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MAJOR ADVISOR
MEGHA K BEDEKAR
SENIOR SCIENTIST
PRESENTED BY
B.MADHUSUDHANA RAO
AAHMA5-07
INTRODUCTION
• Order : Testudines
• Family : Cheloniidae
• Poikilotherms
• 110 million years,
since the time of the
dinosaurs.
Turtles are exposed to a no. of threats
• Degradation, urbanisation &
pollution of nesting habitats &
foraging areas.
• Traditional hunting and egg
harvest
• The impacts of climate change on
the marine and terrestrial
environment.
“Cayman Turtle Farm”
(CTF)
• Grand Cayman island, West
Indies in 1968 with 23 acres.
• Opens the door for – exchange
of views on the pros and cons
of sea turtle farming.
High demand for food
& medicinal purposes.
HERPESVIRUSES
Generally characteristic
features of HV:
 Variable host range,
 Short replication cycle,
and
• Linear, ds DNA
genome with
Icosahedral symmetry
• Replication is within
the nucleus.
HERPESVIRUSES
HERPESVIRUSES
• Greek word herpein , referring to the LATENT.
• Establish latent infection.
During which
viral gene
expression is
minimized
• Expression of these latency-
associated genes may
function to keep the viral
genome from being digested
by cellular ribozymes or being
found out by the immune
system.
HERPESVIRUSES
ChHV 1 (Grey Patch Disease)
ChHV 2
ChHV 3
ChHV 4
ChHV 5 (Fibropapillomatosis)
ChHV 6 (Lung-Eye- and
Tracheal disease)
HV affecting
F.W Turtles
Strains of Chelonid Herpesvirus 5
FIBROPAPILLO
MATOSIS
A
B
D
C
Genome -----23 kb
Atlantic ( Florida &
Barbados)
Middle Pacific (Hawaii)
Eastern Pacific.
Western Pacific (Australia)
FIBROPAPILLOMATOSIS (FP)
• FP - 1st reported in 1938 at Key West, Florida.
• V. limited focus is done on diseases of sea turtles.
But greatest concern -
Green turtles as it has
only reached a panzootic
status in this species
(Williams et al., 1994).
FP is a neoplastic disease characterized by cutaneous, ocular
tumours that has been documented to infect all sea turtle species.
AETIOLOGY
• Research to date suggests
that FP is associated with a
Herpesvirus infection
(Herbst et al., 1995;
Quackenbush et al., 1998,
2001; Lackovich et al.,
1999).
This virus cannot be cultured in vitro and therefore
Koch's postulates have not been fulfilled.
AETIOLOGY
• Agent : Chelonid Herpesvirus 5 (ChHV5) or
"Green turtle fibropapillomatosis” (GTFP)
because it was first recorded in Green turtles.
Family : Herpesviridae
Subfamily : Alphaherpesvirinae
Genus : Scutavirus (ICTV, 2011).
1938
(1.5%)
Disease prevalence and impact
FP emerge in the
Eastern Pacific,
Hawaiian Islands,
Indonesia and
Australia (40%).
PANZOOTIC
Over 140 countries (Groombridge
and Luxmoore, 1989).
50% of the population of green
turtles in the world are affected by
the disease (Balazs 1991, Herbst
1994).
1980s (20-60%)
1990s
Epidemiology
• FP typically occurs in marine turtles inhabiting neritic
areas – most frequently observed in juvenile turtles.
• Horizontal.
• The higher incidence
in females may be –
behavioral ecology
in life cycle.
• FP rates are correl-
ated with degraded
habitat quality.
Epidemiology
• HV have the potential to be maintained on various
surfaces in marine environment (sediments, rubbing
rocks, foods sources, etc.) that could serve as vectors
for transmission.
Chemical pollution can
activate latent viruses or
indirectly increase its
virulence (Aguirre et al.,
1994).
Most prominent in warmer
climates, affecting 50%-
70% of popn.
Epidemiology
• FPHV DNA was detected on the gills of wrasse cleaner fish
(Thalassoma duperrey) – It groom sea turtles - possible
vector for transmission (Lu et al. 2000b).
• Epidemiological links are seen between FP rates,
nitrogen footprints, and invasive macroalgae –
ARGININE.
• Water temperature - lesions of a debilitating size by
autumn.
• Susceptible stages : Juveniles 40 - 70 cms length/ (10–
30 kg) most effected.
