# IBD info (quoted) as some people just don't get the message out there!



## Dextersdad (Mar 28, 2008)

If your rep has it, it MUST be put to sleep and can infect your other otherwise healthy creautures. Care and rehoming is not the answer.It will just end up destroying the lives of reps that WERE previously healthy.

"Inclusion Body Disease

©1995 Melissa Kaplan

Inclusion body disease (IBD) has been increasingly diagnosed in boas and pythons ("boids"). It is believed to be a retrovirus. The way it affects these two groups of snakes is slightly different but the long term effects are the same: the disease is terminal in those animals who exhibit symptoms of the disease.

Pythons, although their symptoms may be somewhat less, are just as affected as boas. There are asymptomatic carriers, so the fact that a boa or python within an infected collection does not show signs of the illness should not be taken to mean that it is immune to it. Boas are most associated with being asymptomatic carriers.

Signs of infection in boas include central nervous system disorders such as paralysis, being unable to right itself when turned over, "star-gazing", inability to strike or constrict. Other signs include chronic regurgitation, extreme weight loss, respiratory infections, and dysecdysis due to the inability to control body movements enough to rub off the old skin. The disease is rapidly fatal in young and juvenile boas, typified by rapid onset of flaccid paralysis.

In pythons, the disease progresses much more rapidly than in boas. Along with the above symptoms (excluding the chronic regurgitation), pythons also tend toward infectious stomatitis ("mouth rot"), heightened or exaggerated reflex responses, disorientation (which may be precipitated by the onset of central blindness) and loss of motor coordination.

What causes this disease? Intracytoplasmic eosinophilic inclusion bodies have been identified in the epithelial cells of the kidneys and pancreas. Neuronal degeneration and lesions form in the spinal cord and brain, and may be accompanied by myelin degeneration and nerve damage. Damage to the spleen is also found, with that organ being grossly atrophied and fibrosed. Electron microscopy has found that the organism falls into the retrovirus category.

The snake mite, Ophionyssus natricis, has been found in collections in which IBD has occurred but it is not implicated in all cases of infection.

As this has been identified as a viral entity, it may spread like a virus, through contact between infectious organisms (such as housing an infected snake with a previously healthy one) or through airborne aerosolized secretions, or by the keeper passing secretions from one snake or enclosure to another during the course of handling or cleaning (when strict quarantine and cleaning procedures are not followed).

There is at this time no treatment for the disease and, as it is at this time always fatal and highly contagious, euthanasia is the course of action recommended. Even if the snake can be kept alive through supportive measures (hydration and force-feeding), the damage to the nerves, brain, spinal cord and internal organs is so great--and progressive--that live is only prolonged with an ever decreasing quality and increasing pain.

Due to the increasing incidence of this disease, it cannot be stated or urged strongly enough to QUARANTINE ALL NEW BOIDS upon acquisition for at least 3-6 months, and to take precautions when visiting other collections, pet stores and expos/swaps."


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## Maureen Collinson (Oct 6, 2006)

Further information which needs to be fully absorbed, not just skim read, if you wish to give your snakes a chance of a long life. Please see below. Please do note that this is from 2007, and that It has also now been diagnosed in colubrids as well.  

Mo.


06WSC12
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The Armed Forces Institute of Pathology
Department of Veterinary Pathology
WEDNESDAY SLIDE CONFERENCE
2006-2007
CONFERENCE 12
10 January 2007
Conference Moderator: Dr. Dick Montali, DVM, Diplomate ACVP
Department of Molecular and Comparative Pathobiology
Johns Hopkins University
Baltimore, MD 21205

