Mastitis of the cow

Front matter

Class J3lF9_A1

Honk TU'sVg G3p>'right N?

COPVRIGHT DEPOSIT.

Preface

This work is based upon the investigation of milk of diseased udders and the subsequent autopsy of such diseased udders.

The material for these examinations consisted principally of samples of milk and specimens of udders sent to the High School for the investigation of tuberculosis.

In addition to this material, milk samples were obtained from acute udder-afFections which were not tuberculous. Most of the material examined, however, was of a tuberculous character. The number of non-tuberculous udders amounted to ca. 50.

In order to study the kinds of udder-infections to be taken up not less than seventy bacterial isolations were made from milk and udders by the plate method. The culture medium was sermn-gelatin-agar or serum-agar. Gelatin plates were poured in only a couple of cases and then for a special purpose.

For study of the histological changes in the diseased udders thirty diiFerent preparations were examined. Most of them were cut with the freezing microtome immediately after fixation in formalin. The remainder, ca. 10 cases, were cut after imbedding in paraffin. The sections were stained with hasmatoxylin and eosin or after the method of Van Gieson. In order to study the bacteria the sections were stained with carbolmethylene blue or after the method of Weigert or Ziehl.

Concerning the clinical description I am supported by clinical material from my veterinary practice (35 cases), and upon the cows with udder tuberculosis, purchased by the Veterinary High School, in which I produced mastitis by artificial infection. In addition other veterinarians have viii PREFACE

contributed data on the clinical symptoms of the questionable or uncommon forms of mastitis.

To all colleagues who have assisted me in my work through material submitted or written information I extend my heartiest thanks. Finally I wish to express my deepest gratitude to my highly esteemed teacher, Professor J. Svensson, who has placed cows at my disposal and guided me in the technic of the bacteriological and pathologichistological investigations.

SVEN WaLI^ Stockholm.

Contents

CHAPTER PAGE

I. The Udder of the Cow 1

Anatomical and Physiological Review.

Chapter I The Udder Of The Cow

Anatomical and Physiological Review

Anatomy. — The udder is a tubulo-alveolar gland. Like other glands, it consists of a true secreting part, the parenchjnma, and a connective-tissue framework, called the stroma.

The parenchyma consists of extensively branched canals or passages as fine as a hair, called tubuli. At their ultimate extremities or blind end they show vesicular dilatations (tubulo-alveolar gland type) which gradually converge into larger collecting ducts that finally terminate in cavities in the teats as large as a hen's egg, called milk cis- ,terns. The milk cisterns empty from the ends of the teats through a canal the size of a match, called the teat canal.

The walls of the finest tubules consist of a single layer of cubical epithelial cells. The collecting tubules, cisterns and teat canals are lined with several layers of epithelium.

The parenchyma is divided by the stroma into round lobules as large as a pea, within which the above mentioned different tubules are imbedded in a very thin, fine connective-tissue network called the intralobular connective tissue (Fig. 1). The part of the stroma which separates the single lobules is called the interlobular connective tissue. From this as a framework the fine intralobular connective tissue is given off. Blood-vessels and nerves lie in the stroma.

The intralobular connective tissue is made up of fine fibrillary connective-tissue tufts containing large lynipli spaces. The interlobular connective tissue on the other hand is made up of firmer fibrilla showing only a few small spaces.

The collecting tubes are surrounded and joined by connective tissue which becomes increasingly firmer and thicker and which constitutes an effectual firm connective-tissue membrane around the epithelium of the cisterns and the teat canals.

The gross anatomical structure of the udder of the cow consists of four parts, the two lateral halves which

are separated from each other by loose connective tissue, a left and a right half. These halves are again divided into two parts, an anterior and a posterior quarter. These are very firmly bound together by connective tissue.

The udder receives blood through Fio. 1— Cross section of three tlic cxtcmal pudic artcry which is a

branch of the crural artery. These external pudic arteries divide into two branches, one for the anterior and one for the posterior quarters. The blood is returned through two blood-vessels: (1) the milk vein or subcutaneous abdominal vein, which runs anteriorly to the internal thoracic vein, and ( 2 ) the external pudic vein, which passes posteriorly (Fig. 2).

The lymph-vessels of the udder are numerous and pass posteriorly to the supramammary lymph-glands and from here out through the internal lumbar-glands to the thoracic duct.

