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 investigative methodologies revealed new highly virulent and antigenically diverse strains referred to as the PPV-27a cluster. This discovery followed an earlier identification of another virulent strain, PPV-Kresse, which also defined its own cluster of “PPV-Kresse-like” strains.

At present, a minimum of seven phylogenetically distinct PPV clusters have been identified. These include two clusters characterized by high virulence, four exhibiting milds to moderate pathogenicity, and one cluster derived from the apathogenic—or minimally pathogenic—reference strain PPV-NADL-2, which serves as the standard in most commercial diagnostic assays and vaccine formulations.

In addition to these PPV1 strains, researchers have identified new PPV viral families, leading to the classification of PPV1 through PPV7. The latter is still not considered pathogenic and is not to be confused with PPV (1). Recently, all the PPV1-7 were renamed into new families with different names, leaving PPV (1) the name Ungulate protoparvovirus 1. However, both are still widely used in both scientific literature and swine veterinary practice, hence also here, PPV is named PPV.

No clinical signs are produced by PPV in the infected host at all. However, infection of fetuses by transplacental or seminal transmission will produce potentially severe reproductive losses. The virus is also transmitted via the oronasal route in secretions and excretions such as feces and fluids from the placenta and mummified piglets. PPV is the major cause of SMEDI syndrome: stillbirth, mummification, embryonic death, and infertility. It also causes weak–born and viremic piglets. Abortion is not a common symptom of PPV. The outcome of PPV infection depends on the virulence, the amount of the virus, and the stage of gestation. PPV is more common in gilt litter with less developed immunity.

PPV is likely the single most important pathogen causing reproductive failure in 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 Leptospirosis, for example, only being identified in 0-1-2% of cases. Other important pathogens are PCV2 (2-25%), PRRS (1-20%), but also Chlamydia spp. (0-2%). Outside of Europe, ADV/PRV is another major reproductive pathogen.

To reveal the true reason for reproductive failure, serology is of little importance. Clinical material is needed: fetuses/mummies/still born piglets including corresponding placentas are collected, frozen and when sufficient material is collected, shipped to a lab capable of reliable PCR testing for at least PPV, PCV2, PRRS, and leptospirosis. Collect AT LEAST: 1 black + 1 brown + 1 white fetus/piglet including corresponding placentas per litter of AT LEAST 3 litters and ensure that the shipment arrives at the lab with the temperature still below 0°C.

It is not possible to evaluate vaccine induced protection against PPV by any known serological methods (i.e. ELISA and VN). As they have not been shown to correlate with clinical disease, the presence of infection and its impact on fetuses in infected pregnant mothers remains uncertain. 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 fetal losses. The vaccine should be administered before breeding. A good vaccination program is crucial to control PPV, as it can survive in the environment for months and is resistant to disinfectants, making it virtually impossible to eliminate.

Swine erysipelas

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 with infected animals, particularly the 30-50% of asymptomatic carriers in endemic farms via feces and oronasal secretion, or from the profuse shedding of clinically affected animals.

Indirect transmission from highly contaminated environments, including Ery embedded in contaminated Ed feed and water, emphasizes hygiene measures as an important control element.

Globally, 80-100% of clinical cases are caused by three highly virulent serotypes: 1a, 1b, and 2.

Virulent Erysipelothrix rhusiopathiae can present in multiple forms, including acute, subacute, and chronic infections. Acute cases may lead to fulminant septicemia within 36 hours, high fever, and sudden death, with fever often causing abortion in gestating sows and gilts. A hallmark sign is the appearance of raised red, diamond-shaped skin lesions—commonly known as “diamond skin disease”—which reflect underlying vascular damage. Subacute infections are often subclinical but can progress to chronic conditions such as degenerative arthritis, resulting in a stilted gait due to painful joints, and endocarditis, an inflammation of the heart lining. These chronic issues may also develop as sequelae in pigs that survive the acute phase. The disease process involves systemic vasculitis, where toxins circulate in the bloodstream and become localized in the skin, joints, and heart, contributing to both visible and internal signs of illness.

Chronic degenerative endocarditis and/or arthritis will most often develop over several weeks before being noticed, without curative treatment possible due to the degenerative nature. High immune status of the dam at the time of colostrum production can protect for up to 12 or more weeks. Inducing strong colostral Ery immunity by pre-farrowing booster vaccination, may alleviate chronic degenerative Ery losses even until 40-50 kg bodyweight, as these infections are initiated several weeks before, when a maximal colostrum protection was potentially achievable.

Triggering factors for disease and outbreaks can be :

poor hygienic conditions

poor climatic conditions (high humidity, sudden changes in weather, especially during hot summer weather)

concomitant Immunosupressive infections

other stressors

The virulence of Ery strains is largely 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 remain viable and multiply 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 act as the major protective elements in swine Ery immunity. These antibodies bind to SpaA protiens and block the non-bacterial phagocytosis like a neutralizing antibody, maintaining the ability of Ery-phagocytotic kill. On top of that, the anti-SpaA antibodies are opsonizing, meaning they attract phagocytes and increase their phagocytic activity against antibody coated Ery.

The SpaA proteins across 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 each 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. Direct disease and protection correlation Anti-SpaA-antibody tests have been developed and maintained functional on an experimental basis at Edinburgh University until a change in staff and equipment calibration in 2018-2019. Since then, there has been reliable tests available for evaluation of Ery protective status of swine.

Vaccination is an integral part of Ery control, and its effectiveness is significantly enhanced by good hygine practices and d climatic control. An ideal vaccine should provide strong protection by inducing high levels of anti-SpaA antibodies, stimulating cell-mediated immunity (CMI), and offering broad cross-protection – at a minimum against stereotypes 1a, 1 b and 2. It should also be suitable for pre-farrowing booster administration to induce maximal colostral protection for piglets.