Shigella and enteroinvasive Escherichia coli: Paradigms for pathogen evolution and host–parasite interactions - Escherichia coli: Pathotypes and Principles of Pathogenesis - page 226

In addition, massive population displacement caused by civil wars in Burundi
and Rwanda in 1993-94 led to explosive epidemics of diarrheal disease caused
by Vibrio cholerae and S. dysenteriae 1 ( Kerneis et al., 2009 ).
Reservoirs and vehicles of infection
Shigella spp. are highly host-adapted pathogens. Humans are the natural res-
ervoir of Shigella infections and non-human primates such as rhesus macaque
monkeys are the only animals in which Shigella cause disease. Interestingly,
several cases of transmission from monkeys to man have been reported. In one
instance, three animal caretakers at a monkey house complained of having diar-
rhea. S. flexneri 1b was isolated from stool samples of these employees and
further investigation showed that four monkeys were shedding the identical sero-
type. The disease was apparently spread by direct contact of the caretakers with
excrement from the infected monkeys ( Kennedy et al., 1993 ). Asymptomatic
carriers of Shigella may contribute to the maintenance and spread of this patho-
gen in developing countries. Two studies, one in Bangladesh ( Hossain et al.,
1994 ) and the other in Mexico ( Guerrero et al., 1994 ), showed that Shigella
could be isolated from stool samples from asymptomatic children under the age
of 5 years. Shigella were rarely found in infants under the age of 6 months.
Clinical features
The incubation period for shigellosis is 1 to 7 days, but the illness usually begins
within 3 days. Signs and symptoms associated with dysentery include fever,
severe abdominal cramps, tenesmus, and diarrhea composed of watery stools
containing mucus and traces of blood. While nearly all patients with shigellosis
experience abdominal pain and diarrhea, fever occurs in about one-third and
gross blood in the stools in about 40% of the cases ( DuPont, 2005 ). The feces
also contain high numbers of PMNs and viable infectious Shigella .
The clinical picture of shigellosis ranges from a mild watery diarrhea to
severe dysentery. The dysentery stage of the disease may or may not be preceded
by watery diarrhea. This stage probably reflects the transient multiplication of
the bacteria as they pass through the small bowel. Enterotoxins produced by
Shigella and EIEC are believed to induce fluid secretion in the small intestine.
In addition, as bacterial invasion and destruction of the colonic mucosa com-
mences, jejunal secretions probably are not effectively reabsorbed in the colon
due to transport abnormalities caused by tissue destruction ( Kinsey et al., 1976 ).
The dysentery stage of disease correlates with extensive bacterial colonization
of the colonic mucosa. The bacteria invade the epithelial cells of the colon,
spread from cell to cell but penetrate only as far as the lamina propria. Foci of
individually infected cells produce microabscesses that coalesce, forming large
abscesses and mucosal ulcerations. Dead cells of the mucosal surface slough
off as the infection progresses, leading to the presence of blood, pus and mucus