On finding a host, larvæ attach themselves by the rostrum, and remain

there for about two days, by which time they are distended, black and

globular. At this time they are easily detached from the host, and have

lost their activity and clinging habits.

=The Pupa.= The possession of eight legs distinguishes the pupa easily

from the larva. The extra pair are placed behind the others. After the

metamorphosis, the pupa takes up its position on the stalks of herbage,

just as the larva had done, for another chance of attachment to a host.

But whereas adult grass ticks seem to confine themselves mostly to

sheep, cattle, and deer, the larvæ and pupæ attach themselves very

readily to various hosts, such as horses, dogs, and even human beings.

After about four days the pupa is again replete with blood, black and

opaque, and again drops to the ground to undergo its second and final

change.

=Adults.= On reaching the adult age, both males and females again wait

on herbage for a passing host. At this time, as well as after distension

of the female on the host, an action which appears to be sexual

intercourse freely takes place, even in confinement. On the host the

females gradually distend (Fig. 202), and in the course of so doing vary

much in colour and appearance. When fully replete, the female _Ixodes

reduvius_ becomes globular and black. One taken in this condition on

April 15th commenced to lay on May 12th, and a few others taken at the

same time commenced shortly afterwards.

Grass ticks never remain on the host to undergo metamorphosis or to lay

eggs. They must therefore during their cycle of existence contrive to

find a fresh host no fewer than three times.

In an article published in the Transactions of the Highland and Ag. Soc.

for 1902 Mr. Wheeler draws attention to the close points of resemblance

between louping-ill, Texas fever, tsetse fly disease, surra,

heart-water, yellow fever, and malaria.

In the article previously referred to he summarises his conclusions as

follows:—

One species only of tick, _Ixodes reduvius_, commonly known as the grass

tick, has been found to carry the louping-ill bacillus to the sheep. It

is easily recognised by the red body of the young females, the legs,

shield, etc., being dark brown.

It lays its eggs, and undergoes its metamorphoses, in coarse herbage,

and after each change seeks a fresh “host” on which to distend itself to

a large size by suction of blood.

[Illustration: $1]

[Illustration: $1]

In all stages grass ticks abstain from all food except when on a host,

and they are endowed with extraordinary powers of fasting until a host

is found.

Ticks soon die of drought where there is no good harbourage among rank

vegetation.

Judging from analogy, it is probable—

That the bacillus can only be obtained from a diseased sheep, and

inserted by the tick into another sheep.

That ticks convey the bacillus through their eggs to their offspring, as

well as retain it through their metamorphoses.

That there is no danger in removing sheep from foul ground to cultivated

lowlands, but that the disease is easily imported from one hill farm to

another.

Strong and fat animals are nearly as susceptible to attack as weakly

ones.

If the land is once free of disease, it can only be re-imported by

diseased sheep, or ticks taken from them.

SUGGESTED MEASURES FOR PREVENTION.

Burning and cutting of long grasses, bracken, rushes, etc.

Salt and sulphur given to the sheep.

Inoculation.

Removal of all diseased sheep to a separate inclosure, where

hand-picking and dipping are carefully attended to, the pasture is kept

short, and damp places are drained. The sheep to be confined to this

inclosure so long as the tick season lasts.

Immediate slaughter and burial of all affected sheep.

BRAXY.

[The following is a very condensed account of a paper published by C. O.

Jensen on the above disease. It first appeared in English in the

_Veterinarian_, Vol. LXIX., No. 825, p. 621, along with the original

illustrations.]

The name Braxy is applied to a disease in some respects resembling

anthrax, which appears as an epizootic, and is best known in Iceland,

the Faroe Islands, and parts of Norway, though it also occurs in

Scotland and Cornwall. Krabbe describes the disease as infectious, very

acute in its course, and as proving fatal within a few hours of the

appearance of certain characteristic swellings about the posterior parts

of the body. Post-mortem reveals extensive dark purplish staining of the

abomasum and distension of the digestive canal with gas, while

decomposition of the cadaver occurs with excessive rapidity, the liver

and kidneys undergoing softening, the skin assuming a bluish tint, the

wool becoming loose, and the entire carcase giving off a most offensive

stench. Krabbe states that the disease was regarded as a form of

anthrax—a view, however, in which he does not coincide. Somewhat later

Messrs. J. Sigurosson, S. Jönsson, and Einarsson, all natives of

Iceland, and the Norwegian State Veterinary Surgeon, Ivar Nielsen,

carefully described the disease, throwing considerable light both on the

conditions in which it appears and on its etiology.

According to them, braxy is an acute, or even exceedingly acute,

infectious disorder, which begins as a hæmorrhagic inflammation of the

mucous membrane of the abomasum, is accompanied by excessive development

of gas in the digestive canal, especially in the stomachs, and proves

fatal in some cases by a kind of general infection, in others by a

specific intoxication, or by dyspnœa due to tympanites.

Braxy commits its chief ravages during the winter months: appearing

first in autumn, the cases increase as winter approaches, to diminish

again in spring; in summer they are exceedingly rare. This fact explains

why the disease was so long regarded as due to climatic influences. Even

at the present day, when it is known to be due to a specific organism,

the action of temperature, etc., must still be regarded as probably

playing an important part in infection. The disease is said not to occur

in mild weather; but whether or not this be true, every one is agreed

that it is principally seen during frost, especially when frost is

unaccompanied by snow.

From experience gained both in Iceland and Norway, the disease appears

to be often localised in certain districts and fields—a fact largely

accounted for when we learn that up to the present little or no attempt

has been made to prevent the spread of infection from the dead bodies.

Braxy chiefly attacks young animals, and is rare in those over three

years of age. Hjaltelin estimates the number of deaths in a single

district during the years 1849–1854 at approximately 6,000, made up as

follows:—

Yearling lambs 2,440

Two-year sheep 2,460

Three-year sheep 1,020

Animals older than three years 80

The younger animals suffer most, and in Norway Nielsen directs attention

to the heavy fatalities amongst lambs.

=Symptoms.= The sheep suddenly appears ill, is dull, lies about, and

cannot be induced to rise; all movement seems to give pain, and from

time to time the animal groans; the posterior parts of the body become

swollen, and a little froth often escapes from the mouth. The pulse

varies between thirty and thirty-five per minute, and is often

imperceptible in the extremities; the temperature may rise to 105° or

even 108° Fahr. This condition may last some hours, and always ends with

the animal’s death; sheep, which overnight had shown no signs of

illness, are often found dead in the morning. The incubation period is

from forty-eight to sixty hours, but ordinary cases seldom live longer

than from five to eight hours after the symptoms declare themselves.

The striking post-mortem appearances, especially the hæmorrhagic

inflammation of the abomasum, were early the subject of remark. This

appearance is very characteristic.

If the animals are slaughtered, the most important change is found to be

a purplish, dark, somewhat swollen patch in the abomasum; during the

course of the disease this increases in size, and if the animal should

be allowed to die of braxy the entire abomasum shows hæmorrhagic or

sero-hæmorrhagic infiltration; the abomasum and the first part of the

small intestine usually contain no food, but may often show a certain

amount of bloody fluid. This hæmorrhagic inflammation may extend in a

forward direction, implicating the other stomachs, or backward, invading

the small or both small and large intestines. The other parts of the

intestinal canal are congested. The pleural and peritoneal cavities

contain a little serous fluid. The blood is dark in colour, but may be

clotted; the spleen is at times somewhat swollen, at others normal. The

liver is usually light-coloured, soft, and degenerated; occasionally

this degenerative process is extremely marked, but due allowance should

always be made for post-mortem change. The kidneys may appear

degenerated; in many cases they are enlarged and soft, or almost fluid

in consistence. The carcase decomposes very rapidly; within a short time

of death the belly is distended with gas, the rectum protrudes at the

anus; the skin assumes a bluish colour in places, and the wool falls

out; sometimes the skin bursts, revealing the presence in the

subcutaneous tissue of a sero-hæmorrhagic fluid.

[Illustration: $1]

Braxy is, then, a primary violent hæmorrhagic inflammation of the

abomasum, with or without secondary general infection.

From careful study it seems quite certain that the Scottish “braxy” is

identical with the Norwegian and Icelandic “bradsot”; it appears at the

same season, and is intimately connected with climatic influences; it

runs its course so rapidly that animals left healthy at night are found

dead in the morning; and the pathological anatomy of braxy is the same

as that of “bradsot.”

To Ivar Nielsen, of Bergen, must be ascribed the honour of elucidating

the etiology of braxy. During the course of investigations, published in

1888, he found, partly in the local lesions of the intestinal track,

partly in the capillaries of the internal organs, a special bacillus,

easy to distinguish from that of anthrax, of which he gives the

following description:

“The bacilli (_B. gastromycocis-ovis_) are oval, of a length varying

from 2 to 6 micromillimètres, and a thickness of one micromillimètre.

They are often in pairs, arranged in a straight line or meeting at an

angle; in the former case, and especially if deeply stained, the pair

may present the appearance of a single bacillus. Occasionally they form

long chains. Near the centre of the bacillus, but not always centrally

placed, may often be found a zone measuring more than half the total

length of the bacillus, and exhibiting little or no colouration. It

appears as though the stained portions gradually contracted, finally

forming two deeply coloured masses at the poles of the lemon-shaped

bacillus, which then somewhat resembles the bacillus of rabbit

septicæmia, except that the unstained part of the braxy bacillus is

larger and more rounded, appearing to be bulged out laterally. In dry

preparations the bacillus is easily recognised on account of the highly

refractile character of the colourless portion; but in sections careful

search is often required, especially if the section be somewhat thick.

Whether the colourless portion represents a spore cannot at present be

said, though such appears probable. The bacillus is always found in the

mucous membrane of the abomasum, and especially in the submucous and

subserous connective tissue. In the other organs the bacillus may be

present in considerable numbers, or, on the other hand, may be

impossible to detect.”

The same bacillus has been found in the tissues of affected sheep both

in Norway and in Iceland; the bacillus, when subcutaneously injected,

produces a violent hæmorrhagic inflammation of the same character as one

finds in the abomasum in cases of spontaneous braxy, and the local

changes at the point of inoculation may, just as in spontaneous braxy,

be accompanied by a general infection with degeneration of different

organs, and with softening of the kidney substance.

The bacillus of braxy is anaërobic. In cultures it develops considerable

quantities of gas, just as it does when inoculated into the tissues. It

is closely related to the bacillus of symptomatic anthrax, which it

somewhat resembles in general appearance, and of which it reminds one by

its ability to produce hæmorrhagic inflammation in the muscular tissues.

It is distinguished from the last named, however, by being pathogenic to

swine, mice, pigeons, and poultry, which are not killed by the bacillus

of symptomatic anthrax.

The bacilli of braxy, malignant œdema, symptomatic anthrax, together

with Ivar Nielsen’s shortly described bacillus of whale’s septicæmia,

and Thoma’s bacillus of malignant emphysema (found in extensive

subcutaneous inflammation and emphysema in man), and certain others less

well known, form a group of closely allied bacilli resembling one

another in form, in being anaërobic, and in producing a sero-hæmorrhagic

inflammation and emphysema, but differing in the manner of producing

their effects.

Experience and analogy both seem to indicate that young animals

occasionally suffer from mild attacks of braxy from which they recover.

Such animals afterwards exhibit a well-marked immunity against the

disease.

Ivar Nielsen attempted to vaccinate against braxy by a method resembling

that used in black-quarter. He dried the diseased kidney tissue, and

injected subcutaneously small quantities of the material thus obtained

suspended in water. A slight local inflammation followed, which appeared

to protect against later “spontaneous” infection. He has used this

method in his own district, and states that it is also practised to some

extent in Iceland. As far as one can judge—and of course a just opinion

is very difficult to form—these inoculations appear of value.

The result of experiment, considered in conjunction with the good

results of inoculation for black-quarter, would seem to indicate that

Nielsen’s method of vaccination against braxy may yet prove of the

greatest possible value, although the method will doubtless require

modification in its details.

These modifications Jensen enumerates at some length.

(Mr. Dollar has been informed that Professor Hamilton and Dr. McCall

have been engaged in an investigation regarding the possibility of

conferring immunity against braxy, and that a Government report will be

issued on the subject. Up to the present time however—April, 1905—he has

not been able to obtain this report or any advance proof sheets of it.)

BILHARZIOSIS IN CATTLE AND SHEEP.

This disease is caused by the bovine blood fluke (_Schistosoma bovis_)

of cattle and sheep. Synonyms: _Bilharzia bovis_; _Bilharzia crassa_;

_Gynæcophorus crassus_; _Gynæcophorus bovis_; _Bilharzia hæmatobia

crassa_; _Schistosomum bovis_.

=Geographical Distribution.= Egypt, Italy, Sicily, India (?).

