The normalized signal change at the driving ssVEP frequency was then evaluated by means of an omnibus mixed-model anova, with CS Type (CS+,CS–), Phase (Baseline, Conditioning, Extinction) and Stimulus (Luminance, Chromatic) as the within-subject factors and Tagging Frequency (14 Hz, 15 Hz) as the between-subjects factor. Rating data obtained after each experimental phase were submitted to the same statistical model. A CS Type × Phase interaction was deemed necessary for inferring

a conditioning effect and served as a prerequisite for conducting follow-up anovas. An alpha level of 0.05 (two-tailed) was employed for all analyses. Ratings of hedonic valence and emotional arousal collected after the end of each experimental phase demonstrated clear evidence of fear conditioning. Across reversal

selleck chemicals llc frequencies and stimulus types, participants rated the CS+ as more unpleasant (i.e., EPZ5676 datasheet lower in hedonic valence) than the CS– solely during the acquisition phase [F1,25 = 35.90, P < 0.001,  = 0.59], resulting in a CS Type x Phase interaction [F2,50 = 19.32, P < 0.001,  = 0.44] in the overall model. No differences were observed during the habituation and extinction phases (all F < 2.52, all P > 0.12). In terms of emotional arousal (intensity), main effects of experimental Phase [F(2,48]  = 12.60, P < 0.001,  = 0.34] and of CS Type [F(1,24] = 32.08, P < 0.001,  = 0.57] were qualified by an interaction of CS Type × Phase [F(2,48] = 18.68, P < 0.001,  = 0.44]. This interaction reflected Fossariinae the absence of CS-related arousal effects during habituation (all F < 2.42, all P > 0.13) and extinction (al F < 2.71, all P > 0.10), and greater rated emotional arousal specifically in response to the CS+ during acquisition [F1,25 = 58.50, P < 0.001,  = 0.71]. Importantly, behavioral ratings were not affected by stimulus type.

Both stimuli evoked strong and reliable ssVEPs at the reversal frequency, with a pronounced posterior topographical maximum (see Fig. 3). Focusing on local ssVEP amplitude over a group of occipital sensors, we observed a significant three-way CS Type × Phase × Stimulus [F2,48 = 6.39, P = 0.003,  = 0.21] interaction. As there were no significant effects involving Tagging Frequency (all P > 0.103), this factor was dropped in subsequent analyses. As suggested in Fig. 4, the crucial CS Type × Phase interaction [F2,50 = 9.80, P < 0.001,  = 0.28] was observed for low-spatial-frequency luminance stimuli only (chromatic stimuli, CS Type × Phase F < 1, P > 0.77). We next conducted a series of follow-up anova contrasts on ssVEPs evoked by the low-spatial-frequency luminance Gabor patches in each experimental phase. These analyses confirmed the visual impression conveyed by Fig. 5; a CS+ specific enhancement at posterior sensors was observed during the conditioning [F1,25 = 6.25, P = 0.019,  = 0.

, 2004b). Unexpectedly, data on fibronectin-binding adhesins and invasins of S. lugdunensis are scarce. Binding to fibronectin has previously been

investigated in a small collection of strains, but all of eleven isolates showed only weak binding to fibronectin compared with that of strain Cowan I of S. aureus (Paulsson et al., 1993). S. lugdunensis has been described as being part of several niches of the human skin flora (Bieber & Kahlmeter, 2010). The clinical presentation of S. lugdunensis-caused infections is similar to infections caused by S. aureus. Staphylococcus lugdunensis can cause potentially fatal endocarditis, osteomyelitis, and skin and soft tissue infections (Vandenesch et al., 1993; Pareja et al., 1998; Patel et al., 2000; Hellbacher et al., 2006; Frank et al., 2008). Staphylococcus lugdunensis is thought to be rarely SB431542 datasheet isolated; nevertheless, the low prevalence of S. lugdunensis in skin infection has recently been questioned (Bocher et al., 2009). We therefore sought to analyze the invasion of epithelial and endothelial cells (human urinary bladder carcinoma cell line 5637 and the endothelial cell line EA.hy 926) using a previously described fluorescence-activated cell-sorting (FACS)-based invasion assay. We correlated these results

with the binding of clinical isolates of S. lugdunensis to fibronectin. The bacteria used were S. aureus Cowan I, Staphylococcus carnosus TM 300 and eight clinical isolates of S. lugdunensis: Stlu 12, Stlu 30, Stlu 33, Stlu 35, Stlu 36, Stlu 39, Stlu 50, and Stlu 108 and the isogenic knockout mutant GKT137831 cell line Stlu 108Δfbl::ermB (Table 1).

