My previous
post on this subject was surprisingly popular. As I asked around for any more information that
might broaden the picture I was sent the article below outlining the current 'official'
position and post it here for further information. The general thrust seems to
be that as yet vets and the scientific community have not enough evidence to be
able to develop a scientific approach and solution. It seems to me that in general frustration and the absence of any
formal accepted regime several falconers and breeders have
found ways to deal with the problem themselves. Its what happened to me as described in
my previous post.
Secondly Nick Wilkinson who breeds a lot of Merlins and has done much of this work himself sent me a booklet from
Australia about cocci in kangaroos. It gives a very clear picture of what they
are dealing with and therefore stimulates ideas that may be helpful to our own
approach. Certainly, although it is primarily about kangaroos, reading this did
much to help me get my mind around my own problem encountered in my tiercel
and thus enabled me to develop my own thoughts for a management program that has
worked for my falcons. It may be misleading to think that treatment techniques used by these people could be applied to birds but it did cause me to think and ask myself appropriate questions.
I attach text only below for what its worth to readers,
diagrams are removed in copying from the PDF but it may at least stimulate readers to look for the original if more clarity is needed.
January 2012
AVS would like to thank the Hawk Board, Honeybrook Animal
Foods, Falcon Mews, M+J Raptors, Mark Stidworthy MA VetMB PhD MRCPath MRCVS, Michael
Lierz Prof. Dr med vet, DZooMed, DipECZM, DipECPVS, Dr. Akbar Dastjerdi and Dr.
Tristan Cogan for their help and support with ongoing research into a wasting
syndrome affecting captive peregrine falcons.
To date this disease has affected a number of falcons up and down the country
(and anecdotally other parts of Europe) and AVS among other avian vets,
pathologists and researchers have been gathering data and pooling experiences
to try and get a better handle on this emerging disease.
We do not as yet have a definitive diagnosis but with falconers and breeders
continued help in submitting cases for investigation we are slowly making
progress.
What follows is a summary of the findings and information we have available at
the time of writing.
1. From our personal observations this syndrome seems only to affect peregrines
or peregrine hybrids even within multi-species collections.
2. Clinical signs include; general poor condition, weight loss despite eating
excessively, screaming, mucoid/slimy diarrhoea, pale feet, cere and talons
(Figs 1 and 2), excessive drinking and vomiting, sadly in many cases
progressing to death despite culture based antibiotic treatment.
3. Some birds with aggressive supportive therapy improve and may even breed,
but recurrent relapses are typical.
4. Despite countless faecal samples and cultures no single bacteria, yeast or
parasite has been consistently identified across the board suggesting that
those pathogens found are secondary invaders to an already inflamed/damaged
gut.
5. We have recently received results from the virologists on both tissue and
faecal samples of affected birds. Viral chip technology that searches for any
viral DNA present in the samples and compares it to a data base of nearly 2000
known viruses, has failed to identify a causal virus in any samples submitted
over the past year.
6. A separate team at Bristol University which has been looking at tissue
samples of both affected and 'normal peregrines' (wild casualties that have
been euthanized on humane grounds) has demonstrated changes consistent with
post infectious inflammatory bowel disease (IBD). This is a similar condition
to ulcerative colitis in people where a historic intestinal insult, be it
viral, parasitic or toxic may result in an 'autoimmune reaction' where the bird
develops antibodies to its own intestinal lining. This damages the gut allowing
secondary infections to proliferate. It is thought this occurs because
'antigens' or protein markers on certain infectious agents (salmonella for
example) may resemble similar structures found on intestinal cells. As such
when antibodies are made in response to infection, they are then stored in the
immune systems 'memory' as a permanent defence mechanism against future
challenge. When under stress or hormonal influences (in a paper on ulcerative
colitis in women, flare ups often occur after giving birth and rarely during
pregnancy) the body can mistakenly identify intestinal cells as invading
infectious agents and attack it accordingly. Also in mammals certain foods can
trigger episodes. As such when a bird demonstrates clinical signs associated
with certain food items it is assumed this must be carrying 'the virus'. It is
equally possible however that certain proteins cause flare ups and others
don't, hence the possible response to exclusion diets (all rat for example).
