Welsh farmers breathed a collective sigh of relief this week after the Welsh Assembly voted not to introduce the contentious 'tabular valuation' system into the Principality.
Cattle compulsorily purchased as bTb reactors in Wales will still be subject to a valuation procedure by a professional, independent valuer rather than an 'all size fits none' figure dreamed up by the Department of Environment, Food and Rural Affairs.
The news was met with relief by the Cymru NFU president, Dai Davies who commented;
"Welsh farmers whose herds are hit with tuberculosis do not want 'compensation' - what they want is for the disease to be eradicated. Compensation should not an issue, and it would become unecessary if the fundemental issue of stopping the spread and eradicating the disease was addressed by government."
Mr. Davies continued: " Valuation tables are based on averages, and are not representative of the animal, as they over compensate poor quality stock, and under value good quality stock".
He added that he hoped the Welsh Assembly would "now put all its efforts into eradicating this business-crippling disease which continues to spiral out of control across Wales".
Other comments on the decision from politicians of various hues included:
Lib-Dem - "tackle the disease, rather than slash farmers' payments"
Plaid Cymru - "valuation 'tables' not only unfair to cattle owners and breeders, especially pedigree cattle breeders, but an inefficient use of taxpayer's money"
The same arguments were levelled at our Minister for Fisheries, Ben Bradshaw, the only member of Deathrow's team to survive the recent parliamentary cull. But he ignored them, and it is now a very strange phenomenon that a pedigree cow in Wales can be valued in £ thousands, but if she has contact with m.bovis in England she's 'worth' just over £900.
Tommorrow, May 31st. Wales' survey of road kill badgers comes to an abrupt - and some say premature - end.
Announced in December and beginning in January, the programme was expected to last a year. Road kill badgers reported to the department of agricluture were to be collected for post mortem, and the results correlated with areas and instances of cattle Tb. But after tomorrow, members of the public have been told "don't report any more thankyou, we have enough" .
These excercises usually involve a 'target' figure with funding to match it and the general concensus from industry commentators is, that the almost 500 badgers collected in just four months, is more an indication of a population explosion in the species than a funding famine.
All commentators expressed "surprise" that a survey which was supposed to last a year, has met its target body count in just four months. But they welcomed the news from the Welsh Assembly that the results of the survey would also be brought forward, and after postmortems are carried out, are due to be published on September 28th.
Tuesday, May 30, 2006
Saturday, May 27, 2006
Spitting badger terrorises staff at sports centre.
Reported in the Western Morning News this week, staff at a watersports centre are nervous after being attacked and chased by a large badger:
"Night staff at a top Westcountry watersports centre are fearing for their safety after a string of attacks... by a three-foot angry badger.
The fearless animal has been terrorising late-shift workers at the Mount Batten Centre in Plymouth.Several members of staff have reported being ambushed by the creature as they make their way home through the car park. The badger, which is thought to be protecting young nearby, lurks in bushes near the centre's car park - and charges at anyone who strays too close. Recent victims have included night porter Glynn Webb and barmaid Tamsin Parish. Miss Parish, 23, had the fright of her life when the stocky animal started thundering towards her as she made her way home at the end of a shift."I was making my way to my boyfriend's car when I caught sight of it out of the corner of my eye," she said. "I've never seen anything move so fast in my life - it was just streaking towards me."I know it sounds silly but I ran as fast as I could. I haven't been to the car park at night since."
Mr Webb, 68, was also left shaken after a run-in with the badger. The former able seaman said the animal has absolutely no fear of humans and is quite willing to launch an attack."I shone my torch at him, and he spat at me. Then he just put his head down and charged. I was so startled I hit my nose on my torch."
Plymouth naturalist Kevin Witts said badgers only became confrontational if they felt their young were threatened - or if they were going senile. He said: "It may be a female with
cubs, or possibly an elderly badger that's losing it a little bit. Either way, it keeps the security staff on their toes."
Well, well well. The passage which we have highlighted in bold is extremely relevant to 'transmission opportunities' for bovine Tb.
So when you hear a scientist in need of further research funding, pleading with his audience:
"but we don't know how bTb is transmitted between badgers and cattle", we do hope that our readers will remember, not only that this animal charged members of the public, attacked them, and generally pursued them around a car park, but that it spat at them. We also suggest that any 'naturalist' wheeled out to comment, will be aware that badgers who behave in this way are not necessarily 'senile', but may be in the later stages of Tb, excluded from their social group and its area, behave 'atypically' (aggressively?) and wander more.
23rd. March 2004 : Col 684W
Mr. Bradshaw: Research conducted by the Central Science Laboratory has identified behavioural differences between badgers excreting M. bovis, and uninfected animals. Badgers excreting M.bovis had a larger 'home range' and were more likely to visit [farm] buildings.
Or sports centres?
"Night staff at a top Westcountry watersports centre are fearing for their safety after a string of attacks... by a three-foot angry badger.
The fearless animal has been terrorising late-shift workers at the Mount Batten Centre in Plymouth.Several members of staff have reported being ambushed by the creature as they make their way home through the car park. The badger, which is thought to be protecting young nearby, lurks in bushes near the centre's car park - and charges at anyone who strays too close. Recent victims have included night porter Glynn Webb and barmaid Tamsin Parish. Miss Parish, 23, had the fright of her life when the stocky animal started thundering towards her as she made her way home at the end of a shift."I was making my way to my boyfriend's car when I caught sight of it out of the corner of my eye," she said. "I've never seen anything move so fast in my life - it was just streaking towards me."I know it sounds silly but I ran as fast as I could. I haven't been to the car park at night since."
Mr Webb, 68, was also left shaken after a run-in with the badger. The former able seaman said the animal has absolutely no fear of humans and is quite willing to launch an attack."I shone my torch at him, and he spat at me. Then he just put his head down and charged. I was so startled I hit my nose on my torch."
Plymouth naturalist Kevin Witts said badgers only became confrontational if they felt their young were threatened - or if they were going senile. He said: "It may be a female with
cubs, or possibly an elderly badger that's losing it a little bit. Either way, it keeps the security staff on their toes."
Well, well well. The passage which we have highlighted in bold is extremely relevant to 'transmission opportunities' for bovine Tb.
So when you hear a scientist in need of further research funding, pleading with his audience:
"but we don't know how bTb is transmitted between badgers and cattle", we do hope that our readers will remember, not only that this animal charged members of the public, attacked them, and generally pursued them around a car park, but that it spat at them. We also suggest that any 'naturalist' wheeled out to comment, will be aware that badgers who behave in this way are not necessarily 'senile', but may be in the later stages of Tb, excluded from their social group and its area, behave 'atypically' (aggressively?) and wander more.
23rd. March 2004 : Col 684W
Mr. Bradshaw: Research conducted by the Central Science Laboratory has identified behavioural differences between badgers excreting M. bovis, and uninfected animals. Badgers excreting M.bovis had a larger 'home range' and were more likely to visit [farm] buildings.
Or sports centres?
Sunday, May 21, 2006
'Failure' redefined ?
This week's Veterinary Times, after leading with Paul Carunana's attack on the Krebs RBCT last week, gives the ISG and John Bourne centre stage and the right to reply.
"The comments from Paul Caruana to the EFRA committee criticised the handling of the trial by the ISG and dismissed the labelling of the trial as "robust".
John Bourne replied to this :
"The explicit scientific approach taken by the ISG in designing the randomised badger culling trial was crucial, as was its implementation, to ensure that appropriate scientific information was collected". He said it was unfortunate that Paul Caruana had failed to grasp the necessity of imposing such scientific discipline to the field work of the WLU when conducting a scientific study. He branded suggestions that the WLU staff and operatives were not consulted as 'utterly false'.
The ISG said that its plan was never to remove all badgers from culled areas and rebutted Mr. Caruana's comment that interference by animal rights activists had affected the trials outcome. He (Professor Bourne) was unequivocal in his opinion of the views of Dr. Gallagher, Dr. Thomas and John Daykin: "The continued dogmatic belief by scientifically uninformed veterinary opinion that failed past bovine Tb control policies should continue to be more vigourously pursued must be challenged by available scientific understanding".
Well that's told 'em then. More on that ISG 'science' later....
Dr. Lewis Thomas said of the ISG's reponse "To embark on a large scale culling trial knowing that 'culling was never expected or designed to remove all badgers from culled areas' is positively breathtaking". Dr. Gallagher and John Daykin added " A salient point of the ISG's response concerns 'failure' of the culling policies of the 1970's and 1980's. They should have better informed themselves on this subject - in fact the original gassing policy was extremely effective in reducing outbreaks more than threefold in just over five years to a national total of 88 confirmed outbreaks in 1981.
The 'Clean Ring' trapping policy which followed was less effective, but maintained some progress until it was halted in 1986 when the total number of outbreaks was 86.
Now under the 'robust' stewardship of the ISG, there were 1,922 new confirmed herd outbreaks during 2005 and a total of 5,539 herds under Tb restriction. So is failure being redefined as well as science?".