• FP is rare (0-12%) among nesting adult females and
lesions tend to be focal and mild.
Epidemiology
Epidemiology
PROTEIN
KINASE C
(PKC)
ACTIVATORS
OKADAIC ACID
LYNGBYATOXIN
A
DEBROMOAPLY
SIATOXIN (DAT)
Prorocentrum lima Lyngbya majuscula
Epidemiology
Note the Fibropapilloma with highly rugose structure (black arrow) and
presence of leeches - Ozobranchus (white arrow).
Photo credit: Tim Collins.
MULTIFACTORIAL AETIOLOGY
U.V LIGHT
(Aguirre, 1991),
CONTAMINATS
(Aguirre et al.
1994a)
METALS
(Monserrat et
al., 2007)
TEMP
(Herbst et al.,
1995)
BIOTOXINS
(ARGININE)
(Landsburg et al.
1999).
PARASITES
(Dailey & Morris,
1995)
CLINICAL SIGNS
Lesions that are comprised primarily of proliferating
epidermis with little or no underlying dermal
involvement are properly called PAPILLOMAS.
Those masses in which both tissues are hyperplastic
are termed FIBROPAPILLOMAS.
While those lesions predominantly comprised of
proliferating dermal components with relatively
normal epidermis are called FIBROMAS.
Severe fibropapillomas in the cervical, periocular, and right
front limb regions of one green turtle
The conjunctiva
(especially bulbar
conjunctiva) is a
common site for GTFP,
and masses may grow
over the cornea.
STAGES OF LESION DEVELOPMENT
(Herbst, 1994; Kang et al., 2008).
• Papilloma
lesions
EARLY PHASE
• Fibropapill
-omas
lesions
INTERMEDIATE
PHASE
• Fibromas
lesions
CHRONIC PHASE
Internal - mouth, heart, lungs, kidneys, liver and gastrointestinal
tract (Mascarenhas and Iverson, 2008).
Occasional visceral Fibromas, Myxofibromas and Fibrosarcomas
HISTOLOGICAL STUDIES
• Histological studies on FP lesions have observed orthokeratotic
hyperkeratosis (a)and varying degrees of epidermal hyperplasia
(b) (upto 30 cells thick), and papillary projections (c)
Key features in FP is proliferative epidermis presenting ballooning cells
with intracellular inclusion bodies (IIBs) suggestive of viral infection,
shown with arrows.
HISTOLOGICAL STUDIES
VIRULENT FACTORS
• Four members of the C-type lectin-like domain
superfamily (F-lec1, F-lec2, F-sial and F-M04) were
found to be present in the ChHV5 genome.
Two of these has been
suggested that these
genes may play a role in
FP pathogenesis & lesions
formation
(Ackermann et al., 2012).
Host response
Thrombospondin
(Tumor suppressor)
Fibropapillomas
GRAY PATCH DISEASE
• Tissues affected – SKIN, SHELL.
• Occurs in two forms
Non spreading
Papules/
pustular like
lesions resolve
spontaneously.
Benign, a
necrotizing
dermatitis of
post-hatching
green turtles
1st Spreading Gray
patches to large
areas of the
epidermal
surface.
Malignent, often
these animals die
2nd
Clinical symptoms
• Necrotizing dermatitis of post - hatching.
• Epizootics of small, circular papular skin lesions that
coalesced into patches were described in young sea
turtles.
• Stressful environmental
conditions such as over
crowding and higher
temp. seemed to enhance
the onset
and severity of lesions.
Proliferative dermatitis lesions on
subadult loggerhead turtle
(A) Early skin lesions with
typical raised white
appearance.
(C) Resolving lesions on
scales of front flipper
(B) Advanced skin lesions
showing area of
discoloration during
healing.
• The first critical time - 2-6 weeks of age.
• At this age – no typical skin lesions of gray-patch
disease; however, there is a consistent level of
mortality (20%).
Affects 90-100% hatchlings
Clinical symptoms
The only obvious clinical sign is impacted fecal material
in the lower intestinal tract.
• The second critical - 8 to 15 weeks of age.
• Mortality is less compare to the first stroke.
Clinical symptoms
• Turtles over I year of age do not have the natural
lesions of gray-patch disease.
• Infection is in higher degree in summer.
• Inactivated vaccine – skin scraping.
• Transmission - horizontal
This is the period of time that we are able to obtain
large amounts of skin scrapings containing the
herpesvirus.
