Muscular dystrophy in dogs: does the crossing of breeds influence disease phenotype?

Golden Retriever (GR) muscular dystrophy is an inherited degenerative muscle disease that provides an excellent model for Duchenne muscular dystrophy in humans. This study defined the histopathologic lesions, including the distribution of type I and II muscle fibers (FTI and FTII), in 12 dystrophic and 3 nondystrophic dogs between 7 and 15 months of age. The authors were interested in studying the influence on disease phenotype from crossing the base GR breed with Yellow Labrador Retrievers. The dystrophic dogs were divided according to breed: GRs and Golden Labrador Retrievers (GLRs). On hematoxylin and eosin staining, histopathologic lesions were more severe in GRs than GLRs. Six of eight GR muscles (75%) had a severe lesion grade (grade 3). In contrast, seven GLR muscles (87.5%) had mild lesions (grade 2), and only one had severe lesions (grade 3). Changes in fiber-type distribution were more pronounced in GRs versus GLRs. FTI:FTII ratio inversion was observed in three dystrophic GRs but only one GLR. The mean diameter of FTI and FTII was smaller in GRs and GLRs than in nondystrophic dogs (P < .01). The FTI of five GR muscles (62.5%) were larger than those of GLRs, whereas only one GLR muscle was larger (P < .05). The differential was less pronounced for FTII, with four GR muscles being larger and three GLR being larger. Observations indicate that crossing the base GR breed with Labrador Retrievers lessened the severity of the GR muscular dystrophy phenotype.

Effects of glycosaminoglycan polysulphate on the organisation of collagen fibres in experimentally induced tendonitis in horses.

An inflammatory process was induced by intratendinous injection of bacterial collagenase into the superficial digital flexor tendon (SDFT) of the left thoracic limb of 10 horses. One week later, the tendons in five of the horses (group 1) were treated with glycosaminoglycan polysulphate (GAGPS), and the tendons of the other five (group 2) were treated with saline solution. The horses were euthanased 150 days after the collagenase injections, and samples of the SDFTs were frozen at -14 degrees C, sectioned at 5 to 7 mum longitudinally and transversely, and stained by the picrosirius red method. Morphometric analysis was used to quantify the organised and disorganised bundles of collagen in the samples from groups 1 and 2. Significantly more organised bundles of collagen were observed in the tendons treated with GAGPS.

Renal involvement in visceral leishmaniasis dogs

Visceral leishmaniasis (VL) is a zoonosis that affects both animals and man. Dogs are the etiological agent’s main reservoir. The aim of this study was to evaluate the clinical laboratory aspects and renal histopathology of VL dogs. Thirty-four symptomatic (case) and 17 asymptomatic (control) VL seropositive dogs of different breeds, sexes, and ages from Teresina, Piauí State, Brazil, were used. Diagnosis was confirmed by enzyme-linked immunosorbent assay and indirect immunofluorescence test. Clinical and laboratory tests included blood cell count and renal function analysis (urea and creatinine). Animals were subjected to euthanasia and necropsy. Renal fragments were prepared by the usual histological techniques and stained with hematoxylin-eosin and periodic acid-Schiff. Physical examination showed that lymph node hypertrophy (85.29%) and skin lesions (35.29%) were frequent in the case group. Anemia was found in 55.88% of the case and in 11.76% of the control group. There was a significant difference between groups by Fisher’s exact test. Two case-group dogs showed azotemia. Renal histopathological evaluation showed that 61.76% case and 17.65% control-group dogs had membranoproliferative glomerulonephritis. Mesangial proliferative glomerulonephritis was seen in 32.35% case and 64.70% control-group animals. There was a significant difference for both types of glomerulonephritis between groups. Amastigote forms of Leishmania were found in the renal parenchyma, in the inflammatory infiltrate of one case-group dog. We concluded that, in canine VL, regardless of the clinical signs at physical examination, the kidneys are frequently compromised