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Compiled by
Cheryl Dooley
January 2003
The purpose of
this paper is:
To communicate information about a blood
parasite, identified in macropods, to carers,
vets and all those interested in the care and
rehabilitation of macropods.
To ask for cooperation from all wildlife groups
to enable further work to identify the parasite
and study cases of the disease as a basis for
its control and thereafter its causes and
possible cures.
Background:
This paper continues investigative work started
in 1994. I have attached a copy of a paper
presented at the Australian Veterinary
Association Pathology Meeting in 1996 by the NSW
Agriculture Regional Veterinary Laboratory at
Wollongbar (RVL Wollongbar), (see Addendum A),
and a paper written in July 1998 by Liz
Drinkwater (FAWNA) (see Addendum B). These
papers could be read first as a background to my
paper.
Many things have changed since
these papers were written, and things will
continue to change. I expect to update this
paper as this work continues.
I am not a veterinarian, and the information
provided here should not be seen as
scientifically proven nor should it replace
advice from your own vet. I am a wildlife carer
of some 2.5 years and
a member of Coffs Harbour WIRES.
I have provided footnotes to show the sources of
documented information wherever possible, and I
have worked to sort the suspected from the
confirmed, and the anecdotal from the clearly
tested and documented. This in no way reflects
on those people who have provided information
that is anecdotal, indeed at times it is all we
have as the basis to develop theories. We need
to use words such as “theory” and “could” and
“may”, and should avoid passing on information
that we do not know to be entirely proven, as
“this is the way it definitely is”. The other
constant danger when information passes from
person to person in an ad hoc way is that old
story that “Send reinforcements we’re going to
advance” becomes “Send three and four pence
we’re going to a dance”. When I say,
“confirmed” in this paper please be assured that
this means confirmed by blood tests and/or
necropsy (postmortem examination).
Some of the information in this paper may
challenge things that some carers have come to
believe as “facts”. This simply shows that
“facts” often change as information grows and
that any changes to treatment today should in no
way suggest we did the wrong thing in the past.
The treatment of native animals is far from
being an exact science and we are all learning
together. Every person I have spoken to has
wanted only the best for the animals in their
care and no one should take anything in this
document as personal criticism. I trust this
paper will be of some benefit to you, and that
it may inspire you to become a part of the
program to investigate this disease further.
What to look
for:
The parasite infects and causes destruction (haemolysis)
of the red cells circulating in the blood. The result is a haemolytic
anaemia. Necropsies have shown that the
parasite localises in massive numbers in the
blood vessels of the kidney and brain.
Signs of anaemia:
White or light pink gums and conjunctival
membranes of the eyes.
Lethargy, weakness.
Fluid build-up in lungs and thoracic and
abdominal cavities.
Other signs reported from suspected cases in
Eastern Greys are:
Tendency to bleed from tick attachment sites or
veins after blood sampling.
Increased consumption of water and frequent
urination (polydipsia and polyuria).
Loss of appetite (though we have one confirmed
case where eating remained normal)
Hot ears
Misshapen and desiccated pellets
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click on
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This is the
"hang dog" look that may be seen in some
animals |
Many of these signs occur in other diseases, so
it is desirable to seek veterinary advice for
diagnosis before treatment is given.
Coccidiosis in macropods also causes anaemia,
due to blood loss into the gut.
In blood loss anaemia a blood
sample will have a low number of red cells
(anaemia) and a low concentration of plasma
protein. In the haemolytic anaemia produced by
the blood parasite there is anaemia but also a
normal concentration of blood plasma
protein.
A blood sample collected in EDTA
anticoagulant is useful for differentiating
these two types of anaemia.
Of course each animal will react individually
and there are probably a wide range of signs
possible.
Could this parasite be the reason for other
“unexplained” deaths where animals have simply
“faded away”?
Prognosis:
At initial examination, it is difficult to
determine whether an animal will live or die.
