Intestinal amoebiasis, Acute amoebic dysentery, Acute amoebiasis, Intestinal amoebiasis

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Acute amoebic dysentery (A06.0)

general information

Short description

Acute amoebic dysentery - the main and most common form of amoebic invasion, characterized by stool disorder with ulcerative lesions of the colon.

Period of flow

Incubation period lasts from 1-2 weeks to 3 months or longer.

Classification

The disease can be severe, moderate and mild form.

Etiology and pathogenesis

When cysts enter small intestine In humans, the destruction of their membranes occurs and from them comes the quadrangular maternal form of amoeba, which, when fission, forms 8 mononuclear amoebas. Under favorable conditions, they multiply, turning into vegetative forms that live in proximal colon.

The amoeba's own enzymes have proteolytic activity, which ensures their penetration into the intestinal wall. In the intestine, cytolysis of the epithelium and tissue necrosis with the formation of ulcers occur. In intestinal amoebiasis, the pathological process is mainly localized in the blind and ascending colon. In some cases, there is a lesion of the rectum, less often - other parts of the intestine.

Epidemiology

Amoebiasis - intestinal anthroponosis. The transmission mechanism is fecal-oral. Various transmission routes are possible: food, water, contact and household.

Sporadic morbidity is characteristic (the possibility of epidemic outbreaks is being questioned). Diseases are recorded throughout the year, with the peak incidence in the hot months.
It is found in all countries of the world, the highest incidence is typical for areas of tropical and subtropical climates, including Central Asia and the Caucasus. The ratio between incidence and carriage in endemic areas is 1: 7, in the rest - from 1:21 to 1:23.

Factors and risk groups

Women are especially susceptible to amoebiasis in the third trimester of pregnancy and postpartum period(it is assumed that this is due to the characteristics of the cellular immune response in pregnant women), as well as persons who received immunosuppressive therapy.

Clinical picture

Symptoms, course

The state of health remains satisfactory for a long time: intoxication is not expressed, body temperature is normal or subfebrile. Only in a small number of cases do patients have general weakness, fatigue, headaches, loss of appetite, feeling of heaviness in the epigastrium Epigastrium - the area of ​​the abdomen, bounded from above by the diaphragm, from below by a horizontal plane passing through a straight line connecting the lowest points of the tenth ribs.
, sometimes - short-term pain in the abdomen, flatulence.

The cardinal symptom of intestinal amoebiasis is stool disorder. In the initial period, the stool is abundant, fecal, with transparent mucus, 4-6 times a day, with a pungent odor. Later, the frequency of bowel movements increases up to 10-20 times a day, the stool loses its fecal character and is vitreous mucus. In the future, blood is added to the feces and they take the form of raspberry jelly.

V acute form diseases, persistent or cramping abdominal pains of varying intensity are possible, which intensify during bowel movements. When the rectum is damaged, painful tenesmus occurs. Tenesmus - false painful urge to defecate, for example, with proctitis, dysentery
.
The abdomen is soft or slightly distended, on palpation it is painful along the colon.

Acute symptoms intestinal amoebiasis usually persists no more than 4-6 weeks. Then, without specific treatment, as a rule, there is an improvement in well-being and relief of colitis. The duration of remission is from several weeks to several months. After remission, all or most of the symptoms of amoebiasis return.

Diagnostics

In the diagnosis of amoebiasis, a carefully collected epidemiological history, anamnesis of the disease, and data from a clinical examination of patients are important.
Disease recognition is assisted sigmoidoscopy Sigmoidoscopy is a method for examining the rectum and sigmoid colon by examining the surface of their mucous membrane using a sigmoidoscope inserted into the intestinal lumen
and biopsy intestinal mucosa, X-ray examination.

Endoscopic examination the colon reveals ulcers ranging in size from 2 to 10-20 mm in diameter, located most often at the tops of the folds. Ulcers have edematous, swollen, undermined edges; the bottom of the ulcer can reach the submucosa, covered with pus and necrotic masses. The ulcer is surrounded by a zone (belt) of hyperemia Hyperemia - increased blood filling in any part of the peripheral vascular system.
... The mucous membrane, free from ulcers, is little changed, sometimes there may be a slight swelling and hyperemia.

Irrigoscopy Irrigoscopy - X-ray examination of the colon with retrograde filling of it with a contrast suspension
reveals uneven filling of the colon, the presence of spasm and rapid bowel movement.

