House of Commons - Environment, Food and Rural Affairs

Select Committee on Environment, Food and Rural Affairs Written Evidence

Further memorandum submitted by M Hancox (BTB 12a)

EXECUTIVE SUMMARY (SECTIONS 1-7)

1. Cattle TB is now worse than in 1960 when the whole of Britain was under annual testing and movement restrictions in a textbook Area Eradication Scheme.

2. Risk to both public health and exports. With some 15% of herds in Devon/Cornwall affected, and 25% in Gloucestershire there should be a total ban on unpasteurised milk, and full availability of BCG vaccination for farmers and their families. This hotspot crisis level is already in breach of EU Directives for export, if BSE restrictions are lifted.

3. The absolute tragedy of the current crisis is that attention has focused to such an extent on badgers as the main TB reservoir over the last 30 years that no-one seems to understand how TB works in cows any longer. Fortunately, Sherlock Holmes has cast some light on the confusion surrounding the scientific rationale for a mass badger cull by exploring the following three scenarios.

4. When you have eliminated the impossible, whatever remains, however improbable must be the truth. Farmers and vets are certain that badgers are the cause of up to 96% of cattle TB herd breakdowns. There is a widespread endemic self-maintaining reservoir of badger TB and cattle testing finds sentinel cases hence locating pockets of badger TB which must be culled to prevent further herd breakdowns11 See section 8.

5. The curious case of the two dogs which failed to bark in the night. As in dozens of countries worldwide which acquired bovine TB from Europe during the colonial era, cattle are the main (or sole) self-maintaining reservoir of cattle TB, which in Britain and Ireland spills over to badgers and other wildlife, and cattle tests serve to locate, control, and contain TB. Relaxing cattle testing and movement restrictions due to foot and mouth (FMD) in 2001 simply allowed TB to spread like wildfire and return to areas TB-free for 50 years. And, secondly, culling over 10,000 badgers in the Krebs/RBCT trial has made no difference to the 18% a year rise in cattle TB. See section 10.

6. It is a capital mistake to theorize before one has data. Insensibly, one begins to wish facts to suit theories, instead of theories to suit facts. Widespread proactive area badger culling decreased cattle TB by 19%, whereas localised reactive culling areas saw a 27% increase via badger perturbation, and similarly immediately outside the proactive areas an increase of 29%. See section 11.

7. Recommendations for tackling the crisis:

(a) four, three and even two year testing intervals are too long. New hotspots may be festering eg in intensive dairying Cheshire, as happened with one or two imports resulting in over 6,000 reactors in Staffs/Derbyshire. The entire national herd should be tested annually for two years at least;

(b) a complete ban on movement from hotspot counties (1 above) until TB is brought under control. Failing that, both pre-movement and post-movement testing (with isolation) is what stops "missed" carriers importing TB into Scotland and the north of England from becoming new hotspots. The pre-movement test from February 2006 of over 15 month old cattle will miss many younger beef stores;

(c) with TB rising exponentially, a fundamental mistake is to de-restrict unconfirmed herds after one clear test: two clear tests from confirmed breakdowns with six month check tests for two years in Ireland (annual testing), or for five years in Michigan (rely more on abattoir surveillance and trace back) 22;

(d) IR Inconclusive Reactors are probably TB positive if other "good" reactors in the herd, so cull at second retest as in EU guidelines, rather than at third retest3;

(e) severe interpretation of skin test with problem herds and "dangerous contacts"24;

(f) IFN in tandem with skin test for problem herds will help remove early cases. However late TB "active spreader" VL cases have an importance out of all proportion to their numbers by exporting carriers from "TB-free" unrestricted herds: and antibody test urgently needed4, 17, 24; (or see g);

