We have already referred to the utter futility of nailing cattle firmly to the floor, while allowing an infected wildlife reservoir to flourish around them in our posting here During what became known as the the 'Downie era', the Republic of Ireland operated cattle controls along the lines of those proposed by the ISG.
At the beginning of these, reactors numbered approx 30,000. And at the end? 35,000.
But in England too, these same measures were tried, and we are grateful for the diligence of those who operated them, for their archive trawls to support their memories of the regime.
Backgrund
In Great Britain after 15 years of a voluntary Attested Herds Scheme, the first Compulsory Eradication Areas were announced. Between 1952 and 1960, more and more CERs were announced until the whole country was covered. By the end of 1960 eradication was deemed complete. Reactor prevalence was reduced from an original estimate of 40% in 1934 to 0.04% in 1965. It was expected that the disease would continue to occur sporadically until the end of the century as a result of animals with walled off lesions developing clinical disease in old age or as a result of stress, but in a few areas, the number of reactors exceeded expectations.
One such was in West Cornwall and a Scottish DVM was parachuted into the Duchy in the early 1970’s, to lance this “ boil” of infection which was blighting the Ministry of Agriculture’s Tb clearance maps.
Much like Professor Bourne, the late William Tait was determined to wipe out the elusive cattle reservoir of bTb. To this end he instigated synchronised Tb testing, more regular testing (see below), applied severe interpretation to all Tb tests, cohort slaughter of a group of cattle if one reactor was found and whole herd de-population. Cattle movements were limited to licensed markets only. He also attempted to ‘disinfect’ farms under his surveillance, and was probably responsible for the demolition of more 'cob' cattle byres in west Cornwall, than anything before or since. Up with steam cleaning, they could not put and collapsed around his ears.
Some of these measures are documented in reports from the CVO 1972 - 1976 as follows:
From The Report of the Chief Veterinary Office 1972
“During the year, a departmental team conducted an enquiry into the persistent bovine tuberculosis problem in the West Penwith area of Cornwall. The report on the team’s findings and recommendations was published in July.”
and from 1973
From The Report of the Chief Veterinary Office 1973
“The recommendations by the departmental team of enquiry into the persistent bovine tuberculosis problem in the West Penwith area of Cornwall were accepted and implemented whenever possible. Thus the discriminating standard of tuberculin test interpretation was continued in West Cornwall and synchronised testing at 3 months intervals was introduced in those areas having the highest reactor incidence in the previous 3 years. Intensive investigations into the incidence of tuberculosis in wildlife, and in particular the badger, continued.”
In the CVL section of the same report:
“…bovine tuberculosis remains a problem in some clearly defined areas in the South West Region. Various investigations of the commonly recognised sources of infection failed to reveal a possible origin and a wild life reservoir of infection was considered to be a possible explanation for its persistence.”
and 1974
From The Report of the Chief Veterinary Office 1974
Records that the Penzance area was on 6 month testing and that there was a continuing problem in the SW region with a reactor prevalence of 0.891% compared with the rest of the country’s 0.015%
So, no dramatic fall in cattle reactors to show for the cattle carnage then?
It goes on to refer to:
“relatively high incidence in young stock that had been turned out to grass while housed calves on the same premises which had not been out remained free.
The reports for 1976 and 7 make no mention of special measures in SW Cornwall but refer increasingly to badger gassing in the SW and a reduction in reactor prevalence.
From their extensive memories of this 'test, condemn and slaughter cattle' spree of the late William Tait, officers who operated the cattle controls say he was 'very fierce' over their implementation. As we see from the CVO reports, 3 month testing in some areas, 6 monthly in others and absolute condemnation if reactors were found.
But no reduction in reactors. For that we have to look to the reports for 1976, which make no mention of any 'special cattle measures' for west Cornwall, but they do report progress and a 'reduction in cattle reactor prevalence' after gassing of badger setts was introduced.
Many of these cattle controls are proposals now resurrected by the ISG. But what has been forgotten, say current and ex DVM’s who operated them three decades ago, is that all these measures, while costing the taxpayers and the cattle industry dearly and severely denting confidence in the Ministry responsible, “had no effect whatsover on the incidence of Tb in cattle, when it came from a wildlife source”.
By 'condemning' the cattle, and ignoring these past cattle-only policy failures, history suggests that those operating the measures proposed by the ISG are condemned to repeat the mistakes of the past.
45 comments:
It's a pity that you keep ignoring the Woodroffe report of October last year - verified by independent international scientists. This clearly showed that after FMD in the area studied,when cattle measures ALONE were re-introduced after FMD (with NO culling of badgers) infection rates amongst badgers decreased dramatically in less than one generation - from 26% to 2%. This not only shows that the infection passes from cattle to badgers (and very little between badgers themselves) but also that cattle controls are an effective way of reducing infection in both cattle and badgers. In contrast, evidence has repeatedly shown that culling of badgers INCREASES infection in badgers, and - overall - in cattle.
Yet you keep stubbornly calling for more and yet more culling of badgers, as if the killing of 12,500 badgers in the Defra trials ALONE were not enough to show us THIS POLICY DOESN'T WORK. Your only answer is that you should kill more, more efficiently and thoroughly, for longer! And yet in Ireland - which you constantly trumpet as a 'success' - why - after killing upwards of 50,000 badgers in a particularly cruel and barbaric way - is the infection rate twice ours? Why do they lose a higher proportion of their national herd to TB?
Further,if you kill badgers at the same time as instituting more rigorous and accurate cattle testing, how could you ever know which was working? What would happen if it just got worse? What if your theory was wrong, and however many badgers you killed, we still had TB in the national herd? How many badgers would you be prepared to kill, and where would you stop?
Badgers have been scapegoated and killed for years in this country, without proper cattle controls in place, and bTB had just got worse. You talk about data from the 70s as if there have been no advances since then in either our knowledge, the science base for this subject or the technology of cattle testing and controls! It's time to move forward and LEARN from our past mistakes, not just go on and on repeating them!
Anon 12.08
We visited Woodroffe's research in October 2006, with several postings which explained our own experiences of the FMD carnage, particularly on the ecology.
Taking several million grazing animals out of the food chain in the spring / summer of 2001 had a devastating effect on the animals (and birds) which depended on this type of habitat for survival.
Any extreme weather conditions from drought to flood will do the same, and the RBCT did it.
FMD caused perturbation of badgers within the clearance areas on a very large scale. It was that which increased the disease level within the badgers. But Woodroffe's paper took no account of that, modelling only the effect of delayed cattle testing.
We do not call for 'more and more culling' of badgers. In this post, we point out the futility of trying to clear cattle bTb without, and we give examples of how others have tried even more stringent cattle measures and failed.
We have also explained that the 'mass culls' of the RBCT were anything but. They made infrequent and quick visits, using an inefficient method of control, open to abuse, thus leaving a fractured community behind to fight for territory and spead disease both between themselves and onwards. Points which managers and operators of the trial agree with and have put on record to Ministers.
We have also said that we favour a 'clean ring' type of control, which would involve the local AHO targetting a group of farms where cattle had been excluded (by slaughter) from the transmission cycle, and using modern technology (PCR and gamma on the badger setts and captured individuals) to work outwards to a clean sett of badgers. Inward movement will always happen, as territorial animals fill a space. The clever bit is to make sure those that do are disease free. To that end we support vaccination of clean badger communities, research for which we understand, is showing good progress.
This approach would, we feel give less killing badgers, not more and a cull only of diseased populations. There are areas of the country still, where the badger population is dense but sentinel tested cattle show no Tb. Conversely, some hot spots show 100 per cent infection of setts (Warwick, PCR, Glos. 2006)and up to 76 per cent infection of post mortemed badgers.(Bourne, Broadway, ISG 4th report) That situation makes a mockery of any cattle measures anyone likes to try.
The incidence of bTb in the R of I is described by the EU overview as 'declining' and under control. That they halved cattle incidence in five years, and been able to halve farmer levies on the back of that is a success. Their methods (snaring) we do not support.
