- 1. Introduction
- 2. Simplified Overview of " The Badger TB Problem "
- 3. Cattle TB Eradication
- 4. Badgers : Victim or Villain ?
- 5. References
- 6. Appendices , Submissions to EFFRA Committee.
Controversy : But Much Heat With Little New Light
This often heated debate has rumbled on for over 40 years and is usually described as a highly complex and emotive issue. Old Brock got the blame for the stalling of GB's textbook Area Eradication Cattle TB Scheme, at the low point (see Figure 1) with the discovery of the "first" TB badger in Gloucestershire in 1971. However, Badger "guilt" was based on rather flimsy circumstantial evidence , that badgers with TB were found after cattle herd TB breakdowns ; with no obvious cattle source ...and supposedly had'nt just caught it from the cows !! With the current cattle TB crisis "out of control" .. explosion to half of GB as in Figures 1 & 2.. clearly policies based on current understanding of TB in both badgers and cattle have failed spectacularly, so a complete reappraisal is urgently needed . I should perhaps declare an "interest" !.. I have been involved with badgers for some 50 years (since 1959); and my Wytham, Oxford ..badger study was cited by Mr. Badger himself : Dr. Ernest NEAL, in his 1977, Badgers , Blandfords , eg. on field ageing badgers by tooth wear (revised ed. 1986 Croom Helm , and 1996, Poyser, with TB chapter by Dr. Cheeseman). Michael Clark's very original Badgers , Whittet, (revised 2011), also incorporated some of my TB ideas. I then represented the National Federation of Badger Groups ( now the Badger Trust) on the government's Consultative Panel on badgers and bovine TB; but left in amused disgust when MAFF tried to use us as political pawns to back the absurd Brocktest culls, as a magic bullet new policy :- antibody blood test 41 % accurate, ie. less use than tossing a coin : 50 % "sensitivity"/100 % specificity (Woodroffe, 1999). So, after some 22 years involvement with the "Badgers & TB" issue, Ive watched with astonishment as MAFF/DEFRA, have painfully attempted to re-discover the very simple basic cattle control measures which were so successful in the Area Eradication Scheme during the 1960s (Macrae, Ritchie, Richards). Indeed, a whole generation of farmers, vets, etc have grown up "knowing" badgers are the main problem, and clearly having NIL Understanding that various basic "assumptions" as to how TB works in cattle are spectacularly wrong.
Self-maintaining disease Transmission source
Going right " back to basics" , in the evolutionary arms race between parasitic disease and host, bovine TB is remarkably successfull. The "reproductive rate" Ro or transmission rate of a disease suggests that if 1 case (individual or herd) produces 1 new case, the disease is self-maintaining..or sustains itself indefinitely. IF more than 1 new cases arises, the disease becomes expansionist, ie. far better than merely self-sustaining, a bit like a human couple producing 2.4 surviving children, the population increases. And if fewer than 1 case results, the disease will die out .. naturally , so the host is merely a dead end spillover host; and eradication schemes work by tipping Ro below 1.
Cattle almost certainly caught TB from humans several thousand years ago (Mycobacterium tuberculosis) when a hunter-gatherer lifestyle switched to fixed communities with an agricultural/pastoralist way of life, in the middle east, and a DNA deletion/ mutation produced M. bovis. Cattle TB was henceforth an extremely succesful Expansionist disease, since cattle are long lived social herd animals with easy spread to new generations, and through the population. Cattle TB spread probably arrived in Britain with Roman imports, additionally 17 th century pedigree stock from Holland etc ; and was exported globally during the colonial era, with spread inexorably amongst national herds .. eradication was achieved entirely by cattle controls, by test and slaughter plus movement controls which minimised spread both within and between herds to below the self-sustaining level. Cattle TB hence represents a textbook Self-Maintaining disease. Pigs, by contrast are a textbook Spillover host .. readily catching bovine, human, avian and other TBs via "dirty feeding" in contaminated environments . The disease is not progressive enough to spread amongst pigs, so dies out when the TB source disappears. In the later stages of area eradication in the USA, abbatoir TB pigs proved a useful "miners canary" for trace -back to otherwise undisclosed cattle breakdowns. Badgers too can catch bovine, avian, & Johnes disease = M. paratuberculosis, plus M. microti and M. chelonei (ICMB 2009)... but one questions the view that high density badger populations are a social, long-lived, ideal self-maintaining host with endemic bovine TB ; Figure 1 Map 2 : as discussed in Sections 2 and 4.
HISTORICALLY, route and extent of transmission has always been a cause of heated debate. After discovering the tubercle bacillus in 1882 placing TB firmly amongst the new "germ theory" view, and TB antigen as the basis of skin test and eradication schemes ; Robert KOCH, then went on in 1901 to suggest bovine TB was not a problem for humans .. it took a Royal Commission to 1911 to prove this wrong .. and GB's leisurly approach to things meant TB controls did not really get started until the 1930s .
