Sugar gliders develop many of the same types of diseases that other mammals do, and many of the same drugs used to treat these diseases in mammals are also used in sugar gliders.
Drug Dosages for Sugar Gliders
Very few pharmacological studies have been performed in sugar gliders. Most published drug dosages have been extrapolated from those determined for cats, ferrets, and hedgehogs. For drugs and dosages commonly administered to sugar gliders, see the table Drugs Commonly Used to Treat Sugar Gliders.
Drugs Commonly Used to Treat Sugar Glidersa
Drug | Dosage | Considerations |
|---|---|---|
Antimicrobials | ||
Amoxicillin (1, 2, 3) | 30 mg/kg, PO or SC, q 12–24 h | For dermatitis |
Amoxicillin–clavulanic acid (1, 2 3) | 12.5 mg/kg, PO, q 12 h | Broad-spectrum against anaerobes and aerobes |
Chloramphenicol (1, 2) | 50 mg/kg, PO, q 12 h | Can rarely cause bone marrow suppression in humans |
Clindamycin (1, 4) | 5.5–10 mg/kg, PO, q 12 h | For periodontal disease |
Enrofloxacin (1, 3, 4, 5) | 2.5–5 mg/kg, PO or IM, q 12–24 h (1, 3, 4, 5) 10 mg/kg, PO, q 24 h (4) | Potential tissue necrosis when injected |
Marbofloxacin (1, 6) | 2–5 mg/kg, PO, SC, or IM, q 24 h | |
Metronidazole (1, 3) | 25 mg/kg, PO, q 12–24 h for 7–10 days | Possible CNS toxicosis at high doses or if underlying hepatic disease; use benzoate form |
Penicillin procaine (2, 3) | 22,000–25,000 IU/kg, SC or IM, q 12–24 h | |
Trimethoprim-sulfonamide (1, 2, 3, 4, 5, 7, 8) | 10–20 mg/kg, PO, q 12–24 h | |
Antiparasitics | ||
Carbaryl 5% powder (2, 3) | Topically or in cage, sparingly | Use small amounts to treat ectoparasites |
Fenbendazole (1, 2, 3, 4, 9) | 20–50 mg/kg, PO, q 24 h for 3 days | For roundworms, hookworms, whipworms, tapeworms, lower dose preferable |
Imidacloprid (9, 10) | 10 mg/kg, topically, q 30 days | Fleas |
Ivermectin (1, 2, 3, 9) | 0.2 mg/kg, PO or SC, once; repeat in 7–14 days for up to 3 treatments | For roundworms, hookworms, whipworms, nematodes, mites |
Metronidazole (1, 2, 11, 12, 13) | 25 mg/kg, PO, q 12–24 h | For intestinal protozoa; possible CNS toxicosis at high doses or if underlying hepatic disease; use benzoate form |
Piperazine (1, 12) | 50–100 mg/kg, PO, q 24 h | For nematodes |
Praziquantel (5, 14) | 5–10 mg/kg, PO or SC, once; repeat in 10–14 days | For cestodes, trematodes |
Pyrethrin powder (12) | Topically, as needed | For ectoparasites; use products formulated for kittens |
Selamectin (1, 2, 11, 15, 16) | 6–18 mg/kg, topically, once; repeat in 30 days | For ectoparasites; not effective against Demodex |
Antifungals | ||
Itraconazole (1, 2, 3) | 5–10 mg/kg, PO, q 12–24 h | For dermatophytes |
Nystatin (3, 4, 9, 11) | 2,000–10,000 IU/kg, PO, q 8 h for 3 days | For Candida |
Analgesics | ||
Buprenorphine (2, 3, 4, 8, 17) | 0.005–0.05 mg/kg, PO, SC, or IM, q 8–12 h | |
Butorphanol (1, 2, 3, 4) | 0.1–0.5 mg/kg, SC or IM, q 6–8 h | Possible sedation at higher doses |
Gabapentin (18, 19) | 3–5 mg/kg, PO, q 8–12 h | For neurotropic pain and anxiety; possible sedation at higher doses |
Tramadol (4, 17, 20) | 2–10 mg/kg, PO or IM, q 12 h | |
Anti-inflammatories | ||
