That was the question posed by Martin Hancox and I enclose his thoughts below - many will know he is a local scientist who has been looking at this issue for many years - see his website:
As I've said before I've not had time to look at the details of this science but have read lots and talked to many people - farmers and vets included - and have been convinced by arguments that question that badgers are the primary cause of TB in cattle - that just does not stand up to scrutiny. Anyway see what you think of this convincing argument - at the very least it warrants proper funded investigations.....
The core rationale behind badger culling is that badgers are The widespread endemic hidden source of TB causing new and repeat herd breakdowns ....BUT this is mainly circumstantial in that no cattle source SEEMS to be present ..hence it is assumed transmission is one-way badger to cattle (Zuckerman p.94, Dunnett para 60, Little 33b , Krebs ) .. and a stated explicitly or implicitly Assumption under-pinning badger-cattle computer models (7, 59, 66). (NB To repeat, cattle supposedly NOT passing TB to badgers, or much to other cattle !).
Astonishingly, over nearly 40 years , narrowly focusing on badgers , and having "forgotten how TB works in cows" NO-ONE Has thought to check whether there were enough TB badgers "out there" or if cattle really can catch TB FROM Old Brock : - ALAS, both "Beautiful hypotheses" would seems to be a couple of Darwin's long enduring "False Facts" !! Addressing these two points,firstly :-
To look at the broader picture, M.bovis originated as a DNA deletion strain caught from humans as M.tuberculosis when man switched from hunter-gathering to farmer in Mesopotamia with a rise in towns and cities (New Sci. 17 Oct 2008, Israel). Bovine TB first arrived in GB with cattle imported by the Romans &/or in the 17-1800s from Europe ..so not endemic in badgers until then ! (18). Cattle still catch human TB in India & Pakistan, in Poland (Pavlic Vet Mic 112;221), and previously Finland thereby upsetting skin test controls. Ironically, humans with bovine TB can also pass it to cattle cases in : Czechoslovakia, Denmark, GB, Germany, Netherlands, Norway, Sweden, recently Switzerland; Canada, USA, N Zld (54 b). Indeed Grange estimated that this might be half by aerosol, and half by folklorist "urinating on feedstuffs to improve mineral content" ; Shades of badgers in barns below!
Very valuable insights on TB transmission arise from comparison with human TB (WITH the critically important difference that in cattle "closed " lesions do not arise, so lesions are progressive/infectIOUS throughout ) (Francis 1958, Myers 1968 but Not Gallagher 2005). Thus, human TB can be acquired either by inhalation Consumption or Phthisis ; OR by ingestion formerly from unpasteurised milk Scrofula with swollen neck glands (Sadly STILL a problem in less developed countries eg Mexico, Africa).Its been known for a century that any mammal can catch bovine TB , but routine abbatoir inspection of millions of cattle, sheep and pigs to safeguard the human food-chain , and study of other species suggests that TB may be either mostly respiratory, or "dietary" (Francis 1958, Dannenberg).Hence the Primary complex lesions are either in the lungs, draining to pulmonary lymph nodes (bronchials ,mediastinals) ; OR in head lymph nodes : submandibulars, tonsils draining to retropharyngeals ,less commonly around gut (mesenterics, ileocaecal with M . avium in deer)... BUT With Secondary lesions in highly vascularised lungs (badger),kidney,(badger & man), meninges, periosteum (badger, dog etc 18 a).
Thus A. Cattle TB is c. 90 % respiratory, 10 % by ingestion (2ndary lesions in lung without necessarily in pulmonary lymph nodes (9 b, 18, 22, 31, 39, 40, 41, 42, 54 b).And being long lived social herd animals, TB is self-maintaining within herds , often with recrudescence from latent cases Section 2. Enormous numbers of bacilli shed in sputum/faeces, uterine discharges, milk if udder TB (18).Cattle TB is mostly a respiratory consumption , a bronchpneumonia caught simply from other cattle as with other "pneumonias" be they viral PI3,RSV,IBR,BVD /bacterial Pasteurella, Haemophilus,Mannheimia / or Mycoplasmal (including the pleuropneumnias). So, being 90 if not often 99 % respiratory it cannot be mainly from badgers !