Physiology. — The udder secretes the milk. It functionates periodically and the period depends upon pregnancy; thus milk secretion begins with great quantities with parturition and continues for ca. 7-8 months. After this

THE UDDER OF THE COW 3

time the milk decreases, the cow loses tone and finally with difficulty gives a negligible quantity of milk which is grayish-yellow, thin and watery.

In general the first milk secretion is produced through reflex stimulations at parturition. The normal milk secretion is only produced through birth.

Milk secretion can be produced however under other circumstances, as during oestrum. This is of little importance, as a rule, and the udder soon loses its tone again (spontaneous milk secretion).

Experimentally it is possible to produce an atypical milk secretion through stimulation of the corresponding nerves.

The above mentioned method of producing milk secretion is maintained j,,^ 2._vesseis of the udthrough mechanical stimulation by v.«.a^'=lnTerk.repia8tric the sucking of the calf or by the hand v.r"'^ vena uben. of the milker. Without these mechani- "." =sup7amamm8ry cal factors the milk quickly diminishes.

The milk secretion is therefore introduced by parturition and maintained through mechanical stimulation (milking).

This mechanical stimulation however cannot sustain the milk secretion indefinitely, as the milk secretion diminishes usually about two months before the next birth.

The lactation period can only be extended by mechanical stimulation when no impregnation has taken place. This can be induced for from fifteen to eighteen months, especially after castration; in every case however a gradual diminution occurs.

In this condition the blood supply is decreased and the udder is poor in liquid and dry (diminished lymph).

The reflexly produced activity of the udder cells disappears simultaneously with the blood supply and in consequence of this lessened nervous stimulation of the gland cells and decreased nutrition a condition of diminished milk secretion results.

The quantity of milk is greatest during the first month after parturition but gradually decreases afterward. The udder decreases in circumference as it is no longer distended with milk and becomes small and quiescent or in the dry or alactiferous state.

In consequence of the diminished work and nutrition the organ undergoes a process called atrophy in pathology but which is physiological in this case. The cell elements become smaller and their number decreases, since part of the cells become retrogressively altered, fatty degenerated and desquamated. The tubules and consequently the lobules become smaller in this way. At the same time, as an indication of retrogressive alterations, great numbers of leucocytes emigrate to the intralobular connective tissue where they assist in the work of absorption.

The atrophic gland cells give off other products of secretion. This secretion is no longer normal milk, it is grayish-yellow and thin, not infrequently viscid and contains a large quantity of albumin so that it coagulates on boiling. INIoreover it is rich in cells, epithelial cells and especially in emigrating leucocytes which are often laden with fat droplets. The secretion is resorbed for the most part, in which work the leucocytes are directly responsible as they re-enter the blood-vessels laden with fat droplets. The atrophic gland cells are capable of producing a yellow coloring matter within their structures which lends a distinct dark yellow color to the cut surface of the yellow udder (yellow atrophy).

At the next parturition the condition is immediately changed. The cells become stimulated to secretion and the atrophic udder is again well nourished with blood, consequently the cells very quickly become functionable again and the milk, especiallj-, very soon becomes normal. The

THE UDDER OF THE COW 5

atrophic pigmentation and likewise the leucoeytic infiltration disappear.

The milk of the first few days, the so-called colostrum, has an albumin and leucoeytic content of great similarity to the milk of the atrophic udders, the " gelt " milk.

During this quick change from the dry to the lactation state circulatory disturbances may easily occur. The functional hypersemia can frequently be so increased that an abnormal transudation occurs inducing oedema of the udder. Following this condition small capillary hemorrhages may occur in the intralobular connective-tissue spaces from which blood may empty into the milk-ducts, mix with the milk and cause bloody milk.

Following these changes functional disturbances may also develop. It is very probable that the atrophic cells also secrete other abnormal products, such as virulent toxins although in insignificant quantities. Following parturition however large quantities of the same toxin may be produced due to the altered condition which may lead to a general intoxication, milk fever. This disease is treated by air inflation with localized cell paralysis due to the effect of pressure.

I. Anatomy of the udder :

A. Microscopic structure.

1. The parenchyma of the udder.

2. The stroma of the udder.

B. Gross anatomical structure.

Arteries and veins.

Lymph-vessels. n. Physiology of the udder:

A. Milking period.

B. Incitation and maintenance of milk secretion.

C. Diminution, dry or alactiferous udder, " gelt " milk.

D. The udder at the time of parturition.

Circulatory disturbances.