Meloxicam (1, 2, 3, 7, 8, 12, 17) | 0.1–0.2 mg/kg, PO or SC, q 24 h 0.5 mg/kg, PO, q 24 h (17) | NSAID |
Prednisolone (1, 2, 3, 21) | 0.1–0.2 mg/kg, PO, SC, or IM, q 24 h | Corticosteroid |
Preanesthetics | ||
Atropine (1, 2, 12) | 0.01–0.04 mg/kg, IM, SC, or IV | To lessen intraoperative secretions, prevent and correct bradycardia |
Glycopyrrolate (1, 2) | 0.01–0.02 mg/kg, IM, SC, or IV | To lessen intraoperative secretions, prevent and correct bradycardia |
Anesthetics | ||
Bupivacaine (2, 22) | 1–2 mg/kg, local infiltration | Local anesthesia |
Buprenorphine (Bu) + midazolam (Mi) + meloxicam (Me) (5) | 0.01 mg/kg Bu + 0.1 mg/kg Mi + 0.2 mg/kg Me, IM | |
Butorphanol (9) | 0.4–1 mg/kg, SC or IM | |
Diazepam (1, 2, 12) | 0.5-2 mg/kg, PO, SC, IM, or IV | Sedative, anticonvulsant |
Isoflurane (1, 5, 23) | 1–5%, via face mask or intubation | |
Ketamine (2, 3) | 20–50 mg/kg, IM | |
Ketamine + midazolam (2, 3) | 10–20 mg/kg + 0.35–0.5 mg/kg, SC or IM | Administer ketamine 10 min after midazolam |
Lidocaine (22, 23) | As a 2% injection, ≤ 0.2 mL/kg (< 4 mg/kg), local infiltration | Local anesthesia |
Midazolam (1, 2, 3, 5, 24) | 0.1–0.5 mg/kg, SC, IM, IV, or intranasal | Sedative, anxiolytic, anticonvulsant; preferred over diazepam for injection |
Sevoflurane (3) | 1–5%, via face mask or intubation | Possible toxicosis; use cautiously |
Anesthetic Reversal Drugs | ||
Flumazenil (18, 25) | 0.02–0.1 mg/kg, SC or IM | For reversal of diazepam and midazolam |
Cardiac Drugs | ||
Enalapril (1, 2, 26) | 0.5 mg/kg, PO, q 24 h | ACE inhibitor |
Furosemide (1, 12, 26, 27) | 1–5 mg/kg, PO, SC or IM, q 6–12 h | Diuretic |
Pimobendan (1) | 0.3-0.5 mg/kg, PO, q 12 h | Positive inotrope and vasodilator |
GI Drugs | ||
Cisapride (1, 3, 4, 27) | 0.1–0.25 mg/kg, PO or SC, q 8–24 h | GI motility enhancer |
Maropitant citrate (2) | 0.2 mg/kg, SC, q 24 h | |
Metoclopramide (1, 3, 4, 9, 28) | 0.05–0.1 mg/kg, PO, SC, or IM, q 6–12 h | GI motility enhancer |
Hormones | ||
Calcitonin (3) | 50–100 IU/kg, SC or IM, q 7 d | Aid to calcium mobilization; calcium levels should be normal before use |
Vitamins and Minerals | ||
Calcium glubionate (1, 3, 27) | 150 mg/kg, PO, q 24 h | Calcium supplement |
Calcium gluconate (1, 27, 29) | 100 mg/kg, SC, q 12 h for 3–5 days | Calcium supplement; dilute to 10 mg/mL solution in saline |
Vitamin A (1, 3) | 500–5,000 IU/kg, IM, once (3) 50–500 IU/kg IM (1) | For dermatitis |
Vitamin B complex (1, 2, 3) | 0.01–0.2 mL/kg, SC or IM | Inject into SC fluids to decrease pain (stings on injection) |
Vitamin E (1, 3, 11) | 25–100 IU/glider, SC, q 24 h | |
Vitamin K (1, 2, 3, 4, 9) | 2 mg/kg, PO or SC, q 24–72 h (1, 2, 3) 2.5 mg/kg, SC, once; then 5 mg/kg, PO, q 24 h for 14 days (4, 9) | For intestinal and liver disease Treatment for anticoagulant rodenticide poisoning |
Other | ||
Dextrose (20%) (9) | 2–5 mL/kg, IV, slow | For hypoglycemia |
Doxapram (1, 2) | 2 mg/kg, SC, IM, IV, or sublingual | Respiratory stimulant |
Abbreviations: ACE, angiotensin-converting enzyme. aData are from the following sources:
bDuration of treatment, when not specified by a referenced study, is at the discretion of the prescriber and depends on the condition being treated. | ||
