Better Pork - August 2006

So says a preliminary study of Ontario farrowing barns. But workplace standards aren’t enforced and many workers don’t wear protection

A preliminary study of noise in Ontario farrowing barns makes a strong case for workers to wear hearing protection and for quieter barn designs, says Kathy Zurbrigg, surveillance analyst for the provincial agriculture ministry.

Prolonged exposure to typical noise levels can cause hearing loss in workers, notes Zurbrigg, after studying noise generated in 36 separate farrowing barns on 24 Ontario farms.

There is also some association between noise and lower farrowing rates, although other pork production parameters were apparently not affected in this pilot study. Barns with a farrowing rate under 85 per cent on average had noise levels three decibels lower than barns where the farrowing rate exceeded 85 per cent.

Noise is measured in decibels with a meter. For every three-decibel increase, the noise level doubles, Zurbrigg says. Exposure to 85 decibels over an eight-hour day will damage a human’s hearing. So will exposure to 100 decibels (a snowmobile) for 15 minutes and to 120 decibels (the sound of a revving chainsaw) for a mere nine seconds.

Some new studies from Germany also show stress hormones in feeder pigs increased when pigs were exposed to more than 90 decibels for two hours three times a week, says Zurbrigg. The pigs exposed to noise spent more time laying down and gained less weight.
Zurbrigg’s study showed a correlation between noisier barns and lower farrowing rates. But Zurbrigg could find no published research on how noise affects farrowing pigs.

On the human side, she says, “hearing loss is irreversible and it adds up.” Outside the barn, noise levels associated with tractors and power tools increase the possibility of hearing damage as well.

More than hearing is affected. Starting at 75 decibels, there is an effect on stress levels in humans, with higher serum cortisol levels in blood (a sign of stress), increased blood pressure and accompanying headaches, insomnia and irritability. Noise in a 450-sow barn before feeding reaches about 83-85 decibels.

Zurbrigg recorded noise levels in pig barns holding between 100 and 2,500 sows. She visited each barn three to five times over two years, recorded ceiling heights, feeding systems, number of pigs in the barns and asked for production information. Half the barns kept farrowing sows in crates and five barns had natural ventilation.

Zurbrigg notes that noise levels in every barn reached 90 decibels “at least for a few minutes a day, usually at feeding.”

Industrial workplace standards in Europe, the United States and Canada call for hearing protection for employees where there is a noise level of more than 85 decibels and also a noise abatement program. These rules aren’t enforced in agricultural settings, Zurbrigg points out.

Zurbrigg says a U.S. study of specific tasks in large farrow-to-wean operations in 2005 showed that piglet processing and heat checking produced the highest noise levels at more than 90 decibels. Feeding pigs averaged 83 decibels.

Two 1970 studies in Europe revealed that pre-feeding noise levels were 61-78 decibels (before the first person entered the barn), and rose to 90-100 decibels and higher during feeding. In a Danish study, power washing produced noise levels of 98 decibels. Feeding grinding produced 88 decibels.

The pros and cons of liquid feeding

Liquid feeding is proving a viable alternative to traditional dry feeding systems common. While it requires a significant capital investment and a higher level of management, it also offers the flexibility of taking advantage of so-called opportunity feeds

Despite considerable effort by dedicated extension agents and industry personnel, producers often say that they garner their most trusted information from peers.

So, what happens when you put a couple of well-versed, experienced pork producers and a well-respected, hands-on researcher in front of a crowd at the London Swine Conference? You get an excellent dialogue on a topic of interest to a growing number of pork producers in Ontario -- liquid feeding.

Liquid feeding of pigs is a science that has developed tremendously over the past 10 years. Since many pork producers have their roots in Europe, where liquid feeding is the norm, it is not surprising that it is considered a viable alternative to traditional dry or wet-dry feeding programs. Driven by opportunity feeds, such as food industry by-products, and interest in feeding high-moisture corn, computer-controlled liquid feeding systems are gaining popularity in Ontario.

The liquid feeding system at the Arkell swine research station of the University of Guelph was installed during the spring of 2004 under the watchful eye of lead researcher Kees de Lange. The system is being used to support North America’s only research program on swine liquid feeding, a project that was developed in close collaboration with the Swine Liquid Feeding Association (SLFA) and a number of sponsors (check the SLFA website at http://www.slfa.ca for more details and a complete list of sponsors).

Like any new system, it took some time to work out the kinks. But after some minor modifications and a substantial learning curve on behalf of the technical staff managing the system, research has begun in earnest. To date, results show that growth performance and feed efficiency of growing-finishing pigs on the liquid feeding system are at least as good as those on a conventional feeding system, where pigs are fed pelleted feed (see Table 1).

