Training a Rat Terrier to Hunt: A novice’s approach that worked

Nifty’s first rat in 2016 (not my usual hunting attire!)

If you have a rodent problem you’ve probably tried every trap made – and then some (Google it, and you’ll find some interesting homemade contraptions) and then watched as after a few mortalities, the rats quickly learned to avoid or even disable the traps. (After finding one trap we had set literally covered up by debris that they had obviously moved over it, I almost worried they would start setting traps for us!) Rats are incredible smart, and for that, as well as their compassion for their own kind (you can Google that too) I admire them. But as farmers we have to try to limit their impact and acknowledge that they are thriving beyond a natural level due to our farming activities. As organic or sustainable stewards, we are not going to use poisons. It then comes down to employing cats, ferrets, or terriers. Cat’s can’t usually take on a full-sized rat and ferrets have their own issues of management, but terriers, in particular rat terriers, can be amazing. (Check out YouTube if you want a demo) Not to mention they are also loving, loyal, snuggly pets.

If you purchase a pup from a reliable breeder – meaning one who takes hunting temperament into consideration rather than primarily show or pet qualities, then you are off to a good start. I found Nifty by asking other farmers on Facebook for recommendations. (I’ll post his breeder’s info at the end of the article). These dogs are born with an instinct to hunt, but that doesn’t mean you don’t need to take an active role in refining that drive. Otherwise, not only will the rats find places to hide, but the dog is likely to want to chase cats, chickens, etc.

Video of Nifty and “his cat”:

The Goal

Again, this was my first rat terrier to work with, the commands I came up with can be altered to your own, but the premise is simply this: You will be working with them as a team. You will be the second set of eyes, the one who can poke a stick into a tight spot, the one who can lift a pallet where a nest of tunnels has been built, and so on. Therefore, you must have a set of commands that informs the dog what you see or what you are about to do to help them.

Start with a Lure

Buy or make a small lure – a stuffed bit, about the size of a rat, made of real animal fur. I bought one online, but you could make one. Don’t let the dog use this as a toy, only use it during training sessions. I tied a long string to mine and placed it behind some bales of straw with the string in my hand. When Nifty showed any interest in sniffing around the straw, I would stand by him and tug on the string. When he noticed the movement, I would say “There it is” and point. Then when he went in for it, “Get it!”.  When he did get the lure, he was praised thoroughly. Sometimes I used treats as a reward, but he loved the praise enough for that to be adequate. Training with the lure started as soon as he showed any interest in chasing the chickens, etc. The praise of hunting for the right thing HAS to happen concurrent or before any scolding for chasing the wrong thing!

A big one!

Look where I’m Pointing

Most dogs watch our hands, looking for the ball to be thrown, the treat to be doled out. I found it very helpful to train Nifty to look where I was pointing. Rats like to hide in odd places, including up in rafters where the dog may not be able to scent them very quickly. By teaching him to look where I was pointing, the rodents have a much harder time avoiding him. In addition to using the lure to help him understand what pointing means, I used treats. I would toss a treat a short distance away and then point, saying “There it is!”. It didn’t take long. It is easy to confuse them, so use this carefully. Even now, I sometimes find myself saying, “I don’t know where it is.” When the “subject” has gotten away. I shouldn’t use this; it is too close to the phrase I want him to understand.

Building on this, and as a way of practice, hiding a favorite toy, chew bone, etc., and then saying “Where’s your bone?”, looking around, then pointing and saying, “There it is, get it” is also fun for everyone.

Go Around

The other very useful phrase tells the dog to go to the other side of something – a drain pipe, a building, a stack of wood, while you stay on the other side and try to flush the rodent out towards them. Teaching this was a bit more difficult, but Nifty learned the concept through trial and error. If he told me that there were rodents under a pallet, for example, I would use my pointing cue along with the term “go around” and then lift the pallet in a way that made the side opposite me easiest for him to access. Now it works for larger spaces, sliding barn doors, sheds, etc.

The whiteboard in the barn July 2020

Team Effort

Without a doubt, using only a single dog to reduce a rodent problem will be the most effective if you plan on working as a team. I count on Nifty to locate the rodents and let me know if he needs help. He has a specific bark that I have come to associate with a located “target”. In fact, even if I don’t see it, he has never been wrong! This included him once going nuts on the outside siding of our barn. He tore and bit at the wood until finally Vern and I went into the tool room on the other side, closed Nifty in with us, and took off the dry wall. Nifty’s score board that day went up by 13 rats. (I did a lot of shrieking as the little buggers ran hither and yon in the small space trying to escape).

There are places on our farm, that despite my best efforts, the rats will always get away. But the regular harassment that Nifty deals out keeps their numbers down even when he can’t actually kill them. As a demonstration of this fact, there was a period of time where we were not able to let him out during the day (we were occupied with caring for aging parents). During that few weeks, rats and ground squirrels proliferated, including moving into an attic space. Oiii.

The Kill

One thing I don’t want to forget to mention is the importance of nurturing the animals kill instinct when they are very young. This is rather tricky if the first thing they chase down doesn’t happen to be a rodent. Nifty’s first kill was a poor little wild turkey poult. He trotted up with it so proudly. I grit my teeth and neither praised nor scolded him. Then I did my best to help him encounter some desired victims. If your farm has rodents, you have this opportunity. When the first appropriate kill is accomplished,  heap on the praise and start using a cue of “that’s a leave-it” or other term to apply to birds, cats, etc. (FYI, Nifty’s best bud on our farm in one of the cats, see video link above).

Nifty and “his” Cat, Dibs

When a kill happens, Nifty’s technique is not to shake-and-break. Rather, he gives it what we call “the massage of death” – rapidly biting up and down the animal’s body. I suspect this is an instinct that helps them rapidly dispatch an animal in a tight burrow or space where shaking wouldn’t be possible.

After it is properly “massaged” I let him confirm this and then take it away from him and praise him. If he is hunting multiple varmints, as in a nest situation, he will drop it as fast as he can and go for another, sometimes coming back later to confirm death. We relegate the poor little critters to the compost pile in the garden.  


Terrier breeds were originally bred to hunt animals that go underground (that’s the origin of the word terrier, for terra or earth). In recent history, many terrier breeds have been used only for show and as pets – or perhaps for agility and other field trials that don’t actually involve dispatching live animals. Rat terriers were quite a popular breed in the early 1900’s (both my parents had them, or crosses, as young people), but then became very hard to find. They have definitely made a comeback, I believe in thanks to people appreciating the organic, relatively humane way they help reduce rodent problems. But other terrier breeds and crosses might also be great ratters. Look for a small to mid-size bloodline (I’d suggest 15- 20 pounds mature weight) as this is a great size to be brave enough to take on a ground squirrel (they are fierce!) and still be maneuverable.

