Feline Heartworm Disease

Dirofilaria immitis infection in cats is a very real clinical problem with a increasing incidence and awareness. Heartworm disease in cats was originally reported in Brazil in 1921; and has been reported worldwide. Cats with heartworm disease are consistently diagnosed in heartworm endemic areas where dogs have the disease.

The increased awareness of the disease has made antemortem diagnosis more common. The frequency of heartworm infection in the cat is generally accepted to correlate with the dog population of the area, but at a lower incidence. The clinical signs and diagnostic approach are different in the cat as compared to the dog; which has impaired the veterinarian's ability to detect this parasite in the cat. New techniques and methodologies have now made the cat owner and veterinarian better able to be aware of this potentially severe disease.
 
 

• Some highlighted words in this text are linked to definitions, not images.

• 1. Biology of the Infection in Cats and D. immitis life cycle

• 2. Pathology and Clinical Presentation
• Clinical Signs
• History
• Physical Examination
• Clinical Pathology

• 3. Diagnosis
• IFA Testing
• Antibody Testing
• Antigen Testing
• Electrocardiogram
• Radiography
• Echocardiogram
• Tracheal Cytology
• Differential Diagnosis

• 4. Clinical Management
• Adulticidal Therapy
• Post Adulticidal Complications
• Efficacy of Treatment
• Conservative Therapy
• Preventative Medication

Ray Dillon, DVM, MS         E-mail Diplomate American College of Veterinary Internal Medicine (ACVIM) Jack O. Rash Professor of Medicine Dept of Small Animal Surgery & Medicine

 

The cat is a resistant, but suceptable host.  Thus they can get heartworms, but it takes a  greater exposure than in dogs.

• If dogs not previously exposed to heartworms are infected with 100 L3 larvae, about 75 adult worms develop in almost 100 % of dogs .

• If cats not previously exposed to heartworms are infected with 100 L3 larvae, about 3-10 adult worms develop in about 75% of cats.

 

(Basic review of D. immitis life cycle- dog & cat)

Incidence maps presented at World Veterinary Congress, Japan 1995 (Japan) (Italy)(US) (US SE)

• Less infective larvae survive to become adults, but most cats can be infected if exposed to L3 larvae.
• Experimentally, heartworm disease is more difficult to produce in cats than in dogs. Moreover, the percentage of infective larvae (L3) developing into adult worms is significantly less in cats (1-25%) than in dogs (40-90%).
• Cats are at greatest risk in a heavily endemic areas where repeated bites by infected mosquitos are common.
• Remember, the average mosquito can only transmit a maximum of 10 infective larvae, therefore an experimental infection with 100 L3 would represent 10 - 20 mosquitoes all biting a cat at the same time.
• However, experimentally, when adequate infective larvae are used, the percentage of infective larvae developing to adult Dirofilaria immitisis low, but the percentage of cats from which adult worms are recovered is high (66-90%).
• Infective larvae in the cat are poorly oriented therefore ectopic sites for the adult (brain, subcutaneous tissue, abdomen) are more common than in the dog.
• The worm burden is less in the cat (range usually 1-9 worms) compared to the dog, but up to 20 adults have been experimentally induced in a cat.
• Although the adult worms reach significant size in the cat, (female > 21 cm, male > 12 cm), their development seems to be slower in the cat than the dog.
• Experimentally, the male cat is easier to infect and the worm burden tends to be higher when exposed to the same number of L3 larvae as in female cats.

Once infected with adult D. immitis, the cat is a poor reservior

• Once infected by adult heartworms via either infective larvae (L3) or transplantation (from experimentally superinfected dogs) the natural resistance of the cat induces a shortened period of patency and a lower concentration or absent microfilaremia.

Microfilaria are bigger in width than a RBC. Although they live for up to 2 years and are present in about 60% of dogs with heartworms, but they are rarely observed in the blood stream of the cat. Therefore the cat is not considered to be a host that can provide mosquitoes with a site to acquire potential larvae. Mosquites that feed on cats rarely if ever infect other cats with heartworms.

