It is wrong to believe and to teach that the parasitic disease is of no

importance, and Moussu declares his belief that the proposed

vaccinations will prove unavailing. He is of opinion, on the other hand,

that when the parasitic invasion can be overcome the mortality will be

checked, and only those animals which are already suffering from severe

infections will succumb. Is not this precisely what has been observed in

human pathology regarding miners’ anæmia or miners’ worm disease

(anchylostomiasis)?

=The diagnosis= presents no difficulty for those who have had a little

practice with the microscope, since the presence of eggs of the parasite

can always be detected in the fæces in cases where external signs have

given rise to suspicion of gastro-entestinal strongylosis.

The macroscopic diagnosis on post-mortem examination is not so easy as

might be supposed, and when very small varieties are in question it is

sometimes necessary to examine the mucous membrane of the abomasum or

intestine very carefully in order to discover the parasite.

=The prognosis= is grave, because before attention has been drawn to

many patients, the entire herd may be more or less infested. It is also

grave because the pastures are infested with eggs or embryos, and the

power of increase of these parasites is enormous.

=Treatment.= The earliest and most energetic means should be adopted in

all cases. Treatment comprises:—

Drainage of swampy pastures.

Dressing of the pastures with chemical manures, preferably with iron

sulphate, at the rate of 40 to 80 lbs. per acre.

Disinfection of manure to destroy the contained eggs or embryos.

The use of chalk, iron sulphate, various acids, etc.

As regards curative treatment, the diseased animals should be grouped

and isolated as far as possible, and should receive doses of the

following vermifuge:—

Powdered areca nut 2 ounces.

Arsenic 30 grains.

The above is sufficient for ten animals, and a dose should be given

daily for a period of six days in a small quantity of bran. Treatment is

completed by abundant nourishment, and by distributing about the

pastures pieces of rock-salt suitably protected.

Many other vermicides or vermifuges have been suggested, but are less

easy to use. They comprise essence of turpentine, mixtures of oil with

essence of turpentine and benzine, picrate of potash in doses of 7 to 20

grains per day, ethereal extract of male fern, etc.

LUMBRICOSIS OF CALVES.

Following the example of human medicine, we apply the term “lumbricosis”

to a disease caused by ascarides in calves, although Neumann separates

the ascarides of calves from the lumbricoid ascarides with which they

are usually confused in current practice.

=Causation.= The disease is exclusively due to infestation with embryos

of the parasite, which in young calves afterwards develop in the first

portions of the intestine and in the abomasum, interfering with

secretion, and producing mechanical disturbance, colic, and digestive

irregularity, eventually followed by marked loss of condition. Death may

even follow, either from rupture of the pylorus or duodenum, or from

secondary septicæmia of intestinal origin, due to the parasites

burrowing into the mucous membrane and facilitating infection. In adults

of all species lumbricosis is rare. It occurs principally in young

animals from the time of weaning up to the age of eighteen months or two

years.

=The diagnosis= cannot usually be formed until the parasites are found

in the fæces, but microscopic examination sometimes reveals the presence

of the eggs, and thus excites suspicion.

Provided the condition is diagnosed early, the =prognosis= is not grave;

but when patients have become exhausted and anæmic they require a long

time to recover, even when freed from parasites.

=Treatment.= Guittard recommends empyreumatic oil as very efficacious,

and gives it in doses of 2½ to 3 drachms diluted with ordinary oil, or

emulsified with any kind of mucilage.

Calomel gives good results, and maybe administered in doses of 15 to 60

grains, according to the animal’s age and size.

Powdered areca nut would probably be easier to administer with the food.

Oil of turpentine is given mixed with ordinary oil, but its action is

less certain.

STRONGYLOSIS OF THE ABOMASUM IN THE OX.

Although well studied by Stadelmann and Ostertag in Germany, and by

Stiles in America, this disease has not yet been regarded in France as

giving rise to accidents.

It is produced by the _Strongylus convolutus rel Ostertagi_, which

becomes embedded under the epithelium of the mucous membrane and causes

the formation of small nodules, the size of a pin’s head or lentil,

which can be detected on palpation. The cavity thus formed beneath the

epithelium communicates with the gastric cavity by a little orifice,

through which the cephalic end of the parasite passes.

PARASITIC GASTRO-ENTERITIS, DIARRHŒA, AND ANÆMIA IN CATTLE, SHEEP AND

LAMBS.

A disease characterised by anæmia with wasting and diarrhœa is sometimes

produced in cattle by the presence in the fourth stomach of small

strongyles varying in size between 3 and 9 millimètres in length,

according to the variety encountered. One variety of the smaller size

has been named by McFadyean _Strongylus gracilis_. Penberthy, who

described the disease in the _Jour. of Comp. Path. and Therap._ for

1894, p. 249, states that in certain cases he also found the _Strongylus

ventricosus_, the _Tricocephalus affiinis_, and minute straight worms

about ²⁄₂₅ of an inch long, which he regarded as anguillulæ. Neumann

declares that pernicious anæmia with catarrh of the abomasum in young

animals is due to _Strongylus convolutus_.

=The symptoms= comprise anæmia, wasting, and diarrhœa of varying

severity. In acute cases, which are common between the ages of six

months and two years, husk is sometimes (accidentally) present. The

disease is rarest in summer. Certain animals lose flesh rapidly, though

appetite is retained. Acute fœtid watery diarrhœa follows. The animal

shows tenesmus, appears dejected, and has a temperature of 103° to 105°

Fahr. The mucous membranes become pale, the pulse small and weak, the

appetite capricious, the eyes sunken, belly tucked up, coat harsh and

dry and hide tight. Wasting is rapid. The animals are listless, and

often lie down for long periods. Death occurs from exhaustion.

=The parasite.= Scrapings from the abomasum and intestine when diluted

with water and viewed under a lens show minute bodies resembling short,

fine hairs. When isolated these are easily visible with the naked eye.

_In situ_ they appear to be lying on the mucous membrane, sometimes with

the head fixed in the latter. They vary in length from ³⁄₂₅ to ⁶⁄₂₅ of

an inch, and are brownish in colour. For a detailed description see

Penberthy _loc. cit._ McFadyean (_Jour. of Comp. Path. and Therap._ for

1896, p. 314) also gives a very full description, illustrated by plates,

of the two species of strongyles which he regards as the cause of

gastritis in cattle in England.

[Illustration: $1]

=The lesions= are those of wasting diseases. The first three gastric

compartments may be thin, but usually show no abnormality. The mucous

membrane of the abomasum shows evidences of catarrh, is sometimes

covered with a loose croupous material, or is denuded of its epithelium

and even extensively destroyed. In acute cases it is more or less deeply

reddened over spots or extensive patches. Occasionally it appears

jelly-like, owing to effusion into its substance. Except for the

catarrhal condition the small intestines may be healthy, but the large,

especially the colon and cæcum, show lesions similar to, but more

pronounced than, those of the abomasum.

=The treatment= comprises administration of the usual vermifuges, of

which Penberthy prefers turpentine. The diet should be nutritious and

easily digestible. Among drugs, non-irritant iron salts, cod liver oil,

bitter vegetable tonics and common salt are recommended. The animals

should be housed and kept warm; the litter, containing parasites, should

be destroyed. The pastures may be dressed with salt and lime; those

worst infected should be ploughed. An uninfected water supply is

essential.

=Parasitic Gastro-enteritis in Sheep and Lambs.= A disease in seven to

eight months old lambs, closely resembling the above, was described by

McFadyean in the _Jour. of Comp. Path. and Therap._ for 1897, p. 48.

Sheep over one year old were not affected.

=The symptoms= comprised diarrhœa, rapid wasting, impaired appetite,

thirst, a tendency to lick and swallow sand or earth, dulness, and

continued fever (105° to 108° Fahr.). There was no evidence of acute

pain or of marked cough.

=Duration.= The disease sometimes proved fatal in one or two days, but

sometimes extended over several days or weeks. The mortality varied from

10 to 20 per cent., but in many cases almost all the members of a flock

exhibited diarrhœa and loss of condition.

=The cause= appeared to be the presence of small nematode worms in the

fourth stomach, which generally exhibited gastritis with inflammatory

congestion of the mucous membrane, though in a considerable number of

cases the lining membrane of the stomach was markedly anæmic. In a large

number of cases the irritation of the mucous membrane was continued into

the duodenum, but as a rule the remainder of the small intestine was not

inflamed.

The worms named by McFadyean _Strongylus cervicornis_ are from 10 to 12

mm. in length, so that although not of microscopic dimensions they

cannot be seen when suspended in the stomach contents. They are readily

detected in microscopical preparations under a low power.

[Illustration: $1]

=The treatment= is similar to that of gastro-enteritis in cattle, but

chief attention should be directed to prophylaxis.

* * * * *

A verminous disease, closely simulating the above, and affecting cattle,

sheep, and goats in Texas, is described by Ch. Wardell Stiles in the

Annual Report of the United States Department of Agriculture for 1900,

p. 356. The disease was of mixed character, and consisted in various

degrees of verminous gastritis, verminous enteritis, and verminous

bronchitis. In the stomach were found the common twisted wireworm

(_Strongylus contortus_) and Ostertag’s encysted wireworm (_Strongylus

Ostertagi_). It appeared to be present in every calf, steer and cow

examined (post-mortem), and was undoubtedly the chief agent in causing

death. The sheep and goats were very similarly affected. In the bowel of

cattle were found the hookworm (_Uncinaria radiata_), nodular disease

worm (_Œsophagostoma columbianum_): in that of sheep the hookworm

(_Uncinaria cernua_) and nodular disease worm (_Œsophagostoma

columbianum_), and the fringed tapeworm (_Thysanosoma actinioides_). In

the lungs of the cattle _Strongylus micrurus_ (the small-tailed

lungworm), and of sheep the threadworm strongyle (_Strongylus filaria_)

were detected.

=Treatment.= Sulphate of copper, gasoline and coal-tar creosote were

tried, but the best results were obtained from doses of 30 grains (for a

lamb) up to 100 grains (for a two-year-old sheep) of thymol in 1 per

cent. coal-tar creosote solution.

INTESTINAL COCCIDIOSIS OF CALVES AND LAMBS (PSOROSPERMOSIS, HÆMORRHAGIC

ENTERITIS, BLOODY FLUX, DYSENTERY, ETC.).

=History.= This disease is very common in the Avalon and surrounding

districts, sometimes assumes the characteristics of a true epizootic,

and affects young bovine animals between the ages of six months and two

years, but is commonest and most contagious in animals of from ten to

eighteen months old.

It attacks animals in good or bad condition, without distinction of

breed or species. It begins towards the end of July, attains its maximum

development towards the end of August and September, and disappears in

October, though occasionally it continues until November. In exceptional

cases Degoix has seen it during January and February in animals which

had returned from the fields to the byres about the end of November. It

develops earlier than verminous bronchitis, in conjunction with which,

however, it often occurs. It is commonest in warm, moist, rainy years,

and amongst animals pastured on swampy ground containing numerous

springs and streams. Year after year it attacks animals occupying

particular pastures in summer. The soil of these pastures is undoubtedly

infested with the germs of the disease, just as in places the soil is

infested with anthrax bacilli. The appearance of symptoms is preceded by

an incubation period of one or two months. The length of this incubation

period is fixed by the observations which Degoix has made during the

past twenty years, and depends on the time which elapses between the

animals being turned into infected pastures and the appearance of the

preliminary symptoms.

=Symptoms.= The disease commences with liquid, serous, fœtid,

greenish-black diarrhœa, the material being voided without special

straining and the animals losing neither their spirits nor appetite.

Fever can scarcely be detected, the temperature ranging between 38° and

39° C. On the second or third day the diarrhœa changes in character.

Though it always remains fœtid, it now becomes mucous, reddish-black, or

sanguinolent, and contains more or less frequent blood clots of varying

size.

The passage of this material causes violent straining, which becomes

more and more common, and is accompanied by very pronounced rectal

tenesmus. The animals stand with their backs arched for one or two

minutes, sometimes longer, and the liquid escapes in large quantities,

soiling the quarters and hocks. The animals are dull, show a certain

degree of colic, and frequently grind the teeth. Appetite is lost,

thirst is severe, and rumination ceases. Wasting makes rapid strides,

the coat stares, the animals have difficulty in standing on account of

their weakness, fever sets in, and the temperature rises to 40° C. This

condition may last from five to ten days and terminate either in

recovery or death. Recovery is frequently rapid in animals which have

continued to eat, and in which the acute period has been of short

duration—five to seven days at most. On the other hand, it is slow if

the appetite has disappeared and the acute period has been prolonged

beyond ten days.