All S. lugdunensis isolates used in this study were confirmed by two reference methods: S. lugdunensis specific tanA and fbl PCRs and by MALDI-TOF MS, as described previously (Noguchi et al., 2009; Szabados et al., 2010; Szabados et al., 2011). Human urinary bladder carcinoma cell line 5637 (DSMZ, Braunschweig, Germany) and endothelial cell line EA.hy 926 (DMSZ) were used throughout this study. Bacteria were grown until the mid-logarithmic phase, as described previously (Szabados et al., 2008). The mutagenesis construct for the homologous recombination cloned into pBT2, and named pMB2503, has previously been described (Marlinghaus Cyclooxygenase (COX) et al., 2011). The homologous recombination of the fbl gene in strain Stlu 108 was also performed as previously described (Marlinghaus et al., 2011). The Δ fbl knockout mutant was confirmed by sequencing (data not shown). Human urinary bladder carcinoma cell line 5637 was cultured in RPMI 1640 with phenol red (PAA, Pasching, Austria). The endothelial cell line EA.hy 926 was cultured in HAT medium (Invitrogen) with addition of HAT medium supplement (hypoxanthine, aminopterin, and thymidine). Both media were also supplemented with 10% heat-inactivated fetal calf serum (PAA) and 1 g L−1 pyruvate (Invitrogen) and 1.5 g L−1 glucose (Invitrogen).

coli strains (Michel et al., 2007). Group II introns in bacteria are usually found only in mobile elements such as transposons (Martinez-Abarca & Toro, 2000). The sequence downstream of aidA reveals the 3′-end of another ORF. The 415-nucleotide sequence is 97% identical to the sequence of a putative large inner membrane associated with a Tn1-transposon. It is therefore highly likely that the aah-aida operon is located within a mobile genetic element. In order to map the beginning of the transcript starting upstream Apoptosis inhibitor of aah, we performed an RT-PCR

on RNA extracted from a culture of 2787 at an OD600 nm of 2.0 using forward primers hybridizing 43, 63, 194 or 247 nucleotides upstream of the aah start codon and a reverse primer hybridizing 140 nucleotides downstream of the start codon. The amplification was successful with the first two forward primers and failed with the last two (data not shown). Controls performed without reverse transcription ensured that there was no DNA contamination in our reactions. This result suggested Selleckchem Akt inhibitor that a transcription start lies between 63 and 194 nucleotides upstream of aah. We then performed 5′ RACE reactions using mRNA extracted from cultures of 2787 at an OD600 nm of 0.7 (mid-log phase) or 2.0 (early-stationary phase). Using aah-specific primers, we obtained one major fragment with both mRNA preparations.

When we performed 5′ RACE reactions with aidA-specific primers, we did not obtain any amplification fragment. ADP ribosylation factor These results suggest that the aah-aidA operon is transcribed as a bicistronic mRNA. The sequences of the fragments amplified with the aah primers were identical and revealed a transcription start 149 nucleotides upstream of the aah start codon (Fig. 1, P149). Analysis of the sequence upstream of this transcription start revealed a putative −10 sequence with the sequence ACTATATTAA, but no −35 sequence. The ACTATATTAA sequence matches the RpoS-specific −10 consensus sequence, and RpoS-controlled promoters are known to have no −35 consensus sequence (Weber et al., 2005). Our results therefore

suggest that the P149 promoter is RpoS dependent. Examination of the sequence chromatograms showed another putative, but weaker transcription start 128 nucleotides upstream of the aah start codon (Fig. 1, P128). Analysis of the sequence upstream of this transcription start revealed putative −10 and −35 sequences. These sequences weakly matched the consensus of RpoD-controlled promoters and are only 15 nucleotides apart. The promoter is therefore expected to be weak, which could explain why the transcript resulting from P128 appeared to be weaker than the one resulting from P149. A number of RpoS-controlled genes are also transcribed by RpoD through overlapping promoter sequences (Bordes et al., 2000). Our work suggests that this is also the case for the aah-aidA operon.

