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Table of contents

1. Escherichiosis. Salmonella. Typhoid fever. Shigellosis (bacterial dysentery). Cholera
2. Diseases caused by Neisseria (Meningococcal infections. Gonococcal infection)
3. Pneumococcal infections
4. staph infection
5. Clostridial infections (Tetanus. Pelvic gangrene. Botulism. Infection caused by anaerobic microorganisms (not clostridia))
6. Diphtheria
7. Pertussis
8. Infections caused by pathogens of the Pseudomonas group (Pseudomonas infection. Diseases caused by other strains of Pseudomonas)
9. Brucellosis
10. yersiniosis (Plague. Diseases caused by Y. enterocolitica and Y. pseudotuberculosis)
11. Tularemia
12. Listeriosis
13. anthrax
14. Viral infections and infections of presumably viral etiology (Measles. Rubella. Herpes simplex. Chickenpox. Cytomegalovirus infection. Epstein-Barr viral infection (infectious mononucleosis))
15. Chlamydial infections (Chlamydia. Chlamydial conjunctivitis and pneumonia in children. Psittacosis (ornithosis). Inguinal lymphogranulomatosis)
16. Tuberculosis

Lecture number 1

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 an infectious-toxic and diarrheal syndrome, less often by damage to other organs or a generalization of the process up to sepsis.

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

They are classified into:

1) enteropathogenic (EPKP) (Escherichia coli). These are specific serotypes of E. coli pathogens that cause diarrhea in young children;

2) enterotoxigenic (ETCP) - produce a toxin that contributes to the development of diarrhea;

3) enteroinvasive (EIEC) E. coli, capable of destroying the intestinal epithelium, which causes diseases resembling dysentery;

4) lining.

Etiology. E. coli is a gram-negative, motile aerobic (facultatively anaerobic) rod, which has more than 150 groups of O antigens, 93 groups of K antigens and 52 groups of H antigens. Each of the groups of antigens can exist independently of the others.

Epidemiology. Enteropathogenic Escherichia coli serve as an ethnological factor in outbreaks of diarrhea epidemics in kindergartens and children's departments of hospitals. After they are administered to the subjects, the latter develop diarrhea, but serotypes of enteropathogenic bacilli can also be detected in individuals without signs of diarrhea, and its outbreaks in children's groups are not necessarily associated with the isolation of this microorganism.

Enterotoxigenic Escherichia coli that produce heat-labile enterotoxin cause disease only with massive infection, so outbreaks develop with significant contamination of food or water supplies.

Pathogenesis. The mechanism of development of diarrhea during infection with EPEC has not been sufficiently deciphered. Some strains that caused diarrhea when infecting volunteers with massive doses were not invasive and did not produce enterotoxin. Others produced an enterotoxin similar to the type 1 dysentery bacillus toxin.

ETCS can produce a thermostable, thermolabile toxin, or both simultaneously, the production of which is genetically controlled by transferred plasmids. Thermolabile enterotoxin is close to cholera toxin. It binds to gangliosides of epithelial cells as their receptor and activates cellular adenylcyclase, resulting in an increase in the intracellular concentration of adenine monophosphate and an increase in the release of water and chlorides. Thermostable enterotoxin activates guanylate cyclase, which enhances the secretory activity of the gastrointestinal tract. The genetic information encoding the resistance of the pathogen to antibiotics is embedded in the same plasmid that carries information about the production of enterotoxin. Therefore, the widespread and uncontrolled use of antibiotics contributes to the spread of both drug-resistant and enterotoxin-producing forms of E. coli.

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. An admixture of mucus and blood appears in the feces, the number of leukocytes increases.

The fourth 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. According to the serological characteristics, these E. coli belong to the type of EPKD.

Clinical manifestations. Diarrhea caused by EPKD is characterized by watery bowel movements, the frequency of which can reach 10-20 times a day, and a slight increase in body temperature. Other general disorders may be absent. There is an admixture of mucus in the stool, but there is no blood. Spontaneous healing occurs after 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. An increase in body temperature and general weakness can be pronounced. The disease caused by heat-stable toxin infection is usually milder, with mild abdominal pain, nausea, and mild fever.

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. Patients complain of abdominal pain, myalgia, chills, headache.

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 caused by ECP can be suspected in the event of a sudden outbreak of an epidemic of diarrhea, especially in a group of children. A presumptive diagnosis can be made when the same serotype of Escherichia coli is detected in several sick children. Similar serotypes of E. coli can also be found in the nasopharynx, pharynx and stomach of patients. Serotyping of E. coli is not carried out under normal conditions; the need for such studies arises only during outbreaks of an epidemic in children's or other closed groups. Identification of ETS and EIKP requires special methods that are currently used only in some research laboratories. An accurate diagnosis of enterocolitis, associated with damage to the surface area of ​​intestinal epithelial cells, can only be made after an intestinal biopsy.

Treatment. The main elements of treatment in children are the correction and maintenance of water and electrolyte balance. Profuse diarrhea and vomiting, causing significant dehydration, are an indication for hospitalization of the child and intravenous administration of fluids.

Neomycin has been effective in treating diarrhea associated with EEC in young children. Relapses after discontinuation of treatment occur in 20% of children.

The results of antibiotic treatment for diarrhea caused by ETEC in children have not been studied.

Traveler's diarrhea (caused by ETEC in 60% of cases) responds well to treatment with trimethoprim-sulfamethoxazole or trimethoprim alone when given early. Against the background of this treatment, the stool quickly normalizes, abdominal pain, nausea and vomiting stop.

The treatment of diarrhea caused by EIRD is not well developed. Usually patients do not need hospitalization and recover after 1 week even without taking antibiotics, in rare cases, ampicillin is required.

Of great importance in the treatment of diarrhea caused by lining strains of Escherichia coli, may have oral administration of neomycin, as well as proper parenteral nutrition.

Prevention. Outbreaks of epidemic diarrhea caused by ECP in children's groups require all measures to prevent intestinal infections. It is necessary to introduce a group system in children's groups. Preventive therapy for traveler's diarrhea may be effective. However, it is usually not recommended due to the rapid development of pathogen resistance and the risk of adverse reactions to antibiotics.

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 heat-labile envelope antigens (Vi), which block the agglutination reactions of O-antigens and O-antibodies. There are more than 2200 serotypes of Salmonella. The currently used nomenclature distinguishes three groups of Salmonella: S. enteritidis, S. typhi and S. choleraesuis. Each Salmonella species is divided into bioserotypes, for example S. enteritidis bio-thyphimurium.

Salmonella are resistant to many physical factors, die at a temperature of 54,4 ° C after 1 hour, and at 60 ° C - after 15 minutes, remain viable in the environment at low temperatures for many days, live for weeks in stagnant water, dried food, pharmaceuticals and faeces.

The properties of Salmonella that determine their pathogenicity remain unclear. Endotoxin increases the resistance of the microorganism to phagocytosis, so strains deficient in this antigen are usually avirulent. The effect of endotoxin on the macroorganism is manifested in general disorders, although they do not play an important role in the development of gastroenteritis. Some types of Salmonella affect mainly humans, causing characteristic signs of the disease. Infection with S. typhosa is observed only in humans, Salmonella groups A and C are also mainly detected in humans, and S. alrortus equi - only in horses.

Epidemiology. Humans become infected by consuming contaminated food or water. The main carrier of salmonella is humans, often serving as a source of food contamination and poisoning. Breast milk can also spread salmonella. Thus, some strains of this pathogen were isolated from milk and feces of donors. In a patient during the acute period of infection, 1-100 salmonella are isolated from 109 g of feces.

Their excretion with feces continues for 2 weeks after the infection in 70-90% of patients, in 50% it lasts up to 4 weeks and in 10-25% - up to 10 weeks.

The duration of the period of bacteriocarrier is the same in symptomatic and asymptomatic forms, but in children under the age of 1 year it is longer than in older children. The terms of bacteriocarrier increase against the background of antibiotic treatment.

Pathogenesis and pathomorphology. The dose of the pathogen required to develop the disease in humans has not been precisely established. For both adults and children, it is determined by the body’s resistance and the virulence of the pathogen.

Salmonella indirectly stimulates the energy system of intestinal epithelial cells, resulting in increased secretion of water and electrolytes. Diarrhea-causing strains of Salmonella contribute to the appearance of neutrophilic cell infiltration in their own membrane. Prostaglandins released from inflammatory exudates can also stimulate the adenylate cyclase system, increasing fluid and electrolyte secretion.

For the development of enterocolitis, the presence of Salmonella in the depth of the intestinal mucosa is necessary. The contents of the stomach with a pH of 2,0 kill pathogens, while higher values ​​have a different effect on Salmonella. At pH 5,0 or more pathogens remain viable. The accelerated passage of food through the intestines, lysozyme and other enzymes are also able to resist salmonella infection.

Salmonella overcome the surface layers of the intestinal mucosa without damaging the epithelial cells. Around them, phagosomes are concentrated, which do not have a noticeable effect on microorganisms penetrating through cells or into the binding membrane. Serotypes that cause diarrhea cause leukocyte infiltration of the basement membrane. The infection does not spread further, and the patient has only diarrhea, sometimes the body temperature rises slightly. The frequency of bacteremia is unknown, but it is usually transient, metastatic foci of infection usually do not form in healthy children.

Systemic diseases caused by salmonella occur mainly in the elderly and in patients with severe disorders of cellular immunity and the function of the reticuloendothelial system. Salmonella septicemia and osteomyelitis often develop in children with sickle cell anemia. Granulomatous disease in children or other disorders of white blood cell function increase the susceptibility to infection. Chronic salmonella bacteremia and bacteriuria are observed in patients with schistosomiasis, also characterized by imperfect phagocytosis.

Clinical manifestations. Gastroenteritis is most often observed in late summer and early autumn, which coincides with an increase in the incidence of foodborne infections. Large epidemics occur at this time, but sporadic cases occur throughout the year.

The incubation period is 8-48 hours. Symptoms often appear in the morning after eating contaminated food the night before. 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 with an admixture of mucus and blood, leaves. Vomiting is usually profuse and short-lived. Body temperature rises to 38-39 ° C in 70% of patients, but chills are less common. Fatal outcomes are rare (about 1%), predominantly in high-risk individuals.

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. Sometimes the symptoms may resemble a picture of typhoid fever, but it is not so long and rarely leads to death. Salmonella can settle in any organ, causing pneumonia, abscesses, empyema, osteomyelitis, purulent arthritis, pyelonephritis, or meningitis.

Complications. Non-typhoidal salmonellosis usually occurs without complications or is limited to extraintestinal manifestations. In rare cases, children have reactive arthritis that develops 2 weeks after the onset of diarrhea, Reiter's disease (conjunctivitis, urethritis, polyarthritis).

Diagnosis is set 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. A preliminary result can be obtained using the method of direct fluorescence of antibodies; microscopic studies of urine, blood, feces, cerebrospinal fluid (CSF) and other affected organs; serological samples that help in the diagnosis of typhoid fever and other salmonellosis.

Differential diagnosis. Salmonella gastroenteritis must be differentiated from other viral and bacterial diseases accompanied by diarrhea, including those caused by rotaviruses, Escherichia coli, Yersinia and Campylobacter. Sometimes clinical findings and radiographic signs suggest ulcerative colitis, which should be excluded.

Treatment. Treatment should be aimed at correcting electrolyte abnormalities and maintaining adequate hydration. Treatment with antibiotics is indicated only in certain cases: when there is a risk of infection spreading (under 3 months of age, in an immunodeficiency state or in severe progressive disease).

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. The choice of antibiotic is determined by the sensitivity of the pathogen.

Forecast with salmonella gastroenteritis is usually favorable, with the exception of very young children and patients with severe comorbidity. With salmonella endocarditis and meningitis, it is unfavorable even with early and intensive therapy.

3. Typhoid fever

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 disease mainly affects people under the age of 20 years. The pathogen is transmitted through household contact, water, food, and flies.

Pathogenesis. Typhoid infection is always accompanied by clinical symptoms. Virulent pathogens of typhoid fever suppress oxidative processes in neutrophils at the final stages of phagocytosis, saving themselves from destruction. In the initial period of infection, monocytes, unable to destroy the pathogen, transport it to the mesenteric lymph nodes and other areas of the reticuloendothelial system in which it multiplies. Inflammatory changes occur in the lymph nodes, liver and spleen. Pathogens quickly penetrate the wall of the upper small intestine without causing pronounced inflammatory changes, and from there into the general bloodstream. Short-term septicemia causes infection of many organs of the reticuloendothelial system, in the cells of which microorganisms concentrate and multiply. Subsequently, local inflammatory changes develop in the lymph nodes, liver and spleen. From these organs, bacteria re-enter the bloodstream. Secondary bacteremia usually lasts longer and leads to damage to many organs. Damage to the gallbladder occurs hematogenously and through the bile duct system. Salmonella multiply massively in its walls, from where they enter the intestinal lumen.

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 during typhoid infection in young children are less pronounced than in adults or children of older age groups. The lymph nodes of the mesentery, liver and spleen are usually full of blood, and foci of necrosis are detected in them. Characteristic features include reticuloendothelial hyperplasia with proliferation of monocytes. Liver cells are swollen. There are signs of inflammation and necrotic changes in the intestinal mucosa and in the lymphatic formations of its walls. Usually, after the ulceration has formed, scars do not remain. Hemorrhages can be observed, sometimes inflammatory changes spread to the muscular and serous membranes, which leads to perforation of the intestinal wall. A mononuclear reaction also develops in the bone marrow, in which foci of necrosis are also visible. Inflammatory changes in the walls of the gallbladder are focal and unstable. The degree of their severity is proportional to the intensity of reproduction of typhoid fever pathogens. Bronchitis is observed in most patients with typhoid fever. Inflammatory processes can manifest as pneumonia, osteomyelitis, abscesses, purulent arthritis, pyelonephritis, endophthalmitis and meningitis. Typhoid bacteria can be found in all organs.

Clinical manifestations. In children, the disease manifests itself as mild gastroenteritis or severe septicemia. Vomiting, bloating and diarrhea are common. Body temperature may rise to 40,5 °C, convulsions may appear, as well as liver enlargement, jaundice, anorexia, and body weight decreases.

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, less often constipation. Nosebleeds and coughing may occur. 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. At this stage of the disease, an enlarged spleen and abdominal pain are determined. In the lungs, scattered dry and often moist rales are heard. 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. Symptoms resolve within 2-4 weeks if complications do not join. Malaise and lethargy may persist for another 1-2 months.

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, but is usually caused by superinfection with other microorganisms. Pyelonephritis, endocarditis and meningitis, as well as osteomyelitis and purulent arthritis, can occur in children suffering from hemoglobinopathies.

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, roseola rash, hepatosplenomegaly and characteristic changes in the peripheral blood, as well as based on the results obtained:

1) laboratory studies, including microscopic and bacteriological methods, based on the detection of the pathogen in the biomaterial and specific antibodies in the patient's blood;

2) serological diagnostics, which makes it possible to detect specific antibodies in the blood or antigens in the biosubstrate using the Vidal reaction and the indirect agglutination reaction;

3) express diagnostics of typhoid fever and bacteriocarrier, aimed at detecting the antigen in feces, urine and other substrates using the immunofluorescence method, the phage titer increase reaction, immunoradiometric analysis, which allow to quickly detect the presence of antigens in the test material.

Differential diagnosis. Typhoid fever in children often has to be differentiated from a typhoid-like form of salmonellosis, paratyphoid fever, infectious mononucleosis, lymphogranulomatosis, yersiniosis, malaria, and in the initial period - with influenza, enterovirus infection and acute intestinal infection (AEI) of another etiology.

Forecast. The prognosis for typhoid fever is determined by the age of the patient, his previous state of health and the nature of the developing complications. Death occurs mainly in the absence of treatment, as well as in the presence of concomitant diseases that reduce the patient’s body’s resistance, intestinal perforation and intestinal bleeding. The infection recurs in 10% of patients who did not receive antibiotics, and appears approximately 2 weeks after the end of treatment, develops acutely, resembles the picture of the primary disease, but is milder and ends faster.

Individuals who excrete typhoid bacilli within 3 months of infection continue to excrete them for at least 1 year, and often throughout their lives. In children, the risk of developing a bacteriocarrier is low, but it increases with age.

Treatment. Patients with typhoid fever are subject to mandatory hospitalization. It is important when treating children with typhoid fever to maintain adequate hydration and electrolyte balance. The development of shock as a result of intestinal perforation or severe hemorrhage is an indication for the administration of large quantities of fluid intravenously. The diet must be complete in calories, of high quality and appropriate for the child’s age. In the presence of diarrhea syndrome, it will be based on the same principles as with other intestinal infections.

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 (diphenhydramine, suprastin, etc.), vitamins C, group B, U, etc. are prescribed. To increase the nonspecific resistance of the body, metacil, immunoglobulin are prescribed intravenously, immunostimulating and immunocorrective drugs . In severe forms of the disease, post-syndromic, symptomatic and pathogenetic therapy is carried out.

Prevention. To prevent typhoid fever, the following are crucial:

1) compliance with sanitary and hygienic requirements;

2) early detection and isolation of patients with typhoid fever and bacteria excretors;

3) final and current disinfection in the focus of infection;

4) active immunization. It is carried out according to epidemiological indications and only in children over 7 years of age with the use of a single subcutaneous injection of a chemical adsorbed typhoid vaccine enriched with Vi-antigen, followed by revaccination no earlier than 6 months and no later than 1 year.

4. 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. Sometimes the disease proceeds like ordinary diarrhea.

Etiology. Shigella are short, non-motile gram-negative rods, the biochemical feature of which is the absence or very slow fermentation of lactose. Other biochemical features help distinguish Shigella from E. coli, which also does not ferment lactose and does not produce gas. The Shigella genus is divided into four groups (A, B, C and D) depending on their biochemical properties and antigenic composition. Group A includes 10 serotypes, of which Shigella disenteriae is the most important. Group B includes 6 serotypes, of which Shigella flexneri is the most common. Of the serotypes of group C, S. boydii is found, and group D includes only one pathogen, most often S. sonnei, which causes half of the cases of the disease.

Epidemiology. Shigella is distributed throughout the world. Most often children aged 1-4 years get sick. The maximum incidence rate is observed at the end of summer, but seasonality is not as pronounced as with salmonellosis.

Man serves as the main reservoir of infection. Infection occurs by direct infection with faeces of sick water or food. Ways of infection: contact-household, food, water. Flies are active carriers of the disease.

Pathogenesis. For the development of the disease, infection with a small number of Shigella (less than 200) is sufficient. Pathogens remain viable in the acidic environment of gastric contents for 4 hours. Infection develops only when the pathogen penetrates the intestinal epithelial cells. Reproduction of the pathogen can occur simultaneously in epithelial cells and the submucosal layer of the lamina propria. In this case, epithelial cells are destroyed, edema, local inflammation and hyperemia develop. The damage is superficial, and therefore intestinal perforation does not occur, and bacteremia is very rare. The symptoms of gastroenterocolitis usually resolve spontaneously after 4-7 days. S. disenteriae produce enterotoxin, but their role in the pathogenesis of the disease is not entirely clear. Toxigenic but minimally invasive forms of Shigella do not cause disease. At the same time, non-toxigenic but highly invasive strains cause severe dysentery. Virulent strains of S. flexneri and S. sonnei are distinguished by the presence of a plasmid that encodes the J antigen, which belongs to the side chain of Shigella O-polysaccharides.

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 Shigella reaches the large intestine. Initially, patients complain of increased body temperature and cramping abdominal pain. Body temperature can reach 40 °C, and the phenomena of general intoxication intensify. 48 hours after the onset of the disease, diarrhea appears, and bowel movements with blood and mucus occur up to 20 times a day. In subsequent days of illness, bloody diarrhea may persist against the background of normalized body temperature or absence of abdominal pain. When examining the child, there is slight abdominal pain on palpation without clear localization.

At high temperature and convulsions, shigellosis may be accompanied by symptoms of damage to the nervous system, resembling meningitis, encephalitis. Significant loss of fluid and electrolytes can lead to dehydration, acidosis, and electrolyte imbalance. Children may have tenesmus. In severe forms of dysentery, especially in debilitated, dystrophic children, rectal prolapse may develop.

If the eyes are contaminated with fingers or other objects, conjunctivitis develops. Bacteremia develops extremely rarely, so local foci of infection outside the intestine usually do not occur. General infection with the development of pneumonia, meningitis, osteomyelitis and arthritis may occur only in young children with significant malnutrition. In such cases, there is severe dehydration, sometimes leading to hemolytic-uremic syndrome and renal failure. Non-suppurative arthritis and Reiter's syndrome due to dysenteric infection are usually associated with the presence of the HLA B27 antigen. Mortality due to bacteremia due to shigellosis reaches 50%, this complication usually occurs with dehydration in non-temperature children with prolonged diarrhea and malnutrition.

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, which is of the greatest importance. It is carried out before the appointment of antibiotic therapy. To study the material, particles of excrement with pathological impurities, except for blood, are selected. Inoculation of the material is carried out on selective media. A negative result is given on the 3-51st day, and a positive result is given on the 5-7th day from the moment the material was delivered to the laboratory;

2) serological methods used in doubtful cases and with negative results of bacteriological examination of feces. They are carried out in two directions: determination of the titer of specific antibodies in the patient's blood serum and antigen in the feces. In the presence of typical clinical symptoms and the detection of a diagnostic titer of specific antibodies (1: 200 and above) or an increase in their titer in the dynamics of the disease, the clinical diagnosis of shigellosis infection is considered established even in the absence of seeding of shigella from the patient's feces;

3) express diagnostic methods based on the detection of Shigella antigen in feces using the direct method of luminescent antibodies or immunoadsorption method;

4) sigmoidoscopy method used to diagnose obliterated forms of the disease and to determine the cause of prolonged bacterial excretion of shigella;

5) coprological method used as an aid in the diagnosis of shigellosis in the presence of colitis. In patients with shigellosis, along with inflammatory changes, signs of a violation of the enzymatic and absorption functions of the intestine are determined;

6) examination of peripheral blood. With all shigellosis, moderate leukocytosis, neutrophilic and stab shift in the blood formula, accelerated ESR are noted.

