Periods of cholera. Causes of cholera
is an acute intestinal infection that occurs when a person is infected with Vibrio cholerae. Cholera is manifested by severe frequent diarrhea, profuse repeated vomiting, which leads to significant loss of fluid and dehydration of the body. Signs of dehydration include dryness skin and mucous membranes, decreased tissue turgor and wrinkling of the skin, sharpening of facial features, oligoanuria. The diagnosis of cholera is confirmed by the results of bacteriological culture of feces and vomit, and serological methods. Treatment includes isolation of the cholera patient, parenteral rehydration, and therapy with tetracycline antibiotics.
Cholera is transmitted by household ( dirty hands, objects, utensils), food and by water by the fecal-oral mechanism. Currently, flies play a special role in the transmission of cholera. A waterway (a contaminated water source) is the most common. Cholera is an infection with high susceptibility; infection most easily occurs in people with hypoacidosis, some anemia, infected with helminths, and alcohol abusers.
Symptoms of cholera
The incubation period for infection with Vibrio cholerae lasts from several hours to 5 days. The onset of the disease is acute, usually at night or in the morning. The first symptom is intense painless urge to defecation, accompanied by an uncomfortable feeling in the abdomen. Initially, the stool has a liquefied consistency, but retains its fecal character. Quite quickly, the frequency of bowel movements increases, reaching 10 or more times per day, while the stool becomes colorless and watery. With cholera, stools are usually not foul-smelling, unlike other infectious diseases intestines. Increased secretion of water into the intestinal lumen contributes to a noticeable increase in the amount of excreted feces. In 20-40% of cases, the stool takes on the consistency of rice water. Typically, stool appears as a greenish liquid with white, loose flakes similar to rice.
Often there is rumbling, seething in the stomach, discomfort, and fluid transfusion in the intestines. The progressive loss of fluid in the body leads to symptoms of dehydration: dry mouth, thirst, then a feeling of coldness in the extremities, ringing in the ears, and dizziness. These symptoms indicate significant dehydration and require emergency measures to restore water-salt homeostasis in the body.
Diagnosis of cholera
Severe cholera is diagnosed based on the clinical picture and physical examination. The final diagnosis is established on the basis of bacteriological culture of feces or vomit, intestinal contents (sectional analysis). The material for sowing must be delivered to the laboratory no later than 3 hours from the moment of receipt; the result will be ready in 3-4 days.
There are serological methods for detecting infection with Vibrio cholerae (RA, RNGA, vibrocidal test, ELISA, RCA), but they are not sufficient for final diagnosis, being considered methods for accelerated tentative identification of the pathogen. Accelerated methods for confirming a preliminary diagnosis can be considered luminescence-serological analysis, dark-field microscopy of vibrios immobilized with O-serum.
Treatment of cholera
Since the main danger with cholera is the progressive loss of fluid, its replenishment in the body is the main goal of treating this infection. Treatment of cholera is carried out in a specialized infectious diseases department with an isolated ward (box) equipped with a special bed (Philips bed) with scales and utensils for collecting feces. For precise definition degree of dehydration, their volume is recorded, the hematocrit, the level of ions in the serum, and the acid-base indicator are regularly determined.
Primary rehydration measures include replenishing the existing deficiency of fluid and electrolytes. In severe cases it is done intravenous administration polyionic solutions. After this, compensatory rehydration is performed. The introduction of fluid occurs in accordance with its losses. The occurrence of vomiting is not a contraindication to continued rehydration. After restoring the water-salt balance and stopping vomiting, antibiotic therapy is started. For cholera, a course of tetracycline drugs is prescribed, and in case of repeated isolation of bacteria, chloramphenicol.
There is no specific diet for cholera; in the first days table No. 4 may be recommended, and after subsiding severe symptoms and restoration of intestinal activity (3-5th laziness of treatment) - nutrition without any special features. Those who have had cholera are advised to increase potassium-containing foods in their diet (dried apricots, tomatoes and orange juice, bananas).
Forecast and prevention of cholera
With timely and complete treatment, recovery occurs after suppression of the infection. Currently modern drugs effectively act on Vibrio cholerae, and rehydration therapy helps prevent complications.
Specific prevention of cholera consists of a single vaccination with cholera toxin before visiting regions with high level spread of this disease. If necessary, revaccination is carried out after 3 months. Non-specific measures Cholera prevention involves compliance with sanitary and hygienic standards in populated areas, at food establishments, and in areas where water is collected for the needs of the population. Individual prevention consists of maintaining hygiene, boiling water, washing food and preparing it properly. When a case of cholera is detected epidemiological focus subject to disinfection, patients are isolated, all contact persons are observed for 5 days to identify possible infection.
Cholera(from ancient Greek χολή “bile” and ῥέω “flow”) - an acute intestinal saprozoonotic infection caused by bacteria of the species Vibrio cholerae. Characterized by a fecal-oral mechanism of infection, damage to the small intestine, watery diarrhea, vomiting, rapid loss of fluid and electrolytes by the body with the development varying degrees dehydration up to hypovolemic shock and death.
3.2 Etiology
The causative agent Vibrio cholerae has more than a hundred serogroups. It was discovered by Koch in the 19th century and has the shape of a comma. Vibrio cholerae can survive on surfaces food products and in cooked food for up to 5 days, can be stored in water, kept in boiling water for 1 minute.
The infection is anthroponotic and epidemic in nature. Of particular importance in the epidemiology of the disease are healthy carriers, that is, people infected with Vibrio cholerae without clinical symptoms of the disease and capable of infecting other people. The greatest danger in terms of cholera infection is drinking undisinfected water and eating contaminated foods, including those that have not undergone heat treatment. Contact-household transmission is also possible. An epidemic danger is posed by stagnant bodies of warm water into which sewage waste flows, since they create favorable conditions for the proliferation of cholera pathogens.
3.3 Epidemiology
The World Health Organization estimates that in 2010 there were between 3 and 5 million cases of cholera worldwide and 100,000 to 130,000 deaths. These diseases occurred mainly in developing countries. In the early 1980s, the death rate was estimated to exceed 3 million per year. The exact number of cases is difficult to estimate because many go unreported due to fears that cholera outbreaks could have an impact negative effect on the influx of tourists in these countries. Currently, cholera continues to be epidemic and endemic in many regions of the world.
All modes of cholera transmission are variants of the fecal-oral mechanism. The source of infection is a person with cholera and a healthy (transient) vibrio carrier, releasing Vibrio cholerae into the environment with feces and vomit.
Healthy vibrio carriers are of great importance for the spread of the disease. The carrier/patient ratio can reach 4:1 with the Vibrio cholerae O1 variant and 10:1 with non-O1 Vibrio cholerae (NAG vibrios).
Infection occurs mainly through drinking undisinfected water, ingesting water when swimming in contaminated bodies of water, while washing, and also when washing dishes with contaminated water. Infection can occur through consumption of food contaminated during cooking, storage, washing or serving, especially non-cooked foods (shellfish, shrimp, dried and lightly salted fish). Possible contact-household (through contaminated hands) transmission route. In addition, Vibrio cholerae can be carried by flies.
