Memorandum submitted by Martin Hancox
BOVINE TB
EXECUTIVE SUMMARY
1. One of the saddest and most depressing
aspects of Cattle TB out of control is that Defra are still consulting
on control measures re-re-identified in your last Report HC432.
There seem to be three main areas of confusion (1-7):
a Transmission "We do not know exactly
how cattle become infected with TB";
b Cattle: Why are current controls not working?
Why do Hotspots develop?; and
c Badgers: role in cattle TB, do culls work?
2. An overview of the vast wealth of information
from Irish work on all 3 issues is presented, since it seems to
be widely unknown here.
3. The future of the Randomised Badger Culling
Trial RBCT, Krebs/Bourne is questioned by the Godfray Review:
"a very expensive academic exercise utilising experimental
approaches inappropriate for the problem", "an uncertain,
ambiguous attitude . . . recommendation for continuing could have
been more clear "(ISG) "lukewarm support" (Mollison).
The hasty and premature fundamentally flawed POLITICAL decision
to abandon the reactive cull (Nov 2003), was taken by Ministers,
Defra Chief Scientist & Vet without the ISG nor consulting
Defra's own expertise within "an ostensibly science-based
government department" (2 : pp 22, 25, 29, 30; ISG response
pp 8-9, 14). The claim that the perturbation effect of culling
made cattle TB 27% worse was not really challenged at either the
ISG Open meeting 19 Dec nor EFRA Committee 10 Dec; and fed into
the Bern Convention Defra annual submission and erroneously into
the "Strategy Consultations" which have had to be extended
to 4 June. Having ruled out a reactive culling policy, the RBCT
cannot now definitively quantify the role of badgers, and proactive
eradication of a legally protected species was deemed politically
unacceptable (Jeff Rooker) and contrary to the Bern Convention.
Krebs noted (1997) that a qualitative effect ought to be evident
after a couple of years (2000)(p 93) Professor Bourne told you
in February last year that (so far we've killed X . . .)"
You would expect that to be having an effect on local incidence
of TB, if it is going to have an effect (Ev 39), so having now
culled 8,379 (Jan 2004 6,313 proactive, 2,066 reactive) results
are still not "statistically significant" which may
indicate they never will be. Using Defra's own figures of 25%
infected and a third infectious the 8,400 badgers amount to 650
infectious in 2000 km2, 1/3 km2, so any effect will be swamped
by cattle spread rising by 20% a year. Most of the badgers have
been culled in some areas eg Exmoor but the Gloucester cull for
example may be under 10% of the population (20 /km2). The Krebs
trial was meant to include two thirds of hotspots but is a mere
fraction now. So rather than an arbitrary 20% reduction it is
admitted para 25 "One has to ask whether it can really be
suggested that a reduction of a few percent in breakdown rates,
the most that is even remotely consistent with the data, will
be of practical value or interest. The Reading University economic
analysis apparently shows such culls will be wildly uneconomic
(Déjá Vu 1986 Dunnet & McInerney still with
ISG, para 96, 102). The 8400 culled so far have cost £25
million, £38,000 per infectious badger, if the trial continues
to 2006 or 2008 (2) a further £21 or £35 million ie
£60 million over a decade on a trial meant to last five years.
So far 57% of traps interfered with, 12% "went missing"
at a replacement cost of £400,000 (apart from costs of re-trapping);
policing and helicopter monitoring of "activists" who
know exactly the cull areas, adding to costs and "confounding
factors" (Farmers Guardian 12.3.04). The interim data on
herd breakdowns and spatiotemporal prevalence in badgers should
be released to Defra to urgently inform policy (1, 2), and probably
already show no demonstrable effect of culls and that badgers
are simply catching TB from cows: the LINK, heretically. ISG para
6 "It cannot be presupposed that badgers represent an external
and independent source of the disease that is continually transmitted
across badger to cattle herds. The likelihood of cattle-to-badger
transmission means that the risk from badgers to cattle could
depend also on the incidence of TB infection in cattle."
