3. Memorandum submitted by
Former Veterinary Officers, State Veterinary Service
Further to my letters of 16 October and 6 November
I enclose a summary of what we would like to present to the Committee.
We are concerned that a number of the assertions
put forward by the ISG whilst theoretically feasible are in fact
implausible in the light of field experience of the realities
of this problem.
In this context we would like to elaborate on
three main areas namely:
1. The nature of TB in the badger.
2. Cattle to cattle transmission.
3. The culling efficiency of the RBCT.
OF TB IN
1. Tuberculosis has a different manifestation
in most species. In the badger it is fundamentally different from
TB in cattle essentially due to the lack of development of a hypersensitivity
response which is a prime feature of infection in cattle. Thus
small numbers of organisms infecting cattle produce a vigorous
cellular response which results in extensive cell death and the
development of large cold abscesses in the affected tissues usually
the lung and respiratory lymph nodes. This is in fact the host
immune reaction to TB. Whilst causing disease and disruption to
the affected organs the changes inside these abscesses strongly
inhibit the TB bacteria and kill many of them.
The badger does not show such a vigorous destructive
reaction but rather a slowly progressive proliferative reaction
which eventually results in cell death as numbers of bacteria
increase markedly. TB lesions are thus relatively much smaller
but contain relatively vastly more bacteria than those of cattle.
TB bacteria do not produce toxins but rather cause lesions as
a result of their highly antigenic cell walls to which different
hosts may respond with greater or lesser aggression.
2. Once a badger develops disease all the
members of that social group are likely to become infected due
to the confined living space in their underground tunnel systems,
their highly gregarious nature and constant mutual grooming. But
that seed of infection (the primary focus) will usually only progress
to produce disease and eventually death in a minority of cases.
Latency is a feature of TB in many species and this is so in badgers
and cattle. The bulk of infections in badgers, usually 70% or
more will become latent or dormant. A small number of badgers
may resolve the infection completely and self cure. But the latent
infections remain fully viable and may breakdown under stress
which may be of nutritional origin, intercurrent disease, senile
deterioration or social disturbance and disruption. Some badgers
may develop fulminating disease (Gallagher et al 1998).
Badgers with terminal generalised tuberculosis
can excrete vast numbers of bacteria particularly when the kidneys
are infected. Counts of several million bacteria in a full urination
have been recorded (Gallagher and Clifton-Hadley, 2000).
When infection is acquired by a bite wound from
the contaminated mouth of another badger, the bacteria are inoculated
either deeply subcutaneously or intramuscularly and rapid generalisation
of infection usually occurs, causing progression to severe and
often fatal tuberculosis which may develop in a matter of several
months (Gallagher and Nelson, 1979). Respiratory origin infections
have a longer duration and cases in an endemically infected population
(Woodchester) have been monitored showing intermittent excretion
of infection for a year, with the longest recorded case excreting
for almost three years before death.
The above ground mortality due to TB is estimated
as about 2% of the population per annum. Thus in the South West
alone with its now extensive endemically infected areas the annual
deaths due to TB will be of the order of at least 1000 to 2000.
Tuberculosis has an unfettered progress in the
badger population and the cycle of infection and disease in the
badger has long been known to be self sustaining (Zuckerman 1980).
Over time the badger has become well adapted as a primary reservoir
host of bovine TB infection.
3. The Thornbury Trial, Gloucestershire
was set up with the agreement of the then Nature Conservancy and
MAFF to test the hypothesis that infected badgers were spreading
TB to cattle. Complete social groups were removed from the trial
area by gassing of setts whilst routine tuberculin testing of
cattle herds continued. Results are shown below.
The trial area was 104 km2 with 158 farms and
over 12,000 cattle. Complete cessation of new cases of TB in cattle
indicated that in this area all infections had been of badger
This trial was replicated in Steeple Leaze,
Dorset by staff at CVL (now VLA) where again complete cessation
of new cases resulted, implying badgers were the sole source of
infections there. This effect lasted seven years as thereafter
the farms switched to arable production so whilst the duration
of the effect may have been longer this could not be determined.
