Clinica Bovina - Acidosis

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F. N. Owens, D. S. Secrist, W. J. Hill and D. R. Gill

Acidosis in cattle: a review

1998. 76:275-286. J Anim Sci

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1P r e se n t ed a t a s ym p os iu m t it le d B u d B r it t on M em or ia lSymposium on Metabolic Disorders of Feedlot Cattle, Ju ly 1996,following the ASAS 88th Annu. Mtg. , Rapid City, SD. Financialsuppor t was provided by Elanco Animal Health . Approved forpublica t ion by the Director, Oklahoma Agr ic . Exp. S ta . Thisresearch was suppor ted under Project H-2123.

2To whom cor respondence should be addressed.Received September 3, 1996.Accepted March 27, 1997.

Acidosis in Cattle: A Review 1

F. N . Ow e ns 2 , D . S . S ec ris t, W. J . Hill, a nd D . R. Gill

Oklahoma Agricul tura l Exper iment Sta t ion, Animal Science Depar tment , St il lwater 74078

ABSTRACT: Acute and chronic acidosis, conditionstha t follow ingestion of excessive am ount s of r eadilyfermented carbohydrate , are prominent product ionproblems for ruminan ts fed diets rich in concentra te.Often occurring during adaptation to concentrate-richdiets in feedyards , chronic acidosis may cont inueduring the feeding period. With acute acidosis, rumi-nal acidity and osmolality increase markedly as acidsand glucose accumulate; these can damage the rumi-nal and intestinal wall, decrease blood pH, a nd causedehydrat ion that proves fa ta l . Lamini t is , pol ioen-cephalomalacia, an d liver a bscesses often accompa ny

acidosis. Even a fter animals recover from a bout of acidosis, nutrient absorption may be r etarded. Withchronic acidosis, feed inta ke typically is reduced butvariable, and performance is depressed, probably dueto hypertonicity of digesta. Acidosis control measures

include feed additives that inhibit microbial st rainsthat produce lactate, that stimulate activity of lactate-using bacteria or starch-engulfing ruminal protozoa,and that reduce meal size. Inoculation with microbials t r a ins capable of p reven t ing glucose or lacta t eaccumulat ion or metabol iz ing lacta te a t a low pHshould help prevent acidosis. Feeding higher amountsof dietar y r oughage, processing gra ins less t horoughly,and l imi t ing the quant i ty of feed should reduce theincidence of acidosis, but these practices often depressperformance and economic efficiency. Cont inuedresear ch concerning gra in pr ocessing, dietary cation-

anion balance, narrow-spectrum antibiotics, glucose orlactat e util izing microbes, a nd feeding mana gement(limit or program feeding) should yield new methodsfor r educing the incidence of acu te and ch ron icacidosis.

Key Words: Acidosis , Grain , Engorgement , Rumen, Osmotic Pressure

1998 Am erican S ociety of Animal Science. All rights reserved. J . Anim. Sci. 1998. 76:275286

Introduction

By definition, acidosis is a decrease in the alkali(base excess ) in body fluids r e la t ive to the acid(hydrogen ion ) content (Stedma n, 1982). Because pHof body fluids is buffered by bicarbonate, the pH of body fluids may or may not be depressed dur ingacidosis , depending on the degree to which bicar-bonate compensat ion is poss ible . Centra l nervoussystem function can be disturbed by low bicarbonateconcentra t ions even i f b lood pH is not depressed.Alth ough clinical diagnosis of acidosis requ ires bloodpH to fa l l below 7.35, other cl in ical s igns such asruminal pH, anorexia, variable feed intake, diarrhea,and lethar gy are the routine diagnostic indications of

acidosis of feedlot cattle. The etiology of ruminal andsystemic acidosis has been descr ibed in excellent

r evie ws b y E la m ( 19 7 6 ), H u be r ( 19 7 6 ), S lyt er( 19 7 6 ), Br it t on a n d S tock ( 19 8 7 ), H u n tin gt on(1988) , E lanco (1993) , and Harmon (1996) . High-lights ar e outlined below t ogether with specific hazar dcontrol points where alterations might help prevent oralleviate acidosis.

Acidosis of Herbivores

An a er obic m icr obe s in t h e r u m en a n d ce cu mferment carbohydrates t o VFA and lactat e. Ruminalproduction of more t han 55 mol of VFA da ily h as beenmeasured in s teers fed feedlot d ie ts (Shar p e t a l .,1982). H erbivores a bsorb t hese organic acids from th erumen an d(or ) cecum for me tabolism by t is sues.When carbohydrate supply is increased abruptly (i.e.,following grain engorgement or during adaptation tohigh-concentrate diets), the supply of total acid andthe prevalence of lac ta te in the mixture increase.Normally, lactate is present in the digestive tract atonly low concentrations, but when carbohydrate sup-ply is increased abrupt ly, lacta te can accumulate ;

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ruminal concentra tions occasionally reach 100 m M .Dunlop and Hammond (1965) coined the term D-lactic acidosis to encompass this metabolic distur-bance variously described as overeating, acute impac-tion, grain engorgement, founder, and grain overload.Today, the term acidosis is used collectively fordigest ive dis turbances of the rumen and intes t ines .However, acidosis of ruminants often is separated into

several forms, including acute, chronic (or subclini-cal ) , and subliminal types . Animals exhibi t acuteacidosis a s an overt illness following consum ption of readily fermen ted carbohydrates in a mounts sufficientto reduce ingesta pH. With chronic acidosis , feedintake an d performa nce are r educed, but animals m aynot appear sick. Clinical diagnosis of acidosis dependson measurements of ru minal or blood acidity, withr u m in a l p H of 5.6 a n d 5.2 oft en be in g u se d a sbenchmar ks for chronic and acute acidosis, respec-tively (Cooper and Klopfenstein, 1996). Britton et al.(1991) has used variation in feed intake between daysas an index of subclinical or chronic acidosis ba sed onthe concept that an increased variabili ty from day today in feed intake by individual animals is associatedwith feeding acidotic diets (Britton and Stock, 1987).

