European outbreak of atypical myopathy in the autumn 2009

Background – Atypical myopathy is an acute, severe rhabdomyolysis occurring in grazing horses. In the beginning of October 2009, a new outbreak occurred in several European countries. Geographic, demographic and clinical data of the reported cases in the month October 2009 are described. Key Findings – The survival rate in this outbreak was 25%. The most frequently observed clinical signs were congested mucous membranes, dyspnea, tachycardia, depression, weakness, stiffness, recumbency, trembling, sweating, and myoglobinuria. Nonsurvivors were significantly more likely to be recumbent than survivors. Prognostic factors, symptomatic treatment, and preventive measures are discussed. Significance – Differences were encountered during the described outbreak of atypical myopathy in October 2009 compared with previous outbreaks reported. Equine practitioners should be aware that previous epidemiological studies have shown that after a high prevalence in the autumn, new cases are likely to occur in the following spring.     

Equine atypical myopathy: a review

Atypical myopathy (AM) is an acute rhabdomyolysis syndrome that occurs at irregular intervals in grazing equines. An increasing number of outbreaks have been reported in recent years, including some from countries where the disease has not previously been diagnosed. In this review, clinical and other details of outbreaks of AM are analysed to better define its epidemiological profile. Potential aetiologies are discussed, the short clinical course of AM is described and the main biochemical and pathological findings are considered. Recommendations for medical management are suggested, based on a review of clinical reports. Biochemical and histopathological findings have been integrated in order to characterise the physiopathology of AM. There is an ongoing requirement to record new cases of this syndrome, ideally through an epidemiological network.     

Concurrent atypical myopathy and equine dysautonomia in two horses

This report concerns 2 horses that suffered typical clinical signs of atypical myopathy (AM) and equine grass sickness (EGS) concurrently. Clinical details and pathological lesions of the cases are described. EGS and AM are relatively rare diseases and the concurrency of the diseases in the same animals is therefore considered unlikely to be a coincidence. However, it is not suggested that the evidence shows a common aetiology but rather the existence of common predisposing causes.     

Morphological alterations in oxidative muscles and mitochondrial structure associated with equine atypical myopathy

REASONS FOR PERFORMING STUDY: There is a lack of well documented studies about muscular lesions in equine atypical myopathy (EAM). OBJECTIVES: To characterise morphopathological changes of striated muscles and myocardium, to progress understanding of this disease. METHODS: Thirty-two horses age 0.5-7 years kept on pasture were referred for a sudden ataxia/myoglobinuria syndrome. Clinical examination (stiffness, muscle pain, muscle fasciculations, abnormal gait, recumbency, myoglobinuria, tachycardia, sweating) and plasma CPK, LDH and AST levels were consistent with extensive myonecrosis and, together with anamnestic data, with so-called 'equine atypical myopathy' (EAM), a disease of unknown aetiology reported since 1939. Macroscopic and microscopic (histology, histoenzymology, ultrastructure) lesions were evaluated. RESULTS: Necropsic examination revealed large areas of muscle necrosis, the extent and severity of which varied between cases and muscles, but which were clearly more constant and severe in respiratory and postural muscles and in the myocardium. Histology highlighted a multifocal and monophasic process compatible with Zenker degeneration/necrosis that mostly and segmentally affected type 1 fibres. Histochemical evaluation revealed a weak and disorganised pattern of NADH tetrazolium reductase staining, the absence of calcium salts precipitates and a dramatic accumulation of lipid droplets. Ultrastructural examination often revealed fibres of which the sole modifications were altered mitochondria and sarcoplasmic lipidosis. CONCLUSIONS: Taken together, the data suggest that a primary alteration of mitochondria should be considered, although secondary mitochondrial abnormalities have yet to be ruled out. POTENTIAL RELEVANCE: The morphological features gathered here reveal that EAM shares most of the characteristics of toxic myopathies.     

Analysing hypoglycin A,methylenecyclopropylacetic acid conjugates and acylcarnitines in blood to confirm the diagnosis and improve our understanding of atypical myopathy

Owing to recent methodological validation studies, we have now the opportunity to determine hypoglycin A, methylenecyclopropylacetic acid–carnitine and acylcarnitines concentrations in equine serum. These analytes are essential to confirm the diagnosis of atypical myopathy but also to improve our understanding of the pathophysiology of the disease. In particular, they might help elucidate why some horses seem more resistant to hypoglycin A poisoning.     

Biochemical and genetic evaluation of the role of AMP-activated protein kinase in polysaccharide storage myopathy in Quarter Horses

OBJECTIVE: To evaluate whether biochemical or genetic alterations in AMP-activated protein kinase (AMPK) play a role in the development of polysaccharide storage myopathy (PSSM) in Quarter Horses. ANIMALS: 30 PSSM-affected and 30 unaffected (control) Quarter Horses. PROCEDURES: By use of an established peptide phosphotransfer assay, basal and maximal AMPK activities were measured in muscle biopsy samples obtained from 6 PSSM-affected and 6 control horses. In 24 PSSM-affected and 24 control horses, microsatellite markers identified from the chromosomal locations of all 7 AMPK subunit genes were genotyped with a fluorescent DNA fragment analyzer. Alleles of 2 of the AMPK gamma subunit genes were genotyped via DNA sequencing. Allele frequencies of DNA markers in or near the AMPK subunit genes were measured in isolated genomic DNA. RESULTS: No differences in basal or maximal muscle AMPK enzyme activities between PSSM-affected and control horses were detected. There were also no differences in allele frequencies for microsatellite markers near any of the 7 AMPK subunit genes between the 2 groups. Furthermore, previously known and newly identified alleles of 2 equine AMPK gamma subunit genes were also not associated with PSSM. CONCLUSIONS AND CLINICAL RELEVANCE: These results have provided no evidence to indicate that AMPK plays a causative role in PSSM in American Quarter Horses.     

