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David W. Horohov Ph.D., Maxwell Gluck Equine Research Center, University of Kentucky

I love the “wow” factor in associations and reminded myself of that experience when I reviewed the tape I made of Dr. David Horohov at the 2010 Mid-Atlantic Nutrition Conference.

Horohov reminded us of the complexities of disease and the circumstances of fact-finding. He gave a talk on rhodococcus equi, a nasty foal disease, but he wove in stories of HIV, the hygiene theory, and the wire walk of how to jump-start one system while leaving another alone.

Rhodococcus equi (RE) is a disease that plagues foals, usually under 2 months, and is known for its distinctive diarrhea and its production of pneumonia. It has veterinary, time, labor and worry costs associated with it and it can kill. Just like the human population, diarrhea and dehydration go hand in hand and little bodies dehydrate pretty quickly; and if the runs don’t get them the lungs drowning in fluid might. Pneumonia is always serious.

The little bugger that causes this disease is ubiquitous. It is everywhere in the ground. Yup, you too are stepping on RE somewhere on your farm. It’s just like ants, if you don’t have them, chances are nothing around you is breathing, including you.

Some farms are plagued more than others and for years the general direction has been cleanliness is akin to healthiness.

Taking a look at RE the first thing that jumps out is that this everywhere-in-the-air disease doesn’t much affect adults. In fact, it is pretty unusual to have an adult with RE.  Turns out the adult horse population has immunity to this little bugger. So the thinking was that the younger horse population had no immunity. And so the thought went until the medical community identified rhodococcus equi in AIDS patients. Huh? The medical community thought the same thing so they started looking into this. (told you the bug was ubiquitous) Human medicine has funding and the results found in that sector were scooped up by the equine medical community.

It was discovered that the foals had immunity, but the immunity just wasn’t kicking in yet. Their bodies had to be “sensitized” to the bacteria, rather like the act of a vaccine. To take a sentence from Horohov’s extract “While most cellular components of the immune system are present at birth, in many cases these cells can be considered immature or lacking full functional capability.”

How do you get an immune system to “grow-up”? One theory (I always want to make sure that people realize we are talking about the discovery phrase, not the we-know-it-for-sure phase.) is that the immature immune cells grow-up to be productive members of the organism by being challenge. This gives some strong meaning to the aphorism, “What doesn’t kill us makes us stronger.”

How do you sensitize a foal? They actually “challenged” their immune system by bringing them into a less than pristine barn for four hours everyday (with mom). This is a scary thing to say because I always worry how others interpret the statement. The foals were getting good management, nutrition, and the barn didn’t have 3 feet of manure in the stalls with no ventilation. It was just dirty, maybe not all the manure and urine out of the stalls, maybe not all the dirt swept from the aisles.

The findings were that these foals didn’t get the disease at the same rates their pasture counter parts did. A lot more work needs to go into this, a lot more blood pulled, conditions researched, etc. But it took the first step in saying maybe these foals need a little challenge in their life. (Horohov discussed the pivotal immunity thruster, interferon gamma, and how it kicks in, but you need lots of cups of coffee to deal with that story.)

It also makes sense in light of the “hygiene” theory.  Human studies that show kids who aren’t exposed to animals, flora and fauna early on in life are much more susceptible to developing allergies later. I see this in the Icelandic horse population where a horse imported from pristine Iceland has a 30% chance of developing summer eczema (allergy) when it hits the states; yet, the domestic-bred Icelandics don’t show this propensity.

If further research confirms these initial findings and theories, the equine community can look into how to beef up immunity faster. It is there, just start the engine earlier. Is there an intra-nasal spray that can be used, a vaccine, a probiotic to feed? But in interfering with a foal’s immunity system can you end up damaging the immunity that mom has passed on? Questions that won’t be answered for a while. But the first step is taken- knowing a bit more about the little bugger and the system it attacks.

Meanwhile, I am starting to see the value in the adage “ you need to eat a pound of dirt before you’re 12.” There just might be something to that.

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You can blow the dust off a piece of paper, but how do you blow the dust off of computer writing? Perhaps letting your fingers absorb the pent-up electrical charges. If so, then it would have to be with fingers vibrating that I write this entry, as it has been a long time between utterances.

Back in the U.S.A.

Not without good reason–– My son came home from Iraq!

But that simple event also required a 2500-mile drive to El Paso. It required stops in Lexington, Kentucky to rubberneck at the border of white and black running board fencing along the highway. Fencing to keep the grazing broodmares and babies from a disastrous highway drift. It required a look across the Mississippi River remembering Tom Sawyer and cogitating on whether there were any horses in his story. It required a stop in Oklahoma City to view an art fair and look at a bevy of beautiful paintings representing the West, and pining after the oils of Michael Swearngin’s cowboys. (Contemporary Cowboy) It required a stop at the Fort Worth Stockyards–– thank you Wildstorm at Backroads Photo Blog for giving me the idea.

