They are not typical for the generalized form of yersiniosis. Yersiniosis. Causes, symptoms, diagnosis and treatment of pathology. Intestinal yersiniosis and its prevention

Krasnoyarsk State Medical Academy

Department of Children's Infectious Diseases

YERSINIA INFECTION

IN CHILDREN

KRASNOYARSK 2000

UDC 616.98- 053.2- 036.22- 07.08

Compiled by: professor L.A. Gulman, associate professors G.P. Martynova, T.S. Krivshich, assistant G.K. Grigorov.

Reviewer: Associate Professor, Ph.D. E.F.Starykh

The problem of yersinia diseases remains quite relevant due to the widespread spread of this infection. Every year from 9 to 10 thousand patients are registered in Russia, of which 80-90% are children. For 1996 and 1997 The incidence rate among children was, respectively, 22.1 and 21.7 per 100 thousand child population. In the Krasnoyarsk Territory in 1998, the incidence rate of pseudotuberculosis was 23.3, and intestinal yersiniosis was 3.17 per 100 thousand children. It must be assumed that the given figures are not true, and we have an underdiagnosis of yersinia infection, since due to the relative “novelty” and polymorphism of clinical manifestations, there are certain difficulties in diagnosing sporadic cases of yersinia infection, especially in a clinic setting. Thus, of the observed patients with yersiniosis, only 20% were sent from the site with suspicion of this disease, and the rest were admitted with a variety of diagnoses: scarlet fever, rubella, measles, enteroviral exanthema, ARVI, meningococcal infection, viral hepatitis, and a diagnosis of yersiniosis infection. placed in the department. But mostly patients with severe and moderate variants of the disease are admitted to hospital treatment, while mild forms are treated in clinics under other diagnoses.

In addition to the underdiagnosis of yersiniosis, attention is drawn to the fact that among pediatricians and infectious disease specialists there is no uniform approach to the interpretation of cases of the disease and to the formulation of the diagnosis.

Considering the relevance of the problem of yersiniosis, the difficulty of diagnosis and the insufficient knowledge of pediatricians in this area, we have prepared these guidelines “Yersiniosis Infection in Children.”

They reflect epidemiological features, clinical characteristics, diagnosis of the disease, and provide approaches to the treatment of children with yersinia infection at the present stage.

Yersiniosis is a group of acute infectious diseases caused by microorganisms from the genus Yersinia and characterized by polymorphism of clinical manifestations, severity and tendency to develop exacerbations and relapses. When we say “yersiniosis,” we mean either pseudotuberculosis or the intestinal form of yersiniosis.

Etiology.

The genus Yersinia is included in the Enterobacteriaceae family. This genus includes the causative agents of plague (Iersinia pestis), the causative agent of pseudotuberculosis (Iersinia pseudotuberculosis) and intestinal yersiniosis (Iersinia enterocolitica). These are Gram-negative rods that do not form spores and capsules, persist and accumulate for a long time at temperatures from 4 to 18 o C and above, survive with minimal amounts of nutrients in a humid environment, which ensures their long-term existence outside a living organism, especially on food. Microbes survive in water for up to 8 months, in oil for up to 5 months, and in soil for up to a year. At the same time, the pathogen quickly dies when it dries out, is exposed to sunlight, chloramine, alcohol, or boils.

There are 8 known serological groups of Iersinia pseudotuberculosis. In humans, the disease is most often caused by serogroups I, III, IV. From the Iersinia enterocolitica group, the disease in humans is caused by serovars 05,09,03,06. Yersinia have pronounced invasive properties, which often leads to generalization of the infection, and they secrete endotoxin, which causes severe symptoms of intoxication.

Epidemiology.

Yersinia diseases are common throughout the world and in Russia. Incidence rates are ambiguous and range from 4000 per 100 thousand population (Chukotka) to 4 - 20.0 per 100 thousand population (St. Petersburg). Pseudotuberculosis is more often recorded than intestinal yersiniosis. In the Krasnoyarsk Territory in 1997, there were 10 cases of pseudotuberculosis per case of intestinal yersiniosis; in 1998, there were 1 to 7.5 cases. Among patients with yersiniosis, 82% are children. Children of school age are most often affected (70%).

The disease is recorded both in the form of sporadic cases and in the form of group outbreaks. In the region in 1998, there were 3 outbreaks involving children from 19 to 43 people.

Yersiniosis affects humans, as well as more than 60 species of mammals and 29 species of birds. But the main reservoir of the pathogen is house and field mice, rats. Animals and rodents, releasing the pathogen into the external environment with feces and urine, infect water, soil, plants, and food products. Human infection occurs through consumption of infected fruits and vegetables (cabbage, carrots, radishes, beets, onions, potatoes), milk, dairy products (cottage cheese, sour cream, cheeses, butter, ice cream), as well as through consumption of meat and baked goods. The main route of infection is the nutritional route. A waterborne route of infection is also possible if unboiled water is used for drinking, especially from open water bodies. M.O. Gasparyan (1993) describes family and nosocomial outbreaks of intestinal yersiniosis with contact-household transmission of infection.

Pathogenesis

Infection with yersiniosis occurs through the mouth. At the site of the entrance gate, a local inflammatory process develops in the form of tonsilopharyngitis and cervical lymphadenitis. Overcoming the gastric barrier, the pathogen enters the small intestine, penetrates into enterocytes, and enteritis can develop (enteric phase of the disease). From the intestine, microbes penetrate through the lymphatic gaps into the regional lymph nodes, and mesadenitis develops (phase of regional infection). When the immunobiological reactivity of the body decreases, Yersinia enters the blood, resulting in bacteremia and toxinemia. The generalization of infection is facilitated by the pronounced invasive properties of the pathogen. First of all, organs and systems rich in reticuloendothelial tissue are affected: liver, spleen, lymph nodes, lungs (parenchymal phase). Toxins and metabolic products of microbes cause symptoms of intoxication. In the pathogenesis of yersiniosis, especially in the development of exacerbations and relapses, great importance is attached to the allergic component and autoimmune processes. Allergic manifestations of the disease include exanthema, erythema nodosum, arthritis, and arthralgia.

Clinic.

The clinic of yersiniosis is characterized by polymorphism of clinical manifestations. Over the past 2 years, we have observed 34 children with yersinia infection. In 20 children (59%) the diagnosis was confirmed serologically, in 14 (41%) it was made on the basis of clinical and epidemiological data. Among children with serological confirmation, 13 were diagnosed with pseudotuberculosis and 7 were diagnosed with intestinal yersiniosis. The patients were distributed by age as follows: 7 children were aged from 3 to 7 years, the rest were of school age, and among them children aged 11-14 predominated.

Clinical symptoms in serologically confirmed cases of pseudotuberculosis and intestinal yersiniosis were absolutely identical, with the exception of intestinal syndrome, which was most common in patients with intestinal yersiniosis. Therefore, we considered it possible to characterize clinical symptoms in general during yersinia infection.

Yersinia infection is characterized by an acute onset of the disease, followed by an increase in clinical symptoms over 5-7 days.

The first symptom in all patients is promotion temperatures s, usually up to high numbers. Every 3 children (35% of patients) had a temperature above 39 0 C, often reaching 40 0 ​​C, in 40% the temperature fluctuated at 38-39 0 C, and only 25% of patients had a moderate increase in temperature (37.5- 38 0 C). The duration of fever in 12 children was 3-7 days, in 12 patients - 8-10 days, in 2 patients, low-grade fever persisted for 4-6 weeks after high fever.

From the very first days the disease developed symptoms of intoxication: headache, weakness, many children complained of dizziness, sleep disturbances, lack of appetite. Almost half of the children had nausea and vomiting. In 5 cases there was repeated vomiting, in 2 children vomiting was observed for 7 days.

The second most common symptom after fever was rash. It was noted in 94% of patients. Most often, it developed on days 2-3 of illness (25 children); on the first day, the rash appeared in only 5 patients, and in 2 cases a late rash was noted - on days 5-6 of illness. The rash was, as a rule, abundant and polymorphic: a pinpoint rash predominated, but in these same patients elements of a small and confluent maculopapular rash were noted. A confluent large maculopapular rash or continuous erythema was located around the ankle, knee, wrist joints, on the face, feet and palms. Symptoms of “hood”, “gloves” and “socks” were noted by us in 60% of patients. Almost 2/3 of the patients had minor diapedetic hemorrhages. The skin was dry, every 4 children had subicteric skin and sclera.

Yersiniosis is characterized by language changes in the dynamics of the disease. When patients were admitted in the early stages, the tongue was dry with a gray or white coating; on the 6-7th day of illness it became brightly papillary. In 70% of cases there was widespread hyperemia of the oropharyngeal mucosa, granularity of the arches, tonsils, small uvula and tuberosity of the posterior pharyngeal wall. Severe catarrhal symptoms with an exudative component are not typical for yersinia infection, i.e. Coughing, sneezing, and nasal discharge were absent in the patients; sore throat rarely developed (in 2 cases lacunar, in 1 patient follicular and in 1 necrotic).

Quite often (in 2/3 patients) it was detected enlarged peripheral lymph nodes, mainly cervical (up to 1.5 cm), less often - other groups.

Almost all children (84%) had severe symptoms scleritis, it usually persisted until the 7-10th day of illness; conjunctivitis was less common. The children complained of pain, pain in the eyes, and photophobia.

Hepatomegaly detected in 80% of patients with yersiniosis. The liver usually enlarged by the 4th-5th day of illness and was 2-2.5 cm higher than the age norm. Only in 2 cases the liver was enlarged by 4-5 cm. In 2/3 patients, the liver size returned to normal after 2 weeks of illness, but in 37% of cases the patients were discharged from the hospital with an enlarged liver. Somewhat less frequently (40%) minor enlarged spleen up to 1-1.5 cm.