3). The spores have smooth surfaces and the selleck chemical chains are spiral in shape. A blast search with partial 16S rRNA gene sequences (∼1252 bp) of BE74 showed similarity (93–99%) to members of the genus Nocardiopsis in the Nocardiopsaceae family. In a phylogenetic tree based on the neighbor-joining

algorithm, BE74 is clustered with all Nocardiopsis typing species (Tamura et al., 2008). The closest strain to BE74 is N. alba DSM 43377 (99% identity). The two formed a clade that was strongly supported by a high bootstrap value (100%). The N. alba strain BE74 was susceptible to rifamycin (∼2 μg mL−1) on AIA. It was isolated from bee guts in all four seasons. However, we can only ascertain that 23% of the sampled bees (N=40) at this location in the winter carried the N. alba strain. The isolate produced medium levels of antagonism (clearing zones ∼3–7 mm) against the B. marisflavi strain. It showed no activities against other organisms in Table 1 except B. cereus. Nocardiopsis species have been isolated from marine sediments (Engelhardt et al., 2010). Antibiotic biosynthetic genes were searched in a draft of the genome of Nocardiopsis dassonvillei DSM 43111 (Wu et al., 2009). One gene cluster proposed for an involvement in

phenazine biosynthesis has been identified in this organism (Mentel et al., 2009). Phenazines are a family of nitrogen-containing tricyclic pigments produced by rhizosphere bacteria including Pseudomonas and Streptomyces Tanespimycin purchase (Pierson & Pierson, 2010). Interestingly, it has been shown that some secreted phenazines of Pseudomonas aeruginosa can promote the anaerobic survival of the producer itself via extracellular electron transfer (Wang et al., 2010). Therefore, we were interested in whether N. alba from the honeybee gut has the phenazine biosynthetic genes and whether they are expressed. The phenazine biosynthetic pathway

is branched from the shikimate pathway in bacteria (Mentel et al., 2009). Five genes, phzB, phzD, phzE, phzF and phzG, are 17-DMAG (Alvespimycin) HCl required for biosynthesis of the core structure, and they are highly conserved in all known phenazine biosynthetic gene clusters. phzF has been used as a genetic marker for analyzing the diversity and evolution of phenazine biosynthetic pathways in many Gram-negative bacteria, most of which are pseudomonads (Mavrodi et al., 2010). The PCR primers for phzF were tested with BE74 genomic DNA but the reactions did not yield products under the suggested conditions. Instead, PCR primers based on the alignments of phzD genes encoding an isochorismatase from Streptomcyes cinnamonensis DSM 1042, Streptomyces anulatus LU9663 and N. dassonvillei DSM 43111 yielded an ∼340-bp fragment with the BE74 DNA. Putative protein sequences encoded by this DNA fragment showed the highest homology to a part of PhzD from N. dassonvillei DSM 43111 and other homologs (similarity ∼70–90%) involved in isochorismate metabolism.

The clinical care of patients with these tumours requires a multidisciplinary approach drawing on the skills and experience of all healthcare professional groups. Moreover, optimal care can only be achieved by the close co-operation of oncologists, haematologists and HIV physicians, and unless all these clinicians are intimately involved in the care of patients it is likely that the outcome will be less favourable. Patients with HIV-associated malignancies should therefore only be managed in a centre dealing with large numbers of patients with these tumours. The minimum number of patients that an HIV

oncology service should manage Apoptosis inhibitor has not been defined. Several studies and a Cochrane review have shown that the more HIV patients treated by a centre, buy R428 the better the outcomes [6–8]. Similarly, Improving outcomes

in haematological cancer published by NICE in 2003 included a systematic review of published evidence suggesting that higher patient volumes are associated with improved outcomes and that outcomes in specialist centres are better. They advocated that all patients with haematological cancer should be managed by a multidisciplinary haemato-oncology team serving a population of at least 500 000 [9]. An audit study in North London confirmed the better management of patients with AIDS-related lymphomas in HIV centres with cohorts of >500 patients [10]. An audit from Canada also showed that clinicians treating larger numbers of patients with AIDS-related lymphoma provided better care [11] and a recent cohort study in the US published in 2013 attributed poorer results in some centres to a lack of access to optimal intergrated cancer and HIV

care [12]. An additional benefit of centralization could be greater uptake of HIV testing amongst patients diagnosed with cancers including lymphomas as advocated in BHIVA testing guidelines [13] and in the US [14]. This remains a concern since UK lymphoma clinicians are often overly reluctant to adopt universal testing [15] and uptake remains low even for AIDS-defining malignancies [16]. In line either with national cancer waiting times, all patients with suspected cancers must be referred urgently and seen within 2 weeks of referral. Moreover, the NHS Cancer Plan sets out the goal that no patient should wait longer than 1 month from an urgent referral with suspected cancer, to the start of treatment [17]. We recommend that all patients with HIV and malignancy should be referred to centres that have developed expertise in the management of these diseases (level of evidence 1B). The multidisciplinary team managing these patients must include HIV physicians, oncologists, haematologists and palliative care physicians along with clinical nurse specialists, specialist HIV pharmacists and specialist chemotherapy pharmacists.