Bacterial Diseases of Sugar Gliders
Sugar gliders are susceptible to infection with common bacteria, including Pasteurella multocida (commonly contracted from pet rabbits), staphylococci, streptococci, Mycobacterium spp (especially in skin), Klebsiella spp, and Clostridiumspp (1). Listeria monocytogenes infection has also been reported in a sugar glider, potentially transmitted from a contaminated cantaloupe (2).
Clinical signs of disease in sugar gliders can be nonspecific; depression, loss of appetite, and weight loss are the most readily detected. Bacterial infections in gliders can present as opportunistic skin infections associated with trauma or can result in sepsis from underlying primary diseases.
Although sugar gliders are hindgut fermenters, broad-spectrum antimicrobial treatment is well tolerated, probably because diets fed in captivity can be digested without fermentation. Suspensions of palatable oral antimicrobials such as amoxicillin or amoxicillin/clavulanic acid have been used successfully in sugar gliders.
If indicated by culture and sensitivity testing or by failure to respond to first-line treatment, compounded formulations of oral chloramphenicol and enrofloxacin are also well tolerated by sugar gliders. These antimicrobials also can be administered intramuscularly into the epaxial muscles or subcutaneously over the shoulders.
Protozoal and Parasitic Diseases of Sugar Gliders
Toxoplasmosis is a common and serious disease of marsupials, and patients typically present with neurological signs and sudden death. Gliders can be infected with toxoplasmosis oocysts found in cat feces. Care should be taken to prevent cat feces from coming in contact with bedding or food of sugar gliders.
Treatment with oral trimethoprim/sulfamethoxazole can be initiated in suspected cases of toxoplasmosis; however, prevention is more successful than treatment.
Internal parasites rarely cause disease in captive gliders; however, giardiasis and cryptosporidiosishave been reported in captive animals (3, 4, 5, 6). For Giardia, metronidazole (compounded into a suspension for oral administration) is the recommended treatment. Coccidia can also cause severe, sometimes fatal diarrhea in young gliders; they can be contracted via fecal-oral transmission from other species. Strongyle eggs have been observed on fecal flotation.
Other internal parasites reported to infect sugar gliders include nematodes of the genus Parastrongyloides and Paraustrostrongylus and a liver trematode of the genus Athesmia. Fecal testing should be performed to identify parasites and appropriate treatment implemented. Injectable ivermectin and oral fenbendazole have been used to treat GI parasites.
Trichomonad infection in sugar gliders can cause diarrhea, wet and “sticky” joeys in the pouch, pouch discharge, and death (particularly in joeys). These clinical signs secondary to trichomonad infection are referred to as “ick” among sugar glider keepers; they were found to be caused by the trichomonad species Simplicimonas. Affected animals can be treated with oral metronidazole and supportive care (7).
