miércoles, 1 de febrero de 2012

Declining Guillain-Barré Syndrome after Campylobacteriosis Control, New Zealand, 1988–2010 - Vol. 18 No. 2 - February 2012 - Emerging Infectious Disease journal - CDC

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Declining Guillain-Barré Syndrome after Campylobacteriosis Control, New Zealand, 1988–2010 - Vol. 18 No. 2 - February 2012 - Emerging Infectious Disease journal - CDC



Volume 18, Number 2—February 2012

CME ACTIVITY

Declining Guillain-Barré Syndrome after Campylobacteriosis Control, New Zealand, 1988–2010

Michael G. BakerComments to Author , Amanda Kvalsvig, Jane Zhang, Rob Lake, Ann Sears, and Nick Wilson
Author affiliations: University of Otago, Wellington, New Zealand (M.G. Baker, A. Kvalsvig, J. Zhang, A. Sears, N. Wilson); Institute of Environmental Science and Research, Christchurch, New Zealand (R. Lake)
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Abstract

Infection with Campylobacter spp. commonly precedes Guillain-Barré syndrome (GBS). We therefore hypothesized that GBS incidence may have followed a marked rise and then decline in campylobacteriosis rates in New Zealand. We reviewed records for 1988–2010: hospitalization records for GBS case-patients and campylobacteriosis case-patients plus notifications of campylobacteriosis. We identified 2,056 first hospitalizations for GBS, an average rate of 2.32 hospitalizations/100,000 population/year. Annual rates of hospitalization for GBS were significantly correlated with rates of notifications of campylobacteriosis. For patients hospitalized for campylobacteriosis, risk of being hospitalized for GBS during the next month was greatly increased. Three years after successful interventions to lower Campylobacter spp. contamination of fresh poultry meat, notifications of campylobacteriosis had declined by 52% and hospitalizations for GBS by 13%. Therefore, regulatory measures to prevent foodborne campylobacteriosis probably have an additional health and economic benefit of preventing GBS.
Guillain-Barré syndrome (GBS) is an autoimmune condition that affects the peripheral nervous system. Patients typically describe ascending weakness and sensory disturbance that evolve over several days; during this acute phase, approximately one third of patients require ventilatory support. The condition is generally self-limiting, but for 3%–10% of patients, it is fatal (1).
An estimated 40%–70% of patients with GBS had an infection before GBS onset; for 6%–39% of these patients, the infection affected the gastrointestinal system (2). Campylobacteriosis is the most commonly identified antecedent infection; several studies have shown that in industrialized countries (Europe, North and South America, Japan, and Australia), Campylobacter spp. infection preceded GBS for 20%–50% of patients (3,4).
During 1980–2006 in New Zealand, incidence of campylobacteriosis steadily increased. The notification rate in 2006 (379 cases/100,000 population) remains the highest national rate reported in the literature (5,6). In 2006, in response to this high incidence, New Zealand introduced an array of voluntary and regulatory interventions to reduce contamination of poultry with Campylobacter spp (7). By 2008, the rate of campylobacteriosis notifications had dropped to 157 cases/100,000 population, a decrease of 59% over 2 years (7); this decline has persisted (8). Given the known association between Campylobacter spp. infection and GBS and the marked recent changes in reported rates of campylobacteriosis in New Zealand, we examined GBS hospitalization data for evidence of responsiveness to trends in campylobacteriosis incidence.

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