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The Great Badger TB Debate; A Final Death ?


BADGER TB RE-TRIAL 2015; VERDICT; WRONGFUL CONVICTION; NOT GUILTY; 18th February 2015. (PLEASE See 2014 Trial, Death of Debate


Scientific and political revolutions occur when a "critical mass" of anomalies or confounding factors become apparent, so a Gestalt shift in "Perception" of the accepted paradigm becomes inevitable. The Great Badgers and Bovine TB Debate has rumbled back and forth , ever since the first "official" badgers with TB were identified in 1971. But whilst farmers and vets are still absolutely certain that "Badgers are the main cause of the spread of TB", so culls or vaccination are essential; it is surprisingly hard to re-discover the rather flimsy "Scientific basis " for this, a whole generation has grown up not really understanding how TB works in cattle, and badgers have been mistakenly blamed at different times for at least four different things where there did not seem to be a confirmed cattle TB source :- giving cattle TB and spreading it within the herd, the obstacle to eradication of TB in the last intractable southwest hotspots, local expansion of these hotspots, and spread back to an area now of half of GB !

Darwin's bulldog, the great Thomas Henry Huxley famously remarked "The great tragedy of science is the slaying of a beautiful hypothesis by an "ugly" fact". Darwin himself in the 1871 "Descent of Man" noted that "False facts are highly injurious to the progress of science and often endure long". Three "Ugly False Facts" underpin the "Science" base of the whole debate. The very successful Area Eradication scheme rapidly shrank TB from countrywide to tiny intractable southwest "islands" of TB, then progress stalled, so clearly there must be a widespread self-sustaining hidden reservoir of TB present there . Incredibly, (and Wrongly), cattle were ruled out as this reservoir, so everyone assumed this reservoir must be badgers for 3 pivotal reasons :-

1. Only "Open Visible Lesion" cattle can spread TB, and they were so rare (2 %) that cattle-to-cattle and explicitly cattle-to-badger spread were unimportant (Gallagher in Zuckerman 1980, p. 86, 94); 2 New early TB cases without Visible lung lesions, so-called Unconfirmed cases were TB-free "False positive" reactors; and 3. Badger TB lesions were often in the lungs or bite wounds, which could account for TB spread within and between badger clans; 100 % wrong on all counts ! This very persistent false idea that badgers have NOT just caught TB from the preceding bad breakdown , proving there must be a widespread self-sustaining badger TB reservoir "out there" is critically important, and why everyone remains so certain badgers are the problem !

The recent review by Godfray HCJ et a, 2013, A restatement of the natural science evidence base re. bovine TB control, Proc.Roy.Soc. http: //; is a vary valuable very wide consultation, with 354 references. It summarises key areas of "Uncertainty", under 36 headings as regards 5 factors; Epidemiology, Testing & Surveillance, Biosecurity, Culls, Vaccines. These Uncertainties as quoted throughout below , with paragraph in brackets (x); are explored under 8 headings . It has been crystal clear all along that there is a "link" between TB in badgers and cattle but surprisingly no-one in 44 years has actually confirmed who has been infecting whom ! (Section 8). The last major review by Krebs in 1997, which led to the RBCT cull, noted that "It is not known if, how, or to what extent badgers might realistically give cattle TB"; and Godfray shed no new light :- (para 14 a, c); "Mycobacterium bovis IS transmitted within and between populations of badgers and cattle "; BUT (para 15), "Little is known about how M.bovis is transmitted between badgers and cattle. Transmission may be indirect; for example, through contamination of pasture, feed and drinking water. Alternatively, direct transmission via aerosol droplets at close contact may occur, possibly inside farm buildings as well as outdoors. No quantitative estimates of any of these transmission rates or their relative importance are currently available. " Astonishingly, DEFRA recently suggested that the badger contribution to cattle TB "Might" be 6, 16, 50, 100 .. or 0 % ! And Dr. Rosie Woodroffe said much the same at two open meetings in 1998 launching the RBCT cull.

CONCLUSION .. BADGERS SIMPLY CANNOT POSSIBLY BE THE MAIN CAUSE OF THE SPREAD OF BOVINE TB ! :- This comprehensive critical reappraisal of the aetiology, pathogenesis, and epidemiology of bovine / badger TB amplifying the "Uncertainties" highlighted by Godfray uncovers why badgers have been wrongly blamed as the main spreaders of Cattle TB. Astonishingly, despite 44 years research, no-one seems to have realised that a Gestalt u-turn in "Paradigm perception" is long overdue. Rather surreally, "Perception of the TB Problem" has continued effectively in 3 separate tendentious "parallel universes"; A. TB has been circulating entirely within the CATTLE population, falls and rises being due to tightening or relaxing cattle controls; B. the very limited actual proven occurrence of TB in BADGERS has been merely as as a temporary spillover host from bad herd breakdowns; C. BADGERS ALLEGEDLY as the Main cause of spread , has been entirely due to missed cattle sources. The only True "Link" between the 3 being that cattle have been giving badgers TB all along; 4 Key Facts:-

1. Cattle TB is entirely a respiratory broncho-Pneumonia caught by prolonged close contact with other cattle; it cannot be coming from badgers ; 2 recent studies of "normal" reactors found that although none had Visible lung lesions, ALL confirmed cases had lesions in the draining lymph nodes (bronchials & mediastinals) , and up to 20 % were sputum positive ie. infectious (McIlroy 1986, Neill 1988; also Liebana 2008)(see Section 1);

2. There is no widespread self-sustaining reservoir of badger TB ( 75 % in Kao 1997, Green 2008, Bieck 2012), Badger TB occurs as a "Dead end" spillover host, a dietary "scrofula" and the tiny numbers of TB badgers in micro-pockets of infection at the epicentre of the preceding herd breakdown dies out unless topped up from cattle , just 6123 TB badgers out of 53,130 sampled 1972-2005 (see Section 5);

3. ALL the new herd breakdowns supposedly "Due to badgers", have actually been caused by Unconfirmed reactors, some 245,000 out of 410,000 cattle removed since foot & mouth 2001, with 20 million farm to farm moves /a (see Section 4.3); and some 2000 Problem herds currently with chronic TB ( skin test non-reactor ie. anergic "active spreader" culprit cow);

4. The cattle TB crisis has been entirely an explosive spread of TB within the cattle population; and cattle controls alone can eradicate TB , without any badger culls, provided Problem herds are eradicated (see Lands End in Section 4.4); as suggested by Kao 1997, Green 2008, ISG 2007, and Evans 2015.

A CRITICAL REAPPRAISAL OF THE GREAT BADGER / BOVINE TB DEBATE :- 1. How TB works in cows... Transmission :- Cattle "Consumption" vs Badger "Scrofula" 2.Cattle TB crisis.. Local spread .. closed herds 3.The Hidden cattle TB reservoir .. self-sustaining after all 4. Two Key Misunderstandings:- A. Open Visible Lesion cases; ....B. Four delays in becoming infectious reactors:- ........1. Incubation/Latency; 2. Are Visible lesion cases more infectious ; .......3. Unconfirmed reactors; 4. Late TB cases, Latency & Anergy, and Problem herds; 5.Badgers .... Deer .... the Edge / Perturbation Effect .... Do culls work ? 6. Further culls / Vaccination / Urgent :- Enhanced cattle controls 7. References 8. An Historical Overview.

1.HOW TB WORKS IN COWS :- Since seemingly even many of the current generation of farmers and vets do not understand this ; a review of the basics might help. Cattle TB is an airborne respiratory lung "consumption", a broncho-pneumonia. The immune system cannot stop the proliferation of bacilli, so increase is seen outwardly in an increase in the number and size of tubercle lung lesions (o to O); with increasing infectiousNESS; Visible Lesions (abattoir inspection or x-ray in man) and skin test positivity by circa 1 year (6-18 months)...




NVL, No Visible Lesions, U=Unconfirmed cases// VL, Visible Lesion= C= Confirmed cases

TESTS;......gamma IFN ....//........SKIN TEST ......................// SKIN negative so ANTIBODY test

MISSED *.. Non reactor..early TB Unconfirmeds//(confirmeds)....//*late TB "Anergics"

SO, TB spreads initially within herds; then these new TB cattle move to cause a random scatter

of new TB herd breakdowns (not completely random, often contiguous spread among a cluster of new herds );

PATTERN of the 3 TYPES of TB herd breakdowns, say 10 in 100 sq. km.per year:-

HOTSPOTS, 60 % U ; 40% C (1P, Problem herd)//..EDGE & LOW RISK AREA, 95-100% U

..........................................................................//.. (No background TB in cattle or badgers )

U U U .... C C..... (P).....................................//.........U U U U ....C

U U U ......C C...............................................//.........U U U U U

** N.B. Badgers have been wrongly blamed for all the herd breakdowns where there was no apparent (ie. MISSED) Confirmed source :- Both A. 60 - 100 % of Early TB Unconfirmed reactors/herds; and B. Problem herds where either A. Chronic TB results from an elderly late TB active spreader, skin test negative ie. anergic culprit cow, easily found with late TB antibody tests such as Chemiluminescent ENFER , ENFERPLEX (especially alpacas), IDEXX Ab test; or PCR on faecal swabs; OR B. Bad breakdowns also produce latent carriers which eventually cause repeat breakdowns in Problem herds.


Natural aerogenous spread of TB broncho-pneumonia amongst cattle usually requires prolonged close "contact" in barns , milking parlours or cattle yards to condense the infectivity to achieve transmission. Just as with other calf winter "pneumonias" be they viral, bacterial or mycoplasmal. And in one school outbreak over 100 hours of shared classes were necessary for fellow pupils to contract TB (Ewer 2003). You wont catch a cold passing someone with a sniffle in the street, but will get a bad dose of flu or swine flu, sharing an office with someone coughing and spluttering the "bugs" about. Breathing heavily on a cold window reveals the tiny aerosolised "droplet" infection in exhaled air. A single bacillus, or more accurately 1 cfu (colony forming unit) , can spread TB among rabbits, cattle, sheep, and humans; 10 cfu in badgers; but it may take the inhalation of 20-30 minimum-sized "droplet nucleii" before infection takes root avoiding macrophage killer cell interceptors in the alveoli (Lesellier 2003, 2012; Dannenberg 2001; O'Reilly 1995). Humans may shed 4 billion bacilli/ day, cattle over 38 million, but badgers only shed 200,000 bacilli/ml of sputum dispersed in exhaled air.

