Mario Modenato

Hepatozoonosis in a dog with skeletal involvement and meningoencephalomyelitis

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.

Clinicopathological features of globoid cell leucodystrophy in cats.

Summary 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.