Differential diagnosis. Bacterial dysentery must be differentiated from other forms of enterocolitis caused by enterotoxigenic Escherichia coli, Salmonella, Campylobacter, amoebic dysentery, viral infections, acute appendicitis, intussusception and mesenteric lymphadenitis.

Treatment. When treated with antibiotics, the duration of the disease and the timing of Shigella isolation are significantly reduced. The choice of antibiotic depends on the drug sensitivity of pathogens that persist in members of a given community. Antibiotics usually clear the gastrointestinal tract of shigella. Long-term bacterial carriage develops very rarely. In such cases, lactulose, a lactose derivative, causes a temporary effect. In acute forms of dysentery, lactulosis is ineffective. Drugs that reduce peristalsis are contraindicated for bacterial dysentery. The need for fluid and electrolyte administration is determined by the patient's hydration status.

Prognosis and prevention. In most previously healthy children, shigellosis progresses favorably and is prone to spontaneous recovery. Pathogens continue to be released for about 3 months after the acute illness. High levels of morbidity and mortality from bacillary dysentery are observed in closed communities in developing countries, where children often suffer from dystrophy.

Strict observance of the rules of personal hygiene and the implementation of sanitary measures are the basis for the prevention of shigellosis. Thorough and systematic handwashing should be the law for all caregivers of patients with bacillary dysentery. In hospitals, it is necessary to strictly comply with all requirements for the isolation of patients. An effective and affordable vaccine has not been created.

5. Cholera

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 rod with a single, polarly located flagellum. There are about 70 serotypes of the pathogen, but true cholera is caused only by serotype 01. Vibrio grows well on various nutrient media. The pathogen of serotype 01 forms opaque, yellow colonies on them. Two different biotypes of V. cholerae 01 have been identified: classic and El Tor. Each of the biotypes, in turn, is divided into two main serotypes: Ogawa and Inaba. Serotype reversion can occur during epidemics.

Epidemiology. Endemic outbreaks and epidemics of cholera are characterized by a pronounced seasonal nature. The source of infection in cholera is only a sick person or a vibrio carrier. Individuals with asymptomatic or mild forms of cholera play an important role in the spread of infection. Long-term carriage of the bacteria, when the reservoir of the pathogen is the gallbladder of adults who have suffered cholera caused by El Tor, does not occur in children. Animals do not play a role in the spread of infection. The mechanism of transmission of infection is through the external environment - the water route of infection is of greater importance, and to a lesser extent - food and household contact.

Pathomorphology and pathophysiology. The entrance gate of infection is the gastrointestinal tract; the main place of reproduction 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 cell membrane receptors. The active subunit of the toxin enters the cell and activates the enzyme adenylate cyclase. This promotes 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.

There may be a so-called toxic factor that plays a role in the pathogenesis of the disease. The disease occurs even in the absence of the gene responsible for the production of the toxin.

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. The excretion of bicarbonates continues even against the background of developed acidosis. Despite some disturbance in the activity of disaccharides, including lactose, glucose absorption does not change.

Clinical manifestations. The incubation period lasts from 6 hours to 5 days, for vaccinated people - 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 abundant, pass freely, and look like rice water and acquire an unusual smell. In less severe cases, the stool has a yellowish tint. Paroxysmal pain in the navel area is observed in 50% of patients, there is no tenesmus. Vomiting is characteristic only of severe forms of infection and usually develops after the onset of diarrhea. The temperature in the rectum in 25% of children rises to 38-39 °C already on the first day of the disease. Severe weakness and adynamia are 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.

Mild forms of cholera are much more common. They usually present as normal diarrhea with little or no dehydration and are more common in children than in adults.

Diagnosis. Cholera is diagnosed based on 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.

Differential diagnosis. Cholera in children is differentiated from Escherichiosis infection, salmonellosis, rotavirus infection, as well as poisoning with mushrooms and chemical poisons.

Complications. In children, complications after cholera are more common and more severe than in adults. With adequate treatment, acute renal failure does not develop. Insufficient replacement of potassium losses can lead to hypokalemia, nephropathy, cardiac arrhythmia, and paralytic ileus. Excessively 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, seizures, or prolonged lethargy. The increased mortality rate of fetuses in the third trimester of pregnancy is explained by severe dehydration and late initiation of appropriate treatment.

Treatment. The main condition for successful treatment is rapid replacement of excreted water and electrolytes. Antibiotics play a supporting role. It is advisable to weigh the patient before hospitalization and then measure the amount of bowel movements. It is necessary to measure the daily amount of urine. The results of systematic studies, hematocrit, serum electrolytes, especially bicarbonates, complement clinical data and help plan transfusion therapy.

At the initial examination of a patient with cholera, it is urgent to assess the degree of dehydration. By the time clinical signs of dehydration develop, the child has lost a significant amount of fluid and electrolytes. The main danger lies in underestimating the magnitude of these losses.

Patients admitted in a state of severe dehydration and hypovolemic shock should immediately begin intravenous fluid administration. The amount of fluid administered and the rate of administration must be specified and varied depending on the changing state of hydration of the patient and ongoing diarrhea. Careful observation of the patient is necessary for the timely detection of signs of hyperhydration. 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 the administration of fluids by mouth, but when it occurs, the fluid should be administered in smaller amounts and more often. 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. In the first hours of treatment, the number of bowel movements may be minimal, but after removing the patient from the state of shock, their volume increases again, reaching 200-350 ml/kg per day. In older children, up to 800 ml of fluid can be excreted through the intestines every hour. Supportive hydration therapy can be carried out by enteral administration of electrolyte and glucose solutions. The exception is children with the most severe disease and malabsorption of glucose, who continue to receive rehydration saline solutions and continue to be monitored continuously until their diarrhea stops. If signs of dehydration reappear and it is impossible to achieve an adequate recovery of the lost amount of fluid, intravenous fluid should be started. Infants should be breastfed as often as possible, older children should be fed with milk diluted with an equal amount of water.

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. Children aged 4-6 months or older who have not previously received semi-solid foods can be started at this time.

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 feces by 50-70%, as well as reduce the period of bacterial isolation. Tetracycline and other etiotropic drugs are prescribed according to age dosages for a 5-day course. Parenteral administration of antibiotics is optional. The appointment of corticosteroids and opium preparations, as well as astringent antidiarrheal drugs, is contraindicated. Blood and plasma transfusions are not required.

Forecast. The outcome of cholera in children is more favorable than in adults, whose mortality rate is less than 1%.

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 sanitization of the pathogen; localization and elimination of the source of infection with a system of quarantine measures, including isolation and examination of persons in contact with the patient, provisional hospitalization of all those suffering from diarrheal diseases in the source of infection.

The cholera vaccine used, containing a suspension of V. cholerae 01 strains of Ogawa and Inaba killed by heat and phenol, is ineffective, since it creates a slight immunity that lasts a short time. A more effective vaccine used in endemic areas provides resistance to infection in 50-80% of those vaccinated for more than 6 months. 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.

Lecture number 2. Diseases caused by Neisseria

1. Meningococcal infections

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 located intra- and extracellularly. It is whimsical to cultivation conditions, sensitive to various environmental factors. Meningococcal infection affects only humans.

The disease develops when these microorganisms enter the bloodstream and spread throughout all organs. Several serological groups of meningococci have been identified. Types A, B, C, D, X, Y, Z, 29E, WI35 differ in specific capsular polysaccharides. The cell wall of meningococci contains lipopolysaccharide, which is responsible for the endotoxin-like action in meningococcemia.

Epidemiology. Meningococcal meningitis is a disease of childhood, more than half of cases occur in children in 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. Susceptibility to meningococcus is low. The contagious index is 10-15%. Meningococcal infection is characterized by periodic increases in incidence - every 8-30 years, high incidence persists for 2-4 years.

Pathogenesis. In the pathogenesis of the disease, the leading role is played by the pathogen, its endotoxin and the allergenic substance. The entry points for infection are the mucous membranes of the nasopharynx and oropharynx. In some individuals, meningococci penetrate the mucous membrane, are captured by white blood cells and spread 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 prolonged bacterial carriage.

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 of serotypes A, B and C. Bactericidal antibodies that cross-react with meningococci can also be formed during infection with other gram-negative and gram-positive bacteria and in many individuals prevent the development of meningococcemia. Children can receive maternal antibodies through the placenta, they are detected in them during the first 3 months of life, after which they are no longer detected until the 8th month of life. In the future, the level of specific antibodies gradually increases.

Pathomorphology. The disease caused by meningococci is accompanied by an acute inflammatory reaction. Endotoxemia can lead to diffuse vasculitis and disseminated intravascular blood coagulation. Small-caliber vessels are filled with clots containing large amounts 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 (Waterhouse-Friderickson syndrome).

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.

Clinical manifestations. The most common manifestation of meningococcal infection is acute respiratory diseases of the upper respiratory tract with bacteremia, reminiscent of common colds. Patients' condition may improve within a few days even without special treatment, but meningococci can sometimes be detected in blood cultures, indicating transient bacteremia. Some patients develop maculopapular rashes on the skin.

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. Sometimes hypotension, oliguria and renal failure, comatose hypotension, disseminated intravascular state, coagulation develop.

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

At the same time, hemorrhages in the adrenal glands, pronounced hematogenous dissemination take place. Treatment of such patients often does not work. 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. Purulent arthritis, which is very characteristic of chronic meningococcemia, can complicate any form of meningococcal infection accompanied by meningococcemia. Acute serous polyarthritis is also observed in some patients with meningococcal bacteremia, which usually occurs on the 5th day of the disease, even against the background of correct and sufficiently intensive treatment. Erythema nodosum often develops. Chronic meningococcemia causes the development of subacute meningococcal endocarditis.

Primary meningococcal pneumonia has been described. Specific endophthalmitis is extremely rare. Their symptoms usually appear 1-3 days after the onset of septicemia or meningitis. Patients complain of photophobia and pain in the eyes. On examination, they show injection of the ciliary body, exudate in the anterior chamber, edema and clouding of the iris.

Vulvovaginitis is rarely associated with meningococcal infection. Its clinical manifestations are the same as for any other vaginal infection: white discharge, irritation and excoriation of the vulva. Infection with meningococci is often accompanied by reactivation of a latent viral infection and is manifested by the so-called catarrhal rashes.

Diagnosis. Meningococcal infection is characterized by an acute onset, high body temperature, headache, vomiting, hyperesthesia, symptoms of meningeal irritation, and hemorrhagic stellate rash. In children of the first year of life, the diagnosis is established on the basis of severe symptoms of intoxication, anxiety, hyperesthesia, tremor of the hands, chin, convulsions, tension and bulging of the large fontanelle, hanging symptom, characteristic posture, etc.

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), enzyme immunoassay and radioimmune research methods.

Differential diagnosis. Meningococcal infection, which occurs as meningococcemia, is differentiated from infectious diseases accompanied by rash, hemorrhagic vasculitis, sepsis, thrombocytopenic conditions with toxic influenza and ARVI, occurring with meningeal and encephalitic phenomena; with other infectious diseases accompanied by meningeal symptoms (typhoid fever, shigellosis, salmonellosis).

Complications. Meningococcal meningitis is often complicated by loss or decrease in vision and hearing, cranial nerve paresis (mainly III, IV, VI and VII pairs), themi and quadriplegia, convulsions, obstructive hydrocephalus and, in rare cases, brain abscesses. Endophthalmitis, observed with meningococcemia, most often accompanies meningococcal meningitis. Panophthalmitis and purulent iridochoroiditis may develop.

Meningococcemia is often complicated by adrenal hemorrhages, encephalitis, arthritis, myo- and pericarditis, pneumonia, lung abscesses, peritonitis, and disseminated intravascular coagulation. In patients with hypotension and purpura, the ability of the adrenal glands to adequately activate further ACTH stimulation is significantly reduced.

Treatment. Penicillin G is prescribed for intravenous administration. If there are any doubts about the etiology of the disease, use ampicillin; if you are allergic to penicillin, use cefuroxime, cefotaxime and ceftriaxone, which give a good effect in the treatment of meningococcal meningitis and other localizations of this infection. Treatment of meningococcemia continues for at least 7 days and at least 72 hours after normalization of body temperature. Pneumonia, pericarditis and other complications are indications for longer treatment. A patient with meningococcal meningitis should be treated for at least 10 days and for at least 5 days after body temperature normalizes.

In acute meningococcal infection, careful and constant monitoring of the patient is necessary. Monitoring of blood pressure at intervals of 30-60 minutes should be continued until the effect of the prescribed treatment appears. 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.

Forecast. The mortality rate from acute meningococcemia may exceed 15-20%. Meningococcal meningitis with adequate treatment is fatal in less than 3% of cases. Survival within 48 hours after initiation of treatment provides hope for a favorable outcome.

2. Gonococcal infection

Gonorrhea is an acute infectious sexually transmitted disease caused by Neisseria gonorrhoeae, which can occur in children of any age due to the possibility of infection through non-sexual contact.

Etiology. The causative agent of gonorrhea - N. gonorrhoeae - is an aerobic gram-negative diplococcus that is difficult to cultivate on artificial nutrient media. Gonococci are divided into four types depending on the colonies they form. Electron microscopy revealed villi in representatives of types I and II, the most virulent for humans. Autotyping of gonococci made it possible to identify about 20 different types, differing in their growth patterns on 11 nutrient media of different chemical compositions. Serological studies identified 16 gonococci with various antigens located in the outer shell of the pathogens. Gonococci infect organs covered with columnar epithelium. Stratified squamous epithelium is affected in children and elderly women.

Epidemiology. Newborns become infected with gonorrhea during childbirth and through contact with contaminated objects. Young children become ill as a result of household contact with parents or service personnel. Teenagers 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 caused by the released endotoxin; they consist of a whitish-yellow discharge consisting of serum, leukocytes and exfoliated epithelium, which often clogs the ducts of the periureteric 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 a 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 enter 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 can determine its antiphagocytic properties. Gonococci have a capsule. The numerous types of pathogens, differing in the composition of the capsule, explain the frequency of relapses of the disease. The thickness of the vaginal walls and the pH of its contents significantly influence the development of gonococci. A common infection most often develops after inoculation of the pathogen in the throat 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.

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

There is no innate or acquired immunity in gonorrhea. Superinfection is observed when a new infection occurs with untreated gonorrhea.

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. Pharyngeal localization of infection may be the result of self-infection with secretions from the genitals or oral-genital contacts.

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.

Girls are more likely to become infected with gonorrhea at the age of 2-8 years from a sick mother, but sexual contact is not excluded. 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. The internal genital organs are rarely involved in the process.

Complications. Complications of gonorrhea include manifestations of the spread of infection from the site of introduction of the pathogen. In this case, acute, subacute or chronic salpingitis, pio- and hydrosalpinx, tubo-ovarian abscesses with subsequent sterility develop.

Gonococci can enter the abdominal cavity and accumulate under the liver capsule, causing perihepatitis, characterized by pain in the right hypochondrium and signs of acute or subacute salpingitis. Gonococcal arthritis is accompanied by destruction of articular cartilage and the development of ankylosis.

Gonococcal ophthalmitis is accompanied by ulceration of the cornea, its clouding, which leads to blindness. Enucleation is often necessary.

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

Treatment 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.

Forecast. With timely, complete treatment, the prognosis is quite good.

Prevention. Prevention of gonorrhea consists of observing hygiene standards and carrying out preventive bactericidal measures immediately after suspicious contact. Specific immunization is currently not possible.

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

Lecture number 3. Pneumococcal infections

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 in the form of individual cocci or chains. Due to differences in the composition of the capsular polysaccharide, more than 80 different serotypes of the microorganism are distinguished. Only smooth capsular strains of pneumococci are pathogenic for humans. Somatic antigens of pneumococcus have been isolated, antibodies to which determine 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 of the rabbit.

On solid nutrient media, pneumococci form non-pigmented, with impressions in the center of the colony, surrounded by a zone of incomplete hemolysis. The pneumococcal capsule can be seen when the microorganisms are treated with a type-specific antiserum mixed with the appropriate capsular polysaccharide.

In this case, the pneumococcus capsule acquires the ability to refract light rays.

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

In epidemiological terms, clones of pneumococci with greater virulence, which are formed in weakened children, matter.

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

Susceptibility has not been precisely established. Pneumococcal disease is usually sporadic, and its frequency and severity is greatest in patients with sickle cell anemia, asplenia, splenosis, humoral (B-lymphocyte) immunity deficiency, or complement deficiency.

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 proliferation of pneumococcus. Pneumococcal diseases often develop after a viral infection of the respiratory tract, which affects the ciliated epithelium and reduces its activity, and also suppresses the activity of alveolar macrophages. Airway secretions may 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.

Deficiency of the terminal complement component (C3-C9) is associated with a tendency to recurrent purulent infections, among which pneumococci also play a role. An increased tendency to pneumococcal infections in patients with a removed spleen or its congenital absence is associated with insufficient opsonization of pneumococci, the lack of a filtering function of the spleen during bacteremia. Pneumococcal infection is especially common in patients with sickle cell anemia and other forms of hemoglobinopathy due to the fact that patients lack the ability to activate C3 in other ways and fix this opsonin to the pneumococcal cell wall.

The efficiency of phagocytosis decreases with a deficiency of T- and B-cell immunity due to the insufficiency of opsonin anticapsular antibodies and the inability to cause lysis and agglutination of bacteria. Pneumococcal disease develops in individuals with transient and pre-existing factor B suppression.

The spread of infection in the tissues of patients is enhanced by the action of the antiphagocytic substance of the soluble pneumococcal capsular antigen. An important role is played by the factor contributing to the development of edema. Subsequently, the number of macrophages in the exudate increases, and the phagocytosis of pneumococci increases. Pneumonia resolution processes are completed in 7-10 days. The introduction of effective antibiotics and type-specific serum can accelerate the healing process.

Clinical manifestations. The clinical symptoms of pneumococcal infection depend on the location of the main pathological process. Most often it involves the upper and deep parts 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 agents of otitis media in children over 1 month of age. The spread of infection can occur through contact, leading to the development of empyema, pericarditis, mastoiditis, epidural abscess and, in rare cases, meningitis. Bacteremia can cause meningitis, purulent arthritis, osteomyelitis, endocarditis and brain abscess. The development of pneumococcal epiglottitis has been described in children with impaired immunity. Subcutaneous abscesses rarely form in pneumococcal bacteremia. Kidney diseases such as glomerulonephritis and cortical arteriolar thrombosis are often associated with pneumococcal bacteremia. Localized gingivitis, gangrenous areas of the face or extremities, and disseminated intravascular coagulation of the blood may also represent pneumococcal bacteremia.

Diagnosis. An accurate diagnosis of pneumococcal infection can be established based on the isolation of pneumococci from the site of inflammation or blood. At the same time, microorganisms found in the nasopharynx of patients with pneumonia, otitis media, septicemia or meningitis may not be the cause of the disease.

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 the diagnosis of 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, and previous antibiotic therapy does not significantly affect their results.

Differential diagnosis pneumococcal infections are carried out with staphylococcal, meningococcal, streptococcal, hemophilic and other bacterial infections. In many ways, it depends on the results of bacteriological and serological studies.

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 advisable in all cases to determine the drug sensitivity of isolated pneumococci using the dilution method to correct treatment tactics. In case of resistance to penicillin, but sensitivity to chloramphenicol, treatment is carried out last. The inability to foresee or predict the drug resistance of the pathogen in advance creates the need to carry out in all cases an appropriate bacteriological study of all strains of pneumococci isolated from the blood and CSF. Erythromycin, cephalosporin, clindamycin and chloramphenicol, sulfadiazine and sulfazoxazole can be successfully used to treat patients intolerant to penicillin.

Forecast. The outcome of the disease depends on the age of the patient, the state of his defenses, the virulence of the pathogen, the localization of the infection, and the adequacy of therapy.

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

Lecture number 4. Staphylococcal infection

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:

a) alpha-toxin with antigenic and immunogenic properties;

b) beta-toxin, causing a violation of the permeability of the vascular wall;

c) gamma and delta toxins causing lysis of erythrocytes and other human blood cells.

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.

Staphylococcus aureus strains produce a yellow pigment.

A constant criterion for the pathogenicity of staphylococci is plasma coagulation, which persists in the process of changing the resistance of staphylococcus.

S. aureus have lysozyme activity;

2) S. epidermidis - epidermal staphylococcus, strains of which can cause various pathological processes in a weakened body, especially in newborns and premature babies. Epidermal staphylococcus 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.

Patients in the acute period of the disease are most dangerous, since they secrete the most pathogenic strains of staphylococcus that are resistant to widely used antibiotics.

The infection is spread by contact, food and airborne droplets.

Staphylococcal infection often occurs sporadically, but group, family diseases, epidemic outbreaks in maternity hospitals, etc. are possible.

The endogenous route of infection (autoinfection) is also allowed.

