Encephalitozoon Cuniculi, Rabbits, Cure

About a dozen years ago, in November of 1999, a very wonderful little bunny named “Snickers” got a very horrible disease called “Wry Neck” or sometimes “Head Tilt”. It is caused by a protozoan named E. Cuniculi. This is an obligatory intracellular parasite of mammals.

The protozoan can be asymptomatic in some animals, have no infective ability in others, or, in some rabbits in particular, be lethal. It can infect the brain of rabbits causing them to lose orientation to up and down, lose control of their limbs, have nystagmus, that involuntary twitching of the eye back and forth at you see in folks who are sea sick, and eventually even death. In those that survive the attack, spores are shed in the urine from infected kidneys and it is those spores that infect other bunnies.

Most likely, Snickers had picked up the spores at the County Fair where she was “on display” with hundreds of other bunnies. We bought her there, and just about the incubation period later, she developed nystagmus, stopped eating, had head tilt, and generally was One Sick Bunny. As I’d bought her for my (then) 12 year old daughter, needless to say, this was a bit traumatic. I made an appointment with the Vet then “hit the computer” and about 2 hours later we were seen by the vet, me with about 1/4 inch stack of printouts in hand and a newly forming understanding of this class of disease.

It is often lethal to Rabbits. So as soon as Snickers started showing symptoms, we ran off to the Vet. We were lucky enough to get a Great Vet named Dr. Sato. She was the only Vet at their office who treated rabbits, and was not strongly familiar (but was somewhat familiar) with E. Cuniculi. That I walked in with a sheaf of web pages printed out (and not just folklore pages, but including scientific papers…) probably did not hurt.

I’d already identified the disease, and the likely cure of Albendazole. But Dr. Sato did a very complete exam. Came to her own conclusion. Checked her own sources, then prescribed the meds she thought were appropriate. Baytril as a general antibiotic (in case it was a bacterial infection of the ear – pasturella), an injection of Albendazole and then Valbazen oral suspension for 10 days (an oral version of Albendazol) to assure long enough treatment to kill off the bugs.

Snickers had also picked up some fur mites, so was given Ivermectin to treat them as well. An injection under the skin, and then a repeat 2 weeks later. Ivermectin kills all sorts of mites and some other odd things too. It can kill Dutch Pattern bunnies. The Dutch rabbit has a panda like look to them. Black eye patches and a white shoulder band.

Dutch pattern Rabbit

Dutch pattern Rabbit

Original Image

Ivermectin works in a rather odd way. Mammals use Acetylcholine as a neurotransmitter in most of the body. We also use something called GABA but mostly in the brain. (Though it does a lot of other interesting things in mammals and is well worth the time spent learning about it). In arthropods, like mites, it is a Very Important Thing, and if you muck it up, they die. So, put something that screws up GABA function into a mammal and the bugs die, but IFF it gets into the brain, you die too… Lucky for us (and most Rabbits) Ivermectin is stopped by the blood brain barrier. Something that the bugs don’t have, and that stops Ivermectin transport. EXCEPT in a few “sensitive” animals like some dogs, and Dutch breed Rabbits…. SO Ivermectin is typically used with caution, or not at all, in those populations.

But Snickers was not a Dutch, she was a Netherlands Dwarf, so “no problem”.

Time Passes

Snickers recovered fully, and lived a normal bunny life, loved and loving. Eventually she died at a normal “old age” time. THE key bit here? She had been cured of E. Cuniculi.

Now I’ve been through dozens (maybe hundreds?) of hours of research on this. There are countless cases and testimonials of treatment of E. Cuniculi with a LOT of different things, including Albendazole, that “help for a while” then the treatment stops being effective and the animal dies. It is widely talked about as a “sometimes cure” but often just a “delay of the inevitable”. I’d just figured we “got lucky”.

Now, a dozen years later, another bunny got E. Cuniculi. Partly I credited the recovery to very early treatment. In later stages, damage has been done, cells are dead, spores are formed on the brain and throughout the body, and often the drugs that kill spores are not the same as the drugs that kill adult protozoans. So I was “quick to act” as with Snickers and wasted no time getting treatment or getting to the vet.

It was 6 pm last Friday, so the regular vet was closed, but I went to the Emergency Animal Clinic that all the Vets pointed to as the “Don’t bother me after 9 to 5, I’ve got dinner plans” place to go.

To say it was a disappointment is not even close. $163 later, we’ve had an inspection, a prescription for Baytril, a subcutaneous saline (that is nice to have as bunnies will die fast from dehydration) and some Meclozine for the potential nausea from the nystagmus. BUT no Albendazole, as they don’t carry it.

Now Albendazol is NOT some odd bizarre drug. It is readily available as sheep wormer at about $40 / pint. The family of Benzimidazole drugs is, IMHO, the most common type of “wormer” used in cattle, sheep, goats, pigs, horses, you name it.

So WHY does THE “emergency clinic” to which the local Vets DUMP their responsibility not have one of the more common wormers, antihelminthics, and the drug that kicks protozoans butts? Is $40 for a few thousand doses too much to spend?

As near as I can tell, they exist to charge twice as much and deal with cats and dogs… so the regular vet can pretend they are not in the medical field and have dinner out without a beeper.

I’d Be Pissed, But…

I’d started the bunny on Valbazen oral suspension at 6:20 pm as soon as I’d done an inspection and diagnosis. I had a small quantity left from 12 years before. Stored carefully all these years in ideal conditions. And not wanting any more neurological damage, started treatment immediately, then went to the Vet for a “confirm and more meds”. Instead I got “Well, donno, we don’t do rabbits and don’t have the meds… here’s your Baytril and go see your Vet tomorrow”…. But maybe the saline was worth the $163…

OK, I figured a Saturday run to Dr. Sato would be OK, and I could keep the “old Valbazen” going for a few days more. It was Friday 10 pm by the time I was done at the Emergency Clinic (having “only” sat for 3+ hours to be “seen and treated”… and told to go see some other vet that actually can treat a rabbit…)

I declined the Baytril (more on why in a later posting. For “non-special knowledge” circumstances, I’d go with it, but this case was “special” in a way I’ll talk about in a few days). And figured Dr. Sato would prescribe ‘next day’.

Next day was several hours of calling and getting a message of “Go away kid, you bother me” as the voicemail said “Open for Saturday appointments only between 9am and 1pm” and nobody ever picks up the phone….

I probably ought to have just driven over and barged in, but had enough Valbazen to make it through the weekend, so why not? Besides, the bunny was responding to treatment and nystagmus was near zero, energy was up, and he was eating and drinking.

Monday Comes

I call Cambrian Vet Hospital and find out “Dr. Sato is off until tomorrow”. After a half dozen “on hold” moments and being dropped and calling back once, I am told they don’t actually HAVE albendazole in stock any more and Dr. FOOBAR who owns the hospital thinks I ought to find “a vet who treats rabbits”. I point out that “I thought I had one”, and hang up.

OK. I’m on my own. Bunny is getting better, but the last dose of Old Valbazen was given. This is day 4. 10 Days is normal. If I stop now, it’s likely just going to come roaring back, but less sensitive to Albendazole…. So (having been told that Cambrian Animal Hospital can’t actually give me a referral to a vet that does treat bunnies, so I ought to just “call arround”…) I start “dialing for dollars”. I eventually find a vet that DOES treat bunnies, and says they have an E. Cuniculi treatment on stock, and I can have an appointment … Thursday… SO I take it. It’s nearly a week after first symptoms, and the bunny would have most likely been dead by then but for my treatment with Valbazen, and I’m out, so there will be a 3 day gap in dosing, but probably “livable” (literally…).

The Quest Begins

But being not so inclined to roll dice with life, I go looking for other sources of Valbazen. NOBODY in 40 miles of me carries it anymore. Some mention “fenbendazole” wormers. I do more research and find out it, too, has been used with E. Cuniculi.

