## 3 Results
\begin{table}
\begin{tabular}{c c c c c c c c c c} \hline \hline \multirow{3}{*}{**Antimicrobial Agents**} & \multirow{3}{*}{**Strain no 1**} & \multirow{3}{*}{**Strain no 2**} & \multirow{3}{*}{**Strain no 3**} & \multirow{3}{*}{**Strain no 4**} & \multirow{3}{*}{**Strain no 5**} & \multirow{3}{*}{**Strain no 6**} & \multirow{3}{*}{**Strain no 7**} & \multirow{3}{*}{**Strain no 8**} & \multirow{3}{*}{**Strain no 9**} \\  & & & & & & & & & \\ \cline{1-1} \cline{6-11}  & & & & & & & & & & \\ \hline \multicolumn{11}{c}{**Mechanism of action: Inhibition of cell wall synthesis ***} \\ \hline
**AMP a** & R - & R & R & R & R & R & R & R \\ \hline
**CEP** & S & S & I & S & I & R & I & R & S \\ \hline
**CEF** & R & S & S & S & S & S & S & S & S \\ \hline \multicolumn{11}{c}{**Mechanism of action: Binding at the 30s ribosomal subunit**} \\ \hline
**AM** & S & S & R & S & R & S & S & S & S \\ \hline
**TET** & R & R & R & R & R & R & S & R & S \\ \hline
**GEN** & I & I & I & S & I & I & S & S & I \\ \hline \multicolumn{11}{c}{**Mechanism of action: Binding at the 50s ribosomal subunit of the 70s ribosome**} \\ \hline
**CHL** & R & S & S & S & S & S & S & I \\ \hline
**STR** & R & I & R & R & R & S & I & S & R \\ \hline \multicolumn{11}{c}{**Mechanism of action: Inhibition of the tetrahydrorofilic acid synthesis**} \\ \hline
**TRI/SU** & S & S & S & S & S & S & S & S & S \\ \hline
**SUL** & S & S & S & S & S & S & S & S \\ \hline \multicolumn{11}{c}{**Mechanism of action: Inhibition of DNA gyrase**} \\ \hline
**NAL** & S & R & S & S & S & R & S & R & S \\ \hline
**CIP** & S & I & R & S & R & I & S & R & S \\ \hline \multicolumn{11}{c}{**Number of classes in which the strains were found resistant**} \\ \hline
3 & 3 & 4 & 3 & 4 & 3 & 1 & 3 & 2 \\ \hline \hline \end{tabular}  
* (-) or (+) for _E. coli_ O157:H7 sorbit (-) or _E. coli_ O157:H7 sorbit (+), respectively; \(\therefore\) for resistant, I for intermediate resistant, and S for susceptible; **: classes of antibiotics against which the _E. coli_ O157:H7 strains were found resistant. Resistance in more than two classes classifies a strain as multi-resistant (MDR). *: Ampicillin (AMP), Amikacin (AM), Tetracycline (TET), Chloramphenicol (CHL), Gentamicin (GEN), Streptomycin (STR), Trimethoprim/Sulfamethoxazole (TRI/SU), Nalidivic acid (NAL), Cephalothin (CEP), Cefotaxime (CEF), Sulfathiazole (SUF), and Ciprofloxacin (CIP).  
\end{table} 
Table 6: Resistance to antimicrobial agents classified by mode of action of the _E. coli_ O157:H7 strains isolated from the different experimental groups. \begin{table}
\begin{tabular}{c c c c c c} \hline \hline
**Group** & \(-\)* & \(+\)** & \(++\) & \(++\) & \(Total\) \\ \hline
**B1*** & 14 & 2 & 4 & 10 & 30 \\ \hline
**C1** & 2 & 1 & 2 & 5 & 10 \\ \hline
**B2** & 8 & 2 & 1 & 2 & 13 \\ \hline
**C2** & 3 & - & 3 & 3 & 3 & 9 \\ \hline
**B3** & 9 & 1 & 4 & 2 & 16 \\ \hline
**C3** & 8 & - & 1 & 5 & 14 \\ \hline
**Total** & 44 & 6 & 15 & 27 & 92 \\ \hline \hline \end{tabular}  
*: (-) not recorded biofilm activity; ** (weak, +), (moderate, ++), and (strong, ++) recorded biofilm activity of increased intensity; **: Experimental group. The interpretation of sampled groups, including the sources of milk samples, is presented in Figure 1.  
\end{table} 
Table 7: Biofilm activity of the isolated _E. coli_ strains in the different experimental groups. _E. coli_ strains involved in mastitisti's acquired resistant features and became MDR (OR = 3.50, CI 95% 1.44-8.55, \(p\) = 0.0058). Table 8 shows the number of non-O157:H7 _E. coli_ strains, isolated from the different groups, representing many potentially pathogenic serotypes. For instance, all the so-called \"big six\" were present in the B groups and remained present--although with reduced prevalence--in the C groups. Mastitis significantly increased the prevalence of the \"O\" serotype strains (OR = 8.43, CI 95% 2.95-24.87, \(p\) < 0.0001) with respect to the controls.