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Its Causes . . . Its Cure


Introduction and Background

Numerous groups and wildlife facilities, as well as individual rehabilitators, have used (or are using) some form of the Modified Jurgelski Diet for opossums (90% kitten chow: 10% raw beef liver), or others with even less clinical evidence behind their recommendation. Many use these innocently thinking they are safe and appropriate. The majority are NEITHER!

Ironically, caregivers strictly following the MJ diet (from 80 grams) are seeing the most rapid onset of dramatic signs of Nutritional Metabolic Bone Disease (NMBD); whereas, caregivers still providing at least some fruit and vegetables, or those who give it to older opossums, are seeing delayed onset of overt signs of NMBD. These latter opossums are often more severely affected by skeletal and systemic complications due to their longer duration on this diet.

In contrast, the diet NOS recommends will not cause NMBD when used exactly as published. However, if its user "improvises" – usually with protein (fish, chicken, etc.) far in excess of that recommended – problems can and do occur (see letter to Editor, Vol. 10, No. 1, "Possum Tales, January, 1996).


  • ANY DIET, when used in specific, INCORRECT ways, can cause NMBD!!
  • CERTAIN DIETS will cause NMBD EVERY TIME, regardless of usage.


This report and a companion one on details of portion quantities in NOS-recommended diets (see "Possum Tales, Vol. 10, No. 2-3, July, 1996) discuss these issues in an effort to provide clarification. This is not intended to be an all-inclusive treatise on NMBD; but it contains the basics to more fully comprehend the nature of the problem with improperly balanced diets .

I sincerely hope all our readers — veterinarians, rehabilitators, orphan care-givers, pet guardians, and wildlife appreciators— will read that which follows . . . then USE THE INFORMATION! Use it in discussions with others, share it on the internet and in Facebook groups, and in communications to friends and those caring for opossums. Each of us – as opossum ambassadors – has the responsibility to get involved!

Eventually, enough people will have the CORRECT information; this will serve as a buffer against the continued spread of this scourge to opossums’ bodies and lives . . . rather like a wide-spread vaccination program which – ultimately – stops an epidemic. For NMBD is becoming a nation-wide epidemic from the proliferation of unbalanced diets.


The Metabolic Bone Disease Complex:

Metabolic bone disease ("MBD") is the term for an entire group of diseases which occur as a result of: (1) defective bone formation, (2) excessive bone resorption, or (3) some combination of the two.

Defective formation, in its "pure" form, is either osteoporosis (insufficient bone formation) or rickets/osteomalacia (defect in mineralization of bone). Excessive resorption, in its "pure" form, results from too much osteolysis (bone breakdown at the cellular level).

In their least complicated presentations, MBD is classified as one of the following disorders (NOTE: in "real life" one frequently sees combinations):

  1. Nutritional secondary hyperparathyroidism, caused by intake of low calcium:high phosphorous foods (i.e., protein in excess); ratios of calcium:phosphorus can reach 1:16 or greater! Most mammals require their diets to have a ratio of 1.0:1.0 to 1.2:1.0. Low calcium intake leads to a fall in blood calcium; this activates parathyroid hormone, which, in turn, stimulates demineralization of bone and release of calcium to maintain blood levels. This is independent of Vitamin D. The activation of the parathyroid hormone also increases urinary calcium loss.

  2. Rickets (in young) or osteomalacia (in adult) is rare, due to widespread availability of Vitamin D in food. Vitamin D deficiency will lead to low calcium:low phosphorus, because of reduced calcium absorption by and use in the body. Vitamin D works best when ingested with Vitamin A. But excesses in A or D can cause functional deficiency in the other (though it may be at adequate levels).

  3. Renal osteodystrophy - accelerated calcium loss from the bones and out via kidneys, due to insufficiency or failure of these organs. Can be temporary (e.g. as a result of medication or certain vitamins), or progressive (e.g. in renal disease).

  4. Hypervitaminosis A osteopathy - Depending on the degree or chonicity of excessive Vitamin A intake, it causes varying amounts of increased bone deposition or accelerates calcium loss from bones and from the body.


Origination and Development of Clinical Metabolic Bone Disease ("MBD"):

The precise circumstances which lead to MBD usually vary from one facility or individual to another. For, although its development involves inappropriate levels of ONE OR MORE of the following, no two situations are exactly the same:

  1. Protein in excess (calcium:phosphorus ratio is too low, sometimes dramatically so!).

  2. Vitamin A (deficiency or excess).

  3. Vitamin D (deficiency or excess).

  4. Miscellaneous. A variety of possible, though less frequently seen, problems. One example is an incident wherein an amoxicillin overdose caused temporary renal dysfunction with resulting accelerated loss of urinary calcium.


