Medical News


Julie K. Levy, DVM, PhD, DACVIM

College of Veterinary Medicine
University of Florida, Gainesville, FL

Feline heartworm (HW) infection is an emerging issue in feline medicine. This is due in part to the recent development of improved serodiagnostic tests for cats, and to increased awareness associated with the promotion of HW preventives licensed for cats. The actual incidence of feline HW infection may also be increasing, paralleling the spread of canine HW infection across the United States.

Pathophysiology of feline heartworm infection

Domestic cats are known to carry at least 4 species of filarial parasites, including Brugia malayi, B. pahangi, Dipetalonema repens, Dipetalonema grassii, in addition to Dirofilaria immitus, the agent of canine heartworm infection. Additional species can be transmitted to cats experimentally. While direct microscopy is often used in the differentiation of filarial parasites, molecular analysis appears to be both more accurate and more sensitive. In the United States, only D. immitus has been reported in cats, with the first case appearing in 1922.

HWs are transmitted to cats when a mosquito that has previously fed on an infected dog subsequently feeds on a cat. Compared to dogs, a much lower percentage of larvae survive to adulthood in cats. HWs survive only 2 to 3 years in cats, compared to 5 to 7 years in dogs, and adult worms are smaller in cats. Cats are much more likely than dogs to have HWs that migrate to unusual locations outside of the heart and lungs where they may be associated with local clinical signs (such as seizures resulting from a HW in the brain) or remain asymptomatic. Cats are much less likely to have circulating microfilaria than dogs. This is due in part to low worm burdens leading to a higher rate of single-sex infections which are incapable of producing microfilaria. However, even male-female HW pairs are associated with amicrofilaremia in cats. Production of microfilaria can be restored when the same HWs are transplanted from cats into dogs, suggesting that the feline environment suppresses HW fertility or that the feline immune response reduces circulating microfilaria.

The organ most often affected by HW in cats is the lung. The pulmonary arteries respond to infection with villous hypertrophy, enlargement (especially in the large caudal arteries), arteriolar muscular hypertrophy, and obstruction by villous hypertrophy, thrombi, or dead heartworms. Eosinophilic interstitial and airway infiltrates are also common. Uncommonly, HWs may lead to right heart enlargement, pleural effusion, or chylothorax. Life-threatening acute collapse may occur in cats with no previous signs of HW infection. This is believed to be associated with the death of a HW which results in massive thrombosis and anaphylaxis.

Significant clinical signs were common in 78 cats diagnosed with natural heartworm infection, including dyspnea (40 percent), vomiting (34 percent), coughing (29 percent), sudden death (19 percent), and neurological signs (14 percent). Sudden death is probably an underreported clinical sign, since most cat owners do not present cats for necropsy when they are unexpectedly found dead at home. The lack of highly reliable serological testing for cats has made it difficult to know the true prevalence of feline dirofilariasis or what proportion of infected cats are symptomatic.

Prevalence of feline heartworm infection

Although cats are naturally resistant to Dirofilaria immitis (D. immitus), feline infection is likely to occur anywhere the parasite is found in dogs. When both cats and dogs are necropsied at animal shelters, worms can usually be found in cats at about 5 percent to 20 percent of the rate they are found in dogs in the same location. Necropsy studies conducted on stray cats from animal shelters in heartworm endemic areas have found adult worms in the heart and lungs in 0-14 percent of cats. This undoubtedly represents the minimum infection rate of cats since many exposed cats fail to develop mature HW infections, and cats are more likely than dogs to have HW located in aberrant sites that would not be detected in routine dissections of the heart and lungs. When 100 pet cats with cardiorespiratory signs were evaluated, 9 percent had confirmed HW infection and 26 percent had positive HW antibody tests indicating exposure.

Feline heartworm prevalence in animal shelter necropsy studies
Year Location No. infected cats Percent infected
1988 Alabama 3/200 2.8 percent
1988 Kentucky 14/100 14.0 percent
1989 Florida 22/712 3.1 percent
1991 Tennessee 3/122 2.5 percent
1992 Louisiana 8/50 10.0 percent
1995 Georgia 5/164 3.0 percent
1995 South Carolina 3/51 5.9 percent
1998 Texas 14/155 9.0 percent
1990 Australia 1/100 1.0 percent
1990 Japan 1/200 0.5 percent
1991 Japan 5/200 2.5 percent
1991 Australia 2/200 1.0 percent
1993 Japan 2/100 2.0 percent
1994 Japan 5/206 2.4 percent
1994 Japan 3/58 5.2 percent
1995 Japan 15/363 4.1 percent
1997 Brazil 1/125 0.8 percent
1997 Japan 15/1840 0.8 percent
2000 Michigan 6/239 2.5 percent
2003 Florida 31/630 4.9 percent
2005 Georgia 4/184 2.1 percent

The University of Florida experience

Our laboratory has necropsied 630 adult cats from our local animal shelter in Alachua County, Florida. Adult HWs were found in the lungs of 5 percent of the cats. Antibodies against heartworms were detected equally in both male and female cats (indicating equal exposure to HWs), but male cats were at slightly increased risk of harboring HWs compared to female cats. There was no association between HW infection and coinfection with FeLV or FIV.

