Campylobacteriosis Decline, New Zealand | CDC EID

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Volume 17, Number 6–June 2011
Research
Marked Campylobacteriosis Decline after Interventions Aimed at Poultry, New Zealand
Ann Sears, Michael G. Baker, Nick Wilson, Jonathan Marshall, Petra Muellner, Donald M. Campbell, Robin J. Lake, and Nigel P. French
Author affiliations: University of Otago, Wellington, New Zealand (A. Sears, M.G. Baker, N. Wilson); Massey University, Palmerston North, New Zealand (J. Marshall, P. Muellner, N.P. French); New Zealand Food Safety Authority, Wellington (D.M. Campbell); and Institute of Environmental Science and Research Ltd, Christchurch, New Zealand (R.J. Lake)


Suggested citation for this article

Abstract
Beginning in the 1980s, New Zealand experienced rising annual rates of campylobacteriosis that peaked in 2006. We analyzed notification, hospitalization, and other data to explore the 2007–2008 drop in campylobacteriosis incidence. Source attribution techniques based on genotyping of Campylobacter jejuni isolates from patients and environmental sources were also used to examine the decline. In 2008, the annual campylobacteriosis notification rate was 161.5/100,000 population, representing a 54% decline compared with the average annual rate of 353.8/100,000 for 2002–2006. A similar decline was seen for hospitalizations. Source attribution findings demonstrated a 74% (95% credible interval 49%–94%) reduction in the number of cases attributed to poultry. These reductions coincided with the introduction of a range of voluntary and regulatory interventions to reduce Campylobacter spp. contamination of poultry. The apparent success of these interventions may inform approaches other countries could consider to help control foodborne campylobacteriosis.

Campylobacteriosis is a common bacterial gastroenteritis reported in New Zealand and many other industrialized countries, with most cases caused by Campylobacter jejuni (1,2). Campylobacteriosis has been a notifiable disease in New Zealand since 1980, and medical practitioners are required to report confirmed or suspected cases to their local public health service (3). Campylobacteriosis notifications rose steadily after campylobacteriosis first became notifiable and peaked in 2006 at >380 per 100,000 population (4). A concomitant increase in campylobacteriosis hospitalizations has been noted, which suggests this rise in notifications is unlikely to be artifactual (3,5).

To help inform prevention and control strategies, research efforts have been directed at establishing the likely contributors to this rise in campylobacteriosis incidence. Consistent with international findings (6–8), New Zealand investigations implicated poultry meat as a significant source of foodborne sporadic campylobacteriosis (9–13). A relatively small case–control study in Christchurch in 1992–1993 reported several poultry-associated risk factors, including consumption of undercooked poultry (10). A larger national case–control study in 1994–1995 reported similar findings, with a combined population-attributable risk of poultry-related exposures >50% (9). A systematic review also concluded that poultry consumption was a prominent risk factor for sporadic campylobacteriosis in New Zealand (11). Reports noted the rise in campylobacteriosis was closely correlated with an increase in consumption of fresh poultry (14).

Microbiological source attribution approaches have also been used to estimate the contribution of different sources and transmission pathways of campylobacteriosis in New Zealand. These techniques involve examining the epidemiology of campylobacteriosis at the genotype level by comparing C. jejuni genotypes from humans with those found in a range of food and environmental sources. In 2005, a major source attribution study for campylobacteriosis was initiated at a sentinel surveillance site in the Manawatu region of New Zealand (12). C. jejuni isolates from cases notified in the region were genotyped by using multilocus sequence typing (MLST) and compared with isolates recovered from food and environmental sources (12,13). Statistical modeling was used to apportion human cases to potential disease sources, thereby estimating each source's relative importance (13,15,16). This modeling revealed that >50% of sporadic campylobacteriosis cases in the region were attributable to poultry (12,13).

On the basis of these findings, public health professionals advocated for more rigorous controls on foodborne pathways of campylobacteriosis, particularly for poultry (5,14). One intervention promoted was the freezing of fresh poultry meat to reduce levels of Campylobacter spp. contamination, with fresh poultry allowed to be sold only when it could be shown to pose a low risk to human health (5,14). In late 2006, the New Zealand Food Safety Authority (NZFSA) released a risk management strategy for reducing incidence of poultry-associated foodborne campylobacteriosis.

New Zealand has a highly integrated, closed system of poultry production, with all poultry meat available for retail sale being of domestic origin. Processors of poultry meat control most aspects of production, processing, and distribution; 3 processing companies supply >90% of chicken meat consumed in New Zealand (2). As a result, interventions applied to the local poultry industry affect all domestically consumed poultry.

A marked decline in campylobacteriosis notifications was observed during 2007 and 2008 (17). We investigated this decline to assess whether it was causally related to the poultry-focused food safety interventions.

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Campylobacteriosis Decline, New Zealand | CDC EID


Suggested Citation for this Article
Sears A, Baker MG, Wilson N, Marshall J, Muellner P, Campbell DM, et al. Marked campylobacteriosis decline after interventions aimed at poultry, New Zealand. Emerg Infect Dis [serial on the Internet]. 2011 Jun [date cited]. http://www.cdc.gov/EID/content/17/6/1007.htm

DOI: 10.3201/eid1706.101272


Comments to the Authors
Please use the form below to submit correspondence to the authors or contact them at the following address:

Michael G. Baker, University of Otago, Box 7343, Wellington 6242, New Zealand; email: michael.baker@otago.ac.nz