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MURDOCH RESEARCH REPOSITORY Http MURDOCH RESEARCH REPOSITORY http://researchrepository.murdoch.edu.au This is the author's final version of the work, as accepted for publication following peer review but without the publisher's layout or pagination. Peacock, R.E. , Hosgood, G. , Swindells, K.L. and Smart, L. (2013) Aplysia giganteatoxicosis in 72 dogs in Western Australia. Australian Veterinary Journal, 91 (7). pp. 292-295. http://researchrepository.murdoch.edu.au/16174 Copyright © 2013 The Authors. Australian Veterinary Journal It is posted here for your personal use. No further distribution is permitted. Aplysia gigantea toxicosis in 72 dogs RE Peacock*, G Hosgood, KL Swindells and L Smart * Corresponding author School of Veterinary and Biomedical Sciences, Murdoch University, 90 South Street, Murdoch, Western Australia, 6150; [email protected] Objectives This study aims to: 1) confirm a temporal association between exposure to the sea hare Aplysia gigantea and the development of a neurotoxicosis in dogs, 2) further characterise the clinical signs in dogs with this suspected toxicosis, and 3) report the treatment and outcome of dogs with this suspected toxicosis. Method The medical records from four veterinary practices within the Geraldton region of Australia were searched for dogs that had been exposed to Aplysia gigantea and were subsequently presented to a veterinarian during the period of January 2001 to March 2011. Signalment, exposure history, clinical signs, treatment and outcome were recorded. Results Seventy-two dogs met the inclusion criteria. Clinical signs included ptyalism, emesis, ataxia, hyperaesthesia, tremors, muscle fasciculations, seizures, nystagmus and respiratory distress. Thirty dogs did not have abnormal clinical signs at presentation. Sixty-nine dogs presented during January to April. Treatment included gastrointestinal and dermal decontamination, and supportive management of seizures, tremors and muscle fasciculations. Sixty-five dogs survived to discharge, four dogs died, and three were euthanised. Information from subsequent examinations was available for 57 dogs and no long-term complications were reported. Conclusions Exposure to Aplysia gigantea was temporally associated with the development of neuroexcitatory clinical signs in dogs. Gastrointestinal and respiratory signs also occurred in some dogs. Dogs with suspected toxicosis mostly presented in the months from January to April. The proportion of dogs that died or were euthanised due to worsening clinical signs was 10%. Keywords: Aplysia, seizure, beach, sea hare, toxicosis, dog. Introduction Veterinarians practicing along the Western Australian coastline near Geraldton have observed that dogs who have had contact with the sea hare Aplysia gigantea can develop neuroexcitatory signs and some dogs die.1 The normal life cycle of the sea hare results in hundreds of dead A. gigantea washing up on Geraldton beaches periodically.2 These events coincide with anecdotal reports of dogs developing neuroexcitatory clinical signs after being at local beaches.1 Sea hares are herbivorous marine molluscs and are a type of sea slug. A distinguishing feature of sea hares is the presence of a pair of large parapodial lobes, which Aplysia species can use for swimming.3 Aplysia gigantea is black or dark brown in colour and is one of the largest sea hares, growing up to 60 cm long and weighing up to 2 kg.3 The documented range of A. gigantea includes the coastal waters of the southwestern corner of Western Australia between Duke of Orleans Bay, east of Esperance, to Bluff Point, north of Geraldton.2 Anecdotal reports of suspected A. gigantea toxicosis in dogs are available.1,4 The purpose of this study was to: 1) confirm a temporal association between exposure to the sea hare A. gigantea and the development of neuroexcitatory clinical signs in dogs, 2) further characterise the clinical signs in dogs with suspected toxicosis after exposure to A. gigantea, and 3) report the treatment and outcome of dogs with suspected toxicosis after exposure to A. gigantea. Materials and Methods The medical records from four veterinary practicesa,b,c,d within the Geraldton region were searched using the keywords: tremor, seizure, shaking, fit, convulsion, hyperaesthesia, toxin, poison, nudibranch, marine, beach, blobbie, Aplysia, Spanish (dancer), snail, slug and hare. Records dated between January 2001 and March 2011 were searched for cases matching the inclusion criteria. Cases were included if a dog had been observed by the owner to have direct contact with A. gigantea, either through licking or rolling, or to have ingested A. gigantea. Information retrieved from records included signalment, body weight, exposure history including ingestion or contact with A. gigantea and time from exposure to the onset of clinical signs, month of the year, owner observations prior to presentation, physical examination findings, treatment, length of hospitalisation, outcome including survival to discharge, death or euthanasia, and details of subsequent examinations. Numerical data were summarised as a median