1325. Natural Immunity Against Invasive Haemophilus influenzae Type A Among Aboriginal Chronic Renal Failure Patients Undergoing Haemodialysis Therapy
Session: Poster Abstract Session: Biomarkers and Correlates of Protection
Saturday, October 5, 2013
Room: The Moscone Center: Poster Hall C
Posters
  • IDWEEK 2013 mini2.pdf (270.6 kB)
  • Background:

    Haemophilus influenzae type b (Hib) was a major cause of invasive bacterial infections such as sepsis and meningitis in children prior to the introduction of a conjugate vaccine.  In the post-Hib vaccine era, non type b serotypes have emerged as significant agents of invasive H. influenzae disease.  Anti-capsular polysaccharide antibodies are the major defence mechanism against invasive infection.  Although invasive disease caused by H. influenzae type a (Hia) is rare, some North American indigenous populations in Alaska, the Arctic and northwestern Ontario (Canada) suffer from high rates of invasive attack relative to the general population. The basis of high rates of infection among certain populations remains unexplained.  However, nearly all adult cases involve patients suffering from a secondary immunodeficiency due to an underlying condition such as chronic renal failure (CRF).  Hia is spread via aerosols and may colonize without causing illness.  As a result individuals may develop natural immunity through asymptomatic carriage while acting as a reservoir for populations vulnerable to infection.

    Methods:

    CRF patients on haemodialysis therapy were categorized as either Aboriginal (n=30) or non-Aboriginal (n=30) and compared with each other as well as their respective healthy controls.  Natural immunity was assessed by measuring the quantity of anti-Hia IgG and the functional activity of antibodies via a serum bactericidal assay (SBA).

    Results:

    Overall, Hia SBA titres were lower in CRF patients compared to controls, i.e.  Geometric mean (95% confidence interval) of 78.2 (42.48-143.9) versus 267.3 (196.1-364.1), p=0.0002.  Aboriginal CRF patients had higher Hia SBA titres: 226.5 (120-426.7) than non-Aboriginal patients: 40.9 (17.7-94.8), p=0.033.  The Aboriginal CRF group also showed higher anti-Hia IgG antibody levels compared to non-Aboriginal patients: 1.23 µg/ml (0.85-1.77) versus 0.66 µg/ml (0.46-0.93), p=0.02.  Aboriginal healthy controls exhibited higher Hia SBA titres compared to non-Aboriginal controls: 371.6 (250-552.3) versus 178.1 (109-291), p=0.007, respectively.

    Conclusion:

    Our results suggest a high rate of Hia circulation within Aboriginal communities rather than an inadequate response to Hia polysaccharide as a major factor contributing to the elevated rates of Hia disease in this population.

    Eli Nix, PhD1, Kylie Williams1, Andrew Cox, PhD2, Frank St. Michael2, William Mccready, MD1 and Marina Ulanova, MD, PhD1, (1)Northern Ontario School of Medicine, Thunder Bay, ON, Canada, (2)National Research Council, Ottawa, ON, Canada

    Disclosures:

    E. Nix, None

    K. Williams, None

    A. Cox, None

    F. St. Michael, None

    W. Mccready, None

    M. Ulanova, None

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