Many plant structures can cause problems for grazing livestock. These structures include awns (hare barley, foxtail barley, needlegrass, medusahead rye, ripgut brome, downy brome, cheat), burrs (burdock, cockle- bur, longspine sandbur), spines (yellow starthistle, puncturevine), and thorns (wild rose). When these plant structures become lodged in the nostrils, eyes, mouth, or digestive tract, they cause animal trauma. In- fections can occur if they become embedded in tissues and form abscesses or ulcers.
Control plants with these structures using the meas- ures discussed in chapter 7. Management information for specific weed species is available in the Pacific
Northwest Weed Management Handbook. See the chapters on “Managing Small Pastures,” “Pasture and Rangeland Weed Control,” and “Control of Problem Species.” Another valuable reference is Weeds of Cali-
fornia and Other Western States. PLANT-INDUCED DISORDERS
Plant-induced disorders include toxicities, digestive problems, and chemical imbalances. Toxicities caused by poisonous plants are due primarily to effects on the animal’s metabolism. Examples include nitrate toxic- ity, prussic acid toxicity, and photosensitization. Exam- ples of digestive and chemical imbalances include bloat and grass tetany.
Many plant-induced animal disorders occur only sea- sonally or sporadically. For example, toxic plant com- pounds vary, depending on the season. In the case of disorders such as bloat and forage mineral imbalances, both the crop (species and stage of growth) and the en- vironment are contributing factors.
Learn to recognize the common symptoms of animals affected by these problems. Immediately remove af- fected animals from the pasture and provide free-choice clean water and good-quality hay. Consult with a veteri- narian about treatment for severely affected animals. Bloat
Bloat (also known as frothy bloat) can be a significant risk for cattle and sheep grazing pastures containing a high percentage of alfalfa and other legumes. Symp- toms include distended rumen, labored breathing, rest- lessness, and frequent urination and defecation. Death
can occur rapidly. Mild “subacute” bloat (rumen dis- tended on one side) frequently occurs. Most individu- als can develop an increasing level of tolerance. Bloat typically occurs in ruminant livestock grazing lush alfalfa or clover, but can also occur on lush grass or cereal pastures such as wheat. Consuming these for- ages without accompanying hay or other low-moisture forage often leads to a severe form of indigestion char- acterized by an abnormally high accumulation of gas. The breakdown of rapidly soluble proteins forms a sta- ble foam over the rumen contents, reducing the ani- mal’s ability to eructate (belch). Bloat results when the animal is unable to eructate the large quantity of gases produced during rumen fermentation.
Contributing factors include:
• Forage species—Alfalfa, white clover, red clover, or wheat is often involved.
• Stage of plant growth—Bloat risk declines with plant maturity.
• Season—Bloat “storms” are more likely in the spring or fall and following rainstorms.
• Concentrations of certain soluble proteins—High ni- trogen (N) fertility increases the risk.
• High rate and amount of forage intake • Low fiber concentration
• Rumen microbial population
• Inflammation of lymph nodes between the lungs—In- flamed lymph nodes compress the esophagus. • An inherited tendency by some animals
Health Disorder Triangle
Animal Environment Presence of a toxic plant, forage mineral
imbalance, disease, pest, or parasite
Figure 12.1. The health disorder triangle illustrates the conditions necessary for development of animal health disorders due to plant toxicities, mineral imbalances, diseases, pests, or para- sites. The presence and severity of the disorder (size of the trian- gle) is determined by the level of each factor.
The complex interactions among bloat-causing factors require a number of preventive measures:
• Establish and manage pastures so that alfalfa and clover make up less than 50 percent of the forage bio- mass.
• Establish a non-bloating legume in pastures, such as birdsfoot trefoil, cicer milkvetch, or sainfoin. • Allow animals to fill on dry roughage before turning
out on bloat-prone pastures.
• When grazing a bloat-prone pasture, feed dry hay or windrow-graze.
• Feed antifoaming agents such as Poloxalene in a mo- lasses-containing block.
• Move animals to a drylot or other area following heavy dew or rain.
• Immediately move distressed animals to another pas- ture (and possibly away from the herd).
• Consult with your veterinarian and plan ahead to be competent in handling a severe bloat event.
