Hypertrophic cardiomyopathy in two captive Bennett's wallabies (Macropus rufogriseus rufogriseus).
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.
Journal of Veterinary Diagnostic
The online version of this article can be found at:
2009 21: 889 J VET Diagn Invest
Adam W. Stern, Stephen Smith and Timothy A. Snider
Macropus Rufogriseus Rufogriseus
Hypertrophic Cardiomyopathy in Two Captive Bennett's Wallabies (
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Hypertrophic cardiomyopathy in two captive Bennett’s wallabies (Macropus
Adam W. Stern,1Stephen Smith, Timothy A. Snider
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.
Hypertrophic cardiomyopathy (HCM) was diagnosed during postmortem examination of 2
Bennett’s wallaby; hypertrophic cardiomyopathy; kangaroos; left ventricular hypertrophy;
The myocardium can be affected by a variety of disease
processes, including primary myocardial disorders, degen-
erative and inflammatory diseases, neoplasia, infarctions,
toxicities, and nutritional deficiencies. Idiopathic or pri-
mary hypertrophic cardiomyopathy (HCM) refers to a
primary myocardial disease characterized by a nondilated
and hypertrophied left ventricle in the absence of a known
precipitating cause of disease. Secondary HCM is a term
used when the cause of the cardiomyopathy is known.
Primary myocardial disease is commonly seen in humans
and domestic animals, particularly in cats and, to a lesser
extent, in dogs,9and has been reported7,10in kangaroos.
Left ventricular hypertrophy (LVH) has been reported7in
the rock kangaroo (Macropus robustus) and is associated
with impaired diastolic function, ventricular arrhythmias,
and sudden death.7,10The etiology remains unknown.
Strenuous jumping was a proposed mechanism; however,
similar findings of LVH were identified in the slow-moving
In cases of secondary HCM in Ragdoll6and Maine
Coon3cats, disease-causing mutations have been identified
in the cardiac myosin binding protein C gene. Numerous
investigations have been undertaken to identify nongenetic
causes of HCM, such as hyperthyroidism and nutritional
deficiencies. Nutritional deficiencies are associated with
dilated cardiomyopathy in some animals.1,4,9In the current
report, the diagnosis of primary HCM, a condition not
previously described in this or any other wallaby species, is
described in 2 adult Bennett’s wallabies (Macropus
In a 1-month period during the summer of 2008, 2 of 3
Bennett’s wallabies on an exotic animal farm in north–
central Oklahoma died suddenly. The animals were fed a
diet consisting of 2 different marsupial feeds: Mazuri
Kangaroo/Wallaby dietaand Booster Hopper Choice feed.b
In addition, the animals received Bermuda grass, apples,
sweet potatoes, carrots, and wheat bread. No nutritional
supplements were given to the wallabies. No clinical signs
of heart disease and/or failure were observed by the owner
prior to the death of the 2 animals. The 3 wallabies were
housed within the same enclosure and observed daily. Both
dead wallabies were female; 1 animal was 3 years old (case
1) and the second animal was 4 years old (case 2). The
remaining living animal was an adult male. Both female
wallabies were submitted to the Oklahoma Animal Disease
Diagnostic Laboratory (Stillwater, OK) for diagnostic
Examination of both animals revealed similar gross
findings, with significant findings limited to the cardiovas-
cular, pulmonary, hepatobiliary, and musculoskeletal sys-
tems. The wallaby in case 1 was moderately obese. The heart
was mildly enlarged and on cut surface,markedthickening of
the left ventricular free wall and moderate thickening of the
interventricular septum were seen. The left ventricular free
wall measured 2.0 cm, the interventricular septum measured
1.5 cm,and the right ventricularfreewall measured 0.7 cmin
thickness. Mild, multifocal hemorrhage and dry musculature
were evident in the right hind limb. There was a single liver
fracture and approximately 20 ml of blood within the
abdomen. The thyroid glands were within normal limits.
In case 2, the wallaby was in an adequate state of
nutritional condition. The heart was mildly enlarged, with
slight rounding of the cardiac apex, and on cut surface,
marked concentric left ventricular hypertrophy of the left
ventricular free wall and interventricular septum was seen
(Fig. 1). The left ventricular free wall measured 2.0 cm, the
From the Department of Pathobiology, Oklahoma State
University, Stillwater, OK.
1Corresponding Author: Adam W. Stern, 250 McElroy Hall,
Oklahoma State University, Department of Pathobiology, Still-
water, OK 74078. Adam.email@example.com
J Vet Diagn Invest 21:889–892 (2009)
Case Reports 889
interventricular septum measured 2.1 cm, and the right
ventricular free wall measured 0.5 cm in thickness. The
lumen of the left ventricle was markedly decreased, and the
left atrium was mildly dilated. Bilaterally, the hind limbs
had a moderate to marked amount of subcutaneous and
intramuscular hemorrhage of the quadriceps muscles and
long digital extensor muscles. The thyroid glands were
within normal limits.
