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Specific prophylaxis: Specific prophylaxis: cholera phages bivalent chemical tabletted cholera vaccine is a mixture of choleragen-toxoid obtained from formalin-inactivated broth culture of Vibrio cholerae 569B or 569 (KM - 76) of serovar Ina-ba, and O-antigens obtained from broth cultures cholera vibrio 569B or 569 (KM - 76) serovar Inaba and M-41 Ogawa. One vaccination dose consists of three tablets. The dose for vaccination of the adult population is 3 tablets, for adolescents 11-17 years old 2 tablets, for children 2-10 years old - 1 tablet. Tablets are taken orally 1 hour before meals, without chewing, washed down with boiled water. This provides antibacterial, antitoxic and local intestinal immunity for up to 6 months. Revaccination in 6-7 months. Registration in the Russian Federation is planned: Ducoral vaccine from Aventis Pasteur, France (oral killed recombinant B-subunit / whole-cell cholera vaccine) Specific treatment - not used.

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Cholera (bile leakage) - especially acute dangerous intestinal infection (quarantine disease) caused byVibrio cholerae, serogroups O1 and 0139, characterized by toxic damage to the small intestine (acute gastroenteritis), impairedin one- salt balance and high mortality.

Cholera as a particularly dangerous infection is capable of:

the sudden appearance of the rapid spread of the mass coverage of the population

characterized by a severe course and high mortality, often occurring in the first hours of the disease.

History

The incidence of cholera since ancient times was recorded on the Indian subcontinent, especially during the period of hostilities. The basins of the Ganges and Brahmaputra rivers in India and Bangladesh are natural foci. Cholera entered Europe and Russia through the Middle East and Egypt. Since 1816, mankind has experienced 7 cholera pandamias, and each of them claimed millions of human lives.

1- India-1816

2- India-1828

3- India -1844-1864

4- India -1865-1875

5- India -1883-1896

6-Arabia - 1900-1926

7- Indonesia - from 1961 to the present.

In 1884 R. Koch discovered Vibrio cholerae ("Koch's comma" or classic cholera vibrio).In 1906 in Egypt, F. Gotschlich isolated a hemolytic vibrio from the corpses of Muslim pilgrims who died with diarrhea at the El Tor quarantine station, which was later named V. eltor. The role of Vibrio eltor in human pathology remains questionable. In 1939 S. de Moor described seasonal diarrhea on the island. Sulawesi (Indonesia), under which V. eltor constantly stood out. In 1961 on the island. Sulawesi suffered a severe epidemic that escalated into the VII pandemic. In 1962, an extraordinary meeting of the WHO expert committee was held, at which the the decision to regard V. eltor as the same cholera agent as classical (Kokhovsky) vibrio.

It used to be customary to call cholera Asiatic. At present, more than half of the total morbidity in the world occurs on the African continent, in a number of countries of which endemic foci have formed, which are a springboard for major epidemics, especially in the context of growing international communication.

In early 1993, there were reports of cholera cases in Southeast Asia caused by vibrios serogroup "0139".

Cholera vibrios of serogroup 0139 "Bengal" are considered to be the causative agents of epidemic cholera.

Bergi classification

Family Vibrionaceae (5 genera):

Vibrio, Aeromonas, Plesiomonas, Photobacterium, Zucibacterium

genus Vibrio (5 species):

V.cholerae, V.parahaemolyticus, V.alginolyticus, V.vulnificus, V.costicola

V. cholerae biovars (4 biovars):

b. cholerae, b. eltor, b. proteus, b. albensis

V. cholerae serogroups

Phagovars V. cholerae - 1, 2, 3, 4, 5 (Mukherjee 1959) Phagovars V.eltor - 1,2,3,4,5,6 (Vazi 1968)

Family Vibrionaceae

genus Vibrio

v. cholerae species

Serogroup 01

Serovary: Inaba-AS Ogawa-AV Gikoshima-ABC

Morphological properties

Vibrio cholerae has the shape of a curved or straight stick, one polar flagellum - its size is several times the length of the cell. AT

hanging or crushed drop, vibrio mobility can be observed, which is compared with the "flight

swallows ". In old cultures, there are

involutional filamentous, coccoid forms. Under the action of penicillin, filterable L-

forms. Have fimbria. Spores and capsules do not form.