Based on the above our current working hypothesis is that a historic gut insult
be it a bacteria, virus, parasite or toxin results in post infectious IBD,
which (as in humans) is then likely to be a lifelong problem with 'flare ups'
managed by identifying and removing apparent trigger factors (certain foods,
parasites etc) in conjunction with supportive fluids, nutrition and medication.
The problem we are up against is by the time obvious clinical signs are
apparent the inciting cause is likely long gone.
As this syndrome seems to be overrepresented on older birds it may be that
chronic or repeated low level intestinal insults by one or a combination of the
above eventually leads to disease.
Current recommendations
If a falcon is displaying such symptoms we would advise you contact your avian
veterinarian ASAP as other easily diagnosed conditions such as coccidia (Fig 3)
can produce similar signs and are very easily treated. In addition collecting
samples as early as possible in the process increases the likelihood of
recovering causal agents. Probiotics have been shown to help maintain a healthy
gut flora and may offer some protection against IBD. As such we have been using
such products on a preventative basis in collections of breeding falcons. If a
falcon seems to have diarrhoea following the ingestion of certain food items or
groups (provided other infectious causes have been ruled out) it may be worth
trying an exclusion diet as discussed above. If things improve on a novel
protein it maybe this bird has a 'sensitivity' or 'intolerance' to certain food
items that may contribute to the development of IBD. As affected falcons appear
to drink copiously, it is recommended fresh water is available at all times.
We will endeavour to keep you informed of any future developments via our
website, the Hawk Board and Falconry club literature and you can make a
donation to the Hawk Board's raptor research fund via their web site. www.hawkboard-cff.org.uk
Text only of Australian booklet
Coccidia a parasitic journey - Gayle Chappell
Everyone has heard of the saying that goes
something like In knowing
an enemy you know how to fight it. That’s how I feel about coccidiosis. The following article explains in
as much detail as I could gather, what coccidia actually is and how it does
what it does. The second part of this lengthy article describes the results of
a small survey carried out amongst shelters experienced with kangaroos. Of
course there are many more of you out there than was surveyed but surveying everyone
is not currently possible. Please feel free to write in and make comments and
share your own experiences.
Coccidia is a
single-celled, protozoan parasite which causes the disease known as
coccidiosis. There are hundreds of different types, or species, of coccidia
which have been divided into two genera; Eimeria and Isospora. Coccidia infect a
large number and variety of animals in the world but the ones that infect the
Eastern Grey (EG) Kangaroo belong to the Eimeria genus. There are perhaps 8 different
species of coccidia that infect the EG roo and perhaps only two of these cause
the disease coccidiosis as we see it. I say perhaps because it is not really known
just strongly suspected.
Each species of
coccidia has distinguishing characteristics that identify it, but these may not
always be obvious or may only be seen at particular stages of the coccidiaís
life cycle. What this means is that the coccidia oocysts that you see in a
faecal sample may not necessarily belong to the species as that will cause
disease in the kangaroo.
Coccidia are
very host specific, and so a species of coccidia may cause disease in one
species of animal but not in another even though they are infected with the
same coccidia.
Coccidia live in
the small intestine of their host, and it only infects the host by ingestion.
That is, a roo has to eat it to get it. Some species of coccidia live on the
surface of the gut lining and cause no ill effects. It is only the species that
burrow into the cells of the gut wall, multiply and rupture, that cause the
problem.
Each oocyst
contains within it 4 smaller bodies, each of which contains 2 even smaller
bodies known as sporozoites.
Doing the maths
- there are 8 sporozoites with in each oocyst.
once in the
small intestine, the outer shell of the oocyst is digested and the 8
sporozoites are released. The sporozoites then invade the lining of the gut
wall.
Once in the
cells of the gut wall, the sporozoites form a membrane about themselves and
start to rapidly multiply by asexual division, which is simpley splitting in
two rather than mating. This division can occur 800 to 900 times. The resulting
bodies of this division are called schizonts. The infected cells of the gut
wall rupture because of the enormous number of schizonts produced within them.
