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For The Love Of Goats
What is the difference between a controlled study and observations that you make on your farm? In this episode, I’m talking to Joan Burke, Ph.D., who has been researching alternative dewormers in small ruminants for about two decades.
In addition to talking about some of her parasite research, we also are debunking some myths that you may have heard. Plus we are talking about the importance of randomly assigning goats to a control group (that receives nothing) to compare to a treatment group, as well as a few others important factors involved in figuring out what treatment caused what response.
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TRANSCRIPT – Basics of Goat Research
Deborah Niemann 0:18
Hello, everyone, and welcome to another episode. I am very excited today to welcome back to the show Dr. Joan Burke from the USDA Research Center in Booneville, Arkansas. Welcome back, Joan!
Joan Burke 0:32
Thanks, Deborah. It’s good to be back.
Deborah Niemann 0:35
So last time we talked, we were talking about all the research that you’ve done on copper oxide wire particles in, like, the last 15+ years, which has made a huge difference for my herd and, I know, the herds of many other people who have dealt with dewormer resistance and barber pole worms. And, one of the things that I face repeatedly when people ask me a question on social media, or they send me an email or something, is, you know, like, they’ve clearly got a problem. And I will say, “Well, it sounds like your goat needs to be dewormed.” And then they say, “Oh, no, I’m not going to do that. The last time I used ‘Dewormer X,’ my goat died.” And then I proceed to try to explain to them, “Well, that dewormer did not kill your goat. Your goat died, probably from worms, but it did not die from that dewormer.” So I want to talk about: What is the difference between research that you do and what people do in their own herds, like, the kind of experiences they have? And so, let’s get started by just talking about, like, how do we know whether or not a treatment that is given to a goat works? How do we figure out those things?
Joan Burke 1:53
A great question. So, sometimes we provide a treatment to our goats. And we think it’s worked. For example, diatomaceous earth. That’s one I get questions on a lot. Diatomaceous earth is fed to goats in a feed supplement as a dewormer, or whatever. Sometimes people feed it for lots of different reasons. And then they say, “The goat looks great, so it works on my farm.” So even if we measure fecal egg count, and the fecal egg count is reduced in these animals getting—I’m going to call it D.E.—we don’t really know that the D.E. treatment worked unless we have a control to compare it with. So, in that regard, a treatment administered to a goat to help her feel better is similar to an experimental treatment given to obtain change in animals. So, my research largely deals with parasite control, health interventions, and improved production, so I’m going to kind of stick with those examples here. So, for experimental treatments, and perhaps farm treatments, we need replicates, because sometimes an animal gets better, or has lower fecal egg count on her own, because her… For whatever reason, her immune system has improved, regardless of whether she was treated or not. So, ideally, we want a group of treated and a group of untreated goats, then we can do a statistical comparison of the means before and after treatment. So this applies even to dewormers like ivermectin; it’s the same concept. If we dose an animal using, in this case, twice the recommended label dose for sheep, because that’s what the American Consortium for Small Ruminant Parasite Control, recommends, and fecal egg counts are reduced—again, we don’t know if it was because the dewormer worked or if she improved because her immune system helped. So, maybe we’re doing some other things to help that. And, of course, we used to be able to rely on the efficacy of a dewarmer, but because of the dewormer resistance of worms, we no longer can, especially in goats, because goats’ immune systems are not very good in that regard.
Joan Burke 3:57
So let me give another example in case that wasn’t quite clear. Let’s say you wanted to know if feeding flaxseed meal to goats improved their health. How would you know if there were improvements? Again, you need a control group and a flaxseed group. It’s best to feed individually, which isn’t always practical. It’s kind of easy with dairy goats, because you bring them in, and you can give them the treatment while they’re milking, but not always practical for meat goats. So you know all of the flaxseed animals get the same amount per unit body weight, compared to the standard feed diet you used before the flaxseed. And classical scientists will say that fat and calories and everything between the two diets has to be identical, except, you know, whatever you’re comparing. But, obviously, that’s not practical on a farm, but we do the best we can. Then you need to consider: What are you going to measure so you know has she been improving? Body weight? You need a scale. Body condition scores? That’s easy enough to do. You can learn how to do body condition scores. Reduced health treatments? Might include reduced amount of antibiotic or dewormer. You could do coat score. Look at, you know, the quality of the coat, the shininess… Again, it’s impossible to say that a treatment works unless you have something to compare it with. So, without sound scientific evidence, we might say there’s anecdotal evidence for a product to make improvements, and sometimes a scientist will use the anecdotal evidence to build justification to conduct an experiment. And I’ve done a lot of that, in my research. I’ll listen to producers when I’m giving talks at conferences, and I’ll say, “Gosh, you know, I’d like to test that. So, I’m going to take their anecdotal evidence and conduct a sound scientific experiment.”
