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Bovine TB and human health

 Added by  Sally
 20 Jul 2010, 5:27 PM

Professor David Torgerson, and academic at York University and co-author of the report 'Public Health and Bovine Tuberculosis - What's All the Fuss About' has been speaking to the Yorkshire Post. He says it would be cheaper to contain the disease, using vaccines, even if that meant giving up some exports into the rest of Europe. Professor Torgerson says the case for trying to eliminate bTB is based on out-of-date fears of transmission to humans. The risk was more or less eliminated by universal pasteurisation of milk and the government is wasting £100 million a year which would be better spent on worse public health threats.. The main risk of transmission of bovine TB to humans was more or less eliminated years ago, by pasteurisation of milk.
'The UK resists vaccination because vaccination interferes with the standard European skin test, which certifies a herd TB-free. But we could get dispensation to vaccinate', said Professor Torgerson. It might mean losing the right to export live cattle to the rest of the EU. But that would cost less than the £100 million a year currently being paid out for testing and culling cattle and compensating farmers.
The Torgersons' report says there is no veterinary case for instantly culling all TB reactors. Most would be ready for the slaughterhouse, at the end of their careers, before they were ever seriously ill anyway. In other countries, animals come through the illness and herds develop resistance to it. And they sell beef to the UK.
Professor Torgerson told the Yorkshire Post: “As far as I can see, Defra has never done a full cost-benefit analysis of its policy and it needs to. It is difficult to see what the benefits are. But there is now a big vested interest in the system. Vets, for example, get quite a lot of income from it.”

There is much confusion regarding whether or not animals with tuberculous lesions can enter the human food chain.
Where post mortem inspection reveals localised tuberculous lesions in more than one organ or area of the carcase, then the whole carcass and its offal and blood should be declared unfit for human consumption. Where, however, tuberculous lesions are found only in a single organ or part of the carcass, the instructions require the removal of the affected organ or part of the carcase as unfit for human consumption. The remainder can then go for human consumption.
If we are reading the TB stats for GB correctly, then the number of whole carcasses condemned is small but we will request figures from the FSA.
See: www.food.gov.uk/aboutus/ourboard/boardmeetoccasionalpapers/2004/tbinmeat0204

The following papers by the ADVISORY COMMITTEE ON THE MICROBIOLOGICAL SAFETY OF FOOD were published in 2010 in light of the alleged increase in M. bovis infection in cattle in the UK. Once again it was concluded that, despite the increase, risk to the public from bovine TB, is very low.
INFECTION (ACM/981a) - www.food.gov.uk/multimedia/pdfs/committee/acm981a_mbovis.pdf
Mycobacterium bovis AND MILK in two parts:
PART I – PASTEURISED MILK AND MILK PRODUCTS (ACM/995 ) - www.food.gov.uk/multimedia/pdfs/committee/acm995mbovis.pdf
PART II – UNPASTEURISED MILK AND MILK PRODUCTS (ACM/1021) - www.food.gov.uk/multimedia/pdfs/committee/acm1021milk.pdf

The contributions to the forum from the poster, Eyes Wide Open, are worth reading at:
The poster is a farmer who runs a beef unit and rears calves.
This has been drawn to our attention by a farmer who believes the risk of bovine TB to human health are being over stated and they would like to see a change of policy and to be able to vaccinate their animals against bTB.
If you look at the map at http://animalhealth.defra.gov.uk/about/publications/pti/pti_uk_map_2011.pdf it reveals the TB parish testing intervals for 2011 showing red areas are tested every 12mths, orange every 24 months, blue every 36 months, beige every 48 months.
The fact that we've been content and are still content in 2011 to leave such large areas of the country for up to 48 months between testing shows that processes like pasteurisation and meat inspection have been considered and are still considered sufficient safeguards.
Also of interest is that despite the fact she picked up the bacteria when she was a child and it remained in her body for many years before causing actual illness /symptoms, she would presumably have been in close contact with many people (and animals), yet did not pass the disease on ...?
Interesting article at www.bbc.co.uk/news/uk-england-shropshire-14531800 about a lady who contracted bovine TB later on in life after drinking raw milk as a child. It is a good example of latency. The bacteria stayed in her body and her immune system must have become compromised so disease was able to develop (similar to what happens with chicken pox/shingles).
Note that Peter Davies, secretary of TB Alert and a recently retired consultant chest physician, said the chance of humans catching bovine TB in Britain was "vanishingly small". He added that the vast majority of TB patients recover from the disease.
