A field outbreak in Ile-de-France sheep of a cardiotoxicosis caused by the plant Pachystigma pygmaeum (Schltr) Robyns (Rubiaceae)

A field outbreak of Pachystigma pygmaeum intoxication in sheep is described. Noteworthy clinical signs were: respiratory distress, apathy and subcutaneous oedema of mainly the head. Gross changes included cardiomegaly, centrilobular hepatic necrosis and effusion of body cavities. Microscopically myocardial fibrosis, affecting predominantly the endocardium of the apex, left free ventricular wall and interventricular septum, was most striking in the majority of animals, whilst myofibre atrophy was present in 1 sheep.     

An ovine hepatotoxicosis caused by the plant Pteronia pallens (Asteraceae) L.f

The hepatotoxicity of Pteronia pallens was demonstrated in 5 sheep which developed lesions that ranged from centrilobular necrosis to diffuse hepatocellular degeneration. Botanical, clinical and pathological data are given and the lesions are briefly compared with those caused by other hepatotoxic plants in South Africa.     

Experimentally-induced Cestrum laevigatum (Schlechtd.) poisoning in sheep.

Dried, milled Cestrum laevigatum plant material was drenched to 6 ewes at doses ranging from 2,5 to 10 g/kg/day for 1 to 47 days. The most noticeable clinical signs were depression, anorexia and ruminal stasis. These signs were accompanied by clinical pathological changes indicative of liver involvement such as increases in the serum activities of aspartate transaminase, lactate dehydrogenase and gamma-glutamyltransferase. Hepatosis characterized by accentuated lobulation, and centrilobular to midzonal coagulative necrosis, haemorrhage and congestion occurred in 2 of the 3 ewes given high doses of plant material. Liver lesions in the other animals included disappearance of hepatocytes and collapse of the reticulin stroma in the centrilobular areas. Spongy changes in the cerebral white matter were evident in the ewes of the high-dose group. Ultrastructural changes in the liver comprised degeneration and necrosis of hepatocytes and occasionally endothelial cells, and disruption of sinusoidal walls.     

The toxicity of myoporum tetrandrum (Boobialla) and myoporaceous furanoid essential oils for ruminants

Boobialla (Myoporum tetrandrum)leaf contains from 0.25 to 0.5% wet weight of furanoid sesquiterpene essential oils of which the main component is dehydrongaione. The plant was toxic when dosed to calves at equivalent dose rates of oils of from 50 to 134 mg/kg, causing mainly extensive haemorrhagic centrillobular necrosis; and to sheep at equivalent dose rates of oil of from 55 to 66 mg/kg, causing either centrilobular or periportal liver lesions with or without acute pulmonary oedema. An essential oil mixture of similar composition derived from Myoporum deserti produced similar syndromes. In addition, treatment of calves with phenobarbitone or Melaleuca linariifolia essential oils prior to dosing with the Myoporum oils caused periportal hepatic necrosis rather than the centrilobular lesion which occurred usually in this species. The liver lesions found in the experimental calves and sheep respectively, were thus similar to those reported in suspected field cases of Boobialla poisoning in cattle and goats in Western Australia. The liver injury that may be expected in intoxication of livestock by myoporaceous plants containing this type of essential oils can thus be either periportal, midzonal or centrilobular necrosis, depending, probably, on the nutritional regime of the animal immediately prior to consumption of the toxic plant.     

An ovine hepatotoxicosis caused by the plant Hertia pallens (DC.) Kuntze (Asteraceae)

A field outbreak of Hertia pallens poisoning in sheep is described. The hepatotoxicity of the plant was experimentally demonstrated in 7 sheep which developed lesions that ranged from a diffuse degeneration to centrilobular necrosis. These lesions occasionally extended to the midzonal area of the lobules. In addition to a lung oedema, a diffuse mononuclear interstitial pneumonia was present in 3 of the sheep. Botanical, clinical and pathological data are given.     

Ovine hepatogenous photosensitivity caused by the plant Nidorella foetida (Thunb.) DC. (Asteraceae)

Following a field outbreak of hepatogenous photosensitivity in sheep, an identical condition was reproduced experimentally by dosing 2 sheep with green, homogenized, Nidorella foetida material, collected from the camp where the outbreak occurred. This is a rare, unpalatable, aromatic shrub found in swampy places in the south-western Cape Province. The main lesion was a hepatosis, characterized by peripheral coagulative necrosis and midzonal degeneration in the 2 acute cases and mild bile duct proliferation and hepatic regeneration in the more chronic field case. Botanical, toxicological, clinical and pathological data are given.     

