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This article was published in 1969-70
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Some Locomotor Disorders of Pigs in Australia

R. H. C. PENNY, B.V.Sc., Ph.D., F.R.C.V.S., University of Sydney, Camden

INTRODUCTION

There are many conditions affecting the locomotor system of the pig and their differential diagnosis is often difficult. The main reasons for this are the problems of handling and examining members of this species, the fact that many of the common causes of lameness in the pig produce similar changes in the gait, and our limited knowledge of some of the conditions involved.

Professor W. Schulze, head of the Section of Pig Medicine, Hanover University, once said, "It is no good discussing the diseases of the pig leaning over the back of a horse", and, as experience is gained with this species the wisdom of his statement becomes increasingly apparent.

There are no figures in the Australian literature relating to the incidence of lameness and paralysis except for a statement by Rose (1926) that lameness leading to paralysis is common in pigs in New South Wales. He suggested that in some areas paralysis was second only to pneumonia as a cause of loss to the industry.

In the United Kingdom, we have some figures to show that lameness and paralysis is an important cause of wastage in pigs. The results of the Pig Industry Development Authority (P.I.D.A. now M.A.L.C.O.M.) Sow Wastage Survey conducted in 1962/1963 showed that about 33⅓ per cent of the sow herd in England and Wales is culled annually (Anon 1963). This is approximately 280,000 sows and gilts out of a population of 840,000. Lameness and paralysis, the fourth most common reason for culling in sows and the second in gilts, accounted for 10.8 per cent of the wastage which would amount to close on 30,250 sows and gilts a year. On individual farms the loss can be higher and I investigated one herd of 400 Sows where the culling rate for lameness had reached the staggering figure of 18 per cent. Other herds investigated showed a very high incidence of lameness in the breeding stock (Penny et al., 1963).

Figures for boars are not available but Melrose (1966) reported that locomotor upsets were the most common single reason for the disposal of boars from A.I. centres in the UK. Fifteen out of 69 boars were culled for this reason. The incidence of lameness in pigs of bacon or heavy-hog weight is unknown, but a slaughterhouse survey into the incidence of lesions on the feet of pigs of bacon-weight (Penny et al., 1963) revealed that about 65 per cent had lesions although admittedly some were very mild.

In this short paper I shall attempt to classify the causes of disease of the locomotor system of the pig. I have divided the subject matter under four main headings:

(1) Nervous System.

(2) Muscles and Tendons.

(3) Bones and Joints.

(4) The Feet.

A number of miscellaneous conditions are also described (5) to (8).

Quite obviously I cannot cover all aspects of the subject, and some of my examples and some of the slides I shall show may not necessarily be the most common or the most economically important condition within the group. I have attempted to remedy this deficiency by marking the conditions I think are the most common with an asterisk.

CLASSIFICATION

(1) Nervous System

Some 80 conditions are known to affect the C.N.S. in pigs and these include such conditions as:

Bacterial meningitis* (commonly Streptococcal)
Swine fever*
Aujeszky's disease
Glasser's disease*
Salt poisoning*
Bowel oedema*
Middle ear disease and cerebellar abscess*
Listeriosis
Arsenilic acid poisoning*
Deficiency of pantothenic acid.

The last-mentioned causes goose-stepping, but so may tarsitis, leg weakness and foot lameness associated with hyperkeratinisation of the heel.

Peripheral Nerves-ascending and descending degenerations occur and they are usually secondary to some other condition (i.e., Teschen/Talfan disease*).

(2) Muscles and Tendons

(a) Leg Weakness* — there are various views on the aetiology of this condition, and one must consider the possible presence of a number of interacting factors:

(i) The degree of congenital splayleg or myofibrillar hypoplasia (see 2b) present at birth.
(ii) The amount of exercise taken during growth.
(iii) The rate of growth.
(iv) The development of severe articular cartilage lesions, i.e. eburnation.
(v) Plate cartilage lesions.
(vi) Infection and hypersensitivity.
(vii) Nutritional and hereditary factors have not been completely absolved.

