Iridophoroma in Leopard Geckos (Eublepharis macularius): Clinical Complications and Histopathology

Abstract

Leopard geckos (Eublepharis macularius) with lemon frost morphologies are predisposed to iridophoroma, attributed to a tumor suppressor gene mutation also associated with melanoma in humans. In this case series, we describe the clinical presentation, diagnostics, complications, and pathology of iridophoroma in 4 adult leopard geckos, including 2 super lemon frost females and 2 lemon frost males. All animals presented with hyporexia, intermittent lethargy, weight loss, submandibular masses, and oral plaques. In addition, females demonstrated asymmetric coelomic distension, and one male developed altered mentation. Initial differential diagnoses included metabolic disorders, gastrointestinal infectious diseases, and neoplasia. During clinical management of these cases, ultrasonography revealed hyperechoic hepatic nodules in all animals. Fine needle aspiration (FNA) of the subcutaneous submandibular masses found clusters of mesenchymal cells with abundant cytoplasm containing fine birefringent granules. Due to continued decline and poor prognosis, animals were euthanized and submitted for necropsy. Gross examination of all 4 geckos demonstrated skin thickening by white masses throughout the body and multifocal white hepatic plaques. Two females showed yellow, enlarged ovaries, and one of the males had hard intraluminal debris in the urinary bladder. Histopathology of the skin throughout the body showed the dermis and subcutis were infiltrated by myriad pleomorphic, ovoid to fusiform, brown-pigmented neoplastic cells characterized by abundant birefringent intra- and extracellular granules. FNA, ultrasound, necropsy, and histopathology results were consistent with diagnosis of malignant iridophoroma with metastasis to multiple visceral organs including the brain and ovary. In addition, both females developed preovulatory follicular stasis (POFS)-associated oophoritis, and one of the males demonstrated urolithiasis; all of which were considered as metabolic imbalance-related pathology due to hyporexia or tumor invasion. This report illustrates the diagnostic features of FNA, ultrasound, and histopathology of malignant iridophoroma in leopard geckos. It also discusses POFS and urolithiasis as multisystemic sequelae to malignant tumors in geckos.

Introduction

The leopard gecko (Eublepharis macularius) has emerged as both a popular companion animal as well as a compelling organism for studying regeneration and various topics of biology, partially owing to the species’ distinctive coloration and genetics.¹ Among its various morphologic variations (morphs), the lemon and super lemon frost varieties are particularly notable for their enhanced white and yellow pigmentation, which arises from a spontaneous semidominant mutation in the Kunitz type 1 (SPINT1) gene. It is thought that these 2 phenotypes are associated with the same mutation, wherein super lemon frost animals are homozygous and lemon frost animals are heterozygous.² In these morphs, mutation leads to an overproliferation of iridophores, cells responsible for white reflective coloration, thereby producing their characteristic bright appearance. This same genetic alteration also predisposes these geckos to the development of iridophoromas, a type of skin tumor, with previous reports² documenting over 80% incidence within 6 months to 5 years of age. Consequently, trade of lemon and super lemon frost morphs has been banned by the International Herpetological Society.³ Association between SPINT1 mutations and oncogenesis is not limited to geckos however; the protein encoded by SPINT1, also known as hepatocyte growth factor activator inhibitor type 1 (HAI-1), is considered a tumor suppressor, and similar links have been established in mice, zebrafish, and humans.² SPINT1 deficiencies are implicated in epithelial tumor growth and poor prognosis in cutaneous melanoma of humans. Thus, the leopard gecko offers a unique opportunity to investigate the genetic basis of pigmentation and its relationship with oncogenesis, providing potential insights into human dermatological conditions.^2,4

Melanophores and iridophores are related lineages, along with xanthophores. These represent the chromatophores of reptiles as pigment-producing neural crest-derived cell populations. Melanophores create black to brown coloration via tyrosine-derived melanin while xanthophores produce red to yellow coloration with either pterinosomes or carotenoid-filled lipid vesicles. Xanthophores may work in conjunction with other chromatophores to produce color change and camouflage. Iridophores can produce various colors, generally ranging from white to blue, with purine or pteridine-containing platelets. Of the 3, iridophores are uniquely iridescent and light reflecting, allowing for identification with polarized light.^5,6

This case report describes the clinical presentation and necropsy findings of malignant iridophoroma in 4 geckos, along with various secondary lesions.

