acidose e sua implicação em laminite nocek

1997 J Dairy Sci 80:1005–1028 1005

Received June 26, 1995.Accepted December 10, 1996.1Present address: Spruce Haven Research Center, Union

Springs, NY 13160.

Bovine Acidosis: Implications on Laminitis

JAMES E. NOCEKAgway Research Center Researchand Development, Tully, NY 13159

ABSTRACT

Bovine lactic acidosis syndrome is associated withlarge increases of lactic acid in the rumen, whichresult from diets that are high in ruminally availablecarbohydrates, or forage that is low in effective fiber,or both. The syndrome involves two separate anatom-ical areas, the gastrointestinal tract and body fluids,and is related to the rate and extent of lactic acidproduction, utilization, and absorption. Clinicalmanifestations range from loss of appetite to death.Lactic acid accumulates in the rumen when the bac-teria that synthesize lactic acid outnumber those thatutilize lactic acid. The systemic impact of acidosismay have several physiological implications, includ-ing laminitis, a diffuse aseptic inflammation of thelaminae (corium). Although a nutritional basis forthe disease exists, etiology includes a multitude ofinteractive factors, such as metabolic and digestivedisorders, postpartum stress, and localized trauma,which lead to the release of vasoactive substancesthat trigger mechanisms that cause degenerativechanges in the foot. The severity of laminitis isrelated to the frequency, intensity, and duration ofsystemic acidotic insults on the mechanisms responsi-ble for the release of vasoactive substance. The criti-cal link between acidosis and laminitis appears to beassociated with a persistent hypoperfusion, whichresults in ischemia in the digit. Management of acido-sis is critical in preventing laminitis. High producingdairy herds attempting to maximize energy intakeare continually confronted with subclinical acidosisand laminitis. Management of feeding and husbandrypractices can be implemented to reduce incidence ofdisease.( Key words: acidosis, rumen, carbohydrate, lamini-tis)

Abbreviation key: AV arterial-venous difference,eNDF = effective NDF.

INTRODUCTION

Several reviews (26, 59, 61, 120) have describedthe process of acidosis in livestock and dairy cattle.Carbohydrates with high ruminal availability appar-ently cause the initial ruminal insult. The severity ofacidosis is related to the frequency and duration ofdiet alteration. Researchers (45, 56, 85) have in-duced acute or subacute acidosis by repeated doses ofhighly available carbohydrate. The critical pHthreshold of the rumen is <5.0 during acute acidosisand is <5.5 during subclinical acidosis (85). As highlyfermentable carbohydrate is introduced to the diet,ruminal VFA production actually increases as pHstarts to decrease. Harmon et al. (56) showed thatintraruminal dosing with glucose decreased pH to<4.5 within 14 h postdosing. The ruminal microbialprofile also changes; Streptococcus bovis and lacticacid production both increase. There is a concomitantdecrease in Megasphera elsdenii and Selenomonasruminantium, and microorganisms that synthesizelactic acid outnumber those that utilize lactic acid(114, 123). As pH continues to drop, growth of S.bovis is also impeded; however, lactobacilli fill thisniche and continue to produce lactic acid as pH drops.Thus, a spiraling effect is initiated (115).

Ruminal changes initiate several systemic changes.Increased organic acid, particularly lactic acid, andreduced pH result in decreased ruminal motility, sta-sis, ruminitis, and hyperkeratosis (33, 93). Thesechanges establish conditions for penetration of certainbacteria ( Fusobacterium necrophorum) through theruminal wall into the liver where abscesses are estab-lished. Other events, which happen simultaneously,are associated with increased ruminal osmotic pres-sure, decreased extracellular volume resulting in de-hydration, decreased cardiac output, decreasedperipheral perfusion, decreased renal blood flow,shock, and death (61).

In many dairy operations, the challenge is notacute acidosis, but rather subclinical acidosis,whereby very little accumulation of lactic acid is de-tected in the rumen; however, pH decreases. Dailyepisodes of pH <5.5 for given periods ultimately pre-dispose cattle to low grade, subclinical acidosis.Symptoms include erratic appetite, body weight loss,diarrhea, and lameness (45, 99).

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Laminitis occurs in acute, subclinical, and chronicforms (13, 53, 72, 100). The link between acidosisand laminitis appears to be associated with alteredhemodynamics of the peripheral microvasculature(15). Various theories have developed to explainevents that occur in the pathogenesis of laminitis.Vasoactive substances (histamine and endotoxins)are released during the decline of ruminal pH and asthe result of bacteriolysis and tissue degradation.These substances cause vasoconstriction and dilation,which ultimately destroy the microvasculature of thecorium (17, 82). Ischemia results, which causes areduction in oxygen and nutrients reaching the ex-tremities of the corium. Ischemia causes physicaldegradation of junctures between tissues that arestructurally critical for locomotion (15). The insidi-ous rotation of the distal phalanx (pedal bone) canresult in permanent anatomical damage. Manifesta-tions of subclinical laminitis are sole hemorrhagesand yellowish discoloration (13, 102). Other clinicalmanifestations include double soles, heel erosion, dor-sal wall concavity, and ridging of the dorsal wall(102).

A challenge for the dairy producer is to identifyoccurrence of subclinical acidosis and laminitis and tomake the appropriate adjustments in feeding andmanagement practices. Acidosis and laminitis can becontrolled by increasing the level and type of dietaryfiber. To maximize energy intake, a proper balance ofnonstructural and structural carbohydrate must beprovided, and the amount of effective fiber must besufficient to promote normal rumen function.

The objective of this review is 1) to characterizeincidence, cause, and mechanistic development of aci-dosis and laminitis, 2) to identify predisposing factorsof acidosis to laminitis, and 3) to present preventivemanagement practices that control these metabolicdiseases.

ACIDOSIS

Acidosis is caused by the ingestion of greater thannormal quantities of ruminally fermentable carbohy-drates. The clinical symptoms of carbohydrate over-load vary, depending upon the types and amounts ofcarbohydrates consumed. As a result of carbohydrateoverload, acids outside physiologically possible limitsare produced and pH is concomitantly reduced, whichoverwhelms the ruminal and host system. The cas-cade effects of acidosis originating from the initialingestion of carbohydrate depend upon the intensityand duration of the insult. Most critical is the pHthreshold, which not only relates to microbial growth

rates and shifts in ruminal populations but also sig-nificantly influences the systemic metabolic state andthe ability to catabolize or excrete certain metabo-lites.

Incidence

Grohn and Bruss (54) evaluated the incidence ofruminal acidosis in >61,000 Finnish Ayrshire cows,which indicated that lactational incidence was only0.3% of animals affected. However, no details weregiven regarding the severity of acidosis or diagnosticmethod used to determine acidosis. The incidence ofacidosis is highest during the 1st mo postcalving andrelatively nonexistent within 3 mo (54). Onset ofacidosis is associated with adaptation to high concen-trate diets containing more highly fermentable carbo-hydrate than cows are accustomed to utilizing duringthe dry period. Also, the high incidence reflects theinability of the system to handle acid overloads dur-ing early lactation.

Acute Acidosis

Acute acidosis results in very sick cows: physiologi-cal functions may be significantly impaired and deathmay occur. Acute acidosis is characterized by a dra-matic reduction in ruminal pH ( ≤5.0), a large in-crease in lactic acid concentration, an increase involatile fatty acid concentration, and a large decreasein total protozoa (86). Huntington and Britton (62)demonstrated a 100-fold increase in ruminal concen-trations of lactic acid of lambs within 48 h of consum-ing a diet of 90% concentrate. By 30 h, blood pHdecreased from 7.44 to 7.20, packed cell volume in-creased, bicarbonate and calcium decreased, and lac-tate increased 6-fold, of which two-thirds was D-lacticacid.

Figure 1 illustrates the developmental and spiral-ing process (115) of lactic acidosis to a systemic andmetabolic state. If the carbohydrate insult persists,the spiraling effect also persists, and irreversiblemetabolic acidosis in inevitable.

During acute acidosis, blood flow to the gastroin-testinal tract is decreased, thereby reducing the ab-sorption of organic acids from the rumen (58).Prolonged exposure of the ruminal epithelium to highacid concentrations can result in hyperkeratosis andparakeratosis, which reduce the absorptive capacityof organic acids, further decreasing pH (96).Although all organic acids accumulate in the rumen,lactate remains the predominant and strongest acid(114). Furthermore, the production and metabolismof D-lactate becomes limiting in the development of

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Figure 1. Sequence of events associated with the induction ofacute ruminal lactic acidosis. CHO = Carbohydrate.

acute acidosis because D-lactate metabolizes moreslowly than L-lactate (47).

Options to Reduce LacticAcid in the Rumen

A generally accepted concept for ruminal lactic acidaccumulation is that lactate producers outnumberutilizing bacteria (114). Critical to this imbalance ispH optimization for growth. Russell et al. (116) illus-trated that growth rate of S. bovis (a major lactic acidproducer) declines dramatically between pH 5.3 and5.1. Also, M. elsdenii, a lactate utilizer, has a reducedgrowth rate from pH 6 to 5.5. This differential resultsin significant accumulation of lactic acid when readilyfermentable carbohydrate is provided. When ruminalpH is maintained >5.5, equilibrium exists betweenproducers and utilizers, such that lactic acid does notaccumulate.

