Part 1. TB Transmission In Cattle and Badgers : - A Critical Review

The Foundation Stone of the whole badger TB saga arose from finding 1 dead badger with TB in April 1971, near Wotton-under-Edge in Glos. , then further moribund or in extremis cases associated with breakdowns. Ironically the initial farmer thought the breakdown came from the contiguous herd , not from badgers ! ""Because OPEN cases of tuberculosis have been extremely rare among reactor animals.. a wild life reservoir of infection was considered to be the possible explanation for the persistence of this disease "" .. in certain fairly clearly defined intractable hotspot areas from Glos. to Thornbury , Still on annual testing, and with many breakdowns of "Obscure" origin . By 1973 TB had been found in 36 out of 165 badgers, and in just 12 of 112 latrine faeces samples, and atypical badger behaviour included visiting barns and eating cattle feedstuffs (Muirhead 1974). Based on such evidence a decade later, verdict :- "Case Unproven ! (Macdonald 1984). Data from the new nearby Woodchester MAFF/CSL study area suggested TB was self-sustaining amongst the badger population , spread being 82 % respiratory and 18 % by bite wounds (Cheeseman 1988, 1989). Recent reviews by Corner 2011, 2012 again emphasise the "apparent" twin transmission routes. Unfortunately this rather simplistic interpretation of the evidence does not stand up to scrutiny.

Cattle "consumption" and badger "scrofula"

Training of biomedical and vet students nowadays rightly devotes much time to the latest "cutting edge" molecular biology, genomic effects, computer simulations etc so many now lack the solid grounding in anatomy , pathology and systematics of older generations necessary to understand transmission and progression of TB :- aetiology and pathogenesis hence confusion over TB spread in either cattle or badgers ! Based on comparison with human TB Francis 1947, 1958 reviewed the exactly matching patterns of infectious cattle TB bacterial excretion with corresponding routes for acquired tubercular lesions. The first cellular immune response produces a granuloma which becomes a tubercle lesion in the lymph nodes (l.n.s ) draining the portal of entry, which may not develop lesions until later in "metastasizing" spread(Jubb 1985; Sisson 1975 ). Airborne droplet nuclei pass especially to the hind (caudal) lung, so primary lesions in the pulmonary l.n.s are in the mediastinal rather than bronchials (see many references below). As in humans (M. tuberculosis), cattle TB (M.bovis) is hence 95 if not 100 % by inhalation , a respiratory (broncho-) Pneumonia :- "Consumption" or "Phthisis", acquired by prolonged contact with other cattle,and NOT from badgers, even those briefly visiting barns or foodstores (Blood , Liebana 2008).
Humans often formerly caught bovine TB by ingestion, from unpasteurised milk , via the tonsils, thence to swollen exciseable l.n.s in the throat, the jugulodigastric l.n. is part of the retropharyngeal l.n.s (literally back of ..mouth) ,.. hence "scrofula" . Pigs (Sus scrofa) as well as wild boar, and warthogs often get TB from "dirty"feeding with tubercles in the head l.n.s ( submaxillary , retropharyngeals) and gut l.n.s (mesenterics). The minority of badgers with generalised advanced TB usually show lung and kidney tubercles , but these are probably secondary spread. Up to 80 % of TB badgers are NVL, early Non Visibly Lesioned cases (just as in cattle), but some 70 % of first clinical detection of excretors are in the lymph nodes under the tongue : Submandibulars , but these often self-heal masking the true "dirty" feeding ingestion transmission route , beetles and worms from under point source cow pats ! (Cheeseman 1985 a & b, 1988, 1989 ; Nolan 1994; Pritchard 1986 ). Overlooked in the ISG and Ulster RTA studies in favour of submaxillary l.n.s (ISG p. 77, Jenkins 2008; Abernethy 2011). Whereas the vast majority of cattle studies found lesions consistently in the pulmonary l.n.s and lungs ; there is a strikingly wider range of early initiating primary TB lesion sites in badgers, suggesting non-respiratory route/s : - a preponderance of head l.n.s (SEE below O'Boyle 1. = submandibulars - submaxillaries), and perhaps why pulmonary l.n.s are bronchial rather than mediastinal which is the opposite of cattle ones (Murphy 2010; Gallagher 1998). Badger TB is a dietary "Scrofula", rather than a "Consumption" from other badgers. Critically important studies which distinguish TB entry early single lesion sites from later multi-lesion badgers include : -