This releases the schizonts to invade even more cells of the gut wall where the
rapid asexual division
continues. It is
in this way that massive cell death in the host occurs and why we see blood
with the
faeces, or
simply blood seeping out from the cloaca.
Coccidia completes
its life cycle outside of the host’s body. Once out of the host’s body the
oocyst must still sporulate - or create the sporozoites. Until it sporulates
the oocyst is not infective. Conditions must be right for the oocyst to
sporulate. If the oocyst is eaten before it sporulates then there are no
sporozoites to infect the cells of the gut wall and the coccidia is harmless.
Once the faeces
carrying the oocysts deteriorates, the oocysts are left on the ground and in
the soil. Some oocysts may become dust born and travel to other areas. Coccidia
oocysts may last in the ground for years waiting for the right conditions to
sporulate. During that time there is an opportunity for oocysts to build up in
enclosed roo areas. In the case of the coccidia in EG roos the right conditions
for sporulation seem to be wet, warm weather. It is very hard to destroy
oocysts in the soil and so the best way to prevent a build up of oocysts is to
regularly pick up roo poo.
Coccidia is
self-limiting, meaning that it cannot asexually divide forever. After a few
generations of asexual division, the coccidia simply stops dividing. This means
oocyst production also ceases and the host becomes essentially free of
coccidia. In order for coccidia to continue to live within the host it must
continue to ingest infective oocysts. Coccidia does not live full time in the
host awaiting an opportunity to multiply and infect. It passes through the host
in order to reproduce. Disease occurs when the normal balance that allows
parasite and host to happily co-exist is disrupted.
This ‘normal’
balance can be affected by:
1.the degree of host immunity (see below for
further information on immunity). If an animal has had prior exposure to
coccidia then it may have a better ability to fight the division of the
coccidia and subsequent oocyst development. As can be seen from the life cycle
of coccidia, oocyst development is essential for reinfection to occur.
2.poor nutrition of the kangaroo may lessen
its ability to cope with, or fight against, the coccidia parasite;
3.the virulence of the infecting coccidia
species;
4.the size of the infecting dose of coccidia.
The larger the number of infective oocysts ingested the greater the risk of
disease occurring. The number of infective oocysts can be increased due to:
- overcrowding;
- faecal contamination of food;
- access to contaminated ground;
After the second
of third division the schizonts begin to reproduce sexually. This means that a schizont
becomes a gamete which is either a male or female fertile cell. The males
fertilise the females and the result of this sexual reproduction is a fertilised
egg otherwise known as an oocyst.
The oocyst
breaks out of the gut wall cell and passes out through the host’s body with the
faeces.
Complications
The disease
caused by coccidiosis is due to the massive destruction of cells of the gut
wall. As the cells of the gut die and slough off the area becomes like a large
ulcer - raw on the inside and red and swollen on the outside. The animal is in
acute pain as a result. However, no toxins are produced by the coccidia. The
damage is mechanical and animals may die from loss of fluid and shock due to
the pain and dehydration alone. Secondary, bacterial infection may flourish
because of the lesions to the gut wall or because of the physical and
psychological stress the animal is under.
Although a
coccidia outbreak may be occurring in the kangaroo, it may not be the disease
which actually kills the animal. There are other bacteria, such as salmonella,
which naturally reside in the kangaroo and will flourish given an opportunity.
Coccidiosis can provide that opportunity as the animal is in a weakened
physical state. Pneumonia is also often seen and can cause death before the
coccidia does.
Diagnosis
Diagnosis of
coccidiosis is not an exact science. The presence of coccidia oocysts in the
faeces is often used as a diagnostic tool but the identification of the genus
of coccidia, let alone the species of coccidia, is not probable unless the
oocyst has sporulated. In other words, as mentioned earlier, the coccidia you
see under the microscope may or may not be the disease bearing one.
High counts of
oocysts in the faeces can, however, be a very strong indicator that a virulent,
disease bearing coccidia is at play.
Referring back
to the life cycle of the coccidia can explain why an animal may die from
coccidia without any oocysts being present in the faeces. If an infective dose
is high enough, or the animal is susceptible enough, the animal may die from the massive trauma to the gut wall due to the
asexual division (and consequent cell destruction) of the coccidia parasites before
they have a chance to sexually reproduce and form oocysts. So you can see
bleeding but no oocysts in the faeces.