Increased Lactate Accumulation

The primary ruminal microorganisms utilizing lac-tic acid are Propionibacterium shermanii, M. elsdenii,and S. ruminantium. Hession and Kung (57) inves-tigated the effects of P. shermanii and M. elsdenii on

ruminal fermentation. Treatments were as follows:108 cfu of P. shermanii/ml of culture, 106 cfu of M.elsdenii/ml, and 107 cfu of M. elsdenii/ml. After ap-proximately 5 h of incubation, pH of the untreatedculture was similar to that of P. shermanii and, for107 cfu of M. elsdenii, was 0.5 pH units greater thanthe control. Lactic acid concentrations were >30 mMfor untreated and P. shermanii cultures. The M. els-denii cultures remained <3 mM throughout fermenta-tion, suggesting that M. elsdenii at 107 cfu/ml was aseffective in elevating ruminal pH and maintaininglower lactic acid concentration as was P. shermanii orM. elsdenii at lower concentrations.

Nisbet and Martin (89) evaluated the effect of pHon rate of L-lactate uptake in the presence of malateby S. ruminantium. Malate substantially increasedlactate uptake at every pH tested. There was no effectof lactate uptake in the presence of 10 mM glucose,maltose, xylose, sucrose, or D-lactate. Nisbet andMartin (89) indicated that stabilization of ruminalpH through the use of an organic feed additive, suchas L-malate, might aid in the prevention of lacticacidosis.

Megasphera elsdenii utilizes 60 to 80% of the lac-tate fermented in the rumen of cattle (25) and ac-counts for 20% of the lactate utilizers in the rumen ofanimals fed high concentrate diets (72). Kung andHession (69) examined the effect of adding two levelsof M. elsdenii on pH, lactate, and VFA concentrationto in vitro batch cultures. Both the low (8.7 × 105 cfu/ml) and high (8.7 × 106 cfu/ml) M. elsdenii levelssustained culture pH at approximately 0.7 pH unitshigher than that of controls. Both levels were moreeffective in utilizing D- and L-lactic acids than wasthe control. However, for the treatment with low M.elsdenii, both D- and L-lactic acid spiked at about 5 hof fermentation and then diminished within 2 h. Cul-tures that were inoculated with M. elsdenii had loweracetate and propionate concentrations than did con-trols. Megasphera elsdenii could be effective in reduc-ing lactic acid accumulation in the rumen by lessen-ing the time for adaptation to high concentrate diets.

Robinson et al. (109) induced acute acidosis insteers that were fed a restricted amount of a 50%concentrate diet. On average, M. elsdenii preventedacute acidosis (pH >5.0) and increased feed intake(24% more DM) following the dietary switch. Thesedata suggest that M. elsdenii can accelerate ruminaladaptation from forage to grain. The implications ofthis type of product in dairy cattle could be significantbecause it relates to the transition period and adapta-tion of high grain levels in early lactation.

As previously mentioned, a major contributory fac-tor to acute acidosis is a greater number of lactic acidproducers compared with utilizers. Russell (114) in-


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dicated that S. bovis and M. elsdenii underwent con-siderable competition. Megasphera elsdenii cannotuse starch, but S. bovis can ferment starch andproduce maltose. Both microbes can use maltose;therefore, both also compete for the substrate, andfactors affecting the relative numbers of S. bovis andM. elsdenii are associated with their relative capacityto use maltose, production of lactic acid by S. bovis,the use of lactate by M. elsdenii, the efficiency ofsubstrate use for growth by both microorganisms, andthe tolerance to low ruminal pH (116). These factorscan all contribute to a shift in population, which cantrigger or sustain ruminal lactic acidosis.

Systemic Lactic Acid Metabolism

Once the physiological conditions in the rumenhave overwhelmed the microbial population to se-quester lactic acid, absorption into the blood streamand systemic acidosis result. Huber (59) indicatedthat lactic acidosis is compartmentalized between thegastrointestinal tract and systemic body fluids. Somephysiological effects include pH ∼5.0 in ruminaldigesta and a decrease in the amplitude and fre-quency of ruminal contractions. A possible mechan-ism involves duodenal hydrogen receptors, which ef-fectively release secretin and, in turn, inhibit motoractivities of the forestomach, ultimately reducing mo-tility (19). Stasis may be beneficial because motilityis required to mix bacteria with substrate, which isnecessary for absorption (59).

Ruminal contents become hypertonic in relation-ship to plasma in acidotic ruminants (36, 58, 124). Akey regulatory method associated with the main-tenance of systemic pH is the bicarbonate bufferingsystem if entry of lactic acid into body fluids is notoverwhelming. The bicarbonate buffering system isusually able to maintain pH within critical limitsuntil the acidotic process has run its course.

L-Lactate Turnover

Between 40 to 65% of L-lactate is derived fromglucose (107, 108). Approximately 20% of the lactatethat enters the system is converted to glucose, and 30to 50% is oxidized to CO2. Conversion of lactate toglucose via the Cori cycle represents 5 to 10% ofglucose (4, 108, 138). L-Lactate is important as aprecursor for fatty acid synthesis as well as glucogen-esis. Approximately 16 to 38% of the acetate used forfatty acid synthesis originates from lactate (47). Thisconversion is particularly important at high intakesduring which the turnover rate of lactate is muchmore rapid than that of acetate (47).

D-Lactate Acid Metabolism

Engorgement of rapidly fermentable carbohydratesinitiates a very rapid elevation of both D- and L-lacticacids within 8 h, peaking at 20 h (56). Giesecke andStangassinger (47) reported that infusion of sugarinto the rumen elevated both isomers within 15 to 20min. The relative proportions of D- and L-lactic acidchange as pH decreases. Normally, D-lactic acid con-stitutes approximately 20% of the total lactic acidconcentration at pH 6, which elevates to about 50% atpH <5; concentrations can be as high as 100 to 150mmol/L (47).

Shifts in ratios of L-lactic acid to D-lactic acid arelargely because of a decline in ruminal concentrationof L-lactate (56). Harmon et al. (56) evaluated thenet portal absorption of lactate in steers that wereruminally infused with glucose or fed a 70% concen-trate diet for ad libitum consumption to mimic acuteand subclinical acidosis, respectively. Ruminal pHdeclined to 4.2 by 18 h and to 6.0 by 14 h for cowsreceiving glucose and concentrate, respectively. Rumi-nal L-lactate and D-lactate concentrations averaged53 and 30.2 mM for glucose and 2.1 and 1.2 mM forconcentrate, respectively. Net portal absorption of L-and D-lactate averaged 96.6 and 10.5 for concentrateand 164.5 and 71.8 mmol/h for glucose, respectively.Animals that were acutely acidotic experienced a6-fold increase in D-lactate absorption, and L-lactateabsorption increased 70%, despite higher rumen con-centrations. Even though absorption rate increasedgreatly, the increase had little effect on the relativeincreases in D- and in L-lactate in arterial and portalblood.

Elimination of D-Lactate

Under normal conditions, removal of D-lactate byoxidation, gluconeogenesis, and renal excretion ac-counts for 45, 14, and 13% of the total elimination,respectively (47). At higher rates of D-lactate entryinto the system, oxidation decreases, and renal excre-tion is enhanced. The kidney threshold for D-lactateconcentration is about 50% of that for L-lactate.Lower absorption rates of D-lactate than of L-lactatefavor faster excretion of D-lactate; the reason for thedifference is unknown (47). The D-lactate concentra-tions in blood need to reach 4.25 mM before urinaryexcretion increases in the cow (119). Harmon et al.(55) demonstrated that most D-lactate elimination incattle was by oxidation (97%), and very little wasexcreted in the urine, although the relative contribu-tion of D-lactate to total oxidative metabolism ac-counted for only 0.014% of the total CO2 expired.



Cattle apparently underwent dynamic changes veryrapidly to alter their metabolism to accommodate D-lactate.

Metabolism of D-Lactate

Limitations of D-lactate compared with L-lactatemetabolism relate to the presence or absence ofspecific enzymes and their location within the cell.The lactate dehydrogenase for L-lactic acid is locatedin the cytosol. The enzyme responsible for D-lactateoxidation is D-2-hydroxy acid dehydrogenase, whichis located in the mitochondria. Therefore, the majorcontrast between the metabolism of the two isomersis that L-lactate can be rapidly oxidized to pyruvate,which can readily translocate the mitochondrial mem-brane for further metabolism. However, D-lactatemust first translocate the mitochondrial membrane tobe oxidized. Another challenge is that D-2-hydroxyacid dehydrogenase is inhibited by increased concen-trations of pyruvate and oxaloacetate. With high lev-els of L-lactate compared with D-lactate, conversion ofpyruvate to oxaloacetate is rapid. The inhibition of D-2-hydroxy acid dehydrogenase by these metabolitesdecreases the relative amount of D-lactate that isremoved via oxidation and subsequently gluconeogen-esis (47).

Under typical acidotic conditions, the primaryroute of D-lactate elimination and the efficiency of itsremoval is associated with entry rate. At high entryrates (>45 mmol/h per kg) (75), oxidation to CO2decreases, and most elimination occurs by renal ex-cretion. However, under conditions of high gastroin-testinal lactate (i.e., acute acidosis), shifts in bodywater to the gastrointestinal tract reduce urine out-put, thereby leaving oxidation and gluconeogenesis asthe major routes for D-lactate elimination (47).

