What is Typhoid Fever?
Typhoid fever is an anthroponotic acute infectious disease with a fecal-oral transmission mechanism. It is characterized by lesions of the lymphatic system of the intestine, bacteremia, severe intoxication, enlargement of the liver and spleen, roseolous rash, and in some cases enteritis.
Brief historical information
The name of the disease, introduced by Hippocrates, comes from the Greek word typhos (fog, confused consciousness). Prior to the discovery of the causative agent of typhoid fever, all feverish states were designated by this term. T. Brovich (1874), N.I. Sokolov (1876) and K. Ebert (1880) found a typhoid bacillus in Peyer’s patches of the intestine, spleen, and mesenteric lymph nodes of deceased people. G. Gaffky (1884) isolated a pure culture of bacteria.
In 1896, M. Gruber discovered the phenomenon of agglutination of typhoid bacteria using specific sera, and later F. Vidal applied this discovery to the development of RA for diagnostic purposes (Vidal reaction). A detailed description of the clinical picture of typhoid fever is further made by I.I. Pyatnitsky (1804), J. Bretano (1820-1829), M. Sokolov and F. Kiyakovsky (1857), as well as S.P. Botkin (1868). A great contribution to the study of typhoid fever was made by Russian scientists – G.А. Ivashentsev, N.K. Rosenberg, G.F. Vogralik, B.Ya. Padalka, G.P. Rudnev, A.F. Bilibin, K.V. Bunin and others
Causes of Typhoid Fever
The causative agent is Salmonella typhi, a Gram-negative movable rod of the Salmonella genus of the family Enterobacteriaceae. Bacteria are unpretentious and grow on ordinary nutrient media. In S. typhi, thermostable somatic O-Ag, thermolabile flagellate H-Ag, thermolabile somatic Vi-Ag, and others are isolated. Bacteria do not form exotoxins. When microorganisms are destroyed, endotoxin is released, which plays a major role in the pathogenesis of the disease. To some extent, the pathogenicity of typhoid bacteria is also determined by “aggression enzymes” – hyaluronidase, fibrinolysin, lecithinase, hemolysin, catalase, etc. More than 100 stable phagovars are distinguished by their sensitivity to typical bacteriophages. Identification of the phagovar of the pathogen is a convenient marker for identifying the epidemiological links between individual diseases, finding out the source and transmission routes of the pathogen. Under adverse conditions, such as in the immune body, bacteria become L-forms. Bacteria are moderately resistant in the external environment – up to 1-5 months in soil and water, up to 25 days in feces, underwear – up to 2 weeks, on food – from several days to weeks. They remain somewhat longer in milk, minced meat, vegetable salads, where they are able to multiply at temperatures above 18 ° C. When heated, the pathogen dies quickly, disinfectant solutions in normal concentrations affect it. If in 1993-1995 phagovars A, K1 dominated , B2, then in 1997 phagovar 28 prevailed, and F4 and 45 phagovars appeared. The presence of antibiotic-resistant strains of the pathogen, capable of causing major outbreaks of the disease, was established.
The reservoir and source of infection is a person (patient or bacterium excreta). The danger of the patient to others in different periods of the disease varies. In the incubation period, an infected person is practically not dangerous.
The danger of the patient to others increases as the disease progresses and reaches its maximum at the 2-3rd week of the disease – during the period of excretion of bacteria with feces, urine and sweat; they can also be found in breast milk and nasopharynx. Most of those who have been ill are released from the pathogen in the first 1 2 weeks or in the next 2-3 months of recovery. Approximately 3-5% remain carriers for a long time, and some – for life. The epidemiological risk of a chronic carrier is determined by his profession and depends on his compliance with the rules of personal hygiene. Carriers that have access to the preparation, storage and sale of food are particularly dangerous.
