Reptile Medicine PDF

Reptile Medicine Marie Kubiak BVSc CertAVP(ZM) CertAqV DZooMed MRCVS RCVS Recognised Specialist in Zoo and Wildlife Medicine Initial consultation  Ensure familiarity with the species  Set aside enough time  to carry out a full assessment of husbandry  To examine the animal Husbandry  Most d...

Reptile Medicine Marie Kubiak BVSc CertAVP(ZM) CertAqV DZooMed MRCVS RCVS Recognised Specialist in Zoo and Wildlife Medicine Initial consultation  Ensure familiarity with the species  Set aside enough time  to carry out a full assessment of husbandry  To examine the animal Husbandry  Most diseases in reptiles develop in association with husbandry deficiencies  Any consultation is a good time to evaluate husbandry and make improvements  Optimise recovery  Address husbandry before clinical disease results Clinical examination  It is important to observe the animal prior to handling  Often history taking is prolonged and allows for assessment of demeanour, respiration and responses to stimuli  Examination should be no different to any other animal  Systematic appraisal and analysis  Develop a personal system for examination  A checklist can help ensure no points are missed Faecal analysis  Performed on every patient where possible  Most parasites have a direct life cycle  Reptiles are not clean!  Debilitated animals are more likely to develop secondary parasitic overgrowth  Both a fresh smear and flotation technique should be used  It is important to be able to identify common parasites Pinworms  Oxyurids common in most reptile species  Species specific  Rarely significant in low numbers  Treat if clinical signs present  Weight loss, poor growth, diarrhoea, anorexia  Fenbendazole 20mg/kg/d for five doses  Beware concurrent disease  Avoid ivermectin in all chelonia and in green tree pythons due to associated neurotoxicity Coccidia  Isospora amphiboluri common in agamids  Pathogenic  30mg/kg TMPS for 5d  10mg/kg toltrazuril (Baycox) for 2 days Ascarids  Common in tortoises  Pathogenic  Impaction, ill thrift and death reported  Fenbendazole effective Protozoa  Tortoise faeces carry a wide variety of motile protozoa  Few are pathogenic  Treat only if clinical signs suggest pathology  Protozoa in carnivorous species are abnormal flora  Metronidazole at 50mg/kg q2d Cryptosporidium  Cause of small intestinal epithelial hyperplasia in leopard geckos and some monitor species  Gastric hyperplasia in snakes  Leads to rapid weight loss  Growth reduction and regurgitation uncommon in geckos  Regurgitation and gastric dilation common in snakes  Asymptomatic dormant state common  Diagnosis by organism detection  Acid-fast faecal/gastric flush preparations  Histopathology Treatment  Potentiated sulphonamides slow progression  Paromomycin and hyperimmune bovine colostrum have shown experimental promise  Not readily available  HIBC no benefit in small intestinal infection  No reliable therapy  Advanced cases should be euthanased  In contacts should be considered infected Salmonella  Captive reptiles frequently carry Salmonella as part of their GI flora  Wild reptiles do not  Treatment is not recommended due to potential for inducing antibiotic resistance  Good hygiene practice will prevent human infection  The HPA has produced a leaflet on this topic Ectoparasites  Ophionyssus natricus  Seen in snakes and lizards  High burdens can lead to anaemia  Vector of disease  Treatment  Fipronil (Frontline) at 2ml/kg  Used with care due to toxicity of alcohol-based solvent  Ivermectin  Do not use with Green tree pythons or near tortoises Pterygosomid mites  Unusual in UK reptiles  Occasionally seen in imported animals  Treated by the same methods Blood sampling  Tortoises  Jugular vein runs superficially from the tympanum to thoracic inlet  Supcarapacial sinus  Dorsal tail vein samples are frequently lymphcontaminated Subcarapacial sinus sample collection Dorsal tail vein sample collection Lizards  Ventral tail vein  Proximal tail contains hemipenes in males  Insert needle midline  Advance until vertebral contact occurs  Withdraw slightly  Easy to sample in most species  Avoid in geckos and juvenile iguanas  Jugular vein  Runs along a line drawn from the mandibular ramus to the shoulder  Difficult to access blind  Ventral abdominal vein  Haemostasis is very difficult Snakes  Ventral tail vein  Palatine vessel  Possible in large, anaesthetised snakes  Cardiac  Visualise heart on ventral body wall  Immobilise