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This paper records a unique ovine encephalomyelopathy seen on several farms in the Otago Region of New Zealand. It occurred in 2-3 month-old Romney lambs as a rapidly progressive posterior paresis leading to flaccid paralysis. Pathologically, it was characterised by severe spongy vacuolation of white matter in both brain and spinal cord. It is suspected that the condition is inherited.

Fatal encephalomyocarditis virus (EMCV) infections in a ring-tailed lemur (Lemur catta), a squirrel monkey (Saimiri sciureus), three mandrills (Mandrillus sphinx), a chimpanzee (Pan troglodytes), a pygmy hippopotamus (Choeropsis liberiensis), and two Goodfellows tree kangaroos (Dendrolagus goodfellowi) occurred at Taronga Zoo. This is the first description of EMCV in a zoological collection outside of the United States. Regardless of species, the most common clinical presentation was sudden death. The gross pathologic changes were diffuse or focal pallor of the myocardium with occasional marked pulmonary congestion. Necrotizing nonsuppurative myocarditis was consistently present. EMCV was isolated from only one of 54 feral rodents examined. No antibodies to EMCV were detected with a serum neutralization test in 79 stored sera from a wide variety of zoo mammals. Titers of 1:16, 1:16, and 1:4 were recorded for a spider monkey (Aeteles geoffroyi), a lion (Panthera leo), and an orangutan (Pongo pygmaeus), respectively. Of seven mandrills tested in 1988, six had measurable virus titers. Later testing indicated that these titers did not persist, and one mandrill with a titer > 1:128 in 1988 subsequently succumbed to EMCV infection in 1991.

Selenium is an essential micronutrient, although ingestion in excess in pigs can cause disease conditions including neurological dysfunction and chronic skin and hoof lesions. Controlled feeding trials in growing swine, using the same Se content in feed sources, resulted in higher concentrations (p < or = 0.05) of Se in blood and organs of pigs fed seleno-DL-methionine compared with those receiving Astragalus bisulcatus or sodium selenate. Clinical signs of Se toxicity including neurological signs of paralysis were more severe and occurred sooner in the A. bisulcatus group than in the sodium selenate or seleno-DL-methionine groups. All five pigs fed A. bisulcatus developed neurological signs of paralysis, and in four the signs occurred within 5 days of the start of treatment. Four of five pigs fed sodium selenate also developed paralysis, but this occurred 4 to 21 days after treatment began. The fifth pig in the group developed signs of chronic selenosis. Two of five pigs fed seleno-DL-methionine developed paralysis on 9 and 24 days, respectively, and the remaining three developed chronic selenosis. Selenium fed to pigs in three forms [plant (A. bisulcatus), sodium selenate, or seleno-DL-methionine] resulted in neurological dysfunction and lesions of symmetrical poliomyelomalacia. These were most severe in the A. bisulcatus group, which also had polioencephalomalacia. Although seleno-DL-methionine caused the greater increase in tissue and blood Se concentrations, this did not correlate with severity of pathological changes, since animals fed A. bisulcatus developed more severe and disseminated lesions.

An echocardiographical and clinical pathological investigation of the rapid loss of weight by a yearling thoroughbred filly revealed an atrial septal defect, a ventricular septal defect and hyperfibrinogenaemia. A post mortem examination confirmed the cardiac abnormalities and revealed a severe thoracic aortitis. It is proposed that the idiopathic thoracic aortitis contributed to the horse's compromised cardiovascular homoeostasis.

Abstract Extract For several months of the summer-autumn of 1994 there were many reports of blindness, particularly in Western Grey Kangaroos on properties extending from north western Victoria throughout western New South Wales. On some properties, up to 20% of macropods were affected. Many animals probably died, mainly from starvation.

The ceroid-lipofuscinoses comprise a group of inherited storage diseases of human beings and animals that are characterised by progressive neurodegenerative disease and the accumulation within cells of a fluorescent lipopigment. A distinct syndrome occurs in Cocker spaniel dogs in which there is a generalised accumulation of a lipofuscin-like pigment, with such a heavy accumulation in smooth muscle that the intestine and other organs have a brown discolouration. Such discolouration is not observed in other forms of ceroid-lipofuscinosis. Dogs are clinically affected in adulthood and show progressive hind limb paresis, incoordination, and deficient postural reactions and proprioception. Spinal reflexes may be exaggerated. Behavioural or temperament changes, seizures or blindness may occur.

