Tortoises and turtles

Chelonia, such as tortoises and their semi-aquatic relatives, terrapins (or turtles), are becom­ing very popular as pets, especially in Europe where there is a long history of keeping the Mediterranean Testudo species as house and garden pets.

The internal anatomy of a tortoise is shown in Figure 12.1.

Exotic Animal Medicine: A Quick Reference Guide

Fig 12-1. Internal anatomy of a tortoise (lateral).

Captive care

As with lizards, the long-term welfare of captive chelonia is intimately dependent on their environment. They must be provided with appropriate temperatures, full-spectrum diet, and correct nutrition, including a calcium supplement (see Chapter 10 for more detail). This especially applies to hatchlings of the Testudo spp., for whom a vivarium is mandatory despite the relative hardiness of the adults.

Importance of lighting

Light in the spectrum of 290 to 315 nm (ultraviolet-B, UVB) is required for endogenous vitamin D₃ production; ultraviolet-A (UVA) spectrum (320 to 400 nm) has been shown to have a beneficial influence on normal behavior.

Endogenous vitamin D₃ production in reptiles is a many-step process that involves not only exposure to UVB but also thermal isomerization and modification in the liver and kidneys. Therefore, correct environmental temperatures and healthy organs are required for normal vitamin D₃ synthesis.

Dietary supplementation with vitamin D₃ alone is not sufficient for chelonia. In addition, dietary calcium supplementation is essential for all captive chelonia. The commercially avail­able leafy greens and vegetables usually offered to tortoises are inherently low in calcium but high in phosphates. Evidence suggests that in the wild tortoise select high-calcium foods. A Ca : P ratio of 3.5 : 1 is recommended.

Consultation and handling

Most terrestrial chelonia can be safely handled without fear of being bitten, but take care with larger terrapins or potentially dangerous species such as snapping turtles. These should be held at the rear of the carapace and, in the case of snappers, at the base of the tail.

Start the examination at the head, as this is likely to be withdrawn into the shell precluding further examination. Grasp the head behind the back of the skull and draw it out to its fullest extent. With most tortoises the mouth can now be opened and examined using the tip of a finger as a gag. With terrapins and similar a gag must be used. The rest of the body can then be examined systematically. Useful auscultation of the lung fields can sometimes be achieved by placing a damp towel over the carapace onto which the stethoscope is placed.

Weight: Length measurement as an indicator of health in Mediterranean tortoises

For Hermann's tortoise (Testudo hermanii) and the spur-thighed complex (T. graeca), an indication of health can be gained by the following (Peter Heathcote, personal communication). This is achieved by the following actions:

1. Weigh the tortoise (in grams).

2. Measure the straight length of the carapace (cm).

3. The weight of the tortoise (g) is then divided by the (straight length of the carapace (cm³)); i.e., tortoise weight (g)/straight length of the carapace (cm)³.

4. The resultant number is compared with the straight length of the carapace:

a. Straight length of carapace >15 cm; normal ratio 0.21 to 0.23.

b. Straight length of carapace Fig. 10-3).

6. Keep individually to minimize intraspecies stress and competition for resources.

Large terrestrial chelonia often appear to have difficulty with transparent barriers and may spend a considerable amount of time attempting to walk through, over, or under glass vivarium sides and doors. Blanking off these sides with tape or paint may reduce this behavior.

With semi-aquatic chelonia such as terrapins, for general care they should be provided with a dry haul-out area that has an overhanging heat source to allow thorough drying of the cara­pace and sufficient water such that the terrapin can rest with its hind feet on the bottom and its nostrils above the surface. A weak terrapin is at risk of drowning. In some cases a terrapin may need to be “dry-docked” for a period of time. Where possible, this can entail only short periods in a deeper bath. This can be combined with feeding because healthy terrapins will often prefer to feed submerged. Alternatively, serious attention to and monitoring of its fluid status should be undertaken if access to water is felt inappropriate (see "Fluid Therapy” below).

Fluid therapy

See "Fluid Therapy” in Chapter 10.

The assessment of dehydration in chelonia can be difficult visually. An obvious sign in chelonia is sunken eyes, so it is better to monitor packed cell volume (PCV). This varies with species, but it should be around 26 to 32 L/L.

Fluid administration

1.

2. Stomach tubing is often feasible in small to medium-sized chelonia (Fig. 12-3). Large chelonia are often physically too strong to hold for stomach tubing (Fig. 12-4).

3. Esophagostomy tubes are often very useful for medium to long-term fluid and nutritional management.

4. All parenteral fluids should be warmed to around 26° C.

5. In chelonia, fluid can be given into the epicoelomic space by passing a 1- to 1.5-inch needle through the pectoral musculature such that the needle is inserted dorsal to and parallel with the plastron but is beneath the pectoral girdle. The needle is directed toward the contralateral hind leg.

6. Another site is by intraosseous catheter into the vertical plastrocarapacial bridge.

7. Whole-blood transfusions can be undertaken using blood obtained from the same or related species.

8. Oxyglobin at 10 mL/kg once only has been used successfully.

Nutritional support

Liquidized normal diet or proprietary support diets can be used, given either by stomach tube or by esophagostomy tube.

Fig 12-3. Measuring a stomach tube for tubing a tortoise.

Fig 12-4. Large terrestrial chelonia such as this leopard tortoise are physically very strong.

Analgesia

• Morphine 1.5 mg/kg PO s.i.d. for 3 days

• Tramadol at 5.0 to 100 mg/kg PO s.i.d. (Baker et al 2011) Also see “Analgesia” in Chapter 10.

Anesthesia

For general notes, see “Anesthesia" in Chapter 10.

Induction and maintenance of anesthesia in Chelonia

1. Propofol at 12 to 15 mg/kg IV delivered into the jugular vein or the dorsal coccygeal vein. Adverse reactions have been noted occasionally when administered via the Subcarapacial jugular anastomosis.

2. Alfaxalone at 2.0 to 5.0 mg/kg IV (Knotek 2014). Can be maintained either with further top-ups at 2.0 mg/kg or by gaseous anesthesia.

3. With prolonged intermittent positive-pressure ventilation the lungs may become permanently expanded, so regular deflation by flexion and compression of all four legs in toward the shell should be undertaken.

4. In chelonia, Doppler ultrasound can be used to monitor heartbeat by placing the ultrasound monitor into the clavicular fossa.

5. For large chelonia in whom IV access is impractical, ketamine at 5 to 10 mg/kg and dexmedetomidine 50 to 100 gg/kg IM. Reverse with same volume atipamazole.

6. Otherwise as for lizards (see Chapter 10)

Skin disorders

The structure of chelonian skin of the legs, tail, neck, and head is as in other reptiles. However, the chelonian shell is unique—in most species there are 54 epidermal scales covering 59 dermal bony plates. The epidermal and dermal seams rarely overlap, possibly giving increased strength to the shell structure. These epidermal scales are often referred to as scutes or shields. Even here, the skin still has epidermal and dermal components.

The scute epidermis consists of:

1. Horny material containing both pigmented and nonpigmented material. This layer contains a mixture of α- and β-type keratin.

2. Pseudostratified columnar epithelium. Occasional melanophores may be seen.

3. Dermis overlies the dermal bone.

4. In the seam between the scutes, the epidermal cell layers are 3 to 4 cells thick, and it is here that differentiation into keratin-producing cells occurs, and so new horny tissue is produced. Unlike in other reptiles, the keratin is usually retained, thereby producing the typical rings on the scutes.

5. Cellular proliferation and keratinization are continuous.

Chelonia generally shed their skin in a piecemeal and uncoordinated fashion. Semi-aquatic chelonia will often shed the older outer scutes.

In some species such as the spur-thighed tortoise (Testudo graeca), there is a hinge between the abdominal and femoral scutes of the plastron, while in others (e.g., the Russian tortoise— T. horsfieldii), there is not. Box turtles (e.g., the Eastern box—Terrapene Carolina) also have a hinged plastron that enables them to withdraw both the head and all four limbs within the shell, protecting them with the trapdoor-like plastron.

Following injury, exposed carapacial or plastral bone, if allowed to dry out, dies off super­ficially; new scutes are formed beneath the exposed bone such that eventually this outer layer is shed.

Differential diagnoses for skin disorders

Abnormal skin shedding (dysecdysis)

• In terrapins a form of dysecdysis is seen where there is a failure of the outer layers of the carapacial scutes to shed and air becomes trapped beneath these, producing silvery patches. This may occur if the terrapin is unable to haul out and bask properly to dry out the shell.

Pruritus

• Ectoparasites

• Dermatitis

Erosions, ulceration, and shell deficits

• Trauma

• Often secondary to damage from another tortoise. Some males, especially the Turkish spur-thighed tortoise (Testudo ibera), are very aggressive to conspecific and heterospecific males.

• Bacterial infection

• Keratinolytic bacteria from soil in the shell

• Other bacteria (e.g., Aeromonas spp. in damp conditions)

• Benekea chitinovora (terrapins)

• Septicemia (opportunistic species)

• Septicemic cutaneous ulcerative disease (SCUD), especially softshell turtles. Often due to Citrobacter freundii or Pseudomonas spp. Other gram-negative organisms may also cause this condition in aquatic chelonia.

• Mycobacteria (see Systemic Disorders)

• Fungal infections

• “Dry” lesions in terrestrial chelonia are often due to soil-derived keratinolytic mycotic infections, such as Geotrichum candidum and Scolecobasidium humicola.

• Fusarium incarnatum (gopher tortoises, Gopherus berlandieri—Rose et al 2001)

• Microsporum spp., Mucor spp. (ulcerative epidermitis in softshell Trionyx spp.)

• Chromomycosis (e.g., Scolecobasidium humicola, Cladosporium herbarum, Phialophora spp.,

Hormodendrum spp., Curvularia spp., Fonsecaea spp., Rhinocladiella spp., and Drechslera spp.)

