Shigella is endemic, hyperendemic, or epidemic in locales with minimal sanitation. Shigellosis is well recognized in southwest and south-central Asia. S. flexneri and S. dysenteriae are more common in southwest and south-central Asia than in the United States, where S. sonnei dominates.
Shigella infection causes an acute diarrheal illness. Symptoms are constitutional; they frequently include malaise and fever, and they immediately involve abdominal bloating, cramping, and diarrhea.
During shigellosis, diarrhea may be nonbloody and watery or bloody; the latter condition is generally termed dysentery. Laboratory examination of stool specimens usually reveals numerous leukocytes. The number of loose stools can range from several per day to more than 20 on the worst day of the illness. Fever and constitutional symptoms typically peak during the period of most severe diarrheal symptoms. The diarrhea may be accompanied by tenesmus, or painful straining while defecating. The illness usually is self-limiting, and patients recover within a week. In the absence of antibiotic treatment, however, shigellosis can be severe or even, rarely, fatal (Bennish 1991).
Diagnosis is based on culture of fecal specimens and very rarely blood. When PCR methods are available, they can be equally valuable. People with acute shigellosis remain culture-positive for up to 4 weeks. Beyond that timeframe, culture is inadequate to confirm or refute any relationship of symptoms with Shigella.
Treatment of all acute gastrointestinal infections must be based first on fluid replacement. The use of antibiotics is recommended because it shortens the duration of shigellosis and the likelihood of transmission to other hosts (Bhattacharya and Sur 2003). Resistance to sulfonamides, chloramphenicol, and tetracyclines is nearly universal, and resistance to ampicillin and trimethoprim-sulfamethoxazole is frequent. Treatment with fluoroquinolines or azithromycin is successful, even in short courses (1-3 days). The use of antimotility agents may induce more severe disease and is contraindicated.
As discussed above, ReA is an acute nonpurulent form of arthritis that complicates infections at other sites of the body. If ReA follows an acute episode of shigellosis, it is usually manifested 2-3 weeks after the gastrointestinal illness (Calin and Fries 1976; Chen et al. 2002; Finch et al. 1986; Good 1979; Noer 1966; Sieper et al. 1993; Simon et al. 1981). It is most common after S. flexneri infection; it also follows infection by S. dysenteriae (Good 1979) but rarely S. sonnei (Good 1979; Kaslow RA 1979; Lewis 1982; Simon et al. 1981). Ankylosing spondylitis occasionally follows ReA and may be considered as a consequence of Shigella-induced ReA. The symptoms of ReA cause up to 25% of affected people to change or curtail their work. Followup studies suggest that some joint symptoms persist in 30-60% of patients for up to a year, but most patients recover within a few months (Calin and Fries 1976; Rongnoparat