LUNG-EYE-TRACHEAL DISEASE(LETD)
• Agent : (LETV) or (Chelonid herpesvirus 6)
• Name implies, the virus affects the eyes and
respiratory tract.
• And has a clinical course of 2-3 weeks.
Characterized by conjunctivitis,
pharyngitis, tracheitis, periglottal
necrosis and pneumonia (Jacobson et al.
1986).
EPIZOOTOLOGY
• Transmission is thought to be vertical or water-
borne.
Affects turtles worldwide, and mortality in post-
hatchling and juvenile - can reach 70%.
MODEL CHELONID HERPES VIRUS
• The virus was cultured in green turtle kidney cells
that helped in further research.
• LETV - gathers information about the general
characteristics of this largely unexplored group of
viruses.
• In addition, the prevalence of LETV infections in wild
populations.
LOGGERHEAD GENITAL-
RESPIRATORY
HERPESVIRUS” (LGRV)
Ulcers in the trachea,
around the cloaca and
on the base of the
phallus.
Venereal transmission.
LOGGERHEAD
OROCUTANEOUS
HERPESVIRUS” (LOCV)
Ulcers in the oral cavity
& cutaneous plaques
that can be covered
with exudate & have an
erythematous border.
------
 Both viruses were thought to be opportunistic in debilitated
turtles.
CONCLUSION
• The longevity of marine turtles, coupled with their
close association with inshore habitats and seagrass
meadows and coral reefs in these habitats, has led to
the proposal that they may act as sentinel indicators
of marine ecosystem health.
• Further investigations has to be carried to rule out
several confusions about remaining viruses which will
in turn inform the management and conservation of a
vulnerable species.
REFERENCE
• Orós, J., Torrent, A., Calabuig, P. and Déniz, S., 2005. Diseases and causes of
mortality among sea turtles stranded in the Canary Islands, Spain (1998–
2001). Diseases of aquatic organisms, 63(1), pp.13-24.
• EAZWV Transmissible Disease Fact Sheet Sheet No. 23 1 FIBROPAPILLOMATOSIS
(FP) OF SEA TURTLES Rachel E. Marschang 2009
• EAZWV Transmissible Disease Fact Sheet Sheet No. 26 GPD
• Select conditions in sea turtle pathology ;Judy St. Leger, DVM, DACVP
• Haines, H.G., Rywlin, A. and Rebell, G., 1974, March. A herpesvirus disease of
farmed green turtles (Chelonia mydas). In Proceedings of the annual
meeting‐World Mariculture Society (Vol. 5, No. 1‐4, pp. 183-195). Blackwell
Publishing Ltd.
• Alfaro-Núñez, A., Bertelsen, M.F., Bojesen, A.M., Rasmussen, I., Zepeda-Mendoza,
L., Olsen, M.T. and Gilbert, M.T.P., 2014. Global distribution of Chelonid
fibropapilloma-associated herpesvirus among clinically healthy sea turtles. BMC
evolutionary biology, 14(1), p.1.
• Jones, A.G., 2004. Sea turtles: old viruses and new tricks. Current biology, 14(19),
pp.R842-R843.
• Stacy, B.A., Wellehan, J.F., Foley, A.M., Coberley, S.S., Herbst, L.H., Manire, C.A.,
Garner, M.M., Brookins, M.D., Childress, A.L. and Jacobson, E.R., 2008. Two
herpesviruses associated with disease in wild Atlantic loggerhead sea turtles
(Caretta caretta). Veterinary microbiology, 126(1), pp.63-73.
• Jacobson, E.R., 1996. Guest editorial: marine turtle farming and health
issues. Marine Turtle Newsletter, 72, pp.13-15.
• Herbst, L., Ene, A., Su, M., Desalle, R. and Lenz, J., 2004. Tumor outbreaks in
marine turtles are not due to recent herpesvirus mutations. Current
Biology, 14(17), pp.R697-R699.
• Greenblatt, R.J., Work, T.M., Balazs, G.H., Sutton, C.A., Casey, R.N. and Casey, J.W.,
2004. The Ozobranchus leech is a candidate mechanical vector for the
fibropapilloma-associated turtle herpesvirus found latently infecting skin tumors
on Hawaiian green turtles (Chelonia mydas). Virology, 321(1), pp.101-110.
