Safeguarding Australia
From mad cows to disappearing bees: safeguarding Australia from emerging diseases of animals
7 August 2007
Dr Mike Nunn
Principal Scientist (Animal Biosecurity)
Biosecurity Australia
Australian Government Department of Agriculture, Fisheries and Forestry
Mike Nunn is a veterinary epidemiologist with extensive overseas and Australian experience in the prevention and control of animal diseases. He has provided advice to a range of regional and international organisations, including the South Pacific Commission, the Asian Development Bank, the Food and Agriculture Organization, and the World Organisation for Animal Health on topics ranging from animal health surveillance systems to emerging zoonoses. He has particular interests in the pathobiology of disease, risk analysis, epidemiology and veterinary public health, including the ecology of emerging infectious diseases and the management of emergency animal diseases.
From mad cows to disappearing bees: safeguarding Australia from emerging diseases of animals
Thank you all for coming out on a cold Canberra night. What I would like to do is to tell you a bit of a story, to take you on a bit of a journey, about what the topic 'From mad cows to disappearing bees' means.
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I want to talk about the biosecurity environment we face now in Australia and the world generally, with some case studies to illustrate the key principles. I would like to talk about foresight, which is something that has become quite important to us where I work in trying to work out what is facing us in the future; how that feeds into policy; some challenges, particularly for the scientists in the audience, because I think science has a particular role here; and some tentative conclusions.
I must point out that this is very much a personal story. These are my views and not necessarily those of my employer – though I hope that they will eventually be.
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What are emerging diseases? I think that Simon Morse, in 1995, gave as good a definition as anybody, that they are those diseases that have been newly recognised in a population, or ones that are known to have existed but are rapidly increasing in either incidence – that is, in how commonly they occur – or their geographical range.
So there are two sorts of things there: those that are new to the world, new to science, and those that we know about but that for some reason have started to be on the march.
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Let's think about typical emerging human pathogens: Michael Woolhouse in 2002 reviewed some 1700 organisms and worked out their characteristics. The typical emerging one is an RNA virus – that is a particular type of virus, characterised by rapid mutation as compared to the DNA viruses – with zoonotic potential. That usually means they have a reservoir host range that is taxonomically and ecologically very broad. They are potentially transmissible between humans, ultimately, and they tend to be found in areas undergoing dramatic change – ecological, demographic or social changes. And about 75 per cent of what he called emerging human pathogens are zoonotic. That is, they come from animals into people or the reverse.
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So what is the environment of biosecurity now? I want to talk about some of the risks, the technologies, how that fits into policy, how we are asking different questions now than we were 10 years ago, and how we have different expectations – at least, the public communities that we deal with have those expectations, as do politicians.
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As to the sorts of risks involved, certainly there is risk of spread or introduction of exotic diseases into disease-free areas. Australia enjoys a very good animal health status, and we are free of many of the major animal plagues that occur around the world – foot-and-mouth disease, highly pathogenic avian influenza, Japanese encephalitis (except for the tip of Cape York peninsula), classical swine fever, and so on.
We certainly have had some cases of re-emergence of endemic diseases. We have seen the dramatic outbreak of Newcastle disease here, several years ago, when we ended up slaughtering-out two million birds to control it. It was an outbreak that went on for several months. It was caused by a virus that had been in Australia since at least 1966 but it had slowly mutated, it had slowly changed over time. In fact, it is used widely as a vaccine around the world, but it changed and eventually the nucleotides lined up and became virulent, and we had a massive outbreak.
We have seen the emergence of new or previously unknown diseases – overseas, Nipah virus, mad cow disease (or BSE), and the one I want to talk about tonight, colony collapse disorder of bees. In Australia, we have had a series of these too: Hendra virus, Menangle virus, porcine myocarditis virus, and I will mention some of those.
There is concern about human-induced risks – inadvertent ones (laboratory escapes, and we would all be aware of the press over the last few days about the UK situation, where it may well be laboratory escape) – and there is concern among different sorts of audiences about deliberately induced risks from acts of bioterrorism: deliberately introducing a pathogen into a population to disrupt it.
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The technologies are changing rapidly. In biotechnology there are some amazing advances – in gene technology, genomics, proteonomics. All of those help us to diagnose diseases better, faster, more accurately, and to track where they have come from.
Nanotechnology is only just beginning. There are potentially extraordinary changes there, in diagnostics and in other things, but there are some risks there as well that have to be thought through.
Other disciplines and new approaches over the past 10 years involve risk analysis, knowledge management, 'ecohealth' or 'ecosystems health' (the buzz word at the moment), 'one medicine', foresight and futures.
And there is the information technology on which we build all these rapid advances, such as geographical information systems (GIS) and mapping, remote sensing, disease modelling. The power of computers on your desk now is much more than that of a whole roomful was when I first joined the department where I now work, and we can do things with simple desktop models that weren't even dreamed of 10 years ago. Communications too is important – but technology is not always the answer; it is often the 'people issues' that are more important.
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The policy context broadly is that we are seeing rapid and continuing growth of globalisation and growth of trade, and with it the potential for what many call 'pathogen pollution', the spread of pathogens and pests with that trade.
We are seeing intensification in livestock industries, particularly in pigs and poultry – but also increasingly in aquaculture and dairy cattle feedlots – and high densities and high numbers of animals attract particular characteristics with respect to diseases.
We have seen in Australia a focus on the quarantine continuum, working not just at the border where you see the sniffer dogs as you come into the country, but also pre-border, with our neighbours and our trading partners, to try and make sure that what comes from there to here is safe, and post-border, in country, trying to get our own farms and our own industries more prepared and more secure.
We have seen a dramatic increase in the amount of time spent on emergency management in Australia in the past 10 years, looking at what is called PPRR – prevention, preparedness, response and recovery. Of course, animal and plant health agencies tend to be the first three – , looking at prevention, preparedness and response – and social services and others tend to focus on the recovery.
As I mentioned, 'one medicine' is becoming increasingly important. Even though the concept was promoted at least 30 years ago, there are more people now starting to advocate the advantages of working together in teams between veterinarians and medicos for diseases that cross between animals and humans.
And a very important factor is that we are seeing greater demands from society. People want increased safety, and increased animal welfare, and these are going to be very important in how we respond to diseases that occur.
