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.

How long do mycoplasma-negative herds stay negative?

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Most hog farms successfully stamp out mycoplasma pneumonia when they work with their veterinarian to eliminate the disease. The challenge is preventing reinfection.

If the herds remain negative after the first 8 months, they became reinfected at a much slower rate over a much longer time than the herds turning positive in 8 months, reported Paul Yeske, DVM, Swine Vet Center, St. Peter, Minnesota.

Yeske and his colleagues looked at all the clinic’s herds taken through a mycoplasma-elimination program. They rated the success of each effort and plotted over time when the herds turned positive, which they called the decay rate.

81% elimination success

They noted a distinct difference between herds that used a closure plan with medication (water medication for sows and injection to piglets) for the elimination versus just medication (injection of both sows and piglets).

“On herds using a closure and medication plan, we were 81% successful,” Yeske said. “In herds with medication and no closure, we were at 62% success.”

The clinic’s protocol for whole-herd elimination required all pigs on the farm to receive a vaccine injection followed with a second dose 2 weeks later. In elimination with no herd closure, animals that become infected with mycoplasma can shed the organism for up to 8 months.

“I believe what happens with no herd closure is some of the herds decay rapidly because we never got mycoplasma totally eliminated,” Yeske said. “If they make it to 8 months, the pigs were done shedding and the herd was able to stay negative going forward.”

More negative herds in future

“Mycoplasma elimination is one program that’s been widely done in a relatively high number of herds and has been successful. I think we will see more and more people adopt elimination and see more herds go to mycoplasma-negative pigs because of the economic benefits with grow-finish production,” he explained.

“The good thing with mycoplasma is we have the tools to eliminate and successfully keep it out of our herds for a long time.”

 

Lessons learned from recent Seneca Valley outbreaks

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The Seneca Valley virus (SVV) is proving to be something of a test case for swine producers’ and veterinarians’ preparedness for foreign animal diseases (FADs).

While SVV is not an FAD, nor does it pose a harsh economic penalty for infected herds, the virus does produce lesions on the pig’s snout, feet and coronary bands that are indistinguishable from FADs, particularly foot-and-mouth disease.

Last summer, Jake Schwartz, DVM, Swine Vet Center, St. Peter, Minnesota, spent time investigating SVV outbreaks in Nebraska. In less than a month, a single packing plant required 124 animal-disease investigations because market hogs started showing up with lesions and vesicles. The good news was the pigs tested negative for FADs; the bad news — they tested positive for SVV.

“There were zero reports of lesions at the originating pig sites, which involved five different states — Kansas, Minnesota, Iowa, Nebraska and South Dakota,” Schwartz told Pig Health Today. “So, either the pigs at the site were never infected or they were infected and the lesions healed relatively fast and we all missed it.”

There is much still to be learned about the virus — the transmission route, infectious period, risk factors, biosecurity effectiveness and more. But hog transport trailers are one suspected route of bringing SVV back to the farm. The linkage has been evident with market hogs as well as some sow-herd cases.

“We learned with the porcine epidemic diarrhea virus (PEDV) that it was not uncommon to have trailers arrive at the packing plant negative for PEDV. But when the trailer left the plant it was positive,” Schwartz said. “Then we drag the virus back to the farm.”

Although the exact steps to prevent SVV from entering a production site have not been scientifically confirmed, for now the best defense is to step up truck and trailer biosecurity protocols. This means wash, disinfect and dry the trailer between every hog transport.

“We don’t know if the thermos-assisted drying process is able to kill SVV, but we know it works quite well for PED and the porcine reproductive and respiratory syndrome virus,” he added. That essentially involves heating the trailer to a surface temperature of 150° F to 160° F for a period of time, say 30 minutes.

“As an industry, we talk about being prepared for an FAD; we talk about vaccine banks and many other strategies,” Schwartz said. “But part of that discussion needs to include how we manage our hog trailers in a way that would slow down or reduce the contamination risk in the event we did get an FAD in the US.”

