LET S WORK THEM UP! EXOTIC COMPANION MAMMAL CASES

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1 LET S WORK THEM UP! EXOTIC COMPANION MAMMAL CASES Anna Meredith, MA, VetMB, PhD, CertLAS, DZooMed, MRCVS Royal (Dick) School of Veterinary Studies University of Edinburgh, Scotland, UK The aim of this presentation is to work through several common case scenarios in exotic companion mammals that are regularly encountered in general practice, using real cases as illustrative examples. Coming up with a species-specific list of differential diagnoses, logical planning of appropriate, targeted, diagnostic tests, and institution of a realistic therapeutic plan are the keystones to successful management of these cases. For future utility, in these notes I have provided information on the main differentials, tests, and therapy to consider for each case scenario, largely in tabular format, rather than the specific individual case reports that will be used to illustrate each scenario these can then be applied to a wide variety of cases that you may encounter in practice. 1. RABBIT WITH URINE SCALD Urine scalding is a common presenting sign in rabbits and can be caused by polyuria, true incontinence (urine leakage), or any illness that results in immobility of the rabbit so that it cannot direct the flow of urine away from the body. In practice it can often be difficult to determine the exact cause of the urine scalding, and a thorough clinical and neurologic examination, assessment of urinary tract function, including urinalysis, and assessment of musculoskeletal function is necessary. Once urine scald is present, a vicious circle occurs, where the painful dermatitis due to the urine scalding makes the rabbit reluctant to adopt the normal urination stance. In these cases, establishing cause and effect can be challenging. Rabbit owners often find long-term care of rabbits with urinary incontinence and scalding very difficult and the stress on the rabbit of prolonged handling and cleaning of the perineum should be taken into account when deciding on a treatment plan. Table 1. Urine Scalding in Rabbits Cause of Urine Scalding Differential Diagnoses Further Investigations Polyuria Renal insufficiency Chronic renal failure Liver disease (hepatic lipidosis) Urinalysis (dipstick, cytology, culture,specific gravity) Hematology

2 Hypokalemia Pyometra Endotoxemia Pyelonephritis Pregnancy toxaemia and ketoacidosis Diabetes mellitus Iatrogenic (diuretics, corticosteroids) Serology (E cuniculi) Ultrasonography Incontinence Encephalitozoonosis/other bacterial meningitis/ encephalomyelitis Spinal fracture/dislocation Intervertebral disk disease Spinal abscess Hormone-responsive incontinence (spayeddoes) Cystitis Urolithiasis/ hypercalciuria Neoplasia Ectopic ureter /CT, including contraststudies (myelography, cystography) Ultrasonography Urinalysis (cytology, culture) Bladder biopsy Serology ( E cuniculi, toxoplasmosis) Response to diethylstilbestrol Inability/reluctance to adopt normal urination stance or direct urine flow away from body Limb fractures Spondylosis/spondylitis Osteoarthritis Pododermatitis Hypovitaminosis E or Se deficiency Floppy rabbit syndrome Obesity Large skin folds Wounds/scarring Perineal dermatitis (the vicious circle ) Treponema cuniculi(syphilis) Any systemic disease leading to severed Serum vitamin E Muscle biopsy

