1. Letter to Mr Roger Williams
MP from Rodger Garratt
Thank you for sending me a copy of the ISG's
report on their investigation into the epidemiology and control
of TB in cattle. It is a comprehensive document and has taken
some time to read and digest. As a result my response has taken
some time to assemble.
You said that you would be grateful for any
input I could offer. Accordingly I would like to offer you my
comments under four separate headings:
GENERAL REMARKS
1. Independent research or not?
The findings of this piece of Government initiated
research by an "Independent Scientific Group" must immediately
be brought into question by a statement apparently innocuously
hidden in this vast document.
How can one seriously trust the independence
of this body when they openly state on page 39 in paragraph 2.27
that "Added to this, the ISG had been given a very explicit
declaration by Ministers that elimination of badgers over large
tracts of the countryside was not acceptable as a future policy."?
With such constraints at the outset, it is unthinkable
that any trial design would be robust or extensive enough to test
the efficacy of culling badgers on anything other than a relatively
restrictive scale.
The only question that this piece of research
has answered, is that if the culling is restricted to such limited
areas (100km2) the benefit is equivocal, although it would appear
that the ISG did admit that persistence in proactive culling began
to show benefits. So, how much better would it have been on a
wider scale?
2. Scientific conclusions, or not?
Looking dispassionately at the report, the overwhelming
impression is that this whole piece of research has been contrived
by statisticians and the subsequent presentation of the results
dictated by statisticians. This may give it the veneer of being
a piece of scientific veterinary research, but we all know how
malleable the interpretation of statistics are to bias and subjectivity.
Reading through the analysis of all these figures it soon becomes
clear how much this may indeed be the case. For a document purporting
to be scientific, it is worrying to notice how frequently phrases
such as "unlikely to", "likely to", "could",
"suggest that", "appear to", "may be",
and "expected to" are used, to name but a few. I find
this alarming and disquieting in trying to assess the true objectivity
and consequential validity of the conclusions that are eventually
drawn.
Adding to this the doubt about the genuine independence
of this research I find it very difficult to be comfortable with
its conclusions.
SPECIFIC REMARKS
1. Historical evidence
I feel that the significance of what happened
back in the seventies has been largely dismissed by the ISG in
terms of its relevance to the present situation. I strongly disagree
with such a view. From 1968 and through the seventies and eighties
I was in practice in one of those problem areas described on page
28 (paragraphs 1.5 and 1.6), namely Wiltshire. We had a number
of problem herds in the early seventies. Following the elimination
of all the setts in the area by repeated gassing, these herds
had no more TB breakdowns up to the time when I left the Practice
in 1990. This was fact as I observed it.
One has only to look at figure 3.1 on page 59
to appreciate that the lowest level of TB disclosure occurred
between 1977 and 1988 after which it began to rise and has done
ever since. The end of the seventies was when gassing became an
unacceptable method of culling as the huge rise in public opinion
following The Badgers Act of 1973 began to influence political
opinion. This was fact.
In the late sixties when TB appeared to be approaching
the point of eradication the only real problem areas were where
there was also the highest densities of Badger populations. This
was also fact and too significant to be dismissed as coincidence.
I also know as a fact that even before and also during the gassing
of the seventies, farmers were carrying out their own assaults
on setts and so by the time the moratorium was called in the early
eighties, the combination of official and unofficial sett destruction
had reduced the badger population, certainly in Wiltshire, to
the lowest level for some time.
From that point forward, the badger population,
totally unchecked, began to recover at a rapid rate. Family groups
grew too large and began to break up, with expelled badgers meeting
other expelled individuals and creating new setts of their own.
Almost certainly, infected badgers with a level of resistance
to the disease established in their own groups, met and infected
badgers with no resistance from other, clean groups. This was
undoubtedly natural perturbation and in my view contributed significantly
to the sudden dramatic rise in TB breakdowns in the early nineties
and has been doing so ever since.
