Psittacine Beak and Feather Disease
Psittacine beak and feather disease (PBFD) was first described in various species of cockatoos in the early 1970s. The disease was characterized by abnormal feather development and loss, beak deformities and eventual death.
In the mid 1980s, researchers at the University of Georgia demonstrated that PBFD was caused by a previously undescribed virus, now designated PBFD virus 1. Several years ago, the same research group identified a variant of this virus (PBFD virus 2) that was originally recovered from lories.
To date, PBFD virus 2 has only been documented in lories. However, other birds may be susceptible to this or other variants. These variants may have a disease progression that is different from that described for PBFD virus 1.
Psittacine beak and feather disease has been documented in more than 40 species of captive and free-ranging Old World psittacine birds (cockatoos, African grey parrots, Eclectus parrots, lovebirds and budgerigars) as well as several species of New World Psittaciformes (Amazon parrots, macaws and pionus). Viruses related to the PBFD virus have been reported in pigeons, Senegal doves, canaries, finches, geese, southern black-backed gulls, ostriches, pigs, chickens and humans.
The PBFD virus is highly infectious and environmentally stable. However, most birds exposed to PBFD virus will have virus in their blood for a brief period (which can be detected using DNA probes), followed by an appropriate immune response that clears the virus before any recognizable feather abnormalities occur. Birds that survive this infection (typically without developing feather abnormalities) can be viewed as naturally vaccinated. Genetic material (DNA) from this virus can be detected in a bird's blood as soon as 2 days after natural exposure to the virus, and weeks to months before an infected bird will develop feather abnormalities.
When the PBFD virus was characterized more than a decade ago, this virus was a common cause for the abnormal development of feathers. Because of improved education, improved aviary management and widespread use of diagnostic tests developed by researchers at the University of Georgia, today most feather abnormalities are caused by problems other than PBFD virus. The notable exception is that many lovebirds, budgerigars and lories with abnormally developing feathers will be diagnosed with PBFD virus.
What to Watch For
Birds may be infected with PBFD for months before developing feather abnormalities.
- Loose feathers. The first outward change that should raise suspicion is the appearance of loose, abnormally formed feathers. The type of feathers initially involved depends on the stage of molt when the feather damage first appears. In young birds less than 2 months old, all of the feather tracts may be affected during a period of several weeks. In older birds, the disease is usually more prolonged, with progressive feather damage occurring during ensuing molts.
- Beak lesions. If beak lesions develop, they may include ulcers and plaques in the roof of the mouth, progressive elongation and fractures of the beak covering.
- Systemic infection. Some young psittacine birds develop a rapidly progressive systemic infection with a sudden onset of depression, loss of appetite, regurgitation, crop stasis, diarrhea and pneumonia. This form of the disease is most common in young cockatoos and African grey parrots and these birds may die before feather abnormalities are easily recognized.
- Dark patches in feather shafts. Other young birds may be depressed for several days followed by a sudden appearance of dark red-brown patches in the shafts of developing feathers or premature shedding of feathers with a deformed or constricted base.
Birds that survive these rapid forms of the disease develop more chronic problems. Most pictures of featherless birds illustrate the chronic form of PBFD, which has progressed for years. The feather loss usually occurs equally in the feather tracts on each side of the body and normal feathers are progressively replaced with abnormally developed feathers during each successive molt. Suspicious changes include retention of feather sheaths, red-brown patches (represents accumulations of dying cells) within the developing feathers, fractures of the feather shaft and deformities or constrictions at the base of abnormal feathers.
Some birds die shortly after the first indication of malformed feathers; others may live for several years in a featherless state. While PBFD is reported most commonly in birds less than three years of age, the disease can also develop in older adult birds that have previously shown no signs of feather abnormalities.
The time period between exposure to PBFD virus and the development of feather abnormalities has been shown to vary among various species and among individuals in the same species. The minimum incubation period is 21 to 24 days. The incubation period in chicks with infections passed to them by the hen has been shown to vary from 32 to 80 days.
Psittacine beak and feather disease should be suspected in any bird with progressive feather loss involving malformed feathers. However, one cannot determine if a bird is infected with the PBFD virus strictly by examining the feathers. Visible feather changes similar to those caused by PBFD virus can be induced by any factor that disrupts the blood supply to the developing feather, including: avian polyomavirus; adenovirus; trauma; bacterial folliculitis; fungal folliculitis; septicemias; malnutrition; endocrine abnormalities and some drug reactions, particularly to penicillins and cephalosporins.
Feather abnormalities identical to those caused by PBFD virus also can be produced by damaging developing feathers at or near the pulp cap. Conversely, birds with normal-appearing feathers can have PBFD virus DNA in their blood stream. A DNA probe-based test can be used to determine if DNA from the virus is in the blood of birds with or without feather abnormalities. However, in birds with feather abnormalities, PBFD virus infections are best confirmed by using a microscope to demonstrate characteristic intracytoplasmic inclusion bodies (virus factories) followed by special stains that demonstrate the affected cells contain DNA from the virus.
Currently, there is no effective therapy for PBFD virus. Since it is caused by a virus, no effective cure for a bird with diseased feathers should be expected. With supportive care, diseased birds can survive for years, but they must be maintained in complete isolation to prevent them from serving as a source of virus for other birds.
In 1989, it was shown that a vaccine developed from the feathers of infected birds could be used to prevent PBFD virus infections in vaccinated chicks. While the vaccine was shown to be effective in preventing the disease, the resilience of the virus made this vaccine much too dangerous for use in companion and breeding psittacine birds maintained in the United States and Europe.
Most birds infected with PBFD develop a transient infection and remain clinically normal. In the vast majority of birds, an appropriate immune response occurs, which clears the virus from the blood with no detectable affect on the host. Birds that do not mount an appropriate immune response either die or develop progressive feather abnormalities.
In general, PBFD associated disease in Old World psittacine birds is considered progressive and fatal. By comparison, some New World psittacine birds with associated severe feather abnormalities caused by PBFD have been known to recover. Apparently, some lories with feather abnormalities caused by PBFD can also recover.