The diarrhœa, which has lost its sanguinolent character towards the

sixth or eighth day, may continue for somewhat longer. The attacks of

straining become rare, and cease between the tenth and fifteenth days.

The appetite remains capricious for a long time.

Convalescence is marked by alternate improvement and retrogression. The

animals are weak, and only recover quickly under energetic treatment and

forced feeding with concentrated digestible foods like milk, soup,

cooked grain, etc., administered for three weeks or more.

Death may occur towards the tenth or fifteenth day from exhaustion. The

patients become very anæmic and thin, the eyes are withdrawn into the

orbits, and the animals appear indifferent to what goes on about them.

They still groan feebly, occasionally grind the teeth, and lie

continually on the chest with the head extended. The body temperature

falls and death follows.

In well-bred animals in good condition the disease sometimes assumes a

much graver and more rapidly progressive form, with peracute symptoms,

and makes as many, if not more, victims than that previously described.

The process is as follows: After suffering for a day from serous

diarrhœa, to which the owners pay little attention, the animals show

sanguinolent diarrhœa and pass blood clots. This is almost immediately

followed by very violent convulsive attacks—true eclampsia. The animals

are then unable to stand, lie on the side with the head outstretched and

resting on the ground, the eyes withdrawn into the sockets and often

showing pirouetting movements (nystagmus), the neck drawn upwards and

backwards (opisthotonos), and the limbs rigidly extended. From time to

time the whole body is shaken by extremely violent convulsive movements.

This condition, which is sometimes preceded by weakness of the hind

quarters and symptoms of locomotor ataxia and inco-ordination, may

continue from six to thirty-six hours; in nine cases out of ten it

terminates in death.

=Causation.= On microscopic examination of the serous dejections one

finds distributed throughout the liquid mass very small numbers of ovoid

corpuscles having a double outline, and contents of varied appearance;

these are the coccidia.

When the diarrhœa has become sanguinolent and muco-fibrinous, the fluid

contains these coccidia in considerable quantities, and large numbers of

them may be found in the mucus, where they are mixed with epithelial

_débris_, blood corpuscles, and lymphatic cells, etc. They are rarer in

the clots. Coccidia cannot be found in the fæces of healthy animals,

even in those occupying the same pastures with the diseased. Should the

clinical symptoms be thought insufficient of themselves clearly to

identify the disease, a simple microscopic examination of the fæces will

remove any doubt.

=Lesions.= Post-mortem examination immediately after death enables one

exactly to identify the habitat of the parasite and the lesions it

produces. These lesions are to be found throughout the large intestine,

from the cæcum to the anus.

The large intestine is almost or entirely empty, the mucous membrane is

reddish-brown in colour, lies in folds, is œdematous, and everywhere

covered with a coating of mucus. This coating varies in character at

different points; in places it forms more or less thickened patches of

greyish or yellowish colour, and of a resistant character, as though

mixed with coagulated fibrin. These patches are fairly well defined,

they are irregular in form, and vary in width from some millimètres up

to several centimètres. They are more or less adherent to the mucous

membrane, from which they can easily be stripped away. The mucous

membrane thus exposed is slightly depressed, and of a whitish colour,

thus markedly contrasting with the surrounding red coloration. This

depression represents a slight ulceration, which, though superficial, is

clearly visible to the naked eye.

Microscopic examination of the mucus patches reveals the existence, both

superficially and in the depths, of epithelial cells derived from the

mucous membrane, of vesicular cells derived from the Lieberkuhnian

follicles, of numerous blood and lymphatic corpuscles, and, distributed

irregularly throughout this mass of cells, of coccidia, resembling those

found in the dejections.

In thin sections of the intestine, made through the ulcerated

mucus-covered patches, and in a direction perpendicular to the mucous

membrane, one finds that the epithelial covering of the intestine has

disappeared.

The Lieberkuhn’s follicles are shortened, their orifices are irregular

and partly blocked with epithelial _débris_. In a large number of these

follicles the blind extremity is dilated, and more or less filled with

coccidia, varying in appearance according to their stage of development.

The epithelial cells normally lining these blind ends seem to have

disappeared, and to have been replaced by the parasites. This, however,

is not really the case. It is easy to prove by suitable dissection

(after maceration of the sections in 30 per cent. alcohol) that the

coccidia are lodged in epithelial cells which have become modified in

shape and undergone hypertrophy as the parasite has grown, whilst the

nucleus has been pushed to one end and undergone atrophy.

Alongside the deceased glands may be found others which are quite

healthy. In the parts which are most markedly affected the

interglandular connective tissue is infiltrated and slightly thickened.

Degoix has never discovered coccidia in the cells of the intestinal

mucous membrane itself. The lesions may be met with throughout the large

intestine, but are more numerous and grave as the rectum is approached.

This disease is characterised by extensive inflammation, affecting the

entire mucous membrane of the large intestine, by more or less extensive

ulceration of this bowel, the ulcers being covered with muco-fibrinous

patches rich in coccidia, by localisation of the parasites in the

epithelial cells of the glandular cul-de-sac, by the appearance of the

disease at a special time of year and in special districts, where it

assumes the form of an enzooty, and by the fact that it always appears

in the same pastures. The mortality varies between 12 and 25 per cent.

from year to year.

=Microscopic appearances.= The protozoa which produce this disease

assume the form of ovoid cysts, varying in length from 18 to 25 µ, and

measuring at the widest part about 13 µ. They possess a hyaline envelope

whose existence is proved by its double contour line, and yellowish,

granular, highly refractile contents. This granular material does not

always occupy the whole of the cavity. At a certain stage of development

it collects towards the centre, forming a nucleus and leaving clear

spaces at the poles of the cell. At a later stage this nucleus divides

into four portions which afterwards separate.

=Treatment.= The protozoa, in their cystic condition, are very resistant

to destructive influences. The most common natural cause of their

destruction is drying in the open air. Unfortunately, in the localities

where the patients usually live, that is, filthy byres, wet pasturages,

etc., this destruction only takes place to a very limited extent.

The disease can be attacked by prophylactic and therapeutic measures.

Prophylaxis consists—firstly, in destroying the parasites contained in

the dejections by the free use of 3 per cent. sulphuric acid solution;

and, secondly, in removing the young animals from infected fields during

the months between June and September.

Therapeutic treatment comprises—firstly, stimulant applications to the

abdomen; secondly, disinfection of the intestine by the administration

of salol, benzo-naphthol, very diluted solutions of creolin, etc.;

thirdly, intestinal irrigation by the administration of mucilaginous

drinks containing bicarbonate of soda, supplemented by general tonic

treatment and the supply of concentrated, very nourishing, and easily

digested food (Degoix, _Revue générale de Médecine Vétérinaire_, No. 28,

February 15th, 1904, p. 177).

* * * * *

McFadyean describes a similar disease to the above in two to three

months old lambs (_Jour. of Comp. Path. and Therap._, March, 1896, p.

31). The mortality reached 10 per cent. The lambs at the time the

disease broke out in the flock were closely folded together with the

ewes on growing roots, which, needless to say, were much soiled with

earth and fæces before they were completely consumed.

INTESTINAL HELMINTHIASIS IN RUMINANTS

(Ox, Sheep, Goat).

[Illustration: $1]

Verminous disease of the intestine is often accompanied by similar

disease of the stomach (gastro-intestinal strongylosis of the sheep,

lumbricosis of the calf), but it also occurs apart from the presence of

gastric parasites. Parasites are more frequent in the intestine than in

the abomasum, because the alkaline intestinal juices prove a much more

favourable medium for their development than do the acid juices of the

stomach.

The actual parasites may include ascarides, strongyles, hooked worms,

œsophagostomes, tricocephales, sclerostomes, and various tæniæ (_Tænia

expansa et alba_). Many of these have already been, or will hereafter

be, referred to.

Helminthiasis due to round worms like strongyles, and the various forms

of hooked worm, is graver than that due to flat worms, but most

extraordinarily varied collections are sometimes met with. Speaking

generally, however, helminthiasis more particularly affects young

animals like calves, lambs, and yearling sheep, is rarer in adults, and

in all cases the complications it produces are of trifling importance in

adults as compared with those caused in the young.

The persistence of verminous diseases in certain infested countries,

districts, farms, or pastures is explained by the enormous number of

eggs or embryos passed with the fæces and disseminated with manure, as

well as by the high degree of resistance of the eggs and embryos to

destructive influences.

=Causation.= The various forms of intestinal helminthiasis are all due

to embryos or eggs of worms obtaining entrance to the stomach or bowels

of susceptible animals. Nevertheless, external conditions largely favour

infestation. The existence of marshes, ponds, and stagnant water on

certain pastures, heavy annual rainfall, the occurrence of wet seasons,

etc., favour the existence and growth of embryos, and, as a consequence,

the infestation of animals.

[Illustration: $1]

=The symptoms= of intestinal helminthiasis are always very vague,

whether the victims be oxen, sheep, or goats. They point to the slow and

progressive development of a pernicious anæmia, characterised primarily

by interference with appetite and digestion, then by anæmia, and finally

by cachexia. The patients are dull, lose condition, suffer from depraved

appetite, and, during the cachectic period, from diarrhœa, and die in a

condition of exhaustion. These forms of helminthiasis are much more

frequent in sheep than in oxen.

=The diagnosis= is only arrived at by discovering parasites in the

fæces, or, in those doubtful cases where one has been led to make a

microscopic examination of the excrement, by the detection of large

numbers of eggs.

From an economic standpoint the =prognosis= is grave, because severely

infected animals recover their condition very slowly, whatever treatment

be adopted.

=Treatment= includes the measures previously indicated regarding the

destruction of germs, eggs, or embryos distributed over the pastures,

and the drainage of wet grounds and stagnant pools. Where such diseases

are common, the pastures should be dressed with iron sulphate, and the

stable manure disinfected or burned.

Curative treatment comprises the administration of such anthelmintics as

can be given with the food. They should not require to be administered

by force, as this proceeding would not only necessitate a great loss of

time, but might result in accidents.

Arsenious acid, in doses of 15 grains per day, and tartar emetic, in

doses of 75 to 150 grains, according to the animal’s size, are among the

best drugs for oxen, and may be given for four or five days running.

Benzine, oil of turpentine, and empyreumatic oil are more difficult to

administer.

In the case of sheep, preference should be given to areca nut, in doses

of 75 to 120 grains, according to the animal’s size, and to tansy, which

are convenient to give, and can be added to bran, oats, or beetroot.

Adult tapeworms of oxen are of relatively minor importance, but one

tapeworm of sheep, viz., the fringed tapeworm (_Thysanosoma

actinioides_), also known as _Tænia fimbriata_; _Moniezia fimbriata_

deserves notice, as at times it forms a veritable scourge to the sheep

industry of North America and South America.

[Illustration: $1]

[Illustration: $1]

=Disease.= The disease in sheep caused by the fringed tapeworm has been

studied in detail by Curtice, who considers that next to scab it is the

most important sheep disease of the western plains of North America. The

financial loss it causes is extensive, and results from the failure of

the lambs to fatten, the small crop of wool, and the weakening of the

animals, so that they cannot withstand cold winter weather. The

parasites develop slowly, and are present in considerable numbers before

their presence is suspected. Toward September the lambs fail to grow as

they should; in November the symptoms are marked. First, the worms

produce local irritation of the intestine, which finally develops into a

chronic catarrhal inflammation; their presence in the gall-ducts

produces similar results, and obstructs the flow of bile; infected lambs

are large-headed, under-sized, and hidebound; their gait is rheumatic,

and they appear more erratic than the other sheep, standing oftener to

stamp at the sheep dogs or herds, and lagging behind the flock when

driven; the general symptoms are those of malnutrition, and Curtice

considers them nearly identical with the symptoms of the “loco” disease;

in fact, he states that it is extremely difficult to distinguish between

the two diseases, and believes that the fact that the worms “may tend to

produce depraved appetites and a morbid craze for a particular food is

also reason for suspecting that the loco disease may depend on the

tapeworm disease.” General systemic disturbances result from

malnutrition; the usual fat is absent; serous effusions are noticed in

the body cavities, serous infiltration in the connective tissue.

=Treatment= is similar to that of parasitic gastro-enteritis of sheep

and lambs (which see).

CHAPTER IX.

DISEASES OF THE LIVER.

From the physiological standpoint the liver is an organ of such

importance that its pathology should be studied as completely as

possible. Furthermore, it is often the seat of a number of varying

lesions, either of parasitic, toxic, infectious, or cancerous origin.