The clinical care of patients with these tumours requires a multidisciplinary approach drawing on the skills and experience of all healthcare professional groups. Moreover, optimal care can only be achieved by the close co-operation of oncologists, haematologists and HIV physicians, and unless all these clinicians are intimately involved in the care of patients it is likely that the outcome will be less favourable. Patients with HIV-associated malignancies should therefore only be managed in a centre dealing with large numbers of patients with these tumours. The minimum number of patients that an HIV

oncology service should manage IDH inhibitor has not been defined. Several studies and a Cochrane review have shown that the more HIV patients treated by a centre, learn more the better the outcomes [6–8]. Similarly, Improving outcomes

in haematological cancer published by NICE in 2003 included a systematic review of published evidence suggesting that higher patient volumes are associated with improved outcomes and that outcomes in specialist centres are better. They advocated that all patients with haematological cancer should be managed by a multidisciplinary haemato-oncology team serving a population of at least 500 000 [9]. An audit study in North London confirmed the better management of patients with AIDS-related lymphomas in HIV centres with cohorts of >500 patients [10]. An audit from Canada also showed that clinicians treating larger numbers of patients with AIDS-related lymphoma provided better care [11] and a recent cohort study in the US published in 2013 attributed poorer results in some centres to a lack of access to optimal intergrated cancer and HIV

care [12]. An additional benefit of centralization could be greater uptake of HIV testing amongst patients diagnosed with cancers including lymphomas as advocated in BHIVA testing guidelines [13] and in the US [14]. This remains a concern since UK lymphoma clinicians are often overly reluctant to adopt universal testing [15] and uptake remains low even for AIDS-defining malignancies [16]. In line Amoxicillin with national cancer waiting times, all patients with suspected cancers must be referred urgently and seen within 2 weeks of referral. Moreover, the NHS Cancer Plan sets out the goal that no patient should wait longer than 1 month from an urgent referral with suspected cancer, to the start of treatment [17]. We recommend that all patients with HIV and malignancy should be referred to centres that have developed expertise in the management of these diseases (level of evidence 1B). The multidisciplinary team managing these patients must include HIV physicians, oncologists, haematologists and palliative care physicians along with clinical nurse specialists, specialist HIV pharmacists and specialist chemotherapy pharmacists.

Selection of clones was performed in E. coli DH5α, Arthrobacter sp. Alectinib 68b and Rhodococcus sp. SQ1

bacteria, which could not utilize 2-hydroxypyridine. E. coli DH5α cells were transformed by ligation mixtures, and kanamycin-resistant clones were grown on NA plates supplemented with IPTG and 2-hydroxypyridine. As the visual inspection of plates did not reveal any coloured colonies, all clones were harvested from agar plates and pooled. The mixture of the recombinant plasmids was isolated and consequently used to transform Arthrobacter sp. 68b and Rhodococcus sp. SQ1 bacteria. A single clone (from ca 4000 clones) was selected on the NA medium supplemented with kanamycin and 2-hydroxypyridine by screening for pigment production. The pHYP1 plasmid containing a 6-kb DNA insert was isolated from the blue pigment producing clone of Rhodococcus sp. SQ1. Sequence analysis of the cloned 6-kb DNA fragment from pHYP1 revealed eight putative ORFs (Fig. 4). Six of them shared the significant (71–87%) sequence homology with hypothetical proteins of the pSI-1 plasmid from Arthrobacter sp. AK-1 (Jerke et al., 2008). Moreover, an identical arrangement of ORFs in both plasmids was observed. The predicted functions of ORFs from pHYP1 are presented in Table 2. New cryptic plasmid, not related to known arthrobacterial

ones, was isolated from A. rhombi PRH1. A conserved sequence found at 45 bp upstream of the repA gene showed remarkable homology to the typical ColE2-type ori (Leret et al., 1998; Yagura et al., 2006). The predicted minimal replication operon of pPRH consisted of repAB genes, which is in accordance with the previous findings that both repA www.selleckchem.com/products/U0126.html and repB are required for replication of pAL5000 (Stolt & Stoker, 1996a), pFAJ2600 (De Mot et al., 1997), pBLA8 (Leret et al., 1998) and pCASE1 (Tsuchida et al., 2009). All these results supported the conclusion that pPRH is a member of the pAL5000 subfamily of ColE2 family (Stolt & Stoker, 1996a), plasmids belonging to the theta replication C

