By Scott J. Stahl, DVM, DABVP-Avian
111-A Center St South
Vienna, Virginia 22180
Telephone: 703 281 3750
The popularity of reptiles has increased tremendously in the last two decades. Over this time many species of lizards have become routinely available and their uniqueness and personality have resulted in their becoming mainstream pets.
With so many species of lizards (> 3000 species) it is difficult for the reptile clinician to be familiar with each species that is presented. This paper will provide the veterinarian with a reference for the most common problems seen in common species or groups of lizards.
The number of conditions and syndromes described for the lizard species discussed here will increase as we continue to see more of these patients in practice, share our clinical experiences and as our diagnostic capabilities improve.
The complexity of care necessary for these diverse lizard species is at the root of most problems seen with pet lizards. A primary goal is to improve husbandry by attempting to provide a captive environment and diet that is similar to the natural history of the lizard. References for natural history, husbandry and captive breeding information for the species of lizards described in this paper are sited at the initial heading for each species.
Bearded Dragons (Pogona vitticeps) 1-4 and Frilled Lizards (Chlamydosaurus kingi) 3,4,
Intestinal Parasitism (Coccidia, oxyurids, flagellates)
Coccidiosis is a common parasitic disease of bearded dragons.5, 6 The bearded dragon has its own species of coccidia known as Isospora amphiboluri. This coccidian lives in the small intestine, replicating in the mucosal lining to produce an oocyst.
Many bearded dragons that are positive for coccidia on fecal flotation are clinically normal and thriving. Thus, there is some debate that Isospora amphiboluri may be a commensal organism. However, in the captive situation the direct lifecycle often allows the protozoa to reach high numbers, which may result in super infections. The large number of organisms invading the intestinal lining may cause gastrointestinal pain, malabsorption and diarrhea. This results in clinical signs, such as anorexia and weight loss, and predisposes dragons to secondary nutritional and bacterial infections.
Routine fecal floats should be done on bearded dragons to look for coccidia. In single pets and small collections, coccidia may be able to be eliminated. In larger collections it may be difficult to eliminate this organism. Eradication is difficult and involves simultaneously treating the lizards and the environment. See Table1. As with coccidia in other animals, re-infection from the environment is the most common cause of treatment failure.
Oxyurids, or pinworms, are common parasites found on fecal examinations in bearded dragons.5, 6 As with coccidia they may not be a concern in wild populations, but in captivity they may reach large numbers and cause problems. Pinworms have a direct lifecycle, and bearded dragons tend to defecate frequently and are often in contact with their stool. This may result clinically in poor growth. As with coccidia, keeping the environment simple and clean during treatment is important for success. See Table 1. Fecal examinations are recommended 3-4 weeks post-treatment to ensure elimination of the organism.
Flagellates are commonly found on direct smears of fresh feces in bearded dragons. In low numbers these trichomonad-like protozoans appear to be normal commensals. But, in conjunction with coccidia and pinworm infections they can reach large numbers, resulting in clinical signs, such as diarrhea, anorexia, and dehydration.5 See Table 1.
Nutritional Secondary Hyperparathyroidism (NSHP)
Juvenile (growing), young gravid female and adult bearded dragons maintained indoors under poor husbandry conditions are susceptible to NSHP.6 As with other reptiles, the disease is usually the result of low dietary calcium and/or insufficient vitamin D. Excessive phosphorous in the diet can also lead to NSHP. Clinical signs of NSHP in bearded dragons include gastrointestinal stasis and bloating, tremors, stunted growth, deformed or fractured bones, soft mandibular and maxillary bones, spinal deviations, and paralysis.6 Radiographs can be useful to identify and characterize fractures and assess the severity of bone involvement. Treatment involves improving the calcium content of the bearded dragon's diet by the proper gut-loading and dusting of feeder insects, providing quality dark green leafy vegetables in the diet, and ensuring exposure to ultraviolet light (UVB) through natural unfiltered sunlight or full spectrum bulbs. Patient treatment for NSHP is similar to the protocols used for other lizard species as described by Mader.7
Female Reproductive Problems
Female bearded dragons often will present with a variety of reproductive related problems.6
Owners may or may not be aware that their dragons are reproductively active. Lizards may develop mature follicles on their ovaries and/or actually ovulate and produce infertile ova without a mate being introduced. Owners often describe their dragon becoming restless in their cage, pacing and climbing, likely looking for potential nesting sites. They may dig in planters or in the substrate in their environment. Owners who are attempting to breed their dragons may present a lizard because she has laid a clutch of eggs, but still appears to have retained some eggs. Or, the lizard has not laid any eggs yet (and showing similar signs as above) but is past her due date, and the owner can see or feel eggs in the lizard.
It is important to differentiate between pre-ovulatory egg stasis and post- ovulatory egg stasis when lizards are presented because treatment for the two syndromes may differ. See the green iguana section for techniques to differentiate the two syndromes and how to manage them.
Reproductive surgery is similar to that described for the green iguana and other lizards.8, 9, 10 Additionally, female bearded dragons presenting with dystocia may have concurrent egg-yolk peritonitis. Also older female bearded dragons may have persistent necrotic ovarian follicles on their ovaries, which may result in coelomic disease and require surgical intervention.6
Hepatic Lipidosis Syndrome
This author has seen a fatty liver-like syndrome in adult bearded dragons commonly.6 Typically, these dragons are obese with large abdominal fat pads. Clinical signs are usually anorexia and depression. Blood work is often unremarkable except sometimes SGOT (AST) is elevated. Bile acids appear to be useful as a more specific liver indicator, but normal values are not well established yet. Radiographs and ultrasound may reveal an enlarged liver and possibly ascites. Endoscopic liver biopsy or exploratory celiotomy and liver biopsy will confirm the diagnosis. Treatment involves supportive care including fluids (15-25ml/kg/day), broad-spectrum antibiotics, lactulose (.05ml/100gm PO daily), and assisted feeding. See Table 2. Daily warm water soaks are also beneficial to help with hydration. Clients may need to continue this support at home for 3-4 weeks before the dragon may begin to accept food on its own. Unfortunately, many of these dragons are presented late in the disease cycle and a diagnosis is made at necropsy. Etiology and techniques for prevention are unknown, but clients should be warned not to over-condition bearded dragons. For an overview of hepatic lipidosis in reptiles see Divers and Cooper.11
Bacterial and fungal dermatitis
Bearded dragons and frilled lizards are prone to bacterial and fungal dermatitis. The condition is usually seen on the head, extremities, lateral body wall and in frilled lizards at the edge of the frill (Fig 1). The skin color may look yellow to grey and often appears moist. As the disease progresses deep ulceration and crusts may form. Burns from a heat source may appear similar and need to be ruled out. A skin biopsy is often the best way to differentiate between bacterial or fungal involvement and possible etiology. Topical treatment with silver sulfadiazine cream and systemic antimicrobials may be necessary to stop progression of the condition and often there is a loss of tissue.See Table 2.