Francis 1947 , 1958 and Bang were aware that cattle did not usually get TB until "they first entered the cowshed" ie. joined the breeding/ milking herd. So badgers popping briefly into a barn for a drink and snack of cattle nuts wont work; most barn visits are in the summer when cattle are out at pasture anyway. Prolonged contact was needed in the only proven case in 44 years of badgers actually giving calves TB in a very artificial yard experiment; 4 calves exposed for under a month seemingly unaffected , although probably autopsied too soon to have developed lesions (Little 1982).

Cattle do not usually catch TB even from pasture super-contaminated with cattle faeces ; even although a cow with advanced TB may shed 38 million bacilli/ day, but cattle naturally avoid grazing near cowpats (Francis 1947; Maddocks 1934; Schellner 1959). Similarly, there are few cases of TB in sheep or rabbits even when they share pasture with tuberculous cattle; selective grazing.Studies a century ago suggested that cattle require an enormous bacillary dose to catch TB by ingestion ; several hundred million , or at least 1 million bacilli .. abundant lymphatic tissues around the gut are an extremely effective barrier to invading pathogens (M'Fadyean 1910; Griffin 1995; Goodchild 2001). Chausse 1910 found a dose of 11 million bacilli was needed by ingestion in sheep; just 1 bacterium by inhalation. So the rare cases in GB or globally were when housed with cattle; orphan lambs reared on unpasteurised milk (Francis 1958). Probably because Brush tailed possums have open skin abscesses and puss may containg 5 billion bacilli/ gram, contaminated pasture caused TB in 18 % of sheep and wild rabbits in New Zealand (Jubb 1985). Inquisitive nosing of dead or moribund possums may be how cattle and deer catch TB ? With somewhat wishful thinking it was suggested that to convert ingested TB to a lung infection might be by "eructatation" (burping) of rumen gases (Mullenax 1964; Waldo 1966).

No one seems to have worked out the dose needed to infect badgers by the ingestion route via cow pats, but judging by raccoon experiments, a few hundred cfu may be enough to get past the limited head lymph node "safety barriers".

Transmission of TB to cattle via badger urine hence seems extremely improbable. A cow would need to drink 3 ml of badger urine to get the minimum dose of 1 million bacilli (300,000 bacilli/ ml); but few badgers reach the infectious urine stage, only 5 badgers in 57 studied and less than 100 cfu/ ml (Corner 2012). Besides, 99 % of urine drains straight into the soil, the residue is diluted by dew & rain, and disinfected by UV in sunlight within 3 days (MAFF 1979). Ironically, Grange (1996) found a small number of cases where farmers themselves reinfected their cattle , half by aerosol and half by urinating on hay according to follklore to improve the mineral content !

Lastly, when cattle and deer get avian TB from contaminated pasture by ingestion , the lesions are around the mouth and gut (retropharyngeals and intestinal lymph nodes eg. ileo-caecals (Jubb 1985). So that applies to bovine TB too in deer, and "dirty feeding" pigs, wild boar (including GB now) , and badgers .. a dietary "scrofula" comparable to human TB caught from unpasteurised milk . Virtually any mammal can get bovine TB, but there is a critical distinction between cattle and other species such as Cape buffalo, Water buffalo, and Bison which being long lived social herd animals can actually spread TB by the respiratory "Consumption" route and be a self-sustaining reservoir; and Dead End spillover hosts which get TB by ingestion "Scrofula", and do not progress to an infectious stage likely to spread TB in a self-sustaining manner.. child bovine TB, pigs, wild boar, And Badgers a wide range of hosts in New Zealand including ferrets, feral cats, stoats, hedgehogs, pigs, rabbits, hares and wild deer (Morris & Pfeiffer 1994).

2. CATTLE TB CRISIS . The key ingredients, and highlighted errors which crept in as to why GB's, cattle and badger controls have failed since 1971 - the mid 1980s, and indeed even why there is a Cattle TB crisis are clear ( Godfray,Box 1, 1986-2012), It is rather obviously simply been due to an explosion of TB within the cattle population . Some 20 million farm-to-farm movements per year (Mitchell 2006; Woolhouse 2005). In epidemiological modelling cattle movements "out performed" all other principal components such as north atlantic weather oscillations or even badgers ! (Gilbert 2005).

And spread of a hidden TB reservoir was via cattle , not badgers ; during the low period 1975 - 1985, with c. 100 breakdowns / a, there were c. 150 TB badgers per 1000 sampled; but the cattle TB crisis magnified the true unconfirmed cattle TB reservoir :-

2002-2014; some 245,000 unconfirmed reactors out of 410 ,000 cattle removed since foot & mouth 2001. Combining the 2012 & 2013 data, there were 9673 breakdowns; 6568 confirmeds (OTF-W) & 3105 unconfirmeds (OTF-S) supposedly due to badgers; so it would absurdly , based on ISG data, have needed 22,000 badgers to yield 3000 with TB, or 220,000 to yield the 1 % of super-excretors which might have posed a risk of causing cattle breakdowns ! AND, by contrast 1972-2005, there were only 6123 TB badgers out of 53,130 sampled is hardly a "major" reservoir of TB (MAFF data to 1996 + RBCT, 1515 in 11,000; not including some 20,000 gassed earlier on ).

A classic U- shaped graph has been repeated in many other unsuccessful Country Eradication schemes, relaxing controls caused a temporary upsurge in many countries for both World Wars . Michigan in the 1960s was particularly interesting, a repeat drop from 6000 reactors to 0 within 6 years and eradication , long before the spillover problem since the 1990s into White Tail deer , first case 1934 ( Clifton-Hadley 1991; Myers 1969).

So, the U-shaped graph for GB reactors was ;

1959 ....................1979..........................................2006 ......................2008................

25, 000 .........//...............................................//back to 25,000...........40,000 reactors

.....................//only 600 reactors in 89 herds //..........................................................

A mistake repeated in many countries worldwide has been to assume at the low point that TB was more or less "cured" . Huge numbers of cattle tested to yield few reactors. So testing relaxed, in practice going prematurely to longer testing intervals, with the proviso of reverting to annual testing if there was any sign of an upsurge in TB. unfortunately ignored in GB because everyone assumed the breakdown spread was now by badgers .

Sadly TB was not truly "eradicated" in the tiny last southwest residual "islands" of TB (c. 1000, testing was relaxed , only 2 million tests / a 1988-1994 (ALL 9 million in 1960s); and with no pre/post-movement tests no wonder TB spread back into recently achieved TB-free areas. And sadly now c. 1/2 of England (60,000 plus whole of Wales is one big "hotspot" (6, Box 1).

Alas, exactly the same in Ireland from the low point (Watchorn 1965). This GB spread was exacerbated by restocking after Mad Cows peaked 1993, disease reintroduced to areas TB-free for 20 years, Exmoor, Hereford/Worcs/Gwent, and the new Derby/Staffs hotspot with 6000 reactors by 2004 (DEFRA 2004) ; and after Foot & Mouth 2001 to areas TB-free 50 years such as Powys, Cumbria, and NE England (Gopal 2005) . Alas, TB was reintroduced to Cheshire after yet another foot & mouth upsurge in the mid-1960s (Richards 1972).

Tragically culling up towards 100,000 badgers in GB & Eire each did not eradicate the residual southwest hotspots, or stop this reintroduction of TB to recently cleared areas , simply because ALL the new breakdowns were caused by imported cattle , particularly unconfirmed reactors. History repeating itself ..badgers nearly wiped out in 1960-1970s in Belgium, Luxemburg, parts of Germany, France and Switzerland trying to stop rabies, but belatedly a realisation that the mobile fox population was the true vector. Both the new 2005 Bovine TB Strategy . and the 2013 Eradication of bovine TB scheme, after wide consultations, had the twin targets of reducing TB levels within hotspots; and stopping the expansion of these hotspots, but continuing to include badger controls is meaningless and futile.. badgers are not the problem.

Jim Paice's data showed in the early 1990s c. 50 % of new breakdowns were in herds TB free 10 years, Avon 15 of 25; Cornwall 103 in 139; Devon 54 in 90; and frontier counties even more ; Shrops. 4 in 5; Derby 6 in 6; Staffs. 29 in 30...clearly bought-in cattle.

LOCAL SPREAD ? A mis-guided belief that badger culls cause edge/ perturbation effects in increasing TB in the ring outside proactive cull areas is why Godfray rather surprisingly claimed that ""the causes for the gradual spread of high-incidence areas are NOT understood "" (outwards spread by c. 10 miles / a; not as suggested by one MP, with armies of badgers determinedly marching outwards ); and yet note spread from high to low TB areas is ALL (especially Scotland), by "local short distance cattle movements or contiguous spread,Plus other cattle-to-cattle transmission/ interactions on nearby / contiguous , or linked (multi-parcel) farms / premises.. which will be unrecorded. Infection can persist in cattle in herds that have tested clear of infection because of limited sensitivity of current tests.. more recurrence in high incidence areas, and hence movement from such higher risk breakdown herds are more likely to seed new breakdowns via undetected infected cattle "" (9, 11, 12, 27 c). A peculiarity in Ulster is the many small farms , broken up into a dozen or so sub-units, greater "edge" , so a 1970s DANI study found 30 % of breakdowns were bought-in, 70 % contiguous spread, and 0 badger (even although a sample then found 36 % of badgers infected, McIlroy 1986). Denny 1999, found 40 % each contiguous / (allegedly) badgers. The Four Areas Donegal reference area flare up was a cluster of contiguous herds (Olea-Popelka 2003).

CLOSED HERDS ? John Bourne famously remarked at one Open ISG meeting "there is no such thing as a truly "closed herd":- no bought-in stock, and even with fully effective double fencing. TB may be brought back from shows (Guernsey, Steger's Germany cases), or hire bulls before AI widespread, inadequate disinfection of premises or vehicles, or slurry spread before properly composted.. and on the tires of post vans going farm yard to farm yard 6 days a week.. leading to a risk of contaminated dust inhalation (which may spread Johnes disease too Allen 2011), shared vehicles, shared watercourses contaminated by slurry pit drainage..cattle biosecurity (28, 29).. back in the 1960s farmers were very aware that a 2-3 yard gap between double barbed wire fencing was essential to stop both TB and brucellosis, inquisitive nosing or "kissing cows", but few implemented this, and as a keen walker in the Cotswolds / on Exmoor I have not seen Any farms so protected ! (Wright 24 Oct. 1985, New Scientist; McIlroy 1986; Richards 1972; Phillips 2003; O'Connor 1986, 1988, 1993; ISG 2007 husbandry / TB 99 studies).