With respect (of course) to all parties in this debate, the only people who can give an 'informed' view of the RBCT are the farmers who took part. It was our fences trashed, and our woods invaded by 'activists' intent on letting out their little furry friends. Paul Caruana was spot on, when he stated that 'it took the teams 4 years to learn how to catch badgers' and avoid such interference. That was assuming that his masters at the ISG directed their little green landrovers in our direction at all. On one of our contributer's farms the 'gap' between any semblance of 'clearance' - which now Bourne says was not not going to happen anyway - was three long years. So much for the ISG acetates in 1997, explaining to participating farmers that the ISG were going to 'Cull ALL Badgers' in the proactive areas, and 'Cull ALL badgers' following a Tb breakdown in the reactive zones. (He lied, Matt, he lied.)
We have quoted PQ's many times as to the level of interference with the Krebs traps:
"57% were 'interfered with, and 12% disappeared" as at October 2003. So of 100% set, 69% were absolutely useless. Defra have estimated the ISG 'badger bag' as somewhere between 20 - 60 percent'. This we suspect is on land made available to the trial teams, and does not take into account the trapping problems. And to compound the problems, as Mr. Caruana stated, the trapping was limited to less than 2 weeks before the team moved on. Sometimes for good. And in Matt 5's case for a good 3 years.
It may be worth recording here the effect on the farm of this totally inadequate attempt to 'cull all badgers'. In the wake of the first foray in 2000, a huge amount of activity was generated among the remaining badgers. Farms became 'motorways' as the groups which had been 'shredded' dispersed, fought and regrouped. And the following disease was devastating, some farms losing 30 animals at a time. And it was three years until the teams returned, and again only for 8 nights. So on balance we would agree with Mr. Caruana and those veterinary practitioners who see the results of Defra's prevarication on a daily basis. Krebs wasn't a trial into the effects of culling badgers at all, it proved to be an excercise in badger dispersal. But hey, what do we know, a Professor calls it 'available scientific understanding' .
Would that be the same Professor who chased 14 million postcards convinced that they were cattle? Yup, it would. And the very same who told farmers in 1997, that he was going to 'Cull all badgers', and now writes that this was never the intention at all. Try, cull as many as we can trap, stir up the rest then - just disappear. That'd be right then. And that's the level of 'available scientific understanding', in dealing with a very serious zoonotic pathogen.
I'm glad I'm not a 'scientist'.
"The comments from Paul Caruana to the EFRA committee criticised the handling of the trial by the ISG and dismissed the labelling of the trial as "robust".
John Bourne replied to this :
"The explicit scientific approach taken by the ISG in designing the randomised badger culling trial was crucial, as was its implementation, to ensure that appropriate scientific information was collected". He said it was unfortunate that Paul Caruana had failed to grasp the necessity of imposing such scientific discipline to the field work of the WLU when conducting a scientific study. He branded suggestions that the WLU staff and operatives were not consulted as 'utterly false'.
The ISG said that its plan was never to remove all badgers from culled areas and rebutted Mr. Caruana's comment that interference by animal rights activists had affected the trials outcome. He (Professor Bourne) was unequivocal in his opinion of the views of Dr. Gallagher, Dr. Thomas and John Daykin: "The continued dogmatic belief by scientifically uninformed veterinary opinion that failed past bovine Tb control policies should continue to be more vigourously pursued must be challenged by available scientific understanding".
Well that's told 'em then. More on that ISG 'science' later....
Dr. Lewis Thomas said of the ISG's reponse "To embark on a large scale culling trial knowing that 'culling was never expected or designed to remove all badgers from culled areas' is positively breathtaking". Dr. Gallagher and John Daykin added " A salient point of the ISG's response concerns 'failure' of the culling policies of the 1970's and 1980's. They should have better informed themselves on this subject - in fact the original gassing policy was extremely effective in reducing outbreaks more than threefold in just over five years to a national total of 88 confirmed outbreaks in 1981.
The 'Clean Ring' trapping policy which followed was less effective, but maintained some progress until it was halted in 1986 when the total number of outbreaks was 86.
Now under the 'robust' stewardship of the ISG, there were 1,922 new confirmed herd outbreaks during 2005 and a total of 5,539 herds under Tb restriction. So is failure being redefined as well as science?".
With respect (of course) to all parties in this debate, the only people who can give an 'informed' view of the RBCT are the farmers who took part. It was our fences trashed, and our woods invaded by 'activists' intent on letting out their little furry friends. Paul Caruana was spot on, when he stated that 'it took the teams 4 years to learn how to catch badgers' and avoid such interference. That was assuming that his masters at the ISG directed their little green landrovers in our direction at all. On one of our contributer's farms the 'gap' between any semblance of 'clearance' - which now Bourne says was not not going to happen anyway - was three long years. So much for the ISG acetates in 1997, explaining to participating farmers that the ISG were going to 'Cull ALL Badgers' in the proactive areas, and 'Cull ALL badgers' following a Tb breakdown in the reactive zones. (He lied, Matt, he lied.)
We have quoted PQ's many times as to the level of interference with the Krebs traps:
"57% were 'interfered with, and 12% disappeared" as at October 2003. So of 100% set, 69% were absolutely useless. Defra have estimated the ISG 'badger bag' as somewhere between 20 - 60 percent'. This we suspect is on land made available to the trial teams, and does not take into account the trapping problems. And to compound the problems, as Mr. Caruana stated, the trapping was limited to less than 2 weeks before the team moved on. Sometimes for good. And in Matt 5's case for a good 3 years.
It may be worth recording here the effect on the farm of this totally inadequate attempt to 'cull all badgers'. In the wake of the first foray in 2000, a huge amount of activity was generated among the remaining badgers. Farms became 'motorways' as the groups which had been 'shredded' dispersed, fought and regrouped. And the following disease was devastating, some farms losing 30 animals at a time. And it was three years until the teams returned, and again only for 8 nights. So on balance we would agree with Mr. Caruana and those veterinary practitioners who see the results of Defra's prevarication on a daily basis. Krebs wasn't a trial into the effects of culling badgers at all, it proved to be an excercise in badger dispersal. But hey, what do we know, a Professor calls it 'available scientific understanding' .
Would that be the same Professor who chased 14 million postcards convinced that they were cattle? Yup, it would. And the very same who told farmers in 1997, that he was going to 'Cull all badgers', and now writes that this was never the intention at all. Try, cull as many as we can trap, stir up the rest then - just disappear. That'd be right then. And that's the level of 'available scientific understanding', in dealing with a very serious zoonotic pathogen.
I'm glad I'm not a 'scientist'.
Defra to 'test' Dutch tuberculin.
The sudden drop in numbers of cattle slaughtered as bTb reactors prompted a flurry of reaction from industry and media, if not from Defra, when figures were published in the second week of May. (see post below)
Farmers Guardian reported the story and gave more information:
Entitled "Dutch tuberculin under scrutiny as TB figures fall", their article continues:
"Defra vets are investigating whether a switch in the type of tuberculin used to test cattle is contributing to the sudden and dramatic decline in recorded incidence of bTb. In the first 3 months of this year there were 954 Tb incidents where cattle reacted to the skin test compared with 1,315 in the first quarter of 2005. A remarkable 27 percent drop.So far there have been 512 confirmed new TB cases [ ] In the first quarter of 2005, there were 802.The figures for January 2006 were broadly unchanged on January last year, indicating that the change happened suddenly in February / March. What makes the decline even more dramatic, is that 2000 more herds, and over 100,000 more animals, were tested in the first three months of 2006, than 2005."
Other reasons for the drop are listed in the article by various sections of the industry:
*Jan Rowe, the NFU TB spokesman highlighted Defra's 'zero tolerance' of overdue Tb tests which was introduced in Feb. 2005 as possibly giving an artificially high comparison figure.
*And Tb levels in badgers could be falling, or the tabular valuations introduced in February 2006 may be encouraging farmers to take the law into their own hands.
*NBA chief executive Robert Forster suggested a colder spring could be an influencing factor.
*BCVA president Andrew Biggs said that the 'knock on ' effect of zero tolerance could be contributory, but that the change to Dutch tuberculin "had to be a possible factor".
*Defra said that changes to the tuberculin was considered as a "possible factor", and analysis was underway to compare the performance of the Dutch Lelystad tuberculin, and the VLA home produced product.
The full text can be viewed at:
http://www.farmersguardian.com/story.asp?sectioncode=1&storycode=2246
As we said in our comments section of the previous thread, many hypotheses may contribute. But that 'something' happened very suddenly, in February / March. Without wishing to dismiss any of the 'possibles' flagged up, we would point out that from Parliamentary questions, the residual effect of exposure to bTb in cattle is "up to 221 days in the UK strains".
So anything that happened to the badgers / cattle interface would have had to have occured, just as dramatically, last autumn and not in February this year. Which is why we suspect, Defra are "monitoring the effect of the tuberculin". By which of course, they may mean checking which batch numbers of Lelystad tuberculin went where. Not publicised is a county or regional breakdown of the figures in a format which allows comparison. Is one region affected by the drop more than another? We have heard figures of 40 percent bandied around for the SW, but Glos. do not seem to have had a similar reduction.
Of the 'zero tolerance' possibility mentioned by the NFU and the BCVA, comparison between Jan/Feb/March 2004 and its introduction in 2005, again using Defra figures which we had fortunately printed off and stored, produced no dramatic upturn. NHI's (New breakdowns) were 1093 in the first 3 months of 2004, compared with 1163 in 2005 - an increase of 50. Confirmed incidents recorded 587 in 2004, against 802 in 2005 and currently 512. Cattle slaughtered as Reactors to the skin test show a drop on 2004 of about 100; 5543 in 2004 and 5455 in 2006 (7731 in 2005) . So February / March 2006 is significantly down even when compared with Defra's 2004 figures.This should be excellent news. So why are we so jittery? And why are Defra (very belatedly) 'testing' the efficacy of Dutch tuberculin (used February / March?) when they have distributed it for almost a year with no apparent problems?