Etiology of Acidosis

The r elevant steps involved with acid production inand output from t he rum en are i l lustra ted in Figure 1.For discussion purposes, reactions have been num-bered.

Starch Concentration and Conversion to Glucose(Items 1 and 2)

Acidosis is most prevalent following engorgement of large amounts of s tar ch or other rapidly fermentedcarbohydrate. Excessive intake of readily fermenteds ta rch oft en occurs when an imal s a re fir s t beingadapted to a high-concentrate (feedlot) diet and(or)wh en a n im a ls a r e s wit ch in g fr om bu lk fill t ochemosta tic inta ke regulation. Acidosis also can occurwhen graz ing an imal s a re fed a l a rge amount of astarch-rich supplement.

Rate of cleavage of star ch to glucose varies withgra in source , gra in p rocess ing, and s t a rch type.Certain grain sources (i .e. , whea t) and grain varietieswith more readily extracted s tarch, as preferred bydisti lleries, presumably are hydrolyzed to glucosemore ra pidly than other sources or varieties. Sta rchgranu les embedded in p rote in in the horny en-dosperm of milo and corn have less surface exposedfor microbial a t tack. Heat and pressure t reatmentexplodes star ch granules into sheets of starch t hat arefermented very rapidly. Heat and pressure processing,particle size reduction, and high-moisture storage of grain increase starch availabili ty and the propensityfor acidosis (J ohns on et al., 1974; Britton an d St ock,

1987; Reinhardt e t a l ., 1993). Glucose is l iberatedfrom starch granules by specific stra ins of microbesthat a t tach to the grain par t icles . Several m ethodshave been developed to quantify flake quality (e.g. ,test weight, birefringence, gas production rate duringin cu ba t ion w it h ye as t or r u m in a l con t en t s, a n dglucose or mal tose re lease dur ing incubat ion withamyloglucosidase or am ylase). These should reflect

the extent of exposure of s tarch a nd (or ) i t s ra t e of fermentat ion. For maximum energetic efficiency, ahigh extent of fermentation is desired. But for acidosisprevention, a slow rate of fermentat ion is preferred.Unfortun ately, among grain sources a nd processingmethods, r a te and extent of d igest ion typical ly arecorre la ted in a posit ive direct ion.

Traditionally, glucose has not been considered to bean important metabol ic in termediate in the rumenbecause rumina l concen t ra t ions normally a re ex-tr emely low. However, in incubations by Slyter (19 76 )and engorgement s tudies by Horn e t a l. (1979),glucose concentra tions in the rumen often exceeded160 mg/dL, a concentration greater than that found inblood. In one of our acidosis studies, ruminal glucoseexceeded 1 ,400 mg/dL. Glucose is l iberated fromstarch by amylase, but whether this elevated concen-tr at ion is simply a result of more r apid hydrolysis or of a r educt ion in the r a t e of glucose u t iliza t ion byrumina l microbes is not cl ea r.

Presence of free glucose in the rumen can have atleas t three adverse effects . Fi rs t , ruminal bacter iatha t normally a re not compet it ive can grow ve ryrapidly when provided with high amounts of glucose.S treptococcus bovis , an inefficient microbe th at thr ivesonly when free glucose is available, was proposed byHungate (1968) as the major culprit in lactic acidosis.However, concen t ra t ions of th is organ ism in therum en of cat tle fed high-concentra te diets a re very low(Leedle, 19 93). Oth er bacteria, th ose directly involvedwith s t a rch fe rmen ta t ion , may be more impor tan tsources of lactate. Indeed, lactate often accumulatesfaster in vitro from starch than from glucose. Second,other opportu nistic microbes, including coliform s an damino acid decarboxylating microbes, may thrive inthe rumen of cattle fed concentrate diets (Slyter andRumsey, 1991; Leedle, 1993) and produce or, duringlysis, release endotoxins or amides (e.g. , histamine;

Huber, 1976; Brent , 1976) when glucose is readilyavailable. Third, free glucose released from starchincreases the osmolali ty of ruminal contents . Anincreased osmolality exacerbates accumu lation of a cidwith in the rumen by inh ib it ing VFA absorp t ion .

Limiting the Supply of Starch and Glucose(Items 1 and 2)

Two common management pract ices that help toprevent acidosis are diluting the diet with roughage orm od ula t in g in t a ke of s t ar ch . Die ta r y r ou gh a gedecreases eat ing ra te and meal s ize . Increas ing the



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ACIDOSIS OF CATTLE 277

Figure 1. Key reactions in acidosis of ruminants. Individual nu mbered reactions are discussed in the text.

concentration of dry roughage increases chewing timean d sa liva pr oduction. Although a n increased extent of mas t ica t ion will decrease s ize of gra in pa r t icle senter ing the rumen and thereby increase i t s ra te of ferm enta tion, an increased input of buffers from sa livafrom a longer chewing time or rumination neutralizesand dilutes ruminal acids. Starch content of the dietalso can be r educed by substituting starch-extra ctedconcentra tes (e.g., distilling or brewing co-productsand middl ings) for cereal gra ins . Total d ie t in takealso can be r es t r icted by using a l imi ted maximuminta ke feeding scheme a s described by Preston (1995 ).

For experimental purposes, researchers often in-duce acute acidosis by withh olding feed for 12 to 24 hand then feeding (or ruminally dosing) 150% of thenormal days feed a l lotment . This shows how anincreased meal size can precipitate acidosis and hasled to the suggest ion tha t da ily va r ia t ion in feedintake a mong days within an animal will increase thepotential for acidosis. Regularity of intake also ha sbeen implicated as a sign of subclinical a cidosis.Fulton et al. (1979) observed that following a bout of acidosis, feed intake by animals typically is low; theysuggested th at a cyclic feed inta ke pattern reflectedrepeated bouts of acidosis . When animals are fed

individually, such fluctuations in intake are detectedreadily. However, when 20 or m ore animals are fedtogether, daily fluctuat ions in intake (or feed deli-v er e d ) m a y n ot be d et ect ed u n le ss a ll a n im a lsexperience acidosis at the same time, as can happenfollowing diet changes or mishaps in processing ormixing.