Deborah Niemann 5:43
Oh, I know. I think one of the ones that you did that you hear a lot of anecdotal evidence is, like, on herbal dewormers. And I know that you actually did a control study with Molly’s Herbals dewormer, where you had a control group that did not get it, and then a group that did get it. And then you compared the outcome of the two groups.
Joan Burke 6:07
Yeah. And we also did a D.E. study, too.
Deborah Niemann 6:09
So, one of the things now that I think is really, really. super important that I want you to talk about is the difference between correlation and cause and effect. Because, you know, like, those people who contact me and say, “Oh, I’m not going to use ‘Dewormer X’ again, because the last time I used it, my goat died.” They’re just looking at a correlation and assuming that, you know, X caused Y. And, that is not always the case. So, can you talk about that a little bit?
Joan Burke 6:43
Yeah, yeah. Cause and effect. So, worms cause disease. That’s the effect. Dewormer kills worms. Flaxseed increases pregnancy rate—I actually don’t know if that’s true, but that’s just an example. People who red meat get cancer. I’m sure you’ve read that somewhere along the way. Sometimes we think we know the cause of the effect, but unless we can control all of the variables, we may not. Could be that people who eat red meat drink more alcohol, or eat more protein, or eat barbecued meat with bits of charred meat and seasoning and maybe there’s some toxins that occur from that, or maybe they eat more potato chips. So unless we can preassign the diet, or the treatment, we can’t know for sure what causes the effect, especially in an observational study. And that really includes most human studies. Here’s another example: If I get my goat a dose of ivermectin—or it might be copper oxide wire particles, or whatever—she’ll die. And yes, I’ve heard this from veterinarians about copper wire. If the goat really died, we cannot know if it was the ivermectin or the copper wire that caused the death. Or, maybe there was a very large load of worms in her gut. So, that’s why we have to have a controlled study of ivermectin treatment in a group of uniformly wormy goats. And I know that’s not always practical on farm. I mean, farmers are focused on production. But, just so you can understand why you can’t say, “Ivermectin killed my goat.” So, we want to characterize what’s going on before the animal is treated. And so we look at the outcome or measures post-treatment. Perhaps look at the proportion of animals that are dewormed that died because they were given treatment too late. We can know that by how anemic the goats were, by measuring the proportion of red blood cells, so… Or FAMACHA scores. Too few red blood cells means that the animal is anemic, and that is caused by the blood-sucking barber pole worm or Haemonchus contortus.
Joan Burke 8:53
Let’s just clarify what happens when a goat is dewormed. So this is more on the cause and effect. First, let’s understand part of the lifecycle of barber pole worm. So, goats ingest infected larvae from pasture or grass. The larva is encased in a protective sheath, which… That comes off once she ingests that in the rumen. This developing worm passes to the abomasum, or the true stomach, of the goat. And both the larval and the adult phases of the worm suck blood. And both of these sucks blood by scratching the surface of the mucosa of the stomach. So the animal will bleed a small—so it scratches it. So it doesn’t sit there and form these suckers on the animal; it scratches. The animal will bleed a small amount, and then the worm or the larva can consume that. And animals can lose as much as 2/10 to 1/2 mil of blood per day per worm. So that’s what causes anemia. Some dewormers target only the adults, such as levamisole and copper wire, whereas other—if they were fully efficacious—target both the adult and developing larvae. So that would be ivermectin, Panacur, and Safe-Guard, for example. So, generally speaking, an effective dewormer will kill the worm, and then the worm’s digested into the gut. So, it’s not like we deworm, they all come off, and come out in the poop. It’s not like that at all. So, of course, we now know, especially in goats due to dewormer resistance, all worms won’t be killed and will survive treatment. The greater the dewormer resistance, the fewer worms will be killed, thus dispelling the misconception that ivermectin will cause worms and release all of them at the same time, and then the goat will bleed to death. And that simply can’t happen. However, if there’s too many worms—too many barber pole worms—a goat can bleed to death. As I said, 2/10 to 1/2 mil blood per day, and you’ve got thousands of worms in there, she can bleed to death from worms.