In animals of the bovine species the liver is placed in the right

retrodiaphragmatic region, so that it is somewhat difficult to examine

by any of the ordinary methods, like palpation and percussion. Under

normal conditions it is entirely concealed beneath the hypochondrium,

except towards the upper margin of the thirteenth rib, where it can be

examined by palpation. When, as in various morbid conditions, it is

considerably increased in size, it extends as far as the margin of the

hypochondriac circle, thus becoming directly accessible to palpation and

percussion. Sometimes it even enters the hypochondriac region, passing

outside the omasum and abomasum, which it then thrusts towards the

middle of the abdominal cavity.

The margin of the liver exhibits a depression lodging the gall bladder

nearly opposite the centre of its vertical depth.

As the liver is so deeply situated, percussion is found to be the method

of examination which gives the best results. Beyond the limits of the

zone of auscultation, percussion gives above a semi-dull sound, then,

proceeding downwards, a dull sound due to the liver, the omasum, and the

collection of liquid in the bowel. When this dulness is well defined,

clear, broad from above downwards, and extends to or beyond the

hypochondrium, it indicates hypertrophy of the liver. By deep palpation

of the posterior margin of the hypochondrium the liver can then be

sounded, and its excessive size detected.

The symptomatology of the liver is still very imperfectly understood,

for in practice the urine is rarely tested for bile pigments, nor

attempts made to ascertain whether the glycogenic function is normal by

the test for alimentary glycosuria.

In this connection nothing has yet been done to assist in diagnosing

certain hepatic conditions. Fortunately, those diseases of the liver

which we have to study are more often of a parasitic nature than true

diseases of the hepatic tissue.

The reported cases of venous or biliary cirrhosis, moreover, are too

ill-defined and too incomplete to be taken as a type for description. We

leave them on one side. In a similar way, apart from parasitic

cholangeitis and cholecystitis, inflammations of the biliary ducts are

little known, and are rare.

CONGESTION OF THE LIVER.

In bovine pathology only passive congestion of the liver, often a result

of various primary affections with cardiac lesions, is well recognised.

Active congestions probably occur during infections or intoxications of

various kinds, but have not been made the object of special research.

Among diseases likely to produce passive congestion must be included all

those which interfere with the return circulation through the posterior

vena cava. All cardiac affections with lesions of the valves or orifices

of the right heart, all forms of pericarditis, tumours or lesions of the

mediastinum compressing the posterior vena cava, produce stasis, passive

congestion, and progressive development of what is called “cardiac

liver.”

=Symptoms.= The liver is considerably hypertrophied, as a consequence of

the stasis of blood and progressive dilatation of the portal system. Its

zone of dulness increases in size, whilst on palpation its borders may

sometimes be detected. This condition is always accompanied by digestive

disturbance.

The function of the liver is more or less interfered with; the urine is

scanty in amount and charged with deposit. Ascites of varying intensity

frequently occurs; cardiac disturbance accompanies or usually precedes

the above symptoms.

=The lesions= of passive congestion are represented by progressive

dilatation of the entire portal venous system (nutmeg liver). In time

this dilatation may produce biliary cirrhosis, as a result of chronic

irritation of the blood-vessels and perivenous inflammation. This

condition is known as “cardiac cirrhosis of the liver.”

=The diagnosis= of this pathological condition is generally easy,

provided that the primary disease which causes it be recognised.

=The prognosis= is always grave, and the practitioner is limited to

treating the primary affection, such as endocarditis, pericarditis, etc.

NODULAR NECROSING HEPATITIS.

This form of inflammation of the liver is somewhat rare in animals of

the bovine species. The disease is difficult to diagnose, and is often

only recognised on post-mortem examination.

Isolated tracts of the liver become inflamed, between which the rest of

the tissue preserves its normal character; the parts affected appear to

undergo complete degeneration, the cause of which is difficult to

explain. On examining affected animals after death, the liver is found

to be greatly enlarged, and apparently invaded by multiple tumours. On

section, the parenchyma generally is of normal colour, but the diseased

parts are represented by dirty greyish-yellow tissue of a lardaceous

character, somewhat resistant to the knife.

The affected spots vary in size, between that of a lentil or hazel nut

and an egg, and are formed of necrotic tissue.

The periphery is the seat of true chronic fibro-plastic inflammation.

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=Causation.= According to Stubbe, these lesions are produced by

microbes, originating in the intestines, and carried to the liver by the

mesenteric veins. The lesions and blood of the liver yield cultures of a

microbe resembling that of necrosis; nevertheless, such lesions have not

been experimentally reproduced.

According to Berndt, infection from the uterus is possible, and indeed

probable. Moussu has only seen three cases of this particular condition

of the liver in living animals. Two of these were in a working ox and a

bull respectively, so that Berndt’s view would not seem to be

exclusively applicable. Moussu is convinced that infection is of

intestinal origin, and that it takes place through the mesenteric veins;

he claims to have found the proof of this in the existence of multiple

pylephlebitis and complete obliteration of the subhepatic veins in some

cases.

=Symptoms.= The symptoms are so vague as to render diagnosis difficult.

Berndt, on the other hand, regards it as fairly easy. He states that the

disease occurs in old cows, which after parturition show loss of

appetite, polydipsia, fever, dyspnœa, and short, feeble cough,

suggesting pneumonia. After a few days the animals appear extremely

weak, remain lying for long periods, and exhibit icterus. Percussion of

the liver detects abnormal sensibility and hypertrophy.

The three cases seen by Moussu showed only slight yellowness of the

membranes, general weakness and difficulty in walking, which at first

glance appeared to suggest laminitis, marked hypertrophy of the liver,

sensitiveness over the hepatic region, and, as complications,

uncontrollable diarrhœa and peritonitis. But these symptoms are also

noted in suppurating echinococcosis, and even in cancer of the biliary

ducts, so that diagnosis does not appear easy. Nevertheless, there is

always marked fever, and on post-mortem examination it is not unusual to

find, in addition to the hepatic lesions, a certain amount of

perihepatitis, partial peritonitis, and even pleurisy in the region of

the diaphragm. The question is of little practical importance, for the

gravity of the disease just described is such that economically no

treatment is possible. The great point lies in correctly diagnosing

disease of the liver, and that is relatively easy.

CANCER OF THE LIVER AND BILE DUCTS.

Cancer of the liver, that is, broadly speaking, the development in the

liver of malignant tumours, capable of becoming generalised throughout

the organism, is comparatively rare when compared with parasitic

diseases of the same organ. It may be primary or secondary in character,

but is much more frequently secondary. In bovines primary cancer assumes

the forms of adenomata, trabecular epitheliomata, or adeno-carcinomata.

Moussu describes a case in which the growths assumed the form of

papillomata or adeno-papillomata extending throughout the biliary ducts,

and partly obstructing the common bile duct, which was greatly dilated.

The real cause of these, as of all other primary tumours, remains

shrouded in mystery.

Secondary cancer is more frequent; it occurs usually in the form of

little isolated tumours (nodular cancer) of varying size and greyish

colour.

=Symptoms.= Clinically the description, or rather the identification, of

cancers of the liver is difficult, and the diagnosis particularly

troublesome in cases of primary cancer.

In secondary cancer (following tumour of the testicle in oxen castrated

by the method of bistournage, for example) the general condition, on the

other hand, is usually so affected that attention is pointedly drawn to

the seat of the secondary growths. The patients lose appetite, the fæces

become fœtid, and diarrhœa sets in without clear signs of enteritis.

Examination of the liver always reveals hypertrophy, and sometimes

sensitiveness. The patients rapidly lose flesh, become cachectic, and

the proportionate number of red blood corpuscles diminishes. From the

normal of six or seven millions the number may fall to one million or

less, while that of the white corpuscles considerably increases. This

leucocytosis, which accompanies all forms of visceral cancer, enables

one to distinguish between cancer and chronic forms of diarrhœic

enteritis; it must not be confused with leucæmia. Moderately developed

ascites is common, in consequence of obstruction in the porto-hepatic

circulation.

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=The diagnosis= of cancer of the liver or biliary ducts is surrounded

with difficulty, and the =prognosis= is extremely grave, because no

treatment is possible.

ECHINOCOCCOSIS OF THE LIVER.

This term is applied to the development in the depths of the hepatic

parenchyma of hydatids of _Tænia echinococcus_.

The echinococcus hydatid is found in man, cattle, sheep, swine, etc. It

represents an intermediate stage of development of the echinococcus

tapeworm of dogs. Since this parasite develops its larval stage in man

also, and further, since it is the most dangerous animal parasite found

in man, it is important to thoroughly understand its life history in

order to guard against infection.

=Adult stage= (_Tænia echinococcus_).

=Hosts.= Dog, dingo, jackal, wolf.

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=Life history.= Starting with the adult tapeworm (Fig. 124) in the small

intestine of the dog or wolf, the eggs are scattered over the ground and

are swallowed by the intermediate host with the fodder or water. Upon

arriving in the stomach the egg-shell is destroyed, and the six-hooked

embryo, which is thus freed, bores its way through the intestinal wall,

and wanders, actively or passively (that is, carried along by the

blood), to various organs of the body—liver, lungs, ovaries, bones,

skull, etc.—where it develops first into an _acephalocyst_, which may

develop further, as shown by the accompanying illustrations. The heads

which are formed, upon being devoured by a dog or wolf, then develop

into adult tapeworms.

Young animals are most exposed to this disease; in adults or aged

animals the migration and development of the embryo are more difficult.

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These embryos perforate the tissue of the liver, become fixed in it, and

derive from it the nourishment necessary for their conversion into

cystic bladders of varying size, either sterile or fertile.

The number of vesicles is rarely large, and when only one or two are

present they seldom produce sufficient disturbance to attract attention.

On the other hand, when numerous they deform the liver, produce

glandular atrophy, increase the total size of the organ, and lead to the

appearance of clearly marked symptoms.

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The cystic vesicles contain a clear, limpid, transparent fluid, in which

float secondary, daughter, or granddaughter vesicles.

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=Symptoms.= Echinococcosis of the liver has no well-marked symptoms, and

is therefore difficult to diagnose in animals whose liver is deeply

seated, and therefore beyond palpation. The signs which may characterise

the period of penetration of the embryos through the intestine and into

the depths of the liver, and which are probably represented by slight

colic, vague pain and diarrhœa, usually pass unnoticed. But later, when

the liver is extensively invaded appetite becomes irregular without

apparent cause, animals show intractable diarrhœa, general feebleness,

dulness, and wasting.

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These symptoms do not point with sufficient clearness to a special

visceral lesion, but as they call for a complete examination, the

practitioner is almost forced to a certain conclusion by the fact that

the examination remains negative except in regard to the liver. The

liver seems large and sensitive, and may sometimes be considerably

hypertrophied, for cases have been seen in the ox where the normal

weight of 10 to 12 lbs. has been increased to 60 or even 100 lbs., while

in the pig, whose liver normally weighs 4 lbs., the weight has been as

high as 20 or 40 lbs. In such cases percussion and palpation show that

the liver extends beyond the right hypochondriac region and invades a

large portion of the corresponding flank. But such great enlargement is

exceptional, and when only a dozen vesicles are present, although the

functions of the liver may be seriously disturbed, the information

obtained by physical examination is seldom sufficient to justify an

exact diagnosis. The liver is found to be enlarged and thickened;

otherwise the examination gives negative results.

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The diarrhœa may result from failure of the liver to secrete sufficient

bile to destroy intestinal toxins, or to carry on its glycogenic

function; but it may possibly be the direct result of chronic

intoxication by the contents of the vesicles.

Experience has shown, in fact, that in man, when a superficial vesicle

becomes ruptured, the peritoneal cavity is flooded with the contents of

the cyst; the daughter cysts adhere to the peritoneum, and that almost

invariably vascular disturbance occurs, accompanied by itching of the

skin and an eruption resembling that of urticaria.

The liquid of the vesicles contains an active toxalbumin.

=Diagnosis.= In certain cases, diagnosis is possible, and even easy, but

in others it is extremely difficult and almost impossible.

=Prognosis.= The prognosis is always grave, for if the lesions in the

liver do not produce death, as usually happens, they so profoundly

affect the animals’ general state, that it is no longer worth while to

keep them alive.

No practical treatment exists. In exceptional cases it certainly might

be possible, although in the large herbivora always difficult, to expose

the liver and to puncture and evacuate the contents of some of the

cysts; but the result would be illusory, because some vesicles would

always be inaccessible, and economically intervention would be

incomplete and useless.

