Lyme Disease in the Equine

By Dr Joyce Harman DVM, MRCVS


Lyme disease (LD) has been recognized for about 40-50 years. It is now the most commonly reported tick-borne illness in the US and Europe and is found in Asia and Australia. The Centers for Disease Control and Prevention (CDC) showed more than 35,000 reported human cases in 2015. Many cases are not reported to the authorities, so the actual numbers are not known and likely higher; equine cases are not reported. Since LD can be found in so many locations, it should be considered as part of a rule-out list when a diagnosis is not clear.

The different stages of a Tick's life

The organism

The Lyme spirochete (Borrelia burgdorferi) is a very mobile, corkscrew-shaped bacterium. Contrary to popular belief, deer are far from the only host for the infected tick as the different tick species prefer different hosts. Many small mammals are part of the host cycle, from the white-footed mouse to the chipmunk, hedgehog and rats, along with humans and dogs. Squirrels of many species worldwide are capable of being carriers and are numerous. Fleas, spiders, mosquitoes, and mites are also possible parts of the life cycle, though the available research has not defined their exact role.

The nymph stage ticks are the source of most infections while the adult tick, which is a little larger and easier to see, may be less important but potentially infective.

Borrelia Burgdorferi

Spirochetes behaviour within the body

Spirochetes possess separate plasmids (DNA strands) and have an inner and an outer protein coat, which is unusual in the bacterial world. The outside coat comes into contact with its host organisms and can be adapted to whichever host the spirochete encounters.

There are many different outer surface protein coats, called OSP ( Outer Surface Protein), and different portions of them are upregulated while the tick is eating its blood meal, even before the spirochete enters the body. The compound decorin essentially hides the outer layer of the spirochete from the host immune system so that it can enter the body undetected. The spirochetes can then modify themselves in a variety of ways to avoid detection by the immune system. The spirochete cells also communicate  in several complex ways, including quorum sensing, plasmid transfer and gene expression to evade antibiotics and immune detection, an event that also occurs with other resistant bacteria.

While in the body, the spirochetes continue to alter their structure from moment to moment. This probably contributes to the various symptoms that are part of the LD picture as well as the resistance to treatment.

Spirochetes are attracted to different kinds of cells in the hosts, particularly collagen. Joints, aqueous humor of the eye, meninges of the brain, skin collagen, and heart tissue (less so in the equine for an unknown reason) are all susceptible. Spirochetes travel faster in collagen than they do in the bloodstream.

The spirochetes are clever opportunists responding to an assault from an antibiotic or the immune system by either changing their protective surfaces, entering a cell, and even forming a protective coating inside the cell. Other evasion tactics include creating a completely different form, usually referred to as a cyst; however, there are also blebs and spheroblastic L-forms. Studies have shown that after antibiotic treatment with various drugs, the DNA of the B. burgdorferi changes, leading to antibiotic resistance, or more likely, a tolerance.

Clinically, many horses seen with later stages of LD seem to mount a poor immune response. This frequently is observed as low white blood cell counts on a traditional CBC. Poor immune responsiveness may be the reason behind the commonly seen low to equivocal Lyme antibody titers.

The longer the spirochetes are in the body prior to treatment, the more adjusted they become to the specific immune situation in that host.


The characteristic bull’s-eye skin lesion is generally missing in the equine and dog, most likely due to the presence of their hair coat. One of the most common signs is lameness that is difficult to specifically identify. In humans, cognitive problems, irritability, fatigue, headaches, disorganization, nerve pain, deficits in memory and retrieval of information, reduced perceptual motor skills, and problem solving are all serious issues. All of these symptoms likely exist in the horse though we usually see irritability, fatigue, lack of interest in work, perhaps stubbornness, or perceived stubbornness, or dullness, all of which are difficult to diagnose. Clinically, about 10-15% of the horses in the author’s practice area become dangerously spooky when infected with the Lyme spirochete


A combination of a thorough history along with a complete physical exam and blood work are required. The history often becomes the most important part of the diagnosis. Many, if not most, of the horses show behavioral changes of various sorts, the most common being lethargy, irritability, or lack of interest in their surroundings. In some cases, as mentioned above, the behavioral changes trend more towards the hyperactive or spooky side. The key is a significant mental change.

The physical part of the history can include shifting leg lameness, stiffness, joint swelling, poor performance, reluctance to turn, and poor jumping performance, etc. In many cases, horses have been worked up for subtle lamenesses and have had traditional treatments such as joint injections and various anti-inflammatory medications but have not responded well. Diagnostic imaging may be inconclusive or may point to joint inflammation, yet treatment of that inflammation yields poor results.

Other signs that have been attributed to Lyme borreliosis are anterior uveitis, neurologic signs, low grade fever, sensitivity to touch, lameness, weight loss, tremors, neck pain, lethargy and laminitis. These signs can be caused by other diseases that are also commonly seen. Those include anaplasmosis, EPM, “tying up,” equine polysaccharide storage myopathy, and many more.


Continue reading the full article by Dr Joyce Harman DVM, MRCVS