Following flowering in the spring and summer, autumn brings the fruiting season and an abundance of fruits, nuts and seeds. Some of these are poisonous and in addition may also be mouldy because of warm, wet autumnal weather. Autumn is also the time that fungi commonly produce their fruit bodies (mushrooms). In addition, to these natural toxins there are also hazards associated with seasonal festivals such as Halloween and, in the UK, Bonfire Night.
Luminous novelties (e.g. glow sticks)
Luminous novelty items such as necklaces, glow sticks and glow bracelets, are often available at fair grounds and similar venues particularly at Halloween and Bonfire Night. They consist of polyethylene tubing filled with a liquid mixture that gives off a light of various colours (Figure 1).
There are usually two components to the mixture within the polyethylene tubing: a luminescer (typically dibutyl phthalate) and an activator (usually comprising dimethyl phthalate, tert-butyl alcohol and hydrogen peroxide). Mixing these components produces the luminescence but in luminous necklaces these components are ready mixed. Pets are usually exposed when they chew these items and break into the tubing.
The chemicals in these products are of low toxicity and present in a low volume. The quantity ingested is usually small because of the unpleasant taste, therefore, systemic effects are not expected.
Clinical signs
Dibutyl phthalate is irritant with an unpleasant taste, and clinical features are a result of these properties, with hypersalivation, hyperactivity and aggressive behaviour (Rosendale, 1999). The signs usually occur immediately and are very short-lived. The liquid in these products is irritant to eyes and skin.
Treatment
Gut decontamination is not required following ingestion of the liquid in these items. Signs usually resolve rapidly, but oral fluids can be given, if required, or a treat which can help to take the taste away.
If the skin or eyes are exposed the area should be thoroughly irrigated. The contents of these glow sticks glow in the dark so examining the animal in a darkened room will help ensure effective decontamination. Treatment of any ocular or dermal effects is supportive.
Fireworks
Fireworks are low explosive pyrotechnic devices available for consumer or professional use. They usually have six components (Gondhia, 2015):
- A fuel that is usually charcoal
- Oxidising agents that provide oxygen for the mixture to burn and are usually nitrates, chlorate or perchlorate
- Reducing agents that burn the oxygen (provided by the oxidising agents) to produce hot gases. Common reducing agents in fireworks are sulphur and charcoal (which produce sulphur dioxide and carbon dioxide, respectively)
- Regulators such as metals that are added to control the speed of the reactions
- Colouring agents that include a variety of chemicals (e.g. copper gives a blue colour, sodium yellow/orange)
- Binders that hold the mixture together in a paste-like consistency. Dextrin (a type of starch) is mostly commonly used. A fuel that is usually charcoal
Sparklers are a common type of firework and comprise a metal wire covered with a combustible material, which is most commonly a gunpowder-type material comprising sodium and/or potassium nitrates (chlorates may be used) with sulphur and carbon. The sparks are provided by powdered metals such as iron, aluminium, or magnesium. The metal powder is coated with paraffin wax to prevent oxidation during storage and to allow the metal to fall off the sparkler as it burns, producing the characteristic sparks (Katz, 2002).
Fireworks can contain a wide variety of different chemicals, but in most cases the exact composition of ingested fireworks is unknown. Few cases of poisoning have been reported in animals. There are reports of firework toxicity in humans involving barium (Rhyee and Heard, 2009; Deepthiraju and Varma, 2012), phosphorous, both white and yellow (Fernandez and Canizares, 1995; Ates et al, 2011; González-Andrade and López-Pulles, 2011; Taskesen and Adiguzel, 2012; Batu et al, 2014; Yilmaz et al, 2015; Türkmen Şamdanci et al, 2016; Yüksekkaya et al, 2019) and arsenic (Brayer et al, 1997). Most of these reports, however, are from countries where fireworks are poorly or unregulated (e.g. Turkey, Philippines, Ecuador, India). Barium (Stanley et al, 2019) and phosphorous (Schrunk et al, 2014) poisoning have been reported in dogs after ingestion of fireworks, but cases are very uncommon. A review of 186 cases of firework ingestion reported to a human poison centre in America found that most patients remained asymptomatic (91%). Signs reported in symptomatic patients were vomiting and abdominal pain (Christian et al, 2011).