Wild sugar glider nests generally contain a range of host-specific mites and fleas; in captivity, however, ectoparasites are uncommon. Dusting with pyrethrin or carbaryl powder (50 g/kg) can control fleas and mites. Both the nest and the animal should be treated. Selamectin also has been used to treat ectoparasites on sugar gliders.
Nutritional Osteodystrophy in Sugar Gliders
Pet sugar gliders maintained on a mainly fruit diet containing few gut-loaded insects or other protein sources are very susceptible to nutritional osteodystrophy (nutritional secondary hyperparathyroidism). This condition results from an imbalance in dietary calcium, phosphorus, and vitamin D and manifests clinically as posterior paresis progressing to hindlimb paralysis, muscle tremors, pathological bone fractures, and, in some advanced cases, seizures.
Chronic malnutrition can lead to increased liver and kidney values, hypoproteinemia, and anemia. Radiography typically reveals osteoporosis of the vertebral column, pelvis, and long bones. Measurement of ionized blood calcium typically demonstrates a low ionized calcium concentration.
Treatment of nutritional osteodystrophy involves cage rest; administration of calcium, vitamin D3, and fluids; assisted feeding; and correction of the diet. Midazolam (IM) or diazepam (IV, IM, intraosseous, or intrarectal) should be administered to stop seizures in sugar gliders. Calcitonin administered intramuscularly to severely affected gliders can decrease calcium resorption from bone after calcium supplementation has normalized plasma calcium levels.
Severe skeletal (especially spinal) deformities may not be reversible.
Dental Disease in Sugar Gliders
Unlike rodent teeth, sugar glider teeth do not grow continuously or require trimming. However, prophylactic scaling and polishing are suggested for sugar gliders because of the frequency of gingivitis and dental abscessation. Providing insects with hard exoskeletons in the diet can also help decrease tartar buildup (3).
Sugar gliders that consume large amounts of soft, sugary foods are prone to tartar buildup and periodontal disease. Tartar can be scaled off under anesthesia. Advanced periodontal disease or traumatic tooth fracture can lead to tooth decay and exposed roots, and, in severe cases, tooth root abscessation, osteomyelitis of the mandible or maxilla, and occasional extension of the abscess into the retrobulbar space (see retrobulbar abscess images).
Courtesy of Dr. Laurie Hess.
Radiography, CT, and oral endoscopy are helpful to delineate the extent of disease.
Fractured and decayed teeth in sugar gliders must be extracted, and tooth root abscesses must be debrided and cultured (both aerobically and anaerobically). Local lidocaine blocks can aid in surgical removal of infected teeth. When removing affected incisors, care must be taken not to cause mandibular symphysial fracture.
Affected animals should be treated with antimicrobials, analgesics, NSAIDs, and antiseptic mouthwash, made either for cats and dogs or (fruit-flavored) for children. Dietary modification to provide softer, more easily chewed foods could be necessary after surgery. Affected animals that do not eat after surgery must be syringe-fed until they eat on their own.
Abscesses have been reported in the gingiva and mucosa of young sugar gliders, and enteric bacteria have been cultured in these cases (3). Antimicrobial treatment should be based on the results of culture and sensitivity testing.
Diarrhea in Sugar Gliders
Potential causes of diarrhea in sugar gliders include the following:
bacterial infection by Escherichia coli, Clostridium spp, and others
GI parasites (nematodes, cestodes, protozoa)
malnutrition
stress
metabolic disease, such as liver or kidney disorders
dietary changes, especially in young animals
Sugar gliders with diarrhea should undergo fecal analysis for parasites, fecal bacterial culture and Gram's staining, blood testing (CBC and chemistry panel), and possibly imaging (radiography or ultrasonography, as indicated). Gliders with diarrhea should be given supportive care with fluids, supplemental feeding, and drug treatment, as dictated by the cause of the GI signs.