When cattle TB gets beyond the "critical mass" NVL/VL
lesion threshold TB spreads like wildfire (answering 1a &
b above), as in many countries worldwide (with or without "wildlife
reservoirs") so that it is unbelievable that Godfray can
think multiple reactor breakdowns might be due to a badger (p
58) and that Bourne reckons cattle-cattle spread MAY be more important
than previously recognised, although within herd spread not proven
by spoligo-typing yet (TBF 93).
4. In fact many aspects of both ISG and
Defra's 5-point strategies show a marked "lack of clarity"
as to their objectives and likely cost-effective policy relevant
impact and should be scrapped (2, see end Conclusions). And given
the spectacular failure and incompetence of the entire ISG in
subscribing to ending reactive culls supposedly via "Robust
Science" (44), they should all be sacked ie given customary
knighthoods, CBEs etc; Regrettably, badger TB "Scientific
Research" is a growth Industry.
5. A major contributing factor in the present
crisis is a shortage of cash for testing and of vets (50); scrapping
the costly pointless past-its-sell-by-date badger cull would release
£21-£35 million infinitely better spent elsewhere.
Transmission, Pathogenesis, Diagnosis
6. Three of the nicest ironies amidst "The
Great Badgers and TB Debate" is that since the M. bovis
genome is smaller than M.tuberculosis cattle must have acquired
this "pneumonia" from man originally; doubts about the
importance of cattle-to-cattle spread have arisen precisely because
annual testing and movement bans stop TB so effectively; and whether
it was due to cock-up or conspiracy the 2001 foot and mouth (FMD)
epidemic has demonstrated serendipitously beyond peradventure,
that abandoning these measures simply lets TB explode out of control
(4-6, 24, 25).
7. Understanding the development of TB and
its transmission is clear from studies of:
7.1. pattern of lesions in abattoir material
shows how TB is acquired and passed on (8-14, 30);
7.2. clinical sampling for infectious sputum
and faeces (both from coughed up lung pus), milky uterine discharges,
urine (15);
7.3. experimental transmission (19-23);
7.4. "in contact" calves experiments
(16-21, 36);
7.5. patterns of spread epidemiologically,
including spoligotyping, RFLP, VNTR genomics: the Furness Cumbria
breakdowns had a rare Shropshire spoligotype, untraced spread.
8. Because bovine TB is evolutionarily younger
than in man, "closed tubercles" are rare, TB is progressive
and failure to control the proliferation of bacilli is reflected
by the growth, multiplication and spread of lesions so the disease
remains "open" infectious at any stage of the disease
with the following implications:
8.1. Infectivity, early microscopic or Non
Visible Lesions (NVL) in the lungs shed few bacilli intermittently,
progressing to Visible Lesions (VL) at gross abattoir inspection
shedding increasing numbers of bacilli continuously up to 38 million
per day (4 billion in man). (14. 22).
8.2. Incubation. It takes about a year to
reach the more infectious VL stager then "sputum positive"
(49 8-11, 26). Calves "in contact" with either cattle
or in a very artificial yard experiment TB badgers, took 6-12
m to become reactors (16, 18, 23), Little or no transmission in
experiments using low doses, lasting under a years or in well
ventilated barns (17, 19-21).
8.3 Tests. Skin test negative then inconclusive
reactor (IR) in early cases: too few bacilli for immune responses
then increasingly positive measurement with progressive lesions
(12); then negative or anergic in late TB: immune system swamped
with bacilli (27). Two specific difficulties arise:
8.3.1 initial infection is overcome
so IR or weak reactors revert to false negative, such as with
juveniles for 2-3 years until the stresses joining main herd.
Singleton IRs are probably false positive, but in herds with other
"good" reactors are probably tuberculous; many skin
test IRs are IFN+ (30). Some latency cases cause outbreaks in
"closed" herds even a decade later (4, 7, 14).
8.3.2 Anergy may be temporary or enduring.
Immunosupression occurs with pregnancy/lactation and TB calves
may be born to temporarily anergic cows "riddled" with
uterine TB (14): critical since cows "need" a calf a
year to keep up milk yield. Susceptibility may be increased with
concurrent disease such as BVD, other pneumonias, or trace element
deficiency (49). Chronic herds arise via non-reactor VL cases:
9% in 36% of 47 depopulated herds (27). Three such anergic cows,18
herd breakdowns in Cornwall including contiguous ones, since many
farmers have forgotten the importance of double fencing to stop
inquisitive nosing soon after juxtaposition (8, 19).