Effects of feed inta ke regularity on acidosis havebeen examined in trials from New Mexico, California,and Nebraska (Ga lyean e t a l ., 1993; Zinn , 1994;Cooper and Klopfenstein, 1996). In these trials, feedsupply for the pen or the animal was purposely alteredor meals were skipped. Al though a l ter ing the dailysupply of feed has adversely altered feed efficiencyslight ly, and performance was reduced in the NewMexico trial , a nimal health was not affected drasti-cally. Stock and Britton (1993), Stock et al. (1995b),and Cooper a nd Klopfenstein (199 6) indicated thatmonensin a nd monensin-tylosin combinat ions reducedda ily va r ia t ion in feed intake by feed lot s t ee r s.I nclu din g m on en s in in t h e d ie t h a s r ed uce d t h eincidence of digestive deaths in pens of feedlot cattle(Pa r r ot t , 1993; Voge l, 1996), p resumably due toinhibition of certain lactate-producing bacteria and



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OWENS ET AL.278

reduced da ily variation in feed intake (Cooper andKlopfenstein, 1996).

Meal frequency may be as important as total feedintake as a cause of acidosis. For example, cattle withimplants typically have greater feed intakes. Weatherchanges and processing cattle to provide implants orinoculations often disrupt feeding patt erns and mayresult in overconsumption and acidosis. Proper timing

of processing so tha t catt le are not deprived of feedma y be useful; intake restr iction following working orweather changes also may be beneficial . Estr ogenicimplants have been shown to increase meal frequency,which in turn may decrease the potential for acidosis.Effects of meal frequency also may explain why moretimid a nimals and certain breeds experience acidosismore frequently. But if meal frequency is important,the incidence of acidosis would be expected to behigher when cattle are limit- or program-fed. To date,a cid os is in cid en ce h a s n ot be en r ep or t ed t o beincreased by limit feeding, perhaps because the totalquan tity of feed supplied is not excessive. However,when excessive amounts of feed are provided, eithermistakenly or during the switch from limit feeding tofree-choice intake, acidosis might be expected.

The roles of ru minal protozoa in acidosis a re notclea r. By engu lfing s t a rch pa r t icle s and s tor ingglucose as polysaccha ride, protozoa delay st ar ch fer-mentation by bacteria, help to retard acid production,and s tabil ize ruminal fermentat ion (Slyter, 1976;Nagaraja et al., 1990). In view of the large amounts of s t a rch consumed by ruminan t s , t he quan t it a t ivesignificance of starch consumption by protozoa seemsquest ionable . However, the populat ion of ruminalbacte r ia normally decreases when p rotozoa a represent; this decrease also could delay fermentation.Protozoal numbers in the rumen typical ly decl inewhen high-concentra te diets a re fed, probably becau selong dietary fiber provides a fibrous mat in the rumento which protozoa attach and remain long enough torepli ca te . F ree fa t ty acids and dete rgen ts r educeprotozoal numbers, as well , and a low pH may causedefaun at ion. H owever, in addition to st abilizing nor-mal fermentat ion, protozoal presence in the rumencan be deleterious. Because they h ave m uch h igheramylase act ivi ty per uni t of prote in than bacter ia(Mendoza and Britton, 1991), protozoa, when ruptur-

ing due to changes in acid or osmolality associatedwith acidosis, release large amounts of amylase thatin tu rn accelerates glucose production from sta rch a ndincreases the l ikelihood of acidosis.

Protozoal stimulants or inhibitors, as indicated inF igure 1 , may have an impact on p ropens ity andseriousness of acidosis. Because protozoal numbers arereduced by high-concentra te die ts and removed byunsaturated fatty acids, high concentrations of dietaryfat often lead to r uminal instability. Huffman et al .( 1 9 9 2 ) s u gge st ed t h a t by coa t in g t h e gr a in a n dreducing i ts ra te of fermentat ion, supplemental fa tshould reduce the incidence of acidosis. However, in

vivo challenge stu dies with corn and wheat detectedno effect of fat level on time that pH fell below 6.0,suggest ing that fa t was ineffect ive in prevent ingsubacute acidosis (Krehbiel e t a l ., 1995b) .

Including lactobaci llus cul tures in the die t mayprolong r umina l ret ention of protozoa (Va n Koeveringet al . , 1994), attenuate fermentation and productionof r u m in a l la ct a t e, a n d h elp m a in t a in a h igh er

ruminal pH (Cooper and Klopfenstein, 1996). Wil-l iams e t a l . (1991) observed that the mean and peak L-lactate concentra tion in r umina l fluid of steers fed abarley-hay diet was lower and ruminal pH was higherwhen the diet was supplemented with a yeast culture.Because yeasts fail to compete and grow in the rumen,frequent dosing is necessary to m aintain activity. Inengorgement stu dies, a yeast culture did not alter thefe rmen ta t ion pa t t ern (Godfrey e t a l ., 1992), bu tspecific yeast cultures, through stimulating growth of la ct a t e u t ilizin g ba ct er ia l s t ra in s in t h e r u m en(Dawson, 1995), may help moderate ruminal pH andavoid acidosis.

Glycolysis (Reaction 3)

Anaerobic microbes typical ly thr ive when freeglucose is available. Yet, the fact that free glucoseconcentrations in the rumen are high during acidosisindicates that glycolysis may be partially blocked. Inour ruminal flu id incubat ion s tudies and those of others (A. Z. Leedle, personal comm unication), lessthan ha lf of the glucose incuba ted with rumina lcontents (1% wt/vol) d isappeared within 6 h; th issupports the concept that free glucose is not beingcatabol ized readily for reasons yet unknown.