We reported the prelude to it's introduction in February 2005 in our posting;
http://bovinetb.blogspot.com/2005/02/ooops.html
A case of shutting the stable door?
Farmers Guardian reported the story and gave more information:
Entitled "Dutch tuberculin under scrutiny as TB figures fall", their article continues:
"Defra vets are investigating whether a switch in the type of tuberculin used to test cattle is contributing to the sudden and dramatic decline in recorded incidence of bTb. In the first 3 months of this year there were 954 Tb incidents where cattle reacted to the skin test compared with 1,315 in the first quarter of 2005. A remarkable 27 percent drop.So far there have been 512 confirmed new TB cases [ ] In the first quarter of 2005, there were 802.The figures for January 2006 were broadly unchanged on January last year, indicating that the change happened suddenly in February / March. What makes the decline even more dramatic, is that 2000 more herds, and over 100,000 more animals, were tested in the first three months of 2006, than 2005."
Other reasons for the drop are listed in the article by various sections of the industry:
*Jan Rowe, the NFU TB spokesman highlighted Defra's 'zero tolerance' of overdue Tb tests which was introduced in Feb. 2005 as possibly giving an artificially high comparison figure.
*And Tb levels in badgers could be falling, or the tabular valuations introduced in February 2006 may be encouraging farmers to take the law into their own hands.
*NBA chief executive Robert Forster suggested a colder spring could be an influencing factor.
*BCVA president Andrew Biggs said that the 'knock on ' effect of zero tolerance could be contributory, but that the change to Dutch tuberculin "had to be a possible factor".
*Defra said that changes to the tuberculin was considered as a "possible factor", and analysis was underway to compare the performance of the Dutch Lelystad tuberculin, and the VLA home produced product.
The full text can be viewed at:
http://www.farmersguardian.com/story.asp?sectioncode=1&storycode=2246
As we said in our comments section of the previous thread, many hypotheses may contribute. But that 'something' happened very suddenly, in February / March. Without wishing to dismiss any of the 'possibles' flagged up, we would point out that from Parliamentary questions, the residual effect of exposure to bTb in cattle is "up to 221 days in the UK strains".
So anything that happened to the badgers / cattle interface would have had to have occured, just as dramatically, last autumn and not in February this year. Which is why we suspect, Defra are "monitoring the effect of the tuberculin". By which of course, they may mean checking which batch numbers of Lelystad tuberculin went where. Not publicised is a county or regional breakdown of the figures in a format which allows comparison. Is one region affected by the drop more than another? We have heard figures of 40 percent bandied around for the SW, but Glos. do not seem to have had a similar reduction.
Of the 'zero tolerance' possibility mentioned by the NFU and the BCVA, comparison between Jan/Feb/March 2004 and its introduction in 2005, again using Defra figures which we had fortunately printed off and stored, produced no dramatic upturn. NHI's (New breakdowns) were 1093 in the first 3 months of 2004, compared with 1163 in 2005 - an increase of 50. Confirmed incidents recorded 587 in 2004, against 802 in 2005 and currently 512. Cattle slaughtered as Reactors to the skin test show a drop on 2004 of about 100; 5543 in 2004 and 5455 in 2006 (7731 in 2005) . So February / March 2006 is significantly down even when compared with Defra's 2004 figures.This should be excellent news. So why are we so jittery? And why are Defra (very belatedly) 'testing' the efficacy of Dutch tuberculin (used February / March?) when they have distributed it for almost a year with no apparent problems?
We reported the prelude to it's introduction in February 2005 in our posting;
http://bovinetb.blogspot.com/2005/02/ooops.html
A case of shutting the stable door?
Thursday, May 11, 2006
Drop in Cattle Reactors - Good News?
A comment on the thread below gave us a wake up call to delve more deeply into the latest slaughter figures from Defra.
The comment we print in full:
"The latest bovine TB figures would appear to be good news!
According to the Provisional TB statistics for Great Britain released on 5 May 2006
TB TESTS CARRIED OUT (in the year to 31st March) increased from
1,649,543 in 2005 to
1,807,805 in 2006
Despite this the number of cows slaughtered as reactors decreased from 7731 to 5455.
I reckon that is about 29% DECREASE
However 6099 herds were under movement restriction on 31 March 2006 (due to a TB incident, overdue TB test, etc), almost half of these
(2994) restricted due to overdue TB tests!
More cattle tested, loads less reactors than last year, and half of the herds under movement restrictions due only to late testing.
Am I missing something, or is this very good news?"
Mmmmm. We really are not sure and for that reason had not explored this too deeply. That's not to say we were unaware of the figures, more listening hard to the many reasons flagged up.
Here are some:
*Defra will no doubt attribute the drop to pre movement testing, but as that only started at the end of March, any cattle involved will not have had a second 60 day test at the posting of these figures. In other words, it has not been around long enough.
*Cynical members of the farming community may have realised that when tabular valuations arrived on Feb 1st., both non pedigree and pedigree cattle values would be severely affected and up with that they would not put.
*Vets were telling us that the Dutch tuberculin, used as we exhausted UK supplies late last year, and mentioned in previous postings, was more sensitive. And in fact it contains 30,000 iu/ ml of bovine antigen compared with 25,000 iu/ml in the UK dose. (25,000 iu/ml of avian in both).
And now we have this amazing drop in cattle numbers. You ask us why. We don't believe in the tooth fairy, and think that the vets may have a point in their concern over the Dutch tuberculin.
The figures have been dropping (they say) since February. But that should have resulted in more reactors if the Dutch serum was more sensitive.
So we are asking some serious and pertinent questions of the specific antigen used and its concentration. Some serum doses are constructed on a broad base to cope at a low level with many strains, but others have a specific 'receptor site' antibody / antigen lock and only identify the strains they are set up to find. And if that were the case, not too many UK cattle wear clogs, or produce Edam cheese. But we return to the earlier veterinary concerns that the Dutch product was TOO sensitive. So if it has it changed, how has it changed from being 'more sensitive' to less? HAS it changed at all? Are they now saying it is not sensitive enough?
The label on the vials still say 25,000 iu/ml for Avian, and 30,000 ph.eur.u/ml for bovine)
Are other factors mentioned above all playing a part?
For the moment the Chancellor may be grateful for small mercies from the Department of the Environment, Food and rural Affairs. His Tb budget is dropping, but if this serum is failing for whatever reason to find reactors, then initially slaughterhouse cases will be seen to increase and eventually, the chickens will come home to roost with an explosion in undiagnosed cases. And that is the worst news.
Defra figures are here: http://www.defra.gov.uk/animalh/tb/stats/detailedstats.htm
'Slaughterhouse' figures have almost doubled from 109 to 189, but the confirmed culture samples from these animals is stable at 68 / 71 respectively.
The comment we print in full:
"The latest bovine TB figures would appear to be good news!
According to the Provisional TB statistics for Great Britain released on 5 May 2006
TB TESTS CARRIED OUT (in the year to 31st March) increased from
1,649,543 in 2005 to
1,807,805 in 2006
Despite this the number of cows slaughtered as reactors decreased from 7731 to 5455.
I reckon that is about 29% DECREASE
However 6099 herds were under movement restriction on 31 March 2006 (due to a TB incident, overdue TB test, etc), almost half of these
(2994) restricted due to overdue TB tests!
More cattle tested, loads less reactors than last year, and half of the herds under movement restrictions due only to late testing.
Am I missing something, or is this very good news?"
Mmmmm. We really are not sure and for that reason had not explored this too deeply. That's not to say we were unaware of the figures, more listening hard to the many reasons flagged up.
Here are some:
*Defra will no doubt attribute the drop to pre movement testing, but as that only started at the end of March, any cattle involved will not have had a second 60 day test at the posting of these figures. In other words, it has not been around long enough.
*Cynical members of the farming community may have realised that when tabular valuations arrived on Feb 1st., both non pedigree and pedigree cattle values would be severely affected and up with that they would not put.
*Vets were telling us that the Dutch tuberculin, used as we exhausted UK supplies late last year, and mentioned in previous postings, was more sensitive. And in fact it contains 30,000 iu/ ml of bovine antigen compared with 25,000 iu/ml in the UK dose. (25,000 iu/ml of avian in both).
And now we have this amazing drop in cattle numbers. You ask us why. We don't believe in the tooth fairy, and think that the vets may have a point in their concern over the Dutch tuberculin.
The figures have been dropping (they say) since February. But that should have resulted in more reactors if the Dutch serum was more sensitive.
So we are asking some serious and pertinent questions of the specific antigen used and its concentration. Some serum doses are constructed on a broad base to cope at a low level with many strains, but others have a specific 'receptor site' antibody / antigen lock and only identify the strains they are set up to find. And if that were the case, not too many UK cattle wear clogs, or produce Edam cheese. But we return to the earlier veterinary concerns that the Dutch product was TOO sensitive. So if it has it changed, how has it changed from being 'more sensitive' to less? HAS it changed at all? Are they now saying it is not sensitive enough?