细粒棘球蚴感染羊肝脏包囊纤维化形成的病理形态学观察

为了探讨细粒棘球蚴感染羊肝脏包囊纤维化形成的病理学过程,本研究通过病理组织学、细胞化学和超微形态学的诊断方法,对羊感染细粒棘球蚴后肝脏的病理组织学变化,以及肝组织纤维化和包囊形成过程进行病理学观察。结果显示:原头蚴感染肝组织后病变沿感染组织的血管周围产生,相继出现肝细胞萎缩、变性、坏死;同时病变组织血管壁出现纤维组织分解、血管管壁出芽,增生出的纤维组织伸向周围炎症区域,血管管腔及炎区大量嗜酸性粒细胞浸润,增生的胶原纤维沿残存的肝细胞周围围绕病变组织,最终形成包囊壁。该研究结果为进一步阐释细粒棘球蚴感染羊肝脏包囊纤维化形成的病理机制奠定了坚实的基础。     

Clinical and pathological features of dilated cardiomyopathy in Holstein-Friesian cattle

Dilated cardiomyopathy is a primary disease of the heart muscle that has been reported in Holstein-Friesian cattle worldwide in the past 20 years. Nine cases of the condition were compared in terms of their clinical and pathological characteristics with nine unaffected animals matched for age, sex and breed. Their clinical signs included right-sided heart failure with severe subcutaneous oedema, ascites and/or hydrothorax and distended jugular veins. There were no characteristic biochemical or haematological changes. Postmortem, the affected hearts were enlarged with all the chambers dilated and walls of variable thickness. In most cases the kidneys were pale with a pitted surface. Histologically there was marked perimysial and endomysial fibrosis, extensive loss of cardiomyocytes by coagulative or colliquative necrosis, increased variation in the cross-sectional area of the myocardial fibres, and multifocal disarray and vacuolation of myocytes. Scanning electron microscopy showed that in all cases there was a mild myocardial inflammatory infiltrate, either diffuse or multifocal, which was identified by immunohistochemical labelling as T cells.     

Observations on three outbreaks of Leptospira interrogans serovar pomona infection in lambs

Sickness and deaths associated with leptospirosis were reported in three lamb flocks in the Manawatu region. The clinical, pathological and serological features of Leptospiru interrogans serovar pomona infection are described. The mucous membranes of affected animals were pale and jaundiced. Haemoglobinuria, haemoglobinaemia and centrilobular hepatocellular necrosis were also consistent findings. All clinically sick lambs had very high titres in the microscopic agglutination test for L. pomona. Circumstantial evidence of pigs being the source of infection was found in one of the three cases.     

The role of antioxidant vitamins (C and E), selenium and Nigella sativa in the prevention of liver fibrosis and cirrhosis in rabbits: new hopes

This experiment was carried out to investigate the role of antioxidants such as vitamin C and E, selenium and Nigella sativa (NS) on the prevention of carbon tetrachloride (CCl4)-induced liver fibrosis in rabbits. It was found that superoxide dismutase (SOD) values in all of the treated groups were significantly lower than those of the control at 12th week of experiment (p < 0.05), while at 6th week and 12th week of experiment glutathione peroxidase (GSH-Px) values in the vitamin C treated group were significantly different from the control (p < 0.05). Histopathologically, hepatocellular necrosis, degeneration and advanced fibrosis were found in the control group. Lesions were minor and only confined to midzonal regions without centrilobular necrosis and fibrosis in the NS treated animals (group B). The lesions observed in the vitamin C treated animals (group C) were similar to that of the control group. Parenchymal changes with fibrosis were less in selenium and vitamin E treated animals (group D) than in those of the control group, but more obvious than in NS group. Histopathological findings demonstrate that NS might, at least partly, be successful in the prevention of liver fibrosis in rabbits. Vitamin E plus selenium had little therapeutic effect and vitamin C seemed to be ineffective, as far as the results of this study are concerned.     