Rather overlooked .. Rats did spread avian TB between poultry and pig units (Myers 1940), so might actually be a more likely vector of bovine TB than badgers. Although they do not develop visble lung lesions, just miliary micro-lesions (Yersins phenomenon), they have been largely ignored in epidemiological studies ( a few cases Steeple Leaze, Little 1982; Delahay 2007), more rats than humans in GB, and they can go 1-2 km farm to farm leaving faeces in the frass of cattle cake in food troughs ; dust inhalation by cattle and probably Michigan White tailed deer "feeding" experiments (Palmer 199, 2004).

This expansion of a "missed" cattle TB reservoir is also clear in DEFRAs 2013 new strategy, p. 28 no recognised wildlife reservoir "out there", and it is simply a clonal expansion of cattle DNA Spoligotype "Home Ranges" p. 74 (Smith 2006). Clear too in Gopal's 2006 northeast reintroductions. And back in the 1980s MAFF realised there was no background TB in either cattle or badgers in the non-southwest areas, so new incidents could only have been via bought-in stock (mostly unconfirmed reactors).. they were unable to Confirm that in c. 75 % of cases, so honestly regarded these as of "Unknown" origin .. Open circles in Zuckerman 1980 maps.. BUT Eureka, midnight on the 31st of December 1978, ALL these became closed circles "Due to Badgers" in the same Dunnet 1986 maps This mistaken identity clear too in Wilesmith's epidemiology studies (1983, 1987).

This tragic and costly explosion outwards could have been prevented :- the last pockets should have been quarantined off until truly tested clear; with NO movements out ; NB. this idea for a c. 5 km radius of new outbreaks in Low risk areas is of critical importance in the new DEFRA Eradication scheme. There should , since the mid-1970s have been both pre- and post-movement testing; these, and purchases from TB-free areas has kept Scotland TB-free OFT status since declaration (27 a, d).. 2-3 bad breakdowns in last few years, all due to bought-in cattle (11, 12)( No badgers culled, only 1 TB badger case ever). Pre-export/post-import tests have stopped TB imports to northern GB from Ireland since the mid-1970s .. up to 40 % of breakdowns back then (Dunnet 1986). Sad, with hindsight that farmers/vets were so opposed to pre-movement cattle tests ( "pointless" because spread is mostly by badgers).. blackmail only agreeing to tests IF badger culls allowed. Likewise, the ISG and many others warning to DEFRA not to permit free movement out of hotspots after FMD ended 2001(see EFRA Committee report), but this was ignored so predictably TB reappeared by restocking in Powys, Cumbria, and the northeast (Gopal 2005). DEFRA 2004, 2005, got it wrong, out of 6 options, pre-movement tests from 2006 on, from 1 & 2 year to 3 & 4 year test areas , is a minor part of the problem.... ever since the mid-1970s there has been a 1-2 parish wide "firebreak / ring fence" of 2 year testing around annual test core hotspots, THAT is where the pre-movement tests would have done most good ! It seems 2015, that DEFRA will At Last bring in pre-movement tests in hotspots, plus post-movement tests from high to edge/low risk (4 year test) areas !

A number of insidious factors have contributed to the development of a southwest Problem area.. a doubling of cattle stocks (Pout 1981), switch to higher producing milk breeds, these were less hardy so more over-wintering in barns , favouring airborne spread, mechanised milking parlours so a normal herd grew from under 50 to 150 .. or now 2-300, 1000 strong, but concomittently a halving of herds overall, with numerous dodgy dispersal sales. Rather amusing to recall that the southwest was NOT a "badger TB hotspot" back in the 1940s, Francis 1958 maps clearly show a northwest "Irish imports" hotspot ! Scotland had higher levels of bovine TB than England back then. The apparent archipelago of southwest high density "Badger Hotspot" islands only became apparent with the increase as high density "Dairying Hotspots" !; and despite decades of badger culling almost identical in the 1970s and the RBCT cull areas. Similarly, in southwest Scotland and Eire. An Irish source clearly seen in an unusual Spoligotype in the Sussex clonally expanded cattle/badgerTB hotspot started in the 1970s ; and the late 1990s Furness Cumbria cattle/farmed deer problem.

The badger "problem" was completely over-looked as TB was eradicated in Germany and Holland in the 1960s even though mysterious respiratory epidemics occured in badgers there (TB ?)..likewise the Isle of Wight eradicated TB before any TB badgers found , also Scotland (just 1).. and fatal ("TB") happened in Shropshire (Francis Pit's pet with "throats" TB ?) 1935, and in Hants & Surrey in the 1960s too. The very "first" TB badger was in London Zoo 1938, another caught TB from Axis deer at Whipsnade in the mid-1950s and ended up at Edinburgh's Royal museum, the first wild TB badgers were mid-1950s in Switzerland via a last spillover to roe deer and eaten as carrion, 1st 3 "official" cases Glos./Glamorgan 1971, 1st Irish TB Brock 1975. Belatedly TB badgers now known as spillovers in Spain, Italy, France.


The textbook GB "Area Eradication scheme" ground to a near halt by 1971, with an intractable "hidden source" of TB in tiny southwest "island" hotspots (Macrae 1961; Ritchie 1964). Since there was no obvious cattle source, everyone assumed there must be a self-sustaining widespread badger reservoir re-infecting herds, but in fact the real hidden "self-sustaining" reservoir has been within the cattle population all along. It was comparatively easy to eradicate diseases such as cattle plague (rinderpest) and foot & mouth where animals show obvious clinical symptoms; but much harder to eliminate diseases reliant on less than 100 % accurate tests for identifying sub-clinical infections such as:- brucellosis, BVD, IBR, leptospirosis,salmonellosis, pleuropneumonias, and TB where thanks to decades of controls, overt clinically ill cases with emaciation, tubercular cough , udder or uterine TB are now very rare ( some 26, 000 such cows removed under TB orders 1955-60, Evans 1981; Pritchard 1982). The simple truth of the matter is that there is "limited sensitivity / specificity of all available diagnostic tests "; all less than 100 % accurate, so false positives and negatives inevitable (1, 21). Obviously, the bigger the herd the more "dodgy" false negative latent TB carriers there will be, so a 1000 strong herd may never test clear, so perhaps a temporary split, and clear subunits separately (Goodchild 2001). Dartmoor became an intractable "badger TB hotspot " (despite low population on moorland), because herds sharing commonage grazings were not treated as one big herd.

Paradoxically , with astonishing pre-cognitive clairvoyance, pioneers of cattle TB eradication schemes c.1900 such as M'Fadyean and Bang solved the current "Badger TB Crisis" over 70 years before the first 3 TB badgers in 1971, Glos. & Glamorgan. Bang said in 1892 "It is found that the tuberculin test is no more perfect than are 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 slight degree of the disease". A view reiterated in Blood's 1989 Veterinary Medicine, "no reliable test exists for the poorly sensitised animals with the early or late stages of the disease which are the usual cause of recrudescence in herds which have been classified as free of TB".........As Godfray also highlights inadequacies in surveillance, "cannot detect the very first stages of infection; some cannot detect very long established infections either (21) ..... and it is precisely these early reactors without TB lesions, Unconfirmed cases late TB skin test non-reactor (ie. Anergic) cases which are the true cause of all the breakdowns supposedly due to badgers. Reviewing country eradication schemes, Francis 1958, noted that Germany's Ostertag Scheme failed bacause it focused Only on cattle with Confirmed Visible lesions. The failure of schemes in GB and Ireland in effect have repeated this error, in not taking enough account of this case of mistaken identity..........ALL the breakdowns allegedly "Due to badgers" have been caused by mis-identified cattle; notably very early TB non-reactors & early TB Unconfirmed cases... plus, assorted late TB cases missed by routine skin tests in Chronic TB herd breakdowns.

4.TWO Pivotal cornerstone MISUNDERSTANDINGS underpin the whole confused Badgers & TB Debate and they crept in when Cattle were bizarely effectively Ruled OUT as the infectious source of TB:-

A. Open Visible Lesion cases; B. Four delays in becoming infectious reactors:-

A. OPEN VISIBLE LESION TB CASES. MAFF vet John Gallagher in Zuckerman 1980 (p. 86, 94) wrongly assumed that "Open Visible Lesion" cases were so rare (2 % of reactors), that cattle-to-cattle and cattle-to-badger spread were Unimportant, so there must be a widespread self-sustaining culprit badger reservoir. A mistake repeated in Dunnet 1986, para. 60; and elsewhere (Hewson 1987).

It was known a century ago that cattle are infectious at any stage of the disease; before they become skin test reactors or have visible lesions (M'Fadyean in Francis 1947, 1958). Francis also noted explicitly that the key difference between human and cattle TB was that cattle do NOT form "closed tubercles"; and so ALL reactors should be considered potentially infectious; and that if a cow with even very slight lesions is left in a herd, then spread of TB will be more or less rapid within the herd. Blood's Vet.Medicine re-iterated this. Re-discovered in recent cattle pathology studies, "normal" reactors may have no visible lung lesions, but do all have lesions in draining lymph nodes (bronchial & mediastinals) so 100 % respiratory , and up to 20 % sputum positive ie. infectious (McIlroy 1986; Neill 1988). This lack of visible lung tubercles early on led to the heated debate a century ago; the Calmette/Guerin School insisted transmission was by ingestion, even 'though there were no "gut lesions" ; entry portals via tonsils or Peyers patches in ileum, so lung TB Secondary. The Bang / Chausse/ M'Fadyean School with Primary lung Ghon foci of respiratory TB was only fully validated with the 1940s understanding of "droplet nucleii" infection (Myers 1940, 1969 versus Francis 1947, 1958; O'Reilly 1995). The clear (and unsurprising) involvement of head lymph nodes (palatine tonsils & retropharyngeals) in high dose nasal inoculation studies almost led to a "resurrection" of the idea of early infectious TB starting in the URT or Upper Respiratory Tract , maybe an"ingestion" transmission route. But it has been known for decades that coughed up and swallowed countless lung bacilli "deglutition", cause Secondary lesions in the retropharyngeal nodes, larynx and gut in cattle and man (Cassidy 1999; Menzies 2001). Confusion too as regards the significance of retropharyngeal lymph nodes since they drain both from around the nasal passages and around the mouth.. but Plum's detailed study showed high involvement with bovine TB via inhalation versus avian TB via ingestion (Francis 1947).