(g) PCR for rapid confirmation of M bovis is suspect lesions in abattoir surveillance in the National Granuloma Submission Programme in Australia5, similarly in Michigan. Huge numbers of bacilli shed in cattle faeces with "open" lung lesions could identify skin test anergics10, but is very unlikely to find bacilli in cattle or badger sputum. There is no evidence environmental bacilli can cause new breakdowns. Although of course huge numbers of bacilli may occur in fresh manure/slurry, so that cattle should not have access to newly contaminated pasture. And uterine discharges and perhaps urine may also add to environmental infectivity in the cowshed25;

(h) Ireland has electronic tagging from birth, a computerised database for full traceability (trace back and forwards) and "at risk" contiguous premises (via subsidy payments), and TB test history on the Blue book "cattle passport"22; and

(i) when cattle schemes reach low levels of TB, many breakdowns are of singleton reactors. When things go wrong however TB becomes entrenched in often big dairy herds. Depopulation was urged if 50 or even 25% of herd affected. The alternative since anergy cases are missed is being restricted for five to 10 years since BSE/FMD until the "missed source" removed amongst the 245,000 cows culled each year due to infertility, mastitis, lameness.

8. Why are farmers, vets and others so certain badgers cause up to 96% of herd TB breakdowns? There are four pivotal claims outlined in policy statements from the NFU, BVA, CLA etc1, 3, 11, 23:

(a) cattle-to-cattle transmission is unimportant, see section 9;

(b) Repeat breakdowns occur in "closed" herds which have tested clear. TB badgers found afterwards, they must be the cause, see section 10;

(d) it is hence entirely logical to regard badgers as the main self-maintaining endemic long- lived social reservoir of TB with ONE-WAY spillover to cattle, and other wildlife, pig, sheep, alpaca, llama, cats and dogs.

9. TB Transmission. John Gallagher ex-MAFF vet was involved with the "first" TB badger 1971, Thornbury, and Zuckerman. (In fact the first wild TB badgers Switzerland 1950's were a spillover from roe deer carrion at the tail end of their cattle TB scheme, others now known Spain and Italy, zoo ones from 1930s London plus Whipsnade in 1950s.) He claims that here is a fundamental difference between TB lesions in badger lungs, kidneys, etc with huge numbers of bacilli making them very infectious in contrast to few bacilli in cattle lung lesions. In the 1970's he found only 21 VL (Visible Lesion) "Open" cases amongst 1,000 reactors so concluded that such cases were so rare that cattle are of little importance in passing TB to other cattle of badgers11,32. Rather awkwardly, at Woodchester Park even with badgers "hooching bacteria" in sputum in the clan, and close contact in sleeping huddles underground, there is very little evidence of spread within the badger group, let alone to cattle!

Cattle "Consumption": Badger "Scrofula". Rather ironically the M bovis genome is smaller than the human M tuberculosis one, so cattle must have got TB originally from man. And just as in man "Consumption or phthisis" is a respiratory lung infection, a progressive bronchopneumonia in up to 95% of cattle10. And just as the aerosol breathed out from a passer-by with a mild cold sniffle won't give you a cold, spending hours in an office with someone coughing and sneezing flu bugs is high risk, so too prolonged exposure is needed to catch TB. Some 130 hours of shared classes in one school outbreak, or several months over-wintering in barns with poor ventilation is ideal to spread TB and other pneumonias amongst cattle (viral, bacterial, mycoplasmal). However, a "superexcretor" patient may infect most contacts, even on a brief plane journey, and a cow with advanced TB may shed 38 million bacilli per day so even brief exposure at agricultural shows or auctions may pass TB back into "closed" herds. TB taken back to Guernsey, and in Germany. Little spread outdoors, cattle often get TB when they first enter the cowshed and breeding herd10. Only the smallest aerosol droplets can stay airborne and reach the inner-most alveoli so avoiding the muco-ciliary escalator on inhalation. The pivotal claim that only "open" visible lesion lung cases are infectious is simply wrong. If lesions occur in the draining pulmonary lymph nodes then if sought for diligently enough there will by lung tubercles, and all such cases are potentially infectious: up to 20% sputum positive20. As in man though lung lesions may occur in up to 10% of cases without any in the lymph nodes suggesting TB was acquitted by ingestion with secondary spread to the lungs. And so just as humans used to catch dietary "Scrofula" via unpasteurised milk, with swollen neck lymph nodes, so badger TB often starts in the submandibular lymph nodes under the tongue. 13. The famous "Link" is that badgers have been catching TB from point source cow pats seeking worms and Dor beetles all along. A fact re-discovered with the most TB badgers linked to the most previous TB cattle (see Table below for DIJ, 30). Up to 85% of badgers with TB at the epicentre of TB herd foci in the clean ring strategy. Cattle may catch TB by ingestion but need a minimum dose of 1 million bacilli, ie 3cc of badger urine with 300,000 bacilli/cc drunk which seems rather improbable! Late TB cases may be infectious via the udder, uterus, or testes with spread at mating and a risk from hire bulls, but such "reproductive" transmission amounts to under 1% of cases. Few reach late TB stage.

