Food-associated toxicoses in dogs and cats
MeSH keywords:food, pets, poisoning
When toxic substances are ingested by a living organism, they may disrupt normal function, resulting in irreparable damage. Several types of food which are safely consumed by humans, can be proven highly dangerous if ingested by companion animals. Such foods are mainly chocolate, coffee, tea, onion, garlic, grapes, raisins, products containing xylitol, avocado, macadamia nuts and dough (ethanol). Each of the resulting food-associated toxicosis develop through a different aetiopathogenetic mechanism, has various consequences upon the affected organism, multiple clinical signs, and requires special management and treatment.
Certain foods, which are completely safe for people and other animals, may cause problems if consumed by dogs and cats, due to metabolic differences in these animal species. Some products are likely to cause only mild digestive disorders, whereas others may result in severe toxicosis or even death. Most of the food-associated toxicosis cases are caused by ingestion of foods, because the owners are not aware of their toxicity. Furthermore, the mechanism of toxicity for some of them remains unknown, therefore they are still under investigation (Handl & Iben 2008, Kovalkovičová et al. 2009, Gugler et al. 2013, Cortinovis & Caloni 2016).
Cases of toxicosis are frequent admitted to veterinary clinics and most of them, according to the literature, during and holidays (Kovalkovičová et al. 2009, Cortinovis & Caloni 2016). Most cases of food-associated toxicosis affect dogs compared to cats (Handl & Iben 2008, Jasani 2011). Due to their particularly curious nature and the tendency to investigate everything in their close environment, dogs are most often exposed to toxic substances and products, whereas cats are rarely affected, because they are attached to their unique dietary habits, which are often limited (Handl & Iben 2008, Cortinovis & Caloni 2016). Cats represent only 11-20% of the recorded cases, a percentage three times smaller than that of canine cases (Kovalkovičová et al. 2009).
The aim of this review is the description of toxicoses caused by ingestion of foods widely consumed by humans, such as chocolate, onions, garlic, grapes, xylitol, avocado, macadamia nuts and dough. All these products are potentially toxic to pets and should not be fed to them. After the ingestion of a toxic food, it is necessary to immediately admit the animal to a veterinary clinician, in order to treat a potentially critical condition. These cases usually require immediate general decontamination measures, mainly induction of emesis when this is deemed safe (Table 1) (Μancintire 2005), as well as specific treatment. Appropriate education of companion animal owners for the risks of food-associated toxicoses contributes to the prevention of such incidents, as well as their immediate and proper management.
Toxic substances: Methylxanthines such as theobromine, caffeine and theophylline, contained in cocoa (chocolate products), coffee beans, as well as tea have been implicated for companion animal toxicosis, after ingestion (Sutton 1981, Stidworthy et al. 1997, Gwaltney-Brant 2001, Agudelo et al. 2003). The majority of methylxanthine toxicoses have been reported in dogs and this is attributed to the canine preference for sweets (Gugler et al. 2013, Cortinovis & Caloni 2016). All types of chocolate are considered to be toxic, however the severity of signs depends on the methylxanthine content of each product (Kovalkovičová et al. 2009, Jasani 2011). In particular, dark chocolate is the most toxic, milk chocolate is less toxic, whereas white chocolate must be consumed in large amounts in order to cause toxicosis (Kovalkovičová et al. 2009, Gugler et al. 2013, Cortinovis & Caloni 2016). The exact amounts of these food products which can result in toxicosis after ingestion have not been fully clarified and vary among studies. Other factors with a key role in causing food-associated toxicosis include body weight, general health condition, stomach content and the type of product that was consumed (Kovalkovičová et al. 2009). The mean lethal dose of caffeine and theobromine for dogs is 100-500 mg kg-1, which corresponds to four bars of dark chocolate. At the low dose of 20-40 mg kg-1 mild clinical signs may occur (hyperactivity, vomiting), the dose of 40–50 mg kg-1 may result in cardiotoxic effects such as cardiac arrhythmias, at the dose of 60 mg kg-1 seizures may be develop, whereas higher doses can be fatal (Gwaltney-Brant 2001, Agudelo et al. 2003, Sudhakara Reddy et al. 2013).
