Dam Parity May Impact Pigs' Immunity Levels
Preliminary results of research at the University of Nebraska suggest that health status, as indicated by circulating immunoglobulin concentrations in baby pigs, may be affected by dam parity.
Researchers investigated the health status of different parities by evaluating the ability of Parity 1 (P1) and Parity 3 (P3) dams to produce and passively transfer immunoglobulins (IgA and IgG) to their offspring.
General observation is that P1 progeny have reduced health status compared to progeny from older sows (Table 1). But these differences in health status of pigs from different dam parities have not been fully clarified.
The objective of the University of Nebraska study was to provide baseline information to gain a greater understanding of parity health differences by evaluating production and transfer of immunoglobulins from dams of increasing parity to their progeny.
Large White x Landrace females were part of an ongoing sow longevity experiment at the University of Nebraska.
After farrowing, 4-5 piglets from five, Parity 3 sows and four, Parity 1 gilts were randomly selected for analysis.
Three parameters were evaluated to assess the health status of progeny derived from different parities:
Circulating concentrations of IgA and IgG in P1 and P3 dams;
Concentrations of IgA and IgG during lactation in colostrum and mid- and late-lactation milk; and
Circulating concentrations of IgA and IgG in P1 and P3 progeny.
Whole blood was obtained from each dam 24 hours pre-farrowing and from dam progeny at 0, 8, 15, 20 (weaning), 29 and 37 days post-farrowing.
The concentrations of IgA and IgG in serum obtained from P1 and P3 females 24 hours prior to parturition are depicted in Figure 1. The values for both immunoglobulins are within normal ranges.
However, P3 females had greater concentrations of both IgA and IgG compared to P1 females. The higher stress load on P1 females may dampen their immune response, researchers noted.
This trend for differences in circulating concentrations of immunoglobulins at the time of parturition did not continue when IgA and IgG concentrations were evaluated in colostrum and milk samples from the same females (Figure 2). The IgA and IgG concentrations observed in colostrum samples obtained within 12 hours of farrowing were greater than immunoglobulin levels detected in milk samples obtained at mid- or late lactation.
“Although differences exist in immunoglobulin concentrations in the serum of these same females, it was somewhat surprising that no differences in colostrum or milk immunoglobulin concentrations were observed during lactation,” says lead researcher Thomas E. Burkey.
Figure 3 depicts circulating IgA and IgG concentrations in P1 and P3 progeny at several time points following parturition. The progeny of P3 females had greater levels of IgG compared to the progeny of P1 females at every time point evaluated, with a similar trend observed for IgA.
Progeny immunoglobulin concentrations from birth to about 2 weeks of age are almost completely due to passive transfer from the dam. Baby pigs rely on passive transfer of immunity via colstrum, and milk from the dam until they can mount their own immune response at 2 to 5 weeks of age.
Researchers: Thomas E. Burkey, Phillip S. Miller, Rodger K. Johnson, Duane E. Reese and Roman Moreno, all of the University of Nebraska. Contact Burkey at (402) 472-6423.
|System 1a||System 2b|
|Parameter||P1 Progeny||P2 Progeny||P1 Progeny||P2 Progeny|
|Weaning wt., lb.||12.10||13.00||11.70||12.60|
|Avg. daily gain, lb.||0.92||0.95||0.91||0.96|
|Avg. daily gain, lb.||1.99||2.01||1.62||1.69|
| aAverages calculated from 242,406 and 677,661 P1 and P2 progeny, respectively. |
bTotal number of progeny were not included.
Circovirus Spread Via Semen Studied
Because porcine circovirus-associated disease (PCVAD) has spread rapidly across North America, boar semen has been implicated as a possible source for dissemination of the virus.
To address this issue, and determine if there are differences in semen shedding of porcine circovirus type 2 (PCV2) isolates, 15, 7-month-old PCV2-negative boars were randomly allotted to three different groups. The first group served as control, the second was inoculated with PCV2a (North American-like virus) and the third group was inoculated with PCV2b (European-like virus).
Semen and serum were collected during the 90-day trial at Iowa State University (ISU).
Research concluded that PCV2a and PCV2b were both shed in low levels in semen in the two groups, of experimentally infected boars. Semen was shed for up to 12 weeks.