• The average time from infective larvae being introduced into the cat until the development of circulating microfilaria in experimental infections is about 8 months and occasionally longer in the cat compared to the typical 5 to 6 1/2 months in the dog. Since the microfilaremia is transient and in very low numbers , the use of concentration tests are recommended and a negative test does not rule-out heartworm disease (see "Diagnosis" below). Microfilaremia is uncommon (< 20% of spontaneous clinical cases), inconsistent and transient when present.Infective larvae developed in about 1% of Anopheles spp. and Aedes spp. mosquitos that fed on cats with patent infections. Thus the cat is a potential but insignificant source as a reservoir for the parasite.

• Some species of mosquitoes will readily feed on both dogs and cats, others prefer only one species. The incidence of heartworms in cats is very high in some areas (18%) and may reflect the willingness of a species of mosquito in the area to feed on both dogs and cats.
• Thus as noted on incidence maps, there is no consistent ratio between the percent of mongrel dogs with heartworms and the percent of cats in the same area with heartworms. (Note (US SE) and (Italy)
• Which cat gets infected depends on a mosquito being willing to feed on a dog and then later feed on a cat. With over 50 species of mosquito being able to transmit heartworms, this is an important variable.

• There is a high mortality of the L5 as they first reach the lungs, 3-4 months after infection. An acute reaction is often noted at this time.
• Evidence supports the premise that adult heartworms in the cat have a relatively short life span (probably less than 2 years) compared to the dog (approximately 5 years). Survival of adult worms after transplantation and after L3 infections would indicate that the cat does not harbor the adult as long and spontaneous recovery is much more likely in the cat than in the dog. A shortened longevity would contribute to an underestimation of the incidence of heartworm disease in the cat based on routine necropsy examination of the general population. A gradual decrease in the number of adult worms found in the heart has been noted when cats are chronologically studied. Thus the cat is a susceptible but resistant host for Dirofilaria immitis with a more transitory disease than in the dog.

The general pulmonary pathology in the cat is similar to that of the dog. Muscular hypertrophy, villous endarteritis, andcellular infiltrates of the adventitia are typically more severe in the caudal pulmonary arteries. Typical of the reaction of the cat, the smaller arteries develop severe muscular hypertrophy . The host's response to the parasite is intense as demonstrated by enlarged pulmonary arteries within 1 week of transplantation.

The cause of the acute crisis in the cat is lung injury resulting in respiratory distress. Often this is associated with the death of an adult heartworm. The lung can become acutely edematous and respiratory failure, not heart failure, becomes the life threatening event. The inflammatory lung changes are much like the effects of a bee sting on a persons finger, the resulting swelling of the tissues make the lung unable to function. This cat had demonstrated no clinical signs before a fatal crisis. Obvious the subclinical disease had been chronic.

Embolization of pulmonary arteries can be a contributing factor to initiation of clinical signs. Although pulmonary hypertension does occasionally occur, right axis EKG changes, radiographic evidence of right sided hypertrophy, and right sided heart failure are infrequent. Indicating that severe cor pulmonale is uncommon in the heartworm cat. Although in chronic cases perivascular reaction and evidence of thrombus formation with recanalization are noted, it would appear in the cat that cardiac changes are minimal. Obstruction of blood flow, especially to the caudal pulmonary arteries causes acute signs and the lung lobe involved becomes hemorrhagic with areas of edema. If the cat survives the initial embolic lesion, recanalization around the obstruction occurs rapidly and the lung is markedly improved within days. The result of the acute lung injury is a Type II alveolar cell hypertrophy. Post-caval syndrome with ascites and right sided heart failure will occur in rare cases with very high worm burdens. Hemglobinurea has not been a consistent finding is these heartworm cats. Poor venous return and tricuspid insufficiency rather than cor pulmonale are considered the pathogenic mechanism of this syndrome in cats.

The hallmark of the disease in the cat is the acute lung injury resulting in a generalized respiratory failure. The inflammation is observed even in lung lobes not associated with embolization. Thus the disease is not a simple obstructive disease associated with blocking of blood flow. The lesions are acute and inflammatory; expecially associated with dead worms.
 