 

Yeske: Multiple factors contributing to rising sow-mortality rates

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The spike in sow-mortality rates in recent years has everyone in the US pork industry searching for answers. Don’t expect any simple solutions, however.  In most cases, multiple factors lead to mortality or declines in sow performance, according to Paul Yeske, DVM, Swine Vet Center, St. Peter, Minnesota.

“Like many different things in the industry, it’s multi-factorial…not just one thing,” he told Pig Health Today.

Not all farms experience high mortality rates. Yeske said he sees a lot of variability among sow herds, and they try to understand why there’s a difference.

Expansion drives higher selection rates

One reason sow mortality increased relates to herd expansion. “As we’ve seen more expansion, we tend to have higher selection rates and sometimes end up with more mortality,” Yeske said.

“Ideally, we’d have a selection rate of 50% to 60%, and sometimes we end up…in the 70% to 80% range,” he explained. “Some of those animals probably shouldn’t have come to the barn to begin with.

“Make sure you bring enough of the animals in to allow for proper selection and not take what’s available,” he added.

In units with internal multiplication, Yeske recommended maintaining a purebred herd large enough to produce the needed replacement gilts. If gilts are outsourced, bring in enough animals for cover selection.

He also suggested making sure sow herds are sized properly. “Sometimes we just have to stand back and make sure the right animals come into the farm,” he said. “If the animal is structurally questionable, it’s going to be more difficult for that animal to stay in the herd.”

Lameness is a leading contributor to higher sow-mortality rates, along with prolapses. “Some research work is actively being done to try and understand what’s going on. We know it’s occurring; we just don’t know exactly why,” he added.

Maintain body condition

Another cause of sow mortality relates to higher production rates and body condition.

“We’re seeing higher levels of [sow] productivity than we’ve ever seen,” Yeske continued. “Are we meeting the needs of this higher-producing animal?” Research on sow diets dates back a number of years when production rates were lower, he noted.

Good body condition is essential for keeping sows in the herd. “If we get the animals into the herd, keep them in the right body condition,” Yeske said. “That’s going to add to their longevity.

“If the animals are yo-yoing a lot on weight, it’s going to add more stress and more challenges. Try to keep them very uniform and consistent on weight.”

Match health status

It’s important to remember that gilts entering a herd are stressed as they begin to develop herd immunity. Producers need to properly acclimate gilts to diseases they may face.

“Understand the health status of the animal coming in, manage it to match your herd and then identify the problems as they show up,” Yeske advised.

“If we don’t get that done right, that just adds more stress to those young-parity animals and ends up having them exit the system faster than they should.”

Fast intervention

Speed is also critical. “Herds that have fast intervention on problem animals tend to have the lowest mortality,” he said.

“Make sure you do individual pig care every day. Go out and check every animal every day. Make sure the animal is getting up and good on all four legs. Make sure the animal is eating and [there are] no other signs of any health problems,” he added.

 

Gilt acclimatization, reduced shedding keys to curbing downstream M. hyo disease

By Paul Yeske, DVM
Swine Vet Center
St. Peter, Minnesota

 

Research shows that if more piglets are positive for Mycoplasma hyopneumoniae (M. hyo) at weaning, there will be more problems in finishers, with decreased average daily gain, increased mortality and poor feed conversion.1 There will be a lower percentage of pigs sent to the primary market as well as higher treatment costs.

The costs of M. hyo can really add up. When actual production numbers from 2007 to 2015 are plugged into an economic model, the cost is $4.99 per pig.2 Data from other farm systems indicate it’s $2.85 per pig.3

To reduce the amount of downstream disease in pigs, we need to reduce the amount of M. hyo shedding. This begins with proper acclimatization of gilts going into the sow herd, which is a challenge.

