Beak and Feather Disease

Psittacine Beak and Feather Disease revisited

by Bob Doneley BVSc FANZCVS (Avian Medicine) CMAV

Psittacine Beak and Feather Disease (PBFD) has been with us for a long time; the earliest reports were in wild Red Rumped Parrots in the late 1800’s and it continues to give both bird owners and vets headaches and heartbreak. As with any common problem, we need to periodically revisit this disease go back and look at it again, and refresh everyone’s memory, particularly with the breeding season just around the corner.

Early thoughts on PBFD ranged from thinking it was caused by an all-seed diet (especially sunflower) to a bacterial infection that would respond to antibiotics. In the late 1970’s Ross Perry, one of the most observant bird vets I know, started to look at this disease and formulated the theory that it was a viral infection. He and David Pass were able to demonstrate that it was an infectious disease and could be transmitted readily from bird to bird. In particular Ross was able to catalogue the range of clinical signs seen with this disease, and gave it a name Psittacine Beak and Feather Dystrophy. Since that early ground-breaking work other researchers have been able to isolate the virus responsible and develop reliable testing methods. The result is that we now know much more about this disease, but there is still much more to learn. In fact, Shane Raidal recently told me that a researcher could easily spend a lifetime researching this virus and the disease it causes, and still not uncover all of its secrets – and this from a man holding a PhD focusing on understanding it!

So what do we know?

PBFD is caused by Psittacine Circovirus, better known as PBFD Virus or PBFDV. This is one of the tiniest viruses known to man a reason why it escaped detection for so long. It infects all parrot species, although South American species (macaws, Amazons and conures) are less frequently affected. Interestingly, cockatiels are rarely affected as well and this is another area waiting for a researcher to devote time to! It is now believed that PBFD is an Australian disease and spread to the rest of the world with the exportation (both legal and illegal) of Australian parrots over the last 200 years. Most Australian, Asiatic and African species are extremely susceptible to PBFD and the disease is now found throughout the world where these species are kept.

The clinical signs vary greatly, depending on the species and age of the infected bird, and the state of moult it was in when first infected.

There is an acute form of this disease, fortunately relatively uncommon. It occurs in juvenile birds, usually at fledging. The virus attacks the bone marrow and destroys it the result is anaemic birds with no defence against disease. Affected chicks often die within days. African Grey babies are particularly sensitive to this form of the disease, and they should never be housed with other susceptible species such as cockatoos and lorikeets.

The more common form is a chronic disease affecting the feathers and, in cockatoos, the beak. Lesions typically develop in order of: powder down, contour feathers, primary feathers, secondaries, tail and then finally crest feathers. This order reflects the rate that these feathers are moulted the powder down feathers are continually turning over so any disease affecting them will quickly become apparent. As feathers are infected they become abnormal (dystrophic) they retain their sheaths, the shaft is full of blood, the base is often constricted and the feather falls out easily. In some birds there may be colour changes green feathers become yellow, blue feathers become white. The bird starts to look untidy and dishevelled. White cockatoos often look dirty with shiny beaks and feet because the powder down, the white dust that keeps them clean, is absent. Lorikeets may simply drop their tail and primary flight feathers. Neophemas just lose a lot of feathers when handled.

Only cockatoos appear to develop beak changes. Both the upper and lower beaks overgrow and become very fragile. The soft issue underlying the horny keratin becomes diseased and dies. The result is that the overgrown beak breaks easily and exposes the underlying sensitive tissue, causing pain and a reluctance to eat.

Many birds become immunosuppressed because of the effect the virus has on the bone marrow. This usually means that infected birds often die within 1-2 years because they cannot resist infection with other viruses, bacteria or fungi. I often liken PBFD to “Bird AIDS” because of this.

There is no treatment for PBFD just as there is no cure for the common cold and many other viral diseases. We can support these birds with good husbandry and nutrition, but they nearly always succumb to the disease in the end.

Likewise, there is no vaccine available. A lot of research has gone into this both here in Australia and also in the USA. Garry Cross at the University of Sydney was able to develop an effective vaccine but Government requirements to test it on all parrot species and the costs involved in doing this have made it cost-prohibitive. At this stage an effective, readily available vaccine still eludes us.

So we come back to preventing this disease by good management to keep it out of our collections, rather than treating it or vaccinating against it. This requires several key points of knowledge:

1. How is it spread?
2. How do we detect infected birds and carriers?

PBFD is spread from bird to bird in feather dust, the droppings and in crop secretions when feeding chicks. It is still unclear whether it is passed through the egg so that the chick is infected when it hatches, but this is suspected by some workers to be the case. Once a bird is infected with the virus the outcome will be determined by the amount of virus that has entered its body, and the state of the bird’s immune system. (Young birds have a relatively immature immune system, and this is why the disease is more common in them.) There are three likely scenarios and outcomes:

• A bird with a good immune system is challenged with a small amount of virus – the bird will mount a strong immune system and eliminate the virus from its body, remaining immune to the disease for the rest of its life;
• A bird with a ‘not so good’ immune system is challenged with a small amount of virus – the bird cannot mount a strong immune response and so it cannot clear the infection. But there is not enough virus to make the bird really sick The result is that the bird becomes chronically infected and intermittently sheds the virus i.e. it is a carrier; and
• A bird with a ‘not so good’ immune system is challenged with a large amount of virus – the bird becomes clinically ill with the virus, shows the clinical signs discussed above, and usually eventually dies.

Another scenario is seen in lorikeets: they become clinically affected, losing their tail and flight feathers; but, after a few months, they appear to recover and re-grow their lost feathers. Anyone looking at them would never know they had been infected. But these birds are probably carriers and will infect other birds they are placed in contact with. This is everyone’s worst nightmare – a bird that appears normal but is carrying a deadly disease.

So it is obvious that, when we are trying to formulate a plan to keep this disease away from our bird, we need to know which of these scenarios a new bird might fit into. Simply quarantining a new bird may not be enough the incubation period for this disease may be as short as 3 weeks or as long as several years. So we need reliable tests to sort out which birds are infected, which are carriers and which are immune. Fortunately, much of this research has been done and tests are available to do this.

DNA testing is strongly advocated in the USA as a reliable test. The only problem with it is that it gives no information about the bird’s immune system. A bird that tests positive may well have the disease but it could also be a case where the virus is just passing through’, as the bird’s immune system is eliminating it (see Scenario 1 above). So birds that appear normal, but test positive will need to be re-tested in 90 days. Another concern is the negative result. Is the bird really free of the virus, or is it a carrier with the virus only intermittently appearing in its blood? Do you know the answer? I certainly don’t just from a DNA test!

Another test that has been developed is the antibody test. This test looks for the antibodies the bird produces to fight disease. When interpreted alongside DNA results it gives a much clearer picture of the bird’s status. A bird that is DNA negative and has high antibody levels is almost certainly immune and not infected. A bird that is positive on DNA and has low or no antibodies almost certainly has the disease. A bird that is negative on both tests has probably never been exposed to the disease, and as such is very susceptible to infection. This is a difficult test to perform unfortunately, bringing its cost up considerably higher than a DNA test. But if you have expensive or rare birds I would strongly recommend that you use this test on all new birds.

Both pet owners and aviculturists alike can benefit from having their birds tested for this disease. Once PBFD gets into an aviary or household it is almost impossible to get rid of it. This is a very tough virus and can live for years outside the bird. Very few disinfectants are effective against it. As with so many diseases we see in birds prevention is the best cure!