He then goes on to mention the human form which is on the increase because of people coming over to the UK from abroad where the human form is rife. Surely this poses a far more significant risk to humans than bovine TB yet we are doing little to either identify or control the human form in this country.
Commenting on the time it takes to diagnose the human form of TB, Mr Davies said: "TB has been increasing in this country over the past 25 years.
"I would have hoped that the message would have got round by now to GPs and hospital doctors that your next patient may have TB."
He added that two-thirds of TB patients in Britain have origins in India and Africa.
An article by Rose Prince in The Telegraph online on 6/8/11 (http://www.telegraph.co.uk/foodanddrink/8684431/Why-shouldnt-we-drink-raw-milk.html) discusses the rights of those who wish to drink raw milk - some 100,000, a tiny minority, in the UK (bearing in mind it is illegal in Scotland. Dairy UK, the association representing the producers and processors of 85% of the milk sold in Britain has demanded that the Food Standards Agency (FSA) ban the sale of unpasteurised milk, citing food safety and the 'safe image of dairy products'
Rose says she finds this baffling as there have been no widespread and regular food poisoning outbreaks linked directly to drinking raw milk. In fact according to FSA figures, not one outbreak has been reported since 2002. Before that, the FSA says, illness due to unpasteurised milk accounted for a ''small proportion’’ of the total number of food-borne outbreaks between 1992 and 2002. I think we can say that raw milk has become a safer, not riskier, product over the intervening years.
Rose says 'I prefer to drink raw milk because I believe it to be more wholesome than standardised, homogenised, pasteurised milk. It can only be obtained direct from one of the 104 farms in England and Wales that are licensed to sell it. Each farm is regularly inspected, at the farmer’s expense, by both local and national authorities. Cattle are rigorously checked for disease, including TB. I would argue that dedicated raw milk producers pay more attention to hygiene than those who rely on the safety net of pasteurisation.'
Email from BF dated 31/7/11:
The best answer to this long running problem would be to vaccinate all cattle and to persuade farmers to block badgers to stop them from joining cattle when they are grouped in barns as pictured in a recent BBC Countryfile programme! Had the farmer concerned not heard of Electric fences etc? As a boy I had Bovine TB from helping deliver untreated milk on my bicycle into jugs and bowls on doorsteps from a stainless steel container. I also caught Scarlet fever. However Vaccination came along and myself and a large family of relatives never succumbed to other deadly diseases simply by being vaccinated by needle and by mouth. So why all the fuss in avoiding such modern methods these days on cattle? Think of the savings to the farmers and taxpayers this ridiculous Government course of action has and still is costing at a time when we need to get the economy thriving again.
Farming Today included a piece about meat from reactors going into the food chain. It said that the carcasses from reactors and inconclusives were sold into the food chain, with the Government receiving the income from these. Carcasses with lesions could legally enter the food chain for human consumption once the area affected was removed and there was negligible risk to human health, even if lesions remained in the meat, as cooking destroyed the bacteria. Surprisingly Defra has only just started keeping figures regarding this area. The programme also referred to the fact that there was negligible risk to humans from bovine TB now most milk is pasteurised so again we ask, why all the fuss about bovine TB?
Information from
Radio 4 Farming Today broadcast 12/7/11

Email dated 18/5/11 from PT re comment above about the Farming Regulation Taskforce and Para 10.25 which says ' We agree with industry that on scientific and safety grounds, the requirements to destroy milk from TB reactors is not evidence based. However, to allow milk from TB reactors to enter the food chain, we must be confident that we can identify TB reactors and know that milk has been pasteurised.We recommend that Defra, the FSA and dairy trade associations should open discussions on how pasteurised milk from TB-reactor cows, could safely enter the food chain.'
PT says 'It is interesting DEFRA's response on milk pasteurisation and TB reactors. The comparative skin test is only 80 sensitive. So for every 4 confirmed reactors there will be one infected cow that is falsely diagnosed as negative for TB. But as she is not a reactor, her milk will be consumed after pasteurization...but despite the numbers of TB positive, reactor negative cowas there msut be (as there are so many cows in the UK that are reactors), there is clearly no danger to public health....'
The links you found are an excellent discovery.
It would seem that there are a number of immune responses.
From the BUPA site, it appears that latent TB is not infectious, nor is full TB after two weeks of antibiotics (always?). The Mantoux test seems to be interpreted by severity to imply actual TB or immunity to TB. But what about latent TB? Surely if someone has latent TB he will need to know and be checked at regular intervals?
Finally reading “Only some people with TB in their lungs are infectious to others ”makes me tend to agree with whoever it was who suggested that Defra were just burying the evidence – too complicated so just kill everything in sight.
