Race Injuries
Wild Herbs
Dry Herbs
Herb Exchange
About Me
Contact Me
Infectious Diseases

         During my life of training and racing horses, I must honestly write that I and my animals have suffered more at the hands of infectious pathogens than anything else in my memory. This is opposite the popular perception that race horses are more likely to die or be adversely affected by breakdowns or common athletic physical injuries in their lives.   My horses have thankfully been spared from both catastrophic breakdowns and the more common tissue failures seen on the track whether by my luck or my skill; however, they have not been so lucky with infections.  Perhaps it is simply the nature of the beast. An animal that is highly tuned and stressed for maximum physical effort on the track most likely will have a depressed immune system because of precisely that life style.  Cortisol, the stress hormone released by the body is one of the strongest immune depresants known to man. Is it any wonder that our youngsters are so vulnerable to barn diseases?  It is very common to hear the word, fraility, bantered around to describe our modern racehorse. This may certainly be accurate if you want to consider the condition of the immune system of our modern racehorse!  Still there may be much that can be done to help strengthen all immune systems, even in the stressed racehorse and there is even more to be done in actually treating an infected horse other than a routine antibiotic protocol.  In many cases, common antibiotics are quite impotent in today's new world of evolved pathogens but, first and foremost, we need to be able to diagnose an infection before it can be successfully treated. On this page, I would like to suggest to you that many of the commonly observed ailments often seen in horses  may not be as they seem.  They may have a microbe based etiology (cause) not commonly accepted in the veterinary literature or by the race track vet.

      My very first taste of what a pathogenic microbe could do to my horses and how ineffective modern veterinary medicine was under such conditions came as a boy back in the 1960s. A little filly of ours came down with sleeping sickness, Equine Encephalomyelitis, a mosquito-borne alpha-virus infection, not that common in my area of Northwest Missouri, but I guess, common enough to do its dirty work. I still recall her to this day trying to hold-on in the front lot of the barn.  From that moment on, I became aware of the horrors, the finality of infections that seemed only moderately affected by modern medicine---at how powerless vets were in fighting many infections.  I became acutely aware that a virus infection was immune to our wonderful array of antibiotics of the 1960s. Those antibiotics that many modern medical soothsayers of that time proclaimed would lead to the total removal of infectious misery from our human and animal's lives.  Later in my racing career, my stable was attacked by the usual array of infections common to all stables, not necessarily fatal, but very troublesome: i.e. Influenza, skin diseases, hoof thrush, etc.  Not only these relatively benign infections, but I would occasionally come into contact with a chronic syndrome that no one seemed to know quite how to treat. One classic example was of a race gelding, I had purchased at a Philadelphia auction.  I shipped him to North Carolina for a winter prep only to find out that he had Colitis X. He had chronic scours. He never seemed to do well and never trained particularly well either. I tried everything on him for that condition to no avail. Had I known what I know now, I would have gone at it in a totally different strategy—live and learn. Then there were those very rare occasions when I actually lost a few horses. My first was while stabled in Pinehurst, North Carolina, and I had a ship-in mare die from a relatively new infectious syndrome that was scaring the dickens out of the horse community back in the early 1980s. The name escapes me now, but the result was a rather horrible death for that nice mare. The second happened to another shipped-in mare when I was racing at Canterbury Downs a few years later. She stepped off the van with a fever and within a few days she was dead, despite the best efforts from the University of Minnesota.  Next, I had a little race mare at Prairie Meadows back around 1990 succumb to what I can only describe of as an unknown type of septicemia. All of these infections did not respond to professional veterinary treatment.  All died. Finally, not so long ago, my nephew purchased a mare and she died within 3 days to what was diagnosed as Blackleg by the local cow vet, but equines do not get black leg! What she died from, who knows, but it was probably a septicemia of some type.

