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Abstract:

The pathogenic species, , , and , are zoonotic agents that cause disease in humans. Human clinical infections caused by and occur after the ingestion of contaminated food or water and manifest primarily as mild gastroenteritis, whereas the etiologic agent of plague, , is transmitted to humans by the bite of an infected flea and results in life-threatening illness. Within the genus, these three species are joined by 14 lesser-known species which are largely considered environmental species and nonpathogenic to humans. Pathogenic species share a highly conserved virulence plasmid and a chromosomal high-pathogenicity island (HPI) and show tropism for lymphoid tissue, where their ability to evade host innate immunity enables extracellular proliferation. Plague is a notorious disease, with strikingly high mortality rates of 40 to 100% if untreated; it is the cause of three major pandemics, including the Black Death of the 14th century, in which an estimated 17 to 28 million Europeans died. was weaponized by the United States, Japan, and the former USSR during and after World War II and remains a high-level biothreat agent. In 2012, was classified as a tier 1 agent, one of 6 bacterial agents considered to present the greatest risk of deliberate misuse with the most significant potential for mass casualties or devastating effects to the economy, critical infrastructure, or public confidence.

Citation: Petersen J, Gladney L, Schriefer M. 2015. , p 738-751. In Jorgensen J, Pfaller M, Carroll K, Funke G, Landry M, Richter S, Warnock D (ed), Manual of Clinical Microbiology, Eleventh Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817381.ch39
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FIGURE 1

(A) Giemsa stain of a blood smear from a patient with infection. Note the bipolar staining of “closed safety pin”-shaped cells. (B) Direct fluorescent-antibody (F1 conjugate) staining of cells grown on sheep blood agar at 37°C. doi:10.1128/9781555817381.ch39.f1

Citation: Petersen J, Gladney L, Schriefer M. 2015. , p 738-751. In Jorgensen J, Pfaller M, Carroll K, Funke G, Landry M, Richter S, Warnock D (ed), Manual of Clinical Microbiology, Eleventh Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817381.ch39
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Image of FIGURE 2
FIGURE 2

(A) and (B) were grown on sheep blood agar at 25°C for 72 h, and was grown on sheep blood agar at 28°C for 72 h (C). doi:10.1128/9781555817381.ch39.f2

Citation: Petersen J, Gladney L, Schriefer M. 2015. , p 738-751. In Jorgensen J, Pfaller M, Carroll K, Funke G, Landry M, Richter S, Warnock D (ed), Manual of Clinical Microbiology, Eleventh Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817381.ch39
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Tables

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TABLE 1

Biochemical reactivities and characteristics of species

Citation: Petersen J, Gladney L, Schriefer M. 2015. , p 738-751. In Jorgensen J, Pfaller M, Carroll K, Funke G, Landry M, Richter S, Warnock D (ed), Manual of Clinical Microbiology, Eleventh Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817381.ch39
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TABLE 2

Reactions of biotypes of after incubation at 25°C for 48 h

Citation: Petersen J, Gladney L, Schriefer M. 2015. , p 738-751. In Jorgensen J, Pfaller M, Carroll K, Funke G, Landry M, Richter S, Warnock D (ed), Manual of Clinical Microbiology, Eleventh Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817381.ch39

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