alumba
Well-Known Member
A disease that is found in oue pythons due to people importing ileagle exotics snakes
i did not write This. HYGIENE, HYGIENE, HYGIENE PEOPLE AND QUARANTEEN.
98 Aust Vet J Vol 76, No 2, February 1998
IBD of snakes in the family Boidae
(boas and pythons) has been
reported 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 disease 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 private and zoological collections
within Australia.3,4
The virus associated with IBD resembles
type C particles of the family
Retroviridae and has been isolated in
Burmese python (Python molurus bivittatus)
and boa constrictor primary
kidney cell cultures. In transmission
studies Koch’s postulates have been
partially fulfilled but full molecular
characterisation of this virus remains to
be completed.1 Retroviral infections
associated with tumours have been
reported previously in non-boid snakes,57
however, the significance of these viruses
remains to be determined.
We report here the clinical signs and
pathological findings of two cases of
IBD in captive pythons. These are the
first published cases of inclusion body
disease of boid snakes in Australia.
Case 1
A 5-year-old female 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 euthanased after failing to respond
to therapy of fenbendazole (100 mg/kg),
praziquantel (15 mg/kg), metronidazole
(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
euthanased for neurological signs which
included agitation, head tilting, incoordination
and episodic convulsions.
Between the time of purchase 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 significant
gross findings. Histological examination
revealed many irregular ovoid, rectangular
or angular variably sized (2 to 10
mm) 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 multifocal gliosis,
mild perivascular lymphoplasmacytic
cuffs and mild lymphoplasmacytic
meningitis. Segmental swelling of
myelin sheaths and axons and mild
multifocal gliosis were seen in the proximal
spinal cord. No significant lesions
were present in the heart, skeletal
muscle, integument, kidney or body fat.
Case 2
A 22-year-old female 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-NOWAKa, N SULLIVANa, M CARRIGANa, C KNIGHTb, C RYANc and ER JACOBSONd
aVeterinary Pathology Services, East Brisbane,
Queensland 4169
bDeception Bay Veterinary Clinic, Deception Bay,
Queensland 4508
cNicklin Way Veterinary Surgery, Warana,
Queensland 4575
dDepartment 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 euthanased after failing to respond to therapy. The diamond python had
flaccid paralysis of the caudal half. It was not treated and became disoriented and died. Hepatocytes from both pythons
contained irregular 2 to 10 mm 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 disease.
Aust Vet J 1998;76: 98-100
IBD Inclusion body disease
Inclusion body disease in two captive
Australian pythons (Morelia spilota variegata
and Morelia spilota spilota)
Aust Vet J Vol 76, No 2, February 1998 99
most of its time coiled, its appetite
remained relatively normal and its girth
had increased. The latter was assumed to
indicate pregnancy. It began to gape
with an open mouth, show signs of
flaccid paralysis of the caudal half of its
body and distension from her mid-body
to cloaca. It became disorientated and
eventually died.
At necropsy, the diamond python was
in good condition with abundant
mesenteric and coelomic fat reserves.
There were occasional petechial haemorrhages
scattered within the scales on the
ventral surface of the body. The body
swelling was caused by about 200 mL of
straw-coloured watery fluid in its
coelomic cavity. The liver was diffusely
pale pink with scattered areas of congestion.
On histological examination, there
was diffuse moderate hepatocytic
swelling and vacuolation and moderate
diffuse congestion. Single and occasionally
multiple variably sized (2 to 10 mm)
eosinophilic intracytoplasmic inclusion
bodies were observed within hepatocytes
(Figure 1). These inclusion bodies were
also occasionally observed within the
renal tubular epithelium. The lungs
were moderately congested. No significant
lesions were found in the heart and
stomach. The brain was not examined.
