The etiology and pathology of grouse disease, fowl enteritis, and some other diseases affecting birds

Front matter

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Preface

Having been engaged for the last five years in collecting data as to the etiology and pathology of grouse disease, I find that the time has arrived when I am enabled to give a coherent account of the subject the number of grouse, dead or dying naturally from the disease, which I have dissected, and which were derived from different parts of England and Scotland, sent to me during several years through the kindness of the Editor of the Field , is very considerable, as will be fully referred to later ; the number of cultivations from the grouse, the number of experiments with cultivations on birds and mammals has been sufficiently large to enable me to draw definite conclusions as to the nature of those cultivations. To the Editor of the Field, and through him to many gentlemen, both in England and Scotland, interested in grouse, my best thanks are due for the valuable assistance which I received from them. The second disease treated here is a

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PREFACE highly infectious and fatal disease of fowls — fowl enteritis, which was at first believed to be fowl cholera, to which it bears a certain resemblance, but from which it materially differs, not so much as to its mortality and high degree of infectiousness, but in respect to its pathology and causation. In order to show these differences I have prefaced the chapters on fowl enteritis with a short chapter on fowl cholera. The first material of fowl enteritis on which I worked was placed at my disposal by Mr. W. Cook of Orpington, the well-known author on, and successful breeder of poultry, through the intervention of Mr. C. Wellington ; both these gentlemen, notably Mr. Cook, have rendered me invaluable service, for which I beg to return them my best thanks.

The third disease, about which I intend to make a few remarks, is the infectious disease of young pheasants known to pheasant - breeders as “the cramps.” While engaged in Ayrshire for the Field, , in the summer of 1887, in inquiring into the pathology and etiology of the grouse disease, I had the opportunity of studying the cramps at Blairquhan, and to the keeper there, Mr. Douglas, my thanks are due for supplying me then and afterwards with materials both as living and dead specimens.

PREFACE

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In conclusion I wish to thank my friend Mr. Andrew Pringle for having kindly prepared many of the micro-photograms, illustrating the microscopic appearances, both of the grouse disease and of the fowl cholera and fowl enteritis, and to my friend and pupil, Mr. E. C. Bousfield, for some of the micro-photograms and of the photograms of the cultivations.

St. Bartholomew’s Hospital, January 1892.

Chapter I

The epidemic disease which affects Red Grouse (Lagopus scoticus ) in Scotland, the North of England, Wales, and Ireland during the spring and the summer, and which, particularly during April, May, and June of some years, makes such sad havoc amongst them, is the one which goes under the name of the Grouse Disease. Not that grouse and allied species are exempt from other affections, but the disease which for years past, in one or another part of the north of the British Isles, has carried away annually large numbers of these birds, is the one known as the “Grouse Disease.” Nor do we mean that this disease occurs amongst the red grouse in spring and summer-time only, for there is good evidence to show that though these are the seasons in which the plague, when occurring, is most conspicuous owing to its extensive mortality, the autumn and winter are not free

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from the presence of the malady, which owing to various circumstances to be mentioned hereafter is then less conspicuous, and may even be altogether overlooked.

The fact that year after year in one or another part of the country the disease is or becomes epidemic, is in itself strong primd facie evidence that it is an infectious illness ; further, the now wellrecognised occurrence of isolated fatal cases of the same illness amongst the grouse in one or another part of a given district during autumn and winter, makes it certain that the disease has become endemic, and is ready, when favouring opportunities offer themselves, to assume the epidemic character. This is the case with some other acute infectious endemic maladies affecting men and animals which, at certain times of the year and under certain other favouring conditions, assume the epidemic character. Such a change is, however, a slow and gradual development. Take, for instance, Asiatic cholera, endemic in Bengal. It is present in isolated cases all the year round in some part or another of Bengal. During the cold season the number of cases gradually increases ; by the end of the cold season, during the spring and beginning of summer, the cases become so numerous, and the spread of the disease so conspicuous, even outside the endemic area, that the disease possesses