The transmission mechanism is fecal-oral, implemented by water, food and domestic routes; in areas with a high incidence of morbidity, the spread is mostly by water. The latter is due to the use of water taken from polluted open or technical reservoirs, as well as due to the poor sanitary and technical condition of water supply and sewage facilities. As a result of the use of contaminated water, acute and chronic water flashes occur, which can last for a long time and cover large groups of the population. Water outbreaks are caused by accidents on water supply networks and structures, pressure drops and irregular water supply, accompanied by the inflow of infected groundwater through leaking network sections. Of the most dangerous foods, milk and dairy products, creams, salads and other products that serve as a favorable breeding ground for bacteria. Infection can sometimes occur through vegetables, especially when they are irrigated with wastewater or fertilized with faeces. Domestic transmission is possible with a low culture of carriers of bacteria or patients with an erased form of the disease. When this occurs, the contamination of surrounding objects, and subsequently – contamination of food.
Natural susceptibility of people. Susceptibility to the disease is high, the disease has a long life-long immunity. Repeated illnesses are extremely rare.
Major epidemiological signs. Typhoid fever is found on all continents, in all climatic zones. The highest incidence rates are recorded in developing countries. In connection with the global spread of typhoid fever is one of the most pressing problems of practical and theoretical medicine. According to WHO, there is not a single country where cases of the disease have not been reported.
About 20 million cases of typhoid fever and about 800 thousand deaths are registered annually in the world. Especially large epidemics are observed in the countries of Asia, Africa and South America. The presence of chronic bacteria carriers in the population and the lack of effective methods for their rehabilitation determine the possibility of sporadic and epidemic spread of typhoid fever in almost any territory at any time of the year. However, the endemicity of the disease is most often determined by the activity of the waterway of infection transmission. It is necessary to distinguish water flashes both by the nature of the water source and by the mechanism of its pollution. Shortage of water, interruptions in its flow also intensify the contact and everyday transmission of the pathogen, as they force the population to use water for industrial plumbing, open reservoirs, rivers, irrigation canals, etc. It is the water factor that causes the high incidence of typhoid fever in Central Asia.
In recent years, the “commercial” coloring of the incidence of typhoid fever has been noted, due to migration processes, the growth of trade relations, and the widespread use of street vending, including food.
The seasonal distribution of morbidity is characterized by rises in the summer-autumn period. The latter is especially characteristic of endemic areas, where, against the background of the generally unsatisfactory quality of drinking water, its deficit is increasing more and more. At present, practically throughout the country, periodic fluctuations in the long-term dynamics of morbidity have not been identified. However, in those areas where conditions still exist for a sufficiently active pathogen circulation, more or less pronounced seasonal rises are noted. The more frequent formation of chronic carrier pathogen in areas with widespread opisthorchosis invasion was noted.
The incidence of residents living in rural areas is higher than that of urban residents, which is mainly due to the presence of conditions for infecting the population. One of the important factors is bathing in reservoirs polluted by fecal waste water. In this regard, the most “threatened” age is the younger and middle school. Among adults, the highest incidence figures are recorded among young people (15-30 years old).
Food outbreaks most often determine the following circumstances:
- the presence in the food enterprise of the source of infection (bacillicarrier or patient of the erased form);
- sanitary and technical defects – the absence or improper operation of utility installations (water supply, sewage);
- unhygienic regime of the food enterprise;
- violations of the technological process of food processing (improper heat treatment, etc.).
In large, well-developed cities, typhoid fever has become an exclusively adult disease. Nosocomial spread of infection is characteristic of neuropsychiatric hospitals.
Pathogenesis During Typhoid Fever
When the pathogen enters the mouth, Salmonella, which have overcome the nonspecific oral protection factors and the acidic barrier of the stomach, penetrate into the solitary and group lymphatic follicles of the small intestine, where they multiply. After reproduction in the latter, as well as in the mesenteric lymph nodes, the pathogen enters the bloodstream, causing bacteremia and endotoxemia. Throughout the disease, typhoid fever is accompanied by intoxication. With the flow of blood, the pathogen disseminates into parenchymal organs (liver, spleen, lymph nodes, bone marrow), forming typhoid granulomas in them, including large typhoid cells with bright nuclei. Granulomas form the basis for the maintenance of secondary waves of bacteremia. Next, the bacteria re-enter the intestine, resulting in the development of GST reactions in the previously sensitized lymphoid tissue of the intestinal wall. Morphologically, HRT is manifested by necrosis of Meyerovich plaques and solitary follicles, which leads to the formation of typhoid ulcers, often in the distal regions of the small intestine. The process goes through a series of successive stages and is determined by a time frame.