1. O'Boyles superb study of some 25, 000 Irish " licence cull" badgers show lesions in 3301 cases , single / multiple sites (up to 8 sites / badger) 6 studies ...1991 - 2005 : - Ingestion : - submandibular, retropharyngeal, parotid 518 / 813; submaxillary 7 / 0; mesenteric 14 / 92; liver 33 / 128, hepatic l.n.s 35/ 179; spleen 1 / 34 ................. AND Surprisingly Few :- kidney 84 / 193 Inhalation : - lung 214 / 602, bronchial-mediastinal l.n.s 329 / 830 Skin : - bite wounds often to neck or "gravel rash" above tail hence .. axillary 22/ 72 , prescapular 142 / 442 , popliteal 298 / 407, inguinal 7 / 3 , "skin" 56 / 16 much rarer genitals , placenta, mammary gland, so "direct" transmission to cubs very rare.

2. And as percentages for head / thorax / abdomen / carcase ie. skin lesions .. Fagan 1993 : 16 / 40 / 15 / 29 .. Murphy 2010 : 22 / 50 / 7 / 12 .. Corner 2012 : 25 / 22 / - / 53 ( a surprisingly high no. in axillary l.ns.).

Controversy ingestion / inhalation

How TB is truly transmitted amongst cattle has been highly controversial for over a century, with two schools of thought .. "Ingestion" and "Inhalation" , the latter school gaining the ascendency with the discovery of airborne "droplet nuclei" reaching the alveoli (Griffin 1995; O'Reilly 1995; see Introduction). Indeed, doubts persisted even into the 1970s ( M'Fadyean 1910; Glover 1941; Myers 1940, 1969 ; Francis 1972), and the controversy has been resurrected in recent years. Unfortunately, experimental transmission studies via low/ high dose inoculation into nasal/ tracheal / or tonsils are "unnatural routes" but have led to misconceptions as to the involvement of tonsils and retropharyngeal lymph nodes (literally behind.. mouth) (Cassidy 1999, Menzies 2000; Neil 2001). True , such experimental studies mimics "natural" transmission in wild deer, which usually acquire both avian and bovine TB from environmental contamination , so involving the retropharyngeal and "gut" mesenteric lymph nodes (particularly via Peyers Patches to ileo-caecal l.n.s )( Clifton-Hadley 1991; Griffin 1994; Johnson 2008; Mackintosh 1994; Palmer 1999, 2004; Ward 2008). But the "normal" airborne/ aerosol route amongst farm deer, via closer contact, including barns and yards (Palmer 2004; Partridge 2008; Stuart 1988). In cattle too a retropharyngeal / mesenteric ingestion pattern for avian TB ( Jubb 1985) or high dose unpasteurised milk (M'Fadyean 1910); and this ought to be the pattern IF TB acquired from badger urine !. Francis 1958 cited Plum's careful analysis of retropharyngeal involvement being 90 % for ingested M. avium, or 88 % for inhaled M. bovis. It seems highly probable both with cattle with even moderate lesions, and man shedding up to 4 billion bacilli / day that coughing up / swallowing , or "deglutition".. with a continuous stream of bacilli causes secondary lesions in palatine tonsils, retropharyngeal l.n.s, larynx, mesenterics , AND Kidneys, and even gut wall (Francis 1947, 1958; Menzies 2000; Neill 2001).

TB transmission in cattle and badgers .. Key References.

CATTLE : - LESIONS .... Asseged 2004; Blood 1989; Cassidy 1999; Corner 1990, 1994; Costello 1997, 1998; Crews 1991; Francis 1947, 1958, 1971, 1972 ; Jubb 1985; Lepper 1973, 1977; Liebana 2008 (also DEFRA 2005, SE 3013) ; McIlroy 1986; Medlar 1940; M'Fadyean 1910; Myers 1940, 1969; Neil 1988; Pritchard 1988; Sisson & Grossman 1975; Stamp 1944, 1946, 1948, 1959; Whipple 1991; White 1997; Wilesmith 1982, 1986; Wright 1985.

