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A new rickettsial disease in the United States.

Received 24 November 2003; accepted 25 November 2003; electronically published 1 March 2004. Reprints or correspondence: Dr. Didier Raoult, Unité des Rickettsies—CNRS UMR 6020, Faculté de Médecine, 27, boulevard Jean Moulin, Marseille 13385, France (Didier. Raoult@medecine.univ-mrs.fr). Clinical Infectious Diseases 2004; 38:812–3 2004 by the Infectious Diseases Society of America. All rights reserved. 1058-4838/2004/3806-0006$15.00 The article by Paddock et al. [1] in this issue of Clinical Infectious Diseases demonstrates that we must be able to change our minds about traditionally established diseases such as Rocky Mountain spotted fever (RMSF) and tickborne rickettsioses. Paddock et al. [1] report the case of an American patient with fever, rash, and an inoculation eschar. The patient had antibodies to Rickettsia rickettsii and to Rickettsia akari. Culture of the eschar biopsy specimen yielded a rickettsia characterized by molecular biology as Rickettsia parkeri, which was discovered in ticks in the United States 60 years ago. This is the first report of an infection with this agent. In the first part of the 20th century, it was established that a single organism, R. rickettsii, was the agent of RMSF. It was considered the only agent of tickborne rickettsial diseases in America. Any other rickettsia obtained from a tick was considered to be nonpathogenic. Among these were R. parkeri (first identified in 1939), Rickettsia montanensis, Rickettsia canadensis, Rickettsia bellii, and Rickettsia rhipicephali, and other isolates without formal description [2]. Even Coxiella burnetii, the agent of Q fever, was first considered to be a nonpathogenic rickettsia (named Rickettsia diaporica) because it was found first in a tick in the Rocky Mountain Laboratory (Hamilton, MT)[2]. In the rest of the world, the same simplification of causality was also observed, and tickborne rickettsial diseases were considered to be caused only by Rickettsia conorii in Europe, Africa, and Asia, by Rickettsia sibirica in Siberia, and by Rickettsia australis in Australia; a single species was considered the agent of all tickborne rickettioses in a specific geographic area. Therefore, only 4 pathogenic species of tickborne rickettsioses were established. Since World War II, the diagnosis of rickettsioses has been made mainly on the basis of serological testing, and indirect immunofluorescence assay has been the reference technique used [2]. After 1976, immunodetection in skin biopsy specimens was also proposed [3]. However, due to the widespread antigenic crossreactions among tick-associated rickettsia, these techniques cannot discriminate among rickettsioses and are rarely able to formally identify new diseases. More sophisticated serological techniques, including cross-adsorption assays and Western blot testing, can differentiate between 2 identified species. However, serological tests can detect only antibodies to the suspected antigens of identified agents and not antibodies to unknown organisms [4]. Starting in 1991, with the introduction of cell culture and molecular biological testing methods, the spectrum of rickettsioses increased dramatically [5]. Eight new species (or new diseases) have been described since 1991: Rickettsia japonica in Japan, Rickettsia honei on Flinders Island (between Australia and Tasmania), Rickettsia africae in Africa and the West Indies, Rickettsia slovaca in Europe, Rickettsia aeschlimannii in Africa and Europe [6], Rickettsia helvetica in Europe and Asia, Rickettsia heilongjanghensis in Asia, and R. parkeri in the United States. Two new subspecies were also reported: Rickettsia conorii astrakhan in Russia, Africa, and Kosovo, and Rickettsia sibirica mongolotimonae in China, Europe, and Africa. New rickettsial diseases have been found mainly under 3 conditions.