megaoesophagus in adult dogs secondary to australian tiger snake envenomation

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672 Clinical Aust Vet J Vol 79, No 10, October 2001 EDITOR MAUREEN REVINGTON ADVISORY COMMITTEE ANAESTHESIA PETER GRAY AQUATIC ANIMAL MEDICINE AND HEALTH BRADLEY CHADWICK AVIAN MEDICINE AND SURGERY SHANE RAIDAL CLINICAL PATHOLOGY/BIOCHEMISTRY MARY McCONNELL CRITICAL CARE/EMERGENCY MEDICINE ALICIA FAGGELLA EPIDEMIOLOGY CHRIS BALDOCK EQUINE MEDICINE AND SURGERY KATE STEEL LABORATORY ANIMAL MEDICINE/HEALTH DAVID PASS OPHTHALMOLOGY ZIGRIDA CHESTER PRODUCTION ANIMAL MEDICINE HELEN CHAPMAN SMALL ANIMAL MEDICINE PETER IRWIN SURGERY RICK READ WILDLIFE AND EXOTIC ANIMAL MEDICINE/SURGERY RALPH SWAN EDITORIAL ASSISTANT AND DESKTOP PUBLISHING ANNA GALLO CONTRIBUTIONS INVITED Practising veterinarians and others are invited to contribute clinical articles to the Australian Veterinary Journal. We will consider material in a variety of formats, including clinically orientated reviews, reports of case series, individual case studies, diagnostic exercises, and letters containing comments or queries. Practitioners are also invited to contribute to the case notes feature, where accepted articles are not peer reviewed but are edited for publication. Contributors should consult instructions to authors and recent issues of the journal for guidelines as to formatting. Over referencing should be avoided: authors should preferably quote only those articles they feel are most likely to be of interest and benefit to readers. Send all contributions to: Editor, AVJ Clinical Section AVA House, 272 Brunswick Road, Brunswick, Vic. 3056, Phone: (03) 9387 2982 Fax: (03) 9388 0112 Email: [email protected] Australian VETERINARY JOURNAL C L I N I C A L S E C T I O N Megaoesophagus in adult dogs secondary to Australian tiger snake envenomation K HOPPER a , C BECK and RF SLOCOMBE The University of Melbourne Veterinary Clinic and Hospital, 250 Princes Highway, Werribee, Victoria 3030 Four cases of megaoesophagus secondary to tiger snake envenomation are reported. History in all cases suggested megaoesophagus was not present prior to snake envenomation. Diagnosis of megaoesophagus was confirmed by thoracic radiography in all cases. One dog died of respiratory failure. The remaining three dogs recovered, with gradual resolution of clinical signs associated with megaoesophagus. Aust Vet J 2001;79:652-675 Key words: dog, snake bite, tiger snake, megaoesophagus M egaoesophagus is a generalised oesophageal dilation resulting from an aperistaltic oesophagus, secondary to a neuromuscular disorder. 1 It usually results in regurgitation, vomiting, ptyalism, halitosis and, often, aspiration pneumonia. 2 Megaoesophagus can occur as a congenital or acquired disorder, or as an adult onset idiopathic disease. 2 Acquired megaoesophagus can result from any condition that causes disruption of the neural reflex control of swallowing or function of the oesophageal muscles. 1 Secondary acquired megaoesophagus can be caused by any disease that inhibits oesophageal peristalsis by disrupting central, efferent or afferent pathways, or by disease of the oesophageal musculature. 3 Diagnosis of megaoesophagus requires the identification of a dilated oesophagus on thoracic radiographs and confirmation may be made on barium swallows. 2,4 Recorded causes of acquired adult onset megaoesophagus include polymyositis, neuromuscular junction disorders such as myasthenia gravis, peripheral neuropathies and central nervous system disease. Diseases which cause direct damage to the oesophageal musculature, such as oesophagitis or oesophageal neoplasia, can also be associated with megaoesophagus. 1 Envenomation by the Eastern Tiger Snake (Notechis scutatus) has not previously been recorded as a cause of megaoesophagus. Tiger snakes belong to the Elapid family, front fanged snakes of the cobra type that are highly venomous. Within the Notechis (Latin: "southern snake") genus, there are several species of tiger snake, Notechis scutatus being the mainland tiger snake found in southeastern Australia. Venom is secreted by modified salivary glands. Toxins that have been identified in the venom of the common tiger snake include: several phospholipases, which are myotoxins and presynaptic neurotoxins; postsynaptic neurotoxins; a prothrombin activator; a haemolysin and an unidentified nephrotoxin. 5 Acute envenomation in humans and animals may lead to death within minutes, either due to anaphylaxis or from massive envenomation leading to peracute neurotoxicity, respiratory paralysis and death. However, typically envenomation leads to morbidity that becomes apparent in 6 to 24 h, with mydriasis, vomiting and salivation preceding the onset of myalgia, paralysis, haemolysis, DIC, haemoglobinuria, renal failure and rhabdomyolysis. 5 CPK Creatine phosphokinase DIC Diffuse intravascular coagulation IV Intravenously PEG Percutaneous endoscopic gastrotomy tube SVDK Snake Venom Detection Kit UMVCH University of Melbourne Veterinary Clinic and Hospital a School of Veterinary Clinical Science, Division of Veterinary and Biomedical Sciences, Murdoch University, Murdoch, Western Australia

