Metabolic Bone Disease
from the Herpetoculturist’s Perspective
In the language of today’s Herpetocultural Community, the phrases calcium deficiency and metabolic bone disease (MBD) are not only used synonymously but have come to mean any condition in which the reptile or amphibian's bones have become soft and/or brittle as evidenced by breakage and/or skeletal deformation. In reality the symptoms that the herpetoculturist refers to as MBD may be the result of several different problems affecting the metabolization of calcium. As there are multiple problems lumped under the heading of MBD, this has created a large amount of confusing and occasionally misleading information being passed through the herpetoculture community regarding the cause and the prevention of MBD in many reptiles and amphibians. This confusion persists despite the attempts of various Veterinarians to inform the public on this topic. I will attempt to review some of the more common causes of the disease known informally as MBD and the ways to avoid them. To keep the phrasing consistent with the current usage in the Herpetocultural Community, I will continue to call these different causes by the title of MBD.
There are several pathways in which an unbalanced diet can cause MBD in reptiles and amphibians. Reptiles and amphibians like other vertebrates require different vitamins and minerals to maintain proper bone growth and strength. Calcium is potentially one of the most commonly unbalanced parts of reptile and amphibian diets. Diets that are lacking in sufficient amounts of calcium may cause abnormal bone development resulting in obvious deformities and if the diet is left uncorrected death as the animal’s bones may become so deformed that feeding becomes impossible. Other symptoms of insufficient dietary calcium are muscle tremors, paralysis, and insufficiently calcified eggs. The problem is that the majority of food items offered to captive reptiles and amphibians are either low in calcium or are imbalanced with respect to the calcium–phosphorus ratio. These issues need to be addressed by appropriate dietary supplementation prior to the reptile or amphibian being offered the food item. Invertebrates can be either dusted with an appropriate vitamin-mineral supplement or fed a suitable calcium loading diet prior to offering the invertebrate to the reptile or amphibian. However, it must be noted that not all reptiles and amphibians may benefit from calcium fed invertebrates as opposed to the vitamin and mineral dusted invertebrates. This may be due to other imbalances in the physiological needs of the animal. Invertebrates fed a calcium-loaded diet may require supplementation of other vitamins and minerals for the proper uptake and usage of the calcium. Herbivorous diets may also be modified through the use of balanced vitamin-mineral mixes. Additionally when choosing the greens for the diet, oxalate containing plants such as spinach, cabbage or beet greens should be only occasionally offered. The oxalates contained in these greens may bind with the calcium preventing its absorption.
Phosphorus is another dietary requirement for proper bone growth that works in conjunction with calcium. However there needs to be a balance between the amounts of calcium and phosphorus contained in the diet. It is possible to have a diet that would be sufficient in calcium to support bone growth yet have MBD develop due to poor calcium to phosphorus ratio. Ideally, the ratio of calcium to phosphorus should be between 1:1 to 2:1. Ratios lower than this can lead to MBD and ratios in excess of this run the risk of hypercalcemia. MBD caused by either insufficient calcium or improper calcium to phosphorus ratios is also more properly called nutritional secondary hyperparathyroidism. As with insufficient dietary calcium the calcium to phosphorus ratio in the diet can be modified through the proper use of vitamin-mineral supplements.
Reptiles and amphibians also require vitamin D to be able to metabolize calcium. However, vitamin D comes in three types; these types are D, D2, and D3. The only one of these that is metabolically useful to reptiles and amphibians is vitamin D3. There are two ways to insure sufficient vitamin D3 in captive reptiles and amphibians. The first way is dietary through an appropriate vitamin/mineral mixture. The herpetoculturist must take care to ensure that vitamin D3 is the D vitamin used in the supplement particularly if the supplement was formulated for animals other than reptiles and amphibians. The reason for this is that D2 is less expensive and is usually substituted for D3 in many non-reptile and amphibian vitamin and mineral supplements. The second method is through exposure to unfiltered sunlight or special UVB (ultraviolet B light) producing bulbs as UVB transforms provitamin D to vitamin D3. UVB is defined as the spectrum of light that has a frequency between 280 and 315 nanometers. Many novice herpetoculturists may make the mistake of trying to use sunlight that passes through glass, either the side of the aquarium or a windowpane as a source of UVB. Unless the glass (and many plastics) was specially formulated to pass UV light, the glass or plastic absorbs the UV light but passes the visible spectrum through the medium. Not only does the herpetoculturist run the risk of overheating the animal, but also the animal is still lacking sufficient UVB for vitamin D3 synthesis. The same problem also applies for many of the glass or plastic panels that are sold with aquarium lighting systems. These panels will filter out the UVB as the