Negative gilts present challenges

Historically, most replacement gilts were born into positive herds, or they were raised internally in the herd and were infected early in life. They had plenty of time for shedding to minimize before farrowing, which helped keep herds stable for M. hyo. By stable, I mean a low percentage of weaning-age pigs are positive for the pathogen within the respiratory tract.

Today, most replacement gilts are negative for M. hyo and aren’t acclimatized until they get to the sow farm. Therefore, the first challenge is getting them infected within a reasonable time frame.

Gilts need to be brought in at a young enough age so there’s enough time following infection for M. hyo shedding to decline. This is critical whether you want to stabilize a positive sow farm and reduce the impact of clinical disease in the finishing phase or if your goal is herd closure and M. hyo elimination.

Ideally, negative gilts would be infected by 84 days of age. Figure 1 demonstrates the time needed to reduce shedding in farrowing gilts and their piglets.

 

Figure 1. Gilt Mycoplasma hyopneumoniae exposure timeline

 

Gilt-exposure methods

There are several methods of exposing negative gilts:

  • Use seeder animals, an approach that’s been utilized in the industry for a long time. It works well if the right animals are used and there’s plenty of time — but it can also be difficult.To achieve a shorter time for infection, such as 30 days, six seeders for every four naïve gilts is needed to be 100% successful. However, if the infection in the seeders dies out, it can be difficult to get the acclimatization program restarted. The result can be problems with M. hyo in finishers and lost performance during the process, and it may take time to re-establish herd stability.
  • Intratracheal inoculation is another way to acclimatize naïve gilts and has been explored in the research arena. I wouldn’t recommend this method because it’s labor intensive and it can pose a danger to staff since restraint of gilts is necessary.
  • Aerosol inoculation is new technology that’s been used in other species for vaccination and may be a possibility for hyo acclimatization of gilts. It’s less labor intensive than intratracheal inoculation and animals don’t have to be restrained. There are some technical steps required. For example, it has to be done in an area with small air space. If you want to consider this approach, it’s imperative to work with your herd veterinarian so all the technical details are addressed.

One of the keys to successful acclimatization is having a good diagnostic protocol to confirm that gilts have in fact been properly exposed. Toward this end, testing every group of exposed naïve gilts is key, whether your goal is M. hyo herd stabilization or elimination.

Considering elimination?

M. hyo elimination is possible using a combination of herd closure, vaccination of the breeding herd and medicating of the breeding herd as well as piglets. Infected piglets also can be treated individually with an injectable antibiotic to help reduce the impact of the disease.

Elimination is recommended when it becomes a struggle to get gilts exposed on a consistent basis, for herds in a filter project and when producers simply become tired of dealing with costly M. hyo clinical problems.

If you’re considering M. hyo elimination, one of the first questions to ask is whether it really will be worthwhile. This might not be possible for farms located in pig-dense areas where reinfection is a strong possibility. However, when we followed 100 sites in pig-dense areas throughout two seasonal periods, we found only 6% of the sites were positive for M. hyo from lateral-source introduction.

Summing up

Proper gilt acclimatization is key to successful herd stabilization and M. hyo management. This applies whether your goal is to stabilize the herd and minimize the load of M. hyo in weaned pigs or to eliminate M. hyo.

A good diagnostic plan is essential. Every group of gilts that enters the herd must be checked after exposure to ensure proper acclimatization. Unfortunately, it takes time, especially in herds receiving adult replacements. Acclimatization of gilts is also more challenging today because most replacement gilts are M. hyo-negative.

Lateral transmission does occur, but it’s not very frequent.  If you are having a problem controlling M. hyo in a herd, it’s likely a problem originating from the source sow herd and not the geographic area.

You’ll have better results managing M. hyo if you work with your herd veterinarian to develop an individualized plan.

 

 

Editor’s note: The opinions and recommendations presented in this article are the author’s and are not necessarily shared by the editors of Pig Health Today or its sponsor.

