Author: Sue Spiegel

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Maintain sound on-farm biosecurity with PRRS ‘season’ approaching

By Brad Leuwerke, DVM, MS

As we creep closer to autumn’s weather change, crop harvest, manure pumping, etc., we also sneak closer to what has become a predictable rise in new cases of porcine reproductive and respiratory syndrome virus (PRRSv) across the country.

For 10 years now, the Dr. Bob Morrison Swine Health Monitoring Project has shown that the swine industry experiences an annual rise in PRRSv cases over an epidemic threshold in the October to November time frame. If history has anything to say, a similar trend should be expected this fall.

Knowing that one of the biggest drivers of profitability for swine producers is reducing nursery and finishing mortality and culls, those swine producers who are able to keep PRRSv out of their herds will have an economic advantage.

As fall arrives and the number of PRRSv cases begins to rise, swine veterinarians will start to get a sense of whether there are any new or more pathogenic “strains” that may become the new virus to be on the lookout for as an industry.

The last two to three years have given rise to PRRSv 1-7-4 and 1-3-4; both viruses caused severe disease in sow herds, leading to aborted fetuses, piglet mortality and sow mortality.

The other challenge these viruses have presented is the difficulty in eliminating them from sow farms. The “traditional” 210- to 240-day closures designed to eliminate PRRSv from a breed-to-wean farm have not been as successful, forcing many producers to make a decision on whether to keep a herd closed longer in hopes of eliminating the virus or to reload the farm and restart the elimination procedures over again in an effort to not miss production targets.

Research on these viruses and how they are transmitted within a herd has shown that these newer strains are shed for a longer period and are shed in higher amounts from infected animals. There also is speculation that new viruses are able to change more quickly within a population. All of these factors have worked to decrease the success of PRRSv elimination in breed-to-wean herds.

The effects of an increasingly pathogenic virus also can be seen in growing pigs. PRRSv 1-7-4 and 1-3-4 infection in growing pigs continues to be severe, causing greater mortality with higher culling rates and increased treatment costs compared to PRRSv strains observed in the past.

Similar to the observations in sow farms regarding the timing of disease, the effects of PRRSv infection seem to extend to longer periods compared to past PRRSv strains. Nursery and finishing sites that are continuous flow struggle tremendously to eliminate the virus and should consider all-in/all-out or, at the very least, site depopulation to eliminate virus from these populations of growing pigs.

Prevention

The cornerstone of preventing new virus introduction still relies on biosecurity, biosecurity, biosecurity.

Even though newer strains of PRRSv act increasingly pathogenic, sound biosecurity practices — including clean/ dirty lines for site entry, controlled supply entry, organized (clean to dirty) personal movement, dedicated trailers, mortality composting, etc. — help limit virus spread from farm to farm.

Air filtration of breed-to-wean farms continues to be successful. Filtration hasn’t been 100% effective in all cases, but when looking at dense areas where sow herds were breaking multiple times each year, the reduction in the outbreak rate has been extraordinary. Updated technologies, including positive-pressure filtration systems and air conditioning, which reduces the amount of air that needs to come into the barn, continue to move the bar on what can be expected for preventing virus introduction into these farms.

A PRRSv vaccine remains an important tool available to producers for virus control. Recent additions of modified live PRRS vaccines on the market give swine producers further options for vaccines.

In many commercial sow herds, especially those in more densely populated swine areas, a modified live vaccine is used to help maintain immunity at least with the goal of lessening the impact a new virus introduction will have on the herd. In many of these cases, the herds and replacement gilts are vaccinated multiple times each year to maintain immunity.

In growing pigs, millions of pigs continue to be vaccinated for PRRSv (either prior to weaning or at some point while in the nursery). PRRSv vaccines continue to show the ability to reduce lung lesions for pigs that become infected with a non-vaccine strain of the virus. In addition, groups that are vaccinated and exposed to a field virus consistently show closeouts that have less mortality and a lower cull rate compared to nonvaccinated groups that become infected with field strains.

As an industry, we’ll start to see the benefits of new diagnostic technologies, including whole-genome sequencing, which will provide more insight than ever before regarding PRRS circulation and change within a population. Take, for example, herds that are unsuccessful at eliminating a resident PRRSv strain from their herd. Whole-genome sequencing will help determine if that virus continues to be the resident strain or if a completely new virus strain has been introduced into the herd.