Case Report

Animals.

Four geckos, 2 females (geckos I and II) and 2 males (geckos III and IV), were adults when transferred to our facility to initiate a new colony of about 150 individuals in total, either sourced from other research institutions or purchased from commercial vendors. While the majority of the colony was wild-type morphs, the subjects of this report were lemon and super lemon frost animals transferred from the same facility. Upon arrival at our institution, the animals were housed in an AAALAC-accredited vivarium (University of Michigan). All work was approved by the University of Michigan IACUC and in accordance with The Guide for the Care and Use of Laboratory Animals. The subjects of this case report remained experimentally naive throughout the course of presentation.

All animals were housed singly in static polycarbonate cages (75 in2; Allentown, Allentown, NJ). Cages were changed biweekly, and temperature gradients were established within each cage by placing a heat source under one end set to 92 °F (Redline Science Heat Tape; Pangea Reptile, Zeeland, MI). The animal room was maintained between 74 and 80 °F, with a relative room humidity between 30% and 40%, and a 12:12 hours light cycle. Geckos were misted with reverse osmosis filtered water 3 times weekly, housed on a paper liner (TechSorb; Shepherd Specialty Paper, Watertown, TN), and given both a moist hide (24-oz meal preparation containers) filled with coconut fiber (Zoo Med Laboratories, San Luis Obispo, CA) as well as a dry hide without. Geckos were fed 2 to 5 crickets (Acheta domesticus) and 2 to 3 mealworms (Tenebrio spp.) per animal 3 times weekly. Insects were both dusted (ReptiVite and Repti Calcium; Zoo Med Laboratories, San Luis Obispo, CA) and fed nutritional supplementation before offering to geckos (Better Bug Gut Loading Diet, Mazuri Exotic Animal Nutrition; Land O’ Lakes, Arden Hills, MN). Geckos were given free access to reverse osmosis filtered water and supplemental nutritional powder (Repti Calcium, Zoo Med Laboratories, San Luis Obispo, CA).

Clinical presentation.

All four animals presented with intermittent hyporexia over 4 months, including both lemon (Figure 1A and B) and super lemon frost (Figure 1C and D) morphologies. This was managed by offering additional feed (mealworms, waxworms) or a slurry of pelleted insectivore diet (Mazuri Exotic Animal Nutrition; Land O’ Lakes, Arden Hills, MN), depending on individual preference. Moderate dehydration and lethargy were noted occasionally but were responsive to oral fluids and NSAIDs (meloxicam: 0.2 mg/kg, PO). All geckos gradually developed freely movable subcutaneous submandibular masses over the first 2 months of presentation. These generally started as dermal thickenings near the rami of the mandible but would progress to be palpable and ranged from solitary to coalescing. All geckos also gradually developed white multifocal to coalescing plaques in the caudal oral cavity and swellings of the axilla. However, some clinical signs were unique to specific animals. Gecko III presented acutely with neurologic clinical signs including markedly altered mentation, right-sided circling with an atypical gait, and mydriasis. On exam, bilateral ventral dermal thickenings running the length of the body (Figure 1B) were also noted. As a result, this animal was humanely euthanized soon after clinical decline was noted. Both females (geckos I and II) gradually developed asymmetric coelomic distension, with pale tan-appearing masses seeming to visibly originate from the cranial coelom on external exam (Figure 1D).

Figure 1.

Presenting Leopard Gecko Appearance. (A) Dorsal and (B) ventral male lemon frost. (C) Dorsal and (D) ventral female super lemon frost. The difference in yellow to white coloration between the morphologies is of note, alongside the presence of clinical signs including (B) bilateral ventral dermal thickening and (D) coelomic mass development.

Initial differential diagnoses included dietary preferences, follicular stasis, nutritional secondary hyperparathyroidism, mild hypocalcemia, hepatic encephalopathy, and cryptosporidiosis. However, other animals in the cohort with the same diet and same housing setup appeared healthy, and the husbandry conditions provided were appropriate for the species. Because all 4 geckos developed submandibular masses and white oral plaques, neoplasia became our primary differential diagnosis.

Antemortem Diagnostics

Fine needle aspiration.

Fine needle aspirate (FNA) was performed on submandibular masses (Figure 2A) for cytologic examination, and the results were analyzed with a Diff-Quik stain set (American Scientific Products, Livonia, MI). Multiple clusters of mesenchymal to spindloid cells were present with mildly basophilic cytoplasm. These contained numerous intracytoplasmic blue-black pigmented granules and identical extracellular granules (Figure 2B). Under polarized light, these clusters appeared birefringent.⁶

Figure 2.

