Bearded Dragon Infectious Disease Slideshow

  • Inland bearded dragon

    Introduction

    Inland bearded dragons (Pogona vitticeps) are native to Australia and are a popular companion animal. Private breeders often select for desirable temperaments and various color morphologies in an effort to provide an ever-increasing variety to the pet trade. Bearded dragons are also bred commercially and sold by large pet retailers making them a widely available pet reptile. Inland bearded dragons are valued for their naturally calm disposition, in addition to their moderate size and ease of handling and husbandry. These characteristics contribute to their increasing popularity as exotic companion animals. As bearded dragon ownership increases, so does the likelihood of presentation of these animals to veterinarians in private practice.

  • Nurse with bearded dragon

    Client Education

    Educating owners on proper husbandry is the cornerstone of good preventative health care for all our exotic patients. As general husbandry for exotic companion animals continues to improve through client education and as owners develop strong bonds with their reptile companions, presentation for infectious disease, neoplasia, and geriatric issues are expected to become more commonplace. The following slideshow is intended as a quick reference guide for the private practitioner on some of the more common infectious diseases of captive Inland bearded dragons.

    Please note this content is not intended to be an all-inclusive list and continued visitation of current literature to identify novel and emerging diseases affecting exotic pet species is recommended.

    Photo credit: Resa McLellan

  • Pinworms

    Oxyurid pinworms (Oxyuris spp.)

    Pinworms are common in captive and free-ranging reptiles.

    Photo credit: Fredric L. Frye, BSc, DVM, MSc, CBiol, FSB, FRSM, Hon DABVP, Hon DECZM

  • Oxyurid pinworms

    Oxyurids: Clinical disease

    More often than not, oxyurid pinworms are considered non-pathogenic commensals and are speculated to aid the host by breaking up cellulose in fecal matter thus preventing constipation (Telfor and Campbell 1981). On rare occasions, heavy parasite burdens can result in colonic impaction.

    Clinical signs: Clinical signs are rarely seen with pinworm infections.

    Pathological findings: Although significant inflammation of the large intestines is not a typical feature of pinworm infection, due to their direct life cycle, rarely pinworm infections can reach high enough parasitic burdens to result in impaction of the large intestine.

    Shown here, Oxyurid adults within a segment of dilated large intestines.

    Photo credit: Fredric L. Frye, BSc, DVM, MSc, CBiol, FSB, FRSM, Hon DABVP, Hon DECZM

  • Oxyurid ovum

    Oxyurids: Eggs

    Diagnosis: Diagnosis is made through identification of eggs in feces by direct smears or flotation techniques. Eggs are large, measuring 130 µm x 40 µm and may or may not be embryonated (Jacobson 2007).

    Shown here, Oxyurid ovum

     

    Photo credit: Fredric L. Frye, BSc, DVM, MSc, CBiol, FSB, FRSM, Hon DABVP, Hon DECZM

  • Oxyurid larva

    Oxyurids: adult worms

    Diagnosis: Sometimes adult worms can be seen in feces.

    Shown here, Oxyurid larva

    Photo credit: Fredric L. Frye, BSc, DVM, MSc, CBiol, FSB, FRSM, Hon DABVP, Hon DECZM

  • Anterior end of pinworm

    Oxyurids

    Shown here, anterior end of pinworm bulbous in green iguana (Iguana iguana).

    Photo credit: Rataj AV et al. Parasites in pet reptiles. Acta Vet Scand 53(1):33, 2011. Posted with permission.

  • Pinworm egg

    Oxyurids: Transmission, Control & Treatment

    Transmission & control: Pinworms are contracted via fecal-oral transmission and undergo a direct life cycle. After ingestion, eggs develop into larvae in the proximal intestinal tract before migrating to the rectum as adults.

    Pinworms are highly host specific. Therefore, there is little risk of transmission between bearded dragons and other pets in the household, including other reptiles. Reptile pinworms are not known to be transmissible to humans. Control is by quarantine of new individuals, routine fecal examinations, and treatment of infected individuals prior to introduction into a collection.