Toxicokinetics: Theobromin and caffeine are easily absorbed by the gastrointestinal tract, widely distributed throughout all tissues (Baile & Garland 1992, Kovalkovičová et al. 2009) and can cross the blood-brain barrier (Handl & Iben 2008). They are metabolised by the liver, in which they undergo enterohepatic circulation, and they are excreted mostly in the urine and in limited amounts in the faeces. It is worthy of note that methylxanthines may directly be transferred into milk and pose a high risk for suckling animals. The half-life of theobromine and caffeine in dogs is 17.5 and 4.5 hours respectively (Baile & Garland 1992, Poppenga 2007, Kovalkovičová et al. 2009, Gugler et al. 2013). The fact that methylxanthine elimination rate in dogs is much slower than in any other animal species is the reason why dogs are so susceptible to this particular toxicosis (Handl & Iben 2008, Jasani 2011).
Mechanism of toxicity: Methylxanthines antagonise cellular adenosine receptors, resulting in severe stimulation of the central nervous system (CNS) and effects on the cardiovascular and respiratory system. Blockade of adenosine effect can induce a positive chronotropic and inotropic effect on the myocardium, vasoconstriction and to a small extent, diuresis. Methylxanthines also increase the intracellular content of calcium which results in increased contractility of the skeletal muscles, antagonise the benzodiazepine receptors, inhibit phosphodiesterase enzyme and increase systemic circulation levels of epinephrine and norepinephrine (Baile & Garland 1992, Gwaltney-Brant 2001, Kovalkovičová et al. 2009, Meola 2010, Jasani 2011). Methylxanthine overdose steadily increases the severity and duration of all these metabolic processes, leading to death by cardiorespiratory failure (Handl & Iben 2008, Cortinovis & Caloni 2016).
Clinical signs: The first clinical signs of toxicosis usually emerge within 2-12 hours after ingestion and usually include salivation, vomiting, diarrhoea, polydipsia and polyuria. Clinical signs develop quickly followed by neurological signs such as restlessness, muscle tremors, ataxia, hyperactivity, seizures, hyperthermia, tachypnoea, cyanosis, tachycardia, arrhythmias and finally death (Baile & Garland 1992, Μancintire 2005, Poppenga 2007, Kovalkovičová et al. 2009, Meola 2010, Gugler et al. 2013).
Diagnosis: Diagnosis is based on history, in combination with clinical signs (Baile & Garland 1992, Handl & Iben 2008). Toxicosis due to organophosphates, mycotoxins, strychnine, nicotine, amphetamines, pseudoephedrine, antihistamines, antidepressants, or generally other CNS stimulants should be included in the differential diagnosis (Meola 2010).
Management-treatment: There is no specific antidote for methylxanthine toxicosis (Μancintire 2005, Jasani 2011). Treatment is symptomatic, supportive and focussed on decontamination (Baile & Garland 1992, Gwaltney-Brant 2001, Jasani 2011). Once the animal is admitted, the first step should be the induction of emesis, if indicated, or when this is not possible or contraindicated, gastric lavage should be performed (Salgado et al. 2011, Mason et al. 2014), followed by the administration of adsorbent agents which prevent further gastrointestinal absorption of toxic substances (Gwaltney-Brant 2001, Poppenga 2007). Furthermore, aggressive intravenous fluid administration is also indicated, aiming in increasing the elimination rate of toxic substances (Μancintire 2005, Kovalkovičová et al. 2009). In cases in which methylxanthine toxicosis has resulted in seizure activity, diazepam as a general measure for seizure control may prove ineffective, because of benzodiazepine receptor antagonism by methylxanthines. Alternatively, phenobarbital, propofol, and inhalational anaesthesia have been recommended in this order for the management of seizure activity (Cope 2005). In cases of cardiac arrhythmias, these are managed according to the type of arrhythmia. Finally, gastroprotective agents are administered if there is refractory vomiting (Μancintire 2005, Poppenga 2007).
Prognosis: It is generally good but can become guarded in cases admitted with severe neurological signs (Baile & Garland 1992, Jasani 2011).
Toxic substances: Onion and garlic belong to the Liliaceae family (Cope 2005, Salgado et al.2011). Onion toxicosis was more frequent in large animals in the past, perhaps due to free-ranging and direct exposure to the plants (Baile & Garland 1992). Due to wide merketing of the products of onion and garlic nowadays, either fresh or in cooked food, the risk of ingestion by companion animals is higher. Onion and garlic toxicosis occur after they have been consumed by pets, in fresh or powdered form, or when they are contained in foods or food products. It is observed in animals which have ingested amounts exceeding 0.5% of their body weight in onions in a single meal (Cope 2005, Kovalkovičová et al. 2009, Cortinovis & Caloni 2016).
