Forty-two dogs with a history of persistent nasal disease were evaluated by a combination of clinical examination, thoracic and nasal radiography, retroflexed endoscopy and biopsy, and anterograde rhinoscopy and blind nasal biopsy. A definitive diagnosis was made in 91 per cent of cases. Neoplasia was the most common diagnosis (33 per cent of cases), followed by inflammatory rhinitis (24 per cent). Other diagnoses included periodontal disease (10 per cent), aspergillosis (7 per cent) and foreign bodies (7 per cent). Adenocarcinoma was the most common tumour diagnosed. The clinical findings were found to be too variable to be used as specific diagnostic criteria. Anterograde rhinoscopy and retroflexed endoscopy had higher specificity and sensitivity than radiology for the diagnosis of neoplasia, inflammatory rhinitis, aspergillosis and foreign bodies. With a systematic approach to the investigation of persistent nasal disease, a definitive diagnosis can be successfully obtained in the vast majority of cases.

Primary hypoadrenocorticism was diagnosed in an eight-year-old neutered male cat. The predominant presenting complaint was dysphagia. Other historical signs included lethargy, weight loss, polydipsia, polyuria, muscle weakness and occasional vomiting. The signs had waxed and waned over the two months before presentation and had improved when the cat was treated with enrofloxacin and prednisolone by the referring veterinarian. On referral, dehydration, depression and poor bodily condition were found on physical examination. Results of initial laboratory tests revealed mild anaemia, hyperkalaemia, hyponatraemia, hypochloraemia and elevations in serum creatinine and creatine kinase. The diagnosis of primary adrenocortical insufficiency was established on the basis of results of an adrenocorticotropic hormone (ACTH) stimulation test and endogenous plasma ACTH determination. Initial therapy for hypoadrenocorticism included intravenous administration of 0.9 per cent saline and dexamethasone, and oral fludrocortisone acetate. Within one week the cat was clinically normal and two years later was still alive and well on fludrocortisone acetate treatment only.

The aim of this study was to investigate the subpopulations of lymphocytes in the colonic mucosa of healthy dogs and dogs with inflammatory bowel disease (IBD). Fourteen normal dogs and 13 dogs with IBD were examined. Endoscopic biopsy specimens of colonic mucosa from each dog were stained specifically for pan T lymphocytes (CD3) and pan B lymphocytes (CD79a), and for plasma cells with methyl green pyronin (MGP) stain. Cells were counted by means of a grid and statistical analysis was performed on the data collected. B and T lymphocytes were also counted in the glandular epithelium of normal dogs and dogs with IBD and the normal and abnormal groups compared statistically. Healthy dogs had significantly lower numbers of T cells in the lamina propria and glandular epithelium and significantly lower numbers of B cells in the lamina propria. Significant group differences for plasma cells were not evident. Our results indicate that in IBD a chronic cellular immune reaction is present in the diseased gut involving increased numbers of B and T lymphocytes.

Three unusual cases of salivary gland enlargement and hypersialosis in the dog that responded to anticonvulsant therapy are reported. Presenting complaints included weight loss, hypersalivation, retching and vomiting of several weeks' duration. Two dogs were presented with enlarged painful mandibular salivary glands. The third dog exhibited bizarre behaviour (including jaw chattering) and developed enlarged painful mandibular salivary glands during hospitalisation. Fine needle aspirate cytology and biopsies from the enlarged salivary glands revealed no significant pathological changes. In one dog, an electroencephalogram revealed changes consistent with epilepsy. Hypersialism and salivary gland enlargement resolved completely during phenobarbital administration in all cases. Two dogs were successfully weaned off treatment six months after diagnosis. The remaining dog relapsed after eight months, but normalised with the addition of oral potassium bromide. It is hypothesised that the syndrome idiopathic hypersialosis may in fact be an unusual form of limbic epilepsy.

AN article in the last issue (September 2002, pp 418-432) discussed the aetiology and pathophysiology of urinary tract infections (UTIs) in dogs and cats and outlined an approach to the diagnostic work-up. This article describes the treatment options for UTIs and the strategies for long-term control as well as control in recurrent cases. It is important that underlying causes are determined (see previous article) and resolved, where possible, prior to the initiation of therapy. UTIs occurring secondarily to underlying conditions may not be appropriately managed by antibiotic therapy alone.