Drought '02 Ohio State University Extension Ohio Veterinary Newsletter - Drought Concerns William P. Shulaw DVM, Extension Veterinarian Kent H. Hoblet DVM, Extension Veterinarian Diane F. Gerken DVM, Veterinary Toxicologist Reminiscent of 1988, we have received several calls in the past few weeks regarding possible problems with feeding drought stressed plants and potential toxic plant consumption by animals that are short on feed because of the drought. Recently, the Ohio Department of Agriculture's Consumer Analytical Laboratory has announced free testing of corn/corn silage for nitrates because of the drought. Although not all areas of Ohio are affected, most concerns center around animals being fed, or allowed to graze, stressed plants or plants not normally used for animals. Some of the most common issues of toxicity and testing are discussed below. NITRATES Nitrate, itself, is not highly toxic. Problems develop when nitrate (N03) is converted to nitrite (N02) in the ruminant animal's digestive system. Plants normally convert soil nitrate to plant protein. However, when stressed by dry weather, plants may be unable to totally effect this conversion and nitrates may accumulate. In the live animal the nitrite which is formed binds to the hemoglobin molecules in red blood cells and produces methemoglobin which prevents oxygen transmission to tissues and cells. Diagnosis of acute nitrate toxicity In the live animal pale to brown mucous membranes, weakness, dyspnea, rapid breathing, rapid pulse, recumbency, and CHOCOLATE-BROWN BLOOD are common signs of acute poisoning. In the dead animal the chocolate brown blood with staining and congestion of the tissues are the predominant finding. Methemoglobin is not stable in blood for more than an hour and nitrite may also rapidly disappear from the blood. Attempts may be made to analyze urine, plasma, serum, aqueous humor and rumen contents for nitrate content if they can be collected immediately after death. Results may vary depending on samples taken and freshness. Samples that must be mailed or held overnight should be frozen. Forage, hay, water or feed samples can be analyzed for nitrate content. Producers should be advised that total nitrate from all sources must be considered. In some cases water sources have been shown to be high in nitrate content. Nitrate concentrations for feed samples are usually reported on a dry weight basis. Plant and soil factors important in nitrate toxicity Species of plant. Certain weeds and forage plants are known to concentrate nitrates. These include: pig weed (Amaranthus spp.), lamb's quarters (Chenopodium spp.), jimson weed (Datura spp.), sweetclover (Melilotus spp. dock (Rumex spp.), nightshade plants (Solanum spp.), Johnson grass, sorghum (Sorghum spp.), oat hay (Avena spp.) barley (Hordeum spp.), wheat (Triticum spp.), and corn (Zea spp.). Soil content of nitrates. The form and timing of nitrogen application to plants, as well as the growth stage of the plant, influences the amount of nitrate accumulation. Other soil factors. For example, soils deficient in sulfur or phosphorous and high soil acidity favor plant nitrate accumulation. Drought. Herbicide use. Some herbicides, such as 2, 4-D, increase plant growth and nitrate uptake in the early period following application. Other determinants of nitrate toxicity Nitrates accumulate in vegetative tissue, not seeds, of plants. Therefore, ruminants are more likely to be exposed than swine. The highest levels occur just before flowering. In corn, stalks are typically higher than leaves in nitrate levels. Oat hay may be particularly high in nitrates. Proper ensiling causes a reduction of nitrates to ammonia so that a majority of nitrates are lost. This process may take several weeks if corn is very high in nitrates when ensiled. Ruminants may adapt to relatively high nitrate levels when doses are spread throughout the feeding period or mixed into the total diet; i.e., diluted. Tolerance also may be increased if ruminants are concurrently fed readily fermentable carbohydrates. Swine are relatively insensitive to nitrates in their diet because they can't convert them to nitrites. They are, however, very sensitive to feeds containing preformed nitrites. Nitrate toxicity is apparently neither reduced nor enhanced by simultaneously feeding urea. Feeding green feeds (e.g., "green chop") or pasturing on forages high in nitrate presents the greatest risk of toxicity. Acute nitrate toxicity may be expected when forage concentrations alone exceed 1.0% nitrate (10,000 ppm) ON A DRY MATTER BASIS. Acute toxicity from nitrate in water alone may be expected at 1,500 ppm (or 1500 mg/l.) The toxic level of nitrates to animals is ADDITIVE from all sources. Because, in a drought year forages may be borderline toxic other