This parasite was discovered by Sonsino (1876) in Egypt in the portal

veins of the ox, and later he found it in sheep, while Grassi and

Rovelli afterwards found it in about 75 per cent. of the sheep

slaughtered at Catania, Sicily.

=Source of Infection.= Clinical observation and analogy point to

unfiltered drinking water as the source of infection.

=Position of the Parasite.= The worms are found in the veins of the

abdomen, the vena porta, vena linealis, vena renalis, and the venous

plexus of the bladder and of the rectum.

=Symptoms.= The young parasites appear to do no injury; in fact, even

the adult worms seem to be inoffensive in themselves. The eggs, on the

other hand, armed with a sharp point, are the exciting cause of the

disease. The position of the parasite in the venous system, and the

consequent location of the agglomeration of eggs, determine the

particular symptoms. Either the genito-urinary system is attacked, in

which case hæmaturia is one of the first symptoms, or the large

intestine is attacked and blood is noticed in the fæces.

[Illustration: $1]

[Illustration: $1]

If the parasites are lodged in the venous plexus of the genito-urinary

system, the chief symptoms are: hæmaturia, pains in the lumbar region,

the left iliac fossa, the thigh, or in the vulva, which may be

spontaneous or may accompany micturition; cystitis, vesical calculus,

urinary fistulæ, vaginal verminous tumours, nephritis.

The eggs accumulate in the capillaries, which they rupture; they

traverse the mucosa and fall into the bladder, thus causing more or less

hæmorrhage; in this way the _hæmaturia_ is established, which is often

the initial symptom. At first the urine is quite bloody, but it

gradually becomes clearer, and it is only at the end of micturition that

muco-purulent flakes are expelled, in which numerous eggs and even

embryos are found; the urine contains also epithelial cells, more or

less pus, eggs, and occasionally embryos. On micturition sharp pains are

felt at the base of the penis or at the gland, possibly due to the

passage of eggs. The passage of eggs through the walls of the bladder

gives rise to _cystitis_; blood becomes more abundant in the urine after

fatigue or coitus; clots may form and cause retention of urine; chronic

urethritis may develop, evidently due to the presence of the eggs. In

Egypt 80 per cent. of the cases of vesical calculus in man coincide with

bilharziosis; the formation of the calculi evidently results from the

presence of the eggs, for the central nodule always contains one or more

of these structures. Urinary fistulæ, opening on the perineum, more

rarely into the rectum, occasionally form. The mucosa of the vagina,

also of the uterus and bladder, becomes impregnated with calcareous

salts. Nephritis develops in grave cases.

[Illustration: $1]

If the parasites lodge in the veins of the rectum the lesions caused are

analogous to those described for the genito-urinary tract.

The heart, lungs, and liver generally remain normal.

=Pathology.= The bladder is reduced in size, while its wall is greatly

thickened, due chiefly to hypertrophy of the muscularis; the mucosa is

also thickened, and at certain points it is indurated by uric or

calcareous deposits, but the principal lesion consists in ulcerations

covered with sanious pus. Lesions analogous to those of the bladder are

also observed in the lower third of the ureters, and may extend as high

as the kidney; the ureter is enlarged and tortuous; the mucosa

irregular; its lumen may remain nearly normal in size, but its wall

becomes very thick: the flow of urine may be obstructed; in short, a

veritable hydro-nephrosis obtains, which results in atrophic lesions of

the kidney, and may finally end fatally.

The mesenteric lymphatic glands may hypertrophy, their substance

becoming tumefied, presenting small hæmorrhagic centres, and containing

eggs. The liver may contain eggs and become somewhat cirrhotic; the eggs

accumulate in the branches of the portal veins, or after piercing the

walls they lie in the hepatic parenchyma. The lungs may also contain

eggs.

=Diagnosis.= The diagnosis may easily be made by a microscopic

examination of the urine to determine the presence of the egg.

=Prognosis, etc.= The severity of the disease varies directly with the

number of parasites (and hence the number of eggs) in the body.

Fortunately, in the majority of cases, the number of parasites is small,

though it may increase from repeated infections to 500 or more. In cases

of comparatively light infection the disease is reduced to a slight

chronic cystitis, with now and then exacerbations, in course of which a

slight amount of blood and pus is passed in the urine. The disease may

last for years without apparent increase. In the most severe cases death

may occur from various causes, rupture of the bladder, ascending

pyelo-nephritis, uræmia, albuminuria; the patient may die in marasmus,

being exhausted by the dysentery or the anæmia.

Bilharziosis is accordingly not such a fatal disease as has sometimes

been supposed.

HEAT STROKE—OVER-EXERTION.

In oxen and sheep heat stroke is rare as a primary accident, but it is

frequently produced by over-exertion resulting from the combined action

of the sun’s rays, heat, and fatigue due to work or travelling.

It is commonest during the hottest months of the year in oxen doing hard

work or in flocks which have been travelled considerable distances. It

may also be seen during cooler seasons as the result of exceptional

fatigue.

The disease results from a general intoxication which reacts most

markedly on the cerebro-spinal centres. It is in fact a complex

intoxication resulting from failure of the natural excretory organs to

perform their function completely, and from excessive central heat

acting on the nervous centres.

Fat animals out of condition are more readily attacked than working

animals or sheep reared in the open air.

=The symptoms= are very characteristic. Oxen when attacked first of all

show extremely rapid respiration and dyspnœa, announcing progressive

asphyxia. They move with the nostrils dilated, the eyes prominent and

injected, the mouth open and the tongue lolling out. Then all of a

sudden they come to a stop beside a wall, or, if at liberty, in a ditch,

and refuse to move. They may die rapidly with symptoms of asphyxia if

they are forced to move until completely exhausted. In others, after a

rest of several hours, the breathing becomes slower, the anxiety less

and normal conditions return.

In sheep the same general signs may be seen: panting respiration,

cyanosed mucous membranes and extreme anxiety, while death follows

rapidly in the same way, with symptoms of asphyxia.

The =diagnosis= is extremely easy. The =prognosis= is grave.

=Treatment= consists in prompt and free bleeding to prevent pulmonary

congestion. The animals should be rested in a shady, sheltered spot.

They should have cool drinks and be sprinkled over the head, neck, or

entire surface of the body with cold water.

To prevent such attacks, fat animals should not be moved for long

distances, or during the hottest hours of the day, while difficult and

prolonged exertion should be avoided.

CHAPTER VI.

DISEASES OF THE LYMPHATIC SYSTEM.

Diseases of the lymphatics are numerous, highly important, and still

imperfectly understood. They follow various accidents, local

inflammations, certain specific diseases, such as tuberculosis, and may

occur in an isolated form without involving any other part of the body.

[Illustration: $1]

Inflammation, usually of infectious origin, may attack lymphatic vessels

(lymphangitis) or lymphatic glands (adenitis), giving rise either to

simple lymphangitis, suppurative lymphangitis, or again to simple or

suppurative adenitis.

It is unnecessary to emphasise this point in general surgical pathology,

for it is identical with that which is observed in other domestic

animals, but in order properly to detect the glandular symptoms in

certain diseases peculiar to the lymphatic apparatus, and in certain

specific diseases, such as tuberculosis, farcy of the ox, etc., it is

necessary to understand thoroughly the topography of the lymphatic

system.

=Topography of the lymphatic glandular apparatus: Examination.= The

lymphatic glands are in some cases superficial, in others deep seated,

and are arranged symmetrically on either side of the body.

[Illustration: $1]

Beginning with the head and fore quarters, the lymphatic apparatus

comprises a subglossal, a preparotid, a subatloid, a prescapular and

several prepectoral glands (Fig. 209).

None of these glands are very deeply placed, and all are easily

accessible to palpation, provided their exact position is known and the

animals are not too fat.

The subatloid is a little more difficult to detect, but in thin animals

the tips of the fingers can easily be passed under the wing of the atlas

so that the condition of the gland can be examined.

In a normal condition, any gland on being examined conveys a sensation

of softness and elasticity of a special character which never varies.

Palpation is painless.

When, however, the gland is diseased, palpation causes pain in the case

of all acute affections. It may, indeed, be impossible to reach the

glands, as they are buried sometimes in œdematous swellings of varying

size. On the other hand, they may be painless on being touched, but

swollen, hypertrophied, indurated, hardened or caseous.

The deep-seated glands of the fore portion of the body comprise the

retro-pharyngeal and the cervical chain running along the posterior

border of the trachea. Normally these glands cannot be examined (Fig.

210); but when the seat of certain morbid processes, they may be so

enlarged as even to be readily visible. The larynx and pharynx are then

displaced downwards, the depression between the head and upper extremity

of the neck disappears, together with the depression known as the

jugular furrow. Such deformities may be either perfectly symmetrical, as

in lymphadenia, or (as is more commonly the case) asymmetrical, as in

tuberculosis; and if inspection leaves any doubt, the glands may be

further examined by palpation.

[Illustration: $1]

To obtain the fullest information both hands should be used, one arm

being passed over the neck and the fingers engaged behind the trachea.

The operator may also stand in front of the animal, whose head should be

lifted so that the points of the fingers can be thrust deeply inwards on

either side of the trachea in the direction of the vertebral column.

In the posterior portion of the body the number of glands that can be

examined is much smaller. The gland of the stifle, also called “gland of

the flank,” is, so to speak, the only one which can readily be detected

by examination or palpation. Nevertheless, in cases of lymphadenitis,

tuberculosis of the glands, etc., it becomes easy to detect lymphatic

glands in the loose fold of skin known as the flank. These glands are

very small, and three in number. They are arranged in a triangle, one

being much more prominent than the two others. In exceptional cases,

little nodular glands, indistinguishable at ordinary times, may become

hypertrophied. This is particularly true of the small glands in the

neighbourhood of the last rib.

[Illustration: $1]

The retro-mammary glands need only be mentioned, but it is important to

know that a deep-seated popliteal gland also exists above the

semi-tendinosus and semi-membranosus muscle in the thickness of the

muscles of the thigh; as also an ischiatic gland opposite the ischiatic

notch, which can only be examined by internal palpation from the pelvis,

and an anal gland situated deeply on the sides and in front of the

sphincter ani.

With the exception of those of the pelvis and of the sublumbar region,

the glands of the thoracic and abdominal cavity cannot be examined, but

change in them is indicated under certain circumstances by clearly

defined clinical symptoms, and moreover it is necessary to be able to

detect changes in these glands on post-mortem examination.

In the thoracic cavity the lymphatic apparatus comprises the mass of the

prepectoral glands, which extends into the anterior mediastinum between

the first ribs (glands of the entry to the chest), the aortic lymphatic

gland situated beneath the dorsal portion of the spine opposite the

bifurcation of the aorta, and the lymphatic glands of the posterior

mediastinum, one of which is relatively small and is lodged in the

concavity of the posterior aorta, the other large, elongated and

situated immediately above the œsophagus in front of its passage through

the diaphragm.

In the abdominal cavity a sublumbar chain is found situated on the sides

of the lumbo-sacral portion of the vertebral column, the mass of the

subsacral lymphatic glands, and, at the entrance to the pelvis,

extending on either side along the course of the external iliac arteries

and veins and resting on the shafts of the iliac bones, the iliac

glands.

All these glands are partly accessible to examination by the rectum.

Last of all, we may mention the gland situated on the hilum of the

liver, the mesenteric glands, and the little lymphatic glands above the

sternum.

In the front limb the only glands of importance from a clinical

standpoint are those of the internal surface of the shoulder, close to

the divisions of the brachial plexus.

When enlarged or invaded by any specific organism, they may, by

compressing the nerve trunks, cause lameness.

THE LYMPHOGENIC DIATHESIS.

(LYMPHADENITIS, LYMPHO-CYTHÆMIA, MYELO-CYTHÆMIA.)

It has been questioned whether the term “lymphogenic diathesis,” which

was employed in human medicine by Jaccoud to describe certain morbid

conditions also found in animals of the bovine species, should continue

in use. At the present moment it is difficult to determine the question.

Under any circumstances it has the advantage of including diseases of

the lymphatic system, indicated by hypertrophy of the lymphatic glands

(adenitis) or by an exaggerated production of white blood corpuscles

(leucæmia), and the passage into the general circulation of products

derived from the lymphatic apparatus. For these reasons it may be

employed here.