     Back in my early racing days, always there seemed to be the rare threat of the dreaded strangles but, now, the newer infectious threats of the herpes viruses (EHV), EPM, Equine infectious anemia (EIA), West Nile Virus, Potomac Horse Fever, and a few others have brought a unique fear/misery into the horse industry, unimagined back in my more innocent times. I dare say that we have only touched the tip of the proverbial iceberg when it comes to recognizing actual occurrences of equine infections, identifying them, and applying appropriate treatment.   By knowing exactly what is infectious and what is not will serve us well in knowing how to treat such conditions. Knowing that there are legitimate alternatives to our increasingly ineffectual antibiotics against bacteria and that even viruses can be treated with efficacy will save life that would otherwise be lost.  In my book, I will outline a number of old and new techniques that have been employed in the past to defeat infectious pathology, all without the use of modern synthetic antibiotics or the modern hopelessness when it comes to viruses and similar "untouchables".   You will discover that despite the wonderful value of many antibiotics of the past and those of the present, this class of drug offers some very worrying aspects to general health of any animal, particularly the horse. Our common antibiotics can actually cause many microorganisms to revert to an L-form, a cell wall deficient form that will allow it to survive antibiotic therapy. Our beloved antibiotics should never be employed indiscriminately. There are viable alternatives to this class of drug, in some cases, the only alternative when a cure is wanted!

     It seems the norm in medicine to view anything that is characteristically acute in pathology as having a likely infectious origin, if other obvious causes are not readily apparent. This is a well accepted characteristic of infections which can often bias diagnosis.  The word, acute, in medicine means a disease that has an abrupt onset often characterized by fever with rapid progression. The word, chronic, on the other hand, is defined as a disease that lasts a long time, often without obvious spiked systemic inflammatory symptoms or an obvious infectious nature of transmission. I would like to present the proposition here that many of the chronic, historically reoccurring diseases that we experience in the horse may not be as they seem and that those diseases which are labeled, cause unknown, may be microbial instigated. Their manifestation may not necessarily be environmentally (non-microbial, that is) or genetically originated as is often put forth in the literature. Ulcers, diabetes, exercise induced bleeding, colitis, laminitis, cancers, degenerative joint/bone syndromes, heart problems, all as commonly seen in horses, may all have an underlying infectious component that modern vets have overlooked.  As an example, some very titillating studies of equine laminitis have been completed suggesting that a factor unique to the bacterium, Streptococcus bovis,  activates the hoof MMP-2 enzyme which has been proven to cause lamellar separationIn reference to calcium forming disorders often seen in the body, a controversial pathogen called nanobacteria, has been theorized in such pathology as arthritis, bone spurs, bursitis, cataracts, heart/ciculatory disease, kidney stones, tendinitis, etc.   Nanobacteria is still being wildly debated as to actually existing as a life form, but it may and it may be very similar to prions (a non-DNA/RNA infection). Nanobacteria was found to be very difficult to culture and just as difficult to detect, encased in a calcified protective shell which does contain a protein, but any presence of RNA is debatable.  Similarly, other microorganism connections can be found in many of the so called chronic equine diseases, if one would look long enough.  Most intriguing of all are those forms of microorganisms that have no cell walls at all and are known as L-forms, CWD bacteria, etc. . Much confusion exists out there on how exactly to classify these forms. They are very similar to mycoplasma. I recently discussed the role of L-forms with a Molecular Diagnostics Coordinator of a local metropolitan Hospital Pathology lab ,and she had no idea exactly what I was talking about. This is typical of how our current medical professionals do not appreciate the importance of cell wall deficient bacteria as a disease causing organism. Did you know that the use of many of the common antibiotics will actually cause normal bacteria to morph into a L-form? And did you know that L-forms are not easily culturable or easily treated?  Dr. Lida Mattman is the current researcher that has taken L-form research to a whole new level. She has linked and cultured L-forms to such human diseases as lyme, Tuberculosis,  Parkinson's, MS, sarcoidosis, and over other so called incurable diseases.  Modern medicine, both human and animal, tends to relegate many of the acute syndromes to infections while declaring chronic conditions to genetics or unknowns.  The modern researcher still considers the use of the Koch's Postulates, the gold standard in classifying something an infection and something not. Koch's Postulates are no longer viable criteria in defining a disease, microbe-based. It is becoming increasingly obvious that there are many microorganisms that exist which are not cultivable under our current traditional lab techniques and are not easily introduced into another individual to cause an identical infection as Koch once believed. The medical establishment must open up their horizons to new types of microbes that defy these Postulates.  Only then can we progress and know truth.

