Chelonians - Veterinary Practice and Husbandry

Sharon Redrobe

Chelonians are a fascinating group of animals. As the only reptiles that possess a shell, they can develop a number of unique diseases. This article will describe the most common shell problems presented to the author's practice.

Introduction

Reptiles that possess a shell belong to the subclass Anapsida and all living species belong to the single order Chelonia within the class Reptilia. This order is considered to contain the most ancient of living reptiles; indeed the structure of the shell has barely changed over 200 million years. There are over 200 species of chelonia recognised today, including the tortoises, turtles and terrapins. In the UK, `tortoise' describes the terrestrial species, `terrapin' the freshwater and `turtle' the marine species. However, in North America all aquatic and terrestrial chelonians are known as `turtle', and `terrapins' are freshwater or marine species.

Anatomy of the Shell

The upper part of the shell is known as the carapace. This is made up of 50 bones which originate from the ribs, vertebrae and dermal plates of the skin. The lower part of the shell, known as the plastron is derived from the clavicles (`collar bone'), interclavicles and gastralia (abdominal ribs). The carapace and plastron are joined by bony bridges between the fore and hind limbs. The entire bony shell is covered by keratin shields (UK) or scutes (USA). These scutes do not exactly overlay the bony pieces of the shell, but are offset so that the seams between the scutes cover the gaps between the bones (known as sutures).

 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).

Shell Diseases

Diseases of the shell are more common in aquatic chelonia than tortoises. The lesions are usually related to poor husbandry practices. These include poor water quality, rough substrates, inappropriate temperatures, lack of ultraviolet light, poor diet and insufficient basking areas. Bite wounds and trauma (road traffic, lawnmowers) also damage the shell and allow pathogens access.

 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.

Dysecdysis

Turtles should shed their scutes regularly as they grow. Retained scutes are a sign of poor husbandry as the animal has not been drying off sufficiently to lose its old scutes. Retained scutes readily become infected with algae, bacteria or more rarely fungi. The newer `healthier' shell underneath becomes vulnerable to infection. The old scutes can usually be lifted off with a blunt probe, taking care not to damage the underlying shell. Soaking the turtle will often help to remove the scutes. The underlying `new' shell should be gently scrubbed to clean off any algae that may have started to grow there.

 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.

Superficial Shell Ulceration

Pitting or discolouration of the shell is caused by erosion or abscessation of the keratin scutes. This mild form of `shell rot' can be treated by removing all the necrotic, infected tissue and treating the lesions with topical antibiotic ointments e.g. silver sulfadiazine, povidone-iodine. If an aquatic species, the animal should be restricted to only 30-60 minutes in water per day to enable the lesions to be kept as clean and dry as possible to speed healing.

Deep Shell Ulceration

If left untreated, superficial abscesses can progress to destroy the full thickness of the keratin scutes and invade the underlying bone plates. It is even possible for the infection to penetrate down to the coelomic membrane, which is the last barrier before the abdominal cavity is entered. The shell debris is necrotic and foul-smelling. The underlying affected bone may feel soft to touch and be moist or bloody. Radiography may reveal extensive infection of the bone (osteomyelitis). The infection may have also spread to other organs of the body, resulting in septicaemia. Petechiation (blood splashes) under the scutes is a sign of septicaemia or trauma in chelonians. This condition is fatal without effective treatment. The severe form of shell rot requires vigorous veterinary treatment to save the animal.

 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.

Renal failure

Chronic renal (kidney) failure can cause the scutes to slough. The bone plates may also loosen and ooze fluid. This has only been reported in two tortoises and two turtles. (Frye FL. Biomedical and Surgical aspects of captive Reptile Husbandry, 2nd Ed. Vol 2. Melbourne Fl. Kreiger Publishing Co. 1991, pp 27-30, 512-525). The failing kidney retains phosphorous. This in turn leads to hyperparathyroidism. This over-activity of the parathyroid gland leads to calcium resorption from the bones. Thus the bony plates of the shell soften and loosen. The scutes may also be shed. The chelonian with renal failure often presents with fluid retention (ascites) and so appears bloated. It may also be drinking and urinating a lot (respectively known as polydipsia and polyuria). A blood test will reveal that the blood urea nitrogen is very high. As the kidney disease is usually irreversible, the prognosis is poor and the animal should be humanely euthanased.

Metabolic Bone Disease.

Metabolic bone disease (MBD) is a term which describes a number of clinical problems (see Table 1) and can be caused by a number of factors (see Table 2).

 
 

Table 1: Clinical Syndromes associated with MBD

Table 2. Causes of MBD

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.

Shell Fractures

The shell can be fractured in many ways; as a result of the chelonian being dropped, stood on, driven over or bitten by a dog to name but a few. Some chelonians have demonstrated the remarkable ability to heal quite severe shell defects without veterinary interference. The author has seen severe defects affecting over a third of the shell resulting from lawnmower and car accidents, yet the healed tortoises were being presented years later for another ailment.

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.

Summary

Table 3: Summary of Signs, Conditions and Treatments

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.

References and Further Reading