POTENTIAL RISK OF METABOLIC BONE DISEASES (MBD) IN CAPTIVE POPULATION OF ROTI ISLAND SNAKE-NECKED TURTLE (Chelodina mccordi)

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1 POTENTIAL RISK OF METABOLIC BONE DISEASES (MBD) IN CAPTIVE POPULATION OF ROTI ISLAND SNAKE-NECKED TURTLE (Chelodina mccordi) Maria Aega Gelolodo 1, Herlina Umbu Deta 1, Yulfia N.Selan 1, Grace Saragih 2 1 Fakultas Kedokteran Hewan, Universitas Nusa Cendana, Kupang; 2 Balai Penelitian dan Pengembangan Lingkungan Hidup dan Kehutanan Kupang ABSTRACT Chelodina mccordi or known as Roti island snake-necked turtle is a freshwater turtle that endemic to the small island of Roti, East Nusa Tenggara. This species nearly extirpated by commercial trade in the recent past. Recently, Chelodina mccordi has been listed by the IUCN red list as critically endangered species and listed in CITES Appendix II. Due to this reason, captive breeding efforts through ex-situ conservation provide hope for saving the species from becoming extinct. However, mostly captive animals facing a high risk of metabolic bone disease (MBD). As one of the most common observed pathological conditions in herpetofauna, metabolic bone disease (MBD) is characterized by metabolic defects affecting the morphology and function of bones. Dietary calcium (Ca) and phosphorus (P) imbalance, a deficiency of Ca and vitamin D in the diet or due to a lack of UVB light exposure and husbandry mismanagement are consider as the cause of the disease. Among these reason, vitamin D deficiency caused by insufficiency of UVB light exposure is essentially a phenomenon of captive animals. MBD is a major killer of young turtle. In past several months, a number of baby Chelodina mccordi with an age range around 4-5 months had died and showed similar clinical sign which were soft shells. This sign is commonly known as pathognomonic sign of MBD. This manuscript will comprehensively review the causes and clinical manifestations of MBD, MBD cases in other herpetofauna, the possibly effects of MBD to Chelodina mccordi conservation program and recommendations to prevent it. Keywords: turtle, Chelodina mccordi, UVB, calsium, Vitamin D ISBN

2 INTRODUCTION Chelodina mccordi or commonly known as Roti island snake-necked turtle is a freshwater turtle that endemic to the small island of Roti, East Nusa Tenggara (Rhodin, Ibarrondo, & Kuchling, 2008). This moderate-sized snakenecked turtle has a very limited distribution and nearly extirpated by international pet trade in the recent past. This condition has pushed it into virtual commercial extinction (IUCN, 2016). Consequently, this species is considered critically endangered by the IUCN red list criteria (IUCN, 2016) and listed in CITES Appendix II since 2005 (CITES, 2005). Fig 1. Chelodina mccordi (CITES, 2005) In Roti, the distribution of this species is restricted to shallow eutrophic lakes and swaps. Rhodin et al. (2008) had indicated that there were only three possible populations along Roti Island. The larger population located in western and central part of the island while the smaller population presented in eastern part of the island, especially in isolated areas at north-eastern. However, as critical endangered (CR) species, Chelodina mccordi facing an extremely high risk of extinction in the wild in the immediate future. The population reduction that manifests in a decline of occupancy area and extent of occurrence and/or quality of habitat due to high level of exploitation has brought this species as one of 25 most endangered freshwater turtle in the world by Turtle Conservation Coalition (Rhodin et al., 2011). Regarding this condition, it is extremely important to apply management action to protect and preserve the endangered species while restore the natural ecosystem (Casazza et al., 2016). Captive breeding through ex-situ conservation provide hope for saving the endangered species from becoming extinct. Oilsonbai research station in Fatukoa, Kupang is the only governmental facility in East Nusa Tenggara that develop Chelodina mccordi ISBN