Jacobson, et. al. 12 reported the first case of this obligate intracellular, unicellular protozoan in the bearded dragon. The organism was found within hepatocytes and associated with hepatic necrosis in one bearded dragon and in two other bearded dragons these microsporidian organisms were found in macrophages that were associated with granulomatous inflammation in the colon, adrenal glands, and ovaries. Clinical signs of bearded dragons with microsporidia are vague, including anorexia, lethargy, depression and acute death. If the organism involves the brain, neurological signs may be noted. Management may be difficult because the organism has a direct life cycle and has resistant spores that may survive in the environment for a long time.5 Also, it can be difficult to diagnose the disease ante mortem. There is no known treatment, and more research is necessary to have a better understanding of this protozoan. Strict quarantine of new bearded dragons for 3-6 months may be the best way to avoid introduction of this organism into a bearded dragon collection
Bearded dragons have acrodont teeth (not rooted, but simply attached to the surface of the mandibular and maxillary bones), which predisposes them to periodontal disease, stomatitis and potentially osteomyelitis.6 This unique dentition results in a gum line along the lateral surface of the mandibular and maxillary bones, which can be readily permeable to bacteria.13 Regular oral exams should be performed to inspect this gum line for signs of discoloration, irregularities, in surface, and loss of tissue. If suspicious lesions are present, gentle curettage with dental instrumentation is useful to assess soft tissue and bone involvement. Radiographs may also be useful to determine bone involvement and presence of osteomyelitis. Deep culture of lesions is important for management, and aggressive surgical debridement and curettage may be necessary. Appropriate systemic antimicrobials (minimum of four-to-six weeks of therapy) and supportive care should be initiated immediately. See Table 2. The prognosis for bearded dragons with periodontal osteomyelitis and loss of bone is guarded to fair depending on severity and progression.
The ingestion of fireflies of the genus Photinus can be lethal to bearded dragons.14 (Glor et. al., 1999). Fireflies contain steroidal pyrones called lucibufagens that are cardenolides. Cardenolides are cardiac glycosides that cause inhibition of sodium, potassium and ATPase activity in cardiac muscle, resulting in stronger myocardial contractions and a decreased heart rate. These Photinus are very toxic to bearded dragons. Eating one firefly may kill an adult bearded dragon.14 Butterflies, such as monarch and queen butterflies, may also contain these cardenolides and should not be fed to bearded dragons or other lizards.
Clinical signs associated with ingestion include gaping and head shaking, color changes from tan to black, dyspnea, and rapid death within several hours of ingestion. No gross changes are typically noted at necropsy.14 If presented early enough, treatment would include attempts to minimize absorption of the toxin by gavaging with activated charcoal and providing support for shock.
Blue tongue skinks (Tiliqua sp.) 3, 4, 15
Difficulty in shedding often results in retained skin that may constrict toes and tail tips. The damage results in necrosis and often loss of toes or part of the tail. Another problem relates to retained skin on the eyelids of skinks, which interferes with eyelid function eventually resulting in conjunctivitis. Also, retained shed skin along the muco-cutaneous borders of the oral cavity may lead to stomatitis, subsequent loss of tissue, and exposure of the mucus membranes.
This condition is related to the need for more humidity in the captive environment of these skinks. Providing a humidity box as described for leopard and fat -tailed geckos may help in conjunction with soaking in a warm water baths during the shedding process until the skink completely sheds.
Using topical medications to soften and protect damaged skin along with ophthalmic ointments when the eye is involved will help. Loss of tissue along the oral cavity may result in chronic exposure of mucus membranes that can be managed by applying oragel (maxigaurd) to protect from periodontal disease.
Indonesian species of blue tongue skinks (ex. Tiliqua gigas) are prone to gastrointestinal parasitism as the majority are still wild caught. The Australian species such as the eastern blue tongue skink (Tiliqua scincoides scincoides) and the northern blue tongue skink (Tiliqua scincoides intermedia), are less likely to be parasitized as Australia does not allow any export of native reptiles, and thus these species are likely to be captive born. Regardless, a fecal fresh mount and flotation to diagnose the presence of parasites should be routinely performed on all blue tongue skinks. See table 1 for treatment protocols.
Blue tongue skinks are often aggressive toward one another, especially with the introduction of a new skink(s) to an existing group or when food is offered. They tend to bite each other's heads, legs and/or feet. Their jaws are very powerful and they tend to bite down, hold on, then roll resulting in a great deal of damage. Aggression can be managed by gradually introducing new skinks, providing a large enclosure with several visual barriers and hiding areas, and providing multiple feeding stations. Management involves separating fighting lizards and systemic and topical treatment of wounds with antimicrobials with a good spectrum against gram-negative bacteria. See Table 2.
Obesity/fatty liver syndrome
Blue tongue skinks are generally good feeders and may become over conditioned. A syndrome associated with anorexia in these skinks results in a fatty-liver syndrome similar to what is seen in the bearded dragon. Diagnosis and management is similar to what is described for bearded dragons.
Collard Lizards (Crotaphytus collaris) 3, 4, 15
Nutritional Secondary Hyperparathyroidism (NSHP)
As desert diurnal insectivorous lizards the collard lizard is very susceptible to NSHP. See the summary of this disease as described for other lizards.
Collard lizards, which are diurnal desert lizards, seem to be prone to respiratory disease. Common clinical signs include "popping sounds", increased respiratory rate, and obvious stridor. Open-mouth breathing and increased fluid or mucus in oral cavity or nares is often noted (Fig 2). A variety of gram-negative bacteria are usually isolated from a tracheal culture or wash. Aggressive treatment with combination antimicrobial therapy over a 4-6 week treatment course is indicated. See Table 2. Husbandry issues, such as ensuring warm enough temperatures (basking site at a minimum of 95F and up to 110F), need to be addressed. Additionally, it is important to make sure the humidity is not too high for these desert lizards.
Female Reproductive Problems
Female collard lizards often will present with a variety of reproductive related problems.
Owners may or may not be aware that their lizards are reproductively active. They may develop mature follicles on their ovaries and/or actually ovulate and produce infertile ova without a mate being introduced. Owners often describe their lizards as becoming restless in their cage, pacing and climbing, likely looking for potential nesting sites. Owners who are attempting to breed their collared lizards may present a lizard because she has laid a clutch of eggs, but still appears to have retained some eggs. Or, the lizard has not laid any eggs yet (and showing similar signs as above) but is past her due date, and the owner can see or feel eggs in the lizard.
It is important to differentiate between pre-ovulatory egg stasis and post-ovulatory egg stasis when lizards are presented because treatment for the two syndromes may differ. See the green iguana and bearded dragon section for techniques to differentiate the two syndromes and how to manage them.
Reproductive surgery is also similar to that described for the green iguana and other lizards.8
This author has seen several collard lizards present with vestibular disease involving head tilt and ataxia. The etiology is unknown but suspected to be bacterial or viral in origin. Minimal response to a variety of long-term antimicrobials has been seen.
Green Iguana (Iguana iguana) 3, 4, 15, 16, 17
Nutritional Secondary Hyperparathyroidism (NSHP)
Low dietary calcium, excessive dietary phosphorus and low levels of dietary vitamin D3 or a lack of proper exposure to sunlight or ultraviolet light in the B range (UVB) may all lead to NSHP. This is a common disease in young growing iguanas and young gravid females, both of which have an excessive demand for calcium.
Clinically, there is usually a history of a poor diet and /or lack of exposure to sunlight or UVB. On physical exam the mandibular and maxillary bones tend to be soft and may be malformed. Growth may be stunted and fibrous osteodystrophy may be evident in many of the long bones. Fractured bones, spinal deviations and paralysis are all common presenting signs.18 Additionally, spinal changes associated with kyphosis and scoliosis, or fractures, related to a weakened spine, may result in gastrointestinal stasis from neurological deficits resulting in bloating, urinary or fecal incontinence and constipation.
Radiographs can be useful to assess the degree of osteodystrophy and loss of mineralization and to locate and characterize fractures.
