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Rainard (1845)
Lafosse (1856) Trasbot (1883)
Saint Cyr (1874) Violet (1888)
Lacteal engorgement. Cellulitis of the udder.
Mammitis
Lucet (1891)
Mammitis
Mammitis
Primary mammitis (properly socalled)
Acute. Chronic.
Acute. Chronic.
Catarrhal. Phlegmonous or interstitial. Parenchymatous.
Acute Galactogenous. Lymphogenous. Chronic Galactogenous. Lymphogenous.
Symptomatic mammitis
Acute Hæmatogenous. Lymphogenous. Chronic Hæmatogenous. Lymphogenous.
All these classifications are justified by the guiding ideas of the writers, yet, as in every case of attempted systematisation, they have the disadvantage of not being in entire agreement with clinical experience.
For instance, the differences between catarrhal and parenchymatous forms of mammitis are only of degree, and it is difficult, therefore, to see why they should be divided into two distinct varieties. The difference is in regard to the prognosis.
Similarly in practice it is difficult and sometimes impossible to distinguish between an interstitial and a parenchymatous mammitis, because all the tissues of the gland may be involved at a given moment. The only factor which allows of differentiation is the discovery of the point from which infection took place. Finally, it is sometimes so difficult to distinguish between galactogenous and lymphogenous mammitis that the attempt has had to be abandoned. In gangrenous mammitis of milch ewes, for example, the infective organism is found not only in the sinus and the galactophorous
canals, but also in the serosity of the interstitial tissue and of the perimammary œdema.
Without doubt the causative agent of mammitis may enter the gland by three principal channels—the galactophorous sinus, the lymphatic plexus (after some injury), and the blood circulation. But from the clinical standpoint it is not at all necessary to identify all the causes in order to establish the classification.
The symptoms allow of a division only into acute and chronic mammitis. Careful examination of the general condition of the patients will afterwards allow cases of primary mammitis to be distinguished from secondary or symptomatic mammitis such as occurs in tuberculosis. Finally, consideration of the conditions under which a particular case of mammitis has appeared, and study of the symptoms in detail (peculiarities of the milk, local temperature, hardness of the tissues, œdematous infiltration, etc.) will in most cases indicate whether the mammitis be parenchymatous or interstitial.
This system really differs little from that adopted by Lucet in his work on Mammitis.
The classification adopted in the following pages is as follows:—
Primary
Acute
Mammitis
Chronic
Parenchymatous or galactogenous.
Interstitial or lymphogenous.
Secondary or symptomatic. Hæmatogenous. Galactogenous.
Primary Simple. Parenchymatous. Interstitial.
Secondary Parenchymatous. Interstitial.
We shall leave on one side everything concerning secondary symptomatic mammitis, the study of which merges into that of the general diseases from which it arises.
ACUTE MAMMITIS.
Causation. The general cause of acute mammitis, like that of chronic mammitis, is infection by pathogenic organisms, whether such organisms enter by the usual natural path, viz., the galactophorous sinus and excretory apparatus, by the lymphatic path, owing to some accidental injury, or, again, by the blood circulation.
Infection of the lymphatics undoubtedly plays a part in superficial and interstitial inflammations, and it is proved that certain microorganisms may pass into the milk, as it has been proved that they pass through the kidney.
But if infection is the determining cause, certain secondary favouring influences must not be overlooked.
Thus lactation is an almost indispensable condition. It is true that some cases of mammary inflammation apart from lactation have been described, but they have been the result of violence, accidental or mechanical.
Accumulation of milk in the udder (overstocking) has unquestionably a certain influence in the large milk-yielding animals, not because it directly produces inflammation, but because milk then escapes spontaneously; and as the udder cannot be entirely evacuated without external assistance, the entrance is kept permanently open for the passage of germs, which are freely transferred to the teat from the litter and surrounding objects.
Cold, or rather chills, also act in a complex manner, particularly by disturbing vaso-motor control. Different forms of mechanical violence, such as blows, crushing strains, wounds, etc., may immediately and directly set up local or general inflammation.