and range. Categorical data were summarised as a frequency. Physical examination findings were divided according to neurologic, gastrointestinal and cardiopulmonary system involvement where possible. A commercially available statistical software packagee was used to summarise data and perform calculations. Results A search of the keywords returned 6,571 records of which 72 cases met the inclusion criteria. The median age of the dogs was 2.5 years (n=64, range 2 months to 13 years). The median weight was 23.4 kg (n=63, range 3.2-50.0 kg). Thirty-four female dogs (22 neutered) and 34 male dogs (21 neutered) were recorded. Breed was recorded for 67 dogs and included mixed-breed dogs (n=25), Labrador retriever (17), Australian cattle dog (4), Staffordshire bull terrier (4), and golden retriever (3). Eleven other breeds were represented by one or two dogs each. Forty dogs had abnormal clinical signs that were observed by the owners prior to presentation. Forty two dogs had abnormal findings on physical examination at presentation. One dog that had an abnormality observed by the owner was normal on physical examination at presentation. Three dogs were reported by the owners to have been normal prior to presentation but had abnormal findings on physical examination at presentation. The number of dogs having contact with an A. gigantea was 37, and the number of dogs that had ingested an A. gigantea was 35. The owners reported tremors (n=17), shaking (12), vomiting (11), seizures (8), ataxia (7), drooling (5), diarrhoea (2), disorientation (1), and oral discomfort (1) in the dogs prior to presentation to the veterinarian. The median time from direct contact to the onset of the signs was 1.75 hours (n=14, range 0.25-18 hours). The median time from ingestion to the onset of the signs was two hours (n=26, range 0.5-12 hours). Dogs were presented in January (n=13), February (29), March (18), April (9), May (1), June (1), and July (1). Clinical signs recorded by veterinarians included tremors (n=29), ataxia (11), hyperaesthesia (10), muscle fasciculation (6), panting or tachypnoea (6), vomiting (5), ptyalism (5), cardiopulmonary arrest (4), seizures (3), and nystagmus (3) (Tables 1, 2, and 3). Pigmenturia was present in two dogs. The median rectal temperature was 40.0oC (n=18, range 33.0-43.9oC). Gastrointestinal decontamination was performed in 15 dogs including emesis (n=12), gastric lavage (2) and activated charcoal administration (2). Material resembling A. gigantea, such as dark slimy material, was present in the vomitus of four dogs and the gastric lavage fluid of one dog. Only one dog received both gastric lavage and activated charcoal. Dermal decontamination via bathing in a mild detergent was performed on 10 dogs at presentation. All dogs displaying signs of toxicosis received more than one drug (Table 4). The most frequent drugs used were intravenous fluids (n=28), diazepam (22) and pentobarbitone (13). The number of dogs that were discharged immediately after consultation was 22 (Table 5). None of these dogs were reported to have returned for repeat consultation. Duration of hospitalisation was less than 24 hours for 64 dogs (Table 5). The number of dogs that survived to discharge was 65 and all were recorded as clinically normal at discharge. Of the remaining seven dogs, two were dead on arrival, two died within 12 hours of presentation due to worsening of clinical signs despite treatment, and three were euthanised within 24 hours due to worsening of clinical signs despite treatment. Three dogs that died had received cardiopulmonary and cerebral resuscitation. All dogs that died had been seen to ingest A. gigantea. Information from subsequent examinations was available for 57 dogs. No owners reported evidence of continued illness that could be related to suspected A. gigantea toxicosis. One owner reported a small amount of skin sloughing in one dog, which the attending veterinarian had suspected was due to extravasation of pentobarbitone. Discussion This study confirms that neuroexcitatory signs in dogs are temporally associated with exposure to A. gigantea. The neuroexcitatory signs are consistent with those seen in other domestic species that have had toxicosis induced by chemical extracts from related sea hares.5,6,7,8 Toxicosis may be due to the presence of cholinomimetic chemicals in the digestive gland and such chemicals have been isolated from other Aplysia species.9,10,11,12,13 Gastrointestinal and respiratory abnormalities were also identified in the present study. It is possible that dogs with other clinical signs may have been missed as a number of the keywords searched were based on anecdotally reported clinical signs.1 Attempts were made to minimise selection bias by using a number of keywords that were not clinical signs. This selection bias may also have led to an over-representation of clinical signs that were also keywords. An under-representation of some clinical signs may also have occurred due to inadvertent omission from the medical records. Tremors were the most frequent neurological manifestation of toxicosis in this study.
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