We will turn your last point around. You ask, if badgers were culled at the same time as more rigourous cattle controls were introduced, how would anyone know which policy was responsible? And more important what would happen if Tb didn't subside in the cattle, after infected badgers were taken out.
The posting on this thread gives the frustratingly stubborn results of a one sided policy (for those involved, now aged 80 - 90) and confirms complete failure of the Tait regime on bTb incidence in SW Cornwall. It was instituted before badgers became implicated and control of infected populations began. Only when infected setts were cleared did incidence of reactors in the area show a decline (CVO report)
When the RBCT started, the ISG dropped their 3 triplets on the hotspots for Tb. And in the last ten years a moratorium on badger culling has prevented any action outside them. The situation now, is that there is more tb outside the RBCT zones than inside. As we have said, Bourne's so called 'edge effect', a phenomenon unique to his trial, is unlikley to have extended 100 miles.
It may be convenient to blame FMD cattle movement and lack of testing for this. But FMD didn't affect all the country and not all of us missed tests. What we missed was our TB 99 inclusion in the RBCT data. From the ISG report, this gave equal measure to cattle contact, bought in cattle and badger activity. In the case of four of the site's contributers the first two were specifically excluded, a point not clear from Bourne's unequivocal conclusions.
The single most important thing to have come from the ISG report is the acceptance that infected badgers will transmit Tb to cattle. And how not to go about clearing this source of infection out.
It is from that point that the debate must move on. Our latest postings report the results of previous ISG-type proposals, instigated with no badger control in the past, together with their results.
Matthew says: "FMD caused perturbation of badgers within the clearance areas on a very large scale. It was that which increased the disease level within the badgers."
What evidence do you have to support this statement?
Anon. 1.54
When that amount (over 11 million)of cattle/ sheep were taken out of the ecosystem in a very short space of time, everything that depended on their presence for survival had to adapt to their absence - or move.
No cattle/sheep meant no dungpats, no placentas, no stilborns. and that meant no beetles, no flies, and fewer earthworms near the surface of long uncropped grass. Farms were at a standstill, growing little corn crops or maize for the whole of 2001, plus unusual 'activity'; fires burning for weeks, guns, men with disinfectant and carcasses meant animals and birds which depended on livestock farming had to move to survive.
The deer stayed. The badgers moved.
The songbirds stayed away. There was nothing to eat and silence. It was indescribably sad and empty.
The badgers moved outwards to where the nearest cattle were, but met indigenous badgers already there. The result was the same sort of territorial scrapping that the RBCT caused. When they returned, as farms restocked they were scarred and battered. Thin and disorientated.
So to answer your question. Observation and talking to farmers who were in the midst of the carnage.
And when that very point was made to an eminent ecologist, his reply was "Just because a scientist didn't see it and hasn't written it up, does not mean it did not happen".
For obvious biosecurity reasons, scientists in the midst of that carnage were thin on the ground, preferring to huddle around the computer and 'model'.
That is just pure supposition, and has absolutely no evidence to back it up at all.
There are so many false premisses here, I don't know where to begin...To take the main ones:
1) Badgers are NOT dependent on domestic animals (or food crops) in order to survive. They are opportunistic omnivores who are known to survive in a huge range of habitats (including ones without humans!) which is why they are such a successful species.It is just a nonsense to suggest they were 'driven out'by the removal of cattle and sheep.
2)The Woodroffe report did not,in any case, claim to be a study of badgers in areas where cattle etc were culled. It was a study of an area where cattle simply stayed put for the duration - and its findings cannot be discounted on the grounds that this wasn't the case everywhere in FMD. I quoted the study because it showed clearly that cattle transmitted infection rapidly to badgers, and that when cattle controls were restarted, infection dropped dramatically in less than one generation. That is in no way changed by the removal of cattle in other areas.
3.Your suggested culling strategy might seem a bit more plausible if the 'modern technology' in the form of vaccination and reliable TB infection testing of LIVE badgers were actually available and effective. But they're not - they may be 'in development' or 'promising'- but we don't have them as working available tools now....So when were you thinking of culling badgers? Now, or at some undefined point in the future when these technologies are actually up and running, and feasible? If now, what are you suggesting instead?
4.We do now however, have a much more effective diagnostic tool for cattle - the gamma interferon test. So thorough cattle testing and controls means something very different now than it did in the outdated results you quote from the 70s and earlier.
And as the ISG report makes clear,all the evidence to date shows that this is what we should now be focussing on.
From the 'supporting information' section of Woodroffe's 'Culling and cattle controls influence tuberculosis risk for badgers'
2.6 Effect of delays to culling on M. bovis infection prevalence
Analyses indicate that the prevalence of M. bovis infection in proactively culled adult badgers was greater following the suspension of routine cattle TB testing during efforts to control the 2001 FMD epidemic. However, badger culling was also suspended at this time (21), and it is conceivable that these delays, rather than the delays to removal of M. bovis infected cattle, could have caused the observed rise in prevalence (although the mechanism whereby this might have occurred remains unclear).'
So it looks to me from that that the increase in badger infection could have led to the increase in cattle infection rather than the other way round. Either is 'conceivable'.
Anon 12.22
1. A comment on another thread, from another Anon may help you grasp the picture of the importance of cattle 'habitat richness' to badgers. Apart from Cheeseman's comments which invariably introduce his speeches: "Where you are farming cattle, you are inevitably farming badgers".
Anon said:
"From Ian Pettyfer, who works on a family farm in mid-Devon:
"Since giving up maize growing 15 years ago, our badger numbers, which had quadrupled over the previous 15 years, have been steadily declining and I have no other explanation. This year the number of occupied setts
seems to be down to almost single figures for the first time since the 1960s, and those that are occupied are nothing like as active as usual."
To which we added, from SW contributer's knowledge of Mr. Pettyfer's farming activities, that he also relinquished a dairy herd and farmed suckler cows more extensively, thus decreasing available food supply to animals which predate on that habitat.
Imagine that dramatic decrease in available food, repeated on a huge scale, in a short time frame and over tightly defined areas.
2. See Jo's comment re Woodroffe's conclusions:
"...However, badger culling was also suspended at this time (21), and it is conceivable that these delays, rather than the delays to removal of M. bovis infected cattle, could have caused the observed rise in prevalence (although the mechanism whereby this might have occurred remains unclear)
3. So everybody push for the authorisation to license new technology, in the shortest possible timeframe. This debate is not about keeping scientists in jobs.
4. The comparative skin test is the world wide primary tool. Not 'was' but 'is'.
Its specificity and sensitivity are as good as it gets, and many countries have completely cleared tb from cattle herds using this test and slaughter. (The UK was so very close.) Tb has not remained as a reservoir in cattle so identified. Countries failing to clear Tb thus, are confined to those experiencing reinfection from wildlife sources, be that badgers,(UK & Ireland) possoms (NZ), white tailed deer(USA) or wild boar (Spain). And all except the UK are making good progress by tackling both sources.
4. We agree with Defra on this. Gamma interferon is far too blunt a tool for use areas of environmental tb. In these areas, those proving positive may have had exposure, but their immune system has overcome the challenge. But they will show antibodies to the blood test. What is the point of taking out cattle who have acquired a degree of immunity?
It is our understanding that gamma is only around 65% specific to bTb, picking up avian, johnnes and skin tb amongst many other micobacteria.
And it is absolutely no help at all if reinfection is inevitable from wildlife sources - as in the case of contributers to this site.
Jo - In the paragraph that immediately follows the one you have quoted, Woodroffe et al. test the hypothesis that the increase in prevalence in badgers was caused by the delays in culling - and find no evidence to support it, concluding that "it is very unlikely that delays between successive culls caused the high prevalence observed after FMD". It's advisable to read a whole paper, not just stop when you've found a bit you like.
And to Matthew who has repeated Jo's quote in #2 immediately above - investigate your sources more thoroughly before quoting from them. It's hard for us to take you seriously when you leap on misquotes like this.
