Predominant immunoglobulin A response to phase II antigen of Coxiella burnetii in acute Q fever.
Diagnosis of acute Q fever is usually confirmed by serology, on the basis of anti-phase II antigen immunoglobulin M (IgM) titers of >/=1:50 and IgG titers of >/=1:200. Phase I antibodies, especially IgG and IgA, are predominant in chronic forms of the disease. However, between January 1982 and June 1998, we observed anti-phase II antigen IgA titers of >/=1:200 as the sole or main antibody response in 10 of 1,034 (0.96%) patients with acute Q fever for whom information was available. In order to determine whether specific epidemiological or clinical factors were associated with these serological profiles, we conducted a retrospective case-control study that included completion of a standardized questionnaire, which was given to 40 matched controls who also suffered from acute Q fever. The mean age of patients with elevated phase II IgA titers was significantly higher than that usually observed for patients with acute Q fever (P = 0.026); the patients were also more likely than controls to live in rural areas (P = 0.026) and to have increased levels of transaminase in blood (P = 0.03). Elevated IgA titers are usually associated with chronic Q fever and are directed mainly at phase I antigens. Although the significance of our findings is unexplained, we herein emphasize the fact that IgA antibodies are not specific for chronic forms of Q fever and that they may occasionally be observed in patients with acute disease. Moreover, as such antibody profiles may not be determined by most laboratories, which test only for total antibody titers to phase I and II antigens, the three isotype-specific Ig titers should be determined as the first step in diagnosing Q fever. (+info
Functional analysis of the active partition region of the Coxiella burnetii plasmid QpH1.
The partition region qsopAB of the Coxiella burnetii plasmid QpH1 was analyzed. Locus qsopA alone appears to fulfill the partitioning function; QsopA represses its own promoter 17-fold. Two partition-associated incompatibility sites were identified: incA in a 200-bp region covering the qsopA promoter and incB in the qsopB locus. (+info
Q fever in Bulgaria and Slovakia.
As a result of dramatic political and economic changes in the beginning of the 1990s, Q-fever epidemiology in Bulgaria has changed. The number of goats almost tripled; contact between goat owners (and their families) and goats, as well as goats and other animals, increased; consumption of raw goat milk and its products increased; and goats replaced cattle and sheep as the main source of human Coxiella burnetii infections. Hundreds of overt, serologically confirmed human cases of acute Q fever have occurred. Chronic forms of Q fever manifesting as endocarditis were also observed. In contrast, in Slovakia, Q fever does not pose a serious public health problem, and the chronic form of infection has not been found either in follow-ups of a Q-fever epidemic connected with goats imported from Bulgaria and other previous Q-fever outbreaks or in a serologic survey. Serologic diagnosis as well as control and prevention of Q fever are discussed. (+info
Coxiella burnetii infection increases transferrin receptors on J774A. 1 cells.
Inoculation with viable, but not inactivated, Coxiella burnetii resulted in the increased expression of transferrin receptors (TfR) in the murine macrophage-like cell line J774A.1. This upregulation was evident in immunoblots as early as 6 h postinfection, with TfR levels continuing to increase through the first 24 h of infection. Fluorescent labeling revealed that TfR upregulation occurred throughout infected monolayers, eliminating the possibility that it reflected a response by a minor subset of host cells. In addition, TfR trafficking did not appear to be affected by C. burnetii infection. Consistent with the increase in TfRs, inoculation with viable C. burnetii resulted in a 2.5-fold increase in total cellular iron by 12 h postinoculation. Our further findings that the chelation of intracellular iron arrests C. burnetii replication and that C. burnetii metabolic activities in vitro are affected by iron concentration suggest that TfR upregulation is a salient factor in C. burnetii infection, and we speculate that it may represent a significant virulence mechanism. (+info
Long term vascular complications of Coxiella burnetii infection in Switzerland: cohort study.
