A. Hepatic lipidosis in reptiles. Proc SEVC, October 2013, Barcelona, Spain.5 West G. Endoscopic hepatic biopsy in Coahuilan box turtles, Terrapene coahuila. J Herpetol Med Surg 2001;11(2):28–29.
Author Drury R. Reavill, DVM, DABVP (Avian and Reptile & Amphibian Practice), DACVP
Herpesviruses
DEFINITION/OVERVIEW
HV are double‐stranded, enveloped DNA viruses. They can cause latent infections and infected animals can shed virus, in some cases without any clinical signs of disease. Infections are associated with various disease syndromes and clinical signs and severity of disease may depend on both the virus strain and the host species. Specific disease processes have been described in sea turtles and tortoises.
ETIOLOGY/PATHOPHYSIOLOGY
HV in the genus Scutavirushave been described in sea turtles, tortoises, and aquatic turtles.
HV infecting sea turtles include various strains of FPTHV, including chelonian chHV5, the type species of the genus Scutavirus, LEDV, and others.
Four different HV have been described in tortoises: testudinid HV 1–4. Transmission is most likely via direct contact.
In sea turtles, virus may survive for some time in sea water, and transmission via the environment may be possible.
Environmental stressors lead to more severe disease, and other infectious agents likely also contribute to the development of severe disease (e.g., mycoplasma infections in tortoises).
Animals that survive initial infection become carriers, and any animal that has been infected should be considered a lifelong carrier.
SIGNALMENT/HISTORY
Can affect all age classes
In sea turtles, fibropapillomatosis has been described in green (Chelonia mydas), loggerhead (Caretta caretta), hawksbill (Eretmochelys imbricata), and olive ridley (Lepidochelys olivacea) turtles around the world.
TeHV has been described in various tortoise species:TeHV1 most commonly in Russian tortoises (Testudo horsfieldii) in Asia and Europe.TeHV2 in California desert tortoises (Gopherus agassizii) in the USA.TeHV3 has been reported from a wide range of species, most commonly Mediterranean tortoise species (Testudospp.). Hermann’s (T. hermanni) and Russian tortoises appear to be highly susceptible to disease, while spur‐thighed (T. graeca) and marginated (T. marginata) tortoises survive disease more often and are more likely to become clinically inapparent carriers.TeHV4 has been described in a bowsprit tortoise (Chersina angluata) and a leopardtortoise (Stignochelys pardalis) in the USA and Europe (although both species are African in origin).
In aquatic turtles, HV have been described in various emydid species, including pond, painted, map, and box turtles as well as in other taxonomic groups of turtles.
Disease can occur year round, although tortoises may be particularly susceptible in the spring and fall.
CLINICAL PRESENTATION
Sea turtles
Fibropapillomatosis: can develop externally on all parts of the body, including the eyes and around the cloaca, leading to difficulties in finding food and/or in defecating. Internal tumors can also occur. Affected animals may be cachectic.
Other HV‐associated diseases described in sea turtles: gray patch disease (skin lesions in young green sea turtles); LETD (respiratory disease in green sea turtles); LGRV, and LOCV in wild‐caught loggerhead sea turtles.
Tortoises
Acute: lethargy, anorexia, caseous plaques on the tongue and palate, dyspnea, hepatitis. Severe disease with high morbidity and mortality associated with TeHV3 infection in various tortoise species. Infection may be clinically inapparent in some cases, although disease can develop in any species. TeHV1 and TeHV4 may be associated with less severe disease or inapparent infections.
Chronic: surviving tortoises may develop CNS signs, including paralysis or incoordination. Clinically healthy carriers are also possible.
Turtles
Sudden death, weakness, nasal discharge, stomatitis, papillomatosis, and hepatitis.
Herpesviruses have also been detected in apparently clinically healthy animals.
RISK FACTORS
Husbandry
Mixing of different tortoise species leads to an increase in the probability of inapparent carriers transmitting virus to highly susceptible species.
In sea turtles, sudden changes in temperature and exposure to environmental pollutants have both been shown to increase susceptibility to HV disease.
Others
N/A
DIFFERENTIAL DIAGNOSIS
In tortoises: depending on the presentation, mycoplasma infections (esp. in cases with upper respiratory disease), ranavirus (family Iridoviridae) infections, topivirus
(family Picornaviridae) infections, bacterial and/or fungal stomatitis.
DIAGNOSTICS
Virus detection
Most commonly done using PCR detection of viral DNA.
A pan‐HV PCR can be used to detect all reptilian HV described so far.
PCRs for specific chelonian HV have also been described.
In sea turtles, material from fibropapillomas should be used for testing; in tortoises oral swabs, tongue, liver and brain can be tested.
Material from any lesions observed should be included in any testing scheme.
Serology