• Arthur, K., Limpus, C., Balazs, G., Capper, A., Udy, J., Shaw, G., Keuper-Bennett, U.
and Bennett, P., 2008. The exposure of green turtles (Chelonia mydas) to tumour
promoting compounds produced by the cyanobacterium Lyngbya majuscula and
their potential role in the aetiology of fibropapillomatosis. Harmful Algae, 7(1),
pp.114-125.
• Sounguet, A.G., Villarubia, A., Balazs, G.H. and Spraker, T.R., 2007.
Fibropapillomatosis confirmed in Chelonia mydas in the Gulf of Guinea, West
Africa. Marine Turtle Newsletter, (116), p.20.
REFERENCE
• Manire, C.A., Stacy, B.A., Kinsel, M.J., Daniel, H.T., Anderson, E.T. and Wellehan, J.F.,
2008. Proliferative dermatitis in a loggerhead turtle, Caretta caretta, and a green
turtle, Chelonia mydas, associated with novel papillomaviruses. Veterinary
microbiology, 130(3), pp.227-237.
• Herbst, L.H., Jacobson, E.R., Klein, P.A., Balazs, G.H., Moretti, R., Brown, T. and
Sundberg, J.P., 1999. Comparative pathology and pathogenesis of spontaneous and
experimentally induced fibropapillomas of green turtles (Chelonia
mydas). Veterinary Pathology Online, 36(6), pp.551-564.
• Coberley, S.S., Herbst, L.H., Brown, D.R., Ehrhart, L.M., Bagley, D.A., Schaf, S.A.,
Moretti, R.H., Jacobson, E.R. and Klein, P.A., 2001. Detection of antibodies to a
disease-associated herpesvirus of the green turtle, Chelonia mydas. Journal of
clinical microbiology, 39(10), pp.3572-3577.
• Curry, S.S., Brown, D.R., Gaskin, J.M., Jacobson, E.R., Ehrhart, L.M., Blahak, S.,
Herbst, L.H. and Klein, P.A., 2000. Persistent infectivity of a disease-associated
herpesvirus in green turtles after exposure to seawater. Journal of Wildlife
Diseases, 36(4), pp.792-797.
REFERENCE
• Duarte, A., Faísca, P., Loureiro, N.S., Rosado, R., Gil, S., Pereira, N. and Tavares, L.,
2012. First histological and virological report of fibropapilloma associated with
herpesvirus in Chelonia mydas at Príncipe Island, West Africa. Archives of
virology, 157(6), pp.1155-1159.
• Reséndiz, E., Flores-Ramírez, S., Koch, V. and Cordero-Tapia, A., 2016. First Record
of Fibropapillomatosis in a Green Turtle Chelonia mydas from the Baja California
Peninsula. Journal of Aquatic Animal Health, 28(4), pp.252-257.
• Warwick, C., Arena, P.C. and Steedman, C., 2013. Health implications associated
with exposure to farmed and wild sea turtles. JRSM short reports, 4(1), p.8.
• EAZWV transmissible disease fact sheet sheet no. 37 Loggerhead genital-
respiratory herpesvirus (lgrv)
• Monezi, T.A., Mehnert, D.U., de Moura, E.M., Müller, N.M., Garrafa, P.,
Matushima, E.R., Werneck, M.R. and Borella, M.I., 2016. Chelonid herpesvirus 5
in secretions and tumor tissues from green turtles (Chelonia mydas) from
Southeastern Brazil: A ten-year study. Veterinary microbiology, 186, pp.150-156.
• Reckseit, S.M., 2016. Volunteer Programs in the Conservation of Sea Turtles in
Costa Rica (Doctoral dissertation, Texas A&M University).
REFERENCE
• Jones, K., Ariel, E., Burgess, G. and Read, M., 2016. A review of fibropapillomatosis in
green turtles (Chelonia mydas). The Veterinary Journal, 212, pp.48-57.
• da Silva, C.C., Klein, R.D., Barcarolli, I.F. and Bianchini, A., 2016. Metal contamination
as a possible etiology of fibropapillomatosis in juvenile female green sea turtles
Chelonia mydas from the southern Atlantic Ocean. Aquatic Toxicology, 170, pp.42-
51.
• Bunkley-Williams, L., Williams Jr, E.H., Horrocks, J.A., Horta, H.C., Mignucci-Giannoni,
A.A. and Poponi, A.C., 2008. New leeches and diseases for the hawksbill sea turtle
and the West Indies. Comparative Parasitology, 75(2), pp.263-270.
