Download Psittacine erythroblastosis - a new disease of Antipodes

Surveillance Vol.18 No.1 1991
Psittacine erythroblastosis - a new disease of Antipodes
Island and New Zealand parakeets
In 1980 a new infectious disease of parrots
was identified in Antipodes Island and New
Zealand parakeets (Cyanoramphus species) held in captizdy on the N e w Zealand
mainland. Although resembling viral
erythroblastosis of poultry, the disease agent
does not appear to belong to theauian leukosissarcoma group of viruses, and has yet to be
identified. To date, thediseaseappears transmissible only to other closely related parrots
and not to poultry.
The first captive populations of Antipodes Island green (Cyanoramphus
unicolor) and red-crowned ( C .
nouaezelandiae hochstetteri) parakeet were
established on the New Zealand mainland, at a Wairarapa bird reserve, in the
southern North Island. Adapting well to
captivity, the numbers of parakeets increased from 12wild-aught birds in 1967
to 30 birds in 1979. Ten captive-bred
birds were transferred to other New
Zealand aviaries in 1979, with the remaining 20 birds held in two separate
aviary blocks, 15metres apart. Adjacent
enclosures held the Antipodes Island
parakeets’ close relatives, the New Zealand red-crowned (C. nouaezelandiae nouaczelandiae) and yellow-crowned ( C .
uuriceps auriceps)parakeet, separated only
by wire mesh. To increase theproductivity of the Antipodes Island parakeets,
clutches of eggs were sometimes crossfostered to New Zealand parakeets. Bird
losses until 1980 consisted of occasional
sporadic deaths. Dead birds were submitted to the Batchelar Animal Health
Laboratory for examination.
In September 1980 an adult female
Antipodes Island green parakeet died
after a short illness. The clinicaland postmortem findings were distinctlydifferent
from any seen previously. Over the next
four years, this disease resulted in the
deaths of 30, out of a total of 37, Antipodes Island parakeets held at this bird
reserve and three other New Zealand
aviaries.
Clinical findings
latter stages of the disease, sequential
blood tests demonstrated a very sudden
drop in haemoglobin (Hb) and packed
cell volume (PCV).
The most consistent post-mortem
finding was a diffusely enlarged liver,
which was three to six percent of body
weight instead of the normal two to three
percent. The colour varied from dull to
bright cherry-red, instead of the normal
dark red-brown, often with a fine pale
reticular pattern over the surface and
larger more irregular areas of necrosis
(Figs 2 and 3). Splenic enlargement was
seen in one bird.
The most distinctive feature was a
change in the eye colour of affected
parakeets, the iris becoming a light yellow instead of the normal orange-red.
Progressively, affected birds became
more lethargic, adopting a sleeping posture, with their feathers ruffled and
breathing deeply (Fig 1). A clear fluid
diarrhoea and regurgitation of crop
contents and clear mucus was seen in
some birds. In the latter stages of the
disease any excess exertion, such as
during handling, resulted in the death of
the bird.
Fig. 2: A normal parakeet liver
Fig. 1 : A clinically affected Antipodes Jsland
green parakeet (C. unicolor).
Laboratory findings
The peripheral blood picture in affected birds was of a severe normochromic anaemia, with red blood cells varying in size from normocytic to macrocytic
(Table 1). Erythroblasts were found in
variable numbers in circulation. In the
TABLE 1: Comparisonof haemoglobin (Hb)
and packed cell volume (PCV) in normal and
affected parakeets
Hb g/l
PCV (%)
140-180
154
27
40-50
45
27
Fig. 3: The liver in psittacine erythroblastosis.
35-100
63
15
4-24
13
15
The two significant microscopic findings were in the bone marrow and liver.
The blood sinuses in the femoral marrow
were tightly packed with multiple layers
of primitive red blood cells, instead of the
Normal
Range
Mean
n
Affected
Range
Mean
n
Surveillance l8(l) 17
Surveillance Vol.18 No.1 1991
normal progression to mature red blood
cells. Very occasionally there was severe
marrow hypoplasia, with the blood s Inuses empty, apart from a narrow lining
of primitive cells. In the liver, similar
immature red blood cells, containing
smallamounts of stainable haemoglobin,
were present clustered within hepatic
sinusoids (Fig 5 ) . Frequently there were
also areas of non-inflammatory liver
necrosis, active erythrophagocytosis,and
increased amounts of iron within
sinusoidal macrophages.
fig. 4: Affected bone marrow showing primitivt,
erythroid cells tightly packed in blood sinuses.
New Zealand red-crowned parakeet
chicks resulted in poor growth rates, a
mild anaemia, a lack of primary tail
feathers and bursal necrosis in all four
birds. One bird died six weeks after
inoculation with liver and bone marrow changes typical of field cases. A
nest-mate inoculated with saline and
held in the same environment for two
months showed no abnormalities.
Naturally occurring disease in
New Zealand parakeets
A similar milder disease causing
anaemia and sporadic deaths was found
in New Zealand red-crowned and yellowcrowned parakeets held at these four bird
reserves. As in the inocuIated redcrowned parakeet chicks, young affected
birds were found well-feathered but
lackingprimary tail feathers, giving them
a lovebird-like appearance. Recently,
over two successive years, young New
Zealand yellow-crownedparakeets with
a similar syndrome have been collected
from the wild at Te Anau. This feathering abnormality has not been observed in
Antipodes Island parakeets.
