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Fly Control


By Madison Seamans MS DVM


To some people, “fly control” involves zippers. However, to those of us who love horses, or to some unenlightened, unfortunate souls who don’t love horses, but live close to someone who does, it means something else. The advent of the wildflower carpet covering the foothills every spring precedes a population of something equally abundant, if less loveable: the fly. The Bible cites Adam as the guy who named all the animals, so he is the one that came up with the name of the fly. I don’t know if he named them that because they could, (which begs the question: where did the name “bird” come from) or did he notice them first because, come to think of it, they are hard to ignore. Maybe there were more flies, or maybe God reserved editorial control for Himself, thus rejecting “@#$&! flies!” …not exactly a Biblical expression. Anyway, all God’s creatures have an important place in the ecosystem, though it is sometimes difficult to understand just what the reason is for some of them: fire ants, snakes and politicians being an integral part of that group.


No matter what you call them, they are very successful life form. They have a reputation for spreading disease, but I can’t tell you how many times a fly has landed on my freshly cut piece of watermelon. I did not throw the melon away nor did I die of some horrible enteric disease, so I think that reputation may be exaggerated. But, in reality, flies are a nuisance to man and beast alike and we spend a fair amount of money every year in an attempt to rid ourselves of these pests.


There are many varieties of flies but he most common ones associated with domestic animals during warm weather are house flies, horn flies and the big fat “horse fly”, or Tabanid, the one that looks like a toy helicopter and bites like a shotgun. The life cycle of most flies is fairly short, just a few days in most cases. Eggs are usually laid in organic matter, a polite word for poop or something dead. The larvae, little “fly students”, those disgusting things that look like mobile rice, emerge from the eggs and eat what they are laid in. Within a few days, the larvae pupate, a process where they form a cocoon, and emerge as adult flies shortly thereafter. The rapid life cycle is the reason that, no

matter what we do to kill the adults today, more keep appearing. Although most fly larvae live in dead stuff, one nasty little beast the, Habronema fly, eats living tissue, but that is the topic of another discussion.


I can’t prove it, but I suspect that Adam invented the fly swatter soon after God invented the fly, and we have been trying different methods of controlling these pests ever since. The first insecticides came into being accidentally around the turn of the nineteenth century. Chemical companies employed by the “war department” (now the United States Department of Defense) were trying to produce antipersonnel compounds—the so-called nerve gasses. Somebody noticed that the roach population in the cafeteria had declined significantly during this research, as

insects are very sensitive to nerve gasses. In fact, very small doses of these compounds with kill insects and even

intestinal parasites in domestic animals without harming the host animal. Among the first of these compounds was called a chemical alphabet abbreviated DDT. We don’t use it any more in this country because the chemical companies don’t pay our politicians enough. They do, however, pay the politicians in Mexicoand South America

very well, as DDT gives the fruits and vegetables we consume all winter that wonderfully distinctive flavor characteristic of foreign produce…but we digress.


These first insecticides, the organophosphates and chlorinated hydrocarbons were very effective and safe for everybody except with less than six legs. Then the U. S. Government, having run out of public sector employment opportunities, invented the Environmental Protection Agency. Their charter was to stifle economic development for the sake of the “environment”. (Who could be against that?) Virtually all effective insecticides were banned from the US. Now we have very few choices in insect repellants or insecticides.


Most fly repellants available at feed stores or on line at any of the horse supply companies contain pyrethrin, an extract of the chrysanthemum plant, or pyrethroid or permectin, synthetic analogues of the naturally occurring compound. The “ready to use” products have very low concentrations of the active ingredients. A careful look at the label will reveal the contents of such products. The amount of the actual repellant, typically one of the synthetic plant extracts, is commonly less than 1%. That means in a twenty dollar, sixteen ounce bottle, there’s less than .16 ounces, or fifty drops of good stuff. The rest is water, alcohol and cheap perfume.


Although all of these products are very effective if you hit the fly directly with a stream of the stuff, none of them have very good residual effects. This is especially true of the stuff that “lasts two weeks”. It’s a lot like the cell phone batteries that last 72 hours, you’re lucky to get 45 minutes out of one. So if these compounds don’t work very well, and are fairly expensive, what do we do? If you must use fly spray, buy the concentrated form, with the highest percentage of active ingredients you can find. (A 10% product is available, Permectrin II, available many places on line). To make a 1% suspension, use one part of the concentrate to nine parts water. Adding a tablespoon of bath oil and some cheap cologne will help the diluted product stick to the hair and make your neighbors think it is some expensive, designer product. The addition of a spoon of something else will wreck the math, but, come on; it’s fly spray, not calculus! Shake well before using, read all the cautionary statements on the label and throw the whole mess away because it is too dangerous to use, and may damage insects.


Other “all natural” products are available, but generally worthless. Citronella has been around for a long time,

but in carefully controlled studies, it has not been found to be an effective insect repellant. Adding garlic to the

diet of the horse may make him smell like Aunt Bertha’s lasagna, but it won’t repel flies.