Pathogenesis. Factors contributing to the occurrence of staphylococcal infection:

1) the presence of entry gates of infection (skin, mucous membranes of the oropharynx and respiratory tract, gastrointestinal tract, conjunctiva of the eyelids and umbilical wound);

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) a toxic component due to the entry of staphylococcal toxin and biologically active substances from a local focus into the blood;

2) an allergic component, which is a consequence of the circulation of damaged microbial cells in the body and changes in the sensitivity of the macroorganism to a foreign protein;

3) staphylococcal invasion due to a sharp decrease in immunological reactivity and an increase in the permeability of the vascular wall as a result of the development of toxicosis and allergies.

In the development of endogenous infection, the state of the child's immunological reactivity, the previous treatment with antibacterial drugs, plays a role.

In the pathogenesis of the development of food poisoning, the value of the infectious dose, the amount of produced enterotoxin is important.

Pathomorphology. Suppuration is the main distinguishing sign of staphylococcal infection. Local proliferation of staphylococci in the tissue leads to the formation of an abscess. The production of hyaluronidase contributes to the further spread of infection. In areas where the pathogen multiplies, a large number of granulocytes appear, thrombosis of blood vessels and the formation of fibrin clots are observed. In the center of the formed area, necrosis occurs, filling with dead leukocytes, fibroblasts are located along the periphery.

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

Clinical manifestations. There are localized and generalized forms of staphylococcal infection.

More often, the infection occurs in a mild localized form with a slightly pronounced local inflammatory reaction and in the absence of a generalized process. Less often, the infection takes on a severe character, is expressed by typical symptoms of intoxication, deep local changes, and is accompanied by bacteremia.

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). A similar clinical symptomatology is observed with secondary infection with staphylococci of wounds and, above all, of the burn surface.

Respiratory diseases. Staphylococci are very often found in the upper respiratory tract, but the corresponding diseases develop relatively rarely. Sinusitis and inflammation of the middle ear caused by Staphylococcus aureus may occur. Purulent parotitis is a rare disease, but if it develops, then the causative agent is usually Staphylococcus aureus. Staphylococcal tonsillitis and pharyngitis are rare - in children with reduced resistance to infection. Staphylococcus aureus can cause tracheitis, which in its clinical symptoms resembles a picture of viral croup. Patients present with marked fever, leukocytosis, and signs of severe upper airway obstruction. Laryngoscopy or bronchoscopy does not reveal changes in the epiglottis, but the subpharyngeal space is sharply narrowed, there is a thick purulent secret in the trachea.

Staphylococcal pneumonias can be primary or secondary if they develop after a viral infection. In children under the age of 1 year, it begins with the appearance of wheezing on exhalation, resembling a picture of bronchiolitis. Most often, body temperature rises sharply, abdominal pain, tachypnea, dyspnea and signs of local or diffuse bronchopneumonia or lobar pneumonia appear. Staphylococci cause necrotizing pneumonitis, often with empyema, pneumatocele, pyopneumothorax, and bronchopleural fistulas. Sometimes staphylococcal pneumonia is accompanied by diffuse interstitial changes, characterized by severe shortness of breath and cyanosis. The cough may be dry. Oxygen therapy only slightly increases the level of oxygenation of the blood.

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. In some cases, disseminated forms of staphylococcal infections develop, accompanied by fever, bone and joint pain, petechial, urticarial, maculopapular, or pustular rashes. Rarely, hematuria, jaundice, convulsions, neck stiffness, and heart murmurs are observed. There may be leukocytosis or leukopenia, proteinuria, in the urine sediment - erythrocytes and leukocytes.

Diseases of muscle tissue. The development of localized abscesses in the muscles, not accompanied by septicemia, is called tropical purulent myositis. Prodromal symptoms include pharyngitis, runny nose, diarrhea, and trauma prior to abscess development. The main components of treatment are the opening of abscesses and the introduction of antibiotics.

Heart diseases. Acute bacterial endocarditis often follows staphylococcal bacteremia and is not always accompanied by changes in the heart valves. Often there is perforation of the heart valves, abscesses develop in the myocardium, acute hemorrhagic and purulent pericarditis, and sudden death syndrome.

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. Staphylococcal meningitis may be due to trauma or infection of the meningomyelocele. Infection after surgical interventions is most often associated with infection with epidermal staphylococci. Staphylococcus aureus can cause brain abscess in 25% of patients.

It also commonly causes epidural abscesses. The staphylococcal nature of CNS disease should be assumed primarily in patients in whom some primary focus serves as the cause of staphylococcal bacteremia.

Disease of the bones and joints. Staphylococcus aureus most often serves as an etiological factor in osteomyelitis and purulent arthritis in children. The disease develops with hematogenous spread of infection.

Diseases of the kidneys. Staphylococci cause the development of abscesses in the kidneys and perirenal tissue. Staphylococcal urinary tract infection is rare.

Diseases of the gastrointestinal tract. Staphylococcal enterocolitis is caused by overgrowth of staphylococci to the detriment of the normal intestinal flora and occurs during enteral treatment with broad-spectrum antibiotics.

This develops diarrhea with blood and mucus in the stool.

Food poisoning can be caused by ingesting large amounts of enterotoxin with staph-contaminated food. 2-7 hours after ingestion of such food, debilitating vomiting suddenly develops, copious watery stools appear, but the body temperature remains within the normal range or slightly increases.

Usually after 12-24 hours these symptoms disappear. In some cases, shock develops and death occurs.

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. In the presence of infectious and inflammatory diseases in the mother, infection of the fetus can occur transplacental. During childbirth - with premature discharge of amniotic fluid and placenta previa. Distinguish localized (vesiculopustulosis, pemphigus of newborns, Ritter's exfoliative dermatitis, pseudofurunculosis, etc.) and generalized forms of infection.

Localized forms of infection can be mild or severe.

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. The primary focus can be catarrhal or purulent omphalitis, pseudotuberculosis, vesiculopustulosis, etc.

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.

The child's condition is disturbed, regurgitation, sluggish sucking, a flat weight curve appear, making it difficult to differentiate from sepsis.

But the disappearance of symptoms of intoxication within 3-7 days against the background of ongoing antibiotic therapy, a decrease in body temperature to normal numbers, rapid sanitation of the local purulent focus, and the absence of damage to other internal organs exclude sepsis.

A feature of staphylococcal sepsis in premature newborns is the presence of mainly septicopyemic forms, less often - septicemia. It can be accompanied by the presence of osteomyelitis of the upper jaw and bones of the extremities, phlegmon, purulent meningitis, staphylococcal pneumonia, secondary enterocolitis, etc. Intoxication is expressed by the lethargy of the child, refusal of the breast, regurgitation, dyspeptic disorders. The skin is pale with a grayish tint, less often icteric, characterized by an enlarged liver, the development of septic hepatitis.

Sepsis can also occur at normal temperatures, changes in the peripheral blood are less pronounced than in children of the older age group. The presence of leukopenia, anemia, thrombocytopenia, toxic granularity of neutrophils and others in the peripheral blood is an unfavorable prognosis.

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 using Gram staining, reactions to coagulase and mannitol. Antibiotic sensitivity and phage typing can be performed if necessary.

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.

Forecast. Untreated staphylococcal septicemia is fatal in 80% of cases or more. The mortality rate with antibiotic treatment is reduced to 20%. An unfavorable prognostic sign is a small number of leukocytes in the blood (less than 5000) or a decrease in the number of neutrophils to 50% or less.

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.

Lecture number 5. Clostridial infections

1. Tetanus

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, motile, non-capsulated rod that forms terminal spores that give it a resemblance to a drumstick. The spores are very resistant to external influences, tolerate boiling, but are destroyed during autoclaving. In soil, protected from sunlight, spores can remain viable for many years. They are found in house dust, soil, salt and fresh water, and feces of many animal species. Both spores and vegetative forms of the pathogen can be found in the human intestine.

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. Several types of tetanus bacilli, different in their antigenic structure, produce tetanospasmin identical in immunological parameters. Neurotoxic and responsible for the clinical symptoms of the disease, the toxin is considered the most powerful organic poison after botulinum toxin. Its lethal dose for humans is 130 mcg.

Epidemiology. The disease tetanus occurs everywhere, but the incidence in different geographical zones is not the same and is associated with the characteristics and level of injuries, the state of active immunity of the population, the development of the healthcare system, etc. Tetanus is characterized by seasonality, with a peak in May-October.

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. Tetanus mainly affects children aged 3-7 years and newborns.

Tetanus is not transmitted from person to person.

Pathogenesis. The disease develops after tetanus spores that have entered damaged tissue 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 oxygen level in the tissues decreases. The site of persistent infection may be the gastrointestinal tract or tonsil crypts. Sometimes tetanus can develop after administration of contaminated serum, vaccine, or enter the body along with suture material.

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 can penetrate into the CNS by being absorbed in neuromuscular synapses and spreading through the perineural spaces along large nerve trunks, as well as with the help of lymphocytes.

Tetanospasmin acts on motor nerve endings at myoneural synapses, on the spinal cord and brain, and on the sympathetic nervous system. In neuromuscular synapses, the toxin inhibits the destruction of acetylcholine, causing disturbances in the processes of neuromuscular transmission. In the spinal cord, its action causes disturbances in the system of polysynaptic reflexes. In the central nervous system, tetanospasmin binds to gangliosides and affects motor and interneurons, removing inhibition of motor neurons and facilitating the spread of excitation processes through the spinal cord. Violation of inhibitory mechanisms in the spinal cord itself significantly weakens the inhibitory effect on the part 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, spasms of peripheral vessels, 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. The antitoxin does not affect the germination of C. tetani spores and the reproduction of vegetative forms of the pathogen in tissues.

Pathomorphology. C. tetani infection remains localized and causes minimal inflammatory changes in damaged tissues. Local pathological changes are secondary. Pneumonia that develops in patients is caused by other pathogens and is associated with difficulty expectorating sputum. Degeneration of striated muscles is often observed, including the diaphragmatic, intercostal, rectus abdominis muscles, etc. The essence of the changes is the disappearance of transverse striations, lysis and death of myofibrils. Hemorrhages into muscle fibers and their rupture are observed. Degenerative changes in the diaphragmatic and intercostal muscles can lead to ventilation failure, as well as myasthenia gravis, which can develop during convalescence. Spinal fractures can be the result of seizures.

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. In some cases, they precede the development of a generalized form of the disease. Local and easily flowing general tetanus is sometimes observed in children with chronic otitis media. The causative agent can be detected in the discharge from the middle ear. Lethal outcomes in a localized form of the disease occur in 1% of cases;

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. Initially, spasms are mild, lasting seconds and punctuated by periods of relaxation. Subsequently, the convulsions become stronger, longer and exhaust the patient. 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. Dysuria, or urinary retention, develops secondary to spasm of the bladder sphincter. There may be involuntary urination, defecation. Excessively strong convulsions often lead to compression fractures of the vertebral bodies and hemorrhages in the muscles. Sometimes there may be weakness of individual muscle groups and loss of sensation caused by peripheral neuropathy. Electrophysiological studies in the initial period reveal conduction disturbances along the nerve trunks. Full or partial recovery occurs in a few weeks or even months.

The body temperature in patients usually rises slightly, its increase to 40 ° C is due to increased energy expenditure during convulsions. Patients have profuse sweating, tachycardia, hypertension, arrhythmia.

During the first 3-7 days, the symptoms of the disease increase, over the next 2 weeks the patient's condition stabilizes, and only after that a gradual improvement is observed. Full recovery occurs after 2-6 weeks;

3) head tetanus. This is an unusual manifestation of the disease. The incubation period is 1-2 days. The disease is usually caused by otitis media, wounds of the head, face and foreign bodies in the nasal cavity. The most characteristic symptoms of the disease include dysfunction III, IV, VII, IX, X and XI pairs of cranial nerves. Most often, the seventh pair (facial nerve) is involved in the process. Following the craniocerebral, a generalized form of tetanus may also develop.

Neonatal tetanus usually begins in a child aged 3-10 days and proceeds according to the type of generalized form. At first, the act of sucking is disturbed in the child, anxiety and strong crying appear. Soon, swallowing disorders join, muscle rigidity appears, convulsions begin. Opisthotonus may be absent.

Complications. Adequate therapy and careful care reduce the frequency and severity of complications that develop with tetanus. Aspiration pneumonia, atelectasis, mediastinal emphysema, pneumothorax due to tetanus are caused by impaired pulmonary ventilation due to spasm of the respiratory muscles, laryngospasm and accumulation of secretions in the bronchi. Mediastinal emphysema and pneumothorax are most common after tracheostomy. Biting the tongue and mucous membrane of the cheek, vertebral fractures, intramuscular hematomas are the result of severe convulsions. With prolonged convulsions, dehydration of the body and general exhaustion occur.

Diagnosis and differential diagnosis. Diagnosis of tetanus is based on clinical data. The results of routine laboratory tests do not have much diagnostic value. Determination of tetanus bacilli in smears from wound discharge or their growth on nutrient media confirms the diagnosis of tetanus only if there are anamnestic and clinical data characteristic of tetanus. The mere detection of tetanus bacilli in a wound does not mean that a person has tetanus or that it will develop in the future.

Tetanus in newborns is differentiated with birth injuries and purulent meningitis, spasmophilia, paratonsillar abscess and other inflammatory diseases in the lower jaw, in which there may be a spasm of masticatory muscles, as well as with strychnine poisoning.

In older children, tetanus is differentiated from hysteria, rabies.

Treatment and nursing. The main goal of treatment for tetanus is to eliminate the source of tetanospasmin formation, neutralize the toxin circulating in the blood and carry out maintenance therapy until tetanospasmin fixed by the nervous tissue is destroyed. Maintenance therapy should be carried out quite intensively and carefully.

Human specific immunoglobunal (SIG) is administered as early as possible at a dose of 3000-6000 IU intramuscularly. Intravenous administration is contraindicated. There are no allergic reactions after the administration of SIG, and the level of antitoxin in the blood is higher than after the administration of immunoglobulins obtained from animals. Re-introduction of SIG is not required. 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 the 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. In the case of a reaction to a foreign protein, desensitization is carried out according to the usual scheme.

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. Wound surfaces are left open.

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. In case of intolerance to penicillin, tetracycline is prescribed.

Careful care includes providing a quiet and calm environment, not exposing the patient to any auditory and visual stimulus, adequate breathing, oxygen administration, suction of bronchial secretions and care of the tracheostomy tube.

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. Drugs with a neuromuscular blocking action help to reduce convulsions while maintaining spontaneous breathing or complete shutdown of muscle function when switching to artificial ventilation.

After the introduction of sedatives and muscle relaxants, patients should be on artificial ventilation and under constant monitoring. It is necessary to control the adequacy of ventilation, systematically suck out the secret from the bronchi and prevent deep depression of the respiratory center.

It is necessary to weigh patients daily, carefully monitor the amount of fluid taken and excreted, maintaining electrolyte and caloric balance. Enteral nutrition is possible only in some patients, in most cases it is necessary to resort to intravenous infusions and the introduction of food through a gastric tube. Sometimes a gastrostomy is necessary. Particular attention should be paid to skin care, oral cavity and to monitor the function of the bladder and intestines.

Of particular concern are mechanical ventilation, sedation, and maintaining adequate hydration in neonates. Their treatment should be carried out as actively as possible with the help of tracheal intubation, muscle relaxation and assisted ventilation. If it is impossible to carry out all these activities in full, they resort to enteral administration of sedatives and muscle relaxants. Children every 6 hours are given to drink syrup with chlorpromazine, an elixir with phenobarbital or mephenesine. Diazepam is administered intravenously, repeatedly depending on the severity of seizures. The additional appointment of pyridoxine has a beneficial effect, contributing to an increase in the production of gamma-aminobutyric acid, which is formed in the region of nerve endings, weakening their sensitivity and reducing spasms. Dissection of the umbilical cord is currently not recommended.

Forecast. The mortality rate from tetanus averages 45-55%, in newborns - 60% or more.

Outcome depends on many factors. In infants and the elderly, the disease usually ends in death; in adolescence and adolescence, recovery most often occurs. Among patients aged 10-19 years, death occurs in only 20% of cases. Adverse signs include widespread muscle damage, high body temperature, short intervals between the time of injury and the development of clinical signs of tetanus, or between the time of trismus and seizures. In severe cases, tetanus ends in death usually within the first week. Intensive and maintenance therapy largely determines the outcome of tetanus.

In surviving children after tetanus, paresis, paralysis of the central type, disturbances in mental development may remain. The causes of brain damage are prolonged states of apnea and anoxia during prolonged spasms.

Those who have recovered from tetanus do not have stable immunity, therefore, even those who have had it in the future must be actively immunized.

Prevention. Active immunization is the best method of preventing tetanus. It is preferable to immunize women before pregnancy, and to immunize unvaccinated women immediately after childbirth.

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 not necessary as SIG does not cause serum sickness. 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.

2. Pelvic 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 causative agents 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, in some cases forming spores both in body tissues and when grown on nutrient media, and are obligate anaerobes. Vegetative forms of bacteria are very susceptible to the action of physical and chemical factors. They secrete a variety of toxins, including lecithinase (a-toxin), collagenase, hyaluronidase, leukocidin, dioxyribonuclease, protease and lipase.

Epidemiology. The frequency of this infection in injuries or in the postoperative period does not exceed 0,1%. Spores of gas gangrene pathogens penetrate wounds from the soil, gastrointestinal tract and female genital organs, where they saprophyte under normal conditions.

Pathogenesis and pathomorphology. The development of gas gangrene is promoted 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. Lecithinase, produced in especially large quantities by C. perfringens, destroys cell membranes and changes capillary permeability. The toxin produced by C. histolyticum rapidly destroys tissues. In the circumference of the wound infected with clostridium, necrosis and vascular thrombosis soon develop. The reproduction of bacteria in tissues is accompanied by the release of gas (hydrogen and carbon dioxide), determined by palpation. At the same time, extensive edema and swelling of the affected tissues appear, severe septicemia and shock develop, usually leading to death.

Clinical manifestations. Clostridia infection syndrome involves the proliferation of pathogens in a wound with minor pain and the absence of general reactions. The surface of the wound is usually uneven, has an untidy appearance, and the serous-purulent discharge is dark brown and foul-smelling. 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. Intact muscles are usually not involved in the process. The general disturbances are expressed poorly. The wound surface looks contaminated, an unpleasant odor emanates from it, serous-purulent discharge, local crepitus is sometimes noted. Pain sensations are expressed slightly. Occasionally, there is swelling and discoloration of the surrounding areas of the skin.

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 general condition of the patient deteriorates sharply, the skin becomes pale, and the patient is covered with sweat. Hypotension, confusion, or agitation may occur. In later periods, jaundice appears. Discharge from the wound becomes serous-bloody, acquires a sweet smell. The amount of gas is minimal, or it is absent. A large number of pathogens are found in the wound, but polymorphonuclear leukocytes may be absent. The muscle tissue in the affected area is edematous and pale. As the infection progresses, the color of the muscles becomes brick red, they lose their ability to contract, and the bleeding from them stops.

Violation of the general condition and functions of other organs is associated with the action of toxins. Septicemia in gas gangrene is a rare and atypical complication. It is most often observed with anaerobic endometritis or with necrotic processes in the gastrointestinal tract. The presence of clostridia in the blood is not always clinically evident. Bacteremia may be accompanied by massive hemolysis of erythrocytes, acute necrosis of the tubules of the kidneys, which leads to the death of the patient.

In infections caused by toxigenic strains of Clostridium, the eyes, brain, lungs, pleura, and liver may be involved. Gas gangrene often develops after penetrating wounds of the chest, when they are contaminated with earth.

Diagnosis and differential 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.

Differential diagnosis of gas gangrene should be made with postoperative gangrene and necrotizing fasciitis.

Treatment. The most reliable method of treatment for gas gangrene is surgical treatment of wounds and removal of all infected tissue. Penicillin G administered intravenously is not a substitute for surgery. If you are intolerant to penicillin, chloramphenicol, erythromycin or cephalosporin are prescribed.

Useful hyperbaric oxygen therapy. The therapeutic effect of polyvalent antitoxin remains controversial.

Prevention. The main methods of preventing gas gangrene include early, correct and thorough treatment of wounds, eliminating the possibility of infection. Parenteral administration of penicillin G is recommended. Reliable methods of active immunization against gas gangrene are lacking. Active immunization against gas gangrene has no effect.

3. Botulism

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) disease of infants, caused by the entry of the pathogen into the intestine, its reproduction and the release of the toxin.

Etiology. C. botulinum is an anaerobic, motile, gram-positive rod 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 of age become ill; the peak of the disease occurs at the age of 2-6 months. The etiological factor may be pathogens of types A and B. The main reservoir and source of infection are warm-blooded herbivores, less often - fish, crustaceans, and 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-prepared canned food. In infants, foodborne botulism may be derived from infant formula. Humans and herbivores are most sensitive to botulinum toxin.

Pathogenesis. The entry point for infection is the gastrointestinal tract. Botulism in young children occurs when C. botulinum spores enter the child's intestines, germinate, multiply, and release a toxin. Spores are constantly present in the soil and in the environment, but in adults a similar genesis of the disease does not occur. Food botulism occurs when botulinum toxin is absorbed from the intestines and entered the body along with improperly prepared 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.

Clinical manifestations Botulism in young children can range from mild forms with only 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. Often there is a need for artificial ventilation of the lungs due to the development of respiratory failure. Often the disease is the cause of the syndrome of sudden death of a child.

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. Weakness, positional hypotension, urinary retention, and constipation may also develop. The patient is oriented in the environment, but at times his consciousness is clouded.

The body temperature and pulse of the patient remain within the normal range. 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, but otherwise does not differ from food botulism.