Along with hepatosplenomegaly and abdominal pain, 7 patients (20%) had loose stool. Moreover, with intestinal yersiniosis, 3 out of 7 patients (43%) had loose stools, and with pseudotuberculosis - 3 times less often (15%). The frequency of stool did not exceed 3-5 times a day, its character was enteritic or enterocolitis, the duration of dysfunction was usually 2-3 days, and only in one case did the stool return to normal after 8 days.

In 12 patients (35%) it was noted joint damage. Moreover, more often these were arthralgia, characterized by pain in the joints and limitation of movements. Pain usually appeared on days 3-5 of illness and persisted for several days. The highest frequency of pain was observed in the ankle joints and small joints of the feet and fingers. 5 children developed polyarthritis, with sequential damage to several joints in different combinations (knees, ankle joints of the feet, wrists, joints of the hand and fingers.). Polyarthritis most often developed in the 2nd week and was characterized by severe pain at rest and during movement, swelling in the joint area, limitation of movement, and sometimes slight hyperemia of the skin. Symptoms of polyarthritis persisted for 7-10 days. If polyarthritis persists for a longer period of time and there is no positive effect on adequate treatment, then it is necessary to remember that yersinia infection can be a trigger for the development of juvenile rheumatoid arthritis or the onset of collagenosis masquerading as yersinia infection.

According to A.V. Gordiets et al., 92% of patients with yersinia infection have signs damage to the cardiovascular system(pallor, cyanosis, tachycardia, bradycardia, rhythm disturbance, muffled tones, systolic murmur). The ECG reveals a dysfunction of automaticity, a decrease in the voltage of the P and T waves. Toxic damage to the myocardium develops more often and less often (7%) infectious-allergic myocarditis.

Among the patients we observed nervous system damage was manifested mainly by symptoms of neurotoxicosis and only one patient developed meningoencephalic syndrome. However, in the literature there is a description of 29 cases of meningitis and meningoencephalitis of yersiniotic etiology (Pilipenko V.V. 1993), and the author notes that with pseudotuberculosis, symptoms of neurotoxicosis often develop, and with intestinal yersiniosis, general cerebral, meningeal, focal symptoms occur, with high cerebrospinal fluid pressure, moderate lymphocytic pleocytosis, protein-cell dissociation, slow sanitation of the cerebrospinal fluid (by 28-34 days of illness).

Classification.

A large number of classifications of pseudotuberculosis and intestinal yersiniosis have been proposed, based on the identification of the leading symptom of the disease (scarlatiniform, arthralgic, abdominal, icteric, generalized, septic, etc.), Drozdov V.N (1991), Gasparyan M.O (1992). , Uchaikin V.F. (1997) formed the opinion that in the classification of yersinia infection the principle of A.A. Koltypin should be used, i.e. determine the type, severity and course of the disease. We completely agree with this opinion, since 80-85% of patients have combined damage to organs and systems and it is difficult to identify the leading syndrome.

Typical shapes Yersinia infection is characterized by the presence of classic symptoms of the disease in various combinations: fever, scleritis, lesions of the oropharynx, rash, symptoms of “socks”, “gloves”, “hood”, enlarged liver, spleen, abdominal pain, etc. loose stools, arthralgia, arthritis.

Typical forms are distinguished by severity: light, medium-heavy and heavy. Severity is determined by the severity and duration of leading symptoms, their totality, and the nature of changes in general blood and urine tests.

Atypical forms(erased and subclinical) can be diagnosed only in foci of infection with serological and bacteriological confirmation.

Among the patients we hospitalized, 10% were diagnosed with a mild form of the disease, 60% with a moderate form, and 20% with a severe form. In 10% of cases, the form of severity is not determined due to late hospitalization of patients.

Based on duration, it is necessary to distinguish between acute, protracted, and chronic course. Moreover, according to the literature, there are discrepancies in determining the duration of the course: V.I. Pokrovsky (1996) considers up to 3 months. -acute course, from 3 to 6 months -protracted course, and more than 6 months -chronic course. We are more impressed by the definition of M.O. Gasparyan et al., who consider an acute course to be up to 1 month, a prolonged course to be more than one month. Having accepted this definition, in 2 cases we could talk about a protracted course of yersinia infection.

The nature of the course can be smooth, with exacerbations, with relapses and with complications. We observed an unsmooth course in 9 patients (27%). Moreover, 6 patients developed exacerbations on days 11-18 against the background of subsiding of the clinical symptoms of the disease, and 3 children had relapses on days 25, 28, and 30 of illness. During the period of exacerbation of the relapse, all patients had a fever again, symptoms of intoxication, pinpoint rash, erythema nodosum and an increase in liver size appeared. Moreover, if in previous years exacerbations and relapses were more severe than the height of the disease, now they look less bright than the onset of the disease.

Gordiets A.V. notes a large percentage of residual effects (in the form of asthenovegetative syndrome, arthralgia, abdominal pain, enlarged liver), especially after pseudotuberculosis and less often in patients with intestinal yersiniosis. Moreover, the percentage of residual effects depends on the severity of the disease. In children who had a mild form of pseudotuberculosis, after a month residual effects were noted in 26%, with a moderate form in 62.% and in a severe form in 78.% of patients.

Diagnostics.

Yersinia infection has clearly defined, manifest signs of the disease, the presence of which allows one to suspect the diagnosis of the disease.

Clinical diagnostic criteria.

High prolonged fever

Increasing symptoms of intoxication

The appearance of a polymorphic, but predominantly pinpoint rash with elements of a maculopapular rash, as well as a diapedetic rash; nested location of the rash, a symptom of “socks”, “gloves”, “hood”.

The appearance of the rash most often occurs on the 2-3rd day of illness.

Hyperemia of the oropharynx and an increase in lymphoid formations, i.e. tuberosity of the posterior pharyngeal wall, granularity of the soft palate, tonsils, and small uvula.

Persistent increase in the size of the liver, less often - the spleen

Joint damage in the form of arthralgia or polyarthritis

There may be abdominal pain and loose stools.

Dry, coated tongue, then papillary or “crimson”

Enlarged peripheral lymph nodes

Considering the combination of the above symptoms, the diagnosis of typical forms of yersinia infection can be made already at the site. Infectious disease doctors today have a fairly good command of clinical diagnostics, therefore, in more than half of patients, a preliminary diagnosis of yersinia infection is made in the emergency room. In the first 2-3, the doctor must determine the type and severity of the disease, then try to decipher whether it is pseudotuberculosis or intestinal yersiniosis. Laboratory examination is used to confirm and etiologically decipher the diagnosis.

Laboratory diagnostics

Includes bacteriological studies and determination of specific antibodies (RSK, RA, RPGA, RNGA) and antigen using ELISA, coagglutination reactions, latex agglutination reactions, as well as determination of specific immunoglobulins. Promising methods for diagnosing yersiniosis are: polymerase chain reaction (PCR), protein immunoblotting. In addition to specific studies, a general blood and urine test is performed, if necessary, a lumbar puncture is performed, and biochemical studies of liver function.

A bacteriological examination of feces, urine, cerebrospinal fluid (if necessary) and blood is carried out in generalized forms, rinsing from the throat, swab swab from the back wall of the pharynx and the root of the tongue in the first 3 days of the disease. It should be emphasized that these studies are very labor-intensive and have little impact.

More diagnostically significant are serological research methods based on the detection of specific antibodies in the agglutination reaction or hemagglutination reaction with erythrocyte diagnosticums. Paired sera are examined: the first blood draw is carried out at the end of the first week, repeated after 7-10 days. Antibodies with a titer of 1:200 or higher are considered diagnostic.

According to literature data, bacteriological research methods confirm the diagnosis in 16-20% of cases, and serological methods in 50-60%. Those. the percentage of bacteriological and serological confirmation is low. This is explained by the fact that the RPGA does not use diagnostics of all Yersinia biovars that can cause human disease. The ELISA method has the greatest information content (90%).

Among the patients we observed, the diagnosis of yersinia infection was confirmed in 59% of cases, and pseudotuberculosis was diagnosed 2 times more often than intestinal yersiniosis (in 13 and 7 patients). Maximum antibody titers ranged from 1:200 (7), 1:400 (6), 1:800 (5) and 1:1600 (2).

In 14 cases, despite repeated examination, the results of RPGA were negative. However, the characteristic clinical picture of the disease and epidemiological data made it possible to make a diagnosis: “Yersinia infection, typical, moderate or severe form.” We draw your attention to the fact that if the diagnosis is not confirmed serologically or bacteriologically, then a general diagnosis of “Yersiniosis infection” should be made, without specifying whether it is pseudotuberculosis or intestinal yersiniosis. If there is serological confirmation, then in the etiological decoding of the diagnosis we are guided by the results of serology.

In foci of infection, infection with two pathogens of Yersinia (pseudotuberculosis and enterocolitica) is possible, if this is confirmed by an increase in the titer of antibodies to both pathogens in paired sera, in these cases the diagnosis should be made: "Yersinia infection, combined form (pseudotuberculosis + intestinal yersiniosis), typical severe or moderate form. If, during the first study, the RPHA is positive in a titer of 1:200 with the diagnosticum of pseudotuberculosis and Yersinia enterocolitica, and subsequently an increase in the titer of antibodies to the diagnosticum of pseudotuberculosis is noted, then a diagnosis should be made: “pseudotuberculosis, typical, moderate or severe,” and if If an increase in the titer of antibodies to Yersinia enterocolitica is noted, but the titer to Yersinia pseudotuberculosis remains the same, then a diagnosis of “Intestinal Yersiniosis, typical, moderate, severe” is made. And both positive tests during the first study are regarded as a manifestation of group agglutination.

