Suspected myelinolysis following rapid correction of hyponatremia in a dog

A dog developed signs of neurological dysfunction five days after rapid correction of severe electrolyte derangements, including hyponatremia, caused by gastrointestinal parasitism (i.e., trichuriasis). History, laboratory findings, and onset of neurological signs following correction of hyponatremia led to a diagnosis of myelinolysis. Myelinolysis is a noninflammatory, demyelinating brain disease caused by sudden, upward osmotic shifts in central nervous system plasma, often a result of rapid correction of chronic hyponatremia. The pathogenesis is complex, but recovery is possible. Iatrogenic damage due to myelinolysis can be avoided by adherence to therapeutic guidelines for correction of chronic hyponatremia.     

Renal concentrating ability in dehydrated hyponatremic dogs

Eleven hyponatremic dogs were unable to concentrate their urine during periods of severe dehydration and azotemia. When normonatremia was reestablished in eight of the dogs, their renal concentrating ability returned. Six dogs, including the 3 dogs in which normonatremia was not reestablished, died or were euthanatized; renal lesions were not found during postmortem examination. Two dogs had hypoadrenocorticism, which has been documented as a cause of hyponatremia and impaired renal concentrating ability. Two dogs had gastrointestinal disease, which has been documented as a cause of hyponatremia, but not of impairment of renal concentrating ability. All dogs without hypoadrenocorticism had clinical and clinicopathologic indications of blood loss, which has not been documented as a cause of hyponatremia or impairment of renal concentrating ability. Hyponatremia (less than 120 mEq/L) was induced by chronic blood removal in a dog maintained on a low-sodium diet. During the period of hyponatremia, the dog became azotemic, hypotensive, and severely dehydrated; renal concentrating ability was impaired. We conclude that hyponatremia may be caused by hemorrhage, but irrespective of the cause, hyponatremia impairs renal concentrating ability.     

Neurologic complications following treatment of canine hypoadrenocorticism

After treatment for hypoadrenocorticism, an 18-month-old dog exhibited marked ataxia and intermittent muscle tremors, progressing to head pressing, dysphagia, and quadraparesis. Serum sodium increased by 38.9 mmol in 48 hours, suggesting myelinolysis. The dog made a complete recovery after intensive treatment.     

Acquired extrahepatic portosystemic shunts in a young dog

A young, male miniature poodle was presented with severe neurological problems. Laboratory tests and ultrasonograph examination were consistent with extrahepatic portosystemic shunts, resulting in hepatic encephalopathy. When surgical correction proved not to be a viable option, the dog was euthanized. Postmortem examination revealed multiple shunts likely acquired after severe hepatitis.     

Neosporosis with cerebellar involvement in an adult dog

A case of an adult dog with multifocal, progressive neurological signs caused by Neospora caninum is reported. Pathological studies showed cerebellar lesions due to the parasite, which was also present in other parts of the nervous system and muscle. Cerebellar atrophy related to Neospora infection has been rarely reported in veterinary medicine, and has been shown to affect ruminants and dogs. The cerebellar involvement and the age of the present dog make this case uncommon.     

Magnetic resonance imaging in two dogs with central nervous system disease

Accurate localization of the lesions in two dogs with progressive neurological disease was demonstrated with magnetic resonance imaging (MRI). The first dog had unilateral cerebellar signs with associated paradoxical vestibular symptoms. The CSF tap and clinical localization suggested a right-sided cerebellar tumour and this was confirmed with MRI scanning. The second dog had predominantly asymmetrical fore-brain signs with circling, personality changes, seizures and contralateral proprioceptive deficits. CSF analysis suggested an inflammatory or neoplastic condition. MRI showed a diffuse oedematous lesion of the left cerebral hemisphere which corresponded exactly with the lesions seen at necropsy. The advantages of MRI over CT scans are discussed.     

Canine cutaneous neosporosis in Brazil

The clinical signs of infection in dogs with Neospora caninum are usually associated with neurological disorders and are seen in young dogs. In this brief case report we observed multifocal ulcerative and exudative skin nodules on the neck and pelvic limbs of a 10‐year‐old cocker spaniel dog. Infection with N. caninum was diagnosed on the basis of cytology and examination of skin tissues by PCR. The dog initially responded to treatment with clindamycin and then relapsed; the dog died. Infection with N. caninum may have been due in part to immune suppression due to hyperadrenocorticism; which either allowed for the development of a primary infection or reactivation of a latent infection by N. caninum with the occurrence of skin lesions.     