Diagnosis and differential diagnosis. Botulism is diagnosed based on epidemiological and characteristic classical manifestations. For laboratory confirmation, the detection of toxins and pathogens is used in biomaterials taken from the patient, as well as in food products using enzyme immunoassay methods and the latex agglutination reaction - specific and highly sensitive methods that, in addition to detecting toxins, allow identifying specific antitoxic and antibacterial antibodies in blood serum of patients.

Botulism in children should be differentiated from food toxic infections of staphylococcal, salmonella and other etiologies, mushroom poisoning, belladonna, atropine, as well as poliomyelitis, viral encephalitis, diphtheria, etc.

Treatment botulism in infants consists of continuous monitoring, basic life support and general intensive care, including respiratory support and nutrition. Recovery usually occurs within a few weeks. Antitoxin is usually not prescribed due to its harm to the body and the good results of properly administered maintenance therapy.

Antibiotics do not shorten the duration of the disease or relieve its symptoms. Aminoglycosides may exacerbate paralysis and exacerbate respiratory failure.

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.

Respiratory and circulatory function should be constantly monitored. Tracheostomy should be performed before severe respiratory failure develops.

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. Before its introduction, an intradermal test is performed for sensitivity to a foreign protein.

To suppress the pathogen, which can continue to produce the toxin, patients are administered an aqueous solution of penicillin G parenterally or enterally after gastric lavage.

Hypotension should be treated with adequate intravenous fluids to maintain adequate hydration and electrolyte balance.

Wound botulism. Wounds should be properly treated and drained. Maintenance therapy, administration of antibiotics and toxins are carried out in the same way as in the treatment of foodborne botulism, with the exception of measures to flush out the toxin from the gastrointestinal tract.

Forecast. Botulism in infants. In newborns, the disease, with proper care and treatment, in most cases ends in recovery.

food botulism. The severity of the disease is determined by the amount of toxin that has entered the body. A short incubation period also indicates the severity of intoxication. The prognosis is more favorable with early treatment. Recovery can be complete with proper supportive care.

Prevention. Boiling food for 10 minutes destroys botulinum toxin. Bacterial spores are killed when heated to 116 °C. The pressure must be varied during cooking.

4. Infection caused by anaerobic microorganisms (not clostridia)

Etiology. Anaerobic bacteria are widespread 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 the degree of 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 an anaerobic infection in children, pathogens can be found 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 frequency of anaerobic infection in children is low. Of all cases of confirmed bacteremia, anaerobic infection is only 5,8%. The main clinical landmarks that allow one to think about the possibility of anaerobic infection in children 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 low virulent for humans. But conditions accompanied by a decrease in the level of oxygen in tissues and a weakening of redox processes create the preconditions for the proliferation 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 surgery, 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 occur and extensive tissue destruction occurs. The localization of lesions determines the characteristics of morphological changes.

Clinical manifestations. A disease caused by anaerobic microorganisms can develop in any organ.

Localization of infection in the upper respiratory tract is not uncommon. Periodontitis usually develops. Periapical abscesses and osteomyelitis of the maxilla or mandible may develop.

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. At first, pneumonia usually develops, and then, due to the melting of the lung tissue, an abscess develops. The sputum has a heavy, putrid odor.

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. The development of these lesions contributes to the inflammatory process in adjacent organs or hematogenous spread of infection from distant foci, such as the lungs or heart. A brain abscess is manifested by headaches, impaired consciousness, stupor, convulsions, focal loss of function of the motor and sensory nerves, and impaired speech. Body temperature remains within normal limits or slightly increases. Swelling of the optic nerve nipple in children is rare. Purulent meningitis is rarely caused by anaerobic microorganisms. Their detection in the CSF in a patient with symptoms of meningitis confirms the diagnosis of a brain abscess or subdural empyema.

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

According to clinical manifestations, anaerobic bacteremia does not differ from aerobic. Fever, leukocytosis, jaundice, hemolytic anemia, and shock may develop. Anaerobic bacteremia often develops against the background of a disease of the gastrointestinal tract or organs of the genitourinary system.

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. Anaerobic microorganisms can be detected by puncturing the middle ear through the tympanic membrane, as well as by examining discharge from the ear with otitis media, chronic or serous.

Diagnosis. Diagnosis of anaerobic infection depends on:

1) the doctor's alertness regarding the possibility of the corresponding infection;

2) correct selection and obtaining of material for bacteriological examination;

3) the use of media and methods to isolate anaerobic microorganisms.

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 the deep layers of wounds, trachea and organ biopsy obtained under aseptic conditions.

Guidelines for bacteriological examination, suggesting an anaerobic infection, include the absence of growth when sowing purulent material on nutrient media; negative culture results in the determination of gram-positive rods in Gram-stained smears; colony growth on thioglycolatol medium or on media containing 100 µg/ml kanamycin, neomycin, or paromomycin; the formation of gas and a putrefactive odor emanating from grown crops; characteristic appearance of colonies incubated under anaerobic conditions.

Rapid diagnosis of a bacteroid infection is possible using an indirect immunofluorescence method using a specific antiserum against B. fragilis capsular polysaccharide and a combined antiserum against different serotypes of these bacteria. It is also possible to quickly establish the diagnosis of anaerobic infection with gas-liquid chromatography of pathological material.

Treatment. Typically, the type of causative agent of an anaerobic infection can be predicted based on the clinical manifestations of the pathological process and its localization. The sensitivity of bacteria is also predictable. In this regard, clinicians have the opportunity to prescribe treatment without waiting for the results of a bacteriological study.

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. A pronounced effect was noted in the treatment of patients with metronidazole - it is effective even with brain abscess in children.

Treatment with penicillin alone is usually sufficient for anaerobic respiratory infections. With a different localization of the infection and suspicion of anaerobic bacteremia, combined treatment with penicillin and chloramphenicol is recommended. Clindamycin is considered a substitute for levomycetin in all forms of anaerobic infection, except for brain abscess, since it does not penetrate the blood-brain barrier.

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.

The doses of all antibiotics used to treat anaerobic infections do not differ from those usually recommended for diseases caused by aerobic pathogens. The duration of treatment varies depending on the specific features of each disease.

Forecast. The age of the patient, the form of the process and the timeliness of diagnosis and initiation of appropriate treatment are of great importance for the prognosis of anaerobic infection. The frequency of deaths in newborns ranges from 4 to 37,5% and depends on the unequal patient population, different approaches to diagnosing infection and the nature of the material sent for bacteriological examination.

Lecture number 6. Diphtheria

Diphtheria is an acute infection caused by Corynebacterium 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 Loeffler's bacillus - is an unevenly stained gram-positive, non-spore-bearing, non-motile pleomorphic bacterium. Flask-shaped swellings at its ends, which are not a true morphological characteristic, reflect the results of cultivation on an inadequate nutrient medium (Leffler). Diphtheria bacilli grow best on special nutrient media containing inhibitors that can inhibit and slow down the growth of other microorganisms.

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. Treatment of diphtheria strains with bacteriophages carrying toxigenicity genes increases the number of toxin-producing pathogens. However, phage multiplication is not a necessary condition for toxin production, which is determined by genetic factors and culture conditions. Apparently, the toxin is formed by those cells in which spontaneous induction of prophages into phages occurs.

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. Diphtheria is a disease common throughout the world, characterized by seasonality: the peak incidence occurs in the autumn and winter months. Infection occurs through contact with a patient or bacteria 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 pathogen strains 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, promoting the enzymatic cleavage of nicotinamide adenine dinucleotide with the subsequent formation of inactive adenosine diphosphoribose transferase. In this case, the synthesis of cellular proteins stops due to disruption of the transfer of amino acids from RNA to elongating polypeptides.

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.

For diphtheria, toxic necrosis and hyaline degeneration of organs and tissues are most characteristic.

Clinical manifestations. The symptoms of diphtheria are 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 based on initial location of infection:

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 color, and then mucopurulent. Excoriations appear on the upper lip and nasal passages, and an unpleasant odor may appear. White films are visible on the nasal septum. Slow absorption of the toxin and weak severity of general disorders cause belated diagnosis;

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. With partial immunity, films may not form. At the beginning of the disease, the film is thin, gray in color, spreading from the tonsils to the soft and hard palate, resembling a thick cobweb. This feature distinguishes diphtheria from other forms of membranous tonsillitis. Subsequently, the films thicken, spread to the walls of the pharynx or larynx and trachea.

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. Edema tissues are soft and painless, warm to the touch. These signs are observed in children over the age of 6 years.

The course of diphtheria of the pharynx depends on the prevalence of films and the amount of toxin produced. In severe cases, respiratory failure and circulatory collapse may develop. The pulse rate increases disproportionately to body temperature, which rises slightly or remains within the normal range. Often there is paralysis of the soft palate. Stupor, coma and death can occur within 7-10 days. In less severe cases, the child recovers gradually, often developing myocarditis or neuritis. In mild cases of the disease, recovery occurs in 7-10 days, shortly after peeling off the films;

3) diphtheria of the larynx develops with the spread of films from the tonsils and from the nasopharynx. Isolated diphtheria of the larynx is rare and often occurs with mild symptoms of intoxication. Clinical symptoms resemble the picture of a common infectious croup: noisy labored breathing, increasing stridor, wheezing and dry cough. Suprasternal, subclavian and intercostal retractions during inspiration indicate severe laryngeal obstruction, which, if left untreated, can be fatal. Sudden and often fatal laryngeal obstruction can occur in mild diphtheria when partially detached membranes obstruct the airways.

Severe cases of diphtheria are accompanied by the spread of films to the entire tracheobronchial tree. Signs of toxemia are mild in children with isolated laryngeal diphtheria. In more severe forms of combined damage to the larynx and nasopharynx, pronounced toxemia and airway obstruction are noted;

4) skin diphtheria is characterized by ulcers with clear edges and a bottom covered with a diphtheria film. This form of the disease is more common in countries with a hot climate and represents a significant epidemic danger;

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

6) diphtheria of the ears is characterized by external otitis media with long-term persistent and foul-smelling purulent discharge.

Cases of vulvovaginal diphtheria have also been described. In addition, diphtheria infection can simultaneously be localized in several places.

Diagnosis. Diphtheria is diagnosed:

1) based on clinical data;

2) when confirming the isolation of the pathogen;

3) using the method of fluorescent antibodies.

Microscopic examination of diphtheria films is considered irrational.

Differential diagnosis. Mild forms of nasal diphtheria must be differentiated from foreign bodies in the nose, sinusitis, adenoiditis and congenital syphilis; diphtheria of the tonsils and pharynx - with streptococcal pharyngitis, usually accompanied by more severe pain when swallowing, high body temperature and very easily detachable films covering only the tonsils. In some patients, diphtheria of the throat and streptococcal pharyngitis coexist; diphtheria of the tonsils and pharynx - with infectious mononucleosis, non-bacterial membranous tonsillitis, primary herpetic tonsillitis, some blood diseases (agranulocytosis and leukemia), post-tonsillectomy changes, toxoplasmosis, tularemia, salmonellosis and cytomegalovirus infection, Vincent's angina; diphtheria of the larynx - with croup of a different etiology, acute epiglottitis, laryngotracheobronchitis, aspiration of foreign bodies, peripharyngeal and retropharyngeal abscesses, laryngeal papillomas, hemangiomas and lymphangiomas.

Complications. Sudden death due to occlusion of the lumen of the larynx or trachea by exfoliated diphtheria film; narrowing of the airways due to significant swelling of the neck tissue; myocarditis after severe and even mild forms of diphtheria, but more often with widespread lesions and delayed diagnosis; neurological complications (soft palate palsy, oculomotor nerve palsy, phrenic nerve neuritis and diaphragm palsy, limb paralysis); damage to vasomotor centers; gastritis, hepatitis and nephritis.

Treatment. The basis of treatment is neutralization of free diphtheria toxin and destruction of the pathogen using antibiotics. The only specific treatment 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. It is administered once in order to avoid sensitization by horse serum upon its repeated administration, having previously tested for sensitivity to foreign proteins. 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. The same dose of antitoxin is administered for multiple sites of infection, massive edema, and disease duration of more than 000 hours.

Antibiotics (erythromycin and penicillin, amoxicillin, rifampicin, clindamycin) are prescribed to stop further production of the toxin by the diphtheria bacillus, and are canceled after receiving negative culture results for diphtheria bacilli three times.

supportive therapy. In order to prevent the development of myocarditis in diphtheria, strict bed rest is prescribed for 2-3 weeks; electrocardiography - 2-3 times a week for 4-6 weeks for the timely diagnosis of incipient myocarditis. Strict bed rest is absolutely necessary in the development of myocarditis. In the presence of symptoms of heart failure, except for cases of diphtheria arrhythmia, patients with myocarditis are prescribed digitalis preparations, in severe cases - prednisolone for 2 weeks at a daily dose of 1-1,5 mg / kg.

It is necessary to maintain the body's hydration at an optimal level, aspirate discharge from the nasopharynx, carefully monitor the swallowing reflex and voice changes, and perform a tracheostomy to ensure airway patency.

Food should be liquid and high-calorie. In case of paralysis of the soft palate or pharyngeal muscles, the child should be fed through a gastric tube to prevent aspiration.

Vaccination should be carried out in people who have had diphtheria, since half of them do not develop strong immunity and relapses of the disease are possible.

Prevention diphtheria includes:

1) immunization with the use of diphtheria toxoid - diphtheria toxin, devoid of toxic properties, adsorbed on aluminum hydroxide (AD-toxoid). Recently, AD-toxoid has been included as a component in the complex vaccines DTP, ADS, ADS-M, etc. Primary vaccination is carried out starting from the age of 3 months with the DPT vaccine three times with an interval of 45 days. The first revaccination - 12-18 months after the third vaccination, the second - after 6-7 years with ADS-toxin, the third - at 16 years and then after 10 years with ADS-toxin;

2) isolation of patients, suppression of the spread of infection and monitoring of contacts. Patients are considered contagious as long as they have pathogens at the site of infection. Isolation is terminated after three negative cultures are obtained.

Forecast and outcomes depend on the severity of primary intoxication and the timing of the start of treatment. A favorable outcome is more likely in localized forms of oropharyngeal and nasal diphtheria. In toxic forms, the frequency and severity of complications depend on the severity of the form and the timing of the started treatment with antidiphtheria serum. Death can occur in case of severe myocarditis or paralysis of the respiratory muscles.

Children with a hypertoxic form of oropharyngeal diphtheria die in the first 2-3 days of illness with symptoms of severe intoxication.

Transferred diphtheria leaves immunity, which persists in 50% of patients for at least 1 year. Relapses are rare, but diphtheria survivors should also be vaccinated.

Lecture number 7. 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. It is characterized by a cyclic protracted course and the presence of a kind of convulsive paroxysmal cough.

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

B. pertussis is a short immobile gram-negative rod, has a capsule, is a strict aerobe, is extremely demanding in terms of nutrient media (it grows on Borde-Gangu medium with the addition of penicillin to suppress the growth of associated flora). Whooping cough bacteria that have just grown on a nutrient medium have antigenic features that allow them to be classified as a type designated as phase I. Phase I strains cause disease and are necessary for the development of a vaccine.

B. parapertussis is morphologically indistinguishable from B. pertussis, it is also demanding on nutrient media, but can be differentiated using special agglutination tests.

Epidemiology. Whooping cough is the most contagious disease, occurring in 97-100% of susceptible individuals. The risk of the disease is highest in children under 5 years of age. A feature of whooping cough is the high susceptibility of children to it from the first days of life, due to the fact that transplacentally transferred antibodies from the mother do not protect the child from this disease. The incidence of whooping cough does not depend on the time of year. Girls get sick more often than boys. The causative agents of whooping cough are extremely rarely isolated from healthy individuals; transmission of infection occurs only through direct contact with a patient.

Pathomorphology. The respiratory tract is the site of primary localization of the pathological process, where mild inflammation such as serous catarrh occurs. The greatest lesions are observed in the larynx and vocal folds: proliferation of epithelial cells with thickening of the epithelial layer, vacuolar degeneration, desquamation of individual cells, swelling of the submucosa. The manifestation of functional disorders is caused by emphysema - a repeated spastic condition of the respiratory tract, as well as atelectasis, a spastic condition of the bronchi. Inflammatory changes are observed in peribronchial, perivascular and interstitial tissues. Inflammatory changes in the lungs are detected against the background of severe disorders of blood and lymph circulation.

Pathological changes can also develop in the brain and liver and consist of hemorrhages, visible both to the naked eye and under a microscope. There may be cases of atrophic changes in the cerebral cortex, probably associated with hypoxia. Pertussis encephalopathy is often accompanied by fatty degeneration of the liver.

Pathogenesis. Pertussis infection occurs through inhalation of phase I bacteria.

In the body of a person infected with whooping cough, agglutinins, hemagglutinin-inhibiting, bactericidal, complement-fixing 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.

In the discharge from the upper respiratory tract in persons immune to pertussis, contains IgA and IgG, which have antipertussis activity. Secretory IgA prevents bacteria from sticking to cells, and serum IgG mediates long-term immunity to whooping cough. The protective effect is also associated with the presence of antitoxic antibodies in the blood serum, which prevent the fixation of the toxin on cell receptors and neutralize toxins. Thus, local and general factors of humoral immunity play an important role in immunity to whooping cough.

The factor that stimulates lymphocytosis also plays an important role in the pathogenesis of the disease, contributing to the mobilization of lymphocytes from the lymphatic organs, B- and T-lymphocytes are also affected. The role of cellular immunity factors in pertussis infection in humans is not well understood.

Clinical manifestations. The incubation period for whooping cough is 6-20 days, more often 7 days. In general, the disease lasts for 6-8 weeks. Clinical manifestations depend on the virulence of the pathogen, the age of the child and his immune status. Diseases caused by B. parapertussis or B. bronchosepta are milder and shorter lasting.

There are three stages of the disease:

1) catarrhal stage. It lasts 1-2 weeks, the characteristic signs are rhinorrhea, injection of conjunctival vessels, lacrimation, weak cough, a slight increase in body temperature, less often abundant viscous mucous discharge from the nose, sometimes leading to blockage of the upper respiratory tract. Whooping cough is usually not diagnosed at this stage;

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, accompanied by a whistling sound due to the forced passage of air through the narrowed glottis. At the same time, the child's face turns red or becomes bluish, the eyes roll out, the tongue hangs down, tears and salivation appear, the veins in the neck swell. Severe bouts of coughing may follow each other until a lump of viscous mucus is discharged, which violates the airway. Vomiting is typical at this stage. The combination of coughing fits with vomiting is a characteristic sign of whooping cough, even if there is no sharp wheezing after coughing. Coughing attacks exhaust the child, frighten him, often he loses weight. Cough-provoking factors can include chewing, swallowing, sneezing, exercise, and in some cases even food and drink offerings. In the intervals between attacks, children feel quite satisfactory and do not give the impression of being seriously ill. Reprises are not observed in all patients with whooping cough;

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. In some patients, coughing fits recur for several years, resuming with subsequent infections of the upper respiratory tract.

On physical examination, changes are usually not detected. In the paroxysmal stage, petechiae may appear on the head, face, conjunctiva and neck of the child. In some patients, scattered dry rales are heard.

Diagnosis and differential diagnosis. Whooping cough is easily diagnosed during the paroxysmal stage of the disease. Indications in the anamnesis of contact with patients help in diagnosis.

An increase in the number of leukocytes in the blood and the absolute number of lymphocytes is not pathognomonic for whooping cough, since similar changes in young children can occur with other infections. Roentgen infiltrates, atelectasis, and emphysema may be seen on chest x-ray.

An accurate diagnosis is made when:

1) bacteriological examination of the material taken from the nasopharynx for sowing with a swab and inoculated directly at the patient's bedside on the Borde-Gangu medium;

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

3) obtaining positive results of serological diagnostics, which can be carried out by determining immunoglobulins M-, A- and G-antibodies to the whooping cough pathogen in serum using an enzyme-like immunosorbent test, etc.;

4) bronchological X-ray examination.

Differential diagnosis is possible by isolating the appropriate pathogen.

With adenovirus infection, an increase in the titer of specific antibodies helps to establish the diagnosis.

Complications. One of the most common and most serious types of complications is pneumonia - the leading cause of death in 90% of children under 3 years of age. The causative agent of pneumonia can be B. pertussis, but most often it is associated with the addition of a secondary infection.

Atelectasis develops secondary due to blockage of the bronchial lumen with mucus. Excessive effort during coughing fits can lead to rupture of the alveoli and the development of interstitial or subcutaneous emphysema. Frequent complications are bronchiectasis, which persists in the future, otitis media caused by pneumococci. Whooping cough provokes the reactivation of a latent tuberculosis infection.

Convulsions and coma are observed, which are manifestations of brain hypoxia due to developed asphyxia. In rare cases, subarachnoid and intraventricular hemorrhages occur. Persistent vomiting leads to the development of alkalosis, may contribute to the occurrence of seizures. Other complications may include tongue ulcers, epistaxis, melena, subconjunctival hemorrhages, spinal cord epidural hematomas, diaphragmatic ruptures, umbilical and inguinal hernias, rectal prolapse, dehydration, and malnutrition.

Treatment. Antibiotics do not shorten the duration of the paroxysmal stage of whooping cough; when administered for 3-4 days, they can eliminate all whooping cough pathogens growing in the nasopharynx of patients, thus preventing the development of whooping cough. Immune pertussis globulin is used to treat children under 2 years of age.

Maintenance therapy - the creation of adequate hydration, nutrition and elimination of factors that provoke coughing attacks, oxygen therapy and suction of a viscous secret from the upper respiratory tract in a patient, especially in children with pneumonia and severe respiratory disorders.