10. Area Eradication Scheme. A critical review of TB schemes14 found that Britain and Ireland had textbook schemes which nearly eradicated TB by the 1970s10, 15, 19, 24-27, 30. Initial tiny microscopic or Non Visible Lesion (NVL) lung cases shed few bacilli intermittently, but as many larger lesions develop and approach the Visible Lesion (VL) stage at abattoir inspection (or human lung X-ray) shedding becomes continuous with up to 38 million per day. Annual testing removes most cases before they reach the more infectious stage (SEE GRAPH).

And working from low to higher TB-level "manageable" regions, areas were gradually cleared reducing TB from countrywide to tiny southwest hotspots by the 1970—early 1990s (SEE MAPS). NB This low point was achieved without any badger culls whatsoever, and the "endemic badger TB" did not reinfect cleared areas, and died out just as dietary TB in pigs dies out when the avian, bovine or human TB source disappears (not self-maintaining). Relaxing cattle testing and movement restrictions prematurely simply allows TB back into cleared areas, as in Ulster and Michigan15; when MAFF were overstretched with FMD in 1967 by restocking to Cheshire24; at the peak of BSE in 1993 with longer test intervals and more restocking movements southwest TB doubled from 121 to 232 herds and the new hotspots of Exmoor, Hereford/Worcs, Staffs/Derby, and Cheshire/Shrops emerged. Hartland also, two year testing, "suddenly" 13 new herds in 19838, 24.

Failure to achieve complete eradication has been blamed on badgers, but the skin test is only 80% accurate, or 65% on retests. It misses early latent cases which can take several years to come "on stream"; lactation may via immunosuppression temporarily make up to 30% of cases non-reactors; and late TB cases may be swamped with bacilli so go "anergic" and are a very potent source of new breakdowns: three such cases caused 18 herd breakdowns or 10% of the 2¼ year total in Cornwall (see 7f and graph, IFN and an antibody test need2, 4, 24. Up to 46% of Irish breakdowns found by abattoir inspection despite annual testing22, 28. And it is scatter of TB cases from such "unrestricted" herds which cause new breakdowns as is clear in the maps of the Four areas trial with no pre-movement tests since 1996 22. Repeat breakdowns may tie up big dairy herds for five years or more, so it was easier in the 1970s with average size of 47 cows to depopulate chronic herds, than now with 70% of dairy herds over 100 cows (routine depopulation if 50 of even 25% herd affected, 25. With 43% of farm-to-farm movements under 20 km, a mean of 58 km, and a significant number up to 1,000 km amongst seven million, it was not surprising hotspots expanded dramatically after FMD leap-frogging in the two year parish testing "cordon sanitaire" (map in Annex E of Preparing A New Strategy). 21. A very particular problem with the last remnants of TB in eradication is NVL cases without M.bovis confirmed either: up to 70% actually have TB8. Shown amongst the 1,099 breakdowns 1972-78: 277 bought-in, including Irish, 37 contiguous, 776 were either unknown or allegedly badger = 78% unknown29. Even West Penwith went clear in 1985, but TB reintroduced three years later and there, with a band south of Redruth, plus Harland with the most intensive dairying became the subsequent hotspots (Dunnet p 8 & 10, 24).