Control of Glycolysis (Reaction 3)

Rate of glycolysis can be l imi ted by inhibit inghexokinase, phosphofructokinase (both of which u seATP), and pyruvate kinase (t ha t yields ATP); lack of oxid ized NAD ( tha t i s r egenera ted with lacta t eproduction) also can limit glycolysis. Certain meta-bolic inhibitors, including iodoacetat e, fluoride, an dmetabisulfi te, by re tarding glycolysis , have beenproposed to reduce ruminal acidosis .

Volatile Fatty Acid Production and Lactate

Production and Utilization (Reactions 4 and 5)Ba ct er ia in t h e r u m en oft en a r e cla s sifie d a s

lactate producers or lactate users. Balance betweenthese t wo groups determines whether lactat e a ccumu-la tes . End products of bacter ia l s t ra ins may changedepending on substrate availability and culture condi-t ions (Russel l and Hino, 1985). Most lacta te-usingmicrobes ar e sensitive to low pH, wherea s m ost lactateproducers are not. Under anaerobic conditions, pyru-vate is conver ted to lacta te to regenerate the NADused in glycolysis. U nder normal conditions, lactatedoes not accumulate in the rumen at concentrations



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above 5 m M . In con t ras t , rumina l concen t ra t ionsexceeding 40 m M are indicative of severe acidosis.Ruminal and silage microbes produce two forms of lactate, the D+ and L form. The L form, identical tothat produced from glucose by exercising muscle, canbe readily metabolized by liver and heart t issue. Incontrast , D+ lactate, typically 30 to 38% of the totalla ct a t e fou n d in t h e r u m en , is n ot p rod uce d by

mam malian tissues. Accumulation of free lactat e ins ilage serves to hal t fermentat ion and s tabil ize thema ss. In addition to D-lactate an d VFA being involvedwith acidosis , other microbial products includingethanol, methan ol, histamine, tyramine, a nd endotox-ins often are detectable during acidosis and can exertsystemic effects (Koers et al ., 1976; Slyter, 1976).

Conversion of pyruvate to VFA involves multiplesteps and generates approximately half the ATP formicrob ia l growth in the rumen; the othe r ha lf i sder ived from convers ion of g lucose to pyruvate .Normally, VFA do not accumulate at sufficient concen-t r a t ion s in t h e r u m en t o r ed uce p H d r as t ica lly.However, when the ra te of acid production exceeds th era te of acid a bsorpt ion, due either to ra pid production,inhibited absorption, or reduced dilution, VFA ac-cumulate to higher concentra tions. In some studies,ruminal pH falls below 5.0 even without lactate beingpresent. This has led to the su ggestion that total acidload, not lactat e alone, is responsible for acidosis(Britton and Stock, 1987), particularly with chronicacidosis.

Control of Lactate Production and Utilization(Reactions 4 and 5)

S treptococcus bovis an d lactobacilli, which producelactate, the coliforms, which seem responsible foranaphylactic shock and sudden death, and the aminoacid degrading microbes associated with tyramine andhistamine product ion a l l may contr ibute to ruminalacidosis; these organisms might be controlled withan tibiotics or bacteriophages. Inoculation with lactate-using microbes that can tolerate a low pH also shouldbe useful for preventing acid accumulation. Repeatedinoculat ion with Megasphaera elsdenii (K u n g a n dHess ion , 1995), Lactobacil lus acidophilus (i nmetabol ism t r ia ls , e .g ., Huffman et a l , 1993; VanKoevering et al ., 1994; but not feeding trials, e.g.,Klopfenstein et a l., 1995; Stock et a l., 1995a ), and thethree species present in Activated Rumen Microbes( AR M ) t h a t G ra ce , I n c. t es t ed e xt en sive ly m a yenhance lactate utilization. Unfortunately, survival inthe face of vigorous competition from other microbialspecies complicates long-term alteration of the rumi-na l microflora . Yet, individual an imals differ an d m ayremain consistently different in ruminal metabolism.During a 6-mo ad l ib itum feeding per iod, lacta teproduct ion by ruminal contents dur ing incubat ionwith cornstarch ranked 10 steers similarly, suggestingthat the mixture of microbial species within an animal

remains s table even though some animals remainedmore prone to acidosis (F. N. Owens, u npubl ishedda ta ) .

To decrease lactate concentra tions, st imulation of microbes that use lactate (e.g., S elenomonas rum inan-tium ) seems beneficial . Dosing cultures or animalswith certain dicarboxylic acids, particularly fumarateand mala te , has decreased lacta t e p roduct ion and

increased pH in vitro and following grain engorge-ment, perhaps through enhanced lactate utilization byS . ruminan t ium (Mart in and Streeter, 1995) . Feasi -bili ty of malate supplementation during diet adapta-t ion to increase lacta t e u t il iza t ion needs fu r thertesting. An inter esting a lterna tive to microbial contr olis to precondition microbes to ha ndle lactat e, either byincluding lactate in the diet or feeding ensiled feedsthat contain lactate. Adding lactate to the adaptationdiet for sheep increased the rate of disappearance of lacta t e in vi tro (Hunt ing ton and Br it ton , 1978),suggest ing that feeding die ts that conta in lacta tebefore an acidot ic chal lenge may be beneficia l.

Feeding ionophores has reduced lactate productionin vi t ro an d in vivo (Newbold and Wallace , 1988;Bauer e t a l ., 1992; Syntex, 1994); effects may beeither thr ough inhibition of lactat e-producing bacteriaor reduced meal s ize. For inhibit ing lactobaci ll i,Tetronasin seems more potent than monensin. Selec-tive inhibition of S . bovis by thiopeptin indicates thatcontrol ling the microbial populat ion can preventacidosis. When catt le were fed virginiamycin theycould be switched u neventfully from a fora ge diet to a100% wheat d ie t within 24 h (Zorr i l la-Rios e t a l .,1991). Virginiamycin may protect animals from rumi-nal and postruminal acidosis (Godfrey et al., 1992) byinhibiting lactate-producing bacteria (Rogers et al .,1995).