SUBCLINICAL ACIDOSIS

Acute acidosis presents specific signs and symp-toms, which, if caught in time, can be treated directly.Symptoms of subclinical acidosis are insidious andconsiderably less overt. Often, subclinical acidosis isdismissed as other problems, such as poor foragequality or poor bunk management. Therefore, acidosiscan cause a tremendous economic loss, drainingproductive efficiency potential from dairy herds. Themajor clinical manifestation of subclinical acidosis isreduced or inconsistent feed intake. Other associatedindications include decreased efficiency of milkproduction, reduced fat test, poor body conditiondespite adequate energy intake, high culling rate,unexplained diarrhea, and episodes of laminitis.

Subclinical acidosis is a consequence of maximizingenergy intake, which requires provision of appropri-ate levels of physical and chemical dietary compo-nents. Often, subclinical acidosis is found in well-managed, high producing herds.

Fate of Ruminal Mucosain Subclinical Acidosis

Ruminal mucosa is the first major metabolicallyactive tissue to which end products of fermentationare exposed. Mucosal tissue has the tremendous abil-ity to transport or metabolize organic acids that havebeen derived from ruminal fermentation. The physi-cal form and energy content of the ration has a pro-found effect on mucosal development (18, 93, 135).Greater mucosal mass is present when diets arepredominantly concentrate, suggesting a greater ca-pacity for metabolism and absorption by the ruminalwall; however, enzymatic activities do not appear tochange (95, 134, 135). The increased mucosal weightstimulated by increased starchy diets may result in athickening of the stratum corneum, resulting in aphysical barrier for VFA to metabolically active sitesand, in fact, may inhibit transport and metabolismwithin the mucosal membrane (95).

Dirksen et al. (34) indicated that adaptation of theruminal mucosal is a critical factor in pH stabiliza-tion with high sugar or high starch diets. In addition,proliferation status of ruminal mucosa had a greaterinfluence on energy supply to the high producing cowduring peak lactation. To maximize pH stabilizationand energy utilization, proliferation of the mucosalepithelium should be established and perhaps max-imized by the time the animal has calved (34).

Leibich et al. (70) compared two groups of cowsduring both the prepartum and postpartum periodsfor changes in ruminal mucosa that were dependenton feed. One group of cows received a low energy dietuntil 14 d before calving and then was switched to alactation diet. The other group of cows received thesame low energy diet until calving and then wasswitched to a lactation diet. Prior to treatment, theruminal mucosal mass of cows in both groups continu-ally declined after the transition to the dry periodration. The mucosal degeneration continued in thegroup of cows that were not switched to a lactationration prior to calving, but cows that were switched toa lactation ration 14 d prepartum exhibited a prolifer-ation of the ruminal mucosa after the dietary change.By 8 wk postpartum, both groups had patterns ofmucosal development that surpassed the initial levelat the end of lactation. A major question remains asto whether mucosal changes ultimately affect the oc-currence of postpartum disease or production perfor-mance.


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Nocek et al. (94) fed diets consisting of 60% con-centrate with hay (ground or chopped) or 100% con-centrate to Holstein calves from 8 to 20 wk of age.Biopsies of ruminal tissue were obtained at 8 and 20wk of age for VFA transport and morphological com-parisons. Acetate transport across the ruminalepithelium increased between 8 and 20 wk for calvesfed hay, but not for calves fed concentrate diets.Propionate transport was highest for calves fedground hay and lowest for calves fed 100% concen-trate at 20 wk of age. No differences in lactate produc-tion in ruminal tissue occurred. Morphology of papil-lae of calves fed 100% concentrate ranged fromclumped to long, flat papillary shapes. Lesions werefrequently visible at the distal tips. Mucosal foldingwas common, and clumping of papillae with imbeddedhair was evident in the anterior ventral region. Esti-mated surface area of absorptive mucosa was approxi-mately halved for calves fed concentrate comparedwith that of calves with 40% ground or chopped hay.Calves fed the 100% concentrate diet had a slightlylower DMI than did calves fed ground hay (2.49 vs.2.74 kg/d), and daily gains were slightly greater(0.80 vs. 0.73 kg/d) (27). Mean ruminal pH waslower (pH 5.6 to 6.7) for calves fed concentrate (96).During the 12-wk period, high concentrate dietscaused no clinical health or performance problems;however, the period was short.

Nocek and Kessler (95) reported morphologicalabnormalities for calves fed a complete calf ration incontrast to those for calves fed a traditional dietbased on hay and grain. After calves were returned toa traditional diet, papillary rejuvenation and develop-ment appeared to be normal for calves that were fedthe complete calf ration within a 4-wk period. Dirksen(33) indicated that approximately 4 to 5 wk wereneeded to achieve a highly stable state for the rumi-nal mucosa after a dietary change from a low to highenergy density. A major question that remains is thethreshold of ruminal pH or physical form that affectsthe ruminal mucosa positively enough to allow ade-quate proliferation for maximal absorption andmetabolism and still not be symptomatically hyper-parakeratotic, thus reducing metabolic activity andability of organic acids to be transported. Duringearly lactation, cows are typically fed a diet consistingof primarily acidic silages with ≥ 60% grain. Thisdietary scenario would appear to be conducive tocausing a slow, insidious reduction of absorptive capa-bility in ruminal mucosa, especially when animalswere maintained on a wet silage diet for the entirelactation cycle. The regulation potential of ruminalmucosa would probably be jeopardized.

Profile of Subclinical Acidosis

Specific parameters need to be identified relatingeither to cow manifestations (milk, urine, blood, andfeces) or dietary characteristics that would aid in thediagnosis or prediction of predisposition to the dis-ease. Often, bulk tank testing for fat is utilized toidentify the onset of subclinical acidosis. Individualacidotic cows demonstrate very low milk fat concen-trations that are not necessarily reflected in the over-all tank test or mean for that group.

Italian researchers (45) studied the effect of nutri-tionally induced acidosis on milk composition. At 15,45, and 90 d postpartum, acidotic cows had less milkfat (2.73 vs. 3.88%) and total milk protein contentthan did controls. The reduction in milk lipids wasrelated to ruminal inversion of the molar ratio ofacetate to propionate. Casein and the ratio of caseinto protein tended to decrease, and the ratio of NPN toprotein tended to increase, for acidotic cows comparedwith those of control cows at each time period (Table1). Also, milk alterations occurred with irregularappetite, transient episodes of diarrhea, and weightloss; no clinical mammary gland alterations were no-ticed.

Kostyra et al. (68) studied changes in N compo-nents in milk after inducing acidosis with sucroseadministration. After 24 h of acute metabolic acidosis,the concentration of total N, casein N, N of wheyproteins, and NPN increased in milk. Between 48 and72 h after sucrose administration, a quantitativechange occurred in N compounds, but concentrationsreturned to preacidosis levels by 6 d.

Intake as an Indicatorof Subclinical Acidosis

For beef cattle, intake patterns are the most impor-tant indicator of subclinical acidosis (120). Fulton etal. (42) evaluated the effect of increased concentratefrom 35 to 90% for cattle fed either dry-rolled corn orhard red winter wheat. Intake profiles for cattle thatwere fed corn appeared to be consistent, indicatingthat those cattle were adjusting normally to highconcentrate diets. However, cattle that were fedwheat diets did not demonstrate increased intake.Evaluation of daily intake data revealed considerablevariation in intake patterns across both groups, butthe variation was not as great for the cattle consum-ing corn until the 90% concentrate level was reached,at which time intake decreased dramatically. Thecattle that were fed wheat experienced acidosis,reduced their intake dramatically for a few days,recovered, ate again, but were unable to adjust to thewheat. These data would suggest that mean intakescan be very misleading values. Extreme variation in



TABLE 1. Milk protein profile of cows induced with nutritionalacidosis.1,2

a,bMeans within a column followed by no common superscriptdiffer ( P < 0.05).

1Gentile et al.(45).2Acidotic state diet is defined as 15 d prepartum to 90 d postpar-

tum: blood pH of 7.3, urine pH of 6.4, irregular appetite, diarrhea,and weight loss.

TimeVariable postpartum Control Acidotic

( d )Protein, % 15 3.92a 3.35b

45 3.28a 2.90b

90 2.94a 2.65b

Casein, % 15 3.47 2.3345 2.56 2.0790 2.32 1.95

Casein protein, mg/ml 15 0.78 0.6945 0.75 0.7190 0.79 0.73

NPN:Protein 15 0.055 0.22045 0.063 0.07090 0.058 0.071

ruminal pH is sufficient to throw cattle off feed. Cat-tle that were fed wheat were able to reduce theirruminal acid load by slowing eating rate. Cattle be-gan eating again when ruminal pH reached ≥5.6.Fulton et al. (43) showed that, when ruminal pH wasmanually adjusted to ≥5.6, for cows that consumedwheat diet, intake patterns were more similar tothose of cattle fed corn. For beef cattle, ruminal pHshould be maintained at ≥5.6 to minimize the intakedepression that is associated with subclinical acidosis;however, no information is available for dairy cowsthat identifies which pH thresholds are associatedwith subtle reduction or variation of intake.