Clinical effects
Ingestion of a sparkler generally, only causes gastrointestinal upset; toxicity is not expected as the quantity of chemicals present is small. Barium poisoning has been reported in a dog that ingested the combustible material from the ends of multiple sparklers (Stanley et al, 2019). A burning sparkler has a high temperature (similar to a welding torch (Singh, 1997)) and will cause burns if chewed or touched.
Unused (unexploded) domestic fireworks are likely to cause only gastrointestinal upset in dogs (Means, 2016). Unused (unexploded) display fireworks could cause more significant signs and possibly chlorate toxicosis (Means, 2016). Although most dogs remain asymptomatic after ingestion of used fireworks there could be vomiting, diarrhoea, abdominal discomfort and ataxia. There is a potential risk of metal or chlorate toxicity, but this is rare.
Ingestion of a used domestic firework is unlikely to result in any significant signs as the chemical components will have been burned or dispersed during the explosion. Spent display fireworks could contain a significant amount of spent ash which could contain toxic components such as barium (Means, 2016).
Barium toxicity results in severe hypokalaemia with vomiting, diarrhoea, hypertension and arrhythmias. In severe cases there may be tremors, convulsions, paralysis, tachypnoea and respiratory failure. Signs can start within an hour and severe signs within 2–3 hours. If there are no signs by 6–8 hours then barium toxicity has not occurred (Gahagan and Wismer, 2018). Chlorates cause vomiting, tachycardia, haemolysis, hyperkalaemia (secondary to methaemoglobinaemia and haemolysis), methaemoglobinaemia and nephropathy (secondary to haemolysis) (Means, 2016).
Phosphorous is not found in fireworks in the UK or the US, but may be in fireworks, particularly firecrackers, from elsewhere. Clinical signs of phosphorous toxicity include haemorrhagic gastroenteritis, abdominal pain, weakness, cardiovascular collapse, hypocalcaemia and renal and hepatic injury. Arsenic toxicity results in severe vomiting and watery diarrhoea, bloody stools, abdominal pain, hypotension, hypothermia, dehydration, weakness and collapse.
There is also a potential for blast injuries, burns, eye injury and inhalation effects with burning fireworks.
Treatment
Owners should be questioned about the origin of the fire-work and whether it was for domestic or professional use, exploded or unexploded.
Gut decontamination is generally not required following ingestion of fireworks. Activated charcoal is not recommended as it does not adsorb metals (the toxic component of fireworks). In most cases the only sign is mild gastrointestinal upset and animals can usually be monitored at home. In cases where the original or type of firework is unknown, and the animal has more than mild gastrointestinal upset it is advisable to monitor electrolytes, liver and renal function.
In most symptomatic animals, rehydration with an antiemetic will be all that is required. If the animal has more significant signs it is important to ensure adequate hydration and monitor renal output. A liver protectant should be considered if liver enzymes are raised. Seek advice from a poison centre if barium or chlorate poisoning is suspected.
Any burn or blast injuries should be managed supportively.
Fungi
Many mushrooms (or toadstools — the terms are used interchangeably) appear in the autumn in warm, wet weather (Figure 2). These are the spore-bearing fruit bodies of fungi. There are many thousands of different fungus species and although most are not considered to be hazardous, some species can cause poisoning. Ingestion of fungi by dogs is quite common and may occur on a walk or with mushrooms growing in the garden.