In addition to lactate, substances toxic to ruminalmicrobes are produced by certain strains of ruminalbacteria grown with excess carbohydrate but insuffi-cient nitrogen (Russell, 1993). Under glucose toxic-ity conditions and accumulation of methylglyoxal,viabi li ty of bacter ia decl ines dras t ical ly (Russel l,unpubl ished dat a) . With lys is of microbial ce lls,endotoxins a lso ma y be re leased. Presence of suchantimicrobial compounds might readily explain thestagnancy of ruminal contents immediately following

a bout of acidosis. Antibacterial activity of ruminalfluid during a cidosis deserves furth er research atten-tion. Toxicants might be neutralized through inocula-tion with toxin-catabolizing or toxin-tolerant strains of microbes, and conditions conducive to toxin produc-t ion, such as a deficiency of specific n i t rogenouscompounds, m ight be corrected by diet modification.

Depression of Ruminal pH (Reaction 6)

Ruminal pH represents the consortium of relativeconcen t ra tions of bases, acids , and buffe r s. Thepr imary ruminal base is ammonia . The two pr imary



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OWENS ET AL.280

Figure 2. Relative contributions of various organic compoun ds to ru minal acidity and osmolality und er n ormal oracidotic conditions. Heights of bars indicate relative contributions to hydrogen ion and osmolality from (bottom totop) butyrate, propionate, acetate, glucose, D-lactate, and L-lactate.

buffers under neutra l pH conditions are bicarbonateand phosphate . In addit ion, VFA and lacta te act asbuffe r s when pH fa ll s below 5 , a s d iscussed byCounotte et al . (1979). The relative contributions of various organic compounds to ruminal acidity and toruminal osmolality under norma l and acidotic condi-t ions a re p resen ted in F igure 2 based on rumina lconcentra tions and calculated extent of ionizationbased on da ta publi shed by Fu lton e t a l . (1979)combined with glucose mea surem ents from H orn et a l.(1979). As indicated in Figure 2, when pH decreasesto 5.0 during acidosis, ionization of acids increasesslightly, but the added lactate is primarily responsiblefor the increased hydrogen ion concentration. Lactatedepresses pH more drastically than similar amountsof other ruminal acids because its pK (the pH point of maximum buffer ing) is considerably lower (3 .8 vs4 .8) . As shown in F igure 2 , with an acidot ic pH,osmotic pressure is increased by greater ionization of

acids and presence of free glucose. Compared withnormal concentra tions, the change during acidosis ismuch greater in osmolality than in the hydrogen ionconcentration.

Absorption from the rumen normally prevents acidaccumulation; however, high osmolality of ruminalcontents reduces the rate of acid absorption (Tabaru

et al., 1990). This exacerbates acidity and osmolality.Fur thermore, acidi ty enhances act ivi ty of lacta tedehydrogenase, increasing conversion of pyruvat e tolactate and complicating recovery from acidosis. Com-bined with the fact that a low pH enhances activity of pyruvate hydrogenase and favors pyruvate conversionto lactate (Russell and Hino, 1985), a severe drop inrumina l pH i s d ifficu lt t o r eve r se .

Control of Ruminal pH (Reaction 6)

Increasing ruminal input of bases or buffers (e.g. ,bicarbonate from the diet or from saliva) or feeds that



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yield bases or buffers (e.g. , ammonia from degradedprotein or nonprotein N ) will help prevent a depres-sion in ruminal pH. Absorption of VFA, by removingun-ionized acid and by the exchange of ionized VFAfor bica r bon a t e d ur in g t h e a bs or pt ion p roce ss(Stevens, 1970), aids in mainta ining pH near neutra l-i ty. Consequently, a reduced rate of VFA absorptioncauses r uminal pH to drop for two reasons: ruminal

VFA accumulate an d bicar bonat e input from t he bloodstream is decreased. Approximately half the bicar-bonate entering the rumen comes from saliva, duringe a tin g a n d r u m in a t ion ; t h e ot h er h a lf e nt er s t h erum en in exchan ge for ionized acids being absorbed.In addition, carbon dioxide produced dur ing fermenta -tion typically saturates ruminal fluid and exchangeswith the bicarbonate pool of the rumen. With concen-t r a t e d ie t s and reduced inpu t of sa liva , a h igherproportion of bicarbonate must be derived from theb lood . Th is r educes the base excess of b lood ; if inadequate ly compensated by respira tory and renalmechanism, this causes metabolic acidosis.

Ruminal Osmolality (Reaction 7)

Osmotic pressure pulls or pushes water throughmembranes depending on relative concentra tions of d issolved mater ia ls . Ruminal osmolali ty normal lyranges from 240 to 265 mOsm/L with roughage dietsand 280 to 300 mOsm/L with concentrate diets (Garzaet al., 1989). Minerals, VFA, lactate, and glucose aret h e p rim a r y s olu t es in r u m in a l flu id . I n blood ,dissolved protein contributes substantially to osmoticpressure that normally ranges from 285 to 310 mOsm.

With the acidotic conditions of engorgement stu dies,we have measured ruminal osmolality as high as 515mOsm. When ruminal osmolality is mar kedly greaterthan blood osmolali ty, water from blood is drawnrapidly inward through the rumen wall . Rapid influxto neutra l ize osmotic pressure swel ls the ruminalp apilla e a n d ca n pu ll p at ch es of t h e r u min a lepi thel ium into the rumen by s t r ipping the in ternalsurface layers of the rumen wall from the underlyinglayers, as illustrated vividly in histological studies byEadie and Mann (1970) . Damage to the wal l of therumen or small intestine due to high osmotic pressure,detected later as sites of abscesses, is a result of thisrapid influx of water. When sepsis occurs , ruminalmicrobes responsible for liver abscesses freely ent erthe blood stream. Subsequently, r epaired tissues of the digestive tract will be thickened (hyperkeratosisor p a r a ke r a t os is ); t h is m a y in h ibit r a t e of VFAabsorption for months or years after the damage hasoccurred (Krehbiel e t a l ., 1995a) . Passage of VFApostr umina lly for absorption is possible, but a boma salpresence of VFA hinders acidificat ion and protein a ndmineral digestion; this may reduce postruminal starchdigestion. Consequently, a single bout of non-fata lacidosis m ay have prolonged effects; t his ma y explain

why subsequent performance is suboptimal for manyof the animals denoted as real izers in feedlots .