From a general blood test, the following changes are characteristic of yersiniosis: leukocytosis occurred in 82% of patients (28), while in 12 children the number of leukocytes ranged from 10 to 17x10 9 \l. In 85%, neutrophilia was noted up to 70-80% and in 56% band shift, including in 9 children the number of band shifts reached 18-50%. Almost all children have an accelerated ESR, in half of the cases from 30 to 50 mm/hour. Changes in the general blood test were persistent. In 10 children they persisted for 3-4 weeks, and 1/3 of the patients were discharged with accelerated ESR and neutrophilia.

Much less frequently (in 1/5 of the patients) changes in urine were detected, in the form of a moderate increase in protein from 50 to 209 mg/l, an increase in the number of leukocytes and erythrocytes. These violations lasted no more than a week.

Treatment.

Complex treatment is carried out taking into account the severity of the leading syndromes, the phase of the disease, and the premorbid background.

Treatment can be done at home or in an infectious diseases hospital.

Indications for hospitalization:

Severe forms of the disease

Combined yersinia infection

Recurrent forms

Moderate forms in young children

Unsatisfactory social conditions

All patients are prescribed bed rest until the temperature normalizes and their general condition improves.

Food: steamed or pureed, depending on whether or not there is damage to the gastrointestinal tract, liver, or kidneys.

Etiotropic treatment should be carried out for all patients, because prevents the generalization of infection, the development of relapses and chronic forms of the disease.

For mild forms, furazolidone or ampicillin is prescribed orally for 6-7 days. For moderate forms, chloramphenicol or ampicillin orally or parenterally is recommended for 7-8 days.

For patients with severe forms of yersinia infection, it is advisable to prescribe sodium chloramphenicol succinate at the rate of 60-80 mg/kg per day in 2-4 injections intravenously, and on the first day it is better to administer the antibiotic intravenously. Gentamicin (4 mg/kg per day IV or IM) or ampicillin (100 mg/kg per day in 4 doses IM) is effective. 3rd generation cephalosporins are also used.

Sometimes it is necessary to prescribe 2 antibiotics. The duration of antibiotic treatment for severe variants of the disease is at least 10-15 days. In addition to etiotropic and detoxification therapy, patients with yersinia infection are prescribed desensitizing drugs and oral vitamins.

In severe forms, for the purpose of detoxification, to restore hemodynamics and eliminate metabolic disorders, intravenous drips of plasma-substituting, glucose-salt solutions (about 50 ml/kg of patient weight) are carried out; proteolysis inhibitors (contrikal, gordox), vascular drugs (trental, Cavinton, Actovegin), vitamins (cocarboxylase, ascorbic acid).

GCS are prescribed in a short course (5-7 days) mainly for severe damage to the musculoskeletal system, myocarditis. In addition, in case of joint damage, non-steroidal anti-inflammatory drugs should be used - indomethacin, methindol, voltaren, brufen, diclofenac.

Also, patients with severe forms of yersinia infection should receive desensitizing drugs.

When the symptoms of intoxication subside, vitamins "A", "E", and "B" complex are prescribed.

Patients should be discharged from the hospital after the disappearance of clinical symptoms and normalization of peripheral blood counts and no earlier than 3-4 days after discontinuation of antibiotics. The average length of hospital stay is 3 weeks.

Dispensary observation.

All patients who have had yersiniosis are observed at the site for 3 months due to the possibility of relapses. Convalescents are also exempt from physical education and physical activity for 3 months. The duration of dispensary observation is individual, and can be extended to a year in case of development of myocarditis, meningitis or polyarthritis.

Yersiniosis I Yersiniosis

infectious, characterized by damage to the gastrointestinal tract, joints, skin and other organs and systems, often with an undulating course with exacerbations and relapses.

More often recorded in areas with temperate climates.

Etiology. The causative agent is a gram-negative motile with rounded ends, belonging to the genus Yersinia, which does not form spores or capsules. Based on their biochemical properties, there are 5 biovars. Based on their antigenic structure, 34 serovars are distinguished; in humans they are caused by serovars 03, 09, 06, 05, 27, 08, 30.

Yersinia has an antigenic relationship with Salmonella, Shigella, Escherichia, Protea, as well as with Vibrio cholerae, the causative agents of tularemia and brucellosis. Growth is optimal at 22-28°, but they can also reproduce at much lower temperatures (for example, in a household refrigerator). Yersinias die when dried out, exposed to sunlight and various chemicals (sublimate, chloramine, hydrogen peroxide, alcohol), and when boiled.

Epidemiology. I. refers to zoonoses. The source of the infectious agent is various wild animals (pigs, cows, dogs, cats), birds (mice, rats, etc.), as well as bacteria carriers.

Group diseases are more often associated with the consumption of vegetables and various vegetable salads (especially cabbage). In addition to food, water transmission is also possible. Family and nosocomial outbreaks of I. have been described, with the source being patients or bacteria carriers from hospital staff or parents caring for children. In these cases, the disease is transmitted through household contact.

Most people who get sick are residents of cities and urban-type settlements, where they often use public catering establishments and consume vegetables and fruits stored in vegetable stores. People of all ages get sick, but more often children 1-3 years old. I. is recorded throughout the year, increasing slightly in October - November.

Pathogenesis. Those that enter a person with food or water partially die in the acidic environment of the stomach, the rest penetrate further into the stomach. The main one develops in the distal small intestine. With sufficient virulence and a sufficient number of pathogens, it is possible for them to penetrate through the lymphatic vessels into the mesenteric vessels and develop mesenteric lymphadenitis. In these cases, I. occurs in the gastrointestinal or abdominal form. With high virulence of Yersinia and a decrease in the immunological reactivity of the body, it develops, clinically manifested by generalization of the infection. The pathogen also penetrates organs and tissues rich in lymphoid elements and fixed macrophages (spleen, lymph nodes). In the case of incomplete phagocytosis, Yersinia persists in the body for a long time, causing new foci of inflammation, from which they re-enter the body. As a result, a secondary focal form may develop with damage to any organ (heart, liver, joints, lungs) or exacerbations and relapses may occur. In the pathogenesis of I. (especially the secondary focal form, exacerbation and relapse), the allergic component and autoimmune processes are of great importance, which is clinically manifested by exanthema, eosinophilia, arthralgia and arthritis.

Pathological anatomy. In deceased I., signs of catarrhal-desquamative or catarrhal-ulcerative lesions are revealed in the gastrointestinal tract; there is an enlargement of the liver and spleen, in which small necrotic nodules are often found. Mesenteric and peripheral lymph nodes are enlarged.

Immunity insufficiently studied. It is known that the acute period is characterized by a decrease in the absolute number of T-lymphocytes and an increase in B-lymphocytes. With a full immune response, there is a gradual increase in the number of T-lymphocytes with their normalization in the period of convalescence. A low level of T-lymphocytes serves as an unfavorable prognostic sign, indicating the possibility of relapse or the transition of the process to a chronic form. In patients with a prolonged course of I., a decrease in the number of T-suppressors was detected. At the 1-2nd week of the disease, specific symptoms appear, the maximum level of which is observed at the 3-4th week of the disease.

Clinical picture. Incubation period from 15 h up to 15 days. The following clinical forms of I. are distinguished: gastrointestinal, abdominal, generalized and secondary focal. All forms of I. have some common clinical signs: acute onset, intoxication, abdominal pain, stool disorder, skin pain, joint and muscle pain, enlargement of peripheral lymph nodes and liver, a tendency to an undulating course with exacerbations and relapses. can be acute (up to 3 months), protracted (up to 6 months), chronic (6 months - 1 1/2 -2 years).

Gastrointestinal form is predominant in adults. The onset is usually acute, in some cases subacute or gradual. Symptoms of gastrointestinal tract damage and signs of intoxication appear. Patients are bothered by abdominal pain of varying intensity, periodic or cramping, localized in the epigastric region or around the navel, and repeated bloating is noted. Stools from 4-5 to 15-20 times a day, stools are liquid, foul-smelling, sometimes mixed with mucus and blood. False urges are possible. Dehydration may develop. , manifested by chills, fever, headache, dizziness, weakness, sweating, loss of appetite, aching muscles and bones, precedes symptoms of damage to the gastrointestinal tract or occurs several hours after the onset of the disease. In some cases, mild catarrhal phenomena are observed (small or sore throat, rare dry throat, hoarseness of voice), which precede gastrointestinal disorders, and sometimes persist against their background.

On examination, a local lesion is often detected in the right iliac region; in almost half of the patients, liver enlargement is detected already from the first days of the disease. There is either pallor of the facial skin, sometimes subicterus, conjunctival hyperemia; in some cases - hyperemia of the mucous membrane of the oral cavity and pharynx, spotted on the soft palate, rarely polyadenopathy. in the first days it is coated, by the 5-6th day it becomes clean, with a “raspberry” tip. The pulse rate corresponds to an increase in body temperature and decreases only with significant dehydration or severe intoxication.

The course of this form of I. is usually mild or moderate. The temperature normalizes by the 4-5th day of illness, clinical symptoms occur in most cases by the end of the 1st week. Rarely, the disease occurs in waves and the duration increases to 3-4 weeks. Exacerbations and relapses are rare. A mild course without intoxication, with normal or subfebrile temperature, with minor, short-term abdominal pain or without pain is possible; stool 2-3 times a day, bowel movements may be pasty. A very severe course with severe intoxication, temperature up to 40°, and severe dehydration is rare.

