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Objectives To report clinical features, gross post mortem and histopathological findings from an investigation into sudden or unexpected death in rabbits that was undertaken during an outbreak of rabbit haemorrhagic disease. Materials and methods Using a standard protocol, veterinarians were invited to submit case histories and results of their post mortem examination of pet rabbits that died unexpectedly. Histopathological examination of heart, lungs, liver, spleen and kidney samples was collated with macroscopic appearance and clinical details. Results Hepatocellular necrosis, characteristic of rabbit haemorrhagic disease, was observed in 185 of 300 (62%) submissions, often accompanied by glomerular thrombosis and changes in other organs. Evidence of rabbit haemorrhagic disease was not apparent on histopathology in 113 of 300 (38%) rabbits. Gross post mortem examination by veterinary practitioners did not always reflect reported histopathological changes. No macroscopic abnormalities were seen in 78/185 (42%) of rabbit haemorrhagic disease cases. Rapid death and death of other rabbits in the household were common features of rabbit haemorrhagic disease. Ante mortem clinical signs included anorexia, collapse, lethargy, seizures, icterus, bleeding from the mouth, dyspnoea, hypothermia, pyrexia, bradycardia or poor blood clotting. Clinical importance Rabbit haemorrhagic disease can be suspected from a history of sudden death, especially if multiple rabbits are affected. There is not always macroscopic evidence of the disease but histopathology is useful to support or refute a diagnosis of rabbit haemorrhagic disease and provide information about other causes of death.

A histological, histochemical and morphometric study was performed on submandibular salivary glands from 13 dogs which had presented with a submandibular mass or swelling that proved to be a portion of non-inflammatory and non-neoplastic submandibular salivary gland. There were no consistent changes in lectin-binding histochemistry or immunohistochemical expression of various cell markers, and, in most cases, there was no measurable difference in acinar size in the affected gland. The possible explanation for the clinical salivary gland enlargement is therefore unclear.

Plexiform vascularisation of a retropharyngeal lymph node is described in an adult cat. The cat presented with a chronic history of inspiratory stridor and a slowly growing mass in the cranial cervical area. Clinical signs resolved after excision of the affected node. This appears to be the first clinical report of plexiform vascularisation of a retropharyngeal lymph node and its treatment in a cat.

Benign connective tumours of the canine salivary glands are rare. This report describes lipomatous infiltration of parotid or submandibular salivary glands in seven dogs in which the glands were enlarged as a result of infiltration by fat cells; they appeared to have been successfully treated by local excision. The precise cause of the lipomatous infiltration in the dogs is unclear but different causes of similar lesions in humans are discussed.

A distinctive lymphadenopathy in nine cats, four of which were of the Longhair breed, was characterized by capillary vasoproliferation and lymphoid atrophy. It occurred in the cervical or inguinal regions. The animals were, apart from local manifestations, healthy at the time and remained so subsequently. In the absence of any clinical or morphological evidence for viral, neoplastic or developmental aetiologies, we postulate an ischaemic pathogenesis for the lesions which may be related to human "vascular transformation of lymph node sinuses". The lesions appear to be by no means a rare cause of non-neoplastic lymphadenopathy in domestic cats, since they constituted over 5 per cent of surgical biopsies of cat lymph nodes seen in the past 5 years. The lesions merit wider recognition and investigation.

The clinicopathological features of tonsillar polyps in eight dogs are described. They occurred in aged animals (mean 12.5 years) and caused gagging and retching in two. In the other six the polyps were an incidental finding during anaesthesia for unrelated surgical procedures. Seven of the polyps were considered to be of inflammatory origin, consisting of a fibrous tissue core containing dilated lymphatics and veins and a variable lymphocytic component. The eighth had microscopic features suggestive of a developmental vascular anomaly (hamartoma).

Two cases of paradoxical vestibular syndrome are described. The principal clinical signs were a persistent head tilt to the right and a progressive ataxia in unrelated 6-year-old Rough Collies. In both dogs the primary lesion found post mortem was a papilloma of the choroid plexus of the fourth ventricle on the left side. This was associated with severe disruption of the cerebellar peduncles, cerebellar folia and the medulla oblongata adjacent to the tumour.

This report describes the clinical, radiological, pathological and genetic features of an inherited dwarfism in the English Pointer. Gross enlargement of the distal ulnar, radial and tibial growth plates occurred in the first 6 weeks of life and radiographic skeletal abnormalities were present at other sites. The enlargement was due to increase in width of the zone of hypertrophic cartilage, but the columns of chondrocytes were well ordered. By 12 weeks of age an unusual type of degeneration was present beneath the surface of articular cartilage; this developed to widespread, patchy erosion of joint surfaces by 32 weeks. The genetics are compatible with a homozygous recessive mode of inheritance.