Printer Friendly

Is chicken meat the most important source of human Campylobacter infection in New Zealand?

It is undisputed that chicken meat plays a role in human campylobacteriosis. However, the claim that "there is overwhelming epidemiological and laboratory evidence that fresh chicken is the dominant source of human infection" (1) is open to question. For chicken as the prime source theory to be accepted, the considerable anomalies associated with this would have to be explained away. Other sources and vectors of campylobacteriosis in New Zealand should at least be properly considered. For instance, the largest reservoir of campylobacter in New Zealand is likely to be the 5.2 million dairy cows (an increase of 79% in 25, producing excrement equivalent to at least 70 million people. This excrement is deposited into our waterways, either directly by cows accessing streams, or indirectly from washing off our clean, green pastures.

Summary of anomalies to chicken as only source of campylobacter infections

* Campylobacter infections have very marked seasonal cycles, but chicken consumption does not.

* The degree of seasonality varies, roughly less seasonal in the North to greater inter-seasonal variation in the South (2).

* Where poultry production has stopped (e.g. Belgium 1999 Dioxin crisis), Campylobacter rates have only dropped up to 40%, leaving at least 60% non-poultry source unexplained.

* These campylobacters cannot grow at all under 30[degrees]C, less than most peak spring and autumn temperatures, so poor food storage multiplication cannot be an issue (unlike other food poisoning bacteria).

* Each 1[degrees]C ambient temperature increase results in a 5% increase in campylobacter infections up to 14[degrees]C (3)--but the bacteria do not multiply below 30[degrees]C, so what cause and what vector?

* Over 80% of human cases are sporadic cases, not outbreak clusters --sporadic incidents have sporadic causes.

* When outbreaks have occurred, the sources have been traced to contaminated water, unpasteurised milk, processed meats and only sometimes chicken.

* New Zealand campylobacter infection rates increased 1995-1999, but dropped dramatically in 1999 and 2000, unlike chicken production and consumption which increased steadily.

* Molecular typing shows the same strains in chickens, humans, animal wastes, water and flies-which came first?

* Food handlers and preparers of "filthy chicken" are not at increased risk of infection.


Campylobacter jejuni is typically found to cause about 80% of campylobacteriosis cases. At least 10% are thought to be from C. coli, with a few cases from other species.

Common features of campylobacteriosis are:

* a marked seasonal variation in cases with a small winter/spring peak and a major summer peak.

* very high rates in infants and the age group 20-40 years.

* higher rates in males, generally across all age groups.

* at least 80% of cases are sporadic rather than outbreak in nature (unlike other food poisoning causative agents).

* relatively low levels of incidence from the 1980s, but growing erratically through to the present.

* the infectious dose is very small, possibly as low as 500 cells (4-6), and

* a very strong and persistent association with chicken consumption.

These features are commonly reported for many countries. New Zealand shows similar trends, but notably at very much higher rates--European and North American rates are of the order of <100/100 000 while New Zealand is >400/100 000 (7).

Campylobacters are also a significant cause of Travellers' Diarrhoea. Foreign travel is such a significant source of campylobacteriosis that some countries record campylobacteriosis separately according to whether it was acquired domestically, or during or after travel. About 25% of cases in the UK are estimated as travel related (8) and up to 38% in Norway (9).

These Campylobacters do not multiply in foods. In fact they cannot multiply at all at temperatures under 30[degrees]C, nor outside of animals or birds (other than very carefully contrived laboratory conditions). Thus they are quite different to many other "food poisoning" bacteria in that the infectious dose is delivered entirely as contamination of the food, not multiplication in foods. Furthermore, symptoms follow the establishment of infection only, and not ingestion of toxins commonly produced by bacteria eg Staphylococcus. Even where foods are at a temperature sufficient to allow Campylobacter growth (optima are at 37[degrees]C and 42[degrees]C, typical body temperatures of mammals and birds respectively), no trials have demonstrated growth in food (10). Growth occurs in the intestinal tracts of birds and mammals - hence jejunum and coli species names. Campylobacter are readily killed at relatively low cooking temperatures--i.e.70[degrees]C (11). They are also only present on the surface of meats (12-13), the only clearly demonstrated exception is liver (14-15). Processed meat products (eg sausages, pates, burgers) therefore mix surface meat contamination into the bulk of the product.

New Zealand evidence

Laboratory evidence in New Zealand is particularly poor as regards chicken as the source of human cases. Routine clinical stool samples are typically identified to genus level only, using a selective medium for C. jejuni and C. coli. When methods suited to identifying other species are used, they are often found in clinical cases (16). Perhaps the advent of multiple species PCR tests now being used in research will assist in clinical diagnosis too[18].

Research laboratory evidence, while indicating a significant commonality between chicken and clinical strains, does not indicate chicken as source, but merely that similar strains are present in both sets of samples. Which came first--the chicken, the egg, the cow, the water, the fly? An early survey showed that some types were indistinguishable between clinical strains and those from chickens and untreated water. However, the strains most commonly isolated were also common in dairy and beef cows, sheep, water and chickens (17-18). Subsequent testing has confirmed the presence of common human isolates in sheep liver (19) and beef, sheep, pork and chicken sources (20).