Predatory insects that destroy the emerging larvae have been used with some success. However, if this is part of your fly control program, using any insecticides or repellants on the premises or horse may kill the beneficial insects. (which sorta defeats the purpose).


Despite all the chemical and biological control methods available, the three most important tools of fly control are the rake, wheel barrel, and shovel. Composting is a very effective method of killing fly larvae and facilitates control of the fly population. Pile the manure some distance from the barn. In dry seasons, wet the piles with a water sprinkler to encourage the bacterial activity that is the composting process. (On cool mornings, you will notice steam rising from the compost pile. This means it is working!) Weekly turning of the piles with a tractor scoop or high school student and aforementioned shovel will keep the bacterial culture actively chewing up the substrate that will turn in to rich mulch that will make your roses, tomatoes or strawberries very happy. Remember, no matter what you do,

your fly control method will be perfect in January. In the mean time, happy shoveling!

EQUINE HERPESVIRUS INFECTIONS:  UPDATE, 6/1/11, DON’T PANIC

by Madison Seamans DVM MS

     The recent outbreak of EHV-1, a neurologic disease caused by equine herpesvirus, has received a lot of press.  The internet, replete with social media and other roads along the information super-highway is responsible for the rapid dissemination of information.  Unfortunately, not all of this “news” is accurate.  Last Friday evening, I spent almost four hours with 60 other veterinarians at UC Davis, along with untold others via a Web cast, to discuss the current outbreak.  The speakers at this meeting included Dr. John Madigan and Dr. David Wilson, two most prolific and respected workers recognized world-wide for their research on EHV-1.  The volume and depth of information provided by all five speakers was impressive.  

     Equine herpesvirus infections (so-called “rhino” infections) have always been a part of equine medicine.  This nasty little bug doesn’t cause any social stigma, as it does in humans, but it can be the source of serious illness in horses and severe anxiety in horse people.  This bug causes four syndromes:  respiratory symptoms--pneumonia, abortion, genital blisters and the one that has everyone freaked out:  neurologic symptoms.  There have been 60 outbreaks in this country since 1970 (the first year for which accurate records are available).  Outbreaks typically occur where large numbers of horses are congregated: shows and sales. No single outbreak has ever lasted more than a month.  There are 75 active cases in 9 states in the current outbreak.  In a population of about nine million horses in this country, it hardly seems like an epidemic.  About 30% of active cases have developed neurologic signs, lack of coordination, especially in the hind limbs, or a complete inability to stand.  Of the neurologic cases, about 85% survive.  In horses surviving severe neurologic symptoms, more than half will return to normal within 6 to 12 months.  Basically, if they can stand, they will survive. So take a deep breath, don’t worry, be happy.  The chances your horse will die from colic are far greater than him developing herpesvirus.  On that comforting note…

     Transmission of equine herpesvirus in horses is usually either airborne (15 to 30 feet), or direct, virtually nose to nose contact with an actively symptomatic case. The virus itself is quite fragile, so transmission by infected trailers, tack or other “fomites” is usually not a problem.  The take home message from this meeting was this:  only horses with direct exposure to an active case have a significant risk for infection.  To make things more complicated, herpes viruses possess some characteristics that make them hard to diagnose, and like most viruses, impossible to treat specifically.       

     Once an animal is exposed, the virus moves to the spinal cord where it may cause disease within 6 to 10 days, or it may lie dormant for years (latency and recrudescence are terms that mean herpes viruses can be found in many horses, but not cause disease until later, or never.) For example, shingles in adult humans is caused by Herpes zoster, the same bug that causes “Chicken Pox” in children.  So most humans are exposed as children, but, as in the case of shingles, the virus may live in the spinal cord for 50 years before causing the disease.  In the horse, the respiratory form of EHV is relatively common in horses under a year of age, but the neurologic form is not seen in juveniles.   In mature horses, the first symptoms include limb edema (swelling in lower legs) and biphasic fever:  one that goes up and down through the day.  This is why the new recommendations for horse show managers includes posting of the horse’s temperature twice daily on the stall door.  Any horse with temperature of 102 will win an all-expense- paid trailer ride off the premises.  This may seem like overkill, but removing febrile horses from contact with others is just good management, no matter what the disease is.    

     The term “stress” is commonly mentioned.  It is especially useful for those of us in the veterinary profession who truly wants to give our clients answers, but clearly has no freaking clue—therefore; stress is vague enough to satisfy most folks.  In reality, few things are more stressful than surgery or foaling, yet there have been no reported outbreaks following these events.  In a small study of apparently normal horses in California, about 3% had herpes virus in nasal swabs.  With this in mind, it is impossible to tell if a horse is a carrier without diagnostic tests, and just because he is a carrier does not mean he is actively shedding the virus. Therefore, it is not wise to test horses in a random screening process as the data generated from the PCR tests are difficult to interpret in normal horses because of the prevalence of subclinical cases (horses testing positive for the virus, but having no clinical symptoms).