Pulmonary Intravascular Macrophages- Specialized cells which are unique to the cat and reside in the capillary bed of the lung. Their phagocytic activity is altered by heartworm disease. They are attached to the endothelial cells by electron dense adhesion sites (See arrow in expanded frame). ACVIM abstract on PIM activity in Heartworm Cats

Because the cat is a resistant but susceptible host as compared to the dog, the increased immunologic response of the cat to the parasite would help explain many of the clinical signs. As the parasite first arrives in the lungs as early as 100 days after being infected by a mosquito, the lung responses with intense inflammation and "asthma- like" symptoms may develop. The cat has a specialized macrophage (designed to envelop and digest foreign materials) in the capillary beds of the lung that are not present in the dog. After the mature parasite develops, the clinical signs may be intermittent or absent. The parasite seems to be able to suppress the immune function. However, at the time of worm death, the lungs become extremely inflamed and the specialized macrophages may become key players in the intense reaction. The result is a non-functioning lung and an acute respiratory distress syndrome. This reaction can occur as the result of even a single worm burden.

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There is no age predilection to Dirofilaria immitis infection in cats and a wide age range of clinically infected cats is reported (6 month - 17 yrs). Indoor and outdoor cats are both represented and indoor cats have a high incidence of positive antibody titers suggesting a successful early infection. (AAVP abstract on clinical study.)A higher incidence in males compared to females in experimental and clinical cases may represent a sex susceptibility.

Feline leukemia virus infection is not a predisposing factor and heartworms are not a common incidental finding at necropsy of cats with FeLV. The arrival of immature heartworms in the lungs and death of adults, are most likely to be associated with clinical signs. The initial arrival (as early as 100 days after infection) of the L5 in the distal pulmonary arteries induces a diffuse pulmonary infiltrate and signs typical of "eosinophilic pneumonitis."

Clinical Signs: The initial clinical signs associated with early infections occur most frequently in the late Fall and early Winter months (4-7 months after the exposure). At this time, because the worms are immature, antigen tests are usually negative. After the initial host response, the signs may abate and become subclinical for a period of time. However, the subsequent death of adult heartworms causes additional severe signs. Infected cats may die acutely, exhibit chronic signs, or be asymptomatic (Table 1). Based on cardio-pulmonary changes and experimental studies, most heartworm cats even with severe heartworm disease are asymptomatic once the infection becomes established.

In the acute cases, death may be so rapid as to preclude diagnosis or treatment. Sudden death has been attributed to circulatory collapse and respiratory failure from acute pulmonary arterial infarction and acute lung injury. Acute collapse may occur with or without previous clinical signs. Cats which die from heartworms can be clinically normal 1 hour before death. All cats with peracute death in heartworm endemic areas should be examined for heartworm disease. In acute cases as few as 1 worm has been found accompanied by severe pulmonary congestion, infarction and edema. The worms in the acute syndrome are not always found embolizing the main pulmonary arteries.

History: The most common historical complaints in cats with clinical signs are coughing, dyspnea, vomiting, lethargy, anorexia, and weight loss. Vomiting and respiratory signs are the predominate complaints in chronic clinical cases, although it is unusual for an infected cat to exhibit both symptoms concurrently. (AAVP abstract on clinical study.) Vomiting tends to be sporadic. The etiology of vomiting in heartworm cats is unknown although the release of inflammatory mediators from the lungs which stimulate the chemoreceptor trigger zone has been hypothesized. The vomitus generally contains food or foam and is rarely bile stained. Retching and severe paroxysmal vomiting is a rare historical findings. Heartworm disease in endemic areas should be included in the differential diagnosis of chronic emesis in the cat. The most common respiratory complaints are coughing and intermittent dyspnea. Hemoptysis is occasionally noted. The coughing can be in severe paroxysmal attacks. Periods of normalcy (days to weeks ) is often seen between episodes. Based on historical data, the coughing is usually temporarily corticosteroid responsive with exacerbation during therapy. The clinical presentation, radiographic pattern, and response to therapy often lead to a tentative diagnosis of bronchial asthma.The dyspnea may be a result of acute emboli formation especially associated with worm death. On occasion, occlusion of a pulmonary artery (right caudal being the most common) is accompanied by a radiographic appearance of lung lobe consolidation and the development of life-threatening acute dyspnea. The non-specific clinical signs are consistent with many feline diseases. Anorexia and/or lethargy can be the only presenting signs in heartworm cats. In these cases, heartworm disease is often an incidental finding on thoracic radiographs during diagnostic screening. Cats with worms found in abnormal locations may have signs attributable to local pathology. Neurological signs are uncommon but can occur in infected cats with or without worms in the CNS.

