Is Acorn Toxicity in Horses Real?

Squirrels aren’t the only ones hoovering up the Fall crop of acorns. Horses love them too. A yummy treat courtesy of Mother Nature – or are they harmful?

Many people report their horses regularly indulge in acorns in the Fall with no ill consequences but a small number of horses develop serious, even fatal, illness as a result.

A study from the UK [Smith et al 2015] reports on a series of 9 horses over a 9 year period treated for suspected acorn toxicity.  Five presented with bloody diarrhea and shock, were rapidly euthanized or died. Four had colic and diarrhea. Three of those survived with medical support and the fourth was euthanized.

Post mortem examination of the 6 dead horses showed extensive intestinal and kidney damage. The authors noted toxicity seems to be more of a problem in some years than others, which has also been reported by others. It is unknown if acorns are more toxic certain years or if it is a matter of larger numbers of them being available.

The details of how acorns cause poisoning remain to be determined. Tannic acid is often blamed but in cattle, which are even more sensitive than horses,  dosing with tannic acid does not reproduce the kidney damage. Gallic acid and phenolic compounds are also believed to be involved. The products of bacterial fermentation of acorns in the rumens of cattle and the colon of the horse may be the most active toxins.

The leaves of oak trees are also potentially toxic.  Cattle have been poisoned by consuming oaks leaves in the spring.  There have not been any recognized cases in horses but it’s possible.

Acorns pose another potential danger to horses, ponies, donkeys and mules with Equine Metabolic Syndrome [EMS]. In this condition, there are exaggerated insulin responses to simple sugars and starch which can result in laminitis.  Acorns average over 40% starch which is way too much for an animal with EMS.

There is no specific treatment for acorn poisoning. Activated charcoal can help if administered immediately after the acorns are consumed but signs don’t usually appear for a few days after ingestion and at that point it’s too late for charcoal. Charcoal also can’t protect an EMS horse from acorn induced laminitis since it doesn’t have any effect on starch digestion.

After the horse becomes ill, the only treatment is supportive care such as intravenous fluids. Even with intensive treatment the fatality rate is high, as much as 67%. Not all horses become poisoned on eating acorns but that high death rate should be strong motivation to avoid exposure to acorns and oak trees.

Removing acorns as they fall is a full time job. It’s preferable to remove the trees entirely or fence off areas containing acorns in the fall and trim the trees so that leaves are not accessible.  If storms bring down branches, be sure to remove them promptly.

Acorns from the mighty oak are a boon to many species but not worth the risk with a horse.

Eleanor Kellon, VMD

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Mid-Pregnancy Nutrition

When an average size mare delivers she will have produced a 100+ lb foal, an 11 pound placenta, and as much as 16 pounds of fluid. She has also greatly increased the size and thickness of her uterus and blood volume increased about 30% during pregnancy.   The raw materials to build these things didn’t come from thin air.

By the halfway point, the foal is about the size of a Beagle, all organs formed, and rapid growth begins

Providing adequate calories is the easy part. Rapidly dividing cells also have critical needs for amino acids, vitamins and minerals which they must obtain from the placenta. It’s true that the dam will rob her own body tissues if necessary to provide for the fetus (not that this is a very smart management tactic!). It’s also true that the dam cannot provide something she herself does not have. If she starts the pregnancy with low body reserves and her diet is not adequate, the foal will be short-changed and the mare become even more deficient.

Extreme deficiencies result in things like White Muscle Disease and goiter with hypothyroidism in foals. More insidious effects include a higher risk for developmental orthopedic disease like OCD and contractures. Chronic copper deficiency has been linked to uterine artery rupture in mares.

Advice on feeding pregnant mares used to be no special attention to nutrition until the last trimester.  The latest (2007) NRC recommendations begin to allow for increased nutrients in the 5th month but since there are still gaps in the research, there are also gaps in their recommendations. For example, they don’t allow for any increase in zinc or manganese but obviously foals have those essential minerals in their bodies.

