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.     

Clinical Phenotype of X‐Linked Myotubular Myopathy in Labrador Retriever Puppies

Background

Seven male Labrador Retriever puppies from 3 different litters, born to clinically normal dams and sires, were evaluated for progressive weakness and muscle atrophy. Muscle biopsies identified a congenital myopathy with pathologic features consistent with myotubular myopathy. Further investigations identified a pathogenic mutation in the myotubularin gene, confirming that these puppies had X‐linked myotubular myopathy (XLMTM).

Objective

To review the clinical phenotype, electrodiagnostic and laboratory features of XLMTM in this cohort of Labrador Retrievers.

Results

Male puppies with XLMTM were small and thin compared with their normal littermates. Generalized weakness and muscle atrophy were present by 7 weeks of age in some puppies and evident to most owners by 14 weeks of age. Affected puppies stood with an arched spine and low head carriage, and walked with a short, choppy stride. Muscle atrophy was severe and progressive. Patellar reflexes were absent. Laryngeal and esophageal dysfunction, and weakness of the masticatory muscles occurred in puppies surviving beyond 4 months of age. Serum creatine kinase activity was normal or only mildly increased. EMG findings were nonspecific and included positive sharp waves and fibrillation potentials. Clinical signs progressed rapidly, with most affected puppies unable to walk within 3–4 weeks after clinical signs were first noticed.

Conclusions and Clinical Importance

Although initial clinical signs of XLMTM are similar to the phenotypically milder centronuclear myopathy in Labrador Retrievers, XLMTM is a rapidly progressive and fatal myopathy. Clinicians should be aware of these 2 distinct myopathies with similar clinical presentations in the Labrador retriever breed.     

Cardiac Troponin I as Compared to Troponin T for the Detection of Myocardial Damage in Horses

Background

Different cardiac troponin I (cTnI) assays give different results. Only 1 manufacturer has marketed troponin T (cTnT) assays. Therefore, cTnT often is preferred for detection of myocardial infarction in human patients. Studies of cTnT in horses are limited.

Objectives

To compare a cTnI and a high‐sensitive cTnT assay (hs‐cTnT) in horses.

Animals

Cardiac troponin I and cTnT were determined in 35 healthy horses (group 1), 23 horses suspected to have primary myocardial damage (group 2a), and 41 horses with secondary myocardial damage caused by structural heart disease (group 2b).

Methods

All cTnI samples were analyzed at laboratory A (limit of detection [LOD]: 0.03 ng/mL), whereas cTnT samples were analyzed at 2 laboratories with the same hs‐cTnT assay (laboratory B, LOD: 10.0 pg/mL; laboratory C, LOD: 4.0 pg/mL).

Results

The median cTnI concentration in group 2a (0.90 ng/mL; range, 0.03–58.27 ng/mL) was significantly higher (P < .001) than in group 1 (0.03 ng/mL; range, 0.03–0.09 ng/mL) or group 2b (0.05 ng/mL; range, 0.03–30.92 ng/mL), and the optimal cut‐off for detection of primary myocardial damage was 0.095 ng/mL (sensitivity: 90.5%, specificity: 100%). Using an LOD of 10.0 pg/mL for all cTnT samples, a cut‐off value of 10.5 pg/mL was found, but sensitivity was low (42.9%). When only samples analyzed at laboratory C (n = 58) were included, a cut‐off of 6.6 pg/mL was found (sensitivity: 81%, specificity: 100%).

Conclusions and Clinical Importance

Despite large quantitative differences, cTnI and cTnT are both useful for detection of myocardial damage in horses.     

拍翅运动诱发肉鸡胸深肌病的血清肌酸磷酸激酶（CPK）水平的变化

强迫ＡＡ肉鸡拍翅运动诱发胸深肌病并测定了诱发过程中试验鸡和对照鸡的血清肌酸磷酸激酶（ＣＰＫ）水平的变化。试验组鸡５天中共拍翅７次，有４／９例发生典型胸深肌病。病变特征为带有绿色坏死区的坏死性肌炎。对照组鸡不拍翅，不发生胸肌坏死。血清ＣＰＫ水平测定表明，试验组ＣＰＫ水平在拍翅后２４小时升高并维持四天，直到实验结束，与对照组保持极显著差异，说明ＣＰＫ是鸡运动应激有实用意义的血清酶指标，测定时间宜在运动后２４小时进行，与猪应激后的情况相似。在试验组内，ＣＰＫ水平仅在０—２天，０—３天，１—２天，１—３天对比组合之间有极显著差异，进一步说明运动应激后２４小时，４８小时之内为测定ＣＰＫ的可选择时间。但发病鸡与不发病鸡的ＣＰＫ水平无显著差异，说明ＣＰＫ水平虽能指示运动应激，却不能揭示胸肌病的发生，对其原因作了简要讨论。     

