Shigella

Categorization
Cell Wall: Gram Negative	Shape: Rod
Biochemistry: Lactose Non-fermenter, Indole Negative	Metabolism: Facultative Anaerobe, H2S Negative

Transmission

Shigella is a purely human pathogen and does not possess an animal reservoir. Transmission is via fecal-oral transmission and infection can occur with a very small infective dose (as low as 100 organisms). Consequently, Shigellosis is usually a disease of cramped quarters with poor sanitation such as campaigning armies and child-care facilities.

Virulence Factors

Shiga Toxin: This is an exotoxin of the A-B toxin family and displays enterotoxin behavior. The B subunit directs absorption of the toxin complex. The A subunit inhibits the mammalian ribosome leading to cell death.

Clinical Consequences

Shigellosis is largely a disease of the GI system although in rare cases systemic spread of Shiga Toxin can cause renal complications. The organisms induce their own phagocytosis by enterocytes after which they then rupture and escape the phagosome. Shigella can then spread from cell to cell but largely remain confined to the GI epithelium and do not spread systemically in macrophages as do typhoidal strains of Salmonella.

This is the major clinical manifestation of Shigellosis and is largely caused by Shiga-toxin-induced enterocyte cell death as well as inflammation of the GI mucosa in response to infection. The resultant infectious diarrhea requires an incubation of several days, is initially watery with little blood or pus, may be accompanied by abdominal pain and fever. In some cases the diarrhea may progress to outright dysentery which manifests as a low-volume bloody and purulent diarrhea with abdominal pain.

Microangiopathic Hemolytic Anemia, classically Hemolytic Uremic Syndrome, can occcur due to systemic spread of Shiga Toxin.

Treatment

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