Morbillivirus-associated unusual mortality event in South Australian bottlenose dolphins is largest reported for the Southern Hemisphere.

Cases of morbillivirus have been recorded in the Southern Hemisphere but have not been linked to significant marine mammal mortality. Post-mortems were conducted on 58 carcasses (44 Indo-Pacific bottlenose dolphins, two common bottlenose dolphins, 12 short-beaked common dolphins) from South Australia during 2005-2013, including an unusual mortality event (UME) in St Vincent Gulf Bioregion (SVG) during 2013. Diagnostic pathology, circumstance of death, body condition, age and stomach contents were documented for Indo-Pacific bottlenose dolphins. At least 50 dolphins died during the UME, 41 were Indo-Pacific bottlenose dolphins and most were young. The UME lasted about seven months and had two peaks, the first being the largest. Effect on the population is unknown. Diagnostic testing for morbillivirus was conducted on 57 carcasses, with evidence for infection in all species during 2011-2013. All tested UME bottlenose dolphins were positive for cetacean morbillivirus (CeMV), and the pathology included interstitial pneumonia, lymphoid depletion and syncytia. Concurrent pathologies, including lung parasite and fungal infections, and severe cutaneous bruising were observed in many dolphins. The event coincided with elevated water temperatures, a diatom bloom and significant fish die-offs. We conclude that the cause for the UME was multifactorial and that CeMV was a major contributor.

A study of the pathology and pathogenesis of the myocardial lesions in gousiekte, a plant-induced cardiotoxicosis of ruminants.

Myocardial lesions were studied in sheep in which gousiekte was induced by experimental dosage of Pachystigma pygmaeum, Fadogia homblei or Pavetta harborii. The single most consistent diagnostic histological feature in 33 animals was hypertrophy of myocardial fibres in the subendocardial region. Fibrosis in the subendocardial region of the apex or left ventricular wall was often scarce or absent in animals with a short latent period, and was not always prominent even in sheep with an intermediate or long latent period. The presence or absence of fibrosis cannot therefore be used to confirm or exclude gousiekte, particularly in cases with shorter latent periods. Light microscopical and ultrastructural lesions in sheep with gousiekte correspond to a large extent to changes reported in humans with dilated cardiomyopathy of unknown cause. It appears that the myocardial lesions in gousiekte represent a final common pathway of cellular damage rather than a manifestation of a specific type of heart disease. The predilection for hypertrophy of myofibres in the subendocardial region is probably related to diminished perfusion that potentiates the primary myocardial dysfunction.

Paratuberculosis in sheep: an emerging disease in South Africa.

During a serological survey for ovine paratuberculosis a total of 145934 ovine serum samples from 2019 farms throughout South Africa were tested by means of the AGID assay. Fifty-two infected farms were identified in the Western Cape and Eastern Cape provinces. Links between infected farms in the two provinces were established. Examination of the distribution of infected farms in the Western Cape indicated a positive correlation between acid soils and occurrence of infection. In an attempt to increase the sensitivity and facilitate screening of large numbers of sera two commercial ELISA systems were evaluated for their potential use in a future monitoring program. Sera from histologically positive sheep and known negative sheep flocks were used. The highest sensitivity (50. 9%) was found if both ELISA systems were run concurrently and the results of both systems combined.

Malignant fibrous histiocytoma of the deep peri-articular tissue of the stifle in a dog.

A Belgian shepherd dog aged 4 years and 9 months was presented with acute onset of non-weight bearing lameness and stifle effusion of the left hind limb, caused by the deep form of a malignant fibrous histiocytoma originating in the deep musculature and fascia surrounding the stifle joint. The tumour progressed rapidly in the tissues along the femoral diaphysis with marked periosteal new bone formation. Cytology of a stifle joint aspirate revealed numerous large polygonal neoplastic cells with considerable anisocytosis and anisokaryosis. These cells were present in clusters, with cytoplasmic projections between the cells, but occasionally also occurred singly. Several cells contained multiple cytoplasmic vacuoles and occasional giant cells were also encountered. Adequate tumour-free margins were not possible with radical limb amputation and the dog was euthanased. Macroscopically the tumour appeared as an extensive pale tan, firm mass with scattered small haemorrhages and foci of yellow discolouration. Histologically the tumour consisted of dense neoplastic expanses or multiple nodules, composed of spindle-shaped fibroblastic cells, polygonal histiocytic cells or cell clusters and scattered giant cells with 2-3 nuclei. The polygonal neoplastic cells were frequently present around and invading lymphatics and blood vessels, causing neoplastic emboli. This is the 1st report of the clinical behaviour, radiography and cytology of the deep form of malignant fibrous histiocytoma in the dog.

