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.

A 15-month-old, female mongrel dog was presented with a 6-week history of inappetence, weight loss, and tetraparesis. Physical examination revealed weakness, poor body condition, mild fever, pale mucous membranes, and diffuse muscle atrophy. The right hind limb was painful and edematous, with large ecchymoses. The femur was irregular on palpation and moderate popliteal lymphadenopathy was evident. Results of a CBC showed severe anemia with mild regeneration, an inflammatory leukogram with 90% of neutrophils parasitized by Hepatozoon sp. gamonts, and moderate thrombocytopenia. A bone marrow aspirate had myeloid hyperplasia and contained a few extracellular Hepatozoon meronts and a few intracellular gamonts within neutrophils. Serum chemistry abnormalities included hypoalbuminemia, hyperglobulinemia, hypoglycemia, hypercalcemia, hyperphosphatemia, and elevated alkaline phosphatase activity. Radiologic findings of the right femur included periosteal bone proliferation and lesions compatible with osteomyelitis. A fine needle aspirate specimen from the bone lesion had neutrophilic inflammation; 36% of the neutrophils contained Hepatozoon gamonts. Results of cerebrospinal fluid analysis included a protein concentration of 37 mg/dL and marked mononuclear pleocytosis (243 cell/microL) with a predominance of lymphocytes. An ELISA was positive for Hepatozoon canis and PCR results with DNA sequencing confirmed infection with this organism. A diagnosis of hepatozoonosis with skeletal involvement and meningoencephalomyelitis was made. The dog recovered almost completely neurologically and had no gamonts in the blood after 60 days of therapy with imidocarb dipropionate and prednisone. This is an unusual case of canine hepatozoonosis involving neurologic signs and a periosteal reaction more typical of H. americanum infection and rarely reported in dogs infected with H. canis.

Summary A 3‐month‐old female Dalmatian dog and a 2.5‐month‐old Poodle dog were referred with a sudden onset of neurological syndrome consistent with hydrocephalus. Clinical signs included depression, severe ataxia, eye abnormalities and skull enlargment in one case. Postmorten examination revealed severe internal hydrocephalus with cavitation of the cerebral white matter associated with necrotizing and inflammatory lesions of the periventricular nervous tissue. Although no bacteria were isolated from cerebrospinal fluid and no infectious agents were detected in the brains, an infectious etiology was postulated.

Clinical and pathological findings consistent with globoid cell leucodystrophy (GLD) were evaluated in two domestic shorthaired cats, aged 3 and 4 months. Both showed neurological signs mainly characterized by progressive pelvic limb ataxia, paraplegia with loss of deep pain perception in the pelvic limb, and intentional tremors of the thoracic limbs. Pathological changes affecting the central and peripheral nervous systems were characterised by diffuse, bilateral and symmetrical myelin loss, and marked astrogliosis. In the leucodystrophic areas there was perivascular accumulation of large PAS-positive, non-metachromatic macrophages (globoid cells), with intracytoplasmic accumulation of crystalloid tubular aggregates. Peripheral nerves showed demyelinating features with thin myelin sheaths, myelin splitting, and ballooning; the nerve fibres had bizarre shapes due to the presence of pale inclusions in the Schwann cells. GLD in cats shares clinical and pathological features with the disease described in other animals and human beings. The neurological signs differed from those of other feline inborn neurometabolic diseases and cerebellar hypoplasia.

SummaryThe purpose of this study was to evaluate the ability of proximal tibial epiphysiodesis to reduce the tibial plateau slope in young dogs with cranial cruciale ligament (CCL) deficient stifles. Of the 14 treated dogs, eight had a bilateral injury, for a total of 22 joints. After physical and radiographical examination and measurement of tibial plateau slope, all of the dogs underwent surgery. Insertion of the screw was placed in the most proximal part of the tibial plateau, in its medio-lateral centre, aiming to the tibial shaft and using a K wire predriven as a guide; correct position of the screw was confirmed with intraoperative fluoroscopy or radiography. In all of the dogs the tibial slope was decreased at the time of physis fusion and the degree of change depended on the age and the breed of the dog at the time of surgery. The minimum change was 4° and the maximum was 24°. There was a statistically significant difference between tibial slope measured before surgery compared to tibial slope measured at the last follow-up visit after surgery. This study shows that the partial proximal tibial fusion in dogs with ACL injuries was effective in reducing the tibial slope during the residual growing time to such an extent to stabilize the joint, provided that the surgery had been carried out when there was still residual growing potential. The technique appeared to be mini-invasive and malalignment complications could be avoided by correct and precise insertion of the screw.