Aust Vet J Vol 76, No 2, February 199898

I
BD of snakes in the family Boidae
(boas and pythons) has been
report ed in captive snakes in the
USA, Africa and Europe over the past
20 years.
1,2
In addition, the disease has
recently been diagnosed in the USA but
not yet reported by one of us (E
Jacobson) in a king snake (Lampropeltis
getulus family Colubridae) which was
housed with boa constrictors (Boa
constrictor). This snake developed clinical signs of central nervous diseas e and
intracytoplasmic inclusion bodies
typical to IBD were found within hepatocytes. Native Australian snakes of the
family Boidae are members of the
subfamily Pythoninae. Boas (subfamily
Boinae) are exotic to Australia but are
present in privat e and zoological collections within Australia.
3,4
The virus associ ated with IBD resembles type C particles of the family
Retroviridae and has been isolated in
Burmes e python (Python molurus bivittatus) and boa constrictor primary
kidney cell cultures. In transmission
studies Kochs postulates have been
partially ful filled but full molecular
characterisation of this virus remains to
be completed.
1
Retroviral infections
associated with tumours have been
report ed previously in non-boid snakes,
5
7
however, the signifi cance of these viruses
remains to be determined.
We report here the clinical signs and
pathological findings of two cas es of
IBD in captive pythons. These are the
fi rst published cases of inclusion body
disease of boid snakes in Australia.
Case 1
A 5-year-old fem ale carpet python
(Morelia spilota variegata), purchased as
an adult in south-east Queensland, was
submitted with a history of anorexia of
12 months duration. Two months prior
to submission, it had been displaying an
open-mouthed stance with her head
raised. She was occasionally disoriented
and intermittently listed to one side. She
was euthanas ed after failing to respond
to therapy of fenbendazole (100 mg/kg),
praziquantel (15 mg/kg), metronidazol e
(40 mg/kg) and a 20 day course of
enrofloxacin injections (5 mg/kg/day).
Six months before submission, her male
carpet python mate had been
euthanas ed for neurological signs which
included agitation, head tilting, incoordination and episodic convulsions.
Between the time of purchas e and death,
both snakes had been directly housed for
2 weeks with a carpet python caught in
the wild and kept under a rescue permit
by another herpetologist.
At necropsy, there were no signifi cant
gross findings. Histological examination
revealed many irregular ovoid, rectangular or angular variably sized (2 to 10
m) eosinophilic intracytoplasmic
inclusion bodies in hepatocytes and
renal tubular epithelial cells, with occasional inclusion bodies in the bronchial
and intestinal epithelium and in splenic
macrophages. Other histological
changes included moderate diffuse
hepatocytic vacuolation and moderate
diffuse depletion of splenic lymphoid
tissue. In the brain, there was spongiform change of grey matter, chromatolytic neuronal degeneration and
neuronal loss, occasional neuronal intracytoplasmic inclusion bodies, occasional
axonal swelling, mild multi focal gliosis,
mild perivascular lymphoplasmacytic
cuffs and mild lymphoplasmacytic
meningitis. Segment al swelling of
myelin sheaths and axons and mild
multifocal gliosis were seen in the proximal spinal cord. No signi ficant lesions
were present in the heart, skeletal
muscle, integument, kidney or body fat.
Case 2
A 22-year-old fem ale diamond python
(Morelia spilota spilota) was obtained 9
years before its illness by her owner in
south-east Queensland. Over the 6
months before presentation, it had spent
MS CARLISLE-NOWAK
a
, N SULLIVAN
a
, M CARRIGAN
a
, C KNIGHT
b
, C RYAN
c
and ER JACOBSON
d
a
Veterinary Pathology Services, East Brisbane,
Queensland 4169
b
Deception Bay Veterinary Clinic, Deception Bay,
Queensland 4508
c
Nicklin Way Veterinary Surgery, Warana,
Queensland 4575
d
Department of Small Animal Clinical Sciences,
College of Veterinary Medicine, University of
Florida, USA, 32610
Two captive Australian pythons, one carpet and one diamond python, presented with signs of central nervous system dysfunction. The carpet python was agitated. Its head was tilting and it was incoordinated and had convulsions. It was treated with
antibiotics and anthelmintics but was eventually euthanas ed after failing to respond to therapy. The diamond python had
fl accid paralysis of the caudal hal f. It was not treated and became disoriented and died. Hepatocytes from both pythons
contained irregul ar 2 to 10 m eosinophilic intracytoplasmic inclusion bodies. The brain of the diamond python was not available for examination. Occasional neurones in the carpet python brain contained similar inclusion bodies and other changes
suggestive of viral infection. The clinical signs and histopathological findings in both pythons were consistent with boid inclusion body diseas e.
Aust Vet J
1998;76: 98-100
IBD Inclusion body diseas e
Inclusion body disease in two captive
Au
stralian pythons (Morelia spilota variegata
and Morelia spilota spilota)

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Supporting Information

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