To Anon 12.22.& 9.39am, some of us can see the day when the only badgers you will be able to see is in Wild life parks! As this country cannot go on protecting these flee infested decease ridden crittors that are protected for what? They dont feed the nation, which one day, sooner than you may think,it is happening,(flood,droughts and the worlds food surplus gone) we shall be only to pleased to have our bellys filled by the now dying country side. I can tell you when needs must the badgers make a very tasty meal,as the old country folk will tell you.So perhaps as you say if cows give badgers TB, we will all look forward to a Sunday roast of badger.
I have no problem with a sunday roast of badger. I did, however, have a problem with Jo taking one paragraph from a paper and presenting it on it's own without the context that it was a hypothesis that was put forward and then discounted. I thought that people who haven't read the SI of the paper might have been interested in the actual conclusion to that particular section.
Anon 3.32pm, replied to your post earlier but it went into orbit somewhere. Cant understand your witterings about 'no problem with eating roast badgers' being a bit of a hyprocrite are you not? your criticisms of the other bloggers is quite sad when all they want is healthy wild life and healthy cattle. Still, never mind, just sharpening my knife for dinner with a difference!!
Ploughing through much of this latest research, we find much of it contradictory, with the word 'suggests' used too many times, to 'suggest' certainty' and thus hypotheses tortured to fit.
What should be of note, and which the RBCT chose to ignore, is the tale of one of our contributer's farms on which BCMS kindly provided confimation of 'No bought in Cattle', a point available from the the TB99 to the ISG, but which we now see was wafted away by the equal weighting given to 'cattle contact, bought in cattle and badger data'.
This farm had 44 casualties among its cattle over 5 years, and data now to hand shows a unique spoligotype in the 3 samples capable of culture. Today we learn that data from the RBCT badger postmortems show that 3 badgers captured either in 2001 or more likely, 2003, (the RBCT's only fleeting visits to this farm) show identical spoligotypes.
That is data which should be taken seriously - by somebody.
I am only responsible for the two most recent anon posts at 9:39am and 3:32pm. All I have done is point out that Jo misrepresented a section of the Woodroffe et al paper. I am not defending badgers or cattle and therefore am not a hypocrite, merely pointing out a (rather severe) error - or was it done on purpose? Only Jo can answer that - let's see what he/she says.
as anon (9.39 3.32 and 7.10) points out, this thread has taken information from a scientific paper very seriously out of context, and the person responsible should apologise for what amounts to spin doctoring it. Anyone quoting it thereafter should also accept some blame in promulgating a falshood: the paper does not say what is suggested.
I declare no particular interest in either badgers or cattle. I am interested in science being carefully done and presented accurately both in original papers and subsequent discussion. It matters to us all that policy decisions are made on the basis of evidence. Not fond hopes about what any given policy will do for badgers, cattle, or indeed anything else. So far as I can see the trial in question did exactly what it set out to do. It is quite right that culling efficacy was lower than hoped (though not as low as some of the wilder estimates on these pages or others) but it does not follow from this that no conclusions can be drawn from the trial. It particularly does not follow that a greater culling efficacy will have any greater beneficial effect. You simply cannot predict that without doing the experiment. Or alternatively you could examine it using a carefully constructed and well validated model. But models are apparently always wrong if they don't tell you something you wanted to hear, so that is out the window as a source of objective enquiry.
I write this in the fond hope of reasoned argument. Please do not write back with inaccurate claims, quotes out of context, figures plucked from PMQs, stories of what happened on one farm on one occasion or what you or a friend saw out the back window during FMD or at any other particular time, and so on and so on. These are not data.
There is a serious matter here, which is that we do not have an effective strategy for dealing with a disease which threatens the livelihoods of many. In trying to devise one, science is the best tool we have got, and it is regularly ridden over roughshod on these pages by people (from both sides) who can scarcely be characterised as objective.
Matthew 8.11
"Imagine that dramatic decrease in available food"
This is just getting ridiculous. You're talking about an animal whose staple food item is earthworms. It's quite possible that growing maize will encourage optimum badger density (which is Mr Pettyfer's explanation for reduced badger numbers) although other natural mechanisms will still limit that density...But it is ludicrous to suggest that badgers cannot survive without the farming of domesticated animals.
Also if, as you say, badger numbers depend on a specific form of cattle farming, are they then declining everywhere else??
Perhaps it would help you to get a better grasp of some basic facts about badgers if you were to read an informative book like 'Badgers' by Ernest Neal and Chris Cheeseman, which covers the whole subject of badger diet and influences on density in some detail.
3. "So everybody push for the authorisation to license new technology, in the shortest possible timeframe"
Doesn't answer my question, which was :
So whay do you think we should be doing in the meantime?
4."The comparative skin test is the world wide primary tool. Not 'was' but 'is'.
Its specificity and sensitivity are as good as it gets....
We agree with Defra on this. Gamma interferon is far too blunt a tool for use areas of environmental tb...
It is our understanding that gamma is only around 65% specific to bTb"
Errrr...to quote from the Defra website:
" The onset of signs of TB in cattle is usually slow, and infected animals may be infectious for months or years before a diagnosis based on clinical signs can be reached. As a result, diagnosis of bTB must rely on detecting infection with the causative bacterium, rather than disease by the use of immunological tests....
{Re gamma interferon test}...By sampling over 1,000 animals in 24 herds considered free of TB in 4 year testing parishes, a specificity value of around 96% was achieved when running the test with the tuberculins as used for skin testing or when using more specific antigenic proteins. When both types of antigens are combined to maximise specificity the test was around 99% specific. When samples from herds who had bought in animals from herds with a recent history of TB were removed from the trial results the specificity figures marginally improved. These results are in agreement with previously published data from other countries around the world.
...the g-IFN test has good sensitivity, appears to detect infected animals earlier than the skin test and can be repeated as often as necessary without the need to wait 60 days between tests. Additionally, the two tests detect marginally different groups of animal with some animals only disclosing to one or other diagnostic test. Therefore, this test is used in many countries in combination with the skin test, to improve the detection of infected cattle
Combined use of skin testing and blood testing resulted in more infected animals being detected than using skin testing alone"
Perhaps you weren't aware of this?
And yet the gamma interferon test has been mandatory for use in conjunction with the skin test since October of last year I believe?
The purpose of the quote I put up was to show that Woodroffe recognised that delays in badger culling could have caused the rise in prevalence of bTB in badgers. Although her model leads her to the view that that is unlikely, that in no way disproves the point.
Whether models tell you what you want to hear or not they are not infallible. As has been well said, there is always a risk of models becoming ‘exercises in mathematical sophistry’.
This thread appears to have veered off topic.
We do not criticise mathematical modelling as a tool, but will question its results if data which some of us have provided has been excluded. By not looking at all input possibilities, results may be seriously skewed. This was explained in a paper on our posting 'The Use and abuse of ..." (below).
A comment from NZ, described their experiences of bTb modelling and told us how such exercises had been extremely accurate there, because much more data on possoms was included.
Matthew(11) said:
"I write this in the fond hope of reasoned argument. Please do not write back with inaccurate claims, quotes out of context, figures plucked from PMQs, stories of what happened on one farm on one occasion or what you or a friend saw out the back window during FMD or at any other particular time, and so on and so on. These are not data."
With respect, what do you think fuels research scientist's models?
Their researchers come onto farms, fill in reams of paper containing specific questions, (some very relevant, some less so and many missing - no box) and then input just such 'observational data', or some of it, into their models.In the case of the ISG, this together with data from CTS the State Veterinary Service and VLA.
What we are saying is that much of that data collected, and in our particular cases important data with regard to the 'weighting' given to various input variables, was excluded.
We also have serious concerns that the area of disease epidemiology appears to been highjacked by this high profile technology, which thus far (BSE, FMD, H5N1 avian flu) has left input from epidemiologists within the field, on the edge, if not excluded altogether.
Hence this thread.
Interesting that the letter posted below this thread from several specialist epidemiologists in the field of bovine tuberculosis, which emphasises Matthew's opinion of the effect of input data and RBCT methodology on the ISG's results, has received no comments.
Jo, your original post misrepresents the paper in question. The hypothesis was considered and was found wanting. It is usual to state the alternatives being considered before saying which one your analysis supports. I am grateful to yesterday's anon for pointing this out, as otherwise it could have been quoted over and again, while being a stark misrepresentation.