Various studies have reaffirmed that cattle TB is almost entirely a respiratory bronchopneumonia, "Consumption or Phthisis". Aristotle's "something pernicious in the air", Villemin 1870s "transmissible" disease , Koch's 1882 new "tubercle bacillus" "GERM". After all, cattle originally caught M.tuberculosis from man with early cattle farming in the fertile crescent X,000 b.c., a DNA deletion produced M.bovis (africanum, caprae, microti, assorted BCG strains, etc); with later spread worldwide, arriving in GB with the Romans and/or Continental breeds in the 17 hundreds, and original spillover to poor old Brock ! (Smith 2006). Interestingly, where cattle get airborne human TB the lung lesions are often small and non-progressive (Lesslie 1960; Jubb 1985).

Rather ironic that the lack of early lung lesions in cattle led to a mistake in understanding the transmission route, whereas, the fact the most badgers do not have any TB lesions (80 %), but the minority that do tend to be in lungs or kidneys led to a simplistic mistaken belief in primary lung TB. Wrong, TB starts in the throat submandibular lymph nodes ie. dietary aetiology ! Hence the key error, Cattle TB is entirely a "Consumption" or respiratory broncho-Pneumonia, Badger TB is a dietary "Scrofula" , TB spread is cow to cow , and cow to badger; NOT, as widely assumed, badger to badger, and badger to cow after all ! More detailed badger autopsies reveal more with TB from a wider range of sites Crawshaw /Corner 2011, 2012. ( Cattle lesions :- McIlroy 1986, Neil 1988, 1992, Liebana 2008, Medlar 1940, Jubbs 1985 Pathology of Domestic animals; Myers 1940; Francis 1947 cites studies by Stamp etc; Pritchard 1982. Crews 1991, found an upsurge in unconfirmeds just when possums allegedly became the problem in N.Zealand).

Various reviews have indeed found that cattle-to-cattle spread is low; but overlook the fact that that is precisely because intensive annual testing is so effective in minimising within herd spread ; c. 50 % of breakdowns at low point GB , Ireland N & S, were just 1 index reactor (singleton herds, Morrison 2000). GB, Irish, Dutch (Fisher) , Argentina (Kantor), N.Zealand (Barlow) studies show just 2-3 reactors /breakdown otherwise (Griffin 1995, Neil 1994, 2001, Goodchild 2001, Menzies 2001). However, IF an active spreader is left in a herd for longer.. there will simply be more reactors in the incident, eg. on 2 year testing, as happened post-FMD, there will be twice the number of breakdowns, and herds with over 6 reactors went from 23 % 2000, to 42 % 2002, back to 17 % 2005. Vets noticed breakdowns were worse when 2-3-4 yr test areas were recruited back to annual testing (2005, 2008 in particular ). This was demonstrated with the Hartland upsurge in the early 1970s, re-re-solved by strict synchronised cattle testing , nothing to do with culling a few badgers (Richards 1972, Krebs 1997). Bad breakdowns initially as re-stocking post-BSE spread TB back into TB-free areas ; Exmoor, Hereford/Worcs, Staffs/Derbyshire, the latter new hotspot had cost 6000 reactors by DEFRA 2004 (Cheeseman 1985; Hewson 1997).

B.FOUR DELAYS IN BECOMING INFECTIOUS REACTORS . The second grave mistake has been the fourfold confusion about:-

1. Incubation/ latency; 2. Are Visible Lesion cases more infectious ? (22); 3. Unconfirmed cases; 4. Late TB cases, Latency & Anergy and Problem herds:-

1. INCUBATION / LATENCY . The assumption that it may take only "several weeks for a positive SICTT test reaction to develop in high dose inoculation experiments was the basis for the claim that the effects of the RBCT cull could be apparent in cattle within 3 months (McCorry 2005; Cassidy 1998; Thom 2012; ISG 2007). Early feeding experiments with raw hi-dose-TB milk were fatal within 2-3 months, (M'Fadyean 1910 ).

It seems that it may take a year or so for TB cattle to reach the more infectious stage, and start spreading TB to fellow herd members.. as shown in bought-in cases in Staffs/Yorks:- Hewson 1987/ Gopal 2008. A classic but sadly long forgotten study clearly showed that 13 calves caught TB by Prolonged exposure to a group of older cattle in a barn, a 2 yard gap so purely airborne spread, 5 reacted at 6 months, the other 8 after 1 year (Svensson 1904 in M'Fadyean 1910).The reason why 32 in-contact calves apparently failed to catch TB was that they were autopsied too soon to have developed lesions:- contrast O'Reilly 1988, with Costello 1998, 40 % in-contacts affected; and a further case in Pollock 2002. And only 1 in 3 in-contacts got TB when exposed to a calf with "reflux" shedding of nasal inoculate, Neill 1989. Likewise, 4 calves exposed to TB badgers in a yard experiment for under a month (Little 1982). And hence the farmer belief that cattle are not catching TB from other cows in barns .. they test clear at spring turn out to pasture, meet those terrible badgers and are overnight riddled with TB !

Delayed "infectivity" , is also very clear from studies of human TB, eg. Dannenberg 1981; O'Reilly & Daborn 1995). On the other hand, a few human cases become super-excretors; and cattle clearly caught TB by brief exposure at agricultural shows to a "super-excretor" cow, taking TB back to Guernsey, or over 50 new TB cases at 1 show in Germany (Francis 1958; Steger 1970). And in the only truly "proven" case of badger to cow transmission ever, It took 9-10 months for calves to become reactors after catching TB from badgers in a very artificial yard experiment (Little 1982).

So it may take c. 1 year for cattle to progress to the reactor stage (range 6-18 months, McIlroy 1986; Neil 1988; White 1997; Gopal 2005). Of course TB can spread among cattle never housed, but "bubble domes" of infectivity may develop above waterholes in Africa or Australia (Lepper 1977); or hypothetically among cattle chewing the cud for hours below shaded hedgerows in GB... but Bang in the 1900s and Francis 1947, were very clear, cattle do NOT usually catch TB sharing pasture with infected cattle; only acquiring the disease when they join the breeding herds and " first enter the cowshed".

No-one seems to fully realise it, but it is because cattle may take c. 12 months to become reactors, Range 6 - 18 months; that in practical terms , a later 6 month check test is vital after herds have 2 clear tests (both confirmeds & unconfirmeds; & IR Inconclusives should be removed at first failed retest EC 64/432); AND using the last annual clear test as a passport to moving stock, in fact may be misleading and a 60 day, 90 day, or 120 day pre-movement test (formerly Eire to 1997) Would be a better guarantee that new early TB cases are not inadvertently sold on . A new initiative , going to 6 monthly testing in Cheshire ( Cox model, ISG 2007), will not find cases any faster, already tried in 1970s Cornwall (Richards 1972).. and no point in surveillance testing of young stock a few months old either. Although formerly, when a minority of calves caught TB "in utero", they could be reactors at birth ( Francis 1958; Myers 1969).

2.ARE VISIBLE LESION CASES MORE INFECTIOUS ?. "The relationship between diagnostic status and infectiousness is not known in detail , although there is an apparent link to late TB with numerous lesions and antibody response" (22, Woodroffe 2005; Pollock 2002). Both cattle and humans become increasingly infectious as they progress from the Incubating non-infectious stage, to No Visible Lesions, to the Visible Lesion stage, the lungs of terminal human cases with florid or fulminating TB are "riddled" with tubercles (Francis 1947, 1958; Jubb 1985; Collins 1997, 2000, Goodchild 2001). Few bacteria are shed intermittently from few initial NVL "granulomas" in cattle and humans; but then infectiousness increases with the increase in the number and size of lung lesions, going from Visible Lesion to cavitation and in man shedding of 4 billion bacilli/day in superexcretors . This increase in bacillary load also shown in increased skin test positivity (Collins 1997, 2000). Steward 1941, in clinical sampling found 399 out of 400 sputum positive cows had Visible lung lesions. He also noted a minimum of 50,000 bacilli /ml were necessary to detect M.bovis in sputum smears; likewise M.tuberculosis in man (O'Reilly 1995). TB Campaigns in Africa and India backed by TB Alert, W.H.O & IUATLD are hampered by poor transport infrastructure, so instead of skin tests rely on smears to find infectious patients to treat with multi-drug therapy. Equating infectiousness with "sputum positivity" is a slight mis-conception, bacilli are shed into bronchioles in exhaled air, later contaminating "sputum".

This increased infectiousness also formerly occured with udder; as well as during pregnancy in, uterine TB in cows, so post-calving "waters" and the shed placenta may contain enormous numbers of bacilli.. how scavenging foxes used to catch TB ! Surprisingly few calves caught TB in utero in the past... although udder TB cases could infect the bulk milk tank so whole batches of calves affected.. cows with udder TB very rare now, so cases worthy of comment, eg. Cornwall (Monies 2006) , the Trioni herd in Wales, 1 case in Eire recently with farmers family infected. NON-Immuno-suppressed pregnancy lesions usually regress postpartum, but some elderly cows may apparently fail to do so, with later calvings hence becoming skin test non-reactor/anergic cases , and the root of chronic herd TB ( Francis 1947, 1958; Myers 1940, 1969; O'Reilly & Daborn 1995; Jubb 1985; Blacks Vet. & Medical Dictionaries).

3. UNCONFIRMED cases (OTF-S, Officially TB Free-Suspended) has been the pivotal misunderstanding since the 1980s (Wilesmith 1987, O'Connor 1986). It was wrongly assumed that early TB reactors without visible lesions, so called unconfirmed reactors, were false positive TB-free cases ( 23 b), even though 70-80 % had been exposed to M. bovis (Dunnet 1986, Wilesmith 1987), so the 60 -100 % , of breakdowns in TB free areas Must be "due to badgers". Skin test (SIT) reactors to avian TB Are "false positives" c. 14 % hence EC derogation to use the SICTT comparative skin test ( Johnes disease or paratuberculosis is a variant of M.avium). Specificity is 99.99 % ie. only 1 in 1000 truly do not have TB; or for IFN 98 % so 20 in 1000; or DIVA 96 % (23, 24, 27 f). Under EC 64/432, ALL reactors mut be assumed to have TB; a fact nearly understood in the TBEG Oct. 2009 Report.

