Feline heartworm disease is recognized as a severe, life-threatening disease. Many cats do not have clinical signs until they die acutely. Thrombi and intense inflammatory reactions in the lungs are characteristic of the disease. Recent studies have implicated the endosymbiont bacteria Wolbachia as part of the cause of the inflammatory reaction. Eicosanoids are produced during the metabolism of arachidonic acid and modulate inflammatory and immunologic responses in mammals. This study investigated the presence of the eicosanoids prostaglandin E2 (PGE2), thromboxane B2 (TxB2), and leukotriene B4 (LTB4) in naturally and experimentally infected cats. PGE2 levels increased significantly during the first 60 days in the experimentally infected cats then decreased until the last time they were checked, postinfection day 180. At that time the PGE2 levels were still higher than before infection. TxB2 and LTB4 levels increased progressively from the beginning of infection. Some of the experimentally infected cats were treated with ivermectin. Fifteen days after the cats were treated, PGE2 and LTB4 levels were both similar to the levels observed in experimentally infected, untreated cats. The levels of PGE2, TxB2, and LTB4 in naturally infected cats were similar to those of experimentally infected cats 180 days after infection. The high levels of TxB2 and LTB4 are consistent with the inflammatory and obstructive reactions that characterize feline heartworm disease.

COMMENTARY: This study explains some of the reasons we see the syndrome we now recognize as in cats known as Heartworm Associated Respiratory Disease (HARD). The American Heartworm Society and the American Association of Feline Practitioners are conducting a joint public awareness campaign, funded by an educational grant from Pfizer Animal Health, to promote awareness of the serious danger of heartworm disease in cats, which reveals itself as HARD.

Details can be found at www.heartwormsociety.org.

Changes in the levels of eicosanoids in cats naturally and experimentally infected with

Dirofilaria immitis

. Mórchon R, Roca F, López-Belmonte J, et al. VET PARASITOL

147:271-275, 2007.