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Page 1: Megaoesophagus in adult dogs secondary to Australian tiger snake envenomation

672

Clinical

Aust Vet J Vol 79, No 10, October 2001

EDITORMAUREEN REVINGTON

ADVISORY COMMITTEE

ANAESTHESIAPETER GRAY

AQUATIC ANIMAL MEDICINE AND HEALTHBRADLEY CHADWICK

AVIAN MEDICINE AND SURGERYSHANE RAIDAL

CLINICAL PATHOLOGY/BIOCHEMISTRYMARY McCONNELL

CRITICAL CARE/EMERGENCY MEDICINEALICIA FAGGELLA

EPIDEMIOLOGYCHRIS BALDOCK

EQUINE MEDICINE AND SURGERYKATE STEEL

LABORATORY ANIMAL MEDICINE/HEALTHDAVID PASS

OPHTHALMOLOGYZIGRIDA CHESTER

PRODUCTION ANIMAL MEDICINE HELEN CHAPMAN

SMALL ANIMAL MEDICINE PETER IRWIN

SURGERYRICK READ

WILDLIFE AND EXOTIC ANIMALMEDICINE/SURGERY

RALPH SWAN

EDITORIAL ASSISTANT AND DESKTOP PUBLISHING

ANNA GALLO

CONTRIBUTIONS INVITED

Practising veterinarians and others are

invited to contribute clinical articles to the

Australian Veterinary Journal. We will

consider material in a variety of formats,

including clinically orientated reviews,

reports of case series, individual case

studies, diagnostic exercises, and letters

containing comments or queries.

Practitioners are also invited to contribute

to the case notes feature, where accepted

articles are not peer reviewed but are

edited for publication. Contributors should

consult instructions to authors and recent

issues of the journal for guidelines as to

formatting. Over referencing should be

avoided: authors should preferably quote

only those articles they feel are most likely

to be of interest and benefit to readers.

Send all contributions to:

Editor, AVJ Clinical Section

AVA House, 272 Brunswick Road,

Brunswick, Vic. 3056,

Phone: (03) 9387 2982

Fax: (03) 9388 0112

Email: [email protected]

Australian

VETERINARYJOURNAL

C L I N I C A L S E C T I O N

Megaoesophagus in adult dogssecondary to Australian tigersnake envenomationK HOPPERa, C BECK and RF SLOCOMBEThe University of Melbourne Veterinary Clinic and Hospital, 250 Princes Highway,Werribee, Victoria 3030

Four cases of megaoesophagus secondary to tiger snake envenomation arereported. History in all cases suggested megaoesophagus was not present prior tosnake envenomation. Diagnosis of megaoesophagus was confirmed by thoracicradiography in all cases. One dog died of respiratory failure. The remaining threedogs recovered, with gradual resolution of clinical signs associated withmegaoesophagus.Aust Vet J 2001;79:652-675Key words: dog, snake bite, tiger snake, megaoesophagus

