=Prognosis.= The prognosis is grave. In calves, obstruction of the bowel

by hair balls inevitably causes death, and in sucking lambs the

mortality may be high: as much as 15 per cent. to 20 per cent. according

to the observations of several observers. The mortality occurs about the

age of six weeks to two months, whilst the licking habit may begin

towards the end of the second week.

=Treatment.= Prophylaxis demands that the mothers (whether cows or ewes)

be well fed. An excellent precaution consists in adding to the food a

sufficient quantity of salt and of phosphate of lime (2 drams to 2½

drams of each). This treatment of the mothers is necessary as soon as

the tendency to licking becomes manifest.

In calves the best method of avoiding fatal results is to prevent the

young animals licking one another; and the method now usually practised

on well-managed farms consists in applying a simple muzzle of wicker

work immediately after each meal.

In lambs treatment is more difficult. As soon as the shepherd sees any

tendency to depraved appetite the lambs should only be left with their

mothers whilst being suckled. The flock should be exercised in the open,

and ordinary salt should be placed at a number of points on the ground

occupied by the animals.

COLIC IN THE OX.

COLIC DUE TO INGESTION OF COLD WATER. CONGESTIVE COLIC.

=Causation.= Congestive colic occurs in the stable, in animals which

have been doing heavy work, and, returning in a heated condition, drink

large quantities of cold water. It is commoner when animals have not

eaten for a considerable time, and when, therefore, the stomach is

nearly empty. Under these circumstances chill of the digestive viscera

is direct and immediate.

=Symptoms.= This form of colic occurs suddenly, soon after the water has

been swallowed, and is characterised by violent pain. At first the

animals show uneasiness, stamp, and continually move about striking

themselves in the flank with the feet or horns, swishing the tail, etc.

They refuse food, lie down and rise frequently, and paw the ground.

As a general rule this form of colic lasts from half an hour to one

hour, and terminates in recovery. In some rare cases where death

occurred Cruzel found on post-mortem examination congestion of the

abomasum, and, in a few, congestion of the small intestine, with or

without rupture.

=The diagnosis= is easy, on account of the suddenness of onset, rapid

development and history of the disease, discovered on questioning the

owner or herdsman.

=The prognosis= is not grave. This form of colic generally cures itself.

Nevertheless precautions are required against possible complications,

such as intestinal hæmorrhage and invagination.

The necessary preventive measures are self-evident. Animals returning

from work should not be allowed to drink freely of cold water, but

should first receive a little food and afterwards water at the

temperature of the atmosphere.

When colic has set in, the patient can be walked about. If pain

persists, the region of the abdomen may be dressed with oil of

turpentine, mustard, or similar counter-irritants. The application of

warm clothing is also useful. Finally, in grave cases, a moderate

quantity (three, four, or five quarts) of blood may be withdrawn from

the jugular. The administration of stimulants like wine, alcohol, etc.,

is also indicated.

COLIC DUE TO INVAGINATION.

Invagination consists in the passage of one portion of the intestine

into the next-following portion. When once the condition has been set up

it tends to become aggravated, the invaginated part being drawn further

and further forwards. Invaginations therefore may vary in length between

a few inches and sixteen to twenty inches.

Law states (Vol. II. p. 347) that in cattle and swine invagination of

the large colon is almost impossible owing to the relation of the bowel

with the layers of the mesentery. The anatomical arrangement is opposed

to the formation of invagination, yet this accident is not uncommon in

cattle and swine. The small intestine can be invaginated into the cæcum

or into itself. The cæcum may become invaginated, or it may pass into

the colon or rectum.

Cartwright, _Veterinarian_ (1829), reports a case of invagination in a

bull calf, and Youatt gives particulars of a similar case which was

followed by sloughing and discharge per anum of the intussuscepted

portion of bowel. (See also Möller and Dollar’s “Regional Surgery,” p.

328.)

=Causation.= This variety of colic is due to a number of somewhat

obscure causes. In a general sense we may say that anything which

increases intestinal peristalsis increases the risk of invagination. The

accident may follow intestinal congestion, but is most frequent in

animals suffering from intestinal worms, or in animals used for heavy

work. Under the influence of violent tractive efforts the peristaltic

movements are stimulated, and the intestine being in an oblique position

on a plane inclined backwards, the contracted portion may slip into the

dilated section behind it.

[Illustration: $1]

Invagination may also occur without any apparent cause, even in animals

standing in the stable.

=Symptoms.= The attack always occurs suddenly, develops rapidly, and is

of an extremely grave character.

Colic comes on while the animal is working, moving about, or resting,

according to circumstances, and at first resembles that due to

congestion. It afterwards becomes very violent; the animals paw, stamp,

show great uneasiness, throw themselves violently down, and rise

suddenly, only to again lie down as before. The face expresses anxiety,

suffering and depression; the tail is often kept lifted, and efforts are

continually made to defæcate, mucus being passed. By passing the hand

into the rectum the invagination may occasionally be discovered.

Colic persists with great intensity for ten to twelve hours, interrupted

only by rare periods of calm. At the end of this time, however, it may

suddenly disappear, and the animal may fall into a semi-comatose state.

This indicates the onset of necrosis in the invaginated section, the

painful reflexes no longer being transmitted to the sympathetic system.

The disappearance of colic is sometimes regarded as a sign of

improvement, but this improvement is illusory. From this time onwards

the animals stand stolidly, obstinately refusing both food and drink. If

they lie down, it is with great care. Palpation of the right side of the

abdomen is painful, and the animal actively resents it. One of the most

important and constant signs at this stage is the absence of defæcation,

due to obstruction of the intestine, which is occluded. The animals may

survive for ten, twelve, or even fifteen days (see also Möller and

Dollar’s “Regional Surgery,” _loc. cit._). The invaginated, necrosed

portion may even be passed with the fæces, and recovery may occur, the

continuity of the intestinal tube being secured by the adhesion of the

serous surfaces; but such spontaneous recoveries are exceptional.

Usually after a few days death results from peritonitis.

Occasionally, trifling invaginations may become reduced spontaneously,

Diarrhœa, with the passage of blood-stained material is then seen for a

time, a sign which alone at this stage would justify the diagnosis of

invagination.

=Diagnosis.= The intensity of the colic and the absence of defæcation

for several days afterwards, justifies the diagnosis of invagination.

Purgatives then remain without effect. In addition, rectal exploration

offers a valuable means of diagnosis. The last portions of the intestine

are found absolutely empty, and the arm when withdrawn is found to be

covered with viscous blood-stained mucus, resulting from the

sero-sanguinolent exudate, due to compression of the blood-vessels.

In cases of this kind accompanied by the above-mentioned symptoms

abdominal exploration by the rectum should always be practised, but it

rarely gives exact information. The hand, when passed towards the right

flank, may sometimes reach the invaginated part, which conveys the

impression of a cylindrical swelling. The invagination, however, can

rarely be reached. If the operator is successful, he will find that as

he displaces this cylindrical mass or attempts to grasp it, the animal

shows signs of exaggerated sensitiveness.

=The prognosis= is of exceptional gravity. Apart from the rare cases

where the invaginated portion becomes necrotic and is eliminated, death

is inevitable. Unless an operation is performed, septic peritonitis may

develop about the fifth or sixth day.

=Treatment.= The only treatment consists in surgical intervention. Some

practitioners have recommended giving large doses of purgatives with the

idea of causing changes in the neighbourhood of the invaginated part;

but such treatment presents little chance of success. The same is true

of the administration of large doses of olive oil, either in the form of

draught or of enema.

Siebert attempted reduction by generating CO_{2} from soda bicarbonate

dissolved in water and diluted HCl, injected successively per rectum. In

time fæces and CO_{2} escaped, and the patient recovered. Siebert claims

to have cured by this method a cow with invagination of five days’

duration; but the effect of his treatment may be doubted, as afterwards

a portion of bowel was found in the cow’s dung.

When diagnosis is certain, the only treatment that can be recommended

consists in performing laparotomy followed by enterotomy. One cannot,

however, operate in all cases, nor do all cases offer the same chances

of success. If the invagination is situated in the first portion of the

small intestine, and is hidden beneath the circle of the hypochondrium,

intervention is out of the question, but if it has been detected by

rectal exploration in the last portion of the intestine, operation may

prove successful. Only in cases of the latter description should it be

attempted.

Laparotomy is performed in the right flank according to the usual method

(see Möller and Dollar’s “Regional Surgery,” p. 313). After opening the

peritoneal cavity, the invaginated loop of intestine must be sought. It

is not always easy to discover amongst the mass of intestines present,

but can be recognised by its hardness and by the congestion of

neighbouring parts. After withdrawing it through the abdominal opening,

the operator may then proceed by one of several methods.

(1.) Some authors recommend grasping the two ends, drawing them apart,

and thus reducing the invagination. The actual manœuvre is not

difficult, but even when unattended by accident or tearing of the

intestine it is by no means always followed by recovery. Although the

intestine may not appear gangrenous externally, necrosis often occurs

eventually.

This method should only be practised during the first twenty-four hours

after the appearance of colic, and even then one must always bear in

mind the possible consequences just mentioned, and the chances of

rapidly fatal septic peritonitis.

(2.) The second method consists in removing the invaginated portion of

intestine. It is best to apply bichromatised catgut or silk ligatures to

all the arteries which pass from the mesentery into the loop to be

removed; after which the loop itself may be simply divided an inch or

two above and below the invagination, in order to be quite certain that

one is operating on healthy tissue, the divided ends being held

meanwhile by an assistant. The intestine is afterwards sutured with a

fine needle and bichromatised catgut or boiled silk. The form of suture

will be found described in Dollar’s “Operative Technique.” It may be

valuable to test the efficacy of decalcified bone tubes for uniting the

ends of the intestine.

The operation is long, delicate and difficult, and it is imperative not

to infect the abdominal cavity during its performance. To prevent this

the liquid and solid materials present in the bowel may be thrust

upwards and downwards away from the diseased part before the section is

made; and in this way the wound and the operator’s hands are preserved

from infection. The intestine should be kept closed during the

application of sutures by means of flat clamps cautiously applied. In

their absence the ends may be held by an assistant, whose hands should

previously have been carefully disinfected.

(3.) In cases where the serous coats of the two portions of bowel

constituting the invagination are to some extent adherent, another

operation of a less perilous character may be performed. This consists

in liberating the invaginated part by means of longitudinal incision,

without previously disengaging the parts, and without resection. The

invaginated (external) portion of intestine is divided longitudinally;

the gangrenous part immediately becomes visible, and may be removed. The

operator has then only to suture the longitudinal wound, an operation

which is much easier and demands much less time than any circular

intestinal suture whatever. These operations must not be attempted

except in response to the express wish of the owner, who should be fully

informed of the dangers to which they expose the animal; for after the

second day of invagination local peritonitis has often developed and one

is then operating on injured or infected tissues, in itself a very

unfavourable modifying condition. The current formula that “the

operation was very successful” is not accepted in veterinary practice

when the patient dies three or four days afterwards. From the economic

standpoint it is better to slaughter animals of any value, for unless

secondary peritonitis has occurred, and the animal is not feverish, the

meat is fit for consumption. “Volvulus,” or twist of the intestine, is

said to be almost unknown in cattle, though Reichert records a case of

volvulus of the ileum.

COLIC AS A RESULT OF STRANGULATION.

The symptoms of this colic differ very little from those of the

preceding with which they are often confused. But in regard to its

causation the condition is essentially different.

=Causation.= Strangulation of the intestine in the ox may be produced in

several different ways: by the passage of a loop of intestine through a

tear in the epiploon, through the diaphragm, mesentery, broad ligament

of the uterus, the serous layer surrounding the spermatic cord, etc., or

by strangulation of an intestinal loop by fibrous bands resulting from

chronic peritonitis, etc. Of these various causes, the three principal

may here be described:—

(1.) Tearing of the mesentery. As a result of mechanical violence the

epiploon or mesentery becomes fissured, and the peristaltic movements

cause a loop of intestine to pass through and become fixed in the

fissure. If the opening is narrow, as is usually the case, the base of

the intestinal loop, riding on the lower lip of the slit, becomes

constricted by the margins of the opening through which it has passed.

[Illustration: $1]

(2.) In pelvic hernia a loop of intestine passes between the spermatic

cord and the walls of the pelvis. The fissure in this case is in the

serous fold which supports the large testicular arteries and the vas

deferens. The fold is often ruptured during castration, especially

during the practice of “bistournage,” in consequence of traction

exercised on the cord.

(3.) Pseudo-ligaments and fibrous bands due to chronic peritonitis.—In

local, subacute or chronic peritonitis false membranes may become

organised, forming fibrous cords or folds connecting the

parieto-visceral or inter-visceral surfaces. If by accident a loop of

intestine insinuates itself beneath one of these fibrous bands, the

passage of digestive material is first impeded and then stopped. The

intestine becomes engorged, and symptoms of strangulation soon follow.

