Dr. Scott Bowridge, associate professor, food animal science at West Virginia University, began a presentation on small ruminant parasites with a quote: “After the symptoms of haemonchosis have been seen, the time necessary for fattening lambs is greatly increased and requires the use of more expensive grains for finishing than non-parasitized lambs. The prime requisite of economical sheep production is raising sheep that don’t suffer from parasitism.”

The quote is from a textbook published in 1949, but haemonchosis, the condition resulting from infection with Haemonchus contortus (barber pole worm), remains a challenge for those raising sheep and goats.

The process of Haemonchus infection in small ruminants begins when animals graze on pasture and pick up parasitic larvae. Larvae are 0.7 mm long and don’t have legs or appendages. Moisture, often in the form of dew, is critical for larvae survival, and sheep are often grazing dewy pasture in mornings and evenings.

Haemonchus larvae travel through the rumen, reticulum and omasum and land in the most inhospitable environment of the GI tract – the abomasum. Once in the highly acidic abomasum, larvae wrap themselves around gut villi and take a small blood meal. There, they ultimately grow into adult worms. Adults mate, and females lay between 5,000 and 10,000 eggs per day on pastures.

Within 24 hours, in a warm, moist humid environment, eggs transition to larvae. It takes three to seven days for an egg to become an L3 larva. “In the L3 stage, larvae are no longer feeding on fecal material they’ve been in,” said Bowridge. “They are metabolically silent, just existing until they get inside the host.”

An important survival feature of Haemonchus is the lancet mouthpart that pierces the host’s mucosal wall. “They poke the sheep in its stomach, open their mouths and feed on blood, move to another spot and poke and feed on blood, and continue to do so,” Bowridge explained.

As the worm feeds, its intestines fill with the host’s blood. The barber pole appearance comes from wrapping itself around the villi. “These worms aren’t moving much,” he said. “They’re crawling on the surface of the abomasum.”

Each adult Haemonchus consumes about 0.5 ml of blood/day, which isn’t as significant for a 200-lb. ewe as it is for a 60-lb. lamb, but there’s a cost to blood loss no matter the age or size of the animal.

As blood is lost, the body replaces blood volume with fluid. This excess fluid often accumulates in the lower jaw area due to the animal having its head down to graze. As animals eat, some of the fluid pushing into the blood volume leaks out of blood vessels. This fluid leakage results in bottle jaw (hyperproteinemia).

The cost of parasitism

As heavily parasitized, anemic animals eat with their heads down, some of the fluid pushing into the blood volume leaks out of blood vessels and results in bottle jaw. Photo by Sally Colby

Losing red blood cells leads to anemia. Chronic anemia leads to lethargy, weakness, anorexia and difficulty maintaining body condition. In some cases, blood loss results in shock and death.

“With parasitism, we typically see something called regenerative anemia,” he said. “Animals have an ability to replace red blood cells, but it takes about two weeks. There’s no way to speed that up so animals have to survive in an anemic condition. There’s a huge nutritional drain on animals to generate an immune response and also to replace the lost blood volume.”

Internal parasites have become a serious problem primarily because the drugs used to treat them are no longer effective. “We used them because we could,” said Bowridge. “If one sheep had diarrhea, we dewormed them all. We’ve been very reliant on chemotherapeutics and have lost the effectiveness of dewormers.”

Sheep and goat producers have three main classes of dewormers to manage internal parasites: macrocyclic lactones such as ivermectin and moxidectin; imidazothiazoles such as Levamisole (Prohibit®); and benzimidazoles (white dewormers) including fenbendazole (SafeGuard®, Panacur®) andalbendazole (Valbazen®).

Researchers found sheep were resistant to benzimidazoles on 23 of 26 sheep farms in a study. “What we’ve seen over the past couple of years is that benzimidazoles simply don’t work,” Bowridge said. “The cattle industry has abandoned benzimidazoles for pour-on drugs.”

Most benzimidazoles don’t work well throughout the U.S. for several reasons, including the way they’ve been formulated and their wide use in feed-throughs and mineral blocks. For most sheep farms in the Northeast, levamisole remains the most effective product.

“The same thing is happening in goat herds,” said Bowridge. “There’s resistance to benzimidazoles and macrocyclic lactones. The one we don’t see much resistance to is levamisole – a neonicotinoid. That’s partially because they’re hard to mix, difficult to dose by weight and don’t last long – it’s out of the system in about 72 hours.”

It’s important to understand that dewormers don’t actually kill internal parasites. “They paralyze worms,” said Bowridge. “If a worm can’t hold position by swimming in the gastrointestinal tract, it’s going to be swept out with everything else. All dewormers are paralytics – they paralyze worms using different mechanisms.”

The best approach for managing parasitism is selective deworming using the FAMACHA system. This method helps to maintain a population of worms that are still susceptible to dewormers, which is key to maintaining effective deworming products.

“The more sheep you deworm, the more you create parasites that are resistant to dewormer,” said Bowridge. “Every time you deworm an animal, you’re changing the genetic structure of the [worm] population and selecting for worms that are more resistant to drugs.”

About 20 years ago, producers were advised to rotate dewormers as a means of staving off resistance. The most recent recommendation to improve efficacy is to use a combination of products from different drug classes and use the same dewormers until they are no longer effective. Each drug should be given individually followed by a separate dose of the second drug.

The problem isn’t going away, and we aren’t getting any new drugs any time soon, Bowridge said.

by Sally Colby