11. DEFRA could not have imagined a more perfect way to show that cattle TB is 99 if not 100% a cattle problem, than the 2001 FMD disaster. It derailed the RBCT cull for 14 months, and the lack of cattle testing and subsequent backlog with no movement restrictions allowed TB to spread like wildfire rising at 18% a year. The 2000 to 2002 jump of confirmed new breakdowns was nearly double 1,039 to 1,902, 8,000 to 23,000 reactors, cost £36 to £75 million. (Hardly attributable to badgers!). 2005 with zero tolerance of overdue tests, now a rise of 35% to 28,000 reactors, cost £90 million.

  The rationale behind any badger cull based on the interim results of the Krebs/RBCT trial are spectacularly flawed for two reasons:too few TB badgers culled, and the analyses rely on the view that ANY effect in cattle is due to the badger cull, ignoring the fact that removing large numbers of TB cattle is what reduces TB in cattle (Rocket Science!). (See 4 above). Reactive area. Only three areas enrolled pre-FMD January 2001 with 319 badgers culled, only another 353 making 672 with three more areas by January 2003. So two thirds of the 2,047 badgers culled in the last five months of the cull in 2003 cannot have had time to make the slightest difference to cattle TB.

Triplet 1st

Proactive

Cull 1st

Reactive

Cull Total TB herds/prev

three years Reactors

prev year

proactive Initial TB badgers proactive

A  Glos/Heref Jan 2000 Jul 2000 130 57 8

B  Dev/Cornwall Dec 1998 Jan 1999 120 70 13

C  E Cornwall Oct 1999 May 2000 51 62 4

D  Hereford Dec 2002 Sept 2003 55 187 102

E  Wilts May 2000 Jun 2002 56 34 29

F  W Cornwall Jul 2000 Aug 2002 62 14 13

G  Staff/Derby Nov 2000 Aug 2002 51 23 29

H  Dev/Somerset Dec 2000 Jan 2003 43 36 12

I  Glos Oct 2002 Oct 2003 74 154 82

J  Devon Oct 2002 — 55 215 65

852 357

The 672 may have been 70 with TB, 20 "superexcretors" (multi-lesion) out of 900 km2. The rise of 30% in cattle was BEFORE the culls started, so the 27% increase was due to cattle spread. And a year later in reanalysis there was no difference between reactive and survey only: 356 vs 358 breakdowns. 6, 17, 18.

Proactive area. By contrast, there were seven areas enrolled pre-FMD, with three follow-ups too, but out of the initial 357 TB badgers with TB culled (table), only 127 possibly superexcretors, and five areas less than 20 TB badgers so hardly a cause of a 19% drop in 1,000 km2 (column 6). This was due to systematic annual testing being in place longer with a drop to 23% after the follow-up cull ie test/slaughter "biting". A rise in all areas after FMD (graphs in 29 September report to Minister). The rise of 29% in the area just outside the proactive area due to more FMD slippage since less prioritised testing, dropping to only 22% after first follow up cull hence mirroring the reactive rise. The most marked effects were "cattle" ones with confirmed breakdowns in the smallest inner area 28 km2 107 herds, outer area 71 km2 297 herds, outside that 97 km2 307 breakdowns. Less marked effects for total confirmed and unconfirmed. Big variation in all areas reflect huge differences in historic TB herds: nine to 54/area, or 43 to 130 for total triplet (table, column 4). These effects had nothing to do with culling a few TB badgers or perturbing a few more to emigrate from reactive of proactive areas31: Alice in Wonderland "Science".

