infectious diseases. Lecture notes: briefly, the most important

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infectious diseases. Lecture notes: briefly, the most important

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Table of contents

Modern understanding of infectious diseases. Vaccination. Vaccination calendar, complications after vaccination (Infectious diseases. Vaccination. Vaccination calendar, complications after vaccination)
Diphtheria. Etiology, clinic, diagnostics, complications. Features of the course of diphtheria
Whooping cough. Etiology, pathogenesis, clinic, diagnosis, treatment
Measles. Rubella. Etiology, pathogenesis, clinical picture, diagnosis, treatment (Measles. Rubella)
Chicken pox. Herpetic infection. Etiology, epidemiology, pathogenesis, clinic, treatment (Chicken pox. Herpetic infection)
Parotitis. Etiology, epidemiology, pathogenesis, clinic, treatment
meningococcal infection. Clinic, diagnostics, differential diagnostics, treatment
Dysentery. Etiology, epidemiology, pathogenesis, clinic, treatment
Salmonellosis. Etiology, epidemiology, pathogenesis, clinic, treatment
Escherichiosis. Rotovirus infection. Etiology, epidemiology, clinic, diagnosis, treatment (Esherichiosis. Rotavirus infection)
Amoebiasis. Balantidiasis. Etiology, epidemiology, clinic, diagnosis, treatment (Amebiasis. Balantidiasis)
Campylobacteriosis. Food poisoning with bacterial toxins. Botulism. Etiology, epidemiology, clinic, diagnosis, treatment (Campylobacteriosis. Food poisoning with bacterial toxins. Botulism)
Cholera. Typhoparatyphoid diseases. Etiology, epidemiology, clinic, diagnosis, treatment (Cholera. Typhoparatyphoid diseases)
Acute respiratory diseases. Flu. Parainfluenza. Etiology, epidemiology, pathogenesis, clinical picture, diagnosis, treatment (Acute respiratory diseases. Influenza. Parainfluenza)
Adenoviral infection. R-s infection. Rhinovirus infection. Etiology, epidemiology, clinic, diagnosis, treatment (Adenovirus infection. R-s infection. Rhinovirus infection)
Acute and chronic viral hepatitis. Etiology, pathogenesis, clinical picture, differential diagnosis, treatment (Viral hepatitis. Chronic hepatitis)
Parasitic diseases. Epidemiology, clinic, treatment (Helminthiasis. Ascariasis. Alveococcosis. Hookworm disease (hookworm and necatoriasis). Diphyllobothriasis. Opisthorchiasis. Taeniasis. Trichocephalosis. Fascioliasis. Echinococcosis. Enterobiasis)
Rabies. Etiology, epidemiology, clinic, diagnostics, treatment
Protozoal infections: malaria, toxoplasmosis. Etiology, epidemiology, clinic, treatment (Malaria. Toxoplasmosis)
Bacterial zoonoses: brucellosis, anthrax, tularemia, plague, psittacosis, yersiniosis. Etiology, epidemiology, pathogenesis, clinical picture, diagnosis, treatment (Brucellosis. Anthrax. Tularemia. Plague. Psittacosis. Yersiniosis)
Hemorrhagic fever. Etiology, epidemiology, pathogenesis, clinic, diagnostics, treatment
Legionellosis. Mycoplasmosis. Etiology, epidemiology, pathogenesis, clinical picture, diagnosis, treatment (Legionellosis. Mycoplasmosis)
Erysipelas. Scarlet fever. Etiology, epidemiology, pathogenesis, clinical picture, diagnosis, treatment (Erysipelas. Scarlet fever)
Tetanus. Etiology, epidemiology, pathogenesis, clinic, treatment
Enteroviral infections. Polio. Etiology, epidemiology, pathogenesis, clinical picture, diagnosis, treatment (Enteroviral infections. Poliomyelitis)
Acquired immunodeficiency syndrome. Etiology, pathogenesis, clinic, diagnosis, treatment

LECTURE № 1. Modern idea of infectious diseases. Vaccination. Immunization calendar, complications after vaccination

1. Infectious diseases

This is an extensive group of human diseases caused by pathogenic viruses, bacteria and protozoa. The essence of infectious diseases is that they develop as a result of the interaction of two independent biosystems - a macroorganism and a microorganism, each of which has its own biological activity.

Infection - this is a complex of interaction between the pathogen and the macroorganism in certain environmental conditions. The third factor of the infectious process - environmental conditions - exerts its influence both on pathogens and on the reactivity of the macroorganism. Forms of interaction of an infectious agent with the human body can be different and depend on the conditions of infection, the biological properties of the pathogen and the characteristics of the macroorganism. An infectious disease is a violation of the function of a macroorganism, the formation of a morphological substrate of the disease, the appearance of clinical symptoms, the formation of specific immunity.

The inapparent form of an infectious disease is a form in which minimal but characteristic morphological changes occur in the tropic organ, and the titer of specific antibodies (AT) increases in the blood.

Healthy carriage - this is the absence of a morphological substrate, clinical symptoms of the disease, an increase in the titer of specific antibodies.

Persistent (latent) infection is a chronic infectious disease with a benign course (with hepatitis B, herpes infection, enterovirus diseases, measles, etc.). Causes of persistent infection in children: depressive state of cellular and humoral immunity, the appearance of L-forms of bacteria and viruses (neurotropic strains with changes in their morphological, biological, antigenic and pathogenic properties).

endogenous infection arises as a result of the activation of the saprophytic flora of one's own organism, the following is observed:

1) in children weakened by previous diseases;

2) in children treated for a long time with antibiotics, hormones, cytostatics;

3) in young children.

According to the type of autoinfection, candida, staphylococcal, proteus, pseudomonas, Klebsiella and other infections proceed.

slow infection - this is a gradual (over many years) progression of the disease, severe organ disorders, an unfavorable outcome is often possible.

According to the type of slow infection, congenital rubella, subacute sclerosing encephalitis, etc.

Sources of infection

1. Mother-child:

1) intrauterine infection;

2) infection during childbirth (during the passage of the birth canal);

3) postnatally (when caring for a child).

2. Attendants of the maternity hospital.

3. Relatives, attendants of orphanages, kindergarten, etc.

Ways of transmission: transplacental, blood contact, food, water, contact-household, drip, fecal-oral.

The most susceptible group: young children, children from 6 months to 2 years old, children with secondary immunodeficiencies.

Classifications and clinical forms of infections (A. A. Koltypin)

1. By type (type - severity of signs, properties of a given disease): typical, atypical, obliterated, inapparent (subclinical, hypertoxic, hemorrhagic).

2. By severity: light, moderate, heavy.

3. By the nature of the course: smooth, non-smooth, with exacerbations and relapses;

4. According to the duration of the course: acute (1-3 months), protracted (4-6 months), chronic (over 6 months).

Principles of treatment: etiotropic therapy elimination of the pathogen and its toxins, pathogenetic therapy, increased specific and nonspecific protection. It is necessary to take into account the age of the patient, background pathology, the period of the disease, the severity of the disease, the nature of the course, the presence of mono- or mixed infection, etc.

Prevention:

1) measures aimed at the source of the disease;

2) measures to create or increase immunity to infectious diseases;

3) measures aimed at breaking the pathways of transmission of the pathogen (depending on the specific disease);

4) isolation of the patient, registration of all infectious patients (an emergency notice is filled in and sent to the CSES).

2. Vaccination

The organization of preventive work among the child population includes, first of all, vaccination (that is, specific immunization), as well as a system of measures aimed at early detection of the disease and dispensary observation of sick and recovered children. Preventive vaccinations are the most important means of specific immunoprophylaxis and effective control of many infectious diseases. Thanks to the widespread introduction of vaccination in the world, smallpox was completely eliminated, and the number of cases of tetanus, whooping cough, and measles decreased tenfold.

What is vaccination? This is the creation in the human body of protection against the causative agent of infection. This method has been known for several hundred years. Even in ancient times, the Chinese inhaled the dried and crushed crusts of smallpox patients. This method was called variolation. It was unsafe and often ended up infecting people. The first physician to vaccinate people with cowpox to protect against smallpox was Edward Jenner, considered the father of the scientific approach to vaccines. He set up the first smallpox vaccination station in London. 100 years later, Louis Pasteur immunized a man against rabies. It was the first successful vaccination against this pathogen. Unfortunately, at present there are no vaccines for all infectious agents, but these methods of protection have been created and successfully applied to many of them - vaccines against tuberculosis, hepatitis, whooping cough, diphtheria, tetanus, rabies, poliomyelitis, rubella, chickenpox, epidemic mumps, measles, etc. In the process of vaccination, a specific immunity to infection is created by simulating the infectious process. Various types of vaccines are used for this purpose. In addition, immunity is acquired after the transfer of an infectious disease. Both after vaccination and after illness, immunity can be lifelong, persistent or persist for a certain time.

Applying immune preparations in practice for the prevention and treatment of infectious diseases, it is necessary to know what they are.

There are drugs for active immunization (vaccines), as well as for passive immunization of the body (immunoglobulins, sera, etc.). All these funds can be used for preventive, therapeutic and diagnostic purposes.

The action of active immunization is preventive. It begins some time after the introduction of the vaccine and lasts for a long time. The action of passive immune preparations is immediate, but short-term, as these preparations are quickly destroyed in the body. In this regard, they are not used for long-term protection against infectious diseases, but they are an excellent tool for emergency prevention of a number of different infectious diseases, including especially dangerous infections (rabies, tetanus, influenza, measles, mumps, tick-borne encephalitis), treatment staphylococcal infections.

Types of immunoprophylaxis

It can be specific, when its action is directed to a specific infectious agent, or non-specific, if its goal is to increase activity, stimulate the protective functions of the body.

Immunization can also be active if immunity arises from the introduction of a vaccine, or passive if gamma globulins, serum preparations are introduced into the body.

Vaccination can be both single and multiple, if the formation of immunity requires several injections of an immunizing agent.

Revaccination is aimed at maintaining and preserving the immunity obtained during previous vaccinations.

"Tour" vaccination. Its plan consists of a one-step vaccination, which is carried out to quickly break the chain of spread of an infectious disease. Conducted in a short time frame. Children who have been vaccinated previously or have been ill are vaccinated within 1 week to 1 month. This event is being carried out by local health authorities.

What determines the effectiveness of vaccination? It is influenced by the following factors:

1) properties of vaccines (purity of preparations, administered dose, antigen lifetime, frequency of administration, presence of protective antigens);

2) properties of the human body (age, the state of the immune system of the individual, genetic characteristics, the presence of immunodeficiency syndrome);

3) external factors (nutrition, living conditions, climate, physical and chemical factors of the environment).

Types of vaccines

Live vaccines. They consist of living but weakened (attenuated) pathogens or selected natural avirulent strains of microorganisms. It has now become possible to create live vaccines using genetic engineering methods. Strains of viruses are taken as pathogens. Examples of live vaccines: rubella, influenza, Sabin's polio, mumps. They contain viruses that, when they enter the human body, cause the production of all parts of the immune response (cellular, humoral, secretory). When using live vaccines, stable, intense, long-lasting immunity is created, but there are also a number of disadvantages.

1. Weakened vaccine virus can acquire virulence, i.e., become the causative agent of the disease (for example, vaccine-associated poliomyelitis).

2. Live vaccines are difficult to combine, as this can mix viruses and the vaccine may become ineffective.

3. Live vaccines have thermolability, i.e., they can lose their properties when the storage temperature changes. Live vaccines also include vaccines containing cross-reacting components that cause a weakened infection in the human body, protecting it from a more severe one. An example of such a vaccine is BCG, which contains Mycobacterium tuberculosis in cattle.

4. Live vaccines have a number of contraindications: they should not be administered to patients with immunodeficiency; patients using steroid hormones, immunomodulators (suppressors); people who have undergone radiotherapy; patients with blood diseases (with leukemia), tumors of the lymphoid tissue (lymphomas), as well as pregnant women.

5. Live vaccines contain up to 99% of ballast substances, therefore they are reactogenic. In addition, they are capable of causing mutations in the cells of the human body, which is especially important for the cells of the reproductive system.

6. Live vaccines contain contaminants - contaminated viruses.

7. They are difficult to accurately dose.

Killed vaccines (inactivated).They contain dead pathogens, they are easily dosed and combined with other vaccines, and are heat stable. Killed vaccines cause the production of several types of antibodies that enhance the phagocytosis of microorganisms, for example, pertussis vaccine. It also has an adjuvant effect, enhancing the immune response to another antigen that is part of the combined (associated) vaccine - DTP. Microorganisms are inactivated using physical methods (temperature, radiation, UV irradiation), chemical methods (alcohol, formaldehyde). But the ballast (preservative) contained in them (90-99%) is reactogenic. These vaccines are not used as often.

Disadvantage: when using these vaccines, only the humoral (unstable) link of immunity arises, therefore they act only for a certain time, require administration in several doses and re-vaccination throughout life. Often administered with an adjuvant (an adjuvant that enhances the immune response), which is an aluminum compound. The adjuvant acts as a reservoir in which the antigen is stored for a long time.

Live vaccines are available in dry (lyophilized) form, with the exception of polio vaccine. Killed vaccines can be in lyophilized and liquid form.

Vaccines that are inactivated by physical or chemical means are also called corpuscular (eg, rabies, pertussis, leptospirosis, encephalitis, hepatitis A).

Chemical vaccines contain cell wall components or other parts of the microorganism. From these parts, antigens are isolated that determine the immune properties of the microbe or virus. These include polysaccharide vaccines (Meningo A + C, Tifim Vi, acellular pertussis vaccines.

Recombinant vaccines. They are also obtained using genetic engineering methods. These are artificially created antigenic components of microorganisms. In this case, the gene of a virulent microorganism is integrated into the genome of a harmless microorganism, which accumulates and produces antigenic properties.

An example of such a vaccine is the hepatitis B vaccine (Combitex or Euvax B). When it is prepared, a subunit of the virus gene is inserted into yeast cells. The yeast is then cultured and HBsAg is isolated from it. It is cleaned of yeast inclusions. This method of preparing a vaccine is called recombinant. This vaccine also contains a preservative and adsorbent in the form of aluminum hydroxide. Biosynthetic vaccines are also being developed. These are artificially created antigenic components of microorganisms (vaccine against viral hepatitis B, rotaviruses).

Ribosomal vaccines - for their production, ribosomes present in each cell are used (bronchial and dysentery vaccines).

Anatoxins. These are substances produced by pathogens. When preparing a number of vaccines, it is impossible to use the pathogen itself, so in these cases its toxin is taken. These are tetanus, diphtheria, staphylococcal and some other toxins.

Anatoxins cause persistent antitoxic immunity, they are easy to combine and dose. They are obtained by treating the toxin with formaldehyde under special temperature conditions. In this case, the toxin is neutralized, but its immune properties are preserved. Chemicals are added to them for weighting, since toxoids contain a very small antigenic fragment. These additives determine the presence of negative properties of the drug (may cause inflammation, abscesses). The immunity produced by toxoids is only antitoxic. When using toxoids, bacteriocarrier and the occurrence of mild forms of the disease are possible.

Immunoglobulins and serums. They contain antibodies in finished form. They are used for emergency prevention, as well as for therapeutic and prophylactic purposes. They can be antimicrobial, antiviral and antitoxic. When sera are administered, a lot of ballast substances enter the human body; in addition, some of the sera are obtained from immunized cattle and horses. To prevent the development of allergic complications, serums are administered according to Bezredka. This method consists of preliminary subcutaneous administration of an immune drug in a dose of 0,1-0,5 ml. Currently, this dose is considered somewhat too high.

Immunoglobulins - together with them, ready-made antibodies enter the body in sufficient quantities and quickly. These are the advantages of immunoglobulins, but they are quickly destroyed, suppress the production of their own immunoglobulins, and can allergize the body.

Destruction of vaccine preparations: ampoules and containers with unused residues of vaccines, sera, immunoglobulins, as well as disposable syringes are not subject to special treatment. All ampoules with immunopreparations unused for any reason should be sent for destruction to the regional center of sanitary and epidemiological supervision.

Formation of an immune response.An important feature of children in the first year of life is that they have innate immunity to some infectious diseases. The origin of this immunity is transplacental. Class G immunoglobulins cross the placenta from the 16th week of pregnancy. Thus, the fetus begins to receive ready-made maternal antibodies, and passive individual immunity is formed during the prenatal period. Passive immunity is called immunity in which the body acquires ready-made antibodies, rather than producing them itself during vaccination or exposure to an infectious disease. After the birth of a child, individual maternal antibodies begin to break down starting at 2 months of age. By the end of the first year of life they completely disappear. Thus, during the first year of life, the newborn’s body is protected from those infections for which antibodies were received from the mother. These antibodies can interfere with the immunity created by vaccination, and this factor is taken into account when developing the vaccination schedule.

Features of the immune response in the human body to the penetration of the antigen determines the main system of histocompatibility. It is located on chromosome VI and is designated HLA. HLA are antigens found on peripheral blood leukocytes. The height of the immune response, the level of suppression of the formation of antibodies depends on them. Various cells are involved in the immune response: macrophages, T-lymphocytes (effector, helper, suppressor, memory T-cells). Also involved in this complex process are B-lymphocytes (memory B-cells), immunoglobulins of classes M, G, A, produced by plasma cells, cytokines. The components of the injected vaccine are taken up by macrophages, which cleave the antigen inside the cell and present parts of the antigen on their surface. T-lymphocytes recognize them and activate B-lymphocytes. B-lymphocytes become cells that form antibodies.

The initial administration of the vaccine goes through three periods.

1. Latent. This is the time between the introduction of the antigen and the appearance of antibodies in the blood. It can last from several days to 2-3 weeks, depending on the type of vaccine, dose, and the state of the child's immune system.

2. Growth period. At this time, the number of antibodies increases rapidly. This period lasts from 4 days to 3 weeks (depending on the type of vaccine). The number of antibodies to the introduction of measles and mumps vaccines increases especially rapidly, which makes it possible to use them for active immunization during emergency prevention. With the introduction of pertussis and diphtheria components of DPT, the level of antibodies increases much more slowly than during the incubation period of the onset of the disease, therefore DTP is not used for emergency prevention.

3. Decrease period. After reaching the maximum level in the blood, the amount of antibodies begins to decrease rapidly, then the process slows down. It can go on for years or decades.

Bacteriophages. Bacteriophages, or bacterial viruses (from the combination of “bacteria” and gr. phagos - “devouring”), are viruses that can invade a bacterial cell, infect it, reproduce in it and cause its destruction (lysis).

At present, a large number of various phages have been created. As a result of the use of antibiotic therapy in the treatment of infectious diseases, microorganisms resistant to many antibiotics have appeared. In addition, with antibiotic therapy, allergic reactions, dysbacteriosis and other complications occur. Phage therapy is a harmless biological method of treatment. In some cases, it is indispensable (if for some reason it is impossible to use antibiotics).

Bacteriophages are available in the form of solutions (in vials and ampoules) and in tablet form. To date, bacteriophage preparations have been created and successfully used against many pathogens (staphylococcus, streptococcus, Klebsiella, Proteus, coli bacteria), which is also of great importance in the treatment of nosocomial infections. Treatment with bacteriophages gives a good effect in the treatment of dysbacteriosis, surgical, urological, ENT infections. The advantage of this therapy lies in the strict specificity of the phage action. It causes the death of only its specific type of microbe, without damaging the rest of the normal microflora of the patient.

The high efficiency of therapy with phages for purulent-septic diseases of newborns and young children has been proven.

To achieve a successful result, it is necessary to first investigate the sensitivity to the bacteriophage of the microorganism. Newborns in the first days of phages are diluted with boiled water 2 times. If there are no side effects in the form of skin rashes, vomiting, then the bacteriophage is used undiluted. Phage preparations are usually taken orally before meals, several times a day (or in the form of microclysters). You can replace one oral dose with a rectal enema.

Dysbacteriosis. Dysbacteriosis is a condition of the body in which the quantitative composition or normal, natural ratio of microorganisms in the intestines is disrupted.

The composition of normal microflora in the human body is formed by aerobic and anaerobic microorganisms. In the oral cavity, aerobes are mainly present, the composition of the intestinal microflora (especially the large intestine) is 95% formed mainly by bifidus and lactobacilli. In addition, there are opportunistic pathogens that, under certain conditions (weakening of the immune system, antibiotic treatment), can become a source of disease. These are Pseudomonas aeruginosa, Proteus, Staphylococcus aureus, fungi of the genus Candida.

Functions of normal microflora: enzyme-forming, protective, synthetic, immunogenic.

Causes of dysbacteriosis: immunodeficiency states, long-term treatment with antibacterial drugs, chronic pancreatitis, hypo- or achlorhydria of the stomach, intestinal obstruction, alcohol abuse.

The main symptoms of dysbacteriosis: diarrhea, anemia, steatorrhea, weight loss.

Diagnosis is based on the patient's complaints (weight loss, periodic pain and discomfort in the abdomen, loose stools, an unpleasant taste in the mouth, there may be skin itching and rashes), endoscopic examination of the large intestine, X-ray data and stool culture on the flora.

Treatment of dysbiosis is long-term, it includes a set of measures aimed at restoring the intestinal microflora, improving its motility and treating concomitant diseases. It is necessary to follow a diet, take bacterial preparations to restore microflora, antispasmodics to normalize intestinal motility, probiotics. The most effective and frequently used drugs are: bacteriophages, bifidum- and lactobacterin, linex, bifikol, enzyme complexes.

Prevention of dysbacteriosis: good nutrition, the inclusion of vegetables, fruits, lactic acid products in the diet, the reduction of fatty meat dishes, the use of bacterial preparations in the process of antibiotic therapy, the refusal to prescribe antibiotics unless absolutely necessary.

3. Vaccination schedule, complications after vaccination

Calendar of preventive vaccinations from June 27.06.2001, XNUMX.

Table 1

Viral hepatitis B vaccination calendar

Newborns in the first 12 hours are vaccinated against viral hepatitis B.

Newborns on the 3rd-7th day are vaccinated with BCG against tuberculosis.

At 1 month - the second vaccination against hepatitis B.

At 3 months - the first vaccination with the DTP vaccine (against diphtheria, whooping cough, tetanus) and the polio vaccine (oral polio vaccine - OPV).

At 4-5 months - the second vaccination with the DTP vaccine and the polio vaccine (OPV).

At 6 months - the third vaccination with the DTP vaccine and the polio vaccine (OPV).

At 12 months - vaccination against measles, rubella, mumps.

At 18 months - the first revaccination against diphtheria, whooping cough, tetanus and polio vaccine (OPV).

At 20 months - the second revaccination against polio.

At 6 years old - revaccination against polio (OPV) + vaccine against measles, mumps, rubella.

At the age of 7 - revaccination against tuberculosis. The second revaccination of ADS-M (against diphtheria, tetanus).

At 13 years old - vaccination against rubella (girls).

At the age of 14 - the third revaccination against diphtheria, tetanus. Revaccination against tuberculosis. Third revaccination against poliomyelitis.

Adults - revaccination against diphtheria, tetanus every 10 years from the last revaccination.

Indications for vaccination

1. Scheduled vaccinations for children according to the calendar and military personnel.

2. Unscheduled vaccinations in cases:

1) threats of occupational disease;

2) residence and upcoming trip to an epidemiologically disadvantaged area;

3) emergency vaccination of persons in contact with the source of infection.

Contraindications for vaccinations

1. Strong reaction (fever, edema at the site of the injected vaccine, hyperemia on the first or second injection).

2. Complications on the first or repeated introduction.

3. Immunosuppression.

4. Immunodeficiency state.

5. Malignant blood diseases, neoplasms.

6. Progressive diseases of the nervous system.

7. Pregnancy.

8. Allergic reactions, anaphylactic shock.

Vaccinations against viral hepatitis B are currently given primarily to children who are at increased risk of infection. If the parents wish, a child of any age can be vaccinated against hepatitis B (according to the scheme 0-1-6 months) three times at intervals of 1 month after the first vaccination and 5 months after the second. The vaccine is given to a healthy child. After examining the child, the doctor sends him for vaccination. Having been vaccinated, it is necessary to observe a sparing regime, contacts with children and adults are limited so as not to infect the child with any infection. In the first days after vaccination, foods containing allergens should be excluded from the child's diet - rich broths, canned food, eggs, fish, citrus fruits, nuts, chocolate. Breastfeeding children are not recommended to introduce complementary foods, change the mode and composition of the diet. You should also be aware of the possibility of a reaction to the introduction of a particular vaccine. In a child, a post-vaccination reaction after vaccination is considered the norm; complications that require a visit to a doctor are extremely rare.

Tuberculosis vaccination. After birth (on the 3-7th day of life), the child receives the first vaccination against tuberculosis in his life with the BCG or BCG-M vaccine. Re-vaccination (revaccination), if necessary, is carried out at 7 and 14 years of age for uninfected children after negative tuberculin tests. If, for any reason, vaccination against tuberculosis in the maternity hospital has not been carried out, it should be carried out as soon as possible. In the event that vaccination has been delayed for more than 2 months, BCG or BCG-M vaccination is carried out only if the tuberculin test - the Mantoux reaction - is negative immediately after its determination. The BCG vaccine is injected intradermally into the outer surface of the shoulder of the left arm. After the vaccination, a normal reaction develops: on the 4th day, a speck of 2-3 mm in size forms at the injection site, and after 1-1,5 months a papule appears in its place (a rise above the skin level up to 5 mm), turning into an infiltrate , sometimes ulcerating in the center. In the future, a crust is formed, after falling off of which there remains a retracted scar measuring 5-7 mm in diameter. The presence of a scar indicates a successful BCG vaccination, a mark is made in the medical record of the child's development and the vaccination certificate. During the period of infiltration and ulceration, parents need to monitor hygiene: the linen that comes into contact with the injection site should be clean, ironed, when bathing the child, the vaccination site should be protected from injury - do not rub with a sponge, washcloth, do not touch it with your hands, you can’t touch the vaccination site apply any bandages.

Vaccine prevention of polio is carried out with the live Sabin polio vaccine, and sometimes with the inactivated Salk vaccine. Two foreign vaccines against polio are approved for use: Complete Sabin Vero - a live vaccine, Imovax Polio - an inactivated vaccine. The Sabin vaccine is dripped into the mouth with a sterile pipette or syringe before meals; the child is not allowed to eat or drink for an hour after vaccination. If the child spits up or vomits, give another dose. Since 2002, children have also been vaccinated three times starting from 3 months of age, but the interval between vaccinations has been increased to 1,5 months (3-4,5-6 months). Revaccination is carried out at 18 months, 20 months and 14 years.

Vaccinal prevention of whooping cough, diphtheria and tetanus is carried out three times at 3-4-5 months, revaccination - at 18 months, since 2002, according to the new vaccination calendar - at 3-4,5-6 months. Immunization can be combined with the polio vaccine. The vaccine is administered intramuscularly, preferably into the anterior outer thigh or buttock. For vaccination, adsorbed pertussis-diphtheria-tetanus vaccine is used - DTP. It contains killed pertussis microbes, diphtheria and tetanus toxoids. In addition to the domestic one, the Tetracoccus vaccine (Pasteur-Merrier, France), containing the pertussis component, diphtheria-tetanus toxoid and killed polio vaccine, is approved for use. After 4 years, when whooping cough ceases to be a life-threatening infection for the child, vaccines without a pertussis component are used: ADS - a vaccine containing diphtheria-tetanus toxoid, ADS-M - a vaccine containing adsorbed diphtheria-tetanus toxoid with a reduced content of antigens, diphtheria-tetanus toxoid (DT VAX). At 6 and 16 years of age, revaccination with the ADS-M vaccine is carried out; at 11 years old - AD-M - adsorbed diphtheria toxoid with a reduced antigen content. Since 2002, revaccination against diphtheria and tetanus has been carried out at 7 and 14 years of age. For revaccination of adolescents and adults, the INOVAX DTADULT vaccine containing diphtheria-tetanus toxoid can be used. After the administration of DPT, ADS, ADS-M, most often in the first 3 days, local and general reactions that are harmless to the child may be observed in the form of redness and a small (no more than 2,5 cm in diameter) compaction at the injection site, which persists for several days, or in the form of short-term malaise, moderate increase in body temperature. These reactions pass quickly, but you must inform your doctor that there has been a reaction.

Vaccine prevention of measles. For immunoprophylaxis of measles, the domestic live attenuated vaccine L-16 is used, as well as foreign ones - the live measles vaccine Ruvax and the trivaccine, which immunizes the child against three infections at once - measles, mumps and rubella. Vaccination of children occurs from 12 months, revaccination - at 6 years. The vaccine is administered subcutaneously under the shoulder blade or in the shoulder area. There are cases when, within 1-2 days, there is slight redness (or swelling of the tissue) at the site of vaccine administration. Occasionally, in the interval from the 6th to the 18th day after vaccination, there may be a state of malaise (decreased appetite, increased temperature, slight runny nose, coughing, and sometimes a measles-like rash). After 3-5 days, all symptoms disappear and the child’s condition returns to normal. Treatment is usually not required. Children who have a reaction to measles vaccination are not contagious.

Vaccination of mumps is carried out with a live attenuated vaccine. It is also possible to use a vaccine against measles, mumps, rubella. Vaccination is carried out for children from 12 months and 6 years. The vaccine is administered once subcutaneously in the area of the shoulder blade or shoulder. In most children, the vaccination process is asymptomatic. Very rarely, from the 4th to the 14th day, there may be a temperature, a slight runny nose, a slight increase in the parotid salivary glands. Within 2-3 days, all symptoms disappear.

Vaccinal prevention of rubella. There is no domestic vaccine against rubella; the live rubella monovaccine Rudivax and the live trivaccine MMR against measles, mumps and rubella are used. Vaccination is carried out at 12 months, revaccination at 6 years. Since 2002, girls from 13 years of age have been revaccinated. The vaccine is administered once subcutaneously or intramuscularly. After vaccination, there is usually no reaction. Adults vaccinated may experience a short-term low-grade fever, enlargement of the occipital and posterior cervical lymph nodes, and sometimes pain and swelling in the knee and wrist joints may be observed. These manifestations do not require treatment and disappear within a few days.

Vaccinal prevention of hepatitis A and B. The foreign vaccine Havrix-720 is used against hepatitis A, which can be vaccinated in all children over 1 year of age living in areas with a high incidence of hepatitis A. The vaccine is administered in two doses: after 6 and 12 months. Vaccination against viral hepatitis B is carried out by various types of recombinant vaccines. The use of these vaccines is permitted in Russia. The vaccine is administered intramuscularly; for newborns and infants it is administered into the anterolateral surface of the upper third of the thigh. For older children and adults, guidance is carried out in the upper third of the shoulder. Vaccination is carried out primarily for children at risk. These are children whose mothers suffered from viral hepatitis B in the last trimester of pregnancy or are carriers of the antigen of this virus, this also applies to children who have patients or carriers of hepatitis B in their family, a contingent of children from boarding schools and orphanages, children who have received repeated blood transfusions, its fractions or hemodialysis was performed. Vaccination is carried out 3 times. According to the new schedule of preventive vaccinations, approved in 2001, all newborns are vaccinated against hepatitis B in the first 12 hours of life. The BCG vaccine is administered secondarily. The second stage of vaccination is carried out at 1 month, the third - at 6 months. Vaccination of previously unvaccinated children is carried out at the age of 11-13 years. The majority of vaccinated people do not experience a reaction to the vaccine. It is important to remember that vaccination is the only way to prevent illness in a child.

LECTURE No. 2. Diphtheria. Etiology, clinic, diagnostics, complications. Features of the course of diphtheria

Diphtheria is an acute infectious disease with an airborne transmission mechanism caused by diphtheria toxigenic corynebacteria, characterized by croupous or fibrinous inflammation of the mucous membrane at the gates of infection (in the pharynx, nose, larynx, trachea, less often) in other organs and general intoxication.

Etiology. The causative agent is a toxigenic diphtheria bacillus, thin, slightly curved with thickenings at the ends, does not form spores and capsules, gram-positive, stable in the external environment, tolerates drying well, is sensitive to high temperature and disinfectants. Diphtheria exotoxin is the main factor in the pathogenicity of diphtheria bacilli. It belongs to potent bacterial toxins, has a tropism for the tissues of the nervous and cardiovascular systems, adrenal glands.

Epidemiology. Sources of infection - a sick person or a carrier of toxigenic strains of diphtheria bacteria. A patient with diphtheria can be contagious on the last day of the incubation period and during the height of the disease. The route of transmission is airborne. Due to the long-term preservation of the viability of microorganisms on household items, transmission of infection through these items is possible, ml. el. household contact. Immunity after diphtheria infection is unstable.

Pathogenesis. Having entered the body, the pathogen stops in the area of the entrance gate (in the pharynx, nose, larynx, on the mucous membranes of the eyes, genitals, etc.). There it multiplies and produces exotoxin, under the influence of which coagulative necrosis of the epithelium, vasodilation and increase in their permeability, sweating of exudate with fibrinogen and the development of fibrinous inflammation occur. The toxin produced by the pathogen is absorbed into the blood and causes general intoxication with damage to the myocardium, peripheral and autonomic nervous system, kidneys, and adrenal glands. Diphtheria bacillus vegetates on the mucous membranes of the pharynx and other organs, where croupous or diphtheria inflammation develops with the formation of films.

