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Original Articles

Effects of monensin and virginiamycin supplementation in finishing diets with distiller dried grains plus solubles on growth performance and digestive function of steers

, , , &
Pages 417-425 | Received 12 Jun 2014, Accepted 10 Oct 2014, Published online: 14 Nov 2014

Abstract

Two trials were conducted to evaluate the influence of virginiamycin (26 mg/kg) and monensin (34 mg/kg) supplementation of a steam-flaked corn-based finishing diet containing 15% distiller dried grains plus solubles (DDGS) on growth performance and digestive function. In Trial 1, 135 steers (257 ± 21 kg) were used to evaluate treatment effects on 145-d growth performance. There were no treatment effects (P > 0.20) on dry matter intake (DMI). Antibiotic supplementation tended to increase average daily gain (ADG; 7%, P = 0.07); increased gain efficiency (11%, P < 0.01) and estimated dietary net energy (NE; 10%, P < 0.01). Carcass marbling score was greater (12%, P = 0.04) for virginiamycin vs. monensin. In Trial 2, three Holstein steers (300 ± 7 kg) were used in a 3 × 3 Latin square to evaluate treatment effects on digestion. Both monensin and virginiamycin depressed ruminal digestion of organic matter (OM; 6%, P < 0.01) and feed nitrogen (N, 15%, P = 0.03) and microbial protein synthesis (15%, P = 0.03). There were no treatment effects of total tract OM and N digestion. Antibiotic supplementation increased (2.3%, P = 0.02) ruminal pH, associated with decreased (7%, P = 0.04) ruminal volatile fatty acids (VFA) concentrations. It is concluded that monensin and virginiamycin supplementation of growing-finishing diets for feedlot cattle may enhance daily weight gain, gain efficiency and dietary energetics. These effects are associated with a shift towards great intestinal OM digestion and decreased ruminal degradation of feed N and microbial protein synthesis.

1. Introduction

Virginiamycin is an antimicrobial derived from Streptomyces virginiae that inhibits growth of Gram-positive bacteria (Cocito Citation1979). In a summary of seven dose–response studies with feedlot cattle (Rogers et al. Citation1995), dietary supplementation with 19 mg to 27 mg virginiamycin/kg (dry matter basis) enhanced average daily gain (4.6%) and gain to feed ratio (3.6%) and reduced (38%) the incidence of liver abscess. The effect on liver abscess incidence is due to direct inhibitory action on growth of Fusobacterium necrophorum and Actinomyces pyogenes (Nagaraja & Chengappa Citation1998). In a 340-d study involving calf-fed Holstein steers, Salinas-Chavira et al. (Citation2009) did not observe an influence of virginamycin supplementation of average daily gain. However, it increased gain efficiency and dietary net energy (NE) by 4%. The basis for improved growth performance is not certain. Virginiamycin inhibits growth of ruminal lactic acid-producing bacteria, limiting ruminal lactate accumulation (Hedde et al. Citation1980; Nagaraja et al. Citation1987; Hynes et al. Citation1997; Clayton et al. Citation1999; Coe et al. Citation1999). Thus, virginiamycin might reduce risk of lactic acidosis and associated digestive dysfunctions following ruminal overload of rapidly fermentable carbohydrate (Owens et al. Citation1998). Salinas-Chavira et al. (Citation2009) did not observe an effect of Virginiamycin supplementation of ruminal lactate concentrations 4 h after feeding steers adapted to a steam-flaked corn-based finishing diet. However, lactate concentrations were low for both unsupplemented and supplemented steers (14.0 mg/dL vs. 13.7 mg/dL, respectively). In swine, virginiamycin enhanced digestion of dry matter, nitrogen (N) and energy (Ravindran et al. Citation1984), metabolizable energy (Vervaeke et al. Citation1979) and minerals (Ravindran et al. Citation1984; Agudelo et al. Citation2007). These benefits were attributable to prolonged intestinal retention time (28%–33%, Ravindran et al. Citation1984) and to reduced intestinal bacterial evolution and corresponding organic acid production (Vervaeke et al. Citation1979). Monensin is a widely used ionophore that is supplemented into feedlot diets to enhance growth performance (Goodrich et al. Citation1984). Incorporation of higher levels of distiller dried grains plus solubles (DDGS) in feedlot diets alter ruminal fermentation in cattle, decreasing of ruminal organic matter (OM) digestion and increasing the acetate to propionate ratio (Carrasco et al. Citation2013). Felix et al. (Citation2012) did not report beneficial effects of monensin supplementation on ruminal pH and volatile fatty acids (VFA) molar proportions in diets with DDGS supplemented with monensin. The object of this study was to further evaluate the effects of virginiamycin and monensin supplementation on growth performance and digestive function in feedlot steers fed diets supplemented with DDGS.

