Jane E. Sykes and Bruno B. Chomel

Etiology and Epidemiology

The genus Yersinia includes 11 different species, three of which are pathogenic in humans, cats, and dogs: Yersinia pestis and the enteropathogenic species Yersinia pseudotuberculosis and Yersinia enterocolitica. Yersinia spp. are nonmotile, gram-negative coccobacilli that belong to the family Enterobacteriaceae. Only Y. pestis is transmitted by arthropod vectors.

Yersinia pestis causes plague, which is maintained in wild burrowing rodents in rural regions of Asia, Africa, and the Americas (Figure 55-1). There is no plague in Australia, and the last case of plague in Europe was reported after World War II. The organism is transmitted between rodents by rodent fleas; humans, dogs, and cats are usually accidental and “dead-end” hosts (although direct transmission can occur through aerosols in humans and cats with pneumonic disease). Fleas become infected when they feed on heavily bacteremic rodents. The organism replicates in the flea intestine and creates a blockage of the intestinal tract, which causes the “starved” flea to repeatedly and aggressively feed and regurgitate bacteria into the bite site of a new host.² A large number of flea species can transmit Y. pestis, but some flea species, such as the Oriental rat flea (Xenopsylla cheopis) worldwide and the ground squirrel flea (Oropsylla montana) in the western United States are particularly efficient vectors. Although nowhere near as efficient as these two fleas as a vector, the cat flea (Ctenocephalides felis) can infest rodent reservoirs and also has the potential to transmit Y. pestis.³ Y. pestis attains very high concentrations in rodent blood (10⁸ organisms/mL) before death of the rodent occurs, which allows fleas to acquire sufficient numbers of bacteria for efficient transmission to other rodents.⁴ Fleas can remain infected for more than a year, which permits transmission long after the death of an infected rodent.

Plague is transmitted to cats or dogs when they ingest infected mammals (especially rodents or rabbits) or less commonly, after the bite of a rodent flea. Humans are infected by (1) the bite of an infected flea; (2) direct contact with contaminated tissues (such as handling dead rodents, rabbits, or other dead wild mammalian carnivores); or rarely (3) inhalation of respiratory secretions by infected animals, especially cats (Figure 55-2). Death of a rodent from plague can cause the rodent’s fleas to bite humans and other animals in a search for an alternative blood meal.

In the United States, plague in humans, dogs, and cats is now uncommon, although it is likely underrecognized in dogs and cats. Cats are considerably more susceptible to disease than dogs. Affected cats can be of any age, breed, and sex, with a mean age of 3 years in one case series.⁵ Most plague cases in humans and cats occur in the southwestern United States, particularly northern New Mexico, but also southern Colorado, northern Arizona, and to a lesser extent California, southern Oregon, and western Nevada (especially in the Sierra Mountain ranges) (Figure 55-3). The probability of an area in the United States being a high-risk plague habitat increases with elevation up to 2300 meters and declines as elevation increases thereafter.⁶ Rodent or rabbit species associated with human cases include white-tailed antelope squirrels, ground squirrels, rock squirrels, cottontail rabbits, jack rabbits, prairie dogs, deer mice, Colorado chipmunks, and wood rats.² The prevalence of antibodies to Y. pestis in a survey of 4115 dogs and 466 cats from California in the mid-1990s was less than 5% in both species.⁷

In general, plague has a seasonal distribution that correlates with the timing of epizootics that lead to a die-off of susceptible rodents. In the United States, most plague cases occur from February through August, when rodents and their fleas are most active and humans and their companion animals are more likely to be outdoors. In general, the organism does not survive well in the environment outside infected hosts, with survival less than 72 hours on hard surfaces.⁸ However, Y. pestis survived at least 24 days in blood-contaminated soil that was protected from UV light.⁹ The extent to which environmental survival of Y. pestis contributes to the geographic distribution and epidemiology of the disease requires further clarification.

Clinical Features