Diseases and Syndromes of Sugar Gliders

Sugar gliders are susceptible to infection with common bacteria, including Pasteurella multocida (commonly contracted from pet rabbits), staphylococci, streptococci, Mycobacterium sp (especially in skin), Klebsiella sp, and Clostridium. Clinical signs may be nonspecific, with depression, loss of appetite, and weight loss being the most readily detected. Bacterial infections in gliders may present as opportunistic skin infections associated with trauma or may result in sepsis from other underlying primary diseases. Although sugar gliders are hindgut fermenters, broad-spectrum antibiotic therapy is well tolerated, probably because diets fed in captivity are digestible without fermentation. Injectable, long-acting penicillin with clavulanic acid is an appropriate first-line antibiotic. If indicated by culture and sensitivity or by failure to respond to first-line treatment, chloramphenicol and enrofloxacin are also well tolerated in this species. Injections can be given IM into the epaxial muscles or SC over the shoulders. Palatable oral medications may also be administered.

Toxoplasmosis is a common and serious disease of marsupials, typically presenting with neurologic signs. Gliders may be infected with toxoplasmosis oocysts found in cat feces. Care should be taken to avoid cat feces coming in contact with the bedding or food of sugar gliders. Prevention is more successful than treatment. Coccidia may also cause severe, sometimes fatal diarrhea in young gliders and may be contracted via fecal-oral transmission from other species.

Internal parasites rarely cause disease in captive gliders, but giardiasis and cryptosporidiosis have been seen in captive animals. Strongyle eggs also have been seen on fecal flotation. Internal parasites reported to infect sugar gliders include nematodes of the genus Parastrongyloides and Paraustrostrongylus and a liver trematode of the genus Athesmia. Wild sugar glider nests generally contain a range of host-specific mites and fleas, but ectoparasites are uncommon in captivity. Dusting with pyrethrin or carbaryl powder (50 g/kg) has controlled fleas and mites. Both the nest and the animal should be treated. Selamectin also has been used to treat ectoparasites on sugar gliders. Ivermectin and fenbendazole have been used to treat GI parasites.

Pet sugar gliders maintained on a mainly fruit diet with 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 a posterior paresis progressing to hindlimb paralysis, muscle tremors, pathologic bone fractures, and sometimes, in advanced cases, seizures. Chronic malnutrition can lead to increased liver and kidney values, hypoproteinemia, and anemia. Radiography reveals osteoporosis of the vertebral column, pelvis, and long bones in particular. Measurement of ionized blood calcium typically demonstrates a low ionized calcium level. Treatment involves cage rest; administration of calcium, vitamin D₃, and fluids; assisted feeding; and correction of the diet. Seizuring gliders should be given diazepam IV, ideally, or if not possible, IM, intraosseously, or intrarectally, to stop seizures. Severely affected gliders may be given calcitonin to decrease calcium resorption from bone once calcium supplementation has normalized plasma calcium levels. Severe skeletal (especially spinal) deformities may not be reversible.

Sugar gliders consuming large amounts of soft, sugary foods are prone to tartar buildup and periodontal disease. Tartar may be scaled off under anesthesia. Advanced periodontal disease or traumatic tooth fracture may lead to tooth decay and exposed roots, necessitating extraction and treatment with antibiotics, analgesics, NSAIDs, and antiseptic mouthwash (either made for cats and dogs or fruit-flavored for children). Unlike rodent teeth, sugar glider teeth do not grow continuously or require trimming.

Potential causes of diarrhea in sugar gliders include bacterial infection (from Escherichia coli, Clostridium sp, and other bacteria), GI parasites, malnutrition, stress, and metabolic disease (such as liver or kidney disorders). Sugar gliders with diarrhea should have a fecal analysis for parasites, fecal bacterial culture and Gram stain, blood testing (CBC and chemistry panel), and possibly radiographs. Gliders with diarrhea should be given supportive care with fluids, supplemental feeding, and drug therapy, as dictated by the cause of the GI signs. Rectal and cloacal prolapse can occur in gliders secondary to diarrhea and straining and is more common in malnourished animals. The prolapsed tissue must be cleaned, checked for necrotic areas (which must be removed if present), and replaced once the glider is anesthetized. Vertical mattress sutures may be placed next to the vent to help prevent recurrence, and the glider should be given postoperative analgesics, antibiotics, and NSAIDs.

Sugar gliders can develop cystitis, crystalluria, and urolithiasis. They may show hematuria, stranguria, and dysuria. Affected gliders should have a urinalysis and urine culture and sensitivity testing and should be properly hydrated. Antibiotics should be administered based on results of culture and sensitivity testing. Cystotomy may be required to remove uroliths. Male gliders may 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, antibiotics, fluids, and NSAIDs. Sugar gliders with renal failure may show weakness, polyuria, and polydypsia and should be treated with standard treatment used in other mammals for renal disease.

Causes of neurologic signs in pet sugar gliders include nutritional secondary hyperparathyroidism, bacterial meningitis, toxoplasmosis, traumatic brain injury, otitis media/interna, encephalitis from aberrant CNS migration of Baylisascaris procyonis, and encephalomalacia from hypovitaminosis E. Gliders exhibiting neurologic signs should undergo a full evaluation, including blood testing (CBC and chemistry), fecal testing for parasites, radiographs, and CT scanning plus CSF analysis, if indicated. Prognosis in many of these cases is poor.

Gliders are prone to neoplastic disease in old age. Hepatocellular tumors and lymphoid neoplasia are common, as is mammary gland adenocarcinoma. Cutaneous melanoma, scent gland tumors, bronchogenic carcinoma, and chondrosarcoma of the jaw also have been reported. A soft-tissue carcinoma associated with a microchip implant was reported in a mahogany glider (Petaurus gracilis). A 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-yr-old male sugar glider.

Sugar gliders may develop cardiomyopathy/myocarditis, cataracts in juveniles (possibly associated with nutritionally imbalanced handfeeding formula, hyperglycemia, and hypovitaminosis A), cloacitis/vaginitis (females), irregularity of ear margins/crusting of pinnae from ear mite infections, and retrobulbar abscesses associated with facial bite wounds in competing males. These syndromes are treated with medications and surgical procedures, when indicated, similarly to those used in other mammals with these conditions.

Sugar gliders live in colonies in the wild and are very social. Thus, they should be kept in captivity 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 stereotypic behaviors, or become aggressive. Anxious gliders will overgroom, causing fur loss, particularly at the tail base. Anorexia, polyphagia, polydipsia, coprophagia, cannibalism, and pacing are also seen in stressed gliders. Sexually mature male sugar gliders without access to females may self-mutilate the tail base, limbs, scrotum, penis, or perineum and may develop paraphimosis, in which the penis remains extruded from the cloaca and becomes traumatized and devitalized, necessitating amputation. These gliders should receive pain relievers, antibiotics, and possibly antidepressants, plus an Elizabethan collar, to enable healing. At least 2 hr per day, preferentially at night, when they are awake, must be spent with pet gliders for proper socialization.

Diseases that may infect sugar gliders, such as salmonellosis, giardiasis, leptospirosis, clostridiosis, and toxoplasmosis, are potentially zoonotic. Sugar gliders are best handled wrapped in a small towel, because they may bite and scratch, and although they are small, their lower incisors, which are designed to bite through tree bark, may inflict significant damage. Biting and scratching can be avoided by gentle handling and proper socialization. All ocular, nasal, GI, and genitourinary discharges should be treated as potentially infectious.