Numerous etiologies or pathophysiologies can be involved in this syndrome, which is reflected by the use of several different names—mastitis-metritis-agalactia (MMA) complex, agalactia syndrome, dysgalactia syndrome, mammary edema, periparturient hypogalactia syndrome, agalactia toxemia, and puerperal mastitis. However, these names are not synonymous and have often been misused. The syndrome can currently be classified according to the number of mammary glands affected, ie, uniglandular or multiglandular mastitis (including postpartum dysgalactia syndrome [PPDS], MMA complex). (Also see Mastitis in Large Animals Mastitis in Large Animals read more .)
Acute or chronic mastitis of only one or two mammary glands (acute or chronic uniglandular mastitis) in sows is present in nearly all herds. If the entire udder is acutely affected, it can be a primary or a secondary mastitis (acute multiglandular mastitis) as well as mammary edema (“hard udder syndrome”), which is common in primiparous sows.
Due to bacterial effects, acute multiglandular mastitis is usually accompanied by systemic signs and agalactia, whereas hard udder syndrome is not. Both conditions occur within the first 3 days after farrowing and rapidly lead to piglet starvation. Although the problem can be sporadic and limited to a few sows, sometimes it can occur in a greater number of sows and become nearly epidemic.
Differentiating acute multiglandular mastitis and hard udder syndrome can be difficult. For this reason, it is often reported by producers as “acute mastitis.”
PPDS is characterized by transitory hypogalactia. It can lead to acute multiglandular mastitis and should be considered as the general cause of lactation failure in the sow. MMA complex is a misnomer and is only part of the more general PPDS. Although the mammary glands are swollen and frequently warmer than normal, grossly detectable primary mastitis is uncommon. Likewise, metritis (more commonly endometritis) is only an occasional finding in some herds. Finally, only rarely is there complete agalactia; most sows continue to produce milk but at a greatly reduced rate (hypogalactia or more correctly dysgalactia). The primary clinical signs of the sow’s inability to produce a sufficient amount of milk to meet the needs of the piglets are growth retardation and increased mortality in piglets.
Mammary glands of sows are anatomically different from those of cows. In sows, there are no well-identified gland cisterns (gland sinus) in the mammary glands. There are usually two complete gland systems and two teat orifices per teat. When three orifices are present, one sinus ends blindly at the base of the teat and does not have glandular tissue. There is no muscular sphincter around the teat orifice. Therefore, intramammary treatment by way of the teat opening is impossible. Mammogenesis occurs almost exclusively during the last half of gestation and during the first days of lactation. New glandular tissues are produced during each gestation. For this reason, feeding and nutrition are of major importance during mammogenesis and the end of gestation, and are less important at midgestation.
Opinions differ as to whether the position of the caudal mammary glands should be considered as a risk factor for mastitis development. Most recent findings seem to reject an increased incidence in caudal glands compared with cranial ones.
Infection of a mammary gland during one lactation has no consequences for the next. However, chronic lesions of the teat canal may be present for multiple lactations.