replied 4 years ago.
First of all, PBFD is caused by a virus that is quite contagious. Viral particles are shed from infected birds in the feathers and feather dust, so it's easily airborne. That means it can be transmitted from one bird to another within one house, for example, if if the birds are kept in separate rooms, because it will travel through the ventilation system.
The virus can also live on fomites (inanimate objects like clothes, dishes, etc.) and be transmitted that way. It's very hardy in the environment and survives for a long time.
All of these things mean that a bird can acquire PBFD (circovirus) without being directly in contact with an infected bird.
It is also possible for a bird to become infected with the PBFD virus (circovirus) and not develop any clinical signs of illness for quite some time. That bird can still infect other birds (be an asymptomatic carrier). I mention that because even though your birds are not around any other birds now, they may have been exposed earlier in their lives, and could have become asymptomatic carriers then. While this is not likely and becomes even less likely with each year that passes during which they remain healthy, it is still possible.
For further understanding, I have attached a useful article below...
A Review of Circovirus, Polyomavirus and Adenovirus in Psittacine Birds and a Future Direction for Australian Research
Final Year Veterinary Science Student, The University of Melbourne, Werribee, Australia
Psittacine circovirus (Beak and feather disease virus) and polyomavirus are able to cause illness and death in captive and wild psittacine birds (Katoh et al. 2010). Relevant literature recognises that these viruses have a worldwide distribution (Shearer et al. 2008; Katoh et al. 2010). Comparatively, the distribution and effects of psittacine adenovirus, particularly on wild populations, but also captive psittacine birds, is still largely unknown, despite some case study literature (Wellehan et al. 2005). This paper reviews these three diseases and highlights the need to readily identify birds ailed by these viruses both clinically and subclinically. It presents a novel direction of study being conducted by a final year Veterinary Science student at the University of Melbourne and the issues associated with conducting such an investigation.
Psittacine beak and feather disease is caused by psittacine circovirus. This virus was first recorded in 1903 in the sulphur-crested cockatoo (Cacatua galerita) population in Australia (Raidal 2012). It has since been documented to occur on a worldwide basis and is now recognised as the most common disease of captive and wild psittacine birds (Raidal 2012). Over 60 species of captive and free-ranging parrot species have been found to be susceptible (Ha et al. 2007).
Aetiology and Epidemiology
Psittacine circovirus is a member of the Circoviridaefamily (Ypelaar et al. 1999; Ritchie et al. 2003). The smallest of viruses yet described, belong to this family of viruses (Greenacre 2005). The virus particles are housed in a non-enveloped, icosahedral capsid measuring between 5 and 26nm in diameter (Ritchie et al. 2003). The capsid contains a single strand of circular DNA, approximately 2000 nucleotides in size (Ypelaar et al. 1999; Ritchie et al. 2003).
This virus is exceptionally resistant to the elements, being likely to remain infective for months to years (Greenacre 2005). Transmission occurs in a horizontal fashion; via inhalation, ingestion or even movement across the bursal epithelium (Phalen 2006). Diseased and carrier birds shed the virus in their faeces, crop secretions and feather dander (Ritchie et al. 2003; Phalen 2006). Contaminated fomites can be a mechanism of indirect horizontal transmission. In the nesting situation, feather dander and crop secretions have a high concentration of virus, and given the immature immune system in a nestling (Ritchie et al. 2003), recently hatched and juvenile birds are the most at risk age group (Phalen 2006). In some instances, viral DNA has been detected in embryonated eggs, suggesting the possibility of vertical transmission (Greenacre 2005).
Pathogenesis and Clinical Signs
Psittacine circovirus targets the host's cell mediated immune system (Ritchie et al. 2003). Replication occurs in the bursa of Fabricus, thymus, gastro-intestinal associated lymphoid tissue, and circulating lymphocytes (Ritchie et al. 1989; Phalen 2006). The ultimate site this virus targets is the epidermis and feather follicles (Raidal 2012).
