Infectious diseases. Cheat sheet: briefly, the most important

Lecture notes, cheat sheets
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Infectious diseases. Cheat sheet: briefly, the most important

Lecture notes, cheat sheets

Table of contents

1. Escherichiosis

Escherichiosis is an acute infectious disease, mainly in young children, caused by various serovars of pathogenic Escherichia coli. They are characterized by the development of pathological processes in the gastrointestinal tract with infectious-toxic and diarrheal syndrome.

Certain strains of E. coli can cause severe diarrhea in children.

They are classified into:

1) enteropathogenic (EPKP) (Escherichia coli);

2) enterotoxigenic (ETCP);

3) enteroinvasive (EICP) E. coli;

4) lining.

Etiology. E. coli is a Gram-negative motile aerobic (facultatively anaerobic) bacillus.

Pathogenesis. ETCS can produce a thermostable, thermolabile toxin, or both simultaneously, the production of which is genetically controlled by transferred plasmids.

EICP can penetrate into the cells of the intestinal epithelium and multiply in them like shigella, resulting in edema, hyperemia, ulceration of the mucous membrane and increased exudation into the intestinal lumen.

Also, the pathogenetic mechanism is adhesion, lining and damage to the villous surface of the intestinal epithelium with a decrease in the activity of parietal enzymes, but without invasion.

Clinical manifestations. Diarrhea associated with EPEC is characterized by watery stools, which can be up to 10-20 times a day, and a slight increase in body temperature. In the feces there is an admixture of mucus, but there is no blood. Spontaneous healing occurs in 3-7 days. Young children may develop vomiting, dehydration, and electrolyte disturbances with acidosis.

Traveler's diarrhea due to ETEC is characterized by the sudden onset of frequent (10-20 times per day) liquid stools 1-2 weeks after arrival in the country. Acute diarrhea is often accompanied by severe cramping abdominal pain, nausea, and vomiting.

In patients with EIKP infection, symptoms develop after 18-24 hours (incubation period), the body temperature suddenly rises, severe diarrhea appears with urges and tenesmus, an admixture of mucus and blood in the feces is observed.

The disease caused by E. coli lining strains is characterized by a gradual onset and a chronic course. Children are slow growing and intolerant of certain foods.

Diagnosis. Gastroenteritis can be suspected with a sudden outbreak of an epidemic of diarrhea, especially in a children's team. Similar serotypes of E. coli can also be found in the nasopharynx, pharynx and stomach of patients.

Treatment. The main elements of treatment in children are the correction and maintenance of water and electrolyte balance.

Neomycin has been effective in treating diarrhea associated with EEC in young children.

Traveler's diarrhea (caused by ETEC in 60% of cases) responds well to treatment with trimethoprimsulfomethoxazole or trimethoprim alone when given early.

2. Salmonella

Salmonellosis is an acute infectious disease of humans and animals caused by Salmonella serovars and occurring in children more often in the form of gastrointestinal, less often typhoid-like and septic forms.

Etiology. Salmonella are motile Gram-negative bacteria that do not have a capsule and do not form spores. The main antigens of Salmonella are flagellar (H), cell wall antigens (O) and thermolabile envelope antigens (Vi), blocking the agglutination reactions of O-antigens and O-antibodies. There are more than 2200 serotypes of Salmonella.

Salmonella are resistant to many physical factors, they die at a temperature of 54,4 ° C after 1 hour, and at 60 ° C - after 15 minutes.

Epidemiology. Human infection occurs through the consumption of contaminated food or water. The main carrier of Salmonella is a person, often serving as a source of food contamination and poisoning.

Salmonella indirectly stimulates the energy system of intestinal epithelial cells, resulting in increased secretion of water and electrolytes.

Clinical manifestations. The incubation period is 8-48 hours. The onset is acute, accompanied by nausea, vomiting, cramping pains in the abdomen, after which a large amount of feces of a liquid consistency, sometimes mixed with mucus and blood, leaves. Vomiting is usually profuse and short-lived. Body temperature rises to 38-39 ° C in 70% of patients.

Infection in some individuals proceeds without fever with minor bowel dysfunction. In other patients, the body temperature rises sharply, headaches appear, consciousness is disturbed, convulsions and meningeal phenomena develop. Sometimes there is a strong bloating, muscle tension, significant local pain.

Hematogenous dissemination of Salmonella is accompanied by chills and fever. It usually occurs in children under 3 months of age. Salmonella can settle in any organ, causing pneumonia, abscesses, empyema, osteomyelitis, purulent arthritis, pyelonephritis, or meningitis.

Complications. Children have reactive arthritis, which develops 2 weeks after the onset of diarrhea, Reiter's disease.

The diagnosis is made on the basis of the results of bacteriological studies, when the material is incubated on a medium enriched with tetrathionate, followed by transfer to a selective medium.

Treatment. Treatment should be aimed at correcting electrolyte disturbances and maintaining adequate hydration. Treatment with antibiotics is indicated only in some cases: when there is a danger of spreading the infection.

With septicemia, high body temperature and metastatic foci of infection, children should be treated with ampicillin, amoxicillin or levomycetin, one of which is prescribed in 4 doses with an interval of 6 hours.

3. Typhoid fever. Epidemiology. Pathogenesis. Pathomorphology

Typhoid fever is an acute infectious disease caused by typhoid bacilli. Characteristic features are the predominant lesion of the lymphatic apparatus of the small intestine, high fever, severe intoxication and bacteremia.

Epidemiology. The transmission of the pathogen is carried out by contact-household, water, food, and also by flies.

Pathogenesis. Typhoid infection is always accompanied by clinical symptoms. Virulent typhoid pathogens suppress oxidative processes in neutrophils at the final stages of phagocytosis, saving themselves from destruction. Monocytes in the initial period of infection, unable to destroy the pathogen, transport it to the mesenteric lymph nodes and other parts of the reticuloendothelial system, in which it multiplies. Inflammatory changes occur in the lymph nodes, in the liver and in the spleen. Pathogens quickly penetrate the wall of the upper small intestine without causing pronounced inflammatory changes, and from there into the general circulation. A short septicemia causes infection of many organs of the reticuloendothelial system, in the cells of which microorganisms concentrate and multiply. Secondary bacteremia is usually more prolonged and leads to the defeat of many organs. The gallbladder is damaged by the hematogenous route and through the bile duct system.

The outer shell of the cell wall of Salmonella is a complex of lipopolysaccharides

(endotoxin). The accumulation of typhoid bacteria and the release of endotoxin cause characteristic histological changes in the intestine, liver, skin, and other organs.

Cellular immunity mechanisms play an important role in resistance to typhoid fever. A significant decrease in the number of T-lymphocytes occurs in patients with especially severe forms of this disease.

Pathomorphology. Morphological changes in typhoid infection in young children are less pronounced than in adults or children of older age groups. Lymph nodes of the mesentery, liver and spleen are usually plethoric, they revealed foci of necrosis. Characteristic features include reticuloendothelial hyperplasia with proliferation of monocytes. Swollen liver cells. Signs of inflammation and necrotic changes on the intestinal mucosa and in the lymphatic formations of its walls are expressed. A mononuclear reaction also develops in the bone marrow, which also shows foci of necrosis. Inflammatory changes in the walls of the gallbladder are focal and unstable. Bronchitis is observed in most patients with typhoid fever. Inflammatory processes can be manifested by pneumonia, osteomyelitis, abscesses, purulent arthritis, pyelonephritis, endophthalmitis and meningitis. Typhoid bacteria can be found in all organs.

4. Typhoid fever. Clinic. Complications. Diagnostics. Treatment

Clinical manifestations. In children, the disease manifests itself as mild gastroenteritis or severe septicemia. Vomiting, bloating, and diarrhea are common.

The incubation period of the disease in older children ranges from 5 to 40 days, more often 10-20 days. It is followed by the initial period of the disease, characterized by a gradual increase in body temperature, malaise, myalgia, headaches and abdominal pain, diarrhea, and less commonly, constipation. Within 1 week, body temperature becomes constant, malaise, anorexia, weight loss, cough, abdominal pain and diarrhea increase. The patient becomes inhibited, he develops depression, delirium and a stuporous state. Maculopapular rashes appear in 80% of sick children. They occur sequentially for 2-3 days and are found on the skin of the abdominal wall and lower chest in the form of spots with a diameter of 1-6 mm.

Complications. Typical complications for typhoid fever are intestinal bleeding and intestinal perforation, less often - neurological complications, acute cholecystitis, thrombosis and phlebitis. Pneumonia often complicates typhoid fever at the height of the disease.

Laboratory research methods. Normochromic normocytic anemia is observed in patients with typhoid fever who have intestinal bleeding or toxic suppression of bone marrow function. Leukopenia is rare. With the development of purulent abscesses, the number of leukocytes increases to 20-000 per 25 ml. Thrombocytopenia can be significantly pronounced and persists from several days to 000 week. Melena and proteinuria are associated with a feverish state.

Diagnosis. Typhoid fever is diagnosed on the basis of prolonged fever, headache, increasing intoxication with the development of "typhoid status", characteristic changes in the tongue, the appearance of flatulence, roseolous rash, hepatosplenomegaly and characteristic changes in the peripheral blood, as well as on the basis of the results obtained:

1) laboratory research;

2) serological diagnostics;

3) express diagnostics of typhoid fever. Treatment. Patients with typhoid fever are subject to mandatory hospitalization. Important in the treatment of children with typhoid fever is the maintenance of adequate hydration and electrolyte balance. The development of shock as a result of intestinal perforation or severe hemorrhage is an indication for the introduction of large amounts of fluid intravenously.

Treatment is carried out with drugs that have a bacteriostatic effect on typhoparatyphoid bacteria (levomycetin, ampicillin, rifampicin, amoxicillin, unazine, amoxiclav). Along with etiotropic treatment, antifungal drugs (nystatin, levorin, etc.), antihistamines are prescribed.

5. Shigellosis (bacterial dysentery)

The disease is an acute inflammatory process in the gastrointestinal tract caused by bacteria from the genus Shigella and characterized by fever, cramping abdominal pain and diarrhea mixed with mucus, pus and blood in the stool.

Etiology. Shigella are short, immobile Gram-negative rods whose biochemical feature is the absence or very slow fermentation of lactose.

Epidemiology. Shigella are common throughout the world.

Man serves as the main reservoir of infection. Ways of infection: contact-household, food, water.

Pathogenesis. Infection with a small number of Shigella (less than 200) is sufficient for the development of the disease. Pathogens remain viable in the acidic environment of gastric contents for 4 hours. The infection develops only when the pathogen penetrates into the epithelial cells of the intestine.

Clinical manifestations. The incubation period depends on the route of infection and the dose of the pathogen and usually ranges from 6-8 hours to 7 days, more often 36-72 hours, during which the Shigella reach the large intestine. Initially, patients complain of fever and cramping abdominal pain. Body temperature can reach 40 ° C, the phenomena of general intoxication intensify. 48 hours after the onset of the disease, diarrhea appears, stools with blood and mucus occur up to 20 times a day. When examining the child, there is a slight soreness of the abdomen on palpation without a clear localization.

At high temperature and convulsions, shigellosis may be accompanied by symptoms of damage to the nervous system, resembling meningitis, encephalitis.

Diagnosis. Dysentery should be suspected in all patients with diarrhea accompanied by fever. The diagnosis of shigellosis is established on the basis of clinical and epidemiological data, with mandatory laboratory confirmation.

For the final diagnosis use:

1) bacteriological method;

2) serological methods;

3) express diagnostic methods;

4) sigmoidoscopy method;

5) scatological method;

6) examination of peripheral blood. Treatment. Significantly when treated with antibiotics

the duration of the disease and the timing of the isolation of shigella are reduced. Prolonged bacteriocarrier develops very rarely. In such cases, lactulose, a derivative of lactose, causes a temporary effect.

Forecast and prevention. In most previously healthy children, shigellosis proceeds favorably and is prone to spontaneous recovery.

Strict adherence to the rules of personal hygiene and sanitary measures are the basis for the prevention of shigellosis.

6. Cholera. Etiology. Epidemiology. Pathogenesis

Cholera is an acute intestinal disease caused by Vibrio cholerae (serotype 01) capable of producing an enterotoxin. Manifestations of cholera range from asymptomatic to extremely severe forms, when the onset of the disease leads to hypovolemic shock, metabolic acidosis and, in untreated cases, death.

Etiology. The causative agent of cholera is a short, slightly curved, mobile Gram-negative bacillus with a single, polarly located flagellum. There are about 70 serotypes of the pathogen, but only serotype 01 causes true cholera. Vibrio grows well on various nutrient media. The causative agent of serotype 01 forms opaque, yellow colonies on them. Two different biotypes of V. cholerae 01 have been identified: classical and El Tor.

Epidemiology. Endemic outbreaks and epidemics of cholera are characterized by a pronounced seasonal pattern. The source of infection in cholera is only a sick person, or vibrio carrier. Individuals with asymptomatic or mild cholera play an important role in spreading the infection. Long-term bacteriocarrier, when the gallbladder of adults who have had cholera caused by El Tor, serves as the reservoir of the pathogen, does not occur in children. The mechanism of infection transmission is carried out through the external environment - the water way of infection is more important.

Pathomorphology and pathophysiology. The entrance gate of infection is the gastrointestinal tract, the main breeding site of vibrios is the lumen of the small intestine, where they attach to the surface of the epithelial cells of the mucous layer and produce enterotoxin, which is fixed on the receptors of the cell membrane. The active subunit of the toxin enters the cell and activates the enzyme adenylate cyclase. This contributes to increased production of cAMP, which leads to a decrease in the active absorption of sodium and chloride and an increase in the active secretion of sodium by crypt cells. The result of these changes is a massive release of water and electrolytes into the intestinal lumen.

A biopsy of the mucous membrane of the small intestine during this period of the disease reveals an intact epithelium with minimal reactive changes in the cells. Histological examination reveals an increase in the size and clarification of goblet cells, which indicates an increase in their secretion of mucus. There is also a slight edema of the lamina propria, an expansion of the blood and lymphatic vessels in the region of the tips of the intestinal villi.

The liquid released into the intestinal lumen is isotonic with plasma, it contains a large amount of sodium and potassium bicarbonate. The feces of children with cholera contain more potassium, and sodium, chloride and bicarbonate - less compared to the feces of adults with cholera. The loss of fluid leads to a deficiency of sodium and water, the development of acidosis and a decrease in potassium levels.

7. Cholera. Clinic. Diagnostics. Complications

Clinical manifestations. The incubation period lasts from 6 hours to 5 days, in vaccinated - up to 9-10 days. Clinical manifestations largely depend on the age of the child. Cholera usually begins acutely: copious watery stools suddenly appear, in the most severe cases they become more frequent, very copious, they pass freely, and they look like rice water and acquire an unusual smell. In less severe cases, the stools are yellowish in color. Vomiting is characteristic only for severe forms of infection, it usually develops after the onset of diarrhea. Sharp weakness and adynamia is one of the most characteristic and early signs of cholera.

Massive fluid loss can be accompanied by a decrease in body weight by 10% or more, which leads to deep dehydration and vascular collapse. In the most severe cases, blood pressure decreases, the pulse on the radial artery is not detected, breathing becomes deep and quickens, urine output stops. The eyes and fontanelles sink, the skin is cold, sticky, its turgor is reduced, it gathers in folds on the fingers. Cyanosis is observed, painful contractions of the muscles of the extremities, especially the calves, appear. Patients are restless, experience extreme thirst. Lethargy may develop, the voice becomes low and quiet.

Diarrhea continues for 7 days. Subsequent manifestations of the disease depend on the adequacy of the therapy. The earliest sign of recovery is the normalization of the color of the stool, after which the diarrhea quickly stops.

Diagnosis. Cholera is diagnosed on the basis of the characteristic clinical picture of the disease, the epidemiological situation and the results of laboratory tests using:

1) bacteriological method, which is of decisive importance and includes microscopy of preparations from the studied biomaterial (feces, vomit, etc.) and its inoculation on a nutrient accumulation medium;

2) express methods of approximate value: luminescent-serological, microagglutination reaction, Polev-Yermolyeva method;

3) serological methods aimed at the detection of specific antibodies in the blood, using the agglutination reaction, the detection reaction of vibriocidal antibodies, the luminescent-serological method and the phage adsorption reaction.

Complications. In children, complications after suffering cholera are more common and more severe than in adults. Inadequate replacement of potassium losses can lead to hypokalemia, nephropathy, cardiac arrhythmias, and paralytic ileus. Too rapid transfusion of large amounts of fluid without correction of acidosis can lead to pulmonary edema. Before or during treatment, 10% of young children may develop coma, convulsions, or prolonged lethargy.

