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Q Fever Outbreak -- Switzerland

On November 18, 1983, the Microbiology and Infectious Diseases Division of the Valais Central Laboratory (VCL) notified the Valais Health Department of an outbreak of Q fever in Bagnes, Switzerland. From October 15 to December 15, more than 300 persons with acute illness characterized by high fever, chills, general malaise, headache, and arthralgias were seen by a physician in Bagnes County (population approximately 4,700). To date, a total of 191 clinical cases of acute Q fever (Figure 1) have been serologically confirmed at the VCL by a fourfold or greater rise in Q fever complement fixation phase II antibody titer or by a 1:20 or greater Coxiella burnetii-specific immunoglobulin M (IgM) titer using an indirect immunofluorescence test on a single serum specimen. Fifty-one specimens with positive titers were sent to the Rocky Mountain Laboratory, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, and all were confirmed. Serum samples from 2,962 well persons from Bagnes were taken during December 1983 for the detection of C. burnetii specific-IgM antibodies; 224 specimens (8%) demonstrated titers of 1:20 or greater, indicating asymptomatic infection.

Patients with symptomatic infections ranged in age from 8 years to 82 years (median 35 years); 10 were children under 15 years of age. One hundred thirteen patients (59%) were male. To date, no deaths have been attributed to acute Q fever. Twelve patients were hospitalized with severe bronchopneumonia; two of these also had myopericarditis, and one had granulomatous hepatitis. After November 20, doxycycline was prescribed for most patients for a period of 14 days and generally resulted in subjective symptomatic improvement.

The movement of sheep flocks has been implicated in the dissemination of the infection. Sheep flocks remained on mountain pastures from June to October 9, 1983, after which they returned to the villages. Higher attack rates occurred among persons living close to the roads on which the sheep traveled. Serum specimens were obtained from 432 sheep distributed in 12 flocks; 166 had C. burnetii antibodies, mainly from six of the 12 flocks. Increased fetal mortality was also noted in infected flocks. On December 3, the Veterinary Department decided to isolate, vaccinate, and shear the sheep, destroy the wool, and disinfect the sheep pens.

To date, milk samples from 12 dairy herds have been evaluated for the presence of antibodies against C. burnetii. One sample was positive. Isolation of the organism was not attempted. Reported by G Dupuis, MD, O Peter, PhD, Infectious Diseases and Microbiology Div, Valais Central Laboratory, J Petite, MD, Martigny County Hospital, M Vouilloz, MD, Valais Health Dept, Sion, Switzerland; MG Peacock, Rocky Mountain Laboratory, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana; Div of Viral Diseases, Center for Infectious Diseases, CDC.

Editorial Note

Editorial Note: Q fever is a zoonosis caused by C. burnetii, a rickettsial organism that is enzootic in a large variety of domestic and wild animals. Domestic ungulates, such as sheep, cattle, and goats, the usual reservoir for man, shed the organism in their feces, milk, urine, and especially their birth products. Humans acquire the infection from inhaling the dessication-resistant rickettsiae in aerosols and dusts, which can remain infectious for months or years (1). Since the disease was first reported in Australia in 1937, sporadic outbreaks and epidemics have been reported from more than 50 countries on five continents, usually occurring in areas where domestic ungulates are raised or animal products are processed (2). Although not a nationally reportable disease, Q fever in humans has been reported from 31 states in the United States. (3). Most recently, four outbreaks have been reported among researchers and staff in urban research facilities using sheep as research animals (4).

It is of particular interest that this large outbreak in Switzerland occurred in the fall months. Most outbreaks in rural communities occur during the spring lambing season when the normally asymptomatic infected ewe can shed as many as one billion organisms per gram of placenta. In this instance, animals apparently shed the organism for many months after the lambing season. It has been suggested that an unusually dry summer and autumn may have encouraged the formation and propagation of infectious dusts and aerosols, especially along the route of sheep movement.

The clinical illness was similar to that reported in previous outbreaks. The infection is often asymptomatic or mistaken for an acute viral illness. After an incubation period of 2-3 weeks, Q fever usually presents with fever, headache, and myalgias. Although often said to be a pulmonary disease, the frequency of clinical pneumonitis is highly variable (5). Occasionally, the illness may be prolonged with severe pneumonitis and hepatic involvement. Tetracycline and chloramphenicol are effective in shortening the course of illness. Although the acute disease is usually self-limited, Q fever endocarditis may occasionally develop 3-20 years following the acute infection and is often fatal (6).

Because of the nonspecific clinical presentation, outbreaks of Q fever undoubtedly go unrecognized. A knowledge of the disease epidemiology and a high index of suspicion are necessary for diagnosis. Both immunofluorescent and complement fixation tests are available that are highly specific for the diagnosis of Q fever (7). Initial evaluations of experimental Q fever vaccines for humans and animals are encouraging (8). CDC is interested in receiving reports of Q fever outbreaks and cases, which should first be reported to local and state health departments.


  1. Leedom JM. Q fever. In: Eichoff TC, ed. Practice of medicine. vol 3. New York: Harper and Row, 1978:1-19.

  2. Hart RJC: The epidemiology of Q fever. Postgrad Med J 1973;49:535-8.

  3. D'Angelo LJ, Baker EF, Schlosser W. From the Center for Disease Control. Q fever in the United States, 1948-1977. J Infect Dis 1979;139:613-5.

  4. Meiklejohn G, Reimer LG, Graves PS, Helmick C. Cryptic epidemic of Q fever in a medical school. J Infect Dis 1981;144:107-13.

  5. Warren JW, Hornick RB. Coxiella burnetii (Q fever). In: Mandell GL, Douglas RG Jr, Bennett JE, eds. Principles and practice of infectious diseases. New York: John Wiley & Sons. 1979:1516-20.

  6. Turck WP, Wowitt G, Turnberg LA, et al. Chronic Q fever. Q J Med 1976;45:193-217.

  7. Hunt JG, Field PR, Murphy AM. Immunoglobulin responses to Coxiella burnetii (Q fever): single-serum diagnosis of acute infection, using an immunofluorescence technique. Infect Immun 1983;39:977-81.

  8. Ascher MS, Berman MA, Ruppanner R. Initial clinical and immunologic evaluation of a new phase I Q fever vaccine and skin test in humans. J Infect Dis 1983;148:214-22.

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