Three cases of a presumptive atypical myopathy in New Zealand horses

CASE HISTORY: Three weanling Thoroughbred fillies were presented during autumn with depression, muscle rigidity and, in one case, colic symptoms and cardiovascular shock.

CLINICAL FINDINGS: All fillies had abnormal physical examinations that included elevated heart rates and respiratory rates coupled with muscle rigidity through the back and rump. Biochemistry revealed markedly elevated creatinine kinase and aspartate aminotransferase which indicated a myopathy.

DIAGNOSIS AND TREATMENT: All three horses were diagnosed with presumptive equine atypical myopathy. The horses received supportive therapy as per the literature available at the time regarding this condition; two responded to supportive therapy and survived, and one was euthanased due to a rapid deterioration in clinical status.

PATHOLOGICAL FINDINGS: Following post mortem of one case, histology of the trapezius muscle demonstrated an acute, severe myofibre degeneration.

CLINICAL RELEVANCE: Atypical myopathy and a very similar disorder termed seasonal pasture myopathy in North America are potentially fatal, pasture-related syndromes that have been described in Europe and America but have not been previously described in New Zealand. This report describes three presumptive cases of this unique syndrome in New Zealand for the first time; it outlines the characteristics of the condition; and includes recently published information regarding diagnosis and treatment.     

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.     

European outbreaks of atypical myopathy in grazing equids (2006-2009): spatiotemporal distribution, history and clinical features

Reasons for performing study: Improved understanding of the epidemiology of atypical myopathy (AM) will help to define the environmental factors that permit or support the causal agent(s) to exert toxicity. Objectives: This European survey of AM aimed to describe spatiotemporal distribution, survival, clinical signs, circumstances in which AM develops and its different expressions between countries and over time. Methods: The spatiotemporal distribution, history and clinical features of AM cases reported to the Atypical Myopathy Alert Group from 2006 to 2009 were described. Comparisons of data from the most severely affected countries and from the large outbreaks were made with Fisher's exact and Welch's tests with Bonferroni correction. Results: Of 600 suspected cases, 354 met the diagnostic criteria for confirmed or highly probable AM. The largest outbreaks occurred during the autumns of 2006 and 2009 in Belgium, France and Germany. For the first time, donkeys, zebras and old horses were affected, and clinical signs such as gastrointestinal impaction, diarrhoea, penile prolapse, buccal ulceration and renal dysfunction were observed. Affected horses spent >6 h/day on pastures that almost always contained or were surrounded by trees. The latency period was estimated at up to 4 days. Overall survival rate was 26%. Although differences between countries in affected breeds, body condition, horse management and pasture characteristics were recognised, the common presenting clinical signs and mortality were similar between countries. Conclusions and potential relevance: This study describes new data on case details, history and clinical course of AM that is of preventive, diagnostic and therapeutic value. However, the true impact of the findings of this study on the development of or severity of AM should be tested with case–control studies.     

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.