- During the first week of the disease, “swelling” of the lymphatic formations in the small intestine is observed; on the incision they are gray-red in color and resemble the brain substance (“brain-like swelling”).
- At week 2, necrotic lesions develop, starting in the central parts of the swollen lymphoid formations (necrosis stage). In some cases, necrosis extends to the entire thickness of the intestinal wall.
- On the 3rd week rejection of necrotic lymphoid tissue begins with the formation of ulcers.
- By the 4th week necrotic masses are rejected from ulcers, leading to the formation of so-called clean ulcers.
In the future, ulcers heal without scarring. During this period, in some cases, the intestinal contents are kept from penetrating into the abdominal cavity only by a thin layer of the serous membrane, which causes the danger of perforation of the intestinal wall.
Against the background of emerging immune reactions, the pathogen is released from the body of a patient with feces already in the initial stage of the disease, reaching its maximum from the 2nd week of illness. Isolation of the microorganism may continue after the end of the clinical manifestations of the disease. In 3-5% of cases, the so-called chronic carriage of the typhoid bacillus is formed, which can last from several months to decades, even for life. The pathogenesis of the bacteria carrier is complex. It is believed that chronic carriage is a chronic typhoid infection. It is believed that important factors in the development of bacterial carriers are the phenotypic features of the immune system, as well as the formation of typhoid bacillus L-forms.
Symptoms of Typhoid Fever
The incubation period varies from several days to 3 weeks (on average, 10-14 days). Previously it was assumed that typhoid fever begins gradually. However, in more than 2/3 of cases, an acute onset of the disease is observed.
The first week of clinical manifestations is designated as the initial period of the disease. If the disease develops gradually, then during the first 3-4 days there is an increase in the temperature reaction, reaching 39–40 ° C by the end of this period. Intoxication syndrome is also gradually developing, manifested by headache, anorexia, progressive general weakness, dizziness, insomnia. In the acute onset of the disease, symptoms of intoxication develop in a shorter time (1-2 days).
When examining a patient in most cases, the paleness of the skin is noteworthy, but in some patients the face may be slightly hyperemic, especially in the case of an acute onset of the disease. Characteristic thickening of the tongue; while in the center it is coated with bloom, while the edges and the tip remain clean. With a large swelling of the tongue, one can observe the imprints of the teeth along its edges. The abdomen is usually swollen due to flatulence, the intestinal peristaltic waves are slow. Constipation is characteristic, however, in the initial stage of the disease, a relaxation of the stool with feces in the form of “pea soup” is possible.
Palpation of the abdomen (care should be taken!) Reveals a slight soreness in the right iliac region, the same rumbling and dullness of the percussion sound can be noted (Padalka symptom). By the 3-4th day of the disease, the patient’s liver and spleen size increase. On palpation, they are somewhat condensed, but painless. Muffled heart sounds. Bradycardia characteristic of the disease usually develops at a later date. The increase in pulse in the initial period does not exclude the diagnosis of typhoid fever.
The peak period is at the end of the first – the beginning of the 2nd week of illness and can last from several days to 2-3 weeks. Characterized by an increase in symptoms of intoxication. Body temperature remains high, acquires a constant, undulating or wrong flow.