    Treatment: Fenbendazole 50 mg/kg PO (Lane and Mader 1996) Imidacloprid and moxidectin (Advantage multi/advocate, Bayer, Shawnee, Mission, KS), topically (Groza et al 2009)

    Shown here, pinworm egg (unidentified species) in the green iguana (Iguana iguana).

    Photo credit:  Rataj AV et al. Parasites in pet reptiles. Acta Vet Scand 53(1):33, 2011. Posted with permission.

  • yellow discoloration of skin on the ventrum of an inland bearded dragon

    Nannizziopsis spp.

    Nannizziopsis guarroi (Yellow Fungus Disease)

    (formerly Chrysosporium anamorph of Nannizziopsis vriesii (CANV) complex)

    The taxonomy of Chrysosporium anamorph of Nannizziopsis vriesii (CANV) complex has recently been reclassified based on molecular sequencing into three genera: Nannizziopsis, Paranannizziopsis, and Ophidiomyces (Sigler et al2013). Fungi within the genera Nannizziopsis are considered the causative agents of yellow fungus disease, with N. chlamydosporaN. draconiiN. barbataN. guarroi, and N. vriesii having been isolated from affected inland bearded dragons. These fungi are keratinophilic and can cause severe and often fatal dermatomycoses (Bowman et al 2007). Nannizziopsis spp. are rarely isolated from the skin of healthy reptiles and are believed to act as primary pathogens.
    Shown here, Characteristic yellow discoloration of skin on the ventrum of an inland bearded dragon. Although highly suggestive, this gross lesion is not entirely specific for yellow fungus disease (next slide).

    Photo credit: Nicholas A. Crossland, DVM, DACVP

  • Nodule overlying the left eyelid of an Inland bearded dragon

    Nannizziopsis: Clinical disease

    Nannizziopsis guarroi: (Yellow Fungus Disease)

    (formerly Chrysosporium anamorph of Nannizziopsis vriesii (CANV) complex)

    Clinical signs: Lesions may begin as localized or multifocal yellow skin discoloration giving this disease the lay moniker “yellow fungus disease.” Lesions progress from multifocal to coalescing irregular patches of thickened skin composed of hyperkeratotic exudate. Less commonly dermal inflammation forms discrete cutaneous nodules (Reavill and Griffin 2013). These thickened and nodular patches of skin can slough, manifesting in ulceration.

    Pathological findings: Initial fungal growth is limited to the superficial epidermal keratin layer represented by hyperkeratosis and yellow discoloration, with fungal growth slowly extending into the underlying dermis, skeletal muscle, and rarely bone associated with extensive granulomatous inflammation and intralesional hyphae.

    Shown here, Nodule overlying the left eyelid of an Inland bearded dragon. Histologically this nodule was composed of granulomatous inflammation surrounding fungal hyphae. Nodules can exfoliate with resultant ulceration.

    Photo credit: Nicholas A. Crossland, DVM, DACVP

  • Nannizziopsis guarroi hyphae within keratinaceous debris

    Nannizziopsis: Diagnosis

    Nannizziopsis guarroi: (Yellow Fungus Disease)

    (formerly Chrysosporium anamorph of Nannizziopsis vriesii (CANV) complex)

    Dermatologic lesions can raise the index of suspicion and presumptive antemortem diagnosis can be made by submission of biopsy samples from affected sites to qualified diagnostic laboratories. Histologic identification of typical hyphae together with isolation of white-powdery fungal colonies containing both solitary aleuroconidia and chains of arthroconidia are highly suggestive of Nannizziopsis spp., however PCR with sequencing is required to reach a definitive diagnosis. Recently, cytologic features of yellow fungus disease have been described, affording clinicians a rapid tool to establish a high index of suspicion (Le Donne et al 2016).

    Author’s note:  Similar yellow discoloration of skin has been observed with concurrent Malessezia sp. and Staphylococcus xylosus infection in Inland bearded dragons, stressing the importance of ancillary diagnostics in obtaining a definitive diagnosis.

    Shown here, Nannizziopsis guarroi hyphae within keratinaceous debris affecting an Inland bearded dragon. Hyphae are highlighted by a Periodic acid–Schiff (PAS) stain.