Poor sanitary and hygienic conditions, overcrowding, and large population migration play an important role in the spread of the disease. Here it is necessary to note endemic and imported foci of cholera. In endemic areas (Southeast Asia, Africa, Latin America), cholera is recorded throughout the year. Imported epidemics are associated with intensive population migration. In endemic areas, children are more likely to get sick because adult population already has naturally acquired immunity. In most cases, an increase in incidence is observed during the warm season.
In approximately 4-5% of recovered patients, chronic carriage of vibrio develops in the gallbladder. This is especially true for older people. After an illness, the body of those who have recovered from the disease develops immunity, which does not exclude infection with other serotypes of Vibrio cholerae.
Clinical picture (symptoms and signs). The incubation period ranges from several hours to 5 days, more often 2-3 days. There are several clinical forms of cholera: enteric, gastroenteric, algid. There is also a gastric form of cholera, when diarrhea is preceded by. The onset of the disease is acute - with a sudden, uncontrollable urge to go down with copious discharge from the intestines. At first, the discharge is liquid, fecal, then watery, odorless. The color of the discharge also changes: at first it resembles beans, peas, then milk soup, later rice water. Stools can sometimes contain mucus, undigested food debris, and blood. This first phase - cholera, cholera, or diarrhea - lasts from several hours to 1-2 days. Sometimes the disease can be limited only to these phenomena.
Subsequently, cholera gastroenteritis develops - the second phase. Repeated and profuse vomiting occurs without nausea. Diarrhea continues. Enormous fluid losses (up to 10% or more of the patient’s body weight) lead to dehydration, loss of sodium salts, etc. The patient’s condition is extremely serious, he is exhausted by continuous vomiting and diarrhea. The tongue is covered with a white coating and is dry. Excruciating thirst. Intoxication phenomena are increasing. deaf, blood pressure decreases sharply. Acrocyanosis is observed. Urine production decreases or completely stops. The stomach is sunken. Sometimes there is moderate pain in the abdomen, more often - a feeling of heaviness. When a large amount of fluid is detected in the intestines. During this period, painful and painful clonic, tonic or mixed symptoms appear.
The third phase is algid. The patient is in prostration, excruciating thirst, hoarse voice (exicosis), even to the point of aphonia. Consciousness is preserved. Acrocyanosis progresses. Facial features become sharper, cheekbones protrude, eyes become sunken, sclera become dull and injected. The skin becomes thinner - it easily folds, becomes wrinkled, cold to the touch, and covered with sticky sweat. The temperature is sharply reduced (to 35-34° and below). continue. A painful hiccup appears. The pulse is threadlike and frequent. Heart sounds are muffled, blood pressure cannot be determined. Urine flow may stop completely (cholera anuria). Due to blood thickening, the amount increases to 6-8 million or more per 1 mm3. Leukocytosis up to 10,000-15,000 and above. The algic phase passes into the asphyxial phase (fourth phase), during which shortness of breath occurs. Consciousness is darkened, and convulsions intensify. With the phenomena of increasing shortness of breath and collapse, the patient dies.
The described phases (forms) of cholera are not observed in all patients. Milder (enteric, gastroenteric) forms are more common, especially with cholera caused by the El Tor biotype. Lightning-fast and “dry” death is described, when death occurs from sudden intoxication even before the development of diarrhea and vomiting.
Clinical picture and course
The duration of the incubation period ranges from several hours to 6 days (usually 2-3 days), less often slightly longer. The onset of the disease is acute, with a sudden urge to go down, often appearing at first at night. The urge is uncontrollable, with copious discharge. Defecation usually occurs without pain or tenesmus. The discharge is initially liquid, fecal, and then after several bowel movements it acquires a thin, watery consistency and loses its odor. The color of the released masses also changes; At first they look like bean soup, then like milk soup, and later like rice water. Sometimes stools contain mucous masses, undigested food debris, and very rarely blood.
The general condition of the patient in this first phase - cholera enteritis, cholera diarrhea, or diarrhea - is slightly disturbed, the disease is carried on the legs, which in epidemiological terms poses a great threat to others. Patients note general weakness, thirst, and lack of appetite. The temperature is not elevated or there is a low-grade fever. The duration of the first period is 1-2 days (G. P. Rudnev, A. G. Podvarko). Sometimes the disease can be limited only to these phenomena.
As the disease continues, the second phase develops - cholera gastroenteritis. Vomiting appears, repeated and in large portions, without preliminary nausea, diarrhea continues. Cholera vibrios are easily detected in feces and vomit (Z. V. Ermolyeva, N. N. Zhukov-Verezhnikov, L. M. Yakobson). The patient is, as it were, likened to a “fountain of infection,” very dangerous from an epidemiological point of view (G.P. Rudnev). Due to profuse diarrhea and repeated vomiting, progressive dehydration occurs.
With a relatively short duration of this period (36-48 hours), some patients lose up to 7 liters of fluid with vomit and up to 30 liters with bowel movements (N.K. Rosenberg). The fluid is removed from the body large quantity protein and a number of salts (especially sodium chloride).
The patient's condition becomes serious, he is exhausted by continuous vomiting and diarrhea. The vomit, which initially contains food impurities, then becomes watery. The tongue is covered with a white coating and is dry. I'm worried about thirst. Intoxication phenomena are increasing. Heart sounds are muffled arterial pressure decreased, acrocyanosis appears, and the amount of urine decreases. The abdomen is soft and sunken. The temperature is normal or decreases significantly. During this period of the disease, painful and excruciating convulsions of a clonic, tonic or mixed nature appear.
Diarrhea, vomiting, dehydration (loss of salts), convulsions are the main symptoms in the clinic of cholera gastroenteritis. However, gastric symptoms (nausea, vomiting) with cholera can sometimes precede the appearance of diarrhea (I. D. Ionin). This is also noted in connection with widespread use antibiotics and for cholera caused by the El Tor variant of Vibrio.
The third phase is algid with the dominant clinical consequences of the second period (G. P. Rudnev). The patient is in prostration, excruciating thirst, the voice is hoarse (exicosis) to the point of complete aphonia. Consciousness is preserved.
Acrocyanosis progresses. Facial features become sharper, cheekbones protrude, eyes become sunken, scleras become dull and injected. Skin turgor is lost, it easily folds, becomes wrinkled, cold to the touch, and covered with sticky sweat. The temperature is sharply reduced (to 36-35-34° and below). Cramps become more widespread, affecting the muscles of the arms, abdomen, chest, chewing and especially the calf muscles. The diarrhea stops, but vomiting is still possible. A painful hiccup appears ( clonic seizures diaphragm).