OBJECTIVE: To evaluate the range of long term vascular manifestations of Coxiella burnetii infection. DESIGN: Cohort study in Switzerland of people affected in 1983 by the largest reported outbreak of Q fever and who were followed up 12 years later. Follow up information about possible vascular disease and endocarditis was obtained through a mailed questionnaire and death certificates. SETTING: Val de Bagnes, a rural Alpine valley in Switzerland. PARTICIPANTS: 2044 (87%) of 2355 people who had serum testing for Coxiella burnetii infection in 1983: 1247 were classed as not having been infected, 411 were classed as having been acutely infected, and 386 were classed as having been infected before 1983. MAIN OUTCOME MEASURES: Relative risk controlled for age and sex and 12 year risk of vascular diseases and endocarditis among infected participants as compared with those who had never been infected. RESULTS: The 12 year risk of endocarditis or venous thromboembolic disease was not increased among those who had been acutely infected. The 12 year risk of arterial disease was significantly higher among those who had been acutely infected (7%) as compared with those who had never been infected (4%) (relative risk 2.2, 95% confidence interval 1.4 to 3.6). Specifically, there was an increased risk of developing a cerebrovascular accident (relative risk 3.7, 1.6 to 8.4) and cardiac ischaemia (relative risk 1.9, 1.04 to 3.4). 12 year mortality was significantly higher among the 411 people who had been acutely infected in 1983 (9.7%; age adjusted relative risk 1.8, 1.2 to 2.6) when compared with the 1247 participants who had remained serologically negative in 1983 (7.0%). CONCLUSIONS: Coxiella burnetii infection may cause long term complications including vascular disease. (+info
Short report: prevalence of antibodies against spotted fever, murine typhus, and Q fever rickettsiae in humans living in Zambia.
The causative agents of rickettsial diseases (Rickettsia conorii, R. typhi, and Coxiella burnetii) have been reported throughout the African continent. However, there have been no reports on epidemiologic surveys of these infections in Zambia. This study was designed to clarify the prevalence of three rickettsioses in 377 humans in Zambia. The seroprevalence of antibodies against R. conorii, R. typhi, and C. burnetii was 16.7%, 5.0%, and 8.2%, respectively. The rates of antibody positivity against R. conorii and C. burnetii were higher in the eastern (23.1% and 11.8%) and western (16.8% and 7.4%) areas of Zambia than in the northern (3.0% and 3.0%) area of this country. There was little difference among the three areas in the distribution of antibodies against R. typhi. Since cattle breeding is more extensive in the western and eastern areas than in the northern area, it is thought that cattle-breeding areas are foci of R. conorii and C. burnetii infections in Zambia. (+info
Coxiella burnetii pericarditis: report of 15 cases and review.
Q fever is characterized by its clinical polymorphism, and pericarditis associated with Q fever has occasionally been described. Herein we report 15 cases of Coxiella burnetii pericarditis, 9 from our data bank and 6 encountered within the past 12 months. Three patients presented with life-threatening tamponade. We compare our cases with the 18 previously reported and with 60 Q fever-matched controls at our center. This study showed that Q fever pericarditis can present as acute as well as chronic disease; we describe relapse after 6 months in association with a serological profile compatible with the chronic form of disease (phase I C. burnetii IgG titer of > or = 800). Discriminant factors among patients and controls are age of > 52 years (adjusted odds ratio [OR], 5.66), the occurrence of general symptoms such as arthralgias or myalgias (adjusted OR, 6.54), and a normal erythrocyte sedimentation rate (adjusted OR, 16.37). No specific symptoms or underlying cardiac predispositions are observed. (+info
Q fever is a zoonosis with a worldwide distribution with the exception of New Zealand. The disease is caused by Coxiella burnetii, a strictly intracellular, gram-negative bacterium. Many species of mammals, birds, and ticks are reservoirs of C. burnetii in nature. C. burnetii infection is most often latent in animals, with persistent shedding of bacteria into the environment. However, in females intermittent high-level shedding occurs at the time of parturition, with millions of bacteria being released per gram of placenta. Humans are usually infected by contaminated aerosols from domestic animals, particularly after contact with parturient females and their birth products. Although often asymptomatic, Q fever may manifest in humans as an acute disease (mainly as a self-limited febrile illness, pneumonia, or hepatitis) or as a chronic disease (mainly endocarditis), especially in patients with previous valvulopathy and to a lesser extent in immunocompromised hosts and in pregnant women. Specific diagnosis of Q fever remains based upon serology. Immunoglobulin M (IgM) and IgG antiphase II antibodies are detected 2 to 3 weeks after infection with C. burnetii, whereas the presence of IgG antiphase I C. burnetii antibodies at titers of >/=1:800 by microimmunofluorescence is indicative of chronic Q fever. The tetracyclines are still considered the mainstay of antibiotic therapy of acute Q fever, whereas antibiotic combinations administered over prolonged periods are necessary to prevent relapses in Q fever endocarditis patients. Although the protective role of Q fever vaccination with whole-cell extracts has been established, the population which should be primarily vaccinated remains to be clearly identified. Vaccination should probably be considered in the population at high risk for Q fever endocarditis. (+info