Prevention. Immunity to whooping cough is not transmitted transplacentally. Active immunity is created using the pertussis vaccine, which is effective in 70-90% of cases. It is part of the complex preparation of DTP vaccine and is administered to all children aged 3 months to 3 years with a course of three intramuscular injections of the drug with an interval of 1,5 months.

Forecast. The mortality rate does not exceed 10 per 1000 cases, but in children under 5 months of age it can reach 40% or more. Death is more often associated with pneumonia or other pulmonary complications. The risk of developing chronic diseases, primarily bronchiectasis, is difficult to account for.

Lecture No. 8. Infections caused by pathogens of the Pseudomonas group

1. Pseudomonas infection

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 protective mechanisms, for example, with cystic fibrosis, immunodeficiency states, malignant neoplasms, other chronic diseases, burns, dystrophy, and also after treatment with immunosuppressive drugs.

Etiology. Among the many well-identified strains of Pseudomonas, only a few are pathogenic to humans. The most common is P. aeruginosa. Others are incidental pathogens: P. cepatica, P. roaltophilia, P. putrefacies. P. mallet causes glanders in horses. All species of the Pseudomonas group are strict aerobes, capable of utilizing various carbon sources and reproducing in a humid environment containing minimal amounts of organic matter.

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. The strains of the pathogen differ in epidemiological significance, serological, phage characteristics, and the ability to produce pyocin.

Epidemiology. Pseudomonas is often found in medical institutions on the skin, clothing and shoes of patients and staff. It can grow in any moist environment, is often isolated even from distilled water, and is present in hospital laundries and kitchens, antiseptic solutions and on equipment used for inhalation and respiratory therapy. In some healthy individuals, Pseudomonas is found in the intestines.

Pathogenesis. For its development, Pseudomonas requires oxygen, the lack of which reduces the virulence of the microorganism. The endotoxin produced by it is significantly inferior in activity to the endotoxins of other gram-negative bacteria, but can cause diarrhea.

Pseudomonas aeruginosa releases large amounts of exotoxins, including lecithinase, collagenase, lipase, and hemolysins, causing necrotic lesions on the skin. One of the hemolytic factors is a heat-resistant glycolipid capable of destroying lecithin, which is part of the pulmonary surfactant. This leads to the development of atelectasis of the lung. The pathogenicity of Pseudomonas aeruginosa also depends on its ability to resist phagocytosis, which, in turn, depends on the production of protein toxins by it. The patient's body reacts to infection by the formation of antibodies to exotoxins (exotoxin A) and lipopolysaccharides of the macroorganism.

Clinical manifestations. In healthy people, Pseudomonas aeruginosa, which gets into small wounds, causes suppuration and local abscesses, which contain green or blue pus. Skin lesions that develop as a result of septicemia or direct inoculation of the pathogen into the skin initially appear as pink spots, which, as the infection progresses, turn into hemorrhagic nodules and undergo necrosis. In their place, scabs form, surrounded by a red rim (ecthyma gangrenosum). Bacteria multiply in affected areas.

Occasionally, healthy children may develop septicemia, meningitis, mastoiditis, folliculitis, pneumonia, and a urinary tract infection. Rarely, Pseudomonas causes gastroenteritis.

Otitis externa caused by P. aeruginosa develops in swimmers who repeatedly use polluted water bodies. Dermatitis and outbreaks of urinary tract infections are possible when using shared baths and showers. Skin lesions appear several hours (up to 2 days) after contact with these water sources, manifesting as erythema, macules, papules, and pustules. Skin lesions may be limited or widespread. Some children have fever, conjunctivitis, rhinitis, and sore throat at the same time.

Other members of the Pseudomonas family rarely cause disease in healthy children. Cases of pneumonia and abscesses in children caused by P. cepacia, otitis media - with P. stutzeri infection, suppuration and septicemia caused by P. maltophila are described.

Shunts, catheters. 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. Pseudomonas can cause abscessing or meningitis in children with dermoid fistulas and malformations of the meningeal membranes, particularly meningomanoceles. These bacteria can cause acute or subacute endocarditis in children with congenital heart disease, both before and after surgery.

Burns and wound infection. Pseuomonas and other gram-negative bacteria are often found on wound and burn surfaces, but their presence does not always lead to the development of an infectious process. Septicemia may be due to the multiplication of the pathogen in necrotic tissues or prolonged use of intravenous or urinary catheters.

Antibiotics that can suppress the microflora sensitive to them do not prevent the reproduction of some strains of Pseudomonas aeruginosa.

cystic fibrosis. Pseudomonas aeruginosa is excreted in sputum in most children with cystic fibrosis, but does not prove an infectious lesion with its characteristic destructive process in the lungs, but may reflect changes in the composition of the microflora due to previous treatment with broad-spectrum antibiotics. Antibiotics sometimes contribute to the elimination of this microflora, sometimes it disappears spontaneously.

Pseudomonas aeruginosa infection in patients with cystic fibrosis is most often limited to the lungs; septicemia develops very rarely.

Malignant neoplasms. Children with leukemia and especially those treated with immunosuppressive drugs are most susceptible to Pseudomonas aeruginosa infection. The leukopenia that develops against the background of such treatment contributes to the activation of the pathogen, usually saprophytic in the gastrointestinal tract, its penetration into the general bloodstream and the development of septicemia. Clinical manifestations of the disease are anorexia, fatigue, nausea, vomiting, fever and diarrhea. Generalized vasculitis develops.

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 in nature, abscesses often develop in the perirectal tissue. Sometimes there may be a picture of ileus and a sharp decrease in blood pressure.

Diagnosis and differential diagnosis. The diagnosis of Pseudomonas infection depends on culture of the pathogen from blood, urine, CSF, or pus obtained from abscesses or areas of inflammation. Specific pneumonia is diagnosed based on the results of a puncture biopsy of the lung or data from a bacteriological examination of sputum.

Bluish nodular skin lesions and ulcerations with an ecchymotic and gangrenous center and a bright halo are pathognomonic of this infection. In rare cases, a similar picture of skin changes is observed with septicemia caused by Aeromonas hydrophila.

Prevention. Of primary importance is the fight against nosocomial infection, timely identification and elimination of its sources, careful adherence to aseptic requirements in the preparation of solutions for parenteral administration, in the disinfection of catheters and the daily replacement of all devices used for prolonged intravenous infusions. Burn patients should be actively immunized with a Pseudomonas polyvaccine to reduce the incidence of septicemia and mortality. The administration of hyperimmune specific globulin prevents the development of septicemia. Timely diagnosis and surgical interventions for dermoid anomalies communicating with the spinal canal can prevent the development of infection with Pseudomonas aeruginosa.

Treatment. In case of infection caused by Pseudomonas aeruginosa, it is necessary to immediately begin treatment with antibiotics to which the pathogen is sensitive in vitro. Antibiotic therapy should be especially intensive and prolonged in patients with impaired immunological reactivity. Many of the new beta-lactam antibiotics have varying degrees of activity against Pseudomonas. Patients with meningitis caused by Pseudomonas aeruginosa infection are treated with intravenous antibacterial drugs. Sometimes it is additionally recommended to administer gentamicin into the ventricles of the brain or under the dura mater.

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

Forecast. The outcome largely depends on the nature of the underlying disease. The immediate cause of death in children with leukemia is sepsis, in half of all cases caused by Pseudomonas. These pathogens are isolated from the lung tissue of most children with cystic fibrosis and in many cases can be the main cause of death. The prognosis for patients who have had specific meningitis is unfavorable.

2. Diseases caused by other strains of Pseudomonas

Sap is a severe infectious disease of horses caused by P. mallet, sometimes transmitted to humans. The disease is most common in Asia, Africa, and the Middle East, but is extremely rare in the United States. Manifestations of infection are acute or chronic pneumonitis, hemorrhagic necrosis of the skin, mucous membranes of the nose and lymph nodes.

Melioidosis is a very rare disease found in Southeast Asia. The causative agent is P. pseudomallei, which lives in the soil and water of tropical countries. Infection occurs by inhalation of dust or contamination of wounds and scratches.

Pulmonary infection in melioidosis can be subacute and mimic tuberculosis. In some cases, septicemia develops, multiple abscesses form in all organs.

Often there is the development of myocarditis, endocarditis, pericarditis, intestinal abscesses, cholecystitis, acute gastroenteritis, septic arthritis, osteomyelitis, paraspinal abscesses, urinary tract infections and generalized lymphadenopathy. Melioidosis may be accompanied by symptoms of encephalitis, high body temperature and convulsions. Antibiotic therapy is usually effective.

The disease can be latent for a long time and manifest clinical symptoms only with a decrease in the resistance of the macroorganism years after the initial infection. Patients with both glanders and melioidosis are treated with tetracycline or chloramphenicol in combination with sulfonamides for several months. Aminoglycosides and penicillins are ineffective. You can prescribe trimethoprim with sulfamethoxazole.

Lecture number 9. Brucellosis

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. There are six known species of Brucella that can cause disease in humans: B. abortus (source: cow), B. melitensis (source: goat), B. suis (source: pig), B. canis (source: dog), V. 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 disease with brucellosis is caused by direct contact with sick animals. People caring for livestock most often fall ill. Sources of infection can be raw milk of sick animals, butter, cream, cottage cheese, ice cream. The pathogen can enter the eye, nasopharynx, and genitals, but intact healthy skin is impermeable to it. Brucella remains viable when infected products are stored in a refrigerator for 3 weeks and during the production (smoking) of ham. They die during pasteurization and boiling.

Brucellosis epidemics usually occur when eating unpasteurized milk, sour cream, butter, cheese, ice cream containing B. abortus.

Children rarely get brucellosis. When conducting mass serological studies, antibodies to B. canis were found in 67,8% of healthy individuals, antibodies to B. canis in 5,7% of newborns came through the placenta. A significant stratum of the population with antibodies to B. canis indicates the prevalence of this infection in humans. Despite the fact that brucellosis pathogens are excreted in the urine of patients, human-to-human transmission has not been reported. Cases of congenital disease are also unknown.

Pathogenesis and pathomorphology. Brucella is an intracellular parasite. After penetration into the human body, they are phagocytosed by leukocytes and macrophages, spreading into the reticuloendothelial tissue. Pathogens can multiply in different cells, including red blood cells.

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. Reproduction of the pathogen in the body is mandatory for the development of immunity. Specific IgM appear first, and then IgC antibodies, the titer of which gradually becomes dominant.

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. The most virulent smooth strains of Brucella continue to multiply in the cells of even individuals immune to brucellosis.

Smooth and intermediate strains of Brucella contain endotoxin, which plays a role in the course of the disease and the results of treatment.

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.

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. Chills, profuse sweating, nosebleeds, abdominal pain and cough appear. Often, body weight decreases significantly.

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.

The number of leukocytes in the peripheral blood may increase, decrease, or remain within the normal range. Relative lymphocytosis and anemia are often observed.

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 (Wright and Huddleson reactions - the main methods for diagnosing brucellosis, CSC, RPHA, antiglobulin test to detect incomplete antibodies (Coombs), etc.);

2) intradermal allergic test Burne, characterized by high sensitivity.

Differential diagnosis. In the acute period, brucellosis is differentiated from tularemia, typhoid, rickettsiosis, influenza, tuberculosis, histoplasmosis, coccidioidomycosis and infectious mononucleosis. Chronic forms of brucellosis are differentiated from lymphogranulomatosis and other neoplastic diseases.

Accounting for anamnestic information, the results of serological and radiographic studies, the isolation of the culture of the pathogen help to correctly establish the diagnosis. In some cases, a diagnostic tissue biopsy may be required.

Complications. The nature of complications of brucellosis is determined by the localization of infectious lesions. The most common complications include osteomyelitis, predominantly purulent spondylitis, accompanied by damage to the intervertebral disc and adjacent vertebrae.

Purulent arthritis often develops, but joint destruction is rare. Neurological complications of brucellosis may appear sooner or later and are expressed in acute or subacute meningitis or encephalitis. Cases of adhesive arachnoiditis have been described.

Myocarditis and endocarditis are among the most serious complications, often leading to death. In the initial period of treatment, signs of the Herxheimer reaction are often observed.

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.

Forecast. Without appropriate treatment, death occurs in 3% of cases.

Most untreated patients survive, but the recovery process is delayed by about six months. With antibiotic treatment, the prognosis is good. With late diagnosis, the treatment time is delayed.

Prevention. Prevention of brucellosis involves eliminating human contact with sources of the disease. Infection in domestic animals with which humans are 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.

Lecture number 10. Yersiniosis

Three types of microorganisms from the Yersinia group are capable of causing disease in humans: Y. pestis, Y. enterocolitica and Y. pseudotuberculosis.

1. Plague

Etiology. Yersinia pestis is a non-motile, polymorphic gram-negative bacterium that does not form spores. The pathogen can be detected in Giemsa-stained smears of pus and other pathological material and in affected tissues. It looks like a short stick with rounded, dense ends and a swollen central part (“safety pin”).

Epidemiology. Plague in domestic and wild animals can appear in two forms:

1) enzootics, reflecting a relatively stable cycle of infection circulation ("rodent - flea - rodent") among a population relatively resistant to this disease and being a long-term reservoir of infection, although they are hardly noticeable;

2) epizootics arising from infection of rodents highly sensitive to plague. In these cases, an epidemic with a high mortality rate develops in the rodent population.

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. In rare cases, the gates of infection are the pharynx and conjunctiva.

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 preventricle. When a flea bites a person, they regurgitate them, and the pathogens enter the lymphatic vessels of the skin, and then into the regional lymph nodes. The latter become denser and increase significantly, forming buboes. In severe forms of bubonic plague, the lymph nodes lose their barrier function, and the pathogens that multiply in them penetrate into the general bloodstream. Developed septicemia can lead to damage to any organ, including meningitis, secondary pneumonia, or cause widespread intravascular coagulation.

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. Drops containing a large number of pathogens are inhaled, the latter enter the lungs, multiply in them, causing pneumonia and septicemia, usually leading to death within the first day.

Once in the human body, Y. pestis undergoes phagocytosis, while the surviving microorganisms are resistant to it. Bacteria that have entered the body of a healthy person from a person who has had the plague are more virulent.

The reaction of tissues to the introduction of Y. pestis is manifested in their purulent melting. Necrotic foci are found in the lymph nodes, spleen, and liver. Hemorrhagic changes are manifested in many organs and tissues with disseminated intravascular coagulation.

Clinical manifestations. The incubation period for bubonic plague is 2-6 days, and for pneumonic plague - 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 without other pronounced signs of intoxication. In the absence or late treatment, septicemia develops, the patient's condition becomes more severe, signs of shock and hemorrhagic pneumonia appear.

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. Signs of lung involvement in the process may be mild, up to death, often occurring within the first day. The disease is manifested by nausea, vomiting, abdominal pain, bloody diarrhea, petechial rash or purpura. During epidemics, there are also milder forms of the disease, manifested by lymphadenopathy, vesicular and pustular rashes on the skin.

Signs of damage to other organs may be absent, recovery occurs spontaneously.

Diagnosis. The diagnosis of sporadic cases of plague is based on a careful assessment of the anamnestic data, the results of an objective examination and the assumption of the possibility of this disease.

Blood, sputum, purulent discharge and aspirate from enlarged lymph nodes should be examined bacterioscopically by staining smears using the Giemsa method, as well as by seeding on blood agar. Serological diagnostic methods can be used only in some patients. Thus, the reaction of passive hemagglutination to the I fraction of the plague pathogen becomes positive only from the 5th day after the onset of the disease and reaches a maximum by the 14th day of the disease.

Differential diagnosis carried out with tularemia and lymphadenitis caused by strepto- and staphylococci. Septicemia in plague does not differ in clinical symptoms from acute, severe forms of sepsis caused by bacterial or rickettsial infection.

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

Persons who have been in contact with patients with pneumonic plague are given prophylactic tetracycline for 10 days.

Forecast. The bubonic form of plague without appropriate treatment is fatal in 60-90% of cases. The pneumonic form of plague leads to the death of all patients.

Timely treatment for bubonic plague reduces the death rate to 10% or more. The prognosis for the pulmonary form is unfavorable if the correct diagnosis is not established and appropriate therapy is not started within the first 18 hours of the disease.

Prevention. The vaccine is indicated only for persons who, due to their occupation, are constantly in contact with sick rodents, as well as laboratory workers working with this microorganism.

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. Additional vaccinations can be carried out at yearly intervals. For children under the age of 11 years, the dosage of the vaccine is reduced: children under 1 year old are given 1/5 of the adult dose, children from 5 to 10 years old - 3/5 of the adult dose in the sequence described above. Even a vaccinated child exposed to the plague should receive a course of chemoprophylaxis, since vaccination does not provide complete protection against the disease, despite the high titer of antibodies in the blood. The main method of preventing plague in urban areas is sanitary measures aimed at reducing the population of rodents and fleas. A person who has the plague must be isolated until cured. Plague pathogens can be excreted in the feces of patients, so their excrement must be disinfected.

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

In recent years, diseases caused by Yersinia have become diagnosed much more frequently.

Y. enterocolitica and Y. pseudotuberculosis are similar to the intestinal group and are Gram-negative rods that are motile at 22°C but lose their motility at 37°C.

These features help distinguish these Yersinia species from Y. pestis and Enterobacteria. 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. Y. enterocolitica serotypes 3, 8 and 9 and Y. pseudotuberculosis serotype 1 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, but diarrhea can last several months.

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

Lecture number 11. Tularemia

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).

Clinical manifestations of this infection depend on the virulence of the pathogen and the route of infection. There are five clinical forms of the disease: ulcerative glandular (80% of all cases of this infection), glandular (10%), ophthalmic (1%), typhoid (almost 6%). The incidence of tularemia pharyngitis and pneumonia in children remains unknown, but oropharyngeal forms occur.

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

F. tularensis strains are antigenically homogeneous, but their virulence is very different: type A strain Jellison is highly virulent for humans, type B of this strain causes only mild forms of the disease in humans.

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 typical for rats, mice, squirrels, beavers, nutmeg rats, moles, birds and the ticks that parasitize them. Tularemia is transmitted by fleas, lice, mosquitoes and horseflies.

Tularemia most often develops in hunters, cooks, fur breeders and other persons who, by the nature of their occupations, most often encounter the pathogen.

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 damaged or healthy skin, mucous membranes, through an insect bite, through the lungs or gastrointestinal tract. After 48-72 hours, an erythematous, maculopapular formation appears on the skin at the site of bacterial penetration, quickly ulcerating, and local lymphadenopathy. The pathogen multiplies in the lymph nodes and causes the formation of granulomas in them. Subsequently, bacteremia may develop, leading to damage to a variety of organs. However, 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.

Cellular immunity responses may be of great importance in resistance to tularemia, the role of circulating antibodies is less prominent.

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

The primary changes on the skin in the 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. Some patients have generalized enlargement of the lymph nodes and splenomegaly.

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 note splenomegaly, sometimes an increase in the liver.

Cases of the development of meningitis, encephalitis, pericarditis, endocarditis, neuralgia, thrombophlebitis and osteomyelitis are described.

Diagnosis. For the diagnosis of tularemia, the following 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 (they are of additional importance and are not always effective).

Differential diagnosis. The ulcerative-glandular form of tularemia is differentiated from cat scratch disease, infectious mononucleosis, sporotrichosis, plague, anthrax, melioidosis, glanders, rat bite fever, or lymphadenitis caused by streptococcus pyogenes or Staphylococcus aureus. The oropharyngeal form of tularemia is differentiated from the same diseases and from acquired cytomegalovirus infection and toxoplasmosis, adenoviral infection and herpes simplex.

Pneumonitis in tularemia is differentiated from other bacterial and non-bacterial pneumonias, especially those caused by mycoplasmas, chlamydia, mycobacteria, fungi and rickettsiae. Their exact differentiation is possible only when the pathogen is isolated.

The typhoid form of tularemia is differentiated from typhoid, brucellosis and other diseases accompanied by septicemia.

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.

Forecast. Death in untreated ulcerative glandular form of tularemia occurs in 5% of cases. If untreated, the disease lasts 2-4 weeks, and within 8-12 weeks there is a decrease in performance.

Pneumonia, both primary and secondary, developed against the background of the bubonic form of tularemia, ends in death in 30% of patients who did not receive appropriate therapy. Those who recover from tularemia acquire immunity to it for life. Relapses are rare and mild. The disease caused by the Jellison type B strain is characterized by a milder course. Properly performed treatment provides a quick and complete cure, while deaths are extremely rare.

Prevention. The main method of prevention is vaccination using the live attenuated anti-tularemia vaccine Elbert-Gaisky. In tularemia-endemic areas and adjacent areas, routine vaccinations cover the entire population over 7 years of age, and in some cases, children under 2 years of age.

In the tularemia focus, a complex of sanitary and anti-epidemic measures is carried out, regulated by a special decree.

Lecture number 12. Listeriosis

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. Unlike animals, the disease in humans is accompanied by a reaction of polymorphonuclear cells in the blood, CSF.

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

Listeria is divided into four serotypes depending on the composition of somatic (O) and flagellated (H) antigens. Groups I, III, IV differ from each other in O-antigens, and group II - in H-antigen. The main groups, in turn, can be subdivided into subgroups. The disease in humans is caused by pathogens belonging to groups I and IV.

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. In pale-stained smears, pathogens look like a gram-negative rod resembling H. influenzae.

Epidemiology. Listeria causes diseases in 42 species of mammals and 22 species of birds. The pathogen was isolated from soil where it had remained for more than 295 days, from springs, wastewater, silage, dust and waste from slaughterhouses. It was isolated from the contents of the intestines and vagina; it was found in the contents of the cervix, nose, ears, blood and urine of apparently healthy individuals. Today it has been established that listeriosis belongs to a new class of infectious diseases - “sapronoses”, a characteristic feature of which is that the source of pathogens is not animals, as in zoonoses, and not humans, as in anthroponoses, but the substrate of the external environment (soil, water natural and artificial reservoirs).