Not to mention that had this not been considered, some people would have been up in arms that it had not been.
And to both Jo and Matthew - your comments suggest that mathematical models can always be dismissed as 'sophistry' if you prefer. This renders them as useless as I suggested. In fact, mathematical modelling is an important part of our armoury. Models can be criticised on such grounds as, for example, being insufficiently robust to variation in parameter estimates. This is perfectly reasonable. A claim of 'sophistry' must be justified. Notably, this work has of course been peer reviewed, and probably by some of the best modellers on the planet who let me assure you NEVER miss a chance to score one off their competitors. It seems likely therefore that the modelling is secure.
Why not collaborate on another model, which considers the likely effect of much better culling on TB. You could submit it to Nature, and if you are concerned that the reviewers would be biased, you can ask that it not be sent to anyone connected with the original trial. If they publish it, well done. Until then, forgive me if I consider comments on this topic speculation.
And finally, there is a large difference between the data used in modelling and that which I mentioned in my previous post. Data are collected in a systematic standardised fashion over many hundreds of farms, with possible confounding factors taken into account for subsequent analysis. Also, there is the rather important factor of data on breakdowns, and at least some estimate of badger numbers.
These data are vastly more thorough than any piecemeal non systematic approach. This can still be useful but only in framing hypotheses. It is not a substitute for a proper study.
Finally, might I ask what would convince you that a cull of badgers, of the sort which is likely to be achievable by the UK government with available funds, would not have a substantial beneficial effect upon TB incidence in cattle over the country as a whole?
Anonymous might be more convincing if he or she relied less on selective quoting and more on looking at the whole picture.
The confident reliance on badger infection data is, at best, insecure. I am not aware of any recent systematic survey of infection rates in badgers.
Those data which are available have an inconsistent and variable base, which precludes any sound conclusions from the different data sets.
Making your "facts" fit your own preconceptions is hardly science.
Thank you Richard, for agreeing with my point that selective quoting is unconvincing. Jo might want to remember that before selecting sentences and quoting them without making the "whole picture" (i.e. the context) clear.
Matthew might also want to remember that before "selecting" quotes from bloggers and reiterating them.
As our colleague said, it is better to see the whole picture.
Matthew (11) asked
"Finally, might I ask what would convince you that a cull of badgers, of the sort which is likely to be achievable by the UK government with available funds, would not have a substantial beneficial effect upon TB incidence in cattle over the country as a whole?"
If you need to ask that, you have not been listening.
Four of the contributers to the site are proof positive of Defra's predicted 20 per cent annual increase in bTb, with what they (Defra) describe as "no new changes in policy".
No interference with badgers occurred prior to their breakdowns.
Tb was identified during routine skin tests.
Matt 1, and his neighbours were given a BRO (Badger Removal Operation) which cleared five neighbouring farms for almost ten years. Tb in rumbling in the area again now, and Matt's cattle were under restriction last year. No cattle have been purchased since the last breakdown, and no one has interfered with the badgers.
Another contributer ran a 'closed' herd and was part of an RBCT 'Reactive' area. This farm was clear at the start and opted for 'survey' only, leaving the badgers alone. A breakdown was identified in 2001 at a routine skin test. All the neighbouring farms were under restriction. None have boundaries which directly touch this farm. The RBCT team came in response to Matt's 2001 breakdown in May 2003. The breakdown lasted almost 5 years. Tb is still rumbling around the area.
Two other contributers,( one in an RBCT Proactive) ran extensive herds, one organic beef and the other a home bred dairy herd. Both had closed herds and both suffered breakdowns.
Epidemiologists will confirm, from Professor Koch in the 1890's, through Evans, and his 'gold standard' of epidemiological postulates and to the present day, that micobacterium bovis, spreads through badger populations and thus to other mammalian species.
It can, it does and it did.
Previous clearances have reduced cattle tb to nil; the last ten years has shown, for the rest of GB, outside the RBCT areas, what happens if this transmission opportunity is ignored. And this thread shows the futility of targetting only one source of the cycle, despite the ISG's confident and persuasive prediction of a 15 per cent reduction per year.
Matthew (8.11),
It is interesting to note that you have not replied to my questions/comments/information from the Defra website re the fact that a much more accurate and effective cattle testing regime is now available (ie gamma interferon in addition to the skin test) - and has begun to be used - than the skin test alone which you claimed in your post to be 'as good as it gets'.
The point of the new regime is precisely that it will pick up infection in cattle that has previously been missed - sometimes, as the Defra website points out, over years in some herds, thus suggesting that these herds were clear when they were in fact reservoirs of infection.
This is precisely why the ISG report recommends focussing on the new regime of improved cattle testing.
You have also again failed to answer my question as to what you are suggesting we should do NOW, in view of the fact that vaccination and effective feasible live badger testing for TB are not yet available.
If you are going to keep claiming - over and over again on this blog - that your suggested solution of 'targeted' culling of badgers is the appropriate one, you must be prepared to answer these kinds of questions if you wish to retain any kind of credibility.
Anon: 3.24
Not deliberately dodging questions, but over time most we have touched on before. Plus day-job.
We said in a previous answer that we 'agreed with Defra' re their targetted use of gamma interferon. In 3/4 year testing parishes it maybe has a place. And yes, you are correct to say it has been in use since October. But not where Defra know they have a wildlife reservoir of Tb; in annual and 2 year testing parishes, they only use Gamma interferon to resolve IR's after their second test. And this is for a very good reason.
Veterinary practitioners with experience of its use in herds within such areas, confirm that reinfection from wildlife precludes its widespread use. What would be the point? Half way through our mammoth dutbreak, we asked to use it and were given a horrified 'No, you'll lose half the cattle". All those who have gained a bit of immunity.
For many reasons a cull of wildlife so infected, has to targetted. Public perception, Bern Convention, achievability and the rest. We have explained our preference for PCR to back up this, and yes, we know Defra are dragging their heels. Short term thinking - they will need this technology to short circuit lab tests for a host of diseases. Farmers could operate the kit - it's soldier proof, but Defra /Imperial colledge hold the assay, so it really is up to them.
Interim, wildlife personal and experienced game keepers do know the signs of a sett with unhealthy occupants. And it is those, and only those which should be actioned. The only thing which stops the social disruption of badgers, is the scent mark of another badger group, thus a healthy and active sett must be left to prevent this.
The intradermal skin test when used on the UK strains of Tb, has a latency prior to testing of 30 - 50 days, but unlike some foreign strains the maximum time from exposure to flagging up an immune reaction, is 221 days. Thus annual testing is extremely successful in weeding out reactors prior to their becoming infectious - should they ever go on to be so.
New pathogenisis report just out - SE 3013 - confirms that of 1006 mucosal swabs taken from 400 paired cattle (Reactors and DCs / IRs) after post mortem to check for onward spread of Tb, all were negative.
Matthew said
"And yes, you are correct to say it has been in use since October. But not where Defra know they have a wildlife reservoir of Tb; in annual and 2 year testing parishes, they only use Gamma interferon to resolve IR's after their second test. And this is for a very good reason.
Veterinary practitioners with experience of its use in herds within such areas, confirm that reinfection from wildlife precludes its widespread use. What would be the point?"
Where does Defra say that the 'reason' you give (i.e.reinfection by wildlife)is THEIR reason for introducing gamma interferon to 'only' resolve IRs after their second test'in 1/2 year testing parishes?
On their website they say, the use of gamma interferon is now mandatory in (among other 'prescribed circumstances'
"Confirmed incidents (with visible lesions) failing to resolve, despite taking bio-security precautions in 1 and 2 yearly tested herds, including those herds where a complete or partial de-population is contemplated
Used at the first inconclusive reactor (IR) retest in unresolved IRs in herds in 1 and 2 yearly tested herds."
Also
"The test continues to be available to use as a disease control tool in TB hotspot areas."
In other words, this is more to do with the appropriate way to use both tests in 'problem' herds and areas, whether wildlife is implicated or not.
"Half way through our mammoth dutbreak, we asked to use it and were given a horrified 'No, you'll lose half the cattle". All those who have gained a bit of immunity."