The first step in treatment is to correct the underlying husbandry problems. Calcium should be increased in the diet and phosphorus limited. Natural unfiltered sunlight is best, but full spectrum lighting (UVB in the range of 290-320 nm) will suffice.
Specific treatment for NSHP is based on the protocol described by Mader.7
The prognosis for NSHP is good for iguanas that have no or minimal spinal involvement. Young iguanas with kyphosis and scoliosis have a more guarded prognosis, especially if neurological deficits, such as poor use of rear limbs, constipation, bloating, are already present.
Abscesses in iguanas are usually secondary to improper husbandry or trauma.18 Bite wounds or scratches from cage mates or other household pets may lead to abscesses. Also, improper temperature and humidity may cause dysecdysis, which can lead to interruption of blood flow to extremities resulting necrosis and abscessation. Deep abscesses in iguanas may become invasive and may penetrate the bone and joints, resulting in osteomyelitis.
Abscesses are also commonly seen along the mandibular and maxillary bones in the green iguana. The origin is often unknown. In most cases these abscesses communicate with the oral cavity along the lateral surface of the mandibular or maxillary bones.
The green iguana is also prone to trauma to the rostrum, which may lead to abscessation, tissue loss and possible osteomyelitis. Typically, the behavior is a result of trying to get out of a cage. An increase in this behavior is often seen with seasonal hormonal changes as both males and females will become more active, presumably looking for a mate.
Treatment of abscesses involves aggressive surgical exploration making a wide excision in the skin over the swelling to allow removal of all purulent material and the opportunity to leave the incision open for continued flushing. Treatment with topical and systemic antimicrobials for 3-4 weeks may be necessary and cases involving bone and osteomyelitis may require bone curettage, placement of antibiotic impregnated methylmethacrylate beads, or amputation when involving limbs, toes, tails.19, 20 See Table 2. Most importantly in the management of this problem is to minimize the reoccurrence of abscesses by separating iguanas that are housed together, minimizing trauma to the rostral area by adjusting or rearranging the cage, increasing the size of the cage or changing the way it opens (cages with screen tops are more likely to cause problems), or by managing hormonal drive by neutering or spaying these lizards.
Renal Disease Syndrome
Renal disease is common in mature green iguanas, though the pathophysiology of this disease is poorly understood. Diets that are high in animal protein, such as dog food, cat food or monkey biscuits may predispose iguanas to renal failure.18 However, renal disease and subsequent failure also occurs commonly in iguanas on more appropriate (herbivorous, non-meat protein) diets. Other possible causes of this syndrome include chronic low-grade dehydration, altered metabolism of vitamin D3, or chronic low- grade bacterial infections. More research is necessary to better understand the cause(s) of renal disease in the green iguana. For a more in depth discussion on the possible pathophysiology of this disease the reader is directed to other sources. 18, 21-25
Common presentations for renal disease are generally non-specific including anorexia, lethargy, weight loss. In more advanced cases signs associated with hypocalcemia are often seen, including muscle tremors and fasiculations, which may progress to front or hind limb paresis and seizures. Constipation is also a common symptom as the diseased kidneys often enlarge filling the pelvic inlet. This blocks the normal passage of stool through the distal colon. Dysphagia is also seen frequently as pharyngeal edema occurs, resulting in difficulty in swallowing.
Physical exam findings include soft mandibular and maxillary bones, injected sclera, hyperemic oral mucosa, muscle twitching, tremors, and fasciculation. Enlarged kidneys may be palpated in the paralumbar region of the coelom, just cranial to the brim of the pelvis whereas the normal sized kidney would reside within the pelvis. Digital rectal palpation in iguanas that are large enough (~1 kg) is a sensitive test to determine and monitor the size of the kidneys. Radiography can also be used to detect the distinct paired masses in this area. Ultrasonography is also useful in diagnosing enlarged kidneys and to evaluate their architecture.
If renal disease is suspected a blood chemistry panel should be performed. Blood chemistry values in iguanas with renal disease will typically reveal normal calcium values or hypocalcemia (calcium < 8.0 mg/dl) and hyperphosphatemia (phosphorus > 10 mg/dl). With kidney disease there usually is a disruption of the normal 2:1 calcium: phosphorus ratio with initially a 1:1 ratio and eventually an inverse ratio. Uric acid values are typically within the normal range or only slightly elevated. Elevations in the white blood cell count may indicate an acute bacterial nephritis, indicating the need for aggressive antibacterial therapy. See Table 2. Boyer et.al.21 summarize the most consistent clinicopathologic findings in twelve cases of iguanas diagnosed with renal disease.
Surgical or endoscopic biopsy with histopathological evaluation is the most specific diagnostic tool for describing the pathology of the kidney.22, 26 The most common histopathological diagnosis described in these cases is severe and extensive interstitial fibrosis.
If the kidneys are enlarged and the plasma phosphorus values are elevated (greater than 15 mg/dl) with a concurrent inverse ratio of calcium to phosphorus values, the prognosis --even with aggressive therapy-- is poor. In some of these severe cases the option of euthanasia should be discussed.
If the owner opts to pursue treatment aggressive fluid therapy should be initiated. A fluid rate of 20-25 ml/kg body weight per day by continuous IV or IO infusion or divided into 2-3 treatments via these routes or intracoelomically is recommended.
If clinical signs of hypocalcemia are severe including tetany and seizures, parenteral calcium may be indicated. Once more stable oral calcium glubionate can be given at 1 ml/kg body weight every 12 hours. The oral calcium may work as a potential phosphorus binder and provide calcium for gastrointestinal absorption .18 A phosphorus binder such as aluminum hydroxide at 1ml/kg orally every 24 hours can be useful to reduce phosphorus absorption.18, 22, 25 Once hydration has been achieved a broad-spectrum antibiotic can be initiated especially in cases where a CBC or biopsy indicates a suspected bacterial nephritis. See Table 2. Having the owner assist with alimentation and oral fluids at home will be important for the long-term prognosis. Calcium and phosphorus values, their associated ratio, the hematocrit and WBC estimates can be monitored to assess response to treatment.
Dystocia / Female Reproductive Disorders
Iguanas often develop mature follicles on their ovaries and/or actually ovulate and produce infertile ova without a mate being introduced. 8, 18 Historically, owners may or may not be aware that their lizards are reproductively active. Owners often describe their pet iguanas as becoming restless in their cage, pacing and climbing, likely looking for potential nesting sites. They may dig in planters or in the substrate in their environment. Appetite and water intake may be greatly reduced or gone. Owners may also have found some eggs that have already been laid.
Clinically, it is important to differentiate between pre-ovulatory egg stasis and post- ovulatory egg stasis when iguanas are presented to the clinician because treatment for the two syndromes may differ.8, 9, 10, 18
In captivity, one common scenario is for the ovarian follicles to become static. They may reach a large ovulatory size but still not be released into the oviduct or resorbed. This is known as pre-ovulatory egg stasis. It is unclear why this occurs, but it may be related to inappropriate environmental cues. It is contraindicated to use oxytocin in iguanas with pre-ovulatory egg stasis. Prior to any use of oxytocin, the clinician must be certain the eggs are in the oviduct.
Post-ovulatory egg stasis occurs when the ovarian follicles are ovulated into the oviduct, but the eggs are not laid or only a portion of the eggs are laid.
Differentiating ovarian follicles from oviductal eggs can be challenging. On palpation, ovarian follicles tend to be more dorsal and spherical and not as mobile as oviductal eggs, which are usually more oblong and ventral/caudal in the abdomen. Radiographs may help to differentiate the two syndromes as the ovarian follicles are usually not calcified and are more spherical and dorsal in their location. Ultrasonography can also be useful to differentiate between the two.