CASE II – XN3076 (AFIP 2988331).
Signalment: 3-year-old, male, red-tailed boa constrictor, snake, Boa constrictor.
History: Two captive bred 3-year-old boa constrictors (Boa constrictor) were
purchased by a reptile collector in the United Kingdom in October 2004, housed
together in a vivarium and fed killed thawed mice, rats and day-old chicks. The
male of the pair had radiologically confirmed spondylosis involving vertebral
segments over a length of 25 cm at mid-body level. This snake exhibited
regurgitation and developed stomatitis one week after purchase. It was treated
with 10 mg/kg enrofloxacin (Baytril 2.5% Oral Solution, Bayer) administered by
daily gavage for one week and appeared to recover. It developed anorexia in early
February 2005 and was found dead on 9 March 2005, four months after purchase.
Gross Pathology: At postmortem examination, the male boa constrictor was 1.6 m
long, weighed 2.9 kg and had adequate reserves of body fat. The lungs contained
frothy greenish brown fluid and there was oedema around the lungs and heart.
Laboratory Results: Bacteriology: Profuse growths of Salmonella enterica serovar
San Diego were recovered from the lungs and intestine at postmortem examination.
Histopathologic Description: Histologically, the snake had a proliferative
pneumonia, with papillary expansion of interconnecting trabeculae lined by ciliated
or non-ciliated columnar epithelial cells, supported by fibrovascular connective
tissue. There were mild multifocal infiltrates of lymphocytes and plasma cells in
the interstitial tissue and mild individual degeneration of epithelial cells. Large
numbers of small bacilliform bacteria were present in the lumen of the lung, but
there were few inflammatory cells in the luminal exudate. Numerous single or
occasionally multiple, ovoid, eosinophilic cytoplasmic inclusion bodies, 1 to 5 mm
in diameter, were detected in epithelial cells in the lungs. Similar inclusion bodies
were also detected in the kidneys, pancreas, stomach and intestine. Pigment
deposits and interstitial fibrosis were evident in the kidneys. There was mild
individual degeneration of renal tubular epithelial cells and occasional sloughing of
cells into tubule lumina. Diffuse vacuolation of hepatocytes, with ballooning
degeneration and moderate numbers of inclusion bodies, was evident in the liver.
Inclusion bodies were also detected in neurons and glial cells in the brain in
association with mild meningoencephalitis. There was lymphoid depletion in the
spleen, with fibrosis and numerous inclusion bodies in lymphoreticular cells.
Contributor’s Morphologic Diagnosis: Lung: Pneumonia, proliferative, diffuse,
severe, with eosinophilic cytoplasmic inclusion bodies, snake, Boa constrictor.
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Contributor’s Comment: Boid inclusion body disease (IBD) is an important
transmissible disease of captive snakes that occurs worldwide.1,2,3 The disease
occurs primarily in boids and pythons (Family Boidae), including the boa constrictor
(Boa constrictor). It has also been diagnosed in colubrids (Family Colubridae) and
viperids (Family Viperidae), but appears to be less common in these groups of
snakes.2,4 Boid IBD is characterised clinically by anorexia, regurgitation, weight
loss, lethargy and neurological signs, including disorientation, incoordination, head
tilting, “star gazing”, tremors, convulsions and flaccid paralysis.1,2,3 Affected
snakes usually die or are euthanased after a prolonged clinical course. The disease
appears to be immunosuppressive, permitting the development of secondary
disease, such as bacterial pneumonia and stomatitis. Histopathological changes in
affected snakes include demyelinating encephalomyelitis, interstitial pneumonia,
hepatopathy with vacuolation and ballooning degeneration of hepatocytes,
pancreatic atrophy and nephrosis.1,2,3 Lymphoid depletion is also evident.