Back from the cattle drive

The Stockyards, Fort Worth, and Texas made me feel like I could stretch out on a horse. In New Jersey I always feel contained. By accident I stopped in at Tesky’s in Weatherford, Texas, the cutting horse capital of the world. I picked up a several pairs of great leather gloves in even greater colors. (Why don’t we find these things back East?)

My simple trip was really a journey. It was not only a journey of miles and friendship (My sister-in-law kept me from falling asleep at the wheel.) it was also a journey of ideas. It is good to open the windows of the mind and let the air blow in the sights and smells of the world outside your own. It is good to let your mind play with those senses and add the spices of information you have stored along the way and come up with new mixes and new ideas.

One of those ideas was from a podcast I listened to during those five days of travel. Simon Sinek on TEDTalks, 5/4/2010 (here’s a link) gave a great talk on what makes leaders. And, of course, great leaders get things done. We need a lot of great leaders in the world of horses right now. Race tracks, trails, competitions, living space, rules and regulations are all presenting problems to people in the horse industry and one of the biggest frustrations I see is getting others to listen and understand the concerns we have. I thought about Sinek’s talk for many miles. I am still thinking about it. I’m thinking we could make better progress if we didn’t talk so much about what we do with our horses and talked more about why we do it. Why we ride, why we like to groom, handle, smell and stand next to them. There are probably as many whys as there are people. Sinek used a phrase, “People don’t buy what you do, they buy why you do it.”

Think about why you ride and the next time someone asks you about your riding consider telling them why you ride, not what you do when you ride.

Raymond Geor, BVMS, College of Veterinary Medicine, Michigan State University

Dr. Raymond Geor, a veterinarian and researcher at the College of Veterinarian Medicine at Michigan State University, gave one of the first presentations I heard at the Mid-Atlantic Nutrition Conference.  His talk had big 6-syllable scientific terms- all delivered with the measured pace of a scientist. He packs a lot of information in his talk, and as a layperson I usually come away thinking, “What was he talking about?”

I am fortunate to have a tape recorder to help me keep track of the stuff I miss. The more I listen to his talk, the more I can skate around the moguls of language and studies: And the more I can see the landscape he is describing. There were no bunny slopes in sight; the good doctor took us to the top of the Matterhorn and it was an hour’s speed race the whole way down to the end.

The verbal description of his talk was only two paragraphs long. It stated that there are anecdotal impressions by veterinarians of a relationship between obesity, insulin resistance, equine metabolic syndrome and laminitis. The second paragraph stated Geor would review the current diet and nutrition management for reducing the risk of laminitis in these animals.

ah, the miracles of photoshop

We start with a wee background from last year where Dr. Nicholas Frank gave a presentation that I summarize as “ Obesity in a horse is a good clinical sign that you are courting problems.” This is where Geor picks up and in a nice way says- it has been noted that the observable characteristic of obesity often indicates a predisposition for pasture-induced laminitis in horses. This, then, would be the laminitic phenotype. These horses seem to respond to changes in dietary and environmental conditions differently than other members of their herd.

We were also reminded of the fact that at the heart of laminitis is inflammation that disrupts life in the laminae resulting in its death and, in some cases, severe coffin bone rotation and the demise of the horse as well. Furthermore, there is a pretty good hunch that there is a connection between a pasture-induced laminitis episode and disturbance in the animal’s hind-gut brought on by rapidly fermenting carbohydrates that in some way (death of microbes, toxin release, gut leakage?) causes an inflammatory response in the horse that takes it over the threshold into laminitis.

Currently there are three main theories scientists are working on.

  1. there is an underlying inflammatory condition in these horses and ponies.
  2. Insulin toxcity
  3. A perfect storm of multiple colliding factors

Why would a fat horse or pony be more susceptible to laminitis? Ah-ha. That’s a good question that has no answers. But, there have been some recent discoveries in other species (us humans for one) that merit consideration (and therefore research) for the equine species.

It would seem that fat, once thought of as a simple collection of  storage cells, actually is ALIVE! ( the monster within- I sense a movie in all of this.) Adipose tissue is very metabolically active. It regulates things like pro-inflammatory cytokines, which makes the scientist wonder if the obese horse is in a constant metabolic state of systemic inflammation. If so it would be easy enough to understand why anything that would contribute more inflammation would tip the horse over the laminitic threshold.

Wondering what insulin looks like?

In other species fat seems to have a pretty strong affect on insulin. Interestingly insulin actually has two pathways, one is use (sensitivity) and the other is production. Fat appears to decrease the use of insulin while increasing the production of it with the result that there ends up being a large concentration of insulin in the blood stream (hyperinsulinemia.) That’s a very bad thing for the circulation and results in vaso-constriction: in other words tissue (such as the laminae) starvation and death.