Whilst these trials were progressing strategic
control of badgers by gassing was being carried out in the problem
areas from 1975 until 1980. In that year a moratorium was introduced
during the Zuckerman review. It was restarted later that year
but halted in 1981 following the review. These control actions
resulted in a more than fourfold reduction in new incidents of
TB in cattle herds over this period of five years as shown in
the graph below (Krebs 1997).
4. Tuberculosis of cattle can be a highly
infectious disease resulting in spread within herds and movement
of infected individuals has been implicated in spread of infection
to other herds. But the frequency with which this occurs in the
field situation remains a matter of debate. Cattle to cattle transmission
is reported to be of low frequency in the field, in a review of
this subject by Menzies and Neil (2000). Features of the current
epidemic which are relevant to the assessment of the frequency
of this mode of infection are:
Over recent years from 40 to
55% of outbreaks involve a single reactor and 60% to 80% involve
less than three reactors.
In the majority of breakdown
herds (65%) reactors are only found at the initial test
Reactor herds are usually identified
during the autumn round of testing as cattle are brought into
the winter housing. Testing during the winter months usually clears
the herd. But if between cattle spread occurred it would be most
likely during this period of confinement in the buildings.
Analysis of testing data during
the Steeple Leaze clearance trial showed a peak of infections
of the circa 600 reactor cattle which occurred in May-June whilst
the cattle were at pasture (Wilesmith et al 1982).
None of the 200 reactor animals
removed from farms in the RBCT for bacteriological sampling were
found to be shedding tubercle bacilli (Sainsbury and Gallagher,
The distribution of different
spoligotypes in the cattle population is highly clustered geographically.
If cattle movements have been spreading the disease around the
country then the types would be randomly distributed and this
pattern would not be seen.
The great majority of the TB
isolates from cattle and badgers (and other mammalian species)
in any area are the same spoligotype, indicating that infection
is cycling between these species.
The ISG appear to assert that if an animal is
infected it will be shedding bacteria. But this is in conflict
with field experience where we have found that unless the animal
has lung disease it is highly unlikely to be infectious and associated
with multiple cases. This is in line with medical experience where
routine tracing of contacts of patients diagnosed with TB is normally
carried out only if they are sputum smear positive.
Compared with badger lesions there is a relative
paucity of bacteria in cattle lesions other than in those with
severe advanced disease.
Whilst the ISG consider cattle to cattle transmission
the main mode of infection they do not elaborate how many of the
outbreaks encountered during the RBCT were considered due to (1)
movements into the herd of infected cattle, (2) to contiguous
cattle contact or (3) to a badger source. Rather, they state they
have assumed equal weighting to all three sources in their estimates.
Yet analysis of on farm outbreak investigations prior to the start
of the RBCT had shown less than 10% to be associated with cattle
movements and approximately 90% considered due to a badger source
(Report 1995, Clifton Hadley 1995). This also correlates more
with the field trial findings at Thornbury and Steeple Leaze where
all outbreaks there were associated with badgers.
The ISG note the importance of translocation
of TB to other areas by movement of infected cattle. They cite
the 30 outbreaks post FMD in the four year testing area of North
East England where in five cases there was evidence of spread
of infection to small numbers of cattle in the recipient herds.
But of course this equates to no spread in 83% of these herds
yet some of the moved cattle had been there for almost two years.
The ISG also express concern over the sensitivity
of the tuberculin test and consider that it is not identifying
significant numbers of what they assume to be infectious individuals
which are fuelling the deteriorating TB epidemic. Two points need
to be considered in relation to this assertion namely:
All but two States in the EEC
have either eradicated TB using this test or are in the final
stages of eradication. Those two States are Britain and Ireland.
Both States have a reservoir of bovine TB infection in wild badgers.
Similar views to those of the
ISG stimulated a draconian test and slaughter campaign in West
Cornwall during the early 1970's using severe interpretation as
standard and partial herd slaughters. After several years this
was abandoned as it made no difference to the incidence of new
outbreaks. A draconian approach was also adopted in Ireland by
the CVO Downie in the late 1970's with the same outcome and was
5. Serious questions remain concerning the
efficacy of the culling approach used in the RBCT which is of
course fundamental to the proper conduct of a culling trial and
significance of its results. Points to consider are:
Minister's reply to a Written
PQ that interference with 57% of traps had occurred and a further
12% had been stolen (Hansard 2003).