    Photo credit: Nicholas A. Crossland, DVM, DACVP

  • Slide 12 Transmission Tx Control

    Nannizziopsis guarroi: Transmission, Treatment & control

    Nannizziopsis guarroi (Yellow Fungus Disease)

    (formerly Chrysosporium anamorph of Nannizziopsis vriesii (CANV) complex)

     

  • Slide 13 Coccidia textCoccidia (Isospora amphiboluri)

    Life cycle (Lane and Mader 1996): Isospora amphiboluri has a direct life cycle and undergoes both asexual and sexual reproduction within the same host. Feces containing unsporulated oocysts are deposited into the environment. Hosts become infected through consumption of mature sporulated oocysts that mature in the environment. Oocysts release sporocysts, which then release sporozoites into the alimentary tract, which colonize and mature into schizonts within epithelial cells of the intestinal mucosa. Mature schizonts cause host enterocytes to rupture, releasing merozoites that can directly infect other epithelial cells again forming schizonts or develop into macro- and microgametocytes. The latter undergo fertilization resulting in formation of oocysts, which are subsequently shed in feces.

    Clinical signs: Bearded dragons with coccidial infections may present with anorexia or diarrhea. In severe cases, the patient may regurgitate, be dehydrated, or experience hemorrhagic enteritis.

    Pathological findings: Replication of Isospora amphiboluri within small intestinal epithelial cells followed by schizont rupture results in necrosis, with possible ulceration, and fibrosis. In severe cases, sepsis is a potential sequel, as ulceration can allow translocation of bacteria from the alimentary tract.

  • Isospora sp. in the bearded dragon (P. vitticeps)

    Coccidia: Diagnosis, Treatment & Control

    Diagnosis: Diagnosis is made by identification of oocysts on fecal examination by direct smear or floatation techniques. Isospora amphiboluri oocysts contain two sporocysts, each containing four sporozoites. Oocysts measure 23 to 26 µm by 23 to 26 µm (McAllister et al 1995).

    Treatment & Control: The current treatment of choice is ponazuril 30 mg/kg  PO q 48 hours for 2 treatments (Bogoslavsky 2007). Previously trimethoprim sulfadiazine administered at 30 mg/kg IM q24h for 2 days, then 15 mg/kg IM q 48h for 5 treatments has been reported (Lane and Mader 1995).

    Control is through quarantine of new individuals, routine fecal examinations, and treatment of positive individuals prior to introduction into a collection. Good hygiene cannot be overemphasized (Gibbons 2014).

    Shown here, Isospora sp. in the bearded dragon (P. vitticeps).

    Photo credit: Rataj AV et al. Parasites in pet reptiles. Acta Vet Scand 53(1):33, 2011. Posted with permission.

  • Adenoviral infection in a juvenile

    Agamid Adenovirus (Agamid AdV1)

    Agamid adenovirus (AdV1) of bearded dragons is a host-specific, non-enveloped double stranded DNA virus that is now endemic throughout the United States (Reavill and Griffin 2014, Schumacher 1996). The majority of cases occur in juveniles ranging from less than a month old to 12 weeks of age, but has also been described in older animals up to 8 months of age (Moormann et al 2009, Doneley et al 2015). Cases can occur as sporadic isolated cases or as outbreaks within colonies (Reavill and Griffin 2014, Schumacher 1996).

    Transmission: Contraction is primarily through direct fecal-oral transmission. Vertical transmission through eggs requires further investigation (Reavill and Griffin 2014, Schumacher 1996).

    Clinical signs: Animals may be presented for intermittent anorexia or lethargy, ill thrift or failure to thrive with opisthotonos, torticollis, or circling. Although less common, stomatitis, pneumonia, and limb paresis have been described. Clinical signs may be more severe in animals that are young, stressed, or that have concurrent infections (e.g. intestinal coccidiosis). Wasting, emaciation, and high mortality are not uncommon in these individuals (Reavill and Griffin 2014, Schumacher 1996).

