Rickettsialpox in Turkey.
The first well-described clinical case of rickettsialpox was documented in New York City in 1946 (1). Historically, most documented rickettsialpox cases have occurred in large metropolitan areas of the United States (2), where the causative agent, R. akari, circulates primarily between the house mouse (Mus musculus) and its mite (Liponyssoides sanguineus). Recently, rickettsialpox cases have been reported from Croatia, Ukraine, South Africa, Korea, and North Carolina (3,4). R. akari was isolated from the blood of a patient suspected o f having Mediterranean spotted fever rather than rickettsialpox; this was the first human isolate of R. akari reported in >40 years (4). Recent reports of a rickettsialpox case in North Carolina (3), R. akari seropositivity found in HIV-positive intravenous drug users in the inner city of Baltimore, Maryland (5), and in Central and East Harlem, New York City (6), as well as rickettsialpox cutaneous eruption in an HIV patient in New York (7), indicate that R. akari rickettsiosis is more common than previously thought and presents the risk of sporadic outbreaks worldwide.
We describe the clinical presentation of rickettsialpox in a 9-year-old boy from Nevpehir, located in the middle region of Turkey. Previously, a report from the Antalya area of Turkey described the prevalence of serum immunoglobulin (Ig) G antibodies in humans directed against R. conorii (spotted fever group Rickettsia) (8); however, rickettsialpox was not reported in Turkey. This report of what we believe to be the first described rickettsialpox case from Turkey further extends the recognized geographic distribution of R. akari.
A 9-year-old boy was admitted to the Kayseri hospital with fever >39[degrees]C and generalized papulovesicular exanthema. One week before admission, fever, profuse sweating, headache, and dysuria were present. On admission, physical examination indicated generalized vesicular, bullouse, and papular exanthema involving the lips and oral cavity. Notable pathologic findings at admission included a black eschar on the boy's penis, bilateral prominent conjunctival ejection, and bilateral lower pulmonary rales. The leukocyte count was 13,300/m[m.sup.3], hemoglobin was 14.49 mg/dL, and the platelet count was 544,000/m[m.sup.3]. Serum electrolytes and blood urea nitrogen levels and results of coagulation study and urine analysis were normal. Routine blood cultures taken 24 hours postadmission were sterile. Specific antibodies (IgG; IgM) against Varicella were not detected in serum samples (Duzen Laboratories, Ankara, Turkey). Additionally, the patient reported mice on the family's farm.
A diagnosis of rickettsialpox was made and doxycycline treatment (200 mg/kg) was initiated. The patient serum sample was tested by indirect immunofluorescence assay (IFA) for IgG and IgM antibodies reactive with R. akari (Kaplan strain), R. typhi (Wilmington), R. rickettsii (Sheila Smith), and R. conorii (Malish 7). Serum IgG titers of 1/1280 and IgM of 1/40 to R. akari were detected and confirmed through cross-adsorption with rickettsial antigens (R. rickettsii, R. conorii) (9,10). Higher reciprocal titers were obtained against R. akari antigens than against R. rickettsii and R. conorii antigens (reciprocol titers of 1,024 vs. 512 and 512, respectively). We observed a difference in reduction in antibody titers against R. akari after adsorption with R. akari (Kaplan) (<16), R. rickettsii (256), and R. conorii (256). Antibodies against R. typhi were not detected. The IFA result confirmed the clinical diagnosis of R. akari infection. After 2 days of doxycycline treatment, the patient was afebrile, and the rickettsialpox infection resolved without scars or complications.
In summary, we present a case in which the presence of an eschar on the patient's penis, the failure of lesions to appear in crops, the sparsity of lesions, and mice on the family's farm led to a diagnosis of rickettsialpox, which was confirmed by cross-adsorption serologic findings. This case indicates that rickettsialpox is an emerging infectious disease in Turkey. We recommend further studies to define the prevalence of R. akari and the worldwide distribution of rickettsialpox.
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(5.) Comer JA, Tzianabos T, Flynn C. Vlahov D, Childs JE. Serologic evidence of rickettsialpox (Rickettsia akari) infection among intravenous drug users in inner-city Baltimore, Maryland. Am J Trop Med Hyg 1999;60:894-8.
(6.) Comer JA, Diaz T, Vlahov D, Monterroso E, Childs JE. Evidence of rodent-associated Bartonella and Rickettsia infections among intravenous drug users from Central and East Harlem, New York City. Am J Trop Med Hyg 2001:65:855-60.
(7.) Sanders S, Di Costanzo D, Leach J, Levy H, Srinivasan K, Zaki SR. et al. Rickettsialpox in a patient with HIV infection. J Am Acad Dermatol 2003;48:286-9.
(8.) Vural T, Ergan C, Sayin F. Investigation of Rickettsia conorii antibodies hi the Antalya area. Infection 1998;26:170-2.
(9.) Eremeeva M, Balayeva NM, Ignatovich VF, Raoult D. Proteinic and genomic identification of spotted fever group rickettsiae isolated in the former USSR. J Clin Microbiol 1993;10:2625-33.
(10.) Eremeeva M, Balayeva N, Ignatovich V, Raoult D. Genomic study of Rickettsia akari by pulsed-field gel electrophoresis. J Clin Microbiol 1995;33:3022-4.
Address for correspondence: Suzana Radulovic, University of Maryland, School of Medicine, Department of Microbiology and immunology, 655 West Baltimore Street, Baltimore, MD 21201, USA; tax: 410 706 4721; email: email@example.com
Mustafa K. Ozturk, *Tamer Gunes, * Mehmet Kose, * Christopher Coker, [dagger] and Suzana Radulovic [dagger]
* Erciyes University, Kayseri, Turkey and [dagger] University of Maryland, Baltimore, Maryland, USA
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|Publication:||Emerging Infectious Diseases|
|Article Type:||Letter to the Editor|
|Date:||Nov 1, 2003|
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