In smears from pure culture, they are arranged in the form of a delicate cobweb. They are well painted with water magenta

Pfeiffer or Ziel's carbolic fuchsin, gram negativemicrobes. They can be located in stained smears from the test material in the form of "schools of fish".

Breathing type: facultative anaerobes, but grow better under aerobic conditions.

Type of food: chemorganotrophs with oxidative and fermentative types of metabolism.

Cultural properties

Grow well in simple nutrient media, but demanding on the pH environment. The medium must be alkaline (pH 8.5-9.0)

On liquid media(enrichment medium - 1% peptone water; accumulation medium - 1% peptone water with potassium tellurite) vibrios grow in the form of turbidity, a superficial delicate film, which collapses upon shaking. On 1% peptone water(pH 9.0) vibrios outpace the growth of enterobacteria and grow in 6-8 hours (in the presence of potassium tellurite, in 12-24 hours).

Cholera is an acute anthroponous intestinal infection caused by Vibrio cholerae and characterized by watery diarrhea followed by the addition of vomiting, the development of dehydration, demineralization and acidosis.

The incubation period lasts 1-5 days. For this period (5 days) quarantine is imposed. Disease periods:

• Cholera enteritis
• Gastroenteritis (vomiting)
• Algid period - a violation of microcirculation leads to the fact that the skin becomes cold.

Disease development options:

1. Recovery occurs when the protective function of the body is sufficiently expressed.

2. When a large number of microbes enter the body and the protective function is insufficiently expressed, an asphyxia form of cholera develops, that is, respiratory failure, impaired central nervous activity (coma) and ultimately death.

Classification of Academician Pokrovsky (according to the degree of dehydration):

• 1 - deficiency of the patient's body weight 1-3%
• 2 - deficit 4-6%
• 3 - deficit 7-9%
• 4 - 10% or more. The fourth degree is hypovolemic dehydration shock.

Typical and atypical forms of the disease are also noted.

Typical forms this is when there is enteritis, followed by the addition of gastritis, there is dehydration.

Atypical form when the changes are insignificant, erased, dehydration practically does not develop. Atypical are also considered such pronounced forms as fulminant, dry cholera (severe dehydration, but without frequent diarrhea, there is a sharp hypokalemia, intestinal paresis, fluid in the pleural cavity).

The onset of the disease is acute. The first symptom is loose stools. Desires are imperative. Features of diarrheal syndrome:

• The temperature does not rise (the maximum temperature rise on the first day is 37.2 -37.5)
• There is no pain syndrome.

The first portions of feces are semi-formed, and later they lose their fecal character, there are no impurities, stool resembles the type of rice broth (whitish, sometimes with a yellowish tinge, with flakes, watery stool). Subsequently, vomiting joins.

The first period is the period of enteritis. After a few hours, sometimes after 12 hours - 24 hours, vomiting (manifestation of gastritis) joins. As a result of the manifestations of gastroenteritis, dehydration and demineralization quickly occur. Fluid loss leads to hypovolemia, and salt loss leads to seizures. Most often these are the muscles, hands, feet, chewing muscles, lower leg muscles.

In case of an unfavorable course of the disease, stool frequency increases, blood pressure decreases, sharp tachycardia is observed, widespread cyanosis appears, skin turgor and elasticity decrease, and the “washerwoman's hand” symptom is noted.

Hypovolemia leads to a decrease in urine output. Oliguria develops, and subsequently anuria.

With the development of hypovolemic shock (grade 4 dehydration), diffuse cyanosis is observed. Facial features sharpen, eyeballs sink deep, the face itself expresses suffering. This is called facies cholerica. The voice is initially weak, quiet, and then disappears (aphonia) with 3-4 degrees of dehydration.

