university press, ames. fifth edition forages · 2010-11-20 · in: forages, volume ii: the science...

Mayland, Henry F. and Peter R. Cheeke. 1995. Forage-induced Animal Disorders. pp. 121-135.In: Forages, Volume II: The Science of Grassland Agriculture Fifth Edition, Iowa StateUniversity Press, Ames. FIFTH EDITION

FORAGESVolume II: The Scienceof Grassland Agriculture

UNDER THE EDITORIAL AUTHORSHIP OF

Robert F Barnes, ASA, CSSA, SSSA

Darrell A. Miller, University of Illinois

C. Jerry Nelson, University of Missouri

WITH 42 CONTRIBUTING AUTHORS

IOWA STATE UNIVERSITY PRESS, Ames, Iowa, USA

1995

121

Forage-inducedAnimal Disorders

HENRY F. MAYLANDAgricultural Research Service, USDA

PETER R. CHEEKEOregon State University

T

HIS chapter presents antiquality fac-tors of forage crops that affect animalperformance. A summary is given of

some herbage minerals that occur in concen-trations deficient or toxic to animals. Signifi-cant attention is given to organic compoundsthat are secondary products (1) of photosyn-thesis or (2) of associated organisms that alterforage quality and reduce animal perfor-mance.

MINERAL DISORDERSMineral element concentrations in herbage

may affect animal health because low levelsmay lead to deficiency, because high levelsmay lead to toxicity, or because one mineralelement interacts with another to reduce therelative availability. Herbage levels and rumi-nant diet requirements are given in Table 9.1.

Grass Tetany (Hypomagnesemis). Grasstetany is a magnesium (Mg) deficiency of zu-minants usually associated with their grazingof cool-season grasses during spring. Next to

HENRY (HANK) F. MAYLAND is Research SoilScientist with the Agricultural Research Service,USDA, Kimberly, Idaho. ills studies center on min-eral cycling in the soil-plant-animal system, withemphasis on magnesium, selenium, silicon, sulfur,and !inc.

PETER R. CHEESE is Professor of ComparativeNutrition in the Department of Animal. Sciences,Oregon State University. His research focus is thestudy of natural toxicants in feeds and poisonousplants. He has also extensively studied the nutri-tion of small herbivores.

bloat, this is probably the most important nu-tritional problem in grazing livestock. Annuallosses in the US are estimated at $50 millionto $150 million (Mayland and Sleper 1993).Grass tetany occurs in all classes of cattle(Boa taurus and Bas inclicus) and sheep (ailscries) but is most prevalent among older fe-males early in their lactation. Magnesiummust be supplied daily because it is excretedin urine and milk.

Plasma Mg levels are normally 18-32 mg /LBlood plasma or serum and urine values lessthan 18 mg IL are considered indicative of hy-pomagnesemia. Increasing concern is ex-pressed when blood plasma or urine levels fallbelow 15 mg/L (Mayland 1988; Vogel at al.1993), and the dramatic signs of tetany areevidenced at levels below 10 mg/L. Physicalsymptoms proceed from reduced appetite,dull appearance, and staggering gait to signsof increased nervousness, frequent urinationand defecation, muscular tremors, and ex..citability followed by collapse, paddling offeet, coma, and death.

Grass tetany is a complex disorder. First;-Mg requirements are greater for lactatingthan for nonlactating animals and greater forolder than for younger animals. Second, thereare differences among bovine breeds in sus-ceptibility to grass tetany with Brahman (Boaindicus) and Brahman crossbreeds beingmore tolerant and European breeds beingleast tolerant (Greene et al. 1989). Third,many factors influence Mg concentration andavailability in the herbage. The principal fac-tor is a high level of potassium (K), which neg-atively affects soil Mg uptake by plants andavailability of herbage Mg to animals. Also,

122 1. PRINCIPLES OF FORAGE MANAGEMENT

TABLE 9.1. Spectrum of nutrient-element concentrations found in grass and legume herbage and aguide to herbage concentrations required by sheep and cattle

Element

Concentrations inHerbage

concentrations forGrasses Legumes Sheep Cattle

(mg/g)Calcium Ca 2-5 2-14 3-4Chlorine' Cl 0.1-20.0 1 2Magnesium Mg 1-3 2-5 1.2 1.9'Nitrogen 10-40 10-50 10-15Phosphorus P 2-4 3-5 2.5 3.0Potassium K 10-30 20-37 2-6

Si 10-40 0.5-L5 not establishedSodium' Na 0.1-3.0 0.1-2.0 1 2Sulfur 1-4 2-5 1-2

(pg)Boron 3-40 30-80Cobalt Co 0.1-0.2 0.2-0.3 0.11 0.08Copper Cu 3-15 3-30 5-6 7-10dFluorine' 2-20 1-2Iodine' 0.004-0.8 0.5 0.5•IronbFe 50-250 50-250 30 40Manganese Mn 20-100 20-200 25 25Molybdenum Mo 1-5 1-10 not establishedSelenium' Se 0.01-1.0 0.03-0.7Zinc Zn 15-50 15-70 25-40

Sources: Herbage data are from the author's files, Gough et al. (1979), and Mayland (1983). Animal da-ta are adapted from Grace 11983), Grace and Clark (1991), and NRC (1984).

'Not required for plant growth.'Values in excess of 100-1501.4g are often reflective of soil contamination.42 mg4 if K and N are high.'Influenced by Mo and S.'2 pg/g in presence of goitrogens.

low levels of readily available energy, calcium(Ca), and phosphorus (P) and high levels of or-ganic acids, higher fatty acids, and nitrogen(N) in the herbage reduce the absorption of orretention of Mg by the animal. Forage Mg lev-els greater than 2.0 mWg dry matter and amilliequivalent 0 ratio of less than 2.2 forK./(Ca + Mg) are considered safe (Grunes andWelch 1989).

Agronomic practices to reduce risk poten-tial of tetany include splitting applications ofN and K fertilizers, liming acid soils withdolomitic rather than calcitic limestone, orspraying Mg on herbage (Robinson et al.1989). One might also use cultivars or specieshaving high Mg and Ca and low K concentra-tions (Sleper et al. 1989; Moseley and Baker1991; Mayland and Sleper 1993). Animal hus-bandry practices include assigning breedsand classes of livestock to pastures that areless susceptible to tetany (Greene et al. 1989).Magnesium could be supplemented throughadditions to herbage, drinking water, stocksalt, molasses licks, or other energy sources(Robinson et al. 1989).

