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New Study Reveals Pathology of Feline Heartworm Disease; Proves Existence of HARD

Washington, D.C., AVMA Annual Convention, July 14, 2007

A landmark study that shows conclusively that heartworms do not need to reach maturity to cause pathology in cats has answered many of the questions surrounding feline heartworm and greatly extended scientific knowledge about the long-misunderstood disease.

Recent efforts by researchers at Auburn University bear out a hypothesis developed through earlier research and confirm fundamental differences in the way heartworms affect cats and dogs. In so doing, these reinforce an emerging consensus that feline heartworm is more insidious than previously thought and underscore the importance of prevention.

The study, which was conducted by A. Ray Dillon, DVM, MS, MBA, DACVIM, and Byron Blagburn, MS, Ph.D., was recently presented at the 2007 American College of Veterinary Internal Medicine Forum, and was published in a special Parasitology Supplement to Veterinary Medicine. Dillon and Blagburn are affiliated with Auburn's College of Veterinary Medicine and are longtime leaders in the field of heartworm research.

"This is a major study from people who already have contributed a tremendous amount to our understanding of heartworm disease in dogs and in cats," says Clarke Atkins, DVM, Professor of Medicine and Cardiology at North Carolina State University's College of Veterinary Medicine.

"What they've done is show in great detail that the effects of feline heartworm infection are more extensive than we previously had known. And because both diagnosis and treatment of the disease are problematic, the study highlights once again the importance of prevention."

Julie Levy, DVM, Ph.D., Professor of Small Animal Medicine at the University of Florida, said, "This work has made a major impact in our understanding of heartworm disease in cats. It has shifted our focus from adult worms to more immature stages, and solidly defined feline heartworm disease as a significant pulmonary syndrome, now defined as Heartworm Associated Respiratory Disease."

Understanding feline heartworm has always been challenging due to the difficulties in testing for it and its frequent asymptomatic presentation. As a result, the affliction—unlike its canine counterpart—for years was thought to be infrequent in occurrence and relatively benign in effect.

But conventional wisdom began to shift after the 1998 Heartworm Symposium, where 60 percent of the papers presented were on feline heartworm disease. One of the presentations was a study by Dr. Tom Nelson, past president of the American Heartworm Society, that showed the prevalence of heartworm infection in a random sample of cats was higher than the rates of feline leukemia and feline AIDS.

In 2005, researchers at the University of Florida reported pulmonary arterial lesions in cats that did not have adult heartworms in the heart and lungs but were antibody positive. This led the scientists to postulate that the lesions were caused by the death of immature heartworm larvae. The hypothesis suggested that the disease followed a fundamentally different course than canine heartworm, since heartworms in dogs typically do not cause significant pathology until they reach the adult stage.

The recent Dillon-Blagburn study sought to document in detail the progression of feline heartworm and better understand the origin of lung lesions. The study also was designed to assess the efficacy of a preventive product.

For the experiment, three groups of approximately 10 heartworm-free animals were used. All three groups were subcutaneously infected with L3 D. immitis larvae. Group 1 received no preventive medication and worms were allowed to develop naturally. Group 2 was regularly treated with ivermectin at 150 ug/kg (Ivomec–Merial) beginning on day 84 of the experiment in an attempt to mimic the natural death of developing heartworms in naturally infected cats. Group 3 was given the preventive product selamectin (Revolution–Pfizer Animal Health) beginning 28 days after infection and continuing through the remaining part of the experiment (240 days).

What the researchers found was that marked lesions and disease do indeed result from the death of immature heartworms in the lungs of cats. Specifically, in Group 2–the cats in which worm larvae were killed to simulate natural death of developing heartworms–lung arterial lesions were consistent with the findings from the Florida study of naturally infected cats. Additionally, lesions in the alveoli, bronchioles and bronchi were observed. The lesions were just as severe as those which developed in Group 1, the untreated animals, despite the fact that no worm fragments were recovered from eight of the nine cats in the group. These findings indicate airway disease, in addition to arterial disease, occurs in cats infected with heartworm larvae, despite the fact the worms may never develop to the adult stage.

Predictably, the cats in Group 1 developed live adult heartworms, with a mean of 4.3 live worms recovered from the animals. In contrast, the cats in Group 3, the animals that had been treated with selamectin, harbored neither adult worms nor evidence of immature heartworms in the lungs.

Matthew W. Miller, Professor of Cardiology in the College of Veterinary Medicine and Biomedical Science at Texas A&M University, said the Auburn study argues against long-held conventional wisdom that heartworm does not pose a significant problem for cats. At the same time, he said, it should raise awareness among practitioners that asthma-like symptoms can, in fact, be heartworm-related.

"I think this will prompt us to be more aggressive and proactive with prevention," he said.

Lynelle Johnson, Associate Professor of Medicine and Epidemiology at the University of California–Davis and an expert on feline respiratory illness, agreed that the Auburn study greatly extends the understanding of feline heartworm's pathophysiology and could help provide greater insight into feline respiratory problems in the long term.

Because of the study, Johnson said, "We may see changes in the incidence of lower respiratory disease over time as more cats in heartworm-affected areas are placed on preventive. But it's important that we understand how much baseline disease there is now and then use that for comparison in the future."

Atkins of North Carolina State University said the Auburn experiment will likely continue to produce new science going forward. "This was a very broad and ambitious study, and I think we're just scratching the surface in terms of what we will ultimately gain from it,'' he said. "I'm sure they have a lot of data that they haven't had time to look into yet."

Levy added, "I hope these results will raise awareness among practitioners that heartworms are a threat to cats even if adult worms never develop. It appears that even transient exposure to immature parasites can leave cats with substantial lung pathology that may persist long after any trace of the parasite has been eliminated. Knowing this, practitioners can take a more aggressive stance in promoting heartworm preventive use in cats."

Nelson of the American Heartworm Society said the work by Dillon and Blagburn should help defeat lingering skepticism in the veterinary community about pathogenicity in infections with juvenile heartworms in cats.

"If you're not able to see something and not able to diagnose it, you're inclined to believe it isn't there," he said. "But you very quickly become a believer when you fully understand what has been demonstrated in these recent studies. It's like smoking. You can't necessarily see it, but the damage is being done."



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