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Experimental Rickettsia typhi Infection in Monodelphis domestica: Implications for Opossums as an Amplifying Host in the Suburban Cycle of Murine Typhus
ABSTRACT.
Murine typhus is an acute undifferentiated febrile illness caused by Rickettsia typhi. In the United States, its reemergence appears to be driven by a shift from the classic rat–rat flea cycle of transmission to one involving opossums (Didelphis virginiana) and cat fleas. Little is known of the ability of opossums to act as a reservoir and amplifying host for R. typhi. Here, we use Monodelphis domestica (the laboratory opossum) as a surrogate for D. virginiana. Opossums were inoculated via the intraperitoneal (IP) or intradermal (ID) route with 1 × 106 viable R. typhi. Blood and tissues were collected on days 6, 13, 20, and 27 or if moribund. Although one ID-infected opossum died, the remainder did not appear ill, whereas half of the IP-inoculated animals succumbed to infection. Rickettsemia was demonstrated in all animals through week 2 of infection and sporadically in weeks 3 and 4. Rickettsia typhi DNA was detected in all tissues, with most animals demonstrating the presence of bacteria into weeks 3 and 4. Histopathology and immunohistochemistry demonstrated typical findings of rickettsial infection. Akin to infection in rats, the demonstration of disseminated infection, typical inflammation, and prolonged rickettsemia with relatively few clinical effects (especially in the more natural route of ID inoculation) supports the potential of opossums to act as a competent mammalian reservoir and component of the zoonotic maintenance cycle of R. typhi. Understanding the dynamics of infection within opossums may have implications for the prevention and control of murine typhus.
Author Notes
Financial support: At the time of this work, Lucas Blanton was supported by the Institute for Translational Sciences at the University of Texas Medical Branch, supported in part by a CTSA Mentored Career Development (KL2) Award (KL2TR001441) from the National Center for Advancing Translational Sciences, National Institutes of Health. This study was funded by a pilot grant provided by the University of Texas Medical Branch Institute for Human Infections and Immunity.
Authors’ addresses: Lucas S. Blanton and Bethany R. Quade, Department of Internal Medicine, Division of Infectious Diseases, University of Texas Medical Branch, Galveston, TX, E-mails: lsblanto@utmb.edu and bequade@utmb.edu. Alejandro Ramírez-Hernández, Veterinary Parasitology Research Group, National University of Colombia, Cra. 30 No. 45-03. Ed. 481. Lab 4. Ciudad Universitaria, Bogotá D.C., Colombia, E-mail: alerrah@yahoo.com. Nicole L. Mendell, Donald H. Bouyer, and David H. Walker, Department of Pathology, University of Texas Medical Branch, Galveston, TX, E-mails: nlmendel@utmb.edu, dobouyer@utmb.edu, and dwalker@utmb.edu. Alejandro Villasante-Tezanos, Department of Preventive Medicine and Population Health, University of Texas Medical Branch, Galveston, TX, E-mail: alvillas@utmb.edu. John L. VandeBerg, Department of Human Genetics, South Texas Diabetes and Obesity Institute, and Center for Vector-Borne Disease, Brownsville, TX, E-mail: john.vandeberg@utrgv.edu.