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This article was published in 1987
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Clinical Items
P.S. Green, Veterinary Inspector, Dubbo
Epiphysiolysis Capitis Femoris
In July 1986 I investigated a case of lameness in pigs. In a group of 50 Large White - Berkshire cross pigs, four months old, some ten pigs had become lame over a period of four weeks.
At first the pig would limp on one hind leg; as the condition progressed it would then 'carry' that leg. In time the other hind leg became lame and the pig would lie on its side unable to rise. It was still interested in eating and drinking but being almost immobile could not compete with the other pigs.
I had seen a somewhat similar lameness in pigs where there was a gross deficiency of Calcium. In such cases the bones are fragile and easily broken. On checking the diet it seemed to be more than adequate; in fact the protein level was 20%. This high level of protein was being fed to get faster growth of leaner pigs. Previously the pigs had been too fat with a slower growth rate. The lameness only became apparent several weeks after the new ration was fed.
I carried out a post-mortem examination on several pigs with varying degrees of lameness. In all cases the head of the femur was detached at the epiphysis. In the more advanced cases both femurs were involved. One pig had a dirty grey fluid surrounding the detached bone but the remainder showed no apparent tissue reaction. The bones in general appeared to be strong.
Specimens were submitted to Orange Regional Laboratory. The Serum Calcium level was 3.0 mmol/L (normal range). Bone density was normal.
The condition fitted the description of Epiphysiolysis Capitis Femoris as given in Proceedings No. 56 of the Post Graduate Committee in Veterinary Science where it is described as essentially a problem of lean fast growing pigs with 'good' management. Overcrowding and slippery floors may precipitate the problem.
In this case the pigs had a pen with the rear portion covered and with a level floor. The front of the pen was uncovered and the concrete floor had quite a steep slope. When this became wet from rain or when hosed it became slippery.
The owner was advised to cut the protein level in the feed to a more conventional level. It was considered preferable to have sound pigs which may grow slower than have faster growing pigs that could not be sold. When the protein level was reduced there were no new cases of lameness.
The pathogenesis of the disease is uncertain but there is some evidence to suggest that there may be an inherited predisposition towards it. On discussing the case with Phil Mort, the local Piggery Officer, he recalled another case which occurred at Wollongbar Research Station in 1973 or 1974. Apparently some gilts were being performance tested when a similar kind of lameness occurred. On investigation it was found that all the lame gilts were sired by one boar. This boar and his female progeny were disposed of over a period and no further cases were experienced even though they continued to feed at a high level.
Some months after investigating this case I did a P.M. on a mature Berkshire sow which had extreme hind limb lameness. She had the heads of both femurs detached. It transpired that the mother of the sow had been purchased in Wellington from the man who owned the other lame pigs. It could of course be just a coincidence but in over thirty years I have only seen this disease on two properties and the pigs were all from the same source.
A SHOCKING MORTALITY IN PIGS
On a cold dark August night, a Saturday, I was called to investigate a mortality in pigs. In a farrowing shed there were twenty Large White Sows with litters from two to six weeks old. The sows were in individual stalls and there was a central aisle between the stalls.
At 1 p.m. that day the owner had fed the pigs and everything was apparently normal. On checking the shed at 5 p.m. he found two sows loose in the aisle; a further sow was caught between the bars of her pen and was assumed to have strangled herself. Further checking revealed another seven sows and twenty four suckers were dead. There were some fifty suckers alive and well. All these pigs had come from one side of the shed. All sows and suckers on the other side of the shed were normal.
The owner had employed 'wide comb' shearers to shear his sheep and foul play was suspected.
As there were no lights in the shed an extension lead and light was brought from a power point in an adjoining shed. Questioning revealed that all pigs in the shed received feed from the same bin and the water supply was the same for all animals.
All dead pigs showed a purple discolouration of the belly and on P.M. the only abnormality noted was excess fluid in the pericardial sac as well as in the thoracic and abdominal cavities plus a mild reddening of the stomach and small intestines. The sow which had died between the bars of her crate showed marked congestion of all organs with pronounced reddening of the stomach mucosa; the small intestines were almost haemorrhagic.
At this stage I too suspected foul play - the dead pigs were on the side of the shed closer to a road. A range of specimens was taken to submit to the Laboratory.
In passing I mentioned an interesting case where an owner had his pigs electrocuted. Even then the 'penny didn't drop'. I can perhaps blame the late hour and the fact that our light came from a power point in another shed.
Early on Sunday morning the owner phoned to say he had given some thought to what I had said. He had gone to the shed and found where two wires had 'shorted' and burned through on the row of stalls where the deaths had occurred. Whilst there were no lights in the shed there was power to provide warmth through bulb heaters for the suckers. Apparently one bulb had become loose and formed a short circuit. I don't know if there were any fuses but the owner has since had a circuit breaker installed.
Out of curiosity I forwarded the specimens to the Laboratory. There was no visible or significant growth on culture of the chilled specimens. On Histopathology there was congestion only in the brain, liver, renal medulla and lung with no other significant changes.
I assume that when the iron rails of the pens became electrified two sows had jumped clear and one became caught in the rails; the suckers which survived had apparently had no contact with the rails. I would have thought that white shedded pigs would have shown some evidence of burning but this was not apparent.
A SCROTUM WITH A RAM ATTACHED.
In November 1983 an owner reported that he had several Merino rams with grossly enlarged scrotums.
There were 70 Merino rams in the mob ranging in age from 16 months to 6 years - they were carrying nine months wool. The rams were running on black soil country with no grass seed problem - there were some scattered Saffron Thistles and abundant Trefoil burrs.
Over a period of four weeks the owner noticed some 20 rams with enlarged scrotums - one scrotum measured 57 cms (23 inches) in diameter. There were very few lesions on the scrotal skin apart from abraded areas on the ventral end - presumably these were caused by dragging in the dirt.
Rams which had recovered, shed their wool from being fevered; the testes were reduced in size and the skin on the scrotum was wrinkled.
As I had never previously seen a similar condition, a typical ram was sent to Orange Regional Veterinary Laboratory for examination. The post-mortem was conducted by the Officer In Charge who reported as follows: 'The scrotum was enormous, hot and had lost all of its wool cover. Dissections showed that the tunica vaginalis on both sides was filled with proteinaceous inflammatory exudate which coagulated on exposure.
The resultant pressure had pushed both testicles up the spermatic cord into the inguinal canal. It appeared that the testicles thus acted as a 'cork' and prevented spread of the infection into the abdominal cavity. The testicles were small in size and soft in texture but otherwise normal. There was no evidence of any epididymal changes.
Cultures of fibrinous material gave a heavy growth of Corynebacterium pyogenes'.
Corynebacterium pyogenes has been described as ubiquitous and widely distributed in healthy cattle, pigs and sheep. It may initiate infection, although more commonly found as a secondary invader superimposed on infection with viruses or other bacteria and generally complicating the clinical and pathological picture.
No portal of entry could be found for the infection but the Saffron Thistles may have played a part.
I did not follow up the fate of the rams but no doubt they would have been infertile for several weeks due to fever and pressure atrophy of the testicles.