Leopard Gecko Clinical Exam. (A) Oral plaques (arrow) and unilateral submandibular mass (square) that initiated as dermal thickening. (B) Multiple clusters of fusiform cells noted on cytology after FNA of submandibular mass. There are several erythrocytes in the periphery. Granules with birefringence were confirmed by microscopic observation under polarized light (not shown).

Ultrasonographic examination.

Ultrasonographic examination (S9 with 16-MHz linear probe; SonoScape Medical USA, Centennial, CO) was performed following detection of coelomic distension (females, Figure 3A) or oral plaques (males). Both females demonstrated space-occupying masses appearing to originate from the midcoelom. Similar masses were identified unilaterally in gecko I and bilaterally in gecko II and appeared in close proximity to the ovaries. These masses demonstrated heterogeneous echogenicity, with hypoechoic pockets that lacked circumferential hyperechoic margins. Pockets demonstrated distal acoustic intensity consistent with an enhancement artifact, suggestive of fluid cavitation (Figure 3A). These masses were interpreted as static preovarian follicles.⁷ Over the course of presentation, masses appeared to grow in size and 2 months later were noted in the caudal coelom at the level of the cloaca. Meanwhile, gecko I demonstrated normal contralateral follicular development over the course of examination with a slightly delayed timeline consisting of approximately 60 days between ultrasonographically noted follicular waves and the production of a single egg.⁸ Cyclicity was not noted in gecko II, which instead demonstrated slow growth of bilateral masses.

Figure 3.

Leopard Gecko Physical and Corresponding Ultrasonographic Exam. (A) A large mass was visualized on external exam of gecko I, prompting further diagnostics. This mass appeared heterogeneous, expansile, and cavitated on ultrasonographic exam both in longitudinal (blue) and transverse (red) views. (B) Representative images of well-demarcated, hyperechoic lesions which were visualized on hepatic ultrasonography of all 4 animals (circle).

Accordingly, the livers of females appeared caudolaterally displaced.⁹ However, all livers demonstrated well-demarcated multifocal to coalescing hyperechoic foci directed toward the serosal surface. Of these, the largest focal lesion measured 0.17 × 0.2 cm in gecko II (Figure 3B, circle).

Postmortem Diagnostics

Gross examination.

Four to 11 months after initial presentation (Table 1), euthanasia was elected for all 4 animals due to a continuing decline in condition, indicated by gradual loss of tail-associated fat,¹⁰ decreased activity, suspected worsening preovulatory follicular stasis (POFS), and inappetence, along with increasing concern for neoplasia. Euthanasia was performed with intracoelomic pentobarbital sodium (1 mL Euthasol; Virbac, Fort Worth, TX) under general anesthesia with inhaled isoflurane (Fluriso, 5% induction, 3% to 4% maintenance; MWI Animal Health, Boise, ID). Blood was collected immediately after euthanasia for cytology of all animals, and cerebrospinal fluid was collected from gecko III.

Table 1.

Summary of Presenting Adult Leopard Geckos, Either Homozygous (Females) or Heterozygous (Males) for the Lemon Frost Mutation

Gecko	Sex	Morph	Interval between intake and necropsy (mo)
I	Female	Super lemon frost	4
II	Female	Super lemon frost	4
III	Male	Lemon Frost	10
IV	Male	Lemon Frost	11

On gross examination, all 4 geckos showed multifocal chalky white plaques or nodules at the submandibular skin and at the hard palate of the oral cavity (Figure 4A). Multifocal white discoloration with skin thickening was found throughout the head, neck, axilla, and the ventrum of the trunk (Figure 4B). Two geckos (geckos III and IV) demonstrated infiltration of similar material, with distension and fluid accumulation in the subcutaneous lymphatic ducts throughout the trunk. Gecko III also demonstrated subcutaneous white plaques above the dorsal spinous processes and around the orbit. All 4 animals demonstrated multifocal to coalescing white plaques expanding the axillary endolymphatic sacs (Figure 4C) and scattered throughout the serosal surface of livers (Figure 4D). A representative lesion (Figure 4D, circle) was then correlated to ultrasonographic lesions (Figure 3B, circle) with similar dimensions on ante- and postmortem measurements.