Classification. Depending on the localization of the inflammatory process, diphtheria of the oropharynx, nose, larynx, eyes, ear, external genital organs, and skin are distinguished. According to the prevalence of raids, localized and widespread forms are distinguished. According to the severity of the toxic syndrome - subtoxic, toxic, hemorrhagic, hypertoxic forms.

Clinic. The following periods of the disease are distinguished: incubation period (from 2 to 10 days), peak period, recovery period. With a localized form of diphtheria, the onset of the disease is acute, with an increase in body temperature to 37-38 ° C. General intoxication is not expressed: headache, malaise, loss of appetite, pallor of the skin. The pharynx is moderately hyperemic, there is moderate or mild pain when swallowing, swelling of the tonsils and palatine arches, fibrinous membranous plaques are formed on the tonsils, regional lymph nodes are slightly enlarged. Plaques on the tonsils look like small plaques, often located in lacunae.

The membranous form is characterized by the presence of raids in the form of a translucent film. They are gradually impregnated with fibrin and become dense. At first, the film is removed easily and without bleeding, later accompanied by bleeding.

The island form of diphtheria is characterized by the presence of single or multiple plaques of irregular shape in the form of islands. Sizes from 3 to 4 mm. The process is often bilateral.

The catarrhal form of diphtheria is characterized by minimal general and local symptoms. Intoxication is not expressed. Subfebrile temperature, there are unpleasant sensations in the throat when swallowing. Hyperemia and swelling of the tonsils are noted, raids are absent.

With a common form of pharyngeal diphtheria, the onset is acute, intoxication is pronounced, body temperature is high, regional lymph nodes are enlarged. Complaints of sore throat, malaise, loss of appetite, headache, weakness, lack of appetite, pale skin. Examination of the oropharynx reveals hyperemia and swelling of the mucous membranes of the palatine tonsils, arches, and soft palate.

Toxic diphtheria of the pharynx: acute onset (with an increase in temperature to 39-40 ° C), severe intoxication. When examining the oropharynx, hyperemia and swelling of the mucous membranes of the palatine tonsils are noted with a sharp increase in the tonsils, significant swelling of the mucous membrane of the pharynx and the formation of plaque 12-15 hours from the onset of the disease in the form of an easily removable film. On the 2-3rd day, the plaque becomes thick, dirty gray in color (sometimes lumpy in shape), moving from the tonsils to the soft and hard palate. Breathing through the mouth may be difficult, and the voice becomes choked. Regional lymph nodes are enlarged, painful, and the surrounding subcutaneous tissue is edematous. An important sign of toxic diphtheria is swelling of the tissue in the neck. With toxic diphtheria of the 39st degree, the swelling spreads to the middle of the neck, with the 40nd degree - to the collarbone, with the XNUMXrd degree - below the collarbone. The general condition of the patient is serious, high temperature (XNUMX-XNUMX °C), weakness. Disorders of the cardiovascular system are observed. Diphtheria of the larynx (or true croup) is rare and is characterized by croupous inflammation of the mucous membrane of the larynx and trachea. The course of the disease progresses rapidly.

The first stage is catarrhal, its duration is 2-3 days. At this time, body temperature rises and hoarseness increases. The cough is rough and barking at first, but then loses its sonority. The next stage is stenotic. It is accompanied by an increase in stenosis of the upper respiratory tract. Noisy breathing is observed, accompanied by increased work of the auxiliary respiratory muscles during inhalation. During the third (asphyxtic) stage, severe gas exchange disorders are observed (increased sweating, cyanosis of the nasolabial triangle, loss of pulse at the height of inspiration), the patient experiences anxiety and restlessness. The hemorrhagic form is characterized by the same clinical symptoms as toxic diphtheria of the oropharynx of II-III degree, but on the 2-3rd day the syndrome of disseminated intravascular coagulation develops. Filmy deposits become saturated with blood and turn black. Nosebleeds, bloody vomiting, and bloody stools occur. Diphtheria of the nose, conjunctiva of the eyes, and external genitalia has almost never been encountered lately. Complications that arise from toxic diphtheria of II and III degrees and from late treatment: in the early period of the disease, symptoms of vascular and heart failure increase. Detection of myocarditis occurs more often in the second week of illness and is manifested by a violation of the contractility of the myocardium and its conduction system. Reversal of myocarditis occurs slowly. Mono- and polyradiculoneuritis are characterized by flaccid peripheral paresis and paralysis of the soft palate, muscles of the limbs, neck, and trunk. A dangerous complication for life is paresis and paralysis of the laryngeal, respiratory intercostal muscles, and diaphragm.

The hypertoxic form of diphtheria is characterized by severe intoxication, body temperature rises to 40-41 ° C, consciousness is darkened, indomitable vomiting may appear. The pulse is frequent, weak, blood pressure is lowered, the skin is pale. Swelling of the oropharyngeal mucosa is pronounced, rapidly spreading from the cervical tissue below the collarbones. The general condition of the patient is severe, the skin is pale, cyanotic, the pulse is filiform, the heart sounds are deaf, the blood pressure decreases, death may occur on the first day.

Diphtheria of the larynx (diphtheria true croup). The clinical syndrome is accompanied by a voice change up to aphonia, a rough "barking" cough and difficult stenotic breathing. The disease begins with a moderate increase in temperature, mild intoxication, the appearance of a "barking" cough and a hoarse voice.

Stenosis of the XNUMXst degree: difficult breathing, noisy breathing, hoarseness of voice, rapid breathing, slight retraction of the compliant parts of the chest. The cough is rough, barking.

Stenosis II degree: more pronounced noisy breathing with retraction of compliant chest areas, aphonic voice, silent cough. Attacks of stenotic breathing become more frequent.

Stenosis III degree: constant stenotic breathing, inhalation is lengthened, difficult, breathing is noisy, audible at a distance, aphonia, silent cough, deep retraction of the chest, respiratory failure. Cyanosis of the nasolabial triangle, cold sticky sweat, frequent pulse. The child is restless, rushing about. Breathing in the lungs is bad. This period of stenosis III degree is called transitional from the stage of stenosis to the stage of asphyxia.

Stenosis IV degree: the child is lethargic, adynamic, breathing is frequent, superficial, general cyanosis. The pupils are dilated. The pulse is frequent, thready, arterial pressure is reduced. Consciousness is obscured or absent. Breath sounds in the lungs are barely audible.

Nasal diphtheria: the inflammatory process is localized on the nasal mucosa. The disease begins gradually, without disturbing the general condition. Discharge from the nose appears, which at first have a serous color, then a serous-purulent or sanious character. When examining the nasal cavity, there is a narrowing of the nasal passages due to swelling of the mucous membrane, erosions, ulcers, crusts, spotting are found on the nasal membrane. The occurrence of edema in the region of the bridge of the nose and paranasal sinuses indicates a toxic form of diphtheria. The course of the disease is long.

Diphtheria of the eyes is divided into croupous, diphtheria, catarrhal. The croupous form begins acutely, the temperature is subfebrile. First, one eye is involved in the inflammatory process, then the other. The skin of the eyelids is edematous, hyperemic. The cornea is not affected. Fibrinous films are located on the mucous membranes, when plaque is removed, the mucous membrane bleeds. The diphtheria form begins acutely, with febrile temperature, intoxication. The raids are dense and are located not only on the mucous membrane of the eyelids, but also pass to the eyeball. The eyelids are closed, the skin of the eyelids is edematous, the color of a ripe plum. Eyelids turn out with great difficulty. There is a moderate serous-bloody discharge from the eyes. The cornea may be affected and vision may be impaired. The catarrhal form of diphtheria of the eyes is characterized by swelling and hyperemia of the mucous membranes, there are no fibrinous films.

Diphtheria of the external genital organs is characterized by tissue edema, hyperemia with a cyanotic tint, the appearance of fibrinous films on the labia majora or foreskin, and an increase in inguinal lymph nodes. Fibrinous plaques are dense, extensive and pass to the mucous membranes of the labia minora, vagina, and surrounding skin. The appearance of edema of the subcutaneous tissue in the inguinal region and on the thighs indicates a toxic form of diphtheria. Complications: myocarditis, nephrosis, peripheral paralysis.

Diagnostics. Based on clinical and laboratory data, the presence of toxigenic diphtheria bacilli is determined, in peripheral blood - leukocytosis with a shift to the left, a decrease in the number of platelets, an increase in blood clotting and retraction of a blood clot.

Differential diagnosis is carried out with tonsillitis, infectious mononucleosis, false croup, membranous adenoviral conjunctivitis (with diphtheria of the eye).

Treatment. Patients with diphtheria are subject to mandatory hospitalization, they are prescribed bed rest, etiotropic treatment, the earliest, intramuscular administration of antitoxic antidiphtheria serum in appropriate doses.

Detoxification therapy is carried out (including fresh frozen plasma, rheopolyglucin, hemodez), as well as non-specific pathogenetic therapy, intravenous drip infusions of protein preparations, such as albumin, glucose solution. Administer prednisolone. Antibacterial therapy, cocarboxylase, vitamin therapy. Diphtheria croup requires rest, fresh air. Sedatives are recommended. The weakening of laryngeal stenosis contributes to the appointment of glucocorticoids. Steam-oxygen inhalations are used in chamber tents. Suction of mucus and films from the respiratory tract with the help of an electric suction can have a good effect. Given the frequency of pneumonia in croup, antibiotic therapy is prescribed. In the case of severe stenosis and during the transition of stage II of stenosis to stage III, nasotracheal intubation or lower tracheostomy is used.

Prevention. Active immunization is the backbone of successful diphtheria control. Immunization with adsorbed pertussis-diphtheria-tetanus vaccine (DTP) and adsorbed diphtheria-tetanus toxoid (DT) applies to all children, subject to contraindications. Primary vaccination is carried out starting from the age of 3 months three times, 0,5 ml of the vaccine with an interval of 1,5 months; revaccination - with the same dose of vaccine 1,5-2 years after the end of the vaccination course. At the age of 6 and 11 years, children are revaccinated only against diphtheria and tetanus with ADS-M toxoid.

LECTURE No. 3. Whooping cough. Etiology, pathogenesis, clinic, diagnosis, treatment

Whooping cough is an acute infectious disease with airborne transmission, characterized by bouts of spasmodic cough. It is observed mainly in children of early and preschool age.

Etiology. The causative agent of whooping cough is a small, gram-negative, hemolytic, immobile, unstable rod in the external environment. The pathogen quickly dies under the influence of high temperature, when exposed to direct sunlight and disinfectants. Retains sensitivity to antibiotics (macrolides, cephalosporins, chloramphenicol). Exotoxin causes death and rejection of the epithelium of the upper respiratory tract. It affects the respiratory and vasomotor centers of the brain, the walls of blood vessels and leads to pronounced disorders of intracellular metabolism, hypoxia.

Pathogenesis. The entrance gate of infection is the upper respiratory tract, where the pertussis bacillus vegetates. The toxin formed by it causes irritation of the mucous membrane of the respiratory tract and has a general effect mainly on the nervous system, resulting in the development of a spastic component (spastic condition of the diaphragm and other respiratory muscles, bronchospasm, a tendency to spasm of peripheral vessels), and in young children - sometimes clonic -tonic spasms of skeletal muscles. In severe forms, hypoxia occurs. Allergic mechanisms play a certain role in the pathogenesis of whooping cough.

Epidemiology. Airborne transmission, sources of infection - a sick person and a bacteriocarrier. The following periods of illness are distinguished:

1) incubation (hidden) period - from 3 to 14 days;

2) catarrhal (prodromal, or preconvulsive) - 7-10 days;

3) the period of the peak of the disease (the period of convulsive cough) - 3-6 weeks;

4) recovery period (period of residual effects) - 2-3 weeks.

Clinic. The incubation period is 5-20 days. The catarrhal period is characterized by a slight or moderate increase in body temperature, infrequent dry cough. This period lasts from several days to 2 weeks. The transition to the spastic period occurs gradually. Attacks of spasmodic cough appear, characterized by a series of short cough jerks, quickly following each other, alternating with a subsequent whistling noisy breath, which is accompanied by a lingering sound (reprise). During an attack, the patient's face turns red, turns blue, the veins of the neck and face swell. The patient stretches his head forward and sticks out his tongue. There is a new series of coughing shocks. This may be repeated several times. The attack ends with the release of a small amount of viscous light sputum, vomiting is often observed, in severe cases - short-term respiratory arrest (apnea). Attacks, depending on the severity of the disease, are repeated up to 20-30 times a day or more. The patient's face becomes puffy, hemorrhages sometimes appear on the skin and conjunctiva of the eyes, and an ulcer forms on the frenulum of the tongue. A severe course at the height of the attack leads to clonic or clonic-tonic convulsions, and in newborns, to respiratory arrest. This period lasts 1-5 weeks or more. In the period of resolution, lasting 1-3 weeks, the cough loses its convulsive character, all symptoms gradually disappear.

Classification. Depending on the frequency of coughing attacks and the severity of other symptoms, mild, moderate and severe forms of whooping cough are distinguished. There are typical and atypical (erased, asymptomatic, transient bacteriocarrier) forms of whooping cough, in which the spastic nature of the cough is not expressed. This form is observed in children who received vaccination and in adults.

Complications. Pneumonia, atelectasis of the lungs, emphysema of the lungs, mediastinum and subcutaneous tissue, encephalopathy, bleeding from the nose, bronchi, as well as hemorrhages under the skin, sclera, retina, brain.

Differential diagnosis is carried out with acute respiratory infections, bronchitis, foreign body aspiration, laryngospasm.

Diagnostics. Based on the anamnesis, clinical and laboratory data, the blood test reveals leukocytosis, lymphocytosis, ESR in the absence of complications is normal or low. The diagnosis is confirmed by the isolation of whooping cough from the tracheobronchial secretion; for retrospective diagnosis in later periods, serological methods are used (agglutination test, RSK, RNGA). During X-ray examination of patients, a horizontal position of the ribs, increased transparency of the lung fields, thickening of the dome of the diaphragm and its low location, increased pulmonary pattern, and the appearance of reticulation are observed.

Treatment is carried out at home. Children under 1 year of age and with severe forms of the disease are hospitalized, in the presence of complications and according to epidemiological indications. Mode - sparing with a long stay of the patient in the fresh air. Diet - by age. Etiotropic antibiotic therapy is carried out with macrolides, penicillins, aminoglycosides for 7 days. In the early stages of the disease, antipertussis gamma globulin is effective (3-6 ml daily for 3 consecutive days). In severe and complicated forms of whooping cough, prednisolone is used. In order to reduce spastic phenomena and coughing attacks, neuroleptic, anticonvulsant, sedative, antitussive drugs and drugs that thin sputum are prescribed. With hypoxia, oxygen therapy is indicated, with apnea - long-term artificial ventilation of the lungs. In case of prolonged repair, stimulating therapy is prescribed (plasma transfusion, immunoglobulin injections, physiotherapy, vitamins).

Forecast. For children of the first year of life, especially with the development of complications, whooping cough remains a dangerous disease. The prognosis worsens in the presence of concomitant diseases.

Prevention. Immunoprophylaxis with DTP vaccine at the age of 3 months three times with an interval of 1,5 months. In children of the first years of life, upon contact with the patient, a specific gamma globulin is recommended (3 ml twice with an interval of 1 day). Isolation of the patient continues 30 days from the onset of the disease. Children under 7 years of age who have been in contact with the patient, who have not previously had whooping cough and are not vaccinated, are quarantined for a period of 14 days from the moment the patient is isolated. If isolation is not carried out, this period is extended to 25 days from the date of illness. Final disinfection is not carried out.

LECTURE No. 4. Measles. Rubella. Etiology, pathogenesis, clinic, diagnosis, treatment

1. Measles

Measles is an acute viral disease with airborne transmission, characterized by cyclical course, fever, intoxication, catarrh of the respiratory tract and membranes of the eyes, maculopapular rash on the skin.

Etiology. The causative agent from the family of paramyxoviruses is quickly inactivated in the external environment. The virus contains RNA, has an irregular shape. Unstable in the external environment, quickly dies under the influence of high temperatures, ultraviolet radiation, ether, and drying. It remains active for a long time at low temperatures and is not sensitive to antibiotics.

Epidemiology. The source of infection is a person with measles. Virus carrying in measles has not been established. The patient is contagious in the last 2 days of the incubation period, the entire catarrhal period and in the first 4 days after the onset of the rash. The infection is transmitted by airborne droplets. After a reactive measles infection, persistent, lifelong immunity is developed.

Pathogenesis. At the end of the incubation period and up to the 3rd day of the rash period, the virus is contained in the blood (viremia). There is a systemic lesion of the lymphoid tissue and the reticuloendothelial system with the formation of giant multinuclear structures. The virus infects the mucous membranes of the respiratory tract and causes perivascular inflammation of the upper layers of the skin, which is manifested by a rash. The role of allergic mechanisms has been proven. Possible persistence of the measles virus in the body after suffering measles with the development of subacute sclerosing panencephalitis, which has a progressive course and ends in death.

Clinic. The following periods of illness are distinguished:

1) incubation (hidden) - 9-17 days. If the child was given immunoglobulin (or blood products) before or after exposure to a measles case, the incubation period may be extended to 21 days;

2) catarrhal (initial, prodromal) period - 3-4 days;

3) period of rash - 3-4 days;

4) pigmentation period - 7-14 days.

The catarrhal (initial) period lasting 3-4 days is characterized by an increase in body temperature to febrile numbers, general intoxication, severe catarrhal inflammation of the upper respiratory tract and conjunctiva. Discharge from the nose is profuse, serous in nature, then a dry, sharp, obsessive cough appears. There are hyperemia of the conjunctiva, photophobia, lacrimation, swelling of the eyelids. A pathognomonic symptom that occurs 1-2 days before the rash is Belsky-Filatov-Koplik spots: small grayish-whitish dots appear on the mucous membrane of the cheeks near small molars (less often lips and gums), surrounded by a red corolla, the size of a poppy seed . They do not merge, they cannot be removed with a spatula, as they are small areas of necrotic epithelium. This symptom lasts 2-3 days. On the 4-5th day of illness, with a new rise in temperature, a rash appears, a period of rash begins, which lasts 3 days and is characterized by stages: at first, the rash is found on the face, neck, upper chest, then on the trunk and on the 3rd day - on limbs. The elements of the rash are large, bright maculopapular, non-pruritic, accompanied by a deterioration in the general condition of the patient, can merge with each other and, after fading, leave spotty pigmentation in the same order as they appeared. The rash lasts 1-1,5 weeks and ends with a small pityriasis peeling. During the period of pigmentation, body temperature normalizes, health improves, catarrhal phenomena gradually disappear. Measles occurs in mild, moderate and severe forms. In seroprophylactic individuals, mitigated (weakened) measles is observed, characterized by the rudimentary nature of all symptoms. The most common complications are laryngitis, which may be accompanied by stenosis of the larynx - an early croup associated with the action of the measles virus, and a late croup with a more severe and prolonged course; pneumonia associated, like late croup, with a secondary bacterial infection and especially frequent in young children; stomatitis, otitis, blepharitis, keratitis. A very rare and dangerous complication is measles encephalitis, meningoencephalitis. Measles in adults is more severe than in children. Symptoms of intoxication, fever, catarrhal manifestations are more pronounced.

Diagnosis is based on anamnesis, clinical and laboratory data. In the blood test - leukopenia, eosinopenia, monocytopenia. A serological examination (RTGA) helps in accurate recognition. For early diagnosis, the method of enzyme-linked immunosorbent assay is used, with the help of which anti-measles antibodies of the IG M class are detected in the blood of a patient in the acute period of the disease, which indicates an acute measles infection, and class antibodies. IG G indicate a previous illness (vaccination).

A differential diagnosis is made with acute respiratory infections, rubella (in which there is no catarrhal period, the rash appears immediately on the first day of illness and quickly spreads to the entire trunk and limbs, is located mainly on the extensor surfaces, is smaller, does not leave pigmentation, does not tend to merge, also typically an increase in the occipital and posterior cervical lymph nodes), allergic and drug rashes.

Treatment. Specific treatment has not been developed. The therapy is based on bed rest until the temperature normalizes and body hygiene. Patients are hospitalized in cases of severe forms of the disease, the presence of complications, and children under 1 year of age are also hospitalized. Posyndromic symptomatic drug therapy is carried out. With complications of a bacterial nature - antibiotic therapy. Treatment of complications is carried out according to the general rules.

Forecast. Deaths from measles are extremely rare. They are mainly found in measles encephalitis.

Prevention. Vaccination is required for all children from 15-18 months of age. For this purpose, live measles vaccine Leningrad-16 is used. The diluted vaccine is administered once subcutaneously to weakened children without age restrictions, as well as to those under 3 years of age. Children under 3 years of age who have had contact with patients with measles are given prophylactic immunoglobulin in the amount of 3 ml. People with measles are isolated until at least 5 days after the onset of the rash. Children who have been in contact with patients and have not been actively immunized are subject to separation from the 8th to the 17th day. Children who have undergone passive immunization are separated until the 21st day from the moment of possible infection. Disinfection is not carried out.

2. Rubella

Rubella is an acute viral disease with an airborne transmission, characterized by a short-term febrile state, a spotted rash and swelling of the posterior cervical and occipital lymph nodes.

Etiology. The virus contains RNA, has a spherical shape, is unstable in the external environment, quickly dies under the influence of high temperatures, ultraviolet radiation and ether, and remains active for a long time when frozen.

Epidemiology. The route of distribution is airborne with a primary lesion of children from 1 to 9 years old. There is a winter-spring peak of incidence. Sources of infection - a sick person or a virus shedder. An infectious patient is 7 days before the rash appears and 5-7 days after it appears. Innate immunity to rubella is present in children of the first six months of life, then it decreases. After the transferred rubella, a stable, lifelong immunity is developed.

Clinic. The incubation period is 11-21 days, sometimes extended to 23 days. The prodromal period is unstable and lasts from several hours to one day; the appearance of enanthema in the form of small spots on the mucous membrane of the soft and hard palate against the background of hyperemia of the mucous arches and the posterior pharyngeal wall is also characteristic. During this period, enlarged posterior cervical, occipital and other lymph nodes appear. Simultaneously with a slight increase in temperature, a rash appears on the skin of the whole body, the duration of the rash is 2-4 days, the elements appear first on the face and spread to all skin integuments in the first day. The rash is small-spotted, soft, pink, plentiful, with even outlines, does not itch, and is mainly localized on the extensor surfaces of the limbs, on the back, lower back, buttocks. The elements of the rash do not tend to merge and disappear after 2-3 days, leaving no pigmentation. The state of health of the patient, as a rule, is almost not disturbed. A constant sign should be considered polyadenitis. Complications of postnatal infection are very rare (arthropathies, encephalitis). Intrauterine infection of the embryo leads to its death or the development of chronic rubella infection with damage to various organs and the formation of intrauterine malformations (microcephaly, hydrocephalus, deafness, cataracts, heart defects, etc.). Intrauterine infection after the end of organogenesis leads to the development of photopathy (anemia, thrombocytopenic purpura, hepatitis, bone lesions, etc.). In these children, the virus persists for a long time.

Diagnosis is made on the basis of complaints, anamnesis, clinical and laboratory data. For early diagnosis, the ELISA method is used, where there is a detection in the blood of a patient in the acute period of the disease of anti-measles antibodies of the IG M class, which indicates an acute rubella infection, and IG G class antibodies indicate a previous disease (vaccination). The diagnosis of congenital rubella can be confirmed by the detection of viral antigens in biopsy specimens of tissues, blood, and cerebrospinal fluid.

Differential diagnosis is carried out with measles, scarlet fever, enterovirus infection, allergic rash. Unlike measles, with rubella, in most cases there is no catarrhal period, Belsky-Filatov-Koplik spots, pronounced staging of the rash; the rash is paler, does not tend to coalesce, and leaves no pigmentation or scaling. An accurate diagnosis is assisted by a serological examination (RTGA).

Treatment is carried out on an outpatient basis, patients with severe course, with complications from the central nervous system, or patients according to epidemiological indications are subject to hospitalization. Assign symptomatic treatment, vitamin therapy.

The prognosis is favorable.

Prevention. Isolation of the patient - at least 7 days from the onset of the disease (appearance of a rash). Contact isolation - for the period from the 11th to the 21st day from the moment of contact. It is necessary to protect pregnant women who have not had rubella from contact with patients for a period of at least 3 weeks. In case of contact of a pregnant woman with a patient with rubella, it is recommended to introduce hyperimmune gamma globulin (up to 20 ml). A woman's illness with rubella in the first 3 months of pregnancy is considered an indication for termination. A method has been developed for active immunization with a live rubella vaccine in children aged 12-15 years, and revaccination is carried out at the age of 6 years and girls at 13 years of age.

LECTURE No. 5. Chicken pox. herpetic infection. Etiology, epidemiology, pathogenesis, clinic, treatment

1. Chickenpox

Chickenpox is a highly contagious acute viral disease with airborne transmission that occurs mainly in childhood and is characterized by moderate intoxication, fever, vesicular rash on the skin and mucous membranes.

Etiology. The causative agent of chickenpox belongs to the herpes group of viruses, contains DNA, has a spherical shape and a diameter of 150-200 nm, is unstable in the external environment. Quickly dies under the influence of high temperatures, ultraviolet radiation, ether. Tolerates freezing well. The virus is volatile and can be transported over considerable distances with air flow.

Epidemiology. The virus causes two clinical variants: chickenpox, herpes zoster. It is believed that chicken pox is a manifestation of a primary infection in a susceptible organism (more often in children), since herpes zoster is a reactivation of an infection in an immune and weakened organism. Ways of transmission of infection - airborne, less often - contact-household and vertical. The source of infection is a person with chickenpox or herpes zoster. The patient is contagious in the last 1-2 days of the incubation period and up to 5 days from the appearance of the last vesicles. The virus is found in large quantities in the contents of the vesicles and is absent in the crusts. After the illness, a strong immunity is developed. After an infection, neutralizing antibodies are produced that do not prevent the development of a latent infection. The virus persists for a long time in the cells of the spinal ganglia, the ganglia of the facial and trigeminal nerves, which is explained by the tropism of the virus to the nervous tissue. Against the background of immunodeficiency conditions, reactivation of the infection in the form of herpes zoster is possible.

Pathogenesis. The pathogen enters the body by airborne droplets through the mucous membranes of the upper respiratory tract. After the end of the incubation period, viremia sets in. Fixation of the virus occurs in the epithelium of the skin and cells of the mucous membranes, resulting in a characteristic rash. The persistence of the virus in the body can occur and under the influence of any provoking factors - its activation. This can be expressed in the form of local rashes on the skin - herpes zoster or shingles.

Clinic. The incubation period can last 11-21 days, with an average of about 14 days. The disease begins acutely: body temperature rises, symptoms of intoxication appear, appetite decreases. At the same time, a rash appears on the whole body with elements in the form of small papules, which quickly turn into vesicles. After 1-3 days, the vesicles dry up, and crusts form in their place, which fall off on the 2-3rd week of the disease. After them, light pigmentation remains on the skin. Scars do not form. Itching of the skin is observed in young children and persons prone to allergic reactions. New elements pour out due to their non-simultaneous maturation; the rash is characterized by polymorphism. Elements of chickenpox rash appear immediately on all skin, including the scalp, as well as on the oral mucosa, conjunctiva. The skin of the palms and feet is not covered with a rash. The elements do not merge. The background of the skin is unchanged. Weakened children are faced with a very rare form - a generalized chickenpox infection with damage to the visceral organs, which can be fatal. The consequence of this form may be treatment with corticosteroids and cytotoxic drugs.

Classification: typical and atypical forms. Atypical include rudimentary, generalized, hemorrhagic, pustular, gangrenous forms. Complications develop rarely and are associated with the addition of a secondary bacterial infection (abscesses, cellulitis, pneumonia, encephalitis, otitis media, sinusitis, conjunctivitis, erysipelas, scarlet fever, lymphadenitis, stomatitis).

The diagnosis is established on the basis of anamnesis, complaints, clinical and laboratory data. In the blood test - leukopenia, lymphocytosis, ESR is normal. If necessary, laboratory methods such as electron microscopy of silver-stained smears of the contents of vesicles, viroscopy, ELISA, RSK, neutralization reaction can be used.

The differential diagnosis is carried out with streptoderma, a generalized form of herpes simplex, insect bites.

Treatment. Treatment is carried out on an outpatient basis, in severe cases with complications from the central nervous system and purulent complications, or according to epidemiological indications, patients are hospitalized in a hospital. Bed rest in the first 2-3 days of illness, vitamin therapy, drinking plenty of water, diet according to age. Hygienic maintenance of the patient with the prevention of secondary infection. Vesicles are lubricated with 1-2% potassium permanganate solution, 1% brilliant green solution, oral mucosa is treated with an aqueous solution of aniline dyes and other disinfectants. Antiviral etiotropic therapy is carried out with acyclovir. In severe cases, the appointment of specific varicellose-zoster immunoglobulin / m. Interferon inducer preparations - cycloferon, neovir - are used for severe immunodeficiency.

The prognosis is favorable.

Prevention. The patient is subject to isolation at home until the 5th day from the moment the last element of the rash appears. Disinfection is not performed. Children under 3 years of age who have been in contact with a patient with chickenpox and who have not had it before are separated from the 11th to the 21st day, counting from the moment of contact.

2. Herpetic infection

Herpes infection - diseases caused by the herpes simplex virus, characterized by damage to the skin and mucous membranes, in some cases can cause damage to the eyes, nervous system and internal organs.

Etiology. The causative agent belongs to the herpes family, is divided into six antigenic groups. Type I is the most common, with the type II virus associated with the occurrence of genital herpes and generalized infection of newborns.

Pathogenesis. The gates of infection are the skin and mucous membranes. Invading, the herpes virus remains in the human body for life as a latent infection, which has the ability to turn into clinically pronounced forms under the influence of factors that weaken the body (flu and other diseases, treatment with immunosuppressants, AIDS, etc.).

Clinic. The incubation period is 2-12 days (usually 4 days). Primary infection usually proceeds subclinically, only 10-20% of patients develop various clinical manifestations. The following clinical forms are distinguished:

1) herpetic skin lesions (localized and widespread);

2) herpetic lesions of the oral cavity;

3) ORZ;

4) genital herpes;

5) herpetic lesions of the eyes (superficial and deep);

6) encephalitis and meningoencephalitis;

7) visceral forms (hepatitis, pneumonia);

8) generalized herpes of newborns.

Localized herpetic skin lesions are the most common, they usually accompany some other disease (ARI, malaria, meningococcal infection, etc.). General symptoms are absent or masked by manifestations of the underlying disease. Bubbles are localized around the mouth, on the lips, wings of the nose. In some cases, there is a common herpetic rash. The defeat of the mucous membranes of the oral cavity usually proceeds in the form of aphthous herpetic stomatitis. Herpes viruses cause 5-7% of all acute respiratory infections; clinically, they differ little from acute respiratory infections of other etiologies. Sexually transmitted genital herpes occurs more often in the form of necrotic cervicitis, herpetic lesions of the vagina and external genitalia. With this form, cervical cancer can occur, in pregnant women it is dangerous for the fetus (severe generalized herpes of the newborn may occur). Herpetic eye damage often occurs in the form of superficial and deep lesions of the cornea. The disease can have a long relapsing course. May cause persistent clouding of the cornea. Herpetic encephalitis is severe and often ends in death. Visceral forms of herpes usually develop as a result of massive treatment with various immunosuppressants, and also in patients with AIDS, they often manifest as hepatitis, pneumonia, encephalitis. Generalized herpes of newborns occurs simultaneously with encephalitis, lesions of the skin and internal organs, without treatment with antiviral drugs, it usually ends in death.

Diagnosis of a herpes infection is facilitated by the presence of characteristic lesions of the skin or mucous membranes. Confirmation of the diagnosis is facilitated by the use of virus isolation from various materials (contents of vesicles, scrapings from the cornea, cerebrospinal fluid, cervical biopsy material, etc.).

Treatment. With localized and uncomplicated forms of herpes, the underlying disease is treated. The elements of the rash are topically treated with a 1% solution of methylene blue or brilliant green. The crusts are lubricated with erythromycin or tetracycline ointment. To prevent the spread of the infectious process, intramuscular injection of 6 ml of normal human immunoglobulin is used. If the elements of the rash suppurate, it is necessary to use antibiotic therapy: oxacillin (3 times a day, 1 g), erythromycin (4 times a day, 0,5 g). To prevent suppuration of the eyes, it is recommended to use a 0,1% solution of 5-iodine-2-deoxyuridine (kerecid). It also has a beneficial effect in herpetic lesions of the mucous membranes. The prognosis for herpes encephalitis and generalized herpes infection is doubtful. Eye damage is promoted by a long relapsing course, which leads to disability.

Prevention. To prevent the generalization of infection, normal human immunoglobulin is administered (6 ml every 3 weeks). Relapses can be prevented with an effective killed herpes virus vaccine. There are no activities in the outbreak.

LECTURE No. 6. Epidemic mumps. Etiology, epidemiology, pathogenesis, clinic, treatment

Mumps (mumps) is an acute viral infectious disease that has an airborne transmission pattern, manifested by inflammation of the salivary glands and other glandular organs and often by the development of serous meningitis, affecting mainly children under 15 years of age.