To shorten a long story, I run off to a “ranch supply store” and buy “Cattle Parasiticide” that is Ivermectin in Giant Size dose ( treats 10 x 550 lb doses) and “Horse Wormer” that is fenbendazole 10% paste suited to treating 1000 lbs of horse.

And figure out that 3.4 “drops” of the Ivermectin “drench” on the skin is enough for my 1.7 lb bunny (guess that $163 also bought a precise weight…) and, knowing the Dutch issue, do one drop per day for 4 days to assess any bad reaction without having a “lethal full dose” in one go as the vet does it… The bunny has tolerated it Just Fine, so as he is all of about 1/2 Dutch, I guess Dad gave him a good non-Dutch blood brain barrier….

I also figured out that 0.17 CC of “paste” was the right fenbendazole dose, and using the 10 CC syringe (that was for making a slurry of the meclozine and administering it… no needle, just a fancy squirt gun into the mouth) made a 0.17 ish sized squirt of the paste and rubbed it on the bunnies teeth / lips where he licked it off.

A Few Days Later

It is now Wednesday. 6 days after first symptoms. The Bunny is symptom free, as far as I can tell. He has a tiny bit of residual head tilt, but even cured bunnies sometimes hold the head a bit tilted. He is full of energy. Eating well. Impatient at being in the cage (he has been ‘free range’ his whole life, and while he did not mind the hutch when dizzy, is looking longingly at the garden now…) On the other hand, he has decided I’m “an OK guy” and even gives “mutual grooming” behaviour as I comb him out. He is rid of fleas and lice ( I’ve been trying to give him that gift for a couple of years, but this is the first time I could pick him up). He is, as near as I can tell, cured.

So I canceled the Vet appointment for tomorrow.

At this point, we will do fenbendazole (“Safe-guard” horse worming paste) for 4 more days, and I’ve given the last drop of Ivermectin.

The Punch Line

Doing some web searching showed some efficacy for Ivermectin against E. Cuniculi. It showed reasonable, but not lasting, effectiveness from the Benzimidazole class of drugs (Albendazole, Fenbendazole, and Oxybendazole – where an oxygen is swapped for a sulphur on the non-active tail of the molecule) but with guarded prognosis and frequent relapse.

So WHY have I had such quick and complete success?

I think it is due to using BOTH Ivermectin and Albendazole / Fenbendazole together. While in the first case (Snickers) it was accidental, in the second case it was a deliberate act. There will be a bit more on why I think the Ivermectin treatment is an important part in “Part Two” of the E. Cuniculi story; but for now, the working thesis is that “each whacks MOST of the bugs but both together are curative”.

Some Links

A nice article that pulls some bits together:


Last fall, while searching online for information on E. cuniculi, a friend discovered Barbi Brown’s article about her experiences treating (and perhaps preventing the spread of) E. cuniculi using Ivermectin. Ms. Brown is a breeder who keeps excellent health records and who believes in regularly treating her rabbits with Ivermectin at three month intervals. She noticed that the rabbits she saw with symptoms of E. cuniculi had either never been treated with Ivermectin or had not been treated for at least six months.

Ms. Brown’s philosophy of regularly treating her rabbits with Ivermectin is similar to the widely-accepted practice of de-worming horses. Twenty years ago, the preferred horse wormer was fenbendazole; today it is Ivermectin. Given the biological parallels between rabbits and horses, it seems worth pursing the possibility that Ivermectin might help stop the spread of E. cuniculi.

Ms. Brown’s article states that Ivermectin “paralyzes the parasite and stops the migration to the brain.” Her protocol calls for a second treatment seven days after the initial treatment, with follow-up treatments every three months, presumably for the remainder of the rabbit’s life.

Despite the current lack of scientific evidence that Ivermectin is effective in treating – and perhaps preventing – attacks of E. cuniculi, this may be an option worth discussing with your rabbit’s veterinarian. Ivermectin has an excellent safety profile, having been used to treat fur mites in many rabbits for many years with very few side effects. The major concern Dr. Allan had with Ms. Brown’s protocol is that her dosage is almost four times greater than the upper limit of the (widely accepted) dose range for rabbits. Dr. Allan has agreed to try this treatment with the rabbits who have joined my family at a young age, but at half the dose used by Ms. Brown.

This was the link that gave me the “Ah Hah!” moment that Albendazole / Fenbendazole WITH Ivermectin might just be the “magic bullet” and would explain my 100% success with a 2 week regimen that has resulted in “cure” instead of “endless treatment and eventual resistance” that others have experienced.

I know I’m being a bit premature, as only Snickers has had the life to show “cure”, but the other bunny has had an astounding return to health (days) and at this point, it’s pretty clear he is “just fine”. There is also “part 2” to give more evidence “soon”.

The same site notes some activity of Baytril against E. Cuniculi, so I’ve got a tiny bit of remorse about declining that baytril for bacteria prescription… part of why I say “get the baytril to assure it’s not Pasteurella” then add the fenbendazole and ivermectin…) but I think it’s not the major part of the “cocktail” that’s doing the heavy lifting.

It goes on to note:

In 2001, a study published in the Veterinary Record (April 14, 2001, pp.478-480) suggested that fenbendazole, a drug used to treat roundworms, might be effective in both preventing and curing E. cuniculi infections. This was a major breakthrough, both because there was scientific data to support the findings and because this was the first treatment that was believed to cure (rather than simply control) the condition. In rare cases, long term treatment with fenbendazole may be associated with the onset of bone marrow failure.

Some veterinarians who had been skeptical of albendazole and oxibendazole because of the lack of scientific data began treating symptomatic cases of E. cuniculi with fenbendazole and others switched to prescribing fenbendazole. I have recently heard from several individuals that their veterinarians were going back to oxibendazole because they considered it to be more effective than fenbendazole once symptoms emerge. Again, however, this conclusion is based on each practitioner’s individual experience rather than on a pooled scientific data.

That was the data that sent me off to the “horse wormer” and let me give up on finding Valbazen in the local “animal feed and cattle stuff” shops. As near as I can tell, at least locally, Fenbendazole has replaced Albendazole thus making it hard to find the Valbazen on the shelf. OK, knowing that, I can “work with that”…

(That same link has a discussion of Albendazole and Oxybendazole as well.)


A little appreciated symptom of E. Cuniculi in Rabbits can be hind quarters paralysis:



Along the way, I had to convert a Ivermectin dose from a 250 ml “drench” or “pour on” for Cattle to a dose the right size for a dwarf bunny. The package lists the dose as “1 ml per 22 lbs of body weight”. Or 1 ml / 10 kg. But if your bunny is less than a kg? … So I needed to take a 1 cc “dose” and meter it even smaller. This site:

Gave me the conversion of 0.05 ml / “drop”. I confirmed that 1 tsp was 100 drops (a tsp is 5 ml, so 100 x 0.05 ml = 5 ml and that was what I found testing my ‘dropper’ against a US tsp. (I also found that it is 4.9289 ml / US tsp, but 5 ml / “metric teaspoon” that seemed rather oxymoronic ;-) and that the English Teaspoon is 1/4 of a tablespoon while the US teaspoon is 1/3 of a tablespoon, so an English Teaspoon is a bit smaller. ( 3/4 of 5 ml or 3.75 ml) so be very careful to use metric measures or be aware of just which teaspoon you are using…)

At any rate, using a ‘dropper’ measured against a tsp standard of 5 ml, I was able to calibrate to 3.4 “drops” / 1.77 lb bunny. Do the math twice. Then do it again twice more. You don’t want to be off by a decimal point and shut down their brain…

Notes on Fenbendizole

The package of “Safe-guard” says:


Safe-Guard (fenbendazole) Paste 10% is administered orally at a rate of 2.3 mg/lb ( 5mg / kg) for the control of large strongyles, small strongyles, and pinworms.

A related “horse wormer” is “Panacure” at 18.75% and ought to work as well, but with slightly harder ‘dilution’ to get the right dose.