• Saprolegnia can infect freshwater aquatic chelonia, often secondarily invading wounds and lesions. Appears as a cotton wool-like covering while submerged that collapses on removal from the water

• Paecilomyces lilacinus (Lafortune et al 2005)

• Iatrogenic hypervitaminosis A (a necrotic dermatitis leading to a full-thickness skin sloughing)

• Burns

• Spirochid flukes (terrapins)

• Renal failure (loss of scutes often accompanied by excess exudation and ascites)

• Shell fractures—see Musculoskeletal Disorders

• Dog or other predator attack

• Rat or rodent attack (gnawed lesions on the legs, especially the lateral surfaces of the front legs—Fig. 12-5)

Nodules and nonhealing wounds

• Abscess

• Granuloma (bacterial, including mycobacteria, fungal)

• Cistudinomyia (Sarcophaga) cistudinis, especially in the axillial and femoral fossae of box turtles (Terrapene spp.)

• Gas bubble disease in aquatic chelonia (rare)

• Spirochid flukes (terrapins)

• Subepidermal mites

• Dermal papillomatosis (sideneck turtles—Platemys spp.)

• Chelonian herpesvirus (CHV—see also Respiratory Tract Disorders)

• Poxlike virus in T. hermanni

Changes in pigmentation

• Erythema (septicemia)

• Burns

Fig 12-5. Rat damage in a Mediterranean spur-thighed tortoise. The elbow joint has been exposed.

• Liver disease (and other possible etiologies for coagulation abnormalities)

• Hemoprotozoans

• Renal failure (often accompanied by excess exudate and loss of scutes)

• Algal growths (aquatic chelonia)

• Scar tissue (depigmented)

• Fusarium semitectum is a cause of whitish skin blemishes in Gopherus berlandieri.

• Failure of the scutes to be able to dry out (semi-aquatic chelonia)

Ectoparasites

• Myiasis (fly strike; maggots)

• Calliphora vicina

• Lucilia ampullacea, L. Coeruleiviridis

• Cistudinomyia (Sarcophaga) cistudinis

• Botfly larvae

• Ticks (e.g., Amblyomma sparsum, A. marmoreum)

• Subepidermal mites (African spurred tortoise Centrochelys sulcata—Nicasio et al 2002)

• Spirochid flukes (terrapins)

• Spirurids

• Leeches (wild-caught or feral freshwater chelonia)

• Barnacles (Balanus spp.) recorded on diamondback terrapins (Malaclemys terrapin) (Werner 2003)

Burns

Neoplasia

Shell deformities

• Excessive protein intake

• Metabolic bone disease (nutritional osteodystrophy)

• Old shell lesions (e.g., traumatic injuries)

• Dyskeratosis—cause unknown, but may be linked to systemic disease (Homer et al 2001)

Findings on clinical examination

• Reddened, thickened areas of skin suggest an underlying infection. These may be moist.

• Loss of dermal structures such as toenails

• Overgrowth of dermal structures such as the toenails, beak, and scutes

• Partial or complete loss of scutes

• Silvery patches on the scutes of semi-aquatic chelonia. Many of these, such as red-eared terrapins (Chrysema scripta elegans), do routinely shed scutes. Failure to do so results in air trapped beneath loosened scutes.

• Exposure of underlying bone

• Flaking and fissuring of the keratin scutes

• Inflammation and exudate accompanied by separation of the scutes from the underlying bone can be indicative of severe septicemia or renal disease.

• Pruritus: The reptile may scratch against objects. The body plan of chelonia means that they are rarely able to scratch themselves in any meaningful manner, nor can they self-mutilate.

• Spirochid eggs cause vascular occlusion, causing focal and coalescing areas of ulcerative necrosis of the carapace and plastron.

• Obvious parasites

• Penetrating injuries through scutes into underlying bone; may reach into coelomic cavity or lungs (dog bites)

• Live maggots on or around open wounds; swellings under the skin (myiasis)

• Exfoliation of skin of head and neck associated with necrotic stomatitis (CHV)

• Papular lesions around the eyes (T. hermanni)—poxlike virus

Investigations

1. Radiography

2. Sterile swabs taken for bacterial or fungal culture

3. Impression smears or other samples taken for staining and cytology

4. Blood samples for general hematology and biochemistry

5. Biopsy of suspect lesions

a. Dracunculid larvae may be present in the skin (spirurids). Adults lie in coelomic cavity.

6. Discuss environmental management with owner:

a. Are calcium and vitamin D₃ supplements offered routinely?

b. Is full-spectrum lighting provided?

c. Are fluorescent tubes changed at the correct frequency (usually every 6 months)?

d. Are high-protein foods being offered?

7. Endoscopy

8. Ultrasonography

Management

1. Any shell lesions should be investigated further by debridement around the lesion to remove fissures that could harbor persistent infections. This is potentially a very painful procedure, and if large areas are to be debrided then general anesthesia (GA) should be considered.

2. Small to medium lesions can be managed with the application of topical iodine and/ or topical antimicrobials.

3. Larger lesions may require dressing:

a. For terrestrial chelonia, application of a topical amorphous hydrogel dressing such as IntraSite Gel (Smith and Nephew Healthcare Ltd.) topically with a covering of a nonadhesive dressing promotes granulation and coverage of the underlying bone.

b. For aquatic chelonia, applying Orabase (Squibb) or bone wax can be used to achieve a relatively watertight protective seal.

4. Consider fluid therapy if large areas of underlying bone are newly exposed and exuding.

5. Attempted covering of exposed bone with products such as methylmethacrylate or fiberglass should be delayed until all signs of infection have resolved.

6. Those chelonia on a high-protein diet may require burring back of excessively long toenails and upper and lower beak.

7. Long-term dry-docking of aquatic chelonia is contraindicated because dehydration and anorexia are common sequelae.

TreatmentZspecific therapy

• Ticks and maggots

• These should be physically or surgically removed. Permethrin-based formulations are safe, although those products with synergists such as piperonyl butoxide should be avoided if possible. Fipronil may not affect a 10% kill of Amblyomma ticks (Burridge et al 2002). Do not use ivermectin as this is toxic to chelonia.

• Note: Ticks are vectors for Babesia/Hepatozoon and Ehrlichia-like organisms.

• Note: The tick Amblyomma marmoreum can transmit heartwater (Cowdria ruminatium) to domestic and native wildlife. This and other ectoparasites may act as vectors for other diseases.

• Bacterial and fungal infections

• SCUD in freshwater terrapins is caused by Citrobacter freundii and other gram-negative bacteria. Often linked to high levels of environmental bacterial contamination so should be addressed

• Antibiotics or antifungals as required

• Saprolegniosis: Salt solutions as low as 10 parts per thousand (ppt) (mg/100 mL) will inhibit infections.

• Paecilomyces lilacinus in the freshwater aquatic Fly River turtle Carettochelys insculpta was controlled (Lafortune 2005) with:

• Permanent salt bath at 5 ppt (0.5%) for 14 days and then increased to 7 ppt

• Malachite green and formalin dips (0.15 mg/L of 0.038% malachite green and 4.26% formaldehyde) for 15 minutes b.i.d. for 33 days

• Itraconazole at 10 mg/kg PO every 48 hours for 20 days

• Spirochid flukes: Praziquantel at 10 mg/kg PO repeat after 4 weeks if necessary

• Address any dietary or environmental deficiencies.

• Dog attack

• Covering antibiotics

• Nonpenetrating injuries: Clean with topical iodine solution.

• Dress any penetrating injuries with nonadhesive dressings. Only once any secondary infection is cleared should the lesion be sealed with synthetic polymers such as polymethylmethacrylate or fiberglass.

• Rat or rodent attack

• Often during or shortly after hibernation when tortoises are sluggish

• Commonly affects the lateral (outer) surfaces of the front legs, which are drawn across in front of the head for protection. Other limbs and the shell may be damaged as well.

• The radius and ulna may be exposed, as may the elbow joint.

• Clean and debride any devitalized tissue.

• Application of topical amorphous hydrogel dressings such as IntraSite Gel (Smith and Nephew Healthcare Ltd.) will encourage secondary healing. A nonadhesive dressing should be applied.

• Healing can take many months before reepithelialization occurs to a sufficient extent.

• If the elbow joint is exposed:

- Strap up the leg so that the tortoise cannot weight-bear on that leg.

- Provide support by the attachment of a prop (e.g., half billiard ball; toy wheel) to the plastron of that quadrant.

- In severe cases, one leg can be amputated at midhumeral or midfemoral level.

• Neoplasia

• Rarely diagnosed or at least reported in the literature

• Chemotherapy in reptiles is in its infancy, and most tumors are managed surgically. Accessible cutaneous tumors can be treated by injecting cisplatin directly into the tissue mass on a weekly basis as a debulking exercise.

See Chapter 10

Respiratory tract disorders

Differential diagnoses for nasal tract disorders

Runny nose syndrome (RNS) is a poorly understood clinical syndrome. Linked with CHV, Mycoplasma agassizii, and various bacteria, but no single pathogenic agent has been estab­lished yet.

Viral

• CHV: A significant cause of RNS. Other commonly associated signs are stomatitis (with diphtheritic membranes on tongue, oropharynx, and nasopharynx), dysphagia, and hypersalivation. Less often there will be cervical edema, diarrhea, and CNS signs, including hind-limb paresis.

• Iridovirus: Can present similarly to CHV, especially with stomatitis and glossitis; may cause hepatitis

• Virus X: An as yet unidentified virus or group of viruses isolated from Testudo and Geochelone spp. that are linked to rhinitis, diphtheroid-necrotizing stomatitis/ pharyngitis, pneumonia, enteritis, and ascites (Marshang and Ruemenapf 2002).

Bacterial

• Often opportunistic bacterial infections—consider occult abscessation

• Mycobacteria (see Systemic Disorders)

• Mycoplasmosis

• M. agassizii identified as a cause of RNS in gopher tortoises

Fungal

• No definitive nasal fungal pathogens have been isolated, but a variety of fungi, regarded as commensals or secondary invaders, have been described in Sulawesi tortoises (Indotestudo forstenii—Innis et al 2003).

