Parvovirosis & Swine Erysipela
Porcine Parvovirus Infection (PPV)
Porcine parvovirus (PPV), a ubiquitous and resistant DNA virus, was considered very stable genetically and antigenically until early 2000’s, when new investigational methodologies revealed new highly virulent and antigenically diverse strains referred to as the PPV-27a cluster. The following years of intense PPV research revealed that this had already happened once before with the identification of the highly virulent PPV-Kresse strain, also defining its own cluster of “PPV-Kresse-like” strains.
Today we consider at least 7 different PPV clusters. Besides the two highly virulent ones, 4 of mild to moderate virulence, and one based on the apathogenic, or at least very low pathogenic commercial reference PPV-NADL-2, used in most commercial tests and vaccines.
Apart from several new PPV field strains, also more, new PPV families were identified in this investigational surge. At some time PPV became PPV1, and PPV2-7 distinct viral families were added. The latter still not considered pathogenic, and not to be confused with PPV(1). Recently all the PPV1-7 were renamed into new families with new different names, leaving PPV(1) the name Ungulate protoparvovirus 1. However, both in still in recent scientific papers, and definitely still swine veterinary practise, hence also here, PPV is named PPV like in “the good old days”.
No clinical signs are produced by from PPV in the infected host at all. However infection of foetuses by transplacental or seminal transmission between will produce potentially sever reproductive losses. PPV is the major cause of the SMEDI syndrome: infertility, embryonic death (return to service), mummified, and stillborn; but also weak-born and viable viraemic piglets. Abortion is not a common trait of PPV. The outcome of PPV infection depends on the virulence and the amount of the virus, and the stage of gestation.
PPV is likely the single most important pathogen as cause reproductive failure in the global swine production. Even in a world of principally 100% PPV vaccinated breeding stock, reproductive failure cases are identified as 4-8% of the cases, as opposed to ie. Leptospirosis only identified in 0-1-2% of cases. Other important pathogens are PCV2 (2-25%), PRRS (1-20%), but also Chlamydia spp. (0-2%). Outside Europe ADV/PRV is another major reproductive pathogen.
To reveal the true reason for reproductive failure, serology is of little use. Clinical material is needed: foetuses/mummies/still borne including corresponding placentas are collected, frozen and when sufficient material is collected, shipped to lab capable of reliable PCR testing for at least PPV, PCV2, PRRS, and leptospirosis. Collect AT LEAST: 1 black + 1 brown + 1 white foetus/piglet including corresponding placentas per litter of AT LEAST 3 litters and ensure that the shipment is appearing at the lab still below zero degree centigrade.
It is not possible to evaluate vaccine induced protection against PPV by any known serological methods (ie ELISA and VN), as they are shown not to correlate clinical disease, the infection of and impact on foetuses in the infected pregnant mother. This supports the potential importance of the early IFN-γ and INF-α activation in PPV infection and a subsequent role of the memory B cells–helper T cell complex of the cell-mediated immunity (CMI) as imperative to PPV protection.
The only way to prevent PPV induced reproductive failure, is by a vaccine building on a PPV strain covering for all relevant field strains and delivering a sufficiently strong protection to avoid foetal losses.
Erysipelothrix rhusiopathiae (Ery) is ubiquitous and the cause of swine erysipelas, an economically significant disease capable of affecting all stages of pork production and causing significant production losses and decreased carcass value.
Ery mainly transmits through direct contact form the 30-50% asymptomatic tonsillar carriers in an endemic farm, or from the profuse shedding of clinically affected animals. Indirect transmission from a potentially highly contaminated environment, including Ery embedded in biofilm, emphasises hygiene measures as an important control element.
Erysipelas in swine is in 80-100% of clinical cases world-wide caused by the three high-virulent Ery serotypes 1a, 1b & 2.
The virulent Ery strains can cause either acute, fulminant septicaemia within 36 hours, erysipelas potential of visual changes in the skin and vascular (diamond skin disease) or sub-acute, most often subclinical, infection potential of chronic degenerative arthritis and/or endocarditis. This may also be the sequelae to the survivors of the acute form.
Chronic degenerative endocarditis and/or arthritis will most often develop over several weeks before noticed, without curative treatment possible due to the degenerative nature. High immune status of the dam at the time of colostral production can protect 12 or more weeks. Inducing strong colostral Ery immunity by pre-farrowing booster vaccination wit an adequate vaccine, may alleviate chronic degenerative Ery losses even until 40-50 kg bodyweight, as these infections are initiated several weeks before, when a maximal colostral protection was potentially achievable.
Triggering factors for disease and outbreaks can be: poor hygienic conditions, poor climatic conditions, as high humidity, sudden changes in weather, especially during hot summer weather, or other stressors, and concomitant immunosuppressive infections.
The virulence of Ery strains is highly dependent on the presence of a particular group of surface protective proteins located on the capsid and responsible for Ery immune evasive properties. These surface protective antigens (Spa’s) will induce a non-bactericidal phagocytotic process of, most importantly, the host macrophages. Such Ery strains remains viable and multiplying inside the host phagocytes, leaving Ery free to induce erysipelas in the host. All swine Ery strains are of the SpaA type.
Specific anti-SpaA antibodies acts as the major protective elements in swine Ery immunity. They are attaching to the SpaA’s, blocking the non-bacterial phagocytosis like a neutralising antibody, maintaining the ability of Ery-phagocytotic kill. On top of that, the anti-SpaA antibodies are opsonising, meaning the attract phagocytes and increase their phagocytic activity against antibody coated Ery.
The SpaA proteins of different strains are similar, but not identical. The cross-protective capacity of a given induced Ery-specific immune response will depend on the quality of the epitope (antigen) used to generate the anti-SpaA antibodies in a given vaccine.
Cell-mediated immunity (CMI) also is important, not only in generating memory & helper T-cells, but also inducing both Ery-specific and general increased macrophage activity. They go out looking more for Ery, and when they connect, the macrophages are more aggressive towards Ery.
Commercial Ery IgG and IgM ELISA kits do not correlate to protection or to anti-SpaA titers. Directly disease and protection correlation Anti-SpaA-antibody tests have been developed and maintained functional at experimental basis at Edinburgh University until a change in staff and equipment calibration in 2018-2019. Since then there have been reliable test available for evaluation of Ery protective status of swine.
Vaccination is an integral part of Ery control, importantly supported by good hygienic measures and climatic control. The vaccine needs to protect the strongest possible against anti-SpaA, induce CMI, provide the best possible cross-protection, as a minimum against serotypes 1a, 1b & 2, and allow for pre-farrowing booster to induce the maximal colostral Ery protection.