Nifty was bred by Clearbrook Kennels in Washington State. I hope they are still breeding when I one day add another.

My Final Novice Advice

If I, without any previous ratter experience, can successfully train a working rodent terminator, you can too. My final advice is to not put it off. Once you get a pup, you must begin to nurture its down-and-dirty, sticking its nose into every cranny, hunting nature. As with all working dogs, from livestock guardian dogs to ratters, you have to keep the ultimate goal in mind when you are raising them. Oh, and get them a good flea collar. (The Seresto 8 month collars are our choice).

DIY – Goat Decks

How to Build Sectional Raised, Slatted Flooring for Goats

Lounging on the deck

 Hands down, raised, slatted flooring for goat housing wins the prize for ease of maintenance, cost over time, and, best of all, goats love it! I call this type of flooring “goat decks”.

Goat decks allow the manure to fall through the slats (mostly) and urine runs through and/or dries. The manure collects without being compacted by the goat’s hooves, meaning it is light and fluffy and super easy to scoop out when the decking is tipped up for cleaning every few weeks. Very little, if any, feedstuffs or other bedding, makes it through the cracks resulting in a higher value manure for gardens and possible sale.

The initial investment, not counting labor, is about 3.00 per square foot. The instructions in this post are for building two 4×4’ sections, or 32 square feet. Given that a bag of shavings will cost most people about 10.00, this one-time investment will save you a lot of money over time. For miniature breeds, space the decking at ½ inch. For standard breeds at 5/8 inch. It works well even with kids in the pen.

I keep one interior space bedded traditionally – with shavings and straw – but am progressively covering the rest of the sheltered space with goat decks. Here in Oregon our coldest winters are only in the teens, usually, and even then, many of the goats prefer the decks to the bedded area for sleeping. There is no draft below them and the manure must build up some heat that makes them comfortable.

We average having to clean under ours about every 6 weeks (that was with a larger herd than we have now), but it depends on the weather – when nice, they don’t spend as much time in the sheltered areas, of course, so manure build-up under the decks diminishes.

Cleaning involves daily raking (with a metal leaf rake) the tops to clear the tops and slats, spraying the undersides with vinegar after cleaning underneath, and occasionally using a hay-hook to clean the spots between the slats where the under-framing prevents manure from falling through. I built the first decks about six years ago and they are still in great shape.

Materials Needed (for two 4’x4’ sections)

5 – 8 foot pressure treated 2×6’s (or 2’x8’s if you want them a little higher, but they will also be heavier)

12 – 8 foot 2×4’s

18 – 3 inch exterior screws

60 – 2 ½ inch exterior screws

2 – ½ – 5/8 inch thick spacers (short pieces of wood to get the deck spacing even)

Construction (takes about 1 ½ hours if you have a bit of experience building)


  1. Cut 4 2×6’s into eight 45” sections
  2. Cut 1 2×6 into two 43 ½ inch sections
  3. Cut  2×4’s in half (24 48” sections)

Assemble Base

  1. Arrange 45 inch sections of pressure treated wood with ends overlapping as shown in 2nd photo from left (alternate the pattern) and connect with 3 of the longer screws at each corner. This will form a square that is 46 1/2 inches on each side. Double check the measurements before assembling to make sure that you have the boards overlapped properly.
  2. Place the 43 ½ inch piece of pressure treated wood in the center and secure through the side with 3 of the long screws.
  3. Check “the square” by running a tape measure diagonally from each corner. They must measure the same distance. If not, adjust by pushing the long side at one corner towards the short side.

Install the Decking

  1. Beginning at one edge (with the decking boards running across the center support board)
  2. Overlap the first board ½ inch at each end and 1 inch along the long edge. Secure in place with 2 of the shorter screws at each end, one in the center support, and a couple along the long edge.
  3. Use the spacers to place the next board and secure it in place.
  4. Continue as in step 3 until all decking is in place.

Repeat for 2nd section.

The newly installed section being properly coated with goat poo. Sections in the back are about 6 years old.

Encounters with Enterotoxemia

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.

enterotoxemia toxoid
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. 


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 2nd 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.

Clostridium Perfringens Types C & D Antitoxin

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.


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:

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.

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


Philosophy of a Vegetarian Butcher

I’m a vegetarian. Lacto-ovo. For almost a quarter century. I also harvest (as it’s so appealingly called these days) meat for my omnivore family. In addition I’ve found it gratifying to teach others how to respectfully take the life of a gentle beast and convert its life into sources of life for others.  I don’t find this a conflict at all.

Vegetarianism in all its forms is a luxury of time and situation. In my case, I have never liked to eat meat. When I was a kid, the only way I enjoyed it was if it was marinated and then cooked to well done. I don’t like the taste of fresh milk or eggs – especially healthy, farm eggs. There is just something about my system that doesn’t crave, enjoy, or seem to need meat. But I am fortunate to have access to homegrown fruits and veggies and an amazing spectrum of local products, rice from our region, beans from many places, organic tofu, amazing cheeses, and numerous other foods and supplements that seem to provide all I need. But to practice abstinence from animal products as a superior lifestyle is to disrespect indigenous cultures throughout time, those living in less bountiful societies, and indeed, our own origins as a species.

To believe that vegetarianism is more evolved and more ethical is the ultimate arrogance. It implies that humankind is above and separate from nature – indeed we seem drawn to this paradigm in almost every aspect of how we treat the planet and its systems. When it comes to eating meat, however, humankind can rise to a level that our non-speaking predator animal kin cannot – we have the potential to take the life of another creature for sustenance with respect, honor, and appreciation. It’s the lack of realizing this potential that is the true tragedy.

To blithely shop the supermarket meat department, its refrigerated cases stacked with tidy rows of bright claret steaks; to selectively dine on primarily just the choice parts of the animal – bacon, chicken breasts, lobster tails; to expect flesh to be inexpensive – all of these things support and create high efficiency, large-scale farming, where the animal, the human worker, and the environment pay the price. Meat, of any kind, should be relatively costly and eaten in proportion to what the animal, the workers, and the land can, without undue compromises, provide.