Mechanism of toxicity: After onions and garlic have been consumed, bisulphites are produced which lead to red blood cell glucose-6-phosphate dehydrogenase deficiency and haemoglobin oxidation (οxidative stress). The denatured haemoglobin (methaemoglobin) forms a residue on the surface red blood cells contributing to Heinz bodies formation, resulting in haemolysis and therefore anaemia (Handl & Iben 2008, Kovalkovičová et al. 2009, Cortinovis & Caloni 2016).
Clinical signs: This toxicosis immediately cause vomiting, diarrhoea, depression, abdominal pain, anorexia and dehydration. After some days, clinical signs pertaining to haemolysis occur, such as pale mucous membranes, tachycardia, dyspnoea, haemoglobinuria, as well as icterus. In cats, marked salivation and vomiting are observed more frequently (Kovalkovičová et al. 2009, Cortinovis & Caloni 2016).
Diagnosis: Diagnosis is initially based on thorough history and clinical signs observed ατ admission, same as in any other toxicosis (Baile & Garland 1992). Laboratory findings characteristically include anaemia with Heinz body formation, haemoglobinuria and neutrophilia (Baile & Garland 1992, Ford & Mazzaferro 2011). It is important to differentiate this from other disorders or conditions causing haemolysis, such as haemoparasites or autoimmune haemolytic anaemia (Cope 2005). However, as long as Heinz body anaemia is rare, onion or garlic toxicosis should be included in the differential diagnosis of such cases (Kovalkovičová et al. 2009).
Management-treatment: There is no antidote for this toxicosis. The primary stage of management of such cases is decontamination and stabilisation. Decontamination occurs through induction of emesis, gastric lavage and administration of laxatives or adsorbent agents. In cases admitted with refractory vomiting antiemetics are administered, considering that it is important to preserve hydration. In severe cases, whole blood or plasma transfusions are recommended, whereas the use of antioxidants such as vitamin E and N-acetylcysteine may prevent Heinz bodies formation (Baile & Garland 1992, Handl & Iben 2008, Kovalkovičová et al. 2009, Ford & Mazzaferro 2011, Cortinovis & Caloni 2016).
Prognosis: Prognosis depends on the severity of anaemia and the effectiveness of supportive care measures. Avoidance of exposure is the best preventive strategy in companion animals. Feeding onions or other species of the Liliaceae family or their products to companion animals should be avoided (Cope 2005, Salgado et al. 2011).
Toxic substances: Xylitol is an artificial sweetener, used as a substitute for sugar in many food items widely consumed by people, such as hard candy, sugar-free gum, cookies, pastries, bread products as well as various products for diabetics. Due to its antibacterial properties and pleasant taste, xylitol is also included in many medical, dental and veterinary products of care, such as toothpastes and mouth washes. The increased selling and use of xylitol as a sweetener have resulted in increased exposure in companion animals (Dunayer 2004, Cortinovis & Caloni 2016). However, it should be mentioned that so far cases of xylitol toxicosis has only been recorded in dogs (Handl & Iben 2008). The toxicity of this substance in cats had been unknown until recently (Mason et al. 2014). Nowadays, regarding the effects of xylitol in cats there have not been found any significant changes in haematological and biochemistry parameters when doses at a level of 0.1, 0.5 and 1 g kg-1have been administered (Jerzele et al. 2018). Dogs ingesting more than 0.1 g kg-1 of xylitol should be considered at risk for hypoglycaemia, whereas doses over 0.5 g kg-1 can be hepatotoxic. Calculating the xylitol dose in various products may prove challenging because even though their xylitol content may be reported, it is more likely only the final content in sugars to be mentioned on the label. It is noted that one cup of powdered xylitol for homemade pastries weighs about 190 g (Dunayer 2006).
Mechanism of toxicity: In people the ingestion of xylitol does not cause significant changes on insulin levels and therefore in blood glucose content. However, in dogs xylitol induces insulin release from the pancreas, which leads to rapid and dramatic reduction of blood glucose levels, resulting in hypoglycaemia (Mason et al. 2014, Oehme & Hare 2014). The ingestion of high amounts of xylitol leads to an increase in insulin excretion within 30 minutes, resulting in hypoglycaemia, hypokalaemia, and potential hypophosphatemia. Furthermore, it may sometimes lead to hepatic necrosis and acute liver failure (Handl & Iben 2008, Kovalkovičová et al. 2009). The mechanisms involved in hepatic damage have not been fully clarified yet (Jasani 2011, Mason et al. 2014, Cortinovis & Caloni 2016).
