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This article was published in 1974
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Encephalomyocarditis Virus in Pigs
by R.I. Walker, B.V.Sc., M.R.C.V.Sc.
Encephalomyocarditis (EMC) virus is a rodent enterovirus, able to infect hosts of many other species, however only in pigs have serious outbreaks been reported. It can cause disease in humans where a polio-like condition is reported and although no deaths have been recorded it is a disease which should be regarded carefully, for those people handling specimens. In rodents, encephalitis and myocarditis occur, in horses an ascending spinalitis has been reported and in cattle and pigs, lesions have been confined to the myocardium, with some evidence of brain changes. The virus can be recovered from heart, brain, spleen, lungs and faeces of pigs and it has been recovered from heart or spleen of cattle, racoons, baboons and chimpanzees.
In America neutralising antibodies to EMC are widespread and it is thought that the disease is very old, although it is has not been commonly diagnosed. (1)
In Australia the EMC virus has been isolated from a water rat in 1959 (2); Rattus rattus on numerous occasions and EMC virus antibody has been detected in pig serums from a survey in Queensland (3). Several isolations are recorded in mosquitos (4), so it would appear to have been in Australia for some time prior to the outbreaks in 1970.
The diagnosis of the disease depends on virus isolation, most easily accomplished in mice or on detection of antibody by neutralisation or haemagglutination inhibition tests.
Mortalities in swine can be very high, in some cases approaching 100%. 214 out of 452 head in 15 piggeries died over a period of 6 years (1); another report states that 30 out of 300 pigs on a feedlot died suddenly (5).
In Australia numerous reports have been received since 1970 with a variation in mortality rates. During the 1970 outbreak in the Cowra district (8), it would appear that the mice and rats first became apparent in Late Spring 1969 and had reached plague proportions by March of 1970 and continued until the cold weather of July, August. Reports of dead mice, where no rodent poison had been employed and sick mice that were seen shivering, huddled up and unwilling to move when approached, were received when plague proportions were evident.
Deaths in pigs were reported from one property early in April 1970 and by May, four other properties within the Cowra district were reported.
It is interesting to note that the mortalities were observed on properties that would not have been less than 10-12 miles apart and also the mortalities ceased when the rats and mice suddenly disappeared.
In several instances, post-mortems revealed parts of mice ingested within the stomachs of dead pigs. Further investigation revealed the presence of rodent excreta in feed stores and in troughs used for feeding pigs, so the transmission of the virus from rodents to pigs is without question. EMC virus was also recovered from healthy and sick mice from the Cowra area (22). The virus from the water race (sic) in Queensland had earlier been found to be extremely pathogenic for pigs. Intracerebral inoculation into pigs produced death with massive myocardial involvement within a few days in experimental pigs.
On one property in Cowra mortalities in piglets from (7) 7-12 weeks were recorded as being 44-78%, while in a group of 2 pens each with a sow and 8x 14 day old piglets, 100% mortality was recorded.
At least eight properties in and around Cowra and Young experienced mortalities during 1970 with EMC in pigs, generally in the order of 40-50% in the age group 10-20 weeks.
In the Northern areas of New South Wales there appears to be some difference in that the disease may not be as severe. Reports from abattoirs in the areas seem to indicate that heart lesions are observed reasonably frequently in pigs at slaughter. Glastonbury (6) feels that EMC is an important cause of neonatal mortality in piglets and lists it as a precipitating cause having an incidence of 1.9% of 157 piglets autopsied.
Abattoir reports from Blayney indicated that a small number of pigs carcases containing myocardial lesions were received at the abattoirs (8) indicating that a number of healthy pigs, containing lesions in the heart, apparently showed some resistance to the virus.
Other reports during 1970 indicated that mortalities were observed in the Parkes and Peak Hill districts.
Recently DVO Narrabri reported Losses in pigs 12 weeks and upwards on a property at Gravesend (Warialda P.P.B.) (Sept. '73).
Clinically: The most striking feature clinically is the fact that death is very rapid; possibly within 4 hours, in pigs that are for all intents and purposes healthy and doing well.
