Feeding to Minimize Acidosis and Laminitis in Dairy Cattle



Subacute rumen acidosis (SARA) is a prevalent problem for dairy herds (Cook et al., 2004; Nordlund et al., 2004), as characterized by having more than 25% of cows sampled via rumenocentesis four to eight hours after a total mixed ration (TMR) meal with ruminal pH less than 5.5 (Nordlund et al., 2004). Ruminal pH is largely a function of the balance between the production of volatile fatty acids (VFA) from the fermentation of carbohydrates, their neutralization by salivary and dietary buffers, and their removal by absorption across the rumen wall or passage from the rumen (Allen, 1997). SARA is caused by the consumption of high amounts of ruminally available carbohydrates, low amounts of effective fiber, or both (Nocek, 1997). Laminitis, an aseptic inflammation of the dermal layers inside the hoof and a major source of lameness for dairy herds, has been linked to SARA (Nocek, 1997; Cook et al., 2004; Nordlund et al., 2004; Stone, 2004).

Despite diet formulation guidelines for neutral detergent fiber (NDF) from forage, total NDF and nonfiber carbohydrate (NFC; Dairy NRC, 2001; Stone, 2004), physically effective NDF (peNDF; Mertens, 1997; Stone, 2004), and starch (Nocek, 1997), along with the feeding of TMR, some degree of SARA may be inevitable in high-producing dairy herds because chewing time, and as a consequence salivary buffer flow, decline per unit of rumen-fermentable organic matter (RFOM) intake or VFA production as RFOM intake increases (Figures 1 and 2; Shaver, 2002).

An increased intake of RFOM as milk production increases is a normal consequence of high milk production because of increases in dry matter intake (DMI) and the feeding of higher concentrate diets to increase dietary energy density (Dairy NRC, 2001). Further, bunk management and cow comfort have been implicated as risk factors for SARA and laminitis in dairy herds (Shaver, 2002; Cook et al., 2004; Stone, 2004). The discussion highlights the challenges that we face in our efforts to minimize SARA and laminitis in today’s dairy herds, and underscores that the margin for error in our feeding programs is small.

Readers are referred to several thorough reviews on SARA/laminitis (Nocek, 1997; Shaver, 2000; Shaver, 2002; Cook et al., 2004; Nordlund et al., 2004; Stone, 2004), as the emphasis of this paper will be to discuss current hot-topic areas.

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Transition Diets

Lead feeding, the practice of increasing the proportion of concentrate in the TMR during the last few weeks prior to calving, has become common practice. Intake of either excessive or minimal amounts of concentrate during the close-up dry period may increase the risk of SARA. Excessive lead feeding is probably not a common risk factor for SARA because low DMI during the transition period (Bertics et al., 1992) would reduce the rate and extent of post-TMR meal decline in ruminal pH, and herd managers tend to be relatively conservative with concentrate amounts for dry cows. Minimal lead feeding may increase the risk of SARA through failure to increase the VFA absorptive capacity of the ruminal papillae (Dirksen et al., 1985) and adapt the ruminal microbial population to starch during the close-up dry period prior to the feeding of high-energy (starch) milking cow diets. Further, fresh-cow transition diets and the relative composition of close-up dry-cow versus fresh-cow transition diets may influence the risk of SARA. Cook et al. (2004) suggested that transition cows may be at an increased risk of developing laminitis following a SARA trigger.

Donovan et al. (2004) evaluated the influence of close-up dry-cow and fresh-cow transition diets on the incidence of laminitis and SARA. Refer to Table 1 for a partial presentation of their data. Cows were fed either low or high-energy diets during the close-up dry period prior to calving for 24 days on average, then postcalving were fed a common energy diet for five days on average, followed by either low or high diets for 16 days on average, followed by the common energy diet again from 21 to 70 days in milk (DIM).