=The symptoms= appear suddenly, and are similar to those of

invagination. They consist of very acute colic, which disappears after

ten to twelve hours.

The peristaltic movements drive the semi-digested food, whether liquid

or gaseous, towards the lower (strangulated) end, from which it cannot

escape. It therefore distends the herniated loop and sets up intestinal

engorgement. This constitutes the first stage of strangulation, and is

accompanied by severe disturbance in the local circulation. The mucous

membrane of the intestine becomes swollen and infiltrated, so that it

alone soon fills the entire neck of the hernia. Necrosis of the loop of

intestine is then only a matter of time.

=The diagnosis= of colic by strangulation is difficult. The condition

cannot often be recognised at an early stage, and may easily and

excusably be confused with invagination. Only in rare cases will rectal

and abdominal examination enable one to detect a pelvic or mesenteric

hernia.

=The prognosis= is even graver than in cases of invagination. Intestinal

hernia progresses very rapidly, necrosis soon sets in, and is followed

by fatal consequences if the condition be not relieved.

=The treatment= is exclusively surgical. As a general rule, whenever

colic is recognised as resulting from strangulated hernia, it is

immediately necessary to perform laparotomy in the right flank, and

after having discovered the cause of strangulation, to divide the

mesentery, epiploon, serous fold supporting the testicular cord, or

accidental fibrous bands, so as to free the herniated loop and avoid

necrosis. If necrosis already exist, the intestine may be resected,

exactly as in invagination.

DISEASES OF THE STOMACH.

In ruminants diseases of the gastric compartments are numerous, and,

although they have been recognised since the earliest times, much

remains to be discovered concerning at least some of them. This fact

results from the imperfect state of our knowledge concerning the

essential phenomena of gastric digestion in ruminants. Digestion really

consists of a number of different acts—some mechanical or neuro-motor,

some chemical; in addition to which must be reckoned the phenomena of

sensation, concerning which patients cannot give any information.

The mechanical phenomena, consisting in the constant movement of

ingested material through the different compartments, rumination,

eructation, evacuation towards the intestine, etc., are well known to

us; and a careful examination of diseased animals enables us to estimate

the importance of changes in them.

On the other hand, the chemical phenomena are little understood. It has

hitherto been considered that the rumen, reticulum, and omasum are only

simple diverticula, with mechanical functions, and that the abomasum is

the reservoir in which the chemical changes take place. Another view,

which is perhaps not altogether justified, presupposes that the chemical

transformation of the food in the abomasum takes place as in other

animals, and in particular as in man, in whom the chemistry of gastric

digestion has been the object of extremely careful research by certain

French and other pathologists. We do not believe (for reasons too long

to be explained here) that the gastric digestion of ruminants, or even

of herbivora in general, can be identified with that of omnivora.

The nature of the food being totally different, the chemical reactions

in the stomach and intestines are also different; in proof of which we

need only cite the single fact that ptyalin is absent from the saliva.

Straw and oats are not digested in the same way as a mutton cutlet.

But even supposing that the broad outlines of physiological action are

the same, nothing has hitherto been discovered in veterinary surgery

respecting possible variations in the chemical processes taking place in

the stomach during different gastric diseases; and it appears not

improbable that in this direction causes might be discovered which

veterinary practitioners have hitherto sought elsewhere. Excess or

insufficiency of hydrochloric acid, and variations in the quantity of

the organic acids, play so important a part in the theory of gastric

pathology in man, that it is scarcely surprising to find similar ideas

recurring in the pathology of domestic animals. The correctness of these

views remains to be proved; and without wishing actually to classify

dyspeptic conditions as in man, we may assert that diseases described

under other names stand in direct relation to variations in the gastric

secretion or to disturbance of gastric movements—_e.g._, simple chronic

tympanites, which, without a doubt, is often a neuro-motor dyspepsia.

The classification we shall adopt in studying the diseases of the

gastric compartments is, therefore, extremely simple. In the first

series we shall consider sudden, accidental, and temporary forms of

indigestion, and in the second series, acute or chronic forms of gastric

inflammation.

INDIGESTION.

GASEOUS INDIGESTION.

Gaseous indigestion, also described as indigestion of the rumen, is

characterised by the rapid accumulation of gases (chiefly carbon

dioxide, carbon monoxide, and marsh gas), due to fermentation in the

upper part of the rumen. It is common in oxen and sheep, and has

received the names of mephitic indigestion, acute tympanites, meteorism,

etc. It occurs during or immediately after feeding.

=Causation.= Numerous causes have been invoked to explain the sudden

occurrence of gaseous indigestion.

The most important is the particular condition of the animal at the

moment when it has been attacked. For if external influences alone were

responsible, there is no reason why all the animals of a given herd or

flock, or of a particular stable, which are under similar conditions as

regards feeding, etc., should not be affected in the same way.

That the external causes cited (cold, excessive heat, stormy weather,

etc.) may affect different animals differently and unfavourably is

beyond doubt. But the temporary morbid condition of the animal itself is

the essential condition to the development of indigestion.

In all probability the animal has in every case been more or less

unwell, except in those attacks of indigestion resulting from

progressive poisoning during the course of a meal, such as occur when

toxic plants like belladonna, veratrine, colchicum, poppies, tobacco,

hemlock, etc., have been eaten. In such temporary abnormal states

movement of the rumen is partly abolished, or at least is markedly

retarded, and, as a consequence of vaso-motor disturbance, the mucous

membrane is probably not so abundantly covered with mucus nor so freely

irrigated with secretion, as usual. Under these conditions, if the

animal, which may appear perfectly well, is allowed to partake of soft,

wet, fermentescible food, gaseous indigestion is very likely to develop.

Cultivated grasses, like lucern, sainfoin, clover, and especially

grasses grown on artificially manured fields, are regarded as

particularly liable to cause gaseous indigestion. This conclusion seems

justified by experience, particularly by the fact that young shoots or

young, tender after-growths are very liable to fermentation.

This exaggerated tendency to fermentation of tender grasses has even

been held exclusively responsible for indigestion, and the cessation of

peristalsis in the rumen has been considered a secondary phenomenon, due

to distension.

Whether atony of the rumen be the primary condition and abnormal

fermentation secondary or inversely, whether fermentation be primary and

atony secondary, is not of importance; for either view may be adopted

without altering the results, and without the theory being invalidated

by the objection that other animals subjected to similar influences had

not contracted the condition.

We have already drawn attention to the importance of the condition of

the animal’s health for the time being. Digestive peristalsis being

diminished, eructation, admixture of food in the rumen, and its onward

movement being impeded, fermentation proceeds rapidly. As a consequence

the rumen becomes distended, and, cause and effect changing places, the

distension in its turn arrests peristalsis, which had previously only

been checked.

Local chills, produced by ingestion of food covered with rime,

hoarfrost, or simply with dew, may favour gaseous indigestion; such

conditions retard or suspend the peristaltic movements by direct local

action, and probably by producing vaso-motor disturbance of the mucous

membrane. In very rare cases chill has an undeniable influence, either

by provoking general vaso-motor disturbance, which reacts on the

secretions, or neuro-motor trouble. Gaseous indigestion is not uncommon

in animals living on dry winter food, which have been moved from their

ordinary quarters and sent on railway journeys or to fairs, etc. As a

general rule this form of indigestion is commonest in spring, when the

transition from dry winter food to grass, etc., has not been carefully

effected. It is also frequent during stormy weather in full summer.

Marked barometric changes seem to have an influence on the general

health, and particularly on the nervous system, thus favouring organic

fermentations.

=Symptoms.= The earlier symptoms of indigestion escape observation, but

they soon begin to develop rapidly, and are then very easy to follow.

They always exhibit the same characters, developing, however, with more

or less rapidity in different cases. Soon after they commence feeding

animals appear to experience special discomfort, which causes those at

grass to stop grazing; even when stabled they stop feeding. From this

time they show eructation, repeated yawning, restlessness, and some

anxiety.

In a quarter of an hour, or less, the left flank begins to project, both

laterally and vertically, so that eventually the walls of that part of

the abdomen may project above the transverse processes of the lumbar

vertebræ. The right flank also becomes swollen, as a consequence of the

intestine being thrust out of position. The animal very rapidly shows

general disturbance; the nostrils are dilated, the mucous membranes

congested, respiration becomes rapid, and asphyxia threatens. The

respiration soon becomes panting, for the distended rumen paralyses the

diaphragm and compresses the lungs. To ease respiration the animals open

the mouth, extend the neck, and stand with the front limbs spread apart;

but this fails to prevent dyspnœa becoming more intense and asphyxia

imminent.

The heart beats more rapidly, the superficial veins appear swollen, and

the mucous membranes cyanotic. The rhythmic contractions of the rumen

can no longer be detected by manual examination of the left flank; and

on auscultation one neither hears the liquid nor the rolling sound, but

only exaggerated crepitation. Finally, there is marked tympanitic

resonance on percussion.

In cases of very grave tympanites the gaseous pressure in the interior

of the rumen appears to stop the crepitation sound. The animals soon

become unable to walk or even to move, suddenly fall to the ground, and

die rapidly from asphyxia.

The rapidity with which gaseous indigestion develops varies greatly.

Sheep and oxen may die from tympanites, within an hour or even half an

hour of their arrival in the field; but more frequently the symptoms

develop slowly, only becoming alarming after some hours and continuing

for twelve or even twenty-four hours without causing death.

As a rule, the gas is voided by a series of eructations which empty the

rumen, and recovery follows; but when distension is extreme eructation

cannot occur, and gaseous indigestion then ends in asphyxia and death.

=Lesions.= It might be imagined that this form of indigestion would only

appear when the rumen contains a large quantity of food; but, in point

of fact, the rumen often contains very little.

On post-mortem examination the rumen is found to contain an enormous

quantity of gas, which, when collected and submitted to analysis,

reveals approximately the following composition:—Carbonic acid, 74 per

cent.; carburetted hydrogen, 24 per cent.; sulphuretted hydrogen, 2 per

cent.; nitrogen, traces. The composition of this mixture varies within

certain limits, according to its origin; but carbonic acid always

predominates.

Lungwitz, after elaborate experiments with different foods kept in

closed vessels at the body temperature and with similar agents fed for

days as an exclusive aliment to oxen provided with a fistula of the

rumen for purposes of collection, found carbonic dioxide the

predominating gas in all cases, though the proportion varied with the

nature of the food.

Marsh gas varied from 16 to 39 per cent., being especially abundant in

cases of abstinence. Hydrogen sulphide was found only in traces. Oxygen

and nitrogen were present in small amount, and were attributed to air

swallowed with the food. In fermentation the oxygen may be completely

consumed.

The abdominal organs, particularly the intestine, are congested, as a

result of impediment to the venous circulation. The thoracic organs

exhibit the lesions of asphyxia.

=Pathogeny.= Death is due to carbonic acid poisoning, brought about in

two different ways—viz., progressive asphyxia, caused by inability to

inflate the lungs, and absorption of carbonic acid gas from the rumen;

by virtue of the laws of diffusion, part of the gas contained in the

rumen passes into the blood.

=The diagnosis= is always very easy, and even farm servants may

recognise the condition.

=The prognosis= varies, according to the rapidity with which the disease

develops. In rapid cases, where the condition is fully established in

thirty minutes to one hour, asphyxia may be threatened from the

beginning; but in others, _e.g._, when the attack follows consumption of

dry food, tympanites may develop slowly, only attaining its maximum

intensity after a considerable lapse of time. In general one may say

that tympanites is grave in proportion to the rapidity with which the

gas is generated.

=Treatment.= From the prophylactic point of view, it is necessary to

avoid suddenly changing animals from dry to green food; the transition

should be effected by giving mixtures of dry and green food.

Curative treatment comprises a large number of methods.

The latest, and one of the most practical, consists in massage of the

left flank. The open hand is applied to the left flank and sharply

pressed directly downwards, care being taken not to injure the parts.

This manipulation excites reflex action, awakens the dormant

contractility of the rumen, and leads to restoration of peristaltic

movement. The gases pass into the omasum and abomasum, or in many cases

make their way into the œsophagus. The sudden impulses sometimes cause

food to be returned into the mouth, eructation recommences, and the gas

accumulated in the rumen is partially and progressively evacuated. This

manipulation is often practised in breeding districts, particularly in

the case of sheep, in which the disease occurs with the same characters.

The shepherd fixes the animal between his legs, and, thrusting the

extended fingers of either hand into the flanks, makes sudden, sharp

movements, which again set up eructation and get rid of the excess of

gas.

In Germany cold douches are often applied to the flanks. These excite

vaso-motor action and reflex peristaltic movements, which result in

eructations and in the evacuation of the rumen. But this is not a very

practical method, and necessitates arrangements which seldom exist on

sheep farms.