Figure 4.

Representative Lesions From Gross Examination of Multiple Animals. (A) White plaques in the caudal oral cavity. (B) Submandibular dermal thickening and focal coalescence of white infiltrate. (C) Axillary infiltration of the endolymphatic sac with white plaques. (D) Multifocal hepatic white plaques (circle). (E) Large space-occupying mass originating from the left ovary, accompanied by multifocal white plaques on the surface of the liver. (F) Two enlarged, yellow ovaries were noted to be firmly adhered to the liver.

The coelomic cavity of the 2 female geckos (geckos I and II) showed cranial displacement of visceral organs by yellow and red mottled, round, 5 to 7 cm in diameter, cystic structure(s) arising from the ovary (Figure 4E and F [gecko I and gecko II, respectively]). These cysts were filled with an excessive amount of yellow to white pasty material. No shelled egg was found in the coelomic cavity of either animal. The retracted lesions in Figure 4E can be correlated to their antemortem appearance in Figure 3A approximately 2 weeks before euthanasia. Furthermore, the liver of one animal (gecko II) was firmly adhered to the ovary, and the parenchyma of the liver adjacent to the adherence site was soft and dark red to black.

Gecko III had a distended urinary bladder containing cloudy urine with pale yellow, flakey, hard masses both free floating in the lumen and embedded in the bladder wall. In this animal, both testicles were firmly adhered to the bladder. Urinalysis was mostly unremarkable with physiologic isosthenuria (specific gravity: 1.009); however, mild proteinuria (1+), alkalosis (pH: 8.5), and granular casts (5/low -powered field) were noted.¹¹

Histopathology.

In geckos I, II, and III, the dermis and subcutis of the skin throughout the body and oral mucosa were expanded by multifocal to coalescing, nonencapsulated, infiltrative, multilobulated light brown masses (Figures 2A, 4A, 4B, 4C, and 5A). These masses had sheets to islands of pleomorphic, round to spindloid neoplastic cells, surrounded by scant fibrovascular stroma. The neoplastic cells contained abundant cytoplasm with variable amounts of brown, intracytoplasmic, birefringent, fine granules, and ovoid nuclei with multiple indistinct nucleoli and coarse chromatin (Figure 5B and C). In gecko IV, the dermal and subdermal masses were composed of similar pleomorphic, round to spindloid neoplastic cells with indistinct intracytoplasmic birefringent granules. The tumor regions in all 4 geckos show approximately 0 to 3 mitotic figures in 10 high-power fields (40×), and the identification of mitosis was heavily interfered with by pigmentation. Intravascular invasion and metastasis to different areas outside of the skin were appreciated, including but not limited to liver, lung, intestine, ovary, bone, eye, and brain (Figure 5D–H; Table 2).

Figure 5.

Histopathology of Malignant Iridophoroma in Leopard Geckos. (A) Dermis and subcutis at the head skin are expanded by neoplastic cells. These cells are also found in the marrow cavity (arrow). (B) High magnification of the skin mass showing sheets of pleomorphic, variously pigmented neoplastic cells supported by fine fibrovascular stroma. (C) Same view as B but under polarized light, showing the various degrees of birefringent, intracytoplasmic, or extracellular granules of the tumor. (D) Tumor mass in the liver. (E) Same view as D but under polarized light, showing the birefringent granules of the tumor. Resident melanomacrophages, which are normally present in the liver of reptiles, do not have birefringent granules. (F) Tumor infiltration in the ovary. (G) Tumor infiltration in the iris of the eye. (H) Tumor at the meninges of the brain. Inset: birefringence of the tumor in the meninges (box).

Table 2.

Summary of Anatomic Locations of Iridophoroma Cell Populations Across all 4 Animals

	Gecko
	Female		Male
Anatomic location	I	II	III	IV
Integument	X	X	X	X
Lymphatics	X	X	X	X
Oral cavity	X	X	X	X
Hepatic	X	X	X	X
Respiratory	X		X	X
Proximal cloaca/distal colon (serosal)			X	X
Heart and aorta	X			X
Ocular (iris and uvea)			X	X
Gonad	X
Meninges			X
Bone and marrow cavity (skull)			X