8. Cholera. Treatment. Prevention

Treatment. The main condition for successful treatment is the rapid replacement of the excreted water and electrolytes.

Patients admitted in a state of severe dehydration and hypovolemic shock should immediately begin intravenous fluid administration. The choice of fluid for intravenous administration to the patient is determined by the nature of the losses. Moderately or slightly severe dehydration allows you to start treatment with enteral fluid. Solutions can be prepared using potable water, but should be prepared daily to avoid bacterial contamination. If necessary, the solution is administered through a gastric tube or nasogastric tube. Vomiting is not a contraindication to oral fluid administration, but fluid should be given in smaller amounts and more frequently. Glucose malabsorption and increased diarrhea occur in 1% of patients. In such cases, it is necessary to switch to an intravenous method of treatment.

After replacing the excreted fluid, it is necessary to continue maintenance therapy, compensating for the consumption of fluid and electrolytes with sweat and feces. Supportive hydration therapy can be carried out by enteral administration of electrolyte and glucose solutions.

Normal and nutritious nutrition, appropriate for age, should be started as soon as the child can eat, in order to prevent further deterioration of the condition of patients associated with malnutrition. High-calorie foods enriched with potassium should be prescribed.

2-6 hours after the start of intensive therapy and the removal of the patient from the state of shock, he is prescribed tetracycline for oral administration, which helps to reduce the duration of diarrhea and the volume of bowel movements by 50-70%, as well as reduce the period of bacteria isolation. Tetracycline and other etiotropic drugs are prescribed according to age dosages for a 5-day course.

Prevention. Cholera prevention is based on a system of measures aimed at preventing the introduction of infection from endemic foci; identification of patients and vibrio carriers, their timely isolation and rehabilitation of the pathogen; localization and elimination of the focus of infection with a system of quarantine measures, including isolation and examination of persons in contact with the sick person, provisional hospitalization of all those suffering from diarrheal diseases in the focus of infection.

Chemoprophylaxis for cholera consists in prescribing tetracycline 500 mg every 6 hours for children over 13 years old, 125 mg for children aged 4–13 years for 2 days, and 50 mg for children under 3 years of age. Simpler methods include a single dose of doxycycline (300 mg for adults and 6 mg/kg for children). Chemoprophylaxis is effective against family contacts. The effectiveness of mass chemoprophylaxis remains questionable.

9. Meningococcal infection. Etiology. Epidemiology. Pathogenesis. Pathomorphology

Meningococcal disease is an acute human infectious disease caused by meningococcus. It is characterized by a variety of clinical forms - from nasopharyngitis and healthy carriage to generalized, occurring in the form of meningococcemia, meningitis and meningoencephalitis.

Etiology. The causative agent of meningococcal infection, Neisseria meningitidis, is a gram-positive diplococcus that is located intra- and extracellularly. Whimsical to the conditions of cultivation, sensitive to various environmental factors. Meningococcal disease only affects humans.

The disease develops when these microorganisms enter the bloodstream and spread throughout all organs.

Epidemiology. Meningococcal meningitis is a disease of childhood, more than half of the cases occur in children of the first 3 years of life. Infection occurs from adult bacteria carriers, less often through contact with patients or bacteria carriers in medical institutions or kindergartens.

Pathogenesis. In the pathogenesis of the disease, the pathogen, its endotoxin and allergenic substance play a leading role. The entrance gates of infection are the mucous membranes of the nasopharynx and oropharynx. In some individuals, meningococci penetrate the mucous membrane, are captured by leukocytes, and are carried through the bloodstream throughout the body, entering the eyes, ears, lungs, joints, meninges, heart, and adrenal glands. Specific group antibodies to meningococci are formed after a long bacteriocarrier.

Carriage in the nasopharynx of non-typable meningococci belonging to serotypes X, Y and Z or producing lactose is accompanied by the production of antibodies to meningococci serotypes A, B and C. Bactericidal antibodies that cross-react with meningococci can also be formed when infected with other gram-negative and gram-positive bacteria and many people prevent the development of meningococcemia.

Pathomorphology. The disease caused by meningococci is accompanied by an acute inflammatory reaction. Endotoxemia can lead to diffuse vasculitis and disseminated intravascular coagulation. Vessels of small caliber are filled with clots containing a large amount of fibrin and leukocytes. Hemorrhages and necrosis are found in all organs, hemorrhages in the adrenal glands are especially characteristic of patients with clinical signs of septicemia and shock.

Meningococcal infection is more common in individuals with a deficiency of the terminal component of complement (C5-C9), as well as in the depletion of the complement system. Fulminant meningococcal infection develops in family members with congenital disorders of the alternative pathway of complement conversion, properdin. Predisposition to meningococcal infections is associated with the presence of leukocyte histoantigen B27, which is statistically confirmed. There is also dependence on immunoglobulin G2 deficiency.

10. Meningococcal infections. Clinic. Diagnostics. Treatment

Clinical manifestations. The most common manifestation of meningococcal infection is acute respiratory infections of the upper respiratory tract with bacteremia, resembling common colds.

Acute meningococcemia can present as a flu-like illness with fever, malaise, and muscle and joint pain. Headaches and dysfunction of the gastrointestinal tract may occur. A few hours or days after the onset of the disease, morbilliform petechial or hemorrhagic skin rashes are detected.

Septicemia may be fulminant, accompanied by exceptionally rapid progression of purpura and shock.

Acute meningococcemia is usually not so violent, the severity of the patient's condition varies, and the ongoing therapy gives a good effect. Metastasis of the process to various organs is noted due to hematogenous dispersion of the pathogen. The development of meningitis against the background of acute meningococcemia is accompanied by the appearance of lethargy, vomiting, photophobia, convulsions and other symptoms of irritation of the meningeal membranes.

Chronic meningococcemia is rare in children and is characterized by loss of appetite, weight loss, chills, fever, arthralgia or arthritis, and maculopapular rash.

Diagnosis. In children of the first year of life, the diagnosis is established on the basis of pronounced symptoms of intoxication, anxiety, hyperesthesia, tremor of the hands, chin, convulsions, tension and bulging of the large fontanel, a symptom of suspension.

Lumbar puncture and the results of laboratory tests are of decisive importance in the diagnosis of meningitis: bacteriological examination of the sediment of the cerebrospinal fluid and blood smears, bacteriological cultures on nutrient media of the cerebrospinal fluid, blood, mucus from the nasopharynx, serological research methods that allow to detect a low content of antibodies (RPHA) and a minimum concentration in blood of patients with meningococcal toxin (VIEF), immunoenzymatic and radioimmune research methods.

Treatment. Penicillin G is prescribed for intravenous administration. If there are doubts about the etiology of the disease, ampicillin is used, with an allergy to penicillin - cefuroxime, cefotaxime and ceftriaxone, which give a good effect in the treatment of meningococcal meningitis and other localizations of this infection. In severe infection and threatening shock, immediate intravenous hydrocortisone is indicated. With the development of shock or disseminated intravascular coagulation, the introduction of a sufficient amount of osmotically active fluids is required in order to maintain an adequate level of blood pressure. In this case, patients are shown the introduction of fresh whole blood and heparin.

11. Gonococcal infection. Etiology. Epidemiology. Pathomorphology. Pathogenesis

Gonorrhea is an acute infectious sexually transmitted disease caused by Neisseria gonorrhoeae.

Etiology. The causative agent of gonorrhea - N. gonorrhoeae - refers to aerobic gram-negative diplococci. Serological studies revealed 16 gonococci. Gonococci infect organs covered with columnar epithelium. Stratified squamous epithelium is affected in children and older women.

Epidemiology. Newborns become infected with gonorrhea during childbirth and through contact with contaminated objects. Young children become ill as a result of domestic contact with parents or caregivers. Adolescents in most cases become infected through sexual contact.

Pathomorphology. Inflammatory changes first appear in the epithelium at the site of penetration of the gonococcus and are due to the released endotoxin, consisting of a whitish-yellow discharge, consisting of serum, leukocytes and desquamated epithelium, which often clogs the ducts of the paraureteral or vaginal glands, causing the formation of cysts or abscesses.

In untreated patients, the inflammatory exudate is replaced by fibroblasts, tissue fibrosis is accompanied by narrowing of the ureter of the urethra.

Gonococci that have penetrated into the lymphatic and blood vessels provoke the development of inguinal lymphadenitis, perineal, perianal, ischiorectal and periprostatic abscesses or dissemination of pathogens and damage to various organs.

Pathogenesis. Pathogens that have fallen on the mucous membranes of the genitourinary tract, conjunctiva, pharynx or rectum are attached to its cells by ciliated structures, which are protein outgrowths on the surface of the microorganism. They protect the pathogen from the action of antibodies and complement and may determine its antiphagocytic properties. Gonococci have a capsule. The multiplicity of types of pathogen, differing in the composition of the capsule, explains the frequency of relapses of the disease. The thickness of the walls of the vagina, the pH of its contents significantly affect the development of gonococci. A widespread infection most often develops after inoculation of the pathogen in the pharynx or rectum.

Gonococcal infection is accompanied by a pronounced immunological restructuring in the majority of patients who develop specific antibodies (normal and secretory IgA) in serum and lymphocytes are sensitized. Despite the presence of serum antigonococcal and secretory antibodies and sensitized lymphocytes, immunity to gonorrhea remains fragile, and reinfections are common.

Gonococci isolated from the disseminated form of the disease require special culture conditions and are more susceptible to low concentrations of antibiotics. In addition, the serum of patients with uncomplicated gonorrhea is more bactericidal than the serum of patients with disseminated forms of the disease.

12. Gonococcal infection. Clinic. Diagnostics. Treatment

Clinical manifestations. The incubation period is 3-7 days, rarely shortened to 2 days or extended to 2-3 weeks.

Clinical forms:

1) fresh gonorrhea - gonorrhea up to 2 months old from the onset of clinical symptoms:

a) acute;

b) subacute;

c) oligosymptomatic;

2) chronic gonorrhea - a disease lasting more than 2 months and of unknown duration.

Symptoms of gonococcal infections depend on:

1) localization of infection;

2) features of the pathogen;

3) reactivity of the macroorganism. Gonococcal carriage is the result of insensitivity of the urethral mucosa and genitourinary apparatus to a strain of gonococcus. At the same time, there is no reaction to gonovaccine, no pathological changes are detected during ureteroscopy.

Gonorrhea in prepubertal boys is manifested by purulent discharge from the urethra, dysuria and hematuria. Edema and balanitis of the penis, epididymitis and periurethral abscesses are rare. Gonococcal proctitis appears when an infection enters the rectum.

Conjunctivitis of gonococcal etiology is detected not only in the neonatal period and is characterized by an acute inflammatory process with abundant yellow or green purulent discharge. Gonococcal arthritis occurs in infants with perinatal infection, is observed in children of puberty, sometimes in the form of arthritis.

The disease in girls is multifocal, with damage to the vagina, vestibule, urethra, rectum, less often - Bartholin's glands. The chronic course of gonorrhea in girls is rare and is more often diagnosed during periods of exacerbation or during a preventive examination. Vaginal examination reveals focal hyperemia and swelling of the vaginal integument.

Diagnostics. The diagnosis of gonorrhea is made on the basis of history, clinical manifestations, the presence of intracellular gram-negative diplococci, and is confirmed by cultural studies.

Treatment is carried out in specialized hospitals. Antibiotics, sulfa drugs, good nutrition, drugs that increase the body's immune defenses, and local treatment are prescribed.

After the end of treatment, all sick children remain in the hospital for 1 month for 2-3 provocations and smear examinations for 3 days. With favorable research results, the child is admitted to children's groups.

Prevention. Gonococcal ophthalmitis in newborns is prevented by instillation of a 1% solution of silver nitrate into the conjunctival sac immediately after birth.

13. Pneumococcal infection. Etiology. Epidemiology. Pathogenesis. Pathomorphology

Pneumococci (Streptococcus pneumoniae) are common inhabitants of the human upper respiratory tract, but under certain conditions they can become pathogens of infectious diseases that are clinically manifested by purulent-inflammatory changes in various organs and systems, more often in the lungs - by the type of croupous pneumonia and in the central nervous system - by type of purulent meningitis.

Etiology. Pneumococci are Gram-positive, lanceolate, capsule-forming diplococci that can be found as single cocci or in chains. For humans, only smooth capsular strains of pneumococci are pathogenic. Somatic antigens of pneumococcus have been isolated, antibodies to which cause an insignificant part of immunity. Antibodies to capsular antigens are of primary importance in protective reactions. Pneumococci produce hemolytic toxin, pneumolysin and toxic neuraminidase. When the pathogen is destroyed, endotoxin is released, causing hemorrhages on the skin and mucous membranes.

Epidemiology. Many healthy individuals are carriers of pneumococci. Serovars that do not have pronounced virulent properties predominate among the carriers. The development of the disease in these cases is possible with a sharp decrease in the immunological reactivity of the body.

The source of infection is a person - a patient or a carrier of pneumococci. The infection is transmitted by airborne droplets.

Pathogenesis and pathomorphology. Pneumococci must be considered as potential pathogens. Nonspecific mechanisms of local immunity, including the presence of other microorganisms in the nasopharynx, significantly limit the reproduction of pneumococcus. Pneumococcal diseases often develop after a viral infection of the respiratory tract, in which the ciliated epithelium is affected and its activity is reduced, and the activity of alveolar macrophages is also suppressed. The secret of the respiratory tract can delay the process of phagocytosis.

In the tissues, pneumococci begin to multiply and spread with the flow of lymph and blood or through contact from the site of infection. The severity of the disease is determined by the virulence of the pathogen, its quantity, especially in bacteremia, and the state of reactivity of the macroorganism. The most unfavorable prognosis is with massive bacteremia and a high concentration of capsular polysaccharide in the blood. A severe progressive form of the disease develops in most patients with antigenemia, despite ongoing intensive antibiotic therapy.

The spread of infection in the tissues of patients is enhanced by the action of the antiphagocytic substance of the soluble capsular antigen of pneumococci. An important role is played by the factor contributing to the development of edema. Subsequently, the number of macrophages in the exudate increases, and phagocytosis of pneumococci increases. The processes of resolving pneumonia are completed in 7-10 days.

14. Pneumococcal infection. Clinic. Diagnostics. Treatment. Prevention

Clinical manifestations. Clinical symptoms of pneumococcal infection depend on the localization of the underlying pathological process. Most often, it involves the upper and deep sections of the respiratory tract, often accompanied by a viral infection. Pneumonia, otitis media, sinusitis and pharyngitis, laryngotracheobronchitis, peritonitis and bacteremia develop. Pneumococci remain the most common causative agent of otitis media in children over the age of 1 month. Spread of infection can occur by contact, resulting in empyema, pericarditis, mastoiditis, epidural abscess, and, rarely, meningitis. Bacteremia can cause meningitis, purulent arthritis, osteomyelitis, endocarditis, and brain abscess. Subcutaneous abscesses rarely form with pneumococcal bacteremia. Kidney diseases such as glomerulonephritis and cortical arteriole thrombosis are often associated with pneumococcal bacteremia. Localized gingivitis, gangrenous areas on the skin of the face or extremities, and disseminated intravascular coagulation of the blood can also be a manifestation of pneumococcal bacteremia.

Diagnosis. The exact diagnosis of pneumococcal infection can be established on the basis of the isolation of pneumococci from the focus of inflammation or blood.

Pneumococci are often found in urine cultures. In the early stages of pneumococcal meningitis, cocci may be found in the CSF. Quantitative immunoelectrophoresis of serum, CSF, or urine using combined pneumococcal serum can be of great help in diagnosing pneumococcal meningitis or bacteremia. Pneumococcal antigens in blood and urine can also be detected in localized pneumococcal disease. Type-specific antiserum significantly improves the accuracy of serological diagnostic methods.

Treatment. Penicillin is the drug of choice for pneumococcal infections. Doses and duration of treatment should vary depending on the location of the infection. It is desirable in all cases to determine the drug sensitivity of isolated pneumococci using the dilution method to correct treatment tactics. The impossibility of foreseeing or predicting the drug resistance of the pathogen creates the need in all cases to conduct an appropriate bacteriological study of all strains of pneumococci isolated from blood and CSF. Erythromycin, cephalosporin, clindamycin and levomycetin, sulfadiazine and sulfazoxazole can be successfully used to treat patients who cannot tolerate penicillin.

Prevention. The polyvalent pneumococcal vaccine "PNEUMO-23" is highly immunogenic and rarely causes adverse reactions; it is recommended for vaccination of children over the age of 2 years from the high-risk group. Children with an immunodeficiency state, if they come into contact with a patient with pneumococcal infection, gamma globulin can be administered.