     Dr. Paul Ewald and Dr. Gregory Cochran have brought new insight into the field of infectious diseases.  Dr. Ewald is a brilliant freethinker, an evolutionary biologist that offers much food for thought when it comes to epidemiology. Before I discuss Ewald, I would like to mention another researcher, Dr. Cochran, who was Dr. Ewald's inspiration. This is all discussed in an exceptional article by Judith Hooper of The Atlantic Monthly.  She quotes Dr. Cochran as saying that widespread, old diseases are infectious, if their incidence in the general population is above one-in-one thousand. Likewise, if he sees a disease that has been observed in a population for many years, he becomes very suspicious that it may well be infectious in nature. His view is that the most "fitness antagonistic diseases" must be of an infectious nature as opposed to genetic.  The word, "Fitness", is defined as simply the survivability of an animal over others on an evolutionary scale. Judith Hooper writes: "Consider a disease with a fitness cost of one percent -- that is, a disease that takes a toll on survival or reproduction such that people who have it, end up with one percent fewer offspring, on average, than the general population. That small amount adds up. If you have an inherited disease with a one percent fitness cost, in the next generation there will be 99 percent of the original number in the gene pool. Eventually the number of people with the disease will dwindle to close to zero -- or, more precisely, to the rate produced by random genetic mutations: about one in 50,000 to one in 100,000."

     This all has major implications to the pathology of the equine as well. You may ask, how does, say, exercise induced bleeding, affect the fitness of survival/reproduction in our modern racehorse when it seems that most all our racehorses are bred with little effort at culling out race bleeding in our breeding stock?  I think this is exactly the key to this question. Bleeding is neither being selected for or against! Thus, it is not realistic to suggest that we are randomly doing exactly that and, additionally, that we are wonderfully successful at achieving increased bleeding in our racehorse population. It is really hard to breed for a trait.   Heritability coefficients can be exceedingly low with success hardly likely even if one is judiciously selecting for it. Only a breeder would appreciate this difficulty. So to make the accusation that our horses are being bred to bleed is ridiculous to me. No one really knows how prevalent bleeding is in our racehorses. There are no accurate statistics and for those that point out that most all of the starters on a card at any race track are on lasix, well, that just means nothing. The mere fact that a horse races on lasix does not confirm a bleeding tendency in the current environment at the American tracks. The first thing, the average American trainer does when a new horse comes into his barn is to get it on lasix as soon as possible. Some states are easier than others in accomplishing this, but any trainer worth his salt can get the job done without ever knowing if his horse is a true bleeder or not. Race track stewards tend to like consistency and having all their horses running on lasix is pretty much a level playing field in their eyes. No wonder lasix is so much abused!  I will discuss lasix (furosemide) further, and how it may relate to improving an infection-induced bleeding syndrome.  I know there are views that almost all racehorses can be scoped after a race and there will be some bleeding present. Well, I am not really sure what this educated opinion means. Certainly this unsubstantiated opinion has no scientific basis to declaring that most all of our horses are bleeders. The time valued system of breeding the best-to-the-best and hoping-for-the-best, should not in itself be a mechanism to breed our modern thoroughbreds into a bleeding genotype. In short, I would hazard to guess that most all of our bleeding racehorses are suffering from an infection.

          So if race bleeding isn't genetic, what is it? Certainly any tendency to bleed in the horse's long ago past would have been bred out by the time that animal evolved up to our current specimens. In prehistoric days, the efficiency of running would have been a life or death trial for selecting the best genes in the primitive horse with bleeding long ago was selected against.  I have no reason to believe that somehow our modern racehorses suddenly acquired a genetic defect for bleeding and that this is being selected and perpetuated by our breeders in a random manner. Nonsense! Dr. Ewald's and Cochran's work seem to concur with this hypothesis as well.  I say that after considering Ewald and Cochran's bio-evolutionary work, exercise-induced bleeding most probably is highly characteristic of a pathogenic syndrome. It seems so crystal clear to me now after so long puzzling why my horses would occasionally bleed. I knew I sent fit horses to the track--so it couldn't be conditioning.   I knew that lasix sometimes helped, but not always. I knew that bleeding was too prevalently seen in a wide diversity of family lines for it to be a genetic thing. Bleeding was seen breed-wide.  After all, one never goes to the auctions and single out specific family lineage as bleeding prone.  It almost has to be environmentally induced, but the question is, what or how? Many people have suggested air pollution could be a reason but, to me, this just didn't make that much sense.  A horse was as likely to bleed in the inner foggy city as he was in the crystal clear air of a country track.  A microorganism cause never seemed to be in question as a general cause of bleeding mainly because bleeding was not obviously infectious by nature or so it seemed. That is the key! An infection can be an infection without being highly transmissible. The Koch Postulates need not apply! Just because our track and University Vets agree that bleeding is not caused by an infection does not make it so.