2. Materials and methods

All procedures involving animal care and management were in accordance with and approved by the University of California, Davis, Animal Use and Care Committee.

2.1. Trial 1

2.1.1. Animals and diets

One hundred thirty-five crossbred steers (approximately 25% Brahman with the remainder represented by Hereford, Angus, Shorthorn and Charolais breeds in various proportions) with an average weight of 257 ± 21 kg were used in a 145-d experiment to compare the effects of virginiamycin and monensin on growth performance, dietary net energy and carcass characteristics. Cattle originated from south-east Texas and were received at the University of California Desert Research Center, El Centro, on 23 October 2012. Upon arrival, steers were vaccinated for bovine rhinotracheitis-parainfluenza (Cattle Master Gold FP 5 L5, Zoetis, New York, NY), clostridials (Ultrabac-7, Zoetis, New York, NY), treated for parasites (Dectomax Injectable, Zoetis, New York, NY), injected subcutaneously with 500,000 IU vitamin A (Vital E–A + D3, Stuart Products, Bedford, TX) and 1200 mg ceftiofur (Excede, Zoetis, New York, NY), branded, ear-tagged and implanted with Revalor-IS (Intervet, Millsboro, DE). Bull calves were castrated and horns, if present, were tipped. During an initial 42-d adaptation period, all steers were fed receiving and transition diets according to schedule given in . On Day 28 of the transition period, steers were given a booster vaccination of Cattle Master Gold. Steers were then blocked by 28-d weight and randomly assigned within weight groupings to 27 pens, 5 steers/pen. All steers received the same basal finishing diet (Control diet, ) for 7 d prior to initiation of the study on 5 December 2012. Pens were 78 m2 with 33 m2 of overhead shade, automatic waterers and fence-line feed bunks. Three dietary treatments were compared: (1) Control (no antibiotic); (2) 34 mg/kg monensin (dry matter (DM) basis; Rumensin 90, Elanco Animal Health, Greenfield, In) and (3) 26 mg/kg virginiamycin (DM basis; V-max 50, Phibro Animal Health, Ridgefield Park, NJ). Diets were prepared at weekly intervals and stored in plywood boxes located in front of each pen. Steers were allowed ad libitum access to their experimental diets. Fresh feed was provided twice daily. On 30 January 2013, all steers were injected subcutaneously with 500,000 IU vitamin A (Vital E-A + D3, Stuart Products, Bedford, TX) and implanted with Revalor-S (Intervet, Millsboro, DE).

Table 1. Diet formulations and feeding programme during 42-d transition period from arrival of steers into the feedlot to initiation of Trial 1.

Table 2. Composition of experimental diets fed to steers.

2.1.2. Estimation of dietary NE

Energy gain (EG) was calculated by the equation: EG = ADG1.097 0.0557W0.75, where EG is the energy deposited (Mcal/d), W is the mean shrunk body weight (BW in kg; NRC Citation1984). Maintenance energy (EM) was calculated by the equation: EM = 0.077W0.75 (NRC Citation1984). Dietary NEg was derived from NEm by the equation: NEg = 0.877 NEm − 0.41 (Zinn Citation1987). Dry matter intake (DMI) is related to energy requirements and dietary NEm according to the equation: DMI = EG/(0.877NEm − 0.41) and can be resolved for estimation of dietary NE by means of the quadratic formula: x = (−b − −b2−4ac)/2c, where x = NEm, a = −0.41 EM, b = 0.877 EM + 0.41 DMI + EG, and c = −0.877 DMI (Zinn & Shen Citation1998).

