Environmental Protection Agency regulations restricting the amount of phosphorus (P) that can be applied to the land have researchers examining ways of reducing P dietary supplementation to swine as well as minimizing the excretion of P.
To reduce P excretion while maintaining animal performance, researchers have studied the requirements for different genotypes and management conditions, plus ways of improving the bioavailability of P through plant sources.
Iowa State University researchers are focusing on the underlying genetic mechanisms behind P utilization and the impact it could have on commercial pork production. Limited research is available on the effects of P nutrition on gene expression in non-agricultural animals, and only a few genes have been studied previously.
Iowa State researchers examined the effects of P nutrition on large-scale gene expression in pigs from two different sire lines – one selected specifically for meat quality, the other for growth rate.
Microarray analysis showed sire treatment effects in gene expression in both liver and muscle tissue. Sire x treatment effects were noted in the expression of genes known to affect bone marrow.
Researchers noted, after only two weeks on the experimental diets, significant sire effects on bone strength and ash percentage. Sire x treatment effects were also seen for average daily gain and feed conversion. However, traditional plasma indicators of P levels, inorganic P concentration and alkaline phosphatase activity did not show any sire or sire x treatment effects, they reported.
Future work will focus on identifying new gene targets for better P utilization and markers for genotype-specific P requirements. The goal is to enable genetic selection of pigs that require less P and excrete less P, and identification of genetic lines to match producers’ waste management strategies.
Researchers: A. Qu, L. Hittmeier, L. Grapes, M.F. Rothschild and Chad Stahl, Iowa State University. Contact Stahl at (515) 294-5990 or e-mail cstahl@iastate.edu.
Timing for artificial insemination (AI) is commonly based on expressions of estrus. Success with AI is largely reliant on the heat-check boars’ abilities to stimulate these expressions of estrus and the breeding technicians’ abilities to recognize them.
However, wean-to-estrus and estrus-to-ovulation intervals are variable. Both are influenced by other factors, such as follicle size, season, parity and lactation length. Researchers at the University of Illinois chose to focus on wean-to-ovulation interval, noting it has not been studied extensively and could be less variable.
If the factors influencing wean-to-ovulation intervals can be more accurately identified, a fixed-timed AI procedure could be developed, and the costs and labor of estrous detection could be eliminated, they speculated.
In an effort to characterize the factors influencing wean-to-ovulation interval, researchers performed a retrospective analysis from eight studies between 1998 and 2005. Sows were divided into two groups – 136 sows that received PG600 at weaning (PGW), and 650 sows that received no treatment at weaning (NOW).
Researchers found little variation in the wean-to-ovulation interval, with most sows ovulating within six days after weaning (6.0 +/- 0.9 days); 85% of sows ovulated within a 36-hour period between Day 5 and Day 6.5. Only 5% of sows ovulated on Days 2 to 4.5. Ten percent ovulated between Days 7 and 10 after weaning (Figure 1).
Wean-to-estrus and wean-to-ovulation intervals were inversely related. As wean-to-estrus inter val increased, wean-to-ovulation interval shortened, researchers reported. Regardless of the wean-to-estrus interval, most sows ovulated within a similar interval from weaning.
Looking closer, researchers found the PGW treatment advanced the wean-to-ovulation interval by more than half a day, and increased the proportion of sows ovulating closer to weaning when compared to the NOW sows (Figure 2). In other words, more of the PGW-treated sows ovulated earlier. Previous studies indicated that about 10% more PGW sows express estrus and ovulate within seven days of weaning. Therefore, insemination times for PGW sows should be altered.
Season and parity did not influence wean-to-ovulation, they noted. However, when lactation length extended beyond 18 days, wean-to-ovulation interval was shorter than sows that nursed less than 18 days.
Researchers concluded it would be difficult to breed 85% of sows within 24 hours before ovulation using a fixed-time insemination procedure. In particular, if single insemination were practiced, those sows ovulating early or late from the norm would likely miss the preferred 24-hour insemination window.
Double insemination would cover a greater percentage of sows ovulating, but would undoubtedly allow for late inseminations of the early-ovulating sows. Late inseminations reportedly cause some reproductive problems.
Likewise, increasing the number of inseminations or shortening the interval between inseminations may be detrimental to conception rates and litter size. In other words, fixed-time inseminations could risk failure due to early- or late-ovulating sows.
Semen extenders or techniques that allow sperm to survive longer within the sow’s reproductive tract, or hormonal treatments that reduce variation in ovulation time, could remedy these concerns.
Researchers agree that further investigation is necessary to refine insemination-timing procedures.
