Walnuts (Juglans Regia)

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Walnut poisoning (Juglans regia) represents a serious intoxication in dogs and cats. This is primarily a mycotoxicosis, meaning poisoning by metabolic products of molds that can grow on the nuts. Dogs are particularly affected, as their less selective eating habits make them more likely to ingest walnuts than cats. The main danger does not come from the walnut itself, but from the mycotoxins, especially Penitrem A, which is produced by the mold Penicillium crustosum. These toxins are effective even in small amounts and can lead to severe neurological symptoms. While fresh, un-molded walnuts are generally harmless to pets in small quantities, nuts lying on the ground, damp, or stored nuts with initial mold growth pose a significant risk.

The most important facts at a glance

Walnut poisoning in dogs and cats represents an acute emergency situation caused by the ingestion of mold toxins, particularly Penitrem A. These mycotoxins are found on moldy walnuts and primarily affect the central nervous system and the gastrointestinal tract. Dogs are more frequently affected than cats due to their less selective eating habits.

Clinical symptoms develop rapidly within 15 minutes to 3 hours after ingestion and include gastrointestinal complaints such as vomiting and diarrhea, as well as neurological abnormalities like tremor, ataxia, and in severe cases, seizures. Diagnosis is primarily based on the history and characteristic clinical picture, as specific diagnostic tests are not available in routine diagnostics.

Therapy is symptomatic and includes decontamination measures such as activated charcoal administration, fluid therapy for circulatory stabilization and promotion of toxin elimination, and pharmacological control of neurological symptoms. Newer approaches such as intravenous lipid emulsion (ILE) can support the binding of lipophilic toxins.

With early and adequate treatment, the prognosis is good, with most animals recovering completely within a few days. Aftercare includes a quiet environment, adapted nutrition, and follow-up examinations to monitor organ functions.

Preventive measures such as regularly collecting fallen walnuts in gardens and safe storage in the household are crucial to prevent recurrent poisoning cases. Pet owners should be informed about the risks and seek immediate veterinary help if walnut poisoning is suspected.

Causes, development and progression

Many dogs enjoy eating walnuts. However, unripe and fresh walnuts, in particular, can be highly toxic to dogs.
The cause is not visible metabolic products of molds (mycotoxin Penitrem A from Penicillium crustosum).
Walnut imports are carefully monitored, so contaminated nuts are unlikely to be found in commercial products. The situation is more critical in home gardens, where dogs should not be allowed to eat nuts lying on the ground unchecked.

Supplements

The main cause of walnut poisoning in dogs and cats is the ingestion of nuts contaminated with mold. These fungi produce highly potent neurotoxins as secondary metabolites, primarily Penitrem A. Contamination of walnuts usually occurs due to improper storage under humid conditions or prolonged lying on the ground, especially during the autumn harvest season. While commercially available walnuts are generally strictly controlled and rarely contaminated, there is an increased risk with nuts from private gardens or public places with walnut trees.

Toxin formation is promoted by various factors:

  • Humidity above 70% relative humidity
  • Temperatures between 20-30°C
  • Damage to the nutshell, facilitating the penetration of fungal spores
  • Prolonged storage under suboptimal conditions

Unripe and fresh walnuts that have fallen to the ground and absorbed moisture are particularly at risk. Even nuts that appear outwardly unaffected can already contain significant amounts of mycotoxins. In dogs, ingesting just a few moldy walnuts is enough to trigger clinically relevant poisoning, while cats are less frequently affected due to their more selective eating habits.

Mechanism of action

In dogs, ingesting even a few moldy walnuts can lead to signs of intoxication.
The mycotoxins are rapidly absorbed in the intestinal tract. The latency period (time between toxin ingestion and the first symptoms of intoxication) is only 15 minutes to 2-3 hours.
They irritate the mucous membrane of the gastrointestinal tract and are toxic to the peripheral and central nervous systems.
The toxic effect of the mycotoxin primarily consists of promoting generalized tremors (tremorgenic effect) by increasing the release of excitatory neurotransmitters in the brain and inhibiting the release of inhibitory neurotransmitters in the brain. The result is tremors and seizures.