Rectal and cloacal prolapse can occur in gliders secondary to diarrhea and straining, and it is more common in malnourished animals. The prolapsed tissue must be cleaned, checked for necrotic areas (which must be debrided), and replaced under anesthesia. Vertical mattress sutures can be placed next to the vent to help prevent recurrence, and postoperative analgesics, antimicrobials, antiparasitics if indicated, and NSAIDs should be administered.
Pouch Disorders of Sugar Gliders
The pouch in female sugar gliders can become infected, and occasionally, secondary pouch prolapse occurs. Infections can be due to yeast or bacteria, as a result of mastitis or excessive grooming.
Culture and sensitivity testing, as well as cytological examination, should be performed on exudate in the pouch to try to identify the cause and guide treatment. The pouch should be cleaned gently with chlorhexidine solution diluted with warm water, inverted, and if prolapsed, placed back into its normal anatomical position.
Temporary stay sutures should be placed until infection and inflammation have resolved. Improving environmental sanitation to minimize the risk of infection, as well as decreasing behavioral stress by eliminating overcrowding or separating incompatible cagemates, might also be warranted.
Urinary Tract Disorders of Sugar Gliders
Sugar gliders can develop cystitis, crystalluria, and urolithiasis.Possible clinical signs include hematuria, stranguria, and dysuria. Affected gliders should undergo urinalysis plus urine culture and sensitivity testing, and should be properly hydrated.
Antimicrobial administration should be based on the results of culture and sensitivity testing. Cystotomy might be required to remove uroliths, which should be sent to a laboratory for analysis. Male gliders can develop urinary tract obstruction from uroliths and require urethrostomy if cystocentesis and flushing of the distal urethra do not relieve the obstruction. These gliders should receive analgesics, antimicrobials, fluids, and NSAIDs.
Sugar gliders with renal failure can show weakness and polyuria/polydipsia, and they should receive the same treatment as other mammals with renal disease. Renal failure is more common in geriatric sugar gliders, and the prognosis is usually guarded because damage could be irreversible.
An intact, adult male sugar glider was diagnosed with bilateral hydronephrosis and hydroureter secondary to functional urinary tract obstruction from inflammation/hyperplasia of the urinary bladder and ureteral epithelium of unknown cause (8).
Paracloacal Gland Impaction in Sugar Gliders
Both sexes of sugar gliders have three paracloacal glands (similar to anal glands in mammals) that can become infected or impacted. Expression of impacted glands can produce thick, mucoid discharge that should be cultured to guide antimicrobial selection and treatment.
Chronically or recurrently infected or impacted glands should be removed. Lidocaine is injected into the skin over each gland, where a single skin incision is made. Each gland is bluntly dissected free of surrounding connective tissue and then removed without rupturing it. Associated blood vessels can be ligated with absorbable suture or cautery. Incisions are closed with a single absorbable suture in a subcuticular pattern with or without tissue glue.
A paracloacal cyst was reported in an adult male sugar glider (9), and bladder herniation was diagnosed in an adult female sugar glider (10). Cancer has also been reported.
Neurological Disease in Sugar Gliders
Causes of neurological signs in pet sugar gliders include nutritional secondary hyperparathyroidism, exposure to toxins (eg, heavy metals; anecdotally, polyvinyl chloride from cages), bacterial meningitis, toxoplasmosis, traumatic brain injury, otitis media/interna, encephalitis from aberrant CNS migration of the nematode Baylisascaris procyonis, and encephalomalacia due to vitamin E deficiency.
Gliders exhibiting neurological signs should undergo a full evaluation, including blood testing (CBC and biochemical panel), fecal testing for parasites, radiography, and CT, plus CSF analysis, if indicated. For seizures, midazolam or diazepam should be administered. The prognosis in many of these cases is poor.
Neoplasia in Sugar Gliders
Several types of benign and malignant tumors have occurred in sugar gliders, including hepatocellular tumors, lymphoid neoplasia, mammary gland adenocarcinoma, cutaneous melanoma, scent gland tumors, dermal hemangiosarcoma, carcinomas, fibroma, histiocytoma, and sebaceous epithelioma. These tumors occur more commonly in older animals (11, 12).
