Herpes zoster-related deaths in the United States: validity of death certificates and mortality rates, 1979-2007.

BACKGROUND: Herpes zoster (HZ) vaccine was recommended in the United States to reduce HZ-associated morbidity. Vaccination may reduce HZ-associated mortality, but no strategy exists to monitor mortality trends. METHODS: We validated HZ coding on death certificates from California, using hospital records as the gold standard, and applied the results to national-level data to estimate HZ mortality. RESULTS: In the validation phase of the study, among 40 available hospital records listing HZ as the underlying cause of death, HZ was the underlying cause for 21 (52.5%) and a contributing cause for 5 (12.5%). Among the 21 hospital records listing HZ as the underlying cause of death, the median age of decedents was 84 years (range, 50-99); 60% had no contraindications for HZ vaccination. Of the 37 available records listing HZ as a contributing cause of death, HZ was a contributing cause for 2 (5.4%) and the underlying cause for 6 (16.2%). Nationally, in the 7 years preceding the HZ vaccination program, the average annual number of deaths in which HZ was reported as the underlying cause of death was 149; however, based on our validation study, we estimate the true number was 78 (range, 31-118). CONCLUSIONS: National death certificate data greatly overestimate deaths in which HZ is the underlying or contributing cause of death. The HZ vaccination program could prevent some HZ-related deaths, but the impact will be difficult to assess using national mortality data.

Evidence of Borrelia autoimmunity-induced component of Lyme carditis and arthritis.

We investigated the possibility that manifestations of Lyme disease in certain hosts, such as arthritis and carditis, may be autoimmunity mediated due to molecular mimicry between the bacterium Borrelia burgdorferi and self-components. We first compared amino acid sequences of Streptococcus pyogenes M protein, a known inducer of antibodies that are cross-reactive with myosin, and B. burgdorferi and found significant homologies with OspA protein. We found that S. pyogenes M5-specific antibodies and sera from B. burgdorferi-infected mice reacted with both myosin and B. burgdorferi proteins by Western blots and enzyme-linked immunosorbent assay. To investigate the relationship between self-reactivity and the response to B. burgdorferi, NZB mice, models of autoimmunity, were infected. NZB mice infected with B. burgdorferi developed higher degrees of joint swelling and higher anti-B. burgdorferi immunoglobulin M cross-reactive responses than other strains with identical major histocompatibility complex (DBA/2 and BALB/c). These studies reveal immunological cross-reactivity and suggest that B. burgdorferi may share common epitopes which mimic self-proteins. These implications could be important for certain autoimmunity-susceptible individuals or animals who become infected with B. burgdorferi.