Organophosphates and Carbamates
Organophosphates and carbamates are among the most common causes of poisoning in our pets. These substances are chemical compounds derived from various phosphoric acids or carbamic acid, respectively, and are found in numerous products in our daily lives. Their primary use is in pest control, where they are used as insecticides, herbicides, and fungicides in fertilizers, as well as direct antiparasitics.
The toxicological mechanism of action of these substances is based on their ability to inhibit the enzyme acetylcholinesterase (AChE). This enzyme is essential for regulating the neurotransmitter acetylcholine at the synapses of the nervous system. In organophosphates, this inhibition is irreversible, while in carbamates, it is reversible—an important difference that explains the lower toxicity of carbamates.
For veterinarians, poisoning with these substances poses a particular challenge, as symptoms can be varied and rapid intervention is required. Knowledge of the pathophysiology, clinical signs, and appropriate treatment strategies is therefore crucial for successful therapy.
The most important facts at a glance
Organophosphate and carbamate poisonings represent a common and potentially life-threatening emergency in small animal medicine. These substances, contained in numerous insecticides, herbicides, and antiparasitics, act by inhibiting the enzyme acetylcholinesterase, leading to overstimulation of the nervous system.
Clinical symptoms include muscarinic effects (hypersalivation, miosis, bronchorrhea, diarrhea), nicotinic effects (muscle tremors, weakness), and central effects (nervousness, ataxia, seizures). In severe cases, respiratory paralysis and death can occur. A special phenomenon is the intermediate syndrome, which can occur 24–96 hours after acute poisoning and is characterized by paralysis of the respiratory muscles.
Diagnosis is based on history, clinical symptoms, and measurement of acetylcholinesterase activity in the blood. Treatment includes decontamination, administration of atropine as a specific antidote against muscarinic effects, and for organophosphates, also the administration of oximes to reactivate cholinesterase, as well as supportive measures.
With early detection and adequate treatment, the prognosis is good, although the toxic effects in dogs and cats can last two to four weeks. Aftercare includes regular check-ups and prevention of further exposures.
It is important for pet owners to be aware of potential hazards in the home and garden and to prevent their pets’ access to these substances. If poisoning is suspected, veterinary help should be sought immediately, as rapid intervention is crucial for successful treatment.
Causes, development and progression
Poisoning with organophosphates and carbamates in pets primarily occurs through three exposure routes: dermal (skin), inhalation (respiratory), or oral (digestive tract). These substances are rapidly absorbed, and initial poisoning symptoms can appear as early as 1–2 hours after ingestion.
Numerous potential hazards for our pets lurk in homes and gardens:
Insecticides and pest control products are the most common source of exposure. These include sprays against ants, cockroaches, or flies, flea collars, spot-on preparations for parasites, and agents against aphids or other plant pests. Products designed for agricultural use are particularly dangerous, as they contain higher concentrations of active ingredients.
Garden fertilizers with integrated insecticides, often containing organophosphates or carbamates, pose a particular risk. Rat poison and slug pellets can also contain these substances and represent a significant danger to curious pets.
The risk of poisoning increases seasonally during the gardening season in spring and summer, when more plant protection products are used. Furthermore, the risk increases in rural areas with intensive agriculture, where these substances are applied over large areas.
A particular problem is that dogs and cats can ingest these poisons not only directly but also by licking treated surfaces or by contact with contaminated paws, which they then lick clean. This explains why even seemingly small amounts of these substances can lead to severe poisoning.
Mechanism of action
Most dogs develop the classic picture of overstimulation of certain functions of the autonomic nervous system (involuntary nervous system), which controls certain bodily functions such as blood pressure, heart rate, respiration, and digestion.
This is due to the inhibitory effect of organophosphates and carbamates on the enzyme acetylcholinesterase (AChE), which breaks down the neurotransmitter acetylcholine at nerve synapses (junctions from nerve cell to nerve cell) and at neuromuscular junctions (junctions from nerve cell to muscle cell). As acetylcholine levels increase, the activity in the autonomic nervous system increases.