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Although there is no useful method of treatment, prophylaxis is possible

and valuable. It consists in preventing the development of tæniæ in farm

and sporting dogs. For this purpose it is sufficient to prevent their

obtaining raw offal containing vesicles of echinococci from sheep, oxen,

or pigs, and also to free them from any helminths which they may

harbour. In this way they no longer spread eggs of tæniæ with their

fæces in the neighbourhood of ponds or drinking places, and the cattle

do not ingest the embryos.

SUPPURATIVE ECHINOCOCCOSIS.

=Causation.= Simple echinococcosis may remain undetected for a long

time, and young animals affected with it may grow up without exhibiting

marked general disturbance. The old echinococci end by degenerating, the

wall of the cyst becomes modified, the liquid it contains, turbid,

lactescent, then caseous; the vesicle becomes wrinkled, and finally

nothing resembling the primary vesicle remains. The liquid is soon

absorbed, and the primary cyst is only represented by a caseous magma,

which undergoes calcareous infiltration and progressive atrophy.

Under other circumstances the development of the echinococcus vesicles

is less regular; they may become accidentally infected and transformed

into encysted abscesses, constituting suppurative echinococcosis of the

liver. The membrane of the vesicles usually resists the passage of

microbes, but the fibrous tissue surrounding the cyst is very vascular;

and if, in consequence of vascular disturbance in the liver (which may

result simply from feeding, trifling infection or other visceral

disease), the blood should for a short time be infected, microbes

penetrate through solutions of continuity in the wall of the vesicle,

which becomes a centre of suppuration. The liquid becomes turbid, the

primary cyst is transformed into an abscess, and suppurative

echinococcosis is set up.

=Symptoms.= The general condition resulting from the development of

suppuration in echinococcus cysts is very different from that of true

echinococcosis. If the abscess develops rapidly, acute generalised

peritonitis or localised peritonitis of the right anterior abdominal

region may almost immediately occur, producing all the characteristic

symptoms of ordinary peritonitis. In all cases, even in the absence of

well-marked peritonitis, perihepatitis occurs, and the liver becomes

adherent to the posterior surface of the diaphragm, to the hypochondriac

region, to the abdominal wall, or to one of the gastric compartments.

This perihepatitis is indicated by exceptional sensitiveness in the

right hypochondriac region, and by respiratory disturbance due to

fixation of the diaphragm.

In certain cases these abscesses seem to develop like “cold”

abscesses—_i.e._, without fever, and this without producing very marked

digestive disturbance; but the patients waste rapidly, become weak, show

slight sub-icteric coloration of the membranes, and appear to lose their

strength. Movement is slow and hesitating, as though the animals were

suffering from laminitis, the anæmia becomes more marked from day to

day, and examination of the blood reveals abundant leucocytosis, the

existence of which often assists in the diagnosis of internal

suppuration. In a few months, at least in the cases we have seen, the

animals become cachectic.

In other and still more obscure cases suppuration of the liver is

accompanied by total hypertrophy, excessive sensitiveness in the right

hypochondriac region, progressive loss of appetite, excessive thirst,

and uncontrollable diarrhœa and fever, although in the case mentioned

above there was little fever and no diarrhœa. The course of these cases,

which probably result from intestinal infection, is much more rapid. In

a fortnight or three weeks, sometimes less, the patients are carried off

by intoxication, generalised purulent infection, or septicæmia.

=Diagnosis.= The diagnosis of suppurative echinococcosis and of primary

abscess of the liver is difficult to establish. It is attained chiefly

by a process of exclusion, though the signs furnished by percussion of

the right flank, and by examination of the blood, are of some

assistance.

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=Prognosis.= The prognosis is extremely grave.

=Treatment= is of little value. Even supposing that the diagnosis has

been exact, surgical intervention is out of the question, and only this

would appear theoretically to offer a chance of success. The abscesses

are multiple, deeply placed, separated from one another, and sometimes

surrounded by enormous tracts of inflamed tissue. In fact, the condition

is of such a character as entirely to prohibit active measures.

CYSTICERCOSIS.

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This disease is produced by the thin- or long-necked bladder-worm

(_Cysticercus tenuicollis_) found in cattle, sheep, and swine. The

cysticercus represents an intermediate stage of development of the

marginate tapeworm (_Tænia marginata_) of dogs and wolves.

It is by no means uncommon in Europe and America, and occurs in the body

cavity of cattle, sheep, swine, and other animals, attached to the

diaphragm, omentum, liver, or other organ.

When eaten by dogs or wolves, it develops into the marginate tapeworm,

which was formerly confused with _T. solium_ of man, and gave rise to

the erroneous idea that the pork-measle tapeworm occurs in dogs as well

as in man.

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=Life history.= In tracing the life history it is best to begin with the

egg, produced by the adult tapeworm in the intestine of dogs. These

eggs, containing a six-hooked embryo, escape from the dog with the

excrements, and are scattered on the ground, either singly or confined

in the escaping segments of the tapeworm. Once upon the ground, they are

easily washed along by rain into the drinking water, ponds, or brooks,

or scattered on the grass. Upon being swallowed with fodder or water,

they arrive in the stomach of the intermediate host (cattle, sheep,

etc.), where the eggshells are destroyed and the embryos set free. The

embryos then traverse the intestinal wall, and, according to most

authors, arrive either actively, by crawling, or passively, by being

carried along by the blood, in the liver or lungs, where they undergo

certain transformations in structure. While still in the finer branches

of the blood-vessels of the liver, which they transform into small,

irregularly shaped tubes about 12 to 15 mm. long and 1 to 1·5 mm. broad,

the embryos lose their six hooks, and develop into small, round kernels,

which are generally situated at one end of the tubes. The embryo can

first be seen about four days after infection. The “scars” (Figs. 140

and 141) described in the liver of animals infested with _Cysticercus

tenuicollis_ are nothing more nor less than these tubes, or altered

blood-vessels, caused by the growth and wandering of the parasites.

Curtice takes a somewhat different view—that is, he considers the liver

as a place of destruction for the young parasites, rather than a normal

place for their development; he also claims that the embryos, which may

even travel the entire length of the intestine of the intermediate host,

traverse the intestine and arrive directly in the position where they

complete their larval development without first passing through the

liver.

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After developing into the full-grown bladder-worm, the parasites remain

unchanged until they are devoured by a dog or wolf, or until, after an

undetermined length of time, they become disintegrated and more or less

calcified.

If the hydatid is devoured by a dog or wolf, either when the latter prey

upon the secondary host or when the dog obtains the cyst at a

slaughter-house, the bladder portion is destroyed, the scolex alone

remaining intact in the digestive fluids. The head holds fast to the

intestinal wall with its suckers and hooks; by strobilation (transverse

division) it gives rise to the segments, which as we have already seen,

together with the head, go to make up the adult tapeworm. Reproductive

organs of both sexes develop in the separate segments, and eggs are

produced, within which are developed the six-hooked embryos, the point

from which we started.

DISTOMATOSIS—LIVER FLUKE DISEASE—LIVER ROT.

In France the name of distomatosis has been given to a disease caused by

the presence of distomata in the bile ducts. It is the “liver rot” of

England, the Eberfäule of Germany, and is produced by the growth in the

biliary ducts of oxen, sheep, and goats of two species of distomata,

viz., the _Distoma hepaticum_ or _Fasciola hepatica_, and the _Distoma

lanceolatum_.

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In 1875 Zundel established the causative relation between the presence

of distomata in the liver and the development of progressive fatal

cachexia in most of the animals affected. This opinion was emphasised by

the works of Leuckart and Thomas on the development of distomata, and at

the present day the parasitic theory is accepted as beyond question.

=Fasciola hepatica= (_Distoma hepaticum_).—The common liver fluke of

cattle, sheep, swine, etc.

=Life history.= The adult parasite, instead of producing young similar

to itself and capable of developing directly into adults in cattle,

produces eggs which develop into organisms totally different from the

adult form, living a parasitic life in other animals. In scientific

language, the parasite is subject to an alternation of generations,

together with a change of hosts. The following summary of the life

history will make this point clear:—

(_a_) _The adult hermaphroditic worm_ (Figs. 144 and 145) fertilises

itself (although a cross fertilisation of two individuals is not

impossible) in the biliary passages of the liver, and produces a large

number of eggs.

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(_b_) _Eggs_ (Figs. 143, 146 and 147).—Each egg is composed of the

following parts: (1) A true germ cell, which originates in the ovary and

is destined to give rise to the future embryo; (2) a number of vitelline

or yolk cells, which are formed in a specialised and independent portion

(vitellogene gland) of the female glands—instead of developing into

embryos the yolk cells form a follicle-like covering for the true germ

cell, and play an important _rôle_ in the nutrition of the latter as it

undergoes further development; (3) a shell surrounding the germ cell and

vitelline cells, and provided at one end with a cap or operculum. The

eggs escape from the uterus of the adult through the vulva, are carried

to the intestine of the host with the bile, then pass through the

intestines with the contents of the latter, and are expelled from the

host with the fæcal matter. Many of them become dried, and then undergo

no further development; but others are naturally dropped in the water in

marshes, or, being dropped on dry ground, they are washed into water by

the rain, or are carried to a more favourable position by the feet of

animals pasturing or passing through the fields. After a longer or

shorter period of incubation, which varies with the temperature, a

ciliated embryo (_miracidium_) is developed. At a temperature of 20° to

26° C. the miracidium may be formed in ten days to three weeks; at a

temperature of 16° C. the development takes two to three months; at 38°

C. it ceases entirely. Experiments have shown that as long as these eggs

remain in the dark the miracidium will not escape from the egg-shell;

accordingly it will not escape during the night. When exposed to the

light, however, or when suddenly brought into contact with cold water,

the organism bursts the cap from the egg-shell, crawls through the

opening, and becomes a—

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(_c_) _Free-swimming ciliated miracidium_ (Fig. 148).—As already stated,

this organism is entirely different from its mother. It measures about

0·15 mm. long; is somewhat broader in its anterior portion than in its

posterior portion; on its anterior extremity we find a small eminence,

known as a boring papilla; the exterior surface of the young worm is

covered with numerous cilia, which by their motion propel the animal

through the water; inside the body we find in the anterior portion a

simple vestigial intestine and a double ganglionic mass provided with a

peculiar pigmented double cup-shaped eye-spot; in the posterior portion

of the body cavity are found a number of germ cells, which develop into

individuals of the next generation.

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Swimming about in the water, the miracidium seeks out certain snails

(_Limnæa truncatula_, _L. oahuensis_, _L. rubella_), which it

immediately attacks (Fig. 148). The miracidium elongates its papilla and

fastens itself to the feelers, head, foot, or other exterior soft

portion of the body of the snail; some of the parasites enter the

pallial (lung) cavity and attach themselves there. After becoming

securely fastened to the snail the miracidium discards its ciliated

covering, and shortens to about half its former length (0·07 mm. to 0·08

mm.). The parasites now bore their way into the body of the snail, and

come to rest in the liver or near the roof of the pallial cavity, etc.;

the movements gradually cease, and we have before us the stage known as

the—

(_d_) _Sporocyst_ (Figs. 149 and 150).—The eye-spots, ganglionic

swellings, and vestigial intestine become more and more indistinct, and

are finally lost. The sporocyst grows slowly at first, then more

rapidly, and at the end of fourteen days or so measures 0·5 mm. The germ

cells mentioned as existing in the posterior portion of the miracidium

now develop into individuals of a third generation, known as—

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(_e_) _Rediæ_ (Figs. 151 and 152).—The rediæ escape from the sporocyst

when the latter are from two weeks (in summer) to four weeks (in late

fall) old. Upon leaving the body of the sporocyst they wander to the

liver of the snail, where they grow to about 2 mm. long by 0·25 mm.

broad. Each redia consists of a cephalic portion, which is extremely

motile, and which is separated from the rest of the young worm by a

ridge; under the latter is situated an opening, through which the next

generation (cercariæ) escape. The posterior portion of the worm is

provided, at about the border of the third and the last fourths of the

body, with two projections. There is a mouth with pharynx situated at

the anterior extremity, the pharynx leading to a simple blind intestinal

sac. The redia, as well as the sporocyst, may be looked upon as a female

organism, and in its body cavity are found a number of germ cells, which

develop into individuals of the next generation, known as—

(_f_) _Cercariæ_ (Figs. 153—155).—These organisms are similar to the

adult parasites into which they later develop. The body is flat, more or

less oval, and provided with a tail inserted at the posterior extremity.

