J. D. Baird

Insulin sensitivity in Belgian horses with polysaccharide storage myopathy

OBJECTIVE To determine insulin sensitivity, proportions of muscle fiber types, and activities of glycogenolytic and glycolytic enzymes in Belgians with and without polysaccharide storage myopathy (PSSM). ANIMALS 10 Quarter Horses (QHs) and 103 Belgians in which PSSM status had been determined. PROCEDURES To determine insulin sensitivity, a hyperinsulinemic euglycemic clamp (HEC) technique was used in 5 Belgians with PSSM and 5 Belgians without PSSM. Insulin was infused i.v. at 3 mU/min/kg for 3 hours, and concentrations of blood glucose and plasma insulin were determined throughout. An i.v. infusion of glucose was administered to maintain blood glucose concentration at 100 mg/dL. Activities of glycogenolytic and glycolytic enzymes were assessed in snap-frozen biopsy specimens of gluteus medius muscle obtained from 4 Belgians with PSSM and 5 Belgians without PSSM. Percentages of type 1, 2a, and 2b muscle fibers were determined via evaluation of >or= 250 muscle fibers in biopsy specimens obtained from each Belgian used in the aforementioned studies and from 10 QHs (5 with PSSM and 5 without PSSM). RESULTS Belgians with and without PSSM were not significantly different with respect to whole-body insulin sensitivity, muscle activities of glycogenolytic and glycolytic enzymes, or proportions of muscle fiber types. However, Belgians had an increased proportion of type 2a and decreased proportion of type 2b muscle fibers, compared with proportions in QHs, regardless of PSSM status. CONCLUSIONS AND CLINICAL RELEVANCE PSSM in Belgians may be attributable to excessive glycogen synthesis rather than decreased glycogen utilization or enhanced glucose uptake into muscle cells.

Presence of the glycogen synthase 1 (GYS1) mutation causing type 1 polysaccharide storage myopathy in continental European draught horse breeds

The purpose of this study was to determine which continental European draught horse breeds harbour a mutation in the glycogen synthase 1 gene (GYS1) that is known to be responsible for type 1 polysaccharide storage myopathy in quarter horses and North American draught horses. Of a non-random selection of continental European draught horses belonging to 13 breeds, 62 per cent (250 of 403) tested were found to carry the mutant allele. The horses were located in Belgium, France, Germany, the Netherlands, Spain and Sweden. The mutation was identified in animals from each of the breeds examined. In the breeds in which more than 15 animals were available for testing, the highest percentages of GYS1-positive horses were found in the Belgian trekpaard (92 per cent; 35 of 38 horses tested), Comtois (80 per cent; 70 of 88), Netherlands trekpaard (74 per cent; 17 of 23), Rheinisch-Deutsches kaltblut (68 per cent; 30 of 44) and Breton (64 per cent; 32 of 51).

Equid Herpesvirus 2-Associated Oral and Esophageal Ulceration in a Foal

A case of a 1-month-old Thoroughbred foal with dysphagia, salivation, pyrexia, oral mucosal pustules, and esophageal ulceration is reported. Swabs from the ulcerated lesions yielded Equid herpesvirus 2 (EHV-2) in virus isolation assays, and histopathology of a biopsy from the esophageal lesion identified nuclear inclusions suggestive of herpesviruses. Immunohistochemical staining with antibodies specific for EHV-2 was positive for epithelial cells in the vicinity of the ulcer but not in more distant mucosa. Electron microscopic evaluation of the biopsy showed herpesviral particles in epithelial cells. The foal recovered over 5 days of supportive and gastroprotective therapy, and the esophageal ulcers healed. Serology and immunohistochemistry indicated that this foal likely had lesions associated with EHV-2 and not EHV-1, −4, or −5.

An Ecotype of Neorickettsia risticii Causing Potomac Horse Fever in Canada

ABSTRACT Neorickettsia (formerly Ehrlichia) risticii is an obligatory intracellular bacterium of digenetic trematodes. When a horse accidentally ingests aquatic insects containing encysted trematodes infected with N. risticii, the bacterium is transmitted from trematodes to horse cells and causes an acute and often fatal disease called Potomac horse fever (PHF). Since the discovery of N. risticii in the United States in 1984, using immunofluorescence and PCR assays, PHF has been increasingly recognized throughout North America and South America. However, so far, there exist only a few stable N. risticii culture isolates, all of which are from horses within the United States, and the strain diversity and environmental spreading and distribution of pathogenic N. risticii strains remain poorly understood. This paper reports the isolation of N. risticii from the blood of a horse with acute PHF in Ontario, Canada. Intracellular N. risticii colonies were detected in P388D1 cells after 47 days of culturing and 8 days after the addition of rapamycin. Molecular phylogenetic analysis based on amino acid sequences of major surface proteins P51 and Ssa1 showed that this isolate is distinct from any previously sequenced strains but closely related to midwestern U.S. strains. This is the first Canadian strain cultured, and a new method was developed to reactivate dormant N. risticii to improve culture isolation. IMPORTANCE Neorickettsia risticii is an environmental bacterium that lives inside flukes that are parasitic to aquatic snails, insects, and bats. When a horse accidentally ingests insects harboring flukes infected with N. risticii, the bacterium is transmitted to the horse and causes an acute and often fatal disease called Potomac horse fever. Although the disease has been increasingly recognized throughout North and South America, N. risticii has not been cultured outside the United States. This paper reports the first Canadian strain cultured and a new method to effectively culture isolate N. risticii from the horse blood sample. Molecular analysis showed that the genotype of this Canadian strain is distinct from previously sequenced strains but closely related to midwestern U.S. strains. Culture isolation of N. risticii strains would confirm the geographic presence of pathogenic N. risticii, help elucidate N. risticii strain diversity and environmental spreading and distribution, and improve diagnosis and development of vaccines for this dreadful disease.

What is your diagnosis? Ascarid impactions.

A 3-month-old Thoroughbred filly weighing 225 kg (495 lb) was evaluated at the Ontario Veterinary College Teaching Hospital for acute respiratory distress and suspected pneumonia. On the morning of the evaluation, the foal was bright and alert and was observed grazing in the field. Late in the afternoon, the foal was found in lateral recumbency. The foal had signs of depression, was anorexic and tachypneic, and had increased intensity of lung sounds; the buccal mucous membranes were cyanotic. No treatment was given prior to referral. The foal had been administered an anthelmintic (an ivermectin product) at the labeled dose of 0.2 mg/kg (0.09 mg/lb) the previous day. On evaluation, the foal was in lateral recumbency, had signs of depression, and was reluctant to rise. On physical examination, the foal was tachypneic (88 breaths/min) and tachycardic (140 beats/min) and was clinically assessed to be severely dehydrated (> 10% fluid loss). The ventral aspect of the abdomen was bilaterally distended. Venous blood-gas analysis revealed severe acidosis (pH, 7.10; reference range, 7.35 to 7.45). Markedly high PCV (70%; reference range, 28% to 47%) and high-normal total solids concentration (70 g/L; reference range, 56 to 75 g/L) were also present. Transcutaneous ultrasonography of the ventral aspect of the abdomen was performed (Figure 1).