Clinical investigation long ago demonstrated that in man certain

pathological conditions were characterised by a peculiar colour of the

blood, due to the presence of white blood corpuscles in excessive

quantities, whence the names “leucæmia” (Virchow) and “leucocythæmia”

(Bennett). In the same way it has been shown that the change in the

blood characterised by a superabundance of white blood corpuscles

generally coincides with engorgement or more or less marked hypertrophy

of the lymphatic system and of the adenoid tissue of the body (lymphatic

glands, spleen, bone marrow, and, in exceptional cases, liver, kidneys,

etc.)—leuco-cythæmic lymphadenitis; but that many cases also occur in

which this hypertrophy of the adenoid tissue or of the lymphatic gland

tissue may exist, without any excessive number of white blood corpuscles

in the blood, whence the name “aleucæmic lymphadenitis or

pseudo-leucæmia.” Cases of true leucæmia without adenitis are much

rarer, the lesions therein being confined to the adenoid tissue of the

bone marrow.

These three morbid conditions—leucæmic lymphadenitis, or leucocythæmia;

aleucæmic or pseudo-leucæmic lymphadenitis, or more simply adenitis; and

true or simple leucæmia—are frequently found in the bovine species.

Whilst stating that these diseases are frequent, we must, however, be

understood to except the numerous cases of tuberculous lesions formerly

included under the same head.

Jaccoud has shown that in reality the causes of these three morbid

conditions are very similar, and that a case which at first appears to

be of the nature of aleucæmic lymphadenitis may later become transformed

into leucæmic lymphadenitis; or, inversely, that a case which at first

appeared to be a simple leucæmia might often become complicated with

lymphadenitis: hence the grouping of these different morbid conditions

under the heading of lymphogenic diathesis.

Investigations have now thrown more light on the subject because of the

more perfect recognition of the varieties of white blood corpuscles, and

the above-mentioned morbid conditions may be defined as follows:—

(1.) The first variety consists of a more or less marked adenitis or

lymphadenitis without leucæmia (aleucæmic lymphadenitis).

(2.) The second variety, consisting of leucæmic lymphadenitis, or

leucocythæmia, is a lymphatic lucæmia or lympho-cythæmia, the anatomical

characteristic of which is enlargement of lymphatic glands, and the

histological characteristic increase in number of the large and small

lymphocytes.

(3.) A third variety, formerly regarded as simple leucæmia without

lymphadenitis, is myelogenic leucæmia or myelo-cythæmia, the

anatomico-pathological characteristic of which is to be found in myeloid

hypertrophy of the bone marrow, giving to the bone marrow on post-mortem

examination a puriform appearance, and in the myeloid condition of the

spleen.

Histologically this variety is characterised by an absolute increase in

numbers of the large mono- and poly-nuclear eosinophile leucocytes.

=Symptoms.= Simple lymphadenitis begins in an insidious manner, and is

characterised by weakness, anæmia, paleness of the mucous membranes, and

wasting without apparent reason, although the appetite is preserved. It

is only at a later stage that the glandular enlargements are discovered

(adenitis), and often this discovery is not made until the veterinary

surgeon is called in.

The existence of the disease is indicated by enlargement of the

superficial glands, and this enlargement, which may commence at any

point, extends along the course of the lymphatic vessels to the

neighbouring glands, until in a shorter or longer time it involves all

the lymphatic glands in the body.

The enlargement of the glands is usually symmetrical, and on clinical

examination it is sometimes easy to detect at the outset an increase in

size of the retro-pharyngeal glands, the glands of the neck, the

prescapular glands, the glands of the flank, etc.

Rectal exploration reveals hypertrophy of the glands of the pelvis and

of the sublumbar region, etc. The animals waste very rapidly, and

sometimes in a few months become incapable of standing. They develop

cachexia, and die in a state of exhaustion, with no other lesions than

those of lymphatic hypertrophy. Neither do they exhibit any marked

increase in the number of white corpuscles in the blood.

In lympho-cythæmia the beginning of the disease is often identical with

that of simple lymphadenitis, the increase in the number of white blood

corpuscles not occurring until later. In other cases, on the contrary,

leucæmia appears first, and the enlargement of the lymphatic gland

follows; but what characterises this form and allows of it being

distinguished from myelo-cythæmia is the great increase in the number of

large or small lymphocytes. The development is identical with, and

sometimes much more rapid than, that of the preceding form. The animals

waste away and become anæmic and cachectic, dying at last in a state of

absolute exhaustion.

Post-mortem examination reveals, as in the previous condition,

symmetrical hypertrophy of all the lymphatic glands; the spleen is very

often enormous, and the liver is sometimes affected, as are also, in

exceptional cases, the kidneys.

It may happen that the spleen alone appears affected, or at least that

it has been first attacked, a fact which explains the existence of

leucæmia before any enlargement of the lymphatic glands.

=Causation.= The causes of lymphadenitis and of lympho-cythæmia are

unknown in veterinary as in human medicine. Apparently these diseases

are more common in adults than in young animals. Some regard them as

infectious in character, but this can hardly be the case, as all

experimental attempts to transmit the diseases have failed. It is more

plausible to compare the development of these morbid conditions with

that of malignant tumours, and although some doubt still exists, simple

lymphadenitis may be described as an aleucæmic lymphoma or

lympho-cytoma, which has gradually become generalised, spreading by way

of the lymphatic channels from the gland first affected through the

surrounding glandular system. Lympho-cythæmia, on the other hand, may be

said to be a leucæmic lympho-cytoma, which spreads both by the blood

circulation and by the lymphatic paths (spleen, hæmatopoietic glands and

organs).

This view of the development of the lesions enables us to class

lympho-sarcomata with lymphomata and lympho-cytomata. The malignant

character and extremely rapid development of lympho-sarcomata appear due

to its extending by contiguity of tissue, and simultaneously by the

lymphatic paths.

This new grouping would consequently place on one side myelogenic

leucæmia, also called myelo-cythæmia, which is perhaps a different

morbid species. This would destroy the unity implied in Jaccoud’s theory

of the lymphogenic diathesis; but for all that this method of grouping

might be justified by reference to specific cellular characteristics. In

myelo-cythæmia the disease appears to commence as a lympho-cythæmia,

_i.e._, it is unaccompanied by enlargement of lymphatic glands or

hypertrophy of the spleen or liver, though the blood appears leucæmic.

The condition is not a leucæmia due to lymphocytes, but rather a

leucæmia produced by mono- and poly-nuclear eosinophile leucocytes,

_i.e._, leucocytes derived from the bone marrow.

The patients are carried off rapidly after persistent wasting, decline

and cachexia, whilst on post-mortem examination the puriform aspect of

the bone marrow is an extremely striking characteristic.

=Diagnosis.= There is rarely much difficulty as regards the diagnosis.

The enlargement of the lymphatic glands, for instance, can readily be

detected, and the only disease with which this can possibly be

confounded is tubercular enlargement.

With the means at present available for diagnosing tuberculosis, such as

microscopic examination of the discharge, inoculation with discharge,

examination of material from the glands, injection of tuberculin, etc.,

the nature of the disease can always be placed beyond doubt.

In lympho-cythæmia and in myelo-cythæmia, the whitish-violet lactescent

appearance of the blood is of unmistakable significance, particularly

when the manifest progressive wasting of the whole system is taken into

account.

Histological examination of the blood after fixation and staining will

in the former cases reveal the presence of very large numbers of

lymphocytes, and in the latter an absolute increase in the number of the

mono- and poly-nuclear lymphocytes. It should be easy, therefore, to

distinguish the two diseases, especially as other symptoms vary.

In the early stages leucæmia may be mistaken for the leucocytosis seen

in infectious diseases. These forms of leucocytosis are very common in

animals of the bovine species. They occur in certain forms of

tuberculosis, in uterine infections, in cases of internal suppuration,

in tumour of the heart, the rumen, etc., and vary in so far as one style

or another of white blood corpuscle predominates. The diagnosis,

therefore, necessitates that the white blood corpuscles should be

counted, and whenever it is found that their variations in number are no

more than between 5,000 and 15,000 per cubic millimètre, the case may be

regarded as one of temporary leucocytosis.

If, on the other hand, those corpuscles number more than from 15,000 to

20,000, or, as may sometimes happen, they attain to from 200,000 to

300,000 per cubic millimètre (one white to two or three red blood

corpuscles), the case is one of leucæmia, and, according to the

predominance of the particular type of cell, it is a lympho-cythæmia or

a myelo-cythæmia.

In leucæmic conditions the red blood corpuscles are also present in

fewer than the normal numbers. They are more irregular, assume giant and

dwarf forms (macrocytes and microcytes), sometimes exhibit lacunæ, and

are always polychromatophile, _i.e._, without special affinity for any

particular constituent of double or triple stains.

=Prognosis.= The prognosis of diseases included in the lymphogenic

diathesis is extremely grave, and in the present state of our knowledge

it may be assumed that sooner or later death is inevitable.

=Treatment.= Treatment can scarcely be considered to exist, for at the

best it can only delay the development of the disease. Nevertheless, and

with this reservation, it is certain that preparations of iron, iodine

and arsenic have a certain effect, probably by acting on the

hæmatopoiesis.

CASEOUS LYMPHADENITIS OF THE SHEEP.

In the sheep the lymphatic glands are sometimes the seat of peculiar

changes, which do not appear to have any marked effect on the general

condition. Thus a post-mortem examination or an examination of animals

in the slaughter-house sometimes shows a certain number of isolated or

symmetrical glands, such as the mediastinal, tracheal, inguinal, pelvic

or sublumbar glands, to be greatly enlarged and completely degenerated.

The precrural, prescapular, and popliteal glands are said to be most

frequently affected. Their contents are caseous and yellowish, enveloped

in a fibrous sheath, and show no signs of peripheral inflammation. The

other organs and viscera may either be healthy or exhibit caseous

lesions identical with those found in caseous broncho-pneumonia.

=The causes= of this disease are imperfectly understood, although Cherry

and Bull (1899, the _Veterinarian_, Vol. LXXII., No. 860, p. 523) have

isolated from the lesions an organism identical with Preisz’s bacillus

and with the microbe of ulcerative lymphangitis in the horse.

Norgaard and Mohler (Annual Report, United States Bureau of Agriculture,

1899, p. 638) have studied the disease. In June, 1897, Turski, at

Danzig, found about 150 breeding ewes, from eight to twelve years old,

suffering from nodules or abscesses the size of a child’s fist in the

inguinal and prescapular regions. They had been sold for slaughter, and

many were in very poor condition. The disease occurs in Europe, Western

America, South America, and Australia. Several thousand cases are

annually seen in the slaughter-houses of the United States.

=The symptoms= generally escape notice, and it is only by accident that

one sometimes detects marked enlargement of the lymphatic glands of the

neck or of the superficial inguinal glands. The patients, moreover, may

remain in very good bodily condition, so that the lesions are only

discovered on the meat being inspected.

Having regard to our imperfect knowledge of this disease, it is

impossible to express an opinion as to its importance or treatment.

GOITRE IN CALVES AND LAMBS.

Although not strictly relevant to the foregoing matter, a few remarks

may here be made on the subject of goitre.

True goitre consists in hyperplasia of the follicles of the thyroid

gland, with colloid change of their contents, which are chiefly

albuminous. The swelling is mainly due to enlargement of the follicles,

and is termed struma follicularis. It may attack the entire organ or

only one-half; less frequently it is confined to certain sections. Other

varieties of goitre are recognised, such as fibrous, varicose and cystic

goitre. (For fuller details see Möller and Dollar’s “Regional Surgery,”

p. 149.)

[Illustration: $1]

=Treatment= by injection of thyroid juice or by feeding on thyroid

extract has given better results than drugs.

The following account of an outbreak in New Zealand is summarised from

the Annual Report of the Chief Veterinarian of New Zealand, 1901:—

The calves affected were born with enlarged thyroids. The farm is of

rich alluvial deposit, and rather below the level of the river, which it

borders. The land has been in occupation, however, for many years, and

no similar condition had been previously noted. At first, as calves only

were affected, it was thought possibly to be due to the bull, a

two-year-old animal, but when a foal was born suffering from a similar

malformation this theory naturally fell to the ground.

The land had been ploughed with a special plough 20 inches deep, but

this is no uncommon practice in the island.

About the same time, a similar disease was discovered affecting lambs at

a farm near Outram. From 450 ewes, 150 lambs had been lost, the glands

being enlarged to the size of a cricket ball. A few had been born dead,

many only lived a few hours, others lived several days, and a

considerable number recovered. There was no connection, directly or

indirectly, between the two farms, they being at least fifty miles

apart. A few of the calves died or were killed, the remainder recovered,

and the foal grew rapidly better. The land on both farms is very similar

in composition.

Mr. Wilkie states, from observation of previous cases in lambs, that “it

appears to be always associated with malnutrition and a condition of

anæmia in the parent, induced in most cases by feeding with watery,

innutritious foods.”

Specimens were forwarded, from a calf and from a lamb, of enlarged

glands. The gland of the calf was enormously enlarged, being at least

twice the size of an orange, dark in colour, flabby in consistency, and

on section a mucous material exuded copiously from the cut surface.

