HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Abstract Full Text (PDF) Interpretive Summary Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Gozho, G. N. Articles by Wittenberg, K. M. Search for Related Content PubMed PubMed Citation Articles by Gozho, G. N. Articles by Wittenberg, K. M.

Subacute Ruminal Acidosis Induces Ruminal Lipopolysaccharide Endotoxin Release and Triggers an Inflammatory Response

Department of Animal Science, University of Manitoba, Winnipeg, Canada R3T 2N2

Corresponding author: J. C. Plaizier; e-mail: plaizier{at}ms.umanitoba.ca.

	ABSTRACT

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS AND DISCUSSION ACKNOWLEDGEMENTS REFERENCES

 
Subacute ruminal acidosis (SARA) was induced in 3 rumen fistulated Jersey steers by offering them different combinations of wheat-barley pellets and chopped alfalfa hay. Steers were offered 4, 5, and 6 kg/d of pelleted concentrate and 6, 5, and 4 kg/d of chopped alfalfa hay for diets 1, 2, and 3, respectively, during 5-d treatment periods and were fed chopped alfalfa hay between treatment periods. Inducing SARA increased blood concentrations of haptoglobin and serum amyloid-A. Dry matter intake of concentrate and hay decreased from d 1 to 5 in each period. Subacute ruminal acidosis was induced in all steers during d 4 and 5 when concentrate was fed, with ruminal pH remaining below 5.6 for an average of 187 and 174 min/d on these days. Lipopolysaccharide concentration increased significantly during periods of grain feeding compared with times when only hay was fed. Inducing SARA by feeding wheat-barley pellets activated a systemic inflammatory response in the steers.

Key Words: steers • subacute ruminal acidosis • ruminal pH • acute phase response

Abbreviation key: Hp = haptoglobin, LAL = Limulus amebocyte lysate, SAA = serum amyloid-A, SARA = subacute ruminal acidosis.

	INTRODUCTION

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS AND DISCUSSION ACKNOWLEDGEMENTS REFERENCES

 
Subacute ruminal acidosis (SARA) is a metabolic disorder characterized by episodes of low rumen pH between 5.2 and 5.6 (Cooper and Klopfenstein, 1996). Clinical signs of SARA are variable and, thus, it is often difficult to identify animals suffering from the disorder. Affected animals may become anorexic, develop intermittent diarrhea, become dehydrated, have unexplained abscesses, and develop laminitis (Nocek, 1997; Kleen et al., 2003). Some of these signs are not specific to SARA and this may lead to SARA being dismissed as other problems such as poor forage quality or poor bunk management (Nocek, 1997). Laminitis cannot be used to diagnose SARA because of the long time lapse between SARA and appearance of signs of laminitis.

Lipopolysaccharide from rumen gram-negative bacteria has been implicated in diseases that are related to feeding high concentrate diets such as sudden death syndrome, ruminal acidosis, and laminitis (Dougherty et al., 1975; Nagaraja et al., 1978). There is a paucity of literature on changes in rumen fluid LPS concentration due to feeding high concentrate diets. Nagaraja et al. (1978) demonstrated that steers fed high concentrate diets had considerably higher rumen fluid LPS concentration than steers fed only hay, whereas a more recent study by Andersen et al. (1994) did not find such a relationship. It has been suggested that the acidic rumen environment, changes in osmotic pressure, and ruminal LPS may render the rumen epithelium susceptible to injury (Brent, 1976; Enemark et al., 2002; Kleen et al., 2003). These changes may result in translocation of rumen LPS into the prehepatic bloodstream.

The presence of LPS in the bloodstream results in the production of multiple proinflammatory cytokines, reactive oxygen and nitrogen intermediates, and bioactive lipids, which affect the host’s metabolic response to inflammation (Baumann and Gauldie, 1994). When released in large quantities, these mediators lead to an acute phase response (Kushner and Rzewnicki, 1994). Profiles of concentrations of some acute phase proteins are used as markers for inflammatory response (Baumann and Gauldie, 1994). Haptoglobin (Hp) and serum amyloid-A (SAA) are 2 such proteins that are used as inflammatory markers in cattle (Alsemgeest et al., 1994). Their concentrations are elevated because of tissue damage (Conner et al., 1988) or due to intradermal and intravascular LPS injections (Boosman et al., 1989), bacterial infections (Deignan et al., 2000), or viral infections (Heegaard et al., 2000).