Clinical signs
Mushroom poisoning can be broadly divided into various different syndromes. Some mushrooms cause only gastrointestinal signs. Others cause neurological signs including those containing psilocybin (e.g. magic mushrooms). Suspected magic mushroom or psilocybin poisoning has been reported in dogs (Kirwan, 1990) and effects include dilated pupils, disorientation and uncharacteristic behaviour (anxiety, aggression, vocalisation, fly snapping), ataxia and tachycardia. Mushrooms that contain muscarine (e.g. Clitocybe rivulosa) or ibotenic acid (e.g. Amanita muscaria, fly agaric) cause neurological and gastrointestinal signs. Dogs appear to be particularly attracted to muscarinic mushrooms (Bates et al, 2014) and ingestion may result in rapid onset of dramatic signs including severe hypersalivation, bradycardia, visual disturbance, increased peristalsis and abdominal tenderness, watery diarrhoea and urination (Reid, 1985; Lee et al, 2009; Seljetun and von Krogh, 2017; Seljetun and Lorentzen, 2018). Deaths have occurred in dogs after ingestion of muscarine-containing mushrooms (Tosterud et al, 2011; Irwin and Leech, 2014; Gleed et al, 2017). Ibotenic acid-containing mushrooms can cause disorientation, ataxia, hallucinations, dilated pupils, muscle spasms and cramps, cycles of lethargy and agitation and hyperactivity, and convulsions. Severe and fatal poisoning has been reported in pets from ingestion of ibotenic acid-containing mushrooms (Hunt and Funk, 1977; Naude and Berry, 1997; Rossmeisl et al, 2006; Lindberg and Holmgren, 2012; Romano et al, 2019).
Some fungi cause delayed poisoning and generally result in severe effects. Mushrooms containing gyromitrin (Gyromitra esculenta, false morel) are associated with gastrointestinal signs and hepatotoxicity (Bernard, 1979; Gulersoy et al, 2020). Orellanine-containing mushrooms (e.g. Cortinarius spp.) cause delayed (sometimes by many days) renal failure. Ingestion of mushrooms containing amatoxins (e.g. Amanita phalloides, death cap) may be fatal in pets (Puschner et al, 2007; Amorin, 2020; Kaae et al, 2021). Signs include delayed severe gastrointestinal effects, liver necrosis and renal failure.
Puffballs (such as Lycoperdon spp.) are of low toxicity by ingestion, but inhalation of puffball spores can cause respiratory signs (cough, sneezing, dyspnoea, tachypnoea), hyperthermia and leucocytosis. A chest x-ray may show bilateral infiltrates. Lung aspirates or biopsy show inflammatory changes and the presence of spores (Alenghat et al, 2009; Rubensohn, 2009; Buckeridge et al, 2011).
Treatment
If mushroom poisoning is suspected, identification of the mushrooms should be attempted. Fungal fruit bodies vary in shape, colour and size and these characteristics can change during development and deterioration. This can make reliable identification of suspect mushrooms difficult and requires specialist knowledge and experience. In addition, there are many thousands of different species. If identification is required in a clinical case, contact a poisons centre for advice. Fungus samples must be stored carefully, ideally by wrapping in paper and refrigerated; plastic wrappings or freezing cause degradation and may render identification impossible.
An emetic and activated charcoal (1–3 g/kg) can be given in pets that have ingested unknown or toxic species. The rapid onset of signs after muscarine poisoning often makes gut decontamination impractical (Puschner and Wegenast, 2018). If there is severe or persistent vomiting, then anti-emetics should be administered. Management is symptomatic and supportive, monitoring fluids and electrolytes. Intravenous fluids can be given for hypotension. Sedation and a quiet environment may be needed for animal with neurological effects from psilocybin poisoning. Liver protectants can be used in poisoning with hepatotoxic fungi.
For muscarine poisoning, animals with severe effects may require atropine which competes for muscarine at receptors. Signs should resolve within 30 minutes of administration. Care should be taken not to give too much atropine as this can result in tachycardia, hyperthermia, behavioural changes and gastrointestinal stasis (Puschner and Wegenast, 2018).
For ibotenic acid poisoning pets should be kept in a calm, quiet and dark environment. It is important to note that some drugs are contraindicated in the management of ibotenic acid poisoning. Sedatives, including diazepam and barbiturates, should be avoided if possible as they may cause respiratory depression or arrest (Rossmeisl et al, 2006; Beug and Shaw, 2009). The agitation or hyperactivity phase can usually be managed without intervention. Ventilation may be required in animals with respiratory depression or arrest. It is important that poisoning from muscarine-containing mushrooms and ibotenic acid-containing mushroom should not be confused. Atropine can rapidly improve the signs of muscarine toxicosis but exacerbate clinical effects of ibotenic acid poisoning (Beug and Shaw, 2009).
Where the mushroom is unknown, monitoring of hydration status, liver and renal function may be required. If fungus samples are not available, toxicological analysis may also be used for confirmation of exposure.