Supplements

Walnuts are not inherently toxic per se, but they can lead to health problems in dogs (less commonly in cats). The potential toxicity depends on several factors:

  1. Mold contamination (production of mycotoxins, especially tremorgenic mycotoxins)

  2. Type of walnut (e.g., black walnut = Juglans nigra)

  3. Rancid or unripe nuts

  4. Fat content and individual intolerance

The actual poisoning problem lies not in the walnut itself, but in microbial or chemical accompanying substances, especially in spoiled or improperly stored nuts.

1. Tremorgenic Mycotoxins (E.G., Penitrem a, Roquefortine C)

  • Formed by molds (especially Penicillium species) on spoiled walnuts.

  • Neurotoxic effect:

    • Blockade of GABA-dependent inhibitory synapses

    • Result: neuromuscular hyperexcitability

  • Symptoms usually begin within 30 minutes to 6 hours:

    • Muscle tremors, seizures, ataxia

    • Hypersalivation, hyperthermia

    • In severe cases: status epilepticus, death

2. Damage Due to Oxidative Stress from Black Walnuts

  • Black walnuts (Juglans nigra) may contain juglone, a phenolic compound with pro-oxidative properties.

  • In dogs, juglone can lead to:

    • Gastrointestinal symptoms (vomiting, diarrhea)

    • Lethargy, muscle tremors, neurological abnormalities.

  • Additionally, juglone is associated with lameness or laminitis in horses – in dogs, this is pathophysiologically less relevant.

3. Fat-related Pancreatitis

  • The high fat content of nuts can trigger reactive or necrotizing pancreatitis in sensitive animals, especially smaller dogs.

  • Pathomechanism:

    • Enzymatic autodigestion of the pancreas due to premature activation of digestive enzymes

    • Release of pro-inflammatory mediators

    • Possible systemic reaction: fever, pain, vomiting, circulatory weakness

4. Mechanical Complications

  • Whole walnuts, if ingested, can lead to foreign bodies in the digestive tract (especially in small dogs).

  • Risk of intestinal obstruction or perforation.

Conclusion

Walnut poisoning in dogs and cats is not caused by the nut itself, but by accompanying factors such as mold toxins, rancid fats, or incompatible ingredients. Tremorgenic mycotoxins, in particular, pose a serious neurological risk. Owners should therefore not feed nuts – especially spoiled ones – to pets. Even small amounts of moldy walnuts can lead to life-threatening seizures.

Symptoms of intoxication

Symptoms affect the gastrointestinal tract and the nervous system. Mycotoxins can damage the kidneys, so kidney function must be carefully monitored in cases of pre-existing conditions.
The symptoms that may be observed include:

  • Drooling (salivation)
  • Vomiting (Vomitus)
  • Diarrhea (Diarrhoea)
  • Weakness
  • Increased body temperature (hyperthermia)
  • Tremor
  • Tonic-clonic seizures
  • Ataxia
  • Hypersensitivity of sensory nerves (hyperesthesia)
  • Noise sensitivity (hyperacusis)
  • Increased respiratory rate (tachypnea)
  • Increased heart rate (tachycardia)
  • Pupil dilation (mydriasis)
  • Rapid horizontal movement of the pupils (nystagmus)
  • Seizures

Supplements

The symptoms of walnut poisoning in dogs and cats usually develop rapidly after ingestion of contaminated nuts. The latency period between ingestion and the first symptoms is only 15 minutes to 3 hours, which is due to the rapid absorption of mycotoxins in the intestinal tract. Clinical signs primarily affect two organ systems: the gastrointestinal tract and the central nervous system.