Also, a century ago, the Behring/ Calmette & Guerin school .. and across the pond, Schroeder & Cotton school were convinced cattle TB was by ingestion, the bacilli passing through the gut without leaving lesions ( palatine tonsils sampling food/water ingested, also Peyers patches into small,intestine =ileum act as "smoke" detectors of pathogens ?).. thence to predilection highly vascularised sites such as lungs and meninges via the blood (dying "killer" macrophages full of bacilli get stuck in microcapillaries creating new foci); ..... the M'Fadyean/ Bang/ Chausse school by contrast; argued strongly for spread by inhalation ( Francis 1947, Myers 1969). It was not until the 1940s that the idea of aerosolised optimum sized droplet infection became widely recognised, dust in barns or yards too probably a very efficient vehicle of aerogenous spread of TB, and Johnes disease (M. paratuberculosis )(Allen 2011). Only droplet nuclei under 5-10 microns likely to remain airborne/ penetrate to outermost alveoli in lung, bacilli may be killed by UV in sunlight within an hour so dark poorly ventilated cattle sheds facilitate spread of TB and other viral, bacterial, Mycoplasmal "pneumonias" (Menzies 2000).
Much confusion still exists as to transmission routes for TB, but comparison with well documented human TB is helpful. Human TB (M. tuberculosis) is a respiratory disease, as recognised as far back as Aristotle " something pernicious in the air "... spread person-to-person by aerosolised droplets in exhaled air .. seen easily when breath condenses on a cold window pane..so the tubercle lesions are focussed in the lungs and draining pulmonary lymph nodes (bronchials, mediastinals). Cattle TB is likewise a bronchopneumonia, acquired by inhalation :- a "Consumption or Phthisis". Experimental infection of calves by intranasal inoculation gives very misleading evidence, calves effectively become nebulisers, with early shedding , tailing off to intermittent later on (ISG 2007, Morrison 2000, Menzies 2000).. BUT with natural spread into lungs , it may then take 6 -12 months before lung "tubercle" lesions build up to become active spreader cases Later on ! (As explained in Section 3 with "becoming infectious" Figure 3).
By contrast, humans formerly caught bovine TB, from unpasteurised milk, the ingestion route revealed by lesions near the gut, particularly via the tonsils to surgically exciseable swollen throat nodes hence so-called "Scrofula" (pig = Sus scrofa... where TB focalises in submaxillary nodes and the gut mesenterics ). Some 2000 human deaths a year in 1940s before pasteurisation removed this bovine TB risk .. probably most Londoners exposed in 1900 (Krebs 1997). Sad that there are still some african, south american "developing countries" which do not take this elementary precaution.
Much confusion STILL exists as to perceived TB transmission route/s ; but Cattle TB is, and always has been a respiratory lung "Consumption" caught from close prolonged contact with other cattle over-wintering in barns or yards, and in milking parlours. It is extremely improbable that it comes from badgers .. brief farm visits for a drink and snack of cattle nuts wont "cut it", most farm visits in summer when cattle at pasture anyway (Ward ). Early studies suggested badger TB was found in the lungs/kidneys, so it was naively assumed spread amongst badgers was 82 % by inhalation, 18 % by bite wounding (Cheeseman 1988, 1989) ; BUT unfortunately , badger TB is rather clearly via ingestion, 70 % start in throat (submandibular lymph nodes), with Secondary lung lesions .. so badger TB is a "Scrofula" and they are Spillover host rather than self-maintaining. It is worth noting that a thigh injection in badgers, or a neck/tail inoculation in cattle ends up as "A Lung Case " ! (Pritchard 1987, Francis 1947). The first wild TB badgers caught it via EATING contaminated roe deer carrion as a last spillover from eradicated cattle TB in the mid-1950s in Switzerland...but the first TB badgers were in fact discovered at London Zoo c. 1938, Whipsnade mid-1950s, maybe from an Axis deer herd outbreak (Clifton-Hadley 1991). ; first Irish TB badger 1974.. cases recently in Spain and Italy, where cattle TB not yet eradicated.
Rather intriguingly, just as AIDS/HIV AND BSE/Mad Cows MAY have been around well before recognised in the 1980s; it seems very probable that badgers with TB were around much earlier than the oft-cited 1971 "first case" in Glos ( also 2 from Glamorgan), but simply not recognised as TB . Badgers with a mysterious disease with coughing, weakness, and often decimation of the local clans occurred in for example Hants 1960; Surrey 1966; Glos 1958; Shropshire 1935; Germany 1965; Holland 1964 .. the latter two countries long before TB eradicated in cattle ..there MIGHT still be museum badger skulls showing superficial acropachia or tooth abscesses due to TB , since bone TB also well known in humans ( mummies !), dogs, lions, etc.(Hancox 1980).