I don’t expect everyone to be able to learn to slaughter and butcher. Even 15 years ago, I harbored a prejudice toward friends who were able to kill their own chickens, it just seemed a bit barbaric. I was raised on a farm by parents who were not from self-sufficient upbringings. But they aspired toward that. In addition to a massive garden, orchards, and a home-scale wheat grinding mill, we also raised animals for milk and meat. But others were paid to kill and process them. It was so hard for my mother, in fact, that she would load me and my sister in the car and take us to town on the day the kill truck came. I took the next step. And my children have a more innate sense of balance regarding life and the food chain than even I do.

In 2003 I told my husband, a happy omnivore, that I wanted to raise a batch of meat chickens. He was uncomfortable with the idea. He was raised on what I call a rural suburb – small lots, dads that worked 9-5 and whose farm skills were topped out by mowing the front lawn. So we made a deal. I’d do the entire processing, serve it up, and if he and our girls could tell me that the meat wasn’t superior, I wouldn’t do it again. You can guess who won – we all did.

The first goat I butchered was named Minerva. She was an adult Nigerian Dwarf doe, but without a good future. Other than being cute, she wasn’t a good milk goat, had an unbalanced personality, and was very noisy. To have given her to a pet home would have likely doomed her to a string of unhappy owners and poor living conditions. I had taken the lives of a few goats before – using a bullet to euthanize them for various sufferings. But I had never processed a larger animal into meat. I printed out instructions from the internet, bought an inexpensive set of butchering tools, and steeled myself.

I made a good portion of the harvest into jerky. I’ll never forget what happened next. I handed a slice to my youngest, an animal lover whose dream was to one day open a cat sanctuary, but who also relished a good steak. She skeptically put a bit in her mouth and chewed. Her eyes widened and she said “Is there anyone else we can off?” The wall had been breached.

It has been my privilege to grow to the point of being able to share these moments with others. Hopefully helping them on their own journeys of returning to balance in the food chain. Life is sacred and so is death. Both must be respected and neither can be avoided. If you aren’t ready for direct involvement with this process, you can still try to honor it. Purchase only “expensive meat” from local farmers who care and are involved with every step of the harvest – even if that means they oversee the animal’s last moments at an FDA approved facility; if you must by from an unknown source, seek out humane certified producers or failing that, organic; don’t eat fast food meat; don’t eat much meat; and finally, try to eat the meat in proportion to what the animal offers, after all there’s much more to a pig than bacon. If you have children, you can guide them toward a level above your own – let them raise an animal, help a farmer harvest meat, learn to cook meat, and above all, never to waste meat.

I sheep farmer friend once taught me the following mantra, and its one omnivores should live by: “Every animal deserves a good life, a good death, a good butcher, and a good chef.” Amen.

The Importance of Monitoring Somatic Cell Counts

Awhile back the FDA raised the maximum number of somatic cells that Grade A goat milk can contain from the former limit of 1,000,000 to 1,500,000.  Our state (Oregon) followed suit just this year and adopted the new limit for goat milk and also lowered the cow level from the FDA level of 750,000 to 500,000. While I applaud the cow levels, I am concerned about the goat levels.

California Mastitis Test

Just what are somatic cells and why do they matter?

I have read and heard somatic cells in milk referred to as “pus”. This is not correct! Somatic cells (SC), by simple definition, are “body” cells.  In milk, these can be normal skin cells (epithelial) shed by the milk ducts (more on that in a bit), portions of the cells (cytoplasmic particles),  or white blood cells (leukocytes) that are present in order to fight off an udder infection (white blood cells are also present in “pus”). So let’s talk about why a healthy udder matters and the difference between the epithelial and white blood cells.

First, udder health correlates with the animal’s health and wellbeing. If you believe in the humane treatment of animals, then this should be important! Second, milk produced by a less than vibrantly functioning udder will not be of superior quality – either for drinking or making cheese.  A healthy udder is created and maintained by a nutritionally, physically, and emotionally balanced animal. (Yes, they do have emotional needs!). While I won’t be covering all of these needs here, it is important that you remember that they are the foundation for the production of superior milk).

White blood cells migrate into the udder in order to fight off microorganisms that could cause, or are causing, an udder infection – the same job they do throughout our own bodies. When they are called to the battle front within the udder their presence is indicative of a problem. The problem could be unseen, meaning you can’t see any difference in the milk or the udder – no swelling, heat, clumps in the milk, etc. This is called “sub-clinical” mastitis and is the most common form of mastitis (udder infection). When a severe udder infection is present, it is called “acute”. Animals can suffer greatly from an acute case of mastitis – including loss of the affected part of the udder to gangrene or even death.

How Cow’s and Goat’s Differ

Now, let’s go over one of the unseen differences between goat and cow milk. Understanding starts with remembering that the udder is a gland. The mammary gland, to be exact. All glands (we have lots of them – from our armpits to our stomach) secrete their products in one of three ways. Two of these are pertinent to milk secretion – apocrine and merocrine. I am not telling you this to add more words to your Scrabble game, but instead to explain some very important differences between cow and goat milk. Glands that secrete via the apocrine system also shed parts of the cell wall lining. Goats and humans secrete milk via the apocrine approach, while cows milk is shed via the merocrine system which keeps the secretory cell intact. Kind of cool, kind of gross, don’t you think? From this you can rightly conclude that goat milk will have a “naturally” higher somatic cell count (SCC) than cow milk (when cells are counted using the same method traditionally used on cow milk).

What is a Normal, Healthy Somatic Cell Level in Goat Milk?

So if goats naturally have a higher SCC, why am I concerned about the legal limit being raised?  In my experience, which is not all encompassing of course, a SCC over 300,000 in our goats, means there is a very low-grade problem. How do I know this? Every month a person comes to our farm and collects a milk sample from each individual milking doe. This sample is then tested at a certified laboratory for many things, including SCC. If the count comes back over 300,00 then we march out to the parlor (as we already do twice daily) and do a California Mastitis Test (CMT) on that doe. The CMT will show the difference in SCC between each half of the udder (or each quarter if you are testing a cow). If they are different, then It is not normal, one side has a problem. By following this policy we have (knock-on-wood) never had an acute case of mastitis and or current herd average (from tests covering about 10 years) SCC is 104,000.

Note: SCC are usually read MINUS three zeros. So 162,000 will appear on test results as 162.  Anything below 1,000 is usually not counted and will appear as zero.

