Changes in the agr locus affect enteritis caused by methicillin-resistant Staphylococcus aureus.

We studied the characteristics of methicillin (meticillin)-resistant Staphylococcus aureus (MRSA) strains that caused enteritis. In a previous report, we demonstrated that both phenotypic and genotypic changes were associated with MRSA enteritis; and we hypothesized that the accessory gene regulator (agr), which is a global regulator of staphylococcal virulence and upregulates several exoproteins, is the key factor associated with the development of MRSA enteritis. In this study, we examined 12 MRSA isolates associated with enteritis from stool samples and 17 MRSA isolates not associated with enteritis that had the following characteristics: the strains associated with enteritis had the same genotype (genotype A), as detected by pulsed-field gel electrophoresis, or the strains were isolated from stools. The differences between strains that caused enteritis and those that did not cause enteritis strains were examined by quantitative reverse transcription-PCR to assess RNAII, agrA, RNAIII, and tst expression and by sequencing of the agr locus. The levels of expression of agrA, RNAIII, and tst were higher by the MRSA isolates associated with enteritis than by the MRSA isolates not associated with enteritis, whether or not they were of the same genotype. The levels of expression of RNAII by almost all the clinical isolates were similar. Sequencing of the agr locus showed that all MRSA isolates that caused enteritis have agr mutations, whereas the MRSA isolates that did not cause enteritis, with three exceptions, did not. Many of the isolates associated with enteritis had the same mutation, especially at the C-terminal end of agrA. These results suggest a trend in which mutations in the agr locus modify the expression of agrA and RNAIII and the production of toxin, all of which may increase the virulence and influence the occurrence of MRSA enteritis.

Bacterial translocation: not a clinically relevant phenomenon in colorectal cancer.

The aim of this study was to identify the risk factors for bacterial translocation and to determine the clinical significance of bacterial translocation in patients with colorectal cancer. Mesenteric lymph node sampling was performed to identify the presence of bacterial translocation in 75 patients with colorectal cancer undergoing laparotomy. Bacterial translocation was identified in 29 patients (39%), with the most common organism being Escherichia coli (31%). Three factors for bacterial translocation were identified, including a preoperative low peripheral lymphocyte count, metastasis to lymph nodes, and invasion depth (= T3). Stepwise regression analysis, however, selected only = T3 [odds ratio (OR) 4.0, 95% confidence interval (CI) 1.2-13.5]. Altogether, 35% of patients with bacterial translocation developed septic complications, compared with 20% in patients without bacterial translocation. In the multivariate analysis, bacterial translocation was not an independent risk factor for infection, with an OR of 1.8 (95% CI 0.56-5.96). Systemic inflammatory response syndrome developed on the first day in 62% of patients with bacterial translocation, compared with 50% of patients without bacterial translocation. Adjusting for the other factors, bacterial translocation was not a significant risk factor in the occurrence of systemic inflammatory response syndrome after surgery (OR 1.1, 95% CI 0.37-3.29). We concluded that in patients with colorectal cancers bacterial translocation does occur and is increased in patients with deep invasion. However, it appears to be of no clinical significance.