B. Sheep TB is very rare because theyre mostly outdoors all year.They dont usually catch TB sharing pasture with TB cattle (nor do selective grazing but otherwise very susceptible rabbits , 11 b), since the minimum dose is c. 13 million bacilli (18).Interestingly high levels in N Zealand may be because puss from open skin lesions in possums on pasture contain 5 million bacilli/gm(68), otherwise cases are either rarely where sheep share barns with cattle (Germany, Uganda, Malone poster 10 Dublin ICMB 4), OR orphans reared on unpasteurised milk (ditto hedgehogs, foals etc in the past ..pasteurisation brought in to stop batches of calves/piglets getting TB originally !).
C. Pigs are the classic example of a spillover "Dead End" host (do not pass it on to fellow pigs or other species). They may catch bovine, human or avian TB by "dirty feeding" but its not self-maintaining , dies out when souce eliminated . Feral pigs hence not a problem eg in Australia , nor mostly N Zld .But useful "sentinels" tracing to otherwise missed herds in USA , and for residual possum TB N Zld after culls.Coyotes are currently indicators of TB in Michigan White-tail deer; badgers have been seen as sentinels for "missed" cattle but in several cases outside southwest hotspot areas, TB was absent in the local herd/s check-tested (beef finishers since gone to join Big Macs !
Wild boar are increasingly blamed as "wildlife reservoirs" of TB, but like farmed/feral pigs may be spillover hosts catching M. bovis, avium, caprae, microti ...including bovis in Cornwall, France,Italy, Spain (high density population May be slf-sustaining ?), and elsewhere in Europe (ICMB5 abstracts 2009). African warthog too get bovine TB...praps thats M africanum ?
Deer are increasingly also blamed as a wildlife TB reservoir, but any species may catch it if in contact with TB cattle (Vet Rec 129;5) . In GB 1972-96 out of 1960 sampled there were just 30 with TB :- 12 fallow, 9 roe, 9 sika. Similarly a DEFRA 2008 study (Paterson) from the southwest out of 719 sampled there were 24 fallow, 2 roe, 1 red... other recent cases in muntjac, and a few red deer on Exmoor (13 b). Clearly they are merely a spillover from cattle ,the species affected being merely the commonest deer locally , and not a maintenance host even in N Zld . Only become such where high stocking & increased close contact occurs eg White tails Michigan , or farmed deer eg Sweden imported from UK .
The two Key Factors determining transmission are dose and a credible route, with 4 main possiblilities discussed below : -
a. aerosol ; b. faeces/urine ; c. other "congenital" . THUS : -
It is widely recognised that a single bacterium may be enough in animals ranging from mice to men, via rabbits to cattle .More likely 5-6 bacilli as a cfu or colony forming unit which would fill the smallest sputum droplet in aerosols most likely to remain airborne long enough to be breathed in by cattle or man (11 b, 12, 22, 52 b, 54 b ). Estimates of sputum positive cattle in studies from Argentina, GB, Germany, India,, Ireland, Netherlands range from 0.7 to 20 % , INCLuding cases WithOUT Visible Lesions (22, 40 and see Appdx 2 f Kissing cows , 47, 64 ). However, detecting bacilli in sputum smears is notoriously difficult in cattle or man (minimum of 100,000 bacilli/cc needed ?) :- so 399 out of 400 clinical sputum + cases were VL (60).Bacilli were present in faeces from swallowed phlegm in over 50 % of cases inoculated into guinea pigs , so cattle may be infectIOUS at Any stage of the disease (18 a ). Aerosolised dust may be nearly as effective as sputum droplets in cattle yards/barns (18).
