CASE STUDY: Early Lactation Production, Body Condition, and Incidence of Disease in Holstein Cows Fed a Low-Potassium Diet Alone or Supplemented with Chloride Prepartum

INTRODUCTION

Clinical hypocalcemia results from the cow's inability to meet increased Ca demands for colostrum production at parturition (Horst et al., 1997). Cows that survive clinical hypocalcemia are at increased risk for other metabolic problems, including retained fetal placenta, ketosis, displaced abomasum, and mastitis (Curtis et al., 1985; Grohn et al., 1989), in part because of the negative effect of Ca status on immune response (Kimura et al., 2006). Milk yield can also be reduced (Block, 1984). Subclinical hypocalcemia (plasma Ca <7.5 mg/dL) can also be economically important, especially if it is not recognized and addressed (Horst et al., 1997). Raising blood Ca levels can improve milk yield even in herds without milk fever (parturient paresis) issues (Beede et al., 1991).

Reducing DCAD can reduce the incidence of hypocalcemia (Block, 1984; Oetzel et al., 1988; Moore et al., 2000). Higher levels of anions in a ration result in metabolic acidosis and reduced urine pH, blood bicarbonate, and blood carbon dioxide (Charbonneau et al., 2006). To buffer the blood, bone Ca is mobilized and exchanged for blood hydrogen ions (Lemann et al., 2003). During metabolic acidosis, kidney and bone are also more responsive to parathyroid hormone (Goff et al., 1991). Vagnoni and Oetzel (1998) observed a strong negative relationship between urinary pH and net acid excretion and suggested monitoring urinary pH to assess adequacy of metabolic acidosis. A prepartum DCAD [mEq/kg = (mEq of Na^sup +^/kg + mEq of K^sup +^/kg) (meEq of Cl^sup -^/kg + mEq of SO^sub 4^^sup -2^/kg)] of below 0 mEq/kg and a urinary pH of 6.2 to 6.8 has been suggested to be most effective for reducing hypocalcemia in Holstein cattle (NRC, 2001; Lean et al., 2006).

Despite positive research with anionic supplements, many nutritionists still do not incorporate them into prepartum diets. A primary concern is the effect of anions on prepartum DMI (Oetzel and Barmore, 1993; Moore et al., 2000; Charbonneau et al., 2006). Low-K prepartum diets (<1.2% DM) are heavily relied upon to control the incidence of hypocalcemia by means of reducing the degree of metabolic alkalosis before parturition (Goff and Horst, 1997). Whether or not the addition of anionic products to low-K prepartum diets would further alleviate hypocalcemia and positively affect performance is a subject of debate (Overton and Waldron, 2004). Anion supplements utilizing hydrochloric acid have proven more palatable than anionic salts and do not affect intake when fed at levels providing up to 2 equivalents of chloride (Goff and Horst, 1998). Chloride has also proven to be a more potent acidifier of blood and urine than sulfates (Goff et al., 2004). The objective of this study was to determine if supplementing a low-K diet, which already reduced metabolic alkalosis and clinical hypocalcemia, using chloride would induce a compensated metabolic acidosis, further improve blood Ca status, reduce disease incidence, or increase milk yield.

MATERIALS AND METHODS

Animals

Two hundred Holstein cows having completed at least one lactation (multiparous cows) and 132 Holstein heifers approaching their first lactation (primiparous cows) were housed in 2 separate pens and fed differing rations for the prepartum period (-21 to 0 DIM) but were comingled after calving. Cows were monitored from 21 d before expected calving date until 90 DIM. The experiment began in March 2006 and ended in September 2006. Cows were housed in a naturally ventilated free-stall barn with fans and misters. Cows were milked 3 times/d at 0200, 1000, and 1800 h, and milk weights were recorded daily. All health events were recorded for all cows assigned to the study. Body condition score was determined using a 5-point scale where 1 = thin to 5 = fat (Wildman et al., 1982) at -30, 0, 30, and 90 DIM. All procedures were in accordance with the guidelines presented in Guidelines for the Care and Use of Agricultural Animals in Agricultural Research and Teaching (FASS, 1999).

Experimental Treatments

Cows were assigned to treatments based on expected calving date, parity (1, 2, 3, and 4+) and previous mature equivalent 305-d milk yield. Treatments were as follows: 1) control treatment consisting of a low-K prepartum diet with a forage base of straw and corn silage, or 2) a low-K prepartum diet with a forage base of straw and corn silage supplemented with SoyChlor 16-7 (West Central, Ralston, IA), a chloride and protein supplement for prepartum cows. Cows received one of the treatment diets from -21 to 0 DIM. Diets were designed according to NRC (2001) recommendations for prepartum cows. The concentrate portion of the control diet contained soybean meal, soyhulls, expeller-processed soybean meal (SoyPlus; West Central), and animal protein (Table 1). The treatment diet was similar except for chloride supplementation.