In a couple of places I saw the dose of “20 mg / kg / day” quoted for use against E. Cuniculi. That is the dose I used. We are not just trying to get a worm to “let go” in the gut and be pooped out, but to kill a bug well inside cells.

While this is higher by a factor of 4 than the “wormer” dose, it looks like it is well tolerated by the patient. Fenbendazole is not as rapidly or efficiently absorbed as Albendazole, so that may be a factor in the toleration of the high dose. It is also the case that I’m only doing a 2 week treatment, not “ongoing” or “months” as others have done.


A landmark study published in the Veterinary Record in April 2001(see reference)offered perhaps the first evidence that treatment of E cuniculi with fenbendazole (Panacur) in rabbits really does work – and has led to a more pro-active approach in treating this problem in rabbits. This study considered the use of fenbendazole (at a dose of 20 mg/kg body weight daily for 28days) for preventing an experimental infection of E. cuniculi in rabbits. Fenbendazole given prior to exposure to the parasite successfully prevented infection, and this may be a way of controlling infection in colonies/groups of rabbits where some animals have the disease and others aren’t yet infected.

The second part of the same paper looked at rabbits with naturally acquired E. cuniculi infection. Following treatment with fenbendazole, E. cuniculi parasites were no longer present (detectable). The authors of the paper went on to suggest that in order to improve the treatment of E. cuniculi in rabbits, the combination of fenbendazole and glucocorticoids (steroids) could be valuable and should be examined in a controlled study.

There’s a catch, though. Although the parasite may be killed by drugs such as fenbendazole, the bunny may not actually get any better. This is because the brain inflammation associated with the parasite may have already caused irreversible damage. This is why steroid treatment has been suggested, in an effort to damp down this inflammatory response. Opponents point out that “damping down” the immune system with steroids could allow the underlying parasitic infection to get worse. Hence, it is probably safest to use steroids only in conjunction with fenbendazole and not as sole therapy, until more evidence is available.

Thus my desire to “jump on it quick”. IF at the very first moment of nystigmus you “jump on it” with immediate administration of a parasiticide ( or 2..) it looks like all the problems are avoided. If you wait a week for a vet to have a “slot” to see you, IMHO, it’s just too late. Again, IMHO, the local vets and the way they run their practice is nearly criminal and amounts to animal cruelty. That I was able to “work around them” does not excuse it for the other 100 folks who are not so “gifted” with technical skills and dogged persistence.


The antiparasitic actions of Safe-Guard (fenbendazole) Paste 10% is believed to be due to the inhibition of energy metabolism of the parasite

In fact, the -bendazoles seem to work by blocking glucose metabolism in the little buggers. SO, a spore is not metabolizing much, and Ivermectin can’t do a lot about it, but the -bendazoles screw up the GABA function and make it not develop correctly, while the Ivermectin causes the active ones to “run out of gas” and be easy prey for the immune system. That, in a nutshell, is my thesis. It may be that a “2 weeks on” and retreat in two weeks; would work best. I’m not seeing the need right now, though.

At any rate, screwing up the GABA internal controls of development and function while shutting of the gas supply looks to me like a darned good “double tap” and the “facts on the ground” seem to indicate it does work well.

In Conclusion

OK, that’s where we are “today”. I’ve got 4 more days of treatment. If I’ve figured this all out correctly, that 10 days of fenbendazole (actually, 4 of Albendazole, 6 of Fenbendazole) is a short fast “wallop” that does not lead to the bone marrow failure of long term treatment, and the adjunct of Ivermecten makes the pair work as a “2 week cure” instead of months long ordeal. So far it has one confirmed success, and a second “sure looks like it at this point”.

I would also note that “Very Early and Immediate” treatment might well be a critical factor to success. I’ll now be “stocking” Ivermectin and “Safe-Guard” just so I never have to deal with “Professional veterinarians” again in this time critical circumstance….

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About E.M.Smith

A technical managerial sort interested in things from Stonehenge to computer science. My present "hot buttons' are the mythology of Climate Change and ancient metrology; but things change...
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28 Responses to Encephalitozoon Cuniculi, Rabbits, Cure

  1. Level_Head says:

    Seems your research and anecdote pickers
    Are well-tuned, though vets twist up their knickers
    If they say you can’t dare
    Dose your friends with the pair
    You can offer them data — and Snickers.

    ===|==============/ Level Head

  2. P.G. Sharrow says:

    Wellcome to the world of the stockman. You contact a vet to learn and then you create a treatment to suit your needs. Livestock raisers can not afford the time and money that use of animal health professionals requires. Good luck on your”practice”. pg

  3. PhilJourdan says:

    The Bunny curer! I am impressed with both your dedication and knowledge!

  4. Tony Hansen says:

    You cover how you think Snickers got the bug, but not how the other bunny acquired same.
    Is the AFAICT un-named bunny called Jimmy?
    (After James Riddle (Jimmy) Hopper who disappeared from the Red Fox?)
    Bunnies should be careful where they eat!!

  5. Pascvaks says:

    Seems there’s a connection between the bunny disorder and MadCow, did your search to help your own pet suggest anything like that? Just curious. “Y”/”N” only appreciated, know this isn’t a good time for you and the family.

  6. R. de Haan says:

    It’s a great story.
    Knowledge combined with practical experience has made you independent.
    That’s the best thing that can happen to any human being.

    So I congratulate you with this really great achievement and thank you for the opportunity for others to learn from that experience.

  7. Level_Head says:


    I’m intrigued by the idea of a connection between prions (aberrantly shaped proteins that trigger other copies to adopt their shape) and the living disease organism involved here, especially considering the so-far incurable nature of prion-based diseases (cf. the experience our host has presented).

    The proteins are a tiny part of cells — in the case of the prions, they are part of nerve cells in brain tissue. The disease here is apparently caused by a “single-celled animal” (a protozoan) that acts as a parasite of the kidneys, then later in the brain. The protozoan is billions of times larger than a prion.

    More details of the E. cuniculi rabbit disease — though not current with treatment, of course, can be seen here.

    Rabbits are not prone to prion diseases, it seems. They happen spontaneously on rare occasion, just as prion diseases happen spontaneously in about one human per million per year, or about 300 people per year in the US. Some other mammals, once this change happens, can pass the changed protein to others of their kind. This is not true of cattle, generally (unless the cattle is actually fed infected nerve tissue), but it is true of deer, and has been responsible for the deaths of huge numbers of deer in the US and Canada.

    Here’s a paper on rabbit prions, and why they might be so hard to transfer.

    A connection seems surprising to me. Where did you see the it suggested?

    ===|==============/ Level Head

  8. E.M.Smith says:



    Interesting citations in that second comment as well.



    The E. Cuniculi is an obligate intracellular paracite.

    “Mad Cow” is a prion disease. It is caused by an “infective protein”. A truely bizzare illness. It isn’t “alive” at all. It is more that the normal protein is somewhat unstable, and in the presence of a “mis folded” one, will refold into the misfolded form. That form is non-functional and forms ‘plaques’ in the brain (that then cause holes and spongiform encephalopathy). There is no way to “kill it” as it isn’t “alive”. However, the protein, if put into the blood of a healthy animal, will cause it to become ill and develop disease too.

    The only thing they have in common is that both can cause damage to the brain, but for E. Cuniculi that looks to be limited to rabbits (and perhaps related exotics). In most species it is a relatively benign parasite or unable to infect the species at all.

    Most of the time E. Cuniculi is not symptomatic and in many species it does not cause any apparent disease at all. It looks like the infection of the brain in Rabbits is a “mistake” by the parasite. In most species, it wanders around the body a bit, looking for the kidneys, where it makes spores that are passed in the urine. Then when some OTHER animal grazes on that place where they peed, a new host is found and the cycle repeats. Works great in other animals (who often show no signs of any illness at all) but for bunnies, the bugs get “lost” and tend to attack the sense of balance (it’s a bit unclear if it is the inner ear or a specific part of the brain) and only sometimes the spinal cord at the point where it controls the hind quarters.