Treatments were as follows: Pre High NEL, Post Low NEL; Pre High NEL, Post High NEL; Pre Low NEL, Post Low NEL; Pre Low NEL, Post High NEL. Average rumenocentesis pH measurements (Garrett et al., 1999) were not affected by treatment (P > 0.05). Lowest ruminal pH for samples taken at 8, 22, and 70 DIM was 0.2 units lower (P < 0.05) for cows fed Post High NEL (ruminal pH of 5.61 on average) than Post Low NEL (ruminal pH of 5.81 on average) diets. The percentage of cows with ruminal pH less than 5.8 at 8 and 22 DIM was greater (P < 0.05) for cows fed Post High NEL (62% on average) than Post Low NEL (34% on average) diets.

Using a more conservative cutoff for SARA (Nordlund et al., 2004), the percentage of cows below ruminal pH of 5.5 were 41% and 24% for Post High NEL and Post Low NEL, respectively. Hoof scores at 60 DIM were worst (P < 0.05) for cows fed the Pre Low NEL, Post High NEL treatment. These results lend support to practice of feeding fresh cow transition diets that stair-step energy content gradually to the high-cow diet, especially when low to moderate energy close-up dry-cow diets are fed.

Heat Stress

Mishra et al. (1970) reported lower ruminal pH for dairy cows in hot-humid (85°C and 85% relative humidity) than cool (65°C and 50% relative humidity ) environments when fed either high-roughage (35% grain; pH of 6.1 vs. 6.4) or high-grain (65% grain; pH of 5.6 vs. 6.1) diets, possibly because of decreased rumination activity (Collier et al., 1982) and increased slug feeding (Mallonee et al., 1985) during heat stress. Leonardi and Armentano (2003) reported extensive sorting away from long TMR particles, and this feeding behavior may increase during heat stress as cows attempt to reduce metabolic heat production by selecting away from forage toward concentrate (McDowell, 1972). Stone (2004) recommended that dietary peNDF content be increased and NFC content decreased during heat stress to reduce the risk of SARA. Heat stress limits the amount of time cows spend in stalls, which may increase risk of laminitis (Cook et al., 2004) since laminitis increased in cows that spent more time standing on concrete rather than lying in stalls (Colam-Ainsworth et al., 1989). Managing facilities to optimize cow comfort and minimize heat stress is an important component of laminitis prevention.

Feed Additives

There are several feed additives available for use in dairy cattle diets that may minimize SARA and/or laminitis.

Rumensin® (monensin sodium) supplementation of dairy cattle diets for increased milk production efficiency was approved recently (FDA-CVM, 2004). Subclinical ketosis was reduced in transition cows treated with a monensin controlled-release capsule (Green et al., 1999). Monensin has been used to prevent lactic acidosis in cattle (Nagaraja et al., 1981), and monensin reduced lactic acid concentrations in vitro through inhibition of the lactic acid producer Streptococcos bovis (Nagaraja et al., 1987), which suggests that monensin may have a role in attenuation of SARA and laminitis.

In dairy cows, monensin increased ruminal pH in one study (Green et al., 1999) but did not influence ruminal pH in others (Mutsvangwa et al., 2002; Osborne et al., 2994; Ruiz et al., 2001). Monensin supplementation of feedlot cattle diets increased meal frequency and reduced average meal size in two trials reviewed by Milton (2000). The efficacy of monensin for minimizing SARA and laminitis in dairy cattle remains to be determined.

Ruminal pH declines following meals with the rate of pH decline increasing as meal size increases and as dietary NDF content decreases (Allen, 1997). Dietary supplementation of sodium bicarbonate attenuates the decline in ruminal pH that is observed postfeeding (Erdman, 1988), and may attenuate SARA. The recommended inclusion rate for sodium bicarbonate is 0.75 to 1.0% of TMR dry matter. Keunen et al. (2003) reported that cows with experimentally induced SARA did not attenuate SARA by consuming free-choice sodium bicarbonate.