Good quality grass hay or pasture should be the bulk of the pregnant mare’s diet. In fact, a hay with 10 to 11% protein and digestible energy (calories) of 0.9 Mcal/lb can meet calorie and protein requirements throughout pregnancy. Even in the last month of pregnancy the  mare would only need to consume a little over 2% of her nonpregnant body weight to meet her needs. For every 1% below 10% in the protein, the mare needs 45 grams of supplemental protein per 10 lbs of hay. For example, if a 9% protein hay and she’s eating 20 lbs, she needs 2 x 45 = 90 grams of supplemental protein. A common range for protein in good quality grass hay is 8 to 12%.

If you don’t know the protein level in your mare’s hay, it’s wise to supplement. “High” (14%) feeds won’t help because they have 2.5 to 3 times more calories than hay but not 2.5 to 3 times more protein so you feed a lot less. Choose a supplement with a blend of vegetable and whey sources, guaranteed levels of lysine and methionine. If you assume 8% protein, a  mare eating 20 lbs/day will need 180 g of protein = 450 g of a 40% protein supplement (1 pound).

You may want to meet part of your extra protein needs with a combination protein and mineral supplement. As a rule of thumb, the pregnant mare will need double her baseline mineral intake at the time of greatest  demand so  look for a supplement with at least 5% calcium and 225 mg copper per 1 lb serving. A pound of it will provide about 112 g of protein if 25% protein.

Do not stop your mare’s  usual mineral supplements when she is pregnant. You still need to have her eating a balanced diet base. The above supplementation is for the additional needs of pregnancy. Compared to what is already invested, this is cheap insurance. A breeding farm client of mine once described foals from mares managed this way as “robust”.  How many 1 week-old foals look like this?

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Do You Need an Oral Sugar Test to Diagnose EMS?

It has been established that high blood insulin is responsible for about 90% of all laminitis cases and best current estimate is 10 to 15% of the equine population is at risk of EMS – Equine Metabolic Syndrome.  A central component of EMS is elevated insulin.

Not all overweight horses have EMS

Some (not all) EMS horses are overweight and have abnormal fat deposits, especially along the  crest of the neck. These are indicators but to confirm you need to document abnormal insulin.

If you have done any reading on EMS diagnostic tests you have probably found many different testing options. A common statement these days is that the oral sugar test is best – but is it?

The original test suggested for documenting abnormally high insulin was a fasting insulin level. The oral sugar test was born after the realization that baseline insulin when fasting missed a lot of cases.  There is no question it’s better than a fasting insulin level, but is it the best and only option?

There are several multi-step tests for insulin function and response to insulin which involve placement of a catheter and evaluating the response to intravenous injection of glucose and/or insulin by taking a varying number of blood samples. Because of their expense and the time involved, simple testing involving minimal time and preferably only one blood draw are more appropriate for screening horses in the field.

The value of field screening tests is established by comparing the results to those obtained from the more intricate but more accurate intravenous tests. The “gold standard” test is the FSIGTT – frequently sampled intravenous glucose tolerance test. Dunbar et al 2016 showed the OST had a 0% sensitivity in detecting insulin resistance compared to FSIGTT when using  the common cutoff for peak insulin of 60 uIU/mL. When the threshold was  lowered to 45 uIU/mL, sensitivity improved to 14%.  This means for every 100 positive horses detected by FSIGTT, only 14 were found with OST.

In 2005, Dr. Trieber’s group used the FSIGTT to develop the proxies RISQI (reciprocal of the square root of insulin) and MIRG (modified insulin to glucose ration). These are calculations using insulin or insulin and glucose results from a single blood draw to approximate the results  from FSIGTT.  When put to the test in a year-long study of 160 ponies being maintained on pasture, either proxy had a sensitivity of at least 64%. When the two were combined with one other marker of EMS such as obesity, sensitivity rose to 74%.  The proxies correctly predicted ponies at risk of laminitis in 84.6% of the cases.