Animals with a slower onset of the disease seem
to have a better chance of survival than those
that go down rapidly.
(That was certainly seen in my
two cases and has been the case for others.) It
would seem that in the cases of a slower onset,
the animal’s bone marrow has a chance to react
to the parasite and start to fight back. These
animals also respond to the use of Imizolâ
(see treatment section). Where the onset is
fast, the immune system does not appear to be
able to cope and Imizolâ
may also not be affective. (Again I saw this in
one of my joeys).
The parasite seems to leave them vulnerable to
internal bleeding and to spontaneous blood
vessel eruption. If a bleed occurs in the brain
the joey may go a bit “lop-sided” or develop eye
ticks/movements. Generally if this happens the
animal cannot be saved. This happened to one of
my joeys, she was found going round in circles.
Within seconds she was down and lost all
coordination and had to be euthanased. It is
important that carers record their cases in a
standard format (see Macropod Examination sheet)
so that we can develop more reliable information
on prognosis and likely response to treatment.
Which animals
are affected and why?
All confirmed cases so far have been from
northern and mid-north coast NSW. This
localisation of cases may simply reflect a
greater awareness of the disease in this area.
Not all kangaroos in a group seem to be
affected. In one group of 8, only 3 were
affected and the first to die was the healthiest
of the group. The majority of cases seem to be
from 5kg upwards, though one anecdotal case is
suspected in a 2kg joey. Both males and females
are affected. Both sick and healthy animals are
affected.
Stress is always a concern in reducing an
animals immunity however in several cases stress
does not appear to have been a factor e.g. 3 x
12kg males that had been in one location for six
months i.e. they had not been moved or changed
handlers and nothing else significant appears to
have happened. Cases also seem to appear at
varied times of the year with confirmed cases
occurring in all seasons. There is a theory
that perhaps more cases occur during drier years
but this cannot be proven at this point.
There are only a couple of reports of this
parasite in wild Eastern Greys, however they are
not confirmed cases. In general outbreaks
seem to be confined to hand-reared orphans and
in “wild” release areas i.e. not in suburban
situations.
Are other
macropods affected?
The disease has been seen almost exclusively in
eastern grey kangaroos. There have been several
suspected cases reported in redneck wallabies
with blood analysis confirming anaemia though
unable to specify this particular parasite
without further testing. In several of these
cases Vets diagnosed a blood parasite and
treated accordingly. In 2002, two cases were
suspected in swamp wallabies. Necropsy (post
mortem) confirmation is required to demonstrate
the organism in these other macropod species.
Could we be assisting this cross over of this
parasite into other species by mixing species at
our release sites? There is not enough
information available to determine this.
Detecting the
parasite:
This is difficult in the live animal. Only a
very small percentage of red cells in the
peripheral blood (rarely more than 5%) contain
the parasite even in severely affected animals.
The parasite is concentrated mainly in the blood
vessels of the brain and kidney of affected
animals. Therefore a negative blood examination
result from an animal with a haemolytic anaemia
does not rule out the disease.
It is certainly worthwhile making smears of
blood taken from the tip of the tail or ears and
sending these smears to a laboratory for
staining and examination under a microscope to
try and detect the parasite.
A blood sample in EDTA anticoagulant is useful
for two reasons:
Testing for severity of anaemia and plasma
protein concentration.
Remainder held frozen for research to identify
the parasite. (See section – what can you do to
help?)
One thing that sets this parasite apart is that
it causes a haemalytic anemia, i.e. only the red
blood cells are affected, and the plasma protein
concentration is normal. (This is not the case
in all anaemias e.g.; in anaemia related to
coccidiosis plasma protein is affected). When
red blood cells are broken down from plasma they
usually constitute 30% of the total, 20% is
considered low and in these cases animals are
seen with as low as 10%.
What is this parasite?
The following brief layman’s guide to microbes
lists them from largest to smallest:
Helminth parasites (e.g. worms).