Physical Examination: The physical examination is usually normal in Dirofilaria immitis infected cats. A systolic murmur over the tricuspid valve area and occasionally a gallop rhythm can be present, but as a general rule are uncommon. Harsh lung sounds (dry rales) are the most frequent abnormal auscultatory finding and can be present in cats without respiratory signs. Ascites, exercise intolerance, and signs of right sided heart failure are rare. There does not seem to be a correlation between the clinical signs, physical findings, and radiographic findings.

Clinical Pathology: Routine complete blood counts may demonstrate a mild anemia (23-33% Hct), occasionally nucleated RBC's, and basophilia (rare). Anemia is present in about one-third the infected cats and is non-regenerative, as in heartworm positive dogs. Peripheraleosinophilia, present in about one-third of client cats at the time of diagnosis, is an inconsistent finding even on serial samples in the same cat and is dependent on the stage of the infective larvae. The eosinophilia occurs 4-7 months post-infection and intermittently thereafter. The absence of eosinophilia does not exclude a diagnosis of feline heartworms.

Cytology of bronchial alveolar lavage fluid may contain eosinophils without the presence of a peripheral eosinophilia. As in the dog, the presence of basophilia is highly suggestive of heartworm disease.

Blood chemistries and urinalysis are usually normal. Although hyperglobulinemia does occur in some heartworm cats, it is neither consistent nor predictable and should not be used to rule out feline heartworm disease. Normal serum globulins and normal electrophoresis are found in cats that are heartworm positive based on Knott's tests, IFA tests and/or antigen tests. Experimental infections produced via L3 larvae or transplantation of adults usually result in a microfilaremia of short duration and low numbers. Thus, a positive blood test for microfilariae is unlikely but diagnostic for heartworm disease. The odds of identifying a heartworm infection are increased by repeated testing (3-4 tests) and using larger quantities of blood (5 ml) for each test. Concentration tests such as Knott tests or milipore filter techniques are best. Even with repetitive testing, occult heartworms represent over 80% of feline heartworm disease. In North & South America, the only filarial disease of cats is heartworms, therefore any microfilaria observed should be considered D immitis.

There are 3 serologic methods which have been used for feline heartworm disease. Rapid advances are constantly changing these assays.

1) IFA for microfilarial antibody

2) ELISA for adult antibody

3) Adult antigen detection by ELISA and colloid gold

Antibody Testing: The ELISA test (detecting feline antibodies to adult heartworm antigen) shows promise and initial concerns related to false positives from cross-reactivity have not been detected. The use of the ELISA (as adapted from the canine ELISA) in the cat to confirm a clinical diagnosis has been very helpful and false positives from cross-reactivity have not been observed. The canine methods for measuring dog antibodies to heartworms cannot be used on cat sera. Initial studies of cats that have eliminated the adult parasite naturally or after adulticidal reveals that a negative ELISA titer develops when the host antibody gradually decreases to negative concentrations (4-6 months). The ELISA test denotes a method of analysis, therefore antigen preparation, antibody sources, and techniques can vary between diagnostic laboratories and titers may differ accordingly. (AAVP abstract on clinical study.)

Because the antibody being detected in produced by the cat in response to the early migration of the L3 or L4 larvae, positive titers are detected about 2-3 months after a successful infection. Detection of antibodies by the antibody test is of clinical significance in symptomatic cats which have negative antigen tests due to the presence of immature worms. However, with the use of macrolides as a preventative medication, the larvae in a cat can initiate a positive antibody response and then be killed by the macrolide; producing a antibody positive but heartworm negative cat. Additionally, the death of adult heartworms may produce a strong antibody response after release of large amounts of antigen. Some of the highest titers are associated with severe clinical signs in cats where the worms have died and the disease may be resolving.

In rare cases, the antibody test can be negative even in the presence of adult worms. There are several different antibody tests currenly available, and there are differences in the specific antibody each appears to quantitate.