The pulse is threadlike and frequent. Heart sounds are muffled, arrhythmia, blood pressure is sharply reduced. On auscultation, there is a friction noise of the pleura and pericardium (exicosis). Urine flow decreases and may stop completely (cholera anuria). Due to blood thickening, the number of red blood cells increases to 6-7-8 million and higher per 1 mm 3. Moderate leukocytosis (up to 10,000-15,000, sometimes higher).
The duration of the algic period is from several hours to 3-4 days.
The algic phase passes into the asphyxic phase, during which shortness of breath appears (up to 40-45 breaths per minute), and uremic and azotemic conditions develop. Consciousness darkens, cyanosis and convulsions intensify. With the phenomena of increasing shortness of breath and collapse, the patient dies. Death can also occur in the algic period during seizure. The mortality rate for the algid form has reached 90% in recent years, although the average mortality rate for cholera is not higher than 50%, and for El Tor cholera it is much lower.
The described phases are not observed in all patients; With timely diagnosis and proper treatment, the disease can transition after the first three phases into the so-called reactive phase.
The division into phases served as the basis for the development by G. P. Rudnev of the following classification of clinical forms of typical cholera.
Classification of clinical forms of cholera
1. Cholera enteritis
2. Cholera gastroenteritis
3. Algid period
Reactive phase Asphyxial phase
Recovery Cholera coma
Death
Lighter ones are possible atypical forms cholera, as well as fulminant and “dry” cholera. Death in these forms of the disease occurs from severe intoxication even before the development of diarrhea and vomiting.
Among the complications that develop especially often in seriously ill patients, it is necessary to note pneumonia, erysipelas, phlegmon, abscesses, sepsis, etc.
TO specific complications diseases include typhoid cholera, in the pathogenesis of which Escherichia coli plays a certain role. Patients have a high temperature, consciousness is darkened (status typhosus), and roseola rashes appear on the skin. Characterized by nausea, vomiting and foul-smelling diarrhea, as in colitis with ichorous stool. It's hard and dangerous complication cholera, the mortality rate of which in the past reached 80-90%.
Cholera is an acute infectious disease, the epidemic spread of which is observed in the summer-autumn period. Characteristic are quick loss fluids as a result of profuse watery diarrhea and vomiting, disturbances in water and electrolyte balance. Refers to particularly dangerous infections.
Etiology. The causative agent is Vibrio cholerae. This is a gram-negative curved rod with a polarly located flagellum, providing high mobility of the pathogen. Does not form spores or capsules. Survives for a long time in open waters, is resistant to low temperatures, can overwinter in frozen water sources. Quickly deactivates when exposed to disinfectants and when boiling. Under the influence of Vibrio cholera exotoxin on the mucosal epithelium small intestine fluid loss occurs in the body. Morphological changes are not observed in epithelial cells and underlying intestinal tissues.
Pathogenesis, clinic. The incubation period varies from several hours to 5 days. The disease begins acutely, with the appearance of diarrhea and subsequent vomiting. Stools become more frequent, stools lose their fecal character and smell, and become watery. The urge to defecate is imperative; patients cannot control the act of defecation. Discharge from the intestines looks like rice water or is a liquid colored yellow or yellow with bile. green color. Often the discharge contains an admixture of mucus and blood. The vomit is similar in chemical composition with intestinal secretions. It is a liquid colored yellow, without sour smell. Loss of fluid during vomiting and diarrhea quickly leads to dehydration of the body, the patient’s appearance changes, facial features become sharper, mucous membranes are dry, the voice loses sonority, normal skin turgor decreases, and it easily gathers into folds, cyanosis develops. Tachycardia, shortness of breath occurs, heart sounds become muffled, blood pressure decreases, and urination decreases. Tonic spasms often appear, as well as muscle spasms of the limbs. Palpation of the abdomen reveals fluid transfusion, increased rumbling, and in some cases the sound of liquid splashing is detected. Palpation is painless. Body temperature is normal. The progression of the disease in the patient is characterized by a severe condition, which is accompanied by a decrease in body temperature to 34-35.5 ° C, extreme dehydration (patients lose 8-12% of body weight), hemodynamic disturbances, and shortness of breath. The skin color of such patients has an ashen tint, there is no voice, the eyes are sunken, the sclera is dull, and the gaze is inactive. The abdomen is retracted, there is no stool or urine output. In the blood, due to the thickening of elements, high leukocytosis, an increase in the content of hemoglobin and red blood cells, the hematocrit index, and an increase in the relative density of plasma are observed.
Diagnosis of the disease in the outbreak in the presence of characteristic signs of the disease is not difficult. The first cases of cholera in an area where it has not previously been observed are often difficult and require mandatory bacteriological confirmation.
Treatment is carried out in a hospital, but in certain cases urgent indications it can be started at home. Patients with extreme dehydration and symptoms of hypovolemic shock (drop in blood pressure, severe tachycardia or absence of a palpable pulse, shortness of breath, cyanosis, lack of urine) to replace the volume of lost fluid and electrolytes, immediately inject warm (38-40 ° C) sterile fluid intravenously saline solution type "Trisol" (1000 ml of sterile pyrogen-free water, 5 g of sodium chloride, 4 g of sodium bicarbonate, 1 g of potassium chloride). In some cases, if venipuncture is difficult, venesection is performed. During the first hour of treatment, patients with symptoms of hypovolemic shock are administered a saline solution in an amount equal to 10% of body weight (for a patient weighing 75 kg - 7.5 liters of solution), and then the patient is transferred to drip administration of the solution at a rate of 80-100 drops per 1 min. The total volume of the replenished saline solution is determined by the amount of fluid released during diarrhea and vomit (for example, if 2 hours after the end of the jet administration of the solution the patient has lost 3 liters of fluid, he needs to be administered an equal amount of saline solution at the same time). In case of a pyrogenic reaction to the injected saline solution (with chills, increased body temperature), the liquid is administered more slowly and prescribed through an IV infusion system, 1-2 ml of a 2% solution of promedol and a 2.5% solution of pipolfen or 1% - solution of diphenhydramine. For more severe reactions, 30-60 mg of prednisolone is administered intravenously. When vomiting stops, patients are prescribed tetracycline 0.3 g orally 4 times a day for 5 days. Material for bacteriological analysis taken before prescribing an antibiotic. Cardiac glycosides, pressor amines, plasma, blood components, colloid solutions are not used to remove patients from hypovolemic shock in cholera.
The prognosis for timely treatment of cholera patients, including those with an extremely severe course, is favorable.
Prevention. If cholera is suspected, patients should be immediately hospitalized. If such patients are identified at home, in hotels and under other circumstances, the doctor, before their hospitalization, must take measures to isolate the sick from others and urgently report the disease to the chief physician of his institution. Chief physician notifies the sanitary-epidemiological station and the department (city, district) of health care about the case of disease. At the same time, a list of people who have been in contact with the patient is compiled; after hospitalization of the patient, they should be placed in the department for contacts. After hospitalization, final disinfection is carried out in the room in which the cholera patient was located.
