Presenting problem: Paresis, Paralysis, and Tremors in Sugar Gliders

Understanding neurologic deficits in the glider

The sugar glider (Petaurus breviceps) is a small, nocturnal marsupial native to New Guinea and Australia. Sugar gliders are omnivores that eat arthropods and plant products, such as eucalyptus phloem sap, manna, honeydew, nectar, and pollen, in the wild (Table 1).

Sugar glider on tree

Figure 1. Sugar gliders (Petaurus breviceps) are omnivores native to New Guinea and Australia. Image by Comfortably Gruntled. Click to enlarge

Table 1. Plant exudate vocabulary
TermDefinition
Acacia gumA hardened sap secreted by the acacia tree in response to plant injury
Eucalyptus phloem sapA highly digestible simple carbohydrate that also serves as a source of minerals
HoneydewExcess sugar secreted by sap-sucking insects
MannaCrusty, white sugar left at the site of plant injury
NectarCarbohydrate-rich liquid produced by nectaries glands within plants

Insects are the main component of the sugar glider diet during the spring and summer (Box 1). Plant exudates make up only a small portion of diet during warm weather seasons, but gliders primarily eat plant exudates during the autumn and winter (Box 3). Acacia gum, secreted in response to plant injury, is a calcium-rich, complex carbohydrate digested by commensal organisms in the glider’s large cecum and colon. Gum makes up a large portion of the wild glider’s diet.

Box 1. Popular insect prey in free-ranging sugar gliders

  • Moths

  • Beetles

  • Insect larvae

  • Spiders

A variety of diets have been described for use in pet sugar gliders, however one regimen commonly recommended by veterinarians consists of (Johnson-Delaney, Ness):

  • 50% insectivore diet such as Mazuri Insectivore Diet (St. Louis, MO), Insectivore-Fare (Reliable Protein Products; Phoenix, AZ) or NutriMax (Vets Pride; Nashville, TN).
  • 50% carbohydrate such as the popular carbohydrate source Leadbeater’s mixture (Box 2), an artificial nectar formula initially formulated to feed captive Leadbeater’s possum (Gymnobelideus leadbeateri). (Ness #3, 13, 16)
Box 2. Leadbeater’s mixture

  • 150 ml warm water

  • 150 ml honey

  • 1 shelled hard-boiled egg

  • 25-gram high protein baby cereal

  • 1 teaspoon multivitamin

Leadbeater’s mixture can be refrigerated for 2-3 days or frozen in ice cube trays. There are many recipes for “modified” Leadbeater’s mixtures, however these have typically been altered for taste and their nutritional content may be suboptimal (Ness). The primary carbohydrate source can be supplemented with products such as Gliderade (Avico; Fallbrook, CA) or lory nectar (Nekton-Lori; Clearwater, FL) several times a week.

  • Insects and diced produce, such as apples, grapes, kiwi, orange with skin, melon, papaya, mango, carrots, leaf lettuce, and sweet potato, should generally make no more than 5% of total diet fed (1 to 2 teaspoons daily.) “Gut load” insect prey, like crickets, mealworms, or waxworms, by offering a high calcium feed before feeding out.
  • Gum arabic, also known as acacia gum, can be purchased in powder form, mixed into a thick paste with fruit juice or lory nectar, and placed in branch holes or on surfaces (Ness) with bits of produce or insects to stimulate foraging and provide enrichment.
Sugar gliders in food cup

Figure 2. Sugar gliders love fruit but this food item should make up no more than 5% of total diet fed. Large amounts of calcium-deficient fruits increase the risk of metabolic bone disease. Image by LostinTexas.

Although there is little medical information available on sugar gliders in captivity, nutritional secondary hyperparathyroidism or metabolic bone disease is recognized as a common problem in this species. Affected animals are often fed diets rich in calcium-deficient fruits and insects.

Presenting signs can include generalized weakness, ataxia, and/or rear limb weakness (Box 3). Neurologic deficits can progress until the sugar glider is unable to walk or climb. Intermittent fine muscle tremors that worsen over time may also be observed. If not corrected, disease can progress to seizures or even tetany. A common presenting sign is acute collapse with the glider found on the cage floor. Affected animals can also suffer from pathologic fractures, and pelvic or spinal deformities but this is relatively rare.

