PBFD-a serious virus
Erik Vloothuis
PBFD is a virus that should not be taken lightly, it is highly contagious
to parrot species especialy cockatoos. This virus is spread through
feather dust, droppings and blood. It has been known to SURVIVE up to
ten years outside of the host with the same devastating potency as
when it was created. Removal of the virus in cages and aviaries etc..
is extremely difficult as it needs a strong disenfectant to kill it, even
then you still could have missed some infected feather dust, that has managed
to get into small cracks in the framework etc..
The virus is originally from Native Sulfur Crested Cockatoos here in
Australia, where it was spread through natural nesting hollows to other
Sulfurs'. But because of forest clearing, other parrots have used these
hollows for nesting purposes and contracted PBFD.
PBFD, Parrot Beak and Feather Disease is a horrible and debilitating
disease. It starts off by causing the bird to lose its feathers and
and replacement ones are malformed and very weak, eventually no more
feathers will grow. While this is happening the beak begins to soften and
degenerate, the bird will not be able feed and die of starvation. If you
though that wasn't enough already, 'Mother Nature' makes the virus
attack the bird's immune system. Very rarely does a bird live long enough
to see it's beak crumble away, by then it would have caught a host
of other infections and diseases.
Currently there is no cure although in Australia research is underway
trying to find a vaccine, so far there has been some sucess, but without
funding nothing will show to fight the virus. Interestingly some
studies have revealed that native Cockatoos are building up a resistance
to the virus with around 20% of birds tested showing immunity to it.
Test breedings have shown that this immunity seems to be hereditery,
fortunatly mother nature has recognised some of these bird's suffering.
I would just like to leave with one statement:
Avoid PBFD like the Plague!!!!!!!!!!!!!
--
Erik Vloothuis ___ |\
/ /__| \
Email : er...@ttq.DIALix.oz.au / \
Fax : +61-3-9800-4050 \ \
-|- \__/--\_*_/ MELBOURNE, AUSTRALIA
----0--(*)--0---- __
"Aviation is a natural high" \/
Spitbird
were capable of contracting PBFD. Is this true? If it is, could you
list the speciaes at risk? I know of course that cockatoos are often
victims, but can any bird get it? I think the magazine said that only 7
or 9 species could get it, but I could very well be wrong. Any
information you could give me would be appreciated.
Cathy Quinones
writes:
:>
:>I read somewhere(possibly bird talk) that only certain species of birds
Scott Lewis posted a great summary (off Harrison & Ritchie's book) a while
back. I saved it and I'll re-post (see below). My understanding is that
there is a list of birds that have been *reported* to have contracted the
disease. A species that is not in the list should NOT be considered to be
immune: it may simply be that no animals were reported to the research team
that compiled the list at publication time. Again, I have never heard that a
given hookbill species is immune to this disease. I HAVE heard that young
birds (under age 2) are most likely to catch the disease if exposed, because
immature immune systems and what not. Therefore, it does seem like a VERY
smart thing to (1) purchase baby birds from VERY trustworthy vendors and (2)
keep birds under age 2 out of risk of contagion as much as possible. Call
Dr. Ritchie's information hotline (1-900-288-4267, 7-10pm Eastern,
$2.95/minute) for the ultimate info scoop and somebody correct me if I am
wrong here!
Begin Scott's post
++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++
Here's a partial summary from Avian Medicine on PBFD. BTW,
I have heard that Ritchie is working on a vaccine, but I don't think
it has finished clinical trials.
===================
A chronic disease characterized by symmetric feather dystrophy and
loss, development of beak deformities and eventual death was first
described in various species of Australian cockatoos in the early
1970's. Free-ranging Psittaciformes with feather abnormalities
suggestive of this disease were noted by Australian explorers at the
turn of the century. The disease has been diagnosed in numerous
Psittaciforme species in addition to cockatoos. The currently used
name, coined by Perry in 1981, is "psittacine beak and feather
disease" (PBFD).