Protozoal

• Intranuclear coccidiosis: Undescribed protozoan found in the mucosal lining of the nares, conjunctiva, and eustachian tubes. May occur elsewhere (e.g., in renal and colonic mucosal epithelial cells). Linked, along with Mycoplasma agassizii, with severe necrotizing sinusitis (Innis et al 2003)

Nutritional

• Hypovitaminosis A (see Nutritional Disorders)

Neoplasia

Other noninfectious problems

• Poor husbandry (including nutrition) plus exposure to suboptimal temperatures

Findings on clinical examination

• Clear, serous to gelatinous or mucopurulent nasal discharge

• Necrosis of external nares, including the nasal septum, that may extend several millimeters caudally. The vomer and palatine bones may be severely damaged, and oronasal fistulae may develop.

• Occasionally accompanied by pharyngeal and tongue lesions

• Other, systemic clinical signs may be seen depending upon etiology.

• Aquatic and semi-aquatic chelonia may swim with one side held lower than the other (pneumonia—asymmetrical or unilateral pulmonary consolidation).

Investigations

1. Examination of discharge: Wet smear plus staining for cytology and Gram staining

2. Culture and sensitivity of discharge sample

a. Submit mucus sample for mycoplasma PCR, isolation, or electron microscopy.

b. Submit mucus sample for virus isolation

3. Radiography

4. Routine hematology and biochemistry

5. Mycoplasma serology

6. CHV serology

7. Endoscopy

8. Biopsy/necropsy

a. Histopathology for intranuclear coccidiosis

9. Ultrasonography

Management

1. Covering systemic and/or topical antibiosis. Consider nebulization.

2. Topical iodine application to any areas of ulceration or exposed bone

3. Flushing of the nares: This should be attempted from both directions, with saline or an antibiotic ointment.

a. With a syringe placed flush with the external nares such that any mucus or accumulated material is displaced caudally into the mouth, from where it can be removed

b. Retrograde flushing can be achieved by placing antibiotic ointment onto the roof of the mouth at the nasopharynx, and displacing the antibiotic up and into the nasal cavity by compression with a cotton bud.

4. Surgical debridement may be required of any necrotic bone.

5. Supportive treatment—may require placement of an esophagostomy tube to bypass the buccal cavity.

TreatmentZspecific therapy

• CHV

• Acyclovir at 80 mg/kg PO s.i.d. for cases of herpesvirus. Efficacy appears variable.

• The author has found that lysine at 125 mg/kg PO b.i.d. PO may be useful to control CHV in some tortoises.

• Other viral infections: Supportive treatment only

• Nonspecific bacterial infections: Appropriate antibiotics

• Mycoplasmosis

• Enrofloxacin at 5 to 10 mg/kg PO, SC s.i.d.

• Doxycycline at 2.5 to 10 mg/kg PO s.i.d. or b.i.d. or 50 mg/kg IM (loading dose) followed by 25 mg/kg every 3 days

• Tylosin at 5 mg/kg IM or PO s.i.d.

• Clarithromycin at 15 mg/kg PO every 2 to 3 days

• Intranuclear coccidiosis

• Potentiated sulfonamides (patient must be well hydrated)

• Toltrazuril at 7.5 mg/kg PO s.i.d. for 2 days. Repeat after 12 days.

Lower respiratory tract disorders

Respiratory anatomy

The glottis is located at the base of the muscular, fleshy tongue relatively caudal in the oro­pharynx. The trachea has complete cartilaginous rings. It bifurcates into two bronchi a rela­tively short distance along the neck, and each of the two bronchi enters a lung dorsally. The lungs occupy the dorsal section of the shell and are adhered to the overlying dermal bones of the carapace. The lungs are paired and saclike with the gas exchanging alveoli situated at the periphery of these organs. The lack of a functional diaphragm allows inflammatory exu­dates to accumulate in the dependent portions of the lungs.

Common respiratory signs

Differential diagnoses of dyspnea:

1. Chelonia are unable to cough, so respiratory disease is likely to present as a dyspnea.

2. Pneumonia

3. Severe stomatitis/pharyngitis

4. Tracheal obstruction

5. Coelomic mass

6. Overheating

Differential diagnoses of respiratory noise:

1. RNS

2. Nasal foreign body

3. Tracheal obstruction/foreign body

4. Esophageal obstruction/foreign body

5. Pneumonia

Differential diagnoses for respiratory disorders

Viral

• CHV

• Iridovirus

• Virus X

Bacterial

• Various, especially environmental contaminants, including Pseudomonas

• Mycobacteria (see Systemic Disorders)

Fungal

• Mycotic pneumonia

• Often secondary to suboptimal temperatures or prolonged antibiotic use

• Many species described, including Candida albicans and Paecilomyces

Parasitic

• Migrant ascarids (often Sulcascaris or Angusticaecum), both in the trachea and the lungs

• Trematodes (aquatic chelonia—fish, amphibians, and crustaceans can act as intermediate hosts)

Nutritional

• Hypovitaminosis A predisposes to secondary lung infections.

Neoplasia

• Metastases

Other noninfectious problems

• Obstruction: Accumulations of mucus and inflammatory material from lower respiratory tract disease can act as obstructions.

• Drowning (typically terrestrial tortoises found in garden pond)

• Hyperthermia (overheating)—collapsed and may be salivating copiously

Findings on clinical examination

• Clearly audible respiratory sounds; may be quite moist in nature

• Dyspnea; exaggerated respiratory movements

• Discharge in mouth or at glottis

• Aquatic chelonia may consistently list to one side while swimming due to asymmetric consolidation in lungs.

• Aquatic chelonia may be reluctant to enter water.

Investigations

1. Radiography

a. Lateral and craniocaudal views more useful than dorsoventral to detect areas of consolidation

b. Compression of the lung fields may indicate an extrapulmonary lesion (e.g., obesity, hepatomegaly).

c. Lung lesions can be accessed for swabbing, biopsy, etc., by carapacial osteotomy once position is ascertained by radiography.

2. Culture and sensitivity

3. Tracheal wash; staining of collected material and/or submission for culture and sensitivity

4. Endoscopy

5. Routine hematology and biochemistry

6. Endoscopy

7. Biopsy/necropsy

8. Ultrasonography

Management

• Systemic antibiosis plus any specific medication

• Nebulization may be effective if there is little build-up of inflammatory material.

• Direct application to lesions via carapacial osteotomy

TreatmentZspecific therapy

• Viral infections: Supportive treatment only

• CHV (see “Differential Diagnoses for Nasal Tract Disorders” in Respiratory Tract Disorders)

• Hypovitaminosis A

• Vitamin A supplementation (see Nutritional Disorders)

• Bacterial pneumonia

• As discussed under “Management” above

• Mycotic pneumonia

• Difficult to treat. Use antimycotics within framework suggested under “Management” above.

• Ketoconazole at 10 to 30 mg/kg PO s.i.d.

• Itraconazole 5 mg/kg PO every other day

• Griseofulvin 20 to 40 mg/kg PO every 3 days

• Ascarids

• Fenbendazole at 50 to 100 mg/kg PO. Repeat every 2 weeks if necessary. Note: Fenbendazole is metabolized to oxfendazole by the liver. Note, however, that it may take up to 31 days to achieve maximum efficacy at 100 mg/kg (Giannetto et al 2007).

• Oxfendazole at 68 mg/kg PO. Repeat every 2 weeks if necessary. Maximum efficacy after 12 days (Giannetto et al 2007)

• Topical emodepside plus praziquantel preparations (Profender, Bayer) at 56 pL/100 g body weight (Mehlhorn et al 2005)

• Prevention: Routine worming every 6 months (prehibernation and posthibernation for Mediterranean and other species where applicable), plus disposal of feces as soon as observed

• Trematodes

• Praziquantel at 10 mg/kg PO or IM. Repeat after 2 weeks.

• Drowning

• Vigorously pump water out of the lungs by holding the tortoise vertically with head downward and repetitively flexing the limbs into the inguinal and femoral fossae, thereby compressing the lungs.

• Place in a high-oxygen atmosphere.

• Furosemide at 5 mg/kg IM b.i.d. to encourage diuresis.

• Hyperthermia

• Place in cool water.

• Dexamethasone at 0.03-0.15 mg/kg IM, IV, or IO may be given.

Ear disorders

Differential diagnoses for tympanic scale (aural) abscess

Bacterial

• Ascending infection from the pharynx up the eustachian tube often reflects normal buccal flora, often gram-negative opportunistic bacteria, especially Proteus vulgaris, Escherichia coli, and Aeromonas hydrophila (Willer et al 2003)

• Mycoplasmosis

Fungal

• Yeasts

Parasitic

• Ascarid (Angusticaecum spp.) described in Mediterranean spur-thighed tortoise Testudo graeca (Cutler 2004)

Nutritional

• Possibly related to hypovitaminosis A

Neoplasia

Other noninfectious problems

• Poor husbandry and suboptimal temperatures

• Exposure to organochlorine pesticides

Findings on clinical examination

• More common in box turtles than other terrestrial chelonia

• Swollen tympanic scale—can be unilateral or bilateral (Fig. 12-6)

• A plug of purulent material may be visible in the pharynx at the site of the eustachian tube.

Investigations

1. Investigate oropharynx—if ascarid present, is likely to be visible

2. Routine culture and sensitivity of purulent material

3. Cytology

4. Radiography

Fig 12-6. Tympanic abscess.

5. Endoscopy

6. Routine hematology and biochemistry

7. Endoscopy

8. Biopsy/necropsy

9. Ultrasonography

Management

1. Remove any ascarid present via the pharynx if possible.

2. Either under GA or local anesthetic, incise through tympanic scale.

3. Remove purulent material and flush. Check that the eustachian tube is patent by monitoring the pharyngeal ostium.

4. Tympanic scale can be sutured but is often left to heal by second intention, thereby allowing repeated flushing.

TreatmentZspecific therapy

• Bacterial infections: Appropriate antibiosis

• Yeasts

• Nystatin at 100,000 units/kg PO daily for 10 days

• Ascarids

• Fenbendazole at 50 to 100 mg/kg PO. Repeat every 2 weeks if necessary. Note: Fenbendazole is metabolized to oxfendazole by the liver.