Protozoan parasites (e.g. coccidia, and many
blood parasites)
Rickettsia
BacteriaViruses (smallest).
The protozoa are Eurcaryotes and have 18S
ribosomal DNA. Preliminary electron microscopic
examination of the parasite in affected Eastern
Grey kangaroos could not confirm its identity as
a Eucaryote. It is therefore possible that it
belongs to another group of microbes such as the
Rickettsia (Prokaryotes with 16S ribosomal
DNA). To investigate this question of the
identity of the parasites we need to collect and
freeze samples of blood in EDTA anticoagulant
from all cases.
How is the parasite spread?
It is not known how this blood parasite
spreads. It could be one of many biting insects
including ticks, flies or even mosquitoes.
Scientists I have questioned seem to favour
ticks as the most likely vector. As an example,
with the Babesia sp blood parasites, (two
types that cause cattle tick fever), the
parasite is taken from infected cattle when
female ticks engorge with blood and transfer the
parasite through tick eggs to the larvae. The
disease spreads when larval ticks attach to a
new host, infecting it by injecting saliva
carrying the organisms1. A
larval tick is the tiniest tick seen and it is
doubtful whether a tick of this size would even
be detected on some animals.
In the areas in NSW where this parasite has been
confirmed, Boophilus microplus (the
cattle tick) does not exist, (or at least it
should not), and cattle ticks do not attach to
native animals. The common ticks seen are
Haemaphysalis longicornis (the bush tick,
also known as the grass or bottle tick), which
make up about 90% of ticks in NSW, and Ixodes
holocyclus (the paralysis tick, also known
as the dog, scrub and shell-back tick), which
make up about 10%. 2 I have
not included detailed information about ticks in
this paper, however I would encourage all carers
to gain further information via websites (e.g.
http://medent.usyd.edu.au is a website created
by the joint work of the University of Sydney
and Westmead Hospital, or www.ozemail.com.au/norbertf
- which is a very detailed site) or from
relevant authorities e.g. NSW Agriculture, so
they can clearly identify the different species
of common ticks.
Could young joeys in the wild be immune?
Let me use cattle tick fever as an example, (and
again I would stress that we are not dealing
with one of the 3 cattle tick fevers here, I
simply use it as an example where we do know how
the organism works), “calves younger than nine
months do not become sick when infected, but do
develop immunity to the organisms.” “Complete
eradication of cattle tick is not recommended
because some ticks are needed to re-infest
cattle continually to help them develop an
immunity to the diseases carried by the ticks.”
“Calves from immune mothers receive temporary
protection (maternal antibody) from the
colostrums which prevents babesiosis. This
protection lasts about 3 months and, in most
cases, is followed by an age resistance, which
lasts until the animals are about nine months
old. Calves exposed to infection when the
maternal or age resistance is high rarely show
clinical symptoms but develop a solid,
long-lasting immunity. It is therefore possible
to have both babesia organisms and cattle
ticks present on a property without animal
losses or clinical disease. This situation is
known as endemic stability.”
3
At this point we don’t know whether this is true
of macropods as well, however as previously
stated there are no confirmed cases of wild
kangaroos only suspected cases. Also this
problem does not seem to happen to carers of
young joeys in what we might call “suburbia” it
only manifests itself in “wild” areas.
In my own situation, I have a mob of some twenty
plus wild eastern grey kangaroos that move
freely around my house and property. They have
come into close contact with the two affected
joeys we have had recently and yet I have seen
no evidence of the problem in the wild mob.
There are also cases where only a few joeys of
those in care developed the problem – could it
be the others had developed an immunity
somewhere in their development – either coming
into care at a later age, or having gained some
bites whilst in care? I also had a red neck
wallaby joey undergoing release that also had
contact with the two eastern grey joeys. He too
showed no signs of the illness, however he had
been exposed to many ticks and flat flies (and
probably mosquitoes) for a calendar month before
their arrival. Could he have built immunity
prior to their arrival?