Aside from tumors, the ovarian follicles of both female geckos (geckos I, II) had large amounts of bright eosinophilic yolk droplets in the lumen, surrounded by a disorganized and severely vacuolated granulosa layer, and mixed with abundant extravasated erythrocytes and fibrous stroma. Several previtellogenic and vitellogenic follicles were identified in the ovarian periphery. In one animal (gecko II), abundant vitellogenic yolk droplets were found outside of the follicle, depositing at the serosal surface of the ovary, oviduct, liver, and lung, and the serosa was lined by thick sheets of large vacuolated cells (mesothelial cells). The parenchyma of the liver at the adhesion site with the ovary contained numerous degenerative hepatocytes and multinucleated giant cells with the presence of yolk droplets. Gram, periodic acid-Schiff (PAS), and Ziehl-Neelsen acid-fast stains did not identify any pathogens in the liver or ovary.

The mucosa and lumen of the urinary bladder of gecko III (male) had multiple granulomas composed of transparent, birefringent, extracellular spicules (uroliths) depositing in its center, surrounded by numerous multinucleated giant cells and macrophages. Histochemistry including Ziehl-Neelsen stain and PAS stain did not identify any pathogen in the urinary bladder of this animal. This, alongside urinalysis, suggested potential dehydration and renal injury. However, kidney tissue from gecko III was not available for histopathologic interpretation. Hematologic cytology from all animals failed to demonstrate neoplastic cells, as did cerebrospinal fluid samples from animal III despite the severe tumor burden.

Final Diagnoses

1. Malignant iridophoroma, skin, with metastasis, all 4 geckos

2. Oophoritis (gecko I, II), yolk egg-induced coelomitis (gecko II)

3. Urolithiasis and visceral gout, urinary bladder (gecko III)

Discussion

Neoplasia in lizards has been estimated to occur in less than 5% of presenting companion reptiles.¹² However, both benign and malignant iridophoromas have been documented in various species.¹³ While early cases of benign iridophoroma of pine snakes (Pituophis melanoleucus) were noted in 1989,⁵ it has since been identified in savannah monitors (Varanus exanthermaticus), veiled chameleons (Chamaeleo calyptratus), and bearded dragons (Pogona vitticeps). Malignant cases have been documented in bearded dragons, pine snakes, green iguanas (Iguana iguana), and dwarf bearded dragons (Pogona henrylawsoni), in addition to betta fish (Betta splendens).^14–18 Previous reports documenting white tumors in both lemon frost and super lemon frost leopard geckos described a young age of onset at about 5 to 6 months; these began on the ventrum and grossly appeared as thickening of the skin that sometimes progressed into protruding masses. White coalescing plaques in the oral cavity and hepatic nodules were noted in severe cases. However, progression beyond dermal thickening has been far more commonly reported in the super lemon frost morph.^2,4 Interestingly, previous reports⁵ have also documented iridophoroma development leading to similar submandibular swelling and hepatic involvement in pine snakes. Similarly, single-animal reports have documented iridophoroma development of oral plaques, submandibular swelling, and liver involvement in dwarf bearded dragons.¹⁴ In addition, while clinical presentation and histopathology of iridophoroma in leopard geckos have been reported previously, it has lacked descriptions of diagnostics, progression to visceral metastasis, and concurrent POFS.^2,4

Some observed clinical signs were conserved between all animals and nonspecific, such as hyporexia, lethargy, or dehydration. However, other signs may be more specific and of potential utility for increasing clinical suspicion of iridophoroma in leopard geckos, including submandibular thickenings and the presence of white plaques in the caudal oral cavity. While both have been previously documented as potential implications to this disease process,² the incidence of these observations in leopard gecko colonies has not. In addition, all animals developed iridophoroma metastasis to the liver (Figures 3, 4G, 4H, 5D, and 5E), suggesting that metastatic disease may correlate with the clinical signs of oral plaques and submandibular masses, both of which have antemortem clinical tools associated with them (for example oral exam, FNA of dermal lesions, ultrasound of coelom). Furthermore, we identified pulmonary metastasis in 3 of 4 animals, which has not previously been documented in cases of iridophoroma in leopard geckos.

The different timelines for clinical progression between male and female geckos should also be noted. There was a 4-month window between initial presentation and euthanasia for both females, whereas males were clinically stable for 10 to 11 months. This could be attributed to the reproductive complications of POFS and egg-yolk-associated coelomitis seen in females along with their super lemon frost phenotype. Without these complicating factors, the lemon frost males progressed to larger tumor burdens, more distant metastases, and alternative complications such as urolithiasis and visceral gout.