A chronic cardiomyopathy in feedlot cattle attributed to toxic levels of salinomycin in the feed.

The clinical signs and pathology in an outbreak of toxicity in feedlot cattle attributed to the ingestion of toxic levels of the ionophore antibiotic salinomycin over an extended period of 11 weeks are described. Thirty-nine out of 380 cattle developed signs consistent with cardiac failure and 8 of these died. Clinical signs included dyspnoea, tachypnoea, tachycardia and exercise intolerance. Two cattle were necropsied and in one there were macroscopic lesions suggestive of congestive heart failure, namely pulmonary oedema, hydrothorax and hepatomegaly. Histopathology revealed a chronic cardiomyopathy characterised principally by extensive myocardial fibre atrophy with multifocal hypertrophy and interstitial and replacement fibrosis. Hepatic and pulmonary lesions were consistent with those of congestive cardiac failure. The myocardial lesions in this outbreak were similar to those encountered in cases of a chronic toxicity associated with the ingestion of litter derived from poultry rations containing ionophores (ionophore-associated poultry litter toxicity). Hence, the clinical and pathological findings in this outbreak indicate that in cattle, the prolonged ingestion of ionophores over several weeks may result in the development of chronic myocardial lesions comparable to those of IAPLT but significantly different from those encountered in the more traditional acute outbreaks of ionophore toxicity as described in the literature.

Two outbreaks of type C and type D botulism in sheep and goats in south Africa.

Two outbreaks of botulism in sheep and goats are described; in one, 329 out of 900 sheep in a feedlot died within 9 d of the onset of the disease and in the other, 100 sheep and goats out of 330 succumbed over a period of about 3 weeks. Animals were found dead or died suddenly, without exhibiting clinical signs. Others stood with lowered heads and showed drooling of saliva or a stiff gait. Paresis and/or paralysis were frequent signs in the terminal stages of the disease. Gross lesions such as the accumulation of fluids in body cavities, pulmonary oedema, foam in the trachea, epicardial haemorrhages and congestion of the mucosa of the small intestine, suggestive of heart failure, were present in animals from both outbreaks. Botulism was confirmed via the mouse toxicity test, by the demonstration of Type C and Type D toxins in the feed and intestinal contents of sheep from the first outbreak and Type D toxin in intestinal contents of sheep from the second. The clinical signs and macropathology in the outbreaks of botulism in sheep and goats in South Africa may resemble "krimpsiekte" and cardiac glycoside and ionophore poisoning, as well as other conditions causing heart failure.

Cardiomyopathy of ruminants induced by the litter of poultry fed on rations containing the ionophore antibiotic, maduramicin. II. Macropathology and histopathology.

This report contains an account of the gross and histopathological lesions of 20 cattle and four sheep in 15 field outbreaks of poultry litter toxicity, one steer fed ad lib. and six sheep dosed with toxic poultry litter, and ten sheep fed experimental rations containing c 2,5 ppm and 5 ppm maduramicin. The principle macroscopic lesions in most cattle that died in field outbreaks were indicative of congestive heart failure. The lesions in sheep were similar, but generally milder. Cardiac dilatation was observed in both sheep and cattle. Microscopically, the cardiac lesions were more pronounced in cattle and comprised varying degrees of atrophy, hypertrophy, degeneration, necrosis of myocardial fibres, and interstitial fibrosis. Skeletal muscle lesions were usually more severe in sheep, particularly in the muscles of the hindquarters which appeared pale, oedematous and mottled. One of the sheep in the poultry litter dosing trial developed signs of congestive heart failure and the hearts of two others were dilated. Extensive hypertrophy and atrophy of myocardial fibres were evident in the steer fed ad lib. with this material. As in field cases, the myocardial lesions of the sheep were less severe than those of the steer. Mild cardiac dilatation was present in four of the seven sheep in the maduramicin feeding trial. Diffuse hypertrophy of myocardial nuclei was present in all seven cases, myocardial fibre atrophy in six, multifocal fibrosis and necrosis in six and two cases, respectively, and focal endocardial thickening in two. The skeletal muscles revealed granular degeneration and foci of necrosis and regeneration. The cardiac and skeletal lesions in the field outbreaks, poultry litter feeding trials and maduramicin feeding trials, were highly comparable. This suggests that this form of poultry litter intoxication is a chronic form of ionophore toxicity the pathology of which is characterized by a dilated cardiomyopathy with congestive heart failure and mild (cattle) to severe (sheep) skeletal muscle lesions.