I the epidemic character ; then, with the commencement of the rainy season, it gradually diminishes again, and reaches its lowest level towards the end of this and the commencement of the cold weather. This same character is observed in countries in which cholera is not endemic, and which remain free from it for years, eg. Syria, Egypt, and European States. Cholera imported into these areas gradually and steadily works

itself up into an epidemic, and equally gradually again declines, the summer and spring being the most favourable seasons in which it thus becomes epidemic. During autumn, and towards the winter, the cases become less numerous and milder, and as such may occur as isolated cases all through the winter. Towards spring they become again more numerous and more severe, and in spring may cause a recrudescence of the epidemic. Scarlet fever, diphtheria, and typhoid fever are other well-known instances in which acute endemic infectious disorders during certain seasons show marked exacerbations. In grouse disease the month of April, and the commencement of May, are the times in which the disease, as a rule, gradually by numbers and intensity (fatal cases) becomes conspicuous. During the end of May and the commencement of June it is at its height, and then again declines during July; but fatal cases occur also during August, September,

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October, and later, but their numbers are, for obvious reasons, smaller during this time. That a moor, or even a whole district, is and remains free from the epidemic during one or more years may be, and as a rule is, due to a variety of conditions which also as regards epidemics of other infectious diseases are known to occur ; some of these we do know and call secondary or accessory conditions. Assuming the disease to be an infectious disease, there is nothing extraordinary in the fact, occasionally observed, and used by some as an argument against the infectious nature of the malady, to wit, that in a given country a series of moors are seriously implicated, while here and there one or another moor is only slightly affected, or apparently remains free from the disease. I say there is nothing extraordinary in this because there may be, for all we know, a variety of circumstances at work which favour, or disfavour, the spread of infection from one moor to the neighbouring moor. In human epidemics this fact is observed repeatedly. One locality becomes a hot-bed for the disease ; the neighbouring locality remains fairly free from disease, or has only few cases. In a third locality at a greater distance the disease is again rife, and so on. Whether, in the case of the grouse disease, birds are in better condition to resist the disease in one locality than in the neighbouring one ;

I whether birds affected with the disease carry it from one locality, not to the one lying next, but to a moor some distance off; whether in one moor there are present conditions as to situation, heather, water, etc., which are favourable or unfavourable to the development and spread of the disease, — all these are points which may, and probably (see below) do, play a part in the dissemination of the plague.

A disease which year after year assumes the character of an epidemic at particular seasons, which commences as isolated cases, and gradually works itself up into a serious epidemic, i.e. spreads from a few to many individuals, and again in the same way gradually declines; further, a disease which has such uniform and typical characters, both as to symptoms and pathology ; bears on the face of it the character of an acute infectious disease.

The late Dr. Cobbold, in his well-known brochure on the grouse disease, enunciated that the cause of the grouse disease is a parasite, in fact a nematoid worm belonging to the group of strongyles ( Stron - gylus pergracilis ), for in the intestines of grouse dead of the disease this parasite was constantly present. Numerous grouse which he examined, and which succumbed either in the epidemic of 1872 or 1873, and others examined in later years, contained these parasites in abundance, though “without doubt”

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(Cobbold, Parasites , p. 439) “the occasional presence of numerous tape-worms ( Tcenia calva) hastened the consequent fatality.” This view has always been strenuously opposed by various writers and observers, both lay and veterinary or medical, inasmuch as it was considered quite insufficient to account for the disease ; for it was pointed out by Dr. Farquharson and Mr. Wilson (see below), and can be easily verified, that the same parasites occur also in birds not subject to the disease. Now, taking into consideration that the disease is well characterised both in its symptoms and its pathology ; that the same parasites undoubtedly occur in grouse not afflicted with the grouse disease ; that grouse dead of the disease are found sometimes plump, sometimes emaciated ; and, above all, that grouse dead of the disease, in several instances when examined, showed no presence of the strongylus : it must be evident that the parasites sometimes present in the intestine cannot be the real cause, the causa causans, of the disease. That cause must be of a different nature. It must be of a nature which works rapidly, or fairly rapidly, which affects the system as a whole, and which easily spreads amongst the birds. We shall presently see that one of the most prominent pathological changes in the diseased grouse is an acute congestion of one or both lungs, and that this change, whether very severe or less

