Infectious deseases of reptiles      Infectious deseases of reptiles   PDF  (293 KB)

Adenovirus infections in lizards and snakes

 It's a common infection in lizards and snakes. In the literature adenoviruses are often mentioned in bearded dragons but they also occur in other breeds of lizards. The clinical picture often is nonspecific. Clinical changes are most often include an acute depression with onset of anorexia, diarrhea, ophistotonus and death in young dragons. Sometimes young dragons die without premonitory signs.

Other species show fatal hepatitis or gastrointestinal changes. Macroscopic lesions associated with adenovirus are often missing. Basophilic intranuclear inclusion bodies have been described in affected animals and are often found in epithelial cells of the gastrointestinal tract, hepatocytes and the epithelium of the bile ducts.

 In snakes fatal hepatitis or gastrointestinal disease in boids, colubrids and viperidae can be found. Clinical signs include regurgitation, diarrhea, or CNS signs. The routs of transmission in reptiles have not been determined yet. The presence of lesions predominately in the liver and gastrointestinal tract strongly suggests fecal-oral transmission though. Ante mortem diagnosis can be confirmed by PCR of feces and cloacal swabs or in liver biopsies.

Post mortem diagnosis by histological examination of the gastrointestinal tract and the liver is an alternative opportunity to diagnose the disease.

Liver of a Bearded dragon (Pogona vitticeps)

Liver of a Bearded dragon (Pogona vitticeps) hepatocytes with large intranuclear basophilic inclusion bodies

Herpesvirus infection in tortoises

Herpesvirus infections can cause life-threatening disease in different species of tortoises e.g. Hermann´s Tortoise (Testudo hermanni), Spurthighed Tortoise (Testudo graeca) and the Afghan Tortoise (Agrionemys horsfieldii).
The route of transmission is through direct contact from one susceptiple individual to another. Horizontal transmission is probably most common in reptiles. A vertical transmission is discussed.
The pathological changes vary by species and among individuals. They may include ulcerative lesions of the gastrointestinal and respiratory mucosa. Furthermore diphteric and necrotizing stomatitis and glossitis, necrotizing bronchitis, pneumonia and hepatomegaly are common signs.

Mortality rates in outbreaks that involve naive populations may approach 100% as has been reported in Hermann`s tortoises (Testudo hermanni) and Leopard tortoises (Testudo pardalis). Herpesvirus infections are typically associated with the formation of intranuclear inclusion bodies in the tissues of affected tortoises. To prevent outbreaks every tortoise introduced into a collection of naive animals should be chekked for herpes. Diagnosis can be confirmed by polymerase chain reaction (PCR) from pharyngeal and tongue swabs or by PCR of tissues (tongue, liver, spleen, esophagus, intestine, trachea, lung and brain. Histological examination from the tissues mentioned above or cytological examination from swabs of the oral cavity is another possibility to look for the inclusion bodies. The lesion should be swabbed with a moist, sterile cotton swab. After collection the swab should be gently rolled along the flat surface of a clean, glass microscope slide. 

Diphteroid-necrotizing stomatitis and glossitis of a Hermann`s tortoise

Diphteroid-necrotizing stomatitis and glossitis of a Hermann`s tortoise (Testudo hermanni)*

Tongue of a Hermann`s tortoise

Tongue of a Hermann`s tortoise (Testudo hermanni), epithelial cells with eosinophilic intranuclear inclusion bodies

Mycoplasmosis in tortoises

Mycoplasma agassizii is a bacterium which leads to upper respiratory tract disease (URTD). Clinical signs, including nasal discharge, conjunctivitis, ocular discharge, and palpebral and periocular edema, may develop as early as 2 weeks after infection. Important to note is that clinical signs may appear alone or in concert with other signs.

Mycoplasmosis is the main differential diagnosis to Herpesvirus and Pasteurella testudinis. The route of transmission for mycoplasmas is via direct contact, particularly when an animal shows a nasal discharge.

Mycoplasma agassizii adheres to the ciliated mucosal epithelium of the tortoise upper respiratory tract and causes severe disruption of the normal tissue architecture and function. Gross examination reveals no apparent clinical signs or a serous to mucopurulent nasal and ocular discharge, edematous and erythemic conjunctiva, and periocular and palpebral edema. Histologic lesions can vary dramatically in severity and may include multifocal to focally extensive subepithelial lymphoid aggregates; a mixed cell inflammatory cell infiltrate; basal cell hyperplasia; mucous and olfactory epithelial metaplasia; and erosion of the ciliated epithelium. Diagnosis can be made by detection of mycoplasmal chromosomal DNA with PCR in a nasal flush or a culture sample.The nasal flush should be filled in a sterile container.  

Hermann’s tortoise

Hermann’s tortoise (Testudo hermanni) with conjunctivitis, ocular discharge, severe palpebral edema and nasal discharge)*

Paramyxovirus in snakes

Paramyxoviruses have been associated with diseases especially in snakes but also in lizards and tortoises. This virus is a very important pathogen in viperids but pathological changes and death have also been documented in nonviperid snakes, including Elapidae, Colubridae, Boidae and Pythonidae.

Paramyxovirus infection should be considered in susceptible species with nasal discharge, open mouth breathing, accumulation of caseous debris in the oral cavity, and harsh respiratory sounds. In addition paramyxovirus infections should also be considered in snakes with emaciation, loss of muscle tonus, unwillingness to move, head tremors, stargazing, heat-seeking behaviour, recurring unresponsive bacterial or fungal pneumonia, mucoid diarrhea, malodorous stools, bowel distention, and severe protozoal infections.