• Oxfendazole at 68 mg/kg PO. Repeat every 2 weeks if necessary.

• Topical emodepside plus praziquantel preparations (Profender, Bayer) at 56 μL∕100 g body weight (Mehlhorn et al 2005)

• Prevention: Routine worming every 6 months (prehibernation and posthibernation for Mediterranean and other species where applicable)

• Hypovitaminosis A: See Nutritional Disorders.

Gastrointestinal tract disorders

Disorders of the oral cavity

Viral

• CHV stomatitis (see also “Runny Nose Syndrome” in Respiratory Tract Disorders)

• Papillomavirus

Bacterial

• Stomatitis (see also “Runny Nose Syndrome” in Respiratory Tract Disorders)

Fungal

• Stomatitis

Parasitic

• Monogenetic trematodes (in semi-aquatic chelonia Chrysemys, Trachemys, and Chelodina spp.)

Nutritional

• Oak leaf toxicity (see Urinary Disorders)

Neoplasia

Other noninfectious problems

• Fractured jaw, especially at mandibular symphysis

• Overheating

• Overgrown beak

Findings on clinical examination

• Inflammation of the oral and pharyngeal membranes progressing to ulcerative lesions involving the palatine area and the trachea. A diphtheritic membrane may be present (CHV, bacterial and fungal stomatitis, oak leaf toxicity)

• Difficulty with prehension or processing of food

• Obvious lesion on lower jaw (fractured mandible); not always visible, however

• Loss of rostral lower jaw, including the intermandibular joint (sequel to bilateral mandibular fractures and∕or osteomyelitis)

• Asymmetry of skull, swelling of one or both mandibles (metabolic bone disease—see Musculoskeletal Disorders, abscess/osteomyelitis, fracture, neoplasia)

• Icterus (see Hepatic Disorders and Cardiovascular and Hematologic Disorders). In some Testudo species (e.g., T. cyrenacea), the mucous membranes are naturally very yellow in appearance.

• Cyanosis

• Excessive ptyalism (overheating, stomatitis)

Investigations

1. Radiography

a. Consider if risk of underlying osteomyelitis

b. Likely to require GA to get head into suitable position for radiography

2. Routine hematology and biochemistry

3. Culture and sensitivity

4. Polymerase chain reaction (PCR) for CHV

5. Cytology

a. Intranuclear inclusions (CHV), fungal hyphae

b. Gram stain (bacteria, yeasts)

c. Modified Ziehl-Neelsen (MZN) stain (mycobacteria)

6. Endoscopy

7. Biopsy

8. Ultrasonography

TreatmentZspecific therapy

• Fractured jaw

• Can be due to traumatic handling (e.g., during stomach tubing) or may be pathological (e.g., infection, metabolic bone disease)

• Placement of an esophagostomy tube will help with fluid and nutritional support during recovery.

• Surgical repair is difficult in smaller chelonia; pins traversing the intermandibular space can interfere with tongue mobility.

• Many terrestrial chelonia can manage surprisingly well following the loss of the intermandibular joint providing food is prepared in smaller pieces for them.

• Bacterial and fungal stomatitis

• Topical antibiotics/antifungals plus topical povidone-iodine daily

• Surgical debridement of necrotic tissue may be necessary, followed by systemic and topical treatment.

• Monogenetic trematodes

• Usually seen in wild-caught piscivorous aquatic and semi-aquatic chelonia

• Probably nonpathogenic

• Praziquantel at 10 mg/kg PO or IM. Repeat after 2 weeks.

• Overgrown beak. Can be associated with:

• Malocclusion following a jaw fracture (can be iatrogenic while stomach tubing)

• Excessive protein intake, often accompanied by relative lack of dietary calcium (i.e., metabolic bone disease—see Musculoskeletal Disorders). In this case, there are often associated skull and shell deformities.

• Burr back the beak into more appropriate shape.

Differential diagnoses for gastrointestinal disorders

Chelonia, like birds, will often produce both fecal and urinary components of their excretions at the same time, mixed to some extent inside the proctodeum of the cloaca. In herbivorous chelonia, the feces should be well formed. Loose feces suggest gastrointestinal disease, a low- fiber diet, excess fruit intake, or anxiety.

In all terrestrial chelonia the bladder is large and acts as a significant organ for water storage. Urination during handling as a sign of anxiety is not uncommon. The urine often consists of a combination of a mucilaginous portion stained white or yellow with urate crystals and a clear watery portion. The urate portion may not be present every time.

Viral

• Reovirus

Bacterial

• Salmonellosis (chelonia can act as asymptomatic reservoirs)

• Campylobacter fetus

• Vibrio spp.

• Clostridium spp.—can be linked to long-term antibiosis

Fungal

• Mycotic enteritis

Protozoal

• Cilates (e.g., Balantidium spp., Nyctotherus spp.)

• Flagellates (e.g., Trichomonas)

• Entamoeba invadens (usually asymptomatic in chelonia but can cause enterocolitis and myositis—Philbey 2006)

• Cryptosporidium spp.

• Caryospora spp.

• Eimeria spp.

Parasitic

• Nematodes

• Ascarids: Angusticaecum and Sulcascaris

• Oxyurids: Tachygonetria spp., Alaeuris spp., Mehdiella spp., Thaparia spp.

• Acanthocephalans (especially aquatic and semi-aquatic chelonia)

• Hookworms: Camallanus spp., Spineoxys spp. (freshwater chelonia)

• Cestodes

• Ophiotaenia spp., Glossocercus spp., Bancroftiella spp. (freshwater chelonia)

• Flukes

Nutritional

• Dysbiosis (lack of fiber, too much fruit in diet, long-term antibiosis)

• Poisoning

• Oak leaf

• Azaleas, rhododendrons, Pieris spp. (Pizzi et al 2005) and other members of the Ericaceae (see Cardiovascular and Hematologic Disorders)

• Heavy metal (e.g., lead, zinc—see Systemic Disorders)

Neoplasia

Other noninfectious problems

• Green, well-formed feces—normal if fed mostly on pelleted foods

• Constipation

• Foreign body

• Gastric dilatation

• Cloacal prolapse

• Cloacitis

• Cloacoliths

• Intestinal foreign body

• Intussusception

• Extraintestinal mass (e.g., renal neoplasm, bladder stone)

• Dystocia

• Hypocalcemia/metabolic bone disease

• Parasitism

Findings on clinical examination

• Diarrhea: Voluminous, runny feces; may be foul smelling (flagellates, dysbiosis)

• Green, well-formed feces (pelleted food)

• Regurgitation (gastritis)

• Dehydration (sunken eyes)

• Lethargy

• Lack of feces (foreign body, bladder stone, renal neoplasia, intussusception)

• Ulceration of the oral mucous membranes

• Petechial hemorrhages (hookworms)

• Edematous swelling at cloaca (cloacal prolapse—differentiate from phallus in male)

• Death

Investigations

1. Microscopy (Fig. 12-7)

a. Fresh fecal sample—“wet prep” (Table 12-2)

2. Radiography

a. Contrast studies

b. Barium sulfate suspension at 5 mL/kg by gavage in the leopard tortoise (Geochelone pardalis) (Table 12-3)

c. Recommended timing for radiography following barium gavage is 0, 10 minutes, 2 hours, 6 hours, 12 hours, 24 hours, and 72 hours.

d. Water-soluble iodine-based contrast media such as Gastrografin (at 1 mL per 130 g in Hermann's tortoise Testudo hermanni (Table 12-4)

Ascarid Oxyurids Hookworm Fluke

Fig 12-7. Common gastrointestinal parasites of chelonia (not drawn to scale).

e. Hernandez-Divers and Hernandez-Divers (2001) suggest similar results with the nonionic iodine-based contrast medium iohexol at 7.5 to 10 mL/kg by gavage, with recommended timing for radiography following iohexol gavage given as 0, 20 minutes, 40 minutes, 60 minutes, 120 minutes, and 240 minutes at 30° C.

f. Colonic contrast studies can be performed by retrograde introduction of the contrast media via a catheter into the colon via the cloaca.

g. Foreign body: Small pieces of gravel or stone can be normal; large numbers suggest a gut stasis, obstruction, or pica.

h. Ileus—common with dysbiosis

3. Routine hematology and biochemistry

4. Culture and sensitivity

5. Endoscopy

6. Biopsy

a. Larvae encapsulated in gut wall (acanthocephalans) or other tissues, such as skin (spirurids—see Skin Disorders)

b. Amebiasis

7. Ultrasonography

Management

• Fluid therapy (see Nursing Care)

• Covering antibiosis

TreatmentZspecific therapy

• Salmonellosis

• Probably best considered as a normal constituent of chelonian cloacal/gut microflora

• Rarely pathogenic to chelonia

• Excretion likely to increase during times of stress (e.g., movement, illness)

• Treatment usually not appropriate as unlikely to be effective long term and may encourage resistance

• Recommendations for prevention of salmonellosis from captive reptiles issued by the Centers for Disease Control and Prevention in the United States include:

- Pregnant women, children 2 minutes.

• Cryptosporidium oocysts are very resistant to chlorine or iodine.

• Ascarids, hookworms, and oxyurids

• Fenbendazole at 50 to 100 mg/kg PO. Repeat every 2 weeks if necessary. Note: Fenbendazole is metabolized to oxfendazole by the liver.

• Oxfendazole at 68 mg/kg PO. Repeat every 2 weeks if necessary.

• Topical emodepside plus praziquantel preparations (Profender, Bayer) at 56 pL/100 g body weight (Mehlhorn et al 2005)

• Prevention: Routine worming every 6 months (prehibernation and posthibernation for Mediterranean and other species where applicable), plus disposal of feces as soon as observed. Note: Oxyuris worms usually have a direct life cycle.