Prepartum cows were fed ad libitum with fresh TMR offered once daily at 1300 h. The weight of feed offered and refused by the treatment groups was recorded daily during the prepartum period. Dry matter intake was characterized but not statistically analyzed because the cows were fed as a group. Forage analysis results were used to adjust both prepartum and lactating rations as needed. Total mixed ration analysis results were used to verify prepartum nutrition.

All cows received the same lactation diets postpartum (Table 1). All cows were in a fresh cow pen for 30 d and then moved to a high production pen. The postpartum diets were designed according to NRC (2001) guidelines and adjusted for changes in forage nutrient contents.

Measurements and Analytical Methods

Weekly TMR and forage samples were obtained and composited by month and analyzed for chemical composition by a commercial laboratory (Dairy One, Ithaca, NY). Samples were analyzed for DM, ash, ether extract, CP, ADF, and lignin (AOAC, 1995). Samples were also analyzed for soluble CP (Krishnamoorthy et al., 1982), NDF with residual ash (using a-amylase and sodium sulfite; Van Soest et al., 1991), and starch (YSI 2700 SELECT Biochemistry Analyzer, Application Note 319; Transition Technologies, Yellow Springs, OH). Nonfiber carbohydrate was calculated as the difference between 100 and the sum of CP, NDF, ether extract, and ash. Analysis of Ca, P, Mg, K, Na, Fe, Zn, Cu, Mn, and Mo were conducted using a Thermo Jarrell Ash IRIS Advantage inductively coupled plasma radial spectrometer (model ICAP 61; Thermo Jarrell Ash, Ithaca, NY). Sulfur was analyzed by combustion using a Leco Model SC-432 instrument (Leco, St. Joseph, MI). Chloride ion was analyzed using a Brinkman Metrohm 716 Titrino titration unit with a silver electrode (model 716; Brinkman Inst. Inc., West bury, NY).

Urine pH was monitored on a subset (5 to 10 cows) of randomly selected multiparous cows from both treatment groups on a weekly basis to assure adequate diet acidification. The feeding rate of the chloride supplement was adjusted up at mid-trial to maintain desired urine pH values (6.2 to 6.8; NRC, 2001). This adjustment was made on June 1, 2006, after 92% of the multiparous cows and 43% of the primiparous cows had completed the prepartum period.

Milk was sampled biweekly for the first 90 DIM. Milk samples were preserved with Bronolab-W II (D & F Control Systems Inc., Dublin, CA), a liquid preservative containing the ac- tive ingredient Bronopol, and sent to Dairy One Milk Laboratories (Ithaca, NY). Milk was analyzed for fat, true protein, total milk solids, SCC, and milk urea nitrogen using an infrared analyzer (Milk-O-Scan 4000; Foss Electric, Hillerød, Denmark).

Blood was sampled from 26 pairs of presumptively normal multiparous cows from the coccygeal vein at calving and at 7 DIM. Any animal treated for milk fever, whether clinical or suspected subclinical (lethargic), had blood drawn before treatment to confirm that milk fever cases were being identified correctly. Blood was collected into 7-mL Vacutainer tubes. Serum samples were refrigerated overnight and centrifuged under refrigeration at 3,000 × g for 25 min. Samples were then stored at -20°C and sent to Michigan State University for spectrophotometric analysis of Ca, Mg, P, and K (Olympus AU 640e, Olympus America Inc., Center Valley, PA).

Statistical Analysis

Statistical analysis was conducted using the PROC MIXED procedure (SAS Institute, 1997). The statistical model was composed of the random effect of cow, fixed effect of parity, fixed effect of treatment, and treatment by parity interaction. Previous mature equivalent 305-d milk yield was used as a covariate for the multiparous cows. The repeated measure was day except in the case if the BCS change that had no repeated measure.

RESULTS AND DISCUSSION

Experimental Diets

The chemical composition of the experimental diets is listed in Table 2. Low K in the control diet (<1.20% DM) was intended to reduce metabolic alkalosis. The objective of significantly reducing dietary DCAD with supplementation of chloride to induce a state of mild metabolic acidosis was achieved. Mean DCAD averaged 6.02 and -10.31 mEq/100 g DM for the control and chloride-supplemented prepartum diets. The recommended urinary pH of 6.2 to 6.8 for Holsteins (NRC, 2001) was attained for the cows fed supplemental chloride. Mean prepartum urine pH was 8.02 (±0.25; SD) and 6.61 (±0.89) for the subset of randomly selected control and chloride-supplemented cows. Mean prepartum DMI was 13.67 kg/d for the control and 13.66 kg/d for the chloride-supplemented cows. All cows received the same lactation diets after calving that provided 17.8% CP, 19.5% ADF, and 37.0% NFC.