Nitrate Poisoning. Nitrate (N0,-) accumu-lates in plant tissue because of luxuriant up-take of soil N when plant metabolism of N is

slow or even stopped. This condition is pro-moted by cool temperature, drought, or otherphysiological stress that slows growth(Wright and Davison 1964). Plant NO,- itselfis not normally toxic to animals, but it is usu-ally reduced to nitrite (NO2-) in the rumen. Ifthe NO,- is not reduced further, the accumu-lated NO2- causes various intensities ofmethemoglobinemia that may cause acutepoisoning of the animal (Wright and Davison1964; Singer 1972; Deeb and Sloan 1975).

Intensive applications of N fertilizer tosilage crops often result in appreciableamounts of NO,- in the herbage. During enail-ing, the NO,- is completely or partially de-graded (Spoelstra 1985). The end products areammonia (NH,) and nitrous oxide, with NO,-and nitric oxide occurring as intermediates.Silage crops containing high NO3- levelsshould be checked for NO,- before the ensiledcrops are fed to livestock.

Silofiller's disease is an illness of farmworkers caused by inhalation of nitric and ni-trous oxides from fermenting forages contain-ing high N concentrations. Good air ventila-tion will reduce the health hazard of thesenoxious gases.

The most common effect of NO,- poisoningis the formation of inetherooglobin that occurs

9. FORAGE-1NDUCED ANIMAL DISORDERS 123

when NO,- oxidizes the ferrous iron of bloodhemoglobin to ferric iron. This produces achocolate-brown methemoglobin that cannotrelease oxygen (0) to body tissue. As the tox-icity intensifies. the brownish-colored bloodcasts a brownish discoloration to the nonpig-inented areas of skin and the mucous mem-branes of the nose, mouth, and vulva. Clinicalsigns progress with staggering, rapid pulse,frequent urinating, and labored breathing,followed by collapse. coma, and death. Sub-lethal toxicity may be evidenced by abortionof pregnant females.

The rate and degree of NO reduction inthe rumen depend on the microflora presentand the energy available for continued reduc-tion of NO to NH,. This interaction of avail-able energy and NO reduction results inmixed responses. Furthermore, cattle andsheep can adapt to some extent to prolongedhigh levels of NO,- feeding (Wright and Davi-son 1964). Sheep have been poisoned by as lit-tie as 500 p.g N/g as NO,-, whereas in other ex-periments 8000 .ig N/g as NO,- had no effect(Singer 1972). Other data show that 2000 ilgN/g as NO,- in forage was the threshold limitfor cattle (Bush et al. 1979) while no problemoccurred with feeding forage containing 4600p.g N/g as NO,- (Davison et al. 1964).

Forages containing 3400 to 4500 ig /lig asNO,- should be considered potentially toxicand should be mixed with safer feeds prior touse (Wright and Davison 1964). Energy sup-plements will help in the complete reductionof inorganic N. Suspect forages should be test-ed for NO levels. Although risky, feeding ad-ditional forages low in NO would dilute theNO intake. Be aware that these test levelsare reported on an elemental N basis.

Sudangrass (Sorghum bicolor (L.1 Moench),sorghums (Sorghum app.), corn (Zea mays L.),and small grains are often indicted in NO,-poisoning. These crops are often heavily fer-tilized and when subject to drought, frost, orother stress may accumulate large concentra-tions of NO,-. Perennial grasses generally areless of a problem because they usually receivelower levels of N fertilizer and have greatertolerance of drought and frost. Legumes fixtheir own N into reduced forms and do notcontribute to NO,- poisoning.

Copper, Molybdenum, and Sulfur interac-tion. Copper (Cu) deficiency significantly af-fects ruminant livestock production in largeareas of North America (Gooneratne et al.1989), mainly in areas where soils are natu-rally high in molybdenum (Mo) and sulfur (S)

(Kubota and Allaway 1972). In ruminant nu-trition, the two-way and three-way interac-tions between these three elements areunique in their complex effects on animalhealth. Different clinical terms describe eachprimary factor affecting Cu nutrition.

Sheep consuming a complete diet, low in Sand Mo and with modest Cu (12-20 mg/kg drymatter), can succumb to Cu toxicity. Sheepgrazing another pasture of similar Cu concen-tration, but high in Mo and S, will produceCu-deficient lambs showing clinical signs ofswayback disease ( Suttle 1991). Copper-defi-cient cattle and sheep appear unthrifty andexhibit poor growth and reproduction. Copperdeficiency reduces the level of melanin pig-ments in hair and wool so that normally dark-colored fibers will be white or grey (Grace1983; Grace and Clark 1991). Low dietary Culevels may limit effectiveness of the immunesystem in animals.

Forage plants growing on soil or peat thatcontain high levels of Mo will produce a scour-ing disease known as molybdenosis. In thepresence of S, high intake of Mo can induce aCu deficiency due to formation of insolubleCu-Mo-S complexes in the digestive tract thatreduce the absorption of Cu. Several path-ways exist by which Cu x Mo x S interactionsmediate their effect on ruminants (Suttle1991). Most clinical signs attributed to thethree-way interaction are the same as thoseproduced by simple Cu deficiency and proba-bly arise from impaired Cu metabolism. Thetolerable risk threshold of Cu:Mo is not fixedat 3:1 but declines from 5:1 to 2:1 as pastureMo concentrations increase from 2 to 10 igMo/g. Risk assessment has been only partial-ly successful because the interactions are notyet fully understood (Suttle 1991).

Cattle are more sensitive than sheep tomolybdenosis; however, sheep are more sus-ceptible to Cu toxicity (Suttle 1991). Sheepshould not be allowed to graze pastures thatrecently received poultry or swine manure.This manure may contain high Cu concentra-tions originating from the Cu salts fed to poul-try or swine to control worms.

Copper-depleted animals should respondequally well to dietary Cu supplements, oralCu boluses or pellets, and Cu injections. Cop-per fertilization of Cu-deficient pasturesshould be done carefully because the rangebetween sufficiency and toxicity is quitesmall.

Selenium Deficiency and Toxicity. Herbageselenium (Se) concentrations are marginal to


severely deficient for herbivores in many ar-eas of the world. These include the PacificNorthwest and the eastern one-third of theUS (Kubota and Allaway 1972; Mayland et al.1989). Herbage Se concentrations of 0.03 gg/gare generally adequate. However, 0.1 gg/gmay be necessary when high S reduces Seavailability. Climate conditions and manage-ment practices that favor large increases inforage yield may dilute Se concentrations tocritical levels in herbage.