Although acute phase proteins have been used as inflammatory markers in various situations where inflammation is the logical development, no studies have investigated inflammatory responses in cattle with SARA. We hypothesize that SARA leads to increased gram-negative bacterial lysis, which increases ruminal LPS concentration. Rumen wall damage associated with SARA further increases ruminal LPS translocation into the bloodstream, resulting in an inflammatory response. Therefore, the objective of this study was to determine changes in rumen fluid LPS, serum Hp, and plasma SAA concentrations in steers due to SARA induced by feeding wheat-barley pellets.

	MATERIALS AND METHODS

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS AND DISCUSSION ACKNOWLEDGEMENTS REFERENCES

 
Three ruminally fistulated adult Jersey steers were kept in metabolism crates at the Animal Science Research Unit at the University of Manitoba throughout the experiment, in accordance with the guidelines of the Canadian Council of Animal Care. The experimental design was a 3 x 3 Latin square with 21-d periods that were divided into a 5-d treatment period and 16-d rest period. During the treatment period, SARA was induced in the steers by offering diets 1, 2, and 3. Diets were combinations of wheat-barley pellets and chopped alfalfa hay, respectively, in the following ratios (as-fed basis): diet 1 (4 kg: 6 kg); diet 2 (5 kg: 5 kg); and diet 3 (6 kg: 4 kg). The concentrate consisted of 50% wheat and 50% barley. Concentrate and hay were offered in separate meals. All animals were offered 1 kg of chopped alfalfa hay at 0900 h followed by two-thirds of their allocation of concentrate at 1100 h. The remainder of the concentrate was offered at 1300 h. At 1700 h, concentrate not eaten was removed and the steers were offered chopped alfalfa hay, to which they had access throughout the night. The steers were fed hay ad libitum during the 16-d rest period between treatments. The last 2 d of the rest period, when only hay was fed, were designated d –2 and d –1. Days when concentrate was fed were designated d 1 to 5. Dry matter (%), CP, and NDF (%DM) content were 84.8, 18.9, and 27.3% for chopped alfalfa hay, and 93.0, 14.9, and 45.7% for wheat-barley pellets.

Rumen pH was measured continuously throughout the treatment period by placing one indwelling pH probe into the ventral sac of the rumen of each steer as described by Cumby et al. (2001). Measurements were taken every second and averaged over 60 s. Rumen fluid pH data were summarized as average pH, time below pH 6.0, and time below pH 5.6, area (time x pH) below pH 6.0, and area (time x pH) below pH 5.6 for each 24-h period. Rumen fluid samples were collected into sterile plastic tubes from the ventral sac of the rumen at 0900 and 1400 h every day during the treatment period. Samples were mixed thoroughly before 25 mL was transferred into sterilized centrifuge tubes and centrifuged for 30 min at 10,000 x g. The supernatant was passed through a disposable 0.22-µm sterile, pyrogen-free filter (Millex, Millipore Corporation, Bedford, MA). Samples were further heated at 100°C for 30 min before being stored at –20°C for the determination of rumen LPS concentration using the Limulus amebocyte lysate (LAL) assay (Levin and Bang, 1964). The assay was performed using a 96-well microplate (BioWhittaker Inc., Walkersville, MD) with absorbance read at 405 nm using a microplate reader (BioRad model 3550, Hercules, CA). Samples were diluted 1000-fold using pyrogen-free water to determine the noninhibitory dilution, with the final dilution being made of 50% diluted sample and 50% ß-glucan blocker (BioWhittaker kit number N190; component number: B50-700). ß-Glucan blocker blocks the reactivity of LAL to ß-1,3-glucans, conferring increased endotoxin specificity to the LAL test. Noninhibitory dilution is achieved when 75 ± 25% of spike is recovered in positive control samples. An average recovery rate of 78.0 ± 8.6% (n = 8) was achieved in positive controls with a sample dilution of 1:60,000.