The oral sucker and acetabulum are present as in the adult, but the

intestinal tract is very simple; on the sides of the body are seen two

large glands, but the complicated genital organs of the adult are not

visible. The cercaria leaves the redia through the birth opening,

remains in the snail for a longer or shorter time, or passes out of the

body of the snail and swims about in the water. After a time it attaches

itself to a blade of grass (Fig. 154) or some other object, and forms a

cyst around itself with material from the large glands, at the same time

losing its tail. It now remains quiet until swallowed by some animal.

Then, upon arriving in the stomach—of a steer, for instance—the cyst is

destroyed, and the young parasite wanders through the gall-ducts or, as

some believe, through the portal veins to the liver, where it develops

into the adult hermaphrodite.

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From the above we see that this parasite runs through three generations,

namely:

(1.) Ovum, miracidium, and sporocyst ... first generation.

(2.) Redia ... second generation.

(3.) Cercaria and adult ... third generation.

During this curious development, which lasts about ten to twelve weeks,

there is a constant potential increase in the number of individuals, for

each sporocyst may give rise to several (five to eight) rediæ, each

redia to a larger number (twelve to twenty) cercariæ, and each adult to

an enormous number (37,000 to 45,000) of eggs. This unusual fertility of

the parasite is necessary because of the complicated life history and

the comparatively small chance any one egg has of completing the entire

cycle.

=Hosts.= An interesting and, from an agricultural standpoint, an

important matter connected with this fluke is that it is found in a

large number (about twenty-five) of domesticated and wild animals, and

this fact probably explains to some degree the wide geographical

distribution of the parasite.

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=Symptoms.= The symptomatology of this disease may clinically be divided

into three well-marked periods:

=I. Primary period.= The primary phase commences with the penetration of

the embryos of the parasite into the body, firstly into the intestine,

and then into the liver by ascending the bile ducts. This phase occurs

during the last months of the year, October, November, and December, and

is rarely accompanied by alarming symptoms. At this time the sheep

appear in good health, the summer being over, and the animals, being

well nourished and fat, are able to resist the first attacks of the

parasite, so that even an observant shepherd only notices a little

dulness, want of condition, and muscular weakness. It requires a

carefully trained eye to note these very general symptoms, for the

bodily condition only changes very slowly and progressively, the

appetite remaining good. Experienced butchers, however, in the districts

where distomatosis is common, readily detect this condition. The animals

make little resistance when handled.

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Nevertheless, even in this primary phase, the conditions are not always

as above sketched, and a certain number of deaths may occur. Gerlach has

mentioned the possibility of death by cerebral apoplexy, in consequence

of the young distomata penetrating to the brain. Moussu has certainly

never seen such a complication, but has seen death from hepatitis,

perihepatitis, and secondary pericarditis in animals gravely infested.

The young embryos, whether they penetrate only by the bile ducts, as has

been stated, or are carried to the liver by the blood stream, often

excavate canals in the substance of the gland before establishing

themselves in the bile ducts. They make their way as far as Glisson’s

capsule, and may even penetrate it; and as they carry with them

innumerable intestinal germs, when they arrive _viâ_ the bile ducts,

they set up hepatitis, perihepatitis, with the formation of numerous

false membranes, or even infectious fibrinous peritonitis. Should the

patients die during this phase one finds young distomata at the surface

of the liver, or even in the thickness of the false membranes.

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When infestation is discrete the appearances are quite different.

Careful breeders have even stated that at this period the young sheep

appear to show a greater tendency to fatten.

=II. Second period.= In the primary phase deaths are exceptional; they

only become common towards the end of the winter. During the second or

middle period (December and January) the patients lose flesh, appear

less active, show less regular appetite and greater thirst. The

conjunctiva becomes pale and swollen, the sclerotic has a bluish tint,

and the eyelids are somewhat infiltrated. The wool appears drier and

less curly; locks of wool part readily from the skin, and the individual

fibres become dry and fragile.

[Illustration: $1]

This phase is accompanied by very marked anæmia, rapid exhaustion during

movement, and inability to run for any length of time.

The different methods of examination reveal nothing specially striking,

except that the valvular sounds of the heart are sharper, and that

trifling œdema occurs under the thorax and abdomen.

Microscopic examination of the fæces reveals the presence of eggs of

distomata. The sheep rapidly become thin from about the end of January,

even although the appetite persists and nourishing food is given.

=III. Third, or wasting, period.= The decline, which sets in about

February, appears extremely obstinate, and resists all treatment.

The patients become feeble, eat less, and digest badly. Submaxillary

œdema, common to advanced wasting diseases, then appears. If the sheep

are removed from the fold to pasture, the swelling of the submaxillary

space is very noticeable. It consists in an indolent œdematous

tumefaction, which disappears when the animals are travelled, but

reappears when grazing on account of the low position in which the head

is then held.

The condition then becomes complicated with diarrhœa, and soon grows

alarming. On examination, extensive dropsy may often be found in the

thorax, pericardium, and abdomen.

Death results from exhaustion; the animals do not appear to suffer, but

become extraordinarily anæmic, and perish without a struggle. The blood

is simply rosy in colour, like gooseberry syrup; the clot is soft and

gelatinous; the number of red blood corpuscles has fallen from about

seven millions to a few hundred thousand.

Icterus is rare, though certain cases have been described where it has

appeared during the last and even during the middle stage.

When animals begin to die in a district which has long been infested,

the losses are enormous, the condition sometimes constitutes a perfect

scourge. It should be remarked, however, that all those affected do not

die; animals kept under good conditions may even survive for several

months, although greatly wasted.

Towards March and April the parasites leave their position, and are

conveyed by the current of bile towards the intestine, to be rejected

with the fæces. This is the period of convalescence and recovery; but

recovery is only relative, for the parasites are never entirely

evacuated. The distomata then recommence their life cycle outside the

animal body.

[Illustration: $1]

Unfortunately the mortality caused by distomata is accidentally

aggravated by other diseases, and the scourge then becomes an absolute

disaster for the districts where such complications occur. Thus Besnoit

and Cuillé, of Toulouse have shown that distomatosis may become

complicated with a form of very rapidly fatal hæmorrhagic septicæmia,

produced by an ovoid bacterium.

Distomatosis, already sufficiently grave, then becomes infinitely more

serious, if only from the fact that it may prove the point of origin of

an absolutely fatal complication.

In bovine animals the symptoms develop exactly as in sheep, though the

cachectic period is uncommon and the injury done is often less important

than in sheep. The patients exhibit irregular appetite, wasting without

appreciable cause, anæmia, and even diarrhœa. In spite of excellent

winter feeding they do not regain condition, and relative recovery only

sets in with the approach of spring. Death from simple distomatosis is

exceptional, but in animals so predisposed enteritis develops more

easily, as do all forms of infection of intestinal origin.

The disease is, however, also grave for bovines because successive

reinfection occurs, and the disease may be prolonged for years.

=Causation.= Distomatosis is due to one cause, viz., the entrance of

embryo flukes into the digestive apparatus of herbivora.

The adult distomata in the biliary ducts continually discharge large

quantities of eggs, though the process is most active between February

and June or July. The eggs are carried away with the bile and fæces and

pass on to the pastures, where they continue their life cycle, thanks to

moisture and the presence of stagnant water. The embryos, having escaped

from the egg, enter the bodies of the snails found in or near stagnant

water (_Limnæa truncatula_), become converted into sporocysts, and

afterwards into rediæ and cercariæ. The cercariæ become encysted on the

lower surface of blades of grass in damp pastures, whence they are

transferred to the animals’ stomachs along with the grass itself.

[Illustration: $1]

As the _Limnæa truncatula_ lives not only in marshy regions, but also in

all damp situations, the embryos of distomata are distributed over

enormous areas, and the disease itself is equally widespread. The

embryo, after ingestion, is set at liberty, and passes from the

intestine into the innermost recesses of the liver, being guided up the

bile ducts by the current of bile. At this point it attaches itself to

the wall of the bile duct, passes through its various stages of

evolution, and attains the adult form. It then begins laying eggs, and

thus starts a new evolutionary cycle.

The life cycle of _Distoma lanceolatum_ is not yet known, and this

variety, moreover, is less widely distributed than the _Distoma

hepaticum_.

The bile ducts are more easily penetrated by the distoma in young

animals, a fact which explains why calves and lambs are particularly

affected. Adults present a less favourable nidus, a fact which renders

them less easily infected, but does not entirely prevent the parasites

from attacking them. Old animals, although unable to resist entirely,

seldom harbour many of the parasites.

Wet years appear to favour the extension and propagation of distomatosis

in an extraordinary fashion, a fact which is easily understood, if we

regard the phases of evolution of the parasite. The autumn appears

particularly favourable to the infection of herds. This is explained by

the fact that, during the summer, the dryness of the fields entirely

prevents the development of such eggs as may be distributed over them;

whilst wet periods during the autumn favour this development.

On the other hand, the grass becomes eaten down in autumn, so that the

animals gather it almost level with the ground. As the cercariæ attach

themselves to the lowest leaves they are then ingested in much larger

quantities. The bad effects of wet seasons are not immediately apparent,

but appear during the following spring.

Distomatosis is common throughout almost the whole of Europe, Africa,

and America. In France it is most serious in the moister regions of

Sologne, in Berry, the mountainous and wet districts of the great

central plateau, and particularly in the Pyrenees. It particularly

attacks oxen in the valley of the Meuse, the marshes of Picardy, the

lower regions of Normandy, and in all the mountainous pastures of the

central plateau.

=Lesions.= The lesions of distomatosis vary with the stage of

development of the parasites. During the primary phase of invasion of

the bile ducts by young distomata one finds interstitial diffuse

hepatitis, due to perforation of the gland by young parasites, adhesive

perihepatitis, with the formation of false membranes, and not uncommonly

slight peritonitis.

Zoologists state that the young distomata penetrate the liver by passing

upwards against the current of bile. It does not appear impossible,

however, that they may penetrate by another path, particularly as

so-called “erratic” forms of distomatosis like distomatosis of the lung,

heart, lymphatic glands, and various other tissues are not uncommon. It

has been suggested that the young distomata, arriving in the bile ducts,

perforate the gland, giving rise to these lesions of perihepatitis,

peritonitis or erratic distomatosis; but this view is scarcely in

harmony with the fact that the parasites are usually found in the bile

ducts.

During the second phase, corresponding to the development of almost

adult distomata, the perihepatitis and peritonitis set up either produce

fatal results by secondary infection or diminish and disappear. The

parasites develop in the bile ducts, in which they attain the adult

condition. They steadily ascend towards the origins of the ducts,

dilating them in their passage in an extraordinary way. The number of

parasites varies greatly: sometimes there are but few, and they are only

discovered on post-mortem examination; in other cases the bile ducts are

crammed with them, as many as six or seven hundred or even a thousand

being present. The distended bile ducts always show chronic peripheral

inflammation, which steadily becomes aggravated, producing

pericanalicular atrophying sclerosis. This condition is followed by

change in and disappearance of a certain quantity of hepatic tissue, and

by various forms of vascular and secretory disease.

This is the period of greatest disturbance, not only in consequence of

the actual presence, but also of the mode of living, of the parasites.

Moussu declares that the parasites live principally on blood, at least

during the first and second stage of their sojourn in the liver,

adducing as proof that if one completely injects the vascular system of

the liver (arteries and veins), some of the injected matter will be

found a day afterwards in the digestive apparatus of the parasites.

The disturbances which they produce are therefore due to their actual

presence and its consequences, to their mode of life, and to the

intercurrent infections of which they are sometimes the initial cause.

It is idle to object that the part played by these parasites is less

important than has been suggested, and that the mortality results from

intercurrent infection, and not from the parasites themselves. It is

equally idle to point out that carcases of animals suffering from severe

infection with distomata, particularly the carcases of sheep, are

frequently found in slaughter-houses, in perfectly fat condition, and

with the appearance of not having suffered in any way. These

observations are perfectly correct and well founded. But it matters

little that death results from an infection superadded to the

distomatosis, if the presence of distomata is the determining factor in

causing the superadded infections, and if such infection is, as Moussu

believes, almost inevitable in animals already exhausted by the action

of the parasites.

The fact that animals suffering from distomatosis and slaughtered for

food are well nourished is not a valid objection; for it has long been

known that wasting and anæmia are not immediate consequences, and that

before they are clearly apparent the distomata must have been present in

the liver for several months. Bakewell and the Marquis of Behague have

shown that in moderately infected animals there is a tendency to lay on

flesh during the first and a portion of the second stage of development

of the disease.

If the animals are slaughtered before the period of progressive decline

sets in, it is quite possible to form entirely wrong views regarding the

importance of these parasites.

