Branson W. Ritchie

Person Preferred Name
Branson W. Ritchie
Model
Digital Document
Description
Important indicators of population health needed for large-scale sea turtle population
recovery efforts include demographics, disease and mortality trends, condition indices, and
baseline blood data. With this comprehensive health assessment of adult female green sea turtles
Chelonia mydas nesting on Juno Beach, Florida, USA, we (1) established baseline health indices;
(2) identified individuals with evidence of infection by chelonid alphaherpes viruses 5 and 6
(ChHV5, ChHV6), which are implicated in fibropapillomatosis and respiratory and skin disease,
respectively; and (3) compared measured health indices between turtles that did versus those that
did not test positive for ChHV5 and/or ChHV6. All 60 turtles included in the study were in good
body condition with no external fibropapillomatosis tumors. Hematological and biochemical reference
intervals were established. Via quantitative PCR (qPCR), 5/60 turtles (8%) tested positive
for ChHV5, and all turtles were negative for ChHV6. Of 41 turtles tested for antibodies to ChHV5
and ChHV6, 29% and 15% tested positive, respectively, and 10% tested positive for antibodies to
both viruses. Notably, there were no statistically significant differences between health variables
for nesting turtles that tested positive for ChHV5 DNA versus those that tested negative; and also
no differences between turtles that tested positive for ChHV5 or ChHV6 antibodies and those that
did not. This suggests that these viruses are enzootically stable in Florida’s adult green turtles.
This study provides a health profile of nesting green turtles in southeastern Florida applicable to
temporal and spatial investigations of this and other populations.
Model
Digital Document
Description
Fibropapillomatosis is a debilitating tumor disease of sea turtles that is sometimes
fatal. This disease is a key concern for sea turtle rehabilitation facilities due to its infectious nature,
as it is associated with a virus called chelonid alphaherpesvirus 5. This is the first study to analyze
antibodies to this virus in loggerhead sea turtles and represents the most complete dataset on
viral detection in sea turtles encountered in the more northern latitudes of their habitat in the
western Atlantic.
Model
Digital Document
Description
Chelonid alphaherpesviruses 5 and 6 (ChHV5 and ChHV6) are viruses that affect wild
sea turtle populations. ChHV5 is associated with the neoplastic disease fibropapillomatosis (FP),
which affects green turtles (Chelonia mydas) in panzootic proportions. ChHV6 infection is associated
with lung-eye-trachea disease (LETD), which has only been observed in maricultured sea turtles,
although antibodies to ChHV6 have been detected in free-ranging turtles. To better understand
herpesvirus prevalence and host immunity in various green turtle foraging aggregations in Florida,
USA, our objectives were to compare measures of innate and adaptive immune function in relation
to (1) FP tumor presence and severity, and (2) ChHV5 and ChHV6 infection status. Free-ranging,
juvenile green turtles (N = 45) were captured and examined for external FP tumors in Florida’s Big
Bend, Indian River Lagoon, and LakeWorth Lagoon. Blood samples were collected upon capture
and analyzed for ChHV5 and ChHV6 DNA, antibodies to ChHV5 and ChHV6, in vitro lymphocyte
proliferation using a T-cell mitogen (concanavalin A), and natural killer cell activity. Despite an
overall high FP prevalence (56%), ChHV5 DNA was only observed in one individual, whereas 20% of
turtles tested positive for antibodies to ChHV5. ChHV6 DNA was not observed in any animals and
only one turtle tested positive for ChHV6 antibodies. T-cell proliferation was not significantly related
to FP presence, tumor burden, or ChHV5 seroprevalence; however, lymphocyte proliferation in
response to concanavalin A was decreased in turtles with severe FP (N = 3). Lastly, green turtles with
FP (N = 9) had significantly lower natural killer cell activity compared to FP-free turtles (N = 5). These
results increase our understanding of immune system effects related to FP and provide evidence that
immunosuppression occurs after the onset of FP disease.