An elevation in osmotic pressure in the rumen issensed by th e wall of the reticulorum en t o inhibit feedin t a ke (C a r t e r a n d Gr ovu m , 1 99 0). I n a d dit ion ,osmotic pressures above 350 mOsm inhibit bacterialdigestion of fiber an d st ar ch, causing rum inal conten tsto become stagnant. High osmolality (> 300 mOsm)

combined with distention of th e abomasum , throughinhibition of outflow, complicates removal of fluid anda cid fr om t h e r u men (S cot t , 1 97 5). Du r in g a22-d trial adapting three heifers to a high-concentratediet, we observed that ruminal osmolality a veraged339 35 mOsmol and peaked over 420 mOsm onseveral days. Although ruminal hypertonicity usuallybut not a lways r educes the fr equency of rumina lcontract ions (Car ter and Grovum, 1990), inhibitedgut mot i li ty or hyper tonici ty a t the abomasum mayhalt flow a nd exacerbate rum inal a cidificat ion; alter edmoti li ty or tonici ty a lso may cause feed in take to

fluctuat e with chronic acidosis.

Control of Osmolality (Reaction 7)

High osmolality from elevated concentra tions of glucose and acids cannot be r eadi ly p reven ted .However, other contr ibutors to osmotic pressur e, suchas ammonia and soluble mine ra ls ( i. e ., sod ium,potass ium, chlor ide) f rom the die t or water can bea lt e red . Sa l t a t 5% of the d ie t increased rumina losmolality to 344 mOsm. Reducing intake of mineralsand sal t might reduce ruminal osmolali ty s light ly.Increasing inpu t of sa liva , a t approximate ly 255

mOsm, also reduces ruminal osmotic pressure. Highmoisture diets or increasing intake of drinking waterprobably do not reduce ruminal osmolality becausefe rmen ted d ie t s oft en have h igh osmola li ty, anddr inking water in take may par t ia lly flush past ther u m en (G a r z a a n d O we ns , 1 98 9). Be ca u se h ighintakes of salt or minerals in feed can exacerbate thesitua tion, a norexia during acidosis sh ould be benefi-cial.

Acid Absorption (Reaction 8)

Lactate and VFA ar e absorbed passively thr oughthe rumen and intestinal epithelium. Rate of absorp-t ion is greater when concentra t ions are high, pH islow, and osmolality is normal (Tabaru et al . , 1990).The lower the pH, the higher the percentage of eachorganic acid in the non-dissociated (a cid) form andthe greater the absorpt ion ra te . During absorpt ion,butyrate is partly metabolized as an energy source forthe rumen wall and glucose is partly converted to D-lactate. Lactate also is produced in and absorbed fromthe intestines (Godfrey et al . , 1992), so total lactateload for the l ive r may grea t ly exceed the l acta t eabsorpt ion from the rumen.



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Control of Acid Absorption (Reaction 8)

Whether i t is desirable t o increase acid absorptionfrom the rumen to a void rum inal acid over load andosmolality or to decrease absorption and temporarilyavoid systemic acidosis depends on the potent ia lseve r ity of the rumina l or sys temic damage . On achronic basis, a cid absorption rat e is reduced most

easily by increasing ruminal pH. Higher bicarbonateinpu t from the d ie t or sa liva will he lp increaseruminal pH and an increased pH s t imulates ut i l iza-tion of lactate in the rumen. H igher ruminal amm oniaconcentra tions from higher dietar y pr otein or ureaconcentra t ions often are associa ted with a higherruminal pH and ruminal buffering capacity (Haa landet al., 1982) even though the ammonia released couldneutralize only 10 to 15% of VFA produced. Increasingt h e ca t ion :a n ion ba la n ce a ls o m a y b e u se fu l t oincrease ruminal pH. However, in research with acuteacidosis induced by a grain overload, including variousbuffers with the diet has not produced a consistent

benefit . This probably relates to th e long t ime lag (6to 10 h ) between a meal and minimum ruminal pH.When combined with outflow of soluble materials fromthe rumen, buffers a re dilu ted too much to have anyresidual effect. Protein or nonprotein N sources t hatre lease ammonia gradually may be beneficia l, cer-ta inly more beneficia l t han urea or bypass prote insources . Enhanced sal iva flow, achieved throughenhancing chewing and rumination time by includinglong roughage in the diet or by a ddition of specificchemicals to the die t (e .g . , s laframine and pilocar-pine) should reduce the incidence of acidosis .

Blood pH (Reaction 9)

Blood acidosis, which is similar in ruminan ts andnonruminan t s , can re su lt from e ithe r excess iveproduct ion or insufficient removal of acid. Withrespirat ory inadequacy, a s can occur during r espira-tory disease, carbon dioxide accumulates in blood; thisdepresses blood pH unless r enal retention of bicar-bonate compensates sufficient ly. In contras t , withmetabolic abnorma lit ies, excess acid production orabsorpt ion decreases pH and bicarbonate in bodyfluids due to accumulation of acids or loss of fixed basefrom the body (as in diarrhea or renal d isease). Innonruminants , lact ic a cidosis i s a specia l type of metabolic acidosis resulting from decreased tissueperfusion, drug reaction, or inhibition of pyruvateconversion to acetyl coenzyme A t hat can occur indeficiencies of specific cofactors (i.e., th iam in or lipoicacid). With arsenite or mercury binding of sulfhydrylgroups of lipoic acid, pyruvate and lactate accumu late.Nutrit ionally deprived alcoholics tha t are thiamin-deficient when administered glucose rapidly accumu-la t e p yr u va t e, a n d t h e la ct a cid em ia t h a t r es u lt sfrequently is lethal. In huma ns, acidosis can occurwith h igh-protein diets with inh ibited m etabolism of

e ithe r p rop ion ic acid (f rom a B 12 deficiency) orisovaleric acid (impa ired isovaleryl dehydrogenase)a s d es cr ibe d by Mu r r a y e t a l. ( 19 9 3 ).

