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Category: Bacterial Pathogenesis
The Genus Shigella, Page 1 of 2
< Previous page | Next page > /docserver/preview/fulltext/10.1128/9781555817541/9781555813420_Chap06-1.gif /docserver/preview/fulltext/10.1128/9781555817541/9781555813420_Chap06-2.gifAbstract:
Shigella is host adapted to the human intestine. In animals, only rare isolations from dogs and sporadic cases or outbreaks in primates have been reported. A variety of primates, including rhesus monkeys, tamarins, and marmosets, are susceptible to shigellosis and have been used as experimental models to study Shigella pathogenesis. The majority of infections in developing countries are caused by S. flexneri (60%), followed by S. sonnei (15%), S. boydii (8%), and S. dysenteriae (8%). Serotyping is always the first epidemiologic test performed, but the prevalence of S. flexneri and S. sonnei mandates the use of other techniques to further define the strains. Techniques used include phage typing, antibiograms, plasmid fingerprinting, ribotyping, pulsed-field gel electrophoresis (PFGE), and polymerase chain reaction (PCR). Most clinical laboratories must rely on commercial sera to confirm their identifications of shigellae. Due to cross-reactions, Shigella should be identified biochemically prior to undertaking serotyping and should never be reported based on serotyping alone. The triad of clinical symptoms (fever, intestinal cramps, and bloody diarrhea) associated with Shigella infection is the result of a series of molecular events triggering invasion of the colonic mucosa and the subsequent elicitation of an intense inflammatory response. Counterindications for treatment include cost (particularly in developing countries) and the development of resistance. This resistance has been facilitated by the emergence of antimicrobial resistance genes, located on plasmids, which are capable of promoting their own spread; insertion of these genes into the chromosome maintains a stable resistant population.
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Smooth and rough colony formation of S. sonnei on heart infusion agar. Large, flat, translucent colonies are rough, avirulent forms caused by the loss of a 180- to 200-kb plasmid.
Smooth and rough colony formation of S. sonnei on heart infusion agar. Large, flat, translucent colonies are rough, avirulent forms caused by the loss of a 180- to 200-kb plasmid.
Evolution of pathogenic shigellae from nonpathogenic E. coli: gain of virulence genes and loss of unnecessary genes.
Evolution of pathogenic shigellae from nonpathogenic E. coli: gain of virulence genes and loss of unnecessary genes.
Nomenclature of the genus Shigella
Nomenclature of the genus Shigella
Differentiation of shigellae from other fecal flora in TSI, LIA, and MIO agars a
Differentiation of shigellae from other fecal flora in TSI, LIA, and MIO agars a
Identifications of Shigella spp. by commonly used commercial systems a
Identifications of Shigella spp. by commonly used commercial systems a