Clinical and laboratory findings: The first clinical signs of xylitol toxicosis develop within a few minutes following ingestion and usually include vomiting, diarrhoea, lethargy, exercise intolerance, ataxia, seizures and coma. Furthermore, sequelae of acute liver failure may be observed such as icterus, prolongation of blood clotting time (prothrombin time and partial thromboplastin time), thrombocytopenia, petechiae and ecchymoses, gastrointestinal tract haemorrhage and elevated liver enzymes (Jasani 2011, Mason et al. 2014, Cortinovis & Caloni 2016). In blood, serum hypoglycaemia, hypokalaemia and hypophosphatemia may be observed (Kovalkovičová et al. 2009, Mason et al. 2014, Oehme & Hare 2014).
Diagnosis: Diagnosis is based on history, clinical signs and laboratory examination. Ingestion of xylitol products should be included in the differential diagnosis of cases with inexplicable hypoglycaemia with or without hepatic dysfunction. Insulinoma, hypoglycaemia due to prolonged starvation and insulin overdose should be included in the differential diagnosis (Handl & Iben 2008, Cortinovis & Caloni 2016).
Management-treatment: The first treatment of this toxicosis is again the removal of the toxic substance either by induction of emesis or gastric lavage. However, the use of activated charcoal as an adsorbent is dubious, considering that in vitro studies showed that the adsorption of xylitol is limited and unreliable (Cope 2004, Oehme & Hare 2014). In asymptomatic animals, small and frequent meals are offered, combined with close monitoring of glucose blood serum levels for at least 6 to 12 hours. In animals with severe hypoglycaemia intravenous administration of dextrose solutions is indicated as well as potassium supplements in cases of concurrent hypokalaemia. The administration of hepatoprotective, antiemetic and gastroprotective agents is also helpful (Handl & Iben 2008, Kovalkovičová et al. 2009, Jasani 2011).
Prognosis: Relatively fair but guarded in patients with hepatic failure (Mason et al. 2014).
Toxic substances: It is worthy of note that grape and raisin toxicosis is considered to be modern in a way, considering that the first cases were reported in the 1990’s, whereas after 2000 it was determined that ingestion of grapes/raisins by companion animals causes renal failure (Poppenga 2007, Jasani 2011). All species of grapes/raisins are considered to be toxic, regardless of type or the way they were produced. The toxic dose calculated by dry matter is at 32-36.4 g kg-1, however studies have indicated that the severity of sensitivity and toxicosis is not the same in all animals (Kovalkovičová et al. 2009). Lethal dose of grapes or grape products has not been determined, whereas case studies have shown no correlation between ingested dose and death in dogs. It has been reported that the minimal dose of grapes that may induce renal failure is 4-5 grapes per 8 kg of body weight or 2.8 g kg-1. Regarding raisins, the minimum dose that may cause renal failure is at 3 g kg-1(Lee 2013). Regardless of these facts, some dogs seem capable of consuming grapes and grape products without any undesirable side effects (Cortinovis & Caloni 2016).
Mechanism of toxicity: The mechanism of toxicity remains unclarified (Eubig et al. 2004). However it has been hypothesised that toxicity in dogs is caused either by their inability to metabolise certain components of this particular fruit (e.g. tannins) or by mycotoxins or contamination by drugs (Handl & Iben 2008, Kovalkovičová et al. 2009).
Clinical signs: Six to 24 hours post ingestion the first clinical signs are observed such as vomiting, diarrhoea, abdominal pain and dehydration, as well as polydipsia. After that, azotaemia develops, and 48-72 hours post ingestion oliguria and/or anuria occur due to acute renal failure. When anuria has been established, the prognosis becomes poor (Baile & Garland 1992, Handl & Iben 2008, Kovalkovičová et al. 2009, Cortinovis & Caloni 2016).
Diagnosis: Much like in all food-associated toxicosis cases, the diagnosis is based on history and evaluation of clinical signs and laboratory findings. Furthermore, it is likely for fruit to be identified in the vomitus, faeces and mouth, a fact which should be an indication to the clinician. In the urine, proteinuria, glycosuria and haematuria may be observed, whereas biochemistry evaluation may reveal increased blood urea nitrogen and creatinine, hyperkalaemia and hyperphosphatemia (Handl & Iben 2008, Kovalkovičová et al. 2009, Cortinovis & Caloni 2016). In animals that underwent histopathological examination of the kidneys, acute tubular necrosis was found (Mazzafero et al. 2004, Morrow et al. 2005, Poppenga 2007).