If the eggs are pre-ovulatory or post-ovulatory and the lizard is normal on assessment, then a nest box can be provided and the lizard may be sent home on calcium glubionate at 1ml/kg PO BID for 21 days. Surgery can also be pursued at this time if the owner prefers. Postovulatory egg-bound iguanas with calcified eggs may present with clinical signs of hypocalcemia, including paresis, tremors, and seizures. These patients are typically critical and must be aggressively treated with fluid therapy and initially calcium at 100mg/kg IM every 6 hours until signs of hypocalcemia resolve.
Medical therapy can be initiated in postovulatory cases to induce oviposition. Calcium at 100mg/kg IM can be given every 6-12 hours followed by oxytocin (approximately one hour after calcium) at 5-20IU/kg IM.8, 9 The higher dose range is used if there is no response to the lower dose. A nest box should be provided after oxytocin injections. If some but not all eggs are laid, dosing can be repeated. If the eggs are not laid within 48 hours, surgery is recommended.9 In this authors opinion there is a short window of opportunity for oxytocin to work. It is appears to be most beneficial within several hours or days of the initial oviposition or completion of the nest and attempt to lay eggs.8 One or two weeks after these events and oxytocin is are rarely effective and may result in oviduct tear or torsion.
See multiple references for the surgical approach to the pre-ovulatory and post-ovulatory reproductive surgery in the green iguana.8, 9, 10
Aggression in male iguanas is a serious and frequent problem for pet owners. Two types of aggression are typically described.9 The most common is known as defensive aggression. This occurs when the iguana is provoked, usually when his personal space has been invaded or if the iguana has been startled or touched. Typically, the iguana will stand erect on all four feet, flatten itself, turn sideways, and fill its lungs with air. The iguana may then lash out with its tail or attempt to bite.
Offensive aggression is when a male iguana actually pursues a person with the intent to attack or becomes aggressive in order to protect his territory. Often, these males are allowed to roam free in an owner's home and they may become extremely territorial during the breeding season. In the northeast, breeding typically occurs from the fall to the spring, but this aggressive behavior can occur anytime of the year.
Male iguanas also have been reported to be aggressive specifically toward women during their menstrual cycle.27 In these cases, female owners may be producing a pheromone that their iguanas can detect.
Management of male iguana aggression should start by evaluating the iguanas' environment. Making changes in the iguana's environment may decrease offensive behavior, especially during the breeding season.
Placing the male iguana in a large cage, instead of allowing it to roam free may be helpful. Reducing the light cycle is also important in trying to reduce aggression. Isolating iguanas from other iguanas (or a reflective image), both physically and visually, may help.
Medical management has not proven very beneficial to date however Mader9 and Funk28 report consistently favorable results in castrating juvenile males. They have found that these iguanas have remained non-aggressive for several years after surgery and will likely remain non-aggressive throughout their lives. Although it does appear that these males do not develop the normal male morphological features, such as large crests and jowls. Typically, these iguanas will be presented for consultation after they have already matured and become aggressive. However, reptile veterinarians should counsel owners of young male iguanas about future aggression so that they can consider juvenile castration.
Castration of the male iguana is similar to ovariosalpingotomy in female iguanas and is described in detail elsewhere.9, 10
Green iguanas may present with the red mites most likely of the genus Hirstiella.23, 29
Clinical signs may include anorexia, depression, lethargy, dysecdysis, and severe ulcerative dermatitis. The owner may or may not have seen the mites moving on the lizard or noticed a change in the lizards skin color to an orange/red with black patches.
On physical exam the orange/red mites are found lined up under scales or in loose folds of skin. They tend to localize around the eyes, under the chin, dewlap, axillary area, inguinal area on limbs in folds of skin associated with joints and on the tail. Severe infestations typically result in deep ulcerative lesions with black necrotic patches of skin, especially over the limbs, abdomen and tail.
Eradication of mites involves the treatment of both the lizard and lizard's environment.
A thorough review of mite biology and other potential mite treatments is described elsewhere. 23, 29, 30
Pinworms or oxyurids are very common in the green iguana and are likely a commensal organism in the wild. However, since these round worms have a direct life cycle and iguanas in captivity are often exposed to their own fecal output, there is a possibility that super infections can occur that may result in pathology.23, 29 See Table 1.
Bladder stones occur regularly in the green iguana.23 These lizards will typically present straining or constipated or just "not right". Radiographs may identify a radiodense bladder stone however some stones may be radiolucent. Bladder stones can become large in size and eventually result in disruption of normal gastrointestinal and genitourinary function. The etiology for these stones is unknown but may be related to inadequate hydration. Most of these stones are composed of urate salts. Surgical removal is usually necessary.
The green iguana will commonly present with the ingestion of a variety of different foreign bodies.23 Historically iguanas that are allowed to free roam in the house are the most likely to ingest a variety of foreign materials including shiny metal items such as coins, nuts, bolts and screws, rocks, plastic toys, etc. The majority of the items can often pass through the gastrointestinal tract without problems, however, lead and zinc toxicity can be a problem with items that contain these heavy metals. Clinical signs are often vague, including anorexia, lethargy, weight loss and possible neurological signs if heavy metals are involved. Radiology is typically necessary to confirm the suspected diagnosis. Surgical removal of items may be necessary and chelation therapy initiated if indicated.
Leopard Gecko (Eublepharis macularius) and Fat-tailed Gecko (Hemitheconyx caudicinctus) 3, 4, 31, 32, 33
Nutritional Secondary Hyperparathyroidism (NSHP)
As insect feeders leopard geckos are prone to calcium deficiencies and the resultant NSHP.31 Since leopard geckos are nocturnal, the benefits of UVB lighting is questionable but it can be provided during the daylight cycle. Most importantly the management should include improving the calcium-to-phosphorus ratio of dietary intake. Feeding invertebrates a high quality, balanced diet, followed by dusting of crickets or worms with a calcium and a vitamin D supplement just prior to feeding them to the geckos, is important. Providing specific feeding stations (such as a deep crock bowl) for geckos allows them to easily catch and consume food items before the dusted supplement falls off.
The most common clinical finding is soft mandibular and maxillary bones and fractures or abnormal growth of long bones.
Follow guidelines for diagnostics and therapy of NSHP in leopard geckos as described for the bearded dragon.
A variety of gastrointestinal parasites can affect leopard geckos, including oxyurids, coccidia, cryptosporidia, and flagellates.31 Clinical signs may include weight loss or "skinny tail" syndrome, diarrhea, or malodorous stools. Diagnostics include fecal direct evaluation, fecal flotation and acid-fast staining of the stool for cryptosporidiosis.
Cryptosporidiosis in lizards tends to involve the intestinal tract instead of the stomach as in snakes, so stomach washes and biopsy are typically not diagnostic.34, 35 Acid fast staining of fecal smears may not be diagnostic for cryptosporidiosis in leopard geckos as they shed oocysts intermittently.34 Intestinal biopsy, or euthanasia followed by histopathological evaluation of the gastrointestinal tract is the most accurate method of diagnosis.
See Table 1 for antiparasitic treatment protocols in lizards. There is no effective treatment for cryptosporidiosis at this time. Decreasing stress by not overcrowding breeding groups of geckos and reducing other husbandry-related stresses may help with management of cryptosporidiosis in leopard gecko colonies.
