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Shigella dysenteriae cause a Bacillary dysentery disease.
The bacteria release the Shiga exotoxin that inhibits
protein sythesis by lysing 28S rRNA.
Shigella belong to the bacterial family, Enterobacteriaciae, and can occur as the four different species:
They are gram-negative, citrate negative, H2S negative, lysine decarboxylase negative, non-lactose fermenting, bile salt resistant, facultative anaerobes that are non-motile and posses a capsule (K antigen) and an O antigen. These bacteria typically effect the higher primates, specifically, humans.
All four species produce a similar disease, shigellosis, which may vary in intensity, but elicits similar symptions in the host. Shigella are said to be the major cause of diarrheal disease and infant mortality throughout the developing nations of the world, and cause an estimated 15-20% of pediatric diarrhea in the United States. The species Shigella sonnei is the most comon cause of the disease, shigellosis in the United States and other developed countries, while Shigella flexneri is the most common cause of shigellosis in underdeveloped nations. However, the species that causes the most serious symptoms (including dysentery) is Shigella dysenteriae. This species occurs most frequently in the Eastern Hemisphere.
Only a small number of cells are required
for infection (200), thus shigella are spread easily via a fecal-oral
route, or even from direct person-to-person contact. Their generation
time is about 40 minutes, and the incubation period is only 1-7 days, averaging
3 days. Ingestion of contaminated food or water is also a mode of
infection, making proper sewage disposal and water treatment necessary
steps for prevention. Because of its association with crowded or
poor living conditions, this bacteria is often spread among people in prisons,
daycare centers, mental institutions, nursing homes, and military camps.
Daycare centers prove especially susceptable to shigellosis because of
the proportion of people under the age of 10yrs.
of the bacteria can occur, and the organism may be carried by its host
for an entire month after convalescence. Shigella can even be carried
by a host for several months by establishing a "chronic carrier condition,"
similar to other enteric bacterial infections.
Fig. 1: Mechanism of entry and dissemination of Shigella
in epithelial cells
Shigella invade the villus cells of the large intestine by penetrating the colonic mucosa, but do not invade the blood, or perforate the intestine beyond the epithelium into the lamina propria. Shigella enter the intestinal mucosa by attaching to, and invading lymphoid cells in Peyer's patches. These specialized lymphoid cells are called "M cells," and normally transport foreign antigens from the intestine to underlying macrophages. The bacteria are internalized by the epithelial cells via a process similar to phagocytosis. This usually occurs with an endosome, but these bacteria have the ability to lyse the phagocytic vacuoles of macrophage cells and replicate in their cytoplasm (Fig 1.). The bacteria are then spread into adjacent epithelial cells by propulsive movements of actin. This way, the bacteria avoid antibody-mediated humoral immunity. Shigella produce Ipa proteins in order to help escape
from the endosome, but also From Parsot and Sansonetti (1996), Fig. 1, p. 27
produce them early on in order http://www.ucs.mun.ca/~cmtulk/shigspread.htm
to initiate a cascade of cellular
signalization that internalizes the bacteria with endosomes.
While present in the mucosa, Shigella typically cause an inflammatory response that results in extensive tissue damage. They release a heat-stabile lipopolysaccharide endotoxin that can cause fever. The LPS of Gram-negative bacteria contains cell wall antigens (O antigens) that can elicit a variety of inflammatory responses in an animal. This endotoxin is part of the outer membrane of the Shigella cell, and has a low degree of specificity and a low degree of potency. It has an MW of 10kDa, and does not show enzymatic activity.
Shigella also use apoptosis in order to intentionally activate the host's inflammatory response. Subsequent infiltration and diapedisis by leukocytes disrupts the tight-junction of the bowel epithelium, thus allowing a massive invasion by bacteria still in the colon, resulting in a massive invasion and degradation of the intestinal mucosa.
Shiga Toxin Molecular Structure