2. Typhoparatyphoid diseases
Typhoparatyphoid diseases (typhoid fever, paratyphoid A and B) are a group of acute infectious diseases with fecal-oral transmission, caused by Salmonella and similar in clinical picture. They are manifested by fever, general intoxication, bacteremia, enlargement of the liver and spleen, enteritis and a peculiar lesion of the intestinal lymphatic system. They are classified as intestinal anthroponoses. Chronic bacteria carriers of salmonella have recently been considered the main source of infection.
Etiology. The causative agents of the disease are several types of Salmonella - Salmonella typhi, S. Paratyphi A, S. schottmulleri. Pathogens are sensitive to chloramphenicol and ampicillin. The infectious dose ranges from 10,000,000 to 1,000,000,000 microbial cells.
Pathogenesis. The pathogen enters the small intestine, where it causes a picture of specific enteritis. The process involves the lymphatic formations of the small intestine and mesenteric The lymph nodes. From the first days of illness, pathogens can be isolated from the blood. When salmonella decompose, endotoxin is released, which causes symptoms of general intoxication and plays a role in important role in the genesis of small intestinal ulcers, leukopenia and can cause the development of infectious-toxic shock.
Clinic. The incubation period lasts from 1 to 3 weeks. The disease develops gradually with a typical course. Symptoms appear and increase: weakness, headache, signs of intoxication, body temperature rises steadily, reaching its highest levels by the 7-9th day of illness. Stool retention and flatulence are more common. With paratyphoid fever, symptoms of acute gastroenteritis may appear in the initial period. Paratyphoid A may cause symptoms of catarrh respiratory tract. During the height of the disease, patients experience lethargy, headache, loss of appetite, slight cough. On examination, a typical typhoid exanthema is revealed. It is expressed in single roseola with a diameter of up to 3-6 mm, plus the tissue has clear boundaries. After 3-5 days, the exanthema disappears without a trace. New lesions may appear periodically. Relative bradycardia and dicrotia of the pulse, decreased blood pressure, and muffled heart sounds are noted. On auscultation, scattered dry rales are heard. The tongue is dry and has a thick brownish coating. The edges and tip of the tongue are clean, with tooth marks. The abdomen is swollen, there is a rough rumbling in the area of the cecum and pain in the right iliac region. The liver and spleen are enlarged. At the height of the disease, the number of leukocytes in the peripheral blood, especially neutrophils and eosinophils. ESR is moderately elevated (up to 20 mm/h). Urine analysis shows traces of protein. Complications: perforation of intestinal ulcers and intestinal bleeding. Pneumonia, infectious psychosis, acute cholecystitis, and, less commonly, other complications are possible. Intestinal perforation can occur in 0.5-8% of patients during the period from the 11th to the 25th day of illness. In recent years, intestinal damage has occurred due to normal temperature and the patient’s well-being, often with dilation motor activity. The onset of perforation is acute: abdominal pain, muscle tension, symptoms of peritoneal irritation, free gas in the abdominal cavity, reduction in size liver dullness. These initial manifestations perforations may vary. As a result, diagnostic difficulties arise early stage. If surgery is not performed within the first 6 hours, development of diffuse peritonitis. Its signs: frequent vomiting, increased flatulence, increased body temperature, rapid pulse, increased symptoms of peritoneal irritation, the appearance of free fluid in the abdominal cavity, leukocytosis. Intestinal bleeding may coincide in timing with perforation intestinal ulcer and is diagnosed when an admixture of altered blood appears in the feces or according to the clinical picture of an acutely developing internal bleeding. Recurrence is possible in some cases 1-2 weeks after normalization of body temperature. Chronic bacterial carriage remains in 3-5% of recovered patients. Diagnostics initial period diagnosis of typhoid paratyphoid diseases is difficult, especially in mild and atypical cases. During this period, it is important to identify the presence of pathogens in the blood (detection using culture in bile broth, immunofluorescence method). With a typical clinical picture, diagnosis is not difficult. In later periods, stool cultures can be used and serological methods(Vidal reaction, RNGA).
Treatment. Antibacterial therapy is prescribed (chloramphenicol 0.5-0.75 g 4 times a day until the 10-12th day of normal temperature). In severe forms, antibiotic therapy is combined with a short course (5-7 days) of glucocorticoids (prednisolone 30-40 mg/day). Pathogenetic therapy is used (vitamins, oxygen therapy, vaccine administration). Bed rest should be observed until the 7-10th day of normalization of temperature. In case of intestinal bleeding, the patient is prescribed strict bed rest, cold on the stomach, Vicasol (1 ml of a 1% solution), aminocaproic acid (200 ml of a 5% solution). In case of intestinal perforation - emergency surgery to prevent intestinal bleeding and related complications. Treatment for chronic bacterial carriage has not been developed.
The prognosis is favorable if treatment is started in a timely manner. In severe forms and the presence of complications (especially intestinal perforation), the prognosis is worse. Working capacity is restored after 1.5-2 months from the onset of the disease.
Prevention. Sanitary supervision of food and water supply. Convalescents are discharged after a triple negative bacteriological examination of stool and urine and a single examination of bile (portions B and C).
Those who have recovered from the disease are registered with the sanitary-epidemiological station for 2 years (workers of food enterprises - 6 years). Isolation of patients stops from the 21st day of normal body temperature. According to indications, specific immunization is carried out. The fireplace is subject to final disinfection.
Cholera (cholera) - acute anthroponotic infectious disease with a fecal-oral transmission mechanism of the pathogen, which is characterized by massive diarrhea with rapid development of dehydration. Due to the possibility of mass spread, it is classified as a quarantine disease that is dangerous to humans.
ICD codes -10 A00. Cholera.
A00.0. Cholera caused by Vibrio cholerae 01, biovar cholerae.
A00.1. Cholera caused by Vibrio cholerae 01, biovar eltor.
A00.9. Cholera unspecified.
Etiology (causes) of cholera
The causative agent of cholera Vibrio cholerae belongs to the genus Vibrio of the family Vibrionaceae.
Vibrio cholerae is represented by two biovars, similar in morphological and tinctorial properties (biovar cholera itself and biovar El Tor).
The causative agents of cholera are short, curved gram-negative rods (1.5–3 µm long and 0.2–0.6 µm wide), highly motile due to the presence of a polarly located flagellum. They do not form spores or capsules, they are located parallel, in a smear they resemble a school of fish, they are cultivated in alkaline nutrient media. Cholera vibrios El Tor, unlike classic ones biological variants, are capable of hemolyzing sheep red blood cells.
Vibrios contain thermostable O-antigens (somatic) and thermolabile H-antigens (flagellar). The latter are group, and according to O-antigens, cholera vibrios are divided into three serological types: Ogawa (contains antigenic fraction B), Inaba (contains fraction C) and intermediate type Gikoshima (contains both fractions - B and C). In relation to cholera phages, they are divided into five main phage types.