• Jacobson, E.R., BUERGETT, C., Williams, B. and Harris, R.K., 1991. Herpesvirus in
cutaneous fibropapillomas of the green turtle Chelonia mydas. Diseases of Aquatic
Organisms, 12(1), pp.1-6.
• Haines, H. and Kleese, W.C., 1977. Effect of water temperature on a herpesvirus
infection of sea turtles. Infection and immunity, 15(3), pp.756-759.
• Rodenbusch, C.R., Almeida, L.L., Marks, F.S., Ataíde, M.W., Alievi, M.M., Tavares, M.,
Pereira, R.A. and Canal, C.W., 2012. Detection and characterization of fibropapilloma
associated herpesvirus of marine turtles in Rio Grande do Sul, Brazil. Pesquisa
Veterinária Brasileira, 32(11), pp.1179-1183.
REFERENCE
AN OUTLINE ON HERPESVIRAL DISEASES IN MARINE TURTLES

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AN OUTLINE ON HERPESVIRAL DISEASES IN MARINE TURTLES

  • 1. MAJOR ADVISOR MEGHA K BEDEKAR SENIOR SCIENTIST PRESENTED BY B.MADHUSUDHANA RAO AAHMA5-07
  • 2. INTRODUCTION • Order : Testudines • Family : Cheloniidae • Poikilotherms • 110 million years, since the time of the dinosaurs.
  • 3. Turtles are exposed to a no. of threats • Degradation, urbanisation & pollution of nesting habitats & foraging areas. • Traditional hunting and egg harvest • The impacts of climate change on the marine and terrestrial environment.
  • 4. “Cayman Turtle Farm” (CTF) • Grand Cayman island, West Indies in 1968 with 23 acres. • Opens the door for – exchange of views on the pros and cons of sea turtle farming. High demand for food & medicinal purposes.
  • 5. HERPESVIRUSES Generally characteristic features of HV:  Variable host range,  Short replication cycle, and • Linear, ds DNA genome with Icosahedral symmetry • Replication is within the nucleus.
  • 7. HERPESVIRUSES • Greek word herpein , referring to the LATENT. • Establish latent infection. During which viral gene expression is minimized • Expression of these latency- associated genes may function to keep the viral genome from being digested by cellular ribozymes or being found out by the immune system.
  • 8. HERPESVIRUSES ChHV 1 (Grey Patch Disease) ChHV 2 ChHV 3 ChHV 4 ChHV 5 (Fibropapillomatosis) ChHV 6 (Lung-Eye- and Tracheal disease) HV affecting F.W Turtles
  • 9. Strains of Chelonid Herpesvirus 5 FIBROPAPILLO MATOSIS A B D C Genome -----23 kb Atlantic ( Florida & Barbados) Middle Pacific (Hawaii) Eastern Pacific. Western Pacific (Australia)
  • 10. FIBROPAPILLOMATOSIS (FP) • FP - 1st reported in 1938 at Key West, Florida. • V. limited focus is done on diseases of sea turtles. But greatest concern - Green turtles as it has only reached a panzootic status in this species (Williams et al., 1994). FP is a neoplastic disease characterized by cutaneous, ocular tumours that has been documented to infect all sea turtle species.
  • 11. AETIOLOGY • Research to date suggests that FP is associated with a Herpesvirus infection (Herbst et al., 1995; Quackenbush et al., 1998, 2001; Lackovich et al., 1999). This virus cannot be cultured in vitro and therefore Koch's postulates have not been fulfilled.
  • 12. AETIOLOGY • Agent : Chelonid Herpesvirus 5 (ChHV5) or "Green turtle fibropapillomatosis” (GTFP) because it was first recorded in Green turtles. Family : Herpesviridae Subfamily : Alphaherpesvirinae Genus : Scutavirus (ICTV, 2011).
  • 13. 1938 (1.5%) Disease prevalence and impact FP emerge in the Eastern Pacific, Hawaiian Islands, Indonesia and Australia (40%). PANZOOTIC Over 140 countries (Groombridge and Luxmoore, 1989). 50% of the population of green turtles in the world are affected by the disease (Balazs 1991, Herbst 1994). 1980s (20-60%) 1990s
  • 14. Epidemiology • FP typically occurs in marine turtles inhabiting neritic areas – most frequently observed in juvenile turtles. • Horizontal. • The higher incidence in females may be – behavioral ecology in life cycle. • FP rates are correl- ated with degraded habitat quality.
