Organophosphates and Carbamates

Author: Dr. med. vet. Gisa Löwe | Last modified: 09.02.2026
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Organophosphates and carbamates are among the most common causes of poisoning in our pets. These substances are chemical compounds that are created as derivatives of various phosphoric acids or carbamic acid and are found in numerous products of 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 the regulation of the neurotransmitter acetylcholine at the synapses of the nervous system. In the case of organophosphates, this inhibition is irreversible, whereas in the case of 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 the symptoms can be varied and rapid intervention is required. Knowledge of the pathophysiology, clinical signs, and appropriate therapy strategies is therefore of crucial importance for successful therapy.

The most important facts at a glance

Poisoning with organophosphates and carbamates is a common and potentially life-threatening emergency in small animal medicine. These substances, which are contained in numerous insecticides, herbicides, and antiparasitics, act by inhibiting the enzyme acetylcholinesterase, which leads to overstimulation of the nervous system.

The clinical symptoms include muscarinic effects (hypersalivation, miosis, bronchorrhea, diarrhea), nicotinic effects (muscle tremors, weakness) and central effects (Nervousness, ataxia, Convulsions). In severe cases, Respiratory paralysis and Death can occur. A particular phenomenon is the intermediate syndrome, which can occur 24–96 hours after acute poisoning and is characterized by Paralysis of the respiratory muscles.

The diagnosis is based on the medical history, the clinical symptoms, and the measurement of acetylcholinesterase activity in the blood. The therapy includes decontamination, the administration of atropine as a specific antidote against the muscarinic effects, in the case of organophosphates also the administration of oximes to reactivate cholinesterase, as well as supportive measures.

With early detection and adequate therapy, the prognosis is good, although the toxic effects in dogs and cats can last two to four weeks. Aftercare includes regular check-ups and the prevention of further exposures.

For pet owners, it is important to know potential sources of danger in the household and garden and to prevent their pets from accessing these substances. If poisoning is suspected, veterinary assistance should be sought immediately, as rapid intervention is crucial for successful therapy.

Causes, development and progression

Organophosphate and carbamate poisoning in pets mainly occurs through three routes of exposure: through the skin (dermal), the respiratory tract (inhalation), or the gastrointestinal tract (oral). These substances are absorbed quickly, and initial symptoms of poisoning can appear as early as 1–2 hours after ingestion.

Numerous potential hazards for our pets lurk in homes and gardens:

Insecticides and pesticides are the most common source of exposure. These include sprays against ants, cockroaches, or flies, flea collars, spot-on parasite treatments, and agents against aphids or other plant pests. Products designed for use in agriculture are particularly dangerous because they contain higher concentrations of active ingredients.

A particularly high-risk group is represented by garden fertilizers with integrated insecticides, which often contain organophosphates or carbamates. Rat poison and slug pellets can also contain these substances and pose a significant risk to curious pets.

The risk of poisoning increases seasonally during the gardening season in spring and summer, when more pesticides are used. The risk is also increased in rural areas with intensive agriculture, where these substances are applied on a large scale.

A particularly problematic fact is that dogs and cats can ingest these poisons not only directly but also by licking treated surfaces or through contact with contaminated paws, which they then lick. This explains why even seemingly small amounts of these substances can lead to serious 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, heartbeat, breathing, 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 the nerve synapses (transitions from nerve cell to nerve cell) and at the neuromuscular junctions (transitions from nerve cell to muscle cell). As the level of acetylcholine increases, the activity in the autonomic nervous system increases.
The effect affects many organs such as the peripheral and central nervous system (CNS), muscles, liver, pancreas, and brain, as well as metabolic processes. The neuronal and hormonal status of the body is permanently disturbed. Acute toxicity results.
With organophosphates, the inhibition of AChE is irreversible; with carbamates, it is reversible. This also partly explains the lower toxicity of carbamates.
The oral LD 50 in dogs is 19 mg/kg body mass.

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With oral ingestion or absorption through the skin, severe intoxication occurs in dogs and cats, mainly 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) – but with important differences in the reversibility and persistence of the 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 stimulus 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 that irreversibly strengthens within hours to days through “aging”
  • Consequence: persistent inhibition of AChE, resulting in 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 endplate, ganglia)
  • CNS receptors (cholinergic pathways in the central nervous system)

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, especially 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 Symptomatik.