Transmission is most likely with prolonged exposure ... in one school study a minimum of 130 hours shared classes was necessary to catch TB from the index case (53 b, Ewer).Hence over-wintering in poorly ventilated dark barns or yards is the most risk scenario; although TB spreads in herds never brought indoors eg clustering round waterholes in africa or australia, also in Cape Buffalo herds Kruger Park. In a barn experiment of elegant simplicity a century ago Svensson found that 5 calves were reactors within 6 mnths, the other 8 within 12 mnths (39);similarly, c. half the contact cattle were infected within 7 mnths (ISG;235); and so latent newly affected cases which are still test negative at spring turnout end up later as reactors "Due to encountering badgers again "!!. Experimental studies of in-contact cattle transmission reveal that it may take around a year or so for "low dose" ie "naturally infected" cattle donors to become infectIOUS and pass on TB (22; also 5, 6,10,38,47 b, 52 a .. Gopal to home bred cattle in ISG;143 ... badger/calf yard experiment 33 ). Doubts over cattle-to cattle transmission have arisen simply because with annual testing underway in most schemes since the war ( 60 yrs) MOST cases are caught before the more infectious VL stage ..thats how eradication works ! .. (Section 4, 22, 24, 29, 42, 52 b ).
N B ...Experimental high dose studies produce misleading results with APParently early infectiousness (6, 29 ,38, 44 ) AND similarly many dont seem to realise that in both cattle and man with advanced TB , the steady stream of coughed up/swallowed bacilli causes secondary lesions in larynx, tonsils, retropharyngeals, lower gut and mesenterics , and probably kidneys ? (18 , 6).
Chris Cheeseman found very little spred even within badger clans with a lung hoocher present , so badger to cattle aerosols in barns a non-starter .
B.FAECES AND URINE TRANSMISSION ?
The various studies of badger to cattle transmission have been focussed mainly on the "risk" from excreta such as urine, faeces, sputum ; either at ; latrines or urination marking crossing points through hedges etc 2, 3, 4, 26, 28, 56, OR
in barns Little, Macdonald , also 20, 55, 58, 63 & Grange as above .
Ironically Littles' study is the Only Proven case of badger-cattle spread in nearly 40 years . And badgers evicted by territorial mates may end up in barns .. 1 or 2 cases annually of sub-dominant young sows having cubs theyre when ousted from the main alpha pairs' main sett (as in meerkats, or wolves). The particular difficulties with such studies are re Dose needed and bacillus survival .
l.Dose, shedding of bacilli may reach 4 billion /day in man so easy to see how plane travellers breathing recycled air at 30,000 ft can get TB on even short flights //possum pus from open skin wounds may have 5 billion bacilli / gm, so inquisitive nosing of moribund possums by cattle or deer a plausible transfer (ingestion though ?) //38 million bacilli in 38 lbs of faeces /day in cattle in one old study ..probably far higher with advanced clinical cases (18) // so badgers with 300,000 bacilli in urine, or 200,000 in faeces or sputum rather a low risk comparatively .
Infective Dose ; - minimum needed in cattle estimated as 400 million M'Fadyean in 22
several thousand million or 10 million (Sigurdsson ) in Francis 1947,
5000 (53, NB pattern of lesions suggests may have been respiratory)
SO , IF the minimum dose is c. 1 million bacilli (39) that would be c. 3 cc of badger urine which seems an unlikely transfer ...unless a sick badger with kidney TB left puddles in barn feed troughs and a cow deliberately seeking extra minerals drank it ! Far more likely are rats visiting barn feed troughs from neighbouring farms , and a faecal/urine /frass with cattle pellets gets inhaled .Most folk dont realise that rat TB presents as numerous micro-lesions "miliary" TB Yersins phenomenon, so overlooked in most studies 13 b ... more rats than humans in GB !
Francis found that cattle rarely caught TB from other cattle at pasture, but often did when first entering the cowshed & breeding herd (18 a , b). Confirmed by studies of limited spread by super-contamination with fresh slurry (37, 57).Suggestions that lung infection can arise by burping of rumen gases (eructation ) from ingested feedstuffs unconvincing (46, 62).