class (Bruand et al., 1993). Usually, repB is located downstream and overlaps with repA of these plasmids, suggesting that both of these genes form an operon. Correspondingly, the start codon of repB in pPRH overlaps with the stop Phosphatidylinositol diacylglycerol-lyase codon of the repA by one nucleotide. A putative rep operon in pPRH may also include ORF4, which overlaps with repB and encodes a hypothetical protein. The function of ORF4 in the plasmid replication and/or maintenance remains unclear. Phylogenetic analysis of RepA and RepB of pPRH showed that they formed a distinct branch on phylogenetic tree suggesting their evident divergence from homologous proteins (Fig. 2a,b). Two putative conserved domains related replicase and primase, respectively, were detected in RepA from pPRH, which is a common structural feature of other RepA proteins associated with theta replication (De Mot et al., 1997; Leret et al., 1998; Sekine et al., 2006; Matsui et al.

The heat shock response in E. coli is positively regulated by σ32, a product of the rpoH, which has been reviewed by Arsene et al. (2000). Several of the genes involved in the heat shock response, including rpoH, groESL, and grpE-dnaKJ, have been characterized in X. campestris (Huang et al., 1998; Weng et al., 2001; Chang et al., 2005). Crosstalk between oxidative stress and heat shock responses has been investigated intensively in the eukaryotic organisms, in which the activity of catalase, a peroxide-degrading enzyme, contributes to protection against heat stress of fungal cells (Noventa-Jordao et al., 1999). Genome-wide analysis in several bacteria

has revealed overlapping and cross-induction of heat shock gene expression by hydrogen peroxide (H2O2) (Stohl et al., 2005; Zeller et al., 2005) and induction of oxidative stress-protective genes by heat stress (Guckenberger et al., 2002; RG7204 molecular weight Gunasekera et al., 2008; Luders et al., 2009). MK-2206 manufacturer These observations indicate the important roles of bacterial heat stress and oxidative stress responses. Xanthomonas campestris

has evolved multiple systems to protect itself from oxidative stress. These well-orchestrated systems require the coordination of several transcriptional regulators, one of which is OxyR, the global regulator of peroxide stress response genes (Mongkolsuk et al., 1998). The known members of the OxyR regulon in X. campestris pv. campestris are katA, katG, and ahpC, encoding KatA monofunctional catalase, KatG catalase–peroxidase, and alkyl hydroperoxide reductase, respectively (Jittawuttipoka et al., 2009). The roles of KatG and KatA in providing protection against H2O2 toxicity in X. campestris pv. campestris have been elucidated. KatG plays a primary role in the Arachidonate 15-lipoxygenase protection

of X. campestris pv. campestris from low levels of H2O2 toxicity, whereas KatA serves a principal function against high concentrations of H2O2 (Jittawuttipoka et al., 2009). Observation in a Gram-positive bacterium Staphylococcus aureus has demonstrated that a catalase-deficient strain is more susceptible to heat injury than its parental wild type (Martin & Chaven, 1987). The current study demonstrates that katG and katA, as well as oxyR, are essential for bacterial survival under heat stress. All X. campestris pv. campestris strains were grown aerobically in Silva–Buddenhagen (SB) medium (0.5% sucrose, 0.5% yeast extract, 0.5% peptone, and 0.1% glutamic acid; pH 7.0) at 28 °C. Overnight cultures were inoculated into a fresh SB medium to yield an OD600 nm of 0.1 . Exponential-phase cells (OD600 nm of 0.5, after 4 h growth) were used in all the experiments. The pBBR1-MCS (Kovach et al., 1995), a medium-copy-number plasmid with the lacZ promoter, was used to complement X.campestris pv. campestris mutant strains. Aliquots of exponential-phase cultures (0.5 mL in each 1.5-mL microcentrifuge tube) were placed in a water bath at 45 °C.