• Hookworms have a direct life cycle; infective larvae can penetrate the skin or infect via contaminated food and water.

• Flukes and cestodes

• Praziquantel at 10 mg/kg IM or PO once only. Repeat after 4 weeks.

• Ciliates

• Usually part of normal gut fauna. Large numbers may indicate gut dysbiosis. Sensitive to metronidazole

• Flagellates

• Metronidazole

- 100 to 257 mg/kg PO body weight. Repeat after 2 weeks if necessary.

- 20 mg/kg every other day until eradicated

• Dysbiosis

- High-fiber diets, reduced fruit intake, fluid and nutritional support

- Antimicrobials often not necessary unless suspect bacterial or mycotic overgrowth.

• Gastric dilatation

• Pass stomach tube to release gas.

- Administer activated charcoal or simethicone through the tube.

- Typically linked to an excess intake of fermentable carbohydrate; may be linked with abnormal gut motility or obstruction

• Cloacal prolapse

• Prevent dessication and trauma by wrapping in nonadhesive protective film-wrap or equivalent.

• Topical sugar may reduce edema by osmosis.

• Place pursestring suture around cloaca for several weeks.

• Limit feeding to reduce straining during defecation.

• If repeated prolapses, consider cloacopexy.

• Attend to underlying etiologies (e.g., uroliths).

• Oak leaf and other poisoning

• If diagnosed antemortem, attempt removal of oak leaves from stomach either by endoscopy or via a coleotomy.

• Supportive therapy, especially fluids, due to renal effects

• Foreign body

• If in stomach may be accessible with endoscopy

• Use of lubricants such as liquid paraffin should be judicious as this may complicate subsequent therapy.

• Surgical enterotomy

• Intussusception

• Surgical enterectomy

Nutritional disorders

• Metabolic bone disease (see also Musculoskeletal Disorders)

• Hypovitaminosis A

• Especially in young semi-aquatic chelonia (e.g., red-eared sliders, Trachemys scripta elegans)

• A variety of ocular lesions, including swollen eyelids due to squamous metaplasia of the orbital glands and their ducts. A whitish cellular mass may develop behind the lower lid. Terrestrial chelonia may appear “bespectacled.”

• Squamous metaplasia also affects the renal tubules, causing kidney damage.

• Affected chelonia are often anorexic, as they cannot see to locate food.

• Treatment is with vitamin A given IM at 1000 to 5000 IU weekly for 4 weeks and the addition of dietary vitamin A supplements.

• Ensure that diet contains natural sources of vitamin A precursors, especially with red, orange, and yellow vegetables, such as sweet peppers, plus leafy greens.

• Poisoning with azaleas, rhododendrons, and other members of the Ericaceae

(see Cardiovascular and Hematologic Disorders)

• Hepatic lipidosis (see Hepatic Disorders)

• Dysbiosis

• Excess fermentable carbohydrate intake, usually combined with insufficient fiber (too much fruit—see Gastrointestinal Tract Disorders)

Hepatic disorders

Viral

• CHV

Bacterial

• Abscessation

• Salmonella typhimurium (Gonzalez Candela et al 2005)

• Mycobacteriosis (granulomas—may be multifocal)

Fungal

Protozoal

• Amebiasis

Nutritional

• Hepatic lipidosis

• Chronic debilitation

• Cholecystolithiasis (gallstones)

Neoplasia

Findings on clinical examination

• Malaise

• Listlessness

• Anorexia

• Weight loss

• Jaundice (icterus). Note: Some Testudo spp. (e.g., T. cyrenacia) naturally have yellowish oral mucous membranes.

• Greenish feces

• Diarrhea

• Death

Investigations

1. Microscopy

a. Fecal examination: Cysts and trophozoites may be present (amebiasis).

2. Radiography

3. Routine hematology and biochemistry

4. Culture and sensitivity

5. Endoscopy

6. Biopsy/necropsy

a. Granulomatous hepatitis (bacterial, fungal infection)

b. Amebiasis

c. Ziehl-Neelsen staining and PCR for mycobacteria

7. Ultrasonography

Management

• Milk thistle (Silybum marianum) is Hepatoprotectant. Dose at 4 to 15 mg/kg PO b.i.d. or t.i.d.

• For ascites try furosemide at 2 to 5 mg/kg PO, SC s.i.d.

• Lactulose 0.05 mL/100 g PO s.i.d.

TreatmentZspecific therapy

• Mycobacteriosis—see Systemic Disorders

• Amebiasis

• Metronidazole 20 mg/kg PO every other day until eradication

• Chloroquine

- 125 mg/kg PO every 48 hours for three treatments

- 50 mg/kg IM every 7 days for 3 weeks

• lodoquinol/diiodohydroxyquin 50 mg/kg PO s.i.d. for 21 days. Note: Possibly toxic to black rat snakes

• Paromomycin

- 300 to 360 mg/kg PO every other day for 14 days

- 25 to 100 mg/kg PO daily for 4 weeks

• Cholecystolithiasis and cholecystitis

• Consider NSAIDs (e.g., meloxicam at 0.2 mg/kg IM, PO once daily or every other day) in the green iguana—see Hernandez-Divers (2006)—and covering antibiosis.

• Surgery to remove gallstones may be feasible.

• Linked to high dietary levels of processed dog and cat food (excessive protein, lipid, vitamin A and D₃ intake)

• Feed a more appropriate herbivorous diet.

Pancreatic disorders

Diabetes mellitus (see Endocrine Disorders)

Cardiovascular and hematologic disorders

Cardiovascular anatomy

• Three-chambered heart consisting of two atria and one ventricle: A series of muscular ridges plus the timing of ventricular contraction tend to functionally divide the ventricle into two (the cavum venosum, the cavum pulmonale, and the cavum arteriosum), thereby separating systemic from pulmonary blood flow.

• The renal portal system (RPV): The RPV is a large vessel arising near the confluence

of the epigastric and external iliac veins. It drains into the kidney. Blood returning from the tail, hind legs, and other closely situated structures may pass through these vessels or may bypass and enter the systemic circulation direct. This appears to depend on various factors, such as hydration status and core body temperature. May be more significant for drugs excreted by tubular secretion than by glomerular filtration.

Differential diagnosis for cardiovascular disorders

Viral

• Iridovirus (epicarditis but associated with other more typical iridovirus signs)

Bacterial

• Endocarditis

Fungal

Protozoal

• Haemogregarina spp.

• Haemoproteus spp.

• Plasmodium spp.

• Pirhaemocyton (may actually be iridoviral inclusions)

Parasitic

• Spirochid flukes, both adults and eggs

Nutritional

• Excessive calcium intake

• Excessive vitamin D₃ intake

• Ingestion of azaleas, rhododendrons, and other members of the Ericaceae (contain several toxins, including cardiac glycosides)

Neoplasia

Other noninfectious problems

• Metastatic mineralization

• Amyloidosis

• Renal disease

• Myocardial disease

• Hyperkalemia

• Pericardial effusion

• Visceral gout (uric acid in pericardial sac—see Urinary Disorders)

Findings on clinical examination

• Anorexia

• Edema

• Weakness

• Weight loss

• Areas of cutaneous mineralization (with metastatic mineralization)

• Spirochid fluke parasitism in freshwater turtles associated with subcutaneous edema, blood-tinged coelomic fluid, and hepatic, pancreatic, and splenic necrosis. Many organs can be affected due to microgranulomas triggered by the fluke eggs.

Investigations

1. Radiography

a. May be useful to diagnose metastatic mineralization but unlikely to be useful for radiographic evaluation of the heart.

2. Routine hematology and biochemistry

3. Cytology (blood smear)

a. Haemogregarina spp.

4. Blood culture and sensitivity

5. Endoscopy

6. Ultrasonography may be useful in large chelonia (Redrobe and Scudamore 2000).

7. Electrocardiography—potentially useful but few normal values established

a. Normal ECG values in anesthetized red-eared slider (Trachemys scripta elegans) using a three-electrode, lead II trace, after Holz and Holz (1995). Some comparative values from conscious terrapins (from Kaplan and Shwartz [1963], cited in Holz and Holz [1995]) are given for comparison (Table 12-5).

b. Note that the QRS complex was always in the form of a large R wave—no Q or S wave deflections were visible.

c. Azalea toxicity: Paroxysmal tachycardia, atrial fibrillation, premature ventricular beats, extrasystoles, ectopic ventricular contractions (Frye and Williams 1995)

d. Atrial fibrillation and first-degree heart block may be indicators of calcium deficiency.

Management

• The usual cardiac drugs are largely untried; therefore, treatment with these is speculative, although still worth attempting.

• Diuretics (e.g., furosemide at 5 mg/kg IM b.i.d. to encourage diuresis)

TreatmentZspecific therapy

• Hemoparasites

• Loading dose of chloroquine phosphate (5 mg/kg PO) and primaquine phosphate (0.5 mg/kg PO)

• Continue with chloroquine at 2.5 mg/kg PO once weekly and primaquine at 0.5 mg/ kg once weekly for 12 to 16 weeks.

• Flukes: Praziquantel

• Azalea poisoning

• Atropine sulfate at 0.04 mg/kg IV

• After 2 minutes give calcium gluconate at 2 mg/kg by slow IV injection over the next

5 minutes

• Once ECG normal, consider gastric lavage.

• Supportive treatment

• Hypocalcemia: See Musculoskeletal Disorders.

Systemic disorders

Viral

• CHV

• Papilloma-like virus (see Drury et al 1998)

Bacterial

• Mycobacteria (see below)

• Chlamydophila pneumoniae

• Chlamydia-like organisms (possibly Parachlamydia acanthamoeba, Simkania negevensis—Soldati et al 2004)

• Spirochetes

Fungal

• Exophiala spp.

