From this time the pericardial symptoms proper commence, the foreign

body having come in contact with the pericardium. This phase, unlike

those which precede it, presents well-defined symptoms. The irritation

of the heart and its ganglionic system by a foreign body in the

pericardium is shown by considerable acceleration of the heart beats

even before there is any exudation into the pericardial sac. Instead of

60 to 70 beats, the normal number, the pulse may rise to 80, 90, 100, or

even 110 beats per minute. The heart sounds are tumultuous, dull and

ill-defined, while the pulse appears bounding and strong.

But this period of cardiac excitement while persisting is soon

complicated by other symptoms. As soon as the foreign body penetrates

the pericardial sac, there is infection, which produces an active form

of inflammation and abundant exudation. From this time the pulse becomes

weaker and weaker, until, under the steadily increasing pressure on the

heart, it is almost imperceptible.

There is only moderate fever. As soon as the exudation becomes

considerable, the symptoms of pericarditis grow very marked: they may be

grouped in the following order, according to their importance.

A. =Cardiac symptoms.= On palpation of the cardiac zone on the left the

impulse of the heart is no longer felt. Percussion, which under normal

circumstances reveals only partial dulness, now seems to give pain, and

indicates abnormal dulness distributed in a vertical plane. The

pulmonary lobes between the pericardium and thoracic walls are thrust

upwards. The distended pericardial sac approaches the parietal layer of

the pleura and may adhere to it, hence the dulness. This dulness extends

as far back as the xiphoid appendix of the sternum, and can be detected

on both sides, marginated above by a convex line.

In rare cases the dulness is absent, being partially replaced by

tympanitic resonance, due to the presence of gases in the distended

pericardial cavity, which gases originate in the digestive reservoirs or

result from putrid fermentation of the pericardial exudate.

Simple or double pleurisy, or even pneumonia of the cardiac lobes

resulting from infection by contiguity, may complicate cases of rapid

pericarditis. The dulness then appears modified, as do the signs

observed on auscultation.

Auscultation furnishes valuable indications. From the outset it reveals

acceleration of the heart. At a later stage, but only for a short time,

it permits of the detection of the pericardial rubbing sound which

precedes serous exudation, and which may persist for several days when

large quantities of false membrane are produced.

If exudate is present in considerable quantities a liquid sound is heard

at each heart beat. The heart appears to be beating in water, but the

liquid note varies considerably. It has been termed the “claclaque”

sound (Lecouturier, 1846), in allusion to the sound produced by the

meeting of water ripples; “clapotement” sound (Boizy, 1858), with

reference to the sound produced under the influence of a light breeze on

the borders of a stream; “glou-glou” sound (Roy, 1875), suggested by the

noise of liquid escaping from an inverted bottle into a resonant vessel,

etc. It is important, however, to remember that cases occur (principally

when the pericardium is greatly distended and entirely filled with

liquid) where, with the animal at rest, these sounds are difficult to

detect. To render them noticeable the patient must be walked for a few

yards.

Vernant, again, has described a sound as of dripping water, of quite

special character; he compared it to that resulting from the fall of

drops of liquid on to a marble table or into a half-filled vessel. So

far as can be ascertained this sound of dripping water greatly resembles

that heard in pneumo-thorax, but it is less resonant and less prolonged.

It appears to be characteristic of the presence of air in the

pericardial cavity, and its special quality varies with the quantity

accumulated in the pericardium. Masked by these pericardial sounds the

beating of the heart seems dull, badly defined, distant and stifled.

[Illustration: $1]

B. =Jugular symptoms.= The “jugular” symptoms are secondary, and result

from the accumulation of liquid in the pericardial cavity. No

intra-pericardial exudate can exist without exerting pressure on the

heart, and as the auricles have very thin walls and are more

compressible than the ventricles, this pressure immediately causes

difficulty in the return circulation, whence venous stasis, varying in

intensity, but clearly visible and appreciable on account of the

distension of the jugulars.

The venous stasis is general, for the pulmonary veins are as much

compressed as the posterior and anterior venæ cavæ, but it is only

apparent in the large superficial veins. This stasis is accompanied by

venous pulse, and particularly by peripheral or internal œdema, œdema of

the lung, intestine, mesentery, etc., of the submaxillary space and of

the dewlap and entrance to the chest. Œdema of the submaxillary space is

specially characteristic, for it appears almost first amongst external

signs. That of the dewlap follows at a later stage, and extends

backwards as far as the umbilicus, rising above this point as high even

as the entrance to the chest and the axillary region.

C. =Pulmonary symptoms.= The pulmonary symptoms result from difficulty

in the return circulation and from the venous stasis. They are due to

passive congestion and œdema of the lung or to hydro-thorax. At rest the

respiration may appear fairly regular, but at the least movement it is

accelerated, and may rise to 40 or even 60 per minute.

Percussion reveals lessened resonance of the parts, and in the case of

hydro-thorax dulness marginated by a horizontal line, as in pleurisy.

On auscultation the vesicular murmur may sometimes have diminished or

even disappeared, while the respiration may be blowing, as in active

congestion, and in exceptional cases a tubal souffle may be observed. In

most cases the animal has a paroxysmal, somewhat frequent cough, due to

reflex irritability of the pneumo-gastric.

Cruzel in addition mentions a double respiratory movement like that

produced in the horse by broken wind. This is really the result of

hydro-thorax, and is not a constant symptom.

D. =General symptoms.= When the disease has lasted a certain time the

patients show certain well-marked general symptoms: they remain standing

in one position for long periods, with the head and neck extended, the

front legs thrust outwards from the trunk and the body rigid, as though

the least movement caused them pain. The general attitude expresses

anxiety, the animals lie down with great care and seldom remain long in

this position, which interferes with the functions of the heart and

lung. In the last stages the animals remain constantly standing,

appetite is almost entirely lost, and they waste rapidly.

=The course= of pericarditis due to foreign bodies is very variable.

Sometimes death occurs in eight or ten days. In other cases the animal

may survive for weeks, provided it is well tended. Everything depends on

the rapidity with which the foreign body moves and on the character of

the infectious organisms which it introduces into the pericardium. Death

is the inevitable termination, and occurs as a consequence of cardiac

and respiratory syncope. It may follow suddenly as the result of a

simple forced movement, even when the animal still seems to retain some

amount of strength. When the organisms introduced into the pericardium

are of marked virulence, complications such as septic pleurisy and

pneumonia may be observed, and death soon takes place.

It has been suggested that recovery might follow a return of the foreign

body towards the reticulum. This view can only have been advanced as a

consequence of errors in diagnosis, either as to the existence of

pericarditis or as to its nature. Pericarditis due to cold or rheumatism

sometimes becomes cured spontaneously.

Death, again, may suddenly occur by syncope when the foreign body

penetrates the myocardium, passes through it, and enters the ventricular

cavities.

The return of the foreign body is not conceivable, at all events after

it arrives in the pericardial cavity. Up to that time the only

disturbance is of a digestive character; no pericarditis exists. But

when for example the disturbance is due to long fragments of iron wire

which may extend from the reticulum as far as the pericardium, it is

clear that the pericarditis is of a kind which cannot be cured without

leaving traces. In our opinion, natural recovery is impossible.

=Diagnosis.= The diagnosis of pericarditis cannot be made until such

pericarditis actually exists, _i.e._, until the disease has arrived at

the third stage of development mentioned above.

As long as the symptoms point only to the first or second stage, the

logical diagnosis is reticulitis produced by a foreign body. At this

time the development of pericarditis, although possible, is not

inevitable.

When, on the other hand, one knows how the digestive disturbance has

originated and developed and thereafter notes signs of cardiac

irritation, disappearance of the cardiac impulse, dulness of the heart

sounds, venous stasis, etc., the diagnosis is easy even thus early.

Mistakes are not very likely. Only in some cases are they liable to

occur, as in acute peripneumonia of the anterior pulmonary lobes,

causing compression of the pericardium of the anterior vena cava and

producing secondarily venous stasis and œdema of the dewlap. Cases of

specific pericarditis due to peripneumonia also occur, and under such

circumstances a mistake would be even more excusable. Nevertheless, the

temperature curve in itself is a sure indication, for whilst in

peripneumonia the fever is always very marked, it is scarcely noticeable

in pericarditis due to a foreign body.

When the diagnosis of pericarditis has been arrived at it is desirable

to determine the exact nature of the disease, for whilst cases of

pericarditis due to foreign bodies are incurable and in the interest of

the owner the animals should be slaughtered, pericarditis due to cold or

rheumatism may be successfully treated. Rheumatism generally affects the

synovial membranes even before it produces pericarditis, and this

indication, supplemented by the history of the case usually ensures one

against mistakes regarding the initial cause.

It is much more difficult to distinguish pericarditis due to a foreign

body from pericarditis due to carcinoma and from the forms of

pseudo-pericarditis produced by lesions in the neighbourhood of the

heart. When considering the latter we shall deal with this particular

point.

=Prognosis.= The prognosis is always fatal.

=Lesions.= When the foreign body is very thin and sharp, the reticulum

may not become attached to the diaphragm. In such cases its passage has

been rapid and the tissues have healed.

Usually the reticulum, diaphragm and pericardium are united by a mass of

fibrous tissue as thick as a man’s arm. It resembles a fibrous sleeve

surrounded by an œdematous zone, usually of slight extent. This mass of

new fibrous tissue is traversed by a sinuous tract resulting from the

irritant action of the foreign body on the surrounding tissues. All

writers describe this fibrous sleeve, which, however, only occurs in

cases where a very long foreign body has occupied a considerable time in

passing from the reticulum to the cavity of the chest.

In very exceptional cases the sinuous tract is ramified, possibly as a

result of displacements of the foreign body.

The orifices of the tract are to be found, one in the reticulum, the

other in the pericardium. On the side of the reticulum there is never

more than one opening, and in many instances the tract is already closed

on that side, either by exuberant granulations or by a cicatrix.

On the contrary, the fistula is more frequently open in the pericardial

cavity. Its walls are of very varying appearance, depending on their

age: they may be red, greyish, soft or hard, and when the lesion is of

old standing they may have been converted into a sclerotic tissue.

[Illustration: $1]

The pericardium appears distended with a considerable quantity of liquid

of a special character—sometimes sero-sanguinolent, sometimes almost or

entirely purulent; sometimes yellowish, or greenish-grey; sometimes

frothy, inodorous, or very fœtid.

These characters depend on the nature and number of the germs which have

invaded the pericardial cavity. They also vary with the gravity and

number of the hæmorrhages produced by the action of the foreign body on

the myocardium.

The quantity of liquid also varies within very wide limits. There may be

scarcely any exudation. In that case the pericarditis is of a partially

adhesive character, with abundant false membranes. As a rule the

quantity of fluid exudation varies between seven and eight quarts, but

sometimes the quantity is much greater. Trasbot described an instance in

which the united weights of the heart and pericardium exceeded 36 lbs.

Hamon mentioned a case of pericarditis in which the liquid exudate

exceeded twenty quarts.

“When inflammation is first set up the liquid is serous, yellowish, or

reddish yellow. It contains fibrinous flocculi in suspension. Little by

little this exudate becomes purulent, whilst the internal layers of the

pericardial serous membrane undergo desquamation. These are next covered

with false membranes of varying appearance; the fibro-albuminous

exudation is wrinkled, villous and tufted. The two layers of serous

membrane are connected at certain points by this exudation, the

adhesions being sometimes very extensive. The pericardial sac properly

so called becomes the seat of marked lardaceous thickening, due to

inflammation. The heart appears entirely covered with a layer of greyish

or earthy-coloured granulation tissue, which appears as though baked,

and was compared by Hamon to the back of a toad. It is atrophied as a

consequence of prolonged compression.

Under the influence of the eccentric pressure of the liquid the

pericardial sac is distended and comes in contact with the walls of the

chest, to which it may adhere. The foreign body, especially if small, is

not always easy to find.

The myocardium often displays interesting lesions. At first there is

thickening, or more commonly sclerous degeneration, of the superficial

layers covering the ventricles, and then appears a crop of little

miliary abscesses. Abscesses of considerable size have several times

been detected in the walls of the ventricles and in the interventricular

septum.

The foreign body, moreover, may not only injure the myocardium, but may

even perforate it completely and produce ulcerative endocarditis

(Cadéac). In this case infectious germs very rapidly invade the

circulation and all the tissues, and the animal dies of pyæmia.

These essential lesions are accompanied by others of varying importance.

Thus the lung is congested throughout, and by contiguity of tissue

inflammation may extend from the pericardium to the lower part of the

pulmonary lobes and to the pleura.