Laboratory diagnostics

The most important for the diagnosis of amoeba dysentery is the identification of a large vegetative form of amoeba in feces, a tissue form of amoeba in sputum, the contents of abscesses and material from the bottom of ulcers. Detection of luminal forms and cysts of amoebas in feces is not enough for a final diagnosis.

The main method detection of amoebas - microscopy of native feces preparations.

Differential diagnosis

Amoebic dysentery is differentiated from other protozoal infections, dysentery, ulcerative colitis, bowel cancer.

Complications

Treatment abroad

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Acute and Chronic Dysentery

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Disease Code (ICD-10) A03.0

Dysentery (syn.: Shigellosis) (dysenteria) - infection caused by shigella, proceeding with symptoms of intoxication and a predominant lesion of the distal colon.

Allocate acute and chronic dysentery.

• Acute dysentery proceeds in several variants (colitis, gastroenterocolitic and gastroenteric), each of which can be presented in mild, moderate and severe forms.
• Chronic dysentery has a recurrent or continuous course and can also be mild, moderate and severe.
• There is also shigellosis bacteria carrier (bacterial excretion), which is considered as a subclinical form of an infectious process.

Acute dysentery

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Colitis variant with mild course the disease is characterized by moderate or mild intoxication. It usually begins acutely with a short-term rise in temperature to 37–38 ° С. In the first hours of the disease, weakness, loss of appetite are observed, later there are moderate abdominal pains. Stool 3-5 to 10 times a day. Stool is semi-liquid or liquid, often with mucus and sometimes streaked with blood. Patients remain able-bodied and often self-medicate. On examination, the tongue is coated. The sigmoid colon is painful and spasmodic, with a rumbling on palpation. With sigmoidoscopy, catarrhal or catarrhal-hemorrhagic proctosigmoiditis and sphincteritis can be detected. Changes in the hemogram are insignificant. The disease lasts 3-5, at least 7-8 days and ends with recovery.

Colitis variant with moderate severity usually begins acutely, with chills, a feeling of "aches" and fatigue throughout the body. The temperature rises to 38-39 ° С and stays at this level for 3-5 days, rarely longer. Anorexia is common, headache, nausea, sometimes vomiting, sharp cramping abdominal pains, tenesmus. Stool frequency 10–20 times a day. Stool quickly loses its fecal character and consists of mucus stained with blood. They can be scanty, rectal spitting, or more abundant, slimy. The phenomena of hemocolitis are observed in 70-75% of patients. Acute phenomena on the 3-5th day of illness gradually weaken. In the stool, the amount of mucus and blood decreases, the stool is normalized, but the coprogram remains pathological. When sigmoidoscopy reveals catarrhal-erosive proctosigmoiditis. Clinical recovery occurs by the end of the 2nd week of illness.

Heavy course of the political option dysentery is characterized by an acute onset with a rise in temperature to 39 ° C and above, a pronounced intoxication. Can be observed fainting, delirium, nausea, vomiting. Abdominal pain is severe and accompanied by excruciating tenesmus and frequent urges on urination. Stool 20–25 to 50 times a day, scanty, colourless, muco-bloody. Sometimes the stool looks like meat slops. Patients are lethargic, adynamic. Dry skin and mucous membranes, blood pressure reduced, there is a constant tachycardia. By the end of 1–2 days, a collaptoid state may develop. Bowel tenesmus and spasms can be replaced by paresis, bloating, anus gaping, and involuntary bowel movements. In the blood, leukocytosis or leukopenia with a shift is observed leukocyte formula to the left and toxic granularity in leukocytes. Palpation of the abdomen reveals spasm, soreness and rumbling of the large intestine (or only sigmoid colon), flatulence. Serious condition patients persist for 7-10 days. During sigmoidoscopy in case of dysentery, the Zone determines catarrhal-hemorrhagic, catarrhal-erosive, less often ulcerative changes in the mucous membrane. At severe course Flexner's dysentery reveals fibrinous-necrotic, fibrinous-ulcerative and phlegmonous-necrotic lesions of the colon mucosa. The disease lasts 3–6 weeks or more.

In persons with immunodeficiency of various origins, severe fever may be absent, but the defeat of the colon is total in nature.