Gastrointestinal symptoms include:

  • Increased salivation (hypersalivation)
  • Vomiting, often repeated and severe
  • Diarrhea, which can be watery to bloody
  • Abdominal pain, recognizable by a tense abdominal wall

The neurological symptoms, caused by the neurotoxic effect of mycotoxins, can be particularly alarming:

  • Muscle tremors, often generalized and exacerbated by movement
  • Coordination disorders (ataxia) with a swaying gait
  • Hypersensitivity to touch stimuli (hyperesthesia)
  • Increased noise sensitivity (hyperacusis)
  • Increased body temperature (hyperthermia)
  • Accelerated breathing (tachypnea)
  • Increased heart rate (tachycardia)
  • Dilated pupils (mydriasis)
  • Rapid, uncontrolled eye movements (nystagmus)
  • Tonic-clonic seizures in severe cases

In cats, symptoms may be more subtle, but neurological abnormalities such as ataxia and tremors are also the main symptoms. Particularly small dog breeds, young animals, and animals with pre-existing conditions may show more severe courses. The intensity of symptoms can vary depending on the amount of toxin ingested and the individual sensitivity of the animal.

Diagnosis

The diagnosis of walnut poisoning in dogs and cats is primarily based on the history and clinical presentation. Since no specific diagnostic test for the detection of mycotoxins is available in routine diagnostics, a thorough history-taking is of particular importance.

The diagnostic process includes the following steps:

A detailed history is crucial, with the pet owner being asked about possible access to walnuts, especially whether the animal was in a garden with walnut trees or if walnuts were accessible in the household. The temporal correlation between possible ingestion and the onset of symptoms provides important clues.

The clinical examination focuses on neurological and gastrointestinal abnormalities. The characteristic picture of tremor, ataxia, and hypersalivation, combined with a history of possible walnut ingestion, strengthens the suspicion. During the neurological examination, reflexes, coordination, and reactions to environmental stimuli are assessed.

Laboratory tests primarily serve to rule out differential diagnoses and assess organ function. A complete blood count, serum chemistry with liver and kidney values, and electrolytes should be performed. In cases of suspected walnut poisoning, elevated liver enzyme levels may occur, but these changes are non-specific.

In unclear cases, a toxicological analysis of vomit or fecal samples for mycotoxins may be considered in specialized laboratories, but this is rarely necessary and time-consuming in practice.

Therapeutic principles

There is no antidote.
Decontamination may involve gastric lavage and administration of activated charcoal. Inducing vomiting is not recommended due to the risk of seizures.
Therapy is symptomatic and focuses on:

  • Intravenous fluid replacement
  • Controlling vomiting
  • Controlling tremors and seizures
  • Anesthesia via continuous drip infusion for persistent seizure tendency
  • Lipid infusion for toxin binding in the blood

The treatment of walnut poisoning in dogs and cats is symptomatic, as no specific antidote exists. The therapeutic management aims to prevent further toxin absorption, eliminate already absorbed toxins, and control symptoms.

Decontamination is the first step in treatment. If presented within the first one to two hours after ingestion, gastric lavage under anesthesia may be considered. Inducing vomiting with emetics such as apomorphine in dogs or xylazine in cats is controversially discussed due to existing or impending neurological symptoms with a tendency to seizures and should only be done under strict veterinary supervision.

The administration of activated charcoal (1-4 g/kg body weight) is an important part of therapy to bind toxins still in the intestine. In severe cases, activated charcoal administration can be repeated every 4-6 hours for 24-48 hours to also capture enterohepatically circulating toxins.

Intravenous fluid therapy with crystalloid solutions (e.g., Ringer’s lactate) is essential to stabilize circulatory function and promote renal elimination of toxins. The dosage depends on the patient’s hydration status, typically 2-4 ml/kg/h.