Interference with the return circulation induces lesions due to venous

stasis: dropsy of the chief serous membranes, œdema of the connective

tissue, pleural and peritoneal exudations, etc. If the hind limbs never

become swollen it is because the skin covering them is very resistant

and does not readily yield. The liver becomes hypertrophied, congested

and engorged with blood, and when the animals live for some weeks, shows

the appearances known as cardiac or nutmeg liver.

=Treatment.= The treatment of pericarditis due to the presence of

foreign bodies is at present merely palliative. Often the only thing to

be done is to slaughter the animal.

We need not go back to the methods formerly recommended. All are

illusory or mischievous, such as the use of purgatives to arrest or

reverse the progress of the foreign body, removal of the foreign body

after opening the rumen, puncture of the pericardium, etc.

In 1878 Bastin successfully opened the pericardium and extracted the

foreign body through a window produced in the thoracic wall.

This operator recommends that after drawing the left limb forward and

incising the skin and muscles, the operator, with his hand bound round

with a cloth, should perforate the pleura, and then having found the

foreign body, proceed to extract it. By this method it seems difficult

to cause perforation of the pericardium, which would certainly lead to

the production of pneumo-thorax complicated with fatal septic pleurisy.

It must be borne in mind that the two pleural sacs, right and left,

descend as far as the sternum (Fig. 173), and that it is not possible to

touch the pericardium directly without perforating the pleura.

Moussu has drained the pericardium through the pleura in the hope of

relieving the pressure on the heart and facilitating the reabsorption of

the œdema, in order to permit of the subsequent slaughter of the animal,

but has had unsatisfactory results. Lastly, he has practised median

trepanation of the sternum in the infra-pericardiac region. Here again

the operation is difficult, because of the œdematous infiltration of all

the substernal region, while it is so dangerous to the patient, which

must be cast and may suddenly succumb, that it is of no use in ordinary

practice.

There is probably only one condition in which it would be possible to

attempt intervention with a fair chance of success, that is, when there

exists a fibrous connection between the pericardium, lung, and wall of

the chest on the right or left side.

In such cases aspiratory puncture or incision of the pericardium in an

intercostal space might prove of service, because it would not expose

the animal to the danger of pneumo-thorax.

The only difficulty lies in ascertaining beyond all question the

existence of such an adhesion before attempting operation, and this is

really very great, even having regard to the form of the dulness and the

absence of all respiratory sound in the lower third of the thoracic

cavity and cardiac zone. The pulmonary lobe between the heart and chest

wall may be thrust upwards and be partially adherent to the pericardium

and to the parietal pleura, and at the same time it may be impossible to

avoid producing operative pneumo-thorax when the cartilages are resected

to admit of incising the pericardium.

The only logical method seems to be puncture of the pericardium through

the xiphoid cartilage, as described below.

The topographical anatomy of the thoracic viscera shows that the point

of the pericardium extends along the sternum to a point close to the

lower insertion of the diaphragm, and that the pericardial sac is only

separated from the xiphoid region, or rather from the region of the neck

of the xiphoid appendix of the sternum, by the fatty cushion at the

point of the heart.

[Illustration: $1]

A glance at the annexed diagram (Fig. 177) will show this.

The diagram, carefully reproduced from an anatomical preparation of an

animal which succumbed to pericarditis, shows that the distended

pericardium extends close to the neck of the xiphoid cartilage.

=First stage.= Identify the three following anatomical guiding points:—

(1.) Xiphoid appendix and white line. (2.) Point at which the circle of

the hypochondrium becomes attached to the sternum. (3.) Point at which

the external mammary vein penetrates the abdominal wall (Fig. 178).

Lines uniting these three points enclose a right-angled triangle, which

the operator must imagine to be bisected by a third line.

The incision, which should be about 8 inches in length, follows this

bisecting line at an equal distance between the white line and the

circle of the hypochondrium, to a point within about 8 inches of the

anterior margin of the mamma. All these points are readily observable

before the animal is cast.

[Illustration: $1]

The cutaneous incision affords exit to large quantities of fluid, and

the pectoral muscles attached to the neck of the ensiform cartilage can

then be divided with the bistoury. The area of operation is thus

uncovered.

=Second stage.= The second phase comprises incision of the tissues

opposite the neck of the ensiform cartilage, about 8 inches in front of

the base of the triangle and at equal distances from the points Nos. 1

and 2; incision through the skin for a distance of 8 inches, and

dissection of the muscles of the ensiform region exposed at the neck of

the cartilage.

By means of the index finger or the index and middle fingers of the

right hand the mediastinal space is explored, and the fatty masses round

the base of the heart broken through. If the pericardium is greatly

distended, the point of the sac can be felt with the tip of the finger,

or its position can be recognised, even from a little distance, on

account of the fluid contents transmitting the impulse of the heart. The

sensation conveyed to the finger is very clear.

The right index finger is then replaced by the left, and, a trocar about

10 inches long and ¼ inch in diameter being introduced along the index

finger used as a director, the pericardial sac is reached. The exudative

fluid transmits the impulse due to the beating of the heart, and the

pulsations can be clearly distinguished when grasping the handle of the

trocar.

=Third stage.= Digital exploration of the course of the puncture and

fatty cushion at the base of the heart, with the object of discovering

the position of the pericardium.

=Fourth stage.= Puncture with a trocar about 10 to 12 inches in length,

puncture of the pericardium, irrigation and dressing.

[Illustration: $1]

The trocar is inclined in a slightly oblique direction from without

inwards and forwards towards the median plane, in order that the point

may not deviate towards the left pleural sac; the left index finger is

then withdrawn, and by a sharp thrust of the right hand the trocar is

pushed forward about 1 to 1½ inches and the pericardial sac is entered.

The position of the canula should not be altered whilst liquid is

escaping, for if it is thrust in too far a considerable quantity of

fluid may remain in the deepest portion of the sac.

The cavity having been drained, a long strip of iodoform gauze is

introduced into the track and a protective surgical dressing applied

over the incision in order to prevent infection by the litter.

In consequence of the introduction of the fingers into the track caused

by puncture and the escape of pericardial liquid along the canula or

after removal of the canula, the operative wound is necessarily

infected; but this is of little importance, because the opening is

inclined downwards, and also because it is impossible to hope for

aseptic healing.

The dressing is renewed after forty-eight hours, and every three or four

days afterwards.

The œdematous infiltration about the front portion of the body

disappears rapidly in two to three days, and should the animal be

slaughtered the meat is quite sound in appearance.

This operation does not aim at effecting a cure, but is simply for the

purpose of allowing animals which would otherwise be valueless to be

slaughtered and sold.

[Illustration: $1]

CHRONIC PERICARDITIS.

Pericarditis when due to tuberculosis may assume the chronic form.

Tuberculous pericarditis, at least in a large number of cases, is only

accompanied by slight exudation, which might remain unnoticed unless the

animals were carefully examined; but it causes the internal surface of

the pericardial sac and the surface of the myocardium to become covered

with exuberant vascular growths, which by setting up adhesions lead to

partial or generalised union of the heart and pericardial sac. Between

these adhesions, which form partitions, are found little cavities filled

with sero-sanguinolent, grumous, or caseous liquid. In time the

adhesions increase in number, pericarditis obliterates the free space,

and the heart becomes wholly adherent to the pericardium.

As in acute pericarditis, the fibrous layer undergoes thickening and

hardening processes. The superficial layers of the myocardium undergo

sclerous transformation, and the tissues forming the adhesions

themselves may assume the characters of fibrous tissue.

In one solitary case Moussu saw another form of chronic pericarditis

with complete adhesion of the heart and pericardial sac, without any

exudation and almost without any false membranes. He was unable to

determine the exact cause, but was strongly inclined to regard the

disease as having followed pericarditis _à frigore_ or pericarditis of a

rheumatic character.

[Illustration: $1]

Adhesions between the heart and pericardial sac are also said to be the

inevitable though delayed result of all punctures of the pericardium

through the ensiform cartilage in cases of pericarditis due to a foreign

body.

=Symptoms.= If the chronic pericarditis is limited to a few partial

adhesions, it remains unnoticed; but when it is more marked it offers

certain signs of acute pericarditis, such as partial dulness of the

cardiac area, which is more extensive than usual, disappearance of the

cardiac shock, weakening of the sounds, feebleness of the pulse, very

marked venous pulse, moderate stasis, extremely rapid and aggravated

dyspnœa when the animal is forced to walk, threatened asphyxia if

exercise is prolonged, and complete asystole.

All these symptoms are due to the existence of adhesions between the

heart and pericardium, which, by destroying the interpericardial space,

interfere with diastole while preventing regular systole.

Sudden death is a frequent consequence.

The =diagnosis= of chronic pericarditis is very difficult. The

=prognosis= is extremely grave, and we do not possess any means of

dealing with the condition.

PSEUDO-PERICARDITIS.

Under this title we purpose grouping a certain number of pathological

accidents due to different causes, but manifesting themselves by

identical symptoms, which symptoms offer so marked a resemblance to

those of pericarditis produced by foreign bodies as to suggest the

presence of that disease. This refers to accidents by which the foreign

body closely approaches, without actually touching, the pericardium, the

lung or the pleural sacs, but in which it causes purulent collections

which displace the pericardium, indirectly compress the heart, and

finally cause symptoms of an apparently pericardial character.

=Causation.= During the development of pericarditis the foreign body

perforates the reticulum and diaphragm, passing along the middle line of

the body, without which it would not come in contact with the

pericardium. If the perforation, however, occurs to the right or left of

the median plane, the foreign body moves forward just as easily, but it

misses the pericardium and passes either into the lung, where it causes

fatal pneumonia; or the pleura, where either it sets up septic pleurisy

in the subpleural connective tissue or produces an abscess.

The abscess is generally lateral, situated in the right subpleural

region, or it may develop below the pericardium. These are the two

varieties of pseudo-pericarditis seen by Moussu.

There is, however, a third variety, which might be called “parasitic

pseudo-pericarditis.” It is extremely rare, and Moussu has only seen one

case. It was due to the presence of an enormous hydatid cyst of the

right lung as large as a man’s head, which was situated towards the

mediastinal plane of the lung and pressed on the supero-posterior

surface of the heart and pericardium. In consequence of the permanent

downward pressure which it exercised it interfered seriously with the

heart’s action and caused symptoms of pseudo-pericarditis.

=Symptoms.= The general and external symptoms are those of

pericarditis—viz., dulness, diminution in appetite, irregular

rumination, wasting, œdema of the dewlap, distension of the jugulars,

marked venous pulse, great anxiety and dyspnœa when the patients are

forced to move, etc.

But the cardiac symptoms differ notably, and moreover vary, according to

the nature of the lesions. Speaking generally percussion reveals

complete dulness on one or both sides, and auscultation always indicates

the absence of sounds due to extravasated fluid in the pericardial sac.

When the abscess is situated below the pericardium, a condition

difficult to diagnose, the dulness seldom extends very high on either

side of the chest, and the sounds heard over the cardiac area, while

much weaker than usual, are audible above the normal points.

An abscess developing beneath the pleura on one side displaces the heart

in the opposite direction. The cardiac beat is weakened by the

compression, but, nevertheless, transmits an impulse to the purulent

fluid, which in its turn conveys it outwards through the intercostal

spaces in the form of movements corresponding in rhythm with the beating

of the heart, so that at first glance one might imagine an aneurism

existed at the base of the large arterial trunks. The lower pulmonary

lobe is thrust upwards, and over the area of dulness pulmonary sounds

completely disappear.

When the heart is compressed by a large hydatid cyst or other lesion,

the general and external symptoms are similar to those above described.

Finally, one last symptom, which appears of some importance, may be

mentioned. When animals suffering from pericarditis due to a foreign

body are forced to move, the heating of the heart becomes so tumultuous

that it can no longer be counted, and even in a state of rest it may

rise to 140 or 150 beats per minute. In cases of pseudo-pericarditis it

rarely rises above 90 or 110.

[Illustration: $1]

=Diagnosis.= The attempt to diagnose this condition accurately must not

be regarded merely as a result of scientific curiosity. Under certain

circumstances the diagnosis may be of very great importance. While the

patient affected with pericarditis due to a foreign body is beyond all

hope of recovery, certain cases of pseudo-pericarditis appear amenable

to treatment.

The diagnosis, therefore, is of great importance, and the practitioner

should spare no effort to confirm it, bearing in mind the symptoms

enumerated, and remembering that the normal sounds of the heart never

completely disappear.

An aseptic exploratory puncture with a long, fine needle will sometimes

prove of great assistance.

=Prognosis.= Although grave, the prognosis is less so than in true

pericarditis.

=Treatment.= If clearly recognised, both subpleural and subpericardial

abscesses seem curable. By freely puncturing the pus-filled cavity

through an intercostal space, the liquid may be evacuated and recovery

may occur. Healing is favoured by carefully washing out the cavity with

a non-irritant disinfectant.

