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.
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
Historically, PMWS in the
A group of
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
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
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
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?
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.