C C H Wielders1, P F M Teunis2, M H A Hermans3, W van der Hoek4, P M Schneeberger5. 1. Department of Medical Microbiology and Infection Control, Jeroen Bosch Hospital, P.O. Box 90153, 5200 ME 's-Hertogenbosch, The Netherlands; Centre for Infectious Disease Control, National Institute for Public Health and the Environment (RIVM), P.O. Box 1, 3720 BA Bilthoven, The Netherlands. 2. Centre for Infectious Disease Control, National Institute for Public Health and the Environment (RIVM), P.O. Box 1, 3720 BA Bilthoven, The Netherlands; Hubert Department of Global Health, Rollins School of Public Health, Emory University, 1518 Clifton Road, Atlanta, GA 30322, USA. 3. Laboratory for Molecular Diagnostics, Jeroen Bosch Hospital, P.O. Box 90153, 5200 ME 's-Hertogenbosch, The Netherlands. 4. Centre for Infectious Disease Control, National Institute for Public Health and the Environment (RIVM), P.O. Box 1, 3720 BA Bilthoven, The Netherlands. 5. Department of Medical Microbiology and Infection Control, Jeroen Bosch Hospital, P.O. Box 90153, 5200 ME 's-Hertogenbosch, The Netherlands; Centre for Infectious Disease Control, National Institute for Public Health and the Environment (RIVM), P.O. Box 1, 3720 BA Bilthoven, The Netherlands. Electronic address: p.schneeberger@jbz.nl.
Abstract
BACKGROUND: From 2007 to 2009, the Netherlands experienced a major Q fever epidemic. Long-term serological follow-up of acute Q fever patients enabled the investigation of longitudinal antibody responses and estimating the onset of the seroresponse in individual patients. METHODS: All available IgG and IgM phase I and II antibody measurements determined by immunofluorescence assay at month 3, 6, 12, and 48 from 2321 acute Q fever patients were retrospectively analyzed. Characteristic features of the antibody response were calculated. To model the seroresponse onset, serological data from patients diagnosed with a positive C. burnetii PCR test (n=364), and therefore with a known time of infection, were used as reference. RESULTS: In 9083 IgG samples and 3260 IgM samples large heterogeneity in shape and magnitude of antibody responses was observed. Phase II reached higher levels than phase I, and IgG antibodies were more persistent than IgM. The estimated seroresponse latency allowed for determining the time since start of the seroresponse from the concentrations of the different antibodies against C. burnetii. CONCLUSIONS: The extraordinary large serological dataset provides new insight into the kinetics of the immunoglobulins against C. burnetii antigens. This knowledge is useful for seroprevalence studies and helps to better understand infection dynamics.
BACKGROUND: From 2007 to 2009, the Netherlands experienced a major Q fever epidemic. Long-term serological follow-up of acute Q feverpatients enabled the investigation of longitudinal antibody responses and estimating the onset of the seroresponse in individual patients. METHODS: All available IgG and IgM phase I and II antibody measurements determined by immunofluorescence assay at month 3, 6, 12, and 48 from 2321 acute Q feverpatients were retrospectively analyzed. Characteristic features of the antibody response were calculated. To model the seroresponse onset, serological data from patients diagnosed with a positive C. burnetii PCR test (n=364), and therefore with a known time of infection, were used as reference. RESULTS: In 9083 IgG samples and 3260 IgM samples large heterogeneity in shape and magnitude of antibody responses was observed. Phase II reached higher levels than phase I, and IgG antibodies were more persistent than IgM. The estimated seroresponse latency allowed for determining the time since start of the seroresponse from the concentrations of the different antibodies against C. burnetii. CONCLUSIONS: The extraordinary large serological dataset provides new insight into the kinetics of the immunoglobulins against C. burnetii antigens. This knowledge is useful for seroprevalence studies and helps to better understand infection dynamics.
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