Infection can occur in the following ways:

1) contact (in contact with sick animals and birds);

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. Abscesses occur, no different from those with other purulent infections. The formation of microabscesses and granulations is possible. Necrotic processes are detected in the kidneys and lungs, especially in the bronchioles and walls of the alveoli.

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

Pathogenesis. The entry point for infection can be any mucous membrane or damaged skin. At the site of initial introduction, Listeria causes an inflammatory reaction involving the lymphatic system. From the site of primary localization, they quickly spread by lymphogenous, hematogenous or neurogenic routes to the internal organs, causing vascular and dystrophic changes in them. First of all, the pathogen and its endotoxin exhibit their hepatoneurotropism. In the affected organs, the pathogen accumulates and characteristic morphological changes of the granuloma-listerioma type are formed. The development of the pathological process depends on the site of penetration of the pathogen.

Listeria are facultative intracellular parasites. Immune reactions in this infection are carried out using cellular mechanisms. Any congenital or acquired dysfunction of T-lymphocytes creates prerequisites for the development of listeriosis.

The disease may be present at birth, later in the neonatal period, or in older children. The early onset of the disease may be due to transplacental infection from a mother who has had a clinically pronounced or erased form of listeriosis. When infected in the early period of pregnancy, a miscarriage usually occurs, and in the later periods, fetal death or premature birth occurs.

Pathogens are often found in a mother whose child has become ill with listeriosis during the first 5 days of life. The disease in a later period is usually not due to infection from the mother. Epidemics of listeriosis among newborns have been described. The onset of the disease in the early neonatal period is associated with listeriosis or bacterial carriage in the mother and usually with serotypes of the pathogen and Ib. The disease of a later period is caused mainly by Listeria serotype IVb, when meningitis develops more often than septicemia.

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

The disease sometimes resembles infectious mononucleosis, and in pregnant women it manifests itself with influenza-like and septic conditions. It is believed that listeriosis is often the cause of spontaneous abortions, but this information is unreliable.

Clinical manifestations of infection in newborns may be different and depend on the time and route of infection. Listeriosis disease in late pregnancy is usually accompanied by miscarriage, intrauterine fetal death, or premature birth of a sick child who dies a few hours after birth.

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. These babies are usually born prematurely and their mortality rate is high.

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. Meningitis can occur against the background of conjunctivitis, otitis media, sinusitis, pneumonia, endo- and pericarditis.

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.

An infectious syndrome resembling mononucleosis was the first human disease to be associated with Listeria infection. The Paul-Bunnel reaction to heterophile antibodies in these patients was negative.

It has been suggested that listeria is a secondary infection that developed against the background of mononucleosis and in a special way affects the production of heterophilic antibodies.

The diagnosis of congenital listeriosis is based on anamnesis data, taking into account the birth of a child with signs of intrauterine infection. In older children, listeriosis can be suspected in the presence of a characteristic pharyngeal lesion with a long course and a mononuclear shift in the blood, as well as in the occurrence of an oculomotor form. In all other cases, the clinical diagnosis of listeriosis is difficult.

The combination of epidemiological and clinical data can only suggest listeriosis. For the final diagnosis, laboratory confirmation is required 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, during which white mice are infected with material from patients. However, using these research methods, it is difficult to confirm the diagnosis due to the difficulty in identifying the pathogen due to its similarity with diphtheroids and some saprophytes;

2) serological research methods, which are the main ones in the diagnosis of listeriosis (RA, RSK, RPGA). In this case, it is recommended that the two reactions indicated above be carried out simultaneously;

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

Differential diagnosis. Isolation of a culture of the pathogen is necessary for the differential diagnosis of listeriosis and other forms of bacterial meningitis and septicemia. Sometimes, with the development of atypical lymphocytosis, it is necessary to exclude toxoplasmosis, viral hepatitis, infections caused by the Epstein-Barr virus and cytomegalovirus. For this purpose, they resort to methods of serodiagnosis and isolation of bacterial flora.

Treatment. The drug sensitivity of different Listeria strains varies. According to laboratory data and animal experiments, 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. Tetracycline should not be given to pregnant women and children under 8 years of age. In children, it causes staining of milk and permanent teeth.

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

Forecast. Transplacental infection with listeriosis almost always leads to abortion of the fetus. The mortality rate for newborns infected shortly before or shortly after birth reaches 50%. Listeria pneumonia, which develops in the first 12 hours after birth, is fatal in 100% of cases. Children who become ill on the 5th-30th day of life die in 20-50% of cases. Timely treatment of listeria septicemia and meningitis in young and older children ensures recovery in 95% of cases. Patients who survive listeria meningitis often remain paralyzed, have mental retardation and signs of hydrocephalus.

Prevention. Listeriosis in newborns can be prevented with timely diagnosis in the mother and intensive treatment.

Since it is nonspecific and mild in pregnant women, its timely diagnosis and prevention are difficult.

The consumption of unpasteurized milk and contaminated water should be avoided.

Lecture No. 13. 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. It got its name from the Greek word for "coal", by analogy with the black color of the scab that forms with the skin form.

Etiology. The causative agent of the disease, Bacillus anthracis, is a gram-positive, immobile rod with a capsule and spores formed under aerobic conditions, resistant to external influences and capable of surviving for years in soil and various products of animal origin.

Epidemiology. Human infection with anthrax is possible through contact, nutritional, aerogenic and transmissible routes. The incidence of anthrax in humans is predominantly sporadic; less often, group diseases may occur. School-age children, especially teenagers, mostly boys, are more likely to suffer from anthrax, which is associated with their participation in caring for animals.

The incidence of anthrax in people increases in the summer-autumn period.

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

The pulmonary form of anthrax develops when spores are inhaled and enter the alveoli. Being phagocytosed, they are transported to regional lymph nodes, where they replicate and produce exotoxin. Subsequently, septicemia usually develops, sometimes meningitis, and death may occur. Intrathoracic lymph nodes are adematous, hemorrhages are observed in them, and due to their increase in size, the bronchi can be compressed. The action of anthrax exotoxin causes depression of the CNS function. Primary pneumonitis after inhalation of the pathogen rarely develops, but respiratory failure and death can occur due to extensive thrombosis of the lung capillaries.

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 spore penetration, quickly turning into a vesicle; as it increases in size, it becomes hemorrhagic, necrosis develops in its center, and a scab forms. Swelling and new blisters appear around the gradually enlarging scab.

Common manifestations of infection are a moderate increase in body temperature, a feeling of malaise, an increase in regional lymph nodes. Sometimes the only manifestations of diseases are atypical changes on the skin: dotted dark spots that do not transform into vesicles. The cutaneous form accounts for more than 90% of all anthrax cases. Lesions of the shoulders and forearm are more common than the fingers, on the legs they are very rare. 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 pulse and respiration become more frequent, body temperature rises, shortness of breath and cyanosis increase. Wet rales are heard, pleurisy develops, and sometimes swelling of the subcutaneous tissue on the neck and chest. Death occurs within a day, usually due to severe respiratory failure.

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. There may be bloody diarrhea and hematomesis. Shock quickly develops and death ensues.

Meningitis can develop with untreated cutaneous anthrax. More than half of all cases of meningitis are complications of the cutaneous form of the disease, although the latter may already subside by the time meningitis develops. The cerebrospinal fluid is usually hemorrhagic in nature, but may also be purulent. B. anthrasis is often found in it. Simultaneously with meningitis, patients often have signs of encephalomyelitis and hemorrhage in the cerebral cortex.

Diagnosis. Anthrax is diagnosed based on characteristic changes on the skin and history of exposure to infection. Isolation of the pathogen from a discharged vesicle or from a scab confirms the diagnosis. The pulmonary form is identified when the pathogen is determined in pleural effusion; it is rarely detected in sputum. Data on the consumption of meat from sick animals should lead to speculation about the gastrointestinal form of anthrax.

Differential diagnosis. The cutaneous form of anthrax must be differentiated from skin diseases caused by staphylococcal infection, tularemia, plague, infection caused by Pseudomonas aeruginosa, A hydrophila, and skin changes after vaccination.

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 novocaine salt of penicillin. Skin lesions are sanitized and bandaged. Cutting them is not recommended due to the risk of progression of the process. For pulmonary and meningeal forms of anthrax, patients are treated with penicillin G, and in some cases a specific antitoxin is administered. Maintenance therapy is necessary.

Forecast. The mortality rate for anthrax meningitis, despite treatment, is 100%, and for pulmonary meningitis it exceeds 90%. The untreated cutaneous form of anthrax is fatal in 10-20% of cases, and with penicillin therapy it decreases to 1%. The gastrointestinal form of infection is fatal in 25-50% of cases.

Prevention. A vaccine has been created, the administration of which is recommended for persons whose occupation is at increased risk of this infection.

Lecture No. 14. Viral infections and infections of presumably viral etiology

1. Measles

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 causative agent of measles is an RNA virus belonging to the Paramyxoviridae family of the Morbillivirus genus. There is only one known antigenic type of virus, structurally similar to the causative agent of infectious mumps and parainfluenza. During the prodromal period and in the first days after the appearance of the rash, it is found in nasopharyngeal discharge, blood and urine. The virus can be grown on tissue cultures of the renal epithelium of a human embryo or rhesus macaque. Cytological changes observed after 5-10 days of cultivation consist in the appearance of multinucleated 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 danger 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 widespread. The source of infection is only a sick person. The route of transmission of the measles virus is airborne, but transmission of infection through objects and third parties 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 are in the skin, mucous membranes of the nasopharynx, bronchi, intestines and conjunctiva. Exudate and proliferating mononuclear and a 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. Occasionally, interstitial measles pneumonitis progresses to giant cell pneumonia. Bronchopneumonia may be due to a secondary bacterial infection.

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 decrease again 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, on the mucous membrane of the cheeks opposite the lower molars, but can be unevenly distributed throughout the shell, less often - on the lips, palate and conjunctiva. Koplik's spots usually disappear after 12-18 hours.

As they wither, they acquire a reddish color, in some places the color of the mucous membrane changes.

Inflammation of the conjunctiva and photophobia suggest measles even before Koplik's spots appear. A clear delimitation of the inflammation of the conjunctiva along the edge of the eyelids and in a direction transverse to the edge can serve as an additional diagnostic sign in the prodromal period of the disease. As the inflammation spreads, this symptom disappears.

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 patient, who was previously in a serious condition, already 24 hours after the decrease in body temperature feels quite satisfactory.

The rash first appears as pale spots on the upper sides of the neck, behind the ears, along the hairline, and on the cheeks (closer to the auricle).

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.

In mild forms, they do not merge; in very mild forms, there are few of them, or they are determined in the form of single elements, mainly on the legs. In severe cases, the rash is confluent, covering the entire skin, including the palmar and plantar surfaces. The face becomes swollen and loses its normal shape.

Often the rash is slightly hemorrhagic in nature. In severe cases, numerous petechiae and ecchymosis are formed. Skin itching is usually minor. At the site of the rash, pigmentation persists for 7-10 days, pityriasis peeling of the skin begins.

The severity of the rash varies greatly. Sometimes they become urticarial in nature. Pale spots or a scarlet-like rash may appear early in the prodrome and disappear quickly as the measles-like rash appears. With measles, accompanied by hemorrhages, bleeding from the mouth, nose and intestines is observed. In milder forms, the rash is not spotty, but punctate and resembles scarlet fever.

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

Mesenteric lymphadenopathy can cause abdominal pain. Characteristic changes in the mucous membrane of the appendix can lead to obliteration of its lumen and cause symptoms of appendicitis. These changes usually resolve after the Koplik spots disappear.

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 and often its fatal outcome.

Diagnosis. To diagnose measles, they mainly use clinical and epidemiological data and, less often, laboratory data, which include hematological data, cytological examination of nasal discharge, virus isolation, and detection of antibodies.

Differential diagnosis. In the catarrhal period, they are differentiated from acute respiratory viral infections; during the period of rash - with rubella, enteroviral exanthema, drug disease, less often - with scarlet fever, pseudotuberculosis, menigococcemia.

Complications. In accordance with the affected organs and systems, complications from the respiratory system are distinguished (pneumonia, laryngitis, laryngotracheitis, bronchitis, pleurisy); digestive (stomatitis, enteritis, colitis); nervous systems (encephalitis, meningoencephalitis, meningitis, psychosis); organs of vision (conjunctivitis, blepharitis, keratitis, keratoconjunctivitis); hearing organs (otitis, mastoiditis); skin (pyoderma, phlegmon); excretory system (cystitis, pyelitis, pyelonephritis).

Treatment. Of primary importance are bed rest, sedatives, and at high temperatures, antipyretics and adequate fluid supply. Humidifying the air in the room may be necessary for laryngitis and severe irritating cough; for 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.

Gamma globulin, hyperimmune gamma globulin, and steroids: Not a big deal.

The effectiveness of modern antiviral drugs has not been confirmed.

Prevention. The most effective means of prevention is vaccination with live measles vaccine (LMV) from 12 months of age, once, subcutaneously.

There is no local reaction to the vaccine, and the general one develops 6-7 days after the introduction of the vaccine in only 10-13% of vaccinated children, representing an infectious process with scattered weakened symptoms in the form of a temperature reaction, catarrhal phenomena, less often a rash.

ZHV is used for emergency vaccination in children's institutions after the introduction of measles in the first 5 days of contact.

Passive immunization or gamma globulin prophylaxis consists in creating temporary immunity to measles by using gamma globulin when measles is introduced into children's medical institutions and when children come into contact with measles who have contraindications to vaccination.

Non-specific or general anti-epidemic measures include early identification and isolation of the source of infection and measures among contacts.

2. Rubella

Rubella is a mildly contagious disease in childhood, characterized by mild general disturbances, rashes resembling those of mild measles or scarlet fever, and swollen lymph nodes in the occipital, parotid, and posterior cervical regions.

In older children and adults, the infection is sometimes severe, with joint involvement and purpura.

Rubella transmitted by a pregnant woman can cause severe fetal malformations. Congenital rubella syndrome is defined as an acute contagious disease that affects many organs and is accompanied by a wide range of clinical manifestations and a long postnatal period of activity with the release of the pathogen.

Etiology. Rubella is caused by a pleomorphic RNA virus. It belongs to the family Togaviridae of the genus Rubivirus. It is usually isolated in tissue cultures, grows well in tissue culture of the renal epithelium of the African gray monkey. The presence of the rubella virus is manifested by the resistance of infected cells to the effects of enterovirus. At the height of the disease, the virus is detected in nasopharyngeal discharge, blood, feces and urine.

In the nasopharynx, it persists already 7 days before the rash appears and for 7-8 days after it disappears. Patients with subclinical forms of infection present an epidemic danger.

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

Boys and girls get sick equally often. In many cases, rubella is hidden. Most often, epidemics begin in the spring. Clinical diagnosis is difficult, since similar symptoms are observed with enterovirus infection. The transferred disease leaves strong immunity.

Clinical manifestations. Incubation period - 14-21 days; prodromal, characterized by minor catarrhal symptoms, usually shorter than with measles, and often goes unnoticed. The most typical is considered to be enlarged occipital, parotid and posterior cervical lymph nodes. Immediately before the skin rash, enanthema may appear in the form of individual pink specks on the soft palate, some of them merge, move to the arches and acquire a dark red color.

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

Eruptions first appear on the face and soon spread to the body, and the evolution of the rash is so rapid that by the time it appears on the trunk on the face, it already fades.

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

Some of them merge, most often on the face. During the 2nd day, they become much smaller, they take on a dotted appearance, resembling a rash with scarlet fever. There may be slight itching. On the 3rd day, the rash turns pale and disappears after a few days, leaving no pigmentation. Skin peeling is very slight. Cases of rubella that are not accompanied by a rash have been described.

The mucous membranes of the pharynx and conjunctiva are somewhat inflamed. Unlike measles, there is no photophobia. The body temperature remains within the normal range or rises for 1-2 days, less often for 3 and only during the period of the rash. Very rarely it exceeds 38,4 °C. Anorexia, headaches, general malaise are not typical for rubella. The spleen is somewhat enlarged, the number of leukocytes does not change or slightly increases, thrombocytopenia, like purpura, is rare.

congenital rubella syndrome. Subclinical intrauterine infection is not uncommon. At birth, the child looks quite healthy, but rubella viruses are found in the nasopharyngeal discharge and urine, and IgM specific to it is also detected. These children can become a source of infection for others. Some of them feel well for several months before the development of severe disease, manifested by interstitial pneumonia, rash, diarrhea, hypogammaglobulinemia, impaired T- and B-cell function, neurological symptoms, and ending in death.

Progressive panencephalitis has been described in several adolescents with congenital rubella syndrome. For many years before the onset of the first symptoms, children developed quite normally.

Diagnosis 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) haematological findings (leukopenia, lymphocytosis, plasma cells, normal erythrocyte sedimentation rate) are helpful in diagnosis, especially when scarlet fever is suspected;

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.

Differential diagnosis. Rubella is differentiated mainly with measles, scarlet fever, and less often with pseudotuberculosis, enterovirus infections ECHO and Coxsackie, adenovirus infections, infectious mononucleosis, allergic and drug rashes.

Complications with rubella in children are rare. Resistance to secondary bacterial infections persists, with occasional neuritis and arthritis. Encephalitis, similar to those developing after measles, is extremely rare.

Forecast favorable, but in congenital forms it varies depending on the severity of the process. Only in 30% of children with encephalitis, after treatment, there are no pronounced changes in motor function and psyche.

Treatment. Typically, ongoing rubella does not require hospitalization or medication. Vitamin therapy, bed rest for 3-4 days are indicated, in combination with ARVI - symptomatic drugs, with streptococcal infection - antibacterial therapy, in the event of meningoencephalitis - urgent hospitalization and complex treatment, including anti-inflammatory, hormonal, detoxification, dehydration, anticonvulsants.

Prevention rubella is based on the complex use of:

1) measures in relation to sources of infection, which come down to identifying and isolating patients and accounting for contacts;

2) means of influencing the mechanisms of infection transmission, which are reduced to ventilation and wet cleaning of the room where the patient is located;

3) means influencing the susceptibility of the population - active and passive immunization. Active immunization in Russia is not provided for in the vaccination calendar. However, vaccinations are recommended to start at 12-15 months of age, regardless of gender. The second dose of the vaccine is administered to girls aged 12-14 years to create protection in those for whom the primary vaccination was ineffective.

Passive immunization or rubella gamma globulin prophylaxis is ineffective and is not carried out in childhood.

3. Herpes simplex

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. The herpes simplex virus contains DNA, reproduces well in the tissues of the chicken embryo in the yolk sac, and causes characteristic cytopathic changes when introduced into a single-layer cell culture. Two types of the 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 is patients and virus carriers. Transmission is carried out by contact, sexual contact, airborne droplets, transplacental transmission of infection is possible, but infection most often occurs during the passage of the birth canal. For the spread of infection, poor sanitary and hygienic conditions, hypothermia, overcrowding, increased solar insolation, and a high incidence of viral infections are important.

Pathology. Pathological changes depend on the location of the infection. On the skin and mucous membranes, characteristic changes include the formation of vesicles resulting from stratification and ballooning degeneration of cells of the spinous 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 shifted 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. Subarachnoid hemorrhages are possible. A picture of leptomeningitis is found with infiltration of the membranes and walls of blood vessels with cellular lymphohistiocytic elements. Similar changes can be found in the liver, lungs, spleen, bone marrow, adrenal cortex.

Clinical manifestations. 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. A scar does not form in their place if a secondary infection does not join and herpes does not recur.

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.

The subsequent spread of infection often occurs along the lymph flow, which is accompanied by an increase in regional lymph nodes and the spread of bubbles to intact skin areas. The developed changes become similar to those in herpes zoster, especially if neuralgia appears. Healing is slow, sometimes delayed for 3 weeks. Eruptions recur at the site of a former injury especially often and can take a bullous form.

Treatment is symptomatic only. Surgical intervention is contraindicated.

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. Less commonly, the process develops gradually with the appearance of a feverish state, irritability, ahead of changes in the oral cavity by 1-2 days. Vesicles form on the mucous membrane, which quickly burst, ulcers 2-10 mm in diameter are formed, covered with a grayish-yellow film. Changes can be localized anywhere in the oral cavity, but most often on the tongue and cheeks. Acute gingivitis is a characteristic symptom and in dentition children may be detected earlier than buccal mucosal changes. The submandibular lymph nodes are usually enlarged.

The acute phase of the disease lasts 4-9 days, pain disappears in 2-4 days until the ulcers are completely healed. In some cases, the tonsils are the first to be involved in the process, which gives reason to suspect the bacterial nature of tonsillitis.

The lack of effect of antibiotics eliminates the suspicion of bacterial tonsillitis, and the appearance of vesicles on the mucous membrane of the oral cavity - to clarify the diagnosis.

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 altered eczematous skin is accompanied by the development of herpetic eczema, which can proceed easily and go unnoticed without special clinical and laboratory studies, in severe form it can result in death. 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. Body temperature rises to 39,4-40,6 °C and remains at this level for 7-10 days, other systemic reactions vary. Recurrent forms are observed in chronic atopic skin lesions. General disturbances in these cases are weakly expressed and are manifested by hyperergic reactions. The disease can be fatal due to severe physiological disorders due to dehydration, excretion of electrolytes and proteins through damaged skin, due to the spread of infection to the central nervous system or other organs, and also due to the addition of a secondary infection.