So what makes you think that badgers don't also develop immunity? Wild populations always tend to develop immunity more readily than captive/domesticated intensively reared ones (as in avian flu, for example).
How do you explain findings (as in the Woodroffe study and others)that culling INCREASES infection in badgers, even within the same social group?
"Interim, wildlife personal and experienced game keepers do know the signs of a sett with unhealthy occupants. And it is those, and only those which should be actioned."
Perhaps you could tell us what conclusive 'signs' there are that a sett has 'unhealthy occupants' (other than tests on a dead badger)? And why you assume that an entire social group will be present in any one sett you gas at any one time? You can gas all the setts you know about at once - but badgers sometimes sleep above ground...And anyway, you said you wanted to keep 'healthy setts'. We have already said that badgers move around from sett to sett, sometimes as individuals and sometimes in small groups. How far out would you go? How would you judge what area to 'ring'? How would you know where one territory ended and another began? If you kill a sett full of badgers who prove clear of infection at post mortem, how will you know which social group they belong to? What if the one infected member of any group happens to be elsewhere that day?
In view of all the above:
How would you ever know where to stop? (And no, you haven't explained this credibly in past posts)
As you couldn't know the exact extent and borders of each badger group and territory without years of painstaking observation, mapping, capture and tagging of individual badgers, how could you avoid the 'perturbation' effect?
I have to say that all your posts on badgers betray the most fundamental ignorance of badger behaviour and social groupings, particularly the ways in which movement between setts in any given badger territory is highly variable and unpredictable, numbers and compositions of groups or subgroups at any one sett are also highly variable and unpredictable,and the uses and types of setts within one badger territory also vary - to the extent that talking about 'healthy' and 'unhealthy' setts makes absolutely no sense at all.
Anon:10,24
Defra do not 'say' that gamma interferon is inappropriate in areas where re infection is likely - veterinary practitioners who have had the pleasure of its use in such areas, do. But it is noteworthy that by so distinguishing its use in 3/4 year testing parishes from annual / 2 year, Defra see a difference too even if they do not spell it out.
They are considering using it to 'de-populate' herds unresolved after several years (ours?), but a caveat is given to land owners advising them 'not to restock with cattle' - or has been
in cases with which we are familiar.
Woodroofe as we have said many times, has not appreciated the effect on badger populations of removing from the ecology, 11 million grazing animals at a time of peak feeding for those who are dependent on that habitat. The result was perturbation and fighting, with attendant increase of Tb in the groups. As Richard pointed out, badger information re infection is very subjective being limited to Woodchester Park's hand fed, regularly trapped population, BRO removals to 1997 and designated area RTA's.
You are correct to assume a degree of immunity to Tb, in badgers where tb has rumbled around for years. But it is our experience that when it moves out from that population, (where the usual reaction in cattle was limited to one or two reactors in a herd), the results are devastating for both species.
The level of infection in 'naive' social groups is greater and as more individuals are infected at the same time, and greater herd losses will result. We saw this in 2002, when our neighbours reported a huge historic set 'closing' down. Instead of 20 or 30 entrances and several chambers active, as had been the case for several decades, this hub was slowly dying. It's occupants were found in various states of death and decay within yards of it. That farm lost 20 or 30 cattle at one test.
A mile away, we had 20 or 30 IR's and just a couple of reactors. We think from the trails into this farm, that thus-far survivors of this group wandered into non-kin territory and from what the WLU told us in 2003, when they trapped two awful results of this, they had fought (bite wounds) with 'our' badgers and amplified the infection through them. This is an area which had been clear of Tb for over twenty years.
Trails tell you which way a badger is travelling from claw marks. State of such claws (sharp and short or flat and long) give an indication of activity and direction of claw marks show the location of the sett responsible - we're told.
Gamma for badgers is very successful, again we are told, and will be a useful aid to identifying healthy setts - apart from the obvious , that is an active area, with clean scratch marks etc.
From www.warmwell. com, Dr. John Gallagher said on this subject:
"Control of tuberculosis in badgers needs to be a mix of culling diseased communities and attempts to raise the immunity of healthy badgers in the surrounds. Culling of infected badgers in new hotspots, as well as endemically infected areas should only begin after investigations have ruled out any other source. The work would consist of surveying all setts in a wide zone, followed by trapping initiated from the outer ring inwards. Badgers testing negative to tuberculosis would be boosted with a BCG injection and protection offered to cubs with oral doses. Any positive testing animals should be euthanased"
Although now retired from direct government employment within the pathology areas of Defra's tb programme, Dr. Gallagher is still in private practise and retains (we assume) information exchange on the development of these technologies with veterinary biologists working on them.
You ask where to stop. Farmers have given much information on the position on their farms of grazing animals relative to badger setts of any size or description. One contributer with 30 setts over a very large moorland farm, has narrowed his problems down to just 3. It is a matter of regret that the ISG report found such information incomplete or changed its format or just too difficult to slot into a mathematical model (as did Warwick last year) and it was therefore not used.
It is vital. No sensible person has the stomach for the sort of carnage we saw in FMD, in any species.
The ultimate back up to identifying such clean populations is regularly tested cattle, and in hotspots that is every 60 days.
And ultimately rtPCR would achieve all this in minutes.
Actually -
Badgers have a reservoir of TB and the pathology tells us they spread it readily.
TB typing shows us that cattle and badgers share the same local types.
Cattle have no proven undisclosed infective reservoir of TB.
Even when they have it, spread from cattle to cattle is uncommon.
It follows that control in both species is needed.
The current skin test has been good enough to eradicate TB from cattle elsewhere, and additional tests are not necessarily the answer, though they may help.
Some sort of badger control is essential - the only realistic question is the method to be employed.
(And in all the control systems and trials used so far, only the ISG have noticed the 'edge effect'.)
Ah George, you haven't been listening (as one of the Matthews is fond of saying)!
If badgers 'readily spread infection amongst themselves' then how do you explain the findings of the 06 Woodroffe study (now mentioned many times on recent posts) that when cattle controls were applied in the studied area, infection rates amongst badgers dropped IN ONE GENERATION from 26% to 2% - without ANY badger culling?
And if the skin test alone is so effective, how come Defra lists the circumstances in which the use of gamma interferon is now mandatory "in order to catch the infection among cattle that has been missed by the skin test alone?"
You can't have any sort of reasoned discussion if you're going to post your opinions as if they were fact, without any kind of back-up evidence - and in the face of already posted evidence that directly contradicts it.
And Matthew says:
"Trails tell you which way a badger is travelling from claw marks. State of such claws (sharp and short or flat and long) give an indication of activity and direction of claw marks show the location of the sett responsible - we're told."
I've seen some pretty absurd claims on this blog, but that must take the biscuit! This is an insult to all our intelligence. And this is the sort of 'information' you want to base your badger cull on???
Anon:
The insult to your intelligence is pictured :
http://bovinetb.blogspot.com/2006/02/badgers-dont-suffer-from-tb.html
and
http://bovinetb.blogspot.com/2007/03/one-cannot-tell-sick-badger.html
Perhaps you would explain how that in any way relates to my post above?
Anon 9.21
You said in response to this observational comment:
"Trails tell you which way a badger is travelling from claw marks. State of such claws (sharp and short or flat and long) give an indication of activity and direction of claw marks show the location of the sett responsible - we're told."
I've seen some pretty absurd claims on this blog, but that must take the biscuit! This is an insult to all our intelligence.
Relevance?
First link. Picture. Half way down. Claws. Picture of.
Long, overgrown, flat, blunt. Leave a different imprint from short, sharp ones, which one would expect to find on an active healthy badger.
Matthew, this is a picture of a DEAD badger. I believe I asked you which 'conclusive signs' of TB infection there were in live badgers, and active setts, as in your claim that
"Interim, wildlife personal and experienced game keepers do know the signs of a sett with unhealthy occupants. And it is those, and only those which should be actioned."
You then offered the length and direction of claw marks in footprints (!)as a 'conclusive sign' of both a TB infected badger and an indication of which sett it came from and which social group/ territory it belonged to !!