On the 8-9th day of the disease, patients with typhoid roseola (roseolae elevatae) can be detected, slightly elevated above the skin surface and located on the anterior abdominal wall and lower chest. The number of roseol is insignificant, sometimes only 2-5 elements. Roseola disappear on the 3-4th day after their appearance, but after the appearance of the first roseol, new drops are possible. The absence of exanthema does not exclude the diagnosis of typhoid fever. The development of bradycardia is characteristic, the pulse rate lags far behind the level of the temperature reaction. Heart sounds, as a rule, are deaf, the pulse of small filling, blood pressure is prone to decrease. In more severe cases, oliguria is observed. With a severe course of the disease, so-called typhoid status can develop with the patient’s prostration, severe weakness, weakness, apathy, stupefaction, and in some cases with motor anxiety. Currently, this condition is rarely met.
The period of convalescence is manifested by a drop in body temperature (sometimes according to the amphibolic type) and the gradual disappearance of signs of intoxication. It must be emphasized that despite the disappearance of symptoms of intoxication, especially under the influence of therapeutic measures, the time frame for the formation of ulcers in the small intestine remains, therefore there remains a risk of intestinal bleeding and intestinal perforations.
It should be borne in mind that the clinical picture of typhoid fever is not always characterized by the specified complex of symptoms; many of them are weak or may be completely absent. Such situations, known as atypical forms, are difficult to diagnose (“outpatient typhoid fever”). Also known abortive form of the disease, characterized by short-term fever in just a few days and the rapid disappearance of intoxication. The erased form of typhoid fever manifests itself in a brief subfebrile condition, absence of exanthema and mild symptoms of intoxication.
In rare cases, the disease can occur in the form of pneumo, meningo, colo, and nephrotiph. In this case, the course of the disease is usually severe, against the background of severe intoxication, signs of damage to the corresponding organs and systems predominate.
Exacerbations and relapses.
In some cases, the disease may become protracted, due to the development of exacerbations. They usually occur against the background of a reduction in the symptoms of intoxication and a decrease in body temperature, which, however, is not reaching normal levels. Against this background, all the symptoms of the disease increase again, the body temperature rises, new elements of the typroid exanthema appear, the liver and spleen increase in size.
Recurrences of the disease differ from exacerbations in that the symptoms of intoxication reappear, fresh roseola appear, the body temperature rises to high numbers after the temperature response has already normalized and the patient is feeling well. In 7-9% of patients relapses occur at the 2-3rd week of apyrexia; in some cases they can be observed at a later date. The number of relapses usually does not exceed 1-2, in rare cases – 3. As a rule, relapses begin acutely, within 1-2 days the full clinical picture of the disease develops. Especially it should be emphasized that in relapses the exanthema can be detected as early as the first day. The course of relapses is easier, and their duration is shorter than the primary disease.
Pathogenetic and most dangerous complications of typhoid fever – infectious toxic shock, perforation of the small intestine and intestinal bleeding.
Infectious-toxic shock develops against the background of pronounced intoxication syndrome; clinically characterized by a sharp decrease in body temperature, tachycardia, a drop in blood pressure, oliguria or anuria, increased sweating, and manifestations of neurotoxicosis.
Perforation of the small intestine and intestinal bleeding more often develop at the end of the 2nd and the beginning of the 3rd week of illness. Following perforation of the intestine, the patient develops peritonitis with the clinical manifestations characteristic of this condition. The task of the infectious disease specialist is to recognize the perforation in the first hours after its appearance, before the development of symptoms of generalized peritonitis.
The perforation signal is abdominal pain. It should be borne in mind that when perforating a typhoid ulcer, the pain may be of the most diverse nature: from minor dullness to “dagger”. On examination of the patient, a slight tension of the abdominal muscles in the perforation area can be noted, and in some cases the symptom of Shchyotkin-Blumberg. However, in some cases, these signs may be absent, then it is necessary to pay attention to indirect symptoms, such as a symptom of “end of silence” (lack of peristalsis noise) during abdominal auscultation, an unexpected sharp drop in body temperature and a change in bradycardia to tachycardia.
