QJM vol. 98 no. 1 © Association of Physicians 2005; all rights reserved.
Long-term persistence of Coxiella burnetii after acute primary Q fever
From the 1Q Fever Research Group, Infectious Diseases Laboratories, IMVS and Hanson Institute, Adelaide, South Australia, and 2Department of Respiratory Medicine, Heartlands Hospital, Birmingham, UK
Received 30 June 2004 and in revised form 27 October 2004
Background: 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.
Aim: 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).
Design: Case follow-up study.
Methods: 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.
Results: 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 
88% of Birmingham patients. No coxiella were isolated from PCR positive samples.
Discussion: 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.
Address correspondence to Professor B.P. Marmion, 14 Birksgate Drive, Urrbrae, South Australia 5064. e-mail: chris.nikolaou{at}imvs.sa.gov.au
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