Overall, the amount of shedding was low and variable among individual boars within groups, and peak shedding occurred approximately three weeks post-challenge.
Detection of PCV2 in semen corresponded well with detection of PCV2 DNA in serum samples and blood swabs.
This trial verified that mature boars shed low quantities of PCV2a and PCV2b in semen, and that semen is a potential route for PCV2 transmission amongst swine herds.
In a second trial, a swine bioassay model was used to determine if PCV2-positive semen was infectious. Twelve, 4-week-old, PCV2-negative pigs were divided into four groups. All of the 4-week-old naїve pigs that were inoculated intraperitoneally (abdominal area) with PCV2-positive semen became infected with either PCV2a or PCV2b.
But when the same semen samples were extended, and used to artificially inseminate PCV2-negative gilts in a third trial, those gilts did not develop PCV2 infection, nor did they show evidence of PCV2-associated reproductive failure. All gilts inseminated with PCV2-positive semen became pregnant and carried pregnancy to term. There was no evidence that fetuses became infected with PCV2.
Researchers concluded that experimental inoculation of boars with PCV2 produces infection; however, it has yet to be determined if PCV2-positive semen is a risk for transmission and dissemination of PCVAD.
Research was funded by the Pork Checkoff.
Researcher: Tanja Opriessnig, Iowa State University. Contact Opriessnig by phone (515) 294-1950, fax (515) 294-6961 or e-mail [email protected] .
Immune Parameters May Signal Why Some Pigs Clear PRRS Virus
Porcine reproductive and respiratory syndrome (PRRS) virus is difficult to rid from herds because infection elicits a weak immune response that is not fully protective.
This results in persistent infection in a subset of pigs, thus providing a continued source of virus circulation within the herd.
Substantial research efforts have not yielded the exact components of a protective anti-PRRS virus immune response, particularly as it relates to persistence.
These shortcomings led researchers at the U.S. Department of Agriculture Agricultural Research Service's (ARS) Beltsville Animal Research Center (BARC) and Kansas State University to use “Big Pig” samples to determine whether immune markers that control PRRS virus persistence can be identified.
The Big Pig project was a PRRS CAP1 (Coordinated Agricultural Project)-supported, multi-institutional (university and commercial), multi-disciplinary experiment initiated in 2005. It was designed to analyze pig responses to PRRS disease, virus replication and immunity in 109 pigs (and 56 control pigs), sampled for up to 203 days post-infection.
Blood samples collected throughout the Big Pig project were evaluated for blood protein levels that might be predictive for pigs that clear PRRS virus rather than pigs that remain persistently infected with PRRS.
The hypothesis was that protective serum cytokine levels 7-42 days post-infection would help predict which pigs were more likely to have persistent viral infection (147-203 days post-infection).
Samples from pigs that apparently cleared PRRS virus from serum and tissues by 28 days post-infection were labeled the Non-Persistent (NP) pigs. Persistent (P) pigs were those that showed evidence of long-term, persistent PRRS infection at 150 days post-infection.
Sera from P and NP pigs collected over the course of the PRRS infection were tested for serum cytokine levels (substances that are secreted by cells of the immune system) following PRRS infection.
NP pigs appeared to have faster and higher levels of serum cytokine Interleukin-8 and anti-viral Interferon-gamma than the pigs with persistent infections. This immune cytokine trend correlated with the clearance of virus from serum and tissues.
Researchers noted this effect might indicate that the NP pig's immune response was faster and more effective than that for pigs with persistent infections, and possibly enabled the NP pigs to prevent PRRS virus infections from becoming persistent.
This conclusion sets the stage for identifying prognostic indicators of persistent infection and for targeting these proteins for anti-PRRS virus biotherapeutics or vaccines.
At present, it is estimated that 60% of U.S. hog operations are infected with PRRS. The National Pork Board calculates PRRS is the most economically significant disease facing the swine industry, costing $560 million annually.
Researchers: Joan K. Lunney, USDA, ARS, BARC; Bob Rowland, Kansas State University. Contact Lunney by phone (301) 504-9368, fax (301) 504-5306 or e-mail [email protected] . Contact Rowland by phone at (785) 532-4631 or e-mail [email protected] .