Predictive value of hypoglycin A and methylencyclopropylacetic acid conjugates in a horse with atypical myopathy in comparison to its cograzing partners

Hypoglycin A (HGA) was detected in blood and urine of a horse suffering from atypical myopathy (AM; Day 2, serum, 8290 μg/l; urine: Day 1, 574, Day 2, 742 μg/l) and in its cograzing partners with a high variability (46–1570 μg/l serum). Over the period of disease, the level of the toxic metabolites (methylencyclopropylacetic acid [MCPA]‐conjugates) increased in body fluids of the AM horse (MCPA‐carnitine: Day 2, 0.246, Day 3, 0.581 μmol/l serum; MCPA‐carnitine: Day 2, 0.621, Day 3, 0.884 μmol/mmol creatinine in urine) and HGA decreased rapidly (Day 3, 2430 μg/l serum). In cograzing horses MCPA‐conjugates were not detected. HGA in seeds ranged from 268 to 367 μg/g. Although HGA was present in body fluids of healthy cograzing horses, MCPA‐conjugates were not detectable, in contrast to the AM horse. Therefore, increasing concentrations of MCPA‐conjugates are supposed to be linked with the onset of AM and both parameters seem to indicate the clinical stage of disease. However, detection of HGA in body fluids of cograzing horses might be a promising step in preventing the disease.     

Mycobacterium fortuitum pneumonia in a cat and the role of lipid in the pathogenesis of atypical mycobacterial infections

Mycobacterium fortuitum is a saprophytic, fast-growing, nontuberculous, and nonlepromatous mycobacterium that can cause infections in animals and humans. In dogs and cats, it is one of the most common agents of ulcerative dermatitides and panniculitides caused by atypical mycobacteria. In humans, it is frequently found in lipoid pneumonias or contaminated surgical sites. We report a cat with granulomatous pneumonia caused by M fortuitum resembling lipoid pneumonia in humans. The similarity between the histopathology of the lung and skin lesions caused by this organism in dogs and cats is emphasized. We discuss the role of lipids in the pathogenesis of mycobacterioses and suggest an association between atypical mycobacteria and lipid-rich environments. We conclude that M fortuitum should be included as a differential in cases of lipid-rich pneumonias that do not respond to common antibiotics.     

European outbreaks of atypical myopathy in grazing horses (2006-2009): determination of indicators for risk and prognostic factors

Reasons for performing study: Appropriate management of atypical myopathy (AM) requires the establishment of an accurate diagnosis and prognosis. Furthermore, preventive measures to avoid AM need to be refined. Objectives: The aims of the study were as follows: 1) to improve the diagnosis of AM; 2) to identify prognostic predictors; and 3) to refine recommended preventive measures based on indicators of risk factors. Methods: An exploratory analysis of cases in Europe between 2006 and 2009 reported to the Atypical Myopathy Alert Group was conducted. Based on clinical data, reported cases were allocated into 2 groups: confirmed or highly probable AM (AM group; further divided into survivors and nonsurvivors); and cases with a low probability of having AM or with another final diagnosis (non‐AM group). Using Welch's test and odds ratios corrected for multiple comparisons, the AM vs. non‐AM groups were compared to identify indicators for diagnosis and risk factors, and survivors vs. nonsurvivors in the AM group were compared to identify prognostic factors. Sensitivity, specificity and positive and negative predictive values were calculated for specific clinical signs related to final diagnosis and outcome. Results: From 600 reported cases, 354 AM cases (survival rate of 26%) and 69 non‐AM cases were identified, while there were insufficient data to categorise the remainder. Variables valuable for diagnosing AM compared with similar diseases were as follows: presence of dead leaves and wood and/or trees on pastures; sloping pastures; full‐time pasture access; no food supplementation; normal body condition; pigmenturia; normothermia; and congested mucous membranes. Nonsurvival was associated with recumbency, sweating, anorexia, dyspnoea, tachypnoea and/or tachycardia. Survival was associated with remaining standing most of the time, normothermia, normal mucous membranes, defaecation and vitamin and antioxidant therapy. Conclusions and potential relevance: This study refines the list of risk factors for AM. Clinical signs valuable for diagnosis and prognosis have been identified, enabling clinicians to improve management of AM cases.     

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.     

蜂蜜酒澄清机理研究

用魔芋精粉作为蜂蜜酒的澄清剂,其作用明显优于其他的澄清剂。魔芋精粉在溶液中形成网状结构,蛋白质分子和杂质被吸附在网膜上,从而使蜂蜜酒得到澄清。     

Fibrotic myopathy of the semitendinosus muscle in a cat

Fibrotic myopathy of the semitendinosus muscle causing a progressive mechanical right hind limb lameness in a cat was treated with a Z-plasty lengthening procedure of the affected muscle. Lameness resolved after surgery; however, recurrence of gait abnormality began 2 weeks later. One year after surgery, the cat's gait was abnormal; this had little effect on ambulation. Histologic examination of biopsy specimens taken from the affected muscle at surgery revealed complete replacement of myofibers with dense fibrous connective tissue. Etiopathogenesis was not determined.