However, growth performance of starter pigs on the liquid feeding system has been somewhat lower, compared to conventional dry feeding systems, and research suggests this is largely due to feed intake restriction.BP

Table 1. Impact of feeding strategy on performance of growing-finishing pigs.
	Conventional feeding, dry pelleted feed	Liquid feeding, dry corn	Liquid feeding, high moisture corn
Initial body weight, kg	23.5	23.7	23.4
Final body weight, kg	104.7	105.8	104.2
Gain, kg/d	982	1011	1009
Feed:gain	2.63	2.64	2.51

Janice Murphy is swine nutritionist with the Ontario Ministry of Agriculture and Food in Fergus. E-mail janice.murphy@omaf.gov.on.ca

Searching out the co-factors that trigger
Porcine Circovirus Disease (PCVD)

By itself, PCV2 is seldom able to cause full blown PCVD. However, the combination of PCV2 with certain co-factors does precipitate the full-blown disease and they can be both infectious and non-infectious in nature

We have known for several years that porcine circovirus type 2 (PCV2), the virus that causes porcine circovirus-associated disease (PCVD), formerly known as postweaning multisystemic wasting syndrome (PMWS), is a necessary factor in causing full-blown PCVD.

But while PCV2 virus has to be present, in most cases it needs help to cause PCVD/ PMWS. What are the key ingredients or co-factors which trigger or help PCV2 to precipitate PCVD? For a start, they can be separated out into infectious and noninfectious co-factors.

Infectious co-factors: the viruses. The PRRS virus tops the list of co-factors that help PCV2 promote PCVD. But before getting into the contribution of the PRRS virus to PCVD, we must first look at the PCV2 virus itself.

At least two aspects of the involvement of PCV2 virus need mentioning at this time. First, the presence of PCV2 is necessary to cause PCVD. Secondly, there is the possibility that more virulent strains of PCV2 virus are responsible for the PCVD epidemic we are experiencing in Ontario and Quebec.

A number of experimental studies have shown that the PCV2 virus has to be present to get PCVD. It should be noted that, in a few of these studies, the PCV2 virus alone was able to produce both the histological lesions and clinical disease of PCVD. In the vast majority of studies, however, another agent or co-factor was introduced which precipitated the full extent of clinical PCVD as is seen in the field.

A key point that must be emphasized is that no one, so far, has ever been able to produce PCVD without involvement of PCV2. The bottom line is that if there is no PCV2, there is no PCVD/ PMWS.

Point #2 is a bit more intriguing. Initial studies showed that any PCV2 virus used from any source produced the same degree of PCVD. This included PCV2 viruses that had been isolated from pigs without PCVD, PCV2 viruses from herds that had never had PCVD and viruses from countries that did not have PCVD nor had any history of ever having had PCVD.

In the last 18 months, however, the PCV2 virus that is being identified in the epidemic cases of PCVD in Ontario and Quebec (designated RFLP 321) has been different from the previous PCV2 viruses present in Eastern Canadian herds for the decade prior (see, PMWS, Better Pork, April 2006).

Furthermore, work done at Iowa State University (ISU) clearly shows that there are differences in the virulence of PCV2 viruses. The researchers at ISU have consistently produced different degrees of severity of PCVD from two different isolates of PCV2 that they use in their experimental studies.

PRRS, however, is the first, the most obvious and by far the easiest culprit to point to as a promoter of PCV2 disease. Long before the epidemic PCVD outbreaks started, we had recognized that herds with active PRRS virus infection were more likely to have PCVD problems. And when they did get PCVD problems, they were more severe than herds that did not have active PRRS virus infections. Concerted efforts must be directed at controlling PRRS virus infection in the growing pig population when it is present as a co-infection with PCV2.

Other viruses. After PRRS, other contributing viruses are less conspicuous. It must be noted, however, that the first virus that was conclusively shown to help PCV2 promote PCVD was not PRRS virus but porcine parvovirus (PPV), an old companion that has been running around in all our herds for decades.

As so often happens, PPV as a co-factor was an accidental, serendipitous discovery. A research team at the University of Saskatchewan in Saskatoon challenged pigs with PCV2 to reproduce PMWS experimentally. They were successful, but at the conclusion of their experiment they found that their PCV2 challenge material, unbeknownst to them, was contaminated with PPV. That accidental discovery has become the basis of at least one predictable and repeatable challenge model for PCVD that is still being used today.

Swine influenza virus (SIV) can also be added to the list, but SIV gets there by field observations and not by rigorous scientific experimental studies. Nonetheless, the field observations are strong enough for us to include SIV as another of the triggering viruses that can precipitate a PMWS outbreak.

