8th July 2011, Volume 124 Number 1337

Michael G Baker, Ann Sears, Nick Wilson, Nigel French, Jonathan Marshall, Petra Muellner, Donald Campbell, Peter van der Logt, Rob Lake

This letter was prompted by a recent paper in the Journal on the epidemiology of campylobacteriosis by Nelson and Harris,1 which we consider distracts from the key issues related to the control of this disease. We also wish to provide an update on the recent decline in campylobacteriosisincidence in New Zealand following successful food safety interventions targeting contaminated poultry.2

In their paper, Nelson and Harris query “...the popular assumption that poultry is the primary source for human campylobacteriosis...”. They also question whether the decline in human cases could be associated with the recently implemented “chicken health scheme”.1

There is however overwhelming evidence that contaminated poultry has been the dominant source for human campylobacteriosis in New Zealand for many years.3-6 In particular, multilocus subtyping techniques have shown that poultry-associated subtypes of Campylobacter are the main contributors to sporadic campylobacteriosis in this country.6 On the basis of this evidence, public health professionals have advocated for more rigorous controls on foodborne pathways of campylobacteriosis, particularly poultry.7

The recent decline in New Zealand’s campylobacteriosis epidemic is further evidence of the dominant role of poultry as the major source. This decline occurred during the second half of 2007, with the 2008 notification and hospitalisation rates >50% lower than the annual average rates for 2002–2006 (Figure 1).2

Our research indicates that this improvement is almost certainly attributable to the implementation of food safety interventions aimed at reducing Campylobacter contamination of poultry, and provides evidence of the success of these interventions.2, 8, 9

In their paper, Nelson and Harris also query the timing of this decline in relation to the implementation of Campylobacter control strategies aimed at poultry.1 They ask the question “If chicken-consumption is truly the source for most cases, why did rates generally decrease in 2007, before the chicken health scheme began...?”. In fact, the New Zealand Food Safety Authority (NZFSA, now the Ministry of Agriculture and Forestry) introduced its first ‘Campylobacter in Poultry Risk Management Strategy’ in August 2006, prior to the decline in human cases. This strategyoutlined a range of voluntary and regulatory interventions to reduce Campylobactercontamination of poultry, which were implemented progressively through 2007 and 2008.

It is important to note that the “chicken health scheme” referred to by the authors was a public health intervention to improve human not animal health, with Campylobacter being a commensal in chickens and not affecting animal health.


Figure 1. Campylobacteriosis notification rates per 100,000 population by year, 1988–2010, and hospitalisation rates per 100,000 population by year, 1996–2010, New Zealand

Baker-1


From April 2007, poultry processors were required to report Campylobacter contamination levels on poultry at the end of primary processing to NZFSA’s National Microbiological Database. From April 2008, mandatory Campylobacter performance targets were introduced, with NZFSA setting maximum limits for Campylobacter contamination on poultry carcasses at the end of primary processing.10

Even before these requirements were in place, the poultry industry had begun monitoringCampylobacter levels, with the proportion of poultry carcasses with detectable Campylobactercounts decreasing from 63.3% in October 2006 to 39.8% in November 2007.11 Therefore, the timing of the decline in human campylobacteriosis is consistent with the implementation of food safety interventions targeting poultry.

Source attribution modelling (based on multilocus subtyping of Campylobacter) provides probably the most definitive evidence that the decline in human campylobacteriosis can be largely attributed to a reduction in infection arising from poultry (Figure 2).2,9

In the pre-intervention period, over 70% of human cases were attributable to poultry, whereas in the post-intervention years, 2008 through to 2010, this estimate declined to 50%, due to an absolute decline in poultry attributable cases.9 Despite the relative increase in the contribution of ruminant sources to human cases, poultry remains the most important source of human infection in the Manawatu (the sentinel site for the source attribution study).2


Figure 2. Poultry, ruminant (combined sheep and cattle) and other source attribution estimates for human cases in the Manawatu for five 12-month periods, 1 July 2005–30 June 2010. Pre-intervention years are shown in red, the transition year in blue, and the post-intervention years in green

Baker-2


Campylobacter is a multi-host pathogen, which amplifies in food-producing animals and wildlife without any evidence of disease in animals. This characteristic provides challenges for the control of human campylobacteriosis. However, there is a clear hierarchy in the relative importance of sources of human disease, with poultry sources identified as being the greatest contributor to human cases.6,12

On this basis, we do not think it is justifiable for authors such as Nelson and Harris to argue that the epidemiology of campylobacteriosis in New Zealand is a complex mystery or that there is an unknown “substantial underlying factor” driving our epidemic.

