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− | ==== Pathogenesis ==== | + | == Introduction == |
| + | Psittacine beak and feather disease is a viral disease affecting all Old World and New World Parrots (Psittacini, Hookbills), caused by the 'Beak and Feather Disease Virus' of the circovirus family. The virus was originally called Psittacine Circovirus. It is circular in shape, measures 16 nm in diameter and consists of a single strand of DNA, between 1992 and 2018 nucleotides in length. |
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− | *Replicates in rapidly dividing beak and feather cells
| + | The virus attacks the feather follicles and the beak and claw growing cells of the bird, causing progressive feather malformation and necrosis. In later stages of the disease, the feathers develop constrictions in feather shafts, cease development early until eventually all feather growth stops. |
− | *Feather loss
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− | *Beak abnormalities
| + | The beak and claws are affected oppositely to the feather. These will overgrow, deform and necrotic tissue will develop. This then increases the risk of secondary bacterial or yeast infection setting in. |
| + | The disease also has a general immunosuppressive effect on the bird, clearing path for secondary systemic viral and bacterial infections which are usually the cause of death, not the PBFD virus itself. |
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− | ==== Epidemiology ====
| + | The first report of featherless, dirty-looking birds in Australian bush was in 1907 by Edwin Ashby. Over the years, Australian people seeing birds like this have thought their condition was caused by exclusive sunflower seed diet, which is often the main source of food for Australian cockatoos in captivity. The first case of chronic PBFD described by a vet was reported in a Control and Therapy article in 1972 for the University of Sydney by Dr Ross Perry. |
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− | *Affects mainly birds under 5 years of age
| + | The disease is transmitted by vertical transmission from parents to their offspring or from other members of the flock by horizontal transmission. The adult birds coming into contact with the virus usually (but not always) develop resistance to it, but the virus is retained in their body and, in most cases, is excreted in feces and feather debris for the rest of their life. No antibodies are transferred to the young, therefore their naive immune system makes them very susceptible to the PBFD virus in their first few weeks of life. The virus may be transferred in crop secretions, fresh or dried feces and feather and skin particles. |
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| + | The virus remains viable in the environment for many years and is resistant to most disinfectants. |
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− | ==== Control ====
| + | BFDV has now been reported on all continents and is increasing in prevalence due to increased legal and illegal bird trade. |
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− | *Import restrictions:
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− | **Quarantine
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− | **PCR screening
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| + | == Clinical Signs == |
| + | The peracute form of the disease is characerised by sudden death with no previous signs of ill health. This usually occurs in hatchlings, particularly in cockatoos. |
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| + | The acute form of the disease occurs most commonly in nestlings or very young birds during their first phase of feather growth. It is manifested by lethargy, depression, abdominal pain, loss of appetite, vomiting and diarrhoea. There is usually a loss of powder down, with resulting shiny black beak in those birds whose beaks are usually dusty grey. The feathers may be abnormally coloured in somecases. Due to the severe suppression of the immune system, multiple secondary viral and bacterial infections will develop, which will cause the death within two to four weeks. |
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| + | The chronic form of disease is the 'classic' form, seen most commonly, and it occurs in older birds, with the feather loss and beak deformity increasing with each moult. The feather loss will eventually affect the whole body, including the head. |
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| + | Some species of birds show no clinical signs yet are carriers of the disease. These are commonly budgerigars, cockatoos and cockatiels. They actively shed the virus in secretions and will infect other birds. |
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| + | == Diagnosis == |
| + | History and clinical signs, especially in the chronic form are highly suggestive of the disease. |
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| + | Blood samples can be taken which may show a severe leucopenia, but definitive diagnosis must be achieved by virus isolation from the bird. |
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| + | A PCR is the most accurate and reliable test avaliable for virus detection. Samples for PCR can include feathers, blood and bone marrow, the latter of which is the most reliable. BFCV is known to occur in different strains and unfortunately not all laboratories doing PCR testing can pick up all strains. |
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| + | Haemoagglutination inhibition can also be performed to detect the virus. However this is not as sensitive as the PCR. |
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| + | == Treatment and Control== |
| + | Currently there is no cure for this condition. |
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| + | Single pet birds in caring homes may be maintained provided quality of life is reasonable and beak deformity is not preventing eating. Supplementing with vitamins, minerals, and probiotics to boost the immune system will help, and treatment of secondary infections will be required regularly. |
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| + | If a bird is infected and is being kept with several other birds, the bird should be quarantined and the pens disinfected to prevent spread to other birds. Infected or positive carrier birds in collections should be culled, and all cages and equipment thoroughly and repeated sterilised. Remaining birds should be tested repeatedly and regularly to detect new infections. Once a group of birds is contaminated, it will prove very difficult to totally eliminate this virus. |
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| + | Therapeutical interventions can only be limited to treating secondary infections (bacterial/fungal), however some veterinarians have injected interferon (an anti-viral drug) from poultry into young parrots in the early stages of infection, with some limited success. Commercially-available interferon derived from cats has not worked. |
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| + | An experimental vaccine has been proven to provide protection against the virus, but is likely to accelerate the disease in parrots already infected with the virus. A new vaccine developed by Dr. Siwo de Kloet protects birds from the virus and does not endanger birds already infected with PBFD. Further development to refine the vaccine and make it commercially available is progressing slowly due to the lack of funding. |
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| + | == References == |
| + | Bridger, J and Russell, P (2007). Virology Study Guide, Royal Veterinary College. |
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| + | Pass, D. A. and Perry, R. A. (1984). The pathology of psittacine beak and feather disease. Aust Vet J, 61, 69–74. |
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| + | Pass, D. A. and Perry, R. A. (1985). Psittacine Beak and Feather Disease: An update. Aust Vet Practit, 15, 55–60. |
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| + | Raidal, S. R. (1994). Studies on Psittacine Beak and Feather Disease, PhD thesis, University of Sydney, Sydney. |
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| + | Raidal, S.R., Johnsen Bonne, N. and Stewart, M. (2005). Development of Recombinant Proteins as a Candidate Vaccine for Psittacine Beak and Feather Disease. Murdoch University, Perth, Western Australia |
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| [[Category:Dermatological Diseases - Birds]][[Category:Avian Viruses]] | | [[Category:Dermatological Diseases - Birds]][[Category:Avian Viruses]] |
− | [[Category:To_Do_-_Clinical/Viruses]] | + | [[Category:To_Do_-_Review]] |