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Abstract
Heartworm disease caused by Dirofilaria immitis, is one of the most pathogenic and deadly parasitic diseases in cats and dogs. There is only one FDA-approved drug for the treatment of heartworm disease in dogs alone, melarsomine dihydrochloride. The American Heartworm Societys recommendation for the treatment of canine heartworm disease utilizes a monthly macrocyclic lactone, 30 days of 10 mg/kg doxycycline twice daily, and the 3-dose protocol of 2.5 mg/kg melarsomine. Despite this, many veterinarians are unable to treat with melarsomine due to either contraindications or the financial burden of this treatment regimen. By refining our current treatment regimens focusing on reducing cost and side effects, the number of dogs that will be able to be successfully treated for heartworm disease may increase, improving the health of these animals. In order to evaluate the efficacy and clinical effects of one slow kill protocol, experimentally-infected beagles were administered 10 months of moxidectin and imidacloprid and 30 days of 10 mg/kg doxycycline BID. Heartworm antigen status, microfilarial concentration, and clinical pathology were documented throughout. This study demonstrated a 95.9% efficacy in the elimination of adult heartworms and no improvement of clinical pathology as compared to non-treated controls. Additionally, minocycline was compared to doxycycline as a cheaper alternative for the reduction of Wolbachia in circulating microfilariae during adulticidal heartworm treatment. This clinical trial evaluated the use of 10 mg/kg or 5 mg/kg of doxycycline and minocycline, administered for 28 days BID. Concentration of heartworm 18S DNA and Wolbachia ftsZ DNA were compared using qPCR. The only group in which all dogs tested negative for the presence of Wolbachia DNA by the end of tetracycline treatment was that given 10 mg/kg doxycycline. The role of antigen-antibody complexes in false-negative antigen testing was evaluated by the addition of polyclonal anti-heartworm antibody to heartworm-positive serum. Resulting serum was evaluated pre- and post-heat treatment. False-negative antigen testing was achieved at high concentration of antibody. Heat treatment of these samples reverted false-negative samples back to positive. Antigen-antibody complexes may play a role in false-negative antigen testing of clinical samples, but this may also not accurately represent every clinical case.