Pathological aspects of Australian Stringhalt.

Nine horses with clinical signs of Australian Stringhalt were killed and tissues collected for a detailed pathological study. Lesions were limited to peripheral nerves and muscles. The most severely affected nerves were the superficial and deep peroneal, distal tibial, plantar digital, volar and recurrent laryngeal nerve with changes characterised by a selective loss of large diameter myelinated fibres with various degrees of demyelination, fibrosis, Schwann cell proliferation and onion-bulb formation. A routine evaluation of the brain and spinal cord by light microscopy failed to reveal any consistent abnormalities. Morphometric analysis of deep peroneal and recurrent laryngeal nerves confirmed the reduced number of large diameter myelinated axons. Teased fibre preparations of these nerves did not show any abnormalities in internodal distance. The most severe muscle lesions were in the long and lateral digital extensors, cranial tibial, dorsal cricoarytenoid, gracilis and lateral deep digital flexor with extensive atrophy of fibres and diffuse fibrosis. Histochemical evaluation of the long digital extensor from 3 affected horses showed an abnormally wide distribution in fibre size and a reduction in type II fibres compared with controls. These lesions are consistent with a distal axonopathy leading to neurogenic muscle atrophy. The distribution of neuromuscular lesions in Australian Stringhalt may be explained by the susceptibility of longer, larger myelinated nerve fibres to injury, but the cause for this distal axonopathy remains unknown.

Feline immunodeficiency virus: prevalence, disease associations and isolation.

Of 467 cat serums tested for antibody to feline immunodeficiency virus (FIV) 120 (26%) were positive. The average age of positive cats was 7.5 years (range 1 to 16 years), and 67% were male. Of 110 serums collected in 1980, 27 (24.5%) were positive. A wide variety of clinical signs including oral cavity disease, anorexia, weight loss, lethargy, depression, fever, respiratory and urinary tract disease, conjunctivitis, abscesses, anaemia and lymphadenopathy were observed in the cats with serum antibody. There was often a history of chronic disease or recurrence of particular or various clinical signs in these cats. FIV was isolated from 4 of 8 FIV antibody positive cats by cocultivation of patient lymphocytes with donor lymphocytes in the presence of interleukin 2.

Australian Stringhalt--epidemiological, clinical and neurological investigations.

An investigation of 78 cases of typical Australian Stringhalt from 52 properties in Victoria was carried out from 1985 to 1987. Horses were either examined in the field (n = 52), referred to the Veterinary Clinical Centre (n = 13) or clinical details were obtained verbally (n = 13). In addition 10 cases of false or atypical stringhalt were examined. Detailed soil and pasture analysis was carried out on 14 properties where Australian Stringhalt had occurred. Information was also obtained on epidemiology of the condition from a survey of practitioners. Fifty of the 52 cases examined in the field occurred in horses that were dependent upon poor quality unimproved dry pasture. In all but a few cases, there was no pasture improvement or fertiliser application, leading to the development of weed-dominated pastures, particularly by flatweed, Hypochaeris radicata. The range of clinical signs exhibited by horses with Australian Stringhalt was described and a grading system proposed to classify horses according to severity of signs. Laryngeal abnormalities were present in 10 of 11 cases examined endoscopically and these horses exhibited increased electromyographic (EMG) activity in the long digital extensor muscle at rest and during hindlimb flexion. To a large extent, the EMG changes disappeared and digital extensor muscle atrophy improved in two horses that were monitored to recovery. Deep peroneal nerve conduction studies in four horses with Australian Stringhalt showed a substantial reduction in nerve conduction velocity and when stimulated at 50 Hz were unable to sustain activation of the long digital extensor muscle. EMG and evoked responses appeared to be sensitive indicators of the state of the disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Use of iohexol for myelography in the horse.

The use of iohexol as a contrast agent for myelography is reported in two groups of horses. Group 1 (n = 6) were used only for myelography and to assess the clinical and pathological effects of intrathecal administration of iohexol. A volume of 20 ml at a concentration of 300 or 350 mg iodine/ml gave satisfactory myelographic detail with no serious clinical or neurological side effects. Only a minimal inflammatory response could be demonstrated in cerebrospinal fluid at four and 14 days after injection. At post mortem examination 14 days after myelography there was no evidence of meningitis nor was any other pathological change detected. Group 2 (n = 19) comprised a series of clinical cases of suspected cervical vertebral malformation. The only untoward sequelae recorded involved two horses in which iohexol was diluted with sterile water prior in intrathecal injection. A progressive necrotising meningitis developed in both cases which necessitated euthanasia. It was concluded that the major advantages of iohexol for use in the horse were its diagnostic quality, safety and low cost.

Fucosidosis in an English springer spaniel presenting as a malabsorption syndrome.