    Even in rabbits, many ‘herds’ have titres showing up to 50% are or have been “infected”. Yet most were never “sick”. One of the problems with the disease is that the test for it only shows if there has ever been an exposure. Does the bunny have antibodies? It does not tell you if they beat the suckers, or not. Add that if the disease runs long enough, the damaged parts stay damaged… now how do you know when you are done with ‘treatment’? You might have killed off the protozoans a month ago, but still have a bunny with head tilt or wobbly gate. THAT is the reason I’m so adamant about the need to “treat it now” and not wait a week to beg audience with the high and holy… when it may well be too late. “We cured the disease, but the patient died”… or just stays broken for life….

    One side bar: E. cuniculi is an ’emergent disease’ of humans in that it is showing up as an opportunistic infection in folks who are immuno compromised. So folks with transplants (taking immunosupressent drugs) and folks with AIDS, among others, need to be aware of that as a potential cause of some ‘strange’ symptoms. In general, humans look to be in the group that is either able to completely kill of the buggers or at least have no symptoms to speak of. Unless your immune system gets shut down.

    As the protozoan lives INSIDE the individual host cells, it is very hard to do a test for them direcly. You would need a tissue sample and lab time. AND you would need to know which patch of tissue was infected. (It may not be broadly disseminated…) So the blood test for antibodies is used.

    The wiki has a fair amount more:


    Encephalitozoon cuniculi is a eukaryotic organism belonging to the phylum Microsporidia, in the kingdom Fungi. An obligate intracellular parasite, E. cuniculi occurs in laboratory mice and rabbits, monkeys, dogs, rats, birds, guinea pigs, and other mammals including humans. At various early times it was thought it was the cause of rabies and polio. This parasite may be transmitted in body exudates or transplacentally. Although damages are minimal, an infection can be fatal, especially in immunocompromised individuals such as AIDS patients.

    A secondary reason for wanting “rapid treatment” is to assure that the orginal host does not reach the spore shedding phase and start to infect the rest of the herd.

    Approximately one month after the rabbit is infected it begins to shed E. cuniculi spores via its urine. Spores continue to be shed for approximately 3 months, but can be shed throughout the rabbit’s life.

    So if it takes about 2 weeks to become symptomatic, then a couple of weeks to get in to see the vet…. cutting that “one month” awful close. I’d rather kill them off while they are sill in the early non-spore shedding phase.

    @Tony Hansen:

    I have no idea what that reference is… It sounds like an interesting story that I’ve never heard…

    As to where the E. Cuniculi came from, that is a good question, but not very relevant right now.


    “It’s what I do”… more “stories” below…

    @P.G. Sharrow:

    I grew up in “Farm Country” and Dad had a ‘toy farm’ on 5 acres outside of town (all of about 2 miles away… it was a very small town ;-) where he had a few head of cattle. He even bought a 1 ton pickup truck with a cattle cage on the back for use on his “farm”…

    And we had rabbits too.

    Every farm kid in town knew you had to “stick your cow” if they got bloat (THEN call the vet to sew them back up…) Anyone with cattle had a belt knife nearby for that purpose.

    (For the non-farmers: Cows can get a kind of sour fermentation that makes a lot of gas, and causes strangulation of one of the stomachs. If you don’t get that gas out, the animal will die. Sometimes in less than an hour. The Vet is usually further than an hour away… So you learn where to “stick the knife”. The “country Vet” in my fram town always had a “hunting knife” on his belt for just that purpose. I remember seeing him teaching one person how to locate the right spot and orient the blade and telling what size knife to get.)

    On one occasion, when I was about 8 years old, two rabbits had been fighting (boy bunnies do that) and one had cut a hole in the hide of the other (middle of the back). Dad took me through the process of how to suture with sewing needle and white thread. Alcohol to sterilize (or flame sterilize the needle if nothing else).

    Bottom line is that I’ve been doing “Stockman” work as long as I can remember. Just not a lot of it. And frankly, I’d rather let the Vet do it. But if they are not up to the task, well, I am.

    At one time we had a very nice stainless steel injection set with a variety of ‘multiple use’ needles. Also a “pill gun” (It’s called a “horse sized pill” for a reason. Some of those things are the size of an apricot and you have to stick them way down past the teeth to get them swallowed… unhappy teeth… so there is this couple of foot long giszmo that holds the pill and is not worried by teeth ;-) along with a banding gun and some other paraphanalia. I suspect my Mom gave it away after my Dad died. Not that I need the stuff to deal with being a Large Animal Vet, but it would be a “connection” to that part of the family history.

    Besides, I don’t think they make quite that quality of gear any more. It was Very Sturdy and fairly expesive.

    At any rate, I grew up with the idea that you “took care of your own” and only called the Vet if you needed them, then watched closely what they did…

    There were two Vets in town. One was the “Large Animal” Vet, the other the “small animal” Vet.. The Small Animals were mostly dogs and cats, but included the folks with rabbits, prized birds (breeding stock), and the odd raccoon, skunk, or lizzard / turtle. Large Animals were mostly horses, cows, sheep, and the occasional goat. (But if you had managed to get a pet Elk, I’m sure they would treat it too…) When it came time to take a 2 week vacation, each Vet covered the other guy’s practice. In an emergency, ANY animal could be treated by each Vet.

    That is why this notion of “we don’t treat rabbits” is so alien to me. Are you a damn Vet or not? Did you sleep through that part of your training? Can’t remember past last year?

    Yes, I know that each species has peculiarities (some antibiotics kill iguanas, for example), that’s why you double check your work and keep that ‘exotic animals’ text book…

    At any rate, it is a point of both dissapointment with the local vets (they don’t deserve a capital letter…) and a bit of personal pride to realize that I am better at this than they are. (I’m sure their surgical skill is far greater than mine. I’ve done minor surgery and I’m just not able to shut off the empathy pain feeling enough, so I’m too tentative with the knife… It took me 3 tries to get the incision large enough to remove the infection and clean the wound. That bunnie went on to live a full life, too. I suppose having some anesthetic would have helped… but oddly, the bunnie seemed to realize I was “fixing the bad spot” and while he would ‘flinch’ just a little, did not fight me or try to escape.)

    For what it’s worth, I think I’ve become a “fair Stockman” and at least on the protozoal diseases better than the local vets.

    FWIW, there are a half dozen similar diseases. Slightly different species, somewhat variable symptoms. Some of them are among the most hideous “tropical diseases” you could get. Leishmaniasis is one of them.


    Giardia is a less onerous one:


    And even malaria is in the same general class:


    Then there are the ones you never heard of unless you know someone who got sick, like Babesiosis and Isosporiasis


    And ones you may have heard of, but not known their nature like Toxoplasmosis and Cryptospordium



    And many more…

    So will this treatment also work for any of THEM?

    It has potential, but only clinical trials will tell.

    I do know that if I was stuck out in the middle of nowhere in some foreign land and got some strange apparently protozoan disease, I’d be quite willing to hit the local animal supply store and measure out a dose of Ivermectin and Fenbendazole as I found out how many weeks it would take to get to the nearest doctor….

    Similarly, if I were an impoverished 3rd worlder who will never be able to pay a doctor, or see one, and came down with such a disease, I’d be more than willing to try a bit of “sheep dip and wormer”… And if I was a 3rd world Doctor, with no budget for medicines and a patient cohort who had zero money either, that $14 carton of “Ivermectin pour on” that will treat 5500 lbs of “patient” is looking like a pretty cheap way to do SOMETHING of benefit (even if it only gets rid of their mites, flies, and lice… that is, even if it fails on the protozoan, it can be helpful).

    All up, I think it was about $25 for the “package” of both drugs. I’ve not calculated the total doses of fenbendazole in the tube on a “human equivalent”, but it’s “one thousand pounds of horse” worth, so probably about the same of humans. So somewhere around $2 / head to treat. Bought in California at western prices. (It WILL be cheaper in other countries). And I bought the smallest package available (so the least cost efficient). Given what I remember of the pricing on the ‘gallon sized’ lots, I’d guess you could get cost down to about 25 cents per person / dose. Certainly worth a try, IMHO, if the alternative is death and disfigurement from some hideous disease where the approved treatment is simply not available in some 3rd world bush country.