Management-treatment: The time from ingestion to admission to the veterinary clinician is of utmost importance, however due to the fact that the fruits are slowly digested, treatment is valuable even after several hours following ingestion. The primary goal is the detoxification via emesis induction, gastric lavage and laxative administration (Handl & Iben 2008, Kovalkovičová et al. 2009). In cases in which animals are admitted with refractory vomiting, antiemetics may be administered, in combination with gastroprotective agents. Intravenous fluid resuscitation should be aggressive, especially when there is concurrent dehydration and should be combined with continuous laboratory monitoring of the renal function for at least 72 hours after ingestion of the toxic substance (Baile & Garland 1992, Jasani 2011). In cases with oliguria, it is indicated other than aggressive fluid therapy to increase diuresis (e.g. administration of furosemide, mannitol or dopamine) in order to preserve renal function (Baile & Garland 1992, Poppenga 2007, Salgado et al. 2011). Finally, in some cases the beneficial effects of haemodialysis and peritoneal dialysis have been proven if these are available to the veterinary clinician (Baile & Garland 1992, Handl & Iben 2008, Kovalkovičová et al. 2009, Mazzaferro 2010, Salgado et al. 2011).
Prognosis: Prognosis is poor in cases with anuria, whereas cases which are admitted quickly after ingestion of toxic products have a fairly good prognosis (Handl & Iben 2008, Mazzaferro 2010).
Toxic substances: Macadamia nuts are produced by trees of the species Macadamia integrifolia and Macadamia tetraphylla, which prosper in mainland USA and Hawaii, and Australia respectively. People can ingest the nuts fresh, roasted and/or salted, in plain form or added to sweets or cookies. They are a valuable food with low cholesterol and sodium content, as well as an excellent source of manganese and thiamine. It is worthy of note that cases of macadamia nut toxicosis have been reported exclusively in dogs and no other animal species (Hansen et al. 2000, Handl & Iben 2008, Botha & Penrith 2009, Kovalkovičová et al. 2009, Gugler et al. 2013, Cortinovis & Caloni 2016).
Mechanism of toxicity: The mechanism of action of their toxicity in dogs is currently unknown and the dose required to induce toxicosis has not been exactly established (Kovalkovičová et al. 2009). Toxicosis can be caused by some unknown element of the nuts or by the presence of contamination and/or mycotoxins (Hansen 2002, Gwaltney-Brant 2012). The minimum toxic dose is at 11.7 g kg-1 body weight, meaning 5 to 6 nuts per kg of body weight (Hansen et al. 2000, Knight 2007).
Clinical signs: Within 12 hours post consumption, gradually emerging signs include lameness, ataxia, muscle tremors, weakness, stiffness and paralysis of the hindlimbs, recumbency, vomiting, abdominal pain, peripheral oedema, hyperthermia and increased heart rate. Deaths that have been attributed to this particular food-associated toxicosis have so far not been reported, considering that all recorded cases recovered fully in the span of 24-48 hours, with minimal veterinary intervention (Hansen et al. 2000, Botha & Penrith 2009, Kovalkovičová et al. 2009, Gugler et al. 2013, Cortinovis & Caloni 2016).
Diagnosis: Patient history and the presence of nuts in vomitus are the main clues pointing to macadamia nut toxicosis (Handl & Iben 2008). The differential diagnosis includes, among other things, toxicoses caused by ivermectin, ethylene glycol, ethanol, bromethalin, benzodiazepines and barbiturate overdose (Hansen SR 2002).
Management-treatment: In most cases no specific treatment is necessary, considering that automatic remission of clinical signs is often observed. However supportive measures and gastric lavage with or without administration of activated charcoal may be required (Kovalkovičová et al. 2009, Cortinovis & Caloni 2016).
Prognosis: Is expected to be good, considering that this toxicosis has not been associated with deaths (Handl & Iben 2008).