(i)-(iii) affect muscular strength and are probably reversible.
(iv) is irreversible when severe enough.
(b) Congenital Splayleg* — myofibrillar hypoplasia. Possibly both hereditary and managemental factors may play a part in this disease. Severe myofibrillar hypoplasia causes splayleg but there are all grades of the condition, the mild forms being symptomless. It is most common in the Landrace and Welsh breeds, the latter having a considerable proportion of Landrace blood.
(c) Iron Toxicity — in young piglets can produce reversible muscular damage, and a vitamin E deficiency in the sow may predispose to the condition. Under such circumstances even the dose recommended by the manufacturer may prove toxic.
(d) Myopathy in Older Pigs — some half dozen conditions are described in the literature but they are not frequently reported.
(e) Diseases involving Tendon — are thought to be extremely rare but perhaps more work should be performed in this field.

(3) Bones and Joints

(a) Arthritis* — There are a number of causes of arthritis and erysipelothrix infection may not be uncommon. In the U.K. there may have been a tendency in the past to over-emphasise the importance of erysipelas as a cause, but in Australia experience would suggest that erysipelas arthritis may be quite common. The figures for condemnation at slaughter tend to support this clinical opinion. Table 1 shows the published figures for the U.K. and some figures obtained from the Queensland Department of Primary Industries.

Table 1—A Comparison of Pig Carcass Condemnations

	All Causes		Arthritis
	%		%
	U.K.	Australia	U.K.	Australia
Total Condemnations	0.48	0.31-0.56*	0.2	0.18-0.51*
Partial Condemnations	1.59	0.94	0.45	0.57

* The figures obtained for one slaughterhouse only.

Provided the standards of meat inspection are comparable in the two countries then the figures indicate quite clearly that there is a higher incidence of condemnations for arthritis in Queensland.

At present there is some doubt about the mechanism producing the arthritic lesions. The lesions may be due to the direct action of the organisms (Shuman et al., 1965) but there is other evidence which suggests that some form of hypersensitivity to the organism may be involved (Freeman et al., 1964). Moreover, a higher incidence of arthritis has been reported in vaccinated than in non-vaccinated pigs (Neher et al., 1958). However, this evidence is as yet not sufficient to warrant discontinuing a vaccination programme, because vaccination undoubtedly reduces the loss from the per-acute and acute forms of the disease. In young pigs, joint-ill is seen and organisms such as mycoplasma, streptococci and E. coli may produce disease. Septic arthritis may be secondary to a chronic infectious process elsewhere in the body, not uncommonly the foot.

(b) Arthrosis* — various irregularities of a non-inflammatory nature occur in the articular cartilages, but they cause no trouble unless eburnation results. Muscular weakness and conformational abnormalities may be predisposing factors. The incidence could be as high as 40-50 per cent in bacon and heavy pigs.

(c) Synovial Fluid — Polyserositis with or without arthritis is very common in the pig. Examination of synovial fluid could be a useful diagnostic tool, and variations in its composition are a predisposing cause of cartilage damage.

(d) Plate Cartilage Lesions

(i) Epiphysiolysis — femoral head detachment.
(ii) Apophysiolysis - tuber ischii detachment.
(iii) Distal ulnar lesions.
Factors such as rapid growth, pressure, trauma and hormonal imbalance may predispose. Epiphysiolysis has some similarities to the condition of "slipped epiphysis" seen in the human male at puberty.

(e) Infections — conditions recognised are:

(i) Osteomyelitis* — secondary to tail biting. foot abscess or infection of the scrotum following castration. Organisms mainly F. necrophorus, C. pyogenes and streptococci. Principal sites last thoracic, first two lumbars and less frequently first two thoracics.
(ii) Spondylitis — possibly associated with erysipelas infection although some degree of spondylitis may not be unusual in long-backed pigs as a sort of supporting brace for the weakened spine.
(iii) Metaphyseal osteoporosis associated with swine fever.

