Tongue and tail necrosis in an atypical case of acute steroid responsive meningitis-arteritis in a dog

Acute steroid responsive meningitis-arteritis (SRMA) is a common neurological disorder in young dogs. Typical clinical symptoms of the acute form of SRMA are neck pain, depression and fever. This case report describes a 1.5-year-old Pointer with uncommon neurological deficits (unilateral multiple cranial nerve deficits and Homer's syndrome) and an exceptional necrosis of the tongue. This was believed to be part of the systemic vasculitis accompanying SRMA. The patient also developed tail necrosis and iatrogenic calcinosis cutis, which complicated further treatment of the dog

Comparative aspects of pulmonary toxicity induced by cytotoxic agents with emphasis on lomustine, and a veterinary case report

In veterinary oncology the use of the nitrosourea compound lomustine is increasing. veterinary oncologists need to be aware of the pulmonary toxicity of this drug. Because of the lack of veterinary publications on this subject, the incidence and pathophysiology in human cancer patients of pulmonary toxicity induced by cytotoxic agents in general and by nitrosoureas in particular are discussed. Three clinical syndromes can be recognized, the most devastating of which is interstitial pneumonitis resulting in pulmonary fibrosis. Disturbances in the homeostatic mechanisms of the oxidant/antioxidant-, immunologic-, matrix repair-, proteolytic-, and central nervous systems are some of the major mechanisms of pulmonary injury in human medicine. Risk factors such as cumulative dose, age, radiation, oxygen administration and multi-drug regimens are recognized. For the first time in veterinarv medicine, a case report of a dog with pulmonary fibrosis, probably caused by chronic lomustine administration, is presented

Evaluation of antibodies in cerebrospinal fluid for the diagnosis of tick-borne encephalitis in dogs

Tick-borne encephalitis (TBE) is caused by the neurotropic tick-borne encephalitis virus (TBEV). In dogs, this virus may affect the central nervous system (CNS), causing meningoencephalitis, meningomyelitis, radiculitis or any combination of these. Diagnosis of TBE relies on a combination of clinical signs of CNS disease and laboratory findings, including CSF pleocytosis and serum TBEV antibody titers. Exposure to TBEV does not necessarily cause clinical disease, and seroprevalence has been reported as high as 40% in endemic areas. This causes concerns of over-diagnosing TBE in dogs with CNS disease. By examining TBEV antibodies in dogs with and without neurological disease in a TBEV endemic area, this study aimed to evaluate the diagnostic value of TBEV antibodies in the cerebrospinal fluid (CSF) in dogs. Eighty-nine dogs were included in the study, 56 with neurological disease and 33 neurologically normal control dogs. A positive TBEV CSF and serum IgG antibody titer (> 126 U/mL) was found in 3/89 dogs (3.4%). A positive serum TBEV antibody titer was found in 11 of the 89 dogs (12.4%). None of the control dogs showed a positive CSF antibody titer, whilst two showed positive serum concentrations. A positive CSF IgG antibody titer supports a clinical diagnosis of TBE in patients with acute onset of CNS disease and may help reduce the risk of over-diagnosis

Favorable outcome of conservative treatment in a cat with T9T10 intervertebral disk disease

A 12-year-old domestic shorthair was presented with acute paraplegia. On the basis of radiography and myelography, a presumable diagnosis of disk herniation at the level of T9T10 was made. The cat was treated conservatively and recovered from paraplegia with only mild residual ataxia. Follow-up for more than one year showed no changes or recurrence of the symptoms

Retrospectieve studie van 20 honden en 1 kat met tetanus (2001-2008)

In 20 dogs and I cat a diagnosis of tetanus was made based on the typical clinical signs and a possible wound history. In 7 animals a tooth abnormality was considered as the entrance way of the bacteria. By means of radiography of the thorax several animals were evaluated for the presence of possible complications such as aspiration pneumonia, megaoesophagus or hiatal hernia. The treatment existed mainly of metronidazole as an antibiotic, acetylpromazine to control the muscle spasms and additional supportive therapy. The survival rate was 71%

Discospondylitis bij de hond: een retrospectieve studie van 18 gevallen

In a retrospective study (1997-2007) of 35 patients suspected of discospondylitis (DS), the diagnosis of discospondylitis was confirmed in 18 dogs. The signalment, the appearance and the clinical presentation of the dogs were comparable to those earlier reported in the literature. Radiography was the most important diagnostic technique, but in some cases further diagnostic investigation was necessary to confirm the diagnosis. Blood- and urine culture was important to identify a possible underlying cause. Medical therapy is the treatment of choice. Most of the dogs (76%) recovered very well after treatment. The results confirm that discospondylitis has a rather favorable prognosis when medical therapy is used

Degenerative encephalopathy in Nova Scotia Duck Tolling Retrievers presenting with a rapid eye movement sleep behavior disorder

BACKGROUND: Neurodegenerative diseases are a heterogeneous group of disorders characterized by loss of neurons and are commonly associated with a genetic mutation. HYPOTHESIS/OBJECTIVES: To characterize the clinical and histopathological features of a novel degenerative neurological disease affecting the brain of young adult Nova Scotia Duck Tolling Retrievers (NSDTRs). ANIMALS: Nine, young adult, related NSDTRs were evaluated for neurological dysfunction and rapid eye movement sleep behavior disorder. METHODS: Case series review. RESULTS: Clinical signs of neurological dysfunction began between 2 months and 5 years of age and were progressive in nature. They were characterized by episodes of marked movements during sleep, increased anxiety, noise phobia, and gait abnormalities. Magnetic resonance imaging documented symmetrical, progressively increasing, T2‐weighted image intensity, predominantly within the caudate nuclei, consistent with necrosis secondary to gray matter degeneration. Abnormalities were not detected on clinicopathological analysis of blood and cerebrospinal fluid, infectious disease screening or urine metabolite screening in most cases. Postmortem examination of brain tissue identified symmetrical malacia of the caudate nuclei and axonal dystrophy within the brainstem and spinal cord. Genealogical analysis supports an autosomal recessive mode of inheritance. CONCLUSIONS AND CLINICAL IMPORTANCE: A degenerative encephalopathy was identified in young adult NSDTRs consistent with a hereditary disease. The prognosis is guarded due to the progressive nature of the disease, which is minimally responsive to empirical treatment