Researchers reported that 20 mg/cow/day supplemental dietary biotin reduced the laminitis-related hoof lesions, white-line separation (Hedges et al., 2001; Fitzgerald et al., 2000; Midla et al., 1998; Potzsch et al., 2003) and sole ulcers (Bergsten et al., 2003), and improved sole ulcer healing (Lischer et al., 2002). Dietary biotin supplementation did not influence ruminal VFA (Zimmerly and Weiss, 2001) or apparent total tract organic matter digestibility (Majee et al., 2003), and it is unlikely that reductions in laminitis-related hoof lesions occur via an attenuation of SARA but rather via biotin’s role in keratization of hoof epidermis (Tomlinson et al., 2004).

Nocek et al. (2000) reported reduced laminitis-related hoof lesions in five commercial dairy herds during the year of dietary supplementation with complexed trace minerals (zinc, manganese, copper, and cobalt) relative to the year prior when these herds were not supplemented with this complexed trace mineral mixture. The role of trace minerals in keratization of hoof epidermis (Tomlinson et al., 2004) could explain this response.

Novel use of direct-fed microbials (DFM) to enhance lactate utilization within the rumen has been reported with specific yeast strains (Dawson, 1995), yeast culture stimulation of Selenomonas ruminantium (Martin and Nisbet, 1992), DFM mixture containing Lactobacillus plantarum, Enterococcus faecium, and yeast (Nocek et al., 2002), Megasphaera elsdenii (Kung and Hession, 1995), and Propionibacterium strains (Parrott et al., 2001; Krehbiel et al., 2003). Controlled research trials demonstrating efficacy for attenuating SARA/laminitis in dairy cows are lacking.

Ration Preparation and Delivery

Extensive variation in DM, NEL and NDF concentrations found within bunker silos is presented in Table 2 (Stone, 2004). This emphasizes the importance of meticulous face management with careful use of loader buckets or face shavers to minimize batch-to-batch variation and for obtaining samples representative of what is being fed. Abruptly switching between silo bags can cause wide swings in nutrient delivery. Errors in nutrient delivery can occur because of failure to routinely determine the DM content of wet forages for adjustment of rations to maintain correct and consistent DM proportions of forage to concentrate. This becomes especially important after periods of heavy rainfall. To ensure consistent and accurate nutrient delivery and minimize SARA, effort should be made to assess and control these sources of error.

Mertens (1997) provided a minimum dietary peNDF guideline of 22% (DM basis). Particle size influences peNDF (Mertens, 1997). Mixing the TMR for too long a period of time reduces particle size of the batch mix and was common in high-incidence laminitis herds (Possin et al., 1995). Leonardi and Armentano (2003) reported extensive sorting away from long TMR particles, which can reduce the peNDF content of the diet consumed relative to the TMR mixed, depending on the proportion of long TMR particles, degree of sorting away from long particles, and the weigh-back proportion. Procedures are available to evaluate forage, TMR, and weigh-back particle size distributions in commercial testing laboratories (ANSI, 1988) or on the dairy (Lammers et al., 1996; Kononoff et al., 2003) to obtain a more accurate assessment of peNDF content of the diet consumed.

Beauchemin and Yang (2005) observed that increasing the peNDF content of diets increased chewing time, but increased chewing time did not necessarily reduce ruminal acidosis. Grain type (corn vs. barley), harvest/storage method (dry vs. high-moisture; DM content), and processing (rolled vs. ground vs. steam-flaked; fineness of grind) and corn silage DM content and processing influence ruminal starch degradability (Nocek and Tamminga, 1991) which is a risk factor for SARA/laminitis (Nocek, 1997).

The guideline provided by Nocek (1997) for ruminal starch degradability was 60 to 70% of total dietary starch. However, analytical procedures for determining ruminal starch degradability of grains, corn, or small-grain silages, or of TMR have generally been unavailable in commercial feed-testing laboratories. Blasel et al. (2005) reported on a laboratory method that provides an index of degree of starch availability (DSA) and ranked samples of corn grain appropriately for differences in particle size, DM content, and vitreousness. Data from corn silage and TMR samples are limited. Research and field experience with DSA as a nutritional diagnostic tool is needed to determine its usefulness for minimizing SARA and laminitis.