Diagnosis of Subclinical RuminalAcidosis: Predicting Ruminal pH

The identification of specific ration parameters forprediction of ruminal pH would assist in the develop-ment of rations that may control the occurrence ofsubclinical acidosis. R. E. Pitt, J. S. Van Kessel, D. G.Fox, A. N. Pell, M. C. Barry, and P. J. Van Soest(1995, unpublished data) utilized the Cornell NetCarbohydrate Protein Model ( 8 ) to predict ruminalpH from a variety of ration nutrient parameters. Themodel considered the effect of pH on microbial growthand yield as well as products of carbohydrate fer-mentation, lactate metabolism, concentration and ab-sorption of VFA and lactate in the rumen, intake,production, ruminal volume, and liquid rate of pas-sage. Reported mean pH were correlated to measure-

ments for dietary rations of various species (dairycows, sheep, and steers). The empirical relationshipbetween ruminal pH and total forage in the dietaryDM was poor (R2 = 0.15). Total ration NDF only ac-counted for approximately 30% of the variation as-sociated with ruminal pH (R2 = 0.30). A factor thataccounted for the most variation associated withpredicting ruminal pH was effective NDF ( eNDF) asa percentage of DMI (R2 = 0.52). The measurementof eNDF used was listed by Barry et al. (8) .

To evaluate the effect of ration NDF ( 8 ) on meanruminal pH of rations for lactating dairy cows, 27studies (1, 5, 20, 21, 24, 30, 31, 40, 41, 44, 46, 49, 50,60, 63, 67, 80, 86, 101, 110, 118, 121, 122, 129, 130,132, 133, 134) were used to determine the effect ofration NDF on mean ruminal pH. The eNDF valueswere obtained from data of Barry et al. (8) . TheeNDF values only accounted for about 5.0% of thevariation that was associated with mean ruminal pH.This relationship does not agree with results of otherstudies (Pitt et al., 1995, unpublished data). Thediscrepancy could be associated with difference inanimal species and thus a wide range of values usedin regressions, lack of validity of mean pH, and themethod of effective fiber determination.

Ruminal pH as a Diagnostic Toolto Detect Subclinical Acidosis

Subclinical acidosis is a temporarily altered stateof the rumen that causes some aberration in fermen-tation patterns and decreased ruminal pH; however,intensity and duration are not sufficient to causeimmediate or overt clinical signs. Therefore, subclini-cal acidosis should be considered a differential diag-nosis associated with a variety of symptoms, includ-ing those listed previously. However, nutritionalalterations (i.e., adequate effective fiber, alteration ofratios of forage to concentrate, and feeding strate-gies) influence ruminal pH, which also can affect theoccurrence of subclinical acidosis. The only diagnostictest for subclinical acidosis is ruminal pH.

Stomach tubing has been used to collect samples ofruminal fluid for pH determination, but this proce-dure often has been falsely interpreted because ofsaliva contamination. Ruminal cannulation is thepreferred method of obtaining representative samplesof ruminal fluid. Although cannulation has tradition-ally been limited to research purposes, dairy fieldprofessionals are beginning to realize its value andapplication.

Nordlund and Garrett (100) discuss rumenocente-sis or percutaneous needle aspiration as a means ofcollecting ruminal fluid for diagnosis of subclinicalacidosis. I evaluated rumenocentesis with the follow-ing objectives: to determine whether one ruminal lo-


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cation would yield a representative ruminal pH andto determine the time of sampling in relation to feed-ing to achieve nadir (J. E. Nocek, 1995, unpublisheddata). The study was a 3 × 3 Latin square with threeforage to concentrate ratios: 30:70, 40:60, and 50:50.Three ruminally cannulated cows were utilized, andruminal samples were taken at hourly intervals twiceprior to feeding, at 7 h postfeeding, and at 12 hpostfeeding (one sample). Sample locations were asfollows: 1) composite of six locations by aspiration(about 200 ml), 2) one location for aspiration of theventral rumen (50 ml), and 3) one point for per-cutaneous needle aspiration (about 5 ml) in the samelocation as the aspiration of the ventral rumen. Thislocation would be the same as that recommended forsampling by rumenocentesis. There were no signifi-cant differences between composites of multiple sam-ples and one sample aspiration of the ventral rumen.Samples taken at 1600 h by rumenocentesis were 0.1to 0.2 pH units higher than the mean values for thecomposite and single samples. Garrett et al. (44)compared needle rumenocentesis versus cannula col-lections and found that needle values for the probeswere approximately 0.35 units lower than those ofsamples obtained via ruminal cannula. The followingequation related cannula pH and needle probing: can-nula pH = 3.257 + 0.506 (needle pH) (r = 0.73, P >0.01).

To reach the nadir when the TMR was fed oncedaily, ruminal samples should be taken 5 to 8 hpostfeeding. These recommendations coincide withthose of Nordlund and Garrett (100) for feeding aTMR. Cows fed forage and concentrate separatelyshould be sampled 2 to 5 h after concentrate feeding(100). Cows should be selected from high risk groupsduring the first 60 d postpartum. Because considera-ble variation is inherent, a minimum of 10 animalsper group should be considered. Nordlund and Gar-rett (100) indicated that, if >30% of the cows withinthe particular subgroup have a pH of ≤5.5, the groupshould be considered as abnormal, and further evalu-ation should be conducted of feeding managementpractices. When pH values were between 5.6 and 5.8,the group was considered to be marginal. Finally, ifall pH were >5.8, the pH status of the group was con-sidered to be normal. These guidelines need to beevaluated further for cows consuming high energydiets (1.72 Mcal/kg) to determine the nadir. Thistype of diagnostic tool should be used in conjunctionwith other factors, such as evaluation of ration,management practices, and herd health problems.

Risk of Acidosis

Although guidelines exist for acidosis risk, highproducing cows that consume large quantities of grain

(55 to 60% of DM) tend to have lower ruminal pHduring the day. It is unknown how low pH can go andfor how long before negative effects are demonstrated.Nordlund (99) described the onset of acidosis asperiparturient cow acidosis and ration formulationand delivery acidosis, which suggest that the differentphysiological occurrences that normally take placeduring transition phases of the lactation cycle predis-pose the cow to acidosis. In addition, managementfactors regarding ration formulation and delivery canmediate the effect of these physiological states andthe risk of contracting acidosis.

In more closely evaluating the transition betweenphysiological states and management practices, thereappears to be considerable overlap from the close-updry period through the peak of DMI. These two majorcausative regions could be designated as cow-mediated acidosis and management-mediated acido-sis, respectively.

Cow-Mediated Acidosis

During the transition from the dry period to lacta-tion, several physiological events and managementpractices occur. The DMI of grain increases from 30 to40% to approximately 60% of the ration DM and ismaximized at approximately 12 to 14 wk postpartum.Microbial adaptation to ration changes can signifi-cantly influence the potential for acidosis develop-ment. During the close-up dry period (1 to 3 d prior tocalving), a reduction in DMI occurs that can signifi-cantly influence the microflora, pH, and endotoxinproduction in the gastrointestinal tract. Cows arepredisposed to metabolic and infectious diseases dur-ing the first 30 to 35 d postpartum. Therefore, cow-mediated acidosis is associated with the normalcourse of events (physiological stress) presented bythe cow. If transition events and stress are notmanaged correctly, some degree of acidosis is likely tooccur.

Management-Mediated Acidosis

Cow- and management-mediated acidosis overlap.During the transition period and through 50 d post-partum, management of the cow-mediated eventsplay an important role in the development of acidosis.

Interpretation of the normal ecological balancewithin the rumen can ultimately assist in predispos-ing the cow to subacute acidosis. When intake isreduced, energy metabolism of the ruminal microor-ganisms as well as the host system is interrupted.Intake is controlled by a balance of physical andchemostatic mechanisms. The challenge is to ensure



Figure 2. Progression of physiological events that link acidosiswith laminitis. CHO = Carbohydrate.

that both mechanisms work in synchrony so that onedoes not overpower the other (i.e., too much grain orfermentable carbohydrate vs. too much forage).

Factors such as the amount and type of grain,grain processing, and forage type, quality, and levelsinfluence intake patterns, energy metabolism, andsubclinical acidosis. The rate and extent of digestionand the amount of starch intake modify the severityof acidosis. Grain mixes containing finely ground orhighly processed cereal grains have the fastest ratesof ruminal digestion of starch. It is critical that thegrain portion of the diet complement the forage typeand quality and contain ingredients with various lev-els of ruminal carbohydrate availability. Both lowroughage and reduced particle size exacerbate acido-sis during the critical transition period.

Although several factors (e.g., heat, cold facilities,management, and diet composition) influence intake,managers ultimately must anticipate and compensatefor intake challenges associated with normal dailypractices.

The Implications of Acidosison the Development of Laminitis

The progression from acidosis to laminitis is as-sociated with several systemic phenomena. Figure 2outlines several aspects that have been associatedwith the development of laminitis. A very strategicand critical apex in this entire cascade process is thereduction of ruminal pH. The effects of pH on thepathogenesis of the rumen, liver, and gastrointestinal

tract ultimately affect hemodynamics and predisposecows to laminitis. The onset of acute acidosis presentsvery hastened and dramatic hemodynamic insultsthat predispose animals to severe but short episodesof acute laminitis. Several severe episodes of shortduration or low insidious levels of acid can create asituation that predisposes the rumen to hyperkerato-sis, pathogen infiltration, and, ultimately, abscessedliver to variable degrees. In addition, changes in gas-trointestinal tract osmolarity, hemoconcentration,and vascular destruction can ultimately result in alow grade but irreversible laminitic process.

