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INSTITUTE OF INSPECTORS OF STOCK OF N.S.W. YEAR BOOK.
Toxoplasmosis in Australia
J. F. Sainty, B.V.Sc., Veterinary Inspector, Mudgee
An attempt is made here to review the position of Toxoplasmosis in Australia; with particular reference to sheep. Little is known about this disease and there are many interesting facets of its processes that possibly can be discovered and reported upon by all of us.
Toxoplasma is a protozoan which multiplies only within living cells. It is a small crescentic or spheroid organism which divides by binary fission. Schizogony has been described, but most authors do not believe this stage is true schizogony and prefer to use the term "pseudocyst": which is in actual fact a resting phase in which the parasites assume a different form within a cyst which has a well developed membrane around it. Toxoplasms are found extracellularly, as well as in most types of parenchymal cells, including heart muscle and nerve cells.
The organism was described first when its occurrence in the Gondi (a North African Rodent) was reported by Nicolle and Manceaux (1908); and in the rabbit in Brazil by Splendor (1908). Since that time naturally occurring Toxoplasmosis has been reported in many species of birds, rodents and larger animals. Several species of Toxoplasma have been described, but most authors are of the opinion that in animals there is probably only one species with some strain variants. In addition to these, there have been reports of diseases caused by Toxoplasma-like organisms in the owl, canary, penguin and some species of sparrows. These organisms, although morphologically similar in some respects to mammalian Toxoplasma, apparently are not infective for mammals.
The exact mode of natural infection is not known. Tick transmission has been suspected, although not substantiated. The disease has resulted from ingestion of an infected carcass and there is evidence to indicate that this is an important mode of infection. The only proven method is that of congenital transmission and this method has been demonstrated in humans, cattle, pigs and dogs in the United States of America and in sheep in New Zealand.
Experimental animals are infected readily by intraperitoneal or intravenous inoculations. The subcutaneous route is less likely to cause infection; and when takes do occur the course is slower.
In a preliminary survey of animal hosts in Queensland, Cook and Pope (1959) found that of 140 bandicoots collected from various regions, 27% were positive to a complement fixation test; of 25 water rats, 91% were positive; and of 268 (black, brown, field and climbing) rats, 7% were positive.
Of 29 cats, 30 dogs, 41 horses, 40 goats, 157 sheep, 109 cattle and 22 pigs, antibodies were detected only in two dogs and one horse from Southern Queensland, and in one cow from Northern Queensland. In this Queensland survey an interesting observation by the authors was that there was no evidence of infection in the 239 animals from places with a rainfall of less than 25 inches: which tends to support the suggestion that Toxoplasmosis is more prevalent in moist, warm areas than in hot or cold, dry areas.
Usually Toxoplasmosis has been diagnosed postmortem: death having occurred after an acute illness lasting a few days or weeks. There is also evidence to suggest that there is a chronic or carrier state in animals and man. In man, neutralising antibodies have been demonstrated in the sera of mothers of infants suffering from Toxoplasmic Hydrocephalus and Encephalitis. The mothers have shown no symptoms of the disease, except in some cases a slight rash on the skin.
Hydrocephalus and encephalitis in infants and encephalomyelitis in older children, and an acute exanthematous disease with a typical pneumonia in adults, are the three syndromes recognised in man.
In Australia the condition has been recorded as occurring naturally in sheep, dogs, once in a cat, once in a native cat, in two colonies of rabbits maintained for scientific purposes, and a marsupial water rat; as well as the Toxoplasma-like organism mentioned previously which has been found in Sydney sparrows.
In the rabbit colonies, young rabbits, one to two months old, were mostly affected. The disease was manifested by rapid emaciation and death within a couple of weeks of the first sign of illness. The kidneys were moderately swollen and showed irregular blotching: with ill-defined paler areas visible in the cortex after stripping the capsule. The urine was commonly cloudy and on centrifugation numerous crescentic, oval or comma-shaped parasites could be demonstrated in the deposit. Toxoplasms were found frequently in clusters in the epithelial cells, particularly of the tubules of the medulla.
In the case recorded by Wickham and Carne (1950) of the disease in the domestic cat, the ante-mortem symptom was paralysis. On post-mortem there was a slight congestion of all the visceral organs and pneumonia. Toxoplasms were found in the brain and the spinal cord.
The first two cases in dogs involved eight-month-old litter mates. They had suffered from persistent diarrhoea for several weeks and had become emaciated before death. In the first, the lungs showed a few shot-like nodules and the liver severe fatty degeneration with some isolated foci of necrosis. The parasites were found in the lung lesions, the liver and the bile duct epithelium. The second dog showed emaciation, congestion of the mucosa of the colon and rectum, which contained blood stained, watery mucoid faeces. Toxoplasms were found in the liver and bile ducts and in the epithelial mucosa of the rectum.
