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Infectious agents usually cause acute gastroenteritis. These agents cause diarrhea by
adherence, mucosal invasion, enterotoxin production, and/or cytotoxin production.

These mechanisms result in increased fluid secretion and/or decreased absorption. This
produces an increased luminal fluid content that cannot be adequately reabsorbed, leading to
dehydration and the loss of electrolytes and nutrients.

Diarrheal illnesses may be classified as follows:

R Osmotic, due to an increase in the osmotic load presented to the intestinal lumen, either
through excessive intake or diminished absorption
R Inflammatory (or mucosal), when the mucosal lining of the intestine is inflamed
R Secretory, when increased secretory activity occurs
R Motile, caused by intestinal motility disorders

The small intestine is the prime absorptive surface. The colon then absorbs additional fluid,
transforming a relatively liquid fecal stream in the cecum to well-formed solid stool in the
rectosigmoid.

Disorders of the small intestine result in increased amounts of diarrheal fluid with a
concomitantly greater loss of electrolytes and nutrients.

Microorganisms may produce toxins that facilitate infection. Enterotoxins are generated by
bacteria (ie, enterotoxigenic ^


 

 ) that act directly on secretory
mechanisms and produce typical, copious watery (rice water) diarrhea. No mucosal invasion
occurs. The small intestines are primarily affected, and elevation of the adenosine
monophosphate (AMP) levels is the common mechanism.

Cytotoxin production by bacteria (ie,   

 

  

 
enterohemorrhagic ^
 ) results in mucosal cell destruction that leads to bloody stools
with inflammatory cells. A resulting decreased absorptive ability occurs.

Enterocyte invasion is the preferred method by which microbes such

as   and  
 organisms and enteroinvasive ^
  cause destruction and
inflammatory diarrhea. Similarly,    and   species also invade cells but do not
cause cell death. Hence, dysentery does not usually occur. However, these bacteria invade the
bloodstream across the lamina propria and cause enteric fever such as typhoid.

Diarrheal illness occurs when microbial virulence overwhelms normal host defenses. A large
inoculum may overwhelm the host capacity to mount an effective defense. Normally, more than
100,000 ^
  are required to cause disease, while only 10 ^ or  cysts may
suffice to do the same. Some organisms (eg, 
 
enterotoxigenic ^
 ) produce proteins
that aid their adherence to the intestinal wall, thereby displacing the normal flora and colonizing
the intestinal lumen.

In addition to the ingestion of pathogenic organisms or toxins, other intrinsic factors can lead to
infection. An alteration of normal bowel flora can create a biologic void that is filled by
pathogens. This occurs most commonly after antibiotic administration, but infants are also at
risk prior to colonization with normal bowel flora.

The normally acidic pH of the stomach and colon is an effective antimicrobial defense. In
achlorhydric states (ie, caused by antacids, histamine-2 [H2] blockers, gastric surgery,
decreased colonic anaerobic flora), this defense is weakened.

Hypomotility states may result in colonization by pathogens, especially in the proximal small
bowel, where motility is the major mechanism in the removal of organisms. Hypomotility may be
induced by antiperistaltic agents (eg, opiates, diphenoxylate and atropine [Lomotil], loperamide)
or anomalous anatomy (eg, fistulae, diverticula, antiperistaltic afferent loops) or is inherent in
disorders such as diabetes mellitus or scleroderma.

The immunocompromised host is more susceptible to infection, as evidenced by the wide

spectrum of diarrheal pathogens in patients with AIDS.

The exact mechanism of vomiting in acute diarrheal illness is not known, although serotonin
release has been postulated as a cause, stimulating visceral afferent input to the chemoreceptor
trigger zone in the lower brainstem. Preformed neurotoxins produced by  


 
 and 
  
 , when ingested, can cause severe vomiting.



 

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