On December 1, 2005, Darmstadt health authorities were notified of a laboratory-diagnosed case of tularemia. The patient had participated in a hare (Lepus europaeus) hunt on October 29, 2005, and cut 1 finger while disemboweling and skinning hares. On November 2, the patient became ill with fever >40°C, axillary lymphadenopathy, arthralgia, and headache. Initially treated as an outpatient, he was hospitalized November 21 for progressive lymphadenitis and recurrent fever; Francisella tularensis infection was diagnosed by lymph node biopsy and specific antibodies. After the Darmstadt-Dieburg Public Health Authority received notification of this index case, that agency initiated an outbreak investigation.

On October 29, 2005, 29 hunters and 10 beaters, who drove hares out of areas of cover, participated in the hunt. Sixty-three hares were shot. Some hares were disemboweled where they were shot; most were later disemboweled and rinsed with a water hose at a hunting lodge. Disemboweled hares were transported to a game chamber and skinned the next day.

We investigated an outbreak of tularemia after a hare hunt in Hesse, Germany, for which epidemiologic, clinical, and microbiologic data indicate an airborne origin. The results of the cohort study support this hypothesis on the basis of the association between case status and presence within 5 meters of the location where disemboweled hares were rinsed. During the afternoon session of disemboweling and rinsing hares, 10 of the 11 case-patients were at the hunting lodge; aerosolization of infectious particles may have been limited to this session. Three case-patients, among them the patient who did not participate in the afternoon session, had a glandular or ulceroglandular form of tularemia. They may have acquired infections through skin lesions. The absence of cutaneous lesions or lymphadenopathy in the remaining 8 patients makes a cutaneous route of infection less likely than a respiratory route. The low incidence of respiratory symptoms among our patients is in agreement with findings from previous airborne outbreaks that involved patients infected with the less virulent subspecies F. tularensis holarctica, in which only a minority of case-patients had symptoms suggestive of pneumonia (8,9).

Two hunters met the probable case-patient definition. The asymptomatic hunter (no. 11) disemboweled hares at a distance from the group. Severity of clinical tularemia has been correlated with infectious dose (20), and this hunter might have been exposed to a smaller pathogen load or exposed on another recent occasion. Case-patient 3 died during the second week of illness. Antibodies against F. tularensis in most patients appear 6–10 days after onset of symptoms (21,22). Serum available for testing from case-patient 3 was from his eighth day of illness; hence, it was possibly taken before a measurable antibody response developed. We further cannot exclude the possibility that the 10 asymptomatic participants who did not undergo laboratory testing had to be considered as probable case-patients if they provided a serum sample.

Detection of F. tularensis in hare specimens, including bone marrow specimens, and lack of F. tularensis detection in samples of the water system used to rinse hares suggest infection of the hares. One or more infected hares, still bloody and wet, may have cross-contaminated additional hares during further processing, e.g., during transport to and storage at the game chamber. All samples taken in the game chamber showed negative results. Case-patient 3 had cleaned the game chamber thoroughly with a pressure washer, possibly exposing himself to a high pathogen load.

Small clusters and outbreaks of airborne tularemia have been associated with hares or rabbits (7–11). However, most cases of tularemia associated with hares are of the ulceroglandular or glandular form (1,22). In a protracted outbreak in Spain, 97% of patients reported previous contact with hares; 71% of these had a glandular or ulceroglandular form of disease (23). Of 577 case-patients treated at a clinic in Czechoslovakia, 194 had direct contact with hares, and an (ulcero) glandular form of disease developed (1). Different frequencies of the diverse clinical forms of tularemia suggest differences in the main route of pathogen acquisition.

In the retrospective cohort study, presence within 5 meters of the place where disemboweled hares were rinsed was the risk factor most strongly associated with infection. Washing of contaminated produce was found to be an effective mechanism of generating infectious aerosols in tularemia outbreaks in sugar beet factories (1–3), and rinsing >1 hares infected with F. tularensis was the most probable way by which an infectious aerosol was generated. However, we cannot exclude the idea that an infectious aerosol was formed through further hare manipulating activities, e.g., transport.

Previous outbreaks in Germany date back to the 1950s, with the last case reported in the outbreak area in 1957 (24). Environmental characteristics of natural foci of tularemia persisting over >30 years have been described (19,25). The outbreak region in Germany shares several features favoring the occurrence or persistence of F. tularensis in the environment. Recently, the presence of F. tularensis in trapped rodents (2.1%) and in water samples from this hunting area was directly confirmed, and >10% of rodents in several German regions not previously considered as endemic foci were infected (19). In addition, F. tularensis was repeatedly detected in 22 hares from 5 federal states (Bavaria, Hesse, Baden-Wuerttemberg, Thuringia, and Lower Saxony) after improved diagnostic tools (real-time PCR) had been applied complementary to standard 48-h bacterial cultivation (W.D. Splettstoesser et al., unpub. data). Together with results obtained from serologic studies in the German population (26), the outbreak reported here suggests that tularemia has either reemerged in Germany or is seriously underreported.