Pleural effusion disease in rabbits. Properties of the aetiological agent

Abstract

The size and heat sensitivity of Pleural effusion disease (PED) agent or virus (PEDV) propagated in rabbits were examined. The infectious particles were estimated to be between 25 and 50 nm by filtration. Residual infectivity of infectious serum was 0.1 per cent after heating at 56 degrees C for 4 hours. PEDV and the Stockholm agent appeared identical concerning pathogenic and immunogenic properties by infection experiments and protection tests in rabbits. Two of the three PEDV isolates were less pathogenic but appeared immunogenically identical to PEDV. The third isolate, obtained from the laboratory, which several years previously had supplied material for demonstration of the Stockholm agent, differed from PEDV in pathogenic and immunogenic properties. Serological examinations of paired rabbit sera did not indicate any antigenic relationship between PEDV and representative members of the two mammalian coronavirus antigenic groups. It is concluded that the aetiological agent of PED is a virus not belonging to the coronaviridae.

Pathogenicity and Persistence of Pleural Effusion Disease Virus Isolates in Rabbits

“…As yet, the agent has not been identified, but it is considered to be a host-specific, enveloped virus, measuring 25 to 50 nm by filtration (Fennestad & MacNaughton, 1983). Observations on the intercurrent disease and experimental studies with the original PEDV isolate suggest that the emergence of PEDV infection as a clinical disease of rabbits is the result of a specific selective pressure on a benign virus population.…”

“…The detailed history of the Stockholm agent since isolation is not known. All nine isolates are considered serologically closely related or identical with PEDV on the basis of crossprotection studies (Fennestad et al, 1980;Fennestad & MacNaughton, 1983). …”

Viral Diseases

“…Immunofluorescent staining of cardiac tissue from diseased rabbits with antisera to 229E virus revealed antigen in myocardial interstitial tissue, and rabbits surviving infection developed antibodies to the virus in a complement fixation assay (Small et al, 1979). In another study, however, surviving rabbits failed to demonstrate antibodies against 229E virus in an enzyme immunoassay and neutralization test, and against OC43 virus in a complement fixation test (Fennestad and MacNaughton, 1983).…”

“…Subsequent inoculation of rabbits with pulmonary tissue and pleural fluid from dead rabbits, previously inoculated with treponemes, resulted in a similar syndrome (Gudjonsson et al, 1970). Differential filtration of pleural fluid and serum from rabbits revealed an infectious particle size of 25-50 nm, which is ether-sensitive and inactivated at temperatures of 65°C or above but not at 56°C (Fennestad and MacNaughton, 1983;Gudjonsson et al, 1972;Small et al, 1979). Sera from rabbits contained pleomorphic virus particles, round or elliptic, 75-100 nm in diameter, bearing club-shaped projections 15-20 nm long (Small et al, 1979), whereas plasma from rabbits contained high concentrations of pleomorphic virus-like particles measuring 51-98 nm in diameter with projections 8-13 nm long (Osterhaus et al, 1982).…”

“…Iridocyclitis has been reported. With virulent strains, a third of infected rabbits die 3-5 days after inoculation, although deaths can occur until 14 days (Baric et al, 1990;Fennestad, 1985;Fennestad and MacNaughton, 1983;Fennestad et al, 1975Fennestad et al, , 1986Fledelius et al, 1978;Gudjónsson and Skog, 1970;Gudjonsson et al, 1970;Small et al, 1979). Generalized or hindquarter muscular weakness was also reported in rabbits surviving the acute phase of infection (Gudjonsson et al, 1970;Small et al, 1979).…”