3 depression Cage too small Management Options The underlying cause should be addressed where possible. Cases with irreversible or progressive neurologic damage should be euthanized. While a diagnosis is being pursued, supportive treatment includes cleaning and drying of perineum including clipping away stained fur. Analgesia is very important, as the inflamed skin is painful and the underlying cause may be due to skeletal pain (e.g., arthritis). Topical or parenteral treatment for any secondary bacterial dermatitis should be instigated. Some spayed female rabbits are responsive to 0.5 mg diethylstilbestrol (DES) one or two times per week. Treatment for encephalitozoonosis can be attempted using fenbendazole (20 mg/kg SID for 4 weeks). Penicillin is used for treating Treponema. Surgical treatment and appropriate antibiosis is indicated for urolithiasis. Surgical resection may also be indicated for removal of large skin folds (dermaplasty) and some cases of neoplasia, and meloxicam may be useful in cases of transitional cell carcinoma. 2. RABBIT WITH HEAD TILT Head tilt or torticollis in rabbits is common and may be sudden or gradual in onset. First, establish whether a true head tilt exists or whether the rabbit is simply holding one ear down due to pain from otitis externa alone. For vestibular disease, the main challenge is in determination of whether the lesion is central or peripheral. A full neurologic assessment should always be carried out; however, findings should be interpreted with care as reactions can be variable and different to those anticipated, due to the stress response and the fact they are a prey species. Rabbits with vestibular pathology (otitis media/interna) will exhibit nystagmus, torticollis, ataxia and/or tremors in addition to the head tilt. Radiographic changes in the tympanic bullae may not be detectable in many rabbits with middle ear disease, and computed tomography (CT) or magnetic resonance imaging (MRI) are superior to radiography in detecting bulla disease. Note that many affected rabbits may also have a positive E cuniculi titer (IgM and/or IgG), which may lead to over-diagnosis of E.cuniculi as a cause of head tilt in the absence of obvious aural disease. The presence of facial nerve paralysis due to damage to CNVII as it passes through the middle ear can aid in distinguishing peripheral from central vestibular disease. There will be ipsilateral paresis/ paralysis of the ear, eyelids, lips and nares and may be corneal lesions due to reduced tear production and the inability to blink. With chronic facial nerve paralysis there may be contracture of the ipsilateral side of the face due to denervation of the facial muscles. However, these lesions can be bilateral and may be subtle and overlooked if both ears are affected. The presence and type of nystagmus does not seem to aid in distinguishing peripheral from central vestibular disease; positional or resting, horizontal or rotary may be seen. There may be ipsilateral

4 strabismus (ventral deviation of the eyeball when the neck is extended) in peripheral vestibular disease. Table 2. Head Tilt in Rabbits Site of Lesion Differential Diagnoses Further Investigations Therapeutic Options Central vestibular disease (cerebellum, medulla oblongata) Bacterial infection Encephalitozoonosis Toxoplasmosis Herpesvirus (Herpessimples 1) encephalitis Cerebrovascular accident Degenerative changes Visceral larva migrans Trauma Toxins Neoplasia Rabies Haematology Serum lead levels CSF analysis/culture Antibiosis Serology (E Fenbendazole cuniculi/toxoplasma) CT MRI Peripheral vestibular disease (CN VIII, inner ear) Otoscopy Cytology Bacterial otitis Culture media/interna Serum lead levels Toxins Radigraphy?idiopathic Ultrasonography of vestibular syndrome bullae Neoplasia CT MRI Antibiosis Myringotomy Surgery - total or partial ECA, bulla osteotomy/ ostectomy External ear Otitis externa Otoscopy Cytology Examination for parasites(psoroptes Antibiosis Antiparasitics(ivermectin/ selamectin) Analgesia

5 cuniclui) Culture Surgery lateral ear canalresection Treatment of otitis media/interna in the rabbit can be attempted using aural cleaning and long term antibiotic therapy based on culture and sensitivity testing, but is frequently best achieved surgically (bulla osteotomy) plus removal of all infected tissue/abscess. Although Pasteurella multocida is frequently cited as being the most common cause of aural infections, many other species of bacteria are frequently isolated and culture and sensitivity testing is always recommended. Yeasts may also be involved in otitis externa. Even with successful elimination of infection, the head tilt and facial paralysis are likely to persist if damage to the vestibular nerve is irreversible, although many rabbits adapt and make an improvement and are able to maintain a good quality of life. Topical treatments should be used with care in rabbits as the epithelium of the external ear canal is very delicate and rabbits may exhibit sensitivity reactions to commercial products designed for cats and dogs. Lateral ear canal resection or total ear canal ablation may be necessary in cases of chronic otitis externa. The incidence of head tilt due to E cuniculi is not known, but it is widely cited as a cause. Diagnosis should be based on methodical ruling out of other causes in addition to the demonstration of antibodies and/or antigen (PCR). E cuniculi can also cause a variety of other clinical signs including paresis/paralysis, seizures and urinary incontinence (neurological or due to renal failure). 3. RABBIT WITH GI STASIS Gastrointestinal stasis is a poorly defined term used to describe any decrease in gastrointestinal motility. An important factor underlying the development of gastrointestinal stasis is a low fiber, high carbohydrate diet. Food intake and GI motility are co-dependent; thus anorexia will cause hypomotility, and hypomotility will cause anorexia. Reduced GI motility leads to accumulation and dehydration of GI contents, which decreases motility further. Gastric stasis leads to dehydration and impaction of the normal stomach contents, which include hair. The impacted material can be palpated as a doughy to firm stomach mass and seen radiographically as a gastric mass surrounded by a halo of gas. True hairballs or trichobezoars can be found in long-haired rabbits such as Angoras, which can ingest excessive amounts of long hair, and these can cause obstruction of the pyloric region and cause mortality. Table 3. Gastrointestinal Stasis in Rabbits Causes of GI Stasis Further Investigations Therapeutic Options

