Identifying nephrotoxic plants, and how to minimize poisoning

Identifying nephrotoxic plants, and how to minimize poisoning

Nov 01, 2007

This is the last of four articles about plants likely to poison horses in North America. Because most horses are selective grazers, they are poisoned less frequently than other livestock, but some plants are palatable or they may be reluctantly accepted when feed selection is limited.

The three previous articles covered hepatoxic, neurotoxic and myotoxic plants. This final installment covers nephrotoxic and miscellaneous toxic plants, with descriptions of poisoning and plant-induced disease, along with recommended treatment and management practices to avoid poisoning.

Nephrotoxic plants

Hemolysis with hemoglobin-induced nephrosis:

Photo 1: Acer rubrum (red maple) is a common ornamental shade tree. It grows to 30 m, bearing large leaves that have three to five lobes with a shiny green topside and silvery-gray underside. The fruit is red and has two wings.
Acer rubrum (red maple — Photo 1)

Red maple is highly toxic for horses; about 1.5 gm leaf/kg BW or 1 kg of wilted leaves will kill a 450-g horse. The wilted and shed leaves are most toxic. Most poisoning occurs in the fall, after storms cause branches to fall into paddocks or when trimmings are fed to animals.

Although only red maple has been associated with poisoning in horses, red-maple hybrids should be considered toxic until proven otherwise.

Red maple leaves contain an unidentified toxin that causes oxidative hemolysis. The clinical signs of poisoning usually develop within 24 hours of exposure and include anorexia, depression, weakness and methemoglobinemia.

Fatally poisoned horses develop intravascular and extravascular hemolysis, icterus, anemia, hemoglobinuria, respiratory distress, Heinz body anemia, colic, laminitis, coma and death. Post-mortem findings include icterus, enlarged and swollen spleen, liver and kidneys and red urine.

Treatment is symptomatic and includes blood transfusions, fluid replacement and oxygen therapy. Because methemoglobinemia is limited, response to methylene blue is minimal. Other antioxidants such as ascorbic acid also may be helpful.

Allium spp. (onion): Onions contain an oxidant (N-propyl disulfide) similar to red maple in that it can cause acute hemolytic anemia. Because only large amounts of onion contain enough toxin, it rarely poisons horses.

Direct nephrotoxins

Photo 2: Quercus spp. (Oak) varies from large trees to shrubs that have large, alternate, simple, lobed leaves. In fall, they produce acorns. In the West, Gambels or scrub oak (shown here) is a shrub that grows in dense clusters on foothills and mountain slopes.
Quercus spp. (oak — Photo 2)

Oaks contain toxic tannins, such as gallotannin. Not all tree parts contain enough tannins to be toxic, but animals have been poisoned from eating flowers, leaf buds or acorns.

Clinical signs begin as depression, acute colic, straining (constipation, frequent urination) followed by bloody diarrhea, hematuria, rapid heartbeat and rapid breathing. Because tannic and gallic acid cause severe renal tubular nephrosis (kidney disease), clinical signs include dehydration, azotemia, hyperphosphatemia, hypocalcemia and hypoproteinemia.

Treatment should include extensive fluid therapy to maintain kidney perfusion, electrolyte and acid-base balances (diuresis).

Oxalate-induced nephrosis and hypocalcemia:

Sarcobatus vermiculatus (black greasewood), western-range plant, 10 percent to 20 percent oxalates.

Halogeton glomeratus (halogeton), invading and expanding desert weed.

Rumex crispus (curly dock) and other dock species.