I have always wondered if perhaps Nigerian Dwarf goats, our breed, have a lower average than the big girls. We have two full sized goats, LaMancha’s. Their average SCC are 109-125,000 (higher than our total herd average). The current average of all dairy goats in the states covered by our testing association is 625,000. When looking at the 2011 summary, where the data is analyzed from several standpoints, Nigerian herds average 121,000 while standard goats average 783,000. If looked at by milk production volume, does producing about 3,000 pounds of milk or more are the highest at 939,000.  Herd size (meaning if you have only a couple of goats versus 31 or more) seems to matter as well, but not as much as milk production volume. So many factors may come into play, but I still have to wonder if this higher limit won’t have the unhelpful effect of causing some producers to ignore even more subclinical mastitis cases instead of jumping on top of the situation before it gets out of hand. Having known commercial producers who have gone from high counts to low by improving techniques and removing animals with chronic subclinical cases does make me feel that the higher limit is a mistake.

What can You Do to Monitor Your Animals and Treat High SCC’s ?

If you have goats or cows and are not on a program where their milk is regularly tested, I highly advise performing a CMT (or other SCC’ing test) EVERY MONTH. By doing this you will find little problems and be able to address them before antibiotics are needed)

So what do we do when one side of the udder has an obvious (decide through CMT) problem? First you must rule out problems with milking equipment and general health of the animal. Of course, when it is just on one side, then you have to assume an udder infection of some sort. Before you resort to antibiotic usage, you can try some organic and old fashioned remedies.  I used to do peppermint oil rubs to the udder and give the doe an oral dose (about 60 ml) of her own milk – to hopefully stimulate an antibody response. I

Garlic cloves in water to make a “tea”

have recently added a common certified organic producer’s technique of orally dosing the animal with garlic “tea”. What a miracle it has been! We soaked peeled garlic cloves in water (be sure to keep refrigerated as botulism is a risk if not) then dosed the doe with 40-60ml 3x a day and her SCC went from 722,000 and 652,000 on the next test (the CMT showed a problem on one side) to, are you ready?  One thousand. Yup. Garlic. Thank you!

Some animals have chronic infections that even garlic cannot clear up. A milk sample should be sent to a certified lab for culture and if appropriate antibiotic therapy can be used. There are some dairy animals now, though, carrying the antibiotic resistant form of Staph aureus (Methicillin-resistant Staphylococcus aureus) these animals should, unfortunately, be culled – removed permanently (not simply passed to another herd!)


So no matter how you feel about the new SCC limit, I hope you will take your animal’s welfare and the quality of your milk so seriously that you will set your own standards. Try to not accept less than the best – no matter what the regulations say!

Making Yogurt to Feed Kids and Calves

Yogurt  not only provides valuable probiotic bacteria to the young ruminant, but it is easy to digest and can remain at room temperature in free choice bucket feeders without fear of growing unwanted pathogens. Making yogurt for kids and calves is a simple and inexpensive process. At Pholia Farm, we feed pasteurized goat milk and goat milk yogurt blended to a feedable consistency and served in free choice bucket feeders. We make the yogurt in the same manner as one would for personal consumption, but with a little less attention to details such as stray goat hairs and incubation temperature.  Here is how we do it:

  1. Heat milk to 180F
  2. Cool to 130F
  3. Stir in about 1-3 TB per gallon of yogurt from the previous batch or store purchased plain yogurt or use 1/2 tsp of powdered yogurt culture (purchased from a culture supply company such as Dairy Connection)
  4. Place pot in an ice chest to hold temperature- add 125 F water for better temperature control. Even easier, you can simply leave the pot to sit on the counter if the room is fairly warm. The resulting yogurt won’t be quite as thick, but it will work for kids.
  5. After 12 hours the yogurt should be set.
  6. Store in refrigerator.
  7. Don’t forget to retain a bit to start your next batch!

There you have it, bon appetit to your young animals!

Feeding Kids with the Free-Choice, Cool Milk Method- Peace in the Barn!

A few years ago we attempted to raise our Nigerian Dwarf kids on the “cool milk, free-choice” method. This way of feeding kids involves providing full time access to a bucket feeder, or other mechanical nursing unit, stocked with cold or cool milk. The idea behind the method is twofold. First-that kids will not overeat when the milk is cool, and second 24 hour access means they will eat frequent small meals, instead of three or four larger bottle fed meals spaced throughout the day. The end result being an unstressed kid who is also less likely to suffer some of the digestive issues associated with  bottle raising.

Unfortunately, our kids became quite chubby and also had trouble making the switch to solids. By weaning time, we had them back on scheduled feedings in an attempt to increase their intake of roughage. I even tried diluting the milk with an electrolyte solution to keep their weight down. That worked, but the resulting volume of urine meant a lot more pen cleaning and ammonia fumes. So we gave up.

I decided to take another look at what could be done to make this method work for us.  I had loved how quiet the kids were when not hungry between bottle feedings. Not only quiet, but they didn’t mob and molest you every time you entered the pen. You could hold and cuddle a kid without risking a fat lip from their flailing heads and hooves down your shirt as their little legs frantically tried to get them closer to that bottle they just knew you had hidden somewhere. I also wanted to decrease the stress a kid experiences during it’s first two months.

Part of our problem had been coming up with a feeder bucket with nipples that the small mouths of Nigerian Dwarf kids could both start on and continue. Red, Pritchard type nipples are just the right size to start these kids on, but our attempts to make them work on a bucket feeder (as directed by companies selling them as usable on a ball valve, square pale type feeder) failed. No matter what we did, the milk leaked out.  In our first attempt we started them on the Pritchard type nipples mounted on a bucket with a small amount of milk (not enough to cover the top the tube on the inside) and then switched them over to the latex nipples designed to go on these bucket types. (See photo). The latex nipples, however, were often the victim of over eager babies trying to figure them out and would “blow out” at the tips, spilling milk everywhere.  The red, rubber versions were much sturdier, but too stiff for the young goats to figure out. “Caprine” type nipples (the long gray or black kind that fit over a soda pop bottle- or beer bottle as I discovered) were too long for all but the older kids. Too bad, as this type is great for a bucket feeder with a long tube that goes down into the milk.  

Last fall I took a new look at the valve set up for the bottom feeding style of bucket feeders. I wondered if I could add a straw type tube to the inside and drill the holes higher in the bucket. I tried it. It was tough to find a small hose that would fit over the tips, but I finally found latex tubing that I could just barely stretch over the tube. I drilled holes in a new square bucket about one third of the way up and fitted the valves with Pritchard nipples. I put water in the bucket and then, guess what, I tested it and got a nice mouthfull of water!  Pritchard nipples have a little metal valve that provides an air vent, so I sealed these with silicone so that milk would stay in the straw- making it easier for the kids to nurse. Armed with this new type of bucket feeder I  was ready for spring.

