Clammy Goosefoot, now commonly treated botanically as Dysphania pumilio, and formerly known as Chenopodium pumilio, is a small, aromatic, sticky or glandular annual plant long associated with the broader goosefoot group. Older references place it within Chenopodium, which is why the name Chenopodium pumilio remains important for older toxic plant databases, herbals, weed references, and pet-poisoning pages. Modern taxonomy generally places the plant in Dysphania, within Amaranthaceae, while older classifications separated this group and its relatives into Chenopodiaceae.

This plant is a member of the broader goosefoot complex, a nearly cosmopolitan group considered by many to contain a wide variety of edible, medicinal, weedy, and forage-associated species. The characteristic shape of the leaves of many species in this group led to the common name “goosefoots,” derived from the Greek chen, meaning goose, and pous, meaning foot. A highly adaptive group, goosefoot species can be found in a variety of soil types and climatic conditions throughout the world and across much of North America.

Clammy Goosefoot itself is native to Australia but has become introduced in other parts of the world, including North America and Europe, often in disturbed ground, roadsides, waste areas, sandy or gravelly soils, streambanks, lots, and other human-altered habitats. Its sticky, glandular surface and low-growing habit help distinguish it from some of the larger lambsquarters-type goosefoots, although common-name confusion remains common.

The leaves and seeds of many members of the goosefoot group are more or less edible when properly identified, harvested, and prepared. As a result, this group has a long history of human use both as a food source and medicinal herb. Native American people of northwestern Mexico reportedly steeped Chenopodium leaves into a concentrated decoction for the treatment of fevers and to remove intestinal worms, while the Navajo used members of the genus as part of a poultice to treat bruises and skin irritation. Native Americans also learned that the long taproot of Chenopodium californicum could be dried, stored, and grated for use as soap.

Even today, many related species are still gathered from the wild and cooked as potherbs. Some species are cultivated for their seeds, which have low gluten content and can be cooked similarly to rice, and others have found use as culinary herbs. That long history of use is important context, because it explains why this group can be confusing: the same general group can include useful edible plants, medicinal plants, pasture weeds, and plants capable of becoming toxic under the right environmental conditions.

These plants, however, can be toxic and, under the right circumstances, quite deadly to humans and livestock alike. The potential toxic ability of these plants is not so much the result of inherently lethal chemicals produced at dangerous levels under all conditions, as it is the result of environmental factors present during growth. It is true that many species in this group may contain oxalates, saponins, nitrates, and in some pasture-forage contexts cyanogenic glycosides. In this group, however, under healthy growing conditions, the amounts are often too small to be toxicologically significant.

The problem is that plants in this group may uptake and hold excess nutrients, specifically nitrate, in response to adverse growing conditions or environmental stress. When that happens, a plant that might otherwise be a low-risk weed or edible green can become toxic enough to cause serious illness or death in livestock. Current weed and livestock-poisoning sources continue to recognize goosefoot-type plants as possible nitrate and oxalate accumulators under certain conditions, particularly in disturbed, rich, fertilized, drought-stressed, or otherwise stressed growing sites.

A quick primer on the nitrogen cycle helps explain the problem. Plants take nitrogen from the soil by absorption through their roots in the form of either nitrate ions or ammonium ions. All nitrogen obtained by animals can be traced back to the eating of plants at some stage of the food chain. If nitrate is absorbed by the plant, it is first reduced to nitrite ions and then ammonium ions for incorporation into amino acids, nucleic acids, and chlorophyll, all of which are essential for plant growth.

Under normal conditions, the conversion of nitrate takes place at about the same rate that nitrate is absorbed by the root system, so nitrate concentration in plant tissues remains low. When plants are stressed, however, excess nitrate accumulation can be triggered, especially in times of drought where plant growth is restricted but absorption of nitrate from soil continues. Under normal conditions, plants may be expected to have safe nitrate levels below 4,400 ppm. Plants that have suffered severe environmental stress, however, can accumulate nitrate at levels reported as high as 70,000 ppm.

Amounts over 15,000 ppm are considered to have serious potential for toxicity in livestock, although cattle have become intoxicated when fed well-fertilized hay with nitrate concentrations as low as 8,250 ppm nitrate. Other factors that can contribute to excess nitrate accumulation include extended periods of reduced sunlight from cloudiness or shading, injury from freezing temperatures below 32°F, extended periods of low growing temperature, acidic soils, deficiencies of essential nutrients such as phosphorus, sulfur, or molybdenum, and certain herbicides including 2,4-D and 2,4,5-T.

It is also possible for plants to accumulate nitrate in the absence of obvious environmental stress when more soil nitrogen is present than the plant needs for maximum growth, as may occur in excessively fertilized soil, rich organic waste areas, manure-heavy locations, barnyards, feedlots, cultivated margins, and disturbed sites. This is why an edible or low-risk plant under one set of conditions may become dangerous under another.

Ruminants, including cattle, goats, and sheep, are the animals most likely to be affected by plants containing high levels of nitrates. When a ruminant ingests nitrates, bacteria in the rumen convert nitrate to nitrite, which is roughly ten times more toxic than nitrate, and then eventually to ammonia. The ammonia is then converted to urea and either recycled to the digestive tract to form bacterial protein or voided in the urine.

In the rumen, the reduction of nitrate to nitrite is rapid, whereas the detoxification of nitrite and subsequent conversion to ammonia is much slower. If the rumen is overwhelmed, it cannot convert incoming nitrate fast enough. Nitrate and nitrite may then be absorbed through the rumen wall and into the bloodstream, producing toxicity.

