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Bacterial Diseases Late from the Water Throughout the Year

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Bacterial Diseases Late from the Water Throughout the Year

Bacterial Diseases Late from the Water Throughout the Year, although most cases of cholera occur seasonally. Pathology and Pathogenesis. Recent studies of cholera indicate that the small intestine is most severely involved. There is an intact gastrointestinal epithelium, even in the acute phase of the disease, but there is mononuclear cell inflammation of the mucosa, vascular congestion, and goblet cell hyperplasia.

This acute stage may be followed by increased “turnover” of the epithelial cells. The occurrence of the disease in impoverished and malnourished persons further suggests this possibility. A mucolytic enzyme is also produced by the vibrio. and may participate in the pathogenesis of the disease. The essential mechanism producing cholera. however, remains unknown. There is no significant loss of albumin into the intestines, as illustrated by the failure of intravenously injected Evans blue dye to appear in the feces. V. cholera infection does not extend beyond the intestinal tract but may invade, to a limited degree, the mucosa of the bowel and, rarely, the regional lymphatics.

Clinical Manifestations. Cholera begins as acute diarrhea with abdominal pain. Vomiting may appear early but is not prominent. Fever and chills are usually absent. The oral and axillary temperature may be depressed, whereas the rectal temperature may be elevated slightly above normal. It is of interest that there may be considerable postmortem elevation of temperature. Over a few hours diarrhea increases in severity, and the volume of feces may be as great as 15 to 20 liters in 24 hours. Initially, the feces are bile-strained, but as diarrhea worsens, the feces become watery, mucoid, and odorless, and occasionally may contain blood. Muscular cramps may be severe.

Thirst is intense, and the ingestion of fluid rarely induces vomiting. Recovery ordinarily is prompt after replacement of fluid and electrolyte, but the patient may continue to have anuria or oliguria and may die in renal failure. The plasma potassium may be slightly elevated or normal, although potassium depletion is severe. Metabolic acidosis is usually severe. Fecal potassium and carbonate Concentrations, however, are higher than those of the plasma. These electrolyte changes in cholera resemble those in another diarrheal disease but are more severe. Many patients with cholera are anemic before the onset of the disease; therefore, the rise in hernia-to crit with dehydration may not be demonstrable. The degree of dehydration in cholera can be clinically estimated but is best measured by the determination of plasma specific gravity and central venous pressure.

Diagnosis. Bacteriologic and immunologic identification of V.cholerae from the feces is usually possible. Microscopic examination of the feces may reveal masses of the microorganism. V. cholera may be cultured from the feces of patients convalescing from cholera but ordinarily disappears within a few days or a few weeks. Serum antibody titers, measured by hemagglutination or virucidal assay, however, rise to maximal levels in about seven days after the onset of cholera. Vibriocidal titers fall rapidly after an illness. Other Vibrio. Infections. V. cholera may be confused with El Tor vibrio, which may also produce diarrheal disease. El Tor vibrio, however, is hemolytic and can be differentiated from the cholera vibrio serologically. The noncholera vibrios are widespread in surface water throughout the world and have been associated with diarrheal disease. Man is infected following occupational exposure to diseased animals or animal ‘products. V. fetus infection of

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