Vanadium air pollution: a cause of malabsorption and immunosuppression in cattle.

An epidemiological investigation into an "illthrift" problem occurring on a dairy farm adjacent to an alloy-processing unit, established that the probable cause of the problem was chronic vanadium poisoning. The disease manifested initially in animals 4-18 months old which showed emaciation, chronic diarrhoea and, in some cases, rhinitis, conjunctivitis and recumbency followed by death. Post-mortem (n = 17) and clinical-pathology findings (n = 60) indicated that malabsorption and immunosuppression were the basis of the pathogenesis in affected animals. Eight months after the commencement of the investigation, adult cows began showing evidence of emaciation, reduced milk production and an apparent increase in the number of abortions, stillbirths and dystocias. Over a 2-year period, 134 surface-soil samples, 134 subsoil samples and 134 grass samples from the farm were analysed for various fractions of vanadium. Thirty-four of each of these samples were collected at different time intervals (autumn 1990, summer 1991 and winter 1991) and at varying distances and directions from the processing unit, in order to gauge the magnitude of the problem, and the distribution pattern of vanadium, and to identify possible seasonal trends. The remaining 100 of each of these samples were taken at 100-m intervals over an area of approximately 1,140,000 m2 directly adjacent to the processing unit so that concentration isolines for vanadium could be drawn and the source more conclusively identified. The levels of vanadium were found to be highest closest to the mine, and surface-soil levels were consistently higher than subsoil levels, suggesting aerial pollution, which was confirmed by air sampling.(ABSTRACT TRUNCATED AT 250 WORDS)

Congenital cardiac defects in two closely related Jersey calves.

This paper describes similar congenital cardiac anomalies in 2 half sibling Jersey calves. Both calves had ventricular septal defects with dextraposition of the aorta and hypertrophy of the right ventricle, consistent with Eisenmenger's complex. One of the calves also had patent foramen ovale. The 2 calves had been sired by the same bull, and collateral relationships existed between the sire and the 2 dams.

An outbreak of narasin poisoning in swine.

An outbreak of narasin poisoning in swine is described. Forty nine out of 108 lactating sows died over a period of one month after being fed a ration accidentally contaminated with narasin. Clinical signs included anorexia, respiratory distress, lethargy and posterior paresis, progressing to lateral recumbency and death. Necropsy examination in 3 pigs revealed extensive myocardial and skeletal muscle damage. Analysis of the feed confirmed the presence of high concentrations of narasin.

Histopathology and morphology of the tissue stages of Haemoproteus columbae causing mortality in Columbiformes.

Two doves from the same aviary died following heavy infections with Haemoproteus columbae. Histopathological examination of various organs revealed numerous schizonts and megaloschizonts. There seemed to be two cycles of schizogony, one within the muscles and another in a wide range of tissues. The shape and size of the schizonts appeared to be a function of the site of formation. The rupture of megaloschizonts, especially in the striated muscles caused extensive fibre necrosis and the resultant muscle damage, is believed to be the major cause of mortality.

Experimental Albizia versicolor poisoning in sheep and its successful treatment with pyridoxine hydrochloride.

Five sheep developed severe nervous signs after being drenched with Albizia versicolor pod-material. Four of these sheep were treated with pyridoxine hydrochloride (a vitamin B6) when the symptoms of toxicity became life-threatening. All the treated sheep recovered dramatically and completely after treatment while the untreated one died 2 h after receiving pod-material. A therapeutic dose of 20-25 mg pyridoxine hydrochloride/kg body mass given twice with an 8 h interval is the recommended treatment regimen. The route of administration will depend on the severity of symptoms. Chemical pathology and post-mortem findings are discussed.