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A summary of how I see it is that when I first came back to Australia some 14 years ago the questions when a new outbreak occurred were, first of all, 'What effect will it have on production or productivity?', 'Will it affect trade?', 'How much will it cost to control it or eradicate it?' – and at about question 4 or 5 was, 'Might it infect people?'
Now the very first question we are asked when a new disease occurs is, 'Can you guarantee it won't affect people?' That is a very different question, and a much harder one to answer, particularly when you have an outbreak where you're not sure what it is, you're not quite sure what is happening, whether you've got the first case or not, and you have people saying, 'Give us a guarantee it won't affect people.' How do you answer that?
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Among the changing expectations we see internationally, slaughter-out responses are no longer as acceptable to society, especially if other options (for example, vaccination) are available. The classic case was in the UK 2001 foot-and-mouth disease response. The calf shown on the right-hand side of this slide was a 'Bambi', and that calf and its owner almost stopped the total eradication program. (The 'Bambi factor' is named after Walt Disney's wonderful deer character which is so photogenic and human-like.) It was front page news and lead TV news for several days that they were going to slaughter that poor calf because it was on an infected premises. There was enormous sympathy from the public about Phoenix, the white photogenic calf. Eventually Phoenix was put down, but it is still a classic case of the power of the media with many lessons for risk communication.
Again, with 'bird flu' in Asia, right across the area we are seeing concerns about the slaughter factor, often for cultural reasons. In Thailand, for example, I have seen veterinarians obliged to slaughter-out infected duck farms in tears as they are obliged to kill animals – If you are a Buddhist, killing animals is not something you wish to do. Even though scientifically they could explain the need, the emotions were very full on.
The other aspect with many areas of developing countries and bird flu is: how long can one continue to slaughter-out and remove from people a very important source of food and employment?
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We are also seeing a change in reading. We now have journals called Future Virology, Future Microbiology, Pharmacogenomics, Nanomedicine, Biosecurity and Bioterrorism – always an interesting read, that one – and a journal called Futures, which looks at some of the more philosophical approaches to how we think about what might happen and how we shape what might happen.
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Among incidents around the world recently in pigs, porcine reproductive and respiratory disease syndrome (PRRS) first occurred in 1985 in the US and has spread worldwide since; post-weaning mortality and wasting syndrome (PMWS) is associated with a group of viruses called the circoviruses, and there are half a dozen diseases associated with that – again it moves rapidly and has spread around the world – and we will talk about Nipah virus in detail.
The poultry disease shown here are ones you may not have heard of, but they have been important in poultry production and again have spread worldwide since they werefirst identified. Chicken anaemia agent may well have been spread worldwide through vaccines, at least to get it into many countries in the first place.
There are a number of diseases in cattle, the most recent one of interest being bluetongue. Bluetongue 8 is spreading in Europe at the moment, and two countries have now said it is probably endemic. That was a disease that was always thought to be an African disease that was never going to get into Europe.
Among crustaceans, crayfish plague is a very important fungal disease that has spread through crayfish stocks in the Northern Hemisphere and there is a whole range of prawn diseases, Taura syndrome being one that is reasonably well known.
There have been incidents in finfish and amphibians. Chytrid fungus has also spread very widely and is actually one of the few diseases that appear to be causing loss of whole species, in particular some of those species of frogs that were quite endangered for other reasons. Perhaps this disease is tipping the balance in a number of endangered species towards extinction..
With humans, we have had SARS and Chikungunya. Chikungunya is a virus that belongs in Africa. It has been spreading from Africa and is now right through India and into Malaysia and Indonesia. It will continue to flare up and is coming this way, being a vector-borne disease.
So these are some examples of things that occur overseas. You'll pick these up in newspapers, and many others. But don't forget it happens in Australia too.
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This is a list here of recent incidents in Australia, from pilchard mortality to anthrax in Victoria, where there was a big outbreak a few years ago. Anthrax occurs periodically in small numbers of animals here every year. Newcastle disease I have already mentioned. Tasmanian devil facial sarcoma appears to be a transmissible tumour spread by biting; it is not an infectious disease per se. Porcine myocarditis caused the loss of between 100,000 and 300,000 young piglets in Australia's largest piggery and has now been associated with what appears to be a 'new' virus, never before found. Abalone herpesvirus was recently found in Victoria in cultured and now in wild abalone. There is also a disease called pearl oyster mortality or oedema disease. We don't yet have an agent for that, but it seems to be very likely to be viral, and it is actually causing very severe losses in the northern pearl farming industry at the moment.
There are other ones there, but when you look at this list it is interesting to see which ones of those have actually been due to incursions, rather than which ones have actually been agents we have had here and that have changed for some reason. One might debate some of those, but quite a number of them have actually been Australian organisms we have known for some time that for some reason – and we will explore some of the possibilities – have recently caused epidemics.
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I would like to focus on these case studies – quickly on BSE, or 'mad cow disease', a bit more on foot-and-mouth disease, avian influenza, the bat viruses and, just to give an example of how one might approach a totally unknown situation, colony collapse disorder of bees.
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BSE is a disease that we now know is transmitted by feeding animals to animals, and is caused by a prion. In 1966, we had prohibited all imports of stockfeed except from New Zealand; that was done because of the concern about introducing anthrax into Australia. In late 1984 – it really hit the presses in 1985 –the first case of BSE occurred in the UK. It became notifiable there in 1988. Australia has a conservative approach to quarantine and disease controls, and we banned imports of live cattle from the UK and Ireland in that same year. So we were fairly quick off the mark.
We started tracing the 131 cattle that had been imported from there in the previous few years, and eventually found most of those except for the ones that either had died or could not be found; they had probably died up north and were never going to be found. So we took fairly early action.
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By 1989 the 'Southwood Report' stated that it was unlikely that BSE was a threat to human health. (It's always easy to be wise in hindsight, to look back and think about what one should have said!) In the early 1990s, we established an expert committee here to advise on and review quarantine controls on a whole range of things: animals, genetic material, animal products including meat and bone meal, pharmaceuticals/biologicals containing bovine material, cosmetics – a lot of bovine material gets into cosmetics – and beef and beef products used for food. So again we were fairly early in trying to work out what the risks were and how we could manage them.
This was consistent with our official policy that we don't have a zero risk policy; we have a managed risk policy. We try to manage risk so that we have got a residual risk that is acceptable.
