What’s the US emergency response to African swine fever?

The emergency response to a possible outbreak of African swine fever (ASF) in the US stands ready for implementation, according to Beth Thompson, DVM, Minnesota state veterinarian and executive director of the Minnesota Board of Animal Health.

Thompson helps plan for potential foreign animal disease (FAD) outbreaks like ASF. She also must help implement plans when an outbreak occurs, like those for the avian influenza (AI) outbreak in 2015.

Thompson laid out the ASF emergency response plans to a group of Swine Vet Center veterinarians and pork producers. These emergency preparations are determined and then practiced during trial runs by the USDA, state boards of animal health and departments of agriculture.

“USDA has had a handful of exercises specific to ASF,” Thompson said. “At least 14 states involved are working through mitigation and response plans.” This fall, USDA will run a full exercise across several days with more than 14 states, covering different parts of the investigation and response process.

Investigate, diagnose

The first step in an emergency response comes when a state veterinarian is notified of a suspected FAD. A specially trained state or federal FAD diagnostician is sent to the site and two sets of samples are taken.  One sample is sent to the University of Minnesota diagnostic lab and the other is flown to the federal diagnostic lab at Plum Island on the East Coast or to a new USDA lab in Manhattan, Kansas, that will open soon.

After collecting samples, FAD diagnosticians begin gathering information from veterinarians and staff about movement onto and off the property including vehicle traffic, biosecurity, employee travel, etc. for the disease investigation.

The university will send preliminary test results back first, but nothing can be made public until the federal lab makes a confirmation and releases the official results, which can be 12 to 15 hours later.

False positives are extremely rare. During the AI outbreak, the university diagnostic lab tested 16,000 samples with zero false positives.

72-hour standstill

At the point of ASF confirmation, the USDA can initiate a temporary state, regional or national 72-hour standstill to all pig movement. Trucks hauling pigs should get to where they are headed and stay put.

“Then we try to figure out what is going on,” Thompson explained. “We’ve got a whole assortment of ways that ASF can be moving around. We have to look at feed mills, animal movement, and so on.”

The standstill may also include feed trucks, depending on individual states. States also may decide not to impose the 72-hour standstill in certain circumstances.

Depending on what is discovered during the standstill, plans for control zones, depopulation and disposal will be determined and put into action.

“To give you an idea of how this works logistically, during AI, I was part of the first initial response found in Polk County in late February 2015,” Thompson explained. “We went to Willmar on Thursday and quarantined the property. We got depopulation going and did surveys around a 10-km control zone (from the outbreak site). We went home on Sunday and thought we were all done. A few weeks later there were more cases.”

The response to the AI outbreak ballooned with cases erupting around the state. “In one day, we had 520 people working just on the response,” she added.

Thompson’s team is able to quickly ramp up when an emergency occurs. “The Minnesota Board of Animal Health has 44 employees. But the state department of ag has 400 employees, and we can also draw from additional resources within the state up to the National Guard,” she said.

Thompson also works with county and local officials to get more feet on the ground where outbreaks occur.

Backyard pigs, garbage feeding

In addition to being prepared for an outbreak, Thompson said the board is working on education with pork producers of all sizes and types.

“We’ve got a large population of people who raise one or two hogs in their backyard for personal use so there’s a lot of education that our agency can get involved in,” she explained.

Minnesota also has a statute that allows permitted garbage feeding but with strict controls, including monthly inspections of the cooking equipment and trucks. Permits have been granted for two classes of feeders; Class A can feed food waste that contains or has been exposed to meat, and Class B can only feed food that’s never had contact with meat. ASF concerns are mostly tied to the Class A holders who generally service grocery stores and restaurants in the Twin Cities.

“I know there’s a lot of interest in this because of possible ASF transmission in meat,” Thompson said. “I support permitted garbage feeding because I know we can achieve a lot more for animal health through cooperation and collaboration than an outright ban of the practice.”

She added that the permit holders are well versed on safe garbage-feeding rules and have visited pork producer meetings to discuss their cooking processes.

Industry involvement

While the state board of animal health will head up the response to an ASF outbreak, Thompson stresses that the entire industry must be involved to make an emergency response successful.

“What keeps me up at night — the amount of damage ASF can do to this commodity group is astounding,” she added. “Not only what would happen with this commodity group but with the related corn and soybean groups if we got ASF. The effects would be devastating.”

 

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.

Download the pdf

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.

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

Download the pdf

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?

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

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

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.