Selenium deficiency causes white muscledisease in lambs and calves. The young maybe born dead or die suddenly within a fewdays of birth because Se intake by the gestat-ing dam was inadequate. A delayed form ofwhite muscle disease occurs in young ani-mals, while a third form is identified asthrift in animals of all ages. Injectable Se, of-ten with vitamin E, or oral supplementation(selenized salt or Se boluses) may meet ani-mal requirements. Selenium fertilization ofsoils is legal only in New Zealand and Fin-land.

In many semiarid areas of the world, grass-es and forbs contain adequate (0.03-0.1 µg/g)to toxic (>5 µg/g) levels of Se for grazing ani-mal requirements. These areas includedesert, prairie, and plains regions of NorthAmerica where Se toxicity is observed in graz-ing animals. Some plants growing in these ar-eas will accumulate 100-1000 gg/g Se. Ani-mals eating these generally unpalatableplants will likely die. Grasses, small grains,and some legumes growing on the Se-richCretaceous geological materials may contain5-20 µg/g. Some animals eating this herbagemay die, but most are likely to develop chron-ic aelenosis called alkali disease. There is hairloss, and hoof tissues become brittle. In theseinstances, some animals may develop a toler-ance for Se as high as 25 µg/g.

A second chronic disorder in ruminants,called "blind staggers," or polioencephaloma-lacia, also occurs in these areas. This disor-der, while historically attributed to Se, is like-ly caused by excess S (Mayland, unpublisheddata). High sulfate levels in the drinking wa-ter and ingested herbage have led to the oc-currence of blind staggers (Beke and Hirona-ka 1990). Changing to high-quality,low-sulfate water and forage has reduced therisk.

Under marginal levels of Se, increased S re-duces the uptake of Se by plants and thebioavailability of dietary Se to animals. How-ever, the S antagonist has not been effectiveagainst Se toxicosis. Replacing high-Se forage

with low-Se forage is the most effective way ofcountering Se toxicity.

Cobalt, iodine, and Zinc. Cobalt (Co) deficien-cies in herbivores have been identified in thesoutheastern US and Atlantic seaboard statesand along the Wasatch Front in Utah (Kubo-ta and Allaway 1972). Cobalt is a metal cofac-tor in vitamin B 12 , which is required in energymetabolism in ruminants. The signs of Co de-ficiency include a transient unthriftiness andanemia leading to extreme loss of appetiteand eventually death. Two other conditionsattributed to Co deficiency are ovine (sheep)white liver disease and phalaris staggers(Graham 1991). The mechanism by whichoral Co supplementation prevents staggers isnot understood. Pasture herbage levels of atleast 0.11 and 0.08 pg Coig will provide ade-quate Co for sheep and cattle, respectively.Cobalt injections or oral supplements can begiven to animals. Pastures may also be fertil-ized with cobalt sulfate. Manganese (Mn) andiron (Fe) are antagonists to Co absorption(Grace 1983).

Plants do not require iodine (I); neverthe-less, herbage in the northern half of the US isgenerally deficient for animal requirements.These deficiencies are noted by the occurrenceof goiter in animals (Kubota and Allaway1972). The use of iodized salt easily meets io-dine needs of animals on pasture.

Zinc (Zn) concentration in pasture plantsranges from 10 to 70 gg/g but is most often inthe 10-30 gg/g range. In one study, cattle graz-ing forage having 15-20 gg/g gained weightfaster when supplemented with additional Zn(Mayland et al. 1980). Blood Zn levels werestatistically higher in supplemented than incontrol animals, but this difference was verysmall and would not be useful as a diagnostictool. There was no other obvious differencebetween the control and Zn-supplementedgroups. More information on Zn requirementsand diagnostic tests is needed.

Fluorosis and Silicosis. Plants do not requirefluorine (F), but herbage generally contains 1-2 p.g Flg, which is adequate for bone and toothdevelopment in animals. At higher levels, thedevelopment of fluorosis is influenced by theage, species, dietary form, and length of expo-sure. Fetuses and young animals are mostsusceptible to excess F. Otherwise, long-termintakes of 30 gg Flg may be tolerated by ru-minants before bone abnormalities appear(Underwood 1977). In areas of endemic fiuo-rosis, plants may be contaminated by nail,

9. FORAGE-INDUCED ANIMAL DISORDERS 125

rally fluoridated dust from rock phosphate orother smelters. During manufacture of super-phosphate and dicalcium phosphate, 25%-50% of the original F is lost. Excess F may al-so be absorbed by plants that are sprinklerirrigated with thermal groundwater. Rockphosphate supplement and naturally fluori-dated drinking water are the primary dietarysources of excess F.

Grasses contain more silicon (Si) than dolegumes and account for the large amount ofSi ingested by grazing animals. Silicon maybe needed in trace amounts by animals but isnot required by herbage plants. Silicon ad-versely affects forage quality and may affectanimal preference of plants. Silicon serves asa varnish on the cell walls, complexes mi-croelements and reduces their availability torumen flora, and inhibits the activity of cellu-lases and other digestive enzymes (Shewmak-er et al. 1989). The net effect of forage Si is toreduce dry matter digestibility by 3 percent-age units for each percentage unit of Si pre-sent (Van Soest and Jones 1968).

Silicon is also responsible for urolithiasis(urinary calculi or range waterbelly) in steers.Waterbeily is correlated negatively with urinevolume and water intake and only weakly re-lated to herbage Si. Management strategiesin high-Si areas include stocking only heifersand providing adequate drinking water. Iffeasible, the Ca:P ratio in the diet should bereduced and urine acidified by supplementinganimals with ammonium chloride (Stewart etal. 1991).

Soli Ingestion. Most grazing animals andsome humans eat soil- The ingestion may beindirect because herbage is dusty. Neverthe-less, animals may actively eat soil for un-known reasons. Ingested soil may serve as asource of minerals. In addition, soil may con-fain. residual chemicals applied to pasture orderived from atmospheric fallout. Some soilparticles are harder than tooth enamel andwill cause excessive abrasion and prematureloss of teeth. Ingested soil, as a possible cont-amnant, must also be considered in experi-mental pasture studies (Mayiand et al. 1977).

NATURAL TOXICANTS IN FORAGESPlanta are protected against herbivory (be-

ing eaten by vertebrate and invertebrate her-bivores) by many diverse physical and chemi-cal - means. Physical defenses include leafhairs, spines, thorns, highly lignifled tissue(e.g., wood), and growth habitat (e.g., pros-trate form), Chemical defenses of plants in-

dude a bewildering array of often complexchemicals that are toxic or poisonous to vari-ous herbivores. These chemicals may be syn-thesized by the plant itself or may be pro-duced by symbiotic or mutualistic fungigrowing with the plant. The defensive chemi-cals produced by the plant are considered sec-ondary compounds, as distinct from the pri-mary compounds that are essential in plantmetabolism. Secondary compounds (e.g., alka-loids) do not function directly in cellular me-tabolism but apparently are synthesized toserve as the plant's defensive arsenal.