The performance of 6 different HW antigen tests and 6 different HW antibody tests revealed a wide disparity in diagnostic accuracy among the various tests. Not all cats with HWs found at necropsy were seropositive for HW antigen or antibody. Using the finding of adult worms at necropsy as the gold standard, antigen tests had a sensitivity of 68 percent to 86 percent and a specificity of 98 percent to 99 percent. Antibody tests had a sensitivity of 32 percent to 90 percent and a specificity of 78 percent to 99 percent. Nine of 31 cats with HWs found at necropsy (29 percent) had at least 1 false-negative antigen test and 4 cats (13 percent) were negative on all antigen tests. Twenty-one cats (68 percent) had at least one false-negative antibody test, and 2 cats (6 percent) were negative on all antibody tests.

Because neither antigen nor antibody tests correctly detected all infected cats, we disagree with testing protocols that eliminate the possibility of HW infection in a cat if a HW antibody test is negative. Our diagnostic evaluation of cats with HW infection as a differential diagnosis includes both HW antigen and antibody testing and a chest radiograph for initial screening. An echocardiogram is included if the index of suspicion is high. In our study, the combination of necropsy and serological testing indicated that 1 in 6 cats had evidence of infection with or exposure to HWs. Because even a single worm can cause disease or death, HW preventive is recommended for all cats seen by the outpatient medicine service at UF.

Permanent lung disease in cats with transient heartworm exposure?

We recently evaluated pulmonary pathology in cats that were free of adult HW but positive for HW antibodies, indicating either very early HW infection, or previous aborted HW infection. Lung lesions characterized by pulmonary artery occlusive hypertrophy were common in cats with adult HW (80 percent) but not in cats free of HW and HW antibodies (10 percent). An unexpected finding was that 50 percent of cats with HW antibodies, but not adult HW, had these pulmonary lesions, suggesting that even transient infection with HW leaves cats with long-lasting pulmonary pathology.

In light of recent information that HW-associated Wolbachia endosymbionts can exert inflammatory effects even after elimination of the host parasite, it is possible that pulmonary pathology is more closely correlated with the presence of Wolbachia than with HW. It is possible that Wolbachia infection is commonly associated with both transient exposure and persistent infection with HW and that the presence of Wolbachia is an independent risk factor for pulmonary lesions characteristic of HW disease. If recently reported positive experiences with antibiotic treatment of human filarial diseases prove to be predictive of responses in cats, then treatment with doxycycline prior to adulticide therapy in dogs may sterilize HW of Wolbachia, leading to fewer inflammatory side-effects, particularly when the adult worms die. Doxycycline therapy may be especially helpful for cats, which suffer substantial and life-threatening effects of HW disease but for which adulticide therapy is associated with high mortality rates and is generally contraindicated. Elimination of inflammatory Wolbachia organisms may allow cats to coexist more comfortably with their HW, even if an actual cure is not feasible.
Regardless of the outcome of studies evaluating the pathogenesis of Wolbachia in HW disease, it is clear that cats in heartworm endemic regions suffer a substantial risk of infection. Infection presents a diagnostic challenge and treatment options at this time are merely palliative. Even transient exposure to HW larvae appears to leave cats with significant lung pathology.

A. Artery from a cat seronegative for heartworm antibodies and lacking adult heartworms at necropsy. Morphometry revealed a ratio of arterial wall area-to-total arterial area of 0.61. B. Artery from a cat seropositive for heartworm antibodies and positive for adult heartworms. Occlusive hypertrophy is characterized by an arterial wall: total area ratio of 0.96.

Frequency of occlusive medial hypertrophy. Arteries with a wall-to-total area ratio ≥0.95 were classified as having occlusive medial hypertrophy. The percentage of cats in each group with at least one vessel in this category is shown. Heartworm antibody-positive cats and heartworm heartworm-positive cats had a greater frequency of occlusive hypertrophy than negative cats.