Swine influenza virus can be found somewhere in the U.S. hog population pretty much year round, yet diagnosing this common ailment is not always easy. That's because of the different SIV subtypes that have emerged and the antigenic variation within those subtypes.

So what's a producer to do?

Veterinarian Kurt Rossow, with the University of Minnesota veterinary diagnostic laboratory, offers some suggestions that you and your veterinarian can use to smooth out SIV's diagnostic rough spots.

He points out that while experience with H1N1 can offer some guidance in addressing other SIV subtypes, the emergence of those new versions have made things more complex. He reminds everyone that SIV is always ready to throw you a curve, and that many questions about the disease remain unanswered.

So, here is Rossow's list of frequently asked questions about diagnosing SIV.

Q  What are specific hemagglutination inhibition (H1) titers?
A  It's difficult to find a list defining SIV H1 titers. Many answers are based on experimental infections or field experiences measuring natural infections. Laboratories often use a titer of > 1:40 as evidence of a specific SIV H1 titer. But, that doesn't mean that a titer of 1:10 or 1:20 is not specific. They may simply represent low-antibody titers in a population facing early infection or with declining antibody levels.

You need to consider H1 titers in the context of clinical findings. For example, in a group of 30 sera from asymptomatic and unvaccinated sows, the H1N1 H1 titers may range from 1:10 to 1:40. If they're composed mostly of 1:10 to 1:20 titers, with only a few 1:40s, a H1N1 ELISA test may help determine whether the H1 titers are nonspecific (negative ELISA results) or if they truly do represent low titers.

However, in a group of 30 sera from asymptomatic, unvaccinated 16-week-old pigs with negative H1N1 or H3N2 titers – exhibiting only a single positive at 1:40 – you could interpret that 1:40 as a nonspecific reaction.

Inaccurate interpretation occurs when the clinical signs and vaccination status are not considered.

Q  H1N1 or H3N2 virus has been isolated, but convalescent sera have negative or low H1 titers. Why?
A  Timing is important when collecting convalescent sera and identifying the correct population. Samples should be collected four weeks after the onset of SIV infection, and they should come from pigs known to have clinical disease.

There also is serological variation among H1N1 and H3N2 viruses when you use the classic H1N1 and the prototype H3N2 A/SW/TX/98 as a measure. Other possibilities are laboratory error and improper sample handling.

Q  When does maternal-antibody decay occur?
A  The maternal antibody persists for 8 to 16 weeks, depending on the initial antibody level. In naturally exposed, unvaccinated sows, 10 weeks is common. Neonatal pigs from vaccinated sows tend to have comparable maternal antibody levels. The higher the sow titer, the later the antibody decay.
If you are basing vaccination protocols on maternal-antibody decay, you need to measure and interpret it for each herd.

Q  Nursery pigs are coughing and we think it's SIV, but we can't get a diagnosis. Why?
A  SIV is shed early during infection, so ideally you should test pigs that are febrile and have been affected for two to three days. A pig with a dry cough is a better candidate than one with a wet, productive cough. Lungs from necropsied pigs offer the best diagnostic sample. However, you also can submit nasal swabs.

Maternal antibody helps alleviate clinical signs associated with SIV infection in nursery pigs. However, pigs with circulating maternal antibodies can still be infected with SIV and shed the virus.
Successful virus recovery is inversely related to maternal antibody levels. Of course, the issue may not be SIV at all, which means you need to investigate further.  

Q Last month, my nursery pigs were diagnosed with SIV. Why are the convalescent titers lower than the acute titers?
A Maternal antibody does not prevent SIV from infecting nursery pigs. It will interfere with antibody production in response to the acute infection. This will result in continued maternal antibody decay and an unexpected decline in the convalescent titer.

Nursery pigs infected with SIV will be susceptible again when the maternal antibody disappears.

Q Which test should my veterinarian use to monitor vaccine compliance?
A He or she can use H1N1 H1 or H1N1 ELISA tests to monitor antibody development, which is an indication of vaccination.

The H1N1 virus in the H1 test would need to react with vaccine antibodies. If needed, you would have to run a separate H3N2 test to measure the response to the vaccine's H3 component. It's important to sample pigs two to four weeks after you've given the vaccine booster dose.

Q Which serological test should we use to monitor my SIV-negative herd?
A H1N1, H3N2 and probably H1N2 infections can occur independently. Although it's not available, a serological test to measure a common Group A influenza antibody would be helpful.

To get the answer, you would have to run tests measuring H1 and H3 antibodies. Also, you would have to test coughing pigs in SIV-negative herds for SIV, because you can detect it prior to seroconversion.  
 
Q We have measured maternal antibody decay, but natural infection occurs before we can vaccinate pigs. Why?
A Generally speaking, the more pigs carrying an infectious agent, the faster it will spread to SIV-nanve pigs. The goal is to reduce the amount of circulating SIV in the nursery at the time of antibody decay. You can do this by improving sow vaccination.

If the sow herd is already well vaccinated, it would be wise to characterize the SIV isolate to see if it's different than the one in the vaccine.

Q Are pigs persistently or latently infected with SIV?
A There is no evidence of either. SIV is maintained in a population by direct contact. Transmission likely occurs throughout the year. However, the minimum population size needed to maintain SIV infection is unknown. Clinical breaks are generally due to the introduction of a new virus or waning herd immunity.

Q How is SIV spread?
A Direct contact between animals or aerosol drop-lets can spread SIV. Aero-solized virus is more likely to survive and spread in cooler months with lower humidity.

Q Is the H or N type important in the animal's immune response to virus infection?
A Resistance to infection or evidence of SIV infection is associated with antibodies to the hemagglutinin (HA) and neuraminidase (NA) glycoproteins. Serum antibody levels of HA and NA correlate to protection from disease and to declining amounts of SIV replication in the respiratory tract. Specifically, HA antibodies can prevent infection, while NA antibodies help reduce virus replication after infection.
 
Q Is protection against one H subtype cross-protective for another within the same subtype?
A Yes and no. Cross protection within an SIV subtype has been documented. But, infection with a swine influenza virus closely related to the previous virus may occur, and protection may depend on the levels of circulating or local antibody.

Also, the initial SIV infection has an antibody response to a limited number of HA glycoproteins. Exposure to additional HA glycoproteins results in a broader range of antibodies produced.

Q  Can I test piglet fetuses for SIV?
A  SIV can only be found in fetuses if the sow was viremic – and viremia is rare in SIV infection. Abortion in sows dealing with SIV is likely caused by a secondary effect of the illness, such as fever. But, fetuses can be used to rule out other possible abortion causes.

Q  Can we detect infection with H types other than H1 and H3?
A  Yes. Most of the tests used to detect SIV infections are directed against a common Group A influenza component. We can identify the infection as influenza virus, but differentiation of an unusual virus requires genetic analysis and serological classification.

Q  Will more unusual influenza viruses turn up?
A  Probably – unusual influenza viruses (non H1 or H3)  will probably infect pigs. However, the significance is not whether they can occur, but how well they can compete and interact with the established SIV population. 

Editor's note: The information within this article was adapted from Rossow's presentation at the 2002 Allen D. Leman Swine Conference.