6 Fluid therapy. If in hypovolemic shock, active warming (warm IV fluids and external heat sources), colloids as well as crystalloids. Monitoring of blood pressure to determine response. Lack of dietary fiber Sudden change of diet Anorexia Chronic dehydration Environmental stressors: Proximity of predators Proximity of adominant/competetive rabbit Change/ destabilisationof group hierarchy Change of housing Transport Extremes ofweather/ temperature Loss of a companion Pain Post-surgical adhesions Ingestion of toxins (e.g.,lead) Foreign body Dietary history Husbandry history Dental examination incl. contrast studies Ultrasonography Hematology Serum lead Laparoscopy Laparotomy Enterotomy/ foreignbody removal Analgesia Buprenorphine mg/kg SC/IV TID, butorphanol mg/kg SC/ IV every 2 4 hours, carprofen 2 4 mg/kg SC/IV SID. Fentanyl 5 10 µg/kg/min plus ketamine 1 2 mg/kg/hr as a constant rate infusion Motility modifiers/ prokinetics Metoclopramide 0.5 mg/kg SC BID, cisapride 0.5 mg/kg PO BID, ranitidine 2 5 mg/kg PO BID. Ranitidine and cisapride have been shown to have a synergistic effect. Nutritional support Commercially available high fiber herbivore recovery diets, ml/kg at least three times a day. Nasogastric tube if syringe feeding is refused or inadequate. Hay and tempting green foods should always be offered to encourage appetite Exercise Helps to stimulate GI motility. Rabbits recovering from GI stasis should be encouraged to exercise as they improve but should not be forced to do so. Clinical signs associated with gastrointestinal stasis where there is no obstruction include a gradual reduction in appetite to anorexia, decreased output and size of fecal pellets,

7 abdominal pain tooth-grinding, hunched posture, reluctance to move dehydration, and shock (hypothermia, depression). Affected rabbits are generally bright initially but without intervention there is progression to depression, lethargy, dehydration and death. Obstruction of the GI tract can be partial or complete. Partial obstruction can present in a very similar fashion to non-obstructive GI stasis and differentiation can be a challenge (Table 4). In some of these cases a moving foreign body could explain the clinical signs. Complete GI obstruction, however, presents as an emergency, with an acute onset of clinical signs and rapid development of shock. Gastric dilation and fluid accumulation is generally associated with obstruction. Rabbits can develop complete or partial obstructions due to small pellets of desiccated ingesta and/or compressed hair, and ingested materials such as locust bean seeds, or pieces of carpet. Less commonly, neoplasia, abscesses or surgical adhesions can cause partial or complete obstruction, and herniation and tapeworm cysts have also been described as causes. The most common sites are the proximal duodenum and ileocecocolic region. Table 4. Factors in Aiding Differentiation of Non-obstructive GI Stasis and GI Obstruction Non-obstructive GI stasis Obstruction Clinical signs: Gradual onset (days to weeks) Gradual reduction in faecal size and output Initially bright, gradual onset of depression and abdominal pain Doughy gastric and caecal contents onpalpation Mild to moderate dehydration Radiographic findings: Compacted material in stomach and sometimes caecum, often with halo of gas. As symptoms progress, entire GI tract gas-filled including stomach Clinical signs: Sudden onset (24-48 hours) Faecal output stops suddenly Gastric dilation and fluid accumulation Severe depression Abdominal pain Reluctance to move Shock slow CRT, pale mucous membranes, bradycardia,hypothermia Severe dehydration Death in hours Radiographic findings: Gastric dilation and tympany Fluid and gas generally proximal to obstruction, although in some cases gas may accumulate distally as well