Eosinophilic inclusion bodies are present in the cytoplasm of epithelial cells in the
lungs, gastrointestinal tract, kidneys and pancreas, as well as in hepatocytes,
neuroglial cells in the brain and lymphoreticular cells in the spleen.1,2,3
The aetiology of boid IBD is currently a matter of controversy. Retroviruses have
been isolated in cell culture and detected by electron microscopy in tissues from
affected snakes.1,5 However, these may be endogenous retroviruses that are not
aetiologically associated with boid IBD.6 Ophidian paramyxoviruses (OPMV), of
which more than 18 types have been recognized, are associated with necrotising or
proliferative interstitial pneumonia, meningoencephalitis and mortality in viperids
and colubrids.7,8,9 Eosinophilic inclusion bodies, along with occasional multinucleate
syncytia, are usually produced in the cytoplasm of infected cells. The degree to
which boids are susceptible to OPMV is uncertain. OPMV type 7 has been isolated
from a reticulated python (Python reticulatus) with respiratory disease in the UK.10
High antibody titres against OPMV were detected by haemagglutination inhibition in
serum from an unaffected reticulated python following an outbreak of disease in
viperids in the USA.9 In situ hybridisation was positive for paramyxovirus
sequences in the brain of a Boelen's python (Morelia boeleni) with
meningoencephalitis and eosinophilic cytoplasmic inclusions in glial cells in the
brain but not in other tissues.11 There is currently insufficient evidence to implicate
OPMV in the aetiology of boid IBD, despite the pathological similarities. The
cytoplasmic inclusion bodies in boid IBD are widely distributed in epithelial, nervous
and lymphoreticular tissues.1 Infection with OPMV may produce inclusion bodies in
the lungs, brain, liver and kidneys, although they are less numerous, multinucleate
syncytia may be present and there is usually a more pronounced suppurative and
necrotising pneumonia.8,9,11
The proliferative pneumonia in the affected snake may be attributable to boid IBD,
since there were only mild lymphoplasmacytic inflammatory infiltrates in the lungs,
06WSC12
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limited necrosis, minimal exudation of heterophils and no evidence of multinucleate
syncytia. A profuse growth of Salmonella enterica serovar San Diego was obtained
from the lungs at postmortem examination and large numbers of bacteria were
present in the pulmonary exudate. The Salmonella isolate may have been an
opportunistic colonist of the lungs in an immunocompromised snake secondary to
boid IBD, possibly related to regurgitation and inhalation of gastrointestinal
contents.
AFIP Diagnosis: Lung: Bronchointerstitial pneumonia, proliferative, heterophilic
and lymphoplasmacytic, diffuse, moderate, with edema, fibrin, and hemorrhage,
numerous epithelial eosinophilic intracytoplasmic inclusion bodies, Gram negative
bacilli and Gram positive cocci.
Conference Comment: The contributor provides a thorough overview of boid
inclusion body disease (IBD) and compares and contrasts it with ophidian
paramyxoviruses (OPMV). The controversial association of a type C retrovirus and
IBD was discussed during conference. Ultrastructurally, the inclusions appear as
electron dense structures that may vary in size and shape. The inclusions may
represent previral material or some type of storage material from a dysfunctional
cell. In one study, an antigenically distinct 68-kilodalton protein was isolated and
characterized from nonviral inclusions in IBD-infected Boa Constrictors.12
As pointed out by the contributor, IBD affects both boids and pythons. Boas may
be inapparent carriers. However, the severity of the disease is significantly worse
in pythons, which have a rapid clinical course that progresses to a fatal CNS
disturbance. There is no treatment for IBD and infected snakes die. Therefore,