Functional disturbances.

Chapter II Mastitis In General

Definition. — Inflammation of the udder or mastitis is a local disease of the udder of a reactive character which manifests itself by an active hypersemia, emigration of cells, and proliferation of connective tissue.

Etiology. — Mastitis is brought about through harmful local influences. These harmful influences are of two kinds : (1) physical, mechanical nature; external force; (2) chemical nature, bacterial toxin ; infection.

Pathogenesis. — The part of the udder exposed to these harmful factors can consequently undergo retrogressive alterations and indeed become so injured that a more or less progressive death of cells super\^enes as the primary lesion.^ The ad j acent living tissue subsequently reacts with an inflammation. In this condition the emigi-ating cells, especially the leucocytes and connective-tissue cells, rid the local diseased area of dead cells and foreign bodies that might be present. The connective-tissue proliferation which occurs at this time is a reparative process and gradually fills all defects existing in the tissue by the process of healing.

This process is supported by a rich blood supply to the diseased part called hyperemia, following which the physiological transudation is increased, and this increased transudate, together with emigrated cells, possibly present foreign bodies and dead cells, is called an exudate.

The real position of the inflammation is in the stroma. The parenchyma is secondarily affected in mastitis following alterations in the stroma.

In consequence of the difference in the structures of the

^ Like Ribbert, I do not classify the retrogressive process with inflammation, but I maintain that it is the incentive factor of the inflammation, wliich therefore may best be called the primary lesion. [Alteration.] 6

MASTITIS IN GENERAL 7

stroma, the intralobular connective tissue is the most severely affected, as it is the most loosely constructed and richest in juices. These spaces become filled with exudate which consists principally of leucocytes and connective-tissue cells. In this condition the tubules become pressed together and the epithelial cells undergo desquamation. Part of the exudate is forced into the tubules and mixed with the milk, which consequently becomes altered in its composition, especially in its cell content. At the same time a proliferation of the connective tissue takes place with thickening of the intralobular connective tissue. Similar alterations but of a lower grade take place in the remaining stroma of the inflamed part.

During the lactation period the udder is most rich in juice and most sensitive, and the inflammations are therefore more severe and often malignant. The dry or alactiferous udder, which is comparatively poor in fluid, is however less sensitive toward the external influences, and its inflammations are therefore milder and more benign.

Termination. — When the irritating matter has been removed by the leucocytes, inflammation recedes. The exudate is resorbed, leucocytes re-enter the blood- and lymph-vessels, and cell infiltration disappears or is reduced to a minimum. The intralobular connective tissue becomes thinner and the tubules are again dilated and enlarged.

The original circumference of the tubules is not attained however, as the intralobular tissue has become thickened by proliferation of the connective tissue, which does not completely reduce following a severe inflammation. As a result of inflammation there is usually a connective tissue proliferation of varying degree which may terminate as sclerosis with subsequent diminution of tubular circumference or atrophy.

Classification. — The causes of mastitis maj^ be divided into: (1) mastitis caused by external force; (2) mastitis caused by infection, infectious mastitis.

Chapter III

MASTITIS CAUSED BY EXTERNAL FORCE This mastitis may be divided into injuries and wounds.

INJURIES OF THE UDDER

An injury of the udder is a destruction of the udder tissues through a more or less uninjured skin covering.

Causes. — Injuries of the udder may be produced by a blow, by squeezing or by being trod upon.

One must discriminate between the primary effect, that is the primarj^ lesion produced by the direct effect of the external force, and the subsequent inflammation.

Primary Lesion. — The force can produce an immediate necrosis of the softer cells, especially the epithelial cells, in a circumscribed area and rupture of blood- and lymph-vessels with an extravasation of blood and lymph into the intralobular connective tissue particularly. This hemorrhage can also get into the milk passages and give rise to bloody milk. As a rule the hemorrhage soon stops. As the tissue becomes distended with blood and lymph the pressure becomes so great that further hemorrhage is mechanically lessened or prevented. Furthermore the destroyed cells liberate fibrin ferment which aids in coagulation of the blood, thus preventing fm'ther hemorrhage. Should the force strike an exposed part which already shows a blood infiltration, a progressive necrosis of the rather poorly nourished cells can easily take place. Seldom is the udder tissue alone affected, as usually the skin is involved at the same time and manifests superficial abrasions of the epidermis and swelling and blood infiltration of the corium and subcutaneous connective tissue.