Protozoal

• Intranuclear coccidiosis

Nutritional

• Hypocalcemia (including metabolic bone disease)

Neoplasia

Other noninfectious problems

• Ivermectin toxicity

• Benzimidazole toxicity

• Anemia

• Gout (renal, visceral, and articular—see Urinary Disorders)

• Hypoglycemia (including posthibernational anorexia)

• Cardiac disease (see Cardiovascular and Hematologic Disorders)

• Heavy metal (e.g., lead, zinc)

Findings on clinical examination

• Weakness

• Emaciation and weight loss

• Anorexia

• Ocular and nasal discharge, stomatitis, with or without bouts of paralysis (CHV)

• Lethargy, anorexia, paralysis following ivermectin administration (ivermectin toxicity)

• Edema

Investigations

1. Radiography

a. Heavy metal poisoning

2. Routine hematology and biochemistry

a. Serum lead and zinc. Consider blood sampling other in-contact chelonia to establish normal ranges.

3. Serology and PCR for CHV

4. PCR for CHV

5. Ziehl-Neelsen staining and PCR for mycobacteria

6. Immunohistochemistry and PCR for Chlamydophila and Chlamydia-like organisms (Soldati et al 2004)

7. Culture and sensitivity

8. Endoscopy

9. Ultrasonography

10. Biopsy/necropsy

a. Single or multiple granulomas (mycobacteria, fungi, Chlamydophila pneumoniae, Chlamydia-like organisms)

b. Eosinophilic intranuclear protozoan-like organisms, typically in the renal epithelial cells, hepatocytes, pancreatic acinar cells, and intestinal epithelial cells (Jacobson et al 1994)

Management

• See Nursing Care.

TreatmentZspecific therapy

• CHV

• No effective treatment, but consider acyclovir at 80 mg/kg PO s.i.d. Efficacy appears variable.

• Supportive treatment only (but see Respiratory Tract Disorders)

• Bacterial infections

• Appropriate antibiosis

• General nursing care

• Mycobacteriosis

• Potential zoonosis. Consider euthanasia.

• No successful treatment for mycobacteriosis in reptiles reported

• Intranuclear coccidiosis

• Potentiated sulfonamides at 30 mg/kg PO s.i.d.

• Ivermectin toxicity

• IV fluids at 5 mL/kg per hour for up to 3 hours and then 5 to 10 ml/kg per day

• Methylprednisolone 1 mg/kg IV s.i.d.

• May require continued support for many weeks (see Divers et al 1999)

• Benzimidazole toxicity

• Overdose with wormers (e.g., fenbendazole)

• Lethargy, anorexia, secondary bacterial or fungal infections secondary to marked leukopenia

• Supportive treatment, including covering antimicrobials

• Care with compromised individuals as studies show (Neiffer et al 2005) an extended heteropenia with transient hypoglycemia, and hyperphosphatemia.

• Heavy metal poisoning

• Remove metallic foreign bodies via endoscope if possible.

• Sodium calcium edetate at 35 mg/kg by slow IV daily for 2 weeks

Musculoskeletal disorders

Bacterial

• Osteomyelitis

• Corynebacterium aquaticum (see Philbey et al 2006)

Fungal

Protozoal

• Amebiasis

Nutritional

• Metabolic bone disease—actually a complex of disorders including:

• Dietary calcium deficiency

• Dietary calcium/phosphorus imbalance

• Protein excess

• Hypovitaminosis D₃

- Lack of exposure to ultraviolet light

- Incorrect environmental temperatures

- Lack of dietary vitamin D₃

• Protein deficiency

• Liver, kidney, and intestinal disease

• Multiple factors may be involved.

• Metastatic calcification of smooth muscle of various organs, including cardiovascular system, pulmonary system, gut, and urogenital system. Typically linked to excess dietary vitamin D₃ intake (e.g., oversupplementation, feeding with dog and

cat food)

Neoplasia

Other noninfectious problems

• Metabolic bone disease (hepatic, renal, and intestinal disease—see also “Nutritional” above)

• Fractures of the shell or limbs (usually traumatic)

• Joint dislocations (traumatic)

• Degenerative joint disease due to:

• Obesity

• Articular gout (see Urinary Disorders)

• Trauma

• Septic arthritis

• Osteochondritis

• Coxofemoral arthritis (Philbey et al 2006)

• Lawn mower trauma

Findings on clinical examination

• Soft shell (Note: In terrestrial chelonia, the shell should be hard by 12 months of age), flattened shell, doming of scutes (metabolic bone disease)

• Weakness—unable to support its own weight, hind legs articulated backward as if sliding rather than held beneath the body (metabolic bone disease)

• Beak abnormalities, including overgrowth

• Soft mandibles (metabolic bone disease)

• Claw abnormalities, including overgrowth (metabolic bone disease)

• Limb swellings (fractures, dislocations, osteomyelitis, myositis, septic or aseptic arthritis)

• Vague signs of ill health (anorexia, lack of movement, lethargy)

Investigations

1. Radiography

a. Reduced bone density, cortical thinning, thickening of limb bones and shell (fibrous osteodystrophy)

b. Fractures (shell, limbs)

c. Lytic bone lesions (osteomyelitis)

d. Areas of abnormal calcification (metastatic calcification)

2. Routine hematology and biochemistry

a. Blood vitamin D₃ (25-hydroxycholecalciferol) levels; also total calcium, ionized calcium, phosphate

b. Acierno et al 2006 measured 25-hydroxyvitamin D₃ in red-eared sliders (Trachemys scripta elegans) (Table 12-6)

3. Culture and sensitivity

4. Cytology (fine-needle aspiration)

5. Endoscopy

6. Biopsy/necropsy

a. Amebiasis

7. Ultrasonography

8. ECG: Atrial fibrillation (see Cardiovascular and Hematologic Disorders)

Management

• Close attention should be paid to environmental parameters, especially exposure to UV lighting, temperature, and dietary supplementation.

TreatmentZspecific therapy

• Amebiasis (see Gastrointestinal Tract Disorders)

• Metabolic bone disease

• Usually due to secondary nutritional hyperparathyroidism linked with either failure to provide sufficient calcium supplementation or exposure to UVB

• Parenteral calcium gluconate or lactate at 1.0 to 2.5 mg/kg daily

• Oral vitamin D₃ at 1 to 4 IU/kg daily

• Dietary calcium supplementation

• Exposure to full-spectrum lighting as a UVB source

• Calcitonin at 1.5 IU/kg SC s.i.d. if normocalcemic

• Metastatic calcification

• No effective treatment

• Reduce hypercalcemia by:

- Calcitonin at 1.5 IU/kg SC s.i.d.

- Fluid therapy: Hartmann's solution at 15 mL/kg intracoelomic until normocalcemic

• Although often linked to excessive vitamin D₃ supplementation, many cases may be due to low levels of calcitrol, commonly secondary to renal disease. This leads to toxic levels of parathormone production with associated abnormal tissue mineralization and further renal damage.

• Osteochondritis

• Arthrotomy and surgical removal of any loose bone fragments

• NSAID therapy (e.g., meloxicam at 0.2 mg/kg once daily or every other day) in the green iguana—see Hernandez-Divers (2006)

• Joint dislocations

• Reduce surgically if possible and immobilize as described for long bone fractures, below.

• Abscessation and osteomyelitis, myositis

• Appropriate antibiosis

• Consider amputation if damage is extensive.

• Fractures

• Long bone fractures: Stabilization by confining the flexed limb into its fossa with strong adhesive tape may be sufficient to allow callus formation and healing; otherwise surgical reduction and internal/external fixation

• Shell fractures may require closure. Some fractures may be reduced by placing clothing hooks attached by epoxy adhesives to the shell and connecting with surgical wire (Bogard and Innis 2008). Other cases may require surgical plating. Once all risk of infection has been ameliorated then shell deficits may require bridging with fiberglass or methylmethacrylate. Those fractures where the coelomic membrane has been breached carry a significantly poorer prognosis.

• Lawn mower trauma

• Tortoises in long grass can be damaged during mowing, especially by “hover-mowers.”

• Injuries usually include injuries to the dorsal carapace, often with exposure of the lungs.

• Because the lungs in tortoises are naturally rigid (attached to the inner surface of the carapace), respiration is usually not compromised.

• Flush the lungs with sterile saline to remove any debris and treat as for Respiratory Tract Disorders.

• As with other shell traumas (see Skin Disorders), do not place a permanent covering (e.g., methylmethacrylate) over the deficit until any infection has resolved.

Neurologic disorders

Viral

• CHV

Bacterial

• Septicemia

• Granuloma/meningitis

• Intracranial/extracranial abscess (vestibular syndrome)

Fungal

• Granuloma/meningitis

Protozoal

Parasitic

• Myiasis (aberrant—Sales et al 2003)

Nutritional

• Hypocalcemia (see “Metabolic Bone Disorder” in Musculoskeletal Disorders)

Neoplasia

• CNS neoplasia

Other noninfectious problems

• Ivermectin toxicity

• CNS gout (uric acid deposition—see Urinary Disorders)

• Heavy metal poisoning

Findings on clinical examination

• Weakness

• Hind-limb weakness; especially common in old female Hermann's tortoises. Often of unknown etiology but consider CHV or CNS gout.

• Lethargy, anorexia, paralysis following ivermectin administration (ivermectin toxicity)

• Vestibular syndrome (head tilt, circling to one side)

• Anorexia

Investigations

1. Radiography

a. Skull

b. Subtle spinal lesions unlikely to be seen on radiography

c. Metallic objects in gut, especially nails, lead shot, etc.

2. Magnetic resonance imaging scan

3. Routine hematology and biochemistry

4. Blood lead or zinc levels

5. Culture and sensitivity

6. Endoscopy

7. Ultrasonography

TreatmentZspecific therapy

• Hypocalcemia (see “Metabolic Bone Disorder” in Musculoskeletal Disorders)

• Ivermectin toxicity (see Systemic Disorders)

• Aberrant myiasis

• No safe systemic insecticidal preparation. Necrosis of dead larva may release toxins.