In conclusion, 15/57 strains of O157:non-H7 serotypes isolated from different sources and geographical regions were found

to carry various eae alleles, suggesting that these strains may be fairly prevalent. Many of the O157:H16 strains found, including strains that were isolated from water in the United States and from meat in France, carried the ɛ-eae allele, shared similar PFGE profiles and had ST-171, a common type in the EcMLST database that, until now, had not included any strains from the O157 serogroup. Clonal analysis also showed that none of these eae-positive O157:non-H7 strains were closely related to the pathogenic O157:H7 serotype and that there is a large genetic diversity within the O157 serogroup. The authors would like to dedicate this work to the memory selleck of Dr Thomas S. Whittam. “
“The potential for microbial fuel cells to act as an alternative, pollution-neutral energy source has generated a major PARP inhibitor cancer increase in the number of publications on this subject. Fundamental to the functioning of a microbial fuel cell, and the efficient transfer of electrons to an associated electrical network, is the formation of specialized biofilms on an electrode surface. Microarray studies

of these biofilms have important considerations that are also fundamental for biofilm gene expression studies in general. Cells in a biofilm exist in a range of different physiological states, but global analysis generalizes transcription across the entire biofilm population. This leads to the common pitfall of a complex system being overly simplified. Bacteria stiripentol are commonly found in the environment as part of surface-associated communities known as biofilms. Through the formation of a biofilm, bacteria gain many advantages, such as an increased resistance to desiccation, resistance to antibiotics, defence against grazing, and increased metabolic function, among others. Biofilms are studied extensively due to their importance in environmental, industrial, and medical processes. They are highly hydrated structures containing cells encased in an extracellular matrix of proteins, DNA, enzymes, and

extracellular polymeric substances. Many bacterial biofilms consist of structured clumps of cells surrounded by channels void of cellular material, in which nutrients and waste can be exchanged, resulting in a diverse range of microenvironments. For example, electrical-producing biofilms in a microbial fuel cell can be >50 μm thick, have been shown to contain proton gradients, and are suspected to contain electrical potential and nutrient gradients. Transcriptional profiling has become the tool of choice for microbiologists to examine changes in gene expression. Microarrays are powerful tools that allow for the examination of genome-wide changes in gene expression in either isogenic mutant strains or different environmental conditions.

To determine if these isolates showed the she PAI associated with the set1 gene, the presence of other genes contained in this PAI, the pic, sigA and sap genes, was studied. Only two isolates carried the three genes indicating the presence of the whole island, 22 showed the pic and sap genes and eight only the pic gene. This indicates the high variability Raf targets in the structure of this PAI. In contrast to the ShET-1 toxin, the ShET-2 toxin encoded by the sen gene was more frequent among isolates collected from patients who had taken quinolones before isolation of the bacteria. This toxin was significantly more frequent among nalidixic

acid-resistant isolates (15% vs. 6%, P=0.046), and 35% of ShET2-positive Navitoclax order isolates belonged to phylogenetic group B1 (P=0.0001). The EAST-1 toxin was more frequently found in the E. coli isolates collected from patients with septic shock (19% vs.

8%, P=0.07). No B2 isolates had this toxin; it was more frequently found among isolates belonging to the A, B1 and D phylogenetic groups (P=0.02). Finally, the AggR transcriptional factor encoded by the aggR gene was more frequently found among isolates collected from patients with chronic renal insufficiency (37.8% vs. 12%, P=0.03) and from patients with pneumonia (33% vs. 12%, P=0.09). The presence of this transcriptional factor was not associated with any phylogenetic group, and it was more frequently found among isolates forming biofilm (18% vs. 9%, P=0.08) (Table 1). The presence of genes encoding enterotoxins and a transcriptional factor involved in virulence were analysed in E. coli isolates collected from patients with bacteraemia. The ShET-1 toxin has been described in S. flexneri 2a and has also been detected in other bacterial taxa such as Y. enterocolitica, S. typhimurium and E. coli (Al-Hasani et al., 2001). This toxin has been found in EAEC causing diarrhoea (Mohamed et al., 2007; Mendez-Arancibia et al.,

2008). In both of these studies, an association was observed between the presence of the set1 gene and biofilm production. Thus, 43% of biofilm producers presented this gene in contrast to 6% of nonbiofilm producers (P=0.0004). These results are in agreement with those obtained in the present study. This ability to form biofilm is a trait that is closely associated with bacterial persistence and virulence, and many persistent Urease and chronic bacterial infections are now believed to be linked to the formation of biofilm (Mohamed et al., 2007). There seems to be a relationship between the presence of the set1 gene and nalidixic acid susceptibility. In fact, set1 was more frequent among nalidixic acid-susceptible isolates. A possible explanation for this phenomenon may be that this gene is contained in the she PAI. This PAI is a chromosomal, laterally acquired, integrative element of S. flexnerii that carries genes with established or putative roles in virulence (Mohamed et al., 2007).