We start the kids out on their mom’s for 3 days. Then we switch them to bottles using Pritchard nipples. When they are taking these well, they are placed in a pen with a bucket feeder stocked with warm milk. After they are comfortable with this setting, we let the milk cool and simply let them work through the adjustment. At about four weeks of age, they move to a pen with two larger nipples, a caprine style and a latex lamb bar (see photo above) type nipple. It usually takes a couple times showing them how to use these (I don’t actually demonstrate this myself…) and then they figure it out just fine.  At weaning time, they are moved to a new pen without a bucket feeder, but with a once a day pail of warm water with probiotic powder and  a pinch of electrolytes.

In addition to milk, we feed our kids homemade goat milk yogurt. (I learned this feeding style from the wonderful Jennifer Bice of Redwood Hill Farm). The yogurt is not only great for their health, but when using the cool milk method, it also provides protection from unwanted bacterial growth by acidifying the milk. Not only that, but it makes it thicker and  slows the hungry little buggers down even more!

Between the new buckets and the yogurt mixture, this years kids are quieter, calmer, look great and best of all, not little fatties!

There are some downsides to free choice feeding: You cannot accurately feed a coccidiostat in the milk and must instead medicate them separately; you will waste some milk when the bucket feeder is emptied daily for cleaning (be sure this is done thoroughly to prevent sickness in the kids); and you will end up with a lot of unused baby bottles.



The De-Horning Dilemma

The De-Horning Dilemma

A few weeks ago I was bumming around on, reading a few of the reviews that readers can post after reading (hopefully thoroughly) someone’s book.  The particular author in whose reviews I was snooping around is a favorite of mine. His book on life with goats is particularly poetic and at the same time realistic and accurate. It is a classic. One of the reviewers wrote of the author’s “barbaric and cruel” treatment of his goats, as he had dis-budded (removed the horn buds of the young kids before actual horns could grow) and fed the babies on a bottle instead of letting the mother raise them. She, as a way of presenting her credentials, cited her own experience with goats.

Do Goats and Cows Really Need to be Disbudded?

For many non-farmers or hobbyists with a strong urban background, the de-horning (or more likely “dis-budding”) of goats and cows that would otherwise grow horns (some animals are born without horns – “polled”) might seem inhumane and even, as the reviewer above said, barbaric. At some level they have a point, but for most domestic livestock, horns are more liability than asset. Now, of course there are some folks out there who would argue that animals should never be kept in captivity and therefore there is no situation when dehorning or disbudding should be performed. If these folks are living on this planet without having any impact to the land, its animals, and the other humans, then I applaud them and admit their superiority. Of course they can’t be doing that and ever read this, so I guess they’ll never know of my admiration.

For goats in the wild, or more primitive domestic settings, horns serve several purposes: First as a means of defense against predators, second as a way to radiate excess body heat when temperatures are high, and lastly as a way to reach that really-itchy-spot between their shoulder blades. For most domesticated goats, though, horns present several life threatening and quality of life issues: The most concerning issue is that horns lead to becoming entrapped in fencing- it is easy to stick one’s head through the fence when horns are present, but all but impossible to extract. When trapped in a fence several horrible things can happen to the animal including becoming a meal for a large predator or having the horn broken off at the base and bleeding, even to death. In the best outcome, the animal must simply be rescued from the fence. But while trapped, they are stressed from being vulnerable and easy targets for other, more dominant herdmates to torment and physically abuse. Then next, only slightly less important issue that horned animals pose is accidental and intentional injury to other goats and to their human handlers. While this can be avoided to a great degree, all of us, who have had goats for any length of time, have a story of being nearly blinded by a goat accidentally hitting our faces with a horn. Some more obstinate goats (What? Goats can be stubborn?) even learn to use their horns as a way to avoid being worked with. Bucks (intact male goats) are especially notorious for this type of behavior.

For the breeder of registered dairy goats, horns limit the animal’s future in another  fashion. In order to enter the ring of a goat show (where prizes can be won that will help the breeder find superior homes for other members of the goat herd and where the breeder can learn more about improving their animals through choosing better genetic traits) dairy goats may not have horns. If animals are not disbudded within a few weeks of birth, then removing horns can be a risky prospect. While many people have no intention of showing their goats, the next owner (and every animal, no matter how loved, is a heartbeat away from a new owner) may not only want to show the goat, but may also have fencing and housing where goats can be harmed.

All that being said, I know several people who quite successfully keep their goats horned. They use electric fencing or large, open range and manage smaller herds. They often use the goats as pack animals, and then the asset of having horns to help lose body heat outweighs the hazards. They also discriminately choose animals with gentle dispositions. So it is possible!

Disbudding in the Most Humane Manner

For those of us who believe that a hornless animal has the best hope for a humane and happy future, the dilemma becomes how to remove the horn growth in the kindest fashion possible. In order to choose the least traumatic method, the goat’s psyche and natural instincts need to be considered. You cannot view it from the standpoint of a predator- any species that naturally eats other animals (that’s us) .Predator and prey animals deal with pain and fear in different fashions.  If you happen to be aware of the writing and teaching of Temple Grandin (whose groundbreaking work studying animal responses as compared to her own autism has led to great changes in how meat animals are managed, especially during slaughter), then you might have already contemplated the fact that for a prey animal fear can be more traumatic than pain. (When compared to predators such as humans, dogs, and cats). Remember all animals feel pain, but the response to pain- in actions, heart rate, blood pressure, etc. is less than a similar pain situation for a human. The opposite is true for fear. When a prey animal is put in a situation of danger- being threatened by a dog, a human yelling and striking at the animal, or being chased, their response- heat rate, blood pressure, etc.- is greater than you would typically see for a human or other predator animal in the same situation.

So how can you use this knowledge to ease the suffering of goats and calves during the procedure of disbudding?

First, let’s review the most common method of disbudding. The quickest, most effective way to disbude involves the use of a hot iron with a circular shaped tip. The iron is heated to approximately 700° F or hotter. If the iron is not hot enough, then it might be held to the head too long and over-heat the skull,  causing damage to the young animal’s brain. It will also not effectively kill the cells that will produce horn growth. So burning-hot-iron-applied-to-animal’s-head. Doesn’t sound too nice, does it? In addition to recalling the knowledge of how an animal handles pain, you must remind yourself that the goat and cow’s skull is designed to take quite a beating (literally) when the animals play and fight by butting each other (goats do this more than cows). When the iron is applied at the right temperature, the procedure is over in a matter of seconds. Recovery time (as measured by vital signs- heart rate and blood pressure) is extremely rapid.

A common electric disbudding iron, the Rhinehart X50 with calf size tip.