Body temperature at the height of the disease drops to 35-34 degrees.

Heart sounds in severe disease are not audible, blood pressure is not detected, shortness of breath increases up to 60 breaths per minute. The auxiliary muscles are involved in the act of breathing. Difficulty breathing is also caused by muscle cramps, including the diaphragm. The convulsive contraction of the diaphragm explains the hiccups in these patients.

Terminal period: consciousness is quickly lost and patients die in a coma.

Diagnostics

A complex of subjective data is taken into account, including epidemiological anamnesis, the dynamics of the development of the disease, the change of enteritis by gastroenteritis, and rapid dehydration.

Objective examination: reduction of turgor, skin elasticity, blood pressure control, diuresis control.

LABORATORY DIAGNOSTICS:

Main indicators: specific gravity of blood plasma, control of hematocrit, electrolytes

specific diagnostics:

1. microscopy of stool - a characteristic type of pathogens (located in parallel in the form of schools of fish, mobile). This allows for a preliminary diagnosis.

2. The classical study at the first stage provides for inoculation of 1% alkaline peptone water, followed by the removal of the film and the setting of a detailed agglutination reaction with anti-cholera 0-1 serum. When a positive reaction with O-1 serum is obtained, a typical agglutination reaction with Inaba and Agave sera is set. This allows you to determine the serotype.

Determination of the vibrio biotype (classic or El-Tor). Phages (typical) phage El-Tor 2 and phage Inkerji 4 are used. Classic biotype, when subjected to lisability to Inkerji phages. El-Tor, when vibrios are lysed by the action of El-Tor2 phages.

ACCELERATED DIAGNOSTIC METHODS

• Method of macroagglutination of vibrios after rearing on peptone water (response after 4 hours)
• Method of microagglutination immobilization of vibrios. When serum is added, vibrios lose their mobility (immobilize). Answer in a few minutes.
• The method of fluorescent antibodies (with a fluorescent microscope). Reply in 2 hours.

Serological methods - detection of vibrocidal and antitoxic antibodies. These methods are less important.

Hospitalization is mandatory. Cases require reporting to WHO.

At the first stage - pathogenetic therapy: replenishment of fluid loss - rehydration, is performed in two stages:

Primary rehydration - depending on the degree of dehydration (in a person 70 kg, 4 degree of dehydration (10%) - 7 liters are transfused.)

Correction of ongoing

losses (those that occur

already in the clinic).

Primary rehydration is carried out by intravenous injection of fluid into 2-3 veins. Use Phillips solution 1 or Trisol solution. It is necessary to heat these solutions to a temperature of 37 degrees. Even if pyrogenic reactions occur in response to the introduction of solutions, further administration is necessary under the guise of the introduction of pipolphene, diphenhydramine and hormones.

After primary rehydration, when health improves, blood pressure rises, diuresis is switched to Phillips solution 2 or disol solution (sodium chloride to bicarbonate 6 to 4, no potassium chloride), since hyperkalemia develops during primary rehydration).

In the first hours in the clinic, the liquid is injected intravenously in a jet (speed 1-2 liters per hour). Subsequently, the frequency of drops becomes usual - 60-120 per minute.

Mild degree diseases - oral rehydration (rehydrol, glucoran) is used. Specific drugs are tetracyclines. Tetracyclines are prescribed 300 mg 4 times a day. The course of treatment is 5 days.

Levomycetin - 500 mg 4 times a day. If there is no effect from these drugs, a good effect is obtained from doxycycline (semi-synthetic tetracycline). On the first day, 1 tab. 2 times a day. For 2-3-4 days, 1 tab. Once a day. Tablets of 0.1.

There are works that indicate a good effect of furadonin at a dosage of 0.1 4 times a day. The diet must include foods rich in potassium (dried apricots, etc.).

