Long term persistence of Coxiella burnetii after acute primary Q fever

B. P. Marmion, P. A. Storm, Jonathan Geoffrey Ayres, L. Semendric, R. J. Harris

    Research output: Contribution to journalArticle

    80 Citations (Scopus)

    Abstract

    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 similar to88% 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 patients immunogenetic back-round to give higher levels of coxiella genomes in bone marrow and increased shedding into the peripheral blood. In Q fever endocarditis, late pregnancy, of during iatrogenic or other immunosuppression, the multiplication cycle is prolonged, and a potential source of live organisms.

    Original languageEnglish
    Pages (from-to)7-20
    Number of pages13
    JournalQJM
    Volume98
    Issue number1
    DOIs
    Publication statusPublished - Jan 2005

    Keywords

    • CHRONIC-FATIGUE-SYNDROME
    • CROHNS-DISEASE
    • HIV-INFECTION
    • ENDOCARDITIS
    • RESPONSES
    • PARATUBERCULOSIS
    • SEQUENCE
    • STRAINS
    • CULTURE
    • PATIENT

    Cite this

    Marmion, B. P., Storm, P. A., Ayres, J. G., Semendric, L., & Harris, R. J. (2005). Long term persistence of Coxiella burnetii after acute primary Q fever. QJM, 98(1), 7-20. https://doi.org/10.1093/qjmed/hci009

    Long term persistence of Coxiella burnetii after acute primary Q fever. / Marmion, B. P.; Storm, P. A.; Ayres, Jonathan Geoffrey; Semendric, L.; Harris, R. J.

    In: QJM, Vol. 98, No. 1, 01.2005, p. 7-20.

    Research output: Contribution to journalArticle

    Marmion, BP, Storm, PA, Ayres, JG, Semendric, L & Harris, RJ 2005, 'Long term persistence of Coxiella burnetii after acute primary Q fever', QJM, vol. 98, no. 1, pp. 7-20. https://doi.org/10.1093/qjmed/hci009
    Marmion BP, Storm PA, Ayres JG, Semendric L, Harris RJ. Long term persistence of Coxiella burnetii after acute primary Q fever. QJM. 2005 Jan;98(1):7-20. https://doi.org/10.1093/qjmed/hci009
    Marmion, B. P. ; Storm, P. A. ; Ayres, Jonathan Geoffrey ; Semendric, L. ; Harris, R. J. / Long term persistence of Coxiella burnetii after acute primary Q fever. In: QJM. 2005 ; Vol. 98, No. 1. pp. 7-20.
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    abstract = "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 similar to88{\%} 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 patients immunogenetic back-round to give higher levels of coxiella genomes in bone marrow and increased shedding into the peripheral blood. In Q fever endocarditis, late pregnancy, of during iatrogenic or other immunosuppression, the multiplication cycle is prolonged, and a potential source of live organisms.",
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    T1 - Long term persistence of Coxiella burnetii after acute primary Q fever

    AU - Marmion, B. P.

    AU - Storm, P. A.

    AU - Ayres, Jonathan Geoffrey

    AU - Semendric, L.

    AU - Harris, R. J.

    PY - 2005/1

    Y1 - 2005/1

    N2 - 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 similar to88% 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 patients immunogenetic back-round to give higher levels of coxiella genomes in bone marrow and increased shedding into the peripheral blood. In Q fever endocarditis, late pregnancy, of during iatrogenic or other immunosuppression, the multiplication cycle is prolonged, and a potential source of live organisms.

    AB - 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 similar to88% 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 patients immunogenetic back-round to give higher levels of coxiella genomes in bone marrow and increased shedding into the peripheral blood. In Q fever endocarditis, late pregnancy, of during iatrogenic or other immunosuppression, the multiplication cycle is prolonged, and a potential source of live organisms.

    KW - CHRONIC-FATIGUE-SYNDROME

    KW - CROHNS-DISEASE

    KW - HIV-INFECTION

    KW - ENDOCARDITIS

    KW - RESPONSES

    KW - PARATUBERCULOSIS

    KW - SEQUENCE

    KW - STRAINS

    KW - CULTURE

    KW - PATIENT

    U2 - 10.1093/qjmed/hci009

    DO - 10.1093/qjmed/hci009

    M3 - Article

    VL - 98

    SP - 7

    EP - 20

    JO - QJM

    JF - QJM

    SN - 1460-2725

    IS - 1

    ER -