These alterations in the udder tissue then call forth an inflammation with emigration of leucocytes. This in-

MASTITIS CAUSED BY EXTERNAL FORCE 9

flammation clears the tissue of extravasated blood and necrotic particles and fills the defects made in the tissue by necrosis and its resorption, with connective tissue.

Similar phenomena occur in the skin as dermatitis when it becomes involved.

Termination. — After resorption of the exudate in the inflamed area, more or less sclerosis remains followed by atrophy of the tubules. If the skin has also been involved in the inflammation, it is no longer movable but is firmly adhered to the udder.

If there is a wound in the skin it may easily become infected. This infection can possibly reach the injured area in the udder through the lymph-vessels and in that way give rise to an infectious mastitis.

Clinical Symptoms. — We see immediately or soon after the impact of the force, as a rule, the formation of a moderate circumscribed swelling which is the primary lesion. In the course of one day the swelling increases, becomes hot (hypersemia), painful and somewhat firm following blood coagulation and cellular infiltration.

After several days the swelling begins to recede and gradually diminishes, after which, however, a somewhat firmer, more circumscribed nodular formed area remains, due to connective-tissue induration.

Treatment. — The condition is not serious. Usually no treatment is necessary. The process heals out rapidly.

In the first few days one can reduce the hypersemia and hemorrhage by the use of cold-water treatment (vasoconstriction) . One can apply a cold water compress to the udder by a suspensory bandage placed around the middle. If the skin is injured one can prevent infection of it by the use of a Burrow's solution compress.

When the swelling begins to recede one can assist the treatment by the use of a skin irritant, as concentrated iodine solution rubbed in as a stimulation to resorption.

WOUNDS OF THE UDDER

Etiology. — Wounds of the udder may be produced by blows, or stabs as by a pitch- fork, hooking, or from a surgical operation such as an incision in an abscess.

This brings us to the discrimination between the primary lesion and the subsequent inflammation.

The wound ruptures the vessels and milk passages, following which the walls of the wound become infiltrated with blood, lymph and milk which flow outward through the mouth of the wound. The hemorrhage may be more or less copious. It is greatest following incisions and least in contused wounds, that is in wounds produced by dull objects, as a tlu'ust from a horn. In contused wounds the vessels of the neighborhood are so injured that thrombosis occurs in most of them. This prevents hemorrhage but predisposes to necrosis.

Inflammation. — The reactive inflammation begins in the immediate vicinity of the wound, that is, the walls of the wound, where a wall of emigi-ating cells [j^hagocytes] is formed which clears the wound of dead tissue and foreign particles. Around this a connective-tissue wall is formed which closes the ruptured tubules and from which connective-tissue cells rapidly proliferate until the wound aperture is gradually filled with young succulent loose connective tissue, gi'anulation tissue.

Termination. — In the most favorable cases the wound heals without any complication. The newly formed connective tissue fills the wound aperture, and the surface is finally covered by regeneration of the epidermis from the margin of the wound. The exudate is resorbed and the loose connective tissue strongly contracts, finally leaving a white fibrous line or scar.

As a rule, however, udder wounds become complicated with infection. In these conditions healing is usually delayed, necrosis of the connective tissue is more widespread

MASTITIS CAUSED BY EXTERNAL FORCE 11

and not infrequently such a condition can develop into a more protracted exudative gangrene.

Treatment. — Our treatment is to avoid an infection when possible and to check its progress when one has taken place.

The wounds are thoroughly disinfected. In the beginning a Burrow's solution compress is applied to the udder ( suspensory bandage ) . Infected wounds are freely opened so that the exudate may have free drainage, necrotic parts are removed, following which a scrupulous antiseptic treatment is carried out.

CHAPTER IV Ports of Infection

The causes of infection may enter the udder: (a) through openings in the udder, and ( h ) through the blood-stream.

The openings which may serve as ports of infection to the udder are of two different types : ( 1 ) natural : the teat canals, and (2) morbid: wounds.

THE TEAT CANAL AS A PORT OF INFECTION

Infectious material enters through the teat canal, so that first the milk and indirectly through it the tissue become infected.