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In 1996, the UK's committee announced that there was a probable link between BSE and variant CJD, its form in humans. We adopted a voluntary industry ban in 1996 on feeding ruminant material to ruminants. It was in legislation in all states and territories a year later. (It is no easy thing to get all seven states and territories to do the same thing at once.) In 1999, the ban was extended to feeding mammalian materials to ruminants as well.
In 1998, we introduced the National TSE [transmissible spongiform encephalopathy] Surveillance Program, where we actively looked for cases of cattle with nervous diseases and examined their brains, to try and get enough surveillance data to convince other countries that we were free.
Eventually, after 17 years of surveillance data and so on, which we showed to the World Organisation for Animal Health (OIE), through its ad hoc group on country categorisation, we finally were amongst the first countries to be accepted as free of what they call 'negligible risk'. (They don't use the term 'free'.)
So we had taken a series of steps fairly early on to try and manage the risk from these products, and we have kept out BSE.
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One of the biggest challenges we had was that as this disease affected the UK and Europe, with very large numbers of animals involved, they tried to amortise that problem to the rest of the world. Basically they were saying, 'Well look, everybody else in the world feeds cattle to cattle and you must do the same.' We spent a lot of time trying to explain to them that we don't raise our cattle that way in Australia. Here they eat grass, and we have very different production systems, but it is very hard to explain that to some colleagues in the north.
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Foot-and-mouth disease is an infectious disease, rather than one that is transmitted by non-infectious material. It occurs throughout most of Africa and Asia and much of South America. Australasia and North America are free, and Europe is usually mostly free. (Some of the eastern states of Europe get regular incursions, but most of western Europe is usually free.)
There are seven serotypes and about 60 subtypes, and that is important because if you are vaccinating to control it you need to use the right vaccine against the particular subtype to get the best immunity.
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This slide helps to give a simple perspective. In about 2003, just before H5N1 avian influenza broke, a group in America looked at the reported outbreaks of the 16 main diseases. This is what the OIE, the World Organisation for Animal Health, calls List A. They looked at all the outbreaks reported around the world. (This excludes China, because China at that stage didn't report.)
You will see that of all the outbreaks – around 17,000 in total – 11,000-odd were foot-and-mouth disease outbreaks in Asia. A total of 14,000 out of about 17,000 outbreaks were foot-and-mouth, as against the other diseases shown: vesicular stomatitis, rindepest, bluetongue, sheeppox, classical swine fever, influenza and Newcastle disease. Now, that would change if we did that figure today because the AI (avian influenza) outbreaks would increase. But it is important because sometimes we forget that the old diseases are the ones that cause a lot of the losses worldwide.
It is also interesting that when we talk about foot-and-mouth disease that I think everyone in this room and most of the public think of the UK, and think of 1969 and 2001, the big outbreaks they have had there. But most outbreaks of foot-and-mouth disease worldwide are small outbreaks and with good veterinary services are rapidly controlled. In developing countries, of course, it is endemic and it continues to cause ongoing losses.
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This slide is just to remind us of that large outbreaks of FMD do occur outside the UK: an outbreak occurred in Taiwan. It is an island country with good veterinary services, which had been free of foot-and-mouth disease for many years, in fact since 1928. It had a pig industry of 16 million pigs, exporting 6 million a year, mainly to Japan, worth about US$1.6 billion.
A pig-adapted strain entered in 1997 and it devastated that industry. More than 6000 farms were infected in four months; 180,000 pigs died and 3.8 million were slaughtered to try and control the disease. More than 30 million doses of vaccine were used, there were direct losses of US$380 million, and they lost 65,000 jobs.
They have had a couple of incursions since, and that whole industry and that economy have been very badly damaged. Yet very few people in Australia would have heard of that outbreak – the Taiwanese don't speak English and they don't play cricket – whereas you do hear about it from England.
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During that period we watched a strain called the 'Pan-Asia' strain starting to move. It was first found in 1990 in India and it spread east and west, reaching Japan in 2000, reaching Greece and the threshold of Europe in 1996. You would see that a couple of countries, Iran and Iraq, don't report much, and Myanmar/Burma doesn't report either, but I am sure it went through there as well. It jumped by ship, by the feeding of ship waste to pigs in South Africa, and was introduced there. And of course that was the strain that in 2001 got into the UK, the one we remember.
We were advising our industry in the years well before 2001 of the movement of this particular virus, and we were very concerned about how rapidly it had been spreading around the world.
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So what happened in 2001? The Pan-Asia strain entered the UK and the outbreak involved were 2020 infected premises (as against 6000 in Taiwan). More than 9300 farms were destocked, about 4 million animals were destroyed, and at the peak of the outbreak they needed something like 1300 vets, 350 slaughtermen, 2500 troops. It had a huge effect on the whole economy – the total losses were as much as £9 billion – and it spread to three other countries in Europe.
The total losses are interesting, because the losses were primarily to the agricultural sector. Hardline economists would tell you that it was of benefit to the economy because there was economic activity in other sectors, but I don't think the farming and tourism industries saw it that way.
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The likely source was swill-feeding of meat to a piggery at Heddon-on-the-Wall, in northern England. There were sheep movements to a Carlisle market, just south of there, on 13 February, and to Devon, where some cattle were infected.
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It was spread further by sheep over the next couple of weeks, from that Devon area through into Northampton and so on. The authorities knew nothing of this. There were 4 million sheep that moved in the UK before they found the first case, which was found at an abattoir.
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By that stage sheep had actually gone from Devon into Europe – legal movements, because there was no evidence of foot-and-mouth disease occurring there.
Foot-and-mouth disease in sheep is a silent infection in most animals. It doesn't cause the classic blisters, sore feet and sore tongues that it usually does in pigs and cattle. The dramatic photos you see in all the textbooks don't apply in sheep, where if you see anything you'll see a bit of what we might call in Australia 'scabby mouth' or some sores in the mouth and a bit of sore feet. It is a relatively silent infection.
The UK first identified it in an abattoir on 20 February, after 4 million sheep had moved around the country.
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The spread continued into Wales and to Northern Ireland and Scotland.
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So by early March there had been more than 100 farms infected; by mid-March, 200; and very soon after that there was a bigger area infected than in the whole of the 1967 outbreak, which went from 1967 to 1969. (That is shown on this slide in red.)
