Tularemia: A Case Report

Rosa Giménez-García1, Mónica de Frutos Serna2, Marta Domínguez Gil2 and Gonzalo Cabezón Villalba1 1Department of Dermatology, Hospital del Rio Hortega, Valladolid, Spain 2Department of Microbiology, Hospital del Rio Hortega, Valladolid, Spain *Corresponding author: Rosa Giménez-García, Department of Dermatology, Hospital del Rio Hortega, Valladolid, Spain, Tel: 0034-670713339; E-mail: rosagim@hotmail.com


Introduction
Tularemia is a serious and potentially life-threatening zoonosis caused by Francisella tularensis, an aerobic catalase-positive, gram negative coccobacilli [1]. It is widespread in the northern hemisphere and it is transmitted by skin contact with infected animals, inhalation, arthropod bites or ingestion of contaminated meat or water. Over the past few years there is new evidence suggesting that tularemia has reemerged worldwide [2]. Tularemia outbreaks occurred in northwestern Spain in 1997-1998 and 2007-2008 [3]. We present a case recently attended at our Department.

Case Report
A 60-year-old woman was admitted to our hospital with a week history of sudden onset of cutaneous lesion on the second finger in her right hand, accompanied by fever, chills, headache and axillary lymphadenopathy. Initial antibiotic therapy with amoxicillin clavulanate was ineffective. The patient history includes recent handling of hares.
Physical examination revealed the presence of a vesiculopustular lesion on periungual region of her second finger (Figure 1), lymphangitis on her inner right arm and tender lymph node in her right axilla. Culture showed colonies 2 to 4 mm in size, greenish-white, round, smooth, and slightly mucoid ( Figure 2). The clinical diagnosis of suspected ulceroglandular tularemia was confirmed by F. tularensis DNA positivity in skin aspirate by polymerase chain reaction. Surgical drainage and a 14-days course of ciprofloxacin 1000 mg/day PO, was given. We observed a gradual improvement and a follow up evaluation one month later revealed that the patient had recovered with no complications.

Discussion
Tularemia was first reported in Spain in 1997, when it caused one of the largest outbreaks in humans ever described and was associated with hunting and handling of hares. Overall 559 cases were confirmed during June 1997-April 1998 in 10 provinces of the northwestern. A second outbreak occurred in the same area in 2007-2008 this time coinciding with a population peak of the common vole [3] especially in our region, Castilla y León. Evidence suggests a worldwide reemerging of tularemia [2,4,5]. In Europe there is only one type of tularemia reported (type B) and it is caused by F. t. Holoarctica [6]. Type A tularemia is caused by F. t. Tularensis, which is more virulent than Holoarctica and has been only reported in North America.
Most cases of tularemia are associated with handling and hunting of hares, however others rodents like the common vole also are a source of infection. Ticks, flies and mosquitoes are vectors of F. tularensis.
There are six clinical forms of tularemia: ulceroglandular, glandular, oculoglandular, oropharyngeal, typhoidal and pneumonic. The most common clinical presentation of tularemia is ulceroglandular form that consists in a painful maculopapular lesion at the entry point that later ulcerates [1]. Erythema multiforme is a common finding in all forms of tularemia. Other dermatological manifestations are urticarial, erythema nodosum and cellulitis [7].
The studied patient had an ulceroglandular form, defined by a painful maculopapular or ulcerate lesion in the spot where the bacteria entered the body, regional lymphadenopathies and systemic symptoms like fever, chills or myalgias. However, lymphadenopathy without the skin lesion can be the only presenting symptom in few cases. Conjunctivitis and pharyngitis may appear in the curse of an ulceroglandular form. The incubation period is typically 3 to 6 days [1].
Because of the difficulty in culturing F. tularensis, most cases of tularemia are diagnosed on the basis of clinical picture and/or serology. The detection of serum antibodies, about 2 weeks after the onset, is most frequently achieved by agglutination or an ELISA. F. tularensis requires enriched medium for growth. Traditionally, cysteine glucose blood agar has been the growth medium of choice, colonies are 2 to 4 mm in size, greenish-white, round, smooth, and slightly mucoid. A range of PCR-based assays have been reported for the detection of F. tularensis for the diagnosis of tularemia. These PCR assays have all used primers directed against genes encoding outer membrane proteins such as fopA or the 17-kDa outer membrane lipoprotein.
The key of a successful treatment is an early diagnosis and the use of appropriate antibiotics. Doxycycline, ciprofloxacin, streptomycin and gentamicin are among the first line of treatment. Azithromycin represents a treatment option for tularemia during pregnancy if there is no resistance to macrolides [10].

Conclusion
Clinical diagnosis of tularemia can be challenging because of its rarity. Tularemia should be included in the differential diagnosis of hand infectious diseases.
Human contact with vectors and reservoirs for tularemia must be avoided.