A case of alpha-fucosidosis in a 2-year-old male English Springer Spaniel presented as a malabsorption syndrome without any clinical neurological abnormalities. The dog had a history of chronic weight loss, diarrhoea, mild anaemia, hypoproteinemia and reduced jejunal absorption of D-xylose. A diagnosis of fucosidosis with intestinal malabsorption was based on these findings, markedly reduced plasma fucosidase levels and the diffuse infiltration of the lamina propria and submucosa of the stomach, small intestine, Peyer's patches and mesenteric lymph nodes by macrophages with finely vacuolated cytoplasm. Cytoplasmic vacuolation was also a feature of cells of the pancreas, thryroid, parathyroid and adenohypophysis and the epithelia lining respiratory airways and the urogenital tract. Neurons of the autonomic plexuses of the gastrointestinal tract and the urinary bladder as well as those of the brain, spinal cord, spinal ganglia and retina were also vacuolated. The profound decrease in sigma-fucosidase activity in the brain, liver and kidney was accompanied by a marked increase in 6 other lysosomal enzymes, especially beta-n-acetyl glucosaminidase.

An unusual incidence of neurological disease affecting horses during a drought.

The clinical, pathological and epidemiological factors were investigated in 12 horses presenting with severe neurological signs. Although the cases involved differing central (n = 1), spinal cord (n = 4) and peripheral nerve (n = 7) deficits in a number of instances, there were similar pathological findings. The possibility of a unifying aetiological factor, such as a toxicosis, is discussed because of the pathological similarities and as the cases appeared during an unusually long dry period.

The effects of dietary T-2 toxin on acute herpes simplex virus type 1 infection in mice.

Young male white Swiss mice were fed control diet or diet supplemented with 20 or 10 parts per million (ppm) of T-2 toxin for two or three weeks. These mice then were inoculated with herpes simplex virus type 1 (HSV-1) (9.6 x 10(6) plaque forming units) intraperitoneally. To compare the effects of T-2 toxin against a known immunosuppressive drug, cyclophosphamide was injected intraperitoneally at 150 mg/kg, 24 hours after treatment with HSV-1, into mice fed the control diet. Mice were necropsied and tissues were collected for microscopic and virologic examination. White Swiss mice which consumed a daily diet containing 20 ppm of T-2 toxin for two or three weeks were highly susceptible to HSV-1 infection and 27 of 36 (75%) died as a result of extensive hepatic and adrenal necrosis. Although HSV-1 was isolated from livers and brains of mice fed 20 ppm of T-2 toxin for two or three weeks, there was little or no inflammatory response found in the adrenals, livers, spinal cords, brains, or ganglia. The necrotizing encephalomyelitis observed in control mice was absent. High levels of dietary T-2 toxin appeared to be more immunosuppressive than cyclophosphamide because only one mouse died after treatment with HSV-1 and cyclophosphamide. Mice treated with cyclophosphamide had changes in brain, spinal cord, spleens, thymus, and bone marrow which were similar to those fed 20 ppm of T-2 toxin and infected with HSV-1, however, liver lesions were much less severe. HSV-1-infected mice on a diet with 10 ppm T-2 toxin had lesions of intermediate severity when compared with HSV-1-infected mice fed a diet with 20 ppm T-2 toxin and HSV-1-infected mice on control diets. Necrosis was less extensive in the livers and adrenals. The infrequent isolation of virus from liver and brain was consistent with the lack of intranuclear inclusion bodies and a more marked inflammatory response. Ten ppm of dietary T-2 toxin only depressed bone marrow and splenic red pulp to a mild or moderate degree. This may have enhanced the necrotizing encephalomyelitis observed in mice killed on days 6 and 8 after HSV-1 infection. Liver lesions were mild and those of the adrenals were moderate in mice fed control diet. The rare isolation of HSV-1 from the liver and brain and the findings of a moderate to severe necrotizing encephalomyelitis in these mice was consistent with an essentially functional immune system.

Experimental T-2 toxicosis in sheep.

Lambs received T-2 toxin at a rate of 0.6 or 0.3 mg/kg body weight per day in a protein reduced diet for 21 days to study the immunological and pathological effects of T-2 toxin in sheep. Blood was collected before T-2 treatment and on days 7, 14 and 21 of the trial for hematological and biochemical examination and for the separation of peripheral blood lymphocytes for the mitogen assay. Myeloid:erythroid ratios were determined from sternal bone marrow samples taken a day before T-2 treatment began, on day 12 and at death (day 22). Lambs treated with 0.6 mg/kg body weight of T-2 toxin daily were leukopenic on day 7 and lymphopenic on days 7 and 14. Also, on day 7, the mitogenic responses of these lambs to the B-cell mitogen, lipopolysaccharide, were significantly depressed and prothrombin times were prolonged. At necropsy, lymphoid atrophy of mesenteric lymph nodes and spleens was most marked in lambs treated with 0.6 mg/kg body weight of T-2 toxin per day. To the authors' knowledge, this is the first report of leukopenia, lymphopenia and lymphoid depletion in ruminants fed T-2 toxin.

