An unusual myopathy in a dog

A nine-month-old Cavalier King Charles Spaniel was examined because it could not withdraw its tongue into its mouth and had difficulty eating and drinking. These clinical signs were first observed when the dog was two months of age. On percussion of the tongue a dimple could be produced and there was electromyographic evidence of myotonia. Histological examination showed replacement of muscle fibres by adipose tissue, focal areas of myonecrosis, neutrophil infiltration and proliferation of sub-sarcolemmal nuclei. These changes were considered to be consistent with a primary myopathy similar to paramyotonia in man. No related dogs were found to be affected.     

An unusual myopathy in a dog

A nine-month-old Cavalier King Charles Spaniel was examined because it could not withdraw its tongue into its mouth and had difficulty eating and drinking. These clinical signs were first observed when the dog was two months of age. On percussion of the tongue a dimple could be produced and there was electromyographic evidence of myotonia. Histological examination showed replacement of muscle fibres by adipose tissue, focal areas of myonecrosis, neutrophil infiltration and proliferation of sub-sarcolemmal nuclei. These changes were considered to be consistent with a primary myopathy similar to paramyotonia in man. No related dogs were found to be affected.     

Centronuclear myopathy in a Border collie dog

A two‐year old, male entire Border collie was presented with a one‐year history of exercise‐induced collapsing on the pelvic limbs. Physical examination revealed generalised muscle atrophy. Neurological examination supported a generalised neuromuscular disorder. Electromyography revealed spontaneous electrical activity in almost all muscles. Unfixed and formaldehyde‐fixed biopsy samples were collected from the triceps brachii, longissimus and vastus lateralis muscles. Histopathological, histochemical and ultrastructural examinations of biopsy specimens were consistent with either centronuclear or myotubular myopathy. The dog clinically improved with supportive treatment with L‐carnitine, co‐enzyme Q10 and vitamin B compound. To the authors’ knowledge, this is the first report of centronuclear/myotubular myopathy in a Border collie.     

Mitochondrial myopathy in a german shepherd dog

A 9-month-old male German Shepherd dog was referred for evaluation of progressive exercise intolerance. Clinical examination revealed a stiff, stilted gait and marked atrophy and hypotonia of skeletal muscle. The dog had raised creatine kinase (181 U/liter), lactate dehydrogenase (510 U/liter), and aspartate aminotransferase (123.6 U/liter) levels, suggesting a muscle disease. Histochemical evaluation of muscle biopsies revealed the presence of subsarcolemmal oxidative activity, reduced nicotinamide adenine dinucleotide, and succinate dehydrogenase, and the absence of cytochrome oxidase activity. Ragged red fibers were demonstrated with Gomori trichrome stain. Ultrastructural examination of the muscle confirmed the presence of subsarcolemmal accumulations of mitochondria and morphologically atypical mitochondria.     

Staphylococcus pseudintermedius necrotizing fasciitis in a dog

Staphylococcus pseudintermedius was implicated as the cause of rapidly progressive and fatal necrotizing fasciitis in a dog. The isolate was methicillin-susceptible and did not contain genes encoding the Panton-Valentine leukocidin. While Streptococcus canis is typically considered to be the main cause of necrotizing fasciitis in dogs, staphylococci should also be considered.     

Fibrotic myopathy of the iliopsoas muscle in a dog

Fibrotic myopathy of the iliopsoas muscle developed in a dog, following extensive migration of a grass awn within the muscle and adjacent subcutaneous tissue. The dog was initially presented for evaluation of a fluctuant swelling over the right flank region. The clinical and imaging findings were suggestive of iliopsoas fibrotic myopathy and the diagnosis was confirmed by histopathology. This is the third report of iliopsoas fibrotic myopathy in a dog, the first report to describe the postmortem pathologic changes and the first report of iliopsoas fibrotic myopathy subsequent to foreign body migration.     

Teres minor myopathy as a cause of lameness in a dog

A case of a teres minor myopathy causing chronic lameness in a flve-yearold working iabrador retriever Is described. Uitrasonography was used to assist in detection of the condition and a definitive diagnosis was made by histological examination after muscle excision. Medical treatment was ineffective, but excision of the affected muscle resulted in complete resolution of the lameness with no apparent adverse affects on joint function. The aetiology of this condition Is unknown.     

Acute selenium toxicosis in a dog

A toxic dose of selenium administered by IM injection to a 3-year-old Chihuahua resulted in pulmonary edema and death. The compound had been dispensed to the owner inadvertently in combination with a vitamin E preparation. Vitamin and mineral products often are considered safe for use in megadoses by the uninformed public. The potential danger of selenium overdosage should not be underestimated.     

Acute nonlymphocytic leukemia in a dog

Acute nonlymphocytic leukemia was diagnosed in a 1-year-old Rhodesian Ridgeback. Clinical signs of disease included weight loss, anorexia, lethargy, lymphadenopathy, splenomegaly, and hepatomegaly. Doxorubicin was administered IV on day 4 at a dosage of 30 mg/m2 of body surface, followed 2 days later by oral administration of cyclophosphamide at a dosage of 100 mg/m2. The cyclophosphamide was given for 4 consecutive days (days 8, 9, 10, and 11), but the WBC count did not respond. The dog was administered 500 ml of blood; but on day 12, it died. Necropsy was not performed, but the presumptive cause of death was related to leukostasis.     

Acute sarcocystosis-like disease in a dog

Two of 8 littermate Rottweiler dogs developed persistent diarrhea at 6.5 weeks of age. Dog 1 was euthanatized at 14 weeks of age and had hepatitis characterized by necrosis and mixed leukocyte infiltrations in association with a previously unrecognized Sarcocystis-like protozoon. The organism was free in the hepatocyte cytoplasm without a parasitophorous vacuole, had divided by schizogony, and stained with anti-Sarcocystis serum, but did not stain with anti-Toxoplasma gondii or anti-Neospora caninum serum in an immunohistochemical test. Dog 2 was euthanatized at 10 weeks of age. This dog had large necrotic, hemorrhagic mesenteric lymph nodes. Numerous T gondii tachyzoites were observed in association with these lesions. The organism divided by endodyogeny and stained specifically with anti-T gondii serum.     

Acute zinc poisoning in a dog

Zinc-induced haemolytic anaemia was diagnosed in a young dog. The origin of the zinc intoxication was the ingestion of a toy material which contained a high percentage of zinc. The level of zinc in the liver and kidneys was resp. 1050 and 1320 ppm.     

Acute myelomonocytic leukemia in a dog

Cytochemical stains and morphologic characteristics were essential in making the correct diagnosis in a dog with acute myelomonocytic leukemia, which initially was diagnosed as lymphoblastic leukemia. Response to a treatment regimen of cytosine arabinoside, thioguanine, vincristine, and doxorubicin, besides accomplishing complete remission, helped revise the initial diagnosis to acute myelomonocytic leukemia. After remission was achieved, the dog died of a fulminating viral infection.