Postpartum dysgalactia syndrome (PPDS) is a primary cause of neonatal problems (eg, diarrhea, crushing, runting, inanition, poor growth) but is challenging to characterize because of its multiple manifestations and the difficulty in making an etiologic diagnosis. In a given herd, PPDS affects ~15%–20% of the sows; a higher percentage is uncommon. It is more common in young sows in their first or second parity.
There are numerous multifactorial etiologies, which complicate the diagnosis and clinical evaluation. Classically perceived as a part of the mastitis-metritis-agalactia (MMA) complex, PPDS should instead be considered a broader pathology. Thus, the MMA complex is essentially a subtype of PPDS, probably the most severe clinically but also the least common.
Evidence suggests that lipopolysaccharide (LPS) endotoxins, a portion of the cell wall of all gram-negative bacteria, play a central role. Bacterial endotoxins can be absorbed from the uterus (eg, endometritis or metritis), mammary glands (eg, acute multiglandular mastitis), or gut (eg, constipation as a consequence of feeding finely ground feed to sows can result in bacterial overgrowth and subsequent absorption of endotoxins from the intestines) and lead to endotoxemia. Identifying the source of the bacterial endotoxins is important to determine the best preventive approach for the particular herd.
The secretion of colostrum is determined by a complex hormonal balance (homeorhesis). LPS endotoxins exert their effects even before farrowing and act with the intervention of the innate immune system (macrophage activation). These changes adversely affect production and secretion of colostrum and milk. In addition, the colostrum is as important for its energy content as it is for its immunoglobulin content. Any decrease in the amount of ingested colostrum will result in consequences for the piglets such as diarrhea, inanition, and poor growth.
Other causes of general hypogalactia that should be considered include acute multiglandular mastitis, udder and teat abnormalities, hypocalcemia (uncommon in sows), and acute (agalactia) or chronic (hypogalactia) ergotism (uncommon in practice). Indeed, ergot derivatives suppress prolactin release.
Risk factors are those associated with stress of the sow and with conditions that lead to bacterial multiplication and subsequent endotoxemia. Such factors are numerous and are linked with different entities (eg, cystitis, metritis, vaginitis, constipation, mastitis).
Genetics can also be a risk factor for PPDS; most recent studies identified susceptibility genes on chromosome 17. Selection among genetic lines should include this parameter.
PPDS is seen almost exclusively within the first 3 days after farrowing. Associated signs are numerous and vary from herd to herd, as well as within herds. PPDS is commonly associated with fat sow syndrome, prolonged farrowings, large litter sizes, and a high postpartum fever. Management practices reported in herds with a high incidence of PPDS include too much manual intervention during parturition or too many parenteral injections to sows (antibiotics, oxytocin, prostaglandins) or piglets (mainly antibiotics). Moving pregnant sows to the farrowing facilities ≤4 days before the expected farrowing, and feeding sows ad lib during lactation also should be considered risk factors. Piglet losses are due to emaciation or diarrhea (or both), as a consequence of poor nutrition during the first few days postpartum.
Diagnosis is difficult and based on clinical signs. Clinical examination is best performed while piglets are nursing; milk ejection in affected sows is either absent or of brief duration, which causes the piglets to actively nurse for an extended time. During the initial stages, piglets repeatedly attempt to nurse at frequent intervals and do not settle after nursing. As a result of vigorous nursing efforts, the teats may be traumatized. As the energy reserves of the piglets are depleted, their attempts to nurse decrease, and they often migrate to the warmest portions of the farrowing crate. Crushing by the sow is common. Therefore, litter behavior should be watched closely for a prolonged time when trying to diagnose PPDS.
Mammary tenderness, swelling, and teat damage are consistent with a diagnosis of lactational insufficiency. The mammary glands vary from grossly normal to swollen, firm, and warm to the touch, sometimes with blotched purple skin. Pure bacterial cultures may be isolated from milk samples. Rectal temperature of the sow varies from normal to markedly increased (>40.5°C [104.9°F]). The concept that postpartum rectal temperatures >39.5°C (103.1°F) predict early lactation problems must be questioned. Physiologic hyperthermia observed in lactating sows should not be confused with fever. Reduced appetite or anorexia, constipation, and depression may also be seen. Abnormal and copious vaginal discharges may be seen in some sows (eg, cervicitis, endometritis). Cystitis, metritis, vaginitis, constipation, or mastitis in the sow and diarrhea in neonatal piglets should be considered as a general syndrome (requiring an overall diagnosis) rather than as individual problems.
Systemic or local therapeutic intervention (antibiotics, NSAIDs) can sometimes be helpful but only on a short-term basis. Flunixin meglumine may help to counteract the effects of endotoxins. Antimicrobial treatment is usually prescribed before susceptibility can be tested. A broad-spectrum antibiotic is therefore recommended. However, if antibiotics are used longterm, a dependence on them for puerperal fevers, acute mastitis, vaginitis, endometritis, or neonatal diarrhea can develop rapidly and lead to multiresistant bacterial infections. Oxytocin or prostaglandins (or both) can be useful in cases of prolonged farrowing or postpartum endometritis. By far the most effective method is to cross-foster the piglets from affected to healthy sows, as long as the health status of the litters are equivalent. Oxytocin (5–10 U/sow) is occasionally effective in reestablishing lactation if used 4 or 5 times at 2- to 3-hr intervals. In herds in which PPDS is a significant problem, incidence may be reduced by inducing parturition with prostaglandin F2α; this results in rapid induction of labor and dilatation of the teats for a shorter period of time. However, the amelioration is not constant among herds and depends on farm circumstances.
As many risk factors as possible should be identified and corrected or minimized. Systematic manual interventions during farrowing or uterine washings should be limited to only those that are necessary. There is no clear evidence that vaccines have a beneficial effect. Good sanitation tends to decrease the incidence of mastitis in the sow and diarrhea in the piglets, but PPDS is also common in herds in overall good health and with a high level of hygiene.
For chronic mastitis, use of partially slatted farrowing pens and cleaning with disinfectants between batches of sows in the farrowing and breeding areas may be helpful. Cutting or grinding the piglets’ teeth after farrowing is not considered a good way to control chronic mastitis. Indeed, it can lead to a high prevalence of mastitis, possibly caused by changes in the oral flora of the piglets or the failure of piglets to suckle as a result of sore mouths from careless cutting of teeth.