As only a very old or injured badger, or a badger in the final stages of a serious disease,would
no longer be able to dig - and as only around 3% of TB infected badgers actually go on to develop any symptoms at all and the majority live out normal lives - this is hardly a reliable diagnostic tool for TB infection! (Even if the 'overgrown claws' could be reliably detected in a footprint)!
Further, how does this answer my point about how you would determine which individual badgers were at which sett at any given time, which badgers were in which social group, and where one territory/social group ended and another began?
In other words, I repeat:
How could you accurately carry out a 'targeted cull' in the absence of any reliable, effective and available tool for diagnosing TB infection in live badgers?
None of the statements in my previous post were just opinions. They are all either facts or hypotheses based on a large body of observational evidence. Science is not just controlled experimentation, this is just a small part of the scientific method. Scientific observations, however, are the bedrock on which science is built and a huge quantity of observational data has been built over the years during the TB control programme in the UK. Analyses have been carried out and many reports written during this period, and it is these that have lead to the current view of most of those involved that badgers, rather than other cattle, are the main source of infection in new breakdowns. The ISG recommendations contradict this view, and it is this that underlies the present concern by most of those working in the field. In a real scientific environment there would be calls for this work to be repeated as experimental work is only really valid if it is reproducible.
Anon: 7.36
Regularly tested cattle are the ultimate messengers. If they are clear then badgers co-habiting that area are likely to be clear of Tb as well.
If not, and after a thorough investigation of cattle movements rules out this as a breakdown source, (and a further 60 day test will usually have been done, to reveal ongoing or 'passing through' infection), then I would be looking at any badger activity which ingresses this farm. This could be from one or more of its own setts, or those on neighbouring land.
SVS / Animal Health have an overview of what is happening to cattle on any neighbouring farms which also influence their decisions.
As I've said, if a sett is active and healthy (scratch marks on trees, bedding regularly moved and clearly marked, sharp clawed trails) I would leave it alone.
I would be looking to identify and remove occupant(s) from, single hole setts, near to farm buildings.
Historic setts, now closing down and limited to one or two very 'lazy' entrances.
Any new area dug near to an 'artificial' feed source.
To locate some of these, needs a degree of knowledge of trail direction etc. as I've described. Defra used coloured peanuts I believe.
A farmer in the SW described an experience with 'his' badgers which was witnessed by his neighbours, when the RBCT moved in.
These badgers were uniquely marked with some almost albino. All the neighbouring farms knew them, and they also knew their main territorial boundaries.
When the WLU started moving around, these badgers swam the river, and took up residence on the opposite side.
The farmer whose land this was, telephoned his neighbour: "I've got your badgers!".
And there they stayed until the RBCT had gone. Then they swam back.
The point of that tale is that both these farmers knew what was happening to badgers on their patch.
The use of PCR and gamma, plus vaccination of badgers testing clear to protect them, is a move we would welcome - ASAP
Heaping up dead cattle, when, depending on who says it - 90 percent (CVO report) or 40 per cent (Bourne) - of outbreaks in hotspots are down to infectious badgers, is not very helpful.
George:
You claim your assertions
"are all either facts or hypotheses based on a large body of observational evidence. Science is not just controlled experimentation, this is just a small part of the scientific method. Scientific observations, however, are the bedrock on which science is built"
I hope another anon will not mind me borrowing his earlier reply to this repeated presentation of personal hypotheses and observations on this blog as if they were established 'facts' or 'science' that could be used to contradict properly validated and peer-reviewed studies:
"Data are collected in a systematic standardised fashion over many hundreds of farms, with possible confounding factors taken into account for subsequent analysis. Also, there is the rather important factor of data on breakdowns, and at least some estimate of badger numbers.
These data are vastly more thorough than any piecemeal non systematic approach. This can still be useful but only in framing hypotheses. It is not a substitute for a proper study."
George also says:
"The ISG recommendations contradict this view,(that badgers are responsible for transmitting infection in new breakdowns) and it is this that underlies the present concern by most of those working in the field. In a real scientific environment there would be calls for this work to be repeated as experimental work is only really valid if it is reproducible."
What are you suggesting here?
Slaughtering another twelve thousand badgers (or more?) to revalidate an already peer validated ten year scientific study (let alone others - such as the Woodroffe study) just because some people refuse to accept findings that don't fit their own personal hypotheses and prejudices?
And Matthew:
So - albino badgers, scratch marks, someone's neighbour's ideas of where one badger territory ends and another begins, setts that are or aren't currently less used, coloured peanuts etc. - are reliable and accurate signs of TB infection in individual badgers and badger social groups are they?
Enough to base an accurate 'targeted' cull on?
I don't think so!
You also say:
" Regularly tested cattle are the ultimate messengers. If they are clear then badgers co-habiting that area are likely to be clear of Tb as well."
So badgers don't give TB to cattle in already 'clean' areas then? I thought the whole point was that in those so-called 'closed herds' where reactors are then found in the cattle, they must have got it from badgers? But the badgers don't have it first?
You are contradicting yourself here.
Oh, and in the interests of 'full and accurate' backgrounds to references, where does that
"40 per cent (Bourne) - of outbreaks in hotspots are down to infectious badgers"
come from?
Anon; 12.27
The last thirty years are littered with published papers on epidemiology, transmission opportunities and badger data. PQ's excavated much of this work.
Having dismissed our (and WLU's)observational signs of infected setts, and nobbled CSL coloured peanut trails with which they determine territory, how would you define an unhealthy badger sett?
Just curious.
You ask:
"So badgers don't give TB to cattle in already 'clean' areas then? I thought the whole point was that in those so-called 'closed herds' where reactors are then found in the cattle, they must have got it from badgers? But the badgers don't have it first?
You are contradicting yourself here".
No. We had to sit and watch as Tb ripped through the badgers and approached our herd at the rate of about 5 miles / year. Until we were surrounded totally. This happened to 3 contributers to this site. The badgers on their farms were clear, as shown by the sentinel and regular cattle tests. They had no bought in cattle and fencing or location which prevented cattle contact.
Eventually, the ingress of and fighting with infected individuals spread the disease very quickly, leading to a complete breakdown in these badgers. The RBCT then stirred up an already heavily infected population.
Did you notice that the postmortems of badgers as examined by the RBCT?
Head lesions : 27 - 28 per cent.
Chest lesions : 41 - 44.8 per cent
Abdominal (including kidney)
19 - 26.7 percent
Peripheral lymph: 20- 28 percent
And did you also notice that the cubs displayed almost double the infection of their older sett mates. In the proactive areas:
Adults with visible lesions 38.5%
Cubs 55.5%
Adults with more than one body lesion 14.7%
Cubs 28.1%
Severely lesioned adults 10.5%
Cubs 23.3%
In reactive areas:
Adults with visible lesions 41.7%
Cubs 40.5%
Adults with more than one body lesion 12.6%
Cubs 26.2%
Severely lesioned adults 7.7%
Cubs 14.3%
You said:
"Oh, and in the interests of 'full and accurate' backgrounds to references, where does that
"40 per cent (Bourne) - of outbreaks in hotspots are down to infectious badgers"
come from? "
In his address to the ISG meeting, Bourne referred to "40 per cent of Tb is driven by badger infection [in hotspot areas]", a comment which led Tb specialist BCVA veterinary practitioner Andrew Biggs, to refer to the situation as 'a no brainer'. Quoting Bourne, he said: "We're saying that we know 40 per cent of the disease is being driven by badgers and we're not going to do anything except kill cows more rapidly ....".
(Interview Vet.Times July 4th)
Just prior to the start of the RBCT, the CVO put the figure at 90 per cent, [in hotspot areas.]
And was this data - in particular the data re increase of infection in cubs - from areas/periods where/when
a) There was increasing infection in cattle,
and/or
b)badger culling was going on ?
Because both culling and an increase of infection in cattle have been shown (most specifically by our old friend the 06 Woodroffe report) to increase infection in badgers, both in the short and longer term - whereas improved cattle controls without culling has been shown to decrease infection in badgers, and particularly their cubs. So - as regards your data - it would not be surprising that in one or both of the above circumstances that infection rates would go up in badgers.
