Changing Epidemiology of Q Fever in Germany; 1947-1999
Changing Epidemiology of Q Fever in Germany; 1947-1999
The epidemiology of Q fever in Germany was examined by reviewing relevant studies since 1947 and by analyzing available surveillance data since 1962. The average annual Q fever incidence nationwide from 1979 to 1989 was 0.8 per million and from 1990 to 1999, 1.4 per million. The mean annual incidence from 1979 to 1999 ranged from a minimum of 0.1 per million in several northern states to 3.1 per million in Baden-Württemberg, in the South. We identified 40 documented outbreaks since 1947; in 24 of these sheep were implicated as the source of transmission. The seasonality of community outbreaks has shifted from predominantly winter-spring to spring-summer, possibly because of changes in sheep husbandry. The location of recent outbreaks suggests that urbanization of rural areas may be contributing to the increase in Q fever. Prevention efforts should focus on reducing sheep-related exposures, particularly near urban areas.
Q fever is caused by the pleomorphic, obligate intracellular rickettsial agent Coxiella burnetii, which has an envelope similar to that of gram-negative bacteria. It is found worldwide except in New Zealand. Its most important reservoirs are ticks and ruminant animals such as cows, sheep, and goats. Although infection rarely causes major clinical symptoms in animals, it has been associated with infertility and abortion, particularly in first-bearing newly infected parturient animals. Birth products from infected animals thus contain high concentrations of C. burnetii and can be an important source of environmental contamination. Transmission to humans and other animals by the aerosol route is facilitated by the tenacity of C. burnetii's survival for months to years in a sporelike state on wool or fur contaminated with infected tick feces, in water, and in soil.
Acute Q fever in humans is characteristically a febrile, flulike illness associated with pneumonia or hepatitis. Rare complications include myocarditis, pericarditis, or meningoencephalitis. The death rate among persons with Q fever pneumonia is 0.5% to 1.5%. Up to half of patients may suffer protracted fatigue and weakness after acute disease. Rarely, more serious forms of chronic disease (most commonly endocarditis but also chronic hepatitis and vascular, osteoarticular, or pulmonary infections) may develop months to years after the acute infection. An increased long-term risk for arterial disease and death has also been observed.
Q fever was first recognized in southern Germany when several large outbreaks occurred in rural communities in 1947 to 1948. Since then, it has been endemic in Germany. In the 1990s, several large outbreaks were recognized and investigated. This led us to review the epidemiology of this disease in Germany.
The epidemiology of Q fever in Germany was examined by reviewing relevant studies since 1947 and by analyzing available surveillance data since 1962. The average annual Q fever incidence nationwide from 1979 to 1989 was 0.8 per million and from 1990 to 1999, 1.4 per million. The mean annual incidence from 1979 to 1999 ranged from a minimum of 0.1 per million in several northern states to 3.1 per million in Baden-Württemberg, in the South. We identified 40 documented outbreaks since 1947; in 24 of these sheep were implicated as the source of transmission. The seasonality of community outbreaks has shifted from predominantly winter-spring to spring-summer, possibly because of changes in sheep husbandry. The location of recent outbreaks suggests that urbanization of rural areas may be contributing to the increase in Q fever. Prevention efforts should focus on reducing sheep-related exposures, particularly near urban areas.
Q fever is caused by the pleomorphic, obligate intracellular rickettsial agent Coxiella burnetii, which has an envelope similar to that of gram-negative bacteria. It is found worldwide except in New Zealand. Its most important reservoirs are ticks and ruminant animals such as cows, sheep, and goats. Although infection rarely causes major clinical symptoms in animals, it has been associated with infertility and abortion, particularly in first-bearing newly infected parturient animals. Birth products from infected animals thus contain high concentrations of C. burnetii and can be an important source of environmental contamination. Transmission to humans and other animals by the aerosol route is facilitated by the tenacity of C. burnetii's survival for months to years in a sporelike state on wool or fur contaminated with infected tick feces, in water, and in soil.
Acute Q fever in humans is characteristically a febrile, flulike illness associated with pneumonia or hepatitis. Rare complications include myocarditis, pericarditis, or meningoencephalitis. The death rate among persons with Q fever pneumonia is 0.5% to 1.5%. Up to half of patients may suffer protracted fatigue and weakness after acute disease. Rarely, more serious forms of chronic disease (most commonly endocarditis but also chronic hepatitis and vascular, osteoarticular, or pulmonary infections) may develop months to years after the acute infection. An increased long-term risk for arterial disease and death has also been observed.
Q fever was first recognized in southern Germany when several large outbreaks occurred in rural communities in 1947 to 1948. Since then, it has been endemic in Germany. In the 1990s, several large outbreaks were recognized and investigated. This led us to review the epidemiology of this disease in Germany.