Three captive banded rock rattlesnakes (Crotalus lepidus klauberi) died at Taronga Zoo, Sydney, Australia, between 1984 and 1987 with similar lesions in each case. Grossly, the liver and kidneys had multiple grey, fleshy nodules replacing much of the parenchyma. Histologically, these lesions were massive accumulations of yeast-like organisms, located mainly within macrophages in capillaries and sinusoids. There was little other inflammatory reaction. Organisms also were seen in the muscle and adventitial coats of the intestine, in the spleen, pancreas, brain, lungs, ovary, and fat body. Apparent budding was observed in fresh smears, and the organisms stained Gram-positive and periodic acid-Schiff positive but failed to grow on routine fungal media. Based on transmission electron microscopy, the organisms were typical yeast cells with thick, apparently single-layered cell walls showing evidence of enteroblastic proliferation. Two of the snakes had concurrent bacterial infections.

Thirteen Tammar wallabies (Macropus eugenii) were dosed orally with 500, 1000 or 10,000 oocysts of Toxoplasma gondii, as part of a vaccination trial. Eleven animals died of acute toxoplasmosis 9 to 15 days after challenge. The lesions were similar in all animals, consisting of foci of necrosis and inflammation in the intestines, lymphoid tissue, adrenal cortex, heart, skeletal muscle and brain, and severe generalised pulmonary congestion and oedema. Free and intracellular tachyzoites of Toxoplasma were associated with the lesions. The remaining 2 animals had shown no signs of disease when euthanased four months after challenge. Small, focal, non-suppurative inflammatory lesions were seen in brain, heart and skeletal muscle of these animals and chronic Toxoplasma infection was confirmed by mouse inoculation.

Sparganosis in the echidna, Tachyglossus aculeatus, is characterized by large subcutaneous masses that may be confused with neoplasms. Plerocercoids, believed to be Spirometra erinacei, were found in the ventral or lateral subcutaneous tissues of three echidnas. In each case there was a prominent fibrous mass < or = 12 cm in diameter enclosing plerocercoids, which were surrounded by an intense inflammatory infiltrate dominated by plasma cells and lymphocytes, with focal suppuration. Multiple, small (< or = 2 mm) plerocercoids were present in the lungs and pleural cavity of a fourth echidna that died due to severe pneumonitis. Several plerocercoids also were found in the lung of a platypus (Ornithorhynchus anatinus) associated with parenchymal compression and focal pneumonia.

This report presents information on the range of diseases and lesions that occurred in sections of livers of macropods held in the Non-Domestic Animal Registry at Taronga Zoo. Of 142 affected livers, 52 were due to parasites, 24 to bacteria, nine to Macropod Herpesvirus, four to fungal agents and ten to tumours. In addition, 17 livers had acute degenerative or necrotic lesions, 22 were affected by fibrosis or other chronic lesions and four had miscellaneous degenerative lesions. Common parasitic diseases included toxoplasmosis, coccidial cholangitis, cestode cholangitis (Progamotaenia sp.), fascioliasis and capillarial hepatitis. Bacterial diseases were varied but lesions due to anaerobic bacteria or Mycobacteria spp. were most common. Many of the acute degenerative lesions were associated with cardio-respiratory disease. Chronic lesions were often of unknown origin, although it was speculated that parasitic and bacterial organisms contributed to the aetiology. There were four primary and six metastatic tumours.

Seven of 30 canaries in an aviary in New Zealand developed ophthalmic problems. Clinically, 5 birds had unilateral and 2 birds had bilateral lesions characterized by conjunctivitis, crusty exudates on eyelids, and collapse of the eyeball. Microscopic lesions in 12 of 14 eyes examined included inflammation of the choroid and retina, with osseous replacement of the globe in some. Numerous Toxoplasma gondii tachyzoites were seen in the detached retina and vitreous humor of acutely affected birds. The diagnosis of toxoplasmosis was confirmed by immunohistochemical staining with T gondii antiserum. Affected birds had encephalitis, and T gondii was localized in the brains of these by immunohistochemical examination and by use of bioassays in mice. Toxoplasmosis should be considered in differential diagnosis of ophthalmitis in canaries.

