A few weeks before the _Field_ induced Dr. Klein to take up the question
of grouse disease and to go to Scotland to investigate, the author had
prevailed upon M. Pasteur to offer to examine the disease, and it was
after this was announced in the _Times_ and _Morning Post_ that Dr.
Klein began his work. The author regretted that he did undertake it,
because it just prevented the necessary grouse being sent to M. Pasteur,
and that great man had a way not only of discovering bacilli but also of
some way of killing them. Dr. Klein may or may not have discovered the
bacillus of the grouse disease, but if so he never gave the disease to a
healthy grouse, nor did he even attempt to discover a cure for or
prevention from the disease, and however interesting to science his
discovery may have been, it was of no use in practice. If he did really
discover the cause of the disease, and if grouse are only subject to
take the disease in the same manner as the creatures to which he
administered his disease, then there appears no escape from the
conclusion that the disease is injected under the skin of healthy
grouse.
Every one knows that grouse disease generally shows signs of its coming,
and yet when it really attacks a bird the latter often dies within a few
hours. The author consequently does not believe that the bare legs and
dull plumage associated with grouse disease always imply that the birds
have the disease, but only that they are in a condition in which they
can more easily take it, or have had and recovered from it. This view is
supported by the fact that, after the last attack of grouse disease in
Badenoch, it was noticed when the birds re-started to breed that the
young ones were well feathered on the legs and the old birds were not.
What had happened to those old grouse? Had they had the disease and
recovered from it, or had they only had that predisposing indisposition
that causes the leg feathers to fall off and the other feathers to look
dull? If they had had the disease, then it is not as fatal as Dr.
Klein’s experiments suggest. The chances are that tapeworm or any other
parasites, or even prolonged wet summers or bad food, will predispose
the grouse to the reception of bacilli, possibly by midge bites on bare
legs conveying disease from the sick to the healthy. This view is
supported by the fact that the grouse never get the disease, however bad
their food and however bare their legs in the hard winter weather, but
only when it is warm and damp and there are lots of midge flies.
It has often been said that all game birds and domestic poultry are
subject to the same diseases, and it is frequently suggested that the
grouse disease, pheasant disease, and fowl diseases are all one and the
same. That is an extraordinary belief, because pheasant disease nearly
always occurs when the foster-parents from the barn door remain
perfectly healthy. These views have had a still further upset in the
summer of 1906, by the fact that a large number of foster-mothers died
of enteritis, but without any of the pheasants becoming sick. It is
quite clear that the pheasant disease of the rearing-fields is as much a
mystery as it was before pathological research began, and is one of
those things that is waiting for investigation. How it is spread is not
even known. Post-mortem examinations without bacteriological research
are freely made, and opinions as freely offered, generally ending in a
recommendation to keep fewer birds. This advice is very wisely not
followed by those who want more, not less, sport. And the preservers
have this in their favour, that pheasants increase in numbers every year
in spite of disease. Game preservers are in these times well aware that
opinions given on a mere inspection of the internal organs can neither
lead to true knowledge of the cause of deaths nor even to wise
suggestions of how infection may be avoided. It is not known whether the
chicks catch the disease from the breath of already diseased birds, from
foul feeding on excretatainted ground, or from inoculation by means of
fleas or other vermin. Although these points could be set at rest in a
week when disease breaks out, it never has been done. It seems more
likely that, as in cramps, the disease bacillus is present in soils
suitable for it, and not in others, or else that some soils favour the
development of the diseases in the birds. The only way known to avoid
either of these diseases is to avoid the ground on which they occur, but
numbers of birds do not create either disease. The perfect health
usually found on the game farms proves this. There they generally have
as many pheasants on 100 acres as sportsmen expect on 10,000 acres. As
with grouse, the greater the stocks the more healthy the birds seem to
be.
Partridges are most attacked by a disease known as “the gapes.”