Epidemiological studies in New Zealand come up with a bewildering array of risk factors. Chicken certainly features prominently, especially raw or undercooked chicken (21). This large case-control study, the most extensive in New Zealand to date, has been criticised for not fully considering other potential sources, such as animal and water-related risks (22). A further problem for this sort of study is the reliance on memory to determine food events and other activities that could affect the resulting risk profile (23). Risk assessments based on reservoir identification have not helped for Campylobacter as they are so widely spread, outbreak data are not representative of a largely sporadic disease, and case-control studies are problematic due to recall bias and long exposure windows (24). The bias towards blaming chicken can be even more blatant, for example a public health questionnaire to obtain information on the source of campylobacteriosis helpfully prompts "Campylobacter infection is most commonly associated with undercooked or left-over chicken meals" (25).

There have been many literature reviews conducted in New Zealand recently. While all mention the chicken/human disease link, none appears able to apply a percentage of cases to chicken specifically, nor do they specify chicken as the definitive major source for campylobacteriosis in New Zealand (26-30). On the contrary, many other sources are acknowledged, particularly dairy and sheep as probable direct and indirect sources. An older study raised the strong potential for domestic pets as a significant risk factor (31), a risk factor receiving renewed interest internationally (32-35). One study even observed that, at least some New Zealanders "live in an environmental sea of Campylobacter" with no significant overlap in types isolated from humans and raw chickens (17).

Outbreaks, while commonly considered to be less than 20% of campyobacteriosis cases, are rather better understood. Common identified sources in these cases are water, unpasteurised milk and processed meats (especially those not cooked after processing and/or that contain liver). Chicken as an outbreak source is still sufficiently uncommon to justify reporting, for example recent events in Australia, Denmark and Japan (36-38). Outbreaks in New Zealand (reviewed in reference 30)) are largely related to water sources, and foods from commercial or other catered events, only some of which included chicken.

Clearly there is no consensus amongst New Zealand campylobacteriosis researchers of any "overwhelming" evidence to indicate that regulation of chicken contamination will control New Zealand's campylobacteriosis epidemic", although it will probably go some way to reduce it.

The marked seasonal pattern of campylobacteriosis cases does not correlate with chicken consumption. The annual growth in cases may correlate with an annual growth in fresh chicken production (1), but this is clearly negated by the quarterly data (Figs 1 and 2). Where seasonal patterns of chicken colonisation have been monitored, they occur at the same time, or slightly after, campylobacteriosis cases (39), strongly suggesting a common source and dispersion agent. Curiously, seasonal campylobacteriosis infection does correlate well with numbers of short term visitors to New Zealand (Fig 3 of reference 40), but the New Zealand notification data does not have this case detail, unlike several overseas countries which show the strong link.


Rates of disease in New Zealand of various age groups are remarkably constant ( report server). The highest rates occur in the under five years group, and the 20-29 years group, across both males and females. It seems unlikely that these age groups will be consuming and/or preparing more chicken meals than other age groups.

Overseas evidence

If the New Zealand data is somewhat sporadic and gives no clear picture of the source of campylobacteriosis, the Iceland and Belgium events are often cited as being definitive against chicken.

Iceland revised its law in 1996 to allow the sale of fresh as well as frozen uncooked chicken meat. The following years showed a massive increase in campylobacteriosis cases, peaking in 1999. Rates dropped subsequently, associated with a major campaign by chicken producers to reduce contamination of retailed chicken meat products and public health campaigns aimed at food and personal hygiene (41). Iceland data must however be considered with some care - not any aspersion on the source, but simply that the population is so small (total 300 000 i.e. less than Christchurch) that a few extra individual cases will have a large impact on the rate calculation. The peak of 1999 was only 426 cases--about a third of the number of cases reported in the Canterbury District Health Board area. In spite of this, other circumstantial evidence, for example the increased consumption of chicken and the growth of the fresh chicken component from <5% in 1996 to 60% by 1999, is strongly indicative of the role of chicken in Icelandic domestically acquired campylobacteriosis (42). However, this occurred within a background of smaller, but similarly timed, peaks in campylobacteriosis in many other European countries. Although campylobacteriosis reports have dropped since intervention measures have been implemented, they only dropped to a level roughly double that pertaining prior to pre-intervention 1996 (Fig 4,


During the 1999 "Dioxin crisis" in Belgium, all Belgian-produced chicken products were withdrawn from the market for a six week period. An approximately 40% reduction in campylobacteriosis reports occurred during those six weeks, returning to trend following the return of chicken meat to market (43). However, many other food products were affected, not just raw chicken meat. May 29th 1999 (week 21) was the date for withdrawal of Belgian-produced poultry and eggs (Belgium is a net exporter of poultry products). June 2nd (week 22) saw the withdrawal of products extended to processed foods containing chicken and egg, and the withdrawal extended again two days later to include processed pork and beef products. Bearing in mind an incubation period of 2-7 days, it is interesting to note that campylobacteriosis reports only dropped from week 23, the week following the withdrawal of processed foods, rather than the week following the withdrawal of chicken. The 40% decline in campylobacteriosis rates cannot therefore be attributed solely to people not eating chicken, and even if it does, the majority 60% of cases are still left with an unexplained non-poultry source. These events also still leave the possibility of disease associated with the style of eating rather than indicating the chicken itself is the source. Indeed, the removal of processed foods eaten without further cooking, and replacement by beef or fish products for chicken in fast food outlets, could indicate a role for food-associated disease (44).