Grass tetany
Grass tetany (also called hypomagnesemia for “low magnesium”) is a common metabolic disease of rumi- nants. It usually is associated with early-spring grazing of lush, grass-dominated pastures, but can occur with grazing of regrowth in intensively grazed pastures. Symptoms include nervousness, stiffness, reduced milk production, staggering, and labored breathing. These symptoms can progress to convulsions and death in as few as 6 hours. Cows or ewes following late-winter parturition are most susceptible to tetany. Tetany occurs when an animal’s level of blood magne- sium (Mg) is too low. Low Mg levels in forage can be a significant contributing factor to tetany.
Magnesium is required at similar levels for both crop and livestock function. Cool-season grasses should contain at least 0.2 percent Mg on a dry weight basis. For proper sheep and cattle growth, livestock diets should contain at least 0.1 percent Mg. For lactating cows, the diet should contain more than 0.2 percent Mg.
In spring, rapidly growing plants typically have low lev- els of Mg and high potassium (K) concentrations (above 3 percent). Potassium reduces the absorption
of Mg in forage plants and the rumen, reducing the amount of animal-available Mg.
Additional factors associated with Mg deficiency in- clude:
• Lactation—Large quantities of calcium (Ca) and Mg are excreted in milk.
• High concentrations of crude protein (greater than 25 percent) or N (greater than 4 percent) in forage. • High levels of N fertilization, especially during poor
plant growing conditions.
• Bad weather (especially storms) or other stresses that cause livestock to go off feed for more than 24 hours.
• Interactions among the above factors, resulting in low blood Mg and Ca.
Pastures can be managed to reduce the risk of grass tetany. On first-pass pastures in the spring, a significant supply of residual growth from the previous year (or some dry hay) can reduce the risk. Split annual N and K applications to avoid high concentrations of these elements.
In extreme cases of tetany, a veterinarian can treat the affected animal with injections of magnesium sulfate or calcium gluconate.
Milk fever
Milk fever (also called hypocalcemia for “low cal- cium”) is a metabolic disorder related to Ca availabil- ity. It occurs most frequently in females at the onset of lactation. Milk fever does not cause a fever. Symptoms include muscle weakness, fatigue, reduced milk yield, and loss of appetite. In severe cases, heart failure can occur. On early-season pastures, both plant Ca and Mg may be low, and the symptoms of milk fever may be in- distinguishable from those of tetany.
Forage tissue levels of 0.3 to 0.4 percent Ca typically meet livestock Ca requirements. Comprehensive for- age testing across the United States has shown that legumes typically have higher concentrations of Ca (1.4 percent) than grasses (0.6 percent). Ideally, the calcium:phosphorus ratio in the diet should be 2:1. Supply Ca in the form of a balanced mineral meal or block prior to parturition and while livestock are on pastures. Severe cases of milk fever may require a vet- erinarian to provide an injection of calcium gluconate.
Nitrate toxicity
Nitrate toxicity is caused by elevated consumption of nitrate (NO3) in pasture crops, weeds, hay, or water. Symptoms include increased heart rate, labored breathing, change in color of tissues from pink to blue, and muscle tremors. Affected animals may stagger, abort fetuses, and die within hours of ingesting toxic levels of nitrate. Gestating ruminants are very suscepti- ble to high levels of NO3.
In the body, nitrite (NO2) is produced as an intermedi- ate step in the conversion of absorbed nitrate to amino acids and protein. Nitrite (NO2) is highly toxic and competes directly with oxygen (O2) in the bloodstream.
A number of plant, livestock, and environmental condi- tions increase the likelihood of nitrate toxicity. These include:
• Stage of plant growth—Many grasses and legumes contain high levels of NO3during their early vegeta- tive growth. During flowering or reproduction, ni- trate is rapidly converted to plant proteins.
• Plant part—NO3is higher in stems than in leaves or reproductive structures. It is highest in the lower stems.
• Plant species—Certain species tend to be nitrate “ac- cumulators,” including oats and other cereals, sudan- grass, and many common weeds, such as pigweed species, nightshade species, common lambsquarters, common mallow, kochia, and wild oat. These species tend to retain high levels of nitrate throughout their entire growth cycle (see table 12.1).