Chemicals synthesized by fungi are knownas rnycotoxim, which may be produced by fun-gi living on or in forage plants. Mycotoxinsare responsible for many disorders of grazinganimals. For example, the endophytic fungi oftall fescue (Festuca arundinacea Schreb.) pro-duce ergot alkaloids that cause fescue foot,summer fescue toxicosis, and reproductivedisorders, while endophytes in perennial rye-grass (Latium perenne L.) produce Iolitrems,which cause ryegrass staggers. In the US, to-tal livestock-related losses attributed to thetall fescue endophyte are estimated between$500 million and $1 billion a year (Ball et al.1993). The economic impact of poisonousplants on livestock production has been re-ported by James at al. (1988).

Tbxins of plant origin can be classified intoseveral major categories, including alkaloids,glycosides, proteins and amino acids, andphenolics (tannins) Alkaloids are bitter sub-stances containing. N in a heterocyclic ring -structure. There are hundreds of different at

Fig,.:. 9.1. An example of ryegrass staff aneurological disorder of livestock grazing ousiow. ,phyts-infected perennial ryegrass paatoresoLalitreni B is the major toxin involved. Cluirtesrof R. E. G. Keogh.


kaloids, which are classified according to thechemical structure of the N-containingring(s). For example, the pyrrolizidine alka-loids in common pasture weeds (Senecio app.)

have a pyrrolizidine nucleus of two five-mem-bered rings, while ergot alkaloids have an in-dole ring structure. Lupins (Lupinus app.)contain quinolizidine alkaloids, which arebased on two six-membered rings.

Glycosides are composed of a carbohydrate(sugar) portion linked to a noncarbohydrategroup (the aglycone) by an ether band. Exam-ples are cyanogenic glycosides, glucosinolates,saponins, and coumarin glycosides. Their tox-icity is associated with the aglycone, such ascyanide in cyanogenic glycosides. Glycosidesare hydrolyzed by enzymatic action. releasingthe aglycone. This often occurs when theplant tissue is damaged by wilting, freezing,mastication, or trampling. A good example ofthis is the production of toxic cyanide whenforage sorghums such as sudangrass arefrosted. The breakdown of cell structure re-leases the glycoside from storage vacuoles, al-

lowing it to be hydrolyzed by enzymes in thecytosol and to release free cyanide.

Many toxic amino acids occur in plants.One of the best known is mimosine, a toxicamino acid in the tropical forage legume Leu-caena leucocephala de Wit. Others includelathyrogenic amino acids in Lathyrus spp., in-dospecine in Indigofera spp., and the brassicaanemia factor, which is caused by S-methyl-cysteine sulfoxide, a metabolic product of for-age brassicas (Brassica spp.).

Phenolic compounds, which include the con-densed and hydrolyzable tannins, are sub-stances containing aromatic rings with one ormore hydroxyl groups. The hydroxyl groupsare chemically reactive and can react withfunctional groups of proteins to form indi-gestible complexes. The tannin-protein com-plexes are astringent and adversely affectfeed intake. All plants contain phenolic com-pounds. In some cases, their type or concen-tration may cause negative animal responses.These include reduced feed intake and pro-tein digestibility of birdsfoot trefoil (Lotus cor-

Fig. 9.2. (a) A steer in Australiathat has been grazing on Leucae-na leucocephala for aeveralmonths. Note the lose of hair andunthrifty appearance due to theeffects of mimosine, a tome aminoacid that occurs in Lescansa. (6)The same steer a few months o

receiving a dose of rumen bac-teria that detoxifies mimosine.These photographs illustratequite dramatically the potential ofrumen microbes to detoxify someof the natural toxins in plants.Courtesy of R. J. Jones.


niculatus L.) and sericea lespedeza (Les-pedeza cuneata (Dum.-Cours.i G. Don). Oak(Quercus spp.) poisoning is caused by tanninsin oak browse. Many tree legumes used intropical agroforestry can contain sufficientlevels of tannins to impair animal perfor-mance.

Toxins and Animal Disorders Associatedwith Forage Legumes. Some animal disor-ders are associated with forage legumes. Forexample, pasture bloat is a very commonproblem with ruminants grazing many foragelegumes, such as alfalfa (Medicago sativa L.)and clovers (Mitchum spp.). Pasture bloat iscaused by rapid release of cell contents of suc-culent, immature legume forage during ru-men fermentation. The succulent materialhas a rapid rate of cell rupture, releasing thesoluble proteins and fermentable carbohy-drates. Soluble proteins are foaming agents,causing the formation of a stable foam in therumen, which prevents eructation (belching)of rumen gases formed by the fermentation.High sugar content of lush legume forage sup-ports a vigorous microbial population, produc-ing large amounts of gas. The combination ofvigorous gas production and presence of foam-ing agents produces a stable frothy foam,which blocks the esophagus, culminating inrumen distention and respiratory paralysis.Bloat can be minimized by maintaining atleast 50% grass in the pasture or by giving an-imals access to blocks containing an an-tifoaming agent (e.g., poloxalene).

Some legume forages, such as birdsfoot tre-foil, cicer milkvetch (Astragalus cicer L.).sericea lespedeza, and sainfoin (Onobrychisuiciifolia Scop.), do not cause bloat. Theseplants contain tannins, which at low concen-trations complex with the cytoplasmic pro-teins and prevent their ability to foam. How-ever, Lespedeza app. and trefoils (Lotus spp.)can contain sufficiently high tannin levels toinhibit animal performance by reducing feedintake and protein digestibility. Althoughsaponins are foaming agents that occur inmost bloat-producing legumes, they do notseem to have a significant role in bloat (Majaket al. 1980).

Phytoestrogens occur in many foragelegumes, including alfalfa, red clover (T.pratense L.), subterranean clover (T subterra-neum L.), and other Trifolium spp. In clovers,the estrogenic compounds are mainlyisoflavones such as formononetin, genistein,biochanin A, and diadzein, while coumestroland other coumestans are the principal estro-

gens in alfalfa and medics, like black medic(Medicago lupuiina L.).

Historically, phytoestrogens have had theirgreatest impact on reproduction of sheepgrazing subterranean clover in Australia."Clover disease" is characterized by a dramat-ic decrease in fertility of ewes, along with ab-normalities of the genitalia. Since the identi-fication of phytoestrogens as the causativeagents of clover disease, Australian plantbreeders have selected for and developed low-estrogen cuitivars of subterranean clover.This has largely eliminated the problem ofclover-induced infertility in Australia.

