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SHIGELLOSIS : CLINICAL ASPECTS
Shigella organisms cause an acute inflammatory colitis and bloody diarrhea, which in themost characteristic state presents as a dysentery syndrome — a clinical triad consisting of cramps, painful straining to pass stools (tenesmus), and a frequent, small-volume, bloody, mucoid discharge. However, most clinical shigellosis due to S. sonnei in the United States is a watery diarrhea that is often indistinguishable from that of other bacterial or viral di-arrheal illness. The disease usually begins with fever and systemic manifestations of malaise, anorexia, and sometimes myalgia. These nondescript symptoms are followed by the onset of watery diarrhea containing the large numbers of leukocytes detectable by light microscopy. The diarrhea may turn bloody with or without the other classical signs of dysentery. The manifestations may be more severe when S. flexneri, the species that predominates in the developing world, is involved and most severe with S. dysenteriae type 1 (Shiga bacillus). Although the vast majority of shigellosis cases resolve sponta-neously after 2 to 5 days, the mortality in Shiga epidemics in Asia, Latin America, and Africa has been as high as 20%.
All Shigella species are readily isolated using selective media (e.g. Hektoen enteric agar) which are part of the routine stool culture in clinical laboratories. These media contain chemical additives empirically shown to inhibit facultative flora (eg, E. coli, Klebsiella), with relatively little effect on Shigella (or Salmonella). They also contain indicator sys-tems which utilize typical biochemical reactions to mark suspect Shigella colonies among the other flora. Isolates are identified with further biochemical tests. Slide agglutination tests using O group specific antisera (A, B, C, D) confirm both the species and theShigella genus.
Several antimicrobics have proved effective in the treatment of shigellosis. Because the disease is usually self-limiting, the beneficial effect of treatment is in shortening the ill-ness and the period of excretion of organisms. Ampicillin was once the treatment of choice, but resistance rates of 5 to 50% have caused a shift to TMP-SMX in many areas. In recent years, quinolones and third-generation cephalosporins have been used in the face of resistance to other agents. Antispasmodic agents may aggravate the condition and are contraindicated in shigellosis and other invasive diarrheas.
Standard sanitation practices such as sewage disposal and water chlorination are impor- tant in preventing the spread of shigellosis. In certain circumstances, insect control may also be important, because flies can serve as passive vectors when open sewage is present. Good individual sanitary practices, such as handwashing and proper cooking of food, are highly protective. Parenteral vaccines have proved disappointing, and current efforts are directed toward finding orally administered live vaccines that can stimulate mucosal IgA. Many strains, including attenuated Shigella mutants, E. coli – Shigella genetic hybrids, and E. coli with genes for some (but not all) the invasive (Ipa) proteins, are vaccine candi- dates. The general idea is to find a strain that will go through enough of the multistage process (see Pathogenesis) to stimulate an immune response but stop short of full penetra- tion and spread.
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