Table of "Psittaciformes Currently Considered Susceptible to PBFD
virus"
Sulpur-crested Cockatoo
Major Mitchell's Cockatoo
Galah
Little Corella
Long-billed Corella
Budgerigar
Cockatiel
Rainbow Lorikeet
Western Rosella
Hooded Parrot
Malee Ring-necked Parakeet
Port Lincoln Parrot
Red-rumped Parrot
Bourke Parrot
Eclectus Parrot
Princess Parrot
Peach-faced Lovebird
Nyassa Lovebird
Fisher's Lovebird
Masked Lovebird
King Parrot
Moluccan Cockatoo
Umbrella Cockatoo
Indian Ring-necked Parakeet
Triton Cockatoo
Citron Cockatoo
Goffin's Cockatoo
Vasa Parrot
Blue-fronted Amazon Parrot
Red-lored Amazon
Red-vented Cockatoo
Senegal Parrot
African Grey Parrot
Myer's Parrot
Black Palm Cockatoo
Red-bellied Parrot
Gang-gang Cockatoo
Scarlet Macaw
Rose-ringed Parakeet
Pale-headed Rosella
Golden-shouldered Parrot
Northern Rosella
Jenday Conure
Green-winged Macaw
Pionus Parrot
Epizootiology
Historically, PBFD was thought to be restricted to Old World and South
Pacific psittacine birds, with the white and pink cockatoos being
particularly susceptible. However, the disease has been documented in
several black cockatoos and New World psittacine birds including
Amazon parrots, macaws and pionus parrots. Investigations indicate
that the actual host range of the PBFD virus remains largely unknown.
PBFD has been documented only in Psittaciformes.
It is postulated that PBFD has historically been enzootic in
free-ranging populations of Old World and South Pacific psittacine
birds, and that the disease has been introduced to other susceptible
populations of both free-ranging and captive birds through the
worldwide movement of birds for the pet market.
As many as 20% of free-ranging Sulphur-crested Cockatoos have clinical
signs of PBFD in any one year. Half of the 20 birds in a free-ranging
flock of Crimson Rosellas were found to have PBFD.
Transmission
Susceptible birds can be experimentally infected with the PBFD virus
through the combined oral, intracloacal and intranasal routes. PBFD
was recovered in the feces and crop washings from various species of
psittacine birds diagnosed with PBFD. ...the possibility of an adult
transmitting the virus to neonates during feeding
activities...deserves consideration. High concentrations of the virus
also can be demonstrated in feather dust collected from a room where
birds with active cases of PBFD are housed.
The demonstration of high concentrations of virus recovered from a
room where PBFD birds were being maintained implicates contaminated
dust from any source as a major vehicle for the environmental
persistence and natural transmission of the virus.
Several reports suggest the possibility of asymptomatic adults
producing progeny with clinical signs of PBFD in successive breeding
seasons. These findings suggest a carrier state may exist with
vertical or horizontal transmission of PBFD from parent to offspring
or a genetic predisposition to the disease; however, in most suspected
cases of parent-to-offspring transmission, epizootiologic
investigations indicate probable exposure to the PBFD virus occurring
through sources other than the parents.
Pathogenesis and Immunity
PBFD is a progressive disease with temporary remission in the
occurrence of new lesions in the periods of nonmolting. Irregular
photoperiods to which many companion birds are subjected may influence
regular molting periods or the lack of them. The lesions of the beak
may progress during the intermolt period. Except for reported
recoveries in budgerigars, lorikeets, lovebirds, a pionus parrot and
some macaw neonates, the clinically apparent form of PBFD virus is
considered fatal. Most infected birds survive less than six months to
one year after the onset of clinical signs, though some birds have
been known to live over ten years in a featherless state. Death
usually occurs either from changes induced by secondary bacterial,
chlamydial, fungal or other viral agents, or from terminal changes
that necessitate euthanasia. Cockatoos with PBFD have
been diagnosed with severe cryptospordiosis infections, which are
generally considered to occur only in patients with
immunodeficiencies.
The predilection for birds to die from secondary or opportunistic
pathogens has been interpreted to indicate an immunosuppression that
is thought to be induced by damage to the thymus and bursa.
