Few viruses have been clearly proved as etiologic agents of disease in reptiles, but several have been linked strongly enough for them to be considered the causative agent until proved otherwise.
Inclusion Body Disease (IBD) of Boid Snakes
Boa constrictors and several species of pythons are most commonly affected by IBD. Boas are considered to be the normal host for this retrovirus because so many are infected, and they can harbor the virus for years without signs. Early signs, possibly precipitated by any factor causing immunosuppression, include a history of unthriftiness, anorexia, weight loss, secondary bacterial infections, poor wound healing, dermal necrosis, and regurgitation. In essence, IBD should be considered in every sick boa. Typical findings in the acute phase of the disease include leukocytosis and a normal chemistry panel. As the disease progresses, WBC counts tend to decline to subnormal levels. Blood chemistry results vary depending on how debilitated and dehydrated the boa becomes, but organ damage may appear. As the disease becomes chronic, some boas exhibit neurologic symptoms ranging from mild facial tics and abnormal tongue flicking to failure of the snake to right itself when placed in dorsal recumbency and severe seizures.
Pythons are thought to be an abnormal host to the IBD retrovirus because the course of disease is more acute and neurologic symptoms more profound. Most pythons present with severe neurologic disease. While the active disease can linger for months or more in boas, most pythons die within days or weeks of the onset of clinical signs.
Exposure to this retrovirus appears to be due to a transfer of body fluids. Breeding, fight wounds, fecal/oral contamination, and snake mites have been implicated as common ways of transfer. A tentative diagnosis is based on the history and clinical signs. Blood work varies depending on the stage of the disease, but few diseases in snakes will cause such elevated WBC counts in the early stages. On blood smears, inclusion bodies are frequently found in the cytoplasm of leukocytes. A definitive diagnosis is obtained via biopsy of internal tissues in which the characteristic inclusion bodies are found, eg, the liver, kidney, esophageal tonsils, and stomach.
IBD is not curable, and many clients choose euthanasia. However, individuals may elect to isolate their snakes and treat with supportive and palliative measures. It is essential to educate clients not to sell infected specimens or their offspring, as this has caused the disease to spread worldwide.
Retroviruses have also been found in Russell's vipers, corn snakes, and California kingsnakes in association with malignant tumors. A retrovirus isolated from a sarcoma in a Russell's viper was designated as viper virus. A related virus was isolated in a corn snake from a rhabdomyosarcoma and designated cornsnake retrovirus.
Adenoviruses have been implicated in fatal hepatic or GI diseases in snakes (gaboon vipers, ball pythons, boa constrictors, rosy boas, and rat snakes), lizards (Jackson's chameleons, savannah monitors, and bearded dragons) and crocodilians.
In bearded dragons, the route of transmission appears to be fecal/oral contamination. Clinical signs are more commonly noted in juvenile dragons but can affect adults, usually to a lesser extent. Signs are vague and include lethargy, weakness, weight loss, diarrhea, and sudden death. The morbidity is high in young bearded dragons, but survival is increased with supportive care. Fluid administration, force feeding, and antibiotics for secondary infections are useful.
As the signs of disease in bearded dragons are vague and similar to those caused by coccidia and nutritional disorders, it is important to confirm the diagnosis. Characteristic intranuclear inclusion bodies are found in several internal organs, primarily the liver. When working with a large breeding group of lizards, it is practical to sacrifice a failing specimen in order to make a diagnosis. Premortem diagnosis can be accomplished by liver biopsy. Identification of adenovirus from fresh feces may be possible in the near future.
Recovered lizards should be quarantined for at least 3 mo. Duration of viral shedding after recovery is unknown, so clients should be discouraged from selling or trading previously infected animals.
Herpesviruses have been isolated from freshwater turtles, tortoises, and green sea turtles. In freshwater turtles, the virus may be associated with hepatic necrosis. In tortoises the virus may cause necrosis of oral mucosa accompanied by anorexia, regurgitation, and oral and ocular discharge. Treatment in tortoises includes isolation, supportive care, and application of 5% acyclovir to oral lesions. Acyclovir given at 80 mg/kg, PO, sid, appeared to improve the lesions in a desert tortoise. Herpesvirus is diagnosed by the presence of intranuclear inclusion bodies and electron microscopic demonstration of viral particles.
