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Public Health Agency of Canada (PHAC)
Canada Communicable Disease Report

Volume 26-03
1 February 2000

[Table of Contents]

  

CAPRINE-ASSOCIATED Q FEVER IN NEWFOUNDLAND

Introduction

Coxiella burnetii is an obligate intracellular pathogen known to be the causative agent of Q fever, a zoonosis with a worldwide occurrence(1,2). The most common reservoirs for infection in humans are domestic farm animals such as cattle, goats, and sheep(3-9). Although C. burnetii can cause abortion and still birth, most animals have a persistent, relatively asymptomatic subclinical infection(10). Infection in humans usually manifests as a self-limiting febrile illness, pneumonia, or hepatitis(11).

Q fever is often difficult to diagnose. The diagnosis is usually established by demonstrating a seroconversion to Coxiella antigens in conjunction with an appropriate clinical history(13). C. burnetii is a small obligate intracellular coccobacillus that can have two distinct antigenic presentations or "phases." Animals and humans develop antibody responses to both phases. Phase II gives rise to an antibody response in acute infection; response to phase I is evident during chronic infections(14,15).

During the spring of 1999, abortions were noted among goats on one of a group of farms belonging to a newly formed cooperative in rural Newfoundland. The cooperative consists of eight goat farms within a 170 km2 area with a total population of approximately 8,000.

Polymerase chain reaction (PCR) analysis of the aborted placental tissue detected the presence of DNA from C. burnetii. At the same time a number of farmers and their workers presented with a non-specific febrile illness associated with severe headaches. Serologic testing revealed that these individuals had titres to phase II antigen > 1/64 suggesting recent infection with C. burnetii. No documented case of Q fever had previously been reported in Newfoundland.

Investigation

An epidemiologic investigation and serologic survey was carried out in April 1999 to determine the number of infections, the nature of the illness, and risk factors for infection associated with this outbreak. A standardized questionnaire was designed to assess the epidemiology, risk factors, and clinical history of participants. Serum samples were collected from 179 farmers, workers, and contacts. Questionnaires were administered to 146 of the participants (33 could not be contacted for questioning). Although locally raised goats were present in the community prior to the establishment of the cooperative, the eight farms received shipments of goats from Ontario, Prince Edward Island, and Maine in the summer and fall of 1998. At the time of the outbreak, there were 174 goats within the cooperative with 10 to 38 animals per herd.

Results

Illness among the goat farmers or their workers was noted in March 1999. Serologic data were available for 179 farmers, workers, and contacts. Eighty (44.7%) of these people had antibodies against the Phase II antigen. Sixty-six (36.9%) had phase II titres of >= 1/64 or had a fourfold rise in titre suggesting recent infection.

Figure 1 shows the epidemic curve suggesting an ongoing source of infection that had a peak during the kidding season. Symptoms associated with infection included sweats, chills, headache, weight loss, malaise, fever, fatigue, myalgia, dyspnea, nausea, and diarrhea. Significant risk factors for infection by multivariate analysis included contact with the placenta (p = 0.0000), tobacco smoking history (p = 0.0010), and eating cheese made from pasteurized goat milk (p = 0.0221).

Figure 1 Epidemic curve for Q fever outbreak, Newfoundland, 1999

Figure 1 Epidemic curve for Q fever outbreak, Newfoundland, 1999

A subsequent survey of 154 members of the surrounding communities revealed a seropositivity rate of 22% with two people who had antibody titres > 1/64. Both of these individuals had had contact with goats. Fourteen percent of the members of this cohort had consumed the pasteurized cheese but did not become infected (titres < 1/64).

Conclusions

These are the first documented cases of Q fever in Newfoundland. The small barns in this cooperative and lack of open fields created confined conditions and an environment which facilitated infection. Although exposure to goats and consumption of unpasteurized milk have been implicated in causing C. burnetii infection in the past(7), this is the first time that a product made from pasteurized milk has been statistically associated with the development of Q fever. Further studies are needed to determine the cause of this epidemiologic association. This outbreak also raises questions about how to control such an outbreak and the interprovicial sale and movement of domestic ungulates.

Acknowledgements

The authors would like to thank the following for their co-operation and assistance: Dr. E. Dumka, Dr. J. Norman, Bonavista, Nfld.; Ms. M. Hayes, Memorial University of Newfoundland, St. John's, Nfld.; Ms. S. Burbridge, Dalhousie University, Halifax, N.S.; Dr. H. Whitney, Newfoundland Department of Forest Resources and Agrifoods, Clarenville, Nfld.

References

  1. Kaplan MM, Bertagna P. The geographical distribution of Q fever. Bull WHO 1955;13:829-60.

  2. Marrie TJ, Raoult D. Q-fever - a review and issues for the next century. Int J Antimicrob Agents 1997;8:145-61.

  3. Luoto L, Pickens EG. A resume of recent research seeking to define the Q-fever problem. Am J Hyg 1961;74:43-9.

  4. Dupuis G, Petite J, Peter O et al. An important outbreak of human Q fever in a Swiss alpine valley. Inter J Epidemiol 1987;16:282-87.

  5. Rauch AM, Tanner M, Pacer RE et al. Sheep-associated outbreak of Q fever. Arch Intern Med 1987;147:341-44.

  6. Akesson A, Macellaro A, Tull P et al. Epidemiology of Q fever in Sweden. Scand J Infect Dis 1991;23:153-57.

  7. Fishbein DB, Raoult D. A cluster of Coxiella burnetii infections associated with exposure to vaccinated goats and their unpasteurized dairy products. Am J Trop Med Hyg 1992;47:35-40.

  8. Aw TC, Ratti N. Occupational infection in an offal porter: a case of Q fever. Ocupp Med 1997;47:432-34.

  9. Gou HR, Gilmore R, Waag DM et al. Prevalence of Coxiella burnetii infections among North Dakota sheep producers. J Occup Environ Med 1998;40:999-1006.

  10. Moore JD, Barr BC, Daft BM et al. Pathology and diagnosis of Coxiella burnetii infection in a goat herd. Vet Pathol 1991;28:81-4.

  11. Tissot Dupont H, Raoult D, Brouqui P et al. Epidemiologic features and clinical presentation of acute Q fever in hospitalised patients: 323 French cases. Am J Med 1992;93:427-34.

  12. Fournier PE, Marrie TJ, Raoult D. Diagnosis of Q fever. J Clin Microbiol 1998;36:1823-34.

  13. Peacock MG, Philip RN, Williams JC et al. Serological evaluation of Q fever in humans: enhanced phase I titres of immunoglobulins G and A are diagnostic for Q fever endocarditis. Infect Immun 1983;41:1089-98.

  14. Raoult D, Marrie T. 1995, Q Fever. Clin Infect Dis 1995;20:489-96.

Source: T Hatchette, MD, Queen Elizabeth II Health Sciences Centre, Dalhousie University, Halifax, N.S.; R Hudson, DVM, Newfoundland Department of Forest Resources and Agrifoods, Clarenville, Nfld.; W Schlech, MD, N Campbell, BSc, J Hatchette, MSc, Queen Elizabeth II Health Sciences Centre, Dalhousie University, Halifax, N.S.; S Ratnam, PhD, MPH, C Donovan, MD, Memorial University of Newfoundland, St. John's, Nfld.; T Marrie, MD, University of Alberta, Edmonton, Alta.

 

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