Neurological symptoms are controlled with anticonvulsants. For tremors and mild seizures, diazepam (0.5-2 mg/kg i.v.) is the drug of choice. For persistent seizures, phenobarbital (2-4 mg/kg i.v.) or levetiracetam (20 mg/kg i.v.) can be used. In therapy-resistant cases, a continuous propofol drip infusion (0.1-0.4 mg/kg/min) or even general anesthesia may be necessary.

A promising newer therapeutic option is intravenous lipid emulsion (ILE). This can help bind lipophilic toxins like mycotoxins in the blood. The dosage is 1.5 ml/kg as a bolus, followed by 0.25-0.5 ml/kg/min over 30-60 minutes.

Supportive measures include antiemetics such as maropitant (1 mg/kg s.c.) for persistent vomiting, temperature management for hyperthermia, and creating a calm environment to avoid additional stimulation.

Prognosis & follow-up care

The prognosis for walnut poisoning is generally good with early and adequate treatment. Most dogs and cats recover completely within 24 to 72 hours, although mild neurological symptoms such as intermittent tremors may persist for up to a week in individual cases. The timing of treatment initiation is crucial for treatment success – the earlier treatment begins, the better the prognosis.

Factors that can negatively influence the prognosis are:

  • Pre-existing liver or kidney diseases
  • Ingestion of large quantities of moldy walnuts
  • Delayed start of treatment (>6 hours after ingestion)
  • Severe neurological symptoms such as persistent seizures
  • Very young, old, or small animals with less physiological reserve

Aftercare plays an important role in complete recovery. After discharge from inpatient treatment, the following aspects should be considered:

Create a calm, stress-free environment for the animal to promote neurological recovery. Activity should be restricted in the first few days, with a slow increase as symptoms improve.

A follow-up examination after 24-48 hours and, if necessary, after one week is recommended to monitor the healing process. On this occasion, blood parameters can be checked to assess liver and kidney function.

The diet should initially consist of easily digestible food in small, frequent portions to protect the gastrointestinal tract. Adequate fluid intake must be ensured.

Preventive measures to avoid renewed exposure should be discussed with the pet owner, especially for animals living in gardens with walnut trees. This includes regularly collecting fallen nuts and safely storing walnuts in the household.

Research outlook

Research in the field of mycotoxicoses in small animals has gained importance in recent years. Current studies focus on several promising areas that could improve the management of walnut poisoning in dogs and cats.

One focus is on the development of rapid diagnostic tests for the detection of Penitrem A and other tremorgenic mycotoxins in blood or urine. Chromatographic methods combined with mass spectrometry show promising results for the sensitive detection of even low toxin concentrations. These could, in the future, refine and accelerate diagnosis.

Intravenous lipid emulsion (ILE) therapy is being intensively researched. Recent studies investigate optimized dosing protocols and the efficacy of various lipid emulsions in binding mycotoxins. Initial results suggest that ILE can shorten recovery time and reduce the severity of neurological symptoms.

In the field of antidote development, specific toxin binders are being investigated that could selectively bind to mycotoxins and prevent their absorption in the intestine. Modified activated charcoal preparations with increased binding capacity for mycotoxins are in the preclinical testing phase.

The role of the microbiome in mycotoxin detoxification is increasingly coming into focus. Studies are investigating whether certain probiotic bacterial strains can metabolize mycotoxins or reduce their absorption. This could enable new preventive approaches.

Epidemiological studies analyze regional and seasonal clusters of poisoning cases in relation to climatic factors. This data could help to better predict risk periods and develop targeted prevention strategies.

The identification of genetic factors influencing individual susceptibility to mycotoxins could enable personalized treatment approaches in the future. Initial studies indicate breed-specific differences in mycotoxin metabolism.

These research approaches promise improved diagnostic and therapeutic options for the future, which could lead to even more targeted and effective treatment of walnut poisoning in dogs and cats.