CATTLE EXPERIMENTAL STUDIES :- Buddle 1994; Cassidy 1998, 1999 a ; Dean 2005; Glover 1941; McCorry 2005; M 'Fadyean 1910 ; Neil 1988, 1989, 1992; O'Reilly 1988; Palmer 1999, 2004; Pollock 2006.

CATTLE-TO-CATTLE TRANSMISSION reviews : - Collins 1987; Goodchild 2001; Griffin 1995; Menzies 2000; Neill 1994, 2001; O'Reilly 1995; Pritchard 1988.

BADGERS : - LESIONS ....Abernethy 2011; Brown 1993; Chambers 2002, 2011; Cheeseman 1985 a & b , 1988, 1989; Clifton-Hadley 1991, 1993; Corner 2010, 2011, 2012; Crawshaw 2008; Dolan 1993; Fagan 1993; Gallagher 1976, 1979, 1980, 1998, 2000; Gavier-Widen 2001, 2009; ISG 2007 p. 77; Jenkins 2008; Little 1982; Monies 1974 (in Gallagher 2000); Muirhead 1974; Murphy 2010; Nolan 1994; O'Boyle 6 reports, 1997-2005 ; O'Keefe 1997; Pritchard 1986 ; Wilesmith 1986.

BADGER EXPERIMENTAL STUDIES :- Lesellier 2003, 2010; Little 1975, 1982 (yard experiment); MAFF Report 13; Mahmood 1987, 1988; Pritchard 1987.

Can badgers really transmit tb to cattle ??

The whole long running badgers and TB Debate saga has been based on the rather Bizarre Surreal ! , key assumption, that cattle are no longer the infectious source of TB , and are NOT transmitting the disease either to other cattle or to badgers (Gallagher in Zuckerman 1980, Dunnet 1986 see quotes in Introduction).

Absurdly untrue, but ...if it were so (nb. a "killer" fact ); then TB spread MUST be one-way, from the supposed self-maintaining badger TB hidden reservoir to other badgers and cattle. It was recognised from the outset that while it is difficult to explain how badgers Might realistically cause a respiratory lung infection in cattle; much simpler to understand spillover from cow to badger via foraging for worms, grubs and beetles under cow pat foci infectious up to 6-12 months (Little 1982 b). Earthworms amount to some 60 % of badger diet, and may act as a passive vector of TB bacilli as shown a century ago (Lortet 1892); perhaps even bringing infection back to the surface from buried carcases (Myers 1940). Most cow pats in a field turned over by badgers (or foxes, rooks ), and as I found in Wytham, 1 scat can contain up to 66 big blue Geotrupes Dor beetles in a dry spell when worms unavailable .. so 1 or 2 badgers per clan almost guaranteed to encounter the handful of infected cow pats from the few Visible Lesion / sputum positive reactor cows in a breakdown herd. Dunnet 1980 (para. 60) suggested cattle faeces were NOT infectious to badgers .. but in the early 1990s 2 in 3 reactors were No Visibly Lesioned NVL without detectable M. bovis, ie. Unconfirmed cases, and why 2 in 3 badger culls embarassingly produced NO TB badgers...also why a mere 46 TB badgers out of 2363 sampled 1972-96 in Wales !