It goes without saying that it has been and will continue to be an interesting time for all swine producers. The industry is already starting to make market pigs for June 2020. It’s paramount to keep PRRSv out of the herd. Those producers who are able to limit new virus entry will have a greater opportunity to keep reducing pig mortality and culls, leading to increased profitability.

PRRSv “season” will be here soon, so it’s important to emphasize that the biosecurity practices producers have used for years for PRRSv and other pathogens still apply.

Reprinted with permission of Feedstuffs.

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Is fogging an M. hyo-elimination option for your swine herd?

Paul Yeske, DVM, with the Swine Vet Center in St. Peter, Minn., has seen repeatable success with Mycoplasma hyopneumoniae (M. hyo) elimination, along with the downstream effect of lower cost of production, better average daily gain, better feed efficiency and lower mortality. He estimates the benefit of M. hyo elimination to be in the $3 to $4 range per pig, conservatively, with some herds seeing a benefit of as much as $10 per pig when other diseases are eliminated at the same time. Now, the relatively new protocol of fogging a barn may make M. hyo elimination even more attractive.

This technology came out of the frustration of trying to evenly and efficiently expose animals to the bacterium, Yeske told Pig Health Today. Fogging allows for faster exposure to establish “time zero” for elimination, so gilts can be stable by the time they enter the sow herd.

“That reduction of time for M. hyo to spread from animal to animal in a natural way is probably the biggest advantage,” he said. Previously, Yeske would use intratracheal exposure of seeder animals, but said, “It’s a lot of work and you still have slow spread from animal to animal. Fogging has been very successful for us, although it’s still new technology and there are some lessons to learn as we go forward.”

Research needed

Fogging appears to be an effective method for M. hyo elimination, but Yeske said critical questions need to be answered on the technology:

  • How long can the inoculums be stored?
  • How long can the lungs used for the inoculum be stored if the herd is kept positive?
  • What’s the best media to use for exposure?
  • Should an M. hyo media be used, or can we use phosphate buffered saline?
  • Which products work best for fogging in terms of storage and/or the fogging procedure?
  • What’s the right dosage and volume level?

“So far it’s been very good, even with the experimental method we’ve used, but I think there’s an opportunity for it to be better,” Yeske said, adding that, “We just need to support the researchers to do the difficult work to answer these questions.”

Other methods also effective

Yeske said depopulation/repopulation is the “tried and true” method that works every time but it’s also the most expensive. It’s difficult for people to invest the money unless there are other compelling reasons, such as additional disease challenges or parity re-distribution, he noted.

The herd closure model is to keep a herd closed (no new introductions) beyond 240 days, Yeske said. Hee recommends medicating the sow herd and piglets at the end of the closure, which allowed the pigs’ immune systems to help as much as possible. Timing varies, but this model has been the most successful and has had the least amount of impact on production.

“We’ve been in the 75% to 80% success rate over time and it’s been the most repeatable system,” he said. “Generally, mycoplasma elimination has been done in conjunction with other diseases, such as porcine reproductive and respiratory syndrome (PRRS). It just adds a little more time to standard PRRS-closure and you also get rid of the M. hyo,” he said.

Another method involves whole-herd medication, without a herd closure, but Yeske said the success rate is closer to 50% when medication is done without herd closure.

“If we do limited-herd closure (150-240 days) and then medicate at the end, the process has been more successful and closer to the long-term closure success rates,” he said.

Useful tool for control or elimination

Fogging may not be a silver bullet, but Yeske said it’s a useful tool for M. hyo control, “whether you’re doing ongoing control and acclimating replacements into the herd, or you’re looking at elimination. The technology is fairly inexpensive, so it’s about having your herd veterinarian help set up the program to make sure you’re doing everything the right way.”

Yeske is often asked how likely a herd is to stay negative if a producer goes through the Mycoplasma-elimination process, especially in pig-dense areas.

“We did some research two years ago and found that lateral introductions happen, but they are rare,” Yeske said. “We saw 94% of the herds stay negative, even in pig-dense areas.”