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)     

A tremorgenic mycotoxicosis of cattle caused by maize sprouts infested with Aspergillus clavatus

An outbreak of disease affecting a herd of 16 dairy cattle which were fed mouldy, sprouted maize is described. Eight of the cattle were affected, 5 of which died. The clinical signs included muscular tremors, hypersensitivity, ataxia, anorexia and salivation. Aspergillus clavatus was the only fungus isolated from the sprouts. Clinical signs that were indistinguishable from those in the field outbreak were reproduced by dosing the mouldy maize sprouts to a steer and a sheep, and by dosing another sheep with maize inoculated with a pure culture of A. clavatus isolated from the mouldy maize on the farm. Light microscopical examination revealed neuronal degeneration and necrosis in the midbrain, medulla oblongata and spinal cord of all 3 of these animals. The disease is clinically and pathologically indistinguishable from the disease caused by the ingestion of sorghum beer residue, and in certain respects it is similar to toxicoses caused by the ingestion of wheat sprouts and malt sprouts infested with A. clavatus.     

The pathology of Cestrum laevigatum (Schlechtd.) poisoning in cattle

The clinical features and pathological findings of 6 steers drenched with dried plant material of Cestrum laevigatum are described. Doses ranging from 0.5 to 10 g/kg/day were given intraruminally for 1 to 38 days. Animals that received 5 to 10 g/kg/day showed nervous signs including ataxia, muscle tremors, hypersensitivity and intermittent chewing. Clinical signs in the steers which received 0,5 to 4 g/kg/day were mild. High doses induced moderate to severe hepatosis characterized by centrilobular to midzonal coagulative necrosis, haemorrhage and congestion. At lower rates only mild hepatic lesions, characterized by disappearance of hepatocytes and collapse of the reticulin stroma in the centrilobular areas were evident. Ultrastructural changes were primarily limited to the hepatocytes and comprised degeneration, necrosis and fatty change. Degeneration and necrosis of endothelial cells and disruption of sinusoidal walls were occasionally observed.     

The pathology of acute Nolletia gariepina poisoning of cattle

Toxicity in cattle by the shrub Nolletia gariepina was induced experimentally by intraruminal administration of 3 g/kg dried, milled plant material as a single dose. The animals had to be starved for 24 hours before dosing, as dosing on a full rumen did not induce any signs of toxicity during 5 days of observation and clinical pathology monitoring. Clinical signs were not specific and varied according to the duration (acute versus subacute) of the toxicological process. Clinical pathological parameters indicated renal and to a lesser extent hepatic damage, with raised serum concentrations of urea, creatinine, aspartate aminotransferase (AST) and gamma glutamyl transferase (GGT). Increased urinary sodium and potassium concentration and GGT activity, as well as proteinuria, were evident. Histological and electron microscopic examinations revealed acute renal tubular epithelial cell degeneration and necrosis, especially of the proximal convoluted tubules. Mild hepatocellular degeneration was also noticeable.     

Cardiomyopathy in broiler chickens congenitally infected with avian leukosis virus subgroup J

Dilated cardiomyopathy and ascites in broiler chickens are frequently associated with rapid growth and pulmonary hypertension, but can be associated with some avian leukosis virus (ALV) infections. The novel subgroup J of ALV has a high cardiac tropism, but dilated cardiomyopathy has not been reported previously. We report a dilated cardiomyopathy incidence of 11.1% in broiler chickens congenitally infected with ALV subgroup J (ALV-J). Gross lesions included severe body weight suppression, cardiomegaly with biventricular dilation, right ventricular hypertrophy, visceral congestion, and ascites. Cardiac myocytes and Purkinje fibers contained 2- to 10-microm intracytoplasmic magenta inclusions that contained ALV-J-specific nucleic acid. Ultrastructurally, inclusions contained ribosomes and immature virions and were associated with myofibril disruption and disarray. Peracute centrilobular hepatic necrosis was present in most cases. ALV-J-associated cardiomyopathy may involve a direct viral effect on cardiac myocytes and Purkinje fibers.     