Etiology. The causative agent is an RNA-containing virus from the paramyxovirus family, stable in the external environment. It remains active for a long time at low temperatures, and at room temperature it remains for several days. It quickly dies under the influence of high temperatures, ultraviolet radiation, and drying. The infection is transmitted by airborne droplets, and the contact route of transmission through objects is also possible. The source of infection is a sick person. The patient becomes contagious in the last 1-2 days of the incubation period and in the first 3-5 days of the disease.

Pathogenesis. The entrance gate of infection is the mucous membranes of the nose, mouth, nasopharynx. Through the bloodstream, the pathogen is introduced into various organs, contributing to tropism in relation to the glandular organs and the central nervous system (mainly the pia mater). Most often, the parotid glands are affected, in which the phenomena of periparotitis develop. The transferred disease contributes to the creation of stable immunity. Clinic: the incubation period lasts 11-21 days (rarely can be extended from 23-26 days). The prodromal period is short and unstable, it is characterized by fever, malaise, loss of appetite, headache. The disease begins with fever and painful swelling of the parotid gland, sometimes simultaneously on both sides. The gland acquires a doughy or elastic consistency. The skin above it is tense, but not hyperemic. There is pain at the points when pressing on the tragus, mastoid process and in the region of the posterior mandibular fossa. The swelling increases within a few days and then subsides within 5-7 days. Suppuration does not occur. During the recovery period, the temperature normalizes, health improves, and the function of the affected glands is restored. In about 50% of cases, the submandibular and occasionally sublingual salivary glands are involved in the process. In adolescents and young men, orchitis often occurs (in women - oophoritis), the pancreas is less often affected (acute pancreatitis), and even less often - other glandular organs (mastitis, bartholinitis, dacryocystitis, etc.). Often the disease is manifested by acute serous meningitis (in the cerebrospinal fluid - lymphocytic pleocytosis, a slight increase in the content of sugar and chlorides). A very rare and dangerous complication is encephalitis or meningoencephalitis, middle ear damage may occur.

Diagnosis is based on complaints, clinical and laboratory data. When diagnosing, secondary bacterial mumps, upper cervical lymphadenitis should be excluded, and in the presence of serous meningitis, enteroviral and tuberculous meningitis. If necessary, use laboratory methods (RSK, RTGA).

Differential diagnosis is carried out with acute, purulent and toxic parotitis, salivary stone disease, lymphadenitis, toxic diphtheria of the oropharynx.

Treatment is carried out on an outpatient basis, in severe cases with complications from the central nervous system, genital organs and other complications, or according to epidemiological indications, patients are hospitalized. Bed rest must be observed during the entire acute period, and for meningitis and orchitis - at least 2-3 weeks. Symptomatic treatment is prescribed. Apply antihistamines, multivitamins. Antiviral therapy is carried out in combination with detoxification (glucose) and dehydration (lasix, diacarb) therapy. Thermal dry procedures (woolen wraps, heated salts, sand, etc.), UHF therapy are applied locally. Compresses are contraindicated. Treatment of orchitis, pancreatitis and meningitis is carried out according to general rules. In severe cases of orchitis, corticosteroid hormones are often used.

Forecast. In most cases, the prognosis is favorable. In rare cases, lesions of the inner ear end with the development of persistent deafness. Bilateral orchitis in some cases leads to testicular atrophy with subsequent reproductive dysfunction.

Prevention. The patient is isolated at home for 9 days from the moment of illness, provided that acute clinical phenomena disappear. They are hospitalized only in severe cases of the disease and for epidemiological indications. Children under 10 years of age who have been in contact with a sick person are subject to separation for 21 days. If the exact time of contact is established, they are not allowed into children's institutions from the 11th to the 21st day from the moment of possible infection. Specific prevention is carried out by active immunization with a live mumps vaccine for children aged 12-15 months simultaneously with vaccination against measles, and revaccination is carried out at the age of 6 years.

LECTURE No. 7. Meningococcal infection. Clinic, diagnostics, differential diagnostics, treatment

Meningococcal infection is an acute infectious disease caused by meningococci, occurring in the form of acute nasopharyngitis, purulent meningitis and meningococcemia. The infection is transmitted by airborne droplets. Healthy carriage of meningococci is widespread.

Etiology. Meningococci are gram-negative spherical formations located in pairs, localized intracellularly in the cerebrospinal fluid and have the shape of a coffee or bean grain. In the external environment, they quickly die, especially under the influence of direct sunlight and ultraviolet rays. There are various serotypes of pathogens (A, B, C, etc.). Sensitive to penicillin and all disinfectants.

Pathogenesis. The entry gates of infection are the mucous membrane of the upper respiratory tract, often the nasopharynx. Some infected people develop acute nasopharyngitis, and in some people, meningococcus with blood flow penetrates into other organs and systems, affecting them (meningococcemia).

Clinic. The incubation period lasts from 2 to 10 days (usually 4-6 days). Acute nasopharyngitis is characterized by low-grade body temperature, moderate symptoms of intoxication (headache, weakness) and nasopharyngitis. Meningococcal sepsis (meningococcemia) begins suddenly and proceeds violently, body temperature quickly rises to 40 °C and above, chills and severe headache are noted. After 5-15 hours from the onset of the disease, a hemorrhagic rash appears. The elements of the rash have the appearance of irregularly shaped stars, at the same time there may be small petechiae and large hemorrhages, reaching 2-4 cm in diameter. Along with hemorrhages, roseolous and papular elements of the rash may appear, blood pressure decreases, tachycardia and shortness of breath appear. Motor excitement, convulsions give way to coma. Meningococcal meningitis begins with an acute increase in body temperature with chills, agitation, restlessness, severe headache, vomiting without previous nausea, and general hyperesthesia. By the end of the first day of the disease, meningeal symptoms arise and increase (stiff neck, Kernig-Brudzinsky symptoms). Delirium, convulsions, blackouts, and tremors are possible. Tendon reflexes are animated, pathological reflexes of Babinsky and Rossolimo appear.

Diagnostics. Based on clinical and laboratory data in the blood, neutrophilic leukocytosis (up to 16-25 109 g/l), accelerated ESR is determined. Cerebrospinal fluid flows out under increased pressure, at the beginning of the disease it is opalescent, then it becomes cloudy, purulent, and cytosis appears. The presence of the disease proves the isolation of meningococcus from the cerebrospinal fluid or blood.

Complications. Infectious-toxic shock, acute adrenal insufficiency, edema and swelling of the brain, leading to brain herniation.

Differential diagnosis should be made with other purulent meningitis.

Treatment. Intensive etiotropic therapy in the treatment of meningococcal nasopharyngitis with the prescription of antibiotics such as ampiox, erythromycin and other macrolides. When treating generalized forms of meningococcal infection, antibiotics, desensitizing therapy, and pathogenetic therapy are prescribed.

The prognosis for early and adequate treatment is favorable. In severe forms and delayed treatment, fatal outcomes are possible.

Prevention. Identification and isolation of patients. The hospital is currently being disinfected. Final disinfection and chemoprophylaxis in the foci is not carried out.

LECTURE No. 8. Dysentery. Etiology, epidemiology, pathogenesis, clinic, treatment

Dysentery

Dysentery (shigellosis) is an infectious disease that affects the large intestine and is characterized by intoxication like neurotoxicosis. Infection occurs via the enteral route.

Etiology. The causative agents are four types of Shigella:

1) shigella dysentery;

2) Shigella Flexner (with subspecies Newcastle);

3) Boyd's shigella;

4) Shigella Sonne.

The most common are Shigella Sonne and Flexner. The pathogens are gram-negative, nonmotile rods that do not form spores or capsules. They can persist for a long time in the external environment (up to 1,5 months). They not only persist on some food products, but can also multiply (on dairy products, etc.). Over time, Shigella resistance to various types of antibiotics increases, and resistance to sulfonamide drugs has developed in almost all strains. The exotoxin produced by Shigella has a pronounced neurotoxic, as well as enterotoxic and cytotoxic effect. Avirulent strains of Shigella have been isolated for enteral immunization. Live attenuated vaccines are obtained from them. The infectious number of bacteria in dysentery is small. The ability of Shigella to parasitize the large intestine has been confirmed.

Epidemiology. The source of infection is a sick person, the mechanism of transmission is fecal-oral, the route of transmission is alimentary, water, contact. Immunity is monotype-specific, not strained.

Pathogenesis. The disease occurs when Shigella toxins enter the bloodstream. Dysentery toxins act on the wall of blood vessels, the central nervous system, peripheral nerve ganglia, the sympathetic-adrenal system, the liver, and the circulatory organs. In severe forms of dysentery, patients usually die from toxic shock.

Clinic. The incubation period is from 1 to 7 days (usually 2-3 days). According to clinical manifestations, dysentery can be divided into the following forms.

1. Acute dysentery:

1) typical (of varying severity);

2) atypical (gastroenterocolitic);

3) subclinical.

2. Chronic dysentery:

1) recurrent;

2) continuous (protracted).

3. Postdysenteric bowel dysfunction (postdysenteric colitis).

Typical forms may flow:

1) with a predominant predominance of toxic phenomena;

2) with predominant predominance of colitis syndrome;

3) in mixed form.

Typical dysentery begins acutely and is manifested by symptoms of general intoxication (fever up to 38-39 ° C, loss of appetite, single or repeated vomiting, lethargy, headache, adynamia, decreased blood pressure) and signs of damage to the gastrointestinal tract (colytic syndrome). Abdominal pain is initially dull, spread throughout the abdomen, constant, then becomes more acute, cramping, localized in the lower abdomen, often on the left or above the pubis. The pain intensifies before defecation. The stool is liquid with an admixture of cloudy green mucus, sometimes streaked with blood, the stool is first abundant, then scanty, 5-6 times a day or more. Tenesmus also appears (this is a false urge to defecate as a result of simultaneous spasm of the sigmoid colon and anal sphincters), drawing pain in the rectal area, radiating to the sacrum. They occur during defecation and continue for 5-15 minutes after it. Tenesmus is accompanied by inflammation of the mucous membrane of the ampullary part of the rectum. Damage to the distal part of the large intestine is associated with false urges and prolonged acts of defecation, a feeling of their incompleteness. When palpating the abdomen, spasm and tenderness of the large intestine are noted, more pronounced in the area of the sigmoid colon. The bowel movements initially have the character of feces, and then admixtures of mucus and blood appear; in more severe cases, only a small amount of bloody mucus is released during bowel movements. In mild forms (up to 80% of all diseases), patients feel satisfactory, low-grade fever (or normal temperature) is noted, abdominal pain is minor, tenesmus and false urges may be absent. Stool - 3-5 times a day; it is not always possible to detect an admixture of mucus and blood in the stool. Subclinical forms of dysentery are usually detected by bacteriological examination; clinical symptoms are mild. Often these patients consider themselves healthy and do not make any complaints. Severe dysentery occurs in 3-5% of cases. It occurs with high fever or, conversely, with hypothermia. Severe weakness, adynamia, and complete lack of appetite are noted. Patients are lethargic, apathetic, pale skin, rapid pulse, weak filling. A picture of infectious collapse may develop (progressive drop in blood pressure, cyanosis, feeling of cold, dizziness, pulse can barely be felt). Stool - up to 50 times a day, mucous-bloody in nature. In severe cases, sphincter paresis sometimes occurs, and the anus may gape, from which bloody mucus is released.

The atypical form has four clinical variants:

1) an erased form, in which there are no manifestations of intoxication, an unstable stool is noted, there is a seeding of the pathogen;

2) dyspeptic form, more often occurring in children of the first year of life, intoxication is mild and is confirmed bacteriologically and serologically;

3) subclinical form, characterized by the release of the pathogen in the absence of clinical manifestations, sigmoidoscopy can detect morphological changes, an increase in antibody titers in the blood;

4) hypertoxic form, occurring with severe neurotoxicosis (hyperthermia, loss of consciousness, convulsions, cardiovascular insufficiency) and the appearance of diarrhea by the end of the first day of illness.

Diagnosis is carried out on the basis of complaints, epidemiological, clinical and laboratory data. Coproscopy reveals mucus, blood macro- and microscopically, and leukocytes. Blood tests revealed leukocytosis, neutrophyllosis, increased ESR. Bacteriological research involves isolating the pathogen from feces, gastric lavage, vomit, and food residues. A serological examination (RSC, RNGA) is possible. There is an increase in antibody titers in the blood serum. During sigmoidoscopy, depending on the severity, changes in the mucous membrane of the large intestine (catarrhal, catarrhal-hemorrhagic, erosive, ulcerative, fibrinous) are revealed to varying degrees of severity. Dysentery is characterized by hemorrhagic and erosive changes against the background of inflammation of the mucous membrane. The fact that the disease is dysenteric is proven by the isolation of Shigella from feces, but this is only possible in 50% of patients (more often during outbreaks). For the diagnosis of chronic dysentery, it is important to indicate acute dysentery during the last 6 months. The initial stage of chronic dysentery occurs in the form of individual exacerbations (relapses), and later turns into a continuous (protracted) form, when there are no periods of remission. Post-dysentery intestinal dysfunctions develop 2 years after dysentery. During this period, Shigella can no longer be isolated from the patient. Complications: specific (intestinal bleeding, intussusception, peritonitis, hemolytic-uremic syndrome), nonspecific (addition of a secondary bacterial infection, pneumonia, cystitis, otitis, etc.).

Differential diagnosis is carried out with acute colitis of another etiology (salmonella, escherichiosis, staphylococcal, yersineosis, etc.), as well as amoebiasis, balantidiasis, ulcerative colitis, colon cancer.

Treatment. Patients with dysentery are hospitalized in an infectious diseases hospital, especially patients with moderate and severe forms, children under 3 years of age, weakened, and also if it is impossible to organize treatment at home. According to epidemiological indications, children attending preschool institutions, food workers, and people living in dormitories are hospitalized. Diet therapy is carried out taking into account age. In the first 2-3 days, reduce the volume of food by 1/4-1/2, depending on the severity of the condition, and use the principles of mechanical sparing. In order to replenish the loss of fluid and electrolytes, correct the acid-base state, metabolic disorders, rehydration therapy is carried out. Antibiotics, sulfonamides, Intetrix, and furazolidone are prescribed as etiotropic drugs. You can use dysentery bacteriophage. A complex of vitamins is prescribed. To restore the microflora, biological products (bifidumbacterin, lactobacterin, linex, bificol, etc.), enzyme therapy, and herbal medicine are prescribed. In case of prolonged course, immunocorrective drugs are used. To prevent relapses of dysentery, careful identification and treatment of concomitant diseases is necessary.

Degrees of dehydration in children. In many infectious diseases, vomiting and frequent stools are among the symptoms. Most often this is observed with intestinal infections caused by shigella, staphylococci, proteus, salmonella, etc. Dehydration often develops in children due to the compensatory capabilities of the child's body.

I degree - easy. Weight loss is up to 5% of body weight. The frequency of stool and vomiting is up to 6 times a day, moderate thirst, patients are capricious, agitated, turgor and skin elasticity are preserved, some dryness of the mucous membranes is observed, heart sounds and pulse quality are within normal limits. Moderate tachycardia is observed, the voice is preserved, diuresis is slightly reduced, body temperature is increased.

II degree - moderate. This is the stage of loss of intracellular potassium and sodium. Weight deficit - up to 9%. The frequency of stool and vomiting is up to 10 times a day, thirst is pronounced, but patients refuse to drink, as nausea is present. The state of anxiety turns into lethargy and lethargy, turgor and elasticity of the skin are reduced, the fold is difficult to gather, the mucous membranes and eyeballs are dry, heart sounds are muffled, significant tachycardia, pulse of weak filling, body temperature is high. Diuresis is reduced. There is a slight hoarseness of voice.

III degree - severe. This is the stage of salt deficiency. The loss of body weight is more than 10%. Stool and vomiting - without counting, patients refuse to eat and drink, there is apathy and adynamia, facial features are pointed, limbs are cold to the touch, loss of consciousness is possible. Skin turgor is sharply reduced, the skin fold does not straighten out, eyes are sharply sunken, soft eyeballs, mucous membranes are dry and bleeding, DIC develops, heart sounds are deaf, bradycardia, diuresis in the stage of oliguria, turning into anuria. Body temperature is below normal, aphonia.

With a mild degree of dehydration, oral rehydration is used with the calculation of the injected fluid 40-50 ml / kg of weight. Rehydration takes 4 hours.

With a moderate degree of dehydration, the liquid calculation is 60-90 ml / kg. Rehydration is carried out within 6 hours, further administration of solutions is prescribed taking into account the loss of fluid with vomiting and stool. For each portion of the lost fluid, a solution is injected at the rate of 10-15 ml / kg.

In severe cases, fluid replacement is 100-120 ml/kg. At this stage, most of the solutions are administered intravenously.

For oral rehydration, the following solutions are used: rehydron, chloralite, glucosolan citrate.

Forecast. The further prognosis for dysentery is favorable. The transition to a chronic form is observed in 1-2% of cases after therapy.

Prevention. Patients who have had dysentery are discharged no earlier than 3 days after complete recovery. In addition, the necessary criteria are the normalization of stool, body temperature, a single negative bacteriological analysis, which should be carried out no earlier than 2 days after antibiotic therapy is discontinued. Food workers and persons equated to them, as well as patients with chronic dysentery, are subject to dispensary observation. The follow-up period is 3-6 months. In cases where the patient stays at home, the current disinfection is carried out in the apartment. Persons who have been in contact with patients are placed under medical supervision for 7 days.

LECTURE No. 9. Salmonellosis. Etiology, epidemiology, pathogenesis, clinic, treatment

Salmonellosis is an acute infectious disease caused by Salmonella, characterized by a variety of clinical manifestations - from asymptomatic carriage to severe septic forms. More often it occurs with a predominant lesion of the digestive organs (in the form of gastroenteritis, colitis), severe long-term intoxication, persistent diarrhea, exsicosis.

Etiology. The causative agent of the disease is gram-negative motile rods with flagella. Salmonella are facultative anaerobes and grow on normal nutrient media. Highly stable in the external environment, for a long time (up to several months) they remain in the external environment, products, and in some of them (milk, meat products) they are able to multiply without changing the appearance and taste of the products, antibiotic resistance is quickly formed.

Epidemiology. The source of infection is sick animals, birds, humans, bacteria carriers. The route of transmission is food, water, contact, rarely airborne. Immunity is mono-specific.

Pathogenesis. The gateway of infection is predominantly the mucous membrane of the small intestine, in which Salmonella are capable of intracellular parasitism in macrophages and reticulocytes. With a generalized form, salmonella penetrate into the blood, and with a septic form they are introduced into various organs, where secondary purulent foci are formed. Endotoxin secreted by Salmonella causes various damage to internal organs. In severe forms, the development of dehydration, as well as infectious-toxic shock, is possible.

Clinic. The incubation period ranges from several hours to 3 days (usually 12-24 hours). The most common forms of Salmonella infection are gastrointestinal forms. Depending on the damage to one or another part of the gastrointestinal tract, the leading syndrome in the clinical picture will be gastritis, gastroenteritis, enterocolitis, gastroenterocolitis, and less often colitis. Gastroenteritis and gastroenterocolitis begin acutely or subacutely, with an increase in body temperature to 38-40 ° C, chills and symptoms of general intoxication. Pain in the epigastric region, nausea, vomiting, and after a few hours - diarrhea also appear. The abdomen is moderately distended. The stool is enterocolitic in nature: frequent, copious, fecal, liquid, watery, fetid, foamy, undigested, up to 10-15 times a day, with an admixture of greenery and muddy mucus like swamp mud. Tenesmus and blood in the stool were not observed. With copious, frequent bowel movements and repeated vomiting, dehydration syndrome may develop (thirst, oliguria, cyanosis of the lips, sunken eyes, wrinkled skin, convulsions, decreased blood pressure). Fever lasts 2-5 days. Children are lethargic, adynamic, and their appetite is sharply reduced.

Enterocolitis is the most common form in children, often in the first years of life, with a burdened premorbid background; it develops as a result of contact and household infection. The disease begins with abdominal pain, anxiety, single vomiting and increased bowel movements. The stool is enteritic in nature (frequent, copious, watery, foamy, undigested, with an admixture of transparent mucus, a sharp sour odor). Flatulence phenomena are characteristic. In children over 3 years of age and in adults, the disease occurs with symptoms of gastritis, gastroenteritis, similar to food toxic infection. In a mild form, the disease is limited to low-grade fever, single vomiting and slight looseness of stool. All phenomena disappear within 1-2 days.

A typhoid-like form of Salmonella infection develops in school-age children and in its manifestations is almost no different from typhoid fever; the diagnosis is clarified after isolating a blood culture of Salmonella. The most severe form of salmonellosis is the septic form. It begins acutely, typhoid intoxication occurs (headache, lethargy, stupor, delirium, confusion), fever of a wave-like or irregular type, with large daily swings, repeated chills and sweat. Lasts for many weeks, bradycardia, roseola rash on the chest and abdomen, and hepatosplenomegaly occur. The disease responds poorly to antibiotic therapy. The development of secondary purulent foci often occurs in the musculoskeletal system, causing osteomyelitis, arthritis, and spondylitis. Sometimes septic Salmonella endocarditis, aortitis with subsequent development of aortic aneurysm, purulent meningitis are detected, and liver abscesses occur less often. The colitic form of salmonellosis is similar to acute dysentery. There may be tenesmus, blood in the stool, catarrhal-hemorrhagic proctosigmoiditis (according to sigmoidoscopy) and other complications (thrombohemorrhagic syndrome, peritonitis), as well as complications associated with the addition of a secondary infection (pneumonia, otitis).

Diagnosis is carried out on the basis of complaints, anamnesis, clinical and laboratory manifestations, epidemiological prerequisites are important (group nature of diseases, connection with a certain product). To confirm the diagnosis by laboratory means, the most significant is the isolation of the pathogen (examine food residues, vomit, feces, blood - in generalized forms, pus - in septic forms of the disease).

Treatment. Hospitalization in a hospital is carried out according to clinical and epidemiological data. Bed rest or semi-bed rest, diet therapy. In case of gastrointestinal form, wash the stomach and intestines with 2-3 liters of water or 2% sodium bicarbonate solution as soon as possible. Lavage is carried out using a gastric tube until clean lavage water is discharged. In mild forms, they are limited to gastric lavage, diet and drinking saline solutions. Typically, a solution of the following composition is used: sodium chloride - 3,5 g, potassium chloride - 1,5 g, sodium bicarbonate - 2,5 g, glucose - 20 g per 1 liter of drinking water. Rehydration therapy is carried out with the appointment of oral rehydration with glucose-salt solutions (Rehydron, Oralit) for exicosis of the I-II degree, and in case of exicosis of the third degree, infusion therapy is carried out simultaneously with oral administration of fluid, taking into account physiological needs and pathological losses.

Aminoglycosides, cephalosporins, etc. are used as etiotropic therapy. Salmonella bacteriophage and a complex immunoglobulin preparation are prescribed as specific etiotropic therapy. In case of moderate severity of the gastrointestinal form of salmonellosis, absence of vomiting and severe hemodynamic disturbances, the liquid can also be administered orally. As dehydration worsens, rehydration is carried out in the same way as for cholera. With the development of infectious-toxic shock, in addition to polyionic solutions, hemodez, polyglucin, rheopolyglucin are administered in 400-1000 ml doses, 60-90 mg of prednisolone or 125-250 mg of hydrocortisone are prescribed intravenously in a bolus, after 4-6 hours they switch to drip administration ( up to 120-300 mg of prednisolone per day). At the same time, deoxycorticosterone acetate is administered at a dose of 5-10 mg intramuscularly every 12 hours. Typhoid-like forms are treated in the same way as typhoid fever. For septic forms, long-term administration of ampicillin (4-6 g/day) is combined with surgical treatment of purulent foci. Biological products, enzymes, and herbal medicine are prescribed at the end of a course of antibiotic therapy.

Forecast. In most cases, recovery occurs. In some patients, a chronic bacteriocarrier is formed in all clinical variants of the course.

Prevention. Veterinary and sanitary supervision over the slaughter of livestock, control over the preparation and storage of meat and fish dishes. Convalescents are prescribed after complete clinical recovery and a double bacteriological examination of stool.

LECTURE No. 10. Escherichiosis. Rotavirus infection. Etiology, epidemiology, clinic, diagnostics, treatment

1. Escherichiosis

Escherichiosis is an acute infectious disease caused by pathogenic Escherichia coli, characterized by damage to the gastrointestinal tract and the development of intoxication and diarrheal syndromes. Occurs with a predominant lesion of the intestine.

Etiology. The causative agent is Escherichia coli, which has many antigenic variants. The most dangerous for children are the following 0-groups: 011, 055, 026, 086, 0119, etc. An adult organism often affects Escherichia 0124. The introduction of bacteria into the body occurs in the small intestine. Severe toxic damage to the intestinal mucosa is caused by Escherichia endotoxin, which has an enterotropic effect.

Epidemiology. Sources of infections are sick people and healthy bacteria carriers, the transmission mechanism is fecal-oral. Children get sick more often.

Clinic. The incubation period lasts 3-6 days (usually 4-5 days). Escherichiosis can occur in the following clinical forms:

1) intestinal diseases of children;

2) intestinal diseases of adults;

3) sepsis.

In children, intestinal forms of escherichiosis occur in the form of varying severity of enteritis and enterocolitis in combination with a syndrome of general intoxication. In mild forms, the body temperature is subfebrile, stools are 3-5 times a day, liquid, sometimes mixed with a small amount of mucus. The moderate form begins acutely, vomiting appears, body temperature rises (38-39 ° C), the abdomen is swollen, stools are up to 10-12 times per day, liquid with mucus. Severe forms are characterized by pronounced toxicosis, stools up to 20 times a day, watery, foamy with an admixture of mucus, sometimes streaked with blood. Body temperature rises to 39-40 °C, there is no appetite, the child is restless, the skin is pale, blood pressure is reduced, and weight loss is noted. In adults, the disease caused by Escherichia 0124 resembles acute dysentery in its course and clinical symptoms. It occurs more often in erased and mild forms; moderate and severe (15%) forms are less common (20-3%). Tenesmus occurs less frequently than with dysentery. The stool is liquid with an admixture of mucus, in some patients with blood. Palpation is accompanied by symptoms of enteritis: pain in the umbilical region, rough rumbling on palpation of the cecum (except for spasm and pain in the colon).

Differentiating escherichiosis with dysentery and salmonella enterocolitis, relying only on clinical data, is quite difficult.

The diagnosis is established on the basis of complaints, clinical and laboratory data of bacteriological examination of feces.

Treatment. In mild forms of escherichiosis in adults, pathogenetic and symptomatic therapy can be limited. Of the etiotropic drugs, mainly amino-glycosides, cephalosporins are used. With watery diarrhea, enterosorbents are prescribed. With severe toxicosis, infusion therapy is used. In severe forms, coli-proteic enteral lactoglobulin, bacteriophages are used.

The prognosis for adults and children over one year of age is favorable; the disease is most severe in children in the first six months of life. Prevention should be especially strict in all medical children's institutions where children are in their first year of life (especially the first six months). Attention is paid to preventing the introduction of infection into these institutions, early detection and isolation of patients. To do this, pregnant women before childbirth are examined for escherichiosis, as well as women in labor, postpartum women and newborns in whom an escherichiosis infection can be suspected, and if detected, the sick are isolated, and personnel are examined for carriage of pathogenic escherichia. For escherichiosis in adults, prophylaxis is carried out in the same way as for dysentery.

2. Rotavirus infection

Rotavirus infection is an acute infectious disease caused by rotaviruses and characterized by damage to the gastrointestinal tract, symptoms of general intoxication, and dehydration with a predominant incidence in children. Causes about half of all intestinal disorders in children in the first 2 years of life.

Etiology. The causative agent - rotaviruses - contains RNA, is divided into two antigenic variants, and is stable in the external environment.

Epidemiology. Sources of infection - a sick person or a virus carrier. Ways of transmission - contact-household, alimentary. A pronounced autumn-winter seasonality is characteristic.

Pathogenesis. Reproduction and accumulation of rotaviruses occurs mainly in the upper gastrointestinal tract, where direct damage to the cells of the intestinal epithelium of the small intestine occurs, leading to the destruction of enterocytes responsible for the synthesis of disaccharidases. In the contents of the intestine, a large amount of osmotically active unsplit disaccharides and sugars accumulates, attracting fluid into the intestinal lumen. The result is osmotic watery diarrhea. After the illness, a short-term immunity is formed. Large losses of fluid and electrolytes are characteristic, which leads to dehydration of the I-III degree.

Clinic. The incubation period lasts from 15 hours to 7 days (usually 1-2 days). The disease begins acutely or gradually. Most patients simultaneously exhibit symptoms of damage to the respiratory tract (coughing, nasal congestion, hyperemia of the palatine arches and the posterior pharyngeal wall). A detailed picture of the disease is formed within 12-24 hours from the onset of the disease. Children usually do not have severe fever. Vomiting is a mandatory symptom of the disease. It appears on the first day and lasts 2-3 days. Intoxication is minor. Characterized by copious, loose, watery stools without mucus or sometimes with a small amount of thread-like mucus, without blood. Diarrhea persists for up to 5-7 days. Abdominal pain is cramping in nature and does not have a clear localization. A more severe course is usually due to the layering of a secondary infection. In adults, with severe intoxication and low-grade fever, pain in the epigastric region, vomiting, and diarrhea appear. Rarely, vomiting recurs on the 2-3rd day of illness. All patients have profuse, watery stools with a pungent odor; sometimes cloudy-whitish stools may resemble the stools of a cholera patient. There is a loud rumbling in the stomach. The urge to defecate is imperative; there are no false urges. In some patients, an admixture of mucus and blood is found in the stool, which always indicates a combination of rotavirus disease with a bacterial infection (shigellosis, escherichiosis). Such patients experience more severe fever and intoxication. With copious loose stools, dehydration may develop; In 95-97% of patients, dehydration is grade I or III; children sometimes experience severe dehydration with decompensated metabolic acidosis. Acute renal failure and hemodynamic disorders are possible here. Palpation of the abdomen is accompanied by pain in the epigastric and umbilical regions, and rough rumbling in the right iliac region. The liver and spleen are not enlarged.

The diagnosis is established on the basis of complaints, clinical and laboratory data: in the blood test at the onset of the disease, there may be leukocytosis, which is replaced by leukopenia during the peak period, ESR is not changed. In the analysis of urine in some patients, albuminuria, leukocytes and erythrocytes are found, the content of residual nitrogen in the blood serum increases. The basis of laboratory diagnostics is the detection of the virus (by electron microscopy, immunofluorescent method, etc.) or its antigens in feces, as well as antibodies in blood serum (RSK, RTGA, etc.). In the coprogram, patients show signs of impaired digestion. With sigmoidoscopy, most patients have no changes.

Differential diagnosis is carried out with cholera, dysentery, escherichiosis, intestinal yersiniosis.

Treatment. Diet therapy (restriction of milk, dairy and carbohydrate-rich foods). The basis is pathogenetic methods of therapy, primarily the restoration of fluid and electrolyte losses, in connection with this oral rehydration is carried out. For degree I-II dehydration, solutions are given orally. According to WHO recommendations, use the following solution; sodium chloride - 3,5 g, sodium bicarbonate - 2,5 g, potassium chloride - 1,5 g, glucose - 20 g/l. The solution is given to drink in small doses every 5-10 minutes. In addition to the solution, other liquids are recommended (tea, fruit drink, mineral water). Enterosorbent therapy (enterodes, polyphepan, smecta), enzyme therapy (mezim-forte, creon) are prescribed. Prescribing antibiotics is contraindicated. Among etiotropic drugs, a complex immunoglobulin preparation or anti-rotavirus oral immunoglobulin is prescribed.

The prognosis is favorable.

Prevention. Patients are isolated for 10-15 days. In cases of mild forms, patients can remain at home under medical supervision if treatment and adequate isolation are provided. The apartment is subject to current and final disinfection. Specific prevention has not been developed.

LECTURE No. 11. Amoebiasis. Balantidiasis. Etiology, epidemiology, clinic, diagnostics, treatment

1. Amoebiasis

Amebiasis is a protozoal disease characterized by ulcerative lesions of the large intestine, with the formation of abscesses in the liver, lungs and other organs and a tendency to a protracted and chronic course.

Etiology. The causative agent is dysenteric amoeba, which can be found in three forms. Cysts are highly resistant to environmental factors; in moist feces and water they are viable for up to 1 month; in darkened and moist soil they live for up to 8 days. High temperatures have a detrimental effect; low temperatures can be tolerated for up to several months. Drying effect is immediate. The large vegetative form (tissue form, erythrophage) phagocytoses red blood cells and is detected only in the patient’s body. The luminal form and stage of the cyst can also be found in carriers.

Epidemiology. The way of transmission of infection is alimentary, fecal-oral, water, and also contact-household. Amoeba cysts are spread by flies, cockroaches.

Pathogenesis. A person becomes infected when cysts enter the digestive system. In the large intestine, the cyst transforms into a luminal form, and carriage occurs. Clinical manifestations appear only when the luminal form transitions to the tissue form. The formation of ulcers in the intestinal mucosa is a consequence of the proliferation of the tissue form in the intestinal wall. In this case, small abscesses first appear in the submucosal layer, which then break into the intestinal lumen. By hematogenous route, dysenteric amoeba can reach the liver, less often - other organs, and cause the formation of specific abscesses in them. As ulcers scar, narrowing of the intestines may occur.