however, as krebs pointed out in the last major review, 1997, and even now "it is not known if, how, or to what extent badgers might contribute to cattle TB !". so, a dozen or so PhD studies have attempted to assess the risk, assuming badgers CAN pass TB to cattle either by direct contact, or indirectly via excreta pasture or in barns as reviewed by Allen 2011, Phillips 2003. After some 42 years research , the ONLY proven case of badger to cattle transmission was in a very artificial yard experiment, in which 21 badgers caught TB and passed it to 8 out of 12 in-contact calves ; it took from 6-10 mnths for the calves to become reactors, and significantly 4 calves exposed to badgers for under a month did not apparently catch TB ( Little 1982).... which supports the view that prolonged contact amongst cattle over-wintering in barns or yards, or in milking parlours is needed for transmission to occur. One school study estimated 130 hours of shared classes required to catch TB (Ewer 2003). So brief badger visits to barns for a drink and snack of cattle nuts wont achieve transmission ! Strikingly low risk of spread even amongst badgers :- even when a sputum positive "hoocher" present in the clan, with ideal conditions for bacillus survival in the sett of constant humidity, temperature and darkness , and with 4-5 badgers in a sleeping huddle in nest chamber, nevertheless often only 1-2 TB badgers per clan (see next section Table). The long forgotten classic study by Svensson found 13 calves caught airborne TB ( 6 m separation) from the main herd in a barn .. 5 were reactors after 6 months, the other 8 by 12 months contact (M'Fadyean 1910 ). Amusingly, farmer concerns that "clean" cattle catch TB at spring turnout to pasture from those terrible badgers .. is simply that TB acquired in the barn does not translate to reactor status until some months later !

Cognitive dissonance : cattle need huge dose by ingestion VS tiny dose likely from badgers e.g. urine on pasture

ALAS, a critical reappraisal of how cattle catch TB suggests that whilst a single bacillus , or CFU (colony forming unit of 6 or so bacilli as they divide and cluster) has long been recognised as enough by inhalation direct to lung alveoli (Francis 1947, Dean 2005) .. which incidentally is why "consumptive" cows with chest TB rarely develop kidney TB and infectious urine, unlike humans and badgers. The minimum dose by ingestion is vastly more to get past batteries of gut lymphatic tissues. Thus, M'Fadyean 1910 noted studies by Kossel 1905 10 mgm amounting to an estimated several thousand million bacilli. Weber 1910 suggested 400 million bacilli (Goodchild 2001, Griffin 1995).. so Francis 1947 claimed a cow would need to eat several pounds of faeces even from a heavily infected cow ( may shed 38 million bacilli/day in 30 lbs of faeces ); and cattle seldom catch TB by ingestion, even from pasture shared with tuberculous companions, so not acquiring TB until they entered the breeding herd /cowshed with aerosol transmission. Sigurdsson suggested at least 10 million bacilli (Palmer 2004). And Francis 1971 suggested 10,000 to a 1 million minimum (Little 1982). Palmer 2004 suggested experimentally , as few as 5000 bacilli orally, but the pattern of lesions was indicative of actual inhalation of cattle pellet dust. M'Fadyean noted easy transmission to calves via TB milk, which may have 100, 000 bacilli / ml, so a few litres a day often causing acute TB and early death within months. Two classic studies showed that cattle MAY catch TB grazing pasture "Super-contaminated" with faeces (Maddocks 1934, 1936; Schellner 1959).. a few farmers DO turn out stock without adequate "weathering" of slurry/manure... and run-off from yards/ manure heaps may pose a risk if draining to farmyard ponds. Contamination of waterholes may be how cattle passed TB to kudu in Africa (Francis 1958). Formerly too, cows with uterine TB may produce a kg of virulent birth waters/pus .. so a potent source of infectivity if ingested via contaminated feed or aerosolised in dust in the cowshed .... foxes may have been catching TB from afterbirth scavenging .

Badger infectivity

Up to 80 % of badgers, similarly to up to 85 % of early TB cattle, are NVL or Non Visibly Lesioned and almost non-infectious (Gallagher 2000); but a critical reappraisal of the levels of shedding of TB bacilli by the minority of badgers with generalised TB ..... excretors/superexcretors ; suggests most would shed far too few bacilli to transmit TB to cattle; OR indeed to other badgers. Studies by MAFF 1979, Gallagher 2000, Corner 2011 & 2012 suggest that infectivity may involve: -