 

 

 

 

1. Schwartz M. Cost of M. Hyopneumoniae in growing pigs. 2015 Allen D Leman conference.
2. Linhares D. A field study on economics of Mycoplasma hyopneumoniae elimination. 2017 Allen D Leman conference.
3. Yeske P. Mycoplasma hyopneumoniae Elimination. Proceedings from AASV annual meeting. 2016:376-381.

 

Practicing precision animal health

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Ross Kiehne, DVM, practices what he calls “precision animal health.”

“I’m only going to provide the vaccine or antibiotic that’s right for the pig at that time in its life to make it as healthy as possible,” the swine veterinarian says in a video produced as part of the Vets on Call series.

Growing up on the family farm, Kiehne says he witnessed the high level of livestock care shown by his father, who taught his son that the farmer is “the guardian of the welfare of the animals first and foremost.”

“We have to speak for them because they can’t speak for themselves,” stressed Kiehne, with the Swine Vet Center in St. Peter, Minn.  “I take that pretty seriously.”

Visiting a farrowing room, Kiehne focuses on the health and welfare of the sow and her recently born piglets.

“We want to find the right environment for them,” he says. “These sows have feed and water at all times; the sow is contained; it’s safe for the piglets to move around her all the time in a warm, dry environment.”

Even though he’s not in every swine barn every day, he can help the people who are by showing them what to look for and how to give the best care possible to the animals.

“Half of my job as a veterinarian is devoted to training the people who will take care of the pigs on a daily basis.”

And that involves treating sick animals. Kiehne says the welfare of the animal is much better if sick animals are treated with the proper antibiotic until they recover.

“We want everyone to understand where their pork comes from; this is how it’s made and we feel pretty good about it,” he says.

 

 

Vets on Call is a video series presented by Zoetis to showcase the important roles veterinarians play in food-animal production.

 

Yeske: Provide better pig care — one animal at a time

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Taking time to walk the pens, make eye contact with each pig and pull the sick ones for individual care seems to conflict with the basic tenets and efficiencies of population medicine.

“It is a big task, but we feel it’s a very important part of doing what’s right for the pig,” said Paul Yeske, DVM, Swine Vet Center, St. Peter, Minnesota.

“Individual pig care [means] to make sure we look at every pig every day — and that we evaluate them essentially from tail to snout — to try to identify any potential problems that pig may have as quickly as possible,” he told Pig Health Today.

Yeske says the approach involves three basic steps: Identifying the at-risk pig, being specific about its symptoms and effectively communicating the situation to others in the operation.

Practically speaking, he adds, that process begins with spotting the outlier — the pig that simply strikes you as somehow unusual.

“I encourage caretakers as they walk through the barn to develop a pattern as they go through each pen, to make sure they get an opportunity to look at every pig,” he said. “Basically, you’re looking for any of the clinical signs that the pig isn’t normal.”

For example:

  • Is he coughing?
  • Does he have diarrhea?
  • Is he gaunt and not eating?
  • Is there nasal discharge?
  • Does he appear stiff or lame when he moves?

Next, individual treatment protocols with an injectable antibiotic — typically already in place and specific for each farm and for each flow and system — can be called into use right away and used under veterinary supervision.

“Early intervention is really the key as we talk about individual pig care,” Yeske said. “We know that if we treat a pig later in the course of the disease, we have poorer response to treatment. If we can treat the pig earlier, we can have a better response.”

Research has proven that, particularly on farms with low health status, training caretakers to identify and treat sick pigs at an early stage of disease can improve growth and productivity during the all-important nursery and growing periods.1

“It does take time,” Yeske conceded, “but the payoff is very high. We get the pig back into production faster. The quicker we can identify that pig, the quicker we can get that pig treated and the better the response. The payback for the producer is very high because we get that early intervention ….  And we know it’s the right thing to do for the pig.”

1. Pineiro C, Morales J, Dereu A, et al. Individual Pig Care program improves productive performance and animal health in nursery-growing pigs. J Swine Health Prod. 2014;22(6):296–299.