We are of course assuming no significant difference between TB and BTB mechanism. BUPA do not even acknowledge that three forms are in circulation.
We have found a couple of interesting links which give some useful and interesting information about the human form of TB.
More than 200 reforms to existing food safety and environmental regulations governing farmers and food producers have been put forward by the Farming Regulation Taskforce set up in July 2010 with the main aim of reducing red tape. Notwithstanding the implications it has for wildlife, which seems to have angered many people, it does include some reference to bovine TB. For full report visit http://image.guardian.co.uk/sys-files/Environment/documents/2011/05/17/FarmingRegulationTaskForcefinalreport.pdf
Para 10.25 says ' We agree with industry that on scientific and safety grounds, the requirements to destroy milk from TB reactors is not evidence based. However, to allow milk from TB reactors to enter the food chain, we must be confident that we can identify TB reactors and know that milk has been pasteurised.We recommend that Defra, the FSA and dairy trade associations should open discussions on how pasteurised milk from TB-reactor cows, could safely enter the food chain.'
8.29 gave the reason why they did not go further into this subject - basically it was outside their remit. Interestingly during the Task Forces's evidence gathering period, they received a lot of comments on TB related issues. However, they felt that as Defra was already working closely with groups involved in bovine TB they did not wish to duplicate this work.
The media have been keen to extract a good story and the Guardian leads with its headlines at http://www.guardian.co.uk/environment/2011/may/17/farming-regulation-tb-cattle-milk 'Environment
Farming 'Easing of farming regulations could allow milk from TB-infected cattle into food chain. Controversial proposal among more than 200 reforms to food safety and environmental regulations put forward by farming regulation taskforce .'
This was quickly followed with a comment from Defra (www.defra.gov.uk/news/2011/05/17/milk-from-tb-cows/)
Under the heading 'Milk from cows testing positive for tuberculosis (TB)' it goes on to state;
'Myth: The Guardian reports that milk from cows testing positive for tuberculosis (TB) would be introduced into the human food chain under reforms suggested by government advisers.
The newspaper also claims that more than 200 recommendations from the Farming Regulation Task Force have been put forward with the aim of scrapping legislation to protect wildlife, the environment and human health.
Fact: The members of the Farming Regulation Task Force are not government advisers. The Task Force, which presented Ministers with a report on regulation today, is completely independent of government. The report clearly states the importance of protecting wildlife, the environment and human health and suggests how high standards can be maintained with less regulation. It’s about reducing red tape, not standards.
One of the recommendations in the independent report is that Defra, the FSA and dairy trade associations should open discussions on whether pasteurised milk from TB-reactor cows could safely enter the food chain. That’s very different from saying that it “would be introduced into the human food chain” as the Guardian claims.
Defra will examine the report’s many recommendations and publish an initial response in the autumn and a full response in the New Year.'

Email from RL dated 8/5/11
Recently, I was talking to a friend about this and she told me her daughter was a 'reactor' too. She thought it may have been because they used to live near Heathrow Airport, where there's increased chance of being exposed to TB from infected immigrants. Her daughter is now a doctor working with children in a hospital in Devon. So apart from being in perfect health herself, apparently the NHS doesn't regard her as any kind of risk to her patients, either.
I am interested in learning more about the parallels that may be drawn to the human form of TB (bearing in mind that the bovine form accounts for less than 0.5% of human TB cases in the UK) and, in particular, the testing of humans using one of the existing skin tests (eg the Heaf or Mantoux test) which is very similar to the skin test used for cattle.
Up until a few years ago there was a regular testing and vaccination programme for teenagers but this is no longer done routinely, though still available privately and for high risk people. It must be noted that all skin tests are only capable of attempting to determine whether or not there has been any exposure to the Mycobacteria that cause TB. As with the cattle test, in humans tuberculin is injected into the skin and the results are read 48 - 72 hours later, by measuring any induration. If there is no induration or it is under a certain depth the person is vaccinated. Over the stipulated measurement and the person is classed as a reactor and not vaccinated.
In human cases these 'reactors' continue to live among us as there is presumably so little risk of them spreading TB. Very few go on to develop the disease. So one would assume the same would apply to cattle?
However, with cattle ALL reactors are assumed to be infected or potentially infectious, so are slaughtered. Interestingly the meat is, in most cases, still sold for human consumption.
So, why do we kill so many cattle just because they are deemed to be 'reactors'? Most milk is pasteurised and meat is cooked - heat destroys any mycobacteria. Why is there so much fuss about cattle and bovine TB?
