Diseases Contributing to Poor Productivity and Profits

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This article is a transcript of a teleconference between five pig veterinary specialists organised by Alpharma. The topics covered include PRRSV and Mycoplasma hyopneumoniae; Clostridium perfringens type A; and circovirus (PCV2)-associated disease.

The pig specialists taking part in the conference were:

• Dr Joseph F. Connor, Carthage Veterinary Service Ltd., Carthage, Illinois
• Dr John Deen, University of Minnesota, St. Paul
• Dr Don Levis, Extension Swine Specialist, University of Nebraska, Lincoln
• Dr Camille Moore, swine consultant, Quebec, Canada and
• Dr Roy A. Schultz, swine veterinary consultant, Avoca, Iowa (moderator)

DEFINING SOW PRODUCTIVITYDr Schultz:Let's start by defining sow productivity and how it should be measured. It's difficult to improve on something unless it can be measured or benchmarked. Common definitions are pigs per sow per year, or pigs weaned per mated female per year. But are these the best methods of defining sow productivity?
Dr Connor:We still typically measure sow productivity by pigs weaned per mated female primarily because it's a recognized measurement and one that we can pull out of Pig Champ and other databases. As we move forward, we're seeing a trend towards measuring pounds marketed per mated female per year, and pounds marketed per square foot per year.
Dr Deen:We're also starting to see more of an emphasis on quality as far as output from the sow unit. There are two measures: one is total pigs per sow per year, and also pigs with certain quality parameters, such as weight or the proportion of pigs that are less than 9 to 10 pounds. That's created a better-quality pig coming through and constrained some of the emphasis on simply producing pigs.
Dr Moore:We're getting geared to look at the weight of marketed weaners or the total weaning weight per sow per year. From that number, pigs weighing less than 3kg or 6.61lb at weaning – let's say less than 7lb – are not included in weaning weights.
Dr Connor:One of the interesting things we were asked to do in our records summary this year was to look at survival from birth through market. Our parameters were to look at the number of pigs slaughtered out of the total born across a number of farms. The percentage of 'top' pigs marketed of the total born was in this measurement, and it accounted for stillborns, mummies [mummified piglets], pre-weaning mortality and, finally, wean-to-finish mortality out of the total born number.
Dr Levis:We have various durations of time that sows are in the herd. I wonder if we don't need to look at life-time pig production in combination with the number of days the female is in the breeding herd. Some younger sows may be more productive, while older sows might fall apart. We have computer technology today to help look at combined pig production as it relates to the number of days the female is in the breeding herd.


DISEASES CONTRIBUTING TO POOR PRODUCTIVITY AND PROFITSPRRSV and Mycoplasma hyopneumoniaeDr Schultz:We could have a three-day seminar on porcine reproductive and respiratory syndrome virus (PRRSV), but can you sum up how significantly it contributes to poor sow productivity and lost profits?
Dr Moore:And poor-quality weaners.
Dr Connor:I would agree that it is still the key insult to sow productivity and pig quality. This year we had some excellent examples of wean-finish groups where individual groups of pigs within a system became PRRSV-positive, without a lot of secondary insults following. We identified a 0.1 difference in feed conversion and about 0.2 difference in average daily gain, indicating that this particular PRRSV strain affects performance. The effect on feed conversion and average daily gain is more dramatic when complicated by Mycoplasma hyopneumoniae, swine influenza, and so forth.
Dr Schultz:We all seem to agree that PRRSV is still the number one problem. Let’s elaborate a bit on these PRRSV problems. What about M. hyo in herds with PRRSV? We know that at least 95% of herds today are positive for Mycoplasma.
Dr Deen, how does this affect pigs in the nursery?
Dr Deen:There is some work being done on risk factors for carriage of Mycoplasma. It looks like gilt progeny are more likely to carry Mycoplasma and other pathogens and that these pigs, like the light-weight pigs, create more risks. We talk about age and size and essentially minimizing age as a method of controlling disease, and what we've seen over the last couple of years with work by Dr Roger Main is that there is a lower limit to that. We set up a very susceptible population where bacteria multiply quite quickly. In many of our systems, we're coming back to the idea of creating a robust pig rather than a disease-free pig, and in many cases that has resulted in success.
Dr Schultz:Let's go into more detail now about solutions to some of the problems we see. We often bring naive gilts into a herd with PRRSV and get them exposed at a young age. Many researchers say that in M. hyo and PRRSV, antibiotic treatment and/or strategic medication for concurrent bacterial infections is often needed and may help more than PRRSV vaccination. In particular, focusing on control of Mycoplasma pneumonia has been shown to be extremely important and quite successful in minimizing disease in porcine respiratory disease complex (PRDC) cases associated with PRRSV, M. hyo, and opportunistic bacteria.