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 (CNS) Overexcitation of cholinergic neurons Seizures, unconsciousness, possibly respiratory depression

Conclusion

Organophosphates and carbamates cause massive cholinergic overstimulation in dogs and cats by inhibiting acetylcholinesterase, which affects all cholinergic receptor types. Organophosphates have an irreversible and long-lasting effect, while carbamates are reversible but still dangerous. Poisoning is a veterinary emergency that requires rapid and targeted treatment with an antidote (atropine ± oximes) and intensive care monitoring.

Symptoms of intoxication

Initial Symptoms: generally appear minutes to hours after ingestion of the toxins. In rare cases, Symptoms: of poisoning may not appear until 1–2 days later.
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
  • Urinary Urgency
  • Intestinal cramps
  • Increase in respiratory rate
  • Shortness of breath
  • Cyanosis of the mucous membrane due to oxygen deficiency
  • 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, a so-called intermediate syndrome has also been described in humans, but also in dogs (two cases).
This involves delayed Paralysis of respiratory muscles, neck muscles, and muscles of the forelimbs, even without previous cholinergic Symptoms:. The causes of this complication are not clearly understood.

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The clinical signs of poisoning with organophosphates and carbamates are diverse and can vary depending on the amount ingested, route of exposure, and individual sensitivity of the animal. The Symptoms: can be divided into three main categories based on the overstimulation of different parts of the nervous system.

The muscarinic-like effects result from the 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. This is often accompanied by Vomiting and Diarrhea, which can lead to rapid dehydration. The pupils constrict (miosis), and the animals suffer from increased Urinary urgency. The respiratory Symptoms: are particularly alarming: increased respiratory rate, wheezing, and shortness of breath due to increased bronchial secretion. 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.

The nicotinic-like effects mainly affect the muscles. Typical signs are muscle tremors, ranging from fine tremors to clearly visible twitching, as well as progressive Muscle weakness, which can lead to Paralysis. These Symptoms: often begin in the hind limbs and progress forward.

The central nervous system (CNS) effects include Behavioral changes such as Restlessness and Nervousness, Coordination disorders (ataxia), Anxiety, and, in the advanced stage, Seizures. Some animals also show impaired consciousness up to coma.

A particular phenomenon is the so-called intermediate syndrome, which can occur 24–96 hours after acute poisoning. This involves delayed Paralysis of respiratory muscles, neck muscles, and muscles of the forelimbs, which can lead to Death without intensive care.

The Symptoms: can occur 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 poisoning by organophosphates or carbamates is based primarily on the medical history, the 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 medical 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 work, pest control measures, or the use of antiparasitics. The possibility of access to storage areas for chemicals 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 indication of poisoning with cholinesterase inhibitors. Measurement of vital signs often shows bradycardia, hypotension, and an increased respiratory rate.

In terms of laboratory diagnosis, 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 the case of organophosphates, this inhibition is long-lasting, whereas in the case of carbamates it is more quickly reversible, which can influence the interpretation of the results.

In the differential diagnosis, other causes of cholinergic symptoms must be excluded, including poisoning with other substances (e.g. nicotine, certain fungi), heart disease, 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 carried out to identify the specific active ingredient. However, these investigations are time-consuming and are usually not available for the acute therapy decision.

Therapeutic principles

Intensive decontamination is absolutely necessary.
In case of skin Contact, extensive bathing of the animals is necessary.
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 Antidot. However, the therapy relies on drugs that can at least partially reverse the cholinergic effects 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 muscarinic-like effects of organophosphates and carbamates and is used repeatedly in dogs and also in cats (in slightly lower doses) depending on the situation.
Under certain temporal conditions, even better results can be achieved in organophosphate intoxication by the simultaneous use of cholinesterase activators (oximes). Oximes do not work for carbamates.
The nicotinic-like effects of organophosphates and carbamates (muscle tremors, muscle cramps, muscle Paralysis) are not affected by atropine, so these effects alone can still lead to the Death of the animals. The use of anticonvulsant drugs is helpful in these cases.
Otherwise, symptomatic therapy focuses on stabilizing the Vital functions: respiration, circulation, water, electrolyte, and acid-base balance.
In some cases, enrichment of the breathing air with oxygen or even artificial respiration is necessary.

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The treatment of poisoning with organophosphates or carbamates 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, whereby the user should wear protective gloves to avoid self-contamination. In case of oral ingestion and if the 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 dosage of 1 to 4 g/kg body weight every 4–6 hours over 24 hours binds the poison in the gastrointestinal tract and prevents further absorption.

The most important specific Antidot 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. The administration is repeated every 3–6 hours until the cholinergic Symptoms: such as hypersalivation and bronchosecretion are controlled. It is important that atropine only affects the muscarinic-like effects, but not the nicotinic-like or central effects.

