A serum sample collected 20 days after onset of the illness was serially diluted to 1 1:4,096 to determine the end-point titer. 106 platelets/L [reference range 140C440 106 platelets/L]), elevated serum alkaline phosphatase (290 U/L [reference range 35C104 U/L]), elevated lactic dehydrogenase concentration (560 U/L [reference range 100C190 U/L]), and elevated antistreptolysin O (E)-Alprenoxime and rheumatoid factor titers. The diagnosis of murine typhus was established by PCR for 17 kDa and citrate synthase (was identified as the causal agent by restriction fragment length polymorphism analysis (RFLP) of the amplified fragment of (382 bp) and 17-kDa Mouse monoclonal to Alkaline Phosphatase gene (434 bp) by using and 17-kDa gene PCR amplicons using BLAST software of the National Center for Biotechnology Information (Bethesda, MD, USA) (genes (Table). Open in a separate window Figure Restriction fragment length polymorphism patterns of (A) and 17-kDa gene (B) PCR products digested with and 17-kDa gene PCR amplicons (from blood sample of infected child); lane 2, human case; lane 3, infection, Yucatan, Mexico, 2007* Wilmington strain100 (“type”:”entrez-nucleotide”,”attrs”:”text”:”AE017197.1″,”term_id”:”51459527″,”term_text”:”AE017197.1″AE017197.1)100 (“type”:”entrez-nucleotide”,”attrs”:”text”:”M28481.1″,”term_id”:”152459″,”term_text”:”M28481.1″M28481.1), 99 (“type”:”entrez-nucleotide”,”attrs”:”text”:”AE017197.1″,”term_id”:”51459527″,”term_text”:”AE017197.1″AE017197.1)256128URRWXCal2NR89 (“type”:”entrez-nucleotide”,”attrs”:”text”:”CP000053.1″,”term_id”:”67003925″,”term_text”:”CP000053.1″CP000053.1)NDSheila Smith92 (“type”:”entrez-nucleotide”,”attrs”:”text”:”CP000848.1″,”term_id”:”157800343″,”term_text”:”CP000848.1″CP000848.1)89 (“type”:”entrez-nucleotide”,”attrs”:”text”:”CP000848.1″,”term_id”:”157800343″,”term_text”:”CP000848.1″CP000848.1)Neg128Hartford strain91 (“type”:”entrez-nucleotide”,”attrs”:”text”:”CP000847.1″,”term_id”:”157799083″,”term_text”:”CP000847.1″CP000847.1)96 (“type”:”entrez-nucleotide”,”attrs”:”text”:”CP000847.1″,”term_id”:”157799083″,”term_text”:”CP000847.1″CP000847.1)Neg64 Open in a separate window *IFA, indirect immunofluorescence assay; Ig, immunoglobulin; NR, not represented in the first 100 sequences with a significant alignment using BLAST (and antigens were fixed on slides. (A positive human serum sample control and IFA slides were provided by the Rickettsial and Ehrlichial Diseases Research Laboratory, (E)-Alprenoxime University of Texas Medical Branch at Galveston.) As a negative control, we used a serum sample (from a healthy donor) that was negative for spp. (microscopic agglutination test and PCR); rickettsiae (IFA and PCR); HIV (microparticle enzyme immunoassay and PCR); hepatitis A, B, and C viruses (microparticle enzyme immunoassay); (ELISA); and (ELISA, PCR). We examined the serum specimens for immunoglobulin (Ig) G and IgM, assessing reactivity of -chainCspecific (E)-Alprenoxime and -heavy-chainCspecific secondary conjugates, respectively, with rickettsial antigens. A serum sample collected 20 days after onset of the illness was serially diluted to 1 1:4,096 to determine the end-point titer. IFA showed antibody reactivity with (Table). The child was treated with intravenous chloramphenicol, 75 mg/kg per day, for 7 days; symptoms were reduced in 48 hours. Conclusions In Yucatan state we have identified several cases of rickettsiosis caused by and infection (is a bacterium that is broadly distributed around the world, and is the cause of many human infections every year (and IgG antibody reactivity with and was established not only by the RFLP pattern of the and 17-kDa gene amplicons, but mainly by the sequence comparison with other rickettsial species. Identity was 100% for (Table). Identification of the species is essential for determining the epidemiology and ecology of the transmission cycle and how the agent is maintained in nature. In addition, species identification is useful for selecting the best preventive program appropriate for each region. This finding of an autochthonous human case of murine typhus in Yucatan Mexico and the finding of in Yucatan state increases the diversity of rickettsioses identified in this ecosystem. Because rickettsioses are treatable diseases, an educational program is critical to instruct the population about these infections and their transmission cycles, as well as to inform the medical community about the rickettsial diseases that must be included in the differential diagnosis of any acute febrile illnesses in the region. Acknowledgments This research was supported by grants from the Consejo Nacional de Ciencia y (E)-Alprenoxime Tecnologia (44064-M) to J.E. Zavala-Velzquez. Biography ?? Dr Zavala-Castro is professor of molecular and cell biology at the Autonomous University of Yucatan. His research interests are host-bacteria-vector relationships, new diagnostic methods, rickettsial evolution, and rickettsial diseases. Footnotes em Suggested citation for this article /em : Zavala-Castro JE, Zavala-Velzquez JE, Sul Uicab JE. Murine typhus in child, Yucatan, Mexico. Emerg Infect Dis [serial on the Internet]. 2009 Jun [ em date cited /em ]. Available from.