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PVC2: Lessons learned and the future
By Raymond Rowland  |  Tuesday, January 01, 2008

Porcine circovirus associated disease has made plenty of headlines, but the attention is not likely to end any time soon. There are many answers yet to find, but some can help us plan for the future.

Let’s start by taking a look at PCVAD. It refers to a group of complex, multi-factorial diseases including two diverse syndromes, porcine multisystemic wasting syndrome and porcine dermatitis and nephropathy syndrome.

In North America, PCVAD has had a sporadic history. After the initial description of PMWS in Canada in the early 1990s, the disease mechanism, its association with porcine circovirus type-2 and other co-factors have been under intense debate.  It seems that for the past 10 years, PCV2 has been a virus looking for a disease. The situation changed in 2005 when Canada reported an increase in PCVD case submissions. This coincided with the appearance of PCV2-321 (also known as PCV2b). 

The current view is that, regardless of its manifestation, PCV2 is a key etiologic factor in PCVAD.  Studies of PCV2 genomic sequences show that most viruses can be divided into distinct genotypes, known as PCV2a and PCV2b. In the United States and in Europe these are known as PCV2 group-2 and PCV2 group-1 viruses, respectively. Comparisons of PCV2a and PCV2b genomes reveal an identity of approximately 95 percent.  A distinct difference between PCV2a and PCV2b is the presence of a signature motif in ORF2. 

Historically, PMWS in the United States has been associated with the PCV2a subtype. The impact of PCV2b in U.S. herds first became apparent with PCVAD outbreaks reported in Kansas and other states.  The outbreaks were characterized by an increased prevalence of PMWS and PDNS as well as increased mortality during the finishing stage. Some herds approached 30 percent morbidity/mortality levels.

A group of Kansas State University scientists, diagnosticians and virologists, under the direction of swine veterinarian Steven Henry, came together to investigate the outbreak.  In 2006, the Kansas State team, in collaboration with others, linked the “severe” PCVD outbreak to the PCV2b genotype, which led to the hypothesis that the two PCV2 genotypes may differ in virulence. In order to track the source of PCVD infection in the field, the Kansas State team developed several differential PCR diagnostic tests.

What we found

Results showed that all PCVD pigs submitted to the Kansas State Veterinary Diagnostic Laboratory possessed the PCV2b genotype. Interestingly, both PCV2a and PCV2b sequences were present in about 25 percent of the clinical samples, demonstrating that pigs can be infected simultaneously with both genotypes.  A logical outcome of co-infection is recombination. In August 2007, the Kansas State team identified a virus that contained the ORF1 from PCV2a and ORF2 from PCV2b. The implications of recombination in disease progression and diagnosis remain to be determined.

In the past year, there have been new developments in our understanding of the disease as a result of using commercial vaccines.  With Steven Dritz, DVM, a Kansas State swine nutritionist, the team initiated the first carefully controlled PCV2 vaccine field study in a 300-head, farrow-to-finish herd in northeastern Kansas.

The results showed more than a 50 percent reduction in mortality in the vaccinated group. In addition, the market weight distribution for the vaccinated population shifted to the right by 8.8 kg, resulting in a significantly lower percentage of pigs that fell below the minimum market weight goal of 111.4 kg. In fact, the producer could have sent the vaccinated pigs to market a week earlier.

A subset of 52 pigs was randomly selected, and blood samples were collected in the nursery through the mid-finishing stages. The resulting serological profile showed an immunological response in vaccinated pigs. Real-time PCR measurement of PCV2 DNA showed an approximate 10-fold decrease in virus load within the vaccinated population. The results from this study demonstrated that vaccination reduces mortality and morbidity, improves performance, induces a measurable serological response and reduces virus replication.

Mortality, growth rate and feed efficiency improvements are calculated to produce an economic benefit well beyond the vaccination cost. Performance gains in vaccinated herds that did not experience overt clinical PCVD signs suggest that the critical lesions associated with PCV2 infection appear to be the loss of pounds.

Questions still remain

Even though vaccines are effective, several questions remain.

1. What is the rate and cause of vaccine failure?  There is early evidence that small numbers of vaccinated pigs are not immune to the virus.  A test that can distinguish vaccinated from naturally infected pigs is needed.

2. Can vaccination lead to virus elimination?  Data show that vaccination reduces virus load, but the biological relevance remains to be determined.  For example, do vaccinated pigs shed virus? Similar to porcine parvovirus, PCV2 is extremely stable. Virus elimination will require a vaccination program that is effective through several production cycles, combined with removing virus from the environment.

3. Are further improvements (or refinements) in the vaccine needed?  Current vaccines incorporate PCV2a capsid protein.  Can improved protection be offered through the incorporation of PCV2b capsid antigen?

The Kansas State approach to address PCV2 illustrates the importance of forming diverse multidisciplinary teams in addressing emerging infectious disease problems. The Kansas State PCV2 team has brought to the industry, in a very timely manner, scientifically sound and useful information which can be integrated into the economics of pork production. We believe that this approach is a useful template to address future pork industry challenges.

Within the context of a much larger conceptual landscape, the modern production system can be viewed as an intricate ecological system involving dynamic and complex interactions between pathogens, opportunists, normal flora, pig genetics and diverse environmental conditions. Experience with PCV2 teaches us that “disease” is the product of the intersection of these biological and physical factors. Applying ecological modeling techniques to pork production systems will have value in developing proactive practices that minimize emerging diseases’ impact. Along with PCV2, there is a vast multitude of viruses circulating in the general pig population that exert unquantified effects. PCV2 taught us that “classical” approaches to understanding an organism’s pathogenic potential are inadequate.

First, we need a definition of disease that, in addition to evaluating lesions and clinical signs, includes the infection’s impact on profitability and animal well-being.

Secondly, we need to widen our study of disease. We need to go beyond the single pathogen in the pig and include the interactions with other disease-associated factors within the ecology of the modern commercial swine population. 

There is plenty of fodder for future strategies.