The following letter, by Professor Paul Torgerson, was published on page 540 of the Veterinary Record (http://veterinaryrecord.bmj.com/content/167/14/540.2.full.html) on October 2, 2010 regarding the cost-effectiveness of bovine TB control.
The major justifications of bovine tuberculosis (TB) control in the UK include protection of public health, protection of animal health and welfare, and reduction of the economic impact of bovine TB (Defra 2005). However, the elimination of bovine TB from the UK has proved elusive and the means of bovine TB control in the UK have been hotly debated. The latest government initiative will allow farmers to cull badgers despite the fact that badger culling is unlikely to be effective at controlling bovine TB (Donnelly and others 2006).
Investment in animal health and veterinary public health should be evidence-based. In a recent extensive review, Torgerson and Torgerson (2010) questioned the need for bovine TB control in its present form. We concluded that the threat to public health is negligible provided that milk continues to be pasteurised, as human infection with Mycobacterium bovis is primarily a foodborne disease. It was also clear that aerosol transmission from cattle to humans is extremely rare even when bovine TB is very common in cattle. We concluded that the present bovine TB programme is an extremely poor cost-effective measure in terms of public health protection, with perhaps over £3 million spent per disability-adjusted life-year (DALY) averted. In addition, it appears that the economic consequences to the livestock industry and taxpayer are largely expensive intervention costs, not direct disease costs. Very little evidence has been reported of direct animal health costs, which are needed to justify the benefits of this elimination programme in terms of agricultural economics.
Large investments in animal or public health could be more effectively targeted against other zoonotic diseases. For example, in the Netherlands, congenital toxoplasmosis results in approximately 2300 DALYs lost per annum (Kortbeek and others 2009). This suggests that, the burden of congenital toxoplasmosis in the UK could also be considerable. Much of this disease could be prevented by implementing a testing programme in the food chain and any meat from Toxoplasma-positive animals could be frozen, which effectively destroys the bradyzoites (Kijlstra and Jongert 2009).
The World Health Organization is undertaking a study of the global burden of foodborne disease (Stein and others 2007), which will indicate priority areas for resource allocation to control such diseases. Presently, the global burden of human tuberculosis caused by M bovis is unknown, but in the UK the burden is extremely low. Human bovine TB in the UK is unlikely to increase beyond a very small handful of cases provided that milk is pasteurized before consumption. And this is regardless of the numbers of infected bovids or badgers blighting the British countryside.
The UK Government, Defra and the veterinary profession frequently hide behind EU legislation as a justification for bovine TB control in its present form. However, derogations from EC legislation can be sought (for example, to allow cattle vaccination) and resources could be diverted into more rewarding areas of public health. Elimination of bovine TB in the UK using current measures is proving intractable, expensive and of negligible benefit to society.
P. R. Torgerson, Division of Epidemiology, Vetsuisse Faculty, University of Zurich, Winterthurestrasse 260, 8057 Zurich, Switzerland e-mail: ptorgerson@vetclinics.uzh.ch
DEFRA (2005) Government Strategic Framework for the Sustainable Control of Bovine Tuberculosis (bTB) in Great Britain. A sub-strategy of the Animal Health and Welfare Strategy for Great Britain. Defra
DONNELLY, C. A., WOODROFFE, R., COX, D. R., BOURNE, F. J., CHEESEMAN, C. L., CLIFTON- HADLEY, R. S. & OTHERS (2006) Positive and negative effects of widespread badger culling on tuberculosis in cattle. Nature 439, 843-846
KIJLSTRA, A. & JONGERT, E. (2009) Toxoplasma-safe meat: close to reality? Trends in Parasitology 25, 18-22
KORTBEEK, L. M., HOFHUIS, A., NIJHUIS, C. D. M. & HAVELAAR, A. H. (2009) Congenital toxoplasmosis and DALYs in the Netherlands. Memórias do Instituto Oswaldo Cruz 104, 370-373
STEIN, C., KUCHENMÜLLER, T., HENDRICKX, S., PRÜSS-USTÜN, A., WOLFSON, L., ENGELS, D. & SCHLUNDT, J. (2007) The global burden of disease assessments – WHO is responsible? PLoS Neglected Tropical Diseases 1, e161
TORGERSON, P. R. & TORGERSON, D. J. (2010) Public health and bovine TB: what’s all the fuss about? Trends in Microbiology 18, 67-72 doi: 10.1136/vr.c5372
Email debate between SH and RW
Email from SH to RW 20/1/11) , having now had yet another read of the HPA report and your comments I must confess to still being confused as to why there is so much emphasis on bovine TB and getting as many cattle identified (does not happen with humans) and killed as possible - especially when skin test only indicates that the animal has mounted an immune response capable of recognising M. bovis and does not conclude actual infection. If it is a matter of a belt and braces approach and we use the skin test then surely it should be used as it was designed - as a herd test - as it misses around 20% of cases? This would mean we would have to cull all herds where there are reactors but this seems to be how they have 'eradicated' bTB in other countries. If we are not prepared to do this (and I hope we don't as I wouldn't want to see yet more cattle killed!) then surely we will always have infection - even if wildlife are culled?TB has ever been !