I severe, is independent of the presence of strongylus. I dissected numerous birds dying or dead of the disease in 1887, and showing the characteristic lung change, and must confess that I was extremely surprised to find the strongylus in some cases entirely absent, in others present in very small numbers, though taenia calva was present in all in large numbers, just as large as in birds killed but not affected with the grouse disease.

Amongst various writers on the grouse disease, none deserve a higher place than Dr. H. Colquhoun and Dr. D. G. F. Macdonald. By selecting the opinions of these two writers amongst a host of writers who, by letters to the Times and the Field or other publications, have contributed to this question, I am practically quoting in a condensed form the most noteworthy summary of the various opinions offered. All these opinions as to the cause of grouse disease do not in reality touch the causa causans at all, but the conditions or secondary causes, which favour, and play an important part in, the appearance of the grouse disease in the epidemic form. Amongst these conditions may be mentioned : — ( a ) bad season ; ( b ) bad or insufficient food ; and ( c ) overstocking. It must be obvious that as in many other acute infectious disorders amongst men or animals these conditions play a very important part, inasmuch as

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they create a less resisting, more susceptible material for the carrying out of infection. The more adverse the season — inclemency of the weather, frost, etc. — the more sparse or inferior the natural food, the less hardy and strong are the birds when the time arrives which is most favourable for the development of the disease, and therefore the more easily do they take infection. This is well understood as applicable to other infectious disorders. A strong individual, not weakened by bad and insufficient food or by bad or inclement weather, will resist the infection much more easily than one previously brought down in general health and strength. Suppose there are, on a given moor, a large number of birds in this weakened state, and suppose there exists on this moor the active cause of the disease, it stands to reason that, there being present a good many birds of no great resisting power, one or the other of them will take the infection, from these others will take it, and so on, so that, after a short time, a large number of foci will thus be started acting not only on the remainder of the weaker but also on the stronger birds. But supposing, on the other hand, the birds in early spring are well and strong ; though the active cause, of the disease be present on this moor, yet it will not easily find, as it were, a susceptible individual, and consequently the disease will show itself either only in

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be absent altogether.

And so also with overstocking and over-preservation. This is admitted by most to have an injurious effect, inasmuch as it is liable to produce too great a struggle for existence and a consequent weakening of the birds on the one hand, and, on the other, a possibility, owing to the great number of birds left, of cases of disease lingering on through the winter as mild cases, but ready in the following spring to cause an epidemic of the severe fatal disease (see below). Dr. R. Farquharson, in a letter to the Lancet , Sept. 1874, was the first to state the opinion that the grouse disease was of the nature of a contagious fever, since “ the idea of an epidemic and infectious fever fits the facts already obtained better than anything else” ( Grouse Disease , Macdonald, p. 129).

He argued that, as great differences prevail in the degree of loss of flesh observed — some dead or dying birds being found as plump as in their healthy condition, whilst others are found reduced to mere skeletons,— this is in favour of its specific or constitutional nature . . . “so that whilst those dying from a very acute attack, or whose constitutions are unable to withstand its debilitating influence for more than a brief period, retain the outward appearance of health, sporadic cases, or will be barely appreciable

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others present all the conditions of excessive exhaustion ” ( l.c . pp. 130 and 1 31).

