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Feline heartworms

The document summarizes key differences in heartworm infection and disease progression between dogs and cats. While cats can develop heartworm infection when exposed to infective larvae, they typically have a lower worm burden of 1-9 worms compared to dogs. In cats, the disease has a more transitory course, with worms having a relatively short lifespan of less than 2 years. Clinical signs in infected cats are often acute and related to inflammatory lung injury from dying worms.

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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. Thus the cat is a susceptable, but resistant host. Anywhere heartworm disease has been found in the dog, it has been observed in cats
Less infective larvae survive to become adults, but most cats can be infected if exposed to L3 larvae . 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. 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.
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 &quot;Diagnosis&quot; 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.
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. 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
The life cycle would then dictate that for a cat to become infected, a mosquito must bite a species of animal with a patent infection (usually a dog) and then after proper climate conditions, bite a cat. The feeding pattern of the mosquito determines which cat get infected. Some species o f 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.
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. Obstruction of blood flow, especially to the caudal pulmonary arteries causes acute signs and the lung lobe involved becomes hemorrhagic with areas of edema.
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.
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 &quot;asthma- like&quot; 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.
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.
Clinical Disease 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. A higher incidence in males compared to females in experimental and clinical cases may represent a sex susceptibility .
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
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.
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. 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 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 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.
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
Diagnosis 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
The IFA test (detecting antibodies to microfilarial cuticular antigen ) is diagnostic in about 33% of positive cases, but the presence of immature or sterile worms, worms of only one sex, or the absence of host response to antigen does not produce a diagnostic titer.
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 serum. 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.
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.
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.