The OST has also been tested to see if it could differentiate between ponies that had previously had laminitis versus never had laminitis. At the usually used dosage of 0.15 mL of Karo syrup/kg of body weight there was no significant difference. There was also no significant difference between groups at 0.30 mL/kg of body weight.  At 0.45 mL/kg there was a significant difference but this would amount to a bit over 4 oz for a 1000 lb horse.  Only 8 ponies were used in this study and sensitivity compared to FSIGTT has not been determined. Cutoff values for determining a positive test have also not been established for this dosage.

Newer is not always better.  The ECIR group https://ecir.groups.io/g/main has been using the proxies since 2006 and before that the G:I (glucose insulin ratio) proxy, which was also shown to have good correlation with FSIGTT in Trieber’s original publication.  Another option is to use nonfasting insulin with the horse having access to hay or pasture only. However, instead of the 20 uIU/mL upper limit of normal currently recommended we use the ranges established by the large pony field trial.  So far, we see no reason to change.

Eleanor Kellon, VMD

 

 

 

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All About Antioxidants

Do you remember when antioxidants were all the rage as the latest and greatest thing in supplements?  Other topics catch most of the headlines these days but antioxidant activity still underlies some of the effects of currently popular ingredients like curcumin and even cannabinoids.

The horse’s natural diet is rich in antioxidants.

Oxygen free radicals, aka reactive oxygen species (ROS) are oxygen-containing products of metabolism which are missing an electron, making them unstable. Normal cellular metabolism, immune system activities, exercise and cellular clean up after injury all generate ROS. Diets high in fat or carbohydrate, metabolism of drugs and toxins also generate oxidative stress, as do chronic health problems.

These substances will attack proteins, DNA, structural  membranes both inside and around cells to steal an electron. The molecule attacked then becomes a free radical itself and a chain reaction can be started. The process weakens and can even destroy the cells under attack.

Antioxidants protect against ROS by donating an electron to stabilize them and prevent attack on the tissues. Antioxidants can be either fat soluble, located primarily inside the structure of membranes, or water soluble, protecting the watery environment inside and outside the cells.

The body has a variety of antioxidant enzymes such as catalase and  SOD – superoxide dismutase. These are manufactured by the cells, as are the important intracellular antioxidants N-acetyl-cysteine, glutathione and alpha-lipoic acid. Vitamins Niacin, C, E and A have potent antioxidant activity.

Foods can also supply plant based antioxidants.  The horse’s diet is naturally rich in plant antioxidants such as carotenoids, flavonoids and polyphenols. Fresh green plants of all types have high levels, even grass. For example, Bermuda Grass is a sacred plant in India, where it is called Durva.

While excess ROS can be harmful, a healthy horse’s body is one that has a correct homeostatic balance between antioxidants and free radicals. This balance is called the cellular redox state. The goal isn’t to eliminate them entirely because at proper levels they have important activities such as stimulating the production of antioxidants, cell to cell signalling, modulation of gene function and enzyme activity.

The first step in ensuring your horse has adequate antioxidant defenses is correct intake of B vitamins, vitamin C, vitamin E and vitamin A/carotene as well as the amino acid L-glutamine and minerals copper, zinc, magnesium and selenium.

If nutrition has been optimized and the horse needs more antioxidant support, look to rich plant sources such as:

  • Grape seed and skin
  • Berries
  • Turmeric
  • Garlic
  • Ginger
  • Ginkgo
  • Boswellia
  • Spirulina

as well as isolated plant compounds such as quercetin or mixed bioflavonoids.

Supporting antioxidant activity is one of the best things you can do in a natural approach to health because it enables the horse’s body to use it’s own homeostatic system of checks and balances to protect itself.

Eleanor Kellon, VMD

 

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Please Stop Anthropomorphizing

A common technique with writers or advertisers is to connect with their audience by using something familiar and important to them. That’s why pet foods are gourmet, stew, dinner, etc. when the dog would actually be happier (and healthier) with a raw chicken neck.  We also need to be careful about making assumptions for our horses based on our own feelings and preferences. Diet issues is a good example here too.