the heart by placing a thumb proximally  Insert needle from caudal aspect Biochemistry  Ensure access to good reference values  Carpenter Exotic animal formulary  Serum or Heparinised plasma suitable  Modern machines can run a profile in 0.1ml serum  6-8% blood volume can be collected  Equates to 0.6ml per 100g (including haematoma)  Less in debilitated animals Hepatic dysfunction  Very common syndrome with non-specific symptoms  Enzymes (AST, GGT, ALT) non-specific  AST elevation with normal CK supports hepatocellular damage  Low albumin and uric acid, elevated urea  Bile acids most reliable marker  Single point measurement  Insensitive with focal/mild hepatopathy  Imaging may identify hepatomegaly  Endoscopic or surgical biopsy is required for definitive diagnosis Renal dysfunction  Urinalysis limited as urine is modified in the lower intestine  Urinary GGT, NAG and AST indicate renal tissue damage  Blood AST non-specific  Elevated uric acid can indicate compromise  Concurrent urea measurement helps with differentiating renal and pre-renal disease  Hypocalcaemia and hyperphosphataemia seen in renal disease (RSHP) Calcium  Total calcium is not a reliable marker of calcium homeostasis  Ionised calcium much more reliable but requires greater sample volume  Phosphate elevation with low ionised calcium consistent with secondary hyperparathyroidism  1,25-Cholecalciferol and PTH levels possible in reptilian species but not commercially available Haematology  Nucleated red blood cells preclude standard haematology machine use  Manual counts simple to perform in-house  PCV  WBC  Heterophilia and leucocytosis common in infectious pathology  Monocytosis in chronic infections  Leucopaenia with chronic disease, viral infection, sequestration with focal inflammation or chronic immunosuppression with inappropriate husbandry  Blood smear evaluation essential  Allows differential count  Assessment of morphology  E.g. toxic heterophil presence, regenerative erythrocyte response Nutritional Secondary Hyperparathyroidism (Metabolic Bone Disease)  Affects all reptiles  Calcium metabolism requires several factors:  Calcium  Vitamin D (dietary or UVB provision)  Appropriate heating  Renal and hepatic function  Husbandry deficiencies are common  Calcium homeostasis aims to keep blood calcium within a narrow range  Reduced availability leads to hypocalcaemia  Parathyroid hormone secretion increases  Osteoclast activity increases  Blood calcium normalises  Bone is demineralised Diagnosis  Clinical presentation is characteristic  Blood calcium may be normal  Blood phosphate is usually elevated  Radiographs can grade severity  Demineralisation, particularly of extremities  Bone remodelling Treatment  Correct deficiency  Intramuscular calcium gluconate  Oral calcium and Vitamin D medication  Correct husbandry  UVB lighting  Supplementation  Correct temperatures  Apply to all animals in group, not only clinical cases  Euthanase cases with permanent mobility or feeding compromise. Post-Hibernation Anorexia  Primarily tortoises  Causes:  Excessive length of hibernation  Poor health prior to hibernation  Low white cell count  Chronic stress  Failing to reach POTZ  Compromises immunity, favours pathogens  Disease or trauma during hibernation  Poor husbandry and management When to intervene?  Loss of 10% body weight during hibernation  Failure to urinate or drink within 4 days  Failure to eat within one week  Presence of any clinical signs  Concurrent runny nose syndrome common Post-Hibernation Anorexia  Treatment  Correct dehydration  Fluid therapy and achieve urination  Prior to initiation of feeding  Increase blood glucose once hydrated  Optimal environmental conditions  Appropriate nutrition  Treat concurrent disease  Improve long-term care and management Oesophagostomy Tube  Allows easy feeding  Medicating  Minimal stress for patient  Very simple for owner  Inexpensive  Long-lasting  Vital for PHA Minimising hibernation problems  Pre-hibernation health check  Visual exam, faecal exam, further tests if indicated  Scan females!  No harm in missing hibernation if tortoise is sick  Discuss hibernation length  Preparation of hibernaculum  Ensure temperatures are appropriate and stable  Monitor throughout hibernation  Be prepared to act if problems arise Can all tortoises hibernate?  YES  NO!  