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https://hdl.handle.net/2440/17156
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Type: | Journal article |
Title: | Long-term persistence of Coxiella burnetii after acute primary Q fever |
Author: | Marmion, B. Storm, P. Ayres, J. Semendric, L. Mathews, L. Winslow, W. Turra, M. Harris, R. |
Citation: | QJM: an international journal of medicine, 2005; 98(1):7-20 |
Publisher: | Oxford Univ Press |
Issue Date: | 2005 |
ISSN: | 1460-2725 1460-2393 |
Statement of Responsibility: | B.P. Marmion, P.A. Storm, J.G. Ayres, L. Semendric, L. Mathews, W. Winslow, M. Turra and R.J. Harris |
Abstract: | <h4>Background</h4>Long-term persistence of C. burnetii in infected animals was established in the 1950s and 60s, but the implications for human Q fever are not fully explored.<h4>Aim</h4>To compare the prevalence of markers of infection in a cohort of Q fever patients in Australia (up to 5 years after infection) with those in the 1989 Birmingham cohort (12 years after infection).<h4>Design</h4>Case follow-up study.<h4>Methods</h4>C. burnetii was tested for by: (i) antibodies to Phase 1 and 2 antigens in the three immunoglobulin classes; (ii) detection of DNA in bone marrow and peripheral blood mononuclear cells by PCR assays directed against several different targets in the genome; and (iii) attempts to isolate coxiellas in cell culture or mice from PCR-positive samples. Amplicon specificity was verified by fluorometric probing and by sequencing. Cross-contamination was excluded by extensive use of non-template controls, and in particular by the use of certain IS1111a target sequences.<h4>Results</h4>Irrespective of clinical state, both groups remained seropositive, principally exhibiting medium levels of IgG antibody against C. burnetii Phase 2 antigen. C. burnetii genomic DNA was detected by PCR in 65% of bone marrow aspirates from Australian patients and approximately 88% of Birmingham patients. No coxiella were isolated from PCR positive samples.<h4>Discussion</h4>We propose a provisional model for persistence. In Q fever without sequelae, the process is largely confined to the bone marrow. In Q fever fatigue syndrome (QFS), it is modulated by the patient's immunogenetic background to give higher levels of coxiella genomes in bone marrow and increased shedding into the peripheral blood. In Q fever endocarditis, late pregnancy, or during iatrogenic or other immunosuppression, the multiplication cycle is prolonged, and a potential source of live organisms. |
Keywords: | Liver Leukocytes, Mononuclear Cells, Cultured Bone Marrow Animals Mice, Knockout Humans Mice Coxiella burnetii Q Fever DNA, Bacterial Antibodies, Bacterial Antigens, Bacterial Follow-Up Studies Polymerase Chain Reaction Carrier State |
DOI: | 10.1093/qjmed/hci037 |
Published version: | http://dx.doi.org/10.1093/qjmed/hci009 |
Appears in Collections: | Aurora harvest 6 Pathology publications |
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