SARA/Cow Comfort Interaction and Laminitis

SARA may or may not result in an increased incidence of laminitis. Environmental factors that influence lying and standing behavior may worsen laminitis-related hoof lesions triggered by SARA (Cook et al., 2004). Nordlund (2000) reported on the diagnosis of SARA without a high corresponding incidence of laminitis in three grazing herds, and attributed this to the fact that the cows were on dirt rather than concrete. Colam-Ainsworth et al. (1989) reported increased laminitis in cows that spent more time standing on concrete rather than lying in stalls. Comparing his findings in grazing herds to diagnostic workups done in confined herds, Nordlund (2000) suggested that the degree of SARA needed to trigger laminitis is greater for cows on dirt than for cows with significant exposure to concrete. Cow comfort and her environment must be evaluated when attempting to minimize laminitis in dairy herds.


Allen, M. S. 1997. Relationship between fermentation acid production in the rumen and the requirement for physically effective fiber. J. Dairy Sci. 80:1447-1462.
American National Standards Institute. 1988. Method of determining and expressing particle size of chopped forage materials by screening. ASAE S424.

Beauchemin, K. A., and W. Z. Yang. 2005. Effects of Physically Effective Fiber on Intake, Chewing Activity, and Ruminal Acidosis for Dairy Cows Fed Diets Based on Corn Silage. J. Dairy Sci. 88:2117-2129.

Bergsten, C., P. R. Greenough, J. M. Gay, W. M. Seymour, and C. C. Gay. 2003. Effects of biotin supplementation on performance and claw lesions on a commercial dairy farm. J. Dairy Sci. 86:3953-3962.

Bertics, S. J., R. R. Grummer, C. Cadorniga-Valino, and E. E. Stoddard. 1992. Effect of prepartum dry matter intake on liver triglyceride concentration and early lactation. J. Dairy Sci. 75:1914-1922.

Blasel, H. M., P. C. Hoffman, R. D. Shaver, and S. M. Offer. 2005. Degree of starch availability: An index to define relative starch digestion potential in corn based feeds. Abstr. In press. Midwest ADSA/ASAS Ann. Mtg. Des Moines, IA.

Colam-Ainsworth, P., G. A. Lunn, R. C. Thomas, and R. G. Eddy. 1989. Behavior of cows in cubicles and its possible relationship with laminitis in replacement dairy heifers. Vet. Rec. 125:573-575.

Collier, R. J., D. K. Beede, W. W. Thatcher, L. A. Israel, and C. J. Wilcox. 1982. Influences of environment and its modification on dairy animal health and production. J. Dairy Sci. 65:2213–2227.

Cook, N. B., K. V. Nordlund, and G. R. Oetzel. 2004. Environmental influences on claw horn lesions associated with laminitis and subacute ruminal acidosis in dairy cows. J. Dairy Sci. 87:(E. Suppl.):E36-E46.

Dawson, K. A. 1995. The use of yeast strain 8417 in manipulating ruminant high concentrate diets. Pages 25-36 in Proc. 56th MN Nutr. Conf. & Alltech, Inc. Tech. Sym. Univ. of MN Ext. Serv., St. Paul, MN.

Dirksen, G. U., H. G. Liebich, and E. Mayer. 1985. Adaptive changes of the ruminal mucosa and their functional and clinical significance. Bovine Pract. 20:116-120.

Donovan, G. A., C. A. Risco, G. M. DeChant Temple, T. Q. Tran, and H. H. van Horn. 2004. Influence of transition diets on occurrence of subclinical laminitis in Holstein dairy cows. 87:73-84. J. Dairy Sci.

Erdman, R. A. 1988. Dietary buffering requirements of the lactating dairy cow: A
review. J. Dairy Sci. 71:3246-3266.

Fitzgerald, T., B. W. Norton, R. Elliot, H. Podlich, O. L. Svendsen. 2000. The influence of long-term supplementation with biotin on the prevention of lameness in pasture fed dairy cows. J. Dairy Sci. 83:338-344.

Food and Drug Administration-Center for Veterinary Medicine. 2004. FDA Approves Rumensin® for Increased Milk Production Efficiency in Dairy Cows. http://www.fda.gov/AnimalVeterinary/NewsEvents/CVMUpdates/ucm048423.htm.