Tyzzer's disease (Bacillus piliformis infection) was diagnosed in nine marsupials (six possums, a koala, a wombat and a dasyurid). All but two of the possums were captive. Five of the seven marsupials, for which ages were recorded, were juvenile. Affected marsupials were either found dead or were showing non-specific illness for up to two days before death. Affected livers and hearts showed gross haemorrhage and scattered areas of white discolouration. Microscopically, areas of coagulative necrosis were often associated with neutrophilic infiltrates. Intracellular, slender, faintly basophilic rods were occasionally detected in HE-stained sections. Rods were shown by silver staining techniques to be associated with the lesions in all affected animals. These rods showed a beaded appearance when stained with methenamine silver and were consistently in packets within cells, on the peripheries of lesions and scattered sparsely and irregularly within the central necrotic regions.

Swainsonine, an indolizidine alkaloid in the locoweeds (certain species of the Astragalus and Oxytropis genera), was fed to young Holstein bull calves in their milk at high elevation (3090 m), and the incidence of high mountain disease (HMD) was compared with locoweed-fed and control calves. Five of 5 calves fed swainsonine and 5 of 5 calves fed fresh Oxytropis sericea showed outward signs of HMD, which included edema under the jaws, throat area and brisket and gross and microscopic lesions of HMD and locoweed poisoning. Grossly there were HMD lesions, including congestion of the liver, right ventricular hypertrophy, and dilatation and excessive fluid in the thoracic and abdominal cavities. Microscopically, the severe centrilobular lesions in the liver, edema of the pulmonary artery, severe edema and/or fibrosis of the roof of the right atrium were suggestive of HMD. The mild to moderate neurovisceral cytoplasmic foamy vacuolation of selected tissues and cerebellar neuroaxonal dystrophy in all calves fed swainsonine and locoweed were indicative of locoweed poisoning. In control calves, 1 of 6 showed equally severe outward, gross, and microscopic lesions of HMD, but none had any lesions indicative of locoweed poisoning. The ratio of right ventricle to left ventricle wall weights were significantly higher (P = 0.033) for the swainsonine-fed calves (1.4) and the locoweed-fed calves (1.3) compared to the controls (0.9). Scores indicating the severity of HMD from observations prior to necropsy were significantly higher for the swainsonine and locoweed-fed calves compared to controls (P = 0.032).(ABSTRACT TRUNCATED AT 250 WORDS)

A penguin (Eudyptula minor) from Tasmania, Australia, died following a 3-day illness. The liver and spleen parenchyma contained grossly visible foci of discoloration. Numerous tachyzoites of Toxoplasma gondii were seen associated with necrosis in sections of liver and spleen. The diagnosis was confirmed by immunohistochemical staining of parasites. This apparently is the first report of fatal toxoplasmosis in a penguin.

Neospora caninum was identified in a calf with spinal cord anomaly in Australia. The calf was full-term and born dead. The caudal cervical and cranial thoracic segments of the spinal cord of the calf were asymmetric because of marked unilateral reduction of ventral gray matter and focal cavitation. Mild focal disseminated nonsuppurative encephalomyelitis was associated with N caninum tissue cysts. Tissue cysts were 16 to 35 microns X 10 to 27 microns, and the cyst walls were 1 to 3 microns thick. In an immunohistochemical test, the parasite stained with N caninum serum but not T gondii serum.

This report describes toxoplasmosis lesions in Australian marsupials. Clinical signs, necropsy findings and histopathological changes are summarized for 43 macropods, two common wombats, two koalas, six possums, 15 dasyurids, two numbats, eight bandicoots and one bilby. Animals either died suddenly without clinical signs or exhibited signs associated with respiratory, neurological or enteric disease. At necropsy, many marsupials had no visible lesions. Where present, common necropsy findings included pulmonary congestion, oedema and consolidation, adrenal enlargement and reddening, haemorrhage and ulceration of stomach and small intestine, and lymphadenomegaly and splenomegaly. Microscopically, affected lungs showed interstitial pneumonia and macrophage accumulation. Myocardial, skeletal and smooth muscle necrosis and neutrophilic inflammation were common. Organs had focal necrosis and/or fibrosis and lymphoid infiltrates. Toxoplasma gondii tissue cysts were common in muscle and nervous tissue. Free tachyzoites were commonly present in areas of necrosis. Selected sections from four macropods, two koalas, two dasyurids, one wombat and one possum stained specifically with avidin-biotin complex and anti-Toxoplasma gondii serum.