LAMINITIS

Definition and Incidence

The scientific name for laminitis is pododermatitisaseptic diffusa, which is an aseptic inflammation ofthe dermal layers inside the foot. Table 2 illustratessurveys that have been conducted to identify the inci-dence of lameness in various parts of the world.Across surveys, mean incidence of lameness rangedfrom 5.5 to 30%. Within surveys, incidence of lame-ness ranged from 0 to 55%. Very few studies havebeen conducted or published to evaluate factors affect-ing lameness in commercial US dairy herds. Wells etal. (136) evaluated the relationship between clinicallameness and risk factors for individual cows in Min-nesota and Wisconsin dairy herds and concluded thatbody weight, body condition score, rear lateral digitangle, nontarsal rear limb superficial swelling, abnor-mal hoof overgrowth, and limb laceration were preva-lent risk factors for clinical lameness. Table 3 illus-trates the types and percentages of foot lesions foundin the largest survey (115). Approximately 62% ofthe total of manifested lesions could be associatedwith laminitis in some form, suggesting the impor-tance of laminitis as a cause of lameness.

To understand the laminitic process as it relates tometabolism and subsequent mechanical and physicaldamage, the basic anatomical components of the bo-vine foot must be understood. Fundamental detailscan be found elsewhere (53, 83, 90).

Causes of Laminitis

Laminitis has a multifactored etiology and isthought to be associated with several, largely inter-dependent factors (83, 100). Nutritional manage-ment has been identified as a key component in thedevelopment of laminitis, particularly the feeding ofincreased fermentable carbohydrate, which results inan acidotic state. Metabolic and digestive disorders


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TABLE 2. Incidence of lameness from surveys.

Study X Range Herds Location

(no.)Russell et al. (113) 5.5 1.8–11.8 1821 United KingdomEddy and Scott (37) 7.3 0–32 150 United KingdomPhilipot et al. (104) 8.0 . . . 160 FranceDewes (32) 14.0 . . . 4 New ZealandWells et al. (136) 13.7/16.7 . . . 17 United StatesTranter and Morris (127) 16.0 2–38 3 New ZealandWhitaker et al. (137) 25.0 2–55 185 England, WalesPrentice and Neal (106) 30.0 . . . . . . England

TABLE 3. Types and percentages of foot lesions: incidence of lami-nitis and associated lesions.1

1Russell et al. (113).2First seven lesions listed account for 61.8% of foot lesions.

Foot lesion2 ( % )

White line abscess 15.6Sole ulcer 13.6Underrun heel 8.7Aseptic laminitis 5.3White line separation 4.7Deep sepsis 3.5Punctured sole 10.4Interdigital hyperplasia 4.8Foreign body in sole 3.5Interdigital foreign body 2.2Overgrown sole 2.2Sandcrack 1.3Other 7.5Total 100.0

can predispose the cow to laminitis. Hormonalchanges associated with parturition and other phasesof the lactation cycle can have an impact on certainphysiological changes. Infectious diseases, such asmastitis, metritis, and foot rot, can impose specificendotoxic insults (76). Environmental aspects, suchas hard surfaces, lack of or little use of bedding, andlack of or excessive exercise on undesirable surfaces,can predispose animals to mechanical damage (13).Other factors, such as body condition, body weight,and feet and leg structure, can unnaturally increasethe weight load and stress on feet, exacerbating theinternal mechanical damage that is associated withlaminitis.

Mechanisms of LaminitisDevelopment

The mechanistic phases of laminitic developmentcan be best described as alternating stages of distur-bances relating to metabolic and subsequent mechan-ical degradation of the internal foot structure (14, 83,100). The process can be segmented into variousphases.

Phase 1

The initial activation phase of laminitis, phase 1, isassociated with a systemic metabolic insult (Figure3). This phase is a result of ruminal and, subse-quently, systemic pH. The reduction in systemic pHactivates a vasoactive mechanism that increases digi-tal pulse and total blood flow. Depending upon theinsult that initiates the process, endotoxins and hista-mine can be released, which create increased vascularconstriction and dilation and, in turn, cause the de-velopment of several unphysiological arteriovenous( AV) shunts, further increasing blood pressure. Theincreased blood pressure causes seepage through ves-sel walls, which ultimately are damaged. Damagedvessels then exude serum, which results in edema,internal hemorrhaging of the solar corium from

thrombosis, and ultimately the expansion of the co-rium, causing severe pain.

Phase 2

As a result of the initial insult, there is mechanicaldamage, phase 2, which is associated with the vascu-lar system (Figure 3). Once vascular edema has oc-curred, ischemia (local anemia) results in hypoemiaof the local internal digital tissue, causing tissuehypoxia, resulting in fewer nutrients and less oxygenreaching the epidermal cells. Ischemia itself can trig-ger a further increase in AV shunting. Trauma,stress, and certain actions releasing hormones andchemicals can increase AV shunting. As a result ofprevious events, increased blood pressure further in-creases vascular seepage in the lower part of the digitas well as edema and ischemia. This cycle continuesas long as the initial insult continues.



Figure 3. The phasic progression of laminitis development. Phase 1, initial activation; phase 2, local mechanical damage; phase 3, localmetabolic insult; and phase 4, progressive local damage of the bone structure. AV = Arteriovenous.


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Figure 4. Stages of laminitis development: severe (acute), sub-clinical, and chronic.

Phase 3

In phase 3, as a result of the mechanical damageassociated with microvasculature and fewer nutrientsprovided to the epidermal cells, the stratum ger-minativum in the epidermis breaks down (Figure 3).These events ultimately cause corium degenerationand breakdown of the laminar region associated withthe dermal-epidermal junction.

Phase 4

Ultimately, in phase 4, local mechanical damageoccurs (Figure 3). A situation develops in which theepidermal junction is broken down, which results inthe separation of the strata germinativum and co-rium. This separation in turn results in a breakdownbetween the dorsal and lateral laminar supports ofthe hoof tissue. Ultimately, the laminar layerseparates, and the pedal bone takes on a differentconfiguration in relationship to its position in thecorium and dorsal wall. As the bone shifts in position,it causes a compression of the soft tissue between thebone and sole, which is extremely susceptible todamage. The compression of this soft tissue results inhemorrhage, thrombosis, and further enhancement ofedema and ischemia, resulting in a necrotic areawithin the solar region of the foot. Small areas of scartissue can accumulate because of the necrotic process.Once this process is triggered, continued potential fortissue degeneration persists because cellular debris isincorporated into the cellular matrix and the produc-tion and integrity of new horn tissue layers are hin-dered. Ultimately, a variety of processes can occur asa result of the incorporation of scar tissue interven-tion, which includes double sole phenomenon, solehemorrhages (red blood patches), bruises, diffuse le-sions, and solar pulp. Figure 4 depicts the anatomicaland physiological aspects associated with develop-ment of the various forms of laminitis: acute, subclini-cal, and chronic (38, 73, 74, 131).

Acute Laminitis

During acute laminitis, the cow is systemically ill.Inflammation of the corium is evident; however, veryfew if any clinical signs are manifested. The cow isprone to recurrences if the metabolic insults persist.Vessel seepage, edema of the capillary beds, and AVshunting are all initiated. Vascular congestion ispresent. The major local clinical signs in addition tointense pain include some swelling and temperaturesthat are slightly warmer than normal above the coro-nary band in the soft tissue area.



Figure 5. Illustration of the lateral digit of a posterior foot thatis broadened, flattened, and possesses elongated sole characteris-tics of a laminitic digit. Sole hemorrhaging, yellow discoloration,and bruised area are visible in contrast to the medial toe (left).

Subclinical Laminitis

Subclinical laminitis can be a long, slow, insidiousprocess that is dependent upon the persistency of lowgrade insults. The horn becomes physically softer dur-ing this period, and the yellowish coloration of thesole is caused by serum seepage from the vessels intothe solar corium. Hemorrhagic stains are manifestedin the solar area, particularly in the white lineregions, the apex of the sole, and the sole-heel junc-tion. Internally, ischemia, hypoxia, and epidermaldamage are key aspects associated with this stage.Arterial-venous shunting becomes an increasing oc-currence. White line separations, frequent dorsal wallridges, and a slight tilting to definite rotation of thepedal bone are characteristic internal manifestations.Sometimes the soles of affected feet are soft and warmbut without visible lesions. This appearance may beassociated with integral hemorrhagic areas. A possi-ble theory about the development of heel cracks anddouble soles may be that hemorrhagic areas, oncewalled off, become a perfect environment for anaero-bic bacteria to grow. As gas and exudate develop, theyare forced by pressure to points of least resistance,which often are at the junction of the sole and heelbulb.

Chronic Laminitis

During the chronic stages, several changes are as-sociated with the localized area of the digit. Thegrowth pattern of the keratinized horn is disrupted,and the shape of the digit is altered, becoming moreelongated, flattened, and broadened (Figure 5).Grooves and ridges on the dorsal wall, giving a rip-pled appearance, become prominent. Internally, the

pedal bone has separated from the dorsal aspect ofthe wall. Often, ulceration can be demonstrated at thesolar region of the foot. Double soles with yellowishdiscoloration continue to be a major clinical sign.Continued ischemia results in destruction of the capil-lary beds and development of AV shunts; arterioscle-rosis is a prominent histopathological feature. Cellu-lar destruction results in the separation of thedermal-epidermal junction and, ultimately, internalfoot destruction. In severe situations, the distal aspector keel portion of the pedal bone can protrude throughthe corium and hard-horned tissue of the sole. Figure6 shows a cow with chronic laminitis. Once the dis-ease process has reached this point, the damage hasbeen done; no therapy can return the foot to a normalconfiguration. The degree of chronic laminitis de-pends on the intensity and frequency of each acuteepisode and, ultimately, the degree of damage eachpreceding episode has caused as a result of the initialmetabolic insult.