     In all likelihood, equine pulmonary bleeding is a symptom of a biofilm infection in the horse's lungs. Biofilms are colonies of bacteria and possibly other microorganism types that have found that living together, protected by a self-secreted polymeric matrix can evade normal immune responses and foster a viable community on a living or non living surface. Dental plaque is probably our best known and studied biofilm, but it is becoming increasingly appreciated that biofilms can be found anywhere in the body.  Biofilms are microorganisms characteristically encased by slimy, gluey films that help these pathogenic microorganisms adhere to moist lung tissue and evade the horse's immune cells and commonly administered antibiotics. Biofilms cannot easily be cultured or detected. It is common to inject lasix, a diuretic to treat EIPH in racehorses. It is generally considered that the diuretic effect of Lasix has a direct bearing on lowering plasma volume and reducing right atrial and pulmonary pressure which discourages lung bleeding. Unfortunately, Lasix is not a sure cure and one often has horses bleeding through their lasix on those hot summer days. I would like to suggest another possibility of why Lasix may be therapuetic for EIPH. A study done by Cross, Ramadan, & Thomas, The impact of Furosemide on Pseudomonas Aeruginsoa Biofilms, found that furosemide (lasix) at 10mg/ml reduced some biofilms by 50% at a pH of 8-9.  Furosemide seemed to destabilize biofilms at pH-dependent concentrations. Perhaps this is why lasix, generally, but not always, seems to help race track bleeders?  It is not so much its diuretic action but rather its biofilm destabilization characteristics that produces efficacy in the bleeding racehorse. Fusomide seems to be only effective at proper pH and specific concentrations which in real life could be quite variable in individual racehorses and racing conditions and may be one reason why we see so much variation in Lasix's efficacy on track.

     It seems quite likely to me that if indeed a biofilm infection is at the heart of our racetrack bleeding problem—that it is in all probablity not a simple bacterial biofilm. It could quite likely be made up of a combination of bacteria and fungal components all working in a synergistic environment to further each's goal of survival to the detriment of our racehorse's health. Not only are biofilms off the radar screen of our racetrack vets but a hybrid biofilm consisting of bacteria and fungi would be totally unheard of by this group! Many times, fungi will be secondary colonizers of a biofilm. It has been written that bacteria in these hybrid biofilms can be up to 4000x more resistant to our common antibiotics and the quencher is that most common antibiotics have very little effect on fungi. A recent study found fungi to be a consistent component in biofilms in sinus mucosal samples from patients with eosinophilic mucin chronic rhinosinusitis (EMCRS) and allergic fungal rhinosinusitis (AFRS). Why should the equine be much different? Certainly, one of the protocols to treating bleeding horses is to be very careful about the hay which is fed, guarding against moldy (fungi infested) hay! Maybe this should be a tip-off of sorts?

     A very popular herbal preparation for bleeding is YUNNAN PAIYAO. Many horsemen swear by this Chinese herbal formulation. If you look carefully into its properties, you will find that it contains powerful anti-infective herbs.  This clouds up the mechanism of why it seems to help bleeding horses. Is it mostly a blood regulator, anti-hemoragic or is it an antibiotic or the combination of the two?

 Dr. Ewald has come to the conclusion that when one finds diseases in populations for many generations which still have a negative impact on fitness--they likely are infection based. Note that the idea that certain diseases are heritable, common to family ancestors, does not necessary mean it is so simply, thus. One can have transference of infections or pathogenic DNA/RNA from one generation to the other, giving all the appearance of being a natural heritable process as far as such processes can be described as "natural". The true genetic diseases tend to disappear in the future generations, not necessarily so, generation-after-generation infections.  He writes: '"A disease-causing gene that reduces survival and reproduction would normally eliminate itself over a number of generations."  Natural selection will weed out any defects that are not advantageous to that individual and the family lineage. This is not particularly true of an inherited infection. An infection will be manifested, generation-after-generation, damn the fitness costs and natural selection. 

     Amy Proal in her article, The Bacteria Boom, writes: "So there is increasing evidence that many of the genetic mutations identified by Human Genome Project researchers are largely induced by bacteria and other pathogens. Rather than serving as markers of particular diseases, such mutations generally mark the presence of those pathogens capable of affecting DNA transcription and translation in the nucleus. This is why, in most cases, the "one gene, one disease" hypothesis has failed to hold water. Instead, geneticists are now stuck examining a perplexing number of different mutations, most of which differ so greatly between individuals that no correlation can be made between their presence and any particular illness. The mutations are nothing but genetic "noise," induced either by random chance or by the pathogens that such researchers fail to factor into the picture." I could not state this conundrum more elegantly! In short, she is saying that what our medical researchers like to suggest are purely genetic markers for a disease from random mutations could quite likely be caused by an infection from a microorganism that can manipulate our genes or insert their own genes into ours or our animal's chromosome—a mind boggling premise!