Ethanol and dough
Toxic substances: Ethanol is a two-carbon alcohol, also known as ethyl alcohol or most commonly alcohol/spirit. Ethanol can be found in a variety of products such as solvents, fuel, paints and drugs. In veterinary medicine, ethanol is commonly used for managing ethylene glycol toxicosis (Jasani 2011, Cortinovis & Caloni 2016). Cases of dietary ethanol toxicosis have been reported following the ingestion of alcoholic beverages or dough but also after consumption of rotting apples (Suter 1992, Kammerer et al. 2001, Kovalkovičová et al. 2009). According to the literature cases of dietary ethanol toxicosis have been noted only in dogs (Means 2003, Gugler et al. 2013).
Mechanism of toxicity:Ethanol is rapidly absorbed by the intestinal tract and passes the blood-brain barrier, leading to various clinical signs from the CNS (Cortinovis & Caloni 2016). Most of the absorbed ethanol is metabolised in the liver and excreted in the urine (Richardson 2006). In cases of dough toxicosis, except for the undesirable effects of ethanol release, the dough itself may act as a foreign body causing obstruction at any point of the intestinal tract or it may even lead to gastric dilatation-volvulus (Means 2003, Gugler et al. 2013).
Clinical signs: Clinical signs usually emerge in under one hour from the time of ingestion and include ataxia, vomiting, diarrhoea, hypothermia, lethargy, depression, with concurrent laboratory findings of metabolic acidosis (Means 2003, Richardson 2006, Cortinovis & Caloni 2016). Animals may develop severe respiratory failure, bradycardia, or they may fall into a comatose state, or present seizure activity, leading to death. The presence of an enlarged painful abdomen caused by excessive gas production may be noted in animals which consumed uncooked dough (Means 2003, Gugler et al. 2013).
Diagnosis: Diagnosis is based on history, clinical signs and confirmed by measuring levels of ethanol in blood (Gugler et al. 2013).
Management-treatment: Initial treatment should be applied with caution and it is only recommended in asymptomatic animals that have recently ingested products containing ethanol (Cortinovis & Caloni 2016). In particular, in cases of dough ingestion it is contraindicated to induce emesis, considering that there is high risk of obstruction of some part of the gastrointestinal tract. In contrast, gastric lavage with cool water may contribute to the delay of fermentation and the consequent undesirable release of ethanol or may even lead to the removal of some of the dough (Means 2003, Cope 2005, Gugler et al. 2013). Treatment of ethanol toxicosis is mostly supportive and is obtained with the intravenous administration of fluids, in order to manage dehydration and support renal excretion (Suter 1992, Kovalkovičová et al. 2009, Gugler et al. 2013). Furthermore, simultaneous monitoring of body temperature is required in order to prevent or manage hypothermia and blood gas analysis to reveal respiratory or metabolic acidosis. Cases should be monitored also for potential seizure activity, which should be controlled immediately (Richardson 2006, Gugler et al. 2013). In rare cases admitted in comatose state with severe respiratory failure, intubation is required followed by mechanical ventilation (Kovalkovičová et al. 2009).
Prognosis: In mild cases of ethanol toxicosis or ingestion of small amounts of dough, with timely intervention, the prognosis can be excellent. Usually with the appropriate supportive measures, clinical signs recede fully within 24 hours. However, patients with severe toxicosis presenting with respiratory failure and metabolic acidosis have a guarded prognosis (Means 2003, Richardson 2006, Gugler et al. 2013).
Toxic substances: The avocado tree grows in tropical areas and its fruit is widely consumed by people all over the world. From the leaves, the fruit, the seeds and the bark of the tree a fungicidal toxin called persin has been isolated, which according to studies is potentially toxic to dogs and cats, as well as other animal species such as mice, rats, birds, rabbits, horses, cattle and goats (Buoro et al. 1994, Handl & Iben 2008, Botha & Penrith 2009, Kovalkovičová et al. 2009). It should be noted that avocado toxicosis has been substantiated by research in most animal species, however very few suspected cases have been reported in dogs and none have been reported in cats (Buoro et al. 1994 Botha & Penrith 2009).
Mechanism of toxicity: The toxic substance persin has been implicated in necrosis of the mammary gland epithelium and myocardial endothelium in cases of avocado toxicosis (Handl & Iben 2008, Botha & Penrith 2009). Furthermore, the consumption of increased amounts of avocado can potentially lead to pancreatitis (Kovalkovičová et al. 2009). Nevertheless, the exact mechanism of this particular toxicosis remains unknown. The severity of clinical signs varies between the different species of avocado plant, with the common Guatemala variety being the most toxic. However, given that these species cannot be differentiated by morphology, the consumption of any part of the plant by companion animals is strictly forbidden (Handl & Iben C 2008).