Problems with shedding skin are common in leopard geckos.31 The retained shed skin is usually associated with extremities such as the toes and the tail, which may lead to constrictions, necrosis and loss of toes or a portion of the tail. Also, shed skin is commonly retained around the eyes in geckos resulting in dysfunction of eyelids and resultant conjunctivitis. Dysecdysis is usually related to improper humidity in the environment. However the author has also confirmed several cases of dysecdysis and associated eye problems with deficiencies of vitamin A. A diagnosis of dysecdysis is made on historical review of environment and diet in conjunction with the physical examination. Usually pieces of white skin are seen still attached to toes and feet, tail or around lips and eyes. Often involved toes have turned dark and may be necrotic. Treatment involves warm water soaks to soften the adhered skin, followed by gentle removal. Systemic antimicrobials may be warranted, depending on severity, and topical antibiotic cream such as silver sulfadiazene cream can be applied to damaged tissue and adhered skin. See Table 2. See old world chameleon section for treating vitamin A deficiency. Providing a humidity box in the environment is also helpful. The owner can place a small plastic sandwich tub with a hole in the side or top for the gecko to crawl into that contains a medium in it that will retain moisture such as shredded paper towels or sphagnum moss which is dampened daily. This will allow the lizard constant access to a humid microenvironment.
Female Reproductive Problems
Reproductive related conditions such as dystocia or pre-ovulatory follicular stasis are common in female leopard geckos.8, 31 Egg yolk celomitis can occur with both pre- and post-ovulatory egg binding. A diagnosis is typically made by historical review, celomic palpation and visualization as calcified eggs (usually only two eggs) can often be seen through the thin skin on the abdomen. Radiology and ultrasonography can also be useful to evaluate these females for any associated pathology with the reproductive tract. Exploratory celiotomy may be performed to remove adhered retained oviductal eggs and to perform a ovarectomy or ovariosalpingectomy. See approach to female reproductive problems in iguanas and bearded dragons for diagnostic and therapeutics considerations.
Problems associated with the ingestion of fine gravel, sand and walnut shell often results in gastrointestinal impactions and cloacal prolapse. 31, 32, 33, 36
The condition is seen most often in juveniles and often in geckos on poor quality diets. Clinically, these geckos present depressed and anorexic with a swollen celom and cloacal prolapse. Celomic palpation usually is diagnostic, but radiographs will confirm ingestion of this foreign material (Fig 3). Mineral oil and warmed saline enemas may help in mild cases but surgery may be necessary in more severe cases.33, 36 Removing these particulate substrates or feeding geckos in a deep bowl or dish to discourage ingestion of substrate, along with correcting any husbandry-related issues is important in preventing these impactions.
Old World Chameleons 37, 38, 39
Nutritional Secondary Hyperparathyroidism (NSHP)
Juvenile (growing) and young gravid female chameleons are the most susceptible to NSHP. As with other reptiles, the disease is usually the result of low dietary calcium and/or insufficient vitamin D.
Clinical signs of MBD in chameleons include stunted growth, deformed or fractured bones, soft mandibular and maxillary bones, spinal deviations, and paralysis.38, 39, 40 Radiographs can be used to identify and characterize fractures and the severity of bone involvement. Treatment involves increasing the calcium content of the chameleon's diet by the proper gut-loading and dusting of feeder insects, and ensuring exposure to ultraviolet light (UVB) through natural unfiltered sunlight or full- spectrum bulbs. Patient treatment for MBD is similar to the protocols used for other lizard species as described by Mader.7 The prognosis can be good depending on severity and duration, however spinal involvement results in a more guarded prognosis.
Clinically, chameleons may present with signs of hypovitaminosis A as described in other reptiles.38, 39, 40 These chameleons typically have a history of low preformed vitamin A supplementation. Usually insects are being fed a poor diet and are only being dusted with a calcium/ vitamin D supplement or a multivitamin that has beta-carotene but no preformed vitamin A.
Clinical signs of hypovitaminosis A include eye problems, respiratory infections, neurological dysfunction, spinal kinking, dysecdysis, and increased formation of hemipenal plugs. Research in the panther chameleon fed a restricted vitamin A diet resulted in these same clinical signs.41 Generally it is recommended to use a multivitamin (for dusting insects) with some pre-formed vitamin A weekly for juvenile (growing) chameleons and every other week in adult chameleons to avoid hypovitaminosis A. Additionally, feeding insects a beta-carotene rich diet, such as green- leafy vegetables, carrots and sweet potato, prior to feeding them to the chameleons, may be beneficial.
Treatment for hypovitaminosis A involves giving a parenteral vitamin A solution (vitamin A palmitate 100,000 IU/ml, vitamin D3 10,000 IU/ml and vitamin E 20 IU/ml). Give 2000 IU vit A/ 30 gm body weight by mouth every 7 days for 2 doses. The parenteral drug works well orally and may be safer when used in this manner.
Organ toxicity associated with the fat-soluble vitamins A and D is a common nutrition-related problem of chameleons. A relationship exists between these two vitamins and their dietary level of supplementation and the amount of ultraviolet exposure (UVB) in chameleons.41
Excess vitamin A supplementation may interfere with the metabolism of vitamin D3, resulting in metabolic bone disease. It may also lead to organ toxicity (renal, hepatic). Gular edema is a common clinical sign of organ dysfunction in chameleons.
Excess vitamin D3 supplementation -- especially in combination with calcium -- may result in organ toxicity. Metastatic calcification and gout are common results. Gular edema is a common clinical sign. Additionally, pseudo-gout has been noted in veiled chameleons fed a heavily-supplemented vitamin D3- and calcium-based diet in combination with restricted levels of vitamin A.38 The pseudo-gout (calcium hydroxyapatite) deposits usually appear as irregular firm swellings over joints in the limbs and on ribs. These lesions are similar to those described by Frye in a chelonian.4 These swellings must be differentiated from true gout, abcesses/osteomyelitis, and cellulitis. Fine-needle aspirate and cytology or biopsy can be used to reach a diagnosis. Radiology may be useful in screening for metastatic calcification and/or pseudo-gout. Bloodwork may indicate extremely elevated plasma calcium values in cases of hypervitaminosis D. Treatment for hypervitaminosis is difficult because the clinical disease is usually well advanced by the time the chameleon is presented (ex. gular edema with renal failure).
One of the most common causes of death in chameleons is renal disease. Renal pathology is commonly noted at necropsy and on histopathology. Similar to the green iguana the etiology for renal disease may be multifactorial and is not yet well understood.21-25 Possible causes include imbalances in the fat soluble vitamins A and D, inadequate exposure to UVB irradiation, chronic bacterial infection (possibly from low grade periodontal disease) or exposure to toxins. Additionally, one of the most likely causes of these renal changes could be chronic dehydration. Exposure to low humidity or inadequate watering methods could lead to renal failure, especially in conjunction with these other possible etiologies. Clinical signs are usually vague, but include anorexia, depression, weight loss, and weakness. Other common signs include gular edema, generalized edema, exophthalmia, and enophthalmia. For diagnostic considerations see renal disease in the green iguana section. Ensuring adequate hydration by maintaining proper humidity -- and providing a method to encourage-- and monitor water intake is critical. Also, "showering" chameleons with a misting system or on a wooden perch in the bathroom shower for 20-30 minutes once to twice weekly may be helpful in avoiding sub clinical dehydration.
Most chameleons are oviparous (some chameleons are live-bearing, such as the Jackson's chameleon) and dystocia is a common problem.38, 39, 40 There are numerous factors that may predispose females to dystocia, including stress, poor nutritional status, and the lack of a proper nesting site.