     Our DNA and our horses' DNA are not what it seems and certainly not how most modern genetic researchers would like to portray genetics.  Dr. Gerald Callahan in his book, Infection, The Uninvited Universe, writes: "Only about 10% of the billion letters is part of human genes. That adds up to about 30,000 genes for each of us. Far, far fewer than most of us expected, but even more interesting, most of the DNA inside of human chromosomes isn't human at all. More than half of the DNA in our chromosomes got there as a result of infection. Inside each of us, there is more viral DNA than DNA in human genes. Nearly 8% of our DNA is intact viral genomes. Another 40-50% is viral fragments. A particular group of viruses, called retroviruses, gave us these genes. "  I would like to suggest further that genetic manipulation can be performed by much more than just the retrovirus. Bacteria have been shown quite capable of inducing changes in a host's genotype as well as other classes of microorganisms.

     Enough genetics for now, but just be aware that we and our horses are affected by a whole host of microorganisms that have the capability to insert and manipulate chromosomes and inhabit our horse's body without portraying themselves as obvious infectious pathogens. These pathogens have the power to evade our horses' immune system, evade our diagnosis when using common lab procedures and remain viable despite modern powerful antibiotics. They are a force to appreciate and to consider in many chronic equine conditions that are normally not viewed infectious at first and second glances and, thus, labeled at best,  Cause: unknown.


Dilute Hydrochloric acid therapy

Sodium Chlorite solution as a unique antibiotic

Liposomal Encapsulated Technology  (LET)

Vitamin C as an amazing antimicrobial par excellence!

The long respected gold standard of classifying infections:

Koch's Postulates:    The bacteria must be present in every case of the disease. The bacteria must be isolated from the host with the disease and grown in pure culture. The specific disease must be reproduced when a pure culture of the bacteria is inoculated into a healthy susceptible host. The bacteria must be recoverable from the experimentally infected host.

     All of these points have been paramount in modern medicine to declare something an infection and something, not. New research shows these postulates are no longer valid, that many exceptions can be found in nature..

     I have studied fresh blood mounts via darkfield and epifluorescence microscopy for a number of years now and have observed some very interesting phenomena which for me seems to suggest that blood contains micro-organisms—perhaps mycoplasma colonies. Under normal circumstances, these micro-organisms are checked inside the circulatory system by the natural immune system  of the host, but if one takes a blood specimen and artificially places it on a sterile glass microscope slide where the host's immune system is no longer viable; we have interesting growths appearing over hours and days of incubation. The above photomicrographs are one such example of what I suspect is a bacterial biofilm growth or a mycoplasma colony. The first photo is a fluorescence photomicrograph stained with acridine orange. The green fluorescence denotes DNA content. The photo to the left is of the same colony, but under darkfield only. This suspected colony showed continual growth over days of incubation. I might add that I followed particularly sterile technique in trying to prevent environmental contamination on my slide and cover slip.

     This is another darkfield photomicrograph of a phenomena often seen in many of my incubated fresh blood mounts. These colonies seem to grow unchecked after hours and days of incubation outside the natural defensive immune response of the host. You see red blood cells to the outside of this growth. Perhaps a mycoplasma colony? These structures also stain with acridine orange to indicate DNA/RNA content.

     These are two photomicrographs of the same cells, one white blood cell with surrounding red blood cells.   The first photo to the left is fluorescence (stained with acridine orange in which DNA will stain green) and the second photo is darkfield of the same identical cell field. You will note that because red blood cells do not contain either DNA or RNA, acridine orange will not stain them and, thusly, they will not appear in the first photo. Only the white blood cell will stain green because of DNA/RNA content of it nucleus.  Bacteria will also stain because of DNA/RNA content and bacteria would also be expected to show on the photo to the left. It is thought by a number of researchers that white blood cells are quite likely parasitized by L-forms of bacteria and able to evade the immune system in this fashion. The above white blood cell with the mysterious sprouting filaments seems to suggest the possibility that this particular cell may be infected by such a microorganism. More study is needed.

Visit the new and improved site at:    www.racehorseherbal.net


Ahart Racing, Unltd

All rights reserved including photographs