Horses have an instinctive drive to eat high starch items

If your horse is obese or has metabolic syndrome are you causing suffering and unhappiness if you don’t feed sweet feed or other grains? The horse has an instinctive drive to select foods with higher starch or sugar content because in pastures that correlates with grasses that have the most calories and better digestibility. Calories = survival.

However, that drive can shoot them, quite literally, in the foot. Given unlimited access to grain any horse will overeat resulting in laminitis, colic and potentially death. They won’t stop until it’s too late. Grains can have a place in the feeding of some hardworking horses but they are not part of the horse’s evolutionary diet and the horse does not naturally need, or crave, very high starch or sugar foods and treats.

What about grazing? Don’t horses need to constantly eat for their mental and physical health? No. Horses in their feral environment spend so much time grazing because grass is about 80% water and often poor nutritional quality. There are no calories in water.  The horse has to eat that much just to get the calories needed.

By comparison, hay is a very concentrated source of calories since it is only about 10% water.  The horse has to eat 4.5 times more grass than hay to get the same number of calories. Furthermore, hay is harvested at the peak of its nutritional value. If the horse is grazing grass that is overly mature and has already gone to seed the horse will need to eat even more.

Horses that do not have EMS can have free choice access to hay and they will limit their intake to what they need to maintain a normal body condition. Those horses are eating a lot less in terms of poundage than they would if they were on pasture. They don’t eat constantly just because it’s there.

The EMS horse on the other hand does not have a normal “Off” switch that tells him when to stop eating.  It’s necessary to restrict his access to only provide what is needed to maintain a normal body condition.  This isn’t a diet.  It’s feeding a normal amount of food for their level of exercise.  If overweight, the vast majority of even EMS horses will gradually reduce to a normal body condition with this approach. Think of it as normalizing, not depriving.

Many people have the most trouble with keeping an EMS horse off pasture or muzzling them.  They think it’s cruel, unnatural, and the horse can’t possibly have a happy life without it. Food is not a substitute for companionship, grooming or exercise. It’s important to provide those things too. When there is a pressing medical need to adjust the horse’s eating, it’s irresponsible to ignore that.

Horses do not use food as a reward or to soothe themselves the way people may. Their instincts don’t always align with the domesticated environment they find themselves in but the horse can have a good life without giving in to providing food choices which can harm them.

Eleanor Kellon, VMD

 

 

 

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Supplementing Fading Pastures

As Autumn settles in, the composition of pasture grasses begins to change. The horses are still interested in grazing, and grasses may still largely be green, but the nutrition is not the same.

All grasses have a natural growth cycle and preferred growing conditions  during which they will take a few weeks to grow to full height, develop and then drop seed.  The stage of active growth and before the grass has set seed is when hay should be cut for peak nutritional value.

After full height is reached and seed begins to form, the caloric value, carbohydrate level and protein in the plant start to drop.  Fiber and lignin begin to rise, decreasing digestibility overall. Mineral levels may drop and the minerals present may be less bioavailable because of complexation with fiber.  Levels of vitamin E and fat progressively fall.  The fat loss is almost exclusively  the more fragile omega-3 fats.

For horses being maintained on pasture, the signs of declining nutritional value include:

  • Weight loss
  • Loss of “bloom” (duller, dry coat)
  • Poor hoof quality
  • Appearance of hoof abscesses
  • Low energy
  • Slowed growth in young animals

Horses with poor hind gut function may show a distended abdomen, increased gas and/or loose manure or increased free fluid with manure.

It’s better to start supplemental feeding before you see any of these signs. Offer hay in a covered feeder or in hay bags in shelters. When pasture quality is adequate, they will eat very little or ignore it. A growing interest in hay is a strong indicator pasture nutrition is lacking.

