Avian cryptococcosis.

Clinical and laboratory findings in 15 unreported cases of avian cryptococcosis from Australia were collated and contrasted with 11 cases recorded in the literature. Cryptococcus species produced localized invasive disease of the upper respiratory tract of captive parrots living in Australia. This resulted in signs referable to mycotic rhinitis or to involvement of structures contiguous with the nasal cavity, such as the beak, sinuses, choana, retrobulbar space and palate. Parrots of widely differing ages were affected and of the seven birds for which sex was determinable, six were male. Cryptococcus bacillisporus (formerly C. neoformans var. gattii) accounted for four of five infections in which the species or variety was determinable, suggesting that exposure to eucalyptus material may be a predisposing factor. In these cases, Cryptococcus appeared to behave as a primary pathogen of immunocompetent hosts. One tissue specimen was available from an Australian racing pigeon with minimally invasive subcutaneous disease; immunohistology demonstrated a C. neoformans var. grubii (formerly C. neoformans var. neoformans serotype A) infection, presumably subsequent to traumatic inoculation of yeast cells into the subcutis. Two similar cases had been reported previously in pigeons domiciled in America. Data for parrots, one pigeon and other birds studied principally in America and Europe (and likely infected with C. neoformans) suggested a different pattern of disease, more suggestive of opportunistic infection of immunodeficient hosts. In this cohort of patients, the organism was not restricted to cool superficial sites such as the upper respiratory tract or subcutis. Instead, infections typically penetrated the lower respiratory tract or disseminated widely to a variety of internal organs. Finally, three captive North Island brown kiwis, one residing in Australia, the other two in New Zealand, died as a result of severe diffuse cryptococcal pneumonia (two cases) or widely disseminated disease (one case). C. bacillisporus strains were isolated from all three cases, as reported previously for another kiwi with disseminated disease in New Zealand.

Central nervous system toxoplasmosis in Roller canaries.

Several birds in a flock of 40 Roller canaries (Serinus canaria) from an outdoor aviary in Victoria, Australia, developed central nervous system signs that included blindness, nystagmus, ataxia, and head rotation. Four died, and four were euthanatized. Two euthanatized birds were submitted for microscopic examination of tissues. Brain lesions in both birds consisted of scattered foci of nonsuppurative meningoencephalitis with gliosis, mild to moderately extensive lymphocytic/plasmacytic perivascular cuffs, and a patchy increased prominence of cerebral blood vessels associated with hypertrophy of the vascular endothelium and/or thickening of their connective tissue walls. These lesions were associated with the presence of Toxoplasma gondii tissue cysts. Lesions in the eyes of both birds were bilateral and consisted of severe plasmacytic/granulomatous ophthalmitis. Surviving birds were treated with trimethoprim and sulfadiazine, no subsequent deaths occurred, and no new cases developed over an 8-month period.

Viral enteritis in cockatoos (Cacatua spp.).

Sulphur-crested cockatoos (Cacatua galerita) and galahs (C. roseicapilla) captured in Victoria, Australia at 7 to 9 weeks of age were found to suffer a profuse diarrhoea and wasting syndrome ending in death. Necropsy revealed dilatation of the duodenum with mucosal thickening. Histologically, the duodenal mucosa had short, fused villi, with marked proliferation of crypt enterocytes compared with normal birds. Electron microscopic examination of faeces and intestinal sections revealed the presence of round, unenveloped viral particles approximately 30 nm diameter, with no surface structures and a smooth, entire edge. Although no virus was cultured, it is likely that an enterovirus infection was associated with a significant enteritis in the cockatoos.

Glucagon and insulin release in the lamb before and after birth: effects of amino acids in vitro and in vivo.

The amino acids glycine, L-serine, L-asparagine and L-glutamine at 5 mmol/l each markedly increased glucagon release from perifused fetal lamb pancreas tissue, whereas the branched-chain amino acids L-leucine and L-valine had no effect. In contrast, only L-leucine and L-valine had any effect on insulin release. With perifused pancreas tissue from newborn lambs (5-9 days of age) glycine, L-serine, L-asparagine, L-arginine and L-lysine caused a similar marked increase in glucagon secretion with glycine having the greatest effect. These stimulatory effects were attenuated little by addition of glucose (20 mmol/l). L-Leucine had little effect on glucagon release, but was the only amino acid tested which caused marked insulin release in the absence of glucagon. Continuous intravenous infusion of glutamine (3 mmol/h per kg estimated fetal weight) or glutamine and asparagine each at this rate for 2 h into chronically cannulated fetal sheep in utero significantly increased plasma glucagon (P less than 0.05) and insulin (P less than 0.01) concentrations, although the effect on glucagon was not great. The results show how a range of amino acids can influence glucagon and insulin release from the pancreas of fetal and newborn lambs suggesting that physiological changes in plasma amino acid concentrations may contribute to regulation of glucagon and insulin release in utero in this species.