Cattle avoid grass contaminated with faeces hence the random scatter of dark green tufts marking former cow pats in recently grazed fields. Likewise cattle may avoid smelly badger faeces and even when short of grazing dont get right down to scat level in dung Pits (2, 28). As regards badger urine, one urination may be 30 cc hence c. 9 million bacilli, but 99 % disappears soaking into the soil, any residual TB on pasture may be disinfected within 3 days in summer, or for sputum 1 week, faeces 2 weeks , about 1 mnth each in winter but cattle in yards then anyway ; badger carcases self-sterilise within weeks also (34, Krebs p.50). Whilst it is often stated that bacilli can survive up to 2 years IN soil (away from UV light), in practice any badger sources accessible to cattle are likely to be of improbably short duration (22).
C. OTHER . "Congenital" , where cattle schemes are absent cattle with advanced clinical TB may transmit trans-placenta in utero but despite huge numbers of bacilli, relatively few cases by this route (calf a reactor at birth).Bulls may have genital TB eg in semen , but hire bulls more likely to have lung TB and spread respiratory (18a ).Far more likely "congenital" spread is via udder TB , a very efficient way to infect batches of calves via bulked milk ; pasteurization first introduced to stop batches of calves/piglets getting TB , only latrer used for human supplies ( 18, 39, more recently 5, 15, 43, Trioni herd Wales ).
B. TB IN BADGERS : PATTERNS AND NUMBERS
Having concluded back in the 1980s that transmission was one-way badger to cattle, it became "accepted wisdom" that badger TB was 82 % respiratory and 18 % by bite wounds (7 c,d, 61 ). But even experimental thigh injections lead to secondary lung lesions (25); and just as with human miners , living underground , badger lungs may be prone to TB due to silicosis (18b, 27, 49), or other damage via adiaspiromycosis or Capillaria lung worms .
Cheeseman found little evidence of spread within groups even with a lung "hoocher" present, and badgers often sleeping in a heap in the bedding filled nest chamber (Badger Watch TV programmes ).Hence usually only 1-2 TB badgers /clan ( 7a, Krebs p.48). A hoocher sow is most likely to achieve pseudovertical transmission by weaning her cub/s on regurgitated earthworm soup with TB flavouring . There are very few sputum + badgers, so fighting wounds more likely to be infected by sett contamination.
So, does the traditional claim that the main hidden reservoir of TB is a widespread, large , endemic /self-maintaining badger TB source with one-way badger TO cattle transmission stand up // Sadly NO ... CONSIDER the following 5 points : --
1. badgers seem to be merely a spillover host just like "dirty feeding" pigs above, catching whatever Mycobacterium spp are available .. including , bovis // avium Zuckerman p. 89// paratuberculosis m.avium, MAFF rept 4;15//microti Moser ICMB 4 ;60//and chelonei 36.
2. a critical reappraisal of badger lesions suggests that in the majority of badgers TB is by ingestion . Most studies note submandibular lymph node lesions (under tongue, which may self-heal thereby hiding the true aetiology , 1) ; and with secondary lesions in lungs and kidneys (QV pig) :- l, 7, 8, 9, 14, 17, 19, 21, 25, 26/ 29 ISG p.77/ 30, 33 a,b , 36 ,48, 49, 50, 59, 61, 65.
Early lesions most likely reveal acquisition pathway , whether in cattle (18a, 40, 41 )or badgers . O'Boyles superb study (50) of some 25,000 Irish badgers culled under licence 1997-2006 show lesions in 3301 cases , clearly separating those with early single lesions //later TB multiple lesion cases (up to 8 sites) per badger . Thus :- (l.n.= lymph node) ...
Ingestion submandibular, pharyngeal,parotid l.n. 518/813 ; submaxillary l.n. 7/0 ; mesenteric l.n. 14/92 ; liver 33/128;
hepatic l.n. 35/179; spleen 1/34; kidney 84/193
Inhalation lung 214/ 602; bronchial,mediastinal l.n 329/830
skin (bite wounds in territorial fights often neck , above tail ) axillary l.n. 22/72; prescapular l.n. 142/442 ; popliteal 298/ 407 ;
inguinal l.n. 7/3 ; skin 56/165
Other :- 1 testes, 1 placenta, 1 mammary gland (so little congenital spread ) ; 1 tonsil, pleura, peritoneum, omerntum, heart/pericardium, adrenals .