There is an acute and a chronic clinical presentation associated with psittacine beak and feather disease. Signs present within 21–28 days of infection and often the only sign is sudden death (Raidal 2012). Alternately, nestlings may be depressed, regurgitate, develop a green diarrhoea, be systemically ill, and if any haematology is conducted, a leucopenia may be identified (Greenacre 2005; Raidal 2012). Newly developing feathers will have annular constricting bands and they can easily break, be pulled out or bleed (Phalen 2006).
The chronic form is the one which is most familiar to clinicians. Chronic infections in the cockatoo (Cacatua) family present in parrots under three years old (Phalen 2006). It is more insidious, progressing only with each subsequent molt (Ritchie et al. 1989; Greenacre 2005). Incubation time is highly variable depending on which stage of the molt the parrot is in at the time of infection. Eventually, dystrophic feathers will replace normal ones. The down and contour feathers are often the first affected, with the primary feathers succumbing to changes later (Greenacre 2005). Growing feathers are short, having a clubbed appearance, with evidence of past or recent haemorrhage in the shaft (Phalen 2006). Clinically, this manifests as a symmetrical feather dystrophy and loss (Katoh et al. 2008, Ritchie et al. 1989). Beak lesions are common in cockatoos and their relatives. A lack of powder down dust on the beak is one of the first signs of beak and feather disease (Phalen 2006). Lesions progress with beak elongation, fractures and eventual necrosis (Ritchie et al. 1989).
Members of the cockatoo (Cacatuaspp.) family and the galah (Eolophus roseicapilla) are the most diverse in their clinical presentations. African grey parrots (Psittacus erithacus) show signs similar to the cockatoo species (Phalen 2006). Comparatively, lovebirds (Agapornisspp.) have no clinical disease and can eliminate the virus. Fledgling budgerigars (Melopsittacus undulatus) tend to lose primary and secondary wing feathers, making its distinction from polyomavirus difficult (Phalen 2006). In Australian rainbow lorikeets (Trichoglossus haematodus), approximately one third will show persistent feather abnormalities, one third die before their first molt, and the remaining develop normal feathers after their molt (Phalen 2006). Other species may only have very easily pluckable feathers or yellow feathers replacing normally green feathers (Raidal 2012). Affected parrots often succumb to secondary infections because of the immunosuppressive effects of the virus (Ritchie et al. 2003).
Circoviral infection in psittacine birds is diagnosed by a combination of methods. Clinicians often reach a presumptive diagnosis based on clinical signs (Phalen 2006). Should the affected bird be fatally affected, or if a clinically affected bird is submitted for post mortem examination, histopathological examination should reveal large basophilic intranuclear and intracytoplasmic inclusion bodies within macrophages, keratinocytes, hepatocytes and other tissues (Ritchie et al. 1989; Raidal 2012). Alternatively, serological methods (haemagglutination assay, haemagglutination inhibition assay and virus neutralisation) can be employed on feathers, blood and faecal matter. Enzyme-linked immunosorbent assay (ELISA), DNA in situ hybridisation and PCR have also been utilised (Kennedy 2005; Katoh et al. 2010). A PCR assay on heparinised blood will often enable confirmation of viral infection (Phalen 2006).
Prevention and Control
Psittacine circovirus is highly resistant to desiccation in the environment and to common disinfectants. Products that are often suitable for inactivating environmentally resistant viruses, such as glutaraldehyde (Raidal 2012) and Virkon-S are recommended when attempting to disinfect contaminated surfaces (Dahlhausen 2010). Where disinfection procedures cannot safely or readily be employed, control is most often limited to preventing introduction of a shedding bird into a naive environment. Appropriate quarantine, biosecurity and routine screening of new birds should enable identification of infected birds (Raidal 2012). Such birds should be immediately removed as they shed massive amounts of virus (Phalen 2006). Any birds exposed to an infected bird should also be quarantined. In-contact birds can be tested initially, and after one month in quarantine, which allows sufficient time for viraemia to develop and be detected (Phalen 2006). An inactivated vaccine has been produced in Australia, although it is not commercially available (Raidal 2012).