The action of massage may be completed by administering stimulants like

wine, alcohol, or infusions of such aromatic plants as cummin, fennel,

peppermint, camomile, etc. These act first of all mechanically, by

clearing the terminal portion of the œsophagus. Furthermore, they

stimulate the mucous membrane of the rumen, causing reflex peristaltic

contractions, and, as a consequence, circulation of the partly digested

food; finally, the majority of them arrest fermentation.

With the latter object, ether and assafœtida are also given. The use of

these drugs, however, entails disadvantages, and if the animal has

finally to be slaughtered renders the flesh unfit for consumption.

The giving of absorbents is probably most widely practised. The ammonia

which many of them contain absorbs carbonic acid, thereby diminishing

the pressure of gas contained in the rumen, and therefore the distension

of the first gastric reservoirs. Unfortunately this action is only

temporary, and if the drug is given in too concentrated a form, the

mucous membrane of the mouth, of the œsophagus, and sometimes even of

the rumen and reticulum, may be irritated and inflamed, producing

lesions of stomatitis, pharyngitis, œsophagitis, contraction of the

œsophagus, etc., which after recovery from the acute condition may

gravely affect the animal’s general health. A further drawback is that

the flesh rapidly acquires an ammoniacal odour.

Perhaps the best internal treatment consists in administering purgatives

such as hyposulphite or sulphate of soda or sulphate of magnesia, in

doses of 10 to 20 ounces, according to the animal’s size, or, in the

case of pregnant animals, in small frequently repeated doses. These

check fermentation, and so arrest the evolution of gas, whilst by their

purgative properties they excite contraction of the gastric reservoirs

and cause eructation.

None of these methods of treatment, therefore, should be used

exclusively, but all may be utilised as auxiliaries to mechanical or

surgical measures, and all should be preceded by the use of the probang

and puncture of the rumen.

The first of these operations, the technique of which scarcely requires

description, is often of little value; for the solids and liquid

contents of the rumen being permeated with gases, rise as a fermenting

mass into the upper portions of the rumen, and continually obstruct the

open end of the catheter, so that very little gas escapes.

Puncture of the rumen is much more effective and easier to perform. The

owner himself often operates with an ordinary pocket knife, sometimes

introducing a couple of fingers or a short length of elder-wood tube

into the wound thus produced.

The incision should be made at one stroke, for any hesitation may cause

the wall of the abdomen to recede from the rumen, which lies immediately

below. Should gas escape under the skin, emphysema, which often extends

to the loins and along the quarters, may be produced, and may be

followed by diffuse subcutaneous suppuration, resulting from pyogenic

germs entering the subcutaneous tissue.

Large quantities of gas escape from the puncture, sometimes with such

force as to drive out the canula. The flow of gas then ceases. In other

cases the tube becomes blocked; because, as the pressure within the

rumen diminishes, the gases dissolved or mixed with the partially

digested food are freed, and the whole contents of the rumen become

converted into an aerated, bubbling mass. Liquid or semi-liquid

materials may be ejected to some distance, or may pass between the skin

and the muscles, or between the walls of the rumen and the abdomen,

producing various complications, like necrosis, abscess formation, etc.

Such accidents can be avoided by exercising firm pressure with the

fingers on the tissues surrounding the canula.

Even when the rumen has resumed its normal size recovery is not certain,

and may not occur for several hours, or even several days, afterwards.

The patients should therefore be kept under observation for some time,

and it is usually best to leave the canula in place for one or two days,

and to put the animal on low diet.

Necrosis of aponeurotic tissues, fistula formation, and local

peritonitis only occur if the instrument is dirty or is introduced in a

wrong direction.

IMPACTION OF THE RUMEN. INDIGESTION AS A RESULT OF OVER-EATING.

In this condition the rumen is over-distended with food. The symptoms

are principally due to abnormal fermentation, the peristaltic action of

the rumen being in abeyance, and the food failing to pass towards the

omasum and abomasum. Rumination is generally suppressed.

The disease usually follows change of diet. When the diet has long been

restricted, as occurs during years of bad harvests, and animals are

afterwards set at liberty in rich pastures, they eat greedily, distend

the rumen with large quantities of green fodder, and set up all the

necessary conditions for this form of indigestion. Similar results

follow when gluttonous animals are freely supplied with rich food.

Working oxen also suffer if withdrawn from work and fed with roots,

beetroot refuse, brewers’ grains, or other manufacturing residue for the

purpose of fattening. These materials can only be absorbed in moderate

quantity, and the large amount of water, etc., they contain is apt to

disturb the animal’s digestive powers, while owing to its fine state of

division such food cannot be returned to the mouth for secondary

mastication, and rumination therefore remains incomplete: the food

accumulates in the rumen, distending and eventually paralysing it. This

is a common result of feeding on semi-liquid pulp, which in order to be

ruminated should be mixed with rough forage.

Insufficiency of drinking water is another and more frequent cause,

especially during the winter, because the ox-herd or cowman is often too

lazy to give a regular and sufficient supply unless water is laid on in

the stable itself. The dry food becomes compacted into a mass, which

cannot be returned to the mouth for rumination. Moreover, less saliva is

then secreted, and Colin has shown that rumination is impossible when

the parotid ducts are ligatured.

=Symptoms.= As may readily be imagined, the symptoms vary, according to

the quantity and digestibility of the food swallowed. In the first place

the appetite falls off: animals suffering from commencing indigestion

only take part of their food; later on appetite ceases, and with it

rumination. Trifling colic sets in, resembling that due to congestion,

and is indicated by unrest, switching of the tail, lifting of the hind

legs, slight groaning, moving from side to side, and lying down and

rising at short intervals. The animals seem oblivious of their

surroundings, anxious, and at times semi-comatose.

When the case has been neglected for several days the animal may

masticate without having any food in the mouth, and may attempt to

eructate and to regurgitate food; but such attempts always fail. It then

absolutely refuses food, and animals which have eaten large quantities

of green forage may show tympanites. If called in at this period of the

disease the veterinary surgeon finds nothing positive except signs

referable to the digestive apparatus. By methodically examining the

digestive tract, and in particular the stomachs, one discovers during

palpation of the left flank that the rumen is distended. This is

characteristic. By deep palpation it is even possible to detect marked

resistance and a certain characteristic firmness resulting from

accumulation of food. The percussion sounds over this region are dull,

and pressure causes pain, as though the rumen and peritoneum were

inflamed. When the open hand is laid flat on the rumen and thrust

downwards, no peristaltic movement can be discovered. Finally, on

auscultation the normal sounds, including crepitation, fermentation, and

rolling sounds are all absent.

There are no well-marked general symptoms. Respiration and circulation

are hardly accelerated, nor is the artery particularly tense.

=Course and Termination.= The course of the disease varies, and the

condition may be divided into two forms, acute and chronic. The first

develops in a single day, and may cause death by the same mechanism as

acute tympanites—_i.e._, asphyxia or carbonic acid poisoning; the other

continues for five, ten, or even twenty or thirty days, according to the

promptitude with which treatment is undertaken.

In protracted cases, however, the indigestion itself ceases to be as

important as the complications. Sometimes spontaneous recovery occurs,

the food passing away towards the intestine, or even being vomited,

though the latter conclusion is rare. Recovery may also follow from

treatment. If the disease is neglected it may become complicated with

gastro-enteritis.

=The diagnosis= is not very difficult. Indigestion resulting from

impaction is distinguished from acute tympanites by its less rapid

course and by the less marked distension of the rumen (in this case due

to solid food), and from acute gastro-enteritis by the varying degree of

fever which accompanies the latter condition.

=Prognosis.= The prognosis is always grave, even in cases of acute

indigestion resulting from eating green food.

In this case gaseous indigestion occurs as a complication, and

necessitates immediate intervention. The other forms may rapidly yield

to proper treatment, or, in spite of every care, may give rise to

prolonged complications.

=Lesions.= On post-mortem examination of animals which have died of

complicated forms of the disease, we find certain lesions peculiar to

gaseous indigestion associated with impaction of the rumen.

If death has followed the consumption of root pulps, we see signs of

poisoning. As a consequence of prolonged stagnation of food in the

rumen, there follows an exaggerated organic fermentation, whose products

are absorbed through the stomach or intestine and pass into the

circulation.

These various fermentations, which may be of the lactic, butyric, and

even putrid order, produce changes in the mucous membrane of the rumen;

wide tracts of the epithelium may be shed, exposing the corium, and

producing enormous ulcerations, which in certain cases implicate the

entire inner surface of the rumen.

=The treatment= must be varied, according to the cause, symptoms, and

immediate complications. When the disease is of an acute type, such as

that produced by over-gorging with lucern and green food, it is best to

proceed as in gaseous indigestion, _i.e._, to puncture the rumen and

give frequent large doses of purgatives until the stomach and bowels

have been freely unloaded. The animals should then be kept for some days

on small quantities of easily digested food, and should be allowed

lukewarm, mucilaginous drinks.

When tympanites and impaction occur simultaneously, immediate surgical

intervention becomes necessary, and gastrotomy may then be performed by

a very simple method.

Two loops of cord are passed around the abdomen, one behind the

hypochondriac circle, the other in front of the angle of the haunch.

Assistants placed on the right side draw these loops tight, so as to

immobilise the left flank. A bistoury is then thrust directly through

the walls of the abdomen and rumen. As a consequence of the pressure

exercised by the ropes, if not of the pressure of gas itself, the food

material contained in the rumen is often expelled in a powerful stream.

As the superposed tissues cannot very readily change their mutual

relations, the author of this suggestion claims that there is little

danger either of infectious materials passing into the subcutaneous

connective tissue, or of peritonitis; but this rude treatment can only

be resorted to in cases of extreme urgency, and it appears by no means

without danger.

Injections of 10 to 15 centigrammes of pilocarpine and 5 to 10

centigrammes of eserine are also useful.

When impaction of the rumen assumes a less acute form, moderate doses of

purgatives may be given and repeated daily, or twice a day, until the

peristaltic action of the rumen is restored and resumes its normal

rhythm. In certain cases, however, recovery is only apparent. The food

in contact with the walls of the rumen breaks down, and passes away into

the abomasum and intestine, while appetite returns. The animals then

resume feeding, and some days afterwards show all their former symptoms.

Low diet should therefore always be continued for some time.

In spite of treatment, or in consequence of treatment being too long

delayed, no improvement may follow. The ingested food is not expelled.

Putrid fermentation results, auto-intoxication sets in, and the

temperature rises to 40° or 41° C. Unless gastrotomy is performed death

is then certain.

This operation should be undertaken whenever the fever rises to 40° C.,

and two-thirds of the contents of the rumen removed. The rumen should

not be completely emptied, as there is danger of collapse of its walls.

Complications in the region of the wound can be avoided by drainage.

If the operation succeeds, the patients must be placed on very low diet

or on milk for some days, and should be given lukewarm farinaceous

drinks, and a little hay of good quality to excite rumination. In old

milch cows this operation is seldom followed by a satisfactory recovery.

Apart from the loss of milk, the animal loses condition, refuses to

feed, and gradually succumbs to exhaustion.

IMPACTION OF THE OMASUM (THIRD STOMACH).

=Definition.= “A form of indigestion, of which the prominent feature is

the drying and impaction of the ingesta between the folds of the third

stomach. It may seem to be a primary disease, but in very many cases it

occurs as a result of some acute febrile or inflammatory affection.”

(Law’s “Veterinary Medicine,” Vol. II. p. 123.)

=Synonyms.= Dry murrain, clew-bound, fardel-bound, stomach staggers,

grass staggers, vertigo, chronic dyspepsia, chronic indigestion.

=Causes.= Torpidity of the omasum, suppression of salivary secretion,

with absence of “waves of liquid floating the finely divided food from

the mouth or rumen to third stomach, are prime conditions of desiccation

of the contents.” The third stomach, like the first and second, has no

provision for liquid secretion, and depends for its supply on constant

flushing by swallowed fluids. Therefore, if feeding and rumination are

arrested and salivary secretion is suppressed, and if movements of the

rumen and resulting overflow into the third stomach are checked, the

ingesta of the third stomach, compressed between its folds, becomes

drained of liquid and converted into a powder or dry mass. All febrile

and inflammatory affections tend to this end, and more or less drying,

with impaction of the contents of the omasum, is a constant feature in

such cases. But in the majority of cases this condition is to be looked

on as a secondary or subsidiary affection, and the real disease must be

sought elsewhere.

The explanation of the susceptibility of the third stomach in

constitutional troubles has been sought in the source of its

innervation. Electric stimulation of the vagus rouses the movements of

the first and second stomachs, but not those of the third. Action of the

third stomach is excited by stimulation of the spinal cord, and of the

sympathetic nervous branches going to the ganglionic cells in the walls

of the omasum (Colin and Ellenberger). Its nerve supply coming from a

different source, derangement of its function may occur independently of

antecedent disorder of the first or second, and its motor supply coming

from a source so closely related to the vaso-motor centres, perhaps

affords some explanation of the connection of disorders of the omasum

with febrile and inflammatory diseases.