Blood pH depends on the relative concentrations of bases , acids , and buffers in solut ion. Low bloodconcentrations make ammonia irrelevant to blood pH,except th at the l iver by urea synthesis m ay alter acid-base s ta tus of the animal . Phosphate plays a minor

role due t o i ts relatively low and constant concentra -t ion. This leaves bicarbonate as the pr imary bloodbuffer (Counot te et al., 1979). A base-excess n orm allyis present in blood, but an acid load can decrease thisbase-excess and can overcome the buffering capacity of bicar bonat e. Acids of concern include those absorbedfrom the digestive tract plus L-lactate produced bymuscular activity. Acid absorption or production is of concern only at the site of absorption or when acidsaccumulate (i .e. , when rate of entry exceeds the rateof m eta bolism). Of the VFA, only acetate normallyreaches the per iphe ra l b lood s t r eam; much of thebutyrate is converted to beta-hydroxybutyrate duringabsorp t ion th rough the rumen wa ll and a l l o f theprop iona te i s conver t ed to glucose by the live r.Presumably, VFA should not accumulate in bloodplasma at sufficient concentra tions to depress bloodpH, but exactly h ow blood VFA concentra tions changeunder acidotic conditions has not been determined.However, metabol ism of th e ruminal wall and theliver may be compromised during acidosis. Fur thercomplicating the situation, the l iver is faced with L-lacta te from t issue metabol ism plus the D- and L-lacta te absorbed from the digest ive t ract . Indeed,when r umina l glucose concentra tions a re h igh, as seenwith acidosis , g lucose being absorbed is par t ia llyconverted to L-lactate by the digestive tract (Seal andParker, 1994); if excessive, capacity of t he l iver tocata bolize lactate may be overloaded (Na ylor et al . ,1984). Individua l an ima ls with a la rge r (whea t -pasture cat t le) or more adapted l iver have greatercapacity for metabolizing lactate and thereby m ay beless l ikely to experience blood acidosis.

Blood usually is saturated with bicarbonate. Bloodacid-base ba lance is r egu la ted by the r e sp ira torysystem (blowing off carbon dioxide), muscular activity(lactate production by muscles), and kidney function(excretion of acid or amm onium sa lts), as described

by Harmon (1996). Balance of absorbed ions can alteracid-base status. Normally determined by measuringconcentrations in feed and designated as the dietarycat ion-anion balance ( DCAB ) , ca t ion s (s od iu m ,potassium, and perhaps ammonia for ruminan t s )increase the base load, whereas anions (chloride, andprobably sulfate for ruminants) increase the acid load.Cattle fed cereal grain diets typically are acidotic andsecrete acid urine partially neutralized by ammoniaand phosphorus. Infused acid increases excretion of amm onium ions but not phosphorus, indicating t hatphosphorus excretion is inconsequential to acidosisand may reflect decreased recycling via saliva to the



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rumen. An increased dietary electrolyte balance hasbeen found to increase ruminal pH of growing steersand to linearly or quadratically increase arterial bloodpH (Ross e t a l ., 1994a ,b ).

Control of Blood pH (Reaction 9)

Increasing the base excess, through a l ter ing t he

ca t ion-an ion ba lance of the d ie t , shou ld a id inprevent ing acidosis . Subst itu t ion of buffers (e .g . ,carbonates and bicar bona tes) for other dietary ionsoften proves beneficial, probably m ore from the addedcat ion than from carbonate or b icarbonate that arelost as carbon dioxide from the rumen, especially whenpH is low. This reduces the impact of added buffer onblood pH or base excess. In contrast, higher levels of u r ea or r u min a lly degr a ded pr ot ein , t h rou ghmetabolism by the l iver, may enhance base sta tus. Toavoid elevating ruminal osmolality, cations should bereadi ly absorbed (Na, K) ra ther than mainta ined inthe rumen (Ca, Mg) in order to increase blood base

status although excesses may increase blood osmolal-i ty and reduce feed in take. Manipulat ion of DCABmay be helpful for increasing feed intake and prevent-ing blood acidosis (Ross et al., 1994a,b; Block, 1994).Because ammonium salts are excreted to counter-balance an acid load, additional sources of ammonia( i .e . , degraded prote in or NPN) may be needed andbeneficial in controlling chronic acidosis. Urinaryammonia, which is derived from glutamine, increasesthe hepa t ic demand for ammonia and energy forglutam ine synthesis.

Blood Osmolality (Reaction 10)

Blood osmolality increases during acidosis for tworeasons . Fi rs t , h igh ruminal osmotic pressure pullsfluid from plasma into the rumen; t his concentra tesblood components, increasing both blood osmolality,packed cell volume, and drinking of water, symptomstypical of dehydration. Second, when rates of absorp-tion of ruminal acids or glucose exceed their rates of metabolism or excretion, these compounds can ac-cumulate in blood and directly increase osmolality.Hoof da mage and laminitis typical of a cidosis havebeen attributed to elevated histamine concentrationsand blood vessel dam age due to uncontrolled eleva-tions in blood pr essure inside the hoof (Vermu nt andGreenough, 1994). Whether blood osmolarity plays arole in lamini t is i s not c lear. Dark l ines around thehoof and rough su r face bands r eadily r evea l anhistor ical record of the animals nutr i t ional s ta tus ,s t ress, and acidosis .

Increased osmolality has numerous physiologicaleffects. Hypertonicity is detected at several sites. It issensed by osmoreceptors in the rumen to inhibit feedin t a ke , in t h e p or t a l s ys t em or live r t o in h ibitrumina t ion , and in the b ra in to inh ib it s a liva t ion(Car te r and Grovum, 1990). The shor t -t e rm feed

intak e depressions noted with subclinical acidosisma y r eflect fluctuat ing blood osmolality. In contr ast ,with clinical or acute acidosis, th e decrease in bloodpH is a l ife-threat ening situation. H ence, acute a ndchronic acidosis, although working from a similar baseof ruminal acidity, probably should be considered asseparate disorders.

