Chronic rhinitis and sinusitis in budgerigars (Melopsittacus undulatus).

The microscopic lesions in the nasal cavity, nasal bones, and infraorbital sinuses of five budgerigars with chronic upper respiratory tract infection are described. All five had chronic inflammation of the lining of the air spaces within the bones surrounding the nares and infraorbital sinuses.

The influence of dietary calcium and phosphorus on tibial dyschondroplasia in broiler chickens.

The incidence and severity of tibial dyschondroplasia in broiler chickens were increased by feeding rations containing high levels of phosphorus relative to the level of calcium. Tibial dyschondroplasia was not eliminated by feeding a ration containing 1.5% calcium and 0.5% available phosphorus. Before typical dyschondroplasia developed, chickens fed a high level of phosphorus had uniformly thickened growth plates at 2 weeks of age. The majority of this thickening was due to an increase in the zone of proliferation, identical to that which occurs in calcium-deficiency rickets.

A papova-like virus infection of splendid parakeets (Neophema splendida).

The lesions associated with a papova-like virus infection in two splendid parakeets (Neophema splendida) are described. The most obvious microscopic lesion in both birds was enlargement of renal medullary collecting-duct epithelial cells. The nuclei of these cells were also enlarged, pleomorphic, and often bizarre, and intranuclear and intracytoplasmic virus-like particles (48 nm in diameter) were demonstrated within them. One bird also had a hepatopathy characterized by hepatocyte enlargement and nuclear pleomorphism.

Fatal pox infection in a rough-legged hawk.

Natural pox infection occurred in a free-living rough-legged hawk (Buteo lagopus) in northeastern North Dakota. Gross, histological and electron microscopic findings were typical of pox infection, and characteristic lesions developed in red-tailed hawks (Buteo jamaicensis) but not in great horned owls (Bubo virginianus) following inoculation with case material. Death of the rough-legged hawk was attributed to starvation rsulting from inability to capture prey and to blood loss from foot lesions.

Beak and feather dystrophy in wild sulphur-crested cockatoos (Cacatua galerita).

Three flocks of wild sulphur-crested cockatoos in southeastern Australia had a 10-20% prevalence of feather and beak deformities. In affected birds, the crest, tail, contour and down feathers were lost or reduced in length owing to a "pinching off" 0.5-1 cm above the skin. The underlying skin was discolored brown. Flight feathers appeared normal and could sustain flight. In mildly affected birds, only the crest and down feathers were involved. Histological examination of affected feathers showed necrosis of developing cells in their epidermal collars. The epidermis was moderately hyperplastic and contained numerous large macrophages, with large intracytoplasmic granules. Electron microscopic examination showed these granules to consist of regular lattices of 17-20-nm-diameter particles, resembling parvovirus particles. In some birds the upper beak was enlarged and had longitudinal cracks. Histological examination of the beak showed necrosis of its epidermis. It was concluded that a viral infection may have caused feather and beak dystrophy in these birds.

Investigations of an enteric infection of cockatoos caused by an enterovirus-like agent.

An enteric infection in cockatoos associated with a 30 nm diameter enterovirus-like agent seen in faeces and intestinal epithelial cells is described. The disease is characterised by intractable, profuse, mucoid diarrhoea, weight loss, dehydration and death. Lesions in the intestine consist of villous atrophy, villous fusion, enterocyte hyperplasia and, in some cases, chronic inflammation. Affected birds so far examined have concurrent psittacine beak and feather disease.

The pathology of psittacine beak and feather disease.

Psittacine beak and feather disease is characterised by loss of feathers, abnormally shaped feathers and overgrowth and irregularity of the surface of the beak. The disease occurs in a number of psittacine species including the Sulphur-crested Cockatoo, Lovebirds , Budgerigars and Galahs . The abnormal appearance of feathers and beak is due to a dystrophic process within the epidermis of the feather and beak. The process consists of epidermal cell necrosis, epidermal hyperplasia and hyperkeratosis. Many of the feather abnormalities are due to retention of a hyperkeratotic feather sheath. A characteristic microscopic finding is the presence of macrophages containing purple intracytoplasmic inclusions in affected epidermis and feather pulp. The inclusions consist of aggregates of particles 17 to 22 nm in diameter. Similar but smaller inclusions occur in epidermal cells. In addition, non-suppurative inflammation occurs in the feather pulp. The findings are suggestive of a viral infection.

Evaluation of tests for the diagnosis of lead exposure in sheep.

Several laboratory tests that are currently used for the diagnosis of lead poisoning in man were evaluated for the detection of lead poisoning in sheep given 3 or 10 mg Pb/kg body weight/day for 7 weeks. Urinary porphyrins and basophilic stippling of erythrocytes were not sensitive indicators of lead poisoning in sheep, while urinary lead and urinary delta-aminolevulinic acid concentrations were too variable to have diagnostic value. However, erythrocyte delta-aminolevulinic acid dehydratase was strongly inhibited by exposure to relatively low doses of lead, while blood lead concentrations gave an indication of the level of exposure to lead poisoning.

The characterisation and pathogenicity of porcine enteroviruses isolated in Victoria.

Approximately 23 viruses were isolated from healthy pigs, pigs with encephalitis, and in cases of reproductive failure. Five viruses were identified as enteroviruses and a total of 10 isolates were shown to cross-react serologically to varying degrees. Twenty viruses were neutralised by a reference antiserum of serotype 8 porcine enterovirus. Intracerebral inoculaton of colostrum-deprived piglets with 2 of the characterised viruses caused lesions of encephalomyelitis which were not induced by oral infection. Intrafoetal inoculation of 2 sows with one characterised faecal isolate caused foetal death and abortion, but no adverse effects followed oral dosage.

Clinical and electrocardiographic findings in suspected viral myocarditis of pups.

Surviving puppies from three separate litters in which deaths had occurred from suspected viral myocarditis were examined clinically and electrocardiographically. Of 11 puppies examined, 5 subsequently died or were euthanised within 11 days of initial examination. ECG changes present in these puppies for 1 to 11 days prior to death were small R waves (less than 0.4 mV in lead II), S-T segment elevation, QRS notching and paroxysmal ventricular tachycardia (PVT). No clinical signs referable to the ECG changes were present before the terminal episodes of apparent sudden death or death following a brief period of dyspnoea. Multifocial subacute myocarditis was present on post-mortem examination. A sixth puppy with small R waves remained clinically normal for a further 4 weeks. It then developed severe dyspnoea which persisted for 24 hours before euthanasia. Extensive fibrosis of the left ventricle was present on post-mortem examination.

Atypical porcine enterovirus encephalomyelitis: possible interraction between enteroviruses and arsenicals.

Porcine enteroviruses were isolated from weaner pigs that had nervous signs and mild non-suppurative meningoencephalomyelitis and ganglioneuritis. The clinical signs and lesions were not typical of enterovirus infection and it is believed that an organic arsenical present in feed enhanced pathogenicity of enteroviruses. Severe non-suppurative polioencephalomyelitis and ganglioneuritis were produced in gnotobiotic pigs by oral inoculation of the viruses.

Poisoning of chickens and ducks by pyrrolizidine alkaloids of Heliotropium europaeum.

The disease produced by feeding chickens and ducks a commercial poultry feed containing heliotrine and lasiocarpine, pyrrolizidine alkaloids of Heliotropium europaeum, is described. Illthrift, ascites and degenerative lesions in the liver were the major findings. Similar lesions occurred in chickens fed a diet containing H. europaeum. The source of the alkaloids in commercial poultry feed was probably the seeds of H. europaeum harvested with wheat.