AJTMH Transactions of the Royal Society of Tropical Medicine and Hygiene
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Am. J. Trop. Med. Hyg., 73(4), 2005, pp. 662-666
Copyright © 2005 by The American Society of Tropical Medicine and Hygiene

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TRANSCRIPTION OF THE RICKETTSIA FELIS OMPA GENE IN NATURALLY INFECTED FLEAS

JORGE E. ZAVALA-CASTRO, MELISSA SMALL, COLETTE KENG, DONALD H. BOUYER, JORGE ZAVALA-VELÁZQUEZ, AND DAVID H. WALKER*
Centro de Investigaciones Regionales Dr. Hideyo Noguchi, e Facultad de Medicina, Departamento de Patologia Tropical, Universidad Autonoma de Yucatan, Merida, Yucatan, Mexico; Department of Pathology, University of Texas Medical Branch, Galveston, Texas

Rickettsia felis is maintained transovarially in Ctenocephalides felis fleas in a widespread geographic distribution and is transmitted to humans and animals, including opossums. This rickettsia is phylogenetically a member of the spotted fever group, most closely related to Rickettsia akari and R. australis. An unusual feature of this rickettsia is that the gene for the outer membrane protein A (OmpA) is interrupted by stop codons. To determine if this putatively dying gene is expressed, mRNA was extracted from laboratory-maintained, R. felis–infected cat fleas. Reverse transcriptase–polymerase chain reaction amplification of three segments of the ompA gene indicated that mRNA of ompA is actively transcribed in fleas. The cDNA sequences expressed represented mRNA of the first 1860-basepair segment of ompA, which includes domains I and II, part of domain III, the region from site 1836 to site 2180, despite the presence of several stop codons, and the open reading frame from site 2788 to site 3837. The detected sequences showed several differences in the amino acid composition when compared with the previously reported sequence.


Received February 6, 2004. Accepted for publication May 24, 2005.

Acknowledgments: This research was supported by grants from the Fogarty International Center of the National Institutes of Health (D43 TW00903) and CONACyT (34436-M).

* Address correspondence to David H. Walker, Department of Pathology, University of Texas Medical Branch, 301 University Boulevard, Keiller Building, Galveston, TX 77555-0609. E-mail: dwalker{at}utmb.edu

Authors’ addresses: Jorge E. Zavala-Castro, Laboratorio de Biología Celular, Centro de Investigaciones Regionales Dr. Hideyo Noguchi, Universidad Autónoma de Yucatán, Avenida Itzaes No. 490 x 59, Centro, CP 97000, Merida, Yucatan, Mexico, Telephone: 52-999-924-6412 extension 120, Fax: 52-999-923-6120, E-mail: zcastro{at}tunku.uady.mx. Melissa Small, Collette Keng, Donald H. Bouyer, and David H. Walker, Department of Pathology, University of Texas Medical Branch, 301 University Boulevard, Keiller Building, Galveston, TX 77555-0609, Telephone: 409-772-2856, Fax: 409-772-1850, E-mails: dobouyer{at}utmb.edu and dwalker{at}utmb.edu. Jorge Zavala-Velázquez, Departmento de Patología Tropical, Universidad Autónoma de Yucatán, Avenida Itzaes No. 498 x 59 y 59a, Centro, C.P. 97000, Merida, Yucatan, 2003 Mexico, Telephone: 52-999-930-0900, zavala{at}tunku.uady.mx.

Reprint requests: Jorge E. Zavala-Velázquez, Facultad de Medicina, Departamento de Pathologia Tropical, Universidad Autónoma de Yucatán, Avenida Itzaes No. 498 x 59 y 59A, Centro CP 9700 Merida, Yucatán, Mexico.




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