Tyzzer's disease-anyone heard of it?

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Sue_C.

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All had been normal at his birth, everything done that should be done, he was a healthy, frolicing, seemingly healthy colt. He just turned a week old, and was found down and too weak to stand. They rushed him to their local vet, where, after testing, he was put onto a round of IV antibiotics.

He seemed to come around...was again up and nursing soon afterwards...the antibiotics continued, yet he again showed signs of distress by that next evening...(that would be yesterday)

They put a call through to the Vet School/Clinic in PEI, and rushed him over, where after checking him over...they found an enlarged liver, which "goes with" their initial diagnosis of "Tyzzer's disease"; which none of us had ever heard of.

Has anyone here ever heard of this disease, and if they had, what was the outcome?

It isn't looking good for this sweet lil guy, so he needs as many healing thoughts as you can afford to send.
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I had never heard of it before, but Googled, and found this from the Merck Veterinary Manual:

Tyzzer’s disease is an acute bacterial infection of a wide range of animals (see also Intestinal Diseases and Gastrointestinal Diseases) that is seen worldwide. Sporadic fatal infection of foals is common, and acute fatal epidemics occur in laboratory animals. The disease is rare in dogs, cats, and calves. It primarily affects young, stressed animals; however, some species appear resistant unless stressed or immunosuppressed, while others are susceptible without immunosuppression. Immunosuppressive drugs and some antibacterials, especially sulfonamides, predispose animals to the disease.

Etiology and Pathogenesis:

The cause is Clostridium piliforme (previously Bacillus piliformis ), a motile, filamentous, gram-negative, sporeforming, obligate, intracellular bacterium. It does not grow in cell-free media but can be cultured in the yolk sac of chick embryos or tissue culture cells. The vegetative phase is very labile; spores may survive in soiled bedding at room temperature for 1 yr and can also survive at ~133°F (60°C) for 1 hr.

The pathogenesis is poorly understood. Infection most likely results from oral exposure. Possible sources include infective spores from the environment, contact with carrier animals, and in foals, ingestion of horse feces. The primary site of infection is the lower intestinal tract with subsequent dissemination via the blood or lymphatics. The bacterium has an affinity for the intestine (epithelial and smooth muscle cells), hepatocytes, and cardiac myocytes. Stress factors such as capture, overcrowding, shipping, and poor sanitation appear to be predisposing. Sulfonamide administration predisposes rabbits to the disease. Mortality is highest at weaning age except in foals, in which the disease is seen between 1 and 6 wk of age, with most cases between 1 and 2 wk. In some species, the disease has been identified concurrently with other diseases, eg, feline infectious peritonitis in cats, distemper and mycotic pneumonia in dogs, and cryptosporidial and coronaviral enteritis in calves.

The disease most often affects well-nourished animals during periods of stress. Under laboratory conditions, stress is created by immunosuppressive drugs or other factors that can be easily identified. With many experiments, stress may be involved as part of the protocol, and when the disease develops, it is devastating.

Clinical Findings:

After experimental infection, the incubation period in foals is 3-7 days; under natural conditions, the period is unknown. Most foals are found in a coma or dead. Clinical signs, if seen, are of short duration (a few hours to 2 days). Signs are variable, but may include depression, anorexia, pyrexia, jaundice, diarrhea, and recumbency. Terminally, there are convulsions and coma. Signs vary slightly between species. Laboratory animals may show depression, ruffled coat, and varying degrees of watery diarrhea; at the start of an outbreak, they often are found dead.

Clinicopathologic tests are of little value in laboratory animals because they die so rapidly. In foals, the serum enzymes sorbitol dehydrogenase, AST, alkaline phosphatase, lactate dehydrogenase, and γ-glutamyltransferase are increased. There is also hyperbilirubinemia, leukopenia, hemoconcentration, and terminally profound hypoglycemia.

Lesions:

Characteristic lesions are seen in the liver, myocardium, and intestinal tract. In the liver, white, gray, or yellowish foci of necrosis, 2 mm in diameter, are few to disseminated. The hepatic necrosis is most marked and disseminated in foals in which the multiple necrotic foci with slightly depressed hemorrhagic centers appear to infect almost every hepatic lobule. In addition, there is marked hepatomegaly, and the hepatic lymph nodes are hyperplastic. In rabbits, severe lesions develop in the intestines and heart. The terminal ileum, cecum, and proximal colon are diffusely reddened. Diffuse (“paint-brush”) hemorrhage is frequently seen on the serosa of the cecum. Patchy areas of mucosal necrosis are present in the cecum and colon, together with marked edema of the wall of the cecum. Mesenteric lymph nodes may be enlarged and edematous. White streaks in the myocardium may be present, especially near the apex. Intestinal and heart lesions are generally milder or absent in other animals.

Microscopically, randomly distributed and coalescing foci of necrosis in the liver are associated with scant to moderate infiltration of neutrophils and macrophages. The causative bacteria are found in a crisscross pattern in viable hepatocytes at the periphery of the necrotic foci. In the cecum and colon of rabbits, patchy areas of necrosis extend as deep as the muscularis externa with associated mucosal and submucosal infiltrates of neutrophils. Organisms may be found in the epithelium, muscularis mucosa, and muscularis externa of the affected intestine. When cardiac lesions are present, they consist of foci of fiber fragmentation, vacuolation, loss of cross-striations, and minimal inflammatory cell infiltration.