A number of other studies raise concerns about the overwhelming expectation that campylobacteriosis comes from chicken consumption. For example, Neal and Slack (45) determined for the Nottingham Health District, UK that foreign travel accounted for 25% of cases, and 15% of cases could be attributed to causes such as contact with puppies, eating chicken and drinking milk from pecked bottle tops, leaving the other 60% unexplained. Note also that eating chicken is only a component of the explained 15% of cases. A large study of the Helsinki, Finland region (46) found a fairly large overlap between PFGE genotypes between humans and chickens, but often not occurring at the same time. Their conclusion was that both humans and chickens probably acquire Campylobacter infection from a common source, rather than indicating chicken as a direct source for humans (or vice versa).

Similarly, a study in Quebec, Canada (47) also showed a high diversity of PFGE genotypes in chickens, but with single growing houses tending to have single strains. Comparison with human sources indicated only 20% of isolates were related to chicken strains. The Czech Republic has campylobacteriosis rates approaching those of New Zealand, rising from 22/100 000 in 1996 to 296/100 000 in 2005 (data.euro.who. int/CISID). Chicken infection patterns are again similar to Finland and Canada with each flock infected with a single clone (48). However, using both PFGE and PCR/RFLP methods, chicken and human genotypes overlapped by only 6%. The authors concluded that "chicken meat does not represent as important a source of campylobacteriosis as was previously believed".

Cross contamination and elimination?

Another anomaly is that handling and preparing chicken does not appear to be a risk factor for disease. Since anything up to 100% of raw chicken can be contaminated, it seems strange that food preparation is not a risky business. Analysis of genetic strains suggests that very small outbreaks are likely being reported as sporadic (49-50), possibly indicating cross-contamination in domestic kitchens. Tests indicate that "during food preparation bacteria become widely disseminated to hand and food contact surfaces" (51) and transfer rates from hands or kitchen utensils to ready-to-eat foods are up to 27% (52). Poultry is a common food item which is contaminated to a high level, with an easily spread and cross-contaminated bacterium requiring a low number of cells needed for infection, yet actual cases of campylobacteriosis are remarkably few compared to the number of chicken meals consumed.

Banning the retail sale of fresh, raw chicken meat has been suggested (1). Reduction of campylobacter numbers on chicken meat can occur during freezing. This is clearly the assumption in the Icelandic experience, both from the ascribed source of the epidemic and one intervention being freezing of meat from flocks testing positive before slaughter (41). Early tests appear to confirm that freezing results in fewer contaminated birds, for example 48% contamination of fresh and 4% of frozen chickens (53), although possibly better isolation tests suggest far higher numbers of frozen chickens are contaminated, for example 94% of fresh and 77% of frozen chickens in a small Irish survey (54). A 0.5 to 3.4 log reduction in Campylobacter following commercial freezing over a 2-week period looks promising, although the authors noted that "refrigeration and freezing are not a substitute for safe handling and proper cooking of poultry" (55). A similar 3 log reduction was noted for contaminated ground beef (11). Apart from contamination in livers, chicken meats are contaminated on the surface. Some chemical treatments applicable for use at slaughter could prove promising to reduce contamination to undetectable levels (56).

If not chicken, what else can be the source and vector?

It has not been our intention to suggest that chicken meat is not a source of Campylobacter, but simply to show that there are significant difficulties associated with ascribing the bulk of the blame to chicken meat. There is certainly no doubt that campylobacteriosis can occur from consuming raw/undercooked chicken meat, or consuming other foods contaminated with raw chicken meat or juices.

Quite clearly, animal (including cows, sheep, pets and humans) and bird excreta are the ultimate source. For human infection to occur, we need both a source and a vector. Other factors, such as different pathogenicity or increased susceptibility (57), including possible immunity reactions (58) play a role in determining actual disease status following colonisation.

Common farm animals, especially cows, must be considered a major source. They are present in large numbers, over 9.5 million cattle in New Zealand, their faeces commonly carry campylobacter that is seldom treated to reduce bacteria. Raw excrement is generally deposited directly into the environment, or is purposely spread to both dispose of it and to fertilise pastures. Dairy cows alone (now 5.2 million) are producing effluent equivalent to at least 70 million humans that is not being treated before discharge into the environment (22). Cows and sheep are clearly major sources for environmental, and especially water, contamination in New Zealand (27,59). These would appear to be the true source of the "environmental sea of Campylobacter" quoted earlier. Further, dairy herds show a marked seasonal pattern of campylobacter shedding (60-61).