Clinic. The incubation period lasts from 1 week to 3 months. The disease begins acutely. Symptoms are manifested in the form of weakness, headache, moderate abdominal pain, the appearance of loose stools with the presence of vitreous mucus and blood, low-grade fever. After the end of the acute period, a long remission may occur, then the disease resumes and takes on a chronic course. Without the appointment of etiotropic antiparasitic treatment, the disease can occur for 10 years or more in the form of recurrent or continuous forms. In this case, there are pains in the abdomen, loose stools, alternating with constipation, sometimes there may be blood in the stool. With a long course of the disease, an asthenic condition develops, weight loss, hypochromic anemia.

Diagnosis is carried out on the basis of epidemiological data and clinical examination of patients. Sigmoidoscopy reveals ulcers up to 10 mm in diameter, deep, with undermined edges. The bottom of the ulcers is covered with a purulent coating. The ulcers are surrounded by a rim of hyperemic mucous membrane. A biopsy of the intestinal mucosa, ultrasound of the liver, and laparoscopy are performed. The main and decisive factor in the diagnosis is the detection of the vegetative form of amoeba in feces, abscess contents, and material from the bottom of ulcers. The study should be carried out no later than 20 minutes after defecation or collection of material. Complications of amebiasis include peritonitis due to intestinal perforation, amoeba, and intestinal bleeding. Liver abscess (extraintestinal complication) can develop both during the acute period and after a long time, when there are no longer significant intestinal lesions. The acute course of an abscess is manifested by hectic fever, chills, and pain in the right hypochondrium. An x-ray reveals a high position of the diaphragm (or its local protrusion). Even minor abscesses can be detected with a liver scan. Mild intoxication and fever are observed with chronic abscess. The possibility of an amoebic abscess breaking into surrounding organs can lead to the formation of a subphrenic abscess, peritonitis, and purulent pleurisy. Laboratory diagnosis is confirmed when a large vegetative form of amoeba with phagocytosed red blood cells is detected in the stool. Serological diagnostic methods are available. Amebiasis must be differentiated from dysentery, balantidiasis, ulcerative colitis, and neoplasms of the large intestine.

Treatment. Prescribe a 2% solution of emetine hydrochloride, 1,5-2 ml IM 2 times a day for 5-7 days. A week later the cycle is repeated. In the intervals between zmetin cycles, khingamin (delagil) is prescribed 0,25 g 3 times a day, quiniophone 0,5 g 3 times a day. Metronidazole (Trichopolum, Flagyl) is considered the most effective and non-toxic drug for the treatment of patients with both intestinal and extraintestinal manifestations of amebiasis. It is prescribed 0,5-0,75 g 3 times a day for 5-7 days. Antibacterial therapy is prescribed as an adjunct in order to change the microbial biocenosis in the intestine. For amoebic liver abscesses, the drug is prescribed for a longer period - until the abscess resolves (based on the results of a liver scan). For large liver abscesses, surgical treatment methods are used.

The prognosis for intestinal amebiasis is favorable. Possible residual effects in the form of narrowing of the intestine. With an amoebic abscess of the liver or brain, a fatal outcome is possible, but modern therapy has made the prognosis more favorable.

Prevention. Isolation, hospitalization and treatment of patients. Amoeba carriers are not allowed to work in the public catering system. General preventive measures are the same as for dysentery.

2. Balantidiasis

Balantidiasis is a protozoal disease characterized by ulcerative lesions of the colon and symptoms of general intoxication, severe course and high mortality in late therapy.

Etiology. The causative agent - balantidia - belongs to the class of ciliates, occurs in a vegetative form and in the form of cysts that are stable in the external environment. The natural carriers of balantidia are pigs.

Epidemiology. The route of transmission is fecal-oral. The reservoir of pathogens are pigs.

Pathogenesis. Infection occurs when balantidia enter the human digestive tract, mainly in the small intestine, where they stay for a long time without causing a clinical picture of the disease. Some of the infected balantidia enter organs and tissues. At the same time, ulcers, foci of necrosis, and hemorrhages are formed there. The ulcers are irregular in shape, the edges are thickened and indented. Their bottom is uneven, with a purulent-bloody coating. Perforation of ulcers may occur and the development of peritonitis is not excluded.

Clinic. The incubation period lasts 1-3 weeks. Acute forms of the disease are characterized by fever, symptoms of general intoxication and signs of intestinal damage (abdominal pain, diarrhea, flatulence, tenesmus is possible). The stools are characterized by an admixture of mucus and blood. Spasm and soreness of the large intestine, enlargement of the liver are characteristic. In severe cases, general intoxication, high fever, stools up to 20 times a day with an admixture of mucus and blood with a rotten smell are observed. Patients quickly lose weight, sometimes there are symptoms of irritation of the peritoneum. Chronic balantidiasis occurs with mild symptoms of intoxication, body temperature is normal, stools - up to 2-3 times a day, liquid, with mucus, sometimes with an admixture of blood. On palpation, pain is found predominantly in the blind and ascending colon.

Diagnosis is based on epidemiological data and clinical examination data of patients. Sigmoidoscopy reveals a focal infiltrative-ulcerative process or extensive ulcerative lesions. The diagnosis is confirmed by the detection of parasites in feces, biopsy specimens of the edge of ulcers, and in smears of ulcerative contents.

Treatment. Etiotropic drugs are used in the form of 2-3 5-day cycles. Assign monomycin 0,15 g 4 times a day, oxytetracycline 0,4 g 4 times a day, metronidazole 0,5 g 3 times a day. The interval between cycles is 5 days.

The prognosis for modern therapy is favorable. Without the use of antiparasitic therapy, mortality reached 10-12%.

Prevention. Compliance with hygiene measures when caring for pigs. Identification and treatment of people with balantidiasis. General preventive measures are the same as for dysentery.

LECTURE No. 12. Campylobacteriosis. Food poisoning with bacterial toxins. Botulism. Etiology, epidemiology, clinic, diagnostics, treatment

1. Campylobacteriosis

Campylobacteriosis is an acute infectious disease of a zoonotic nature, characterized by an acute onset, general intoxication, fever, and a predominant lesion of the gastrointestinal tract. In newborns, it often occurs in the form of a septic disease.

Etiology. The causative agent is various serotypes of Campylobacter. Gram-negative curved rod, does not form spores, is immobile, has one or two flagella. The optimum growth of the pathogen is 37 °C. The causative agent is well preserved in the external environment at a temperature of 4 ° C, in soil, water, milk - for several weeks, frozen meat - up to several months. Pathogens are sensitive to drying and exposure to sunlight, and die when boiled and chlorinated.

Epidemiology. The reservoir is domestic and farm animals (rabbits, pigs, cows, etc.). When animals are slaughtered, the infection of meat comes from the intestinal contents. The route of transmission is fecal-oral, alimentary.

Pathogenesis. The pathogen enters the body mainly through the gastrointestinal tract with alimentary infection, penetration through damaged skin is possible. In the site of the entrance gate of infection, inflammatory changes in the mucous membrane occur. In pregnant women, transplacental transmission of infection is noted, which is the cause of abortion and intrauterine infection of children. In weakened people, the disease takes a septic course with the formation of secondary foci.

Clinic. The incubation period lasts about 6 days, usually 1-2 days. According to clinical manifestations, the following forms are distinguished:

1) gastrointestinal;

2) generalized (septic);

3) chronic;

4) subclinical (bacteriocarrier).

In most cases, the gastrointestinal form occurs. The disease is characterized by an acute onset in the form of fever, symptoms of intoxication and gastroenteritis. Patients begin to experience nausea, vomiting, and pain in the epigastric region. The stool is copious, liquid, foamy, and does not contain pathological impurities in adult patients. In children, the symptoms of intoxication are more pronounced; there may be mucus and blood in the stool; dehydration of the body often develops, characterized by dry skin and mucous membranes, decreased skin turgor, and decreased urination. The generalized (septic) form most often develops in newborns, sometimes in weakened adults. Characterized by irregular fever, weight loss, and anemia. Subsequently, this is accompanied by pneumonia, peritonitis, abscesses in the liver and brain. In the subclinical form, the pathogen is isolated from feces, and an increase in antibody titer in the blood is observed. Chronic forms occur without an acute phase, with the gradual development of symptoms in the form of low-grade fever, general weakness, asthenic syndrome, weight loss, and eye damage. Women may develop disorders in the form of vaginitis, vulvovaginitis, and endocervicitis. In rare cases, inflammation of the joints, pleura, and endocardium occurs.

Diagnosis is based on the isolation of the pathogen from feces, blood, cerebrospinal fluid, pus, abscesses, tissue of an aborted fetus, as well as serologically (RSK, RNGA, etc.).

Treatment is carried out with antibacterial drugs, the most effective are erythromycin and gentamicin. The duration of the course of antibiotic therapy is 7-10 days. In chronic forms, repeated courses of treatment are carried out.

Prevention. Elimination of infection among animals, observance of sanitary and hygienic rules during the processing, transportation, storage and preparation of food products, compliance with animal slaughter standards, personal hygiene, protection of products from contamination.

2. Food poisoning with bacterial toxins

Food poisoning with bacterial toxins - diseases caused by the consumption of foods contaminated with various microorganisms and containing bacterial toxins. These include poisoning with botulism toxins, Cl. perfringens and staphylococcal poisoning. This section describes poisoning with staphylococcal toxin and Cl. perfringens (see also Botulism).

Etiology, pathogenesis. Food poisoning of staphylococcal origin is associated with strains of pathogenic staphylococci capable of producing enterotoxin. They are also capable of producing hematoxins, hyaluronidase, and give a positive plasma coagulation reaction. Getting into products (from patients with pustular diseases or aerogenously from healthy carriers of staphylococci), they have the ability to multiply, which leads to the accumulation of enterotoxin in products. Staphylococcal poisoning is mainly associated with the consumption of milk, dairy products, meat, fish, vegetable dishes, cakes, pastries, and canned fish in oil. Products containing enterotoxin do not differ in appearance and smell from benign ones. Staphylococci tolerate high concentrations of salt and sugar. If staphylococci die when heated to 80 °C, then enterotoxin can withstand heating to 100 °C for 1,5-2 hours. Kittens and puppies on which a biological test is performed are very sensitive to enterotoxin.

Microbes Cl. perfringens are large gram-negative rods. They grow in anaerobic conditions and are capable of forming spores. Based on antigenic properties, they are divided into six serotypes (A, B, C, D, E, F). Poisoning is most often associated with the pathogen type A. Staphylococcal poisoning is caused only by toxins, and can occur in the absence of the pathogen itself (for example, poisoning with products containing enterotoxin). Enterotoxin is resistant to digestive enzymes and can penetrate the mucous membranes of the gastrointestinal tract. Considering the short incubation period (up to 2 hours), one might think that the toxin is already absorbed in the stomach. The toxin causes activation of gastrointestinal motility and affects the cardiovascular system (significant reduction in blood pressure). In case of poisoning with clostridia toxins, lecithinase C (alpha toxin) is of greatest importance. Toxins lead to damage to the intestinal mucosa, disrupt its absorption function, penetrate hematogenously into various organs, and bind to the mitochondria of the cells of the liver, kidneys, spleen, and lungs. The vascular wall is damaged, which leads to the development of hemorrhagic syndrome. In severe cases, anaerobic sepsis may develop.

Clinic. The incubation period for staphylococcal poisoning often lasts 1,5-2 hours, for poisoning with clostridia toxins - from 6 to 24 hours. With staphylococcal poisoning, the most characteristic signs are cutting, cramping pain in the epigastric region, and vomiting. Body temperature is normal or subfebrile. Diarrhea may not be present, a short-term disorder of the stool is observed in about half of the patients. Typical signs such as increasing weakness, pallor of the skin, cold extremities, lowering blood pressure. A collapsed state may develop. However, even with a pronounced symptomatology of the initial period, recovery occurs by the end of the day from the onset of the disease, only in some patients weakness persists for 2-3 days. Poisoning caused by Clostridial toxins is much more severe.

The disease begins with cramps in the abdomen, mainly in the umbilical region. There is an increase in general weakness, stool frequency increases up to 20 times or more, it is copious, watery, sometimes in the form of rice water. Repeated vomiting and uncounted loose stools lead in some cases to severe dehydration. In some cases, a picture of necrotic enteritis occurs. Mortality reaches 30%. The diagnosis of staphylococcal poisoning is based on a combination of characteristic symptoms and epidemiological history (taking into account the group nature of poisonings and connections with certain products). To confirm the diagnosis, it is desirable to isolate enterotoxin-producing staphylococcus from food debris or the contents of the patient’s stomach. In case of poisoning by heat-processed food, the presence of enterotoxin is determined by means of a biological test on laboratory animals or by performing a precipitation reaction. Confirmation of poisoning by clostridia toxins is the detection of the presence of these pathogens in food products, washing waters or vomit.

Treatment. To cleanse the body of toxins, the stomach is washed with water or a 5% solution of sodium bicarbonate, after which the use of a saline laxative gives a good effect for the elimination of staphylococcal toxin. With a significant loss of fluid by the body (with clostridial toxin poisoning), a set of measures is taken to restore the water and electrolyte balance. If the patient's condition is assessed as moderate, an isotonic solution of sodium chloride or its equal volumes with a 5% glucose solution in an amount of 1000-1500 ml are injected intravenously. When the condition is aggravated, a good restoring effect is given by the use of the Trisol solution. Its composition is as follows: 1000 ml of pyrogen-free sterile water, 5 g of sodium chloride, 4 g of sodium bicarbonate and 1 g of potassium chloride. "Trisol" is recommended to be combined with colloidal solutions, which help to remove toxins from the body, restore microcirculation. The principles of rehydration are the same as in the treatment of cholera patients. In case of staphylococcal poisoning, antibacterial drugs are used, but, given the anaerobic nature of the action of clostridia and the risk of developing sepsis, broad-spectrum antibiotics (tetracyclines, chloramphenicol, erythromycin) are prescribed.

The prognosis for staphylococcal poisoning is favorable. In case of poisoning with Clostridial toxins, the prognosis is serious, especially with the development of anaerobic sepsis.

Prevention consists in taking measures to reduce and eliminate staphylococcal carriage among food service workers (for the prevention and treatment of pustular skin diseases, the treatment of chronic inflammatory diseases of the nasopharynx, upper respiratory tract). Persons with pustular diseases are not allowed to work. An important factor is the proper storage of ready meals, excluding the reproduction of these staphylococci. Prevention of poisoning with Clostridium toxins consists in controlling the slaughter of livestock, as well as in observing the rules for storing, processing and transporting meat.

3. Botulism

Botulism is a severe toxic infectious disease, characterized by damage to the nervous system, mainly the medulla oblongata and spinal cord, occurring with a predominance of ophthalmoplegic and bulbar syndromes.

Etiology. The causative agent - clostridium botulism - is an anaerobic microorganism that forms spores and produces a strong toxin (a dose of 0,3 mcg is lethal for humans). There are seven antigenic types of pathogens, the antitoxins of which are specific to each type and protection against one of them does not provide protection against the effects of other types. The spores can withstand boiling for up to 5 hours (when canning food at home, the spores are preserved). Botulinum toxin, one of the most powerful natural poisons, is a toxic complex consisting of the neurotoxin itself, hemagglutinin and a non-toxic protein with unstudied biological properties. The toxin is destroyed when heated to 80 °C for 30 minutes, to 100 °C for 10 minutes.

Epidemiology. A person becomes infected when eating home canned products (mushrooms, fish, meat, etc.).

Pathogenesis. The botulinum toxin that has entered the digestive tract is not destroyed by enzymes, but is absorbed through the mucous membranes of the stomach and intestines and spreads hematogenously throughout the body. When infants are infected with botulism, the toxin is formed in the intestines, and with wound botulism, in necrotic tissues. Botulinum toxin has a selective effect on the cholinergic parts of the nervous system. The cessation of the synthesis of acetylcholine in nerve synapses leads to muscle paralysis. With paralysis of the larynx, pharynx, respiratory muscles, the act of swallowing and breathing becomes difficult, which contributes to the occurrence of aspiration pneumonia due to the addition of secondary microflora.

Clinic. The incubation period can vary from a few hours to 2-5 days. The following syndromes are defined: paralytic, gastrointestinal and general toxic. The latter does not have a bright clinical picture. Gastrointestinal syndrome is the most common manifestation of the initial stage of botulism. It is manifested by nausea, vomiting, diarrhea and lasts about a day. Neurological symptoms increase against the background of gastrointestinal syndrome, and in some patients it appears only after 1-2 days. There are general weakness, dry mouth, visual disturbances (blurred vision near, fog, grid before the eyes, diplopia). On examination, dilated pupils, their weak reaction to light, anisocoria, insufficiency of the action of any of the oculomotor muscles (with diplopia), ptosis, nystagmus are revealed. Often there is paralysis of the soft palate (speech acquires a nasal tone, when you try to swallow, the liquid pours out through the nose). Paralysis of the muscles of the larynx causes the occurrence of hoarseness and aphonia. Violation of the act of swallowing occurs due to paralysis of the muscles of the pharynx. Paresis of mimic muscles is often observed. In some cases, there are paralysis of the masticatory muscles, muscles of the neck and upper limbs. In severe cases, respiratory failure quickly sets in due to impaired activity of the respiratory muscles. Sensitivity disorders are not typical. Consciousness is completely preserved. Body temperature is not elevated. In severe forms, death occurs from respiratory arrest on the 3-5th day of illness. Complications: acute pneumonia, toxic myocarditis, sepsis, various myositis and peripheral neuritis.

Diagnosis is based on characteristic clinical symptoms.

Differential diagnosis is carried out with stem encephalitis, bulbar form of poliomyelitis, diphtheria, cerebrovascular accident, poisoning (atropine, henbane, fly agaric, ethanol, etc.), and in the presence of gastrointestinal syndrome - with gastroenteritis of another etiology. Epidemiological anamnesis is taken into account (the use of certain foods, the group nature of diseases). Laboratory confirmation of the diagnosis is retrospective. The presence of botulinum toxin or clostridia is determined in food, gastric contents, serum.

Treatment. Patients with botulism are shown washing the stomach, intestines with a 2% sodium bicarbonate solution, siphon enemas, saline laxatives (30 g of magnesium sulfate in 500 ml of water). The introduction of specific serum (A, B, E) should be carried out as soon as possible. Type A serum is administered in an amount of 10-000 IU, type B - 15-000 IU and type E - 5000 IU. The serum is preheated to 7500 ° C and injected intravenously (after a preliminary intradermal test with diluted 15: 000 serum). In severe forms of the disease, serum is administered in the same dosages intramuscularly 37-1 times with an interval of 100-1 hours. A 2% glucose solution is also prescribed s / c or / in, isotonic sodium chloride solution (up to 6 ml) , diuretics. In the case of an increase in asphyxia due to paralytic closure of the upper respiratory tract, a tracheotomy is performed. The presence of respiratory paralysis suggests that the patient must be transferred to artificial ventilation.

The prognosis is serious. Even with modern methods of therapy and diagnostics, mortality in botulism is high and amounts to 15-30%. The length of stay of the patient in the hospital is at least 1-2 months.

Prevention. Checking canned products before use, destroying bomb cans. Explanation of the rules for home canning and storage of canned food. Heating home-canned mushrooms and canned vegetables to 100 °C (for 30 minutes) before use (to destroy botulinum toxin). Persons who have eaten an infected product together with a sick person are given serums for the purpose of prevention (i.m. A, B, E, 1000-2000 IU of each type and observation is carried out for 10-12 days).

LECTURE No. 13. Cholera. Typhoid diseases. Etiology, epidemiology, clinic, diagnostics, treatment

1. Cholera

Cholera is an acute infectious disease, the epidemic spread of which is observed in the summer-autumn period. Characteristic are rapid loss of fluid as a result of profuse watery diarrhea and vomiting, and disturbances in water and electrolyte balance. Refers to particularly dangerous infections.

Etiology. The causative agent is Vibrio cholerae. It is a gram-negative, curved rod with a polarly located flagellum, providing high mobility of the pathogen. Does not form spores or capsules. It survives for a long time in open water bodies, is resistant to low temperatures, and can overwinter in frozen water sources. It quickly deactivates under the influence of disinfectants and when boiled. Under the influence of exotoxin of vibrio cholera on the epithelium of the mucous membrane of the small intestine, fluid is lost by the body. Morphological changes in epithelial cells and underlying intestinal tissues are not observed.

Pathogenesis, clinic. The incubation period varies from several hours to 5 days. The disease begins acutely, with the appearance of diarrhea and subsequent vomiting. Stools become more frequent, stools lose their fecal character and smell, and become watery. The urge to defecate is imperative; patients cannot control the act of defecation. Discharge from the intestines looks like rice water or is a liquid colored yellow or green by bile. Often the discharge contains an admixture of mucus and blood. Vomit is similar in chemical composition to intestinal secretions. It is a yellow colored liquid with no sour odor. Loss of fluid during vomiting and diarrhea quickly leads to dehydration of the body, the patient’s appearance changes, facial features become sharper, mucous membranes are dry, the voice loses sonority, normal skin turgor decreases, and it easily folds, cyanosis develops. Tachycardia, shortness of breath occur, heart sounds become muffled, blood pressure decreases, and urination decreases. Tonic spasms often appear, as well as muscle spasms of the limbs. Palpation of the abdomen reveals fluid transfusion, increased rumbling, and in some cases the sound of liquid splashing is detected. Palpation is painless. Body temperature is normal. The progression of the disease in the patient is characterized by a severe condition, which is accompanied by a decrease in body temperature to 34-35,5 ° C, extreme dehydration (patients lose 8-12% of body weight), hemodynamic disturbances, and shortness of breath. The skin color of such patients has an ashen tint, there is no voice, the eyes are sunken, the sclera is dull, and the gaze is inactive. The abdomen is retracted, there is no stool or urination. In the blood, due to the thickening of elements, high leukocytosis, an increase in the content of hemoglobin and red blood cells, the hematocrit index, and an increase in the relative density of plasma are observed.

Diagnosis of the disease in the focus in the presence of characteristic signs of the disease is not difficult. The first cases of cholera in areas where it has not previously been observed are often difficult and require mandatory bacteriological confirmation.

Treatment is carried out in a hospital, but in certain cases, for urgent reasons, it can be started at home. For patients with extreme dehydration and symptoms of hypovolemic shock (drop in blood pressure, severe tachycardia or absence of a palpable pulse, shortness of breath, cyanosis, lack of urine), to replace the volume of lost fluid and electrolytes, a warm (38-40 ° C) sterile fluid is immediately injected intravenously. saline solution of the Trisol type (1000 ml of sterile pyrogen-free water, 5 g of sodium chloride, 4 g of sodium bicarbonate, 1 g of potassium chloride). In some cases, if venipuncture is difficult, venesection is performed. During the first hour of treatment, patients with symptoms of hypovolemic shock are administered a saline solution in an amount equal to 10% of body weight (for a patient weighing 75 kg - 7,5 liters of solution), and then the patient is transferred to drip administration of the solution at a rate of 80-100 drops per hour. 1 min. The total volume of the replenished saline solution is determined by the amount of fluid released during diarrhea and vomit (for example, if 2 hours after the end of the jet administration of the solution the patient has lost 3 liters of fluid, he needs to be administered an equal amount of saline solution at the same time). In case of a pyrogenic reaction to the injected saline solution (with chills, increased body temperature), the liquid is administered more slowly and prescribed through an IV infusion system, 1-2 ml of a 2% solution of promedol and a 2,5% solution of pipolfen or 1% - solution of diphenhydramine. For more severe reactions, 30-60 mg of prednisolone is administered intravenously. When vomiting stops, patients are prescribed tetracycline 0,3 g orally 4 times a day for 5 days. Material for bacteriological analysis is taken before the antibiotic is prescribed. Cardiac glycosides, pressor amines, plasma, blood components, colloid solutions are not used to remove patients from hypovolemic shock in cholera.

The prognosis for timely treatment of patients with cholera, including those with extremely severe course, is favorable.

Prevention. If cholera is suspected, patients should be immediately hospitalized. When such patients are identified at home, in hotels and under other circumstances, the doctor, before their hospitalization, must take measures to isolate the sick from others and urgently report the disease to the chief physician of his institution. The chief physician informs the sanitary-epidemiological station and the department (city, district) of health care about the case of disease. At the same time, a list of people who have been in contact with the patient is compiled; after hospitalization of the patient, they should be placed in the department for contacts. After hospitalization, final disinfection is carried out in the room in which the cholera patient was located.

2. Typhoparatyphoid diseases

Typhoid and paratyphoid diseases (typhoid fever, paratyphoid A and B) are a group of acute infectious diseases with fecal-oral transmission caused by salmonella and similar in clinical presentation. They are manifested by fever, general intoxication, bacteremia, enlargement of the liver and spleen, enteritis and a peculiar lesion of the intestinal lymphatic apparatus. They are classified as intestinal anthroponoses. The main source of infection in recent years is considered to be chronic Salmonella bacteria carriers.

Etiology. The causative agents of the disease are several types of salmonella - Salmonella typhi, S. Paratyphi A, S. schottmulleri. Pathogens are sensitive to chloramphenicol and ampicillin. The infectious dose ranges from 10 to 000 microbial cells.

Pathogenesis. The pathogen enters the small intestine, where it causes a picture of specific enteritis. The process involves the lymphatic formations of the small intestine and mesenteric lymph nodes. From the first days of illness, pathogens can be isolated from the blood. When salmonella decompose, endotoxin is released, which causes symptoms of general intoxication and plays an important role in the genesis of small intestinal ulcers, leukopenia and can cause the development of infectious-toxic shock.

Clinic. The incubation period lasts from 1 to 3 weeks. The disease develops gradually with a typical course. Symptoms appear and increase: weakness, headache, signs of intoxication, body temperature steadily rises, reaching its highest levels by the 7-9th day of illness. Stool retention and flatulence are more common. With paratyphoid fever, symptoms of acute gastroenteritis may appear in the initial period. With paratyphoid A, symptoms of respiratory tract catarrh may occur. During the height of the disease, patients experience lethargy, headache, loss of appetite, and a slight cough. On examination, a typical typhoid exanthema is revealed. It is expressed in single roseola with a diameter of up to 3-6 mm, plus the tissue has clear boundaries. After 3-5 days, the exanthema disappears without a trace. New lesions may appear periodically. Relative bradycardia and dicrotia of the pulse, decreased blood pressure, and muffled heart sounds are noted. On auscultation, scattered dry rales are heard. The tongue is dry and has a thick brownish coating. The edges and tip of the tongue are clean, with tooth marks. The abdomen is swollen, there is a rough rumbling in the area of the cecum and pain in the right iliac region. The liver and spleen are enlarged. At the height of the disease, the number of leukocytes in the peripheral blood, especially neutrophils and eosinophils, decreases. ESR is moderately elevated (up to 20 mm/h). Urine analysis shows traces of protein.

Complications: perforation of intestinal ulcers and intestinal bleeding. Pneumonia, infectious psychosis, acute cholecystitis, and less often other complications are possible. Intestinal perforation can occur in 0,5-8% of patients during the period from the 11th to the 25th day of illness. In recent years, intestinal damage occurs against the background of normal temperature and good health of the patient, often with increased physical activity. The onset of perforation is acute: abdominal pain, muscle tension, symptoms of peritoneal irritation, free gas in the abdominal cavity, and a decrease in the size of hepatic dullness appear. These initial manifestations of perforation may vary. As a result, early diagnosis becomes difficult. If surgery is not performed within the first 6 hours, diffuse peritonitis may develop. Its signs: frequent vomiting, increased flatulence, increased body temperature, rapid pulse, increased symptoms of peritoneal irritation, the appearance of free fluid in the abdominal cavity, leukocytosis. Intestinal bleeding can coincide in timing with perforation of an intestinal ulcer and is diagnosed when an admixture of altered blood appears in the feces or according to the clinical picture of acutely developing internal bleeding.

Recurrence is possible in some cases 1-2 weeks after normalization of body temperature. Chronic bacterial carriage remains in 3-5% of recovered patients. Diagnosis of the initial period of typhoparatyphoid diseases is difficult, especially in mild and atypical cases. During this period, it is important to identify the presence of pathogens in the blood (detection using culture in bile broth, immunofluorescence method). With a typical clinical picture, diagnosis is not difficult. In later periods, stool cultures and serological methods (Vidal reaction, RNGA) can be used.

Treatment. Antibacterial therapy is prescribed (chloramphenicol 0,5-0,75 g 4 times a day until the 10-12th day of normal temperature). In severe forms, antibiotic therapy is combined with a short course (5-7 days) of glucocorticoids (prednisolone 30-40 mg/day). Pathogenetic therapy is used (vitamins, oxygen therapy, vaccine administration). Bed rest should be observed until the 7-10th day of normalization of temperature. In case of intestinal bleeding, the patient is prescribed strict bed rest, cold on the stomach, Vicasol (1 ml of a 1% solution), aminocaproic acid (200 ml of a 5% solution). In case of intestinal perforation, urgent surgical intervention is required to prevent intestinal bleeding and associated complications. Treatment for chronic bacterial carriage has not been developed.

The prognosis is favorable with timely treatment. In severe forms and the presence of complications (especially intestinal perforation), the prognosis is worse. Ability to work is restored after 1,5-2 months from the onset of the disease.

Prevention. Sanitary supervision of food and water supply. Convalescents are discharged after a triple negative bacteriological examination of stool and urine and a single examination of bile (portions B and C).

Those who have recovered from the disease are registered with the sanitary-epidemiological station for 2 years (workers of food enterprises - 6 years). Isolation of patients stops from the 21st day of normal body temperature. According to indications, specific immunization is carried out. The fireplace is subject to final disinfection.

LECTURE No. 14. Acute respiratory diseases. Flu. Parainfluenza. Etiology, epidemiology, pathogenesis, clinic, diagnostics, treatment

1. Acute respiratory diseases

Acute respiratory diseases (ARI, acute respiratory viral infections, ARVI) are widespread, characterized by general intoxication and predominant damage to the mucous membranes of the respiratory tract. They belong to anthroponotic infections with an airborne transmission mechanism. Children get sick more often. They occur as sporadic cases and epidemic outbreaks.

Etiology. ORZ are caused by:

1) influenza viruses of various antigenic types and variants;

2) parainfluenza viruses - four types;

3) adenoviruses - thirty-two types;

4) reoviruses - three types;

5) rhinoviruses - over a hundred types;

6) coronaviruses - four types;

7) respiratory syncytial virus;

8) enteroviruses - about seventy types;

9) herpes simplex virus.

The main bacterial pathogens of acute respiratory infections are opportunistic pneumotropic microorganisms (streptococci, staphylococci, mycoplasmas, chlamydia, etc.).

Pathogenesis. The entrance gates of infection are various parts of the respiratory tract, where inflammatory changes occur.

The clinic is characterized by moderately severe symptoms of general infectious intoxication, fever, syndrome of damage to the upper respiratory tract at various levels and local inflammatory changes in the form of rhinitis, pharyngitis, laryngitis, tracheitis, bronchitis and their combinations. The localization of the most pronounced changes in the respiratory tract depends on the type of pathogen. For example, rhinoviral diseases are characterized by a predominance of rhinitis, adenoviral diseases - nasopharyngitis, parainfluenza is manifested by a predominant lesion of the larynx, influenza - the trachea, respiratory syncytial viral disease - the bronchi. Some etiological factors, in addition to damage to the respiratory tract, lead to other symptoms. The consequence of adenoviral diseases can be conjunctivitis and keratitis, with enteroviral diseases - signs of epidemic myalgia, herpangina, exanthema. The duration of acute respiratory infections not complicated by pneumonia usually ranges from 2-3 to 5-8 days. If there are inflammatory changes in the lungs, the disease may drag on for 3-4 weeks.

Rhinitis is subjectively felt in the form of a runny nose, a feeling of nasal congestion and itching, and sneezing. Rhinoscopy reveals hyperemia, swelling of the nasal mucosa, the presence of serous, mucous or mucopurulent discharge in the nasal passages. Pharyngitis is manifested by dryness, sore throat, coughing, and pain when swallowing. Pharyngoscopy reveals hyperemia of the mucous membrane of the posterior and lateral walls of the pharynx, mucous or mucopurulent discharge along the posterior wall of the pharynx, hyperplasia or hypertrophy of the tonsils. Hyperemia, granularity and injection of blood vessels in the mucous membrane of the soft palate are typical. Laryngitis is characterized by complaints of hoarseness, a rough, “barking” cough, soreness and soreness in the throat, which worsens with coughing. Laryngoscopy reveals diffuse hyperemia of the laryngeal mucosa, hyperemia and infiltration of the vocal cords, incomplete closure of the vocal cords during phonation, and the presence of viscous mucus in the larynx. Tracheitis is characterized subjectively by the patient as rawness and burning behind the sternum, aggravated by coughing. The cough at the beginning of the disease is dry, unproductive and painful, not bringing relief to the patient; after a while, sputum appears. When auscultating hard breathing, wheezing may be heard, which quickly disappears when coughing up sputum. Bronchitis is characterized by the presence of a dry or wet cough with the discharge of mucous or mucopurulent sputum. On auscultation, harsh breathing and moist or dry rales are heard throughout all lung fields. An X-ray examination of the chest organs can detect an increase in the pulmonary pattern.

