You never learn a lesson quite so well as when personal experience is involved. My goat keep giving me these learning opportunities, whether I want them or not. A few weeks ago I had my first up close experience with the disease process called enterotoxemia.

Vaccine for two types of Enterotoxemia and tetanus

What is Enterotoxemia?

Toxemia means that a toxin is present in an animal’s system and is causing illness. Entero means having to do with the intestinal tract. All beasts are prone to different toxemias. Toxins might be directly introduced to the animal, but more often than not they are produced by microbes that are either accidentally ingested or reside normally in the animal’s system. In the case of those accidentally eaten, during digestion they release their toxins, with varying results depending upon the type of toxin. Microbes that normally reside in the animals system can be triggered to grow more rapidly than the animal can handle, resulting in the production of large amounts of toxins, and subsequently illness.

When it comes to enterotoxemia in the goat, the bacteria we are concerned with is Clostridium perfringens. This microbe, from the same large family as t

he one that causes tetanus – Clostridium tetani, is a normal part of the farm environment. Like C. tetani, it is anaerobic – living in conditions with little or no oxygen. This means that it can readily reside in the goat’s intestinal tract.

There are five types of C. perfringens, A, B, C, D, and E. Although types C and D are thought to be the primary ones affecting goats, type A and B have also been implicated in cases. The exact rates of each, though, are impossible to document, as most cases of the disease are never fully investigated. This is an important aspect for us to consider since the primary vaccine labeled for goats is for C. perfringens is based on types C and D only.

	Frequency in Goats	Alpha toxin	Beta Toxin	Epsilon Toxin	Iota Toxin
Type A	Rare	Yes
Type B	Rare	Yes	Yes	Yes
Type C	Uncommon	Yes	Yes
Type D	Most Common	Yes		Yes
Type E	Unknown	Yes			Yes

Each C. perfringens type specializes in the production of one or more toxins: alpha (α), beta (β), epsilon, and iota. As if that isn’t confusing enough, a variation on the β toxin has also been discovered and has been dubbed β2. 

Vaccination

Let’s talk about vaccination for enterotoxemia. As a reminder, vaccines are for prevention of disease, not treatment. Vaccines cause the animal to produce antibodies which are meant to protect the animal against disease. Vaccines for toxin induced disease are called toxoids. (versus anti-toxin which is a treatment and meant to inactivate the toxin produced during the disease). Most veterinarians and most literature will tell you that vaccination, for Clostridium perfringens type C and D (usually given in conjunction with the tetanus vaccine and so called C,D, and T) is a critical part of goat husbandry. You might also get the impression that if you follow a strict annual vaccination regimen, that your herd is protected. Unfortunately, when it comes to goats, this is not strictly true. The vaccine is acknowledged to be less effective in goats – not maintaining adequate antibodies in the animal’s system for long enough to protect the animal in between yearly doses. (See Goat Medicine 2^nd Edition, by Mary Smith and David Sherman, page 411) It is recommended that for vaccination to be effective a goat should be “receive booster doses every three or four months throughout their life” after the initial two vaccinations as kid. Because of this as well as the possibility of other types of C. perfringens being the problem, many producers in consultation with their vets are taking a different approach that focusses on management only. This has been my approach for the last 15 years. During that time we’ve had up to 124 kids per year and at peak milked 40 does. I’ve just had our first case of enterotoxemia – and it was avoidable.

Causes and Our Case

Earlier I mentioned that for enough toxin to be produced, something must trigger the bacteria to grow out of control. The number one reason is the sudden availability of highly nutritious food in the animal’s gut – namely proteins and carbohydrates. It’s for good reason that the condition is known as overeating disease. The rapid intake of more grain, milk, or even lush pasture than the animal is accustomed to can trigger the disease and cause death within hours. Overfilling of the stomachs can lead to undigested matter, containing starches that haven’t had time to be fermented by the rumen, moving on to the gut where they provide nutrients for C. perfringens. Fast growing, healthy kids are more often the victims of this disease simply due to their success at being vigorous, aggressive eaters.

So what happened on our farm? As a part of my current herd management strategy, I keep kids over a certain age off of their moms at night, milk the mom’s all or part of the way out, and then recombine them for the day. The moms rarely let the kids nurse for long – a few sips over a few seconds and then they walk away. I’ve noticed this behavior seems to be directly linked to the age of the kids. It appears to begin when the kids are about two weeks old. Perhaps the kids are just too annoying and rough by then, or perhaps instinct has the mother’s not allowing them to overeat – given that by then they are eating roughage and ruminating. The kid I lost was one of triplets, the biggest and most vigorous. With three kids, I didn’t really worry about anyone overeating, but I should have. On the morning in question I was teaching the last day of a three-day class at our creamery, in other words, in a hurry with my focus elsewhere. To save time and the distraction of hearing kids yell, I let the kids out before milking. When their mom came up on the stand, she was much emptier than usual when the kids had been allowed to nurse before milking on other occasions.