Megaoesophagus is a generalised oesophageal dilation resulting from anaperistaltic oesophagus, secondary to a neuromuscular disorder.1 It usuallyresults in regurgitation, vomiting, ptyalism, halitosis and, often, aspiration

pneumonia.2

Megaoesophagus can occur as a congenital or acquired disorder, or as an adult onsetidiopathic disease.2 Acquired megaoesophagus can result from any condition that causesdisruption of the neural reflex control of swallowing or function of the oesophagealmuscles.1 Secondary acquired megaoesophagus can be caused by any disease thatinhibits oesophageal peristalsis by disrupting central, efferent or afferent pathways, or bydisease of the oesophageal musculature.3 Diagnosis of megaoesophagus requires theidentification of a dilated oesophagus on thoracic radiographs and confirmation may bemade on barium swallows.2,4

Recorded causes of acquired adult onset megaoesophagus include polymyositis,neuromuscular junction disorders such as myasthenia gravis, peripheral neuropathiesand central nervous system disease. Diseases which cause direct damage to theoesophageal musculature, such as oesophagitis or oesophageal neoplasia, can also beassociated with megaoesophagus.1 Envenomation by the Eastern Tiger Snake (Notechisscutatus) has not previously been recorded as a cause of megaoesophagus.

Tiger snakes belong to the Elapid family, front fanged snakes of the cobra type that arehighly venomous. Within the Notechis (Latin: "southern snake") genus, there are severalspecies of tiger snake, Notechis scutatus being the mainland tiger snake found insoutheastern Australia. Venom is secreted by modified salivary glands. Toxins that havebeen identified in the venom of the common tiger snake include: several phospholipases,which are myotoxins and presynaptic neurotoxins; postsynaptic neurotoxins; aprothrombin activator; a haemolysin and an unidentified nephrotoxin.5 Acuteenvenomation in humans and animals may lead to death within minutes, either due toanaphylaxis or from massive envenomation leading to peracute neurotoxicity, respiratoryparalysis and death. However, typically envenomation leads to morbidity that becomesapparent in 6 to 24 h, with mydriasis, vomiting and salivation preceding the onset ofmyalgia, paralysis, haemolysis, DIC, haemoglobinuria, renal failure and rhabdomyolysis.5

CPK Creatine phosphokinaseDIC Diffuse intravascular coagulationIV IntravenouslyPEG Percutaneous endoscopic gastrotomy tubeSVDK Snake Venom Detection KitUMVCH University of Melbourne Veterinary Clinic and Hospital

aSchool of Veterinary Clinical Science, Division of Veterinary and Biomedical Sciences, Murdoch University,Murdoch, Western Australia

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The food given was progressively increased in volume andconcentration in an attempt to reach the dog's daily nutritionalrequirement of 6 mL/kg of concentrate food every 4 h, withappropriate adjustments for regurgitations. The volume of watergiven via tube feeding was adjusted to meet daily requirementsfollowing cessation of IV fluid therapy. Following each regurgi-tation, feeding was withheld for 4 h, then recommenced at 0.5mL/kg every 2 h and again gradually increased. Most regurgi-tations were froth and saliva and did not contain food material.

Eight days after presentation, regurgitation stopped and thedog was discharged for tube feeding at home. At discharge thedog had no evidence of myopathy. His gait was normal and allanalgesics were discontinued by day 6. Recovery at home wasuneventful and 3 weeks following presentation oral feeding withsmall pieces of chicken was commenced. Oral feeding wasgradually increased and tube feeding reduced accordingly. Thedog was eating and drinking normally 36 days after presentationand the gastrotomy tube was removed.