possible nitrate sources must also be scrutinized. Chronic nitrate toxicity, although suspected, has not been documented in controlled studies. In a Wisconsin, study dairy cows were exposed to 400 ppm of nitrate in their water for 35 months without significantly affecting either health or production. Laboratory Diagnosis - A number of public and private laboratories will analyze forages and water for nitrate levels. IT' accurate interpretation of results are expected extra care should be taken in obtaining representative samples. Most laboratories will report nitrate content as either ppm of nitrate (NOD or nitrate nitrogen (N03-N). To convert N03-N to N03 multiply by 4.4. For livestock owners it is wise to sample to forages with a worst case scenario in mind. This means to 1) always test before feeding if there is any question about the potential for nitrate levels in the feed, 2) sample areas of a field that may represent the most stressed plants if grazing them is anticipated, 3) sample corn to be ensiled in the most stressed areas, ensile under moisture and other conditions that promote ideal fermentation, allow 30 days of fermentation, and do not feed until the silage is tested for nitrates, and finally 4) be sure enough samples are taken to be representative of what is to be fed. Field test kits have been recommended for use in screening corn and other forages for nitrates. Their accuracy is unknown. The old field test based upon diphenylamine and sulfuric acid does not have a lower limit of detection capable of detecting nitrate at the lower levels that may still cause poisoning. Color change indicates more than 2% nitrate. One percent is lethal. Some other kits have been developed to test water for nitrates and do not report results on a dry weight basis. This may make interpretation of the result for forages difficult. Be sure the sampling procedures and test method used to determine nitrate level are reliable. CYANIDE (Prussic Acid Toxicity) Usual plants involved: wild cherry (Prunus spp.) Sudan grass, Johnson grass, and other Sorghum spp. elderberry (Sanbucus spp.) The clinical course is very rapid with prussic acid toxicity; death can occur within 30 minutes. Clinical signs are similar to nitrate poisoning except the blood is cherry- red. Sodium nitrite and sodium thiosulfate are antidotes. Rumen contents can be examined for presence of these plants to aid in the diagnosis. In the authors' experience, animals poisoned by nitrates may be more likely to be seen alive and experiencing signs than animals experiencing prussic acid toxicity. OTHER PLANTS WHICH ARE POTENTIALLY TOXIC Jimson weed (Datura spp.) nervous system; no antidote Pigweed (Amaranthus spp.) renal system; no antidote Oak (Quercus spp.) gastrointestinal and renal systems; no antidote Cocklebur (Xanthium spp.) gastrointestinal including liver; no antidote Nightshade (Solanum spp.) gastrointestinal, and nervous system; no antidote Poison Hemlock (Conium spp.) nervous system: no antidote Black locust (Robinia spp.) gastrointestinal and nervous; no antidote Bittersweet (Celastrus spp.) gastrointestinal; no antidote Note: The local county extension agent may be consulted for help in identifying unknown plants. Avoid using jargon terms to designate a plant when seeking information since many different plants may have the same jargon name depending on locality. Treatment Because specific antidotes are often not available, several principles of general treatment should be considered: Prevent further absorption by cathartics, mineral oil, or activated charcoal. Activated charcoal can increase excretion by preventing enterohepatic cycling. Remember the rumen serves as a large depot for continued absorption of toxicant. Large quantities of activated charcoal can be obtained by contacting your local water treatment plant. Obviously we haven't covered all the possibilities and potential problems that may be observed as a result of this year's drought. Furthermore, if alternative and damaged feeds will be used by producers, this will be a year to highly encourage forage testing for its nutritive value as a basis for ration formulation. Please feel free to call us if you have questions. - William P. Shulaw DVM, Extension Veterinarian; Kent H. Hoblet DVM, Extension Veterinarian; Diane F. Gerken DVM, Veterinary Toxicologist. All educational programs conducted by Ohio State University Extension are available to clientele on a nondiscriminatory basis without regard to race, color, creed, religion, sexual orientation, national origin, gender, age, disability or Vietnam-era veteran status. Keith L. Smith, Associate Vice President for Ag. Adm. and Director, OSU Extension. TDD No. 800-589-8292 (Ohio only) or 614-292-1868   | C.O.R.N. | Newsletter | Ohioline | Publications |