Frequently asked questions (FAQs)

  1. Are all walnuts toxic to dogs and cats?
    Not all walnuts are toxic. The danger mainly comes from moldy walnuts that contain mycotoxins. Fresh, unmoldy walnuts in small quantities are generally harmless, but due to their high fat content, they can cause gastrointestinal upset.
  2. How quickly do symptoms appear after ingesting moldy walnuts?
    The first symptoms usually appear within 15 minutes to 3 hours after ingestion. The rapid development of symptoms is characteristic of this poisoning and underscores the need for prompt veterinary treatment.
  3. Can cats also get walnut poisoning?
    Yes, cats can also be poisoned by moldy walnuts. However, due to their more selective eating habits, they are less frequently affected than dogs. The symptoms and treatment are similar in both animal species.
  4. How can I tell if a walnut is contaminated with mold?
    Mold contamination is not always visible to the naked eye. Outwardly, mold can appear as whitish, greenish, or bluish discoloration. However, nuts can also be internally contaminated without being outwardly visible. Moist, musty-smelling, or unusually looking walnuts should generally not be fed.
  5. What should I do if my pet has eaten moldy walnuts?
    Seek veterinary attention immediately, even if no symptoms are yet visible. If possible, take any remaining walnuts that were eaten with you to allow for a better assessment of the situation. Do not attempt to induce vomiting without veterinary instruction.
  6. Are there long-term consequences after recovering from walnut poisoning?
    With timely and adequate treatment, long-term consequences are rare. Most animals recover completely. In very severe cases with persistent seizures, permanent neurological deficits could theoretically occur, but this is an exception.
  7. Which dog and cat breeds are particularly susceptible to walnut poisoning?
    There are no specific breeds that are particularly susceptible. However, small breeds and young animals may show more severe courses due to the unfavorable ratio of body weight to the amount of toxin ingested. Animals with pre-existing liver or kidney diseases also have an increased risk of complications.
  8. How can I protect my pet from walnut poisoning?
    Regularly collect fallen nuts in gardens with walnut trees. Store walnuts safely out of reach of pets in the household. When out walking, make sure your pet does not eat any nuts lying on the ground. Train a reliable “leave it” command for emergency situations.
  9. Are other types of nuts as dangerous for pets as walnuts?
    Different types of nuts pose different risks. Macadamia nuts can lead to weakness, tremors, and hyperthermia in dogs. Almonds and pistachios can cause gastrointestinal upset due to their high fat content. In general, nuts should only be given in very small quantities and under supervision.
  10. Is intravenous lipid emulsion an effective treatment method for walnut poisoning?
    Intravenous lipid emulsion (ILE) shows promising results in the treatment of poisoning with lipophilic toxins such as mycotoxins. Initial clinical experience suggests faster recovery and milder neurological symptoms. However, the method is still being researched and is not available in every veterinary practice.

Literature

  • https://www.vetpharm.uzh.ch/GIFTDB/PFLANZEN/0198_tvm.htm
  • Fritz, L., Miklis, A., Bitter, V., & Neiger, R. (2020). Suspected intoxication by tremorgenic mycotoxins in twelve dogs after ingestion of moldy walnuts. Kleintierpraxis, 65(9), 476-481.
  • Manwaring, G., Graves, T., & Schott, H. (2021). Intravenous lipid emulsion therapy for treatment of mold toxicosis in dogs: A retrospective case series (2010-2020). Journal of Veterinary Emergency and Critical Care, 31(3), 345-352. https://doi.org/10.1111/vec.13058
  • Peterson, M. E., & Talcott, P. A. (2022). Small Animal Toxicology (4th ed.). Elsevier Health Sciences, 612-615.
  • Puschner, B., & Reimschuessel, R. (2021). Toxicosis caused by tremorgenic mycotoxins in companion animals. Veterinary Clinics of North America: Small Animal Practice, 51(6), 1299-1315. https://doi.org/10.1016/j.cvsm.2021.06.006
  • Löwe G, Löwe O. Poisoning in Dogs and Cats – A Veterinary Guide. 2nd edition. Kreuztal: Kynos-Verlag. 2021; 208 p.
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