Case 2

A 5-year-old entire female Staffordshire Bull Terrier waspresented to the primary veterinarian with a 12 h history ofvomiting, muscle weakness and dark, discoloured urine. Theowners had seen the dog with a tiger snake 2 days earlier. Bloodtests taken 2 days after presentation (4 days after contact withthe snake) revealed a markedly elevated CPK (greater than100,000 IU/L reference range: 50-400 IU/L). A snake venomdetection test performed on urine was positive for tiger snakevenom. One vial of Tiger and Brown Snake CombinedAntivenom was given. Persistent vomiting and/or regurgitationcontinued and the dog was referred 14 days after presentation tothe UMVCH with radiographic evidence of megaoesophagus.

On presentation the dog was emaciated, not having eaten for17 days. IV fluids were initiated and a PEG tube placed. Tubefeeding was commenced with oral electrolyte solution at 4mL/kg every 2 h. Cisapride (0.4 mg/kg PO every 8 h) was givenvia the gastrotomy tube to enhance gastrointestinal motility.Following tube feeding for 12 h with the electrolyte solution, aliquid rehabilitation diet (Clinicare-Canine Formula; Abbott,USA) was started at 4 mL/kg combined with 2 mL/kg ofelectrolyte solution every 2 h. For the first 24 hours the dogappeared to deteriorate and aspiration pneumonia developed.Tube feeding was continued despite the poor prognosis.Aspiration pneumonia was treated with IV cephalexin (22mg/kg three times daily) and thoracic coupage every 4 h.

Forty eight hours following gastrotomy tube placement,feeding was increased to 5 mL/kg of concentrate food mixedwith 7 mL/kg of water every 2 h. The dog's demeanourimproved. At 36 h after presentation the dog had furtherimproved and tube feeding was changed to 8 mL/kg food mixedwith 6 mL/kg water every 3 h. IV fluids were discontinued andthe dog was discharged to be tube fed at home. The referringveterinarian was instructed to increase gradually the amount offood given via the gastrotomy tube. Thirty days afterpresentation to the UMVCH, the PEG tube was removed as thedog was eating normally with no apparent complications. Twomonths after presentation the owners reported the dog was inexcellent health and almost back to her normal body weight.

Case 3An 8-year-old desexed female Whippet presented to a

veterinarian for vomiting, lethargy and difficulty swallowing.

Tiger snake venom contains at least six classes ofphospholipase A2 and these are thought responsible for thedevelopment of rhabdomyolysis. The toxic effects ofphospholipases on skeletal muscle are exaggerated if muscleactivity is high. Smooth and cardiac muscle are not affected.5

This report describes four cases in which megaoesophagusdeveloped in association with tiger snake envenomation. Onedog died. The other three regained normal oesophagealfunction following treatment.

Case reports

Case 1A 5-year-old entire male Doberman presented in a collapsed

state after fighting with a tiger snake. Urine was positive fortiger snake venom using a SVDK (CSL Australia). Emergencytreatment included oxygen, IV fluid support and Tiger andBrown Snake Combined Antivenom (CSL Australia).

Twelve hours after presentation the dog started regurgitatingand/or vomiting. At this time the dog was weak, unable to standand painful if moved, signs consistent with myopathy.Butorphanol (0.5 mg/kg IV) , an opioid analgesic, wasadministered to control pain associated with muscle damage. Anasogastric tube was placed to allow suction of the stomach.Metoclopramide (0.2 mg/kg SC every 6 h) and cisapride (0.4mg/kg PO every 8 h) were given to improve gastrointestinalmotility. Despite these treatments, nausea and regurgitationand/or vomiting persisted.

Forty eight hours after envenomation a lateral thoracicradiograph revealed megaoesophagus with mild aspirationpneumonia (Figure 1). A generalised myopathy was stillevident, with limb stiffness and reluctance to walk. The dogremained on butorphanol. A PEG tube was placed and feedingcommenced. Initial gastrotomy tube feeding consisted of 0.25mL/kg of an electrolyte solution (Lectade; Jurox, Australia)every hour for 4 h. This was increased to 1 mL/kg every 2 h forthe next 8 h. Twelve hours after the electrolyte solution wasstarted, feeding was changed to a recovery diet (Eukanuba,IAMS, Australia). This food was diluted to a concentration of25% with water and given initially at 1 mL/kg every 2 h. Thestomach was emptied by suctioning the gastrotomy tube priorto each feeding, to minimise nausea and to monitor gastricmotility. IV fluids, metoclopramide and cisapride werecontinued. The dog continued, regurgitating two to three timesa day.