    Pathological findings: The liver is typically diffusely swollen and pale. Histologically, multifocal areas of hepatic necrosis are associated with intranuclear, eosinophilic to amphophilic inclusion bodies within hepatocytes (Reavill and Griffin 2014, Schumacher 1996).

    Shown here, Adenoviral infection in a juvenile Pogona henrylawsoni. Infection in P. vitticeps appears to be morphologically identical.

    Photo credit: Fredric L. Frye, BSc, DVM, MSc, CBiol, FSB, FRSM, Hon DABVP, Hon DECZM

  • Swollen and pale liver

    Adenovirus: Diagnosis

    Antemortem diagnosis is made with PCR performed on cloacal swabs. For postmortem diagnosis, PCR testing on liver and intestinal swabs is preferred. A diagnosis is readily made histologically by the presence of hepatic necrosis with large intralesional basophilic intranuclear inclusions (Reavill and Griffin 2014, Schumacher 1996).

    Photo credit: Fredric L. Frye, BSc, DVM, MSc, CBiol, FSB, FRSM, Hon DABVP, Hon DECZM

  • Transmission electron micrograph of adenoviral paracrystalline arrays in Pogona henrylawsoni

    Agamid Adenovirus: Pathology

    Pathological Findings: Similar intranuclear inclusion bodies most prominent in hepatocytes may be observed in biliary, renal, small and large intestinal, pancreatic, or oral mucosal epithelium. Electron microscopy can demonstrate viral particles with icosahedral nucleocapsids measuring 80 to 110 nm in diameter arranged in paracrystalline arrays (Reavill and Griffin 2014, Moorman et al 2009, Schumacher 1996).

    Shown here, transmission electron micrograph of adenoviral paracrystalline arrays in Pogona henrylawsoni

    Photo credit: Fredric L. Frye, BSc, DVM, MSc, CBiol, FSB, FRSM, Hon DABVP, Hon DECZM

  • Electron micrograph of adenoviral paracrystalline arrays in Pogona henrylawsoni

    Agamid Adenovirus: Electron Microscopy

    Electron microscopy can demonstrate viral particles with icosahedral nucleocapsids measuring 80 to 110 nm in diameter arranged in paracrystalline arrays (Reavill and Griffin 2014, Moorman et al 2009, Schumacher 1996).

    Shown here, electron micrograph of adenoviral paracrystalline arrays in Pogona henrylawsoni

    Photo credit: Fredric L. Frye, BSc, DVM, MSc, CBiol, FSB, FRSM, Hon DABVP, Hon DECZM

  • Adenoviral infection in a juvenile inland bearded dragon with prominent basophilic intranuclear viral inclusions within hepatocytes.

    Adenovirus: Treatment & Control

    Treatment & control: Currently there is no antiviral treatment acceptable for adenovirus infections in bearded dragons and no vaccine is available. Antibiotics should be considered for secondary bacterial infections and antiparasiticals for concurrent infections (Reavill and Griffin 2014, Schumacher 1996).

    Shown here, Adenoviral infection in a juvenile inland bearded dragon with prominent basophilic intranuclear viral inclusions within hepatocytes.

    Photo credit: Nicholas A. Crossland, DVM, DACVP

  • Cryptosporidium attached to mucosa, highlighted by a Giemsa stain.

    Cryptosporidium spp.

    Cryptosporidium are a coccidian protozoal parasite.

    Transmission: Cryptosporidium is spread by fecal-oral transmission or by contaminated fomites. Sporulated oocysts can be shed intermittently in feces by infected hosts, which are immediately infective. Although this parasite is not species-specific, reptilian cryptosporidium is not known to be infectious to humans. Small mammal prey items are not believed to be a source of exposure for pet reptiles (Lane and Mader 1996, Cranfield and Graczyk 1996).

    Clinical signs: To date, cryptosporidium has not been reported to cause clinical signs or lesions in inland bearded dragons. Cryptosporidium is known for causing severe proliferative gastritis in snakes. In lizards, enteritis is more common. Animals may become severely emaciated and dehydrated and can exhibit diarrhea that may or may not be hemorrhagic. Chronic wasting may precede death (Reavill and Griffin 2014, Cranfield and Graczyk 1996). Shown here, Cryptosporidium attached to mucosa, highlighted by a Giemsa stain.