8.3.3 Detailed comparisons of IFN, skin
test, pathology have been made, but with present antigens IFN
can only be a backup to skin tests (12, 16, 20, 21, 30, 31). A
radical rethink on testing may include caudal fold skin test,
use of only bovine PP antibody tests for anergics, rapid PCR for
faster herd derestriction etc (20, 29, 32-5)
Why Are Current Cattle Controls Not Working?
Why Do Hotspots Develop?
9. The absolute imperative in cattle TB
eradication schemes is to remove reactors before they reach the
more infectious VL stage. Annual testing surveillance locates
TB herds early enough that 60 day repeat testing can then clear
TB from the herd and pick up any potential new herds arising via
contiguous spread or sold on carriers, and gradually clear an
area of TB as explained previously (4, 8-11). The superb Area
Eradication Scheme overseen by Macrae, Ritchie and Richards (5)
hence cleared most of the country by the early 1970s, and because
the test is only 80% accurate the movement ban into newly TB-free
areas was the only way of guaranteeing they stayed that way. So
in Glos only 2% of cattle were VL 1971-7.
Things began to go insidiously wrong when both
KEY Measures: annual tests/movement bans were gradually relaxed,
and exacerbated when MAFF were over-stretched with BSE then FMD.
Longer test intervals and more replacement stock movements at
the height of BSE in 1992-93 doubled the SW herds from 121 to
232 and the suspension of testing during FMD plus two years subsequent
backlog of overdue tests with unrestricted restocking and other
movement of untested cattle completed the debacle. Although 1997-98
52% of breakdowns were still single reactors, importantly some
15% had over five reactors so local flare ups occur, and there
was a rise in clusters of repeat/contiguous hotspot breakdowns
1987-96 (Krebs maps p 54, 91). Also whereas TB had been semi-contained
in the tiny SW blackspots 1976-909 by 1999 over 50% of breakdowns
were in areas TB-free for 10 years: Avon 15 out of 25, Cornwall
103 in 139, Devon 54 in 99, and "frontier" counties
spreading northwards. Derby 6 in 69 Shropshire 4 in 5, Staffs.
29 in 30. Quite clearly there has been an expansion and infilling
of hotspots, so the two year test "cordon sanitaire"
(1, Annex E) has been leaking like a sieve given the virulence
of fulminating breakdowns at the epicentre, where most of the
herds in a neighbourhood have gone down, according to farmer comments
Devon, Wilts, Derby. 25% of herds Glos. 15% Cornwall. Rise 1997-2002
from average of 1.9 to 4.7 reactors/breakdown and period under
restriction 215 to 292 days (1).
Critically, in areas with up to 3-4 year testing
a number of new hotspots had got going before they were discovered,
1993 both Exmoor, 25 herds 14 confirmed, and Hereford/Worcs. with
a bad VL breakdown (28), followed by Staffs/Derby in 1995-97,
plus Shrops; and in 2000 a Hatherley/Okehampton cluster of 16
herds, some with 300 dairy cows, and the nearest TB 18 m previously
being nine miles away, and like Exmoor a parish which hadn't seen
TB for 20 years. The Staffs hotspot started with one (or 2) index
oases and has now cost 6,000 reactors, one 2001 herd 62 dairy
cows (35 VL). Pre and Post movement tests miss 1 in 1,000, so
of the 2002 528,000 cattle exported from the 10 worst TB counties
that could mean 528 new breakdowns and potential hotspots (1).