Pathogenicity factors:
· mobility;
chemotaxis, with the help of which the vibrio overcomes slime layer and interacts with epithelial cells of the small intestine;
· adhesion and colonization factors, with the help of which vibrio adheres to microvilli and colonizes the mucous membrane of the small intestine;
· enzymes (mucinase, protease, neuraminidase, lecithinase), which promote adhesion and colonization, as they destroy substances that make up the mucus;
· exotoxin cholerogens - main factor, which determines the pathogenesis of the disease, namely, recognizes the enterocyte receptor and binds to it, forms an intramembrane hydrophobic channel for the passage of subunit A, which interacts with nicotinamide adenine dinucleotide, causes the hydrolysis of adenosine triphosphate with the subsequent formation of cAMP;
· factors that increase capillary permeability;
· endotoxin is a thermostable LPS that does not play a significant role in the development of clinical manifestations of the disease. Antibodies formed against endotoxin and having a pronounced vibriocidal effect - important component post-infectious and post-vaccination immunity.
Vibrios cholerae survive well at low temperatures; stored in ice for up to 1 month, in sea water- up to 47 days, in river water- from 3–5 days to several weeks, in soil - from 8 days to 3 months, in feces - up to 3 days, on raw vegetables- 2–4 days, on fruits – 1–2 days. Cholera vibrios die at 80 °C in 5 minutes, at 100 °C - instantly; highly sensitive to acids, drying and direct sun rays, under the influence of chloramine and other disinfectants they die in 5–15 minutes, are preserved well and for a long time and even reproduce in open waters and Wastewater ah, rich in organic matter.
Epidemiology of cholera
Source of infectious agent- human (sick and vibrio carrier).
Especially dangerous are those that save social activity patients with erased and mild forms of the disease.
Mechanism of transmission of infection- fecal-oral. Routes of transmission: water, nutritional, contact and household. The waterway has crucial for the rapid epidemic and pandemic spread of cholera. At the same time, not only drinking water, but also using it for household needs (washing vegetables, fruits, etc.), swimming in an infected reservoir, as well as eating fish, crayfish, shrimp, oysters caught there and not passed heat treatment, can lead to cholera infection.
Susceptibility to cholera is universal. People with reduced acidity of gastric juice are most susceptible to the disease (chronic gastritis, pernicious anemia, helminthic infestations, alcoholism).
After an illness, antimicrobial and antitoxic immunity is developed, which lasts from 1 to 3 years.
The epidemic process is characterized by acute explosive outbreaks, group diseases and individual imported cases. Thanks to wide transport connections, cholera is systematically introduced into the territory of countries free from it. Six cholera pandemics have been described. The seventh pandemic caused by Vibrio El Tor is currently ongoing.
Classic cholera is common in India, Bangladesh, Pakistan, El Tor cholera is common in Indonesia, Thailand and other countries of Southeast Asia. Mostly imported cases are recorded in Russia. Over the past 20 years, more than 100 cases of importation have been recorded in seven regions of the country. The main reason for this is tourism (85%). There have been cases of cholera among foreign citizens.
The most severe cholera epidemic was in Dagestan in 1994, where 2,359 cases were registered. The infection was brought by pilgrims performing the Hajj to Saudi Arabia.
As for everyone intestinal infections, cholera in countries with temperate climates is characterized by summer-autumn seasonality.
Cholera Prevention Measures
Nonspecific prevention
Aimed at providing the population with good-quality drinking water, disinfecting wastewater, sanitary cleaning and improvement of populated areas, and informing the population. Employees of the epidemiological surveillance system carry out work to prevent the introduction of the pathogen and its spread throughout the country in accordance with the rules of sanitary protection of the territory, as well as a planned study of water in open reservoirs for the presence of Vibrio cholerae in sanitary protection zones of water intakes, public bathing areas, port waters, etc. d.
An analysis of data on the incidence of cholera, examination and bacteriological examination (as indicated) of citizens arriving from abroad are carried out.
According to international epidemiological rules, persons arriving from cholera-affected countries are subject to five-day observation with a single bacteriological examination.
A comprehensive plan of anti-epidemic measures is being carried out in the outbreak, including hospitalization of sick people and vibrio carriers, isolation of contacts and medical supervision followed them for 5 days with 3-fold bacteriological examination. Carry out current and final disinfection.
Emergency prevention includes the use antibacterial drugs(Table 17-9).
Table 17-9. Schemes for the use of antibacterial drugs for emergency prevention cholera
| A drug | Single dose orally, g | Frequency of application per day | Daily dose, g | Course dose, g | Course duration, days |
| Ciprofloxacin | 0,5 | 2 | 1,0 | 3,0–4,0 | 3-4 |
| Doxycycline | 0.2 on the 1st day, then 0.1 | 1 | 0.2 on the 1st day, then 0.1 | 0,5 | 4 |
| Tetracycline | 0,3 | 4 | 1,2 | 4,8 | 4 |
| Ofloxacin | 0,2 | 2 | 0,4 | 1,6 | 4 |
| Pefloxacin | 0,4 | 2 | 0,8 | 3,2 | 4 |
| Norfloxacin | 0,4 | 2 | 0,8 | 3,2 | 4 |
| Chloramphenicol (chloramphenicol) | 0,5 | 4 | 2,0 | 8,0 | 4 |
| Sulfamethoxazole/biseptol | 0,8/0,16 | 2 | 1,6 / 0,32 | 6,4 / 1,28 | 4 |
| Furazolidone + kanamycin | 0,1+0,5 | 4 | 0,4+2,0 | 1,6 + 8,0 | 4 |
Note. When vibrios cholerae are isolated that are sensitive to sulfamethoxazole + trimethoprim and furazolidone, pregnant women are prescribed furazolidone, children - sulfamethoxazole + trimethoprim (Biseptol).
Specific prevention
For specific prevention, cholera vaccine and cholera toxin are used. Vaccination is carried out according to epidemic indications. A vaccine containing 8–10 vibrios per 1 ml is injected under the skin, the first time 1 ml, the second time (after 7–10 days) 1.5 ml. Children 2–5 years old are administered 0.3 and 0.5 ml, 5–10 years old - 0.5 and 0.7 ml, 10–15 years old - 0.7–1 ml, respectively. Cholerogen toxoid is administered once annually strictly under the skin below the angle of the scapula. Revaccination is carried out according to epidemic indications no earlier than 3 months after primary immunization.
Adults need 0.5 ml of the drug (for revaccination also 0.5 ml), children from 7 to 10 years old - 0.1 and 0.2 ml, respectively, 11–14 years old - 0.2 and 0.4 ml, 15– 17 years old - 0.3 and 0.5 ml. The international certificate of vaccination against cholera is valid for 6 months after vaccination or revaccination.
