As the chelonian grows, new scutes are either retained (tortoises) or shed (some terrapins). It is often suggested that one can age a chelonian by counting the growth rings of the scutes. However, these growth rings only indicate a distinct growth period, not a single year or season. An animal may have many rings in one year. Alternatively, a captive turtle may grow relatively continuously and so have few obvious growth rings. Further, many species of terrapin shed their scutes, further confusing the accuracy of counting growth rings.
The scutes of the carapace and plastron have given names. Using the correct terminology is useful for veterinarians to describe the position of shell lesions and surgical sites, and zoologists use them to identify species. The scutes are named according to their position relative to the body within, e.g. femoral scutes overlay the femurs, anals are by the cloaca.
In general, the shell should feel firm and unyielding. A healthy hatchling should develop a firm shell in 12 months. A few species have evolved variations of the shell. Leatherbacks, softshell turtles (Trionychidae) and Fly River turtles have a reduced bony shell with the keratin scutes replaced with leathery skin. Pancake tortoises (Malachochersus tornieri), male and immature female giant Asian river turtles (Batagur baska, Kachuga kachuga and K. dhongoka). Some chelonia have developed hinges in their shells so that their rear legs can be protected from predators e.g. the hingeback tortoises (Klinxys) and some mud turtles (Klinosternon).
A healthy shell should be symmetrical in shape without any obvious dents or bumps and firm and unyielding to the touch. Infections of the shell can penetrate to the underlying bone plates causing systemic life-threatening illness. It is important to seek veterinary advice when shell lesions are first noticed. A delay in providing effective treatment may merely allow the disease to progress. Previous home treatment using antiseptics may even hinder recovery as it may alter microbiological results leading to inappropriate antimicrobial selection. The owner can and must work with the veterinarian to achieve a successful and permanent cure by eliminating those factors which played a part in the development of the condition. These steps may include improving the filtration and cleanliness of the water, providing a larger basking area, correcting the diet to prevent any nutritional disorders and the provision of ultra-violet light.
This cleaning of the shell should be carried out
weekly on captive turtles. It is also an excellent way of ensuring the
turtle and its shell are checked frequently for signs of disease and that
any problems are noticed as early as possible. The husbandry should be
reviewed and a larger basking area, or more hot spots, should be added
as required. In the author's experience, terrapins will bask in the water
if it is too warm rather than come out of the water and dry off on the
basking platform. It is wise in these cases to lower the water temperature
(maintaining it within the temperature range for that species) to encourage
them to emerge and bask for a greater part of the day.
The animal will require sedation and analgesia so that the lesions can be debrided thoroughly without causing the patient undue suffering. The lesions should be swabbed and sent for bacteriological and fungal culture and sensitivity testing. In the terrestrial chelonians, bacteria tend to be isolated from wet shell ulcers, and fungus from dry lesions. Ulcerative shell disease or `shell rot' in aquatic species was thought to be caused by Beneckea chitovora, a bacterium from shell fish. It is now thought to have a multifactorial aetiology including poor husbandry and Gram negative bacteria (especially those from the gut known as Enterobacteriacae). The lesions should be topically treated with antibiotic and cleaned daily. Systemic rather than merely topical treatment is required if the animal is Septacaemic.
If extensive shell defects have occurred, shell repair may be attempted, but only after the infection has been eliminated. Once the defect has been repaired, topical treatment or monitoring of the underlying infection is not possible. A full blood haematology and biochemistry panel will reveal the extent to which the animal has been compromised. Supportive therapy should be instigated as required. If systemic disease is indicated either from clinical examination (osteomyelitis) or haematology results, then appropriate antibiotic therapy will be required. Supportive care including fluid therapy and nutritional support are also required to restore the animal to health. In advanced cases the prognosis is poor, so any affected animals should be treated as early in the course of the disease as possible.
In the case illustrated, Citrobacter freundii was isolated from the lesions. This organism was sensitive to gentamicin. The lesions were debrided then cleaned daily with povidone-iodine before being topically treated with gentamicin drops. The animal was given 10 mg/Kg gentamicin intra-muscularly every 48 hours for 10 doses. After 5 days the lesions were swabbed and sent for bacteriology culture. The results were negative and so it was deemed safe to close the shell defect whilst continuing systemic antibiotic therapy.
A proprietary fibreglass product is used to apply several layers over the multiple defects. A final coat of resin is applied to ensure the fibreglass is waterproof. The patches are then allowed 24-48 hours to harden before the animal is placed in water. The shell takes 1-2 years to heal. In adult turtles, the patches may be left in place. However, the patches should be `scored' along the edges of the scutes in juveniles to allow for expansion and growth.
|nutritional secondary hyperparathyroidism||dietary induced MBD|
|osteoporosis||loss of bone density|
|osteomalacia||adult failure of bone calcification|
|rickets||juvenile failure of bone calcification|
|hypocalcaemia||low blood calcium level|
|fibrous osteodystrophy||excessive bone resorption and secondary fibrosis|
Less Common Causes
|diet deficient in calcium||diet deficient in vitamin D|
|a negative dietary calcium/ phosphorous ratio||lack of exposure to ultraviolet light|
|disruption of vitamin D metabolism||disease of liver, kidney, intestine, thyroid, parathyroid|
The clinical signs of MBD in chelonia depend upon the stage of shell development which is affected by the disease. If the young growing chelonian is maintained on an inadequate diet the shell may fail to calcify and so remain soft, rather than becoming firm at around 12 months of age. The muscles of the pectoral (shoulders) and pelvic (hips) girdles pull on the relatively weak shell as the disease progresses. The rear end of the carapace is pulled downwards and the carapace edges curl upwards. MBD is implicated in the cause of pyramidal shell growth of tortoises. As the turtle continues to grow, it begins to look too small for its shell. The scutes show uneven growth. The animal will also show reduced weight gain, small size for age and overgrowth of rhamphotheca (beak) and claws. The turtle may also have difficulty lifting the shell from the ground when walking.