Clinical signs of tumors in sugar gliders vary depending on the location and type of tumor. In most cases, metastatic disease has not been reported; however, the prognosis is usually poor.
Sugar gliders with tumors are usually treated with supportive care as needed, analgesia, antimicrobials if infection is present, and surgery to remove the primary tumor, if possible.
Hepatocellular carcinoma was reported simultaneously with adrenocortical carcinoma in a 15-year-old female sugar glider. Hepatic carcinosarcoma was also reported in a sugar glider (13). Dermal hemangiosarcoma was diagnosed in an 11-year-old female glider at the margin of the patagium. Soft tissue carcinoma associated with a microchip implant was reported in a mahogany glider (Petaurus gracilis). Malignant testicular interstitial cell tumor in a mahogany glider was managed by hemicastration. Transitional cell carcinoma with squamous differentiation was noted pericloacally in a 10-year-old male sugar glider. Paracloacal gland carcinoma was diagnosed in a male sugar glider that was self-mutilating its cloacal region, and a 9-year-old female sugar glider was found to have mammary adenocarcinoma that metastasized to sublumbar, axillary, and pouch lymph nodes, as well as to the lungs (3, 12, 14).
Behavior Disorders of Sugar Gliders
Sugar gliders live in colonies in the wild and are very social. Thus, in captivity they should be kept in groups of two or more. Gliders love to crawl into pockets or pouches, where they feel safe and more relaxed. Behavioral disorders can develop in sugar gliders housed alone, with incompatible mates, or in inappropriate cages. When housed singly, not given enough social stimulation, or not provided with a nest box or pouch in which to hide or enough room to exercise, they may self-mutilate their fur and skin, develop stereotypical behaviors, or become aggressive.
Anxious gliders can groom excessively, causing fur loss, particularly at the tail base. Anorexia, polyphagia/polydipsia, coprophagia, cannibalism, and pacing also occur in stressed gliders. A full workup that includes a thorough examination, blood work, and imaging should be performed to rule out underlying conditions that could be causing pain or discomfort, which can manifest as self-mutilation and excessive grooming.
Sexually mature male sugar gliders that lack access to females might self-mutilate the tail base, limbs, scrotum, penis, or perineum and can develop paraphimosis, in which the penis remains extruded from the cloaca and becomes traumatized and devitalized, necessitating amputation. These gliders should be treated with pain relievers, antimicrobials, and possibly antidepressants, plus an Elizabethan collar, to enable healing. Gabapentin, as both analgesic and anxiolytic, can also be useful in these cases. For proper socialization, self-mutilating gliders should spend at least 2 hours per day with other pet gliders, preferably at night when they are awake.
Miscellaneous Disorders of Sugar Gliders
Sugar gliders can develop cardiomyopathy/myocarditis, cataracts in juveniles (possibly associated with nutritionally imbalanced hand-feeding formulas, hyperglycemia, and vitamin A deficiency), cloacitis/vaginitis (females), mastitis (females), irregularity of ear margins or crusting of pinnae from ear mite infections, trauma (ocular injury/corneal abrasion, fractures, wounds, and lacerations), and retrobulbar abscesses associated with dental disease or facial bite wounds in competing males.
Endocrine-mediated alopecia has been reported primarily in older female sugar gliders (3). Diabetes has also been reported in a sugar glider, possibly secondary to acute pancreatitis that was treated with diluted NPH insulin (15). Gastric dilatation and volvulus due to unknown causes can also occur in sugar gliders presented for acute abdominal distention. Reproductive tract infection and pyometra have occurred in older female sugar gliders (16, 17). As in other mammals, these syndromes in sugar gliders are treated with medications and surgery, when indicated.