Within an hour or so the kid was in severe distress. There is a cry a goat kid makes that lets you know it is in serious agony. Once heard, never forgotten. This kid was making those sounds, lying on her side, and extending her back legs stiffly. When stimulated, she would get up and walk to a new spot and lie down again. The fact that she could walk seemed to rule out a spinal injury. Her temperature was normal, rumen not distended as in bloat, inner eyelids nice and pink (no anemia as in a severe case of coccidiosis), but rumen sounds and movement were diminished. I gave her Banamine (flunixin meglumine) for pain, B vitamins for rumen support, electrolyte liquid, probiotics, put her in a pen alone, put a goat coat on her, and went in to return to my responsibilities to the class. My husband kept checking in on her and reporting back to me. The Banamine helped with the pain. One of this drug’s side effects is to calm the lining of the gut, so I was hoping if it was a case of colic or some other gastric upset, that there would be hope, but given how she had sounded earlier, my hope was low.

By the class lunch break, I could hear that her distress had not only resumed, but had turned a corner from which she could not return. I went to sit with her, trying to decide if there was even time to perform that last act of euthanasia. I sedated her to at least remove her awareness of the final pain, and she died quickly in my arms. From first symptoms to death only 3 hours had passed.

Enterotoxemia type C and D antitoxin (not toxoid) can be used if a case is suspected. I had been dissuaded by vets as to its effectiveness, but I sure wish I had had some to try, just to know. It is also used in some cases as a preventative, repeated every few weeks, to maintain antibody antitoxin levels in the animal. Be aware that when being used as a treatment for an active case, the dosage is at least two times that as for a preventative! See Goat Medicine (info at end) for suggested dosages for treatment of different degrees of the disease – peracute, acute, and chronic. Be aware that this dosage instruction includes follow up injections.

Necropsy and Diagnosis

If you’ve read much of my work, you know that I always try to perform my own, albeit amateur, field necropsy on any goat that dies from unknown causes. In this case, I waited until the class had dispersed, with the exception of one student that was staying on our farm to also learn about goat farming. I offered for her to watch if she wanted to. It’s not an easy thing to do or to see, the investigation of the inside of an animal, but she was game. In my book I teach you how to perform a field, or gross, necropsy and tell you that you don’t know if you will learn anything that answers that particular animal’s mystery, but you will learn something. This case was proof of that.

When talking about the case with a friend and fellow goat farmer a few days later, she said “Was it enterotoxemia?” That diagnosis hadn’t even been on my radar. I honestly didn’t know that milk could cause it. I talked to my vet, and she said that yes, in some species it is even called milk toxemia. So I sat down with my books and correlated the necropsy findings and symptoms with the information and concluded that yes, she most certainly died of enterotoxemia.

These are the abnormal things I found on the kid’s necropsy:  A small amount of clear fluid in her abdominal cavity (peritoneal cavity) that drained with the first incision; her abomasum (fourth or true stomach) contained large pieces of undigested matter (by the time the contents get to the abomasum they should be very broken down from rumen activity and rumination as well as the work of the omasum); the first portion of her lower intestines (the duodenum) had areas of taupe/brown color on the outside; the next section (the jejunum) had light, milky green liquid in it. Everything else appeared to my non-veterinarian eyes as normal. I didn’t think to check her kidneys for a change in texture – “pulpy kidney” is associated with this disease, but is seen more often in sheep than in goats. Often a section of the lower intestines is found to be red and inflamed (hemorrhagic), but this kid’s appeared normal to the naked eye, but no doubt was damaged at the microscopic level.

In reading different cases (see references at end), you find a variety of symptoms, some that correlate with the type and toxin, and others that seem interchangeable. Without a full necropsy with lab work, there is no way to know for certain which C. perfringens is the culprit, but enough of this kid’s results, and of course how she exhibited pain along with her sudden death make it an easy conclusion. Being a superior eater, she had filled her rumen with roughage, her abomasum was no doubt already full. Then she filled up on milk. The overeating caused two things to happen, roughage passed on to the abomasum before it was ready and the milk moved on to the intestines before it was ready. This provided a sudden, rich source of nutrients for the C. perfringens bacteria. The bacteria grew swiftly and released toxins that caused the neurological symptoms (back legs stiffening).  One of the effects of the bacteria is a rapid thinning of the intestinal wall, causing the leakage of serum into the abdominal cavity – which was seen on necropsy.

Conclusion

I always tell folks in my classes that the longer you have goats the more you will learn, and many of the lessons will be quite painful. There will always be something waiting to humble you and remind you of your own lack of full control. It’s important to accept this fact, but at the same time keep adding knowledge to our collection – and sharing it with others. Oh, and I ordered a bottle of anti-toxin, hopefully it will sit unneeded for another 15 years.

Review on Pulpy Kidney Disease, Dinsefa Jemal, Mohazeba Shifa and Bedaso Kebede, Journal of Veterinary Science and Disease:  https://www.omicsonline.org/open-access/review-on-pulpy-kidney-disease-2157-7579-1000361.pdf

Clostridium perfringens type A and type A and β2 toxin associated with enterotoxemia in a 5-week-old goat, Tammy Dray. The Canadian Veterinary Journal. http://www.scielo.br/pdf/jvatitd/v13n4/a17v13n4.pdf

Goat Medicine 2^nd Edition, Mary Smith and David Sherman, Wiley Blackwell, 2009, pages 406-412