Another interesting finding was metastasis to the central nervous system, as observed in the animal with the largest number of metastatic sites. Neoplasia arising from the nervous system is rare in reptiles, with most reports from chelonians, crocodilians, and lizards. Instead, the hematopoietic and integumentary systems are likely the most commonly affected systems for reptilian neoplasia, and although there is some discrepancy, lymphoma has historically been the most commonly reported hematopoietic neoplasm in reptiles.^12,19 Instead, chromatophores are of neural crest origin, migrating to the dermis during development.⁶ In addition, while lymphoma tends to have hematogenous spread, this was not observed in our report of iridophoroma. Neoplastic cell populations were not observed in hematologic cytology prepared from all animals nor in the cerebrospinal fluid from gecko III. However, lymphatic chains appeared dilated and expanded by neoplastic cell populations. It has been suggested that the endolymphatic sacs can be terminal intrameningeal dilations of otic structures in amphibians and some reptiles, extending from the inner ear to the meninges of the brain in geckos.²⁰ All examined geckos appeared to have involvement of the lymphatic system, and the largest neoplastic burden was associated with meningeal metastasis of one animal. This suggests that the lymphatic system is a potential route of metastasis of iridophoroma in geckos. In human melanoma, 3 potential hypotheses have been posed for the potential spread of melanoma, one of which suggests that melanoma may initially spread lymphatically to adjacent nodes before progressing to hematogenous dissemination. However, more study is currently needed. Another hypothesis suggests that cell populations within the heterogeneous tumor may be predisposed to specific routes of spread, and it may be that lemon frost leopard geckos are a model to study this mechanism.²¹

Outside of neoplasia, reproductive disorders are commonly seen in captive reptiles including follicular stasis.²² Generally speaking, stasis is described as either pre- or postovulatory, as designated by the impaired step of development and location. Preovulatory follicles are not mineralized and associated with the ovary directly. Static postovulatory follicles, colloquially referred to as “egg-binding,” may be associated with dystocia as this condition includes stasis along the oviduct and distally. Pathogenesis of preovulatory follicular stasis in captive reptiles is complex and usually involves several environmental and animal-associated factors. These may include nutritional imbalance, absence of appropriate environmental cues, and underlying systemic diseases, such as metabolic bone disease or infections. Generally, the recommended treatment for POFS is oophorectomy as ultimately and unfortunately, static follicles may eventually become inspissated, necrotic, and even rupture- leading to yolk-associated coelomitis.^7,9 Cases of preovulatory follicular stasis have historically also been associated with estrogen toxicities such as anemia, as vitellogenesis is partially under the control of ovarian estrogens. Because of this process, some transient hepatic lipidosis and organomegaly are considered physiologically appropriate for vitellogenesis and should be considered when imaging reptiles with potential disease.^7,22,23 CBC and chemistry of the blood tests were not performed as part of this case series.

In terrestrial reptiles, concurrent renal disease can be seen with other disease processes due to their physiology. For example, urolithiasis, characterized by the formation of urinary calculi, is frequently associated with chronic dehydration, excessive dietary protein intake, and renal dysfunction. These conditions promote the accumulation and precipitation of uric acid salts, leading to stone formation within the urinary tract. Treatment generally relates to the location and removal of calculi, whereas prevention involves adequate hydration and husbandry.¹¹ Neoplastic processes in reptiles may predispose individuals to these metabolic disorders by affecting hepatic and renal functions, disturbing endocrine balance, or simply resulting in lethargy and inappetence.

In this case, we speculated that the large load of the tumor, either directly within the oral cavity or indirectly via multisystemic involvement, resulted in reduced appetite and secondary metabolic imbalance.¹⁷ Both multisystemic invasion of the tumor and the associated metabolic disorders significantly complicate the clinical management and most likely result in ineffective treatment, leading to euthanasia in animals.^24,25

Taken together, this case series highlights the incidence, clinical progression, and potential diagnostic tools for the detection of iridophoroma in leopard geckos. This case report also found POFS or urolithiasis in these tumor-affected animals, emphasizing the fact that metabolic dysregulation is a confounding factor for poor prognosis in addition to tumor malignancy.

Conflict of Interest

The authors have no conflict of interest to declare.

Funding

This work was internally supported by the Unit for Laboratory Animal Medicine (ULAM) at the University of Michigan.