    But that’s wandering a bit…

  9. Pascvaks says:


    The connection was personal, the MadCow problem came up after I’d returned from the UK and the RedCross had a problem taking my blood anymore;-)

    Since then I’ve kept half of a deaf ear cocked to “Creutzfeldt-Jakob Disease (Variant) and Bovine Spongiform Encephalopathy (Prion Diseases)”

    So far so good for me, guess I got lucky.

  10. Level_Head says:


    I’m glad you were unaffected, but the restrictions are silly. Since the quarantine and reduction of consumption of infected nerve tissue, the low rate of infection has dropped to a level below that of random spontaneous chance. As epidemics go, this was a fizzle.

    I would avoid eating scrambled eggs and cow brains in England (well, I do anywhere), but I would not be concerned about a steak there.

    And we must be aware that no matter what we do, the occasional human, and cow, will spontaneously develop the disease even with no contact to any other infected being.

    It is not an “organism” at all; it is a random bit of damage (perhaps even cosmic ray) to a certain type of protein molecule that then catalyzes the same damage to others of the same type.

    The proteins become unrecognizable as originals, so the cell makes more. And the “destroy excess protein” mechanisms no longer work either, since they don’t recognize the mis-bent molecule. So the cells make more and more until they destroy themselves; the neurons physically burst.

    The deer/elk version is a particular problem, since it is all but unkillable and is passed even by nose-to-nose or grazing contact. This “cervid chronic wasting disease” is pretty serious, though it is not apparently transmissible to humans.

    The cattle version, happily, has not been known to be passed even between cows, except for the humans’ odd habit of using cow nerve tissue in cattle feed. Cows are not normally cannibalistic.

    ===|==============/ Level Head

  11. Pascvaks says:

    Chiefio –
    After I went to and read the article at the first link Level-Head mentioned above, I sent them an e-mail giving the link here and suggested they might want to take a peek. Their article seemed a little dated at –

  12. Tony Hansen says:


  13. Tim Clark says:

    Ivomec works on pinworms humans get from eating oysters. Stick your finger into the bottle and dab some on the inside of your wrist. Cures within three days. Horse treatment for “thrush” works great on athletes foot and ringworm. Most people can’t do the math for dosage conversions, or understand the phylogenetic tree to know what to use. A little common sense can go a long way.

  14. E.M.Smith says:

    @Tony Hansen:

    Ah! Got it… Didn’t know the “Riddle” part, only indexed as “Jimmy Hoffa”, and had taken Red Fox to be the probably name of some (fictional?) character who was a real animal fox named “Red”… rather than connecting to the restaurant name ” Machus Red Fox Restaurant”. For whatever reason, I tend to index things on the first letter, and this was in “M”s instead of “R”s… One of the few downsides of the ways my brain functions. It is sensitive to search kiey rather a bit more than I’d like….

    OK, now I get it…


    IMHO, the whole area of protozoan parasitology “needs work”… even in humans.

    The House Rabbit Society folks have a better handle on things than most, and they are a key resource. My first Vet visit with Snickers included a multipage print-out from their site. As I’ve only just had the “Ah Hah” moment that it’s using both drugs at once which game my better results, I can’t fault them for not sharing that moment with me in real time.

    Even Dr. Sato who prescribed both was prescribing Albendazole for the E. Cuniculi and Ivermectin for fur mites; not thinking they were synergistic for E. Cuniculi. It was only after recreated that “2 fer” treatment (and for the same two reasons) and getting the same “near instant” improvement that I started to ponder “Why?”.

    So now other folks can look, try it, and see if I’ve just been incredibly lucky with my two bunnies; or, if there is something to this speculative assertion: the “Two Fer” treatment can start being diseminated.

    With luck, your letter to them can help get that particular round of “trials and reports” going.

    Per CJD, mad cow, and prions:

    There was an interesting article I’d read back when the whole Mad Cow thing was in the news (and I attended a lecture on it at Roche in Palo Alto… they things I do for “fun” ;-) which looked at inter-species transmission. The results were fascinating.

    Often it is highly limited in transmission between one species and another. That depends on the degree of similarity of the two species versions of that particular protein. HOWEVER, once you get a transmission, that infected new species makes a varient that is now more infective inside their tribe. (That is, if you get “cow to mink” it’s a bit hard, but once you have it in the mink, getting mink to mink is now easy.) In some cases, they had a “over and back” transmission through a couple of species that resulted in an even more damaging version in the first species. This is due to subtile variations in the mis-folding of the protein.

    It was just such a change that makes the “spontaneous” form of CJD different from the “Varient CJD” of mad cow. (Clinical signs are largely the same, but some minor differences).

    For some folks, they have a particular genetic variation in the base protein that makes it a bit more senstive (more prone) to making the ‘mis-fold’ form. This can happen spontaneously (cosmic rays? random chance?) and you get that random case of CJD with no contact with any contaminant. THEY, then, can become a source of infection to others with the more “normal” form. Thus the Kuru form. (The canibals ate the brains of their dead relatives as an ‘honor’… so once any one of them got the spontaneous CJD, it started being persistent in the tribe. As soon as they stopped, Kuru stopped.)


    Scrapie is the form in sheep. As near as can be figured out, it is not transmissible to humans. (Folks had it in sheep herds for generations and it stayed in sheep). The “working thesis” last time I looked was that the scrapie from sheep made the leap into cows in Britain as the dead sheep were used to make ‘protein meal’ for use in cattle feed. That they could infect cows (not humans), but then the cow form could infect some small number of humans. Once in cows, then the “canibal cow” cycle could start as sick cows were sent off to be “protein meal suppliment” for more cows…


    There are now folks working on the transmisibility map to figure out what species can transmit to which other species. This matters as it determines if you just need to not feed cows and sheep to cows, or if, for example, putting their proteins into pig or chicken feed is “a bad idea” too… As there sometimes can be more than one mis-folding, with more than one transmissibility map, this can be a bit hard to figure out.

    Basically, it’s just a whole lot better to not feed meat to herbivores… and the UK ban on “canibal cows” looks to have been a great success.

    Final note:

    There are 4 major variations on CJD / BSE and they are each related to the transmission history.

    1) Spontaneous in individuals with predisposing genetics. (Some folks just make a version of the protein that “mis-folds” all on it’s own.) Seen in “familial incidence” in very small populations.

    2) Spontaneous in individuals with NO predisposing genetics. Very rare, but enough “insult” to the protein can sometimes get a ‘mis-fold’ going, then it’s all down hill.

    3) Contagious, human to human, probably from 1 or 2: Kuru (and related forms).

    4) Contagious, human to human, from animal origin. Mad Cow, for example.

    You could possibly add a “5” of “Number 4 but with different animal species to different animal species first. There are some more virulent forms that look like the mis-fold is a slighly different form and may be due to the particular species path taken causing a differnt folding pattern. There are small variations in the amino acid sequence in #1 vs the other 3. There are small variations in the actual folding pattern of the protein and / or clinical signs between #2, #3, and #4-5. Some of the folding patterns are much more “infective” than others (per the presentation I saw at Roche).

    From the “good news / bad news” department:

    Opportunities to study these variations and figure out how important they are, or exactly what they are, are dwindling. Kuru is essentially erradicated. There is not much “material” to work with. Mad Cow is vanishing and likely erradicated in many variations (such as the postulated “sheep to cow” varient in the UK – though likely still present in the US “Downer Cow” version that may be a ‘deer to cow’ or ‘elk to cow’ variation and has not been shown to cause vCJD, or maybe we just havn’t looked very well…) There is a “Scrapie erradication” effort that is working well to erradicate scrapie from sheep herds. (It had simply been ignored or thought of as a random illness before). As this is both removing sources of infective protein AND selecting for individuals with any genetic variation that makes them less prone to ‘mis-folding’, eventually it, too, will succeed.