Antibiotic therapy is given orally. If the patient has severe gastroenteritis, vomiting, then oral therapy will be ineffective. Prescribed chloramphenicol succinate 1 g 3 times a day intramuscularly.

Discharge of patients is made after their recovery and a three-fold negative bacteriological examination of feces. The study is done 7 days after antibiotic treatment three times with an interval of 24 hours (inoculation on 1% alkaline media). If this is a decreed contingent (doctors, work with children, food workers), then it is necessary to obtain a negative culture of bile.

TYPES OF HOSPITAL DEPLOYING IN CHOLERA OUTBREAK

• Cholera hospital - patients with a confirmed bacteriological diagnosis of cholera.
• Provisional hospital - in patients with diarrhea syndrome; bacteriological research has not yet been carried out. Bacteriological examination is carried out. If there is Vibrio cholerae, they are transferred to a cholera hospital, if this salmonellosis is transferred to the usual infectious diseases department.
• Observatory hospital - all contact persons are hospitalized for 45 days. Bacteriological research and observation are being carried out.

Prevention

Preventive measures are aimed at preventing the introduction of the causative agent of cholera from abroad and its spread on the territory of the country, which is regulated by the "Rules for the sanitary protection of the territory." The second preventive measure is a study for the presence of Vibrio cholerae in the water of open reservoirs in the area of \u200b\u200bwater intakes, bathing areas below the wastewater discharge. According to the indications, a specific vaccination is performed with a corpuscular vaccine and cholerogen-toxoid.

In the outbreak of cholera, a set of restrictive measures is carried out, including restriction of entry and 5-day observation of those leaving, with medical supervision and bacteriological examination. They carry out measures to control water sources, disinfect water, control catering establishments, sanitary-preventive work, etc.

After hospitalization of the patient, final disinfection, identification and provisional hospitalization of contact persons, their examination and chemoprophylaxis with tetracycline, rifampicin and sulfatone are carried out.

The causative agent of cholera belongs to the genus Vibrio. It is a curved, gram-negative, non-spore-forming rod with one polar flagellum. By sensitivity to a specific phage (type IV according to Mukherjee), two biotypes of Vibrio cholerae are distinguished (the causative agent of Asian cholera) and El Tor. Each of them on the 0-antigen is divided into 3 serological types: Ogawa (AB), Inaba (AC) and the rare Gikoshima (ABC), which some authors consider as a variant of the Ogawa serotype. Vibrio cholerae H antigen is common for all serotypes. Vibrios cholerae form the heat-labile exotoxin cholerogen (relative molecular weight 8284 cd). It consists of a complex of the heavy subunit A, which activates adenylate cyclase, and the subunit B, represented by 46 light chains, and provides the binding of cholerogen with the receptors of the epithelial cells of the small intestine.

Biological and pathogenetic properties of the pathogen Having passed the gastric barrier, vibrios enter the small intestine with a favorable environment for them and colonize (colonize) the surface of the intestinal epithelium. The colonization process includes chemotaxis of vibrios to the layer of mucus covering the tops of the villi of the small intestine, penetration through this mucus, adhesion to receptors on the striated border of intestinal epithelial cells, and proliferation of villi and crypts on the surface of the epithelium. In patients with cholera, the pathogen can be found throughout the gastrointestinal tract. In the stomach at a pH of at least 5.5, vibrios are not found, in the stool their concentration reaches (sometimes ^ 109).

Having multiplied to a certain concentration, the pathogen causes the disease through the cholerogen it produces. The main role in the development of the disease is played by vibrios, which are in close connection with the mucous membrane of the small intestine, since they secrete cholerogen in the immediate vicinity of its receptors on the epithelial cells of the GM1 ganglioside. After the attachment of the cholera toxin to the ganglioside, the A subunit passes through the membranes into the epithelial cell, where the A1 fragment is released. The latter enzymatically cleaves NAD and transfers its ADP-ribose half to the regulatory protein of the adenylate cyclase complex located on the inner side of the epithelial membrane. As a result, adenylate cyclase is activated, leading to an increase in the cAMP content of one of the intracellular stimulants of intestinal secretion. The binding of cholera toxin to receptors on epithelial cells occurs extremely quickly (after 13 minutes); biochemical changes in the cell are irreversible. The resulting disease is accompanied by the loss of huge amounts of fluid with a low protein content and high concentration of sodium, potassium, chloride, and bicarbonate ions. This liquid differs in composition from both exudate and transudate and is closer to the composition of intestinal secretions.