boas and pythons should not be mixed in the same collection. The snake mite,
Ophionyssus natricis, is suspected as a vector associated with the spread of
disease. Other modes of transmission include direct contact and venereal spread.13
Gross lesions are frequently limited to changes associated with secondary bacterial
infections, such as pneumonia, stomatitis, and bacterial granulomas within the liver
and kidneys. In some species, such as Boa Constrictors, fibrous changes and
splenic atrophy may be observed.12
Some conference participants favored OPMV. The moderator preferred a diagnosis
of IBD since the inclusions were widespread in other organs and there was a lack
of a pronounced suppurative and necrotizing pneumonia as pointed out by the
contributor. Additionally, in his experience, it is uncommon to see so many
inclusions with OPMV infections. He also added that the syncytial cells seen in
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OPMV infections are typically striking and the inclusions are more pleomorphic
similar to those seen with canine distemper virus.
Gram stains performed at the AFIP revealed myriad Gram negative bacilli as well as
chains and pairs of Gram positive cocci within the pulmonary exudate and were
most likely opportunistic pathogens in this debilitated snake.
Contributor: Division of Pathological Sciences, Institute of Comparative Medicine,
University of Glasgow Veterinary School, Glasgow G61 1QH, Scotland, United
Kingdom, http://www.gla.ac.uk/faculties/vet
References:
1. Schumacher J, Jacobson ER, Homer BL, Gaskin JM: Inclusion body disease in
boid snakes. J Zoo Wildl Med 25:511-524, 1994
2. Carlisle-Nowak MS, Sullivan N, Carrigan M, Knight C, Ryan C, Jacobson ER:
Inclusion body disease in two captive Australian pythons (Morelia spilota variegata
and Morelia spilota spilota). Aust Vet J 76:98-100, 1998
3. Orós J, Tucker S, Jacobson ER: Inclusion body disease in two captive boas in
the Canary islands. Vet Rec 143:283-285, 1998
4. Raymond JT, Garner MM, Nordhausen RW, Jacobson ER: A disease resembling
inclusion body disease of boid snakes in captive palm vipers (Bothriechis marchi). J
Vet Diagn Invest 13:82-86, 2001
5. Jacobson ER, Orós J, Tucker SJ, Pollock DP, Kelley KL, Munn RJ, Lock BA,
Mergia A, Yamamoto JK: Partial characterization of retroviruses from boid snakes
with inclusion body disease. Am J Vet Res 62:217-224, 2001
6. Huder JB, Boni J, Hatt JM, Soldati G, Lutz H, Schupbach J: Identification and
characterization of two closely related unclassifiable endogenous retroviruses in
pythons (Python molurus and Python curtus). J Virol 76:7607-7615, 2002
7. Franke J, Essbauer S, Ahne W, Blahak S: Identification and molecular
characterization of 18 paramyxoviruses isolated from snakes. Virus Res 80:67-74,
2001
8. Jacobson E, Gaskin JM, Page D, Iverson WO, Johnson JW: Illness associated
with paramyxo-like virus infection in a zoologic collection of snakes. J Am Vet Med
Assoc 179:1227-1230, 1981
9. Jacobson ER, Gaskin JM, Wells S, Bowler K, Schumacher J: Epizootic of
ophidian paramyxovirus in a zoological collection. Pathological, microbiological, and
serological findings. J Zoo Wildl Med 23:318-327, 1992
10. Manvell RJ, Drury SE, Geach M, Lewis JC: Isolation of ophidian paramyxovirus
type 7 from a reticulated python in the UK. Vet Rec 147:696, 2000
11. West G, Garner M, Raymond J, Latimer KS, Nordhausen R:
Meningoencephalitis in a Boelen's python (Morelia boeleni) associated with
paramyxovirus infection. J Zoo Wildl Med 32:360-365, 2001
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12. Schumacher J: Inclusion body disease virus. In: Reptile Medicine and Surgery,
ed. Mader DR, 2nd ed., pp. 836-840. Saunders Elsevier, St. Louis, Missouri, 2006
13. Bennet RA, Mehler SJ: Neurology. In: Reptile Medicine and Surgery, ed. Mader
DR, 2nd ed., pp. 248-249. Saunders Elsevier, St. Louis, Missouri, 2006