The milk is a nutritious fluid and contains water, salts, albumin, carbohydrates, and fats. It is an excellent source of nourishment for bacteria and therefore difficult to preserve, especially in summer, since it easily undergoes acid fermentation in vessels.

The udder keeps the milk warm, like a thermostat, and offers very favorable conditions for bacterial development.

Under normal conditions, however, the milk in the udder is practically sterile. The reasons for this are of two types: (a) physical nature, and (b) biological nature.

Physiological causes of sterility of milk in the udder. The teat canal is closed between milkings by bundles of smooth muscle tissue imbedded in the walls which maintain a definite moderate tension. Thus under physiological conditions the external opening of the teat canal is small, usuallj^ rendering infection more difficult.

Furthermore, the teat canal is directed downward, or to the side when the cow is lying, but never upward, as the dorsal position is not physiological to the cow. Thus usually the bacterial infection takes place in a direction opposite to that of gravitation, never in the direction with it, wliich usually is an obstacle to infection.

Finally the milk stream passes only in one direction, outward from the udder through the teat canal by sucking or milking. A retrogressive stream does not occur. The udder is mechanically distended by the milk and collapses like an empty glove after milking, without the influence of any in-sucking force. Thus the infection must enter against the stream, never with it.

Biological causes for sterility of milk in the udder. In spite of the before mentioned obstacles to infection one or more bacteria may gain entrance, but these may be taken up and destroyed by the ever-present leucocytes which are more or less numerous. The leucocytes play a very important part inasmuch as they inhibit the invasion of the milk by bacteria. [The normal healthy udder of the cow harbors bacteria throughout its whole extent (Ward). The healthy udder always gives milk which is entirely bacteria free (Kitt., vol. i, 2d ed., p. 227).]

Predisposing factors to infection through the teat canal. These factors are of two types: {a) physical nature, and ( b ) biological nature.

Predisposing Causes of a Physical Nature. — Arrest of milk secretion is produced by neglecting to milk or from poorly regulated milking hours. For the same reasons the cisterns can become so distended with milk that the pressure finally overcomes the tension of the sphincter muscle and the teat canal fills with milk which continuously drops from the end of the teat. A rapidly growing or motile bacillus can now easily gain entrance against the stream, grow in the milk in the teat canal, and finally infect the entire milk.

A paralysis of the sphincter muscle following age, as in old milch cows, or a more severe affection, as a chill or fever,^ causes the same alteration, and dilatation of the milk canal takes place and predisposes to infection.

Infection may be induced by the introduction of instruments, as a milk tube in the teat canal, or spontaneously with foreign bodies, as a straw which may be forced into the teat canal when the cow lies down.

Predisposing Factors of a Biological Nature. — \Vlien a very virulent rapidly growing bacillus gains access to the mouth of the teat canal it can always find spaces in that passage containing moisture from the physiological capillaries in which it can grow. Through its own virulence it can withstand the leucocytes (negative chemotaxis) [aggressins], and infect the milk. This explains the distinctly contagious character of many cases of mastitis.

Prophylactic Measures Against Infection Through the Teat Canal. — Avoid aiTest of the milk secretion by wellregulated milking hours and punctuality in milking. Use the milk tube cautiously. Keep the teats clean and dry. In cases of contagious mastitis isolate the diseased individual, milk it last and disinfect the morbid milk in order to avoid the possibility of spreading the infectious material in the cow stable.

UDDER WOUNDS AS PORTS OF ENTRANCE

Udder wounds may already be infected from the beginning, that is, the infectious material is injected at the same time that the wound is made. Such is often the case in stab wounds. In other cases a wound may be sterile at first and become infected later.

In fresh wounds the exterior of the wound itself and also the milk through the ruptured tubules may become

^ Both appear to be followed by paresis of the involuntary muscles which among other things produces diminished peristaltic action.

infected. In old wounds tliis is prevented by the inflammatory connective-tissue formation.

Protection of Wounds Against Infection. — The leucocytic wall forms the most important protection against infection of the wound. But since the wall of leucocytes is only an evidence of inflammation, that process plays a very important part against infection.

Finally the inflammatory connective-tissue wall forms a very good obstacle to the progress of infection, as it circumscribes it.

Predisposing Factors to the Infection. — The nutrient fluids, blood, lymph, and milk which infiltrate the udder wound, predispose it to infection more than any other wound because of the favorable nutrient conditions for the infectious organisms and because the wound itself is a good thermostat.