All horses should receive vitamin E, 1000 to 2000 IU/day, preferably in an oil base.  Begin supplementing a high omega-3, flax based product at 2 to 6 oz/day. Horses on mature stands of grass should all be supported with an essential amino acid supplement of L-lysine, D,L-methionine and L-threonine.  As the pasture ages and begins to lose the bright green color, a concentrated quality protein supplement based on soy and whey should be added if supplemental feeds are not meeting protein requirements.  When in doubt about protein and fiber levels, a short pasture analysis can be obtained very inexpensively. Ask your local agricultural extension agent.

If you know when and what to supplement, your pastured horses can keep that Spring glow of health all year long.

Eleanor Kellon, VMD

 

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Insulin Problems – Forget about NSC

Hay or pasture is a major component of any horse’s diet, and is likely to be virtually the complete diet in animals that are obese.  Since insulin resistance is often part of the reason why a horse or pony becomes obese, it’s important to know how to determine if their diet contains a safe amount of carbohydrate but not all carbohydrates are created equal.

Carbohydrates in forage plants include soluble and insoluble fiber (cellulose, hemicellulose, pectins, galactans, beta-glucan), starch, simple and complex sugars and fructans. NSC = Non-Structural Carbohydrates. These are plant cell carbohydrates that are free in the cell and not part of the cell wall.  NSC includes starch plus water soluble carbohydrates – simple sugars, plant sugars and fructans.

So far it sounds like looking at NSC would be smart if you have a horse with high insulin. The problem is, NSC also includes things that do not influence insulin, most  notably fructans. https://wp.me/p2WBdh-gn.  By including fructans in the evaluation of a forage’s safety/suitability, many perfectly appropriate hays are being rejected and owners are spending a lot more time, analysis fees and energy than they need to be.

The answer is to look at the tests that are most relevant to insulin rising – starch and ESC.  ESC = Ethanol Soluble Carbohydrates.  It is the best measure of the simple sugars that can trigger an insulin response when they are digested and absorbed.

Does it make that much difference?

Evaluation of 221 grass  hay samples from Oregon (K. Gustafson, personal communication) showed if using 10% NSC as a cutoff for hays that would need to be soaked or not used, 87% would be called a problem. If the threshold is raised to 12% NSC, 70% were identified as problematic.  When 10% ESC + starch was used as the guideline, only 4% were an issue. Hays passing the 10% or less ESC + starch test were subsequently fed to horses diagnosed as having Equine Metabolic Syndrome without issues.

An argument is sometimes made that NSC should be used because the other carbohydrates contribute calories and most of these horses need to lose weight or have their calorie intake controlled.  However, a lot more than fructan goes into determining the DE [Digestible Energy = calories] of a forage and the hay analysis also actually provides a DE number. That is what should be used to determine caloric content and how much to feed, not NSC.

The take-home message here is that the scientific studies on Equine Metabolic Syndrome and laminitis are all now clearly showing that insulin is the issue. When evaluating possible hays for these horses, the focus needs to be on elements that can cause an insulin rise – ESC + starch. It’s time to stop talking about NSC.

Eleanor Kellon, VMD

 

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The Equine Intestinal Microbiome

The intestinal microbiome is trending, and judging by interest in pre- and probiotics it’s a rather longstanding interest too. Research has actually generated quite a lot of interesting information recently but we are light years away from really understanding how the teeming microbial population in the gut can interact with the horse’s body at large.

The composition of an individual’s microbiome is as unique as a fingerprint, complicating efforts to try manipulating it in ways that are deemed to be healthful [electron microscopic image of bacteria]

Some bacteria, like Salmonella, Shigella and certain strains of E.coli or Clostridia, are known to directly cause disease and we want to avoid them. For the vast majority though, their functions in fermentation of various types of equine foods is understood but any other effects are not well described and what’s good for GI and general health in a dog or human might not be in a horse.

