The Auxotrophic Nature of Streptococcus uberis

Kitt, A.J.; Leigh, James A.

doi:10.1007/978-1-4899-1825-3_151

Cited by 23 publications

(3 citation statements)

References 6 publications

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“…1 . It has been postulated that S. uberis is dependent on casein cleavage to obtain nutrients during IMI, 47 but shifts in protein and peptide distributions persist beyond resolution of infection so casein cleavage is not dependent on the pathogen.…”

Section: Discussionmentioning

confidence: 99%

Mastitomics, the integrated omics of bovine milk in an experimental model of Streptococcus uberis mastitis: 1. High abundance proteins, acute phase proteins and peptidomics

et al. 2016

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Section: Discussionmentioning

confidence: 99%

Mastitomics, the integrated omics of bovine milk in an experimental model of Streptococcus uberis mastitis: 1. High abundance proteins, acute phase proteins and peptidomics

et al. 2016

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“…Different serine proteases that activate host plasminogen to plasmin, generating activity needed for the degradation of extracellular matrix proteins and subsequent colonization, have been described. In addition, the activation of endogenous plasminogen present in milk would lead to hydrolysis of milk proteins and thereby release of peptides from which S. uberis could obtain essential amino acids (Kitt & Leigh, 1997). We found that the skc gene was harboured by 65.3% of the strains.…”

Section: Discussionmentioning

confidence: 99%

Distribution of virulence-associated genes in Streptococcus uberis isolated from bovine mastitis

Reinoso

Lasagno

Dieser

et al. 2011

FEMS Microbiology Letters

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Streptococcus uberis is an important pathogen that has been implicated in bovine mastitis but the virulence factors associated with pathogenesis are not well understood. The aim of this work was to examine 11 putative and known virulence-associated genes by PCR in 78 S. uberis strains isolated from infected animals in Argentina. Additionally, the distribution of virulence patterns over various herds was determined. Not all genes were present in the strains but all of the detected virulence-associated genes were present in combination. Forty-seven (60.3%) isolates carried seven to 10 virulence-associated genes. Further analysis revealed 58 virulence patterns. Different patterns were found within the same herd and among herds, demonstrating that strains with different virulence patterns were able to cause mastitis. Despite the large number of strains with different virulence patterns, strains with identical patterns was found. Detection of virulence-associated genes in individual S. uberis strains isolated from infected animals revealed one to 10 virulence genes. This may indicate that other virulence factors could be involved. The present study reveals the occurrence and distribution of 11 virulence-associated genes among S. uberis isolates from bovine mastitis in various herds and contributes to a better understanding of the pathogenicity of this bacterium.

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“…Given that milk, and probably the interior of the mammary gland, does not in the first instance provide all of the nutritional requirements of Str. uberis (Kitt and Leigh, 1997) and that in vitro growth in milk has a lag phase up to seven hours (Kliem and Hillerton, 2002), the timing of introduction of these bacteria may affect the establishment of infection and subsequent disease. This has been examined by experimental infection of an infectious dose of Str.…”

mentioning

confidence: 99%

Timing of entry of Streptococcus uberis into the mammary gland of the dairy cow

Hillerton¹

2020

Journal of Dairy Research

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Streptococcus uberis do not colonise the teat canal and appear to invade the mammary gland of the dairy cow by direct entry though the canal. When they enter the mammary gland, and the early resulting processes, are unclear. Experimental infusions of the lactating mammary gland have been made to determine outcomes of infection, mastitis and disease. Infusion of 500 cfu bacteria was made immediately after milking (8 and 16 h intermilking interval) and 1, 4 or 12 h prior to milking. A mastitis resulted from all infusions, probably in response to the skim milk carrier. Infusions post milking resulted in clinical mastitis in more than half of the quarters, whereas infusion 1 h premilking created no clinical mastitis. Infusion 4 or 12 h pre milking resulted in the most severe reactions, with all quarters developing moderate to severe clinical mastitis. This was more rapid with the 4 h pre milking group. The results demonstrate that the initial inflammatory response caused by an invasion of the mammary gland is not necessarily protective against establishment of a pathogen, and that especially the response to invasion in the intermilking interval is often insufficient to prevent infection and/or disease.

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The Auxotrophic Nature of Streptococcus uberis

Cited by 23 publications

References 6 publications

Mastitomics, the integrated omics of bovine milk in an experimental model of Streptococcus uberis mastitis: 1. High abundance proteins, acute phase proteins and peptidomics

Mastitomics, the integrated omics of bovine milk in an experimental model of Streptococcus uberis mastitis: 1. High abundance proteins, acute phase proteins and peptidomics

Distribution of virulence-associated genes in Streptococcus uberis isolated from bovine mastitis

Timing of entry of Streptococcus uberis into the mammary gland of the dairy cow

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