Bacteriological investigation has proved that numerous and varied microorganisms can be found in the milk or interstitial exudates in cases of mammitis, but only a few special forms have been proved to be specific: streptococcus of contagious mammitis of milch cows, and micrococcus of contagious gangrenous mammitis of ewes (Nocard).
Pathology. The pathogenic results produced by infective organisms depend on their number and power of reproduction, and on the activity of their life products.
The most immediate and regular result of acute mammary infection is coagulation of the milk within the udder by
decomposition of the lactose, and the formation of lactic or even of butyric acid. The acini and excretory canals are dilated by coagula, and can no longer expel their products of secretion, so that the colonies of microorganisms develop there in full security. The active epithelial cells undergo granular degeneration and disappear, whilst the walls of the glands become infiltrated and large numbers of leucocytes are poured forth around the glandular culs-de-sac.
The tissues being thus affected, the virulent organisms penetrate from the acini into the interstitial tissue, and from this time onwards the lesions become mixed.
Inversely, should infection originate in the lymphatic spaces, a time arrives when the organisms make their way from the interstitial tissue into the acini, with a similar result in the end.
The development of the lesions may be arrested or may pass on to suppuration, or even gangrene, of the parenchymatous lobules. Cases happen in which infection is so rapid and severe that the successive stages cannot even be identified, and gangrene appears without any preliminary stages at all. Luckily the commonest forms are less serious.
Symptoms. Acute mammitis is characterised by its sudden appearance, more or less acute general symptoms (dulness, fever, and loss of appetite), and variable local symptoms. When the practitioner is able to follow the development of the disease throughout, he may sometimes distinguish well-marked signs, which permit the two clinical varieties to be distinguished.
A. Interstitial Mammitis.—This form, which might perhaps also be termed peri-mammitis when it primarily affects the subcutaneous lymphatic spaces, has also received the names of phlegmonous and lymphogenous mammitis.
It is characterised by alarming general symptoms, and particularly by a rise in temperature of 2°, 4°, or even 5° Fahr., with all its consequences, such as loss of appetite, stoppage of rumination, acceleration of breathing and circulation, slight tympanites, constipation, and by the thrusting of the hind limb on the affected side away from the centre line. The animals groan when forced to move.
These symptoms sometimes precede by a considerable interval the appearance of the local changes, which consist in painful swelling of one or two quarters, rarely of more.
The perimammary subcutaneous tissue is infiltrated, œdematous, painful on palpation and preserves the imprint of the finger. The teat is tense, swollen, very tender, and of reddish colour. In the grave forms the swelling extends forwards under the abdomen in the direction of the umbilicus, and backwards towards the perineum. The local temperature is abnormally high, the secretion of milk in the diseased gland is modified or checked, and sometimes this phenomenon extends by reflex action to the neighbouring quarters, although the latter may not themselves be affected. The inflammation rarely extends from one quarter to another, because the lymphatic plexuses do not anastomose (Fig. 237).
The animals lose appetite and fall away rapidly.
Resolution may occur after from five to eight days. By degrees all the symptoms then become less marked. The appetite returns, pain diminishes, the fever drops, and the lesions gradually disappear, but the yield of milk rarely regains its former amount.
Suppuration may occur; sometimes a superficial subcutaneous abscess forms, more rarely, a deep-seated, interstitial abscess, originating in the connective tissue or lymphatic spaces. With a superficial abscess, the local symptoms again revive to a slight extent; these are present in a more marked degree where the abscess is deep-seated. An extremely sensitive œdematous swelling forms, the skin covering which is at some point of a deep-red tint, whilst fluctuation gradually appears.
In cases of deep-seated abscess formation the general condition becomes alarming; the affected quarter is tense throughout, hard and very sensitive.
Deep-seated suppuration is difficult to detect, and exploratory punctures with a fine needle may be necessary before the diagnosis can be made.
Local or diffuse gangrene forms a rare complication. It is due to the vessels of one or several glandular lobules becoming obliterated or thrombosed.