Box 3. Signs of metabolic bone disease in the sugar glider can include:

  • Generalized weakness

  • Ataxia

  • Rear limb paresis

  • Rear limb paralysis

  • Muscle tremors

  • Tetany

  • Seizure activity

  • Pathologic fractures

  • Pelvic or spinal deformities

Key points of urgent care

Consider nutritional secondary hyperparathyroidism in sugar gliders as a medical emergency. Whenever possible collect blood for chemistry analysis before starting treatment (see diagnostics below). Administer injectable calcium when indicated (Table 2) and provide supportive care such as nutritional support and fluid therapy.

Table 2. Medical mgmt. of metabolic bone disease in sugar gliders
DrugDoseRouteFrequencyComments
Calcium glubionate150 mg/kg POq8-24h
Calcium gluconate100 mg/kgSCq12hDilute in saline 1:1
100-150 mg/kgIV,IO
PO: per os, SC: subcutaneous, IV: intravenous, IO: intraosseous, q: every; h: hour

Sugar glider drug dosages are generally extrapolated from use in other species and are anecdotal. Intravenous injections are difficult, but can be given under sedation (midazolam 0.05-0.35 mg/kg IM) or inhalant anesthesia (sevoflurane, isoflurane) into the lateral saphenous or cephalic veins.

Anticonvulsant therapy may be needed for patients that have been seizuring for a long time. Dosages are extrapolated from small animal treatments, and can be administered parenterally, per os, or into the rectum via cloacal infusion.

Administer warmed fluids by the intraosseous, intraperitoneal, or subcutaneous route. Maintenance fluid requirements are estimated at 60-100 ml/kg/day (Corriveau).

  • Subcutaneous fluids should be given over the dorsal midline of the thorax to prevent fluids from settling into the patagium or wing web where they will be absorbed slowly.
  • Place intraosseous catheters into the proximal tibia via the tibial crest or into the proximal femur by way of the trochanteric fossa. A 25-to 23-gauge needle can serve as an intraosseous catheter in the sugar glider.
  • Inject intraperitoneal fluids into the lower left abdominal quadrant. Viscera may be displaced cranially by placing the patient on a binder with its head directed down.

Provide supplemental heat to hypothermic patients using heating pads, forced air warming devices, and incubators. Radiant heat sources and hot-water bottles can also be used but the patient must be monitored especially well to prevent overheating under the heat lamp or rapid cooling as the water bottle cools.

Nutritional support can be easily provided by syringe feeding Leadbeater’s formula, Smart HPW (Vets Pride; Nashville, TN) and/or commercial insectivore diet gruel

Any fractures present should be stabilized using external coaptation techniques.

 

Case management

Clinical signs and dietary history are often enough to develop a strong clinical suspicion. Use additional testing to confirm your suspicions.

 

History

Obtain a detailed history that includes information on patient diet and husbandry:

  • What is the diet offered?
  • What does the sugar glider actually eat and in what proportions?
  • Is vitamin-mineral supplementation provided?
  • Are insects “gut-loaded” or fed a calcium-rich diet prior to feeding?
  • Describe the cage setup in detail including cage size and the materials used to construct the cage. Galvanized wire incorporates zinc and lead components.
  • What is the cage substrate? The aromatic oils in cedar and pine shavings can be toxic.
  • Are there cats in the household? (If the answer is yes, this pushes toxoplasmosis higher on the differential diagnosis list.)
  • Has the glider been reluctant to move? Has it missed landings, bounced off walls, or fallen frequently?
  • Describe the glider’s appetite and water intake.

Hands off examination

Careful visual exam should gather as much information as possible including:

  • Degree of mental alertness
  • Ability to grip with all four feet
  • Truncal lift
  • Gait: Is lameness observed? Does the sugar glider drag its pelvis and/or tail?

Physical examination

Healthy sugar gliders normally vocalize extensively when restrained. Obtain a body weight using a gram scale (Table 3), and measure vitals.

Table 3. Average body weights in sugar gliders
Male113-160 grams
Female80-142 grams
  • The normal heart rate is 200 to 300 beats per minute.
  • Cloacal temperature is typically 89.6°F (32°C). Ness recommends gently directing the thermometer dorsally into the rectum. Rectal temperature is typically about 97.3°F (36.3°C).
  • In addition to normal skin turgor over the dorsum, the hydrated sugar glider should display good elasticity of the patagium or gliding membrane.
  • Palpate the limbs and joints. Closely inspect the toes.
  • The semi-prehensile tail should display tone.
  • Evaluate body condition. Malnutrition can lead to obesity, weight loss, blindness, cataracts, and alopecia.
  • Evaluate proprioception, tail and toe pinch, and the righting reflex.
  • Assessment of spinal reflexes is difficult to impossible since sugar gliders tend to cling to the handler while resisting limb or joint manipulation (Ness).
  • Palpate along the spine for lumps, bumps, or deviations.