On one property in Cowra piglets 10-12 weeks old were observed to eat normally and be found dead prior to the next feeding. In any group of piglets it seems impossible to nominate, by clinical appearance, which pigs will die. On one occasion a pig (12-14 weeks old) died while being taken out of a pen for examination after a degree of difficulty in catching the said pig.
Post-Mortem Findings: Hydrothorax, Hydropericardium and Ascites with varying amounts of fibrinous material are almost always observed. Strands of fibrin are usually observed in the folds of the intestine, and fibrin tags can mostly be found adhering to the liver. Some degree of fibrinous pleurisy may be observed, and lungs may or may not be congested, or inflamed. Fibrinous pericarditis can usually be seen with a variation from an excess of fluid containing a fibrin clot to a very strong fibrinous attachment of the pericardial sac to the epicardium. Kidneys may show congestion.
The most obvious lesions are those of a myocarditis. Areas of pale white to yellow necrosis 1-2mm wide by 4-8mm long either as discrete or diffuse lesions. These are usually found over the ventricles and vary in number from one to many or as a diffuse paleness of the heart muscle and extending to the myocardium. They are not always present. Histologically, the myocardial lesions were focal areas of necrosis, degenerating muscle fibres, interstitial accumulations of mononuclear cells and interstitial oedema.
In the brain, mild changes are seen, from areas of demyelination and perivascular cuffing, to localised non-purulent meningoencephalitis.
Both Nancy Wickham and Glenfield observed Toxoplasma cysts in the brain and possibly the heart, unassociated with any lesions, but one wonders on their significance in the light of Spradbrow's comments (10) that not all the variability in the host can be attributed to the virus. In rats, concurrent trichinosis has a synergistic effect and further in mice during pregnancy EMC virus grows to a higher level in heart muscle in pregnant mice than in non-pregnant mice, and myocarditis accounts for the high mortality in pregnant mice. Possibly environmental factors would be important in porcine populations at risk to EMC virus.
Where the rodent population is basically endemic, such as on the north coast and presumably where the EMC virus is endemic within the rodent population, some degree of resistance could well be seen in the pig population and this may account for the variation in severity of the disease in such areas.
None of those eight properties in the Cowra and Young district which suffered both the rodent plague and EMC virus in pigs, have had any known or suspected cases since 1970. I have seen only one piglet presented this year (1973) that appeared to have died as a result of E.M.C. This was from a piggery which does have a continual rodent problem.
E.M.C. then is a disease which will probably remain in the rodent population and as a disease entity in pigs, will be observed when susceptible pigs are exposed to large numbers of rats and mice.
On the basis of the work done by Glastonbury, it would be noteworthy to suspect EMC as a significant entity in any differential diagnosis of neonatal mortalities.
Encephalomyocarditis is a disease in pigs in Australia, while only recently recognised, has been present for some time and will continue to be seen sporadically unless a rodent plague is again observed, when outbreak proportions in pigs could again be reached.
References
(1) Gainer, J.H. (1967) J.A.V.M.A. 151 (4): 421-425
(2) Pope, J.H. (1959) Aust.J. exp. Biol. 37:117
(3) Spradbrow, P.B. (1968) A.V.J. 44,320
(4) Dickinson, L. & Griffiths, A.J. (1966) Brit. J. exp. Path 47: 35
(5) Murnane et al. (1960) Science 131:498
(6) Glastonbury, J.R.W.(1973) Proc. of Course for Veterinarians. Post. Grad.Committee in Vet.Sc., No. 20: p 237,
242(a)
(7) Ackland, H.M., Littlejohns, I.R & Walker, R.I. (1970) A.V.J. 46:348
(8) Departmental Report (1970) B.P. Healy - Orange
(9) Departmental Report (1973) DVO Narrabri
(10) Spradbrow, P.B. (1972) Proc. of Course for Veterinarians. Post Grad.Committee in Vet.Sc., No. 16:35
(11) Veterinary Notes (1972) Vol.7. No. 1.