Authored by: Christina Miller CAHT/RVT, RLAT, BSc

In Part 1 of Metabolic Bone Diseases in Reptiles and Amphibians, we explored how a healthy herp will maintain normal calcium levels in the blood, and touched on how it goes wrong with inappropriate husbandry. Now, we’ll take a closer look at what malfunctions in the affected animal’s body in response to those husbandry errors, how it manifests clinically in an animal, how it’s treated, and how we prevent this avoidable condition.

Pathophysiology and Clinical Signs

Previously, we looked at how the body maintains appropriate levels of calcium in the blood. Refer to Figure 1 for a repeat appearance of the diagram illustrating how the body accomplishes calcium homeostasis. They key part of this process that leads to bone pathology is the loop concerning parathyroid hormone (PTH) and hypocalcemia: If all of PTH’s mediating effects cannot raise blood calcium to an acceptable level, the parathyroid gland will continue to produce it. PTH will continue to stimulate bone resorption until the calcium “stores” of the skeleton are essentially depleted (Wedekind et al. 2010).

Bones that continually lose their mineral structure become weakened and brittle. This condition is known as osteomalacia. The body, still lacking calcium to “end” the PTH negative feedback loop, will try to reinforce the skeleton (notably the humerus, femur, and mandible) by laying down fibrous scar tissue. This process is called fibrous osteodystrophy, and gives a swollen appearance to the affected bones (Figures 2 and 3). Despite this desperate attempt to fortify the skeleton, pathological fractures are common (Mader 2006) as seen in Figures 4 and 5. Osteomalacia in humans (called “rickets” when it involves a vitamin D3 deficiency and afflicts children) is painful and affected people often experience muscle weakness (Mayo Clinic 2014); this may certainly contribute to the lethargy we see in afflicted reptiles and amphibians. When MBD occurs in young, rapidly growing animals, spinal deformities appear to be more common.

This manifests as scoliosis and kyphosis, lateral and vertical distortions of the spine respectively, in varying severities and combinations (Mader 2006), visible in Figures 5, 6, and 7 in the gallery below. In advanced stages of the disease where the bones have been depleted of minerals, blood calcium levels will continue to drop. Neuromuscular signs begin to occur as there is not enough calcium for nerve-to-muscle signals to continue to function. Twitching of the digits, from muscular spasms in response to hypocalcemia, tends to be an early clinical sign, and will progress to muscular tremors and larger spasms, often with a loss of balance (termed ataxia) as the animal’s condition declines. Gastrointestinal bloating occurs from the effects of hypocalcemia on the muscle of the digestive tract.

Cloacal prolapse can occur secondary to the lack of intestinal muscle tone combined with pressure from the gas distension involved in bloat. Muscle tremors/spasms, weakness, and ataxia worsen. The final stage is hypocalcemic tetany, where the extremely low levels of blood calcium cause “misfiring” of nerve endings to muscle; seizures and death are imminent without emergency treatment (Mader 2006).

See Table 1 below for a summary of clinical signs associated with MDB and the severity of the disease. Please note that these clinical signs may vary greatly depending on the individual, as there is no one set of guaranteed deformities that occur in every patient (Mader 2006).

Scoliosis, Kyphosis, lateral and vertical distortions of the spine scoliosis and kyphosis, lateral and vertical distortions of the spine respectively, in varying severities and combinations in blue tongue skink (Tiliqua sp., green Iguana (Iguana iguana), and Chinese water dragon (Physignathus cocincinus) (Mader 2006) Related Another Chinese Water Dragon, with a pathological fracture of the front left limb evidenced by the “extra joint” that is visible in this photo. This animal also has severe scoliosis and is obviously dehydrated. Unfortunately, he was for sale in a pet store (returned by a client for being “defective”), for full price. This juvenile blue-tongued skink, Tiliqua sp., is presenting with a severe spinal deformities (kyphosis) due to NSHP during the critical growth period as a juvenile. Despite the dramatic appearance of this animal, it may recuperate to live a long and relatively healthy life. Photo provided by Vanier College’s Animal Health Technology department. This Green Iguana (Iguana iguana) had poor husbandry for the first few months of his life, and suffered severe skeletal deformities as a result. Fortunately, he was stabilized with good husbandry and he now has a normal bone density.

Summary of clinical signs in various stages of MBD

Early Progression Moderate to Severe Progression Advanced Progression Clinical Signs Digits of the hands are not held straight, the hands may begin to "roll" on their sides.



Slight, bilateral swelling and/or softening of the mandible.



Mandible begins receding.



Small bumps may be palpated along the vertebrae and long bones (especially the femur).



Young animals may display the beginning of spinal deformities. All of the previous column’s symptoms, to a greater degree.



Jerky gait when walking.



Repeated tremors and twitching in the limbs and toes when at rest.



Shakiness noticeable when handled.



Spine and tail may warp and twist.



Bone fractures and breaks are very common due to reduced bone density.



Lethargy (arboreal animals will avoid climbing and spend most of their time on the floor). All symptoms previously listed, deformities to a greater degree.



Constipation.



Anorexia (refusal to eat).



Cachexia (weight loss).



Animal may be presented in hypocalcemic tetany. Treatment Prompt correction of dietary and/or environmental factors.



Oral calcium supplement added to the diet. Diet and environmental corrections are vital.



Oral calcium supplements.



Treatment of bone fractures and breaks. Diet and environmental corrections are vital.



Oral calcium supplementation.



Injectable calcitonin once plasma levels of calcium have returned to normal through diet correction and supplementation.



Treatment of bone fractures and breaks. Prognosis Excellent: These minor symptoms will either subside or reverse (although depending on the severity of the skeletal deformity, it may remain). Good: Skeletal deformities cannot be reversed, but the animal can still potentially have a relatively normal life. Varies: Animals with severe deformities may recover with prompt, aggressive treatment, although deformities may prevent a normal lifestyle; euthanasia should be considered for severely debilitated and deformed animals

References

Mayo Clinic. 2014. “Osteomalacia Definition.” Mayo Clinic. <http://www.mayoclinic.org/diseases-conditions/osteomalacia/basics/definition/con-20029393> Accessed 3-Sept-2014.

Mader, DR. 2006. Metabolic Bone Diseases. In: Reptile Medicine and Surgery, 2e (Affiliate Link) Dr. Mader (editor). Saunders Elsevier, St. Louis, Missouri, USA.