(f) Rickets and osteomalacia — basically, enough ground substance is formed but this is poorly ossified.

Normal Low (sic)	Serum Ca Level	10 mg./100 ml.
Normal Low (sic)	Serum P Level	7 mg./100 mil.

Product of these is 70. When product <40, rickets results. These causes are:

(i) Vitamin D or phosphorus deficiency or unavailability.
(ii) An extreme deficiency or unavailability of Ca.
(iii) Phytic acid, iron and beryllium precipitate P and alkaline mediums reduce solubility and hence absorption. Rickets is very uncommon in the pig in the U.K. but I have no figures for Australia.

(g) Osteoporosis — two little ground substance adequately ossified. Blood serum-mineral values frequently normal, but alkaline phosphatase levels may be below normal. The causes are:

(i) Ca deficiency with adequate P and Vitamin D.
(ii) Possibly a protein deficiency.
(iii) Oxalates and possibly phytic acid, precipitate Ca and alkaline mediums reduce its solubility.
(iv) Deficiencies of Vitamins A and C, thiamine, Cu, Mn, and food generally, and also overboiled swill may reduce protien (sic)availability.
(v) Arsenilic acid poisoning and swine fever.

(h) Fractures and disc protrusions are seen in the pig.

(4) Feet*

Foot lesions are common in the pig and in the U.K. the incidence in pigs of bacon-weight might be around 65 per cent. They are also commonly seen in pigs in New Zealand and Australia. The common primary lesions of foot-rot in pigs are:
(a) Heel, sole and toe erosions.
(b) White-line lesions.
(c) False sand-cracks.
These can themselves cause lameness, but if perforation of the horny-hoof occurs, a "bush" may develop. The causes of the condition are:
(a) Trauma to the feet (from concrete floors particularly).
(b) Wet dirty conditions underfoot.
(c) Infection.
(d) Other predisposing factors may be irregularities in claw size, faulty conformation, new concrete and whey feeding.
Treatment is directed at:
(a) Reducing trauma by turning outdoors or providing ample bedding.
(b) Hardening the feet with 5-10 per cent solutions of formalin or copper sulphate. The latter would seem to be the most satisfactory.
(c) Antibiotics have proved of little benefit in my experience.
The condition can be prevented by the regular use of a copper sulphate footbath, but attention to floor surfaces and better hygiene are also worthwhile preventive measures. If carefully sited, pigs can readily be trained to use a footbath.

(5) Laminitis has been reported in pigs, mainly sows, but it is uncommon.

(6) Bursitis of the Hocks*

Bursitis of the hocks is common in pigs of all ages but rarely leads to lameness. A small adventitious bursa is present in a high proportion of pigs, at the back of the hock on a level with the lower row of tarsal bones in the lateral aspect of the leg. It is usually bilateral and the main causes are:
(a) Continued trauma.
(b) Lack of bedding.
Other bursae may be affected (i.e., hock, knee).

(7) Necrosis of the knees*

This is a common condition in young piglets particularly in intensive units. The causes are not fully understood although trauma with infection plays at least some part. The fetlocks and hocks may also be involved. (Nipple necrosis may be associated.) Suggested treatments are as follows:
(a) More bedding.
(b) Better hygiene.
(c) Less abrasive floor surfaces.
(d) Strips of plaster to protect joints.
(e) Outdoor rearing.

(8) Congenital abnormalities

These occasionally involve the skeleton and nervous system. There are many other conditions that could of course have been mentioned but in conclusion do not forget that Foot-and-Mouth disease occurs in pigs and can be introduced into a country through unboiled swill. It has not been seen in Australia since 1871 (Seddon, 1958) but we must always be on the alert.