    All of which is great for food safety, but making it ever harder to get “natural forbidden experiments” to study and harder to get “material”. (In once case a mink farm had a large outbreak traced to a particular other species used as food. Very interesting study results, but that practice is now banned, so no more “material” will arrive…) One of the more facinating bits is that whole question of which species transmits to which other and the very complicated bit that sometimes, A infects B can NOT infect C; but…. D infects B and it CAN infect C… That ‘folding history’ matters.

    All of this is from what I remember from about a decade back. It was quite new then. I’m sure more is known now, and any newer work ought to be taken ahead of my rememberance of “cutting edge ideas” from one seminar a decade ago.

    The “bottom line” for me was that I decided to eat a lot of lamb and chicken for a couple of years till the “canibal cow” feed issue was all dealt with, and as of now with the requirements for ruminant feed to be vegetarian see no reason to avoid beef at all in the USA or in the UK.

    For blood donation:

    The restrictions of the time were “a good idea” as we simply did not know how many folks in the UK had the protein mis-folding in the early stages and were headed for vCJD “real soon”. It can have a modestly long ‘ramp up’ if the initial exposure was low, and folks had not yet sorted out the ‘spontaneous’ form from the BSE form, so estimates of “incubation” were highly variable.

    At this point, IMHO, any remaining restrictions would be just silly. It’s been several years since the feed changes were put in place. For BSE, it’s about 8 years:


    so any infected cow ought to have shown up some time ago. Folks are still not sure what the “lag time” is for CJD and vCJD (and the ‘new varient CJD” or nvCJD) and some estimates range up to 50 years, so maybe being a bit paranoid about it is “OK”…


    New concerns

    In The Lancet (June 2006), a University College London team suggested that it may take more than 50 years for vCJD to develop
    , from their studies of kuru, a similar disease in Papua New Guinea. The reasoning behind the claim is that kuru was possibly transmitted through cannibalism in Papua New Guinea when family members would eat the body of a dead relative as a sign of mourning. In the 1950s, cannibalism was banned. In the late 20th century, however, kuru reached epidemic proportions in certain Papua New Guinean communities, therefore suggesting that vCJD may also have a similar incubation period of 30 to 50 years. A critique to this theory is that while mortuary cannibalism was banned in Papua New Guinea in the 1950s, that does not necessarily mean that the practice ended. 15 years later Jared Diamond was informed by Papuans that the practice continued. Kuru may have passed to the Fore through the preparing of the dead body for burial.

    These researchers noticed a genetic variation in some kuru patients that has been known to promote long incubation periods. They have also proposed that individuals who contracted CJD in the early 1990s represent a distinct genetic subpopulation, with unusually short incubation periods for BSE. This means that there may be many more vCJD patients who have longer incubation periods, which may surface many years later.

    In 1997 a number of Kentuckians developed CJD. It was discovered that all the victims had consumed squirrel brains
    , although a coincidental relationship between the disease and this dietary practice may have been involved.. See: http://www.guardian.co.uk/uk/2008/aug/03/bse.medicalresearch for recent concerns.

    So don’t go eating a lot of squirrel brains either…

    Though that would explain a lot about some folks I knew back in “the rural country” ;-)

    At any rate, we have some clue about CJD, but there’s still a goodly ways to go on it.

    One final note: Kosher practices forbid feeding dead animal parts to cows. So one simple way to avoid BSE is to simply eat Kosher Beef. Yes, for years we’ve bought Hebrew National Hotdogs for just that reason… from shortly after the scare begain and I learned what there was to know about it. “Kosher is your friend”… Expensive, but you get what you pay for. Halal also ought to be the same, but i’ve not looked into it enough to know if the practice extends to “what the animal ate” to the same extent that Kosher rules do. “At the time” I contacted a Rabi or two and got an official pronouncement that feeding reprocessed animal parts in feed would make beef non-Kosher. Grass or grain was all that was allowed. So if you are really worried, just eat Kosher.

  15. PhilJourdan says:

    I always learn something totally unexpected in reading your columns and comments! Now I know why the question “Family history of CJD” is on the questionaire!

    That being said, the one thing no one can accuse the vampires of (in this area it is VBS – Virginia Blood Service – but most have the Red Cross) is being rash. They err on the side of caution so much that a great number of people are disqualified that in all statistical likelihood should not be. So I do not see them changing the UK questions in the near future (perhaps another 10-20 years). A shame really. A friend got a false positive for HIV once (in the early days). Yet they will not take his blood even to this day.

  16. Re the connection with BSE (Mad Cow Disease), etc., – Mark Purdey’s story and research might interest you. I just looked at his site and saw that his brother had a book published that tells the story. (Mark died in 2006 at age 52.)

    I don’t have the book (yet), but IIRC from communication with him and from reading his articles online, there would have to be a combination of factors to lead to the occurrence of the disease. He was another of those never-say-die researchers who did their own digging into the literature and whatever resources were available. He wasn’t about to let the Powers That Be dictate how he handled his animals.

  17. Level_Head says:

    It’s probably worth noting that the transmission of prions within a given species is quite variable. For example, cows — other than the peculiar “cannibal cow” arrangements we’ve subjected them to — don’t seem to pass the disease to each other. But deer and elk do, and quite readily.

    Humans, too, don’t seem to pass CJD to each other, except again by cannibalism. And, well, by tissue transplants, and apparently by growth hormone injections made from people who had died of CJD.

    But the prion is hard to destroy, and surgical instruments that have operated on CJD brains will cause the disease in the next patient, even after autoclaving. Much higher temperatures and caustic chemicals are required for prions, and that practice has now been adopted.

    Because the prion is natively a nerve-tissue protein, it tends to concentrate there. But this varies somewhat by species (brain neurons exclusively versus some in other locales), and the minor details make a major difference.

    Prion diseases are currently incurable, untreatable, and 100% fatal. Imagine, for a moment, a human version as transmissible as deer prion; a sneeze would be enough to pass it along. And unlike bacteria, the prions spread by sneezing or whatever remain infectious for centuries, and require 600°F temperatures to deactivate. That’s the way it is now for deer in North America.

    ===|==============/ Level Head

  18. Pascvaks says:

    Been eating them ‘Hebrew National Hotdogs’ for years;-) I guess I became addicted to the ‘other’ kinds over my lifetime, initially, they didn’t ‘taste’ quite right – guess they didn’t add all the ‘secret’ ingredients I’d become addicted to.

    Over the years, my better half and I developed a number of lopsided unscientific guesses about prions. One of our better ones, in our humble opinion, was that prions were bits and pieces of DNA/RNA –it sort of hit us that stuff was all over the planet after 500+ million years of evolution and, like dust and ChickenMan, it was EVERYWHERE and IN everything. That it was a genetic WildCard or Joker and might have more to do with evolution than cosmic rays. You understand, if you don’t know if you got “IT”, and you don’t know what “IT” is, you tend to think about “IT” and look at each other real close to see if you can detect any “CHANGES” in behaviour that would indicate the person in bed with you wasn’t quite right in the head. We’ve both thought the other had “IT” on numerous occassions over the years. (Especially when one of us thinks the other is crazy, which seems to be happening more often the older we get;-)

  19. E.M.Smith says:


    Well, just swap “protein” for “RNA/DNA” and your “story” still holds. So far, every critter we’ve looked at has the protein. (Don’t know if they have looked at non-mamalian species). It is not fully denatured by the typical sterilization processes. “It” is in everything. (As the number of places where “protein powder” is added has become astounding… Even, as pointed out in one of the articles, cakes and candies may have gelatine in them.

    Yeah, “IT” is a big issue…

    @Level_Head & LauraTheSurvivor:

    One of the “other factors” is the exact sequence of amino acids in the individual species version of the protein. Even near trivial changes can effect the degree to which the protein is “willing” to “mis-fold”. Protein folding is a very complicated (and only modestly understood) process; but the particular pattern of electric charges from the particular amino acids plays a roll. THEN those same charges play a roll in holding the package in the final shape. So each species is different.