  • 15. Epidemiology • HV have the potential to be maintained on various surfaces in marine environment (sediments, rubbing rocks, foods sources, etc.) that could serve as vectors for transmission. Chemical pollution can activate latent viruses or indirectly increase its virulence (Aguirre et al., 1994). Most prominent in warmer climates, affecting 50%- 70% of popn.
  • 16. Epidemiology • FPHV DNA was detected on the gills of wrasse cleaner fish (Thalassoma duperrey) – It groom sea turtles - possible vector for transmission (Lu et al. 2000b).
  • 17. • Epidemiological links are seen between FP rates, nitrogen footprints, and invasive macroalgae – ARGININE. • Water temperature - lesions of a debilitating size by autumn. • Susceptible stages : Juveniles 40 - 70 cms length/ (10– 30 kg) most effected. • FP is rare (0-12%) among nesting adult females and lesions tend to be focal and mild. Epidemiology
  • 19. Note the Fibropapilloma with highly rugose structure (black arrow) and presence of leeches - Ozobranchus (white arrow). Photo credit: Tim Collins.
  • 20. MULTIFACTORIAL AETIOLOGY U.V LIGHT (Aguirre, 1991), CONTAMINATS (Aguirre et al. 1994a) METALS (Monserrat et al., 2007) TEMP (Herbst et al., 1995) BIOTOXINS (ARGININE) (Landsburg et al. 1999). PARASITES (Dailey & Morris, 1995)
  • 21. CLINICAL SIGNS Lesions that are comprised primarily of proliferating epidermis with little or no underlying dermal involvement are properly called PAPILLOMAS. Those masses in which both tissues are hyperplastic are termed FIBROPAPILLOMAS. While those lesions predominantly comprised of proliferating dermal components with relatively normal epidermis are called FIBROMAS.
  • 22. Severe fibropapillomas in the cervical, periocular, and right front limb regions of one green turtle
  • 23. The conjunctiva (especially bulbar conjunctiva) is a common site for GTFP, and masses may grow over the cornea.
  • 24. STAGES OF LESION DEVELOPMENT (Herbst, 1994; Kang et al., 2008). • Papilloma lesions EARLY PHASE • Fibropapill -omas lesions INTERMEDIATE PHASE • Fibromas lesions CHRONIC PHASE Internal - mouth, heart, lungs, kidneys, liver and gastrointestinal tract (Mascarenhas and Iverson, 2008). Occasional visceral Fibromas, Myxofibromas and Fibrosarcomas
  • 25. HISTOLOGICAL STUDIES • Histological studies on FP lesions have observed orthokeratotic hyperkeratosis (a)and varying degrees of epidermal hyperplasia (b) (upto 30 cells thick), and papillary projections (c)
  • 26. Key features in FP is proliferative epidermis presenting ballooning cells with intracellular inclusion bodies (IIBs) suggestive of viral infection, shown with arrows. HISTOLOGICAL STUDIES
  • 27. VIRULENT FACTORS • Four members of the C-type lectin-like domain superfamily (F-lec1, F-lec2, F-sial and F-M04) were found to be present in the ChHV5 genome. Two of these has been suggested that these genes may play a role in FP pathogenesis & lesions formation (Ackermann et al., 2012).
  • 29. GRAY PATCH DISEASE • Tissues affected – SKIN, SHELL. • Occurs in two forms Non spreading Papules/ pustular like lesions resolve spontaneously. Benign, a necrotizing dermatitis of post-hatching green turtles 1st Spreading Gray patches to large areas of the epidermal surface. Malignent, often these animals die 2nd
  • 30. Clinical symptoms • Necrotizing dermatitis of post - hatching. • Epizootics of small, circular papular skin lesions that coalesced into patches were described in young sea turtles. • Stressful environmental conditions such as over crowding and higher temp. seemed to enhance the onset and severity of lesions.
  • 31. Proliferative dermatitis lesions on subadult loggerhead turtle (A) Early skin lesions with typical raised white appearance. (C) Resolving lesions on scales of front flipper (B) Advanced skin lesions showing area of discoloration during healing.
  • 32. • The first critical time - 2-6 weeks of age. • At this age – no typical skin lesions of gray-patch disease; however, there is a consistent level of mortality (20%). Affects 90-100% hatchlings Clinical symptoms The only obvious clinical sign is impacted fecal material in the lower intestinal tract.