    Photo credit: Nicholas A. Crossland, DVM, DACVP

  • Ziehl-Neelson staining of Cryptosporidium.

    Cryptosporidium: Clinical disease

    Although cryptosporidium appears to be asymptomatic in inland bearded dragons, carriers may spread the parasite to susceptible species (e.g. leopard geckos, snakes) in collections or households (Cranfield and Graczyk 1996). In spite of treatment, mortality approaches 100% in those animals diagnosed with cryptosporidiosis. Concurrent infections (e.g. adenovirus) may increase severity of clinical signs and chance of death.

    Shown here, Ziehl-Neelson staining of Cryptosporidium.

    Photo credit: Fredric L. Frye, BSc, DVM, MSc, CBiol, FSB, FRSM, Hon DABVP, Hon DECZM

  • Cryptosporidium lining the intestinal epithelium of an Inland bearded dragon.

    Cryptosporidium spp.: Pathological findings

    In accordance with the absence of clinical disease, no significant inflammation is associated with cryptosporidium protozoa. Organisms are readily observed lining the apical surface of enterocytes, predominating within the distal third of the intestinal tract. Organisms are highlighted by a Giemsa stain. Organisms are intracellular, but extracytoplasmic when viewed by electron microscopy.

    Shown here, Cryptosporidium lining the intestinal epithelium of an inland bearded dragon.

    Photo credit: Nicholas A. Crossland, DVM, DACVP

  • Unstained wet mount illustrating Cryptosporidium serpentis.

    Cryptosporidium: Diagnosis

    Cryptosporidiosis is diagnosed by observation of oocysts in stained fecal smears. Cryptosporidium oocysts contain four sporozoites without sporocysts and are less than 4 microns in diameter. Period acid Schiff (PAS) or Mayer’s hematoxylin are recommended to help identification (Cranfield and Graczyk 1996).

    Shown here, Unstained wet mount illustrating Cryptosporidium serpentis.

    Photo credit: Fredric L. Frye, BSc, DVM, MSc, CBiol, FSB, FRSM, Hon DABVP, Hon DECZM

  • methiolate-stained Cryptosporidium.

    Cryptosporidium: Treatment & Control

    Paromomycin, a poorly absorbed oral aminoglycoside, administered at 360 mg/kg q 48h for 10 days was successful at eliminating fecal shedding (Grosset et al 2011). Oocysts are hardy and environmental decontamination requires 18 hours of contact with 5% ammonia. Potential fomites should be disinfected with ammonia solutions and allowed to air dry for up to 3 days prior to use (Cranfield and Graczyk 1996).

    Shown here, methiolate-stained Cryptosporidium.

    Photo credit: Fredric L. Frye, BSc, DVM, MSc, CBiol, FSB, FRSM, Hon DABVP, Hon DECZM

  • Summary

    This bearded dragon slideshow reviews important infectious diseases of this popular lizard species, including yellow fungus disease, agamid adenovirus, oxyurid pinworms, and cryptosporidium. The clinical picture seen with these conditions ranges from asymptomatic, as with oxyurid pinworms or cryptosporidium, to dermatologic lesions associated with Chrysosporium anamorph of Nannizziopsis vriesii (CANV) complex or yellow fungus disease. A host of clinical signs have been seen with agamid adenovirus, including non-specific signs of illness, neurologic deficits, stomatitis, and/or pneumonia, particularly in animals that are young or suffering from concurrent stressors.

    Photo credit: Mariposa Veterinary Wellness Center

Inland bearded dragons are native to Australia and are a popular companion animal. Private breeders often select for desirable temperaments and various color morphologies in an effort to provide an ever-increasing variety to the pet trade. They are also bred commercially and sold by large pet retailers making them a widely available pet reptile . . .


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References

Bogoslavsky B. The use of ponazuril to treat coccidiosis in eight Inland bearded dragons (Pogona vitticeps). Proc Annu Conf Association of Reptilian and Amphibian Veterinarians 2007: 8-9.