Mineral Status of Multiparous Cows

Plasma Ca levels at calving in the 26 pairs of normal multiparous cows were higher (P = 0.01) for cows fed supplemental chloride than for those fed the low-K control diet with means of 7.94 vs. 8.56 mg/dL for control vs. chloride-supplemented cows (Table 3). At 7 DIM, prepartum supplemental chloride had no effect on plasma Ca levels. The higher plasma Ca levels at parturition observed in cows fed supplemental chloride are comparable to those of Moore et al. (2000) who reduced DCAD from 0 to -15 mEq/100 g dietary DM and observed that urine pH was reduced from 7.3 to 6.0 and plasma ionized Ca concentrations at calving were increased from 3.8 to 4.3 mg/dL.

There was no effect of prepartum diet on plasma P, Mg, and K at 0 and 7 DIM in normal multiparous cows. Others have observed no effect of DCAD on P, Mg, and K concentrations in blood plasma (Oetzel et al., 1988; Vagnoni and Oetzel, 1998). Beede et al. (1991) measured higher serum P levels when an anionic diet was fed before calving (4.4 vs. 3.6 mg/dL, P < 0.01). Although blood Mg concentrations were within the normal range at calving, the concentration of Mg in the blood of all cows was below normal at 7 DIM. This may not have impacted Ca metabolism at calving, but it may have impacted feed intake and performance in early lactation. Low plasma Mg concentration in the lactating cows suggests there was inadequate available Mg in the lactating cow ration.

Body Condition and Disease Incidence in All Cows

Cows were thin at the start of the study (-30 DIM; BCS = 2.92) and lost some body condition during the first 90 DIM (BCS = 2.75; Table 4). No differences were observed in BCS or the change in BCS due to prepartum dietary treatments at any time point. Given this result, it is possible that the hydrochloric acid based anion source had no negative effect on energy status. Moore et al. (2000) observed that cows fed a diet with a DCAD of -15 mEq/100 g dietary DM with more traditional anionic salts (CaCl^sub 2^, CaSO^sub 4^, and MgSO^sub 4^) consumed less DM and had a lower adjusted BW at calving than those fed a zero DCAD diet.

Prepartum diet had no effect on incidence of clinical milk fever, clinical ketosis, retained placenta, and mastitis (Table 5). There were no incidences of clinical milk fever in multiparous cows fed supplemental chloride, and only 1.2% of multiparous cows fed the control diet experienced clinical milk fever. Prevalence of clinical ketosis was numerically higher in cows fed the control diet (10.1% vs. 7.9% in control vs. chloride-supplemented cows, respectively). The incidence of mastitis and SCC of milk of cows fed supplemental chloride prepartum were numerically lower than in control cows (Tables 5 and 6). This result is interesting considering the work of Kimura et al. (2006) that associated a poor Ca status with a negative effect on immune cells of dairy cows.

Milk Yield and Milk Components

Milk yield of cows with 3 or more lactations was positively affected by addition of supplemental chloride to the prepartum diet (39.9 vs. 38.6 kg/d), but treatment had no effect on milk yield of first and second lactation cows (Table 6). Cows with 3 or more lactations fed supplemental chloride during the prepartum period produced significantly more milk protein and milk solids than the control animals, although protein and solids percentage of milk was not affected by treatment. There was no effect of treatment on milk fat percentage or milk fat yield (Table 6).

The increases in yield of milk, milk protein, and milk solids in cows with 3 or more lactations fed supplemental chloride in the prepartum diet are interesting in light of the variation of responses seen in the literature with traditional anionic salts. Beede et al. (1991) observed that addition of anionic salts to the prepartum diet increased milk yield in the following lactation by 3.6%. Moore et al. (2000) fed anionic salts and had no effect on milk yield from 7 to 70 DIM. Ostergaard and Larson (2000) observed no relationship between blood plasma Ca levels at calving and subsequent milk yield.

IMPLICATIONS

Typically, nutritionists use anionic products only when low-K prepartum diets cannot be formulated or clinical milk fevers persist in a herd. This study reveals that further reducing subclinical hypocalcemia with supplemental chloride added to low-K prepartum diets can improve Ca status and have productive benefits for third and greater lactation cows, even in a herd with no noticeable clinical milk fever problem.

© 2008 American Registry of Professional Animal Scientists Provided by ProQuest LLC. All Rights Reserved.