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It spread out of the UK, the first cases being in France, then in the Netherlands and one in Ireland. The French got onto it very quickly, because by that stage they were on full alert, and they slaughtered their properties out. The Dutch had a number of farms infected, mainly dairy farms. They chose to vaccinate around the infected farms, whereas the UK didn't choose to vaccinate; they took the infected animals out and did destroy them, ultimately, but did so in better conditions, in the sense that they were taken to abattoirs rather than field-shot.
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The outbreak in the UK dragged on for months and months. It is always hard in the last phase of an outbreak to get those last few cases. There was enormous political flak – it delayed the general elections there, there were huge debates between experts – modellers coming from mathematical disciplines, epidemiologists coming from the veterinary area – and a plethora of people advising COBRA, the relevant UK emergency group.
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What did Australia do? First of all, we did something very sensible: we sent vets across to help in the outbreak. That both helps our colleagues overseas and also gives us experience in managing these diseases. We also sent lab technicians and stock inspectors and some others.
We worked with some other countries – the United States, Canada and New Zealand, the 'Quads' countries – to develop better standards and to look at carcase disposal and how one could do that better, and we looked at criteria for country and zonal freedom, if it were to occur in any of our Quads countries.
We increased the awareness and engagement of industries here, and held a series of workshops around the country over a number of years to try to raise awareness and get biosecurity plans in place and better planning and preparedness here.
We also reviewed new technologies and what impact they might have on our current policy, and commissioned specific work by a company called Ausvet and the CSIRO laboratory at Geelong, the Australian Animal Health Laboratory, to try and look forward a bit about what new technologies are there now that might enable us to adopt better and more innovative policy approaches if it were to occur in Australia.
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We reviewed our contingency plans. We have a national plan called Ausvetplan, which covers the planning details for a whole range of diseases, including foot-and-mouth disease. It has manuals about control centres and how you run those, communications, and so on – a very detailed set of manuals, all available on the internet and debated at length in 'peacetime' so that in 'wartime', if they are needed, we are better prepared.
We also exercised those plans, with a series of short desktop exercises around the country – I think all states and territories had at least one. These culminated in a five-day national exercise called Exercise Minotaur, where we simulated a major national outbreak at some length – simulating Day 1, Day 3, Day 7 and three weeks later – to see how our response would work. It involved something like 1000 people around the country and was at that time probably the biggest disease simulation exercise ever conducted.
We certainly looked at new diagnostic techniques. We both developed some of these at the Australian Animal Health Laboratory at Geelong and introduced new ones there, and distributed some of those techniques to other laboratories around the country so that in the event of need they could actually bring them on line quickly.
And we started doing some very serious spatial disease modelling, looking at real datasets from farming systems in Australia, across the different farming systems and landscapes, to provide two things: realistic scenarios for training and also decision-support tools for use if an incursion occurred. They are probability-based models, based on realistic simulations. You can feed in things such as, 'I only have 200 vets. Where do I put them? Do I put them into the field, do I put them onto quarantine of properties, or do I put them into managing slaughter teams?' You can very quickly work out where your resource constraints occur, and this is a fairly powerful way of advising policy makers.
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Let's move on to the current 'celebrity disease', avian influenza, or bird flu. It is a viral disease caused by influenza viruses, of which there are 15 H types and nine N types. H is haemagglutinin and N is neurominidase, so it is just like the licence plates of a car: we talk about H5N7 and so on, to tell you what particular strain you are dealing with.
The virulent form is called high-path avian influenza, HPAI, or fowl plague. It causes, basically, sudden death. If the birds survive, they get generalised haemorrhages, oedema et cetera. There are less virulent forms, called low-path, which cause respiratory disease, egg drop and so on. Some low-path strains, if they are allowed to continue, will mutate and turn into high-path and become virulent.
Some strains, the H5 ones and H7 ones, are potentially zoonotic. H5N1, which is the current 'celebrity disease' worldwide, has killed 192 people out of the some 320 that are known to have been infected since 2003.
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There is a wide range of hosts, both birds and mammals. The important thing on this slide is that the species with the highest frequency of carrying these viruses are the water birds, the waterfowl. Wild ducks, geese and swans tend to carry these viruses more commonly. That is important here for epidemiology, and important in why Australia so far has remained free.
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If you looked at the literature you would see that before 2000 there had been a total of 19 outbreaks of bird flu worldwide – excluding China, which again didn't report. There have almost certainly been outbreaks there that were not been reported. Five have been in Australia, two in Italy, et cetera, and three of those had been associated with low-virulent strains mutating to become highly pathogenic.
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We had five outbreaks, from 1976 to 1997. They were all H7s of different sorts. The total costs are shown here. All of those were linked to wild waterfowl; all of those farms were low-biosecurity farms where there were ducks walking amongst the chickens et cetera. But in none of those outbreaks did we actually find those particular strains in those wild birds at the same time. We have found them before and since, but there wasn't a direct chronological link involved.
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Since 2000, there has been an explosion of outbreaks around the world – Hong Kong in 2001 and 2002 (the first human cases were there, with H5N1, and from memory seven people died then), Chile, the United States et cetera. Europe in 2003 had a big outbreak, when 60 million birds were slaughtered and there was one human death, with the H7N1 strain. Going down the list, the big strain is H5N1, and that has spread from Asia into Europe and Africa.
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So what happened? In late January–early February 2004, a number of countries reported they had HPAI. We had fairly good intelligence that it was happening well before that, because for the first time ever we were getting requests from laboratories overseas for avian influenza diagnostics from our national laboratory at Geelong, and we also had a variety of people working in the region in the poultry industry who were telling us it was occurring. We were able to advise our industry that it was almost certainly there, well before the official reports occurred. So that sort of disease intelligence is quite important.
The illusion was that it happened all at once in half a dozen countries in Asia, and I would put it to you that it was in part an illusion of reporting. Indonesia, for example, didn't report till late February, but now officially admits that they certainly had cases as early as August the year before. We know the same applied in Thailand and a number of other countries. China, just the day before the first international meeting on aid for this disease, announced that it had the disease. So it was really quite an interesting political disease, as much as a biological phenomenon.
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The apparent map was like this, showing the outbreaks in the three months before each date.
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In March more of those lit up.