The only precaution required in making such punctures is to avoid the

internal thoracic artery and vein, the intercostal artery, and the lower

cul-de-sac of the pleura.

CHAPTER III.

ENDOCARDITIS.

If the symptoms of pericardial diseases are well defined, we cannot say

the same of diseases of the heart, properly so-called. Such affections

often pass unnoticed, being detected only on post-mortem examination.

Moreover, cardiac diseases are rare. Very frequently they are only of a

secondary nature, accompanying or following better recognised

conditions, such as infectious diseases, post-partum infections, etc.

=Causation.= Endocarditis, _i.e._, inflammation of the endocardium and

valves, is rarely primary, simple and benign. It was formerly thought to

be the result of chills or of the rheumatic diathesis. These simple

forms of endocarditis usually escape observation, though careful

examination in the first instance reveals them.

Much more frequently, however, endocarditis is secondary, malignant,

infectious and infecting. This variety occurs as a complication of

post-partum infection or of very serious general conditions, such as

peripneumonia, gangrenous coryza, aphthous fever, tuberculosis, etc. To

detect it, not only must the original disease be accurately diagnosed,

but all the changes the disease is producing in important organs must be

followed.

While it is generally admitted that all forms of endocarditis, even of

the most benign character, are originally due to infection, it is

certain that in those of the second group the organisms which have

entered the bloodstream through a lesion of the uterus, lung or other

tissue, are endowed with very great virulence. They attack some point on

the endocardium, and produce either ulcerations which become covered

with fibrous clots, or exuberant new growths of a pathological nature,

which generally are papilliform, fragile, and prone to become detached

by rupture of their pedicle and thus to be launched into the general

circulation and to form emboli. The surface of these infected

vegetations, like that of the ulcerations, becomes covered with

fibrinous clots, which are readily loosened, form emboli in their turn,

and infect distant organs.

=Symptoms.= The general symptoms of infectious endocarditis are by far

the most important. They consist of prostration, loss of appetite,

severe thirst, and high temperature. The local symptoms consist

principally of murmurs: soft murmurs due to insufficiency of the

auriculo-ventricular valves, heard during systole, particularly opposite

the point of the heart where the cardiac shock is most clearly felt.

This fact differentiates them from the murmurs of chronic endocarditis,

which are usually due to aortic contraction, and are accompanied by a

systolic sound heard at the base of the heart, more in advance and at a

higher point than those now under consideration.

These murmurs or souffles furthermore vary in intensity and in

character, according to whether the endocarditis results from

post-partum infection, pyæmic disease, or some other cause.

=Diagnosis.= The diagnosis of endocarditis has not yet been the object

of really careful study in bovine pathology, but there is no doubt that

it can often be detected by patient examination.

=Prognosis.= The prognosis is very grave, and patients may die in a few

days.

=Treatment= comprises vigorous local stimulation over the cardiac area,

the administration of antithermic and antiseptic drugs, such as

salicylate of soda, or of digitalis, sparteine or other cardiac tonics.

Pathologists have also described, chiefly as post-mortem curiosities of

interest to pathological anatomists, various diseases and lesions due to

insufficiency or contraction of the auriculo-ventricular, aortic, and

pulmonary openings, lesions due to infectious myocarditis, to the

presence of parasites and to other causes.

The symptoms of these various diseases or lesions in bovine animals are

still too imperfectly understood to permit of more than a very limited

description.

In the present state of our knowledge, diagnosis would always be of an

uncertain character, and for this reason we do not propose to deal with

them at present.

CHAPTER IV.

DISEASES OF BLOOD-VESSELS.

Diseases of vessels, arteries or veins, in animals of the bovine and

ovine species are frequently nothing more than localisations of grave

general disorders, and rarely admit of treatment. This is specially the

case in regard to arteries, but a study of the diseases of veins has

some practical importance.

PHLEBITIS.

Phlebitis, _i.e._, inflammation of a vein, is of interest only in the

case of bovine animals. In them certain conditions may occur which the

practitioner should understand, with a view either to prevention or

treatment. Inflammation of the veins may be due to external causes, such

as surgical or accidental wounds (phlebotomy wounds, accidental wounds,

local inflammations, etc.), or to internal causes of infectious origin

(general infection, puerperal infection, etc.).

ACCIDENTAL PHLEBITIS.

The jugular vein may become inflamed as a result of accidental wounds or

of phlebotomy, but the mammary vein in cows is much more frequently

affected. In both cases the disease is due to infection of the clot

which seals the vessel; it may assume the form of either adhesive

phlebitis or suppurative phlebitis. Whether produced directly by the use

of infected instruments or whether it is of a secondary character,

traceable to the clot being infected by germs entering from without

being conveyed to the wounds by the head-stall chains, by litter,

manure, etc., the result is the same. The inflammation, at first

confined to the endothelium, extends to the wall of the vein and causes

fibrin to be precipitated over the inner wall of the inflamed vein for a

distance varying with each case.

If the microorganisms do not produce suppuration, the vein appears

simply thrombosed and inflamed, the phlebitis remains of an adhesive

character, and may disappear spontaneously, provided the animal be kept

quiet. If, on the other hand, suppuration is set up, the clot gradually

breaks down, the internal surface of the vein develops granulations and

undergoes suppuration, and the phlebitis is then said to become

suppurative. The clot may even become entirely detached, transforming

the suppurative phlebitis into a very grave form of hæmorrhagic

phlebitis.

The jugular is the commonest seat of adhesive phlebitis, the mammary

vein of suppurative phlebitis.

=Symptoms.= The symptoms are easy to recognise. The accidental or

instrumental wound is the seat of a painful œdematous swelling. It

discharges a reddish offensive serosity, or exhibits blackish-violet

bleeding granulations surrounding a little central sinus.

The affected vein, whether the jugular or mammary, soon becomes swollen,

is sensitive to the touch and very rapidly becomes indurated in the

direction of its origin for a greater or less distance.

Phlebitis has then set in, and according as one or other complication

predominates, it is described as suppurative or hæmorrhagic.

=Diagnosis and prognosis.= The diagnosis presents no difficulty. In

phlebitis of the jugular the neck is held stiffly, and the jugular

furrow is partly obliterated.

The prognosis is somewhat serious, particularly in phlebitis of the

mammary vein, for obliteration of the vein interferes with the function

of the venous plexus from which it springs, and, although there may be a

limited vicarious circulation, the secretion of milk is indirectly and

secondarily checked owing to difficulty of irrigation.

The extension of phlebitis of the jugular towards the head and the

venous sinuses of the cranial cavity, is quite exceptional.

When the mammary vein is inflamed it appears collapsed in the direction

of the heart and swollen, indurated, and painful in that of its origin

in the mammary gland.

=Treatment.= The first point requiring attention is so to fix the animal

as to prevent the clot from being pressed upon or crushed, though,

unfortunately, this cannot always be properly done. The difficulty is

obviated by applying vesicants, which cause swelling and pain, and so

reduce natural movement of the parts to a minimum.

At first, when the parts surrounding the operative wound are simply

swollen and phlebitis is threatened, repeated application of tincture of

iodine or a liquid vesicant is useful, and may prevent the disease

developing.

In existing cases a blister applied over and around the whole of the

hardened tract may prevent the mischief from proceeding beyond the

adhesive stage. In such case the clot becomes organised, the vein

remains obliterated, and recovery follows.

Similar treatment may also be employed in suppurative phlebitis, but as

the clot gradually breaks down in consequence of the action of bacteria

it is useful and almost indispensable to disinfect the vessel. For this

purpose the opening of the sinus must be enlarged, and, by means of a

sterilised or very clean syringe with a curved nozzle, the parts washed

out daily with warm boiled water, followed by an antiseptic injection

containing 2 per thousand of iodine, 3 per cent. of carbolic acid, or,

better still, glycerine containing 1 per thousand of sublimate.

If in spite of this treatment the phlebitis extends towards the origin

of the jugular or mammary vein, a counter-opening may be made at the

point where the clot still remains adherent, and a strip of iodoform

gauze saturated with tincture of iodine or with blistering ointment

diluted to one-eighth with oil may be passed. Needle firing is also of

value. Finally, as a last resource, a ligature may be applied to the

vein above or beyond the clot.

This operation, which in the horse is confined to hæmorrhagic phlebitis,

is especially applicable to phlebitis of the mammary vein in the cow. As

the vein is subcutaneous, the operation may easily be performed in the

standing position; the successive stages are as follows:—

The patient is firmly secured and its hind limbs hobbled by passing a

rope around the hocks in a figure of eight. It is steadied on one side

by an assistant who presses on the quarter.

One cubic centimètre of a 10 per cent. solution of cocaine is

subcutaneously injected on each side of the vein at the point chosen.

Ten minutes later a button-hole incision is made through the skin and a

loop of thick catgut passed around the vein by means of a curved needle.

The ligature is tied firmly with a surgical knot and the little wound

afterwards covered with a mass of cotton wool secured by collodion.

INTERNAL INFECTIOUS PHLEBITIS (UTERO-OVARIAN PHLEBITIS).

The internal forms of phlebitis of parasitic or infectious origin are as

yet little understood, but mention may be made of phlebitis of the

utero-ovarian veins which frequently follows parturition and post-partum

infection. This is probably in many instances the real cause of the

post-partum paraplegia without gross or apparent material lesions.

This form of infectious phlebitis may extend to the large internal and

external iliac veins and produce embolism and septicæmia, as is shown by

recorded cases.

The mechanism of the disease is easily understood. The infective agents

penetrate the veins of the uterine mucous membrane and pass from the

lumen into the wall of the vein. Here they cause inflammation of the

vascular endothelium, followed by the deposit of a fibrous clot of

cylindrical form, which sets up partial thrombosis of the vein. This

thrombosis becomes complete by the formation of a central clot due to

venous stasis.

It is not necessary for the germs to penetrate at a number of points.

The thrombosis progresses until it gains a large trunk beyond the

original point of infection.

=Symptoms.= Phlebitis of the veins of the pelvis is frequently

misunderstood or overlooked, because the practitioner is apt to confine

his attention to external signs, the paresis and paraplegia of the hind

quarters.

The symptoms usually appear from five to eight days after normal

parturition or parturition in which there is retention of the

after-birth followed by metritis. The animals show fever and lose

appetite, signs which may be due to metritis, but soon after they

experience difficulty in rising, and some days later remain permanently

recumbent.

The circulation is weak, and the entire intra-pelvic region painful; the

large nervous trunks are affected, exertion becomes difficult, and the

animals refuse to rise. At this stage they should not be forced to do

so.

In two to three weeks improvement may occur and lead to recovery but in

many instances various complications in the nature of purulent infection

or septicæmia set in, or the animals are previously slaughtered.

=Diagnosis.= The diagnosis can only be determined after the symptoms

develop. Confirmation might in some cases be obtained by rectal

exploration made methodically and gently.

=Prognosis.= The prognosis is grave.

=Treatment.= Treatment should be based on disinfection of the uterus by

injections of boiled water or warm iodised solutions and drainage by

means of strips of iodoform gauze. The animals should be placed on a

thick and scrupulously clean bed, and as far as possible be spared any

considerable exertion for a fortnight. By changing their position once

or twice a day complications may be avoided.

UMBILICAL PHLEBITIS OF NEW-BORN ANIMALS.

One of the most serious conditions met with in practice is that known as

umbilical phlebitis of new-born animals. Whilst in fact it is easy to

deal with phlebitis of the jugular or mammary vein, surgical or medical

assistance becomes extremely difficult in this case, because the

inflamed vein is deeply situated in the abdomen and passes through one

of the most important internal organs, viz., the liver. When it is added

that umbilical phlebitis is in 95 per cent. of cases of a suppurative

character, the reader may form some idea of its gravity.

Unless the condition is early diagnosed and measures are at once taken,

such complications as infectious hepatitis, purulent infection, and

septicæmia cannot be avoided. Death is then inevitable.

In order clearly to understand this phlebitis, however, it is necessary

to recall the anatomical formation of the umbilical region in the

new-born animal.

At birth the umbilical cord is represented by a cylindrical mass,

surrounded by the terminal portion of the amnion. It enters the abdomen

through a circular perforation in the abdominal wall known as the

umbilical ring. This ring may be divided into two parts, one deeply

seated, the fibro-aponeurotic ring, consisting of an aperture in the

white line; the other the superficial or cutaneous ring, formed by the

skin, which is wrinkled all round it, and constitutes a kind of sleeve

about an inch in length. This cutaneous sleeve is continuous with the

amniotic tissues. The entire umbilical cord is therefore enveloped in an

amniotic-cutaneous sheath.

[Illustration: $1]

It is composed of four principal structures—the umbilical arteries, the

umbilical vein, the urachus, and the interstitial mucous tissue.

The umbilical arteries and vein consist of two parts—the extra-fœtal

part, which co-operates in forming the cord, and the intra-fœtal part.