Getting the blame it is hence astonishingly "UNbelievable" , that at the 1970's low point, the idea took hold that cattle-to-cattle transmission was unimportant, so suddenly cattle TB was NOT a self-maintaining infectious disease !! .. but it was all down to badgers:
Gallagher in Zuckerman 1980 pp. 86, 94 "in the context of the total bovine population , the number of cattle excreting tubercle bacilli appears of no consequence in the maintenance of tuberculosis in badgers, and of very little consequence in its maintenance in cattle ".... only 21 "open" or visible lesion cases in 1000 reactors.
DUNNET 1986 para . 60 "It is assumed that transmission of the tubercle bacilli from cattle to badgers is very infrequent. Prior to 1950, cattle with open lesions were found frequently, but now, as a result of regular testing, open cases are so rare as to be insignificant as a source of infection to badgers. Where such cases do occur in cattle the infection is usually pulmonary, and very close contact is required for aerosol transmission. The organism is not excreted by cattle onto pasture in urine or faeces. (*). The pulmonary route of transmission is more likely to affect other cows, rather than passing the infection from cow to badger. We accept this premise." (* 100 % wrong , see later). AND so, having RULED OUT Cattle as the hidden reservoir, it was entirely reasonable to assume there must be another, ie. badger self-maintaing reservoir in the last intractable hotspot TB pockets shown in Figure 1, Map 2. AND , henceforth as shown in above "Transmission Box" , the Inner cycle , TB spread was entirely one-way: - badger-to-badger-to -cow... and critically NO spillover cow to badger, also the explicit or implicit assumption underpinning models of the textbook endemic Woodchester study area (eg. Smith, Shirley, Wilkinson) . Interestingly, this same mistake has been made claiming wild boar in Spain/ Corsica are a self-sustaining reservoir of TB .. since they havent just caught it from the latest herd breakdown (Gortazar, Boschiroli in Viale 2011). Unbelievably farmers leaders are STILL saying cattle-to-cattle spread is unimportant, when clearly the current crisis has been entirely an explosion amongst cattle to an area now of half GB.
IT seems surreal, but everyone will have to re-discover that cattle do become infectious to other cattle, and since despite 4 decades study no-one has realistically shown how badgers Might give cows TB, (it is 100 % respiratory, from other cows !); SO, Having RULED OUT Badgers, there has been a perfectly valid SELF-SUSTAINING "Hidden Reservoir" of cattle TB .. so in truth , the Outer cycle in the above "Transmission box " has been true all along , its cow-to-cow; with a quite efficient Spillover TO BADGERS, neatly reflecting the severity of the preceding herd breakdown. Pointers to this version of "truth" have been available right from the begining of cattle TB Eradication schemes ...diagnosis /tests MISS both active spreader cases and a substantial self-maintaining "Hidden Reservoir "......as known to pioneers such as :-BANG 1892 "It is found that the tuberculin test is no more perfect than other things in this world. Sometimes it fails. Animals with a very real degree of tuberculosis will sometimes fail to react, and the same applies to animals with a very slight degree of the disease . ...but it would be the greatest folly to reject this method because it is not able to give everything we desire."
BLOOD's Veterinary Medicine 1989 "..no reliable test to detect the poorly sensitized animals in the early or late stages of the disease which are THE USUAL CAUSE OF recrudescence in herds which have been classified as being free of the disease " ... ALSO "If the incidence of reactors is high at the first test or if "open" lesions are found in culled animals, emphasis must be placed on repeat testing at short intervals or the spread of the disease may overtake the culling rate." M'FADYEAN , 1888, knew that cattle without visible lesions were infecTIOUS .. AND warned against the simplistic emphasis on "Open Visible Lesion" cases in TB spread.
Francis 1947, "It is known that the primary focus in cattle may remain latent for many years or at the most progress very slightly (Bang 1899, M'Fadyean 1899) .. but the lesions remain open .. if any animal reacting to the tuberculin test , EVEN with very SLIGHT lung lesions, is left in the herd spread will be more of less rapid." Also (p.124), "The primary lung lesions are a bronchopneumonic focus which may progress rapidly or may remain quiescent for many years . Despite this, however, it would appear that the complete healing of lesions which often occurs in man seldom takes place in cattle . This is a fundamental difference and in practice all tuberculin positive cattle are regarded as infectious to other cattle ." (apparently "closed" catlle tubercles DO in fact seep exudate at the edges, into bronchioles, so there is "intracanalicular spread .. Jubb). Francis 1958, re. the failure in ultimate eradication in cattle TB schemes .. "Problem herds in which infection continues to show up on retests indicate the need for identifying non-reactor spreader cows ".