Gastroenterocolitic variant dysentery proceeds as food toxicoinfection with a short incubation period, a violent onset of the disease. The main syndrome at the onset of the disease is gastroenteritis, which is accompanied by severe symptoms of intoxication. In the future, the symptoms of enterocolitis begin to dominate. For the initial period, typical vomiting, profuse diarrhea, profuse watery bowel movements without blood and mucus, diffuse pain in the abdomen. Subsequently, the stool becomes less abundant, impurities of mucus and blood are found in it. This option can be mild, moderate, and severe. When assessing the severity of the course of the disease, the degree of dehydration of the body is taken into account. In the case of a mild course of dysentery, there are no symptoms of dehydration. The course of the disease of moderate severity is accompanied by degree I dehydration (fluid loss is 1-3% of body weight). In severe cases of dysentery, dehydration of the II – III degree develops (fluid loss is 4–9% of body weight).

The gastroenteric variant is close downstream to the initial period of the gastroenterocolitic variant. Its difference lies in the absence of colitis symptoms in the later period of the disease (after 2-3 days of illness). The leading symptoms are gastroenteritis and signs of dehydration.

Erased flow dysentery occurs in all variants of the disease. It is characterized by minor abdominal pain and short-term (1–2 days) bowel dysfunction. The stool is semi-liquid, without blood, and often without mucus. Body temperature is normal, but may be subfebrile. Often, on palpation, an increased sensitivity of the sigmoid colon is determined. In the coprogram, the number of leukocytes exceeds 20 in the field of view. With sigmoidoscopy, catarrhal proctosigmoiditis is detected. The diagnosis is established after a thorough collection of an anamnesis of the disease, an epidemiological history, as well as a timely laboratory examination.

Prolonged course of acute dysentery characterized by the preservation clinical signs diseases for 1.5–3 months. At the same time, in most patients, there are phenomena of a sluggish inflammatory process in the intestine with the absence of its functional and morphological recovery in terms of up to 3 months.

Complications: formidable, but relatively rare complications of the disease include toxic-infectious and mixed (toxic-infectious + dehydration) shocks. They develop during the height of the disease and have a serious prognosis. The complications of acute dysentery include its relapses, which are observed in 5-15% of cases. Some patients experience exacerbation of hemorrhoids, anal sphincter fissures. Weakened patients may develop complications associated with the addition of secondary flora: pneumonia, ascending urogenital infection, as well as severe intestinal dysbiosis.

Rarer complications include perforation of intestinal ulcers followed by peritonitis, toxic bowel dilatation, mesenteric vascular thrombosis, and rectal prolapse.

Acute dysentery relatively rarely turns into chronic (with Flexner's dysentery in 2-5%, with Sonne's dysentery - in 1% of cases).

Chronic dysentery

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There are two forms of chronic dysentery - recurrent and continuous.

Recurrent form occurs much more often continuous and is characterized by the alternation of remissions and relapses of dysentery. The duration of each new return of the disease and light intervals may be different. Symptoms of lesions of the distal colon predominate. However, a systemic examination of a patient with chronic dysentery can reveal signs of involvement in the pathological process of the stomach, small intestine, pancreas, hepatobiliary system.

Clinical picture recurrence is similar to that in mild or moderate acute dysentery. Bowel dysfunction is characterized by persistence and duration.

To a greater or lesser extent, the central nervous system... Patients are irritable, excitable, their performance is reduced, sleep is disturbed, headaches are frequent. Some of them have expressed autonomic disorders (symptoms of vagotonia are more common).

When sigmoidoscopy reveals polymorphic changes in the mucous membrane of the rectum and sigmoid colon. During an exacerbation, the sigmoidoscopic picture resembles the changes characteristic of acute dysentery. However, their intensity in different areas is not the same. It is possible to alternate bright hyperemia with paler areas of the mucous membrane, on which the expanded vascular network is clearly visible. The mucous membrane in these places is thinned, dull, and easily wounded.

• A03.0. Dysentery due to Shigella dysenteriae.
• A03.1. Shigellaflexneri dysentery.
• A03.2. Dysentery due to Shigella boydii.
• A0Z.Z. Shigella sonnei dysentery.
• A03.8. Other dysentery.
• A03.9. Dysentery, unspecified.