Antigen Testing: Heartworm antigen detection tests utilizing blood or serum have been successful in dogs and have been positive in cats within days of transplantation of mature adult worms from dogs into cats. Since the antigen being detected seems to be derived primarily from the adult female reproductive tract, immature infections, a low worm burden, a male infection, or sexually immature worms may not produce enough antigen to be detected. The elimination of the adult parasite will also cause a negative antigen test. Cats may develop positive antigen tests 6 months after the experimental introduction of large numbers of infective larvae.

However, clinical cats and experimentally infected cats with active heartworm disease and high antibody titers can be negative on antigen testing. The low number and slow maturation of adult worms in clinical infections and the clinical signs associated with immature worms make it prudent to consider a positive antigen test diagnostic but not to rule out heartworms based on a negative antigen test. Most cats with heartworm disease are antigen negative.

There are now several different assays for antigen in the blood, and each should be reviewed for strengths and weaknesses. However, currently the antigen tests appear to be detecting the same basic glycoprotein.

Electrocardiogram: Although subtle signs of right ventricular enlargement are occasionally noted (with unipolar chest leads) a right axis vector (>120 degrees) on a standard 6 lead EKG is rare. Ectopic ventricular beats and other arrhythmias have been infrequently seen after adulticide in asymptomatic cats.

Radiography: Radiology is a screening tests for feline heartworms. The pulmonary parenchymalchanges are non-specific and can change rapidly in infected cats. The lung changes include diffuse or coalescing infiltrates, perivascular densities, and lung atelectasis. The most distinctive radiographic sign is enlarged pulmonary arteries with ill-defined margins.This is most prominent in the caudal lung lobes on the VD view. Blunting and tortuosity of the pulmonary arteries are occasionally seen, but not as common in cats as in dogs. An enlarged main pulmonary arterial segment extending beyond the cardiac border on the VD or DV view is not a classic feature of feline heartworms. Arteriograms as a diagnostic tool may demonstrate the enlarged pulmonary arteries and embolus. A non-selective angiocardiogram is a simple and safe method of confirming a tentative diagnosis of heartworms. A radiographic exposure 5-6 seconds after injection of a contrast material into the jugular vein will provide good visualization of the pulmonary vasculature and on occasion the presence of worms. There does not seem to be a correlation between the severity of lesions based on angiocardiogram and the severity of clinical signs or post-adulticide reaction. Some cats with heartworm disease have normal radiographs. Because of the changing nature of the disease over time, repeated radiographs are often necessary.

Echocardiogram: Parallel hyperechoiclines, representing an image from the heartworm cuticle, may be observed in the pulmonary arteries (PA), right ventricle (RV), or rarely the right atria (RA). These lines are generally not over 0.5-1 cm in length because of the angle of the probe and curved nature of the worms in the heart. Heartworms in the most distal pulmonary arteries often cannot be visualized (distal to LPA & RPA). Echocardiography (images: Dr. C. Atkins, NCS) is useful to confirm a tentative diagnosis of heartworms.

Actual videos of the echocardiogram pictured above are available in several different formats below. These are large files and may take a considerable length of time to download over a modem connection. The file size is listed next to each available version.

The right parasteral view gives the best view of the pulmonary outflow tract. The most common location of the adult worm is the pulmonary outflow tract.

Tracheal Cytology: The finding of eosinophils on a tracheal wash is common in heartworm disease, asthma and parasitic lung diseases. In feline heartworms, the presence of eosinophils on the wash seems to occur 4-7 months after L3 infection and often may not be present later in the infection even when adult worms are present.Tracheal cytology typical of chronic inflammation may be present after the eosinophilic reaction resolves. Careful fecal examination should be performed before the tracheal wash. Fecal flotation and direct smears may reveal the large operculated egg of Paragonimus kellicotti or the larvae of Aelurostrongylus abstrusus.

In the cat with respiratory signs, heartworm disease must be differentiated from Aelurostrongylus abstrusus or Paragonimus kellicotti infection, asthma, cardiomyopathy, and other diseases associated with dyspnea (pyothorax, pleural effusions, pneumothorax, anemia, etc). Although each in various stages can mimic the clinical and radiographic pulmonary parenchymal changes, the pulmonary arterial changes of heartworm disease are unique, if present, and can be enhanced by contrast procedures.