15. Staphylococcal infection. Etiology. Epidemiology. Pathogenesis. Pathomorphology

Staphylococcal infection is a large group of diseases from mild localized forms to severe septic process caused by staphylococci.

Etiology. Staphylococci are spherical cells that grow in clusters and are facultative anaerobes, although they can grow under aerobic conditions. There are two types of staphylococci.

1. S. aureus (Staphylococcus aureus) - pathogenic, producing four types of exotoxin:

1) alpha toxin;

2) beta-toxin;

3) gamma and delta toxins.

In addition, they can also produce enterotoxins.

S. aureus produce enzymes capable of destroying cell membranes, and the released fatty acids disrupt the process of oxidative phosphorylation;

2. S. epidermidis - epidermal staphylococcus, strains of which can cause various pathological processes in a weakened body, especially in newborns and premature infants. Staphylococcus epidermidis produces a white pigment.

Staphylococci are resistant to environmental factors, in addition, they quickly acquire resistance to widely used antibiotics.

Epidemiology. The source of infection are patients and carriers of pathogenic strains of staphylococcus aureus.

The infection is spread by contact, food and airborne droplets. Pathogenesis. Factors contributing to the occurrence of staphylococcal infection:

1) the presence of the entrance gate of infection;

2) exceeding the threshold of sensitivity of the organism by irritation caused by the pathogen;

3) the absence of specific and nonspecific protection in the body.

At the site of the entrance gate, a local inflammatory process occurs. In cases of high specific reactivity of the organism, the pathological process may not develop or be limited to a local inflammatory reaction. With a decrease in specific immunological reactivity, a generalization of the process with the development of septicemia and septicopyemia is possible, especially in newborns and children in the first months of life.

The pathogenesis is determined:

1) toxic component;

2) an allergic component;

3) staphylococcal invasion.

Pathomorphology. Suppuration is the main distinguishing sign of staphylococcal infection. Local proliferation of staphylococci in the tissue leads to the formation of an abscess.

In the cavity of the abscess are living bacteria and leukocytes. Abscess rupture is accompanied by bacteremia and dissemination of infection.

16. Staphylococcal infection. Clinic

There are localized and generalized forms of staphylococcal infection.

Skin diseases. Purulent skin diseases are primary or secondary, manifested by impetigo, folliculitis, boils, carbuncles, bullous impetigo (pemphigus of the newborn, Ritter's disease) and toxic epidermal necrolysis (Lyell's disease).

Respiratory diseases. Sinusitis and inflammation of the middle ear caused by Staphylococcus aureus may occur. Purulent parotitis is a rare disease.

Staphylococcal pneumonias can be primary or secondary if they develop after a viral infection.

Sepsis can occur at any localization of this infection and develops acutely with fever, chills, nausea, vomiting, and muscle pain. Subsequently, microorganisms can be localized in the lungs, heart, joints, bones, kidneys or brain.

Diseases of muscle tissue. The development of localized abscesses in the muscles, not accompanied by septicemia, is called tropical purulent myositis.

Heart diseases. Acute bacterial endocarditis often follows staphylococcal bacteremia and is not always accompanied by changes in the heart valves.

CNS diseases. Meningitis caused by S. aureus often develops after staphylococcal bacteremia, sometimes with direct infection from the middle ear, with osteomyelitis of the bones of the cranial vault or spine.

Disease of the bones and joints. Staphylococcus aureus most often serves as an etiological factor in osteomyelitis.

Diseases of the kidneys. Staphylococci cause the development of abscesses in the kidneys and perirenal tissue.

Diseases of the gastrointestinal tract. Staphylococcal enterocolitis is caused by excessive reproduction of staphylococci to the detriment of the normal intestinal flora.

Staphylococcal infection in newborns and children of the first year of life. Infection of a child is possible in the antenatal period, during childbirth or after birth.

Mild forms are characterized by the presence of a local focus and slightly pronounced intoxication, without disturbing the general condition and pathological changes in other internal organs.

Severe forms are characterized by severe intoxication, high body temperature, the presence of a localized purulent focus in the form of phlegmon, abscess, etc.

The most severe manifestation of infection is phlegmon of newborns, accompanied by an extensive suppurative-necrotic process in the subcutaneous fat of the back, neck, lumbar region, chest, and abdomen.

A feature of staphylococcal sepsis in premature newborns is the presence of mainly septicopyemic forms, less often - septicemia.

17. Staphylococcal infection. Diagnostics. Treatment. Prevention

Diagnosis. Staphylococcal infection is diagnosed based on isolation of the pathogen from lesions on the skin, abscess cavity, blood, CSF, or other sites. After isolation, the pathogen is identified by Gram stain, coagulase and mannitol reactions. Antibiotic sensitivity and phage typing can be done if needed.

The diagnosis of staphylococcal food poisoning is usually established on the basis of clinical and epidemiological data. The food that served as the source of food poisoning should be subjected to bacteriological examination and tested for the content of enterotoxin, which is determined using gel diffusion reactions, passive hemagglutination inhibition and the method of fluorescent antibodies.

Antibodies to teichoic acid can be detected using the agar double diffusion method. This test is important in the diagnosis of staphylococcal endocarditis or septicemia.

Diagnostic value in infections accompanied by staphylococcal bacteremia may have a determination of staphylococcal peptidoglycan and a test for antibodies to IgG.

Treatment is carried out taking into account the form, severity, period of the disease and the age of the child.

With mild and isolated forms of infection in older children, they are limited to symptomatic and local therapy. In moderate and severe forms of infection, complex therapy is prescribed, aimed at eliminating the pathogen, detoxification, restoring metabolic disorders and increasing the body's defenses. If necessary, surgical methods of treatment are used.

For the treatment of infection, especially in severe and generalized forms, broad-spectrum antibacterial drugs are used.

Complex therapy of severe forms of infection includes the use of anti-staphylococcal immunoglobulin, hyperimmune plasma, staphylococcal bacteriophage, blood transfusion from donors immunized with staphylococcal toxoid.

Nonspecific therapy is reduced to the use of detoxification agents, protein preparations, desensitizing agents.

In young children with prolonged sepsis, accompanied by depletion of the function of the adrenal cortex, steroid hormones are indicated (contraindication - septicopyemia with a low index of body reactivity).

To prevent and treat dysbacteriosis, nystatin, levorin, B and C vitamins, bacterial preparations are prescribed, the choice of which depends on the age of the child and the nature of microflora disorders.

Prevention includes a complex of anti-epidemic and organizational measures aimed at preventing staphylococcal infection in maternity hospitals, medical hospitals and physiological children's institutions.

Children who have had a staphylococcal infection are under dispensary observation for 6-12 months.

18. Tetanus. Etiology

Epidemiology. Pathogenesis. Pathomorphology

Tetanus is an acute toxemic disease caused by the action of an exotoxin (tetanospasmin) produced by the bacteria Clostridium tetani. The toxin is produced by vegetative forms of the microorganism at the site of its penetration into the tissues of the body, and then enters the central nervous system and is fixed there.

Etiology. The causative agent of tetanus is an obligate anaerobe, a thin Gram-positive mobile non-encapsulated rod that forms terminal spores, which give it a resemblance to a drumstick.

Vegetative C. tetani are sensitive to heat and disinfectants.

Tetanus bacilli are themselves harmless, their disease-causing effect is associated with two toxins they produce: tetanospasmin and tetanolysin.

Epidemiology. The sources of infection are animals and humans, in the intestines of which tetanus bacillus saprophytes, which enters the soil with the feces of animals and disperses in the environment.

Tetanus is a wound infection, the disease occurs when the pathogen enters the body through the wound surface. In newborns, the umbilical wound, infected in violation of the rules of asepsis and antisepsis, can serve as an entrance gate.

Pathogenesis. The disease develops after tetanus spores that have fallen into damaged tissues begin to germinate, multiply and produce tetanospasmin. Germination and reproduction of spores occurs at the site of the entrance gate of infection and only when the level of oxygen in the tissues decreases.

From the site of the entrance gate, the infection spreads throughout the body:

1) on the surrounding tissues;

2) through the lymphatic system;

3) along the nerve trunks.

Tetanospasmin acts on motor nerve endings at myoneural synapses, on the spinal cord and brain, and on the sympathetic nervous system. At neuromuscular synapses, the toxin inhibits the destruction of acetylcholine, causing disturbances in the processes of neuromuscular transmission. Disruption of inhibitory mechanisms in the spinal cord itself significantly weakens the inhibitory influence of the higher parts of the central nervous system. The toxin causes an increase in the activity of the sympathetic nervous system: tachycardia, unstable hypertension, arrhythmia, peripheral vascular spasms, profuse sweating, hypercarbia and an increase in the excretion of catecholamines in the urine.

Tetanospasmin, adsorbed in the tissues, binds strongly with them, and is not subsequently destroyed or neutralized by antitoxin. Tetanus antitoxin may prevent the binding of tetanospasmin to the CNS if the latter is located in the peripheral nerve trunks.

Pathomorphology. C. tetani infection remains localized and causes minimal inflammatory changes in damaged tissues. Local pathological changes are secondary.

19. Tetanus. Clinic. Diagnostics

Clinical manifestations. The incubation period for tetanus is 3-14 days after injury, less often - from 1 day to several months.

There are three clinical forms of tetanus:

1) local tetanus, manifested by pain, prolonged rigidity and muscle spasm proximal to the injury site, which can persist for several weeks and disappear without a trace.

2) general tetanus, usually beginning imperceptibly, but trismus can be detected in 50% of patients. Spasm of the chewing muscles is often combined with neck stiffness and difficulty swallowing. Early symptoms include anxiety, irritability, and headaches. Spasm of facial muscles causes a sardonic smile. Short tonic contractions of different muscle groups appear. The lumbar and abdominal muscle groups become rigid, spasms of the back muscles begin, leading to opisthotonus. Tetanus cramps are characterized by the sudden appearance of tonic contractions of different muscle groups, causing flexion and adduction of the arms, squeezing of the hands, and extension of the legs. Seizures are provoked by almost any visual, auditory or tactile stimulus. During the entire period of illness, the victim retains consciousness, he experiences severe pain. At the same time, there is a pronounced feeling of fear. Spasms of the muscles of the pharynx and respiratory tract can lead to closure of the airways, cause cyanosis, asphyxia.

Body temperature in patients usually increases slightly; its increase to 40 °C is explained by increased energy expenditure during convulsions. Patients experience profuse sweating, tachycardia, hypertension, and arrhythmia. During the first 3-7 days, the symptoms of the disease increase; over the next 2 weeks, the patient’s condition stabilizes. Full recovery occurs after 2-6 weeks;

3) cephalic tetanus. This is an unusual manifestation of the disease. The incubation period is 1-2 days. The most characteristic symptoms of the disease include dysfunction of the III, IV, VII, IX, X and XI pairs of cranial nerves. Most often, the VII pair (facial nerve) is involved in the process. Neonatal tetanus usually begins in a child aged 3-10 days and occurs in a generalized form. Initially, the child's act of sucking is disrupted, anxiety and severe crying appear. Swallowing problems soon develop, muscle rigidity appears, and convulsions begin.

Diagnosis. Diagnosis of tetanus is based on clinical findings. Determination of tetanus bacilli in swabs from wound discharge or their growth on nutrient media confirms the diagnosis of tetanus only with anamnestic and clinical data characteristic of tetanus.

20. Tetanus. Treatment. Prevention

Treatment. The main goal of treatment for tetanus is to eliminate the source of tetanospasmin formation, neutralize the toxin circulating in the blood, and conduct maintenance therapy until the tetanospasmin fixed by the nervous tissue is destroyed.

Human specific immunoglobunal (SIG) is administered as early as possible at a dose of 3000-6000 IU intramuscularly. Antitetanus immunoglobulin does not penetrate the blood-brain barrier and does not affect the toxin fixed in the nervous tissue. Its therapeutic effect is reduced only to the neutralization of tetanospasmin circulating in the blood.

In the absence of SIG and unchanged reactivity of the patient in accordance with the data of an intradermal test with tetanus antitoxin (CAT), the latter is recommended to be administered at a dose of 50-000 IU: half the dose - intramuscularly, the other half - intravenously.

Surgical measures for the treatment of wounds are carried out after the introduction of antitoxin and sedatives. Remove necrotic tissue and foreign bodies from the wound.

Antibiotic therapy helps to eliminate the vegetative forms of tetanus bacillus located in dead tissues. Usually large doses of penicillin G are prescribed intravenously in 6 doses for at least 10 days and try to ensure sufficient penetration of it into the lesions.

Muscle relaxants should be administered to all patients with tetanus. Diazepam (sibazon) is effective in reducing increased muscle tone and prevents convulsions. You can enter chlorpromazine or mefenesin, but their effect is less pronounced. Prevention. Active immunization is the best way to prevent tetanus. It is best to immunize women before pregnancy.

Children 6 years of age and older are immunized according to the method recommended for adults. Tetanus and diphtheria toxoids are administered intramuscularly in 3 divided doses. Primary immunization should be with tetanus toxoid. The introduction of at least 4 doses provides a sufficient level of immunity to tetanus.

Preventive measures after injury are determined by the immune status of the patient and the nature of the lesion itself. Surgical treatment of the wound should be carried out immediately and carefully. Patients who have not been actively immunized or who have been incomplete should be administered intramuscularly with human tetanus immunoglobulin at a dose of 250-500 IU. Skin allergy testing is optional. In the absence of SIG, tetanus antitoxin is injected intramuscularly at a dose of 3000-5000 IU, having previously tested for sensitivity to foreign proteins. The introduction of maintenance doses of toxoid is indicated when a child receives an injury 5 years or more after a full course of active immunization.

21. Gas gangrene

Gas gangrene is a severe anaerobic infection of soft tissues, primarily muscles, accompanied by the formation of gas and severe intoxication.

Etiology. There are six most common pathogens of gas gangrene: Clostridium perfringens, Clostridium novyi, Clostridium septicum, Clostridium histolyticum, Clostridium bifermentans, Clostridium fallax. All these microorganisms are small (0,5-5 microns) Gram-positive rods.

Pathogenesis and pathomorphology. The development of gas gangrene is facilitated by:

1) getting into the wound clostridia;

2) dead tissue, in which the level of oxygen is reduced.

Factors predisposing to the development of infection include trauma, ischemia, foreign bodies in the wound, or infection with other microorganisms. Gas gangrene syndrome is caused by the action of toxins produced by multiplying clostridia. The reproduction of bacteria in tissues is accompanied by the release of gas (hydrogen and carbon dioxide), determined by palpation.

Clinical manifestations. Clostridia infection syndrome consists in the multiplication of pathogens in the wound with minor pain and the absence of general reactions. The surface of the wound is usually uneven, has an untidy appearance, serous-purulent discharge is dark brown in color and fetid. The healing process is slow. Along with clostridia, anaerobic streptococcus can be released from the wound.

Anaerobic cellulitis often develops initially, but may complicate other forms of wound infection. The incubation period is 3-4 days. Clostridia multiply in already dead tissues affected by trauma and subsequent ischemia.

Anaerobic myonecrosis is the most severe form of gas gangrene. The incubation period can last from several hours to 1-2 months, more often - no more than 3 days. The disease begins acutely, there are severe pain in the wound, local swelling and swelling. The muscle tissue in the affected area is edematous and pale. As the infection progresses, the muscles become brick red and lose their ability to contract.

Diagnosis. The diagnosis of gas gangrene must be established in the early stages of the disease, based on clinical data, the results of laboratory tests, including microscopy and bacteriological examination, and x-ray examination.

Treatment. The most reliable method of treatment for gas gangrene is surgical debridement and removal of all infected tissues. Penicillin G given intravenously is not a substitute for surgery.

Prevention. The main methods of preventing gas gangrene include early, correctly and carefully performed wound treatment, which excludes the possibility of infection.

22. Botulism. Etiology. Epidemiology. Pathogenesis

Botulism is an acute infectious disease with a leading enteral route of infection, caused by C. botulinum exotoxins and characterized by a severe course with a predominant lesion of the central and autonomic nervous system. There are three forms of botulism:

1. food, caused by food intake, in which botulinum toxin accumulates during storage;

2. wound, caused by infection of wounds by the causative agent of this disease, which produces a toxin;

3. a disease of infants caused by the pathogen entering the intestines, its reproduction and the release of a toxin.

Etiology. C. botulinum is an anaerobic, motile Gram-positive bacillus that produces heat-resistant spores.

If the spores survive the cooking process, they germinate, multiply, and produce toxins. Seven antigenically distinct toxins (A, B, C, D, E, F, and G) have been identified, of which only types A, B, E, F, and G are responsible for human disease.