Diagnosis is
usually based on observations of the Kangaroo (generally joey). A disinterest
in milk is an early warning sign as is a hunched stance, which generally
indicates gut pain, and dull eyes. More detail about the physical signs that
may be seen before coccidia is clinically diagnosed is given in the following
section about carer experiences with the disease.
Immunity
It is thought
that the production of antibodies against coccidia only plays a very minor role
in the body’s fight against the parasite. The body has several different types
of immune responses and immunoglobulins are the stuff responsible for telling
the body what immune response to engage.
The main immune
response against coccidia is cell-mediated as the body must defend itself
against an organism which is actually living in the cells themselves. T
lymphocytes are what the body uses for this type of immune response.
Prior exposure
to coccidia primes the T lymphocytes for response to subsequent exposures. Dr
Anne Fowler describes the T lymphocyte cells as army scouts that know what the
enemy look like and have made an army ready for war. When war comes (coccidia)
the troops are all ready to mobilise rather than trying to build an army from
scratch.
So, unlike
antibodies which are like a standing army, T lymphocytes are like an army in
reserve.
It has been
found in chickens that exposure to very low levels of virulent oocysts in
chicken’s first few weeks of life promotes the best immune response against
coccidia. Kangaroo joeys in the wild are likely to be exposed to fairly
constant, low doses of coccidia from a very early age. The rate of occurrence
of coccidia in wild populations of kangaroos is unknown. The virulence of the
coccidia and the amount of oocysts ingested remain the primary factors in
causing coccidiosis to flourish.
Treatment And
Prevention
There are no
cures for coccidia only prophylactics that reduce the number of coccidia
produced.
Baycox uses a
drug called Toltrazuril which kills coccidia parasites at several stages of
their life cycle attacking the schizonts in and outside of the gut cell and
also the fertile gametes. The parasites ability to produce oocysts is severely
compromised. but the oocysts themselves are not actually killed by the Baycox.
If Baycox is administered after oocysts have been produced, then the oocysts
will still pass through the body in the faeces and reinfection can still occur
once the sporulated oocysts is ingested. Other drugs used to treat coccidia are
trimeth and sulfa based drugs. These are effective against the coccidia at the schizont
stage in the gut cell. (NB: the drug monensin which goes under the brand name
of Rumensin, is used in the treatment of coccidia in cattle and is fatal to
macropods).Amprolium products, such as coccivet, is active against the schizont
stage in the gut cell and the oocysts. This is why Amprolium is used as a ‘preventative’
- because it reduces the oocyst numbers in the faeces and therefor reduces the
rate of coccidia oocyst build up in confined areas.
These
prophylactic drugs are most effectively administered when an animal undergoes
periods of stress and change. The dose rates and length of administration of
these drugs is somewhat dependent on the circumstances and environment. The
following is a guide only:
Baycox is
effective when early symptoms of the disease appear. General dose rate is 0.8ml
per kg of roo; sometimes given as a one off dose or over three consecutive
days. This appears to be up to carer experience and preference.
Baycox is not
usually used as a preventative as it may interfere with the body’s ability to
formulate its own immune response while exposed to low doses of coccidia.
However, in some circumstances, such as if a kangaroo has just been transferred
or there is a coccidia infection in other nearby roos, a one off dose of Baycox
may be fortuitous.
Amprolium is
often used to reduce numbers of coccidia on an ongoing basis. It is unsure as
to weather or not it does inhibit kangaroo coccidiosis. It should also be noted
that coccidia species (particularly in poultry) have shown resistance build up
to drugs when used in high, on-going doses. Sulfa based drugs are often
administered when coccidiosis is apparent and this used to be the best
treatment there was. They attack the schizont stage of the coccidia cycle.
A course of
antibiotics is used to help prevent infections, salmonella and pneumonia from
causing further complications during the illness. Baytril and Trivetrin are two
antibiotic brand names often used. Your vet must be consulted for appropriate
dose rates. Good nursing is essential to the animals’s survival. Warmth,
hydration and quiet are essential to helping nurse the roo through the illness.