The phytoestrogens owe their physiologicalactivity to their structural resemblance to en-dogenous estrogens. allowing them to bind toestrogen receptors and elicit an estrogen re-sponse (Adams 1989). The activity of phytoe-strogens is altered by rumen fermentation.Biochanin A and genistein are converted to in-active compounds in the rumen, while for-mononetin is bioactivated to the more potentcompounds daidzein and equal (Adams 1989).

Toxins associated with specific foragelegume species will be briefly described. Fur-ther detail is provided by Cheeke and Shull(1985).

RED CLOVER (Trlfolium pretense L.) When in-fected with the black patch fungus (Rhizocto-nia leguminicola Gough & ES Elliott), redclover hay may contain the indolizidine alka-loid slaframine. Slaframine is a cholinergicagent that causes excessive salivation (cloverslobbers), eye discharge, bloat, frequent uri-nation, and watery diarrhea. These effects aredue to stimulation of the autonomic nervoussystem. The fungal infection and potentialtoxicity develop most rapidly in periods ofhigh humidity. Prompt removal of the toxicforage from livestock generally alleviates allsigns of intoxication.

WHITE CLOVER (Taonum repens L). Whiteclover may contain cyanogenic glycosides.These may have some importance in confer-ring resistance to slugs and other pests. Theconcentration of cyanogens in white clover isnot sufficiently high to cause livestock poison-ing but may contribute to lower midsummerpalatability of the clover.

ALSIKE CLOVER (Tiff°Hum hybricium L). Poi-soning from alsike clover has been reported inCanada and the northern US. It has not beenconclusively proven to be caused by the clover,but circumstantial evidence strongly suggests


that it is clover caused (Nation 1991). Toxici-ty signs include photosensitization, neurolog-ical effects such as depression and stupor, liv-er damage, and contradictory effects on liversize. Sometimes, the liver is extremely en-larged, in others, it is shrunken and fibrotic.

SWEETCLOVER (Meiliatus app.). Sweetcloverpoisoning has been an important problem inNorth America. Sweetclover containscoumarin glycosides, which are converted bymold growth to dicoumarol. Dicoumarol is aninhibitor of vitamin K metabolism, thus caus-ing an induced vitamin K deficiency. Sweet-clover poisoning causes a pronounced suscep-tibility to prolonged bleeding and hemor-rhaging because of the essential role of vita-min K in blood clotting. Wet, humid weatherthat favors mold growth during curing ofsweetciover hay increases the likelihood ofpoisoning. Cattle are the main livestock af-fected.

Moldy sweetclover hay should not be fed orshould be used with caution. Ammoniation ofstacked hay with anhydrous ammonia re-duces dicoumarol levels. Animals with signsof sweetciover poisoning are treated with in-jections of vitamin K. Low-coumarin cultivaraof sweetclover have been developed andshould be used in areas where sweetcloverpoisoning is a problem. Coumarin has a vanil-lalike odor and is responsible for the charac-teristic smell of sweetciover.

OTHERS. Additional forage legumes containvarious_ toxins. As already mentioned, birds-foot trefoil and lespedeza contain tannins.Crownvetch (Corona la varies L.) contains gly-cosides of 3-nitropropionic acid, which are me-tabolized in ruminants to yield NO,-. Concen-trations are rarely sufficient to cause NO,-poisoning, but the glycosides contribute to alow palatability of crownvetch. Cicermilkvetch, a minor forage legume in thenorthern US, has caused photosensitizationin cattle and sheep (Marten et al. 1987, 1990).

The seeds of common (VIcia sativa L) andhairy vetch (V villosa Roth) are poisonous.They contain toxic lathyrogenic amino acids,which cause damage to the nervous system,with signs such as convulsions and paralysis.This occurs primarily in nonruminants thatconsume seeds as a contaminant of grain.Hairy vetch poisoning of ruminants has beenreported in the US (Kerr and Edwards 1982)and South Africa (Kellerman et al. 1988).Signs include severe dermatitis, skin edema,conjunctivitis, corneal ulcers, and diarrhea.About 60% of affected animals die. The toxic

agent in hairy vetch has not been identified.Many Lathyrus spp. contain toxic amino

acids that cause neurological problems andskeletal defects known as lathyrism. Flatpea(L. sylvestris L.) has potential as a forage cropfor degraded soils such as reclaimed strip-mined areas. Flatpea is nearly free of toxicity;but Foster (1990) notes that 'the question offiatpea toxicity must be answered conclusive-ly before this plant can be recommended foruse by livestock producers." Toxicity of ilatpeahay to sheep, with typical signs of neuro-lathyrism, has been reported by Rasmussenet al. (1993).

Lupinus app. contain a variety of alkaloidsof the quinolizidine class. The sweet lupinessuch as L. albus L. and L. angustifolius L.contain low levels of various alkaloids (e.g.,cytisine, sparteine, lupinine, lupanine). Thesecause feed refusal and neurological effects.Sheep are frequently poisoned by wild lupineson rangelands, as they avidly consume theseedpods. On rangelands in western NorthAmerica, there are many species of wildlupines that are toxic to livestock. Speciessuch as L. sericeus Pursh., L. caudatus Kel-logg, and L. argenteus var. tenellus (Dougl. exG.Don) D.Dunn (also known as L. laxiflarus)contain anagyrine, an alkaloid that is terato-genic in cattle. It causes crooked calf disease,if consumed by pregnant cows during days 40-T0 of gestation. Severe skeletal deformationsin the fetuses may occur. This teratogenic al-kaloid does not occur in domesticated Lupi-nus app.

In Australia., sweet lupines are extensivelygrown as a grain crop; sheep are grazed onthe lupine stubble after harvest. Often thestems of lupines are infected with a fungus(Phomapsis leptostromiforrnis [Kahn] Bubakin Kab. & Bubak) that produces toxic pho-mopsins. These mycotoxins cause liver dam-age, including fatty liver and necrosis, even-tually leading to liver failure and death. Thiscondition is referred to as lupin/ma.

Leucaena contains a toxic amino acid,. mi-=eine. In the rumen, mimosine is convertedto various metabolites, including 3,4-dihy-clroxypyridine (DHP). Both mimosine andDHP are toxic to ruminants, causing dermati-tis and poor growth (mimosine) and goitro-genic (thyroid-inhibitory) effects. Australianresearchers (Jones and Megarrity 1986)learned that Hawaiian ruminants, adapted toa leucaena diet, had mimosine-degrading ru-men bacteria that eliminated the toxicityThese bacteria have now been introduced intocattle in Australia, allowing leucaena.to beused as a productive source of high: protein


forage (Quirk et al. 1988). Hammond et al.(1989) in Florida also reports detoxification ofmimosine by rumen microbes.