Research to date has shown the three major bacterial phyla in the hind gut, in descending order, are Bacteroides, Firmicutes (some studies show Firmicutes more abundant) followed by Fibrobacteria or Verrucomicrobia in most horses, with many different genus and species within them. However, there is tremendous individual variation by sex, breed, diet, geographical location, level of exercise and things like antibiotics. Because of this, it is extremely important that strict experimental conditions be used to minimize those influences when trying to determine any changes present in a disease state.

There is also limited information to be gained from manure. The microbiome of the cecum and ventral colon are similar but very different from the dorsal colon and small colon. Comparing information between studies and even samples within any given laboratory is  hindered by alterations that occur due to sample handling [Beckers et al 2017].

An area of high interest now is any connection with obesity since mouse and human studies seem to show a clearly different intestinal microbiome in the obese. A few  studies detected some changes in horses but they used subjects not standardized for breed, location and diet. In two well controlled recent studies, Morrison et al 2018 from UK and Coleman et al 2019 USA showed no differences between normal weight and obese horses in their bacterial phyla. Unlike in humans and mice, bacterial diversity is higher in obese horses. Some studies showed an increase in isolated genera like Verrucomicrobia or Pseudoflavonifractor in obese horses but no two studies showed the same thing and others showed no significant differences.

What does all this mean? For one thing, it’s complicated! Even when a pattern is found, as in people and mice, it is still unknown what is cause or effect, chicken or egg. It also  means that services cropping up that claim to diagnose health issues in your horse from a fecal microbial profile have no solid scientific ground to stand on.

There are several companies I know of, in UK, USA, AU, offering fecal cultures or fecal genetic  material profiling which claim to identify disease risk. Among the things claimed to be detected are influences on metabolism, gut wall renewal, dysbiosis/colitis, gut wall integrity linked to diet or “stress”, inflammation/immune function and bloating.  Claims are made that they can identify changes in your horse linked to disruption in those functions, as well as outlandish advice such as supplementing your horse with vitamins and minerals will kill off beneficial microbes.

These tests are very expensive, as are the variety of prebiotics, herbs and anti-acidity products they sell to go along with them and cure the problems.  Don’t be taken in or your horse may suffer along with your wallet.

Eleanor Kellon, VMD

 

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Fall Laminitis

Your horse should be kicking up her heels in the cool, crisp autumn air but every year some are struck by laminitis.  There are several distinct groups of horses at risk and they all have EMS/high insulin in common.

A recent blog described the rise in ACTH hormone which occurs in late summer and fall https://wp.me/p2WBdh-Iy and can trigger laminitis in uncontrolled PPID. Horses with EMS may also be pushed over the edge by this seasonal hormonal shift. Be vigilant for changes in crest, other fat deposits, weight and activity.

Fall laminitis has also been blamed on increased fructan levels in pasture grasses which occur when nights turn cooler. However, grass fructan has never actually been proven to cause laminitis and the higher sugar levels in stressed grasses and fall regrowths are the  real cause. This is only an issue for EMS horses.

EMS horses can also develop laminitis after free access to acorns. Very high intakes can cause poisoning in any horse but EMS horses develop laminitis with no other signs of toxicity because acorns are high in starch. It happens every year.

Another risk group is pregnant mares. Pregnant mares develop insulin resistance as pregnancy advances. This combined with increasing weight and pasture changes in the fall may result in laminitis.

Management of at risk horses should include:

  • make sure ACTH is controlled in PPID horses
  • feed a suitably low sugar and starch diet
  • limit or avoid pasture time when nights are below 40 F or there is obvious new green growth
  • prevent access to acorns

It’s always important to supplement correctly to support healthy hooves. The horse can be assisted nutritionally by supplements which encourage the production of nitric oxide. Nitric oxide is a vessel dilating messenger that is the natural counterbalance to the vasoconstrictor endothelin-1.  The herb Gynostemma pentaphyllum (Jiaogulan) is a powerful support for nitric oxide. This is helped by providing the precursors for nitric oxide in the form of L-arginine and L-citrulline. Antioxidants also combat oxidative stress which inhibits the activity of the enzyme that produces nitric oxide inside blood  vessels [eNOS – endothelial nitric oxide synthesis].