Two blood samples (7 mL) were collected by tail venipuncture from each steer on d –2, –1, 1, 2, 3, 4, and 5 into serum and plasma tubes at 0900 h. Serum and plasma were harvested by centrifuging samples at 3000 rpm for 30 min. Haptoglobin and SAA were determined in serum and plasma, respectively, using ELISA Tridelta Phase range kits (Tridelta Diagnostics Inc., Cedar Knolls, NJ; catalog numbers TP-801 and TP-802, respectively) (Makimura and Suzuki, 1982; McDonald et al., 1991). For Hp, serum samples were diluted 1:5 with PBS and vortexed. Seventy-five microliters of diluted serum was added to duplicate wells of a 96-well microtiter plate. Stabilized hemoglobin diluted 1:1 with hemoglobin diluent, was added (100 µL) to the diluted sample. Chromogen and substrate, mixed in a ratio of 9:5 (140 µL), were added to the reaction mixture and incubated at room temperature (25°C) for 5 min. Absorbance was read immediately at 630 nm using a microplate spectrophotometer (Spectra Max 340 PC, Molecular Devices Corporation, Sunnyvale, CA). For SAA, plasma samples were diluted 1:500 in diluent buffer and vortexed. Fifty micro-liters was added to each well of a 96-well plate coated with 50 µL of biotinylated antiserum amyloid-A monoclonal antibody (diluted 1:100 in 1x diluent buffer). The microtiter plate was covered and incubated at 37°C for at least 1 h and then washed 4 times with diluted wash buffer to remove unbound material. Streptavidin-horseradish peroxidase conjugate was diluted 1:4000 in diluent buffer and added (100 µL) to each well. The plate was incubated at room temperature (25°C) in darkness for 30 min. The microtiter plate was washed (as described above) and tapped dry. Substrate (100 µL) was added to the plate, which was then incubated at room temperature (25°C) in darkness for an additional 30 min. Stop solution was added, and the plate was read in a microplate reader (BioRad model 3550) at 450 nm.

Statistical Analyses
Data were analyzed using mixed model analysis with the first-order autoregressive covariance structure in Proc Mixed in SAS (SAS Institute, 1996). The following model was used:

where Y_ijkl = observations for dependent variables; µ = overall mean; _i = average effect of period i; ß_j = average effect of the animal j; D_k = average effect of dietary treatment; ( x ß)_ij = animal x period interaction, which was the main plot error; T_l = average effect of time in days for feed intake, or hours since the beginning of feeding concentrate for blood metabolites or endotoxin concentration; (D x T)_kl = interaction between time and dietary treatment; and e_ijkl = subplot error. Lipopolysaccharide concentrations were log transformed because of nonhomogeneous residual error. Orthogonal contrasts were used to compare Hp, SAA, and log-transformed LPS concentrations during the period when only hay was fed with those when concentrate was fed to induce SARA. Mean differences for rumen pH data and DM intake were separated using Tukey’s multiple comparison procedure.

	RESULTS AND DISCUSSION

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS AND DISCUSSION ACKNOWLEDGEMENTS REFERENCES

 
Average rumen fluid pH, time, and area with pH below 6.0 or 5.6 did not differ among the diets (Table 1). However, feeding concentrate decreased average daily pH from d 1 to a nadir on d 4. Both time below pH 6.0 and time below pH 5.6 increased from d 1 to a peak on d 4. Area below pH 6.0 increased from d 1 to a peak on d 4 but area below pH 5.6 showed only numerical increases (P = 0.096; Table 1). Because the steers spent 187 and 174 min/d with pH below 5.6 on d 4 and 5, respectively, we concluded that SARA was successfully induced on these days. The severity of SARA was less than that experienced by cows used in studies by Krajcarski-Hunt et al. (2002), who reported time and area below pH 5.6 of 594.4 ± 188.9 min/d and 228.0 ± 88.8 min x pH/d, respectively. The rumen fluid pH that defines SARA is still a controversial issue, with various threshold values having been arbitrarily set to define SARA. For example, threshold values of 5.5 (Hibbard et al., 1995), 5.6 (Cooper and Klopfenstein, 1996), 5.8 (Beauchemin et al., 2001), and 6.0 (Kriehbiel et al., 1995) have been used to define the upper bound of pH that defines SARA. The duration for which the pH must remain below this threshold has not been properly defined.

View larger version (11K): [in this window] [in a new window]   Figure 1. Concentrations of ruminal LPS (log10 endotoxin units/mL; panel A), haptoglobin (Hp; panel B), and serum amyloid-A (SAA; panel C) in steers fed chopped alfalfa hay only (d –2 and d –1) and during concentrate feeding (d 1 to 5). Orthogonal contrasts were used to determine which concentrations differed from baseline values. Lipopolysaccharide concentrations measured in samples collected before feeding concentrate on d 1 were taken as baseline. Bars indicate SE, and significance was declared at the 5% level of significance.