Epidemiology. Botulism in young children. Most often, children under 1 year old get sick, the peak of the disease occurs at the age of 2-6 months. The etiological factor can be pathogens of types A and B. The main reservoir and source of infection are warm-blooded herbivores, less often - fish, crustaceans, mollusks.

From a sick person to a healthy person, the disease is not transmitted. The main route of infection is food, more often with the use of home-made canned food. In infants, foodborne botulism may be derived from infant formula.

Pathogenesis. The entrance gate of infection is the gastrointestinal tract. Botulism in young children occurs when C. botulinum spores enter the child's intestines, germinate, multiply, and release the toxin. Spores are constantly present in the soil and in the environment, but in adults such a genesis of the disease does not occur. Food botulism occurs when botulinum toxin is absorbed from the intestines, which has entered the body along with improperly cooked food. Wound botulism is characterized by the formation of a toxin in the wound itself.

It is assumed that the transport of the toxin to the nerve endings occurs not only with the blood flow, but also with the participation of lymphocytes. Different toxins have different affinity for nervous tissue. It is most pronounced in type A toxin, less in type E and weakly in type B. The last toxin circulates in the blood longer than others and is determined in it even 3 weeks after ingestion of contaminated food.

The toxin selectively acts on the endings of motor nerve fibers, inhibiting the formation of acetylcholine. Its inhibitory effect on the motor neurons of the spinal cord has been proven. The effect of the toxin on the brain is slightly pronounced, the endings of the cranial nerves are affected early, and therefore the patients develop shortness of breath or asphyxia and arrhythmia.

23. Botulism. Clinic. Diagnostics. Treatment. Prevention

The clinical manifestations of botulism in young children can range from mild forms, manifested only by constipation and anorexia, to very severe forms, characterized by neurological symptoms with sudden death. Usually, an outwardly healthy child develops constipation, sucking and swallowing worsens, crying and screaming weaken, he stops smiling, hypotension develops, and the heart rhythm is disturbed. Within a few hours or days, descending-type paralysis progresses with damage to the cranial nerves, trunk and legs. Intestinal paresis, atony of the bladder, ptosis, mydriasis, weakening of salivation and lacrimation are noted.

food botulism. The incubation period lasts from several hours to 8 days, most often 12-36 hours.

Characteristic signs of botulinum toxicity are nausea, vomiting, dysphagia, diplopia, dysarthria, and dry mouth. Ptosis, miosis, nystagmus and paresis of the eye muscles are detected. The mucous membranes of the oral cavity, pharynx and tongue are dry, lacrimation stops, respiratory movements are disturbed, sensitivity does not change. Respiratory failure progresses rapidly due to impaired mechanical functions and breathing capabilities.

The course of wound botulism is milder and slower, depending on the nature of the wound.

Diagnosis. Botulism is diagnosed on the basis of epidemiological and characteristic classical manifestations. For laboratory confirmation, the detection of a toxin and a pathogen in biomaterials taken from a patient, as well as in food products using enzyme-linked immunosorbent assay methods and latex agglutination reactions are used - specific and highly sensitive methods that allow, in addition to detecting toxins, to identify specific antitoxic and antibacterial antibodies in blood serum sick.

Treatment of botulism in infants consists of continuous monitoring, basic life support, and general intensive care, including respiratory support and nutrition.

food botulism. All persons who have consumed products contaminated with botulinum toxin should be hospitalized. They urgently need to provoke vomiting, gastric lavage and then administer a saline laxative, high enemas are required to remove unabsorbed toxin.

A pronounced effect is observed after the introduction of a specific antitoxin. There are three types of antitoxin derived from horse serum. Prior to identifying the type of botulinum toxin, a polyvalent antitoxin must be administered.

To suppress the pathogen, which can continue to produce the toxin, patients are given an aqueous solution of penicillin.

Wound botulism. Wounds should be properly treated and drained.

Prevention. Boiling food for 10 minutes destroys botulinum toxin. Bacterial spores are killed when heated to 116 °C.

24. Infection caused by anaerobic microorganisms. Etiology. Epidemiology. Pathogenesis. Pathomorphology

Etiology. Anaerobic bacteria are widely distributed in the soil, are part of the normal human microflora, and are constantly found on mucous membranes, especially in the oral cavity and gastrointestinal tract. Anaerobic microorganisms usually die in the presence of oxygen, but their sensitivity to it varies. Some pathogens of anaerobic infections can grow in the presence of oxygen, although less intensively than without it (facultative anaerobes).

Obligate anaerobes do not develop in an environment containing oxygen. In humans, obligate anaerobes dominate.

Epidemiology. With the development of anaerobic infection in children, pathogens can be detected in the blood, abdominal cavity and soft tissues, from where, in addition to blood, several strains of anaerobic and aerobic microorganisms are usually isolated.

The main clinical landmarks are:

1) prolonged labored delivery, accompanied by early rupture of the membranes of the membranes of the membranes;

2) peritonitis or septicemia due to intestinal obstruction and intestinal perforation or appendicitis;

3) congenital or acquired diseases that violate the child's body resistance to infection;

4) subcutaneous abscesses and infection of the female genital organs;

5) infection of the oropharynx, nasopharynx;

6) aspiration pneumonia.

Pathogenesis. Under normal conditions, anaerobes are of little virulence for humans. But conditions accompanied by a decrease in the level of oxygen in tissues and a weakening of redox processes create prerequisites for the reproduction of anaerobic flora and the manifestation of its pathogenic properties. Diseases of the lungs and pleura caused by anaerobic microorganisms usually develop against the background of existing extrapulmonary foci of anaerobic infection, after penetrating wounds of the chest and heart operations, against the background of systemic diseases that weaken the body's resistance.

Brain abscesses can occur with chronic otitis media, mastoiditis, sinusitis, lung abscess, congenital heart defects with right and left shunts, bacterial endocarditis, infections and injuries of the face and head, and brain surgery. Peritonitis and bacteremia develop after perforation of the small or large intestine, appendicitis, cholecystitis, or gastroenteritis.

Anaerobic infection in newborns is usually observed after prolonged labor, accompanied by early rupture of the membranes of the membranes, or with necrotizing enterocolitis.

Pathomorphology. Conditions for the development of anaerobic infection appear when abscesses and extensive tissue destruction occur. Localization of lesions determines the features of morphological changes.

25. Infection caused by anaerobic microorganisms. Clinic. Diagnostics. Treatment

Clinical manifestations. Anaerobic bacteria are commonly found in chronic sinusitis, otitis media, mastoiditis, peritonsillar and pharyngeal abscesses, mumps, and cervical lymphadenitis.

Fusobacteria play an important role in the development of Vincent's angina, characterized by ulceration of the tonsils and the appearance of a brown or gray fetid coating on them. Rapidly developing necrosis and fusion of surrounding tissues can lead to perforation of the carotid artery.

Ludwig's angina is an acute inflammation of the tissue in the sublingual and submandibular regions. The infection spreads rapidly, without involvement of the lymph nodes and the formation of abscesses. Airway obstruction may occur, requiring urgent tracheostomy.

Anaerobic infection of the lower respiratory tract usually takes the form of necrotizing pneumonia, lung abscess, or purulent empyema.

Anaerobic infection of the CNS is manifested by a brain abscess, subdural empyema, or septic thrombophlebitis of the veins of the cortex or venous sinuses. A brain abscess is manifested by headaches, impaired consciousness, stupor, convulsions, focal loss of function of the motor and sensory nerves, and impaired speech.

The penetration of intestinal contents, which is very rich in anaerobic flora, into the abdominal cavity often leads to the development of anaerobic peritonitis.

Infection with anaerobic microorganisms can cause osteomyelitis, septic arthritis, urinary tract disease, subdiaphragmatic and hepatic abscesses, lymphadenitis, skin and soft tissue diseases, orbital and perinephric, periorbital and peritonsillar abscesses.

Diagnosis. The objects of bacteriological examination are the blood of patients, bile, exudate from the pleural, abdominal cavities or from the pericardial cavity, CSF, the contents of abscesses, aspirate from deep layers of wounds, trachea and biopsy of organs obtained under aseptic conditions.

Treatment. Penicillin G is effective in almost all infections caused by gram-positive and gram-negative anaerobic bacteria. The exception is B. fragilis, which is resistant to penicillin, ampicillin, and cephalosporin. Combined treatment with penicillin and levomycetin should be carried out with anaerobic bacteremia and localization of infection in other organs. Most anaerobic pathogens are sensitive to chloramphenicol, clindamycin, carbenicillin.

Erythromycin has an effect on anaerobic cocci. Aminoglycosides do not affect anaerobic bacteria. Cefoxitin has a bacteriostatic effect on B. fragilis (in 80% of cases) and C. perfringes, but does not affect other types of clostridia.

With a mixed aerobic and anaerobic infection, especially when it is localized in the abdominal cavity, gastrointestinal tract, retroperitoneal space or organs of the genitourinary system, treatment with chloramphenicol or clindamycin in combination with gentamicin or kanamycin is recommended.

26. Diphtheria. Etiology. Epidemiology. Pathogenesis and pathomorphology

Diphtheria is an acute infection caused by Corynеbacterium diphtheriae, the symptoms of which are due to the production of a toxin - an extracellular protein product of a toxigenic strain of the pathogen.

Etiology. The causative agent of diphtheria, Corynebacterium diphtheriae, or Leffler's bacillus, is an unevenly stained gram-positive, non-spore-bearing, immobile pleomorphic bacterium.

Toxigenic and non-toxigenic microorganisms are found among smooth and rough strains, the production of exotoxin is determined in any of the three types of Corynebacterium colonies.

Diseases are caused by toxigenic and non-toxigenic strains of diphtheria bacillus, but only the first, toxigenic, are responsible for the development of complications such as myocarditis and neuritis.

Epidemiology. Infection occurs through contact with a sick person or a carrier. Bacteria are transmitted by airborne droplets, the role of the household route of infection is small.

Pathogenesis and pathomorphology. Initially, the infection is localized on the mucous membranes of the upper respiratory tract, less often on the conjunctival membrane, wound surfaces of the skin or in the genital area. After 2-4 days of the incubation period, the strains of the pathogen with the bacteriophage begin to produce a toxin, which is first adsorbed on the cell wall, then overcomes it and interferes with the processes of protein synthesis of the cell.

Tissue necrosis is most pronounced along the periphery of the breeding zones of diphtheria pathogens. In these areas, an inflammatory reaction develops, which, together with the processes of necrosis, contributes to the formation of characteristic plaques, which are initially easily removed. As toxin production increases, the affected area becomes wider and deeper, fibrinous deposits appear on its surface, quickly transforming into dense, firmly fixed films from gray to black, depending on the blood content in them. They also include fibrin and surface epithelial cells. The separation of the film causes bleeding, since the epithelial layer is firmly included in its composition. In the process of recovery, the films peel off on their own.

Swelling of the surrounding soft tissues can become rampant. Films and edematous soft tissues can hang over the airways, disrupting their patency and causing suffocation, which may be accompanied by expansion of the larynx and tracheobronchial tree.

The toxin formed at the breeding site of diphtheria bacilli enters the bloodstream and spreads throughout the body. When the tonsils, pharynx and pharynx are already covered with diphtheria films, toxemia begins.

The toxin has a destructive effect most of all on the heart, nervous system and kidneys. After fixation of the toxin in the cells, a latent period passes before the development of clinical symptoms. Myocarditis usually develops in 10-14 days, and diseases of the nervous system - not earlier than 3-7 weeks after the onset of the disease.

27. Diphtheria. Clinic. Diagnostics. Treatment

Clinical manifestations. The symptomatology of diphtheria is determined by the localization of the infection, the immunological status of the macroorganism and the severity of toxemia. The incubation period is 1-6 days. Classification:

1) diphtheria of the nose occurs mainly in young children. Initially, it is characterized by mild rhinorrhea in the absence of general disorders. Gradually, discharge from the nose becomes serous-bloody in color, and then mucopurulent;

2) diphtheria of the tonsils and pharynx - a more severe form of the disease. The onset of the disease is characterized by an inconspicuous, gradual increase in body temperature, anorexia, malaise and pharyngitis. After 1-2 days, films appear in the throat, the prevalence of which depends on the immune status of the patient.

Cervical lymphadenitis in some cases is accompanied by swelling of the soft tissues of the neck, in others it can be very pronounced, resembling a bull's neck. The course of pharyngeal diphtheria depends on the prevalence of films and the amount of toxin produced;

3) diphtheria of the larynx develops with the spread of films from the tonsils and from the nasopharynx. Clinical symptoms resemble a picture of a common infectious croup: noisy labored breathing, increasing stridor, wheezing and dry cough;

4) diphtheria of the skin is characterized by ulcers with clear edges and a bottom covered with a diphtheria film;

5) diphtheria of the conjunctival membrane is usually limited to a local process, with reddening of the eyelids, their swelling and film formation;

6) ear diphtheria is characterized by otitis externa with long-term persistent and foul-smelling purulent discharge. Diagnosis. Diphtheria is diagnosed:

1) based on clinical data;

2) when confirming the isolation of the pathogen;

3) using the method of fluorescent antibodies. Treatment. The basis of treatment is the neutralization of free diphtheria toxin and the destruction of the pathogen with antibiotics. The only specific therapeutic agent is diphtheria antitoxin, obtained from the serum of hyperimmunized horses.

Antitoxin should be given intravenously as early as possible and in amounts sufficient to neutralize all circulating toxin in the body. Doses of antitoxin are selected empirically: in mild forms of diphtheria of the nose or pharynx, 40 units are prescribed, and in more severe forms, 000 units. A dose of 80 units is prescribed for the most severe forms of diphtheria of the pharynx and larynx.

Antibiotics (erythromycin and penicillin, amoxicillin, rifampicin, clindamycin) are prescribed to stop further production of the toxin by the diphtheria bacillus.

28. Whooping cough

Whooping cough is an acute respiratory disease that can develop at any age, but it occurs and becomes most severe in young children.

Etiology. The causative agent of whooping cough is Bordetella pertussis and, less commonly, B. parertussis.

B. pertussis is a short immobile gram-negative rod, has a capsule, a strict aerobe.

Epidemiology. The causative agents of whooping cough are extremely rarely isolated from healthy individuals, the transmission of infection occurs only through direct contact with the patient.

Pathomorphology. The respiratory tract is the site of the primary localization of the pathological process, where a mild inflammation such as serous catarrh occurs. In the larynx and vocal folds, the greatest lesions are observed: proliferation of epithelial cells.

Pathogenesis. In the body of a person infected with whooping cough, agglutinins, hemagglutinin-inhibiting, bactericidal, complement-binding and immunofluorescent antibodies begin to be produced, but resistance to whooping cough does not correlate with them. The existence of a protective antigen in the cell wall of the pathogen suggests that antibodies that act on this antigen are capable of conferring immunity.

Clinical manifestations. The incubation period of whooping cough is 6-20 days, more often - 7 days. In general, the disease proceeds within 6-8 weeks.

There are 3 stages of the disease:

1) catarrhal stage. Lasts 1-2 weeks, characteristic signs are rhinorrhea, injection of vessels of the conjunctival membrane, lacrimation, weak cough;

2) paroxysmal stage. Lasts 2-4 weeks or more. There are characteristic repeated series of 5-10 strong cough shocks during one exhalation, followed by an intense and sudden breath;

3) the stage of recovery. Passes within 1-2 weeks. During this period of time, attacks of coughing, reprises and vomiting are easier and occur less frequently. The cough may continue for several months.

Diagnosis. An accurate diagnosis is made when:

1) bacteriological examination of the material;

2) study of material from the nasopharynx using the method of fluorescent antibodies;

3) obtaining positive results of serological diagnostics;

4) bronchological X-ray examination. Treatment. Antibiotics do not shorten the duration of the paroxysmal stage of whooping cough. Immune antipertussis globulin is used to treat children under 2 years of age.

Prevention. Active immunity is created with the pertussis vaccine. It is part of the complex preparation of the DTP vaccine and is administered to all children aged 3 months to 3 years.

29. Pseudomonas infection - an infection caused by Pseudomonas aeruginosa (Pseudomonas)

Representatives of Pseudomonas - numerous gram-negative bacteria that live in soil and in water, are a common flora of wet rooms, including hospitals. They cause diseases mainly in newborns and children with insufficient defense mechanisms.

Etiology. Pseudomonas aeruginosa is a Gram-negative bacterium that causes hemolysis on blood agar. More than 90% of bacterial strains produce a bluish-green phenazine pigment (blue pus), as well as fluorescein, which is yellowish-green, diffusing into the nutrient medium, which stains around the colonies.

Epidemiology. Pseudomonas is often found in medical institutions on the skin, clothes and shoes of patients and attendants. It is able to grow in any humid environment.

