In 1991, velogenic viscerotropic Newcastle disease (VVND) was diagnosed in domestic psittacine birds in six states: Illinois, Indiana, Michigan, Texas, California, and Nevada. In the first four states, the disease assumed outbreak proportions. The affected psittacine birds--yellow-headed Amazon parrots (Amazona ochrocephala oratrix), yellow-naped Amazon parrots (Amazona ochrocephala auropalliata), cockatiels (Nymphicus hollandicus), and conures (unknown species)--exhibited respiratory and/or central nervous system signs. The velogenic viscerotropic Newcastle disease virus (VVNDV) was isolated from cloacal and tracheal swabs and various tissues, such as the lung, trachea, distal intestine, and spleen. The origin of the birds could not be established. The disease in the six states was promptly controlled, with no evidence that domestic poultry had been exposed. Also, VVNDV was isolated from quarantined birds intended for importation into the United States. Included were 53 moustached parakeets (Psittacula alexandri fasciata), a mynah (Gracula religiosa), a drongo (Dicrurus sp.), and three partridges (family Phasianidae). Groups of birds that yielded VVNDV were denied entry into the United States. Birds that are illegally imported and therefore not tested for the presence of foreign animal pathogens are a potential source of VVNDV and a threat to domestic poultry and caged birds.
An epizootic of duck plague occurred in early 1973 in a population of 163,500 wild waterfowl, primarily mallards (Anas platyrhynchos), wintering on Lake Andes and the nearby Missouri River in southeastern South Dakota (USA). The diagnosis was based on pathologic lesions and confirmed by virus isolation. Control measures included quarantine, attempts to reduce virus contamination of the area, dispersal of waterfowl, and monitoring of wild waterfowl populations for mortality. The epizootic resulted in documented mortality of 18% and estimated mortality of 26% of the waterfowl at risk. Prompt implementation of control measures might have limited mortality to approximately 8%. Losses during the epizootic were equivalent to 0.12% of the annual mortality in the North American 1996 fall population of 80,000,000 wild ducks. The most likely sources of the infection were free-flying wild mallard or American black duck (Anas rubripes) carriers from the upper midwestern or northeastern United States. Duck plague serum neutralization antibodies were demonstrated in 31% of 395 apparently healthy mallards sampled prior to dispersal of the flock at Lake Andes, suggesting that tens of thousands of potential duck plague carriers entered the wild waterfowl populations of all four major flyways. Consequently, the absence of major epizootics of duck plague in wild waterfowl in the subsequent two decades is evidence that substantial numbers of duck plague carriers can occur in wild waterfowl populations without resulting in epizootic mortalities. The failure to isolate duck plague virus from apparently healthy mallards sampled during the epizootic raises questions concerning the validity of conclusions regarding the status of duck plague in wild waterfowl based upon negative results of random surveys conducted in the absence of epizootics.
A trial was conducted to determine the suitability of using a pelleted diet containing chlortetracycline (CTC) for treatment of chlamydiosis in macaws. Macaws, normally fed seed and fruit diets in captivity, are notoriously difficult to treat with CTC-medicated mash diets. Healthy macaws fed a pelleted diet containing 1% or 1.5% CTC for 30 or 45 days maintained adequate food intake and mean blood concentrations of 1-2 CTC micrograms/ml blood throughout the treatment period. There were no significant differences between blood concentrations induced by the different dietary CTC concentrations. Blood concentrations of 1 microgram/ml are considered therapeutic, so it is likely that 1% CTC-medicated pellets will be adequate for treating chlamydiosis in these species.
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