MBD is more difficult to diagnose in the turtle or tortoise which has already formed a normal shell. An adult chelonian presenting with a history of a deficient diet, broken bones, anorexia and lethargy is suspicious of MBD. If the animal has been affected for a longer period, the carapace may curl at the edges and the animal will appear small for its shell. The bridge can grow abnormally; rather than horizontally its grows vertically. This increases the distance between the carapace and the plastron. Diagnosis of MBD requires radiography of the whole chelonian. The bones will show decreased opacity, especially in the pelvic (hip) and pectoral (shoulder) regions in the early stages progressing to irregular cortical thickening of soft tissue density (fibrous osteodystrophy) in the later stages.
MBD is fatal without the appropriate treatment. The disease takes months or years to produce clinical signs and so often requires months of treatment when it is presented to the veterinarian. Caring for and treating an animal with MBD requires patience and dedication on the part of the owner, working in partnership with the vet. Mild cases of fibrous osteodystrophy can cure completely but more severe cases may be left with permanent changes. The husbandry, especially the diet, must be corrected for treatment to be successful.
Home treatment includes careful handling to reduce the risk of fractures, force-feeding as required, provision of an adequate, balanced diet, correct temperature and UV light. If the animal is not eating readily, it may require hospitalisation for stomach tubing or placement of a pharygostomy tube for a short period. Blood should be taken and analysed for calcium and phosphorous levels as well as assessing dehydration, signs of infection, liver or renal disease. Calcium therapy should be initiated, by injection if the animal is not eating (100mg/Kg 10% calcium gluconate) then oral calcium therapy on the food for 2-3 months or until radiographic signs are resolving. Care should be taken when supplementing MBD patients with mixed supplements containing both calcium and phosphorous. Some patients are already hyperphosphataemic (high blood phosphorous levels) and this can be worsened by the incorrect use of supplements. Vitamin D is involved in the body's absorption of calcium from the gut. It is useful to give the animal two weekly vitamin D injections (1000 IU/Kg) initially.
Recent reports have suggested that calcitonin can speed recovery in iguanas suffering from MBD. 50 IU/Kg is given into the muscle every 7 days for two treatments. This hormone stops calcium being resorbed from bone and it is released naturally in the body when plasma calcium levels are high. If it is used to treat an animal with MBD, the animal must have a normal blood calcium level or this treatment can be fatal. Mader ( Mader 1993) thus recommends treating the animal with oral calcium for 7 days before calcitonin treatment. In the UK, this treatment is still quite expensive.
Generally though, when a shell fracture occurs it should be treated as an emergency. The fractured pieces of shell may have caused damage to the underlying organs causing shock, haemorrhage, pulmonary contusions or spinal cord damage. The animal requires supportive therapy which may include intravenous fluids and placement of a pharygostomy tube to facilitate feeding the collapsed animal. Radiographs will reveal the extent of the fracture.
As chelonia lack a diaphragm, air is moved in and out of the lungs by contraction of smooth muscle within the lungs and the movements of the limbs. This means that even when the body cavity is opened during surgery or from a shell fracture, respiration can continue as it does not depend upon maintaining a vacuum within the cavity. Thus the chelonian does not suffer from a `collapsed lung' as mammals do. However, animals so severely damaged present a poor anaesthetic risk and so require stabilisation and supportive therapy before surgery. Whole body radiographs including a dorsoventral view and horizontal beam projections of the cranio-caudal and lateral views are most useful in revealing damage to the shell and skeleton.
Fractures of the dorsal midline carry a poor prognosis as the vertebrae are fused to the shell in this area. Fractures here may result in damage to the spinal cord leading to irreversible hindlimb paralysis.
Most Common Condition
|retained scutes||Dysecdysis||remove old scutes
|pitting of shell||Superficial Shell Ulceration||debride necrotic areas
|large areas of dead shell
foul smelling lesions
|Deep Shell Ulceration||debride necrotic areas under sedation
clean and apply topical treatment
give appropriate systemic therapy
shell "too small"
|Metabolic Bone Disease||correct diet and husbandry
shell plate loosening
|Renal Failure||no treatment - euthanasia|
Many of the common shell diseases are unfortunately caused by poor husbandry and a lack of appropriate knowledge. The treatment plan must include corrections and optimisation of the diet and husbandry as well as pure `veterinary' treatment. As with most reptile diseases, the vet and owner must work closely together to detect, treat and cure diseases of the captive chelonian.
Mader DR. Use of calcitonin in green iguana (Iguana iguana) with metabolic bone disease. Bull Assoc Reptil Amphib Vet 3(1):5, 1993
Mader DR. 1996. Reptile medicine and Surgery. WB Saunders Company.
Quesenberry KE, Hillyer EV. 1993. The Veterinary Clinics of North America, Small Animal Practice. Exotic Pet Medicine 1. WB Saunders Company.
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