APPENDIX 6
Memorandum submitted by Mr Martin Hancox
(P6)
In your 2000 Report my memorandum (with above
title) listed 3 key control measures needed
1. Annual testing (all cattle),
2. Movement ban,
3. Centralised scheme and concluded "There
will be nil progress until measures 1-3 above are relaunched—badger
culls are a waste of money because they don't work" 1 These
views were based on the 4 classics Francis 1947, 1958, Myers 1940,
1969 as reviewed elsewhere and with various warnings and criticisms
of the Krebs trial submitted to the Committee in the interim,
many being available on the web 2-12.
Sadly, the two years impact of 2001 foot and
mouth has meant effectively abandoning the 3 controls—Cattle
TB is out of control, back to 1960s levels, with increased risk
to man6,9 The government, DEFRA, ISG response, specifically the
autumn package (news releases 9 Oct. 407/02, 21 Nov. 476/02) is
a too little too late compromise. It is still claimed (wrongly)
that it is not known how TB is transmitted so "robust science"
husbandry risks/controls cannot be launched 13,14, so two main
topics are addressed:
CATTLE TB CONTROL
In textbooks, bovine TB is simply a slow but
progressive broncho-pneumonia, hence :
1. If unchecked, TB spreads slowly but inexorably
at 3 levels :
(a) Individual—the initial
lung lesion/s grow and spawn secondary lesions in the lungs, then
kidneys, uterus, udder, etc. The older the animal the more advanced
the TB is in size/number lesions, test positivity, infectiousness:
few bacilli shed intermittently, then with multiple gross lesions
up to 38 million/day;
(b) Population—1. Within herds,
2. Local cluster of herds, 3.Distant herd via missed—carrier,
producing new "hotspot" cluster—clusters grow
and merge eventually;
(c) Respiratory—spread via
aerosolised sputum, just like human colds, flu, TB and other cattle
"pneumonias" (Viral RSV, Bacterial Pasteurella etc,
mycoplasmal).
2. The two Checks are determined by the
long incubation of the disease
(a) Annual Testing—on "average"
it takes about two months to become a reactor, eight to 65 days
then about a year to reach the more infectious visible lesion
stage (one and a half—15 m) 15-l7 However the classic studies
noted that depending on challenge dose TB may heal fully . . .
remain latent for years . . . progress slightly with remissions
and exacerbations, a chronic TB—or become acute and fatal
in months. A group of calves infected in 1987 had one reactor
then, 1989 17 in Apr., 2 Jun., l Aug., then 1 each in 1990-92,
so 24 reactors, 14 VL in six yrs showing the danger of leaving
inconclusives in-situ. Also, around 9% may be infectious by 6
months, 17% by 12 m, 26% by 18 m, 34% by 24 m 19 . In Ulster with
annual testing reinstated in 1982 only 20% infectious. Spread
of TB may then be rapid; many breakdowns now with reactors in
double figures.
(b) Movement Ban—apart from
false positives, this latency is partly why the test is only 80%
accurate (68% on retests) so a movement ban is the only guaranteed
way of preventing spread to TB-free areas. Less useful is sourcing
from allegedly TB-free areas, pre-movement tests, or the option
so far, post-movement test which can never be better than catch-up.
Restocking already taken TB to areas TB-free up to 50 years:—Powys/Dumfries,
Ayr, Banf ?/Cumbria, Northumberland, Durham, Yorks, Leic, Sussex.
3. Widely overlooked is why annual testing
is the gold standard worldwide and under EC Directives, but it
has three critical impacts on TB control:
(a) Minimising Spread—Reactors are
removed at the early legion stage before they can pass on TB to
any extent, both within the herd and in sold on stock. Both factors
apply to contiguous or bought-in stock in local or distant herds—if
these are on longer test intervals TB will simply build up within
the herd—some breakdowns now 60% of herd affected.
(b) Respiratory Spread—The microscopic
NVL lesion/s are almost 100% in the lungs or lymph nodes associated
with the respiratory tract, these early lesions show spread by
inhalation—abbatoir material14,15-17,20 and contact studies,
14,21,22. Stage of urinogenital, udder late TB not reached, avoiding
maternal-calf transmission.
(c) Demographic—after some
years of annual testing older tuberculous stock removed, so the
ongoing problem is confined to younger stock. Older cows may be
anergic superexcretors; three such caused 18 breakdowns or 10%
of total, early 1970s Penwith. And activation of latent TB in
older cows may cause breakdown in herd "closed" 10 yrs
+ .
CONCLUSION
The autumn package of measures meant to curb
the spread from hotspots is too late—2b above. Until the
national herd has been tested at least once it wont be known where
TB has got to. The "official" backlog of herd tests
has only fallen from 27,000 to 10,000 herds (Nov.) but with usually
some 35,000/a the whole test programme is way behind. Several
years of annual testing in hotspots are needed to even begin to
bring spread under control, let alone get ahead of it. It is absurd
that it is taking some 53-320 days to remove reactors to slaughter.
The initial freeze on recruiting extra vets has been lifted. The
idea of lay testing has been raised again (Oct, and recently)
but would be a disaster . . . testing interpretation is subjective,
and long experience of a herd desirable as with the inconclusives
above.
ALTERNATIVE TESTS
GB and Ireland have derogation to use the comparative
intradermal, but Francis warned of false positivity; the single
(bovine PPD) used on the continent might be better. IFN also too
many false +, never better than a backup to skin tests.