The first is formed of two arteries and two veins, in contra-distinction

to the condition in solipeds, where the cord only contains one vein. In

the second, the arrangement is as follows: The two umbilical allantoid

arteries on entering the abdomen curve backwards towards the entry of

the pelvis, passing over the sides of the bladder enveloped in the

lateral ligaments, and extend upwards towards the bifurcation of the

aorta, finally pouring their contents into the internal iliac arteries.

In the adult they may still be traced as annexes of these latter

vessels. The two umbilical veins on passing through the ring unite to

form one within the abdomen. This vessel passes forwards, rising along

the lower abdominal wall, then becomes lodged in the thickness of the

inferior middle ligament of the liver, and finally penetrates that organ

where it unites with the portal vein. It is also connected with a vessel

known as “the vein of Arantius,” which places it in communication with

the posterior vena cava, a vein not found in solipeds.

The fœtal blood is purified by exchanges between it and that circulating

in the maternal placenta, and when re-arterialised it returns by the

umbilical vein.

The urachus, found in the embryo and fœtus, eventually gives rise to the

bladder. In new-born animals this viscus is therefore open at its base,

and communicates with the allantoid cavity through the urachus. The

urachus starts from the base of the bladder, and, extending along the

median plane of the lower abdominal wall between the two umbilical

arteries as far as the umbilical opening, takes its place in the cord

alongside the vessels. Through it the secretions of the fœtal kidneys

drain into the allantoid cavity. The interstitial mucous tissue, also

called “Wharton’s jelly,” is a gelatinous material which unites these

different vessels and helps to support and protect them in the umbilical

cord. It is particularly abundant opposite the umbilicus.

Immediately after birth the umbilical cord ruptures of itself as a

result of the fall which the young animal experiences or of movements

made by the mother, as for instance when she attempts to rise. In

certain other cases it is divided by the mother biting it, or it may be

ligatured by some person present. However the rupture may be brought

about, it always occurs at a distance of 2 to 4 inches from the

umbilicus. The immediate result is to produce thrombosis of the

umbilical vessels and obstruction of the urachus. The two umbilical

arteries rarely bleed, for hæmostasis is brought about by stretching,

and these arteries, being very elastic, almost immediately retract and

close. The umbilical veins simultaneously become blocked, and the single

intra-abdominal vein having no further _raison d’être_, gradually

becomes obliterated. The urachus should normally be obliterated at the

moment of delivery (Colin and Saint-Cyr), or at any rate soon

afterwards, as a consequence of rupture of the cord (Chauveau and

Zundel).

Immediately after delivery another change sets in. The extra-fœtal

portion of the cord, which remains attached to the umbilicus, dries on

contact with the air, the Wharton’s jelly retracts, the whole undergoes

a kind of necrosis, assumes the appearance of a dry scab, and in eight

or ten days falls away, leaving in its place the umbilicus, which should

be half cicatrised on the fall of the cord. Thus the umbilical cord

presents an extra-fœtal degenerated portion and a persistent portion

about ½ to 1 inch only in length, buried in the cutaneous ring of the

umbilical region.

If all the changes indicated occur normally and physiologically, the

little wound in the region of the umbilicus cicatrises in a perfectly

regular way. But unfortunately this is not always the case. At times the

cicatrix becomes contaminated by manure, urine or dust, suppurates, and

may then become the seat of various complications, such as umbilical

phlebitis, omphalitis or persistence of the canal of the urachus.

UMBILICAL PHLEBITIS OR OMPHALO-PHLEBITIS.

=History.= Umbilical phlebitis, and in a more general sense all

pathological conditions of the umbilicus, in new-born animals have been

the object of numerous investigations by Lecoq, Bénard, Loiset (1843),

Bollinger (1874); and more recently by Morot (1884), Uffredizzi (1884),

Chassaing (1886), etc.

Omphalo-phlebitis may occur as a primary condition or may appear as a

complication of omphalitis and of persistence of the urachus. It

consists essentially in suppurating inflammation of the umbilical vein,

but is not infrequently accompanied by omphalitis, arteritis,

peritonitis, and cystitis.

=Causation.= The disease results from infection of the (normal) clot and

of the wound resulting from severance of the cord. The infection may

only cause simple phlebitis of the umbilical vein, but if the organisms

are virulent the phlebitis almost inevitably degenerates into

suppurative phlebitis.

Formerly omphalo-phlebitis was thought to be caused by the mother

licking the foal, by irregular tearing of the cord, by crushing and

separation of the obliterating clot, etc. The truth is that all these

causes favour infection of the umbilical wound, which is the primary

cause, suppurative phlebitis being secondary only.

When the cord is ruptured both the veins and arteries become plugged,

and bleeding ceases. This plugging should end in organisation of the

clot and obliteration of the vessels. If, however, the wound is

infected, microorganisms make their way between the clot and walls, and

extend along the inner surface of the vein, infecting first the clot and

then the vein, and thus setting up suppurative phlebitis.

If suppuration does not continue, recovery may occur spontaneously.

Infection may be confined to the clot, producing simple phlebitis, but

it often extends along the umbilical vein to the liver, causes

infectious hepatitis and purulent infection or septicæmia. Similar

results may be produced by infection of the arteries, the organisms

making their way as far as the bifurcation of the aorta, and thus

gaining the general circulation. Moussu believes that this is the

commonest method by which septicæmia is produced in calves.

=Symptoms.= In these cases it is usually the general symptoms which

first attract attention, the local lesion passing unnoticed for a

greater or less time.

The animal shows intense fever, due to either suppurative phlebitis,

infectious hepatitis, or, as often happens, to generalised infection.

Appetite is lost, diarrhœa is abundant, the respiration and circulation

are accelerated, and the temperature rises to 104° Fahr., or even 105°

Fahr.

The local symptoms are those usually associated with omphalitis or

phlebitis. An examination of the umbilical ring reveals an œdematous,

hot, sensitive swelling, the lower part of which exhibits a chronic,

suppurating, fungoid, blackish wound of unhealthy appearance.

This wound is the seat of one or more sinuses which penetrate the vein,

arteries, or urachus. If only one sinus exists, it always passes upward

and forward into the umbilical vein. The utmost precaution should be

employed in examining the parts. Should it be thought desirable to probe

the sinus in order to discover its direction, the probe must be very

cautiously introduced, and only for a short distance, because rough

handling would tear the tissues and carry infective material to deeper

seated points.

=Complications.= These are numerous and very grave. Long ago Lecoq

described a disease suggestive of laminitis, which beyond doubt was only

a form of purulent infection. At a later date Loiset studied a disease

following omphalitis, in which interstitial abscesses developed in the

cord. This also was simply purulent infection.

More recently complications such as pleurisy, pneumonia, infectious

endocarditis, diarrhœic enteritis, and especially suppurative

polyarthritis of young animals have been referred to omphalo-phlebitis.

All these complications result from infection. The microorganisms

themselves or the toxins they secrete appear to have a particularly

injurious action on the serous membranes, a fact which throws light on

the frequency of such complications as pleurisy, peritonitis,

endocarditis and arthritis.

Intoxication also plays a certain part, and microbic toxins are

responsible, at least at first, for the uncontrollable diarrhœa,

arthritis with sterile exudations, etc.

=Diagnosis.= This presents no difficulty. The alarming general symptoms

seen at the outset immediately suggest in the case of young animals the

possibility of disease in the umbilical region.

=Prognosis.= The prognosis is grave, it may be said very grave, because

treatment is difficult to apply, and dangerous complications, which

almost always prove fatal, may already have been set up.

One must always distinguish, however, and take into account in forming

the prognosis, the special characteristics of the phlebitis, and weigh

carefully the signs of complication. The fistula should be cautiously

explored, and its depth, etc., noted, while the temperature,

circulation, respiration, etc., should be carefully studied.

=Treatment.= A very important item of treatment consists in regularly

and scrupulously cleansing the region of the umbilicus after the cord

has separated and until the wound has completely cicatrised. The parts

are washed with boiled water and dusted with boric acid, iodoform, etc.

A still better plan, and one that almost certainly guards against this

disease, is to apply an antiseptic dry dressing as soon as the new-born

animal has become dry. This need only consist of a small sheet of

antiseptic cotton wool fixed to the umbilicus by four pitch bandages or

by two pieces of webbing passed over the back. In this way contamination

of the cord and the risk of infection are avoided.

In cases of fully-developed phlebitis the old generation of

practitioners used to recommend local dressings with adhesive plasters,

astringent and vesicant applications, etc. All such methods are useless,

because they only act on a part of the diseased structures and cannot

reach the blind ends of the sinuses. The classic treatment of

suppurative phlebitis also is out of the question.

All that can be done, therefore, is slightly to open up the sinuses and

wash them out frequently with antiseptic solutions, such as boiled

water, sublimate glycerine, carbolic glycerine, etc., afterwards

applying antiseptic dressings. These methods, however, are scarcely

likely to put an end to infectious complications such as suppurative

polyarthritis.

There is no danger in using strong carbolic solution, 3 per cent.

creolin, 4 per cent. chloride of zinc, sulphate of copper, etc. Should

there be several sinuses and should one of them extend in a backward

direction, it is necessary to make certain that no communication exists

between the urachus and the bladder. For this purpose some boiled water

may be injected into the sinus. If a communication exist, this water

will fill the bladder and distend the urachus. The treatment necessary

in this case is similar to that of persistence of the urachus.

It is well in all cases to be guided by the following principle: never

to resort to treatment unless suppuration has occurred and the sinus is

blind. To check suppuration a blister may be applied around the

umbilical region while means are taken to prevent the animal licking the

parts.

Chassaing in 1886 suggested a rather original method of operation which

deserves description. It is founded on the permanent treatment of

sinuses, and consists in introducing a flexible osier stick, a kind of

bougie, enveloped in tow and moistened with the following mixture:

Collodion 3 parts.

Sublimate 1 part.

This is introduced for a distance of 3 to 4 inches into the fistula, and

is fixed to the skin with gutta-percha or pitch. The dressing is renewed

every five or six days, and healing takes place, it is said, in one,

two, or at most three weeks.

It is very likely that if the sinuses were previously cleared and simply

plugged with antiseptics or treated by introducing pencils of salol,

nitrate of silver, sulphate of copper, iodoform, etc., at least as good

results might be obtained.

CHAPTER V.

DISEASES OF THE BLOOD.

SEPTICÆMIA OF NEW-BORN ANIMALS.

The above title is given to that exceedingly fatal disease commonly

known as “white scour,” etc., the mortality in which often rises to 95

per cent.

The disease was studied by Poels in Holland in 1889, Dèle in Belgium in

1891, Perroncito in Italy, Galtier in the centre of France in 1891–92,

and quite recently by Nocard in Ireland in 1901.

It occurs throughout all the breeding districts of France, and in some

parts causes enormous losses, the mortality comprising two-thirds or

even three-fourths of all new-born calves. In certain breeding

establishments in Normandy all the new-born animals without exception

die unless special precautions are adopted.

In foals, septicæmia of the new-born is very rare, because

horse-breeding establishments are much better cared for, and breeding

mares are segregated. In byres, on the other hand, the greatest

promiscuity exists. The disease is equally uncommon in lambs, although

it makes numerous victims in folds which have once been attacked. It is,

however, quite common in young pigs.

=Symptoms.= The development and course of the disease are in certain

respects characteristic.

The disease usually appears within two or three days after birth, and

only in rare cases after the second week. Calves which at birth appeared

vigorous and in good health are found dull on the second day; after the

second or third meal they suffer from diarrhœa, and from that time

refuse all nourishment, lie down as though exhausted, and sometimes die

very rapidly.

Some even perish in ten to twelve hours without showing diarrhœa;

although apparently well at night, they are found dead or dying the next

morning. This is the peracute form.

Most frequently the young creatures suffer for two or three days,

sometimes a week. Appetite is partly preserved; at first the diarrhœa

resembles that due to inability to digest milk, but the fæces soon

become greyish or blackish and very fœtid. The hair of the tail,

quarters and hocks is soiled and matted, the skin irritable and reddish;

the patients lose strength, appear unsteady on their limbs, and develop

rapid respiration and tumultuous action of the heart.

They take little food, become weaker by degrees, and die in a condition

of exhaustion.

Fever, well marked at first, frequently diminishes, and the temperature

may remain normal for several days, falling to 97° Fahr., or even 95°

Fahr., twenty-four hours before death.

This is the commonest form of the disease. It lasts three to five days,

and is always grave.

Cattle-men recognise the disease chiefly by the diarrhœa and loss of

appetite.

