Cats infected with Dirofilaria immitis, with or without clinical signs, are defined as having heartworm infection (HWI). If clinical signs (eg, historical, physical, radiographic) are present, then the syndrome is defined as heartworm disease (HWD). Heartworm infection may also be referred to as dirofilariasis or dirofilarosis.
Heartworm-associated respiratory disease (HARD) refers to respiratory signs associated with HWD that may indicate mature, immature, or aborted infection. When associated with infections that fail to reach maturity (aborted), this syndrome has been referred to as pulmonary larval dirofilariasis since immature L5 (early 5th-stage larvae; also termed young adults) produce disease in the pulmonary arteries, and probably, on the basis of experimental infections, alveolar and bronchial lung disease.
Incidence/Prevalence. The feline prevalence is generally believed to approximate 10% of the unprotected canine prevalence in any given region. This percentage varies with the predominant mosquito species in a region because feline infection requires a species that feeds on both cats and dogs. Figures 1 and 2 demonstrate the proven prevalence in cats by necropsy and by exposure, respectively. Although only 10% to 20% of exposed cats have mature HWI, it is important to remember that all these antibody-positive cats are at risk for pulmonary larval dirofilariasis.
Geographic Distribution.Feline HWI is recognized wherever canine HWI is prevalent, particularly in the southeastern United States and the Mississippi River Valley (Figure 3). HWI has been diagnosed in cats in most states.
Age and Range. Cats of any age may be infected with D immitis. The median age at diagnosis is approximately 6.5 years. Clinical signs may be recognized within 3 to 4 months (pulmonary larval dirofilariasis) to 7 to 8 months for mature infection.
Gender. Male cats are thought to be at greater risk due to outdoor roaming habits. In addition, experimental infections produce heavier infections in male cats than in females despite equal larval exposure.
Causes & Risk Factors
Risk factors for cats include male gender, short hair coat, and outdoor exposure. Of course, the risk is increased in highly endemic heartworm areas and in situations where neighborhoods have a high prevalence due to standing water or low socioeconomic conditions. Immunosuppression is associated with human HWI, but to date, cats with feline leukemia or feline immunodeficiency virus have not been shown to be predisposed.
As in the dog, immature adult heartworms (also termed immature L5) may create pulmonary and pulmonary vascular disease in cats prior to maturation. Uniquely, the disease process develops even in cats that ultimately resist mature infection. A severe myointimal and eosinophilic response produces pulmonary vascular narrowing and tortuosity, thrombosis, and possibly hypertension.
Although uncommon, cor pulmonale and right heart failure can be associated with chronic feline HWD. Right heart failure is manifested by pleural effusion (hydro- or chylothorax) or ascites. The lung itself also is insulted by HWI, with eosinophilic infiltrates in the lung parenchyma (pneumonitis) and pulmonary arteries. The pulmonary vessels may leak plasma, producing pulmonary edema (possibly acute respiratory distress syndrome) and type II cell proliferation, both potentially altering oxygen diffusion. In addition, radiographic findings suggest air-trapping, compatible with bronchoconstriction.
The end result to this multifaceted insult is diminished pulmonary function, hypoxemia, dyspnea, cough, and even death. Recently, a symbiotic bacterium, Wolbachia, has been found within filarid parasites and their microfilariae. This bacterium is essential for filarial reproduction and well-being. It has been hypothesized that antigens from these bacteria are proinflammatory, contributing to HWD (particularly upon the death of the adult heartworm) and that tetracycline might be a possible treatment strategy for adult dirofilariasis.
History. Historical findings range from none (28% of cats diagnosed with HWI infection have no signs related to this syndrome) to fulminant respiratory failure and death. The most common signs are those associated with the respiratory tract (coughing, wheezing and dyspnea). Clinical signs are listed in the Table.
Physical Examination. Signs may range from mild wheezing and coughing to profound dyspnea and respiratory collapse. Vomiting is frequently recognized in cats with HWI, but the mechanism is unclear. Neurologic signs (eg, seizures, blindness, paresis/paralysis), due to aberrant worm migration to the brain, eye, or spinal cord are also noted. Heart failure, if present, is typically associated with dyspnea, abdominal distention, diminished lung sounds, and fluid line evident by percussion, jugular venous distention, tachycardia, ashen mucous membranes, and weak pulses. A heart murmur or gallop may be present.
Dirofilariasis (mature HWI) in cats can be diagnosed definitively by several means. Necropsy is considered the gold standard. However, antemortem diagnosis can be assumed with a positive microfilaria test (modified Knott or Millipore filter technique), positive antigen test (indicates mature adult female worms are present), and echocardiographic parasite identification by someone with expertise in this area.
Pulmonary larval dirofilariasis (HARD) is diagnosed by the clinical finding of respiratory signs, antibody-positive status, and suggestive radiographic findings. By definition, these cats will be antigen-negative and will not have worms identifiable by echocardiography.
The antigen test recognizes fewer than 50% of cases because of low female worm burden or immature infection. Consequently, the diagnosis must often be made on a combination of clinical findings (eg, cough or dyspnea), antibody-positive status (indicating exposure, with larval development to the L4 stage and possibly beyond), and radiographic findings.
Eosinophilia is noted in approximately 33% of cases, with occasional basophilia.