REFERENCES

Introduction

Anon (1963) Sow Wastage Survey, P.I.D.A., London.
Melrose, D. R. (1966). Vet. Rec., 78, 159.
Rose, A. L. (1926). Aust. vet. J., 2, 98.
1. Nervous System

Done, J. T. (1957). Vet. Rec., 69, 1341.
Gordon, W. A. M. and Luke, D. (1955). Vet. Rec., 67, 591.
Harding. J. D. J., Done, J. T., and Kershaw, G. F. (1957). Vet. Rec., 69, 824.
Huck, R. A. (1962). J. Comp. Path., 72, 380.
O'Hara, P. J., and Shortridge, E. H. (1966). N.Z. vet. J., 14, 1.
O'Hara, PJ., and Shortridge, E. H. (1966). Ibid., 14, 13.

2. Muscles and Tendons

(a) Bullough, P. G., and Heard, T. W. (1967), Br. vet. J., 123, 305.

Cunningham, B. (1966). Irish vet. J., 20, 66.
Duthie, I. F. and Lancaster, M. C. (1964). Vet. Rec., 76, 263.
Walker, T.Fell, B. F., Jones, A. S., Boyne, R., and Elliott, M. (1966). Vet. Rec., 79, 472.

(b) Dobson, K. J. (1968). Aust. vet. J., 44, 26.
Thurley, D. C., Gilbert, F. R.. and Done, J. T. (1967). Vet. Rec., 80, 302.

(c) Arpi, T., and Tollerz, G. (1965). Acta Veterinaria Scandinavica, 6, 360.
Patterson, D. S. P. Allen, W. M., Thurley, D. C. and Done, J. T. (1967). Vet. Rec., 80, 333.

3. Bones and Joints

(a) Freeman, M.J., Segre, D., and Berman, D. T. 1964). American Journal of Veterinary Research, 25, 135.

Freeman, M. J. (1964). Ibid., 25, 599.
Grabell, I Hansen, H. J., Thal, E., and Wellmann, G. (1965). J. Comp. Path., 75, 275.
Grabell, I. Hansen, H. J., Olsson, S. E., Orstadius, K., and Thal, E. (1952). Acta Veterinaria Scandinavica, 3, 33.
Moore. R. W. Redmond, H. E. and Livingston, C. W. (1966). American Journal of Veterinary Research, 27, 1649.
Neher, G. M., Swenson, C. B., Doyle, L. P, and Sikes, D. (1958), Ibid., 19, 3.
Shuman, D., Wood, R. L. and Moniur, W. S. (1965). Cornell Vet., 55, 523.
Sutherland, A. K., and Simmons, G. C. (1947). Aust. vet. J., 23, 91.
Webster, D. J. (1966). O. agric. J., 92, 206.

King. S. J. (1968). Aust. vet. J., 44, 227.

(d) Sabec, D., Schilling, E., Schultz, L. C. (1961). Dtsch. tierarztl. Wschr., 68, 231.

See also: Muscles and Tendons.
(h) Vaughan, L. C. (1966). Vet. Rec., 79, 2.

4. Feet

Osborne, H. G., and Ensor, C. R. (1955). N.Z. vet. J., 3, 91.
Penny, R. H. C., Osborne, A. D. and Wright, A. I. (1963). Vet. Rec., 75, 1225.
Penny, R. H. C. Osborne, A. D., Wright, A. L. and Stephens, T.K. (1965). Ibid., 77, 1101.
Pugh, 0. L., and Penny, R. H.C. (1966). Vet. Rec., 79, 390.

5. Laminitis

Nilsson, S.A. (1964). Nordisk veterinærmedicin, 16, 128.
Maclean, C. W. (1968). Vet. Rec., 83, 3. 71-75.

6. Bursitis of the Hocks

Penny, R. H C. Osborne, A. D., and Wright, A. I. (1963). Vet. Rec., 75, 1225.

7. Necrosis of the knees

Penny, R. H. C., Osborne, A. D., and Wright, A. I. (1963). Vet. Rec., 75, 1225.