2.1.3. Carcass data

Hot carcass weights (HCW) were obtained at time of slaughter. After carcasses chilled for 48 h, the following measurements were obtained: Longissimus muscle (LM) area (cm2) by direct grid reading of the LM at the 12th rib; subcutaneous fat (cm) over the LM at the 12th rib taken at a location ¾ the lateral length from the chine bone end (adjusted by eye for unusual fat distribution); KPH as a percentage of HCW; marbling score (USDA Citation1997; using 3.0 as minimum slight, 4.0 as minimum small, 5.0 as minimum modest, 6.0 as minimum moderate, etc.) and estimated retail yield of boneless, closely trimmed retail cuts from the round, loin, rib and chuck (percentage of HCW; Murphey et al. Citation1960) = 52.56 – 1.95 × subcutaneous fat − 1.06 × KPH + 0.106 × LM area − 0.018 × HCW.

2.1.4. Statistical design and analysis

For calculating steer performance in Trial 1, BW was reduced by 4% to account for digestive tract fill. Final shrunk LW was adjusted for HCW by dividing HCW by the decimal fraction of the average dressing percentage (0.64). Pens were used as experimental units. The experimental data were analysed as a randomized complete block design experiment according to the following statistical model: Yij = μ + Bi + Tj + εij (Hicks Citation1973), where μ is the common experimental effect, Bi represents initial weight group effect (df = 8), Tj represents dietary treatment effect (df = 2) and εij represents the residual error (df = 16). Treatment effects were tested using the following contrasts: (1) control vs. monensin and virginiamycin; (2) monensin vs. virginiamycin. Significant effect was considered at P < 0.10 (Stastix 9, Analytical Software, Tallahassee, FL).

2.2. Trial 2

2.2.1. Animals and sampling

Three Holstein steers (300 ± 7 kg) with cannulas in the rumen (3.8 cm internal diameter) and proximal duodenum (Zinn & Plascencia Citation1993) were used in 3 × 3 Latin square experiment to study treatment effects on characteristics of digestion. Treatments were the same as those used in Trial 1 (). All steers were fed the same basal control diet with 0.30% chromic oxide added as a digesta marker. Dietary antibiotic treatments (virginiamycin and monensin) were top-dressed on the individual steer's feed allotment at the time of feeding. Steers were maintained in individual pens (4 m2) with automatic waterers. Diets were fed at 0800 and 2000 h daily. In order to avoid the complications of feed refusals, DMI was restricted to 6.7 kg/d (equivalent to 2.2% of LW). This value is 97% of average observed DMI intake for steers in Trial 1 (2.27% of LW). Experimental periods were 3 weeks, with 10 d for dietary treatment adjustment, 4 d for collection and 7 d of drug withdrawal (steers were fed only the basal diet with no added virginiamycin or monensin for 1 week before switching to new dietary treatment assignments of the subsequent experimental period). During collection, duodenal and faecal samples were taken twice daily as follows: Day 1, 0750 and 1350 h; Day 2, 0900 and 1500 h; Day 3, 1050 and 1650 h and Day 4, 1200 and 1800 h. Individual samples consisted of approximately 700 mL of duodenal chime and 200 g (wet basis) of faecal material. Samples from each steer within each collection period were composited for analysis. During the final day of each collection period, ruminal samples were obtained from each steer via ruminal cannula 4 h after feeding. Ruminal fluid pH was determined on fresh samples. Samples were strained through four layers of cheesecloth. Two millilitres of freshly prepared 25% (wt/vol) meta-phosphoric acid was added to 8 mL of strained ruminal fluid. Samples were then centrifuged (17,000 × g for 10 min), and supernatant fluid was stored at −20°C for VFA analysis (gas chromatography; Zinn Citation1988). Upon the completion of the experiment, ruminal fluid was obtained via the ruminal cannula from all steers and composited for isolation of ruminal bacteria by differential centrifugation (Bergen et al. Citation1968).