The third case was in a young dog in good condition. All lymph nodes were congested, the liver pale and more pliable than normal and the lungs were oedematous.
The fourth dog died suddenly and on post-mortem showed bilateral, even consolidation of the lungs with white focal lesions 2-3 mm. in diameter scattered throughout. The parasites were demonstrated in the lung tissue and in the brain of a mouse injected intraperitoneally with material from the dog's lung.
Generally the symptoms recorded as common to most cases in the dog have been emaciation, dyspnoea and diarrhoea.
In adult sheep the principal symptoms have been those of acute encephalitis. Olarson and Monlux (1942) record the occurrence of nervous symptoms, characterised mainly by muscle rigidity and a semi-flexed position of the legs; as well as noting a marked dyspnoea with some nasal discharge.
Wickham and Carne (1950) report a case in Australian sheep in which the condition suspected was "Circling Disease". Sections of brain showed congestion and perivascular cuffing, and the presence of Toxoplasma in pseudocysts.
The strain or strains of Toxoplasma occurring in Australia do not appear to be as virulent as those in America, as in Australia the disease has been recorded only the once in adult sheep; the limited Queensland survey showed a low incidence in the domestic animals tested. Whereas in America, Cole et al. (1954) inoculated a strain of Toxoplasma into ten pregnant ewes, a systemic reaction was produced in the ewes with respiratory distress. Two ewes died, two aborted. two had still lambs and two lambed normally. Toxoplasma were recovered at birth or autopsy from all lambs born from infected ewes and some lambs showed focal necrosis and microglian nodules; with pseudocysts in sections of spinal cord and cerebrum. New Zealand workers, also, have recorded Toxoplasmosis as a cause of perinatal mortality in the sheep and research there indicates that Toxoplasmosis is the most widespread and probably the most important cause of infective ovine perinatal mortality in that country.
Osborne (1959) described two outbreaks of abortion in ewes associated with Toxoplasma in the New England District of New South Wales; one in Merino stud ewes and the other in Merino/Border Leicester cross ewes pregnant for the first time.
The abortions in both outbreaks occurred in the fourth month. The foetal membrane showed lesions similar to those in New Zealand. These lesions were associated with the cotyledons, which were slightly larger and firmer in consistency than normal, and tended to be convex, bright to dark red in colour, with numerous greyish white flecks or small soft greyish-white nodules 1 to 3 mm. in diameter amongst the soft "pile" that is in such close contact with the cotyledons in the uterus. These scattered greyish-white areas give the cotyledons a mottled appearance. In some cases there was slight oedema affecting the placenta, but not as extensive as that seen in Brucellosis.
In the foetuses found, no significant lesions were seen; but in New Zealand in comprehensive histological examinations of lambs from both field and experimental cases the abnormalities so far detected have been in the brain, lungs and heart. These abnormalities consisted mainly of Toxoplasma pseudocysts and microglial nodules, some of which showed central caseous necrosis.
A positive diagnosis of Toxoplasmosis depends on complement fixation tests, as well as the culture of the parasites in mice; although the latter of itself is strong evidence for such a diagnosis.
On the other hand, there appears to be a typical change associated with the foetal cotyledons seen in histological sections. Similarly changes have been seen in Australia, New Zealand and United States of America. With increased knowledge this change, and possibly others, may be found to be pathognomonic for the disease.
It would appear that bandicoots are important hosts of Toxoplasma in Queensland, and possibly in the other areas where bandicoots exist. Evidence from Queensland also tends to support overseas thought that the disease is more common in moist, warm areas than in hot or cold, dry regions.
Toxoplasmosis is widespread in New Zealand and could possibly be an important cause of perinatal and neonatal loss, particularly in the coastal and tablelands areas, in Australia.
REFERENCE:
- Beverley, J. K. A. (1957) — Vet. Rec., 69: 337
- Cook, I. and Pope, J. H. (1959) — Aust. J. exp. Biol., 37: 253
- Hartley, W. J. and Marshall S. C. (1957) — N.Z. vet. J., 5: 119
- Olafson, P. and Monlux, W. S. (1942) — Cornell Vet., 32: 176
- Osborne, H. G. (1959) — Aust. vet. J., 35: 424
- Pope, J. H., Bicks, V. A., and Cook, I. (1957) — Aust., J. exp. Biol., 35: 48
- Thompson, S. W. and Reid, T. H. (1957) — J. Am. Vet. Med. Ass., 131: 545
- Wickham, Nancy and Carne, H. R. (1950) — Aust. vet. J., 26: 1