RVL Wollongbar have seen this parasite in the
kidney of a wild kangaroo (brought in for
testing for another reason). This animal showed
no signs of anaemia so it is possible that, as
is the case with coccidia, animals carry this
parasite but have a natural immunity to it.
This then raises the question - could this
problem be as a result of joeys being raised in
care, not being exposed to the range and number
of ticks and other biting insects that would be
a normal part of their wild world? This
question is also raised in the report by Cook,
Fraser and Hartley and the Liz Drinkwater
Paper. Although it is natural for carers to
want to protect joeys from such biting insects,
perhaps some exposure to bites at an early age
is as necessary to develop immunities, as dirt
is in developing good gut flora?
How would we solve this problem, given we need
our suburban carers? One suggestion may be to
cut grasses and bushes from the wild and to take
them into suburban carers to enable exposure.
(Ticks are…common in ground and shrub layers….
contrary to popular belief ticks do not fall out
of trees).
This may not solve the problem though given such
things as flat flies seem to be a very rare
event in suburbia and may not travel on branches
or in grasses? Also what degree of exposure is
needed? Is one tick enough? Probably not.
It is easy to forget that we should be thinking
and acting like eastern grey kangaroos rather
than letting our own motherly instincts take
over – this could be fatal to our charges e.g. I
have heard of carers who test milk warmth by
popping the teat into their own mouths before
popping it into the joeys mouth. This may be
fine for human babies, but what diseases might
we pass on to a kangaroo joey via our saliva?
In the same way too sterile an environment might
set animals up for later failure. It is a sad
fact that we often do not know what happens to
our joeys once they are released but we must try
to ensure they have the same chance as wild
joeys and that may mean treating them like wild
joeys and exposing them to wild elements from an
early age.
Treatment
Two things must always be considered when
treating eastern grey kangaroos:
They have a lower body temperature than domestic
animals “Kangaroos, like most marsupials, try to
maintain their core body temperatures near 36ºC,
slightly lower than most placental mammals.”
5
They have a lower metabolism than domestic
animals. “As a general characteristic,
kangaroos have basal metabolic rates that are
about 70% of those of comparable placental
mammals.” 6
This means there can be the risk of prescribing
too much medication, which could do immediate or
long-term damage. The following are
treatments being used by four different groups
who have seen this infection.
Group 1
– Gives one shot of Imizolâ
subcutaneously (no specific location for shot),
using the dosage rate of 0.12ml per 5kg (0.024ml
per kg). Vets sometimes also prescribe
antibiotics if there are signs of fluid
build-ups or chest infections. They keep fluids
up, using Lectade or by administering Hartmann’s
subcutaneously. They use pentavite with iron or
Incremin. Prior to the use of Imizolâ
this group managed to save about half of the
joeys that suffered from this problem using
various treatments including vitamin supplements
such as pentavite, cellvite E and also
antibiotics.
Group 2
– Two shots of Imizolâ.
One shot and then a second given 24 hours
later. Dosage rate 0.1ml per 2 kg (0.05ml per
1kg). Shot is given in the back of the neck.
Antibiotics are given on the 1st and
3rd days into the muscle. Anabolic
steroids were given to one animal, as it was
very debilitated. They sometimes also use a
natural tonic (similar to pentavite) and vytrate
(similar to lectade) to keep fluids up.
Group 3
– Pentavite with iron, Incremin, keep them well
fed and watered. This group has lost 2 out of 5
joeys in the past 10 years that have presented
with the problem.
Group 4
– Two shots of Imizolâ,
one day one, the second one week later. Dosage
rate is 0.2ml per 4kg (0.05ml per kg). Given
subcutaneously, no specific location.
The use of Imizolâ
When this drug was initially used, the main
concern was its possible toxic effect on
macropods. Given the number of animals that
have now been treated with the drug, and in
varying amounts, it could probably be safely
concluded that it does no short-term damage to
the animal being treated. (Group 2 has seen
side effects of localized swelling and a scab
that falls off).