Discussion
The clinical signs in both of the
snakes presented in this report are
similar to those previously reported for
IBD. Neurological signs are more severe
in pythons than in boas and include
head tremors, incoordination, disorientation,
head tilting, loss of righting
reflex, opisthotonos, progressive loss of
motor function (particularly of the
caudal half of the snake) and flaccid
paralysis in some cases.1,8 In boas, clinical
signs usually start with chronic
regurgitation followed by anorexia. The
neurological signs are milder than in
pythons.1,8 The course of the disease may
be longer in boas (months) than
pythons (weeks to months).8 Chronic
regurgitation is usually not seen in
pythons8 and was not present in these
two pythons. The carpet python was
anorectic.
Both snakes showed mouth gaping
with or without head raising. This clinical
sign in snakes can be related to
stomatitis and/or respiratory distress.4 A
proliferative pneumonia with intracytoplasmic
inclusion bodies within airway
epithelial cells has been observed in boas
with IBD.1 There was no gross evidence
of stomatitis or blocked nares and no
significant inflammatory changes within
the pulmonary tissue sections examined
in either snake. The possibility of a peracute
secondary septicaemia leading to
respiratory distress4 cannot entirely be
ruled out as a cause of the openmouthed
stance in these two pythons.
The presence of occasional petechial
haemorrhages in the ventral scales of the
diamond python is suggestive of septicaemia
in snakes,4 but this was not
confirmed by blood culture in these two
snakes. Secondary bacterial infections
are reported to be common in pythons
and boas affected with IBD.1,8
Necropsy findings in IBD are variable
with a diffusely pale liver associated with
hepatocytic swelling and vacuolation
being found in some cases.1 This was
present in the diamond python. The
ascites in the coelom of the diamond
python has not been previously recorded
in cases of IBD. It could have been the
result of portal hypertension secondary
to the liver disease. Other possible
causes include hypoproteinemia or
vascular damage from peracute
secondary septicaemia.
The eosinophilic intracytoplasmic
inclusion bodies associated with IBD are
usually present in hepatocytes, epithelial
cells of many visceral organs and within
neurones in the brain.1 Eosinophilic
intracytoplasmic inclusion bodies were
seen in hepatocytes of these two pythons
and similar intracytoplasmic inclusion
bodies were observed within some
neurones in the carpet python’s brain.
The brain of the diamond python was
not available for histopathological examination.
The nature of these intracytoplasmic
inclusion bodies remains
unknown. However, in previously
reported cases of IBD, suspected retroviral
particles have been demonstrated
in cells containing intracytoplasmic
inclusions.1 In the carpet python, the
brain had inflammatory and degenerative
changes and the spleen showed
lymphoid depletion. These findings
have also been reported previously in
cases of IBD.1
Until the causative virus has been fully
characterised and serological and/or
molecular biological techniques such as
polymerase chain reaction have been
designed, diagnosis of IBD in clinically
affected boid snakes and detection of
carriers remains difficult. Biopsies of
liver or kidney can be evaluated histologically
for the presence of eosinophilic
intracytoplasmic inclusion bodies.1
The length of time this disease has
been present in Australia and the
method of introduction are impossible
to define until the agent is characterised
and molecular or serological tools are
available for evaluation of archival
samples. Necropsy and histopathological
examination of snakes with signs consistent
with IBD would be needed to
differentiate causes of these signs9 and to
establish the extent of infection in
captive and wild Australian pythons.
Unpublished cases of Australian pythons
with clinical and histological findings
consistent with IBD have been recorded
in the Taronga Park pathology register
(W Hartley personal communication).
The route of transmission of this
disease is unknown. Infestation with
snake mites (Ophionyssus natricis) is a
common finding in many affected
snakes and may play a role in viral transmission.
1,8 In common with the other
viral infections of reptiles, there is no
specific treatment available for IBD.8
Despite supportive therapy, the disease
is considered to be fatal.1 Euthanasia of
boid snakes diagnosed with IBD and
Figure 1. Photomicrograph of the liver
from diamond python. Diffuse hepatocytic
vacuolation can be seen and there
is an intracytoplasmic inclusion body
within hepatocyte (arrow). Haematoxylin
and eosin, x 1160.