Often larger roos will go back into a pouch but the pain may be so intense that
they can only stand. Oral hydration, using a rehydration formula, such as
lectade, is most effective if the fluid is taken in small amounts given often
over time. Replacement fluids should start at 5% of body weight per day but
could be as high as 10% depending on the severity of the diarrhoea and
bleeding.
Maintaining good
gut health is essential. Probiotic products provide healthy gut bacteria so
that a healthy digestive balance is maintained, and promote the absorption of
iron and other micronurients. Colustrum products, such as Wombaroo Impact, work
to feed the intestinal cells. Colostrum also contains immunoglobulins which may
be useful in promoting a strong immune response to the infection of coccidia.
The bacteria in probiotics are destroyed by antibiotics so they are best given
after a course of antbiotics is finished. The colostrum may be given at a time
of stress, illness or recovery. Vitamin B-12 is also important in the
maintenance of intestinal health.
Pain relief is
difficult to administer to a kangaroo once the gut wall is ulcerated which it
essentially is
with
coccidiosis. Non steroidal anti-inflammatory drugs (NSAIDS) could cause more
irritation and make the ulceration even worse. Cortisone will suppress the
immune system, so that’s out. The opiate drugs, which vets are often reluctant
to use anyway, will cause sedation, depression of respiration and the
possibility of stopping the gut from moving (constipation). Codeine has been
used in very limited quantities and it is essential to consult with a vet
before administering anything. Codeine will also slow down gut movement.
The two most
essential preventative measures remain hygiene and stress reduction. Picking up
roo poo to help prevent coccidia concentration; not putting feed on the ground
to help prevent ingestion of large numbers of oocysts from contaminated food;
removing as many stress inducing events as is possible. If the roo is becoming
very distressed during the illness Valium may be given to help calm the animal.
Again, consult with your vet first.
Once the
coccidiosis has passed, a product that will sooth the intestine can be given.
Slippery elm tea has been used as has scourban and dolomite (see next section).
Coccidia
- a carer’s journey. by Gayle Chappell
Ten shelters in
Victoria who are experienced with kangaroos were surveyed about their
encounters with
coccidia.
Occurrence
These figures
are based on confident diagnosis and do not reflect the number of cocci cases
that have been avoided, missed or cured because of the fast action and sound
preventative measures from the shelters. It is often the case that after the
first few cases prevention measures begin to work very well.
They were found
to have the following confirmed cases.
7 in last two
years
5 in last two
years
3 in last two
years
2 in last two
years
2 in last two
years
The shelter
which had 7 cases had three unusual cases. The three roos had all been released
for a couple of years and were about 3.5 years old. No classic symptoms were
present but autopsies claimed the cause of death to be coccidia. The carers
feel strongly that coccidia was a secondary infection brought about by a
weakened state from another primary infection. Further investigation confirmed
that at least one roo had a Yersinia infection. A protozoan affecting the lymph
and the immune systems. It is often carried in wild duck droppings. The three
roos that became ill were the only ones in a sizeable mob that fell ill and the
only observable element they had in common was that they had all been eating
from the same food bowl.
One other
shelter found on autopsy that strongaloides was the primary cause of illness
and coccidiosis was able to develop as a secondary infection.
These examples
echo the concerns of some shelter operators - what is really going on when a
roo succumbs to coccidiosis? Autopsies are not often extended (for obvious
financial reasons) past the most obvious cause of death (coccidiosis) but this
does not always explain what else the kangaroo may have been dealing with.
Age
Most carers said
that the time when a joey emerges from the pouch to eat grass is when they are
at their most vulnerable to coccidiosis. The carers collectively had cases in a
broad range of ages. The youngest case being a small pinkie and the oldest
being a healthy released 3.5 year old. Most of the roos are in a 4 to 7kg
weight range. Roos in larger weight ranges of 8 to 15kg generally tend to be ‘transfers’.
Younger transfers appear to be equally susceptible to the older ones. Further
data needs to be collected before any real patterns can be revealed.