PBFD-positive birds with inclusion bodies located only within the
nucleus of infected epithelial cells have been found to spontaneously
recover. On the other hand, larger psittacine birds with
intracytoplasmic inclusion bodies located in macrophages usually
succumb to the disease. Because the macrophage is critical for the
initial processing and presentation of viral antigen to the immune
system, it can be postulated that the determining factor in whether an
infected bird develops a chromic fatal PBFD virus infection, or
develops a protective immune response is based on how the body
processes the virus before it begins to persist in the cytoplasm of
macrophages.
Some birds exposed to the PBFD virus remain clinically normal. In
fact, the detection of anti-PBFD virus antibodies in most adult
Psittaciformes of a susceptible species suggests that these birds were
exposed to the virus at some point in their lives and that the
exposure resulted in a subclinical infection with the development of
an effective immunologic response. The factors that determine whether
a bird mounts an immune response or is fatally infected could depend
on the age at the time of exposure, the presence and levels of
maternal antibodies, the route of viral exposure and the titer
(concentration) of the infecting virus.
An age-related susceptibility to the virus has been suggested by some
experimental transmission studies. Neonatal budgerigars infected at
less than seven days of age were found to develop severe disease,
while birds infected at 10 to 14 days were reported to experience
lower levels of morbidity, and some remained asymptomatic.
Incubation Period
Infected chicks and fledglings may show the first signs of disease
during their feather development after replacing the neonatal down.
Following experimental infection, the minimum incubation period is 21
to 25 days. The maximum incubation period may be months to years.
Clinical Disease
It appears that the avian species listed [above] are of various
susceptibilities; therefore, clinical (and pathological) signs may
vary greatly. Generally, PBFD is a disease of young birds (up to three
years), but older individuals (up to 20 years of age) may also develop
clinical lesions. Older birds that develop clinical signs later in
life may have been infected at a young age and remained latently
infected.
In some Psittaciformes with pigmented feathers, abnormal coloration
has been associated with histologic lesions consistent with PBFD virus
infection. This is particularly true in African Grey Parrots, where
affected feathers may be red instead of grey.
The feather changes, typical lesions of the beak (if present), and
more rarely also of the nails, occur symmetrically in most instances.
Based on markedly different clinical presentations, peracute, acute
and chronic forms of PBFD have been described. The type of clinical
disease appears to be influenced by the age of the bird when clinical
signs first appear.
Peracute disease is suspected in neonatal psittacines that show signs
of septicemia accompanied by pneumonia, enteritis, rapid weight loss
and death. Histologic lesions in these cases may be limited. The
peracute syndrome appears to be particularly common in young cockatoos
and African Grey parrots.
The acute form of PBFD, commonly called French moult in Australia, is
most frequently reported in young or fledgling birds during their
first feather formation after replacement of the neonatal down, and
chicks as young as 28 to 32 days of age have been described with
classic lesions. Acute infections are characterized by several days of
depression followed by sudden changes in developing feathers,
including necrosis, fractures, bending, bleeding or premature shedding
of diseased feathers.
Experimentally infected Rose-breasted Cockatoo neonates became acutely
depressed and anorectic approximately four weeks post-infection.
Twenty-four hours later, the feathers appeared to lose their luster
and became pale and brittle. Subsequently, dystrophic feathers began
to appear as the neonates developed their adult plumage. A similar
disease progression has been defined for experimentally infected
Umbrella Cockatoos and African Grey Parrot chicks.
Chronic PBFD is characterized by the progressive appearance of
abnormally developed feathers during successive molt. Gross changes
include retention of feather sheathes, hemorrhage within the pulp
cavity, fractures of the proximal rachis and failure of developing to
exsheathe. Shot, clubbed feathers, deformed, curled feathers, stress
lines within vanes and circumferential constrictions may also be
present. Replacement feathers become increasingly abnormal, and if
birds live ling enough they will eventually develop baldness as the
feather follicles become inactive.
In older birds, the first sign of PBFD is the replacement of normal
powder down and contour feathers with dystrophic, necrotic, non-viable
feathers that stop growing shortly after emerging from the follicle.
