Under the heading “mammitis” are included different forms of inflammation of the mammary tissue, whether such inflammation attack the parenchyma of the gland or the interstitial tissue. Generally the whole gland is invaded at the end of a few days, whatever the point of origin, and the inflammation is therefore of a mixed character.

Mammitis has been recognised from very early times. In his researches on “contagious mammitis” Nocard in 1884 showed that infection was the principal factor in its evolution.

Numerous classifications, based on the causes or on the pathological anatomy of the condition, have been suggested; but most appear too rigid, and therefore, without discussing them, we confine ourselves to giving the following résumé:—

Rainard (1845) Lacteal engorgement.
Cellulitis of the udder.
Mammitis Acute.
Chronic.
Lafosse (1856)
Trasbot (1883)
Mammitis Acute.
Chronic.
Saint Cyr (1874)
Violet (1888)
Mammitis Catarrhal.
Phlegmonous or interstitial.
Parenchymatous.
Lucet (1891) Primary mammitis (properly so-called) 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.