Dr Thacker found that Aureomycin® (chlortetracycline) decreased pneumonia in cases of Mycoplasma and PRRSV. She used a program of 10 mg/lb body weight of Aureomycin in her model for 14 days starting at the time of exposure to M. hyo and PRRSV, and it reduced or eliminated the potentiating effects of M. hyo on PRRSV pneumonia. More specifically, pneumonia decreased at days 10 and 32 by about 80%, and microorganism numbers of Mycoplasma and PRRSV were significantly reduced in that same range. This is new work that is yet to be published and it looks like there are some real potential benefits. Have any of you had experience with this type of regimen?
Dr Connor:We have and I agree fully. We look at adaptation and acclimation as critical factors and segregate incoming gilts from the PRRSV-positive herd. In these herds, we try to develop natural immunity when the gilts are very young. It’s been a work-in-progress on each herd to get the timing of natural exposure to PRRSV vs exposure to Mycoplasma or circovirus so that we control mortality and have adequate growth. One of the things we've had to do in addition to the vaccination programs pre-exposure is to pulse with antibiotics such as chlortetracycline just prior to when we would expect a respiratory insult to occur from Mycoplasma, Pasteurella, Lawsonia, or other pathogens.

We've put Aureomycin in very early in the course of what we expected to be repeated or consistent respiratory outbreaks on grow-finish pigs with relatively good success.
Dr Schultz:Does it control ileitis as well? Dr Connor:It does, and in those systems respiratory signs and ileitis are occurring at the same time because of the sequence of events and the way we're moving gilts out of the nursery after an 8- or 9-week period and into a continuous-flow grower-finisher section.
Dr Schultz:That's my experience too. Any other comments?
Dr Connor:The key part of that is inclusion at time of exposure. Frequently, inclusion occurs considerably longer after exposure and then the analysis of the results is unsatisfactory.
Dr Schultz:Because they don't get the medication in at the time of exposure?
Dr Connor:Correct.
Dr Schultz:Again, that's what I would suggest happens in the real world. Everything doesn't get exposed at the same time as happens in an experimental model. You must get the medication in and leave it in for a little longer than in an experimental model.


Clostridium perfringens type ADr Schultz:What about Clostridium? Dr Glenn Songer of the University of Arizona, in his paper 'Neonatal clostridial infections: new problems or same old, same old?' says that C. perfringens is the most important cause of neonatal enteritis, and that although type C infections are well known, strains of type A predominate today. Do any of you have experience with C. perfringens type A? Are you seeing this infection as a cause of light-weight pigs?
Dr Connor:We've had quite a problem over the last 18 to 24 months with C. perfringens type A. It is clinical in about 10% of the herds we service. The general scenario is that there are stresses either involving poor ventilation or sanitation resulting in an increase in pre-weaning mortality and a reduction in weaning weights, or an increase in weaning weight variability.
Dr Schultz:Dr Connor, you mentioned that you use autogenous vaccines for Clostridium, and I've used them too. I've found them to be less effective with type A than with type C. We've also seen a decrease in the incidence of type C Clostridium, except for the chronic form.

I was recently in a high-health unit where they recognized they had Clostridium type A disease and were having trouble managing it with autogenous vaccines. They went back to basics, such as improved sanitation combined with BMD® (bacitracin methylene disalicylate) fed to the sows, and were able to control it very well. What has been your experience?
Dr Connor:I would agree with your observations. Part of our group has conducted studies with different companies looking at the response to type A vaccines. In many cases, we're getting a serological response, but it's not adequate to prevent Clostridium type A effects without other interventions.

Typically, we still use BMD pre-farrowing and through lactation as an adjunct to control. If we do this and watch for other stressors, such as inadequate ventilation or sanitation problems, we can get satisfactory control. It collectively takes more input than what we would like.

What we've found during that time period is that we've had to intensify sanitation to the point of removing the creep mats that we normally use. We're pretty gung-ho on using hot boxes where the pigs are put in at birth to improve survivability. However, if sanitation of the boxes is not excellent, they can become the source of clostridial contamination.

Historically, we could achieve control through improved sanitation and with BMD pre-farrowing through lactation or combined with a vaccine, but recently, excellent control has been more challenging.