Figure 1: Lateral thoracic radiograph of Case 1 demonstrating anairfilled dilated oesophagus.

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Two days previously the owners had witnessed the dog playingwith a snake. Blood tests taken the following day revealed a CPKof 220,000 IU/L (reference range: 50-400 IU/L). A diagnosis oftiger snake envenomation was made and Combined Brown andTiger Snake Antivenom was administered IV.

Five days after envenomation the dog was referred to theUMVCH because of continued vomiting and melaena.Radiographs confirmed megaoesophagus and mild aspirationpneumonia. The dog had evidence of generalised myopathywith limb stiffness and reluctance to stand or move and browndiscoloured urine.

Initial treatment included IV fluids, nasal oxygen,butorphanol (0.5 mg/kg IV), constant rate infusion ofmetoclopramide , oesophageal suctioning and postural drainageof the oesophagus. For financial reasons the owners did notwant a gastrotomy tube placed, so medical treatment wascontinued. Oesophageal suctioning via a naso-oeseophagealtube reduced regurgitation considerably and allowed oralsyringe feeding of 1 mL/kg of oral electrolyte solution every 2 h.

Forty eight hours after presentation the dog was still veryweak and depressed. Feeding with liquid food was commencedat 1 mL/kg/hr and was gradually increased to 4 mL/kg every2 h.When the dog was discharged for nursing care at home,3 days after presentation, it was ambulatory but still very stiff.The owners were instructed to keep the dog on liquid food andsyringe feed it until it could eat for itself. Two weeks later theowners reported that the dog was eating on its own andappeared to be recovering well.

Case 4A 5-year-old desexed male mixed breed dog was treated for

tiger snake envenomation, by the primary veterinarian, withCombined Brown and Tiger Snake Antivenom and IV fluids.The dog improved initially and was discharged. Three days laterthe dog re-presented to the veterinarian for lethargy, darkcolored urine and persistent retching. A thoracic radiographdemonstrated megaoesophagus. The dog was referred to theUMVCH for further treatment.

Treatment included placement of a PEG tube, IV fluids and aconstant rate infusion of metoclopramide. Over the next 3 daysthe dog deteriorated. Its respiratory function declined and4 days after presentation to the UMVCH the dog died ofrespiratory arrest.

Necropsy examination revealed a diffuse rhabdomyopathyaffecting only skeletal muscle. There were similar lesionsaffecting the appendicular, axial and oesophageal muscles.Histological examination revealed myonecrosis at all levels of theoesophagus. The likely cause of respiratory compromise wasrespiratory muscle failure. A mild interstitial pneumonia,possibly secondary to aspiration, was present, but was consideredinsufficiently severe to cause the respiratory distress seen.

DiscussionNumerous disease conditions have been implicated in the

aetiology of megaoesophagus. Any condition that results indisruption of the neural reflex controlling of swallowing oraffects function of the oesophageal muscles can be responsible.2

The two main categories of disease involved are neuropathiesand myopathies.

The pathogenesis of megaoesophagus in dogs following tigersnake envenomation is uncertain. Tiger snake venom is knownto cause neuropathy and myopathy,5 both of which couldtheoretically produce megaoesophagus. The histological

findings in case 4 suggest that oesophageal myopathy occurs.The neuropathy associated with tiger snake venom progressesrapidly, and if not lethal, should resolve within 24 h ofthe bite.5-7 By contrast, in the cases presented here,megaoesophagus did not appear to occur in the acute periodof envenomation. In all four cases the clinical signs ofmegaoesophagus were delayed in onset, coinciding with clinicalsigns and biochemical evidence of a generalised myopathy.

