Postgenomics Characterization of an Essential Genetic Determinant of Mammary Pathogenic
            <i>Escherichia coli</i>

Blum, Shlomo E.; Goldstone, Robert; Connolly, James P. R.; Répérant-Ferter, Maryline; Germon, Pierre; Inglis, Neil F.; Krifucks, O.; Mathur, Shubham; Manson, Erin; McLean, Kevin; Rainard, Pascal; Roe, Andrew J.; Leitner, Gabriel; Smith, David George Emslie

doi:10.1128/mbio.00423-18

Cited by 46 publications

(65 citation statements)

References 31 publications

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“…g_Enterorhabdus is a common conditional pathogen that can cause intestinal infections. Meanwhile, it is also signi cantly enriched in milk from mastitis cows [40]. Overall, the above bacteria increased in rumen during CM may not only re ected the invasion of pathogens, the occurrence of in ammation or rumen damage, but also revealed the resistance to in ammation.…”

Section: Discussionmentioning

confidence: 89%

Rumen microbiome structure and metabolites activity in dairy cows with clinical and subclinical mastitis

Wang

Nan²,

Zhao³

et al. 2020

Preprint

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Background: With high prevalence and complex etiology, bovine mastitis (BM) often causes serious damage to dairy cows’ health and milk quality. Although the shift in milk has been the main research interest on mastitis, recent studies have suggested that gastrointestinal microorganism has a crucial effect on the inflammation of the tissues outside the gut, such as mammary gland. However, studies related to the variation of rumen inner-environment during mastitis were limited. This study compared the differences of rumen microorganisms and metabolites under different udder health conditions, in order to investigate the correlation between udder health status and rumen microbiome structure and metabolites activity. Based on the somatic cell counts (SCC), California mastitis test (CMT) parameters and clinical symptoms of mastitis, 60 lactating Holstein dairy cows with similar body conditions (excepted for udder health condition) were divided into 3 groups (n = 20 per group): healthy (H) group, subclinical mastitis (SM) group and clinical mastitis (CM) group. Lactation and rumen fermentation parameters were detected, and rumen microbiota and metabolites were analyzed via 16S rRNA amplicon sequencing and untargeted metabolomics, respectively. Results: As the degree of mastitis increased, milk SCC and milk protein were significantly increased (P < 0.01). Milk yield, milk fat and lactose (P < 0.01), and rumen lactic acid (LA) (P < 0.01), acetate, propionate, butyrate, valerate (P < 0.001), total volatile fatty acids (TVFAs) concentrations (P < 0.01) and pH value (P = 0.024) were significantly decreased. In the rumen of CM cows, the significantly increased pathogens related to intestinal and oral inflammation, such as g__Lachnospiraceae_UCG-006 (P = 0.03), g__Moraxella and g__norank_f__Neisseriaceae (P < 0.01), etc., were accompanied by a significant increase in 12-oxo-20-dihydroxy-leukotriene B4 and 10beta-Hydroxy-6beta-isobutyrylfuranoeremophilane (P < 0.01). Meanwhile, in the rumen of SM cows, the g__Ruminiclostridium_9 (P = 0.04) and g_Enterorhabdus (P = 0.01) were increased with methenamine, 5-Hydroxymethyl-2-furancarboxaldehyde (5-HMF) and 6-Methoxymellein (P < 0.01). During mastitis, the decrease of short-chain fatty acids (SCFAs)-producing bacteria and intestinal probiotics in rumen, including g__Prevoterotoella_1 and g__Bifidobacterium (P = 0.03), etc., were significantly reduced, accompanied by a reduction in 2-Phenylbutyric acid (2-PBA) (P < 0.01).Conclusion: This study suggested that the microflora and metabolites associated with pathogen invasion, inflammatory response and rumen wall damage in the rumen of cows suffered mastitis were prominent.

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Section: Discussionmentioning

confidence: 89%

Rumen microbiome structure and metabolites activity in dairy cows with clinical and subclinical mastitis

Wang

Nan²,

Zhao³

et al. 2020

Preprint

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“…It will also allow systematic review and meta-analysis of studies examining the association between strain or lineage and infection characteristics such as infection severity, infection duration, transmission, and cure rate after antimicrobial therapy. Comparative genomics with strains isolated from humans or other animals may also lead to the identification of loci important for pathogenicity in each specific host, an approach that has already shown much promise (Lowder et al, 2009;Guinane et al, 2010;Blum et al, 2018). The cost and labor requirements of WGS means this technique is likely to remain a research tool in the short term.…”

