Is Allium Toxic To Dogs

What dosage of allium renders dogs toxic?

Since the beginning of time, both wild and domesticated Allium species have been employed in food and traditional medicine.

Since the beginning of time, both wild and domesticated Allium species have been employed in food and traditional medicine. In North America, there are about 95 species of native or cultivated leeks, chives, garlic, shallots, scallions, and onions. Additionally, there are more than 80 species of ornamental Allium. Dogs and cats can be harmful to all Allium species and their products1, but only a small number of Allium species are of significant toxicologic concern.

Domesticated varieties of Allium cepa (onion), Allium porrum (leek), Allium sativum (garlic), and Allium schoenoprasum are frequently engaged in toxicosis (chive). When crushed, the plants release an onion or garlic scent and develop solitary or clustered bulbs. Allium species can be distinguished from dangerous plants with visually identical leaves by their distinctive odour, especially death camas (Zigadenus species). 1


Numerous organosulfoxides, in particular alk(en)ylcysteine sulfoxides, are present in allium species. Chewing or other plant trauma transforms organosulfoxides into a complicated brew of organic molecules that contain sulfur. Many of these substances, or their metabolites, are in charge of giving these plants their distinctive scents, tastes, and pharmacological effects. Many of the organosulfur compounds found in Allium species seem to be easily absorbed by the digestive system and are converted into highly reactive oxidants. 2 Allium species’ potential toxicity is not diminished by cooking or rotting. 1

Mechanism of action

The main toxicologic mechanism for organosulfur compounds formed from Allium species is oxidative hemolysis, which happens when the amount of oxidants in an erythrocyte exceeds the capability of the metabolic pathways that produce antioxidants. Dog erythrocytes have low catalase antioxidant activity3, and cat normal hemoglobin is about two to three times more vulnerable to oxidative damage than normal hemoglobin in other species. 4

Sulfhemoglobin is created when exposed beta-93 cysteine residues in hemoglobin undergo oxidation.

5 Sulfhemoglobin precipitates, aggregates, and attaches to the cell membrane to form Heinz bodies because it is less soluble than hemoglobin. The production of eccentrocytes and membrane cross-linking processes are the results of other forms of hemoglobin oxidation. 6 Erythrocyte fragility and extravascular hemolysis are increased by the development of Heinz bodies and eccentrocytes. Cell lysis is also caused by direct oxidative damage to the erythrocyte cell membrane and its sodium-potassium pump or by the oxidative synthesis of hemin. Oxidation of the heme ion and related methemoglobinemia cause the hemoglobin-oxygen dissociation curve to move to the left, blood oxygen transport capacity to be reduced, and eventually poor oxygen delivery to the tissues.

Thus, the start of anemia, methemoglobinemia, and reduced oxygen transport are caused by the oxidative hemolytic process generated by ingestion of Allium species. A day after eating onions, there may be noticeable Heinz body formation, but the anemic nadir usually appears several days later.

The pharmacologically active components of garlic, allicin and ajoene, are strong vasodilators, hypotensive, and cardiac and smooth muscle relaxants.

7-9 Additionally, onions’ organosulfur components, such as ajoene, are effective antithrombotic medicines. 10 Therefore, hypotensive and antithrombotic actions may make anemia and poor oxygen transport worse from a physiological standpoint. Unaged garlic formulations directly harm the stomach and ileal mucosa, causing discomfort and diarrhea. 11

Exposure and susceptibility

The most frequent cause of allium species toxicosis is oral ingestion. In addition to ingesting fresh plant material, dogs and cats may be poisoned by drinking juice, fresh and aged dietary supplements, powdered cookery preparations, dried material, or food preparations made with or containing Allium species. 1 Allium species toxicosis often develops following consumption of either a single big quantity or repeated little doses of the substance. Onion toxicosis is quite dangerous for dogs and cats. Even a little amount of onion consumption—5 g/kg for cats and 15 to 30 g/kg for dogs—has been linked to clinically significant hematologic alterations. Animals who consume more than 0.5% of their body weight in onions at once are frequently recognized to develop onion toxicosis.

Dogs with heritably high levels of potassium and erythrocyte reduced glutathione are more vulnerable to the hematologic effects of onions.

12 Japanese breeds are comparatively prone to this characteristic. An animal’s sensitivity to the toxicity of Allium species may be increased by further inborn metabolic flaws or dietary inadequacies, such as zinc or glucose-6-phosphate dehydrogenase insufficiency, which lower erythrocyte antioxidant defenses. 13 An animal’s susceptibility to Allium species toxicosis is likely to be increased by concurrent treatment with xenobiotics, medications, or dietary elements that cause erythrocyte oxidative injury (e.g., propofol, propylene glycol, dl-methionine, sulfonamides, sulfapyridine, high doses of vitamin K3, benzocaine) or weaken erythrocyte oxidative

Clinical signs and laboratory findings

If considerable amounts of the substance have been consumed, clinical signs of Allium species toxicosis in dogs and cats may arise within a day of intake; however, it is more typical for clinical signs to appear after a delay of several days. Depression, hemoglobinuria, urinary casts of hemosiderin and/or hemoglobin, icterus, tachypnea, tachycardia, weakness, exercise intolerance, and cold sensitivity are common clinical symptoms. Additionally possible symptoms include nausea, diarrhea, and stomach pain. The sick dog or cat may have an onion or garlic breath odor if they recently consumed something.

Clinical pathology results support the presence of intravascular and extravascular hemolysis, Heinz body anemia, eccentrocytosis, hemoglobinemia, hemoglobinuria, hyperbilirubinemia, methemoglobinemia, and, if the animal survives long enough, a concomitant regenerative response.


Hemolytic anemia is often diagnosed through necropsy and histologic findings. Gastrointestinal erosion or Allium species in the gut content may not be seen due to the typical delay of several days between consumption and the onset of clinical indications. The presence of hemosiderin in the phagocytic cells of the liver, spleen, and renal tubular epithelium; renal tubular pigment necrosis; and the presence of nephrotubular casts and hemoglobin casts in the renal tubules are histopathologic findings that, while consistent with hemolytic anemia, are not specific to Allium species toxicosis. 1

Differential diagnoses

Other typical toxicoses such as brassicaceous vegetables, propylene glycol, acetaminophen, benzocaine, vitamin K3, dl-methionine, naphthalene, zinc, and copper are differentially diagnosed. Diabetes mellitus, particularly if ketoacidosis is present, hepatic lipidosis, hyperthyroidism, lymphoma and other neoplasms, as well as hyperthyroidism are common feline diseases linked to the development of Heinz bodies.