Susceptibility People of all ages are susceptible to Vibrio cholerae. People who abuse alcohol or have undergone gastric resection are more likely to suffer from cholera. The acidity of gastric juice plays an important role in determining the minimum infectious dose in experiments on volunteers when neutralizing gastric juice with sodium bicarbonate, the number of vibrios required to reproduce a specific process in humans decreases from 10 "to 10410b microbial cells.

Clinical features The incubation period for cholera lasts from 1 to 5 days. The clinical manifestations of cholera are highly variable, and the severity of the clinical course is determined by the degree of dehydration. The disease usually begins suddenly. The first clinical sign of cholera is diarrhea. Typical cholera stools are a watery, cloudy-whitish liquid with floating flakes, rice-like in appearance and odorless. Muscle weakness and cramps in the calf muscles are early symptoms of cholera. Loose stools are followed by profuse repeated vomiting, rapidly leading to decompensated exicosis. The skin becomes cyanotic, cold to the touch, facial features sharpen, eyes and cheeks sink. The skin of the hands is wrinkled (“the hands of the washerwoman”), the voice is hoarse, up to aphonia. Patients with severe cholera have hypothermia. Because of its constancy, the terminal form of cholera (IV degree of dehydration) was called "algid". Algid (decompensated dehydration) is accompanied by a disruption in the activity of the main systems of the body, cardiovascular, respiratory, and urinary.

Immunological diagnostics Antigen detection. The causative agent of cholera and its specific antigens (corpuscular, soluble, cholerogen) are detected in feces, vomit, blood, duodenal and intestinal contents, gallbladder, in environmental objects (washings from various objects), in open water, sewage, hydrobionts and etc.

Of the modern methods of indication of Vibrio cholerae antigens, the most widespread is RNGA, the sensitivity of which with antibody erythrocyte diagnosticums is "bacteria in 1 ml or 0.04 μg / ml of 0-antigen. In clinically expressed forms of cholera, when the feces of patients contain a huge number of vibrios ( 10'109 in 1 ml), a direct study of the filtrates of feces heated in a water bath in the RNGA with an antibody diagnosticum makes it possible to give an answer about the presence of a specific antigen already after 2-3 hours. it is advisable to investigate after a preliminary 6-hour growth on 1% peptone water. In the study of feces and vomit, it turned out that only in 52% of cases, the diagnosis of cholera was bacteriologically confirmed in patients, in the history of a significant part of whom there was an indication of the use of antibiotics when the first signs of the disease appeared. With the help of RNGA, cholera disease was additionally established in another 21% of patients [Polyakov II and others, 1973]. When examining the feces, contents of the intestines and gallbladder of those who died from acute intestinal diseases, feces of healthy individuals and water samples, in practical conditions, complete coincidence of the results of serological and bacteriological research methods was usually observed, which makes it possible to consider RNGA with an antibody erythrocyte diagnosticum as a rather reliable express method for mass examination for cholera.