    From a “casual observation” it looks like the common predator species are less prone to the disease. (That would make sense, as, for example, eating a lot of sick deer would have large selective pressure to weeding out the predators prone to ‘catching it’…


    The paticular ‘Mis-folded’ version also matters. That pattern of electric charges on it pull the regular folded version into the “new” shape. As that particular mis-fold depends on:

    1) The original species version of the protein (i.e. “sheep” version)
    2) The particular mutation of the individual with the mis-fold (i.e. any variation)
    3) The folding history of the one that caused IT to mis-fold (small shape variations)
    4) The target species version of the protein
    5) The target individual particular mutations
    6) The particularly mis-fold shape of the prion that hits the target and any charge variations from any amino acid substitutions.

    You end up with each species having a different tendency to be infected by each OTHER species (including itself) and variable depending on ‘from which species you start the infective chain’. So Mink, a predator species, have been infected by other mammal meat. Perhaps as Mink like to eat fish more than mammals, so didn’t have much evolutionary pressure in that regard. People don’t seem very sensitive and do not show much tendency to get it from sheep at all. (Scrapie has been in sheep herds for thousands of years and folks have been eating lamb the whole time without much effect). But we get it quite easily from each other (Kuru) if eaten, and intermediate from cows. While a particularly infective form in Mad Cow was suspected of easier human transmission even if it then went through other species (such as a speculation that running it back through sheep would be a bad idea…)

    “Grazers” look to pick it up from eating grass with some body cell contamination on it. One thesis is that in the birth process, the placenta et.al. is consumed (so that predators are not attracted to the herd) and to the extent other herd members join in that process, or graze grasses that have been contaminated, they get exposed.

    The end result of this is that there are now a couple of variations just in cows. Depending on what species was in the feed that had given it to them, and what THAT species had been fed… Some of these variations are MUCH more infective than others…

    One (slightly speculative about a decade ago when Iast I looked) idea was that the version in Canibal Cows may have originated from sheep with scrapie being ‘recycled’ into animal feed, but that the way that changed the shape in Cows was particularly infective BOTH to humans AND to other cows, so when those cows went back into the ‘feed mill’, a feedback loop started that lead to the Mad Cow epidemic in Britain.

    In the USA, we had (and last I looked, still have!) “Downer Cows”. These are not called “Mad Cows” (for no good reason) and are shipped off to the reprocessor… Yet we did not have Mad Cow or vCJD breaking out all over. To explain this, the notion was floated that our low consumption of sheep led to low levels of Scrapie, and the “Downer Cows” were getting their BSE from some other source (deer?, cow form? Pigs?) and that particular mis-fold was less infective both to other cows (so the feedback loop was muted) and to humans (thus the low CJD disease levels).

    So I was watching this film about the extreme levels of erradication effort in Britain, and how at the same time the USA “Downer Cows” were still going off to the recycler… (this was about a decade ago… or maybe 15 years) and then this desctription of them both being BSE and just what was different again? Didn’t bring me alot of comfort to think we were being “saved” by a bit of random chance mixed with subtilties of protein folding history….

    FWIW, last I looked, “Downer Cows” and sheep with scrapie could still be recycled into protein meal for non-mamalian species. IIRC, “Fish Chow” was the prefered stuff as they had not shown transmission between wrarm and cold blooded species. Just too far different.

    Oh, and “just for fun”, think on this:

    The incubation period in cows is up to 8 years.
    Feed with that form from those cows was fed to pigs.
    Pigs are slaughtered at a year or two old and rarely kept for 8 years.
    The cow form was demonstrated to be transmissible to pigs.

    So you could easily have it in a pig population and never see the symptoms develop.

    Enjoy that ham sandwich…

    I gained a newfound appreciation of Kosher Food Law when looking into prions and realizign that it does prevent the whole problem. Even the prohibition on what parts to eat. The major nerves that have partical infectivity are in the “forbidden” parts of the cow. Only the forequarters can be Kosher:


    Only the forequarters of the cow can be kosher-certified. The precise parts of the cow where kosher meat comes from is the shoulder, the rib, the leg, under the rib and behind the leg.Rabbi Seth Mandel, Rabbinic Coordinator,The Orthodox Union said, “Only the 13th rib is disqualified. In the US, most productions take the 12th rib and the meat between it and the 13th (rib).”

    According to our interview with Rabbi Reuven Stein of the Atlanta Kashruth Commission, the portion of kosher beef that is in the hindquarter leg of the cow is not used in the United States, but is used in Israel. This is because the non-kosher sciatic nerve runs through this meat, and it is both labor-intensive and costly to remove. In Israel, where there is less of a market for non-kosher meat, and meat prices are much higher, it makes economic sense to take the time and effort to remove the sciatic nerve and sell the rest as kosher meat.

    Notice that it is the presence of nerve tissue that makes it Kosher, or not…

    Now what I want to know is how Jews knew to avoid Prions in this way, before they were even discovered. It is either one heck of a coincidence, or I need to read up on my Old Testament…

  20. Pascvaks says:

    We don’t give much credit to “civilization” prior to the Greeks do we? Moses got all those dos and don’ts from somewhere. It is amazing how well the old biblical admonitions turn out to be a VERY good guide for staying healthy. What book did the main character of H.G. Wells’ The Time Machine take back to the future? For some strange reason, I always thought it was a Bible.

    (Chiefio, love it when we bounce all over creation connecting dots and dashes in one of your pieces. Reminds me of that old show on PBS years ago called “Connections”;-)

  21. Pascvaks says:

    An example of happenstance “Connections” and off-shoots,
    “The Immune Systems of Archaic Humans”
    Honest Injun! I was bouncing around to my regular haunts and there it was at the top of Hawks’ homepage.

  22. Lyndal says:

    I just want to say thank you for your post. My beloved bunny Cadbury has had a titer tested positive for EC but my vet isn’t completely convinced that it is curable. At my insistence however (I too, went in with a bunch of papers), she agreed to try putting him on a panacur (fenbendazole) + Orbax (family of Baytril) treatment. We tried for a week, nothing happened and so I asked for an extension. Anyway, long story short, we tried that course of treatment for almost 6 weeks and changes, if any, were miniscule. Now Cadbury is having major incontinence issues and runs around in circles trying to get his bearings together. I brought this up with my vet again and she doesn’t want to “drug him up.” I actually like my vet a lot, but I think her indifference to treating EC shows just how misunderstood this disease is and how bunny owners are almost expected to just roll over and call it quits when the EC titer comes back positive. Your post gave me hope that there are other forms of treatment out there for him and I’ve decided to seek another vet who is more willing to take the risk and try out different options of treating EC. Thanks for sharing your experience.

  23. E.M.Smith says:


    I loved that show…


    Unfortunately, by this time, and with ‘tepid’ treatment by the vet, there has likely been some irreversible neurological damage to your bunny. Still, I think it would be ‘worth a shot’ at treatment. I went with the Do It Yourself approach so as to get the best treatment as fast as possible. While I wish you luck with your search for a vet, a visit to the nearest ‘Tractor Farm Supply’ might work better for you…

  24. Linda says:

    Wow I lost you when you got into the mad cow stuff, which by the way cant be determoned a cause of death unless you inspect the brain post mortem. What I need to figue out is I am rescuing a young bunny who is in a herd with EC and likely had it passed to him from birth. I plan to quarantine him from my 4 other rabbits but if its like TB where you have been exposed but its not active, by the time there are symptoms its active and too late, past the contagious part. I cant figure out if the spores are only spread in urine for 3 months max, cant it activate anytime and the spores spread.? I read it completes it life cycle in 3-5 weeks and can stay on the ground a month but can a positive testing bunny be active anytime? I need to figure out how to protect my other bunnys from it Thanx

  25. E.M.Smith says:


    Per MadCow: One can also do a brain biopsy, but that’s typically not done unless there are extreme issues.