In case of poisoning with organophosphates (not with carbamates), oximes such as pralidoxime (2-PAM) can be used as cholinesterase reactivators. They reactivate the inhibited enzyme, provided they are 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 in case of respiratory impairment, and possibly mechanical ventilation in severe cases. In case of Seizures, anticonvulsants such as diazepam (0.5-1 mg/kg IV) or phenobarbital are used. The body temperature must be monitored, as hyperthermia can occur due to muscle activity or hypothermia due to central effects.

Intensive care 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 the fatty tissue.

Prognosis & follow-up care

Naturally, the earlier the animals are treated, the better the Prognose.
The toxic effects can last two to four weeks in dogs and cats. During this time, the animals require careful monitoring and therapy, but recover in most cases as a result
The Prognose is good.

The Prognose for dogs and cats with organophosphate or carbamate poisoning depends on several factors: the type and amount of poison ingested, the time until the start of therapy, the intensity of the clinical Symptoms:, and the general health of the animal before the poisoning.

With early detection and adequate treatment, the Prognose is generally good. Animals that are treated within the first hours after exposure and show 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 Prognose is less favorable in animals with severe Symptoms: such as Respiratory paralysis, persistent Seizures, or the intermediate syndrome. Here, the mortality rate may be increased despite intensive care. Very young, old, or pre-existing animals as well as those with liver or kidney dysfunction, which impair the detoxification and excretion of the toxins, are particularly at risk.

Aftercare plays a crucial role in complete recovery. After the acute phase of poisoning, regular check-ups should be carried out to monitor the normalization of organ functions. This includes:

  1. Regular clinical examinations to assess general well-being and detect possible residual symptoms.
  2. Laboratory tests to monitor acetylcholinesterase activity, which may not fully recover for weeks in organophosphate poisoning.
  3. Liver and kidney function tests, as these organs may be affected by the toxins or the therapy.
  4. 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 consequences, 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 Prävention of further exposures. Pet owners should be comprehensively informed about the risks of organophosphates and carbamates in the household 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 poisoning in small animals is constantly evolving. Current studies are focusing on several promising areas that could improve the management of these poisonings in the future.

An important focus of research is the development of improved antidotes. While atropine and oximes have been the mainstays 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. Enzyme replacement therapies are also being researched, in which recombinant butyrylcholinesterase or specific phosphodiesterases are administered to directly neutralize the toxins.

Biomarker research aims to identify more sensitive and specific indicators of exposure to organophosphates and carbamates. In addition to the classic measurement of acetylcholinesterase activity, newer biomarkers such as specific Protein adducts in the blood or metabolic signatures in the urine are being investigated. These could enable earlier diagnosis and also detect more subtle, chronic exposures.

In the area of long-term consequences, studies are investigating the neurological and immunological effects 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 therapy approaches such as the use of antioxidants to reduce the 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 the development of 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 poisoning in small animals in the coming years and possibly reduce the incidence of these poisonings through safer alternatives.

Frequently asked questions (FAQs)

  1. How quickly do symptoms appear after organophosphate or carbamate poisoning?

The first symptoms can appear within minutes to a few hours after the 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.

  1. Can pets fully recover from organophosphate or carbamate poisoning?

Yes, with early detection and adequate therapy, a 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 therapy was delayed or the poisoning was very severe.

  1. How can I protect my pet from poisoning with these substances?

Keep all insecticides, herbicides, and antiparasitics out of the reach of your pets, ideally in locked cabinets. Read the instructions for use carefully and keep treated areas inaccessible to your animals for the recommended time. Consider using more pet-friendly alternatives for pest control. Learn about the ingredients in products and avoid those with organophosphates or carbamates.

  1. 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. There are no clear breed predispositions in dogs, but very young, old, or animals with pre-existing conditions are particularly at risk. Animals with low body weight may also be more affected at the same dose.

  1. 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 the event of skin contamination, you can bathe the animal with lukewarm water and mild shampoo, wearing gloves. Do not induce Vomiting without veterinary advice, especially if the animal is already showing symptoms or is confused. Transport the animal calmly and try to take a sample of the suspected poison with you for the veterinarian.

  1. How long does the treatment for organophosphate or carbamate poisoning last?

The acute therapy 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 on.

  1. 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 can also occur. Pay attention to changes in your animal’s behavior, coordination, or general health and discuss them with your veterinarian.

  1. 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 to cats. It is important to check the specific ingredients and learn 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. Poisonings in Dogs and Cats – A Veterinary Guide. 2nd Edition. Kreuztal: Kynos-Verlag. 2021; 208 p.