PATHOGENESIS OF LAMINITIS

Vasoactive Substances

Destruction of the normal hemodynamic processhas been identified as a major etiological factor as-sociated with the development of laminitis (14, 76).Histamine has long been identified as a potentvasodilator and arterial constrictor (22) and is natur-ally found in tissues and blood. Early works by Dainet al. (29) showed a direct correlation between thepH of the rumen, histamine concentration in the in-gesta, and health of the animal. Sanford (117) alsoindicated a similar relationship between histamineconcentration and pH of the ruminal fluid and sug-gested that histamine formation was a result of achange in microbial population. Histamine can beformed by the decarboxylation of histidine in severallactobacilli species (111).

The hemodynamics that are associated with thecirculatory effects of histamine on laminitis coincidewith mode of action. Early detection of laminitis andtreatment with antihistamine has had good results(64). Maclean (75) indicated that histamine wasslightly elevated during acute laminitis of cattle feddiets that are high in concentrate; however, hista-mine is somewhat higher in the serum of cows inchronic stages of laminitis. Once histamine is ab-sorbed into the portal circulation, it is rapidlymethylated or oxidized to various inactive forms(48). Oral administration of histamine has had noeffect on causing laminitis because histamine ismetabolized by the liver, the gastrointestinal wall,and the intestinal bacteria (48). A more feasible


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Figure 6. Illustration of “slipper foot”; concave sole, elongatedtoe, dorsal wall concavity, and ridging and swelling of the coronaryband are characteristic of a chronic laminitic digit.

explanation for the elevation of serum histamine dur-ing the occurrence of chronic laminitis might be therelease of histamine as the result of the corium tissuebreakdown, stress, or protein degradation that is as-sociated with other necrotic diseases such as mastitisand metritis. Dougherty et al. (35) injected sheepwith histamine but were not able to reproduce charac-teristics of lambs dosed with the ruminal contents ofacidotic sheep. Anaerobic bacterial growth in develop-ing abscesses and hemorrhagic areas of the foot mightalso contribute to histamine production.

Acidosis creates ruminal conditions that are ap-propriate for a chain of events associated with theliberation of Fusiformis necrophorus. These bacteriapermeate the wall of the rumen as a result of rumini-tis or hyperkeratosis and enter the portal circulation,predisposing the cow to liver abscesses. The degenera-tion process associated with this chain of events canalso cause release of histamine. The primary target ofendotoxins appears to be vascular arterial tissues,which affects the release of vasoactive mediators,thus inducing an acute inflammation of the dermisand associated vascular responses (51). Endotoxins,released from lysed bacteria as a result of low rumi-nal pH, have been extracted from ruminal fluid (84).

Controversy also exists about the specific action ofhistamine and vasoactive substances on the processaffecting hemodynamics. Brent (17) indicated thathistamine increases capillary permeability and arteri-olar dilatation. The Merck Index (81) identifies hista-mine as a potent vasal dilator, and Chavance (22)identified histamine as a potent arterial constrictor. Ifhistamine is an arterial constrictor and vasal dilator,blood pressure and flow would increase to the capil-lary beds and allow pooling, vessel rupture, serum

seepage, and hemorrhaging. If the reverse were thecase, then pooling would also occur because of con-striction of veins rather than arteries. In any event,the impedance of blood flow and pressure buildingwithin the capillaries forces fluid through the vesselsinto the interstitial tissue spaces setting up ischemia.

When the microvasculature of the corium is af-fected by vasoactive substances, vascular destructionis inevitable. When blood is not returned to circula-tion by the musculature of the vascular system,seepage and hemorrhage can result. The anatomicalfeatures of the corium vascular network play a veryimportant role in the development of various stages oflaminitis (83).

The involvement of histamine and endotoxins fitswell with the nutritional theory of laminitis develop-ment. However, histamine release can be caused by avariety of factors other than nutritional origin, suchas environmental stress, concussion, trauma as-sociated with concrete floors, overcrowding, and infec-tious diseases, causing tissue breakdown. Thisprocess accentuates the dynamics of the etiology oflaminitis, particularly because many of these eventsoccur during the first 50 d postpartum (112).

Even though histamine and endotoxins havereceived much of the attention that is associated withvasoactivity, other substances may be importantseparately or in conjunction with histamine in creat-ing an altered hemodynamic state. Serotonin is foundin the mucus membranes of the intestinal tract and isliberated by blood platelets (81). The specific mode ofaction can be associated with smooth muscle contrac-tion as well as dilation of capillary beds and contrac-tion of arterioles. Hormonal changes associated withparturition ( 2 ) have been associated with vasculardynamics. Estrogen has peripheral dilation activityand also enhances catecholamine-mediated vesselconstriction, which could have a significant impact onhemodynamics (2) .

Characterization of Laminitis

Philipot et al. (104) conducted a survey to charac-terize clinical laminitis and to identify risk factorsthat are associated with affected cows. A total of 4896cows from 160 French dairy farms were evaluated.Very few (11%) cows were free from foot lesions, and>25% of the cows were affected by at least one of thefollowing lesions: heel erosion, sole hemorrhage, dor-sal wall concavity, and yellow sole coloration. Three ofthe lesions that are associated with laminitis did notcause lameness: yellow discoloration of the sole, brit-tle horn, and dorsal concavity of the wall. Eightypercent of the cows were lame during the survey, andat least one foot lesion was identified in 89% of the



Figure 7. Illustration of various degrees of sole hemorrhaging appearing in order from top to bottom, left to right: 0 = no hemorrhage, 1= light hemorrhagic permeation in small area (<50% surface), 2 = light hemorrhagic permeation in large area (>50% surface), 3 = darkhemorrhagic permeation in small area (<50% surface), 4 = dark hemorrhagic permeation in large area (>50% surface), and 5 = soleulceration (at any location:exposed corium).

cows. The relationship between podolesions and lami-nitis identifies the presence of a subacute and chronicphase. The subacute phase is characterized by yellow-ish colorization of the sole, white line separation,double soles, and sole ulcers; the chronic phase ischaracterized by wall ridges and concavity of thedorsal wall. Other researchers (126) have indicated

that yellowish colorization is more specific to lamini-tis because this colorization represents serum exuda-tion from the corium; solar hemorrhaging can be as-sociated with a variety of disorders, includingmechanical injury. Subacute laminitis was furthercategorized into a benign or serious phase. The be-nign phase did not include lameness, but consisted of


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Figure 8. Depicts a cross sectional view of a digit; note theseparation of the dorsal aspect of the pedal bone.

yellow colorization of the sole. The serious phase wascharacterized by yellow colorization of the sole plus atleast one of the three subacute components of whiteline separation, double soles, and sole ulcers. Yellowcolorization of the sole was a higher risk factor oflaminitis than hemorrhaging of the sole (128).

Subclinical Laminitis: Involvementof Sole Hemorrhaging

Sole hemorrhaging is very common and often isrelated to the incidence of subclinical laminitis.Enevoldsen et al. (39) indicated that 29.7% of firstlactation cows and 24.7% of cows in second and thirdlactations have sole hemorrhages in >1 foot. Otherresearchers (6, 82, 102, 128) also found a >25% inci-dence of sole hemorrhaging. Laminitis is associatedwith inflammation of the local corium, a process thatinvolves vascular breakdown, hemorrhaging, and exu-dation of the serum from capillary beds. As the horntissue of the sole grows, the hemorrhaging moves tothe external surface, and ultimately, the externaltissue of the sole is a prominent clinical sign thatinternal hemorrhaging has occurred. The interval be-tween occurrence and appearance of a hemorrhagicarea is a function of growth rate. Growth rate of thehorn is approximately 5 to 6 mm/mo (53, 77). Solethickness ranges from 10 to 12 mm. Depending upontrimming objectives, the expected time needed for ahemorrhage to externalize is approximately 2 mo.

Bargai and Levin ( 6 ) indicated that sole hemor-rhaging and white line separation are sequel lesionsof subclinical laminitis. Inflammation of the coriumresults in hemorrhaging, which is a clinical sign oflaminitis (11). Hemorrhages of the sole are com-monly found 2 to 3 mo postcalving and are verycommon in first calf heifers (11, 52).

The severity of hemorrhages is related to the inten-sity and duration of the insult that caused the vascu-lar disruption. Bergsten (12) developed a photomet-ric method of scoring to record sole hemorrhages: 0 =no hemorrhage, 1 = slight hemorrhage in small area,2 = slight hemorrhage in large area, 3 = moderatehemorrhage in large area, 4 = severe hemorrhage insmall area, and 5 = severe hemorrhage in large areaor with ulceration. A consistent methodology to evalu-ate sole hemorrhages is important in characterizingthe pathogenesis of laminitis. Evaluation betweentwo assessors for sole hemorrhages indicated goodcorrelation (r2 = 0.78; P < 0.001). Figure 7 illustratesvarious degrees and locations of sole hemorrhaging.The site of sole hemorrhaging or ulceration is a reflec-tion of the severity of the disease process. For exam-

ple, if sole hemorrhaging was relatively light in inten-sity but diffuse throughout the entire region of thesole (score 2), vascular damage was neither severenor associated, in particular, with mechanical damageassociated with shifting bone structure at this time.More specific intense hemorrhaging at a specific locus(score 3) would suggest a mechanical degradationassociated with pedal bone separation and irritation.

