Biology Reference
In-Depth Information
In addition to temperature regulation of genes required for invasion,
Shigella
relies on post-invasion signals following contact with host cells to cue expression
of virulence genes required for intracellular growth and survival (
Demers et al.,
1998
). Growth at 37°C is not sufficient for expression of
ipaH
and
virA
. Expres-
sion of these genes and at least four additional T3SS secreted effectors is induced
after entry into host cells (
Kane et al., 2002
). Expression of 13 “post-invasion”
genes is regulated by the transcriptional activator MxiE along with the co-activator
IpgC (
Kane et al., 2002
;
Mavris et al., 2002
;
Le Gall et al., 2005
). Included among
these genes are the
osp
genes which dampen the host inflammatory response (see
Table 7.1
). Thus, this second level of virulence gene regulation ensures expression
of factors where they are most effective and maximizes pathogen fitness in host
tissues while reprograming the host cell to serve the pathogen's needs.
CLINICAL MANIFESTATIONS OF DISEASE
Infectious dose and transmission
An important aspect of
Shigella
pathogenesis is the extremely low ID
50
, i.e. the
experimentally determined oral dose required to cause disease in 50% of volun-
teers challenged with a virulent strain of the organism. The ID
50
for
S. flexneri
,
S.
sonnei
, and
S. dysenteriae
is approximately 5,000 organisms. Volunteers become
ill when doses as low as 200 organisms are given (
DuPont et al., 1989
). The low
infectious dose of
Shigella
underlies the high communicability of bacillary dys-
entery and gives the disease great explosive potential for person-to-person spread
as well as foodborne and water borne outbreaks of diarrhea. In contrast, at least
10
8
EIEC must be ingested to produce disease (
DuPont et al., 1971
). The reason
for the significantly higher infectious dose for EIEC remains unknown.
Person-to-person transmission of
Shigella
is by the fecal-oral route with
most cases of shigellosis being caused by the ingestion of fecally-contaminated
food or water. The highest incidence of shigellosis occurs during the warmer
months of the year.
Shigella
can spread from infected carriers by several routes
including food, fingers, feces, and flies. The latter usually transmit the bacteria
from fecal matter to foods. Many types of raw and cooked foods have been
implicated as sources and outbreak settings have included restaurants, social
gatherings, airlines and cruise ships. The major factor for contamination is the
poor personal hygiene of food handlers. Improper storage of contaminated
foods is the second most common factor that accounts for foodborne outbreaks
due to
Shigella
(
Nygren et al., 2012
).
Epidemiology
Shigella
and EIEC are frank pathogens capable of causing disease in other-
wise healthy individuals. Certain populations, however, may be predisposed to
infection and disease due to the nature of transmission of the organisms. The
annual number of cases of shigellosis worldwide has been estimated to exceed
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