Such a termination is indicated by extreme aggravation of the general symptoms, feebleness of the heart and great weakness of the patients, who fall into a condition of coma. Locally the udder remains œdematous, the skin becomes of a blackish-violet colour, whilst the local temperature falls and the animals die from exhaustion and intoxication.
Parenchymatous Mammitis.—Parenchymatous mammitis when mild is also termed catarrhal mammitis. It is in reality true primary mammitis; interstitial being primarily and practically perimammary lymphangitis.
In this case infection occurs through the teat, and may be localised in the sinus or excretory apparatus, giving rise to galactophoritis, but it usually extends to the acini. Inflammation of the mammary tissue is therefore direct and primary. It rapidly extends, however, through the glandular wall into the interstitial tissue, thus setting up (from the anatomo-pathological standpoint) a mixed mammitis. Clinical distinction between this form and interstitial mammitis is at first easy.
The symptoms usually occur in the following order:—Swelling of the affected quarter or quarters; appreciable increase in size and sensitiveness; the presence at first of curdled milk in the galactophorous sinus, then of clots mixed with slightly red tinged serosity; complete cessation of the yield of milk, and suppuration in the secreting portions of the gland.
The general symptoms appear only after the objective signs, and vary greatly in intensity, according to the case. As in the interstitial form, there may be marked fever, loss of appetite, cessation of rumination, groaning, and difficulty in walking.
In some grave forms, where development is peracute, infection spreads rapidly from the glandular to the interstitial tissue, and subcutaneous, subabdominal, or perineal interstitial œdema occurs secondarily.
The udder is turgid, tense, shining, and of reddish-violet colour in places, as if a deep-seated abscess were developing.
Pressure on the galactophorous sinus causes the flow of reddishgrey milk, sometimes fœtid or of gangrenous odour. The animals
seem exhausted, show signs of profound intoxication, are unable to rise, and appear paralysed.
But besides these grave forms are others, in which the patients seem scarcely to suffer: appetite is preserved and all the vital functions are in full activity. Only the local signs are of importance.
This variability in the clinical symptoms of acute forms of mammitis is entirely due to differences in the pathogenic infecting organisms.
Parenchymatous mammitis may end in resolution in three to four days, with progressive but slow return to the physiological condition. This termination is announced by the gradual disappearance of all the symptoms and the return of milk secretion. It is, however, quite exceptional for the former condition to be fully restored, and in many cases the affected quarter must be regarded as lost from the physiological standpoint.
It gradually becomes hardened, sclerotic and atrophied.
Suppuration is very common. It attacks the galactophorous sinus, the excretory canals, and even the acini. If obstructions occur in the course of the collecting vessels, or if evacuation is not artificially stimulated by milking, the pus collects in the depths of the gland, and enormous diffuse abscesses may form at the expense of the mammary tissue.
Circumscribed or diffuse gangrene, as a primary condition, is rarer. Infective organisms rapidly invade even the depths of the gland, the interstitial and subcutaneous tissue, and thrombosis due to infection or intoxication occurs, followed by gangrene. Death results from infection or intoxication.
Complications such as necrosis of the abdominal tunic, of the fibrous tissue enveloping the mamma, and of the muscular layers on the inner surface of the thighs, may occur in the suppurative forms.
Diagnosis. The diagnosis of acute mammitis is easy, and the interstitial forms (mammary lymphangitis) can be distinguished from the parenchymatous forms very early in the attack.
Careful examination suffices to differentiate between this condition and mammary congestion or primary chronic mammitis. The examination, however, must be much more thorough and
searching when a specific disease (such as tuberculous mammitis) is in question.
Prognosis. The prognosis of acute mammitis is always grave, whatever form the disease may assume, for, if the animal’s life is not invariably endangered, its economic value is always affected. Moreover, should superficial or deep-seated abscesses form, prolonged suppuration may follow, resulting in loss of condition and enormous depreciation.