Lastly, a third and rarer form occurs during which appetite is

maintained in spite of the diarrhœa. The animals remain thin, develop

poorly, but survive for a month, six weeks or two months. The diarrhœa

diminishes or disappears, but its disappearance is followed by

complications such as broncho-pneumonia, pleuro-pneumonia, endocarditis,

acute arthritis, etc., a fact which led Prof. Galtier to give the

disease the name of “septic pleuro-pneumonia in calves.” These

complications, again, are extremely grave, and generally prove fatal

after a period of varying length. They are due to local development of

microorganisms of the kind which produce septicæmia, and similar to

those described under the name of broncho-pneumonia of intestinal origin

in sucking calves.

They differ, however, as regards their cause, from the primary

affection, and may be due to very varied organisms, the commonest being

those of suppuration. These organisms, in fact, are alien to the primary

disease, and obtain entrance from without, very probably by the

tracheobronchial tract.

In young pigs septicæmia assumes the same forms as in the calf. In lambs

the chronic form seems more frequent than the peracute and the ordinary

forms.

=Causation.= The septicæmia of calves, and possibly of all new-born

animals, of whatever species, is produced by a microbe which flourishes

in the manure and litter of stables, and which Nocard included in the

group of Pasteurella. It can be found in the blood from the moment the

first external symptoms appear until the time of death. During the last

hours, however, the bacterium _Coli communis_ also invades the

circulation in many instances, and if cultures are not made until some

hours after death, the colon bacillus and bacteria of putrefaction are

more particularly discovered.

The microbe of calf septicæmia can be readily cultivated in jelly or in

ordinary liquid media. Injected into the veins of experimental animals,

it reproduces the clinical symptoms, and causes death more or less

rapidly, according to the dose injected.

The virulence of cultures grown in defibrinated calf’s blood seems more

intense, and Moussu has been able to reproduce the clinical form of the

disease by applying to the umbilical cord of a new-born animal a pledget

of cotton wool saturated with such a culture, and covering it with a

dressing. The germs of the disease are spread throughout the byres

through the medium of fæces. When the umbilical cord has become dry,

that is, after the third day, the application of virulent cultures to

the stump no longer causes infection.

=Pathogeny.= The pathogeny of this septicæmia of calves and of new-born

animals is easy to explain.

At birth the young animals fall on the litter, and the umbilical cord

becomes contaminated. The infective agent, finding an excellent culture

medium in the tissues of the cord, at once begins to develop, increases

in enormous numbers, steadily ascends along the cord, and sets up

septicæmia. It grows in the gelatinous Wharton’s jelly and in the

fibrinous plug closing the arteries and umbilical vein, and soon enters

the true circulation. Septicæmia is then fully established, general

disturbance sets in, and with it the diarrhœa by which it is externally

indicated.

It is important to remember, however, that infection occurs most readily

through the medium of the cord, and during the first few days after

birth: it may occasionally be brought about towards the eighth or tenth

day, when the shrivelled portion of the cord falls; in this case its

entrance is effected through the little umbilical wound.

=Lesions.= The lesions are sometimes so obscure that the practitioner

may hesitate to deliver an opinion.

In acute cases, where death occurs in two or three days, or even in ten

to twelve hours, post-mortem examination reveals only increased

vascularity of the serous membranes—the peritoneum, pleura, pericardium,

etc.; and it may be almost impossible to discover anything abnormal in

the cord, for although the clots closing the arteries and veins are

infected, they are neither separated from the walls of the vessels nor

broken up.

On the surface of the urachus, at the base of the bladder, and in the

depths of the peritoneal folds supporting the allantoid arteries

(sometimes also the hepatic vein), unequivocal signs of local ascending

infection may, however, almost always be found, together with intense

injection of the capillaries, little hæmorrhagic spots, and commencing

formation of false membranes, etc.

The infection extends also by the lymphatic vessels contained in these

peritoneal folds, and finally attains the sublumbar region.

When the disease develops less rapidly the peritoneal cavity contains a

certain quantity of blood-stained serosity, as do the pleuræ and

pericardium, whilst vascular engorgement of the serous membranes is

extremely marked. The intestine shows traces of congestion and

inflammation throughout its length, and its contents contain the

specific organism in very large numbers.

Finally, in the chronic forms, the serous membranes and the intestine

seem only slightly attacked, possibly because the lesions have undergone

retrogressive changes. The striking features are the secondary lesions,

such as those of pneumonia, broncho-pneumonia, pericarditis, and abscess

formation in the lung.

Nocard gives the following description of the lesions found during his

investigation of “white scour” of calves in Ireland (_Veterinarian_,

April, 1902, p. 171; see also Prof. Mettam’s paper, _Veterinarian_,

June, 1902, p. 307):—“The lesions found on autopsy vary according to

whether the evolution of the disease has been rapid or slow. One lesion,

however, is never absent—that of the navel and the navel vessels. In all

the calves attacked we found a large umbilicus with hardened coats

enclosing a clot easily broken down, sometimes soft and purulent. In

every case, also, we observed blood suffusions, often very extensive,

along the course of the umbilical vessels and of the urachus, invading

often the posterior third of the bladder. In cases where the evolution

had been rapid we found the lesions of true hæmorrhagic septicæmia. All

the viscera were congested to excess; their surface was studded with

petechiæ, ecchymoses, or subserous blood suffusions. The capillary

network of the peritoneum, pleura, and pericardium appeared strongly

injected. This lesion was especially marked on the epiploon. The

intestine was the seat of intense congestion, especially at the level of

the ‘floating colon.’

“The mucous membrane was thickened, gorged with blood, and friable; the

solitary glands, thick and protruding, were sometimes transformed into a

kind of bloody magma, or they were ulcerated, as in anthrax; the

contents of the bowel were mixed with a large quantity of blood. The

mucous membrane of the fourth stomach was altered nearly to the same

degree; it was studded with interstitial hæmorrhages, especially above

the level of the open edge of its folds. The mesenteric

glands—especially those of the colon—were enormous, gorged with blood,

reddish, and often hæmorrhagic. The mucous membrane of the bladder was

often covered with petechiæ, the urine which it contained was clear and

limpid, but always rich in albumen. [In one sample which was analysed,

the urine contained more than 4 grammes of albumen to the litre.] The

lungs were gorged with blood, like the intestines; sometimes they were

manifestly œdematous, but generally their tissue was still supple,

elastic, permeable, and without apparent lesion.

“In the subacute forms the lesions are much less marked. The mucous

membrane of the intestine is less congested; sometimes œdema of the

submucous tissue exists. The mucous membrane of the fourth stomach is

often punctuated with brownish-red patches, traces of the capillary

hæmorrhages which were produced at the onset of the disease. The

mesenteric glands are swollen, gorged with serum, but not hæmorrhagic;

the liver is large and of a yellowish tint; the spleen is little

altered; the urine always contains albumen; the lungs are seldom quite

sound; they usually contain here and there small diffuse centres of

catarrhal pneumonia, of nodular bronchial pneumonia, or simply of

atelectasis.

“These lesions are more constant and more dense if the animals have

resisted the disease for some time; they then constitute the transition

stage between the simple collapse at the beginning of the disease and

the suppurating lesion of lung disease. The joint lesions when they

exist are very interesting. At the beginning all the periarticular

tissues are infiltrated with a yellowish gelatinous serosity. The

synovial membrane is covered with vascular aborisations of an extreme

richness, which extend on to the articular cartilages. The synovial

capsules are distended by a considerable quantity of thick synovia of a

deep yellow or brownish tint, holding in suspension flakes of fibrous

exudate more or less dense and abundant. When the lesion is older the

synovia is replaced by a thick fibrous exudate, which fills

sacculations, and extends between the articular surfaces. In this case

the lesion appears identical with that of the arthritis seen in

pleuro-pneumonia of sucking calves.”

=Diagnosis.= The diagnosis presents no difficulty, for the development

and acute course of the disease (the majority of patients die within a

week of birth) leave little room for doubt.

This disease is easily distinguished from dysentery in new-born animals,

which appears at birth, as also from simple diarrhœic enteritis; in the

latter disease the symptoms are delayed, sometimes occurring only when

the animals are weaned; moreover, the disease is never so grave as that

now under consideration.

Should, however, the post-mortem appearances seem indecisive, the

diagnosis can be based simply on the high mortality.

=Prognosis.= The prognosis is extremely grave. About 95 per cent. of the

animals attacked die, and among those which survive many show thoracic

complications, that render them useless.

=Treatment.= Treatment of animals already affected is useless, and,

moreover, too costly. Drugs administered through the digestive apparatus

to a large extent miss their mark, because the digestive symptoms are

secondary, primary infection having occurred through the circulation.

The administration of purgatives and internal antiseptics can,

therefore, only prove illusory.

On the other hand, prophylactic treatment is of the greatest value; all

that is necessary is to prevent the umbilical cord from becoming

infected.

The great mortality, which causes such severe loss to breeders, is

simply due to want of proper care of new-born animals. Even in carefully

kept byres the mortality may be high, for the specific agent develops in

litter contaminated with fæcal matter, by lying on which young animals

become fatally infected.

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To check or prevent this septicæmia in breeding establishments, it is

merely necessary to take the same precaution as is taken in dealing with

young children, _i.e._, to apply an aseptic or antiseptic dressing to

the stump of the cord after ligation. As soon as the young animal has

been dried by the mother or by artificial means, a carefully boiled

ligature is applied to the cord at a distance of about 1 inch from the

umbilical ring. The portion of the cord below the ligature is snipped

off, the remaining part is carefully washed with boiled water or boric

solution, and is surrounded with a mass of iodoform wool, kept in place

by a bandage passed over the back.

The cord will shrivel a little less rapidly than it would if exposed to

the air, but will be protected from all infection. The young animal

should be separated from the mother to prevent her from displacing the

dressing by licking the parts.

In a few days all danger is at an end. This method is very simple, and

can be carried out even by the breeder and in an infected byre. Nocard

recommends the use of umbilical dressings containing collodion, and the

practitioner can choose whichever method he pleases.

In grave outbreaks involving large establishments, the byres should be

rigorously disinfected, and it is sometimes well to segregate cows about

to calve in a special byre, from which the calves are not allowed to

pass until the umbilicus is cicatrised.

TAKOSIS: A CONTAGIOUS DISEASE OF GOATS.[4]

Footnote 4:

Annual Report, U.S.A. Bureau of Animal Industry, 1902, p. 354 (Mohler

and Washburn).

This disease has been seen in Angora goats brought from Texas into

Pennsylvania, U.S.A.

=Symptoms.= The disease presents many of the symptoms usually

accompanying a parasitic invasion, and is characterised by great

emaciation and weakness, with symptoms of diarrhœa and pneumonia. In the

early stages of the affection there is usually little to indicate that

anything is seriously amiss with the animal. The first observable

symptom manifested is the listless and languid appearance of the animal,

evidenced by its lagging behind the flock, and is usually accompanied by

a drooping of the ears and a drowsy appearance of the eyes. The pulse is

slow and feeble, and the temperature is elevated slightly at first, but

becomes subnormal a few days before death. The highest temperature

observed in the natural disease was 104·1°, and the lowest, in a

prostrated animal a few hours before death, registered 99·7° Fahr.

Snuffling of the nose, as in a case of coryza, with occasional coughing

is sometimes in evidence.

As the disease advances the animal moves about in a desultory manner,

with back arched, neck drawn down toward the sternum, and with a

staggering gait. Rumination is seldom impaired. The appetite, while not

so vigorous, is still present, though capricious, and the affected

animal shows plainly that the ravages of the disease are rapidly

overcoming the restorative elements derived from the food. The fleece is

usually of good growth, and presents a surprisingly thrifty appearance

when the condition of the animal is taken into consideration. All the

exposed mucous membranes appear pale, and the respirations are

accelerated and laboured. The goats finally become so weak that they are

readily knocked down and trampled upon by their fellows. If picked up

they may move off slowly and eat a little, but within a few hours are

down again, and in this way linger for several days, shrinking to about

half their natural weight, and occasionally bleating or groaning, with

head bent around on the side or drawn down to the sternum. A fluid

discharge from the bowels of a very offensive odour is usually observed

in the last few days of life, but this symptom is not constant.

=Course and Susceptibility.= This disease may assume a subacute or

chronic type, usually the latter. The animal dies of inanition in from

eight days to six or eight weeks. Several owners have reported deaths

after only two or three days of illness, but the goats doubtless had

been affected for a longer period, although not noticed on account of

their mingling in the flock. Many of the animals live for weeks, but

gradually become weaker and more debilitated, finally dying in a

comatose condition. In no instance has the natural recovery of an animal

after once the symptoms of takosis were noticed been observed or heard

of.

The younger goats seem to be the most susceptible to the disease,

although the old animals are by no means immune.