Hermann’s tortoise  Tunisian tortoise  Spur-thighed tortoise  Red-eared terrapins  Marginated tortoise  Box turtles  Horsfields tortoise  Hingeback tortoises  Desert tortoise  Leopard tortoise  African spurred tortoise  Red/Yellow foot tortoise Hibernation Preparation  Mimic late autumnal conditions  Decrease temperature gradually initially  Maintain at consistently low temperatures (<15oC)  Decreasing light and UVB exposure  Starve for 3-4 weeks  No necrotic food in gut  Usually tortoises do this themselves  Bath regularly to ensure hydration Hibernation  Hibernate between 3oC-7oC  Too cold: frost can cause blindness and limb damage  Frequently seen in ‘free hibernating’ UK tortoises  Too warm: energy stores are rapidly used up so tortoises lose weight, dehydrate and accumulate toxins  1% weight loss per month is acceptable Management during hibernation  Tortoises can and should be handled and checked  Weight check  Every two days  Signs of activity  Urination or significantly disturbed bedding suggests increased temperature and a break in hibernation  Early hibernation – ensure temperatures low enough  Mid/late hibernation - Stop hibernation  Monitor ambient temperature at least once daily  Ideal is auto-monitoring, data-storing thermometer  Any other signs of illness  Predator injury in outbuildings Traditional hibernaculum Fridge method  Stable temperatures  Easy monitoring  Preferable  Beware fridges with ice formation! Ending Hibernation  Outdoor hibernated tortoises will naturally awake in late spring  Prolonged hibernation is the most common factor in posthibernation anorexia  Utilisation of all energy stores  Lack of time to reaccumulate stores before next hibernation  Failure to recover from prolonged dormant state  UK tortoises are commonly hibernated for 5-6 months  Far longer than in their natural climate  4-12 weeks is recommended  Hibernation should never exceed 16 weeks Ending Hibernation  Tortoises need temperatures >15oC to kickstart the metabolism  Warming should occur over several hours  Once responsive movement is seen move to normal enclosure  Increase temperatures from 15oC to POTZ over 48hrs  Provide 8hrs light with UVB  Bathe daily  Many tortoises require water to stimulate urination  Allow hydration via drinking/bladder absorption  Monitor weight, urination, defaecation and appetite until normal Post-Hibernation Exam  Discuss hibernation protocol used  Check weight  Physical examination  Assess summer management  Intervention as necessary  Further tests e.g. blood profile  Fluid therapy  Pharyngostomy tube placement  Specific treatment Runny Nose Syndrome  Any tortoise species, often Testudo sp  Causes:  Viral  Mycoplasma  Bacterial  Fungal  Hypovitaminosis A  Poor husbandry n Diagnosis  Clinical appearance distinctive  Identify specific causative factors  Chelonian herpes PCR  Geochelone/Stigmochelys species and Hermann’s tortoises appear particularly sensitive, many others may act as carriers  Mycoplasma PCR  Chlamydia serology/PCR  Dietary and husbandry assessment  Bacterial culture and sensitivity Treatment  Antibiotics  Secondary infections are often cause of symptoms even with herpes and hypovitaminosis A  Nasal flushing  Antibiotics  Saline  F10  Improve husbandry  Severe cases will require hospitalisation for assist feeding, fluid therapy, nebulisation and flushing. Pneumonia  This may be an extension of RNS in tortoises or stomatitis in snakes  Viral, bacterial and fungal agents all reported  Radiography especially useful in tortoises  Horizontal beam views most rewarding  Tracheal wash indicated in all reptiles  Cytology  Culture  PCR  Lung biopsy/flush can be carried out endoscopically Treatment  Antimicrobial therapy based on microbiology  Nebulisation  1:250 F10  Antibiotic solutions  Clearing of secretions important in snakes  Coupage  Encourage activity  High humidity Tortoise trauma  Common in outdoor tortoises  Lawnmowers  Children  Dogs, foxes and rats  All wounds should be considered contaminated  Maintain as open wounds initially  Soft tissue injuries require protection to granulate Shell Fracture Repair  Wet-to Dry Bandages  Gauze and saline +/chlorhexidine  Short-term to clear infection  Long-term use traumatises granulation bed  Vacuum assisted closure  Constant negative pressure of ~125mmHg  Excellent for chronically infected wounds  Expensive equipment, not practical in all cases  Epoxy resin  Cannot be used for contaminated wounds  Can hinder shell growth  Often used together with screws/wires/plates  External fixation  Cannot replace deficits  Good positioning of