The effects of dietary T-2 toxin on the immunological function and herpes simplex reactivation in Swiss mice.

T-2 toxin, a trichothecene mycotoxin, is a potently cytotoxic and immunosuppressive secondary metabolite produced by Fusarium fungi. Young male white Swiss mice were fed a diet supplemented with T-2 toxin at levels of 5, 10, or 20 ppm, control diet ad libitum, or control diet at a restricted rate for 1, 2, 3, 4, and 6 weeks. The effect of the toxin on the immune system of these mice was assessed by counting total spleen cell numbers and the in vitro proliferative response of spleen cells from these mice to the polyclonal mitogens, concanavalin A (Con A), and lipopolysaccharide (LPS). Body weight gains were also measured. Initially, the ingestion of T-2 toxin and restricted diet depressed total spleen cell counts, but after 3 weeks, only the spleen cell counts of mice fed 20 ppm of T-2 toxin were significantly lower. Consumption of 20 ppm of T-2 toxin by mice for 1 to 4 weeks depressed the spleen proliferative responses to the T-cell mitogen Con A; however, the response to LPS, a B-cell mitogen, was depressed in mice fed 10 and 20 ppm of T-2 toxin as well as in mice fed a control diet at a restricted rate. In order to determine whether T-2 toxin could induce reactivation of herpes simplex virus type 1 (HSV-1), latency was established in the trigeminal ganglia of mice. Feeding of T-2 toxin at 5, 10, and 20 ppm levels for 3 or 6 weeks did not reactivate virus; however, treatment with liquid nitrogen and cyclophosphamide did reactivate virus. These results demonstrate that although T-2 can cause immunosuppression, this response is not sufficient to reactivate HSV-1.

Effect of infectious bovine rhinotracheitis virus infection of calves on cell populations recovered by lung lavage.

Calves were challenge exposed with infectious bovine rhinotracheitis (IBR) virus, and experiments were carried out to determine the presence of virus in the lungs, virus or viral antigen in alveolar macrophages, and alterations in immune functions of alveolar macrophages. In experiment 1, calves were challenge exposed intranasally with IBR virus. Although clinical signs of IBR occurred in all challenge-exposed calves, there was minimal evidence of virus or viral antigen in cells lavaged from their lungs, and macrophage Fc- and complement-receptor activities, phagocytic activity, and ability to mediate antibody-dependent cell cytotoxicity were unaltered. In experiment 2, calves were challenge exposed intranasally or by aerosol with IBR virus strains Colorado-1 and 108, and samples were collected 4 and 6 days after challenge exposure. Virus was isolated from the lungs, and pathologic lesions of greater severity occurred in those calves challenge exposed by aerosol. Less than 0.1% of lavaged cells from challenge-exposed calves produced infectious centers on susceptible cell monolayers. In 1 sample of lavaged cells, approximately 5% of the cells, mainly macrophages, had viral antigen in the cytoplasm, as detected by immunofluorescence. Because of the small proportion of macrophages that appeared to become infected after challenge exposure of calves with IBR virus, it is believed that the effect of IBR virus in predisposing calves to pneumonic pasteurellosis is an indirect, rather than a direct, manifestation of viral infection of macrophages.

Postanesthetic myonecrosis in horses.

Two horses died of massive myonecrosis following surgery. The hematological, biochemical and pathological changes are described and compared with those previously reported in the literature.

Experimental Eimeria bovis infection in calves: a histopathological study.

Eight male holstein calves, four to six weeks of age, were infected with 100,000 sporulated oocysts of a culture containing Eimeria bovis. The calves were injected with steroids on days 13, 14 and 15 and killed on days 16, 18, 19, 20, 21, 22, 24 and 26 postinfection. The lesions caused by experimental E. bovis infection in the small and large intestines are characterized by a diphtheritic typhilitis and colitis. Severe lesions were also seen in the last metre of the ileum in a calf killed 19 days after infection. Most of the damage of the intestinal mucosa is caused by the sexual stages. There is destruction and loss of epithelial cells with subsequent exposure of lamina propria and formation of diphtheritic membranes.

Mycobacterium intracellulare infection in a water monitor.

Mycobacteriosis caused by Mycobacterium intracellulare serotypes Davis (8) and Altman (18) is described in a water monitor (Varanus semiremex). Infection with this of organism has not been reported previously in reptiles in Australia.

Pulmonary lesions induced by Pasteurella hemolytica in cattle.

Twelve four month old calves were inoculated intratracheally with a large dose of Pasteurella hemolytica and the lungs examined 18 hours, three days and seven days later. The gross and microscopic lesions were graded in each calf. The most extensive gross lesions were present at three days and were characteristic of a fibrinous pneumonia. Discrete areas of coagulation necrosis were present at three days and granulation tissue had formed around these by seven days. Characteristic swirly dark cells accumulated in alveoli and alveolar ducts and were observed from three days onwards. The gross and microscopic lesions were similar to those seen in field cases of pneumonic pasteurellosis.