The effect concerns many organs such as the peripheral and central nervous systems, muscles, liver, pancreas, and brain, as well as metabolic processes. The neuronal and hormonal status of the body is permanently disturbed. An acute toxicosis develops.
In organophosphates, the inhibition of AChE is irreversible, whereas in carbamates, it is reversible. This partly explains the lower toxicity of carbamates.
The oral LD50 in dogs is 19 mg/kg body weight.
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In dogs and cats, oral ingestion or dermal absorption leads to severe intoxications, primarily characterized by overstimulation of the parasympathetic nervous system.
The common toxicological target mechanism of both substance classes is the inhibition of the enzyme acetylcholinesterase (AChE) – however, with important differences in the reversibility and persistence of binding.
1. Physiological Function of Acetylcholinesterase
Acetylcholine (ACh) is a central neurotransmitter in the parasympathetic nervous system, at neuromuscular endplates, and in the CNS. It mediates impulse transmission by binding to cholinergic receptors.
Acetylcholinesterase rapidly breaks down ACh in the synaptic cleft into choline and acetate, terminating signal transmission.
2. Mechanism of Action of Organophosphates
Organophosphates (e.g., parathion, diazinon, chlorpyrifos) act by:
- Irreversible phosphorylation of the serine residue in the active center of AChE
- Formation of a stable phosphorus-enzyme bond, which irreversibly strengthens within hours to days through “aging”
- Result: sustained inhibition of AChE, leading to accumulation of acetylcholine in the synaptic cleft
This leads to a continuous overstimulation of cholinergic synapses – with sometimes life-threatening overstimulations at:
- Muscarinic receptors (smooth muscle, glands, heart)
- Nicotinic receptors (neuromuscular junction, ganglia)
- CNS receptors (central nervous cholinergic pathways)
3. Mechanism of Action of Carbamates
Carbamates (e.g., carbaryl, propoxur, methomyl) also bind to AChE, but:
- The binding is reversible and not subject to aging
- Carbamylated inhibition of AChE occurs with a time-limited effect (hours to a few days)
- Clinically, the symptoms resemble those of OP poisoning, but are often milder and shorter
4. Clinical Effects – Cholinergic Syndrome
A) Muscarinic Symptoms (via M-receptors):
- Hypersalivation
- Miosis (constricted pupils)
- Bradycardia
- Bronchorrhea and bronchospasm
- Diarrhea, vomiting, colic
- Urinary incontinence
Mnemonic: SLUDGE (Salivation, Lacrimation, Urination, Defecation, Gastrointestinal signs, Emesis)
B) Nicotinic Symptoms (via N-receptors):
- Muscle tremors
- Fasciculations
- Weakness
- Muscle paralysis (possibly respiratory paralysis!)
C) CNS Symptoms:
- Restlessness
- Ataxia
- Seizures
- Coma
5. Species-Specific Characteristics
Dog:
- Sensitive, especially with dermal exposure (e.g., flea treatments).
- Rapid onset of action (30 min – 3 h).
- Symptoms usually in full manifestation: muscarinic, nicotinic, central nervous.
- Life-threatening primarily due to respiratory paralysis, circulatory shock, seizures.
Cat:
- Very sensitive, especially with improper use of flea treatments for dogs (e.g., permethrin-OP combination).
- Pronounced skin absorption (thin epidermis, high liver sensitivity).
- Even small amounts can lead to massive symptoms.
6. Summary of the Toxic Mechanism
| Substance Class | Effect on AChE | Reversibility | Clinical Significance |
| Organophosphates | Phosphorylation of the enzyme | Irreversible after “aging” | Persistent, potentially fatal overstimulation |
| Carbamates | Carbamylation of the enzyme | Reversible | Short-term symptoms, usually less severe |
| Target Structure | Effect | Consequence | |
| Muscarinic Receptors | Overactivation of glands, smooth muscles | Salivation, bronchorrhea, bradycardia, diarrhea | |
| Nicotinic Receptors | Sustained excitation of the motor endplate | Muscle tremors, paralysis, respiratory arrest | |
| Central Nervous System | Overexcitation of cholinergic neurons | Seizures, unconsciousness, possibly respiratory depression |
Conclusion
Organophosphates and carbamates cause massive cholinergic overstimulation in dogs and cats by inhibiting acetylcholinesterase, affecting all cholinergic receptor types. Organophosphates have an irreversible and long-lasting effect, while carbamates are reversible but still dangerous. Poisoning is a veterinary emergency requiring rapid and targeted treatment with an antidote (atropine ± oximes) and intensive medical monitoring.
