By Jamie M. Studer, Zoe E. Kiefer, and Jason W. Ross

Sow longevity is a crucial factor in the contribution towards efficiency and profitability of commercial swine operations, as the reproducing females represent the most valuable animals in the herd (Díaz et al., 2015).

Increased rates of sow mortality and culling indicate a decline in sow longevity in recent years, as approximately 54% of breeding females are removed annually in the US swine industry (Lucia et al., 2000).

The period surrounding farrowing represents the greatest risk for sow health, as previous reports indicate approximately 30% to 42% of sow deaths occur from three days prior through six days post-farrowing (Díaz et al., 2015). During this timeframe, sows are vulnerable to morbidity and mortality caused by conditions such as urogenital infections, retained piglets, and uterine prolapse.

Furthermore, conditions affecting lactation performance also represent a threat to sow retention rates, as culling of sows due to poor litter performance is estimated to account for an average of 20% to 30% of sow removals (Díaz et al., 2015).

Removals due to poor litter performance include reasons such as small litter size at weaning, low piglet weaning weights, udder problems, and poor mothering ability.

POSTPARTUM DYSGALACTIA SYNDROME

Postpartum dysgalactia syndrome (PDS) is a major puerperal disease in sows characterized by reduced or insufficient milk production.

Before the establishment of PDS as the predominant lactation disorder in sows, multiple names were associated with lactational insufficiency, including mastitis-metritis-agalactia (MMA), agalactia toxemia, agalactia complex, periparturient hypogalactia syndrome, and puerperal septicemia and toxemia, among others.

The numerous variations in names used to describe lactational insufficiency reflect the multitude of etiologies associated with decreased milk production in sows.

Nonetheless, PDS contributes to reduced longevity of sow herds, as insufficient milk production reduces piglet growth and survival during the pre-weaning period, ultimately compromising sow and piglet productivity and increasing rates of premature sow removal.

However, the prevalence of PDS and removals due to PDS are not well understood in the swine industry, partially due to insufficient records of sow removals. Additionally, variations in the definition of PDS as well as in the criteria used for determining PDS between farms make it challenging to accurately estimate PDS prevalence (Maes et al., 2010).

Identification of PDS in sows is challenging, as this condition is often subclinical and symptoms may be subtle and difficult to recognize.

Additionally, signs of PDS are non-specific and highly variable, adding to the complexity of this condition. Signs of PDS include lack of udder fill, elevated rectal temperature, belly-laying, decreased appetite, vaginal discharge, mastitis, and lack of milk secretion (Maes and Farmer, 2024).

Observations in piglets include mortality, diarrhea, poor growth, variation in body weight, and remaining close to the sow between nursing periods (Maes and Farmer, 2024).

At the herd level, PDS may reduce productivity as observed by low or variable piglet weights at weaning or decreased piglets weaned per sow per year (Farmer et al., 2019).

Another indication that a herd may be affected by PDS is a higher incidence of sows being weaned early (between days 2 and 12 of lactation), as this may indicate poor lactation performance. In this case, piglets may be transferred to a “nurse” sow, although this depends on availability.

EVALUATION OF CIRCULATING FACTORS ASSOCIATED WITH PDS

To better understand the physiology underlying PDS development, we conducted a study (Studer et al., 2024) on a commercial farm with a history of sows being weaned early due to poor lactation performance. The objective of this study was to evaluate circulating immune cells, analytes, and inflammatory markers in PDS-affected sows compared to healthy herd-mates before symptoms of PDS were observed and at PDS diagnosis (Figure 1).

Blood samples were collected from sows within 24 hours post-farrowing (timepoint 1) to obtain a bank of samples before identification of PDS. Sows were subsequently monitored for signs of PDS, including elevated rectal temperature (>102.9 °F), lack of udder fill, laying on underline (on the udder) to prevent piglets from suckling, gaunt piglets, and piglets demonstrating milk-searching behavior.

When a sow met the criteria for PDS, a healthy sow of the same parity and day of lactation was identified for use as a control, and blood samples were collected again from both sows (timepoint 2). Identification of PDS occurred 9.3 ± 2.7 days after farrowing.

From the 374 sows sampled at timepoint 1, 36 sows with PDS symptoms were identified and matched by parity and day of lactation with 36 healthy control sows.

Sow parity in the PDS group ranged from one to six (Figure 2), with the average parity being 3.0 ± 1.3.

Additionally, records were collected of sows that had previously experienced a shortened lactation, defined as piglets being weaned less than 16 days into lactation. This data revealed that 47.2% of PDS-affected sows had been weaned early in previous lactations, whereas only 8.3% of control sows had previously experienced a shortened lactation.

This finding agrees with an early study stating that sows affected with agalactia in the previous parturition were more likely to experience agalactia at the next parturition (Hermansson et al., 1978).

PIGLET PERFORMANCE AND SOW RECTAL TEMPERATURE

Piglet performance was utilized as an indirect measurement of sow milk production. It revealed that average daily gain was 55% lower and mortality was 5-fold higher in litters from PDS-affected sows compared to control (P < 0.01), indicating reduced milk production in PDS-affected sows.