Control of Blood Osmolality (Reaction 10)Increased salivation, achieved through higher in-

ta kes of coar se pa rt icles from roughage or wh ole corn,and higher intake of water should serve to buffer anddilute ruminal contents to r educe ruminal osmolality.Reduced ruminal osmolality will avoid the influx of fluid from blood that causes an elevation in bloodosmolality. Sim ilarly, su pply of cofactors involved withVFA metabolism (B 12 , thiamin, a nd lipoic acid) mustbe adequate to prevent accumulation of these acids.

Acid Metabolism and Excretion

(Reactions 11 and 12)Metabol ism of VFA to glucose for s torage or to

carbon dioxide to yield energy typically proceedsrapidly so that b lood concentra t ions remain low.Traditionally, acidosis was att ributed strictly to lac-tate because lactate is 10 times stronger an acid thanVFA. Huber (1976) reviewing ear lier s tudies indi-cated that D-lactate was not metabolized by tissues asrapidly or extensively as L-lactate; he suggested thatit was removed from blood only by excretion throughthe kidney. In contrast , more recent studies indicatethat D-lacta te is metabol ized by rum inant t i ssues

(Giesecke and Stangass inger, 1980; Harmon et a l .,1983), a l though ra te of metabol ism under acidot icconditions have not yet been measured. Presence of butyra te reduces conversion of L-lactate to glucose bycalf hepatocytes (Reynolds et al ., 1992), so interac-t ion s a m on g a bs or bed a cids m a y a lt er r a te of metabolism.

Enhancing Acid Metabolism and Excretion(Reactions 11 and 12)

Kidney clea rance of flu id can be increased byelevat ing dietar y concentra tions of salt or digestible

prote in . Al though VFA should be resorbed by thekidney, D-lactat e is part ially excreted. Deficiencies of cofactor s and adapta t ion to me tabol ize VFA andlactat e m ay increase the maximum rat e of metabolismof these acid end-products. Specific cofactors of in-terest include vitamin B 12 , l ipoic acid, and thiamin.The latt er could explain why polioencephaloma laciaoccasionally is l inked to acidosis. In contra st , Brent(1976) indicated that ruminal thiaminase developedafter acidosis and suggested that bacter ia l th iamindestruction was enhanced by acidosis. Concentrationsof VFA and lactate in plasma of animals dying fromacidosis need to be measured to determine whether



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OWENS ET AL.284

Table 1. Subclinical acidosis checklist, scale of risk, and apparent impact und er various conditions

a Cation-anion balance.

Da nger sca le Impa ct

Fa ctor Low H igh La b In vivo Feedlot

ManagementCa t t le disposit ion Ta m e Fligh ty ? ? Modera teMea l size Sma ll Hu ge St r ong St r ong St rongF eed a ccess Limited Unlim ited St ron g St rong Lim ited

Diet compositionConcent ra te level 0% 100% St rong St r ong St rongGr a in Cor n , Milo Whea t St rong St rong St r ongGr a in processing Whole Steam -fla ked St rong St rong St r ongF eed type Unferm ented F erm ented Wea k ? ?DCAB a Acid Ba sic Weak ? ?

AdditivesIonophor es P resen t Absent St rong St ron g St rongBicar bona te Pr esen t None Weak Wea k Wea k F a t Up to 8% None Wea k Nega t ive NoneP robiot ics La ctoba cilli None Modera te Som e ?P rotozoa l st imula n ts P resen t Absent St rong St rong ?P rotein level H igh Low Wea k Weak ?Thia m in Supplem ented None Weak Wea k ?Virgin ia m ycin P resen t Absent St rong St ron g Modera teMa la te/F uma ra te Pr esen t Absent St r ong Modera te Wea k

ra tes of a cid metabol ism are l imi ted. Naylor e t a l .(1984) indicated that hepat ic metabol ism of lacta tema y be limited. Only with absorption or liver m alfunc-t ion would one expect butyra te or p rop iona te toaccumulate in peripheral blood. Relative concentra -t ions of ace ta t e and D and L lacta t e cou ld r evea lwhether catabol ic ra tes are being exceeded.

Overview

F a ct or s t h a t m igh t be m od ifie d t o r ed uce t h eincidence of subclinical and clinical acidosis are listedin Table 1 together with a re la t ive danger scal ingconcerning the expected effect on the incidence of acidosis. Effectiveness of modifying certain factors hasbeen studied only in ruminal fluid incubation studies,whereas other factors have been tes ted with cannu-la t ed an imals or have been obse rved in feed lot ;relative degrees of testing and effectiveness underthese three scenar ios are es t imated. Inhibit ing lac-

tat e-producing microbes and enhancing activity of lactat e-using m icrobes and new procedures in feedmanagement ( limi t or program feeding) m ay helpreduce the incidence of acute and subacute acidosis.

Implications

Acute and chronic acidosis cont inues to plaguefeedlot rum inant s. Steps involved with accumu lationof ruminal acids and elevated osmolality of ruminalconten ts an d blood a re outlined a nd contr ol proceduresare proposed. Promising control measures include

specific feed additives that inhibit the lactate-produc-ing bacterial strains, that stimulate activity of lactate-using bacteria or starch-engulfing ruminal protozoa,and that reduce meal size. Ruminal inoculation withmicrobial strains capable of preventing glucose orlactate accumulation or of meta bolizing lactat e at alow pH may help . Cont inued research concerninggrain processing, dietary cation-anion balance, nar-

row-spectr um an tibiotics, glucose- or lactate-utilizingmicrobes , sa liva ry flow s t imulan t s , and feed ingman agement should yield new methods for reducingthe incidence of acute and chronic acidosis .

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