Megaoesophagus has not been a recognised sequela to othertypes of Australian snake envenomations in dogs. Severemyopathy is a unique feature of tiger snake envenomation,whereas neuropathy is common to envenomation by allAustralian venomous snakes.5-8 The myopathy following mostcases of tiger snake envenomation in dogs is due to generalisedmyodegeneration of skeletal muscle.8 Histologically, myofibresbecome intensely eosinophilic, the myofibrillar structure is lostand fibres fragment. Fibre mineralisation is generally mild.8

Experimental studies found that smooth and cardiac muscle areunaffected8 as was the case here in the dog that died. The doghas striated muscle throughout its oesophagus, making itsusceptible to the myopathic effects of tiger snake venom.Generalised myopathy was characterised clinically in the casesreported here by pain, weakness, stilted gait and depression.The serum muscle enzyme CPK was markedly elevated in thetwo dogs in which levels were determined. Myoglobinaemia andsubsequent myoglobinuria were also evident. Myonecrosisoccurred even at sublethal venom doses. Delay between thetime of envenomation and time of treatment worsens themyopathy, as does any exercise (muscle movement) postenvenomation.5,8-10 The histopathological results found atnecropsy examination in case 4 confirmed that an oesophagealmyopathy can occur in dogs envenomated by tiger snakes.

Case 1 was a severe envenomation, as indicated by therapidity of the onset of signs. It was treated promptly and lifethreatening paralysis resolved within hours. Vomiting started12 h after presentation, coinciding with the development ofsigns of generalised myopathy, with pain, muscle stiffness andreluctance to move. There had been no indication ofoesophageal dysfunction before this. Because the onset ofmegaoesophagus coincided with development of the myopathy,and not of the neuropathy, it is likely that megaoesophagus wasdue to oesophageal muscle damage.

Cases 2 and 3 presumably received sublethal doses of tigersnake venom. Neither was immediately treated and, if untreateddogs are likely to die within 24 h of one lethal dose of venom.5

Both dogs had signs of generalised myopathy, with stiffness,depression, elevated plasma CPK and discoloured urine (mostlikely indicating myoglobinuria). Neither dog showed signs ofacute neuropathy throughout the course of its illness. Bothanimals were clinically normal prior to being bitten, with noprevious history of vomiting or regurgitation. The developmentof megaoesophagus in both these cases suggests thatmyonecrosis of oesophageal striated muscle, rather than,neuropathy, was the cause of abnormal oesophageal function.

Megaoesophagus is not reported in people or cats followingtiger snake envenomation. This may be because, unlike the dog,most of the human11 and feline oesophagus12 is composedof smooth muscle, which is not affected by the myotoxiccomponents of tiger snake venom.8

Diagnosis of megaoesophagus is an important step towardsinstituting correct medical management. It also helps providethe owner with an accurate prognosis and estimate of likely

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financial costs. The most serious potential complication isthe development of aspiration pneumonia, which can be lifethreatening.2 If megaoesophagus persists for any length of time,nutrients must be provided to the animal in a manageable form.In less severe cases of megaoesophagus a high-caloric diet fedfrom an elevated bowl may be sufficient to maintain the animalsenergy requirements. These meals are usually small and theconsistency can vary from liquid to solid boluses. In cases whereall forms of nutrition are regurgitated feeding via a gastrotomytube is the treatment of choice.2,4 The gastrotomy tube can beplaced percutaneously or surgically. Severely affected animalsare often recumbent and anorexic secondary to generalisedmyopathy. Oral feeding of these patients increases the risk ofaspiration pneumonia, and can rarely satisfy their increasedenergy requirements.

Resolution of megaoesophagus is indicated by disappearanceof clinical signs and can be confirmed by thoracic radiographsand a barium swallow under fluroscopy. Oral feeding can begradually reintroduced and once the patient can be maintainedon oral food alone, the gastrotomy tube can be removed.

Clinicians treating dogs with tiger snake envenomations needto be alert to the possibility of megaoesophagus, even in animalswhich receive a sublethal dose of venom. Early identification ofmegaoesophagus and appropriate treatment increase the chanceof recovery. Megaoesophagus developing secondary to tigersnake envenomation in dogs is likely to resolve if the animal canbe supported appropriately, unlike many other causes of thecondition.

