Substantial mortalities in pigs due to encephalomyocarditis (EMC) virus infection in the central west and north coast of New South Wales have been reported. The usual finding on affected piggeries was sudden death of about 10% of young pigs. On post-mortem examination, pale areas a few mm to 1 cm in diameter could be readily seen in the myocardium. This paper is to describe experimental infections produced by I. R. Littlejohns and myself in pigs with this virus.
The first experimental infection was performed to confirm the pathogenicity of the virus for pigs. Four pigs were given a high dose of virus intramuscularly in a mouse tissue inoculum. They died 2, 3, 5 and 11 days after inoculation and had severe gross heart lesions.
In this first experimental infection and in later infections, rectal temperatures were recorded twice daily. In most cases, there was a brief temperature rise to 41°C for 24 hours or less, usually 2-4 days after exposure. This was so brief, and clinical abnormalities were so infrequently apparent, that illness would not have been observed under normal husbandry conditions.
In the second group of experimental infections, an intramuscular dose of mouse tissue about 3000 times less potent than that in the first experiment was used. Three of the 4 pigs died within 3 days of inoculation and were clinically and pathologically comparable to those that died in the first group. The fourth pig had a brief febrile response, but following this was clinically normal. It was destroyed 28 days post-inoculation. This pig provided high titre pig antiserun to the virus and allowed resolving lesions to be examined. The small fibrous scards in the myocardium bore resemblance to the lesions seen in a few hearts from abattoirs and to those in a field case that died some weeks after its pen mates died with typical acute heart lesions.
Two pigs were inoculated intramuscularly with virus in cell culture and they died within 5 days with typical lesions.
In an attempt to provide more natural exposure, 4 pigs were fed on the carcases of mice that died after EMC virus infection. The pigs played with the carcases, chewing them and tossing them around from one to another before eating them. All 4 pigs died within 6 days of exposure. Transmission by contact was attempted. Four pigs were given tissue culture virus orally and held under conditions that allowed good contact with 2 unexposed pigs. Three of the pigs given virus had gross heart lesions when they died or were killed, but the in-contact pigs had no clinical or serological evidence of infection 21 days after exposure.
Intranasal exposure to an aerosol of tissue culture fluid was used, 4 pigs being given undiluted fluid, and 4 pigs being given a thousand fold dilution of fluid. (In) The high-dose group, one pig died and two others had minor lesions when they were destroyed. In the low-dose group, all pigs were destroyed 14 days post-exposure and one had severe heart lesions, while one had mild lesions.
A field report that vitamin E supplementation increased the resistance of pigs to EMC virus infection was the basis of a further trial. Results were not conclusive because of the small number of intramuscularly inoculated pigs used. However, it appeared that although vitamin E supplementation did not affect the susceptibility of pigs to infection with EMC virus, the outcome was less likely to be fatal in supplemented pigs. Further trials with EMC virus and vitamin E supplementation are being undertaken in mice.
There were no substantial differences in the clinical and post-mortem findings in disease induced in pigs by the various virus preparations or routes of exposure, the range of clinicopathological manifestations after intra-nasal exposure approached that seen in the natural disease. Possibly more moderate doses for oral exposure may have similarly approached the natural spectrum of disease intensities.