The changing clinical and radiographic pattern of disease make the diagnosis difficult and over the time course of the disease, there will be differences in diagnostic results. The peripheral eosinophilia, eosinophilic tracheal cytology, and chronic cough of feline heartworms is consistent with a diagnosis of "bronchial asthma." However, an apparent higher incidence of asthma has not been reported in heartworm endemic areas. The enlarged pulmonary arteries and muscular hypertrophy of Aelurostrongylus abstrusus and Toxocara cati infection is clinically uncommon.

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• CBC
• Knott test
• Thoracic radiographs
• Fecal examination
• EKG
• Echocardiography
• Serology for feline antibody against adult antigen
• Serologic detection of adult antigen
• Tracheal wash or BAL
• Arteriogram

After the diagnosis of feline heartworm disease, the veterinarian and client are in a lose - lose proposition. One can let the adult worms die on their own over the next several years and run the risk of continued problems and on occassion an acute crisis. Or one can use an adulticide and eliminate the worms and run the risk of acute complications associated with the worm(s) dying all at once with severe consequences.

Mechanical removal of heartworms through surgery or special forceps and brushes has been successful. Mechanical removal should only be attempted in cats where worms have been demonstrated in the rights ventricle or pulmonary arteries by echocardiogram.

The nature of feline heartworm disease to cause chronic vomiting, intermittent respiratory signs, or to be asymptomatic often misleads the client into thinking the disease is not severe. Spontaneous acute complications and death in a small percentage of cats can occur. Therefore, the client must be warned that withholding therapy can be lethal in a minority of cases. In the asymptomatic cat, this risk appears to be small compared to the complications of adulticidal therapy. Because the adult heartworm has a shortened longevity in the cat compared to the dog, the possibility of spontaneous recovery should also be discussed. However, the natural death of the adult worms can be associated with severe respiratory signs. Cats which have been managed conservatively by intermittent corticosteroid therapy have developed peracute signs and died from heartworm disease. In the cat with recurrent dyspnea that is life-threatening or with clinical signs that are unacceptable to the owner, adulticidal therapy has been used safely and should be considered.

Adulticidal Therapy: Treatment of feline heartworm disease with thiacetarsamide sodium (2.2 mg/kg IV, bid, two days) is tolerated by cats without immediate complications of hepatotoxicity or renal toxicity. The use of ketamine as a sedative to aid in careful administration of thiacetarsamide is recommended in active cats. There are occasional reports of acute symptoms after thiacetarsamide injections, but slow injections have not caused acute collapse in normal healthy cats in this author's experience. Pulmonary edema as a complication during the two days of injections has been observed and oxygen therapy and corticosteroids should be considered if dyspnea and/or cyanosis occurs. This complication cannot be predicted and attempts to reproduce the acute lung injury have been unsuccessful.

In the symptomatic cat, clinical signs tend to improve after therapy. However, anorexic cats may require hyperalimentation. Although the presence of circulating microfilaria is uncommon, ivermectins have both been used successfully as microfilaricides. Imidicide at the dog dose should not be used in cats.

Post Adulticidal Complications: Complications after therapy are usually related to embolization. The complication of pulmonary edema and cyanosis warrants further consideration but has not been consistent with this author's experience. Sudden death from embolization can occur especially within the first 10 days after adulticide administration. Embolization can induce severe lung injury, hemoptysis and dyspnea. Severe thrombocytopenia and disseminated intravascular coagulation has not been noted. Based on the assumption that heartworm mass is related to antigen load, a cat with a "strong positive" antigen test would be more likely to develop post-adulticide complications than a cat that has a low worm burden and is antigen negative or "weakly positive." Embolization most often affects the caudal lung lobes and thoracic radiographs may demonstrate a lung lobe with increased density. Oxygen therapy is indicated if dyspnea occurs. High doses of corticosteroids (1-2 mg/lb of prednisolone three times a day) with careful IV fluid therapy will often support the cat through the crisis. The routine use of corticosteroids is not recommended before or after thiacetarsamide in cats. Aspirin is contraindicated in feline heartworm disease. Based on current information, there is evidence that aspirin may inhibit prostaglandin formation and thus increase leukotriene production in the lung; the result would be increased inflammatory mediators, bronchospasm and pulmonary hypertension. Because of the potential protective effects of ketamine as an serotonin antagonist, a single IM injection of ketamine has been recommended before administration of the first dose of thiacetarsamide. The peracute nature of the post-adulticide reaction dictates that the cat be under constant attention, especially during the first two weeks. The clinical and radiographic signs of acute embolization can resolve over one to two days. However, death can occur before therapy can be instituted. The client should be aware that the risk of complications in the cat seems to be greater than in the dog. The severity of the post-adulticidal reaction poses a dilemma for the veterinarian and the risk of post-adulticide complications is probably greater than the risk of spontaneous death in the asymptomatic, heartworm infected cat. The advantage of treating a cat is being able to observe the cat during two week period after thiacetarsamide therapy while the worms are dying compared to not knowing when the heartworms will die on their own in an untreated cat.