Symptoms of intoxication
Initial symptoms generally appear minutes to hours after toxin ingestion. In rare cases, poisoning symptoms may only appear after 1–2 days.
The symptoms are typical of cholinergic overstimulation (acetylcholine excess).
They can be divided into three categories.
Muscarinic effects (effects similar to the mushroom poison muscarine),
nicotine-like effects, and central effects.
Muscarinic effects:
- Drooling
- Loss of appetite
- Pupil constriction
- Vomiting
- Diarrhea
- Urge to urinate
- Intestinal cramps
- Increase in respiratory rate
- Difficulty breathing
- Cyanosis of the mucous membrane due to lack of oxygen
- pulmonary edema
- Respiratory failure
Nicotine-like effects:
- Muscle tremors
- Weakness
Central effects:
- Nervousness
- Ataxia
- Anxiety
- Seizures.
In addition to the acute cholinergic crisis and the delayed neurological effects in organophosphate and carbamate intoxications, an intermediate syndrome has also been described in humans, and in two cases in dogs.
This involves delayed paralysis of the respiratory muscles, neck muscles, and forelimb muscles, even without prior cholinergic symptoms. The causes of this complication are not clearly understood.
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The clinical signs of organophosphate and carbamate poisoning are diverse and can vary depending on the amount ingested, the route of exposure, and the individual sensitivity of the animal. Symptoms can be divided into three main categories based on the overstimulation of different parts of the nervous system.
Muscarinic effects result from overstimulation of the parasympathetic nervous system and typically manifest first. Affected animals show excessive salivation (hypersalivation), which can be so severe that saliva literally drips from the mouth. Vomiting and diarrhea are also common, which can lead to rapid dehydration. The pupils constrict (miosis), and the animals suffer from increased urination. Particularly concerning are the respiratory symptoms: increased respiratory rate, wheezing, and shortness of breath due to increased bronchial secretions. In severe cases, pulmonary edema can develop, recognizable by the bluish discoloration of the mucous membranes (cyanosis) and frothy discharge from the nose and mouth.
Nicotinic effects primarily affect the muscles. Typical signs include muscle tremors, which can range from fine tremors to clearly visible twitching, as well as progressive muscle weakness that can lead to paralysis. These symptoms often begin in the hind limbs and progress forward.
Central nervous system effects include behavioral changes such as restlessness and nervousness, coordination disorders (ataxia), anxiety, and in advanced stages, seizures. Some animals also show impaired consciousness up to coma.
A special phenomenon is the so-called intermediate syndrome, which can occur 24–96 hours after acute poisoning. This involves delayed paralysis of the respiratory muscles, neck muscles, and forelimb muscles, which can lead to death without intensive medical care.
Symptoms can appear within minutes to hours after exposure, depending on the severity of the poisoning, and progress rapidly without treatment. The toxic effects can last two to four weeks in dogs and cats, requiring long-term monitoring and therapy.
Diagnosis
The diagnosis of organophosphate or carbamate poisoning relies primarily on history, clinical examination, and specific laboratory diagnostic procedures. Due to the potentially life-threatening nature of these poisonings, a systematic and rapid approach is crucial.
In the history, information about possible contact with insecticides, pesticides, or other potential sources of organophosphates and carbamates is of great importance. Pet owners should be asked about recent gardening activities, pest control measures, or the application of antiparasitics. The possibility of access to chemical storage areas should also be investigated.
The clinical examination focuses on the characteristic symptoms of cholinergic overstimulation. The presence of the classic symptom complex—hypersalivation, miosis, bronchorrhea, diarrhea, and muscle tremors—is a strong indicator of poisoning with cholinesterase inhibitors. Measurement of vital parameters often shows bradycardia, hypotension, and an increased respiratory rate.