Mortality
All shelters but
two had 100% mortality. Opinions were expressed that if a roo recovers from a
suspected case of coccidiosis, then it probably wasn’t coccidiosis. Most
shelters felt that if a roo got to the bleeding stage then it had no chance of
survival. One shelter has a very high survival rate (nearly 100%). This shelter
has pulled roos through the bleeding stage and they have made a complete
recovery. Carers have also heard of other cases of such recovery. Even at the
bleeding stage it is shock and dehydration that a roo must survive with
coccidiosis. The injury is internal, it is painful and horrible, but so is
concussion, broken limbs and any number of external injuries. Injured animals
are nearly always treated for shock and dehydration when they come in, and they
are protected from bacterial infection with antibiotics. The same principles
apply when treating coccidiosis.
Symptoms and
detection
Nearly all
carers said it is almost an intuitive knowledge that they detect something is
wrong with the roo. It was expressed that the early warning signs of
coccidiosis for transferred roos are often missed because the new carer does
not know the roo well enough to know if something is wrong. All carers said
that you can see it in the eyes first when a roo is ill with coccidiosis.
One carer
observed one little roo became very clingy and sooky before it became obvious
that there was something amiss.
6 in 7 years
4 in 10 years
1 in 15 years
5 in 40 years
none in 10 years
Also in the
early stages the kangaroos were often observed by carers to go off their milk
but not always or sometimes not enough to be sure that something was wrong. It
was generally found that if a roo went off their milk over several feeds,
offensive smelling and bloody diarrhoea followed after about two days and the
roo was usually dead in 3 to 4 days. Carers also observed a number of kangaroos
that showed no sign of diarrhoea or bleeding but went entirely off their milk
between one feed and the next and they suddenly appeared to be pain. In these
cases death was very rapid, within 24 to 48 hours. There was occasionally fresh
bleeding (red blood) immediately prior to death but not always.
The offensive
smelling dark diarrhoea is caused by the partial digestion of the blood in the
intestine. The colour of the blood may be a good indicator as to where the
infection is occurring in the gut. Bright red blood indicates there is little digestion
occurring and perhaps the infection is lower down in the gut. The survey had
hoped to find a connection between where the coccidia infection occurred,
indicated by the colour of the blood, and the virulence of the infection.
As it is
considered that there are two species of coccidia that cause coccidiosis in EG
roos it is not unreasonable to think that one may be more virulent than the
other or cause slightly different symptoms. Would this make a difference to
treatment? Perhaps, perhaps not. The survey sample was not large enough to form
any real picture on this.
It does appear
that the slower the onset of the symptoms then the better the chance of
survival. Remember though that even a ‘slow’ onset is fairly rapid.(24 hrs).
Most shelters
showed little to no confidence in faecal float tests. As was explained earlier
the presence or lack of presence of oocysts may not be a sure indicator of what
is going on. The coccidia may not have reached a stage of sexual reproduction
and so little or no oocysts would be present in the farces at that particular
stage. or the oocysts present may not belong to the coccidia species which is
causing the coccidiosis.
One problem with
faecal floats of course is that if you are not doing them yourself then you may
not have time to wait for a diagnosis (which may be incorrect anyway) from
a vet or laboratory. One shelter surveyed does faecal floats at the shelter and
has found them to be a very good indicator of coccidiosis. The carer has been
able to observe the massive increase of oocysts in the faeces over time. The
essential elements to proper diagnosis in this situation is a) being able to do
faecal floats at regular intervals and b) being able to match symptoms with
observations of oocysts in the faeces.
One carer has
observed that roo droppings accompanied by a dark wet fluid stain is an early
sign of coccidiosis. The droppings may still be pelleted but sometimes a little
soft.
One shelter felt
that coccidiosis was often misdiagnosed as any sign of diarrhoea can often be
jumped upon as coccidiosis. There is a fairly consistent set of symptoms that
are indicative of coccidiosis but they do not all present in every case nor do
they present in a set order. The carer must often weigh up the symptoms that
are (or are not) presenting with recent circumstances
and weather
conditions. To not act very quickly could be fatal for the roo and to act
prematurely is not very harmful with the treatments for coccidiosis. The worst
effect of acting too quickly is giving the Roo an application of unnecessary antibiotics.