The disease then progresses to involve the contour feathers in most
tracts, followed by dystrophic changes in the primary, secondary, tail
and crest feathers. Primary feathers are usually the last to manifest
the disease.
(Watch out for cockatoos with shiny beaks. Indicates a lack of powder
down--DSL.)
Clinical changes in the beak and oral mucosa of PBFD-positive birds
are characterized by progressive elongation, transverse or
longitudinal fractures, palatine necrosis and oral ulceration.
Classically, beak deformities develop in birds following a protracted
course of PBFD where substantial feather changes have occurred;
however, some individuals develop severe beak lesions with relatively
minor feather pathology...
Diagnosis
Feather lesions that appear grossly similar can be caused by PBFD
virus and avian polyomavirus. Feather lesions seen with polyomavirus
typically resolve after one or two molts whereas PBFD lesions as a
rule progress from molt to molt.
PBFD should be suspected in any psittacine bird with progressive
feather loss involving malformed feathers...Because several viruses
may result in similarly appearing intranuclear inclusion bodies, a
confirmatory diagnosis of PBFD requires the use of viral-specific
antibodies to demonstrate PBFD virus antigen or the use of DNA probes
to detect PBFD virus nucleic acid. Viral-specific DNA probes are most
sensitive for detecting PBFD virus and can be used on biopsy samples
to confirm an infection or on blood samples from a live bird to detect
viremia.
Therapy
Numerous therapeutic trials have been attempted for PBFD
virus-infected birds. Recoveries have been reported principally in
birds with only intranuclear inclusion bodies. While feather lesions
can be tolerated as long as the animal is kept in a controlled
environment, beak lesions (also nail lesions) can be painful,
particularly when secondarily infected. Euthanasia is suggested under
these conditions. Secondary infections should be treated accordingly,
and special examinations for cryptospordisois might be indicated.
(Picture caption: some birds can live with PBFD virus for many years.
Birds with long-term infections frequently appear bald as feather
pathology progresses through successive molts.)
Control
The chicken anemia agent (CAA), which is similar...to PBFD, has been
found to be environmentally stable, and infectivity remains unchanged
when the virus is heated to 60 C for one hour and following treatment
with detergents, enzymes and many commercial disinfectants. While the
environmental stability of the PBFD virus is unknown, it would be
prudent to consider its stability to be similar to that described for
CAA. Psittacine neonates, which seem to be most susceptible, should
definitely not be exposed to areas that may have been contaminated by
feces or feather dust from a PBFD-positive bird.
DNA probes should be used for ... all birds of a susceptible species
should be tested to determine if they are latently infected with the
PBFD virus. This is particularly true with respect to breeding birds,
birds being sent to pet shops and birds being evaluated during
post-purchase examinations.
The DNA probe can also be used to screen walls, caging, air
circulating ducts and equipment in the home or hospital.
A positive test in a bird that has feather abnormalities suggests that
the bird has an active PBFD viral infection. A positive blood test in
a bird that does not have feather abnormalities may indicate that the
bird is latently infected or that it recently has been exposed to the
PBFD virus and is viremic (has virus in the blood). A bird that tests
positive and has no feather abnormalities must be retested in 90 days.
If the bird is still positive, then it should be considered to be
latently infected. A negative test 90 days later would indicate that
the viral nucleic acid was no longer detected in the blood and that
the bird has probably eliminated the virus.
A companion bird that is diagnosed as a PBFD virus carrier can live a
long life when provided a stressor-free environment and supportive
medical care. PBFD virus-infected birds should not be maintained in
breeding facilities or where they may expose susceptible neonates or
adults. Infected birds should be removed from the breeding collection
and nursery immediately.
======================================================
Linda and Scott Lewis 512/928-1200
Old World Aviaries sle...@bga.com
Austin, Tx
======================================================
++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++
End of Scott's post
p.s.
Thanks Scott! And to everyone who takes the time to quote big chunks of
H&R's book: maybe someday I'll have a complete pirate copy ;) ;) ;)
===========================================================
Cathy Quinones quin...@mindspring.com
http://www.mindspring.com/~mintz/coverpg.html = bird care info
Poicephalus rule!!