From a laboratory diagnostic perspective, the determination of acetylcholinesterase activity in the blood is the most specific test. A reduction in enzyme activity of more than 25% compared to the normal value is considered diagnostic for exposure to cholinesterase inhibitors. In organophosphates, this inhibition is long-lasting, while in carbamates, it is more rapidly reversible, which can influence the interpretation of the results.
Differential diagnoses must exclude other causes of cholinergic symptoms, including poisoning with other substances (e.g., nicotine, certain mushrooms), heart diseases, or neurological disorders. Infectious diseases with gastrointestinal and neurological symptoms can also cause similar clinical pictures.
In special cases, toxicological analyses of stomach contents, vomit, or suspicious substances can be performed to identify the specific active ingredient. However, these investigations are time-consuming and usually not available for acute treatment decisions.
Therapeutic principles
Intensive decontamination is absolutely necessary.
In case of skin contact, extensive bathing of the animals is required.
If oral ingestion occurred less than 2 hours ago, inducing vomiting is indicated, provided the animal is awake and shows no seizures or paralysis.
Otherwise, gastric lavage and repeated activated charcoal treatment are performed.
There is no primary antidote. However, therapy relies on medications that can at least partially counteract the cholinergic effect of organophosphates and carbamates. In a broader sense, they can be understood as antidotes.
These are muscarinic receptor blockers and cholinesterase reactivators.
Atropine is the drug of choice. It blocks the central and peripheral muscarine-like effects of organophosphates and carbamates and is used repeatedly in dogs and also in cats (in a slightly lower dosage) depending on the situation.
Under certain time conditions, even better results can be achieved in organophosphate intoxication by the simultaneous use of cholinesterase activators (oximes). Oximes do not work with carbamates.
The nicotine-like effects of organophosphates and carbamates (muscle tremors, muscle cramps, muscle paralysis) are not affected by atropine, so animals can still die from these effects alone. The use of anticonvulsant medications is helpful in these cases.
Otherwise, symptomatic therapy focuses on stabilizing vital functions: respiration, circulation, water, electrolyte, and acid-base balance.
In some cases, oxygen enrichment of the breathing air or even artificial ventilation is necessary.
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The treatment of organophosphate or carbamate poisoning requires a rapid and targeted approach. It comprises several components: decontamination, specific antidote therapy, and supportive measures.
Decontamination is the first and crucial step. In case of skin contact, the animal must be thoroughly bathed with lukewarm water and mild shampoo, with the handler wearing protective gloves to prevent self-contamination. In case of oral ingestion and if exposure occurred less than two hours ago, vomiting can be induced in awake animals without neurological symptoms. Alternatively or additionally, gastric lavage under general anesthesia is indicated. The administration of activated charcoal at a dose of 1 to 4 g/kg body weight every 4–6 hours for 24 hours binds the poison in the gastrointestinal tract and prevents further absorption.
The most important specific antidote is atropine, a muscarinic receptor antagonist that blocks the peripheral effects of acetylcholine accumulation. The initial dose is 0.1-0.2 mg/kg intravenously for dogs and 0.05-0.1 mg/kg for cats. Administration is repeated every 3–6 hours until cholinergic symptoms such as hypersalivation and bronchial secretion are controlled. It is important to note that atropine only affects muscarinic effects, not nicotinic or central effects.
In organophosphate poisonings (not with carbamates), oximes such as pralidoxime (2-PAM) can be used as cholinesterase reactivators. They reactivate the inhibited enzyme if administered within 24–48 hours after exposure. The recommended dose is 20–50 mg/kg slowly intravenously, followed by repeated doses every 8–12 hours or as a continuous infusion.
Supportive measures include fluid therapy to correct dehydration and electrolyte imbalances, oxygen supply for respiratory impairment, and possibly mechanical ventilation in severe cases. For seizures, anticonvulsants such as diazepam (0.5-1 mg/kg i.v.) or phenobarbital are used. Body temperature must be monitored, as hyperthermia due to muscle activity or hypothermia due to central effects can occur.
Intensive medical monitoring should be continued for at least 48–72 hours, as relapses can occur, especially with organophosphates with a long half-life or with fat-soluble compounds that are slowly released from adipose tissue.