Pathogenesis. For its development, Pseudomonas needs oxygen, the lack of which reduces the virulence of the microorganism.

Pseudomonas aeruginosa releases large amounts of exotoxins, including lecithinase, collagenase, lipase, and hemolysins, causing necrotic lesions on the skin.

Clinical manifestations. In healthy people, Pseudomonas aeruginosa, which has fallen into small wounds, causes suppuration and local abscesses, which contain green or blue pus. Skin lesions that develop during septicemia or direct inoculation of the pathogen into the skin initially look like pink spots, which, with the progression of the infection, turn into hemorrhagic nodules and undergo necrosis. In their place, scabs form, surrounded by a red rim (ecthyma gangrenosum). The reproduction of bacteria occurs in the affected areas.

Septicemia most often develops in children after the introduction of intravenous or urinary catheters. Pneumonia and septicemia are more common in children who are on artificial or assisted breathing. Peritonitis and septicemia develop when instruments used for peritoneal dialysis are contaminated. Pseuomonas and other Gram-negative bacteria are often found on wounds and burns.

Hemorrhagic necrosis can appear in all organs, including the skin in the form of purple nodules or areas of ecchymosis, rapidly undergoing necrosis. Inflammatory changes are usually hemorrhagic and necrotic.

Diagnosis and differential diagnosis. The diagnosis of Pseudomonas infection depends on the culture of the pathogen from blood, urine, CSF, or pus obtained from abscesses or sites of inflammation.

Treatment. Antibiotic therapy should be especially intense and prolonged in patients with impaired immunological reactivity. Patients with meningitis caused by Pseudomonas aeruginosa are treated with intravenous antibiotics.

Abscesses should be opened and drained, without which even long-term antibiotic treatment remains ineffective.

30. Brucellosis. Etiology. Epidemiology. Pathogenesis and pathomorphology

Brucellosis is an acute or chronic disease of livestock transmitted to humans mainly by four types of brucella - from cows, goats, pigs and dogs.

Etiology. Six species of Brucella are known that can cause disease in humans: B. abortus (source - cow), B. melitensis (source - goat), B. suis (source - pig), B. canis (source - dog), B. ovis (sources - sheep and hare) and B. neotome (source - wood rat).

The causative agents of brucellosis are small gram-negative, immobile, aerobic rods that do not form spores and capsules, characterized by slow growth on nutrient media.

Epidemiology. Human brucellosis is caused by direct contact with sick animals. Most often, people who care for livestock get sick. Raw milk of sick animals, butter, cream, cottage cheese, ice cream can be sources of infection. The pathogen can enter the eye, nasopharynx, genitals, but intact healthy skin is impervious to it. Brucella remain viable when storing infected products in a refrigerator for 3 weeks and during the production (smoking) of ham. They die during pasteurization and boiling.

Pathogenesis and pathomorphology. Brucella are intracellular parasites. After entering the human body, they are phagocytosed by leukocytes and macrophages, spreading in the reticuloendothelial tissue. Pathogens can multiply in different cells, including erythrocytes.

Infection with brucellosis is accompanied by the development of delayed-type hypersensitivity to the brucellosis antigen. The patient's body reacts to a brucellosis infection by producing antibodies, among which are agglutinins, bacteriolysins, opsonins, precipitins and complement-fixing antibodies.

Serum or plasma of healthy individuals and patients in the acute phase of the disease, when complement is added, has a pronounced non-specific bactericidal activity against Brucella. In chronic forms of infection, specific antibodies appear that prevent the action of the "serum-complement" system, act as opsonins and increase the phagocytic activity of polymorphonuclear and mononuclear cells, due to which Brucella quickly disappear from the blood of patients with a high antibody titer, but remain in the cells, in which the action of antibodies is not manifested.

All types of Brucella cause granulomatous changes detected by histological examination of the liver, spleen, lymph nodes and bone marrow. There are signs of central lobular necrosis and cirrhosis of the liver. Granulomatous inflammation develops in the gallbladder, there are signs of interstitial orchitis with scattered areas of fibrous atrophy. Endocarditis with thickening of the aortic valve and atrioventricular orifice is also commonly found, and granulomatous changes in the myocardium, kidneys, brain, and skin have been described.

31. Brucilosis. Clinic. Diagnostics. Treatment. Prevention

Clinical manifestations. The incubation period varies from several days to several months. The disease most often begins unnoticed, but acute sudden development of clinical signs of infection is possible; in endemic areas, the disease in children usually proceeds unnoticed. Prodromal symptoms are weakness, fatigue, anorexia, headaches, myalgia, and constipation. As the disease progresses, there is an increase in body temperature in the evening, which soon reaches 41-42,5 ° C. There are chills, profuse sweating, nosebleeds, abdominal pain and coughing. Often there is a significant decrease in body weight.

Physical examination reveals an enlarged liver and spleen, hyperplasia of the cervical and axillary lymph nodes. Wheezing may be heard in the lungs, in which case changes in them are visible on chest radiographs.

Chronic forms of brucellosis are difficult to diagnose and are often interpreted as a fever of unknown origin. Patients complain of fatigue, muscle and joint pain, sweating, nervousness and lack of appetite. Cases of depression and psychosis have been described. A maculopapular (more rarely, morbilliform) rash may appear. Brucellosis is often accompanied by the development of uveitis, endocarditis, hepatitis, cholecystitis, epididymitis, prostatitis, osteomyelitis, encephalitis and myelitis.

Diagnosis. Diagnosis of the disease is carried out on the basis of anamnestic data, epidemiological history, an objective examination of the patient, as well as a number of laboratory tests, including:

1) serological research methods;

2) intradermal allergic test Burne.

Treatment. Patients with brucellosis are prescribed bed rest and an easily digestible high-calorie diet. Treatment with tetracycline is carried out for 3-4 weeks. Relapses of the disease occur in 50% of patients.

In these cases, increase the dose of tetracycline and add streptomycin for a period of 2 weeks. During the 2nd week, the initial dose of drugs is halved. It is also recommended to prescribe rifampicin in combination with trimethoprim-sulfamethoxazole or moxalactam.

Other third-generation cephalosporins have been reported to have an effect on Brucella in vitro, but clinical studies are not yet available.

Limited abscesses must be opened and drained.

Corticosteroids may be useful only in the initial period of treatment to prevent the Herxheimer's reaction.

Prevention. The prevention of brucellosis consists in the exclusion of human contact with the sources of the disease. Infection in domestic animals with which a person is in constant contact can be prevented by vaccination.

Along with the vaccination of animals and the pasteurization of milk, it is necessary to periodically carry out agglutination reactions with the blood and milk of animals, which makes it possible to identify infected animals. The latter are to be slaughtered. Eating unpasteurized milk and products from it should be excluded.

32. Plague is an acute infectious disease caused by a plague bacillus

Etiology. Yersinia pestis is an immobile, polymorphic, Gram-negative bacterium that does not form spores. It looks like a short stick with rounded dense ends and a swollen central part ("safety pin").

Epidemiology. A person becomes ill with plague after being bitten by a flea that previously sucked the blood of a sick rodent, or when processing the carcass of a sick animal. This usually results in the bubonic form of the plague. Infection from a sick person by aerogenic route is also possible, and the most severe pulmonary form of plague develops.

Pathomorphology and pathogenesis. The causative agents of plague, having entered the body of a flea with the blood of a sick animal, multiply in the digestive tract and clog the lumen of the anterior ventricle. When a flea bites a person, it regurgitates them, and the pathogens enter the lymphatic vessels of the skin, and then into the regional lymph nodes. In a severe form of bubonic plague, the lymph nodes lose their barrier function, and pathogens that have multiplied in them penetrate into the general bloodstream.

The primary form of pneumonic plague is caused by aerogenic infection from a sick person; it also develops in case of accidents during laboratory tests.

The reaction of tissues to the introduction of Y. pestis is manifested in their purulent melting.

Clinical manifestations. The incubation period for the bubonic form of plague is 2-6 days, and for the pulmonary form - 1-72 hours.

The bubonic form of plague begins acutely or subacutely. The first manifestations of the subacute form are an increase and compaction of one of the groups of lymph nodes and an increase in body temperature.

The acute form of bubonic plague, in addition to lymphadenitis, is manifested by high body temperature, tachycardia, myalgia. The disease progresses rapidly, there is a violation of consciousness, shock and death within 3-5 days.

The course of primary pneumonic plague is even more acute. The disease is manifested by nausea, vomiting, abdominal pain, bloody diarrhea, petechial rash or purpura.

Diagnosis. The diagnosis of sporadic cases of plague is based on a careful assessment of the history, physical examination findings, and the possibility of the disease.

Blood, sputum, purulent discharge and aspirate from enlarged lymph nodes should be examined bacterioscopically.

Treatment. Treatment with streptomycin for 5-10 days is indicated, under the influence of which a massive lysis of bacteria occurs, as a result of which reactive phenomena can be observed already at the beginning of treatment. After 2-3 days of treatment with streptomycin, tetracycline or levomycetin is additionally prescribed for 10 days. The bubonic form of plague responds well to treatment with tetracycline for 10 days or chloramphenicol.

Prevention. Primary immunization of adults and children over 11 years of age begins with a dose of 1 ml. After 4 weeks, the second dose is administered - 0,2 ml, and after another 6 months - the third (0,2 ml). In the future, three of the same doses are administered at 6-month intervals.

33. Diseases caused by Y. enterocolitica and Y. pseudotuberculosis

Y enterocolitica and Y pseudotuberculosis resemble the intestinal group and are Gram-negative rods that are motile at 22°C but lose the ability to move at 37°C.

These features help distinguish these Yersinia species from Y pestis and Enterobacteriaceae. It is possible to differentiate these pathogens from each other using biochemical methods, agglutination reactions with specific antiserum, and interaction with a bacteriophage specific for Y. pseudotuberculosis. Serotypes 3, 8 and 9 of Y enterocolitica and serotype 1Y of pseudotuberculosis are most often pathogenic for humans.

Y. enterocolitica has been found in many species of wild and domestic animals, in raw milk, oysters, and water sources. Most often, young children get sick. The disease is characterized by diarrhea, acute inflammation of the mesenteric lymph nodes, pharyngitis, abscesses, arthritis, osteomyelitis, hepatitis, carditis, meningitis, ophthalmitis, hemolytic anemia, Reiter's syndrome, septicemia, and skin rashes up to erythema nodosum. The most severe manifestations of yersiniosis are accompanied by a high mortality rate (up to 50%) even after antibiotic treatment. Abdominal pain in the gastrointestinal form of yersiniosis can be severe enough to suggest acute appendicitis. A common symptom is acute diarrhea for 1-2 weeks. The stools are watery, slimy, or colored with bile, but without blood. A large number of polymorphonuclear leukocytes are found in the feces of patients. Children with severe forms of diarrhea may develop hypoalbuminemia and hypokalemia associated with widespread changes in the mucous membrane of the small intestine. The disease proceeds within 2-3 weeks.

The diagnosis of yersiniosis can be confirmed by isolating the pathogen (Y. enterocolitica) from the faeces of patients. Positive results of the passive hemagglutination reaction also confirm the diagnosis. Antibodies in the blood of patients appear on the 8-10th day after the onset of the disease and can remain in it for several months. In children under the age of 1 year, positive results of serological tests are obtained much less frequently than in older children.

Diarrhea due to Y. enterocolitica usually resolves over time without special treatment.

Most strains of Yersinia are sensitive to streptomycin, tetracycline, chloramphenicol and sulfonamides.

Diseases caused by Y. pseudotuberculosa are accompanied by symptoms of acute mesadenitis and terminal ileitis. Abdominal pain is usually severe, often suggesting acute appendicitis. Septicemia rarely develops. The development of postdiarrheal syndrome of hemolysis and uremia associated with yersinia infection is described. The pathogen is sensitive to ampicillin, kanamycin, tetracycline and chloramphenicol.

34. Tularemia. Etiology. Epidemiology. Pathomorphology and pathogenesis

Tularemia - a typical zoonosis, is a natural focal infectious disease that occurs with symptoms of general intoxication, fever and the development of specific lymphadenitis, less often without pronounced disorders. The causative agent is Francisella tularensis (Pasteurella tularensis).

Etiology. The causative agent of tularemia is a short Gram-negative immobile bacterium that does not have a capsule and does not form spores. When grown on nutrient media, the bacteria show pronounced signs of polymorphism. Working with cultures of the pathogen requires special care due to the risk of infection.

Epidemiology. The causative agent of tularemia has been isolated from one hundred different species of mammals and arthropods. Type A bacteria are commonly found in white-tailed rabbits and ticks. Type B is more characteristic of rats, mice, squirrels, beavers, nutmeg rats, moles, birds and ticks that parasitize them. Carriers of tularemia are fleas, lice, mosquitoes and horseflies.

The disease can occur in children who consume contaminated food (rabbit meat or proteins) or water. Often the disease occurs after being bitten by infected ticks, mosquitoes, or other carriers of the disease.

Pathomorphology and pathogenesis. A person becomes infected with tularemia when the pathogen penetrates through the affected or healthy skin, mucous membranes, with an insect bite, through the lungs or the gastrointestinal tract. After 48-72 hours, an erythematous, maculopapular formation appears on the skin at the site of bacteria penetration, rapidly ulcerating, and local lymphadenopathy. The causative agent multiplies in the lymph nodes and causes the formation of granulomas in them. Subsequently, bacteremia can develop, leading to the defeat of a variety of organs. Nevertheless, the most pronounced changes occur in the reticuloendothelial system.

With the inhalation route of infection, bronchopneumonia develops, less often lobar pneumonia. Inflammatory changes are localized in the places where bacteria settle, accompanied by necrosis of the walls of the alveoli. In some cases, bronchitis rather than pneumonia may occur after inhalation exposure.

The causative agent of tularemia, which has entered the lungs, is phagocytosed by alveolar macrophages and enters with them into the lymph nodes of the root of the lungs, and from there into the general circulation. Typhoid forms of tularemia are caused by aspiration of chewed contaminated food.

The factors that determine the virulence of the causative agent of tularemia have not yet been studied. F. tularensis does not produce exotoxin, and no relationship between virulence and antiphagocytic activity of individual strains of these bacteria was noted.

The causative agent of tularemia is an intracellular parasite that can persist for a long time in monocytes and other cells of the macroorganism, which creates the risk of a chronic course and subsequent exacerbations of the infection.

35. Tularemia. Clinic. Diagnostics. Treatment

Clinical manifestations. The incubation period for tularemia varies from a few hours to 1 week. The disease begins acutely with an increase in body temperature up to 40-41 ° C, chills, pain in the muscles and joints, nausea, vomiting and sweating. Headaches are often very severe, but in young children they are usually absent. Sometimes there is photophobia, a maculopapular rash appears. Mild anemia may develop. The number of leukocytes in the peripheral blood may be within the normal range, increased or decreased, ESR may not change. There is transient proteinuria.

Primary changes on the skin with ulcerative-glandular form of tularemia during the first 3 days are maculopapular in nature. By the 4-5th day of illness, they ulcerate and become painful. Healing occurs within 4 weeks. Lymphangitis around the ulcers is usually absent. Enlarged regional lymph nodes are dense, sensitive, in 25% of cases, if left untreated, they melt.

The oropharyngeal form of tularemia is characterized by the development of purulent tonsillitis and pharyngitis, and sometimes ulcerative stomatitis. The general manifestations of the disease are the same as in the ulcerative glandular form.

The glandular form of tularemia does not differ from the ulcerative glandular, a characteristic feature is the absence of changes in the skin and mucous membranes. The oculoglandular form of tularemia is similar to the cutaneous glandular one, but the primary lesion in it is represented by severe conjunctivitis and an increase in regional lymph nodes.

The typhoid form of tularemia resembles typhus. The febrile state is kept for a long time, changes on the skin and mucous membranes may be absent. There are dry cough, severe chest pain, hemoptysis. The clinical picture of bronchitis, pneumonitis or pleurisy is observed in 20% of patients. In most patients in these cases, X-ray examination reveals the involvement of lung tissue and pleura in the process, an increase in the lymph nodes of the lung root. Often noted splenomegaly, sometimes an increase in the liver.

Diagnosis. For the diagnosis of tularemia are of great importance:

1) allergic (intradermal, dermal) test with tularin, which is put according to the type of Pirquet and Mantoux reactions. The reaction is recorded after 1-2 days and is considered positive in the presence of infiltrate and hyperemia of at least 0,5 cm;

2) serological RA with high specificity, but the late appearance of agglutinins in the blood reduces their value as an early diagnostic method; as well as RPHA and ROP - strictly specific and reliable for the diagnosis of tularemia and the retrospective diagnosis of this infection;

3) bacteriological diagnostic methods. Treatment. Positive results are obtained with treatment with streptomycin, as well as tetracycline and chloramphenicol, however, when treating the latter, relapses often occur, requiring repeated courses of treatment with tetracycline.

