Clinical Manifestations and Pathology

The bacterial infection is limited to the intestinal tract; no microbes are found to invade the body tissues. The low bacterial population normally in the small intestine as well as its high alkalinity contribute to the cholera vibrio's ability to survive and grow there, usually in massive numbers. They adhere to the intestinal wall and secrete a toxin that inhibits the absorption of water and electrolytes (salts) from the intestine into the circulation. Since the blood delivers large amounts of water and salts into the intestinal tract, which are then normally reabsorbed back into the bloodstream, failure of this reabsorp-tion results in the loss and excretion of many liters of fluid in the course of a single day. This loss presents as a massive, debilitating diarrhea, which is the major clinical feature of cholera. All other symptoms of the disease are attributable to this water and salt depletion. These symptoms and clinical findings include weakening and finally loss of palpable pulse, thickening of the circulating blood, suppression of urination, loss of tissue fluids giving the face a sunken appearance, cyanosis, muscular spasms, and a disastrous fall in blood pressure leading to profound shock, which represents the fatal conclusion of the disease. The mind is ordinarily clear throughout the course of the disease. Recovery, when it occurs, is marked by the return of the capacity to reabsorb and retain fluids and salts, and a reversal of the signs and symptoms discussed above.

Pathological changes observed in the past on examination of the body at autopsy can now be attributed to postmortem changes. Early reports describe an erosion of the intestinal wall leading to the fluid loss mentioned, with the intestinal lining being found shed into the excreta. But in 1960, Eugene J. Gangarosa of the Walter Reed Hospital was able to observe the intestinal walls of cholera patients directly and found no evidence of any structural damage to cells in this area. Thus was research directed toward damage at an enzymatic or molecular level, pathologically caused by the cholera toxin already discovered by De in 1959.

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