Tremorgenic mycotoxins
Tremorgenic mycotoxins are commonly produced by the fungus Penicillium which is found in decomposing organic material. Most cases of tremorgenic mycotoxicosis involve dogs, as cats have more discriminating eating habits (Warantuke, 2017). Sources include food waste including composted waste, and rotting, fallen fruits and nuts. Wet, warm weather is ideal for fungal growth.
Clinical effects
Signs of tremorgenic mycotoxicosis occur within 30 minutes to 3 hours with whole-body muscle tremors, vomiting, pyrexia, convulsions, ataxia, twitching and hyperaesthesia. There may also be hypersalivation, rigidity with hyperextension of extremities, hyperactivity, tachycardia, panting, diarrhoea and nystagmus. In severe cases, severe tremors and opisthotonos, status epilepticus and coma with paddling can occur. Aspiration is also a risk. Complications of prolonged seizure activity include severe pyrexia and rhabdomyolysis which can lead to acute kidney injury and disseminated intravascular coagulation (DIC). These complications can lead to multi-organ failure.
Treatment
The mainstay of treatment in dogs with tremorgenic mycotoxicosis is decontamination and control of increased muscle activity and seizures to prevent complications from prolonged seizure activity.
An emetic could be considered if ingestion was recent (within 1 hour) but only if the dog is asymptomatic. Alternatively, a gastric lavage could be considered if the quantity of mouldy material ingested is large or the animal is symptomatic. Repeat dose activated charcoal (1–3 g/kg every 4 hours) should be given, if practical, as the mycotoxins undergo enterohepatic recirculation. An antiemetic should be given to reduce the risk of vomiting and aspiration pneumonia.
The respiration, neurological status and temperature should be monitored. Comatose animals should be turned regularly and positioned to reduce the risk of aspiration. Ventilatory support may be required in dogs with severe respiratory depression. In many cases of tremorgenic mycotoxicosis in dogs, diazepam is ineffective and other sedatives and anticonvulsants will be required. Propofol, ketamine, levetiracetam or barbiturates can be used. If tremors/convulsions are not controlled, then general anaesthesia may be required. Inhalant anaesthetics can also be used, particularly where lipid emulsion is used (as barbiturates and propofol are themselves lipid soluble). Lipid emulsion has been shown to be beneficial in cases of suspected tremorgenic mycotoxicosis in dogs (Kormpou et al, 2018). Early use of lipid emulsion is recommended if the exposure is thought to be significant, there are significant neurological signs or there is failure to respond to other therapies.
Autumn plants
Many fruits and nuts are produced in the autumn as these are part of plant reproductive processes and function to spread the seeds or to attract dispersers. Windfall fruits are also a potential hazard as they are readily accessible to pets and may fall to the ground in large numbers during windy weather. If they are left, there is a risk they may become mouldy or in the case of some fruits, such as apples, ferment which may lead to alcohol intoxication if ingested. Fatal ethanol intoxication was reported in a dog that ate rotten apples in the garden (Kammerer et al, 2001) and tremorgenic mycotoxicosis occurred in a dog that ingested mouldy walnuts (Munday et al, 2008). Also some toxic plants, such as autumn crocus, may flower in the autumn, rather than the spring or summer.
Pumpkins
Pets may eat discarded flesh or carved Halloween pumpkins (Figure 3). This is usually not a concern although there may be mild gastrointestinal upset. Pumpkins and related fruits (e.g. courgettes) can contain extremely bitter-tasting compounds but they have been bred out of crop varieties. Very occasionally these compounds can occur in cultivated species through mutation, environmental stress or an outcross with a wild species (this does not occur in the UK as wild species are not native). Ingestion of bitter roots or fruits can cause more pronounced signs and significant gastrointestinal effects with severe abdominal discomfort, diarrhoea (which may be haemorrhagic), vomiting and collapse. Management is supportive.
Conkers
Conkers (Figure 4a) are the seeds of the horse chestnut tree (Aesculus hippocastanum). They ripen from late summer to autumn, and this is when most cases of accidental ingestion in dogs are reported.