ICD-10 code

A03 Shigelez

A03.0 Shigellosis due to Shigella dysenteriae

A03.1 Shigellosis due to Shigella flexneri

A03.2 Shigellosis due to Shigella boydii

A03.3 Shigellosis due to Shigella sonnei

A03.8 Other shigellosis

A03.9 Shigellosis, unspecified

What causes dysentery?

Shigella is ubiquitous and a common cause of inflammatory dysentery. Shigella is the cause of 5-10% of diarrheal diseases in many regions. Shigella are divided into 4 main subgroups: A, B, C and D, which in turn are divided into specific serological types. Shigella flexneri and Shigella sonnei are found more frequently than Shigella boydii, and especially the virulent Shigella dysenteriae. Shigella Sonnei is the most commonly found isolate in the United States.

The source of infection is the feces of sick people and recovering carriers. Direct distribution is carried out by the fecal-oral route. Indirect spread is through contaminated food and objects. Fleas can serve as carriers of Shigella. Most often, epidemics occur in densely populated populations with inadequate sanitary measures. Dysentery is especially common in young children living in endemic regions. In adults, the onset of dysentery is usually less severe.

Convalescent and subclinical carriers can be a serious source of infection, but long-term carriers of this organism are rare. Dysentery leaves almost no immunity behind.

The causative agent penetrates the mucous membrane of the lower intestines, which causes mucus secretion, hyperemia, leukocyte infiltration, edema, and often superficial ulceration of the mucous membrane. Shigella dysenteriae type 1 (not found in the US) produces Shiga toxin, which causes severe watery diarrhea and sometimes hemolytic uremic syndrome.

What are the symptoms of dysentery?

Dysentery has an incubation period of 1-4 days, after which the typical symptoms of dysentery appear. The most common manifestation is watery diarrhea, which is indistinguishable from diarrhea that occurs with other bacterial, viral and protozoal infections, in which there is an increased secretory activity of intestinal epithelial cells.

In adults, dysentery may begin with episodes of cramping abdominal pain, urge to defecate, and defecation with formalized feces, followed by temporary relief of pain. These episodes are repeated with increasing severity and frequency. Diarrhea becomes pronounced, while the stool can be soft, liquid, contain an admixture of mucus, pus and often blood. Rectal prolapse and subsequent stool incontinence can cause acute tenesmus. In adults, the manifestation of infection can proceed without fever, with diarrhea, in which there is no admixture of mucus or blood in the stool, and with little or no tenesmus. Dysentery usually ends with recovery. In the case of a moderate infection, this occurs after 4-8 days, in the case of acute infection- in 3-6 weeks. Severe dehydration with loss of electrolytes and circulatory collapse and death usually occurs in debilitated adults and children under 2 years of age.

Rarely, dysentery begins suddenly with rice-water diarrhea and serous (in some cases bloody) stools. The patient may vomit and quickly become dehydrated. Dysentery may manifest as delirium, seizures, and coma. In this case, diarrhea is poorly expressed or completely absent. Death can occur within 12-24 hours.

In young children, dysentery begins suddenly. Fever, irritability or tearfulness, loss of appetite, nausea or vomiting, diarrhea, abdominal pain and bloating, and tenesmus occur. Within 3 days, blood, pus and mucus appear in the stool. The number of bowel movements can reach more than 20 per day, and weight loss and dehydration become acute. If untreated, the child can die within the first 12 days of the illness. In cases where the child survives, the symptoms of dysentery gradually decrease by the end of the second week.

Secondary bacterial infections, especially in debilitated patients and in patients with dehydration. Acute ulceration of the mucous membrane can lead to acute blood loss.

Other complications are uncommon. These can include toxic neuritis, arthritis, myocarditis, and rarely intestinal perforation. Hemolytic uremic syndrome can complicate shigellosis in children. This infection cannot take chronic course... It is also not an etiological factor in ulcerative colitis. Reactive arthritis is more common in patients with the HLA-B27 genotype after shigellosis and other enteritis.

How is dysentery diagnosed?

Making diagnostics simpler high index suspicion of shigellosis during outbreaks of infection, the presence of the disease in endemic regions and the detection of leukocytes in feces on examination of smears stained with methylene blue or Wright's dye. Stool culture is diagnostic and should be done. In patients with symptoms of dysentery (presence of mucus or blood in the feces), differential diagnosis of dysentery with invasive E. coli, salmonella, yersiniosis, campylobacteriosis, as well as amebiasis and viral diarrhea is necessary.