Mycoplasma co-infection. Mycoplasma hyopneumoniae is a common infection of pigs around the world and hence also a common co-infection with PCV2 in the field.
Researchers at ISU have clearly demonstrated that M. hyopneumoniae infection increases the severity and duration of PCVD. Control of M. hyopneumoniae in the face of PCV2 infection is critical in minimizing the losses associated with PCVD.

Haemophilus parasuis (the Glässer’s Disease organism), Strep suis and other bacteria that are common to many swine herds act as secondary infections, worsening the severity of PCVD and necessitating efforts to control these bacterial secondaries.

Non-infectious co-factors: vaccine adjuvants. An adjuvant is a substance that helps and enhances the pharmacological effect of a drug or increases the ability of an antigen to stimulate the immune system.Considerable research on the impact that adjuvanted vaccines might have on PCVD has shown that vaccines adjuvanted with mineral oil-in-water adjuvants, given at the time that PCV2 virus infection is occurring, do enhance PCVD.

All adjuvants stimulate the immune system by activating immune cells in the host. That’s what they are supposed to do. However, activation of the pig’s immune cells seems to encourage proliferation of the PCV2 virus in these same immune cells.
The most common adjuvanted vaccines administered to pigs are the mycoplasma vaccines. All adjuvanted vaccines have been shown to encourage uptake of PCV2 when given at the time of PCV2 infection. Vaccines containing mineral oil-in-water adjuvants have been shown to go further than other adjuvants to the point of actually triggering PCVD.

However, the same mineral oil-in-water adjuvanted vaccines, administered two to four weeks prior to the time of infection with PCV2, have been shown to be safe and do not trigger PCVD. Thus, timing of vaccination is the important aspect to look out for. When dealing with PCVD, timing of all vaccines should be addressed so that they do not coincide with PCV2 infection.

Genetics. Several studies have documented dramatic differences in certain genetic lines in their susceptibility to developing PCVD. At the same time other genetic lines show considerable resistance to developing PCVD.

There are several reports documenting progeny from the Pietrain boar which have resistance to developing PCVD. Conversely, there are a few studies that have not been able to show this resistance in pigs sired by the Pietrain boar, but the majority of controlled and field observational studies, so far, have shown that pigs from a Pietrain boar do show resistance to PCVD.

Some caution is advisable, however, as there are also some undesirable carcass characteristics present in the Pietrain progeny that would have to be weighed against any possible benefits of PCVD resistance. Furthermore, since some studies have not shown this Pietrain beneficial effect, it may be that the resistance to PCV2 resides in some lines of Pietrain and not in the entire Pietrain breed.

On the susceptibility side of the equation, pigs from Landrace dams seem to be more prone to developing PCVD. In several experimental studies, Landrace pigs have repeatedly come out with higher infection and mortality rates when exposed to PCV2 infection than do the Large White and Duroc breeds. Even cross-bred pigs containing Landrace fare worse than cross-breeds that do not contain Landrace.

Agent X is another postulated, but as yet unproven, possible co-factor. If an Agent X does exist, it straddles the fence as being potentially infectious or noninfectious. For the most part, Agent X is believed to be a virus of some sort, and hence an infectious co-factor, but there is the possibility that it could be an as-yet-undetected environmental or management factor, and hence non-infectious. So far no Agent X has surfaced from any source and remains just a theory.

In short, by itself PCV2 is seldom able to cause full blown PCVD. However, the combination of PCV2 with certain co-factors is able to precipitate full-blown PCVD. The contributors are represented by a selection of infectious and non-infectious co-factors. PRRS virus, SIV and Mycoplasma are the main infectious co-factors. Adjuvanted vaccines, specifically mycoplasma vaccines containing mineral oil-in-water adjuvants, are the main representatives of the non-infectious co-factors.

Certain breeds and genetic lines show increased resistance and other genetic lines show susceptibility to developing PCVD. Pigs sired by Pietrain boars seem to be resistant to developing PCVD. Landrace pigs seem to be more susceptible. Then there is Agent X, an as-yet-unidentified virus or environmental factor which is purported to be a possible co-factor.BP

Noisy barns can cause hearing loss in workers
and stress their animals

The pros and cons of liquid feeding

Searching out the co-factors that trigger
Porcine Circovirus Disease (PCVD)

Noisy barns can cause hearing loss in workers and stress their animals

The pros and cons of liquid feeding

Searching out the co-factors that trigger Porcine Circovirus Disease (PCVD)

Noisy barns can cause hearing loss in workers
and stress their animals

Searching out the co-factors that trigger
Porcine Circovirus Disease (PCVD)