Food is an important cause. Impaction of the omasum is a winter

disease—the time of dry feeding. Dry, fibrous, innutritious fodder, and

scarcity of water contribute to its production. It attacks cattle in

spring or autumn on pastures in which fresh grass grows among the dead,

dried, or withered stems of a previous growth. It occurs when stock are

fed on corn or corn stalks (maize stalks) affected with smut or ergot,

or on cereals or grasses similarly damaged, and in both cases especially

when the water supply is deficient or restricted.

Sheep and goats, which habitually drink little, suffer less than do

cattle, which drink freely.

=Other causes.= Fermented foods, microbian ferments and their products,

which tend to induce torpidity of the omasum, fever, and lessened

secretion of saliva, with diminished supply of liquid from mouth or

rumen.

Pericarditis, by causing vascular stasis in the omasum, may induce

torpor and impaction.

Lead poisoning paralyses action and favours impaction. Finely divided

food stuffs—meal and bran—eaten greedily, may pass in quantity directly

into the omasum and induce impaction. “The most acute and fatal forms

occur in connection with a sudden change from dry to rich, luscious,

green food in spring, the unwonted stimulus giving rise to general

irritation of the whole gastric mucosa, with disordered and impaired

function of all four stomachs, but especially of the third. Such cases

are usually congestive and inflammatory, and the suspension of the

gastric movements is a grand cause of impaction. In such cases, too, the

brain or spinal cord, or both, are seriously involved, and the early

death is preceded by torpor, paralysis, violent delirium or convulsions,

following largely the type of acute lead poisoning.” (Law, _loc. cit._)

=The symptoms= depend on the degree of impaction, and vary from simple,

irregular, or suspended rumination to severe gastric and nervous

disorder. The less acute cases are marked by failure to re-establish

regular rumination or partial convalescence from fever or inflammation.

The fever subsides, but the appetite remains capricious, the muzzle dry,

eyes dull, spirits low, and breathing accelerated; the condition is

sometimes accompanied by moaning. Slight tympanites may appear, and the

contents of the rumen may feel solid, the mouth hot, clammy, and fœtid.

The bowels are constipated, the fæces small in quantity, hard, covered

with mucus or blood-streaked, and containing particles of undigested

food; in other cases diarrhœa may set in, to be followed later by

constipation. Alternations of constipation and diarrhœa may be repeated

again and again. Exploration by pressure of the closed hand over the

omasum will give an impression of solid resistance. There may be slight

shivering, the ears and limbs are cold, the hair is erect in patches,

dry and lustreless.

In cases occurring independently of previous disease, diarrhœa may be

the first symptom observed, the malady being preceded by local

irritation and congestion; but this soon gives place to constipation or

diarrhœa and the symptoms above mentioned. The animal is found lying

apart on its left side, with its nose in its right flank, the pulse and

breathing quickened, the eyes congested; expiration is accompanied by a

grunt. The patient walks with its back arched and dragging its limbs.

The appetite may continue, but only in an impaired and irregular form,

and as rumination ceases grinding of the teeth becomes common. The

secretion of milk is diminished or arrested, emaciation advances day by

day. Fœtid eructation may be a marked symptom. This form may last from

ten to fourteen days, and merge finally into paralysis of the hind

limbs, drowsiness and stupor, or delirium and convulsions.

“In more acute cases (from sudden access of green food, change of water,

or ingestion of irritant plants), the affection partakes more or less of

the nature of congestion or inflammation of the viscus (omasitis), and

may run a rapidly fatal course” (Law, _loc. cit._). The animal is seen

apart from the herd in a characteristic recumbent position, the eyes are

red and glassy, the eyelids semi-closed, the patient shows much

drowsiness and stupor, but when raised may still feed in a sleepy,

listless manner. The bowels are loose or confined, the pulse and

breathing accelerated, the right hypochondrium is firm and tender, and

the sound of fermentation absent or subdued over the omasum. Soon

nervous disorder appears, the eyes glare wildly, the animal seeks relief

in motion—sometimes in a straight line, sometimes to one side—and being

blind and unconscious of obstacles, may fall into pits or ditches, knock

against trees, fences, gates, or buildings, and continue pushing against

resisting objects, breaking its horns or teeth; and otherwise sustaining

injury through violent muscular contractions.

=Course.= Chronic cases may continue indefinitely, with symptoms of poor

health, impaired digestion, and gradual loss of condition. After death

the omasum may contain dried food which the animal consumed several

months before the attack.

In cases ending in early recovery there occurs abundant diarrhœa, “the

fæces are mixed with flattened, dark, solid, and polished masses, the

impacted ingesta from the omasum. Tympany subsides; movement in rumen

and omasum and rumbling in bowels can be heard. Appetite returns.”

(Law.)

=Diagnosis.= The condition of the pulse and respiration, and the

grunting with expiration may lead to confusion with pneumonia.

At first there is no fever, tenderness is confined to the right flank;

there is an absence of pulmonary crepitation, of pleural effusion, and

of movement in the rumen and omasum. Signs of gastric and intestinal

disorder can be detected.

=Lesions.= The omasum is gorged—it may be twice its normal size—solid,

resistant, almost stony. The spaces between the leaves are packed with

dried food, which, when removed, carries a layer of epithelium from the

mucous membrane. (This (layer on contents) is not inconsistent with

health.)

The rumen contains ingesta packed in masses, more or less offensive from

putrefaction.

The abomasum is empty of food, but contains much mucus. Its mucous

membrane is congested.

The small intestine is red in places, empty and collapsed.

The larger intestine contains a quantity of dry, glistening pellets, and

much mucus.

=Treatment= follows the lines of impaction of rumen, though the response

is usually less certain, and always slower. Flax-seed tea, several

bucketfuls per day, will often succeed.

Epsom and common salts, with sol. ammoniæ, excite thirst; liquids should

be supplied freely.

In obstinate cases, and in absence of gastric or cerebral congestion, 20

croton beans, or 20 drops of croton oil, may be added to the purgative.

Nux vomica stimulates the nervous supply. Enemata may be given freely.

Other remedies, stimulating contractility and secretion, are: Eserine,

1½ grains; veratrine, 1 grain; barium chloride, 10 to 15 grains; or

pilocarpin, 3 grains, hypodermically.

The patient may be days or even a week without alvine discharge and

recover.

If fever and symptoms of gastric congestion appear, a blister may be

applied to the right side over the omasum.

Nervous symptoms, such as dilated pupils, blindness, congested mucous

membrane, hot horns and ears, drowsiness or excitement, are combated by

applying cold water or ice to poll, etc.

When free action of the bowels is restored, laxative diet, roots

(pulped), green food, plenty of common salt, and free access to drinking

water should be prescribed.

During convalescence a course of tonics, including nux vomica, is

advisable to help in restoring normal gastric functions.

ABOMASAL INDIGESTION.

Primary indigestion in the abomasum appears to be rare in adults, for

until the present time no one has given a sufficiently characteristic

description of this disease to enable it readily to be recognised. On

the other hand, it is to be presumed, although final proof has certainly

not been furnished, that in cases of gaseous indigestion, or of

impaction of the rumen, the abomasum, whose physiological action is

predominant, must simultaneously suffer.

Primary abomasal indigestion, on the contrary, is common in young

animals before weaning, so that the condition has been given the name of

“milk indigestion.” It could not very well be otherwise, for the

abomasum is the only one of the gastric divisions which in ruminants is

active during the first few weeks of life. At this period it is larger

than the other gastric reservoirs; and the rumen, the reticulum, and the

omasum do not undergo great development till weaning begins.

=Causation.= Milk indigestion attacks young animals, under varying

conditions.

In animals suckled by the mother the disease rarely occurs, but yet when

the mothers are good milkers, like the Flemish, Norman, Jersey, and

Holland breeds, and when there is too long an interval between the

feeds, calves, which are naturally greedy, and in addition are hungry,

are apt to take too large a quantity of milk—in fact, they often gorge

to the fullest possible extent. Owing to its over-distended state the

abomasum either fails to secrete sufficient of the rennet ferment

necessary for coagulating the milk or secretes an insufficiently active

ferment. The first stage of digestion remains incomplete, giving rise to

so-called “milk indigestion.”

When the cows are employed in ploughing, etc., or in drawing carts, not

only are the calves fed at long intervals, but the milk is not always of

proper chemical composition even in the udder. As a result of work,

fatigue, over-exertion and irregular feeding, the cow’s yield of milk

for the time is less digestible than the normal supply, or may even

prove irritant to the calf’s stomach. Milk indigestion is thus set up.

When the cows are fed on factory waste, like beetroot-pulp or brewers’

grains, toxic or irritant products may even find their way into the

milk, which then irritates the little creature’s abomasum and produces

gastric indigestion. Just as in the production of congenital alcoholism

in man, the young animal is then ingesting, unknown to those responsible

for its well-being, chemical substances which produce various

pathological changes.

But milk indigestion is commonest of all in calves fed by hand. The food

usually given is a mixture of milk from the previous night, and skim

milk or even butter milk. It contains lactic ferments and various

microbes, some capable of producing toxic principles.

When swallowed and brought directly in contact with the mucous membrane

these cause abomasal indigestion.

=Symptoms.= Soon after feeding, the little animal appears dull and

somnolent, and shows moderate abdominal pain, suggesting trifling colic.

This stage is soon followed by nausea; the breathing and the heart’s

action become rapid, vomiting efforts are made, and finally milk, in the

form of firm or partially softened curds, depending on the time which

has elapsed since the last feed was taken, are vomited. The quantity

ejected varies. Pressure over the right side of the abdomen produces

pain, and tympanites of the abomasum may sometimes be detected on

percussion.

The sensitiveness and gaseous inflation are confined to the middle and

lower zone of the hypochondrium. Soon after vomiting the animal begins

to improve. The patient seems brighter, relief is very marked, and in

some cases proves permanent; but more frequently a certain degree of

depression persists, the mouth emits a sourish odour, and for a time the

appetite remains poor. This temporary irritation of the abomasum has a

tendency to become permanent; or even to extend to the intestine, in

which the conditions appear more favourable to the development of

microorganisms than do those in the stomach. Indigestion then becomes

complicated with diarrhœic enteritis.

=The diagnosis= presents no difficulty.

=The prognosis= is not serious, provided that the young animals are

carefully attended to; but such complications as diarrhœic enteritis may

become very grave if neglected.

=The treatment.= To prevent recurrences:

(1) The periods of feeding should be regulated;

(2) The cows should not be worked, or should be worked as little as

possible;

(3) Mixed milk, or milk which has already undergone lactic or other

fermentation, should be avoided.

If the calves must be reared by hand, the mixed milk should at least be

boiled or relatively pasteurised by heating to 70° or 80° C., and the

buckets used for feeding should be kept scrupulously clean. These

precautions become absolutely necessary when diarrhœa exists amongst the

calves. Curative treatment consists in placing the animals on low diet

for two or three days after the attack of indigestion, or in giving them

boiled milk diluted with from one-half to two-thirds of boiled water.

The addition of a mild saline purgative like sulphate of soda, in doses

of one-half to three-quarters of an ounce, usually ensures a cure.

Infusions of lime-tree flowers, peppermint, camomile, etc., may

advantageously be used to replace boiled water in diluting the first

foods.

ACUTE GASTRIC INDIGESTION IN SWINE.

=The causes= comprise putrid food, swill, spoilt turnips, potatoes,

apples, succulent vegetables, frozen food, and the admixture of caustic

alkaline powders (used in washing table dishes) with the swill.

Indigestible matters—hoof, horn, hair, bristles, tree bark, etc.—when

not rejected by vomiting, cause gastritis and indigestion. Lastly,

medicinal substances and poisons, paint and lead, sometimes produce the

disease.

Among the symptoms may be mentioned dulness, arching of the back,

standing with the feet brought together, erection of the bristles,

hiding under the litter, grunting, uneasiness, shifting from place to

place, tenseness of the abdominal wall, borborygmus; these may be

followed by diarrhœa and recovery. Speedier relief is afforded by

copious vomiting of irritant matters.

=The treatment= should commence with the free administration of emetics.

To combat alkaline poisoning vinegar may be given, followed by a

laxative. Prophylaxis calls for greater care in feeding.

CHAPTER V.

ACUTE INFLAMMATION OF THE GASTRIC COMPARTMENTS.

RUMENITIS—RETICULITIS—GASTRITIS.

=Causation.= Acute primary inflammation of the first gastric reservoirs,

viz., the rumen and reticulum, is not common. It sometimes accompanies

such infectious disorders as foot-and-mouth disease, gangrenous coryza,

etc., but then constitutes an added phenomenon which should be studied

along with the original disease itself. Rumenitis or reticulitis may

however follow the ingestion of irritant foods or plants, of very hot

liquids, and more frequently still of unskilfully compounded medicines.

