Summary Background During 2016–2018, 15 critically ill neonatal foals with acute respiratory distress associated with Chlamydia psittaci infection were presented to three referral hospitals in New South Wales. Chlamydia psittaci has not previously been associated with the development of neonatal respiratory disease. Objectives To investigate and describe the clinical features and outcome of C. psittaci infection in neonatal foals. Study design Multicentre retrospective case series. Methods The clinical, clinicopathological, necropsy and histological features of 15 foals with confirmed C. psittaci infection were reviewed and reported. Results Thirteen foals with C. psittaci infection died or were subjected to euthanasia within 36 h of hospitalisation and two foals survived to discharge. Findings during post‐mortem examination of nonsurviving foals included bronchopneumonia, pulmonary congestion, hepatic congestion and hepatic inflammation. Detection of C. psittaci was achieved using polymerase chain reaction (PCR) testing of swabs of nasal secretions (4/6) and rectal mucosa (5/7) from live foals, lung tissues of foals at necropsy (11/14) and foetal membranes (4/5). Main limitations Small numbers of confirmed cases of neonatal C. psittaci infection and inconsistent sampling methods. Conclusions Chlamydia psittaci should be considered a differential diagnosis for neonatal foals with signs of severe systemic disease, including equine neonatal acute respiratory distress syndrome (EqNARDS). Chlamydia psittaci is a zoonotic pathogen and a personal protective equipment (PPE) should be worn for the management of foals with suspected or confirmed infection.

Psittacine beak and feather disease virus (PBFDV) was administered to adult galahs (Eolophus roseicapillus) by mouth or by intramuscular injection. Concentration of PBFDV antibodies in serum and excretion of PBFDV were monitored by haemagglutination inhibition (HI) and haemagglutination (HA) respectively. After oral administration, 17 of 18 galahs remained clinically normal and a small rise in antibody titre was detected in 3 of 18 birds. After intramuscular administration, antibody was detected in all birds. PBFDV was not detected in the feather dander of birds in either group. One bird developed diarrhoea and high faecal HA titres within 4 days of oral administration and then died. Adult and nestling cockatoos were vaccinated with an experimental inactivated double-oil emulsion vaccine. PBFDV antibody responses are comparable to those induced by a primary-oil emulsion vaccination regimen using Freund's adjuvants. Both vaccines protected nestlings. Three sibling wild-caught sulphur-crested cockatoos were vaccinated but died of PBFD before experimental challenge despite antibody responses in all birds. Unvaccinated control chicks developed acute PBFD within 4 weeks of challenge, probably from PBFDV-induced hepatitis since high concentrations of PBFDV were detected in their livers.

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