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Letter
Rickettsialpox in Turkey
Mustafa K. Ozturk,* Tamer Gunes,* Mehmet Kose,* Christopher Coker,†
and Suzana Radulovic†
*Erciyes University, Kayseri, Turkey; and †University of Maryland, Baltimore,
Maryland, USA
Suggested citation
for this article:
Ozturk MK, Gunes T, Kose M, Coker C, Radulovic S. Rickettsialpox in
Turkey. Emerg Infect Dis [serial online] 2003 Nov [date cited].
Available from: URL: http://www.cdc.gov/ncidod/EID/vol9no11/03-0224.htm
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 (1–3). 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.
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