Parvovirosis & Swine Erysipela

Porcine Parvovirus Infection (PPV)

Porcine parvovirus (PPV), a ubiquitous and resistant DNA virus, was considered highly stable both genetically and antigenically until the early 2000s, when new analytical methods revealed highly virulent and antigenically diverse strains grouped within the PPV‑27a cluster.

This discovery followed the identification of another virulent strain, PPV‑Kresse, which defined its own “PPV‑Kresse‑like” cluster. To date, at least seven distinct phylogenetic clusters of PPV have been identified:

• 2 highly virulent clusters,
• 4 clusters of low to moderate pathogenicity,
• 1 cluster derived from the reference apathogenic or low-pathogenic strain PPV‑NADL‑2, used in most diagnostic tests and commercial vaccine formulations.

In addition to these PPV1 strains, researchers have identified new PPV viral families, leading to a classification from PPV1 to PPV7.
PPV6‑7 are not considered pathogenic and should not be confused with PPV1.
Recently, PPV1‑7 have been renamed according to new viral families, and PPV1 is now referred to as Ungulate protoparvovirus 1. However, in the scientific literature and in swine veterinary medicine, the term PPV is still widely used, and we will retain it here.

Clinical signs and economic importance

PPV does not cause any clinical signs in the infected animal.
However, infection of fetuses through transplacental transmission or via semen can result in severe reproductive losses.

The virus is also transmitted:

• via the oronasal route,
• through secretions and excretions (feces, placental fluids, mummified fetuses).

PPV is the main cause of the SMEDI syndrome:

• Stillbirth
• Mummification
• Embryonic Death
• Infertility

It also causes weak or viremic piglets.
Abortion is not a frequent sign of PPV.

The outcome of an infection depends on:

• strain virulence,
• viral load,
• stage of gestation.

PPV is more common in gilts, whose immunity is less developed.
PPV is likely the most important pathogen causing reproductive failure in global swine production, even in environments where nearly 100% of breeding females are vaccinated.

Cases of reproductive failure attributable to pathogens are approximately identified as follows:

• PPV: 4–8%
• PCV2: 2–25%
• PRRS: 1–20%
• Chlamydia spp.: 0–2%
• Outside Europe: ADV/PRV is also a major agent.

Diagnosis

Serology is of limited value in identifying the real cause of reproductive failure.
Clinical material must be analyzed:

• fetuses
• mummies
• stillborn piglets
• corresponding placentas

Recommendations:

• Collect at least 1 black + 1 brown + 1 white per litter
• Collect at least 3 litters
• Freeze, then ship to the laboratory (PCR PPV, PCV2, PRRS, leptospirosis)
• Ensure the sample arrives below 0 °C

There is no serological method (ELISA or VN) that allows assessment of protection induced by PPV vaccination.
Protection appears to be more related to:

• early activation of IFN‑γ and INF‑α,
• the role of memory B cells – helper T lymphocytes,
• and cell-mediated immunity (CMI).

Control and vaccination

The only way to prevent PPV-related reproductive losses is to use a vaccine based on a strain that covers all relevant field strains, providing sufficient protection to prevent fetal losses.
Vaccination must be administered before breeding.
A strong vaccination program is essential because PPV:

• survives for months in the environment,
• is resistant to disinfectants,
• and is therefore virtually impossible to eliminate.

Swine erysipelas

Erysipelothrix rhusiopathiae (Ery) is ubiquitous and responsible for swine erysipelas, an economically important disease that can affect all stages of production and lead to significant losses and reduced carcass value.

Transmission

Ery is mainly transmitted through:

• Direct contact with infected animals, including:
  • 30–50% asymptomatic carriers in endemic farms,
  • oronasal and fecal secretions,
  • massive shedding by clinically affected animals.
• Indirect transmission: heavily contaminated environment, contaminated feed/water.

Hygiene is therefore a key factor in control.
Worldwide, 80–100% of clinical cases are caused by three highly virulent serotypes: 1a, 1b and 2.

Clinical forms of erysipelas

Ery can occur in: acute, subacute, and chronic forms.

Acute form

• Fulminant septicemia within 36 hours
• High fever
• Sudden death
• Abortions in pregnant sows
• Red diamond-shaped skin lesions (diamond skin disease) → typical vascular signs

Subacute form

• Often subclinical
• May progress to chronic forms

Chronic form

• Degenerative arthritis → stiff gait
• Endocarditis
• Gradual development over several weeks
• No curative treatment once lesions are established

Chronic infections often begin several weeks before clinical signs appear, sometimes at a time when maximal colostral protection could have been achieved. A strong colostral immunity in the sow (through vaccination before farrowing) can protect piglets up to 12 weeks and beyond, reducing losses linked to chronic forms up to 40–50 kg body weight.

Outbreak triggering factors

• Poor hygiene conditions
• Poor environmental conditions (high humidity, sudden changes, heat)
• Concurrent immunosuppressive infections
• Various stress factors

Virulence and immunity

Virulence largely depends on a group of protective surface proteins (Spa) located on the capsule, which allow Ery to evade immunity.
Anti‑SpaA antibodies are the main components of protection against Ery:

• they neutralize immune evasion,
• they promote opsonization (increased macrophage activation),
• they restore effective phagocytosis of the bacteria.

SpaA proteins are similar but not identical between strains.
Cross-protection capacity therefore depends on:

• the quality of the vaccine epitope,
• the ability of the vaccine to generate strong anti‑SpaA antibodies.

Cell-mediated immunity (CMI) also plays a major role:

• generation of memory T cells and helper T cells,
• overall macrophage activation
  → macrophages become more aggressive and faster at targeting Ery.

Commercial IgG/IgM ELISA tests do not correlate with protection or anti‑SpaA titres.
An anti‑SpaA test correlated with protection existed at the University of Edinburgh until 2018–2019, but no reliable commercially available test exists today.

Control and vaccination

Vaccination is an essential component of erysipelas control.

Its effectiveness also strongly depends on:

• hygiene,
• environmental control.

The ideal vaccine must:

• induce high anti‑SpaA antibody titres,
• strongly stimulate CMI,
• provide broad cross-protection, at minimum against serotypes 1a, 1b and 2,
• be suitable for pre‑farrowing booster use to maximize colostral protection.