Serum amyloid-A concentrations were not significantly different among the different diets but concentrations in blood plasma increased from 33.6 ± 36.53 (when only hay was fed) to 170.7 ± 36.53 µg/mL on d 5 (P < 0.001), when concentrate was offered in addition to hay (Figure 1). Serum amyloid-A is the other major acute phase protein, and is a more sensitive marker of inflammatory challenge than Hp (Horadagoda et al., 1999). The acute phase protein profiles obtained in the present study indicate that as time with pH below 5.6 increased, the intensity of the acute phase response increased (Figure 1). This could be due to formation of extensive microlesions on the ruminal epithelium leading to increased LPS translocation across the ruminal epithelium into the systemic circulation, which would amplify the acute phase response associated with SARA. To our knowledge, this is the first study that has examined an acute phase response due to SARA.

Therefore, in conclusion, offering steers wheat-barley pellets and chopped alfalfa hay successfully induced SARA, particularly on d 4 and 5 of our study, although DM intake declined from d 1 to 5. Inducing SARA increased the concentration of LPS in rumen fluid, plasma SAA, and serum Hp concentrations. Although SAA concentrations increased within 24 h of feeding concentrate, Hp levels did not change until the third day of feeding concentrate. Inducing SARA increased rumen LPS concentration and initiated an acute phase response. Causal factors for inflammatory response may be an increase in LPS and bacterial translocation into the prehepatic circulation. Further work needs to be done under controlled feed intake conditions to remove possible confounding of LPS concentration with variable feed intake.

	ACKNOWLEDGEMENTS

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS AND DISCUSSION ACKNOWLEDGEMENTS REFERENCES

 
Financial support (to JCP) of the Natural Sciences and Engineering Research Council of Canada (NSERC) is gratefully acknowledged. We thank Dale Rosner, staff at Glenlea Research Station, and Robert Stuski for looking after the animals, Terri Garner and Ricki Araneda for technical assistance, and Gary Crow and Loreen Onischuk for help with statistical analyses.

Received for publication October 15, 2004. Accepted for publication December 9, 2004.

	REFERENCES

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS AND DISCUSSION ACKNOWLEDGEMENTS REFERENCES

 


Alsemgeest, S. P., H. C. Kalsbeek, T. Wensing, J. P. Koeman, A. M. van Ederen, and E. Gruys. 1994. Concentrations of serum amyloid-A (SAA) and haptoglobin (HP) as parameters of inflammatory diseases in cattle. Vet. Q. 16:21–23.[Medline]

Andersen, P. H., B. Bergelin, and K. A. Christensen. 1994. Effect of feeding regimen on concentration of free endotoxin in ruminal fluid of cattle. J. Anim. Sci. 72:487–491.[Abstract]

Baumann, H., and J. Gauldie. 1994. The acute phase response. Immunol. Today 15:74–80.[Medline]

Beauchemin, K. A., W. Z. Yang, and L. M. Rode. 2001. Effects of barley grain processing on the site and extent of digestion in beef. J. Anim. Sci. 79:1925–1936.[Abstract/Free Full Text]

Boosman, R., T. A. Niewold, C. W. A. A. Mutsaers, and E. Gruys. 1989. Serum amyloid A concentrations in cows given endotoxin as an acute phase stimulant. Am. J. Vet. Res. 50:1690–1694.[Medline]

Brent, B. E. 1976. Relationship of acidosis to other feedlot ailments. J. Anim. Sci. 43:930–935.

Conner, J. G., P. D. Eckersall, A. Wiseman, T. C. Aitchison, and T. A. Douglas. 1988. Bovine acute phase response following turpentine injection. Res. Vet. Sci. 44:82–88.[Medline]

Cooper, R., and T. Klopfenstein. 1996. Effects of Rumensin and feed intake variation on ruminal pH. Update on Rumensin / Tylan / Micotyl for the Professional Feedlot Consultant. Elanco Animal Health, Greenfield, IN.

Cumby, J. L., J. C. Plaizier, I. Kyriazakis, and B. W. McBride. 2001. Effects of subacute ruminal acidosis on the preference of cows for pellets containing sodium bicarbonate. Can. J. Anim. Sci. 81:149–152.