Various other tropical legumes contain tox-ic factors. Many Indigofera app. contain thetoxic amino acid indospecine (Aylward et al.1987). The jackbean (Canavalia ensiformis[L.] DC) contains canavanine, an amino acidanalog of arginine (Cheeke and Shull 1985).Generally, the grazing diet contains otherspecies that dilute the effects of the toxins.

Toxins and Animal Disorders Associatedwith Grasses. In contrast to herbaceousplants, grasses are generally not well defend-ed chemically. Most grasses have coevolvedwith grazing animals and by growth habitsurvive frequent defoliation. Hence, there arefew intrinsic toxins in common forage grasses.More frequent are mycotoxins produced byfungi living in or on grasses. Fungi livingwithin plant tissues or tissue spaces arecalled endophytes. Many livestock syndromesare attributed to endophyte toxins. Examplesof toxins intrinsically present in grasses arethe alkaloids of Phalaris spp., cyanogens inforage sorghums (e.g., sudangrass), and ox-alates in many tropical grasses. These havebeen reviewed by Cheeke (1995).

PHALARIS POISONING. This poisoning pro-duces two syndromes in livestock: a neuraldisorder (phalaris staggers) and a suddendeath syndrome. These are disorders of bothsheep and cattle consuming various Phalarisapp., either by grazing or as hay or other con-served feed. Phalaris poisoning has particu-larly y been reported from Australia and. NewZealand, primarily in animals grazing pas-tures containing P. aquatics L. (formerly P.tuberose L). In the US, phalaris poisoning ofsheep P. earoliniana Walt. is associated withP..1:oroliniana Walt. (Nicholson et al. 1989)and. P. aquatics L. (East and Higgins 1988).Reed canarygrass (P. arundinacea L.) poison-inv.:of sheep has been observed in NewZialand (Simpson et al. 1969). Contaminationoisa -sheep feedlot diet with a source ofphalaris alkaloids led to an outbreak of stag-ger!, in California (Lean et al. 1989).

Phalaris staggers is characterized by con-vulsiousland.other neurological signs due tobrain:damage, culminating in mortality. Thesyndrome is caused by tryptamine alkaloidsin:Phalaris app., which are believed to inhibitserotonin.. receptors in specific brain andsphial cord nuclei (Bourke et al. 1990). Thesetryptamine alkaloids are responsible for thelow palatability of the grass and poor perfor-

mane of animals on reed canarygrass pas-tures (Marten et al. 1976). Low-alkaloid culti-vars of reed canarygrass have been developedthat give improved animal productivity(Marten et al. 1981; Wittenberg et al. 1992).The cause of the phalaris sudden death syn-drome has not been conclusively identifiedbut appears not to be the tryptamine alka-loids (Bourke et al. 1988). As many as four dif-ferent factors, including a cardiorespiratorytoxin, thiarninase and amine cosubstrate,cyanogenic compounds, and NO,- compounds,have been implicated (Bourke and Carrigan1992).

HYDROCYANIC ACID (HCN) POISONING. For-age sorghums such as sudangrass containcyanogenic glycosides, from which freecyanide can be released by enzymatic action.The glycosides occur in epithelial cells of theplant, while the glycoside-hydrolyzing en-zymes are in mesophyll cells. Damage to theplant from wilting, trampling, frost, droughtstress, etc., results in the breakdown of theplant structure, causing exposure of the gly-cosides to the hydrolyzing enzymes and for-mation of free cyanide (Fig. 9.3). Cyanidecauses acute respiratory inhibition by inhibit-ing the enzyme cytochrome oxidase. Signs ofpoisoning include labored breathing, excite-ment, gasping, convulsions, paralysis, anddeath.

The cyanide potential and risk of poisoningdecrease as forage sorghums mature (Wheel-er et al. 1990). The likelihood of acute cyanidepoisoning may be greater when feedingsorghum hay than when grazing the freshplant because of the more rapid dry matterintake. Ground and pelleted sorghum- haymay be especially toxic because of the rapidrate of intake and cyanide release (Wheelerand Mulcahy 1989). Ensiling markedly re-duces the cyanide risk.

Nitrogen fertilization of forage sorghumsenhances the cyanide risk. Special caution isneeded when livestock is grazing lush, inuna-hire forage sorghums and when frost has oc-curred. Laboratory analysis of the cyanide po-tential of sorghum hay is advisable (Wheelerand Mulcahy 1989). Cattle deaths onsorghum pastures occur most frequently inlate summer or early fall, following anovernight frost.

OXALATE POISONING. Many tropical grassescontain high levels of oxalate. Upon ingestionby ruminants, the oxalate complexes dietaryCa and forms insoluble calcium oxalate. Thisleads to disturbances in Ca and P metabolism


FIg. 9.3. Forage sorghums likesudangrass are excellent feeds forgrazing animals. However theymust be managed carefully toavoid cyanide toxicity. Courtesy ofC. Mukohy.

involving excessive mobilization of bone min-eral. The demineralized bones become fibroticand misshapen, causing lameness and "big-head" in horses. Ruminants are less affected,but prolonged grazing by cattle and sheep ofsome tropical grass species can result in se-vere hypocalcemia, i.e., Ca deposits in the kid-neys and kidney failure. Tropical grasses thathave high oxalate levels include Setaxia spp.,Brachiaria spp., buffelgrass (Cenchrus cil-iaris L.), Tangola' digitgrass (Digiteria eri-antha Steud.), and kikuyugrass (Pennisetumclandestinum Hochst. ex Chiov.). Provision ofmineral supplements high in Ca to grazinganimals overcomes the adverse effect of ox-alates in grasses.

FACIAL ECZEMA. Many livestock poisons arecaused by fungi growing on or in grass. Otherorganisms like nematodes, insects, and bacte-ria are sometimes involved. Facial eczema ofgrazing rwninants is a classic example of sec-ondary or hepatogenous photosensitization,due to liver damage. Facial eczema is a majorproblem of sheep and cattle on perennial rye-grass pastures in New Zealand and has beenreported sporadically in other countries.

The fungus Pithomyces chartarum (Berk. &M.A. Curtin) M.B. Ellis grows on the dead lit-ter in ryegrass pastures and produces largenumbers of spores. The spores contain a he-patotoxin, sporidesmin, which is only slowlybroken down in the liver. Spores are con-

slimed during grazing of infected pastures,which leads to sporidesmin-induced liverdamage. The damaged liver is unable to me-tabolize phylloerythrin, a metabolite ofchlorophyll, which then accumulates in theblood. Phylloerythrin is a photodynamicagent that reacts with sunlight, causing se-vere dermatitis of the face, udder, and otherexposed areas.