Liz Day
>I read somewhere(possibly bird talk) that only certain species of birds
>were capable of contracting PBFD. Is this true? If it is, could you
>list the speciaes at risk?
I think most parrots can get it. It might be better to ask which ones
CAN'T. It's also worth noting that usually such data are gathered by
noting which species have been seen to get the disease so far, rather
than by testing every species by inoculating it - so if some species
isn't noted as getting PBFD, I wouldn't be overconfident about that...
Dr. Ritchie would know. Anyone else know?
Liz Day
Indianapolis, Indiana, central USA
LD...@indy.net (use this address - not the 'r' key)
JSKD
>I read somewhere(possibly bird talk) that only certain species of birds
>were capable of contracting PBFD. Is this true? If it is, could you
>list the speciaes at risk? I know of course that cockatoos are often
>victims, but can any bird get it? I think the magazine said that only 7
>or 9 species could get it, but I could very well be wrong. Any
>information you could give me would be appreciated.
For some time, people thought that only Old World birds were susceptible
to PBFD, but now the list of affected birds includes many of the New World
species as well. The list is *much* longer than just 9 species. I
believe any psitticine is considered at risk as a youngster.
Judy D in WV
Scott Lewis
>I read somewhere(possibly bird talk) that only certain species of birds
>were capable of contracting PBFD. Is this true? If it is, could you
>list the speciaes at risk? I know of course that cockatoos are often
>victims, but can any bird get it? I think the magazine said that only 7
>or 9 species could get it, but I could very well be wrong. Any
>information you could give me would be appreciated.
According to RH&H the following species are CURRENTLY considered
susceptible. This doesn't mean that other species aren't susceptible.
It means PBFD has been documented in the following:
Sulphur-crested Cockatoo
Major Mitchell's Cockatoo
Galah
Little Corella
Long-billed Corella
Budgerigar
Cockatiel
Rainbow Lorikeet
Western Rosella
Hooded Parrot
Malee Ring-necked Parrot
Port Lincoln Parrot
Red-rumped Parrot
Bourke Parrot
Eclectus Parrot
Princess Parrot
Peach-faced Lovebird
Nyassa Lovebird
Fisher's Lovebird
Masked Lovebird
King Parrot
Moluccan Cockatoo
Umbrella Cockatoo
Indian Ring-necked Parakeet
Triton Cockatoo
Citron Cockatoo
Goffin's Cockatoo
Vasa Parrot
Blue-fronted Amazon Parrot
Red-lored Amazon
Red-vented Cockatoo
Senegal Parrot
African Parrot
Meyer's Parrot
Black Palm Cockatoo
Red-bellied Parrot
Gang-gang Cockatoo
Scarelt Macaw
Rose-ringed Parakeet
Pale-headed Rosella
Golden-shouldered Parrot
Northern Rosella
Jenday Conure
Green-winged Macaw
Pionus Parrot
RH&H say, "Investigations indicate that the actual host range of the
PBFD virus remaines largely unknown."
Regards,
Scott
=====================================================
Scott & Linda Lewis Phone: 512/928-1200
Old World Aviaries FAX: 512/928-8738
e-mail: sle...@bga.com
=====================================================
V...@one.net
>
>I read somewhere(possibly bird talk) that only certain species of birds
>were capable of contracting PBFD. Is this true? If it is, could you
>list the speciaes at risk? I know of course that cockatoos are often
>victims, but can any bird get it? I think the magazine said that only 7
>or 9 species could get it, but I could very well be wrong. Any
>information you could give me would be appreciated.
PBFD virus is highly infectious and affects ALL species of psittacine
birds!!! However old world species appear more susceptible than new
world species. The maturity and competency of the hosts immune system
at the time of exposure appears to affect the clinical course of the
disease. An execellent test is available to screen birds for this
virus. Don't take chances with this disease!!!
VET
soha...@std.pharma.cu.edu.eg
I read now that there is on disinfectant usable for this virus other than a brand named virkon s
which I have no access too .. do I still get rid of the cage
Hope you reply sorry for intruding
