Anthelmintic

Many early treatments were herbal, such as the oil of herbs of the genus Chenopodium that were given as anthelmintic treatment for centuries. In 1908 it was found that the active constituent was ascaridole. From the 1920s to the 1970s, halogenated hydrocarbons (such as chloroform, carbon tetrachloride, tetrachloroethylene and hexachloroethane) were used in a string of continually more efficacious anthelmintics, until their underlying host toxicity was revealed. Historically, there have been three main classes of broad-spectrum anthelmintics. These are benzimidazoles, imidazothiazoles/tetrahydropyrimidines, and macrocyclic lactones. • Benzimidazoles disrupt parasitic worms' microtubules, a critical part of their cells' cytoskeletons. and also possesses antiprotozoal effects. This is also an ascaricide. • Oxamniquine – effective against flatworms (e.g., tapeworms and schistosoma) • Praziquantel – effective against flatworms (e.g., tapeworms and schistosoma) • Octadepsipeptides (e.g. Emodepside) – effective against a variety of gastrointestinal helminths • Monepantel (aminoacetonitrile class) – effective against a variety of nematodes including those resistant to other anthelmintic classes • Spiroindoles (e.g. derquantel) – effective against a variety of nematodes including those resistant to other anthelmintic classes • Artemisinin – shows anthelmintic activity ==Anthelmintic resistance==

Anthelmintic resistance occurs when a heritable genetic change occurs in the parasite's DNA, rendering it insensitive to a previously effective anthelmintic drug. This is a particularly serious problem in helminth parasites of small ruminant farm animals. This is a major threat to the sustainability of modern ruminant livestock production, resulting in reduced productivity, compromised animal health and welfare, and increased greenhouse gas emissions through increased parasitism and farm inputs. However, resistance is not seen as often in the parasitic helminths that affect cattle, compared to sheep. Reasons for this include the fact that cattle receive anthelmintic drugs less frequently than sheep, and the different nature of their faecal pats that could leave different numbers of resistant infective larvae on the pasture. Both in vitro (egg hatch assay, larval development test, larval motility test, polymerase chain reaction and in vivo methods (fecal egg count reduction test) can be used to detect anthelmintic resistance.[11] Treatment with an antihelmintic drug kills worms whose phenotype renders them susceptible to the drug, but resistant parasites survive and pass on their "resistance" genes. Resistant varieties accumulate, and treatment failure finally occurs. The ways in which anthelmintics are used have contributed to a major anthelmintic resistance issue worldwide. From the 1950s to the 1980s, new classes of effective and inexpensive anthelmintics were made available every decade, leading to excessive use throughout agriculture and disincentivizing alternative anti-nematodal strategies. Other methods include using a combination of multiple different anthelmintics, and the use of refugia based strategies. Refugia refers to the portion of the parasite population not being exposed to anthelmintics. This population is therefore not undergoing selection for resistance. Use of refugia helps to slow down the speed of evolution of resistance to anthelmintic drugs. Due to the problem of anthelmintic resistance, research into alternatives is continuing, including in the field of rational drug design. == See also ==