Differential diagnoses

Common causes of metabolic bone disease (MBD) include diets rich in calcium-deficient fruits and insects and improper calcium: phosphorus ratios. Since sugar gliders are nocturnal, gastrointestinal absorption of vitamin D3 is much more important than full-spectrum light (Johnson 2008).

Less common causes of MBD include disease processes that interfere with normal vitamin D metabolism such as renal, liver or gastrointestinal problems, as well as thyroid or parathyroid disease.

Other important potential causes of weakness or neurologic deficits in the sugar glider include hypoglycemia, toxic exposure, or trauma (Table 4).

Table 4. Potential causes of weakness and neurologic deficits in the sugar glider*
Disease categoriesDifferentials
DDegenerative
AAnomalous
MMetabolic

  • Hypoglycemia

NNutritional

  • Nutritional secondary hyperparathyroidism

  • Hypovitaminosis E causing encephalomalacia

Neoplasia

  • Structural neurologic disease

IInfectious

  • Otitis media

  • Toxoplasma encephalitis

  • Baylisascaris procyonis larval migrans (outdoor gliders)

  • Cryptococcosis

Inflammatory


Idiopathic

  • Involuntary Tremoring Syndrome of Sugar Gliders

TTrauma

  • Involuntary Tremoring Syndrome of Sugar Gliders

Toxic

  • Long bone fractures or dislocations

  • Soft tissue trauma

  • Heavy metal toxicity

  • Aromatic oils in wood shavings

*The most important differentials are bolded.

A newly emerging condition that causes neurologic signs in sugar gliders is called “Involuntary Tremoring Syndrome”. Affected gliders are typically young (3-6 months of age). The cause of this syndrome does not appear to be congenital or husbandry-related because affected sugar gliders are from a wide range of sources and are fed a variety of diets considered acceptable. Organic and inorganic toxicity related to cage wiring is one of the prevalent theories. Onset of neurologic signs is acute and can progress to death within days.

 

Diagnostics

  • Venipuncture can be challenging and is not always possible until the patient is warm and rehydrated. Whenever possible perform a complete biochemistry panel and complete blood count. Although hypocalcemia and hyperphosphatemia are classic findings in metabolic bone disease, plasma or ionized calcium and phosphorus levels can be within normal limits in early, even symptomatic, cases. Other common findings in the sugar glider with malnutrition can include hypoproteinemia and anemia.If only a small blood sample can be collected, measure blood calcium and phosphorus levels. If anything else is available, make a blood smear and fill a microhematocrit tube to measure packed cell volume and total protein.
  • Use survey radiographs to evaluate bone quality and assess the patient for the presence of fractures.It may be possible to radiograph conscious gliders when they are severely debilitated. In other patients, administer light inhalant anesthesia using isoflurane or sevoflurane or sedate with midazolam (0.05-0.35 mg/kg IM) (Lennox, Ness).

Therapeutics

Management of nutritional secondary hyperparathyroidism is described above, and relies upon calcium administration and supportive care. If there is no response to calcium, consider treatments used in the management of tremor syndrome.

  • Move the sugar glider to a new cage.
  • Continue aggressive supportive care.
  • Administer injectable vitamin B complex 0.01 ml SC (0.01-0.02 ml/kg IM) while the glider is anesthetized or diluted.
  • Additional medications tried have include heavy metal chelation (calcium EDTA 25 mg/kg SC BID x 5d), prednisone (1 mg/kg PO SID x 7d, then taper), and/or metronidazole (15 mg/kg PO SID x 14d).

The majority of animals affected with this syndrome improve after the cage environment is changed and aggressive supportive care is provided. Visit the Association of Sugar Glider Veterinarians website for additional advice.

Injectable vitamin E/selenium (10 IU/kg) can also be administered to sugar gliders when hypovitaminosis E is suspected (Pye 2009).

 

Prognosis

The prognosis for nutritional secondary hyperparathyroidism is best when disease is recognized early. Advanced cases can be fatal since the patient may not respond to treatment.

References