• The amount and availability of soil N—In intensively managed pastures, N applications must be split. • Soil conditions—NO3uptake is favored by low soil
temperatures and low or deficient plant levels of phosphorus (P), sulfur (S), and molybdenum (Mo). • Drought, cloudiness, or extreme heat or cold condi-
tions that restrict normal plant growth
• Livestock condition—NO3toxicity risk usually is higher for females on a low plane of nutrition, in ges- tation, or under other stress.
• Rapid change in the diet of gestating or stressed live- stock from a low-quality roughage to a diet contain- ing high levels of NO3
Over time, livestock can tolerate increasingly higher levels of forage NO3, as the rumen microflora adapt. In a managed rotational grazing system, livestock can adapt to elevated NO3levels multiple times during the year, including during winter when hay is fed. Due to the potentially rapid onset of NO3toxicity, be careful when initiating grazing on suspect pastures, es- pecially in the case of pregnant mares, foals, and other juvenile animals. Test forage that is likely to be high in NO3, especially if it has been heavily fertilized with N or is drought stressed. A recently developed product (www.lallemand.com) containing high concentrations of propionic bacteria can be administered to animals before feeding high-NO3roughages.
Animals suspected of having NO3poisoning should be kept stress-free. Remove the suspect feed source from
Winter tetany
“Winter tetany” is caused by feeding hay with ex- cessive (or unbalanced) K levels. A “tetany risk ratio” is often used to evaluate the potential risk. If the milliequivalent (meq) ratio of K to (Ca + Mg) is above 2.2, the hay has a high risk of inducing tetany. To es- timate the tetany risk ratio, obtain laboratory analy- ses for K, Ca, and Mg (100 percent dry matter basis). Calculate the meq values by multiplying the concen- trations (percent) of K, Ca, and Mg by 255.74, 499.00, and 822.64, respectively.
For example, from a barley hay analysis, the labora- tory reported that the forage contained 3.09 percent K, 0.24 percent Ca, and 0.2 percent Mg. Using the equations above, the tetany risk ratio is:
Since 2.8 is greater than 2.2, this hay is at risk for in- ducing tetany.
You can use soil or forage tissue analysis to monitor Mg concentrations. However, it may be more effi- cient to provide Mg in a complete mineral supple- ment. Begin supplementation 3 weeks before tetany is anticipated (the turnout date in some circum- stances). Many mineral formulations are available. An economical choice is a 1:1:1 mixture of trace mineral salt, magnesium oxide, and cracked grain or dry molasses. Monitor mineral intake frequently. Daily consumption is required, because Mg is not stored in the body.
3.09 x 255.74
(0.24 x 499.0) + (0.2 x 822.64) = 790.2 284.3= 2.8
Table 12.1. Toxicities and associated common plant species in the inland Pacific Northwest.
Impact on animal
Chemical/
symptom group Potential plants involved
Potential for sudden death
Cyanogenic glycosides (HCN)
Sudangrass and other sorghums (Sorghum spp.), white clover (Trifolium repens), ser viceberr y (Amelanchier alnifolia), hydrangeas (Hydrangea spp.), flaxes (Linum spp.), birdsfoot trefoil (Lotus spp.), crabapple leaves (Malus spp.), lima bean (Phaseolus lunatus), chokecherries (Prunus spp.), elderberries (Sambuccus spp.), mountain-mahogany (Cercocarpus montanum), brackenfern (Pterid- ium aquilinum), arrowgrass (Triglochin maritima), vetch seed (Vicia sativa), corn (Zea mays)
Nitrate toxicity Ragweeds (Ambrosia spp.), pigweeds (Amaranthus spp.), tame oat and wild oat (Avena spp.), sugarbeet (Beta vulgaris), rape (Brassica napus), common lambsquar ters (Chenopodium album), Canada thistle (Cirsium ar vense), field bindweed (Convolvulus ar vense), jimsonweed (Datura stra- monium), barnyardgrass (Echinochloa crus-galli), sunflower (Helianthus annuus), barley (Hordeum vulgare), kochia (Kochia scoparia), flaxes (Linum spp.), mallows (Malva spp.), alfalfa (Medicago sativa), sweetclovers (Melilotus spp.), millets (Pennisetum, Pannicum, and Echinochloa spp.), smar tweeds (Polygonum spp.), curly dock (Rumex crispus), Russian thistle (Salsola kali), feral or cereal r ye (Secale cereale), sudangrass and sorghums (Sorghum spp.), nightshades (Solanum spp.), goldenrods (Solidago spp.), wheat (Triticum aestivum), corn (Zea mays)
Toxic alkaloids Larkspurs (Delphinium spp.), monkshood (Aconitum columbianum), poison hemlock (Conium mac- ulatum), waterhemlocks (Cicuta spp.)