In such cases the mucous membrane is directly attacked, and pathological

congestion, infiltration, and desquamation may follow, or even vesicles

and ulcerations may rapidly be formed.

=Symptoms.= Inflammation of the rumen or reticulum is announced by loss

of appetite, suspension of rumination or of regular peristalsis, slight

tympanites, and particularly by excessive sensitiveness to palpation.

This sensitiveness is general, but is more specially marked in the left

lower third of the abdominal cavity, and in the retro-ensiform region

which corresponds to the position of the reticulum. Moderate fever is

present.

These symptoms, which indicate the gravity and intensity of the

inflammation, may persist, become aggravated, provoke vomiting from the

rumen, and leave as a legacy motor dyspepsia, or even more serious

consequences. On the other hand, they may progressively diminish and

disappear for good.

=Lesions.= The lesions comprise hyperæmia of the walls of the rumen and

of the mucous membrane, extensive local exfoliation of epithelium, and

sometimes true ulceration of the mucous membrane.

=Diagnosis.= The diagnosis is based on the exceptional sensitiveness of

the gastric compartments on palpation, and also on the history, provided

reliable information can be obtained.

=Prognosis.= The prognosis should be reserved, because it is never

possible to foretell whether acute lesions may not give place to chronic

disease, which, though apparently unimportant, may terminate in grave

consequences.

=Treatment.= Owing to their local action demulcent drinks and teas are

indicated. Cooked food is useful, because it makes little demand on the

digestive powers; steamed hay and farinaceous substances are given, both

on account of their nutritious qualities and of the slight local

irritation they cause when swallowed.

Lukewarm drinks and saline laxatives, such as the sulphate of soda, and

carbonate of soda or Carlsbad salt in small doses of 1½ to 2 ounces,

seem most useful in combatting the reflex atony of the digestive

compartments.

=Inflammation of the omasum=, like that of the rumen and reticulum,

occurs as a secondary phenomenon in conditions like rinderpest, Texas

fever, foot-and-mouth disease, anthrax, and gangrenous coryza (malignant

catarrh); but primary inflammation is much rarer even than that of the

rumen and of the reticulum.

This is accounted for by the deep position of the omasum, which is thus

sheltered from external violence, early contact with irritant foods and

from the effect of chills, etc. It can only become inflamed by the

prolonged action of irritant food and drink, which have already produced

lesions in the rumen and reticulum; or as a consequence of the prolonged

stagnation of dry food in cases where animals have been deprived of

water.

Under these conditions inflammation of the omasum develops slowly, and

from the clinical point of view is identical with what was formerly

known as obstruction of the omasum. Obstruction or impaction is probably

much rarer than has been stated, in so far at least as it constitutes a

primary condition, for in the great majority of cases it is consecutive

to impaction, inflammation of the rumen, or inflammation of the

abomasum. Obstruction of the omasum, which was formerly invoked in all

doubtful and ill-defined cases of digestive disturbance, seldom occurs

as an isolated disease.

It has been suggested that the omasum, being supplied with nerves solely

by the sympathetic system, and provided with a relatively weak muscular

coat, was more susceptible than the other reservoirs to the reaction of

abdominal reflexes, and therefore more subject to inflammation,

indigestion and obstruction. We do not hold that view, because, as a

result of its general situation and the position of its orifices of

communication, this compartment is easily able to expel its contents so

long as they are liquid. Its function appears chiefly to be to complete

the trituration of food after rumination.

We do not consider that inflammation of the omasum never occurs, for we

are well aware of the contrary, and that the inflammation assumes a

subacute course and is accompanied by stasis of the semi-digested food

between the mucous leaves which partly fill the cavity. We simply wish

to emphasise the view that the condition is not a primary and isolated

inflammation.

=Symptoms.= The symptoms are always vague and very difficult clearly to

define.

Inflammation of the omasum is indicated by relative loss of appetite,

marked thirst, general atony, and diffuse and vague sensitiveness in the

inferior half of the right hypochondrium (zone of the asternal ribs).

There are no pathognomonic symptoms.

Obstruction has also been described as accompanied by loss of appetite,

constipation, the passage of black, coated, fœtid and sometimes

blood-streaked fæces, symptoms of chronic tympanites with fœtid

eructations and sometimes vomiting. These sometimes accompany

hydrochloric acid dyspepsia, a form of chronic gastritis, and, from our

standpoint, the stagnation of food in the omasum is only secondary. We

therefore interpret the facts in quite a different manner, and believe

that only by a rational and physiological interpretation of the symptoms

observed can one diagnose the condition.

=Diagnosis.= The diagnosis of inflammation of the omasum can only be

made by a process of exclusion; and although we are admittedly dealing

with a condition secondary to disturbance of the rumen and reticulum, or

on the other hand consecutive to inflammatory states or to modifications

in the secretion of the abomasum (dyspepsia), the diagnosis does not

present insuperable difficulties.

=The prognosis= is only grave when the primary acute or chronic

conditions of the other gastric compartments are serious.

=The lesions= comprise abnormal vascularity of the mucous membrane and

desquamation, and even gangrene, of the leaves. The partially digested

food is not passed on, becomes dry and hard, and in time aggravates the

local condition.

=The treatment= does not essentially differ from that of other gastric

inflammations. The object to be attained is to evacuate as completely as

possible, not only the omasum, but all the gastric reservoirs, for which

purpose one may freely administer demulcent drinks—linseed gruel, bran

mashes and lukewarm liquids containing laxatives. At first such

alkaloids as arecolin and pilocarpine may be subcutaneously injected to

ensure energetic and speedy evacuation.

Later on slightly stimulant aromatic infusions, like infusions of sage,

peppermint, hyssop, thyme, etc., stimulate the functions of the stomach

and hasten the return of normal conditions.

ACUTE GASTRITIS.

The term “acute gastritis,” sometimes “gastro-enteritis,” is used in

bovine pathology to indicate inflammation of the abomasum. If this

inflammation is confined to the superficial epithelial layers it is

defined as superficial catarrh of the abomasum; if, on the contrary, it

extends to the deep epithelium of the gastric glands and to the mucous

corium, it is termed deep-seated gastritis.

Clinically it is impossible to make these distinctions. We simply

recognise degrees of gravity, and only in this way can one diagnose

acute gastritis, phlegmonous gastritis, ulcerative gastritis, etc.

=Causation.= The abomasum frequently becomes inflamed as a consequence

of irritant foods, apart altogether from lesions of the rumen or

reticulum, the mucous membrane lining the abomasum being so much more

delicate than that of either of the two first compartments.

Irritant plants, parasites, acid drinks, very cold water, certain acid

or toxic industrial residues like mouldy brewers’ grains, fermented

vegetable pulp, decomposed beet, etc., and mouldy or spoilt forage of

any kind may all produce acute gastritis.

Intense feeding—_i.e._, feeding with farinaceous materials, with large

quantities of beans, roots, peas, given regularly—may also cause

gastritis by overtaxing the functions of the organ. Frozen or fermented

roots and sudden changes in feeding produce similar results. Chills have

also been blamed, but it is probable that they only act as favouring

causes.

=Symptoms.= It is necessary to consider these very carefully in order to

arrive at a correct diagnosis.

Inflammation of the abomasum is attended with moderate fever, diminution

in appetite, irregularity in rumination and some tension of the rumen,

without, however, true tympanites.

At first the bowels are constipated, but in time fœtid diarrhœa sets in.

Examination of the digestive apparatus on the left side and in the right

posterior abdominal region reveals nothing abnormal, but pressure over

the lower portion of the abdomen and along the cartilages of the right

hypochondriac region produces, on the contrary, well-marked pain. This

region corresponds to the position of the abomasum.

The conjunctiva appears reddish yellow, as in most visceral

inflammations.

Some authors have described attacks of extreme excitement, but these are

no more pathognomonic than is grinding of the teeth, which is a constant

symptom, or the metallic sound noted on auscultation of the rumen. This

sound occurs in all cases of inertia of the rumen, and indicates

distension and emptiness of the viscus (acute peritonitis, chronic

adhesive peritonitis, inflammation of the reticulum as a consequence of

the presence of foreign bodies).

Dull colic and groaning are not uncommon. Finally, Thierry and others

have all mentioned an alliaceous smell of the eructations as

pathognomonic.

Acute gastritis develops regularly in ten to fifteen days, after which

the symptoms diminish and disappear, giving place to normal health. In

grave cases, despite proper treatment, acute gastritis more frequently

ends in a chronic condition, finally leading to gastric atrophy, and the

insufficient secretion of hydrochloric acid, with all the consequences

of these conditions. The glands of the stomach degenerate; the secretion

becomes abnormal and dyspepsia is set up.

=Diagnosis.= The diagnosis is rather difficult, for the condition is

very apt to be confused with primary dyspepsia, or with inflammation of

the gastric compartments. It might also be mistaken for acute enteritis

of the first part of the small intestine; but as gastritis is very often

complicated with duodenitis, such a mistake is without serious

consequences.

=Prognosis.= The prognosis is grave, not because death is a frequent

termination, but because the disease very often leads to chronic

incurable lesions.

=The lesions= consist of congestion of the vascular network of the

mucous and sub-epithelial coats, serous infiltration of the corium and

submucous connective layers, desquamation, and later in excessive

proliferation of the epithelium.

When the inflammation is deep seated the epithelium of the gastric

glands becomes swollen and cloudy, and undergoes a kind of atrophic

degeneration. In very grave cases, petechiæ, superficial capillary

hæmorrhages, and slight ulceration may be noted. The mucous folds are

always thickened and infiltrated.

=Treatment.= In cases of gastritis or acute gastro-duodenitis moderate

bleeding (three to four quarts) and local stimulation were formerly

recommended. This practice certainly has its advantages, provided it is

not pushed to excess. Sinapisms give good results, but as they must be

left in position for a considerable time, it is often better to apply

vesicants over the lower right hypochondriac region. At first purgatives

are useful, because they unload the digestive tract, arrest the organic

fermentation which results from stagnation in the movement of food along

the alimentary tract, and diminish the tendency to intoxications or

infections.

At a later stage small doses of laxatives and bicarbonate of soda should

be given daily, the diet being of an emollient character, and consisting

of milk, starchy or farinaceous foods, and small quantities of good hay.

Linseed, bran, cooked grain, decoctions of pellitory, barley and various

cereals may also be administered with advantage.

CATARRHAL GASTRITIS IN SWINE.

=Definition.= Inflammation of the gastric mucosa, with muco-purulent

discharge.

=The causes= comprise irritants, fermented or putrid swill, decomposed

food, excess of brine, alkalies (washings from table dishes, hotels,

etc.), gastric parasites.

The condition occurs also in hog cholera, swine plague, rouget, etc.

The chief =symptoms= are: Inappetence, vomiting, uneasiness, colic,

constipation or diarrhœa, fever, stiffness, tense and tender abdomen,

arched back, frequent grunting, limpness of the tail. Sudden vomiting

may bring about a rapid recovery.

=Treatment= calls for a complete change of food, which may include

freshly cooked roots, linseed or meal, butter milk, boiled milk, etc.

As an emetic 30 grains of ipecacuanha may be given. Constipation can be

relieved by a dose of calomel or jalap. If diarrhœa is persistent small

doses of grey powder should be given, and to combat the irritation of

the gastric mucous membrane bismuth subnitrate is also useful.

The piggery should be cleansed and disinfected, and the litter

frequently changed.

ULCERATIVE GASTRITIS.

Ulcerative gastritis (ulcer of the abomasum) is recognised after death,

but hitherto it has been impossible to so clearly identify the symptoms

as to permit of diagnosis during the animal’s life. It has been found

after death in adults and in calves (Ostertag).

=Causation and Pathogeny.= The cause of gastric ulceration is decidedly

obscure, though we know that certain forms occur during infectious

diseases like cattle plague, foot-and-mouth disease, gangrenous coryza,

and as a consequence of certain direct local infections; other forms

result from the administration of drugs; and finally some are of

secretory origin.

In human medicine at the present day there is a tendency to refer the

development of round ulcer and ulcerative gastritis to the secretion of

an excess of hydrochloric acid. Probably the same cause may be at work

in domestic animals, but the proof has not yet been given.

With regard to the pathogeny, the theories of embolism or of thrombosis

of capillary vessels find favour with few authorities at the present

day. Yet these explanations are logical enough, for if we prevent

physiological irrigation of any given part, it is possible to conceive

that ulcer formation may follow from auto-digestion, _i.e._, from the

simple action of the gastric juice on a surface which is no longer

protected.

The theory of microbic origin has been advanced; but although it may be

accepted in relation to the intestine, where the most varied organisms

abound, it is scarcely so applicable to the stomach, in which acidity is

always very marked and must exercise a very energetic antiseptic action.

In sucking calves, however, this theory appears the most plausible.

It is quite certain that ulceration may result from the unwise use of

drugs, like tartar emetic or arsenious acid, especially if these be

administered for long periods; but such ulceration always occurs at the

same points, viz., at the deepest portion of the rumen, reticulum, or

abomasum.