Garrett, E. F., M. N. Pereira, K. V. Nordlund, L. E. Armentano, W. J. Goodger, and G. R. Oetzel. 1999. Diagnostic methods for the detection of subacute ruminal acidosis in dairy cows. J. Dairy Sci. 82:1170-1178.

Green, B. L., B. W. McBride, D. Sandals, K. E. Leslie, R. Bagg, and P. Dick. 1999. The impact of a monensin controlled-release capsule on subclinical ketosis in the transition dairy cow. J. Dairy Sci. 82:333-342.

Hedges, J., R. W. Blowey, A. J. Packington, C. J. O’Callaghan, and L. E. Green. 2001. A longitudinal field trial of the effect of biotin on lameness in dairy cattle. J. Dairy Sci. 84:1969-1975.

Keunen, J. E., J. C. Plazier, I. Kyriazakis, T. F. Duffield, T. M. Widowski, M. I.
Lindinger, and B. W. McBride. 2003. Effects of subacute ruminal acidosis on free-choice intake of sodium bicarbonate in lactating dairy cows. J. Dairy Sci. 86:954-957.

Kononoff, P. J., A. J. Heinrichs, and D. R. Buckmaster. 2003. Modification of the Penn State forage and total mixed ration particle separator and the effects of moisture content on its measurements. J. Dairy Sci. 86:1858–1863.

Krehbiel, C. R., S. R. Rust, G. Zhang, and S. E. Gilliland. 2003. Bacterial direct-fed microbials in ruminant diets: Performance response and mode of action. J. Anim. Sci. 81:(E. Suppl. 2):E120-E132.

Kung, L., Jr., and A. O. Hession. 1995. Preventing in vitro lactate accumulation in ruminal fermentations by inoculation with Megasphaera elsdenii. J. Anim. Sci. 73:250-256.

Lammers, B. P., D. R. Buckmaster, and A. J. Heinrichs. 1996. A simple method for the analysis of particle sizes of forage and total mixed rations. J. Dairy Sci. 79:922-928.

Leonardi, C., and L. E. Armentano. 2003. Effect of quantity, quality, and length of alfalfa hay on selective consumption by dairy cows. J. Dairy Sci. 86:557-564.

Lischer, Ch. J., U. Koller, H. Geyer, Ch. Mulling, J. Schulze, and P. Ossent. 2002. Effect of therapeutic dietary biotin on the healing of uncomplicated sole ulcers in dairy cattle – a double blinded controlled study. Vet. J. 163:51-60.

Majee, D. N., E. C. Schwab, S. J. Bertics, W. M. Seymour, and R. D. Shaver. 2003. Lactation performance by dairy cows fed supplemental biotin and a B-vitamin blend. J. Dairy Sci. 86:2106-2112.

Mallonee, P.G., D. K. Beede, R. J. Collier, and C. J. Wilcox. 1985. Production and physiological responses of dairy cows to varying dietary potassium during heat stress. J. Dairy Sci. 1985. 68:1479-1487.

Martin, S. A., and D. J. Nisbet. 1992. Effect of direct-fed microbials on rumen microbial fermentation. J. Dairy Sci. 75:1736-1744.

McDowell, R. E. 1972. The animal body in warm environments. Page 65 in Improvement of Livestock Production in Warm Climates. W. H. Freeman and Co.. San Francisco, CA.

Mertens, D. R. 1997. Creating a system for meeting the fiber requirements of dairy cows. J. Dairy Sci. 80:1463-1481.

Midla, L. T., K. H. Hoblet, W. P. Weiss, M. L. Moeschberger. 1998. Supplemental dietary biotin for prevention of lesions associated with aseptic subclinical laminitis (pododermatitis aseptica diffusa) in primiparous cows. Am. J. Vet. Res. 59:733-738.

Milton, T. 2000. Managing nutritional disorders with high-grain rations in beef cattle. Pages 65-80 in Proc. Inter-Mountain Nutr. Conf. Salt Lake City, UT. Utah State Univ., Logan, UT.