You also say that there is no contradiction between saying on the one hand that badgers are the source of infection in new areas, but on the other that a clear cattle test is a reliable indication of uninfected badgers, because
"The badgers on their farms were clear, as shown by the sentinel and regular cattle tests. They had no bought in cattle and fencing or location which prevented cattle contact.
Eventually, the ingress of and fighting with infected individuals spread the disease very quickly, leading to a complete breakdown in these badgers"
So where cattle tests are clear, we can assume badgers are clear too....that is, unless infected individuals have arrived and are fighting? Is that what you're saying? So I ask again, according to you, how can a clear cattle test be a reliable sign of no TB in badgers? Are we now adding on 'unless the farmer happens to be aware of new badger individuals arriving and fighting'?
And how could we be sure of that?
Because he can tell one badger from another?
You also ask how I would identify an "unhealthy sett".
I've already explained earlier in this thread why the concept of an 'unhealthy sett' makes no sense - primarily because different badgers are present at different setts at different times. I could only identify an 'unhealthy individual badger' (live, as opposed to dead) if I saw one who was obviously wounded, or who was lying in a weak and enfeebled condition and finding it difficult or impossible to move, particularly at the approach of humans or dogs.
Anon: 6.19
Data re. lesions: from RBCT final report. (p.76) from post mortems over the trial time.
Cattle reactors were decreasing in the proactive area by over 20 per cent, (RBCT) and with constant testing were likely to mirror the recently released Pathogenisis report, which showed 100 per cent negative for over 1000 culture samples taken from cattle, some from within the RBCT area.
Badger dispersal was going on. We would not refer to the RBCT as a culling trial, as you must know. It broke the social groups by trapping the strongest first, then leaving a fractured community after a very short time (8 nights). And that's without the interference which rendered 70 per cent of traps empty or disappeared (up to Oct 2003) Underground gassing achieved the complete cull of a group, so no peturbation, and no further spread of disease.
Re. cattle tests / clean badgers. Yes, that is what we are saying. Of the contributers to this site, most had been clear for 40 years since the eradication programme of the 1950's, another having moved farms and been introduced to bought-in reactor, took great care not repeat that experience, by not purchasing any cattle at all.
No BRO's had been carried out in the areas of our contributer's farms in recent times, but slowly Tb overtook surrounding herds and caught up with our contributer's cattle. Some had found dead badgers in the months prior to their test, in fields, buildings or near setts, in various states of wounding, emaciation or both. We can say that we are sure badgers are responsible, because we have deliberately excluded the 'cattle' option.
The 'leave it all alone' option does not seem to have worked outside the areas covered by the RBCT - unless the 'edge effect', unique it has been pointed out, to Bourne's trial, - extended 100s of miles. Badgers have been 'left alone' in these areas for ten years, since the moratorium on BROs.
That Tb is endemic in badgers is indisputable. That they can and do pass it to cattle is also fact. It does not 'go away' if left, and 'culling' how the RBCT went about its business is how not to deal with it.
That cattle controls alone will not work, in the presence of an infected badger population was the subject of this thread. On another posting we have noted the NI 'drop' but pointed out that it occurred from an unusual spike, post FMD. 2001 - 2006 show a straight line of 6.5 % incidence. The drop which the Badger Trust are so excited about is from 10 % in 2002/3. The Republic has achieved a sustained drop (part of NI is now increasing steadily) by a combination of measures, including culling infected populations of badgers, when cattle contact has been ruled out.
Your description of an 'unhealthy' badger matches exactly the experience of one farmer in mid Devon, who has had great success 'managing' an endemically infected population. As we understand it, he leaves the main historic setts and occupants, and concentrates any action on the animals such as you describe, who have been excluded from the group.
But instead of a curious 'will you show us how', this approach was met with derision and personal attack. This is very sad as it the sort of management strategy we would welcome.
"But instead of a curious 'will you show us how', this approach was met with derision"
Well frankly I'm not surprised!
To repeat: a badger in the state I described would either be badly injured or in the last stages of a disease. We can already test a dead badger for TB in any case. This would be of no use whatsoever in "managing an endemically (TB) infected population" as you put it, as so few badgers go on to develop this stage of the disease even if they are infected (around 3%), and it would say nothing about particular setts or social groups.
The whole point is: there IS NO RELIABLE WAY that is yet available for establishing TB infection in live badgers.
It is clear from this blog that the 'Matthews'do not know some quite basic details about badger social groupings and behaviour, and yet continue to insist they would be able to carry out an accurate targeted cull.
" We can say that we are sure badgers are responsible, because we have deliberately excluded the 'cattle' option."
And that just about sums up the attitude of this blog!
The whole blog seems to dismiss, distort or ignore virtually all the scientifically validated trials and evidence to date, while vilifying the scientists concerned, or indeed anyone who dares to be guided by them and their findings.
It all boils down to:
Never mind the evidence, we're farmers, so we're right.
Anonymous, after saying 'so few badgers go on to develop this stage of the disease even if they are infected (around 3%)', says 'It all boils down to:
Never mind the evidence.....' .
May I suggest he / she reads The Spatio -Temporal Distribution of Mycobacterium bovis (Bovine Tuberculosis) Infection in a Badger Population
by Delahay et al.
It's an interesting study from Woodchester Park, where the infectious status of badgers was determined on the basis of a serological test (ELISA). The figures quoted are conservative. (‘Since infected badgers shed M. bovis bacilli intermittently, clinical sampling has a lower capacity to detect infection on any one capture than does necropsy.’ Woodroffe et al 2006)
'From 1982 to 1999 the annual prevalence of test positive badgers (i.e. positive on serological or microbiological tests) was 4.2% - 18.9% of the population, although only 1.4% - 8.8% were confirmed to be infectious'.
If he / she is then interested enough to look at the accompanying figures he / she will see that out of more than 20 setts it is only five or so which have high rates of infectiousness, which would make the percentage in those setts much higher.
Look at figure 1 , the rate of infectiousness goes up and down, but the peak for culture positives in 1996 is higher than it was in 1982. The line for test positives follows the same up and down, but rising even more sharply.
Then look at supporting data for Woodroffe 2006 fig. 12. Her graph relates to Male or Female 'badgers newly detected as shedding (i.e. infectious with) M. bovis' between 1990 and 2005. She doesn’t use data earlier than 1990, as ‘ minor changes were made to diagnostic procedures in 1989. These changes were considered to have had a marginal impact on test sensitivity; nevertheless we excluded the earlier data to be conservative.’ It’s a pity, because her graph would then show clearly that rates of infection do go up and down. One thing that strikes me about Woodroffe’s graph is that these badgers are ‘newly detected’ and the graph does not include those with ongoing infectiousness. If badgers can live for some time with the disease how many of those noted as being infectious earlier were alive in later years? I assume that Woodchester Park have done research on this but I haven’t found it so far. Perhaps Anonymous could let me know?
Anon; 6.44 said
" We can say that we are sure badgers are responsible, because we have deliberately excluded the 'cattle' option."
And that just about sums up the attitude of this blog!"
Yes. When farmers have done the biosecurity bit, and still suffer prolonged tb breakdowns, wouldn't you say we have a point? Obviously not. It's all cattle to cattle, you've been told, so it must be.
and
"The whole blog seems to dismiss, distort or ignore virtually all the scientifically validated trials and evidence to date, while vilifying the scientists concerned, or indeed anyone who dares to be guided by them and their findings."
Nope. Just the RBCT trial - formerly known as the 'Krebs' trial, - which was carried out in such a way as to achieve exactly the opposite of what its author intended and in so doing, created precisely the problems its author predicted.
We fully support VLA's work on spoligotypes and have said so. And of course the recently published pathogenisis project. It is a matter of regret however, that when making reference to the 32 candidates of that £2.8 million study, which were found with lung lesions, in the ISG final report, it was not made clear that those 32, among 1006 other mucosal samples all totally failed to culture m.bovis. All were negative.