Lastly – although we probably should have expected this in our parity flows where we have all Parity 1 on one farm – C. perfringens type A has been more difficult to control.
Dr Schultz:Dr Moore, Dr Connor noted that C. perfringens type A is more of a problem in Parity 1 gilts. Do you have more in your Parity 1 system?
Dr Moore:No, I could not say that we’ve seen an increase in Clostridium over the past 2 years. However, we are feeding them BMD to get heavier pig weights. We’re still having a battle with some tough Escherichia coli strains.
Dr Schultz:Sometimes I think producers don't realize they have Clostridium type A and it can become a diagnostic nightmare because Clostridium type A is a normal inhabitant. How do you determine if it’s the cause of disease? Dr Mike Yaeger of Iowa State University (ISU) and Dr Songer are developing an ante-mortem test using a rectal swab that is based on finding the beta 2 toxin in the intestinal tract of type A clinical cases. It's in the jejunum about 90% of the time and can be recovered on rectal swabs about 80% of the time. So they are developing a capture enzyme-linked immunosorbent assay (ELISA) and dot blot test to get a rapid turnaround because quite often, we get scouring pigs and we don't know whether it's E. coli or Clostridium. They are finding that what we normally thought was E. coli is Clostridium and that it’s taking predominance over E. coli in neonatal pigs, causing low weaning weight on affected pigs. We have something to look forward to in this test.

I'd also like to share some recent work from Dr Yaeger at ISU. Data from the ISU Veterinary Diagnostic Laboratory are shown in Tables 1 and 2. You'll see that Clostridium type A is far more predominant than type C, or than E. coli for that matter.

Table 1. Pathogens detected in piglets under 2 weeks of age with diarrhoea.
Pathogen	Number of cases	% of total neonatal diarrhoea cases
C. perfringens type A	100	30
Rotavirus	77	23
C. difficile	67	20
E. coli	40	12
C. perfringens type C	36	11
TGE	13	4

Retrospective study; ISU VDL 2003-2004, Dr Michael Yaeger

Table 2. Pathogens detected in piglets under 7 days of age with diarrhoea.
Pathogen	Number of cases	% of total neonatal diarrhoea cases
C. perfringens type A alpha and beta 2 toxin (small and/or large intestine)	52	68
C. difficile	37	48
C. perfringens type A alpha and beta 2 toxin (small intestine only)	36	47
Rotavirus	10	13
E. coli	2	3
C. perfringens type C	0	0
TGE	0	0

Prospective study; ISU VDL 2000-2001, Dr Michael Yaeger

Circovirus-Associated Disease (PCV2)Dr Schultz:What about porcine circovirus type 2 (PCV2) and circovirus-associated diseases? We're hearing more about them today as causes of post-weaning multisystemic wasting syndrome (PMWS) and PRDC, and they have also been blamed for sporadic cases of reproductive failure. Have any of you seen PCV2 as a cause of reproductive failure and, if so, how significant is it in this stage of production or other areas of production?
I'd like to hear from Dr Moore about what's going on in Quebec.
Dr Moore:We have been experiencing a major outbreak of what we believe is circovirus, but it's in the grower stage. It started probably back in January and in the neighborhood of one-third of herds are affected. There are some scours and fading pigs. As you know, diagnosis of circovirus is very difficult and it is hard to understand why it is blooming.
We have not seen reproductive effects so far. There is nothing in the sow herd and it is mild in the nursery. It is affecting mostly 12- to 18-week old pigs. Dr Schultz:What about managing circovirus? Dr Halbur says that since it usually occurs with other pathogens such as PRRSV and M. hyo, treatment should be aimed at reducing the prevalence of these. Do you agree, and how would you approach PCV2?
Dr Deen:Directly controlling PCV2 is tough. I think that the emphasis should be on stabilizing and reducing the number of gilt litters and reducing the amount of mixing.
Dr Moore:Yes, circovirus-related problems are very difficult to understand and, as of now, no specific strategy has been found. What has helped the most is going back to basics, trying to have all of the other pathogens under control and reviewing management for each herd.
Dr Schultz:On a global basis, PCV2 is causing major problems, more severe than we are experiencing in the US at this time. It is usually a late nursery or more often a grow-finish disease. Dr Pat Halbur recently reported using Aureomycin at the rate of 10mg/lb of body weight (500g/ton of feed) in his experimental co-infection model of Mycoplasma and PCV2. Treatment decreased the lung lesions and clinical expression of the disease to almost zero.
Dr Moore:This is part of our current or standard strategy for those herds at risk where we believe that they will be exposed to either PRRSV, circovirus or both – to use some strategic medication.

Aureomycin at 10 mg/lb body weight is one of our preferred choices. We try to do it toward the end of the nursery phase to avoid problems in the beginning of the grower phase. That’s a strategy that has been commonly used and has a very good benefit.
Dr Schultz:What other diseases do you see as leading causes of poor productivity?
Dr Connor:It's interesting that we see more short-term parvovirus outbreaks, and I think that's directly related to changes in gilt rearing and pig flows. We see parvo-negative gilts entering herds and with a low prevalence of parvo within the sow herd, our natural acclimatization is ineffective.

Those outbreaks are generally 2 to 3 weeks duration. Clearly, the incidence is higher than what we would have seen in our traditional systems.
A further extract from the teleconference - covering breeding issues - will appear in a future article on ThePigSite.