Cardiomyopathy of ruminants induced by the litter of poultry fed on rations containing the ionophore antibiotic, maduramicin. I. Epidemiology, clinical signs and clinical pathology.

The epidemiological, clinical and clinical pathological findings in 20 cattle and 4 sheep from 15 outbreaks of poultry litter toxicity in South Africa over the past 6 years are documented. In 6 outbreaks, the litter emanated from batteries where maduramicin had been incorporated into rations of broilers. According to circumstantial evidence the litter involved in the 9 other outbreaks was also derived from broilers which had been fed on rations containing an ionophore. The litter was fed ad libitum to the affected stock or constituted 30-80% by volume of their rations. The principal sign manifested was sudden mortality of up to 70% of the herd or flock, usually within 20-40 days of commencement of feeding of poultry litter. A few cattle developed signs of congestive heart failure, and stiffness was commonly seen in sheep. In a dosing trial with poultry litter involving 1 steer and 6 sheep, the steer and a sheep died suddenly and a second sheep was destroyed in extremis. Tachycardia and/or cardiac arrythmia were recorded in 5 sheep, and the activity of aspartate transaminase (AST) and/or lactate dehydrogenase (LD) in the sera of 4 was elevated. Since the cardiac lesions in field cases were similar to those of ionophore poisoning and broiler rations containing maduramicin was a common factor in several outbreaks, toxic litter from some of these outbreaks were tested for the presence of this compound. Analysis by high performance liquid chromatography of litter from 2 specimens of outbreaks revealed that they contained 2.5 ppm and 6.1 ppm maduramicin.(ABSTRACT TRUNCATED AT 250 WORDS)

Copper toxicity in ruminants: air pollution as a possible cause.

Pathological findings and liver and kidney analyses confirmed that cattle had died of chronic copper poisoning on a farm in the north-eastern Transvaal. This is the first known published record of chronic copper intoxication of cattle in southern Africa. An epidemiological study revealed that a source of copper was air pollution which could have arisen from a nearby copper smelting unit. Buffalo and impala in an adjacent area of the Kruger National Park were found to have significantly higher liver copper levels than animals elsewhere in the Park. Prophylactic licks, containing zinc sulphate and sulphur, seemed to be successful in protecting cattle against the effects of the copper in the contaminated grazing.

Pathological findings in a natural outbreak of aflatoxicosis in dogs.

The gross and histopathological lesions of 10 cases in a natural outbreak of aflatoxicosis amongst dogs in the Republic of South Africa are reported. The 10 cases were classified as acute (1 case), subacute (7 cases) and chronic (2 cases) on the basis of the nature, degree and extent of the following histopathological fractures: hepatocellular fatty degeneration, necrosis or regeneration; proliferation of bile ductules; accumulation of bile within the canaliculi; fibroplasia; and, mucoid degeneration, necrosis or segmental atrophy of the larger intrahepatic bile ducts. Fatty degeneration was noted grossly in the livers of all 10 cases and bile stasis in 4. Varying degrees of fibrosis were present depending on the stage of the disease. In the 2 chronic cases in which nodular regeneration was also observed fibrosis was pronounced. Other macroscopic findings included icterus, anaemia, ascites, hydrothorax, hydropericardium, anasarca, pulmonary oedema, gastro-enterorrhagia and nephrosis.

The pathology of a case of biliary atresia in a foal.

The pathological features of biliary atresia in a foal are described. A 4-week-old American Saddler foal was presented for autopsy following an illness characterised by clinical features indicative of hepatic failure. The significant macroscopical lesions occurred in the liver which was extremely enlarged, mottled in appearance and indurated. Bile stasis was evident. Lobular distinction was absent and on sectioning, large bile ducts were absent. A moderate ascites, hydrothorax and hydropericardium and a mild anasarca and intermuscular oedema accompanied the hepatic lesion. The diagnosis of biliary atresia was determined by the histo-pathological features of bile duct proliferation and extensive replacement fibrosis. The condition is compared to extrahepatic and intrahepatic biliary atresia of man and evidence is presented for regarding this case to be one of extrahepatic origin.