Lesions. The lesions of interstitial mammitis are similar to those of ordinary lymphangitis, the condition originating near the teat and gradually extending to the layers of connective tissue between the acini, mammæ, etc.
In the parenchymatous form the inflammation may remain partial, and be localised in particular tracts of glandular tissue. The secreting epithelium, when infected, exhibits cloudy swelling, becomes loosened, and disappears; the margin of the gland and the interstitial divisions become infiltrated with enormous numbers of white blood corpuscles, and are the seat of suppurative processes which end in the production of small acinous abscesses. By the union of neighbouring abscesses large branching collections of pus are produced, and lead to partial or total destruction of tracts of the parenchyma, of the connective tissue divisions, vessels and aponeuroses.
The abscess tends to break through the skin, which becomes inflamed and ulcerated, or, when the microorganisms are of slight virulence, the tissues may react, so that the abscess becomes surrounded with a thick indurated wall, and finally encysted.
Treatment. Very numerous methods of treatment have been proposed, an admission which, in itself, suggests that no perfect one has been discovered. No infallible system, in fact, exists of arresting the disease and restoring the parts to their normal condition.
From a prophylactic standpoint, mammitis can be avoided by placing the animals under proper hygienic conditions, paying special attention to cleanliness, avoiding overstocking, and treating excoriations or injuries to the teat or udder as soon as they appear.
Once acute mammitis has developed, general and local treatment must both be attempted.
The older practitioners were in the habit of bleeding from the mammary or jugular vein. Since their time, however, objections have been made to bleeding because acute mammitis has been proved to be of an infectious character, and, therefore, it is undesirable to lower the patients’ resisting power.
This reasoning, however, appears to be erroneous. Little by little the advantages of bleeding, both in intoxications and infections, have been recognised, and one thing at least is beyond dispute, namely, its action on fever. Undoubtedly, it must not be resorted to without judgment, nor should it be freely employed in debilitated animals; but in well-nourished patients its effect on fever and on the accompanying respiratory and circulatory disturbance is immediate.
We, therefore, recommend moderate bleeding from the jugular.
Bleeding from the mammary vein entails too great a risk of infection to be commendable.
Purgatives and diuretics diminish or prevent accidents such as intoxication and the complications resulting from temporary suspension of the digestive function.
Local treatment is more or less efficacious in mammary infection. To relieve pain and check infection it should be of an emollient and antiseptic character. Ointments containing 10 per cent. of carbolic acid, boric acid or iodine, or 12½ per cent. of camphor, opium or belladonna, are of real service during the first stages, particularly of mammary lymphangitis and interstitial mammitis.
Repeated applications of 10 per cent. carbolic glycerine have similar advantages.
In the less acute forms originating in the parenchymatous tissue, mild ointments of plumbic iodide, Goulard’s extract, or mercury may also be used if precautions are taken to prevent the animals from licking, and so poisoning themselves.
When the tendency to suppuration is marked, vesicants hasten the development of the abscess and facilitate puncture. The most commonly used are the 33 per cent. tartar emetic ointment or the 10 per cent. biniodide of mercury ointment.
If, on the other hand, the mammitis is of the interstitial type, with severe subcutaneous œdema, extending over the belly and towards the perineum, good results often follow deep firing in points over the
swollen region. The points should be widely spaced, venous branches being avoided. In this way numerous ducts are formed by which the toxic and septic liquid which causes the œdema is enabled to escape.
This method of treatment can be supplemented by the simultaneous use of antiseptic ointments.
Finally, in mammitis of the parenchymatous type, where there is no marked tendency to invade the interstitial tissue, the most important point is to wash out the interior of the gland, and even the acini as far as possible, with antiseptic fluids. Practically this is difficult to effect, because such irrigation must be performed aseptically, and cannot properly be left to the cowmen.
In current practice, therefore, one often has to be content with stripping the udder every hour. Milk clots which accumulate in the sinuses and galactophorous canals are broken down by soft pressure, and withdrawn with more or less difficulty. By repeated milking they are prevented from accumulating in the galactophorous sinus and canals, a very important point. Neglect of this precaution enables the colonies of microorganisms to develop uninterruptedly in the culsde-sac, whereupon the coagula formed of casein obstruct the excretory channels and complications develop despite all external treatment.
