These studies clearly demonstrate the existence of an avian reservoir of remarkably diverse bornaviruses and provide a compelling candidate in the search for an etiologic agent of PDD.

Background: Proventricular dilatation disease (PDD) is a fatal disorder of psittacine birds worldwide. The disease is characterized by lymphoplasmacytic infiltration of the central and peripheral nervous systems, leading to gastrointestinal motility and/or central nervous system dysfunction. Recently, we detected a significant association between avian bornavirus (ABV) infection and clinical signs of PDD in psittacines. However, it remains unclear whether ABV infection actually causes PDD. To address this question, we examined the impact of ABV inoculation on the cockatiel (Nymphicus hollandicus).

Proventricular dilatation disease (PDD) is a fatal inflammatory disease that affects mainly, but not exclusively, psittacine birds (Order: Psittaciformes). PDD has long been suspected to be a viral disease, but its causative agent, a novel Bornavirus, was only identified in 2008.

Susceptibility of North American owls to WNV is associated with native breeding range.

This study describes the macroscopic and microscopic lesions and the viral antigen distribution in 82 owls (Family: Strigidae) of 11 North American and one Eurasian species that died following natural West Nile virus infection. The range of lesions seen was greater than that previously reported for owls, and involved more organs. Two patterns of antigen distribution were identified: one that involved the blood and all major organs; and a second where antigen was sparse, localized, and absent from the blood. The first pattern was associated with species of northern natural breeding range, while the second was seen in owls of a more southern distribution and appeared to be associated with a more prolonged course of illness. Further differences in lesion and antigen distribution appeared to be either species related or individual. The findings underline the complexity and variability of West Nile virus pathology within birds of a relatively narrow taxonomic group.

The quantitative mechanistic acid-base approach to clinical assessment of acid-base status requires species-specific values for [A]tot (the total concentration of nonvolatile buffers in plasma) and Ka (the effective dissociation constant for weak acids in plasma). The aim of this study was to determine [A]tot and Ka values for plasma in domestic pigeons. Plasma from 12 healthy commercial domestic pigeons was tonometered with 20% CO2 at 37 degrees C. Plasma pH, Pco2, and plasma concentrations of strong cations (Na, K, Ca), strong anions (Cl, L-lactate), and nonvolatile buffer ions (total protein, albumin, phosphate) were measured over a pH range of 6.8-7.7. Strong ion difference (SID) (SID5=Na+K+Ca-Cl-lactate) was used to calculate [A]tot and Ka from the measured pH and Pco2 and SID5. Mean (+/-SD) values for bird plasma were as follows: [A]tot=7.76+/-2.15 mmol/l (equivalent to 0.32 mmol/g of total protein, 0.51 mmol/g of albumin, 0.23 mmol/g of total solids); Ka=2.15+/-1.15x10(-7); and pKa=6.67. The net protein charge at normal pH (7.43) was estimated to be 6 meq/l; this value indicates that pigeon plasma has a much lower anion gap value than mammals after adjusting for high mean L-lactate concentrations induced by restraint during blood sampling. This finding indicates that plasma proteins in pigeons have a much lower net anion charge than mammalian plasma protein. An incidental finding was that total protein concentration measured by a multianalyzer system was consistently lower than the value for total solids measured by refractometer.

Lead toxicosis induced significant changes in the values of commonly measured hematologic parameters in waterfowl. These changes may be useful indicators of severe lead intoxication during routine laboratory assessment. Changes in clinical chemistry values, although statistically significant, were too inconsistent to serve as indicators of lead toxicosis.

Diabetes mellitus was diagnosed in a 5-year-old male chestnut-fronted macaw (Ara severa) and an 8-year-old female Military macaw (Ara militaris) based on persistent hyperglycaemia and glucosuria. Hepatic biopsies showed marked hepatic haemosiderosis, while pancreatic biopsies showed no inflammatory lesions. Repeatable and titratable responses to bovine or porcine protamine zinc insulin were recorded in both patients, who were followed up for more than 2 years. In addition, ironelimination therapy was initiated by chelation or phlebotomy, and the birds' diet was changed to lowiron content pellets. Both birds responded favourably to this therapy, showing a decreased demand for extrinsic insulin. Follow-up biopsies demonstrated marked reduction in hepatic haemosiderin. Plasma fructosamine and b-hydroxybutyric acid levels were measured periodically in both birds and compared with euglycaemic psittacines. Both tests appeared useful for monitoring treatment success. The potential association between diabetes mellitus and excessive iron storage in birds should be further investigated.