Matthew said: "And that's without the interference which rendered 70 per cent of traps empty or disappeared (up to Oct 2003)". Where did this figure come from? And how do you then explain the 8.1% of trap nights lost through interference for the whole trial (p.51 final report).
Matthew also said: "It broke the social groups by trapping the strongest first, then leaving a fractured community" - what evidence do you have that trapping got the strongest badgers first?
And Matthew also said: "Underground gassing achieved the complete cull of a group, so no perturbation, and no further spread of disease." Have you not quite understood what perturbation is? It would not be avoided by taking out an entire social group. Perturbation is caused when either part of OR a whole social group are taken out leaving badgers in bordering social groups to wander more freely into the empty space (and hence infect cattle in that space). One could argue it's MORE likely to happen when you remove an entire social group. Now explain how gassing or any method of culling would avoid perturbation...? The only one I can think of is either a complete nationwide cull or one which managed to cull ONLY infected badgers so uninfected badgers could freely be left to roam as far as they like without causing infection - and, as has very clearly been established, it is not (yet) possible to detect an infected badger without killing it first.
I apologise for my enforced absence from commenting on this. I hope to make up for it now.
Some time ago I enquired "what would convince you that a cull of badgers, of the sort which is likely to be achievable by the UK government with available funds, would not have a substantial beneficial effect upon TB incidence in cattle over the country as a whole?"
Interested people can find the question, its context, and the response earlier in this thread. I found the response intriguing, but depressing.
The substance was that some people the author knew, 4 of them, had had some experiences which suggested badgers were involved in the epidemiology of bTB, which is not in dispute as far as I am aware. It then went from that to stating that a cull was necessary - and it is quite clear that nothing at all would convince the author of any contrary opinion.
This sort of debate is religious, not scientific in nature. That is to say it is a faith position, rather than one come to by open enquiry, and from which one can change one's mind.
I suggest that scientists stop bothering to feed the trolls who run this blog. They simply enjoy it and it makes them think there is a debate to be had. There is not, at least not one in which people with such scant understanding of scientific method are qualified to participate. There are saner voices, listen to them, and deprive these here of the oxygen which helps them get up in the morning and angry enough to waste all our time.
Considering myself, I cannot understand why I have already devoted such time to responding to the nonsensical arguments presented here. So now I will stop. I wouldn't bother responding matthews, I'm not going to read it. This is rather a plea to my fellow rationalists.
Anon: 10.30
PQ's 8th Dec 2003; Col 218W [141971]
(re trap removal, interference)
"Management records indicate that over 116 culling operations, across 19 trial sites Dec 1998 - Oct 2003, during which 15,666 traps were sited, there were 8,981 individual occasions where a trap was interfered with, and 1,827 occasions when a trap was removed." This was confirmed by WLU manager Paul Caruana's submission to EFRAcom when he explained to the committee that for the first four years of the trial, the last thing it achieved was catching badgers due to 'constraints'.
We couldn't possibly comment on the ISG final report's figures, but note they specify 'trap nights' not traps set, which is a different set of data.
In any animal community, there is a 'pecking' order. The most inquisitive, strongest and dominant members are usually leaders of it. They are the most dominant feeders too. First in. With badgers, it is these which will go for the peanuts laid as trial bait in the open cages ahead of trapping proper. In our experience of cattle, it the most lively, inquisitive group leaders who have become reactors, precisely because it is they who have investigated either smell of or activity of 'something which contained m.bovis'.
Peturbation, or the movement of a group to fill a space will happen. If the trapping was unable due to time constraints (8 nights only) to account for the whole group, and (as in our cases) specifically missed the single hole disperser setts, then what they left behind was the remnants of the group. Leaderless and often weak, or sick (dispersers)
Of course badgers will expand territory to fill any vaccuum left. After the original scent marks have dissipated, (about 4-8 weeks) their (now wider) boundaries will become the next scent marked area. The problem the RBCT caused was not removing all the group, leaving a few to scrap.
If incoming badgers are free of Tb which some will be, there is no problem with a slow recolonistaion. This happened at Thornbury, after an intense clearance lasting several months. That kept the area clear of Tb for 12 years. Badger numbers recovered naturally to pre-cull levels.
We think there is some milage in gassing, as setts are then unavailable for recolonistation - at least for a time. It is pretty stupid, knowing that m.bovis can lurk in damp humid conditions for several months if not years, to leave such an area to reinfect healthy incoming badgers.
Your final sentence is probably correct. Depressing but correct.
A 'nationwide cull' or one which identified only infected badgers (groups?).
The former would work, but I think, like you we would find it abhorrent. This site has been pushing for the latter since its inception. And will continue to do so. PCR will identify such setts / latrines without even handling badgers, but we understand that gamma bloods are more specific to bTb on badgers than in cattle. If a couple of trapped and tested individuals prove positive then that infection will spread through the group, sooner or later.
We've had several comments saying "only 3% of badgers die from Tb". But figures given in the Bourne's 4th ISG report to the Bern convention offer a figure of over 70 % infection rate obtained from badgers taken in BRO's up to 1997. And the ISG final report describes up to 55% of the RBCT badgers as having visible lesions and over 14% 'severly lesioned' with multiple body parts affected.
Any mammal with TB, will eventually either from stress, food shortage, weather induced pressure, fighting or a secondary disease challenge, suffer a breakdown of closed Tb lesions.
Matthew (11)10.48
That a reservoir of a highly infectious zoonosis can be left alone and may not then infect many other species including mankind, is irresponsible.
Our point was that having done just that, (left an increasing and infected badger population) we all found our cattle experiencing prolonged Tb breakdowns.
This is not a 'religious' debate. It does however support the PQ's which form the basis of this site and which go a long way to satisfying both the Koch and Evans postulates of epidemiology.
Any other conclusion is the triumph of hope over (bitter) experience.
Matthew said "We couldn't possibly comment on the ISG final report's figures, but note they specify 'trap nights' not traps set, which is a different set of data.". Think about this logically - if you were to use some sort of measure to assess how much impact interference had on the quality of trapping, how could the absolute number of traps inferred with possibly provide what you want? One trap that is destroyed can be replaced by another one and how many times was that trap successfully used before it was destroyed? The ONLY measure which makes sense is number of trap NIGHTS - i.e. one trap night is one trapping opportunity, so one that is interferred with was (potentially) a trapped badger not trapped. What has happened to individual traps is meaningless, only a measure of trapping OPPORTUNITIES can possibly tell us what we need to know. And that figure is 8.1%, rather different to your 70%. You surely aren't trying to misrepresent statistics are you? 'gasp!'
You said "The problem the RBCT caused was not removing all the group, leaving a few to scrap.". As I already said in my last post, this is not a reasonable argument, as removing whole social groups, if anything would cause more of a problem with perturbation. The scrapping is not the main problem, it's the fact that the badgers move further and so are able to spread their infection further - it's as simple as that. Your lack of appreciation of this is why you (in a rather petty fashion) refer to the RBCT as a dispersal trial. Fact is even if it didn't take out as many badgers as it should have done, the reality is that taking ALL of them out would not have reduced the perturbation effect, it made have even made it worse. To not acknowledge this is foolish when deciding how/if to cull badgers.
You do however, then go on to agree with me and state that "If incoming badgers are free of Tb which some will be, there is no problem with a slow recolonistaion.". Of course this is true - but it is a huge IF (and of course the "some" is simply not enough, you need ALL to be free). The fact is, we know infection rates in badgers are high and to naively assume that a neighbouring badger social group is free of infection is foolish to say the least.
As regards gassing, you say there is some mileage in it and then say that "It is pretty stupid, knowing that m.bovis can lurk in damp humid conditions for several months if not years, to leave such an area to reinfect healthy incoming badgers.". Rather contradictory I think and the conclusion is that gassing isn't really a very viable option.
I agree with you that possibilities for identifying an infected badger (while it's still alive) should be looked in to. As should vaccines (but who knows when they materialise). In the meantime, dismissing the results of the CULLING trial is irresponsible and naive as is misrepresenting (or selectively quoting) statistics from it. (By results I refer to effects of culling, not the recommendations for just looking at cattle based controls).
Post a Comment