Memorandum submitted by Martin Hancox
Your February Report on the ISG's 2007 final
report on badgers and bovine TB (2) shows that Defra science infrastructure
and collaborative subcontracting is "fit for purpose",
but unfortunately had too narrow a remit to achieve the desired
results. The best science is an art form in that asking the right
questions gets results. What should have been asked was why is
there a cattle TB crisis, how does it fit in with schemes elsewhere
(13) or indeed why GB nearly eradicated TB without any badger
culls (15), and why is everyone so certain badgers are the problem.
The ISG team started with the preconceived notion
that badgers are the main reservoir of bovine TB, and hence concluded
that the rises and falls in cattle TB were due to the badger culls.
In particular that perturbed badger populations had more contact
with cattle hence the "edge effect" and a rise in TB.
The compromise between this ISG view that partial culls would
make things worse contrasted with Professor King's view that culls
work, led to the idea that any cull would need to be over some
300 km2, be sustained for many years, and preferably be within
impermeable boundary areas. This accidentally renders any cull
policy unworkable and uneconomic: a perfect political fudge.
It is very sad that neither the ISG nor the
EFRA Committee reports were able to recognise that like the Emperor
with no clothes, they have in fact at long last proven badgers
to be completely irrelevant to solving cattle TB. They have failed
to note two key facts:
1. Too few badgers with TB. Out of nearly
11,000 badgers culled over seven years from 2,000 km2
there were only 1,515 with TB (1,204 proactive, 311 reactive
ISG p 50, 74, 75, 205-9) and ONLY 166 with severe lesions
which might have been a risk to cattle (p 77). In nearly half
of the 51 proactive culls there were 15 or fewer TB
badgers per 100 km2
hardly a major reservoir or cause
of anything. And since the cull removed c 70% of badgers, there
would have been some 500 left and perturbed, so 50 per
100 km2 area which supposedly rushed across the boundary
to cause the rise in cattle TB there (about 1 per km!).
2. It seems almost beyond belief, but the
ISG have completely ignored the fact from cattle TB schemes worldwide,
that removing TB cattle by test annually and slaughter reduces
cattle TB, any relaxation of such measures allows cattle TB to
explode out of control via cattle-to-cattle spread (1, 3, 5-11,
13). Lack of testing due to 2001 foot and mouth and a huge
backlog of tests meant from 2000 to 2002 a doubling
of herds and a 3-4 fold rise in reactors. The number of herds
with over six reactors doubled from 23% to 42%, but had dropped
back to 17% by 2005 as intensive testing began to bite. Zero
tolerance on overdue tests led to a peak of 30,000 TB cattle
in 2005 (twice as bad as 1960) but these measures dropped
TB by 30% in 2006 whereas the apparent rise last year is
simply because more herds and cattle are being tested: cattle
controls are working!
The drop of 23% in proactive areas is due to
this, especially "by the fourth badger cull", and is
most marked where annual tests have been in place longest (Cornwall)
nothing to do with impermeable boundaries. The rise in reactive
areas happened BEFORE the cull (p 109) so it's daft to claim it
was due to perturbed badgers. Only three areas ran long enough
for any "effect" to appear, and only 32 TB badgers
culled (ABC). Doubts as to any reactive perturbation factor elsewhere
(King and 12). A decisive rebuttal of reactive perturbation effects
is hidden in Defra Project Report SE 3108 which found too
few TB badgers, too few badger movements and only to next door
clan, and the cattle TB DNA spoligotypes were NOT the same as
local badgers ie from brought in cattle! As to proactive
perturbation
in fact there were transient cattle rises both
inside and outside these AND the survey only (no cull) areas (p
88, 94, 97, 100).
The two key misunderstandings underpinning the
entire badger TB debate are that annual testing removes cases
before they reach the more infectious stage (not recognised by
ISG 17), (1, 5, 6-11, 13). And when such measures have been in
place some years most cattle are caught very early so it is not
possible to confirm TB via lesions or M bovis culture. These NVL
or non visible lesion cases comprise a HUGE undetected reservoir
of TB and are the real source of new or repeat herd breakdowns
hence the Australian NGSP National Granuloma Submission program
(4, 6, 14, 16).
Rather ironically the ISG also accidentally
showed that doubling cattle TB meant twice the spillover TO badgers
more widely or with less clustering: Victim not Villain.
March 2008
REFERENCES
1. Blood R, 1989, Veterinary Medicine
2. Bourne J, 2007, ISG final report on
bovine TB
3. Clark M, 2007, Badgers, Whittet
revised ed.
4. Cousins D, 2001, Australia, Tuberculosis
81.5
5. Francis J, 1947, Bovine Tuberculosis
6. Hancox M, 2000, Agric Committee Appd.
15 (maps, graphs are in 4 letters annexed to 2002 Anderson
& Follett Royal Soc Foot & Mouth Inquiries
7. Hancox M, 2003 EFRA Com report
Bovine TB Ev 66-69
8. Hancox M, 2004 EFRA Com ev 37-44
9. Hancox M, 2006 EFRA Com Ev 52-58
10. Hancox M, www.badger.org.uk News 31 May
2006 and October 2006 Badger Trust news "No
such thing as closed herds".
11. Hancox M, www.stopwaronbadgers.org
12. More S, 2007, Vet Rec. 161: 208
13. Myers J, Steele J, 1969, Bovine tuberculosis
control in man and other animals
14. Neill S, 1994, IFN test, Proc. Soc. Vet Epidemiol:
1; and Vet Rec 135:134
15. Ritchie J, in Stableforth A 1959, Infectious
diseases of animals Vol 2:713
16. Wilesmith J, 1987, NVL cases at least 70%
with TB Epid Inf. 99:173 (Dunnet Report para 32 claims
80% have TB)
17. Woodroffe R, 2005, Cattle-badger spillover,
J An Ecol 42:861
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