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In September, we are seeing further extent, particularly coming down into Indonesia.
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And since then we have seen it getting into Europe and Africa. The map for this year is much the same, different countries lighting on or off, depending on the time of the year. The concern at the moment is primarily that it is endemic, continuing uncontrolled in a number of countries, particularly in northern China, Vietnam, Indonesia and Africa, both in Egypt and in Nigeria.
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Quite a number of things might have changed. There have certainly been very big increases in the numbers of birds raised. Husbandry systems have changed in some countries. Migration patterns? Have they changed with climate change? There has certainly been a change in some of the viruses circulating. Trade patterns? Possibly. And vaccines. Remember, the vaccines we are using for this disease are the same vaccines that were around in the 1960s. They are not new, modern-technique vaccines; they are very old vaccines with only one exception, really. Now there is a lot of work being done by vaccine manufacturers worldwide, but for 30 years nobody looked at this disease, because it wasn't affecting countries that could afford to pay for vaccines.
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One of the interesting things to plot is the number of ducks and 'chickens' – or chooks, in Australian parlance – per agricultural person in South-East Asia. We have seen very big increases in Thailand, with significant increases in Malaysia and China, between 1990 and 2000. The poultry sector has exploded in those countries, both commercially and in the village areas.
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The very important species are ducks. This graph from the Food and Agriculture Organisation (FAO) shows, just to give an impression, the growth in numbers of ducks between 1993 and 2003, from Laos through to Vietnam. Ninety per cent of the world's ducks occur in China, Vietnam and Thailand, and so we are talking about something like 800 million ducks. Ducks are really the key to this particular disease.
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FAO defined different sectors. Sector 1 is the high-end, industrial, integrated farms, which have a high level of biosecurity, and these birds are marketed commercially. In many countries that are affected, those birds are perfectly safe. They are either well-vaccinated by the companies that own those flocks, or they are left alone and they are an island of disease-free birds in a sea of virus. Certainly in countries like Thailand we saw innovative companies buying out village birds for three kilometres around them, and providing meat and eggs to the villagers, as a means of keeping their birds free.
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Sector 2 are the ones that are more commercial, non-integrated, with moderate to high biosecurity, and they are marketed commercially as well. So the birds tend to get into a commercial chain and be cooked, et cetera.
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Sector 3 are commercial smallholders. They have minimal biosecurity, and their birds tend to be marketed in live bird markets. They will eat some themselves, but they will take their excess each day to a live bird market. And of course the ones they don't sell, they take back. So you mix your birds at the markets, take them back, and you spread the disease. Motorbikes are said to be the most frequent means of spreading this disease in South-East Asia.
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The last sector is your true village birds, where poultry are raised for home consumption and if there are any sold, it is more by informal marketing with the neighbours rather than to a formal market.
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Of course, in real life it's not so simple. Here are some farms that have various levels of biosecurity. You can see ibis under the sheds of chickens, ducks right outside the chicken sheds, and the manure going straight into the ponds to feed fish, and a pig farm in one of them at the back. So it is not always as simple as the FAO classification in real life.
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How do humans get the disease? At the moment you really have to try hard to catch it. Cultural practices are important. A significant percentage of the people who have caught the disease in Thailand and Indonesia got it from fighting cocks. If you fight with fighting cocks you do two things: if they are wounded you suck the blood to sew them up, at the end, and also if you are betting on them you will get the bird and blow into it and suck back to get an idea of its tidal volume, how well it can breathe. If you do things like that, you are likely be exposed to large amounts of virus and should not be surprised if you get the disease. The other custom in parts of Vietnam and southern China, at wedding feasts, is drinking raw duck blood, which is said to increase your virility – not recommended.
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The big risk is live bird markets. When you think of markets here it is not quite the same as what you see in places like South-East Asia. There are enormous opportunities for exposure to contaminated manure, blood et cetera as people slaughter birds in less than ideal environments.
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As to wild birds, what is their role, what type are involved, what are the implications, what are the key messages to people? There have been great concerns from ornithologists about blaming wild birds and shooting them. I have no doubt that wild birds have played a role in the spread of disease, and there is good evidence for that, but they are not the only means of spread.
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You would all have seen flyways diagrams like this one, which shows flyways of birds from north to south, with some going across south-west. One can imagine how some of the spread is occurring, and there is certainly good evidence of the east–west spread there and concerns about the north–south ones. You'll see many diagrams like that showing the Australian flyways.
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The important thing for us to remember from this slide is that the largest flyways is the flyway of the shorebirds and waders. These birds have a very low prevalence of AI; that is, only a very low percentage of them are infected with any sort of AI. The one that is important is the flyway for the anatids – ducks, swans and geese. Note that they do not come as far south as Australia.
The concern is that if we get infection in Indonesia, which we have, and if we get incursions into Papua New Guinea, there are some birds that periodically go from Papua New Guinea into northern Australia and across the Torres Strait, and back. But while it is only in the swans and the anatid family, Australia is relatively protected. Many people ask why we haven't become infected, and I think that is one of the key reasons why we haven't so far.
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What have we done here? We have increased our border quarantine measures; we have increased surveillance of both domestic flocks and the wild birds; we have run exercises to test our preparedness plans for this disease; we have certainly had a lot of communication and intelligence with industry, both here and overseas; we have increased our extension and awareness to raise industry biosecurity; and we have also put some money into diagnostic tests to give us better differentiation of the different strains that are out there, so we can be sure, if we find one, exactly what strain it is.
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What is the role of vaccines? There is a great debate internationally about this. Do you vaccinate or not? Do you vaccinate this species or not? I suspect that more and more countries will be looking to vaccination. The international agencies opposed it originally because of concern that it could hide or 'mask' infection, but more countries are realising they have to live with this disease, which is going to be around for a long time, it is not going to go away soon.
Village birds: the question there is the R value. R is the reproductive ratio: if each bird infects one other bird or more than one bird, the disease will spread. If that ratio is less, it will die out. There is some evidence in countries like Cambodia and Laos, where you have very low populations and very low density of populations, if the disease gets into a village those birds that get it die, they are dead and eaten by dogs or whatever, and the disease dies out.
Ducks are the big question. Not only do they get disease but some act as silent reservoirs. Almost certainly, there are ducks and ducks – some types or breeds of ducks, at some ages, if infected get clinical disease, whereas other ducks seem to show no signs of disease but excrete the virus and are a source of infection to chickens et cetera.
