189. Cholera: etiology, pathogenesis, morphological characteristics, outcomes.

Cholera is an acute infectious disease with a predominant lesion of the stomach and small intestine. Cholera is a severe anthroponosis, belongs to the group of quarantine or conventional infections and is extremely contagious.

Etiology:

The causative agent is a vibrio isolated by R. Koch. The most important are vibrio Asiatic cholera Koch and vibrio El Tor, which was previously considered conditionally pathogenic. Vibrio El Torus, compared with vibrio Koch, causes milder forms of the disease, gives a lower mortality rate.

Pathogenesis:

Vibrions multiply in the small intestine and secrete exotoxin (cholerogen). Abundant secretion of fluid as a result of  the interaction of cholerogen with the enzyme systems of the cell;  impaired reabsorption.  profuse diarrhea, rapid loss of water and electrolytes (sodium, potassium, bicarbonates),  Dehydration,  Oliguria and a drop in body temperature, hypovolemic shock and metabolic acidosis, blood thickening and hypoxia  cholera coma.

Morphological characteristics:

There are 3 stages (periods) in the development of cholera: cholera enteritis, cholera gastroenteritis and algid period.

Cholera enteritis has a serous or serous hemorrhagic character. The mucous membrane is swollen, edematous and full-blooded; hypersecretion of goblet cells is noted, the cytoplasmic membranes of which are torn and the secret exits into the lumen of the intestine. Against this background, single or multiple hemorrhages appear.

In choleric gastroenteritis, enteritis phenomena increase, epithelial cells are vacuolized and lose microvilli, some of them die and desquamate. Enteritis is accompanied by serous or serous hemorrhagic gastritis. Progressive dehydration during this period is associated not only with diarrhea, but also with vomiting.

In the algid period, morphological changes are most pronounced. In the small intestine, there is a sharp fullness, edema, necrosis and peeling of epithelial cells of the villi, infiltration of the mucous membrane by lymphocytes, plasma cells, neutrophils, foci of hemorrhages. The loops of the intestine are stretched, their lumen contains a lot (3-4 liters) of colorless, odorless liquid in the form of rice broth. Vibrions can be detected in this liquid. The serous lining of the intestine is dry, with spot hemorrhages, matte, colored pinkish yellow. A transparent, sticky mucus stretching in the form of threads is found between the loops of the small intestine.

Outcomes:

Death of a cholera patient usually occurs in the algid period from dehydration, coma, uremia, intoxication. Due to early and adequate treatment (administration of fluids and electrolytes, taking antibiotics), mortality in cholera algid is significantly reduced. Death is also possible from complications of cholera, of which uremia is the most common.

190. Acute enteritis (salmonellosis, staphylococcal, caused by Escherichia coli).

Etiology. Acute enteritis often occurs in infectious diseases (cholera, typhoid fever, colibacillar, staphylococcal and viral infections, sepsis, giardiasis, opisthorchiasis), food toxicoinfections (salmonellosis, botulism), poisoning (chemical poisons, poisonous mushrooms). Acute enteritis of alimentary (overeating, eating coarse food, spices, spirits) and allergic (idiosyncrasy to food, medicines) origin is known.

Pathological anatomy. Acute enteritis can be catarrhal, fibrinous, purulent, necrotic ulcerative. In the most frequent catarrhal enteritis, the full-blooded and edematous mucous membrane of the intestine is abundantly covered with serous, serous-mucous or serous-purulent exudate. Edema and inflammatory infiltration cover the mucous membrane and submucosal layer. Dystrophy and desquamation of the epithelium are noted, especially at the tips of the villi (catarrhal desquamative enteritis), hyperplasia of goblet cells (goblet transformation), minor erosions and hemorrhages. In fibrinous enteritis, often ileitis, the intestinal mucosa is necrotized and permeated with fibrinous exudate, as a result of which gray or gray-brown filmy overlays appear on its surface. Depending on the depth of necrosis, inflammation can be croup or diphtheria, in which deep ulcers form after rejection of fibrinous films. Purulent enteritis — diffuse impregnation of the intestinal wall with pus (phlegmonous enteritis) or the formation of pustules, especially at the site of lymphoid follicles (apostematous enteritis). In necrotic ulcerative enteritis, the group and solitary lymphatic follicles of the intestine are susceptible to destruction, as in typhoid fever, or the mucous membrane is out of connection with the lymphatic apparatus of the intestine. At the same time, necrosis and ulceration are common (influenza, sepsis) or focal (allergic vasculitis, nodular periarteritis). Regardless of the nature of inflammation of the mucous membrane, hyperplasia and reticulomacrophagal transformation of the intestinal lymphatic apparatus develop in acute enteritis. Sometimes it is extremely pronounced (for example, cerebral swelling of group and solitary follicles in typhoid fever) and causes the subsequent destruction of the intestinal wall.

In mesenteric lymph nodes, reactive hyperplasia of lymphoid elements develops, their plasmocytic and reticulomacrophagous transformation, and often inflammation.

Complications of acute enteritis: bleeding, perforation of the intestinal wall followed by peritonitis (for example, with typhoid fever), dehydration and demineralization (for example, with cholera). Sometimes acute enteritis turns into chronic.