• Vestibular syndrome

• Consider surgical removal or debridement if due to a contributing abscess, if feasible.

• Heavy metal toxicity

• Remove metallic foreign body if possible.

• NaCa-EDTA at 35 mg/kg IM s.i.d. until clinically normal (see Chitty 2003)

Ophthalmic disorders

Chelonia have both rods and cones but lack a fovea. Instead they have an area centralis or area temporalis: sections of retina sensitive to detail, edges, or movement. There is no conus papillaris. Chelonia have both lachrymal and harderian glands.

Examination of the posterior segment of the eye is difficult as the iris muscle fibers are striated and partly under voluntary control. Therefore, parasympatholytics (e.g., atropine) and sympathomimetics (e.g., phenylephrine) will not work. Consider examination by:

1. Using low light levels

2. General anesthesia

3. Nonparasympatholytic mydriatics such as vecuronium

Viral

• CHV

• Poxlike virus

Bacterial

• Secondary infection

• Eyelid granuloma (mycobacteriosis)

• Pasteurella

Fungal

• Keratitis (Fig. 12-8)

• Exophiala spp.

Parasitic

• Nematode larvae (red-eared slider, Trachemys scripta elegans)

• Microfilariae

Nutritional

• Hypovitaminosis A (especially semi-aquatic chelonia—Fig. 12-9)

Neoplasia

Other noninfectious problems

• Aging (cataracts)

• Subzero temperatures (cataracts, vitreal haze)

• Nutritional deficiencies (cataracts)

• Trauma

• Poor water quality (aquatic chelonia, especially snapping turtle—Chelydra serpentina)

Fig 12-8. Fungal keratitis in a red-footed tortoise.

Fig 12-9. Hypovitaminosis A in a hatchling red-eared slider.

• Exposure to ultraviolet C (incorrect UV lighting)

• Congenital defects

• Cyclopia

• Microphthalmia

• Anophthalmia

• Arcus senilis

• Chronic hypertrophy of the nictitating membrane

• Coagulative keratopathy

Findings on clinical examination

• Conjunctivitis

• Blepharitis

• Ocular discharge

• Corneal ulceration

• Deep ulceration followed by perforation and iris collapse

• Hypopyon

• Uveitis

• Keratitis

• Cataracts

• Grossly swollen eyelids; unable to open one or both eyes (hypovitaminosis A, infection)

• In terrestrial chelonia, the eyelid lesions give a semblance of spectacles.

• A whitish cellular mass may develop behind the lower lid.

• Anorexia (cannot see to locate food). Note: Renal disease may be concurrent with hypovitaminosis A (see Urinary Disorders).

• Nematode larvae within the choroid (red-eared slider Trachemys scripta elegans)

• Obvious worm in the anterior chamber (microfilariae)

• Panophthalmitis

• Ocular signs possibly accompanied by stomatitis and rhinitis (CHV)

• Yellow papular lesions of the eyelids in Testudo hermanni (poxlike virus)

Investigations

1. Ophthalmic examination

2. Radiography

3. Routine hematology and biochemistry

4. Culture and sensitivity

5. Endoscopy

6. Biopsy/necropsy

a. Ziehl-Neelsen staining and PCR for mycobacteria

7. Water quality testing for aquatic chelonia (especially pH, ammonia, nitrites, nitrates, temperature)

8. Ultrasonography

9. Reassess lighting (exposure to UVC).

Management

1. Many nonspecific ocular lesions respond well to vitamin A supplementation at 1000 to 5000 IU IM weekly for 4 weeks and the addition of dietary vitamin A supplements.

2. Enucleation may be required for severely damaged or infected eyes.

TreatmentZspecific therapy

• Hypovitaminosis A (see Nutritional Disorders)

• Eyelid granuloma

• Topical treatment

• Consider resection.

• Fungal keratitis

• Topical antimycotics (e.g., clotrimazole)

• Systemic antimycosis may be required.

• Congenital defects

• No treatment

• Consider incubation parameters (temperature, humidity, etc.) as well as genetic factors when considering cause.

• Cataracts

• Phacoemulsification (see Kelly et al 2005)

• Lens extraction

• Arcus senilis: Age related; no treatment

• Chronic hypertrophy of the nictitating membrane

• Lavage of the conjunctival space

• Topical application of ophthalmic corticosteroid preparation

• Coagulative keratopathy

• Topical ophthalmic ointment containing proteolytic enzyme

• May occur posthibernation

• Poor water quality

• Identify abnormality and correct (see Chapter 15).

• Microfilariae and helminths

• Fenbendazole at 50 to 100 mg/kg PO. Repeat every 2 weeks if necessary.

• Do not use ivermectin (see Systemic Disorders).

• Exposure to UVC

• Provision of incorrect lighting (e.g., UV-sterilization tubes, blacklights for tanning beds instead of the correct full-spectrum lighting)

• Correct lighting; provision of a darkened area during the initial recovery period may be beneficial.

• Supportive treatment as may be anorexic due to compromised vision

Urinary disorders

Bacterial

• Cystitis

• Pyelonephritis

Fungal

• Cystitis

• Pyelonephritis

Protozoal

• Hexamita

• Myxidium spp. (Myxozoa—crowned river turtle Hardella thurjii; see Garner et al 2003)

Parasitic

• Monogenetic trematodes (in semi-aquatic chelonia Chrysemys, Trachemys, and Chelodina spp.)

Nutritional

• Hypovitaminosis A (squamous metaplasia of the renal tubules)

• Oak leaf toxicity (see Gastrointestinal Tract Disorders)

Neoplasia

Other noninfectious problems

• Bladder calculi/stones

• Gout (renal)

• Iatrogenic (nephrotoxic drugs, such aminoglycosides)

• Pelvic obstruction (foreign body, coxofemoral arthritis—see Musculoskeletal Disorders, retained eggs)

• Interstitial nephropathy

• Tubulonephropathy

• Glomerulonephropathy

Findings on clinical examination

• Anorexia

• Lethargy

• Weight loss

• Polydipsia/polyuria

• Polyuria

• Urinary tenesmus

• Yellow urates (denotes prolonged retention)

• Anuria

• Edema

• Hind-limb weakness (see also Neurologic Disorders)

• Pale mucous membranes

• Ocular disease, especially in semi-aquatic chelonia (hypovitaminosis A)

• Mortalities

Investigations

1. Radiography

a. Soft-tissue mineralization; increased soft-tissue or mineral density in renal region

b. Uroliths. Note: The bladder is voluminous in chelonia, and bladder stones may appear farther cranial and more lateral than expected.

c. Pneumocystography may help to differentiate eggs in the bladder from eggs in the reproductive tract (see Reproductive Disorders).

Pneumocystography in larger chelonia

1. Catheterize the urethra.

2. Flush out the bladder contents.

3. Infuse 10 to 20 mL/kg of air (stop if resistance encountered).

4. Administer 2 to 5 mL of iohexol to produce a double-contrast pneumocystogram.

(Hernandez-Divers S, Hernandez-Divers S 2001 Diagnostic imaging of reptiles. Practice 23:370-391.)

Intravenous urography

1. Fast chelonian for 2 to 3 days.

2. Maintain at 30° C.

3. Place IV catheter into right jugular vein.

4. Use suitable urography medium—inject 800 to 1200 mg iodine into the jugular vein.

5. Lateral and dorsoventral radiographs taken at 0, 1, 3, 5, 15, 30, and 60 minutes.

6. As an adjunct, inject medium into dorsal coccygeal tail vein. Radiographs taken after 30 seconds.

(Hernandez-Divers S, Hernandez-Divers S 2001 Diagnostic imaging of reptiles. Practice 23:370-391.)

2. Routine hematology and biochemistry

a. Blood uric acid levels, urea, creatinine, calcium, and phosphorus

3. Urinalysis including cytology

a. Renal casts

b. Inflammatory cells

c. Centrifuged urine (supernatant)

4. Detectable levels of alkaline phosphatase, aspartate transaminase (AST), alanine transaminase (ALT), urea, calcium, creatine kinase (CK), creatinine, glucose, lactate dehydrogenase (LDH), magnesium, ammonia, phosphorus, total bilirubin, total protein, and uric acid

5. Parameters raised with renal disease: AST, urea, calcium, CK, creatinine, glucose, LDH, ammonia, and phosphorus. Uric acid may be significantly raised or lowered than normal (Koelle and Hoffman 2002).

6. Culture and sensitivity

7. Endoscopy

8. Biopsy/necropsy

9. Ultrasonography

Management

• Fluid therapy (see Nursing Care)

TreatmentZspecific therapy

• Bacterial pyelonephritis and cystitis

• Appropriate antibiosis

• Fungal pyelonephritis and cystitis

• Appropriate mycosis (see Respiratory Tract Disorders)

• Myxozoans

• No effective treatment

• Flukes

• Probably nonpathogenic

• Praziquantel at 10 mg/kg once. Repeat after 4 weeks if necessary.

• Hexamitiasis

• Cause of renal tubular damage

• Metronidazole

- 100 to 257 mg/kg PO body weight. Repeat after 2 weeks if necessary.

- 20 mg/kg PO every other day until eradicated

• Dimetridazole at 40 mg/kg PO s.i.d. for 5 days

• Gout

• Fluid therapy

• Allopurinol at 10 mg/kg PO s.i.d. Note: This will only prevent subsequent uric acid deposition.

• Very guarded prognosis

• Uroliths/bladder calculi

• Adults: Surgical cystotomy; note that the chelonian bladder is very thin and difficulty can be experienced during closure. One method is by marsupialization of bladder to the body wall at the inguinal fossa.

• Hatchling/small chelonia: Success can be achieved by long-term treatment with allopurinol at 10 mg/kg PO s.i.d. indefinitely; this helps prevent enlargement of the stone such that in time the growing chelonian may be able to pass the calculus.

