Because the virus also affects the thymus and Bursa of Fabricius, slowing lymphocyte production, immunosuppression occurs and the bird becomes more vulnerable to secondary infections.

In wild red-rumped grass parakeets (Psephotus haematonotus), a case of feather loss syndrome that was highly suggestive of PBFD was first recorded in South Australia in 1907.

[3] The first case of chronic PBFD was reported in a Control and Therapy article in 1972 for the University of Sydney by Ross Perry, in which he described it as "beak rot in a cockatoo".

Like other circoviruses, BFDV possesses a small, circular single-stranded DNA (ssDNA) genome (approximately 2.0 kb in length) that is encapsidated into a non-enveloped, spherical icosahedral virion.

However, it is thought that the BFDV encodes proteins that actively transport the viral genome into the nucleus, as well as factors that direct the precursor DNA exit to the cytoplasm, where it causes large globular intracytoplasmic paracrystalline arrays.

[8] BFDV infection was thought to be restricted to within Psittaciformes, but evidence of host switching among distantly-related Australian avian species was recently demonstrated in the rainbow bee-eater (Merops ornatus),[12] powerful owl (Ninox strenua)[13] and finches.

[14] A large number of other non-psittacine birds are likely susceptible to sporadic spill-over infection,[15] and there is unpublished evidence of BFDV-associated feather disease in the laughing kookaburra (Daceolo novaeguineae), columbids, corvids and raptors including the wedge-tailed eagle (Aquila audax), white-breasted sea eagle (Haliaetus leucogaster), peregrine falcon (Falco peregrinus) and whistling kite (Haliastur sphenurus).

Knemidokoptes mites have recently been shown to concentrate BFDV within their faeces[17] which raises the possibility of ectoparasites such as hippoboscid flies acting as fomites and vectors of transmission particularly to insectivorous bird species such as the rainbow bee-eater.

In wild bird populations, transmission of infection most likely occurs within nest hollows by oral or intracloacal ingestion of the virus possibly sourced from feather dust, crop secretions, or faeces.

The disease presents as an immunosuppressive condition with chronic symmetrical irreversible loss of feathers as well as beak and claw deformities, eventually leading to death.

[24] A recently developed sLAMP assay may serve as a rapid, sensitive, and specific diagnostic field test for the detection of BFDV in clinical samples.

[15][43][23][24][16][44][45][20][25][13][12][46][excessive citations] It has the potential to become a significant threat to all species of wild parrots and to modern aviculture, due to international legal and illegal bird trade.

[24] A large number of psittacine and non-psittacine bird species globally are currently affected by BFDV both in captivity and in the wild, and the disease has the potential to disrupt vital ecosystem processes and services.

[15][22][24][13][12] A recent study has shown the importance of an accurate evaluation of avian diseases in wild populations, since invasive parrots may introduce BFDV without showing any visually detectable clinical signs.

[19] The Environment Protection and Biodiversity Conservation Act 1999 developed a threat abatement plan (TAP) with two broad goals: ensure that PBFD does not escalate the threatened species status of affected birds; and minimise the likelihood of PBFD becoming a key threatening process (KTP) for other psittacine species.

[48] PBFD has the potential to become a major threat to all species of wild parrots and to modern aviculture, due to international legal and illegal bird trade.

Epidemiological studies have shown a high seroprevalence in wild and captive flocks, indicating that infection does not always lead to the development of feather lesions.

[16] This article was adapted from the following source under a [ ] license (2020) (reviewer reports): Subir Sarker; Jade Forwood; Shane Raidal (20 September 2020).