In addition, six adult sugar gliders with lethargy, tachypnea, and dyspnea were found to have pulmonary hyalinosis at necropsy, similar to lesions documented in the lungs of old dogs after death (18). Complications secondary to microchip implantation have been reported in sugar gliders and include self-mutilation resulting in wounds requiring medical and surgical intervention and ultimately leading to death in one case (19).
Hepatic copper accumulation has been reported on postmortem evaluation of sugar gliders with hepatopathy. Clinical signs included anorexia, lethargy, weight loss, neurological signs, icterus, and sudden death. Liver masses, particularly hepatic carcinomas, were commonly associated with increased copper accumulation. The cause is unknown (20).
Zoonoses of Sugar Gliders
Diseases that can infect sugar gliders, such as salmonellosis (21), giardiasis, leptospirosis, clostridiosis, Baylisascaris infection, and toxoplasmosis, are potentially zoonotic.
To prevent transmission of zoonotic diseases through a bite or a scratch, sugar gliders are best wrapped in a small towel when handled. Although their lower incisors are small, they are designed to bite through tree bark and can inflict substantial damage. Biting and scratching can be avoided by gentle handling and proper socialization.
All ocular, nasal, GI, and genitourinary discharges of sugar gliders should be treated as potentially infectious.
Key Points
Sugar gliders have specific nutritional requirements that predispose them to the development of nutritional deficiencies in captivity.
Many surgical procedures performed in mammals, such as spaying, castration, and dental surgery, can be performed in sugar gliders; however, these procedures must be adapted to the unique anatomical features of gliders.
Sugar gliders tend to self-mutilate postoperatively; therefore, subcuticular sutures and skin glue are recommended.
Sugar gliders are prone to many infectious and neoplastic diseases recognized in mammals, including dental abscesses, toxoplasmosis, and hepatocellular carcinoma.
For More Information
Johnson-Delaney CA. Sugar gliders. In: Quesenberry KE, Orcutt CJ, Mans C, Carpenter JW. Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery. 4th ed. Elsevier; 2021:385-400.
Brust DM, Mans C. Sugar gliders. In Carpenter JW, Harms CA, eds. Carpenter’s Exotic Animal Formulary. 6th ed. Elsevier; 2023:496-510.
Johnson-Delaney C. Sugar glider disease update: "ick". LafeberVet. January 22, 2016. Accessed October 30, 2024.
Johnson-Delaney CA, Lennox AM. Reproductive disorders of marsupials. Vet Clin North Am Exot Anim Pract. 2017;20(2):539-553.
Pignon C, Mayer J. Zoonoses of ferrets, hedgehogs, and sugar gliders. Vet Clin North Am Exot Anim Pract. 2011;14(3):533-549, vii.
Also see pet owner content regarding disorders and diseases of sugar gliders.
References
Varriale L, Russo TP, Pace A, et al. Microbiological survey of sugar gliders (Petaurus breviceps) kept as pets in Italy. Lett Appl Microbiol. 2019;69(6):399-402. doi:10.1111/lam.13233
Nichols M, Takacs N, Ragsdale J, et al. Listeria monocytogenes infection in a sugar glider (Pretaurus breviceps) - New Mexico, 2011.Zoonoses Public Health. 2015;62(4);254-257. doi:10.1111/zph.12134
Johnson-Delaney CA. Sugar gliders. In: Quesenberry KE, Orcutt CJ, Mans C, Carpenter JW. Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery. 4th ed. Elsevier; 2021:385-400.
Brust DM. Gastrointestinal diseases of marsupials. J Exot Pet Med. 2013;22(2):132-140. doi:10.1053/j.jepm.2013.05.005
Barbosa AD, Egan S, Feng Y, Xiao L, Balogun S, Ryan U. Zoonotic Cryptosporidium and Giardia in marsupials—an update. Parasitol Res. 2024;123(1):107. doi:10.1007/s00436-024-08129-w
Takaki Y, Takami Y, Watanabe T, Nakaya T, Murakoshi F. Molecular identification of Cryptosporidium isolates from ill exotic pet animals in Japan including a new subtype in Cryptosporidium fayeri. Vet Parasitol Reg Stud Reports. 2020;21:100430. doi:10.1016/j.vprsr.2020.100430
Johnson-Delaney C. Sugar glider disease update: "ick". LafeberVet. January 22, 2016. Accessed October 30, 2024.