Again it is no coincidence that these dramatic
rises have been seen in exactly the same areas that gave the problems
in the sixties. What is different is that these areas have grown
more extensive as the unchecked rise in badger population has
created natural perturbation into widening contiguous areas. One
of the most indicative signs of this increasing population is
the dramatic rise in the number of dead badgers seen on the roadside.
One rarely saw a dead badger in Wiltshire in the sixties and seventies.
I know that this section is reiterating known
facts, but I have included it to emphasise that I believe that
the culling of badgers would significantly contribute to the reduction
of TB in cattle, but only if carried out on a large and efficient
enough level. It did in the past and would do so again. The level,
efficacy and persistence of culling carried out in the ten proactive
and ten reactive trial areas were on an inadequate scale to show
this to be so.
What makes it even more difficult is that we
have a far higher badger population to deal with than was the
case forty years ago, because with no official or unofficial control,
badger numbers have risen exponentially.
2. Proactive culling in the trial areas
The ISG conclusions dismissed this option as
being ineffective in reducing cattle TB in these areas.
However I would question how thorough the culling
really was in these areas. Access was only allowed on to 70% of
these areas. (Page 169 paragraph 10.35ii) That's only just in
excess of two thirds. Traps were placed along the edges of the
prohibited areas, but compared to traps placed close to setts
and pre-baited before being set, not very satisfactory. It was
admitted that there had been reduction in the trapping numbers
due to sabotage.
Nowhere in the tables or text could I find a
clear indication of the estimated badger removal by proactive
culling as a percentage of the original population.
Unless one can quantify the efficacy of removal
how can the failure of cattle TB reduction be blamed simply on
perturbation? I would suggest that is a biased conclusion.
3. Perturbation
The ISG report cites perturbation as a counterproductive
effect of culling within a trial area (cf paragraph 2). However
there is absolutely no recognition of the fact that natural perturbation
due to the unchecked growth in badger population may be a factor
in the contiguous spread of cattle TB radially from the traditionally
troublesome areas (cf paragraph 1).
I find this a very unbalanced view.
4. Epidemiology—Cattle to Cattle transmission
The evidence of respiratory transmission between
cattle is based on the intranasal inoculation of the donor animals
with M bovis. Such experiments have then shown that these artificially
infected cattle can transmit disease to clean in-contact cattle.
This is making an initial assumption that this is how infection
occurs in the field; but does it?
What if, because of the idiosyncratic grooming
habit of cattle, infection is transferred from the mouth to the
nose by the tongue? Cattle are the only domestic species to push
their tongues into their nostrils as part of their normal grooming
process and they do this on a very regular basis.
If cattle do transfer infection from their alimentary
tract to their respiratory tract in this manner would they necessarily
be equally likely to transmit infection to the respiratory tract
of other cattle as they are shown to do when artificially infected?
Although this would account for the transfer of infection to their
own respiratory tract would it necessarily result in equal risk
to other cattle. I am not at all convinced.
I believe that this doubt needs to be investigated,
because it could alter the long-standing and I suspect somewhat
spurious assumption that the transmission of M bovis closely models
that of M tuberculosis in humans.
The ISG report mentions that increased movement
of cattle within high-risk areas and from high-risk to low-risk
areas is undoubtedly a significant source of increased herd breakdowns.
What I looked for, but couldn't find was whether there were any
tables identifying further spread within the herds that had broken
down as the result of importing an infected animal.
I must deduce from my failure to find such evidence
that any consequential spread within these herds was not observed.
The text from page 175-178 (paragraphs 10.64-10.75) seems to confirm
this. If cattle to cattle transmission really is a significant
cause of the escalation of the disease generally then surely the
failure to find significant evidence to this effect is most surprising?
5. Epidemiology—Cattle to Badger transmission
Until the 1930s the main site of cattle TB was
the mammary gland and in humans the site of M bovis infection
were the lymph glands of the throat, a condition known as scrofula.
The introduction of milk pasteurisation eliminated this human
condition, but it wasn't until the eradication of cattle TB gathered
momentum together with a greater understanding of milking hygiene
that TB mastitis was eliminated.