Abdominal form(appendicular, pseudoappendicular) form is more often observed in children. Initial manifestations may be the same as with the gastrointestinal form: fever, intoxication, moderate abdominal pain, nausea, vomiting, frequent loose stools, and sometimes catarrhal symptoms. After 1-3 days, vomiting stops, but pain appears (or intensifies) in the right abdominal region or around the navel. may begin with the occurrence of severe abdominal pain without a specific localization, which in a period of several hours to 1-2 days is localized in the right iliac region. On palpation of the abdomen, in addition to sharp pain in the ileocecal angle, muscle tension and other symptoms of peritoneal irritation are revealed. In children, it is sometimes possible to palpate painful, enlarged mesenteric lymph nodes. Blood tests reveal. With the described clinical picture, acute is often diagnosed. In half of the patients with the abdominal form, it is noted on the skin, sometimes the peripheral lymph nodes become enlarged, pain in the muscles and joints appears, and the liver becomes enlarged. The duration of this form is usually 3-4 weeks, the disease usually ends with recovery.

Abdominal and gastrointestinal forms of I. can become generalized.

Generalized form begins acutely, in some cases gradually. The most common early manifestations of the disease are chills or headache, pain when moving the eyeballs, weakness, loss of appetite, muscle aches, fever combined with catarrhal symptoms (sore throat, nasal congestion, dry cough). After a few days (sometimes from the 1st day), pain appears in the epigastric region or around the navel, sometimes in the right hypochondrium and nausea. In half of the patients, stools become more frequent up to 2-3 times a day, stools are mushy or liquid, without impurities; Vomiting is less common (1-2 times a day). Characterized by aversion to food, unpleasant taste, bitterness and dry mouth, loss of taste. The height of the disease in this form usually occurs by the 3-4th day of illness, sometimes later. The temperature can rise to 39-40°, chills recur, headaches and other symptoms of intoxication intensify. The temperature curve most often has a wave-like, less often constant or. The duration of the febrile period varies widely: from 2 days to 7 months, in most patients it does not exceed 2 weeks.

One of the most common symptoms in the generalized form of I. is a rash. Most often, skin rashes appear on the 2-3rd day from the onset of the disease, but are possible within a few hours to the end of the 2nd week. They are located on the chest, stomach, back, arms and legs; A rash on the palms and soles is typical, while patients feel a burning sensation (sometimes regardless of the presence of a rash), swelling and hyperemia of the skin occur. Often the rashes are localized on the face and can be grouped around the knee, elbow, ankle, and shoulder joints. Almost half of the patients have mild skin. By nature, the rash is most often small-spotted, less often small- and large-spotted, sometimes papular, petechial, urticarial, such as erythema nodosum, polymorphic. Individual elements of the rash may merge into continuous erythema. The duration of the rash is most often 1-4 days, but the rash may be ephemeral or persist for 1-2 weeks. Possible rashes occur at different stages of the disease, and the nature and location of the rash may be different each time. From the 12-15th day of illness, large and small lamellar skin of the fingers and toes or pityriasis-like peeling of the skin of the face, thighs, and shoulders usually begins.

The second most common symptom is joint pain. Typically, arthralgia develops on the 3-4th day of the onset of the disease, sometimes after 2-4 weeks. Affects the knees, shoulders, ankles, wrists, and interphalangeal joints. Pain occurs in several joints at once. The intensity of arthralgia is from weak to moderate, the duration is from several days to 1-2 months, they are characterized by their undulation. It is possible, especially in small joints, that pain of varying intensity appears in the muscles of the back, legs, neck, heels and soles when walking.

When examining patients in the initial period, they reveal hyperemia of the skin of the face and neck, injection of the sclera, hyperemia of the conjunctiva, sometimes spotted enanthema on the soft palate, from the 3-4th day of illness - “crimson”. In some patients, peripheral lymph nodes enlarge and become painful, more often anterior and posterior cervical, submandibular, less often axillary and inguinal, and possibly enlarged tonsils. Dry sounds are often heard in the lungs. There are stabbing pains in the heart area (even at normal temperature), and changes indicating dystrophic changes in the myocardium, infectious cardiopathy, and in rare cases myocarditis. In the vast majority of patients, from the 3-6th day of illness, the liver, less often the spleen, enlarges. On palpation of the abdomen, 1/3 of patients experience pain and rumbling in the ileocecal area. Sometimes patients notice cramps and pain when urinating, which becomes more frequent. At the height of the disease, vision may deteriorate due to the development of uveitis and iridocyclitis. Various vegetative disorders are characteristic: severe, feeling of heat, coldness of the hands and feet, paresthesia, blood pressure and pulse rate, dizziness; and they usually occur at the beginning of convalescence. Some patients lose weight up to 5-10 kg even with a short course of the disease. The period of convalescence is long, weakness, decreased performance, vegetative-vascular, sleep disturbances, pain in the joints, muscles, and heart area persist for a long time.

In some cases, a septic variant of the generalized form of yersiniosis is observed. It usually develops in individuals with various concomitant diseases (diabetes mellitus, liver cirrhosis, tuberculosis, chronic alcoholism, blood diseases, endocrinopathies) and immunodeficiency conditions (congenital or acquired). Characterized by a severe, long-term acyclic (2 1/2 -6 months and longer) course with high (40° and above) hectic-type fever, severe intoxication, stunning chills, profuse sweats, hepatosplenomegaly, jaundice, severe abdominal pain, profuse ( often hemorrhagic rash, polyarthritis, myocarditis, pneumonia, pyelonephritis. The syndrome is usually detected, and in some cases, focal symptoms of damage to the central nervous system, which indicates the development of meningoencephalitis. characterized by neutrophilic leukocytosis with a shift in the leukocyte formula to the left, up to myelocytes, a significant increase in ESR, and often anemia. with these variants of the course, I. reaches, despite antibiotics, 30-60%. In favorable cases, recovery occurs very slowly. The total duration of the disease is from 2 months. up to 1 1/2 -2 years.

Secondary focal form is not independent, but can develop after any of the described forms of I. In this case, the disease can occur subclinically, or the first manifestations of I. (for example,) and the focal lesions that then arise are separated from each other by a long period, during which health remains good. In these cases, the first pronounced clinical manifestation of the disease is damage to any organ (heart, liver, joint, meninges).

The most common variant of this form is with damage to 2-3 joints or; arthralgia in 50-80% of cases is preceded by (abdominal pain, nausea, vomiting) and symptoms of intoxication. Particularly characteristic is asymmetrical damage to the joints of the legs. Usually 2-3 joints are successively affected with an interval of several days to 2-3 weeks. The intensity of arthralgia is usually very high, even unbearable at the slightest passive or active movement. with I. they are reactive and are often combined with heart damage, which does not give pronounced changes on the ECG and has a favorable outcome. With this variant of the disease, an increase in ESR is often observed in the blood (up to 30% of cases). Arthralgia and arthritis can be combined with erythema nodosum, which is more common in women over 20 years of age. Elements of the rash appear in half of the patients after 2-3 weeks. after acute gastroenteritis. The course of this variant of I. is favorable, recovery, as a rule, occurs without residual effects, and relapses usually do not occur. Myocarditis is manifested by low-grade fever, weakness, fatigue, discomfort or pain in the heart, palpitations, shortness of breath, tachycardia, weakening of the sonority of heart sounds, the appearance of systolic murmur at the apex, expansion of the boundaries of the heart, changes in the ECG, similar to those with myocarditis of other etiologies. The course is benign and does not develop, but the duration can be several months.

Yersiniosis can be not only a manifestation of the generalized form, but also a variant of the secondary focal form of I. With the latter, it appears from the very beginning of the disease. The content of bilirubin in the blood increases moderately due to the bound fraction, liver function tests are usually within normal limits, transaminases are slightly increased. , as a rule, is short-lived and not intense, and the fever and intoxication with which the disease begins can be severe and prolonged.

Meningitis can also be a variant of the secondary focal form; it is usually serous, the course is usually not severe, and is rare. Rare variants of the secondary focal form of I. include Reiter's syndrome , cervical, ophthalmitis, osteitis.

Diagnosis difficult. Laboratory tests are required, which include the pathogen from blood, feces, urine, bile, cerebrospinal fluid, sputum, pharyngeal swab, mesenteric lymph nodes and detection of antibodies to Yersinia using an agglutination test or passive hemagglutination. Before sending to the laboratory, tubes with the test material in the accumulation medium must be kept in the refrigerator. Determination of the titer of antibodies to Yersinia should be carried out in paired blood sera taken at intervals of 5-7 days. in a diagnostic titer of 1:400 and above are usually detected only at the end of the 2nd week of illness.

When examining blood, some patients reveal leukocytosis (especially at the onset of the disease and during exacerbation) and an increase in ESR to 35-60 mm/h. Protein is detected in urine (0.03-0.24 g/l), and the height of the disease is microhematuria, . In a biochemical blood test, in addition to an increase in free bilirubin, bound bilirubin is occasionally determined, as well as a moderate increase in the activity of alanine aminotransferase and aspartate aminotransferase.

The polymorphism of clinical manifestations in I. makes it necessary to carry out a differential diagnosis with a number of infectious and non-infectious diseases. In this case, one should pay attention to the epidemiological history, the dynamics of the clinical picture of the disease, the severity of certain symptoms, the results of bacteriological and serological (over time) studies, as well as the effectiveness of etiotropic therapy.

In everyday practice, differential diagnosis is most often carried out with salmonellosis (Salmonellosis) , food toxic infections (food toxic infections) , dysentery (Dysentery) , viral hepatitis (viral hepatitis) , typhoid-paratyphoid diseases (see Typhoid fever , Paratyphoid) , brucellosis (Brucellosis) , Sepsis , Rheumatism , acute appendicitis , polyarthritis.