Efficacy of Treatment: Although heartworms in cats may not live as long as in dogs, clinical signs and even death may occur. The efficacy of thiacetarsamide cannot be evaluated in many client cats because of the occult nature of the disease. However, of cats that have had microfilariae, repeated attempts to eliminate microfilariae have failed and repeated adulticidal therapy has been required in some. However, current research seems to indicate that the adulticide is effective and clinical signs usually abate during the initial weeks after thiacetarsamide. As is known in the dog, immature worms are probably resistant to thiacetarsamide. If a cat was antigen positive before therapy, the antigen test should be negative 12 weeks after adulticide therapy. A positive test at this time would indicate the presence of adult heartworms after the adulticide.

Conservative Therapy: In cats with intermittent clinical signs or if the owner will not accept the potential risk of adulticidal therapy, the owner should be educated as to the nature of the peracute signs of embolization. Alternate day prednisolone therapy (5 mg/kg) has been used successfully to prevent clinical signs of coughing and vomiting. However, progression of radiographic lesions have been observed during corticosteroid therapy. In addition, acute respiratory distress and death have occurred in cats on conservative glucocorticoid therapy. An emergency dose of oral or injectable glucocorticoid should be dispensed to the owner to be administered if collapse or dyspnea are noted. The onset of acute respiratory signs in a heartworm cat is a true emergency requiring immediate care. The radiographic signs of severe lung pathology should not be over-interpreted as "consolidation or pneumonia." The initiation of intra-nasal oxygen therapy, cage rest, small volumes of intravenous fluids, and injectable prednisolone has resulted in clinical improvement and resolution of radiographic signs within 24 hours of presentation in cats with life-threatening dyspnea and collapse.

Preventative Medication: In endemic areas with vector populations (dogs) providing the mosquito with a reservoir, the incidence of heartworms in cats indicates that preventive medication are needed. Infection from D. immitis in cats can be prevented with the newly released feline product Heartgard for Cats, (24 mcg/kg of ivermectin; Merial Limited, Iselin, NJ, 07065). administered per os once a month. In endemic areas, it is suggested that preventative medication be administered as early as 6 weeks of age and continued for the life of the cat.

Selamectin (Revolution®—Pfizer Animal Health) was approved by the U.S. Food and Drug Administration (FDA) as a heartworm preventative for cats and dogs at a dose (6 mg/kg) applied topically once a month starting within one month of the pet’s exposure to mosquitoes.  Although other heartworm preventatives have been combined with additional products to gain label claims for internal parasites, selamectin as a singular topical product in cats prevents heartworms, treats and controls fleas and ear mites, and is indicated in treatment of hookworms and roundworms. Selamectin can be initiated at 6 weeks of age.
 

Because current antigen testing is inconsistent in cats, especially those with a low worm burden, antigen testing before instituting preventative therapy in an asymptomatic adult cat would not seem to be cost effective. Although heartworm disease may be of low incidence in many areas, the high rate of complications associated with feline heartworm disease makes preventative medication an attractive alternative. Sub-clinical signs of heartworms may precede the more obvious clinical syndromes of allergic lung disease in cats. Heartworm positive cats may be safely placed on preventative medication. A positive antibody test reflects that the cat has been successfully infected and that the parasite has lived several months and may or may not have developed to be an adult. A positive antibody test does not preclude administration of preventative medication. Although heartworm disease can be self-limiting in many cats, the potential to initiate inflammatory lung disease and predispose to bronchial asthma may prove to be adequate indications for preventative medications for cats in endemic areas.