Mishra, M., F. A. Martz, R. W. Stanley, H. D. Johnson, J. R. Campbell, and E. Hilderbrand. 1970. Effect of diet and ambient temperature-humidity on ruminal pH, oxidation reduction potential, ammonia and lactic acid in lactating cows. J. Animal Sci. 30:1023-1028.

Mutsvangwa, T., J. P. Walton, J. C. Plazier, T. F. Duffield, R. Bagg, P. Dick, G. Vessie, and B. W. McBride. 2002. Effects of monensin controlled-release capsule or premix on attenuation of subacute ruminal acidosis in dairy cows. J. Dairy Sci. 85:3454-3461.

Nagaraja, T. G., T. B. Avery, E. E. Bartley, S. J. Galitzer, and A. D. Dayton. 1981. Prevention of lactic acidosis in cattle by lasalocid or monensin. J. Anim. Sci. 53:206–216.

Nagaraja, T. G., M. B. Taylor, D. L. Harmon, and J. E. Boyer. 1987. In vitro lactic acid inhibition and alterations in volatile fatty acid production by antimicrobial feed additives. J. Anim. Sci. 65:1064-1076.

National Research Council. 2001. Nutrient Requirements of Dairy Cattle. 7th rev. ed. Natl. Acad. Sci., Washington, DC.

Nocek, J. E. 1997. Bovine acidosis: Implications on laminitis. J. Dairy Sci. 80:1005-1028.

Nocek, J. E., A. B. Johnson, and M. T. Socha. 2000. Digital characteristics in
commercial dairy herds fed metal-specific amino acid complexes. J. Dairy Sci. 83:1553-1572.

Nocek, J. E., W. P. Kautz, J. A. Z. Leedle, and J. G. Allman. 2002. Ruminal supplementation of direct-fed microbials on diurnal pH variation and in situ digestion in dairy cattle. J. Dairy Sci. 85:429-433.

Nocek, J. E., and S. Tamminga. 1991. Site of digestion of starch in the gastrointestinal tract of dairy cows and its effect on milk yield and composition. J. Dairy Sci. 74:3598-3629.

Nordlund, K. 2000. Sore feet, sour rumens, clinical quandaries. Pages 58-64 in Proc. 33rd Ann. Conf. Of Amer. Assoc. Bov. Pract. Rapid City, SD.

Nordlund, K. V., N. B. Cook, and G. R. Oetzel. 2004. Investigation strategies for laminitis problem herds. J. Dairy Sci. 87:(E. Suppl.):E27-E35.

Osborne, J. K., T. Mutsvangwa, O. Alzahal, T. F. Duffield, R. Bagg, P. Dick, G. Vessie, and B. W. McBride. 2004. Effects of monensin on ruminal forage degradability and total tract diet digestibility in lactating dairy cows during grain-induced subacute ruminal acidosis. J. Dairy Sci. 87:1840-1847.

Parrott, T. D., T. G. Rehberger, and F. N. Owens. 2001. Selection of Propionibacterium strains capable of utilizing lactic acid from in vitro models. J. Anim. Sci. 79(Suppl. 1):80(Abstr.).

Possin, I., C. DeCorte, and R. D. Shaver. 1995. Particle length of forages and total mixed rations on commercial dairies. J. Anim. Sci. Midwestern Sec. Mtg. Abstr.

Potzsch, C. J., V. J. Collis, R. W. Blowey, A. J. Packington, and L. E. Green. 2003. The impact of parity and duration of biotin supplementation on white line disease lameness in dairy cattle. J. Dairy Sci. 86:2577–2582.

Ruiz, R., G. L. Albrecht, L. O. Tedeschi, G. Jarvis, J. B. Russell, and D. G. Fox. 2001. Effect of monensin on the performance and nitrogen utilization of lactating dairy cows consuming fresh forage. J. Dairy Sci. 84:1717-1727.