Herpesvirus infection of farmed green sea turtles have been associated with gray patch disease, and lung-eye-trachea disease, while fibropapillomas plague certain free-ranging populations. Gray patch disease (Chelonian herpesvirus 1) causes epizootics of small, circular papular skin lesions that coalesce into patches and is associated with young turtles maintained in crowded, warmer, stressful situations. Biopsies of the skin reveal basophilic intranuclear inclusion bodies in epidermal cells; viral particles are noted in the cytoplasm by electron microscopy. There is no specific treatment, but reduction of crowding and stress appears to decrease the incidence. Lung-eye-trachea disease causes harsh respiratory sounds, with ulcerations and caseous debris over the globe and throughout the oropharynx and trachea. Buoyancy problems and high mortality are reported.
Fibropapillomatosis has been reported from free-ranging sea turtles, especially around Hawaii. The route of transmission is not known. The light gray to black masses range in size up to 20 cm in diameter. The location of the masses seems to dictate the severity of signs. Masses occurring on periocular tissue can obscure vision. Growths on the flippers can interfere with swimming and the ability to forage for food. Internal masses also occur, primarily in the lungs, liver, kidneys, and GI tract. Diagnosis is made by characteristic lesions and histology. Treatment consists of surgical removal, with wide margins to help reduce recurrence. Some turtles recover spontaneously, while those with internal lesions usually perish. It is suspected that fibropapillomas are caused by a herpesvirus, and infected specimens should be isolated from healthy turtles.
Paramyxovirus infections are more common in viperid snakes, but have been reported in nonvenomous snakes as well. This highly contagious virus causes predominantly respiratory signs; transmission appears to be from respiratory secretions. Secondary bacterial infections are common due to the severe inflammation initiated by the virus, and it is not unusual to note nasal discharge, open-mouth breathing, caseated pus in the oral cavity, and labored breathing. Neurologic involvement, including tremors and opisthotonos, is occasionally noted.
Paramyxovirus should be suspected in any respiratory infection that does not respond to treatment with supportive care, antibiotics, and nebulization. Endoscopic biopsies and postmortem samples of lung can be submitted to detect viral particles by histology and electron microscopy. A hemagglutination inhibition test is available to measure antibodies against ophidian paramyxovirus in zoos and private collections; a positive titer should be used as a screening tool to aid in eliminating infected animals and preventing carriers from entering noninfected collections.
There is no specific treatment, but supportive care and antibiotics may prove useful. Affected specimens should be isolated and strict hygiene employed. Although a vaccine is under development, it is currently not effective.
Viral particles appear to be transmitted from one European green lizard to another via bite wounds. The resulting papillomas are 2–20 mm in diameter and may be single or multiple. While there are no signs in the initial phase, affected lizards may become lethargic, anorectic, and die. Diagnosis involves detection of viral particles by electron microscopy. Treatment consists of surgically removing single masses, although regrowth is common. Isolating affected lizards is perhaps the only means to prevent spread.
A papilloma-type virus also appears to affect Bolivian side-neck turtles and appears as white, oval skin lesions distributed over the head. Ulcerative shell lesions are also seen, primarily on the plastron. Diagnosis is made by identifying viral particles on electron microscopy. Treatment is supportive and palliative, and affected animals should be isolated.
Iridoviruses have been reported in various chelonians, snakes, and lizards. An iridovirus was found in a Herman's tortoise, which died without prior signs of disease. Progressive anemia in Australian geckos has been linked to an iridovirus. Clinical signs range from none to stomatitis, rhinitis, conjunctivitis, tracheitis, edema, and cutaneous abscessation. In some cases, the recovered iridoviruses have been closely related to amphibian ranaviruses. While the clinical importance of several of these viruses remain unclear, iridoviruses deserve close attention, especially in chelonians.
Many other viruses have been reported, but little information exists regarding their diagnosis, control, and treatment. Two nonpathogenic rhabdoviruses were isolated from Ameiva sp lizards. In addition to herpesviruses and adenoviruses, parvoviruses and picornaviruses have been found in the intestinal tract of snakes, but their exact role is unknown. A poxvirus-like virus has been isolated from circumscribed cutaneous lesions in a caiman and from dermal lesions in a tegu. A reovirus isolated from Chinese vipers was associated with death without prior signs of illness.
Last full review/revision July 2011 by Stephen J. Divers, BVetMed, DZooMed, DACZM, DECZM (herpetology), FRCVS