It is sad to recall farmer disinclination to participate in the VLA IFN trials (ISG 2007) because "they throw up too many "False positives". And most recently JW Simpson Sussex, had 2 IR Inconclusive reactors plus 8 further reactors, and was told "all perfectly healthy" after abattoir inspection. A reply from vet Andy Paterson (APHA,Southeast, 2 Jan.2015, Farmers Guardian) clearly recognised that only 1 in 5000 reactors are truly false positive, and these unconfirmeds have'nt yet developed visible lesions.......tragic that over the last 40 years vets have not been explaining this to understandably angry despairing farmers losing pedigree stock built up over generations.

Sad to recall that at an open briefing for MPs, in the early 1990s, with BSE replacement reintroductions rife, 95 % of breakdowns were unconfirmed, so a MAFF/VLA vet happily told everyone that 95 % of herd breakdowns were "Due to badgers". It is a great pity more use is still not being made of fast PCR/Spoligotype tests for M.bovis in suspect unconfirmeds tissue samples.... rapid confirmation, plus the added bonus that the true source can be identified, eg French spoligotype in the Derby/Staffs 2004 new hotspot . Focussing on early/ late TB cases, with intensive annual testing has been crucial elsewhere:-

Australia achieved final eradication via the NGSP scheme, National Granuloma Submissions Programme, to track down the last cases. New Zealand too, now nearing eradication with draconian movement restrictions and testing regime (10 a; Griffin 1994). Even in Eire, the "sudden" halving of reactors has nothing to do with culling 6000 badgers /a, but a highly sophisticated IT database (TB history, contiguous premises etc), and routine use of both IFN & ENFER tests (early & late TB), has meant that controls can be focussed on the localised pockets of high infection in CVERA's bienninial "kernel" mapping of TB density. A tragedy pre-movement tests not re-introduced (as for brucellosis)...English & Eire models suggest only c. 15 % of breakdowns prevented But, these are just the confirmed ones (Goodchild 2001; Clegg 2008; 27 a,d) :-

1959 ...................1999.....................2008........................2013


Ulster too halved TB within 5-6 years post FMD. Sad to recall they got down to just 173 reactors in 1971, prematurely relaxed to 3 year testing, TB shot up rapidly to 2500 / a. (O'Connor 1986). Although 36 % of badgers had TB back then they've always been regarded as a spillover host (McIlroy 1986). Alas until last year (2014) , the hugely costly labour intensive and futile T V R Scheme, launched ; Test badgers (IFN & DPP Dual Path Platform), Vaccinate healthy ones, Remove TB ones, 180 badgers so far, a mere 35,000 to go). Wales similarly. TB was nearly eradicated in Wales by the early 1980s, just a few problem herds left in Dyfed. However, thanks to FMD, TB doubled from 2006-8, 6000 to 12,000 reactors. The dramatic halving from 2008 to 2014, back down to 6000 reactors was due to a return to annual testing nationally , nothing to do with vaccinating a few thousand badgers in the IAA area. England, even many farmers are now aware that 4 yearly testing is too long; bad breakdowns in Staffs, Leics, Notts, etc as well as a few in Scotland since it went OFT-Free .. a couple of years of annual testing needed to find out if these english areas really are TB-free.

Godfray repeats the ISG 2007 view that (30 d & Box 2, iv) ""RBCT CULLS HAD NO EFFECT ON THE INCIDENCE OF UNCONFIRMED BREAKDOWNS ""( c. 30 % in hotspots).... well, is'nt that simply because they are caused by unconfirmed (TB +) Reactors, NOT by badgers after all; A QUICK CHECK OF the ISG raw data should show that there WERE NO TB badgers in culls after unconfirmed breakdowns !!?? And CVERA could do a rapid check on their so-called "Greenfield study" breakdowns too. Earlier studies reveal almost no background TB in badgers, in Wales, and the Staffs & Sussex studies. In the early 1990s in Wilts, 2 in 3 breakdowns were unconfrmeds, and 2 in 3 culls had 0 TB badgers. Thornbury gassed out badgers, but in the following decade there were still 1-2 unconfirmed breakdowns each year (Clifton-Hadley 1995).

4. LATE TB CASES , LATENCY & ANERGY AND PROBLEM HERDS. Strikingly , Godfray highlights the inadequacies of test surveillance, (1,21-25), But did not mention antibody tests as the simple answer for SICTT non-reactors / anergics; for chronic herds, some 2000 currently, ENFER, ENFERPLEX, IDEXX Ab test , or even more simply using rapid PCR on faecal swabs .. a bad TB cow may shed 38 million bacilli/day in faeces (no wonder poor old Brock gets TB turning over cow pats seeking beetles, grubs and worms which may be TB "vectors !, Lortet & Despeignes 1892; so moles can get TB "worming" underground !).

The skin test has been pivotal to eradication schemes for a century, but is perhaps past its sell by date. Fast blood tests are now available which only require 1 farm visit, and combined use of 1 sample for early/late TB are much simpler , IFN/ENFER , or other tests in New Zealand (Griffin 1994). Perhaps the Single Intradermal ( just M.bovis) Skin test should be used for mass surveillance as on the Continent, then for 60 day re-tests to achieve clear status in affected herds , the blood IFN/ENFER tests would be more accurate ; as routine now in Eire. Greater use of fast PCR/ Spoligotyping of tissue samples, would have the added bonus of more closely elucidating source of TB. New developments; "Synergy" produce ENFERPLEX for alpacas and goats; "LGC Forensics" use PCR/ DNA tests (Courtenay 2006, 2007, 2008).

Godfray did not stress enough that 1/3 of cows go temporarily anergic around the time of calving (23 b) .. presumably vets know it is daft to herd test then !? (Blood's Vet. Medicine). Immunosuppression also occurs with BVD (Monies 2006), cattle BIV (HIV/Aids, with co-infection behind TB problem in Africa, also malaria), and liver fluke ( 23 b; O'Reilly 1995). There is recurrence due to residual cases even in supposedly clear herds (11, 12, Blood's Vet.Medicine), Incredibly (!?) the SICTT (23 ) IS Only 49 % accurate as a herd test ( 66 -80 % sensitivity, may miss 1 in 3, Monaghan 1994) , So, up to 25 % of breakdowns ONLY picked up at abattoir inspection ..More (2006), found it could be nearly 50 % in Eire)(25)....when annual testing is working effectively there are hardly any cases left to be picked up by the abattoir "safety net"...GB in 1980s just 20-30 /a, but since FMD in the hundreds. Corner's studies of abbatoir gross quick checks of carcases found that they may miss 50 % , unsurprising, lesions may be only pin head sized in a lung volume the size of a cows "chest" , needles in haystacks . Adequate to protect human food chain, but wholly useless for critical epidemiological purposes.

The minority of "Problem herds" , 5-15 % breakdowns are a disproportionate obstacle to area eradication schemes. Bad breakdowns often in occur big dairy herds, which are the most likely to take longer to "apparently go clear"; but since the SICTT retests are only 66 % accurate, about 1 in 3 will have repeat breakdowns via latent carriers such as IR Inconclusive Reactors 18 m to several years, or even 7 years later (11, 12, ISG 2007 the IFN trial , DEFRA 2013 new scheme, Conlan 2012, Karolemeas 2011, 2012, Hewson 1987; Good 1994). "Active spreader" elderly cows may be anergic, so pass all skin tests and remain in the herd undetected until culled for other reasons,such as mastitis, lameness, poor fertility (c. 250,000 cows/a)..but may be "riddled" with lesions at abattoir inspection, Adam Henson of Cotswold Rare Breeds had a case, another at Gelli Aur university farm under restriction 10 years.

A third of Gopal's 2006 northeast breakdowns came from 1 problem Cheshire herd. Dr. Glossop noted dispersal sales from a 4 year test area breakdown caused 15 new breakdowns in Wales. The 1972 Richards report on Lands End (the infamous West Penwith intractable area, found 3 skin test non-reactor/ anergic cows caused 18 herd breakdowns in Madron Parish. ; 10 % of the total for the 2 1/4 year study. So no wonder depopulating a dozen or so chronic herds allowed the area to go clear in 1985, and it was not immediately re-infected by badgers , but stayed clear 2-3 years. Depopulation was the answer where 50 % or even 25 % of a chronic TB herd affected, but is unnecessary now with better late TB antibody tests ( Costello 1997, Good 2011; DEFRA 2014 error).


BADGERS . GB's very successful Area Eradication scheme shrank TB from countrywide down to a dozen or so intractable southwest "island" pockets. It was assumed (wrongly) that since "Open Visible Lesion"cattle were so rare, cattle-to-cattle, and explicitly cattle-to-badger spread was unimportant, so there must be a widespread self-maintining reservoir of TB in the high density badger population preventing eradication in these areas. And since TB was often found in a. the lungs, there must be by respiratory spread within clans; b. in bite wounds, so clan to clan spread; and c. in urine with spread back to cattle.

Unfortunately, this over-simplified idealised scenario was simply wrong. TB in badgers occurs in incredibly tiny micro-pockets; with just 1-2 TB badgers per clan, in 1 to several clans, as a spillover from cattle at the epicentre of the preceding herd breakdown. As was very clear from the "clean ring" culls 1982 - 1986 (Krebs 1997), and in the early detailed studies of badger populations in the last intractable TB hotspots in Avon, Cornwall, Dorset, Glos.(Woodchester), Staffs and Sussex (Cheeseman 1981, 1985, 1988; Wilesmith/Pritchard 1982, 1986).