There are species differences in susceptibil-ity to sporidesmin: for example, goats aremuch more resistant to facial eczema thansheep, probably because of a faster rate ofsporidesmin detoxification in the liver (Smithand Embling 1991).

ERGOT. Ergotism is another mycotoxicosisassociated with grasses. Seed heads of manygrasses are susceptible to infection with Ckiv-iceps paspali F Stevens & JO Hall and otherClaviceps spp. In the US, dallisgrass (Pas-paium dilatatum Pair.) poisoning is the majorC/aviceps-caused ergotism. Ergot alkaloidscause vasoconstriction and reduced blood sup-ply to the extremities, resulting in sloughingof ear tips, tail, and hooves. There are alsoneurological effects, including hypereircitabil-ity, incoordination, and convulsions. Ergotismcan be avoided by not allowing grasses to setseed.

TALL FESCUE TOXICOSIS. Tall fescue infect-ed with the endophytic fungus (Aereinaniu,m


coenophialum Morgan-Jones & Gams) is re-sponsible for three types of livestock disorderswhen animals consume forage or seed. Theseinclude fescue foot, summer fescue toxicosis,and fat necrosis. Animal performance is re-duced, and reproduction is impaired.

Tall fescue toxicity is caused by ergot alka-loids such as ergovaline, which is produced bythe endophyte growing systemically withinthe plant tissues. One effect of ergovaline isthe inhibition of prolactin from the pituitarygland. Physiologically, tall fescue toxicosisand its associated reproductive effects are ex-plained by reduced prolactin levels that, viaeffects on brain neurotransmitters, inhibitsmooth muscle contraction. Because prolactinalso stimulates lactation, agalactia, i.e., lackof milk production, occurs with consumptionof endophyte-infected tall fescue. This is par-ticularly severe in horses (Porter and Thomp-son 1992). The problems associated with en-dophyte-infected tall fescue are furtherdescribed in Chapter 28, Volume 1.

RYEGRASS TOXICITY. There are several live-stock disorders associated with consumptionoLryegrass. Besides facial eczema (alreadydescribed), two other major syndromes areperennial ryegrass staggers and annual rye-grass (L. multiflorum Lam-) toxicity.

Perennial ryegrass staggers is caused bycompounds called tremorgens. Affected ani-mals exhibit various degrees of incoordinationand other neurological signs (head shaking,stumbling and collapse, and severe musclespasms), particularly when disturbed orforced to run. Even in severe cases, there arenoepathological signs in nervous tissue.feitted animals usually spontaneously recover.Withisheep, ryegrass staggers is primarily aproblem in animal management, as affectedanimals are difficult to move from one pas-

: biretta another. Growth rate of the animal is.. r- riliere reduced (Fletcher and Barren 1984). InArsitralia and New Zealand, ryegrass stag-

- game:curs in sheep, cattle, horses, and deer.Itthas been reported in sheep and cattle in

(Gaffey et a1.1991). It also occurs in!.; sheep,-grazing winter forage and stubble

;.i. realdue of endophyte-enhanced turf-type rye-; passer in Oregon.nerramain causative agents of ryegrasa stag-gess-areca group of potent tremorgens calledlolitrems, the most important of which is

B (Gallagher at al. 1984). Lolitrem Bice• potent inhibitor of neurotransmitters inthekbraim. The lolitrems are produced by anelidophytic fungus, Acremonium Witt, which

is often present in perennial ryegrass. Turfcultivars of both tall fescue and perennial rye-grass are often deliberately infected with en-dophytes because the endophyte increasesplant vigor, in part by producing ergot alka-loids (A. coenophialum) and tremorgens (A.

While the presence of the endophyte isadvantageous when the grass is used for turfpurposes, it has negative effects on animalperformance when the grass is consumed bylivestock.

In Australia and South Africa, annual rye-grass toxicity is a significant disorder of live-stock. It has an interesting etiology; involvingannual ryegrass, a nematode, and bacteria.Although the neurological signs are superfi-cially similar, annual ryegrass toxicity andryegrass staggers are totally different disor-ders. In contrast to the temporary incoordina-tion seen with ryegrass staggers, there isbrain damage with annual ryegrass toxicity.The neurological damage is evidenced by con-vulsions of increasing severity that terminatein death.

Annual ryegrass toxicity is caused bycorynetoxins, which are chemically similar instructure to the tunicamycin antibiotics.Corynetoxins are produced by a Ckwibacterspp. (formerly designated Carynebacteriumspp.). This bacterium parasitizes a nematode(Anguina agrostis) that infects annual rye-grass. Ryegrass is toxic only when infectedwith the bacteria-containing nematode. Thenematodes infect the seedling shortly aftergermination, and the larvae are passively car-ried up the plant as the plant stem elongates.They invade the florets, producing a nema-tode gall instead of seed. When consumed byanimals, corynetoxins inhibit an enzyme in-volved in glycoprotein synthesis, leading todefective formation of various blood conrpo--nents of the reticulo-endothelial system; Thisimpairs cardiovascular function and vascularintegrity, causing inadequate blood supply tothe brain.

Corynetoxins have been identified in othergrasses besides annual ryegrass, includingPolypagon and Agrostis spp. (Finnie 1991;Bourke at al. 1992). Annual ryegraas toxicitycan be avoided by not allowing animals tograze mature grass containing seed heads orby-clipping pastures to prevent seed head de-velopment. In Australia, these measures are-often impractical because of the extensiveland areas involved.

OTHER GRASS POISONS. Kikuyu grass is acommon tropical forage that is occasionally


toxic to livestock (Peet et al. 1990). Clinicalsigns include depression, drooling, muscletwitching, convulsions, and sham drinking(Newsholme et al. 1983). There is a loss of ru-men motility and severe damage to the mu-cosa of the rumen and omasum. In many butnot all cases, kikuyu poisoning occurs whenthe pasture is invaded by armyworm(Spodoptera exempta {Walker) [Lepidoptera,Noactuidael). The causative agent has notbeen identified, and it is not conclusivelyknown if the armyworm has a role in the tox-icity.

Photosensitization of grazing animals oftenoccurs with Panicum and Brachiaria spp.(Bridges et al. 1987; Cornick et al. 1988;Graydon et al. 1991). The condition is usuallyaccompanied by crystals in and around thebile ducts in the liver. Miles et al. (1991) haveshown that the crystals are metabolites ofs aponins, which are common constituents ofPanicum spp. The crystals impair bifiary ex-cretion, leading to elevated phylloerythrinlevels in the blood, causing secondary (hepat-ic) photosensitization, as previously de-scribed.