Email from RW to SH 20/1/11), irstly it is important to understand that immune response to M bovis if it is truely positive does equal infection with M bovis. Either the infection progresses from the point when it is first established allbeit mostly pretty slowly, whilst some other infected cattle may maintain the infection in a latent state that could re-emerge as an active infection at any time though in some cattle it may never re-activate. In humans the proportion of latent infections, and those that never re-emerge in an active state, with or without shedding and infective potential, is quite high over all infections but what this is in cattle I do not know.
This concept may seem strange to you. In virology it is quite normal, we actually go on accumulating different virus infections all our lives. DNA viruses persist in us as do some RNA viruses. If you have antibody to herpes simplex virus 1 then you have been and are infected with it and will remain so for the rest of your life. Even if you never suffer a cold sore. But should you require severe immunesuppression as in a bone marrow transplant for example the virus will re-emerge. Hence we do not screen prospective BMT patients with the question 'have you ever had a cold sore?' but we do a specific antibody test. If it is positive then the patient is given prophylactic acyclovir to prevent reactivation that will occur and be associated with a painful gingivostomatitis. The virus remains even after treatment with acyclovir which merely suppresses the clinical consequences of reactivation.
M bovis and M tuberculosis are very interesting bacterial infections because they do behave like viruses in this respect, which rely on reactivations to ensure the infection of the next generation of the host. They are not the only bacteria that persisit, Q fever is another but not perhaps in all the animals it infects.
Luckily we don't go in for slaughtering entire herds in the UK which would be useless because of re-infection from other animals in the environment such as most importantly badgers. I guess if there were no other animals infected in our environment or contact was occasional only (infected lynxes in Spain, but actually wild boar are infected too) we might go in for herd slaughter particularly if after culling the skin test positive animals more positive animals were revealed on subsequent testing. I guess this is what happens in the USA. The infected white tailed deer seem to be confined to a few areas and infection in a bovine herd is occasional.
There has not been a conscious TB eradication program for humans but I think it has been surprising how little TB is transmitted in the UK nowadays. I think the treatment program is actually very impressive- very few cases of isoniazid resistant TB were identified as arising in the UK. The USA is copying our DOTS program, directly observed treatment supervision.
Of course anti-microbial treatment of humans for TB can prevent shedding and infectivity, treat active infection so that is is controlled and bacteria cannot be isolated at a later time nor re-emerge, also I read that treatment of 'latent' infection can prevent re-activation. This is very powerful for infection control, and cannot be done with viruses! The anti-microbial treatment kills the organisms even it would seem the latent ones. Anti-viral agents are only virostatic not virocidal. Hence treatment of HIV for life for example.
Skin testing in humans is said to miss overall about 10% of cases. I do not know if on repeat skin testing of herds one would miss more than this. Where does 20% come from? The problem is that with infection from cattle movement or from animals in the environment wild and domestic that are infected and infectious (farm cats may be disproportionaltely important!) the farm animals are not an isolated herd.
It is useless to try to eliminate TB in cattle by testing them if they can be infected from other animals in our UK farmed environment. We are tied into this thinking by many strands, very strong ones for trade and membership of the EU that seem to so disort any initiative and direction that might be taken by the UK. I think the Welsh are attempting to be innovative in their intensive treatment area.
Email from SH to RW dated 22/1/11), so why does a BCG vaccinated animal react to the skin test? I thought that if the immune system was functioning perfectly it resisted the infection – so none was present after the episode – but left antibodies giving enhanced future immunity - although this may not be the case with TB? However, your first sentence seems to be saying that the animal will always have the infection, albeit in a latent form for some?
Email from RW to SH dated 23/1/11) Natural infections that persist. Life is not simple. Our immune systems do not cleanse our bodies of all infections. Persistent infections have evolved means of not being completely eliminated by the immune system, even one that functions perfectly. TB is one of those infections. Once infected with TB, M tuberculosis or M bovis, the animal remains infected though in some the infection may remain latent, inactive, for the rest of the animal's life after an initial clinically inapparent infection. At present it is presumed that organisms can reactivate from latent infections in all such individuals but old studies on human post mortems and attemps to isolate mycobacteria from the gohn's focus, the primary infection site in the lung, there are some cases from whom the mycobacteria cannot be isolated.