Providing exposure to ultraviolet light (UVB) and adequate levels of vitamin A and vitamin D3 may be the most important factors in preventing dystocia and other reproductive problems.41
Gravid female oviporous chameleons typically present with an enlarged abdomen, and gentle palpation of the abdomen usually reveals the presence of eggs. Ultrasound or radiographs can be used to confirm the diagnosis. An egg-bound chameleon is usually presented well past her due date and in distress.
Retention of eggs will usually result in death, so medical and/or surgical intervention is indicated to avoid the loss of the chameleon.
For diagnostic and therapeutic considerations see reproductive problems and dystocia in the green iguana, bearded dragon and leopard gecko sections.
Bacterial infections of the respiratory system are common in chameleons. Signs of respiratory disease include increased mucus in the oral cavity, increased stridor with breathing, open-mouth breathing, and hyperinflation of the lungs. Frequently, the sinuses of the head are involved and bumps or swellings on top of the head between the eyes will often occur. Respiratory and sinus infections are typically associated with eye problems.38, 39 Discharge from an affected eye(s), swelling in the retrobulbar and periocular areas, and/or holding the eye(s) closed are all common clinical signs of ocular disease.
Tracheal culture, deep culture of the lining of the involved sinus, or culturing fluid from the sinuses are useful techniques to direct antimicrobial treatment. Treatment of respiratory infections with systemic antimicrobials should be initiated early and combination therapy is recommended. See Table 2. Swellings involving the sinuses should be opened for drainage; and purulent material should be removed when possible. A review of the diet may indicate the need to supplement with vitamin A (see hypovitaminosis A).
Stomatitis in chameleons usually involves the mucous membranes along the lips, the commisures of the mouth, or sometimes the tongue. Clinical signs include anorexia, inability to close the mouth completely, loss of symmetry to the mouth, and inability to use the tongue. Chameleons have acrodont teeth (not rooted, but simply attached to the surface of the mandibular and maxillary bones), which predisposes them to periodontal disease and potentially osteomyelitis (Fig 4) .13 See bearded dragon section for diagnostic and therapeutic considerations. The prognosis for chameleons with periodontal osteomyelitis and loss of bone is guarded-to-fair depending on severity and progression.
Abscesses are common in chameleons and are typically the result of damage to the skin. Trauma from sharp edges in cage materials, bite wounds, or scratches from cagemates or other animals will often result in abscesses. Damaged nails from screen injuries or from pulling chameleons off branches, or dysecdysis of the toes often results in abscessation of toes, subsequent cellulitis, and osteomyelitis.
See iguana and bearded dragon section for diagnostic and therapeutic considerations for abscesses.
Nematodes, cestodes, coccidia, flagellates, and amoebae are all intestinal parasites commonly found in chameleons.38, 39, 42 Clinical signs of parasitism include weight loss, anorexia, regurgitation and vomiting, and malformed and malodorous stools. Parasitic infections are not seen as often in the more commonly captive-bred species, such as veiled chameleons and Jackson's chameleons. But nematodes (primarily oxyurids) and coccidia can still be found in these captive- born animals, and fecal exams should be performed. Flagellates, amoebae, and other nematodes may also be present in captive chameleons that live in mixed collections or facilities with poor isolation and quarantine practices. See Table 2.
A case of cryptosporidia was described in a panther chameleon and this organism will likely will be found in other species of chameleons.35 Screening fecal samples for cryptosporidia, especially in animals showing signs of gastrointestinal disease, is recommended (see leopard gecko section). Currently no effective drug exists to treat cryptosporidiosis in lizards and infected chameleons should be isolated or removed from the collection.
Prehensile-tailed Skinks (Corucia zebrata) 3, 4, 43, 44
Juvenile sudden death syndrome
A syndrome has been described in young prehensile-tailed skinks associated with neonates suddenly dying several days or weeks after birth.45
This problem is difficult to manage because the juveniles appear to be doing well and then suddenly succumb. A thorough evaluation of newborns should be done after birth to look for any health concerns and with specific attention to any obvious abnormality of the yolk sac.
In some cases but not all there have been problems associated with the umbilicus.45 This problem is usually related to a retained or unabsorbed yolk sac. The abnormal yolk material often becomes infected and may lead to bacterial pyelonephritis. Surgical removal of any enlarged, poorly absorbed yolk sac should be performed. For a description of this procedure see Wright.45
Many of captive prehensile-tailed skinks were originally wild caught and often have heavy parasite loads with a variety of nematode parasites and protozoal overgrowth. In one study, the most common gastrointestinal parasites found in fecal samples from 56 positive skinks were reviewed.45 Ascarid ova were found to be the most common parasites with flagellates, coccidia, and Strongyloides found less frequently. A thorough evaluation of the feces including a direct mount and flotation should be routinely performed on these skinks.
Amoebiasis may also cause problems for prehensile-tailed skinks, and direct mounts and prophylactic treatment with metronidazole may increase survivability especially in recently imported prehensile-tailed skinks. See Table 1.
Prehensile-tailed skinks have a distinct odor to their fecal output and an orange pink color is often normally associated with urates and urine. See Table 1 for parasitic treatment protocols. Remember that this species of skink is known to be coprophagic in the wild so removing fecal material quickly during treatment is important.
Prehensile-tailed skinks are a live bearing species generally producing between one and three young. Problems with pregnancy may occur and confirming pregnancy with radiology or ultrasonography is useful. Surgery may be necessary in cases of dystocia or death of the fetus during the pregnancy. Due to a desire to reproduce these lizards in captivity, reproductive surgery may involve removing the fetus or an abnormal ovarian follicle while attempting to maintain a functional reproductive tract. See section on reproductive surgery for the green iguana and bearded dragon.
Cage mate aggression
Similar to blue tongue skinks, this species of skink can also be very aggressive toward one another, especially when introducing new lizards to an existing group or into a cage with a single skink.45 Wounds from fighting can be severe and may need surgical debridement, systemic antibiotics and topical treatment (Fig 5). See Table 1. Providing multiple visual barriers and hiding places, including elevated perches within the cage, can reduce cage-mate aggression. Also, a slow introduction of a new skink can be more safely achieved by placing the new lizard in the cage within another smaller cage made of wire mesh to allow exposure and exchange of pheromones but within the safety of a physical barrier.
These skinks are also prone to bacterial stomatitis with purulent discharge often found along the gum line. The associated swelling and inflammation often results in an inability for the mouth to close properly. Stomatitis may become severe and result in osteomyelitis. Aggressive surgical debridement followed by topical and systemic antimicrobials, may be necessary to resolve these problems. See Table 2.
Respiratory disease may be associated with stomatitis or a separate problem. Noting mucus production and abnormal breathing sounds such as wheezing and popping sounds may be noted. Open-mouth breathing and nasal and ocular discharge may also be seen.
A tracheal culture or lung and tracheal wash with culture and sensitivity can be useful for diagnosing potential pathogens and helping to direct treatment. Medical therapy consists of aggressive systemic antimicrobials for a minimum of 4-6 weeks. See Table 2.
The skin of skinks is similar to that of snakes, making them susceptible to the snake mite Ophionyssus natricis. Skinks that have been housed near infected snakes will often become infested. These mites can cause a life-threatening anemia and become a vector for possible bacterial and viral diseases. Typically, the black mites are noted on the skink or on the hands of the handler after holding the skink. Also, a white dust -- which is the fecal material of the mites -- may be noted on the skin of these lizards. Eradication of mites involves the treatment of both the lizard and lizard's environment.