We also need to reconsider the vector(s). In New Zealand, it would appear that water and flies, however currently unfashionable compared to chicken consumption, are strong candidates as significant vectors. Sparrows are a very mobile vector for transferring campylobacter from rural to urban areas, although what part they might play in human infection is less clear (62). The reason for water is that significant sections of the New Zealand population are normally, or frequently, exposed to untreated drinking water supplies (including shallow groundwater wells), and even treated water can have detectable levels of Campylobacter contamination (63). This could also go some way to explain the correlation between campylobacteriosis and visitor numbers since many small water supplies service holiday and visitor attractions for both potable water and recreational/swimming activities.

Addressing the anomalies in the chicken story and considering other possible sources and vectors is u n I i kely to generate a "miasma viewpoint" likely to be "paralysing and easily exploited by interest groups"(64). We would hope to stimulate research into other sources, possibly more likely to offer a means of reducing campylobacteriosis infection rates more significantly.


Chicken meat is undoubtedly one significant source for Campylobacter causing human disease. Where detailed studies have been conducted to establish chicken as the direct source of disease, results indicate from 6% to possibly 40% of cases should be attributed to chicken consumption. Of greatest significance for New Zealand is the growing data indicating why New Zealand has such a high rate of disease, and the environmental sources driving the pattern of infection.

Poultry meat has gained an unenviable public perception as the essential cause of almost all campylobacter cases, and there are also many scientific and industry vested interests surrounding this. But, for this concept to have reasonable scientific credibility, all the serious anomalies listed would have to be credibly debased. We need to address some sacred cows before we put all our eggs into one basket if we are going to topple ourselves off the perch of leaders of the OECD for campylobacteriosis.


Thanks to the Institute of Environmental Science and Research for campylobacteriosis statistics, and to the Poultry Industry Association of New Zealand for statistics on chicken production, and to Statistics New Zealand for short term visitor and dairy cow numbers.

European country campylobacteriosis rates from CISID/.


(1.) 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.

(2.) Heamden M, Skelly C, Eyles R, Weinstein P. The regionality of campylobacteriosis seasonality in New Zealand. Int J Environ Health Res 2003; 13: 337-48.

(3.) Tam CC, Rodrigues LC, O'Brien SJ, Hajat S. Temperature dependence of reported Campylobacter infection in England, 1989-1999. Epidemiol Infect 2006; 134: 119-25.

(4.) Robinson DA. Infective dose of Campylobacter jejuni in milk. Br Med J (Chn Res Ed) 1981; 282: 1584.

(5.) Black RE, Levine MM, Clements ML, Hughes TP, Blaser MJ. Experimental Campylobacterjejuni infection in humans. J Infect Dis 1988; 157: 472-9.

(6.) Riordan T, Humphrey TJ, Fowles A. A point source outbreak of campylobacter infection related to bird-pecked milk. Epidemiol Infect 1993; 110: 261-5.

(7.) Baker MG, Sneyd E, Wilson NA. Is the major increase in notified campylobacteriosis in New Zealand real? Epidemiol Infect 2007; 135: 163-70.

(8.) Neal KR, Slack RC. The autumn peak in campylobacter gastroenteritis. Are the risk factors the same for travel- and UK-acquired campylobacter infections?. J Public Health Med 1995; 17:98-102.

(9.) Kapperud G, Aasen S. Descriptive epidemiology of infections due to thermotolerant Campylobacter spp. in Norway, 1979-1988. APMIS 1992; 100: 883-90.

(10.) Arumugaswamy RK, Proudford RW, Eyles MJ. The response of Campylobacter jejuni and Campylobacter coli in the Sydney rock oyster (Crassostrea commercialis), during depuration and storage. Int J Food Microbiol 1988; 7: 173-83.

(11.) Stern NJ, Kotula AW. Survival of Campylobacter jejuni inoculated into ground beef. Appl Environ Microbiol 1982; 44: 1150-3.

(12.) Luber P, Bartelt E. Enumeration of Campylobacter spp. on the surface and within chicken breast fillets. J Appl Microbiol 2007; 102: 313-8.

(13.) Bosilevac JIM, Guerini MN, Brichta-Harhay DM, Arthur TM, Koohmaraie M. Microbiological characterization of imported and domestic boneless beef trim used for ground beef. J Food Prot 2007; 70: 440-9.

(14.) Scates P, Moran L, Madden RH. Effect of incubation temperature on isolation of Campylobacter jejuni genotypes from foodstuffs enriched in Preston broth. Appl Environ Microbiol 2003; 69: 4658-61.

(15.) Kramer JIM, Frost JA, Bolton FJ, Wareing DR. Campylobacter contamination of raw meat and poultry at retail sale: identification of multiple types and comparison with isolates from human infection. J Food Prot 2000; 63: 1654-9.

(16.) Miller WG, Parker CT, Heath S, Lastovica AJ. Identification of genomic differences between Campylobacter jejuni subsp. jejuni and C. jejuni subsp. doylei at the nap locus leads to the development of a C. jejuni subspeciation multiplex PCR method. BMC Microbiol 2007; 7: 11.