  • 33. • The second critical - 8 to 15 weeks of age. • Mortality is less compare to the first stroke. Clinical symptoms • Turtles over I year of age do not have the natural lesions of gray-patch disease. • Infection is in higher degree in summer. • Inactivated vaccine – skin scraping. • Transmission - horizontal This is the period of time that we are able to obtain large amounts of skin scrapings containing the herpesvirus.
  • 34.
  • 35. LUNG-EYE-TRACHEAL DISEASE(LETD) • Agent : (LETV) or (Chelonid herpesvirus 6) • Name implies, the virus affects the eyes and respiratory tract. • And has a clinical course of 2-3 weeks. Characterized by conjunctivitis, pharyngitis, tracheitis, periglottal necrosis and pneumonia (Jacobson et al. 1986).
  • 36. EPIZOOTOLOGY • Transmission is thought to be vertical or water- borne. Affects turtles worldwide, and mortality in post- hatchling and juvenile - can reach 70%.
  • 37. MODEL CHELONID HERPES VIRUS • The virus was cultured in green turtle kidney cells that helped in further research. • LETV - gathers information about the general characteristics of this largely unexplored group of viruses. • In addition, the prevalence of LETV infections in wild populations.
  • 38. LOGGERHEAD GENITAL- RESPIRATORY HERPESVIRUS” (LGRV) Ulcers in the trachea, around the cloaca and on the base of the phallus. Venereal transmission. LOGGERHEAD OROCUTANEOUS HERPESVIRUS” (LOCV) Ulcers in the oral cavity & cutaneous plaques that can be covered with exudate & have an erythematous border. ------  Both viruses were thought to be opportunistic in debilitated turtles.
  • 39. CONCLUSION • The longevity of marine turtles, coupled with their close association with inshore habitats and seagrass meadows and coral reefs in these habitats, has led to the proposal that they may act as sentinel indicators of marine ecosystem health. • Further investigations has to be carried to rule out several confusions about remaining viruses which will in turn inform the management and conservation of a vulnerable species.
  • 40. REFERENCE • Orós, J., Torrent, A., Calabuig, P. and Déniz, S., 2005. Diseases and causes of mortality among sea turtles stranded in the Canary Islands, Spain (1998– 2001). Diseases of aquatic organisms, 63(1), pp.13-24. • EAZWV Transmissible Disease Fact Sheet Sheet No. 23 1 FIBROPAPILLOMATOSIS (FP) OF SEA TURTLES Rachel E. Marschang 2009 • EAZWV Transmissible Disease Fact Sheet Sheet No. 26 GPD • Select conditions in sea turtle pathology ;Judy St. Leger, DVM, DACVP • Haines, H.G., Rywlin, A. and Rebell, G., 1974, March. A herpesvirus disease of farmed green turtles (Chelonia mydas). In Proceedings of the annual meeting‐World Mariculture Society (Vol. 5, No. 1‐4, pp. 183-195). Blackwell Publishing Ltd. • Alfaro-Núñez, A., Bertelsen, M.F., Bojesen, A.M., Rasmussen, I., Zepeda-Mendoza, L., Olsen, M.T. and Gilbert, M.T.P., 2014. Global distribution of Chelonid fibropapilloma-associated herpesvirus among clinically healthy sea turtles. BMC evolutionary biology, 14(1), p.1. • Jones, A.G., 2004. Sea turtles: old viruses and new tricks. Current biology, 14(19), pp.R842-R843. • Stacy, B.A., Wellehan, J.F., Foley, A.M., Coberley, S.S., Herbst, L.H., Manire, C.A., Garner, M.M., Brookins, M.D., Childress, A.L. and Jacobson, E.R., 2008. Two herpesviruses associated with disease in wild Atlantic loggerhead sea turtles (Caretta caretta). Veterinary microbiology, 126(1), pp.63-73.
