Skip directly to site content Skip directly to page options Skip directly to A-Z link Skip directly to A-Z link Skip directly to A-Z link
Volume 9, Number 11—November 2003

Rickettsialpox in Turkey

On This Page
Article Metrics
citations of this article
EID Journal Metrics on Scopus

Cite This Article

To the Editor: Rickettsialpox is often described as a chickenpox-like disease and is caused by Rickettsia akari, a spotted fever group Rickettsia that is transmitted to humans by the bite of mites (Liponyssoides sanguineus). Although the mite host (typically a mouse) is widely distributed in cities, the disease is infrequently diagnosed. It is typically characterized in patients by the appearance of a primary eschar at the site of a mite bite followed by fever, headache, and development of a papulovesicular rash. Symptoms normally appear 9–14 days after the mite bite and are often unnoticed by the affected person. In documented rickettsialpox cases, the presence of a papule that ulcerates and becomes a scar approximately 0.5–3.0 cm in diameter is reported (13). Three to 7 days later, symptoms are more pronounced, with patients experiencing the sudden onset of chills, fever, and headache followed by myalgia and the appearence of generalized vesicular skin rashes. Less frequently, photophobia, conjunctival injection, cough, generalized lymphadenopathy, and vomiting are reported.

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 of 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°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/mm3, hemoglobin was 14.49 mg/dL, and the platelet count was 544,000/mm3. 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.


Mustafa K. Ozturk*, Tamer Gunes*, Mehmet Kose*, Christopher Coker†, and Suzana Radulovic†Comments to Author 
Author affiliations: *Erciyes University, Kayseri, Turkey; †University of Maryland, Baltimore, Maryland, USA



  1. Shankman  B. Report of an outbreak of endemic febrile illness, not yet identified, occurring in New York City. N Y State J Med. 1946;46:21569.PubMedGoogle Scholar
  2. Kass  EM, Szaniawski  WK, Levy  H, Leach  J, Srinivasan  K, Rives  C. Rickettsialpox in a New York City hospital, 1980 to 1989. N Engl J Med. 1994;331:16127. DOIPubMedGoogle Scholar
  3. Krusell  A, Comer  JA, Sexton  DJ. Rickettsialpox in North Carolina: a case report. Emerg Infect Dis. 2002;8:7278.PubMedGoogle Scholar
  4. Radulovic  S, Feng  HM, Morovic  M, Djelalija  B, Popov  V, Crocquet-Valdes  P, Isolation of Rickettsia akari from a patient in a region where Mediterranean spotted fever is endemic. Clin Infect Dis. 1996;22:21620.PubMedGoogle Scholar
  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;60:8948.PubMedGoogle Scholar
  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;65:85560.PubMedGoogle Scholar
  7. Sanders  S, Di Costanzo  D, Leach  J, Levy  H, Srinivasan  K, Zaki  SR, Rickettsialpox in a patient with HIV infection. J Am Acad Dermatol. 2003;48:2869. DOIPubMedGoogle Scholar
  8. Vural  T, Ergan  C, Sayin  F. Investigation of Rickettsia conorii antibodies in the Antalya area. Infection. 1998;26:1702. DOIPubMedGoogle Scholar
  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;10:262533.PubMedGoogle Scholar
  10. Eremeeva  M, Balayeva  N, Ignatovich  V, Raoult  D. Genomic study of Rickettsia akari by pulsed-filed gel electrophoresis. J Clin Microbiol. 1995;33:30224.PubMedGoogle Scholar


Cite This Article

DOI: 10.3201/eid0911.030224

Related Links


Table of Contents – Volume 9, Number 11—November 2003

EID Search Options
presentation_01 Advanced Article Search – Search articles by author and/or keyword.
presentation_01 Articles by Country Search – Search articles by the topic country.
presentation_01 Article Type Search – Search articles by article type and issue.



Please use the form below to submit correspondence to the authors or contact them at the following address:

Suzana Radulovic, University of Maryland, School of Medicine, Department of Microbiology and Immunology, 655 West Baltimore Street, Baltimore, MD 21201, USA; fax: 410 706 4721

Send To

10000 character(s) remaining.


Page created: January 21, 2011
Page updated: January 21, 2011
Page reviewed: January 21, 2011
The conclusions, findings, and opinions expressed by authors contributing to this journal do not necessarily reflect the official position of the U.S. Department of Health and Human Services, the Public Health Service, the Centers for Disease Control and Prevention, or the authors' affiliated institutions. Use of trade names is for identification only and does not imply endorsement by any of the groups named above.