36. Listeriosis. Etiology. Epidemiology. Pathomorphology and pathogenesis

Listeriosis is a disease manifested by septicemia or meningitis more often in newborns or those with reduced immunological reactions. The human causative agent is Listeria monocytogenes.

Etiology. The causative agent of listeriosis is a small gram-positive rod that does not form spores. It has mobility at room temperature, but loses this ability at 37 °C. When growing on blood agar, it causes beta-hemolysis, but occasionally has the ability to alpha-hemolysis.

When grown on conventional nutrient media, Listeria is often mistaken for diphtheroid bacteria and described as non-pathogenic microorganisms. When stained by Gram material obtained from patients, listeria is often found in the form of cocci, and therefore they are treated as streptococci.

Epidemiology. The pathogen has been isolated from soil where it has lived for more than 295 days, springs, sewage, silage, dust and slaughterhouse waste. It was isolated from the contents of the intestines, the vagina, it was found in the contents of the cervix, nose, ears, blood and urine of apparently healthy individuals. Listeriosis belongs to a new class of infectious diseases - "sapronosis", a characteristic feature of which is that the source of pathogens is not animals, as in zoonoses, and not a person, as in anthroponoses, but the substrate of the external environment.

Infection can occur in the following ways:

1) contact;

2) food (when eating food);

3) aerogenic (in contaminated rooms);

4) transmissively (through insect bites);

5) vertical (transplacental);

6) sexual (during sexual intercourse);

7) intrapartum (during childbirth). Pathomorphology. The disease is accompanied by damage to many organs, including the liver, lungs, kidneys, adrenal glands and brain. There are abscesses that do not differ from those in other purulent infections. Formation of microabscesses and granulations is possible. Necrotic processes are detected in the kidneys and lungs, especially in the bronchioles and the walls of the alveoli.

Listeria causes purulent meningitis and can be the cause of purulent epididymitis, encephalitis, choroiditis, and gliosis.

Pathogenesis. The entrance gates of infection can be any mucous membranes and damaged skin. At the site of the primary introduction of Listeria, they cause an inflammatory reaction involving the lymphatic apparatus. From the place of primary localization, they quickly spread by lymphogenous, hematogenous or neurogenic way to the internal organs, causing vascular and degenerative changes in them. First of all, the pathogen and its endotoxin show their hepatoneurotropism. In the affected organs, the pathogen accumulates and characteristic morphological changes are formed according to the type of listerioma granulomas. The development of the pathological process depends on the site of penetration of the pathogen.

37. Listeriosis. Clinic. Diagnostics. Treatment

Clinical manifestations. Listeria can cause meningitis or sepsis in newborns and young children. Listeriosis can present with pneumonia, endocarditis, localized abscesses, papular or pustular skin changes, conjunctivitis, and urethritis.

With an early onset in a live-born child, the disease in the 1st week of life is manifested by the formation of whitish granulomas on the mucous membranes, widespread papular or petechial rashes on the skin, as well as anorexia, lethargy, vomiting, jaundice, respiratory disorders, infiltrative changes in the lungs, myocarditis, cyanosis, hepatomegaly. Often septicemia or meningitis develops.

With a late onset of the disease, the child looks healthy at birth, but within the 1st month of life he develops septicemia or meningitis, which manifests itself as ordinary purulent meningitis.

Older children may develop meningitis or meningoencephalitis. Clinically, meningitis does not differ from that in other purulent infections, but in some cases it begins subacutely - with headaches, a slight increase in body temperature and a feeling of weakness a few days before the onset of signs of CNS damage.

Oculo-glandular syndrome is characterized by keratoconjunctivitis, corneal ulceration, and regional lymphadenitis.

Listeriosis can also present with pneumonia, a flu-like condition (especially in pregnant women), endocarditis, localized abscesses, conjunctivitis, urethritis, and papular or pustular skin changes. For the final diagnosis, laboratory confirmation is necessary after performing:

1) bacteriological research methods for the purpose of isolating listeria, taking cultures of mucus from the throat, nose, blood, cerebrospinal fluid and other pathological materials on a normal nutrient medium or using a biological sample;

2) serological research methods, which are the main ones in the diagnosis of listeriosis (RA, RSK, RPGA);

3) intradermal test with listeriosis antigen to confirm the diagnosis.

Treatment. The drug sensitivity of different strains of Listeria is different. Most of them are sensitive to erythromycin, tetracycline, penicillin G and ampicillin. Many strains are also sensitive to chloramphenicol.

Treatment usually begins with the appointment of ampicillin in the usual doses, taking into account the form of the disease and the age of the patient. It is necessary to conduct studies of the sensitivity of the pathogen during treatment and make appropriate changes to it, if necessary.

Some strains of L. monocytogenes are resistant to ampicillin; in these cases, treatment with a combination of ampicillin and gentamicin is quite effective.

38. Anthrax

Anthrax is a well-known animal disease that is transmitted to humans and proceeds as an acute infectious disease characterized by severe intoxication, damage to the skin and lymphatic apparatus.

Etiology. The causative agent of the disease Bacillus anthracis is a gram-positive immobile bacillus with a capsule and spores that form under aerobic conditions, are resistant to external influences and can persist for years in soil and various products of animal origin.

Epidemiology. Human infection with anthrax is possible by contact, alimentary, aerogenic and transmissible routes.

Pathogenesis and pathomorphology. The cutaneous form of anthrax is caused by the introduction of spores of the pathogen into the subepidermal layer. The spores multiply and produce an exotoxin that causes tissue necrosis and the formation of a black eschar.

The pulmonary form of anthrax develops when spores are inhaled and enter the alveoli.

The gastrointestinal form of anthrax develops when spores of the pathogen enter the stomach. This form of the disease is manifested by hemorrhages and necrosis of the terminal ileum and caecum as a result of the multiplication of bacteria and the production of a toxin by them.

Clinical manifestations. The incubation period for cutaneous anthrax is 2-5 days. Initially, a small spot appears at the site of penetration of the spores, which quickly turns into a bubble, as it increases in size, it becomes hemorrhagic in nature, necrosis develops in its center, and a scab forms.

Common manifestations of infection are a moderate increase in body temperature, a feeling of malaise, an increase in regional lymph nodes. The incubation period for the pulmonary form is 1-5 days. Initially, there is a general malaise, a moderate increase in body temperature, muscle pain. Then a dry cough may join, and wheezing begins to be heard.

After 2-4 days, a picture of severe respiratory failure develops.

The gastrointestinal form of infection most often occurs when eating the meat of sick animals. After an incubation period of 2-5 days, anorexia, nausea, vomiting appear, and body temperature rises.

Meningitis can develop with untreated cutaneous anthrax. More than half of all cases of meningitis are complications of the cutaneous form of the disease.

Diagnosis. Anthrax is diagnosed on the basis of characteristic changes in the skin and a history of contact with the infection. Isolation of the pathogen from the detachable vesicle or from the scab confirms the diagnosis.

Treatment. Penicillin is the drug of choice. In mild forms of the disease, patients can be treated with penicillin V; in severe and severe forms, patients should be treated with penicillin novocaine salt. In pulmonary and meningeal forms of anthrax, patients are treated with penicillin G.

39. Measles. Etiology. Infectivity. Epidemiology. Pathology

Measles is an acute contagious disease characterized by periods of:

1) incubation, lasting 10-12 days, sometimes accompanied by individual symptoms;

2) prodromal, during which enanthema (Koplik spots) appears on the mucous membrane of the cheeks and pharynx, body temperature rises, conjunctivitis, rhinitis develop, and a painful cough grows;

3) final, accompanied by maculopapular rashes on the face, neck, torso, arms and legs and high body temperature.

Etiology. The measles RNA virus belongs to the Paramyxoviridae family of the Morbillivirus genus. Only one antigenic type of virus is known, which is similar in structure to the causative agent of infectious parotitis and parainfluenza. During the prodromal period and in the first days after the onset of the rash, it is found in the discharge from the nasopharynx, blood and urine. The virus can be grown on tissue cultures of the renal epithelium of a human embryo or rhesus monkey. Cytological changes observed after 5-10 days of cultivation are the appearance of multinuclear giant cells with intranuclear inclusions. By the time the rash appears, specific antibodies circulate in the blood of patients.

Infectivity. Measles is spread by airborne droplets. The virus is localized in the respiratory tract of the patient. The maximum risk of infection exists during the prodromal period.

Susceptible individuals are most likely to become infected before the first case is diagnosed. An infected person becomes dangerous to others on the 9th-10th day after contact, less often - on the 7th day, therefore, isolation of patients and persons in contact with them is necessary from the 7th day after contact. 5 days after the disappearance of the rash, quarantine is removed.

Epidemiology. Measles is ubiquitous. The source of infection is only a sick person. The route of transmission of the measles virus is airborne, but the transmission of infection through objects and a third person should also be taken into account.

Natural susceptibility to measles can be considered universal, with the exception of children of the first 3 months of life with innate immunity obtained from a mother who had measles or was vaccinated.

Pathology. The most characteristic changes in the skin, mucous membranes of the nasopharynx, bronchi, intestines and conjunctiva. Exudate and proliferating mononuclear and few polymorphonuclear cells appear around the capillaries. Lymphoid tissue is hyperplastic. On the skin, these changes are most pronounced around the sebaceous glands and hair follicles.

Koplik's spots are composed of serous exudate and proliferating endothelial cells, similar to those in areas of skin rashes. Often develops diffuse inflammation of the mucous membrane of the oral cavity, pharynx, spreading to the lymphoid tissue of the mucous membranes of the trachea and bronchi.

40. Measles. Clinic. Diagnostics. Treatment

Clinical manifestations. The incubation period is 10-12, less often 6-10 days, and the rash appears after 14 days. Body temperature may rise slightly on the 9-10th day, and then again decreases for a day or more.

The prodromal period, usually lasting 3-5 days, is characterized by fever, dry, "barking" cough, rhinitis, and conjunctivitis. 2-3 days before skin rashes, a symptom pathognomonic for measles appears - Koplik's spots (grayish-white spots the size of a grain of sand, surrounded by a reddish rim), usually located on the hard and soft palate.

Occasionally, the prodromal period is difficult, starting with a sudden increase in body temperature, convulsions, and even pneumonia.

Usually, rhinitis, fever and cough gradually increase, reaching a maximum by the time the rash appears.

Body temperature rises to 39-40,5 ° C simultaneously with a rash on the skin. In uncomplicated cases, after 2 days, when the rash covers the entire trunk and legs, the symptoms begin to disappear quickly.

The rash first appears as pale spots on the upper sides of the neck, behind the ears, along the hairline.

Within 24 hours, it rapidly spreads to the entire face, neck, arms, and upper chest.

Individual elements become maculopapular in nature. Over the next 24 hours, the rash spreads to the back, abdomen, and extremities. On the 2nd or 3rd day, it appears on the feet and at the same time begins to turn pale on the face. The rash turns pale and disappears in the same sequence as it appears. The severity of the disease is directly dependent on the severity of the rashes and their tendency to merge.

Lymph nodes in the angle of the mandible and the posterior neck are usually enlarged, and the spleen may also be slightly enlarged.

Young children with malnutrition are more likely to experience otitis media, bronchopneumonia, and gastrointestinal disturbances such as diarrhea and vomiting. Measles often affects children under the age of 1 year, and malnutrition contributes to the severe course of the disease.

Diagnosis. For the diagnosis of measles, mainly clinical and epidemiological data are used, and less often laboratory data, which include hematological data, cytological examination of nasal discharge, virus isolation, and detection of antibodies.

Treatment. Of paramount importance are bed rest, sedatives, and at high temperature, antipyretics and adequate fluid supply. Humidification of the air in the room may be necessary for laryngitis and severe irritating cough, with photophobia, the patient is protected from exposure to bright light.

When complicated by otitis media and pneumonia, appropriate antibacterial treatment is required. Children with encephalitis, sclerosing panencephalitis, giant cell pneumonia, disseminated intravascular coagulation require an individual approach and qualified care.

41. Rubella

Rubella is a moderately contagious disease in childhood, characterized by mild general disorders, rashes, and swollen lymph nodes in the occipital, parotid, and posterior cervical regions.

Rubella transmitted by a pregnant woman can cause severe fetal malformations.

Etiology. Rubella is caused by a pleomorphic RNA virus. It belongs to the family Togaviridae of the genus Rubivirus. The presence of the rubella virus is manifested by the resistance of infected cells to the effects of the enterovirus. At the height of the disease, the virus is determined in the discharge from the nasopharynx, in the blood, feces and urine.

Epidemiology. Man is the only reservoir of infection. It spreads by airborne droplets or is transmitted transplacentally.

Clinical manifestations. Incubation period - 14-21 days; prodromal, characterized by minor catarrhal symptoms, usually shorter than measles, and often goes unnoticed. The most typical is an increase in the occipital, parotid and posterior cervical lymph nodes. Immediately before the skin rash, an enanthema may appear in the form of separate pink specks on the soft palate, some of which merge.

Lymph nodes increase at least 24 hours before skin rashes and remain in this state for 1 week or more.

The rash first appears on the face and soon spreads to the body.

The rashes are numerous and look like maculopapular formations, covering the body especially abundantly during the first 24 hours.

The mucous membranes of the pharynx and conjunctiva are somewhat inflamed.

The diagnosis of rubella is established on the basis of clinical and epidemiological data:

1) the clinical method includes the data of the anamnesis of the disease and an objective examination;

2) hematological data (leukopenia, lymphocytosis, plasma cells, normal ESR);

3) the virological method consists in isolating the virus from nasopharyngeal swabs, blood, urine, feces;

4) the serological method allows you to determine the state of immunity and identify its dynamics during the course of the disease.

Treatment. Rubella usually does not require hospitalization and prescription of drugs. Vitamin therapy, bed rest for 3-4 days are shown, in combination with ARVI - symptomatic agents, with streptococcal infection - antibacterial therapy, in the event of meningoencephalitis - urgent hospitalization and complex treatment, including anti-inflammatory, hormonal, detoxification, dehydration.

Rubella prevention is based on the complex use of:

1) measures in relation to sources of infection;

2) means of influencing the mechanisms of infection transmission;

3) means that affect the susceptibility of the population - active and passive immunization.

42. Herpes simplex. Etiology. Epidemiology. Pathology. Diagnostics. Treatment

Herpes simplex infection is clinically manifested by the defeat of many organs and tissues, accompanied by the appearance of clustered blisters on the skin and mucous membranes. It has a tendency to a long latent course with periodic relapses.

Etiology. Two types of virus (HVH-1 - most often cause damage to the skin of the face and mucous membranes of the oral cavity, HVH-2 - damage to the genitals, meningoencephalitis) differ in antigenic and biological properties.

Epidemiology. The source of infection are sick and virus carriers. Transmission is carried out by contact, sexual, airborne, a transplacental route of infection is possible, but infection occurs especially often during the passage of the birth canal.

Pathology. Pathological changes depend on the localization of the infection. On the skin and mucous membranes, the characteristic changes are the formation of vesicles resulting from stratification and ballooning degeneration of the cells of the spiny layer of the epidermis. Specific features include intranuclear inclusions - homogeneous masses located in the center of a significantly altered nucleus, the chromatin substance of which is displaced to the periphery, to its membrane.

With generalized forms, small foci of coagulation necrosis are formed in many organs and systems. In the central nervous system, changes occur in the cortical, less often in the white matter and subcortical centers. Typical diffuse vasculitis, glia proliferation, necrosis of individual nerve cells. Diagnostics. Diagnosis is based on two of the following:

1) typical clinical picture;

2) isolation of the herpes virus;

3) determination of specific neutralizing antibodies;

4) characteristic cells in prints or biopsy. Treatment. With localized lesions of the skin and mucous membranes, locally 0,25% oxolinic ointment, 0,5% Florenal ointment, 0,25-0,5% tebrofen ointment, 0,25-0,5% rhyodoxol ointment, as well as Acyclovir ointment and other antiviral drugs. With keratitis - the antiviral drug JDUR (5 iodine-2-deoxyuridine) in the form of ointments, solutions, as well as adenine arabinoside. The treatment of affected areas of the skin and mucous membranes is carried out using antiseptic agents: 1-2% alcohol solution of brilliant green, 1-3% alcohol solution of methylene blue, with herpetic stomatitis - 3% hydrogen peroxide solution. Locally used painkillers (anesthesia, lidocaine).