To date, there is no published data regarding normal
gross or histologic cardiac parameters for any wallaby
species. When compared to available cardiac measurements
from healthy red kangaroos (Macropus rufa) obtained
utilizing echocardiograms,11the wallabies in the current
report had enlargement of the interventricular septum and
left ventricular free wall (Table 1). Additionally, there was
asymmetric hypertrophy of the left ventricular free wall in
wallaby 1 and symmetric hypertrophy of the left ventricular
free wall and interventricular septum in wallaby 2.
Based primarily upon the gross findings of the present
case, the diagnosis and cause of death were HCM.
Histopathologic examination was performed, and histo-
logic changes were observed in the heart, lungs, liver, and
skeletal muscles. In case 1, sections of the left ventricular
free wall were examined. Histologic lesions of the heart
included mild myofiber disarray, mild myofiber diameter
asynchrony, and marked myocardiocyte hypertrophy with
no evidence of myocardial necrosis, mineralization, and/or
fibrosis. Microscopic findings of the lungs and liver
consisted of marked pulmonary and centrilobular conges-
tion, respectively. Skeletal musculature exhibited mild
multifocal myonecrosis and multifocal hemorrhage. All
other tissues examined were within normal limits. In case 2,
sections of the left ventricular free wall, interventricular
septum, and right ventricular free wall were examined.
Lesions consisted of marked myocardiocyte hypertrophy,
with no evidence of myocardiocyte necrosis, mineralization,
and/or fibrosis. There was marked pulmonary and centri-
lobular hepatic congestion. Skeletal musculature exhibited
mild multifocal hemorrhage. Heart failure cells were not
observed within the lungs in either case. All other tissues
examined (haired skin, uterus, ovary, spleen, brain, and
kidney) were within normal limits.
Left ventricular free wall and/or interventricular wall
thickening are consistent gross findings in HCM of domestic
animals. Pulmonary congestion and edema are commonly
associated with left-sided heart failure. Additional, but
inconsistent, findings of HCM include left atrial dilation,
atrial thrombosis, and aortic thrombosis. The histopatho-
logic hallmarks of HCM are myocardiocyte disarray, cardiac
with LVH, myocardial fibrosis has not been observed.8
As a result of the grossly observed skeletal muscle
hemorrhage and dry texture of the hind limb musculature
in case 1, fluorescent antibody testing for Clostridium
chauvoei, the causative agent of blackleg disease, was
performed and was negative. Additional diagnostic testing
was undertaken for this case to elucidate a cause of HCM.
Although there was no gross or histologic evidence
(multiphasic myocyte necrosis, mineralization, and/or
fibrosis) to support a nutritional myopathy, vitamin E
and selenium analyses were performed on the liver of case
1. Results were 24.45 mg/g dry weight and 1.8 mg/g dry
weight for vitamin E and selenium, respectively. No
published reference values using dry weight are available
for any wallaby species; however, these results were
interpreted as within normal limits, as most species have
reference ranges of 20–40 mg/g dry weight and 1.0–2.5 mg/g
dry weight for hepatic vitamin E concentrations and
selenium concentrations, respectively.8Pelleted feed was
analyzed for ionophores (monensin, lasalocid, and salino-
mycin) and sodium fluoroacetate (1080); none were
detected. Analyses of plasma levels of taurine and carnitine
rufogriseus), case 2. Markedly thickened left ventricular free wall
and interventricular septum with decreased size of the left
ventricular lumen. Section removed from left ventricular free wall
for histopathologic studies. The pale discoloration is due to
formalin fixation. Bar 5 1.0 cm.
Heart; Bennett’s wallaby (Macropus rufogriseus
ratio [(left ventricular free wall [LV] + interventricular septum [S])/
(right ventricular free wall [RV])] compared to healthy mature
Comparison of heart measurements and ventricular
(mm)S/LV (LV + S)/RV
NA 3.26 (2.39–5.12)
NA 2.78 (2.43–4.00)
* NA 5 not available. Measurements for the dog and cow are to
be interpreted as mean 6 2 standard deviations.
were not performed because appropriate samples for testing
were not available.