Joan Burke 11:04
Sometimes, there’s published reports based on observational studies. So, as I said, in human studies, a lot of those are observational studies. Here’s an example of an observational study that I conducted. It’s not published, and I’ll explain why. So, I gathered data over a two-year period on deworming lambs. So, lambs were based on FAMACHA scores. If the FAMACHA score was three, the lamb got only copper wire particles. If the FAMACHA score was four, then she got a two-way combination: copper wire and a dewormer. And if the FAMACHA was a five, then she got a three-way combination: copper wire and two different dewormers from a different class. It’s an observational study, because treatments were not assigned ahead of time or randomly assigned. I used the untreated lambs as a negative control. But again, it wasn’t assigned ahead of time. The fecal egg count and level of anemia were much higher in the three-way treatment than the two-way or the copper alone. And that kind of makes sense, because we know that FAMACHA scores and level of anemia are correlated. So, ideally, when an experiment begins, you want the means of each group to be the same. A study like this can’t be published in a scientific journal, because there’s no randomization or proper control. However, we could use this study as preliminary data and then conduct a study with animals randomly assigned to the three treatments. So, I can include this in my report, but I’ve got to have something to back up the treatments that are randomly assigned to the groups. So, you asked about correlations. So, we know from scientific studies that fecal egg count and FAMACHA scores and anemia are correlated. Fecal egg counts and FAMACHA scores are positively correlated, so as one goes up, the other goes up. And we looked at thousands of observations to statistically determine that correlation was significant. So, we can’t just look at ten animals and kind of get a feel whether it’s correlated or not. I mean, it takes a lot of observations to really find something significant. An obvious correlation—another one—is body weight and body condition. So, obviously, when you consider animals of similar age, reproductive stage, or feeding group, you kind of get a feeling in your mind, “Okay, as body weight increases, the body condition is going to increase.” So they’re positively correlated, again. And body condition score and pregnancy rate are also positively correlated. And that’s why we recommend flushing before we breed animals, to increase pregnancy rate and increase ovulation, right? So as one goes up, the other goes up, or vice versa.
Deborah Niemann 13:50
Oh, that’s great. Thank you for explaining all of that. Those are all a lot of really good examples. And I’m really glad that you talked about that myth about ivermectin causing animals to bleed to death, because that is, unfortunately, something that I see get repeated quite a lot, that if a goat has a really, really bad case of barber pole worm, and you give them oral ivermectin, that all of the worms will release at one time and the goat will bleed to death. When you… I mean, like, you just explained how that is impossible, because they’re not… barber pole worms are not like leeches that sit there and just suck blood all day.
Joan Burke 14:27
Yep. They’ll scratch the surface several times, but they don’t sit there and just latch on.
Deborah Niemann 14:34
So, another thing that I think is, like, really important for people to understand is the possibility of conflicting variables, because, you know, like, I get emails and messages from people who have said things like, “Oh, my mentor in Arizona says there is no such thing as dewormer resistance.” And I’m like, “Well, you know, in Arizona, people don’t have trouble with barber pole worms. So, I have no doubt that your mentor does not have a problem with worms. And, if she’s doing all these things like deworming regularly, that’s not controlling her worms. Like, she’s just wasting her money, because barber pole worms thrive in wet, grassy environments, not in the middle of a desert.” So, can you talk a little bit about either conflicting variables or, like, other factors that are important to consider when you’re trying to figure out a valid experimental approach?
Joan Burke 15:34
Yeah, and considering conflicting variables… So, as I mentioned earlier, the immune system of goats isn’t as good as other livestock species, because goats were raised in the desert. So they didn’t have to adapt to worms. And, when they were exposed to worms, you know, in their natural environment, they choose to eat browse, so up away from where the worms are. But, when we force them to eat grass, it’s a whole different story. And you mentioned not having worms in, you know, a lot of the western states. There are worms on irrigated pastures. But otherwise, when we talk about worm control, we have to think of the environment that we’re in. And I suppose, you know, there’s other variables in an experimental study that we have to consider. So, we have to be practical when we listen to recommendations. Does this apply to me? Am I in the middle of a desert? Do I have to worry about worms? No. Or, even if you’re in a Mediterranean climate, let’s say if you’re in Oregon or Washington, you’re not going to have the same parasites and the same parasite issues as people in the Southeast or, again, on irrigated pastures.
