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Hypertrophic cardiomyopathy in two captive Bennett's wallabies (Macropus rufogriseus rufogriseus)
Adam W Stern1, Stephen Smith, Timothy A Snider
1Department of Pathobiology, Oklahoma State University, Stillwater, OK 74078, USA. Adam.stern@okstate.edu
Insights
Postmortem examinations revealed hypertrophic cardiomyopathy (HCM) in two Bennett's wallabies. These findings highlight potential cardiac issues in captive macropods, similar to kangaroos.
Area of Science:
- Veterinary Pathology
- Cardiology
- Zoological Medicine
Background:
- Hypertrophic cardiomyopathy (HCM) is a primary cardiac disorder.
- Captive wildlife may experience unique health challenges.
- Bennett's wallabies (Macropus rufogriseus rufogriseus) are susceptible to various conditions.
Observation:
- Two captive adult Bennett's wallabies died spontaneously.
- No clinical signs of heart failure were observed prior to death.
- Necropsy revealed concentric left ventricular hypertrophy, pulmonary edema, and hind limb edema.
Findings:
- Postmortem diagnosis of hypertrophic cardiomyopathy (HCM) in both wallabies.
- Histopathology showed cardiac myofiber hypertrophy and mild disarray.
- Etiology of HCM remains undetermined.
- Cardiac changes resemble those seen in kangaroos.
Implications:
- This case report expands the understanding of cardiac diseases in Bennett's wallabies.
- Highlights the importance of considering HCM in captive macropods.
- Suggests potential shared etiologies or predispositions for left ventricular hypertrophy in related species.
Abstract:
Hypertrophic cardiomyopathy (HCM) was diagnosed during postmortem examination of 2 captive adult Bennett's wallabies (Macropus rufogriseus rufogriseus). The wallabies were members of a mob (herd) of 3 wallabies, and 2 died spontaneously without clinical signs of heart failure being detected. Gross lesions in both cases included marked concentric hypertrophy of the left ventricle, pulmonary edema, and multifocal hemorrhage and subcutaneous edema of the hind limbs. Histologic lesions of the heart were limited to mild cardiac myofiber disarray and marked cardiac myofiber hypertrophy. A specific etiology for the HCM was not determined in either animal. The cardiac changes are similar to the left ventricular hypertrophy previously described in kangaroos.