3.endemic high density badger population ? TB may be "endemic" within a clan in so far as an infected long lived individual is present (7 a,c.d ; Krebs p.48); but TB nearly died out in the Woodchester study population in 1984/1993 (13 b). Modelling attempts to explain the persistence of TB in populations such as by threshold group size fail to recognise the error of the original solely badger -cattle transfer assumption, and badger TB prevalence simply reflects spillover via the severity of the preceding cattle breakdown (59 b, 29)...with prevalences ranging from 0 to 100 % (7a, Krebs p.46 , 67 , see Appendix 3 b ). A bad breakdown in four "inner ring" farms in Woodchester in the mid-1980s with over 90 reactor cattle spilt over to a new clan (13 b, 48 ); hence cattle TB "Seemed" to peak BEFORE that in badgers !! (65) .
4. Not surprising then that badger TB levels in the 1980s were c. 15 % from culls, but under 5 % from RTAs. The clean ring culls clearly showed a random scatter of micro-pockets of TB badgers at the epicentre of the farm breakdowns , but not in the intervening area (see Appendix 3 e). The dramatic shrinking of cattle TB from countrywide in the 1950s down to tiny southwest hotspots (of high density dairying ) seemingly left NO RESIDUAL TB badgers (died out ?) (Section 4 ). Hence the survey of 23,032 RTA badgers 1972-96 found 1066 with TB , of which 942 were in the 7 southwest hotspot counties (Cornwall, Devon, Avon, Glos, Dorset, Somerset, Wilts ); the rest in Herefd./Worcs, Sussex, Staffs, Dyfed, Gwent, 1 Glamorgan old record), just 1 in Scotland Lothians (34):24 counties with additions since of Derbyshire, Powys, probably to be discovered Leics, Yorks.
The textbook expansion of cattle TB since the mid-1980s (Section 4) is beautifully documented with Krebs report colour maps pp.. confirmed breakdowns 57, unconfirmed more widely 156-7, repeat breakdowns 58, 91; as reflected by expansion of TB badgers via culls/RTAs 165-8 ; including DNA spoligotypes of cattle then badgers 67, 173-4 (cf.Ireland , 51). The RTA southwest hotspot 1972-90 (Cornwall, Devon, Glos) has "moved" to least controlled cattle TB AREAS : Herefd/Worcs. Powys in recent English/Welsh RTA surveys (ISG p.75, 83-4).
5. a. Too few TB badgers to be a major reservoir
RBCT /Krebs cull only 1515 (311 reactive, 1204 proactive) out of 11,000 culled from 2000 sq.km (see Table Sect.6 (3))
Offaly cull only 141 out of 1232 culled in 600 sq.km
Four areas cull only 450 out of 2360 culled , but only 240 VL possibly infectious , and adjusted to exclude buffer zone ones
just Cork 115, Donegal 37, Kilkenny 59, Monaghan 75, ie just 286 out of 960 sq.km. (24 b).Just 37 TB badgers in
Donegal with an alleged impact on cattle of 96 % (BUT in fact a flare UP in reference cattle !) (24 b,51 b)
b. Too few infectIOUS badgers :- Woodchester, study since 1970s , c. 300-350 badgers in 9 sq.km with clinical sampling of live badgers , yielded only 49 excretors by 1990 (37 % with urine TB)(65) ; later on over 14 years just 188 were
infected of which 41 were infectious and 17 superexcretors (the only ones usually suggested as capable of passing on
TB ) (59 a).
The RBCT cull of 11,000 badgers found just 166 superexcretors out of 9919 detailed autopsies (ISG p.77, 30).
In CONCLUSION , MAFF admitted back in 1982 that it was far easier to explain how cattle pass TB to badgers than how badgers Might give cows a respiratory lung infection (33 b). And as MAFFs' John Wilesmith said at a Consultative Panel meeting c. 1992, if badger to cattle transfer happens at all its such a rare event as to be little practical relevance !
