Hindawi Publishing Corporation
Case Reports in Infectious Diseases
Volume 2012, Article ID 916142, 3 pages
AClassic Presentation of a CommonlyMisdiagnosedDisease
1Career Epidemiology Field Officer Program, Centers for Disease Control and Prevention (CDC), Atlanta, GA 30333, USA
2Communicable Disease Control and Prevention Bureau, Montana Department of Public Health and Human Services,
Helena, MT 59610, USA
3St. Peter’s Medical Group, Helena, MT 59601, USA
4Rickettsial Zoonoses Branch, CDC, Atlanta, GA 30333, USA
Correspondence should be addressed to Randall J. Nett, firstname.lastname@example.org
Received 15 March 2012; Accepted 6 June 2012
Academic Editors: R. Colodner, M. de Gorgolas, and S. Yazar
Copyright © 2012 Randall J. Nett et al.Thisisanopenaccess articledistributedundertheCreativeCommonsAttributionLicense,
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
We describe the case of a man presumptively diagnosed and treated for Rocky Mountain spotted fever following exposure to
of acute Q fever as the etiology. This case represents a potential tickborne transmission of Coxiella burnetii and highlights the
importance of considering Q fever as a possible diagnosis following tick exposures.
Coxiella burnetii is an enzootic and endemic bacterial
pathogen in the United States and causative agent of Q fever
. Cattle, sheep, and goats are the most common animal
reservoirs, and C. burnetii is shed in the birth products
of infected animals [1, 2]. While humans typically become
infected through inhalation of contaminated aerosols and
dust, possible tickborne transmission of C. burnetii has been
The incubation period of Q fever is usually 2–3 weeks
. Approximately half of persons infected with C. burnetii
will remain asymptomatic. The most common clinical
manifestation of acute Q fever is a nonspecific and febrile
flu-like illness ; thus, the diagnosis is challenging and
few patients receive appropriate treatment. Acute Q fever
is treated with doxycycline and is most successful when
initiated within three days of symptom onset. Approximately
commonlymanifestingasendocarditis in thosewithvalvular
heart disease or immune compromising conditions .
Rickettsia rickettsii is an arthropod-borne bacterium and
part of the spotted fever group rickettsiae (SFGR). The SFGR
are transmitted through the bites of infected ixodid ticks
. R. rickettsii infection causes Rocky Mountain spotted
fever (RMSF). RMSF generally occurs 2–14 days following
infection and is characterized by fever, rash, headache, and
abdominal pain . Approximately 20% of patients do not
with doxycycline increases the likelihood for recovery.
A 57-year-old male presented on June 29, 2011 with a five-
day history of fever, headache, nausea, rash, and fatigue. The
patient had no history of immunosuppression. He reported
exposure to multiple ticks and mosquitoes while riding
horses in South Dakota in early June 2011. On examination,
the patient was afebrile, diaphoretic, and had left upper
on his trunk, no other rashes were present. The remainder
of the physical examination was unremarkable. Laboratory
results from serum collected at the time of presentation
showed a mild leukopenia, acute renal failure, elevated liver
transaminases, and elevated anti-SFGR immunoglobulin
(Ig)G; initial testing for Q fever was negative (Table 1). The
patient was treated with doxycycline for 14 days for the
presumptive diagnosis of RMSF and subsequently recovered.
2 Case Reports in Infectious Diseases
Table 1: Case-patient laboratory test results, Montana, 2011.
White blood cell count (g/L)
Platelet count (g/L)
Blood urea nitrogen (mg/dL)
Aspartate aminotransferase (IU/L)
Alanine aminotransferase (IU/L)
Alkaline phosphatase (IU/L)
Coxiella burnetii antibody titers†by specimen
IgG∗/IgM phase I
IgG/IgM phase II
IgG/IgM phase I
IgG/IgM phase II
SFGR antibody titers†by specimen
Borrelia burgdorferi antibody¶(IgG and/or
IgM) by specimen
West Nile virus antibody¶
∗IgG: immunoglobulin G; IgM: immunoglobulin M; SFGR: spotted fever
†Testing performed using indirect immunofluorescence assay.
‡Acute specimen collected on June 29, 2011.
§Convalescent specimen collected on July 12, 2011.
¶Testing performed using enzyme-linked immunosorbent assay (ELISA);
therefore, no titers reported.
However, convalescent testing on July 12 revealed that the
patient experienced no subsequent increase in anti-SFGR
antibody, while a significant increase in phase I and II anti-
C. burnetii IgG occurred (Table 1). The patient was judged
unlikely to have been a case of RMSF as there was no
demonstrable anti-SFGR IgM and no change in IgG titers.
However, the patient was laboratory confirmed as infected
with C. burnetii as demonstrated by a four-fold rise in phase
II IgG-specific antibody titer between acute and convalescent
The patient’s symptom onset began approximately 2–3
weeks after exposure to multiple ticks suggesting possible
tickborne disease transmission. The most common mode of
human transmission is inhalational, but cases of tickborne
transmission have been described [7, 8]. Over 40 tick species
are naturally infected with C. burnetii and tick transmission
to various mammals has been documented . Although the
patient did not report livestock contact, it is not possible to
the organism can become windborne and carried for long
distances . Ticks from the patient or from the area of
exposure were not available for testing so it is not possible
to prove that C. burnetii infection occurred because of a
tick bite rather than exposure to contaminated aerosols and
The patient’s initial diagnosis of RMSF was based on an
elevated SFGR IgG antibody in the acute specimen. This was
a reasonable assumption as the patient had a history of tick
exposure, a compatible clinical presentation for RMSF and
met the CDC surveillance case definition for a laboratory
supportive SFGR case. However, the patient’s SFGR IgG
antibody did not show a significant rise in titer in the
convalescent sample and no IgM antibody was detected. An
acute serum specimen taken during the first week of illness is
often negative as a rise in antibody titer does not typically
occur until at least 7 days after symptom onset. For these
reasons, it is more likely that the patient’s titer to SFGR was
caused by a previously undiagnosed infection rather than an
acute infection as SFGR IgG response can be elevated for
extended periods following acute infection .
This case of Q fever suggests a potential tickborne
transmission of C. burnetii and highlights the importance
of evaluating patients with suspected tickborne disease for
Q fever in areas known to be endemic for C. burnetii .
Considering the diagnosis of Q fever is especially important
for patients who are pregnant, immunocompromised, or
have valvular heart disease as prompt antibiotic treatment
can prevent life-threatening complications.
Conflict of Interests
The authors report no conflict of interests.
The patient provided written informed consent for this case
The findings and conclusions of this report are those of the
authors and do not necessarily represent the views of the
Centers for Disease Control and Prevention or the institu-
tions with which the authors are affiliated.
The authors thank the Lewis and Clark City-County Health
Department for their assistance in this investigation, Dr.
Steven Helgerson for paper review, and Drs. Jennifer
McQuiston and Robert Massung for discussions and helpful
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