fragments usually achieved  Platelet Rich Plasma  Platelets store and release growth factors and chemotactic molecules involves in haemostasis and cell proliferation  Sodium citrate anticoagulant  Add calcium gluconate to trigger clot formation and apply as a gel  Acts as a barrier and promotes local healing  Analgesia  Antibiotic therapy  Secure loose fragments  Sterile dressing changes daily  Consider patching large defects once confident the area is not infected  Fibreglass or non-heating resin Stomatitis  Causative factors vary:  Herpes virus related in tortoises  Snout trauma in lizards  Immunosuppression in snakes  ?OPMV-1 involvment  Culture, cytology and biopsy can aid specific diagnosis  Often broad spectrum antibiotic therapy is initiated  Topical treatments can help  F10 flushes  Silver ointments for open lesions  Analgesia necessary Periodontal disease  Agamids and chameleons have acrodont teeth  These are housed in an exposed section of the jaw bone  Teeth are not shed and replaced  Soft diet or trauma predispose to gingival inflammation and recession  Osteomyelitis eventually results  Prevention  Feed harder diet (avoid soft fruits)  Prevent trauma  Treatment  Remove plaque  Debride necrotic tissue and bone  Administer topical and systemic antibiotics Neurological disease in snakes  Typically presents as:  Loss of righting reflex  Stargazing  Paresis  Tremors  Seizures  Aggressive behaviour Differential diagnoses  Heat or mechanical trauma  Metabolic abnormalities  Renal/hepatic disease  Hypocalcaemia unusual in snakes  Toxin exposure  Nicotine  Insecticides Infectious causes  Paramyxovirus (Ferlavirus)  Seen in colubrids and elapids  Predilection for venomous species  May cause respiratory or neurological disease  Difficult to diagnose reliably  Can have an incubation period of up to 1yr  1/3 positive cases asymptomatic  1/5 grossly normal on post-mortem exam  Diagnosis by serology  Seroconversion takes 6-8 weeks, demonstrate rising titre  PCR on oral and cloacal swabs can be used  Lung>intestine>liver>kidney for inclusions on histopath Inclusion Body Disease of Boids  Due to infection with arenavirus  Pythons highly susceptible and develop acute neurological symptoms  Single case report in corn snakes  Boas can act as subclinical carriers  Serology and PCR available for ante-mortem testing  Histopathology IBDB  Clinical syndrome not necessarily single pathogen  Large eosinophilic protein inclusions, NOT viral particles  BCI most commonly diagnosed histopathologically  47% of post-mortem BCI cases were positive  95% of these had detectable hepatic inclusions  Other Boinae and Pythoninae less commonly affected  Very low clinical incidence in pythons  Beware assuming diagnosis with ‘typical’ symptoms Agamid adenovirus 1  Cause of neurological signs, poor growth, immunosuppression and death  The virus has been demonstrated in clinically healthy bearded dragons  18.5% PCR +ve for agamid adenovirus 1  Breeding groups should be screened to maintain clean colonies  Combined choanal and cloacal swabs for PCR Autotomy  Tail autoamputation is a natural defence  Rough handling, Acute stress or tail trauma triggers vertebral cleavage  Ongoing contractions focus attention on the tail  Keep the stump clean but do not apply medication or suture the site  House the gecko alone, on paper  Feed daily as energy and fluid storage is compromised  Within 8 weeks a primitive tail will reform  Autoamputation can be used to minimise bleeding for tail amputations Osteomyelitis  Requires initial entry wound  Skin trauma common  Bacterial emboli block smallest capillaries  Toes typically affected  Other joints may less commonly be involved  Swelling and pain results  Aspiration and radiography needed for diagnosis  Analgesia should be prescribed  Broad-spectrum antibiotic therapy pending culture  Cytology of joints assists in diagnosis  Gout  Mycoplasmosis  Mycobacteriosis  Fungal infections Urolithiasis in bearded dragons  Urates are semi-solid waste produced by the kidneys  Urates are stored in the rectum and cloaca until they are voided with faeces  Infrequent defaecation predisposes to dessication of urates refluxed into the colon  The colon absorbs fluid to leave a solid urolith Treatment  Uroliths are usually easily flushed by instilling fluid into the cloaca and rectum via a blunt ended tube  Prevention  Adequate fibre  Appropriate temperatures  Hydration  Calcium and UVB provision Any questions?