In the 3 groups using it, all believe that a
majority of the animals recover with the use of
Imizolâ,
though some confirmed cases did die and a
greater number of cases are “suspected” rather
than confirmed and so some recovering animals
may not have had the parasite. As previously
stated, those with a regenerative anaemia (even
with haemocrits as low as 0.11 and 0.12 L/L) do
seem to improve clinically with the use of
Imizolâ
7.
Anecdotally it would seem that those that are
going to die usually do so within a few days and
those that will recover respond to the Imizolâ
within 24 hours.
A single dose sterilizes Babesia spp.
infections and is effective, though less so
against Anaplasma spp. Therefore if the
drug is active against the kangaroo organism a
single dose may be sufficient treatment. One
Vet I discussed this with said in some cases
where a second dose was given it appeared that
the animal was probably going to recover anyway
and that the 2nd dose probably had
little effect. This may be confirmed by the
Department of Agriculture (WA), which states
“Imidocarb (the active ingredient in Imizolâ)
is highly effective for treating tick fever.
However a single dose steralises the bloodstream
for up to 12 weeks, negating the development of
immunity” 8. This then raises
the question of immunity in those cases which
have survived. So far there have been no cases
reported of second infections, however given
surviving animals are released to the wild, not
all animals can be tracked for the duration of
their life. One Vet I spoke to felt if their
immune systems have started to fight the problem
then they should gain a degree of immunity
despite the use of Imizolâ.
The Department of Primary Industry Queensland
states the recommended dosage of Imizolâ
when used for the treatment of vaccine reactions
in cattle as follows:
For the two babesia strains:
“Imizolâ
dose rate: 1ml/100kg (0.01ml/1kg) live weight
(treatment). Imizolâ
must be given under the skin, preferably in the
neck. Depending on the volume given, it may
cause some tissue damage and it is advisable to
split the dose into two inoculations if it
exceeds 5mls.”
For anaplasma reactions and if using it as a
short-term preventative:
“Imizolâ
dose rate 2.5ml/100kg (0.025ml/1kg) live weight”
9.
With regard to where the dose should be given,
the scientific consensus seemed to be it
probably doesn’t matter where it is given but it
should certainly be subcutaneous and not
intravenous. Because of the difficulty of
obtaining Imizolâ
in the affected area, sometimes it may have been
used when passed its use by date. The
manufacturer’s advice is that this should not
happen. I have been unable to ascertain, at
this point, what changes may occur in the
product after it expires. There are drugs whose
properties change post expiry and may create
neurological problems. It is probably safest
not to use Imizolâ
past its use by date if possible.
The use of antibiotics
The use of antibiotics will not kill the
parasite, but could be helpful if there are
secondary problems such as fluid build-up
(oedema) within the lungs, which can predispose
to pneumonia. Antibiotic use is the same in
animals as in humans in that most may have some
toxic effects, and over use may reduce future
resistance. Whether antibiotics should be
given subcutaneously or intra-muscularly depends
on the type of antibiotic used.
Is Imizolâ
the only drug?
At this point it would seem so. In some of my
research I came across reference to quinuronium
sulphate (Ludobalâ)10.
This drug is an old babesiacide developed in the
1930s and no longer available. It is,
however, very stable and old stock of this
product has still worked for cattle tick fever.
Recovery:
May takes two weeks or longer, with the animal
slowly gaining energy. Meanwhile, their heart
may be under strain, as it is working so much
harder to pump the blood around. Rest with
plenty of fluids and food is recommended. Some
animals are so lethargic that they cannot move
themselves out of the sun and this obviously
needs to be monitored.
Preventative
Measures:
ImizolÒ
is only used as a preventative on cattle as a
temporary measure (e.g. the cattle tick vaccine
can create problems for pregnant cows and
therefore ImizolÒ
may be used as a temporary measure, but does
wear off after a short time.) It is registered
with the claim of providing protection for 4
weeks. The conclusion seems to be that it
should only be given to macropods as a treatment
and not as a preventative.