A thorough review of mite biology and mite treatments is described elsewhere.30
Savannah Monitor (Varanus exathematicus) 3, 4, 15, 46
Obesity/hepatic lipidosis syndrome
Savannah monitors typically have an aggressive appetite. Pet owners tend to overfeed these voracious lizards. Coupled with a reduced activity level in captivity, these lizards may become obese. In their natural environment these large lizards are active, diurnal, and are opportunistic feeders. They tend to cover a large range, plodding along looking for anything edible. Investigations into dietary intake from stomach samples include a very wide range of small food items, such as invertebrates, small rodents, bird eggs, fecal material of other lizards, etc. Limiting intake and feeding a variety of smaller lower energy foods may help to reduce over conditioning. Limiting rodents to 1-2 times weekly and increasing exercise and activity can help. A hepatic lipidosis-like syndrome is seen in savannah monitors and is very similar to what is described for the bearded dragon. See the bearded dragon section on hepatic lipidosis for diagnostic and therapeutic considerations.
Nutritional Secondary Hyperparathyroidism (NSHP)
Young savannah monitors eat a diet of primarily invertebrates, so they are prone to problems with calcium metabolism. Rapid growth in conjunction with the poor calcium- to-phosphorus ratio of most invertebrates results in nutritional secondary hyperparathyroidism. The clinical signs, diagnosis and management are similar to what is described for the green iguana and bearded dragon.
Sub adult and adult savannah monitors typically will not have problems with NSHP because they will begin to eat the more balanced rodents as a staple part of their diet. Exposure to proper lighting that includes UVB is important for these diurnal lizards and should be addressed when reviewing husbandry management.
Savannah monitors seem to be very susceptible to a variety of different neoplasms, especially reproductive and liver-related neoplasms. Often, these masses result in a distended celom, and in most cases, the presence of free celomic fluid. Many of these lizards will present with celomic distention. Radiology, -specifically ultrasonography- can be very useful in diagnosing organ involvement. Exploratory celioscopy or surgery is often necessary to allow biopsy and histopathology to confirm a diagnosis and assist with possible therapy.
Since the majority of savannah monitors are still wild caught, intestinal parasites are common. Nematodes, cestodes and protozoa are all commonly found. A variety of non-specific signs such as anorexia, poor body condition, and weight loss may be noted. Occasionally, diarrhea or malodorous stools may be noted. Routine fecal examination, including direct mounts and flotation, are important in diagnosing gastrointestinal parasitism. Tapeworm eggs may not be found on routine examination, so prophylactic treatment may be necessary. See Table 1 for antiparasitic drug dosages. Additionally, a case of cryptosporidia has been reported in the Savannah monitor.35 See leopard gecko section for a discussion on cryptosporidiosis in lizards.
Savannah monitors like many other lizards are prone to abscesses. See abscess description for other lizards for clinical signs, diagnostics and therapeutics. A unique abscess syndrome involving the feet is commonly seen in savannah monitors.46 The syndrome is likely related to a high humidity environment. Both the substrate used for the lizards and the large size of these lizards may also play roles. A variety of gram-negative bacteria have been isolated from these abscesses. The plantar surfaces of the hind feet are the most commonly affected, but the front feet can be involved as well. Typically, the entire foot, including the toes, becomes swollen with cellulitis and caseated purulent material (Fig 6). In severe cases osteomyelitis occurs, and radiographs are useful to determine the extent of bone involvement. Aggressive treatment, including surgical debridement, flushing, and the initiation of topical and systemic antimicrobials based on culture and sensitivity results, is important. See Table 2. Bandaging may also be useful to protect the feet during healing since lesions typically involve the weight bearing portions of the foot. In cases of osteomyelitis, toes or part of the foot may have to be amputated. The use of surgically placed antibiotic impregnated methylmethacrylate beads may also be useful.20
This author has seen a vestibular like syndrome in savannah monitors. The lizards often present with a mild to severe held tilt and often are ataxia or recumbent. Etiology is unknown and the syndrome responds poorly to antimicrobials and supportive care. Bloodwork may show an elevation of the WBC with a left shift, but bloodwork is often unremarkable. Etiologies suspected include bacterial and parasitic involvement, however the author suspects a possible viral disease due to the poor response to treatment. More research is necessary to further define this syndrome.
Savannah monitors are prone to respiratory infections usually from husbandry problems such as improper heat or inadequate ventilation in their enclosures. They typically present with increased mucus in the mouth and nares. They may keep their eyes closed, and wheezing and bubbling sounds may be noted. Gaping, open-mouth breathing or a distended gular area is common with severe respiratory infections. Tracheal culture or tracheal/lung wash for culture and sensitivity is useful for determining appropriate long-term systemic antibacterial treatment. See Table 2.
Husbandry issues must also be addressed to ensure response to therapeutics and prevent recurrence.
Tegus (Tupinambis sp.) 3, 4, 15, 46
Tegus generally are native to areas with high humidity (South America) and need some consistent moisture in the environment to shed properly. However, too much moisture can lead to bacterial or fungal dermatitis.
Difficulty in shedding often results in retained skin that may constrict toes and tail tips. The damage results in necrosis and often loss of toes or part of tail. Another problem relating to difficulty with shedding includes retained shed on the eyelids resulting in conjunctivitis. Also retained shed along the commisure of the mouth and along the muco-cutaneous border oral cavity results in a stomatitis-like syndrome that can result in a loss of tissue and exposure of the mucus membranes.
Providing a humidity box as described for leopard and fat-tailed geckos may help, along with frequently soaking in a warm-water bath throughout the shedding process. Alternatively, providing a water bowl that is large enough for the tegu to lie in often results in them soaking themselves.
Topical medications to soften and protect damaged skin and ophthalmic ointments for eyes is often beneficial.
Bacterial and fungal dermatitis
Problems with shedding or with humidity (to much or too little) often result in bacterial or fungal dermatitis. Areas that are typically involved include extremities, such as toes and tail, areas around the oral cavity, and the inguinal and axillary regions. Skin biopsy may be the most effective way to determine the underlying etiology. Changing the husbandry by increasing humidity or decreasing humidity based on the history is important, along with topical and parenteral antimicrobials depending on histopathology and culture and sensitivity results. See Table 2.
Egg yolk celomitis/dystocia
Tegus are prone to reproductive-related abnormalities and specifically egg yolk celomitis, which primarily involves females in a pre-ovulatory stage rather than complications with oviductal eggs. The reason for the rupture and leakage of these ovarian follicles is unknown. Diagnosis is difficult, as these lizards tend to deteriorate suddenly without obvious signs. Radiology and ultrasonography may help with a diagnosis. Elevated white-blood cell counts with toxic cells; along with elevations of blood calcium values support the diagnosis. Endoscopic celioscopy may also be useful in diagnosis, but exploratory celiotomy will be necessary to flush out these females and remove or attempt to repair affected ovaries.
Tegus have a ravenous appetite and are often overfed. The decreased activity associated with captivity then results in over conditioning and obesity. Obesity may place additional stress on organ systems, which may result in a shortened life span. Obesity may also reduce the breeding activity of tegus and may contribute to reproductive problems, such as the egg yolk celomitis. Monitoring and regulating the dietary intake of these lizards is important. An exclusive diet of rodents for adult tegus can lead to obesity. Therefore, tegus should also be offered some fruit such as melon, papaya, and berries, along with lean cooked meat; tuna fish packed in water, invertebrates and occasional low-fat wet dog food. Encouraging exercise is also valuable.