On the other hand, ulceration due to secretory disturbance occurs at

different points, and the figure opposite shows that the mucous folds

themselves may be injured and perforated.

=Lesions.= Ulceration of the abomasum varies in severity. The case

referred to showed excavated ulcers from the site of which a portion or

the whole of the epithelium and glandular layer had been shed; true

round ulcers, which had destroyed the entire depth of the mucous

membrane and had produced chronic inflammation and sclerosis of the

muscular layer; and finally perforations resembling cleanly punched-out

holes.

=The Symptoms= are those of a mild form of ordinary acute gastritis,

without marked fever, and without special injection of the conjunctiva.

The appetite is diminished and irregular, but more as a consequence of

excessive reflex sensibility of the injured organ than from absence of

hunger. This excessive reflex sensibility of the abomasum causes

relative or absolute gastric intolerance, so that only a small amount of

the food ingested passes towards the intestine.

Absolute intolerance on the part of the abomasum may even occur, as in a

case described by Moussu in 1895, which produced a very special form of

impaction of the rumen, absolutely different from primary impaction.

Intolerance of the abomasum for food already ingested and ruminated may

extend to the omasum. Peristalsis of the rumen then ceases, and slight

tympanites occurs. The most characteristic condition is the existence of

obstinate constipation. If ulceration takes place without producing any

important vascular lesion, which, however, is rare, the fæces are hard

and coated, but without other peculiarity; if, however (and this appears

to be the rule), local hæmorrhage occurs, the extravasated blood is

modified by the gastric and intestinal juices, and the fæces appear of a

black, tarry colour. This coloration is very significant, and differs

from that produced by the bile. It occurs only in gastric hæmorrhage,

and at intervals.

=Diagnosis.= The diagnosis of gastric ulcer is difficult, and can only

be arrived at with confidence when the above-mentioned coloration of the

fæces can be detected.

=Prognosis.= From an economic standpoint the prognosis is grave. The

patient may recover; the ulcers may heal, but cicatrisation is always

prolonged, and as, on the other hand, the glandular apparatus of the

abomasum is generally more or less injured, complete recovery is

impossible.

[Illustration: $1]

=Treatment= should be directed towards checking hæmorrhage, diminishing

intolerance to food, and assisting the healing of the lesions. These

objects are facilitated by prolonged complete rest in the stable, by

injecting ergotine, or, ·7 per cent. saline solution, at the time when

the hæmorrhage occurs, and, if possible, by placing the animals on milk

diet or on emollient food, like gruels, emollient infusions, barley,

milk, cooked roots, etc.

Stimulation over the region of the abomasum is also of value. At a later

stage, when the acute symptoms have diminished, Carlsbad salts, in doses

of 1 to 2 ounces per day, can be given. Bicarbonate of soda is also of

considerable value.

CHRONIC TYMPANITES.

Chronic Indigestion—Obstruction of the Abomasum—Chronic

Gastritis—Dyspepsia.

Among pathological conditions of the stomach in ruminants a certain

number are clinically marked by one constant symptom, viz., chronic

tympanites, a fact which was formerly recognised as indicative of

chronic indigestion.

It is evident that such titles have only the significance accorded them,

and the term chronic indigestion used only to mean that gastric

digestion was badly performed, and that the condition was more or less

permanent. It being granted, on the other hand, that the term

indigestion is used to characterise temporary conditions during which

digestion is suspended, and produces immediate disturbance, it would

appear that the term gastric dyspepsia is more exact and more in

conformity with the present state of our knowledge of general

physiology. In studying this question it is clear a number of facts

still require explanation, for, as has been previously indicated, we

know almost nothing concerning the variations in the chemical phenomena

of gastric digestion under different morbid conditions; nevertheless,

the dominant fact, the imperfect or irregular digestion, is easily

appreciable. Future discoveries will no doubt enable us more exactly to

differentiate several dyspeptic conditions due to chemical or mechanical

causes and with or without anatomical lesions. At present it is

sufficient to indicate the limits of inquiry.

=Causation.= The symptom of chronic tympanites accompanies a great

number of very different conditions—some due to disease of the digestive

tract itself, others to general diseases or lesions of neighbouring

parts. In the latter cases the tympanites is only indicative of

secondary dyspepsia; in the former, on the other hand, the dyspepsia is

primary.

Secondary dyspepsia occurs very commonly during tuberculosis, diseases

of the liver, subacute or chronic peritonitis, gestation, lesions of the

mediastinum, etc., etc.

=(a) Secretory or Chemical Dyspepsia.= In primary dyspepsia it is

impossible to discover any lesion sufficient to explain the disturbance.

Chronic tympanites, for instance, follows prolonged consumption of rough

or bad food (in years when forage has been scarce or winter food has

been lacking), and too short a supply of water for weeks in succession.

It also occurs as a consequence of acute inflammation of one or other of

the gastric compartments—rumenitis, reticulitis, gastritis. Sometimes it

assumes an insidious, slow, progressive form, without any apparent cause

whatever.

In these various conditions, the mucous membrane of the gastric

compartments suffers from the deferred results of the bad feeding or

want of water. Its secretory powers and anatomical structure becoming

modified, it is no longer able regularly to elaborate the juices

necessary for digestion, and chronic indigestion, imperfect digestion,

or dyspepsia result. Similar results follow acute inflammation of the

omasum, reticulum, or rumen. Integral repair becomes impossible.

Anatomical injury is done, disturbance of secretion follows, and

dyspepsia is a necessary consequence.

=(b) Motor Dyspepsia.= Finally, it would appear that general bad health,

abstinence and exhausting work, may produce a form of dyspepsia,

unconnected with secretory disturbance, but resulting from mechanical

disturbance due to general enfeeblement and to atony of the muscular

walls of the gastric compartments. The rumen ceases to perform its work

of mixing the food, the reticulum also acts badly, and the abomasum

receives imperfectly prepared material. The result is what might be

described as motor dyspepsia, in opposition to those forms which are of

chemical origin.

The condition may vary in degree, peristalsis being diminished (one

contraction every two or three minutes instead of two per minute), or

being simply intermittent and occurring only for a few hours during the

day, or finally being altogether suppressed. Suppression is never

absolute, but atony may be so marked that the mixing of the food is very

imperfectly performed.

=Symptoms.= The most constant symptom present in all dyspeptic

conditions is chronic tympanites, indicated by a certain degree of

tension or by permanent dilatation of the rumen.

Rumination is impeded and irregular, the distended rumen loses its power

of contraction, and no longer causes eructation nor passes gas into the

intestine. It becomes progressively inert, whether the inertia be

primary and occur suddenly, as a result of some particular condition of

the sympathetic system (motor dyspepsia), or secondary and of slow

development in consequence of disturbance in the gastric secretions and

of abnormal organic fermentation (secretory dyspepsia).

This symptom of tympanites is always accompanied by irregularity,

diminution, and frequently also by depravity of appetite.

Wasting occurs, but to a very varying degree, according to the nature of

the primary condition and the method of feeding.

These general symptoms are accompanied either by constipation or by

diarrhœa; and as stagnation of food leads to fermentation, which always

forms products differing from those of normal digestion—toxic materials

in fact—a chronic auto-intoxication results, which in its turn, if not

remedied, becomes a cause of irritation, and aggravates the bad general

condition.

In many cases fever is absent, except during the final complications, in

animals in the last stages of wasting; but some signs always exist on

which the diagnosis may be founded.

The most frequent clinical type of these dyspeptic conditions is motor

dyspepsia, consisting in relative atony of the rumen without disturbance

in the secretion of the gastric mucous membranes. Luckily, this is the

most easily curable form, and is only marked by distension, dulness and

constipation.

Dyspeptic diseases of secretory origin are little understood. Their

essential causes have been badly described, and their clinical symptoms

are ill-recognised.

We cannot prove whether the forms said to be due in man to excess of

hydrochloric acid and insufficiency of hydrochloric acid really occur or

are well defined in domestic animals: nor are we better informed as to

the exact part played by the organic acid of fermentation (lactic,

butyric, acetic acid, etc.); but the most complete investigations which

have yet been made justify our supposing there is some parallel.

Moussu described primary ulcerative gastritis in 1895; and as this

form is almost certainly associated with excess of pepsin, the

occurrence of an excess of hydrochloric acid also seems possible, the

more so as the symptoms noted resemble the general symptoms of that

condition—preservation of appetite and of the motor power of the

rumen, accumulation of food in the rumen as a consequence of reflex

intolerance of the abomasum, constipation, and vomiting.

In addition to these two morbid conditions, a third occurs with some

frequency. It is characterised by chronic tympanites, alimentary

diarrhœa (the food being badly digested), and progressive wasting. This

condition seems due to an insufficiency of hydrochloric acid, brought

about by chronic gastritis, the epithelial cells of the mucous membrane

appearing incapable of producing sufficient hydrochloric acid for

digestion.

=Diagnosis.= In the present state of our knowledge regarding digestion

in ruminants the precise diagnosis of these pathological conditions must

always remain difficult; but it is indisputable that with the above

grouping of symptoms we are more likely to succeed than by confining

ourselves to the diagnosis formerly common, viz., that of chronic

tympanites or chronic indigestion.

The difference between primary and secondary dyspepsia should always be

borne in mind, and careful examination will often reveal the special

condition which has served as the point of departure for gastric

disturbance. Thus generalised tuberculosis, or tuberculosis of the liver

or mediastinum, should always be sought for, and the possible existence

of such conditions of the liver as echinococcosis, cancer of the bile

ducts, tumours, etc., and diseases of the kidneys should be borne in

mind. The influence of gestation, which so frequently causes gastric

disturbance complicated with albuminuria, should never be overlooked,

and in these secondary forms of dyspepsia the determining cause, and not

the objective symptoms should receive chief attention.

=Prognosis.= The prognosis of secondary forms of dyspepsia varies with

the gravity of the primary disease. The prognosis of primary dyspeptic

conditions varies greatly, and that state in which hydrochloric acid is

too sparingly secreted is certainly the gravest.

=Lesions.= The lesions have not been carefully studied, but it is

probable that in many cases they might afford a key to the symptoms

noted. Like all mucous lesions, they are difficult to demonstrate

histologically. Infiltration and thickening of the mucous corium and

submucous layers have been described. Such lesions indicate nothing; but

in some cases new growths have been found in the gastric compartments or

contractions about the pyloric orifice, the essential importance of

which cannot be doubted.

=Treatment.= If our knowledge is still insufficient to enable us

precisely to diagnose what we have termed “gastric dyspepsia,” or what

is still currently described as “chronic dyspepsia,” the difficulty is

even greater when attempting to lay down lines of treatment, because of

the lack of known facts and the want of a base for reasoning. Thus we

find, without being able to explain why, that some prescribe tartar

emetic, others rapid and energetic purgatives, others, again, laxatives;

whilst German authors, apparently without any justification, recommend

oil of turpentine. It seems to us, however, that one might do better

than this and attempt to lay down some rational indications for

treatment.

(_a_) In cases characterised only by chronic tympanites, without

diarrhœa, without manifest constipation (motor dyspepsia), and without

any other apparent organic disturbance, drugs calculated to stimulate

peristalsis of the rumen seem indicated. The most promising comprise

ipecacuanha in doses of 1 to 2 drams per day, tincture of nux vomica in

similar doses, powdered nux vomica in doses of 45 to 75 grains, and

laxatives like Carlsbad salts in doses of 8 to 10 drams.

Little by little peristalsis returns, becomes regular, and the chronic

tympanites disappears for good. This is frequently the case during

gestation, when the condition simply consists in motor dyspepsia without

anæmia.

(_b_) If, on the contrary, chronic tympanites is accompanied by

constipation, and the fæces are hard or, as is usually the case, covered

with mucus, suggesting the probability of excess of hydrochloric acid,

salines are indicated—not to the point of producing purgation, which

would not lead to any lasting improvement, but still as laxatives,

continued daily for ten, fifteen, or twenty days, or, if necessary, even

longer.

Carlsbad salts in doses of 8 to 10 drams, or one-ounce doses of sulphate

of sodium associated with 2½ drams of bicarbonate of potash after each

meal, are to be recommended in preference to bicarbonate of soda alone,

because they act on the secretions, on the muscular system, and also on

the liver.

(_c_) Finally, when chronic tympanites is accompanied by diarrhœa, a

condition which usually indicates insufficient secretion of hydrochloric

acid, the administration of that acid tends to arrest or check organic

fermentation and to facilitate digestion in the abomasum by

supplementing the diminished physiological secretion. The dosage is an

important point. At first small quantities should be given, 2½ drams per

day, divided into two doses and freely diluted in the drinking water;

but this amount may, if necessary, afterwards be doubled or trebled. The

drinking water is not rendered irritant by these doses, for it is

admitted, and Moussu has confirmed the fact by analysis, that the

quantity of HCl in the gastric juice may rise as high as ·2 to ·3 per

cent. Chloride of sodium, the excito-secretory action of which on the

gastric mucous membrane is well known, may be given for long periods in

doses of 1 to 1½ ounces per day.

