Toxins

๐Ÿ Honeybee Venom (Apitoxin)

Toxic Components

  • Melittin (major peptide): causes membrane disruption, pain, hemolysis.

  • Phospholipase Aโ‚‚: hydrolyzes membrane phospholipids โ†’ cell lysis, inflammation.

  • Hyaluronidase: promotes toxin spread through tissue.

  • Histamine, serotonin, kinins: cause vasodilation and pain.

Mechanism of Action / Pathophysiology

  • Local effects: pain, erythema, edema due to histamine and kinins.

  • Systemic effects (multiple stings):

    • Hemolysis and rhabdomyolysis โ†’ hemoglobinuria/myoglobinuria โ†’ renal injury.

    • Hypotension and shock due to histamine and melittin-induced vascular permeability.

    • Anaphylaxis (immune-mediated): rapid onset respiratory or cardiovascular collapse.

Target tissues

  • Cell membranes (melittin + phospholipase Aโ‚‚)

  • Vascular endothelium โ†’ shock

  • Kidneys (secondary to pigment nephropathy)


๐ŸŒฟ Top Plant Toxins in Dogs

Plant

Toxic Principle

Mechanism / Pathophysiology

Sago palm (Cycas revoluta)

Cycasin (hepatotoxin)

Causes centrilobular hepatic necrosis โ†’ vomiting, icterus, coagulopathy.

Lilies (Lilium, Hemerocallis)

Unknown nephrotoxin

Renal tubular necrosis โ†’ acute kidney failure (especially cats; less so in dogs).

Oleander, Foxglove

Cardiac glycosides

Inhibit Naโบ/Kโบ-ATPase โ†’ arrhythmias, hyperkalemia.

Ricinus communis (Castor bean)

Ricin

Ribosome inactivation โ†’ inhibition of protein synthesis โ†’ GI, liver, kidney damage.

Grapes/Raisins

Unknown nephrotoxin

Proximal tubular necrosis โ†’ acute renal failure.

Autumn crocus (Colchicum autumnale)

Colchicine

Binds tubulin โ†’ inhibits mitosis โ†’ GI ulceration, bone marrow suppression.


๐Ÿซ Top Food Toxins in Dogs

Food

Toxic Principle

Pathophysiology / Mechanism

Chocolate / Cocoa

Methylxanthines (theobromine, caffeine)

Inhibit phosphodiesterase โ†’ โ†‘ cAMP, โ†‘ catecholamines โ†’ tachycardia, CNS excitation, tremors.

Xylitol

Artificial sweetener

Stimulates massive insulin release โ†’ profound hypoglycemia; may cause acute hepatic necrosis.

Onions / Garlic

Thiosulfates

Oxidative damage to erythrocytes โ†’ Heinz body hemolytic anemia.

Grapes / Raisins

Unknown

Acute tubular necrosis โ†’ acute renal failure.

Macadamia nuts

Unknown

Causes weakness, ataxia, hyperthermia, vomiting (non-fatal, self-limiting).


๐Ÿงผ Top Cleaning Product Toxins

Type

Active Agents

Mechanism / Pathophysiology

Bleach (sodium hypochlorite)

Corrosive alkali

Liquefactive necrosis of mucosa โ†’ vomiting, esophageal burns, aspiration pneumonia.

Phenolic disinfectants

Phenol compounds

Direct hepatotoxin and corrosive; causes CNS depression, liver necrosis.

Cationic detergents (quaternary ammonium compounds)

Benzalkonium chloride, etc.

Caustic โ†’ oral/dermal ulceration, respiratory distress if inhaled.

Drain / Oven cleaners

Strong alkali (NaOH, KOH)

Liquefactive necrosis of oral/esophageal tissue โ†’ perforation, strictures.


๐Ÿœ Pesticides

Class

Toxic Component

Mechanism of Action

Pathophysiology

Organophosphates / Carbamates

Acetylcholinesterase inhibitors

Accumulate ACh at synapses

Muscarinic (SLUD signs), nicotinic (tremors, paralysis), CNS (seizures).

Pyrethrins / Pyrethroids

Synthetic insecticides

Prolong Naโบ channel opening in neurons

Tremors, hyperexcitability, seizures; cats especially sensitive.

Metal phosphides (e.g., zinc phosphide)

Produces phosphine gas

Cellular respiration inhibition

Vomiting, pulmonary edema, acidosis.

Rodenticides (anticoagulant)

Warfarin, brodifacoum

Inhibit vitamin K epoxide reductase

Hemorrhage (delayed).


๐Ÿšจ Acute Toxic Causes of Vomiting

Xylitol

  • Mechanism: Rapid absorption โ†’ potent stimulator of pancreatic ฮฒ-cells โ†’ insulin surge โ†’ hypoglycemia within 30โ€“60 min.

  • Pathophysiology: Low blood glucose โ†’ weakness, seizures, collapse.

  • High doses: Hepatic necrosis due to ATP depletion and oxidative stress.

  • Toxic dose: As low as 0.05 g/kg (hypoglycemia); >0.5 g/kg (liver injury).

Nicotine

  • Mechanism: Nicotinic acetylcholine receptor agonist โ†’ initial stimulation โ†’ receptor blockade with high doses.

  • Pathophysiology: Vomiting (early), tremors, tachycardia โ†’ then bradycardia, respiratory paralysis.

  • Toxic dose: ~1 mg/kg can cause signs; 9โ€“12 mg/kg lethal.


๐ŸŒพ Herbicides

Compound

Mechanism

Pathophysiology / Effects

2,4-D (2,4-dichlorophenoxyacetic acid)

Interferes with oxidative phosphorylation and neuromuscular conduction

Vomiting, ataxia, myotonia, nephrotoxicity; delayed muscle necrosis.

Glyphosate (Roundupยฎ)

Surfactant toxicity (not glyphosate itself)

GI irritation, hypersalivation, vomiting, diarrhea; rarely systemic toxicity.


๐Ÿชฒ Blister Beetle (Cantharidin Toxicity)

Toxic Compound

  • Cantharidin (a potent vesicant produced by Epicauta species beetles).

Source

  • Beetles contaminate alfalfa hay, especially in horses; dogs can be affected if they ingest contaminated feed or insects.

Mechanism of Action

  • Cantharidin inhibits serine/threonine phosphatases (PP2A) โ†’ cell junction disruption โ†’ vesicle and blister formation in mucosa.

Pathophysiology

  • Direct mucosal damage: Ulceration of oral, esophageal, gastric, and urinary mucosa.

  • Systemic effects:

    • Hypocalcemia (binding and loss in damaged tissues).

    • Myocardial necrosis.

    • Renal tubular damage due to excreted cantharidin.

Clinical signs

  • Salivation, vomiting (dogs), colic, hematuria, shock.