This syndrome is seen in all types of herds, including those with excellent hygiene and adequate disinfection practices. It occurs mainly during the first 3 days after farrowing and has major consequences for the piglets. Acute multiglandular mastitis can also follow a specific systemic disease of the sow (eg, septicemia, pseudorabies [see Pseudorabies], porcine reproductive and respiratory syndrome [see Porcine Reproductive and Respiratory Syndrome]).
Etiology and Pathogenesis
The etiology is multifactorial. Infections of the mammary gland are more often secondary, and many microorganisms have been identified, including Escherichia coli, Klebsiella spp, Enterobacter spp, Citrobacter spp, Staphylococcus spp (eg, S epidermidis), and Pseudomonas aeruginosa. All these microorganisms are common in the environment of sows.
Although many sows in a herd may be severely affected, this type of mastitis is not contagious. After farrowing, the mammary gland is infected by an environmental opportunist. Very few bacteria (often <100) are enough to colonize the mammary gland.
Major herd risk factors are the sow (see PPDS, see Postpartum Dysgalactia Syndrome and Mastitis in Sows: Postpartum Dysgalactia Syndrome in Sows), the piglets (uncommon primary form), or the environment (eg, some beddings such as wood shavings can be contaminated by Klebsiella pneumoniae).
Systemic signs such as anorexia, constipation, fever, and depression are common. Local signs include acute induration of the mammary glands as well as severe edema and skin congestion of the mammary region. However, many sows (especially primiparous sows) develop mammary edema without any signs of acute mastitis. Circumstantial evidence suggests that this is usually associated with increasing milk production (often the milk drips during and right after farrowing) to such an extent that piglets are unable to consume all the available milk.
Once acute multiglandular mastitis is established, the secretion (with oxytocin) of milk is no longer possible. Affected sows deny piglets access to the teats by lying on their mammary glands. General signs result from bacterial multiplication and resorption of toxins. Common consequences for the litter include an increase of stillborn piglets, weak piglets, neonatal diarrhea, starvation, hypoglycemia-induced weakness, an increased incidence of crushing by the sow, and increased susceptibility to other diseases and other problems (eg, runt pigs).
Early diagnosis is not always easy. Most problem litters are thought to be due to early lactation problems. The primary differential diagnoses are peripartum mammary edema, which is often seen in primiparous sows without any systemic signs, and PPDS, which is less spectacular but affects a greater number of sows. A thorough physical examination, including careful palpation of the mammary glands, should be performed. However, it is necessary to be cautious in the interpretation—hard mammary glands without systemic signs do not always indicate acute mastitis. Although frequently seen, peripartum mammary edema is poorly documented. The sows often appear to be in discomfort and lay down, as do sows with mastitis. However, peripartum mammary edema can certainly lead to an acute multiglandular mastitis. In contrast to the situation in cows, interpretation of cellular modifications in the milk is very difficult in sows.
Treatment and Control
Systemic antibiotic therapy should be started as soon as possible (see PPDS, see Postpartum Dysgalactia Syndrome and Mastitis in Sows: Postpartum Dysgalactia Syndrome in Sows). Longterm control of a herd problem also requires identification and correction of risk factors. General antibiotic therapy as well as corticosteroids are useful to reduce the intensity of the inflammatory reaction. Management techniques to improve hygiene should be implemented as soon as possible. Cross-fostering is often the only effective way to save a litter.
Last full review/revision July 2011 by Guy-Pierre Martineau, DVM, DECPHM