PCV2 is considered ubiquitous and domestic and feral swine are considered the natural hosts. Natural infection occurs via the oronasal route. Disease occurs in all types of herds. Risk factors that trigger a worsening of disease may include, but are not restricted to, co-infection with PRRSV and porcine parvovirus, mixing of litters (which stresses pigs and exposes them to other new infectious agents), early vaccination against certain diseases and environmental factors, such as poor ventilation, overcrowding, or possible other ‘stressors’. Seroconversion of piglets to PCV2 generally occurs at 3-4 weeks post weaning. It can therefore be concluded that pigs are exposed when they are transferred to the fattening unit. While it seems that the virus is mainly transmitted horizontally, evidence exists to suggest that the virus can also be transmitted vertically
(dam to offspring). The virus is very resistant in the environment and a substantial number of disinfectants are ineffective against it.
There are a number of “known unknowns” concerning PCVD including the following:
• Disease occurs in a percentage of the infected animals only. Furthermore, while pigs diagnosed with PMWS are always PCV2 positive, not all PCV2 positive herds develop PMWS– why these are the case is currently unknown
• Severity of the disease can also vary enormously between countries or indeed regions. For instance, in some countries a high incidence of PCV2 positive herds is seen along with very few cases of PMWS. Significant effort has been made to differentiate strains to align with disease causing ability (pathogenicity) but, as yet, has not yielded any meaningful results.
• Seroprevalence, excretion patterns, incubation period and host range for PCV2 have not been fully elucidated. Excretion of PCV2 has been detected in faeces and saliva for up to one month post infection and possibly persists for longer