Hand-reared birds can be dealt with more or less successfully by means
of fumigation. Carbolic acid crystals are volatilised on a hot shovel
within a closed coop containing the affected birds. However, this is a
clumsy way of dealing with the matter, and the best plan is to move the
birds that show signs of being troubled with the disorder to the woods,
where they can get lots of insect food as it falls from the trees. This
applies to both partridges and pheasants. In the wild state the former
are most subjected to “gapes” when the weather is very hot and dry. It
is not known how the worm that is the cause of the trouble gets into the
air passages.
There is a large number of other diseases to which game birds are
subject, but a preserver who can avoid those mentioned need not trouble
about the others. That is the reason they are not mentioned in this work
on Shooting.
But an additional word may perhaps be said on grouse disease. A
Departmental Committee of Investigation has been formed by the late
President of the Board of Agriculture to investigate the disease. One of
its first acts was to issue a pamphlet to correspondents to show what
had already been said and thought about the disease. None of these old
faiths are in agreement with Dr. Klein’s conclusions as they stand, but
it only needs one factor to be assumed to bring them into agreement, as
will be seen by the following table:—
┌─────────────────────┬──────────────────────────────────────────────┐
│A list of supposed │A list of supposed causes of grouse disease │
│ causes of grouse │ that are in agreement with Dr. Klein’s │
│ disease that are in│ conclusions, provided subcutaneous injection│
│ disagreement with │ of the bacilli by an insect is │
│ Dr. Klein’s │ assumed—probably the midge fly. │
│ conclusions. │ │
├─────────────────────┼──────────────────────────────────────────────┤
│Tapeworm. │Tapeworm. │
│Cobbold’s Strongylus.│Cobbold’s Strongylus. │
│Bad food. │Bad food. │
│Over stocking. │Bad water. │
│Bad water. │Wet warm weather. │
│Wet warm weather. │Bog or floe ground. │
│Bog or floe ground. │The first four acting by debility to │
│ │ impoverish the blood and the plumage, so as │
│ │ to allow the midge to get at the skin, │
│ │ especially of the legs. The last two acting │
│ │ by enabling the insects to breed. │
└─────────────────────┴──────────────────────────────────────────────┘
It may be remarked that it is no answer to say that tapeworm cannot be a
cause of predisposition to disease, because it is always present. It is
greatly more in evidence some years than in others. The author never in
any other year than 1873 saw quantities of shot grouse from which
tapeworms exuded in yards of entangled mass from the shot wounds of the
dead birds. Then, however, they did so, and had to be withdrawn from the
birds before the latter could be bagged. The birds could not have been
left upon the moor, because the dogs would have gone back for them. Yet
with all these worms the only evidence of disease was an absence of much
leg feathering. The owner of Glenbuchat has been good enough to tell the
author that disease broke out there in 1872 after the shooting season,
but he never before heard of any disease in that year, and as a matter
of fact the grouse at Aldourie, in Inverness-shire, not far away, bred
well in 1873, and only were attacked by the disease later than the
shooting season of that year. But even 1874, the great disease year, was
by no means universally bad. That autumn they had a splendid crop of
grouse in perfect health at Crossmount, in Perthshire. The Rannoch Lodge
ground was only fair that year, but the author’s party there was
credited in the Scotch papers with the record bag for that season,
probably wrongly, as there was not one bird for five compared with the
little moor of Crossmount. 1873 was very wet in the August and September
shooting season, and the writer never before or since saw so many midges
as in that season. That grouse disease does not attack in winter
(although many grouse die then and in the spring of various complaints)
also tends to prove that the bacilli must have an intermediate host that
is not in evidence in the cold weather. Then the disease is not known in
Ireland and in the Lews, where the climate is mild and damp and
encouraging to midge flies. But there is really no place that the midge
can attack a grouse as long as he is full feathered, and in the mild
climate even if there were starvation there would not be bad food. But
it may very well be that the bacilli do not exist in Ireland or the
Lews, and until it is proved that they do exist there it is beside the
mark to set aside the evidence to be had where they do exist, only
because it does not conform to that of a place where they are unknown.