I may here at once state that this explanation offered by Dr. Farquharson, as to the difference of condition observed in birds dead of the grouse disease, is one which I think perfectly correct and one for which I shall be able to offer direct experimental evidence. Moreover, it is one which from analogy, i.e. such as is observed in other infectious fevers, would, a priori , suggest itself. The next noteworthy contribution made to our subject is by Mr. Andrew Wilson, Lecturer on Zoology and Comparative Anatomy, Edinburgh, who in the Edinburgh Medical Journal gave the first accurate description of the pathology of the disease. “ Mr. Wilson has had many opportunities (Macdonald, pp. 145 and 146) afforded him for the examination of grouse dying from the disease, and he states that, in most of the birds he examined, he observed a markedly congested appearance of the mucous surface of the digestive and respiratory tracts. Repeated dissections and careful observations satisfied him beyond doubt of the almost invariable presence of this lesion in birds.” Mr. Wilson “unhesitatingly” prefers the theory of Dr. Farquharson, i.e. that the grouse disease is an infectious fever ; “ and the reasons for enlistment

under the banner of the epidemic hypothesis, rather i NATURE OF THE DISEASE n

than under that of parasitism, are chiefly those derived from the consideration that the former theory fully comprehends all the conditions which the phenomena of the grouse disease may present ; and further, that the theory may be applied to the explanation of points and facts, of which the theory of helminthiasis can take no heed.

“ We thus find that these birds are almost invariably affected by both kinds of entozoa — most specimens to a moderate extent, some to a very great degree. But it is exceedingly rare to meet with a bird in which not a single parasite of either kind is present. Out of many cases examined not a single bird was found actually free from the characteristic tape-worm, and in one or two doubtful instances only could it be asserted or suggested that none of the round worms were present.

“ That the presence of these parasites was unconnected with the death of the great majority of the birds examined is, I think, proved by the want of any causal or obvious relationship between the infestation and the fatal issue ; and also by the absence, in most cases, of the signs of fatal parasitism — such as inanition, producing the ‘ pining ’ condition, actual perforation, morbid appearance of the muscular tissues, etc. No one can deny that the presence of parasites in large numbers undoubtedly causes death in a

CHAP. I specific and readily understood manner ; but this fact will not explain the nature of the cause or disease which operates so fatally, without any exceptional development of parasites , and certainly without the slightest appearance of inanition or other concomitant symptoms of helminthiasis. Outside the parasitic hypothesis, applicable as that theory is to a certain class of cases, there lies, I am convinced, the great bulk of fatal instances, the exact cause of which fatality must be sought for in some lesion analogous to that involved in the idea of the epidemic theory. We must thus account for the death in numbers of grouse which, with what one may consider a normal and

actual degree of parasitism, yet die and succumb to disease, and which on examination present wellnourished bodies, firm, healthy, muscular tissue, and other signs of presumed health ” (Macdonald, pp. 147 and 148).

Chapter II

It must be obvious that in a disease affecting birds that cannot be kept in captivity for any sufficient time, the accurate and systematic observation of the symptoms of the disease is fraught with great difficulties, and it is therefore impossible to give a connected account of the course of the disease. From what I can gather of shrewd and observant keepers, and what I myself observed on the grouse in 1887 while staying on the moors in Ayrshire and in Cumberland, thanks to the editor of the Field , and the kind and generous hospitality of Mr. G. Bailey Worthington, then holding Blairquhan, and of the late Sir Frederick Graham of Netherby Hall, on the borders of Cumberland, and also from what I observed of ammers and other birds experimentally infected with the disease in the laboratory, I fully agree with Dr. Farquharson that the grouse disease is an acute infectious fever — being, in fact, an acute

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infectious pneumonia. In the severe forms, such as are observed during epidemics in May and June, the birds, once affected, rapidly, in a. day or two, show great loss of muscular power and seek the water. The loss of muscular power is apparent by the impeded flight, this being sluggish, being performed with unwillingness, and not for any normal time, that is to say, if on the wing the birds soon drop again. Wherever there is a trace of water the affected birds will seek this, and in many instances in severe epidemics their bodies are picked up in numbers on the shores of such water. As the post-mortem examination shows, the congestion of the lungs forms a conspicuous pathological symptom ; and it is therefore clear that, as in acute congestion of the lung in man and animals, also in the grouse, under these conditions, fever must be a prominent symptom, and the above appearances during life easily account for this.