In these various chemico-pathological states the food should receive the

closest attention. The forage, which should be good, may be supplemented

by the addition of cooked roots, demulcent drinks, and, if possible,

milk.

GASTRIC DISTURBANCE DUE TO FOREIGN BODIES.

These morbid conditions are extremely complex, but the facts that they

are due only to one cause, and that they possess certain symptoms in

common, permit of a certain grouping. It would obviously be illogical to

speak of traumatic indigestion of the rumen, reticulum, and abomasum, as

has been done in more than one book on this subject; for the gastric

disturbances described below should be considered as complications, and

not as diseases.

=Causation.= In young animals foreign bodies may be composed of hairs,

wool, bristles, cotton, and clover hairs.

Hair balls are common in the rumen, and are sometimes met with in the

fourth stomach. They cause irritation, indigestion, sometimes pyloric

obstruction, dilatation, and eventually death.

Wool balls in lambs, bristle balls in young pigs, cause much gastric

irritation. Cotton balls occur in lambs fed on cotton-seed cake; the

fibre constitutes a foreign body. The hairs of clover leaves may form a

ball in the abomasum of lambs.

Under the influence of depraved appetite animals of the bovine species

consume, apart from their regular food, the most varying substances,

such as linen, fragments of wood, nails, stones, gravel, sand, etc.

Moreover, forage, even when of good quality, often contains foreign

bodies like nails and pins (when the fields are near factories), sewing

or knitting needles (when the animals are looked after by women),

fragments of iron wire derived from bales of compressed forage, etc.,

etc. The ingestion of such objects is followed by various consequences,

which may be studied in three divisions, in the first of which the

foreign object is soft in character, in the second is blunt at one

extremity and pointed at the other, and in the third is pointed at both

ends.

(1.) =Soft objects.= The movements of the rumen, the warmth and the

action of the digestive fluids, may cause soft objects to be broken up;

the disturbance they produce is then insignificant.

Of such substances, however, some are quite incapable of digestion

(clothing, sacks, linen, etc.), and may produce obstructions; others are

both indigestible and heavy (gravel and sand), and may fall into the

depressions of the compartments, where they remain, or, if passed into

the reticulum, may become arrested in the deepest lying part. They then

produce atony of the muscular coats, slowing of peristaltic movements,

diminution in the frequency of eructation, and, as an additional

consequence, chronic tympanites, sometimes visible at the flank.

=The symptoms= are vague and common to a number of the digestive

diseases already described. The animals masticate without having

anything in the mouth; rumination becomes irregular or is altogether

suppressed, but this is not characteristic, being a symptom common to

many visceral diseases.

Later, as a result of auto-infection, diarrhœa sets in; under the

influence of abnormal fermentation in the gastric compartments the

eructations become fœtid; the animals fall into a condition of marasmus.

Death usually results after a varying time—when large quantities of

foreign substances have been ingested, in twenty to thirty days.

=The diagnosis= chiefly rests on the history, and can only be of a

confident character when one knows what quantity and what kind of

foreign body has been swallowed.

=The prognosis= is grave, because the animal usually dies of progressive

exhaustion.

=Treatment.= There is only one rational form of treatment—viz.,

gastrotomy, followed by examination of the rumen and reticulum and

removal of the foreign body. Before undertaking operation the surgeon

should be fully informed as to the cause and the probable results to be

expected.

(2.) =Foreign bodies with one pointed extremity.= These usually consist

of large-headed nails, or fragments of iron wire rolled up at one end,

which have been swallowed during primary mastication along with forage.

When ingested, they may become implanted at any point in the gastric

apparatus without necessarily penetrating deeply. When fixed across the

division of the reticulum, they cause slowing of its physiological

action. Should they penetrate the wall either of the reticulum or of the

rumen, they may attack on the right the liver, or on the left the

diaphragm or spleen, producing suppurating hepatitis, splenitis, or

respiratory disturbance. The hypochondriac region then appears

sensitive. The muscular portion of the diaphragm is partly paralysed,

and costal respiration set up, while frequent coughing of reflex origin

is provoked by irritation of the pneumo-gastric and diaphragmatic

nerves, and may give rise to suspicion of some thoracic disease, from

which, however, it is distinguished by the absence of discharge,

expectoration, and pulmonary symptoms.

Finally, if implanted in the lower wall or sides of the rumen or

reticulum, foreign bodies may carry with them infectious agents and set

up localised or generalised peritonitis.

=Early diagnosis= is a matter of great difficulty, as it can only rest

on the diaphragmatic disturbance or on the symptoms of peritonitis.

=Lesions.= Small-sized sharp bodies cause lesions of trifling extent,

which in most cases are only indicated by retardation of movement of the

gastric compartments, between which and the diaphragm, and between the

diaphragm and the posterior portions of the lung, various adhesions are

set up. In such cases the peripheral inflammation ends by producing a

fibrous sleeve, which prevents the pleural cavity becoming infected.

Other cases show patches of adhesive peritonitis or signs of generalised

peritonitis, the real cause of which often evades discovery during life.

=Treatment.= Gastrotomy is the sole means of effecting a cure, but we

are forced to admit that it only gives good results when the operator

knows what he is trying to find. Without this information he acts in the

dark, is obliged to abandon himself to chance, and although luck

sometimes favours him, it more often leaves him in the lurch.

(3.) =Foreign bodies pointed at both ends.= Bodies like needles, pins,

straight fragments of iron wire, knitting needles and broken hairpins,

become implanted in the gastric walls and travel in the most diverse

directions, in obedience to the varied movements of the organ injured.

They produce results similar to those just described. Most frequently

they fall into the lower part of the gastric compartments, pass near the

ensiform cartilage, between the pleura and the triangularis sterni into

the thickness of this muscle, or into the mediastinum, and there produce

either an abscess in the region of the ensiform cartilage, an abscess of

the thoracic wall, or a collection of pus in the subpericardial or

subpleural region (pseudo-pericarditis). They may even reach the

pericardium, causing pericarditis, and sometimes, when adhesions are set

up between the heart and pericardial sac, carditis.

By deviating to the right or left, the foreign body may produce pleurisy

or even pneumonia. If it moves towards the right, it involves the liver

and produces suppurative hepatitis; if to the left, suppurative

splenitis. Travelling in a downward direction, it encounters the

abdominal wall, and after producing an abscess may be eliminated;

passing backwards, it falls into the peritoneum, and may lead to

peritonitis. In those exceptional cases in which foreign bodies reach

the abomasum they generally become implanted towards the greater

curvature, producing in the abdominal wall an abscess which breaks

externally, and through which the foreign body is discharged; gastric

fistula is then a common sequel.

=The symptoms= vary, according to the complications. The earliest

comprise digestive disturbance, which coincides with the passage of the

sharp object through the rumen or reticulum, and depends on whether such

passage produces local peritonitis and pain, rendering movement of these

compartments impossible. Later, when the diaphragm has been penetrated,

respiratory disturbance occurs, and is succeeded by apparent

improvement, which in its turn may be followed by the occurrence of

pericarditis, pleurisy, or abscess formation.

In other cases where suppurative hepatitis or splenitis, or even

peritonitis may be present, the symptoms are extremely vague and very

difficult to refer to their real cause.

=Diagnosis= is difficult, unless the owner is able to supply exact

information that at some previous time the animal had swallowed such and

such an object.

=The prognosis= is grave, though cases occur where a foreign body is

tolerated, and may for a long time be retained without producing

accidents.

=Treatment.= Gastrotomy should not be performed unless the operator is

possessed of very precise information. In such case the rumen and

reticulum should be emptied and the foreign body sought for and removed.

When the symptoms strongly point to the presence of a foreign body

exploratory gastrotomy may be performed, but the operator will do well

to employ the operation only as a last resort.

Many complications, like septic peritonitis, hepatitis, and splenitis,

are practically hopeless; but others show a tendency to recovery. This

is the case when abscesses form in the thoracic or abdominal wall, or

beneath the pleura or pericardium. The entire difficulty consists in

diagnosis, for when once this is clearly defined intervention is fully

justified. As, however, the surgical measures vary in every case, the

exact course to be adopted must be left to the initiative of the

surgeon.

TUMOURS OF THE GASTRIC COMPARTMENTS.

=Papillomata= result from hypertrophy of normal papillæ; they resemble

those of the pharynx and œsophagus. The growth may attain the size of a

fist. It often resembles a cauliflower in appearance. When very large,

such growths may cause obstruction. A very striking illustration of a

papilloma of the mucous membrane is given on p. 180 of Möller and

Dollar’s “Regional Surgery.”

=Sarcoma= has been noted by Paule, Kitt, and Schütz as forming in the

subserous tissue of the omasum, and later bulging out as a wounded

swelling of irregular size.

=Actinomycosis of the abomasum= has been reported by Professor Axe.

CHAPTER VI.

ENTERITIS.

Enteritis consists in inflammation of the intestine, or, more precisely,

in inflammation of the intestinal mucous membrane. All the constituent

portions of the intestinal tube may be affected (duodenum, jejeunum,

ileum, colon, cæcum); but clinical distinctions and localisation of

inflammation in the various parts are very difficult in the domesticated

animals, and at present it is impossible to describe with any accuracy

the differences between duodenitis, enteritis of the jejeunum and ileum,

colitis or typhlitis. Without doubt certain symptoms suggest that some

regions are more affected than others; but clinically we are only able

to distinguish between acute and chronic enteritis. Acute enteritis may

assume different forms, according to its intensity, rapidity of

development, and lesions, so that it is possible to distinguish between

such conditions as simple acute enteritis and hæmorrhagic enteritis.

Chronic enteritis, an abstraction founded on our knowledge of such

specific forms of enteritis as are due to tuberculosis, distomatosis,

helminthiasis, etc., usually assumes the diarrhœic form.

ACUTE ENTERITIS.

As acute enteritis, whether localised in one portion of the intestine or

involving the whole intestinal tube, is produced by varying causes, and

assumes very varying degrees of intensity, its clinical symptoms are

equally diverse.

=Causation.= The various forms of enteritis result from two great series

of causes: infections and intoxications. Normally the intestine contains

an extremely large number of different microbes, which may prove of

service so long as circulation, secretion, and peristalsis continue

normal; but as soon as any perturbation occurs, either in the blood

supply or in the movement of the bowel, normal secretion is impeded;

abnormal organic fermentation commences, producing irritant principles

or toxins which at once set up local irritation, or, being absorbed,

produce that complex of symptoms which we recognise as enteritis,

intoxication of intestinal origin, or even infection.

Bearing in mind these facts, we are better able to understand the part

played by cold, by damaged fodder, by intense, stimulating feeding, or

sudden changes in the food, as well as by the action of drastic

purgatives, which modify beyond physiological limits the condition of

the glands, or even cause local desquamation of epithelium.

Toxic substances or plants act similarly by modifying either the

circulatory, secretory, or motor systems.

=Symptoms.= The first appreciable external symptoms appear to result

from fever—loss of appetite, suspension of rumination, dryness of the

muzzle and of the mouth, earthy-red colour of the conjunctival mucous

membrane, etc.

On manipulating the left flank one notes neither tympanites nor

sensitiveness—in a word, there is no indication of functional

disturbance of the rumen.

On the right side, on the contrary, palpation causes the animal to

resist and to show signs of pain. According as this sensitiveness is

more marked in the middle or upper region or towards the hypochondriac

circle, we infer that the inflammation is most acute in the large or

small intestine, either in the middle portions or, again, in the most

anterior portion. The temperature always rises at the commencement,

attaining 103° to 104° Fahr. (39·5° or 40° C.), but rarely a higher

point, a fact which negatives the idea of a rapidly progressive

infectious disease. Slight colic appears, and is accompanied by

constipation; the fæces are covered with mucus, or false membranes, or

are completely enclosed in fibrinous tubes. After four or five days the

fæces change in character. Constipation gives place to a liquid,

blackish, very fœtid diarrhœa. Finally the mouth exhales a stercoraceous

odour, resulting from fœtid eructation.

The passage of flat or tubular false membranes continues for a certain

time.

When false membranes constitute the chief symptom, the condition is

termed “pseudo-membranous, croupal, or diphtheritic enteritis.” This

form is only a variety of acute enteritis, but is grave, because

complications due to hæmorrhage or infection are very liable to occur.

In certain cases movement causes groaning. In the slighter forms the

patient may recover spontaneously. If fed with easily digested

materials, the symptoms diminish in intensity. Towards the eighth day

the fæces become normal, appetite and rumination reappear, and the

secretion of milk which had fallen off rises to its normal amount.

Resolution has occurred.