Where to from here?
There is a need to:
Identify the organism (from DNA studies using
EDTA blood samples collected from cases and
frozen for future testing. For this work we
need to collect samples from a substantial
number of cases.
Collect clinical and treatment data in a
standard format for ease of collation.
Inhibitors to further progress in this area
include:
Sometimes poor documentation of cases by carers.
Information not shared between wildlife groups.
Unclear definition of cases (anecdotal versus
confirmed cases). It is important to have
laboratory tests done to support the diagnosis
and be sure of what the problem is. If we are
tempted to see this parasite as the possible
cause of all ills and ImizolÒ
as the cure we run the risk of losing animals to
other diseases as well as being unable to come
to scientific conclusions.
Lack of funding for research for native animals.
What can you do to help?
1. When
you have a LIVE suspected case,
you are encouraged to collect the following
information in a standardised format and samples
for diagnosis and research:
Air-dried blood smears
from tip of tail or ear (for staining and
detection of the organism).
EDTA blood sample.
A
blood sample in EDTA anticoagulant is useful for
two reasons:
a.
Test immediately to assess severity of anaemia
and plasma protein concentration
b.
Freeze remainder for research to identify the
organism.
Collect any ticks from affected
animals
and hold them in a 70% by volume alcohol mix.
(This can be pure alcohol, or even mentholated
spirits can be used, but in a 70%
alcohol/30%water mix). In a clean jar. These
do not require freezing.
Complete the Macropod Exam Sheet attached
so we can gain consistent information from all
sources
Arrange for these frozen EDTA blood samples,
ticks in 70% alcohol, and Macropod Exam Sheets
and any other details to be sent to or collected
by:
Cheryl Dooley, 1647 Orara Way, Glenreagh NSW
2450
Ph: (02) 6654 3793,
Email:
dooleydy@ozemail.com.au
2. When
you have a DEAD suspected case,
you are encouraged to arrange necropsy (a
postmortem examination). Bodies for necropsy
should be chilled NOT FROZEN (i.e.
use the fridge not the freezer). The
approximate cost is $100 (current January 2003).
Post mortem examination can be by a local
veterinarian who can collect specimens to send
to the laboratory, (these should include fresh
and formalin-fixed kidney and brain at minimum.
Fresh faeces and a range of other
formalin-fixed tissues – heart, lung, liver,
intestines, bone marrow – should also be
collected to diagnose other possible diseases
such as coccidiosis), or the chilled carcass can
be sent directly to the laboratory, e.g.:
NSW
Agriculture Regional Veterinary Laboratory
Bruxner Highway. Wollongbar NSW 2477
Ph: (02) 6626 1261; Fax: (02) 6626 1276
3. Send
all information to Cheryl Dooley (contact
details above). This will enable us to have a
central contact point so that this paper can be
updated 11.
4. Distribute
this paper to all known macropod carers and vets
who may be involved in macropod care.
References
Acknowledgments:
I have spoken to almost 40 people in the course
of this initial investigation. Everyone has
been extremely helpful and I obviously cannot
acknowledge everyone by name or another page
would be added to this report. I must, however,
particularly thank a number of people, Dr Roger
Cook and his colleagues at RVL Wollongbar; Dr
Karrie Rose of Taronga Zoo; Dr Anton Sluyters of
the Yamba Vet Clinic; Dr Michael Featherstone of
the Blue & White Vet Clinic, Coffs Harbour;
Kerry Cranney (without whom this research would
not be happening as she initially alerted me to
the problem); Judy Petersen; Liz Drinkwater;
Joyce Skinner; Lyn Davies; Carol Riley; Diane
Ward and all of the many other wildlife carers I
talked to as well as other vets and interested
persons.
Thank you all for your advice, support, precious
time and continued interest in this problem. |