=Pathological Anatomy.= As already indicated, the general appearance of

the carcase simulates that produced by a wasting disease. The visible

mucous membranes are pale and anæmic, while the fleece, which appears

somewhat dry and lustreless, furnishes a shroud for the extremely

emaciated condition, that becomes plainly perceptible on skinning. The

same anæmic condition of the subcutaneous and muscular tissues is

observed on eviscerating the carcases. The lungs in most cases are the

seat of a peculiar diversified inflammation, never of a remarkable

extent. The external appearance of these organs is at times mottled,

caused by a few congested areas, several patches of an iron-grey colour

similar to areas of pneumonia during the process of absorption, and

normal tissue. On section through the reddened patches, a frothy mucus

may exude from the bronchioles, and in one case numerous punctiform

hæmorrhages were observed on the sides of the incision. This tissue,

while not so buoyant as a normal portion would be, nevertheless floats

when placed in water.

The heart in all cases is pale and dull, its tissue soft and flabby,

while inflamed areas, more or less penetrating, are present at times on

the epicardium about the auricular appendages, and at other times on the

endocardium, especially that lining the ventricles. These hæmorrhagic

patches consist of either pure extravasated blood or blood mixed with

serum, which gives them a more diffuse appearance and a gelatinous

consistence. The pericardium is slightly thickened, and usually contains

a small increase of fluid tinged with blood. The liver usually appears

normal, although the gall bladder is frequently distended with

pale-yellow watery bile. The kidneys are anæmic and softened. The cortex

appears slightly thicker and paler than normal, and contrasts strongly

with the darker pyramids. The capsule strips off easily from the

parenchyma of the organ. In one instance several pale areas simulating

anæmic infarcts were observed under the capsule extending into the

cortex, which probably resulted from the compression of the capillaries

by the swollen parenchymatous cells. The presence of albumin in the

urine was detected by the nitric-acid test. The spleen appears atrophied

and indurated, and on section the fibrous tissue far exceeds the splenic

pulp. Attachments by fibrous adhesions may fix the spleen to the

diaphragm or the neighbouring organs. The intestines may contain normal

fæcal matter or semi-fluid fæces of a disagreeable odour. The surface of

the mucous membrane is at times covered with a slimy mucus or plastic

exudate, and the appearance is that of a chronic catarrh associated with

necrosis of the mucosa.

=Bacteriology.= Examination of cultures and slides showed the presence

of a micrococcus, usually arranged in the form of a diplococcus, which

was found in pure cultures from the heart’s blood, spleen, kidneys, and

pericardial fluid, and essentially so in the tubes inoculated from the

other organs.

The specific organism of takosis appears in fresh bouillon cultures as a

spherical or oval micrococcus with a diameter of 0·8 to 1 µ. In these

cultures it is single or in chains of two, three, or four elements, but

most frequently in pairs, as diplococci, with a diameter transverse to

the axis of the chain greater than the longitudinal diameter.

=Treatment: Prophylaxis.= Sudden climatic changes should be avoided as

far as possible, and when shipments of goats for breeding purposes are

to be made which necessitate their transportation over considerable

distances the changes should be made during the months of summer or late

spring, and not in the fall or winter, when the contrast of temperature

will be so much greater.

Angora goats should be provided with stables that are thoroughly dry,

erected upon ground that has perfect natural drainage.

As a third measure of prevention may be mentioned careful feeding.

The segregation or isolation of all affected animals as soon as they

evince any symptoms of the disease will be found a most valuable means

of protection for those that remain unaffected, and a strict quarantine

over all of the diseased members of the flock should be maintained so

long as the disease remains upon the premises.

=Medicinal treatment= has proved unsatisfactory in many of the cases of

takosis to which it has been applied. The best results have been derived

from the administration of calomel in 0.1 gram doses twice daily for two

days, followed by arsenic, iron, and quinine, as follows:

Arsenious acid 1·40 grams.

Iron, reduced 12·00 „

Quinine sulphate 6·00 „

Mix and make into twenty powders, giving one to each adult goat morning

and evening at the conclusion of the administration of calomel. After an

interval of two days this treatment is repeated. In case the diarrhœa

persists, the sulphate of iron has been substituted for the reduced

iron, with beneficial effects.

=Conclusions.= After preliminary investigation, the following

conclusions have been reached:—

(1.) The disease described as takosis has appeared in many parts of

America, but particularly in the Northern States, where it has caused

great loss to many breeders of Angora goats.

(2.) It is a progressive, debilitative, contagious disease,

characterised by great emaciation and weakness, with symptoms of

diarrhœa and pneumonia, and causes a mortality of 100 per cent. of those

affected and from 30 to 85 per cent. of the whole flock.

(3.) From the carcases of numerous animals that have succumbed a new

organism, _Micrococcus caprinus_, has been recovered in purity, and is

presumably the etiological factor.

(4.) This micrococcus possesses pathogenic properties for goats,

chickens, rabbits, guinea-pigs, and white mice, but not for sheep, dogs,

or rats.

(5.) Medicinal treatment was attempted with varying success, while the

immunising experiments thus far conducted (although too few to permit of

any conclusive statement or accurate estimate as to their protective

value) have shown highly encouraging results. When accompanied with

measures of isolation and disinfection, the treatment may prove of great

assistance in the suppression and eradication of the disease in an

infected flock.

BLOOD POISONING (MALIGNANT ŒDEMA) IN SHEEP AND LAMBS IN NEW ZEALAND.

This disease, which occurs during the operations of shearing sheep and

of castrating and docking lambs, is the cause of considerable loss

annually to sheep breeders in several districts of New Zealand. In 1893

J. A. Gilruth, Chief Veterinarian for New Zealand, issued a leaflet

dealing with the disease and the preventive measures to be adopted.

Generally the first thing that draws the owner’s attention seriously to

the condition of his flock is the discovery, in from thirty-six to

forty-eight hours after docking or shearing, of a few dead sheep lying

in various parts of the paddocks. Next morning he finds a few more dead,

and so on for three or four days, when, as a rule, the mortality ceases.

=Symptoms.= In the early stages of this disease the animal seems

listless, disinclined to move about, and, if the sun is shining

strongly, prefers to lie in the shade. If forced to move, the hind legs

are drawn forward with a peculiar stiff, dragging motion, as if there

were no joints. There are slight muscular tremors all over the body,

which become spasmodic as the disease progresses. If the flock be driven

about much, the diseased animal soon shows signs of great fatigue,

ultimately dropping to the ground thoroughly exhausted. The breathing is

fast and painful, being maintained more by a series of spasmodic jerks

than by any regular act. The pulse is quick and weak; the temperature is

very high, registering 106° to 108° Fahr., showing acute fever; the eyes

close, and the whole face is expressive of pain. Gradually the spasms

cease and coma sets in, resulting in death. The scrotum and surrounding

skin right along the floor of the abdomen and between the hind legs

become swollen and black. This gangrenous tissue, when present before

death, can be peeled off without pain to the animal. On post-mortem

examination various conditions are met with. The animals are generally

found to be among the best of the flock and in fairly good condition.

The scrotal and perineal regions in lambs (between hind legs and below

tail) are always, or almost always, gangrenous, this condition extending

along to the floor of the chest, and sometimes implicating the tail.

Many of the muscles, generally those of the shoulders, haunches, and

loins, are dark in colour and infiltrated with a black, watery fluid.

The intestines are generally healthy, though sometimes the peritoneum is

inflamed. The spleen and liver are in the usual condition after death,

due to febrile disturbance. In the chest, either the pleuræ (coverings

of the lungs) or pericardium (covering of the heart) are often inflamed,

with occasionally a fibrinous exudation, causing surfaces to adhere.

=Cause.= In Gilruth’s report for 1900 he demonstrated the cause of blood

poisoning to be a microbe known as the malignant œdema bacillus

(_Vibrion septique_ of Pasteur). This organism, which is found in many

dirty yards, swampy soils, etc., on gaining entrance to the system of

almost any animal by means of a wound, rapidly increases in numbers,

producing gangrene, or death, of the part affected first, and ultimately

the death of the animal.

=Curative treatment= is practically useless.

=Preventive measures.= Destruction of the carcases of animals which have

succumbed to this disease by efficient burial or by fire. Disinfection

of surface soil of yards, etc., by quick-lime. Cleansing of floors and

walls of sheds with strong hot lime wash containing crude carbolic acid

in the proportion of 1 to 50. Disinfection of flesh cuts made by the

shears or the docking or castrating knife. Boiling of docking and

tailing knives before use. Observance of antiseptic applications even

when temporary yards are employed. Sheep and lambs after operation to be

kept in a paddock free from swampy patches.

PIROPLASMOSIS.

Under the title piroplasmosis is included a group of diseases caused by

hæmosporidia, and found in animals of the bovine and ovine species.

These affections are far from having the same importance in temperate as

they have in tropical countries; nevertheless, it is very important to

be able to recognise them.

BOVINE PIROPLASMOSIS.

Bovine piroplasmosis has been described under different names, such as

hæmoglobinæmia, hæmoglobinuria, Texas fever (U.S.A.), tick fever

(Australia), tristeza (Argentine Republic), African coast fever, East

Coast fever, redwater, Rhodesian fever (Cape), and bovine malaria.

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It was first described by Babès in 1888, in animals inhabiting the

Danube Valley, and was termed by him bacterial hæmoglobinuria of the ox.

Afterwards it was well described by Smith and Kilborne (in 1889) under

the title of Texas fever. It was rediscovered in Finland by Krogius and

Van Hellens in 1894; in Sardinia by San Felice and Loi; in Australia in

1895 by Pound; and it has been the object of remarkable investigations

by Koch in South Africa (1898–1904).

[Illustration: $1]

Nicolle and Adil-Bey (1899) state that it exists in a latent form in

European Turkey and Asiatic Turkey; and Lignières (1900), after a series

of researches in Argentina, suggests the final solution of the questions

which it raises.

=Symptoms.= Babès describes it as an acute febrile disease, clinically

distinguished by the passage of blood-stained urine. The urine is

coloured by dissolved hæmoglobin; red blood corpuscles are not found.

Smith and Kilborne, and afterwards Stiles, described two forms: an

acute, rapidly fatal form, in which the _Piroplasma bigeminum_ is found

in the blood of the general circulation, in the spleen and kidneys; and

a chronic form, in which, notwithstanding the absence of clinical signs,

the parasites may be discovered in the blood under the form of

diplococci.

Lignières describes a grave and a benignant form. The grave form is

indicated by dulness, loss of appetite, and considerable fever. In

twenty-four hours the temperature rises to 104° or 105° Fahr., and the

pulse to 100 or 120 per minute, while the respiration is greatly

accelerated.

The urine is of a light-red or brownish-red colour, resembling

coffee-grounds, but it contains no blood corpuscles. The animals die in

from three to eight days with symptoms of asphyxia; but this termination

is not inevitable, and recovery may occur spontaneously. Improvement is

indicated by a fall in temperature, disappearance of the blood-stained

urine, and a return of appetite, together with marked thirst.

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Drs. Smith and Kilborne describe the symptoms as follows:—“The beast

when first observed to be amiss appears to be dull and sluggish, with a

disinclination to move, and hence it is generally found apart from the

rest of the herd. The hair stands erect like that of an animal on a cold

day (a staring coat), the ears hang, and the eyes have a dull and

lustreless appearance. In some cases the animals cease to feed, or

ruminate, in others they continue to nibble at the herbage until nearly

the last, but in a languid, indifferent manner, indicating that they

have little relish for their food, and they fall off very rapidly in

condition. There is generally a dribbling of saliva from the mouth, the

muzzle may appear quite moist during the early stages of the disease,

but it invariably becomes dry and crusty as the disease advances. Later

on the animal manifests a strong reluctance to move, and when compelled

to do so, it walks with a dragging, straddling gait, as if weak across

the loins. In severe cases, when the sick beast is left undisturbed, it

will remain almost constantly in one place, standing with its head

depressed and ears hanging in a drowsy semi-comatose condition, looking

the very picture of complete nervous prostration. Other animals will lie

down the greater part of the time and scarcely move, and when dead the

limbs will be found in their natural position, and the head doubled

round on the shoulder as if asleep. On making a post-mortem examination

of some of these cases the carcase was found to be pale and bloodless,

as if the animal had been bled to death.

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“In other acute cases a twitching and quivering of the muscles will be

observed, especially of those situated in the flank and behind the

shoulder. The pulse and breathing are much quickened, and the animal

will stand and grind its teeth and curl up its upper lip, indicating

great uneasiness and pain. The fæces during the early stages of the

disease are very often soft, with a tendency to diarrhœa, more

especially in transport oxen on the road, but they invariably become

hard as the disease advances; but whether hard or soft, they have

generally a brownish tinge, and often mixed more or less with blood and

mucus. In some severe cases which recover, the favourable crisis is

often ushered in by a salutary diarrhœa.”