Prognosis & follow-up care
The earlier the animals are treated, the more favorable the prognosis naturally is.
The toxic effects can last two to four weeks in dogs and cats. During this time, the animals require careful monitoring and therapy, but in most cases, they recover as a result.
The prognosis is good.
The prognosis for dogs and cats with organophosphate or carbamate poisoning depends on several factors: the type and amount of poison ingested, the time until therapy begins, the intensity of clinical symptoms, and the animal’s general health status before poisoning.
With early detection and adequate treatment, the prognosis is generally good. Animals treated within the first few hours after exposure and showing only mild to moderate symptoms usually recover completely. However, the toxic effects can last two to four weeks in dogs and cats, requiring careful monitoring and continued therapy.
The prognosis is less favorable for animals with severe symptoms such as respiratory paralysis, persistent seizures, or the intermediate syndrome. Here, the mortality rate may be increased despite intensive medical care. Very young, old, or pre-existing conditions, as well as those with liver or kidney dysfunction that impair detoxification and excretion of toxins, are particularly at risk.
Aftercare plays a crucial role in complete recovery. After the acute phase of poisoning, regular follow-up examinations should be performed to monitor the normalization of organ functions. This includes:
- Regular clinical examinations to assess general well-being and detect possible residual symptoms.
- Laboratory controls to monitor acetylcholinesterase activity, which may take weeks to fully recover in organophosphate poisonings.
- Liver and kidney function tests, as these organs may be affected by the toxins or therapy.
- Neurological examinations to detect subtle neurological deficits that may persist in some animals as a long-term consequence.
Pet owners should be informed about possible long-term effects, including subtle behavioral changes, reduced resilience, or increased sensitivity to other toxins. In rare cases, chronic neurological damage may also persist, requiring long-term therapy.
An important aspect of aftercare is the prevention of further exposures. Pet owners should be comprehensively educated about the risks of organophosphates and carbamates in the home and garden and encouraged to store such products safely or to refrain from using them.
Research outlook
Research in the field of organophosphate and carbamate poisonings in small animals is continuously evolving. Current studies focus on several promising areas that could improve the management of these poisonings in the future.
A key research focus is on the development of improved antidotes. While atropine and oximes have been the cornerstones of therapy for decades, they have known limitations. Newer approaches include the development of modified oximes with better blood-brain barrier penetration to more effectively treat the central nervous system effects of poisoning. In addition, enzyme replacement therapies are being explored, where recombinant butyrylcholinesterase or specific phosphodiesterases are administered to directly neutralize the toxins.
Biomarker research aims to identify more sensitive and specific indicators for exposure to organophosphates and carbamates. In addition to the classic measurement of acetylcholinesterase activity, newer biomarkers such as specific protein adducts in blood or metabolic signatures in urine are being investigated. These could enable earlier diagnosis and also detect more subtle, chronic exposures.
In the area of long-term effects, studies are investigating the neurological and immunological impacts of subacute and low-dose exposures. There is increasing evidence that even exposures below the threshold for acute poisoning symptoms can have long-term effects on neurological development, cognitive functions, and possibly also on the immune system.
Innovative therapeutic approaches such as the use of antioxidants to reduce oxidative stress caused by organophosphates, or the use of neuroprotectants to prevent long-term neurological damage, are also being researched. Some studies are investigating the potential benefits of melatonin, N-acetylcysteine, and other antioxidants as adjuvant therapy.
Last but not least, research is also dedicated to developing safer alternatives to organophosphates and carbamates in pest control and plant protection. Biological control methods, more selective insecticides with lower toxicity for mammals, and innovative formulations that reduce the risk of accidental ingestion by pets are in focus.
These research approaches promise to improve the management of organophosphate and carbamate poisonings in small animals in the coming years and potentially reduce the incidence of these poisonings through safer alternatives.
Frequently asked questions (FAQs)
- How quickly do symptoms appear after organophosphate or carbamate poisoning?
The first symptoms can appear within minutes to a few hours after exposure. With skin contact, it may take a little longer, typically 1–2 hours. In rare cases, especially with low doses or slow absorption, symptoms may not become visible until 24–48 hours later.
