Chapter 6 : The Genus

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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 pathogenesis. The majority of infections in developing countries are caused by (60%), followed by (15%), (8%), and (8%). Serotyping is always the first epidemiologic test performed, but the prevalence of and 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, 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 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.

Citation: Janda J, Abbott S. 2006. The Genus , p 65-80. In The Enterobacteria, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817541.ch6

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Restriction Fragment Length Polymorphism
Random Amplified Polymorphic DNA
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Figure 1

Smooth and rough colony formation of on heart infusion agar. Large, flat, translucent colonies are rough, avirulent forms caused by the loss of a 180- to 200-kb plasmid.

Citation: Janda J, Abbott S. 2006. The Genus , p 65-80. In The Enterobacteria, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817541.ch6
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Figure 2

Evolution of pathogenic shigellae from nonpathogenic : gain of virulence genes and loss of unnecessary genes.

Citation: Janda J, Abbott S. 2006. The Genus , p 65-80. In The Enterobacteria, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817541.ch6
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Table 1.

Nomenclature of the genus

Citation: Janda J, Abbott S. 2006. The Genus , p 65-80. In The Enterobacteria, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817541.ch6
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Table 2

Differentiation of shigellae from other fecal flora in TSI, LIA, and MIO agars

Citation: Janda J, Abbott S. 2006. The Genus , p 65-80. In The Enterobacteria, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817541.ch6
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Table 3

Identifications of spp. by commonly used commercial systems

Citation: Janda J, Abbott S. 2006. The Genus , p 65-80. In The Enterobacteria, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817541.ch6

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