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The big question is whether we are going to get a human pandemic. That really depends on the sorts of systems shown here: the production systems, the ecology of the viruses and the human exposure risks.
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Where does all that take us? On to bats.
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We have seen a variety of 'new' viruses coming out of bats in the past few years – new to science, that is, not necessarily really new. A number of them are listed on this slide.
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I just want to touch on Nipah virus, in particular. It was first found in 1998. More than 260 cases of encephalitis occurred in people in Malaysia. Initially, it was thought to be Japanese encephalitis, because they see that periodically there, and the signs in humans are very similar. So they misdiagnosed it, in the sense that they didn't have a diagnostic test anyway. More than 105 of those people died.
Very quickly they linked it to a disease in pigs that was coming from bats – a spillover. It causes respiratory signs ('barking pigs', a very harsh cough), encephalitis in some and high mortality in young piglets. There was some evidence of spillover into cats, dogs and possibly even horses, but they weren't really of epidemiological significance.
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The index farm was in central Malaysia near Ipoh. It was a large piggery, 30,000 animals, right next to primary forest of fruit bat habitat. To pretty the farm up they had mangoes and other trees – fruit crops – growing through the farm rows. The bats would come in and eat those, drop the mangoes, defecate et cetera, and that is almost certainly how the pigs were exposed and got the infection initially. And it spread through them.
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It resulted in the culling of more than a million pigs, more than 800 pig farms were destroyed, $120 million of exports were lost and 36,000 jobs were lost. This was a fairly significant outbreak. The Malaysians went in 'boots and all' and really did a very good job cleaning it up. The problem now is: do they continue with a pig industry, or do they work out different farming systems where you can have pigs without attracting bats?
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The disease gets more interesting because in Bangladesh and India there have also been outbreaks. The recent outbreaks in Bangladesh are of some potential concern. There have been five major outbreaks since 2001 – seasonal – and 102 human cases have been confirmed (there may well have been more) and 75 of those died. Again there was a pteropid reservoir, a fruit bat; and transmission was associated with risk factors such as climbing trees, contact with sick animals, contact with sick people, and drinking raw palm juice. Just recently, they have retrospective data that gives first evidence of human-to-human transmission there, not necessarily bat-to-human. It may well be that this agent is starting to break through the next level of its journey to becoming a human pathogen. It is certainly one to watch.
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Pteropid bats are very widespread, from Madagascar, near Africa, right through the Pacific Islands. But they don't migrate. They're not like birds – they don't move backwards and forwards. They are panmictic; they live in colonies and breed, and mix at the edges of those colonies.
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So one of the research issues we have been looking at is tracking studies. Peter Daszak, Hume Field and others, with the Australian Biosecurity CRC, have been doing some fundamental work trying to find out how far these animals fly to forage each night. You will see that they fly right across the Straits of Molucca with gay abandon – they don't worry about international borders – and some of these go rather long distances. They have been fitted with radio collars to track them through that area, and they can certainly go more 200 kilometres in 10 days.
It seems that one of the reasons they are flying more there than had previously been described is that there has been loss of rainforest habitat and so they have to travel further to forage. They don't like too much oil palm fruit, but they certainly like other fruits and rainforest fruits, and we are finding a relationship between the ecology of those animals, their habitat destruction, and where they are moving.
We have some people working on the same sorts of studies in Australia.
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If we look at wildlife diseases and a host of others, we see some lessons for us generally. They are of growing importance, both for other animals and for humans, and also intrinsically for the value in biodiversity and sustainability.
Compared to livestock diseases, not much is known about them. There is not much monitoring and surveillance done anywhere. There is very poor collation of the information and poor reporting. The costs are possibly quite high but they are not well documented, so you can't prove to somebody how much wildlife diseases cost.
And many of them are complex and multifactorial, and certainly need interdisciplinary teamwork to work them out.
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The last case I want to talk about is a 'new' disease, colony collapse disorder. It is a new syndrome in bees that started being reported late last year in the US.
There have been die-offs of bees in the northern hemisphere for some years, and they get different names – 'disappearing disease' and so on – but no-one has been really quite sure how bad they are and what they are doing. But this has been a very large die-off. People report going out, leaving their hives, coming back a week later and finding them absolutely, totally empty but with the honey still there. So the bees have been alive and well, and are actually dying quite quickly. They are not making it back to the hive. There is a complete absence of adult bees but the brood colony is left untouched, and food stores are there.
The causes proposed are numerous, everything from malnutrition to mobile phones, which are supposed to upset their navigation systems. It is almost certain to be multifactorial.
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What have we done in Australia about it? We picked this issue up in our 'foresight' scanning, trying to track what is happening around the world. We talked with industry groups here to see if there was anything like it happening here, and so they could increase their surveillance. We reviewed our import requirements of what is coming in to Australia and what is not. We are looking at increasing our sentinel hives scheme here, as we have hives that are monitored for other diseases here. We are monitoring the literature – both the formal literature and the grey. Also, much of this information is on websites and electronic news lists and blogs, and we are monitoring these. It is now included in an inquiry here into the honeybee industry, and we are certainly continuing to liaise with experts in the United States and Europe.
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That brings me to foresight, which is an activity that I think we need to think more about, particularly in regard to developing better policies. Joe Voros, who works at Swinburne University of Technology, in Melbourne, puts up this model. To him, foresight is that box that says to look and see what is happening, then work out what is really happening, work out what you might need to do, and then finally decide how you are going to do it and who will do it.
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To think of it from an animal health point of view: we do things like environmental scanning, tracking what is happening in the literature and around the place; we do some scenario planning and some backcasting, thinking of what it might look like in 10 years' time and what would have to happen now to get there. It involves systems thinking approaches and a range of other techniques. The idea is to try to get a range of strategic options to feed into public policy.
Very often, in government departments, with the sorts of issue I am talking about we are looking at planning horizons of three to 12 months, rather than three years or, better, 10 years, needed for considering emerging diseases threats.
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Richard Slaughter claims that strategic foresight is the 'ability to create and maintain viable forward views and to use the insights arising in organisationally useful ways'.
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The sorts of approaches we are looking at are based on these seven themes, which we have been looking at since 1993: emerging diseases, sustainability et cetera, down to new technologies and so on.
