Abstract

Nuclear magnetic resonance spectroscopy was applied to investigate the association between milk metabolome and udder quarter health status in dairy cows. Mammary gland health status was defined by combining information provided by traditional somatic cell count (SCC) and differential SCC (DSCC), which expresses the percentage of neutrophils and lymphocytes over total SCC. Quarter milk samples were collected in triplicate (d 1 to 3) from 10 Simmental cows, 5 defined as cases and 5 defined as controls according to SCC levels at d 0. A total of 120 samples were collected and analyzed for bacteriology, milk composition, SCC, DSCC, and milk metabolome. Bacteriological analysis revealed the presence of mostly coagulase-negative staphylococci in quarter milk samples of cows defined as cases. Nuclear magnetic resonance spectra of all quarter samples were first analyzed using the unsupervised multivariate approach principal component analysis, which revealed a specific metabolomic fingerprint of each cow. Then, the supervised cross-validated orthogonal projections to latent structures discriminant analysis unquestionably showed that each cow could be very well identified according to its milk metabolomic fingerprint (accuracy = 95.8%). The comparison of 12 different models, built on bucketed 1-dimensional NOESY spectra (noesygppr1d, Bruker BioSpin) using different SCC and DSCC thresholds, corroborated the assumption of improved udder health status classification ability by joining information provided by both SCC and DSCC. Univariate analysis performed on the 34 quantitated metabolites revealed lower levels of riboflavin, galactose, galactose-1-phosphate, dimethylsulfone, carnitine, hippurate, orotate, lecithin, succinate, glucose, and lactose, and greater levels of lactate, phenylalanine, choline, acetate, O-acetylcarnitine, 2-oxoglutarate, and valine, in milk samples with high somatic cells. In the 5 cases, results of the udder quarter with the highest SCC compared with its symmetrical relative were in line with quarter-level findings. Our study suggests that increased SCC is associated with changes in milk metabolite fingerprint and highlights the potential use of different metabolites as novel indicators of udder health status and milk quality.

Highlights

  • In recent decades, the ability to monitor udder health in lactating cows, especially in terms of mastitis and milk somatic cells, has become one of the key points for the entire dairy chain

  • Milk somatic cell count (SCC) has been widely adopted as an indicator to screen for subclinical mastitis at population level (Harmon, 2001; Pyörälä, 2003) and to perform indirect selection for animals endowed with lower susceptibility toward mastitis (Weigel and Shook, 2018)

  • Differential somatic cell count (DSCC), which expresses the percentage of neutrophils and lymphocytes over total SCC, has been proposed as a novel trait to screen for udder health on a wide scale (Damm et al, 2017)

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Summary

Introduction

The ability to monitor udder health in lactating cows, especially in terms of mastitis and milk somatic cells, has become one of the key points for the entire dairy chain This issue is of particular interest for (1) farmers, to increase profit through milk quality payment systems and reduction of veterinary interventions; (2) processing industries, as optimal cheese-making properties and cheese yields are favored by low milk somatic cells; and (3) consumers, due to increased sensibility and awareness toward animal health and welfare (Halasa et al, 2007). Bobbo et al.: MILK METABOLITES AND UDDER HEALTH milk SCC and decreased milk yield and quality (Xi et al, 2017) In these circumstances, the development of large-scale tools for identification of animals affected by subclinical mastitis is of great interest, as this would help farmers in the management of this disease and in the prevention of serious clinical outcomes. The study of the metabolic profile of cow milk with high and low SCC is a quite novel approach in the livestock sector, which is shedding light on the physiologic pathways at the basis of mastitis onset (Sundekilde et al, 2013)

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