PCR with IS6110 or MPB70 probes can confirm
small samples in two days. An Edinburgh vet J.Gamgee (D.Mail 26
Ap.02) said the overzealous removal of BSE risk materials at abattoirs
means that this vital complement to tracing TB herds from TB lesions
lost.
1. Badger Involvement?
The 1991 Krebs Report concluded that is not
known IF, how, or to what extent badgers MIGHT give cattle TB;
nor if culls work. The Bourne trial is meant to solve both issues
by 2005 , but the Crisis is already out of control, and 4 things
are already clear:
1.1 Cattle TB respiratory—transmission
is almost entirely by inhalation as shown by the early primary
lesion complex 3b above, so badgers are an improbable source.
The study of badgers in barns widely hailed as The Answer 23 failed
to mention an earlier study which showed that even if TB badgers
and calves co-habit long-term transmission is difficult; unlikely
under field conditions of brief sporadic visits to barns. Four
calves exposed under one month failed to get TB . 22
1.2 Very few badgers reach the infectious
stage:—at Woodchester over 14 yrs 1981-94 with c. 300 badgers
in 9 km2, Only 188 infected, 41 infectious, 17 superinfectious
ie. 58 (31%). Hence little spread within or between clans, let
alone to cattle, indeed clear spillover from cattle (which isn't
supposed to happen) 25. Extrapolating these figures to the eventual
Krebs/Bourne cull of c. 12,500 badgers, would give 2,500 with
TB, 750 infectious, in relation to c, 3,000 farms in 2,000 km2
cull area, ie one infectious badger per 13 km2, or 1 per 20 herds.
No cull, fertility control or vaccination will ever be remotely
cost-effective or practicable (even if very rarely such a superinfectious
badger living in a barn caused a breakdown).
1.3 Ulster had some 50% of badgers with
TB in some 1970s samples but have always regarded badgers as merely
a spillover host, irrelevant to cattle TB, not culled.
1.4 GBs textbook cattle TB scheme 1-12 brought
TB down to tiny southwest "cattle hotspots" rather than
high-density badger ones, with almost no culling, the low of 89
herds /600 cases 1979. TB has spread far and wide beyond these
supposedly important badger hotspots revealing them as spectacularly
irrelevant now. By Nov. 2827 new incidents and over 21,000 cases
. . . Nothing to do with Old Brock.
REFERENCES
1. Select Committee, 2000, Badgers and bovine
TB, HC 92, Appdx. 15, p. 75.—Hancox M, 2002 refs 2-12—and
earlier ones.
2. Biologist 49 :144 www.iob.org/biologist.Letterbox,
Badgers and bovine TB, and 42 :159.
3. Foot and Mouth Inquiries, www.fmd-lessonslearned.org.uk/A-submissions,
Hancox 4 lett.
4. ditto, www.royalsoc.ac.uk/inquiry/evidence—ind—h.htm,
Hancox 4 submissions.
5. J.Agric.Sci. 139:1-4 Great Debate,
and 135:333 revw. Bourne 2, 125:441 transm.badgr.
6. Lancet 359:706 health risk.
7. Lett.Appl.Miorobiol. --, and 31:87-93
cattle schemes, transmission cattle 28:242,
and in badgers 24:226.
8. Microbiol.Today 29:166 , www.socgenmicrobiol.org.uk/QUA!mtaugO2.htm.comment
9. Respir.Medec. 96:842-5 cattl.TB crisis,
www.idealibrary.com ; &94:1007 schemes, 93:220 transmission
cattle
10. Sci.in Parliament 59:22 bov.TB, 58:19
culling to end?
11. Small Carnivore Conservation 27:32 TB
Politics, 26:22 Great Debate/Bern Convtn.
12. Tuberculosis—and 81:185-7 cattle
schemes .
13. Bourne J. 2001 , 3rd Report, www.defra.gov.uk/animalh/tb/isg.
14. Goodchild A, 2001, Tuberculosis 81:23
cattle transmission.
15. McIlroy S, 1986, Vet.Rec. 118:718.
16. Neill S, 1988, Vet.Rec. 122:184.
17. Cassidy J, 1999, Vet.Rec. 144:139.
18. Good M, 1994, ERAD Selected Papers 1993:
45.
19. Griffin J, 2002, ERAD Selected Papers
2000-01 :54.
20. White P, 1997, ERAD Selected Papers
1996:64
21. Costello E, 1998, Vet. J. 155:
245.
22. Little T, 1982, Vet.Rec. 111: 550.
23. Garnett B, 2002, Proc. Royal Soc. B
269: 1487.
24. Smith G, 1995, Mammalia 59:639.
25. Delahay R, 2000, J. Anim.Ecol.
69: 428.
POSTSCRIPT
Having been on the TB Panel, and involved for
12 years, it is very depressing that a whole generation of farmers,
vets, biologists, and politicians have grown up being told for
30 years that badgers are the problem. Current research has accordingly
failed to understand the simplicity of spread once a "critical
mass" of lung lesions arises. Cause and cure of the crisis
is clear but politically difficult. My suggestion to ministers
(tongue in cheek) is to sack the Bourne-ISG team and the trial
is taking too long (5 yrs so far) to understand TB in cows will
doubtless go unheeded.
27 January 2003
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