Differential diagnosis of acute respiratory infections is difficult; therefore, in the work of a practicing physician, the etiological characteristics of the disease often remain undisclosed. During epidemic outbreaks, the characteristic clinical picture suggests the presence of the disease. Confirmation of the diagnosis is an increase in the titer of specific antibodies in paired sera. The first serum is taken before the 6th day of illness, the second - after 10-14 days.

The diagnosis is confirmed by an increase in titers by 4 times or more. Use RSK and RTGA. Detection of pathogens using the immunofluorescent method is a quick method for deciphering the etiology of diseases. Similar clinical manifestations of past diseases leave behind only type-specific immunity. Because of this, the same person can endure acute respiratory infections 5-7 times during the year. This is especially true in children's groups.

Treatment. For uncomplicated acute respiratory infections, patients are treated at home. Hospitalization is subject to patients with severe and complicated forms of the disease, as well as persons from organized groups. Antibacterial drugs are prescribed only with the addition of a bacterial infection and the presence of microbial complications (otitis media, pneumonia, sinusitis, etc.). During the febrile period, the patient must comply with bed rest. Vitamin therapy is prescribed (vitamin C - up to 300 mg). To reduce cough use steam inhalation, expectorants. With severe rhinitis, galazolin, naphthyzin, sanorin, etc. are instilled into the nose. If necessary, other symptomatic agents are prescribed. You can use antigrippin, which is a complex of symptomatic drugs. In severe forms of the disease, it is possible to administer normal human immunoglobulin (gamma globulin) in the first days of the disease, 6 ml o/w. With the development of false croup syndrome in children, it is necessary to moisten the air in the room (hang wet sheets, put dishes with warm water), apply warm or hot compresses to the neck area.

The prognosis is favorable. The average duration of disability is 5-7 days.

Prevention. Isolation of the patient from others, the allocation of individual dishes that should be disinfected. Activities in the foci of infection are the same as with influenza. Preventive measures also include hardening, restorative procedures, a full-fledged summer vacation, a healthy lifestyle (observance of the daily routine, regular walks, age-appropriate sleep, eating fresh fruits, garlic and onions).

2. Flu

Influenza is an anthroponotic disease of a viral nature. It is characterized by an acute onset, fever, symptoms of general intoxication and damage to the respiratory tract, and is transmitted by airborne droplets.

Etiology. The causative agents of influenza are RNA viruses that belong to the orthomyxovirus family, which includes the genus of influenza A viruses, the genus of influenza B and C viruses. Influenza A viruses are divided into many serotypes. New antigenic variants are constantly emerging. The influenza virus has a spherical shell covered with spines formed by two glycoproteins: neuraminidase, which is a protein enzyme that facilitates the penetration of the virus into the host cell, and hemagglutinin, a protein. The influenza virus is quickly killed by heating, drying and under the influence of various disinfecting agents.

Pathogenesis. The portal of infection is the upper parts of the respiratory tract. The influenza virus selectively infects the columnar epithelium of the respiratory tract, especially the trachea. By multiplying in columnar epithelial cells, it causes their degenerative changes, using the contents of epithelial cells to build new viral particles. Also, the release of mature viral particles is accompanied by the death of epithelial cells, and necrosis of the epithelium and the associated destruction of the natural protective barrier leads to viremia. The toxins of the virus, together with the decay products of epithelial cells, have a toxic effect on the cardiovascular, nervous and other systems of the body. Damage to various organs and systems during influenza is often caused by circulatory disorders, which are the result of disturbances in the tone, elasticity and permeability of the vascular wall. Increased permeability of vessel walls leads to impaired microcirculation and the occurrence of hemorrhages (hemoptysis, nosebleeds, hemorrhagic pneumonia). Flu helps reduce immunological reactivity. This leads to an exacerbation of various chronic diseases - rheumatism, chronic pneumonia, pyelitis, cholecystitis, dysentery, toxoplasmosis, as well as the occurrence of secondary bacterial complications. The virus persists in the patient’s body for 3-5 days from the onset of the disease, and when complicated by pneumonia - up to 10-14 days.

Epidemiology. The disease is ubiquitous. The reservoir of infection is a sick person who is dangerous to others from the end of the incubation period and the entire febrile period. The incubation period lasts from 12 to 48 hours. The route of transmission is airborne. Susceptibility to influenza is universal. After an infection, type-specific immunity is formed. Classification: typical course and atypical course; according to the severity of the course: mild, moderate, severe forms.

Clinic. A typical flu begins acutely, often with chills or chills, the body temperature rises rapidly, and already on the first day the fever reaches its maximum level (38-40 ° C). There are signs of general intoxication (weakness, weakness, sweating, muscle pain, severe headache, eye pain) and symptoms of respiratory tract damage (dry cough, sore throat, rawness behind the sternum, hoarseness). Examination reveals flushing of the face and neck, injection of scleral vessels, increased sweating, bradycardia, and a decrease in blood pressure. Revealed the defeat of the upper respiratory tract in the form of rhinitis, pharyngitis, laryngitis, tracheitis. The trachea is more commonly affected, while rhinitis may be absent. Characterized by hyperemia and a kind of granularity of the mucous membrane of the pharynx. The tongue is coated, there may be a short-term liquid stool. Complications from the side of the central nervous system are expressed in the form of meningism and encephalopathy. Characterized by leukopenia, neutropenia, ESR in normal cases is not increased. Mild forms of influenza can sometimes occur without fever (afebrile form of influenza). Complications are associated with the addition of bacterial flora (pneumonia, frontal sinusitis, sinusitis, otitis media, sinusitis, toxic myocarditis).

Diagnostics. During an influenza epidemic, diagnosis is not difficult. In inter-epidemic times, this disease is rare and occurs in the form of mild and erased forms. In these cases, influenza is difficult to distinguish from acute respiratory infections of other etiologies. To confirm the diagnosis of influenza, the detection of the virus in the material from the pharynx and nose, as well as the detection of an increase in the titer of specific antibodies in the study of paired sera, is used: the first serum is taken before the 6th day of the disease, the second after 10-14 days. Diagnostic is the increase in antibody titers by 4 times or more.

Treatment. Patients with influenza are treated at home. Patients with severe forms of influenza, with complications and severe concomitant diseases, as well as for epidemiological indications (from hostels, boarding schools, etc.) are sent for inpatient treatment. Those being treated at home are placed in a separate room or isolated from others using a screen. For them, separate dishes are allocated, which are disinfected with boiling water. Persons caring for the patient should wear a four-layer gauze mask and change it every 4 hours. During the febrile period, the patient is recommended to rest in bed and drink plenty of alkaline fluids.

To prevent complications, especially for older people with high blood pressure, it is necessary to include in the diet green tea, chokeberry jam or juice, citrus fruits, as well as P vitamins (rutin) in combination with 500 mg of ascorbic acid per day. An effective remedy is anti-influenza donor gamma globulin, which is used for severe forms of influenza in the earliest stages (adults 6 ml, children 0,15-0,2 ml/kg). You can use normal human immunoglobulin, which is administered intramuscularly in the same doses. Antibacterial therapy is indicated only for complications. Synthetic penicillins and broad-spectrum drugs are most often used. Pathogenetic and symptomatic drugs are widely used. To reduce headaches and muscle pain, analgesics and others are used. Antihistamines (pipolfen, suprastin, diphenhydramine) have a therapeutic effect to relieve sensitization. To improve the drainage function of the bronchi, alkaline inhalations, expectorants and bronchodilators are used.

For symptoms of rhinitis, naphthyzin, galazolin, sanorin, etc. are used topically. Cupping and mustard plasters are prescribed for convalescents. In extremely severe, hypertoxic forms of influenza (with a temperature above 40 °C, shortness of breath, cyanosis, severe tachycardia, decreased blood pressure), patients are treated in intensive care wards with detoxification therapy. These patients are injected intramuscularly with anti-influenza immunoglobulin (6-12 ml), and broad-spectrum antibiotics are prescribed (oxacillin, methicillin, ceporin 1 g 4 times a day). A mixture containing 2-200 ml of hemodez or 300% glucose solution, 40-0,25 ml of 0,5% strophanthin solution, 0,05 ml of 2% Lasix solution is administered 1 times a day intravenously. 250-300 mg of prednisolone, 10 ml of 2,4% aminophylline solution, 10 ml of 5% ascorbic acid solution, 10 ml of 10% calcium chloride solution, 400 ml of rheopolyglucin, 10-000 units of contrical. If breathing becomes more frequent (more than 20 respiratory movements per minute), or breathing rhythm disturbances occur, the patient is transferred to artificial ventilation.

Forecast. With influenza without complications, the ability to work is restored after 7-10 days, with the addition of complications - not earlier than 3-4 weeks. The prognosis for life is favorable, severe forms with encephalopathy or pulmonary edema are extremely rare, while patients (usually during epidemics) are hospitalized.

Prevention of influenza is carried out using specific vaccine prophylaxis. Vaccination with live (intranasal) or inactivated (intradermal and subcutaneous) vaccines is used. Vaccination should precede the onset of an influenza epidemic, since vaccines are created based on the circulating influenza viruses in a given season. Special vaccines are used for children of different age groups, adults and the elderly. Sometimes the reaction to the vaccine occurs in the form of short-term malaise and low-grade fever. It is much milder than the disease, and you should not be afraid of it. The formation of immunity occurs only against influenza, so a child who has been vaccinated may well become ill with another viral disease. All people sick with the flu should be isolated from healthy people, the room where the patient is located should be ventilated, and wet cleaning should be carried out regularly. Anyone who is in contact with a person with the flu is recommended to instill interferon into the nose for a week; you can give aflubin, ascorbic acid or dibazole. Adults are recommended to take rimantadine in appropriate dosages. Children over 1 year of age can be prescribed Algirem. To prevent influenza A, you can use rimantadine, which is given throughout the epidemic outbreak. Current and final disinfection is carried out in the fireplace (dishes are doused with boiling water, laundry is boiled). Isolate the patient from others, allocate individual dishes, which should be scalded with boiling water.

3. Parainfluenza

Parainfluenza is a disease of the respiratory tract, characterized by moderate intoxication with a primary lesion of the mucous membranes of the nose and larynx.

Etiology. Viruses belong to the paramyxovirus family. They are distinguished from influenza viruses by the stability of the antigenic structure and the absence of visible variability in the virion genome.

Epidemiology. The highest incidence is recorded in children of the first 2 years of life, which can be explained by the narrow lumen of the larynx, looseness of the submucosal layer in the subglottic space, children over 7 years of age rarely get parainfluenza. The factors predisposing to the development of croup syndrome include lymphatic-hypoplastic diathesis. The source of infection is a sick person who is dangerous during the entire period of illness (up to 10 days). The route of transmission is airborne. The incubation period is from 2 to 7 days.

Pathogenesis. The entrance gates of infection are the mucous membranes of the nose, pharynx, larynx, where inflammatory changes occur. The virus reproduces in the epithelial cells of the respiratory tract, destroying the cells. Viruses and decay products of epithelial cells partially penetrate the bloodstream, which contributes to the development of fever and intoxication.

Clinic. The disease begins gradually with an increase in body temperature to 38 ° C, the appearance of hoarseness, and persistent cough, which occurs with the development of laryngeal stenosis. Stenosing laryngotracheitis is manifested by a triad of symptoms: a rough, “barking” cough, noisy stenotic breathing, and a hoarse voice. Croup syndrome can occur with all acute respiratory viral infections. It occurs due to swelling and inflammatory changes in the airways, preglottic space and vocal cords, which leads to a narrowing of the lumen of the larynx. Laryngeal stenosis develops acutely, usually at night. The child wakes up with a rough “barking” cough, noisy breathing, and becomes restless and frightened. There are four degrees of laryngeal stenosis. I degree laryngeal stenosis is manifested by a rough, “barking” cough, hoarseness, and inspiratory shortness of breath during physical exertion. II degree laryngeal stenosis is manifested by pallor of the skin, perioral cyanosis, and tachycardia. Children are restless, excited, noisy breathing with retraction of the jugular fossa and auxiliary respiratory muscles, a rough, “barking” cough, a hoarse voice. III degree laryngeal stenosis is manifested by respiratory failure, cyanosis of the lips, acrocyanosis, pallor of the skin, and sweating. Breathing is noisy with a sharp retraction of the compliant areas of the chest.

Children are restless, rush about, feel a sense of fear. Heart sounds are muffled, tachycardia. Stenosis of the larynx of the IV degree (asphyxia) is manifested by the serious condition of the patient, the skin is pale gray, cyanotic, the extremities are cold. Breathing is frequent, shallow, periodically with deep breaths, apnea, bradycardia. Consciousness is absent, death from asphyxia may occur.

Treatment. Etiotropic therapy, sedative therapy, hormonal therapy, desensitizing therapy, infusion therapy, symptomatic therapy. Inhalation, physiotherapy. Nasotracheal intubation is possible.

LECTURE No. 15. Adenovirus infection. RS infection. Rhinovirus infection. Etiology, epidemiology, clinic, diagnostics, treatment

1. Adenovirus infection

Adenovirus infection is an acute respiratory disease characterized by fever, moderate intoxication, severe exudative lesions of the mucous membranes of the respiratory tract, often the conjunctiva of the eyes, and lymphoid tissue.

Etiology. Virions of adenoviruses have a diameter of 70-90 nm, contain double-stranded DNA covered with a capsid. Epidemiology: the focus of infection are patients with clinically pronounced or erased forms of the disease. The virus is excreted in the acute period of the disease with nasal or nasopharyngeal mucus, and at a later date with feces.

The transmission of the disease is airborne. With adenovirus infection, the main clinical syndromes are distinguished: pharyngoconjunctival fever, tonsillopharyngitis, catarrh of the upper respiratory tract, keratoconjunctivitis, diarrhea, swollen lymph nodes. According to severity, mild, moderate, severe forms are distinguished. By the nature of the course - without complications, with complications.

Pathogenesis. The entry point for infection is the mucous membranes of the upper respiratory tract. Adenoviruses multiply in the mucous membrane with gradual involvement of the descending parts of the respiratory tract in the pathological process. Reproduction of the virus can occur in intestinal tissue and lymph nodes. Reproduction in lymphoid tissue is accompanied by multiple enlargement of lymph nodes. The ability of adenoviruses to reproduce in epithelial cells of the respiratory tract, conjunctiva, and intestines with the occurrence in some cases of hematogenous dissemination creates a wide range of clinical manifestations of this infection, including the manifestation of generalized lymphadenopathy and widespread exanthema.

Clinic. The predominant season is the summer-autumn period. The incubation period is 5-8 days. The onset of the disease is acute, with a characteristic combination of exudative inflammation of the mucous membranes of the oropharynx, eyes with systemic enlargement of the lymph nodes. Characterized by hyperemia of the pharynx with the development of acute tonsillitis, diarrhea is possible.

2. Rs-infection

Rs-infection is an acute viral disease that occurs with a predominant lesion of the lower respiratory tract with frequent development of bronchitis, bronchiolitis. Rs-viruses are considered the main cause of broncho-obstructive syndrome in children of the first year of life. The causative agent is a respiratory syncytial RNA virus.

Epidemiology. The source of infection is a sick person at the beginning and at the height of the disease. The disease is transmitted by airborne droplets.

Pathogenesis. Inflammatory changes develop on the mucous membrane of the nose and pharynx. In children under the age of one year, bronchithiols and lung parenchyma are usually affected with the presence of necrosis of the tracheobronchial epithelium and necrotizing obstructive bronchiolitis, which leads to blockage of the bronchi. The resulting spasm leads to the formation of atelectasis and emphysema. These phenomena contribute to the development of viral-bacterial pneumonia. Seasonality for this disease is the cold season. The incubation period lasts 3-6 days. The distal parts of the respiratory tract are affected with a pronounced bronchospastic component, duration is 2-3 weeks. Characterized by a persistent paroxysmal cough, first dry, then productive. Respiratory failure appears, often complicated by bacterial pneumonia.

3. Rhinovirus infection

Rhinovirus infection is an acute viral disease of the respiratory tract, occurring with a predominant lesion of the nasal mucosa. The causative agent is an RNA-containing virus.

Epidemiology. The source of infection is patients and virus carriers. The virus is shed in the nasal secretion at the end of the incubation period and throughout the acute period of the disease. The route of transmission is airborne, possibly through infected objects. Seasonality is autumn-winter, the incubation period is 1-3 days.

Clinic. Rhinitis with profuse serous and later mucous discharge.

Diagnostics includes express methods for detecting pathogens in various biological environments of the body, isolation and identification of pathogens, as well as serological studies.

Treatment. Correct treatment regimen, rational therapeutic nutrition, vitamin therapy, antiviral therapy (leukocyte interferon, arbidol, amiksin, influenza, viferon, immunoglobulins), antibacterial therapy. Pathogenetic therapy: detoxification therapy, improvement of microcirculation, bronchodilators, correction of the body's defenses, symptomatic therapy, antipyretic therapy, antitussive and expectorant drugs. Physiotherapeutic treatment. Rehabilitation and medical examination of those who have recovered from the disease.

LECTURE № 16. Acute and chronic viral hepatitis. Etiology, pathogenesis, clinic, differential diagnosis, treatment

1. Viral hepatitis

Viral hepatitis (Botkin's disease) is a disease of a viral nature that occurs with symptoms of general intoxication and a predominant lesion of the liver. These include viral hepatitis A, viral hepatitis B, hepatitis C, hepatitis D. Acute hepatitis is an inflammatory disease of the liver. The introduction of the hepatitis A virus occurs through the mucous membranes of the gastrointestinal tract. The hepatitis B virus enters the body during transfusion of blood or blood products (except for albumin and donor immunoglobulin), during medical manipulations, tattoos, contacts with blood (from surgeons, laboratory assistants); there is sexual transmission of the infection.

Etiology. The hepatitis A virus is built from protein subunits that form a cavity in which a single-stranded RNA molecule with a diameter of 28 nm is tightly packed. The virus persists for a long time in water, soil and on household items. The virus is resistant to ether, acids, chlorine, sensitive to formaldehyde, and is inactivated by boiling within 5 minutes. It is excreted in feces from the end of the incubation period and during the pre-icteric period. With the onset of jaundice, the virus cannot be detected in the stool. Hepatitis B virus is a complex virus from a non-taxonomic group; a DNA-containing virus primarily affects liver cells. The virus has a double-stranded DNA polymerase, which is necessary for completing the internal DNA chain, and antigens (surface, core, infectious). The virus is stable in the external environment, persists at room temperature for up to 6 months, can withstand heating up to 60 °C for up to 10 hours. It loses the ability to cause infection at a temperature of 120 °C after 45 minutes, sterilization with dry steam at a temperature of 180 °C - within 60 min, boiling for 30 minutes. It is insensitive to acidic pH values, but is destroyed in an alkaline environment. Hydrogen peroxide, UV irradiation, chloramine, formalin, phenol have a detrimental effect on the virus; the virus is resistant to chemical factors. The virus can persist in the human body for several years.

The most common acute liver injury in humans occurs with viral hepatitis. Acute hepatitis can be caused by enteroviruses, intestinal microbes, the causative agent of infectious mononucleosis, and septic bacterial infection. There are also acute toxic drug-induced hepatitis caused by MAO inhibitors, hydrazine derivatives, PAS, isonicotinic acid derivatives, male fern extract and other industrial poisons (phosphorus, organophosphorus insecticides, trinitrotoluene, etc.), mushroom poisons of inedible mushrooms (muscarine, aflatoxin, etc. .). Acute hepatitis can occur as a result of radiation injury, with extensive burns of the body, severe infectious diseases, and toxicosis of pregnant women.

The pathogenesis consists in the direct impact of a damaging factor on the hepatic parenchyma or in immunological disorders that occur in response to a primary liver lesion, followed by cytolysis of affected and intact hepatocytes. In some cases, disturbances in blood flow in the liver and intrahepatic cholestasis are important.

Clinic. The incubation period for viral hepatitis A can range from 7 to 50 days (usually 15-30 days), for hepatitis B - from 50 to 180 (usually 60-120 days). Viral hepatitis can have icteric, anicteric and subclinical forms. The duration of viral hepatitis is divided into acute (up to 3 months), protracted (3-6 months) and chronic (over 6 months). The development of the disease is gradual, the pre-icteric period lasts 1-2 weeks. There are influenza-like, dyspeptic, asthenovegetative and arthralgic variants of the pre-icteric period. At the end of it, the urine darkens, the feces become discolored, an enlargement of the spleen is observed, and the activity of liver enzymes increases, especially ALT. During the icteric period, patients experience general weakness, nausea, loss of appetite, dull pain in the liver area, and itchy skin. Jaundice may increase, but this is not a criterion for the severity of the disease; there may be severe forms with slight jaundice. The severity is determined by the severity of intoxication symptoms. Often not only the liver is enlarged, but also the spleen. With viral hepatitis A, the icteric period lasts 7-15 days, and recovery occurs within 1-2 months. Viral hepatitis B can have a protracted and chronic course. With hepatitis B, the development of acute liver failure (hepatic coma, hepatic encephalopathy) may occur. Signs of increasing liver failure: memory impairment, increased general weakness, dizziness, agitation, increased jaundice, increased vomiting, decreased liver size, the appearance of hemorrhagic syndrome, ascites, fever, neutrophilic leukocytosis, decreased cholesterol levels (below 2,6 mmol/l, coefficient esterification below 0,2, sublimate titer less than 1,4, prothrombin index below 40%, fibrinogen below 2,93 µmol/l, platelets less than 10 x 106 µmol/l. In mild cases, acute hepatitis is practically asymptomatic, being detected only by chance examination. In more severe cases (with toxic hepatitis), clinical symptoms of the disease develop quickly, simultaneously with signs of general intoxication and toxic damage to other organs and systems. The height of the disease is characterized by icteric staining of the skin and mucous membranes, whitish-clay color of stool, deep dark color (beer-colored) urine, hemorrhagic phenomena, orange or saffron-colored skin. In mild cases, jaundice is visible only in daylight; icteric staining of the sclera and mucous membrane of the soft palate appears most early. Sometimes nosebleeds and petechiae appear. Patients are concerned about skin itching, bradycardia, depressed mental state, increased irritability, insomnia and other signs of damage to the central nervous system. Enlargement of the liver and spleen is slightly painful on palpation.

Diagnostics. Based on clinical, epidemiological and laboratory data, hyperbilirubinemia (100-300 μmol / l or more), an increase in the activity of a number of serum enzymes (aldolase, aspartate aminotransferase and especially alanine aminotransferase (significantly above 40 units), lactate dehydrogenase), hypoalbuminemia, hyperglobulinemia are detected. Indicators of protein-sedimentary samples (thymol, sublimate, etc.) are deviated from the norm. One of the functions of the liver is disturbed - the production of fibrinogen, prothrombin, coagulation factors VII, V, as a result of which hemorrhagic manifestations appear. Laboratory confirmation of the diagnosis is an immunofluorescent method, by which antibodies to the hepatitis A virus are detected in the patient's blood serum. In hepatitis B, detection of the surface antigen of the hepatitis B virus or antibodies to it is of diagnostic importance.

Differential diagnosis is carried out with liver damage in other infections (leptospirosis, infectious mononucleosis, pseudotuberculosis, salmonellosis, ornithosis, sepsis), with toxic hepatitis (poisoning with carbon tetrachloride, dichloroethane), drug-induced jaundice (from chlorpromazine, anti-tuberculosis drugs, etc.), hemolytic and mechanical jaundice, functional hyperbilirubinemia (Gilbert syndrome, Dubin-Johnson syndrome). Of great importance are a thorough history taking, identification of possible professional or domestic intoxications, the epidemiological situation when a disease is detected and its cause is identified. In unclear cases, the presence of viral hepatitis should be assumed. The determination of the so-called Australian antigen is a marker for serum hepatitis B (it is also detected in virus carriers). Mechanical (subhepatic) jaundice usually occurs with cholelithiasis as a result of blockage of the common bile duct by a stone. But in this case, before the appearance of jaundice, an attack of biliary colic occurs. Direct bilirubin is found in the blood, the stool is discolored. With hemolytic adrenal jaundice, free (indirect) bilirubin is present in the blood, the color of the stool is normal, and the osmotic resistance of red blood cells is usually reduced. With false jaundice (due to staining of the skin with carotene during prolonged and abundant consumption of oranges, pumpkins, carrots), the sclera are usually not stained, hyperbilirubinemia is absent.

Treatment. Hospitalization in special departments of infectious diseases hospitals is mandatory, and sanitary and epidemiological measures are carried out at the source of infection. Prescribe bed rest, a gentle diet with limited fat and increased carbohydrate content, and a large amount of fruit juices. The basis of treatment is gentle treatment and nutrition (table No. 5). Liquid - up to 2-3 liters per day in the form of juices, alkaline mineral waters. A complex of vitamins is prescribed. For moderate forms, it is advisable to administer 5% glucose solution and Ringer-Locke solution 250-300 ml intravenously. In severe cases, hemodez or rheopolyglucin 200-400 ml are administered intravenously, and treatment continues in intensive care wards. A 10% glucose solution (up to 1 l/day), Lobari solution is administered intravenously (1 l of pyrogen-free water contains 1,2 g of potassium chloride, 0,8 g of magnesium sulfate, 0,4 g of calcium chloride and 100 g glucose) up to 1-1,5 l/day. In case of acute liver failure, prednisolone is administered (IV or IM 60-90 mg/day. A 20% sorbitol solution (250-500 ml/day), a 15% albumin solution (200-300 ml) is used. /day), 2-3 units of contrical (trasylol) are administered intravenously 10-000 times a day. To suppress opportunistic intestinal microflora, neomycin 30 g 000 times a day or kanamycin 1 is taken orally g 4 times a day. A siphon enema is done daily with a 0,5% sodium bicarbonate solution. An exchange blood transfusion is recommended. Hyperbaric oxygenation with a session regimen of 4 to 2 atm, lasting 1,5 minutes, as well as hemosorption using activated carbon. In severe cases, detoxification therapy is carried out.

The prognosis is determined by the etiology of the disease, the severity of liver damage, and the timeliness of the treatment started. The prognosis for life is generally favorable. After the transfer of hepatitis B, in some cases, the development of chronic hepatitis and cirrhosis of the liver is possible.

Prevention of acute hepatitis consists in observing the rules of personal hygiene, carrying out sanitary and epidemiological measures, ensuring appropriate sanitary and technical supervision at enterprises, which prevents the possibility of industrial poisoning with hepatotropic poisons. Do not eat unknown mushrooms. For the prevention of viral hepatitis B, it is necessary to examine donors (persons with the presence of an antigen to the hepatitis B virus or antibodies to it in the blood are excluded), careful processing of instruments is necessary.

2. Chronic hepatitis

Chronic hepatitis is a polyetiological liver disease of a chronic nature, expressed in inflammatory-dystrophic changes with moderate fibrosis and generally preserved lobular structure of the liver, occurring without positive dynamics for at least 6 months. Clinically, chronic hepatitis is characterized by asthenovegetative, dyspeptic syndromes, an increase in liver size, impaired liver function, morphological persistence of necrosis, an inflammatory process, and the development of fibrosis while maintaining the overall structure of the liver.

Etiology. The most important are the viral, toxic and toxic-allergic occurrence of liver damage.

Pathogenesis. The direct impact of an etiological factor (virus, hepatotoxic substance) on the liver parenchyma causes degeneration and necrobiosis of hepatocytes and reactive proliferation of mesenchyme. One of the mechanisms for the transition of acute viral and toxic hepatitis into a chronic form and further progression of the process has an immunological specific nature.

Clinic. Pain in the liver of a dull nature, constant. There is an increase in the liver, pain or a feeling of heaviness, fullness in the right hypochondrium, dyspepsia, less often jaundice, pruritus, low-grade fever are detected. Enlargement of the liver, enlargement of the spleen is absent (or it is slightly enlarged). Lethargy, fatigue, decreased appetite, belching, nausea, poor fat tolerance, flatulence, unstable stools, general weakness. The skin is pale, dryish, sometimes in some patients mild (subicteric sclera and palate) or moderate jaundice is detected.

Diagnostics. Based on clinical and laboratory data, moderate hyperbilirubinemia is determined. Positive results of protein-sedimentary tests - thymol, sublimate, etc. In the blood serum of patients, the content of aminotransferases (ALAT, AST and LDH) is increased, with difficulty in the outflow of bile - alkaline phosphatase. Ultrasound of the liver and scanning of the liver can determine its size. In hepatitis, sometimes there is a reduced or uneven accumulation of the radioisotope in the liver tissue, in some cases there is an increased accumulation in the spleen. Methods of laparoscopy and puncture biopsy of the liver make it possible to more accurately differentiate these two forms of hepatitis and distinguish them from other liver diseases.

Treatment. Compliance with a diet with the exception of hot, spicy seasonings, refractory animal fats, fried foods, excess meat dishes. It is recommended to use cottage cheese (daily up to 100-150 g), mild cheeses, boiled fish and meat, bread. With toxic and toxic-allergic hepatitis, it is extremely important to completely stop contact with the corresponding toxic substance. The use of hepatoprotectors (Karsila, Essentiale, etc.), cytostatics, antiviral drugs, immunocorrectors.

LECTURE No. 17. Parasitic diseases. Epidemiology, clinic, treatment

1. Helminthiases

Helminthiases are diseases caused by parasitic worms (helminths) and their larvae that have settled in the body.

Classification of helminthiases

According to the biological principle: nematodoses (roundworms), cestodoses (tapeworms), trematodoses (flukes).

According to the epidemiological: geohelminthiases, biohelminthiases, contact.

2. Ascariasis

The causative agent is the roundworm, which parasitizes in the adult stage in the small intestines. The lifespan of roundworms is about a year. In the migratory stage (the first 6-8 weeks after infection), roundworm larvae have a mechanical and sensitizing effect, causing hemorrhages and eosinophilic infiltrates in the tissues of various organs. In the intestinal phase (8 weeks after infection), adult roundworms cause general toxic-allergic and neuro-reflex reactions of the body and a variety of local mechanical effects.

Clinic. The migratory phase often proceeds under the guise of acute respiratory infections, bronchitis (with malaise, dry cough or scanty sputum, subfebrile temperature, dry and moist rales in the lungs).

Urticaria, vesicular rash on the hands and feet may occur, volatile eosinophilic infiltrates in the lungs are possible. In the intestinal phase, the gastrointestinal form is distinguished (the main symptoms are salivation, nausea, loss of appetite, cramping pains around the navel, sometimes disorders of the stool and gastric secretion), hypotonic (decrease in blood pressure, weakness) and neurological (the main symptoms are dizziness, headache, fatigue, sleep disturbance, vegetative-vascular disorders) forms.

Complications. Ascariasis intestinal obstruction, ascariasis appendicitis, perforative peritonitis, liver ascariasis with the development of jaundice, subdiaphragmatic abscess, pancreatic ascariasis with symptoms of acute pancreatitis, creeping of ascaris into the respiratory tract with the development of asphyxia.

The diagnosis is made on the basis of laboratory data, based on the detection of nematode larvae in sputum and antibodies in the blood, in the late intestinal phase - roundworm eggs in feces.

Treatment. For the expulsion of young individuals and adult roundworms, piperazine, levamisole, and combantrin are used. Piperazine is taken after meals 2 times a day with an interval between doses of 2-3 hours for 2 days in the amount of 1,5-2 g per dose (3-4 g / day). The effectiveness of therapy increases when taking piperazine after dinner at night.

Levamisole (Decaris) is prescribed after meals at a dose of 150 mg once, it is also recommended to take combantrin once after meals at a rate of 10 mg/kg. Oxygen treatment is carried out on an empty stomach or 3-4 hours after a meal for 2-3 days in a row.

The prognosis in the absence of complications is favorable.

Prevention. It is necessary to conduct a mass examination of the population, identify and treat all those infected with ascariasis, as well as protect the soil of vegetable gardens and orchards from contamination with feces. Thorough washing under running water and scalding vegetables and fruits with boiling water. Compliance with personal hygiene measures.

3. Alveococcosis

Etiology, pathogenesis. The causative agent is the larval stage of alveococcus. Infection occurs when oncospheres enter the mouth after contact with contaminated skins of foxes, arctic foxes, dogs, with water from stagnant bodies of water and by eating wild berries collected in endemic areas. The larvae (usually in the liver) infiltrate tissues and grow into them, thereby disrupting the blood supply to organs and causing degenerative and atrophic changes in them.

Clinic. The disease remains asymptomatic for a long time, there is a progressive enlargement of the liver, heaviness and pressure appear in the right hypochondrium, dull aching pain. After a few years, the liver becomes bumpy and very dense. Jaundice may develop, sometimes the spleen is enlarged. With the disintegration of the nodes, the body temperature rises, sweating is observed.

The diagnosis is made on the basis of laboratory data (leukocytosis, eosinophilia, increased ESR, hyperproteinemia, hypergammaglobulinemia). Put serological reactions with alveococcal antigen. To clarify the localization, X-ray and ultrasound examinations, as well as liver scans, and computed tomography are used. Trial puncture is not performed due to the risk of infection of other organs.

Differential diagnosis is carried out with tumor processes, echinococcosis and cirrhosis of the liver.

Methods of treatment: surgical and symptomatic.