Researchers: S.M. Breen and R.V. Knox, Department of Animal Sciences, University of Illinois. Contact Knox at (217) 244-5177 or e-mail rknox@uiuc.edu.
The most important disease affecting U.S. pork production is porcine reproductive and respiratory syndrome (PRRS). With losses estimated at nearly $600 million annually, the identification of genetically-resistant breeding stock would be a significant advancement in controlling the disease.
Work conducted at the University of Nebraska, led by Rodger Johnson, has proven that genetic variation in resistance to PRRS virus infection exists. In a recent manuscript, Johnson’s group reported differences in responses to PRRS virus infection in two genetic lines of pigs.
Pigs from the Nebraska Index line (NEI), selected 20 generations for litter size, and commercial Hampshire-Duroc cross pigs (HD), selected for lean growth, were compared for responses to PRRS virus infection.
At 26 days of age, pigs were infected intranasally with PRRS virus. Viral load (viremia); weight; and rectal temperature at 0, 4, 7, and 14 days post-infection (dpi) were recorded for PRRS-infected and litter-matched control pigs. Lung, bronchial lymph node, and blood were collected at necropsy (14 dpi).
Infected NEI pigs had greater weight gain, decreased viremia, and decreased clinical signs than infected HD pigs. D.B. Petry and his colleagues concluded that line differences, and line by treatment (infection) interactions across days, indicate genetic variation in responses to PRRS virus. Overall, NEI pigs were more resistant to PRRS virus than HD pigs.
Researchers then used principal component analyses to rank pigs for phenotypic response to PRRS virus. Pigs were classed either as low (L) responders (low viremia, few lung lesions, and high weight change) and high (H) responders (high viremia, many lesions, low weight change).
Infected (+) low-responder NEI pigs (LNEI+) had the lowest viremia at day 14 (Table 1), low clinical signs in their lungs, and greater weight gain than high responder NEI pigs (HNEI+) and either low- or high-responder HD pigs (LHD+ or HHD+).
If underlying genetic variation determines whether pigs will effectively limit virus replication after infection with PRRS virus, the next challenge is identifying the genes involved.
Likely targets for control of most viral infections are immune genes (Table 2). There are innate immune factors, those that react immediately to infections but are non-specific. Most viruses require more specific responses, such as interferon-gamma (IFNG) related genes, termed T helper 1 (Th1) genes.
Alternately, some viruses decrease the host immune response by stimulating regulatory T cell genes, such as interleukin-10 (IL10), that can turn off immune responses.
To evaluate the role of these immune genes, a collaboration funded by the USDA PRRS Coordinated Agricultural Project (PRRS-CAP) grant was established between Nebraska scientists and Joan Lunney’s lab at the USDA’s Beltsville Agricultural Research Center.
For these immune gene studies, RNA was prepared from frozen lung and lymph node tissue of seven pigs in each group: LNEI+, HNEI+, LHD+, HHD+, and their control littermates; cDNA expression of the 12 genes noted in Table 2 was performed and data were statistically evaluated.
Overall, HD pigs had greater magnitude of difference in expression of immune genes in their lung and lymph node tissue at 14 dpi than NEI pigs. To confirm these results, serum protein levels of a subset of the Table 2 immune markers were tested. These tests affirmed the lung gene expression differences.
Thus, following PRRS virus infection, low expression of IFNG in cDNA and in serum were correlated with resistance. This low IFNG, along with low serum antibodies, is the opposite of what might be expected. One might predict that a “better” immune response would produce higher levels of IFNG and antibodies. But PRRS virus-resistant pigs had lower levels of IFNG and antibodies.
An additional immune marker was identified: PRRS virus-resistant pigs had high pre-infection serum levels of the innate cytokine interleukin-8 (IL8). This suggests that pre-activation of the innate immune system may help to prevent viral expansion.
These data outline targets for future studies of genetic association, to determine if specific immune gene alleles are associated with PRRS virus resistance. Such studies will help determine the actual causative alleles, thus enabling producers to decrease breeding of PRRS-susceptible pigs, and specifically select for PRRS-resistant stock.
Because of the likely involvement of important immune genes, it will be essential to determine whether PRRS-resistance alleles are also associated with resistance to other viral infections.
Researchers: Rodger Johnson, University of Nebraska, Lincoln, NE; Derek Petry, Monsanto Choice Genetics, St. Louis, MO; Joan K. Lunney, Animal Parasitic Diseases Laboratory, ANRI, ARS, USDA, Beltsville, MD. Contact Lunney at (301) 504-9368 or e-mail jlunney@anri.barc.usda.gov.