The clinical progression may be peracute, acute, or chronic. The gross lesions associated with respiratory tract infections include the accumulation of caseous debris in the trachea, and nasal passages and the lung. These lesions are particularly observed in snakes with more chronic forms of disease.

Histologically, proliferation of alveolar typ II cells in the lungs with infiltrates of heterophils and lymphocytes is suggestive for Paramyxovirus. Syncytial cells may be noted in some patients, and interstitial fibrosis is common in snakes with chronic infections. Some snakes have an enlarged pancreas with ductal epithelial necrosis or hyperplasia of the pancreatic ducts. Hepatic necrosis, pyogranulomatous hepatitis and neurologic lesions are characterized by multifocal gliosis and perivascular cuffing in the brain and ballooning degeneration of axonal fibres in the brain stem and proximal spinal cord. Ingestion of contaminated materials and direct contact with contaminated respiratory secretions is considered the primary route of transmission.

Diagnosis can be confirmed by polymerase chain reaction (PCR) of secretions, excretions, oral and cloacal swabs and tissues (lung, intestine, liver and kidney) and suspect patients. 

Boa constrictor

Boa constrictor with hemorrhagic pneumonia and bloody discharge in the oral cavity*

Retrovirus infection of snakes

A retrovirus was associated with inclusion body disease of boid snakes (IBD).

IBD is common in captive boas and pythons. Clinical signs are including CNS symptoms like head tremors, opisthotonus, and loss of righting reflex.

The clinical changes associated with IBD vary with the species and individual. However, IBD should be considered in any snake, particularly boids, with chronic wasting, regurgitation, loose feces, stomatitis, ulcerative or necrotizing dermatitis, pale mucous membranes, respiratory disease, cutaneous neoplasia and leukemias. This signs may be noted with or without concurrent CNS signs. Most young snakes have an acute infection develop, with a mortality rate that approaches 100%. Infections in adults tend to be more protracted and debilitating. Subtle head tremors, depressed tongue flicking and dull mentation have been described as early signs, followed by anorexia, lethargy, weight loss, and dehydration as the disease progresses.

Disease progression is typically more rapid and severe in pythons than boas. Frequently regurgitation is the first sign in Boas, followed by slowly progressive CNS signs that worsen over a period of 1 to 2 years. Other affected boas may regurgitate partially digested food and then die within several weeks. The routes of transmission in reptiles are documented poorly. Contaminated aerosols or excrement have been implicated in the transmission of IBD.

Infections spread rapidly when an affected snake is introduced to a susceptible group. Snake mites may be involved in virus transmission in large groups of infested snakes. Snakes with IBD typically have eosinophilic intracytoplasmatic inclusion bodies in epithelial cells of affected tissues. Inclusion bodies are particularly common in the pancreas, liver, kidneys, brain and spinal gray matter. Further on inclusions were found in pulmonary epithelia cells, heart, spleen and neuronal cells. PCR is not yet available for diagnosis.

For cytological diagnosis a blood smear (buffy coat) and a swab of the esophageal mucosa taken with a moist, sterile cotton swab is recommended. After collection the swab should be gently rolled along the flat surface of a clean, glass microscope slide. The slides will then be checked microscopically for evidence of inclusion bodies. For histological ante mortem diagnosis a liver biopsy is the sample of choice. Post mortem diagnostic could be done by examining tissues of pancreas, liver, kidneys, the gastrointestinal mucosa and brain. 
Boa constrictor with CNS

 Boa constrictor with CNS signs loss of righting reflex and stargazing *

Intrazytoplasmatische Einschlüsse in den Epithelien der exokrinen Pankreas (Boa constrictor)

 Pancreas of a Boa constrictor with large intracytoplasmatic eosinophilic inclusion bodies 




Test Material

Examination time




anorexie, depression, diarrhea, opisthotonus, hepatomegaly  

PCR: Feces and Cloacal swab
Histology: gastrointestinal tract, liver

2 - 3 days

2 days





anorexie, depression, diarrhea, hepatomegaly, regurgitation, CNS signs, necrotizing hepatitis  

PCR: Feces and Cloacal swab

2 - 3 days



nasal discharge, open mouth breathing, accumulation of caseous debris in the oral cavity, harsh respiratory sounds, pneumonia, CNS signs (loss of muscle tonus, unwillingness to move, head tremors, stargazing), recurring unresponsive bacterial, fungal and protozoal infections  

PCR: Oral and Cloacal swab
- post mortem: tissue samples (liver, gastro-intestinal mucosa)

2 - 3 days


 CNS signs like head tremors, opisthotonus, loss of righting reflex, depression, depressed tongue flicking, regurgitation, stomatitis, progressive pneumonia  

Cytology: Buffy-coat blood smears, esophageal smear
- ante mortem: liver biopsy
- post mortem: tissue samples (liver, pancreas, kidneys, gastro-intestinal mucosa, brain, lung)  

1 day

2 days  




Mycoplasma agassizii

Conjunctivitis, ocular and nasal discharge, palpebral and periocular edema


PCR : Nasal flush

2 - 3 days


anorexia, depression, diphteric and necrotizing stomatitis and glossitis, necrotizing bronchitis, pneumonia and hepatomegaly

PCR : Oral swab post mortem: tissue samples (tongue, liver, spleen, esophagus, intestine, trachea, lung and brain)

2 - 3 days


 *Macro photos with permission of the "Gemeinschaftspraxis Rüschoff / Christian, Hamburg" .


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