(17.) Baker M, Ball A, Devane M, Garrett N, Gilpin B, Hudson A, et al. Potential transmission routes of campylobacter from environment to humans. Inst Environ Sci & Res 2002;

(18.) Hudson JA, Nicol C, Wright J, Whyte R, Hasell SK. Seasonal variation of Campylobacter types from human cases, veterinary cases, raw chicken, milk and water. J Appl Microbiol 1999; 87: 115-24.

(19.) Cornelius AJ, Nicol C, Hudson JA. Campylobacter spp. in New Zealand raw sheep liver and human campylobacteriosis cases. Int J Food Microbiol 2005; 99: 99-105.

(20.) Wong TL, Hollis L, Cornelius A, Nicol C, Cook R, Hudson JA. Prevalence, numbers, and subtypes of Campylobacter jejuni and Campylobacter coli in uncooked retail meat samples. J Food Prot 2007; 70: 566-73.

(21.) 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: 686-91.

(22.) Till DG, McBride GB. Potential public health risk of Campylobacter and other zoonotic waterborne infections in New Zealand. In: Cotruvo JA, Dufour A, Rees G, Bartram J, Carr R, Cliver DO, et al, eds. Waterborne Zoonoses: Identification, Causes and Control. IWA Publishing, London; 2004: 191-207.

(23.) Skelly C, Weinstein P. Pathogen survival trajectories: an eco-environmental approach to the modeling of human campylobacteriosis ecology. Environ Health Perspect 2003; 111: 19-28.

(24.) Batz MB, Doyle MP, Morris GJ, Painter J, Singh R, Tauxe RV, et al. Attributing illness to food. Emerg Infect Dis 2005; 11: 993-9.

(25.) Leighton K. Improving enhanced surveillance of notifiable enteric illnesses. MPH Thesis. University of Western Australia; 2004.

(26.) Wong T, On SLW, Michie H. Campylobacter in New Zealand: reservoirs, Sources and the labyrinth of transmission routes. N Z J Environ Health 2006; 29: 1-6.

(27.) McBride G, Meleason M, Skelly C, Lake R, van der Logt P, Collins R. Preliminary relative risk assessment for Campylobacter exposure in New Zealand: 1. National model for four potential human exposure routes 2. Farm environmental model. Nat Inst Water & Atmos Res 2005;

(28.) Lake R, Hudson A, Cressey P, Nortje G. Risk profile: Campylobacter jejuni/coli in poultry (whole and pieces). Inst Environ Sci & Res, 2003.

(29.) Lake R: Transmission routes for campylobacteriosis in New Zealand. Inst Environ Sci & Res 2006;

(30.) Wilson N. A systematic review of the aetiology of human campylobacteriosis in New Zealand. NZ Food Safety Authority 2005;

(31.) Brieseman MA. A further study of the epidemiology of Campylobacterjejuni infections. NZMedJ 1990; 103: 207-9.

(32.) Keller J, Wieland B, Wittwer M, Stephan R, Perreten V. Distribution and genetic variability among Campylobacter spp. isolates from different animal species and humans in Switzerland. Zoonoses Public Health 2007; 54: 2-7.

(33.) Siemer BL, Harrington CS, Nielsen EM, Borck B, Nielsen NL, Engberg J. On SLW: genetic relatedness among Campylobacter jejuni serotyped isolates of diverse origin as determined by numerical analysis of amplified fragment length polymorphism (AFLP) profiles. J Appl Microbiol 2004; 96: 795-802.

(34.) Karenlampi R, Rautelin H, Sch(5nberg-Norio D, Paulin L, Hanninen M. Longitudinal study of Finnish Campylobacter jejuni and C. coli isolatesfrom humans, using multilocussequence typing, including comparison with epidemiological data and isolates from poultry and cattle. Appl Environ Microbiol 2007; 73: 148-55.

(35.) Wieland B, Wittwer M, Regula G, Wassenaar TM, Burnens AP, Keller J, et al. Phenon cluster analysis as a method to investigate epidemiological relatedness between sources of Campylobacter jejuni. JAppl Microbiol 2006; 100: 316-24.

(36.) Yoda K, Uchimura M. An outbreak of Campylobacter jejuni food poisoning caused by secondary contamination in cooking practice at a high school. Jpn J Infect Dis 2006; 59: 408-9.

(37.) Mazick A, Ethelberg S, Nielsen EM, Molbak K, Lisby M. An outbreak of Campylobacter jejuni associated with consumption of chicken, Copenhagen, 2005. Euro Surveill 2006; 11: 137-9.

(38.) Black AP, Kirk MD, Millard G. Campylobacter outbreak due to chicken consumption at an Australian Capital Territory restaurant. Commun Dis Intell 2006; 30: 373-7.

(39.) Hald B, Skovgard H, Bang DD, Pedersen K, Dybdahl J, Jespersen JB, et al. Flies and Campylobacter infection of broiler flocks. Emerg Infect Dis 2004; 10: 1490-2.