The label on the vials still say 25,000 iu/ml for Avian, and 30,000 ph.eur.u/ml for bovine)
Are other factors mentioned above all playing a part?
For the moment the Chancellor may be grateful for small mercies from the Department of the Environment, Food and rural Affairs. His Tb budget is dropping, but if this serum is failing for whatever reason to find reactors, then initially slaughterhouse cases will be seen to increase and eventually, the chickens will come home to roost with an explosion in undiagnosed cases. And that is the worst news.
Defra figures are here: http://www.defra.gov.uk/animalh/tb/stats/detailedstats.htm
'Slaughterhouse' figures have almost doubled from 109 to 189, but the confirmed culture samples from these animals is stable at 68 / 71 respectively.
Monday, May 08, 2006
The iron has it - Mark Purdey on bTb
Mark Purdey, an organic farmer who plays a clarinet to his cows in Somerset had some interesting theories on the origins of BSE. While he was including organophosphates in the equation, our casualties fitted his thesis, but when he jumped to ley lines and the phases of the moon, Matt 5 got a bit lost. anyway, a comment on the previous thread reminded us of Mark's brush with bTb and his theories on that.
As we replied after the comment, if the facts don't fit our contributer's particular situation - and here they did not, then a theory it must remain.
TUBERCULOSIS ALERT** --
"Despatches from behind the iron curtain of a British "biohazard" zone."By Mark Purdey, High Barn Farm, Elworthy, Taunton, Somerset, TA43PX,UK.
European livestock farmers dread the day when their cattle succumb to a tuberculosis breakdown. The implications are severe; a ruthless cull of infected cattle and badgers(not since 1997 Mark!), with all remaining healthy cattle impounded behind an iron curtain of government mandated movement restrictions and red tape. The knock on effects have virtually paralysed small farming businesses into a state of financial melt down. /**/But the official procedures of TB control are archaic and outmoded.They are founded upon the age old hypothesis that humans develop TB as a sole result of exposure to TB infected animals, whilst failing toaccommodate the more recent front line revelations in the multifactorial science surrounding mycobacterial disease. In this respect, we need to be questioning whether such cruel and costly strategies that are currently involved in TB control programmes are actually fulfilling their desired effect -- to protect the human population against the TBagent.
Earlier this summer , I was forced to come to terms with my own cattle joining the ever increasing ranks of TB infected herds that are currently blighting the UK.
TB Breakdown; a testing time.
At dawn I scaled the hill to collect the cattle from the furthest fields. The earth still held the heat of the previous day, and I was forced to coerce the cows a little, for they seemed more reluctant to rise and amble the few feet to the green lane than usual. Perhaps the cows were more perceptive than me, their sixth sense receptive to the fate that was about to befall them in a few hours time. As we reached the steeper gradients of the shillet track, the cattle accelerated a little, rutting up the dust with their hooves. The tailswish of a cow disturbed an early morning bee, that droned off beyond the bank of bluebells and into the haze of the dazzling sun. Gradually, the entire caravan of cattle snaked its way down the track to the valley bottom below. On the last stretch to the farm, a patch of giant foxgloves towered over us like an array of mauve lanterns, their luminescence still resonating the brilliance of first light. But I failed to heed their red alert, and just drove the cows on without a second thought. Back at the yard, the vet was ready and we led the cows straight down to the inspection pens. The procedure was simple - to measure the size of any lumps that had erupted on the cows' necks which served as a yardstick for gauging the extent of allergic response to the TB skintest - an intradermal injection of tubercle bacillus that had been administered by the vet three days earlier. After a few minutes I saw the vet stand back abruptly. "Oh" he said in a despondent, drawn out tone, popping on his spectacles slightly askew."We could have a problem here, Mark". I watched him fumbling through his pockets for the callipers, and now knew that he had to take a more precise measurement of what obviously looked like a colossal reaction lump on the cow's neck. I became anxious, and my mouth was beginning to parch up in anticipation of what was coming next.The air was heavy, like that period of suspense before a thunderstorm. Even the robins who had been busy in the yard a minute earlier rustling up the brittle leafs, seemed to have stopped in their tracks. The vet raised his glasses and wiped the sweat off his forehead. "You have a reactor, I'm afraid Mark". A few minutes later there was another reactor, and then several more. My mouth had parched up completely now and my stomach felt nauseaous.
I became angry at the thought of these fine young pedigree animals just into their prime, now condemned to slaughter under the government's animal health diktat. Furthermore, like many other cattle farmers in the UK, I was confused by the perfect condition of the TB reactor cows, since I had always assumed that TB was a debilitating disease. Although these cows had reacted tothe skin test and were therefore deemed to carry TB, I began to wonder whether they had successfully adapted to the infection by knocking out the greater majority of the invasive mycobacteria. In this respect, TheTB slaughter programme could actually be annihilating the resistant animals -- culling the genetically robust individuals that we really needed to be keeping as breeding stock for future generations.
Badgering the true evidence.
The next stage of the so called 'crisis' procedure was to retire to the farmhouse for a tree's worth of form filling, where I was presented with several sheets of a TB questionnaire. I was amazed by the reductionist contents of the questions that followed. Each one had been designed on the assumption that the transmission of the TB agent from infected badgers to cattle was the sole cause of bovine TB. In this respect,*/baddie the badger/* had been dubbed the guilty culprit before the necessary detective work had even begun. ( If this was the TB 99 form, we found only one paragraph of the many sheets referred to badgers - ed) The exact same 'back to front' investigation was applicable to the questionnaire which the government presented to farms that had experienced a case of mad cow disease (BSE) where every question was based on the assumption of a meat and bone meal feed cause - despite the diversity of evidence which indicated that this theory was totally flawed.
The search for susceptibility factors -- the seeds of TB ?
The real question was why had my farm always boasted a TB-free status, despite being surrounded by TB affected cattle / badgers for many years. I began to wonder what changes had been integrated into our farming practises over recent years: changes that could be responsible for switching on the susceptibility of our cattle to the TB agent ? I felt that this was the relevant question that I should be asking right now.TB is virtually endemic in the soils, waters and atmospheres of themajority of ecosystems, where mycobacteria have co-existed with mammalian life for centuries. Despite its widespread prevalence, the TBagent has produced relatively few major outbreaks across the world. It seems that an epidemic of clinical TB can only erupt once some anti-TBcomponent of our immune defence has been disrupted. In this respect, the primary event is a disruption of immunity which enables the TB agent to breach the body's defences and opportunistically take a hold. A historical study of the epidemiology of TB demonstrates that epidemics of TB have occurred since the iron age, and that this disease has always been rife amongst specific population groups who are nutritionally impoverished in some way. For example, TB was rife amongst city slum dwellers who had no choice but to breath the industrially polluted air 24 hours a day, as well as the half starved Scottish / Irish crofterswho were evicted and forced onto boats bound for North America. Another more recent example involves AIDS victims whose immune systems are so severely compromised that they invariably develop TB as a secondarycomplication.
A Limey's view of TB cause.
So what is the key factor that has suddenly unleashed TB susceptibility amongst my cattle following so many years of TB-free status ? After much thought about the specific changes that I had integrated into my farming system over recent years, I began to wonder whether the TB breakdown in my herd could be connected to the drastic cost-cutting measures which I have been forced to adopt in order to survive the current agri-economiccrisis. Along with most other hard pressed livestock farmers across the UK, we had foolishly cut back on the use of the so called '*/non essential'/*lime / calcified seaweed based fertilisers. Furthermore, the trend in reduced usage of lime based fertilisers has been exacerbated by recent conservation measures that have debarred the harvesting of Cornish calcified seaweed altogether - thereby preventing future usage of this material on the farm. It is the general reduction in use of lime fertilisers, combined withthe recent increases in winter rainfall across the western UK, that has acidified the top soil as a result; whilst other eco-influences such as acid rain and the continued use of so called '*/essential'/* artificial fertilisers will undoubtably be playing their contributory roles in the acidification of Agricultural ecosystems. The pH alkaline/acidic value of the soils on our farm has dropped from an acceptable neutral pH 6 to an acidic pH 5 over the last three years -evidenced by the invasion of buttercups into our pastures where clover used to flourish. Research has shown that there is a correlation between areas of high mycobacteria incidence and regions where the soils are acid. This association is strengthened by the results of studies where lime was spread on farms in Michigan that were suffering from high rates of mycobacterium infection ( albeit the paratuberculosis strain of mycobacterium ). The study concluded that the lime treatment had produced a ten-fold reduction in the infection of cattle after a three year period had passed. [ Johnson-Ifearulundu and Kaneene 1997 ].
*/Branding the Iron on TB/*/cause/*
The relevant issue in respect of TB infection and soil acidity hinges on the fact that acidification of the topsoil leads to an excessive accumulation of available iron [ Pais and Benton Jones 1997] --particularly in the regions where soil iron is naturally elevated and rainfall is high. The iron is taken up by the pasture herbage (especially ryegrass, plantain [ McDonald and others 1973 ], bluebell tubers, etc) as well as percolating into the local water supplies as aresult; which, in turn, is taken up by any animals who thrive upon the local iron rich ecosystem -- particularly those individuals who are genetically predisposed to an increased uptake/retention of iron within their biosystems. Interestingly, the key hotspot zones of bovine TB across the UK are the Forest of Dean, Exmoor, Cornwall, Devon and the Mendip hills. These regions all correlate with the areas where iron has been mined in abundance [ Flett 1935 ] and rainfall is high. Preliminary pasture sampling from the specific fields on my own farm (June 2005) where the TB reactors had been pastured has consistently demonstrated an */excessive/* elevation of iron ( average 378 mg/kg), in relation to the levels of 143 mg/kg recorded three years previously.This research is being expanded to cover TB-free and TB farms across the key TB cluster areas of the UK .
