Peregrine virus 2

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