Treatment. Patients are hospitalized according to clinical indications. For uncomplicated gastrointestinal forms, diet and pathogenetic therapy similar to treatment for other acute intestinal infections (oral or parenteral rehydration depending on the degree of dehydration) are sufficient. For moderate and severe cases, as well as for a protracted, undulating course of this form, in addition, chloramphenicol is prescribed or in medium therapeutic doses for 10-12 days.

For all other forms of I. (abdominal, generalized, secondary focal), etiotropic is mandatory. If the above antibiotics are ineffective, gentamicin is prescribed (40-60 mg 2-3 times a day intramuscularly) and doxycycline hydrochloride (0.1 G 1 time per day).

Antibacterial therapy affects not only the duration of the febrile period and the severity of intoxication, but also significantly reduces the percentage of relapses and in some cases prevents the transition of localized forms of I. to generalized. The complex of treatment for patients with I. also includes detoxification and desensitizing therapy (antihistamines). In the abdominal form, in some cases (yersinia appendicitis), surgical treatment is necessary (). In the postoperative period, a course of antibiotic therapy must be carried out. In the generalized form, antibiotics are prescribed parenterally (for example, chloramphenicol succinate), usually several courses of treatment are carried out sequentially with different drugs (better taking into account the sensitivity of Yersinia isolated from the patient). In order to increase immunogenesis, drugs containing ready-made antibodies (polyglobulin, immunoglobulin, plasma) are used.

For arthritis, treatment is carried out with anti-inflammatory non-steroidal drugs (indomethacin, chlotazole, ibuprofen, voltaren, naproxen, acetylsalicylic acid, butadione, delagil, etc.) in individually selected doses for several months (the duration of treatment depends on the clinical effect and ESR indicators). In cases of persistent monoarthritis, intra-articular administration of corticosteroids (hydrocortisone, Kenalog, etc.) is indicated. For erythema nodosum and myocarditis, the same drugs are used as in the treatment of arthritis; in case of prolonged and severe course, prednisolone is also prescribed (30-40 mg per day orally). In case of yersinia hepatitis, in addition to etiotropic therapy, diet is important. For meningitis, preference should be given to chloramphenicol succinate in a daily dose of 50-100 mg/kg body weight, administration at intervals of 8 h; detoxification and dehydration therapy are carried out simultaneously.

Forecast. In the vast majority of cases, the disease ends in recovery. In individuals with reduced resistance, septic conditions develop; in some patients, the disease takes a protracted or chronic course.

Prevention includes early detection, treatment, isolation and hospitalization of patients and bacteria carriers; identification of sick animals (especially pigs and cows); measures aimed at exterminating rodents and preventing their entry into canteens, vegetable stores, food warehouses and stores, etc. It is also necessary to monitor the safety of vegetables and fruits in vegetable stores. To prevent nosocomial outbreaks, bacteria carriers and patients with mild forms of AI should be identified among hospital staff.

Bibliography: Guide to Zoonoses, ed. IN AND. Pokrovsky, s. 150, M., 1983; Enterobacteria, ed. IN AND. Pokrovsky, s. 220. M., 1985.

II Yersiniosis

acute infectious disease caused by Yersinia enterocolitica; characterized by a variety of clinical forms, and in typical cases - fever, intoxication, symptoms of gastroenteritis or enterocolitis, damage to the mesenteric lymph nodes.

1. Small medical encyclopedia. - M.: Medical encyclopedia. 1991-96 2. First aid. - M.: Great Russian Encyclopedia. 1994 3. Encyclopedic Dictionary of Medical Terms. - M.: Soviet Encyclopedia. - 1982-1984.

Synonyms:

Yersiniosis (intestinal yersiniosis; entereritis caused by Yersinia enterocolitica) - belongs to the group of yersiniosis, is an acute zoophilic sapronotic bacterial infection with a fecal-oral transmission mechanism, with a predominant lesion of the gastrointestinal tract (but multiple organ lesions are also possible) occurring against the background of a feverish-intoxication syndrome.

The causative agent of yersiniosis

The pathogen and its pathogenicity factors (ability to cause morbidity):

Gram negative rod (when stained by gram it turns pink), the color of which indicates the presence of a capsule;

There are also flagella, which cause active movement after introduction into the body;
There is also an adhesin that binds to collagen, resulting in arthritis;
The ability to synthesize serine protease, which ensures the destruction of secretory IgA of the mucous membranes and facilitates penetration through the protective barrier, since IgA is the first line of defense on the mucous membranes (and not only the intestines).
Like pseudotuberculosis, the causative agent of intestinal yersiniosis has outer membrane proteins that ensure penetration through the intestinal mucosa in a non-invasive way (i.e. without violating the integrity of the intestinal wall);

The last two factors explain the unimpeded penetration through the mucous barrier and further into the underlying tissues.

Yersinia enterocolitica dies when dried, boiled, exposed to direct UV rays and various chemicals (sublimate, chlorine, alcohol). Pasteurization and short-term exposure to temperatures up to 80°C do not always lead to death.

Susceptibility to the disease is high. The risk group includes people working in livestock farming, poultry farming, and food processing units. Children aged 3-6 years old are 4 times more likely to get sick, possibly due to the fact that local immunization is not developed, and maternal IgA has already been exhausted from the last feeding.

Prevalence: countries of Western and Northern Europe, Great Britain, USA, Canada, Japan and Russia, Africa, Asia, South America, Eastern Europe are under threat.

There is no specific seasonality; the disease is recorded throughout the year, but recently epidemic outbreaks and/or sporadic incidences have been noted from March to July, and at the end of the year.

Causes of yersiniosis

Reservoir (guardians) - soil, rodents, pigs, cattle, rabbits, birds, cats and dogs. Sources: animal reservoirs and patients of various forms, as well as bacteria carriers. Mechanism of transmission: fecal-oral (through food, i.e. through nutrition), infections have also been recorded after blood transfusion from an infected person.

Symptoms of yersiniosis

The incubation period is the time from the beginning of the introduction of the pathogen into the body until the first clinical manifestations; with yersiniosis it can last from 15 hours to 6 days, but more often 2-3 days. During this period, the pathogen penetrates the intestines through the gastrointestinal tract, where it is fixed and multiplies. There it is captured by tissue macrovags, part of it dies, releasing endotoxin, and part is carried by the same macrophages (due to incomplete phagocytosis) throughout the lymphoid system, and then through the circulatory system - causing dissemination, which is the trigger for the period of clinical manifestations.

The duration of the incubation period and the course of all other processes will depend on the following factors: the immunological reactivity of the body, the strain and infectious dose of the pathogen, and the route of penetration.

Period of clinical manifestations - the symptoms are very diverse, because the same clinical manifestation can be either isolated or be the beginning of the next form. And because of this, there is still no generally accepted classification, and at the moment, to separate and simplify the understanding of yersiniosis, the syndromic principle is based (as in pseudotuberculosis, the division of clinical forms is identical):

Gastrointestinal (characterized by the manifestation of gastroenteritis, enteritis, enterocolitis);
abdominal form (presence of mesenteric lymphadenitis, terminal ileitis, acute appendicitis);
generalized form (can be mixed and septic);
secondary focal manifestations (arthritis, erythema, Reiter's syndrome).

In any form, the disease begins with acute gastroenteritis against the background of intoxication, on days 4-5 the temperature normalizes, and by the end of the second week there is complete recovery.

Additional symptoms may also be present: catarrhal; diuretic; exanthema; scarlet fever-like symptoms (“gloves, sock and hood”, “crimson tongue”); hepatosplenomegaly.

At gastrointestinal form There is abdominal pain of varying intensity, constant or cramping. Localization is often in the right iliac region or in the navel, and can also be in the epigastrium. Also. as with pseudotuberculosis, an increase in stool frequency is observed, but unlike it, with yersiniosis an admixture of mucus and blood is found in the stool. Let me remind you that the gastrointestinal form can either occur separately or indicate the onset of a generalized form, combining all the symptoms listed below - so you always need to be on alert.

Abdominal form of yersiniosis: the onset of the disease is identical to gastrointestinal, and after 1-3 days, symptoms of appendicitis appear and increase (pain in the right iliac region and/or around the navel, pain on palpation of this area, diagnostic symptoms are also positive - increased pain when turning from the right side to the left , increased pain when raising the right leg in a supine position, etc., these symptoms may be accompanied by symptoms of peritoneal irritation).

Mesenteric lymphadenitis: against the background of feverish-intoxication syndrome, mild, often diffuse pain in the abdominal area occurs on days 2-4, lasting for 2 months.

Generalized form: occurs in a mixed or septic variant. This form is characterized by “combined symptoms” from each different form:

Acute onset against the background of the same symptoms as the gastrointestinal form;
catarrhal phenomena that appear against the background of a feverish-intoxication syndrome that lasts for 2 months;
a scaratina-like rash appears on the 2-3rd day and lasts for a week, with possible itching and rashes;
Arthralgia of varying intensity and duration, with damage to joints of different sizes, with inflammation of the plantar aponeurosis;
Hepatosplenomegaly with the ensuing consequences - icterus (yellowness) of the sclera and skin, pain on palpation in the right and left hypochondrium.
Dry wheezing in the lungs, which may indicate small focal pneumonia.
With a long course - signs of infectious cardiomyopathy or myocarditis, manifested by stabbing pain in the heart, a feeling of increased heartbeat, tachycardia not associated with fever.

Septic form of yersiniosis: It is also characterized by an acute onset, but in addition to gastroenteritis, the symptoms of ITS (infectious toxic shock) and DIC (disseminated intravascular coagulation) come to the fore.