4. Ankylostomiasis (ankylostomiasis and necatoriasis)

Etiology, pathogenesis. The causative agents are hookworm and necator, which parasitize the human small intestine, mainly in the duodenum. Invasion occurs when larvae enter through the skin or through food with contaminated vegetables, fruits, and water. The larvae migrate for 7-10 days through the systemic and pulmonary circulation. In the small intestine they turn into sexually mature individuals and after 4-6 weeks begin to lay eggs. Hookworms can live from several months to 20 years. During the migration of larvae, toxic-allergic changes occur in the body. Adult helminths are hematophagous. When fixed to the intestinal mucosa, they injure tissues, lead to the formation of hemorrhage, cause bleeding, anemia, support the state of allergies, gastrointestinal dyskinesia and dyspepsia.

Clinic. Skin itching and burning, asthmatic phenomena, fever, eosinophilia. In the late stage, nausea, hypersalivation, vomiting, abdominal pain, intestinal disorders (constipation or diarrhea), flatulence join.

The diagnosis is confirmed as a result of the detection of eggs of the pathogen in the feces and sometimes in the intestinal contents.

Treatment. For deworming use combantrin or levamisole. With symptoms of anemia (hemoglobin below 67 g / l), iron preparations, red blood cell transfusions are used.

The prognosis is favorable in most cases.

Prevention. In the foci of ankylostomiasis, you can not walk without shoes and lie on the ground without bedding. It is necessary to thoroughly wash and scald fruits, vegetables, berries with boiling water before use, water for drinking must be boiled.

5. Diphyllobothriasis

Etiology, pathogenesis. The causative agent is the broad tapeworm. Its lifespan can be several decades. A person becomes infected by eating fresh, insufficiently salted caviar and raw fish (pike, perch, omul, etc.). The parasite attaches to the intestinal mucosa with its bothria, injuring it. Clusters of tapeworms can close the intestinal lumen. The waste products of the helminth sensitize the body.

Clinic. Characterized by nausea, weakness, dizziness, abdominal pain, unstable stool, excretion of scraps of strobilus during defecation.

The diagnosis is confirmed by the detection of lentelets eggs and strobila fragments in the feces.

Treatment. In case of severe anemia, before treatment with antiparasitic drugs, vitamin B12, B6, 300-500 mcg intramuscularly, 2-3 times a week for a month, iron supplements, hemostimulin, etc. are prescribed. To destroy the parasite, fenasal, male fern extract, and a decoction of seeds are used. pumpkins.

The prognosis in the absence of complications in most cases is favorable.

Prevention. Do not eat fish and caviar that has not undergone high-quality heat treatment.

6. Opisthorchiasis

Etiology, pathogenesis. The causative agent is the feline fluke, which parasitizes in the bile ducts of the liver, gallbladder and pancreatic ducts of humans, cats, dogs, etc. The parasite lives in the human body for 20-40 years. Infection occurs when eating raw and insufficiently thermally processed carp fish. Opisthorchiasis damage the mucous membranes of the pancreatic ducts and bile ducts, creating bile stasis, and contribute to the formation of cystic enlargements and neoplasms of the liver. They have a toxic and neuro-reflex effect.

Clinic. The incubation period is about 2 weeks. In the early period, there may be an increase in body temperature, muscle and joint pain, nausea, vomiting, hepatomegaly, splenomegaly, loose stools, leukocytosis and severe eosinophilia, and skin allergic manifestations. In the chronic stage - complaints of pain in the epigastric region, right hypochondrium, radiating to the back and left hypochondrium, attacks of pain such as gall bladder colic. Frequent dizziness and various dyspeptic symptoms. Muscle resistance in the right hypochondrium, liver enlargement, occasionally icteric sclera, enlarged gallbladder, and symptoms of pancreatitis are detected. Most often, with opisthorchiasis, a picture of cholecystitis, biliary dyskinesia, chronic hepatitis and pancreatitis develops; symptoms of gastroduodenitis and enterocolitis are less often observed. Opisthorchiasis can be asymptomatic.

The diagnosis is made upon detection of helminth eggs in the feces and duodenal contents.

Treatment. Deworming with mebendazole (Vermox)

Prevention. Explanation to the population of the danger of eating fish food that has not undergone sufficient heat treatment.

7. Teniasis

Etiology. The causative agent is pork tapeworm, it can be in the human body not only in the sexually mature, but also in the larval stage, causing cysticercosis. The adult parasite can reside in the small intestine for many years. The reason for infecting people with taeniasis is the consumption of raw or half-baked meat containing Finns.

The diagnosis is confirmed after a double examination of feces and the detection of parasite segments and mucus from the perianal folds by scraping and the detection of helminth eggs.

Treatment is carried out with the drug "vermox". Sometimes male fern ethereal extract and pumpkin seeds are used.

Prevention. Eating pork that has undergone sufficient heat treatment.

8. Trichuriasis

Etiology, pathogenesis. The causative agent is the whipworm, which parasitizes the human large intestine. The lifespan of the parasite is about 5 years. Whipworms injure the intestinal mucosa, are hematophagous and promote inoculation of microflora, causing reflex reactions in other organs of the abdominal cavity. The products of their metabolism cause sensitization of the body.

Clinic. Patients complain of salivation, decreased (rarely increased) appetite, pain in the right side of the abdomen and epigastric region, nausea, constipation or diarrhea, headache, dizziness, sleep disturbances, irritability are sometimes noted. In the blood there is a moderate hypochromic anemia, a slight leukocytosis is possible. Whipworm infestation can also be asymptomatic.

The diagnosis is made when whipworm eggs are found in the feces.

Treatment. Prescribe mebendazole and other drugs. Previously, the patient is given a cleansing enema.

The prognosis is favorable.

9. Fascioliasis

Etiology, pathogenesis. The causative agents of the disease are liver and giant flukes. The main source of infection for humans is farm animals. A person becomes infected in the warm season when the larvae enter the body with water, greens. The life span of helminths in the body lasts about 10 years. Traumatization and toxic-allergic damage to the hepatobiliary system play an important role in pathogenesis. It is possible for the parasite to enter other tissues and organs.

Clinic. The disease is characterized by eosinophilia in the blood, allergic symptoms, dysfunction of the liver and gallbladder, similar to the symptoms of opisthorchiasis (jaundice and attacks of gall bladder colic are more common).

Diagnosis at an early stage of the disease is difficult, since helminth eggs begin to be released only 3-4 months after infection. Immunological methods are used. In the late stage, the diagnosis is confirmed by the detection of fasciol eggs in the duodenal contents and feces.

Treatment. Anthelmintic drugs are prescribed, and after deworming, cholagogues are prescribed for 1-2 months. A long-term (at least 1 year) medical examination of patients is necessary.

The prognosis for treatment is favorable.

Prevention. It is necessary to prohibit the use of water from stagnant reservoirs, but you need to thoroughly wash and scald the greens with boiling water.

10. Echinococcosis

Etiology. The causative agent of hydatous echinococcosis is the larval stage of a small cestode that has a scolex with 4 suckers and hooks and 3-4 proglotids filled with eggs. The larva is a single-chamber bubble, the wall of which consists of two layers (outer and inner) of cells that form small parietal protrusions. The bubble cavity is filled with liquid. Echinococcus eggs are highly stable in the external environment, withstand drying and exposure to low temperatures.

Epidemiology. The disease is widespread throughout the world, infection of the population is very widespread, shepherds, hunters and persons who have constant contact with the final owners of echinococcus are more likely to get sick.

Reservoir and source of invasion. The final hosts are carnivores, domestic animals (dog, fox, wolf), in which a mature worm parasitizes in the intestines. Its segments, containing eggs, are excreted with feces into the external environment. Intermediate hosts are herbivores and omnivores (sheep, goats, pigs, horses, rodents).

The mechanism of transmission of invasion is fecal-oral (as a result of ingestion of invasive echinococcus eggs upon contact with dogs, sheep, on whose wool there may be helminth eggs), the route of transmission is food, water, household.

Pathogenesis. When a person swallows echinococcosis eggs in the stomach and intestines, the latter are released from the oncospheres, penetrate through the intestinal wall into the blood, then into the liver, where the larval stage of echinococcosis is formed. The growing bubble causes compression of the surrounding tissues of the lung, bronchi, and vessels and involves the pleura in the pathological process with the appearance of symptoms of a space-occupying formation. The death of the parasite leads to the addition of a bacterial infection and the formation of a lung abscess.

Clinic. Chest pain of various types, dry cough, then with purulent sputum, hemoptysis, shortness of breath. If a bubble breaks into the bronchus, severe coughing, cyanosis, and suffocation appear, and the contents of the bubble may be detected in the sputum. When echinococcal blisters suppurate, a lung abscess develops. With echinococcosis of the liver, patients lose their appetite, develop weakness, weight loss, headaches, decreased performance, a feeling of heaviness in the epigastrium, pain in the right hypochondrium, liver enlargement, thickening, pain on palpation, nausea, vomiting, stool upset. In rare cases, subicteric skin and jaundice may appear.

Diagnostics. Based on clinical and laboratory data using serological reactions (RSC, RNGA, latex agglutination reaction with antigen from echinococcal bladder fluid), additional research methods, chest X-ray, computed tomography of the lungs, ultrasound of the lungs, a diagnosis is made.

Treatment. Usually by surgery.

Prevention. Prevention of infection of animals and humans, observance of personal hygiene rules, periodic helminthological examination of dogs and timely deworming of infected animals and humans. Information from medical and veterinary institutions is of particular importance.

11. Enterobiasis

Etiology. The causative agent is pinworm. The female has a length of 9-12 cm, males - 3-4 cm. Males die after fertilization, females come out of the anus and lay eggs on the perianal region and in the perineum. Infection occurs as a result of ingestion of invasive eggs. Possible autoinvasion. In the upper small intestine, infective larvae leave the egg shells and reach sexual maturity in the large intestine. Pinworms stick to the intestinal mucosa and penetrate to the muscle layer, producing toxins.

Clinic. With a slight invasion, complaints may be absent. There is itching around the anus, scratching, infection, rapid stools with pathological impurities. Symptoms of intoxication, girls have vulvovaginitis.

Diagnosis is based on the detection of pinworm eggs in the stool or by scraping on the pinworm eggs. In the blood - eosinophilia.

Treatment. Mebendazole (Vermox): from 2 to 10 years, 25-50 mg/kg taken once, pyrantel (Combantrin) - 10 mg/kg once after breakfast (must be chewed), piperazine - up to 1 year 0,2 g 2 times during 5 days; 2-3 years - 0,3 g; 4-5 years - 0,5 g; 6-8 years - 0,5 g; 9-12 years - 1,0 g; 13-15 l - 1,5 g.

Prevention. Compliance with personal hygiene.

LECTURE No. 18. Rabies. Etiology, epidemiology, clinic, diagnostics, treatment

Rabies is an acute viral disease that occurs after contact with the damaged skin of the saliva of an infected animal, is characterized by the development of damage to the central nervous system (encephalitis) with a fatal outcome.

Etiology. The causative agent - a neurotropic virus - belongs to the group of rhabdoviruses. It has a bullet shape, reaches a size of 80-180 nm. The nucleocapsid of the virus is a single-stranded RNA. The virus is unstable in the external environment, boiling kills it within 2 minutes, quickly dies in chloramine. The virus is resistant to low temperatures. The virus is dangerous for many warm-blooded animals, which, when infected, begin to secrete the virus with saliva 7-8 days before the onset of clinical symptoms.

Epidemiology. Rabies is a zoonotic infection. The main reservoir of the virus is carnivores (foxes, wolves, jackals, dogs, cats). The virus is excreted with saliva in the last 7-10 days of the incubation period and throughout the disease. Infection occurs when sick animals bite or saliva on damaged skin and less often mucous membranes. The virus is not transmitted from person to person. Susceptibility to rabies is universal. The highest incidence was noted in the summer-autumn period, due to more intensive contacts of people with wild animals.

Pathogenesis. After penetration through the damaged skin, the virus reaches the brain along the nerve trunks, where it is fixed and replicated in the neurons of the medulla oblongata, in the nodes of the base of the brain and in the lumbar part of the spinal cord, causing edema, hemorrhages, and degeneration of the nerve cells of the spinal cord. This leads to an increase in reflex excitability with the subsequent development of paralysis. The defeat of the higher autonomic centers in the hypothalamus, subcortical areas, in the medulla oblongata with an increase in their excitability causes convulsive contractions of the respiratory and swallowing muscles, hypersalivation, increased sweating, disorders of the cardiovascular system and respiratory activity characteristic of this disease. From the central nervous system, the virus enters various organs: the kidneys, lungs, liver, as well as the salivary glands and is released into the external environment with saliva.

Clinic. The incubation period ranges from 7 days to a year (usually 1-3 months). There are stages of premonitions, excitement and paralysis. During the prodromal period, a precursor stage is distinguished, which lasts 1-3 days. During this period, the patient is accompanied by unpleasant sensations in the area of the bite or salivation (burning, nagging pain, itching), despite the fact that the wound has already healed, causeless anxiety, depression, insomnia. The excitation stage is characterized by hydrophobia, aerophobia and increased sensitivity. Hydrophobia (phobia of water) manifests itself in the fact that when trying to drink, and then only when a glass of water approaches the lips, the patient is characterized by convulsive contraction of the muscles of the pharynx and larynx, breathing becomes noisy in the form of short convulsive breaths, and short-term cessation of breathing is possible. Convulsions may occur as a result of blowing a stream of air into the face (aerophobia). Body temperature is subfebrile. The skin is covered with cold, sticky sweat, the limbs are cold. Salivation is increased, the patient cannot swallow saliva and constantly spits it out. Excitement increases, visual and auditory hallucinations appear. Sometimes there are attacks of violence with aggressive actions. The paralytic period is characterized by mental calm. Fear and anxious melancholy mood disappear, attacks of hydro- and aerophobia stop, and after 2-3 days the excitement is replaced by paralysis of the muscles of the limbs, tongue, and face. Death occurs 12-20 hours after the onset of paralysis. The bulbar form with pronounced symptoms of damage to the medulla oblongata, paralytic (begins with paralysis, sometimes Landry type) and cerebellar with cerebellar disorders are considered to be variants of the course.

Diagnosis is based on the clinical picture. When examining a patient, attention is paid to the presence of scars from bites, salivation, sweating, the appearance of symptoms of mental disorders, etc.

Differential diagnosis is carried out by tetanus, encephalitis, encephalomyelitis, hysteria. After the death of patients, the diagnosis is confirmed by histological examination of the brain.

Treatment. There is no specific therapy for rabies. After the onset of clinical symptoms, it is not possible to save patients. Treatment is symptomatic and aimed at reducing the suffering of the patient. Patients are placed in a darkened soundproof room. Re-introduce pantopon, chlorpromazine, diphenhydramine.

Prevention. They combat rabies among animals and prevent rabies in people bitten by infected animals. In case of a bite, the wound is washed with soapy water and cauterized with tincture of iodine. Surgical excision of the wound edges and suturing in the first days should not be performed. At Pasteur stations, anti-rabies vaccinations and serotherapy are carried out according to a special scheme approved by the USSR Ministry of Health.

LECTURE No. 19. Protozoal infections: malaria, toxoplasmosis. Etiology, epidemiology, clinic, treatment

1. Malaria

Acute protozoan disease with manifestation of febrile attacks, anemia, with enlargement of the liver and spleen. The source of infection is only a person with malaria, or a gametocarrier. Transmission of infection occurs through the bites of various types of mosquitoes.

Etiology. There are four types of pathogens that cause malaria: Plasmodium falciparum - the causative agent of tropical malaria, P. vivax - the causative agent of 3-day malaria (vivax-malaria), P. ovale - the causative agent of oval malaria and P. malariae - the causative agent of 4-day malaria. A complex cycle of development in the body of a vertebrate host (tissue and erythrocyte schizogony) and in the body of a mosquito-carrier (sporogony) is performed by Plasmodium malaria.

Pathogenesis. Sporozoites enter the body when infected during a mosquito bite and transform into tissue schizonts in liver cells. They divide many times, forming a large number (up to 50 from each schizont) of tissue merozoites. The duration of the preerythrocyte cycle is 000-6 days. Then the parasites penetrate the red blood cells, and erythrocyte schizogony begins. The duration of schizogony for the causative agents of 9-day malaria is 4 hours, for the rest - 72 hours. The resistance of the causative agent of tropical malaria to drugs is of great importance. In some countries of Southeast Asia, resistance of half of the strains of tropical malaria pathogens to hingamine (delagil, chloroquine), as well as to chloridine and quinine, is more often observed. Drug resistance of tropical malaria pathogens is also observed in other regions. The pre-erythrocytic development cycle of the parasite does not occur simultaneously with clinical manifestations. The attack begins simultaneously with the moment of massive destruction of the affected red blood cells and the release of the parasite into the blood. An attack is a peculiar reaction to a foreign protein penetrating into the blood. The destruction of red blood cells leads to anemia. The development of immunity in malaria occurs only in relation to the homologous species of plasmodium.

Clinic. The duration of the incubation period for tropical malaria is 10-14 days, with a 3-day incubation with a short incubation - 10-14 days, with a long one - 8-14 months, with a 4-day incubation - 20-25 days. The onset of the disease may be accompanied by a fever of the wrong type, and after a few days the correct alternation of attacks is established. During an attack, periods of chills, heat and sweat are distinguished. Attacks usually occur in the morning with a maximum temperature in the first half of the day (with oval-malaria attacks begin in the evening after 18-20 hours). The onset of chills occurs suddenly, it can be amazing, lasting 1,5-2 hours. The duration of the entire attack in the case of 3-day malaria and oval-malaria is 6-8 hours, 4-day - 12-24 hours, with tropical malaria the attack is longer , and the period of apyrexia is so short that it can only be detected with thermometry every 3 hours. Chills are replaced by fever, and when the temperature drops, the patient begins to sweat heavily, which leads to an improvement in well-being, the patient calms down and often falls asleep. During the period of apyrexia, the patient's state of health remains good, often he retains his ability to work. With 3-day, tropical and oval malaria, attacks occur every other day, and with 4-day - after 2 days. The temperature during attacks usually reaches 40 ° C and above. After 2-3 attacks, there is an increase in the liver and especially the spleen, it is painful on palpation. Perhaps the appearance of a herpetic rash. The breakdown of red blood cells is the cause of pallor and icteric staining of the skin. Without antiparasitic treatment, the duration of 3-day malaria reaches 2-3 years, tropical - up to a year and 4-day - up to 20 years or more. Complications: malarial coma, rupture of the spleen, hemoglobinuric fever.

Diagnostics. Of great importance is a blood test that reveals hypochromic anemia, poikilocytosis, anisocytosis, an increase in the number of reticulocytes, leukopenia, and an increase in ESR.

Differential diagnosis should be made with diseases that are accompanied by paroxysmal fever (sepsis, brucellosis, leptospirosis, visceral leishmaniasis). The proof of the diagnosis is the detection of malarial plasmodia in the blood. Swabs and a thick drop are taken before antimalarial treatment.

Treatment. For tropical malaria, quinamine (chloroquine, delagil) is prescribed on the 1st day, 1 g and after 6 hours another 0,5 g of the drug, then 4 g/day for 0,5 days. In the case of treatment of 3- and 4-day malaria, a 3-day course of treatment with hingamine is first carried out: on the 1st day, give 0,5 g 2 times a day, on the 2nd and 3rd days - 0,5. 10 g in one dose. This course stops attacks of malaria, but has no effect on the tissue forms of the parasite. Radical treatment after finishing taking hingamine is accompanied by a 0,027-day course of treatment with primaquine (0,65 g/day). To treat tropical malaria caused by drug-resistant plasmodia, quinine sulfate is used at a dose of 3 g 10 times a day. for 1 days in combination with sulfapyridazine (on the 1st day 4 g, in the next 0,5 days 1 g). An effective combination of hingamine (on the 0,5st day 2 g 3 times a day, in the next 4-0,5 days 1 g / day) with sulfapyridazine (1st day 4 g, the next 0,5 days 0,65 .250 g/day). Other drugs are also used. The preferred start of treatment for malarial coma is the intravenous drip of quinine dihydrochloride at a dose of 500 g in 8-2 ml of isotonic sodium chloride solution. Repeated infusion can be carried out after 5 hours. The daily dose should not be more than 5 g. A 10% delagil solution (available in 6 ml ampoules) is also used, 8 ml every 30-30 hours, but not more than 3 ml/day. In severe forms, pathogenetic treatment is carried out. Glucocorticoids are prescribed (prednisolone XNUMX mg XNUMX times a day), infusion therapy, antihistamines, etc. In uncomplicated forms of malaria, there is a favorable prognosis. Deaths are common in cases of splenic rupture and malarial coma.

Prevention. Elimination of mosquito vectors, protecting people from mosquito bites (use of repellents, nets). Persons traveling to malaria-endemic areas are given chemoprophylaxis (given 0,25 g of hingamin 2 times a week). The drug is prescribed 3 days before arrival at the outbreak, and it is continued for 4-6 weeks after departure. Those who have had malaria are monitored in accordance with the instructions.

2. Toxoplasmosis

Toxoplasmosis is a parasitic disease that manifests itself in a chronic course, damage to the nervous system, lymphadenopathy, mesadenitis, frequent damage to the myocardium, muscles and eyes. The main host of the parasite is cats, whose feces contain oocysts that can persist in the soil for up to a year. Human infection occurs when oocysts enter the digestive tract. Other animals are not dangerous, except when eating raw meat (minced meat). A sick person is also not dangerous. Infection during pregnancy leads to intrauterine infection of the fetus.

Etiology. The causative agent is Toxoplasma, a protozoan. The shape of the body depends on the phase of the process.

Epidemiology. Toxoplasmosis is a zoonosis with predominantly fecal-oral (sometimes vertical) transmission mechanisms. The reservoir is domestic and wild mammals. The ultimate host of the parasite is domestic cats, which excrete Toxoplasma oocysts in their faeces. In humans and other intermediate hosts, it exists as trophozoites, which are characterized by intracellular reproduction. These forms are very unstable to the external environment, they are inactivated under the influence of chemotherapeutic drugs. Cysts are being formed in the body, i.e., accumulations of a large number of parasites surrounded by a dense membrane and very resistant to the effects of chemotherapeutic drugs.

Pathogenesis. The gateway to infection is the digestive organs. The site of entry of the pathogen is the small intestine. Toxoplasma enters regional lymph nodes through the lymph flow, where the protozoa multiply, causing inflammatory changes with the formation of granulomas. Next, the parasites hematogenously penetrate into various organs and tissues, where cysts are formed that remain in the human body for decades and for life. Allergization of the body occurs simultaneously with the production of antibodies. The course of the infection most often occurs in a latent form, but when the body’s defenses are weakened, an exacerbation of the disease may occur, and a sharp suppression of the immune system (taking immunosuppressants, AIDS) can lead to a generalized infection with severe encephalitis.

Clinic. The incubation period lasts about 2 weeks. Depending on the mechanism of invasion, acquired and congenital toxoplasmosis is distinguished. Downstream can be acute, chronic, latent. Toxoplasmosis begins as a primary chronic disease, many months can pass from the moment of infection to the first manifestations of the disease. The development of congenital toxoplasmosis can only occur as a result of infection of a woman during pregnancy with transplacental transmission of the pathogen. Often, its manifestation occurs in the form of encephalitis and eye damage. Toxoplasmosis infection of a woman before pregnancy does not lead to congenital toxoplasmosis. In many infected, the course of toxoplasmosis is latent, without any clinical manifestations. Acquired toxoplasmosis: with acute development, the onset of the disease is acute, fever, intoxication, enlargement of the liver and spleen, damage to the central nervous system in the form of encephalitis, meningoencephalitis. The course of the disease is severe, with a fatal outcome. The chronic form can last for many years with periodic exacerbations and remissions. It is characterized by subfebrile condition, symptoms of chronic intoxication. Its most frequent manifestations are: prolonged subfebrile condition, generalized lymphadenopathy, myositis, mesadenitis, liver enlargement, ECG changes, functional changes in the central nervous system (in 50-90% of patients), enlargement of the spleen, chorioretinitis, miscarriage (in 10-20 % of patients).

Diagnosis is carried out on the basis of clinical data, laboratory research methods. To detect infection, an intradermal test with toxoplasmin and serological tests (usually RSK) are used. Positive specific reactions are uninformative for diagnosis, since about 20-30% of the total population is infected. In case of negative reactions (especially with an intradermal allergic test), toxoplasmosis may be excluded.

Differential diagnosis is carried out with other chronic diseases (rheumatism, chronic tonsillitis, etc.).

Treatment. The main form of treatment in the case of acute forms of toxoplasmosis is etiotropic therapy. Prescribe chloridine 0,025 g 2-3 times a day and sulfadimezin 2-4 g per day for 5-7 days. Three courses are carried out with an interval of 7-10 days. Etiotropic therapy is practically ineffective in chronic forms. There is a complex treatment, which includes one course (5-7 days) of etiotropic treatment (tetracyclines, metronidazole, delagil, chloridine with sulfadimezine, biseptol) in combination with nonspecific desensitizing therapy (antihistamines, corticosteroids), vitamin therapy. An important factor is vaccine therapy (toxoplasmin therapy), an individual dose of toxoplasmin dilution is selected, and then administered intradermally with increasing dosage under the control of individual sensitivity. Pregnant women who have positive reactions to toxoplasmosis, but without clinical manifestations of the disease, are not subject to treatment. Chemotherapy drugs (especially chloridine and sulfadimezine) are not prescribed in the early stages of pregnancy (the first 3 months), as this can cause deformities.

Forecast. One course of complex therapy for chronic acquired toxoplasmosis leads to a stable recovery of 85% of patients; 15% relapse at various intervals requiring treatment. In some patients, residual phenomena may occur that contribute to a decrease in working capacity (decreased vision, damage to the nervous system). In acute forms, the prognosis is serious.

Prevention. Compliance with the rules of hygiene when keeping cats, the prohibition of the use of raw minced meat and meat dishes without the necessary heat treatment.

LECTURE No. 20. Bacterial zoonoses: brucellosis, anthrax, tularemia, plague, ornithosis, yersiniosis. Etiology, epidemiology, pathogenesis, clinic, diagnostics, treatment

1. Brucellosis

Zoonotic infectious-allergic disease, with the manifestation of general intoxication, damage to the musculoskeletal system, nervous and reproductive systems.

Etiology. Currently, six species of Brucella are known. The main carriers are goats, sheep, cattle, pigs. Brucella are microorganisms that have a spherical shape, their size is 0,3-0,6 nm. Gram-negative and grow on normal nutrient media. Under the influence of antibiotics, they are able to transform into L-forms. Brucella are characterized by a high capacity for invasion and intracellular parasitism. As they break down, endotoxin is released. The resistance of the pathogen in the external environment, as well as in food products (milk, cheese) is characteristic. High temperatures lead to death when boiled. Low temperatures contribute to the preservation of a long time. They die quickly when exposed to direct sunlight and common disinfectants.

Epidemiology. The focus of infection is large and small cattle. For infection, the alimentary or contact route is characteristic. Immunity is not strained and short-lived, on average lasts 6-9 months, is not strictly specific.

Pathogenesis. For infection, the alimentary route or microdamages of the skin are characteristic (during assistance with calving, lambing, etc.). The spread of the pathogen occurs throughout the body by the hematogenous route, which is the cause of allergopathy and the formation of foci in various organs and systems.

Clinic. The duration of the incubation period ranges from 6 to 30 days. Brucellosis is characterized by polymorphism of clinical manifestations. In some infected people, a primary latent form occurs without clinical symptoms, the manifestation of which is characterized by immunological reactions. For others, the course of the disease occurs in acute (acuteseptic) or chronic (primary chronic metastatic and secondary chronic metastatic) forms. From the moment the clinical symptoms disappear (while Brucella remains in the body), the disease transitions into a secondary latent form, which can again lead to an exacerbation and again turn into one of the chronic forms when the body weakens. The acute form of brucellosis is characterized by high fever (up to 40 °C), during which patients feel well (sometimes they even remain able to work). There is a moderate headache, repeated chills, increased sweating, and fatigue. All groups of peripheral lymph nodes (micropolyadenitis), liver, and spleen are moderately enlarged.

At the end of the prodromal period, the symptoms of intoxication increase, and at the height of the disease there is a temperature of remitting type with a rise in the afternoon or in the evening hours. As the toxic-septic process develops, changes in the respiratory system such as catarrhal inflammation of the upper respiratory tract, bronchitis, bronchopneumonia, and bronchoadenitis are revealed. When the nervous system is damaged in the midst of an acute form of the disease, headaches, irritability, emotional instability, and sleep disturbances are present. In severe cases, mental disorders, the phenomena of meningism and meningitis are observed. The course of meningitis is sluggish, without pronounced cerebral and meningeal symptoms. In the case of chronic forms, against the background of subfebrile (less often febrile) temperature and reticuloendotheliosis (micropolyadenitis, enlarged liver and spleen), various organ changes appear. Large joints (periarthritis, arthritis), muscles (myositis), peripheral nervous system (mono- and polyneuritis, radiculitis, plexitis), and reproductive system (orchitis, oophoritis, endometritis, spontaneous abortion) often occur. The course of chronic forms of brucellosis is long, exacerbations are replaced by remissions. In some patients, even after sanitization of the body from Brucella, there may be persistent residual effects (residual brucellosis).

Diagnosis is based on epidemiological data and characteristic clinical manifestations.

Differential diagnosis should be made with sepsis, malaria, tuberculosis, rheumatoid arthritis. Specific reactions that are used include the Wright, Huddleson, intradermal allergy test with brucellin (Burnet test).

Treatment. In the acute form, the main is etiotropic therapy, the duration of which is up to 3-4 weeks. Antibiotics of the tetracycline group, streptomycin, levomycetin, rifampicin are prescribed. In chronic forms, a complex of restorative therapeutic measures is carried out simultaneously with vaccine therapy. For the purpose of immunocorrection, various immunomodulators are prescribed. Sanatorium treatment can be carried out no earlier than 6 months after the disappearance of the clinical symptoms of brucellosis.

The prognosis for life is favorable, but often the disease is the cause of partial disability.

Prevention. Control of brucellosis in farm animals. Specific prevention is achieved by using a live anti-brucellosis vaccine, which provides immunity for 1-2 years. Vaccination is carried out in areas where there is an incidence of brucellosis among animals. Persons at risk (caring for farm animals and workers in enterprises processing livestock products) are subject to immunoprophylaxis.

2. Anthrax

An acute infectious disease from the group of zoonoses, characterized by intoxication, the development of serous-hemorrhagic inflammation of the skin, lymph nodes and internal organs and occurring in the form of a cutaneous (or septic) form. In humans it occurs in the form of skin, pulmonary, intestinal and septic forms.

Etiology. The causative agent is a relatively large anthrax gram-positive bacillus that forms spores and a capsule. The death of the vegetative form of the pathogen occurs without air access, during heating, exposure to disinfectants. In the external environment, the spores of the pathogen are very stable.

Epidemiology. The focus of infection are cattle. It is most often transmitted by contact, less often by alimentary, airborne dust.

Pathogenesis. The entry point for the anthrax pathogen is usually damaged skin. At the site of penetration of the pathogen into the skin, an anthrax carbuncle appears in the form of a focus of serous-hemorrhagic inflammation with necrosis, edema of adjacent tissues, and regional lymphadenitis. The local pathological process is caused by the action of anthrax exotoxin, individual components of which cause severe microcirculation disorders, tissue edema and coagulative necrosis. Further generalization of anthrax pathogens with their breakthrough into the blood and the development of a septic form rarely occurs in the cutaneous form.

Clinic. The duration of the incubation period ranges from several hours to 14 days (usually 2-3 days). The most common form of anthrax in humans occurs in the form of a cutaneous form (95-99% of cases) and only in 1-5% of patients in the form of pulmonary and intestinal. The characteristic manifestations of cutaneous anthrax occur at the site of infection. Initially, a red itchy spot appears, quickly turning into a papule, and the latter into a vesicle with transparent or hemorrhagic contents. Continued itching leads to the patient's rupture of the vesicle, in its place an ulcer with a dark bottom and copious serous discharge is formed. Along the periphery of the ulcer, an inflammatory ridge develops, in the area of which daughter vesicles form. At the moment, swelling (can be quite extensive) and regional lymphadenitis develop around the ulcer. There is no sensitivity in the area of the bottom of the ulcer; in addition, there is no pain in the area of enlarged lymph nodes. By the time the ulcer forms, a fever appears, the duration of which is 5-7 days, general weakness, headaches, fatigue, and adynamia are observed.

Local changes in the affected area increase over approximately the same period as fever, and then a reverse development occurs: first, a decrease in body temperature is observed, the removal of serous fluid from the necrosis zone ceases, a decrease (until complete disappearance) of edema begins, and gradually at the site of necrosis a scab forms. On the 10-14th day, the scab is rejected, leading to the formation of an ulcer with a granulating bottom and moderate purulent discharge, followed by scarring. The pulmonary form of anthrax is characterized by an acute onset and severe course. Manifested by chest pain, shortness of breath, tachycardia (up to 120-140 beats per minute), cyanosis, cough with foamy bloody sputum. Body temperature quickly reaches febrile levels (1 °C and above), blood pressure decreases. The intestinal form of anthrax is characterized by the manifestation of general intoxication (fever, pain in the epigastric region, diarrhea and vomiting). Abdominal bloating, severe pain on palpation are also characteristic, and there are often signs of peritoneal irritation. An admixture of blood appears in the vomit and intestinal discharge. Any of the described forms of anthrax can lead to the development of sepsis with bacteremia and secondary foci (damage to the liver, spleen, kidneys, meninges).