Also the peculiar alteration in the call of the diseased birds, this being somewhat feeble and hoarse, would be a natural result of the lung congestion, since this condition would prevent the birds from uttering their call with normal force, and the congested state of the mucous membrane of the larynx would cause the sound to be less clear and sharp, and more hoarse. The more or less ruffled ii SYMPTOMS AND PATHOLOGY 15

condition of the feathers of the back and throat, or rather the absence of the smooth condition and metallic lustre of the feathers of the back observed in diseased birds, could also be accounted for by their feverish condition.

The colour of the eyelids, bright in the normal state, is not of the normal bright orange colour in birds dead of the disease. In every severe congestion ■ of the lungs, such as obtains in the severer forms of the grouse disease, there is a general venous congestion of all parts consequent on the engorgement of the venous part of the heart supplying the pulmonary artery ; and therefore also the skin all over the body, including the eyelids, would participate in this venous congestion. The natural aspect of the bright pigment of the eyelids would therefore become altered by the presence of this venous congestion, and the eyelid would look duller.

Pathological appearances. — The birds that die during a severe epidemic, such as obtains in the spring and early summer, show the following post-mortem appearances : the crop is generally more or less full of undigested heather; as a rule this is the more conspicuous the better nourished and the plumper the bird, and the better preserved the pectoral muscles are. I have dissected birds which were emaciated, the legs bare of feathers, and in which i6

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the crop contained only little or no food ; and in such cases the disease of the lungs is as a rule, but not without exception, not very extensive, only a portion of one or both lungs being congested. Such is the case in some birds in the spring and summer epidemic ; such is the case in birds that die in the autumn. In the majority of instances in which the dead birds are found plump — as for instance during the height of the spring epidemic — the lungs show a great deal of congestion, the crop is full, and the legs are not bare. I conclude from this that, in these cases the disease being severe, it rapidly kills the animal, or more correctly, if the animal rapidly succumbs to the disease it will show less loss of flesh, and the crop more full of heather than when the animal lingers on for some time — for then the fever would inevitably cause great loss of flesh, and the animal, as is to be expected, would present appearances of emaciation. This view, enunciated by Dr. Farquharson and Mr. Wilson, seems to me the best to harmonise with the facts.

The chief changes are undoubtedly those found in the lungs. The mucous membrane of the larynx and trachea is of a dark colour, hypersemic ; this is the more pronounced the more marked the lung change. The latter shows deep coloration in the greater part of either one or both organs,

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1 7 the hind portions being, in these cases, the ones chiefly affected; or both lungs are uniformly congested, being in some cases of a dark purple-red colour. On microscopic examination it is found that in the congested parts the large and small blood-vessels are uniformly distended and filled with blood, and that the air-spaces of the more deeply affected parts are uniformly filled either with a homogeneous or granular exudation, or with blood ; so that in these parts we have a solidification of the lung which compares with the condition known as the red hepatisation in Pneumonia. There is, however, no fibrine in the form of threads noticeable in the air - spaces ; the smaller air-spaces contain blood en masse , while the large ones are filled with a homogeneous albuminous exudation. From this we conclude that rupture of small vessels had taken place during life

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The spleen is not enlarged, and appears of a dark colour. The liver is uniformly congested and soft ; it is either of dark red colour or appears almost black. On microscopic examination the large blood-vessels as well as the capillaries of the lobules are distended and filled with blood corpuscles. In some cases the liver, on post - mortem examination, is blackish, or rather is of a dark olive-green colour. In these instances the liver cells appear granular and more or