Cardiovascular system
Cardiac glycosides Hemp dogbane (Apocynum cannabinum), lily-of-the-valley (Convallaria majalis), garden foxglove (Digitalis purpurea), oleander (Nerium oleander), milkweeds (Asclepias spp.), yews (Taxus spp.), deathcamas (Zigadenus spp.)
Digestive system
Excessive salivation Physical structures: foxtail barley (Hordeum jubatum), hare barley (Hordeum leporinum), needle- grass (Stipa spp.), ripgut brome and downy brome (Bromus spp.), squirreltail (Sitanion hystrix), foxtails (Setaria spp.), sandbur (Cenchrus longispinus), medusahead r ye (Taeniatherum asperum), burdock (Arctium minus), cocklebur (Xanthium strumarium) Chemical irritants: clover or alfalfa in- fected with Rhizoctonia leguminicola Protoanemonins: buttercups (Ranunculus spp.), marsh marigold (Caltha palustris), clematis (Clematis spp.), baneberr y (Actaea arguta)
Vomiting Orange sneezeweed (Dugaldia hoopesii), Colorado rubber weed (Hymenoxys richardsonii), bitter- weed (Hymenoxys odorata)
Nightshade poisoning (steroidal glycoalkaloids causing colic, constipation, or hemorrhagic diarrhea)
Nightshades, buffalobur, horsenettle, and bull nettle (Solanum spp.), jimsonweed (Datura stramo- nium), deadly nightshade (Atropa belladonna), black henbane (Hyoscyamus niger), buffalobur (Solanum rostratum), ground cherries (Physalis spp.)
Diarrhea, gastrointestinal poisoning
Yarrow (Achillea milleflorum), leafy spurge (Euphorbia esula), irises (Iris spp.), horsetail (Equisetum arvense), bitterweeds (Helenium spp.), tulips (Tulipa spp.), numerous mustards (Brassica spp.), rho- dodendrons (Rhododendron spp.), common boxwood (Buxus sempervirens), laurels (Kalmia spp.)
Skin and liver disorders
Primar y
photosensitization (directly affects skin)
Buckwheat (Fagopyrum esculentum), St. Johnswor t (Hypericum per foratum)
Secondar y photosensitization (liver function damaged—compounds or their components cause secondar y skin and organ disorders)
Pyrrolizidine alkaloids: fiddlenecks (Amsinckia spp.), houndstongue (Cynoglossum officinale), tansy ragwor t and groundsels (Senecio spp.)
Alsike clover poisoning: Trifolium hybridum
Other: tame oat and wild oat (Avena spp.), rape (Brassica rapus), kale (Brassica oleraceae), sand- bur (Cenchrus longispinus), tansy mustard (Descurainia pinnata), flixweed (Descurainia sophia), wild carrot (Daucus carota), milk purslane (Euphorbia maculata), barley (Hordeum vulgare), kochia (Kochia scoparia), cocklebur (Xanthium strumarium), perennial r yegrass (Lolium perenne), panic grasses (Panicum spp.), alfalfa (Medicago sativa), hair y vetch (Vicia villosa), parsnip (Pastinaca spp.), knotweeds (Polygonum spp.), buttercups (Ranunculus spp.), sudangrass (Sorghum spp.), puncturevine (Tribulus terrestris), clovers (Trifolium spp.)
Mycotoxin (aflatoxin): Moldy hay, straw, or grain infected with Aspergillus or Penicillium spp. Blue-green algae poisoning in stagnant ponds: (Microcystis, Anabaena, and Aphanizomenon spp.)
