To date, several DNA viral infections have been reported in psittacine birds. Psittacine beak and feather disease (PBFD) is characterized by symmetric feather dystrophy and loss and development of beak deformities. PBFD is caused by beak and feather virus, which belongs to the Circoviridae, and is the most important infection in psittacine birds worldwide. Avian polyomavirus infection causes acute death, abdominal distention, and feather abnormalities. Pacheco's disease (PD), which is caused by psittacid herpesvirus type 1, is an acute lethal disease without a prodrome. Psittacine adenovirus infections are described as having a clinical progression similar to PD. The clinical changes in psittacine poxvirus-infected birds include serious ocular discharge, rhinitis, and conjunctivitis, followed by the appearance of ulcerations on the medial canthi of the eyes. Internal papillomatosis of parrots (IPP) is a tumor disease characterized by progressive development of papillomas in the oral and cloacal mucosa. IPP has been suggested to caused by papillomavirus or herpesvirus. However, information about these diseases is limited. Here we review the etiology, clinical features, pathology, epidemiology, and diagnosis of these DNA viruses.

Equine Herpesvirus Type 9 in Giraffe with Encephalitis

Susceptibility of DT40 cells to pathogenic field strains of infectious bursal disease virus (IBDV) including very virulent and classical virulent strains were studied. After the first and second passage of the virus in DT40 cells, IBDV-specific antigen was readily detected in DT40 cells inoculated with the pathogenic field strain infected bursal homogenates. Nucleotide sequence analysis in the VP2 hypervariable domain, which is critical for the virulence of IBDV, revealed no common amino acid substitutions among the pathogenic IBDVs in accordance with the propagation in DT40 cells. These results indicate that DT40 cells are a useful tool for rapid isolation of pathogenic field strains and successive in vitro analysis of IBDV.

Two attenuated infectious bursal disease virus strains used as commercial live vaccine were passaged five successive times in specific-pathogen-free chickens and chicken embryo fibroblast (CEF) cells. Both attenuated strains increased in virulence during the passage in susceptible chickens as evidenced by the decrease in bursa/body weight ratios. A direct nucleotide sequence analysis of the VP2 hypervariable domain amplified by the reverse transcription-polymerase chain reaction revealed that the nucleotide at position 890 (T) in both strains was A after the passage in chicken. In addition, the nucleotide at position 890 (A) was T or C after the subsequent passage in CEF cells. Because of the nucleotide differences, the amino acid residue at position 253 (His) in both vaccines was Gln after the passage in chickens, and the amino acid residue Gln was changed back to His during the subsequent passage in CEF cells. The digestion of the amplified fragment with restriction endonucleases Stul and Ncol, which recognize the sequence difference at position 890, showed that the population of the virus that had amino acid Gln at position 253 was gradually increased during the passage in chickens. Conversely, the population of the virus that had amino acid His at position 253 was gradually increased during the subsequent passage in CEF cells.