When indicating specific antigens of Vibrio cholerae, some authors prefer RTNGA. Cholera diagnostics for this reaction are prepared from mutton or human O (I) group of erythrocytes sensitized with cholera O antigens. The sensitivity of the bacterial method in 1 ml in the study of native feces and 10'105 after preliminary rearing. The minimum amount of 0-antigen detected by RTNGA is 0.040.16 μg / ml. RTNGA gives positive results in 91% of patients with cholera, in 40% of re - convalescents and 12% of those who were in contact with patients, 0-antigen of Vibrio cholerae can be determined 1 month after the onset of the disease in the feces of all people who have been ill, and after 56 months in half of the examined people, which apparently indicates a longer excretion of specific antigen in a non-viable form. The coincidence of the results of the bacteriological method and RTNGA, according to various sources, is observed in 63,100% of cases. The available materials give reason to consider it expedient to test the RTNGA. ° in 1 ml. It is advisable to use MFA in the study of native material from the sick and corpses. In patients with cholera, positive results using MFA were obtained within 2 hours in 7090% of observations, in full agreement with the results of bacteriological analysis. The use of MFA in the study of water and washings is possible only after preliminary growth or concentration of the material. The use of immuno-extinguishing coloration of vibrio cholerae seems promising.

Immunity After an illness, a person develops a pronounced immunity, which lasts for a long time, therefore, cases of repeated cholera diseases are extremely rare. Experiments on volunteers showed that for 3 years (observation period), people who had been ill with cholera as a result of experimental infection remained resistant to re-infection with cholera vibrios.

The main role in immunity to cholera belongs to antibodies produced locally (in the intestine), although circulating antibodies at high concentrations make a certain contribution to protection when they penetrate into the intestinal lumen from the blood, which is confirmed by animal experiments. A higher level of protection is observed with the synergistic action of antibacterial and antitoxic antibodies in the intestine. The main role of antibacterial SIgA is to inhibit the chemotaxis of vibrios to the epithelium and adherence to the surface of the intestinal mucosa by blocking adhesion structures (ligands) on the surface of bacterial cells. A decrease in the colonization and adhesion of Vibrio cholerae contributes to their more rapid elimination from the intestine during peristalsis and thereby reduces the possibility of the pathogen engraftment in the intestinal tract. The effect of intestinal IgA antibodies against cholerogen is mainly due to the blockade of its B-subunit, which prevents the binding of the toxin with the GM1 ganglioside on the surface of epithelial cells. Antibodies that block the toxic site on the A-subunit of choleragen have less protective effect.

List of used literature 1. LB Khazenson, N.A. Chaika: Immunological bases of diagnosis and epidemiological analysis of intestinal infections. "Medicine", V.D. Timakov, V.S. Levashev, LB Borisov: Microbiology. "Medicine", Lecture on the topic. 4. Methodical development of the department.

Pathogenesis: Passing through the gastrointestinal tract, part of the cholera vibrios dies in the acidic environment of the stomach, part penetrates into the small intestine, where the alkaline environment and protein breakdown products contribute to their reproduction.

IVs colonize the intestinal mucosa without penetrating into enterocytes. Accumulating in large quantities, CW produceexotoxin ... The mechanism of action of cholera toxin is the transformation of enterocyte adenylate cyclase into a constantly active form, whichviolates the reabsorption of sodium and chlorine ions and increases the secretion of chloride ions. Following an increase in the osmotic pressure of the intestinal contents, water rushes into the intestinal lumen.

Profuse diarrhea leads to increased dehydration, loss of potassium and sodium.

The balance of electrolytes is disturbed, hypovolemia develops.

CHOLERA

CLINICAL MANIFESTATIONS

The loss of fluid, reaching 8-10% of the patient's body weight, as well as salt deficiency, lead to the development of algid (from the Latin algidus - cold).

Clinically, algid is characterized by drop in blood pressure(up to his

disappearance), a decrease in body temperature to 34 ° C, severe shortness of breath (up to 55-60 breaths per minute), expressed by a generalcyanosis skin,convulsions muscles of the limbs, abdomen, face, aphonia. Skin turgor sharply decreases, a symptom is noted"The hands of the washerwoman".

But mostly there are cases of moderate and mild cholera, manifested by diarrheal syndrome with stool frequency from 5 to 20 times a day and dehydration. Stools watery, mixed with mucus, reminiscent of rice water.

