Malformation of the elbow joint in an Afghan hound litter

An abnormal development of the elbow joint in an Afghan Hound litter is described. Four out of nine littermates showed abnormalities on radiographs. Incongruity between the joint surfaces of the radius/ulna and the humérus were demonstrated in three of the dogs, while in the fourth, a calcified body was found in front of the joint space in both elbows. No account of a similar defect could be found in the literature. Résumé. On a déterminé par diagnostic clinique deux cas d'insuffisance primaire adrénale chez le chien, en corrélationnant les signes non-spécifiques de vomissement, diarrhée, anorexie et faiblesse musculaire avec un déséquilibre d'électrolytes du sang d'hyponatrémie et d'hyperkaliémie. L'amélioration clinique chez les deux chiens, après l'administration de stéroïdes a, de plus, donné appui à ce diagnostic. Les signes cliniques chez les deux chiens ont été associés avec une destruction primaire des tissus adrénocorticaux. Zusammenfassung. Zwei Fälle von primärer adrenaler Insuffizienz waren klinisch diagnostiziert in dem man die unspezifischen Anzeichen von Erbrechen, Durchfall, Anorexie und Muskelschwäche korrelierte mit Blutelektrolyte Ungleichheiten von Hyponaträmie und Hyperkaliämie. Klinische Besserung in beiden Hunden nach Steroid Verabreichung bekräftigte weiter disse Diagnose. Die klinischen Anzeichen in beiden Hunden waren mit primärer Zerstörung des Adreno-corticogewebes verbunden.     

Canine adenovirus-induced ocular lesions in the Afghan hound

A series of referred cases of CAV-1-induced ocular disease suggested increased susceptibility of the Afghan Hound. Of a litter of Afghan Hound puppies inoculated with a commercial vaccine containing attenuated CAV-1, three developed corneal edema and the litter as a whole showed marked febrile and serological responses to the virus. Under experimental conditions Afghan Hounds inoculated with CAV-1 at two levels of attenuation showed more profound clinical responses than Beagles receiving similar inocula. An enhanced generalized susceptibility to infection is suggested as a possible explanation for the greater incidence of CAC-1-induced ocular lesions in this breed.     

Pancreatic insulin-secreting neoplasia in a 9-year-old Afghan hound

An Afghan hound was presented with recurring episodes of weakness progressing to seizures after exercise. Insulinoma was diagnosed by demonstrating excessive insulin secretion in the presence of hypoglycemia. A pancreatic mass was identified and removed during an exploratory laparotomy. Surgical and pathological findings, diagnosis, and clinical management are discussed.     

Congenital central diabetes insipidus in two sibling Afghan hound pups

Congenital central diabetes insipidus was determined to be the cause of polydipsia and polyuria in sibling pups. Both pups were lacking adequate plasma arginine vasopressin concentration, compared with that in control dogs. Microscopic abnormalities were confined to the brain and pituitary gland in one pup. Without breeding trials of these dogs or their relatives, it cannot be determined whether the cause was familial.     

Cerebellar granuloprival degeneration in an Italian hound

A severe atrophy of the cerebellum was observed in a 7-month-old male Italian hound with a history of progressive ataxia and head tremor from the age of 3 months. On clinical examination, signs included severe hypermetric gait, head tremors and proprioception deficits in all limbs. At necropsy, a pronounced symmetrical reduction in size of the cerebellum was the only gross lesion observed. Histological examination of the cerebellum revealed marked thinning of the granular and molecular layers with almost complete loss of granule cells. Purkinje cells had normal morphology and distribution. These findings differ from those of previous reports of cerebellar cortical abiotrophy in dogs, which were mainly characterized by prominent Purkinje cell degeneration and loss.     

Lafora's disease in an epileptic Basset hound

A 6-year-old Basset hound developed a progressive central nervous system disease culminating in epileptic seizures. Histologically, Lafora bodies were found in neurones of the middle and deeper cerebral cortex and midbrain, in Purkinje cells and their processes, and in glial cells of the molecular layer of the cerebellum. Many were also observed free in the neuropil. The ultrastructural and histochemical characteristics of the bodies were similar to those described in previous human and canine cases of Lafora's disease.     

Lafora's disease in an epileptic Basset hound

A 6-year-old Basset hound developed a progressive central nervous system disease culminating in epileptic seizures. Histologically, Lafora bodies were found in neurones of the middle and deeper cerebral cortex and midbrain, in Purkinje cells and their processes, and in glial cells of the molecular layer of the cerebellum. Many were also observed free in the neuropil. The ultrastructural and histochemical characteristics of the bodies were similar to those described in previous human and canine cases of Lafora's disease.     

Avulsion of the popliteal muscle in an Afghan Hound

The diagnosis and successful surgical correction of avulsion of the origin of the popliteus muscle is reported in a 4–month–old female Afghan Hound.     

Permanent transvenous pacemaker implantation in an Ibizan hound cross with persistent atrial standstill

An Ibizan hound cross was referred with a 1-year history of syncope and exercise intolerance. An electrocardiogram showed bradycardia and no P waves; atrial standstill was diagnosed. A permanent artificial endocardial pacemaker was implanted. The lead dislodged and was reimplanted into the right ventricular apex. Capture was once again achieved.     

Chronic myocardial infarction due to arteriosclerosis of coronary arteries followed by acute thromboembolism of caudal abdominal aorta in a cat

A 10-year-old cat with the paresis of hind limbs was initially diagnosed as a hypertrophic cardiomyopathy followed by acute thromboembolism of caudal abdominal aorta from the findings of the medical examinations. However, this case was proved to be an chronic myocardial infarction due to arteriosclerosis of coronary arteries by the pathologic diagnosis. In the left ventricular, the hypertrophy and the narrowing were slight, and a coagulative infarction was seen obviously. The intramural coronary arteriosclerosis showed thickening of the wall due to medial hyperplasia by fibrosis, and arterial stenosis. Myocardial infarction and arteriosclerosis are scarcely any reports of these lesions in cats. This case is valuable for an extremely rare case of myocardial infarction in the cat.     

Meningoencephalitis in an adult cow due to Mortierella woifli.

A 7-year-old dairy cow presented with clinical signs of neurologic disease. Despite treatment with penicillin, the cow died 36 hours after initial presentation. Necropsy examination revealed multiple foci of hemorrhage within the cerebrum and thickened meninges. Additionally, endometritis and consolidation of approximately 30% of both lungs was observed. Histology revealed necrotizing vasculitis, infarction, and hemorrhage within sections of the brain, uterus, and lung. Large numbers of intralesional fungal hyphae were visible. Because only formalin-fixed tissue was available, polymerase chain reaction was used to make an etiologic diagnosis of Mortierella wolfii.     

Cerebral arteriosclerosis in an aged captive polar bear (Ursus maritimus).

Cerebral arteriosclerosis was observed upon necropsy of a 36-yr-old female captive polar bear (Ursus maritimus) that developed a sudden onset of seizure-like activity and died. The medium and large cerebral arteries of the meninges had moderate to severe diffuse discoloration and mineralization of the matrix of the tunica media, with little or no associated cellular reaction. Scanning electron microscopy of the affected arteries showed discrete crystalline calcified deposits in the media and sclerosis of the arterial wall. There were no lesions in the brainstem. The findings suggested a sudden and rapidly fatal loss of blood flow to the brain caused by long-standing arterial lesions. Incidental findings included numerous 0.1- to 10-cm-diameter, hepatic cysts lined with hyperplastic biliary epithelium, a unilateral, unipolar, 3-cm-diameter renal tubular adenoma, and approximately 250 active Baylisascaris sp. nematodes in the intestines.