The wasting process commences towards the end of the second phase of the

disease, and then makes rapid progress. The parasites, which have then

been continuously drawing on the blood for their nourishment for a long

time, produce anæmia, and some infection of the bile ducts, and usually

a certain degree of icterus.

The third phase is accompanied by general signs of cachexia, which need

not again be described. They are similar to those of all progressive

cachexias. In animals which survive this phase and are ultimately

slaughtered the liver always shows very marked sclerosis, commencing

around the biliary ducts. Even after the parasites have been evacuated,

these ducts appear indurated, thickened, fibrous, and sometimes

encrusted with biliary deposits or obstructed with true calculi. These

calculi may or may not contain parasites; sometimes they simply contain

eggs: they are open, tubular, and perforated, but always irregular on

the surface.

When in addition complications have appeared, one usually finds general

lesions of septicæmia and blood infection.

In erratic distomatosis, which is of no importance clinically, distomata

may become encysted in the lung or other viscus, and in time die. The

cysts, which only contain one and rarely two parasites, present a

fibrous shell, enclosing a blackish, pultaceous, grumous magma, which

sometimes has undergone a certain amount of calcareous infiltration. The

parasite may be entirely destroyed.

=Diagnosis.= Early diagnosis is difficult, and can only be established

by microscopic examination of the excreta and the discovery of eggs. On

an average one may find one egg in each preparation when the liver

contains 80 to 100 flukes. When wasting is very marked, and particularly

when there has already been a number of deaths, diagnosis becomes

extremely easy. It is sufficient to find flukes in any form (_Distoma

hepaticum rel lanceolatum_) to be assured as to the cause of disease.

=Prognosis.= In severely infested cases the prognosis is extremely

grave, because no efficient method of treatment exists. Embedded in the

liver, the parasites resist the action of all drugs, and we know of no

anthelmintic eliminated by the bile which in any way affects their

vitality. When the disease is recognised early, the most economical

method is to fatten the animals as rapidly as possible and prepare them

for slaughter.

=Treatment.= There is no reliable curative treatment. The drugs which

one might employ would kill the animal before poisoning the parasites

embedded in the liver. Various mixtures containing sulphate of iron,

juniper leaves, etc., have been recommended; but rich food constitutes

the best of all treatment, both from a curative and a prophylactic

standpoint.

With the view of preventing the disease, however, and protecting flocks

from attack in places where the disease is common, certain precautions

should be adopted. They comprise—(_a_) providing a free supply of

rock-salt, either in masses placed in the mangers or distributed with

the food; the salt increases gastric secretion, and has a slight action

on the parasites: (_b_) adding to the food during the first months of

winter branches of birch, juniper, willow, and broom; the leaves of

these plants contain aromatic or resinous principles which act on the

liver, are eliminated by the bile, and may have valuable results.

But of all preventive measures the most effective consist in draining,

cleansing, and drying low, moist, or marshy lands, because the molluscs

which are essential to the life cycle of the parasites are unable to

develop where the soil is dry. The manure containing the eggs of the

parasites may be disinfected by adding to it lime, sulphate of iron, or

common salt. Common salt and lime spread over the pastures has a double

beneficial influence, acting both as a manure and as a parasiticide.

From May to August is the best time for spreading this dressing.

The fluke embryos are destroyed by 1 to 2 per cent. solutions of common

salt, and by ¾ per cent. solutions of lime.

In over-stocked fields the animals are obliged to graze very close to

the ground, and are thus more exposed to infection. Over-stocking should

therefore be avoided. Animals should not be left too long on the same

ground. If infected they should at once be driven to higher pastures.

Raised water tanks can be placed in the pastures—they are less likely to

become infected. Animals from known infected flocks or herds should not

be purchased. Livers from infected animals should be cooked or

destroyed. If eaten raw by dogs the eggs pass uninjured through the

dog’s intestine and infect fresh pastures.

Sulphate of iron distributed in quantities of 250 to 400 lbs. per acre

is valuable as a manure, and would probably have a greater effect in

destroying the embryos.

SECTION III.

RESPIRATORY APPARATUS.

CHAPTER I.

EXAMINATION OF THE RESPIRATORY APPARATUS.

From the clinical standpoint a study of the respiratory apparatus

implies the examination of the nostrils, nasal cavities, frontal and

maxillary sinuses, larynx, trachea, and, for the purpose of ascertaining

the condition of the lungs and pleura, of the chest.

=Nasal cavities.= Examination of the external portion of the nasal

cavities is extremely simple. The observer notes the degree to which the

orifices are dilated, the frequency of the respiratory movements and the

condition of the muzzle. He may find various eruptions, crusts due to

discharge, etc., and will remark any peculiarities presented by these.

The depths of the nasal cavities can only be examined through the

nostrils to a very limited extent; but the condition of the pituitary

mucous membrane, its degree of vascularity, and the existence of

ulcerations or of vegetations can be observed.

Digital examination is sometimes useful in discovering the condition of

the lower portions of the turbinated bones. The electric light does not

greatly assist the observer, on account of the narrowness of the air

passages. On the other hand, examination of the face, and palpation and

percussion over the region of the frontal sinuses is of considerable

value. By inspection, one discovers deformity caused by tumours, by

ossific inflammation, or other lesions; and detection is rendered easier

by the fact that deformities are usually asymmetrical, only occurring on

one side.

Palpation reveals the degree of resistance and flexibility of the

external bony wall as well as the condition of the subcutaneous tissues.

Percussion sometimes discloses absolute dulness, due to tumours of the

mucous membrane, of the turbinated bones, or of the bones of the face.

The pharyngeal portion of the nasal cavities is difficult to reach, but

can be examined by passing the hand, palm upwards, into the pharyngeal

cavity, when the fingers may be slipped behind the soft palate and thus

introduced into the posterior nasal chamber. The animals should first be

very carefully secured and a strong gag introduced into the mouth.

=Sinuses.= _Frontal sinus._—The frontal sinus occupies the greater part

of the anterior cranial region and the summit of the head, extending

from the highest point of the poll as far forward as a line drawn

between the two orbits. Above, it directly communicates with the sinus

of the horn core. In this upper region, where it abuts on the sinus of

the opposite side along the median line, it is of greatest size. Below,

on the other hand, it is very narrow, much broken up and incompletely

divided into a series of cells, by thin, bony plates running in all

directions.

[Illustration: $1]

It is in direct communication with the nasal cavity.

The frontal sinus, then, occupies all the supero-lateral portion of the

cranial box, which is thus provided with a double wall. At one point,

however, over a lozenge-shaped area, the cranial cavity is only

protected by a single wall. It is in this region that the slaughterman

strikes the animal when killing it.

The frontal sinus may be examined by inspection and palpation.

Inspection sometimes reveals deformity of the external wall of the

sinus. Such deformity, however, is rare, and Moussu has only observed it

in two cases of tuberculosis of the bones forming the cranial wall.

By percussion one detects abnormal sensibility, and partial or complete

dulness over certain areas.

[Illustration: $1]

_Maxillary sinus._—The maxillary sinus occupies the whole lateral region

of the face, from the inferior extremity of the maxillary spine as far

as the sub-orbito-palatine region. In front its external wall is very

solid, but behind, below the orbit, is extremely thin. Externally the

sinus is largely protected by the anterior insertion of the external

masseter muscle, a fact which explains how rarely it is injured.

=Larynx.= In consequence of its deep situation, the larynx can scarcely

be examined except by inspection, external palpation, internal digital

palpation, and auscultation.

External examination presents no difficulty, and enables one to detect

lesions around or near the larynx.

Palpation reveals the existence of œdematous swellings, enlargements of

the retro-pharyngeal lymphatic glands, inflammatory engorgements, etc.

Internal digital examination, like examination of the pharynx, can only

be performed after very firmly fixing the animal in position, and

inserting a gag in the mouth.

[Illustration: $1]

The hand is introduced, palm downwards, and passed as far as the

pharyngeal cavity. The index finger can then easily be slipped into the

glottis. Exploration must be effected rapidly and without violence. It

reveals the condition of the glottis, the presence, position and form of

growths like myxomata and of new tissues, due to the presence of

actinomyces, as well as tuberculous vegetations or ulcerations.

By auscultation we discover the presence of normal or abnormal laryngeal

sounds—roaring, whistling, or bubbling sounds, etc.

=Trachea.= The trachea may be examined by palpation and auscultation.

Palpation reveals the degree of sensitiveness, abnormalities in position

or form, the presence of peripheral inflammations, fractures of rings,

etc.

Auscultation indicates whether the tracheal sound be normal or

otherwise, or accompanied by abnormal sounds, like mucous _râles_, or by

pathological sounds conveyed from the chest.

=Thorax.= The thorax can be examined by inspection, palpation,

percussion, and auscultation.

By inspection we discover whether the formation of the thorax as a whole

is normal, or whether there exist congenital or acquired deformities,

asymmetry like that produced by pneumo-thorax or deviations of ribs from

the normal line, etc. One also notes the breathing movements, the manner

in which the sides expand and contract, the respiratory rhythm, and any

special peculiarities of inspiration or expiration.

Palpation reveals the degree of sensitiveness of the thoracic wall and

of the intercostal spaces, the existence of more or less extensive local

œdematous infiltration, and the presence or disappearance of thoracic

conditions like hydro-thorax.

Percussion indicates the degree of sonority of the chest in different

parts. It can either be practised directly with the hand or through the

medium of a pleximeter. The latter method is preferable when dealing

with fat animals. Percussion, however, gives slightly different results,

according to the degree of fatness of the subjects. It should be

practised both in a vertical as well as in a horizontal direction.

At all points where the muscles are thick or well developed the results

produced are negative, in the sense that only a dull sound is obtained.

This is the result obtained in auscultating the areas marked =1=, where

one meets with the ileo-spinal and common intercostal muscle, and in

that marked =4=, where the olecranian muscles are encountered (Fig.

166). Over the middle and inferior zones, however, the results are much

more instructive.

On the right side percussion of the middle zone gives, under normal

conditions, a clear sound and perfect resonance from above downwards,

and from in front backwards, between the fourth intercostal space and

the ninth rib. Beyond this point lies the liver, which gives a partial

dull sound, and absolute dulness from the ninth to the twelfth rib, in

consequence of its position, and of the projection of the diaphragm

towards the thoracic cavity.

Percussion of the inferior zone produces less marked resonance, which

diminishes more and more towards the base, in consequence of the

thinness of the pulmonary lobes at this point. This resonance does not

extend as far as the hypochondriac region, because the lower part of the

abomasum insinuates itself beneath the costal cartilages and causes a

region of dulness.

On the left side percussion gives precisely similar results, except in

the upper portion of the middle zone. Beyond the ninth intercostal space

the sound changes, and has a tympanic character; because here the

anterior and upper portions of the rumen are encountered, as they are

lodged beneath the hypochondrium. Below, the sound is dull, on account

of the gastric compartments generally being full of food.

Certain trifling modifications of this normal condition may be noted,

depending on the degree of fatness or thinness of the subjects. The

pathological changes which may occur are as follows:—

A tympanic sound, with or without metallic character, may be found at a

point where normally one would expect a clear sound (pneumo-thorax,

diaphragmatic hernia). A dull sound may be met with in the same regions,

all resonance being lost (pneumonia, broncho-pneumonia, pleural exudate,

etc.). Partial dulness and partial loss of resonance may occur in

regions which ought to give a resonant sound (deep pneumonia,

tuberculous lesions, the presence of echinococcus cysts, etc.).

Auscultation—_i.e._, examination by means of the ear—is the most

valuable method of discovering and localising pulmonary, pleural, or

cardiac lesions.

Various sensations are conveyed to the ear, depending on the method in

which the normal or pathological sounds are produced.

The deductions to be drawn as regards the nature of existing disease are

based on the intensity, character, duration, and special attributes of

the sounds noted.

Direct auscultation is the most certain method, but the ear cannot be

applied with equal facility at all points. Under such circumstances a

simple or binaural stethoscope, or the phonendoscope, may be used with

advantage.

To properly appreciate the sounds heard it is essential to be exactly

acquainted with the relation between the lung and thorax. On the left

side (Fig. 60) the anterior pulmonary lobe occupies the space between

the first and fourth ribs, in front and above the base of the heart. The

middle, or cardiac, lobe covers the left upper and postero-lateral part

of the heart from the fourth to the sixth rib. The posterior lobe

occupies all the region beyond the sixth rib as far as the twelfth.

On the right side the arrangement is similar, but the anterior lobe and

the cardiac lobe are more developed (Fig. 62).

