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in the stools. Bacillary dysentery is also characterized by massive amounts of
PMNs which migrate from the subepithelium into the intestinal lumen. The
intense host inflammatory response is initiated by
Shigella
and sustained by
release of pro-inflammatory mediators.
S. dysenteriae
1 causes the most severe disease while
S. sonnei
produces
the mildest.
S. flexneri
and
S. boydii
infections can be either mild or severe.
Volunteer studies and clinical reports show that EIEC produce dysentery with
a clinical presentation indistinguishable from that produced by
Shigella
with
symptoms ranging from mild to severe (
DuPont et al., 1971
;
Tulloch et al.,
1973
). Despite the severity of the disease, shigellosis is self-limiting. If left
untreated, clinical illness usually persists for 1 to 2 weeks (although it may be
as long as a month) and the patient recovers.
Complications
Dysentery can be a very painful and incapacitating disease and is more likely to
require hospitalization than other bacterial diarrheas. It is not usually life-threaten-
ing and mortality is rare except in malnourished children, immunocompromised
individuals, and the elderly (
Bennish et al., 1990
). However, serious complica-
tions can arise from the disease and include severe dehydration, intestinal perfo-
ration, toxic megacolon, sepsis, seizures, HUS, and Reiter's syndrome (
Bennish,
1991
). HUS is a rare but potentially fatal complication associated with infection
by
S. dysenteriae
1 (
Butler, 2012
). The syndrome is characterized by hemolytic
anemia, thrombocytopenia, and acute renal failure. Epidemiological studies sug-
gest that Shiga toxin produced by
S. dysenteriae
1 is the cause of HUS. This
hypothesis is supported by the fact that HUS is also caused by strains of
E. coli
,
especially enterohemorrahagic
E. coli
, that produce high levels of Shiga toxin
(see Chapter 5) (
Melton-Celsa, et al., 2012
). Shiga toxin causes HUS by entering
the bloodstream and damaging vascular endothelial cells such as those in the kid-
ney (
O'Loughlin and Robins-Browne, 2001
). Reiter's syndrome, a form of reac-
tive arthritis, is a post infection sequela to shigellosis that is strongly associated
with individuals of the HLA-B27 histocompatibility group (
Simon et al., 1981
).
The syndrome is comprised of urethritis, conjunctivitis, and arthritis with the lat-
ter being the most dominant symptom. Reactive arthritis is an ill-defined clinical
syndrome that also results from infections by several other Gram-negative enteric
pathogens (
Townes, 2010
). A PubMed search of the literature (November 2012)
yielded no reports of reactive arthritis as a complication of infection with EIEC.
Treatment, control, and prevention
Stool fluid losses with dysentery are not as massive as with other bacterial diar-
rheas. However, the diarrhea associated with dysentery, combined with water
loss due to fever and decreased water intake due to anorexia, may result in
severe dehydration (
Bennish et al., 1990
). Although intravenous rehydration
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