Intestinal bleeding may be clinically asymptomatic, in which case it is determined by the presence of blood in the feces and a decrease in the hemoglobin content. Massive bleeding is accompanied by a sudden drop in body temperature, the emergence of a feeling of thirst, an increase in pulse rate, a decrease in blood pressure. With massive bleeding, fecal masses acquire the character of melena. Appearance of vomiting is possible, emetic masses look like “coffee grounds”. With the simultaneous development of perforation and bleeding in most cases there is no pain syndrome.
Diagnosis of Typhoid Fever
Typhoid fever must be differentiated from diseases accompanied by prolonged fever and the development of signs of intoxication – typhus, malaria, brucellosis, pneumonia, sepsis, tuberculosis, Hodgkin’s disease, etc. pallor of the skin of the face, pain and rumbling on palpation in the right iliac region, hepatolienal syndrome, bradycardia, an increase in the size of the tongue ntru, the appearance on the 8th-9th day of the illness of a scanty rosole-like rash on the abdomen and lower part of the chest, with a more severe course, the development of typhoid status. Establishing the correct diagnosis causes considerable difficulties, especially with atypical forms of typhoid fever. Therefore, each case of unclear fever lasting more than 3 days requires appropriate laboratory tests, including the isolation of the pathogen from blood and feces, the determination of pathogen antigens in the blood serum and feces. Getting typhoid hemoculture is an absolute confirmation of the diagnosis of typhoid fever. Detection of typroid sticks in fecal masses is less informative.
At the height of intoxication in patients with typhoid fever, hemogram changes are characterized by leukopenia, aneosinophilia, relative lymphocytosis and a moderate increase in erythrocyte sedimentation rate (ESR). In the early stages of the disease, you can also observe moderate leukocytosis with a shift of the leukocyte formula to the left. In the analysis of urine can detect protein and an increase in the number of red blood cells, as well as cylinders.
The most reliable method for the diagnosis of typhoid fever is the isolation of the pathogen. To do this, sow 10 ml of blood per 100 ml of medium containing bile (10-20% gall broth, medium Rappoport). Hemoculture excretion is most effective in the first week of the disease, however, for diagnostic purposes, the study is conducted during all periods of the temperature reaction. The cultures of feces (coproculture) and urine (urinoculture) are also carried out during all periods of the disease, especially at the 2nd or 3rd week. However, it must be remembered that the typhoid bacillus from feces and urine can be distinguished not only in patients with typhoid fever, but also from bacterial carriers in various febrile conditions. Crops of excrements and urine are carried out on dense nutrient media.
In addition to bacteriological studies, it is possible to detect typhoid O-Ag in feces or serum in the RCA, RLA, as well as by methods of immunofluorescence microscopy and ELISA from the first days of the disease.
Serological diagnosis (RNGA in paired sera with an erythrocyte typhoid O-diagnosticum) is carried out from the end of the first week of the disease, but the minimum diagnostic AT titer (1: 200) can be detected for the first time in the later stages of the disease (at the 3rd week of illness). RNGA with erythrocytic typhoid Vi-diagnosticum in patients with typhoid fever has an auxiliary value (minimum diagnostic titer of 1:40). Most often, this reaction is used to select individuals suspicious of bacteriocarrier. When the credits AT 1:80 and above, these individuals conduct repeated bacteriological research.
Treatment of Typhoid Fever
In all cases, even with suspected typhoid paratyphoid disease, patients must be hospitalized. The diet of patients should be mechanically and sparingly chemical. Usually, patients are prescribed table No. 4 (in the infectious hospital it is often referred to as table No. 4abt). Dishes should be boiled and rubbed through a sieve. Meals are shown fractional, in small portions; food should be washed down with plenty of liquid.
Bed rest of the patient is caused by the need to avoid tension of the abdominal muscles, which can provoke bowel perforation or bleeding. A sparing diet and bed rest should continue until the end of the 4th week of illness, i.e. until the onset of reparation of the intestinal mucosa. Diet and regimen must be observed regardless of the timing of the disappearance of intoxication.