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## Dextersdad (Mar 28, 2008)

Maureen Collinson said:


> Further information which needs to be fully absorbed, not just skim read, if you wish to give your snakes a chance of a long life. Please click on link below.
> 
> Mo.


There is no link below.

My original message was meant to get some people thinking.


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## Maureen Collinson (Oct 6, 2006)

You will note the reference to OPMV above which is short for Ophidio Paramyxovirus. Look below, and click on link to learn more about this. It is also doing the rounds here in the UK, and will explain to those of you that have had it, the fact that it can go through a collection and leave some species unscathed, which I know has beena puzzle to some of you.

Mo.

Ophidio Paramyxovirus (OPMV) / Reovirus in Australian Reptile Collections.


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## Maureen Collinson (Oct 6, 2006)

Here's another one also well established in the lizards here in the UK, and now snakes as well. There are other retro-viruses too, as well as Cryptosporidium out there, so please quarantine for as long as you can, remembering that some of the above have at least a year's incubation period and longer.

Mo.

PART 1.

JOURNAL OF VIROLOGY, Dec. 2004, p. 13366–13369 Vol. 78, No. 23
0022-538X/04/$08.000 DOI: 10.1128/JVI.78.23.13366–13369.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
Detection and Analysis of Six Lizard Adenoviruses by Consensus
Primer PCR Provides Further Evidence of a Reptilian Origin for
the Atadenoviruses
James F. X. Wellehan,1* April J. Johnson,1 Bala´zs Harrach,2 Ma´ria Benko¨,2 Allan P. Pessier,3
Calvin M. Johnson,4† Michael M. Garner,5 April Childress,1 and Elliott R. Jacobson1
Department of Small Animal Clinical Sciences1 and Department of Pathobiology,4 College of Veterinary Medicine,
University of Florida, Gainesville, Florida; Veterinary Medical Research Institute, Hungarian Academy of
Sciences, Budapest, Hungary2; Department of Pathology, Center for Reproduction of Endangered
Species, Zoological Society of San Diego, San Diego, California3; and Northwest ZooPath,
Monroe, Washington5
Received 29 May 2004/Accepted 9 July 2004
A consensus nested-PCR method was designed for investigation of the DNA polymerase gene of adenoviruses.
Gene fragments were amplified and sequenced from six novel adenoviruses from seven lizard species,
including four species from which adenoviruses had not previously been reported. Host species included Gila
monster, leopard gecko, fat-tail gecko, blue-tongued skink, Tokay gecko, bearded dragon, and mountain
chameleon. This is the first sequence information from lizard adenoviruses. Phylogenetic analysis indicated
that these viruses belong to the genus Atadenovirus, supporting the reptilian origin of atadenoviruses. This PCR
method may be useful for obtaining templates for initial sequencing of novel adenoviruses.
Adenoviruses (AdVs) are categorized into four genera: Mastadenovirus
(from mammals) (7, 42), Aviadenovirus (from
birds) (19), and two recently accepted genera, Atadenovirus (5,
9) and Siadenovirus (13). Atadenoviruses from ruminants (3, 8,
11, 32, 33), birds (21, 23), snakes (4, 15, 34), and a marsupial
(44) were isolated and studied. The two siadenoviruses were
from a frog (14) and poultry (39). The mixed-host origin of
these genera suggests that host switches may have occurred.
Prior to the availability of reptile AdV phylogenetic information,
a reptilian origin of atadenoviruses was proposed on the
basis of comparison of phylogenetic trees of the adenoviruses
and host rRNA (18). A fifth genus is proposed for a sturgeon
adenovirus (4).
AdV-like particles have been identified in many reptile species,
including 10 snake species (22, 28, 36, 38, 40, 43, 47), 4
lizard species (24, 27, 29, 30), and 1 crocodilian species (25).
Lesions in reptiles associated with AdV-like agents include
hepatitis (25, 27, 29, 43), enteritis (22, 30, 47), esophagitis (24,
40), splenitis (22), and encephalopathy (41). The only reptile
adenovirus previously further classified was a corn snake
(Elaphe guttata) isolate (15) which was consistent with the
genus Atadenovirus. A Boa constrictor isolate was identical to
the corn snake isolate (34).
Methods previously used for diagnosis of AdV infection in
reptiles include virus isolation (26), electron microscopy (22),
DNA in situ hybridization (ISH) (38), and plaque reduction
neutralization (PRN) (34). Virus isolation requires further diagnostics
for speciation. Electron microscopy and available
ISH protocols do not speciate reptile adenoviruses (38). The