Badger TB is a dietary "scrofula" comparable to bovine TB in man, the Kings Evil, from unpasteurised milk; TB in badgers in 70 % of cases starts via the tonsils (palatines), in "throat" lymph nodes (submandibulars) , TB in the lungs and kidneys is by secondary spread (Cheeseman 1985, 1988, 1989; O'Boyle 1997-2005; Nolan 1994; Anderson & Trewhella 1985). Given that much of badger feeding entails "grubbing" in soil for invertebrates, damaged and lost teeth are common; up to 6 % of badgers may have dental abscesses which provide an easy entry portal for germs; and skulls with periodontal disease, and peripheral/ superficial osteomyelitis/ acropachia are not uncommon in TB areas, as found also in dogs, lions and horses (Francis 1958; Sleeman The idea of silicosis/ immunosuppression and higher susceptibility to lung TB in badger miners seems unfounded, TB is not caught initially by inhalation anyway (Higgins 1985). Badgers do not after all catch TB mainly from other badgers; but have been a spillover from cattle "dead end" host all along; and TB dies out among badgers when not topped up from cattle. Badger primary TB of the submandibular lymph nodes often self-heal so have been overlooked in aetio-pathological epidemiological studies including the RBCT/ISG, Jenkins 2008; Corner 2011, 2012; DARDNI RTA study (Abernethy 2013).

One of the most astonishing tunnel vision blind spots in the whole 44 year Badger TB Debate, is that many many thousands of herds have gone clear, and stayed clear for 5-10 years when normal herd demographics change eg. replacing a cohort of "clapped out" milker cows with a new batch of heifers; They DID NOT immediately become re-infected by badgers, so the whole mythical widespread self-sustaining badger TB reservoir risk "out there" is a Mirage ! As most of the country eradicated TB in cattle, TB died out in badgers accordingly, so there were almost no TB badgers in the county apart from those associated with the last problem herds in Staffs or Sussex (Cheeseman 1985, Hewson 1987; Wilesmith/Pritchard 1986). TB had almost been eradicated in Wales by the early 1970s, just a cluster of problem herds in Dyfed. So there was almost no background TB in badgers. But 1972-1996 there were c. 700 herd breakdowns, mostly unconfirmeds, "Mostly due to badgers" according to MAFF, but only 46 TB badgers out of 2363 sampled, and none from Powys where strikingly there were 25 % of RTAs with TB after cattle restocking after FMD reintroduced TB. Almost no TB badgers in counties until Cattle TB re-introduced by BSE replacements in the early 1990s on Exmoor, and in Hereford/Worcs/Gwent. In the previous 20 years there were only 11 TB badgers out of 1204 sampled in Somerset, but then 85 % affected. In Hereford/Worcs. there were only 10 TB badgers out of 876 sampled, but then 55 % affected.

"The dog that did not bark in the night" :- the Woodchester study area of 9, with c.350 badgers in 32 clans, and a dozen cattle herds has been the textbook example of a high density , supposedly high risk population with "endemic" TB, but there has not been even a single Proven breakdown since 1975, where herd A, caught TB from badger clan B. With 20 : 20 hindsight, not surprising since there were so few super-excretors within the population; just 17 or 24 among some 900 individual badgers over 14 years (Cheeseman 1989; Smith 1995; Rogers 1998). Hence there was very little "environmental contamination" from these badgers.. 1983-7 just 32 out of 4023 latrine faecal samples, and similarly very low incidence in the Staffs and Sussex studies, and very few badgers producing infectious urine 1991, Wilesmith had found just 18. Corner (2011, 2012) found that there were only 5 amongst 57 detailed badger autopsies, and all had under 100 cfu /ml of urine. So even in supposedly high density /high risk badger populations there was actually almost zero risk of passing TB to cattle. In fact TB in badgers is not self-sustaining (14 c); it nearly died out 3 times in the area, and only persisted within certain clans for 5-6 or up to 14 years (Delahay 2000). Spillover TB in badgers peaked After the peak in cattle, as regards 5 studies :-

A. the Beech Tree (first TV "Badgerwatch") clan; B. whole of Jacks Mirey clan tuberculous, caused by 4 bad inner ring farms with 93 reactors 1987-8, but there was 1 TB badger in 1984 at the true start of the incident, (Krebs 1997, p. 48, Wilesmith 1991, Newell 1997); C. North Woodchester clans both in 1979 & 1988-9 (Cheeseman in Hayden 1993) ; initially there were only 14 TB badgers out of 67 culled from 6 out of 11 clans removed; and D. the Sussex badger population study found no TB badgers remaining over most of the county after cattle TB eradicated; but all 8 study clans were infected after the 1984 peak in new herd TB, but only 4 groups subsequently culled had TB (Wilesmith / Pritchard 1986); E. Staffs. likewise, (Cheeseman 1985; Hewson 1987).

Godfray still claims that "badgers are the most important wildlife reservoir (in GB), and a major reservoir in Ireland"; and that "Mycobacterium bovis IS transmitted within and between populations of badgers and cattle may cause 50 % of breakdowns" (14 a). A hypothetical 4-way transmission Box :-


4 ...< to..................................................2 >

Badgers ...................3 .. < to ..................Badgers

When badgers initially got the blame for the last intractable southwest problem of TB in cattle , it was clearly (but wrongly )assumed that only 3 & 4 were happening (Zuckerman 1980,Dunnet 1986); but transmission has been 1 & 2 all along ! So badgers Cannot after all possibly be the MAIN Hidden reservoir, Godfray, "LITTLE Known re. badger to cow transmission "(15), but clearly cows ARE still giving badgers TB (14 a , b).

Just as in cattle and humans, badger TB too shows a progression; over 80 % of TB badgers are found in the early No Visible lesion stage; only late TB multi-lesion cases shedding for example in "sputum", faeces and urine are super-excretors which might pose a risk to other badgers or cattle, but they are very rare. These studies actually found little evidence of TB spread either within / or between clans .. either supposedly 82 % via the respiratory route within social groups, or 18 % by bite wounds or emigration to neighbouring new groups; and it seems far more likely that bite wounds get secondarily infected with TB from environmental contamination in the sett & bedding rather than actually by biting as with fox rabies (Cheeseman 1989). Indeed, TB was initially confined to the western half of the study area, and did not arise in the eastern half until further herd breakdowns there (Delahay 2000; Garnett 2005. Whole clan breakdowns, 1 in Cornwall, plus Jacks Mirey (above; resulting from bad herd breakdowns ), sparked the plausible idea that "pseudo-vertical" transmission sow to cub might be important; although the RBCT cull found no extra incidence in cubs (Jenkins 2008, 2011). IF a sow with bad lung TB swallowing bacilli weans cubs by regurgitation of earthworm soup with TB flavouring, that would be an option.. so accounting for clans where TB persists beyond the initial TB badgers lifetime ( Cheeseman 1981; 1984, Delahay 2000).

Chris Cheeseman and Dez Delahay were puzzled that even when a badger "hooching" lung TB was present in a clan, there were still often only 1-2 TB badgers in the clan; it seems surprisingly that badgers are only transiently clinically infectious excretors or super-excretors, some 42 % reverted to non-excretor status by the next sampling; so badgers often do self-heal and may even form "closed lung tubercles "(Clifton-Hadley 1993; Gallagher 1998; Newell 1997; Pritchard 1986).Often also, such really sick badgers stayed in subsidiary setts, not sleeping in group huddles in underground nests in the main sett.

The Woodroffe 2006 PNAS conclusion that "cattle pose a risk to badgers" and cows ARE still giving badgers TB (14 a, b), is of absolutely Critical importance, since both the Zuckerman 1980 and Dunnet 1986 Assumption of badger guilt ( a self-sustaining hidden reservoir), explicitly claimed that badgers had NOT just caught TB from the preceding herd breakdown !

One of the clearest results of the RBCT, was that the level of TB in badgers has no link to badger density, nor indeed for a minimum clan size to sustain TB; so any idea of controlling bovine TB by badger fertility control seems somewhat ill-founded (White 1995; Woodroffe 2009; Tuyttens 2000). The tiny southwest high density badger TB hotspot "islands" were actually limited to the highest density dairying hotspots, so were almost identical between the 1970s and the same 1998-2005 RBCT triplet hotspots. Badger TB prevalence is overwhelmingly a result of spillover from variable preceding cattle TB ; badgers are a very sensitive Miners canary to cattle TB, like wolves and coyotes for Michigan white tail deer TB, or lions badly affected by TB via Cape Buffalo mixing with TB cattle herds in the Kruger Park in South Africa. The first sign of bad breakdowns in areas long TB-free has been finding dead or moribund badgers behaving erratically Beech Tree sett above , Gelli Aur university farm Wales (Cheeseman 1981, Muirhead 1974). In MAFF's 1972-1996 sample of 42,130 badgers , there were just 5608 with TB ; the vast majority derived from the last 7 southwest hotspot counties, with a scatter of the occasional TB badger elsewhere just as with spillover deer cases. So some 27 counties in GB affected , and all 32 in Ireland.

Some 15 % of breakdowns have active spreader Confirmed Visible lesion cows, which produce infected cow pats, and hence c. 15 % of badgers catch TB from cattle. The RBCT result too, just 1515 TB badgers out of 11,000 culled. But, early Unconfirmed reactors are less infectious, probably do not produce infectious cow pats (Dunnet 1986 para. 60), so NO Spillover to these badgers. In the early 1990s in Wilts, 2 in 3 breakdowns were Unconfirmeds, so 2 in 3 badger culls produced none with TB !

The numbers of cattle reactors preceding TB badgers found in the RBCT 10 triplets first culls (Woodroffe 2005) were :-

A, B, C, D, E, F, G, H, I, J ..............................

57, 70, 62, 187, 34, 14, 23, 36, 154, 215 total 852.............

8, 13, 14, 102, 29, 13, 29, 12, 82, 65 total 357..............

The last 3 Recruited, AFTER Foot & Mouth Upsurge in cattle, D, I, J , had the most spillover TB badgers .

Strikingly, the Avon, Cornish, Glos. Sussex & Staffs population studies found only 1-2 TB badgers / clan ..23 out of 32 clans , or in 168 RBCT culls. But, if there is only 1 "more infectious" Visible Lesion cow in a group of 20, then only 5 out of a scatter of 100 cow pats in a field will be infectious to the 1-2 badgers in the 6-12 strong clan unlucky enough to find Dor beetles etc under those particular TB point source pats infectious for up to a year . During dry summers, with worms aestivating underground, badger scats can contain 70 + Dor beetles. "Fossil" cow pats obvious from tufts of greener ungrazed longer grass ! Unsurprisingly, pigs /wild boar being "dirty feeders" have caught Mycobacterium bovis, avium, tuberculosis, microti, caprae, etc ...........badger likewise with records of bovis, avium, & the Johnes paraTB variant, microti, chelonei, xenopi (ICMB 2009; Windsor 2015).. but like badgers, are "dead end" spillover hosts, no evidence they can spread TB back to cattle.