Serum Sampling is Best PRRS Diagnostic Tool
Serum samples provide the best sample to detect porcine reproductive and respiratory syndrome (PRRS) virus during acute infection, with the blood swab sample performing almost as well in research conducted by the University of Minnesota in collaboration with South Dakota State University, PIC and Boehringer Ingelheim Vetmedica, Inc.
Boar studs are regularly monitored for the presence of the PRRS virus, testing different biological samples by reverse-transcription polymerase chain reaction (RT-PCR).
Usually, samples are run in pools to reduce the cost of submitting individual samples, even though the impact of pooling on the sensitivity of RT-PCR is unknown.
To assess the impact of pooling and collection method on PRRS virus by detection, 29 boars were inoculated with a low virulent PRRS strain. Serum, blood swab and semen samples were obtained from each boar every two to three days for two weeks and tested by RT-PCR.
Eleven of the 29 boars did not appear to become infected from the inoculation. Data from the other 18 boars showed that serum provided the best sample, followed by blood swab.
Other results showed that semen samples failed to detect PRRS infection in most of the cases.
For most of the samples, pooling did not affect the performance of the test. But PRRS detection was missed in a small proportion of pooled samples. The impact of pooling on the sensitivity of PCR was higher in samples taken when infection started. Sensitivity was decreased by 6-8% when serum or blood swab samples were run in pools of five.
This decrease in sensitivity should be taken into account when designing surveillance protocols for boar studs by proportionally sampling more boars.
Researcher: Albert Rovira, DVM, University of Minnesota. Contact Rovira by phone (612) 625-7702, fax (612) 625-1210 or e-mail [email protected] .
Seeking Answers for Postweaning Diarrhea
Porcine postweaning diarrhea (PWD), caused by enterotoxigenic Escherichia coli (ETEC), is one of the most economically significant swine diseases. It causes an estimated $90 million in annual losses due to death of up to 5% of young pigs.
Symptoms of PWD include severe diarrhea, dehydration, slow growth and weight loss.
Despite its importance, there are no commercially available vaccines or treatment options to protect weaned pigs from PWD.
Key virulence factors for PWD are believed to be bacterial fimbriae and enterotoxins produced by ETEC strains. Bacterial fimbriae attach E. coli strains to the small intestine and cause bacterial colonization. Then the colonized E. coli strains secrete enterotoxins, which cause an overproduction of fluid secretions and result in diarrhea.
However, recent studies at South Dakota State University's Center for Infectious Disease Research & Vaccinology indicate that factors causing PWD could be more complicated, and that other virulence factors could be contributing to the disease, making the development of treatment options even more difficult.
K88 and F18 fimbrial strains of E. coli are the dominant pathogens found in pigs with PWD. These E. coli strains produce one or more enterotoxins.
A study of 304 E. coli strains isolated from pigs with PWD suggests that other E. coli toxins and non-fimbrial adhesions could contribute to PWD.
The study found that fimbrial E. coli strains isolated from pigs with PWD express mainly K88 (64.6%) and F18 (34.3%), but also heat-labile (57.7%) and a variety of heat-stable toxins, all of which remain the dominant fimbriae and enterotoxins associated with PWD.
But it is noticeable that enteroaggregative E. coli toxin is commonly associated with PWD, and that the porcine attaching and effacing-associated factor is showing high prevalence in PWD.
To understand the virulence factors for PWD, a study model was developed using genetically engineered E. coli strains with one fimbria and one enterotoxin. Animal challenge studies were conducted using gnotobiotic (germ free) pigs.
It was found that a K88 E. coli strain and a heat-labile toxin cause severe diarrhea in all pigs, and a strain producing K88 fimbria and heat-stable toxin (STb) causes disease in 60-70% of pigs. Other enterotoxins are being investigated for virulence.
An ongoing research project for vaccine development funded by USDA shows promise. So far the vaccine protects pigs from K88 fimbrial ETEC strains. Work continues to add vaccine protection against heat-stable toxins, and acquisition of funds to complete this research project.
Researcher: Weiping Zhang, South Dakota State University. Contact Zhang by phone (605) 688-4317, fax (605) 688-6003 or e-mail [email protected] .