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Plague exists worldwide as continuing
enzootic sylvatic disease in rodent-flea cycles that occasionally
spreads into the human population. Yersinia pestis, the
causative organism, is a nonmotile, gram-negative, non–spore-forming,
coccobacillus.
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The geographic distribution of plague is largely confined to
the semiarid areas of most continents, with the exception of Australia. Enzootic
North America foci are the largest in the world, occurring primarily
in the southwestern United States (extending east as far as Dallas,
Texas) and the Pacific coastal region, extending from Coahuila,
Mexico, to Alberta and British Columbia, Canada. The disease exists
almost entirely in the sylvatic form, with rodent-flea cycles among
a number of wild rodent species.1 Urban plague,
the cause of the epidemics of the European Middle Ages, is dependent
upon the Norwegian rat and flea (Xenopsylla cheopis),
but is now quite rare. The last epidemic of urban US plague occurred
in 1925 in Los Angeles. Rarely, pneumonic plague is transmissible
from person to person, bypassing both the rat reservoir and the
flea vector.1,2
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In the United States and Canada, the epidemiology is more complex
and involves a number of different rodent hosts and flea vectors, as
well as domestic animals. Most commonly, the infection is acquired
by human exposure to infected tissues or from the bites of fleas
of wild rodents such as prairie dogs, ground squirrels, chipmunks,
rabbits, and other wild rodent species. Contact with squirrels accounts for
nearly half of the exposures. Domestic animals, especially cats,
may become infected after contact with wildlife and may transmit the
infection to humans.2 Prior to 1977, no cat-related
cases had occurred, but since that time 18 cases have been reported,
with 28% of the cases causing direct pneumonic plague. Therefore,
direct contact with wild animals or their fleas is not required
for plague transmission. With the exception of cats, most other carnivores,
including dogs, are relatively resistant to plague and therefore
are rarely involved in plague transmission.
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Plague is considered a select agent and a potential bioterrorism
agent. Therefore, its isolation in most clinical laboratories in
the United States is restricted to genus and presumptive species
based on phenotypic criteria, but final specific identification
is performed in appropriate public health laboratories.
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Clinical Manifestations
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In the United States, most human plague cases occur from May
to September and usually present as 1 of 3 primary forms: bubonic,
septicemic, or pneumonic. Bubonic plague accounts for 78% of
US cases, the remainder are septicemic (13.2%), pneumonic
(4.4%), and meningitic or unknown (3.4%).3,4 In
recent series, the incidence of septicemic plague has been as high as
25%.
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The incubation period of bubonic and septicemic plague is often
difficult to determine but is usually within 2 to 6 days (range
1–10 days) of contact. Skin lesions are infrequently present
at the site of initial infection ...