Researchers Assess Deworming’s Link to Inflammation in Horses
Cyathostomins, or small strongyles, are the most pervasive internal parasites of horses and the primary targets of adult deworming programs. The larval stages of this species, which become encysted in the large intestine’s mucosa, are what cause disease and clinical signs in horses. In large numbers they can cause a rare, life-threatening disease called larval cyathostominosis—a mass eruption of encysted larvae that leads to a profound inflammatory response in the horse’s gastrointestinal tract.

“Concerns have been raised that killing larvae while encysted within the mucosal walls could lead to adverse (e.g., inflammatory) reactions,” said Ashley E. Steuer, DVM, PhD, assistant professor of parasitology at Texas Tech University’s School of Veterinary Medicine, in Amarillo.

She and a team from the University of Kentucky recently performed a study to assess horses’ inflammatory response to deworming. “We were especially keen on evaluating the difference between a product that kills those pesky encysted larvae (moxidectin) and a product that does not (ivermectin),” Steuer said. She presented their findings at the 2020 American Association of Equine Practitioners’ virtual convention.

“It’s important that we discuss this inflammatory response, because this can cause disease—not necessarily the parasites themselves, but the reaction to their existence within the host,” Steuer said, adding that very few studies have looked at post-deworming inflammation in horses.

The team conducted a two-part study involving 36 healthy, pastured horses with large worm burdens. They divided the horses randomly into three groups of 12: One received a label dose of the larvicidal moxidectin; one received a label dose of the adulticidal ivermectin; and one served as untreated controls. The researchers collected blood from all horses weekly and collected tissue samples from their cecum, ventral colon, and distal colon (all part of the large intestine) two and five weeks post-treatment.

In Phase 1 of the study, the team evaluated tissue samples under a microscope and graded the level of inflammation, especially surrounding any larvae. One aspect they assessed was the amount of hyperplasia (enlargement) in intestinal mucosal epithelial cells called goblet cells, which play a role in the host’s natural defense against parasites.

“We did not see many significant differences in inflammation between treatment groups,” said Steuer. “However, we did note significant differences between goblet cell scores—they were higher at two weeks post-treatment and lower at five weeks.”

She said they also found a significant correlation between worm burdens and goblet cell score, “meaning we would typically find more of an inflammatory response when more worms were present.”

In Phase 2, the researchers evaluated gene expression of the horses’ tissues, looking at pro-inflammatory, anti-inflammatory, and goblet cell responses on a local and systemic level. They found  “horses that receive anthelmintic treatment have a lower inflammatory response because their larval burdens are less,” Steuer explained.

Systemically, they noted a small amount of “spillover” of genes—particularly goblet-cell-associated genes—that you normally wouldn’t find circulating in the blood. She said this systemic effect might be useful information for future studies.

Based on these results, Steuer said her team confirmed that:

  • Goblet cells do respond to cyathostomin larvae burdens.
  • Inflammatory response depends not on the dewormer used but on the worms present.
  • Pro-inflammatory reactions are minimal in otherwise healthy, but heavily parasitized horses.

“Larvicidal therapy is not associated with a measurable effect on pro-inflammatory response,” Steuer said. “Just because you’re treating with that larvicidal dose and eradicating the larvae doesn’t mean there’s going to be an inflammatory response and cause larval cyathostominosis.”