Micro-examination showed the acini to be larger than normal, filled with

the usual mucous material, and lined with cubical epithelium. The

connective tissue surrounding the alveoli was, however, crowded with

round-cells, so much so that the whole parenchyma seemed to be

practically composed of these cells.

A specimen of an enlarged thyroid from the lamb was about the size of a

sheep’s kidney, and very much the same shape and colour. Sections

microscopically examined showed a different condition to that of the

calf’s thyroid. Here the acini were filled with epithelial cells loosely

arranged as if the lining epithelium had been proliferating rapidly,

while the connective tissue surrounding the acini was fairly normal. The

section had a somewhat adenomatous appearance.

SECTION V.

NERVOUS SYSTEM.

CEREBRAL CONGESTION.

According to Cruzel, cerebral congestion is somewhat frequent in working

oxen subject to continued concussion from the yoke, especially among

animals working on a rocky soil. The condition may also be produced by

prolonged exposure to the sun, as well as by sudden and intense cold.

Passive cerebral congestion by stasis may be produced by any cause

markedly interfering with the return circulation (pericarditis due to

foreign bodies). Clinically it is of no importance.

The animals, previously in good health, suddenly appear comatose. They

are insensible to stimulation of any kind, the head is rested on any

convenient object or is held stationary, the animal looks drowsy, the

gait is hesitating or vacillating, the respiration slow or irregular.

Left at liberty, the animal does not seem to know where it is going;

indeed, sometimes it is absolutely blind and strikes against any

obstacle in its path, or falls and suffers from epileptiform

convulsions. The cranial region is abnormally warm. The =course= of the

attack is rapid, and the animal either dies in a state of coma or

convulsions or else recovers rapidly.

=Diagnosis.= The diagnosis is decidedly difficult; and the =prognosis=

should be reserved.

=Treatment= commences with free bleeding, the amount of blood drawn

being proportioned to the animal’s size. The sides of the body may then

be stimulated and a purgative administered.

MENINGITIS.

The generic term “meningitis” includes all inflammations of the

arachnoid, pia mater and internal surface of the dura mater.

These forms of inflammation occur in diseases such as tuberculosis and

in parasitic diseases of the brain. Under other circumstances, they are

rare, and may be produced by very varying causes.

An epizootic cerebro-spinal meningitis of the bovine species has also

been described, principally in Germany. It seems almost unknown in

France, and French literature contains no well-authenticated case.

Furthermore, an epizootic cerebro-spinal meningitis of sheep, or rather

of lambs, has been described in Germany, in Italy, and in France. These

descriptions are all open to many objections. It seems that under the

term “cerebro-spinal meningitis” have been grouped cases of enzootic

tetanus, doubtful cases of poisoning, and particularly cases of

cœnurosis in the first stage of development. We therefore discard these

descriptions, which differ too much among themselves to be of any value.

=Causation.= Meningitis occurs in the ox and sheep as a complication of

wounds in the cranial region, accompanied by fissuring of the bone,

periostitis, abscess formation, etc.

It is also seen as a complication of fractures of the horns, and

old-standing catarrh of the facial sinuses. In the sheep it follows

parasitic catarrh due to the larvæ of œstridæ.

The meningitis appears, according to circumstances, in the forms of

local meningitis, anterior frontal meningitis, basilar meningitis, etc.

Finally, it may develop as a complication of different diseases, such as

gangrenous coryza, purulent infection, subparotid abscess, suppurative

phlebitis, suppuration of the eye or of the orbit, etc.

=Symptoms.= It is difficult to detect and interpret the first symptoms

shown, because these chiefly consist in dulness, want of appetite and

constipation, without any particular fever. At a later stage, excessive

excitability is produced by noises, by changes of light, or by handling.

Careful examination of the patients shows a change in their expression,

rapidly followed by contraction and inequality of the pupils or

deviation of the visual axis (strabismus, squinting). The pulse becomes

irregular, as also the respiration. The appetite is entirely lost, and

it is not uncommon to note a contraction of the muscles of the neck and

jaws, as well as inability to move about and symptoms similar to those

of dropsy of the cerebral ventricles.

The chronic form is rare.

=Lesions.= The lesions comprise local or general hyperæmia and exudative

inflammation of the pia mater and arachnoid, together with the formation

of false membranes or of pus in the subdural space. The meninges are

partially adherent, and the superficial layers of the brain are also

inflamed by contiguity of tissue.

=Diagnosis.= The diagnosis must be based on the disturbance of vision,

movement, and appetite, and on the course of the symptoms, as well as on

the external signs in the case of such diseases as are prone to become

complicated with meningitis.

=Prognosis.= Sooner or later the case is likely to end fatally, and

there is no practical use in treating the patient.

=Treatment.= If in exceptional cases slaughter is objected to, setons

and blisters may be applied to the poll or the parotid region, or the

parts may be enveloped in ice bags or compresses of iced water

frequently renewed.

ENCEPHALITIS.

Encephalitis, _i.e._, inflammation of the cerebral substance, is very

closely allied to meningitis; in a great number of cases meningitis and

encephalitis co-exist. In other cases encephalitis may be found apart

from meningitis, and _vice versâ_. Moreover, many of the symptoms of

meningitis are to be found in cases of encephalitis.

Encephalitis may develop as a complication of meningitis. Encephalitis

may also follow abundant parasitic infestation, as in cœnurosis (which

will be particularly studied as it affects sheep), or microbic

infection, the commonest form of which in the ox is tuberculosis. The

encephalitis may be diffuse or circumscribed, according to the cause,

while the symptoms are varied and numerous. Very frequently,

particularly in cases of tuberculosis, encephalitis assumes a chronic

form.

=Symptoms.= The earliest symptoms are extremely difficult to detect,

because they are scarcely characteristic and because it is impossible to

ascertain the sensations of the animal.

It is only when the disturbances in walking, in the eyesight, in

swallowing, etc., are noted that suspicion is aroused.

The symptoms may appear suddenly. Nevertheless it is beyond doubt that

there are certain slightly marked prodromata, indicated by diminution of

appetite, wasting, and changes in vision. Soon afterwards occur other

forms of disturbance, which may be classified under the heading of

“motor, visual, nervous, and impulsive.” The patients appear stunned,

their movements are slow and hesitating, they partially lose control

over their limbs and display lameness, with spasmodic movements of one

or two limbs. Examination of the joints shows no injury. The lameness

may simultaneously affect two diagonal limbs or two fore and two hind

limbs, or even three limbs. This lameness is of central origin.

The ocular disturbance is marked by diminution or loss of vision, by

strabismus, or by frequent unconscious movements of the eyes and

eyelids, and also more particularly by inequality, contraction or

dilatation of the pupils.

Nervous, impulsive disturbance is most readily noted when the animals

are at liberty. Even when the sight remains, they seem quite incapable

of avoiding obstacles or as though absolutely forced to move to the

right or left, etc.

Attacks of giddiness, moreover, are not unusual under the influence of

the slightest excitement. During such attacks the animals thrust the

head against a wall, or they involuntarily recoil or make lateral

movements. In many cases these vertiginous attacks end by the animal

falling and showing epileptiform convulsions, during which it may die.

The symptoms are never the same in two different animals, but they may

easily be classed according to the above indications. The indications

furnished by the condition of the eyes and by the peculiar impulsive

movements are particularly significant.

On the other hand, there are modifications in breathing without apparent

local cause, and difficulty or even impossibility of swallowing, etc.,

although there exists no material obstacle.

=Diagnosis.= The condition is often confused with meningitis, and the

mistake is not serious, because meningitis and encephalitis frequently

accompany one another.

=Prognosis.= The prognosis must be regarded as fatal. The patients very

seldom recover, and there is no reason for keeping them alive.

=Treatment.= Here, again, blisters may be applied to the upper extremity

of the neck, or setons may be passed. Cooling applications to the

cranial region have also been suggested. None of these methods produces

more than a temporary palliative effect.

CEREBRAL TUMOURS.

The brain may be injured and compressed by various tumours of other than

parasitic origin. Such tumours may originate in the bones, the meninges

or the choroid plexus, or they may simply be due to generalisation of a

previously existing tumour. Whilst of very varied origin and nature, all

tumours of the cranial cavity have one common effect, viz., to compress

the brain. This continuous compression causes progressive atrophy of the

brain, but its existence is not always suspected, because the lesions

may not give rise to any marked symptoms.

The hind portions of the hemispheres and the white substance are

generally very tolerant. The front portions, on the other hand—the

frontal lobes and the grey substance—resent compression, which provokes

various symptoms in consequence.

=The symptoms= of compression and atrophy of the brain differ greatly, a

fact which is easily understood, inasmuch as the seat of the change may

vary, and therefore it is possible only to trace the chief

manifestations, which suggest the existence of a cerebral tumour.

The general changes are indicated by signs precisely similar to those so

common in horses with dropsy of the ventricles (general depression,

inability to back, long intervals between the prehension of successive

mouthfuls of food, sudden cessation of mastication, etc.), by an

impulsive or automatic gait, and by the assumption of strange attitudes

(kneeling down in front, etc.). When at rest the animals appear to be in

a state of continual torpor.

Special symptoms sometimes occur, which enable the seat of the injury to

be localised in more or less exact fashion. These symptoms affect the

vision (amblyopia, amaurosis, strabismus, nystagmus), general

sensibility (hyperæsthesia, anæsthesia, etc.), and the power of movement

(total, partial or crossed hemiplegia, want of co-ordination of

movements, etc.).

Trifling stimuli almost always lead to marked and even epileptiform

attacks.

=The diagnosis= of cerebral tumours is very difficult, particularly when

attempts are made to indicate their exact seat, but that of other

cerebral lesions is somewhat easier.

=The prognosis= is very grave, and in the case of domestic animals

nothing can be done. In the ox intra-cranial operations are difficult,

by reason of the presence of the sinuses which obstruct the approach to

the brain cavity; economically surgical treatment is seldom advisable.

INSOLATION.

Insolation is an exceptional accident in animals of the bovine, ovine,

or porcine species. If at liberty these animals move about, and always

seek shelter when the sun is fierce. If, on the contrary, they are

harnessed and kept standing for long, exposed to the full midday sun

during June, July or August, they may suffer from insolation.

During the International Cattle Show attached to the Exhibition of 1900

in Paris, a considerable number of cases of insolation occurred in

animals of one class, exposed to the full midday sun, in an

ill-ventilated spot. The other classes only received sunlight from the

sides, and in them not a single case occurred.

Death may follow in a few hours; it is difficult to say precisely how it

is brought about, but it is always accompanied by congestion of the

cerebro-spinal centres and general blood stasis.

=The symptoms= of the development of insolation occur very rapidly. In

animals of the bovine species there is accelerated respiration, which

soon amounts to dyspnœa. The mucous membranes then become cyanotic. The

animals attacked seem anxious, although not agitated, and soon

afterwards the eyes water, the mucous membrane and the lips of the vulva

display œdematus infiltration and congestion, and areas of cutaneous

congestion, closely resembling mud fever in the horse, appear over the

mammæ. At this stage the animals move with difficulty, and show all the

symptoms seen at the outset of gangrenous coryza.

All these symptoms develop in one, two, or three hours, and death may

follow if nothing is done. They disappear, however, as rapidly as they

appear. In an hour or less we have seen in some cases a complete return

to the normal condition. Given the facts, the =diagnosis= is extremely

easy.

=Treatment.= Treatment should be commenced by immediately removing the

animal to a cool, airy, shady place. It may then be bled, and the head

and neck should be freely drenched with cold water. The symptoms

generally disappear as though by magic.

POST-PARTUM PARALYSIS—MILK FEVER—MAMMARY TOXÆMIA—PARTURIENT

APOPLEXY—DROPPING AFTER CALVING.

For a great part of the following short account we are indebted to an

excellent report by J. J. Repp, V.M.D., in the _Journal of Comp.

Medicine and Veterinary Archives_, September, 1901:—

The word “fever” in connection with the terminology of this disease is

not very appropriate, because in the majority of cases fever is not

present, but the animal has a subnormal temperature. The term milk fever

is very misleading and indefinite, as it is also used by the laity to

designate other diseases, such as parturient septicæmia and the various

forms of mammitis. Parturient paralysis must be clearly differentiated

from parturient septicæmia, which is a disease of an entirely different

character and which may occur in any of the domestic species, whereas

parturient paralysis occurs only in the cow.

=Distribution.= Parturient paralysis occurs wherever milch cows are

kept. It is more prevalent in dairy districts, because it is the heavy

milking strains of cows that are most subject to the disease.