(40.) Nelson W, Harris B. Can we change the hymn sheet? Campylobacteriosis not just from chicken. N Z Med J 2006; 119 (1244): U2299.

(41.) Stern NJ, Hiett KL, Alfredsson GA, Kristinsson KG, Reiersen J, Hardardottir H, et al. Campylobacter spp. in Icelandic poultry operations and human disease. Epidemiol Infect 2003; 130: 23-32.

(42.) Reiersen J, Briem H, Hardardottir H, Gunnarsson E, Georgsson F, Gudmundsdottir E, et al. Human campylobacteriosis epidemic in Iceland 1998-2000 and effect of interventions aimed at poultry and humans. FAO/WHO Global Forum of Food Safety Regulators, Marrakech, Morrocco 2002.

(43.) Vellinga A, Van Loock F. The dioxin crisis as experiment to determine poultry-related campylobacter enteritis. Emerg Infect Dis 2002; 8: 19-22.

(44.) Nelson W, Harris B. Flies, fingers, fomites, and food. Campylobacteriosis in New Zealand--food-associated rather than food-borne. N Z Med J 2006; 119 (1240): U2128.

(45.) Neal KR, Slack RC. Diabetes mellitus, anti-secretory drugs and other risk factors for campylobacter gastro-enteritis in adults: a case-control study. Epidemiol Infect 1997; 119: 307-11.

(46.) Hanninen ML, Perko-Makela P, Pitkala A, Rautelin H. A three-year study of Campylobacter jejuni genotypes in humans with domestically acquired infections and in chicken samples from the Helsinki area. J Clin Microbiol 2000; 38: 1998-2000.

(47.) Nadeau E, Messier S, Quessy S. Prevalence and comparison of genetic profiles of Campylobacter strains isolated from poultry and sporadic cases of campylobacteriosis in humans. J Food Prot 2002; 65: 73-8.

(48.) Nebola M, Steinhauserova I. PFGE and PCR/RFLP typing of Campylobacter jejuni strains from poultry. Br Poult Sci 2006; 47: 456-61.

(49.) Gillespie IA, O'Brien SJ, Adak GK, Tam CC, Frost JA, Bolton FJ, et al. Point source outbreaks of Campylobacter jejuni infection-are they more common than we think and what might cause them?. Epidemiol Infect 2003; 130: 367-75.

(50.) Gilpin B, Cornelius A, Robson B, Boxall N, Ferguson A, Nicol C, et al. Application of pulsed-field gel electrophoresis to identify potential outbreaks of campylobacteriosis in New Zealand. J Clin Microbiol 2006; 44: 406-12.

(51.) Cogan TA, Bloomfield SF, Humphrey TJ. The effectiveness of hygiene procedures for prevention of cross-contamination from chicken carcases in the domestic kitchen. Lett Appl Microbiol 1999; 29: 354-8.

(52.) Luber P, Brynestad S, Topsch D, Scherer K, Bartelt E. Quantification of campylobacter species cross-contamination during handling of contaminated fresh chicken parts in kitchens. Appl Environ Microbiol2006; 72: 66-70.

(53.) Hood AM, Pearson AD, Shahamat M. The extent of surface contamination of retailed chickens with Campylobacter jejuni serogroups. Epidemiol Infect 1988; 100: 17-25.

(54.) Moore JE, Wilson TS, Wareing DRA, Humphrey TJ, Murphy PG. Prevalence of thermophilic Campylobacter spp. in ready-to-eat foods and raw poultry in Northern Ireland. J Food Prot 2002; 65: 1326-8.

(55.) Bhaduri S, Cottrell B. Survival of cold-stressed Campylobacter jejuni on ground chicken and chicken skin during frozen storage. Appl Environ Microbiol 2004; 70: 7103-9.

(56.) Zhao T, Doyle MP Reduction of Campylobacter jejuni on chicken wings by chemical treatments. J Food Prot 2006; 69: 762-7.

(57.) Cogan TA, Thomas A0, Rees LE, Taylor AH, Jepson MA, Williams PH, et al. Norepinephrine increases the pathogenic potential of Campylobacterjejuni. Gut 2006; doi: 10.1136/gut.2006.114926.

(58.) Jones FR, Bagar S, Gozalo A, Nunez G, Espinoza N, Reyes SM, et al. New World monkey Aotus nancymae as a model for Campylobacterjejuni infection and immunity. Infect lmmun 2006; 74: 790-3.

(59.) Journeaux P. Microbial contamination of waters from livestock farming in New Zealand. In : OECD Workshop on Agriculture and Water: Sustainability, Markets and Policies, Adelaide, South Australia 2005.

(60.) Meanger JD, Marshall RB. Seasonal prevalence of thermophilic Campylobacter infections in dairy cattle and a study of infection of sheep. N Z Vet J 1989,; 37: 18-20.

(61.) Stanley KN, Wallace JS, Currie JE, Diggle PJ, Jones K. The seasonal variation of thermophilic campylobacters in beef cattle, dairy cattle and calves. J Appl Microbiol 1998; 85: 472-80.