Differential diagnosis with eczema after smallpox vaccination is made by excluding the fact of recent vaccination, and also on the basis of the typical herpetic appearance of the vesicles. It is possible to accurately and quickly confirm the diagnosis by examining them under an electron microscope.

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. Newborns may develop cataracts, chorioretinitis, and uveitis.

The diagnosis can be suspected by the appearance of herpetic vesicles on the eyelids and confirmed by isolation of the virus. The differential diagnosis is with highly contagious keratoconjunctivitis caused by one of the adenovirus serotypes.

7. Herpes in the vulva is most common in adolescents and young adults through sexual contact and is usually caused by HVH-2. Between 5 and 10% of individuals become infected with HVH-1. If the patient does not have antibodies to the herpes virus, then he develops general disorders (body temperature rises, regional lymph nodes increase, dysuria begins). In women, the vagina and vulva may be involved in the process, but the primary infection is localized on the cervix. Frequent relapses appear only on the part of the cervix, are not accompanied by clinical symptoms and serve as a source of infection for a newborn passing through the birth canal.

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. Many of these children do not have the characteristic skin manifestations of herpes, and some may have other lesions (hyaline membrane disease, bacterial pneumonia that does not respond to antibiotics, or septicemia). The diagnosis of systemic herpetic infection in these cases can only be made with special alertness in relation to this disease and after appropriate laboratory tests have been carried out.

Clinical manifestations develop during the first 2 weeks and consist of characteristic skin lesions, lethargy, poor breastfeeding, persistent acidosis, liver enlargement, pneumonitis, meningoencephalitis, and bleeding.

With insufficient treatment or its absence, the disease progresses and ends fatally. Clinical manifestations of meningoencephalitis usually develop on the 11-20th day after birth in a full-term baby.

About 70% of children hospitalized for only skin manifestations of herpes subsequently acquire a systemic form of this infection. Localized forms end in death only in rare cases, but 12% of these children develop neurological disorders.

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 to the herpes simplex virus circulate.

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.

Differential diagnosis. Herpes simplex infection is differentiated from herpes zoster, enterovirus infection, adenoviral keratoconjunctivitis, and eczema vaccinatum.

Forecast depends on the clinical form. With localized forms, the prognosis is favorable. With generalized - serious, especially severe with herpetic encephalitis, meningoencephalitis, congenital herpes and diseases of the newborn.

Treatment. For localized lesions of the skin and mucous membranes, 0,25% oxolinic ointment, 0,5% Florenal ointment, 0,25-0,5% tebrofen ointment, 0,25-0,5% are prescribed locally. riodoxol ointment, as well as Acyclovir ointment and other antiviral drugs. For keratitis - the antiviral drug IDUR (5 iodine-2-deoxyuridine) in the form of ointments, solutions, as well as adenine arabinoside. Treatment of affected areas of the skin and mucous membranes is carried out using antiseptics: 1-2% alcohol solution of brilliant green, 1-3% alcohol solution of methylene blue, for herpetic stomatitis - 3% solution of hydrogen peroxide. Painkillers (anesthesin, lidocaine) are used locally.

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. Corticosteroid hormones are contraindicated. Acyclovir is prescribed to prevent dissemination of mucocutaneous herpetic manifestations in children with immune deficiency. Local application of acyclovir promotes healing of ulcers, oral and intravenous - to reduce the frequency of relapses.

Prevention. Hardening children and developing general hygiene skills is of great importance. To prevent intrauterine infection of the fetus in the presence of clinical signs of herpetic infection in a pregnant woman, it is recommended to administer immunoglobulin; if an infection is detected immediately before birth, a cesarean section is recommended.

4. 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, but people of any age, including newborns, get sick. Secondary cases of diseases among persons susceptible to chickenpox who were in contact with a sick person in the family are approximately 90%. The complement fixation test is the most widely used test, but its sensitivity is low. A test with fluorescent antibodies to membrane antigens, immunohemagglutination, and enzyme-linked immunosorbent assay are considered more informative.

The infection is spread by drop or contact, its outbreaks are observed from January to May. The causative agent is contained in the fluid of the vesicles, but unlike natural smallpox, it is not determined in the crusts. 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. Epidemics often occur after contact with a patient with herpes zoster. Recurrent cases of the disease are rare.

Clinical manifestations. The incubation period is 11-21 days, but more often 13-17 days. Towards 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, loss of appetite, sometimes accompanied by a scarlet fever or measles-like rash and preceded 24 hours by rashes typical of chickenpox. Their characteristic feature is the speed of their appearance.

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. In the mildest cases of the disease, there are a very small number of vesicles. There is a pronounced tendency to their predominant localization in places of greatest skin irritation and pressure on it. 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 some cases, they are localized on the mucous membranes of the genital organs, conjunctiva and cornea, which threatens with loss of vision. The mucous membrane of the larynx is rarely involved in the process. Generalized lymphadenopathy may develop.

The severity of the flow can vary greatly. 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. Systemic manifestations persist no more than the first 3-4 days during the rash.

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. A transient purpura may develop, usually at the end of the 1st week of illness, often leading to gangrene, which is probably a Schwartzmann-type reaction.

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. The rest of the course of the disease does not change.

Congenital chickenpox manifests itself already at birth or in the first days of life of a child whose mother is ill with an active form of the infection.

Complications are specific, due to the direct action of the virus itself, and may occur as a result of the layering of a bacterial infection. Among specific complications, the leading ones are varicella encephalitis, meningoencephalitis, less often - myelitis, neuritis, myocarditis, etc. Among bacterial complications, phlegmon, abscess, impetigo, bullous streptoderma, erysipelas, lymphadenitis occur. Less common are pneumonia, croup syndrome.

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

From laboratory methods use:

1) microscopic examination method (detection of virus accumulations in smears of vesicular fluid stained with silver according to Morozov using conventional or electron microscopy);

2) serological methods (immunofluorescence, complement fixation reaction and ELISA).

Differential diagnosis. Chickenpox is differentiated from impetigo, strophulus, generalized forms of herpetic infection, and less often with scarlet fever and other rash diseases.

Forecast. In typical cases, the disease ends in recovery.

Fatal outcomes are possible with malignant forms, as well as with the development of severe bacterial complications, mainly in young children, newborns and with congenital smallpox.

Treatment. Strict adherence to the hygienic care of the child, bedding, and clothing. The vesicles are lubricated with a 1% solution of brilliant green or a 1-2% solution of potassium permanganate. General hygienic baths with a weak solution of potassium permanganate, rinsing the mouth with disinfectant solutions after meals are indicated, in case of purulent complications - antibiotics, in severe forms - immunoglobulin.

Corticosteroids are prescribed only if encephalitis or meningoencephalitis occurs. In severe forms, immunoglobulin is prescribed.

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

Treatment with these drugs is also effective in the development of complications of chickenpox.

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 previously been ill are isolated from 11 to 21 days from the moment of contact.

After isolating the patient, it is enough to ventilate the room and do a wet cleaning.

In the presence of massive (more than 1 hour) contact, passive immunization with specific Varicella Zoster immunoglobulin is indicated in susceptible children with immunodeficiency; newborns from mothers who fell ill with chickenpox 5 days before delivery or within 2 days after them; premature babies from mothers who do not have information about the transferred chicken pox, regardless of history; healthy susceptible adolescents 15 years of age and older, and seronegative adults.

Active immunization is not widely used.

5. Cytomegalovirus infection

Infection with cytomegaloviruses often goes unnoticed, but infection before, during, or shortly after birth usually causes severe illness resembling infectious mononucleosis and is most commonly seen in individuals with cellular immune deficiency.

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

Epidemiology. Cytomegalovirus infection is common throughout the world. The source of infection is only a person, a patient or a virus carrier.

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

Pathology. According to electron microscopic examination, cytomegalovirus particles are no different from varicella zoster virus, herpes simplex virus and Epstein-Barr virus. Light microscopy reveals large intranuclear inclusions in tissues with a high titer of the virus. Their large size in the cells of the liver, kidneys, lungs, and in urine sediment allows for an accurate diagnosis. However, tissue culture is a more sensitive and reliable method for detecting cytomegalovirus.

Clinical manifestations. The incubation period appears to range from 15 days to 3 months. There are congenital and acquired cytomegaly, according to the course - acute and chronic.

congenital infection. More than 90% of newborns with cytomegalovirus infection are asymptomatic. In other cases, its severity varies considerably, but death is rare. 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. Signs of dysfunction of the central nervous system in the neonatal period are usually not observed.

The assumption of congenital cytomegalovirus infection should arise when a child develops a petechial rash on the first day of life, especially in combination with an enlarged spleen.

For many children, the only symptoms are developmental delays and irritability. Isolated congenital anomalies, such as clubfoot, strabismus, deafness, palatal deformity, and microcephaly, occur predominantly in children with severe clinical signs of congenital infection.

The most common and important sign of a congenital infection is a violation of the central nervous system function, while the underdevelopment of psychomotor functions a few years after birth is equally common in children with or without pronounced signs of it at birth. Changes in the liver, lungs and kidneys are completely reversible and their function is almost completely restored.

Vision is lost extremely rarely due to chorioretinitis and optic nerve atrophy.

Hearing loss is much more common. In the most seriously ill children, the disease is accompanied by spasticity and muscle hypotension.

CNS dysfunction ranges from a slight decrease in intelligence, which makes learning difficult, to severe brain damage that prevents the normal development of psychomotor functions in early childhood.

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.

The asymptomatic course is explained by the presence of maternal antibodies to this infection in the blood of the newborn.

However, the virus causes them to develop pneumonia, coughing fits, petechial rash, enlargement of the liver and spleen. In some cases, the function of the central nervous system is impaired.

Muscle spasticity is not characteristic of cytomegalovirus infection.

Chorioretinitis develops only in children with suppressed immune mechanisms.

In older children and adults, mononucleosis due to cytomegalovirus is the main manifestation of the disease recognized by the doctor. Its clinic varies, but general malaise, myalgia, headaches, anorexia, abdominal pain, enlarged liver and spleen are usually determined.

Liver function is often impaired. The mucous membrane of the pharynx is edematous, but there is no plaque on it, the symptoms of angina are not expressed.

The feeling of weakness and fatigue persists for a long time, some patients sleep 12-15 hours a day. Chills and daily fever up to 40 °C or more may last for 2 weeks or more. An early and important sign is atypical lymphocytosis.

After transfusion of blood components, especially whole fresh blood, a seronegative recipient may develop post-transfusion cytomegalovirus mononucleosis in 3-4 weeks.

After transfusion of such blood to a premature newborn, his skin becomes pale grayish, respiratory failure develops, the spleen enlarges, atypical lymphocytosis and a virus in the urine are determined.

After the introduction of ampicillin in patients in this case, a maculopapular rash appears, resembling that of infectious mononucleosis. Both diseases are characterized by the same type of serological reactions, including agglutination in the cold, antinuclear antibodies, cryoimmunoglobulins.

Diagnostics. It is impossible to make a diagnosis of cytomegalovirus infection based on clinical data alone. Laboratory diagnosis is based on:

1) cytological studies, when virus-affected cells (cytomegals) are easily detected in urine sediment, saliva, cerebrospinal fluid, sputum, gastric lavage and other secrets and excretions;

2) virological studies, when a primary embryonic culture of human fibroblasts or a line of diploid human embryonic lung cells is used to isolate cytomegalovirus, as well as detection of viral DNA by a polymerase chain reaction;

3) serological studies using RSK, RN, TPHA, platelet aggregation reaction, ELISA, etc.

Differential diagnosis it is necessary to carry out with toxoplasmosis, rubella, herpes simplex and bacterial sepsis, infectious mononucleosis.

Forecast with congenital cytomegaly, it is often unfavorable, the disease can end in death, and in case of survival, dysfunction of the central nervous system is possible. Acquired cytomegalovirus infection, proceeding as mononucleosis, often ends in recovery, with a generalized form, death is possible.

Treatment. A complex of medications is used depending on the organ affected.

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. In view of the immunosuppressive effect of the virus, immunostimulants are prescribed (decaris, sodium nucleinate, taktivin, etc.).

Prevention. For active prevention, the proposed live and killed vaccines have not received practical use. It is important to observe good personal hygiene when caring for a newborn.

It is advisable to examine all pregnant women for cytomegaly, as well as women who have had ARVI during pregnancy, newborns with jaundice or toxic-septic disease.

In order to prevent parenteral infection, it is advisable to use blood and its components only from seronegative donors or to transfuse washed erythrocytes, as well as blood freed from leukocytes. During organ transplantation, it is mandatory to examine donors for the presence of antibodies to cytomegalovirus and to prevent organ transplantation from seropositive individuals to seronegative recipients.

6. Epstein-Barr virus infection (infectious mononucleosis)

Infectious mononucleosis is an acute infectious disease caused by the Epstein-Barr virus from the herpetiform group, characterized by fever, tonsillitis, enlarged lymph nodes, liver and spleen, the appearance of atypical mononuclear cells in the peripheral blood and heterophilic antibodies.

Etiology. The virus is no different in its morphological structure from the herpes simplex virus. The virus was first discovered by electron microscopy of a cell culture of malignant Burkitt's lymphoma. The first cultures of the virus were obtained by Epstein and Barr. Until now, the virus could only be transferred to lymphocytes or lymphoblasts.

Now the virus can be cultivated in several types of epithelial cells.

Although the majority of atypical lymphocytes are T-lymphocytes, viral replication occurs only in B-lymphocytes.

After in vitro virus infection of lymphocytes, the latter acquired the ability to grow indefinitely. This is characteristic only of lymphocytes obtained from persons previously infected with the Epstein-Barr virus.

Epidemiology. EBV is ubiquitous. Infection occurs differently depending on age. When EBV enters a child’s body, it is most often not accompanied by any clinical symptoms or occurs as an acute respiratory infection (atypical form).

Infectious mononucleosis is considered a typical clinical manifestation of acute EBV infection.

In children of the first 3 years of life, the primary entry of EBV into the body often manifests itself as acute respiratory infections with the so-called mononucleosis-like syndrome.

When EBV first enters the body of older children, then in 45% of cases a typical clinical picture of infectious mononucleosis occurs.

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 unnoticed and gradually. The patient complains of weakness, fatigue, headaches, nausea, and sore throat. The prodromal period can last 1-2 weeks. Gradually, the sore throat intensifies, the body temperature rises, which forces the patient to 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 at 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.

Other clinical signs include eyelid swelling and rash. Maculopapular rash occurs in 3-15% of patients. Severe clinical symptoms persist for 2-4 weeks, after which the condition of patients gradually improves.

Weakness, fatigue and decreased performance persist for several months. Recurrence has not been serologically documented. The prognosis is good unless complications develop.

Severe forms of the disease, accompanied by severe clinical symptoms, are more common in children. Clinically, they may resemble diseases in adults, often manifesting as tonsillitis, fever of unknown origin, and unidentifiable respiratory diseases.

The younger the child, the less characteristic the symptoms that develop in him are, first of all, this refers to an increase in the liver, spleen and lymph nodes.

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. Some patients complain of weakness, fatigue, and fever for 1 year or more after infectious mononucleosis.

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) (in Africa and Asia) and nasopharyngeal carcinoma (mainly in the male population, in China).

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

Nasopharyngeal carcinoma is a malignant tumor of the nasopharynx.

Recently, an association of polyclonal B-cell lymphomas with Epstein-Barr virus has been found in immunocompromised patients. The DNA of this virus has been found in tumors and tumor cells. Such tumors were observed in patients with congenital and acquired immunodeficiency after organ transplantation. Primary B-cell lymphomas in the CNS may be associated with the Epstein-Barr virus.

Complications. The most serious complications include splenic rupture, which occurs mainly during the 2nd week of the disease; swelling of the tonsils and pharyngeal mucosa, which can cause blockage of the upper respiratory tract; meningitis with a predominance of mononuclear cells in the cerebrospinal fluid, transverse myelitis, paralysis, encephalitis and Guillain-Baré syndrome; sometimes patients have impaired perception of space and the size of objects (Alice in Wonderland syndrome); myocarditis and interstitial pneumonia; hemolytic anemia with a positive Coombs test and cold agglutination reaction with antigen i, specific for erythrocytes; thrombocytopenic purpura and aplastic anemia, which significantly complicate diagnosis; hepatitis, etc.

Diagnosis. The polymorphism of clinical manifestations and the involvement of the immune system in the pathological process force the diagnosis to be confirmed using laboratory research methods, in particular using serological diagnostic methods, which make it possible to identify heterophilic antibodies in the blood serum of patients in relation to the erythrocytes of various animals. Heterophilic antibodies in infectious mononucleosis belong to the class of immunoglobulins M.

Differential diagnosis. Infectious mononucleosis is differentiated:

1) with diphtheria of the oropharynx, accompanied by tonsillitis;

2) with acute respiratory viral infections, especially adenovirus etiology, when a mononucleosis-like syndrome can be expressed;

3) with acute leukemia, when infectious mononucleosis is accompanied by high leukocytosis and lymphocytosis;

4) with viral hepatitis, accompanied by jaundice.

Treatment. There is no specific treatment. Symptomatic and pathogenetic therapy is prescribed depending on the form of the disease. For all forms of the disease, antipyretics, desensitizing drugs, antiseptics to stop the local process, vitamin therapy are used as basic therapy; for functional changes in the liver, choleretic drugs are used. Antibacterial therapy is prescribed if there are significant deposits in the oropharynx or complications occur.

In severe cases, with a sharp increase in the lymphadenoid tissue of the nasopharynx and oropharynx, corticosteroids are prescribed.

For the treatment of protracted forms of the disease, it is advisable to prescribe immunocorrectors.

Prevention. Specific prevention of infectious mononucleosis has not been developed. Anti-epidemic measures are not being taken at the source of infection.

The patient in the acute period is isolated. Hospitalization for mild forms of the disease is optional.

Lecture number 15. Chlamydial infections

1. Chlamydia

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. Both infections occur predominantly in humans and are usually accompanied by local changes;

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

The causative agents of both groups differ in common antigens detected by the complement fixation reaction, but the immunofluorescence test is highly specific for each group and for individual pathogens.

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

Trachoma is commonly associated with overcrowding and unsanitary living conditions. Nonspecific non-gonococcal urethritis in almost 40% of cases due to chlamydial infection. Chlamydia also causes cervicitis, salpingitis, endometritis, and epididymitis. About 20-30% of infections occur in adolescents, some of whom do not feel any signs of the disease.

Acute salpingitis syndrome and perihepatitis, usually attributed to gonococcal infection, may be caused by chlamydia.

Some cases of Reiter's disease are caused by chlamydia. Occasionally, these microorganisms are the causative agents of endocarditis, otitis media, choroiditis, or erythema nodosum.

2. Chlamydial conjunctivitis and pneumonia in children

Clinical manifestations. Conjunctivitis usually begins in the 2nd week of life, less often developing 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, but can take a chronic course.

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

In children, chlamydia can cause a kind of pneumonic syndrome, which is detected at the age of 3-16 weeks.

Body temperature and general appearance remain within the normal range, but a cough appears, tachypnea, cyanosis, and vomiting develop.

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

Some children had concurrent infection with cytomegaloviruses.

Clinical symptoms do not differ from the clinic in chlamydial pneumonia.

Recovery occurs gradually without treatment, but some signs and positive culture results may persist for several weeks or even months.

Chronic cough, wheezing, and impaired lung function are more common in patients hospitalized for chlamydia-induced pneumonia (or bronchiolitis) than in controls with lesions of a different etiology.

Diagnosis and differential diagnosis. Clinically, a chlamydial infection can be suspected if a newborn consistently develops conjunctivitis with a long persistent course, bronchitis with bouts of painful coughing, small-focal pneumonia, as well as if eosinophilia and a significantly accelerated ESR are detected in 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.

Chlamydial conjunctivitis must be differentiated from conjunctival damage by silver nitrate, conjunctivitis caused by gonococci or other bacteria and viruses.

For differentiation, bacterioscopic, bacteriological and virological research methods are used. Pneumonia in children can be caused by a variety of bacteria and viruses.

Bacterial pneumonias are usually accompanied by high leukocytosis against the background of a reduced or unchanged number of eosinophils. Blood or sputum cultures often detect the pathogen.

Viruses can only be isolated using an appropriate shadow culture technique.

Treatment. For conjunctivitis, antibacterial drugs are prescribed in the form of an ointment; for pneumonia, erythromycin and other antibacterial drugs are prescribed in age-specific dosages.

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 to the source of infection, the route of transmission and the susceptible organism. Active prophylaxis has not been developed.

3. 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 often occurs in a latent form. The pathogen is excreted by birds in feces and respiratory secretions. The main transmission routes are airborne droplets and airborne dust. Children become infected 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 using anamnestic data on contact with sick birds at production or on 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 on the basis of a single determination of the complement fixation reaction with a titer of 1: 32 and above.

Treatment. Antibiotics are usually prescribed (erythromycin, sumamed, chloramphenicol, rulid in an age-specific 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.

4. 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. The causative agent, close to Chlamydia trachomatis, was classified as a virus in the past. It differs from the causative agent of trachoma in greater invasiveness, epithelial and lymphotropism.

Epidemiology. The disease occurs mainly in countries with tropical and subtropical climates; imported cases are possible in Russia.

Pathology. The primary lesion is an ulcer localized in the area of ​​the external genitalia. The most characteristic changes develop in the regional lymph nodes, which enlarge, fuse together, and then melt, resulting in the formation of abscesses of irregular shape.

Polymorphonuclear leukocytes and macrophages are found in their contents.

In chronic processes, rough scars and long-lasting fistulas are found.