  • 41. • Jacobson, E.R., 1996. Guest editorial: marine turtle farming and health issues. Marine Turtle Newsletter, 72, pp.13-15. • Herbst, L., Ene, A., Su, M., Desalle, R. and Lenz, J., 2004. Tumor outbreaks in marine turtles are not due to recent herpesvirus mutations. Current Biology, 14(17), pp.R697-R699. • Greenblatt, R.J., Work, T.M., Balazs, G.H., Sutton, C.A., Casey, R.N. and Casey, J.W., 2004. The Ozobranchus leech is a candidate mechanical vector for the fibropapilloma-associated turtle herpesvirus found latently infecting skin tumors on Hawaiian green turtles (Chelonia mydas). Virology, 321(1), pp.101-110. • Arthur, K., Limpus, C., Balazs, G., Capper, A., Udy, J., Shaw, G., Keuper-Bennett, U. and Bennett, P., 2008. The exposure of green turtles (Chelonia mydas) to tumour promoting compounds produced by the cyanobacterium Lyngbya majuscula and their potential role in the aetiology of fibropapillomatosis. Harmful Algae, 7(1), pp.114-125. • Sounguet, A.G., Villarubia, A., Balazs, G.H. and Spraker, T.R., 2007. Fibropapillomatosis confirmed in Chelonia mydas in the Gulf of Guinea, West Africa. Marine Turtle Newsletter, (116), p.20. REFERENCE
  • 42. • Manire, C.A., Stacy, B.A., Kinsel, M.J., Daniel, H.T., Anderson, E.T. and Wellehan, J.F., 2008. Proliferative dermatitis in a loggerhead turtle, Caretta caretta, and a green turtle, Chelonia mydas, associated with novel papillomaviruses. Veterinary microbiology, 130(3), pp.227-237. • Herbst, L.H., Jacobson, E.R., Klein, P.A., Balazs, G.H., Moretti, R., Brown, T. and Sundberg, J.P., 1999. Comparative pathology and pathogenesis of spontaneous and experimentally induced fibropapillomas of green turtles (Chelonia mydas). Veterinary Pathology Online, 36(6), pp.551-564. • Coberley, S.S., Herbst, L.H., Brown, D.R., Ehrhart, L.M., Bagley, D.A., Schaf, S.A., Moretti, R.H., Jacobson, E.R. and Klein, P.A., 2001. Detection of antibodies to a disease-associated herpesvirus of the green turtle, Chelonia mydas. Journal of clinical microbiology, 39(10), pp.3572-3577. • Curry, S.S., Brown, D.R., Gaskin, J.M., Jacobson, E.R., Ehrhart, L.M., Blahak, S., Herbst, L.H. and Klein, P.A., 2000. Persistent infectivity of a disease-associated herpesvirus in green turtles after exposure to seawater. Journal of Wildlife Diseases, 36(4), pp.792-797. REFERENCE
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Editor's Notes

  1. found today have been around for
  2. Ingestion of marine debris. Nest and hatchling depredation by wild, feral and domestic animals, boat strike, and entanglement in fishing nets and lines.
  3. Severely debilitating disease
  4. disease has a worldwide, circumtropical distribution in florida, mexico, costa rica, australia. Perhaps due to limited funding or human resources, FP has gone unnoticed in other parts of the world until current times.
  5. These new recruits may be exposed to several stressors associated with migration, adaptation to a new environment, and changes in population density, diet and pathogen exposure, which may all combine to reduce the efficacy of the immune system and make these immature and  juveniles more susceptible to infection.
  6. There appears to be a link between the development of FP and the immune system. Immunosuppression is strongly correlated with FP in captive green turtles
  7. Arginine is a regulator of immune activity & promote herpesviruses and contribute to tumour formation
  8. Okadaic acid is a known tumor promotor and is produced by the Prorocentrum dinoflagellate that grows on sea grasses. Similarly, lyngbyatoxin A & debromoaplysiatoxin (DAT) are produced by Lyngbya majuscula (filamentous cyanobacterium found in marine and estuarine environments). act as protein kinase C (PKC) activators and are potent tumour promoters
  9. Persistent chlorinated compounds, such as polychlorinated biphenyls(PCBs) and chlorinated pesticides,
  10. interfere with the hydrodynamics and locomotion.
  11. These three proliferative lesions are the hallmarks of the disease referred to as green turtle fibropapillomatosis (GTFP).
  12.  hypertrophy of the stratum corneum of the skin No nucleus is seen in the cells.
  13. Conjunctivitis, also known as pink eye, is inflammation of the outermost layer of the white part of the eye and the inner surface of the eyelid.
  14. In addition, this research has provided the means to assess the prevalence of LETV infections in wild populations and the threat such infections may present for marine turtle health and conservation via serodiagnosis.