Clinical pathological changes in gousiekte, a plant-induced cardiotoxicosis of ruminants

Twenty sheep were dosed with either Pachystigma pygmaeum or Fadogia homblei belonging to the Rubiaceae. The experimentally-induced cardiotoxicoses were monitored by various clinical pathological parameters and heart function tests. Elevated AST (aspartate transaminase) activity in the serum proved to be a more reliable indicator of cardiac damage in gousiekte than either LD (lactate dehydrogenase) or CK (creatine kinase). Persistent increases of AST activity were recorded from c. 14 days after commencement of dosing, and this activity sometimes peaked as late as 30 days after the dosing had ceased. Tachycardia and diminished heart function were registered only terminally. Lesions of gousiekte were present in all the sheep that were exposed to the plants. In a field outbreak of P. pygmaeum, where 60 out of 90 sheep died, 14 out of the 15 animals examined had increased AST levels compared with none of the 15 controls. These results indicated that increased enzyme levels can be of use to identify affected animals during latency in a natural outbreak of gousiekte.     

Clinical and pathological studies in adult sheep and goats experimentally infected with Wesselsbron disease virus

The clinical symptoms and pathology in 33 adult sheep and 31 adult goats experimentally infected with Wesselsbron disease virus are described. There was moderate to severe hyperthermia in most animals, but no other clinical signs of disease or deaths were recorded. Eleven sheep and 6 goats were sacrificed for pathological studies at various stages during the febrile response. The macroscopic and microscopic lesions in these cases are described. Microscopic studies revealed that the liver was consistently affected and showed small foci of necrosis. These were sparsely distributed and associated with a marked localized Kupffer cell response ("retothelial nodules"). In addition, acidophilic bodies and small groups of necrotic hepatocytes were evident in some lobules. Apart from the hepatic lesions, mild to moderate pyknosis and karyorrhexis of lymphocytes were seen in the spleen and lymph nodes. This report also compares the microscopic lesions in the livers of adult sheep and goats with those of new-born lambs for Wesselsbron disease as well as with those reported for Rift Valley fever in adult sheep.     

Acute Hepatic Necrosis And Liver Failure Associated With Benzodiazepine Therapy In Six Cats, 1986–1995.

A retrospective analysis was conducted of all feline necropsies performed during a nine year period to identify cases of sever, acute, centrilobular (periacinar), hepatic necrosis (ACHN). After exclusion of cats with anemia, a series of seven cases of ACHN was identified. In addition, two similar cases were identified from tissue submitted for histopathology following, and eight had bile duct hyperplasia. Seven of the nine cats received diazepam prior to dath, and one received zolazepam. Of the seven cats that received diazepam, five were healthy prior to treatment and received oral diazepam for the treatment of inappropriate urination, intercat aggression, or skin disease. Two cats which received diazepam exhibited other clinical signs: one had chronic vomiting, and the other received diazepam after biochemical evidence of hepatocellular necrosis was present. Onset of clinical sings in cats receiving oral diazepam occurred 7–13 days following the initiation of treatment. Clinical signs and clinical biochemical analysis were compatible with severe hepatocellular necrosis and acute liver failure. All cats had lesions in other organs: five had pancreatic disease, five had cardiac disease, and five had renal disease. All cats died, or were euthanized, within 4 dyas of the onset of clinical signs and 2 days after presentation to a veterinarian. Fatal, acute, centrilobular hepatic necrosis appears to be a serious adverse reaction to diazepam therapy in certain cats.     

绵羊感染伪狂犬病的病理学观察与病毒分离鉴定

为了确诊1例疑似绵羊伪狂犬病病例,本试验以上海郊区某羊场发病绵羊的病料为研究对象进行了病理学观察、病毒分离和鉴定。病理组织学变化显示,发病羊大脑组织神经元发生广泛性变性、坏死并伴有嗜神经现象,神经元周围出现胶质细胞增生。病料接种BHK-21细胞,细胞出现病变,间接免疫荧光试验和荧光定量PCR检测结果证实所分离的病毒为伪狂犬病病毒。流行病学调查结果表明,绵羊伪狂犬病可能是由猪伪狂犬病病毒感染引起的。通过免疫接种猪伪狂犬病弱毒疫苗,绵羊伪狂犬病疫情得到及时控制。     

Scrapie in goats in Cyprus

Ovine scrapie was first recorded in Cyprus in 1985. Subsequently four dairy goats kept in two mixed flocks with affected sheep developed characteristic clinical signs similar to those seen in sheep. Fifteen goats from the two flocks were examined histologically and neurological lesions consistent with a diagnosis of scrapie were found in the four animals and in three others which had subsequently developed early neurological signs. These lesions were similar to those of naturally-affected sheep although neuronal degeneration and vacuolation were more severe in some cases.