By repeated friction of the udder as in milking the advantages that would be produced by washing out the gland from the direction of the acini are secured, and thus the ascending infection is checked.
The diseased udder must always be emptied before making antiseptic injections, which would otherwise be useless.
Should the practitioner decide to face the practical difficulties of injections, he must take care that his instruments are aseptic; that the solutions employed are always at or about bodily temperature; that these solutions are incapable of irritating even tissues so tender as the epithelium of the acini or of the galactophorous canals; and, finally, that the drugs employed will not coagulate the milk within the gland.
Bearing in mind these points, the practitioner will do well to restrict himself to the use either of boiled water, physiological salt solution (·9 per cent.); alkaline 3 per cent. solution of borate of soda; or ·05 per cent. of fluoride of sodium. Every precaution having been
taken, from 12 to 20 ounces of liquid can be injected into each quarter, according to its size. The solutions should be made to penetrate as far as possible into all portions of the gland by gently manipulating the parts, and should again be withdrawn in about a quarter of an hour.
It must always be remembered that failure to observe the above precautions may make matters worse instead of better, and therefore that intra-mammary injections can only be of value when carried out by a skilled person.
In otherwise hopeless cases there remains as a last resort total or partial ablation of the mamma. This operation is advisable in cases of diffuse gangrene, or of intense massive suppuration, where there is imminent danger of death from infection.
Directions for its performance will be found in Möller and Dollar’s “Regional Surgery” (uniform with the present volume), p. 454.
CONTAGIOUS MAMMITIS IN MILCH COWS.
Although its cause was unknown before the investigations of Nocard and Mollereau in 1884, this disease is of very common occurrence in England, in large dairies in the environs of Paris, and is also seen, though more rarely, in Normandy, in Brie and the Soissonnais, causing serious losses on account of its transmissibility.
It had been described in Germany by Gerlach as early as 1854, and Kitt in 1885 recognised it as common, and proposed for it the title of “contagious catarrhal agalaxia.” It also occurs in Denmark, Italy, and England.
Contagious streptococcic mammitis of cows always assumes a chronic form, during the course of which indurated centres appear, varying in size between that of a hazel-nut and a walnut.
Causation. The cause is always to be found in contagion, the disease being due to a streptococcus, which has been carefully studied by Nocard. Its transmission from a diseased to a healthy udder is explained by the fact that the milkers are careless as to cleanliness, and thus directly convey the germs to healthy teats and facilitate infection.
Symptoms. As in chronic mammitis, general symptoms are not well marked, though some cases are ushered in with cough, slight nasal discharge, and offensive diarrhœa. The first appreciable indication is a change in the milk, which diminishes in quantity, and, although normal to all appearance, coagulates rapidly if left undisturbed. Infection has already taken place, although nothing can be detected on examining the udder.
Next appears a nodule of hardened tissue above the teat. This nodule is of rounded or ovoid shape, ill-defined towards its periphery, and it becomes progressively enlarged without any sign of acute inflammation. The milk becomes watery and of a bluish colour. Microscopical examination reveals numerous streptococci. The hardening process proceeds slowly. At the end of several months the sclerosis may only have extended to one-third of the height of the infected quarter. With the appearance of these lesions the character of the milk again changes. It becomes yellowish in colour and fœtid, and contains a fibrous reticulum, whilst its reaction is distinctly acid. The lesions, which at first had been confined to one quarter, successively extend to the others unless precautions are taken.
Lesions. The lesions consist in mammary sclerosis, with nodules which progressively increase in size. This sclerosis originates in the galactophorous canals, and extends first to the periphery, then to the interstitial connective tissue; the latter undergoes hyperplasia and confines within its tracts the true glandular elements, destroying their secretory power. Locally, catarrhal mammitis exists.