" Sputum " ( as evidenced by clinical samples of tracheal/bronchial / larynx mucus) 200, 000 cfu/ml ( 75,000- 1 million cfu/ml); rather strikingly Gallagher assessed "sputum" risk via the minority of badgers with advanced TB from 2 sub-studies :- 30 TB badgers with VL lungs shed bacilli in rectal faeces in 19 cases, 14 of which had advanced miliary or acute tuberculous pneumonia // and sampling 43 TB badgers he found shedding in 16 by lung lavage ( 8 miliary, 4 with lungs VL, other 4 NVL ) .. and 12 had urine TB +, 11 also with kidney lesions . Corner 2012 found that out of 57 TB badgers from a "natural cull sample" only 14 had VL lungs, so only 2 had TB faeces, with under 100 cfu / gm .. whilst there were only 4 with kidney lesions, so just 5 with TB + urine, and only 3- 93 cfu /ml; supposedly badger sputum dribbles might contaminate mineral feed blocks too but low numbers ingested by cows at licks;

Faeces 75,000 cfu/ gm ( 68 - 100,000 cfu/gm) (NB clearly derived from swallowed lung exudates) . Corner 2012 found VL lung cases in only 14 of 57 TB badgers, hence only 2 with infectious (rectal) faeces , and under 100 cfu / ml, so rather a low risk ;

Urine 300, 000 cfu / ml ( 100 - 217,000 , 250,000- 300,000 cfu/ml ; NB. Corner 2 para. above); it has been suggested that faeces and urine accumulating at badger latrines may pose added risk, particularly as cows ingest considerable amounts of soil annually (Hutchings 1999), but there is degradation loss of viability, and cattle avoid latrines (Benham 1993);

Bite wounds .. N.Zealand possums may have open fissures with 5 billion bacilli/gm in pus, so possible transmission by inquisitive nosing/licking by cattle or deer .. but badgers do not develop such markedly suppurating lesions . Most badgers, both boars and sows MAY have bite wounds from territorial fighting particularly associated with cubbing / peak rutting in spring and late summer,.. fights characteristically result in wounds to face, neck and chest, with a "gravel rash" above the tail, hence secondary infection of wounds is frequently via tuberculous lesions in the nearest draining skin lymph nodes :- prescapular, axillary, popliteal, and inguinal l.n.s ( Jenkins 2008, O'Boyle 1997-2005 ; see Table above ). However, very few will actually pass on TB directly ...given the tiny minority of badgers with infectious "sputum" from the few with advanced generalised lung/kidney TB .The same doubts apply to mutual grooming which has been suggested as another way TB might spread. So, it seems likely the vast majority of bite wounds become secondarily infected with assorted "septicaemia " bacilli including TB from within the contaminated sett environment eg. bedding ( Courtenay 2006; Gallagher 1979). Bite wounding may give a more rapid progression of TB (Gallagher 2000; Newell 1997; MAFF Report 13); but true transmission by bite wounds is quite rare : - 20 badgers out of 146 or 15 out of 27 which died of TB Gallagher 1979, 2000; 7 out of 78 Murphy 2010; 5 among 56 Corner 2012; and in Woodchester over 14 years 1981-1994, out of 868 known individuals, there were ONLY 25 Superexcretors , 12 boars (with clinical M. bovis + samples = 10 bite wounds, 7 tracheal aspirate ) and 13 sows ( clinically 3 bite wounds, and 12 tracheal aspirate) Smith 1995, 2001. Even with fox rabies only a minority with viral positive sputum resulting in actual bite wound transmission ;

Badger bedding turned out onto sett spoil heap 5000- 6000 cfu/gm.. cows Might eat it, but low dose wont affect them .

"Reproductive spread "....whilst amongst cattle, bulls may have genital TB , spread from hire bulls is more likely to be via aerosol as they have generalised TB. Cows may formerly have passed TB to unborn calves from infected uteri ( under 1 %).. but affected udder a far more potent route of transmissiion since bulk milk can infect whole batches of calves (Francis 1947, Monies 2006). Genital TB of either boars or sows is extremely rare amongst badgers , also as regards mammary infection . So emphasis on "pseudo-vertical" transmission from sow to cubs in badger TB models is vastly exaggerated .. perhaps one clear case each Woodchester / Staffs studies .. and the apparent high number of TB cubs in some clans more likely caught as spillover from bad cattle breakdowns ! ( Cheeseman 1981; Delahay 2000; Gallagher 2000; Newell 1997; Shirley 2003; Wilkinson 2009). The ISG study did not find a particularly high proportion of tuberculous cubs (Jenkins 2008). Everyone seems to have overlooked the rather obvious transmission route from a sow with bad lung TB weaning her cubs by regurgitation of a rich soup of semi-digested worms with coughed up/swallowed TB flavouring !