Uromastyx Lizards (Uromastyx sp.) 3, 4, 15, 47
Nutritional Secondary Hyperparathyroidism (NSHP)
Because these desert diurnal lizards eat an omnivorous-based diet as juveniles and then a primarily herbivorous diet as adults they are very susceptible to NSHP. See the summary of this disease as described for other lizards.
The uromastyx lizard is a desert diurnal lizard that is prone to a variety of dermatological conditions typically related to an environment that is too humid. The skin can become thickened and have a yellow moist appearance to it. On skin biopsy both fungal and bacterial conditions can be found.
A specific dermatological condition has been described in the uromastyx lizard causing a chelitis associated with a filamentous gram-positive bacterium.48 The disease is characterized by a chronic hyperkeratotic dermatitis involving predominantly the lip region, but has also been associated with dorsolateral skin folds, the nuchal region, and the tail spines. Culture and sensitivity is unrewarding and a diagnosis is made on histopathology with the presence of gram-positive pleomorphic filamentous bacteria. Treatment involves systemic and topical antimicrobials based on biopsy and culture and sensitivity. See Table 2. It is important to ensure proper humidity in the environment and for these lizards to have a very high basking temperature (110-120F).
As more uromastyx lizards are bred in captivity we will likely deal with less gastrointestinal parasitism, however many of the lizards are still wild caught and often are heavily parasitized. Nematodes, cestodes and an overgrowth of protozoa can all be of concern. Fecal examinations should be performed routinely on uromastyx lizards and treatment initiated based on theses findings. See Table 1.
Uromastyx lizards, which are desert lizards, seem to be prone to respiratory disease. Common clinical signs include "popping sounds", increased respiratory rate, and obvious stridor. Open-mouth breathing and increased fluid or mucus in oral cavity or nares is often noted. A variety of gram-negative bacteria are usually isolated from a tracheal culture or wash. Aggressive treatment with combination antimicrobial therapy over a 4-6 week treatment course is indicated.See Table 2. Husbandry issues, such as ensuring warm enough temperatures (basking site at a minimum of 110F and up to 120F), need to be addressed. Additionally, it is important to make sure the humidity is not too high for these desert lizards.
Egg Yolk Coelomitis
Uromastyx lizards are also prone to reproductive-related abnormalities; specifically egg yolk celomitis primarily involving females in a pre-ovulatory situation rather than oviductal egg abnormalities. The reason for the rupture and leakage of these ovarian follicles is unknown. Radiology and ultrasonography may help with a diagnosis. Elevated white blood cell counts with toxic cells along with elevations of blood calcium values may be helpful diagnostically. Endoscopic celioscopy may also be useful in diagnosis, but exploratory celiotomy will be necessary to flush out these females and remove or attempt to repair affected ovaries.
Uromastyx lizards are prone to problems associated with oversupplementation of vitamins and minerals resulting in metabolic disease such as renal failure and gout. See the section on hypervitaminosis in old world chameleons for a summary of history, clinical signs, diagnostics and management.
Water Dragon (Physignathus cocincinus) 3, 4, 49, 50
Nutritional Secondary Hyperparathyroidism
See syndrome as described for the bearded dragon.
Rostral Trauma/Periodontal Disease
Water dragons are highly stressed lizards that typically will respond to approach by diving into the water along the rivers edge in their natural habitat. Thus, when they are startled in captivity they may "jump" forward into the side of the cage, smashing into the glass, which results in trauma to the rostrum. When this trauma is repeated over and over, the rostral tissue is often severely damaged, leading to a loss of tissue, stomatitis, exposure of bone, and osteomyelitis (Fig 7). Due to their acrodont dentition, damage to the fragile gum line often results in periodontal disease and osteomyelitis (see description of this condition above in the bearded dragon). Treatment involves minimizing trauma to the rostral area by providing visual barriers, such as construction paper around the sides at the bottom of the cage, to minimize the lizard smashing into the glass. Also, larger cages with adequate room to move around and branches for climbing and retreats will help to minimize trauma.
Water dragons are prone to gastrointestinal parasitism, especially as most are still wild caught. A variety of nematodes can be present. Fecal flotation to diagnose presence of parasites should be routinely performed on these lizards. For treatment refer to Table 1.
Female Reproductive Problems
Female water dragons will often present with reproductive-related problems including dystocia.
Refer to reproductive problems in the green iguana and the bearded dragon for history, clinical presentation, diagnostic approach and options for management.
See abscesses in green iguanas and bearded dragons for a description and management of this problem in water dragons.
Adult water dragons are prone to hepatic lipidosis. The syndrome is very similar to what is seen in bearded dragons. It is seen most frequently in over-conditioned water dragons and in females with reproductive activity. For a summary of clinical signs, diagnostic considerations and management see bearded dragon section.
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Table 1. Commonly Used Antiparasitic Agents in Lizards
Fenbendazole (Panacur, 100mg/ml) 50-100 mg/kg q 7days x 3-4 doses. For nematodes.
Ivermectin (Ivomec, 10mg/ml) 0.2 mg/kg p.o. q 10-14 days x 2-3 doses. For attempting to treat lungworms, such as pentastomids, or migrating nemtodes, such as filarids. In most cases, fenbendazole is safer and just as effective for other nematode infections. There have been reports of deaths in chameleons 42 and prehensile-tailed skinks51 given this drug, so it should be used with caution.
Praziquantel (Droncit, 56.8 mg/ml) 8-10 mg/kg s.c. q 14 days x 2-3 doses. For cestodes.
Metronidazole (Metronidazole Benzoate, 100mg/ml) 40-60 mg/kg p.o. q 7 days x 2-3 doses. For flagellates and amoebae.
Sulfadimethoxine (Albon, 50 mg/ml) 90 mg/kg (first day) p.o. followed by 45 mg/kg p.o. s.i.d. x 9 days. For coccidia.
This author has had some success in treating sick or unthrifty individual bearded dragons with coccidiosis with the regimen of sulfadimethoxine above along with thorough daily cage cleaning. This protocol, in conjunction with other supportive treatment (fluids, assisted feeding, appropriate husbandry changes), often results in the clinical improvement of a sick dragon. However, failure to eliminate coccidia with this regimen is common.
Another treatment for bearded dragons utilizes sulfadimethoxine orally at 50mg/kg (or trimethoprim-sulfa at 30mg/kg), daily for five days, then every other day until the coccidia is eliminated based on follow up fecal examinations.5
Table 2. Commonly used Antibiotics in Lizards
Amikacin (Amyglide-V): 2.5-5.0 mg/kg i.m. or s.c. q 48-72 hr. Ensure that the animal is well-hydrated prior to and during treatment.
Enrofloxacin (Baytril): 5-10 mg/kg i.m., s.c., or p.o. q 24-48 hrs. Subcutaneous or the intramuscular route initially followed by oral treatment seems to be the most effective method. Be aware that parenteral dosing may cause damage to the skin and/or muscle resulting in skin color changes. Giving an injection of subcutaneous fluid then placing the initial injection of baytril into the fluids will help to minimize tissue damage.
Ceftazidime (Fortaz) 20-40 mg/kg i.m. or s.c. q 48-72 hrs.
Carbenicillin (Geopen) 100 mg/kg i.m. q 24 hr.
Metronidazole 20 mg/kg po q 24-48 hrs.
Trimethoprim sulfa 30 mg/kg q 24-48 hrs.
The author often uses combination therapy if culture and sensitivities indicate it is necessary or to gain a broader spectrum (e.g. enrofloxacin and ceftazidime or amikacin and ceftazidime).
Copyright 2007 Scott J. Stahl, DVM, DABVP-Avian
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