Feline heartworm disease: Solving the puzzle - Veterinary Medicine
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Feline heartworm disease: Solving the puzzle
Does that cat you suspect of having asthma really have a heartworm infection? In cats, heartworm disease manifests quite differently than in dogs and has an altered infective cycle. These researchers are seeking to create a definitive model for feline heartworm disease to improve our overall understanding.


Figures 3A & 3B
Cats with abbreviated infections (Group 2) had demonstrable pulmonary vascular lesions, although they were not as severe as lesions observed in the control cats. Vascular morphometry findings in the selamectin-treated cats appeared normal. Statistical analysis supported the fact that lesion scores were significantly lower in selamectin-treated cats than in both nontreated cats and cats with abbreviated infections.

Figures 4A & 4B
Lesions typical of feline heartworm disease were not observed in cats in which selamectin was used as a preventive. Although seemingly intuitive, these studies again demonstrate the benefits of prevention, and there appears to be no evidence that immature heartworms reach the pulmonary vasculature.

The number of heartworms and fragments recovered from untreated control cats confirms and corroborates the results of prior experimental infections. A mean of 4.3 live adult heartworms (range = 1 to 12) were recovered from eight Group 1 cats at necropsy. Six of these cats also harbored worm fragments (mean = 8.5 fragments; range = 2 to 13). Two cats harbored live adult worms but did not harbor fragments. Two cats did not harbor live adult worms but did harbor pulmonary fragments (one fragment and 12 fragments, respectively).

A cat in Group 2 died with respiratory disease presumably in response to immature worm death (one immature worm was present in the heart and two immature worms were present in the lungs at necropsy). No worm fragments of live adult heartworms were recovered from eight of the remaining nine cats in Group 2 cats at necropsy. One affected cat harbored one dead worm fragment attached to the tricuspid valve and one small degenerate worm in the lungs. These numbers strongly support the success of the strategy to kill immature worms in the lungs and the success of the laboratory model.

None of the cats in Group 3 harbored adult heartworms or any evidence of immature heartworms in the lungs.

Preliminary examination of radiographs suggests that radiographic findings correlate with histologic lesions in the lungs. Preliminary data based on thoracic radiographic findings in cats in which development of immature worms was interrupted (Group 2) reveal similarities between these cats and cats with other bronchial diseases, including feline asthma. Consequently, as noted earlier, early death of heartworms in cats is important both pathogenically and in its potential for misdiagnosis. Recall that in early infections, antigenic confirmation of heartworm would not be possible and that antibody responses inconsistently reflect adult heartworm infection. Radiographic and laboratory data (results of antigen and antibody tests, complete blood counts, serum chemistry profiles, and bronchoalveolar lavages) will be made available in a future report.

The results of our experimentally induced infections appear to correlate to a recent assessment of pulmonary lesions in uninfected and naturally infected cats subjected to necropsy examination.8 In that study, pulmonary arterial lesions (occlusive medial hypertrophy) were most severe in the caudal lung lobes of cats that were positive for the presence of adult worms and antibodies to developing stages of D. immitis (19/24 cats; 79%).8 Cats in that group would correlate to our experimentally infected control cats (Group 1). The inherent problems with the poor correlation of antibody testing, radiographic lesions, and the presence or absence of adult heartworms at necropsy have been demonstrated in other experimental infections in which radiographic lesions were present and no adult heartworms were present at necropsy.9 Pulmonary arterial lesions in the cats with spontaneous disease were also severe in cats without evidence of adult worms but with positive antibody responses (12/24; 50%).8 Cats in that group would correlate to our cats in which infections were abbreviated while in the lungs (Group 2). Pulmonary arterial lesions were least severe in cats that were negative for both adult worms and antibody responses (3/24; 13%).8 Those cats could correlate to our Group 3 cats, which were receiving selamectin. However, pulmonary arterial lesions due to other causes would likely be more prevalent in cats in the referenced study because those cats came from random sources and were more likely to be exposed to other potential pathogens. The comparative results of the two studies add further validity to our established laboratory model.

*These results are part of a comprehensive study assessing both short- and long-term effects of experimentally induced abbreviated and nonabbreviated heartworm infections in cats. The results of the short-term study are presented here. An additional three groups of cats were studied for 16 months after infection.


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