The procedure can be made even less traumatic through a few simple choices that address the fear factor of being held down as well as any residual pain that the animal will feel (even if they don’t show the effects of pain the same as you and I would).  To help reduce anxiety and fear, the following things should be addressed:

  1. Is the animal afraid of you and fearful of being handled?
  2. Can you provide a low stress environment where the procedure is to be done? For example, the area should be near their usual housing, free of other fears such as dogs, loud noises, etc.
  3. Are you competent in performing the procedure? Quick, confident action will provide the shortest exposure to pain and fear.
  4. Can the animal be restrained in the least traumatic, most comfortable fashion?
  5. Can the animal be returned to a low stress, comforting situation? For example, if the kid or calf can return to a pen with its litter or pen mates or mother or be given a bottle of milk, then anxiety will be reduced. Be aware that it is not uncommon for mothers to temporarily or permanently reject a recently disbudded baby due to the scent change. If the mother rejects the baby, then stress will be increased.

Using Pain Medication, Sedation, and other Pain Reduction Methods

Here at Pholia Farm we sedate (put to sleep) the kids during the procedure. We use a medication that is legal for the veterinarian to prescribe to the producers they feel are accomplished in accurately dosing strong medications as well as monitoring the vital signs of the animal. If I was only disbudding, I might not choose to do this, but we also tattoo the kids at the same time. Tattooing seems to be equally or more painful to the young kid, so for us it makes sense to provide the least fear and pain possible.   Many breeders choose not to sedate as when the kid awakes, they are disoriented and seem quite anxious. In that case, it makes sense, given what I talked about earlier, that it is likely that the groggy state caused by the medication might be more traumatic for the animal than the brief moment of strong pain. Fortunately, we figured out a simple remedy for this. After the procedure is finished we place the kid in a small pen with other “sleeping” kids and cover it to keep the space dark. The kids wake feeling safe and quiet- making almost no sounds and recovering fully without any apparent signs of stress. If you are interested in using sedation, you will need to first become competent in other areas of herd management and then develop a plan with your veterinarian.

Analgesics (pain killers) can be given to young animals about 30 minutes before the procedure to help minimize the after effects of the burning. Again, you should consult your veterinarian to decide upon the medication and dosage.

A cool, antiseptic (kills bacteria) spray should be applied immediately after the procedure is completed (as each bud is finished burning, spray that area). This will help cool the animals head.  Some people also use an icepack to apply to the head of the animal.

Again, distracting the baby with a bottle of milk or nursing on their mother, will help shift them away from any fear or anxiety that had been being experienced.

Public Perceptions

However you decide to approach the horn issue, you owe it to your animals and the survivability of small farms to both educate the public and deal with the issue in the most civilized, humane approach possible. Beware of treating the concerns of others with a cavalier attitude- nothing good will come of such an approach. Even with the right attitude, keep in mind that many people are greatly distanced from any of the less savory realities that most farmers deal with without a second thought. People cannot be exposed too suddenly to things that they might not understand or be able to put into context. Even watching a live birth, without any complications, can be too traumatic for some people. So be alert, be aware, be knowledgeable, and be kind!

Doing your own Plate Counts

I finally plugged in the little petri-film incubator we purchased from Nelson Jameson and I am, at the moment, cooking our first anaerobic plate counts.  It took me a long time to get around to this, but I think it will go a long way toward making sure our milk is super clean, as well as our process.

The films must incubate for 48 hours, so I don’t have any exciting things to share with you guys, other than I am pleased that I finally tried it!  My friend at Rogue Creamery, Shawn Fells, showed me how to do these simple, on-site quality tests for milk and environment, but I was still intimidated, I have to admit! Turns out it is as easy as squirting 1ml of milk on a plate and sticking it in to cook (much simpler than making dinner, right?).

I’ll write a full description of how to do it (maybe a YouTube video for you all too?) once I figure it out and have a better idea on how to implement it as a part of our quality assurance program.

Oh, the little incubator was under 100.00 and the plates are about 7.00 each. Still cheaper than shipping samples out for testing (or having your inspector let you know your milk is not as clean as hoped).

So pictures and updates to come, unless I botched the entire process….

Mycoplasma, The Lurking Menace

Every few weeks I receive a phone call, email, or a FAX from someone in the US with a goat kid (dead or alive) with a diagnosed case of mycoplasma. They find me through finding online an article I wrote in 2008 about our experiences with the disease. I am sharing the article again here along with an added Q&A section that follows the article. I based the Q &A on the most common questions I get from these folks. I always remind people, of course, that I am not a veterinarian, but as many have found out, just because you are consulting a licensed DVM does not mean that you will get all of the correct answers. Still, you should always work with a vet you trust and that will do some research and stay current with updates regarding the disease. There, enough disclaimers!  Here is the old article:

Mycoplasma: This Time it’s Personal!

By Gianaclis Caldwell

Appearing in Dairy Goat Journal, Volume 86 Number 6, Nov/Dec 2008

 Authors Note:  The author is not a veterinarian. All references to medications used in this article are for reference only as they relate to the author’s personal experience.  Please consult a licensed veterinarian when dealing with this or any other medical problem.

Mycoplasma is one of those diseases that most goat owners have heard of, but may not be able to tell you much about.  Like so many problems, until it threatens your own animals, it remains a word in a book, a definition waiting to be looked up.  Unfortunately, I know a lot more about mycoplasma than I would like to known thanks to the pathogen calling on our herd in the spring of 2005.

 Before I tell the story of our own loss and learning, let me give you a short course on mycoplasma.  I would first like to reassure you that mycoplasma is not the killer that it once was. The microorganism has apparently lost much of its virulence. Also, it poses no threat to humans, either in the milk or via the carrier animal. So please read on without too much trepidation!

Mycoplasma – In a Nut-Shell

Mycoplasmas are simple microbial organisms (not true bacteria or viruses) that lack a true cell wall.  While this makes it sound as if they should be easy to be rid of unfortunately they are not.  Most antibiotics work by attacking the cell wall, thus destroying the microorganism.  Since mycoplasmas do not have a cell wall, not as many antibiotics are effective against them.

There are many members in the mycoplasma family.  The most common typically cause mastitis and respiratory problems.  Many animals never sicken after exposure, but remain capable of passing the pathogen to their offspring in their milk (the most common route of transmission). While many adults can remain asymptomatic, kids, especially those under stress, are the most susceptible to becoming ill after exposure.