Treatment and Control:

Little is known about the effectiveness of antibiotics for treatment; some antibiotics are known to aggravate the disease. C piliforme is sensitive to tetracycline and partially sensitive to streptomycin, erythromycin, penicillin, and chlortetracycline; it is resistant to sulfonamides and chloramphenicol. In foals, the disease seems to be nearly 100% fatal, although it is likely that some foals survive. A definitive clinical diagnosis is not possible due to the lack of a definitive diagnostic test. Once the disease is present on a farm, it may be seen sporadically year after year. Animals suspected of being infected may be treated IV initially with 50% dextrose, followed by 10% dextrose (slowly), other fluid therapy, and antibiotics. Most foals respond dramatically to the dextrose therapy but relapse into a coma and die in a few hours. Rarely, an occasional foal appears to survive the disease after prolonged treatment with dextrose given slowly IV with antibiotics.

Because the disease in foals is sporadic and not highly contagious, specific preventive measures are usually not indicated. Reducing factors that cause stress and immunosuppression lessens the incidence. When the disease is seen in a colony, treatment is not recommended because it prolongs the disease and possibly produces carrier animals. It is best to destroy all animals in the colony and attempt to restock with disease-free animals.

I also found another link, its REALLY technical, way over my head, but some folks might be interested... History and Technical Info
 
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Thank you...It is a scary thing from the sounds of it.

Altough we've read the information on it...what I REALLY want to know, is if anyone else has had experience with it?

What were the symptoms, the treatments, and most importantly...what was the outcome??
 
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Sorry, double post for some reason...

We just don't understand. The barn, pastures, yards are cleaned regularly...the foal hadn't been stressed by anything, seemed like a happy, healthy foal, normal in every way?
 
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I hadn't heard of it before and unfortunately the prognosis doesn't sound good. As to stress factors, some foals seem to stress for reasons we can't see. Our first of the year colt ended up on Gastroguard for 30 days....he's in a stable environment, is not a timid easily frightened colt, had no other health or developmental issues, and yet he got ulcers.

The seizure foal I have currently seems to have his episodes when he has been resting - and is stressed by being held for meds, etc.

I hope your friend's foal bucks the odds and pulls through, and I'm glad you posted here. At the very least, we have learned something.

Jan
 
I had not heard of clostridium in horses but have lost goat kids to clostridium perfringes. Luckly for goats there is a vaccine that does seem to help prevent it. Clostridium is everywhere so its not something your friend did wrong. Seems most animals can fiend off the bacteria, some are just unlucky enough to not be able to.
 
I have seen three cases of Tyzzer's, two in our own foals (though about 15 years apart) and one in a client foal at the vet clinic where I work.

From what I understand, your friend''s foal is a little young, usually they're 2-3 weeks old. And he's doing very well for a Tyzzer's foal.

The first one we had, we noticed she was a little dopey, called the vet, loaded her on the trailer, and by the time we got to the clinic, she was down and non-responsive. Despite all the treatment they could give her, she started seizing in a few hours and died soon after.

The quarter horse foal that I saw with it was actually AT the clinic for breeding with his dam and set to go home. When we went to get them to load on the trailer, the baby didn't want to get up, which wasn't unusual (he was a super quiet, cuddly type) but did and then trotted to the trailer after his mom looking completely normal. By the time the owner got home (which was just across the highway, less than 10 minutes) the foal was down and non-responsive and she turned around and came back, but he died in a few hours.

Just last year I went out just after lunch (had seen the filly at 10 or so, and she was normal) and found Juliette's filly flat out, if we got her up she'd just flop back down. I rushed her to the clinic, but she was dead by the time I got there.

There's nothing you can do to prevent it, but it's super rare. Apparently the clostridium lives in the soil everywhere, but just a very few foals are succeptible. The clinic has at least 80 foals come and go each spring, and I've been there 10 years, and that is the only foal that's died of Tyzzer's. It destroys their liver, and does so extremely fast.

The fact that your little guy is still alive make's me wonder if it really is Tyzzer's.
 
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This does sound amazingly like what happened to my filly last year. A full autopsy was done, so I shall forward this link to my Vet, who was baffled.

Even cutting all the costs as far as they could, this cost me over $3,000.00 so I should like to get to the bottom of it.

My filly was at the upper age limit, 7 weeks, and I had just started halter training, but she was really OK with it all.

Just goes to show you can never tell what stresses a foal.
 
As of 3pm, he was still alive...and if they think he is strong enough, they soon plan to take a liver biopsy, which is the only way to be 100% sure. So far, the only way it has been positively diagnosed, has been after a necropsy. Hopefully, this little guy will be the exception...

You mention goats...that is curious, because this mare and foal have not shared a pasture with the other horses...but were turned out in a large goat pen. The goats hadn't been out in it since late fall, until just that morning, prior to his evening collapse. Makes me wonder if the goats could be carrying it???
 
I just got this in an e-mail from my buddy...looks like her little colt is gonna make it.
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Just received another up date from the Vet College. The first thing the doctor said to me was “ Well it is looking like your little fellow is going to make history”
 
I had never heard of it until today - I have a filly in the vet clinic right now and it sounds like this is what she has. Very poor prognosis - I am just sick.
 
I thought someone else here had posted about this awhile back? Did you try doing a forum search?
 

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