Psittacine Beak and
Feather Disease
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Psittacine beak and feather disease (PBFD) was first recognized
and described thoroughly in 1975 by Dr Ross Perry, a veterinary
practitioner in Sydney. It has since been recognised as the most
significant disease of psittacine birds in Australia.
Numerous reasons were put forward from veterinarians around the world
to explain the cause of PBFD. Some blamed "sunflower seeds", whilst
others thought that the disease was caused by in-breeding.
Research at Murdoch University by Drs David Pass, Ross Perry and
Sarah Wylie demonstrated that PBFD was caused by a new type of
virus which has since been characterised by researchers at the
University of Georgia.
Recent research at the University of Sydney by Drs Garry Cross
and Shane Raidal demonstrated that the disease is widespread in
some wild parrots and other psittacine birds. They also demonstrated
that the disease can be prevented by vaccination.
PBFD is caused by a relatively simple virus which infects and
kills the cells of the feather and beak. The virus also kills the
cells of the immune system. Consequently many diseased birds
succumb to bacterial and other infections.
Psittacine circovirus measures 16 nm in diameter and the genome
is a circular single-stranded DNA molecule. These characteristics
make it the smallest known virus capable of causing disease.
The psittacine circovirus only causes problems for psittacine
birds. As far as we know, no other bird or animal species is
susceptible. A similar PBFD-like disease recently seen in doves
is probably caused by similar but antigenically different
circovirus.
PBFD has distinct features and in most circumstances a diagnosis
can be achieved by veterinary examination alone. PBFD generally
affects young psittacine birds. However, birds all ages can
succumb to the disease.
Chronic PBFD is insidious in its development and progression;
dystrophic feathers replace normal ones as they are moulted. In
this manner, a PBFD-affected bird can gradually lose its plumage
without other signs of illness.
In some parrots such as this gang gang too (the birds chest is
to the left, its tail is to the right) the powder-down feathers
are often the first feathers affected. PBFD-affected feathers are
fragile or develop an abnormally thickened outer sheath.
Destruction of powder-down feathers creates bare areas of skin
like that in the photograph and the decreased production of
powder causes the plumage to become dull and the beak to become
glossy.
The pattern of feather abnormality which develops is related to
the stage of moult that the bird is in when the disease first
begins and is usually slowly progressive. Abnormal feathers are
usually short and have one or more of the following
characteristics; fault lines; a thickened or constricted feather
sheath; clotted blood attached to the formed feather quill.
In Neophema spp., apparently normal feathers which fall out or
are effortlessly plucked, may be the only clinical sign. The
first clinical sign in birds with green plumage (such as Princess
parrots) may be the development of yellow feathers which
otherwise appear normal. This is probably the result of
microscopic changes in the feather structures.
Secondary disease problems commonly exist. These include
bacterial, fungal and viral infections. Most birds with chronic
disease eventually have difficulty eating, lose weight and die.
Acutely affected birds often have mucoid or green diarrhoea.
These signs are often clinically diagnosed as secondary bacterial
or chlamydial infections. However, the virus can cause acute
hepatitis, particularly in some parrots. Some birds may die of acute
hepatitis without obvious feather lesions.
Diagnosis
Severe on-going PBFD is not difficult to diagnose. The difficult
cases to diagnose are those birds (and species) which only
showing subtle signs either because of their age or immunity.
Histological examination of feather follicles has been routinely
used to confirm clinical disease but it is not suitable for
diagnosing incubating infections.
Psittacine circovirus can be detected in affected feathers by
haemagglutination assay (HA) and HI antibodies can be detected in
blood, serum, plasma or yolk.
Virus detection by HA is currently the best method available in
Australia for detecting circovirus. It is a valuable tool for
detecting virus in feathers, liver and faeces. It can be
performed on actively growing feather pulp or dry feathers. In
some parrots the powder-down feathers are the best feathers to test
for HA because they are often the first to become affected.
Feather testing is preferred over faecal because acutely
PBFD-affected birds do not excrete high concentrations of virus
in faeces and some chronically affected birds only excrete
intermittently.
