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| Journal of the New Zealand Medical Association,
22-September-2006, Vol 119 No 1242
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New Zealand should control
Campylobacter in fresh poultry before
worrying about flies
The possible role of flies in the aetiology of human
campylobacteriosis in New Zealand was the focus of a recent
Journal article by Nelson and Harris.1
This is not a new hypothesis,2 so we were surprised to see it being raised again
without specific data to support it.
Such speculation contrasts with the well established role of
contaminated food products (and particularly fresh poultry) as the major risk
factor for campylobacteriosis in New Zealand as detailed in recent reviews.3 4
This evidence is based on New Zealand case-control studies of sporadic disease,
one of which was a large multi-centre study.5
Other published and unpublished New Zealand epidemiological
studies of sporadic campylobacteriosis, and of outbreaks, provide additional
support for the importance of food-borne transmission.4 Further to the
epidemiological evidence, serotyping has revealed strains common to cases and
poultry from New Zealand stores (including those stores at which cases
shopped),6–9 and links with sausage,10 sheep liver,11 and sheep and beef
offal.12 However, such serotyping work may still be of somewhat limited value
owing to the likely
genetic instability of
the
Campylobacter
genome (e.g.
uptake of extracellular DNA and DNA recombination). Even when considering
campylobacteriosis outbreaks alone, food dominates over water-borne
transmission.4
None of the 13 published outbreak and 16 unpublished
outbreak reports in New Zealand (that met the quality criteria for inclusion in
a review) identified flies or fly-contaminated environmental surfaces as risk
factors for campylobacteriosis.4
Nelson and Harris suggest cow faeces as the major
environmental source with a flies-fomites-fingers link to humans. If this was
the case, we would expect to see much higher rates of illness in rural areas.
Such a pattern is not observed.13
There is no need to propose a role for flies to explain the
elevated summer rates of campylobacteriosis in New Zealand.
Many other factors may be more important, including:
However, the impact of the latter
point may be minor, since notification and hospitalisation rates are highest in
New Zealand cities,13 again consistent with the importance of food-borne
transmission rather than from contaminated environments.
Nelson and Harris’ article also failed to explain how
flies could account for the huge rise in campylobacteriosis over the past 20
years. Instead, it presented data showing how the rise in campylobacteriosis
notifications appeared closely correlated with increased consumption of chicken,
which is a far more plausible explanation.
Informed scientific debate is highly desirable, but the kind
of unsubstantiated speculation contained in the Nelson and Harris article can
have negative consequences for public health. Indeed, it can reinforce a public
perception that the sources of human
Campylobacter infection are highly
speculative, that every surface in their home environment is potentially
contaminated, and that this disease is virtually unstoppable. This
‘miasma’ viewpoint is paralysing and easily exploited by interest
groups which seek to divert attention from potential interventions.
Given the research evidence detailed above, the emphasis in
this country should continue to be on reducing the levels of
Campylobacter contamination in the food
supply (e.g. particularly on poultry farms, in poultry processing plants, and in
poultry in the distribution system). In fact, the bulk of government-funded
research into campylobacteriosis control appears to relate to the food-borne
transmission pathway (see the New Zealand Food Safety Authority website: http://www.nzfsa.govt.nz/).
Studies on the possible role of flies might be justified in
the distant future, but only once the major sources of campylobacteriosis have
been successfully controlled and control programmes evaluated.
Nick Wilson, Michael
Baker
Public Health Physicians Wellington School of Medicine and Health Sciences, University of Otago Wellington (nick.wilson@otago.ac.nz) Greg Simmons
Public Health Physician Auckland Regional Public Health Service Auckland Phil Shoemack
Medical Officer of Health Bay of Plenty District Health Board Tauranga References:
ResponseEating raw or undercooked chicken and associated food
contamination is not disputed as a risk for campylobacteriosis. Neither is
suggesting another transmission route to be taken as justification for the
chicken industry to make no attempt to reduce or eliminate
Campylobacter contamination of their
product. If we are to get on top of the problem though, we need to have an
honest evaluation of facts.