Vitamin A or D Deficiency as a Cause of NMBD:

"Pure" deficiencies of Vitamins A or D are essentially non-existent in orphan care. Infant wildlife formulas all contain some form of these nutrients in sufficient quantities to augment the orphan’s own body stores. Some formula mixes actually contain very high levels which can lead to MBD (see below).

In the late infant juvenile period, prior to release, "pure" deficiency of Vitamin A or D can theoretically occur. But most diets fed opossums in captivity prior to release are rarely deficient in either vitamin due to wide-spread fortification in commercial chows. Although they are lower in A than opossums appear to require (NOTE: cat chow is higher in Vitamin A than are dog chows), they are usually sufficient to augment whatever body stores remain until they are released . . . but only if they are not fed protein in excess! Appropriate deworming with levamisole by injection removes the potential drain of vitamins and nutrients by parasites. NOTE: Actually, excess Vitamin A is a greater potential danger; it is involved in MBD caused by the "MJD" or similar diets (see below)!

Deficiency of one or both vitamins may be present in adult opossums having the so-called "emaciation syndrome", where cachexia (malnutrition, wasting), parasitism and prolonged nutritional deprivation is frequently associated with states of systemic infection, trauma, etc. In these cases, body muscle, organ mass and fat depot sites are reduced. Vitamin A and D stores are reduced or near absent, too. It is uncommon to find clinical evidence of bone density loss of any significance, however, unless there is associated renal insufficiency (see renal osteodystrophy discussion). Most of these animals – were they not treated appropriately – would die of all their other problems long before fractures or other bone damage might occur. A proper and balanced diet is of extreme importance, of course, for recovery of these animals.

Vitamin D deficiency leads to rickets. It is seldom recognized now in human populations in developed countries – unless nutrition is inadequate and the individual receives no sunlight (the best means to our bodies of forming Vitamin D). Although opossums in infancy may be exposed to some sunlight, they seldom are for the bulk of their lives. Their primary source of this vitamin is their food – predominantly from insects, slugs, snails, mammals, etc., which comprise approximately 70% of their diet. A slightly analogous situation exists in humans: The more pigment in one’s skin the longer exposure to sun is required to form adequate levels of Vitamin D; dietary sources can play a vital role in these circumstances.


Calcium:Phosphorus Ratio less than Minimum of 1:1 as a Cause of NMBD:

Many foods, in addition to beef, chicken, fish, eggs, or organ meats, contain protein. Even vegetables! The difference is, the calcium:phosphorus ratio is usually better (i.e. closer to the desired ratio) in vegetables and, of course, dairy foods, than it is in "pure protein" foods. Additionally, not all proteins are "created equal". For example, organ meats and mackerel have a much lower ratio than do sardine, salmon or chicken, and are also disproportionately higher in Vitamin A and D. One must examine more than a few constituents of the foods we feed to fully assess their suitability.


Vitamin A and/or D in EXCESS as a Cause of NMBD:

Paradoxically, these vitamins . . . which, in deficiency, can lead to bone calcium loss, weakened and fractured bones, mobility problems, septemic illness via organ damage and pain . . . these vitamins in EXCESS will also lead to these same problems and often far worse organ damage! It may also happen more quickly than with other possible causes of NMBD.

Vitamin A, in excess, increases osteoclast (cells which resorb bone) activity. This leads to hypercalcemia (overload of calcium in the blood stream) and, initially, more bone formation (possibly fusion) along certain joints and the spine. It also damages renal tubules which, if it continues, causes excessive calcium excretion and, ultimately, hypocalcemia (shortage of calcium in the blood stream). The animal experiences deep bone pain, has flaky, dry skin, a poor appetite, nausea, and diarrhea. The liver may be enlarged; there is often excessive urine output. Discontinuing the vitamin will usually reverse all signs within days. But, bone damage may or may not be fully reversible, depending upon the presence and degree of deformities.

Vitamin D in excess is the most toxic vitamin. It, too, increases osteoclast activity, and causes hypercalcemia and urinary calcium excretion. Additionally, it leads to calcium deposition in heart and skeletal muscles, artery walls and the lungs. The animal is anorexic, nauseated, and may vomit. Continued excess may cause hypertension and severe kidney damage from calcium deposition in the tubules. Discontinuation of excess Vitamin D results in quick recovery from all signs, except for any deformities in bone.