=Cause.= No definite cause can be assigned for this disease. Schmidt’s

theory is that parturient paralysis is caused by the evolution in the

mammary gland of a poisonous substance through the over-activity of the

epithelial cells of this gland excited by the determination to the udder

after birth of large quantities of blood which was supplied to the

uterus and the fœtus before birth, but which now goes to the udder

because of the natural demand for milk secretion. This poisonous

substance being carried in the circulation to various parts of the body,

brings on the symptoms which characterise the disease. It is well

recognised that living cells may, under certain circumstances, produce

poisonous substances. Schmidt’s theory, therefore, is in accord with an

established principle.

=Pathogenesis, or generation, of the disease.= Parturient paralysis, as

a rule, occurs in cows which give a heavy flow of milk and which are in

a high state of nutrition. It may develop at any age, but is extremely

rare in cows before they have reached adult age and have given birth to

several calves. It is also rare in old cows. It occurs, then, in cows

which are of middle age and in the full height of their activity as milk

producers. The disease attacks the cow after she has given birth to a

calf, usually within twenty-four hours thereafter, but in some cases not

until a week or even a month after parturition. In a few cases the

disease has its inception a short time before parturition. Cows which

are stabled and deprived of exercise are said to be more prone to the

disease than those which are permitted to exercise at will. There are

many exceptions to this statement, although it is the usual teaching.

Further observation may show that it is not correct. In Iowa more cows

take this disease while at pasture than in any other circumstance. This

doubtless arises from the fact that in Iowa cows are given more freedom

than is customary in older dairy States. The disease may arise at any

time in the year, but, on account of the fact that spring-time is

pre-eminently the calving season, most cases originate at this season.

=Morbid anatomy.= The morbid alterations are limited and variable, and

offer nothing characteristic. The blood is irregularly distributed, a

condition which probably indicates marked vaso-motor disturbance

resulting from the profound interference with the nervous functions

which accompanies the disease. The abdominal organs are usually filled

with blood. The brain may be anæmic, œdematous, easily torn, and

yellowish in colour. In other cases it shows hyperæmia of the meninges

and of the brain substance.

=Symptoms.= The disease usually appears within twenty-four to

forty-eight hours after parturition. In extreme cases it may not occur

until two months or even six months after parturition. It may rarely

occur before birth. It usually follows an easy birth. At the onset of

the disease the cow manifests some uneasiness; it moves about in a

restless manner, stamps, strikes the abdomen with its hind legs, perhaps

bellows, grinds the teeth, and may have spasms of groups of muscles or

even a general convulsion. After this period, which may be unnoticed,

the symptoms of paralysis come on. The cow shows weakness, staggers, and

at last falls. As the paralysis advances it stretches on the ground,

lying on its side usually with the neck bent to one side so as to bring

the nose into the flank or the costal region. This is the characteristic

position in parturient paralysis. If the head is brought into the normal

position, it at once returns to the unnatural position in which it was

found. The animal is in a state of partial or complete unconsciousness,

does not respond to blows or calls, and takes no note of its

surroundings. The eye is dull and not sensitive to the finger touch,

sunken, pupil dilated, and the upper lid is drooping; the tongue is

paralysed, saliva runs from the mouth, the pharynx and œsophagus have

lost the power of motion, so that the animal is unable to swallow; the

peristalsis of the stomachs and intestines is in abeyance, and as a

result digestion is arrested, fermentation sets in, and the animal

becomes tympanitic; the contents of the rectum and colon are hard and

dry, and may be covered with mucus or blood, urination is suspended; the

os uteri is almost invariably dilated if the disease occurs within a day

of parturition; pulse small, often imperceptible, 60 to 120 per minute;

temperature, usually normal or below normal, may be as low as 95° Fahr.,

in some cases may be as high as 105° Fahr. Such a high temperature

probably does not occur in a case of pure parturient paralysis, but only

when there is a complication of parturient septicæmia. The extremities

are cold. The after-birth is sometimes retained. There may be

accompanying prolapse of the uterus.

=Course.= Without treatment, and, indeed, with most kinds of treatment

which have been applied in the past, the disease usually runs rapidly to

a fatal issue. It lasts two to three days, and in some cases longer, the

condition gradually becoming more and more aggravated. Death results

from sudden failure of the heart or brain, and is often preceded by

profuse diarrhœa. In milder cases the cow may linger as long as two to

four weeks and then die of pneumonia, which results from the inhalation,

or introduction through attempts at medication, of foreign substances

into the lungs during the period of paralysis of the pharynx and

œsophagus. If recovery occurs, the animal is entirely well in two to

five days. In rare cases paralysis of the hind parts may persist for a

long while.

=Diagnosis.= This is made by a study of the history and symptoms. It is

comparatively easy.

=Differential diagnosis.= It must be distinguished from ante-partum

paralysis, broken-back, parturient septicæmia; but one familiar with the

character of these diseases will find no difficulty in making this

differentiation.

=Treatment.= This may be considered under two distinct subdivisions,

viz., preventive treatment and curative treatment.

(_a_) _Preventive treatment._—By considering what has been said under

the head of “generation of the disease,” one can easily infer what

measures should be adopted to prevent the disease. Cows in the later

stage of gestation should be fed moderately, grain especially being

given sparingly or entirely withheld; the animals should be given an

opportunity to take plenty of exercise; the bowels should be kept in

good condition by the administration of such salines as magnesium

sulphate, sodium chloride, and sodium bicarbonate. The after-birth

should be removed soon after parturition and several uterine douches

administered.

(_b_) _Curative treatment._—The older methods of treatment comprised:

warmth and friction to the mammary gland; the administration of

sedatives, such as opium, chloral and bromide of potassium; stimulants,

including ammonia, ether, turpentine and alcohol; washing out the uterus

with water or disinfectant solutions; the relief of tympany by the use

of the trocar and canula (by which instrument medicines may also be

injected directly into the rumen); the removal of fæces from the rectum;

warm clothing of the body and general attention to the animal’s comfort,

and to the teachings of hygiene. For all these widely diversified

methods good results have been claimed, and, we may add, bad ones at

times recorded. F. T. Harvey (Cornwall) estimates the average mortality

at from 40 to 66 per cent., though he claims for his more recent

practice a lessened mortality of only 20 per cent.

Schmidt does not claim that his method of treatment disposes bodily of

the morbid condition, but that it does measurably assist Nature in her

efforts to restore the animal to the normal physiological state. It is

well known that after the beginning of the attack the animal, if left to

itself, rapidly grows worse until the crisis of the disease is reached,

at which time death occurs or convalescence begins, usually the former.

It has been observed, however, that if the treatment is applied within a

few hours after the inception of the disease its progress is modified in

such a way that convalescence at once begins, as a rule, and the animal

hastily recovers its health, usually within twelve hours, although in

extreme cases it may be as late as forty-eight hours. The following is

an outline of the plan of treatment of parturient paralysis suggested by

Schmidt. The operator should disinfect his hands and the udder and teats

of the cow by washing with a 5 per cent. solution of carbolic acid or

creolin, or a 1½ per cent. solution of lysol or trikresol. The apparatus

needed for the treatment consists of a small glass funnel, a rubber hose

three feet long and one-eighth inch in calibre into which the funnel

fits, and an ordinary milking tube over which the rubber hose fits. This

apparatus should be sterilised immediately before it is used by boiling

or soaking in such a solution as recommended for washing the udder.

Dissolve from 2 to 2½ drachms of potassium iodide—the size of the dose

depending upon the size of the cow and the character of the attack—in

about one quart of clean water previously boiled to sterilise it, and

allow the solution to cool to a little above body temperature, or 40° C.

or 104° Fahr. The temperature may be determined with the clinical

thermometer. Withdraw all the colostrum or milk from the udder. Then

insert the milking tube, with hose and funnel attached, into one of the

teats, elevate the funnel about two feet above the teat and slowly pour

in one-fourth of the solution, allowing the funnel and hose to become

empty several times during the process in order to permit the entrance

of a liberal quantity of air. Repeat this infusion with the other three

quarters of the udder. After all is introduced, knead the udder

carefully so as to cause the solution to permeate the ducts and acini as

much as possible.

As the condition of the cow is usually such as to call for additional

treatment, the veterinarian should not be content with injecting the

potassium iodide solution, but should resort to any and all other

measures which promise assistance.

As the cow is usually unable to urinate, the bladder will be found

filled with urine. This should be removed with the catheter, and its

removal accomplished at intervals until the recovery of the cow renders

this procedure no longer needful.

It may be advisable that catharsis be brought about. As the cow is

usually unable to swallow, it is dangerous to attempt to give medicines

by the mouth. This may be done if assurance that the cow can swallow is

obtained. Some have given medicines successfully through a probang

inserted into the stomach. The plan is feasible. Schmidt says that he

usually resorted to an aloe powder. If this is done 1 ounce to 1½ ounces

of aloes may be given. It would seem preferable to give the aloes in a

bolus, capsule, or drench. Some have given linseed oil or Epsom salts.

If the animal cannot swallow and a probang is not at hand, one may

administer 1½ to 2 grains of physostigmine salicylate subcutaneously,

repeating the dose in about three hours if purgation is not produced.

Rectal injections should be given at short intervals in order to get rid

of the accumulation of hard, dry fæces in the rectum. These injections

may be of linseed oil, cotton-seed oil, or warm soap solution. Schmidt

recommends, also, enemata of sodium chloride solution. Meanwhile the cow

should be kept propped up on the sternum by means of bags of straw or

pieces of wood. If the temperature is below normal, as it usually is,

the cow should be thickly clothed with blankets and straw heaped up

about it. Schmidt used powdered digitalis given by the mouth when the

heart was rapid and weak. It would seem much better in every way to give

the tincture of digitalis subcutaneously. He has also resorted to

subcutaneous injections of camphor and caffeine. This is good treatment.

If the cow does not show marked improvement within eight hours the

potassium iodide infusion may be repeated. Schmidt has found that as

much as 6 drachms may be injected into the udder without harm to the

cow. Schmidt, in his first report, made in 1898, recorded 50 cases

treated for parturient paralysis by this method with but two deaths from

the disease. There were, however, only 46 recoveries, as two cows were

slaughtered for beef during the first day of convalescence. A short time

later a report was made by Jensen showing that in Denmark up to that

time sixty-five veterinarians of that country had treated 412 cases by

the Schmidt method, 90 per cent. of which recovered. Such results seem

to indicate this as the treatment _par excellence_ for parturient

paralysis. It still remained to secure the introduction of this

treatment into the United States and to determine what results could be

obtained. In all 166 cases were reported; of these 166, 119 resulted in

recovery, while 47 were fatal. Of the fatal cases, in eight of the cows

death may be traced to some complication, such as prolapse of the

uterus, foreign-body pneumonia, etc. In these cases the Schmidt

treatment cannot be said to have failed, for it is not in any way

intended that it shall be able to overcome such accidental conditions.

If the cow has recovered from its condition of paralysis as a result of

the Schmidt treatment far enough to be out of danger from that source

and to promise recovery, but later falls a victim to some complication

that is in no measure a part of parturient paralysis, but only a result

of that disease, it may with justice be said that the Schmidt treatment

was a success so far as the malady against which it was directed is

concerned. Looking at the reports from this generous point of view, in

127 cases out of 166, or 76·5 per cent., the Schmidt treatment was

successful so far as the parturient paralysis was concerned.

In a paper published in the _Berliner Thierärztliche Wochenschrift_ in

August, 1902, Schmidt reviews the results of his treatment as evinced by

914 patients treated by thirty-one different practitioners: 884, or 96·7

per cent., recovered, twelve died and six were slaughtered during the

course of the disease. Twelve others were slaughtered at a later period

in consequence of complications. Jensen reported the results of 1,744

cases.

Schmidt also found that the simple injection of air was in many cases

sufficient to produce recovery, and subsequent observation tends to show

that the fluid injected is of less importance than was first

anticipated. A large number of unirritating solutions may be employed.

Schmidt, however, still counsels the use of a quart of 1 per cent.

solution of iodide of potassium, in which can be dissolved 5 grammes of

caffein sodio-salicylate if the heart’s action is weak. About 10 ounces

of this solution are injected into each quarter, and are followed by a

liberal injection of air. The parts should afterwards be freely

massaged.

CŒNUROSIS (GID, STURDY, TURN-SICK).

Cœnurosis is a disease due to invasion of the animal body by embryos of

larvæ of the _Tænia cœnurus_ of dogs and wolves. These embryos only

develop freely in the brain substance (_Cœnurus cerebralis_) and medulla

oblongata. The hosts of the larvæ include the calf, sheep, goat,

roedeer, reindeer and horse.

The disease was formerly erroneously called “turn-sick,” for the turning

is only a manifestation, and even a tardy manifestation, of the disease,

while in addition it is not invariably present.

Cœnurosis principally attacks lambs of from three to six months,

although it occurs up to eighteen months, and sometimes even two years.

It is exceptional, however, in adults. Similarly in the bovine species

it usually affects young animals up to the fourth or fifth year.