The site of sole necrosis depends on the angle atwhich the pedal bone descends. If the distal point ofthe pedal bone descends first, compression and des-truction of the corium of the sole can cause hemor-rhaging or ulceration. If detachment between the dor-sal aspect of the pedal bone and corresponding walloccurs, the distal tip of the bone could eventuallycause ulceration in the toe region. Figure 8 depicts afoot with separation of the dorsal aspect of the pedalbone.

Bergsten (13) evaluated 11 laminitic and controlherds for 2 consecutive yr. Sole hemorrhages werescored for each digit and were related to clinical lami-nitis. Herds with a high incidence of laminitis hada greater tendency for lesions than did controlherds, and hind digits were affected more thanfront digits. Primiparous heifers were more prone tosole hemorrhage than were multiparous cows.Primiparous heifers had a higher score, regardless ofwhether they came from a laminitic or control herd;hind feet were twice as susceptible as front feet for allcows. Higher hemorrhage scores for cows were as-sociated with housing on hard concrete floors withlittle or no use of bedding. The occurrence of solehemorrhaging was about 80 to 90% during the 2 yr.Others have also shown a high incidence (16). Solehemorrhages of the front feet were more prevalent onthe medial than the lateral digits; the reverse wastrue for the hind feet. Other factors that were related



Figure 9. Illustration of the development of the clinicalmanifestations of chronic laminitis. Adapted from Boosman et al.(15).

to sole hemorrhages were associated with feedingpractices, which included fewer than four daily feed-ings of concentrates, the short time allocated for cowsto consume concentrates, and the feeding of concen-trates as the first meal in the morning or afternoon(13). The incidence of sole hemorrhages was posi-tively correlated with clinical laminitis, which agreedwith results of Livesey and Fleming (71), suggestingthat sole hemorrhaging can be used to gain informa-tion relating to the etiology of subclinical and clinicallaminitis (13).

Greenough and Vermunt (52) showed a distinctpattern of changes in severity of sole hemorrhagewith respect to calving and parity. Primiparous heif-ers demonstrated more severe sole hemorrhagingthrough calving, and then the incidence decreaseddramatically; the incidence and severity tended toincrease during the dry period and continued to in-crease during the postpartum period for multiparouscows. This trend may be associated with recurringepisodes of solar hemorrhaging and scar tissue fromprevious occurrences.

Histology of Bovine Laminitis

Specific vascular changes that were associatedwith laminitis included dilation of the capillaries andvenules, proliferation of the tunica intima, hyper-trophy of the tunica media, and fibrosis of the tunicadventitia of arteries and arterioles; arteriosclerosisoccurred mainly in the corium (3) . Boosman et al.(14) investigated the histopathology of chronic bo-vine laminitis in 20 rear lateral digits. Fivehistopathological parameters were used to evaluatedigits that had clinical signs of chronic laminitis.Digits with chronic laminitis were no more severelyaffected with chronic degenerative changes than weredigits of cows in the control group. The number of AVshunts increased as age increased. In the digitalcushion area, more severe abnormalities occurredwith respect to arteriosclerosis, AV shunts, and solehemorrhages. However, only minor influences of ageon laminitis were shown. In addition, no pathologicalchanges, such as thrombosis, which is correlated withlaminitis, were evident. Chronic bovine laminitis maybe related to the altered hemodynamics in the under-lying foot without specific pathological events (14).The study was also characterized by the fact that the20 specimens were obtained from the slaughterhouse,and the age differential was identified by examiningthe teeth.

Boosman et al. (15) evaluated the arteriographicaland pathological changes associated with chronic

laminitis in 76 hind digits that were obtained fromthe slaughterhouse. Lateral digits clearly had agreater total score for laminitis than did medialdigits. Differences between medial and lateral clawswere explained by the fact that horn tissue in thelateral digit grew faster because of overburdening.More severe arteriographical lesions (i.e., arterial di-lation, tortuous and irregular vascular course, andconstriction of vessels at the exit of the pedal bone)were present in lateral than in medial toes. Primaryclaw arteries were often either dilated or constricted;however, constrictions were particularly prominent inthe toe region. The correlation ( P < 0.05) between thetotal laminitis score and arterial abnormalities in theclaw was positive. This relationship did not changewhen the score for sole hemorrhages was subtractedfrom the total laminitis score, suggesting that solehemorrhaging might not be important in themanifestation of subclinical laminitis. Boosman et al.(15) identified ridges in the dorsal wall as the bestcriteria to predict the presence of arteriographic le-sions because they were more reliable than solehemorrhaging. Mortensen (83) also agreed with thissuggestion. Figure 9 illustrates findings of Boosmanet al. (15) on the development of manifestations ofchronic clinical laminitis. A subclinical episode oflaminitis results in muralthrombosis, which causesarteriosclerosis. Arteriographic lesions can also be in-fluenced by other factors including aging, hyperten-sion, mechanical stress, and hypoxia. These changescan influence pododermal hemodynamic changes,causing loss of vascular integrity, sole hemorrhaging,poor quality horn tissue, and dorsal wall concavity.Therefore, development of chronic laminitis isthought to be associated with continuous hypoperfu-sion of the digits.


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Nutrition and Laminitis

Although the etiology of laminitis is multifactorial,nutrition has received considerable recognition as thecause. A major challenge regarding nutrition is a lackof information to specify threshold levels of carbohy-drate that initiate nutritional insult (i.e., acidosis).Carbohydrates constitute approximately 70 to 80% ofthe dairy cow ration; therefore, the level and availa-bility in various rations can have a significant impacton ruminal metabolism.

The amount of feed that is necessary to induceruminal acidosis depends on the type of carbohydrateprocessing, the adaptation period, the nutritional sta-tus of the cow, and the frequency with which thecarbohydrate is fed (42, 86, 91, 92, 93). Nocek andTamminga (98) show the rate and extent of ruminaldigestion of various feedstuffs. Barley, wheat flour,oats, and steam-flaked corn all have ruminal starchavailabilities >85%. However, processing (grinding,steam-flaking, or chemical treatment) can have amajor influence on availability (98, 125). Ruminaladaption is critical in determining the amount ofcarbohydrate that induces acidosis (86). Telle andPreston (124) showed that, for undernourishedsheep, 50 to 60 g of wheat/kg of body weight producedclinical signs of acute acidosis, but well-nourishedsheep required 75 to 80 g/kg.

Relatively few studies have evaluated the directinfluence of carbohydrate per se on the incidence oflaminitis. Manson and Leaver (79) offered a diet ofconcentrate and silage (60:40 or 40:60 ratio) to cowsduring wk 3 to 26 of lactation. The TMR of 60:40concentrate and silage was restricted to yield thesame metabolizable energy intake between treat-ments. Hooves of half of the cows for each treatmentwere trimmed prior to the experiment; the other halfremained untrimmed. The 60:40 diet increased loco-motion scores, increased number and duration of clin-ical lameness, decreased hoof hardness, and increasedmilk protein; the diet had no effect on milk productioncompared with the higher forage diet. Trimminghooves reduced the incidence and duration of clinicallamenesses. In addition, hoof growth was signifi-cantly increased by trimming. For cows fed the lowconcentrate diet, 8 cows had an incidence of lameness3.3 wk in duration; for cows fed the high concentratediet, 11 cows had an incidence of lameness 3.9 wk induration.

Because intake was restricted with the 60:40 dietand with grain fed in a TMR, the major differencebetween dietary treatments was concentrate intake(9.1 vs. 5.8 kg concentrate or 5.7 and 1.7 kg ofbarley). Cows fed a high amount of concentrate

produced 1.2 kg more milk, 0.15 percentage unitsmore protein, and 0.16 kg more milk/kg of DM thandid cows fed low amounts of concentrate. This study,therefore, demonstrated the effect of carbohydratelevel and availability on lameness, but also showedthat increasing nonstructural carbohydrate levels en-hanced production performance, at least temporarily.

In another study, Manson and Leaver (77) com-pared 7 versus 11 kg of concentrate/d from 3 to 22 wkinto lactation. Cows fed diets that were high in con-centrates had more lameness; sole lesions were themajor problem. However, cows fed more grainproduced 3.2 kg more milk/d that had 0.06 percentageunits higher milk protein. Other researchers (71, 83)have shown a relationship between high carbohydratediets, feeding frequency, and severity of digital le-sions.

The incidence of laminitis can be controlledthrough good nutrition management (high fiberdiets) and use of good feeding and management prac-tices. Increasing concentrate intake to a certainthreshold maximizes milk production and milk com-ponents.