Only time, a properly balanced diet, and a planned exercise program will enhance recovery and assist the patient in remodeling damaged bones.


Calcium Supplementation:

Calcium supplementation in the opossum should be limited to high calcium food sources in controlled amounts for a restricted length of time. NO PURE calcium supplements should be used, EXCEPT in severe cases of NMBD for only the first few days of treatment.

There is NO ADVANTAGE to continuing calcium supplements; the opossum is extremely efficient at absorbing and utilizing dietary calcium from a BALANCED diet. Supplements can lead to hypercalcemia, depressing of osteoclast activity, and depression of bone and cartilage remodeling and maturation. In other words: TOO MUCH OF A "GOOD THING" – even calcium! – CAN IMPAIR DEVELOPMENT AND REMODELING OF BONE!


Typical Sequence of Signs, According to Degree or Duration of NMBD:

Once signs of NMBD are recognized, regardless of the duration or extent, ONE MUST IMMEDIATELY STOP THE DIET AND/OR SUPPLEMENTS OF ANY TYPE. One must institute an appropriate diet, deficient in protein, in a planned management program! Consultation with someone experienced in care of these patients is STRONGLY URGED, so that recovery can be as uncomplicated and as complete as the animal is able to achieve. DO NOT DELAY!

    1. Peracute-Acute (days to two weeks, approximately, from start of cause):

      a. Usually limited to infants and young juveniles (up to approximately 1 lb. body weight).

      b. Hypocalcemia may be the first sign (hyperactive behavior, tremors, inappropriate fear, sometimes inappropriate jaw snapping, twitching. (Some of these signs might be confused with the opossum that is in need of levamisole).

      c. Other signs will progress, as below, if cause is not removed/corrected immediately.

    NOTE: THIS IS ONE CAUSE OF SO-CALLED CANNIBALISM. These animals will attack anything, including litter mates or cage mates. This is not true cannibalism; but can maim or kill others, REGARDLESS! You will only see this in human-fed infants.

    2. Acute to chronic (days to weeks to months):

      a. Can occur at any age through adulthood; but always sooner and often more extensive in young, rapid-growing animal.

      b. Sequence from earliest (mild NMBD) to advanced (severe and/or chronic NMBD):

      (1) Slight to significant depressed grip in hands/feet and in strength of limbs or tail; reluctant to climb.

      (2) Depressed activity level. Tends to sleep more; cranky when awake; will not run when active. (Pain begins here.)

      (3) Appetite may begin to change; grip markedly reduced.

      (4) Stands with restricted stance; walks with short mincing steps, variously described as "walking on egg shells." Can’t climb. (Pain increases.)

      (5) Early signs of systemic changes (e.g. urinary output may rise, dilute urine, sometimes increased water intake).

      (6) Limbs appear to have become stocky or chubby; palpation (examining by touching) of the long bones causes significant pain. Changes are due to thinning of the cortex (outer portion of the bone) while the diameter of the limb widens.

      (7) If blood calcium is fluctuating, may see tremors and jerky movements. Or blood level may be normal and phosphorus may be elevated.

      (8) Fractures are possibility at any time from 5 or 6 above– digits first, then long bones, spine, etc.

      (9) Walks in crouched posture with creeping movements of limbs; down on elbows and/or knees and ankles; hands and feet have abnormal postures with little use.

      (10) Distortion of limbs, loss of appetite, further changes in urine and bowel habits.

      (11) Skull changes, including, but not limited to, inability to effectively use mouth/jaw parts; bulging of eyes, etc.

      (12) Depending on the severity of the diet, site of fractures (e.g. thoracic (chest) area has potential for extremely grave prognosis), age of animal, and other problems (e.g. parasites, infection, etc.), the animal is ill enough to die at any point if intervention is not immediate and aggressive.

    NOTE: It is always worth treating and rehabilitating these opossums to whatever level of functional recovery they may attain – particularly since WE caused this animal’s distress and pain, regardless of how sincere our intentions were to help. WE must accept responsibility, correct the problem, and assist this patient back to health.

    Recovery takes at least as long to accomplish as did the damage to occur. Complications or residual problems can arise; but their extent is unknown until one reaches the late recovery phase of rehabilitation. If the disorder is recognized early and halted, opossums will completely recover!