3 conservation programs. Under the Ministry of Environment and Forestry, this research station applies captive breeding for some important endemic wildlife in East Nusa Tenggara likes Chelodina mccordi. Unfortunately, in past several months several young Chelodina mccordi with an age range around 4-5 months died and showed similar clinical signs such as fatigue, reluctant to move and soft shell or carapace. A soft carapace is known as the pathognomonic sign of Metabolic Bone Disease (MBD) (Mitchell & Tully Jr, 2008), the most common observed pathological conditions in herpetofauna (Hoby et al., 2010) and a major killer of young turtle. Mostly captive herpetofauna facing a high risk of MBD (Donoghue, 1998). METABOLIC BONE DISEASE (MBD) Basically, Metabolic bone disease (MBD) is a term that used to define a miscellaneous medical disorder. This disease is characterized by metabolic defects affecting the morphology and function of bones causing defects of morphology and function of bones (Hoby et al., 2010; Johnson, 2004). However, other shell pathological changes also can be caused by trauma or variety of bacterial and fungal infections (Hernandez-Divers et al., 2009). In general, husbandry mismanagement likes inappropriate temperature, humidity, lighting, and dietary, is considered as cause of MBD in many captive herpetofauna (Hernandez-Divers et al., 2009; Johnson, 2004). Among these predisposing factors, dietary calcium (Ca) and phosphorus (P) imbalance, a deficiency of Ca and vitamin D in the diet, or a lack of UVB light exposure followed by the effects of secondary hyperparathyroidism are mostly recognised as major factor of MDB. Juveniles and reproducing females, are most affected by the disease because in their life stages there are intensive growth and enhanced demands on Ca and P metabolism (Hoby et al., 2010). Calcium is a mineral that needs to be consumed in a herptile s diet which is critical for bone development and maintenance, egg production, and cellular or muscle activity including the heart, the gastrointestinal tract (GIT), and the brain. Calcium absorption is regulated by the type of calcium, levels of phosphorus in the diet, the health of the GIT, cholecalciferol (vitamin D3) levels, calcitonin levels, and PTH levels. Calcium and phosphorus form a conglomeration, called hydroxyapatite, which is the main component of bone and teeth (Klaphake, 2010). Under natural conditions, the body synthesizes its own vitamin D when it is exposed to sunlight. Light from the ultraviolet spectrum 290 to 320 nm (UVB) reacts with the body s skin to activate the cholecalciferol pathway (Mader, 2000). Provitamin D3 (7-dehydrocholesterol) in the skin is ISBN

4 converted by UV-B to pre-vitamin D3. Pre-vitamin D3 is thermochemically isomerized into cholecalciferol in the skin, with higher temperature increasing the rate of isomerization (Antwis & Browne, 2009). Once cholecalciferol is inside the body, methodwhether from diet or from UV-B conversion, the next steps are the same. Cholecalciferol travels to the liver, where it is hydroxylated into calcidiol (25-hydroxycholecalciferol), then travels to the kidney for a final hydroxylation to become calcitriol (1,25- dihydroxycholecalciferol) the biologically active form of vitamin D3. Calcitriol is what increases calcium and phosphorus absorption from the GIT, increases bone release of calcium (demineralization) and induces immune system stimulation in mammals at least (Klaphake, 2010; Stanford, 2006; Watson & Mitchell, 2014). In the wild, exposure to natural sunlight is not a problem for most diurnal animals. Animals in a captive environment do not always get the proper exposure to natural unobstructed sunlight. Important to note is that the part of the spectrum of ultraviolet light that is necessary for vitamin D synthesis in the skin may be filtered out as it passes through ordinary glass. Animals kept in aquaria next to a window that is exposed to sunlight may not get adequate ultraviolet light and as a result are unable to synthesize the needed vitamin D (Mader, 2000). There are two types of MBDs, NSHPT (Nutritional secondary hyperparathyroidism) and RSHPT (Renal secondary hyperparathyroidism). NSHPT presents in most cases as a juvenile or immature herptile such as lizards and aquatic turtles. NSHPT happens because of husbandry or dietary mismanagement, for instance inadequate oral calcium, a poor calcium/phosphorus ratio, inadequate oral cholecalciferol/uv light, inappropriate heating/humidity, or often a combination of several of these factors leads to a physiologic response to depleted calcium levels by increasing PTH production. Because needs are not met, calcium depletion from bone becomes clinical and the overall shortages start affecting muscle calcium needs. The most commonly implicated factors are a prolonged deficiency of dietary calcium or vitamin D3, an imbalance of the calcium-tophosphorus ratio in the diet (usually an excess of phosphorus), or inadequate exposure to ultraviolet (UV) radiation in diurnal animals (Mader, 2000). In contrast, RSHPT tends to be a condition of older animals, where a slow decline in kidney function eventually leads to an inability to respond to signals for the kidneys to selectively retain calcium and secrete extra phosphorus. Often gastrointestinal absorption can compensate for this declining function, but eventually the combination of this issue and the inability to hydroxylate calcidiol to calcitriol leads to a non-responsiveness of ISBN