Then there is the perfect storm theory, fat, inflammation, insulin, gut mobility, gut bio-environment, gut motility, gut permeability, forage composition factors other than carbohydrates, genetics, climate, life-style. Whew. Oh, and what about the obese mom that predisposes her foal to metabolic disorders? Happens in humans – could the same be true in horses?

And here’s my own wild card questions. How about how the whole digestion process works in these laminitic phenotypes.  Does their system empty slower or faster than their healthy counterparts? There is always talk of the role of  GI micro-organisms in creating laminitis.

coprophagia: foal eating mom's manure

Well, perhaps the genetic pre-disposition component is the foal eating mom’s bacteria laden feces.Mom could have “laminitis-making-bacteria” in her GI track. Maybe it’s not a gene, maybe it’s being in a stall with predisposed, obese, laminitic mom and the foal’s natural and needed coprophagia.

So many of these conditions are tightly intertwined that it will be a galactic challenge to investigate. And, of course, there is very little money to support this research.

I have an insulin resistant horse and another overweight pony. After listening to Geor’s presentation I renewed my efforts to reduce their weight as I have seen and heard the devastation of laminitis.

And, personally, I’m going on a diet lest I become even more inflammatory in my remarks.

new research on livestock nutrition

One of my annual March sojourns is to partake of the Mid-Atlantic Nutrition Conference. I come away filled with adrenaline and excitement: my brain neurons firing away at all the paths those little research tidbits lead me down. None of my conjectures  have any scientific backing, but they are still worth a moment  or two of wonder. I noticed some interesting directions from the conference this year.

It might help for you to understand what this conference is all about–– livestock nutrition. Primarily dairy cattle, poultry and equine. This is where the academic researchers, feed mills, veterinarians and large livestock producers go to find out what are the newest research studies and theories on animal nutrition. You are not going to get razzle-dazzle slides here; you are going to get charts and ugly photos. But you walk out with a good sense of what isn’t known, what needs to be studied and a few sentences of something that has finally been proven.

It always reminds me the road to knowledge is a long one and that the body is blessedly complex.  I hope to post a number of entries over the next several weeks on specific topics covered at the conference along with my thoughts and questions. But for now I am still cogitating on a number of overall directions and impressions from my time in Maryland.

  • There was a new word thrown around quite liberally phenotype. Phenotype refers to the OBSERVABLE characteristics of an organism that has resulted from the interaction of its genotype and environment. It is an old word, but is being picked up and used more regularly in the scientific community. One might say that I am a phenotype for heart attacks; I have a chicken physique. (we’re using silly examples here, folks.) All fat lands in a plumb Buddha belly with nary an ounce going into my legs or butt. Observable characteristics are the belly fat. My mother and father had the same structure. This predisposition is most likely a genetic code of where my family line should store fat. Environment characteristics are the incessant putting of a full fork into my mouth. And now we have research to show that belly fat is hormonally active and a leading cause of heart attack. So I could stand as a phenotype for humans courting heart attacks. Or I could be a fat horse and the phenotype for laminitis.

There was a lot of discussion of the laminitic, IR and obese horse phenotype.

  • I think this word is being used more often because of another trend- the researchers are looking really small. Better technology has helped here as well as directions in human medicine. And in looking really small they are finding that the organism is REALLY connected. A cure for laminitis isn’t going to come by just looking at the inflammation of the feet. That is a sign, but now they are realizing that there are a lot of things on the cellular level that might cause inflammation in a body structure that might send hormone signals to other parts of the body that might start another cascade of seemingly unrelated events that end up in the feet. In looking really small, researchers are broadening their horizons.
  • Researchers are starting to whisper in the hallways about the failures. No one studies the failures in a research project. Part of that is due to the “system” of publishing papers where talking about failures is likely to result in a failure of the paper to get published. One of the speakers mentioned that in a clinically induced challenge of horses with genetic predispositions for laminitis, 20% of them never get laminitis. Their results are left in the paper trail that hits the circular file. Yet, this researcher had the strength to pause and say, folks someone should study these failures- what have they got in their systems that the other horses don’t have. (Please remember a failure is what does not prove the hypothesis. So if the hypothesis is that lush green grass will produce laminitis and these predisposed horses didn’t get it. Well, they “failed” in that they did not prove the point where as the other 80% did get it and proved the hypothesis.- Okay, okay- it’s a very simplistic explanation to help get across a very complex point.)

I’m not a scientist, but I find this thrilling stuff.  Finally the research industry is connecting the smaller dots that make up the larger ones. I also find it overwhelming- the amount we now know we don’t know. Dr. Raymond Goer from the University of Michigan School of Veterinary Medicine said it nicely,

“I know a lot less than I did a year ago. And I know a whole lot less than I knew two years ago.”

We are having to step back to go forward, but it is putting us on a better path.

Oh, and that word “phenotype” bet you see it everywhere now.