Characteristics of a coronavirus causing vomition and wasting in pigs

Abstract

Some characteristics of a virus, isolated from the tonsils of 2 pigs with clinical signs of inappetenee and vomition and designated VW572 were examined. It induced the formation of syneytia in primary pig kidney cell cultures, caused hemadsorption and hemagglutination using chicken, turkey, rat and mouse erythrocytes. In growth curve experiments, infectious virus was produced intracellularly starting at 6 hours after inoculation and was followed by rapid release of the virus from the infected cells. The virus contains ribonucleic acid, is ether sensitive and has a size between 100 and 220 nm. At 37 ~ C, the infectivity titer decreased about 2 lOgl0TCIDs0 per 24 hours. The viral population was heterogeneous as indicated by the rate of inactivation by U.V. irradiation and acid pH. Some hemagglutinating activity was left after complete loss of infectivity by ether-, temperature-and U.V. treatment. The VW 572 isolate is antigenically related if not identical to isolates from Canada, U.S.A. and England which were classified as a porcine eoronavirus.Oronasal and intracerebral inoculation of the VW572 isolate in colostrum deprived pigs resulted in clinical disease after an incubation period of 6 and 4 days, respectively. Signs were characterized by depression, vomition, loss of appetence with rapid weakness in young pigs and vomition with progressive wasting in older pigs. Virus was isolated from nasal and pharyngeal swabs, nasal mueosa, tonsils, lungs and hind brains but not from rectal swabs or other organs tested. Virus could not be isolated later than 8 days after inoculation. Hemagglutination inhibiting and neutralizing antibodies were detected in sera at 6 days and 9 days after inoculation, respectively.

Detection and genetic analysis of porcine hemagglutinating encephalomyelitis virus in South Korea

“…The clinical signs of VWD are characterized by sneezing, coughing, depression, loss of appetence, weakness, and marked vomition [15,16]. On the other hand, the encephalomyelitic form may start as VWD signs but pigs soon develop severe neurological signs such as muscle tremor, hyperesthesia, incoordination, paddling, or paralysis and in most cases, they precede death [15].…”

“…Since then, more PHEVs were isolated from 30 different outbreaks of encephalomyelitis in Canadian pigs over the following few years [4]. Apart from North America, another type of PHEV, characterized by vomition, inappetence and loss of condition, was reported in Belgium in 1973 [16]. PHEV infection is now known to be widespread in worldwide but it usually remains subclinical because pigs are protected by colostral antibodies and subsequently they develop age-related resistance against PHEV [15].…”

Antigenic relationship of the feline infectious peritonitis virus to coronaviruses of other species

“…Coronaviruses are 60 to 220 nm in diameter, have a buoyant density in sucrose of 1.16 to 1.23 g/cm 3, are sensitive to lipid solvents, contain a large single strand of ribonucleic acid, have regularly spaced surface projections N.C. PEDERSEN, J. WAI~D, and W. L. MESrG~LL~G: t h a t are 12 to 24 n m in length, and bud from profiles of endoplasmic reticulum into cytoplasmic vesicles in the infected cells (23). Coronaviruses cause bronchitis in chickens (5), humans (7,10) and rats (14), acute enteric infections in b a b y pigs (22), calves (21) a n d puppies (1), hepatitis in mice (4), and encephalomyelitis a n d chronic vomition and wasting in swine (6,18).…”

Development of a triplex real-time RT-PCR assay for detection and differentiation of three US genotypes of porcine hemagglutinating encephalomyelitis virus

“…PHEV was first isolated from suckling piglets suffering from encephalomyelitis in Canada in 1962 (Greig et al, 1962). PHEV has since been identified in many countries of Europe, Asia, and America (Cartwright et al, 1969;Dong et al, 2014;Forman et al, 1979;Hirahara et al, 1987;Mengeling, 1975;Pensaert and Callebaut, 1974;Quiroga et al, 2008;Rho et al, 2011). Although PHEV infection has been endemic in different countries for decades and the primary route of PHEV infection is through upper and lower respiratory tracts, only few reports suggest an association of the virus with respiratory disease in swine (Cutlip and Mengeling, 1972).…”