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Worldwide, there are a lot of people looking at foresight. There have been very large programs in Europe; there are programs in the United States, Canada and New Zealand. A range of information sources have started to appear. ProMED is an emerging diseases list on the internet. GOAN and GPHIN are United Nations-run information networks on diseases.
In Australia, we provide a number of these lists. One, called Belly-up, is for fish diseases – that is how the fish end up if they are sick – and there are others on particular diseases. NAHIS is the National Animal Health Information System, on livestock diseases, and the other one is the Australian Wildlife Health Information System. We are trying to collate data and information, to package and analyse it, to see what is going on. If something unusual is going on, then one hopes it will be investigated – earlier rather than later.
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Emerging issues analysis is another technique, where you track issues over time. If you look at the quantity of information published, you will often find early on that the sorts of things we are talking about are picked up in science fiction and then gradually get into the scientific literature. Then they get into the mass media and so on. You can track issues arising, be it antimicrobial resistance or emerging diseases.
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All this helps contribute to what I call the changing science–policy interface. I just want to touch briefly on how science and public policy work together, post-normal science and trans-science.
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Science is a very broad discipline and integrates information of a range of medical-type disciplines and their new technologies. It provides a framework for analysing and synthesising. It leads to outputs that can be provided into public policy, but it is still largely based on classical, reductionist approaches.
I would put it to the scientists in the room that as we grapple with these issues of greater complexity and more uncertainty, we need to think of other approaches.
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Funtowicz and Ravetz talk about post-normal science, that you need different science for different problems. We are very comfortable as scientists working in the first sector of this figure, with relatively low uncertainty and low decision stakes. As we work in the areas of emerging diseases we are working in the outer sector, with higher uncertainty, more judgment, and potentially very high decision stakes. Many scientists are uncomfortable with that, because there is judgment – but the judgment is often the policy-maker's rather than the scientist's.
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Weinberg argues that there is a difference between 'science' (or 'research science') and 'trans-science' (or 'policy science'). He recognises a grey zone between science and policy, and says there are questions that are to be asked of science but cannot be answered by science, questions that are largely due to the questions and issues that are more complex and more uncertain. He argues that one has to 'democratise' – a terrible word – how one 'does' science.
He argues in particular that scientific ways of knowing break down where there is a high 'dread' factor, where people are fearful of the consequences. Certainly in risk analysis we see that very strongly, that people are concerned about 'what affects me, what affects my children': we think individually, rather than at the population level.
All that compels scientists to look beyond the known facts to make judgments and determinations, and nowhere is rawer than in the face of an outbreak, where you have the first case of a disease and you have to make a decision that day, on limited information, about what you are going to do. Judgment there is very important.
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Going further than that, some people argue that you should focus on expertise rather than science. Collins and Evans, and Carolan, are the major proponents of this theory.
The important point in their argument is that public expertise is the explicit incorporation of values into your decision-making processes, with a change in the focus of the question from 'what is' – the science question – to 'what should be done', which is more a policy issue. I think that many scientists are not exposed to some of these ideas, and probably more exposure would help us to meet some of these challenges.
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We are very good as scientists at measuring things: we measure production efficiency, productivity and profit. We do it very well, and in great detail. But what should we be measuring? For emerging diseases, what should we be measuring about the risk factors and the thresholds – things like population size and density, inter-connectedness and so on? What about resilience and sustainability of our production systems? What should we be measuring there? Surely we should be looking at inputs such as ecological footprints, energy, water, fuel et cetera.
Importantly, how much do we need to know before we act? What cautionary measures – or, as some would say, precautionary measures – should we be taking with the knowledge we have? If we are going to try to stop emerging diseases, we should be looking at how and where we put our farms and how we locate our industries. How do we affect the planning process of separating our modules and our farms by greater distances, decreasing animal densities and farm sizes, keeping them away from wildlife, where many of these diseases are coming from? This leads into strategic planning, land use planning and zoning, and these involve are societal influences and decisions, and are not just for technocrats.
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In conclusion, diseases will continue to emerge. There will be new or newly recognised ones, and known ones that have broken through. They will occur and will cause losses in livestock and aquatic animals, in wildlife and humans (zoonoses), at local, national and international levels.
Their effects will include pathogen pollution and changes to biodiversity. The small island countries in the Pacific et cetera are particularly vulnerable to the latter, and 'islands' in the sense of islands of biodiversity in countries like Australia are also quite vulnerable.
There will be increasing concerns, I suspect, about the responses to animal diseases: what are the options, what are the costs, what are the animal welfare implications? By the options, I mean looking at options to vaccinate rather than to slaughter-out, for example.
There will be continued and growing concerns about consumer confidence, about the safety of animal produce – 'Is it safe to eat this?'
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All that will need better interdisciplinary cooperation, better intersectoral planning and better collaboration, particularly internationally, to look at the threats that are on our doorstep.
It needs early identification and prompt reporting, through better monitoring and surveillance, diagnostic capacity, information systems et cetera.
In doing that, we also need to consider what factors favour emergence, when we are planning changes to production systems. Certainly there are opportunities and a need for targeted applied research into risk factors for disease emergence. The Australian Biosecurity CRC, amongst others, has taken a lead in trying to get some of those risk factors analysed, but there is more to be done there.
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We certainly live in an increasingly interconnected world, with unprecedented opportunities for more diseases to emerge. But I do think we can take some cautionary approaches now. We should use classical science and technology where appropriate, but acknowledge that they do not have all the answers. And we need to improve our ability to provide better input into policy, by improving our ability to deal with uncertainty and complexity – and by being prepared to make judgments and determinations based on what we know when we are asked.
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If I could leave you with one take-home message, it is STEEP. STEEP is an acronym to remember: Social, Technical/scientific, Economic, Environmental, Policy/political. All of those things are involved in responding to and preparing for emerging diseases. We need not just the 'T' but each of those elements. The solutions to biosecurity, I put it to you, are more than just 'T'; you need to have all the other elements of STEEP.
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I thank you for your attention.
Discussion
Hugh Tyndale-Biscoe: Thank you very much, Mike, for a really wonderful talk. There was a lot of material there for discussion and questions.