In the benign form the animal for the space of about a week shows

indifference to its surroundings, loses its appetite, wastes, and, less

frequently, has slight feverish symptoms, without discoloration of the

urine. The only reason for the belief that this trifling disturbance is

due to piroplasmosis is furnished by examination of the blood, in which

the parasites may be found in very small numbers in certain blood

corpuscles.

Calves seldom take the disease except in the benign form.

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=Lesions.= At first glance the lesions appear to resemble those of

anthrax, but may be differentiated from them in many details.

The skin is covered with ticks or shows traces of their punctures.

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The myocardium appears as if boiled, the spleen is invariably

hypertrophied and two or three times as large as in the normal state.

The kidneys are violet in colour and congested, and the adipose layer

surrounding the kidney is infiltrated with a yellowish serosity. The

urine may present a variety of tints, derived from hæmoglobin. The liver

is often engorged with blood and the gall bladder always distended.

When convalescence sets in, icterus appears; but it is a special kind of

icterus, depending on changes in the hæmoglobin—in fact, a hæmaphæic

icterus. Histological examination of the blood furnishes the explanation

of the disease by revealing the presence of the parasite.

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=Pathogeny.= The parasite is the _Piroplasma bigeminum_, which is easily

demonstrated by drying the blood, fixing it and staining with very weak

methylene blue. The blood is light in colour and pale, and the serum is

tinted by the dissolved hæmoglobin. The blood corpuscles diminish in

number with extreme rapidity while the parasites are developing, and in

twenty-four or forty-eight hours may fall from some six millions and a

half, the normal number, to one million or even to two or three hundred

thousand red blood corpuscles per cubic millimètre.

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This destruction is due to the action of the piroplasmata, as may be

shown by staining with a ·5 per cent. methylene blue or carbolised

thionine. These parasites usually assume a simple pyriform shape, and

two or three may be found in one blood corpuscle. The number of

parasites and infected blood corpuscles is generally in direct ratio to

the intensity of the infection. These parasites are found throughout the

blood, but principally in that of the spleen, kidneys, and mesenteric

veins. They are only abundant whilst the temperature is rising or at the

moment when it reaches its highest point, and they often disappear

before death or convalescence.

The pyriform shape is only temporary, and corresponds to the acute phase

of the disease, but the parasite assumes the round form as soon as

convalescence sets in. This round form gives birth to one, two or three

spherical spores, which are set free in the plasma after the destruction

of the maternal protoplasm, and are able after transference to a fresh

red blood corpuscle to again assume the pyriform shape peculiar to the

grave forms of disease.

The parasite can only be cultivated in defibrinated blood from a

hæmoglobinuric subject, and the cultures do not always yield more than

reproductions of the round form, the pear-shaped form only being

produced with red blood corpuscles in the living animal body.

Regarding the method of growth of the piroplasma in the body and in

cultures, Lignières believes that the parasite may produce two forms of

spores differing in their nature. One, the active spore, has little

resisting power. It soon degenerates outside the animal body, forms

rapidly at the expense of one of the pear-shaped parasites, and may

immediately reinfect another red blood corpuscle. The other, called the

passive spore, is very resistant, and retains its vitality for a long

time outside the body, being produced at the expense of spherical

parasites already withdrawn and incapable of producing the disease.

The form of piroplasmosis at present under consideration is peculiar to

the ox, and none of the other domestic animals or experimental subjects

can be inoculated with it.

Subcutaneous or intravenous inoculation of the ox with 5 to 10 cubic

centimètres always gives positive results when made with blood or active

products, such as the pear-shaped parasites or active spores, but is

ineffectual when the parasites have already begun to retract in order to

form passive spores.

Calves seldom contract more than the benign form of the disease, and do

not die.

In the grave form following experimental infection the temperature

begins to rise between the third and sixth day, and corresponds with a

marked increase in the number of parasites to be found within the red

blood corpuscles. The urine at first becomes albuminous, then

hæmoglobinuric, whilst the red blood corpuscles diminish in number to a

very marked extent, falling from about six or seven millions to one

million, or even a few hundred thousands, in the course of a few days.

The temperature, which may previously have risen to above 105° Fahr.,

suddenly falls, indicating the approach of death.

If an immediate autopsy is made, the spleen is always found to be

enlarged, the intestinal mucous membrane reddish in tint or

blood-stained, and the serous membranes, particularly the endocardium,

covered with petechiæ.

Few or no parasites can be discovered except in the blood from the

cardiac muscle and the kidneys.

The grave form may end in recovery. This end is indicated by the

temperature remaining normal after defervescence, the appearance of

hæmaphæic icterus of an obstinate character, and the progressive return

of appetite.

The disease is usually transmitted by adult and larval ticks carrying

the parasite from infected animals. Lignières has proved that this

transmission occurs through the medium of passive spores, which, though

themselves incapable of producing the disease, become active and

infective in consequence of the local irritation produced by the

poisonous saliva of the ticks.

The pathogeny of Texas fever may be shortly summed up as

follows:—Animals suffering from the disease carry in their blood a

protozoan organism called the _Piroplasma bigeminum_, analogous to the

parasite of human malaria; once introduced into the blood, this organism

remains there in an active condition throughout the animal’s life; it is

transferred to susceptible cattle either within or without the infected

district by the Southern (U.S.) cattle tick _Boophilus annulatus_;

Southern cattle, although carrying the protozoa, are harmless unless

infested by this particular tick: the mature ticks and their eggs

contain the protozoa, and the mystery of certain grounds over which

infected animals have passed being first dangerous, then harmless, and

again dangerous depends on—(_a_) the infestation of the ground with

mature infected ticks; (_b_) the destruction or death of the mature

ticks; and (_c_) the hatching out of new (infected) ticks from the eggs

laid on the ground by the mature female ticks.

Dr. Salmon states that in Texas a successful method of protection is in

practice based on the observations that young cattle do not suffer so

severely as adults, and that the disease always assumes a milder form in

winter. Young animals introduced during the winter are inoculated with

virulent blood. They contract a mild form of disease, and afterwards

resist. In this way the losses, which previously amounted to 90 per

cent. of all freshly introduced stock, have been reduced to about 10 per

cent.

A remarkable and very interesting observation (if absolutely reliable)

deserves to be mentioned, viz., that the ticks develop regularly in the

natural prairie, but do not develop in parts artificially sown with

grass such as lucern, and that when contaminated or diseased animals are

transferred to artificial meadows they do not convey the disease to

other animals already there; the latter are proof against it.

=Diagnosis.= The disease is so typical that it cannot be mistaken for

anthrax. In anthrax the urine is never hæmoglobinuric and very rarely

hæmaturic, and the fæces are sometimes blood-stained, a symptom never

present in piroplasmosis. Anthrax can be transmitted to experimental

animals, but piroplasmosis cannot.

=Prognosis.= The prognosis is generally grave.

=Treatment.= Van Hellens recommends the use of quinine in large doses.

He give 5 drachms in one dose, and repeats it for the next two, three,

or four days.

Lignières says that he has never obtained the slightest success with

quinine, though it is true he has never given higher doses than 2½

drachms.

Attempts have been made to confer immunity by injecting animals with

serum from others which have recovered. Vaccination with the blood of

patients arrived at the period of convalescence has also been tried. The

results, however, have not been very satisfactory.

Lignières has formulated an efficient method of vaccination, of which he

has not yet published the full details, but which appeared by reason of

its simplicity likely to render great service. Nevertheless, his most

recent reports seem to show that vaccination is not always efficacious,

and that in the Argentine Republic alone several varieties of the

disease exist, two being caused by allied but different parasites. The

vaccine used against one variety is powerless against the other. The

problem of vaccination would therefore appear to be much more complex

than in the case where one form only occurs in any particular country.

The immunity arising from attacks of piroplasmosis is in direct ratio to

the gravity of the disease, and according to Lignières’ views this

acquired immunity is due to the secretion by the piroplasma of a

substance which is toxic for the red blood corpuscles. This toxic

substance provokes, as in other diseases, an organic antitoxic reaction.

BOVINE PIROPLASMOSIS IN FRANCE.

Until recent years it did not seem that piroplasmosis occurred in

France. It had been detected in Algeria, although its existence had not

been conclusively proved. Mathis claims to have met with it in the

department of the Loire in 1896 and in the Ain in consequence of the

importation of Algerian cattle, but its ravages were comparatively

trifling.

Having good reason to suspect that certain morbid conditions, known as

_mal de Brou_, might be due to piroplasmosis, Lignières endeavoured to

verify his theory, and discovered that sometimes, but not often, this

disease was mistaken in France for anthrax and _mal de Brou_.

Piroplasmosis in France appears less grave than in America, and is

rarely fatal.

As regards its =symptoms=, it usually develops suddenly with fever, loss

of appetite, acceleration of the pulse and respiratory movements,

suppression of the milk secretion, and the passage of red hæmoglobinuric

urine. In exceptional cases death may occur in from three to five days.

On post-mortem examination a varying number of ticks (_Ixodes

hexagonus_) are found on the skin, the spleen is always increased in

size, and the kidneys are black and hæmorrhagic.

The disease transmitted by ticks, as in Texas fever, seems due to the

presence of a round parasite, different from the well-known _Piroplasma

bigeminum_.

The elucidation of this disease, which occurs towards the northern

frontier of France in the neighbourhood of Maubeuge, calls for further

investigation. It never appears to be very fatal, and it attacks more

especially animals imported into the infected region. A method of

vaccination identical with that used by Lignières against one of the

forms of the American disease may perhaps in the future prove available

against the disease in France. Until then the best =treatment= would

appear to consist in free subcutaneous injection of saline solution and

the administration of evacuants, sulphate of quinine, and laxatives.

OVINE PIROPLASMOSIS.

=Causation.= The existence in France of this disease has not yet been

clearly established, for in the only communication on the subject (by

Leblanc in 1899) the writer seems to have confused the toxic

hæmoglobinuria produced by feeding on decomposed beet pulp with the

parasitic hæmoglobinuria due to piroplasmosis.

In Italy ovine piroplasmosis was described by Bonomo in 1896 under the

title of parasitic icteric hæmaturia of sheep. It is said to be due to a

parasite of the red blood corpuscles (_Amœba sporidium polyphagum_), the

said parasite being of oval form, very refractile, always occupying an

outer position near the free margin of the corpuscle, and sometimes

floating freely in the plasma.

According to Babès, who described it under the name of _gurceac du

mouton_, the same disease appears to occur in the islands and low parts

of the Danube valley.

=Symptoms.= The development of this parasite produces in the patient

loss of appetite and high fever, accompanied by the passage of dark

coloured hæmoglobinuric urine. Icterus is frequently present. The

animals rapidly become exhausted, collapse and die.

On post-mortem examination carried out immediately after death the

spleen is found to be large, the pulp being like wine lees. The liver is

soft and yellowish; the kidneys are soft and black.

The disease is said not to be transmissible by direct transfusion (?).

It would appear that this disease has also been seen in Turkey by

Nicolle and Laveran, near Constantinople, in 1899. The parasites

(_Piroplasma oris_) are round or slightly elongated and occur near the

periphery of the red blood corpuscles. It is to be hoped in the interest

of breeders in localities where this disease rages that Lignières’

method of vaccination against bovine piroplasmosis may prove reliable

and equally applicable in the case of sheep.

DISEASES PRODUCED BY TRYPANOSOMATA.[5]

Footnote 5:

An interesting article and a series of figures on the “Evolution of

the _Trypanosoma Evansi_” were published in the _Jour. of Comp. Path.

and Therap._ for September, 1904, p. 210. The same number also

contained articles on several piroplasmic diseases.

In 1904 Professor Koch delivered an address, from which the following is

a summary, to the Berlin Medical Society regarding his experiences and

observations on diseases produced by trypanosomata in Africa:—

A wide field of study has recently been opened by the discovery of

various pathological protozoa. Three discoveries especially have

directed attention to these special disease organisms—

(1.) Laveran’s discoveries regarding malaria. Ross has shown that the

malaria parasites are carried by mosquitoes (_Anopheles claviger_).

(2.) The discovery of the protozoa of Texas fever by Smith. In this case

ticks (_Rhipicephalus_ (_boophilus_) _annulatus_) convey the disease.

(3.) The discovery of the trypanosoma of the tsetse disease, which is

conveyed by a stinging fly (_Glossina morsitans_).

These discoveries were followed by numerous others indicating protozoa

as causes of disease.

The trypanosomata are morphologically distinguished by the existence of

a flagellum. When fresh blood is examined it is scarcely possible to

overlook the protozoa in the preparation, for attention is at once

attracted by the energetic way in which the red blood corpuscles are

continually being displaced. The peculiar form of the protozoa, however,

can only be detected in stained preparations. Romanowsky’s staining

method is probably the best. Trypanosomata stained by this method show a

fish-shaped body, the front end of which carries a flagellum. The body

of the trypanosoma is coloured blue. At the anterior end may be seen a

red-stained nucleus; at the opposite end a much smaller red spot, which

has been termed the nucleolus, but is more properly described as the

centrosome. From the centrosome a red thread extends along the outer

margin of the body as far as the front extremity, where it becomes

continuous with the flagellum.