BCG vaccine. This is a live bacterium so when the it is given as a vaccine it causes a local infection. Interestingly it does not persist for life in the vaccinated animal. Amongst the casettes of genes lost in its creation to deliberately create a nonpathogenic M bovis derived organism, called Bacille Calmette Guerin after its makers, it has lost the ability to persist. The immune response to BCG is the full immune response that is made to M bovis or M tuberculosis that it why it was hoped this would protect against disease. There is some protection against disease, that is the dissemination of the infection that gives rise to tuberculous meningitis and generealised disease that could result in shedding from various infected organs. Unfortunately its protection against disease is only partial and it does not apparently offer any protection against lung disease. As I have mentioned before the protection against infection in the first instance in exposed vaccinees has been difficult to prove but is thought to occur especially in young individuals not yet exposed to environmental mycobacteria. Envrionmental mycobacteria subvert the immune response in that cytokines are made that inhibit the release of those that are concerned in the killing of M bovis or M tuberculosis in macrophages raised by the vaccine.
When the skin test is done the tuberculin protein is placed in the skin. The immune response from BCG or M bovis will recognise this protein as a foreign protein that it has already formed an immune response to so that immune cells particularly T-cells go to the site and give rise to the indurated bump. Actually that to the BCG will be quite small and tends to diminish over a few years considerably.
Antibodies in mycobacteria infection are useless, they may actually help the entry of the organism into macrophage cells where it wants to be. Antibodies in a detectable quantity or titre appear late in an infection when there is a high load of M bovis or M tuberculosis and are the result of the immune system's switch from T-cells producing cytokines such as gamma interferon to make macrophages kill the M bovis they contain, to producing antibodies from B-cells. Different cells in the immune system are activated and de-activated so the immune system no longer has any protective value. An interesting strategy by the organism to ensure it is more likely to be shed and infect other animals before that animal is killed by the infection. You could liken this to shingles in the old to ensure infection of a new generation with chicken pox.
Email from SH to RW dated 23/1/11, it is now getting clearer in my mind - but also clearer why it is such a difficult disease to deal with! I wonder why the majority (even in countries where it is rife), even those who come in contact with obviously infected infected individuals, do not all succumb?
Email from RW to SH dated 23/1/11, for some reason it is not easy to be infected with TB even when one is potentially exposed, though sometimes one is infected through what seems to be casual exposure (in a night club for instance). The likelihood of infection is high when one is exposed for considerable periods of time such as in class at school or in the home all day or night with someone who is shedding. TB does not spread like a cold or the flu. Then most people who are infected have an inapparent illness associated with the primary infection and then the organism is latent clinically for a long period of time- a small % of humans will present within one year of exposure and primary infection with clinical TB. Occasionally there are re-infections so that one or more strains of TB are found.
Email from SH to RW dated 24/1/11, this is what I thought, and understood from reading books on subject. This surely then a very important consideration when implementing a policy to deal with a disease. If so few become infected then why this obsession with 'eradication' and a policy that is disproportionate and so rigid it is causing far more suffering to cattle owners and animals than the disease itself, particularly when its very foundation is a test that is not perfect?
Email from RW to SH dated 24/1/11, I think it is because the disease is not shed by so many infected animals and is not so 'catching' that the skin test (which is not a bad test) has been successful in eradicating bovine TB in some countries where there is not a wild life reservoir, and it is possible that there may be factors that interfere less with the specificity of the skin test (such as no fluke) and the organism may not remain viable so long in the environment. I am thinking of Australia for instance.
I notice with great interest in an article in the Telegraph that there is an article in Nature about a new vaccine that will prevent reactivation of latent infection. This will be very interesting. At the moment it is in the laboratory rodent stage of development but is anticipated to be of great use in humans where latent infection is so common. I don't know how common latent infection is in cattle or badgers with M bovis.
I understand this development rests upon the molecular bilogy of sequencing, examining the function of encoded individual proteins, and they have identified proteins that are important for stimulating immune responses that prevent the mycobacteria from re-emerging in an active state thus maintaining latency.
I believe the EU is important in forcing a policy of eradication upon us even supposing we might choose another path.

We have been asked to point out that virtually all the UK's cases attributed to bovineTB are either a) in old people who probably have reactivated old lesions that were acquired before there was compulsorily milk pasteurization or b) immigrants who were infected overseas. Thus transmission to humans in the UK is virtually zero at the present time.