The antibiotics may, however, also be appropriate for other possible bacterial
infections that show similar symptoms. Knowing when to treat for coccidia is
often a matter of experience and intuition rather than diagnostic certainty.
A proper
diagnosis is of course preferable and still necessary to ensure any other
disease or infective
parasite is
being adequately dealt with. Make sure that a faecal sample is gathered BEFORE
any drugs are administered. Discuss your chosen treatments with your vet before
applying them to a roo.
Treatment
drug regime
Once treatment
is decided upon the shelters surveyed tended to go one of two ways;
1)
administration of a sulfa based drug and/ or amprolium product. either with;
i) a broad
spectrum antibiotic such as Trimethiprim, Trivetrin or Baytril
ii) no
antibiotic
2)
administration of Baycox. either with;
i) a broad
spectrum antibiotic such as Trimethiprim, Trivetirin or Baytril
ii) no
antibiotic.
One shelter
administers Vitamin B as this has been known to arrest oocyst development in infected
poultry.
The most
successful treatment was by far the immediate administration of a course of
antibiotics together with Baycox
at 0.8ml per kg
for three consecutive days.
A few shelters
mentioned the use of a coagulant if bleeding occurs but Dr Anne Fowler says
that in theory this should not make much difference. A coagulant acts to help
the blood to clot because it lacks a clotting agent.
The roo with
coccidiosis is bleeding due to trauma and has not had its ability to clot blood
compromised at all.
Pain killers are
not currently used by any of the carers surveyed because of the difficulty in
prescribing an appropriate pain killer and also because they have sometimes
been tried and found to be ineffective. Buscopan has been tried by a couple of
carers but with no satisfactory result. Valium has been used in a couple of
survival cases but only to sedate a distressed roo not as a pain killer.
Scourban is very
successfully used by one shelter for easing the gut after the coccidiosis has
cleared and the antibiotic course is complete. The roos are given a daily dose
until scouring stops. Scourban can have a soothing affect as it coats the
lining of the intestine. It also has some antibiotic affect. One carer uses
unrefined dolomite powder sprinkled on dry feed as it forms a protective
coating of the gut.
Two shelters had
used Salazapryin but only once. It is a drug used in humans to treat ulcerated
cholitus which presents some very similar symptoms to coccidiosis. Salazapryin
is not an antibiotic but works to change the PH levels in the gut and to form a
soothing coat to the intestinal wall. Not much is known of its effectiveness in
treating coccidiosis.
It was mentioned
by a few carers that stress reduces the health of mucous elements and that the
use of vitamin A is beneficial to restore and maintain mucous elements in the
body, particularly the intestine. Dr Anne Fowler says that stress does not
actually affect the production of mucous and that vitamin A is more helpful to
those mucous linings that are exposed to air such as for the nose and mouth. Dr
Fowler says that Vitamin B12 is important for the health of intestinal
microbes. Also very good for healthy intestinal microbes is a probiotic powder
added to fluids. This is used by a number of carers. No carers mentioned the
use of colostrum supplements either as a preventative or during the illness.
Nursing
All carers were
very aware of the need to keep the roo’s fluids up. Nobody found this easy. It
was found to be best to give up on milk altogether and offer electrolytes such
as Lectade and Vytrate. Other things that were tried to entice the roo to drink
were glucagon, nutrigel and cold black tea with glucagon. It was found that
fluids had to be forcefully given in small but regular doses. Just to get 5ml
in at a time was considered a success. Such small doses may need to be given
every half hour to hour.
Some carers felt
that the stress of forcing fluids into a roo could be harmful. One carer
mentioned the possibility that too much fluid in the gut when it is so badly
ulcerated could cause further problems such as herniation. Dr Fowler believes
this to be very unlikely and that any herniation would be caused by continuous
straining from the diarrhoea.
A bottle was
usually used to give fluids as it was felt that using a syringe was too risky
in case of fluid aspiration. As pneumonia is a common secondary illness any
fluid aspiration could be very dangerous. It was felt that to maintain a
rehydration level of 10% was nearly impossible. Persistence and patience are
essential in getting what fluid you can into the roo.