Cœnurosis with diffuse parasitic encephalitis often remains

unrecognised, the animals being regarded as affected with epizootic

meningitis of unknown cause or septic intoxication, and when they die

the owners are ignorant as to the cause of death. The stage

corresponding to turn-sick, which is an advanced phase of the disease,

is only seen in animals which have been infested to a slight extent, and

in which three or four parasites only, sometimes only one, have attained

the brain and developed there. Such cases exhibit all the classic

symptoms of turn-sick, viz., turning movements, heaviness, vertigo, etc.

=Causation.= Cœnurosis is due solely to one cause, viz., the ingestion

of eggs or embryos in feeding or drinking.

The _Tænia cœnurus_ lives in the dog, and fertilised segments are passed

with the fæces in yards, pastures and fields, and on the margins of

roads, ditches and ponds. Amongst damp grass or in water the eggs, which

contain more or less well-developed embryos, may retain their vitality

for several weeks, and when swallowed the embryos are set at liberty in

the intestine.

The six-hooked embryos perforate the walls of the intestine, pass into

the blood stream or chyle ducts, and from these points are carried in

all directions. Those which gain the nervous centres, the brain or

spinal cord, continue to develop; the others, dispersed through

different tissues, degenerate and disappear.

Experimental infection with these parasites shows that the brain is

invaded after about a week’s time. From the twentieth day the presence

of embryos can easily be detected in the superficial layers of the

convolutions. They make their way through the grey substance, leaving

behind them greenish-yellow sinuous tracts with caseous contents.

The cyst or finn undergoing development can be found at the end of one

of these tracts in the form of a little transparent bladder, of a size

varying between that of a pin’s head and that of a lentil or a small

hazel-nut.

Later the tracts, with their caseous contents, disappear, and the

development of many of the vesicles proves abortive. At the end of a

month the vesicles, continuing to develop regularly, attain to about the

size of a pea. Between the fiftieth and sixtieth days heads or scolices

appear in the interior of the vesicle, which then reaches the dimensions

of a hazel-nut. From this time the vesicles continue to increase in size

until the death of the patient. Usually they become as large as a

walnut, or even larger, and the interior contains hundreds of scolices,

each showing a head.

[Illustration: $1]

The cystic phase only develops completely in animals whose brains

contain a limited number of cysts, and in such the signs of turn-sick

are well developed. In others, where the numbers are large (ten to

fifteen embryos or more), death occurs during the primary stage, usually

towards the end of the first month, in consequence of acute encephalitis

and without any of the symptoms of turn-sick.

[Illustration: $1]

The number of animals attacked is sometimes enormous. Moussu has

recorded cases where fifty, one hundred, and even four hundred lambs of

one flock were affected. The enormous mortality in such cases is very

apt to cause errors in diagnosis. Cœnurosis occurs most frequently

during rainy seasons, moisture favouring the preservation of the eggs.

Young animals become infected, particularly during the spring and

autumn, more rarely in the summer, as prolonged desiccation, say for a

period of twelve to fifteen days, destroys the vitality of the eggs, but

animals may become infested at any time through drinking contaminated

water. Moussu has seen cœnurosis (acute encephalitis) from the

last-named cause in the middle of January.

=Symptoms. First phase.=—_Disseminated encephalitis._—The symptoms vary

with the phases of evolution of the parasite and of the disease which it

causes. After the six-hooked embryos have penetrated to the brain, the

animals affected lose appetite and show a certain degree of dulness,

which is all the more marked inasmuch as the animals usually affected

are young, and therefore should appear bright and alert. Then follow

wasting and depression; the animals remain stationary for whole hours

together, the head being carried low or inclined to one side. At this

stage disturbance in vision and irregularities in movement may appear.

[Illustration: $1]

[Illustration: $1]

The eyesight is almost always affected, but the symptoms may vary

widely. In some cases the patients seem to be absolutely blind, and

strike against any obstacle in their way; in others the power of vision

seems to be lost only on one side. All that can be discerned objectively

is an inequality in the pupils, together with retraction or dilatation,

convergent or divergent strabismus, nystagmus, etc. The humours of the

eye appear infected, but examination with the ophthalmoscope reveals

lesions of more or less extensive neuro-retinitis.

The visual disturbance is of central origin. The powers of movement may

be affected in numerous ways, which at times are extremely difficult to

estimate with accuracy. Sometimes the gait is uncertain, inco-ordinated,

and hesitant; at others the animal shows lameness or loss of control

over a front or hind limb, or over two limbs simultaneously (either the

two front or hind limbs or the diagonal limbs), or it may be absolutely

unable to stand.

It walks obliquely, or the front or hind limbs collapse; or again, it

may persistently lie down, a fact which makes the shepherd think it is

suffering from paralysis. On examination, however, no true indications

of paralysis can be found; sensation and motor power are both preserved

in a modified form.

[Illustration: $1]

Death is very frequent at this stage of the disease; the animals eat

little or nothing, refuse drink, and die of exhaustion.

All this general disturbance is of central origin, and is due to

disseminated parasitic encephalitis, but up to this point the seat of

the disease is not yet clearly apparent.

=Second phase.=—_Turn-sick._—The central symptoms are slow of

development, and are due to the progressive growth of one or two, more

rarely three or four, fertile vesicles. These are the true symptoms of

turn-sick, and it is only after this phase of the disease has developed

that the term becomes appropriate.

Left at liberty, the patient usually walks in a circle towards the right

or left in an impulsive and irresponsible fashion. Sometimes it

describes a circle, always of the same size. In other cases, on the

contrary, it travels along a spiral track, getting further from or

nearer to the centre as the case may be. The turning movement may become

so accentuated that the animal appears to revolve as on a pivot, and if

it is confined in a field or straw-yard its legs become caught in the

litter and it falls to the ground.

Attempts have been made under these circumstances to discover the exact

point of compression, _i.e._, the point at which the cyst exists, by

noting the direction of the turning movement. The diagnosis, however

arrived at in this way is frequently illusory, because it is not

uncommon to find two or three vesicles, and in any case the most

important information in regard to diagnosis is to be derived from the

ocular symptoms.

When only one vesicle exists, the turning movement usually occurs

towards the side on which it is situated, and the eye of the opposite

side is affected with amaurosis.

[Illustration: $1]

If the cyst is situated near the olfactory lobes, the animal marches

with a high-stepping movement and the head drawn back towards the body.

If the cyst is in the cerebellum the animal is incapable of moving,

because it can no longer co-ordinate its movements. Finally, if the cyst

develops in the occipital region, animals turn towards the wind, with

the neck raised and the head extended.

At the moment when they fall to the ground they sometimes have

epileptiform convulsions, grind their teeth, and salivate profusely. In

a severe attack even death may supervene at this point.

=Cœnurosis of the Medulla.= The embryos may develop in the medulla

oblongata as well as on the brain itself. Compression and atrophy of the

medulla then give rise to true paralysis.

The animals exhibit paralysis of the hind quarters, unilateral paralysis

only, or still less marked signs. Everything depends on the degree of

development of the cysts.

=Bovine Animals.= Cœnurosis in oxen is less important than in sheep.

Moreover, it very rarely affects a large number of young animals

belonging to one farm. Loss of appetite, dulness and depression are the

earliest indications, as in sheep. The gaze seems fixed, the neck is

held stiffly and almost rigidly, the animal shows a tendency to vertigo,

pushes its head against a wall, or leans the head or neck on the manger

or trough.

[Illustration: $1]

Inequality in the size of the pupils, amaurosis, hesitating and

inco-ordinated movements may also be seen developed in different

degrees. The animals have the appearance of horses suffering from

“_immobilité_”—that is, the very peculiar general condition produced by

dropsy of the brain ventricles, or from encephalitis. They forget to eat

or do not attempt to chew unless handfuls of food are thrust between the

molars; they plunge the muzzle into a bucketful of water and do not

drink, etc. They take little notice of what passes around them, although

they may become greatly excited if an attempt is made to move them, to

give them medicine from a bottle, or to set them at liberty, etc. Such

attacks of excitement often end in vertigo and in the animals falling to

the ground and showing epileptiform movements. All these symptoms may

occur with extraordinary variations, due in reality to the peculiar

position which the cœnurus occupies.

=Second phase.= If set at liberty during the first phase of the disease,

the animal’s gait appears only slightly disordered, but when a single

vesicle has become well developed in one of the hemispheres (and this is

usually the case with oxen), the symptoms of turn-sick appear as in

sheep, and are equally varied. The patients seem impelled to move in a

given direction, whatever obstacles may be in their way. It is not at

all uncommon to see them thrusting their heads against walls or trees,

falling into ponds or ditches, or attempting to force their way through

blind alleys between hay or straw stacks.

After the cyst develops in the cerebellum, the animals are soon unable

to move. They may be able to stand in one position, but on any attempt

to move they fall.

=Lesions.= The lesions develop successively from the moment the embryos

arrive in the mass of the brain. At first the six-hooked embryos only

excite a slight disseminated encephalitis. Their course through the

brain is marked by short, greyish-green caseous tracts, the thickness of

a needle, which are readily discoverable in the superficial layers.

Later these caseous deposits become absorbed, the lesions of

disseminated encephalitis diminish and disappear, while a certain number

of vesicles after partial development undergo atrophy and disappear.

Before long nothing remains but local atrophic encephalitis caused by

the development of the vesicles, and from this time the central symptoms

begin to appear.

=Diagnosis.= When the turning movement has developed the diagnosis is

generally easy, but it is more difficult during the first period, when

encephalitis alone exists; or at least, it is very difficult at this

period to discover whether the symptoms are attributable to

encephalitis, meningoencephalitis, cœnurosis, tuberculosis, or to some

injury.

[Illustration: $1]

=Prognosis.= The prognosis is grave, and very few animals recover. Zürn

estimated the cases of recovery in flocks at 2 per cent. In these cases

the cysts degenerate and disappear.

=Treatment.= At the present moment there is no really practical curative

treatment.

The best plan appears to be to trephine the skull and remove the cyst,

provided its exact position can previously be determined. That, however,

is the great difficulty. Its solution presupposes a perfect knowledge of

the central nervous system and of the real purport of any apparent

symptoms.

On the other hand, in sheep at least, the position of the cyst must

always remain somewhat uncertain, because there are generally several,

and the symptoms are of a mixed character.

The only treatment, therefore, which would be likely to succeed is

difficult to carry out, and more difficult in the ox than in the sheep

because of the great development of the frontal sinuses.

It has been mentioned that under exceptional circumstances the cœnurus,

if very superficially placed, may cause atrophy of the cranial wall in

the sheep by the outward pressure it exerts, and that the points of

least resistance may be detected by the touch. In such cases

intervention is necessary and is greatly facilitated; but they must be

extremely rare, and Moussu declares he has never seen one.

Hartenstein has suggested continuous cooling of the cranium by

irrigation or by applications of ice, the local lowering of temperature

serving to impede the development of the cœnurus. This method should be

tried in animals of high value, and, if the symptoms have not yet become

too alarming, recovery is possible. On the other hand, when the symptoms

indicate the presence of an old-standing cyst, there is little chance of

success. Moreover, the treatment could not be applied where a large

number of animals are affected.

It is much better to send the animals to the butcher if they are in good

condition. In Scotland, however—particularly in Caithness—operation is

said to be frequently practised with success.

=Prophylaxis.= In well-managed establishments it is easy to avoid the

appearance of cœnurosis.

The development of this condition being due to the _Tænia cœnurus_ of

the dog, which passes ripe segments containing eggs with its fæces in

the pastures, the first indication is to prevent the development of this

tænia in sheep dogs, sporting dogs and house dogs, and the sole

precaution required is to avoid giving them as food sheeps’ heads

containing the bladder-worms. But, as despite these precautions they may

accidentally contract infection with _Tænia cœnurus_ by eating the offal

of slaughtered animals, it is a wise precaution to administer to all

farm dogs, twice a year at least, a dose of some tænicide.

They should be starved and kept in for twenty-four hours, and should

then receive a full dose of some energetic vermifuge, such as areca nut,

kamala, kousso, powdered pomegranate root, extract of male fern, etc.,

followed by a purgative. The material passed and the fæces should be

burned or mixed with quick-lime. By these simple precautions the losses

which formerly proved so heavy may entirely be prevented.

“TREMBLING,” OR LUMBAR PRURIGO, IN SHEEP.

The above term is applied to a disease peculiar to sheep, and

characterised by neuro-muscular disturbance, which always ends fatally

after a longer or shorter period.

