April 1997

Feline Heartworm Disease

As a follow-up to the February, 1977 Antech News which focused on canine heartworm disease, we present a summary of current views on the clinical, diagnostic, prophylactic and treatment aspects of this disease in cats.

Cats are susceptible but resistant natural hosts to heartworms. Dirofilaria immitus is the causative agent for feline heartworm disease and has the highest incidence rate in the south- eastern United States. The prevalence of feline heartworm disease is generally stated to be 10 percent (10%) of that seen in dogs in a particular region. A vigorous immune response to all stages of the parasite is mounted in host species other than dogs, with that of cats being intermediate between that of humans and dogs. A relatively small percentage of migrating heartworm larvae ever reach the heart in cats. Many migrating worms end up in various other body sites where they die and elicit local inflammatory reactions. If adult worms do reach the heart, microfilariae usually appear in the cat’s blood for just a few weeks. Thus, most cats have occult heartworm infections.

Pulmonary vascular lesions are usually more severe on radiographic and histopathologic examinations of affected cats in comparison to dogs. Radiographic signs are usually lobar, with pulmonary artery enlargement and a mixed bronchial interstitial pattern. Mild to moderate cardiac enlargement is seen in about 50% of affected cats. Aberrant migration of worms to other body tissues produces associated tissue reactions and disease more commonly in cats.

The clinical syndromes are seen in feline dirafilariasis:

• Asymptomatic, self-limiting infections;
• Clinically apparent pulmonary disease, and
• Miscellaneous symptoms associated with aberrant or ectopic heartworm migration, such as neurologic disease.

In experimentally infected cats, 40% of infections are asymptomatic and self-limiting. They are likely to be more common in naturally exposed cats. This type of infection occurs when larvae never migrate beyond the subcutaneous tissues or when adults reach the heart but are subsequently destroyed by the strong immunologic response they elicit. Even though pronounced abnormalities may be seen on radiographs, cats rarely show outward signs of heartworm disease.

Pulmonary dirofilariasis in cats is usually associated with a small number of adult worms (1-7) located in the right ventricle, right atrium, or main pulmonary arteries. When cats are experimentally infected with large numbers of third-stage larvae, 60% will develop pulmonary signs. The incidence of pulmonary disease reported for 156 heartworm positive cats was about 50% with signs of coughing, gagging, dyspnea and tachypnea. In 80-90% of cases, infection is occult due to lack of mating pairs or immune-mediated microfilarial destruction. Up to 1/3 of these infected cats can die suddenly or develop acute, often fatal, respiratory distress. Most cats with the pulmonary form of heartworm disease have a more chronic disorder which can last up to a year or more. Vomiting, weight loss, listless- ness, gagging and a chronic cough can be seen. Vomiting without diarrhea has actually been a more consistent sign than coughing, and has a ready explanation. One study reported that 70% of infected cats were males. Aberrant migration of heartworms (also called "spurious" migration or ectopic heartworms) in cats occurs most commonly in the brain, and to a lesser extent, the spinal cord.

• Nonspecific blood tests, such as the modified Knott’s test, are typically negative in 80- 90% of cats and so are likely to be nondiagnostic. Hematologic changes such as eosinophilia, or eosinophilia and basophilia, occur about 10 weeks after infection, especially if the worm burden is more than 10. The absence of eosinophilia does not rule out infection.

• Heartworm Antibody Testing is available using ELISA or IFA technology. Cats develop antibodies to filaria 2-3 months after infection. Once cleared, seroconversion to antibody negative status typically occurs after 9-12 months. A recent survey of 215 stray cats from the southeastern United States showed that 28 were heartworrn antibody positive and three were both heartworm antigen and anti- body positive. However, only eight of these cats were infected with adult heartworms at necropsy. Of these, 7 were antibody positive and 3 were antigen positive. The conclusion of the study was that a negative antibody test strongly suggests the cat does not have heartworms in the heart, lungs or pulmonary vessels. Reasons why heartworms were not found in 20 of the 28 antibody positive cats include: antibody test became positive before adult heartworms reached the heart and pulmonary vessels; persistence of antibody titers after heartworm infection has spontaneously cleared or larvae have been exposed to monthly preventative; and ectopic heartworms in other tissues not detected at necropsy.

Antibodies to dirofilarial antigens are not generated in cats with unisex or sterile infections.

• Heartworm Antigen Testing has also become available. It cannot detect male heartworms, and may be negative in the presence of only one or very few female heartworms. The antigen tests used for detecting canine heartworms have recently been approved for use in cats. Immature infections can be detected as early as 2 months post-infection with the antibody test whereas antigen testing detects only adult heartworms. Therefore, unlike the anti- body tests, antigen tests detect current infections and not larvae or previous infections.

If the heartworm antigen test is negative and the cat has symptoms compatible with heartworm disease, additional testing with the heartworm antibody test, radiographs, blood profile and ultra- sonography may be indicated. On the other hand, most cats that test heartworm antigen positive have occult infections with substantial pathologic changes in the lung and heart.

Treatment

Cats with heartworm disease are treated in the same manner as infected dogs (see February, 1997 Antech News). When severe pulmonary vascular disease is present, prednisolone (or equivalent) is given at 2 mg/kg P.O. daily for at least 2 weeks before treatment with arsenical adulticides. Discontinue corticosteroid use several days before arsenical treatment to avoid reducing the toxicity of arsenic for the adult worms. Toxic effects of arsenicals tend to be greater in cats than dogs. The main complication arises 7-14 days after treatment when the adult worms begin to die. Acute pulmonary thromboembolism and death can occur in up to 30% of cats, especially if corticosteroids are not used first and the cat is not kept strictly confined. Strict cage rest, oxygen treatment as needed, and high doses of corticosteroids are used for several days for cats that become dyspneic after treatment. A typical arsenical protocol is: Caparsolate (Thiacetarsamide) [Rhone-Merieux] at 2.2 mg/kg IV daily for 2 days. A single treatment course is usually successful in eliminating adult worms in 75-100% of cats.

Heartworm preventives such as daily diethylcarbamazine (several manufacturers) or monthly livermectin (Heartgard for cats, Merck) are now being recommended for cats. Manufacturers recommend diagnostic screening for existing heartworm infection prior to use of preventative. Routine use of these preventatives is debatable, however, because the incidence of feline heartworm infection is quite low even in highly enzootic areas. Furthermore, most of these infected cats recover spontaneously after mounting an efficient immune response. For outdoor cats in areas of high heartworm exposure risk, use of routine preventive treatment may be warranted.

Abstracts from Heartworm Society Meeting, 1995. Feline Practice (24(1): 32-33, 1996.; Feline Heartworm Disease, Round Table Discussion, Part 1. Feline Practice 24(6): 12-16, 1996. Ibid, Part 2. Feline Practice 25(1): 26-30, 1997; Goodwin, JK: Diagnosing FHD in Cats. Vet Prod News, Feb. 1997, pg. 22.