Section: Genomics Of Imi Pathogensmentioning

confidence: 99%

“…The protein products of this locus allow the bacteria to capture iron from ferric citrate and were subsequently demonstrated to facilitate growth of E. coli in milk. They were additionally shown to be required for E. coli to cause IMI as deletion of the fec genes rendered the MPEC strain P4 nonpathogenic, whereas their introduction into the nonpathogenic strain K71 rendered this strain capable of causing IMI (Blum et al, 2018).…”

Section: E Colimentioning

confidence: 99%

Symposium review: Intramammary infections—Major pathogens and strain-associated complexity

Keane

2019

Journal of Dairy Science

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Intramammary infection (IMI) is one of the most costly diseases to the dairy industry. It is primarily due to bacterial infection and the major intramammary pathogens include Escherichia coli, Streptococcus uberis, and Staphylococcus aureus. The severity and outcome of IMI is dependent on several host factors including innate host resistance, energy balance, immune status, parity, and stage of lactation. Additionally, the infecting organism can influence the host immune response and progression of disease. It is increasingly recognized that not only the infecting pathogen species, but also the strain, can affect the transmission, severity, and outcome of IMI. For each of 3 major IMI-associated pathogens, S. aureus, Strep. uberis, and E. coli, specific strains have been identified that are adapted to the intramammary environment. Strain-dependent variation in the host immune response to infection has also been reported. The diversity of strains associated with IMI must be considered if vaccines effective against the full repertoire of mammary pathogenic strains are to be developed. Although important advances have been made recently in understanding the molecular mechanism underpinning strain-specific virulence, further research is required to fully elucidate the cellular and molecular pathogenesis of mammary adapted strains and the role of the strain in influencing the pathophysiology of infection. Improved understanding of molecular pathogenesis of strains associated with bovine IMI will contribute to the development of new control strategies, therapies, and vaccines. The development of enabling technologies such as pathogenomics, transcriptomics, and proteomics can facilitate system-level studies of strain-specific molecular pathogenesis and the identification of key mediators of host-pathogen interactions.

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“…Peak bacterial counts in milk were observed at 24 h [4], following a steep decrease in citrate between 16 to 24 h after challenge and concomitant to a significant increase in lactoferrin in milk. The ability to assimilate iron from citrate is a key feature of MPEC [3] and therefore it is possible that the exchange of citrate to lactoferrin as main iron chelator in milk contributes to reduce bacterial load.…”

Section: Discussionmentioning

confidence: 99%

“…Escherichia coli is the main pathogen causing acute mastitis in cattle, a disease of significant economic and animal welfare impact in dairy production worldwide. Upon entry into the mammary gland, mammary pathogenic strains of E. coli rapidly grow using milk as a nutrient source, in a manner highly dependent on the expression of the ferric-dicitrate system by these bacteria [1-3]. The resulting infection leads to an acute inflammation that causes a sharp decrease in milk yield and deep changes of milk properties and constituents [4].…”

Section: Introductionmentioning

confidence: 99%

The physiological response in the mammary gland to Escherichia coli infection reflects a conflict between glucose need for milk production and immune response

Jacoby

et al. 2019

Preprint

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30Upon entry into the mammary gland, mammary pathogenic strains of Escherichia 31 coli rapidly grow using milk as a nutrient source, in a manner highly dependent on the 32 expression of the ferric-dicitrate system by these bacteria. Intra-mammary challenge with 33 distinct mammary pathogenic E. coli (MPEC) strains result in development of clinical 34 acute mastitis, with peak bacterial counts in milk at 16-24 h post-challenged and profound 35 immune changes found in the milk. The main biochemical changes measured in milk 36 were partially in accord with lipopolysaccharide-induced mastitis, with increased 37 glucose-6-phosphate and lactate dehydrogenase activity or prolonged lactate 38 dehydrogenase, and Glu6P/Glu alterations. Changes also reflect physiological responses 39 to inflammation in the mammary gland, as in the balance between aerobic and anaerobic 40 metabolism (citrate to lactate ratios). Some alterations measured in milk resolved with 41 days after challenge but other remained for above one month, regardless of bacterial 42 clearance. The results suggest that E. coli mastitits can be divided into two stages: an 43 acute, clinical phase, as an immediate response to bacterial infection in the mammary 44 gland and a chronic phase, independent of bacteria clearance, and in response to the tissue 45 damage caused in the first phase. 46 47

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Postgenomics Characterization of an Essential Genetic Determinant of Mammary Pathogenic Escherichia coli

Cited by 46 publications

References 31 publications

Rumen microbiome structure and metabolites activity in dairy cows with clinical and subclinical mastitis

Rumen microbiome structure and metabolites activity in dairy cows with clinical and subclinical mastitis

Symposium review: Intramammary infections—Major pathogens and strain-associated complexity

The physiological response in the mammary gland to Escherichia coli infection reflects a conflict between glucose need for milk production and immune response

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