- Can pets fully recover from organophosphate or carbamate poisoning?
Yes, with early detection and adequate treatment, full recovery is possible. However, the recovery process can take two to four weeks, depending on the severity of the poisoning. In some cases, subtle neurological deficits may persist, especially if treatment was delayed or the poisoning was very severe.
- How can I protect my pet from poisoning with these substances?
Store all insecticides, herbicides, and antiparasitics out of reach of your pets, ideally in locked cabinets. Read the instructions carefully and keep treated areas inaccessible to your animals for the recommended time. Consider using more pet-friendly alternatives for pest control. Inform yourself about the ingredients of products and avoid those with organophosphates or carbamates.
- Are certain animal breeds or species more susceptible to these poisonings?
Cats are generally more sensitive to many toxins because they lack certain detoxification enzymes in the liver. In dogs, there are no clear breed predispositions, but very young, old, or pre-diseased animals are particularly at risk. Animals with low body weight can also be more severely affected by the same dose.
- Can I administer first aid myself if I suspect my pet has been poisoned?
If you suspect poisoning, you should contact a veterinarian immediately. In case of skin contamination, you can bathe the animal with lukewarm water and mild shampoo, wearing gloves. Do not induce vomiting without veterinary instruction, especially not if the animal is already showing symptoms or is disoriented. Transport the animal calmly and try to take a sample of the suspected poison for the veterinarian.
- How long does the treatment for organophosphate or carbamate poisoning last?
The acute treatment phase typically lasts 24–72 hours, depending on the severity of the poisoning and the specific toxin. However, full recovery can take two to four weeks. During this time, regular check-ups are important to monitor progress and detect possible complications early.
- Are there long-term consequences I should watch out for after a poisoning?
Possible long-term consequences include subtle neurological deficits, behavioral changes, reduced resilience, or increased sensitivity to other toxins. In rare cases, chronic liver or kidney damage may also occur. Pay attention to changes in your pet’s behavior, coordination, or general health and discuss them with your veterinarian.
- Are biological or “natural” insecticides safer for pets?
Not all products marketed as “natural” or “biological” are automatically safe for pets. Some plant-based insecticides, such as pyrethrins, can also be toxic, especially for cats. It is important to check the specific ingredients and inform yourself about their safety profile. If in doubt, consult your veterinarian before using such products near your pets.
Literature
- Klainbart, S., Grabernik, M., Kelmer, E., Chai, O., Cuneah, O., Segev, G., & Aroch, I. (2019). Clinical manifestations, laboratory findings, treatment, and outcome of acute organophosphate or carbamate intoxication in 102 dogs: A retrospective study. The Veterinary Journal, 251, 105349.
- Karami-Mohajeri, S., & Abdollahi, M. (2011). Toxic influence of organophosphate, carbamate, and organochlorine pesticides on cellular metabolism of lipids, proteins, and carbohydrates: a systematic review. Human & experimental toxicology, 30(9), 1119-1140.
- Klainbart, S., Grabernik, M., Kelmer, E., Chai, O., Cuneah, O., Segev, G., & Aroch, I. (2019). Clinical manifestations, laboratory findings, treatment, and outcome of acute organophosphate or carbamate intoxication in 102 dogs: A retrospective study. The Veterinary Journal, 251, 105349.
- Brutlag, A. G., & Puschner, B. (2020). Small Animal Toxicology (3rd ed.). Elsevier Health Sciences.
- Gupta, R. C., Malik, J. K., & Milatovic, D. (2022). Organophosphate and carbamate pesticides. In R. C. Gupta (Ed.), Biomarkers in Toxicology (2nd ed., pp. 515-548). Academic Press. https://doi.org/10.1016/B978-0-12-819233-6.00028-9
- Fikes, J. D. (2018). Organophosphorus and carbamate insecticides. Veterinary Clinics of North America: Small Animal Practice, 48(6), 1133-1146. https://doi.org/10.1016/j.cvsm.2018.07.002
- Löwe G, Löwe O. Poisoning in Dogs and Cats – A Veterinary Guide. 2nd edition. Kreuztal: Kynos-Verlag. 2021; 208 p.