Secondary focal form: can develop after any other form and in this case damage to any organ comes to the fore, so the symptoms are extremely diverse, but the most common are the following manifestations:

Polyarthritis (interphalangeal joints, wrist, intervertebral, scapuloclavicular, hip joints are affected);
monoarthritis (knee, ankle, elbow joints are affected in combination or isolated from each other). In this case, joint damage is often asymmetrical.
Difficult-to-control astheno-vegetoneurotic reactions develop.

Immunity is weak and intraspecific, that is, for a certain strain, that is, after an illness you can become infected again.

Diagnosis of yersiniosis

Diagnosis is carried out taking into account epidemiological, clinical and specific laboratory data. Clinical data are often based on differential diagnosis, taking into account the comparison of a number of data (the onset of the disease, the severity of intoxication-febrile symptoms, the presence of catarrhal phenomena, the presence of exanthema and its characteristics, dyspeptic symptoms) and require specialized training of an infectious disease specialist.

Lab tests:
Hemogram (Lc and Nf with a shift of the formula to the left, E and ESR, ↓Lf)
Biochemical blood test: ALT, AST and alkaline phosphatase, as well as bilirubin
Specific laboratory diagnostics:
- the bacteriological method is the main one, but it is not very convenient, because the final diagnosis becomes known after 10 days. This method is based on taking biological material and preferably a different substrate (feces, blood, urine and swabs from the back of the throat)
- immunological method: RA, RIGA is aimed at determining specific antibodies on days 6-10, ELISA determines specific antibodies already on day 3 - therefore it is an express method.
Instrumental methods: X-ray of the chest and joints, ECG, EchoCG, survey ultrasound of the abdominal cavity and retroperitoneal space where the kidneys are located, sigmoidoscopy, colonoscopy, CT, laparoscopy, sonography.

Treatment, complications and prevention are similar to those for pseudotuberculosis.

General practitioner Shabanova I.E.

Methodological development of a practical lesson for students.

Practical lesson No. 7

Subject: Yersiniosis

Lesson objectives: The relevance of the topic is related to the spread of pseudotuberculosis and intestinal yersiniosis in many countries of the world, including Russia. The incidence occurs both in the form of individual sporadic cases and in the form of outbreaks. Taking into account the polymorphism of clinical manifestations and possible chronicity, a general practitioner needs knowledge of this topic for timely diagnosis and implementation of complex therapeutic and anti-epidemic measures. The student, based on knowledge of the clinic, diagnosis, treatment of pseudotuberculosis and yersiniosis, should be able to substantiate the clinical diagnosis, draw up an examination and treatment plan for these diseases, carry out anti-epidemic measures.

Lesson duration: 4 hours (180 minutes).

Location of the lesson: Department of Infectious Diseases, classrooms, patient wards

Methodological equipment– textbook E.P. Shuvalov “Infectious diseases” M., 2001.

Material and technical equipment– tables, stands, extracts from the medical history, regulatory documentation.

Timing of the practical lesson:

teacher's introductory speech – 10 minutes

checking the initial level of knowledge (test-control) – 15 minutes

analysis of theoretical questions on the topic “esiniosis” – 60 minutes

supervision of patients and their analysis – 60 minutes

solving situational problems – 25 minutes

summing up the lesson – 10 minutes

Questions on the topic for self-study:

1. Etiology of yersiniosis.

2. Epidemiological features of yersiniosis.

3. Pathogenesis of yersiniosis.

4. Classification and features of the clinical course of yersiniosis

5. Complications of yersiniosis.

6. Syndromic differential diagnosis of yersiniosis.

7. Laboratory diagnosis of yersiniosis.

8. Treatment of yersiniosis.

9. Prevention of yersiniosis.

10. Features of anti-epidemic measures for yersiniosis.

Clinical classification of yersiniosis

There is still no unified classification of yersiniosis.

Based on pathogenesis, they distinguish:

1. Gastrointestinal form:

Gastroenteritis

Enterocolitis

Gastroenterocolitis

2. Abdominal form:

Mesenteric lymphadenitis

Terminal ileitis

Acute appendicitis

3. Generalized form:

Mixed option

Septic option

Septicopyemic variant

4. Secondary focal form:

• Erythema nodosum

  Myocarditis

• Meningitis

  Reiter's syndrome

Severity of the current:

• Medium-heavy,

Course of the disease:

Acute (up to 3 months),

Prolonged (up to 6 months),

Chronic (6 months – 1.5-2 years)

Laboratory diagnosis of yersiniosis

1. Express diagnostics:

Determination of Yersinia Ag in coproextracts, saliva, urine and blood of patients in RCA (coagglutination reaction), RLA, RNIF, ELISA. The effectiveness of RCA increases with the severity of the clinical picture, exacerbations and relapses of the disease; the frequency of positive results ranges from 55 to 90% (for the gastrointestinal form of the disease).

2. Molecular biological method - PCR

3. Bacteriological method

Material for research - feces, swabs from the throat, urine, sputum, cerebrospinal fluid, blood, bile, surgical material (mesenteric lymph nodes, intestinal sections), as well as sectional material. Pathogens can also be isolated from environmental objects - vegetables and fruits, from salads, milk, fish and dairy products, as well as from washes from equipment and containers.

Positive research results are obtained in 9-15% of cases with sporadic diseases and in 25-30% with outbreaks. The low efficiency of isolation is due to the small amount of Yersinia in the test material (especially in the blood) and the high contamination of the test objects with accompanying microflora. Bacteriological analysis requires quite a long time - from 7 to 30 days.

4. Serological diagnosis (Table 1):

From the 6-7th day of illness, RA and RNGA are used with their re-appointment after 5-7 days. RNGA gives 40-70% positive results; The minimum diagnostic titer of AT is 1:200. However, it is necessary to take into account the possibility of the appearance of AT in diagnostic titers only in the later stages, after the 21st day from the onset of the disease. When staging RA with live cultures of Yersinia, it is possible to detect antibodies to a greater number of serovars than in RNGA and in a higher percentage of cases. The minimum diagnostic titer of AT is not less than 1:160.

(Central Research Institute of Epidemiology)

Treatment plan for patients with yersiniosis

I. Indications for hospitalization

Patients are required to be hospitalized for the following clinical indications:

Severe and moderate forms of yersiniosis;

Yersiniosis in people who are severely weakened and burdened with concomitant diseases;

Age (children under 1 year old, adults over 60 years old).

II. Bed rest (for the period of intoxication, in severe forms of the disease).

III. Diet – gentle (schistochromia table) for the gastrointestinal form of yersiniosis.

IV. Etiotropic therapy.

A course of etiotropic treatment until 10-12 days of normal body temperature. Prescribing drugs after the 3rd day of illness does not prevent the development of exacerbations, relapses and chronicity of the disease. In the generalized form of yersiniosis, preference is given to combined parenteral antibacterial therapy; in cases of relapse, it is necessary to conduct repeated courses of antimicrobial therapy with a change in drugs.

The choice of antibacterial agents in the treatment of yersiniosis

Antibiotic group	Generic name	Daily dose
First line antibiotics Fluoroquinolones	Ciprofloxacin Ofloxacin	0.5 g x 2 times a day 0.4 g x 2 times a day
Second line antibiotics Semi-synthetic tetracyclines	Doxycycline Metacycline	0.1 g x 2 times a day 0.3 g x 3 times a day
Alternative drugs: Combined sulfonamides Aminoglycosides III generation cephalosporins	Co-trimoxazole Gentamicin Ceftriaxone	0.960 g x 2 times a day 0.240 g x 1 time per day 2.0 g x 1 time per day

Note. Semi-synthetic tetracyclines, aminoglycosides and co-trimoxazole should not be prescribed for icteric forms.

V. Pathogenetic therapy.

Detoxification therapy using crystalloid and colloid solutions is carried out according to generally accepted schemes. Rehydron, citro-glucosolan, quartasol, 5% glucose solution, hemodez, reopolyglucin are prescribed.

Desensitizing therapy – prescribed for the development of a secondary focal form; in this case, etiotropic therapy becomes secondary. Antihistamines are indicated; for persistent erythema nodosum, prednisolone is recommended in a short course for 4-5 days at 60-80 mg/day.

Antioxidants (eg vitamin E).

Immunocorrectors (cimetidine, methyluracil, pentoxyl, etc.) and immunostimulants (normal human immunoglobulin, polyglobulin).

Probiotics, given the high likelihood of developing intestinal dysbiosis.

VI. Symptomatic therapy: enzymes (hilak-forte), tranquilizers, cardiovascular drugs.

V. Treatment of polyarthritis. Antirheumatic drugs, physical therapy, and physiotherapeutic measures are prescribed; temporary relief comes from local administration of glucocorticoids.

Discharge from hospital and follow-up

Patients are discharged from the hospital after complete clinical recovery, no earlier than the 10th day of normal body temperature and when laboratory parameters are normalized. One-time control tests before discharge are advisable only for intestinal yersiniosis. Bacteria carriers are treated on an outpatient basis without release from work. For the period of outpatient treatment, carriers working in catering units are transferred to another job not related to food preparation. Children who have suffered from pseudotuberculosis and yersiniosis, especially severe forms, are subject to dispensary observation by a local pediatrician to prevent relapses, protracted course and complications. If the course is favorable, observation is carried out for 21 days; when complaints or clinical manifestations appear, a laboratory examination is prescribed, and if indicated, hospitalization and treatment.

Persons belonging to decreed categories are subjected to a bacteriological examination before discharge (1 stool test 2 days after the end of treatment). If the examination result is negative, they are immediately allowed to work. After discharge, clinical observation of all patients who have been ill is recommended for at least 3 months. In this case, depending on the organ damage, clinical blood tests, urine tests, biochemical tests (bilirubin, cholesterol, liver function tests, ALT and AST, total protein and its fractions), and RIGA should be performed. If necessary, consultations with a therapist, rheumatologist, gastroenterologist and other specialists are prescribed.

