Human Rickettsialpox, Southeastern Mexico | CDC EID

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Volume 15, Number 10–October 2009
Dispatch
Human Rickettsialpox, Southeastern Mexico
Jorge E. Zavala-Castro, Jorge E. Zavala-Velázquez, Gaspar F. Peniche-Lara, and Justo E. Sulú Uicab
Author affiliation: Universidad Autónoma de Yucatán, Mérida, Mexico

Suggested citation for this article

Abstract
The detection of Rickettsia akari in 2 human patients increased the diversity of rickettsioses affecting the public health in the southeast of Mexico. Rickettsialpox should be considered in the differential diagnosis with other febrile illnesses for the correct diagnosis and accurate treatment of this potential threat to human health.

Rickettsialpox is an illness characterized by fever, headache, papulovesicular rash over the trunk and extremities, and, in 80% of cases, appearance of an eschar. Rickettsia akari, the etiologic agent of rickettsialpox, is commonly transmitted by the bite of the house-mouse mite, Liponyssoides sanguineus. Human cases of rickettsialpox, as well as infected mites and potential reservoirs of R. akari, have been found in several countries, including the United States, Turkey, Croatia, and Ukraine (1–5). Despite the presence of the house mouse (Mus musculus) around the world, in Latin America human cases caused by R. akari have not been reported, and rickettsial diseases caused by antigenically related rickettsiae have been confined to R. rickettsii, R. felis, R. prowasekii, R. typhi, and R. parkeri (6–11). We report 2 human cases of R. akari infection in the Yucatan Peninsula of Mexico.

The Study
Patient 1 was a 9-year-old girl who came to the public hospital in Merida, Yucatan, in May 2008. Her illness had started abruptly with high fever and headache, then evolved over a 12-day period to include nausea, vomiting, hemorrhagic conjunctivitis, excessive lacrimation, and epistaxis. She was treated empirically with antipyretic drugs and had a slight improvement; 3 days after beginning treatment, fever and epistaxis returned with myalgia; irritability; papulovesicular rash involving the extremities, thorax, and oral mucosa; vaginal and gingival bleeding; and disseminated ecchymoses. Clinical laboratory studies showed hemoglobin 9.9 g/dL and hematocrit 29.0% (reference ranges 12–18 g/dL and 31%–51%, respectively), thrombocytopenia (45 × 103 platelets/mL [reference range 140–440 × 103 platelets/mL]), prolonged prothrombin and thromboplastine times (20 s and 64 s [reference range 10–15 s and 25–35 s, respectively]), neutrophilia, and elevated transaminase (aspartate transaminase 100 mU/mL [reference range 14–36 mU/mL], alanine transaminase 148 mU/mL [reference range 9–52 mU/mL]). The girl was hospitalized in the intensive care unit with a preliminary diagnosis of shock from dengue hemorrhagic fever.

Patient 2 was a 32-year-old woman in whom rickettsialpox was diagnosed in July 2008. She reported visiting a suburban area and being bitten by an unidentified arthropod. Her illness started abruptly with fever, headache, myalgia, and arthralgia in her extremities. The patient showed signs of dengue fever and was treated symptomatically. Three days after the first symptoms, a papulovesicular rash appeared on her extremities and thorax. Clinical laboratory results showed thrombocytopenia (100 × 103 platelets/mL [reference range 140–440 × 103 platelets/mL]) with slightly prolonged clotting times of thrombin and prothrombin, and neutrophilia.

Rickettsiosis was diagnosed on the basis of PCR amplification and sequencing of bacterial genes; immunofluorescent assay (IFA) and restriction fragment length polymorphism (RFLP) analyses confirmed the diagnosis and identified the Rickettsia species. Blood was collected in 3.8% sodium citrate as anticoagulant, and DNA was extracted immediately by QIAamp DNA kit (QIAGEN, Valencia, CA, USA) following the manufacturer's instructions. PCR amplification was performed by using genus-specific primers for the rickettsial 17-kDa protein gene (5´-GCTCTTGCAACTTCTATGTT-3´ and 5´-CATTGTTCGTCAGGTTGGCG-3´) (434-bp PCR fragment) and the outer membrane protein B (ompB) primers (5´-ATGGCTCAAAAACCAAATTTTCTAA-3´ and 5´-GCTCTACCTGCTCCATTATCTGTACC-3´) (996-bp PCR fragment). The positive controls used were DNA of R. felis, R. rickettsii, R. akari, R. typhi, R. conorii, and R. honei, provided by the Rickettsial and Ehrlichial Diseases Research Laboratory (University of Texas Medical Branch, Galveston, TX, USA); 1 reaction without DNA was used as a negative control. To avoid contamination, DNA of the positive controls and the patients was handled separately.

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Human Rickettsialpox, Southeastern Mexico | CDC EID