=Symptoms.= Clinically the disease occurs in two forms, one termed the

convulsive form, the other the pruriginous form. In the convulsive form

the patients rapidly lose appetite, soon appear unable to stand, fall on

their sides, and exhibit spasmodic contractions of certain groups of

muscles. After a time the clonic contractions may give place to

persistent rigidity. The patients are carried off rapidly in a week or

two without other important symptoms. This disease appears to exhibit

certain analogies with louping-ill, but these do not seem to be

recognised in France, where it chiefly occurs.

In the pruriginous form the beginning of the attack is obscure, and only

the shepherd is able to note anything unusual. The animals move in a

jerky way, the hind limbs being lifted at times after the manner of a

horse suffering from stringhalt. They are excitable, exhibit trembling

movements when touched, with convulsive movements of the head, and

present an anxious and vacant appearance. The development of these

symptoms, which constitute what may be termed the first phase of the

disease, is sometimes prolonged, and in winter may last from one to two

months. In summer it rarely lasts longer than a week or two.

At this stage a special pathognomonic symptom develops, viz., intense

and permanent pruritus of the hind quarters, which causes the animals to

rub the croup against any projecting objects, walls, mangers, etc. They

thrust themselves backward against the object, and rub with such

violence that the wool is torn away and the skin itself often

excoriated, although the irritability appears to be in no wise

diminished thereby. In the fold the animals sometimes rub against one

another, making their sides raw, and bite themselves on the croup, the

quarters, and the tail.

When the affected parts are touched with the hand, peculiar movements of

the head and the lips are immediately excited, similar in character to

those caused by mange. Up to this time the animals continue to feed, but

they progressively lose condition, become weak in the hind quarters, and

fail to keep up with the other animals in the flock. Their gait becomes

hesitating; they move with a trotting step and appear semi-ataxic.

All these symptoms develop without fever, but become aggravated from day

to day, until they end in paraplegia and death. This second phase lasts

for a period of from two to four months in winter.

=Lesions.= No lesions can be detected on a simple examination of the

dead bodies. Gilbert has mentioned a change in the blood; Trasbot,

chronic inflammation of the pia mater and of the lumbo-sacral portion of

the spinal cord. German writers have described sclerotic changes in the

posterior portions of the cord. Moussu has carried out a large number of

examinations, but has never found these lesions, either on anatomical or

on histological investigation, and he considers that they are not by any

means present in all cases.

Besnoit and Morel, who carried out a very remarkable anatomical and

pathological study of the disease, used Nissl’s staining method, but

only found very discrete changes in the cord (vacuoles in the motor

cells of the anterior horns). They found, however, significant lesions

of neuritis in the peripheral nerves.

=Causation.= The cause is as yet little understood, and it is difficult

to prove how the forms of neuritis described by Besnoit are brought

about.

The disease was not known in France before the introduction of Merinos,

and former investigators referred it to heredity, consanguinity,

precocity, and even to sexual excitement. German writers declare that it

seems more particularly to attack rams and the better-bred varieties. In

reality, the disease occurs in all flocks, and in all kinds of sheep

indiscriminately; it attacks ewe lambs and young castrated lambs as well

as rams. Moussu is absolutely of this opinion, and for want of more

precise information agrees with Trasbot, and, he believes, with Besnoit,

that the symptoms shown may possibly be referred to a chronic

intoxication.

=Diagnosis.= The diagnosis is difficult during the early stages, but

when the pruritus becomes manifest there can no longer be room for

doubt.

Cases of paraplegia might perhaps be mistaken for paraplegia due to

cœnurosis, but in the latter case there is no pruritus.

=Prognosis.= The prognosis is extremely grave, observation having shown

that all the patients die after a longer or shorter time.

=Treatment.= Until now treatment has proved absolutely useless, and it

would seem the best course to slaughter the animals before wasting

becomes marked.

SECTION VI.

DISEASES OF THE PERITONEUM AND ABDOMINAL CAVITY.

CHAPTER I.

PERITONITIS.

Peritonitis, _i.e._, inflammation of the peritoneum, may attack any of

the domesticated animals. It must, however, be regarded as an almost

accidental and relatively infrequent disease. It is due to infection of

very varying character, and from the clinical standpoint may assume one

of two forms—acute peritonitis or chronic peritonitis.

ACUTE PERITONITIS.

The microorganisms which produce peritonitis have not been the subject

of special investigation in the domesticated animals, though the colon

bacillus and streptococci, so frequently found in the female genital

tract after parturition, seem to be the most frequent causative agents.

Certain putrefactive organisms may also bring about the disease.

The peritoneum may become infected, and acute peritonitis ensue under

various circumstances.

All operations in which the peritoneal cavity is opened, such as

castration of the cow and of the sow, laparotomy, gastrotomy,

enterotomy, etc., may be followed by acute peritonitis if performed

without sufficient regard to aseptic precautions. Peritonitis then

usually assumes an acute septic form.

Even simple puncture of the rumen, though usually quite harmless if

carefully performed, may by followed by local or general peritonitis

should food material escape from the rumen and find its way into the

peritoneal cavity.

One of the most frequent causes is infection from the genital tract soon

after parturition. Here the agents of infection are not introduced

directly into the cavity, but find their way there in consequence of a

diseased condition of the mucous membrane and the uterine walls.

Ascending infections of this character and infections by contiguity of

tissue may only give rise to local peritonitis, though in too many

instances they become generalised.

Acute peritonitis may follow infection from the stomach or bowel, should

a foreign body perforate the rumen or reticulum and pass backwards

towards the peritoneal cavity, or a serious intestinal inflammation

(enteritis, invagination, etc.) facilitate the passage of microbes

through the thickness of the intestinal wall.

Abscess of the liver, suppurative echinococcosis, renal infection,

pyelo-nephritis, acute cystitis, rupture of the bladder, etc., may in a

similar way become complicated with acute peritonitis.

Finally, abdominal wounds may cause interstitial ruptures and lesions in

the serous membrane, accompanied by local exudation (kicks,

horn-thrusts, blows from cart-poles, etc.), and if microbic agents are

brought within the region of the lesion by the general circulation or

otherwise, peritonitis may follow.

=Symptoms.= At first the symptoms are vague and imperfectly defined, and

diagnosis is always very difficult during the first few days, except in

cases where there exists a lesion or a condition previously recognised

as likely to become complicated with peritonitis.

The early symptoms comprise fever, loss of appetite, arrest of

rumination, rigors, constipation, etc., but these symptoms only attain

full significance when accompanied by what has been termed “peritonism.”

The patient appears to be suffering from tympanites, as may really be

the case, but the tympanites of the rumen and gaseous distension of the

loops of bowel are not primary, and only result from the arrest of

peristalsis. The primary condition is peritonism, _i.e._, distension of

the peritoneal cavity, this being indicated by a symmetrical fulness of

the right and left flanks.

The patients suffer from dull colic, and from this time always assume an

attitude indicating pain. They remain in one position, with the back

arched, the limbs gathered together, and the lower abdominal wall

shortened. The face expresses suffering, the respiration is short and

rapid and of the costal type, movement is painful and causes groaning,

and the animals do not shrink when the lumbar region is pressed upon.

Palpation of the abdomen causes pain, and if practised at certain points

may be followed by groaning. This method of examination, however, gives

no further information, because the abdominal wall is rigid, tense, and

as though tonically contracted.

Percussion is followed by tympanic resonance in the right and left upper

zones, due to accumulation of gases of fermentation, and to distension

of the peritoneal cavity itself. Towards the lower parts, however,

percussion produces a dull sound. The presence of liquid can here be

detected by the manner in which impulses are transmitted, particularly

at the period of crisis and when much exudation exists.

Abdominal auscultation shows that the digestive movements are arrested.

Peristaltic movement ceases, and the movements peculiar to the rumen and

to the progress of food through the intestine are absent. Fermentation

sounds, however, can be detected.

The heart beats are strong, rapid and violent, and yet the pulse remains

feeble, though the artery is tense.

At a later stage, when the disease becomes aggravated, pain is less

acute, depression is extreme, the animals no longer even drink, the

abdominal wall becomes relaxed, and diarrhœa is succeeded by

constipation. Palpation of the abdomen is less painful and does not

cause groaning, but the pulse becomes feebler, much more frequent,

imperceptible, and at last the animal dies from intoxication and

exhaustion, caused by the fever and pain.

When peritonitis is due to rupture of the intestine or escape of

alimentary material from the rumen into the peritoneal cavity, as may

occur after puncture of the rumen or gastrotomy, etc., fever is not

always very marked. The temperature may even fall below the normal

point. Some cases vary greatly from the type described as regards their

development, but the important features are always present, and the

difference is chiefly found in the course of the disease.

=Diagnosis.= The diagnosis is rather difficult, but when there is colic,

together with persistent peritonism, exaggerated sensitiveness to

palpation and arrest of the functions of the digestive apparatus, there

is little room for doubt.

=Prognosis.= The prognosis of acute peritonitis is very grave.

=Lesions.= The lesions vary with the primary cause (traumatism,

metritis, suppurative echinococcosis, foreign bodies escaping from the

digestive tract into the peritoneal cavity, etc.).

The parietal and visceral layers of the serous membrane are always

inflamed, vascular, roughened, dull, and in places covered by

vegetations. Between the loops of intestine and in the peritoneal

pockets there are discovered more or less numerous and more or less

thickened false membranes, presenting the characteristics of the false

membranes seen in acute pleurisy.

The liquid varies in quantity and in colour, being sometimes

lemon-yellow, sometimes purulent, sanguinolent, or even blackish, and of

putrid odour.

The lesions may appear more marked at a particular point, such as the

uterus, rumen, hypochondrium, etc., and the intestinal loops may become

partly fixed in position by false membranes. In time these false

membranes may solidify and undergo transformation into fibrous tissue.

=Treatment.= Treatment is generally useless in cases where peritonitis

results from rupture of the bladder or intestine or from eventration.

Complete and perfect cleansing of the infected abdominal cavity is

impossible in large animals.

In other cases the animals should be left completely at rest, and

purgatives should be avoided. Movement or the administration of

purgatives provokes peristalsis, and, as a consequence, almost

inevitably leads to generalisation of a lesion which might otherwise

have some chance of remaining localised, as in pelvi-peritonitis and

peritonitis due to foreign bodies issuing from the rumen or reticulum.

If the movements of the intestinal loops disperse the septic liquids

beyond the points originally injured, the whole cavity becomes

inoculated and generalised peritonitis is set up.

Emollient and diuretic drinks containing opium, and oatmeal or linseed

gruels, have the advantage of soothing the colic and preventing

stagnation in the bowel. These should be given from the first and solid

food entirely avoided.

The sides of the abdomen should be mildly stimulated, provided the

operation does not give rise to undue pain and cause the animals to

struggle. Vesicants are preferable to mustard, though mixtures of

mustard and linseed meal may be used, and, if found advantageous, can be

repeated.

Mercurial salts, though much used in earlier times, are now entirely

given up. Diuretics, such as bicarbonate of potash, nitrate of potash,

alcohol, and acetate of ammonia, should be used, according to

circumstances.

Aseptic washing out of the peritoneal cavity would be advantageous, but

in large animals cannot easily be effected.

CHRONIC PERITONITIS.

=Causation.= Chronic peritonitis may occur as a termination of the acute

form, but it may also develop gradually as a result of disease of the

kidney (pyelo-nephritis), of the uterus or ovaries (chronic metritis,

tumour of the ovary), of the liver (suppurative echinococcosis), or of

any other lesion in neighbouring parts which is capable of setting up

continued irritation.

It also accompanies tuberculosis of the peritoneum, cancer of the

peritoneum, chronic disease of the bladder, etc. Further, it appears,

but more rarely, in certain chronic diseases, such as chronic dysentery

and lymphadenitis.

=Lesions.= The lesions consist of local thickenings of the peritoneal

layers, and numerous papilliform vegetations scattered very irregularly

over the parietal peritoneum, mesentery, epiploon, etc.

If the disease has existed for a long time, fibrous bands or solid

adhesions may be discovered, connecting various parts of the digestive

apparatus with one another, or with the abdominal walls.

Sometimes the intestinal contents seem almost entirely adherent to the

abdominal walls.

The primary lesions of the liver, spleen, kidneys, or genital organs,

from which the disease originated, are also found.

The quantity of exuded liquid varies greatly; sometimes there is a great

quantity of a transparent or lemon-coloured liquid, resembling that of

ascites. In other cases the liquid is scanty, and may be confined

between layers of bowel, which are connected by an inflamed layer of

epiploon.

These old-standing lesions cause atrophy of the abdominal organs,

contraction of the intestine, and sometimes true obstruction.

In chronic tuberculous peritonitis the adhesions between the intestine

and the abdominal walls may be enormous. The peritoneum is generally

covered with great masses of tuberculous new growth, while the

mesenteric and sublumbar lymphatic glands are attacked.