Another problematic aspect is that there are no laboratory tests that guarantee your animals are mycoplasma free. The pathogen is capable of lurking undetected within an asymptomatic host.  Unless an animal is “shedding” during the test your results will be negative. So while you may never have had any animals ill or with symptoms of mycoplasma, you cannot kno w for sure that your herd is mycoplasma free.  Only when symptoms appear AND are tests are done specifically for mycoplasma will you know.  Not a very cooperative little pathogen, is it?

The Stealth Killer

Even when an animal has symptoms that might be indicative of mycoplasma, it could easily be a bacterial or viral problem- and more often than not it will be.  So you might treat the animal for what you think is pneumonia, joint-ill, or bacterial mastitis.  The animal recovers and you never know that it might have been mycoplasma.  Here’s an example using one kid with 3 different treatment approaches:

Scenario 1: A six week old wether kid goes off his feed.  You watch him, he looks okay so you wait until the next morning. You take his temp.  It is 105.3. You give him a little Banamine (a pain killer, and fevere reducer) and check your antibiotic stock.  If you are like most of us, you have LA 200 or Biomycin (both are oxytetracyline) on hand.  You double check the dosage for this age and weight and start him on a course of treatment.

He is still taking his bottle, although with less than a kid’s usual vigor, and his temperatuire is dropping. He doesn’t like to stand up, but you figure he is just feeling poorly. By the next day, the antibiotics and Banamine seem to be helping. His temp is down and he is back to eating well.  You figure he had a touch of pneumonia.  You continue with the oxytetracycline and he recovers completely, never having any more problems.

Scenario 2:  Your six week old wether goes off his feed.  You watch him and he looks okay, but the next morning he looks a little listless.  You take his temp, it is 105.3.  You give him a little Banamine and call your vet.  You also notice that he doesn’t seem to want to stand up.  After closer inspection, you see that his knees are a bit swollen, or is it your imagination?- they are not soft and squishy, and he is very fuzzy.  You mention all of this to your vet who suspects joint-ill (an infection that enters through the newborns umbilical cord). Even though you dipped his cord right after birth the vet says that it can still happen.  So he starts the kid on Naxcel (a newer, powerful antibiotic) and has you continue the Banamine.  You have the little guy in your house to watch him closely and keep him taking fluids.  By the next day, you think he is getting better, as his temp. is within normal at 103.2.  But he isn’t eating and seems so uncomfortable.  You keep up the antibiotics.  He won’t stand at all by the end of the day and it is obvious the joints are tender. If you bend his knees for him, he cries out in horrible pain.  That night, his temperature plummets, and he dies in your arms.

You are horribly sad, but know you have done all you can.  You let your vet know. He suggests a post-mortem joint fluid culture taken to rule out other possibilities.  He asks if the dam has had mastitis.  She hasn’t, so he suspects a bacterial infection which led to polyarthritis.  The cost for the culture is high, you don’t want to haul this dead kid to the vet, you have no other symptoms in your herd, so while you feel bad, your budget dictates that you pass on the cultures and bury him.

Scenario 3: A six week old wether kid goes off his feed a bit.  By morning he looks worse, so you take his temperature.  It is a elevated at 105.3.  He also seems a bit stiff when he moves.  You decide take him to the vet. The vet gives you the possible causes after she notices that his knee joints are tender.  One possibility is bacterial polyarthritis (also known as joint-ill), which she thinks is the most likely cause, even though his cord was properly dipped at birth. Since you have no mastitis in your herd, mycoplasma is not her first suspect.  But just to be sure, you decide to go ahead and have a joint fluid sample taken.  It is painful for the kid and you feel badly about the potential cost.  The vet shows you the fluid under the microscope it is obviously filled with pus, as it would be for bacterial polyarthritis.  You and the vet decide that a sample should be sent to a lab for culture, just to be sure.  The vet starts the baby on oxytetracyline (which is effective against mycoplasma) and sends you home with some Naxcel as well to switch to if he doesn’t improve.  The culture will take 7-10 days.     Fortunately the kid improves within a day or two. The bill is 250.00.

Then the culture comes back positive for mycoplasma.


Our Story

Our story is similar to both Scenario 2 and 3.  Our first kid to get sick was treated as was the kid in example two.  He was a little buckling that we were keeping intact and were quite impressed with. When he died it was very difficult, both from the standpoint of the loss of the potential as well as watching a creature suffer.  I know now that we didn’t have to lose him or let him suffer.  At the time I was convinced it was “joint-ill” as everything I read seemed to indicate that diagnosis and our vet thought so too.  It was only when a few weeks later that another kid, a little wether, developed the same symptoms that I felt there must be something else was going on.  Even then, I was very doubtful of it being mycoplasma.  We had never had a clinical case of mastitis.  We milk all of our does twice a day, even when they have kids on them part time, so we are quite aware of their udder health.  Everything I read and the vets that I talked to at the time, confirmed these feelings.  Then the test came back positive for mycoplasma.

 At first I felt like quitting the business.  We had THOUGHT our herd was so healthy.  We had THOUGHT we were free of any contagious pathogens.  We did annual CAE and Johnes testing, put tarps up at shows, hadn’t bought any new stock in some time, all of it.  I was humbled.

We decided to have the sample cultured farther to determine out what exact mycoplasma we were dealing with.  This took another few weeks and more funds.  We also took milk samples from all our does and had them cultured for mycoplasma as well.  Although, by this time we knew that the shedding of the microorganism can be intermittent and asymptomatic.  We also knew that there was a possibility that we had spread it to other does via the milking machine.  I felt so dismayed.  I wondered how we could deal with this and still enjoy the farm.

The milk samples all came back negative.  Nice in one way, not in another- at least a positive sample would have told us who our culprit was and given us something to act upon.

The joint fluid sample came back positive for Mycoplasma mycoides mycoides Large Colony (or MmmLC).  This is the one that I had come to suspect after spending the intervening weeks reading everything I could find on mycoplasmas.  It is also the one I hoped for (if you could hope for such a thing) as it seemed to be the least pathogenic of all of them.

Changes.  We had to make them.  We had to for our own assurance as well as for our buyers.  We started pulling kids at birth and feeding heat treated colostrum and pasteurized milk.  For the does in the milking string, we implemented a manual “back-flushing” regimen to sanitize the inflations between animals.  We had more samples of milk taken and cultured after all of the fall fresheners were milking. All samples are negative and none of the other spring kids that received mixed milk have ever sickened.