Whilst the "first" official TB badger was in 1971 in Glos, 1975 in Ireland , in fact TB badgers occurred at London Zoo in 1938, at Whipsnade in the 1950s (now at Edinburgh museum ); the first wild TB badgers in Switzerland caught it eating infected roe deer as a last spillover from cattle in the 1950s . Some 50 % of Ulster badgers had TB in the 1970s , but were regarded merely as a spillover host ; Thus Nobadger culls , yet cattle controls nearly eradicated TB by 1971 just 174 reactors (see Appdx 3 e )..alas premature switch to 3 yr tests allowed upsurge. TB has now been found in badgers in Spain , Italy .. further search eg in Poland ,Russia etc might find more.
Interestingly, with 20 : 20 hind-sight, the mysterious coughing illness which decimated some clans back in the 1935-60s era in Glos., Hants, Shropshire, Surrey, Germany , Netherlands was probably TB but unrecognised back then ! ( Mamm.Rev. 10;151).
Thus it seems crystal clear that CATTLE TB is a respiratory "Consumption" caught mainly from other cows , and NOT mainly from badgers ..... BADGER TB is essentially a "dietary" "Scrofula" caught by spillover FROM cattle, with little spread to other badgers , let alone TO cattle . AND there are simply too few TB badgers and even fewer likely to be infectIOUS by some unexplained route to cattle .. for them to be even a minor reservoir contributing to cattle TB .
SOooo alas Old Brock dead end spillover : Victim not Villain !
REFERENCES (NB. IF these shortened citations are unclear, just ask : hancoxm(at)live.co.uk)
1 Anderson 1985 Phil Trans R Soc 310; 327 model and lesions
2 Benham 1989 Br Vet J 145; 226, 1991 Br Vet J 147;517, 1993 in Hayden ;189 ... latrines
3 Bohm 2008 Ecography doi , & J An Ec doi , & White Trend Mic 16; doi ...2009 Plosone 4 ; doi ....latrines
4 Brown 1994 Trend Mic 2; 43 .. 1993 in Hayden; 139 ..latrines
5 Buddle 1994 N Zld Vet J 42; 167 experimental transfer
6 Cassidy 1999 J Comp Path 121; 321 (& 119;27) lesions exptlly, Vet Rec 144; 139 tonsils
7 Cheeseman a. 1981 J Appl Ec 18;795 4 areas / b. 1985 Mam Rev 15; 125 Staffs /c & d. 1988 Mam Rev 18; 61 , 1989 Epid Inf
8 Clifton-Hadley 1993 Epid Inf 111;9 lesions
9 Corner 1990 Aust Vet J 67; 389 cattle lesions , 2006 Vet Mic 112;303 badgers etc
10 Costello 1998 Vet J 155; 245 calf expt
11 Dannenberg a. similarity man/animals 1984 Microbiology ;344 ; b. also in Tuberculosis 2001, 81; 87 rabbit models
12 Dean 2005 Inf Immun 73; 6467 dose by aerosol
13 Delahay a. 2000 J An Ec 69; 428 Woodchester ; b. (other spp) 2001 Tuberculosis 81;43 & 2007 Vet J 173;287
14 Dolan in Hayden ;108 lesions
15 Doran in ERAD 2006-7 papers milk TB
16 Dunnett et 1986 report
17 Fagan in Hayden ;117 lesions
18 Francis a. 1947 Bovine tuberculosis ...b. 1958 Tb in animals and man (NB Myers & Steele same 1968)
19 Gallagher 1976 Vet Rec 98;9 //1979 Vet Rec 105;546 // 1980 in Zuckerman // 1998 Vet Rec 142;710//2000 Res Vet Sci
69;203 // 2005 Vet Times 35;14 // 2009 Cattle Practice 17;45
20 Garnett 2002 Proc R Soc 269; 1487, 2003 appl An Biol 80;1 , (2003 see Roper) ... barns