The association between the sudden death as a result of
HCM and the hind limb subcutaneous and intramuscular
hemorrhage (cases 1 and 2), myonecrosis (case 1), and liver
fracture (case 1) is purely speculative. However, the authors
theorize that these changes likely represent acute traumatic
injury that occurred prior to death. This may be due to a
predator–prey interaction either within the enclosure or
surrounding the enclosure, given that coyotes (Canis
latrans), bobcats (Lynx rufus), and wild dogs are all present
within this region of Oklahoma. The decreased cardiac
output secondary to the HCM may have led to exacerba-
tion of the animal’s heart disease during forced exertion,
resulting in acute left-sided congestive heart failure. The
presence of myonecrosis is supportive of capture myopathy
as a cause of sudden death in wallaby 1. Another factor
that may have exacerbated the existing heart disease in
these animals is the weather at the time of death. The
average temperature in central Oklahoma during this time
was 26.6uC, with temperatures as high as 44.3uC, accom-
panied by high humidity (http://climate.mesonet.org/
The diagnosis of HCM in these 2 wallabies rests
predominantly upon the gross cardiac findings accompanied
by a comprehensive effort to rule out other causes of sudden
death and to rule out etiologies of some lesions seen. Cardiac
and the interpretation of cardiac histology of these 2 cases
should not be considered definitive. Like many other animal
species, peer-reviewed literature establishing normal ranges
of gross and histologic cardiac parameters of any macropod
species is not available, and such data would assist in the
diagnosis of similar cases in the future.
Unfortunately, the inciting cause of the HCM for these 2
cases is not known. According to the owner, all wallabies
on this farm are from different source farms and are not
genetically related. However, because written pedigree
information confirming this fact was not available and
because any wallabies outside of Australia are part of a
limited and unvarying gene pool, a genetic basis for this
disease process cannot be excluded. What seems more
likely, however, is that the cause of HCM in these animals
is environmental. This assumption is based on the
occurrence of 2 cases at the same facility, the short time
frame between the 2 deaths, the lack of chronic changes,
and the degree of the cardiac changes observed. With
genetically based (long-term) HCM, more chronic changes,
such as cardiac fibrosis, would be expected. One potential
source of an environmental cause for development of HCM
could be ingestion of a toxic plant. Plants that are found on
this farm and potentially ingested by the wallabies include
oak (Quercus species), buffalo bur nightshade (Solanum
rostratum), mulberry (Morus species), and pokeweed
(Phytolacca americana). These plants do have toxic
principles but are not known to be associated with cardiac
disease. If these cases truly have an environmental source, it
is quite possible that the remaining wallaby that is alive at
the time of this report has HCM as well. The remaining
third wallaby on this farm was lost to follow-up.
With appropriate gross lesions, HCM should be sus-
pected as a cause of mortality in wallabies without clinical
signs, and a diagnosis can be made at necropsy. The gross
lesions of HCM in the wallabies on this farm are similar to
the lesions reported in other domestic animal species;
however, histologically, the lack of cardiac fibrosis in
kangaroos with unexplained LVH is strikingly similar to
that of the wallabies reported in the current case.
Additional gross lesions, such as aortic and atrial thrombi,
were not observed in the wallabies in the present study.
There are no reports of thrombus formation in kangaroos
In these 2 cases, no specific etiology for the HCM was
identified. Whether there is an underlying infectious agent,
nutritional or toxic component, or genetic cause for the
HCM is currently not known. As stated previously, the
limited export of Australian native species does contribute
to a lack of genetic diversity within existing populations of
these animals outside of Australia and lends support to a
potential genetic cause. Genetically related HCM in
domestic cats often occurs in middle-aged cats, and this
process could be similar in wallabies. Assuming an average
life span of 10–12 years, these wallabies (at 3 and 4 years of
age) were approaching middle age. There may also be
environmental factors of which the authors are unaware
that contributed to the development of HCM in these 2
animals. Alternatively, the changes found in these wallabies
may represent LVH similar to that seen in the kangaroo.
Although not suspected in the cases reported in the present
study, other myocardial diseases in wallabies that may
result in acute death include toxoplasmosis and nutritional
myodegeneration,2both of which exhibit typical histologic
findings of inflammation and necrosis (toxoplasmosis) and
polyphasic myodegeneration and necrosis (nutritional
myodegeneration). None of these findings were present in
these 2 cases.
To the authors’ knowledge, HCM has not been
previously reported in Bennett’s wallabies. Based on the
information reported herein, further studies should be
performed to document normal gross and histologic
cardiac parameters in macropods, to elucidate the
cause(s) of cardiac changes in wallabies, and to determine
whether the wallaby may serve as a potential model for
HCM in humans (similar to the use of the kangaroo for
studying fatal rhythm disturbances). Such studies
should employ electrocardiography, echocardiography,
and histopathology to fully evaluate wallabies with cardiac
Sandra Morgan and Kelly McCracken for their help in
working up this case.
Sources and manufacturers
a. MazuriH, PMI Nutrition International LLC, St. Louis, MO.
b. Booster Feed Mill LLC, Tulsa, OK.
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