Impact on animal
Chemical/
symptom group Potential plants involved
Blood disorders
Red blood cell damage Onion and wild onion (Allium spp.), kale, rape, and turnip (Brassica spp.)
Inhibition of blood clotting
Brackenfern (thiaminase) and dicoumarol, an anticoagulant in sweetclover infected by Aspergillus, Penicillium, or Mucor spp.
Goiter, hypothyroidism Glucosinolate poisoning: whitetop (Lepidium draba), mustards (Brassica spp.)
Ner vous system
“Locoism” alkaloids Milkvetches (Astragalus spp.), point vetch (Oxytropis spp.)
Essential oils, sesquiterpene lactones, or monoterpene toxins
Fringed sage (Ar temisia frigida—horses only), big sagebrush (Ar temisia tridentata), yellow star this- tle (Centaurea solstitialis), Russian knapweed (Centaurea repens)
Other Horsetails (Equisetum spp.), sudangrass (Sorghum spp.), sweetpea (Lathyrus spp.), hemp (Cannabis sativa)
Kidney failure Oxalate poisoning (sodium or potassium oxalate accumulation)
Pigweeds (Amaranthus spp.), sugarbeet (Beta vulgaris), lambsquar ters (Chenopodium album), halogeton (Halogeton glomeratus), kochia (Kochia scoparia), sheep sorrel (Rumex acetosella), purslane (Por tulaca oleraceae), curly dock (Rumex crispus), rhubarb (Rheum rhaponticum), Russ- ian thistle (Salsola kali), greasewood (Sarcobatus vermiculatus)
Congenital defects and reproductive disorders
Abor tion Milkvetches (Astragalus spp.), Oxytropis spp., Brassica spp., poison hemlock (Conium macula- tum), spotted hemlock (Conium maculatum vars. angustifolia and bolanderi), fescue (Festuca spp.), halogeton (Halogeton spp.), juniper (Indigofera glomeratus and Juniperus spp.), alfalfa (Medicago sativa), tansy (Tanacetum spp.), goldenrods (Solidago spp.), clovers, false hellebore (Veratrum spp.)
Pine needle abortion: ponderosa pine (Pinus ponderosa) Nitrate accumulators: see “Nitrate toxicity,” previous page
Teratogens (cause fetal death or deformity)
Milkvetches (Astragalus spp.), Oxytropis spp., spotted hemlock (Conium maculatum vars. angusti- folia and bolanderi), sweetpea (Lathyrus odoratus), lupine (Lupinus spp.), poppies (Papaveraceae spp.), Senecio spp., false hellebore (Veratrum spp.), periwinkle (Vinca rosea)
Phytoestrogens
(cause infer tility) Clovers (Trifolium spp.), alfalfa (Medicago sativa)
Muscle and bone system
Selenium poisoning, alkali disease
Milkvetches (Astragalus spp.), rayless goldenweed (Oonopsis engelmannii), woody aster (Xylor- rhiza glabriuscula), white fall aster (Aster falcatus), prince’s plume (Stanleya pinnata), broom snakeweed (Gutierrezia sarothrae), gumweed (Grindelia spp.), saltbush (Atriplex spp.), Indian paintbrush (Castilleja spp.), beard tongue (Penstemon spp.)
Plant toxins in milk
Above compounds and symptoms transferred in milk
Pyrrolizidine alkaloids: fiddleneck (Amsinckia spp.), houndstongue (Cynoglossum officinale), tansy ragwor t and groundsels (Senecio spp.)
Indolizidine alkaloids: milkvetches (Astragalus spp.), Oxytropis spp. Glucosinolates: whitetop (Lepidium draba), mustards (Brassica spp.)
Source: Adapted from Knight, A.P. and R.G. Walter. 2001. A Guide to Plant Poisoning of Animals in Nor th America. Teton NewMedia.
the diet. If a case is severe but diagnosed early, a veterinar- ian can inject the affected animal with methylene blue. Prussic acid poisoning
About 2,000 plant species produce cyanogenic glyco- sides (table 12.1). These compounds can cause prussic acid (hydrogen cyanide, or HCN) poisoning within 20 minutes of ingestion. HCN is released when plant cells are chewed, crushed, digested, wilted, or frozen. It is highly toxic and inhibits cells’ ability to utilize oxygen. Early symptoms of prussic acid poisoning include ex- citement and labored breathing. Convulsions, stupor, coma, and death follow. Chronic HCN poisoning, which is caused by sublethal doses over time, causes loss of nerve function.