Joan Burke 16:50
And, to answer the rest of the question, you know, what are other important factors to consider in experiments: As I mentioned earlier, we want the experimental groups to be as uniform as possible. So, we don’t want to compare a group of goat kids versus nannies. So, you know, “Well, I was feeding my animals the other day, and I noticed that the goat kids, they just really didn’t look good. But the nannies in a different group on the pasture, they look great. So that pasture must be much better.” You have to consider, well, the goat kids, they’re growing, they’re more susceptible to parasites; it might not have anything to do with pasture at all. You know, their body weight and their production phases are going to be different, their immune system is going to be different. So, similarly, we don’t want to compare a group of buck kids to doe kids, because the buck kids are going to be fighting, more active. And we have to be careful, even when we have them in the same group comparing buck kids to doe kids, because the bucks are—as anyone who has goats knows—they’re gonna harass the females, whether they’re adult or young does. So, yeah, we have to be careful of considering all the different variables in the animals that we want to compare. And, you know, I mentioned about breeds. Let’s say we’re conducting a study, and we’ve got Boer goats and Spanish goats, and, it’s okay to have them on the same treatment, as long as your treatment versus control has similar numbers. But be careful about favoring one. Let’s say I like spotted goats, so I’m going to treat the spotted goats more special. If you think about it, you know in your mind you don’t want to do that, because just treating them special is going to make her feel good. And maybe she’ll get the extra handout that you have in your hand, or whatever. And, the last thing, I talked about randomization. You know, why do we randomize animals to treatment? And again, using that example in my observational study with the copper wire and the two-way or three-way deworming treatment—they were not randomized. And so the outcome is going to be different, even before the treatments administered. You know, we can affect the outcome of the experiment.
Deborah Niemann 19:07
That was great. This is a lot of really good information. One of the things that I know, and this is, like, a really embarrassing story to tell, because I started reading your research, and all of the other research of the Consortium, back well over 10 years ago when we had dewormer resistance in our herd. And the dewormers were not working anymore. And I decided to do my own little study, and came up with some horrible conclusions., because I did not randomize my groups. And, I have a master’s degree, and I took courses in research design, and I knew when I did this, like, my professors in grad school never would have approved this study, because there was no randomization of groups. And I don’t even remember what my groups were anymore, but I do remember the first one was all the goats that kidded in January were going to get D.E. And all the goats that kidded in February we’re going to get… I think maybe it was an herbal one. And then, in March, something else, and in April, they were going to get Cydectin. And then, in May, they were going to get nothing. That was going to be my control group! And, I’m in Illinois, you know, and I even said this—because I wrote this in my blog, my old blog. And I said that, “I know people might say that there’s some effect on which month a doe kids, but I’ve never noticed it before. And I’m sure I would have noticed it if there was, so I’m not really worried about having a conflicting variable.” But, the reality is, that’s exactly what happened. Because, like, all the January goats did great. So I’m like, “Wow, that means the D.E. works.” And then the February goats, you know, almost as good, but not quite. And I’m like, “Oh, the herbal dewormer works, too, but not quite as good.” And then, you know, like, by April, it’s like, all the goats… Like, it was terrible. They were all having serious problems. And I’m like, “Well, that just shows me that the Cydectin definitely does not work anymore. We’ve got resistance to that.” And in May, the poor goats were also in really bad shape. Well, looking back on that now, I realize—because this is actually what got us out of our dewormer resistance problem was—it was the month they kidded. In January and February, our ground is frozen. We’ve got snow everywhere. There’s no worms on pasture at all. And that was really it. Like, it wasn’t the D.E., because then I tried, you know, like, giving D.E. to other goats and, like, “Oh, it doesn’t work, and the herbal doesn’t work.” And I finally realized, like, “Oh, no, it was January and February. That’s the answer.” And so that’s what we did for several years to break that cycle with the barber pole worm so that our goats… Well, I always say, “Mother Nature culled my herd.” The ones that were not very resistant to worms just died. But then, ultimately, what got us out of that mess was multiple years of kidding in January and February when the worms were extremely low on pasture.