2.2.2. Sample analysis and calculations

Samples were subjected to all or part of the following analysis: dry matter (oven drying at 105°C until no further weight loss), ash, ammonia N, Kjeldahl N (AOAC Citation1984); NDF (Goering & Van Soest Citation1970; adjusted for insoluble ash), chromic oxide (Hill & AndersonCitation 1958); purines (Zinn & Owens Citation1986); and starch (Zinn Citation1990). Microbial OM and N leaving the abomasum were calculated using purines as a microbial marker (Zinn & Owens Citation1986). OM fermented in the rumen was considered equal to OM intake minus the difference between the amount of total OM and microbial OM reaching the duodenum. Feed N escape to the small intestine was considered equal to total N leaving the abomasum minus ammonia-N, microbial N and endogenous N, assuming endogenous N is equivalent to 0.195 W0.75 (Ørskow et al. Citation1986). Methane production (mol/mol glucose equivalent fermented) was estimated based on the theoretical fermentation balance for observed molar distribution of VFA (Wolin Citation1960).

2.2.3. Statistical design and analysis

Treatment effects on characteristics of digestion in cattle were analysed as a 3 × 3 Latin square design (Stastix 9, Analytical Software, Tallahassee, FL). The statistical model for the trial was as follows: Yijk =µ + Si + Pj + Tk + Eijk, where: Yijk is the response variable, µ is the common experimental effect, Si is the steer effect (df = 2), Pj is the period effect (df = 2), Tk is the treatment effect (df = 2), and Eijk is the residual error (df = 2). Treatments effects were tested using the following contrasts: (1) control vs. monensin and virginiamycin; (2) monensin vs. virginiamycin. Significant effect was considered at P < 0.10.

3. Results and discussion

Treatment effects on growth performance of feedlot steers (Trial 1) are shown in . There were no treatment effects (P > 0.20) on DMI. Antibiotic supplementation (virginiamycin and monensin) tended to increase average daily gain (ADG) (7%, P = 0.07), gain efficiency (11%, P < 0.01), estimated dietary NEm (9%, P < 0.01) and NEg (11%, P < 0.01).

Table 3. Treatment effects on growth performance of feedlot steers and NE value of the diet.

Growth performance responses to supplemental monensin have been variable. Barreras et al. (Citation2013) also observed increased ADG (6%), gain efficiency (5%) and dietary NEm (3%) and NEg (4%) in beef heifers fed a steam-flaked corn-based finishing diet supplemented with monensin. Likewise, monensin supplementation of a high-fibre finishing diet containing 60% DDGS, 10% corn silage and 10% haylage increased ADG and G:F by 5% and 4%, respectively (Felix & Loerch Citation2011). However, in numerous other studies involving feedlot cattle fed energy dense finishing diets based on steam-flaked corn with urea as the principal source of supplemental N, monensin supplementation did not improve ADG or G:F (Zinn & Borques Citation1993; Zinn et al. Citation1994; Depenbusch et al. Citation2008; Salinas-Chavira et al. Citation2009). The basis for the variable response is not certain. Rogerio et al. (Citation1997) observed that monensin supplementation did not affect ADG and G:F of Holstein steers fed a cracked corn-based finishing diet with urea as the supplemental N source. However, with soybean meal as the supplemental N source, monensin supplementation increased both ADG and G:F. In a 228-trial summary, Goodrich et al. (Citation1984) observed that monensin supplementation numerically increased ADG and G:F by an average of 1.6% and 8.0%, respectively. However, the coefficient of variation for those measures were high (531 and 87%, respectively), with responses tending to decrease with increasing ADG of control (non-supplemented) cattle, with increasing dietary energy density, and when non-protein N (NPN) was the principal source of supplemental N. Based on generalized equations of Zinn et al. (Citation2008; ADG = 1.628 + 0.00287 IW − 0.00000107 IW2 − 0.461 Frame), the expected ADG for the average-frame (2.0) steers used in this study (IW = 313 kg) is 1.50 kg, in good agreement with observed (). Thus, the observed gain response to monensin was in addition to control performance that equaled or was slightly better than expected.