*/What is the relationship between elevated iron and increasedsusceptibility to TB ?
Much research is published in the scientific literature which demonstrates that Iron represents an essential prerequisite in the pathogenesis of TB , enabling TB and other strains of mycobacterium to proliferate, metabolise and survive within the mammalian biosystem [Ratledge 2004 ]. In this respect, it is the supply of 'free' iron within the host which provides the TB agent with its 'fire power' capacity to unleash its deleterious pathogenicity, thereby invoking the often fatal, devastating consequences that result from TB infection. Although TB victims adapt to their parasitic attacks by stashing away their iron supplies in tissues that are inaccessible to the mycobacteria, the grand finale of the TB disease process usually culminates in the parasite getting the upper hand; whereby the host develops the classic iron deficient anaemic state that is a central clinical feature of TB. Mycobacteria acquire their iron from the host's own transferrin /ferritin molecules -- the iron binding transport / storage proteins thatare integral to the healthy metabolism of iron within the mammalian biosystem. The mycobacteria rob their host's iron by releasing a type of iron-capturing siderophore called an exochelin; which, in turn, transfers and donates the iron back to the mycobactins which exist inthe cell walls of the mycobacteria themselves [ Gobin and Horwitz1996 ].This hijaking of the host's iron supply is beneficial for the survivalof the TB mycobacteria in more ways than one. Not only does the TB agent utilise the host's iron for its own proliferation and survival, but it also utilises this metal to indemnify its own long term security within the host; by disabling the host's immune defence against itself. The parasite achieves this means of self protection by curtailing the viable synthesis of the iron binding beta-2-microglobulin molecules whose role is to activate the killer T lymphocytes [ Schaible and others 2002 ] -the host's main line of immune defence against mycobacteria infection.This could explain why individual humans whose T immune systems have become compromised through nutritional deprivation or AIDS toxicity areat a significantly greater risk of developing TB as a secondary complication. But TB is not the only pathogen that depends upon the host's iron for its maintenance and growth within the body. The infamous Clostridium Botulinum ( implicated in grass sickness of horses ), Leprosy, HIV,Candida , Listeria, Salmonella, Malaria etc, are all members of this insidious family of */ironmonger /*pathogens to which TB belongs[Weinberg 1999] Only last week, champion horsebreeder Gail Dunsbee had been in touch with me over the sudden death of one of her horses as a result of grass sickness -- a devastating paralysis of the autonomic nerve endings inthe horse's gut due to infection with clostridium botulinum. But much like TB, Botulinum is virtually endemic in the gastro tract of horses where it rarely produces any adverse health effects at all. So what environmental factor had suddenly switched on the susceptibility of her horse's gut to the infection ? Dissatisfied with the professional ignorance surrounding the root causes of grass sickness, Gail had taken matters into her own hands in order to safeguard the future of her surviving horses. And once again, it looks like the results of her preliminary soil analyses have provided the causal clues that might address this catastrophic problem for horsebreeders. Apart from the low potassium readings, the extremely excessive readings for Iron ( at 1344 ppm ) was the only other element of the twelve elements tested which had deviated from its respective reference range.This result could explain why grass sickness, like TB, has invariably remained confined to acid soil districts where iron levels are generally elevated.
*/Ironing out the TB pathogen./*
Since elevated iron increases TB risk , it is easy to understand how the management of dietary iron can influence the outcome of TB [ Ratledge2004, Cronje and Bornman 2005 ]. For example. when TB infected mice weretreated with the iron chelating lactoferrin protein ( a natural ingredient of colostrum milk ) , there was a one hundred fold reduction in the number of pathogens present in the mice. [ Schaible and others 2002 ]. Likewise, TB diseased individuals used to be regularly treated with the iron-chelating compound p-aminosalicylate with some success [ Ratledge2004 ]. In this respect, it could prove beneficial from a preventativeas well as a curative perspective to introduce copper or zinc bicarbonate supplements into the diet of TB affected populations [ Paisand Benton Jones 1997 ]. Whilst these anionic compounds do not act as iron chelators as such, they will impair the absorption of iron across the gastrotract by competing for its uptake system of transport proteins. Furthermore, any foodstuffs containing phytic acids, such aslegumes ( alfalfa, clover, etc ) and grains [ McDonald and others 1973 ]will produce the same anti-iron effects. Use of inorganic phosphorus as an inclusion in fertilisers or mineral feed supplements would also assist in reducing the amount of free iron that is rendered 'available' in the soil or taken up into the animal respectively [ Underwood 1977 ]. The phosphorus competes for the ironbinding site on the transport proteins that normally convey iron acrossthe gut wall; thereby arresting the uptake of iron at its initial pointof entry into the body. It is also important to consider the knock-out effects that iron chelators might impact upon the */horror chamber/* of other pathogens which need to bite the */iron bullet/* before they can trigger disease.For instance, it has already been demonstrated that the iron chelating compounds, deferoxamine and 8-hydroxyquinoline-5-sulfonic acid have produced beneficial effects in the treatment of leprosy and clostridiumbotulinum respectively .[Weinberg 1999][ Bhattacharyya and Sugiyama 1989]
*/Iron in the Ecosystem. /*
It is proposed that badgers and cattle that co-exist within the same environments will both develop TB due to their separate co-exposure to the same iron-rich foodchain, and not necessarily due to across-infection from one animal to the other. Bluebell and other iron-rich tubers constitute a large part of thebadger's diet and these will gradually load up the badger's biosystem with a concentrated source of iron until threshold levels are exceeded - thereby providing any mycobacterial pathogens that are present with the sustenance to proliferate to pathogenic levels. Likewise, the high incidence rates of human TB that have been recorded amongst steelworkers and slum dwellers ( who lived beside their workplaces during theindustrial revolution ) could have been induced by the high levels ofiron in the atmospheres of their local environment.
*/The politics of TB. /*
I believe that government ministers in the UK have been correct in resisting pressures to re-enact wholesale slaughter of badgers as a means of controlling TB in the bovine / human populations. For the badger culls of bygone years have achieved nothing in terms of eradicating TB. (Thornbury? 100% eradication for 12 years? - ed)The disease has kept on re-occurring irrespective of the various slaughter measures that have been put in place. In this respect, we need to consider what is actually achieved each time that we re-enact this final farcical solution for TB control --eg; badger gassing and blanket cattle culls ?Furthermore, it is scientifically naïve to think that we will ever be able to eradicate a pathogen that is endemic in the environment at large. As long as optimum eco-conditions for the survival of TBmycobacterium are allowed to exist ( eg; high iron / soil acidity ),then TB epidemics will continue to rear their ugly head, as and when alterations in weather conditions and husbandry methods permit. In respect of consumers who are anxious about exposure to TB pathogens in their foods, they need to be aware that modern methods of foodprocessing safeguard consumers from exposure to the TB agent -- methods that did not exist half a century ago. For example, any milk that is taken from a TB affected animal today is automatically pasteurised in the modern dairy set up. (prohibited from the food chain including calves from January 2006- ed) Although pasteurisation produces some negative health effects -- by switching our immune response to TB and other pathogens into 'sleep mode' - this ultra efficient sterilisation process provides a guarantee of biosecurity for those who are concerned about TB exposure.
Whilst it is high time that governments should say farewell to their archaic strategy for TB control, some viable alternative will be needed to replace it. In this respect, governments should begin to examine the considerably cheaper / animal welfare friendly option of encouragingfarmers ( via subsidies) to adopt husbandry practices which prevent cattle from succumbing to TB infection in the first instance. Eg; by subsidising the spreading of lime fertilisers across the TB endemic/highiron regions, as well as promoting feeding / fertilising with iron-chelating/ anti-iron compounds on farms in the TB risk areas. This would reduce the amount of iron that is flowing up the farm foodchain, which, in turn, would reduce the levels of TB mycobacteria.Such a radical approach which curtails the susceptibility of cattle to the TB agent could produce some major advantages over the existing system which slaughters out the end results of TB infection. This would achieve a considerable reduction in the overall incidence rates of TB ,thereby reaping major savings for both human and animal life, farmers' livelihoods and the tax payer. Since the incidence of TB is increasing amongst the human population, it is high time that we adopted a more intelligent, civilised and updated strategy for dealing with the prevention of TB. In this respect, we need to be taking a closer look at the underlying causes of 'iron overload' in the human foodchain and ecosystem at large. This would entail looking at the impacts of acid rain and how it brings about a rise in the levels of available iron within the soil and water supplies. Issues surroundingthe industrial emission of iron particulates into the atmosphere, as well as the supplementation of our foods with iron additives representimportant areas that warrant investigation and the development of controls. Likewise, the indirect impact of various toxic or mutagenicenvironmental agents upon the metabolic processes that regulate iron homeostasis is an area that also needs to be considered. For a whole range of environmental chemicals /metals are recognised to disrupt or mutate the body's capacity to regulate the balanced uptake, storage and/or excretion of iron; thereby representing an alternative means through which iron levels could become elevated in the biosystem; which in turn, switches on an increased susceptibility to TB infection.