Most badger to cattle

Indirect transmission studies have focussed on badger urine as the most likely transmision route to cattle .. but "Badger Urine Risk" to catttle has been vastly exaggerated (by default since no other plausible transmission route !). Over emphasised thus : --

1. Far too few badgers with kidney TB .. 51 out of 1166 badgers ISG / Jenkins 2008; 6 out of 36 and 9 out of 146 Gallagher 1976, 2000; 4 among 72 Nolan 1994 ; and in Irish studies 68 out of 664 Dolan; 3 among 42 Fagan; 4 among 57 Corner 2012; rare in Ulster RTAs Abnernethy 2011; and badgers with advanced generalised TB among 21 experimental badgers 11 had kidney TB but only 2 M.bovis + urine Little 1982;

2. Often cited 300, 000 bacilli / ml urine, but Corner 2012 among 57 TB badgers found just 5 with TB urine and only 3-93 cfu / ml . In the Woodchester study, between 1981-1994, out of some 300 badgers recovered for PM, just 47 had TB , 20 had kidney TB, and out of 25 clinical cases with most data only 4 had TB urine (Clifton-Hadley 1993). Wilesmith 1991, similarly noted amongst 49 clinical excretors to 1990, just 18 (37 %) had M. bovis + urine, and data from 12 excretors in 1990 had just 2 with TB urine. The Staffs study found TB in 8 of 45 badgers culled, only 2 with TB urine (Cheeseman 1985). The Sussex study found 10 TB badgers among 47 culled, 4 with kidney TB, but none giving positive urine (Pritchard & Wilesmith 1986 ).

3. Some 99 % of urine will drain straight into the soil, rest disinfected within 3 days by UV in sunlight ( airborne droplet nuclei can be sterilised within 20 minutes ; King 1999; O'Reilly 1995), and a cow would need to "drink" c. 3 cc to achieve a minimum dose of 1 million bacilli (as above) ... even though 1 urination of 30 cc could contain 9 million bacilli initially ! All rather improbable. Having said that, rather ironically, in a number of countries just after bovine TB was largely eliminated do record cases of farmers with bovine TB re-infecting their herds .. seemingly half by aerosol, and half by urination on hay which according to folklore "improves the mineral content " for cows; but probably with enormous bacillary load ( 1 human lung case shedding 4 billion bacilli/day.. hence kidney infection via swallowed bacilli ) (Grange 1996). It seems that cattle suffering from mineral deficiency/ ketosis may actively drink urine as well . So, IF a really sick badger with kidney TB, took up residence in a barn as happens occasionally (Cheeseman 1989, Macdonald 1984), and did leave urine puddles in food troughs, risk to mineral deficient cows... about as likely an event as winning the lottery if you do not buy tickets !

4. Cattle do catch avian TB by ingestion, but route clearly shown in lymph nodes near mouth/ gut (retropharyngeals, mesenterics )..this ought to be the pattern if transmission was truly via badger urine, BUT it is not so. An ingenious hypothesis to convert ingested TB to a lung infection is by eructation ie burping of rumen gases .. but highly unlikely that would yield the critical droplet infective particles needed (Mullenax 1964/ Waldo 1966). Also improbable is the idea that cattle may snort at and then by "investigative " inhalation acquire TB via aerosolised particles from faeces/urine on pasture.