We repeat, chicken production interruption in both Belgium
(1999) and the Netherlands (2003) cut reported
Campylobacter rates significantly, a
calculated 40% reduction. That still leaves 60% with an unexplained source. Our
flies/fomites/fingers hypothesis offers an alternative transmission route to
explain a chicken-consumption link to illness, while at the same time also
taking into account the many factors strongly discounting the source as being
only and directly chicken.
Chicken as a direct source is heavily entrenched in the
medical mindset. The “well established direct link” claimed is, at
best, circumstantial. In its favour is the common knowledge that chicken meat is
frequently contaminated, very low levels of organism constitute an infectious
dose, and people who get sick have commonly eaten chicken recently. Chickens can
provide some of the same strains as found in human cases, but this is not
evidence of direction of
transmission.
Outbreaks and their associated food or water-borne
transmission routes represent about 10% of campylobacteriosis cases. Our paper
focussed solely on the much more common
sporadic cases. Food-borne causes of
gastroenteritis frequently result in outbreaks of cases, not sporadic incidents
as is usual with Campylobacter.
We made no claim to be first to involve flies in the
transmission of Campylobacter to
humans, nor for the idea that dairy cows are a significant source for
Campylobacter in the environment. Prior
credit is clearly indicated. We do however propose a fomite, finger addition to
the transmission pathway.
The rural/urban aspect needs investigating, but no New
Zealand city is far from a rural source of disease. Urban pets may yet prove a
more common source than is currently fashionable to consider. An interesting
coincidence to fomites and fingers is the hand to mouth suggestion recently
postulated, although this retains chickens as source.1
The marked increase in campylobacteriosis cases over the
last 20 years was not part of our investigation. However, the increase in
chicken consumption noted fits our hypothesis of food-associated transmission.
The increase in dairy cow numbers also shows a somewhat similar trend (Figure
1). Far from being a paralysing viewpoint, washing hands before touching food is
a key hygiene factor. We have merely tried to determine a plausible transmission
route that also fits the known epidemiology and risk factors associated with
eating chicken and sporadic campylobacteriosis.
Figure 1.
Campylobacter data as before, with
dairy cow numbers added
 Data from Livestock
Improvement Company (http://www.lic.co.nz).
Least squares linear regression fitted.
The supposed genetic instability of
Campylobacter is not supported by
evidence. Specific subtypes are common from the Far East to Europe.2 Genotype
overlap between humans and chickens has been reported as between 20%3 and 6%.4
Some virulence markers in Campylobacter
jejuni show little commonality between humans and chickens.5 This should
come as little surprise as a chicken flock is often colonised by a single or
very few strains of Campylobacter.6
Flies being eaten or contaminating food are a known source
of Campylobacter for chickens.7,8 Flies
are therefore a highly plausible vector between other environmental sources and
chickens, or between chicken houses. Thus cows are a plausible source of
environmental Campylobacter for both
chickens and humans. Flies represent a common transmission agent too, although
direct consumption by humans of flies is rare, hence the indirect fomite/fingers
suggestion.
Recent calls for banning the sale of fresh chicken meat in
New Zealand based on our high rate of campylobacteriosis do not have
experimental evidence on their side.9 The weekly pattern of disease in the UK
supports a hypothesis of food-associated (but not necessarily food-borne)
transmission.10 Unfortunately, we cannot repeat this here as New Zealand
statistics are on a monthly basis.
With the bulk of research funding already going on a
food-borne approach, yet with only rising rates over 20 years to show for it,
perhaps a broader target is justified.
Campylobacter-free chicken meat is a
desirable aim, but this is likely to only target the outbreak (10%) side of the
equation. Chicken-association appears to be about 40% of cases.
Wilson et al seem to have missed the point of our paper and
the authors apologise for apparent obscurity of expression. We hope this
response will also aid others who might have missed these points. However, we
are delighted with the widespread uptake of our main points by the popular press
as it is individual diners who control what they ingest from their own
fingers.
Warrick Nelson
Research and Management Consultant 888 Management Ltd (a technical, consulting, and publishing agency) Christchurch (warrick.nelson@gmail.com) Ben Harris
Medical Laboratory Scientist and General Manager Southern Community Laboratories Christchurch References:
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