This report catalogues all spontaneous proliferations in dasyurids and bandicoots held by the Comparative Pathology Registry at Taronga Zoo. Proliferative lesions were present in 70 dasyurids and three bandicoots. Hyperplastic or benign neoplastic masses in adrenals and livers were common in dasyurids. In addition, previously misdiagnosed splenic haematopoietic hyperplasia was common. A variety of mammary proliferations was present in dasyurids. Dasyurids often had multiple proliferative lesions. Lymphoid neoplasia was common, especially in the smaller dasyurids. No obvious aetiological factors have been identified in any of the tumour conditions in dasyurids although there is some evidence to suggest a genetic predisposition to lymphosarcoma in the fat-tailed antechinus.

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.

A probable neurovisceral lysosomal storage disease is reported, for the first time, in immature red and grey kangaroos (Macropus rufus and M. giganteus). Foamy, pale eosinophilic, periodic acid-Schiff positive, intracytoplasmic material was stored in the liver, lymphoid tissue, kidney, adrenal gland, stomach, blood vessels and central nervous system. Extensive Wallerian-type degeneration was present in the central nervous system. Electron microscopic study of one animal revealed electron dense, cytoplasmic lamellar bodies in neurons and foamy visceral cells. The disease differs from other reported storage diseases in the distribution and nature of the lesions.

Toxoplasma gondii-like organisms were seen in the heart, kidney, liver, lung, lymph node, spleen, small intestine, and stomach from 2 koalas that died suddenly in a fauna park in Sydney, Australia. Diagnosis was confirmed by immunohistochemical staining. This is the first confirmed report of toxoplasmosis in an arboreal marsupial.

Neospora caninum tissue cysts were found in the brain and spinal cord of a 1-wk-old lamb that was unable to stand after birth. The lamb was originally diagnosed as having toxoplasmosis, but ultrastructural and immunohistochemical techniques used in the present study permitted a definitive diagnosis of Neospora caninum tissue cysts in the brain and spinal cord of this lamb. This is the first report of N. caninum in sheep.

A 2-week-old Angora kid goat developed diarrhoea and was treated with parenterally administered antibiotics and saline. The kid rapidly became moribund and died within 6 hours of the first signs of illness. No bacterial or viral agents were detected in the intestinal content. On histological examination large numbers of small haematoxylin-staining bodies were detected associated with the brush border of small intestinal enterocytes. Associated with these bodies there was variable shortening of intestinal villi, some congestion and focal leucocyte infiltration in the lamina propira of the villi and focal epithelial erosions, sloughing or cell transition to more immature enterocyte forms. The location and features revealed by light microscopy and scanning and transmission electron microscopy indicate these bodies are cryptoporidia.

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)

Bilateral laryngeal paralysis is described in 5 Arabian and part-Arabian foals aged between 23 and 35 days. Tracheotomies resulted in complete relief of dyspnoea. Two cases showed recovery of abductor function of the right arytenoid cartilage after 3 weeks and one of these cases later recovered left abductor function. Four of the foals were autopsied at various times from one week to 6 months after the onset of respiratory obstruction. Histology of the recurrent laryngeal nerves showed active Wallerian degeneration and loss of nerve fibres in many fascicles in cases affected for one to 2 weeks. In the longer standing cases there was a severe deficiency of myelinated fibres. Histology of the dorsal and lateral cricoarytenoid muscles showed no abnormalities in the cases affected from one to 5 weeks. However, in the foal affected for 6 months there was variation in fibre diameter in the left dorsal cricoarytenoid muscle; in sections stained for myosin ATPase there was evidence of muscle fibre type grouping in both left and right dorsal cricoarytenoid muscles. It is postulated that the most likely cause of the condition was oral haloxon administration which was given to the foals at a dose rate of 1 to 2 g at fortnightly intervals, beginning at 2 days of age.

Five central nervous diseases are described and their relationships to previously recorded conditions are discussed. The conditions are congenital inclusion-body encephalopathy probably caused by a paramyxovirus infection, idiopathic neuraxial oedema of a newborn calf, focal symmetrical encephalomalacia of a young calf, yacca (Xanthorrhoea spp) poisoning of adult cattle leading to spinal demyelination, and focal demyelination and neuropathy in an adult cow.

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.