The Activation of Bovine Plasminogen by PauA Is Not Required for Virulence of Streptococcus uberis

Abstract

A mutant of Streptococcus uberis carrying a single copy of ISS1 within pauA was unable to activate bovine plasminogen. Contrary to a hypothesis postulated previously, this mutation did not alter the ability of the bacterium to grow in milk or to infect the lactating bovine mammary gland

Vru (Sub0144) controls expression of proven and putative virulence determinants and alters the ability of Streptococcus uberis to cause disease in dairy cattle

“…The sequences downregulated in the absence of Vru responsible for production of capsule, hasA and hasB1 (Ward et al , 2001), plasminogen activator, pauA (Leigh, 1994; Rosey et al , 1999), lactoferrin-binding protein, lbp , and collagen-like protein, Sub1095 (Ward et al , 2009), have been subject to previous investigation to determine their individual roles in virulence (Field et al , 2003; Leigh et al , 2010; Ward et al , 2003). While Lbp and the collagen-like protein have been shown to be required for the full expression of the virulent phenotype of S. uberis (Leigh et al , 2010), the absence of PauA or capsule alone was not deemed to affect virulence in lactating cattle (Field et al , 2003; Ward et al , 2003).…”

“…While Lbp and the collagen-like protein have been shown to be required for the full expression of the virulent phenotype of S. uberis (Leigh et al , 2010), the absence of PauA or capsule alone was not deemed to affect virulence in lactating cattle (Field et al , 2003; Ward et al , 2003). …”

“…Whilst attractive as virulence determinants, neither has been shown independently to alter the virulence of S. uberis (Field et al , 2003; Ward et al , 2003), implying that either these proteins do not have a function in pathogenesis or that they exert any effect in a highly redundant manner alongside other molecules.…”

“…Parallel evolution and/or acquisition and retention of such CDSs imply the utility of the activity, a view that is further reinforced by the apparent lack of variation within a selection of PauA sequences analysed (Ward & Leigh, 2004). However disabling mutations of PauA in S. uberis have no effect on virulence in lactating dairy cattle, indicating that any role for this activity is not linked to virulence within the lactating bovine mammary gland (Ward et al , 2003). Again, the presence of PauA (or PauB) is not ubiquitous in S. uberis , although it appears to be present in more than 90 % of the isolates investigated (Ward & Leigh, 2002), a greater proportion than have acquired (and retained) the hasAB1 gene cluster.…”

“…The sub0145 , sub0826 , sub0888 and sub1095 mutants were isolated following PCR screening of an S. uberis 0140J/pGh9: ISS1 mutant bank, as previously described (Egan et al , 2010; Leigh et al , 2010; Ward et al , 2001). The vru mutant, containing an insertional disruption in the reverse orientation to the CDS, was isolated from the same mutant bank using a phenotypic screening method by identification of zones of clearing on Todd–Hewitt agar containing skimmed milk (1 %, v/v) and bovine plasminogen, as previously described (Ward et al , 2003). Southern analysis and DNA sequencing were used to confirm the nature and location of mutation events (data not shown).…”