For etiotropic therapy, chloramphenicol is usually administered at 0.5 g 5 times a day, on the 2nd day after the normalization of body temperature (inclusive), then 0.5 g, 4 times a day, on the 10th day of apyrexia. In severe cases, the disease is prescribed chloramphenicol succinate intramuscularly at 3 g / day. Considering the increasing resistance of typhoid bacillus to chloramphenicol, in the treatment of patients, ampicillin is also taken in doses of 0.5 g orally 4 times a day, azithromycin 500 mg per day, and then 250 mg / day orally, III generation cephalosporins (ceftriaxone 2 g each) / day intramuscularly) and fluoroquinolones (ciprofloxacin orally 500 mg 2 times a day). The duration of the courses of these drugs with their clinical effectiveness can be reduced to 5-7 days of apyrexia.
Given the presence of intoxication syndrome, all patients need to conduct active detoxification therapy by intravenous administration of colloid and crystalloid solutions.
In cases of intestinal bleeding, the patient is prescribed absolute rest in a dorsal position, hunger, a limited amount of fluid (not more than 500 ml, in teaspoons) for 12-24 hours. The expansion of the diet is possible not earlier than the 2nd day from the onset of bleeding; in the diet include meat and fish broths, juices, jelly, jelly, soft-boiled eggs. In the case of cessation of bleeding diet for 3-5 days gradually expand to the table number 4abt. From the first hours of bleeding, the patient needs to hang up an ice pack, slightly touching the front wall of the abdomen. From drugs to stop bleeding apply aminocaproic acid solution, blood substitutes, fibrinolysis inhibitors. For the prevention of rebleeding prescribed vikasol.
In the diagnosis of perforation of the intestine, the patient comes under the supervision of a surgeon.
Release of convalescents from the hospital with full clinical recovery is possible after the 21st day of normal body temperature, but the day of discharge can not be earlier than the end of the 4th week of the disease.
Prevention of Typhoid Fever
Epidemiological surveillance should be based on sanitary inspection, including sanitary and hygienic control of the external environment, sanitary and epidemiological regime at food facilities, etc. It is aimed at gathering information, dynamically assessing risk factors and living conditions, and includes monitoring the incidence of typhoid fever, taking into account the prevalence of various modes of transmission, as well as determining the phage-like landscape of isolated pathogens. Of great importance is the systematic control of chronic carriers of typhoid fever with periodic laboratory tests. In the implementation of epidemiological surveillance of typhoid fever, the most attention is paid to water supply facilities and dairy processing enterprises, as well as to the control of cleaning, sewage and disposal of sewage, the fight against flies. In the context of epidemiological diagnosis, a retrospective and operational epidemiological analysis is carried out. The main prerequisites for the complication of the epidemiological situation are the phenomena of social life that can activate the leading routes of transmission of the pathogen (water and food).
A harbinger of the complications of the epidemiological situation in typhoid fever and other intestinal infections may be the deterioration of bacteriological indicators of water and food, changes in the phage type and biological properties of the circulating pathogen.
Preventive measures are reduced primarily to the detection of bacterium carriers of typhoid bacilli and suppression of transmission routes. The most effective measures to eliminate water and food routes of transmission of pathogens that ensure the establishment of adequate water supply, sewage and good work of catering. Maintaining water supply and sewage facilities in proper sanitary and technical condition, compliance with sanitary and anti-epidemic norms and rules for their operation, cleaning and disinfection of wastewater before they are discharged into open water bodies serve as a guarantee of calm epidemic conditions for typhoid fever and other intestinal infections. Of great importance is the health education of the population, the mastery of sanitary minima by catering and food trade workers. In order to identify carriers among people entering the work on food and similar to them objects (not previously ill with typhoid fever), before admission to work, blood serum is tested in RPHA with O and Vi erythrocyte diagnostics and a single bacteriological examination of feces is performed. In case of negative results, the examined persons are allowed to work.