Cusack L, Schnellbacher R, Howerth EW, Jiménez DA, Mayer J, Divers S. Bilateral hydronephrosis in a sugar glider (Petaurus breviceps). J Zoo Wildl Med. 2016;47(3):886-889. doi:10.1638/2016-0007.1
Thomas M, Parkinson L, Shaw G, Mans C. Paracloacal cyst in a sugar glider (Petaurus breviceps). J Exot Pet Med. 2019;29:40-44. doi:10.1053/j.jepm.2018.02.046
Chu M. Surgical management of posterior perineal urinary bladder herniation and cystolithiasis in a sugar glider (Petaurus breviceps). In: Venice ICARE: 3. International Conference on Avian, Herpetological, and Exotic Mammal Medicine, March 25th–29th, 2017 Italy: Proceedings. International Conference on Avian, Herpetological, and Exotic Mammal Medicine; 2017.
Stans J. Oncology of the sugar glider (petaurus breviceps): a comprehensive review. Veterinaria. 2023;72(2):135-141. doi:10.51607/22331360.2023.72.2.135
Kubiak M. Sugar gliders. In Kubiak M, ed. Handbook of Exotic Pet Medicine. John Wiley & Sons; 2021:125-139.
McCready JE, Fisher J, McCleery B. Clinical, imaging and pathological features of hepatic carcinosarcoma in a sugar glider (Petaurus breviceps). Vet Rec Case Rep. 2024;12(1):e764.
Gentz EJ, Richard MJ, Crawshaw G. Neoplasia in sugar gliders (Petaurus breviceps): thirty-three cases. In: 2003 Scientific Proceedings, 34th Annual Meeting of the American Association of Zoo Veterinarians. American Association of Zoo Veterinarians; 2003:132-134.
Lofgren N. Treatment of type II diabetes in a sugar glider. In: Proceedings. ExoticsCon 2023:305.
Bassan T, Cobos A, Mallol C, Abarca ML, Martorell J. Reproductive tract infection caused by Kocuria kristinae in an entire female sugar glider (Petaurus breviceps). Vet Rec Case Rep. 2022;10(4):e507. doi:10.1002/vrc2.507
Koizumi I, Okumura N, Kondo H. Pyometra in a sugar glider (Petaurus breviceps): surgical treatment and postoperative complications. J Vet Med Sci. 2023;85(11):1252-1256. doi:10.1292/jvms.23-0117
Sokol SA, Agnew DW, Lewis AD, Southard TL, Miller AD. Pulmonary hyalinosis in captive sugar gliders (Petaurus breviceps). J Vet Diagn Invest. 2017:29(5):691-695. doi:10.1177/1040638717703683
Fisher CJ, Tovar-Lopez G, Schiavone S, Muñoz Gutiérrez JF, Watson AM, Sadar MJ. Microchip implant induced dermatitis and self-mutilation in four sugar gliders. J Exot Pet Med. 2022;42:20-25. doi:10.1053/j.jepm.2022.04.003
Yuschenkoff D, Graham J, Barton BA, Garner MM. Evaluation of the clinical presentation and histologic lesions of hepatic copper accumulation in sugar gliders (Petaurus breviceps). J Exot Pet Med. 2021;39:51-56. doi:10.1053/j.jepm.2021.06.007
Nur Diana H, Saleha AA, Azlan CM, Bejo SK, Zunita Z, Fauziah N. Oral microbes of pet sugar gliders and detection of Salmonella in their faeces. J Vet Malaysia. 2016;28(2):24-25.