Bowman MR, Pare JA, Sigler L, et al. Deep fungal dermatitis in three inland bearded dragons (Pogona vitticeps) caused by the Chrysosporium anamorph of Nannizziopsis vriesii. Med Mycol 45(4):371-376, 2007.

Cranfield MR, Graczyk TK. Cryptosporidiosis. In: Mader DR (ed). Reptile Medicine and Surgery. City: WB Saunders; 1996: 359-363.

Doneley RJT, Buckle KN, Hulse L. 2015. Adenoviral infection in a collection of juvenile Inland bearded dragons (Pogona vitticeps). Aust Vet J 92(1-2):41-45, 2015.

Gibbons PM. Therapeutics. In: Mader DR, Divers SJ (eds). Current Therapy in Reptile Medicine and Surgery. St. Louis, MO: Elsevier Saunders; 2014: 57-69.

Grosset C, Villeneuve A, Brieger A, et al. 2011. Cryptosporidiosis in juvenile bearded dragons (Pogona vitticeps): effects of treatment with paromomycin. J Herpetol Med Surg 21(1):10-15, 2011.

Groza A, Mederle N, Darabus G. Advocate-therapeutical solution in parasitical infestation in frillneck lizard (Chlamydosaurus kingie) and bearded dragon (Pogona vitticeps). Lucrari Stiintifice – Universitatea Stiinte Agricole Banatului Timisoara, Med Vet, 105-108, 2009.

Jacobson ER. Infectious Diseases and Pathology of Reptiles: Color Atlas and Text. Boca Raton, FL: Taylor & Francis Group; 2007:589.

Lane TJ, Mader DR. Parasitology. In: Mader DR (ed). Reptile Medicine and Surgery. City: WB Saunders; 1996:185-203.

Le Donne V, Crossland N, Brandão J, et al. Nannizziopsis guarroi infection in 2 Inland Bearded Dragons (Pogona vitticeps):  clinical, cytologic, histologic, and ultrastructural aspects. Vet Clin Path 45(2):368-375, 2016.

McAllister CT, Upton SJ, Jacobson ER, et al. A description of Isospora amphiboluri (Apicomplexa: Eimeriidae) from the Inland bearded dragon, Pogona vitticeps (Sauria: Agamidae). J Parasitol 81(2):281-284, 1995.

Moormann S, Seehusen F, Rechling D, et al. Systemic adenovirus infection in bearded dragons (Pogona vitticeps): histologic, ultrastructural and molecular findings. J Comp Path 141(1):78-83, 2009.

Paré JA, Coyle KA, Sigler L, et al. Pathogenicity of the Chrysosporium anamorph of Nannizziopsis vriesii for veiled chameleons (Chamaeleo calyptratus). Med Mycol 44(1):25-31, 2006.

Reavill DR, Griffin C. Common pathology and diseases seen in pet store reptiles. In Mader DR, Divers SJ (eds). Current Therapy in Reptile Medicine and Surgery. St. Louis, MO: Elsevier Saunders; 2014:13-19.

Schumacher J. Viral diseases. In: Mader DR (ed). Reptile Medicine and Surgery. St. Louis, MO: WB Saunders; 1996: 224-234.

Sigler L, Hambleton S, Paré JA. Molecular characterization of reptile pathogens currently known as members of the Chrysosporium anamorph of Nannizziopsis vriesii complex and relationship with some human-associated isolates. J Clin Microbiol 51(10):3338-3357, 2013.

Telfor SR JR, Campbell HW. Parasites of the American alligator, their importance to husbandry and suggestions toward their prevention and control. Proceedings of the First Annual Alligator Production Conference 1981; 46-51.

Van Waeyenberghe L, Baert K, Pasmans F, et al. Voriconazole, a safe alternative for treating infections caused by the Chrysosporium anamorph of Nannizziopsis vriesii in bearded dragons (Pogona vitticeps). Med Mycol 48(6): 880-885, 2010.

To cite this page: Crossland N, DiGeronimo P. Bearded dragon infectious disease slideshow. LafeberVet web site. Available at https://lafeber.com/vet/bearded-dragon-infectious-disease-slideshow/
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