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Winter 2005 Newsletter

Canine Zinc Intoxication
Disseminated Intravascular Coagulation
Equine Enteric Salmonellosis
Murine Respiratory Mycoplasmosis
in Animals


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     Zinc Intoxication in a dog

History:  A female Pekingese dog, six months of age, was found dead by its owner.  The dog had been lethargic for approximately one week, but was still eating.  There was no history of diarrhea or vomiting.  The puppy was current on all of its vaccines.  A physical exam and fecal exam, performed five weeks prior to death, were both normal.

Gross necropsy lesions: The proximal portion of the duodenum at the junction with the pyloric sphincter contained five and ½ coins.  The coins consisted of three pennies, one each from the years 1986, 1992, and 1978, and one half of a penny with a roughened surface, teeth marks, and an irregularly serrated edge with a year that was not visible.  The other two coins were dimes.  Significant gastrointestinal lesions were not found at the location of the coins.  The serosal and mucosal surfaces of the bladder were discolored dark purple to black.  The bladder contained approximately 20 ml of a thin, dark red to purple fluid.  The liver was diffusely discolored dark red.  The visceral surface of the kidneys was diffusely and bilaterally discolored dark red.  No other lesions were found in the musculoskeletal, respiratory, cardiovascular, digestive, genitourinary, lymphatic, endocrine, or nervous systems or in the organs of special senses.

Toxicology testing: The penny with the serrated edge was cut longitudinally.  The core of the penny was a silver metallic substance indicative of zinc.  An ICP-MS zinc analysis of the liver revealed a zinc concentration of 236.087 ppm (normal  range for liver zinc at the laboratory used by the ADDL is 30-90 ppm).

Microscopic lesions:  The peripheral acini of the pancreas were necrotic and occasionally infiltrated with neutrophils, macrophages, and lymphocytes with individualization and destruction of acinar cells.  Interlobular septa within the pancreas contained occasional neutrophils, macrophages, and lymphocytes.  Hepatocytes within the liver were vacuolated and sinusoids were distended with edema fluid.  There was intrahepatic cholestasis.  The lungs were edematous.  Lymphoid follicles within the small and large intestines were diffusely depleted of cells.  The red pulp of the spleen contained multiple foci of extramedullary hematopoiesis.

Diagnosis:  The gross findings (pigmented urine, icterus), microscopic findings (pancreatic necrosis), and liver zinc level support a diagnosis of canine zinc toxicity.

Discussion:  Following the ingestion of zinc containing objects, zinc forms soluble salts in gastric acid and is absorbed mainly in the proximal small intestine.  Approximately 67% of the zinc is bound to plasma proteins and carried to the liver.  Protein-bound zinc is transported to the liver where approximately 30-40% of the zinc is extracted and returned to the bloodstream where it accumulates in high levels in the liver, kidney, pancreas, and bone.  The remainder of the zinc is absorbed by hepatocytes and storied in the liver.  Zinc is normally excreted in the feces via pancreatic secretions, intestinal mucosal secretions, and bile.

  Zinc objects are directly irritating to the gastrointestinal tract.  However, clinical signs at presentation are usually associated with severe intravascular hemolysis and organ damage (liver, kidney and pancreas).  The pathogenic mechanism in dogs is not well-understood but oxidative damage to red blood cells plays a major role.  Affected animals may appear asymptomatic prior to the hemolytic crisis.  Clinical signs of zinc toxicity can be vague and non-specific or these animals may present with signs that are suggestive of hemolytic anemia and multiple organ damage.

  Antemortem diagnosis of zinc intoxication is confirmed with elevated serum/plasma zinc levels.  Either whole blood or serum can be submitted for zinc analysis.  Whole blood can be collected into EDTA or heparinized collection tubes.  It should be noted that the rubber in syringes and red-top tubes can contribute zinc to the sample and falsely elevate the serum zinc level.  Trace element-free tubes (Vacutainer, Venoject, royal blue stopper tubes) are preferred for sample collection.  If these are not available, then the serum/plasma should be separated as soon as possible and placed in plastic-stoppered containers. Samples need to be refrigerated.  The laboratory performing the zinc testing should be contacted for information regarding sample collection, storage, and shipping.  Normal serum zinc level varies by laboratory but is usually less than 2mg/ml or approximately 0.7-2.0 ppm.

  Typical gross necropsy lesions include icterus, splenomegaly, nodular appearance to the pancreas, and large, diffusely discolored red/brown kidneys.  Postmortem diagnosis of zinc toxicity is confirmed by elevated tissue zinc levels.  Sections of pancreas, kidney, and liver can be tested for zinc.  Tissue samples should be stored frozen until analyzed.  The testing laboratory should be contacted for information regarding tissue collection and submission.  Normal liver zinc level varies by laboratory but is usually within the range of 30-90 ppm.

  The main source of zinc toxication in dogs is pennies that were minted after 1982.  These coins are composed mainly of zinc wafers (98% zinc) with a thin copper coating.  Pennies minted before 1982 are composed mainly of copper.  Other sources of zinc include galvanized coating on iron and steel (dog crates, carriers, and fencing), zinc nuts used in collapsible transport cages, automotive parts, batteries, fungicides, zinc-based paints (can be 50-55% zinc), shampoos, and zinc-containing topical medications (zinc-oxide lotions).

-by Dr. Chris Hoppe, ADDL Graduate    Student


  1. Ettinger SJ and Feldman EC: 2000. Textbook of Veterinary Internal Medicine, 5th ed. Philadelphia: W.B. Saunders Co., p. 362

  2. Hardy A, Krimer :M, Latimer KS. College of Veterinary Medicine, University of Georgia, Athens, GA. Department of Pathology: Canine Zinc Toxicosis. http://www.vet.uga.edu/vpp/clerk/Hardy

  3. Plumlee KH: 2004. Clinical Veterinary Toxicology. St. Louis: Mosby, Inc., pp 221-226.




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