10. It is worth highlighting three main
factors which underpin these problems:
10.1 NVL/VL, Francis 1947 warned very clearly
"If any animal reacting to the tuberculin test, even with
very slight lung lesions is left in a herd spread will be more
or less rapid" and may affect 75% of the herd. Well shown
by a 150 strong Chippenham, Wilts dairy herd, a small breakdown
2000. 1 carrier must have been missed, no test March 2001 due
FMD, so by 2002 there were in Feb 34 (28 VL), Mar 189 Jul 4 =
56 reactors or 40% of the herd, clear Dec, but May 2003 another
20, so 102 lost (Farmers Weekly 9 Aug 2002, 9 May & 5 Dec
2003). Most of the neighbours affected, and clearly if the first
wave of reactors are VL mostly, in a big herd, there will be many
more to come.
10.2 Herd Size. Francis also noted, since
1900, the bigger the herd the greater the risk cases will be missed.
Clearly an 80% accurate test may miss 2 in 10 herds with 1-2 cases;
and herds with 6 or 40 reactors have a 4 or 9% chance of an infected
animal remaining in the herd after 2 clear tests, so that a subsequent
6 m check test may in 100, 101-200, 200+ strong herds have recurrent
herd incidents in 6.9, 10.4, 14.2% of cases. The incidence, duration
of incident, number of reactors, and repeat breakdowns all increase
with herd size, and there is a greater chance of "time bomb"
anergy cases (25). Some 500 or 1,000 strong dairy herds have endemic
chronic TB for over a decade. Average dairy herd size 47 in 1975,
now almost 70% are over 100 animals (versus only 24% of beef herds)(1).
10.3 Other contributory factors may be: greater
stock movement (QV FMD), the drop from 260,000 GB herds 1960 to
100,000 now meant many dispersal sales, and the consolidation
often of several village farms into one necessitates hired distant
grazings and exposure to more contiguous risks; susceptibility
via immunocompromisation by stress intensification/productivity;
rise in diseases such as BVD; greater test inaccuracy due to rise
in Johnes disease or trace element deficiencies (49).
11. Clearly fulminatingly active persistent
hotspots get going when a new herd cluster remains undiscovered
for a few years, VL cases can spread TB widely in bigger herds
so that many more latent cases then come on stream. Years of intensive
testing are needed to bring them down off "the boil",
but even then long established are like semi-dormant volcanoes
waiting their chance to erupt into life with any relaxation of
testing. The success of the 1960s and 70s to be repeated (4, 5).
OLD BROCK:
VICTIM OR
VILLAIN?
12. The rationale justifying badger culling
is that being social and long lived, they are an ideal self-maintaining
reservoir host of TB, and the cause of cattle herd breakdowns
in the APPARENT absence of a cattle source. Three flaws in this
view:
12.1
Transmission. Cattle TB is 90% respiratory, 10% by
ingestion (6, 14) so it is improbable badgers can be guilty by
either route.
Inhalation. Only the smallest aerosol sputum droplets
can reach the innermost upper alveoli, lower down in cattle and
man the muco-ciliary lift sweeps them along to be harmlessly ejected
(13). Prolonged exposure needed to ensure transfer: 130 hours
shared classes in a school, over a month in the badger/calf experiment
(31, 36, missed by 37). Superexcretors may infect folk in air
flights, or cattle at shows.
Ingestion. Calves can catch TB via a 1 million bacilli
dose in raw milk, but are hardly likely to ingest 3 cc of badger
urine (300,000 bacilli/cc) (14,24). Farmers with progressive bovine
TB can infect cattle, half respiratory, half urinating on hay
to "improve the salts" according to folklore (43).
12.2
Too few infectious badgers to be self-maintaining
and most TB badgers have simply caught TB from the preceding cattle.
Woodchester study. Over 14 years only 58 infectious
in 188 infected. The 1986-89 breakdown of 94 cattle caused new
clan infection, as in N Woodchester 1979, 32% of badgers with
TB, like Hereford 70%, Exmoor 85% with TB (38-41), Similarly out
of 1960 deer between 1971-96 only 30 had TB (12 fallow, nine roe,
nine sika), Plus eight red and one muntjac since . . . a spillover
from cattle, although TB can be spread in farmed deer (42).
