Author’s note: I am not a veterinarian. All references to medications used in this article are for reference only as they relate to my 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 know 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. So please read on without too much trepidation!
MycoplasmaIn 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 a-symptomatic 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 know for sure that your herd is mycoplasma free. Only when symptoms appear and 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 problemand 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 three 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°F. You give him a little Banamine (a pain killer and fever 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 temperature 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°F. 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 swollenor 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 newborn’s 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 range at 103.2°F. 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 an elevated at 105.3°F. He also seems a bit stiff when he moves. You decide to 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.
Then the culture comes back positive for mycoplasma.
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 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 further to determine 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 anotherat 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 asymptomatic 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 came 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 affected, with firm swelling, and seem painful 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 (seven kids in addition to these two) that received the same milk at the same time, have never showed signs. But we will suspect them as carriers and not ever feed their raw milk to their kids.
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 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 becomes stressed or is 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.
Gianaclis, along with her husband Vern and their daughter Amelia, own Pholia Farm Nigerians and Pholia Farm Creamery, LLC in Rogue River, Oregon.