Studies of badger risk to cattle include : --Allen 2011; Benham 1989, 1991, 1993; Bennett 2005 ; Brown 1992, 1993, 1994; Bohm 2008; Cheeseman 1981 (atypical behaviour); Courtenay 2006; Drewe 2013; Garnett 2002, 2003, 2005; Grange 1996 (human risk); Hutchings 1996, 1997, 1999; Judge 2009; King 1999 ( urine viability cited by Delahay 2000, Goodchild 2001); Kruuk 1979; Little 1982; Maddocks 1934, 1936; MAFF 1979; Palmer 2004; Phillips 2000, 2003 ; Roper 2003; Scantlebury 2004; Schellner 1959; Sleeman 1993, 2008; Tolhurst 2009; Ward 2006, 2008, 2010; White 1993 . Roper's 2010 revision of Ernest Neal's "Badgers" found no clear convincing explanation of mode of badger "guilt".

Early studies by Kruuk and Benham suggested that badgers avoid cattle at pasture, so attention focussed on badger excreta particularly urine/faeces. Ingenious studies used spool and line tracking of nightly badger movements, with fluorescein dye marking of urine which glows under UV light .. 1 cow did graze a urine patch within 8 hours (Brown 1994). Much emphasis was placed on likelihood of cattle grazing patterns.. field edges, high or low status cows use of over-grazed pastures.. less avoidance of contaminated pasture by a tiny minority ( 5 out of 50 ) cows , sward length relation to optimum "worming" by badgers, strip or sett stocking ( Benham, Hutchings, Bohm, Kruuk ). However, most cattle avoided both urine and smelly faeces on pasture .. so attention switched to "contacts" between badgers/ cows, particularly in barns/ farmyards .. cattle transponders, proximity data loggers, and radio-tracking plus video surveillance....Garnett recorded 139 badger visits, Ward 71, 18 contacts, some even "nose to nose" .. with occasional urination/defaecation even in food troughs ! Given this evidence from over 200 "farm visits", with a very low likelihood of transmission risk even in barns, it seems doubtful that the latest new FERA study (2013) will shed much further light . Most farm visits in dry summers, for a drink as well as food sources (cattle cake etc) when worms scarce, BUT cattle out at pasture then anyway... so "contact" further limited. Use of electric fencing to exclude badgers from barns/foodstores (Tolhurst 2009 ). In truth, brown rats are a more probable transmission risk.. said to out-number the human population of GB now, an influx to barns / farmyards in autuumn, may travel a km or more per night, do leave a frass of faecal pellets in food troughs , they DID spread avian TB amongst fowl flocks (Myers 1940) , and very under-estimated as carriers of bovine TB since they exhibit tiny micro-lesions of miliary TB easily missed ie. Yersins phenomenon (Little 1982; Francis 1958). Concern that switch to maize silage with high Selenium content might be behind southwest problem area .. apart from an abundance of "linear features" ie. hedges with crossing point territorial urine sites (Brown 1994, White 1993). The latest field study by Drewe, found approaches to within 1.4 m between cows/badgers amounted to just 4 in 500,000 contacts over a year, and only 1716 visits near badger latrines .. so hardly a frequent contact-transmission route . It has always been the case that most cows avoid grazing contaminated pasture .. recently grazed fields have a random scatter of greener longer grass tufts marking former cow pat sites ! Rabbits are prone to TB, but very few wild ones catch TB since both they and sheep selectively graze away from contaminated areas.

In conclusion

It seems rather clear that Badgers get "Scrofula" by spillover from cattle; and NOT to any great extent as a self-sustaining reservoir spread from other badgers ; Cattle get a respiratory "Consumption" from other cows. So, Cattle- to -Cattle transmission is 95 if not 100 % The Problem after all:- reviews which re-discover a low rate of transmission seem to have overlooked the fact that the whole point of annual testing is to minimise within and between herd spread by removing cases before they get to the more infectious VL stage (Goodchild 2001; Griffin 1995; Menzies 2000; Neill 2001) . At the low point in GB and Ireland both south and north, c. half of breakdowns with just a singleton reactor (Morrison 2000); and only some 3 reactors / breakdown (2-4 ), whether in Argentina, GB, Holland , or New Zealand ( Fischer 2005, Goodchild 2001, Perez 2002, Wilesmith 1986). Slippage to 2 year testing , as happened with Foot and Mouth (Cattle Section 3 ), simply allows more spread within herds .