Meanwhile back on the farm, the knacker man had arrived to collect theTB reactors at nightfall. I lead the unsuspecting cows to the loading pen, feeling guilty that I had betrayed them by failing to mount any kind of resistance against the government's strategy of senseless slaughter. The cows waited, absorbing their final moments of life in the half light. Their backs were steaming and heads held low.The monster lorry rattled in like an aluminium alien, and then backed upto the loading pen. The ramps came down, and after a rapid fire of whelpings and whip lashings, the cattle reluctantly surrendered themselves to their fate; hooves sliding and clattering up the steely ramp into the dark hold of the lorry. As the truck turned the top corner, I caught my last glimpse of the cows, their noses frantically pressing through the six inch slats - a last ditch attempt to escape their premature and pointless execution.Tonight they will be sectioned to the post mortem bench, abattoired into oblivion..As I walked back to the farmhouse in the half light, I caught a glimpse of the patch of foxglove petals glowing like red hot irons on the hill, still resonating with the evening sun. It was a timely reminder that our TB problem had not been extinguished by the removal of our reactor cows from the farm, but was still very much alive and well, and rooted in the acidity of our soils. As I walked back to the farmhouse, I remembered that the presence of foxgloves indicates high iron and high manganeselevels in the soil. Mark Purdey 15/8/05
As we pointed out, Mark's withdrawal of lime from his land for monetry pressures and the subsequent increase in iron levels does not necessarily apply to all of us. And in our case, it did not. Ph levels were 5.8 - 6.2 at the last testing session. we would hope that Mark has rectified the acidity of his land since last August. Did it have any affect in subsequent tb tests I wonder? Conversly the 'cause' of his problem may have died or gone to pastures new.
A farmer in the north feeds 'his' badgers with selenium and reckons it protects them and his cattle. Time will tell.
As we replied after the comment, if the facts don't fit our contributer's particular situation - and here they did not, then a theory it must remain.
TUBERCULOSIS ALERT** --
"Despatches from behind the iron curtain of a British "biohazard" zone."By Mark Purdey, High Barn Farm, Elworthy, Taunton, Somerset, TA43PX,UK.
European livestock farmers dread the day when their cattle succumb to a tuberculosis breakdown. The implications are severe; a ruthless cull of infected cattle and badgers(not since 1997 Mark!), with all remaining healthy cattle impounded behind an iron curtain of government mandated movement restrictions and red tape. The knock on effects have virtually paralysed small farming businesses into a state of financial melt down. /**/But the official procedures of TB control are archaic and outmoded.They are founded upon the age old hypothesis that humans develop TB as a sole result of exposure to TB infected animals, whilst failing toaccommodate the more recent front line revelations in the multifactorial science surrounding mycobacterial disease. In this respect, we need to be questioning whether such cruel and costly strategies that are currently involved in TB control programmes are actually fulfilling their desired effect -- to protect the human population against the TBagent.
Earlier this summer , I was forced to come to terms with my own cattle joining the ever increasing ranks of TB infected herds that are currently blighting the UK.
TB Breakdown; a testing time.
At dawn I scaled the hill to collect the cattle from the furthest fields. The earth still held the heat of the previous day, and I was forced to coerce the cows a little, for they seemed more reluctant to rise and amble the few feet to the green lane than usual. Perhaps the cows were more perceptive than me, their sixth sense receptive to the fate that was about to befall them in a few hours time. As we reached the steeper gradients of the shillet track, the cattle accelerated a little, rutting up the dust with their hooves. The tailswish of a cow disturbed an early morning bee, that droned off beyond the bank of bluebells and into the haze of the dazzling sun. Gradually, the entire caravan of cattle snaked its way down the track to the valley bottom below. On the last stretch to the farm, a patch of giant foxgloves towered over us like an array of mauve lanterns, their luminescence still resonating the brilliance of first light. But I failed to heed their red alert, and just drove the cows on without a second thought. Back at the yard, the vet was ready and we led the cows straight down to the inspection pens. The procedure was simple - to measure the size of any lumps that had erupted on the cows' necks which served as a yardstick for gauging the extent of allergic response to the TB skintest - an intradermal injection of tubercle bacillus that had been administered by the vet three days earlier. After a few minutes I saw the vet stand back abruptly. "Oh" he said in a despondent, drawn out tone, popping on his spectacles slightly askew."We could have a problem here, Mark". I watched him fumbling through his pockets for the callipers, and now knew that he had to take a more precise measurement of what obviously looked like a colossal reaction lump on the cow's neck. I became anxious, and my mouth was beginning to parch up in anticipation of what was coming next.The air was heavy, like that period of suspense before a thunderstorm. Even the robins who had been busy in the yard a minute earlier rustling up the brittle leafs, seemed to have stopped in their tracks. The vet raised his glasses and wiped the sweat off his forehead. "You have a reactor, I'm afraid Mark". A few minutes later there was another reactor, and then several more. My mouth had parched up completely now and my stomach felt nauseaous.
I became angry at the thought of these fine young pedigree animals just into their prime, now condemned to slaughter under the government's animal health diktat. Furthermore, like many other cattle farmers in the UK, I was confused by the perfect condition of the TB reactor cows, since I had always assumed that TB was a debilitating disease. Although these cows had reacted tothe skin test and were therefore deemed to carry TB, I began to wonder whether they had successfully adapted to the infection by knocking out the greater majority of the invasive mycobacteria. In this respect, TheTB slaughter programme could actually be annihilating the resistant animals -- culling the genetically robust individuals that we really needed to be keeping as breeding stock for future generations.
Badgering the true evidence.
The next stage of the so called 'crisis' procedure was to retire to the farmhouse for a tree's worth of form filling, where I was presented with several sheets of a TB questionnaire. I was amazed by the reductionist contents of the questions that followed. Each one had been designed on the assumption that the transmission of the TB agent from infected badgers to cattle was the sole cause of bovine TB. In this respect,*/baddie the badger/* had been dubbed the guilty culprit before the necessary detective work had even begun. ( If this was the TB 99 form, we found only one paragraph of the many sheets referred to badgers - ed) The exact same 'back to front' investigation was applicable to the questionnaire which the government presented to farms that had experienced a case of mad cow disease (BSE) where every question was based on the assumption of a meat and bone meal feed cause - despite the diversity of evidence which indicated that this theory was totally flawed.
The search for susceptibility factors -- the seeds of TB ?
The real question was why had my farm always boasted a TB-free status, despite being surrounded by TB affected cattle / badgers for many years. I began to wonder what changes had been integrated into our farming practises over recent years: changes that could be responsible for switching on the susceptibility of our cattle to the TB agent ? I felt that this was the relevant question that I should be asking right now.TB is virtually endemic in the soils, waters and atmospheres of themajority of ecosystems, where mycobacteria have co-existed with mammalian life for centuries. Despite its widespread prevalence, the TBagent has produced relatively few major outbreaks across the world. It seems that an epidemic of clinical TB can only erupt once some anti-TBcomponent of our immune defence has been disrupted. In this respect, the primary event is a disruption of immunity which enables the TB agent to breach the body's defences and opportunistically take a hold. A historical study of the epidemiology of TB demonstrates that epidemics of TB have occurred since the iron age, and that this disease has always been rife amongst specific population groups who are nutritionally impoverished in some way. For example, TB was rife amongst city slum dwellers who had no choice but to breath the industrially polluted air 24 hours a day, as well as the half starved Scottish / Irish crofterswho were evicted and forced onto boats bound for North America. Another more recent example involves AIDS victims whose immune systems are so severely compromised that they invariably develop TB as a secondarycomplication.
A Limey's view of TB cause.
So what is the key factor that has suddenly unleashed TB susceptibility amongst my cattle following so many years of TB-free status ? After much thought about the specific changes that I had integrated into my farming system over recent years, I began to wonder whether the TB breakdown in my herd could be connected to the drastic cost-cutting measures which I have been forced to adopt in order to survive the current agri-economiccrisis. Along with most other hard pressed livestock farmers across the UK, we had foolishly cut back on the use of the so called '*/non essential'/*lime / calcified seaweed based fertilisers. Furthermore, the trend in reduced usage of lime based fertilisers has been exacerbated by recent conservation measures that have debarred the harvesting of Cornish calcified seaweed altogether - thereby preventing future usage of this material on the farm. It is the general reduction in use of lime fertilisers, combined withthe recent increases in winter rainfall across the western UK, that has acidified the top soil as a result; whilst other eco-influences such as acid rain and the continued use of so called '*/essential'/* artificial fertilisers will undoubtably be playing their contributory roles in the acidification of Agricultural ecosystems. The pH alkaline/acidic value of the soils on our farm has dropped from an acceptable neutral pH 6 to an acidic pH 5 over the last three years -evidenced by the invasion of buttercups into our pastures where clover used to flourish. Research has shown that there is a correlation between areas of high mycobacteria incidence and regions where the soils are acid. This association is strengthened by the results of studies where lime was spread on farms in Michigan that were suffering from high rates of mycobacterium infection ( albeit the paratuberculosis strain of mycobacterium ). The study concluded that the lime treatment had produced a ten-fold reduction in the infection of cattle after a three year period had passed. [ Johnson-Ifearulundu and Kaneene 1997 ].
