Although porcine reproductive and respiratory syndrome (PRRS) was recognized in the U.S. swine population as early as 1989, the porcine respiratory disease complex (PRDC) was not recognized until the middle of the following decade.
Among the pathogens associated with PRDC, Mycoplasmal pneumonia and swine influenza virus (SIV) were most commonly seen when finishing pigs hit the “respiratory disease wall” at ages 14 to 17 weeks. Clinical disease is more severe in pigs that are infected with both agents.
In 1997, a wasting disease associated with porcine circovirus type 2 (PCV-2) infection was described. Within the last two years, several investigators have confirmed PCV-2 as the main cause of postweaning multisystemic wasting syndrome (PMWS). Due to its ability to suppress the immune system of the pig, it can also be a major contributor to PRDC.
Until PRDC was recognized, pigs were not routinely vaccinated for SIV. It was realized that control of SIV in the growing pig could minimize the impact of PRDC, and pig vaccination became common. Using an existing commercial vaccine and proper timing, control was easily accomplished through vaccination of sow herds and growing pigs.
More recently, producers were confronted with another disease that looked like SIV, but did not respond to vaccination against H1N1 SIV. A new subtype of SIV, H3N2, was first confirmed in 1998 in a new 2,400-sow herd experiencing a massive abortion storm and excessive sow mortality.
For the next year, H3N2 SIV was responsible for over two-thirds of the respiratory disease outbreaks in U.S. herds. In that time, a conditionally licensed vaccine was developed for the new subtype, and was used extensively. Within two years after the emergence of H3N2 SIV, H1N1 SIV had reemerged as the primary pathogen associated with SIV outbreaks.
Along with the return of H1N1 SIV as the primary influenza pathogen, a new subtype of SIV emerged throughout the country, H1N2. Its emergence was predicted at the time H3N2 SIV became dominant in U.S. herds.
When pigs are simultaneously infected with both H1N2 SIV and H3N2 SIV, re-assortment of the segmented genome of the two viruses can occur in the infected pig. The new virus, possessing the H1 and other proteins of H3N2 SIV, was then able to spread to other pigs. Diagnostic and research laboratories have confirmed the presence of H1N2 SIV in all of the major pork-producing states.
In the United Kingdom (UK), H1N2 has become the major subtype of SIV associated with respiratory disease in producers' herds. The H1N2 SIV of the UK is much different than the U.S. version. At this time, we don't know if the American H1N2 subtype will become a significant cause of SIV in U.S. pigs.
Because it is derived from two viruses for which vaccines are already available, disease may be minimal for herds vaccinated against both H1N1 and H3N2 SIV.
Due to the presence of three different subtypes of SIV in U.S. herds, it is very important to determine which subtype is causing disease in your herd. Serologic testing alone for H1N1 and H3N2 will not confirm the presence of H1N2 SIV, nor will polymerase chain reaction (PCR) testing of either infected tissues or swabs or viral isolates from those specimens.
Only specific typing of the viral isolate will confirm infection due to H1N2, H1N1 and H3N2 SIV subtypes.
To make subtyping possible, submit the proper samples for diagnostic evaluation. In all cases, pigs or pig specimens should only be submitted for virologic evaluation when pigs or sows are febrile (body temperatures of 104° F or higher with a clear nasal discharge). Pigs or sows with white nasal discharge should not be submitted.
Viral shedding is very brief for SIV and typically doesn't exceed five days from the time of exposure (the first 2-3 days of clinical illness). Affected nursery pigs will be reluctant to rise or will move very slowly and will be hot to the touch.
If abortions occur as a result of SIV, sows will be off feed and feverish.
For lab submissions to confirm the presence of SIV, swab sows near aborted sows that appear normal but have a fever of 104° F or higher. Deep nasal swab specimens should be collected with dacron or polyester swabs, being certain to insert the swab towards the center of the nose to assure sampling of the nasal septum epithelial lining. Discard swabs with a lot of blood.
Swab samples should be kept moist and cool after collection for submission to the laboratory. Place swabs in a closed tube with a few drops of non-chlorinated water or saline.
When growing pigs are examined for lesions, SIV-infected lungs typically have a blotchy red lesion pattern due to a bronchopneumonia. The lesion areas and a small amount of adjacent, normal-appearing lung tissue should be submitted for laboratory examination.
Fresh lung can be examined by the fluorescent antibody tissue section test or by direct antigen capture enzyme-linked immunosorbent assay (ELISA). Both procedures are rapid and can provide confirmation of SIV within a matter of minutes to a few hours.
Serologic testing with either the hemagglutination inhibition (HI) test or by ELISA is needed to determine if vaccination is properly timed to prevent clinical disease in both sows and pigs. Even when the proper subtypes are included in a vaccination program, results may not always be satisfactory. Two of the most common causes of failure to control clinical disease by vaccination are improper gilt immunization and vaccination of growing pigs when residual colostral immunity is present.
Pigs with HI antibody titers as low as 1:10 may not respond to vaccination against H1N1 SIV. Unlike H1N1 SIV, pigs can be effectively immunized against H3N2 SIV in the presence of low residual maternal antibody titers of either 1:10 or 1:20, and possibly as high as 1:40. The impact of maternal immunity on piglet vaccination for protection against H1N2 SIV is unknown at this time.