More frequently, either because the animals have less power of

resistance or because decomposition is taking place more actively in the

intestine, or, again, because intoxication is setting in, the disease

becomes aggravated. Constipation is more marked, and the fæces passed

are in small masses, covered with layers of epithelium, or sometimes

streaked with blood. In other cases the diarrhœa becomes exaggerated and

assumes a mucous or sero-mucous character; the temperature rises, and

death results from exhaustion and infection, microorganisms passing from

the lumen of the intestine through its walls and invading the general

circulation.

=Lesions.= To study the lesions to advantage the autopsy must be

performed as soon as possible after death.

In slight cases they consist of trifling generalised congestion of the

intestinal mucous membrane. The points most affected show infiltration

of the submucous coat, and sometimes of the muscular coat; the wall of

the intestine is double its normal thickness, but the thickening never

equals that seen in cases of rapidly fatal intestinal congestion.

At a more advanced stage the mucous membrane clearly is inflamed, its

surface is covered with a fibrous exudate, and the glandular and

epithelial cells proliferate, assume the embryonic form, and produce the

new tissue which one recognises under the form of false membranes.

The false membranes are generally but slightly adherent, and are readily

expelled.

In other cases, however, they adhere firmly, and when detached by the

friction caused by movement of semi-digested food through the bowel,

produce rupture of capillary vessels; this explains the presence of

blood streaks in the fæces.

=The diagnosis= is relatively easy, especially at the onset, on account

of the special character of the fæces and the sensitiveness of the right

flank.

=The prognosis= is seldom grave. If the enteritis is taken at the

beginning, recovery is usual; but if the animal has been ill for eight

or ten days and is exhausted, and if fever and diarrhœa are intense, the

prognosis should be guarded.

=The treatment= is that of all acute inflammatory diseases. Mustard

plasters may be applied to the chest and abdomen and left in position

for some hours, or may be repeated. Some practitioners prefer hot

blankets or dry friction, or, again, rubbing with essence of turpentine,

but this substance should be spread over large surfaces, in order to

prevent injury to the skin. Bleeding is only justifiable in plethoric

animals, and should never be exhaustive.

To relieve the digestive symptoms purgatives are at first given, even

though diarrhœa is marked from the onset; for purgatives still

constitute the best intestinal antiseptics, because they get rid of the

intestinal contents and microbes. The diet should be carefully selected,

and may consist of gruel, mucilaginous materials, linseed tea, cooked

roots, etc.

Of drugs, sulphate of sodium in doses of 10 to 15 ounces is probably the

best. It can gradually be replaced by 2 to 3 drachm doses of bicarbonate

of soda or of ordinary salt per day. Laudanum, camphor, and bismuth

relieve persistent colic and diarrhœa. Pilocarpine, veratrine and

eserine, though recommended by some authors, present no advantage in our

opinion. The first two of these substances certainly cause purgation,

but the action is quite temporary. The last induces violent contraction

of the striped muscular tissue, and may produce grave lesions or

invagination when the bowel is diseased, thickened or infiltrated.

HÆMORRHAGIC ENTERITIS.

This form of enteritis derives its name from the dominant symptom, which

consists in the passage of unaltered or clotted blood in the fæces. In

the former case the blood is bright in colour, as if it came directly

from an open vessel. In the second it is coagulated, and assumes the

form of fibrinous clots, which seem to result from the superposition, in

the intestinal tract of their constituent elements, viz., serum, blood

corpuscles, and fibrin.

=Causation.= Hæmorrhagic enteritis is rarely seen except during the

hottest days of summer, and in young animals which have previously shown

nothing abnormal. The high temperature seems to favour its appearance,

but is always supplemented by another cause, viz., the ingestion of

irritant food, particularly of weeds and toxic plants or herbage of bad

quality; amongst such may be mentioned dog’s mercury, and plants of the

order Papaveraceæ, Euphorbiaceæ, etc. Otherwise the often rapid manner

in which the disease develops indicates toxic enteritis.

In other cases, more benign in appearance, but quite as grave in

reality, blood is passed continually, and the disease assumes a chronic

form. It is then of parasitic origin, and is due to intestinal

psorospermosis.

=Symptoms.= The primary symptoms are similar to those of acute

enteritis, and consist of fever, dryness of the muzzle and of the mouth,

colic and constipation. This is soon followed by loose motions

containing blood or blood clots, according as the hæmorrhage occurs at a

greater or less distance from the rectum. The fæces are then ejected

violently to a considerable distance, on account of the exaggerated

intestinal peristalsis.

The disease may produce death in twenty-four hours, though usually the

end is deferred for several days, or, in cases due to sporozoa, for a

considerably longer time. In these cases there is some chance of

recovery, provided that treatment be prompt.

=The diagnosis= is very easy.

=The prognosis= is in all cases grave.

=The lesions= are ill-recognised. The animals die rapidly, and if not

immediately examined show no characteristic lesions. The changes to be

looked for consist in intense congestion or ulceration of the intestine,

or even in ulceration of arterioles and of arteries of considerable

size.

In parasitic enteritis one finds localised inflammation and, in the

epithelial interstices, sporozoa, which cause the rupture of

blood-vessels.

=Treatment.= It is necessary to act energetically from the outset, and

to arrest hæmorrhage by acting on the intestine, on the vascular system,

and on the skin. Mustard plasters or other external stimulant

applications are therefore indicated. Internally, small doses of

astringents like tannin, preparations of opium, 25 per cent. solution of

sulphuric acid in alcohol, etc., are given to produce constriction of

the vessels, though they seldom arrest the discharge of blood for long.

In most cases it is necessary to have recourse to subcutaneous

injections of ergotine, in doses of 5 to 10 grains in young animals, and

15 to 45 grains in adults. The dose may be given in two parts to prevent

an unduly severe action. The smooth fibres of the small vessels are thus

directly excited, and hæmorrhage ceases in consequence of clotting in

the contracted vessels.

One may give for the same purpose injections of arseniate of strychnine,

which has the advantage of sustaining the tone of the heart and

preventing syncope. The dose should not exceed 1·5 grains in large

animals.

Finally, a stimulating diet containing milk, alcohol, soup, cooked

vegetables, and small quantities of vegetable pulp is useful.

With early treatment animals sometimes recover in a few hours.

Intravenous or subcutaneous injections of physiological salt solution (2

drachms of sodium chloride in one quart of water) may prove of value

when hæmorrhage has been abundant and vascular pressure is low.

CHRONIC ENTERITIS (CHRONIC DIARRHŒA).

Chronic diarrhœa is common in byres. It appears suddenly, often fails to

attract attention, and assumes the form of simple diarrhœa, a fact which

accounts for it frequently being described as chronic diarrhœa,

dysentery, etc.

=Causation= and =pathogeny=. This form of diarrhœa occurs sporadically

throughout France, and under exceptional circumstances may permanently

attack a number of animals in a given place.

The immediate cause is not known, but without doubt the disease is of

microbic origin. Like Lignières, Moussu at one time believed that this

disease was very probably identical with that known in Argentina under

the names of diarrhœa, _entéqué_, or bovine pasteurellosis. The

hypothesis has not been verified, and Lignières’ treatment, said by him

to have succeeded in Argentina, always failed in Moussu’s hand.

[Illustration: $1]

The only point which seems admissible is that this disease, which Moussu

considered to have analogies with chronic sporadic dysentery in man, is

due to one or several organisms, which develop in the intestine and

produce toxins, causing diarrhœa, without, however, marked inflammation

of the intestinal mucous membrane.

=Symptoms.= The onset is often overlooked. The diarrhœa gradually

increases without appearing to be very serious; but it persists in

varying degrees of intensity. The patients do not appear to suffer, and

do not lose their appetite or spirits, but in time the diarrhœa becomes

exhausting; they waste, and after some months become excessively thin

and poor.

Intestinal peristalsis becomes exaggerated without the existence of

colic or tympanites. The evacuations are frequent, and little by little

the abdomen retracts, until, in horseman’s parlance, “the belly is up to

the back,” even in cows of four, seven, and eight years’ bearing.

The diarrhœa is serous, always fœtid, and without tenesmus.

The fæces may either be very soft or be passed in veritable jets. They

are always a little discoloured, and frequently contain grain or

undigested forage. They always contain numerous bubbles of gas.

The wasting during later periods of the disease is absolutely

characteristic, and different from that of other wasting diseases, such

as chronic broncho-pneumonia, tuberculosis, etc. The patients finally

become walking skeletons. The red corpuscles of the blood progressively

decrease, until the number may fall as low as 800,000 or even 500,000

red corpuscles instead of six millions, the normal figure. The œdema

common to wasting conditions appears, and the animals die without

suffering, in a condition of absolute exhaustion.

[Illustration: $1]

Complications are rare, though occasionally intestinal hæmorrhage or

broncho-pneumonia occurs. The temperature, which remains normal or shows

very slight changes throughout the course of the disease, may then

oscillate between 101° and 103° Fahr. (38° and 39·5° C.).

[Illustration: $1]

=Lesions.= At the first glance no lesions can be detected on post-mortem

examination except those of generalised wasting, but when the autopsy is

carried out immediately after death all the interior of the intestine

appears affected. The mucous membrane of the abomasum and the mucous

folds appear infiltrated, thickened, and with moderate sub-epithelial

congestion. The intestine seems friable, and tears with the slightest

traction. The sub-epithelial portions of the mucous folds are

infiltrated and congested, while the more prominent parts of the folds,

which are exposed to the friction of semi-digested food, become eroded.

Throughout the length of the jejeunum and ileum the mucous membrane

exhibits multitudes of small ulcerations.

Histologically, the epithelium and the glands seem atrophied, without

any inflammatory change having occurred in the mucous or submucous

coats.

The colon and the cæcum show similar lesions, and in addition brown

deposits of pigment under the mucous membrane and along the course of

the small blood-vessels. This lesion resembles that found in chronic

dysentery in man, and suggested to Moussu a possible connection between

the two diseases.

The liver is less than the normal size. In the heart Moussu has seen one

case of sclerosis of the auricles and calcareous infiltration of the

sub-endothelial lining of the aorta.

In several instances he has noted calcareous infiltration of the

mesenteric lymphatic gland.

=Diagnosis.= It is easy to diagnose this condition, and quite possible

to distinguish it from the diarrhœa of tuberculous enteritis, infectious

hepatitis, and other conditions.

=Prognosis.= The prognosis is very grave, and the disease almost always

proves fatal.

=Treatment.= At the present moment no curative treatment is known.

Lignières’ treatment—viz., the injection of physiological salt solution

and serum from healthy oxen, and saline solution or defibrinated

blood—has never given permanently successful results.

All the drugs usually employed against diarrhœa, the antiseptics,

astringents, etc., fail, or confer merely momentary benefit.

Economically, nothing is to be gained by keeping the patients alive.

With great care existence may be prolonged for months, or even for

several years, but the animals never regain condition, and are never of

any use.

The most rapid and lasting good effects follow the administration of 2½

to 8 fluid drachms of hydrochloric acid per day, given in two portions

and very freely diluted.

DYSENTERY IN CALVES.

This disease sometimes appears on the first day after birth, frequently

on the second or third. It may be mistaken for septicæmia of umbilical

origin.

=Symptoms.= The young animal may be born vigorous and in good condition,

though this is exceptional. More frequently it is puny and below normal

weight. The first evacuation (of meconium) may exhibit the diarrhœic

character; in other cases this peculiarity only appears on the second or

third day, when half-digested milk is passed. The fluid is greyish,

extremely fœtid, and rapidly becomes brownish and blood-stained.

Evacuation is frequent and accompanied by tenesmus.

The patients at once become very dull, refuse to suck, and resist

efforts to feed them by hand. The temperature rises, and the diarrhœa,

which at first was of an alimentary character, becomes mucous, serous

and blood-stained. The little patients appear “tucked up,” the flanks

sink in, the strength diminishes, and in twenty-four hours, or two or

three days at most, they die of exhaustion.

Recovery is exceptional, and when the disease assumes this character it

usually attacks a considerable proportion of the other animals in the

byre.

=Causation.= The exact cause of this form of dysentery in new-born

calves has not yet been identified, but the disease is undoubtedly a

microbic enteritis, and may even be a primary septicæmia of puerperal

origin.

For a very long time this dysentery was mistaken for simple diarrhœa,

though it exhibits neither the characteristics, course, nor termination

of the latter disease.

The co-existence of epizootic abortion and dysentery in certain byres

has led some authors to believe that a connection exists between the two

diseases, and that the young are infected with dysentery at birth.

Evidently, intra-uterine infection is not exceptional, and it seems

quite natural that the new-born calf may equally suffer when the fœtal

envelopes and fluids are infected before parturition. Epizootic abortion

is probably not the only disease which may produce this condition.

=The diagnosis= is very simple. The course of the disease and its rapid

development prevent it from being mistaken for ordinary diarrhœa. It is

more difficult to distinguish from septicæmia of umbilical origin,

although this disease also has well-marked characteristics.