A 9.5-kilobase plasmid of Yersinia pestis, the causative agent of plague, is required for high virulence when mice are inoculated with the bacterium by subcutaneous injection. Inactivation of the plasmid gene pla, which encodes a surface protease, increased the median lethal dose of the bacteria for mice by a millionfold. Moreover, cloned pla was sufficient to restore segregants lacking the entire pla-bearing plasmid to full virulence. Both pla+ strains injected subcutaneously and pla- mutants injected intravenously reached high titers in liver and spleen of infected mice, whereas pla- mutants injected subcutaneously failed to do so even though they establish a sustained local infection at the injection site. More inflammatory cells accumulated in lesions caused by the pla- mutants than in lesions produced by the pla+ parent. The Pla protease was shown to be a plasminogen activator with unusual kinetic properties. It can also cleave complement C3 at a specific site.
From 1970 to 1991, 295 indigenous cases and one imported case of human plague were reported in the United States. Eighty-two percent of the total indigenous cases occurred in New Mexico, Arizona, and Colorado. Ninety-three percent of these cases had onset in the months of April through November. Most cases (89%) presented as bubonic or septicemic plague, or both. Cases were reported more frequently in males (58%), and male mortality exceeded that of females (17 versus 11%). Ground squirrels were the most frequently implicated sources of infection in cases associated with flea bites, and domestic cats were found to play an increasingly important role in transmission of disease to humans during these decades.
A plague (Yersinia pestis) epizootic spread through Gunnison's prairie dogs (Cynomys gunnisoni), and possibly other rodent species, in the Moreno Valley in north-central New Mexico between winter 1984-1985 and autumn 1987. We observed the progress of the epizootic and subsequent population recovery at four prairie dog towns within the valley during this period. At two towns (Midlake and Val Verde) the prairie dogs were marked prior to the epizootic. At two additional towns (Vega and South Entrance) prairie dogs were marked following the epizootic. In 1988, a second epizootic occurred at Vega. One hundred thirty-nine serum samples were collected from prairie dogs and other rodents and 1,750 fleas were collected from animals and burrows. Fleas infected with Y. pestis were collected from prairie dogs, deer mice (Peromyscus maniculatus), and thirteen-lined ground squirrels (Spermophilus tridecemlineatus). Prairie dog fleas included Oropsylla hirsuta, O. labis and O. tuberculata, deermouse associated fleas were Aetheca wagneri and Rhadinopsylla sectilis, and Oropsylla bacchi was associated with thirteen-lined ground squirrels. All of the above flea species were collected from prairie dog burrows. All rodent species shared some flea species. Thirteen-lined ground squirrels disappeared shortly before plague was identified in prairie dogs at Midlake. Meadow voles were rare following the epizootic at Vega in 1986, became abundant in 1987, and disappeared at the time of the second prairie dog epizootic in summer 1988. Although we collected serum from Gunnison's prairie dogs, thirteen-lined ground squirrels, deer mice, and meadow voles (Microtus pennsylvanicus), we identified elevated serum titers against Y. pestis only in Gunnison's prairie dogs. Prairie dog mortality at all towns affected by plague was in excess of 99%. Serum antibody titers indicate that more than 40% of the few prairie dogs left to establish colonies following epizootics survived plague infection.
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