Endocrine disorders

Thyroid activity in chelonia can be affected by temperature; low temperatures (10° C for 15 days) inhibit thyroid activity, whereas high temperatures (32 to 34° C) stimulate thyroid activity in soft-shelled turtle Lissemys punctata punctata (Sengupta et al 2003).

Nutritional

• Thymic hyperplasia (goiter associated with iodine deficiency)

Neoplasia

• Multicentric lymphoblastic lymphoma (thyroid)

Other noninfectious problems

• Thymic hyperplasia (not diet related; possibly antigenic stimulation)

• Diabetes mellitus

Findings on clinical examination

• Marked swelling of ventral neck (goiter)

• Polydipsia, polyuria, inappetence (diabetes mellitus)

Investigations

1. Radiography

2. Routine hematology and biochemistry

a. Hyperglycemia, normal renal parameters (diabetes mellitus); differentiate from stress hyperglycemia

b. Serum insulin

c. Serum glucagon (may be more important in glucose regulation than insulin)

d. Serum thyroxine levels (consider sampling conspecifics to establish normal ranges)

e. Normal T₃(_total) < 0.0154 nmol/L

f. Normal T₄(_total) = 0.05 to 0.1 nmol/L

g. However, Hulbert (2000) cites T₄(_total) values for growing red-eared sliders (Trachemys scripta) of 80 to 145.0 nM/L.

h. Note: Thymic hyperplasia can occur with normal T₃ and T₄ levels (Fleming et al 2004).

3. Culture and sensitivity

4. Endoscopy

5. Biopsy/necropsy

6. Ultrasonography

TreatmentZspecific therapy

• Thymic hyperplasia (nutritional)

• Supplement with iodine.

• Sodium or potassium iodide solution at 0.25 to 0.5 mg/kg IV or PO every 7 days

• Lugol's iodine solution at 0.5 to 2.0 mg/kg PO every 7 days

• Other dietary supplements high in iodine include kelp tablets.

• Usually associated with feeding high volumes of Brassicas (cabbage family), which contain goitrogens that antagonize thyroid function

• Volcanic island herbivores (e.g., Galapagos tortoises) especially predisposed

• Thymic hyperplasia (nonnutritional)

• Investigate other, nonnutritional, causes

• Diabetes mellitus

• Rare but very guarded prognosis

• Commercial insulin unlikely to work—reptilian insulin is different from mammalian.

• Attempt feeding high-fiber, low-carbohydrate diet to allow natural modulation of glucose uptake.

Hibernation-associated disorders

Many species of chelonia undergo a seasonal period of dormancy. Typically this is a period of hibernation (brumation) to survive times of low temperatures and poor food resources, but occasionally it may be to survive times of high temperatures or drought (estivation).

Commonly kept species suitable for hibernation

1. Mediterranean species that are safe to hibernate include Testudo ibera, T. whitei, T. marginata, T. hermanni, and T. horsfieldii. Of the T. graeca graeca group, the Moroccan and Algerian races are safe to hibernate.

2. North American gopher tortoise Gopherus agassizi

3. Northern populations of the ornate box turtle (Terrapene ornata) and eastern box turtle (T. Carolina)

4. Some populations of Bell's hinge-back tortoise (Kinixys belliana) will estivate during periods of drought.

5. Painted terrapins (Chrysemys spp.) and some sliders (Trachemys spp.—red-eared sliders, T. scripta elegans)

Commonly kept species that should not be hibernated

1. Mediterranean species: Egyptian tortoise (Testudo kleinmanni) and the Tunisian tortoise (T. nabulensis). The Libyan race of T. graeca graeca should either not be hibernated or should only be allowed to do so for a relatively short time, such as 6 to 8 weeks.

2. Indian star tortoise (Geochelone elegans), red-footed tortoise (G. carbonaria), yellow-footed tortoise (G. denticulata), leopard tortoise (G. pardalis), and African spur-thighed tortoise (G. sulcata)

3. Serrated hinge-back tortoise (Kinixys erosa) and Homes' hinge-back tortoise (K. homeana)

4. Vietnamese leaf turtle (Geoemyda spengleri)

5. Keeled box turtle (Pyxidea mouhoti)

Hibernation triggered bγ environmental stimuli

1. Reducing ambient temperatures

2. Reducing photoperiod

3. Reducing light intensity

Testudo spp. during hibernation lose around 0.2 to 0.4 g/day, so expect a loss of around 1% of body weight per month. Water is lost via respiration, so PCV rises from 0.28 to 0.29 L/L to 0.34 to 0.38 L/L, while urea levels rise from id="Picutre 269" class="lazyload" data-src="/files/uch_group31/uch_pgroup24/uch_uch7218/image/image131.jpg">

Fig 12-10. Prolapsed phallus in a red-eared slider.

3. Urine sample: High levels of spermatozoa in sexually active male tortoises

4. Routine hematology and biochemistry

5. Culture and sensitivity

6. Endoscopy

7. Biopsy/necropsy

8. Ultrasonography

a. Place probe into inguinal fossa to pick up ova in POOS.

b. Eggs in the bladder

TreatmentZspecific therapy

• POOS

• Medical management with levothyroxine at 50 pg/kg PO s.i.d. This treatment can be prolonged over several months; monitor follicular regression with regular ultrasound scans.

• Ovariectomy

• Egg stasis

• Provision of correct environment, including appropriate temperature, humidity, and nesting chamber, may induce normal egg laying. Supplement with calcium (e.g., calcium gluconate at 1 mL/kg PO b.i.d.).

• May be linked with stress

• Medical induction

- Calcium at 100 mg/kg IV, IM every 6 to 12 hours

- 1 to 10 lU/kg oxytocin IM given 1 hour after last calcium. Unlike in snakes there appears to be a wide “window” of many weeks where oxytocin is effective for induction.

- Repeat over 2 to 3 cycles if the reptile is otherwise healthy.

- If some eggs still retained after 48 hours, consider surgery.

- Vasopressin at 0.01 to 1.0 pg/kg IM, IV (more potent than oxytocin in reptiles)

* Salpingotomy

- Plastral coeliotomy

- Prefemoral coeliotomy

* Ovariosalpingectomy (as for “Salpingotomy")

• Egg retention in the urinary bladder

• Cystotomy: Temporary marsupialization of the bladder via the inguinal fossa. Bladder closure can be problematic.

• Ultrasound-guided snaring of eggs per cloaca

• Fractured egg

• Risk of egg yolk serositis and trauma from sharp shell fragments

• Consider either endoscopic or surgical retrieval.

• Egg yolk serositis

• Coeliotomy followed by extensive lavage and removal of any egg fragments; surgical repair of oviduct or salpingectomy if necessary

• Hypersexuality

• Delmadinone acetate at 1 to 2 mg/kg SC. Repeat after 4 to 6 weeks if needed.

• Supplementary feeding (e.g., tube feeding) for tortoises with anorexia and weight loss

• Environmental modification may be possible by shortening day length and dropping ambient temperatures by 2 to 3° C for a period of time for those tortoises kept inside.

• Prolapsed phallus

• If fresh and relatively nontraumatized, replace and retain with a pursestring suture.

• If badly damaged or if pursestring unsuccessful, consider resection. This will only interfere with reproduction, not with urination.

Pediatric and neonatal disorders

Bacterial

• Systemic infections

Fungal

Protozoal

Parasitic

• Nematodes (see Gastrointestinal Tract Disorders)

Nutritional

• Metabolic bone disease

• Uroliths (Fig. 12-11)

Other noninfectious problems

• Prolapse of the umbilicus

• Congenital abnormalities

Fig 12-11. Bladder urolith in a hatchling spur-thighed tortoise (plastron removed).

Findings on clinical examination

• Lethargy

• Loss of appetite

• Cryptic behavior (hiding)

• Bulging of tissue at the umbilicus of newborn or newly hatched chelonia. Bulge may contain coelomic lining, yolk sac remnant, and coelomic fat.

• Edema

Investigations

1. Radiography

2. Routine hematology and biochemistry a. Serum calcium and ionized calcium

3. Culture and sensitivity

4. Endoscopy

5. Biopsy/necropsy

6. Ultrasonography

TreatmentZspecific therapy

• Systemic infections

• Difficult to diagnose in hatchlings as small size precludes adequate sampling.

• Covering antibiosis often gives a good clinical response.

• Metabolic bone disease—see Musculoskeletal Disorders

• Note: Hatchling chelonia are naturally soft and somewhat flexible.

• Often accompanied by hypovitaminosis A (especially semi-aquatic chelonia) and other signs of disease (e.g., anorexia, lethargy)

• May be delayed if calcium status of female was good; signs only once calcium reserves utilized

• If very early onset, may be due to poor calcification of egg, a reflection of poor calcium status of the mother

• Prolapsed umbilicus

• Clean and replace prolapse. Suture in place.

• May require surgical resection of yolk sac remnant

• This is particularly prevalent in hatchlings with incomplete yolk sac resorption, where the yolk sac membranes adhere to dry surfaces or to the inside of the shell (especially if the humidity is too low). Keep hatchlings with pronounced egg sacs in moist, clean surroundings until resorption takes place. Do not attempt to separate the hatchling from the egg, but increase humidity and/or remove the hatchling plus egg to a warm, humid environment to allow natural separation.

• Edema

• Occasionally seen in hatchling Testudo spp.

• Swollen body

• Soft shell

• On postmortem the carcass is edematous; uroliths may be present.

• Unknown etiology

• Uroliths

• See Urinary Disorders for treatment.

• Can occur individually or in groups

• May be linked to poor environmental conditions (e.g., marginal chronic dehydration)

• In some cases hatchlings may have inherited susceptibility (clutch mates under different husbandry regimens developed uroliths—personal observation).

Husbandry-related disorders

• Water quality

• Poor water quality, especially high ammonia levels, can cause skin and ophthalmic disorders and mortalities in young semi-aquatic chelonia. (See Chapter 15 for details in “Management.”)

• Metabolic bone disease (see Musculoskeletal Disorders)

• Posthibernational anorexia (see Hibernation-Associated Disorders)