The lesions can easily be recognised on microscopic examination, and, when the section is suitably stained, numerous streptococci can be detected in the acini, which are blocked with proliferating epithelial cells. These lesions are due to the invasion of colonies of microorganisms, which spread from below upwards.
The streptococcus causing this mammitis colours readily with thionin and methylene blue. It can be cultivated in liquid and solid media containing sugar or glycerine, but growth is impeded by the presence of peptone or common salt. Under ordinary circumstances the culture dies after some weeks, but if the acidity of the medium is neutralised by the addition of powdered carbonate of lime, it preserves its vitality for six or eight months. The culture when injected into the udder of a healthy cow or she-goat reproduces the
disease. The microorganism is not pathogenic for any of the smaller animals used for purposes of experiment.
Diagnosis and prognosis. The diagnosis is easy, the presence of the sclerotic nodules being characteristic, whilst in doubtful cases a microscopical examination can always be made.
The treatment should be prophylactic and curative.
Prophylactic treatment comprises disinfection of the milkers’ hands, which are the ordinary vehicles of contagion, and disinfection of the cow’s udder. Diseased animals in a byre should be milked last of all, and the milk should be destroyed.
Curative treatment is confined to local antiseptic injections. Warm concentrated boric solution gives good results. The injections may be repeated three or four times a day after milking, the liquid being left for a certain time within the udder. In this way animals suffering only from a slight attack may be cured, but when the disease is already somewhat advanced injections lose their effect.
Injections of fluoride of sodium (·1 to ·5 per cent. strength) appear to be much more effectual. Moussu claims to have cured by this means several old-standing cases where all four quarters of the gland were diseased.
These injections necessitate the same precautions as those above indicated for securing perfect asepsis. In grave cases it is very difficult to prevent the disease from extending in infected stables, because the necessary precautions cannot be observed.
CHRONIC MAMMITIS.
Chronic inflammation of the udder may form a termination of ordinary acute mammitis, or it may result from infection with organisms of a less virulent type.
In cases of acute mammitis, where severe injury of the interstitial tissue or mammary parenchyma has occurred, its physiological function is partially destroyed. The circulation is disturbed, the vessels undergo change, the layers of connective tissue are indurated and sclerotic, the epithelial tissue is not fully restored, and chronic inflammation of the udder persists.
Clinically, it is impossible to distinguish all the variations that may occur, because the constituent tissues are all injured, and the disease is of a mixed type, with very numerous variations.
Symptoms. When chronic mammitis follows the acute form its onset is only indicated by gradual diminution in the signs of acute inflammation. The appetite is regained, and all the important vital functions are properly performed.
Nevertheless, it is possible to distinguish two different clinical forms. In one, the secretion of milk is almost entirely suspended, the udder becomes atrophied, shrivelled and sclerotic; the hardening gradually continues, and the patients, being useless as milch cows, can only be fattened for slaughter. The induration may be partial, nodular, or diffused.
In the other form the udder is large, but the milk is replaced by a purulent secretion which permeates the acini and galactophorous canals. Although they eat well, the patients remain thin, and are with difficulty fattened for slaughter.
The suppuration may be diffuse or local. In rarer cases it is localised in the form of “cold abscess.”
Treatment. No treatment can perfectly restore the udder after chronic mammitis with sclerosis and atrophy.
In the suppurating forms of chronic mammitis the morbid secretion may be checked by internal irrigation of the udder and antiseptic injections, but, as this treatment necessitates careful and continued attention, it is usually out of the question.
If only one quarter is diseased the animal may be kept for milking purposes, but where two or three quarters are attacked it should be prepared for the butcher.
In cows suffering from chronic purulent mammitis of all four quarters, Kroon suggests removing the teats in order to facilitate fattening. The teats are removed with the bistouri or scissors, by which means a large opening into the galactophorous sinus is produced, through which the purulent secretion escapes freely and continuously; the retention of pus and intoxication in consequence of resorption are prevented and the animal can be fattened, which would be difficult without the operation.
GANGRENOUS MAMMITIS OF MILCH EWES.