(62.) Adhikari B, Connolly JH, Madie P, Davies PR. Prevalence and clonal diversity of Campylobacter jejuni from dairy farms and urban sources. N Z Vet J 2004; 52: 378-83.

(63.) Savill MG, Hudson JA, Ball A, Klena JD, Scholes P, Whyte RJ, et al. Enumeration of Campylobacter in New Zealand recreational and drinking waters. J Appl Microbiol 2001; 91: 38-46.

(64.) Wilson N, Baker M. New Zealand should control Campylobacter in fresh poultry before worrying about flies. N Z Med J 2006; 119 (1242): U2242.

Warrick Nelson, MSc, Principal Research Consultant 1888 Management Ltd., Christchurch

Ben Harris, MNZIML Medical Laboratory Scientist and General Manager Microbiology, Southern Community Laboratories Canterbury, Christchurch

Correspondence: Warrick Nelson, 888 Management Ltd., PO Box 6393, Upper Ricarton, Christchurch. Email:

Response to Nelson and Harris' article by Michael Baker and Nick Wilson

Reading the article by Nelson and Harris (1) one could easily come to the conclusion that they are arguing for the affirmative, that chicken meat is indeed the most important source of human Campylobacter infection in New Zealand. They repeatedly cite evidence showing the importance of fresh chicken meat as a source of this infection. Nowhere do they refer to a body of evidence that supports an alternative source as being more important in New Zealand.

The main proposition that Nelson and Harris appear to be arguing for is that chicken meat is not the only source of human campylobacteriosis. For example, their first subheading reads "Summary of anomalies to chicken as only source of Campylobacter infections" (1). Of course we can only agree with this statement, given the numerous studies cited in both of our papers that describe these other sources. However, this statement was not the one we were meant to be debating so it makes the logic of their article rather bewildering. Nevertheless, we wish to address some of the particularly spurious arguments that are raised by these authors.

Environmental reservoirs vs sources

New Zealand is not short of mammalian and avian reservoirs for Campylobacter infection. But for such reservoirs to be important, they need plausible pathways that link them to regular human ingestion of infectious organisms, hence the need to focus on sources of infection. As we discussed in our paper, fresh chicken meat provides a well-documented pathway for such transmission in the New Zealand setting (2). It is heavily contaminated by chicken faeces during slaughter and processing. The organism survives well at refrigeration temperatures. Fresh chicken meat has been found to be heavily contaminated at the point of sale, far more than any other meat. The volume of sales has risen to the point where it is now the most commonly eaten meat and so consumers have many opportunities to be exposed to it. Preventing cross-contamination in kitchen settings is very difficult. Nelson and Harris have not presented evidence-based arguments that challenge the plausibility and important of this source and pathway.


Campylobacter infection has a seasonal component and the mechanisms for this seasonality have received considerable scrutiny (3). These mechanisms are likely to be driven by either seasonal variations in human behaviour linked to exposure, or seasonal variation in the prevalence of Campylobacter in reservoirs and sources (3). Barbecuing chicken, which is known to be a risk factor (4), is more common in summer months. Studies in other temperate countries have found both chicken flocks (5) and fresh chicken meat for sale (6) to be more heavily contaminated in summer. The fact that consumption of chicken itself is not especially seasonal is therefore not particularly relevant.

Sporadic vs. outbreaks

The observation that most campylobacteriosis cases occur 'sporadically' rather than as recognised outbreaks is also entirely consistent with the importance of chicken meat as a major source. Campylobacter infection requires only a small infectious dose. Many New Zealanders are likely to be regularly exposed to foods and surfaces that have been cross contaminated from chicken meat, both in their homes and in commercial food outlets. This combination of circumstances creates the conditions for large numbers of sporadic cases. To quantify the sources of sporadic disease usually requires an analytical epidemiological investigation such as a case-control study. As we have noted, such studies carried out in New Zealand point to chicken as the dominant source of infection (4,7).

Effects of host immunity

The observed patterns of Campylobacter infection are a product of both exposure and the human immune response. No single exposure, no matter how dominant, can explain the full pattern of disease distribution that we observe. Nelson and Harris appear to imply that the higher rates of disease in young children, for example, count against chicken as an important source whereas this distribution is almost certainly influenced by patterns of immunity as well as exposure. In developing countries where the levels of environmental exposure are very high, almost all cases are in young children and it is hypothesised that this results in some level of immunity that extends into adulthood (8).


The 'debate' about the sources of New Zealand's campylobacteriosis epidemic is not simply an academic matter. If we fail to act on the important sources then the human health and economic consequences will remain considerable (2). Consequently, we are alarmed that these authors appear stuck in the hypothesis-generating stage and continue focusing on a succession of minor sources, such as overseas visitors, without a strong evidence base for their assertions. For example, they are incorrect in stating that New Zealand's notification system does not record whether a case was travel associated (it is on the standard case report form). In 2006, only 6% of cases who were asked about travel reported that they had been overseas during their incubation period (9). The caption to their Figure 3, which talks about the "uncanny correlation between New Zealand campylobacteriosis cases and tourist arrivals ..." is nothing more than 'pseudoscience'.