Now that the burden of disease from contaminated poultry has reduced we are beginning to develop a picture of other sources and vulnerable groups. Such groups include children living in rural areas as we have previously reported.2 More research is underway in New Zealand, in addition to the extensive literature already published, examining the contribution of other, albeit less important, sources. An updated Campylobacter Risk Management Strategy has also been released.10

New Zealand still has one of the highest campylobacteriosis rates among developed countries,8and source attribution studies continue to show that poultry remains the dominant source.9 This situation suggests that ongoing efforts are required by poultry producers, with the support of regulators and researchers, to further reduce the disease burden from this source.

Michael G Baker, Ann Sears, Nick Wilson
Department of Public Health, University of Otago, Wellington
michael.baker@otago.ac.nz

Nigel French, Jonathan Marshall
mEpiLab, Massey University, Palmerston North

Petra Muellner
mEpiLab, Massey University, Palmerston North / Epi-interactive, Wellington

Donald Campbell, Peter van der Logt
Ministry of Agriculture and Forestry (formerly New Zealand Food Safety Authority) Wellington

Rob Lake
Institute of Environmental Science and Research Ltd, Christchurch

Author Information

Michael G Baker, Ann Sears, Nick Wilson, Department of Public Health, University of Otago, Wellington, Nigel French, Jonathan Marshall, mEpiLab, Massey University, Palmerston North, Petra Muellner, mEpiLab, Massey University, Palmerston North / Epi-interactive, Wellington, Donald Campbell, Peter van der Logt, Ministry of Agriculture and Forestry (formerly New Zealand Food Safety Authority) Wellington, Rob Lake, Institute of Environmental Science and Research Ltd, Christchurch

Correspondence Email

michael.baker@otago.ac.nz

References

  1. Nelson W, Harris B. Campylobacteriosis rates show age-related static bimodal and seasonality trends. N Z Med J. 2011; 124(1337):33-9.
  2. Sears A, Baker MG, Wilson N, Marshall J, Mueller P, Campbell D, et al. Marked Campylobacteriosis Decline After Interventions Aimed at Poultry, New Zealand. Emerg Infect Dis. 2011; 17(6):1007 - 15.
  3. Baker M, Wilson N. The compelling case for urgent action to control New Zealand's foodborne campylobacteriosis epidemic. Proceedings of the Food Safety, Animal Welfare and Biosecurity Branch of the NZVA. 2007; 265:67–76.
  4. Wilson N. A systematic review of the aetiology of human campylobacteriosis in New Zealand (Report to the Food Safety Authority of New Zealand). Wellington: Food Safety Authority of New Zealand; 2005; Available from:http://www.foodsafety.govt.nz/elibrary/industry/Systematic_Review-Literature_Evidence.pdf
  5. Eberhart-Phillips J, Walker N, Garrett N, Bell D, Sinclair D, Rainger W, et al. Campylobacteriosis in New Zealand: results of a case-control study. J Epidemiol Community Health. 1997; 51(6):686–91.
  6. Müllner P, Spencer S, Wilson D, Jones G, Noble A, Midwinter A, et al. Assigning the source of human campylobacteriosis in New Zealand: A comparative genetic and epidemiological approach. Infect Genet Evol. 2009; 9:1311–9.
  7. Baker M, Wilson N, Ikram R, Chambers S, Shoemack P, Cook G. Regulation of chicken contamination is urgently needed to control New Zealand's serious campylobacteriosis epidemic. N Z Med J. 2006; 119(1243):U2264.
  8. Mueller P, Marshall J, Spencer S, Noble A, Shadbolt T, Collins-Emerson JM, et al. Utilising a combination of molecular and spatial tools to assess the effect of a public health intervention. Spatial and Spatio-temporal Epidemiology. 2011; In Press.
  9. French N, Marshall J and Molecular Epidemiology and Public Health Laboratory. Source attribution July 2009 to June 2010 of human Campylobacter jejuni cases from the Manawatu. Wellington: New Zealand Food Safety Authority; 2010; Available from: http://www.foodsafety.govt.nz/elibrary/industry/campylobacter-jejun/final-report.pdf
  10. New Zealand Food Safety Authority. Campylobacter Risk Management Strategy 2010 - 2013. Wellington: New Zealand Food Safety Authority; 2010; Available from: http://www.foodsafety.govt.nz/elibrary/industry/Campylobacter_Risk-Comprehensive_Aimed.pdf
  11. Chrystal N, Hargraves S, Boa A, Ironside C. Counts of Campylobacter spp. and prevalence of Salmonella associated with New Zealand broiler carcasses. J Food Prot. 2008; 71(12):2526–32.
  12. Müllner P, Collins-Emerson JM, Midwinter AC, Carter P, Spencer SE, van der Logt P, et al. Molecular epidemiology of Campylobacter jejuni in a geographically isolated country with a uniquely structured poultry industry. Appl Environ Microbiol. 2010; 76(7):2145–54.