Question 1: My understanding, as a scientist, is that traditionally the role of the scientist is to gather data – in this case concerning zoonotic diseases et cetera – and the role of the policy-maker is to use data to make policies. I am trying to wrap my brain around the idea of 'post-normal'. How does post-normal work in terms of the role of the scientist?
Mike Nunn: I suppose in the sort of environment where I work there are three levels of input. There is a science input, there is a policy input, and there is a political input, and a good scientist is providing the best scientific advice possible to the policy-maker.
Now, the policy-maker may also be a scientist, if someone has come from a science background, but that person is working at the interface between the politicians and the scientists. That role is a difficult one. You are trying to convey to the scientists what questions that the policy makers and society want asked (and thus what research you should do), and also you are trying to convey to the decision-makers, often politicians, what the uncertainties of that science are.
Funtowicz and Ravetz argue that there is a role for scientists to step out of their normal lab coat environment, if I could put it that way – that is the popular image – and the certainties of science with robust trials, statistical analysis and so on. There are certain types of decisions that you have got to take by looking at the problem a different way.
I think that in emerging diseases and disease responses you never have the all the information you want. You can't stop an outbreak and say, 'Whoa! Let's do some research and work out the best approach.' You have to make a judgment call. It is that nexus or interface between science, policy and decision-makers, if I could put it that way.
I think they are trying to say that more science is going to be at that policy interface than in the past, because you won't have the luxury of doing all the research you might want to do. You are going to have to make a call.
Hugh Tyndale-Biscoe: That has been the dilemma for medicine for some time, that the practitioner has to make a decision with the available evidence. Clearly, in the quarantine area that you are in, the same dilemma applies: you have to work with what information is already available.
Mike Nunn: Certainly you do in an outbreak response, but you also often have to do it in 'peacetime' too. So if you are doing an import risk analysis, you can't afford to take 25 years to do more and more research. You have got to say, 'On the information available, this is what we think happens.' You certainly try to find the key factors, the critical factors that would make something likely to get in or not, and focus your research on those areas. But we have to accept that we are going to have to make decisions in uncertainty. And as issues get more complex and more diseases are more complex– some of the examples I hope drew that out – that is going to be challenging us more, as professionals.
Question 2: I wonder about the problem over having to deal with politicians constantly getting in the way of the sort of work that you are trying to do. Obviously, you will not want to speak out on that issue. But, for example, I find it very difficult to believe that there is any value in having quarantine dealt with as a trade issue. I have attended CRC for National Plant Biosecurity meetings. Here in Canberra they tend to be dominated by scientists who now work in the ministries, and they are quite happy with the fact that quarantine is being dealt with as a trade issue.
Trade is a very short-term thing. It is a political thing. And also, in this time of climate change, there is likely to be a change in the very short term as to what is the best trade that Australia can do. I have heard the discussion, for example, of plum pox virus. People are saying, 'Oh, there's no need to worry about that. Stone fruit isn't a big trade issue in Australia.' Now, who knows whether or not, in a very short time, Australia will need to grow plums for overseas?
So you have got a long-term subject, which is quarantine, in a short-term context, which is politics and trade.
Mike Nunn: It is not entirely trade. Certainly we are members of the WTO, the World Trade Organisation, and under that there are a number of agreements that we are signatory to, the SPS Agreement on the Application of Sanitary and Phytosanitary Measures being the major one. But for each of those agreements you have a scientific basis. So there is the International Plant Protection Convention, the Codex Alimentarius for food, and the World Organisation for Animal Health for animals.
We have scientifically based rules around trade, and it is very important for Australia to help shape those rules. We sit on a number of international committees for different diseases, shaping the rules of the science for trade. So it is not just a matter of rolling over to trade priorities. The issue you are touching on there, about emerging industries – industries that we don't have yet but might have in the future – is a difficult one, because how does one value those? There are no easy answers there. Again it is a decision beyond science, a societal decision.
Think of the aquaculture industries. Are we likely ever to have an industry for some particular finfish that we don't have at the moment but might want to have in 10 or 20 years' time? If so, how do we protect it now? It is difficult, as a society, to make those decisions.
Question 3 (Hugh Tyndale-Biscoe): In relation to the example you gave of the practice you did for foot-and-mouth disease spread, in Ausvetplan, did you include in that plan the possibility of the virus getting into the feral pig population?
Mike Nunn: Feral pigs have been put forward by some people as a major risk to Australia because of a potential for acting as a reservoir of infection for foot-and-mouth disseas. The key factor epidemiologically is that the animals with carrier status – that is, the animals that can carry the virus but not get sick from it, and can spread it – are actually ruminants: cattle and buffalo.
When pigs get foot-and-mouth disease, they get very bad blisters on the feet and the mouth, and they get very sick. The virus stays in them for only about three days and they don't have carrier status, whereas in some cattle it can last for many days.
All the modelling work we have done suggests that yes, FMD may well get into feral pig populations, but it is probably going to die out. The risk is that if they get sick and sit down, they might sit near a waterhole where ruminants might come to drink. We have quite considerable debate about whether, if an outbreak occurred here, the best thing to do would be to leave the pigs alone, or whether you should be going out there and trying to shoot them out. If you are trying to shoot them out, you might be spreading them even further and dissipating it.
In my judgment, the modelling work we have done suggests that feral pigs are not as great a risk as some would maintain, because the dynamics of the virus are such that they are not going to be the main game.
Question 4: Mike, at the end of your talk you were advocating, using some sort of cautionary approach. How do you see the precautionary principle as fitting with the SPS Agreement?
Mike Nunn: I don't. The SPS Agreement talks about a 'cautionary' approach, not 'precautionary'. The reason I put '(pre)cautionary' in the slide is that many in the environmental field use the word 'precaution', and the precautionary principle in environment legislation tends be used to say, 'If you don't know, you do nothing.' I don't believe you can adopt this approach, certainly not in the area where we work.
We talk about a cautionary approach. That is, you look at the best evidence you have, and if you are uncertain you might do some more work but if you have to make a decision you make it on the best evidence you have at the time. That is the difference between the WTO SPS Agreement, and some of the environmental agreements. There is a tension in the international agreements, international law, because one says you should not act unless you have got perfect information, and the other says you should act on the best information you have because you never will have perfect information.
On the slide I put the 'pre' in brackets because some scientists see it one way, as coming from the environment sciences, and other scientists see it more the WTO way.