Looking at the 24 counties with TB badgers (culls
+ RTAs), the numbers (to 91) mirror the cattle breakdowns in the
15 years to 1993: counties with 15 breakdowns: Glos 940, Cornwall
540, Avon 363, Devon 224, Wilts 179, Dorset 99, Dyfed 17; 10-14
breakdowns: Somerset 11, Shrops 2, Cumbria 2, Heref/Worcs 10,
Cheshire 10 Staffs 21, Sussex 56; under 10 breakdowns: Essex,
Kent, Oxford, Suffolk, Surrey, Warks, Clwyd, Glamorgan, Gwent,
Lothian. Whilst the RTAs to 1996 alone out of 22,323: 961 with
TB (890 SW, 49 rest England, 21 Wales, one Scotland).
12.3
Culls Work? (See Tables)
12.3.1
RBCT. The reactive cull was ended supposedly
because it caused a 27% increase in cattle TB consistent across
the nine areas (44). But there are three flaws in this view:
calves take six to 12 months to become reactors and
extra time lags occur for the cull to reduce density to decrease
or perturb badgers to initially increase cattle TB and for transmission
to occur, and the annual test to come due. Two thirds of the 2,047
badgers were culled in the last 4½ months, and of the areas
which had run over 15 months, ABCE that was 520 out of the 981.
Using MAFF data as in Summary, 2,047 would include
150 infectious or 1/6 km2, only areas BCE with over 100 culled
by January 2003 ie 15 infectious each, hardly "causal"
.
Statistical validity is outlined in Krebs pp 58-91,
87-96, 128-30; your report pp 4-129, 47-9, 93, and Godfray Box
3 & 6, The pivotal error is that the analysis assumes Poisson
ie independent incidents, when it is perfectly clear that repeat
and contiguous ones are NON-INDEPENDENT, hence the small difference:
231 control TB herds, 331 in reactive ones . . . or arisen "by
chance" (2). So much for Robust Science and Statistical Rigour,
or indeed plain commonsense.
12.3.2
Offaly. The drop in cattle TB either as number
of reactors or reactor rate (APT ) was similar in the project/control
areas: 1,458 out of 55,000 cattle, 5,646 out of 150,000. Three
times the number of cattle the impact less. And it is just silly
to claim culling 141 TB badgers versus 7,000 reactors made the
slightest difference, one badger/4 km2, Over half culled in first
year but no one off drop. (45). The four areas trial also claims
a 90% drop in cattle TB due to badger culls, but is likely to
equally unbelievable.
12.3.3
Steeple Leaze, Dorset. 1973-75 , five tests/a.
244 reactors (83 VL) so 1976-77 only one case. That solved cattle
TB, gassing afterwards irrelevant (46). The Thornbury cull analysis
failed to recognise the role of NVL cattle, 70% infected, or contiguous
effects, and if there were 2,000 badgers in the 104 km2 that is
only 160 infectious or under two per km2, Hartland was merely
a success because of area synchronised testing (47). Badger culling
"proof" stories are in fact a perfect demonstration
that systematic intensive cattle testing will eradicate cattle
TB. The "scientific" explanations of this are entertaining
(48).
13. Two side issues: Milk Pasteurization/Public
Health. Most countries with TB eradication schemes ban un-pasteurised
milk (N & S Ireland, Scotland), with rise in hotspots needs
full GB ban. NVL/VL data used to be given in Chief Vet Animal
Health reports, then unconfirmed/confirmed; those by J Scudamore
lack either . . . this data plus slaughter-house state are a barometer
of improving/worsening TB.
14. Godfray reviews the verdicts of Krebs,
your HC432, hence exposing the ad hoc nature of the 5 Point &
ISG strategies. Many issues are "Lacking in Clarity"
as to objective, value, point in continuing with their pursuit
cost-wise:
— RBCT Reactive cull impact was NOT
consistent across areas, did not prove a perturbation effect,
a link or anything at all. Far from being a "scientific"
reason to stop culls (WITHOUT admitting there is 0 evidence badgers
CAN give cows TB) farmers "rightly" concluded, "a
link", badgers "missed" = MORE culls needed, ie
a political own goal through lack of joined up thinking. A faint
idea of a 1-2% drop due to culls with cattle spread going up 20%/a
. . . scrap the waste £.