Clinical signs: In the two cases that have so far been reported in dogs, clinical signs included vomiting, diarrhoea due to irritation of the gastrointestinal mucosae, abdominal distension, exercise intolerance, and respiratory distress (Kovalkovičová et al. 2009, Buoro et al. 1994). Clinical examination, electrocardiography and laboratory examinations revealed findings consistent with right congestive heart failure. The two dogs died, and necropsy confirmed the clinical findings (Buoro et al. 1994). The exact lethal dose remains unknown and the effect may vary depending on animal species.
Diagnosis: Diagnosis is based purely on history, considering there are no pathognomonic clinical or laboratory findings nor any known diagnostic test that may prove avocado toxicosis (Handl & Iben 2008).
Management-treatment: The treatment of avocado toxicosis is purely symptomatic based on clinical signs (Handl & Iben 2008).
Prognosis: When clinical signs originate from the cardiovascular and/or respiratory system the prognosis is guarded (Handl & Iben 2008).
Other than the previously mentioned foods, any other substance which has not yet been studied or is of unknown origin may potentially lead to companion animal toxicosis. Furthermore, there is a variety of foods commonly consumed by people such as potatoes and tomatoes, which are believed to be responsible for milder but just as undesirable gastrointestinal signs in animals. It is therefore obvious that the increase in dietary needs and demands in the human consumer population, will lead to a corresponding higher frequency of toxicosis cases in animals caused by food, the toxic effects of which have not been reported yet. Of course, the occurrence of new potential toxicosis cases due to foods which are currently commonly ingested by people, which is what happened due to grapes in the past, cannot be ruled out.
Conflicts of Interest
The authors declare no conflicts of interest.
Agudelo CF, Filipejova Z, Schanilec P (2003) Chocolate ingestioninduced non-cardiogenic pulmonary oedema in a puppy: a case report. Vet Med 2, 109–112.
Albretsen JC (2004) Methylxanthines. In: K.H Plumlee, eds. Veterinary Clinical Toxicology. Mosby, St. Louis, pp.322–326.
Baile ME, Garland T (1992) Toxicologic emergencies. In: R.W Reinhardt, eds. Veterinary Emergency and Critical Care Medicine. Mobsy, St.Louis, pp.427-452.
Bates N, Rawson-Harris P, Edwards N (2015) Common questions in veterinary toxicology. J Small Anim Pract 56, 298-306.
Botha CJ, Penrith ML (2009) Potential plant poisonings in dogs and cats in southern Africa. J S Afr Vet Assoc 80, 63–74.
Buoro IB, Nyamwange SB, Chai D, Munyua SM (1994) Putative avocado toxicity in two dogs. Onderstepoort J Vet Res. 61, 107-109.
Cope RB. (2004) A screening study of xylitol binding in vitro to activated charcoal. Vet Hum Toxicol 46, 336-337.
Cope RB (2005) Allium species poisoning in dogs and cats. Vet Med 100, 562–6.
Cortinovis C, Caloni F (2016) Household Food Items Toxic to Dogs and Cats. Front Vet Sci 3, 26.
Dunayer EK (2004) Hypoglycemia following canine ingestion of xylitol-containing gum. Vet Hum Toxicol. 46, 87-8.
Dunayer EK (2006) New findings on the effects of xylitol ingestion in dogs. Veterinary Medicine, 791-797.
Ford RB, Mazzaferro EM (2011) Emergency care. In: A.J Winkel, eds. Kirk and Bistner’s Handbook of Veterinary procedures and Emergency treatment. 9th ed. Saunders Elsevier, St.Louis, pp.1-291.
Gugler K, Piscitelli C, Dennis J (2013) Hidden dangers in the kitchen: common foods toxic to dogs and cats. Compend Contin Educ Vet 35, E2.
Gwaltney-Brant S (2001) Chocolate intoxication. Vet Med 96, 108–111.
Gwaltney-Brant SM (2012) Macadamia nuts. In: M.E Peterson et al., eds. Small animal toxicology. 3rd ed. Saunders Elsevier, St. Louis, pp.817-821.
Handl S, Iben C (2008) Foodstuff’s toxic to small animals-a review. Vet Med, 95, 235–242.
Hansen SR, Buck WB, Meerdink G, Khan SA (2000) We01akness, tremors, and depression associated with macadamia nuts in dogs. Vet Hum Toxicol 42, 18-21.
