2010 was anything but a banner year for forage and hay crops. Incessant rain, early frost and delayed harvesting reduced the quality of most legume stands and the quality of cereals destined for winter forage. Volunteer crops mixed with weeds like kochia are being bailed on land that went unseeded, adding to the inventory of substandard forage. Lurking in the mix of poor-quality hay and silage is nitrate. If not managed properly, the risk of acute and chronic nitrate poisoning in cattle can be high.
Plant roots absorb soil nitrogen in the form of nitrate. Under normal growing conditions a balance is maintained between nitrate gathered by roots and its conversion to protein by the plant, but during abnormal growing conditions like drought, frost, unseasonable or prolonged cool temperatures, hail, disease, high levels of soil nitrogen, soil mineral deficiencies or herbicide damage nitrate accumulates in forages. The upper plant, unable to utilize nitrate as efficiently, accumulates it in stems and leaves where it remains unless new growth occurs. If the plant dies or is harvested, accumulated nitrate is permanently trapped.
All plants contain nitrate, but nitrate levels toxic to livestock are mostly associated with forages (hay, fodder, silage, pasture or weeds). The risk of nitrate toxicity is highest when livestock graze standing greenfeed or fed green-chop. Hay poses a medium risk and silage is the least hazardous feed. Ensiling forage usually lowers the nitrate level 10 to 60 per cent. Immature plants have a tendency to concentrate nitrates more so than those in later stages of growth. Nitrate concentrations are highest in stems, are maintained at intermediate levels in leaves and are practically non-existent in grain. Producers should never assume any forage is safe if crops have been exposed to adverse growing conditions.
While nitrates (N03) by themselves are not very toxic, nitrites (N02) are. In ruminants nitrate is converted to nitrite by rumen bacteria. Normally, nitrite is converted to ammonia that is absorbed from the rumen and metabolized into protein. Nitrate poisoning occurs when rumen nitrite levels exceed the capacity of microbes to convert it to ammonia. At this point, both nitrate and nitrite collect in the rumen and are absorbed.
When nitrite is absorbed through the rumen wall into the bloodstream it combines with hemoglobin, the oxygen-carrying protein of red blood cells, to form methemoglobin. Methemoglobin is unable to transport oxygen to organs and tissues throughout the body. Oxygen starvation is the result.
The absorbed nitrate component does not initially create problems but as it is recycled back into the rumen via saliva and intestinal secretions it is converted to nitrite, which after absorption enhances methemoglobin concentration in the bloodstream. The amounts of recycled nitrate combined with the rate of nitrite breakdown influences the difference recognized in tolerance of individual animals and groups of animals to nitrate poisoning.
The effects of sublethal nitrate levels on livestock health and performance are not well defined. Winter diets of hay containing nitrates can create chronic symptoms like abortions, poor winter health, reduced appetite and lower weight gains. Although safe and unsafe levels of nitrate in livestock feed have been established they should only be considered guidelines because the effects of nitrate will vary among individual animals, condition and age of livestock, other feeds in the diet and weather. Low-grade nitrate poisoning affects newborn calf vigour and survival. Groups of animals can develop varying degrees of tolerance to nitrates in feed, creating situations where clinical signs may appear after several weeks on a given feed when there is a change in feed intake induced by conditions like inclement weather. Production problems associated with low-grade nitrate toxicity can be obscure and may go unrecognized when nitrate levels are borderline e. g. in the range of 0.5 to 1.0 per cent of feed consumed (on a dry basis).
Conversion of nitrate to nitrite in the rumen can be rapid with large amounts absorbed into the bloodstream over short periods of time. Affected animals can die within a few hours of initial ingestion of high-nitrate feed. Typically, maximum methemoglobin levels in cattle fed once a day occur approximately eight hours after consuming hay containing nitrates. Clinical signs of acute poisoning in cattle include: dark chocolatecoloured blood, increased heart rate, muscle tremors, weakness, blue-grey mucous membranes, excess salivation and tear production, depression, laboured breathing, inco-ordination, frequent urination, low body temperature, disorientation and inability to get up. Affected animals not uncommonly collapse when being handled.
If producers suspect nitrate poisoning they should contact a veterinarian immediately. Individual animal treatment of nitrate poisoning is limited to intravenous therapy of a drug like methylene blue. A critical step is removal of the offending feed until all control options can be considered.
The most important preventive step cattle producers can take this fall is testing forages for nitrates and nutrient quality. We move into fall knowing forage quality is poor in many areas. Growing conditions have been less than ideal and nitrate toxicity is a very real threat. Beef extension specialists and veterinary practitioners can advise on where and how to conduct feed testing. These same people can help developing strategies for utilizing high-nitrate feeds.
Dr. Ron Clarke prepares this column on behalf of the Western Canadian Association of Bovine Practitioners. Suggestions for future articles can be sent to CANADIAN CATTLEMEN ( [email protected]) or WCABP ( [email protected]).