— RTA SURVEY a woolly idea that badger
prevalence needed re. reducing density and maintenance of TB/vaccines
etc, but huge study already 12.2, Scrap it.
— IFN PILOT already known IFN can de-restrict
quicker, 8.3.1/8.3.3. Scrap it.
— PATHOGENESIS ISG have focused on
Neill (22), 2nd Report, and conclude infectivity peaks early then
declines, so early cases missed by test (20) are a problem. Overlooks
huge infectivity later NVL/VL stage. Their calf contact study
uses intranasal inoculation which turns calf into a "nebuliser"
(better if natural infection 16, 18), and study too short for
much transmission to occur. The alternative, sputum positive cases
amongst older abattoir cases already done (9).
— MODELS based on Woodchester, assume
badger TB self-maintaining at 11-22%. Without topping up from
cattle, even Woodchester 32% AFTER cattle 12.2 so models are rather
silly despite being in "peer review" journals (7), Incidentally
Derby is a 25th county with TB badgers AFTER cattle breakdowns
12.2.
— VACCINES "03 Scoping study,
Still 10-15 years away, neither badger or cattle one likely to
work, badger contribution too small, a better cattle test will
be available long before any vaccine viable 8.3.3.
Table 1
BADGERS CULLED IN REACTIVE TRIAL AREAS: 1998-2003
| |
| January
2001 | January
2003
| September
2003 |
A | Glos/Herefd
| Blaisdon | 34 | 34
| 117 |
| B | Devon/Cornwall | Hartland
| 107 | 165 | 301
|
| C | E Cornwall | Otterham
| 178 | 206 | 394
|
| D | E Herefd | Puddlestone
| — | — | 122
|
| E | N Wilts | Cold Ashton
| — | 56 | 169
|
| F | W Cornwll | Stithians
| — | 62 | 435
|
| G | Stafs/Derby | Nettley Knowle
| — | 149 | 256
|
| H | Devon/Somst | Brandon Hills
| — | — | 159
|
| I | Glos | Alderton
| — | — | 94
|
| J | Devon | Cadbury
| — | — | —
|
Totals |
| 319 | 672 | 2,047
|
| |
| | |
|
(From EFRA 2003 Ev 48 & Donnelly 2003 Nature 426: 834-7)
Table 2
THE EAST OFFALY BADGER CULL
Year | Project zone
| | Control zone |
| No of reactors | APT
| Badgers cull/TB + | No of reactors
| APT |
1988 | 326 | 3.91
| (107/7) | 910 | 3.39
|
| 1989 | 362 | 3.51
| 700/86 | 982 | 3.34
|
| 1990 | 299 | 2.89
| 197/24 | 904 | 3.16
|
| 1991 | 194 | 2.69
| 117/13 | 979 | 4.47 (a rise)
|
| 1992 | 89 | 1.35
| 108/7 | 594 | 2.53
|
| 1993 | 54 | 0.80
| 62/8 | 404 | 1.90
|
| 1994 | 54 | 0.79
| 48/3 | 443 | 2.11 (a rise)
|
| 1995 | 30 | 0.46
| — | 430 | 2.10
|
Totals | 1,458 |
| 1,232/141 | 5,646
| — |
| (1996 | 60 | 0.92 (up)
| | 327 | 1.76)
|
| (1997 | 20 | 0.31
| | 333 | 1.74)
|
| (APT = Animal reactors per thousand tests) |
| | |
| |
| | |
| | |
CATTLE DATA | 559,000 (excludes buffer zone)
| 150,000 |
| 1988-95 | 1,458 reactors |
5,646 reactors |
| No reactors 32630 = drop 91%
| 910430 = drop 53% |
| APT 3.910.46 = drop 88% |
3.392.10 = drop 38% |
| (by 1997 no reactors 20, APT 0.31 = drop 92%
| 3,331,74 = drop 49%) |
| (Eves, 1999, Irish Vet J 52:199 & Dolan ERAD paps'97)
| |
BADGER DATA cull 1989-94, six years, 1,232 of which 141 TB+; in 600 km2
ie 1/4 km2 over half in first year. NB some culls in "control" zone re bad breakdowns and farmer DIY and 501 in buffer zone of which 41 TB+
|
|
| |
PS In 2002 6.3% of Offaly herds were under restriction, as bad
as Eire average of 6.5 . . . so culls didn't solve anything.