This disease occurs in different parts of France, and has also been seen in Germany.
Causation. Lafosse in 1856 attributed it to the dark and dirty condition of the sheep-folds, a cause which certainly contributes to its propagation, though it is not the determining cause of the disease itself. The latter is a specific micrococcus discovered in 1875 by Rivolta, and thoroughly studied by Nocard in 1886 and 1887.
Symptoms. The course of the symptoms offers a certain analogy to that of septic engorgements and interstitial mammitis or mammary lymphangitis. As a rule only one gland is infected, but generally symptoms at once appear, indicating an extremely dangerous condition, viz., peracute mammitis. The patient suddenly becomes dull and entirely loses appetite, rumination ceases and respiration is short and jerky, although the bodily temperature does not always rise to any marked extent.
Local symptoms soon develop. The udder assumes a violet-red tint and becomes the seat of an erysipelatous swelling; the local temperature rises, but as the disease progresses it gradually falls again. Milk secretion ceases.
All these appearances rapidly become aggravated. The patient lies down; the œdematous swelling extends to the belly and even to the chest and thighs; the local temperature falls, indicating the imminence of gangrene; the teat becomes contracted, and the pulse is very frequent and almost imperceptible. From time to time the animal grinds its teeth.
The bodily temperature next falls to 98° or even 96° Fahr. (37° or 36° C.), and the animal shows extreme prostration. The subcutaneous swelling extends as far as the sternum in one direction and the quarters and perineum in the other. The udder crackles under the finger. Death occurs without a struggle.
All these symptoms follow as a rule in barely more than twentyfour hours. Nevertheless, in certain cases, the disease lasts for three, four or five days. Cases of spontaneous recovery are exceptional. The gangrenous part may become delimited and slough away, leaving an enormous suppurating wound, which slowly cicatrises. Even though
the animals survive, they never recover condition, but remain weakly, so that, from a monetary standpoint, death would have been preferable. Moreover, the lambs are starved and require a fostermother.
Lesions. Post-mortem examination reveals œdematous infiltration of the udder and surrounding connective tissue, and often extensive, diffuse gangrene. The serosity is of a reddish colour, and sections of the diseased udder of a violet tint. The tissues of the udder and the serous liquid contain the specific micrococcus.
It is very small, and stains readily by the Gram-Nicolle method. It grows rapidly in liquid and solid media, liquefies gelatine, and quickly renders neutral media alkaline.
The injection of a few drops of culture into the udder of a milch ewe reproduces the typical disease. In any other species it is without effect. Infection occurs through the open extremity of the teat, or the medium of a wound, and the microorganism is so virulent that it rapidly invades all the tissues.
Treatment. No antiseptic treatment appears capable of checking the course of the disease.
Surgical treatment alone is of any value, and consists in ablation of the udder, followed by antiseptic dressing. Only a portion of the gland is removed: an elliptical incision is made, including the diseased teat, the skin is then dissected free so as to form a flap; the diseased tissue is isolated; last of all, the vessels are ligatured. The consequences of operation are less grave than might be expected, considering the size of the wound, which heals with fair rapidity.
Moussu has frequently practised this radical method of treatment without losing a single case. The remaining portion of the udder becomes hypertrophied, and is often quite capable of secreting sufficient milk for the nourishment of one lamb.
GANGRENOUS MAMMITIS IN GOATS.
Goats suffer from a form of mammitis which presents symptoms precisely similar as regards development and termination to that of ewes. The disease occurs in a sporadic form in animals giving milk,
whatever their breed or the conditions under which they are kept. It has been seen at Alfort, as well as at Lyons.
Moussu has seen it in an enzootic form in herds of milch goats near Bizerta (Tunis), and considers that contagion results from kids sucking healthy animals after having been suckled by diseased ones. Fifty milch goats out of a total of three hundred were affected at the time of Moussu’s visit, and two had already succumbed.
The diagnosis presents no difficulty.
The prognosis is very grave.
The treatment is precisely similar to that of gangrenous mammitis of milch ewes, viz., ablation of the diseased udder.
