Unique Strain of Rickettsia parkeri Associated with the Hard Tick Dermacentor parumapertus Neumann in the Western United States

In 1953, investigators at the Rocky Mountain Laboratories in Hamilton, Montana, described the isolation of a spotted fever group Rickettsia (SFGR) species from Dermacentor parumapertus collected from black-tailed jackrabbits ( Lepus californicus ) in northern Nevada. Several decades later, investigators characterized this SFGR by using mouse serotyping methods and determined that it represented a distinct rickettsial serotype, related closely to Rickettsia parkeri; nonetheless, the parumapertus agent was not further characterized or studied. No extant isolates of the parumapertus agent remain in any rickettsial culture collection around the world which precludes contemporary phylogenetic placement of this enigmatic SFGR. To rediscover the parumapertus agent, adult-stage D. parumapertus ticks were collected from black-tailed jackrabbits shot or encountered as road-kills in Arizona, Utah, or Texas during 2011-2016. A total of 339 ticks were collected and evaluated for infection with Rickettsia species. From 112 D. parumapertus collected in south Texas, 16 (14.3%) contained partial omp A sequences with closest identity (99.6%) to Rickettsia sp. Atlantic rainforest, a recently identified pathogenic SFGR that causes a mild rickettsiosis in several states of Brazil. A pure isolate, designated strain Black Gap, was cultivated in Vero E6 cells and sequence analysis of the rrs , glt A, sca 0, sca 5 and sca 4 genes also revealed closest genetic identity to Rickettsia sp. Atlantic rainforest. Phylogenetic analysis of the five concatenated rickettsial genes place Rickettsia sp. Black Gap and Rickettsia sp. Atlantic rainforest with R. parkeri in a distinct and well-supported clade. Importance. We suggest that Rickettsia sp. Black Gap and Rickettsia sp. Atlantic rainforest represent nearly identical strains of R. parkeri , and that Rickettsia sp. Black Gap, or a very similar strain of R. parkeri , represents the parumapertus agent. Close genetic relatedness among these taxa, as well as the response of guinea pigs infected with Black Gap strain, suggest that R. parkeri Black Gap could cause disease in humans. The identification of this organism could also account, at least in part, for remarkable differences in severity ascribed to RMSF among various regions of the American West during the early 20 th century. We suggest that wide variation in case-fatality rates attributed to RMSF could have occurred by the inadvertent inclusion of cases of milder disease caused by R. parkeri Black Gap.