Pathogenesis of cholera
The entry point for infection is digestive tract. The disease develops only when pathogens overcome the gastric barrier (this is usually observed in the period of basal secretion, when the pH of the gastric contents is close to 7), reach the small intestine, where they begin to multiply intensively and secrete exotoxin. Enterotoxin or cholerogens determines the occurrence of the main manifestations of cholera. Cholera syndrome is associated with the presence of two substances in this vibrio: a protein enterotoxin - choleragen (exotoxin) and neuraminidase. Cholerogen binds to a specific enterocyte receptor - ganglioside. Under the action of neuraminidase, a specific receptor is formed from gangliosides. The choleragen-specific receptor complex activates adenylate cyclase, which initiates the synthesis of cAMP.
Adenosine triphosphate regulates the secretion of water and electrolytes from the cell into the intestinal lumen through an ion pump. As a result, the mucous membrane of the small intestine begins to secrete a huge amount of isotonic fluid, which does not have time to be absorbed in the large intestine - isotonic diarrhea develops. With 1 liter of feces, the body loses 5 g of sodium chloride, 4 g of sodium bicarbonate, 1 g of potassium chloride. The addition of vomiting increases the volume of fluid lost.
As a result, the volume of plasma decreases, the volume of circulating blood decreases and it thickens. Fluid is redistributed from the interstitial to the intravascular space. Hemodynamic disorders and microcirculation disorders occur, resulting in dehydration shock and acute renal failure. Metabolic acidosis develops, which is accompanied by convulsions. Hypokalemia causes arrhythmia, hypotension, changes in the myocardium and intestinal atony.
Clinical picture (symptoms) of cholera
Incubation period from several hours to 5 days, more often 2–3 days.
Classification of cholera
According to the severity of clinical manifestations, they distinguish between erased, mild, moderate, severe and very severe form cholera, determined by the degree of dehydration.
IN AND. Pokrovsky identifies the following degrees of dehydration:
· I degree, when patients lose a volume of fluid equal to 1–3% of body weight (erased and mild forms);
· II degree - losses reach 4–6% (moderate form);
· III degree - 7–9% (severe);
· IV degree of dehydration with a loss of over 9% corresponds to a very severe course of cholera.
Currently, degree I of dehydration occurs in 50–60% of patients, II in 20–25%, III in 8–10%, IV in 8–10% (Table 17-10).
Table 17-10. Assessing the severity of dehydration in adults and children
| Sign | Degree of dehydration, % body weight loss | |||
| worn and light | moderate severity | heavy | very heavy | |
| 1–3 | 4–6 | 7–9 | 10 or more | |
| Chair | Up to 10 times | Up to 20 times | More than 20 times | No bill |
| Vomit | Up to 5 times | Up to 10 times | Up to 20 times | Repeated (indomitable) |
| Thirst | Weak | Moderately expressed | Sharply expressed | Insatiable (or unable to drink) |
| Diuresis | Norm | Reduced | Oliguria | Anuria |
| Convulsions | No | Calf muscles, short-term | Long lasting and painful | Generalized clonic |
| State | Satisfactory | Moderate | Heavy | Very heavy |
| Eyeballs | Norm | Norm | Sunken | Sharply sunken |
| Mucous membranes of the mouth, tongue | Wet | Dryish | Dry | Dry, sharply hyperemic |
| Breath | Norm | Norm | Moderate tachypnea | Tachypnea |
| Cyanosis | No | Nasolabial triangle | Acrocyanosis | Sharply expressed, diffuse |
| Skin turgor | Norm | Norm | Decreased (skinfold straightens >1 s) | Sharply reduced (skinfold straightens >2 s) |
| Pulse | Norm | Up to 100 per minute | Up to 120 rpm | Above 120 per minute, thread-like |
| BPsyst., mm Hg. | Norm | Up to 100 | 60–100 | Less than 60 |
| Blood pH | 7,36–7,40 | 7,36–7,40 | 7,30–7,36 | Less than 7.3 |
| Voice sound | Saved | Saved | Hoarseness of voice | Aphonia |
| Relative plasma density | Norm (up to 1025) | 1026–1029 | 1030–1035 | 1036 or more |
| Hematocrit, % | Normal (40–46%) | 46–50 | 50–55 | Above 55 |
Main symptoms and dynamics of their development
The disease begins acutely, without fever or prodromal phenomena.
First clinical signs are a sudden urge to defecate and the passage of mushy or watery stools from the very beginning.
Subsequently, these imperative urges are repeated. The stool loses its fecal character and often has the appearance of rice water: translucent, cloudy white in color, sometimes with floating flakes gray, odorless or with odor fresh water. The patient notes rumbling and discomfort in the umbilical region.
In patients with mild form cholera defecation is repeated no more than 3–5 times a day, general health remains satisfactory, minor feelings of weakness, thirst, dry mouth. The duration of the disease is limited to 1–2 days.
For moderate severity(second degree dehydration) the disease progresses, diarrhea is accompanied by vomiting, increasing in frequency. The vomit has the same rice-water appearance as the stool. It is typical that vomiting is not accompanied by any tension or nausea. With the addition of vomiting, exicosis rapidly progresses. Thirst becomes painful, the tongue is dry, with a “chalky coating”, the skin, mucous membranes of the eyes and oropharynx become pale, skin turgor decreases. Stools are up to 10 times a day, copious, and the volume does not decrease, but increases. arise single convulsions calf muscles, hands, feet, masticatory muscles, unstable cyanosis of the lips and fingers, hoarseness of voice.
Moderate tachycardia, hypotension, oliguria, and hypokalemia develop.
The disease in this form lasts 4–5 days.
Severe form of cholera(III degree of dehydration) is characterized by pronounced signs of exicosis due to copious (up to 1–1.5 liters per bowel movement) stool, which becomes so from the first hours of the disease, and the same copious and repeated vomiting. Patients are bothered by painful spasms of the muscles of the limbs and abdomen, which, as the disease progresses, move from rare clonic to frequent and even give way to tonic spasms. The voice is weak, thin, often barely audible. Skin turgor decreases, folded skin does not straighten out for a long time. The skin of the hands and feet becomes wrinkled (“washerwoman’s hand”). The face takes on the appearance characteristic of cholera: sharpened features, sunken eyes, cyanosis of the lips, ears, earlobes, nose.
When palpating the abdomen, fluid transfusion through the intestines and the sound of liquid splashing are determined. Palpation is painless. Tachypnea appears, tachycardia increases to 110–120 per minute. The pulse is weakly filled (“thread-like”), heart sounds are muffled, blood pressure progressively drops below 90 mm Hg, first maximum, then minimum and pulse. The body temperature is normal, urination decreases and soon stops. Blood thickening is moderate. Indicators of relative plasma density, hematocrit index and blood viscosity on upper limit normal or moderately increased. Pronounced hypokalemia of plasma and erythrocytes, hypochloremia, moderate compensatory hypernatremia of plasma and erythrocytes.