Shaver, R. D. 2002. Rumen acidosis in dairy cattle: Bunk management considerations. Pages 75-81 in Proc. 12th Int. Symp. on Lameness in Ruminants. Orlando, FL.

Shaver, R. D. 2000. Feed delivery and bunk management aspects of laminitis in dairy herds fed total mixed rations. Pages 70-77 in Proc. III Int. Conf. on Bovine Lameness. Parma, Italy.

Stone, W. C. 2004. Nutritional approaches to minimize subacute ruminal acidosis and laminitis in dairy cattle. J. Dairy Sci. 87:(E. Suppl.):E13-E26.

Tomlinson, D. J., Mulling, C. H., and T. M. Fakler. 2004. Formation of keratins in the bovine claw: Roles of hormones, minerals, and vitamins in functional claw integrity. J. Dairy Sci. 87:797-809.

Yang, W. Z., K. A. Beauchemin., and L. M. Rode. 2000, Effects of barley grain processing on extent of digestion and milk production of lactating cows. Journal of Dairy Sci. 83: 554-568.

Zimmerly, C. A. and W. P. Weiss. 2001. Effects of supplemental dietary biotin on performance of Holstein cows during early lactation. J. Dairy Sci. 84:498-506.

Figure 1. Relationship between total chewing time per kilogram of rumen-fermentable organic matter intake and intake of rumen fermentable organic matter.

Figure 2. Calculated fermentation acid production and salivary buffer flow at varying intakes of rumen-fermentable organic matter.

Table 1. Transition diets and laminitis/SARA (Donovan et al., 2004)1.
  Pre High NEL
Post Low NEL
Pre High NEL
Post High NEL
Pre Low NEL
Post Low NEL
Pre Low NEL
Post High NEL
Diet Concentrate (% DMB)
Prepartum, 24 Days 50 50 45 45
Postpartum, 5 Days 60 60 60 60
Postpartum, 16 Days 60 65 60 65
Postpartum, 21-70 DIM 60 60 60 60
Diet NDF (% DMB)
Prepartum, 24 Days 40 40 45 45
Postpartum, 5 Days 34 34 34 34
Postpartum, 16 Days 36 30 36 30
Postpartum, 21-70 DIM 34 34 34 34
Diet NEL (Mcal per lb. DM)
Prepartum, 24 Days 0.74 0.74 0.69 0.69
Postpartum, 5 Days 0.79 0.79 0.79 0.79
Postpartum, 16 Days 0.77 0.81 0.77 0.81
Postpartum, 21-70 DIM 0.79 0.79 0.79 0.79
Rumenocentesis pH
-14 DIM 6.25 6.04 6.18 6.23
8 DIM 6.00 5.82 6.07 5.93
22 DIM 5.92 5.79 5.84 5.73
Lowest Postpartum pH2 5.84a 5.59b 5.78a 5.64b
% pH < 5.83 35b 58a 32b 65a
Hoof Score4 2.0a, b 1.4b 1.0b 2.6a
a, bMeans in the same row with different superscripts differ (P < 0.05).
1Ninety-eight cows completed the study.
2Lowest ruminal pH for samples taken at 8, 22, and 70 DIM.
3Percentage of samples taken at 8 and 22 DIM with pH less than 5.8.
4Means of sum of hoof scores (0 = no hemorrhages or discoloration; 1 = slight discoloration or yellow staining; 2 = moderate hemorrhages; 3 = severe hemorrhages or secondary horn disintegration; 4 = exposed corium/sole ulcer) at zones 3 (abaxial wall-bulb junction) and 4 (sole-bulb junction) of sole at 60 DIM.

Table 2. Percentage deviations from minimum analytical result for lower, middle, and upper face samples within nine haylage and 11 corn silage bunkers on nine commercial dairies in New York (Stone, 2004).
% Deviation DM NEL NDF
21.0 9.9 14.7
5.2 1.6 5.4
44.7 20.0 24.8
Corn Silage
12.3 3.1 8.6
1.3 1.4 0.5
55.0 5.6 18.6


Randy D. Shaver
University of Wisconsin – Madison
University of Wisconsin – Extension