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This report catalogues all spontaneous proliferations in macropods, koalas, wombats, and possums and gliders held by the Comparative Pathology Registry at Taronga Zoo. Proliferative lesions were present in 14 macropods, 26 koalas, two wombats and 22 possums and gliders. Most neoplasms recorded in macropods were singular and many were found incidentally. Lymphoid neoplasia, cranio-facial tumours and apparent mesotheliomas were common in koalas. Hyperplastic or benign neoplastic masses in adrenals and livers were common in possums. In addition, previously misdiagnosed splenic haematopoietic hyperplasia was common in these animals. Mammary proliferations were present in macropods and gliders. No obvious aetiological factors have been identified in any of the tumour conditions, although there is some evidence to suggest a viral involvement in lymphosarcoma in koalas.

Perinatal lamb mortality, associated with malformations of the CNS due to Akabane viral infection, occurred in 4 of 9 flocks of ewes lambing on 3 farms between 26 May and 14 November, 1976. Cases were restricted to ewes conceiving prior to the second week of March and lambing between 26 May and 19 July. As judged by seroconversion in sentinel flocks on 2 of the farms, field infection with Akabane virus occurred mainly between mid-February and mid-April. Malformations of the CNS occurred in 42.5%, 51.2%, 100% and 31.0% of the dead lambs examined in the affected flocks respectively. Prevalence in the 4 affected flocks, expressed as the proportion of ewes lambing which delivered at least one malformed foetus, was 6.1%, 8.4%, 88.9% and 5.7% respectively. Lamb mortality due to malformations of the CNS was 7.1%, 5.5%, 92.3% and 5.7% of lambs born. Age-specific prevalence was calculated for 3 of the 4 flocks and 2-year-old ewes accounted for 71.4% and 76.9% of total cases respectively in 2 flocks, whereas in one flock malformations occurred at equivalent frequencies throughout several older age groups. Birthweights of affected lambs were usually significantly lighter than those of unaffected lambs of similar sex and birth-type, and their mean duration of gestation was slightly, and significantly, prolonged. Micrencephaly (88.1% of cases) and hydrocephalus (68.7% of cases) were the outstanding pathological features of the malformations with hydranencephaly, microgyria, porencephaly and attenuation of the spinal cord occurring at much lower frequencies.(ABSTRACT TRUNCATED AT 250 WORDS)

Calves, lambs, and kittens given milk from cows fed locoweeds developed microscopic lesions typical of locoweed poisoning. Serum aspartate aminotransferase activities increased markedly during the feeding period in both the cows given the locoweed and the animals receiving their milk. The results of this experiment indicate that the toxin in locoweed can be secreted in the milk.

Certain plants accumulate selenium at levels that render them toxic. One of the principle groups of selenium-accumulating plants is the selenium-accumulating Astragalus. Reports in early literature suggest that selenium is the only toxin in these plants. Sheep fed Astragalus bisulcatus, a selenium-accumulating plant, had signs similar to those observed in locoweed poisoning, and the microscopic lesions from tissues collected from these sheep were similar to those of locoweed poisoning rather than selenium poisoning. This suggests this group of plants contains toxin compounds in addition to selenium.

Pollens collected from Astragalus lentiginosus and Oxytropis sericea were fed to mice. At the end of the feeding period, uterine weights were taken to determine estrogenic activity, and tissue was collected for microscopic examination. The pollen from A lentiginosus, but not from O sericea, induced lesions similar to those of locoweed poisoning. The pollen from neither plant was estrogenic. Seeds from A lentiginosus produced toxicosis when fed to rats.

Locoweed (Astragalus lentiginosus) fed to mature rams induced transient degenerative changes in the seminiferous, epididymal and vas deferens epithelium. There were changes in behavior and loss of condition in the treatment rams. Observed libido was reduced. Estimated percent abnormal sperm was significantly (P less than 0.05) higher in the locoweed-fed rams than in the controls. Increased retained proximal cytoplasmic droplets, separation of the heads and tails of the spermatozoa, and reduced sperm motility were observed. Serum SGOT (serum glutamic oxaloacetic transaminase) levels were significantly (P less than 0.01) elevated, and WBC (white blood cell) counts were decreased (P less than 0.01). Grossly no changes were observed. Histologically there were advanced lesions of foamy cytoplasmic vacuolation in all tissues taken at necropsy, but particularly in the epithelium of the seminiferous tubules, epididymis and vas deferens. Reduced spermatozoa production was evident. Testicular changes were transient and rams appeared clinically normal 70 days after locoweed feeding was terminated; however, there was slight residual atrophy of the germinal epithelium at necropsy.

Locoweed (Oxytropis sericea), when fed to calves at high elevations, increased the prevalence and severity of congestive heart failure. Forced exercise did not increase the prevalence of congestive heart failure, but it did increase severity. Calves consuming locoweed at high elevations developed signs and gross lesions of congestive heart failure and microscopic lesions of congestive heart failure and locoweed poisoning. Calves fed locoweed at low elevations developed only signs and lesions of locoweed poisoning.