Joan Burke 22:16
Yeah, it’s really hard to include time in your research or observations, as you just described. I mean, there’s so much that changes. If you’re grazing, you’ve got forages that they change so dynamically. And, even if you’re… Let’s say you’re looking at the first half of kidding versus the second half. Well, the second group of kids are going to weigh a lot less, because they’re younger, and it takes them a little while to catch up. I’ve got an experiment that’s been going on for a number of years looking at fall lambing versus winter lambing. So I’m not just comparing the two different times, but, you know, now we’ve got different forages between the groups, and a whole slew of variables, not to mention that sheep—they typically don’t breed out of season. So, that’s a consideration as well. The parasite—and this is actually the reason for the study—is that the parasite load is much less in fall lambing. So I have to describe all the different variables between the two groups. So, not just that we’ve got the two timeframes, but all those other things. And still, I’m not going to be able to make these two groups as similar as I want. And so, sometimes, you just have to describe things the best you can and go from there.
Deborah Niemann 23:42
Yeah. So, I know a lot of people get really frustrated about all of the different information that they find online. And I always tell them, “Well, that’s because there’s a lot of research that’s been done in the last 20 years.” Since goats are a minor breed in the United States, we didn’t really have a lot of solid research prior to the 2000s that we could base practices on. And a lot of stuff has changed in the last 15 years because of all the research that’s done. Can you talk a little bit about some of the things that we now know, and some of the things that are now considered best practices because research has showed us that the way we used to do it 20-30 years ago doesn’t really work?
Joan Burke 24:32
Yeah, let me try to answer that. So, we’ve discovered dewormer resistance. Twenty years ago—well, I think we started seeing that in the 1960s and probably didn’t pay enough attention to it back then. But, now we know how widespread dewormer resistance is, and especially in goats, and especially if you don’t consider refugia. So we’ve learned a lot about refugia. Why is refugia important? And refugia is just, you know, keeping a population that hasn’t been exposed to dewormer or whatever treatment you have. We’ve also—and this isn’t necessarily new, because again, if you look way back in the literature, you’ll see some examples of this—but we’ve made a lot of progress on genetics. So again, I’m going to stick with talking about worms. Worm resistance in the animal is a genetic trait, and it’s a heritable trait. And it has to do with, you know, a better immune system. So, when we select goats or sheep or even cattle for improved health traits, like worm resistance, we can make a lot of progress so that we don’t have to have as many health interventions. Sometimes it might take 10 years, sometimes 20 years, but, you know, starting somewhere, having a good program to do that… And we do have the National Sheep Improvement Program, which allows both goats and sheep to submit data to help you make those decisions. Some other things that were learned: coccidiostats. We learned how to use, you know, the use of coccidiostats, like Deccox and Bovatec can prevent coccidiosis, which is a protozoan parasite that causes diarrhea, poor weight gains, and sometimes death. And, with any of the health problems, it’s much easier to prevent a disease than to treat it. Vaccines. Look at the research that went into preventative vaccines. And, whenever we look at any of these scientific treatments or research, we don’t just look at “Did we fix it?” We also want to look at the economic advantage of doing something. We always consider economics and animal welfare when conducting research. And sometimes there’s accidental discoveries while doing research, such as using copper oxide wire particles to eliminate barber pole. And I think I alluded to that in the last podcast that, you know, while scientists who were studying alleviating copper deficiency by using copper oxide, they found that the worm load was lower. So…
Deborah Niemann 27:15
This has been really good. And, hopefully, it has helped people understand more about why you shouldn’t just base your management decisions on something that happened with a single goat. Because there are so many things that could have caused whatever it was that happened, you know, that there’s other things that could have caused it. It may not be as simple as, you know, “Oh, I gave a dewormer and the goat died. So this is why it happened.” And that’s another thing, too, I always tell people. If you… You see people on Facebook going, “Why did my goat die?” And it’s like, “Well, if you really want to know, go get a necropsy.” Because people are just guessing. And I will tell people that, like, “I would just be guessing if I tried you to tell you how your goat died.” Like, if you really want to know, you have to get a necropsy. So…
Joan Burke 28:05
There’s also some good videos—if your producer can stomach it—to do your own necropsies, because you can’t always get a dead animal to a vet. But, I actually have my crew—who’ve never done necropsies—I have them do a necropsy if they’ve got time, and they’re willing, and you’d be amazed at the things that are just so obviously wrong: lungs, liver. If you compare YouTube videos, then you got an “Well, oh, gosh, I know that the lungs were involved.” And then you can call your vet and say, “Here’s what I found,” or take some pictures. That’s been really useful for us.
Deborah Niemann 28:44
Well, thank you so much for joining us today! This has been very interesting, and hopefully also very helpful to people.
Joan Burke 28:52
Yeah, well, thanks! I appreciate you asking me to do it. That was a lot of fun.