Toxins in Other Forages. Most common for-ages are legumes or grasses. A few others aresometimes used, including buckwheat(Fagopyrum esculentum Moench.), spinelesscactus (Opuntia spp.), saltbush (Atriplexspp.), and forage brassicas such as kale (B.oleracea L.), rape (B. napes L.), cabbage (B.oleracea L.), and turnips (B. rapa L.).

Brassica app. contain glucosinolates (goitro-genii) and the brassica anemia factor. Glucosi-nolates are primarily of concern in the bread-caa grown for seed, such as rapeseed andmustard. Forage brassiest:, contain a toxicamino acid, S-methylcysteine sulfoxide (SM-CO), the brassica anemia factor. Ruminantsoften develop severe hemolytic anemia onkale or rape pastures, and growth is marked-ly reduced.

S-methylcysteine sulfoxide is metabolizedin the rumen to dimethyl disulfide, an oxidantthat destroys the red blood cell membrane-This leads to anemia, hemoglobinuria (redurine), and liver and kidney damage. Mortal-ity frequently occurs. Because the SMCO con-tent of brassicas increases with plant maturi-ty, it is not advisable to graze mature brassicaor to use these crops for late winter pasture intemperate areas. Avoiding the use of S andhigh N in fertilizer reduces SMCO levels andtoxicity. Brassica anemia is reviewed byCheeke and Shull (1985) and Smith (1980).

Buckwheat is a fast-growing, broad-leavedannual sometimes grown as a temporary pas-ture. Buckwheat seed and forage contain aphotosensitizing agent, fagopyrin. This com-pound is absorbed by the body and moved tothe surface of the skin, where it reacts withsunlight, causing photodermatitis (photosen-sitization). Light-skinned animals are partic-ularly susceptible.

Acute bovine pulmonary emphysema mayoccur when cattle are moved from sparse drypasture to lush grass, legume, or brassicapasture. The abrupt change in pasture typeresults in a disturbance in the rumen mi-crobes, leading to excessive conversion of theamino acid tryptophan to a metabolite, 3-methyl indole (3-MI). The 3-MI is absorbedand is toxic to the lung tissue, causing pul-monary edema and emphysema (Carlson andBreeze 1984). The condition, also called sum-mer pneumonia, may be fatal. Provision ofsupplementary feed before moving cattle ontolush meadows is helpful in preventing the dis-order.

Animal Metabolism of Plant Toxins. Plantsand animals have coevolved. As plants havedeveloped the enzymatic means to synthesizedefensive chemicals, animals have evolveddetoxification mechanisms to overcome theplant defenses. The most fundamental ofthese are the drug-metabolizing enzyme sys-tems of the liver, such as the cytochrome P450system. This enzyme system (also called themixed function oxidase system) oxidizes hy-drophobic, nonpolar substances such as planttoxins and introduces a hydroxyl group. Thehydroxyl group increases the water solubilityof the compound, mainly by providing a site toreact (conjugate) with other water- solublecompounds such as amino acids (e.g., glycine),peptides (glutathione), and sugars (e.g., ght-curonic acid). These conjugated compounds,such as glucuronides, are much less toxic andcan be excreted in the urine or bile (e.g.,saponin glucuronides in the bile of animalsconsuming Panicum app.). Most differences insusceptibility among livestock species to planttoxins are due to differences in liver metabo-lism. Some toxins are bioactivated, or mademore toxic, because of liver metabolism (e.g.,afiatoxin or slaframine). The relative rates atwhich the active metabolites are formed anddetoxified determine the extent of cellulardamage.

On an evolutionary basis, browsing animalssuch as sheep and goats have been exposed togreater concentrations of plant toxins than

9. FORAGE4NDUCED ANIMAL DiSORDERS 133

have grazing animals such as horses and cat-tle. As a result, these browsing species gener-ally are more resistant to many plant toxinsthan are the strict grazers, and they findplants containing toxins more palatable thando cattle and horses (Cheeke 1991). Some-times, as with pyrrolizidine alkaloids inSenecio spp., the resistance of sheep andgoats is due to a lower rate of bioactivation ofthe compounds in the liver to the toxicmetabolites (Cheeke 1988).

Browsing animals are better able thangrazers to resist adverse effects of dietary tan-nins and phenolic compounds, which are com-

mon constituents of shrubs, trees, and otherbrowse plants. For example, deer, which arebrowsers, have salivary tannin-binding pro-teins that counteract the astringent effects oftannins (Austin et al. 1989). These salivaryproteins are absent in sheep and cattle.Mehansho et al. (1987) reviews the roles ofsalivary tannin-binding proteins as animaldefenses against plant toxins. Resistance totannin astringency would result in tannin-containing plants being more palatable tobrowsers than to grazers, which lack the tan-nin-binding proteins.

In ruminants, metabolism of toxins by ru-men microbes is an important factor in alter-ing sensitivity to plant toxins. in some cases,e.g., cyanogenic glycosides and the brassicaanemia factor, the toxicity is increased by ru-men fermentation. Sometimes, e.g., mimosineor oxalate toxicity, the compounds are detoxi-fied by microbial metabolism. The toxic aminoacid mimosine in Leucaena spp. has been ofparticular interest in this regard. As dis-cussed earlier, the successful use of leucaenaas a high-protein forage was not possible inAustralia and many other areas until nuni-nants were dosed with mimosine-degradingbacteria.

QUESTIONS

1.What is the genetic potential of various foragespecies for increased palatability, digestibility,and bioavailability of elements like Mg, Ca, andSe?

2. What is the empirical relationship of bioavail-able Cu to forage Cu, Mo, and S concentrations?

3. What affect does Si and soil ingestion have ondigestive processes and bioavailability of traceelements?

4.What is the toxicity of excess S in herbage andits role in animal nutrition and health, specifi-cally polioencephalomalacea?

5. Bow does the element requirement for nutrition(production functions) differ from that requiredfor adequate immune response in animals?

6. Why do many plants contain toxic substances?7. Why does pasture bloat occur more often with

legumes than with grasses? Why are somelegumes nonbloating?

8. How have the problems associated with Leucae-na leucocepiutla toxicity been overcome? Doesthat technique have potential application withother plant toxins?

9. What are endophytes? What is the role of endo-phytes in perennial ryegrass staggers?

10. Under what conditions is sudangrass most tox-ic? How can toxicity be prevented?

11.Why do cattle, sheep, and goats differ in theirsusceptibility to plant toxins?

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