Leishmania infantum and Neospora caninum simultaneous skin infection in a young dog in Italy.

Leishmania infantum, the agent of canine leishmaniasis in Mediterranean countries, and Neospora caninum, a recently recognized protozoal pathogen in dogs, were diagnosed in a 9-month-old Argentine Dogo dog. Both skin lesions and neurological signs were present. Histopathology of cutaneous lesions revealed a suppurative, diffuse dermatitis with numerous intracellular protozoa. Serology was positive for both L. infantum (1:640) and N. caninum (1:800). Double-label immunohistochemical staining of skin samples with hyperimmune serum from L. infantum-infected dogs was positive for protozoa within macrophages, while the polyclonal antibody specific for N. caninum showed positive reactions for protozoa in endothelial cells and fibroblasts. Transmission electron microscopy (TEM) confirmed the infection with both protozoa. This is, to the authors' knowledge, the first case of simultaneous infection with L. infantum and N. caninum in a dog. It is possible that the immunosuppressive effects of Leishmania infection or long-term steroid therapy may have been a contributing factor to the development of N. caninum in this dog.     

Acute myelomonocytic leukemia (AML-M4) in a dog with the extradural lesion

A two-year-old dog having presented with neurological signs showed marked leukocytosis and appearance of blast cells in the peripheral blood. Hematological and bone marrow examination showed an increase in blasts having both myeloid and monocytic cells characteristics. The dog was diagnosed with acute myelomonocytic leukemia (AML-M4) on the basis of bone marrow findings. Although the dog was treated with a multi-combination chemotherapy, the neurological abnormalities progressed and the dog was euthanized. Myelographic examination and necropsy revealed the extradural lesion formed by AML-M4 around the cervical spinal cord and this lesion was considered as a cause of the neurological signs.     

An outbreak of lead poisoning in dogs

SUMMARY An outbreak of lead toxicosis in working dogs on a sheep farm is described. The affected dogs exhibited neurological signs which appeared to be initiated by straineous physical activity. Radiological examination and estimation of urinary delta aminolevolonic acid (U-ALA) was not found to be useful for clinical diagnosis but blood lead estimation was helpful in detecting and confirming dogs that were exposed to lead. Gross pathological lesions were absent in a lead poisoned dog. However, histopathological lesions were seen in brain and bone. Acid-fast lead inclusion were not detected in liver and kidney epithelial cells but were present in osteoclasts.     

Adipsia and hypernatraemia in a dog with focal hypothalamic granulomatous meningoencephalitis

A 7-year-old Doberman was presented with a history of progressive neurological disease of 4 weeks duration. Initially there were episodes of aimless wandering and uncharacteristic aggression, however, the dog was obtunded at presentation. Serum biochemical analysis revealed profound hypernatraemia and moderate hyperproteinaemia. Despite correction of the hypernatraemia by the infusion of hypotonic fluids, the dog continued to periodically exhibit pacing and head pressing. A patchy, ill-defined contrast-enhancing area was evident in the ventral midbrain on computed tomography of the brain. Analysis of the cerebrospinal fluid revealed a mild increase in protein concentration, positive Pandy's test and mild pleocytosis. Because of the poor prognosis, euthanasia and necropsy were performed. Histopathological analysis of the brain revealed a severe focal meningoencephalitis affecting hypothalamic nuclei and mammillothalamic tracts. Destruction of osmoreceptors in the hypothalamus responsible for recognition of thirst is believed to have resulted in adipsia and subsequent hypernatraemia.     

Severe respiratory compromise secondary to cervical disk herniation in two dogs

Two dogs presented with acute tetraparesis, hypoventilation, and bradycardia with a second-degree atrioventricular heart block. Neurological examination localized both lesions to the cervical spine. Diagnostic imaging revealed a ventral extradural compression at the second to third cervical (C(2)-C(3)) region in one dog and at the third to fourth cervical (C(3)-C(4)) region in the other. Following surgical correction of the extruded disk, the hypoventilation and bradycardia resolved. Cervical disk extrusions are a common cause of acute tetraparesis in the dog. This report shows that respiratory and cardiac complications may occur concurrently. The authors recommend screening dogs with cervical myelopathies for respiratory and cardiac dysfunctions and treating appropriately. Prompt surgical intervention and supportive care can improve the prognosis.     

