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Herpesviruses

BASICS

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

DIAGNOSIS

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

 Virus neutralization tests have been used for the detection of antibodies against TeHV1 and 3 in tortoises.

 An ELISA has also been described for the detection of antibodies against these two viruses and against TeHV2, but may not be commercially available.

PATHOLOGICAL FINDINGS

 Ballooning degeneration and necrosis may be noted in infected epithelial cells, necrosis and inflammation in affected tissues.

 Fibropapillomas consist of a hyperplastic epidermis and a thickened hypercellular dermis.

 Infected cells may contain eosinophilic to amphophilic intranuclear inclusions.

TREATMENT

APPROPRIATE HEALTH CARE

 There are no standardized protocols for treating HV‐infected reptiles.

 Strict quarantine, biosecurity, and hygiene are essential for the prevention of HV infections.

 Autovaccination with inactivated material from surgically removed fibropapillomas has been suggested.

 Keeping animals at the high end of their POTZ may help in recovery, as well as treatment of secondary bacterial infections.

NUTRITIONAL SUPPORT

 Herpesvirus infected reptiles may be anorexic and nutritional support may be necessary.

 In animals with oral lesions, esophagostomy tubes may be necessary.

CLIENT EDUCATION/HUSBANDRY RECOMMENDATIONS

 Testing for both virus and antibodies (in tortoises) should be in place.

 An effective quarantine regimen should be in place.

 Mixing of tortoise species should be avoided.

 Infected animals must be isolated

SURGICAL CONSIDERATIONS

For fibropapillomas—surgical removal of lesions.

MEDICATIONS

DRUG(S) OF CHOICE

 Acyclovir 80 mg/kg PO q24h (famciclovir has been shown to be safer in mammals and may be an alternative choice for treatment).

 Acyclovir topically on lesions or topical disinfection (e.g., with 0.5% chlorhexidine solution) have also been suggested.

 The use of immunomodulators (e.g., Zylexis (Pfizer AG, Zurich, Switzerland)) has been suggested in HV infected tortoises, but its efficacy is unproven.

PRECAUTIONS/INTERACTIONS

 Affected animals should be barrier nursed and in‐contact animals should be placed in quarantine.

FOLLOW‐UP

PATIENT MONITORING

 Development of disease in contact animals may take several weeks, so monitoring of a collection (and barrier nursing of contact animals) should remain active for at least one season.

 There is some indication that brumation may provoke disease outbreaks, and intensified health monitoring should be carried out in the spring and again before the next brumation.

EXPECTED COURSE AND PROGNOSIS

 Morbidity and mortality can be high, depending on the virus strain and host species involved, although it can take an extended period of time for the disease to run its course within a collection.

 Surviving animals remain carriers

MISCELLANEOUS

COMMENTS

N/A

ZOONOTIC POTENTIAL

Herpesviruses of reptiles have not been shown to be zoonotic.

SYNONYMS

Fibropapillomatosis (FP) in sea turtles

ABBREVIATIONS

 chHV5 = chelonid alphaherpesvirus 5

 CNS = central nervous system

 ELISA = enzyme‐linked immunosorbent assay

 FPTHV = fibropapillomatosis‐associated turtle herpesvirus

 HV = herpesvirus

 LETD = lung = eye = and trachea disease

 LEDV = lung = eye = and trachea disease virus

 LGRV = loggerhead genital–respiratory herpesvirus

 LOCV = loggerhead orocutaneous herpesvirus

 PCR = polymerase chain reaction

 POTZ = preferred optimal temperature zone

 TeHV = testudinid herpesvirus

Suggested Reading

1 Gandar F, Wilkie GS, Gatherer D, et al. The genome of a tortoise herpesvirus (testudinid herpesvirus 3) has a novel structure and contains a large region that is not required for replication in vitro or virulence in vivo. J Virol 2015;89(22):11438–11456.

2 Marschang RE. Virology. In: Divers SJ, Stahl SJ, eds. Mader’s Reptile and Amphibian Medicine and Surgery. St. Louis, MO: Elsevier; 2019:247–269.

3 Marschang RE. Viruses infecting reptiles. Viruses 2011;3:2087–2126.

Author Rachel E. Marschang, PD, Dr. med. vet., DECZM (Herpetology), FTÄ Mikrobiologie

Blackwell's Five-Minute Veterinary Consult: Reptile and Amphibian

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