He recommended producers and veterinarians work on herd stabilization, with consideration given to elimination if other issues are impacting the herd.

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The changing face of PCV: Virus experts compare notes on evolving pathogen in US swine herds

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Clinical disease due to porcine circovirus type 2 (PCV2) has been dramatically reduced thanks to vaccination, but concern remains about the persistence of PCV2 subclinical infection, even in vaccinates, and the virus’s propensity for change.

Furthermore, PCV3, a newly identified porcine circovirus that is genetically different from PCV2, is believed to be widespread in US herds and, so far, there’s no consistent evidence it causes disease.

Darin Madson, DVM, PhD

Those were among the observations shared by SVC’s Laura Bruner, DVM, and academicians, scientists diagnosticians at “The Changing Face of PCV,” a roundtable held at the 2018 Leman Swine Conference.

The panel agreed that new genotypes of PCV2 are expected to emerge, although currently the predominant genotype circulating in US herds is PCV2d, according to Darin Madson, DVM, PhD, Iowa State University, a leading PCV expert who tracks the virus’s evolution.

He explained that PCV2 replicates at a high rate for a DNA virus. PCV2a and PCV2b were major players in the US from 2005 until 2012, when a genetic shift to PCV2d occurred. Additional genotypes that have been identified include PCV2e and PCV2f.

‘Pretty unique’

“It’s pretty unique to have a DNA virus mutate to the level [PCV2] has,” Madson said.

Albert Rovira, DVM, PhD

Albert Rovira, DVM, PhD, a diagnostician at the University of Minnesota, said sequencing of PCV2 field strains in 2017 showed that more than 50% were PCV2d.

“What’s interesting is that about 35% were PCV2a, about 12% were PCV2b and about 3% were PCV2e. So, PCV2d is definitely the main genotype, but PCV2a and PCV2b are not gone; they are still there,” he said.

The pattern in Europe has been similar, said Joaquim Segalés, DVM, PhD, of the Universitat Autònoma de Barcelona, another PCV authority. There were big outbreaks of systemic disease that occurred with the shift in genotype from PCV2a to PCV2b around 2000 to 2001, and now it appears PCV2d is increasing in prevalence.

‘Success story’ but…

Despite the shift in the predominant genotype of PCV2, panel moderator and practitioner Clayton Johnson, DVM, Carthage Veterinary Service, said, “Vaccination against PCV2 has been a success story in the industry…but we always ask if things could be better. Subclinical PCV2 disease remains a problem.”

Joaquim Segalés, DVM, PhD

SVC’s Laura Bruner, DVM, of the Swine Vet Center (SVC), said, “Subclinical PCV2 disease is super hard to find…I wasn’t worried about it before, but I think that’s probably what concerns me the most now…PCV2 wasn’t a big deal at first, then all of a sudden it became a really big deal. I don’t want to [go] back there,” she said.

Similar concern was voiced by Vitelio Utrera, DVM, PhD, a swine respiratory disease specialist with Zoetis, who said subclinical infection may be underestimated. “If the vaccines are working well, that brings the genetic shift into question. If there’s no immune pressure, why is the virus genetically changing?”

He referred to a study in herds with no clinical PCV2 disease that had improved average daily gain and growth performance after PCV2 vaccination. “So, in that way, they showed there was a subclinical infection associated with PCV2.”

‘Incomplete’ cross-protection

Segalés believes current vaccines are controlling subclinical infection and said there’s no need to update vaccines.

However, Meggan Bandrick, DVM, PhD, a Zoetis scientist, said cross-protection is not complete. If heterologous vaccine strains are used — vaccines that aren’t matched to field strains — “we see [more] viremia and fecal shedding” compared to the use of vaccines that match field strains.

“So, you may still see protection against disease where the vaccine and challenge strain are mismatched, but that subclinical disease is still there.”

Clayton Johnson, DVM

As genetic shifts occur, there’s a growing gap between vaccine and field strains, Bandrick maintained. That gap, substantiated with results from epitope analysis, is what prompted Zoetis to develop the first PCV2 vaccine with two genotypes — PCV2a as well as PCV2b. The vaccine is also effective against PCV2d and is expected to provide broader coverage against current and emerging genotypes of PCV2.