Interesting that Irish badger clans may have up to 3 different M.bovis genotypes (Costello 2006 ; RFLP/VNTR) from 3 different previous herd breakdowns, similarly, some farmers buying up cheap cattle to use up spare grazings, may end up with up to 6 different M.bovis Spoligotypes in the next breakdown (Krebs 1997).

DEER (16, 17 , Ward 2012). The modelling idea that GB deer may be a self-sustaining reservoir rather foolishly Assumed 5 % might be due to deer, so "proved" deer might cause 5% of TB herds. But in truth the tiny numbers of TB deer have obviously only been an occasional sporadic spillover from cows. MAFF found just 30 TB deer in a sample of 1960, 1972-96; 12 fallow, 9 roe and 9 sika... DEFRAs recent survey found the most TB deer, in the commonest species locally..even 1 muntjac; and with the reappearance of TB on Exmoor, now red deer too affected, also Cumbria & Scotland farmed reds. Aetiology is clearly by ingestion from contaminated pasture , lesions in head (retropharyngeal) & gut lymph nodes (Johnson 2008). Secondary lung lesions rare, so spread to other wild deer improbable Perhaps surprisingly in New Zealand, despite widespread TB in several introduced wild deer species they are not regarded as a major source of cattle TB, simply because there is little evidence that limited "contact" could transmit the respiratory disease. It is doubtful if shared supplementary feeds with Michigan white tailed deer could give cattle TB either, dust inhaled in experimental studies (Palmer 1999, 2004 ). TB can be self-sustaining in high stocking deer farms or deer parks in N.Zealand, Sweden, Eire , GB, and the USA and Canada ( Clifton-Hadley 1991; Griffin 1994; Partridge 2008; Stuart 1988; More ed. 2006 ).


PERTURBATION . Since decades of badger culls have failed to stop the spread of TB to an area now of 1/2 of GB Godfray still implies that since badgers supposedly may cause 50 % of herd breakdowns , "Culls can affect the incidence of Confirmed bTB in cattle; and the idea has gradually become established that this failure must be due to perturbation:- (14 a, 31, 32; Macdonald 2006; Carter 2007; White 2008). "Culling badgers disrupts social structure.. so increasing disease transmission to other badgers and to cattle ..consistently increased the prevalence of M.bovis in badgers ...especially marked in the RBCT cull re.weaker barriers, close to area boundary .. culls not simultaneous . Hence the prediction that a 70 % cull of badgers in 150 over 5 years would after 9.5 years have a net benefit reduction of bTB, of 12-16 % (- 27 inside, + 25 outside) hence preventing 47 out of an expected 292 breakdowns; so further culls and/or vaccination may be necessary even if culls may make things worse (14 a, 19, 30-34, Box 2 ):-

These conclusions are a rather a selective interpretation of the data:- ISG 2007 clearly realised the doubling of badger TB prevalence was due to twice the spillover from cattle TB after the FMD 2001 upsurge , even in "Unculled " RTAs , (Woodroffe 2006, "cattle pose risk to badgers"); the non-simultaneous culls were at this peak jump; hard boundaries ?; lowest jump eg. in Lands End triplet F, the longest on annual testing (see Spillover numbers above)... badgers can swim over rivers eg. Harris/Cresswell Bristol study, and badgers immigrated across both the M4/M5 to recolonise Thornbury; and it is simple maths, most of the badgers were removed in inner small area initially, inevitably more in outer bigger areas nearer edge in later culls, which had just had the doubling spillover from cows .

The Results of the RBCT 1998 - 2011 are shown in BOX 2 ... BUT , the "Perturbation Proof" seems to be overlooking a few flaws; as regards both proactive and reactive culls. The BOX 2 Graph summarises confirmed results for PROACTIVE culls :-

YEAR .............................1998-2002 // 2007 // 2008 // 2009 // 2011

OUTSIDE 2km ring........ +43.............//-25.....//+38....//....0.......// -10....


INSIDE Cull area ............0...............//-50....// -25....//.....0....// -10....

PROACTIVE CULLS, the 2008 brief outside rise (38 % ) was clearly a one off with maximum of 40,000 reactors for GB, due mainly to bringing more areas back into annual testing ; so the 43 % START "rise" (10 triplets enrolled in different years 1996-2002) was merely accumulative ( heavily skewed by triplets D,I ,J rise above ) of the FMD increases, and was before the culls happened , so not due suddenly to perturbed badgers ( it takes c. 1 year for cows to become reactors, so a cull effect would not appear within 3 months ); hence it took longer for these cattle controls to reduce TB outside by 2007;

BUT in fact these cattle controls had a greater effect in the longer term since fewer baseline herds ..outside vs inside 1998 to 2007 a 70 vs 49 % drop, and 2007 to 2011, a 42 vs 4 % drop. NB cattle controls brought both outside & inside areas back to zero in 2009, with an identical final drop by 2011. ALL these Outside rises (in Box) cross 0, = non-significant ie. a random blip By Chance ; how are badgers immigrating INTO cull areas supposed to cause the rise in 2 km outside ring ?; Worth remembering that the dozen or so previous cull studies occurred when TB levels were falling, so none showed any "perturbation" effect, the RBCT cull was the only one during a widespread foot & mouth induced rise. The interim ISG reports actually showed this rise both inside and outside ALL the cull / no cull areas, so rather dubiously unscientific to focus just on reactive & the 2 km outside proactive ring.

REACTIVE CULLS, again the (22 %) rise happened before the culls; there was a rise in the Wilts. Triplet E, Perturbation study (DEFRA Report SE 3108) in both cull / no cull areas , which was clearly due to imported cattle, with a different DNA Spoligotype to that in the previous cattle / badgers !

DO CULLS "work" ? Previous culls did Not actually reduce cattle TB or stop its spread ( 34) .Cattle controls had virtually eradicated TB ..before gassing started in Thornbury, Avon and Steeple Leaze Dorset (Clifton-Hadley 1995; Little 1982); and the 40 % drop occurred nationally not just in gassed areas (Dunnet 1986). It seems rather improbable that a 50 % drop in Irish cattle TB was due to the removal of just 148 TB badgers from 550 in East Offaly; or 286 TB badgers from 960 in the Four Areas trial (Eves 1999; Griffin 2003, 2005; Kelly 2008, 2011); just 30 from 250 in Donegal where the 97 % "drop" actually reflected a flare up in a cluster of contiguous herds in the reference area (Olea-Popelka 2003 ) . Godfray in summarising the RBCT results noted the " LARGE uncertainty as regards the figure of 50 % "due to badgers"; which sugested an extended cull might reduce bTB by 12-16 % (Box 2) (which) is currently in review " (14, bibliography); Donnelly Oct. 2013 Plosone reduced it to just 5.7 %. NB. the Final ISG Report 2007, p. 103 clearly concluded by 2005, it was - 116 inside / + 102 breakdowns outside proactive areas (with perturbation) so a NET difference of just 14 fewer, or 1.4 breakdowns per 190 In fact , the True result of the RBCT cull of 11,000 badgers ( raw data in Sections 4 & 5 , in ISG 2007; ..see Appendix 7, in ) was that there was NO Difference between accumulated breakdowns 1562 vs 1668 herds, cull vs no cull areas, a mere 10 / 200; IF the cull caused a 50 % drop then there should have been 834 vs 1668, and if perturbation caused a 25 % rise it should have been 2032 vs 1668; so there was in fact no positive "beneficial" or negative "detrimental" effects of the cull after all (Donnelly 2007); Cattle control effectiveness was the cause of these statistical trends, with both inside/ outside areas returning to ZERO by 2009 in Graph !;


PILOT BADGER CULLS. It is a pity the IEP Independent Expert Panel , and Natural England monitors/licensors; allowed the two 2014 Pilot culls to go ahead....numbers culled, Glos. 274, Somerset 341; which with 2013's 1879 came to 2494 total , with less than half the "required" apocryphal target of 70 % of a largely unknown baseline badger population in Glos.; due to animal rights protestors disrupting shooting of "free running badgers" (extra policing wasted several million pounds). Of these extrapolating from RBCT figures, maybe 400 TB +; but at most 25 super-excretors which Might have been a risk to other badgers or cattle; from c. 300 which cannot possibly have made the slightest difference to cattle TB . Alas, Chief Vet Nigel Gibbens & Minister Liz Truss seem to think another 2 years worth of these Pilots will "help" .. since farmers still think they are "essential" to stop TB spread !

PILOT BADGER VACCINATION. "It is reasonable to expect a reduction in cattle TB but there has been no trial yet to assess the magnitude of any effect (36). Donnelly Oct. 2013 (Plosone).. noted vaccinating some 5000 badgers in the Glos. BVDP /Badger Vaccination Deployment Project, or Welsh IAA/ Intensive Action Area ( 1300 vaccinated in 2014; an eye watering ? 650 / badger) , has had no demonstrable effect on cattle TB. Although neither trial completed yet, it would surely be easy even now to show that there is no difference in the accumulated number of new breakdowns in trial areas compared to equal sized non-vaccinated areas nearby; so continuing these costly trials utterly pointless . The Kilkenny Eire trial too has so far had no demonstrable effect (Byrne 2012).

In the National Trust, Killerton Estate (Exeter) trial there were 6 new herd breakdowns in 2014; so vaccinating c. 539 badgers (most of population ?) in 20 did NOT stop this incursion (36, bibliography). The ? 2 million Lands End Pilot vaccine study will fail too; this was Triplet F , but the RBCT cull found only 118 TB badgers out of 1614 culled over 200 hardly a major TB source.

Ring vaccination (Chambers 2013) in Edge areas would be sensible if badgers really are the main cause of TB spread; but Donnelly 2013, suggests they might only account for 5.7 % of breakdowns, so the other 94.3% must be local spread by brought-in cattle, so ring vaccination spectacularly meaningless ! And a monumental wasteof ? 25 million from the EU , December 2014. The ultimate absurdity as regards the widely favoured badger (BACVI) "vaccine solution" is that vaccination does not stop badgers from catching TB , so the whole concept is flawed from the outset (Chambers 2013; Lesellier 2012).