CHOLERA

Development stages:

1. Cholera enteritis

2. Cholera

gastroenteritis

3. Algid period

CHOLERA

Cholera enteritis:

1. Edema and congestion of the mucous membrane

2. Goblet cell hypersecretion

3. Focal hemorrhages in the mucous membrane

Cholera gastroenteritis:

1. Vacuolization of epithelial cells and their loss of microvilli

2. Desquamation of the epithelium

3. Serous-hemorrhagic enteritis and gastritis

CHOLERA Algid form

1. Early and pronounced rigor mortis. The corpse looks like a "wrestler or boxer pose".

2. Sunken cheeks and eyes, dry cornea, protruding mouth and chin.

3. The skin is earthy, cyanosis on the tip of the nose, fingers, earlobes. Cadaveric spotspurple-purple color. On the cut, the skin, subcutaneous tissue, and muscles are dry.

4. The blood is dark, thick, reminiscent of "currant jelly".

5. Serous membranes (peritoneum, pleura, pericardium) are full-blooded, with punctate hemorrhages, dry. The serous membrane of the small intestine can have a "marbled appearance" (unevenly plethoric). Possible mucous effusion on the serous cover of the peritoneum and intestines.

6. In the small intestine there is a significant amount of flocculent contents, colorless and odorless, reminiscent of "rice water", sometimes mixed with blood or bile.

CHOLERA Algid form

7. The mucous membrane of the small intestines is swollen, full-blooded, swollen, with small-focal hemorrhages and pityriasis plaque.

8. Lymphatic follicles and Peyer's plaques are swollen, often surrounded by a hemorrhage rim.

9. Lymph nodes at the mesenteric root are enlarged, dense, juicy on a cut.

In general, changes in the small intestine are designated as acute serous or serous-hemorrhagic enteritis. 10. In the stomach there is acute serous-hemorrhagic gastritis. The mucous membrane is swollen, hyperemic, with focal hemorrhages.

11. The large intestine is often without visible changes. There may be congestion and swelling of the mucous membrane, minor hemorrhages.

CHOLERA Algid form

12. The gallbladder is distended with cloudy or light watery bile ("white bile"). In other cases, the contents are thick, black in color. The mucous membrane of the bladder is full-blooded, with hemorrhages.

13. In the liver, dystrophic changes of fatty and proteinaceous nature.

Decreased skin turgor

Cholera typhoid

- A complication resulting from the attachment of a secondary, mainly bacterial microflora.

- Signs of dehydration disappear, rigor mortis is less pronounced, there is no wrinkling of the skin, cyanosis, the blood in the vessels is liquid.

- Changes in the small intestine may be. only in limited areas in the form of foci of diphtheria inflammation.

- At the site of Peyer's patches, the mucous membrane is necrotic to the mucous layer.

- In the lumen of the intestines, liquid or semi-liquid contents of the usual color and smell.

- The main changes develop in the small intestine in the form of fibrinous, more often diphtheria, inflammation of the mucous membrane withgrayish-green overlays and possible ulceration, reminiscent of changes in dysentery. Catarrhal changes in the mucous membrane of the colon are possible.

Cholera typhoid

- The kidneys are enlarged, the capsule is tense, easily removable. The cortical substance is expanded, in the medullary - plethora of pyramids, mucous membrane of the pelvis.

- Liver with signs of granular and fatty degeneration.

- The spleen is usually enlarged, sometimes with heart attacks.

DIPHTHERIA

Diphtheria is an acute infectious disease

characterized by local fibrinous inflammation, most often of the mucous membranes of the oropharynx and nasopharynx, as well as the phenomena of general intoxication, damage to the cardiovascular, nervous and excretory systems.

Causative agent - Corynebacterium diphtheriae

Source of infection: a patient with diphtheria, convalescent and a carrier of bacteria.

Transmission mechanism: mainly by airborne droplets, but it is also possible by contact and household means (through infected objects).

The main sign of the pathogenicity of diphtheria bacteria is the ability to produce exotoxin. Diphtheria toxin belongs to potent poisons, second only to botulinum and tetanus.