cross-reactivity of neutralizing antibodies to reptile adenoviruses
in PRN is not known. PRN also requires that a virus had
been previously cultured, making this a poor method for novel
virus discovery. Consensus PCR is a rapid way to obtain a
sequencing template from clinical samples (45). A PCR
protocol used for the snake atadenovirus (15) did not work
with gecko samples; a technique usable for diverse novel
adenoviruses was needed. The protocol described here has
been used to amplify these atadenoviruses as well as a mastadenovirus
and an aviadenovirus (J. F. X. Wellehan, unpublished
data).
Samples. The eublepharid gecko sample was obtained from
a disease outbreak. Fat-tail geckos (Hemitheconyx caudicinctus)
were wasting, with a high mortality rate. Histologically,
lymphoplasmacytic enteritis with intranuclear inclusion bodies
and multifocal lymphocytic pancreatitis were seen. Leopard
geckos (Eublepharis macularius) in this collection did not have
a high mortality rate, but a few did suffer weight loss and death.
In these leopard geckos, both eublepharid gecko adenovirus
and Cryptosporidium spp. were found.
The Tokay gecko (Gekko gecko) sample was collected from a
cloacal wash of an animal with marked weight loss and regurgitation.
Histologically, there was severe proliferative gastritis with
myriad intralesional protozoa consistent with Cryptosporidium
spp. No inclusion bodies were observed in tissue sections.
The Gila monster (Heloderma suspectum) adenoviral sample
was collected from a cloacal wash of an animal with signs of
regurgitation.
The blue-tongued skink (Tiliqua scincoides intermedia) sample
was extracted from paraffin-embedded tissue of an asymtomatic
neonatal animal euthanized for a spinal deformity.
Histologically, the small intestine had numerous intranuclear
* Corresponding author. Mailing address: Zoological Medicine Service,
Department of Small Animal Clinical Sciences, College of Veterinary
Medicine, University of Florida, Gainesville, FL 32610. Phone:
(352) 392-4700. Fax: (352) 392-4877. E-mail: [email protected]ed
.ufl.edu.
† Present address: Department of Pathobiology, College of Veterinary
Medicine, Auburn University, Auburn, AL 36849.
13366
Downloaded from jvi.asm.org by on June 17, 2007
basophilic inclusions. Transmission electron microscopy demonstrated
adenovirus-like particles.
The bearded dragon (Pogona vitticeps) sample was extracted
from paraffin-embedded tissue. Histologic examination revealed
that the intestinal mucosa, hepatocytes, and bile ducts
contained intranuclear inclusions.
The mountain chameleon (Chameleo montium) adenoviral
sample was extracted from paraffin-embedded tissue from a
previously described infection (30).
PCR and sequencing. DNA was extracted with a DNEasy kit
(QIAGEN, Valencia, Calif.). Nested-PCR amplification of a
partial sequence of the adenoviral DNA polymerase gene was
performed. For the first amplification, the 20-l reaction mixture
contained 2 l of extracted DNA, 5% dimethyl sulfoxide,
1 M concentrations for each primer (forward primer, pol-
Fouter [5-TNMGNGGNGGNMGNTGYTAYCC-3, where
Y  C or T, N  A, C, G, or T, and M  A or C]; reverse
primer, polRouter [5-GTDGCRAANSHNCCRTABARNG
MRTT-3, where R  A or G, M  A or C, D  A, G, or T,
S  G or C, H  A, T, or C, and B  G, T, or C]), 200 M
(each) for dATP, dCTP, dGTP, and dTTP, 2.5 U of Pwo DNA
polymerase (Thermo Hybaid, Franklin, Mass.), and PCR buffer
(Thermo Hybaid). The mixtures were amplified with an initial
denaturation at 94°C for 5 min followed by 45 cycles at 94°C for
30 s, 46°C for 60 s, and 72°C for 60 s. There was a final extension
at 72°C for 7 min. For the second round, 2 l of product from the
above-described reaction mixture was used with forward primer
polFinner (5-GTNTWYGAYATHTGYGGHATGTAYGC-3,
where W  A or T) and reverse primer polRinner (5-CCANC
CBCDRTTRTGNARNGTRA-3) and amplified under the
same conditions. Purified products were sequenced directly using
a Big-Dye terminator kit (Perkin-Elmer, Branchburg, N.J.) and
analyzed on ABI 377 automated DNA sequencers.
PCR amplification resulted in products that consisted of 318
to 324 bp before primer sequences were edited out. Sequences
from the fat-tail gecko and leopard gecko samples were identical
and were considered to represent the same virus. On the
basis of naming conventions, these adenoviruses were named
eublepharid adenovirus 1 (EuAdV-1, from the leopard and
fat-tail geckos), gekkonid adenovirus 1 (GeAdV-1, from the
Tokay gecko), agamid adenovirus 1 (AAdV-1, from the
bearded dragon), helodermatid adenovirus 1 (HeAdV-1, from
the Gila monster), chameleonid adenovirus 1 (ChAdV-1, from
the mountain chameleon), and scincid adenovirus 1 (ScAdV-1,