Serology is useful for detecting PBFDV-infected flocks and for
demonstrating antibodies in individual birds. The presence of
antibody means that the bird has been exposed to circovirus and a
high HI antibody titre in an adult bird is a good indicator that
it does not have chronic PBFD. Nestlings with incubating
infection or acute disease may have low and declining antibody
titres. The test fails to detect passively derived maternal
antibody.
Blood can be collected directly onto filter-paper - only a few
drops are required, thus small parrots can be easily tested. The
paper is allowed to dry and does not have to be refrigerated for
transportation to the laboratory. The blood test detects
antibodies to the virus.
HA and HI testing cannot identify young birds which are
incubating the infection.
Psittacine circovirus can also be detected by Polymerase Chain
Reaction (PCR).
The incubation period of PBFD can be as short as 21 days but it
is probably dependent on the dose of virus; the age of the bird;
the stage of feather development; and the absence of immunity.
Primary circovirus replication probably occurs in the bursa of
Fabricius and/or gastrointestinal tract lymphoid tissue.
Secondary virus replication occurs in the liver and thymus and
probably other tissues. The target organ is the epidermis and the
manifestation of skin disease requires a moult. Consequently,
birds which become infected after feather development has
completed may not develop clinical signs until their next moult.
This could take six or more months.
Most birds which succumb to PBFD are less than 2 years of age.
However, all age groups should be considered susceptible to
circovirus infection. Chronic exposure to high concentrations of
virus and/or stress are probably required for infection and
seroconversion in adult birds.
Prognosis
Spontaneous recovery from acute PBFD can occur in many species,
including budgerigars, lorikeets and lovebirds. Some acutely
affected birds also recover. However, the majority of chronically
affected birds do not recover from the disease.
A report in 1907 by Ashby described probably the earliest report
of an outbreak of PBFD which occurred in wild red-rumped parrots
(Psephotus haematonotus) in the Adelaide hills in 1888.
PBFD has been confirmed in wild galahs, sulphur-crested
corellas, rainbow lorikeets, orange-bellied parrots,
rosellas, ringneck parrots, Major Mitchell's gang gang,
king parrots, swift parrots and many other species.
There is evidence that PBFD occurs in wild budgerigars,
red-rumped parrots, yellow-tailed black toos and Narethra
bluebonnets.
Flocks of wild toos may have a disease prevalence of 20% and
a seroprevalence of 60- 80%. Infection is probably maintained in
a population by diseased birds. Epidemics can occur in
susceptible wild or aviary flocks. Virus transmission is probably
predominantly by horizontal spread but carrier birds may
contribute by vertical transmission. Virus infectivity probably
persists in contaminated nests for many months or years.
PBFD in aviary birds
Aviary flocks with a history of PBFD usually have a high
seroprevalence. In these situations PBFD-affected birds are often
the progeny of hens with low or non-detectable serum antibody
levels.
Prevention and control
Aviculturists should be advised to maintain a closed flock or
purchase birds from PBFD-free flocks and to breed birds in
quarantine.
The appropriate use of disinfectants which are suitable (eg
glutaraldehyde) for inactivating environmentally resistant
viruses (ie parvoviruses) should be recommended for disinfecting
contaminated utensils, cages and rooms. PBFD is difficult to
quarantine. Carrier birds may appear clinically normal but
produce diseased young. Therefore it is necessary to breed birds
in quarantine.
Vaccination (Inactivated vaccine)
A killed-virus vaccine has recently been developed. When given
to normal healthy birds the vaccine stimulates immunity to the
psittacine circovirus. The vaccine is not a treatment for birds
already affected by PBFD because it does not cure birds already
infected with PBFDV. In fact it can exacerbate the disease
process.
It is important to vaccinate pet birds at an early age. Birds as
young as 14 days of age can be vaccinated. All vaccinated pets
need to have a booster one month after their first vaccination.
After this pet birds should be examined every six months until
they are 3 years of age.
Breeding birds should also be vaccinated one month prior to
breeding.
Article From: Murdoch University
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