=Symptoms.= The disease develops without marked fever or grave

interference with the chief functions, and the first approach of the

disease may, therefore, easily be overlooked. Chronic peritonitis,

moreover, may remain strictly localised.

When the disease assumes the ascitic form the dominant sign is readily

detected. Where new membranes form the principal lesions the symptoms

are much less definite, and the existence of disease is chiefly

indicated by digestive disturbance, such as diminished peristalsis, the

occurrence of colic, diarrhœa, etc.

It is well to remember, however, that these troubles often follow an

ascitic stage, which may gradually disappear owing to the fluid becoming

absorbed. Even in the fibrous form, where the intestines appear

completely glued together by adhesions, the volume of the abdomen is

increased and the belly is deformed, as in ascites.

In time patients suffering from primary lesions of an important internal

organ are affected in their digestion, lose flesh and become anæmic, and

finally cachectic.

=Diagnosis.= The diagnosis is by no means easy, particularly in the

fibrous forms, owing to the great difficulty of discovering the primary

lesion.

=Prognosis.= The prognosis is grave, though it must not be regarded as

necessarily fatal. In cases resulting from genital diseases, and in

localised chronic peritonitis resulting from persistent, but not

excessive, mechanical violence, complete and perfect recovery may occur.

On the other hand, in cases of chronic lesions of the liver, kidneys,

heart, etc., and in tuberculosis, carcinoma, etc., recovery cannot be

expected.

=Treatment.= Treatment should be directed towards combatting the chronic

inflammation. With this object resort may be had, when necessary, to

persistent stimulation of the sides of the abdomen, mild blisters and

mustard plasters, or friction with turpentine.

The food should be easy of digestion, and of first-rate quality. The

most useful drugs comprise mild, unirritating diuretics, general

stimulants, and tonics.

Animals affected with incurable lesions should not be treated.

ASCITES.

True ascites consists in dropsy of the peritoneum, unaccompanied by

inflammation of that membrane, or by the presence of infectious

microorganisms in the transuded liquid. Properly speaking, it is not a

morbid entity, but only a symptom common to several very complex

diseases.

=Causation.= The diseases which produce it may be set forth under five

principal heads:—

(1.) Cardiac affections in general, particularly chronic lesions of the

heart, interfering with venous circulation, and causing prolonged stasis

of blood in an organ or tissue.

(2.) Pericarditis due to foreign bodies, and the various forms of

pseudo-pericarditis, _i.e._, lesions in the neighbourhood of the heart,

causing compression of that organ and of its vessels.

(3.) Generally speaking, all lesions which interfere with the return

circulation, particularly lesions of the liver (distomatosis,

echinococcosis, and interstitial hepatitis). These produce compression

of the portal vein or other obstacle to circulation, and the

transudation is exclusively localised in the abdominal cavity. The

connective tissue does not become infiltrated.

(4.) Diseases of the kidneys (nephritis, pyelo-nephritis), which

secondarily produce cardiac disturbance.

(5.) Gestation, which causes compression of certain digestive viscera,

and of certain veins of the pelvic cavity.

Ascites was formerly regarded as always forming a complication either of

anæmia or of hydræmia. We now know that the primary cause of these three

collections of symptoms (ascites, anæmia, and hydræmia) is the

development of certain chronic wasting diseases or chronic lesions of

the heart, liver, and kidney, which act and react upon each other.

=Symptoms.= True ascites is unaccompanied by fever. The condition

develops slowly, insidiously, and therefore escapes notice at first.

Only when the exuded liquid is present in considerable quantities is the

condition apparent. The symptoms are similar to those of ascites

following chronic peritonitis.

The transuded liquid progressively accumulates in the peritoneal cavity,

the lower portion of which it distends. When the animal is viewed from

behind the enlargement appears symmetrical, despite the position of the

rumen. The intestinal contents float on the liquid and are thrust

upwards towards the lumbar region. On palpation, the abdominal cavity

seems unusually full, the tension differing in proportion to the

quantity of liquid. The accumulation of liquid may become considerable

and interfere with respiration, circulation, and movement. Very marked

anæmia always exists, the mucous membranes are extremely pale, the

respiration is rapid, the pulse feeble, all these symptoms being

consequent on the primary disease of the heart or liver. Percussion of

the lower part of the belly produces a dull sound. On the left side this

dulness often extends from the linea alba as high as a horizontal line,

uniting the external angle of the ilium and the hypochondriac circle. On

the right it is bounded by a horizontal line. Percussion or, better

still, palpation provokes on one side of the abdomen a wave or impulse

of the liquid, perceptible to the touch or even to the view at the

opposite side.

=Diagnosis.= In general diagnosis is easy, thanks to the slowness with

which the disease develops.

=Prognosis.= The prognosis varies in each case, more especially

according to the more or less marked debility of the animal. Ascites due

to gestation is usually of a very simple character, but if it is the

result of pericarditis produced by a foreign body, or of nephritis, the

outlook is very gloomy; lesions of the kidney in particular showing

little tendency to recovery. Finally, the prognosis varies when the

ascites follows disease of the liver, for certain exceptional cases have

been noted in which an attack of hepatitis has led to the disappearance

of the transudate.

=Lesions.= The lesions peculiar to this disease are very trifling.

Transudation takes place without inflammation of the peritoneum,

although the veins of the abdominal cavity are abnormally dilated. The

abdominal wall is thin and distended, and the tissues are colourless as

though soaked in water. The cavity is distended with a clear

lemon-coloured albuminous liquid free from blood corpuscles.

=Treatment.= The treatment must vary according to circumstances, _i.e._,

having regard to the primary cause. Ascites due to gestation, which is

always slight, calls only for simple hygienic treatment; but when the

disease is attributable to lesions of the heart, pericarditis, or

chronic affections of the kidney or liver, it is generally incurable in

common with the original lesions themselves.

If, finally, no clearly defined cause can be detected, or if the ascites

is due to chronic peritonitis, treatment should be attempted. The first

step may consist in evacuation of the liquid for the purpose of reducing

the excessive pressure on the diaphragm and facilitating respiration.

For this purpose an aseptic puncture is made with a fine trocar on the

right side of the abdomen in the flank region, about equidistant from

the umbilicus and the loose flap of skin in front of the stifle. The

absorption of liquid may afterwards be assisted by administering

diuretics, such as digitalis, bicarbonate of potash or nitrate of

potash, and by giving lukewarm drinks, tonics, etc. In Germany

injections of pilocarpine have been suggested, but it is doubtful

whether they have proved satisfactory.

PERITONEAL CYSTICERCOSIS.

The above name has been given to a parasitic disease caused by the

infestation of young animals, such as calves, lambs and young pigs, with

embryos of the _Tænia marginata_ of the dog.

=Symptoms.= Peritoneal cysticercosis is often of so mild a character,

and the number of embryos which penetrate the body so small, that in the

majority of cases there are no visible symptoms. It is not until the

meat comes to be dressed by the butcher that little cysts (_Cysticercus

tenuicollis_) are discovered in the abdominal cavity.

Unfortunately, in exceptional cases it may also happen that the number

of embryos in the abdominal cavity is so great as to produce lesions of

acute hepatitis, acute peritonitis, and sometimes pleurisy. These grave

forms are more common in young pigs and lambs.

The animals appear dull, feeble, exhausted and without appetite, but

exhibit marked thirst, lose flesh and become anæmic in a few days. Soon

afterwards they show symptoms of acute peritonitis, with exudation of

fluid, and death may follow in a week or two.

In cases where infestation is less marked, the animals may exhibit only

progressive anæmia, without well-developed symptoms of peritonitis,

until death occurs.

=Lesions.= On post-mortem examination a sero-sanguinolent exudation is

seen, together with more or less numerous false membranes, and a varying

number of young cysticerci floating freely in the liquid or enclosed in

the folds of the mesentery. The cystic vesicles are spherical, ovoid, or

elongated, and translucid or opalescent. They are some millimètres in

diameter, and in some cases are very numerous, ranging from a few

hundreds up to several thousands, but in others comparatively few.

The liver shows signs of intense hepatitis, caused by embryos burrowing

into its tissue.

=Causation.= The causes are limited to a single fact, viz., ingestion of

the eggs of _Tænia marginata_, which are spread over the fields in the

excrement of dogs suffering from that parasite.

=Diagnosis.= The diagnosis can only be arrived at by a post-mortem

examination, when cysticerci in various stages of development are

discovered.

=Prognosis.= The prognosis is difficult to indicate, because everything

depends on the intensity of the infestation.

=Treatment.= No curative treatment is possible, direct action on the

developing parasites being impracticable. Nevertheless, some patients

survive, and after having shown grave general disturbance may gradually

improve.

The only efficacious treatment is of a prophylactic nature, as in

cœnurosis and echinococcosis. Dogs suffering from tæniæ should

periodically be treated and freed from their parasites.

CHAPTER II.

HERNIÆ.[6]

Footnote 6:

For a fuller description of herniæ and their treatment, see Möller and

Dollar’s “Regional Surgery,” pp. 263–309.

CONGENITAL HERNIÆ.

PERINEAL HERNIA OF YOUNG PIGS.

This variety is very common in young pigs, on account of their

anatomical peculiarities and of the persistence and enlargement of the

inguinal canal. Loops of intestine, impelled by their own weight,

accumulate at the lowest point and readily pass into the canal.

It is usually when the little pig begins to eat, _i.e._, a fortnight or

three weeks after birth, that the symptoms become plainly apparent.

The hernia is indicated by a swelling which commences in front of the

pubis and extends backwards behind the hind limbs. When the herniated

loop of intestine is examined by palpation, the presence of liquid in it

can be detected, particularly after a meal, while a characteristic

gurgling sound is heard.

=Diagnosis.= To confirm the diagnosis, the animal is placed on its back,

whereupon reduction as a rule is easily effected. As soon as the animal

rises again the hernia returns.

=The prognosis= is not grave.

=The treatment= is exclusively surgical, and the hernia can be reduced

and castration performed at one and the same time. The animal being

placed on its back and firmly held, an incision of about 2 to 3 inches

in length is made in the inguinal region, dividing the skin and

subcutaneous connective tissue only. The vaginal sheath is then

completely isolated, the hernia reduced, and a ligature applied to the

sheath and the spermatic cord close to the abdominal wall. The testicle

is then removed.

If adhesions have been set up, which is quite exceptional, the vaginal

sheath is incised and the loop of adherent intestine liberated, when it

can readily be returned. The vaginal sheath and spermatic cord are then

twisted as high as the level of the inguinal ring and tied with catgut.

To prevent this ligature becoming displaced, it should be fixed by

passing a sterilised thread through it and through the mass of tissue;

the hernial sac should be divided immediately below. In order to ensure

greater security, it may even be desirable to pass a suture through the

margins of the inguinal ring.

UMBILICAL HERNIA.

Umbilical hernia is less common in young animals of the bovine, ovine

and porcine species than in the foal, and when existing almost always

disappears at the period of weaning. The rumen then assumes its full

development, the loops of intestine are displaced and thrust towards the

sublumbar region, and the hernia disappears. The same is true of the

young pig, the development of the stomach producing the same favourable

result.

In the rare cases where this hernia is not reduced spontaneously, it may

be necessary to utilise the methods so frequently employed in the foal,

and, despite the number of these, there are only two which can

thoroughly be relied on to give good results.

In the first, irritants are employed.

Subcutaneous injections of concentrated solution of common salt,

_filtered and sterilised_, or 10 per cent. solution of chloride of zinc

produce enormous engorgement of the connective tissue, which thrusts

back the herniated loop of intestine and later causes the development of

very resistant fibrous tissue, which prevents the hernia returning.

To ensure this result, however, it is indispensable that perfect asepsis

should be observed in the injections, for if germs are introduced severe

suppuration occurs at the point of injection. The injections are made at

four opposite spots in the subcutaneous tissue surrounding the hernia, 1

to 2 drachms of saline solution being injected at each spot; of the

chloride of zinc solution half a cubic centimètre is used. This method

is only of value in small herniæ, which may sometimes be cured by the

application of sinapisms alone.

The second method is applicable to larger herniæ, and aims at destroying

the hernial sac.

The application of clams is simplest, and can be recommended. The

patient is placed on its back, reduction is effected, the hernial sac is

drawn upwards vertically, and the clams placed as near the abdominal

wall as possible, after care has been taken that no portion of the

intestine is included in the sac. The clams are kept in place by a

suture passed through the neighbouring tissues.

In other cases where a radical cure is necessary, because of adhesions

within the hernial sac, the patients are similarly placed on their

backs, the hernial sac is opened aseptically, the adherent parts

liberated, the herniated portions of intestine reduced, and the hernial

ring sutured with sterilised strong silk, the skin being afterwards

brought together with silk sutures after removal of the sac itself. A

surgical dressing can then be applied to the umbilicus. The patients

should be carefully dieted.