light passes through the panel. Light either from the sun or from a UVB producing bulb needs to be allowed to reach the animal without passing through glass or plastic unless the glass or plastic is labeled as UV transparent. Even if the glass or plastic is UV transparent, it still may absorb some of the ultraviolet light thus decreasing the effectiveness of the bulb. Additionally, UV transparent materials need to be replaced at certain intervals as specified by the manufacturer as the UV transmission may decrease over time. Another issue that many herpetoculturists fail to take into consideration is the distance of the bulb from the animal. With fluorescent bulbs, the bulb needs to be within 18 to 24 inches (45.7 to 60.96 cm) of the animal for the light to be of any benefit. At distances greater than 24 inches, the amount of UVB received by the animal is insufficient for the conversion of provitamin D to vitamin D3. At this time there are many bulbs whose manufacturers claim to produce "full spectrum lighting". Frequently these bulbs produce ultraviolet light of the wrong frequency (either below 280 or above 315 nanometers). These bulbs may produce ultraviolet light (UVA) that is behaviorally important in some reptiles but does not contribute to vitamin D3 synthesis. The only recommendation that can be made is that the spectral emission of the bulbs be checked for an output peak between 280 and 315 nanometers. Many manufacturers will provide a spectral emissions chart upon request. Once a choice has been made for the type of bulb to be used, the bulbs will need to be changed according to the manufacture's specifications, as the UVB output decreases over time. Failure to follow the manufacturer's specifications can result in insufficient synthesis of vitamin D3. UVB lighting may be used to supplement dietary sources of D3 to provide a margin of safety in preventing hypovitaminosis of D3. The reptile will only synthesize as much vitamin D3 as needed for proper growth. If done properly the use of UVB can greatly decrease or eliminate the risks of MBD in many reptiles.
Another potential cause of MBD is over supplementation of Vitamin A. Vitamin A competes with vitamin D3 for absorption in the digestive tract in reptiles and amphibians. If the ratio of vitamin A to vitamin D3 is greater than 10 to 1 then the animal may not be absorbing sufficient oral vitamin D3 to permit normal bone formation. The herpetoculturist needs to be aware of the vitamin A levels in both the offered diet as well as the dietary supplements. Some food items such as obese mice fed on commercial diets containing high levels of vitamin A can cause improper vitamin A to D3 ratios. Once again, a proper ratio of vitamin A to vitamin D3 can be reached through the use of a proper supplement or alternatively adequate exposure to unfiltered UVB.
In trying to prevent MBD from these different sources, the herpetoculturist must be careful to not oversupplement the animal as all of these dietary requirements have a narrow window of safety. Over supplementation of these dietary supplements can be as dangerous to the health of the animal as under supplementation. If the calcium supplement is more than 2.5% of the diet* then hypercalcemia may result. This can result in conditioned deficiencies of different trace minerals as well as calcium soaps forming in the digestive tract if simultaneously offered a high fat diet. The maximal amount of phosphorus that should be offered is about 1.6% of the diet**. Excessive phosphorus in the diet can result in MBD as mentioned above, as well as bone reabsorption, and calcification of the heart and kidneys. Vitamin D3 levels in excess of 5,000 IU/kg can cause soft tissue calcification, anorexia, depression, and renal failure and excessive exposure to UVB has been linked to scarring of exposed tissues. To avoid problems caused by too little or too much of any supplement the herpetoculturist needs to monitor the levels in the chosen vitamin-mineral mix(es). As always, the freshest supplements should be used. However the herpetoculturist should be aware that many of the premixed vitamin/mineral mixes have a shortened shelf life as the minerals may catalyze decomposition of the other ingredients. Ideally, all vitamin-mineral mixes should have a shelf life printed on the container and the opened container should be stored in a cool dark location to maximize the shelf life of the contents.
The information provided in the above article should help the herpetoculturist to avoid the problems commonly labeled as MBD as well as enhance the understanding of the multiple routes that can lead to MBD. In all cases, if the herpetoculturist believes that an animal in their collection may be suffering from MBD or another nutritional or metabolic disorder then a Veterinarian should be consulted as soon as possible.
Boyer, Thomas H., Metabolic Bone Disease, In Reptile Medicine and Surgery, edited by Mader, Douglas R., 1996, W. B. Saunders Co., Philadelphia
Frye, Fredric L., 1991, Reptile Care, an Atlas of Diseases and Treatments, TFH Publications, INC., Neptune
Donoghue, Susan; Langenberg, Julie, Nutrition, In Reptile Medicine and Surgery, edited by Mader, Douglas R., 1996, W. B. Saunders Co., Philadelphia
Mader, Douglas R., 1990, Metabolic bone disease in captive reptiles, part 1, Vivarium 2(3): 12-14
Mader, Douglas R., 1990, Metabolic bone disease in captive reptiles, part 2, Vivarium 2(4): 12-13
Wright, Kevin M., Whitaker, Brent R., 2001, Amphibian Medicine and Captive Husbandry, Krieger Publishing Co., Malabar
article by Ed Kowalski