Background and History

Porcine circovirus (PCV) is a common virus of pigs found throughout the world. Porcine circovirus Type 1 is widespread in commercial swine but is nonpathogenic.

PCV1 was identified in 1974 as a contaminant in a pig kidney cell line but has not been shown to cause disease in pigs. In 1997, PCV2 was recognized as the cause of a novel wasting disease affecting Canadian pigs. In 2016, PCV3 was detected in tissues from sows from North Carolina that died with PDNS-like clinical signs and aborted fetuses. Evidence suggests that known PCVs have been circulating in swine long before they were detected.

PCV2 is strongly associated with post weaning multi-systemic wasting syndrome (PMWS), also known as porcine circovirus type 2 systemic disease (PCV2-SD) and porcine circovirus type 2 subclinical infection (PCV2-SI). PCV2 has become widely distributed in most developed swine industries around the world. While most swine are infected with PCV2, only a smaller portion of pigs show signs of the disease. There are 8 proposed PCV2 genotypes labeled PCV2a-h. PCV2 virus genotypes (a, b, d, etc.) are genetically similar and contain two major structural proteins - the replicase encoded by ORF1 and the capsid encoded by ORF2. Recombination occurs in 20–35% of PCV2 viruses and has been observed across most genotypes. Ongoing genetic change has led to molecular diversity within PCV2. Initial PCV2 infections were identified as PCV2a. Now, there there have been two major genotype shifts resulting in a switch of predominant circulating virus from PCV2a to PCV2b to PCV2d in many parts of the world. PCV2c, e–h are detected less often. PCV2g and PCV2h have been more recently identified recombinant genogroups mostly stemming from gene segments from PCV2a, b, and d. Genotypes a, b, and d are clinically relevant and most often associated with clinical disease.

PCV3 has been associated with signs similar to PCV2, however, many infections seem to be subclinical. PCV3 has been associated with neurological disease, reproductive failure, respiratory disease, enteric disease, and porcine dermatitis and nephropathy syndrome (PDNS). Epidemiological studies have found that infection is widespread, with prevalence up to 100%. A few studies have shown that prevalence is highest in piglets/weaners and decreases with age, but PCV3 has been detected in pigs up to 23 weeks of age. PCV3 is distinctly different from other PCAVs and is closely related to canine and bat circoviruses.

Clinical Signs

PCV2 (PCVAD): Loss of body condition and enlarged lymph nodes, rough hair coat, polypnea, dyspnea, pallor, diarrhea and occasionally icterus. Affected pigs usually die; clinical survivors are severely stunted. Signs and lesions vary considerably. Hallmarks of severe PCV2 infection include high viremia levels, high virus titers within tissues, and lymphoid depletion/granulomatous inflammation. The severity of infection can be complicated by common co-infections with other viruses or bacteria.

Diagnosis

PCVAD: Diagnosis is made on clinical features, gross lesions, microscopic lesions, and demonstration of PCV2 within lesions. Using microscopy, characteristic lesions may be observed, and virus inclusion bodies can often be identified in depleted lymph nodes, spleen, tonsils, or Peyer’s patches.

Immunohistochemical tests or in situ hybridization are used to confirm diagnosis of disease associated with PCV2. PCR will confirm the presence of virus but does not confirm the presence of disease. Isolation and identification of a circovirus is not useful for diagnosis since asymptomatic infection is widespread in swine populations.

PCVAD must be differentiated from other bacterial or viral diseases, especially PRRSV which has similarities in clinical signs and lesion. Concurrent infections are common.

PCV3: First identified by metagenomic sequencing. Many PCR assays have been developed for PCV3 in the research setting. Virus can be demonstrated in lesions by immunohistochemistry (IHC) or in situ hybridization (ISH). PCV3 can be detected in many tissues and organs. Heart, lung, and lymphoid tissue are important for histology and IHC or ISH. When PDNS is suspected, skin lesions should be submitted, and in cases of reproductive failure, fetal tissues should be submitted.

Cause

PCV DNA is unique for its small size (~1800 bp), nonenveloped, single stranded circular genome, and hardiness in the environment.

Both PCV2 and PCV3 spread through vertical and horizontal transmission. Virus is shed in most secretions and excretions. Direct contact is the route of most significance but spread can also occur via fomites and ingestion.

Exposing pigs to other pigs or boots, clothing, or equipment that has been around other pigs greatly increases the risk for disease transmission. Visible bodily secretions (blood, urine, feces, or mucus) from pigs can contain infectious disease organisms.

Treatment

There is no specific treatment for pigs with PCVAD. However, anti-inflammatory agents and/or antimicrobials are sometimes used with some success in groups of pigs experiencing disease. All in/all out pig flow, thorough cleaning and disinfection between batches of pigs and early segregation and euthanasia of affected pigs are measures that may help control the disease. Antibiotics in feed or water may suppress secondary infections.

The ubiquitous nature of PCV2 makes it unlikely that commercial farms can be maintained free of the virus. The use of total depopulation as a control strategy is not often recommended.

PCV2 vaccines became commercially available in the US in 2006. Field experience demonstrates that the vaccines are effective in reducing the severity and incidence rate of PCVAD on many farms. The timing of vaccination and population to be immunized (breeding herds, replacement stock, growing pigs) varies between farms depending on the characteristics of the affected populations and the physical operation of the farm.

There is no cross-protection between PCV2 and PCV3. No commercially available PCV3 vaccines exist.