Shigellosis pathophysiology
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Overview
Pathophysiology
Shigella infection is typically via ingestion (fecal–oral contamination); depending on age and condition of the host as few as ten bacterial cells can be enough to cause an infection. Shigella cause dysentery that results in the destruction of the epithelial cells of the intestinal mucosa in the cecum and rectum. Some strains produce enterotoxin and Shiga toxin, similar to the verotoxin of E. coli O157:H7.[1] Both Shiga toxin and verotoxin are associated with causing hemolytic uremic syndrome.
Shigella invade the host through epithelial cells of the small intestine. Using a Type III secretion system acting as a biological syringe, the bacterium injects Ipa protein into cell, triggering bacterial invasion, and the subsequently lysis of vacuolar membranes. It utilizes a mechanism for its motility by which its IcsA triggers actin polymerization in the host cell in a "rocket" propulsion fashion for cell-to-cell spread.
The most common symptoms are diarrhea, fever, nausea, vomiting, stomach cramps, and straining to have a bowel movement. The stool may contain blood, mucus, or pus (e.g. dysentery). In rare cases, young children may have seizures. Symptoms can take as long as a week to show up, but most often begin two to four days after ingestion. Symptoms usually last for several days, but can last for weeks. Shigella is implicated as one of the pathogenic causes of reactive arthritis worldwide.[2]
Severe dysentery can be treated with ampicillin, TMP-SMX, or fluoroquinolones such as ciprofloxacin.
Histopathology of Shigellosis (Bacillary Dysentery)
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References
- ↑ Hale TL, Keusch GT (1996). Shigella. in: Baron's Medical Microbiology (Baron S et al, eds.) (4th ed. ed.). Univ of Texas Medical Branch. ISBN 0-9631172-1-1.
- ↑ Hill Gaston JS, Lillicrap MS (2003). "Arthritis associated with enteric infection". Best practice & research. Clinical rheumatology. 17 (2): 219–39. PMID 12787523.