It is my view that until this point the only
plausible source of TB infection in badgers was via the licking
up of TB infected milk that had leaked out from cows lying at
pasture. In those days most grass was permanent pasture. Permanent
pasture is a rich source of earthworms and earthworms are a favourite
food of badgers. Added to this, I know for an observed clinical
fact that milk leaks out from the swollen quarters of recumbent
cows affected with mastitis.
It is also my view that since the eradication
of TB mastitis in cattle there has been very little transfer of
disease from cattle to badger.
There has been no research to investigate possible
cattle to badger transmission whatsoever. Any prolonged close
contact between badgers and cattle either at pasture or in buildings
has not even been investigated let alone assessed under experimental
conditions.
I therefore believe that to glibly make the
assertion on page 173 (paragraph 10.49) that the most likely cause
of reciprocal transmission between the two species is via the
respiratory tract is a very unscientific assumption. Not only
that, but it also demonstrates a serious ignorance of significant
clinical knowledge that might serve to widen the perception to
alternative hypotheses.
6. Epidemiology—Badger to Cattle transmission
What we do know is that the worst areas of cattle
TB are associated with the highest density of badger population.
We also know that the most common point of contact between cattle
and badgers is grassland, particularly permanent pasture.
Whilst admitting that there is much scope for
further research into the transmission of infection from badgers
to cattle the overwhelming circumstantial evidence suggests that
pasture is the most significant place of transmission and that,
if there were no badgers on the pasture TB in cattle would not
be a problem, as indeed it isn't where badgers are uncommon.
ANECDOTAL OBSERVATIONS
These case studies are taken from a paper I
gave to Powys LVIs in the autumn of 1995 at the request of the
then DVO. I include them to support my concern regarding the assumptions
about M bovis transmission that have been made since the very
inception of Inset 23 and that have been perpetuated ever since,
up to and including the conclusions drawn by the ISG.
Case History 1
A farmer in Hay on Wye raised beef cattle for
show. In order to augment each calf's milk consumption he would
move the calf from the dam to suckle a "spent" milking
cow purchased at market.
In this particular instance the cow had been
purchased some four months (from October to January) when a routine
test of the cow's herd of origin disclosed TB. I was asked to
test this cow as a tracing. She was a reactor and I carried out
the PM at slaughter. She had open TB (visible lesions in the lung
tissue), which were culture positive. These lesions were severe,
being of considerable size and number and could reasonably be
assumed to be resulting in the exhalation of considerable amounts
of M bovis infected material.
The herd was then tested. There were no reactors
or indeed inconclusive reactors, not even the calf she had been
suckling. A similar result pertained at the ensuing short interval
tests and the herd was duly released from restrictions. Subsequent
six month and annual tests also proved to be negative.
The infected cow had been indoors, in a building,
sharing air space with several other cattle and in extremely close
contact twice a day with the suckling calf, but there was no transmission
of infection.
Case History 2
A farmer moved from Hereford to Powys in September
with the intention of building up a 100 cow suckler herd. He purchased
the same month 24 Hereford x heifer calves to bucket rear. The
following May he sent these calves plus two home-bred calves to
rented grassland in Herefordshire close to the farm he had left.
In October these 26 heifers returned to Powys
and were housed together with five other purchased heifers, one
homebred heifer and one homebred steer all summered at his farm
in Powys. These 33 cattle were all housed in the same pen and
in the same building as older homebred store cattle.
Four months later, in January, I carried out
a routine herd test. From this group of 33 only the 29 purchased
heifers had to be tested.
Of the 29 there were 17 reactors and one inconclusive
reactor. All 18 came from the group of 24 that had summered in
Herefordshire and of the 17 reactors five of them were open cases
and culture positive. The subsequent whole herd test revealed
no further reactors or inconclusive reactors at all. Nor were
there any at the short interval or subsequent tests.