The greater the blood infiltration, the more widespread the death of cells, and the more saturated with fluids the wound is, just so much better it is for infection. It is broken down by the bacteria which as a rule live more easily on dead than on living media. In the latter case they are more directly exposed to healthy phagocytes.

THE BLOOD AS A PORT OF INFECTION

In order that the blood coming into the udder may be a port of infection, it is necessary that we have a blood-infection, that is, that the infectious organisms be in the blood stream.

Blood-infection. — The blood can become entirely or partially infected, that is, general blood-infection (bactersemia), or partial blood-infection.

A partial blood-infection is possible in this way, that the infectious organism be deposited in the organs or be transported to the organs from the blood by leucocyies.

The local blood-infection, which is of importance to the udder, is through infection of the blood of the aorta.

Causes. — A blood-infection can be produced in different ways. Infectious material may be picked up by the leucocytes in an infected area in the intestines or in other organs rich in bacteria and be carried by them into the blood stream. In a wound infectious organisms can grow directly in ruptured vessels. In the infection of an organ the primarj" lesion (necrosis) may become permeated with infectious organisms, which surround the vessels of the primary lesion, inducing deep necrosis, so that a blood-infection may take place through the walls of these vessels. Blood-infection can be induced through infectious ulceration of a vessel wall. Should the lymph become infected (lymph-infection) this fluid can finally infect the blood.

The usual causes of infection of the blood of the aorta is a lung-infection or an infectious endocarditis.

If the blood of other organs, for instance of a wound or of a uterus, as in infectious metritis, be infected the blood of the aorta can still remain sterile, since the infectious material is filtered out in the lungs. This is the rule for infectious organisms of positive chemotaxic action, while on the contrary infectious organisms of negative chemotaxic action easily pass through the lungs.

With infectious pnemnonia usually a blood-infection is brought about thi-ough ulceration of a vein wall with emptying of infectious fluid material into the blood of the veins.

The exudate discharges itself into the vein gradually and thus divides itself minutely. It becomes further comminuted in its passage in the vessel by impact against the vessel wall, and through the action of the current eddies in the vessel ramifications. A drop of exudate discharged into the vein can become so finely divided in this way that it can be distributed over an incredibly large area.

Infection of the blood stream is not of long duration as the blood soon deposits the infectious organisms and thus purifies itself again. Infection of the blood can recur, however.

An acute fatal general blood-infection like anthrax naturally cannot give rise to a local diseased process, such as inflammation of the udder. A non-fatal generalized blood-infection can, however, produce different infectious local disease processes, such as pneumonia, pleurisy, arthritis, nephritis, and perhaps mastitis.

Infection of the Blood of the Udder. — The possibility of one of these emboli reaching the udder is very great, since both external pudic arteries are fairly large, have no important curves, and are incipient at the aorta. [External iliac, femoral artery, external pudic or mammary artery.]

As the aorta runs on the left side [anterior part], the most direct course is to the left half of the udder which is therefore most exposed to a blood-infection. It is clear, however, that the situation and the time during which the emboli are passing in the blood are of great importance. If, for instance, a cow stands with her posterior extremity inclined toward the left, the right external pudic artery is the most direct course. For the emboli to reach the posterior quarters the most direct way seems to be through the external pudic arteries.

Thus the left quarters of the udder are more exposed to a blood-infection than the right, and the posterior quarters more so than the anterior. The left posterior quarter therefore is the most severely exposed.

The small infectious emboli, if they be sufficiently large, may be caught in the capillaries or fine arterioles and at these points produce a thrombus with infectious necrosis and the formation of infectious metastatic foci. In other cases very small emboli may be taken up and carried into the loose intralobular connective tissue where the leucocytes degenerate, remain and die when the infectious organisms are the stronger. Here a metastatic infectious focus is produced. On the other hand, if the leucocytes are the stronger, the infectious organisms are destroyed without the production of tissue alterations.

In tliis manner, as a rule, through infection by the blood to the udder a great number of small foci, distributed throughout the connective-tissue stroma of the udder, are formed.

Infection of the Udder in General

The infection of the udder may be divided - into milk' infection and stroma-infection, depending upon the position of the infectious organisms.

milk-infection [Parenchymatous Mastitis] .

Definition. — Milk- or parenchyma-infection is an infection of the udder in which the bacteria are only found in the milk, or rather in the parenchymatous passages.