Porcine Respiratory Coronavirus (PRCv)
Occurrence: Europe and N. America since 1986.
Age affected: All ages.
Causes: Virus related to TGE.
Effects: Often no signs, may be cough, inappetence, fever.
PRCv is a coronavirus very closely related to TGE and causes cytopathic effects (damage) and syncytia (fused cells) in cell cultures. It can be isolated from the lungs of infected pigs. Antibody to it neutralises TGE virus and the syncytia fluoresce with sera specific to TGE but monoclonal antibodies to TGE virus exist which do not react with PRCv. The differences between TGE and PRCv result from a genetic change to the spike (S) protein (used in attachment) which changed the tissue infected from gut to lung and altered the antigenicity. Infection is by aerosol and the virus multiplies chiefly in the lungs.
Virus has been demonstrated in nasal mucosal epithelial cells, those of the trachea, bronchi, bronchioles and alveoli. Alveolar macrophages are also affected. Varying degrees of interstitial pneumonia result from infection. The virus is shed as an aerosol and in nasal secretions for 1-6 days after infection. It does not appear to cross the placenta but has been found in the semen for up to 6 days post infection in boars. Antibody to the virus becomes detectable in sera within a week. When PRCv is present with another virus, lesions in the lung are more severe than with PRCv alone.
Mode of transmission
Transmission is by direct contact and aerosol, the disease spreads rapidly within a herd once introduced. Transmission between farms is usually by means of carrier pigs.
Infection with PRCV may result in the production of serum antibody at 3-5 months of age in some herds, in which maternal antibody is present but coughing and inappetence have been reported in others. Inappetence, reluctance to move, laboured respiration and fever (40°C, 104°F) have been reported 1-5 days following experimental infection of antibody free conventional pigs. No clinical signs were noted in germ-free pigs in some studies. Experimental infection with PRCv alone or together with influenza virus has little effect on growth rate.
The clinical signs are not sufficiently consistent to reach a diagnosis. The spread of mild respiratory disease throughout a herd previously free from TGE, coupled with seroconversion to TGE virus in the absence of enteric signs suggests the presence of PRCv. Specific serological tests for PRCv have been produced using a blocking ELISA tests using monoclonal antibodies specific for TGE.
The pathology in infected pigs may suggest PRCv. Lesions have not been found in some cases and in others severe catarrhal bronchopneumonia has been seen. Lesions are restricted to the lung and bronchi. They include mild interstitial pneumonia, hyperplasia (overgrowth) of the bronchiolar epithelium and epithelial cell loss. Syncytia occur in the alveoli and airways.
Virus may be demonstrated in the bronchiolar and bronchial epithelial cells, in alveolar macrophages and septal monocytes using immunoperoxidase, biotin labelled monoclonal antibody which detects viral proteins and in situ hybridisation which detects nucleic acid. Viral nucleic acid can also be identified in tissue by tests related to the Polymerase Chain Reaction (PCR). The demonstration of the virus or its nucleic acid confirms the diagnosis.
Treatment and prevention
The only indication for control at present is that infected pigs are seropositive for TGE and infection therefore interferes with the certification of herd for freedom from TGE. This problem has been approached by founding and maintaining antibody-free herds by rigorous testing and isolation. This experience confirms that it is possible to obtain and maintain herds free from the infection, but there is no other commercial reason to do so. Disinfect as for TGE. An experimental vaccine has been produced but none are available commercially.