Determination of indicators indicating the threat of relapses and chronicity of the disease (methodological recommendations of the Ministry of Health of the Russian Federation on yersiniosis (1995)):

Detection of Ag HLA-B27.

Decrease in the activity of polymorphonuclear leukocytes during the period of convalescence.

Increased levels of PGE2 and PGF2 in the stage of early convalescence.

Long-term circulation of bacterial O-Ag and CEC in the blood.

Dysbacteriosis of the 3rd and 4th degrees.

If at least two of the above indicators are detected, dispensary observation of convalescents is recommended to be extended to 1 year with monthly examinations, laboratory tests (clinical blood test, protein and its fractions) and the involvement of relevant specialists for consultation - a rheumatologist, gastroenterologist, etc.

At the end of the dispensary observation, persons of the decreed categories undergo two control bacteriological analyzes of stool with an interval of 2–3 days.

Prevention of yersiniosis

Nonspecific prevention of yersiniosis:

In the prevention of yersiniosis, rodent control measures and compliance with hygienic food preparation rules come first.

Rules for preventing yersiniosis:

Places for storing vegetables and other products should be inaccessible to rodents.

If signs of spoilage by rodents are detected, food products are not suitable for human consumption.

The vegetable storage area must be disinfected before planting a new crop.

Vegetables contaminated with soil must be thoroughly washed and blanched in boiling water for 10-30 minutes or rinsed with boiling water before eating fresh.

For children, it is not recommended to use old harvest vegetables in spring and summer for salads and juices.

Drinking water should be consumed only after boiling.

Prevention of yersiniosis in animals involves strict adherence to veterinary, sanitary and zoohygienic rules for the care and feeding of animals and the prevention of their infection through environmental objects.

Specific prevention of yersiniosis: not developed.

List of basic literature for students:

1. Yushchuk N.D., Vengerov Yu.Ya. Infectious diseases: Textbook. - M.: Medicine, 2003. - 544 p.

List of additional literature for students:

1. Order of the USSR Ministry of Health No. 475 of August 16, 1989 “On measures to further improve the prevention of acute intestinal infections in the country”

2. Acute intestinal infections. Collection of normative and methodological materials. – M.: GRANT, 1999. – 64 p.

3. Belyakov V.D. Epidemiology / V.D. Belyakov, R.Kh. Yafaev.- M., 1989.- P. 365-370.

4. Kazantsev A.P. Differential diagnostics / A.P. Kazantsev, T.M. Zubik, K.S. Ivanov, V.A. Kazantsev. – M.: MIA, 1999.

5. Lobzin Yu.V. Selected issues in the treatment of infectious patients: a guide for doctors / Yu.V. Lobzin. – St. Petersburg: Foliant, 2005. – 912 p.

6. Pokrovsky V.I. Infectious diseases and epidemiology: textbook. for universities / V.I. Pokrovsky, S.G. Pak, N.I. Brico, B.K. Danilkin. – M.: GEOTAR-MED, 2004. – 816 p.

7. Sazonova N.S. Pseudotuberculosis / N.S. Sazonova. – Kyiv, 1984.

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The methodological development of practical classes was considered at the department meeting dated “__” ________ 2012 (Minutes No.__)

Head of the department ___________________ L.I. Ratnikova

Yersiniosis is an acute intestinal infection characterized by multifocality: damage to the intestines, bones and joints, liver, kidneys, lymph nodes and myocardium. This is an anthropozoonosis, characterized by transmission of the pathogen from animals to humans and accompanied by a toxic-allergic reaction.

Since yersiniosis affects various internal organs, its clinical manifestations are very diverse. Due to such a variety of symptoms, certain difficulties arise in diagnosing the disease. This is the danger of this disease, which is often complicated by other pathologies that pose a threat to the lives of patients.

Yersiniosis occurs in people of any age, but most often it affects the body of young children. Patients develop signs of intoxication syndrome, maculopapular rash, dyspepsia, hepatosplenomegaly, arthropathy, abdominal pain. Diagnosis of pathology is based on the results of microbiological examination of biological material in which Yersinia, the causative agent of pathology, is found.

Men are more susceptible to yersiniosis than women. The disease is widespread, but is more common in regions with temperate climates. Sporadic cases of infection usually occur, but outbreaks are also possible. The incidence reaches its maximum in the winter-spring period, which is associated with an increase in the biological activity of rodents at this time of year.

Etiology

The causative agent of yersiniosis is the microorganism Yersinia, which belongs to the Enterobacteriaceae family. This motile polymorphic bacterial rod stains negatively for Gram and survives in facultative anaerobic conditions - oxygen-free. Yersinia have peritrichous flagella that provide motility and do not form spores.

The microbe tolerates low temperatures well: it grows and multiplies in food products at 4-6 °C. Thanks to this characteristic of bacteria, yersiniosis is popularly called “refrigerator disease.” The favorite habitats of microbes are confectionery and bakery products, milk and butter. Yersinia actively reproduces in vegetable salads at an ideal temperature of 25 – 29°C.

Yersinia is resistant to environmental factors: it survives freezing and thawing, and retains its pathogenic properties in water and soil for a long time. Direct sunlight, boiling, ultraviolet irradiation, oxidizing agents and chemical disinfectants have a bactericidal effect on Yersinia.

Due to pathogenicity factors, microbes cause the development of pathology. During their life, bacteria release three types of toxins - enterotoxin, cytotoxin and endotoxin. Enterotoxin activates adenylate cyclase of enterocytes, increases the permeability of their membranes to water and electrolytes, causes diarrhea and dehydration.

Yersinia pathogenicity factors:

1. A negative Gram stain indicates the presence of a capsule.
2. Flagella, which determine the active movement of the microbe after introduction into the human body.
3. The ability of the pathogen to adhere and colonize the intestinal mucosa.
4. Adhesins causing arthropathy.
5. A protease that destroys IgA and facilitates penetration through the mucous membrane of internal organs.
6. Outer membrane proteins that ensure unhindered penetration of microbes into deep-lying tissues.
7. Cell wall lipopolysaccharides cause the toxicity of Yersinia.

The complex antigenic structure of bacteria explains the unique pathogenesis of the disease, the variety of clinical manifestations, the wide range of severity of toxicosis and the polymorphism of organ lesions.

Epidemiology

Bacteria live in the soil and enter the human body through carriers - various animals: pigs, cats, dogs, cattle, birds, rabbits. Infection from a sick person is possible, but it is extremely rare and has no epidemiological significance. The source of infection during outbreaks in cities is rodents, the accumulations of which form the epicenter. Sick rats and mice live in cellars and vegetable stores. Their feces end up on vegetables and in water tanks.

The transmission mechanism is fecal-oral, realized through the alimentary and waterways.

• Infection occurs when eating food that has undergone inadequate heat treatment: poorly cooked meat, unboiled milk, as well as raw water contaminated with Yersinia.
• There is a contact and household route of transmission of infection among people with poor hygiene standards.
• Cases of yersiniosis after transfusion of infected blood have been described.

Animals become infected by consuming food or water contaminated with soil infected with Yersinia. The contact route of transmission of the pathogen is due to keeping animals in unsanitary conditions.

People have a low susceptibility to yersiniosis. Individuals with a healthy immune system practically do not suffer from clinical forms of infection. Children, elderly people and people with weakened defenses are difficult to tolerate the disease. Bacteria, penetrating the body, attach to the epithelium of the intestinal mucosa and destroy it. Such processes lead to the formation of a detailed clinical picture of the disease. The risk group includes people working in livestock farming, poultry farming and food processing units.

Mechanism of occurrence and course of the disease

The pathogenesis of yersiniosis is caused by the following factors:

1. The state of immunity and factors of nonspecific resistance of the body,
2. The presence of chronic gastrointestinal dysfunction,
3. The magnitude of the infectious dose of the microbe,
4. Pathogenicity and virulence of Yersinia.

Yersinia Enterocolitica

Pathogenesis links in yersiniosis:

• Infection is the penetration of a pathogen into the body through food,
• Formation of a food bolus and its entry into the stomach,
• Death of some microbes under the influence of gastric juice,
• Penetration of Yersinia into the small intestine,
• Reproduction of bacteria
• Damage to intestinal epithelial cells and lymphatic formations,
• Development of catarrhal-desquamative or ulcerative inflammation - enteritis,
• Violation of the relief of the intestinal mucosa,
• Formation of erosions and ulcers,
• The occurrence of multiple point hemorrhages,
• Damage to all layers of the intestinal wall,
• Development of enterocolitis or colitis,
• Invasion of infection into the lymph nodes of the mesentery with the development of mesenteric lymphadenitis,
• Overcoming the lymphatic barrier and penetration of microbes into the blood,
• Bacteremia is a general toxic syndrome,
• Spread of infection by hematogenous route,
• Parenchymal diffusion - incomplete phagocytosis, diffuse metastatic focal damage to internal organs,
• The formation of new inflammatory foci with the development of cholecystitis, arthritis, hepatitis, nephritis, conjunctivitis,
• The appearance of granulomas and microabscesses in the affected organs,
• Freedom from infection - phagocytosis, specific antibodies.

Periodic entry of the pathogen into the blood leads to an exacerbation of the disease and the formation of new infectious foci. Excessive accumulation of toxins in the blood and long-term presence of bacteria in the body results in the formation of stable sensitization and autoimmune processes, accompanied by intoxication and allergic manifestations.

Classification

Morphological forms of the disease:

Yersiniosis can acquire an acute, chronic and recurrent course with periods of attenuation and exacerbation.