A common question concerns the relationship of an ELISA S/P (sample to positive) value to HI titers in terms of ability to vaccinate pigs. At this time, a commercial antibody test kit is only available for H1N1 SIV. According to the manufacturer, and in correlation testing by HI, an ELISA S/P of 0.40 correlates with a HI titer of 1:10.
When using ELISA serology to evaluate sow herd vaccination programs, it is very important to evaluate gilts and low parity sows to determine if their serologic profiles match those of the older sows in the herd.
Gilts and sows should be bled 2-3 weeks after their 30-day pre-farrow booster immunization. By testing at that time, antibody levels are highly reproducible and represent the peak immune response to the booster vaccination. No less than 10 gilts, 10 parity 1 sows and 10 parity 2 sows should be bled and compared to 30 serum samples evenly distributed across all older parity sows. From 10 to 20, 3- to 4-week-old nursery pigs should be bled for herd evaluations.
ELISA data should be evaluated by determining the geometric mean S/P ratio for each parity tested. A geometric mean is different from a arithmetic mean (adding all S/P values and dividing by the number of pigs tested). Geometric mean values involve the addition of logarithmic values, divided by the number of samples. Geometric mean S/P compensates for changes in antibody development in the pig during its immune response to infection.
Evaluation of the geometric mean S/P for each parity will determine if gilts are being properly immunized before entry into the sow herd. Herds with little disease due to H1N1 SIV typically have geometric mean S/P values of 1.50 to 1.60, with most parities having mean S/P values of 1.50 to 1.55.
Older parity sows (P-6 or higher) are most likely to have S/P values of 1.60 or greater. Geometric mean S/P values for gilts, P-1 and P-2 sows should be very similar, and should be nearly the same as those obtained for older parity sows.
Routine use of the H1N1 ELISA in our laboratory has resulted in the development of guidelines for producers utilizing a 30-day pre-farrow booster immunization program and is compared to S/P values obtained for 3- to 4-week-old nursery pigs.
Maternal antibody S/P values in 3-week-old pigs will mirror the overall sow herd geometric mean S/P. For example, a sow herd mean S/P of 1.50 will typically result in a 3-week-old nursery pig S/P value of around 1.4. It appears that the colostral antibody “half life” or uniform decay pattern by ELISA is a linear decay curve of 2-week increments.
USDA-licensed vaccines have been proven to be effective against both H1N1 and H3N2 SIV infection of pigs and sows. As implied above, herd immunity must be uniform to protect growing pigs through the nursery. Typically, this is achieved by the administration of at least two doses of vaccine in the gilt developer, followed by a third dose of vaccine 30 days prior to farrowing.
In some cases, replacement gilts are vaccinated once as grow-finish pigs. It is important to realize that a single dose of SIV vaccine will only prime the pigs for a secondary immune response to either a second dose of vaccine or natural infection with SIV. For that reason, a gilt that receives a single dose as a growing pig should also receive two doses of SIV vaccine either later on in the gilt developer prior to shipment or in isolation prior to addition to the sow herd.
When clinical losses are occurring due to SIV in the middle of the finishing period, some producers and practitioners choose to adopt a finishing pig vaccination program against SIV. Remember that inclusion of the subtype of SIV causing disease, in the vaccine administered, is critical to long-term control of SIV on the farm.
The sow herd vaccination program must be coordinated with grow-finish vaccination. Sow herds using a 30-day pre-farrow booster immunization program will provide pigs long-lasting immunity through the nursery. This means that finishers will have to be vaccinated at a heavier weight. Most commonly, immunization with SIV vaccine will not be possible until 12-16 weeks of age.
If SIV hasn't been a problem in sows or nursery pigs for some time, sow revaccination can be changed to a weaned-sow booster program. Such a change results in lower maternal antibody transfer to pigs, thereby providing an opportunity for younger grow-finish pig vaccination.
Antigenic drift has been mentioned many times over the past two years as a possible reason why vaccines sometimes fail to protect sow herds and pigs against SIV. This is caused by amino acid changes in the surface proteins of SIV. If the change is due to infection of partially immune pigs, then the virus can gain an edge to infect those pigs. This would require a change to a newer strain of SIV in the vaccine.
There still is no scientific basis for such a claim of antigenic drift regarding H1N1 SIV. All detailed investigations have failed to turn up enough change in H1N1 strains to cause vaccine failure.
The situation is not nearly as clear for H3N2 SIV. Three different genetic groups of H3N2 SIV have been reported in the U.S. One is represented by a single reference strain from Colorado, and has not been reported as a common strain in field isolates. The other two groups are represented by the triple re-assortment H3N2 SIV strains recovered from the major pork-producing states in 1998 and 1999. The Texas 1998 prototype isolate recovered by the National Veterinary Services Laboratories in Ames, IA, in 1998 represents one group. The second group is represented by four 1999 isolates from Wisconsin, Oklahoma and Indiana.
Whether these variances represent major antigenic drift among H3N2 SIV isolates is unknown.
To date, there is no indication that H1N2 SIV isolates are different from each other. Since all viral proteins are derived from the currently circulating H1N1 and H3N2 SIV strains that are present in USDA-licensed vaccines, one would predict protection from infection if both H1N1 and H3N2 vaccines are given to pigs.