For some reason that the author is not aware of, the _Field_, which
commissioned Dr. Klein’s investigations, seems to have thrown over his
conclusions entirely. Without any remark upon the wisdom or otherwise of
this course, it is necessary to show how thoroughly it disagrees with
them. At random the author takes the issue of October 6th, 1906, and he
finds therein these four references to grouse disease. At page 581 is
stated that “pneumo-enteritis is the technical name of the grouse
disease.” On page 591, Mr. W. B. Tegetmeier writes: “During the present
year the number of grouse that I have seen affected by disease has been
unusually small, not half a dozen from all parts of the kingdom. The
extension of the disease to blackcock is an interesting fact that should
be known. The disease appears to confine itself almost exclusively to
gallinaceous birds.”
On the same page the _Field_ says: “Partridges were practically exempt
from pneumo-enteritis as long as they were allowed to breed naturally,
but overcrowded on foul ground they will become as subject to it as
pheasants.” And on page 592, in reference to pheasants it is said, “The
birds died from very severe pneumo-enteritis.” On September 22nd, page
531, Mr. Tegetmeier has an article in which he seeks every means of
discovering why foster-mothers have died of the disease and the
pheasants have not died. Consequently, it is evident that the journal
treats this disease as one and the same in all species of gallinaceous
birds. But Dr. Klein said at page 38 of his book on grouse disease, “In
pigeons and fowls the subcutaneous inoculation is not followed by any,
not even a local, positive result; the animals remained lively and
well.” In fact, Dr. Klein failed to give the disease he had discovered
to fowls or any gallinaceous birds whatever, but he said, “The most
striking results were obtained on the common bunting and the
yellow-hammer, for the injection of a small drop of the broth culture
into the leg is followed by fatal results.”
Obviously, if the _Field_ is right now, Dr. Klein did not discover the
grouse disease bacillus. And if he did discover it, any fowls dead from
or sick with disease may at once be regarded as victims of something
else; and other gallinaceous birds must be suspected in consequence of
being refractory to the grouse disease.
The author’s belief is that Dr. Klein did discover the bacillus,
although he failed to prove it, and that his experiments on buntings,
fowls, and other creatures went to suggest that the grouse is not a
natural host of the bacilli, that it or its virus becomes attenuated or
weakened every time it passes through a grouse, but that, on the
contrary, it becomes more virulent in passing through buntings and
yellow-hammers. This was suggested by the weakness of the virulence from
the bacilli cultivated from the diseased autumnal grouse after a severer
spring outbreak, and it is also suggested by the fact that in such cases
the grouse do not die rapidly, and that it is a slow disease from which
perhaps some grouse recover; whereas they do not recover in the spring.
The writer’s suggestion is, therefore, that when the bacillus is carried
from grouse to grouse it may be weakened, but that in spring it is not
originated in the grouse, but in some creature unknown, and possibly a
migrant bird of the bunting, hammer, or finch families. The importance
of finding this out, and testing the attenuation theory more thoroughly
in live grouse, is obvious, for if it is true that the blood of
successive grouse gradually weakens the bacilli or their virus, then it
is clear that the safety of grouse will be the constant presence of some
few diseased grouse on the moor.
The author only dwells on this aspect because it is not receiving as
much attention as some others, which are constantly being discussed, and
are therefore less necessary to mention.
At present thought is mostly in the contrary direction. But it is to be
hoped and believed that the Commissioners will investigate every
possible view from a scientific standpoint, and more important still,
from a practical one. For instance, if on a disease affected moor grouse
can be kept in health in a pen of midge-proof netting, we shall hardly
need to know where the midge gets his poison, but shall be exceedingly
likely to dry up his breeding-places and exterminate him as nearly as
may be.