Original Research
Fecal pH and Microbial Populations in Thoroughbred Horses During Transition from Pasture to Concentrate Feeding

https://doi.org/10.1016/j.jevs.2012.06.004Get rights and content

Abstract

Abrupt dietary transitions and feeding of rapidly fermentable diets are common practices in the horse industry and have been associated with digestive and metabolic disorders that can impair the performance of horses. The present study investigated the effect of dietary transition from pasture grazing to confinement with concentrate feeding, and back, on fecal pH and bacterial populations of Streptococcus spp and Lactobacillus spp. Six Thoroughbred fillies, previously grazing perennial ryegrass and white clover-based pasture, were housed in individual stalls and fed an increasing ratio of concentrate to conserved forages for 13 days (days 1-13), followed by an abrupt transition back to only pasture-grazing for 3 days (days 14-16). The concentrate was initially offered at 0.83 kg dry matter (DM)/d and increased to 5 kg DM/d, whereas ensiled alfalfa was initially offered at 0.61 kg DM/d, increasing to 1.22 kg DM/d. Meadow hay was initially offered at 6.73 kg DM/d, decreasing to 1.6 kg DM/d. Fecal specimens were collected daily for determination of pH, and every 2 days for quantitative analysis of Streptococcus spp and Lactobacillus spp. Mean fecal pH increased significantly from pasture baseline values (pH 6.18) during the initial confinement and supplementation on day 1 (6.37), day 2 (6.52), day 3 (6.58), and day 4 (6.43) (standard error of mean [SEM]: 0.056; P < .001). By day 5, mean fecal pH values had decreased to, and remained at, baseline values until the horses returned to pasture, when another increase occurred at day 15 (6.45). Fecal colony forming units (cfu) of Streptococcus spp and Lactobacillus spp increased linearly (r = 0.94; P < .001) from 6.0 and 6.1 log10 cfu/g on day -4, to 7.8 log10 cfu/g on day 14 (SEM: 0.2 P < .001), respectively. Fecal cfu decreased on return to a pasture-only diet (P < .001). In this study, the increment of bacterial populations was associated with a relatively stable fecal pH and highlights the difficulty in identifying the effects of dietary transition on the equine hindgut health, without microbial culture.

Introduction

Intensive management of horses for sport and racing is often associated with dietary transition and the feeding of rapidly fermentable carbohydrates. In New Zealand, the preparation of young horses often involves rotations of short periods (2-3 weeks) of stall confinement and concentrate feeding, followed by a return to the pasture environment [1], [2]. During the period of transition from pasture to confinement and concentrate feeding, the concentrate component of the diet is commonly increased by as much as 500 g/d [3]. This is significantly higher than the 200 g/d for a 550-kg horse recommended internationally to minimize digestive and metabolic disorders [4].

The equine hindgut microflora can be highly and rapidly reactive to abrupt changes in diet, with changes in colon and cecum microflora observed as early as 5 hours after the introduction of concentrate to horses previously fed a hay-based diet [5]. Abrupt dietary changes, especially those involving pastures rapidly increasing in levels of water-soluble carbohydrates (WSC), or feeding excess levels of starch-containing grain, or cereal concentrates, are the known risk factors for the development of digestive and metabolic disorders such as hindgut acidosis and laminitis [6], [7], [8]. Equine hindgut acidosis occurs when resistant starch escapes digestion in the small intestine, or dietary starch or WSC concentrations exceed the prececal digestive and absorptive capacity. The starch or WSC are then rapidly fermented in the hindgut by anaerobic bacteria that excessively produce lactate, causing a rapid decrease in hindgut pH (hindgut acidosis) [9], [10].

Various studies monitoring changes in cecal microbial populations of the equine hindgut in response to excess starch, or fructan (oligofructose), suggest that gram-positive bacteria such as Lactobacillus spp [6], [11], Streptococcus bovis [6], [11], [12], and Streptococcus equinus [12] play an integral role during the onset of hindgut acidosis and laminitis. Recent advances in the identification of equine gut microbiology show that specific members of the Streptococcus genus, collectively described as equine hindgut streptococcal species, may be involved in the series of events that lead to lactic acidosis and subsequently to laminitis in the horse, proliferating in response to carbohydrate administration, before rapidly declining in numbers [13], [14]. Even mild lactic cases of acidosis and laminitis can affect the well-being and performance potential of horses owing to subtle radiographic changes [15]. Therefore, monitoring of equine gut health can assist with the early detection of unfavorable changes and identifying those horses at risk of developing acidosis.

Acute and subacute hindgut acidosis cases are not distinctly separate disorders, thereby making diagnosis difficult. The critical hindgut pH threshold for the development of subacute or acute acidosis in horses is related to the optimal pH for lactate using bacteria to establish. An intestinal and hindgut pH of ≤6.0 is known to inhibit cellulolytic bacteria and protozoa and favors the rapid growth of acid-tolerant bacteria such as Streptococcus bovis/equinus and Lactobacillus spp [12], [16]. A cecal pH of 6.0 in horses is considered to represent subclinical acidosis [17], and a hindgut pH of <6.0 is associated with clinical conditions, such as osmotic diarrhea, overgrowth of gram-positive bacteria, and lyses of gram-negative bacteria, which may culminate in laminitis in horses [6].

Direct measurement of gastrointestinal changes in pH and microbial populations requires fistulation [18], which is invasive and not practical in a nonlaboratory setting. In several species, measurement of fecal pH and microbial culture has been validated as an indirect measure of gastrointestinal changes [19], [20], [21]. In the horse, fecal pH and fecal microbial culture have been successfully used to monitor changes in the equine hindgut in response to carbohydrate challenges and evaluation of different feeding strategies [22], [23].

Despite the general view linking the composition of the intestinal microflora with the development of acidosis, the microbial changes in the equine hindgut during transition from the feeding of concentrates with conserved forage to the grazing of fresh pasture, or vice versa, are poorly understood. The aim of the current study was to investigate the effect of abrupt dietary transition from pasture grazing to confinement with concentrate feeding, and back, on fecal pH and bacterial populations of Streptococcus spp and Lactobacillus spp in the hindgut of a young Thoroughbred horse.

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Materials and Methods

This study was conducted in early spring (September) 2005 and was approved by the Massey University Animal Ethics Committee (Palmerston North, New Zealand).

Feed Intake

The chemical composition of feedstuffs and the mean feed intake of horses are detailed in Table 1, Table 2. Overall similar compositions were observed between the pasture diet pre- and post-treatment and hay offered and refused. The mean intake of DM, organic matter, CP, HWSC, gross energy, and DE increased significantly over time of treatment (P < .001) (Table 2). The maximum starch intake per meal was between 2.9 and 3.3 g DM/kg body weight (BW) on days 11-13.

The minimum recommended fiber

Discussion

The aim of this study was to investigate the effect of dietary transitions on fecal pH and bacterial populations of Streptococcus spp and Lactobacillus spp in young Thoroughbred horses. Despite a rapid increase in the amount of barley/concentrate fed to the horses, acute acidosis was not observed in this study. Although significant changes associated with the development of acidosis and laminitis occurred in the hindgut of the horses in this study, as determined by microflora populations, no

Acknowledgments

Funding for this project was kindly provided by the New Zealand Equine Research Foundation (NZERF) and Massey University. The authors thank Dr. John O'Brien and Newmarket Lodge for their kind assistance in providing horses and facilities. The authors also acknowledge Cecile Mathieu for assisting during the experimental work, and the technical staff of the Infectious Disease group, IVABS, Massey University, for their help in the laboratory.

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