Cholera is caused by the enterotoxin
elaborated by Vibrio cholerae, a gram-negative bacillus.
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The organism proliferates in the lumen
of the small intestine and causes profuse watery diarrhea, rapid
dehydration, and (if fluids are not restored) shock and death within
24 hours of the onset of symptoms.
Enterotoxins of other vibrios (for
instance V. parahemolyticus) also cause diarrhea and mimic cholera,
but symptoms are milder.
In the 19th century cholera
was common in most parts of the world, but it periodically
“disappears”.
There have been major pandemic -
(1961-74) : Extended throughout Asia, the Middle East, southern
Russia, the Mediterranean basin, and parts of Africa.
V. cholerae is a curved gram-negative
bacillus with a polar flagellum that moves in a helical path, with a
characteristic wobble.
V. cholerae is destroyed by gastric
acid.
Successful colonization in the small
intestine depends on (a) a reduction or dilution of gastric acid, (b)
bacterial motility, pili, and production of enzymes (colicins,
mucinase, neuraminidase), and (c) availability of binding sites for
the organisms and the enterotoxin. Pathogenic strain adhere to cells
of the intestinal mucosa.
Drinking
water contaminated with Vibrio cholerae.and food prepared with
contaminated water are infectious.
Those with a
normal gastric acidity are much less susceptible than those with low
levels of stomach acid as result of a gastrectomy or other cause.
Vibrios
traverse the stomach, enter the small intestine and propagate.
They remain
in the lumen and do not invade the intestinal mucosa.
They do,
however elaborate an enterotoxin, which contains A and B subunits.
The B subunit
binds the toxin to GM1 ganglioside in the cell membrane at the brush
border of the small intestine.
The A subunit
enters the cell and activates adenyl cyclase, thereby initiating a
chain of reactions in the membrane.
Symptoms
begin when the massive secretion of water and sodium in the small
intestine, a consequence of the activation of cyclic AMP, exceeds the
resorptive capacity of the colon.
The small
intestine, however, is not damaged morphologically either by the
vibrios or by the enterotoxin.
The loss of sodium and water causes
severe diarrhea, called “ricewater stool”. Fluid loss may exceed 1
liter per hour.
Acute dehydration , hypovolemic shock,
and metabolic acidosis follow quickly.
The patient exhibits dry skin, sunken
eyes, lethargy, cyanosis, a weak pulse, faint heart sounds,
hemoconcentration, and elevation of serum proteins.
The hematocrit may rise to 55-65 and
the plasma specific gravity to 1.035-1.050.
Patients are usually afebrile , body
temperature may be subnormal.
Treatment is prompt rehydration, and
under such circumstances most patients survive.
After the onset of diarrhea, urine
production ceases, but renal function improves when fluid and
electrolytes are replaced.
Inadequate replacement, however, leads
to prolonged renal failure, with acute damage of tubules and the
vacuolar lesions of hypokalemia.
For many years, the intestinal changes
in cholera could be studied only at autopsy.
Degenerative changes in the intestinal
epithelium, although observed repeatedly in victims of cholera, could
not be distinguished from the autolysis that begins in the intestine
at the moment of death.
Specimens of the small intestine taken
promptly after death have now shown that cholera patients have an
intact intestinal epithelium and, except for minor, nonspecific
changes, a morphologically normal mucosa.
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