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“Is parasite resistance a concern with EPM treatments?”

This is a question I often get and find particularly puzzling. While the equine industry faces challenges with antimicrobial and anthelmintic resistance, concern about antiprotozoals inducing resistant parasites can likely be crossed off the list.

There are 2 primary reasons. First, for resistance to develop, antiprotozoal drugs would need to be overused, selecting hardier organisms for survival. In my mind, that is not happening in the equine industry. Second, the life cycle of Sarcocystis neurona – the primary causative organism of EPM – shows us that even if resistance is selected, the parasite will die with the host. The rare exception would be if opossums scavenged the horse. Let’s take a closer look.

BIOLOGY OF S. NEURONA MAKES RESISTANCE HIGHLY IMPROBABLE

Sarcocystis neurona has a 2-host life cycle – a definitive host, the opossum, and several intermediate hosts, with skunks, raccoons, armadillos and cats among the most common. Opossums are commonly infected with S. neurona and are a major source of infection for horses. The horse is a dead-end host and becomes infected with S. neurona by ingesting food or water contaminated with opossum feces (see Figure 1). S. neurona cannot be transmitted horizontally among horses, nor can it be spread by nonequine intermediate hosts.

The life cycle of S. neurona is the primary reason concerns with antiprotozoal resistance are unjustified. The parasite’s life cycle endswith the horse unless the opossum scavenges the horse, which isunlikely.

Although limited evidence exists that the horse may serve as a natural intermediate host for S. neurona 1 , it is unlikely that horses are normal intermediate hosts that contribute to the parasite’s life cycle. This is because S. neurona sarcocysts typically are not found in the tissue of horses, and equine carcasses are rarely accessible to opossums.

Hence, a horse treated with an antiprotozoal drug is highly unlikely to harbor resistant forms of S. neurona that can then be ingested by opossums, completing the parasite’s life cycle. Furthermore, all drugs that are FDA-approved for the treatment of EPM have been shown to yield concentrations at steady state that are in excess of what is needed to inhibit S. neurona growth. There are likely strains of S. neurona that are less susceptible to antiprotozoals, but that does not make them resistant.

WHAT HAPPENS IN THE HORSE, STAYS AND DIES IN THE HORSE

Resistance is often a result of product overuse (or incorrect use), as we have seen with antibiotics and deworming compounds. However, the same comparison cannot be made with EPM treatments. Not only is overuse of EPM treatments unlikely, but the biology of the inciting parasite makes resistance highly improbable. In the words of the late President Harry S. Truman, [when it comes to S. neurona in the horse] “the buck stops here.”

ABOUT THE AUTHOR

Nicola Pusterla, DVM, PhD, DACVIM, DAVDC-Equine is a professor of equine internal medicine and dentistry at the University of California, Davis, School of Veterinary Medicine. His research focus is on equine infectious diseases with an emphasis on molecular epidemiology. Dr. Pusterla also leads the UC Davis Equine Infectious Disease Research Laboratory.

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1. T. Mullaney, et al. Evidence to support horses as natural intermediate hosts for Sarcocystis neurona. Vet Parasitol. 2005;133:27-36.