Locoweed (Astragalus lentiginosus) was fed to ewes from 70 to 100 days of pregnancy. Ewes were killed at 100, 115, 130, and 145 days, and selected tissues were collected from both the dam and the fetus for histologic examination. Neurovisceral cytoplasmic vacuolation and neuroaxonal dystrophy decreased in dam and fetus with time after the feeding of locoweed was discontinued.

Two outbreaks of an encephalitis apparently induced by an attenuated live distemper vaccine occurred in a large ferret breeding establishment in New Zealand. Approximately 350 of 6,000 young ferrets 16-22 weeks old died. Many were found dead with no premonitory signs, others showed severe neurological signs. Some with central nervous system (C.N.S.) signs recovered. Pathological examination showed no gross abnormalities except for a few with mild conjunctivitis, rhinitis and lung emphysema. Microscopically there was a moderate to massive non-inflammatory necrosis of hippocampal nerve cell bodies. In those animals which survived for several days with CNS signs there was also a mild to moderately severe non-supportive encephalitis, and in some of these distinct neuronal intranuclear and intracytoplasmic eosinophilic inclusion bodies were seen. Some ferrets also had a bronchiolitis with intracytoplasmic eosinophilic inclusion bodies in bronchiolar epithelium. All these lesions suggest that a distemper like condition was involved. About half of the ferrets also had a mild to severe inflammatory myocardial necrosis.

Ten Devon cattle from a single property were affected with blindness from 14 months of age. Severe retinal degeneration progressing to atrophy was associated with widespread intracellular accumulation of pigment in the retinal ganglion cells, central nervous system and major organs. The pigment was consistent with ceroid-lipofuscin granules on histological, histochemical and ultrastructural examination. Although a familial relationship existed between affected individuals, a pattern of inheritance could not be established by examination of available breeding records. The disease is compared to similar disorders reported in man and other species.

Three groups of 5 pigs each were fed a high selenium (Se) diet by mixing either Astragalus praelongus (31.6 ppm Se in feed), A bisulcatus (31.7 ppm Se in feed), or sodium selenate (26.6 ppm Se in feed) with commercial hog feed. Ten control pigs were fed only commercial hog chow containing trace selenium (0.44 ppm Se). Pigs were fed for 9 weeks and necropsied when they had ataxia or paralysis. Blood was collected for hematologic and serum biochemical determinations, and samples of various tissues were collected and fixed in neutral-buffered 10% formalin for histologic evaluation or frozen for determination of selenium concentration. All forms of selenium induced clinical signs of weight and hair loss, with cracked hooves and inflamed coronary bands developing in all Na2SeO4-fed pigs and 1 A praelongus-fed pig, but not in A bisulcatus-fed pigs. Serum calcium, phosphorus, and albumin concentrations were unchanged or significantly decreased from prefeeding values in groups fed selenium. Serum aspartate transaminase (AST) activities in Astragalus species-fed groups, and amylase activities and PCV in all groups of pigs fed selenium, were increased. Serum alkaline phosphatase and creatine kinase activities were significantly increased in the A praelongus-fed pigs and significantly decreased in Na2SeO4-fed pigs. Terminal tissue and body fluid selenium concentrations were determined in all groups of pigs fed selenium and compared with values in control pigs. Urine and bile concentrations were increased by the greatest factor (40 to 100x), with tissue concentrations of selenium increased by a lesser factor (6 to 17x).(ABSTRACT TRUNCATED AT 250 WORDS)

Twenty-nine cases of EHV1 infection occurred on a property, mainly in full term foals. Some foals were stillborn, some were born alive but weak and soon died and others were healthy at birth, became ill and died within 3 days of birth. Apart from voluminous, oedematous and atelectic lungs there were no gross lesions. Microscopically the lungs showed oedema, pneumonitis and bronchiolitis with intranuclear inclusions and, in many of the foals that survived over 6 hours, there was also hyaline membrane formation. Microscopic lesions were also seen in the liver, adrenal, thymus and spleen of some of these foals.

Various species of nitro-containing Astragalus, and the toxic principle of these plants, 3-nitropropionic acid or 3-nitro-1-propanol, were fed to sheep and cattle at doses which produced chronic or acute intoxication. The signs of intoxication produced were similar to those observed in poisoning that occurs under field conditions. The signs of intoxication were emphysema and difficulty in locomotion. Primary microscopic lesions were observed in the lungs and CNS. The lungs had varying degrees of alveolar emphysema and there were varying degrees of wallerian degeneration of the spinal cord.

Six new species of Klossiella are described in the kidneys of Australian marsupials: Klossiella rufogrisei in Bennett's Wallaby, Macropus rufogriseus; Klossiella rufi in the Red Kangaroo, Macropus rufus; Klossiella thylogale in the Red-Bellied or Tasmanian Pademelon, Thylogale billardierii; Klossiella beveridgei in the Spectacled Hare-Wallaby, Lagorchestes conspicillatus; Klossiella bettongiae in the Tasmanian Bettong, Bettongia gaimardi; and Klossiella schoinobatis in the petaurid Greater Glider, Petauroides volans. It is concluded that the genus Klossiella has radiated widely among Australian marsupials, and that since it is present in American marsupials, it may have an ancient association with the subclass.