    Per bunnies:

    For E.C. the neurological symptoms are reversible “for a while”. It is not like TB. The parasite lives INSIDE a cell. So first you get ‘no problem’. Then you get some impairment of the cell and some function impairment. At that point IMHO treatment that kills the parasite can still result in recovery.

    After that, the reproductive cycle kicks in, in some cases to excess, and some cells are ruptured / killed. At that point, some of the impairment becomes permanent.

    That’s why part of what I stressed in the article was the fact that in both cases I started fairly aggressive treatment as soon as symptoms showed. IMHO, it is delaying by a week or two to get the appointment with the vet and an “OK” to use the right drugs that is a major part of the tendency for ‘treatment’ to fail.

    Time is of the essence in starting treatment as from the moment symptoms show, you are having more damage each day that can not be reversed. If treatment is started inside a couple of days OF SYMPTOM ONSET, it ought to be the best possible outcome.

    That was why I was unwilling to wait for a 2 week interval to get an appointment with a new ‘bunny vet’ and just went to the local farm store (something like a ‘Tractor Supply” or “Feed and Fuel” in farm country) and got the meds myself and did the treatment myself.

    Per contagion:

    Any bunny that has not had the parasite killed off can make spores and be a source of infection. Yet, a bunny who has had neurological damage may be “symptomatic” forever even though you killed off all the parasites. Similarly, they “blood titer” may show positive antibody after the infection is all killed.

    Neither blood titer nor symptoms tell you if they can be a source of infection.

    What I did:

    IMMEDIATE treatment of the newly symptomatic bunny. Kill the bugs now and stop spore formation in the urine.

    Isolate the infected bunny from the others and clean up the urine location (with bleach – 1 TBS / gallon) if possible.

    IFF you suspect the other bunnies were the source of infection, treat them as well to eradicate the parasite.

    You have 2 goals:

    Kill off the live parasites in the potential hosts ( Ivermectin, bendazoles)

    Kill off spores in the “run”. Sanitation / washing. Soil UV exposure. Relocation to a new “run” area for a few months. Anything that might kill off spores.

    FWIW, my bunny got it from a source that had not infected the others, and I treated it fast enough that they did not pass spores. No other bunnies got infected and everyone is doing fine even without aggressive treatment of the ‘run’ area and / or bleach washing things. Another data point for “fast treatment” being a very important aspect.

    Hope that helps.

  26. jennabelle says:

    Hi E.M,

    I was wondering if you could help me as I stumbled upon your E. Cuniculi information and need help in working out how to dose my bunny who has head tilt. I can’t readily get the medicines I need here but I have managed to get some Ivermectin and some Panacur. I have been trying to work it out as best I can from all the information available on the internet as our vet knows absolutely nothing about rabbits.

    I started out by giving him 14 days worth of Panacur 18.75 % as per the dosage on the packet (it is already graduated) and then I found Barbi’s information on Ivomec 1%. I managed to find someone who stocked Ivermectin and when I checked, she said it is a 0.8g/L ready to use Ivermectin. I stopped giving him Panacur and used the Ivermectin instead.

    The bottle of Ivermectin doesn’t have much information on it but it does say the following: “Worm dose: 0.3 of a ml per kg orally every 3 months; Mange dose: 0.5 of a ml per kg orally every 7-10 days until resolved” so I decided to try 1ml every 7 days. He has had 3 doses of the Ivermectin and I don’t see much improvement as far as the head tilt goes. He is eating and drinking as normal however and although he kind of curls up when you pick him up or just put him down on the ground, he can get around quite well even with his head tilted.

    How do you think I should proceed? Can I combine the two and if so, what do you recommend as far as the dosage goes? We are of course metric over here (Australia). The rabbit weighs 2 kg so I was wondering if I could give him the 1 graduation of Panacur along with some Ivermectin each day…just not sure how much of the Ivermectin would be suitable?

    Sorry for all the questions.

    Thanks in advance. I really appreciate any suggestions you may have.

  27. E.M.Smith says:


    In the above article I speculated that part of why I’d had such good results was the use of BOTH the bendazoles and Ivermectin at the same time. So Panacure is a bendazole and I would use it with the Ivermectin.

    The doseage is something you must calculate from the information on the package (as your package might be different from the one I bought). I’m not near my package at the moment so I can’t read it to see the gm/kg, but there are web sources on dose available (or I can find a vet supply store if you need help with that). I did Panacure according to package directions along with the “drench” according to package directions (it is just put on the skin, not swallowed, so I think it’s a larger dose)

    IVERMECTIN for cattle is a clear, blue colored liquid containing 5 mg of Ivermectin per mL (0.5% w/v) Ivermectin is formulated to deliver the recommended dose level of 500 ug of Ivermectin per kg. of body weight in cattle when applied along the top line from the withers to the tail head at the rate of 1mL per 10 kg.

    So that says it’s 500 ug or 0.5 mg / kg of weight. You have a 2 kg bunny, so I make that 1 mg of pure Ivermectin. Look on your package, find the ‘mg per unit’ and figure out what gives you 1 mg. You said yours was 0.8 g / L so thats 800 mg / 1000 ml or 0.8 mg / ml. I make that 1.25 ml as the “dose”.

    I think I was applying that one time each week. The first time, I metered it out over 4 days as my bunny was 1/2 Dutch and that breed sometimes has “issues’ with Ivermectin (and I didn’t want to kill him with one big dose if he WAS one of the odd ones). Later I swapped to just one dose each 7 days.

    For Panacure

    A related “horse wormer” is “Panacure” at 18.75% and ought to work as well, but with slightly harder ‘dilution’ to get the right dose.

    In a couple of places I saw the dose of “20 mg / kg / day” quoted for use against E. Cuniculi. That is the dose I used.

    You have a 2 kg bunny, so that’s 40 mg. Panacure is 18.75% so you need 40 x 100/18.75 = 40 x 5.3333 = 213 mg of Panacure a day. I would measure out 1 CC of it and see if it’s close to a gram ( i.e. check that the density is close to that of water at 1.0) then you can measure by volume which is a lot easier at those small doses. 0.2 cc is easier to get right with a syringe. (You could also look on your package for “mg / cc” and figure the volume to get 213 mg directly). That is given daily for a couple of weeks.

    Hopefully that is specific enough.

    Key points:

    You must calculate the dose from the data on YOUR package to be sure it is the right mg/ kg since different strengths might be available in different places / types.

    Ivermectin is persistent. A full dose is done once per week. If your bunny is a Dutch or Dutch hybrid, watch out as some are sensitive to Ivermectin (I did 1/4 doses over 4 days to watch for problems and be safer).

    Using BOTH Ivermectin and Panacure (or other fenbendazole source) together was, IMHO, important. They each help the other to be a more effective cure.

    And, sadly, time is of the essence. It may well be that your bunny now has a permanent balance problem as those parts of his brain have been damaged. One can hope that killing off the parasites will let it heal, but sometimes the bugs are killed and the balance issue remains. For me, I acted within a day or two and got a full cure. I don’t know how many days is too many for full recovery. “Snickers” took a couple of months to slowly get her head back to fully straight up and down, but was mostly straight up and down inside 2 weeks. So there is some hope for longer term healing.

    Best of luck!

  28. jennabelle says:

    Hi E.M,

    Many thanks for your advise. I have given the bunny his first 0.2 mg/ml dose of Panacur 18.75% Oral Paste. I will do this daily and will continue with the Ivermectin every 7 days (1.25ml instead of the 1 ml I was giving him). I will let you know if he improves. I didn’t have anything to weigh the Panacur with but I measured 5mls of water and 5 mls of the Panacur to compare them. The side of the Panacur packet says, as you have found, 20mg/kg fenbendazole daily. I have little syringes and I am just squirting it into those so I can measure an accurate dose. I find it very difficult to get precise doses with the graduated syringe.

    Many thanks. I’ll be sure to update you all.

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