In severe forms of the disease, bonafton, local bonafton ointment, intravenous administration of YDUR, antiviral drugs (adenine arabinoside, highly active leukocyte interferon, acyclovir, virolex, ribavirin, etc.) are prescribed to prevent the progression of local manifestations and prevent dissemination of infection.

With a recurrent course of the disease, general strengthening and stimulating agents are indicated. Antibacterial therapy is carried out only with the layering of a secondary bacterial infection.

43. Herpes simplex clinic

The incubation period is 2-14 days, on average - 6. Clinical manifestations depend on the location of the lesion and its prevalence.

1. Damage to the mucous membranes and skin. On the skin, the changes look like conglomerates of thin-walled vesicles with an erythematous base, they rupture, crust and heal in 7-10 days.

2. Traumatic skin injuries predispose to the development of herpetic eruptions. In this case, the primary infection is more often manifested by single vesicles, and the recurrent one - by their clusters, the vesicles appear at the site of infection after 2-3 days.

3. Acute herpetic gingivostomatitis. In children aged 1-3 years, the primary infection is manifested by stomatitis. Symptoms develop acutely, pain in the mouth, salivation, bad breath appear, the child refuses to eat, his body temperature rises to 40-40,6 ° C. Vesicles form on the mucous membrane, which quickly burst, ulcers 2-10 mm in diameter are formed, covered with a grayish-yellow film.

4. Recurrent stomatitis is characterized by isolated changes localized in the soft palate or near the lips and accompanied by fever.

5. Massive infection with the herpes virus of the altered eczematous skin is accompanied by the development of herpetic eczema. In typical cases, numerous vesicles appear at the site of eczematous changes. New rashes may appear within 7-9 days. At first they are isolated, but then they are grouped and directly adjacent to the healthy skin area. The epithelium may slough off. Healing usually occurs with scar formation.

6. Infection of the eyes. Primary infection with the herpes virus and its relapses are manifested by conjunctivitis and keratoconjunctivitis. In a primary infection, the parotid lymph nodes enlarge and thicken.

7. Herpes in the vulva is most common in adolescents and young adults through sexual contact and is usually caused by HVH-2. If the patient does not have antibodies to the herpes virus, then he develops general disorders

8. Systemic infection. Newborns in most cases become infected during childbirth when passing through the birth canal infected with the HVH-2 virus, or when the fetal bladder ruptures.

Clinical manifestations develop during the first 2 weeks and consist in characteristic skin lesions, lethargy, the child does not take the breast well, persistent acidosis, liver enlargement, pneumonitis, meningoencephalitis are noted.

9. Meningoencephalitis. In newborns, it is usually caused by HVH-2, and in older age groups by HVH-1. Its pathogenesis remains unknown, but it can develop even in immune individuals in whose blood antibodies circulate.

44. Chickenpox

A characteristic feature of chickenpox is the consistent appearance of typical vesicles on the skin and mucous membranes against the background of minor general disorders.

Epidemiology. The disease is highly contagious. The peak incidence occurs in the age group of 5-9 years.

The infection is spread by drop or contact, the causative agent is contained in the fluid of the vesicles. The patient is an epidemic danger one day before the appearance of rashes and for the next 7-8 days, until all the bubbles are covered with crusts.

Clinical manifestations. The incubation period is 11-21 days, but more often 13-17 days. By the end of it, prodromal symptoms appear, with the exception of mild cases of the disease, manifested by malaise, a slight increase in body temperature.

Usually rashes are abundant, appear within 3-4 days, first on the trunk, then on the face and scalp, and minimally on the distal extremities. Varicella is characterized by polymorphism of the rash, observed at the height of the disease and associated with different periods of the appearance of its individual elements. The rash is accompanied by constant and irritating itching. Vesicles on the mucous membranes, especially in the oral cavity, quickly macerate and ulcerate.

In mild forms, a meager number of vesicles scattered throughout the body and mild general disturbances are observed. In severe forms, their number is huge, symptoms of intoxication are expressed, body temperature rises to 39,4-40,6 ° C.

Sometimes the rash becomes hemorrhagic due to moderate thrombocytopenia. A more severe degree of it and hemorrhage most often occurs with the development of complications.

The bullous form is rare, mainly in children under the age of 2 years.

In this case, instead of characteristic bubbles, large flabby bubbles form on the skin.

Diagnosis. The diagnosis is based on the detection of a typical vesicular rash.

From laboratory methods use:

1) microscopic research method;

2) serological methods.

Treatment. Vesicles are lubricated with 1% brilliant green solution or 1-2% potassium permanganate solution. Showing general hygienic baths with a weak solution of potassium permanganate, rinsing the mouth with disinfectant solutions after eating, with the appearance of purulent complications - antibiotics, in severe forms - immunoglobulin.

A good effect is given by the appointment of antiviral drugs: adenine arabinoside, acyclovir, virolex, ganciclovir.

Prevention. A patient with chickenpox is isolated at home until the 5th day after the last rash. Children with severe and complicated forms of the disease are subject to hospitalization. Contacted children who have not been ill before are isolated from 11 to 21 days from the moment of contact.

45. Cytomegalovirus infection

Cytomegalovirus infection often goes unnoticed, but infection before, during, or shortly after birth usually causes severe illness.

Etiology. Cytomegalovirus is a species-specific agent, similar in its physicochemical and electron microscopic properties to the herpes virus.

Epidemiology. The source of infection is only a person, a sick person or a virus carrier.

Transmission is carried out, apparently, mainly by contact, less often by airborne and enteral routes, as well as parenterally, newborns can become infected through mother's milk; transplacentally.

Pathology. Under light microscopy in tissues with a high titer of the virus, large intranuclear inclusions are determined. Their large size in the cells of the liver, kidneys, lungs, in the urine sediment allows you to make an accurate diagnosis.

Clinical manifestations. The incubation period seems to range from 15 days to 3 months.

congenital infection. Commonly observed symptoms, in decreasing order of frequency, are hepatosplenomegaly, jaundice, purpura, microcephaly, brain calcification, and chorioretinitis. Any of the manifestations can occur in isolation.

For many children, the only symptoms are developmental delays and irritability.

The most common and important sign of congenital infection is a violation of the function of the central nervous system.

Acquired infection, as well as congenital, is most often asymptomatic.

It is not uncommon for babies to become infected from their mother during the 2nd stage of labor, and the virus begins to be shed in their urine after a few weeks.

In older children and adults, mononucleosis due to cytomegalovirus is the main manifestation of the disease.

The feeling of weakness and fatigue persists for a long time. Chills and daily fever of 40°C or more may last for 2 weeks or more. An early and important sign is atypical lymphocytosis.

Diagnostics. Based on clinical data alone, it is impossible to make a diagnosis of cytomegalovirus infection. Laboratory diagnostics is based on:

1) cytological studies;

2) virological studies;

3) serological studies.

With generalized cytomegaly, the use of corticosteroid hormones, intramuscular use of interferon or reaferon, the introduction of vitamins C, K, P, group B are indicated, antibiotics are prescribed when a bacterial infection is layered and complications occur. Due to the immunosuppressive effect of the virus, immunostimulants are prescribed.

Prevention. It is advisable to examine all pregnant women for cytomegaly, as well as women who have had ARVI during pregnancy, newborns with jaundice.

46. Epstein-Barr virus infection (infectious mononucleosis)

Infectious mononucleosis is an acute infectious disease caused by the Epstein-Barr virus from the herpetiform group.

Etiology. The virus in its morphological structure does not differ from the herpes simplex virus.

Epidemiology. EBV is ubiquitous. Infection proceeds differently depending on age.

The source of infection is patients with asymptomatic and manifest (erased and typical) forms of the disease, as well as virus carriers. The main route of transmission is airborne, often through infected saliva, less often vertically (from mother to fetus).

Clinical manifestations. The incubation period in adolescents and young men is 30-50 days, in children it is shorter, but the exact timing has not been established. The disease begins imperceptibly and gradually. The patient complains of weakness, fatigue, headaches, nausea, sore throat. The prodromal period can last 1-2 weeks. Gradually, the pain in the throat intensifies, the body temperature rises, which makes the patient consult a doctor. During the examination, signs of moderate or severe pharyngitis are found, a significant increase in the tonsils, sometimes covered with plaque. In some patients, enanthema is often detected in the form of petechiae, localized mainly on the border of the hard and soft palate. Body temperature rises to 39 ° C in 85% of patients.

The characteristic signs include an increase in lymph nodes, liver and spleen. Most often, nodes on the back of the neck increase.

Atypical lymphocytosis in children is usually absent, but antibodies in the blood appear much later, often only during the period of convalescence. Before the age of 2 years, infectious mononucleosis is usually asymptomatic.

Oncogenic activity of the Epstein-Barr virus. The causative agent of infectious mononucleosis is one of the factors contributing to the development of Burkitt's lymphoma (BL).

Burkitt's lymphoma is a malignant disease of lymphoid tissue localized outside the lymph nodes - in the upper jaw, kidneys, and ovaries.

Recently, an association of polyclonal B-cell lymphomas with Epstein-Barr virus has been found in immunocompromised patients.

Diagnosis. The diagnosis is confirmed using laboratory research methods, in particular, using serological diagnostic methods that make it possible to identify heterophilic antibodies in the blood serum of patients with respect to the erythrocytes of various animals.

Treatment. There is no specific treatment. Assign symptomatic and pathogenetic therapy depending on the form of the disease. In all forms of the disease, antipyretics, desensitizing drugs, antiseptics for stopping the local process, vitamin therapy are used as basic therapy, and choleretic agents for functional changes in the liver. Antibacterial therapy is prescribed in the presence of pronounced overlays in the oropharynx, the occurrence of complications.

47. Chlamydia. Chlamydial conjunctivitis and pneumonia in children

Chlamydia is an infectious disease of humans, animals and birds caused by chlamydia.

Etiology. Chlamydia are obligate intracellular parasites with a discrete membrane similar to that of Gram-negative bacteria.

They include RNA and DNA. Their activity is suppressed by some antibiotics.

Parasites do not stain according to Gram, they perceive Giemsa stain, which makes it possible to detect them in the form of characteristic cytoplasmic perinuclear inclusions.

The genus Chlamydia is divided into two groups:

1) group A includes C. trachomatis and the causative agent of inguinal lymphogranuloma;

2) group B includes pathogens of psittacosis (ornithosis), Reiter's disease, pneumonia and encephalomyelitis in cows and polyarthritis in sheep.

Epidemiology. Chlamydia is widespread throughout the world. Infection occurs sexually (in adults) with the development of inguinal lymphogranuloma or non-specific non-gonococcal urethritis, by contact when the pathogen is transferred by hand. Newborns become infected during the passage of the fetus through the birth canal of a sick woman.

Chlamydial conjunctivitis and pneumonia in children

Clinical manifestations. Conjunctivitis usually begins in the 2nd week of life, rarely develops after 3 days or after 5-6 weeks.

The child becomes irritable, the body temperature does not rise, the eyelids swell, pus begins to stand out from the eyes, and pseudomembranous formations appear in them.

The bacterial flora is usually not detected during sowing of the discharge. After 2-3 weeks, conjunctivitis resolves, sometimes even without appropriate treatment.

Local application of antibiotics is accompanied by an effect, but does not protect against recurrence of the disease.

Physical examination reveals dry rales. Conjunctivitis develops in 50% of children.

Diagnosis. Chlamydial infection can be clinically suspected if the newborn consistently develops conjunctivitis with a long persistent course, bronchitis that occurs with bouts of painful coughing, small-focal pneumonia, and also if eosinophilia and a significantly accelerated ESR are detected with a relatively mild general condition.

Laboratory confirmed by methods that allow:

1) identify chlamydial antigen in biological material;

2) isolate chlamydia in cell culture;

3) determine specific anti-chlamydial antibodies of class G and M, etc.

Treatment. With conjunctivitis, antibacterial drugs are prescribed in the form of an ointment, with pneumonia - erythromycin and other antibacterial drugs in an age dosage.

In severe cases, combined treatment with two or more drugs (erythromycin with biseptol, other sulfanilamide drugs or furazolidone) is prescribed. With a recurrent course, immunostimulating therapy is indicated.

Preventive measures should be directed at the source of infection, the route of transmission and the susceptible organism. Active prophylaxis has not been developed.

48. Psittacosis (ornithosis)

Ornithosis is an infectious disease caused by Chlamydia psittaci, transmitted to humans from birds, characterized by symptoms of intoxication and lung damage.

Epidemiology. The natural reservoir is wild and domestic birds, in which the infection occurs more often in a latent form. The causative agent is excreted by birds with feces and respiratory secretions. The main routes of transmission are airborne and airborne. Infection of children occurs through contact with indoor and domestic birds, as well as pigeons, etc.

Clinical manifestations. The incubation period is from 5 to 30 days, usually 1-2 weeks. The onset of the disease is usually acute.

There are chills, fever, severe headaches, muscle pain, weakness and blackout of consciousness. Pneumonia often develops, less common anorexia, vomiting, photophobia, and an enlarged spleen.

In some rare cases, hepatitis, pulmonary embolism, disseminated intravascular coagulation are noted. Body temperature can reach 40,5 °C.

Auscultation of the lungs reveals scattered dry rales, and x-rays show signs of diffuse interstitial pneumonia. Changes in the blood formula are uncharacteristic.

A serious condition can last for 3 weeks, after which a pronounced improvement occurs. Mortality does not exceed 1%.

Diagnosis and differential diagnosis. A similar clinical picture develops with pneumonia caused by mycoplasmas, influenza bacillus and some viruses. The diagnosis is established by anamnestic data on contact with sick birds at work or in the market.

Isolation of chlamydia from blood and sputum with appropriate laboratory capabilities facilitates diagnosis. A 4-fold increase in the titer of complement-fixing antibodies is also of great importance.

A presumptive diagnosis can be made based on a single determination of the complement fixation reaction when its titer is 1:32 or higher.

Treatment. Antibiotics are usually prescribed (erythromycin, sumamed, levomycetin, rulid in the age dosage and depending on the nature of the course).

With bacterial complications, penicillin, cephalosporins, aminoglycosides are prescribed.

In severe cases of psittacosis, corticosteroid hormones are indicated. Symptomatic and stimulating treatment is prescribed.

Prevention is aimed at identifying ornithosis in birds, observing sanitary and hygienic skills when caring for poultry. Hospitalized patients should be kept under the conditions of isolation used for airborne infections.

49. Inguinal lymphogranulomatosis

Inguinal lymphogranulomatosis is an infectious disease caused by chlamydia, sexually transmitted, manifested by an ulcer at the site of the pathogen, regional lymphadenitis with suppuration and scarring. Children usually get sick after contact with an adult patient.

Epidemiology. The disease occurs mainly in countries with tropical and subtropical climates.

Pathology. The primary lesion is an ulcer localized in the vulva. The most characteristic changes develop in the regional lymph nodes, which increase, solder to each other, and then melt, resulting in the formation of irregularly shaped abscesses.

Clinical manifestations. The incubation period is 3-30 days in cases where the primary ulcer is considered the end of it at the site of penetration of the pathogen.

The primary lesion has the appearance of a small erosion, pustule or papule, but often goes unnoticed due to asymptomatic and small size. Secondary lesions develop 1 week to 1 month after the primary lesion and represent the most characteristic symptom of the disease.

Lymph nodes are initially dense, elastic and mobile, but then solder.

The skin above them turns red, becomes cyanotic, flaky and thinner. Soon, fistulas open in these areas, functioning for many weeks and months.

Inguinal lymphogranulomatosis is accompanied by general malaise, fever, headaches, anorexia, etc. Sometimes meningoencephalitis develops, and the pathogen is determined in the cerebrospinal fluid.

The number of leukocytes and ESR are often elevated, there is a slight anemia, a decrease in albumin, an increase in globulins, and an increase in liver enzymes.

Diagnosis and differential diagnosis. The disease is diagnosed on the basis of the presence of a primary lesion, regional lymphadenitis in the inguinal region, proctitis.

The diagnosis is confirmed by the detection of the pathogen in the contents of the suppurating lymph nodes or the discharge of fistulas, the isolation of the pathogen in the cultures of developing chicken embryos and cultured cells, the identification of group- and species-specific antibodies, etc.

Treatment. Antibiotics of the erythromycin and tetracycline groups, as well as levomycetin, etc. are effective. Sulfanilamide preparations are prescribed for a period of 3-4 weeks. With severe cicatricial changes and strictures, lidase is prescribed by electrophoresis on the affected area, injections of aloe, vitreous body, etc. In severe cases, they resort to surgical treatment.

Prevention. All measures taken to prevent sexually transmitted diseases are also effective against inguinal lymphogranulomatosis. There are no vaccines.