In a seven-trial summary of feedlot cattle growth performance, Rogers et al. (Citation1995) observed that virginiamycin supplementation at the rate of 19 mg/kg−27 mg/kg dietary DM increased ADG and G:F by 5% and 4%, respectively. In a 340-d growing-finishing trial involving calf-fed Holstein steers, virginiamycin supplementation did not affect ADG, but increased G:F and dietary NE by 4% and 5%, respectively (Salinas-Chavira et al. Citation2009).

Treatment effects on carcass characteristics of feedlot steers are shown in . Antibiotic supplementation increased carcass weight (3%, P = 0.05). Effects of monensin and virginiamycin on carcass weight were similar (P = 0.91). There were no treatment effects (P > 0.10) on carcass dressing percentage, KPH, fat thickness, LM area, marbling score and retail yield. However, marbling score was greater (12%, P = 0.04) for virginiamycin than for monensin-supplemented cattle. This treatment effect on marbling score is surprising. In the previous studies (Goodrich et al. Citation1984; Salinas-Chavira et al. Citation2009), effects of monensin or virginiamycin on carcass characteristics were not apparent.

Table 4. Treatment effects on carcass characteristics of feedlot steers.

Treatment effects on characteristics of ruminal and total tract digestion (Trial 2) are shown in . There were no treatment effects (P = 0.47) on ruminal starch digestion. Both monensin and virginiamycin supplementation depressed (6%, P < 0.01) ruminal OM digestion. This effect was associated in part with depressed ruminal digestion of feed N (15%, P = 0.03), and a tendency (10%, P = 0.09) for depressed microbial efficiency (g microbial N entering the small intestine per kg OM fermented). Although virginiamycin supplementation, like monensin, also decreased microbial N flow to the small intestine (P = 0.03), the magnitude of the effect tended to be less (9% vs. 21%; P = 0.07) for virginiamycin than for monensin. Likewise, the depression in ruminal OM digestion was lesser (5%, P = 0.02) for virginiamycin than for monensin supplemented diets. Hence, flow of non-ammonia-N (combination of microbial and feed N) to the small intestine was greater (6%, P < 0.01) for virginaimycin than for monensin supplemented diets. Ruminal OM digestion (P = 0.02) and N efficiency (g non-ammonia-N entering the small intestine per g N intake; P < 0.01) were greater (5% and 9%, respectively) for virginiamycin than for monensin-supplemented diets. There were no treatment effects (P ≥ 0.19) on total tract digestion of OM, starch and N.

Table 5. Treatment effects on characteristics of ruminal and total tract digestion in Holstein steers.

The effect of supplemental monensin on ruminal OM digestion of growing-finishing diets for feedlot cattle has been fairly consistent. As with the present study, there are numerous reports of small decreases (4%–6%) in ruminal OM digestion with monensin supplementation (Zinn & Borques Citation1993; Zinn et al. Citation1994; Surber & Bowman Citation1998; Salinas-Chavira et al. Citation2009). In contrast, Zinn (Citation1987) did not observe an effect of monensin supplementation on ruminal OM digestion. Reduced ruminal feed protein degradation (Poos et al. Citation1979; Zinn & Borques Citation1993; Zinn et al. Citation1994; Surber & Bowman Citation1998) also has been a consistent response to monensin supplementation. This effect is apparently due to a marked reduction in monensin sensitive amino acid fermenting bacteria (Yang & Russell Citation1993). Nevertheless, the effect of supplemental monensin on ruminal feed N degradation has been observed independently of effects on net ruminal microbial N synthesis. In some cases, as with the present study (), supplementation reduced net ruminal microbial N synthesis (Poos et al. Citation1979; Zinn et al. Citation1994), whereas in others, effects were small or non-appreciable (Zinn & Borques Citation1993; Surber & Bowman Citation1998).