The number of tuberculosis cases in the UK topped 9,000 in 2009 - the highest for nearly 30 years - ONLY 0.5% of these cases were identified as bovine TB.
Diagnoses of human form have been rising almost continuously since the 1980s, with many of the new cases thought to be among people who caught the disease abroad.
Comment from Professor PT (email 19/01/11)
Perhaps they should spend the £100 million a year in bTB control on this problem including screening potential immigrants with a chest x-ray before giving a visa - this the standard practice by the Americans if one is seeking an immigration visa to the USA. The high rate in immigrants is not surprising as TB is an enormous problem in many low income countries and it seems these infected people are then transmitting it within their own ethnic communities.
It is also of note:
Species identification
Among culture-confirmed cases, 99% (5014/5075) were due to infection by Mycobacterium tuberculosis; 0.5% (25) were identified with M. bovis and 0.7% (36) with M. africanum. Within England, the number of cases attributable to M. africanum has increased in recent years from around three cases per year between 2000 and 2005 to 31 cases in 2009 (UK data not available); the number of cases due to M. bovis has remained relatively stable.
Finally, BCG vaccine is not and never has been anywhere close to 100% effective in humans, cattle or any other species. Just because many of the cases of human TB had been vaccinated with BCG does not say it is ineffective….there may have been many many more without the BCG vaccination. BCG vaccination in cattle would lower transmission rates and such lowering of transmission at a population level would almost certainly help to ameliorate the problem in the UK
Comment from Dr RW (email dated 19/01/11)
I have quickly looked at the HPA document. Some of the paragraphs seem alarmist. More than half the cases weren't infectious pulmonary cases: half the total cases were extrapulmonary so were not infectious.
The document does not say but if one looks at protocols of TB management family or school class members, any significant contacts would be followed up for infection, isolation made if possible and treated if diagnosed . Obviously if the case is homeless contact tracing cannot be done. Isolation negative cases would also be diagnosed and treated in contacts and other cases.
It is striking how very few cases of M bovis were identified. There were more cases of M africanum. The typing to identify species of Mycobacterium is done when organisms can be grown, and organisms can be grown from sputum if enough are shed but can also be cultured from urine or liver biopsy or lymp node for example. Unfortunately no details on the whereabouts of the M bovis cases is given, whether in England or Wales or the South West, whether they were all in non-UK born persons or any could have been acquired in the UK, whether any were pulmonary and infectious, and whether any were in contacts, and the typing of M bovis isolates is not given nor will it be done. Were any drug resistant? I do notice that in the relatively small number of cases of TB in Wales the commonest reason for not completeing treatment was death and about half and half were UK acquired or non-UK acquired. Obviously if contacts are identified with acute disease in the UK when the exposure was to someone who probably acquired it outside the UK that would be a UK acquired case. Such distinction may not always be clear, I should have read the definitions in the appendix. I guess the genotyping of M tuberculosis will be of interest to match with genotypes in country of origin or known exposures and identify chains of infection and so on.

The Health Protection Agency's report on tuberculosis surveillance in the UK 2010; 'Tuberculosis in the UK' makes interesting reading. Of great significance is that bovine TB accounted for JUST .5% of the total TB cases.
It is also significant to note that TB in the UK has risen by 4.2% rise and now affects around 15 per 100,000 people - mainly young adults 15-44 years old and 60% are non UK.
Interesting too that many cases from abroad are not diagnosed for two or more years - so these cases could well be spreading the disease to others throughout this time -so if there is such a fuss being made re bovine TB and spread of disease why is there little fuss being made re the human form? Also one in five are said to not complete treatment (although 6% of these died!) so surely these people too will presumably be spreading the disease if they are not fully cured!
There are some concerns over drug resistance and with the increasing cases maybe all bTB funding should be transferred over to dealing with the human forms of TB as the health risk is far greater than bovine TB has ever been !

Email from Ruth 23/7/10
Switching from TH1 to TH2 for Mycobacterial infection with M bovis or M tuberculosis would lead to missing the diagnosis by skin testing or gamma interferon testing- however I don't think there are enormous numbers of such cases in cattle and they have tended to turn up in old dairy cows being slaughtered (negative on all tests during life but with gross lesions of TB PM).  They can certainly be a reason for repeated breakdowns on a farm.  They could be detected by antibody testing but the standards of such testing should be high ie an antigen matrix or some other test for specificity of antibody.  However I can't answer his point about parasitic infections switching TH1 to TH2 response; if he says it does well he certainly should know.  I think this may occur individually for each infection whether parasitic, bacterial or viral, rather than be so for all simulatneously in the infected host.  After all in many parts of the world all humans have parasitic infections all their lives, indeed it was the normal state for humans to have such and they can and do have TH1 responses to other types of infection, for instance a positive skin test response if they have latent TB.  Perhaps in parasitic infections it happens when there is a high burden of infection and not at all levels of infection?  I don't know.