    The most severely affected opossums can still live quite happy, comfortable lives in captivity — as non-releasable captives in homes, or in education programs. As has been pointed out in prior articles, mobility impairment results in the need to MONITOR CLOSELY FOR UTI (urinary tract infections)...for life. A female must have ovario-vaginal-hysterectomy as soon as she is in recovery and otherwise healthy (see ’Possum Tales, Vol. 8, No.1-2, 1994 articles on female anatomy and genital tract infections).


    Comments on the Jurgelski , or Similar Diets, in View of Tabulated Data Provided in Table 1 and Discussion Above:

    Although Table 1 only includes major components of the foods listed, one must not make the assumption these are their only important constituents (see note with Table ). One ordinarily begins evaluation of any given diet by examining these values; either in relation to another diet or as compared with what one knows of the species’ requirements. But, more extensive analysis is necessary to ascertain precise dietary needs of any given species. Unfortunately, this would dictate an EXPERIMENTAL STUDY which, by its very nature, leads to detriment (sometimes illness and death) of many subjects in the study – in this case, opossums. For we do not know their full dietary requirements! We only know a few of the extremes (i.e., too much or too little of something causes a specific problem), and data from post mortem examination of stomach and intestinal contents of urban opossums in two separate studies (see reading list at end).

    I believe the "experiment" of the MJD diet for opossums has failed! It has harmed more than it has helped; and it has especially done so at their most vulnerable point in life: the rapid-growth months. And, when it is given – EVEN FOR A FEW DAYS! – just prior to release, one ensures damaged and at-risk animals are in the environment... because the care-giver is apparently incapable of recognizing the subtle signs of VERY EARLY NMBD! These just-released 200-gram plus opossums are prey to any animal that comes upon them. In pain, weak, unable to run or climb, they are caught, injured or killed. Guilt can be a powerful motivator to effect positive change in our behavior . . . if we acknowledge it, instead of denying it or misdirecting it elsewhere.

    Please note, from Table 1, that kitten chow:raw beef liver APPEARS to have a "wonderful" calcium:phosphorus ratio. For the "MJD" diet, hypervitaminosis A (over-dose of Vitamin A) is of FAR GREATER SIGNIFICANCE, and the prime (not exclusive) mode of NMBD in opossums fed this UNBALANCED DIET. Beef liver, particularly RAW beef liver (which retains all its – high – Vitamin A content!) is the ABSOLUTELY WORST PROTEIN TO PROVIDE OPOSSUMS! ... Besides, how many times have you seen an opossum bring down, kill and eat a cow?? Opossums certainly can and do kill and eat chickens and other birds. But COWS??! Any proposed diet for opossums MUST be analyzed for all nutrients of known importance to opossum nutrition.


    This report’s companion article (and also in ’Possum Tales, Vol. 10, No. 2-3, July, 1996) discusses the content and amounts National Opossum Society recommends in its Infant Formula and Adult Diet and gives seven sample days’ basic diet. It also touches upon comparisons between Esbilac, MultiMilk, and Milk Matrix 33/40 used in infant formulas. As a result of preparing for both these articles, we also have some specific comments on recommendations and "pit-falls" to avoid.

    Suggested Reading:

      Ettinger & Feldman, Editors. Joint and Skeletal Disorders, Section XVI, Textbook of Veterinary Internal Medicine; Diseases of the Dog and Cat. 4th Ed. (1995). WB Saunders; p. 2146.

      Hamilton, WJ. The Food of the Opossum in New York State, Journal of Wildlife Management, Vol. 15, #13 (July 1951), pp. 258-264.

      Hopkins, DD and Forbes, RB. Dietary Patters of the Virginia Opossum in an Urban Environment, The Murrelet, Vol. 61 (Spring 1980), pp. 20-30. Portland, OR.

      Kirschmann, JD and Dunne, LJ. Nutrition Almanac, 2nd Ed. (1984), pp. 313. [Note: There is a 4th Ed, which contains many new categories, but the 2nd Ed. Is actually more complete for foods used for wildlife.]

      Pennington, JA. Bowes & Church’s Food Values of Portions Commonly Used, 16th Ed. (1994). JB Lippincott, p. 483.

      Watt, BK and Merrill, AL. Agriculture Handbook No. 8, Composition of Foods, Raw, Processed, Prepared. (Dec. 1963) USDA, Wash, DC, p. 190; and the Revised version (1967-1991).


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