We document columbid herpesvirus-1 (CoHV-1) infection in two barking owls (Ninox connivens), a powerful owl (Ninox strenua) and an Australian hobby (Falco longipennis). Antemortem signs of infection were non-specific and the birds either died soon after they were identified as ill or were found dead unexpectedly. Gross postmortem findings were also not specific. Microscopically, marked to massive splenic and hepatic necrosis with the presence of eosinophilic inclusion bodies in remaining splenocytes and hepatocytes was found in all birds. Herpesvirus virions were identified in liver sections from one of the boobook owls by electron microscopy. Using CoHV-1-specific primers and polymerase chain reaction, CoHV-1 DNA was amplified from tissue samples from all birds. A comparison of these sequences to previously reported sequences of CoHV-1 found them to be identical or to vary by a single base pair. These findings increase the number of known species of birds of prey that are susceptible to CoHV-1 infection and indicate that rock pigeons (Columbia livia) should not be included in the diet of captive Australian birds of prey.
Transfer of maternal immunoglobulin G (IgG) to the yolk and nestling was investigated in the budgerigar. Specific antibodies to avian polyomavirus and Newcastle disease virus could be detected in 82% of yolk extracts of eggs from seropositive hens. Using a double immunodiffusion assay with anti-chicken IgG antibodies, IgG could also be detected in yolk supernatants with virus neutralizing activity. In all assays, IgG concentrations in the yolk extracts were significantly less than those of the adult budgerigar serum. No antiviral activity was detected in nestling serum. Examination of nestling serum with the double immunodiffusion assay and an immuno-dot-blot technique specific for IgG showed that detectable concentrations of IgG are not present in nestling serum until after the yolk sac is fully absorbed. This observation, coupled with the absence of specific anti-viral antibody in nestlings of seropositive hens, indicated that none of the yolk sac antibody reached the nestling circulation.
Objective
To assess the efficacy of a commercially available in‐water amphotericin B treatment for Macrorhabdus ornithogaster.
Design
Clinical treatment trial.
Methods
Faecal shedding of 16 naturally infected budgerigars (Melopsittacus undulatus) was monitored while they were being treated using in‐water amphotericin B, as per the manufacturer's instructions, for 10 days. Any birds that remained positive after 10 days received a further 10 day course of treatment. All birds were rechecked 16 days after the end of the second treatment period.
Results
At the conclusion of treatment, 11 birds had stopped shedding M. ornithogaster, and 5 birds were still shedding. Sixteen days after the conclusion of the second treatment period, four birds that were negative after 10 days of treatment were shedding again, and two of the birds that were treated for 20 days were shedding. In addition, one bird from each treatment group died after treatment and before follow‐up testing.
Conclusion
These findings represent a 36% treatment failure, suggesting that treatment with the commercially available, water‐soluble amphotericin B has inconsistent efficacy against M. ornithogaster in some budgerigars in Australia and is not effective for eliminating it from budgerigar aviaries.
Adult budgerigars (Melopsittacus undulatus) with 2 years of breeding experience were removed from an aviary with enzootic avian polyomavirus (APV) disease and maintained in an isolation unit. Following a 7-month respite from breeding, these birds were allowed to breed without interruption for 2 years. Although the adults were seropositive both at the beginning and end of the experiment, all 102 of their offspring were seronegative. These data suggest that APV can be eliminated from a budgerigar aviary with the use of simple management techniques.
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