No carers
mentioned the provision of warmth and quiet. This was probably an oversight or
perhaps taken for granted. As an animal goes into shock, as they may with
coccidiosis, their ability to maintain their body temperature is weakened.
Warmth may also provide comfort to a hurting body. Quiet and removal from any
stress causing factors is needed for the comfort of the roo. It was strongly
felt that the sick roo benefited greatly from the security and reassurance that
their carrer gives. Trust and affection between the roo and the carer reduces
stress and allows the carer to nurse the roo properly.
Prevention
Preventative
measures are taken by most shelters. These range from regular doses of
amprolium , to doses of amprolium only during wet warm weather, to never using
amprolium. No one was certain of the affectiveness of amprolium as a
preventative.
One shelter uses
a one off low dose of Baycox at 0.2ml per kg if she suspects anything,
especially after dramatic changes in weather conditions. If suspicious signs
persist she will dose the roo again, at the same dosage, after 3 days. Another
shelter doses roos eating spring grass with Baycox when the weather turns warm
and wet. At this time they may dose the roos once every 4 weeks for up to
several months.
All the carers
recognise that good hygiene practices help prevent coccidiosis. Most shelters
regularly poo scoop enclosures, sometimes once or twice a day, with one shelter
picking up dropping at every milk feed if necessary (she hasn’t had cocci in 15
years). The actual outside release of the roos varies, some being penned,
others free ranging when they step out of the pouch and some having nursery
pens only. It does appear that the earlier a roo can free range, the less
likely the occurrence of coccidiosis. This makes sense as the concentration of
oocysts in faecal matter is reduced in free ranging areas. There may be other
factors influencing kangaroo health as they pick and choose for themselves the
foods they prefer to eat.
Stress events
were identified by everyone as a major cause for coccidiosis. There are obvious
stress events such as moving location or contact with a strange dog, however,
most carers were also at a loss to identify exactly what those stress events
were that brought on the coccidiosis in their own roos. Stress could be chronic
rather than acute but then you would expect to see other signs that the roo is
not thriving.
Some carers
stressed the importance of trying to raise a roo by mimicking development as
closely as they could the roos in the wild. Knowing when to start popping a
joey from their pouch and for how long are as important as providing wild foods
for the pouched joey.
Most carers said
it was all about knowing the kangaroos. Knowing how far you can push them,
knowing their likes and dislikes, feeding and toilet habits. Knowing their
emotional needs. Every roo is an individual and needs be treated as such. In
many cases of coccidiosis there is reason to hope and work towards recovery.
Many thanks to
the shelters who participated in the survey:
Ivy Hawkins
Mara Chambers
Brenda Cheers
Clare Davis
Manfred and
Donna Zabimskas
Carol Bainbridge
Gayle Chappell
Pam Turner
Jane and Doug
Ward
Chris Litchfield
and Mrcus Ward
Many thanks to
Dr Anne Fowler for answering my many questions.
References:
Bayer company (2003) Mode
of action. Influence of Toltrazuril on the development of coccidia. http://www.baycox.com
Carmichael I. (1998) Coccidiosis. http://www.marsupialsociety.org.au./coccidiosis
Latham E. (1997) Coccidia from a layman’s point of view. http://www.ozark.wild.net.au/coccidia
WILDLIFE
MATTERS December 2003 19
Spring cleaning is somehow
infectious once it takes hold, simply keeping going and coping with the
accumulated clutter from our wet winter is no longer enough, the fresh emerald
green and sticky buds inspire a dormant set of feelings that thrust me forward
into clearing up, moving stuff from one pile to another, having a bonfire of
what is left and then seeing that there are numerous jobs still to do. Our
eyasses grow at a fantastic rate and then quite suddenly growth is almost over,
a period of patient calm arises whilst new feathers emerge from white down,
excitement in daily inspection of what colour each will turn out to be? For Emma
the most hectic part is completed, feeding changes to three times a day, then
two as full crops are slower to digest, she can sunbathe on the front shelf,
drying herself from a longed for bath after the weeks of incubation and
brooding.
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