Under ordinary circumstances the extensive movement of the lung which

occurs during inspiration produces a special sound known as the

respiratory or vesicular murmur. Contrary to what has been written, and

said, this sound in animals possessing absolutely sound lungs ends with

inspiration. Expiration is silent, though it is easy to estimate its

duration.

In auscultating the lung, we may distinguish four zones, a superior

zone, a middle zone, an inferior zone, and a scapular zone.

The superior zone is bounded by the vertebro-costal gutter, descends

approximately as far as the inferior line of insertion of the common

intercostal muscle, and extends from the summit of the scapula in front

to the hypochondrium behind.

Auscultation of this region through the ileo-spinal and common

intercostal muscle will always reveal, except in very fat animals, the

vesicular murmur to a point as far back as the eleventh intercostal

space. Nevertheless, this vesicular murmur is relatively feeble, and

becomes imperceptible beyond the eleventh rib.

The middle zone comprises the most convex portion of the ribs, and at

this point the wall of the thorax is thinnest, while the lung below is

thickest.

[Illustration: $1]

For these reasons the vesicular murmur is heard at its maximum intensity

at this point. Towards the upper and lower limits of this zone are found

the great bronchial divisions, so that auscultation should always be

practised with the greatest care at this point. The middle zone occupies

approximately one-third of the total depth of the thorax. The vesicular

murmur becomes weaker as one passes backwards, and finally disappears at

a considerable distance from the angle of the hypochondrium, following a

curved line the convexity of which is directed forwards, and which is

continuous with that limiting the upper zone.

These peculiarities are due to the anatomical arrangement and mode of

insertion of the diaphragm on the internal surface of the hypochondrium.

The inferior zone is very limited, and corresponds externally to the

inferior third of the thorax, and topographically to the cardiac lobe or

middle lobe of the lung and to the inferior portion of the posterior

lobe.

As these pulmonary lobes are of comparatively slight thickness, the

vesicular murmur is feeble. It can be heard over a trapezoidal space,

forming a prolongation of the middle zone, but not below in the region

of the sternum or pectoral muscles.

The fourth zone extends over the mass of the olecranian muscles. It is

of triangular form, in consequence of the inclination of the scapula and

humerus. Except in very fat animals the vesicular murmur is readily

audible through the muscular mass on the right side better than on the

left, on account of the development of the right anterior pulmonary

lobe.

On the left side the beating of the heart is heard above the pulmonary

sounds.

Clinically one may hear an exaggeration of the ordinary respiratory

murmur whenever the lung is actively exercised, as, _e.g._, immediately

after trotting. This exaggeration, however, is often pathological. It is

known as “juvenile or supplementary respiration,” when due to the fact

that some other portion of the lung is not acting.

The respiratory murmur may be lessened in certain morbid conditions,

such as emphysema and congestion of the lung, and may completely

disappear in pneumonia or broncho-pneumonia, a fact which is even of

greater significance.

In various pathological conditions the respiratory murmur may also be

modified. On the other hand, the movement of air in the bronchi also

produces various sounds of importance.

A number of different bronchial sounds may be distinguished; these

include both inspiratory and expiratory sounds, for sometimes an

expiratory sound may become audible and clearly appreciable, or may

acquire characters of the greatest importance.

The inspiratory sound may be strong, rough, rasping, painful, moist or

rattling. The pathological expiratory sounds may vary between audible,

strong, rough, prolonged, or rattling. The varieties of souffle, or

rattle, are the tubal souffle of inspiration or expiration (met with in

pneumonia or broncho-pneumonia); the soft, deep-seated pleuritic souffle

(peripneumonia); the continuous cavernous souffle (met with in

tuberculosis); the broad amphoric souffle, in which the vibrations are

extensive and of metallic character (met with in pneumo-thorax).

As to the varieties of _râles_ which usually accompany these souffles,

they may all be met with in tuberculous animals, and comprise crepitant

and sub-crepitant, mucous, cavernous, snoring and sibilant _râles_.

CHAPTER II.

NASAL CAVITIES.

SIMPLE CORYZA.

Simple acute coryza, or inflammation of the mucous membrane of the nasal

cavities, is of comparatively trifling importance in bovine animals,

and, were it not for the possibility of gangrenous coryza being confused

with it, there would scarcely be any necessity for a special

description.

The onset of coryza is indicated by repeated sneezing and coughing, by

congestion of the pituitary mucous membrane, which soon begins to

secrete abnormally, and by difficulty in respiration, which becomes

snoring or whistling.

The discharge, transparent at first, then mucous and muco-purulent, is

abundant in quantity; the inflammation is arrested at this point or

extends towards the facial sinuses, the pharynx and larynx; the eyes are

swollen and watering, and almost all the characteristic symptoms appear

which mark the onset of gangrenous coryza. Two signs, however, are

wanting. The appetite is fairly well maintained, and the temperature

little above normal. Simple coryza occurs at all times of the year in

consequence of sudden chills, but is commonest in spring and autumn.

At first the distinction between this condition and gangrenous coryza

can only be ascertained after taking the temperature.

=The prognosis= is absolutely favourable, and often in forty-eight hours

every symptom disappears.

=Treatment= is confined to keeping the animals in stables at a suitable

temperature, sheltered from draughts. Emollient fumigations and

inhalations of turpentine, creosote, or eucalyptus oil rapidly check the

more alarming symptoms. Warm drinks and foods and cooked roots are

recommended.

In sheep, acute coryza as a consequence of chills, etc., occurs in

autumn, but is more commonly due to a parasitic cause, viz., invasion of

the nasal cavities by larvæ of certain œstridæ. During the succeeding

winter it continues under the form of chronic coryza, as a result of the

larvæ retaining their position in the sinuses.

Treatment of this parasitic coryza consists in trephining the sinuses

and destroying the larvæ.

GANGRENOUS CORYZA.

Gangrenous coryza is a grave disease of diphtheritic character, which at

first seems to be localised in the mucous membrane of the upper

respiratory passages, but which exhibits a tendency to affect all the

mucous membranes of the system.

The term “gangrenous coryza,” adopted in France, has been replaced in

other countries, especially in Germany, by such descriptions as

“contagious disease of the head,” and “malignant catarrhal fever of the

ox.” Old writers describe gangrenous coryza as a disease common in the

Jura, the eastern parts of France generally, and in the valley of the

Saône. In reality this disease occurs everywhere, both in the centre,

west and north of France, as well as in the eastern regions. Serious

outbreaks frequently occur in Germany and Italy.

=Symptoms.= Gangrenous coryza assumes three different forms, which,

however, only represent successive degrees of intensity of the attack.

In the peracute form death occurs in three to five days, even when the

characteristic signs are not all as yet apparent. In the acute, and by

far the most frequent form, the disease lasts from fifteen to twenty

days, and also ends in death in by far the greater number of cases.

Finally, in the form usually termed chronic, the disease lasts from four

to eight weeks, and most frequently ends in recovery.

_Acute and peracute forms._—The onset is marked by very striking

symptoms, which precede the local symptoms by some hours, or by a day or

more.

The temperature rises rapidly from the normal to 103° or 105° Fahr.

(39·5° to 41° C.), or even higher. Appetite and rumination are entirely

suspended; the respiration becomes rapid and difficult, while the heart

beats strongly and tumultuously; the muzzle is dry, the mouth hot, and

salivation so abundant as to suggest an attack of foot-and-mouth

disease. Fæces and urine are only passed at long intervals, and dysuria

is present.

At first everything seems to indicate the development of an acute

infectious disease; but soon afterwards appear local indications

affecting the respiratory, ocular, digestive, urinary, nervous and

cutaneous systems.

The respiratory symptoms are most important, and almost characteristic.

Respiration becomes difficult, rough as in acute coryza, but soon

assumes a snoring character, and is accompanied by a discharge,

containing false membranes, from both nostrils.

The serous and muco-purulent discharge becomes rusty or reddish-brown,

soon acquires a very fœtid smell, and is found to contain epithelial

_débris_ and yellowish-green false membranes. After the least effort to

cough or the slightest touch on the membranes themselves—sometimes

without any visible cause at all—epistaxis sets in, the blood being

mixed with the discharge or simply escaping in the form of reddish

strings, like that occasionally seen in glanders.

The mucous membrane of the nasal cavities is red, turgid, apt to bleed,

and painful to the touch.

Percussion of the nasal cavities, sinuses, and even of the horns reveals

everywhere exceptional sensibility.

Sometimes, but only in certain subjects, the lower portions of the head,

including the muzzle, nostrils, lips and forehead, become infiltrated,

as though the case were one of purpura. Thoracic complications are

rarely absent, unless the disease is treated. Towards the end of the

first week the respiration, still painful and snoring, becomes more

rapid; and auscultation reveals at various points in the lungs areas of

bronchitis and of broncho-pneumonia, indicated by bronchial _râles_,

rattling breathing, and tubal souffles, etc. These complications are

accompanied by attacks of coughing, which increase the discharge, and

may threaten to end in suffocation. This happens when large masses of

false membranes from the bronchi are thrown into the larynx and cannot

readily be ejected through the glottis, which has been reduced in size

by œdematous infiltration and inflammation.

Percussion is generally useless. The appearance of the eyes is also very

significant. These symptoms develop simultaneously with the respiratory

disturbance, and are marked by infiltration of the eyelids, œdematous

conjunctivitis, and ophthalmia. The cornea becomes whitish, infiltrated,

opaque, and sometimes shows ulcerative keratitis; or, on the other hand,

it remains simply semi-transparent, and through it the media of the eye

may be seen to have become opalescent. Ulcerative keratitis may develop

rapidly and end in perforation of the cornea.

In certain rare instances examination with the ophthalmoscope has

revealed the existence of exudative iritis; this condition may be

complicated with syncchia, intra-ocular hæmorrhage, and result in

permanent loss of vision.

These ocular symptoms are accompanied by continuous, abundant and

prolonged discharge of tears, intense photophobia, and exceptional

sensitiveness to manual examination, etc.

Digestive disturbance appears less important, and may be regarded as

consequent on the febrile reaction, the general disturbance, or the

condition of the respiratory apparatus. But complete examination will

show that from the onset of the disease a special form of stomatitis

occurs. From the first the mouth is hot and dry: soon afterwards

abundant reflex salivation occurs, and the discharge, like that from the

nose, becomes excessively fœtid. This stomatitis differs entirely from

ordinary forms of stomatitis and from the stomatitis peculiar to

foot-and-mouth disease, and is characterised by the necrosis of

fragments of epithelium forming false membranes. These on being shed

leave exposed numerous ulcers distributed over the tongue, cheeks, and

lips. Neither vesicles nor pustules are produced, but merely false

membranes of small dimensions.

The false membranes and ulcerations occur on the soft palate and in the

pharynx.

When the patients survive for a certain time, croupal enteritis and

ulcerative enteritis, sometimes accompanied by hæmorrhage, develop. The

administration of enemata is followed by the passage of fæces containing

considerable fragments of epithelium or of streaks of blood. From the

outset these digestive complications are indicated by failure to

ruminate, by cessation of peristalsis and by constipation, which is

usually succeeded by abundant fœtid diarrhœa.

Functional disturbance of the genito-urinary apparatus is rarer, or at

least more difficult to detect. The animals refuse drink; micturition

seems to be suspended or very difficult. The urine may be albuminous or

rose-coloured, in consequence of the presence of hæmatin; more rarely it

is purulent or sanguinolent. There may also be urethritis, cystitis,

pyelitis, and nephritis, with the passage of hyalin cylinders in the

urine, although this is not always the case.

In females the mucous membrane of the vagina and lips of the vulva

usually seem congested and œdematous; but it is rare to find

diphtheritic false membranes, as on the buccal and nasal mucous

membranes, etc. On the other hand, vaginitis and exudative metritis are

common.

Cutaneous outbreaks also constitute important symptoms by which this

disease is recognised. At points where the skin is fine, on the inner

surface of the thighs, around the girth, on the inner surface of the

forearm, and on the mammæ, etc., an exanthematous eruption occurs,

followed later by the development of pustules, which at first sight

might suggest cow-pox.

These pustules are prominently apparent, and can readily be detected on

palpation. They are more or less confluent, hard, and without a

peripheral œdematous zone.

In the case of the mammæ these pustules occur most commonly on the

teats, are round or slightly oval in form, bright red in colour, and

sometimes violet-red. They never become converted into vesico-pustules,

as in cow-pox, or into vesicles; and in no way resemble the skin

eruption peculiar to foot-and-mouth disease.