There is limited information regarding the effects of virginiamycin supplementation on characteristics of site and extent of digestion in cattle. In a previous study conducted at this centre (Salinas-Chavira et al. Citation2009), virginiamycin supplementation of a steam-flaked corn-based finishing diet did not affect ruminal digestion of OM and feed N and net microbial N synthesis, whereas in the present study, virginiamycin supplementation of a steam-flaked corn-based diet containing higher levels of supplementation intact protein as DDGS, virginiamycin supplementation markedly increased (26%) flow of feed N to the small intestine. Likewise, Ives et al. (Citation2002) observed a protein-sparing effect of virginiamycin on ruminal feed protein degradation, associated with decreased ruminal deaminase activity. Although, in contrast with the present study, they did not observe this effect with supplemental monensin.

The partial substitution of DDGS for steam-flaked corn in feedlot diets reduces ruminal OM digestion and increases flow of feed N to the small intestine (Carrasco et al. Citation2013). In the present study, both monensin and virginiamycin, likewise, reduced ruminal OM digestion and increased flow of feed N to the duodenum, but they also decreased ruminal microbial N efficiency and net flow of microbial N to the small intestine.

Treatment effects on characteristics of ruminal pH and VFA molar proportions are shown in . Antibiotic supplementation increased (2.3%, P = 0.02) ruminal pH. Ruminal pH was not different (P = 0.17) for virginiamycin vs. monensin. Consistent with decreased ruminal OM digestion, ruminal VFA concentrations were lower (7%, P = 0.04) for antibiotic supplemented diets. Although there were no treatment effects (P ≥ 0.12) on individual ruminal VFA molar proportions, both monensin and virginiamycin supplementation tended (8%, P = 0.09) to decrease estimated ruminal methane production.

Table 6. Treatment effects on ruminal fermentation characteristics in Holstein steers.

Previously, the biological activity of monensin on cattle performance was attributed largely to its effects of decreased methane energy loss associated with a shifting fermentation of end-products towards greater propionate and lesser acetate and butyrate (Richardson et al. Citation1979). The magnitude of the effect has been variable, with numerous studies showing decreases in acetate:propionate molar ratios (Wedegaertner & Johnson Citation1983; Ricke et al. Citation1984; Rogers et al. Citation1991; Zinn & Borques Citation1993; Surber & Bowman Citation1998; Guan et al. Citation2006). However, in other cases (Zinn Citation1987; Zinn et al. Citation1994; Salinas-Chavira et al. Citation2009; Felix & Loerch Citation2011), supplemental monensin did not influence VFA molar proportions.

As with monensin, the effects of virginiamycin supplementation of end-products of fermentation have been variable. In a grain challenge study, Al Jassim et al. (Citation2003) observed decreased acetate:propionate molar ratio with virginiamycin supplementation. More commonly; however, the effects of virginiamycin on ruminal VFA molar proportions has been negligible (Ives et al. Citation2002; Candanosa et al. Citation2008; Salinas-Chavira et al. Citation2009).

The inclusion of DDGS in feedlot diets increases acetate and reduced propionate, consequently increasing acetate:propionate molar ratio and methane production (Carrasco et al. Citation2013). In the present study, the supplementation with monensin or virginiamycin did not influence molar proportions of these VFA, although methane production tended to reduce with these feed additives.

4. Conclusion

It is concluded that monensin and virginiamycin supplementation of growing-finishing diets with DDGS for feedlot cattle may enhance daily weight gain, gain efficiency, and dietary NE value. These effects are associated with a shift towards great intestinal OM digestion, and decreased ruminal degradation of feed N and microbial protein synthesis.

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