The surface of the mucous membrane when viewed with a rectoscope is diffusely erythematous with a large number of small ulcers. Despite the fact that the number of leukocytes is reduced at the onset of the disease, on average it is 13x109. Hemoconcentration and metabolic acidosis associated with diarrhea are common.

Definition Shigellosis (dysentery) is an infectious human disease caused by bacteria of the genus Shigella. It proceeds with diarrhea syndrome with a predominant lesion of the mucous membrane of the distal colon. 2

Etiology Bacterial dysentery is caused by microorganisms united in the genus Shigella, which, according to modern classification is subdivided into 4 species: Shigella dysenteriae (Grigorieva - Shiga, Stutzer-Schmitz, Large-Sachs). Shigella flexneri subspecies Newcastle. Shigella boydii. Shigella sonnei. 3

Each of these species, except for the Sonne Shigella, consists of several serotypes. All Shigella are motionless; do not stain by gram, do not ferment lactose, with the exception of Zonne. Microscopically, these are rods with a rounded end, 2-4 microns long, 0.5-0.6 microns wide. They have an antigenic structure (somatic O-antigen and surface K-antigen). 4

Shigella are relatively resistant to the effects of some physical and chemical environmental factors: when exposed to ultraviolet irradiation, they die after 10 minutes, direct sunlight - after 30 minutes. ; quickly stop functioning under the influence disinfectants; can maintain their viability in the external environment for up to 3-4 months, in water for up to 7 days and food products for 5-14 days and longer. At a temperature of 100 C they die instantly, at a temperature of 60 C - after 20 -30 minutes. 6

Epidemiology The source of the causative agent is a bacterial excretory agent. - a sick person or a sick person is most dangerous in the first days of the disease, when a large number of shigella is excreted with frequent loose stools. The transmission mechanism is fecal-oral. The main routes of transmission for dysentery of Grigoriev-Shiga are household, Flexner, Newcastle - water, Sonne - food. 7

Transmission factors: infected water, milk, sour cream, as well as those dishes where these products are included in the form of components (mashed potatoes, salads, etc.). eight

Clinic The duration of the illness ranges from several days to three months. The incubation period is 2-5 days, but can be shortened to 3-12 hours and lengthened to 710 days. nine

Classification of bacterial dysentery: 1. in form: acute up to 1 -1, 5 months chronic from 3 months to 1 -2 years (in 2 -3% of cases, recurrent continuous) shigellosis bacterial carriage. 2.on option: colitis gastroenterocolitic gastroenteric 10

3. by severity: mild (up to 60 -70% of all cases) moderate - with dehydration of I-II degrees (20 -30%) severe with dehydration of III-IV degrees (1, 52%) 4. along the course: obliterated lingering (1, 5 -3 months) recurrent continuous subclinical convalescent 11

Complications: more often in children: ndysphagia, notitis, nstagmus, prolapse of the rectum. in adults: ITSH, OSSN, exacerbation of hemorrhoids, anal fissures. Mortality before a / b therapy is 10 -15%. Mortality in children 0, 2 -0, 6% in children, elderly and senile people. 13

The disease begins acutely. A short prodromal period may be present, manifested by a short feeling of discomfort in the abdomen or mild chills, headache, malaise, weakness. The first sign of developing acute dysentery is usually persistent or recurrent pain in the abdomen, localized in its lower part, mainly on the left in the region of the sigmoid colon. fourteen

A feature of the pain syndrome is its connection with the act of defecation, the intensity of pain decreases and even it disappears for a while after a bowel movement. Following the pain syndrome, or simultaneously with it, stool disorders and signs of intoxication appear - severe fever, headache, increasing weakness. 15

The stool initially has a mushy character, then its quantity rapidly decreases, it becomes scarce. V feces impurities of blood and mucus appear (bloody cords, streaks, point inclusions). In the midst of the disease, the stool is scanty and consists of a small amount of mucus with blood - "rectal spitting". Stool frequency depends on the severity of the disease. 16

Chronic dysentery Flexner's dysentery becomes chronic in 2 - 5%, Sonne's dysentery in 1% of cases. Chronic dysentery lasts more than 3 months. It is caused by the presence of the same pathogen in the human body. Immunity is not persistent specific. eighteen