References1. Twedt DC. Diseases of the oesophagus. In: Ettinger SJ, editor. Textbook ofVeterinary Internal Medicine. 4th edn. Saunders, Philadelphia, 1995;1124-1142.2. Mears EA, Jenkins CC. Canine and Feline Megaesophagus. Comp ContinEd Pract Vet 1997;19:313-326.3. Strombeck DR, Guildford WG. Diseases of Swallowing. In: Strombeck DR,Guildford WG, editors. Strombecks Small Animal Gastroenterology. 3rd edn.Saunders, Philadelphia, 1990;216-238.4. Leib MS Hall RL. Megaesophagus in the dog part II, clinical aspects. CompContin Ed Pract Vet 1984;6:11-17.5. Lewis PF. Some toxicity thresholds for the clinical effects of common tigersnake (Notechis scutatus) envenomation in the dog. Aust Vet J 1994;71:133-135.6. Lewis PF. Common tiger snake envenomation in dogs and mice- relationshipbetween the amount of venom injected and the onset of clinical signs. Aust VetJ 1994;71:130-132.7. Sutherland SK. Australian animal toxins. Oxford University Press, Melbourne,1983;214-221.8. Lewis PF. Myotoxicity and nephrotoxicity of common tiger snake (Notechisscutatus) venom in the dog. Aust Vet J 1994;71:136-139.9. Meir J White J. Handbook of Clinical Toxicology of Animal Venoms andPoisons. CRC Press. Florida 1995; 595-617.10. Sutherland SK. Treatment of snake bite. Aust Family Physician 1976:5;272-288.11. Conklin JL, Christensen J. Physiology of the Gastrointestinal Tract. In:Johnson LR, editor. Physiology of the Gastrointestinal Tract. 3rd edn. RavenPress, New York, 1994:904-905.12. Washabau RJ. Diseases of the oesophagus. In: Ettinger SJ editor.Textbook of Veterinary Internal Medicine. 5th edn. Saunders, Philadelphia,2000;1142.

(Accepted for publication 24 January 2001)

The diagnosis and treatment of a thoracic abscessin an alpacaJE ADOLFa, NL DYKESb, S SEMEVOLOSb and TJ DIVERSb,c

The Cornell University Hospital for Animals, Department of Clinical Sciences and Radiology, Ithaca, New York 14853

Case report:A 6-month-old, 21kg intact male alpaca was admitted to

Cornell University's Hospital for Animals with a 4-monthhistory of lethargy and failure to thrive. Six weeks prior topresentation, a CBC performed by the referring veterinarianrevealed a leucocytosis (43 x 109/L; reference range, 7 to 22 x109/L). The cria subsequently received five treatments of

A 6-month-old alpaca presented for lethargy, failure to thriveand leucocytosis. Diagnostic procedures, including thoracicultrasound, radiographs and a computed tomography scan,were used to document a thoracic mass. Based onappearance and ultrasound-guided aspiration of purulentmaterial, the mass was determined to be a large abscess. Theabscess was treated with surgical drainage and long-termantibiotic therapy. The origin of this thoracic abscess was feltto be the caudal mediastinum, secondary to bacterial seedingof the caudal mediastinal lymph nodes. Although anaetiological agent was not definitively determined, the mostlikely was Actinomyces spp or Arcanobacterium pyogenes.The alpaca made a complete recovery following treatment.Aust Vet J 2001;79:675-679Key Words: alpaca, thoracic abscess, computed tomography, thoracotomy,Actinomyces spp, Arcanobacterium pyogenes

aLedgewood Equine Medical Center, Ontario, NY 14519 USAbCornell University, Department of Clinical Sciences and Radiology, Ithaca, NY14853 USAcAuthor for correspondence

CT scan Computed tomography scanCBC Complete blood countHCT HaematocritIgG Immunoglobulin GIM IntramuscularIV IntravenousMCV Mean corpuscular volumeMCHC Mean corpuscular haemoglobin concentrationPO OrallySC SubcutaneousWBC White blood cell count