*/Branding the Iron on TB/*/cause/*
The relevant issue in respect of TB infection and soil acidity hinges on the fact that acidification of the topsoil leads to an excessive accumulation of available iron [ Pais and Benton Jones 1997] --particularly in the regions where soil iron is naturally elevated and rainfall is high. The iron is taken up by the pasture herbage (especially ryegrass, plantain [ McDonald and others 1973 ], bluebell tubers, etc) as well as percolating into the local water supplies as aresult; which, in turn, is taken up by any animals who thrive upon the local iron rich ecosystem -- particularly those individuals who are genetically predisposed to an increased uptake/retention of iron within their biosystems. Interestingly, the key hotspot zones of bovine TB across the UK are the Forest of Dean, Exmoor, Cornwall, Devon and the Mendip hills. These regions all correlate with the areas where iron has been mined in abundance [ Flett 1935 ] and rainfall is high. Preliminary pasture sampling from the specific fields on my own farm (June 2005) where the TB reactors had been pastured has consistently demonstrated an */excessive/* elevation of iron ( average 378 mg/kg), in relation to the levels of 143 mg/kg recorded three years previously.This research is being expanded to cover TB-free and TB farms across the key TB cluster areas of the UK .
*/What is the relationship between elevated iron and increasedsusceptibility to TB ?
Much research is published in the scientific literature which demonstrates that Iron represents an essential prerequisite in the pathogenesis of TB , enabling TB and other strains of mycobacterium to proliferate, metabolise and survive within the mammalian biosystem [Ratledge 2004 ]. In this respect, it is the supply of 'free' iron within the host which provides the TB agent with its 'fire power' capacity to unleash its deleterious pathogenicity, thereby invoking the often fatal, devastating consequences that result from TB infection. Although TB victims adapt to their parasitic attacks by stashing away their iron supplies in tissues that are inaccessible to the mycobacteria, the grand finale of the TB disease process usually culminates in the parasite getting the upper hand; whereby the host develops the classic iron deficient anaemic state that is a central clinical feature of TB. Mycobacteria acquire their iron from the host's own transferrin /ferritin molecules -- the iron binding transport / storage proteins thatare integral to the healthy metabolism of iron within the mammalian biosystem. The mycobacteria rob their host's iron by releasing a type of iron-capturing siderophore called an exochelin; which, in turn, transfers and donates the iron back to the mycobactins which exist inthe cell walls of the mycobacteria themselves [ Gobin and Horwitz1996 ].This hijaking of the host's iron supply is beneficial for the survivalof the TB mycobacteria in more ways than one. Not only does the TB agent utilise the host's iron for its own proliferation and survival, but it also utilises this metal to indemnify its own long term security within the host; by disabling the host's immune defence against itself. The parasite achieves this means of self protection by curtailing the viable synthesis of the iron binding beta-2-microglobulin molecules whose role is to activate the killer T lymphocytes [ Schaible and others 2002 ] -the host's main line of immune defence against mycobacteria infection.This could explain why individual humans whose T immune systems have become compromised through nutritional deprivation or AIDS toxicity areat a significantly greater risk of developing TB as a secondary complication. But TB is not the only pathogen that depends upon the host's iron for its maintenance and growth within the body. The infamous Clostridium Botulinum ( implicated in grass sickness of horses ), Leprosy, HIV,Candida , Listeria, Salmonella, Malaria etc, are all members of this insidious family of */ironmonger /*pathogens to which TB belongs[Weinberg 1999] Only last week, champion horsebreeder Gail Dunsbee had been in touch with me over the sudden death of one of her horses as a result of grass sickness -- a devastating paralysis of the autonomic nerve endings inthe horse's gut due to infection with clostridium botulinum. But much like TB, Botulinum is virtually endemic in the gastro tract of horses where it rarely produces any adverse health effects at all. So what environmental factor had suddenly switched on the susceptibility of her horse's gut to the infection ? Dissatisfied with the professional ignorance surrounding the root causes of grass sickness, Gail had taken matters into her own hands in order to safeguard the future of her surviving horses. And once again, it looks like the results of her preliminary soil analyses have provided the causal clues that might address this catastrophic problem for horsebreeders. Apart from the low potassium readings, the extremely excessive readings for Iron ( at 1344 ppm ) was the only other element of the twelve elements tested which had deviated from its respective reference range.This result could explain why grass sickness, like TB, has invariably remained confined to acid soil districts where iron levels are generally elevated.
*/Ironing out the TB pathogen./*
Since elevated iron increases TB risk , it is easy to understand how the management of dietary iron can influence the outcome of TB [ Ratledge2004, Cronje and Bornman 2005 ]. For example. when TB infected mice weretreated with the iron chelating lactoferrin protein ( a natural ingredient of colostrum milk ) , there was a one hundred fold reduction in the number of pathogens present in the mice. [ Schaible and others 2002 ]. Likewise, TB diseased individuals used to be regularly treated with the iron-chelating compound p-aminosalicylate with some success [ Ratledge2004 ]. In this respect, it could prove beneficial from a preventativeas well as a curative perspective to introduce copper or zinc bicarbonate supplements into the diet of TB affected populations [ Paisand Benton Jones 1997 ]. Whilst these anionic compounds do not act as iron chelators as such, they will impair the absorption of iron across the gastrotract by competing for its uptake system of transport proteins. Furthermore, any foodstuffs containing phytic acids, such aslegumes ( alfalfa, clover, etc ) and grains [ McDonald and others 1973 ]will produce the same anti-iron effects. Use of inorganic phosphorus as an inclusion in fertilisers or mineral feed supplements would also assist in reducing the amount of free iron that is rendered 'available' in the soil or taken up into the animal respectively [ Underwood 1977 ]. The phosphorus competes for the ironbinding site on the transport proteins that normally convey iron acrossthe gut wall; thereby arresting the uptake of iron at its initial pointof entry into the body. It is also important to consider the knock-out effects that iron chelators might impact upon the */horror chamber/* of other pathogens which need to bite the */iron bullet/* before they can trigger disease.For instance, it has already been demonstrated that the iron chelating compounds, deferoxamine and 8-hydroxyquinoline-5-sulfonic acid have produced beneficial effects in the treatment of leprosy and clostridiumbotulinum respectively .[Weinberg 1999][ Bhattacharyya and Sugiyama 1989]
*/Iron in the Ecosystem. /*
It is proposed that badgers and cattle that co-exist within the same environments will both develop TB due to their separate co-exposure to the same iron-rich foodchain, and not necessarily due to across-infection from one animal to the other. Bluebell and other iron-rich tubers constitute a large part of thebadger's diet and these will gradually load up the badger's biosystem with a concentrated source of iron until threshold levels are exceeded - thereby providing any mycobacterial pathogens that are present with the sustenance to proliferate to pathogenic levels. Likewise, the high incidence rates of human TB that have been recorded amongst steelworkers and slum dwellers ( who lived beside their workplaces during theindustrial revolution ) could have been induced by the high levels ofiron in the atmospheres of their local environment.
*/The politics of TB. /*
I believe that government ministers in the UK have been correct in resisting pressures to re-enact wholesale slaughter of badgers as a means of controlling TB in the bovine / human populations. For the badger culls of bygone years have achieved nothing in terms of eradicating TB. (Thornbury? 100% eradication for 12 years? - ed)The disease has kept on re-occurring irrespective of the various slaughter measures that have been put in place. In this respect, we need to consider what is actually achieved each time that we re-enact this final farcical solution for TB control --eg; badger gassing and blanket cattle culls ?Furthermore, it is scientifically naïve to think that we will ever be able to eradicate a pathogen that is endemic in the environment at large. As long as optimum eco-conditions for the survival of TBmycobacterium are allowed to exist ( eg; high iron / soil acidity ),then TB epidemics will continue to rear their ugly head, as and when alterations in weather conditions and husbandry methods permit. In respect of consumers who are anxious about exposure to TB pathogens in their foods, they need to be aware that modern methods of foodprocessing safeguard consumers from exposure to the TB agent -- methods that did not exist half a century ago. For example, any milk that is taken from a TB affected animal today is automatically pasteurised in the modern dairy set up. (prohibited from the food chain including calves from January 2006- ed) Although pasteurisation produces some negative health effects -- by switching our immune response to TB and other pathogens into 'sleep mode' - this ultra efficient sterilisation process provides a guarantee of biosecurity for those who are concerned about TB exposure.
