Host antibodies develop in response to the early migration of the L3 or L4 larvae and are first detected serologically about
two to three months after exposure.34 If an appropriate antibody response occurs, the larvae may be eliminated and may never reach the L5 stage, yet antibodies
can persist for several months.35 So positive antibody test results can simply be an indication of exposure without an actual heartworm infestation. Traditionally,
antibody tests have been used for heartworm screening because they were reportedly more sensitive (true positive results)
than antigen tests,35 but in a recent study, antigen tests outperformed antibody tests when used to identify true positive cases of naturally
heartworm-infested cats. Thus, antibody tests should not be used as a stand-alone screening test; rather antigen and antibody
tests should be used in combination to increase the sensitivity of heartworm detection.31 Eosinophilia and basophilia are supportive hematologic abnormalities noted in some cats with heartworm infestations.37
Figure 5: A short-axis right parasternal view echocardiogram showing the aorta (AO), left atrium (LA), right ventricle (RV),
and main pulmonary artery (MPA) in a cat. The double echogenic linear structures (arrows) within the right ventricle and main
pulmonary artery represent the heartworms.
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Other methodologies for detecting or supporting a diagnosis of a heartworm infestation include thoracic radiography and echocardiography.
Caudal pulmonary artery enlargement greater than or equal to 1.6 times the diameter of the ninth rib at the ninth intercostal
space is supportive evidence of heartworm infestation.38 Echocardiography is most useful in instances in which antigen test results are negative but cats display clinical and radiographic
signs or in cases in which antibody test results are positive and suggest heartworm disease (Figure 5).39
Prevention and treatment
Feline heartworm prevention is recommended during the transmission period, which is year-round in the southern United States
and variable in the northern United States.40 In the Northeast, transmission is from June through November. Infection from D. immitis can be prevented with 2 mg/kg of milbemycin oxime, 0.024 mg/kg of ivermectin administered orally once a month, or 6 mg/kg
selamectin applied topically once a month. Prophylaxis can be started at as early as 4 weeks of age. Heartworm-positive cats
can receive these preventives without complications, so heartworm testing before administration is not necessary in asymptomatic
cats.34
Adulticide therapy with thiacetarsamide sodium (2.2 mg/kg intravenously b.i.d. for two days) is unpredictable and may cause
sudden death from embolism of worms. Acute collapse, pulmonary edema, pneumonitis, dyspnea, cyanosis, anorexia, pulmonary
thromboemboli, hemoptysis, thrombocytopenia, and sudden death have all been reported from adulticide therapy.34 Therefore, the American Heartworm Society does not recommend arsenical therapy in cats.41 Oxygen therapy, supportive nursing care, and corticosteroids have been advocated in such reactions with variable success.
Right heart catheter procedures using various retrieval techniques have successfully removed adult worms from the right atrium,
right ventricle, and pulmonary arteries of cats and dogs with caval syndrome. Special care is necessary to avoid tearing worms
and causing an acute anaphylaxis reaction. Heartworms in cats have a relatively short life span (two years) compared with
heartworms in dogs (five to seven years) because cats are not the normal hosts.34 So in an asymptomatic cat, benign neglect with periodic antigen and antibody monitoring is reasonable. Corticosteroids are
often helpful to treat clinical signs resulting from heartworm disease. Preventing an infestation is optimal because it is
easier than treatment.41 (For comprehensive guidelines on managing feline heartworm infection, see www.heartwormsociety.org.)
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