100 Aust Vet J Vol 76, No 2, February 1998
quarantine of newly acquired boid
snakes are recommended to prevent the
possibility of the infection spreading to
other susceptible snakes in a collection.
In addition, since boas often show
milder clinical signs than pythons and
could act as potential carriers of boid
IBD,1,8 separation of boas from pythons
is advisable.8
Acknowledgment
We are grateful to Mrs Jennifer
Coombs for necropsy/histopathology
technical assistance.
References
1. Schumacher J, Jacobson ER, Homer BL,
Gaskin JM. Inclusion body disease in boid snakes.
J Zoo Wldlf Med 1994;25:511-524.
2. Collett MG, Verseput MP, Maree CC. Newly
identified virus disease of captive snakes in South
Africa. In: Herpetological symposium on captive
propagation and husbandry of reptiles.
Herpetological Association of South Africa,
1988:23-24.
3. Cogger HG. Family Boidae. In: Reptiles and
amphibians of Australia. Reed Books Australia,
Melbourne, 1996:600-614.
4. McCracken H. Husbandry and diseases of
captive reptiles. In: Wildlife. Proceedings,
University of Sydney Post Graduate Committee in
Veterinary Science, 1994;(233):461-545.
5. Lunger PD, Hardy WD, Clark HF. C-type particles
in a reptilian tumour. J Natl Cancer Inst
1974;52:1231-12330.
6. Zeigel RF, Clark HF. Electron microscopic
observations on a “C”-type virus in cell cultures
derived from a tumour-bearing viper. J Natl
Cancer Inst 1969;43:1097-1102.
7. Andersen PR, Barbacid M, Tronick SR, Clark
HF, Aaronson SA. Evolutionary relatedness of
viper and primate endogenous retroviruses.
Science 1979;204:318-321.
8. Schumacher J. Viral diseases. In: Mader DR,
editor. Reptile medicine and surgery. WP
Saunders, Philadelphia, 1996:230-231.
9. Lawton MPC. Neurological diseases. In:
Beynon PR, editor. BSAVA Manual of reptiles.
British Small Animal Veterinary Association,
Gloucestershire, 1992:128-133.
(Accepted for publication 24 October 1997)
Benefits of castration
Dogs are castrated for two main reasons:
contraception and elimination or reduction
of unwanted male behaviour. Castration
is an effective contraceptive; the degree of
success in eliminating problem behaviours
is not so clear. In addition, it has been questioned
whether the dog’s age and the duration
of behaviour affect the success of castration.
A team of researchers from University of
California, Davis, did a follow-up study on
on 57 castrated dogs with the aid of a telephone
survey. Each dog had one or more of
the following problem behaviours: urine
marking, mounting, roaming, fear, aggression
towards family members, aggression
towards other people, aggression towards
other dogs in the household or aggression
towards people intruding the territory. The
dogs were over 2 years old at the time of
castration.
As expected, castration was most effective
in reducing the highly sexual behaviours
of urine marking, roaming and mounting
people, objects and other animals.
These behaviours diminished to a half in
over 60% of the dogs and more than 90% in
over 25% of the dogs.
Although the effect was not as profound
in reducing aggressive behaviours, in about
one third of the aggressive dogs these
behaviours were reduced by half, except
aggression towards unfamiliar people. That
and fear of inanimate stimuli were not significantly
affected.
For the five problem behaviour patterns
that were significantly reduced after castration,
the dog’s age at castration and the
duration of the problem did not affect the
degree of improvement. In fact, there was a
slight tendency for greater improvement in
older dogs and dogs with a long-lasting
problem. These results indicate that prior
sexual experience does not interfere with
the success of eliminating unwanted male
behaviour and that castrating older dogs is
feasible.
Neilson JC, Eckstein RA, Hart BL. Effects of castration
on problem behaviours in male dogs with
reference to age and duration of behaviour. J Am
Vet Med Assoc 1997;211:180-182.