Epidemiologic observations
f i g . 5: Affected liver with similar primitive cell.5
within hepatic sinusoids
The failure of red blood cell matumtion in the marrow, and the presence of
primitive red-blood cells in the liver were
interpreted as neoplasia, rather than a
response to anaemia.',* Neither feature
was observed in an experimentally-induced blood-loss anaemia in New Ze,aland red-crowned parakeets (Anne L R
Southern, unpublished data).
Research findings
* Experimental inoculation of infected
tissue into ten-day-old SPF domestic
fowl embryos, and one-day old and
six-week-old chicks, failed to produce
any lesions.
* Tissues from diseased parakeets and
blood samples from in contact birds
were tested at the CSIRO, Melbourne,
and found to be negative for avian
leukosis-sarcoma group specific antigen.
*.
No agent has been identified on electron microscopic examination of tissues from a number of affected birdls.
* Intraperitoneal inoculation of liver
homogenate into four, six-week-old
18 Surveillance 18(1)
As with erythroblastosis in poultry,
the incubation period of this disease appears to be long, in the order of three-tofour months, with the time between the
first and second case being 140 days.
Close contact between birds appears
necessary for the spread of the disease,
with deaths occurring only in the second
aviary at the Wairarapa bird reserve,
when birds of the two aviaries were
mixed. Initially, the disease resulted in
deaths in adult birds, but in 1983 this
pattern changed,with survivingclinically
normal Antipodes Island parakeets producing successive clutches of offspring
that died with erythroblastosis at threeto-six months of age. These deaths occurred even when eggs were incubated
and chicks reared by clinically normal
New Zealand red-crowned parakeets in
separate aviaries. This observation raises
the possibility that there may also be
vertical transmission of the agent from
parent to offspring. The disease was later
identified in three other New Zealand
aviaries with Antipodes Island parakeets.
In two aviaries it appeared to be the
result of introducing clinically normal
but infected Antipodes Island parakeets
from the Wairarapa. In the third aviary,
the disease appeared to have arisen independently. As in the Wairarapa bird
reserve, there were numerous New Zealand red-crowned and yellow-crowned
parakeets held in adjacent enclosures
separated only by wire mesh.
Discussion
It seems this new and often fatal disease of Antipodes Island parakeets may
have been present undetected in New
Zealand parakeets, and possibly other
parrots, for many years. In the past, bone
marrow and blood was seldom examined in parrots, which hasprobably meant
that the liver changes were confused with
other neoplastic and inflammatory diseases. Even with a correct diagnosis, the
infectious nature of the disease would
not have been obvious, with only sporadic deaths in birds other than Antipodes Island parakeets.
This disease appears to be present not
only in captive parakeets, but also in wild
parakeets on the New Zealand mainland. The role this disease has played in
previous declines in wild parakeets, or
other native parrots, has yet to be determined, but could prove important for
future wildlife management in this
country.
Last century native parakeets were
common on both main islands, with the
red-crowned parakeet in particular, occurring in large flocks, and considered a
crop pest. In the 1880s there was a sudden decline following the release of Australian parrots and parakeets on New
Zealand's twomain islands3Onoff-shore
islands, where these liberations did not
occur, parakeet populations have remained healthy, despite islands such as
Stewart Island having most of the introduced predators that occur on the New
Zealand mainland. This has led to
speculationthat introduced avian disease
may have been involved in these declines,
rather than just simply the spread of introduced predators? Comparisons of
susceptibility between mainland parakeets and those from off-shore islands
may eventually establish whether these
islands have, indeed, acted as refuges
from avian disease.
There are still very large gaps in our
knowledge of this new disease of parrots,
with further research necessary to identify the agent and the range of avian
species affected. The relationship, if any,
between this and "beak and feather" disContinued next puge
Surveillance Vol.18 No.1 1991
Psittacine erythroblastosis
Corrtinuedjrom page I8
ease, a viral disease occurring mainly in
Australian parrots, where feathering
abnormalities and occasionally
myelogenous leukaemia has been seen,
seems worthy of in~estigation.~
From the little we do know, it seems
that there are avian diseases on the New
Zealand mainland which could pose a
significant threat to species occurring on
isolated island habitats. This threat must
be taken into consideration not only when
bringing birds to the New Zealand
mainland, but also in any future
liberations of mainland bird species onto
New Zealand's outer islands.
Acknowledgements
W J Hartley. A F Julian. D J Tisdall, A Slieker, A
L R Southern and the CSIRO, Melbourne.
References
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anaemias of the fowl. A ( , h i \ ~ofPothology
s
12:
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Purchase, H G, 1975: Leukosis andSarcomas.
In I.\olotion and Identification of Aviun
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Hutton, F W, Drummon, J , 1923. TheAnimu1.t
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Buller. W L, 1967: Buller's Birds of NeM,
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Mark C Vickc,i-s
Ruakura Animal Health Laboratory
Surveillance 18(1) 19