These five "open case" reactors had
been in the same air space as more than 30 "clean" other
cattle for more than four months, but despite the amount of infective
material they would have been assumed to have been disseminating
there was no transmission of infection. I must also add that this
particular building was very poorly ventilated.
Case History 3
This farmer had his home farm in Powys comprising
50 suckler cows plus followers.
He takes summer keep each year from May to October
on the same land in Herefordshire for around 60 strong stores,
roughly half heifers and half steers. These cattle were then finished
over the next nine months at the home farm and sold fat when ready.
The following history is very revealing:
|
| May '92 | TB was detected in a fat animal at slaughter.
| | | |
| Jun '92 | TT
| Powys | 4 Reactors (summered at Hereford previous year)
|
| | Hereford
| Clear test |
|
| Aug '92 | TT
| Powys | 2 Reactors (summered at Hereford previous year)
|
| | Hereford
| Clear test |
|
| Oct '92 | TT
| Powys | 1 Reactor (summered at Hereford previous year)
|
| | Hereford
| 3 Reactors |
|
| Summered cattle moved back to Powys
| | | |
| Dec '92 | TT
| Powys | 1 Reactor (NVL culture -ve)
|
| Feb '93 | TT
| Powys | Clear test
| TB10 served |
| May '93 | c. 60 store cattle moved to Hereford
| | | |
| Oct '93 | c. 60 store cattle moved back to Powys
| | | |
| Oct '93 | TT
| Powys | 1 Inconclusive reactor
|
| Dec '93 | TT
| Powys | IR clear
| TB10 served |
| May '94 | c. 60 store cattle moved to Hereford
| | | |
| Oct '94 | c. 60 store cattle moved back to Powys
| | | |
| Oct '94 | TT
| Powys | 5 Reactors (all summered at Hereford)
|
| | |
3 Inconclusive reactors
|
| Dec '94 | TT
| Powys | Clear test
| |
| Mar '95 | TT
| Powys | Clear test
| TB10 served |
| May '95 | c. 50 store cattle moved to Hereford
| | | |
| (all to be sold fat from keep)
| | | |
| Oct '95 | TT
| Powys | Clear test
| |
|
There are two very interesting facts that are demonstrated
by this breakdown.
i) All the animals that were reactors over the 3½
years of this breakdown had been to Herefordshire for summer grazing
and despite coming back at the start of each winter and being
housed in the same air space with other cattle there was absolutely
no transmission of infection to any other cattle.
ii) The 60 or so cattle that went to Herefordshire each
summer were roughly half heifers and half steers. These two groups
were separated and grazed on different ground for the whole of
the summer period, but within a few hundred yards of each other
and there was a large badger sett close to both groups. In the
case of the '94 outbreak all five Reactors and three Inconclusive
reactors came from the heifer group. What was so interesting was
that the heifers were grazing old orchard, ie earthworm rich permanent
pasture, whilst the steers on the other hand were grazing short
term leys that alternated with corn crops and would have had very
few earthworms.
I feel that this case history makes these two points very
nicely.
CONCLUSIONS
The comments I have made in this letter are intended to make
a number of points in response to this report by the ISG and can
be summarized as follows.
1. The true independence of this report is in question.
2. The deductions made from the statistical data have
a whiff of political expedience.
3. There is no progress whatsoever in understanding the
true pathogenesis of M bovis.
4. There is no indication that any veterinary thought
from a clinical point of view has been applied to the problem
of epidemiology as a whole. Viz. i) The construction of the trial
took little notice of the available history from the seventies
and eighties. ie that reducing the badger population sufficiently
did markedly reduce the incidence of cattle TB. ii) That the assumption
that the transmission of M bovis in cattle mirrors that of M tuberculosis
in humans may actually be flawed.
5. The whole exercise was an expensive delaying tactic
to avoid doing anything until a vaccine is available.
For good measure I have enclosed further copies of the documents
I handed to you when I first came to see you in 2004.[1]
Reading through them again nothing seems to have changed.
August 2007
1
Not printed. Back
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