The manner in which feeds are fed can have asignificant impact on the stability of ruminal pH. Asthe amount of concentrate goes up in the diet or thediet increases in fermentable carbohydrates, salivaproduction and rumination time decrease, whichdecreases ruminal pH. Kaufmann et al. (65) showedthat feeding frequency of concentrates has a signifi-cant impact on maintaining a stable ruminal pH.Nocek (92) found that feeding the same ingredientsand forages in different strategies during the day caninfluence the time ruminal pH remains below a giventhreshold. The influence of carbohydrate on ruminalpH is the critical link among nutrition, acidosis, andlaminitis. Although excessive amounts of ruminallyavailable carbohydrate have been blamed for in-creased acid production and for overwhelming thebicarbonate buffering systems, a lack of effective fibercan significantly influence ruminal motility, salivaproduction, and ruminal pH (Figure 10). RuminalpH is a balance between acid production from carbo-hydrate substrates and saliva production (bufferingaction). Substantially more information is needed toquantify physically effective NDF. Digestible NDFcan contribute to acid production, especially im-properly fermented, wet forages with high nonstruc-tural and carbohydrates and lactic acid levels.

The relationship between ration nonstructural car-bohydrate, ruminally available starch, NDF, andeNDF is critical in maintaining proper ruminal func-tion. Poore et al. (105) fed diets that were similar in



Figure 10. Illustration of structural (NDF) and nonstructuralcarbohydrate (NSC) on buffering in the rumen. eNDF = EffectiveNDF.

NDF (30%) in a factorial study in which sorghumwas either dry-rolled or steam-flaked and wheatstraw was substituted for alfalfa hay. Chopped wheatstraw substituted for alfalfa hay did not affect milkyield or composition. Increasing starch degradabilityincreased milk yield and protein, regardless of fibersource. These researchers suggested that a ratio offorage NDF to ruminally degradable starch should bemaintained at about 1:1 (wt/wt) to avoid depressionin fiber digestion and to maintain normal ruminalfunction. Nocek and Russell (97) showed milk yieldto be maximized when the ratio of nonstructural car-bohydrates to NDF was between 0.9 and 1.2.

The addition of hay to diets does less to enhancethe effective fiber of the diet than to increase theparticle size of silage (10). Although small amountsof hay added to the diet increased intake more thanincreased silage particle length did, milk productionand composition were unaffected by diets that werelow in eNDF (10).

Mean values for daily ruminal pH are of questiona-ble validity in evaluating the potential of a given diet

to predispose cows to acidosis. More critical to thedetriment of certain physiological events is the dura-tion spent under a given pH threshold. Dado andAllen (28) fed diets containing 25 and 35% NDF withand without ruminally inert bulk. Cows fed diets thatwere low in NDF without ruminally inert bulk had asignificantly lower mean ruminal pH. More impor-tantly, the daily minimum pH was lower, and thehours spent at pH <5.5 were higher, for cows thatwere not fed ruminally inert bulk. Khorasani et al.(66) found that mean ruminal pH was the same (pH6.06) on diets differing in protein degradability;however, daily minimum pH was significantly differ-ent.

Guidelines for Carbohydrate Fractionsin Dairy Cows Rations

Based on studies of lactating dairy cows producing>30 kg of milk (88, 99), general guidelines for differ-ent carbohydrate fraction concentrations can be consi-dered (percentage of total ration DM): NDF, 25 to30% (75% from forage); nonstructural carbohydrates,35 to 40%; and starch, 30 to 40%. When parameters ofruminal degradability are considered, the followingare general guidelines: ruminally degradable starch,60 to 70% of total starch; ruminally degradable NDF,50 to 60% of total NDF; and ruminally degradablecarbohydrate, 50 to 55% of total carbohydrate. Theseguidelines should only be considered after total rationenergy (NEL) requirements (87) are met for thespecific animals in question.

Other guidelines regarding physical form and theratios of structural to nonstructural carbohydrate in-clude forage NDF to ruminally degradable starch >1:1; NDF:nonstructural carbohydrates >0.9 and <1.2,and eNDF (forage) with 15 to 20% of particles ≥3.8cm in length.

The method of determination of starch and non-structural carbohydrate contents and the procedureutilized to determine ruminal degradability can havea significant influence on the analytical measure de-veloped. Particle size, processing method, andmoisture content can also significantly influence de-terminations of ruminal availability. In addition,storage and processing procedures of both structuraland nonstructural carbohydrate can dramatically in-fluence ruminal degradability and should be consi-dered in ration formulation. Appropriate N fractionsmust also be provided with these various carbohy-drate fractions for optimal ruminal function and car-bohydrate utilization to occur.


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TABLE 4. Effect of protein level1 on laminitis in calves.2

aDifferent ( P < 0.05) from affected farm.bSignificantly different ( P < 0.05) from affected animals within

affected farm.1Protein level: 15.3% versus 18.0% on normal farms versus

farms affected by laminitis.2Bargari et al. (7) .

Normalfarm

Affected farm

Item Normal Affected

Blood urea, mg/dl 15.9a 24.6 25.5Globulin, g/dl 3.0 2.8b 3.9Total protein, g/dl 6.1 6.1b 7.1Packed cell volume, % 29.4a 32.2b 33.9Hemoglobin, % 8.9a 9.6 10.1

Protein in the ration. The amount of protein inthe ration has been suggested to influence the inci-dence of laminitis. Manson and Leaver (78) com-pared diets with 16.1 versus 19.8% crude protein. Thehigh protein diet significantly influenced locomotionscores and the incidence and duration of clinical lame-ness for dairy cows between 3 and 26 wk postpartum.Bargari et al. ( 7 ) studied the influence of 15.3 versus18% dietary crude protein on healthy calves and onthose affected with laminitis (Table 4). Blood urea Nwas elevated for both normal and affected calves.Total protein globulin and packed cell volume wereelevated in affected calves. Therefore, high percen-tages of ruminally degradable protein have been iden-tified in association with lameness and laminitis;however, the role of protein is not yet clear.

Little information is available to identify what roleprotein might play in the development of lameness.Several postulations involve allergic histaminic reac-tions to certain types of proteins (88) or a link be-tween high protein supplementation and proteindegradation end products (9) .

Husbandry Factors Associatedwith Controlling SubclinicalAcidosis and Laminitis

Although carbohydrate nutrition has a direct linkto acidosis and laminitis, other factors—includinghousing, stage of lactation, and age—have an in-fluence on the predisposition of cows to subclinicalacidosis and laminitis.

Separation of primiparous heifers intospecific groups. Often, laminitis in primiparousheifers is associated with changes in management,such as introduction to groups of mature cows aroundcalving and to stalls with inadequate bedding or poordesign such that ease of maneuvering in and out ofthe stall is difficult. There is a relationship among thetime spent standing, the use of stalls, and the inci-dences of sole ulceration and laminitis in primiparousheifers (52). Colan-Ainsworth et al. (23) showedthat supplying additional bedding to stalls eliminatednew cases of laminitis and sole ulceration of heifers.

Provision of adequate exercise. Locomotion hasa significant influence on the hemodynamics of theperipheral circulation of the foot. Too little exercise(i.e., standing) can cause sluggish blood flow, edema,and swelling. Too much exercise and concussion onconcrete floors, especially for heifers that have beenaccustomed to pasture, can cause trauma andmechanical damage and a greater incidence of soleulceration (13).

Stall comfort. First, adequate stall space must beprovided to allow reclining and ruminating for ap-

proximately 12 to 14 h/d. The dimensions of the stallmust be proper for the size of animal that is beinghoused, especially stall length, width, and lungespace. Sand is an optimal stall bedding, providing cowcomfort, traction, and lack of organic matter for bac-terial growth that may predispose cows to mastitis.However, management of sand may be a challengebecause of burrowing and destruction to manure sys-tems. In addition, sand must be free of small stones,which can penetrate the sole horn. An earthen basewith shredded tires covered with polyethylene sheetsalso works effectively in providing a cushioned base.However, this material must not be of an abrasivenature and must not scrape hocks or knees as cowsrise and lie down. The use of sawdust with wood chipson these polyethylene surfaces can also be abrasive,causing hock lesions.

Age and stage of lactation. In a survey con-ducted in the United Kingdom, Rowland et al. (112)showed that susceptibility to lameness increased asage increased; 10-yr-old cows were four times aslikely to develop lameness than were 3-yr-old cows.The most prevalent lesions were white line abscesses,sole ulcers, and underrun heels. The incidences ofthese diseases with age were thought to be caused bycumulative factors (scar tissue).

The same study showed that lameness was morecommon during the first 120 d postpartum, account-ing for 5l% of all cases. Ulcers of the soles weresomewhat more common during the 30 d after calvingthan before calving; white line abscesses, however,were more common toward the end of lactation.

CONCLUSIONS

Bovine lactic acidosis and laminitis are linkedthrough imbalances in carbohydrate nutrition: an ex-cess of ruminally fermentable carbohydrate in con-



junction with inadequate effective fiber. However,laminitis in particular is multifactorial in etiology. Inaddition, laminitis and acidosis are prevalent duringthe transition period and are associated with an in-creased incidence of metabolic and infectious diseases,nutritional mismanagement, and an environmentthat did not provide cow comfort. The subclinicalphases of both disease processes are most costly anddamaging because symptoms are often dismissed forother problems. Critical areas of management includepractices of feeding and feed management, comforta-ble cow environment, and routine trimming and careof hooves. More information is needed in order todevelop accurate physiological diagnostic indexes thatwill alert managers to subclinical acidosis and lamini-tis in the herd (i.e., incidence of sole hemorrhaging,ruminal pH, and milk parameters) before there is apermanent negative influence on production, perfor-mance, and health.

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