CATTLE VACCINATION + DIVA Test . Sad this has been available for over a decade, but DEFRA wrongly thought trials were not possible in GB under EU rules (EFRA 2013); so the Ethiopian trial found a 56-68 % drop (35). Current local 10 year trial in GB with DIVA test (distinguishes infected from vaccinated) for licensing validation underway . A great pity it is not being used as part of routine cattle controls eg. in whole counties ( accepting no possibility of export).. this is "TVR" for cows instead of badgers, Test, Vaccinate healthy ones, & microchip, Remove infected reactors (Mike Rendle ).

It is blindingly obvious that Badger culls, vaccines, fertility controls will simply never work; because embarassingly, badgers cannot possibly be the "Problem ". Or, as vet David Coffey noted back in 1977; Political expediency pursued way beyond the point of absurdity. A Wonderfully Insane "Solution" to a Non-Existent Problem !!


The twin goals of both the 2005 New Strategy, and the 2013 Eradication Strategy were to A. reduce the level of TB in High Risk Areas ; and B. to stop the spread of TB from these hotspots to Edge and Low Risk areas . Purely cattle measures Will work:-

A. Pre-movement testing , 2 clear tests to derestrict both confirmed and unconfirmed breakdowns, remove Inconclusive reactors at first re-test , avoid testing around calving time, greater use of IFN and ENFER/ENFERPLEX tests for early /late cases and of PCR /Spoligotyping in tissue sample confirmation of TB, cattle vaccination across whole county trials (as above), it will be politically unacceptable, but it would make sense to include recent TB testing results as an MOT certificate on cattle passports, as in Ireland the IT cattle TB database could be greatly enhanced so that at a click of a mouse TB history, neighbouring farms, movements etc would enable much more precise rapid targetting of problem herds;

B. pre- and post-movement testing, quarantining a 5 km ring around new breakdowns until index herd and neighbours test clear, 4 yearly testing in Low Risk Areas is too long.. a couple of years of annual testing needed to discover whether area is really TB-free (as in Wales from 2008).

Fig2 Fig3


1. Hancox M.;
A. WWW.BADGERSANDTB.COM, SEE "Death of Great Debate" new section ; and NB ALL cited authors above, are given in References there ;
B. Ev W8 mss in EFRA Committee, 2013, Vaccine Report, www.efracom.parliament ;
C. articles in LAM Lett.Appl.Mic.; RM Resp.Medic. cattle TB schemes 2000, LAM 31; 87; 2002, RM 96; 842; 2001, Tuberculosis 81; 185/ 2003, latency, LAM 97;1075 cattle transmission 1999 LAM 28;242; 1999 RM 93;220; badger aetiology 1997 LAM 24;226; Also 2006 J.Agric. Sci. 144;167; 1995 Biologist 42;159
My Wytham Oxford thesis 1973 was used extensively by Ernest Neal, 1977, Badgers & revised 1986 Natural History of Badgers With my figures for simple ageing badgers from tooth wear. Nice that in my Cotswold Stroud study area badgers often get to 10 years old, ie. despite "unfriendly" farmers, gamekeepers, the Hunt, so live to natural old age, sadly Ernest Neal's Rendcomb/ Cirencester setts are often illegally hard stopped. Interesting that early studies overlooked the earthworm "specialist" diet of many western Europe badgers.. no-one noticed that worm chaetae were easy to spot in faecal samples .. my 2000 scat diet analysis , contrasts with George Barker in Neal also from Wytham, and David Macdonald too found worms in his 1980 study. These Ageing & diet figures are added in web Death of Debate.
2. Godfray HCJ et a, 2013, A restatement of the natural science evidence base relevant to the control of bovine tuberculosis in Great Britain; Proc.Royal Soc.; also Godfray 2004, review of ISG science.
3. DEFRA 2013, New Eradication strategy ; and , both : badger cull consultation (2011) & bovine TB.
4. Four Classics ......Francis J, 1947 , Bovine TB, & 1958 Bovine TB in animals and man ; Myers & Steele 1969, Bovine TB in man and other animals, updating Myers 1940, Mans greatest victory over tuberculosis... Area Eradication ..Macrae, 1961, Symp.Zool.Soc. 4;81; Stableforth 1959, Infectious diseases of animals; Ritchie 1964; Watchorn 1965; Richards 1972, Inquiry into bovine tuberculosis in West Cornwall.
8. AN HISTORICAL OVERVIEW . It seems crystal clear that :-
CATTLE TB is simply a brocho-pneumonia or respiratory "Consumption" caught 100 % from other cows aerogenously ; BADGER TB is dietary "Scrofula ", so badgers are simply a "dead end" spillover host catching TB from cows via contaminated " dirty feeding" turning over cow pats for worms & beetles... with little evidence of spread to other badgers or cattle. Fascinating that a dozen "expert" opinions over 4 1/2 decades of research have overlooked this :-
1. DARD, 2014, DEPARTMENT OF AGRICULTURE AND RURAL DEVELOPMENT ; ULSTER :--" Science has established a link between TB in badgers and TB in cattle. The exact means of spread between the species and the relative importance of potential routes of infection has not been established. The proportion of the disease in cattle which can be directly attributed to badgers has not been quantified ." (Allen 2011 review);
2. DAFM, 2014, DEPARTMENT OF AGRICULTURE, FARMING AND THE MARINE; EIRE :- "Route of transmission not fully understood " ; "Culls , a stop gap measure that will not eradicate TB in cattle; SO, switch to vaccine trials instead, but it will be some years before culling will be abandoned"; and rather absurdly , "Culls, only in areas where badgers are a likely source of infection"........IN Fact, TB most likely to occur in badgers as a spillover FROM bad herd breakdowns, so with superbly irrational circular logic the veterinary epidemiologists investigating, base whether to licence culls or not on how bad the breakdown was !
Amusing that Dr Liam Downey of ERAD TB Unit told the first International Conference on M. bovis, in Dublin way back in 1991, that "OF COURSE, WE'VE KNOWN FOR YEARS THAT BADGER CULLS DO NOT WORK ." SO a tragic folly that culling over 100,000 badgers has not stopped the spread of cattle TB, more than halved the 1990S badger population to no avail. GB too, towards another 100,000 badgers culled since 1971, had nil effect of spread back into TB free areas;
3. DEFRA 2013, admitted , Most recently, IN written response to EFRA Vaccine Report 2013, "We lack precise data on transmission routes";
4. GODFRAY 2013, Proc. Royal Soc., para. 15 :- "Little is known about how M.bovis is transmitted between badgers and cattle .Transmission may be indirect ; for example, through contamination of pasture, feed and drinking water. Alternatively, direct transmission via aerosol droplets at close contact may occur, possibly inside farm buildings as well as outdoors. No quantitative estimates of any of these transmission rates or their relative importance are currently available ";
5.Prof. John BOURNE, Chair of ISG, in the Guardian, 27th May 2013; repeated these uncertainties from the 2007 Final Report, saying "badger culls can make no meaningful contribution to the eradication of TB in cattle", and even suggested that ""Badger infections are following, not leading, TB infections in cattle"... Woodroffe 2006, the Proc. Nat Acad. Sci. paper admitted a doubled spillover cow to badger as a result of the foot & mouth upsurge;
STRIKINGLY, TOO, John Wilesmith (1991, ICMB N.Zealand) was "puzzled" that in the Woodchester Jacks Mirey whole badger clan infection ( from 4 inner ring contiguous farms outbreak), "" the TB peak in cattle preceded that in badgers !!
6. Patrick BARKHAM, 2013 "Badgerlands", noted that "Without conclusive scientific proof of badgers transmitting the disease to cattle " (Phil Drabble); nevertheless, the badger contribution to cattle TB "Might" be c. 30 % , Chris Cheeseman; or 15 - 75 % Tim Roper.
7. ASSORTED Reviews and various research projects have failed to unravel these uncertainties as to transmission, and hence relevance to husbandry, management and "biosecurity" factors .......... Drewe 2013, Allen 2011, TBEG Oct 2009; Ward 2008 and Garnett badgers in barns ; the DEFRA Strategy consultations, 2004/2005; & 2013 ; PHILLIPS 2003 & Husbandry Report to DEFRA & section in ISG 2007 TB99 studies; O'Connor 1993. Studies of transmission also by Benham, Bohm, Brown, Garnett, Hutchings, Judge 2012, Palphramand, Roper, Scantlebury, Tolhurst, Ward, White, Wilson 2011.
8. Tim Roper , 2010, BADGER (New Naturalist) "WE DONT NOT KNOW HOW BADGERS TRANSMIT TB TO CATTLE"; NB. he was one of Independent Expert Panel IEP advisers .. also to Chief "Scientist" Prof. King 2007 enquiry;
9. Prof.John KREBS, 1997, Review , re-discovered ""A LINK" ; but was very careful to state :- ""IT IS NOT KNOWN IF, HOW, OR TO WHAT EXTENT BADGERS MIGHT GIVE CATTLE TB "; Pity , that several co-authors here went on to oversee the RBCT/ KREBS cull trial; WITH the start assumption that badgers DO give cows TB, Culls may bring about a 50 % drop in cattle.
10. Neal & Cheeseman, 1996, BADGERS p. 203; "What proof is there that badgers infect cattle with TB ? The simple answer has to be that there is no scientific proof of a link. It would actually be very difficult to prove beyond doubt that badgers are the source of infection in cattle.. but given the weight of circumstantial evidence .. (research and culls are ) .. based on the Assumption" thatr badgers "ARE" a wildlife reservoir of TB in cattle.
11.HAYDEN, 1993, THE BADGER, (Proc. of the 1991 first International Conference on M. bovis ):- "TB: epidemiological darkness is plight enough ... ""The role of the badger in the aetiology of tuberculosis in bovines is still not quantified , ( and notes ) the lack of even a simple model of pathways through which M.bovis circulates through wildlife and domestic livestock """.............Tom Hayden reviewed the early studies by Benham on the improbability of cows catching TB from badgers : mutual avoidance at pasture ; and by cattle of badger latrines too !... also in Kruuk's The Social Badger;
12. MAFF VETS were perfectly aware of the difficulty in explaining how badgers Might give cows a respiratory lung infection, Dorset study, Little 1982; indeed I recall John Wilesmith saying with frank candour at one early 1990s Consultative Panel meeting, that IF badgers do give cows TB it is such a rare event that for all practical purposes should be ignored !!!.