Krebs 1997 " it is not known if, how , or to what extent badgers might contribute to cattle TB ".
Rather astonishingly, with 20 ; 20 Hindsight, the whole Badgers guilty Saga, has been simply a case of Mistaken Identity as to the True self-maintaining "Hidden TB Reservoir"; and very simply everyone needs to RE-Discover this Infectous Reservoir amongst catte !
"No Country Has Eradicated TB Without Tackling The Wildlife Reservoir "
DEFRA , Ministers and farmers/vets in justifying the "Need " for badger culls , frequently state that no country has eradicated cattle TB Without tackling the Wildlife Reservoir ... but this is simply a Wrong misinterpretation of half truths. Cattle TB WAS Eradicated without any badger culls in Scotland, now EU Officially "BTB-FREE" on 4 year testing.. it had nearly gone clear, before wildlife sampling prevalent , so no subsequent spillover to wildlife and up to 2006, there had only been 2 sika, 1 roe, 1 red deer and 1 badger with TB , plus 1 Red deer in 1964 (Vet.Rec)... more "reds" recently. Ulster nearly eradicated TB too, just 174 reactors in 1971 .. badgers always regarded as spillover host and not culled. Wales very nearly clear by 1980s ; no badger culls and incredibly few with TB anyway 1972-96 , just 46 TB+ out of 2363 sampled. :-- see Maps in Figure 1 & 2 ... Note Also, Even hotspot pockets in England such as the Isle of Wight, and West Penwith/Lands End went clear without culls (Figure 6 too).
It is true that cattle-like "wildlife" with similar herd life-styles to cattle DO represent a risk .. Water buffalo in Australia, Cape buffalo in South Africa /Kruger Park ; Bison in USA/Canada ....and the "problem" of deer is revealing. Now clearly recognised that dispersed populations of wild deer do not represent a self-sustaining reservoir in New Zealand or Scotland with several hundred thousand red deer... but high stocking/close contact farmed deer are another matter.... amusingly one Irish sika farm study believed the odd TB badger found nearby must have been the problem source ! (Partridge 2008). There were 1972-96 just 30 TB deer out of 1960 sampled in GB.. 12 fallow, 9 roe, 9 sika . And simply spillover from cattle to the commonest local deer :- roe in Wilts, Glos. even Hants recently; fallow Chilterns, Savernake forest, Herefordshire, Glos.; sika on Purbecks & Scotland; red Exmoor recently; 1 muntjac Glos. Amusingly a recent southwest deer survey found just 24 fallow/ 2 roe/ 2 red = 28 TB + out of 720 sampled, and "Assumed" c. 10 % deer-to-deer spread; so "Proved" it might be self-sustaining (Ward 2008, Delahay 2007). White tailed deer in Michigan are a recent "problem". Ironically Michigan, 151,000 sq.km. was a textbook case where relaxing catle controls due to the war allowed TB to explode out of control, with a classic U-shaped graph as in Figure 1; resuming tight controls dropped cattle TB from 6000 reactors 1959 to just 136 in 1966.. 7 years (Myers 1969). TB in white tails not noticed back then as a problem, despite first case 1934 Levine (Clifton-Hadley 1991). The current problem is blamed on high stocking for hunting, supplementary food the possible contact point with cattle (Palmer, More 2006); and wolves act as a "concentration sampler" to TB presence in deer/cattle !
Brush tail Possums (Trichosurus vulpecula) ; first TB case Bolliger 1948 (Francis 1958), but NOT a problem in its arid natural Australian home. Seemingly the wet/forest edge proximity of introduced possums in New Zealand favours cross-species spread ..but possums are extremely susceptible to TB, develop open skin abscesses, and pus may contain 5 billion bacilli / gram, so inquisitive nosing of moribund possums by cattle/deer a plausible transfer route, Contamination of pasture may be why up to 18 % of sheep affected (Jubb); whereas TB in sheep very rare in GB and elsewhere .. either orphan lambs reared on unpasteurised milk or "unusually" housed eg. in Uganda, Germany ; Chausee found a century ago that 1 bacillus enough for respiratory transfer, but 11 million needed by ingestion.. batteries of lymph nodes around gut .. and like also susceptible wild rabbits, selective grazing avoids cow pats ; AS DO cows : tufts of darker green dung -fertilised longer grass show scatter of former cow pats on pasture ! (Francis 1958). QV. A rather melancholy and moth eaten Possum in Natural History Museum, South Kensington, London !.