Very severe form of cholera(previously called algid) is distinguished by its stormy sudden development an illness that begins with massive continuous bowel movements and profuse vomiting. After 3–12 hours, the patient develops a severe condition of algid, which is characterized by a decrease in body temperature to 34–35.5 ° C, extreme dehydration (patients lose up to 12% of body weight - IV degree dehydration), shortness of breath, anuria and hemodynamic disorders of the type hypovolemic shock. By the time patients are admitted to the hospital, they develop paresis of the muscles of the stomach and intestines, as a result of which the patients stop vomiting (replaced by convulsive hiccups) and diarrhea (gaping anus, free flow of “intestinal water” from the anus with light pressure on the anterior abdominal wall). Diarrhea and vomiting occur again during or after rehydration. The patients are in a state of prostration. Breathing is frequent, shallow, and in some cases Kussmaul breathing is observed.
The color of the skin in such patients acquires an ashen tint (total cyanosis), “dark glasses around the eyes” appear, the eyes are sunken, the sclera is dull, the gaze is unblinking, and there is no voice. The skin is cold and clammy to the touch, easily wrinkled and long time(sometimes within an hour) does not straighten (“cholera fold”).
Severe forms are more often observed at the beginning and at the height of the epidemic. At the end of the outbreak and in the inter-epidemic time, lungs and erased forms, indistinguishable from forms of diarrhea of other etiologies. In children under 3 years of age, cholera is most severe: they tolerate dehydration less well. In addition, children experience secondary damage to the central nervous system: adynamia, clonic convulsions, impaired consciousness, and even the development of coma are observed. It is difficult to determine the initial degree of dehydration in children. In such cases, one cannot rely on the relative density of plasma due to the large extracellular volume of fluid. It is therefore advisable to weigh patients at the time of admission in order to most reliably determine their degree of dehydration. The clinical picture of cholera in children has some features: body temperature often rises, apathy, adynamia, and a tendency to epileptiform seizures due to the rapid development of hypokalemia are more pronounced.
The duration of the disease ranges from 3 to 10 days, its subsequent manifestations depend on the adequacy of replacement treatment with electrolytes.
Complications of cholera
Due to disorders of hemostasis and microcirculation in older patients age groups myocardial infarction, mesenteric thrombosis are observed, acute failure cerebral circulation. Phlebitis is possible (during venous catheterization), and pneumonia often occurs in severely ill patients.
Diagnosis of cholera
Clinical diagnosis
Clinical diagnosis in the presence of epidemiological data and a characteristic clinical picture (onset of the disease with diarrhea followed by vomiting, absence pain syndrome and fever, the nature of the vomit) is not complicated, however, mild, erased forms of the disease, especially isolated cases, are often viewed. In these situations, laboratory diagnosis is critical.
Specific and nonspecific laboratory diagnostics
Main and decisive method laboratory diagnosis of cholera is bacteriological examination. Feces and vomit are used as material; feces are examined for vibrio carriage; From persons who died from cholera, a ligated section of the small intestine and gall bladder is taken.
When conducting a bacteriological study, three conditions must be observed: · culture material from the patient as quickly as possible (Vibrio cholerae persists in feces for a short period of time); · the containers in which the material is taken should not be disinfected with chemicals and should not contain traces of them, since Vibrio cholerae is very sensitive to them; · exclude the possibility of contamination and infection of others.
The material must be delivered to the laboratory within the first 3 hours; if this is not possible, use preservative media (alkaline peptone water, etc.).
The material is collected in individual vessels, washed from disinfectant solutions, at the bottom of which a smaller vessel or sheets of parchment paper are placed, disinfected by boiling. When shipping, the material is placed in a metal container and transported in a special vehicle with an accompanying person.
Each sample is provided with a label indicating the first and last name of the patient, the name of the sample, the place and time of collection, the intended diagnosis and the name of the person who took the material. In the laboratory, the material is inoculated onto liquid and solid nutrient media to isolate and identify a pure culture.
The results of the express analysis are obtained after 2-6 hours (indicative answer), the accelerated analysis - after 8-22 hours (preliminary answer), the full analysis - after 36 hours (final answer).
Serological methods are of auxiliary value and can be used mainly for retrospective diagnosis. For this purpose, microagglutination in phase contrast, RNGA, can be used, but it is better to determine the titer of vibriocidal antibodies or antitoxins (cholerogen antibodies are determined by ELISA or immunofluorescent method).
Differential diagnosis
Differential diagnosis is carried out with other infections that cause diarrhea. Differential features are given in table. 17-11.
Table 17-11. Differential diagnosis cholera
| Epidemiological and clinical signs | Nosological form | ||||
| cholera | PTI | dysentery | viral diarrhea | traveler's diarrhea | |
| Contingent | Residents of endemic regions and visitors from them | No specifics | No specifics | No specifics | Tourists to developing countries with hot climates |
| Epidemiological data | Drinking undisinfected water, washing vegetables and fruits in it, swimming in polluted waters, contact with a sick person | Consumption of food products prepared and stored in violation of hygienic standards | Contact with a sick person, consumption of mainly lactic acid products, violation of personal hygiene | Contact with the patient | Consumption of water, food purchased from street vendors |
| Fociality | Often based on general epidemiological characteristics | Often among those who used the same suspicious product | Possible among contact persons who consumed the suspect product | Often among contact persons | Possible based on general epidemiological characteristics |
| First symptoms | Loose stool | Epigastric pain, vomiting | Abdominal pain, loose stools | Epigastric pain, vomiting | Epigastric pain, vomiting |
| Subsequent symptoms | Vomit | Loose stool | Tenesmus, false urges | Loose stool | Loose stool |
| Fever, intoxication | None | Often, simultaneously with dyspeptic syndrome or before it | Often, simultaneously or before dyspeptic syndrome | Often, moderately expressed | Characteristic, simultaneously with dyspeptic syndrome |
| Character of the chair | Calcless, watery, without a characteristic odor | Fecal, liquid, foul-smelling | Fecal or non-fecal (“rectal spit”) with mucus and blood | Fecal, liquid, foamy, sour smelling | Liquid stool, often with mucus |
| Stomach | Bloated, painless | Bloated, painful in epi- and mesogastrium | Retracted, painful in the left iliac region | Bloated, slightly painful | Moderately painful |
| Dehydration | II–IV degrees | I–III degrees | Possibly I–II degrees | I–III degrees | I–II degrees |
An example of a diagnosis formulation
A 00.1. Cholera (coproculture of Vibrio eltor), severe course, third degree dehydration.
Indications for hospitalization
All patients with cholera or suspected of having it are subject to mandatory hospitalization.
Treatment of cholera
Mode. Diet for cholera
No special diet is required for cholera patients.
Drug therapy
Basic principles of therapy: · replacement of fluid loss and restoration of the electrolyte composition of the body; · impact on the pathogen.
Treatment must begin within the first hours of the onset of the disease.
Pathogenetic agents
Therapy includes primary rehydration (replacement of water and salt losses before treatment) and corrective compensatory rehydration (correction of ongoing losses of water and electrolytes). Rehydration is seen as resuscitation event. In the emergency room, during the first 5 minutes, the patient must measure the patient’s pulse rate, blood pressure, body weight, take blood to determine hematocrit or relative density of blood plasma, electrolyte content, acid-base status, coagulogram, and then begin jet injection saline solutions.