The poisonous principle is generally described as aesculin (or esculin), a saponin glycoside but over 210 compounds have been isolated from Aesculus spp. and the mechanism of toxic effects seen in animals following ingestion of conkers is unclear. Vomiting is the most common effect in dogs. Other signs include abdominal discomfort, diarrhoea, lethargy, ataxia, pyrexia, depression and tremor. Less common effects include haematemesis, dehydration, rigidity, constipation, ileus and/or obstruction of the gastrointestinal tract.
Gut decontamination is generally not required in dogs after ingestion of conkers and activated charcoal is not recommended as it could increase the risk of constipation. Treatment is supportive, particularly ensuring adequate hydration. If there is severe or persistent vomiting, an antiemetic can be given, and a laxative may help passage of plant material through the gastrointestinal tract. Laparotomy and surgical removal of impacted plant material may be required in dogs with suspected or confirmed gastrointestinal obstruction.
Acorns
Acorns (Figure 4b) are the nuts of oaks (Quercus spp.). They ripen from August onwards and autumn is when most cases of exposure in dogs occurs. Oak poisoning is a serious problem in ruminants and horses, and severe cases are occasionally reported in dogs (Bosseler et al, 2017; Camacho et al, 2021).
The mechanism of acorn toxicity is not clear. Oaks contain tannic acid, which can cause increased vascular permeability and subsequent fluid loss. It is postulated that ingestion of a large quantity of oak results in an astringent effect on the gut increasing absorption of toxic compounds. The absorbed tannins are metabolised to toxic components which results in tissue damage at the sites of highest concentration (e.g. the kidney). Damage to the gut is exacerbated by the effects of uraemia.
Vomiting and diarrhoea (occasionally haemorrhagic) are the most common signs in dogs after acorn ingestion. There may also be abdominal tenderness, inappetence and lethargy. Less commonly, melaena, haematemesis, pale mucous membranes and pyrexia may occur. There is a risk of choking or gastrointestinal obstruction following ingestion of acorns, but these are not common in dogs. Liver and/or kidney injury occurs in a small number of cases.
In most cases gut decontamination is unlikely to be necessary following ingestion of acorns since spontaneous vomiting often occurs. Owners should be advised to observe for signs of obstruction (e.g. repetitive vomiting, weakness, inappetence, bloating, inappetence) and if signs are pronounced or persist beyond 48 hours the renal and liver parameters should be checked. X-ray, endoscopic evaluation and/or surgery may be required in cases of suspected obstruction. Liver or kidney injury is managed supportively (e.g. intravenous fluids, liver protectants).
Rowan (mountain ash)
Rowan (Sorbus aucuparia) is a common tree with large clusters of orange-red (Figure 4c), or sometimes yellow berries. The plant and its berries are considered of low toxicity, but ingestion may cause gastrointestinal upset and irritation of the mucous membranes. Effects are usually mild and self-limiting (Veterinary Poisons Information Service (VPIS) case data).
Cherry laurel
Cherry laurel (Prunus laurocerasus, Figure 4d) is a common plant that contains cyanogenic glycosides, which produces cyanide when the plant material is chewed or crushed. Owners may be very concerned if this plant is eaten. Cyanide poisoning, however, is much more of a concern in ruminants, as the rumen contains enzymes that hydrolyse the glycosides and the higher pH of the rumen increases the rate of conversion releasing more cyanide. Signs of cyanide poisoning are rarely seen in cats and dogs after ingestion of plant material containing cyanogenic glycosides. Most dogs and cats that ingest cherry laurel develop gastrointestinal signs with vomiting, diarrhoea and abdominal discomfort, these effects are unrelated to possible cyanide release. There may also be panting, constipation and there is risk of gastrointestinal obstruction depending on the quantity and size of the fruit eaten. The stones may be passed in the faeces and faeces may be discoloured (depending on the colour of the fruit).
