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Dispatch
Rickettsialpox in North Carolina:
A Case Report
Allan Krusell,* James A. Comer,† and Daniel J. Sexton‡
*Northeast Medical Center, Concord, North Carolina, USA; Centers for
Disease Control and Prevention, Atlanta, Georgia, USA; and ‡Duke University
Medical Center, Durham, North Carolina, USA
We report a case
of rickettsialpox from North Carolina confirmed by serologic testing.
To our knowledge, this case is the first to be reported from this region
of the United States. Including rickettsialpox in the evaluation of
patients with eschars or vesicular rashes is likely to extend the recognized
geographic distribution of Rickettsia akari, the etiologic agent
of this disease.
Rickettsialpox is caused by infection with Rickettsia akari. Disease
in humans was first described in 1946 in residents of apartments clustered
in a three-block area in the borough of Queens, New York City (1).
Subsequently, small outbreaks of rickettsialpox were recognized in several
U.S. cities, including Boston, Cleveland, Philadelphia, Pittsburgh, and
West Hartford (2). Most cases to date have occurred in
large metropolitan areas of the northeastern United States; about half
the described cases have occurred in New York City. However, rickettsialpox
is likely more common in the United States than suggested by the relatively
small number of reported cases during the past 50 years (3,4).
R. akari is transmitted among house mice (Mus musculus)
and to humans by the house mouse mite (Liponyssoides sanguineus)
(2). Recently, cases of rickettsialpox have been reported
in residents of the Ukraine (5) and Croatia (6).
Isolations have also been made from Korean voles in an area where rickettsialpox
has not been reported (7). These data suggest that silent
sylvan cycles of R. akari infection exist and that the organism
is more widely distributed than currently appreciated. To our knowledge,
rickettsialpox has not previously been reported in patients in the southern
United States. We describe a recently diagnosed R. akari
infection in a man who resides in a suburban area of North Carolina.
Case Report
A 48-year-old man who worked at a golf course was admitted to a North
Carolina hospital with fevers, chills, headaches, and a rash. Seven days
before admission, he noted discomfort on the back of his right calf. The
patient stated that he thought something had bitten him at this site,
although he had not seen any insects or ticks. Over the next 2 days, thigh
tenderness and a papule developed at the site of the original discomfort.
Three days before admission, the papule began to ulcerate, and fevers,
chills, headaches, and general malaise were present. Two days before admission,
several red macules appeared over the anterior chest. Over the next 24
hours, vesicles appeared near the center of these macules.
The patient had a pet dog and cat and had not traveled outside North
Carolina in the 3 months before admission. He reported that he had no
known exposures to ticks or recent tick bites. He was unaware of any rodents
in his house or any local rodent extermination projects. However, he recalled
that a stray cat periodically brought dead mice to the general area where
he worked, although he never directly touched them.
On admission, the patient appeared ill and was febrile. An eschar was
present on his posterior right lower leg (Figure 1).
Approximately 30 erythematous macules were noted on his trunk, arms, and
legs (Figures 2 and 3).
Many of these macules had small central vesicles. Laboratory testing showed
normal values for electrolytes and creatinine, hematocrit, and leukocytes.
His platelet count was 85,000/mm3. Routine blood cultures were
sterile.
A diagnosis of rickettsialpox was made, and therapy was started with
doxycycline and cefazolin. After 48 hours, the patient became afebrile,
and his constitutional symptoms abated. He was discharged, took doxycycline
orally for an additional 7 days, and recovered completely.
Two serum samples were submitted to the Centers for Disease Control and
Prevention for confirmatory testing. Samples were tested by a standard
immunofluorescent antibody assay (IFA) for immunoglobulin G antibodies
reactive with R. akari and R. rickettsii antigens.
Because of cross-reactivity among the spotted fever group rickettsiae,
confirmatory cross-adsorption testing was done as described (8).
Higher reciprocal titers were obtained to R. akari antigens
than to R. rickettsii antigens in both samples (reciprocal
titers of 1,024 versus 512 on August 29 and 512 versus 256 on October
11, respectively). Adsorption with R. akari greatly reduced
titers to both antigens (<16 to both antigens for both samples), whereas
adsorption with R. rickettsii only partially lowered titers
to both antigens (512 versus 256 for the first sample; 128 versus 64 for
the second sample). This pattern of differential reduction in titers is
confirmatory for a serologic diagnosis of rickettsialpox (9).
This patient's illness was typical of rickettsialpox. He had a classic
eschar, and his vesicular rash, severe headache, and thrombocytopenia
are characteristic findings of infection with R. akari.
However, not all patients with rickettsialpox have a vesicular rash. Although
isolation of R. akari was not attempted and a skin biopsy
was not performed, the results of the IFA testing confirmed the diagnosis.
Rickettsialpox may have occurred sporadically in North Carolina in the
past, but the incidence of this disease in this state is probably extremely
low. As Figures 1–3 illustrate,
infection with R. akari produces unusual and characteristic
skin abnormalities. Because cases of rickettsialpox may be confused with
chickenpox or other viral exanthematous diseases, misdiagnosis may occur
when sporadic cases occur in areas where the disease is unknown to local
practitioners. The vesicular rash of rickettsialpox may be easily confused
with the skin rash seen in patients with chickenpox; however, the presence
of one or more eschars at the site(s) of inoculation, the lack of successive
crops of vesicles over time, and the presence of thrombocytopenia should
lead clinicians to exclude varicella-zoster virus (formal name: Human
herpesvirus 3) as the etiologic agent.
In large cities, R. akari is maintained in a cycle that
includes the house mouse and its associated mite (2).
Although our patient did not recall direct exposure to rodents, he did
recall a stray cat’s bringing mice into the work area. The patient may
have been exposed to infected mites in this manner, although he may also
have been unknowingly exposed to rodents and their mites at some other
location.
Evaluation of patients with eschars or vesicular rashes for rickettsialpox
is likely to extend the recognized geographic distribution of Rickettsia
akari, the etiologic agent of this disease.
We thank J.E. Childs, C.D. Paddock, and J. O'Connor for thorough review
of the manuscript.
Dr. Krusell is medical director of infection control and hospital epidemiology
at the Northeast Medical Center in Concord, North Carolina. His research
focuses on rickettsial diseases.
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