from the blue-tongued skink) (7).
Phylogenetic calculations. The sequences were compared to
known sequences in GenBank (National Center for Biotechnology
Information, Bethesda, Md.), EMBL (Cambridge,
United Kingdom), and Data Bank of Japan (Mishima, Shiuoka,
Japan) databases by use of TBLASTX (2). All sequences
except for that of EuAdV-1 showed the highest score with duck
adenovirus 1 (DAdV-1) DNA polymerase (GenBank accession
FIG. 1. Alignment of predicted homologous 89- to 91-amino-acid sequences from GenBank corresponding to the complement of bases 6458
to 6732 of human adenovirus 1 (GenBank accession number AF534906) or from our own studies. Sequences were aligned using MultAlin (10).
Members of the same species are shown with black characters on a gray-shaded background. Genera are separated by lines. Viruses new to this
study are in bold.
VOL. 78, 2004 NOTES 13367
Downloaded from jvi.asm.org by on June 17, 2007
no. BK000404.1) (12). EuAdV-1 showed the highest score with
bovine adenovirus 4 (BAdV-4) DNA polymerase (GenBank
accession no. AF036092) (11). DAdV-1 and BAdV-4 are both
in the genus Atadenovirus.
An alignment of predicted homologous sequences is shown
(Fig. 1). Phylogenetic analyses of the predicted alignment were
performed with PHYLIP (Phylogeny Inference Package; version
3.572c) program software (17) as described earlier (20).
The phylogenetic tree (Fig. 2) shows the presently accepted
species clustering. Similar AdV serotypes are classified as
members of a species (7). While the two snake isolates studied
so far are identical (34), these lizard AdV sequences are adequately
different (less than 90% sequence identity) to be considered
distinct adenovirus species. The tree also shows that
these lizard AdVs group with the genus Atadenovirus. Further
characterization would help confirm this. The classification of
multiple species of reptile adenoviruses, all in the genus Atadenovirus,
supports a reptilian origin for Atadenovirus.
The lizard sequences show a balanced GC content (43.75
to 58.09% over the region sequenced) in contrast to results
seen with the ruminant, marsupial, and bird atadenoviruses, so
named because of their biased genome (32.35 to 47.43% GC
over the comparable region). Following a host switch, viral
genes would undergo rapid evolution as they adapt to a new
host. DNA containing CG dinucleotides is recognized by the
innate immune system (1). In the absence of a previous hostadapted
function of a sequence, there could be strong selective
pressure away from CG dinucleotides. An AT bias in genome
composition could signify that a virus had evolved in a
secondary host (6).
Phylogenetic analyses of mammalian herpesviruses suggest
that the branching patterns of Herpesviridae are often congruent
with those of host species (35). While reptilian herpesviruses
fit well with herpesvirus phylogeny (46), the herpesviruses
of amphibians and fish are highly divergent (31) and
phylogenetic comparison with other herpesviruses is challenging.
The fish and amphibian “herpesviruses” may have diverged
long before the divergence of their hosts. In contrast,
the adenoviruses are more clearly of a continuous lineage (6),
providing the possibility to study coevolution of viruses
through all vertebrate classes. The low resolution in this study
emphasizes the need for additional sequences from more
hosts.
Nucleotide sequence accession numbers. Sequence data
were submitted to GenBank; the accession numbers are
AY576677 to AY576682.
We thank Darryl Heard and Sylvia Tucker at the University of
Florida and Molly Pearson at Micanopy Animal Hospital for their
assistance. We also thank the Lincoln Park Zoo, Chicago, Ill., and the
University of Illinois Zoological Pathology program for generously
donating the mountain chameleon adenovirus tissue sample.
The work was partly supported by Hungarian research grants OTKA
T034461 and MEH 4767/1/2003.
REFERENCES
1. Aderem, A., and D. A. Hume. 2000. How do you see CG? Cell 103:993–996.
2. Altschul, S. F., T. L. Madden, A. A. Scha¨ffer, J. Zhang, Z. Zhang, W. Miller,
and D. J. Lipman. 1997. Gapped BLAST and PSI-BLAST: a new generation
of protein database search programs. Nucleic Acids Res. 25:3389–3402.
3. Bartha, A. 1969. Proposal for subgrouping of bovine adenoviruses. Acta Vet.
Acad. Sci. Hung. 19:319–321.
4. Benko¨, M., P. E´ lo¨, K. Ursu, W. Ahne, S. E. LaPatra, D. Thomson, and B.
Harrach. 2002. First molecular evidence for the existence of distinct fish and
snake adenoviruses. J. Virol. 76:10056–10059.
5. Benko¨, M., and B. Harrach. 1998. A proposal for a new (third) genus within
the Adenoviridae family. Arch. Virol. 143:829–837.


