Suspected acute myopathy of pigs

Following sudden exposure to extreme cold, a group of 15-week-old pigs exhibited strange nervous signs which included arching the back, a high stepping gait, violent tremors of the whole body and screaming. The animals lowered themselves and once sitting, the tremors and screaming stopped. But if forced to rise, these signs recurred. When the pigs returned to a warmer environment, they rapidly recovered. An acute clinical myopathy caused by a marginal vitamin E deficiency was suspected. Other stress-induced factors, such as circulatory collapse caused by movement from a warm to a cold environment, were also thought to have contributed towards the myopathy.     

Inherited myopathy of great Danes

A hereditary, non-inflammatory myopathy occurring in young great Danes with distinctive histological features in muscle biopsy specimens is reviewed. Onset of clinical signs is usually before one year of age and both sexes are affected. Clinical signs are characterised by exercise intolerance, muscle wasting, and an exercise-induced tremor. Although most affected dogs have a severe form of the disease, occasional dogs may have a less pronounced form and survive into adulthood with an acceptable quality of life. Litters containing affected puppies are born to clinically unaffected parents, and an autosomal recessive pattern of inheritance is likely. All recorded cases have had fawn or brindle coat coloration. Elevated serum creatinine kinase concentrations and spontaneous electrical activity in skeletal muscles are frequently found. While originally reported (Targett and others 1994) as a central core myopathy in this breed, the histochemical characteristics of the distinct cytoarchitectural structures differ from those of the well-characterised central core myopathy in human beings. In fact, these structures differ from any known myopathy in human beings and likely represents a unique non-inflammatory myopathy affecting dogs. Until this myopathy is characterised further, the name inherited myopathy in great Danes is suggested.     

Nutritional myopathy in goats

A nutritional myopathy in unweaned fibre goats aged 2 to 4 mths is described in 3 flocks from the tablelands of New South Wales. Clinically affected animals were illthrifty and in circulatory failure prior to being found dead. At necropsy, there was pronounced ascites, pulmonary congestion and marked mottling of the liver. Chalky white streaks and patches were obvious in the myocardium, particularly in the right ventricular wall. Skeletal muscles varied from grossly normal to generally pale. Histologically, the myocardium exhibited areas of severe acute myonecrosis with mineralisation and adjoining areas of phagocytosis and fibrosis. In 2 of 3 flocks, some skeletal muscles showed a mild subacute myopathy. Marked hepatic congestion extended to periacinar haemorrhage and necrosis in some areas. Dietary imbalances of selenium, vitamin E and polyunsatured fatty acids were probable factors in the pathogenesis of the condition.     

Hypokalaemic myopathy in Burmese kittens

AIM: To describe the microscopic and immunohistochemical findings in a case of pulmonary hyalohyphomycosis in a Kemp's ridley sea turtle (Lepidochelys kempi).

METHODS: Samples of lung, liver and kidney from a stranded, dead Kemp's ridley sea turtle were routinely processed for histopathological studies. Two monoclonal antibodies that reacted specifically with antigens of Aspergillus spp and the Mucorales (Zygomycetes) group, and a panel of polyclonal antibodies raised against Aspergillus fumigatus, Candida albicans, Geotrichum candidum, Fusarium solani, and Scedosporium apiospermum were used for immunohistochemical or immunofluorescence staining.

RESULTS: Histologically, a severe multifocal granulomatous pneumonia associated with fungal infection was diagnosed. All hyphae were identified as Fusarium spp because a strong and uniform reactivity was obtained only with a heterologously-absorbed polyclonal antibody raised against somatic antigens of Fusarium solani.

CONCLUSIONS: Fusarium spp should be included in the differential diagnosis of mycotic pneumonia in Kemp's ridley sea turtles.

CLINICAL RELEVANCE: This is the first report of a pulmonary mycotic infection in a sea turtle diagnosed using immunohistochemistry. Wildlife rehabilitators and pathologists should be aware of the availability of immunohistochemical techniques for identifying fungi in sea turtles.     

