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| Journal of the New Zealand Medical Association,
26-January-2007, Vol 120 No 1248
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Tularaemic cervical lymphadenopathy
Oguz Karabay, Fahrettin Yilmaz, Saban Gurcan, Nadir
Goksugur
A 38-year-old previously healthy man presented with fever
(39.1°C), fatigue, and weakness. He had suffered sore throat, neck pain,
and cervical lymphadenopathy for 10 days (Figure 1). Before admission to our
clinic, he had received cefuroxime axetil 2×500 mg PO 10 days for treatment
of a painful cervical mass, however there was no improvement.
Physical examination revealed painful right cervical
lymphadenopathy. Laboratory tests revealed a WBC count of
12,000/mm3 (65 % neutrophils, 30% lymphocytes,
2% eosinophils, and 3% monocytes) and the erythrocyte sedimentation rate was 93
mm/h. The microagglutination test was positive for antibody of Francisella
tularensis at 1/640 titres.
Thereafter, we started gentamicin 5 mg/kg /day IM for a
10-day period. The patient’s sore throat improved with this therapy, and
the cervical lymphadenopathy spontaneously suppurated (Figure 2).
DiscussionTularaemia, sometimes known as rabbit fever, is a zoonotic
bacterial disease caused by the facultative intracellular, gram-negative
bacterium Francisella tularensis that multiplies within macrophages.
F. tularensis, infects humans by direct contact
with infected rodents (e.g. squirrels, voles, rabbits, and muskrats), aerogenic
exposure, ingestion of contaminated food or water, or by arthropod bites (e.g.
ticks, mosquitos, and deer flies acting as vectors of the
disease).1
Although person-to-person transmission does not occur with
F. tularensis, the organism is extremely infectious, with as few as
10–50 inhaled organisms producing disease. It is therefore an organism
that can infect laboratory technicians working with the organism, and it is a
potential biological weapon.1
Tularaemia occurs endemically in most countries of the
Northern Hemisphere, within a range of 30 to 71 degrees
latitude.2 The worldwide incidence of
tularaemia is not known, and the disease is probably greatly under-recognised
and under-reported.1
F. tularensis can infect humans through the skin,
mucous membranes, gastrointestinal tract, and lungs. The major target organs are
the lymph nodes, lungs and pleura, spleen, liver, and kidney. Bacilli inoculated
into skin or mucous membranes multiply, spread to regional lymph nodes, then may
disseminate to organs throughout the body.1,3
Tularaemia is divided into six clinical (ulceroglandular,
glandular, oculoglandular , oropharyngeal, pneumonic, and typhoidal) forms.
These forms of tularaemia in humans largely depend on the infectious route. For
example, ulceroglandular tularaemia is most frequently caused by vector-borne
transmission and oropharyngeal tularaemia is contracted by ingestion of
contaminated food or water.3
In Turkey, where this case occurred, the oropharyngeal form
of the disease is the most common, in contrast to most European countries and
the United States where the ulceroglandular form is more
prominent.3 Illness usually begins 3 to 5 days
after inoculation, with fever (38°C–40°C), generalised body
aches, headache, chills, and malaise.4 In
oropharyngeal tularaemia, the primary ulcer is localised in the mouth, and lymph
nodes of the neck region are enlarged. If appropriate treatment is not afforded
in time (<2 weeks after onset of disease), the risk of abscess development
will be >20%.2
Extreme caution should be maintained when handling infected
tissues or culture media, and bacterial cultures should be handled in a
biosafety Level 3 facility.5 Serology is most
commonly used for diagnosis. Most laboratories use tube agglutination or
microagglutination tests that detect combined immunoglobulin M and
immunoglobulin G. A four-fold change in titre between acute and convalescent
serum specimens, or a single titre of at least 1:160 for tube agglutination, or
1:128 for microagglutination is diagnostic for F. tularensis
infection.1–2
Therapy against tularaemia has consisted of aminoglycosides
(streptomycin is considered the drug of choice), tetracycline, quinolones, and
(in the early days) chloramphenicol. Betalactams, macrolides, lincosamides, and
cotrimoxazole are not reliable for treatment of
tularaemia.1–2
Treated tularaemia has a mortality rate of less than 1%.
Lifelong immunity is usually conferred after
infection.4
Author information: Oguz Karabay, Associate
Professor, Department of Infectious Diseases and Clinical Microbiology, Izzet
Baysal Medical Faculty, Izzet Baysal University, Bolu; Fahrettin Yilmaz,
Assistant Professor, Department of Otorhinolaryngology, Izzet Baysal Medical
Faculty, Izzet Baysal University, Bolu; Saban Gurcan,
Associate Professor, Department of Clinical Microbiology, Medical
Faculty, Trakya University, Edirne; Nadir Goksugur, Assistant Professor,
Department of Dermatology, Izzet Baysal Medical Faculty, Izzet Baysal
University, Bolu; Turkey
Correspondence: Associate Professor Oguz
Karabay, Department of Infectious Diseases and Clinical Microbiology, Abant
Izzet Baysal University Medical Faculty, 14280 Golkoy –Bolu, Turkey. Fax:
+90 374 253 4615; email: drkarabay@yahoo.com
References:
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