Diagnosis is based on epidemiological data (the patient's profession, contact with sick animals or contaminated raw materials of animal origin) and characteristic clinical skin lesions. Laboratory proof of the diagnosis is the isolation of the causative agent of anthrax. An allergic test with anthraxin has an auxiliary effect.

Differential diagnosis is carried out with glanders, boils, plague, tularemia, erysipelas.

Treatment. In mild forms of the disease, penicillin is prescribed at a dose of 200-000 IU 300-000 times a day for 6-8 days. An increase in a single dose of penicillin is carried out in extremely severe forms with a septic component up to 5-7 IU 1-500 times a day. The most effective is the treatment with antibiotics in combination with a specific antiulcer immunoglobulin at a dose of 000-2 ml / m. Cancellation of antibiotics occurs after a significant decrease in edema, cessation of the increase in the size of skin necrosis and separation of fluid from the affected area. The removal of the patient from infectious-toxic shock in severe forms of anthrax is facilitated by intensive pathogenetic therapy.

The prognosis for the skin form and with timely treatment is favorable. With intestinal and pulmonary forms, the prognosis is questionable even in the case of early and intensive treatment.

Prevention. A patient with anthrax is hospitalized in a separate ward with the issuance of individual care items, linen, dishes. Allocations of patients (feces, urine, sputum), as well as dressings, are disinfected. The patient can be discharged after complete clinical recovery with epithelialization of ulcers. When recovering from the transfer of intestinal pulmonary forms, the patient is discharged after a double negative bacteriological examination of feces, urine and sputum for the presence of anthrax.

3. Tularemia

An acute infectious disease, the signs of which are an increase in body temperature, symptoms of general intoxication, damage to the lymphatic system, skin, mucous membranes, and in case of aerogenic infection - lung tissue. Tularemia refers to zoonoses with natural foci. The prevalence is observed in many regions of Russia, many types of rodents serve as a source of infection.

Etiology. The causative agents are small cocci-like rods with a thin capsule, gram-negative, not forming spores. Contain two antigenic complexes: shell and somatic. Resistant in the external environment, slightly resistant to drying, ultraviolet rays, disinfectants.

Epidemiology. Tularemia has multiple portals of infection. The pathogen is transmitted to humans through transmissible, contact, and aspiration routes. The following routes of infection are distinguished: through the skin (contact with infected rodents), the transmission mechanism is through ticks, mainly ixodid, in addition, there is a route of transmission through the mucous membranes of the digestive tract when consuming contaminated water and food and the respiratory tract (inhalation of infected dust). The clinical forms of the disease are closely related to the portal of infection. With the contact and transmissible mechanism of infection, bubonic and cutaneous-bubonic forms of the disease appear, with aspiration - pneumonic, with alimentary - intestinal and anginal-bubonic forms of this infection. When infected through the conjunctiva, the oculobubonic form develops. After surviving the disease, immunity is formed.

Pathogenesis. The causative agent of tularemia enters the human body through damaged skin, mucous membranes of the eyes, respiratory tract, gastrointestinal tract, and its lymphogenous spread occurs. The entry of bacteria into regional lymph nodes and their proliferation cause a picture of inflammatory changes. When bacteria die, endotoxin is released, which enhances the local pathological process, and when it enters the bloodstream, it causes symptoms of intoxication. Specific tularemia granulomas are formed in the lymph nodes of the affected internal organs. Under microscopy, areas of necrosis are visible in the center, surrounded by epithelioid cells and a shaft of lymphoid elements with a small number of leukocytes. When the buboes suppurate and open, a long-term non-healing ulcer appears on the skin.

Clinic. The incubation period lasts from several hours to 14 days (usually 3-7 days). The disease has an acute onset and is manifested by chills, a rapid increase in body temperature to febrile levels. Patients complain of severe headache, weakness, muscle pain, insomnia, and possibly vomiting. The skin of the face and neck is hyperemic, the vessels of the sclera are injected. In some patients, from the 3rd day of illness a rash appears, often of an erythematous nature. In bubonic forms, regional lymph nodes, especially cervical and axillary ones, are significantly enlarged. In abdominal forms, symptoms of acute mesadenitis may occur. With tularemic buboes, there is no periadenitis; the buboes fester rarely and at a later stage (at the end of the 3rd week of the disease). The duration of fever ranges from 5 to 30 days (usually 2-3 weeks). During the period of convalescence, prolonged low-grade fever may persist. The oculobubonic form, in addition to the typical damage to the lymph node, is characterized by pronounced conjunctivitis with swelling of the eyelids and ulcers on the conjunctiva. Usually one eye is affected. The process lasts up to several months, vision is completely restored. In the anginal-bubonic form, in addition to the presence of typical buboes, specific tonsillitis is observed in the form of pain when swallowing with necrotic changes on the tonsils, palatine arches, and the appearance of fibrinous plaque on the affected areas, reminiscent of diphtheria. Ulcers heal very slowly. The abdominal form is characterized by abdominal pain, flatulence, constipation, and tenderness in the area of the mesenteric lymph nodes upon palpation. The pulmonary form of tularemia is characterized by prolonged fever of the wrong type with repeated chills and profuse sweating. Patients experience pain in the chest area, complain of a cough, initially dry, then with the presence of mucopurulent and sometimes bloody sputum. X-ray is determined by focal or lobar infiltration of the lung tissue. Pneumonia has a sluggish, protracted course (up to 2 months or more) and a tendency to recur.

Diagnosis of tularemia at the onset of the disease before the appearance of buboes is quite difficult. When buboes appear, diagnosis becomes easier. To confirm the diagnosis, serological methods are used - agglutination reaction, RNHA and specific skin tests with tularin.

The differential diagnosis is carried out with the bubonic form of the plague, with the disease of cat scratches and purulent lymphadenitis.

Treatment. Antibiotics are prescribed: streptomycin IM 0,5 g 2 times a day, tetracycline 0,4 g every 6 hours or chloramphenicol 0,5 g every 6 hours. Antibiotic therapy is carried out until the 5-7th day of normal temperature. In case of a prolonged course of the disease, killed tularemia vaccine is used (in a dose of 1 to 15 million microbial bodies at intervals of 3-5 days, a total of 6-10 sessions). If a symptom of fluctuation appears during palpation of the buboes, their opening and cleansing of pus is indicated.

The prognosis is favorable.

Prevention. Rodent control, protection of food and water from them. According to epidemiological indications, specific prophylaxis is carried out in some cases.

4. Plague

An acute infectious disease caused by the plague bacillus - Yersinia pestis. A natural focal disease, it is a particularly dangerous infection. There are several natural foci on earth where plague is constantly observed in a small number of rodents living there. Epidemics of plague among people were often caused by the migration of rats infected in natural foci. The transmission of microbes from rodents to humans is carried out by fleas, which, in the event of mass death of animals, look for a new host. In addition, one of the methods of infection is infection when people process the skins of infected animals. The method of transmission of infection from person to person, carried out by airborne droplets, is fundamentally different.

Etiology. The causative agent of plague is a small, immobile rod. It is a facultative anaerobe, does not form spores, is gram-negative, is highly resistant in the external environment, can persist in soil for up to 7 months, on clothing for 5-6 months, in milk for 3 months, and is stable at low temperatures and freezing. It is destroyed immediately when boiled, and at 55 ° C - in 10-15 minutes. It is quickly destroyed by disinfectants and is sensitive to antibiotics of the streptomycin and tetracycline series. Contains about 30 antigens, including heat-stable somatic and heat-labile capsular.

Epidemiology. The hosts of the plague are rodents (marmots, ground squirrels). Plague refers to diseases with pronounced natural foci. A person, getting into a natural focus, can be exposed to the disease through the bites of blood-sucking arthropods. In rodents that hibernate during the cold season, plague occurs in a chronic form. A person becomes infected with the plague microbe in several ways: through the bites of infected fleas, by contact (when removing the skins of infected commercial rodents), by the alimentary route (by eating foods contaminated with bacteria), by aerogenic route (from patients with pneumonic plague).

Pathogenesis. The pathogen enters the body through damage to the skin with a flea bite, mucous membranes of the respiratory tract, digestive system, conjunctiva. When a person is bitten by an infected insect, a papule or pustule is formed at the site of the bite, filled with hemorrhagic contents (in the case of a cutaneous form). Further, the infection spreads through the lymphatic vessels without the manifestation of lymphangitis. Bacteria proliferate in the macrophages of the lymph nodes, leading to the massive enlargement, fusion, and agglomeration that is characteristic of the bubonic form. Further generalization of the infection, which does not always develop, can lead to the development of a septic form, which is characterized by damage to almost all internal organs. From the point of view of epidemiology, screening of the pathogen into the lung tissue plays an important role, which leads to the pulmonary form of the disease. The development of this pneumonia leads to the fact that a sick person becomes a source of infection, but at the same time transmits the pulmonary form of the disease to other people. It is extremely dangerous, characterized by a lightning-fast course.

Clinic. With the bubonic form of plague, sharply painful conglomerates appear, most often in the inguinal lymph nodes on one side. The incubation period ranges from 2 to 6 days (less often 1-12 days). The disease begins acutely, with an increase in body temperature to 39 °C, chills, a feeling of heat, myalgia, headache, and dizziness. The appearance of the patient is also characteristic: the face and conjunctiva are hyperemic, the lips are dry, the tongue is swollen, dry, trembling, covered with a dry, thick white coating. The patient's speech is unintelligible, blurred, the patient is inhibited or excited, delusions and hallucinations appear, coordination of movements is impaired, and a feeling of fear arises. Over the course of a few days, the conglomerate increases in size, and the skin over it often becomes hyperemic. At the same time, other lymph nodes—secondary buboes—enlarge. The lymph nodes in the primary focus soften, when they are punctured, purulent or hemorrhagic contents are obtained, which, upon microscopy, reveals a large number of gram-negative rods with bipolar staining. If antibacterial therapy is not used, the festering lymph nodes are opened and the fistulas gradually heal. The condition of patients gradually worsens by the 4-5th day, the temperature may rise, sometimes to febrile levels, but nevertheless, at first, patients may feel satisfactory. But at any moment the bubonic form can become a generalized process and turn into a secondary septic (or secondary pulmonary form). In these cases, the condition of the patients very quickly becomes extremely serious. Symptoms of intoxication increase very quickly. The temperature is accompanied by severe chills and rises to febrile levels. All signs of sepsis are observed: muscle pain, severe weakness, dizziness, congestion of consciousness, up to its loss, headaches, often agitation and sleep disturbance. With the addition of pneumonia, cyanosis and shortness of breath increase, and a cough occurs with the release of foamy, bloody sputum containing a large number of plague bacilli. It is this discharge that becomes the source of infection from person to person with the development of the primary pulmonary form. Septic and pneumonic forms of plague have all the signs of sepsis and occur with symptoms of disseminated intravascular coagulation syndrome: minor hemorrhages on the skin, gastrointestinal bleeding (vomiting of bloody masses, melena), severe tachycardia, and a rapid drop in blood pressure are possible. Auscultation shows all the signs of bilateral focal pneumonia.

Diagnosis. The most important role in the diagnosis of plague in modern conditions is played by epidemiological anamnesis. Arrival from zones endemic for this disease (Vietnam, Burma, Bolivia, Ecuador, Turkmenistan, Karakalpak ASSR, etc.), or from anti-plague stations of a patient with the signs of the bubonic form described above or with signs of the most severe (with hemorrhages and bloody sputum) pneumonia with severe lymphadenopathy is a serious enough argument for the doctor of the first contact to take all measures to localize the alleged plague and accurately diagnose it. It is important that under the conditions of modern medical prophylaxis, the probability of illness of medical personnel in contact with a coughing plague patient is very small. Currently, there are no cases of primary pneumonic plague among medical personnel.

Diagnosis is based on bacteriological studies. Materials for bacteriological examination are punctate from a festering lymph node, sputum, blood, discharge from fistulas and ulcers. Laboratory diagnostics is carried out using fluorescence microscopy methods. In this case, a fluorescent specific antiserum is used, which stains the taken material.

Treatment. If plague is suspected, the patient is immediately hospitalized in the isolation ward of the infectious diseases hospital. However, in certain cases, it is more advisable to carry out hospitalization (before establishing an accurate diagnosis) in the institution where the patient is at the time of making the preliminary diagnosis. Therapeutic measures and prevention of infection of personnel must be combined. Personnel should immediately put on anti-plague suits or three-layer gauze masks, shoe covers, scarves made of two layers of gauze that completely cover the hair, and protective glasses to prevent splashes of sputum on the mucous membrane of the eyes. All personnel who had contact with the patient continue to provide assistance. A special medical post isolates the compartment in which the patient and the personnel treating him are located from contact with other patients and personnel. The compartment should have a toilet and a treatment room. All personnel urgently undergo prophylaxis with antibiotics throughout all days of their stay in the isolation ward.

In the bubonic form of plague, the patient is prescribed intramuscular streptomycin 3-4 times a day. (daily dose 3 g), tetracycline antibiotics IV 6 g/day. In case of severe intoxication, saline solutions and hemodez are administered intravenously. When blood pressure decreases, which is regarded as a sign of sepsis in this form of the disease, resuscitation measures are carried out (administration of dopamine, installation of a permanent catheter). In pneumonic and septic forms of plague, the dose of streptomycin is increased to 4-5 g/day, and tetracycline - up to 6 g. In forms resistant to streptomycin, it is replaced with chloramphenicol succinate up to 6-8 g/day. i.v. If the dynamics are positive, the dose of antibiotics is reduced: streptomycin - to 2 g/day. until the temperature normalizes, but for at least 3 days, tetracyclines - up to 2 g/day. daily orally, chloramphenicol - up to 3 g/day, in the amount of 20-25 g. Biseptol is also used with great success in the treatment of plague.

In case of pulmonary, septic forms of development of hemorrhage, they immediately begin to relieve disseminated intravascular coagulation syndrome: plasmapheresis is performed (intermittent plasmapheresis in plastic bags can be carried out in any centrifuge with special or air cooling with a container capacity of 0,5 l or more) in the volume of removed plasma 1-1,5 liters when replaced with the same amount of fresh frozen plasma. In the presence of hemorrhagic syndrome, daily infusions of fresh frozen plasma are necessary. Plasmapheresis is performed daily until the acute signs of sepsis disappear. Relief of hemorrhagic syndrome and stabilization of blood pressure in sepsis are indications for stopping plasmapheresis sessions. The effect of plasmapheresis in the acute period of the disease is observed almost immediately, the symptoms of intoxication decrease, the dose of dopamine decreases, muscle pain becomes less intense, and shortness of breath decreases. The medical team must include an intensive care specialist.

Forecast. In modern conditions of therapy and diagnosis, mortality in the bubonic form does not exceed 5-10%, but in other forms the recovery rate is high if treatment is started in a timely manner. If plague is suspected, the sanitary and epidemiological station of the area is urgently notified. The notification is filled out by the doctor who suspects the presence of the disease, and its forwarding is ensured by the chief physician of the institution where the patient was found.

5. Ornithosis

An acute infectious disease caused by chlamydia. It manifests itself in the form of fever with general intoxication, damage to the pulmonary system, central nervous system, hepato- and splenomegaly. Refers to zoonotic infections. The reservoir of infection and the source of infection are domestic and wild birds. The disease is most often recorded in the cold season. It was revealed that 10-20% of all acute pneumonias have ornithosis etiology.

Etiology. The causative agent - chlamydia - is an obligate intracellular parasite, has a coccal shape and shell and is sensitive to some antibiotics (tetracycline, chloramphenicol). Chlamydia develop intracellularly, forming cytoplasmic inclusions. In the external environment, they remain up to 2-3 weeks. They die when heated and exposed to ultraviolet rays.

Epidemiology. Birds are the reservoir and source. The transmission mechanism is aerogenic, the main ways of infection are airborne, airborne. Human infection occurs through contact with sick birds. The transferred disease leaves unstable immunity.

Pathogenesis. The site of infection is predominantly the mucous membrane of the respiratory tract: infection occurs through airborne dust. Often the pathogen invades the small bronchi and bronchioles, causing peribronchial inflammation. The pathogen penetrates into the blood at high speed, causing symptoms of general intoxication and damage to various organs - the liver, spleen, nervous system, adrenal glands. Less commonly, the mucous membrane of the digestive tract serves as the gateway to infection. In these cases, chlamydia also penetrates into the blood, causing severe intoxication, hepato- and splenomegaly, but secondary hematogenous pneumonia does not develop. As a result, the disease proceeds atypically, without affecting the lungs. In some cases, chlamydia penetrates the central nervous system, causing a picture of serous meningitis.

Clinic. The incubation period lasts from 6 to 17 days (usually 8-12 days). Pneumonic forms of psittacosis have an acute onset with fever and symptoms of general intoxication, which at a later stage are joined by signs of damage to the respiratory system. In most patients, the temperature reaches febrile levels, accompanied by chills, severe headache, pain in the muscles of the back and limbs, weakness, vomiting and nosebleeds are possible. On the 2-4th day of illness, signs of lung damage become noticeable: a dry cough appears, sometimes stabbing pain in the chest. After 1-3 days, the release of scanty mucous or mucopurulent sputum begins, sometimes mixed with blood. On examination, pallor of the skin, absence of pronounced symptoms of damage to the upper respiratory tract, decreased blood pressure, bradycardia, and muffled heart sounds are noted. In most patients, the lower parts of the lungs are affected, most often on the right. A shortening of the percussion sound over the affected area is determined, dry and fine moist rales are heard, and in some patients there is a pleural friction noise. Radiographs reveal peribronchial and parenchymal changes characteristic of focal and segmental pneumonia. At the end of the first week, hepato- and splenomegaly are detected in half of the patients. The duration and severity of individual symptoms are determined by the severity of the disease.

In mild forms, intoxication is moderate, and the fever lasts 2-5 days; in severe forms, it can reach a month. The fever is of the wrong type with large daily fluctuations, repeated chills and profuse sweat, sometimes wavy. During the period of convalescence, asthenic syndrome with impaired ability to work persists for a long time (in severe forms up to 2-3 months). During the period of early convalescence, relapses and complications (myocarditis, thrombophlebitis) may occur. In some patients, the disease becomes chronic. The atypical course of acute ornithosis is manifested by meningeal syndrome, which can occur against the background of ornithosis pneumonia (meningopneumonia), or serous meningitis with a long course (with fever for up to a month, sanitation of the cerebrospinal fluid after 2 months). Sometimes ornithosis occurs in the form of an acute febrile illness with severe intoxication, hepato- and splenomegaly, but without signs of damage to the respiratory system.

differential diagnosis. When diagnosing, it is necessary to differentiate with pulmonary tuberculosis and pneumonia of another etiology: meningeal forms are differentiated from tuberculous and viral meningitis.

Confirmation of the diagnosis is the presence of specific antibodies (titer 1:16 - 1:32 and above) in paired sera.

Treatment. Assign tetracyclines 0,3-0,5 g 4 times a day until the 4th-7th day of normal temperature. If suspected and there are signs of an incomplete pathological process, tetracycline continues to be taken until the 9-10th day of normal temperature. You can prescribe chloramphenicol, erythromycin with intolerance to the tetracycline group, but they are less effective. Penicillin, streptomycin and sulfanilamide preparations do not have a therapeutic effect in ornithosis. Pathogenetic therapy is used: bronchodilators, oxygen therapy.

Complications: myocarditis.

The prognosis is favorable.

Prevention. Fighting disease in birds, regulating the number of pigeons, limiting their contact with people, observing the rules for processing poultry meat. The patient is not contagious to others.

6. Yersiniosis

Acute infectious disease related to zoonoses. The main route of human infection is alimentary. A sick person does not pose a danger to others.

Etiology. The pathogen (Yersinia) is similar in its properties to the pathogens of plague and pseudotuberculosis. Yersinia is divided into five biotypes, ten phagotypes, and according to the 0-antigen - more than thirty serotypes. Biotypes 2, 4, serotypes 3, 5, 8, 9 are of greatest importance in the structure of human morbidity. The microorganism is characterized by polymorphism, bipolar coloring, gram-negative, does not form capsules or spores. Can exist at a temperature of +5 °C. Highly sensitive to antibacterial drugs (chloramphenicol, tetracyclines, aminoglycosides).

Pathogenesis. The pathogen enters the body in the lower parts of the small intestine, where terminal ileitis begins to develop, there may be ulceration. In the lymphogenous way, the pathogen reaches the mesenteric lymph nodes, where lymphadenitis is formed with a tendency to abscess formation.

Clinic. The incubation period is from 15 hours to 4 days (usually 1-2 days). The main clinical forms are:

1) gastroenterocolitic;

2) appendicular;

3) septic;

4) subclinical.

The disease begins acutely, with an increase in body temperature to 38-40 °C. Fever lasts up to 5 days, with septic forms longer. There are symptoms of general intoxication (chills, headache, muscle and joint pain). In the gastroenterocolitic form, against this background, pain appears in the abdomen of a cramping nature, mainly in the lower parts on the right or in the navel area. Nausea and vomiting may be present, loose stools with an unpleasant odor, up to 10 times a day, may contain pathological impurities in the form of mucus (usually there is no blood). Unlike dysentery, there is no tenesmus, the sigmoid colon is not spasmodic and painless. In the appendicular form, symptoms of appendicitis (sometimes purulent) occur. The septic form can develop in weakened patients, occur with attacks of fever of the wrong type, with repeated chills, profuse sweating, hepato- and splenomegaly, increasing signs of anemia, jaundice of the skin. This form is fatal.

Diagnostics. In the blood test - leukocytosis, ESR increased. Laboratory confirmation of the diagnosis is the isolation of the pathogen from various environments of the body: from feces, blood, pus, removed appendix, and also RNGA. Yersiniosis must be distinguished from gastroenterocolitis of various etiologies (dysentery, escherichiosis, salmonellosis), appendicitis, pseudo-tuberculosis.

Treatment. Antibacterial drugs are used: levomycetin (0,5 g 3-4 times a day), tetracyclines (0,3-0,4 g 4 times a day) for 5-7 days.

Prevention. See Salmonella.

LECTURE No. 21. Hemorrhagic fever. Etiology, epidemiology, pathogenesis, clinic, diagnostics, treatment

Hemorrhagic fever with renal syndrome (hemorrhagic nephrosonephritis) is an acute viral disease that occurs with a peculiar renal syndrome and symptoms of intoxication, fever, hemorrhagic manifestations. This is a natural focal disease.

Etiology. The causative agent belongs to the group of arboviruses, spherical RNA-containing viruses.

Epidemiology. HFRS is a typical zoonotic natural focal infection. The reservoir of viruses on the territory of Russia is rodents and insectivores, which have latent forms of infection. The virus is excreted into the external environment mainly with urine (less often with feces, saliva). The transmission of infection from rodent to rodent is carried out through ticks and fleas. Transmission of the virus to humans is carried out by aspiration by inhalation of air containing suspended infectious excretions of rodents. There may be a contact route - when an infected material gets on abrasions, cuts, scratches, an alimentary route - when eating food contaminated with infected secretions of rodents. After the illness, a strong immunity is acquired. Relapses are extremely rare.

Pathogenesis. After entering the human body through damaged skin and mucous membranes, the virus is localized in the vascular endothelium, where it replicates and accumulates intracellularly. Then comes the viremia phase, which coincides with the onset of the disease and the appearance of general toxic symptoms. The virus has a capillary toxic effect in the form of destructive arteritis with increased permeability of the vascular wall, impaired microcirculation, development of disseminated intravascular coagulation syndrome, and organ failure, especially of the kidneys. During the febrile period of the disease, the virus is in the blood, causing infectious-toxic damage to the nervous system and severe hemorrhagic capillary toxicosis. Kidney damage with the development of acute renal failure is typical.

Clinic. The incubation period is from 11 to 23 days. There are four stages of the disease: febrile, oliguric, polyuric, convalescent stage. The febrile stage begins acutely. Fever (38-40 °C), headache, insomnia, myalgia, and photophobia appear. The face, neck, and upper parts of the body are hyperemic, the vessels of the sclera are injected. By the 3-4th day of illness, the patient’s condition worsens, vomiting, abdominal pain, hemorrhages in the form of a rash, nosebleeds, and hemorrhages at the injection sites appear. The rash may appear in stripes that resemble a whiplash. Subsequently, nasal, uterine, and stomach bleeding are possible, which can cause death. From the cardiovascular system, bradycardia, muffled heart sounds, and decreased blood pressure are observed. In severe cases of the disease, the development of infectious-toxic shock is observed. Pain appears in the abdomen and lower back, intensifies to unbearable, palpation of the abdomen reveals pain (usually in the hypochondrium), the liver is enlarged, tapping on the lower back is sharply painful.

The oliguric period begins on the 3-4th day of illness; against the background of high temperature, the patient’s condition worsens: severe pain in the lower back appears, forcing the patient to take a forced position. Headaches and vomiting appear, leading to dehydration. Palpation of the kidney area is painful. Spontaneous kidney rupture may occur. The amount of urine decreases, its relative density is low (up to 1,004), urinary retention may occur, azotemia increases, and the resulting renal failure in some cases ends in uremic coma. From the 6-7th day of illness, the body temperature begins to decrease to normal, but the patient’s condition does not improve. Toxicosis progresses (nausea, vomiting, hiccups), insomnia, and meningeal symptoms appear. Characterized by the absence of jaundice, enlarged liver and spleen. Transporting the patient during this period must be very careful. The polyuric stage occurs from the 9-13th day of illness. The patient's condition improves: nausea and vomiting stop, appetite appears, diuresis increases to 5-6 l, nocturia is characteristic. Lower back pain becomes less intense, but persists for several weeks, sometimes several months. During the recovery process, the symptoms of the disease are gradually reduced, but asthenia in the body may persist for a long time. During the period of convalescence, polyuria decreases and body function is restored. The convalescent period lasts up to 3-6 months. Recovery comes slowly. Complications: infectious-toxic shock, pulmonary edema, uremic coma, eclampsia, kidney rupture, hemorrhages in the brain, adrenal glands, heart muscle, pancreas.

Diagnosis is based on characteristic clinical symptoms; specific methods of laboratory diagnostics are not widely used.

Differential diagnosis should be made with leptospirosis, Q fever, pseudotuberculosis.

Treatment. There is no etiotropic therapy. Bed rest, a dairy-vegetable diet, and vitamins are recommended. Hormone therapy is prescribed, prednisolone from 50 to 120 mg/day. After normalization of body temperature, the dose is gradually reduced. Course duration is 8-15 days. In the first days, a 5% glucose solution or an isotonic sodium chloride solution is administered intravenously with the addition of a 1% potassium chloride solution (50 ml per 1 liter of isotonic solution), a 5% ascorbic acid solution (20 ml/day. ) and 4% sodium bicarbonate solution (50 ml per 1 liter of solution). 1-1,5 liters are administered per day. In the absence of arterial hypotension in the oliguria phase, mannitol or furosemide (Lasix) is prescribed. Gastric lavage with a 2% solution of sodium bicarbonate and siphon enemas are advisable. During attacks of intense pain, pantopon is prescribed. If signs of renal failure increase, the patient needs extracorporeal hemodialysis.

The prognosis is favorable, sometimes there are complications in the form of ruptured kidneys, uremic coma, meningoencephalitis. Ability to work returns slowly, sometimes after several months.

Prevention. Destruction of rodents, protection of foodstuff from their penetration. Patients are isolated. Current and final disinfection is carried out in the wards.

LECTURE No. 22. Legionellosis. Mycoplasmosis. Etiology, epidemiology, pathogenesis, clinic, diagnostics, treatment

1. Legionellosis

An acute infectious disease caused by the action on the body of various types of legionella. The main symptoms: fever, severe intoxication, severe course, damage to the lungs, central nervous system, digestive system.

Etiology. Legionella are gram-negative bacteria that are widespread and persist for a long time in the external environment (in water - up to 1 year). Legionella are highly sensitive to antibiotics, especially erythromycin, chloramphenicol, ampicillin, are not very sensitive to tetracyclines and are not sensitive to a number of penicillins and cephalosporins.

Epidemiology. Infection occurs by inhaling tiny droplets of infected water (in showers, from air conditioner sprayers, etc.). The sources of infection have not been established. Middle-aged and elderly people are more likely to get sick; the disease is promoted by smoking, alcohol consumption, diabetes mellitus, the use of immunosuppressants, and AIDS.

Pathogenesis. The entry gates of infection are the lower parts of the respiratory tract; the pathological process develops in the terminal and respiratory bronchioles, as well as the alveoli. The pulmonary infiltrate consists of macrophages and polymorphonuclear cells, which are located in the alveolar spaces along with a large amount of fibrin deposits. The breakdown of microbes leads to the release of endotoxin, which causes damage to a number of organs and systems of the gastrointestinal tract, nervous system, and the possible development of endocarditis and lung abscess. In severe cases, infectious-toxic shock develops, accompanied by symptoms of respiratory and cardiovascular failure, hypoxia, and respiratory acidosis.

Clinic. The incubation period is 2-10 days (usually 5-7 days). The disease begins acutely. A significant increase in body temperature is accompanied by chills. General weakness, fatigue, and muscle pain quickly increase. From the first days, patients complain of a painful cough and stabbing pain in the chest area. Signs of pneumonia, shortness of breath, and tachypnea are detected. The respiratory rate reaches 30-40 respiratory movements per minute. There may be vomiting and loose stools. The central nervous system is affected, which is manifested by dizziness, delirium, disturbance of consciousness, loss of coordination, cerebellar ataxia, and dysarthria. Tachycardia is noted, blood pressure is reduced. The skin is pale, hemorrhagic syndrome may develop. The tongue is dry, covered with a brown coating, the abdomen is soft on palpation, moderately painful in the epigastrium and navel area. The liver and spleen are not enlarged. The amount of urine is sharply reduced. In severe cases, respiratory and cardiovascular insufficiency quickly increases, and infectious-toxic shock develops. Death occurs by the end of the first week of illness.

Legionellosis does not always occur in the form of pneumonia. The so-called Pontiac fever is expressed in a short-term increase in temperature (2-5 days), moderate general intoxication. Symptoms of bronchitis and pleurisy may be detected, but pneumonia as such is absent. No deaths were observed with this form of the disease. Legionellosis must be remembered when severe pneumonia develops at an unusual time of year (late summer) in middle-aged and elderly men in the presence of predisposing factors (smoking, alcoholism, diabetes, etc.). The lack of therapeutic effect from antibiotics commonly used for pneumonia (penicillin, streptomycin, tetracycline) is also important.

Differential diagnosis should be made with other pneumonias. Serology and bacteriology methods are used to confirm the diagnosis.

Treatment. The most effective therapy is erythromycin 0,4-0,5 g 4-6 times a day. until stable temperature normalization. In severe cases, you can use erythromycin phosphate intravenously (2-3 times a day, 0,2 g each). The effectiveness of therapy increases with the combination of erythromycin with rifampicin.

The prognosis of the disease is serious. In the United States, mortality reached 20%, with the use of erythromycin it decreased to 4%.

Prevention. Disinfection of water, bathrooms, showers and nets, control of air conditioning. Patients are in isolated wards. The current disinfection of the patient's secretions is carried out.

2. Mycoplasmosis

Acute infectious disease caused by the presence of mycoplasmas. It proceeds in the form of acute respiratory infections and pneumonia, less often other organs are affected.

Etiology. Damage to the respiratory system is caused by the properties of mycoplasma pneumoniae. M. hominis and T-mycoplasmas parasitize the genitourinary organs. Mycoplasmas are gram-negative, contain DNA, RNA, and are facultative anaerobes. Mycoplasmas are resistant to sulfonamides, penicillin, streptomycin, sensitive to tetracycline antibiotics, and quickly die when heated, exposed to ultraviolet rays and disinfectants.

Epidemiology. Sources of infection - a sick person or a carrier of mycoplasmas. Infection occurs by airborne droplets. The maximum rise in incidence is observed in the autumn-winter period.

Pathogenesis. The entrance gates of infection are the mucous membranes of the respiratory or genitourinary tract (depending on the type of mycoplasmas). There, in the first place, a pathological process occurs. The pathogen is transmitted by airborne droplets or through sexual contact. In pregnant women, the fetus can become infected in utero.

Clinic. The incubation period ranges from 4 to 25 days (usually 7-14 days). The infection occurs in the form of an acute respiratory disease, acute pneumonia, abacterial (non-gonococcal) urethritis, gynecological inflammatory manifestations. Mycoplasmal acute respiratory infections are characterized by exudative pharyngitis and rhinopharyngitis. The general state of health of patients is satisfactory, the temperature is often subfebrile. Acute pneumonia begins with chills, fever, symptoms of general intoxication. With the methods of examination used for pneumonia, mycoplasmal pneumonia differs little from acute bacterial pneumonia.

Diagnostics. For laboratory confirmation of the diagnosis, serological tests are used (complement fixation - RSK and indirect hemagglutination - RNHA). The diagnosis is confirmed if the antibody titer increases by more than 4 times.