Evaluation of sow rectal temperature revealed that PDS-affected sows did not have significantly higher temperatures than control sows until the fourth and fifth days of lactation (Figure 3).

This observation emphasizes the importance of evaluating sow rectal temperature along with piglet weight gain, as early studies relied heavily on elevated rectal temperature within 12 to 24 hours post-farrowing as the main criterion for identification of PDS.

CIRCULATING FACTORS ASSOCIATED WITH PDS

Hematology analysis revealed that differences in immune cell populations were not observed between PDS-affected and control sows at timepoint 1.

However, lymphocytes were 11.6% higher (P = 0.06), and neutrophil percentage was 6.9% lower (P = 0.03) in PDS-affected sows compared to controls at timepoint 2.

Interestingly, hemoglobin (HbC) was 4.1% higher (P = 0.04) in PDS-affected sows at timepoint 2, and average HbC was > 10 g/dL in both PDS-affected and control sows at both timepoints. Similarly, Nachreiner and Ginther (1972) reported that sows that developed agalactia had higher HbC within 48 hours prior to farrowing and within 24 hours post-farrowing compared to the unaffected sows.

In regard to the clinical chemistry analysis, differences in liver enzymes were observed, with alanine aminotransferase being 8.9% higher in PDS-affected compared to control sows at timepoint 1 (P = 0.06).

Additionally, aspartate aminotransferase was 26.6% higher at timepoint 1 (P < 0.01) and 23% higher at timepoint 2 (P = 0.06) in PDS-affected sows compared to controls.

Furthermore, blood urea nitrogen was 12.1% higher at timepoint 1 (P = 0.08) and 15.7% higher at timepoint 2 (P = 0.01) in PDS-affected sows.

Differences in serum protein levels were observed at timepoint 2, with albumin levels being 5.7% lower (P = 0.01) and globulin levels being 28.7% higher (P < 0.01) in PDS-affected sows.

Evaluation of inflammatory markers revealed that the acute phase protein haptoglobin was 21.4% higher (P = 0.04) at timepoint 1 in PDS-affected sows compared to controls. Similarly, Kaiser et al. (2018) reported elevated haptoglobin in PDS-affected sows within 12 to 36 hours post-farrowing compared to healthy sows. Lastly, lipopolysaccharide binding protein was 48.3% higher in PDS-affected sows compared to controls at timepoint 2 (P = 0.07).

In summary, this study demonstrated that differences in circulating analytes and inflammatory markers exist within 24 hours post-farrowing in sows that subsequently developed PDS compared to healthy herd-mates. Additionally, differences in hematological factors observed at diagnosis of PDS may provide insight into the physiology underlying this multifactorial syndrome.

FUTURE DIRECTIONS

In addition to this work, we have characterized alterations to the serum metabolome and have evaluated differences in the fecal and vaginal microbiota of PDS-affected sows compared to healthy herd mates. These studies are in preparation for publication.

References

Díaz, J. A. C. et al. Sow longevity. In: The gestating and lactating sow. 423–452. (2015). doi:10.3920/978-90-8686-803-2_19

Farmer, C. et al. Mammary System. In: Diseases of Swine. 11th ed. 313–338. (2019). doi:10.1002/9781119350927.ch18

Hermansson, I., S. Einarsson, K. Larsson, and L. Bäckström. On the agalactia post partum in the sow. A clinical study. Nord. Vet. Med. 30:465–73. (1978).

Kaiser, M. et al. Inflammatory markers before and after farrowing in healthy sows and in sows affected with postpartum dysgalactia syndrome. BMC Vet. Res. 14:83. (2018). doi:10.1186/s12917-018-1382-7

Lucia, T. et al. Lifetime reproductive performance in female pigs having distinct reasons for removal. Livest. Prod. Sci. 63:213–222. (2000). doi:10.1016/S0301-6226(99)00142-6

Maes, D. and C. Farmer. Postpartum Dysgalactia Syndrome in Sows: A Review. In: Production Diseases in Farm Animals. (2024). 319–338. doi:10.1007/978-3-031-51788-4_14

Maes, D. et al. Postpartum dysgalactia in sows: pathophysiology and risk factors. Tierärztliche Prax. Ausgabe K Kleintiere / Heimtiere. (2010). 38:S15– S20. doi:10.1055/s-0038-1622890.

Nachreiner, R. F., and O. J. Ginther. Porcine agalactia: Hematologic, serum chemical, and clinical changes during the preceding gestation. Am. J. Vet. (1972). Res. 33:799–809. doi:10.2460/ ajvr.1972.33.04.799.

Studer, J. M. et al. Evaluation of circulating immune cells, analytes, and inflammatory markers in sows affected with postpartum dysgalactia syndrome. J. Anim. Sci. 102:skae270. (2024). doi:10.1093/jas/ skae270.

Jamie M. Studer
Iowa State University

Jamie Studer is a postdoctoral researcher in swine reproductive physiology at Iowa State University. She received her Master’s (2021) and PhD (2025) in Swine Reproductive Physiology at Iowa State University under the direction of Dr. Jason Ross.