Genetic aspects of Labrador Retriever myopathy

Labrador Retriever myopathy (LRM) has become a relatively common muscular disease. The objective of our prospective study was to determine by segregation analyses a plausible mode of inheritance within a Labrador Retriever population. Therefore we performed neurological examinations, as well as electromyographic and histopathological evaluations of 58 closely related dogs. Seven dogs with an average age of 27.8 months had clinical signs consistent with LRM including exercise intolerance or fatigue. The diagnosis was based on neurological deficits and confirmed by histopathological results of muscle biopsy. We found in all cases obvious differences in fiber calibre size associated with texture disturbances. In addition, we found 41 clinically normal dogs with histological findings consistent with LRM. Three genetic models, the major gene, the mixed inheritance as well as the environmental model, were evaluated by segregation analyses. They were applied to an extended pedigree including 164 non-randomly ascertained related Labradors. According to phenotype the clinically examined dogs were divided into two different data sets. One data set distinguished between clinically normal and abnormal dogs, the second data set between histopathologically normal and abnormal dogs. We concluded that the clinical form of LRM is transmitted by a major gene and controlled by an autosomal recessive mode of inheritance. Furthermore, for expression of the subclinical form an additional gene or an environmental factor is responsible. Our findings suggest that LRM is similar to limb-girdle muscular dystrophy in man and therefore, may be used in the future as an animal model.     

Hereditary myopathy of Devon rex cats

Six closely related Devon rex cats afflicted with a congenital muscle disease were investigated over a three-year period. Physical findings included passive ventroflexion of the head and neck, dorsal protrusion of the scapulae, megaoesophagus, generalised appendicular weakness and fatigability. Signs became evident at three to 23 weeks of age and then usually progressed slowly or remained static. Plasma levels of creatine kinase and aspartate aminotransferase were not elevated. Histological examination of tissues from affected cats showed changes indicative of a primary myopathy, with neither nerve nor spinal cord involvement. Four of the six cats died suddenly of laryngospasm after obstruction of the pharynx or larynx with food.     

Thermopsis montana-induced myopathy in calves

Six heifer calves were administered the dried and ground whole plant of Thermopsis montana by gavage once daily for 2 to 4 days at an initial dosage rate of 1 g/kg of body weight. Two of the 6 heifers died after the second dose, and the remaining 4 calves were humanely killed and their tissues were examined. Serum creatine kinase and aspartate transaminase activities were significantly (P less than 0.05) increased after initiation of plant administration. All calves had skeletal muscular degeneration or evidence of regeneration and repair of damaged myofibers in all skeletal muscle groups examined. Myoglobinuria and cardiac muscle degeneration were not detected in any of the calves.     

Atypical myopathy in 2 Bactrian camels

Atypical myopathy (AM) is an acute seasonal rhabdomyolysis seen primarily in equids, caused by the ingestion of sycamore maple samaras containing hypoglycin A (HGA) and methylenecyclopropyl-glycine (MCPG). Toxic metabolites inhibit acyl-CoA dehydrogenases and enoyl-CoA hydratases, causing selective hyaline degeneration of type I muscle fibers. Two zoo-kept Bactrian camels (Camelus bactrianus) with a fatal course of AM had sudden onset of muscle pain and weakness, recumbency, and dysphagia, accompanied by increased serum creatine kinase activity and detection in serum of HGA, MCPG, and metabolites. Medical treatment was ineffective. At postmortem examination, sycamore maple tree material was found within the first gastric compartment of the 2-y-old gelding. Although musculature was macroscopically normal, histologically, monophasic hyaline degeneration was marked within type I fibers of intercostal and hypoglossal muscles of the gelding, and in neck, tongue, and masticatory muscles of the cow. The ingestion of sycamore maple material can cause AM in Bactrian camels, and trees of the Sapindaceae family should be avoided in enclosures.