Hansen SR (2002) Macadamia nut toxicosis in dogs. Vet Med 97, 275-276.
Jasani S (2011) Toxicological Emergencies. In: F Nind, eds. Small animal emergency medicine. Saunders Elsevier, St. Louis, pp.152- 175.
Jerzele Α, Karancsi Z, Paszti-Gere E, Sterczer A, Bersenyi A, Fodor K, Szabo D, Vajdovich P (2018) Effects of p.o. administered xylitol in cats. J Vet Parmacol Ther. 41, 409-414.
Kammerer M, Sachot E, Blanchot D (2001) Ethanol toxicosis from the ingestion of rotten apples by a dog. Vet Hum Toxicol. 43, 349- 50.
Keno LA, Langston CE (2011) Treatment of accidental ethanol intoxication with hemodialysis in a dog. J Vet Emerg Crit Care 21, 363-368.
Knight PA (2007) Μacadamia. In: a guide to poisonous house and garden plants. Teton Νew Μedia, pp.181-182.
Kovalkovičová N, Sutiaková I, Pistl J, Sutiak V (2009) Some food toxic for pets. Interdiscip Toxicol 2, 169-176.
Lee AJ (2013) Emergency Management and Treatment of The Poisoned Small Animal Patient. Vet Clin Small Anim 43, 757-771.
Mazzafero EM, Eubig PA, Hackett TB et al. (2004) Acute Renal failure associated with raisin or grape ingestion in 4 dogs. J Vet Emerg Crit Care 14, 203-212.
Mazzaferro EM (2010) Raisin and Grape Toxicity. In: E.M Mazzafero, eds. Blackwell’s Five-Minute Veterinary Consult Clinical companion. Small animal emergency and critical care. Blackwell Publishing. Ames, pp.667-674.
Μancintire DK, Drobatz KJ, Hakins SC, Saxon WD (2005) Toxicologic Emergencies. In: D.B Troy, eds. Manual of Small Animal Emergency and Critical Care Medicine. Lippincott Williams & Wilkins. Baltimore USA, pp.384-387.
Mason JA, Khan SA, Gwaltney-Brant SM (2014) Recently Recognized Animal. In: Kirk’s Current Veterinary Therapy XIV. Bonagura J, Twedt D (ed), (14th edn), Saunders-Elsevier 31, 138- 143.
Means C (2003) Bread dough toxicosis in dogs. J Vet Emerg Crit Care 13, 39-41.
Meola SD (2010) Chocolate toxicity. In: E.M Mazzafero, eds. Blackwell’s Five-Minute Veterinary Consult Clinical companion. Small animal emergency and critical care. Blackwell Publishing. Ames, pp.141-145. • Morrow CMK, Valli VE, Volmer PA, Eubig PA (2005) Canine Renal Pathology Associated with Grape or Raisin Ingestion: 10 Cases. J Vet Diagn Invest 17, 223-231.
Oehme FW, Hare WR (2014) Urban Legends of Toxicology: Facts and Fiction. In: J Bonagura et al., eds. Kirk’s Current Veterinary Therapy XIV. 14th ed. Saunders Elsevier, St.Luis, pp.109-111.
Poppenga RH (2007) Toxicological emergencies. In: L.S King et al., eds. BSAVA Manual of Canine and Feline Emergency and Critical Care. 2nd ed. BSAVA. Gloucester, pp.278-294.
Richardson JA (2006) Ethanol. In: M.E Peterson et al., eds. Small animal toxicology. 2nd ed, Saunders Elsevier, St. Luis, pp.698-701.
Salgado BS, Monteiro LN, Rocha NS (2011) Allium species poisoning in dogs and cats. J Venom Anim Toxins Incl Trop Dis 17, 4-11.
Stidworthy MF, Bleakley JS, Cheeseman MT, Kelly DF (1997) Chocolate poisoning in dogs. Vet Rec 141, 28.
Sudhakara Reddy Β, Varaprasad Reddy LSS, Sivajothi (2013) Chocolate Poisoning in a Dog, Int J Vet Health Sci Res 01, 16-17.
Suter RJ (1992) Presumed ethanol intoxication in sheep dogs fed uncooked pizza dough. Aust Vet J. 69, 20.
Sutton RH (1981) Cocoa poisoning in a dog. Vet Rec 109, 563-564.
How to Cite
Copyright (c) 2020 Elisavet Panagopoulou, Ageliki Vorloka, George Kazakos
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.