Deignan, T., A. Alwan, J. Kelly, J. McNair, T. Warren, and C. O’Farrelly. 2000. Serum haptoglobin: An objective indicator of experimentally induced Salmonella infection in calves. Res. Vet. Sci. 69:153–158.[Medline]

Dougherty, R. W., K. S. Coburn, H. M. Cook, and M. Allison. 1975. A preliminary study of the appearance of endotoxin in the circulatory system of sheep and cattle after induced grain-engorgement. Am. J. Vet. Res. 36:831–832.[Medline]

Enemark, J. M., R. J. Jørgensen, and P. Enemark. 2002. Rumen acidosis with special emphasis on diagnostic aspects of subclinical rumen acidosis: A review. Vet. Zootec. 20:16–29.

Heegaard, P. M. H., D. L. Godson, M. J. M. Toussaint, K. Tjørnehøj, L. E. Larsen, B. Viuff, and L. Rønsholt. 2000. The acute phase response of haptoglobin and serum amyloid A (SAA) in cattle undergoing experimental infection with bovine respiratory syncytial virus. Vet. Immunol. Immunopathol. 77:151–159.[Medline]

Hibbard, B., J. P. Peters, S. T. Chester, J. A. Robinson, S. Kotarski, W. J. Croom, and W. M. Hagler. 1995. The effect of slaframine on salivary output and subacute and acute acidosis in growing beef steers. J. Anim. Sci. 73:516–525.[Abstract]

Horadagoda, N. U., K. M. G. Knox, H. A. Gibbs, S. W. J. Reid, A. Horadagoda, S. E. R. Edwards, and P. D. Eckersall. 1999. Acute phase proteins in cattle: Discrimination between acute and chronic inflammation. Vet. Rec. 144:437–441.[Abstract/Free Full Text]

Kleen, J. L., G. A. Hooijer, J. Rehage, and J. P. T. M. Noordhuizen. 2003. Subacute ruminal acidosis (SARA): A review. J. Vet. Med. A Physiol. Pathol. Clin. Med. 50:406–414.[Medline]

Krajcarski-Hunt, H., J. C. Plaizier, J. P. Walton, R. Spratt, and B. W. McBride. 2002. Effect of subacute ruminal acidosis on in situ fiber digestion in lactating dairy cows. J. Dairy Sci. 85:570–573.[Abstract]

Kriehbiel, C. R., R. A. Britton, D. L. Harmon, T. J. Wester, and R. A. Stock. 1995. The effects of ruminal acidosis on volatile fatty acid absorption and plasma activities of pancreatic enzymes in lambs. J. Anim. Sci. 73:3111–3121.[Abstract]

Kushner, I., and D. L. Rzewnicki. 1994. The acute phase response: General aspects. Baillieres Clin. Rheumatol. 8:513–530.[Medline]

Levin, J., and F. B. Bang. 1964. A description of cellular coagulation in the Limulus. Bull. Johns Hopkins Hosp. 115:337.[Medline]

Makimura, S., and N. Suzuki. 1982. Quantitative determination of bovine serum haptoglobin and its elevation in some inflammatory diseases. J. Vet. Sci. 44:15–21.

McDonald, T. L., A. Weber, and J. W. Smith. 1991. A monoclonal antibody sandwich immunoassay for serum amyloid A protein. J. Immunol. Methods 144:149–155.[Medline]

Nagaraja, T. G., E. E. Bartley, L. R. Fina, and H. D. Anthony. 1978. Relationship of rumen gram-negative bacteria and free endotoxin to lactic acidosis in cattle. J. Anim. Sci. 47:1329–1336.

Nocek, J. E. 1997. Bovine acidosis: Implications on laminitis. J. Dairy Sci. 80:1005–1028.[Abstract]

SAS Institute. 1996. SAS System for Mixed Models. 4th ed. SAS Inst., Inc., Cary NC.