This disorder is relatively rare on well-managed perma- nent pastures. The highest risk of HCN poisoning oc- curs on annual pastures containing sudangrass or sorghums (all now classified as S. bicolor (L.) Moench). The risk is greatest when grazing young growth or regrowth following drought or frost. High HCN levels can occur sporadically in pastures with high densities of white clover, vetch (seed), or birds- foot trefoil, or where animals have access to arrow- grass, brackenfern, chokecherry, serviceberry, western waterhemlock, or apple trees.
In grass-legume pastures containing white clover or birdsfoot trefoil, maintain a good balance of grass and legume foliage. Follow guidelines for proper grazing heights, rest periods, and fertilizer application. Pay close attention to grazing animals in the early spring and fall.
The only treatment for HCN poisoning is injection of an appropriate antidote, such as sodium thiosulfate or sodium nitrate.
Fescue and ryegrass toxicoses
The causes of these long-known animal disorders have only recently been fully recognized. Previously re- ferred to as “fescue foot,” “summer slump,” or “rye- grass staggers,” these disorders are very important because of the widespread use of tall fescue and peren- nial ryegrass in improved pastures.
Symptoms in cattle and sheep include lack of appetite; reduced weight; low milk production; high body tem- perature; dull, rough haircoat or reduced wool produc- tion; excessive salivation; and reproductive problems. Under high N fertilization, affected cattle can develop fat necrosis—hard masses in the fatty tissues
surrounding the intestines. This condition causes di- gestive problems and can interfere with calving. In horses, mares are particularly susceptible to fescue and ryegrass toxicoses. Symptoms include prolonged gestation, difficult or abnormal labor or delivery (dys- tocia), retained placenta, stillborn foals, late-term abor- tions, and greatly reduced milk production (agalactia). Foals born to affected mares may be uncoordinated and have limited immunity to infection.
Fescue and ryegrass species live in a mutually benefi- cial (symbiotic) relationship with an endophytic (in- side-the-plant) fungus Neotyphodium spp. The fungus, in combination with the plant, produces alkaloids simi- lar to those produced by the ergot fungus. The alka- loids provide the plant with increased tolerance to numerous stresses, including drought, cold, salinity, grazing, and pests. However, they also cause animal health problems.
The fungus is seed-borne, so the major preventive measure is to establish new pastures with endophyte- free seed. Seed of endophyte-free varieties of tall fes- cue and perennial ryegrass is now available, as are new varieties containing novel endophytes. These endo- phytes convey agronomic benefits without adverse ani- mal health effects.
When renovating an infested pasture, remove vegeta- tion mechanically or chemically. Do not replant with fescue or ryegrass for at least one season.
Grass-legume mixes reduce the impact of the toxins. Overseeding with red or white clover can be a tempo- rary measure to reduce animal health problems by di- luting forage with a high-quality, toxin-free species. Photosensitization
Photosensitization is induced by numerous compounds in a variety of plants (table 12.1). It resembles severe sunburn. In severe cases, the animal’s skin can slough off. Light-skinned animals and white areas on multicol- ored livestock (e.g., Hereford cattle) are most suscepti- ble.
In primary photosensitization, dermatitis and other skin disorders occur when plant compounds react with ultraviolet (UV) light in the animal’s blood. Plants asso- ciated with primary photosensitization include tall and creeping buttercup, buckwheat, St. Johnswort, and spring parsley.
Secondary photosensitization is more common than primary photosensitization. This disorder is due to
liver disease. Numerous plant compounds, such as pyrrolizidine alkaloids, destroy liver tissue. The weak- ened liver cannot break down phylloerythrin (a prod- uct of chlorophyll), allowing this compound to circulate through the blood. It interacts with UV light to cause severe symptoms on nonpigmented skin. Live-