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Background: Q fever caused by Coxiella burnetii is transmitted to humans by inhalation of aerosols from animal birth products. Q fever in pregnancy is suspected to be a potential cause of fetal and maternal morbidity and fetal mortality but the pathogenesis is poorly understood, and even in Q fever endemic areas, the magnitude of a potential association is not established.We aimed to examine if presence of antibodies to C. burnetii during pregnancy or seroconversion were associated with adverse pregnancy outcomes., Methods: The Danish National Birth Cohort collected blood samples and interview data from 100,418 pregnant women (1996-2002). We sampled 397 pregnant women with occupational or domestic exposure to cattle or sheep and a random sample of 459 women with no animal exposure. Outcome measures were spontaneous abortion, preterm birth, birth weight and Small for Gestational Age (SGA).Blood samples collected in pregnancy were screened for antibodies against C. burnetii by enzyme-linked immunosorbent assay (ELISA). Samples positive for IgG or IgM antibodies in the ELISA were confirmed by immunofluorescence antibody test (IFA)., Results: Among the 856 women, 169 (19.7%) women were IFA positive; 147 (87%) of these had occupational or domestic contact with livestock (IFA cutoff > =1:128).Two abortions were IFA positive vs. 6 IFA negative (OR: 1.5; 95%CI: 0.3-7.6). Three preterm births were IFA positive vs. 38 IFA negative (OR: 0.4; 95% CI: 0.1-1.1). There was a significant difference in birth weight of 168 g (95% CI: 70-267 g) with IFA positive being heavier, and the risk of being SGA was not increased in the newborns of IFA positive women (OR: 0.4; 95%CI: 0.8-1.0).Most seropositive women were IgG positive indicating previous exposure. Seroconversion during pregnancy was found in 10 women; they all delivered live babies at term, but two were SGA., Conclusion: We found no increased risk of adverse pregnancy outcome in women with verified exposure to C. burnetii.To our knowledge, this is the first population-based seroepidemiologic study evaluating pregnancy outcome in women with serologically verified exposure to C. burnetii against a comparable reference group of seronegative women.

Background: Q fever is a zoonosis caused by Coxiella burnetii. The disease is emerging in many parts of the world, likely in part due to increased awareness and the availability of better diagnostic tests. The clinical diagnosis of Q fever is difficult, and most confirmed cases rely on serology., Methods: This study compared the sensitivity, specificity, and performance of 2 commercial enzyme-linked immunosorbent assay (ELISA) kits, with a commercial microimmunofluorescence antibody test (IFA) used as reference., Results: One of the ELISA kits showed a higher sensitivity and a lower cross-reactivity than the other kit. Likewise, the same kit was superior when comparing the area under the receiver operating characteristic curves., Conclusions: The results support the continued use of IFA as a primary serological test for Q fever; for large numbers of samples, an ELISA kit can be used as a screening tool, if followed by a confirmatory IFA test.

Q fever is a ubiquitous zoonosis caused by Coxiella burnetii. The disease is emerging in many parts of the world, likely because of increased awareness and availability of better diagnostics. The diagnosis is primarily based on serology. Because the prevalence of the disease varies worldwide, the establishment of local cutoff values is needed. A baseline for antibodies against C. burnetii in Denmark was defined by testing sera from healthy Danish volunteers using a commercially available immunofluorescence antibody test. Cross-reactivity was studied on sera obtained from patients experiencing clinically related diseases. The cutoff titers suggested by the manufacturer were found to result in very low specificity of the test. The specificity was, however, effectively increased by using cutoff titers based on the local baseline and equal to immunoglobulin M (IgM) phase I > or =128, IgM phase II > or =256, IgG phase I > or =512, and IgG phase II > or =1024.