Cholera (Asiatic Cholera) Leighton E. Cluff



Cholera is a specific infectious dis-ease of man-caused by Vibrio cholera. It is characterized by severe diarrhea with fluid and electrolyte depletion and now occurs endemically and epidemically in Asia. Etiology. In a classic study in 1857, Snow described an outbreak of cholera in London and incriminated contaminated water as the source of disease. In 1883, Koch identified Vibrio cholerae in the feces of a large number Of patients with cholera. The cholera vibrio is a comma-shaped, gram-negative, nonhemolytic, flagellated, and motile micro-organism that grows aerobically on nutrient media at 37° C., preferentially at an alkaline pH. V. cholerae can be characterized and differentiated from noncholera vibrios by its fermentative, nonhemolytic, pathogenic, and anti-genic reactions. Incidence and Prevalence. Cholera is endemic in India, China, Burma, Pakistan, Thailand, and a few other” areas in Asia. It has occurred in epidemics throughout the world.

Prior to the nineteenth century, cholera was unknown outside India, but during that century it was observed sporadically and as an epidemic in Europe, England, Russia, and North America. In the twentieth century, cholera has largely disappeared from the Western Hemisphere and Europe but continues to occur endemically and epidemically in Asia, primarily along the Ganges River in India and in Pakistan. The last pandemic of cholera began in 1902.

During the period 1898 to 1907 cholera was responsible for at least 370,000 deaths in India. Epidemiology. The only man is naturally infected with V. cholerae. The infection is transmitted most commonly by contaminated water, but it can be transmitted by contamination of fresh leafy. or root vegetables and fruit fertilized With human feces or contaminated with water containing the micro-organism. V. cholerae has been isolated from flies, roaches, and other insects, but these may be an unimportant source of contagion. Doctors and nurses caring for patients with cholera rarely contract the disease, suggesting that direct contact under hygienic conditions is an uncommon mode of transmission of the infection. Cholera is primarily a disease of persons who live in love y or who have poor standards of living and sanitation. Outbreaks of cholera usually appear during dry, hot weather preceding a rainy season. The reason for this seasonal occurrence of cholera is unexplained.

Although sporadic cases may occur throughout the year, there are rare chronic carriers of V. cholera, as there are of typhoid bacilli, and the principal reservoir of the organism in int. epidemic periods is unclear. In endemic areas around river basins, V. cholerae can be iso-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. These morphologic changes are similar to those seen in nonspecific diarrhea but do not explain the clinical features of the disease. Chronic atrophic enteritis may precede and persist after the infection. It is likely that nutritional and other chronic affections of the intestine and stomach are predisposing causes of cholera. The occurrence of the disease in impoverished and malnourished persons further suggests this possibility. A cholera-like disease has been produced in dogs by feeding vibrio cultures (10″ bacteria) in bicarbonate.

The cholera vibrio elaborates a substance altering sodium transport that produces intestinal intoxication, diarrhea, and fluid and electrolyte depletion. 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. The primary difficulty in cholera is severe fluid and electrolyte depletion. The feces contain mucus, epithelial debris, large quantities of water, sodium, potassium, and bicarbonate, but little plasma protein.

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.

The feces of patients with cholera may resemble rice water or starch water and may contain cellular debris and masses of cholera vibrios. The patient becomes rapidly dehydrated, the skin is cold and withered, and the face becomes drawn. As dehydration increases, the patient becomes stuporous, comatose, hypotensive, and cyanotic, and may die in shock. Urine output decreases, mouth and eyes become dry, but lacteal and sweat secretion may persist. 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 renal insufficiency may be attributable to hypokalemia, shock, or reduced renal blood flow owing to dehydration. With severe dehydration the hematocrit, leukocyte count, and specific gravity of the plasma rise. This plasma sodium chloride and total serum protein are increased above normal. The plasma potassium may be slightly elevated or normal, although potassium depletion is severe.

Metabolic acidosis is usually severe. In cholera, the fecal sodium and chloride concentrations are increased above normal, as is fecal osmolarity, but these are consistently lower than the plasma values. 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.

In endemic areas and during epidemics, cholera is easily recognized clinically. Sporadic cases must be differentiated from other diarrheal diseases such as typhoid fever, bacillary dysentery, amebiasis, other forms of intestinal parasitism, viral enteritis, staphylococcal food poisoning, and chemical poisoning. The epidemiologic and fulminant characteristics of cholera, however, are helpful diagnostically. Bacteriologic and immunologic identification of V. cholerae from the feces is usually possible. Microscopic examination of the feces may reveal masses of the micro-organism. V. cholerae may be cultured from the feces of patients convalescing from cholera but ordinarily disappears within a few days or a few weeks. Many patients have a positive serologic test for V. cholera antibodies on the day of onset of disease.

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