Diagnosis The diagnosis of dysentery can typically be made on the basis of clinical and epidemiological data, pending the availability of special studies. 19

Special diagnostic methods: 1. Bacteriological diagnostics: examination of feces (from 22 to 80%). 2. Serological diagnostics (RNGA, diagnostic titer 1: 200). Blood should be taken from the 5th day, the maximum titers at the 2nd week of illness. The research is carried out in dynamics. twenty

Non-specific methods are of auxiliary value, but can establish the etiology: n n scatological examination (mucus, leukocytes, erythrocytes, epithelial cells); sigmoidoscopy. 21

Treatment The question of hospitalization is decided by the doctor who identified the patient. If the patient is left at home, it is necessary to notify the territorial center of the State Sanitary and Epidemiological Supervision. More than 60% of patients are usually hospitalized. Indications for hospitalization: clinical epidemiological social welfare. 22

Among all patients, the following must be hospitalized: collectives, § as well as in the absence of the necessary conditions for treatment at home. 23

Treatment of dysentery should be comprehensive, including etiotropic and pathogenetic therapy, medical and protective regimen, diet therapy and immunostimulating therapy. Diet of patients with dysentery: § First, diet No. 4 is prescribed, which provides mechanical and chemical sparing of the digestive tract. § After stool normalization, diet No. 4 is indicated. § With the advent of appetite and the subsidence of colitis, the patients are transferred to diet No. 2. § Before discharge, they are transferred to diet No. 15. 24

Antibacterial therapy The name of the medication Furazolidone Application form Table. 0.1 Daily dose Dose for a course of treatment 0. 4 2. 0 -2. 8 Ciprofloxacin Tab. 250 mg 1, 0 5, 0 Co-trimoxazole Tab. 4 tab. 20 -28 tab. Doxycycline Caps. 0.1 0.2 -0. 1 0.6 Gentamicin 80 mg. 40 mg. 160-240 mg 960 mg. 25

Detoxification therapy Name of medication Form of application Daily dose Oralit, Package for 1 rehydron, liter of water citroglucosolan 30 -70 ml / kg. Trisol, quartasol, chlorosalt, lactosolt 60 -120 ml / kg Vials of 400.0 and 200.0 ml Dose per course of treatment Up to 2-3 liters per day in 2-3 vials 26

Medicines additional assortment Name of medication Dysenteric bacteriophage Application form Per os bottle In enema Daily dose 100.0 Dose per course of treatment 500.0 Herbal infusions and decoctions (St. John's wort, chamomile, oak bark, blueberries, bird cherry) Glass 2-3 cups 6-10 cups Activated carbon Tab. 15 tab. 45 -50 tab. Enemas with vegetable oil, fish oil, vinyline Bottles 50 ml 100 -200 ml 28

Medicines of additional assortment Name of medication Form of application Daily dose Dose for a course of treatment Vitamins gr. A Vitamins gr. Vitamins gr. With Dragee 3 -4 40 15 doses 360 doses Eubiotics Vials of 5 doses (bificol, bifidumbacterin) 29

Criteria for recovery § Disappearance of normalization of the tract. symptoms of intoxication and the function of the gastrointestinal § The recovery of persons in the decreed group is confirmed by negative results of bacteriological examination of feces. thirty

Prognosis In the treatment of patients with dysentery, as a rule, the prognosis is favorable. However, with a severe form of the disease in elderly people, especially with concomitant chronic diseases deaths are also possible. In case of dysfunction immune system in 20 - 25% the disease is protracted. Of these patients, as a rule, in 2 - 5%, acute dysentery becomes chronic. 31

Prevention and measures in the outbreak Those who have had acute dysentery are discharged from the hospital no earlier than 3 days after clinical recovery and a negative result of a single control bacteriological study of feces, which is performed no earlier than the 2nd day after the end of etiotropic therapy (decreed group of persons). Employees of food enterprises are allowed to work if they have a doctor's certificate from a hospital about recovery without additional bacteriological studies. 32

They are all subject dispensary supervision for up to 1 month, with double sowing at the end of observation with an interval of 2 - 3 days. For persons who were in contact with patients with dysentery, medical supervision is established for 7 days. When a patient with dysentery is identified in an organized group, persons in contact with him are subjected to a control bacteriological study. Chemoprophylaxis in contact with the patient is not performed. 33