Once in the bloodstream, excess nitrite combines with hemoglobin in the red blood cells and oxidizes its ferrous iron into the ferric state, forming methemoglobin. Methemoglobin is incapable of transporting oxygen. A normal, non-intoxicated animal will generally have methemoglobin values in the range of 1 to 3 percent of hemoglobin content, while severely intoxicated animals can have methemoglobin levels upward of 70 percent. When an animal dies from nitrate poisoning, death is ultimately due to oxygen deprivation and multiple organ failure, even though the animal may be breathing.

The excess nitrate in the bloodstream does not, in and of itself, create the main toxicity problem, but it can contribute to the overall syndrome when it is recycled back into the rumen through saliva or gastrointestinal secretions. Once returned to the rumen, it can be converted again into more toxic nitrite and then reabsorbed into the bloodstream.

Nitrate reduction and nitrite production also occur in the cecum, or hindgut, of equids such as horses and donkeys, but not to the same extent as in ruminants. As a result, horses are generally much more tolerant of high nitrate concentrations than cattle, sheep, or goats. Nitrate poisoning in horses is considered rare and is more often associated with fertilizer spills, contaminated water, or unusual exposure than with ordinary grazing on plants containing high nitrate levels.

Nitrate poisoning in ruminants may be either acute or subacute, and in many cases the first indication of a problem will be the discovery of a dead animal in the field. Affected animals may die suddenly without appearing ill, sometimes within an hour of ingesting high-nitrate forage. In other cases, clinical signs may persist for a few hours to a few days before death, often culminating in terminal anoxic convulsions due to lack of oxygen to the brain.

In most cases, the symptoms of nitrate poisoning appear suddenly as a result of tissue hypoxia and low blood pressure due to vasodilation. In the early stages of intoxication, when methemoglobin levels begin to exceed 20%, vaginal and other mucous membranes may turn from pink to gray-brown as a result of tissue hypoxia. As nitrite continues to be released into the blood, methemoglobin levels continue to rise.

At methemoglobin levels of approximately 30 to 40 percent, animals may exhibit a rapid, weak heartbeat with subnormal body temperature, muscular tremors, weakness, and ataxia. Freshly drawn blood from an animal affected by nitrate poisoning will often be dark chocolate-brown. Once total methemoglobin content exceeds approximately 50%, dyspnea, air hunger, tachypnea, anxiety, and frequent urination are common, and seizures or death become likely.

Monogastric animals, meaning animals with a single-chamber stomach such as humans, dogs, cats, horses, and rabbits, more commonly suffer nitrate intoxication from non-plant sources such as fertilizers or contaminated water. When affected, they may exhibit depression, inappetence, hypersalivation, moderate to severe gastrointestinal upset, vomiting, diarrhea, abdominal pain, gastric hemorrhage, and possibly death.

Some animals may not exhibit adverse effects until after they have eaten high-nitrate forage for days to weeks, at which point the progression from clinical signs to death may be rapid. Severely intoxicated animals that develop marked dyspnea may recover, only to then develop interstitial pulmonary emphysema and continued respiratory distress. Many of these animals will recover fully within one to two weeks, but recovery depends heavily on the severity of the exposure, speed of diagnosis, and access to treatment.

Unfortunately, the symptoms of cyanide poisoning are very similar to those of nitrate toxicity. In cases where livestock may have had access to pasture containing plants known to be a source of cyanogenic glycosides, one must determine whether nitrate or cyanide is the culprit. Potential cyanogenic plant sources include arrow grass, velvet grass, sorghum species such as Johnson grass, Sudan grass, and common sorghum, Prunus species such as apricot, peach, chokecherry, pincherry, and wild black cherry, elderberry, apple, corn, and flax.

In the field, the simplest distinction is the appearance of freshly drawn blood. Cyanide-contaminated blood will generally turn a brilliant cherry red upon exposure to air, whereas methemoglobin-contaminated blood from nitrate poisoning will be dark brown or chocolate in color. This distinction is practical and important, because nitrate poisoning and cyanide poisoning require different therapeutic approaches.

Nitrate accumulation may also affect a plant’s accumulation of oxalate. A number of studies have shown that nitrate can efficiently induce accumulation of high levels of oxalates in plants, although the exact mechanism is not fully understood. Typically, concentrations of oxalates may be in the range of 1 to 2%, but nitrate accumulation can result in oxalate accumulation above 20%. As a plant matures, oxalate levels in the leaves may increase while levels in the stems decrease.

Current livestock references describe soluble oxalate poisoning as a significant concern in grazing animals consuming large amounts of oxalate-accumulating plants. Signs of oxalate intoxication may occur abruptly a few hours after consumption of contaminated plants, and animals may die within 12 hours. There is typically a progression of symptoms from depression, weakness, tremors, weak pulse, and labored respiration to recumbency, prostration, coma, and death in a few hours.

Prevention is the best medicine. If you are unsure of a plant’s nitrate content, have it tested. If plants have been subjected to drought conditions, excessive fertilization, herbicide stress, frost injury, prolonged cloud cover, low growing temperatures, nutrient deficiency, or other unusual stresses, forage samples should be tested before animals are allowed to graze the area.

References:
Ozmen O, Mor F, and Ayhan U (2003) Nitrate poisoning in cattle fed Chenopodium album hay. Veterinary and Human Toxicology 45:83–84.
University of Wisconsin, “Nitrate Poisoning in Cattle, Sheep and Goats”; Dan Undersander, Dave Combs, Randy Shaver, and Dave Thomas.
Robert Smith, DVM and Glenn Selk, Nitrate Toxicity: Diagnosis and Treatment.