Email from Prof. P.T. dated 203/7/10 I am an expert on disease economics and disease burden (my role with the WHO) and an epidemiologist which is a cross disciplinary expertise. I am also well aware of the weaknesses (and strengths) of modelling. The modellers actually got it right during the Foot and Mouth Epidemic (although the veterinary profession in their ignorance were screaming that “something else must be done”). And unlike most modellers, who publish a model saying do this and this will happen (but with NO data), the modelling I have undertaken hads actually utilised large amounts of field data to challenge the models...The journals I published my opinions in were Nature and Trends in Microbiology. These are both very high impact journals and all the articles underwent extensive peer review before publications (including by “TB experts”) and so the scientific community at large clearly thought that the articles make a good case.
It might be helpful if some of the bTB protagonists took courses in evidence based medicine and epidemiology. They might then be able to see the bigger picture. Many who sometimes cannot see the wood for the trees repeatedly miss two very important points I made in my articles. The first is the protection of exports. It is simply uneconomic to spend a sum many times greater than the value of the live exports simply to protect these live exports....The protection of live export argument is completely non viable. We also import beef from many endemic countries....
The other point is maybe less obvious but equally important. (some make) the point about the disease getting into wild life in south Africa etc and posing a huge threat to HIV infected people and others. But even in the UK, in the 1930s when 40% of dairy cattle were infected with bTB (many magnitudes higher than in south Africa), there was virtually NO aerosol transmission to humans. bTB in humans is foodborne (milk borne), and pasteurisation will prevent human infection regardless of the amount of HIV or other concomitant disease. Indeed I was at a WHO meeting in Tunisia last week. A report was tabled regarding bovine TB and aerosol transmission, but was just simply dismissed as not relevant. As the head of the CDC infectious diseases in the USA said “we have long recognised that bTB it is an entirely foodborne disease”. Africans need pasteurisation facilities not (bovine) TB testing (although some countries such as Ethiopia are getting the latter, funded by the British ODA and being overseen by the same bTB protagonists that run the UK programme.
I am well aware of the current (and woefully inadequate) Welsh echinococcus control programme –give out a few worming tablets and hope for the best. Echinococcosis is a very severe (much more so than human bTB) disease and can be eliminated (unlike bTB). To eliminate you need compulsory dog registration, compulsory and supervised treatment of all dogs in the endemic area on a regular basis, surveillance of sheep and cattle at abattoirs and trace back when hydatid cysts are found in animals (sounds a bit similar to bTB control). It can and has been done in other countries. A serious effort on echinococcus control might actually make a contribution to public health unlike the bTB control! Unlike bTB, Echinococcus granulosus transmission in the UK is not self sustaining in wild life – it is an anthropogenic problem (i.e. mainly dogs and sheep).
Also “He was unaware that infected cattle late during the course of infection may be negative on skin testing and on gamma interferon testing because they have switched from TH1 to TH2” (not refering to me) – but this is possibly one reason why the present diagnostic tests have such a poor sensitivity and hence some infected cows are not removed (but then one can always blame Mr badger). And I have worked fairly extensively on immunology. Parasites switch immune responses from Th1 to Th2, and parasitic infections are pretty common in UK livestock.
My passion is for (veterinary) public health, but most funding is hijacked by rather pointless programmes for bovine TB (and Trichinella – another none disease the EU spends half a billion EUROs a year undertaking surveillance and never finding it!)
Email from Prof. P.T. dated 20/7/10 refers to a surveillance report (from May 2010) in the Veterinary Record (July 19 2010 issue). This reported a case of hydatid disease in a cow in Carmarthen. He stressed that Hydatid disease (Echinococcus) is one of the nastiest zoonoses known to man. If a child had been infected with that cyst major surgery at the very least would have been the result. Instead of making a detailed investigation of trace back with this cow, and dealing with the source of infection (as would be done with bTB), the vet record waxes lyrically of the 'unusual clinical presentation'! Now echinococcus can be eliminated from any island nation as has been successfully achieved in New Zealand, Tasmania, Iceland (by periodically compulsorily worming dogs and strict abattoir controls). But the BVA and other veterinary authorities ignore it. It is not even notifiable. And it is no exaggeration to say that as far as zoonoses goes, only rabies is more dangerous.


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