Detection of hypoglycin A in the seeds of sycamore (Acer pseudoplatanus) and box elder (A. negundo) in New Zealand; the toxin associated with cases of equine atypical myopathy

CASE HISTORY AND CLINICAL FINDINGS: During April and May 2014 four horses aged between 5 months and 9 years, located in the Canterbury, Marlborough and Southland regions, presented with a variety of clinical signs including recumbency, stiffness, lethargy, dehydration, depression, and myoglobinuria suggestive of acute muscle damage. Two horses were subjected to euthanasia and two recovered. In all cases seeds of sycamore maple (Acer pseudoplatanus) or box elder (A. negundo) were present in the area where the horse had been grazing.

LABORATORY INVESTIGATION: The samaras (seeds) of some Acer spp. may contain hypoglycin A, that has been associated with cases of atypical myopathy in Europe and North America. To determine if hypoglycin A is present in the samaras of Acer spp. in New Zealand, samples were collected from trees throughout the country that were associated with historical and/or current cases of atypical myopathy, and analysed for hypoglycin A. Serum samples from the four cases and four unaffected horses were analysed for the presence of hypoglycin A, profiles of acylcarnitines (the definitive diagnosis for atypical myopathy) and activities of creatine kinase and aspartate aminotransferase.Markedly elevated serum activities of creatine kinase and aspartate aminotransferase, and increased concentrations of selected acylcarnitines were found in the case horses. Hypoglycin A was detected in the serum of those horses but not in the healthy controls. Hypoglycin A was detected in 10/15 samples of samaras from sycamore maple and box elder from throughout New Zealand.

DIAGNOSIS: Cases of atypical myopathy were diagnosed on properties where samaras containing hypoglycin A were also found.

CLINICAL RELEVANCE: Sycamore and box elder trees in New Zealand are a source of hypoglycin A associated with the development of atypical myopathy. If pastured horses present with clinical and biochemical signs of severe muscle damage then the environment should be checked for the presence of these trees. Horses should be prevented from grazing samaras from Acer spp. in the autumn.     

Neuromyotonia in a horse

This article describes the clinical and electromyographic findings of neuromyotonia in a 19‐month‐old male crossbred Quarter Horse that presented with stiffness and muscle asymmetry in the hind limbs as well as sacrococcygeal, paravertebral, and gluteal myokymia. An electromyographic study showed spontaneous continuous muscle fiber activity with high‐frequency discharges, fibrillations, positive sharp waves, fasciculation potentials, and complex repetitive discharges. Histological examination of the gluteal muscle showed a mixed neurogenic and myopathic pattern. The findings are consistent with neuromyotonia.     

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.     

Effect of dietary starch, fat, and bicarbonate content on exercise responses and serum creatine kinase activity in equine recurrent exertional rhabdomyolysis

To determine the effect of dietary starch, bicarbonate, and fat content on metabolic responses and serum creatine kinase (CK) activity in exercising Thoroughbreds with recurrent exertional rhabdomyolysis (RER), 5 RER horses were fed 3 isocaloric diets (28.8 Mcal/d [120.5 MJ/d]) for 3 weeks in a crossover design and exercised for 30 minutes on a treadmill 5 days/wk. On the last day of each diet, an incremental standardized exercise test (SET) was performed. The starch diet contained 40% digestible energy (DE) as starch and 5% as fat: the bicarbonate-starch diet was identical but was supplemented with sodium bicarbonate (4.2% of the pellet): and the fat diet provided 7% DE as starch and 20% as fat. Serum CK activity before the SET was similar among the diets. Serum CK activity (log transformed) after submaximal exercise differed dramatically among the diets and was greatest on the bicarbonate-starch diet (6.51 +/- 1.5) and lowest on the fat diet (5.71 +/- 0.6). Appreciable differences were observed in the severity of RER among individual horses. Postexercise plasma pH, bicarbonate concentration, and lactate concentration did not differ among the diets. Resting heart rates before the SET were markedly lower on the fat diet than on the starch diet. Muscle lactate and glycogen concentrations before and after the SET did not differ markedly among the diets. A high-fat, low-starch diet results in dramatically lower postexercise CK activity in severely affected RER horses than does a low-fat, high-starch diet without measurably altering muscle lactate and glycogen concentrations. Dietary bicarbonate supplementation at the concentration administered in this study did not prevent increased serum CK activity on a high-starch diet.     

Survival time with pacemaker implantation for dogs diagnosed with persistent atrial standstill

Objectives

To evaluate survival time in dogs with persistent atrial standstill after pacemaker implantation and to compare the survival times for cardiac-related vs. non-cardiac deaths. Secondary objectives were to evaluate the effects of breed and the presence of congestive heart failure (CHF) at the time of diagnosis on survival time.