Treatment. Antibacterial drugs of the tetracycline group are prescribed, 0,3 g 4 times a day. within 6-8 days. For genitourinary mycoplasmosis, local treatment with tetracycline is used. For pneumonia, the entire range of pathogenetic therapy is carried out (oxygen therapy, bronchodilators, exercise therapy, massage, physiotherapy, etc.).

The prognosis is favorable.

Prevention. Patients with mycoplasmal pneumonia are isolated for 2-3 weeks, patients with acute respiratory infections - for 5-7 days. Preventive measures are the same as for other types of respiratory infections.

LECTURE No. 23. Erysipelas. Scarlet fever. Etiology, epidemiology, pathogenesis, clinic, diagnostics, treatment

1. Erysipelas

An acute infectious disease characterized by skin lesions with the formation of a sharply limited inflammatory focus, as well as fever and symptoms of general intoxication, recurrence.

Etiology. The causative agent is hemolytic streptococcus. These are facultative anaerobes, they are resistant to environmental factors. But when exposed to heat, antiseptics and antibiotics quickly die.

Epidemiology. The source of infection is a patient with erysipelas, as well as a carrier of b-hemolytic streptococcus. Infection occurs as a result of the penetration of the pathogen through damaged skin or mucous membranes. Immunity after erysipelas does not occur.

Pathogenesis. The causative agent penetrates through small breaks in the skin. Exogenous infection is possible (through contaminated instruments, dressings). In the occurrence of recurrences of erysipelas in the same place, allergic mood and skin sensitization to hemolytic streptococcus matter.

Clinic. The duration of the incubation period lasts from several hours to 5 days (usually 3-4 days). According to the nature of local lesions, erythematous, erythematous-bullous, erythematous-hemorrhagic and bullous forms are distinguished, according to the severity of the course - mild, moderate and severe, as well as primary, recurrent and repeated; according to the nature of local phenomena - localized, widespread and metastatic. Primary erysipelas begins acutely, with symptoms of general intoxication. Body temperature rises to 39-40 °C, general weakness, chills, headache and muscle pain appear; in severe cases, convulsions, impaired consciousness, and symptoms of irritation of the meninges may appear. After 10-24 hours from the onset of the disease, local symptoms develop: pain, burning and a feeling of tension in the affected area of the skin; upon examination, hyperemia and swelling are revealed. Erythema is often uniform, rising above the skin level. The severity of edema is mainly observed when inflammation is localized in the eyelids, lips, fingers, and genitals. Sometimes, against the background of erythema, blisters are formed filled with serous (erythematous-bullous erysipelas) or hemorrhagic (bullous-hemorrhagic erysipelas) contents. Lymphangitis and regional lymphadenitis are also noted. At the site of inflammation, peeling of the skin subsequently appears.

Local changes persist for 5-15 days; pastiness and pigmentation of the skin may persist for a long time. Recurrences of erysipelas can occur from several days to 2 years after the infection. With a later (over 2 years) appearance of erysipelas, we are talking about recurrent erysipelas. It is usually localized in a new area of skin. Recurrence is promoted by insufficient treatment of primary erysipelas, residual effects after erysipelas (lymphostasis, etc.). With frequent relapses, fever and symptoms of intoxication are mild. Complications and consequences of erysipelas may be the same as with other streptococcal diseases (rheumatism, nephritis, myocarditis), but may be more specific: ulcers and skin necrosis (gangrenous erysipelas), abscesses and phlegmons (abscess erysipelas), impaired lymph circulation leading to to elephantiasis of the affected limb. In the case of clinical diagnosis, differentiation is necessary with other diseases in which local redness and swelling of the skin may occur (vein thrombosis, erysipiloid, cellulitis and abscesses, acute dermatitis, etc.). In the blood there is a slight leukocytosis with a shift to the left, acceleration of ESR.

Treatment. The most effective action is provided by antibiotics of the penicillin series. For primary erysipelas and rare recurrences, penicillin is prescribed at a dose of 500 IU every 000 hours for 6-7 days; With significant residual effects, to prevent recurrence, bicillin-10 must be administered within 5-1 months (500 IU every 000 weeks). In case of intolerance to penicillin, erythromycin (5 g 4 times a day) or tetracycline (6-1 g 500 times a day) can be used, the duration of the course is 000-4 days. With persistent and frequent relapses of erysipelas, antibiotics are combined with corticosteroid hormones (prednisolone 0,3 mg / day).

The prognosis is generally favorable. With often recurrent erysipelas, elephantiasis may occur, partially disrupting the ability to work.

Prevention. Prevention of injuries and scuffs of the legs, treatment of streptococcal diseases. With a pronounced seasonality of relapses, bicillin prophylaxis is carried out, which begins a month before the start of the season and continues for 3-4 months (Bicillin-4 is injected every 5 weeks at 1 units). With frequent relapses of erysipelas, year-round bicillin prophylaxis is advisable. There are no activities in the outbreak. Specific prophylaxis has not been developed.

2. Scarlet fever

Acute airborne anthroponosis, affecting mainly children under the age of 10 years, but cases of the disease are also observed at a later age. The infection is characterized by fever, general intoxication, sore throat symptoms, characteristic elements on the skin and changes in the pharynx. The incidence increases in the autumn and winter months.

Etiology, pathogenesis. The causative agent is beta-hemolytic toxigenic group A streptococcus; it settles in the nasopharynx, less often in the skin, causing local inflammatory changes (sore throat, regional lymphadenitis). The exotoxin it produces causes symptoms of general intoxication and characteristic local manifestations. Streptococcus, under conditions favorable to microbial invasion, causes the development of a septic component, manifested by lymphadenitis, otitis, and septicemia. In the development of the pathological process, sensitizing mechanisms involved in the occurrence and pathogenesis of complications in the late period of the disease play an important role. The development of complications is often associated with streptococcal superinfection or reinfection.

Clinic. The incubation period lasts 5-7 days. The disease begins acutely. The body temperature rises, a pronounced deterioration in the child’s condition, headache, and sore throat when swallowing appear. A typical and constant symptom is tonsillitis, characterized by bright, circumscribed hyperemia of the soft palate, enlarged tonsils, in the lacunae or on the surface of which plaque is often found. The upper cervical lymph nodes are enlarged and painful. Vomiting often occurs as a symptom of intoxication. On the 1st (less often on the 2nd) day, a bright pink or red pinpoint rash appears on the skin of the entire body, predominantly localized on the chest, in the area of the extensor surfaces of the forearms. The nasolabial triangle remains pale (Filatov's symptom), white dermographism is detected, and pinpoint hemorrhages are common in the bends of the limbs. The rash lasts from 2 to 5 days, and then turns pale, while the body temperature drops. In the second week of the disease, peeling of the skin appears - lamellar on the palms and soles, finely and coarsely scaly - on the body. The tongue is initially coated, from the 2-3rd day it clears and by the 4th day it takes on a characteristic appearance: bright red color, sharply protruding papillae (crimson tongue). In the presence of severe intoxication, damage to the central nervous system is observed (excitement, delirium, blackout). At the beginning of the disease, symptoms of increased tone of the sympathetic nervous system are noted, and from the 4-5th day - of the parasympathetic nervous system.

With a mild form of scarlet fever, the symptoms of intoxication are mild, fever and all other manifestations of the disease disappear by the 4-5th day; This is the most common variant of the modern course of scarlet fever. The moderate form of scarlet fever is characterized by greater severity of symptoms, including symptoms of intoxication; the febrile period lasts 5-7 days. The severe form, currently very rare, occurs in two main variants: in the form of toxic scarlet fever with pronounced symptoms of intoxication (with high fever, symptoms of central nervous system damage - blackouts, delirium, and in young children, convulsions, meningeal signs), all symptoms from the pharynx and skin are pronounced; in the form of severe septic scarlet fever with necrotizing tonsillitis, violent reaction of regional lymph nodes and frequent septic complications; necrosis in the pharynx can be located not only on the tonsils, but also on the mucous membrane of the soft palate and pharynx.

The toxic-septic course of scarlet fever is characterized by a combination of symptoms of these two severe forms. Atypical forms of the disease include erased scarlet fever, in which all symptoms are rudimentary, and some are completely absent. If the entrance gate of infection is the skin (burns, wounds), then the development of an extrapharyngeal, or extrabuccal, form of scarlet fever occurs, in which such an important symptom as tonsillitis is absent. With mild and erased forms of scarlet fever, changes in the peripheral blood are insignificant or absent. In moderate and severe forms, leukocytosis, neutrophilia with a shift to the left and a significant increase in ESR are observed. From the 3rd day of the disease, the content of eosinophils increases, however, in severe septic form, their decrease or complete disappearance is possible. Complications: glomerulonephritis (mainly in the third week), synovitis, the so-called infectious heart, less often myocarditis, which is a serious manifestation of the disease in children. In the presence of a septic component of the disease, purulent complications may occur (lymphadenitis, adenophlegmon, otitis, mastoiditis, sinusitis, septicopyemia). Pneumonia may develop. Relapses of scarlet fever and tonsillitis are associated with streptococcal reinfection. In recent decades, the incidence of complications has decreased sharply. After scarlet fever, lifelong immunity is usually maintained. However, recently the frequency of recurrent diseases has increased slightly. Difficulties in diagnosis arise with atypical forms of the disease.

Differential diagnosis is carried out with measles, rubella, drug rash, scarlet fever-like form of pseudotuberculosis. Cases of staphylococcal infection with scarlatiniform syndrome are observed.

Treatment. In the presence of appropriate conditions, therapy is carried out at home. Patients are hospitalized with severe and complicated forms of scarlet fever, as well as according to epidemiological indications. Bed rest is always observed for 5-6 days (in severe cases or more). Antibiotic therapy is carried out: benzylpenicillin is prescribed at the rate of 15-000 IU / kg per day. in / m for 20-000 days. At home, with a mild form of scarlet fever, phenoxymethylpenicillin can be used orally, doubling the indicated daily dose. In the toxic form in a hospital, intravenous infusions of neocompensan, gemodez, 5% glucose solution with vitamin therapy are used. With a septic form, intensive antibiotic therapy is indicated. Treatment of complications (lymphadenitis, otitis, nephritis) is carried out according to the usual rules.

The prognosis is favorable.

Prevention. The patient is isolated at home or (according to indications) is hospitalized. The wards in the hospital are filled simultaneously for 1-2 days, contacts of convalescents with patients in the acute period of the disease are excluded. Convalescents are discharged from the hospital in the absence of complications on the 10th day of illness. Children who have been in contact with a sick person and have not previously had scarlet fever are allowed to preschool or the first two grades of school after 7 days of isolation at home. In the apartment where the patient is kept, regular current disinfection is carried out; under these conditions, the final disinfection is unnecessary. It must be remembered that scarlet fever is transmitted through clothing, underwear, toys and other things, that is, through third parties.

LECTURE No. 24. Tetanus. Etiology, epidemiology, pathogenesis, clinic, treatment

Tetanus is an acute infectious disease characterized by severe toxic damage to the nervous system with tonic and clonic convulsions and disturbances in thermoregulation.

Etiology, pathogenesis. The causative agent is a large anaerobic bacillus, spore-forming, producing exotoxin. Often found in the soil, where it persists for years. Spores of the pathogen enter the human body with various injuries and minor damage to the skin, especially the lower extremities. Under anaerobic conditions, the spores turn into vegetative forms, which begin to multiply and secrete an exotoxin that causes damage to the anterior horns of the spinal cord and the corresponding symptoms.

Epidemiology. The causative agent is widespread in nature and is a permanent inhabitant of the intestines of herbivores; it enters the soil with feces, infects it for a long time, transforming into a spore form. The main route of transmission is contact (through damaged skin and mucous membranes). The disease is associated with trauma (cuts, skin punctures with rusty objects, etc.).

Clinic. The incubation period lasts from 3 to 30 (usually 7-14) days; with a short incubation period, the disease is much more severe. The disease begins with manifestations in the area of the wound (pulling pain, twitching of the muscles around it). The most characteristic symptom is seizures. Early convulsive contraction of the masticatory muscles (trismus), as well as facial muscles, occurs. Tonic muscle contraction is replaced by attacks of clonic convulsions, the muscles of the back and limbs are seized, and opisthotonus occurs. The characteristic position of the patient's body is in the position of an arc, curved outward. Seizure attacks are triggered by the slightest external irritation. Convulsive contraction of the respiratory muscles, diaphragm and laryngeal muscles can lead to the death of the patient from asphyxia. Characterized by headache and muscle pain, fever, increased sweating, drowsiness, and weakness. Complications: pneumonia, muscle rupture, compression fracture of the spine with convulsions that reach unusual strength. Tetanus must be differentiated from hysteria, tetanus, strychnine poisoning, rabies, and meningitis.

Treatment carried out in specialized anti-tetanus centers. The patient is transported by a doctor working in this center. Before transportation, the patient is injected with an antipsychotic mixture of the following composition: 2,5% solution of chlorpromazine - 2 ml, 2% solution of pantopon - 1 ml, 2% solution of diphenhydramine - 2 ml, 0,05% solution of scopolamine - 0,5 ml. After 30 minutes, 5-10 ml of a 10% solution of hexenal or thiopental is injected intramuscularly. For treatment, in the first 2-3 days, antitetanus serum is administered intramuscularly at 100-000 IU (preferably antitetanus gamma globulin). The neuroleptic mixture is administered 150-000 times a day. To reduce seizures, chloral hydrate is prescribed in enemas (3-4 ml of a 50-150% solution). In anti-tetanus centers, a complex of resuscitation measures is carried out (total muscle relaxation in combination with artificial ventilation of the lungs, etc.).

The prognosis is favorable.

LECTURE No. 25. Enteroviral infections. Polio. Etiology, epidemiology, pathogenesis, clinic, diagnostics, treatment

1. Enteroviral infections

Acute infectious diseases caused by intestinal viruses are often accompanied by damage to the muscles, central nervous system and skin. May occur as sporadic cases or epidemic outbreaks. Transmission is predominantly airborne.

Etiology. Enteroviruses, in addition to polio viruses, include twenty-three types of Coxsackie A virus, six types of Coxsackie B virus, thirty-two types of ECHO viruses and four more human enteroviruses (enteroviruses 68-71). All of them can cause disease in humans. Enterovirus 70 is the causative agent of acute hemorrhagic conjunctivitis.

Pathogenesis. The entrance gates of infection are the mucous membranes of the respiratory and digestive tract. In the place of implementation, inflammatory changes may occur. Viruses quickly penetrate the bloodstream, spread throughout the body, gaining a foothold mainly in the nervous system, muscles and epithelial cells, causing their changes.

Clinic. The incubation period lasts from 2 to 10 days (usually 3-4 days). Enterovirus infection causes a variety of clinical manifestations. The most common are acute respiratory infections and “minor illness”, serous meningitis, herpangina, epidemic myalgia, hemorrhagic conjunctivitis, myelitis with paralysis, encephalitis, pericarditis, myocarditis, infectious exanthemas, enteroviral diarrhea are sometimes observed. The disease begins acutely. ARI can be caused by any enterovirus, but most often the causative agent is the Coxsackie A-21 virus. “Minor disease” is a short-term, mild enteroviral disease without a picture of organ damage and symptoms of acute respiratory infections. Serous enteroviral meningitis begins acutely, with an increase in temperature (up to 39-40 ° C) and the appearance of symptoms of general intoxication. By the end of the 1st day or on the 2nd day, the whole complex of meningeal symptoms appears: severe headache, stiff neck, Kernig's symptoms, etc. Sometimes exanthema is observed. The cerebrospinal fluid is clear, cytosis is about 200-300 in 1 μl, neutrophils are up to 50%, the amount of sugar and chlorides is within normal limits. Herpangina. The disease is characterized by an acute onset, body temperature is elevated to 39-40 ° C, but the general condition of the patients does not suffer too much. Fever lasts 3-5 days. Sore throat is mild or may be absent. The pharynx mucosa is hyperemic, single (from 1 to 20) papules appear on it, they quickly turn into vesicles with a diameter of about 5 mm. Soon, in their place, superficial ulcerations appear, covered with a grayish coating and surrounded by a narrow rim of the mucous membrane. Individual ulcers may merge with each other. They are usually localized on the anterior arches.

Treatment. Both symptomatic and pathogenetic therapy is prescribed. With serous meningitis, prednisolone is included in the therapy for 5-7 days.

The prognosis is favorable. Enteroviral encephalomyocarditis in newborns has a severe course.

Prevention. Timely detection and isolation of patients (for a period of 14 days). In children's groups, all contacts are given normal human immunoglobulin (gamma globulin) at a dose of 0,3 ml/kg.

2. Polio

Infantile spinal paralysis is an acute infectious disease that is caused by one of the three types of the polio virus and is characterized by a wide range of clinical manifestations - from abortive to paralytic forms.

Etiology. The virus belongs to the family Picornaviridae, genus Enterovirus. Virions have a diameter of 18-30 nm. The viral particle consists of single-stranded RNA and a protein shell. Three main serotypes: 1 (Brunhild), 2 (Lansing), 3 (Leoon). Viruses tolerate freezing well and persist for several years. They are sensitive to the action of ordinary disinfectant solutions and ultraviolet rays; at a temperature of 60 ° C they die within 30 minutes, and when boiled - instantly. Resistant to all known antibiotics and chemotherapy drugs.

Pathogenesis. The primary reproduction of the virus occurs in the nasopharynx or intestines. Dissemination of the virus occurs through the lymphatic system, and viremia develops. The reproduction of the virus occurs in various organs and tissues (lymph nodes, spleen, liver, lungs, heart muscle, brown fat), the pathological process can be interrupted at this stage - inapparent and abortive forms of the disease. The virus enters the central nervous system through the endothelium of small vessels and peripheral nerves. Within 1-2 days, the titer of the virus in the central nervous system increases, and then begins to fall and soon disappears completely. Poliovirus infects motor neurons located in the gray matter of the anterior horns of the spinal cord and the nuclei of the motor cranial nerves in the brainstem. An inflammatory process similar to serous meningitis develops in the membranes of the brain.

Clinic. Forms of poliomyelitis without damage to the central nervous system. The incubation period lasts approximately 4-30 days (usually 6-21). The inapparent form occurs as a carrier state and is not accompanied by clinical symptoms. The abortive (“minor disease”) form is characterized by general infectious symptoms without signs of damage to the nervous system (moderate fever, intoxication, slight headache, sometimes minor catarrhal symptoms of the upper respiratory tract, intestinal dysfunction). Forms of poliomyelitis with damage to the central nervous system. Meningeal: the disease begins acutely and can have a one- or two-wave course. Severe headache, repeated vomiting and meningeal symptoms accompanied by high fever are noted. In a two-phase course, the first wave occurs without signs of damage to the meninges, reminiscent of the symptoms of the abortive form, but on the 1st-5th day, against the background of normal temperature, the second wave develops with the clinical manifestations of serous meningitis. Pain in the limbs, neck and back, positive symptoms of tension and pain on palpation along the nerve trunks may occur.

paralytic forms. During the course of the disease, four periods are distinguished: preparalytic, paralytic, restorative, residual. The preparalytic period lasts from the onset of the disease until the first signs of damage to the motor sphere appear. The disease begins acutely, with an increase in temperature to high numbers, the appearance of weakness, anorexia. Half of the patients have moderate catarrhal phenomena, intestinal dysfunction. The meningoradicular syndrome is characteristic: headaches, repeated vomiting, pain in the extremities and back, hyperesthesia, neck muscle stiffness, positive Kernig, Brudzinsky syndromes, tension of the nerve trunks and roots, and periodic twitching in certain muscle groups. The paralytic period lasts from the moment of the appearance of paresis and paralysis and during the time of their stabilization. The clinic of the paralytic period is determined by the localization of the lesion in the nervous system. There are spinal, bulbar, pontine and mixed forms (pontospinal, bulbospinal).

Spinal form (the most common form of the disease). Typically, the rapid development of paralysis in a short time - from several hours to 1-3 days. Paralysis is sluggish in nature (low muscle tone, hypoareflexia, subsequently developing muscle atrophy). The lower extremities are most commonly affected. Pyramidal signs, loss of functions of the pelvic organs do not happen, sensitivity disorders are not characteristic. The asymmetric distribution of paralysis and paresis is characteristic, associated with the mosaic nature of the damage to the nuclei of the spinal cord. The paralytic period lasts from several days to 2-4 weeks. Differential diagnostic signs of flaccid paresis and paralysis in acute poliomyelitis:

1) the period of increase in motor disorders is very short (from several hours to 1-2 days). An increase in paresis over 3-4 days is a rare exception and is a reason to doubt the diagnosis;

2) the proximal limbs suffer more often;

3) paresis and paralysis have an asymmetric (mosaic) arrangement;

4) sensory, pelvic disorders and pyramidal symptoms are absent;

5) muscle atrophy appears early, on the 2-3rd week of the disease and further progresses.

Bulbar form, as a rule, has a severe course with a short preparalytic period, accompanied by dysfunction of vital organs. The onset of the disease is acute, the condition from the very beginning of the disease is severe: high fever, vomiting, weakness, malaise. Paresis and paralysis of the soft palate, swallowing and phonation disorders are noted. Patients experience a sharp increase in the formation of mucus with obstruction of the airways (wet form), shortness of breath, cyanosis, and bubbling breathing. Patients develop respiratory rhythm disturbances, pathological types of breathing, tachy- and bradyarrhythmias. A soporous, comatose state quickly develops.

The pontine form develops with a separate lesion of the nucleus of the facial nerve (VII pair of cranial nerves). Clinically, this is one of the least severe forms of paralytic poliomyelitis, its course is most favorable. Upon examination, loss of movements of the facial muscles, facial asymmetry, and exophthalmos will be noted. Patients do not complain of pain or lacrimation. The recovery period for the spinal form begins 2-3 weeks from the onset of the disease. As a rule, deeply affected muscles do not provide complete recovery or do not show any tendency to reverse the development of paralysis. Uneven and mosaic recovery of the affected muscles leads to the development of skeletal deformities and contractures. The period of residual effects usually occurs 1-1,5 years from the onset of the disease. Characterized by muscle atrophy, bone deformities, contractures, osteoporosis.

differential diagnosis. In the meningeal form, a differential diagnosis is made with serous meningitis of a different etiology. In the spinal form, a differential diagnosis is made with osteoarticular pathology, polyradiculoneuropathy, myelitis, and poliomyelitis-like diseases. The pontine form requires differential diagnosis with neuritis of the facial nerve.

Diagnosis is based on data from clinical, laboratory and instrumental diagnostic methods. Virological examination: a study of nasopharyngeal swabs, feces, less often cerebrospinal fluid, blood is carried out. The first sample of faeces is taken at the time of diagnosis, the second - after 24-48 hours. Serological methods: a blood test for paired sera with an interval of 2-3 weeks. A 4-fold increase in antibody titer is considered diagnostic. CSF examination: in the preparalytic and at the beginning of the paralytic period, lymphocytic cytosis is noted (sometimes neutrophils predominate at the very beginning) up to 100-300 cells per 1 μl, a moderate increase in protein levels (up to 1 g / l). By the end of the third week in the cerebrospinal fluid, against the background of a decrease and normalization of cytosis, there is an increase in protein up to 1-2 g/l (protein-cell dissociation replaces cell-protein dissociation). Elevated protein levels sometimes persist for up to 1,5 months. Complete blood count: there may be moderate neutrophilic leukocytosis at the onset of the disease. Electromyography: a straight line is recorded in severely affected muscles, which indicates the death of neurons.

Treatment. Dehydration and removal of edema of the brain substance (diacarb, lasix, magnesium sulfate, etc.). Detoxification therapy in the mode of dehydration using hypertonic glucose solutions, colloidal solutions (hemodez, etc.). Desensitizing drugs. Glucocorticoids are used only in the presence of vital indications (with cerebral edema, collapse). Antibiotics are used in the development of bacterial complications. At the end of the paralytic period, the complex of therapeutic measures includes anticholinesterase drugs (prozerin, galantamine, kalimin), strychnine, dibazol, B vitamins, glutamic acid. During the rehabilitation period - nootropic drugs, anabolic drugs (carnitine, retabolil, etc.), actovegin, etc. Exercise therapy and massage are of great importance in the treatment of poliomyelitis.

Prevention. Since 1959, Russia has used the live trivalent Seibin vaccine from attenuated strains of the polio virus. Vaccination is carried out from 3 months of age with an interval of 1,5 months three times. Revaccination is carried out in the second year of a child’s life and before school. Criteria for vaccine-associated polio (WHO, 1964):

1) the onset of the disease is not earlier than the 4-6th day and not later than the 30th day after taking the vaccine. For contacts with vaccinated, the maximum period is extended to the 60th day;

2) flaccid paralysis or paresis develops without a violation of sensitivity with persistent residual phenomena (after 2 months);

3) there is no long-term progression of paresis (more than 3-4 days);

4) isolation of a polio virus related to the vaccine strain, and at least a fourfold increase in specific antibodies to it in the blood.

LECTURE No. 26. Acquired immunodeficiency syndrome. Etiology, pathogenesis, clinic, diagnosis, treatment

Acquired immunodeficiency syndrome (AIDS) is a particularly dangerous viral infection with a long incubation period. It is characterized by suppression of cellular immunity, the development of secondary infections (viral, bacterial, protozoal) and tumor lesions, resulting in the death of patients.

Etiology. The causative agent of AIDS is a human T-lymphotropic virus of the retrovirus family. The virus was isolated in 1983 and was initially designated LAV and also HTLV-111. Since 1986, it has been called human immunodeficiency virus (HIV). Retroviruses have a reverse transcriptase enzyme. Viruses are grown in cell culture. Heating at 56°C kills viruses. Two types of human immunodeficiency virus have been discovered. Many of their properties have not been studied enough.

Pathogenesis. The entrance gates of AIDS are microtraumas of the skin (contact with blood) and the mucous membranes of the reproductive system or rectum. From the moment of infection until the appearance of the first symptoms of the disease (latent (incubation) period) can take from 1 month to 4-6 years. Persistence and reproduction of the virus occurs in lymphoid tissue. However, already at this moment the virus periodically penetrates the blood and can be detected in secretions. Such individuals without severe AIDS symptoms can be sources of infection. The intensity of viremia determines clinical manifestations. The pathogenesis of AIDS is based on the T-lymphotropic nature of the virus. AIDS viruses, replicating in T4 cells (helpers), inhibit their proliferation and disrupt the structure of the T-helper plasmalemma proteins. A change in their structure prevents the recognition of infected T4 cells and their destruction by cytotoxic T8 lymphocytes. There is a suppression of proliferation and a decrease in the absolute number of T4 cells. A defect in the mechanism of recognition of AIDS virus antigens is manifested by increased synthesis of antibodies of classes A and G, which, however, do not have the ability to neutralize the pathogen.

Deficiency of immunity leads to the development of latent infections or the addition of an opportunistic (random) disease caused by opportunistic microbes. It is these diseases that determine the outcome and lead to the death of patients in the next 1-2 years after the appearance of the first clinical symptoms of AIDS. A decrease in cellular immunity also leads to the occurrence of some malignant tumors (Kaposi's sarcoma, brain lymphoma). The most common associated infections include Pneumocystis pneumonia, gastrointestinal and pulmonary forms of cryptosporoidosis, generalized toxoplasmosis, which often occurs in the form of encephalitis, generalized manifestations of herpetic and cytomegalovirus infections, mycoses, and bacterial infections.

Russian classification of HIV infection (V.I. Pokrovsky, 2001)

1. Stage of incubation.

2. Stage of primary manifestations, course options:

1) asymptomatic;

2) acute HIV infection without secondary diseases;

3) acute infection with secondary diseases.

3. Latent stage.

4. Stage of secondary diseases, course options:

1) weight loss less than 10%; fungal, viral, bacterial lesions of the skin and mucous membranes, shingles; repeated pharyngitis, sinusitis;

2) weight loss of more than 10%, unexplained diarrhea or fever for more than 1 month, hairy leukoplakia, pulmonary tuberculosis, recurrent or persistent viral, bacterial, fungal, protozoal lesions of internal organs, recurrent or disseminated herpes zoster, localized Kaposi's sarcoma;

3) cachexia, generalized bacterial, viral, fungal, protozoal and parasitic diseases, pneumocystis pneumonia, candidiasis of the esophagus of the bronchi, lungs, extrapulmonary tuberculosis, atypical mycobacteriosis, disseminated Kaposi's sarcoma, lesions of the central nervous system of various etiologies.

Phases: progression (against the background of the absence of antiretroviral therapy, against the background of antiretroviral therapy), remission (spontaneous, after previous or against the background of antiretroviral therapy).

5. Terminal stage.

Clinic. The incubation period usually lasts about 6 months. The onset of the disease is gradual. The initial (prodromal, nonspecific) period is characterized by an increase in body temperature (above 38 ° C) with profuse sweating and symptoms of general intoxication (lethargy, depression, decreased performance). Damage to the digestive system is also observed; esophagitis (pain when swallowing, ulcers of the esophagus) of candidal etiology, less often viral (herpetic, cytomegalovirus) may develop. Enteritis is characterized by abdominal pain, diarrhea; sigmoidoscopy shows no changes. Enteritis is most often caused by protozoa (Giardia, Cryptosporidae, Isospora) and helminths (Strongyloidiasis), less often by cytomegaloviruses. Colitis is most often caused by salmonella, campylobacter, sometimes dysenteric amoebae and chlamydia. Homosexuals may first of all show signs of proctitis of gonococcal origin, syphilitic, and less commonly, damage by cytomegaloviruses and herpes viruses. Characteristic of the initial period of AIDS is the presence of generalized lymphadenopathy. The process begins mainly from the cervical, axillary and occipital lymph nodes.

AIDS is characterized by damage to the lymph nodes in at least two places for 3 months or more. They can increase up to 5 cm in diameter and be painless. During the development of the disease, the lymph nodes may merge. Splenomegaly is detected in 20% of patients with lymphadenopathy. More than half of the patients experience skin changes - maculopapular elements, seborrheic dermatitis. Fever, resistant to steroid drugs, etc. appears. The presence of AIDS can be confirmed based on the simultaneous detection of two or more clinical signs that make up this complex, and two or more laboratory diagnostic signs. Next, it is necessary to conduct a set of special studies that will confirm the final diagnosis.

Symptom complex related to AIDS.

1. Clinical signs (for 3 months or more):

1) unmotivated lymphadenopathy;

2) unmotivated loss of body weight (more than 7 kg or 10% of body weight);

3) unmotivated fever (constant or intermittent);

4) unmotivated diarrhea;

5) unmotivated night sweats.

2. Laboratory and diagnostic signs:

1) reduced number of T-helpers;

2) change in the ratio of T-helpers and T-suppressors;

3) anemia, leukopenia, thrombocytopenia or lymphopenia;

4) an increase in the amount of immunoglobulins A and G in the blood serum;

5) decrease in the reaction of blast transformation of lymphocytes into mitogens;

6) the absence of a delayed-type hypersensitivity skin reaction to several antigens;

7) increase in the level of circulating immune complexes.

The manifest period of AIDS (the period of the peak of the disease) is characterized by the predominance of clinical manifestations of a secondary (opportunistic) infection. Almost half of the patients develop lung lesions (pulmonary type of AIDS), most often caused by pneumocystis. Pneumocystis pneumonia is severe, mortality is 90-100%. There are pains in the chest, aggravated by inhalation, shortness of breath, cough, cyanosis. The radiograph shows multiple infiltrates in the lung tissue. Lung diseases caused by legionella and various bacterial pathogens are also severe. The lungs are also affected in generalized cytomegalovirus infection. When lung abscesses form, a fungal infection can develop in their cavities. In 30% of patients, CNS lesions in the form of encephalitis caused by generalized toxoplasmosis infection, less often cytomegalovirus and herpetic, come to the fore. Signs of encephalitis may be combined with a picture of serous meningitis. Primary or secondary brain lymphoma may also develop. In some cases, AIDS patients are dominated by prolonged fever and general intoxication. Fever is often of the wrong (septic) type. This is usually a rare disease in older people with a primary lesion of the skin of the lower extremities. The disease is steadily progressing. Patients with manifest forms of AIDS die within the next 1-2 years.

Diagnostics. Examination of the contingent, as well as the stages and scope of clinical and laboratory studies, are regulated by the Decree of the Presidium of the Supreme Soviet of the USSR of August 25.08.1987, XNUMX, and the rules for medical examination for the detection of infection with the AIDS virus, established by the USSR Ministry of Health in accordance with the provisions of this Decree. Research is carried out in specially designated laboratories.

Treatment. Effective etiotropic agents currently do not exist. Antiviral drugs (azidothymidine, virazole) are prescribed. With the development of a secondary infection, drugs are used to treat it. Treatment also includes the use of immunomodulators. At best, the improvement is only temporary, then a new infectious factor joins, and the disease recurs.

Prevention. General preventive measures are carried out in accordance with the Decree of the Presidium of the Supreme Soviet of the USSR of August 25.08.1987, 70 "On measures to prevent infection with the AIDS virus." Patients are placed in separate boxes, they are cared for by specially assigned instructed personnel. The sampling of blood and other materials, as well as their processing, is carried out in rubber gloves. If infectious material gets on the skin, it must be treated with medical alcohol with a strength of 1% or a XNUMX% solution of chloramine. Laboratory glassware containing blood and other materials must be specially marked. Work is underway to create specific immunoprophylaxis.

Author: Gavrilova N.V.

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