Vaccine versus vaccination failure

Several panelists said an important key to successful PCV2 control is proper use of available vaccines.

Segalés acknowledged that vaccination isn’t perfect, “especially if we use a single shot. Try two doses and you will improve results from vaccination, for sure.”

Madson added, “I’m not sure I can singly point to vaccine failure. There’s vaccination failure. There’s a difference.”

Similar experience was cited by Rovira, who said he hadn’t dealt with any cases he thought were real vaccine failures.

Laura Bruner, DVM

“We know that in most cases the vaccines work really well, if we use them well,” but he cautioned about cutting corners at times when the swine industry isn’t as profitable. “When we tried to cut corners on PCV2 vaccination, we started seeing it again.”

SVC’s Bruner said, “Everything starts with the sow herd. If you have a really good PCV2 vaccination program on your sow farm, those instances of vaccine failure or vaccination failure are less just because you started with a lower amount of PCV2 on the sow farm being transmitted to piglets.”

More PCV3 circulating

Panelists emphasized that PCV3 and PCV2 are different viruses. PCV3 appears to be widespread but went largely undetected until recently, they said.

Rovira said there are reports of PCV3 as far back as 1996 in Spain, and in Sweden, PCV3 was found later in a sample collected in 1993. “I think we would all agree this is a virus that has been among us for a long time.”

Vitelio Utrera, DVM, PhD

Jianfa Bai, PhD, a molecular diagnostician at Kansas State University, said in his lab, the PCV3-positive rate has gone up, indicating a close eye should be kept on prevalence changes in the field.

Nevertheless, Bai, as well as Segalés, Madson and Utrera, said that so far, PCV3 is merely a finding and proof is lacking that this virus causes disease. Johnson added, “…it’s the classic question of infection versus disease. I have absolutely found infection. I have not yet found anything I would characterize as a disease…”

Bruner, however, expressed concern about PCV3 and said she’s finding a lot in all types of tissue and in processing fluids. She described a case she had involving a sow herd with a high mummy rate. Lab testing showed high levels of PCV3 in mummy tissue as well as epicarditis and myocarditis. Other pathogens were not found.

‘Very common’

Meggan Bandrick, DVM, PhD

Madson said PCV3 is often seen at the Iowa State Diagnostic Lab, and although it’s been found in higher quantities in reproductive cases testing negative for other pathogens, the causative pathogen may have cleared by the time samples were submitted.

Rovira said his lab is likewise finding PCV3 to be “very common,” now in over 34% of samples that come through. There have been a few myocarditis cases associated with PCV3 from different farms and different clients. “That builds confidence for us that the first reported case was not just a fluke.”

In some of the cases, there was an influx of gilts. It could be that PCV3 is subclinical and does nothing, but if an imbalance of immunity occurs in the herd, problems may occur and then resolve. His overall impression about PCV3 is that it can be relevant in a very small percentage of cases.

PCV3 can also occur along with other pathogens, such as PCV2, reproductive and respiratory disease virus and parvovirus, panelists reported.

PCV3 vaccine?

Because PCV3 and PCV2 are less than 40% genetically similar, Bandrick and others said PCV2 vaccines would not cross-protect against PCV3. That brought up the question of whether a vaccine for PCV3 is needed.

Bandrick said at this time, a PCV3 vaccine would not be of great benefit to the industry, but she stressed the situation needs to be carefully monitored. So far, it’s not been possible to culture PCV3 in the lab, but there are other ways to develop a vaccine if one is needed.

Jianfa Bai, PhD

Bruner said if a PCV3 vaccine were available, she’d probably try it out when there’s a herd with a high mummy rate and the only pathogen that can be found is PCV3. Similarly, Rovira said he believes other practitioners would try a PCV3 vaccine for cases of abortions or mummies if they thought PCV3 was involved.

Despite all the questions that remain about the significance of PCV3, Segales said, “Certainly, PCV3 can be added into the pile of pathogens you are looking for…I would say let’s try to isolate it so we can perform experimental infections.”

Utrera agreed and said for now, “…we need to have the virus, we need to reproduce the [signs] and lesions, and we need to identify any associated cofactors and then record them.”

Editor’s note: For a copy of the roundtable proceedings booklet, click here.