White sweet-clover-Melilotus alba-Poisonous plant

White sweet-clover

General poisoning notes:

White sweet-clover (Melilotus alba) is a cultivated and naturalized plant that occurs as a weed across most of Canada. This plant contains a glycoside with a coumarin fraction. When sweet-clover is harvested for feed, the succulent stems usually mold before drying. The molds metabolize the glycoside into dicoumarol, which interrupts vitamin K activation of prothrombin, necessary in blood clotting. Levels of dicoumarol at more than 10 ppm are suspected of possible poisoning. Dicoumarol levels are usually higher in small and round bales than in stacks. Cattle, horses, and sheep have been poisoned. However, cattle are almost exclusively poisoned by sweet-clover (Blakely 1985, Cheeke and Schull 1985).

Description:

Annual, erect, 30-150 cm tall. Leaflets narrowly oblong-obovate to sub-orbicular, serrate. Stipules entire. Inflorescence a peduncled raceme, peduncle up to 4 cm long, raceme 4-10-(15) cm long. Calyx c. 2 mm long. Corolla 3.5-5 mm long, white, wings and keel subequal, shorter than the vexillum. Fruit c. 3-5 mm long, reticulately veined, glabrous.

Nomenclature:

Scientific Name: Melilotus alba Desr.

Vernacular name(s): white sweet-clover

Scientific family name: Leguminosae

Vernacular family name: pea

Geographic Information:

Distribution: Pakistan, India, Kashmir; Tibet, Persia, Afghanistan, Central Asia, Turkey, Arabia, Europe, introduced in America and Australia.

Canada: Alberta, British Columbia, Labrador, Manitoba, New Brunswick, Northwest Territories, Nova Scotia, Ontario, Prince Edward Island, Quebec, Saskatchewan, Yukon Territory.

Notes on Poisonous plant parts:

Moldy sweet-clover is produced through insufficient drying of bales and silage. Dicoumarol production by molds is not likely to occur if animals ingest living plants.

Toxic parts:

Stems, leaves.

Notes on Toxic plant chemicals:

A glycoside, melilotoside, contains an ether and coumarin. The coumarin is metabolized by various molds (e.g., Penicillium spp.) into dicoumarol. Dicoumarol inhibits vitamin K, which causes hemorrhaging. Sweet-clover has a succulent stem, which makes molding common after cutting. Round bales have been found to have significantly higher dicoumarol (mean of 22.9 +/- 3.10 mg/kg) than stacks of silage (means 1.8 of +/- 6.3 and 0.6 +/- 2.1 mg/kg). The outer parts of round bales had a higher concentration of dicoumarol (Benson et al. 1981, Cheeke and Schull 1985).

Toxic plant chemicals:

Dicoumarol, melilotoside.

Chemical diagram(s) are courtesy of Ruth McDiarmid, Biochemistry Technician, Kamloops Range Station, Agriculture and Agri-Food Canada, Kamploops, British Columbia, Canada.

Animals/Human Poisoning:

Note: When an animal is listed without additional information, the literature (as of 1993) contained no detailed explanation.

Cattle

General symptoms of poisoning:

Abortion, anemia, elevated, heart rate, hemorrhage.

Notes on poisoning:

Symptoms of moldy sweet-clover poisoning may appear without any obvious cause. Trauma and surgery are often followed by severe hemorrhage and death. Hemorrhage may result after uncomplicated parturition. Newborn calves may die during the first few days of life if their dams have been fed on toxic feed. In Saskatchewan 286 animals from 56 herds were affected in 1983. The mortality rate was 12.1%. Aborted fetuses and calves less than 2 weeks old were affected most often. Poisoning usually occurred between January to April. Sweet-clover fed as bales was more of a problem than when fed as silage (Radostits et al. 1980, Blakely 1985). Treatment using vitamin K1 was effective at dosages of 1.1-3.3 mg/kg of body weight after poisoning by sweet-clover containing dicoumarol at a minimum of 90 ppm. Vitamin K3 was ineffective as treatment (Alstad et al. 1985).

Horses

General symptoms of poisoning:

Anemia, hemorrhage.

Notes on poisoning:

In one case in Saskatchewan, a Percheron mare was anemic and was hemorrhaging from the left nostril at 60 drops per min. Mucous membranes were blanched. Subcutaneous edema extended from the intermandibular space to the pectoral region. The animal was treated with an injection of 4.2 g of menadione sodium bisulphate and with 4 L of whole blood preserved in acid citrate dextrose solution. Complete recovery resulted. The mare had been fed weathered sweet-clover hay free-choice with access to pasture (McDonald 1980).