BADGERS have been increasingly blamed for causing cattle
TB since 1971 . . . because supposedly badger TB is endemic and
widespread, and culled since 1975 . . . HOWEVER, flaws in this
view support a purely CATTLE explanation.
1. Cattle TB was countrywide at the start of Area Eradication;
annual testing and banning cattle movement into newly TB-free
areas brought it down to tiny southwest hotspots by the 1970s,
without any badger culling;
2. Why didn't the "endemic" badger TB reservoir
reinfect these areas then?
3. Badger culls 1975-90 made no difference, about 100
TB herds/a . . . graph.
4. The expansion of cattle TB northwards was by more
movements linked to BSE/FMD.
5. The 1940s Midlands hotspot was via Irish cattle imports
. . . the southwest was not a hotspot then (nor SW Wales). Parishes
either have/have not got TB badgers so solid blocks in map an
artefact . . . actually a denser cluster of TB herds. The SW became
a hotspot because of a 50% increase in stocking 1964-74. Mild
wet climate favours permanent pasture: intensive dairying AND
lots of worms for Brock.
6. Northern Ireland have always regarded badgers as a
Spillover from cattle TB, so are neither blamed nor culled . .
. same curves in graph—long term climate changes.
REFERENCES 1. Consultation,
New GB Strategy on bovine TB, Defra/Welsh/Scottish versions.
2. Godfray H, 2004, Independent Scientific Review RBCT,
& ISG Response.
3. Hancox M, 2004, submission to 1, includes both in
4 . . . available to public; Defra,
4. Hancox M, 2003, EFRA Cttee Appd 6 & 7, & 2000
Report Appd.15 ALSO 5-7.
5. Cattle TB Schemes Lett Appl Mic 31:37, Resp,Xed 94:1007,
Tuberculosis 81:185
6. Transmission Cattle LAM 28:242, Resp M, 93:220, Badger
LAM 24:226, J Agric.125:441
7. Trial compromised/Models J Agric. 139:223 Great Debate,
142: in press oulls, Resp M 96:842 Cattle crisis, 97:1075 Latency,
Microbiol Today 29:166.
8. McIlroy S, 1986, Vet Rec 118:718 reactors.
9. Neill S, 1988, Vet Rec. 122:184 reactors.
10. Cassidy J, 1999, Vet Rec 140:139 reactors.
11. White P, ERAD Selected Papers 1996:64 abbatoir.
12. Collins J, ERAD Selected Papers 1996:55 abbatoir.
13. Medlar E, 1940, Amer Rev Tuberculosis 41:283 lung lesions.
14. Francis J, 1947, Bovine TB, Staples Press pp 89-90, 93,
95.
15. Steward J, 1941, Vet Rec 53:521 clinical samples.
16. Costello B, 1998, Vet Journal 155:240 calf contacts.
17. O'Reilly L, 1988, Irish Vet News 10:11 contacts.
18. Svensson in 23, calf contacts.
19. Neill S, 1989, Vet Rec 124:269 calf Contacts.
20. Neill S, 1992, Vet Rec 131:45 calf contacts.
21. Cassidy J, 1999, J Comp Path 121:321 calf contacts, also
119:27 early lesions.
22. Neill S, 1988, Vet Rec 123:340 experimental dose.
23. M'Fadyean J, 1910, J,Comp Path Therap 23:239 & 289
inhalation/ingestion.
24. Griffin J, 1995, Irish Vet J 48:228 cattle-to-cattle transmission.
25. Goodchild A, 2001, Tuberculosis 81:23 cattle-to-cattle
transmission.
26. Griffin J, ERAD Selected Papers 2000-1 :54, infectivity.
27. Costello E, 1997, Vet Rec 141:222, anergy in depopulated
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Martin Hancox
May 2004
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