Feline heartworm disease: Assessing the danger for owners

Figure 1: three-Month disease cycle
An owner depends on the veterinarian to assess the danger of any potential disease to his or her dog or cat. In some instances, these dangers are well known by the general public (rabies, distempter, FeLV), and owner's may request these "preventative measures". In other diseases, the consequences of the disease are not as well defined or understood by owners, and the veterinarian serves the role as an advisor to the owners by increasing their awareness. Whether we like to consider it this way or not, the veterinarian serves in the capacity of a risk manager, much like selling insurance, and he or she has to lay out the gravity of the consequences of not using a preventative medication (insurance). Owners have to often visually "see" the dire consequences of not using a preventative (dehydrated cat with parvovirus for example) or be advised of these dangers. In the center of the awareness issue is being able to accurately determine the current disease status of a pet, as in "is it protected" or "is it currently infected".

Figure 2: Serology of Heartworm Infections
The testing issue in feline heartworm disease is to many veterinarians the center of the problem in making owners appreciate the dangers of heartworm disease in cats. Because we have become so dependent on simple antigen testing for the presence of adult heartworms in dogs, the absence of simple unambiguous definitive heartworm testing in cats has led the practicing veterinarian to avoid discussions of the disease. Consider that in 2002, there were $351 million dollars of heartworm preventative medications sold in the United States, and feline heartworm prevention was only $14 million (4 percent) of this total. Yet, in almost every survey performed, feline heartworm disease is more common in the general cat population than feline leukemia virus infection in the United States. One obvious difference is that we currently have a definitive test for FeLV which although as a screening test has some nuances, practitioners feel secure in using the test and interpreting the results. If we consider feline health over the last 30 years, hyperthyroidism, FeLV, FIV and hypertrophic cardiomyopathy are "new" diseases which have become "main stream" concerns of cat owners mainly because diagnostic methods have been developed which give the veterinarian and owner some security in the ante mortem prediction of the "disease status." Many other feline diseases with real consequences are "off the radar" at this point simply because there is no easy diagnostic method.

Photo 1: Although adult heartworms can develop in cats, disease can be induced months before the heartworm develops into a mature adult worm.
Three-month disease cycle In feline heartworm disease, the diagnostics require more interpretation and the clinical signs are often demonstrated at a different time in the life cycle of the heartworm compared to the dog (Figure 1, p. 23). When the heartworm life cycle is described by parisitologists, veterinarians are often conditioned to consider heartworm disease as a six-month life cycle. However, it should be considered a three-month disease cycle. Just 90 to 100 days after a mosquito has infected a dog or cat with stage 3 larvae, immature L5 (adults) arrive in the right side of the heart. These immature heartworms are only 2 cm in length at 3-month-old immature worms. These small worms are carried out into the pulmonary circulation. Because of the pressure and direction of the flow, these small immature heartworms are deposited into primarily the distal left and right caudal pulmonary arteries. Thus, three months before there is any presence of antigen or microfilaria, heartworm disease is being induced (Figure 2, p. 23). In the dog, this timeframe is rarely associated with clinical disease although evidence can be demonstrated radiographically and histologically. However, in the cat, this three-month disease cycle (three to six months after infection) is often associated with marked increases in interstitial and bronchial disease on radiographs and the cat is much more likely than to the dog to have clinical signs of coughing and/or dyspnea with this early immature infection. A plausible explanation for the difference is that in dogs almost all of the immature L5 that arrive in the pulmonary arteries survive and develop into adults heartworms, resulting in minimal clinical signs during this three- to six-month period after infection. However, in the cat many of the immature L5 in the pulmonary arteries at three months die over the next several months, resulting in inflammation and peribronchial infiltration. (Photo 1) Some cats will develop this early infection, have immature L5 in their lungs, develop clinical disease, and yet never develop fully mature adult heartworms. Thus, the disease sequence is abbreviated in the cat, but there is a consequence of this infection, but compared to the dog, it is just over a shorter timeframe. Heartworm disease in the cat is not necessarily only associated with fully mature adult heartworms.

Determining heartworm status Taking the three-month disease cycle into account, it is not surprising that cats with this early form of heartworm disease are all antigen negative. Given the fact that cats rarely have microfilaria, the standard diagnostic methods for the presence of circulating antigen or microfilaria do not apply to cats. Thus, a cat presented for coughing, dyspnea or sporadic vomiting unrelated to eating may have radiographic signs typical of a bronchial infiltrate with perhaps enlarged caudal pulmonary arteries, yet will be heartworm antigen negative. Because blood, tissue and fluids all have the same radiographic density, the enlargement in the caudal pulmonary artery is often not a consequence of enlargement of the pulmonary artery itself, but a combination of the pulmonary artery and all the inflammation around the distal pulmonary arteries associated with the death of immature L5 heartworms in these sites (Photo 2). Therefore, it is not surprising that in some cats, the apparent enlargement of the pulmonary arteries abate over time, even in the face of a continued adult infection. The spontaneous death of immature adult heartworms in cats causes an inflammatory pattern in the lungs of cats in a similar pattern to the death of heartworms in dogs after adulticidal therapy. The timeframe heartworm death is simply different in the cat (Photo 3, p. 25).