This article has been cited by other articles:

				E. Khafipour, S. Li, J. C. Plaizier, and D. O. Krause Rumen Microbiome Composition Determined Using Two Nutritional Models of Subacute Ruminal Acidosis Appl. Envir. Microbiol., November 15, 2009; 75(22): 7115 - 7124. [Abstract] [Full Text] [PDF]

				E. Khafipour, D. O. Krause, and J. C. Plaizier Alfalfa pellet-induced subacute ruminal acidosis in dairy cows increases bacterial endotoxin in the rumen without causing inflammation J Dairy Sci, April 1, 2009; 92(4): 1712 - 1724. [Abstract] [Full Text] [PDF]

				E. Khafipour, D. O. Krause, and J. C. Plaizier A grain-based subacute ruminal acidosis challenge causes translocation of lipopolysaccharide and triggers inflammation J Dairy Sci, March 1, 2009; 92(3): 1060 - 1070. [Abstract] [Full Text] [PDF]

				O. AlZahal, M. M. Or-Rashid, S. L. Greenwood, M. S. Douglas, and B. W. McBride The effect of dietary fiber level on milk fat concentration and fatty acid profile of cows fed diets containing low levels of polyunsaturated fatty acids J Dairy Sci, March 1, 2009; 92(3): 1108 - 1116. [Abstract] [Full Text] [PDF]

				S. K. Bhandari, S. Li, K. H. Ominski, K. M. Wittenberg, and J. C. Plaizier Effects of the Chop Lengths of Alfalfa Silage and Oat Silage on Feed Intake, Milk Production, Feeding Behavior, and Rumen Fermentation of Dairy Cows J Dairy Sci, May 1, 2008; 91(5): 1942 - 1958. [Abstract] [Full Text] [PDF]

				Q. Zebeli, J. Dijkstra, M. Tafaj, H. Steingass, B. N. Ametaj, and W. Drochner Modeling the Adequacy of Dietary Fiber in Dairy Cows Based on the Responses of Ruminal pH and Milk Fat Production to Composition of the Diet J Dairy Sci, May 1, 2008; 91(5): 2046 - 2066. [Abstract] [Full Text] [PDF]

				T. G. Nagaraja and E. C. Titgemeyer Ruminal Acidosis in Beef Cattle: The Current Microbiological and Nutritional Outlook J Dairy Sci, June 1, 2007; 90(13_suppl): E17 - E38. [Abstract] [Full Text] [PDF]

				S. K. Bhandari, K. H. Ominski, K. M. Wittenberg, and J. C. Plaizier Effects of Chop Length of Alfalfa and Corn Silage on Milk Production and Rumen Fermentation of Dairy Cows J Dairy Sci, May 1, 2007; 90(5): 2355 - 2366. [Abstract] [Full Text] [PDF]

				G. N. Gozho, D. O. Krause, and J. C. Plaizier Ruminal Lipopolysaccharide Concentration and Inflammatory Response During Grain-Induced Subacute Ruminal Acidosis in Dairy Cows J Dairy Sci, February 1, 2007; 90(2): 856 - 866. [Abstract] [Full Text] [PDF]

				J. J. Loor, H. M. Dann, N. A. J. Guretzky, R. E. Everts, R. Oliveira, C. A. Green, N. B. Litherland, S. L. Rodriguez-Zas, H. A. Lewin, and J. K. Drackley Plane of nutrition prepartum alters hepatic gene expression and function in dairy cows as assessed by longitudinal transcript and metabolic profiling Physiol Genomics, January 12, 2007; 27(1): 29 - 41. [Abstract] [Full Text] [PDF]

				G. B. Penner, K. A. Beauchemin, and T. Mutsvangwa Severity of Ruminal Acidosis in Primiparous Holstein Cows During the Periparturient Period J Dairy Sci, January 1, 2007; 90(1): 365 - 375. [Abstract] [Full Text] [PDF]

				D. G. V. Emmanuel, A. Jafari, K. A. Beauchemin, J. A. Z. Leedle, and B. N. Ametaj Feeding live cultures of Enterococcus faecium and Saccharomyces cerevisiae induces an inflammatory response in feedlot steers J Anim Sci, January 1, 2007; 85(1): 233 - 239. [Abstract] [Full Text] [PDF]

				G. N. Gozho, D. O. Krause, and J. C. Plaizier Rumen lipopolysaccharide and inflammation during grain adaptation and subacute ruminal acidosis in steers. J Dairy Sci, November 1, 2006; 89(11): 4404 - 4413. [Abstract] [Full Text] [PDF]

This Article Abstract Full Text (PDF) Interpretive Summary Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Gozho, G. N. Articles by Wittenberg, K. M. Search for Related Content PubMed PubMed Citation Articles by Gozho, G. N. Articles by Wittenberg, K. M.