Table 1.
Characterization of the bovine SDSD isolates collected and for control SDSE isolates HSME53 and COI289 and control Streptococcus pyogenes GAP58, GAP90, and GAP447 isolates
| Isolate codea | Host | Samples Origin | Clinical | Hemolysis | Lancefield | S. pyogenes virulence genesb | Adhesin genes | Resistance phenotype | Reference |
|---|---|---|---|---|---|---|---|---|---|
| VSD5 | Bovine | Milk from udder | Subclinical mastitis | α | Group C | sdn sagA | fbpA | TET | Rato et al., (2010, 2011, 2013) |
| VSD9 | Bovine | Milk from udder | Subclinical mastitis | α | Group C | sagA | fbpA | TET | |
| VSD13 | Bovine | Milk from udder | Subclinical mastitis | α | Group C | speC speK speL speM spd1 sagA | fbpA | ERY + TET | |
| VSD21 | Bovine | Milk from udder | Clinical mastitis | α | Group C | sdn sagA | fbpA | ERY + TET + GEN | This study |
| VSD23 | Bovine | Milk from udder | Clinical mastitis | α | Group C | sagA | fbpA | TET, GEN | |
| VSD24 | Bovine | Milk from udder | Clinical mastitis | α | Group C | speC speK spd1 sagA | fbpA | GEN | |
| HSM53 | Human (adult) | Blood | Invasive infection | β | Group G | — | fbpA znuA | n.d. | Rato et al. (2010, 2011, 2013) |
| COI289 | Human (adult) | Pharyng | Non‐Invasive infection | β | Group G | — | fbpA znuA | n.d. | |
| GAP58 | Human (adult) | Blood | Invasive infection | β | Group A | speA speB speF speJ smeZ sagA | n.d. | TET | Pires et al. (2012) |
| GAP90 | Human (child) | Blood | Invasive infection | β | Group A | speC speK speL speM spd1, sagA | n.d. | ERY + TET | |
| GAP447 | Human (adult) | Pharingytis | colonization | β | Group A | speC speK speL speM spd1, sagA | n.d. | TET |
a
VSD5, VSD9, and VSD13 were collected in 2002–2003 and VSD21, VSD23, VSD24 were collected in 2011–2013.
b
speC, speK, speL, speM—encode streptococcal pyrogenic exotoxins; spd1—DNase; sdn—streptodornase (DNase); fbpA—Fibronectin‐binding protein A znuA, high‐affinity zinc uptake system protein precursor).