Gastrointestinal and abdominal forms develop if the Yersinia strain has a low invasive ability, and the human immune system reliably protects the body from the infectious process. Pathology is formed at the gastrointestinal tract level without further spread of infection.

Highly virulent Yersinia strains are causative agents of a generalized form of infection in individuals with severe immunodeficiency. Microbes enter the blood through the intestinal wall, spread throughout the body and reach internal organs, which become inflamed and cease to function normally. During the treatment process, the immune system defeats the infection and the patient makes a full recovery. If this does not happen, the generalized form becomes secondary focal, proceeding like an autoimmune disease - vasculitis, Crohn's disease, rheumatoid arthritis, thyroiditis.

Symptoms

Incubation of yersiniosis is 1-6 days. Microbes enter the gastrointestinal tract, actively multiply in intestinal epithelial cells and damage them. Symptoms of yersiniosis in a patient will appear very quickly if the dose of bacteria and their virulence are high and the state of the immune system is weak. Bacteria are captured by tissue macrophages. Some of them die, releasing endotoxin, and the other part enters the lymphoid and circulatory system. The dissemination of microorganisms throughout the body is the trigger for the period of clinical manifestations.

The clinical picture of the disease is represented by several syndromes.

Yersiniosis begins acutely and proceeds like gastroenteritis. After all the symptoms of the disease appear, the intestinal infection can acquire a generalized form with damage to internal organs not related to the digestive system. During the height of the disease, taking into account the characteristics of the clinical picture, the form of infection is determined - gastrointestinal, abdominal, generalized, secondary focal, as well as the severity of the pathological process.

After etiotropic treatment, recovery occurs, during which pathogenic microbes are completely killed and the affected cells of the internal organs and their functions are restored. Mortality with yersiniosis is relatively low.

Morphofunctional forms of pathology:

1. Gastrointestinal form occurs most often and is manifested by signs of intoxication, dyspepsia, skin rash, catarrh, arthropathy, hepatosplenomegaly, lymphadenopathy. Patients complain of constant or cramping pain in the epigastrium and near the navel, nausea, vomiting, foul-smelling diarrhea, chills, myalgia, and weakness. The frequency of stool varies from 4 to 20 times a day. The stool contains mucus, blood and pus. Then arthralgia, runny nose and cough, conjunctivitis, and dysuric disorders appear. The disease lasts from 2 to 14 days and ends with complete recovery. The wave-like nature of the infection leads to dehydration of the body.
2. Abdominal form proceeds as mesenteric lymphadenitis, acute appendicitis or terminal ileitis. The pain syndrome is accompanied by signs of intoxication and dyspepsia. In patients, the liver, spleen and lymph nodes become enlarged, myalgia, arthralgia and exanthema appear.
3. At generalized form clinical symptoms are very diverse. In patients, the body temperature rises above 40 degrees, there are signs of arthralgic and catarrhal syndromes. On the third day of illness, a rash appears on the palms and soles. Among the dyspeptic symptoms, abdominal pain, nausea, vomiting, and diarrhea predominate. Then blood pressure decreases, consciousness is impaired, shortness of breath, tachycardia, pale skin occurs, and a hemorrhagic rash appears. The septic form is characterized by high mortality.
4. Mixed form manifests itself as symptoms of a generalized yersinia infection with progression of hepatosplenomegaly and damage to internal organs. Patients develop inflammation of the liver, lungs, kidneys, and meninges of yersinia etiology with characteristic clinical manifestations. The cervical lymph nodes become enlarged, myalgia, palpitations, cardialgia, and dysuria occur.
5. Secondary focal form is a consequence of one of the above forms. It develops a month after an acute intestinal infection. Pathological reactivity is formed in the body of patients, and autoimmune inflammation of internal organs develops. Asymmetric polyarthritis or monoarthritis occurs with swelling of the joints, pain and hyperemia of the skin; erythema nodosum with subcutaneous nodules on the thighs; enterocolitis with abdominal pain and stool disturbances. Myocarditis does not last long and has a favorable course. Possible development of Crohn's disease, osteitis, conjunctivitis, thyroiditis, enterocolitis.

Complications of yersiniosis are quite diverse. These include:

• Therapeutic pathology – inflammation of the liver, gall bladder, myocardium, pancreas;
• Surgical pathology - inflammation of the appendix, adhesions in the abdominal cavity, perforated intestinal ulcer, inflammation of the peritoneum, sepsis;
• Diseases of the central nervous system - meningitis, encephalitis, arachnoiditis;
• Diseases of the urinary system - glomerulonephritis;
• Pathology of the osteoarticular system - arthritis, osteomyelitis.

The disease has a predominantly favorable prognosis and a benign course. The patients recover completely. The mortality rate of the disease is low.

Diagnostic measures

Diagnosis of yersiniosis begins with listening to complaints, collecting anamnesis and external examination of the patient. Specialists collect information about the symptoms and the time of their appearance, the course of the disease and the circumstances under which the infection occurred - contact with sick animals, consumption of raw water and poorly cooked food.

1. Laboratory diagnostics consists of conducting a blood test and drawing up an immunogram. The hemogram shows anemia, leukocytosis, lymphopenia, eosinophilia, increased ESR; in the immunogram - antigens and antibodies to the causative agent of yersiniosis.
2. The main method for diagnosing yersiniosis is bacteriological. The pathogen is isolated from the feces, blood, bile and liquor of sick people. The laboratory examines sputum or rinsing from the mucous membrane of the throat. The biomaterial taken from the patient is inoculated on special nutrient media on which the infectious agent grows and multiplies freely. First, inoculate in liquid accumulation media and place the tubes in the refrigerator. On the 3rd or 5th day, the culture is reseeded onto Endo and Ploskirev plate selective media, and the dishes are placed in a thermostat. After incubation under special conditions, bacterial colonies are assessed. Then a pure culture is isolated and the microbe is identified to genus and species by sowing in a variegated His row to study its biochemical properties. Final typing is carried out using diagnostic agglutinating sera. Yersinia is also isolated from environmental objects and food products. Bacteriological diagnostics give good and accurate results, but take a lot of time.
3. Serodiagnosis allows you to get results in a shorter time. Pathogen antigens are determined in the blood using ELISA, RIF, RAL and RNIF. Serological diagnosis of yersiniosis includes a detailed Widal agglutination reaction with the appropriate diagnosticums and a passive hemagglutination reaction with an antigenic erythrocyte diagnosticum.
4. Genetic analysis- detection of pathogen DNA in the test material by performing PCR.
5. All patients require consultation with specialists in the field of gastroenterology, cardiology, nephrology, and neurology.
6. To identify existing complications, an ECG, echocardiography, ultrasound of internal organs, CT, MRI, and radiography are performed.

Treatment

Treatment of yersiniosis is carried out in an infectious diseases hospital. Drug treatment consists of prescribing various groups of drugs.

• Etiotropic therapy is aimed at destroying Yersinia in the human body. Patients are prescribed broad-spectrum antibacterial agents from the group of fluoroquinolones, macrolides, cyphalosporins, and protected penicillins. Antibiotics are prescribed after receiving the results of determining the sensitivity of isolated bacteria from the biomaterial. The most effective are Ciprofloxacin, Chloramphenicol, Ceftriaxone, Amoxiclav, Azithromycin.
• Detoxification treatment helps remove toxins from the body and eliminate symptoms of intoxication - intravenous administration of colloid and crystalloid solutions: “Gemodeza”, “Reopoliglyukin”, “Regidron”.
• Symptomatic therapy aimed at reducing pain, inflammation, swelling, heat - antihistamines: Suprastin, Tavegil; NSAIDs: Ibuprofen, Diclofenac; glucocorticosteroids: Prednisolone, Hydrocortisone.
• General restorative treatment allows patients to recover faster and recover from a serious illness - vitamin therapy; enzyme preparations: “Pancreatin”, “Creon”; pre- and probiotics: “Linex”, “Acipol”.
• Immunomodulators increase the body’s overall resistance to pathogenic pathogenic agents - “Imunofan”, “Methyluracil”.

Surgical intervention is performed for inflammation of the appendix or peritoneum, intestinal perforation, or intestinal obstruction.

All patients with yersiniosis are discharged from the hospital after a repeat diagnostic examination and receipt of the results of a three-time stool examination in a bacteriological laboratory.

In the absence of timely treatment, yersinia infection becomes chronic. In patients, the risk of developing severe complications increases, the recovery period is prolonged and undesirable consequences appear.

Prognosis and prevention

Intestinal yersiniosis has a benign course and a favorable prognosis. Fatalities are extremely rare. The prognosis becomes unfavorable after the development of yersinia sepsis, which can lead to the death of the patient.

Specific prevention of yersiniosis has not currently been developed. Measures to prevent the development of pathology:

1. Maintaining a healthy lifestyle,
2. Maintaining personal hygiene rules
3. Complete thermal processing of animal products,
4. Proper food storage
5. Compliance with sanitary and hygienic conditions in catering establishments and vegetable stores,
6. Destruction of rodents and protection against them,
7. Veterinary surveillance to identify sick animals.

To prevent seasonal outbreaks of yersiniosis, anti-epidemic measures are taken. If there are rodents in the outbreak, unscheduled deratization is necessary, and to destroy harmful bacteria, total disinfection is necessary.

Yersiniosis is characterized by polymorphism of clinical manifestations, damage to the gastrointestinal tract, a tendency to generalization, septicopyemia and damage to various organs and systems. This bacterial zoonosis is manifested by a variety of clinical symptoms: fever, dyspepsia and toxic-allergic manifestations.

Video: yersiniosis in the program “About the Most Important Thing”