50. Tuberculosis. Etiology. Epidemiology. Immunology

Etiology. Tuberculosis is caused by tubercle bacilli belonging to the family of mycobacteria, a group of actinomycetes. In humans, the leading role is played by M. tuberculosis, responsible for most cases of the disease; M. bovis is the causative agent of tuberculosis in cattle, rabbits, M. avium causes disease in birds and white mice. All mycobacteria are non-motile, aerobic, polymorphic rods that do not form spores. They are difficult to stain due to the high lipid content in their cell wall, but once stained, they are no longer discolored by alcohol and acids. A feature of Mycobacterium tuberculosis is their very slow growth on nutrient media. Under the influence of various environmental factors, the causative agent of tuberculosis exhibits a wide range of variability in the morphology of bacterial cells - from the smallest filtering particles and grains to giant branched forms, which affects their functional properties.

Epidemiology. Tuberculosis is a relatively common disease, with adults with active tuberculosis and tuberculosis-affected cattle being the main source of infection in children.

The most dangerous are patients with bacterial excretion. The main route of infection transmission is airborne. The rest - alimentary, contact, through damaged skin and mucous membranes - are rare and do not have great epidemiological significance.

Immunology. Immune responses in tuberculosis are a complex set of interactions between the pathogen, specific populations of lymphocytes, and tissue macrophages. Various types of antibodies produced during the development of infection do not play a significant role in suppressing the growth of mycobacteria and in the development of anti-tuberculosis immunity. Cellular reactions of immunity begin to manifest themselves after the ingestion of live and pathogenic mycobacteria. Lung macrophages phagocytize them, but are unable to destroy them. In macrophages, the pathogen continues to multiply, with them mycobacteria enter the regional lymph nodes. Subsequently, the infection spreads along the hematogenous and lymphogenous pathways with the formation of numerous extrapulmonary foci.

Immunological processes are completed within 6-10 weeks, leading to the development of primary infection and elimination of metastatic foci.

The development of natural immunity to this life-threatening infection depends on the influence of:

1) genetic factors;

2) age determining the severity of tuberculosis;

3) factors affecting the function of T-lymphocytes and thereby contributing to the development of severe forms of the disease: malnutrition, various infections, primarily measles and whooping cough, pregnancy, diseases of the reticuloendothelial system, lymphocytic leukemia.

51. Diagnostic skin tests

Diagnostic skin tests. Skin reactions to the administration of tuberculin are based on the detection of delayed-type hypersensitivity to antigens of tuberculous mycobacteria and are of great importance in the diagnosis of tuberculosis infection. Positive reactions appear 6-10 weeks after pathogens enter the body. The test involves intradermal injection of an antigen drug into the patient. A positive reaction is expressed by the appearance of indurate at the injection site. It is caused by migration of activated lymphocytes and macrophages to the area of antigen injection. Two different tuberculin preparations are used: old Koch tuberculin (alt-tuberculin, ATK) and purified protein-free tuberculin PPD.

Mass screening of tuberculosis infection in pediatric practice is carried out using multiple puncture methods. The disadvantage of this relatively sensitive method is the weak specificity, therefore, in cases of a positive or doubtful reaction, it is usually necessary to additionally examine using the Mantoux test. The most common is the Tine-test, which involves the use of a plate with four steel spikes soaked in ATK. The test results are taken into account after 48-72 hours. A positive reaction is expressed by the appearance of vesicles or more often papules with a size of at least 2 mm at the site of one or more punctures.

The Heaf test involves the use of a special device that simultaneously produces 6 skin punctures to a depth of 1 mm through a layer of concentrated PPD tuberculin. The sample can be taken into account within the next 3-7 days. A positive reaction is expressed by the appearance of 4 or more papules at the puncture site. False positive reactions are not uncommon with all multiple puncture techniques. In addition, all positive and doubtful reactions require confirmation of the Mantoux test.

The Mantoux test is more complex than multiple puncture methods, but more accurate, since it introduces a strictly defined amount of antigen. The results of the reaction are taken into account after 48-72 hours. The appearance of an indurat with a diameter of 10 mm at the injection site indicates an infection with tuberculosis and is regarded as a positive reaction.

With an indurate of 5 to 10 mm, the reaction is regarded as doubtful, and with an indurate diameter of up to 5 mm, as negative.

Under certain circumstances, an indurat of 5 to 10 mm can be interpreted as a dubious reaction and treatment can be prescribed. False-negative Mantoux test results can occur for many reasons: they are negative in the early stages of the disease, even with the introduction of 250 IU; as a result of technical errors in the storage of tuberculin and during the test; as a result of the suppression of tuberculin reactions by preventing activation by lymphocytes and the development of delayed-type hypersensitivity.

Any reaction to intradermal administration of tuberculin larger than 10 mm, occurring 3 years or more after BCG vaccination, should be considered as an indicator of tuberculosis infection.

52. Clinical forms of tuberculosis. Intrathoracic tuberculosis

Pathogenesis and pathomorphology. Primary infection develops most often after inhalation of live virulent mycobacterium tuberculosis. The body of a non-immune child reacts to the penetration of infection with certain cellular reactions. Pathogens are phagocytized by macrophages, in these cells their further reproduction occurs, macrophages bring mycobacteria into regional lymph nodes. Subsequently, lymphogenous and hematogenous dissemination of the infection occurs with the appearance of metastatic foci in the lungs, in the reticuloendothelial system and in other organs.

During this period, when cellular immunity reactions to tuberculosis infection have not yet developed, tissue damage is minimal, and clinical symptoms may be absent. In the vast majority of cases, acquired immunity reactions form 6-10 weeks after infection and are accompanied by recovery, calcification of pulmonary and extrapulmonary foci occurs. Dormant tuberculous infection persists in these residual tuberculous changes, usually located in the apical and subapical regions of the lungs.

Any factors that damage the response of cellular immunity can lead to the reactivation of tuberculosis infection, to the multiplication of pathogens in these foci and the development of pulmonary or extrapulmonary lesions.

Primary pulmonary tuberculosis

Clinical manifestations. In children aged 3 to 15 years, primary tuberculosis is usually asymptomatic, may not be accompanied by changes on chest radiographs, and manifests itself only by a tuberculin test. General symptoms are mild and non-specific, manifested by slight fever, loss of appetite, weight loss, rarely erythema nodosum and phlyctenular conjunctivitis.

Additional symptoms may develop later with a massive increase in intrathoracic lymph nodes, characteristic of a primary tuberculosis infection. In these cases, the enlarged lymph nodes are displaced, squeezed, impair patency or destroy various adjacent organs of the mediastinum. In most children, primary lung infection is mild, asymptomatic, and resolves within a short time even without chemotherapy.

In older children and adolescents, primary pulmonary tuberculosis usually manifests itself as pronounced infiltrative changes in the upper parts of the lungs with the development of destruction, while there are no signs of calcification and enlargement of the intrathoracic lymph nodes. Less commonly, there is a lesion of the middle and lower parts of the lungs with involvement of the intrathoracic lymph nodes, which is characteristic of young children. In younger children, against the background of the described symptoms, a picture of lympho- and hematogenous dissemination may develop, leading to miliary tuberculosis and meningitis.

53. Clinical forms of tuberculosis. Progressive primary pulmonary tuberculosis

tuberculosis reactivation. Effusion in the pleural cavity

1. Progressive primary pulmonary tuberculosis

In some cases, the primary focus formed in the lungs does not heal, but increases in size. Damage to the entire lower or middle lobe of the lung may develop. Typically, this course of the disease is observed in patients with suppressed immunity. The increase in intrathoracic lymph nodes in such patients is natural, endobronchial spread of infection and the development of destructive changes in the lungs are often observed. Clinical symptoms are pronounced: febrile body temperature, malaise, anorexia, weight loss, cough with sputum. Physical examination and radiographs reveal hilar adenopathy, inflammatory changes in the middle or lower lobes of the lungs, and cavern formation. The diagnosis must be confirmed by bacteriological data.

2. Reactivation (reinfection) of tuberculosis Reactivation of tuberculosis (or "adult" tuberculosis) is not typical for childhood, especially with the development of primary tuberculosis at the age of about 3 years. Lesions in these cases are localized in the apical and dorsal segments of the upper lobes or in the apex of the lower lobe. An increase in hilar lymph nodes is rare. The most characteristic symptom is subfebrile temperature and night sweats due to a decrease in temperature. On physical examination, gentle rales are found predominantly in the apical regions of the lungs, especially after coughing. The earliest radiographic findings are usually homogeneous, well-demarcated opacities at the apex of the lungs.

3. Pleural effusion

The development of pleurisy can occur as a result of the penetration of tuberculosis mycobacteria into the pleural cavity from peripherally located tuberculosis foci in the lung, as a result of hematogenous dissemination of the pathogen.

It is bilateral, accompanied by pericarditis and peritonitis. Often these lesions resolve spontaneously. Often, a few years after suffering pleurisy, patients observe reactivation of pulmonary tuberculosis. Such patients are shown prophylactic administration of anti-tuberculosis drugs.

A biopsy of the pleura should be performed in all cases and preferably at the same time as the first pleural puncture. In the absence of effusion in the pleural cavity, pleural biopsy is difficult. Histological examination of the pleural biopsy material in most cases reveals granulomatous changes. The appearance of pleural effusion in children with positive tuberculin reactions in all cases should raise the suspicion of tuberculosis and serve as the basis for an appropriate examination. Similarly, pleurisy of unknown etiology in a child with negative tuberculin tests requires a repeat tuberculin diagnosis after 2-3 weeks.

54. Clinical forms of tuberculosis. Extrathoracic and miliary tuberculosis

1. Extrathoracic tuberculosis

Tuberculosis of the upper respiratory tract. Tuberculosis of the larynx in a child almost always occurs against the background of cavernous pulmonary tuberculosis, its symptoms are persistent cough, sore throat and pain when swallowing, hoarseness of voice.

Tuberculosis of the lymph nodes. The defeat of peripheral and deep lymph nodes is considered a characteristic feature of tuberculosis infection.

In children, the hilar lymph nodes are most often affected first, from which the process can subsequently spread to paratracheal, supraclavicular, deep cervical or intraperitoneal groups of lymph nodes.

Clinical manifestations. Tuberculosis of the lymph nodes usually begins gradually and imperceptibly. Only in children highly sensitive to tuberculosis infection, an acute onset of the disease is possible with an increase in body temperature and the development of local signs of inflammation. Most children have positive tuberculin tests, and chest radiographs show signs of primary pulmonary tuberculosis.

Diagnosis. An accurate diagnosis is possible on the basis of histological or microbiological examination.

Treatment. Tuberculous lesions of the lymph nodes respond well to treatment with isoniazid and rifampicin or ethambutol given for at least 18 months.

2. Miliary tuberculosis

Miliary tuberculosis occurs more often in children under 3 years of age with hematogenous dissemination of mycobacteria with the development of granulomas in many organs that undergo caseous necrosis.

Clinical manifestations. The onset of the disease in children can be acute. Body temperature rises, weakness, malaise, anorexia, weight loss develop. On physical examination, nonspecific changes are noted in the form of lymphadenopathy, enlargement of the liver and spleen. Subsequently, respiratory disorders increase. With the development of meningitis, headaches, lethargy, stiffness of the neck muscles join.

In the case of periodic penetration of a small number of pathogens into the bloodstream, a picture of chronic hematogenous disseminated tuberculosis usually develops, which is more typical for adult patients, and not for children. Its clinical symptoms are short or long periods of fever, weakness, weight loss, growing over a long time.

Diagnosis. Diagnostic methods are:

1) x-ray examination;

2) cultures of blood, urine, gastric contents and cerebrospinal fluid in order to detect myco-bacteria;

3) transthoracic lung biopsy.

Treatment. The appointment of isoniazid and rifampicin in combination with ethambutol or streptomycin is shown.

55. Tuberculous meningitis

Epidemiology. The disease most often develops within six months after infection with tuberculosis.

Pathophysiology and pathomorphology. Hematogenous generalization of infection, characteristic of this disease, leads to the formation of metastatic foci of tuberculosis infection. In the central nervous system, solitary tubercular foci (tuberculomas) may occur, the membranes of the brain and spinal cord are affected. Tuberculous meningitis occurs when tuberculous tubercles localized subependymal or large tuberculous foci located near the meninges break into the subarachnoid space, emptying their infected contents into it. In this case, a severe inflammatory reaction develops in the immune organism, primarily from the side of the central nervous system.

Clinical manifestations. Symptoms of the disease develop gradually. There are three stages of the process:

1) the prodromal phase, characterized by nonspecific symptoms: apathy, mood deterioration, poor school performance, loss of appetite, nausea, vomiting, and low-grade fever;

2) the stage of onset of clinical symptoms, which occurs after a couple of weeks and is characterized by the appearance of neurological symptoms. Irritability increases, older children complain of a headache. Neck stiffness may appear in combination with Kernig's and Brudzinski's symptoms. Loss of function of the cranial nerves is characteristic: pathology of pupillary reactions, diplopia, decreased visual acuity, hearing impairment, facial paralysis. Often there are speech disorders, aphasia, disorientation, hemiplegia, ataxia, involuntary movements and convulsions. Intracranial pressure at this stage of the disease is increased. At the same time, there may be an increase in the volume of the head, bulging of the fontanelles, and in older children - swelling of the nipple of the optic nerve;

3) the stage of impaired consciousness up to stupor and coma, characterized by an increase in signs of diffuse cerebral dysfunction. Stupor, coma, decerebration or decortication, irregular breathing, pupils fixed or dilated develop.

Diagnosis. In all doubtful cases, after a thorough and comprehensive study of the anamnesis, clinical examination, it is necessary to resort to diagnostic lumbar puncture, to the study of cerebrospinal fluid for mycobacterium tuberculosis, direct bacterioscopy using the flotation method or using crops and infection of the guinea pig.

Treatment. Isoniazid and rifampicin are recommended for the first 2 months of treatment with additional streptomycin or ethambutol. Subsequently, treatment with isoniazid and rifampicin is continued for another 10 months.

56. Treatment of tuberculosis

Anti-tuberculosis drugs. Isoniazid is the drug of choice in the treatment of all forms of tuberculosis, prescribed for all therapeutic regimens, if pathogens remain sensitive to it. Side effects of the drug are rare.

Rifampicin is a broad-spectrum antibiotic that is available for oral use and is prescribed in the most active phase of the tuberculous process once a day at a dose of 1-15 mg/kg. The side effect of the drug is expressed by orange staining of teeth, urine and saliva, symptoms of the gastrointestinal tract, toxic changes in the liver, especially in the first weeks of therapy.

Ethambutol has an effect only on mycobacteria. The drug is administered orally 1 time per day at a dose of 15-20 mg/kg. A side effect is expressed by reversible visual impairment - narrowing of the visual fields and a change in the perception of color. Ethambutol can serve as a substitute for isoniazid in combination with streptomycin in cases of isoniazid drug resistance.

Streptomycin is significantly less effective against Mycobacterium tuberculosis than isoniazid and rifampicin, but is superior in this regard to ethambutol. In severe forms of tuberculosis, streptomycin is administered intramuscularly once a day at a dose of 1 mg / kg along with isoniazid and rifampicin during the first few months of therapy. Most often, the side effect is manifested by a violation of the function of the VIII pair of cranial nerves, especially their vestibular department.

Pyrazinamide, administered simultaneously with isoniazid, has a bactericidal effect on Mycobacterium tuberculosis. The drug is administered orally, its daily dose (30-40 mg / kg) is divided into 2-3 doses. The disadvantages of the drug are the tendency to more rapid development of drug resistance.

Ethionamide has a pronounced effect on Mycobacterium tuberculosis, is prescribed in combination with other drugs in the treatment of relapses of the disease and the ineffectiveness of standard chemotherapy regimens. The drug is taken orally 1 time per day at a dose of 15 mg / kg.

Monotherapy. Isoniazid chemoprophylaxis is indicated for all apparently healthy individuals younger than 35 years of age with positive tuberculin tests, who have no changes on chest radiographs or have traces of past tuberculosis. To prevent reactivation of the infection with the development of a general disease, such persons are recommended treatment for 12 months. Prophylactic monotherapy with isoniazid can also be given to children at high risk of developing tuberculosis. Treatment in such cases is prescribed even for children with a tuberculin-negative reaction. The usual practice is to give isoniazid for 3 months and then repeat tuberculin tests. If a turn occurs, then treatment is continued for up to 12 months.

Treatment regimens with two and three drugs. Most cases of tuberculosis in children respond well to treatment with a dual combination of anti-tuberculosis drugs. The most commonly used isoniazid and rifampicin, less often - ethambutol.

Author: Pavlova N.V.

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