Minister's reply to a Written
PQ that trapping efficiency had been as low as 30% (Hansard
Statement by DEFRA that culling
efficacy in the RBCT was 20% to 60% (DEFRA,2005).
Submission by a trapping team
supervisor (P Caruana) to this committee that trapping approaches
required by the ISG were seriously flawed (EFRACOM 2006).
ISG Final Report data showing
5 of the crucial initial 10 proactive culls were carried out in
midwinter which is well known to be the least successful time
Trapping was carried out for
eight days on average and only once a year.
The average annual rate for
the removal of badgers was 1.8 badgers per km2 with a variation
from 0.7 to 2.91.
Our local knowledge that trapping
success was poor.
Poor culling efficiency would be expected to
cause social disruption and dispersal (perturbation) of infected
badgers most of which would have been in a state of latent infection.
As discussed under 1. above stress caused by such disruption is
likely to cause latent infections to become activated and may
produce fulminating disease. Culling rationally must always aim
to remove the entire social group, as the infected unit. It should
avoid dispersing infection to make the situation worse both in
the badger population as well as for cattle and of course all
other species sharing the badger's habitat.
It is noteworthy that cage trapping was used
in the Hartland, Devon control exercise in 1984 and resulted in
a fall in confirmed herd outbreaks in cattle from 15% to 4% in
1985 (Krebs 1987). Thereafter annual incidence declined and held
at around 1% for nearly 10 years. In excess of 80% to almost 90%
of badgers were removed which required protracted trapping efforts
in some of the area. In some difficult parts trapping continued
for up to three months. The area involved was 62 km2 and no so
called edge effect was seen during or after this removal.
Dr J Gallagher, former
Senior Veterinary Investigation Officer, Devon and Cornwall, former
Independent Consultant to DEFRA TB Research Division.
R M Q Sainsbury, former
Specialist TB Veterinary Officer, Truro.
A T Turnbull, former Head
Notifiable Diseases Section, Tolworth, former Veterinary Advisor
to Krebs TB Review Group.
Clifton-Hadley, R S, Wilesmith, J W, Richards, M
S, Upton, P and Johnston, S (1995) The occurrence of Mycobacterium
bovis infection in cattle in and around an area subject to extensive
badger (Meles meles) control. Epidemiol Infect, 114, 179-93.
DEFRA (2005) Controlling the Spread of Bovine Tuberculosis
in Cattle in High Incidence Areas in England: Badger Culling.
Accessed 10 April 2006.
Gallagher, J and Clifton-Hadley, RS (2000) Tuberculosis
in badgers; a review of the disease and its significance for other
animals. Res Vet Sci, 69, 203-217.
Gallagher, J, Monies, R, Gavier-Widen, M and Rule,
B (1998) The role of the infected non diseased animal in the pathogenesis
of tuberculosis in the badger. Vet Rec 142, 710-714.
Gallagher, J and Nelson, J (1979) Causes of ill health
and natural death in badgers in Gloucestershire. Vet Rec, 105,
Hansard (2003) Bovine
TB. 8 December 2003, column 218W. London, Hansard.
Hansard (2004) Bovine
TB. 29 April 2004, column 1189. London, Hansard.
Menzies, FD and Neill, SD (2000) Cattle to cattle
transmission of bovine tuberculosis.
Vet Journal, 160, 92-106.
Krebs, J R (1997) Bovine tuberculosis in cattle and
badgers. Report to Rt Hon Dr Cunningham MP. London: HMSO.
Report (1995) Bovine Tuberculosis in Badgers, 18th
report by The Ministry of Agriculture, Fisheries and Food, London,
Sainsbury, RMQ and Gallagher, J (2007) TB policy
and the ISG's findings. Vet Rec 161: 495-496
Wilesmith, J W, Little, T W A, Thompson, H V and
Swan, C (1982) Bovine tuberculosis in domestic and wild mammals
in an area of Dorset. 1. Tuberculosis in cattle. J Hyg (Camb),
Zuckerman, Lord (1980) Badgers, Cattle and Tuberculosis.
Report to the Rt Hon Peter Walker MP. London: HMSO.
3 Not printed. Back