8 Fluid only present late in disease Diagnosis is based on clinical signs, abdominal palpation and radiographic findings. is the single most important diagnostic tool for evaluation of the rabbit GI tract and for monitoring response to treatment. Ultrasonography may also be useful in some circumstances but the presence of gas reduces its utility. Hematology and serum biochemistry are useful for assessing dehydration, and other abnormalities such as anemia, hypoproteinemia, hypo- or hyperglycemia or azotemia. 4. FERRET WITH HIND LIMB PARESIS In ferrets, hind limb or posterior paresis is indistinguishable from hind limb weakness (Table 5). Generalized weakness in ferrets is more pronounced and visible in the hind limbs, as they lose the normal arched back stance, and can often be mistakenly attributed to a primary neurologic problem. Paresis should be distinguished from ataxia (incoordination) and can be due to cerebellar or vestibular disease, where weakness/ paresis is not present, or spinal disease, where proprioceptive deficits are present. The most important initial rule out is hypoglycemia, which is commonly due to insulinoma, although prolonged seizures due to other causes can cause hypoglycemia. Any weak ferret should have a fasting blood glucose taken, levels <60 mg/dl (3.4 mmol/l) are generally diagnostic. Abdominal discomfort or pain may also result in hind limb paresis. 5. GUINEA PIG WITH ABDOMINAL SWELLING Guinea pigs can make challenging patients they seem exquisitely sensitive to any discomfort or pain and often appear to lose the will to live and not respond even to aggressive supportive treatment in some situations. Adequate analgesia and intensive supportive care in the form of high-fiber assisted feeding, fluid therapy, GI motility modifiers, warmth and stress-free surroundings with a dark secure hide-box are essential. The presence of a known companion is also highly beneficial as separation is very stressful, and low dose midazolam (2 5 mg/kg) can be a useful adjunct in minimizing stress during hospitalization. Abdominal enlargement/distention is a common presenting sign and for the novice, palpation of a normal guinea pig abdomen can be confusing, due to the presence of the large cecum and elicitation of vocalizations even on gentle manipulation (Table 6). Table 5. Hind Limb Paresis in Ferrets

9 Cause of Paresis Further Investigations Therapeutic Options Neurological Spinal trauma/abscess Other musculoskeletal trauma Intervertebral disk disease Aleutian disease Myelitis Neoplasia, e.g., chordoma Disseminated idiopathic myositis Systemic granulomatous inflammatory syndrome Toxicity, e.g., ibuprofen, botulism Neuronal ceroid lipofuscinosis(rare; inherited) Neurologic examination Hematology AD serology/pcr CSF analysis CT MRI Myelography Muscle biopsy Supportive care Surgery Penicillin (botulism) Non-neurological Hypoglycemia: Insulinoma, food deprivation, vomiting, sepsis, seizures, severe hepatic disease Hypocalcemia (lactation) Pregnancy toxemia Thromboembolism Anemia (e.g., AGD, hyperestrogenism) Cardiac disease Hypoxia Proliferative bowel Blood glucose Hematology Bone marrow analysis Ultrasonography Echocardiography Ilial or colonic biopsy PCR for Lawsonia Supportive care Insulinoma therapy surgery, diazoxide, prednisolone Calcium supplementation Blood transfusion Surgery Chloramphenicol (PBD)

10 disease Splenomegaly Caudal abdominal mass Cystic calculi Peritonitis Prostatomegaly Urinary obstruction Table 6. Abdominal Swelling in Guinea Pigs Cause of Abdominal Swelling Further Investigations Therapeutic Options Cystic ovarian disease Gastric bloat Ileus Ascites Organomegaly Pregnancy Neoplasia Abscess Lymphadenopathy e.g.,yersiniosis. Lymphoma/ lymphosarcoma GI foreign body Gastric trichobezoar GI Impaction Uterine hyperplasia/neoplasia Pyometra/metritis Abdominal fat Dental examination Hematology includingcontrast studies Ultrasonographyincluding US-guided FNA/biopsy Peritoneal tap Laparoscopy Exploratory laparotomy Supportive care( fluids, feeding) Ovariohysterectomy Stomach tube/decompression GI motility modifiers (ranitidine, cisapridemetoclopramide) Gastrotomy/enterotomy Chemotherapy Antibiosis