Of the above-mentioned herd, twenty animals were operated on, and all recovered without accident. Among the others treated by less radical methods, such as scarifications, incisions, antiseptic injections, etc., eight died. The only justifiable treatment, therefore, is ablation.
CYSTS OF THE UDDER.
Cysts of the udder may assume one of two forms, milk or galactocelous cysts and serous cysts; possibly the latter are only hydatid cysts.
Both varieties are of the nature of retention cysts, and result from accidental obliteration of a milk conduit, which has been obstructed by coagulated casein, or from atresia due to contraction of inflamed connective tissue. The acini are isolated and become dilated, the milk undergoes changes in composition, the secretory epithelium degenerates, and the cyst is produced.
The serous or milk cysts may vary considerably in size, and always show a rapid tendency to suppuration.
The diagnosis is based on the detection of uniform fluctuation without excessive sensibility, and can be confirmed by an exploratory capillary puncture.
The prognosis is grave, for recovery can only occur after the lining membrane of the cyst has been destroyed.
Treatment. Puncture followed by irrigation is insufficient, whatever the nature of the cyst.
Free incision, or simple puncture with a bistoury, produces suppuration within the cystic cavity, which continues until the lining membrane is completely destroyed; but this takes a very long time.
Removal of the entire cyst, either with the bistoury or by tearing through the surrounding connective tissue, is the best method of treatment. The wound thus produced heals regularly and rapidly under an antiseptic surgical dressing.
TUMOURS OF THE UDDER.
Tumours of the udder have been little studied in the larger domestic animals, the reason being that immediately animals cease to yield milk they are fattened and despatched to the butcher. Clinically, therefore, these tumours are not of great practical importance.
Without entering into general considerations of a pathological anatomical character, by which different varieties of these tumours are differentiated, we may say that they assume one of three different forms. The first is sharply circumscribed, of clearly defined shape, and easily separated from neighbouring tissues, to which it adheres but slightly. Such tumours are benign, and have no tendency to return after removal.
The second is ill-defined, very adherent, and appears to infiltrate the surrounding tissue. It is malignant in character, is often impossible to completely remove, returns after extirpation, and infects neighbouring lymphatic glands.
Between these two varieties may be placed a third, occupying an intermediate position as regards both its characteristics and gravity.
Practically a knowledge of the above facts is a sufficient guide in dealing with lesions of this character.
Canalicular Papillomata.—There exists another variety of tumours which is of much more frequent occurrence, and which is apt to cause mistakes. This variety consists of inter-canalicular papillomata.
These show no sign of their existence on external examination of the diseased udder, and can be diagnosed only by reasoning based on the signs observed.
They are of very small size, and grow from the internal wall of the galactophorous sinus or excretory canal. They increase in length, finally extending for some distance along the sinus, where they remain unrecognised until some external manifestation arouses suspicion as to their existence.
Under the mechanical contraction due to milking they easily become excoriated, and their existence is then suggested almost solely by the fact that the milk is tinted with blood, for palpation of the udder very seldom gives more than negative results.
The diagnosis is always doubtful. The prognosis is grave, because it is impossible to remove the tumour, which is often deeply placed within the udder. There is no curative treatment.
VERRUCOUS PAPILLOMATA OF THE UDDER.
In cows suffering from cutaneous papillomata the udder is often covered with a varying number of little sessile warts, which are spread over a considerable surface, are very sensitive, and bleed at the lightest touch. Milking is thus rendered extremely painful and difficult; the animals struggle, kick, and become dangerous.
The condition is extremely troublesome, and in spite of every precaution the milk is always soiled.
The best method of treatment consists in removing the warts individually with fine, sharp-bladed curved scissors.
The animals must be firmly secured, if necessary cast, and the operator should avoid removing more of the skin covering the udder than is absolutely necessary. The bleeding which follows is trifling, and stops of itself. After washing the parts with an antiseptic solution, the little wounds may be powered with a mixture in equal proportions of tannin and boric acid.