The volume of solutions administered to adults is calculated using the following formulas.
Cohen's formula: V = 4 (or 5) × P × (Ht 6 – Htн), where V is the determined fluid deficit (ml); P - patient’s body weight (kg); Ht 6 - patient's hematocrit; Htн - normal hematocrit; 4 is the coefficient for a hematocrit difference of up to 15, and 5 for a difference of more than 15.
Phillips formula: V = 4(8) × 1000 × P × (X – 1.024), where V is the determined fluid deficit (ml); P - patient’s body weight (kg); X is the relative density of the patient’s plasma; 4 is the coefficient for a patient’s plasma density up to 1.040, and 8 for a density above 1.041.
In practice, the degree of dehydration and, accordingly, the percentage of body weight loss are usually determined according to the criteria presented above. The resulting figure is multiplied by body weight to obtain the volume of fluid loss. For example, body weight 70 kg, degree III dehydration (8%). Therefore, the volume of losses is 70,000 g 0.08 = 5600 g (ml).
Polyionic solutions, preheated to 38–40 °C, are administered intravenously at a rate of 80–120 ml/min at II–IV degree of dehydration. Various polyionic solutions are used for treatment. The most physiological are Trisol® (5 g sodium chloride, 4 g sodium bicarbonate and 1 g potassium chloride); acesol® (5 g sodium chloride, 2 g sodium acetate, 1 g potassium chloride per 1 liter of pyrogen-free water); Chlosol® (4.75 g sodium chloride, 3.6 g sodium acetate and 1.5 g potassium chloride per 1 liter of pyrogen-free water) and Laktasol® solution (6.1 g sodium chloride, 3.4 g sodium lactate, 0. 3 g sodium bicarbonate, 0.3 g potassium chloride, 0.16 g calcium chloride and 0.1 g magnesium chloride per 1 liter of pyrogen-free water).
Jet primary rehydration is carried out using catheterization of central or peripheral veins. After replenishing losses, increasing blood pressure to physiological norms, restoring diuresis, and stopping seizures, the infusion rate is reduced to the required level to compensate for continuing losses. The administration of solutions is crucial in the treatment of seriously ill patients. As a rule, 15–25 minutes after the start of administration, pulse and blood pressure begin to be determined, and after 30–45 minutes, shortness of breath disappears, cyanosis decreases, lips become warmer, and a voice appears. After 4–6 hours, the patient’s condition improves significantly, and he begins to drink on his own. Every 2 hours it is necessary to monitor the patient’s blood hematocrit (or relative density of blood plasma), as well as the content of blood electrolytes to correct infusion therapy.
Error entering large quantities 5% glucose® solution: this not only does not eliminate the deficiency of electrolytes, but, on the contrary, reduces their concentration in the plasma. Blood transfusions and blood substitutes are also not indicated. It is unacceptable to use colloidal solutions for rehydration therapy, as they contribute to the development of intracellular dehydration, acute renal failure and shock lung syndrome.
Oral rehydration is necessary for cholera patients who are not vomiting.
The WHO Expert Committee recommends the following composition: 3.5 g sodium chloride, 2.5 g sodium bicarbonate, 1.5 g potassium chloride, 20 g glucose, 1 l boiled water(the solution is oral). The addition of glucose® promotes the absorption of sodium and water in the intestines. WHO experts have also proposed another rehydration solution, in which bicarbonate is replaced by a more stable sodium citrate (Rehydron®).
In Russia, a drug glucosolan® has been developed, which is identical to the WHO glucose-saline solution.
Water-salt therapy is stopped after the appearance of fecal stools in the absence of vomiting and the predominance of the amount of urine over the amount of feces in the last 6-12 hours.
Etiotropic therapy
Antibiotics - additional remedy therapy, they do not affect the survival of patients, but shorten the duration of clinical manifestations of cholera and accelerate the cleansing of the body from the pathogen. Recommended drugs and regimens for their use are presented in table. 17-12, 17-13. Use one of the listed drugs.
Table 17-12. Schemes of a five-day course of antibacterial drugs for the treatment of patients with cholera (I–II degree of dehydration, no vomiting) in tablet form
| A drug | Single dose, g | Average daily dose, G | Course dose, g | |
| Doxycycline | 0,2 | 1 | 0,2 | 1 |
| Chloramphenicol (chloramphenicol®) | 0,5 | 4 | 2 | 10 |
| Lomefloxacin | 0,4 | 1 | 0,4 | 2 |
| Norfloxacin | 0,4 | 2 | 0,8 | 4 |
| Ofloxacin | 0,2 | 2 | 0,4 | 2 |
| Pefloxacin | 0,4 | 2 | 0,8 | 4 |
| Rifampicin + trimethoprim | 0,3 0,8 |
2 | 0,6 0,16 |
3 0,8 |
| Tetracycline | 0,3 | 4 | 1,2 | |
| 0,16 0,8 |
2 | 0,32 1,6 |
1,6 8 |
|
| Ciprofloxacin | 0,25 | 2 | 0,5 | 2,5 |
Table 17-13. Schemes for a 5-day course of antibacterial drugs for the treatment of patients with cholera (presence of vomiting, III–IV degree of dehydration), intravenous administration
| A drug | Single dose, g | Frequency of application, per day | Average daily dose, g | Course dose, g |
| Amikacin | 0,5 | 2 | 1,0 | 5 |
| Gentamicin | 0,08 | 2 | 0,16 | 0,8 |
| Doxycycline | 0,2 | 1 | 0,2 | 1 |
| Kanamycin | 0,5 | 2 | 1 | 5 |
| Chloramphenicol (chloramphenicol®) | 1 | 2 | 2 | 10 |
| Ofloxacin | 0,4 | 1 | 0,4 | 2 |
| Sizomycin | 0,1 | 2 | 0,2 | 1 |
| Tobramycin | 0,1 | 2 | 0,2 | 1 |
| Trimethoprim + sulfamethoxazole | 0,16 0,8 |
2 | 0,32 1,6 |
1,6 8 |
| Ciprofloxacin | 0,2 | 2 | 0,4 | 2 |
Clinical examination
Patients with cholera (vibrio carriers) are discharged after their recovery, completion of rehydration and etiotropic therapy and receiving three negative results of bacteriological examination.
After being discharged from hospitals, those who have suffered from cholera or vibrio carriage are allowed to work (study), regardless of their profession, they are registered with the territorial departments of epidemiological surveillance and clinical health clinics at their place of residence. Dispensary observation is carried out for 3 months.
Those who have had cholera are subject to bacteriological examination for cholera: in the first month, bacteriological examination of stool is carried out once every 10 days, then once a month.
If vibrio carriage is detected in convalescents, they are hospitalized for treatment in infectious diseases hospital, after which dispensary observation of them is resumed.
Those who have had cholera or are vibrio carriers are removed from the dispensary registration if cholera vibrios are not isolated during the dispensary observation.