Our two kids that sickened, received commingled (mixed from the whole herd) raw milk. One of the does had to be an asympotomatic carrier.  She may never shed again, or she might.  Had she passed it to other kids who never sickened, but are now carriers as well?  We were suspicious of one doe whose SCC (somatic cell count) was higher than normal during the time the kids would have received her milk.  Her tests all come back negative, but we placed her in a pet home anyway.  We are now (at the time of writing) over three years out from our experience.  None of the other goats that received the mixed milk at the same time as the ones that were ill, have ever had any problems.  We continue to not allow their kids to nurse and if we feed commingled milk, it is always pasteurized.

Mycoplasma Arthritis- How it Happens

When a kid receives milk with the MmmLC in it, the mycoplasma most often attacks the joints first.  When this happens the kid’s temperature spikes (a spike means a sudden increase followed by a rapid decrease). The front knee joints are often the first to be effected, with firm swelling and seem painful to him when touched.  Their gait becomes tentative and stiff.  Very rapidly they become septic (a body-wide infection) and their temperature begins to drop (this is why you do not see extremely high temperatures with mycoplasma, it attacks so rapidly that their systems begin failing before their body can attack it with extended fever).  For the less observant herdkeeper, the kid can even look as though it has enterotoxemia- with its hunched posture and painful cries.

For all animals with mycoplasma in their system, including the asymptomatic ones, stress can cause an active, symptomatic case.  An unstressed animal can remain asymptomatic and healthy, but still shed the pathogen.

For our two kids, one developed it after a long transport (when you would also suspect “shipping fever” and might treat for that instead) and the other sickened just shortly after castration.  All others though, (seven kids in addition to these two) that received the same milk at the same time, and have never showed signs.  But we will suspect them as carriers and not ever feed their raw milk to their kids.

Other Stories

In doing the research for this article, I called upon other breeders who had experienced mycoplasma in their herds.  I received several private communications from breeders who have had proven cases of mycoplasma.

In all of the stories there was a common theme of unpredictability. For example, one doe had two kids with only one that sickened and died.  The other kid never showed symptoms and never passed it on to her kids, nor did that dam ever have any kids sicken from it.  In another small herd, one doe spiked a high SCC (somatic cell count) then died a few months later. Her necropsy cultures were positive for mycoplasma.  She apparently never passed it on to her adult herd-mates or to her kids. These breeders felt strongly that mycoplasma is very opportunistic..  It may be out there in many herds, but only strike the occasional animal that become stressed or are immune suppressed for some reason.

All of the breeders who kindly shared their experiences with me asked that they remain anonymous.  Due to the past virulence of the disease and the stigma associated with mycoplasma positive animals, they are hesitant to openly share their experiences. Understandably so.


We live in a world where disease can spread rapidly and cause great financial loss to farmers and breeders.  This fear of both the disease and the potential financial loss can lead to the lack of open information and therefore education for breeders.  By sharing our experience openly I knew that we might lose sales.  But I feel strongly that sharing information will lead to a healthier population of animals and a more informed buyer or breeder.

Given the fact that we had a “closed herd” that appeared vigorous and healthy yet one of the animals was a carrier, you can draw the conclusion that there must be many undocumented carriers of mycoplasma. Therefore, learning to identify the symptoms, prevent further spread, and gain knowledge of the organism is critical.  Even if it is never eliminated, suffering can be alleviated and losses cut if we know what we are dealing with.

Once you come to terms with the likelihood that many herds could have undetected mycoplasma carriers; that these carriers might never spread the disease; that if spread the disease is not the death sentence; and that you can implement a highly effective preventative program if you choose, then the fear changes to knowledge and power.  We owe it to our animals and to our fellow human-herdmates to share our experience.


Updates and Q&A

Q: Can the joint swelling be in only one knee?

A: Yes, recently veterinarians have diagnosed some cases of joint arthritis from mycoplasma in only one knee (front leg) or joint,of an animal. These cases were accompanied by the same symptoms of initial high fever, general malaise (not feeling good, no appetite, depressed attitude, etc), and death if not treated.

Q: I bought a doe whose adult daughter had kids who came down with mycoplasma. Should I assume the doe I bought (the mother of the dam whose kids got mycoplasma) is a carrier?

A: While you can’t know for certain, I think it would be wise to assume she is and consider not allowing her to raise her own babies. They should not nurse from her or be fed any un-heat treated colostrum or unpasteurized milk.

Q: Can a buck infect a doe through his semen?

A: To my knowledge passing of MmmLC (the type that seems to be the most common here in the US and the only type I have any experience with) is primarily passed through the milk of a carrier doe who is shedding the microorganism. In theory it can be passed other ways, but that seems to be quite rare. We still have a doe that was symptomatic as a kid (the full sister of the little buck that died here in 2005 from the disease). She has never been allowed to nurse her kids and we continue to pasteurize all milk fed to kids that is not from their mom’s only, but she is not segregated from the herd in any way. We have not had any cases since 2005.

Q: I suddenly had three cases of mycoplasma in kids this spring, but I have had all of the mom’s for many years, how is that possible?

A: It is entirely possible for a doe to not shed the microorganism until something causes extra stress, and then the babies have to be nursing her (or you feed the milk to them raw) at the same time.  This is why it is so difficult to be able to say that it is not present in your herd. For all we know, we all have a carrier or two, and they may never shed it, or the kids could become carriers but not have any symptoms.

Q: Our vet told us to give the kids (from a doe that we worry might be a carrier, although she has never had any symptoms) a shot of LA 200 (oxytetracycline) to make sure that they don’t get mycoplasma, does that make sense?

A: I am never in favor of giving antibiotics without any diagnosis, especially just one treatment. You are in essence exposing every microbe in the animal’s body to an ineffective dose that will only cause the ones that you want to kill (someday) to grow a bit more resistant. If the kid does have mycoplasma, one treatment won’t kill it off, and even if the kid has an active case and you treat them with a full course, you are not going to get rid of all of the microorganisms, they will still be a carrier. So it makes more sense to be observant and watch these kids for symptoms and then treat them properly.  Also, don’t forget to feed probiotics when giving any antibiotics.

Q: Speaking of probiotics, won’t giving those at the same time as antibiotics kill the antibiotic?

A: No, probiotics do not kill off antibiotics, they simply help replace some of the good bacteria in the animals digestive tract that the antibiotic will be killing.

Q: What is your best advice if I am worried about having mycoplasma in my herd?

A: First, be observant for the symptoms. Second, only feed the raw milk and colostrum of any mother to her own kids (that is assuming she is free of other diseases transmitted via milk). Last, if you feed milk from more than one mom to a group of kids, always pasteurize it.  I think I am hearing so much more about mycoplasm because, as people’s herds become free of CAE, they are beginning to feed raw milk to kids again. I think this is just proof that mycoplasma has never gone away and never will.