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Q Fever among Slaughterhouse Workers -- California

During May 1985, five cases of hepatitis were reported to the Solano County (California) Health Department among workers at a local meatpacking plant that processes sheep. Illnesses were characterized by fever, malaise, myalgias, severe headache, and abdominal pain, but no jaundice. Symptoms lasted at least 1 week, then gradually resolved. Hepatitis was suspected because all cases had moderately elevated SGOT values. However, none had serologic evidence of acute infection with either hepatitis A or B (i.e., negative immunoglobulin M (IgM) antibody to hepatitis A and hepatitis B surface antigen). Since all five patients were exposed to domestic animals in the course of their work, the differential diagnoses included Q fever, brucellosis, and leptospirosis. Sera from four of the patients who were originally thought to have had hepatitis from other causes were positive for IgM antibody to Q fever by the immunofluorescent antibody test (IFA), indicating recent infection.

A serosurvey was conducted to identify the extent of the outbreak. Forty-two of approximately 100 employees agreed to be surveyed, including the five employees described above. Twelve (29%) had complement-fixation (CF) titers to Q fever rickettsiae; eight (67%) of the 12 had recently experienced a clinical illness compatible with Q fever. Nineteen (45%) of the surveyed employees were positive by IFA test (but negative by CF test) for IgG antibody. Eleven of the 42 employees were negative both by CF and IFA. The 31 persons with serologic evidence of infection worked in a variety of jobs in areas throughout the plant, but no further investigation was performed to determine areas of highest risk.

Employees were educated about the illness through printed material and a question-and-answer session. A letter was mailed to physicians in the vicinity of the meatpacking plant informing them about Q fever. An investigation conducted by the California Occupational Health and Safety Administration resulted in the implementation of a surveillance program that included screening for Q fever by serology and for valvular heart disease among new employees. No feasible environmental control measures were identified. Reported by E Lopez, MD, Solano County Health Dept, M Ascher, MD, Viral and Rickettsial Disease Laboratory, R Roberto, MD, Infectious Disease Br, J Chin, MD, State Epidemiologist, California State Dept of Health Svcs; Viral and Rickettsial Zoonoses Br, Div of Viral Diseases, Center for Infectious Diseases, CDC.

Editorial Note

Editorial Note:Q fever, caused by the rickettsial organism Coxiella burnetii, is found in at least 51 countries on five continents. The primary reservoirs are cattle, sheep, goats, and ticks, but many species of animals, both wild and domestic, are susceptible to infection. The infection in animals is usually subclinical, although organisms are excreted in milk, urine, and feces. In the infected parturient ewe, rickettsiae are found in especially high numbers in amniotic fluid, placenta, and fetal membranes (the placenta may contain 10((9)) organisms per gram during late gestation) (1). A single inhaled organism is sufficient to initiate infection. Because they are extremely resistant to desiccation and to physical agents, organisms survive for long periods in the inanimate environment (2).

Humans are usually infected by inhalation of aerosolized particles from contaminated environments. Disease resulting from sheep occurs most commonly during the lambing season because of the high numbers of organisms shed at this time. Humans are at risk at other times as well, since the organism may be shed periodically from domestic animals and may be found in raw milk, arthropods, and other animal products, e.g., wool. Other occupational exposures to sheep have accounted for four reported outbreaks among employees in urban research facilities (3).

The incubation period for Q fever in humans is 14-39 days, averaging 20 days. Most commonly, Q fever causes a mild influenza-like illness that rarely requires medical attention. Q fever may manifest as a systemic illness, as in the first four cases, with symptoms characterized by sudden onset of severe headache, retrobulbar pain, a fever of 40 C (104 F) or greater, chills, general malaise, myalgia, and chest pain. Other more severe manifestations may include pneumonia and hepatitis. Although the acute disease is usually self-limited, Q fever endocarditis occassionally develops, typically 3-20 years following the acute infection, and is often fatal (5,6). Patients with underlying heart disease are at particular risk, because it affects previously damaged heart valves. Prompt treatment with tetracycline or chloramphenicol is effective in shortening the course of acute illness (7).

Q fever has also been described among children. Infection with C. burnetii was diagnosed in 18 children under 3 years of age who were hospitalized in the Netherlands during a 16-month period (8). These patients presented most commonly with fever of unknown etiology or with pneumonia. Four of the children had relapsing episodes of fever that lasted 2-11 months before presentation. The duration of hospitalization averaged 25 days, and ranged from 4 days to 80 days.

Q fever is difficult to diagnose clinically, and radiologic findings of the lungs, when present, may not be diagnostic. However, the diagnosis is readily made serologically (9,10).

Q fever is reportable in 24 states (Figure 1). Because Q fever may be mild and self-limited or mistaken for an acute viral illness, diagnosis requires a high index of suspicion. An occupational history should be obtained; contact with animals should suggest Q fever or another zoonoses. Q fever should be considered in the differential diagnosis of patients with atypical pneumonia, an influenza-like illness during periods of low influenza activity, in patients with abnormal liver function tests when serologic evidence for hepatitis A or B is absent, and in children with fever of unknown origin (8). To facilitate diagnosis, a pilot state laboratory-based Q fever surveillance program has been initiated in California, Colorado, Idaho, Iowa, Montana, New Mexico, and Oregon. Participating state laboratories have volunteered to test selected serum specimens for Q fever antibody. Positive specimens are reported both to the physician and to the state epidemiologist, who subsequently completes a case history form. Physicians in these seven states are encouraged to report such cases through their local/state health departments to the Viral and Rickettsial Zoonoses Branch, Division of Viral Diseases, Center for Infectious Diseases, CDC.


  1. Welsh HH, Lennette EH, Abinanti FR, et al. Air-borne transmission of Q fever: the role of parturition in the generation of infective aerosols. Ann NY Acad Sci 1958;70:528-40.

  2. Ormsbee RA. Q fever rickettsia. In: Horsfall FL Jr, Tamm I, eds. Viral and rickettsial infections of man. 4th ed. Philadelphia: JB Lippincott, 1965:1144-60.

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

  4. Ellis ME, Smith CC, Moffat MAJ. Chronic or fatal Q-fever infection: a review of 16 patients seen in North-East Scotland (1967-80). Q J Med 1983;52:54-66.

  5. Turck WPG, Howitt G, Turnberg LA, et al. Chronic Q fever. Quart J Med 1976;45:193-217.

  6. Wilson HG, Neilson GH, Galea EG, et al. Q fever endocarditis in Queensland. Circulation 1976;53:680-4.

  7. Leedom JM. Q fever. In: Eickhoff TC, ed. Practice of medicine. vol. III. Hagerstown, Maryland: Harper & Row, 1978:1-19 (chapter 47).

  8. Richardus JH, Dumas AM, Huisman J, Schaap GJP. Q fever in infancy: a review of 18 cases. Pediatr Infect Dis 1985;4:369-73.

  9. Dupuis G, Peter O, Peacock M, Burgdorfer W, Haller E. Immunoglobulin responses in acute Q fever. J Clin Micro 1985;22:484-7.

  10. Peter O, Dupuis G, Burgdorfer W, Peacock M. Evaluation of the complement fixation and indirect immunofluorescence tests in the early diagnosis of primary Q fever. Eur J Clin Microbiol 1985;4:394-6.

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