Severe brain damage after punitive training technique with a choke chain collar in a German shepherd dog

The features of severe ischemic brain damage after strangulation by the owner of a 1-year-old German shepherd dog are described. The dog was disciplined by the owner during training by holding the dog off the ground by his choke chain collar. At first, the dog behaved normally, but he became increasingly ataxic and started circling to the left and showed reduced consciousness. The neurological examination revealed severe disorientation, left lateral pleurothotonus, and circling. The neurological findings were consistent with a multifocal brain lesion. A magnetic resonance imaging scan was performed and showed changes in the T2- and diffusion-weighted images, consistent with severe cerebral edema resulting from ischemia. Because of the severity of the clinical features, the dog was later euthanized. To the author's knowledge, this is the first report of a severe brain ischemia after strangulation in a dog.     

Cerebellar infarcts in two dogs diagnosed with magnetic resonance imaging

Two dogs presented with severe, peracute-onset, neurological signs. Neuroanatomical localization was cerebellovestibular. Magnetic resonance imaging (MRI) was performed and revealed focal, wedge-shaped lesions in the cerebellum. Diagnosis of cerebellar infarctions was made based on peracute-onset, clinical signs, MRI, and outcome as well as ancillary diagnostic information. Both dogs recovered completely. Cerebellar infarction should be included in the differential of any dog with peracute-onset, central cerebellovestibular signs regardless of severity of clinical signs. Outcome was excellent in these dogs.     

Disc extrusion in a Rottweiler dog with caudal cervical spondylomyelopathy after failure of intervertebral distraction/stabilisation

A Rottweiler dog was presented with an 8 week history of hindlimb ataxia. Neurological examination localised the lesion to the cervical spinal cord. Myelography demonstrated dynamic compressive lesions at C5-6 and C6-7 consistent with a diagnosis of caudal cervical spondylomyelopathy. Distraction/stabilisation of both discs was performed using interbody polymethyl methacrylate. Both implants subsequently failed leading to extrusion of the remaining dorsal annulus fibrosus of the C5-6 intervertebral disc and nonambulatory tetraparesis. A ventral slot combined with distraction/stabilisation using screws and polymethyl methacrylate was performed and resulted in nearly full neurological recovery.     

Histological diagnosis of mucopolysaccharidosis IIIA in a wire-haired dachshund

A four-year-old wire-haired dachshund developed progressive neurological signs of ataxia, intention tremor and finally dysuria. Two years later, histopathology showed that neurons throughout the brain and spinal cord were distended with lipopigment which was also present in macrophages. Ultrastructurally, the pigment in the neurons occurred predominantly as electron-dense membranous whorls and stacks. There were a few vacuolated macrophages in the meninges. Hepatocytes were highly vacuolated and electron microscopy suggested that they were empty membrane-bound vesicles. The disease was diagnosed as mucopolysaccharidosis IIIA because of its similarity to other biochemically confirmed cases in the same breed and in a New Zealand huntaway dog. Additional lesions included calcium oxalate uroliths, severe secondary calcification of tissues including the brain and storage deposits in some neurons, and lesions which may have been associated with high levels of the substrate, heparan sulphate.     

Stereotactic CT-guided brain biopsy in the dog

This study evaluated the accuracy of a new stereotactic CT-guided brain biopsy (SCTGBB) device on 23 client-owned dogs which presented with a brain lesion. Biopsy of the lesion was achieved in 95 per cent of cases. The target tissue was not sampled in one dog. Complications were observed in six dogs. Two dogs with highly vascularised brainstem tumours died after SCTGBB. Minor complications (slight variation in the neurological status) were observed in a further four cases. A diagnosis was reached in 16 dogs after cytological examination and in 21 dogs after histological evaluation. SCTGBB is an accurate diagnostic method for the diagnosis of brain lesions.     

Coccidioidomycosis in dogs and cats: a review

The dimorphic fungi Coccidioides immitis and Coccidioides posadasii are the causative agents of coccidioidomycosis. Dogs and cats residing in and visiting endemic areas are at risk of exposure to infectious arthrospores. The primary infection is pulmonary and frequently results in chronic cough. Disseminated disease is common and causes cutaneous, osseous, cardiac, ocular, nervous system, or other organ disease. Radiographic changes include a variable degree of interstitial pulmonary infiltration, hilar lymphadenopathy, and osseous lesions. Serological titers support the diagnosis, but definitive diagnosis relies on identification of Coccidioides in cytological or tissue samples. Coccidioidomycosis should be considered in any dog or cat that has been potentially exposed during the previous 3 years and is presented with chronic illness, respiratory signs, lameness, lymphadenopathy, nonhealing cutaneous lesions, or neurological, ocular, or cardiac abnormalities.