12. The other cases which supposedly "prove that badger culls work" are likewise fundamentally flawed. Simply too few TB badgers versus the impact of removing large numbers of TB cattle:

Offaly 141 TB badgers out of 600 km2 and 1,458 reactor cattle from 55,000 cattle versus 5646 reactors out of 150,000 cattle in the control area. Three times the population yield three times the reactors. 7, 9, 17 Four area trial. Only 286 TB badgers out of 960 km2 vs 5,000-10,000 reactor cattle. There were twice the number of confirmed breakdowns in the reference area (393) as in the removal area (193) so the same cattle measures did half as well. The new breakdowns were scattered across the area maps (see section 10). And the famous 96% "drop" in cattle TB "due to badger culls" was in fact a flare UP in the reference area (12, 22 p 23-6). The Thornbury area was down to a single herd before the cull, again a small cattle flare-up before gassing, so nothing to do with badger gassing11. And NOT clear until 1990's—odd unconfirmed breakdowns yearly.

No-one has shown how badgers are supposed to give cattle a respiratory lung disease, and the supposed effects of badger culling are in fact due cattle culling. Case for any culls unfounded, Old Brock victim not villain. Possums "not guilty" in native Australia5; overly blamed in New Zealand recently re-discovering area cattle scheme "works"! Regards to the melancholy moth -eaten possum in Mammal gallery of Natural History Museum where nearby dwells the other great "scientific" hoax/fraud: Piltdown Man!

REFERENCES:

1 Badger Trust, Strategy/Policy briefing—www.badger.org.uk

2 Blood D, 1989, Veterinary Medicine (Copy at Bristol University Library)

3 British Vet Association—www.bva.co.uk

4 Costello E, 1997, anergy, Vet Record 141 : 222

5 Cousins D, 2001, Australia, Tuberculosis 81 : 5

6 Donnelly C, 2003, reactive cull, Nature 426 : 834 & reanalysis 7 Oct 20 05 www.defra

7 Donnelly C, 2005, positive and negative impact proactive cull 14 Dec Nature online

8 Dunnet G, 1986, Badgers and Bovine TB

9 Eves S, 1999, Offally cull, Irish Vet. J, 52 : 199

10 Francis J, 1947, Bovine Tuberculosis, Staples Press

11 Gallagher J, 2005, TB: Tracing the dilemma, Vet Times 35 : 14

12 Griffin J, 2005, Four areas cull, Prev Vet Med 67 : 237 & Irish Vet J 58: 629

13 Hancox M, 1995, Badger TB, J Agric Sci. 125 : 441 also Lett, Appl Mic 24 : 221

14 Hancox M, 2000, Cattle TB schemes, Lett Appl Microbiol 31 : 87; also Resp Medic 94:1007, Tuberculosis 81:185

15 Hancox M, 2000, Agricultural Committee Badgers & Bovine TB Report HC 92 Appdx 15 NB Maps & graphs in http://www.royalsoc.ac.uk/inquiry/index, four submissions: FMD enquiry.

16 Hancox M, 2003, EFRA Committee Badgers & Bovine TB Report HC 432 Appdx 6&7.

17 Hancox, M, 2004, EFRA Committee, Bovine TB Report HC 638 Ev 37-Ev 44

18 ISG, 2005, Fourth Report

19 Macrae W, 1961, cattle scheme, Symp Zool Soc Lon 4 : 81

20 McIlroy S, 1986, cattle lesions, Vet Record 118 : 718; also Neill S, Vet Rec 122 : 184

21 Mitchell A, 2005, cattle movements, Animal Science 80 : 265

22 More S, 2004, Four areas trial, Report to Mary Coughlan (& Vet. Microbiol in press)

23 National Farmers Union, policy leaflet—www.nfuonline.com

24 Richards R, 1972, Inquiry into bovine TB in west Cornwall, MAFF

25 Ritchie J, 1959, In Stableforth, Infectious Diseases of Animals, Vol.2: 713 (Copy at Surrey University, Guildford, also articles Paterson/Stamp)

26 Ritchie J, 1964, cattle scheme, Conquest 52 : 3

27 Watchorn R, 1965, Bovine TB Eradication Scheme, Dublin