Variation of drug timing and its effect on "susceptibility gap" larvae in canine heartworm disease treatment
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Abstract
Canine heartworm disease is a serious disease effecting domestic canines and is potentially fatal if left untreated. In the United States it is caused by parasitic filarial nematodes, Dirofilaria immitis, that infiltrate the canine cardiovascular system and accumulate to cause obstructions within the pulmonary arteries and right heart. Mature adult worms give live birth to tiny worms called microfilariae that only molt into infective stage larvae within a mosquito vector. Infective larvae can infiltrate a new host and progressively mature into adults while traveling towards the heart and lungs. The obstructions are not readily reachable through surgery, except in life threatening disease states, so drug treatments are relied on to limit disease progression. The recommended drug protocol for most cases combines the use of macrocyclic lactones and melarsomine dihydrochloride to target the immature and adult stages of parasite development, respectively. As per product labels of both, there exists a gap in larval development from 2-4 months old post infection where the parasite is not effectively treated, thus generating a “susceptibility gap”. Due to this “gap”, macrocyclic lactones are started two months prior to melarsomine. This prevents more larvae from entering the “gap” while those within it progressively age out. However, experimental studies have shown that both drugs are effective on larvae within the “susceptibility gap” to a lesser extent. This poses the potential to reduce the treatment length without sacrificing worm clearage outcome, which can be more beneficial overall for dogs and owners alike.