Gut decontamination is usually not required following ingestion of the fleshy fruits or if the seeds (stones) are swallowed whole. It could be considered if the stones are crushed and swallowed. Animals should be monitored for signs of gastrointestinal obstruction (e.g. vomiting, diarrhoea, abdominal discomfort, inappetence, constipation). Also, depending on what has been ingested (e.g. crushed rather than whole stones), monitoring for signs of cyanide poisoning may be appropriate. In animals with signs of collapse and/or respiratory distress it is important to determine whether signs are a result of gastrointestinal pain or cyanide poisoning (where signs are caused by hypoxia). Lactic acidosis is a common (but non-specific) biomarker of cyanide poisoning and could be measured if cyanide poisoning is suspected (and facilities allow).
Management of gastrointestinal signs is supportive with analgesia, rehydration and an antiemetic, as required. Any animal with persistent gastrointestinal signs should be assessed for possible gastrointestinal obstruction. If cyanide poisoning is suspected, 100% oxygen should be administered. Treatment of cyanide poisoning in companion animals is supportive as cyanide antidotes such as hydroxocobalamin or sodium thiosulphate and sodium nitrite are generally unavailable in veterinary medicine and may be prohibitively expensive.
Yew
Yew (Taxus spp., Figure 4e) is a common conifer containing taxine, a complex mixture of alkaloids, which have cardiotoxic effects, and an irritant volatile oil that can cause gastrointestinal irritation and diarrhoea.
All parts of yew are toxic, except the fleshy part of the ‘fruit’ (the aril) (Wilson et al, 2001). The fruits appear in the autumn, but poisoning can occur at any time of the year as plant material remains toxic after drying. Most cases of poisoning in animals usually occur in herbivores following ingestion of hedge trimmings or grazing on yew. Few cases of poisoning have been reported in companion animals (e.g. Evans and Cook, 1991).
In dogs, signs after yew ingestion are usually limited to vomiting and diarrhoea. Other signs occasionally reported include lethargy, ataxia, abdominal tenderness and dilated pupils. Aggressive behaviour may occur (Evans and Cook, 1991). In severe cases collapse, bradycardia (or tachycardia), pyrexia, tremor, dyspnoea, hypotension and convulsions and arrhythmias may occur (Cope, 2005).
There is no specific antidote and treatment of animals with yew poisoning is supportive.
Autumn crocus
Autumn crocus (Colchicum autumnale) as its common name suggests, flowers in the autumn, unlike the spring crocus (Crocus spp.) which flowers in the spring. The flowers of autumn crocus appear before the leaves (Figure 5). All parts of the plant are toxic and contain colchicine which has an anti-mitotic effect and inhibits cell division and therefore has most effect on cells with a high turnover rate such as bone marrow cells and the epithelial cells of the gastrointestinal tract.
Clinical signs following ingestion of autumn crocus include severe gastrointestinal irritation with dehydration, inco-ordination, recumbency, collapse and shock. In severe cases there may also be bone marrow depression and multiorgan failure. Severe cases are not common in pets, but fatal cases are reported (VPIS cases data).
Treatment is supportive with gut decontamination, and, if required, aggressive rehydration, monitoring of haematological parameters, liver and renal function, blood transfusion and broad-spectrum antibiotic cover.
Conclusions
Autumn is associated with specific seasonal poisoning risks, such as the sudden profusion of mushrooms (particularly if the weather is wet and warm) and the risk of exposure to mouldy foodstuffs or fallen fruits and nuts. There is also an abundance of fruits, nuts and seeds which may be hazardous and the additional risk of exposure to luminous novelty items commonly available around Halloween and Bonfire Night. In the majority of cases treatment of autumn seasonal hazards is supportive. Expert identification of mushrooms is highly recommended to identify animals at risk of severe poisoning and those that can be managed at home. Contact a poisons information service for advice on this and the management of other poisons, if required.
KEY POINTS
- Autumnal poisoning risks include fungi, Halloween and Bonfire night novelties and autumn fruits, seeds and nuts.
- Ingestion of luminous novelties is low risk but will produce a taste reaction. The liquid is irritant to eyes and skin.
- In cases of ingestion of a mushroom, expert identification is highly recommended — contact a poisons information service.
- Moulds producing tremorgenic mycotoxins may flourish in warm, wet weather with the risk of poisoning for dogs with indiscriminate eating habits.
- Pets, particularly dogs, commonly eat autumnal fruits, nuts and seeds. In most cases only gastrointestinal signs occur, but there is a risk of more severe poisoning.