     Diagnosis of symptomatic horses is made by clinical examination and a PCR test from a nasal swab and blood.  This test detects the actual presence of viral DNA.  A messenger RNA test determines viral load and active shedding, transmitting the disease.  The traditional antibody tests can only indicate exposure and are not useful in detecting active disease in most cases.  Treatment involves nursing care: iv fluids and anti-inflammatory drugs. The anti-herpes drugs like acyclovir have not shown any promise in treating this disease in the horse.   Although there are several vaccines on the market for equine “rhino”, none of them have label claims of preventing neurologic infection. 

     In conclusion, this crisis will blow over in a few weeks, and horses will soon be on the road again just like every summer despite the five-dollar-diesel-blues.  If you are worried, stay home and wait for reports of additional cases


If you have more questions, feel free to contact me:

559-689-3343 or madisonseamans@gmail.com


There is no "Weight Watchers" for horses!

EQUINE METABOLIC SYNDROME

By Madison Seamans MS DVM


     In order to get along in this world, we must learn to be kind.  That is why somebody invented the euphemism:  a cleverly indirect way of saying something bad.  Like:  “Is that back in style?”, or: “You don’t sweat much, for a fat guy, do ya’.”  So when somebody calls your horse an easy keeper, what they’re really thinking is:  “Wow, you could ride that horse without a saddle, you’d just sink right in to her back like a really soft couch.  I wonder if it would leave a dent”.  I must confess I have used the term “easy keeper”, because: “I don’t know” doesn’t qualify as a good answer for the overweight horse.  Thanks to some recent studies in equine endocrinology and nutrition, there are some answers to the cause and potentially dire effects of equine obesity.

     Many horse lovers show their affection through bag of feed.  However, most folks are pretty savvy about how much a horse should eat, and will know they have one that seems to gain weight on the thought of eating a carrot.  We can cut ‘em back to bread and water without the bread, and they still gain weight!  So, for those readers who think a healthy diet is a gallon of molasses and a Costco bag of carrots, you can stop reading now.  For the rest of us, hang on.  Equine Metabolic Syndrome (EMS) is a relatively new term used to encompass a series of complex metabolic relationships between glucose and insulin metabolism (insulin resistance), thyroid hormones (hypothyroidism), and plasma cortisol (Cushing’s syndrome/old horse laminitis).

     Not too long ago, our approach to obesity in human and veterinary medicine involved measuring blood levels of thyroxin, one of several hormones produced by the thyroid gland.  We could measure these compounds, and we thought we knew what the “normal” levels were, so, armed with sharp objects and glass vials, we proceeded to partially exsanguinate the unsuspecting horse population of the world.  Surprise!  Most of the clinically obese horses we tested showed “normal” thyroid hormone levels.  Like many things, a “simple” blood test wasn’t. 

     Recent research has revealed that some animals (horses, people, lab rats, politicians) are genetically programmed with “thrifty genes”.  This is God’s way of making sure they survive harsh winters with no forage or “stimulus” checks until times get better.  Horses with this genetic makeup will thrive during lean times due to their ability to store energy in fat cells, but become morbidly obese on a normal diet.   There are many horses like this.  I know, the prettiest color on a show horse is FAT, but it is also dangerous.  Obese horses are prone to laminitis (founder) and other diseases of blood vessels.  (note the radiographs and photographs of the paint mare)  Fat tissue secretes a hormone called leptin that is toxic to the lining of blood vessels.  My 450 pound uncle Albert has cardiovascular disease, not because of the extra load on his heart, but because the leptin from his fat cells have damaged the lining of his heart and arteries.   The “easy keeper” mare crippled with chronic laminitis (founder) has cardiovascular disease just like Uncle Albert.

     Treating obese horses can be a challenge, but there is hope.  We must start by identifying the patient, and this diagnosis has little chance of damaging his self-esteem.  We must limit dietary sugars and starches.  (Purina makes a low sugar diet for horses, and it really does help).  In our area, there are rich grasses from January through June, so restricting grazing is imperative, either by stall confinement or using a grazing muzzle—a stupid name because horses can’t graze with it.  Soaking hay in water for 8 to 12 hours will rinse out up to half the sugars, so this provides a cheap and easy way to restrict caloric intake in horses.  There are some packaged hay products available which can be a good source of low-carbohydrate forage because they are 50% “plant juices” ( a great euphemism for water).  However, care should be taken as the packaging has resulted in problems with mold.  Horses fed forage with high water content, either soaked or packaged hay will feel full, but receive only half the calories of regular hay. I strongly recommend thyroid hormone supplement for at least the first six months of the weight loss program.

     Finally, you can monitor your horses’ progress with a weight tape.  These may not be real accurate in measuring the exact weight of your horse, but a weight tape is an excellent way to determine changes in weight.  A strict regimen of low starch/sugar diet and thyroid supplementation has shown promising results in obese horses even without increased exercise.  Be patient, progress will not be noted immediately, but most horses will achieve the desired results within six months.  

Mare below shows signs of equine metabolic syndrome.

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