5 the system to PTH and the hypertrophy of the parathyroid glands (Klaphake, 2010). Generally, clinical signs consistent with MBD vary depending on the age and species of the patient (Acierno, Mitchell, Roundtree, & Zachariah, 2006). Young animals with active bone growth are the most affected. MBD in young water turtles present several clinical manifestation such as fatigue, inability to raise body off of ground, hypocalcemic tetany, soft shells and abnormal shell formation (Flanagan, 2014) like pyramidal mounding of the carapace, premature cessation of shell growth, and scoliosis of the spine (Rosskopf & Shindo, 2003). The most common clinical finding in the aquatic turtle is softshell. Aquatic turtles may also exhibit extensive secondary erosive infections of the plastron and carapace. Contrary, Adult chelonians have large calcium reserves in the bones of the carapace, plastron, and limbs; therefore, they typically exhibit non-specific signs of illness. These clinical signs include dystocia, anorexia, cloacal prolapse, abnormal fecal character, muscular weakness, collapse of the femoral head, renal compromise, hepatic lipidosis, and constipation (Acierno et al., 2006). Due to the universality of problems among captive water turtle, these turtles rarely possess normal-appearing shells RECOMMENDATION Basically, the focus on treatment for MBD especially NSHP has been to correct husbandry and nutritional problems and provide exposure to natural sunlight. Treatment program such as increase dietary calcium, administer calcium gluconate parenterally; provide a source of ultraviolet radiation, increase environmental temperatures; address cause of renal failure; and treat symptomatically provide hope to MBD patients (Flanagan, 2014). In term of dietary composition, a balanced diet with adequate calcium is crucial to good health. An unsuitable calcium-phosphorus ratio of the diet should be corrected. It is suggested to include the following Ca : P ratio of 1.5 : 1 to 2 : 1, suitable amounts of calcium and phosphorus (Ca: 0.6%-1% dry matter, P: 0.5%-0.8% dry matter), and appropriate mineral and vitamin supplementation. To maintain UVB exposure, there are 2 method that can be applied in captive conservation. The first is via natural exposure to direct sunlight and the second is via artificial supplementation with UVB-producing light bulbs. The UV index of natural sunlight is highly variable based on latitude, time of day, and time of year. Studies have shown that the exposure to UVB radiation must be direct, or through air permeable membranes. Glass or acrylic materials (non-permeable) absorb or obstruct UVB radiation, ISBN

6 preventing the animal from gaining any exposure to the UVB radiation. Artificial sources of UVB light will also degrade over time because of the degradation of the phosphorus in the bulb. Even if the bulb is still emitting visual light, it may not be emitting wave lengths within the optimum spectrum for vitamin D synthesis, and for this reason, current recommendations include replacing the bulbs every 6 months to 1 year (Watson & Mitchell, 2014). When positioning these lights in the animal s cage, placement of the lights close enough that they are still effective is crucial. All ultraviolet light sources should be placed within 16 to 24 inches of the animal for maximum effect. Moreover, in situations in which the animal cannot be provided with proper exposure to ultraviolet light, vitamin D must be supplemented in the diet (Mader, 2000). Initial supplementation of parenteral vitamin D3 once weekly for 2 weeks has proved useful. Calcitonin administration has been used in the treatment of NSHP in other herpetofauna (Klaphake, 2010). However, it must be done carefully because administration of calcitonin to hypocalcemic patients can be fatal (Antwis & Browne, 2009). The main objective of long-term treatment, once a patient is stable, is to correct the underlying predisposing factors that led to the development of MBD (Rivera & Lock, 2008). REFERANCES Acierno, M. J., Mitchell, M. A., Roundtree, M. K., & Zachariah, T. T. (2006). Effects of ultraviolet radiation on 25-hydroxyvitamin D3 synthesis in red-eared slider turtles (Trachemys scripta elegans). American journal of veterinary research, 67(12), Antwis, R., & Browne, R. (2009). Ultraviolet radiation and vitamin D 3 in amphibian health, behaviour, diet and conservation. Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology, 154(2), Casazza, M., Overton, C., Bui, T.-V., Hull, J., Albertson, J., Bloom, V.,... Olofson, P. (2016). Endangered species management and ecosystem restoration: finding the common ground. Ecology and Society, 21(1). Donoghue, S. (1998). Nutrition of pet amphibians and reptiles. Paper presented at the Seminars in Avian and Exotic Pet Medicine. Flanagan, J. P. (2014). Chelonians (Turtles, Tortoises). Fowler's Zoo and Wild Animal Medicine, 8, 27. Hernandez-Divers, S. J., Hensel, P., Gladden, J., Hernandez-Divers, S. M., Buhlmann, K. A., Hagen, C.,... Camus, A. C. (2009). Investigation of ISBN

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