Magnesium and phosphorus are common deficiencies and important for energy generation and storage in metabolically active cells in the hoof.  Selenium and iodine are common deficiencies also and both critical to normal functioning of the thyroid gland. Acetyl-L-carnitine and alpha lipoic acid are antioxidants which also support normal glucose tolerance, as do fenugreek and chromium. Zinc, copper and biotin are often suboptimal and play important roles in normal hoof wall production and hoof integrity.

Proper management and supplementation can assist the horse in maintaining good blood delivery and avoiding nutritional roadblocks to normal  hoof health and metabolism.

Eleanor Kellon, VMD

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Rethinking Deworming Strategy

Deworming by fecal egg count (FEC) is advocated as a way to avoid overexposure of parasites to deworming drugs. It’s important to understand the effect of deworming by FEC is primarily to minimize environmental contamination, not optimally protect the individual.

Young horses, PPID horses and seniors in general are at high risk for parasitism. Even some young adult horses have poor parasite resistance.  Much damage is done by immature forms that are not even laying eggs yet.

The problem with FECs is their limited capacity to detect parasites.

– they only reflect adults that are actively laying eggs at the time of the test
– egg-laying activity may vary seasonally
– tapes often missed because eggs are laid in packets/segments, not evenly mixed in the manure
– can’t detect tissue forms or immature stages in the lumen but these can be the most harmful for the host
– bots missed
– pinworms missed (lay their eggs on the perianal skin)
– Strongyloides in adults not detected

None of that matters in terms of herd health because small Strongyles are the major threat and the only mode of transmission is contamination of the environment by fecal shedding, but it sure matters to the individual.

The other problem is technical limitations. Samples sent through the mail are useless. Samples not collected as soon as they are passed then kept cold are likely inaccurate. The reason is that eggs hatch and flotation methods do not pick up larvae.

As for resistance, helminths come equipped with drug metabolizing enzymes which in some individuals transform the dewormers to harmless compounds. Obviously those genetically fortunate enough to possess those enzymes are the most likely to become resistant by upregulating enzyme activity when they are exposed to the drug – if it doesn’t kill them first.

Any parasitologist will tell you the major way resistance develops is underdosing. (Ditto for antibiotics and bacteria.) What doesn’t kill them makes them stronger. Frequent exposure can cause a dewormer to go from a 20% failure rate to 80% or higher.

It’s also true they can’t be fully resistant to a drug they have never been exposed to so there is an argument in favor of not automatically exposing parasites to a variety of dewormer drugs (rotation).  On the other hand dead parasites do not develop resistance or pass it on to their descendants.

In any case,  it’s wise not to attempt to deworm with drugs that are known to have widespread resistance in the species you are treating. This includes the following reported resistances:

  • Roundworms (Ascarids): Ivermectin, moxidectin, pyrantel
  • Strongyles: Fenbendazole, pyrantel, albendazole
  • Pinworms: https://wp.me/p2WBdh-G5

Last but far from least, there is growing evidence that the practice of only deworming by FEC is leading to reemergence of Strongylus vulgaris – “bloodworms”.

https://www.ncbi.nlm.nih.gov/pubmed/22703964

These are the large Strongyles which do significant damage to the intestine and arterial system when they are migrating. Back when I was starting out as a veterinarian we still had to deal with many horses with S. vulgaris damage and it wasn’t pretty – severe recurrent colic, intestinal infarction, debilitating lameness, even to the point of euthanasia. If you wait to see the eggs in feces, it may be too late. Regular deworming with ivermectin or moxidectin had all but wiped them out.

Deworming strategies have gone from one extreme to another – from frequent, regularly scheduled treatments to deworming only on evidence of egg-laying adults on FECs.  Neither is ideal.  Speak to your vet about developing a program that is optimal for your individual horse.

Eleanor Kellon, VMD

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