Johnson grass (Sorghum halepense) poses a significant danger to livestock, including cattle and sheep, because its toxicity is not constant. This aggressive, perennial grass contains compounds that convert into a rapid-acting poison when the plant is under stress. The safety of a pasture depends entirely on the environmental conditions and the physical state of the plant. While a healthy, actively growing stand may be tolerated, specific weather events can quickly transform it into a lethal forage, causing livestock deaths within minutes to hours of consumption.
Identification and Characteristics of Johnson Grass
Johnson grass is a tall, warm-season perennial that can reach heights of four to eight feet. Its leaves are notable for a prominent white or light green midrib running down the center of the blade. The plant spreads rapidly and aggressively through an extensive network of thick, fleshy, horizontal underground stems called rhizomes.
It produces large, open seed heads, or panicles, which often display a purplish tint as they mature. Prolific seed production, combined with the spreading rhizomes, contributes to its persistent nature. Although originally introduced as a forage crop, its potential toxicity has made it a management concern for ranchers.
The Chemical Cause of Poisoning
The toxicity of Johnson grass originates from a cyanogenic glycoside called dhurrin, which is stored within the plant’s cells. In a healthy, undamaged plant, dhurrin is physically separated from an enzyme that can break it down. The glycoside itself is harmless, but its breakdown product is deadly.
When the plant’s cell structure is ruptured—such as through chewing, wilting, or crushing—the dhurrin and the enzyme combine. This chemical reaction releases hydrogen cyanide (HCN) gas, also known as prussic acid. Ruminant animals, like cattle and goats, are particularly susceptible because their rumen microflora accelerate the conversion of dhurrin into free cyanide.
Once absorbed into the bloodstream, hydrogen cyanide acts as a cellular toxin. It binds to the enzyme cytochrome oxidase within the animal’s cells, blocking the cell’s ability to use oxygen. This inhibition of cellular respiration means oxygen carried by the blood cannot be released to the tissues. This leads to internal suffocation, or anoxia, despite the blood being saturated with oxygen.
Environmental Factors Affecting Toxicity
The concentration of cyanogenic glycosides increases dramatically when Johnson grass is subjected to environmental stress. Severe drought is a primary factor, as the lack of water slows growth and favors the accumulation of toxic compounds. Wilting caused by drought physically damages the plant cells, prematurely releasing the poison.
A hard frost is another significant trigger, as freezing temperatures rupture the plant cells, instantly releasing hydrogen cyanide. After a frost, the entire plant remains dangerous until the toxin dissipates, which can take up to two weeks. The tender, young leaves and new shoots contain the highest concentrations of dhurrin, making them the most dangerous parts of the plant.
Rapid regrowth following a period of stress, such as after a drought-ending rain or a light frost, is also highly toxic. Grazing on plants shorter than 18 to 24 inches is especially risky because the toxin concentration is higher in immature tissue. Producers should wait several days after substantial rainfall or until regrowth reaches a safe height before grazing.
Signs of Exposure and Emergency Response
Signs of cyanide poisoning in livestock have a rapid onset, typically appearing within 15 to 20 minutes of consuming a lethal amount. Early symptoms include rapid and labored breathing (dyspnea) and excessive frothing at the mouth. As poisoning progresses, the animal may experience muscle tremors, staggering, and dilated pupils.
A distinctive indicator is the bright, cherry-red color of the animal’s mucous membranes, such as the gums. This color is due to the high oxygen content trapped in the blood. Death from internal asphyxiation can occur within one to two hours after the first clinical signs are observed, and affected animals are often found dead without prior symptoms.
Immediate action is necessary to save an exposed animal, and a veterinarian must be contacted immediately. The antidote involves the rapid intravenous administration of a combination of chemicals, typically sodium nitrite and sodium thiosulfate. Moving unexposed animals away from the toxic forage source is an immediate preventive step while waiting for professional help.