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## Maureen Collinson (Oct 6, 2006)

PART 2. Conclusion.

Mo. 

6. Benko¨, M., and B. Harrach. 2003. Molecular evolution of adenoviruses.
Curr. Top. Microbiol. Immunol. 272:4–35.
7. Benko¨, M., B. Harrach, and W. C. Russell. 2000. Family Adenoviridae, p.
227–238. In M. H. V. van Regenmortel, C. M. Fauquet, D. H. L. Bishop,
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## Fangio (Jun 2, 2007)

Sorry Mo but even I have trouble trying to absorb all the jargon and waffle there. It doesn't make for easy reading (the last 2 posts that is).


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## RasperAndy (Sep 21, 2007)

just hope nobody uses the quote button


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## Dextersdad (Mar 28, 2008)

Fangio said:


> Sorry Mo but even I have trouble trying to absorb all the jargon and waffle there. It doesn't make for easy reading (the last 2 posts that is).


Hence the original one I put up I was hoping would be an easy read without scaring the bejesus out of folk!


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## slither61 (Nov 18, 2006)

HI all,

Poeple know IBD it is about, some take precautions when aquireing a new snake some don't.

I think the problem is if someone has got IBD in there collection and after a PM on snake it is proved how many will admit to it online if big breeder they will sign there own death warrent.

I think the only thing you can do is be very careful and do your home work on the person or shop you are going to buy off.

I think the problem lies with people who are out to make a quick buck, and dont give a dam about the snakes, bad conditions no hygene no quarentine if a snake dies no PM to find out why a lot of it boils down to money.

And take all precautions you possibly can and a very long quarentine eg up to 2 years.

There are snakes I would like but I am just holding fire and doing my research.

PS intresting posts Mo, but very hard work and need to be read

slither61:snake::snake::snake::snake:


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