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less disintegrating, and contain dark brown pigment granules ; besides, numerous clumps of dark greenish pigment masses are found in the spaces of the intralobular capillary vessels, while the large vascular branches are full of blood. Evidently in these cases the disease is of longer standing than a few days, for the capillary blood-vessels are not found filled with blood corpuscles, as would be the case in recent cases, but contain the remnants of disintegrated blood corpuscles,. viz. masses of amorphous pigment. The dark greenish-black condition of the liver is always associated with great emaciation of the animals, and, as is proved by microscopic examination, is associated with a large amount of blood pigment, so that from this we conclude that there must have existed, some time before death, stasis in the blood-vessels, disintegration of the blood corpuscles, and change of the blood pigment. This is in agreement with what wre mentioned on a previous page as to the emaciation of birds indicating that the disease must have lasted for some time. In all instances, however, the liver cells themselves contain brown pigment granules. The kidneys are congested, in some instances leading to haemorrhage into the tissue of the kidney. The intestinal mucous membrane shows patchy congestion, and the same is the case with its serous covering, which in most instances is congested in many places,

II sometimes to a considerable extent. In some cases the peritoneum appears very moist in these localities ; that is to say, there is a small amount of exudation. I have seen a few cases in which haemorrhage has taken place, showing itself in the form of petechiae in the peritoneum.

From this we see that the grouse dead of the disease show a definite series of pathological appearances, in which the congestion of the lungs and liver is very conspicuous.

The above considerations led me to conclude that the disease was an acute infectious disease, and owing to the constantly congested and diseased condition of the lungs and liver, I thought it possible that the disease belonged to the group of diseases in which the microbe caused the disorder by its multiplication in the blood. The first birds dead of the disease which I dissected in June 1887, in Ayrshire, were examined with the view of discovering the microbe in the blood. Cover-glass specimens were made of the heart’s blood and of the blood of the lung, i.e. a thin film of blood was dried on cover-glasses and then stained in the usual manner with aniline dyes — methyl blue or gentian violet ; but on microscopic examination no bacteria could be discovered. Numerous tubes, some containing nutrient gelatine, others nutrient Agar, were inoculated in the usual

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manner with the heart’s blood ; they all remained sterile on incubation and free of any growth. The heart’s blood of at least half-a-dozen grouse dead of the disease, or killed while diseased, was thus examined, but no bacteria could be discovered in it. Lungs, liver, and kidneys were taken out from the animals after death, and were cut into small bits and preserved in spirit or Muller’s fluid. Sections were then cut and stained with aniline dyes and mounted in the usual way, but here also no bacteria could then be found. This was the position of things which I described in my first report in the Field in July 1887. I have in 1888, 1889, and 1890 examined many birds that died of the disease in April, May, June, or July; and also in them I could not discover in the blood of the general circulation, either in cover-glass specimens or by cultivation, any bacteria. From this I am enabled to say that in a large number of the grouse dead of the grouse disease in the spring and summer, — that is, dead with the characteristic pathological appearances of the lungs and liver, — the blood of the general circulation does not contain any microbes discoverable by the cover-glass or culture test. In 1888 therefore I directed my attention to examining in the same way, in the fresh condition, the tissue of the lung and liver; and, with the exception of one or two doubtful cases, in

II all others, whose number is considerable, I obtained, by the culture test in nutrient gelatine, evidence of the presence in the lungs and the liver of numbers of bacteria belonging to one and the same species ; for when a particle of the lung or liver tissue is rubbed over the slanting surface of nutrient gelatine, or when it is shaken up in a test-tube with melted sterile nutrient gelatine, and the latter is then poured into a sterile glass dish, allowed to set and then incubated — that is if a plate cultivation in gelatine is made — colonies of one single bacterial species are obtained. By making sections through the inflamed lung or liver, after hardening, and staining these sections for several hours in methyl blue, or better still in rubin and methyl blue, it is found that in some parts some of the capillary blood-vessels, both in the lung and in the liver, contain continuous masses, plugs or emboli, of the same bacterial species (Figs. 2, 3, 4, 15 and 16).1 But there are seen under the microscope extensive parts in which the blood-vessels do not contain them. It is from this easy to see why I failed in 1887 to obtain the microbe from the lung or liver in cover-glass specimens or in culture, viz. I used in both cases a droplet of the blood of the lung or liver,