Clinical manifestations. The incubation period is 3-30 days in cases where the end is considered to be a primary ulcer at the site of penetration of the pathogen (on the genitals, oral cavity, lips, tongue).

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.

In 2/3 of patients, lymphadenitis is unilateral. 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.

Sometimes swollen lymph nodes can shrink without proper treatment. Exacerbations of lymphadenitis are very frequent.

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

Laboratory research methods can detect hypergammaglobulinemia due to an increase in the level of IgA and IgG.

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.

Along with this, autoimmune disorders appear, a positive Coombs test is noted, an anticomplementary factor is isolated, and false positive results are obtained when conducting serological tests for syphilis.

Diagnosis and differential diagnosis. The disease is diagnosed based on the presence of a primary lesion, regional lymphadenitis in the groin area, and 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.

Inguinal lymphogranulomatosis is differentiated with felinosis, tularemia, plague, lymphadenopathy caused by pyogenic bacteria, soft chancre.

Treatment. Antibiotics of the erythromycin and tetracycline group, as well as chloramphenicol, etc., are effective. Sulfonamide drugs are prescribed for a period of 3-4 weeks. In case of pronounced scar changes and strictures, lidase is prescribed by electrophoresis to the affected area, injections of aloe, vitreous, etc. In severe cases, surgical treatment is resorted to.

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

Lecture No. 16. Tuberculosis

Etiology. Tuberculosis is caused by tuberculosis bacilli belonging to the Mycobacterium family, a group of actinomycetes. In humans, the leading role is played by M. tuberculosis, which is responsible for the majority of cases of the disease; M. bovis is the causative agent of tuberculosis in cattle and rabbits; M. avium causes disease in birds and white mice. All mycobacteria are nonmotile, aerobic, non-spore forming polymorphic rods. They are difficult to stain due to the high lipid content in their cell wall, but once they take on color, they are no longer discolored by alcohol and acids. A feature of Mycobacterium tuberculosis is its very slow growth on nutrient media (on average, a response is obtained after 21 days). 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 filterable particles and grains to giant branched forms, which affects their functional properties. Mycobacterium tuberculosis may develop resistance to all specific antibiotics and chemotherapy drugs, which prevents effective treatment of the disease.

Epidemiology. Tuberculosis is a relatively common disease; the main sources of infection in children are adults with active tuberculosis and cattle affected by tuberculosis.

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 reactions in tuberculosis are a complex set of interactions between the pathogen, special 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 immune responses begin to appear after live and pathogenic mycobacteria enter the body. Pulmonary macrophages phagocytose them, but are unable to destroy them. The pathogen continues to multiply in macrophages, and with them mycobacteria enter the regional lymph nodes. Subsequently, the infection spreads through hematogenous and lymphogenous routes 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 that have a certain influence on the development of the disease and its outcome;

2) age, which determines the severity of tuberculosis infection. Children under 3 years of age are most often prone to miliary tuberculosis and meningitis with a fatal outcome;

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. The appointment of immunosuppressive drugs, in particular corticosteroids, may contribute to the development of particularly severe forms of primary tuberculosis infection or the reactivation of a dormant infection.

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. ATK is a crude product obtained by sterilizing the filtrate of a culture on which tuberculous mycobacteria were grown. This drug is used only in a multiple skin prick test.

For all tuberculin skin tests, including the Mantoux test and the multiple puncture test, tuberculin PPD is preferred.

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 Apli-test is performed using tuberculin PPD with phenol.

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. In the latter case, it is necessary to exclude the possibility of allergy, for example, by conducting skin allergy tests to infectious mumps allergens (after vaccination) or to Candida antigens.

Questionable reactions to tuberculin are most often associated with infection with atypical mycobacteria, since tuberculin PPD contains antigens that are common with antigens of non-tuberculous mycobacteria. Cross-reactions are most often observed with the introduction of large doses of tuberculin (250 IU).

Under certain circumstances, an indurat of 5 to 10 mm can be interpreted as a dubious reaction and treatment can be prescribed. False-negative results of the Mantoux test 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 (due to infancy, severe diseases of any type, intercurrent infections of viral etiology, administration of an attenuated viral vaccine, immunosuppressive therapy, malnutrition, neoplastic processes, sarcoidosis, chronic renal failure) .

False-positive results of the Mantoux test can be observed with repeated injections of tuberculin PPD or ATK, as well as after BCG vaccination. BCG vaccination leads to positive tuberculin reactions, which are difficult to distinguish from reactions that occur with tuberculosis infection. 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.

Clinical forms of tuberculosis

1. Intrathoracic tuberculosis

Pathogenesis and pathomorphology. Primary infection most often develops after inhalation of live virulent tuberculous mycobacteria. The body of a non-immune child reacts to infection with certain cellular reactions. Pathogens are phagocytosed by macrophages, their further reproduction occurs in these cells, and macrophages carry 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. In contrast to the primary infection, reactivation, or, as it is also called, post-primary tuberculosis or "adult tuberculosis", occurs against the background of pronounced reactions of cellular immunity. Most often, it is localized and is accompanied by severe symptoms and tissue 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 x-rays and manifests itself only by changes in tuberculin tests. General symptoms can be mild and nonspecific, manifesting themselves as slight increases in temperature, loss of appetite, weight loss, and less commonly 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.

Diagnosis. Primary pulmonary tuberculosis is diagnosed in children during examination regarding the incidence of tuberculin tests. The diagnosis of tuberculosis requires bacteriological confirmation.

2. 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.

3. 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. Additional symptoms: malaise, weakness, weight loss. The development of caseous necrosis, its melting and emptying with the formation of cavities are manifested by a cough with sputum, often with a slight hemoptysis. 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. With an increase in infiltrative changes, lesions of the lobar length may occur. After melting and rejection of caseous necrosis, classical thin-walled cavities are formed, sometimes with a liquid level in them.

4. 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.

The differential diagnosis of tuberculous pleurisy should be carried out with pleural effusions due to heart failure, malignant neoplasms, malnutrition and metabolism, with collagen vascular lesions and parapneumonic nonspecific pleurisy due to other infections. Pleural effusion in tuberculous pleurisy is characterized by a significant specific gravity, high protein content, increased activity of lactate depidrogenase and adenosine deaminase, and low glucose levels. In a cytological examination, neutrophils can be detected in it in the early stages, lymphocytes predominate, mesothelial cells are usually absent. Mycobacterium tuberculosis in the pleural effusion with bacterioscopy usually cannot be detected, but when sowing exudate and pleural tissue, pathogens are detected in almost half of the cases. With repeated punctures and centrifugation of the removed fluid, the effectiveness of the seeding method increases. 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. Under normal conditions, nonspecific pleural effusion quickly resolves, thoracocentesis and drainage are not indicated.

5. 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 middle ear is accompanied by hearing loss, diffuse otorrhea, absence of pain and enlargement of the parotid lymph nodes. Often, there are violations of the facial nerve and signs of mastoiditis. Otoscopy reveals thickening of the tympanic membrane and its perforation in one or more places. Treatment of upper respiratory tract tuberculosis depends on the extent of the pulmonary lesion. Isoniazid and rifampicin are usually indicated for 18-24 months. Surgical interventions are indicated for the development of paralysis of the facial nerve, with mastoiditis and with subperiosteal abscesses.

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. The defeat of the axillary and inguinal lymph nodes is much less common and usually with the localization of the primary focus on the corresponding limbs.

Adenopathy sometimes develops as a result of hematogenous or lymphogenous dissemination of tuberculosis mycobacteria in the initial phase of primary tuberculosis infection before the development of specific immunity. In these cases, changes are found in the peripheral and deep groups of lymph nodes.

Tuberculosis of the peripheral lymph nodes is the most common of all extrapulmonary forms of tuberculosis, characterized by the localization of multiple, often bilateral lesions mainly in the neck.

Clinical manifestations. Tuberculosis of the lymph nodes usually begins gradually and unnoticeably. Only in children highly sensitive to tuberculosis infection is an acute onset of the disease with an increase in body temperature and the development of local signs of inflammation possible. The history often contains indications of contact with patients with active tuberculosis. Most children have positive tuberculin tests, and chest x-rays show signs of primary pulmonary tuberculosis. A significant increase in nodes and compression of neighboring organs is observed only in exceptional cases. Melting of enlarged surface nodes can lead to the spread of the process to surrounding tissues and the formation of external fistulas.

On palpation, the nodes are compacted, can be hard, not soldered to each other. Less often, when melted, they are soft and solder with surrounding tissues or with the skin. Sometimes fistulas are found.

Diagnosis and differential diagnosis. An accurate diagnosis is possible based on histological or microbiological examination. However, histological examination does not allow differentiating tuberculous lymphadenitis from lesions that occur when infected with atypical mycobacteria. Therefore, in all cases, it is advisable to send biopsy material for microbiological examination for inoculation on appropriate nutrient media.

Tuberculous lymphadenitis must be differentiated from non-tuberculous mycobacteriosis, diseases caused by viruses, fungi, toxoplasma, bacteria and the causative agent of cat scratch disease, as well as malignant lesions, sarcoidosis and reactions to certain drugs.

Treatment. Tuberculous lesions of the lymph nodes respond well to treatment with isoniazid and rifampicin or ethambutol, which are prescribed for a period of at least 18 months.

6. 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. The development of miliary tuberculosis is facilitated by the presence of chronic diseases, immunosuppressive therapy and AIDS.

Clinical manifestations. The onset of the disease in children can be acute. Body temperature rises, weakness, malaise, anorexia, and 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 in the form of shortness of breath, tachypnea, cough, and scattered wheezing in the lungs. With the development of meningitis, headaches, lethargy, and stiffness of the neck muscles occur. Metastatic skin lesions and the appearance of tuberculous tubercles in the fundus are rare symptoms of miliary tuberculosis.

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, increasing over a long time (weeks and months). As a rule, diffuse lymphadenopathy, enlargement of the liver and spleen are noted.

Diagnosis. Diagnostic methods are:

1) X-ray examination, in which diffuse widespread rashes of a characteristic type are determined in the lungs. But in the initial period of the disease, changes on radiographs are not yet visible, so the study should be repeated in case of the slightest suspicion of this disease;

2) cultures of blood, urine, gastric contents and cerebrospinal fluid in order to detect Mycobacterium tuberculosis;

3) transthoracic lung biopsy performed during bronchoscopy performed using fine-fiber optics in order to detect specific granulation tissue, sometimes with signs of caseous necrosis, as well as acid-fast bacilli.

Treatment. The use of isoniazid and rifampicin in combination with ethambutol or streptomycin is indicated. In severely ill patients with signs of respiratory failure and hypoxemia, corticosteroids are simultaneously recommended.

7. Tuberculous meningitis

Epidemiology. The incidence of tuberculous meningitis depends on the prevalence of tuberculosis in a given area. The disease most often develops within six months after infection with tuberculosis, so it is usually considered a childhood disease.

Pathophysiology and pathomorphology. Hematogenous generalization of infection, characteristic of this disease, leads to the formation of metastatic foci of tuberculosis infection. Solitary tuberculous foci (tuberculomas) can occur in the central nervous system; 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 body, primarily from the central nervous system. Soon a thick gelatinous effusion appears, lining the basal surface of the brain in a thick layer, as a result of which the cerebral arteries and veins are compressed, the cranial nerves are damaged, and the basal cisterns and interventricular foramina are obliterated.

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 and clinical examination, it is necessary to resort to a diagnostic spinal puncture, including counting cellular elements, determining the content of protein, sugar and chlorides, examining the cerebrospinal fluid for tuberculous mycobacteria, direct bacterioscopy using the flotation method or using cultures and infection of the guinea pig.

Treatment. It is recommended to prescribe isoniazid and rifampicin during the first 2 months of treatment with additionally prescribed streptomycin or ethambutol. Subsequently, treatment with isoniazid and rifampicin is continued for another 10 months.

Forecast. The outcome of tuberculous meningitis depends on the patient’s condition at the time of treatment. With treatment started in the 1st stage of the disease, cure occurs in all patients, and residual changes are minimal. Optimal results of treatment started in the 2nd stage of the disease are obtained in 85% of patients, and half of the survivors still have significant impairments. Treatment started in the 3rd stage of tuberculous meningitis saves the lives of only 50% of patients, and they usually remain severely disabled.

8. Tuberculoma of the central nervous system

Single or multiple tuberculomas can form at any stage of the course of tuberculosis infection and are manifested by symptoms of a slowly growing volumetric process in the brain. Headaches, increased intracranial pressure, visual disturbances are noted. On radiographs of the skull, signs of calcification in tuberculomas are occasionally found. Computed tomography in the early stages reveals contrasting shadows surrounded by an annular edema zone. In the anamnesis of sick children, there is usually information about contact with patients with active tuberculosis. Most of them also have tuberculous changes in the lungs in the form of hilar lymphadenopathy, infiltrative changes in the lower lobes, and pleurisy. Tuberculin reactions are positive.

Often, the diagnosis of brain tuberculoma is established only during surgery. Usually, treatment is carried out with three anti-tuberculosis drugs for 12-18 months. Corticosteroids are prescribed in the first weeks of treatment, mainly to reduce cerebral edema.

Chemotherapy for tuberculosis. Studies to determine the optimal duration of chemotherapy and the most effective anti-tuberculosis drugs in children show that simply transferring the principles of adult chemotherapy to pediatric practice can lead to “overtreatment” of children, since adults have to deal with a much larger bacterial population in cases of destructive tuberculosis.

In many cases, effective treatment of tuberculosis infection in children is possible on an outpatient basis. Hospitalization is recommended for:

1) the need for repeated cultures and biopsies to confirm the diagnosis;

2) severe, life-threatening processes to start treatment and select adequate therapy;

3) the selection of chemotherapy at the initial stage in infants and young children;

4) the need for surgery or corticosteroid therapy;

5) overcoming severe drug intolerance reactions;

6) concomitant diseases requiring inpatient treatment;

7) difficult domestic and social conditions that prevent adequate treatment at home.

In these cases, the transfer of a sick child to outpatient treatment can be carried out only after the establishment of therapy and the organization of subsequent monitoring of its implementation.

Anti-tuberculosis drugs. Isoniazid is the drug of choice for the treatment of all forms of tuberculosis; it is prescribed for all therapeutic regimens if the 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. The risk of hepatotoxicity is greatest when rifampicin is given concomitantly with isoniazid. In these cases, the dose of the latter drug is recommended to be reduced to 20 mg/kg. Intermittent treatment with rifampicin often results in thrombocytopenia, leukopenia, and a flu-like syndrome.

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. The use of ethambutol in young children is limited due to insufficient knowledge of its pharmacokinetics and difficulties in visual control at this age.

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.

The results of this action are ataxia, balance disorders and, less commonly, hearing loss.

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 of the pathogen against the background of its administration, the hepatotoxic effect - sometimes provokes the development of jaundice.

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. Side effects of ethionamide usually affect the gastrointestinal tract (such as nausea, vomiting, abdominal pain).

Monotherapy. Chemoprophylaxis with isoniazid is indicated for all practically healthy persons under 35 years of age with positive tuberculin tests, in whom no changes are detected on chest x-rays or where there are traces of previous tuberculosis. To prevent reactivation of the infection with the development of a general disease, such individuals are recommended to be treated for 12 months. Children at high risk of infection with isoniazid-resistant strains of the pathogen require careful follow-up along with isoniazid chemoprophylaxis. Preventive monotherapy with isoniazid can also be administered to children at high risk of tuberculosis. Treatment in such cases is prescribed even to children with a tuberculin-negative reaction. In usual practice, isoniazid is prescribed for 3 months and then tuberculin tests are repeated. If a turn occurs, treatment is continued for up to 12 months. If skin reactions to tuberculin remain negative, and the source of infection has already been eliminated during this time, then chemoprophylaxis is gradually completed. Lack of effect from chemoprophylaxis can be observed during infection with isoniazid-resistant strains of Mycobacterium tuberculosis.

Two- and three-drug treatment regimens. Most cases of tuberculosis in children respond well to treatment with a dual combination of anti-tuberculosis drugs. The most commonly used drugs are isoniazid and rifampicin, and less commonly, ethambutol. The duration of such therapy in children is 12 months. A triple combination of drugs (isoniazid, rifampicin and streptomycin) is indicated in the initial stages of treatment of children with the most severe, life-threatening forms of tuberculosis. In the presence of drug resistance to isoniazid, treatment is carried out with rifampicin, streptomycin and ethambutol.

Children with destructive bacillary forms of pulmonary tuberculosis stop excreting mycobacteria in sputum already 2 weeks after the start of treatment according to chemotherapy regimens with rifampicin. A longer period of isolation is necessary in cases where there is contact with healthy children or infection with resistant strains of the pathogen is suspected.

Prevention. Prevention of tuberculosis involves the following measures:

1) prevention of contact with patients with active forms of tuberculosis;

2) carrying out specific chemoprophylaxis;

3) BCG vaccination in high-risk groups;

4) general improvement of social and economic conditions.

The anti-tuberculosis vaccine is a preparation of live attenuated harmless mycobacteria of the BCG vaccine strain (Bacillus Calmette and Guerin) and is used as the most effective and economical intradermal method of vaccination. An important indicator of the quality and effectiveness of BCG vaccination is the post-vaccination reaction:

1) a local reaction during intradermal vaccination is characterized by the appearance of a small infiltrate with pink staining of the skin above it with a diameter of up to 12 mm. The infiltrate may look like a nodule with a cyanotic tinge; pustules - a slight enlightenment due to thinning of the skin over the infiltrate, which can dry out and resolve, or can be converted into a crust like smallpox; small ulceration with serous-purulent discharge, spontaneously healing. The described nature of the reactions is considered as normal, reflecting the individual reactivity of the organism. The reverse development of changes at the site of vaccination occurs within 2-4 months, less often - in longer periods. Superficial scars from 2 to 10 mm remain at the healing site;

2) post-vaccination allergy - an objective indicator of the immunological restructuring of the body under the influence of the BCG vaccine, develops in 50% of the Mantoux test.

Contraindications to vaccination of newborns: prematurity, intrauterine infection, purulent-septic diseases, hemolytic disease of the newborn, severe birth injuries with neurological symptoms, generalized skin lesions, acute diseases, generalized BCG infection in other family members.

Revaccination is contraindicated in children and adolescents infected with tuberculosis or who have had tuberculosis in the past, with a positive or questionable Mantoux test, who had complicated reactions to previous injections of the BCG vaccine, with malignant blood diseases and neoplasms, immunodeficiency conditions, treated with immunosuppressants, with acute diseases, with allergic diseases in the acute stage (vaccinated 1 month after recovery or remission on the conclusion of a specialist).

The frequency of post-vaccination complications is 0,02-0,03%.

Author: Muradova E.O.

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Artificial leather for touch emulation 15.04.2024

In a modern technology world where distance is becoming increasingly commonplace, maintaining connection and a sense of closeness is important. Recent developments in artificial skin by German scientists from Saarland University represent a new era in virtual interactions. German researchers from Saarland University have developed ultra-thin films that can transmit the sensation of touch over a distance. This cutting-edge technology provides new opportunities for virtual communication, especially for those who find themselves far from their loved ones. The ultra-thin films developed by the researchers, just 50 micrometers thick, can be integrated into textiles and worn like a second skin. These films act as sensors that recognize tactile signals from mom or dad, and as actuators that transmit these movements to the baby. Parents' touch to the fabric activates sensors that react to pressure and deform the ultra-thin film. This ... >>

Petgugu Global cat litter 15.04.2024

Taking care of pets can often be a challenge, especially when it comes to keeping your home clean. A new interesting solution from the Petgugu Global startup has been presented, which will make life easier for cat owners and help them keep their home perfectly clean and tidy. Startup Petgugu Global has unveiled a unique cat toilet that can automatically flush feces, keeping your home clean and fresh. This innovative device is equipped with various smart sensors that monitor your pet's toilet activity and activate to automatically clean after use. The device connects to the sewer system and ensures efficient waste removal without the need for intervention from the owner. Additionally, the toilet has a large flushable storage capacity, making it ideal for multi-cat households. The Petgugu cat litter bowl is designed for use with water-soluble litters and offers a range of additional ... >>

The attractiveness of caring men 14.04.2024

The stereotype that women prefer "bad boys" has long been widespread. However, recent research conducted by British scientists from Monash University offers a new perspective on this issue. They looked at how women responded to men's emotional responsibility and willingness to help others. The study's findings could change our understanding of what makes men attractive to women. A study conducted by scientists from Monash University leads to new findings about men's attractiveness to women. In the experiment, women were shown photographs of men with brief stories about their behavior in various situations, including their reaction to an encounter with a homeless person. Some of the men ignored the homeless man, while others helped him, such as buying him food. A study found that men who showed empathy and kindness were more attractive to women compared to men who showed empathy and kindness. ... >>

Random news from the Archive Robot waiter Servi 04.10.2020 Bear Robotics, a robotics and artificial intelligence company, and SoftBank Robotics Group, a leading robotics manufacturer and solution provider, have jointly unveiled a new robot. It is called Servi and is intended for the catering industry. According to the partners, Servi was designed to be the new go-to in the food service industry, assisting staff and improving the customer experience. It has already been tested in several institutions in the US, South Korea and Japan. Measuring 445 x 430 x 1046 mm and weighing 33 kg, the robot is designed for a payload of up to 30 kg. Without recharging, it works 8-12 hours. The robot can move around the hall, detecting obstacles and avoiding them, in particular, avoiding collisions with visitors. He is able to deliver orders and act as an assistant waiter, taking dirty dishes to the sink. The versatility of the robot is provided by interchangeable trays. Several robots can work simultaneously. As stated, the use of Servi allows you to increase the efficiency of the institution and the quality of customer service.

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