The trypanosomata increase by longitudinal fission. The centrosome and

then the nucleus divide, and finally a second flagellum is formed.

Sometimes the young trypanosomata remain connected, producing the

so-called “rosettes.”

The disturbance produced by trypanosomata seldom becomes acute, but

often continues for years. The only sign of disease consists in

ill-defined fever with long intermissions. The destruction of the red

blood corpuscles causes anæmia, the animals or men become weak and waste

away, œdema and sometimes erythema occur at varying points in the body,

and occasionally the lymphatic glands become swollen.

The classical land of the tsetse disease is in the neighbourhood of the

Zambesi. There it was seen and very well described by Livingstone; but,

unfortunately, further investigations have shown that tsetse disease

extends over the whole of Africa.

Whilst the trypanosomata of rats can only be conveyed to the one

species, those of tsetse disease thrive in all mammals, particularly in

the horse, mule, ox, dog, rat, and mouse.

The tsetse organism has been shown to kill both horses and mules, but to

be less dangerous for oxen. A certain relative immunity exists in some

races. As regards the ass, observers are not agreed; Koch failed to

infect it. Sheep and goats are also but slightly susceptible. The

conveyance of trypanosomata from the blood to uninfected animals occurs

through the medium of a stinging fly (the _Glossina morsitans_).

Surra is endemic in the Philippines, Java, and the island of Mauritius.

Koch regards the trypanosomata of surra as strictly analogous with the

parasites of tsetse disease. Horses (and, in India, elephants)

especially suffer from surra. Although the _Glossina morsitans_ does not

occur in India, other stinging flies replace it and convey the disease.

Another variety of trypanosomiasis is _mal de caderas_, seen in South

America, particularly in Argentina and Brazil. It affects horses.

According to Koch, the parasites of _mal de caderas_ exactly resemble

the tsetse and surra parasites. Other observers, however, declare that

the _mal de caderas_ parasites are distinguished from those before

mentioned by their particularly small centrosome. _Mal de caderas_

affects not only horses, but all the other animals which suffer from

tsetse.

Another variety of trypanosoma, the trypanosoma Theileri, is especially

striking on account of its size. It is only found in oxen, and exhibits

a very slight degree of virulence.

Koch divides trypanosomata into two great groups.

The grouping is based on three important peculiarities: firstly, the

morphology of the parasite; secondly, its virulence; and, thirdly, its

relation to the host.

The first group only exists in one species of animal. They have become

so completely accustomed to this method of life that they cannot exist

under other circumstances. Their virulence is slight but constant. This

group comprises the trypanosoma of rats and the trypanosoma Theileri.

The second group (to which all other trypanosomata belong) shows great

variation in virulence and in form. These trypanosomata are not peculiar

to any one species, but may affect dogs, rats, horses, etc. Their

morphological peculiarities also vary according to the animals in which

they are found. Thus, the tsetse parasites when cultivated in the bodies

of dogs and rats become much smaller than usual, and the centrosome

appears near the end; when cultivated in horses the end appears pointed,

and the centrosome lies near the centre; in the pig the parasites lose

their peculiar short flagellum. Their virulence also varies within wide

limits.

It has been found possible, as in the case of bacteria, to modify the

virulence of trypanosomata by successive passages through different

animals. By inoculating dogs with comparatively innocuous trypanosomata

and conveying the disease from dog to dog the virulence is markedly

increased. On the other hand, parasites which prove very virulent for

oxen become much less active for these animals after passages through

rats and dogs. This apparently trifling discovery laid the foundation

for protective inoculation experiments. Parasites of the second group

can also exist in the bodies of almost all mammals.

Koch is of opinion that the parasites of surra in India and of tsetse

disease in Africa are absolutely identical. Laveran, on the other hand,

states that he has protected animals against tsetse, and that they have

nevertheless suffered from surra.

That this in no way disproves the identity of the two parasites is shown

by other experiments.

Koch, whilst in Dar-es-Salaam, made some interesting experiments for the

purpose of discovering a method of protective inoculation. He had found

that the virulence of the ox parasites could be modified. He therefore

inoculated oxen first with these weakened parasites and afterwards with

others of high virulence. All the control animals died while those

treated as above remained alive.

Veterinary Surgeon Schmidt kept these animals under observation, and

reinoculated them from time to time with highly virulent material,

notwithstanding which they were still perfectly well six years after the

first inoculation.

In practising this method, however, the trypanosomata used for the first

inoculation must not be unduly weakened. The method would have appeared

fully successful were it not for the fact that the protected and

apparently quite vigorous animals still suffered from the presence of

parasites in the blood. To extend its use, therefore, meant that one

would not suppress, but would spread the disease. The effect would be to

produce herds harbouring the parasite, which herds, though exhibiting no

signs of illness, would nevertheless in a sense be propagating the

active cause. Further observation has also shown that the protection so

conferred is only relative. Dogs can always be infected with the blood

of such animals. It has long been known in Africa that antelopes and

buffaloes harbour trypanosomata in their blood without showing external

signs of disease.

Another method of protection must therefore be sought, such as

destroying the various stinging flies; but this offers little hope of

success. Koch admits that he sees no method of dealing with them. The

other method is directed against the parasite, and here he seems more

hopeful. The disease can be rooted out by killing all diseased animals

suspected of disease. The line of procedure is indicated by the

experience gained in Mauritius and Java. When surra broke out in

Mauritius almost all the oxen died in two years. In Java the nature of

the disease was early recognised, and all suspected animals were at once

slaughtered or isolated until slaughtered; in this way the disease was

soon stamped out.

LOUPING-ILL.

The close analogy between the convulsive form of the disease described

as “trembling” (which disease is well known in France) and the condition

known in Britain as louping-ill lead us to give here a short account of

the latter condition. For a great part of what follows we are indebted

to articles by Meek and Greig Smith, published in the _Veterinarian_,

Vol. LXIX, Nos. 820 and 840.

=Nature and Symptoms of the disease.= The disease known usually as

louping-ill or trembling has long been of annual and sometimes of

biennial recurrence in certain parts of Great Britain. In these places

sheep farmers look for the appearance about the middle of April, to its

continuation during May, and to its gradual disappearance early in June.

Lambs are most liable, but sheep are also quite susceptible to the

disease, and in both the symptoms are the same. The disease under

consideration is rendered quite distinct by certain well-known symptoms.

Though these have been described in various ways, the disease can be

recognised by the more or less complete paralysis of the body and limbs.

Symptoms may succeed one another very rapidly, or may be spread over

some length of time. The animal at first loses control over the muscles,

which are seen to twitch convulsively. It may fall down and struggle on

the ground, sometimes jumping up again, often to some height. Between

the fits it is often seen to stand trembling. These symptoms are

frequently accompanied by frothing at the mouth. Some such appearances

are the usual onset to the disease, and are followed by a paralysis

which usually affects the hind limbs, but may also include more or less

of the body and the head and neck. The fore limbs are often similarly

paralysed. The affected limb or limbs become cold to the touch. The

paralysis necessarily brings the animal to the ground, though it may be

able to crawl about by the aid of the unaffected legs. When the head and

neck are affected the former is usually drawn to one side, and the eyes

often become oblique. Excitement is greatly increased when the animal is

disturbed. The symptoms, then, in a few words are more or less complete

paralysis, preceded as a rule by fits and trembling.

The small number which recover present “a wry neck, stiff joint, high

back, or other deformity.” During recovery swellings occur at the

joints; these may be pierced with good results, giving a large discharge

of pus. According to Fair, in the _Veterinarian_, Vol. VIII., “these

abscesses usually appear in the neighbourhood of the joints, but

sometimes above the arms, the brisket, or any neighbouring part of the

body.”

While the disease is characteristically a sheep ailment, other animals

are also liable. Swine fed with the carcases or blood of sheep which

have succumbed to louping-ill die with every characteristic of the

disease in a short time. If the carcase has been boiled this does not

occur. Swine will also frequently take the malady if allowed access to

the grass of affected fields. Cattle are said to take the disease, and

in the North Tyne district it is said that if a cow takes louping-ill,

the milk will give the illness to a calf or lamb. One or two cases of

horses being attacked are also reported.

Regarding the infectious character of louping-ill, the following is very

well known. Sheep bred on diseased places are not nearly so liable to

the disease as sheep which have been introduced from unaffected places.

Louping-ill may be introduced into a new place, but in such cases,

unless the importation from affected farms be continued, the malady may

disappear.

=Distribution of the disease.= In Great Britain it is confined to the

North Tyne district of Northumberland and to the contiguous border

counties of Scotland, extending into Kirkcudbrightshire and certain

valleys of Dumfriesshire. It is rare in Berwickshire, common in the

north and west of Roxburghshire and the similar hilly districts of

Selkirkshire and Peeblesshire. It occurs in Ayrshire, to a slight extent

in Lanarkshire, and is found in the western parts and islands of

Argyleshire and Inverness-shire.

Not only is the disease very circumscribed in its distribution as a

whole, but locally in the places mentioned infected and non-infected

spots are pointed out. These may be quite contiguous. The flocks in the

North Tyne district feed up and down the hills in limited “cuts,” and it

is one of the features of the illness that certain “cuts” are very

liable to it, while others, even on the same farm, are just as free. In

many cases the nature of the pasture is such as to suggest to an

experienced man the probability of its being subject to the disease. A

dry and foggy pasture seems best suited for harbouring the cause of the

malady. These infected places have remained wonderfully constant, but a

peculiar feature about them is that some may be very bad for louping-ill

one year, and others bad another year. Of two adjoining farms, one may

be badly attacked and the other mildly, while in the following year the

conditions may be reversed. Districts may present the same

peculiarities. Thus, though the disease is essentially endemic, it is

not absolutely constant in its recurrence. There seem to be certain

circumstances capable of favouring or retarding it.

[Illustration: $1]

[Illustration: $1]

=Lesions.= The chief lesions are localised in the membranes of the brain

and spinal cord, which are congested or inflamed, and contain an

increased amount of cerebro-spinal fluid or a jelly-like, sometimes

blood-stained exudation. Softening and hardening of the spinal cord have

both been observed. Inflammation of the pleura and pericardium, with

fluid or jelly-like exudation, are common; lobar congestion of the

lungs, endocarditis, gastritis, and enteritis have all been described;

some observers have mentioned congestion of the kidneys and liver and

swelling of the spleen. Lesions of the nerve-centres are the most

constant and reliable.

=Etiology.= Depressing and weakening influences of all kinds have been

blamed for producing the disease, but the general consensus of opinion

points in the direction of infection with microorganisms carried and

introduced into the sheep’s system by the common sheep tick or “grass

tick” (_Ixodes redurius_). The following remarks on, and illustrations

of, this parasite are from an article by Mr. Wheeler, of Alnwick

(_Veterinarian_, Vol. LXXIII., No. 867, p. 141).

=Life History of the Grass Tick.= Sheep ticks (which must not be

confused with the sheep-ked, or keb, a wingless six-legged fly,

universal on sheep everywhere) are allied to the spiders. They pass

through four stages of existence: the egg—the six-legged larva—the

eight-legged pupa—and, finally, the eight-legged adult male or female.

[Illustration: $1]

[Illustration: $1]

In each of the three stages of larva, pupa, and adult female, all

species of ticks attack some “host” or animal, either beast, bird, or

reptile, to which they attach themselves by the “rostrum” or beak, and

become greatly distended by suction of the host’s blood. When replete

they fall to the ground—if a larva or pupa, in order to undergo its

metamorphosis to the next stage of its existence, and afterwards seek a

fresh host; if an adult female, to lay its eggs amongst herbage. The

adult male is not capable of distension by suction, though it equally

attaches itself to a host.

After undergoing metamorphoses, grass ticks, with the exception of

males, are light in colour, soft and lethargic, and remain concealed for

some time while recovering strength before seeking a fresh host.

Professor Neumann alludes to the fact that a fresh host is sought by

ticks three several times during their existence.

=The Larva.= When first hatched out from the eggs, which are supposed to

be laid at the roots of coarse herbage, the young ticks are white and

soft, but soon gain strength. Provided the weather is favourable, they

climb up the stems, and, holding by their two posterior pairs of legs,

await the passing of a host, employing their two front legs as insects

use their antennæ.

In this, as in other “free living” stages of their existence, the young

larvæ show great activity, attaching themselves and clinging tenaciously

to any moving object. They appear to be more numerous on the rank rushes

growing in damp, undrained places.

[Illustration: $1]