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22 Goodchild Tuberculosis 81; 23 cattle-cattle spread questions
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25 Hancox both cattle & badgers see Section 7 "my refs" ; & Appdcs 3 b & c ( & Mam Rev 10;151 parasites and diseases )
26 Hayden 1993 The Badger (ICMB Dublin 1991)
27 Higgins 1985 Inf Immun 48; 252 silicosis
28 Hutchings 1997 Vet J 153; 149 ... 1999 Epid Inf 122; 167 .. latrines
29 ISG 2007 Final Report
30 Jenkins 2007 Epid Inf badger lesions doi
31 Jubb 1985 Pathology of domestic animals
32 Krebs 1997 Report
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34 MAFF Consultative Panel Badger Reports .. 1979 No 3 // No.4 ;15 paratb // 1996 No 20 summary TB badgers from
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37 Maddock 1933, 1934 see in ref 22 super-contaminated pasture
38 McCorry 2005 Vet Rec 157; 613 exptl transmission
39 McFadyean 1910 J Comp Path 23 ; 239 & 289 an old but valuable classic on cattle transmission
40 McIlroy 1986 Vet Rec 118;718 early lesions and see Appdx 2f Kissing cows
41 Medlar 1940 Am Rev Tuberc 41; 283 early cattle lesions
42 Menzies 2000 Vet J 160; 92 cattle-cattle ?
43 Monies 2006 Gov Vet J 16;81 BVD and TB via milk
44 Morrison 2000 Vet Rec 146; 236 ISG view on " problem" of transmission
45 Moser in Dublin ICMB4 Handbook; 60.. microti in badgers
46 Mullenax 1964 Am J Vet Res 25; 1583 eructation
47 Neill A 1988 Vet Rec 122;184 lesions// B 1989 Vet Rec 124;269 && 1992 Vet Rec 131; 45 calf contacts
C 1994 Vet Rec 135; 134 sputum + D 2001 Tuberculosis 81;79 cattle-cattle
48 Newell 1997 Epid Inf 118; 173 new clan Woodcheter
49 Nolan 1994 Vet Micr 40; 179 lesions
50 O'Boyle ERAD Papers : -- 1997; 37 // 1998; 10 // 1999 ;55 // 2001; 19 // 2003 ;13 // 2005 ;106 :- Badger Lesions !!!
51 Olea-Popelka a. 2005 Prev Vet Med 71; 57 ...b. Donegal ERAD 2006-7;21 & Ir Vet J 59;683
52 O'Reilly 1988 Ir Vet News 10;11 contacts // & Daborn 1995 Tubercle & Lung 76;1 overview incl man See Ewer 2003 in
Lancet 361;1168 school outbreak
53 Palmer 2004 Amer J Vet Res 65; 1483 white tail deer transmission
54 Pritchard a. 1987 Epid Inf 98; 145 lesions Sussex study // 1988 J Comp Path 99; 357 centenary overview whole history
55 Roper 2003 Cattle Practice 11;9 barns
56 Scantlebury 2004 J Dairy Sci 87; 330 latrines
57 Schnelllner .. see in ref super-contamination pasture
58 Sleeman 2008 Vet Rec 163; 724 barns
59 Smith a. 1995 Mammalia 59; 639 Woodchester ... b. models 2001 Tuberculosis 81;51
60 Steward 1941 Vet Rec 53;521 clinical samples
61 Stuart 1988 Rev Sci tech OIE 7; 929 lesions
62 Waldo 1966 J Dairy Sci 44 ;1766 eructation
63 Ward 2008 Vet Rec 163; 107 badgers in barns
64 Whelan 2009 in N Zld Handbook abstracts ;136 .... Also Conlan ;58 RE-Think assumptions latency/infectiousness
65 Wilesmith 1991 N Zld Symposium ;95 lesions & Woodchester
66 Wilkinson 2004 J Appl Ec 41; 492 models
67 Woodroffe 2005 J Appl Ecol 42; 852 patterns badger TB , dont accept VL cows more infectIOUS !
68 Zuckerman 1980 report