With a positive result of serological tests put a sample with cysteine; with its positive result, these people are not allowed to work. If these individuals in the past have suffered from typhoid fever, the serum is examined in RPHA with cysteine; feces, urine and bile should be examined using the bacteriological method. With positive results, bacteriological and serological studies of these individuals are considered as chronic carriers, they are registered and are not allowed to work.
Immunization carried out according to epidemiological indications among the population, starting from 3 years in areas unsuccessful in typhoid fever (incidence rate exceeds 25 cases per 100,000 population), and also to adults from risk groups: workers of sewage treatment plants, infectious diseases hospitals, bacteriological laboratories, etc. Vaccination is indicated for people traveling to countries in Asia, Africa and Latin America, where the incidence of typhoid fever is high. For this purpose, killed cellular vaccines with a protection ratio of 50-88% and subcellular (based on Vi-Ar) with a protection ratio of 62-75% are used.
Typhoid alcohol vaccine is administered twice in the subscapular region. The first dose is 0.5 ml, the second is 1 ml (after 25-35 days). Revaccination is carried out after 2 years at a dose of 1 ml. Vaccines VIANVAK and Tifim V are administered once subcutaneously in the outer surface of the upper third of the shoulder. Single dose for persons of any age – 0.5 ml. Revaccination is carried out every 3 years.
Activities in the epidemic focus
Information about the disease is sent to the territorial Center of State Sanitary and Epidemiological Surveillance in the form of an emergency notice.
Hospitalization of a patient or a person suspicious of the disease is obligatory due to the possibility of life-threatening complications – perforative peritonitis and intestinal bleeding. After clinical recovery, the patient is discharged from the hospital no earlier than the 21st day of normal body temperature. Before discharge, 3-fold bacteriological examination of feces and urine for the presence of the pathogen is necessary. All patients after discharge are subject to medical observation with thermometry once a week for the first 2 months, then once every 2 weeks for 1 month. 10 days after discharge from hospital, convalescents are examined 5 times for bacteriocarrier (feces and urine) at intervals of 1–2 days. Then for 3 months monthly once subjected to bacteriological examination of feces and urine. On the 4th month of observation, the bile was bacteriologically examined, and in the PHA with cysteine - blood serum. When the negative results of all studies have recovered removed from the dispensary observation.
Those who have been ill from among the employees of food enterprises and persons equivalent to them are not allowed to work for 1 month after discharge from the hospital. During this time, they are subjected to 5-fold bacteriological examination. With negative results of the study they are allowed to work, but monthly bacteriologically examined within the next 2 months. By the end of the 3rd month, bile and serum were examined in RPHA with cysteine. In the next 2 years, they are examined quarterly, and later throughout the work activity – 2 times a year (they examine the feces and urine). If during any of the surveys carried out after 3 months after recovery, at least once the pathogen is isolated, such persons are classified as chronic carriers of bacteria and are excluded from work. All chronic carriers of the causative agent of typhoid fever are registered in the centers of sanitary and epidemiological surveillance. They are trained in the preparation of disinfectant solutions, the current disinfection, proper hygienic behavior.
Work in the outbreak of typhoid paratyphoid infection is aimed at identifying the source of infection (mild patient, convalescent, chronic carrier), protecting people who have communicated with the patient, and observing them for a maximum incubation period (21 days) to identify new patients. The children of preschool age who attended child care facilities, food industry workers, and persons equated to them reside in the outbreak, are suspended from work and visits to the KPI until receiving a one-time negative result of the carrier study. For protection against the disease of typhoid fever and paratyphoid fever of persons who have interacted with patients or convalescents in the outbreak, a typhoid bacteriophage is used. It is prescribed 3 times with an interval of 3-4 days; however, the first dose is administered after the material is collected for bacteriological examination.
Given the persistence of Salmonella in the environment, disinfection is carried out in the foci. The current disinfection is carried out by relatives during the entire period of stay of the patient or bacillicarrier in the focus of infection, the final disinfection is performed by the disinfection service workers after the patient is hospitalized.