Fortunately, agencies such as the New Zealand Food Safety Authority have accepted that contaminated chicken meat is the main source of New Zealand's campylobacteriosis epidemic (10). There are even encouraging signs that the Poultry Industry Association takes the same view, based on their recent press releases.

Even so, we also support other approaches to controlling this disease including: improving drinking water quality; education about the risks of untreated surface water and unpasteurised milk; promoting good hand washing after touching animals, contaminated foods, and other potential sources; travel health advice; and general efforts to improve the microbial safety of all foods through 'paddock-to-plate' food safety programmes. However, none of these efforts is unlikely to have much impact compared with taking the essential steps to manage the dominant source of infection in New Zealand (11).

We also advocate more research on New Zealand's serious campylobacteriosis epidemic. Given its estimated cost, there is an economic justification for investing tens of millions of dollars a year in researching and controlling this hazard. But to get the best value for money, let's make this research highly focussed on dealing with the dominant source. This country is well positioned to carry out a controlled intervention trial of the impact of reducing contamination of chicken meat eg, by freezing and/or chemical treatments. Discussing how to design and run such a trial--now that would be a debate worth having!

Competing interests

There was no external funding for this work. One of the authors (MB) has provided technical advice to the NZFSA and the other (NW) has had two previous research contracts with the NZFSA in 2005.


(1.) Nelson W, Harris B. Is chicken meat the most important source of human Campylobacter infection in New Zealand? N Z J Med Lab Sci, 2007; 61.xx

(2.) Baker MG, Wilson NA. Chicken meat is clearly the most important source of human Campylobacter infection in New Zealand. N Z J Med Lab Sci, 2007; 61.xx

(3.) Nylen G, Dunstan F, Palmer SR, et al. The seasonal distribution of campylobacter infection in nine European countries and New Zealand. Epidemiol Infect, 2002; 128: 383-390.

(4.) Ikram R, Chambers S, Mitchell P, et al. A case control study to determine risk factors for campylobacter infection in Christchurch in the summer of 1992-3. N Z Med J, 1994; 107: 430-2.

(5.) Bouwknegt M, van de Giessen AW, Dam-Deisz WD, et al. Risk factors for the presence of Campylobacter spp. in Dutch broiler flocks. Prev Vet Med, 2004; 62: 35-49.

(6.) Meldrum RJ, Griffiths JK, Smith RM, et al. The seasonality of human campylobacter infection and Campylobacter isolates from fresh, retail chicken in Wales. Epidemiol Infect, 2005; 133: 49-52.

(7.) Eberhart-Phillips J, Walker N, Garrett N, et al. Campylobacteriosis in New Zealand: results of a case-control study. J Epidemiol Community Health, 1997; 51: 686-91.

(8.) CokerAO, Isokpehi RD, Thomas BN, et al. Human campylobacteriosis in developing countries. Emerg Infect Dis, 2002; 8: 237-44.

(9.) Institute of Environmental Science and Research Limited. Notifiable and other diseases in NewZealand: Annual report 2006. Wellington: Institute of Environmental Science and Research Limited, 2007.

(10.) New Zealand Food Safety Authority. Campylobacter in poultry--Risk management strategy 2006-2009. Wellington: New Zealand Food Safety Authority, 2006.

(11.) Baker M, Wilson N, Ikram R, et al. Regulation of chicken contamination is urgently needed to control New Zealand's serious campylobacteriosis epidemic. NZMed J, 2006; 119: U2264.
COPYRIGHT 2007 New Zealand Institute of Medical Laboratory Science
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 2007 Gale, Cengage Learning. All rights reserved.

Article Details
Printer friendly Cite/link Email Feedback
Author:Nelson, Warrick; Harris, Ben
Publication:New Zealand Journal of Medical Laboratory Science
Geographic Code:8NEWZ
Date:Aug 1, 2007
Previous Article:Laboratory diagnosis of malaria infection--a short review of methods.
Next Article:Chicken meat is clearly the most important source of human Campylobacter infection in New Zealand.

Related Articles
Campylobacter jejuni--An Emerging Foodborne Pathogen.
The dioxin crisis as experiment to determine poultry-related campylobacter enteritis. (Research).
Human campylobacteriosis in developing countries. (Synopsis).
A case-case comparison of campylobacter coli and campylobacter jejuni infection: a tool for generating hypotheses. (Research).
Campylobacteriosis, Eastern Townships, Quebec.
Salmonella and Campylobacter spp. in northern elephant seals, California.
Fresh chicken as main risk factor for campylobacteriosis, Denmark.
Chicken meat is clearly the most important source of human Campylobacter infection in New Zealand.
Use of fly screens to reduce Campylobacter spp. introduction in broiler houses.
Population-attributable risk estimates for risk factors associated with Campylobacter infection, Australia.

Terms of use | Copyright © 2018 Farlex, Inc. | Feedback | For webmasters