Whilst it is high time that governments should say farewell to their archaic strategy for TB control, some viable alternative will be needed to replace it. In this respect, governments should begin to examine the considerably cheaper / animal welfare friendly option of encouragingfarmers ( via subsidies) to adopt husbandry practices which prevent cattle from succumbing to TB infection in the first instance. Eg; by subsidising the spreading of lime fertilisers across the TB endemic/highiron regions, as well as promoting feeding / fertilising with iron-chelating/ anti-iron compounds on farms in the TB risk areas. This would reduce the amount of iron that is flowing up the farm foodchain, which, in turn, would reduce the levels of TB mycobacteria.Such a radical approach which curtails the susceptibility of cattle to the TB agent could produce some major advantages over the existing system which slaughters out the end results of TB infection. This would achieve a considerable reduction in the overall incidence rates of TB ,thereby reaping major savings for both human and animal life, farmers' livelihoods and the tax payer. Since the incidence of TB is increasing amongst the human population, it is high time that we adopted a more intelligent, civilised and updated strategy for dealing with the prevention of TB. In this respect, we need to be taking a closer look at the underlying causes of 'iron overload' in the human foodchain and ecosystem at large. This would entail looking at the impacts of acid rain and how it brings about a rise in the levels of available iron within the soil and water supplies. Issues surroundingthe industrial emission of iron particulates into the atmosphere, as well as the supplementation of our foods with iron additives representimportant areas that warrant investigation and the development of controls. Likewise, the indirect impact of various toxic or mutagenicenvironmental agents upon the metabolic processes that regulate iron homeostasis is an area that also needs to be considered. For a whole range of environmental chemicals /metals are recognised to disrupt or mutate the body's capacity to regulate the balanced uptake, storage and/or excretion of iron; thereby representing an alternative means through which iron levels could become elevated in the biosystem; which in turn, switches on an increased susceptibility to TB infection.
Meanwhile back on the farm, the knacker man had arrived to collect theTB reactors at nightfall. I lead the unsuspecting cows to the loading pen, feeling guilty that I had betrayed them by failing to mount any kind of resistance against the government's strategy of senseless slaughter. The cows waited, absorbing their final moments of life in the half light. Their backs were steaming and heads held low.The monster lorry rattled in like an aluminium alien, and then backed upto the loading pen. The ramps came down, and after a rapid fire of whelpings and whip lashings, the cattle reluctantly surrendered themselves to their fate; hooves sliding and clattering up the steely ramp into the dark hold of the lorry. As the truck turned the top corner, I caught my last glimpse of the cows, their noses frantically pressing through the six inch slats - a last ditch attempt to escape their premature and pointless execution.Tonight they will be sectioned to the post mortem bench, abattoired into oblivion..As I walked back to the farmhouse in the half light, I caught a glimpse of the patch of foxglove petals glowing like red hot irons on the hill, still resonating with the evening sun. It was a timely reminder that our TB problem had not been extinguished by the removal of our reactor cows from the farm, but was still very much alive and well, and rooted in the acidity of our soils. As I walked back to the farmhouse, I remembered that the presence of foxgloves indicates high iron and high manganeselevels in the soil. Mark Purdey 15/8/05
As we pointed out, Mark's withdrawal of lime from his land for monetry pressures and the subsequent increase in iron levels does not necessarily apply to all of us. And in our case, it did not. Ph levels were 5.8 - 6.2 at the last testing session. we would hope that Mark has rectified the acidity of his land since last August. Did it have any affect in subsequent tb tests I wonder? Conversly the 'cause' of his problem may have died or gone to pastures new.
A farmer in the north feeds 'his' badgers with selenium and reckons it protects them and his cattle. Time will tell.
Friday, May 05, 2006
Hold the Front Page
The headline and front page of this weeks' Veterinary Times highlights the submission by Paul Caruana who was part of Defra's Wildlife Unit, and who entered a personal submission to the EFRA commmittee, describing the Krebs' RBCT as "having too many flaws to be taken seriously".
In our posts below, we forecast the demise of this highly competent unit. Mr. Caruana's statement is also listed.
"Defra Employee Blasts ISG over Culling trials."
A submission to the EFRA committee by a Defra employee has slammed the Independent Scientific Group's (ISG) badger culling trials.
Veterinarians and bovine tb experts, Dr. John Gallagher and John Daykin called the information contained in Paul Caruana's submission "dynamite".
Dr. Gallagher told the Veterinary Times "This submission shows how the ISG badly mismanaged this trial and refused to listen to those with practical knowledge who could have done the job properly, if allowed".
Defra's badger culling consultation has attracted more than 41,000 responses: the biggest interest to date in a public consultation. most of the responses are thought to have been promoted by public campaigns orchestrated by the RSPCA and the Badger Trust.
Dr. Gallagher said that these groups had used (the first year results ) the ISG's badger culling trial to back up their arguments. "Assertions based on the findings of the recently completed culling trials have been used as 'hard factual evidence' by welfare groups who've been saying that culling (badgers) does not resolve the TB problem in cattle"
Paul Caruana, field manager at the Defra wildlife unit, Polwhele, Cornwall was unapologetic when offering his submission to the EFRA committee. ........ He outlined that the Krebs trial had too many anomalies and weaknesses in its strategy for it to be successful. "It took us four years to steer away from trapping setts that had been interfered with by animal rights activists, to being able to trap badgers anywhere in order to eliminate them. That was only one of a raft of operational problems we faced and had to endure".
Mr. Caruana said he did not believe scientists had all the answers, and added "most certainly, Krebs doesn't". According to him, the trial had far too many flaws to be trusted to produce meaningful evidence. ......... The whole basis of the trial was to remove badgers off the ground and this, said Mr. Carauna was "farcical " due to restrictions that were placed on staff.
Professor John Bourne, chairman of the ISG has repeatedly stated that the trials represent 'robust science', but Mr. Caruana disagreed with this assessment of events. His condemnation of the trial is unequivocal. "How much weight do we give the latest ISG report detailing 'robust' findings to the minister? If it were down to my staff and myself - very little".
John Daykin who is based in East sussex, said "The evidence in Paul's statement is a shocking indictment of the implementation of badger culling in the experimental triplets. It provides clear evidence that the ISG refused to change course despite repeated entreaties from from operatives carrying out the work at the sharp end. It is vital, that such significant information is looked at in depth by Parliament, before any pronouncements are made on the badger culling consultation."
Dr. Gallagher said that all other badger culling trials conducted in Britian and Ireland had been carried out to a proper standard. He concluded "It is only the ISG's trials that have produced these totally spurious findings, and it is these that the RSPCA and Badger Trust have used".
This front page article also carries a comment:
Where are we now?
"New evidence questioning the efficiency of the ISG's culling trials .... brings many questions to the surface about the ongoing bTb debate.
Do the criticisms that have been levelled at the trials mean that the ISG has in effect, misled ministers and therefore Parliament?
And does this new evidence mean that that the results of the RBCTs are totally discredited?
Ends.
In our posts below, we forecast the demise of this highly competent unit. Mr. Caruana's statement is also listed.
"Defra Employee Blasts ISG over Culling trials."
A submission to the EFRA committee by a Defra employee has slammed the Independent Scientific Group's (ISG) badger culling trials.
Veterinarians and bovine tb experts, Dr. John Gallagher and John Daykin called the information contained in Paul Caruana's submission "dynamite".
Dr. Gallagher told the Veterinary Times "This submission shows how the ISG badly mismanaged this trial and refused to listen to those with practical knowledge who could have done the job properly, if allowed".
Defra's badger culling consultation has attracted more than 41,000 responses: the biggest interest to date in a public consultation. most of the responses are thought to have been promoted by public campaigns orchestrated by the RSPCA and the Badger Trust.
Dr. Gallagher said that these groups had used (the first year results ) the ISG's badger culling trial to back up their arguments. "Assertions based on the findings of the recently completed culling trials have been used as 'hard factual evidence' by welfare groups who've been saying that culling (badgers) does not resolve the TB problem in cattle"
Paul Caruana, field manager at the Defra wildlife unit, Polwhele, Cornwall was unapologetic when offering his submission to the EFRA committee. ........ He outlined that the Krebs trial had too many anomalies and weaknesses in its strategy for it to be successful. "It took us four years to steer away from trapping setts that had been interfered with by animal rights activists, to being able to trap badgers anywhere in order to eliminate them. That was only one of a raft of operational problems we faced and had to endure".
Mr. Caruana said he did not believe scientists had all the answers, and added "most certainly, Krebs doesn't". According to him, the trial had far too many flaws to be trusted to produce meaningful evidence. ......... The whole basis of the trial was to remove badgers off the ground and this, said Mr. Carauna was "farcical " due to restrictions that were placed on staff.
Professor John Bourne, chairman of the ISG has repeatedly stated that the trials represent 'robust science', but Mr. Caruana disagreed with this assessment of events. His condemnation of the trial is unequivocal. "How much weight do we give the latest ISG report detailing 'robust' findings to the minister? If it were down to my staff and myself - very little".
John Daykin who is based in East sussex, said "The evidence in Paul's statement is a shocking indictment of the implementation of badger culling in the experimental triplets. It provides clear evidence that the ISG refused to change course despite repeated entreaties from from operatives carrying out the work at the sharp end. It is vital, that such significant information is looked at in depth by Parliament, before any pronouncements are made on the badger culling consultation."
Dr. Gallagher said that all other badger culling trials conducted in Britian and Ireland had been carried out to a proper standard. He concluded "It is only the ISG's trials that have produced these totally spurious findings, and it is these that the RSPCA and Badger Trust have used".
This front page article also carries a comment:
Where are we now?
"New evidence questioning the efficiency of the ISG's culling trials .... brings many questions to the surface about the ongoing bTb debate.
Do the criticisms that have been levelled at the trials mean that the ISG has in effect, misled ministers and therefore Parliament?
And does this new evidence mean that that the results of the RBCTs are totally discredited?
Ends.
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