Certain nervous symptoms have also been described, comprising trembling,

epileptiform convulsions, and paraplegia of the hind quarters.

Moussu has never seen nervous disturbance assume the form of

epileptiform convulsions, and it is possible that the paraplegia

referred to simply marks the last stage of the disease.

=Causation.= The essential cause of gangrenous coryza has not yet been

definitely ascertained. Within recent years teachers of the highest

authority have represented the disease as a general affection belonging

to the hæmorrhagic forms of septicæmia (Nocard and Leclainche). Nocard

has found ovoid bacteria in the false membranes of the larynx, and

Leclainche a paracoli-bacillus in the mesenteric ganglia and the

intestines, but the disease has never been reproduced in a

characteristic and complete form similar to the clinical type.

Other microbes have also been described as occurring in the blood or

discharges; but attempts to transmit the disease by using cultures or

the different morbid products which observers have collected have

invariably failed, and it has therefore been concluded that the disease

is not contagious, but merely infectious.

Moussu does not regard this disease as a hæmorrhagic septicæmia, because

the blood proves sterile unless grave pulmonary, intestinal or renal

complications occur, and because the disease appears capable of being

cured in a short time by simple methods. In the present state of

knowledge he prefers to regard it as an infectious disease of

diphtheritic form, at first localised in the upper respiratory and

digestive tracts, always tending towards a grave toxæmia, and towards

complications due to various other infections.

Even though direct contagion has not been proved, it is impossible to

doubt that stables may become infected. This is sufficiently proved by

the continued appearance of the disease when disinfection is neglected

after the occurrence of the first case.

It is possible that the causes formerly assigned—viz., chills, the

influence of draughts, and a morbid predisposition—may increase

susceptibility in animals otherwise well cared for, but it is quite

certain that infection of the stable is an important factor.

=Lesions.= The lesions vary with the complications, but those shown in

the beginning are always identical. The mucous membrane of the nasal

cavities is congested, inflamed, sphacelated, and ulcerated at different

points. The turbinated bones and the ethmoid cells may become necrotic;

in the larynx the region of the glottis is always most markedly

affected; the mucous membrane becomes ulcerated in the neighbourhood of

the vocal cords, and the tissues may become more deeply attacked.

In the trachea and bronchi the mucous membrane undergoes desquamation,

and may become ulcerated at the points where false membranes have

formed. The mucous membrane of the sinuses is always affected, but is

rarely ulcerated.

Such complications as capillary bronchitis, broncho-pneumonia, and

gangrene of the lung may be noted.

The mucous membrane of the mouth presents a violet-red or blackish-red

colour; the tongue and gums are swollen, and ulcers as large as a lentil

or a halfpenny may occur either singly or in a confluent form.

The genito-urinary apparatus reveals signs of croupal cystitis,

submucous effusions of blood, vaginitis with the formation of false

membranes, acute pyelitis, etc.

=Diagnosis.= When the symptoms are fully developed the diagnosis of

gangrenous coryza is extremely simple, but the absence of some of these

may justify hesitation in forming an opinion. If the examination is

carefully carried out, it is always possible to distinguish this disease

from simple coryza, which is only accompanied by trifling fever, and in

which appetite is preserved; from foot-and-mouth disease, with its very

characteristic buccal eruption and absence of lesions from the upper

portions of the respiratory tract; and from contagious ophthalmia.

=Prognosis.= Up to the present time the prognosis has always been

regarded as extremely grave, the mortality being sometimes as high as

from 90 to 100 per cent., and moreover the cases which recover are

invariably those of what is considered the chronic form. Sudden sinking

of temperature during the disease is an unfavourable sign. From 1894 to

1900 Moussu never cured a single case, whatever his method of treatment;

nevertheless, it now seems possible to regard the condition a little

more hopefully, provided that no incurable complication occurs before

the beginning of treatment.

=Treatment.= Of all the modes of treatment suggested—viz., anti-febrile

agents, general stimulants, purgatives, diuretics, external stimulant

applications, etc.—none have succeeded. Antiseptics injected into the

nasal cavities, antiseptics given internally, milk diet, and all the

methods hitherto suggested are equally useless.

The only treatment which appears to have achieved any degree of success

is that of injecting physiological salt solution in large doses (up to

six quarts per day, divided into three parts). All the animals treated

by this method recovered, provided they presented no broncho-pulmonary

complications.

The sole inconvenience of this treatment is the difficulty in carrying

it out when the animals are at a distance from the practitioner. It is

indispensable that they should be close at hand, in order that he

himself may make the injections at the proper time. There is some reason

for hoping, however, that serum from animals which have recovered will

prove to be more active than saline injections.

This method of treatment should be followed up by the most rigid

hygienic precautions. The mouth, nasal cavities and eyes should

frequently be washed with antiseptic solutions. The stables should be

freely ventilated, and the floors and bed kept in the cleanest possible

condition, etc.

Whenever a case of gangrenous coryza is observed it should be isolated,

and the stables should most carefully be disinfected.

TUMOURS OF THE NASAL CAVITIES.

Apart from actinomycosis of the upper jaw, tumours of the nasal cavities

or of the sinuses are not frequent in bovine animals. They are, however,

occasionally met with, and present symptoms which must be carefully

studied in order to avoid errors of diagnosis. Usually they are of the

nature of myxomata, more rarely of fibro-myxomata.

[Illustration: $1]

=Symptoms.= The dominant symptom is difficulty in breathing, both when

moving and eating, a difficulty which is sometimes so considerable as to

cause snoring respiration or roaring. Nevertheless, examination of the

trachea and of the lung, visual examination of the lower portions of the

nasal cavities, and manual examination of the pharynx, larynx and

glottis give only negative results. It may even happen, as occurred in

the case from which the illustration herewith was taken, that percussion

of the maxillary sinus reveals normal resonance.

In the case of tumours of small size the forehead is not deformed. When,

on the other hand, the tumour partly obstructs the nasal cavities it may

thrust on one side the septum nasi and externally cause well-marked

asymmetry of the face. Sero-mucous or muco-purulent discharge then

occurs.

=The diagnosis= is somewhat difficult, for continuous or temporary

roaring (or at any rate difficulty of respiration), being the dominant

symptom, must be distinguished from roaring due to a laryngeal lesion

like paralysis or tumour formation, from perilaryngeal compression due

to enlarged retro-pharyngeal glands, and from tracheal or pulmonary

lesions; and its origin must be located in the nasal cavities.

[Illustration: $1]

=The prognosis= is grave, in consequence of the difficulty of exploring

the depth of these cavities and of the possible nature of the tumour.

Nevertheless, in the case of simple myxomata permanent recovery usually

follows extirpation.

=Treatment= is confined to extirpation, which is quite possible in the

case of pedunculated tumours; in the case of sessile tumours free

trepanation of the roof of the nasal cavities becomes necessary. The

operation is quite safe.

PURULENT COLLECTIONS IN THE NASAL SINUSES. NASAL GLEET.

From the clinical point of view two varieties of this condition may be

distinguished—inflammation of the mucous membrane of the maxillary sinus

and inflammation of the mucous membrane of the frontal sinus and of the

horn core. These forms of inflammation frequently lead to suppuration.

The pus collects in the depressions and divisions of the frontal or

maxillary sinus.

PURULENT COLLECTIONS IN THE FRONTAL SINUS.

=Causation.= In the majority of cases inflammation of the mucous

membrane of the frontal sinus is produced by external causes: fractures

of the horns and horn core accompanied by hæmorrhage into the horn core;

fractures of the horn with exposure of the sinus of the horn core;

wounds and violent blows on the occipital region or the frontal bone;

cracks or depressions of the external wall of the sinus, etc.

In all these cases, whether blood is effused or the mucous membrane of

the sinus is merely infiltrated with serum, infection may be produced by

germs being deposited from the air passing through the nasal cavities

and causing suppuration.

Purulent collections in the frontal sinus may result from continued

irritation, like that due to a badly fitting yoke. They also occur as an

accidental complication of general diseases like gangrenous coryza.

=Symptoms.= The catarrh or purulent collection in the sinus may be

unilateral or bilateral, and the symptoms vary, according to the form

which it assumes.

_Unilateral collections._—Nasal hæmorrhage is often the first symptom,

but this is often regarded as of little importance, because the

formation of pus does not occur until very much later. The animal shows

ill-defined pain, loses appetite, remains dull and somnolent, and

carries its head on one side. The horn on the injured side is hot and

sensitive, and at a later stage the eye becomes affected by contiguity

of tissue. It is then swollen, closed, and watery; the conjunctiva is

infiltrated, and somewhat inflamed. Sensibility and partial or complete

dulness of the affected side may be detected by palpation and

percussion. On the animal being made to cough, a yellowish or

greyish-white discharge of very fœtid and sometimes putrid character

escapes.

_Bilateral collections._—Catarrh is rarely bilateral at first; but if

the unilateral lesion is not treated, it affects the median septum

dividing the two cavities, and the inflammation extends to the second

sinus. The animal then shows dull pain, and exhibits marked depression;

sometimes it appears quite prostrate. The head is carried low and

inclined towards the ground, while the above-mentioned ocular symptoms

and the indications furnished by palpation and percussion extend to both

sides. Coughing produces momentarily a double discharge, which the

animal disposes of after the fashion of horned cattle.

=Diagnosis.= The diagnosis only presents difficulty in the early stages.

Later the warmth and sensitiveness of the horns, the partial dulness,

offensive character of the discharge, etc., render diagnosis easy.

The disease is not likely to be mistaken for gangrenous coryza, despite

the condition of the eyes, because it develops slowly, progressively,

and without marked fever.

=Prognosis.= If treated early, unilateral or bilateral collections of

pus in the sinuses are capable of cure, but later when bodily health is

impaired and the local lesions of the mucous membrane very pronounced,

there is less chance of success.

=Lesions.= The initial lesions consist in cracks, fissures, or fractures

of the bones of the face or exostoses of traumatic origin. In other

cases the mucous membrane alone is affected. As a result of chronic

irritation it becomes thickened, inflamed, and ulcerated, and granulates

freely. The depressions in the sinuses contain grumous, fœtid pus, which

irritates the surrounding tissues and produces pain and general symptoms

of cerebral irritation, which are sometimes very disquieting.

=Treatment.= Numerous methods of treatment were formerly recommended,

such as absolute rest, bleeding, cold affusions, perforation of a horn,

section of a horn, etc. None of these is of any value.

At first, provided only a certain degree of sensitiveness and simple

catarrh without suppuration exist, antiseptic fumigations with tar,

carbolic acid, thymol, etc., are useful; but later, when pus has formed,

they are useless. At this period the only rational and efficacious

treatment consists in trepanation. In unilateral collections three

openings are necessary.

The first is an opening into the sinus of the horn core. It is made ⅜ to

¾ of an inch above the horn-secreting band of the horn. It must not be

forgotten, however, in planning such an opening that the sinus of the

horn core only exists in a rudimentary condition in young animals, and

that it is scarcely possible to trephine the horns before the patient is

three years of age.

The second opening is made towards the upper part of the frontal sinus

about ¾ inch below the horn-secreting ring at the base of the horn and

in a line with the axis of the horn core itself. Whatever the animal’s

age and however little the sinuses may be developed, this opening is

certain to expose the cavity of the frontal sinus.

In old animals where the frontal sinus is enormously developed, and

where very large depressions exist in the orbital region, a third

opening should be made just above a transverse line uniting the upper

margins of the two orbits and inside the suborbital suture.

These openings having been made, treatment consists—firstly, in

completely washing out the cavity with boiled water, cooled to 95° or

100° Fahr.; and, secondly, in injecting antiseptic and astringent

solutions so as to check the formation of pus. Among such may be

mentioned 3 per cent. carbolic solution, 5 per cent. carbolic glycerine,

2 per cent. solution of iodine in iodide of potassium, etc.

Whatever the drugs employed, the cavities should be washed out every

day, first with plain sterilised water, and then with antiseptic

solutions at the body temperature, since cold solutions often cause

inflammation of the mucous membrane of the opposite sinus.

PURULENT COLLECTIONS IN THE MAXILLARY SINUS.

This disease is much rarer than that of the frontal sinus, and only

within the last few years (Ries, 1899) has a really good description

been given of it.

=The causation= is imperfectly understood. Injuries to the suborbital

region and maxillary ridge, caries of the molar teeth, and inflammation

occurring during the development of general diseases represent the

principal causes.

The dominating and characteristic symptom of the presence of pus in the

maxillary sinus consists in incessant snorting, accompanied by violent

movements of the head and the discharge of purulent or muco-purulent

material.