“…Resistance to carbapenems in B. fragilis is usually caused by the expression of the class B metallo-betalactamase encoded by the c A gene, located on the chromosome. Accordingly, if an insertion sequence is located in its upstream region, it will be expressed and will cause carbapenem resistance (4,34). In a study conducted by Soki et al, B. fragilis isolates (n = 10) contained the c A gene, of which seven isolates were resistant to imipenem (35).…”
Section: Discussionmentioning
confidence: 99%
“…Among various species of this genus, Bacteroides fragilis (B. fragilis) has been also introduced as the most abundant opportunistic anaerobic bacterium isolated from clinical specimens (3). The bacteria form 1-2% of the normal ora of the gastrointestinal tract and, if dislocated into other anatomical sites, develop various infections such as abdominal infections, abscesses, and bacteremia with a mortality rate of about 19% (1,4).…”
Background: Bacteroides fragilis is a part of the normal gastrointestinal flora and the most prevalent anaerobic bacteria causes’ infection. It is highly resistant to antibiotics and contains abundant antibiotic resistance mechanisms. Methods: The antibiotic resistance pattern of 78 isolates of B. fragilis (56 strains from the gastrointestinal [GI] tract and 22 strains from clinical samples) was investigated using agar dilution method. The gene encoding Bacteroides fargilis toxin bft, and antibiotic resistance genes were targeted by PCR assay. Results: The highest rate of resistance was observed for penicillin G (100%) followed by tetracycline (74.4%), clindamycin (41%) and cefoxitin (38.5%). Only a single isolate showed resistance to imipenem which contained cfiA and IS1186 genes. All isolates were susceptible to metronidazole. Accordingly, tetQ (87.2%), cepA (73.1%) and ermF (64.1%) were the most abundant antibiotic-resistant genes identified in this study. MIC values for penicillin, cefoxitin and clindamycin were significantly different among isolates with the cepA, cfxA and ermF in compare with those lacking such genes. In addition, 22.7% and 17.8% of clinical and GI tract isolates had the bft gene, respectively. Conclusions: Therefore, it is of utmost importance to determine the antibiotic resistance patterns of B. fragilis periodically in different geographical areas to provide a suitable treatment profile for patients and to prevent improper antibiotic prescriptions.
“…Resistance to carbapenems in B. fragilis is usually caused by the expression of the class B metallo-betalactamase encoded by the c A gene, located on the chromosome. Accordingly, if an insertion sequence is located in its upstream region, it will be expressed and will cause carbapenem resistance (4,34). In a study conducted by Soki et al, B. fragilis isolates (n = 10) contained the c A gene, of which seven isolates were resistant to imipenem (35).…”
Section: Discussionmentioning
confidence: 99%
“…Among various species of this genus, Bacteroides fragilis (B. fragilis) has been also introduced as the most abundant opportunistic anaerobic bacterium isolated from clinical specimens (3). The bacteria form 1-2% of the normal ora of the gastrointestinal tract and, if dislocated into other anatomical sites, develop various infections such as abdominal infections, abscesses, and bacteremia with a mortality rate of about 19% (1,4).…”
Background: Bacteroides fragilis is a part of the normal gastrointestinal flora and the most prevalent anaerobic bacteria causes’ infection. It is highly resistant to antibiotics and contains abundant antibiotic resistance mechanisms. Methods: The antibiotic resistance pattern of 78 isolates of B. fragilis (56 strains from the gastrointestinal [GI] tract and 22 strains from clinical samples) was investigated using agar dilution method. The gene encoding Bacteroides fargilis toxin bft, and antibiotic resistance genes were targeted by PCR assay. Results: The highest rate of resistance was observed for penicillin G (100%) followed by tetracycline (74.4%), clindamycin (41%) and cefoxitin (38.5%). Only a single isolate showed resistance to imipenem which contained cfiA and IS1186 genes. All isolates were susceptible to metronidazole. Accordingly, tetQ (87.2%), cepA (73.1%) and ermF (64.1%) were the most abundant antibiotic-resistant genes identified in this study. MIC values for penicillin, cefoxitin and clindamycin were significantly different among isolates with the cepA, cfxA and ermF in compare with those lacking such genes. In addition, 22.7% and 17.8% of clinical and GI tract isolates had the bft gene, respectively. Conclusions: Therefore, it is of utmost importance to determine the antibiotic resistance patterns of B. fragilis periodically in different geographical areas to provide a suitable treatment profile for patients and to prevent improper antibiotic prescriptions.
“…The resistance to carbapenems is mediated by cfiA gene which codes a metallo β-lactamase. The presence of IS elements in the upstream of the cfiA gene is required for its expression [16,25]. The most common mechanism of B. fragilis resistance to metronidazole is the expression of nitroreductases (nim genes dependent mechanism), which reduces the nitroimidazoles drug's nitro group to an inactive amino group [24].…”
Section: Discussionmentioning
confidence: 99%
“…Therapeutic considerations for anaerobes are broadening as more species are identified to play active role in human infections. This is compounded by emergence of antibiotic resistant strains that have made treatment more difficult [16][17][18]. Adding to this dilemma is the relative lack of rapid and cost effective methods for routine AST for anaerobes.…”
The propensity to develop resistance to antibiotics has accounted for the predominance of Bacteroides and Prevotella in infections due to anaerobic bacteria. The observed differences in resistance pattern across geographical boundaries underscored the timeliness for this study to review data on antibiotic susceptibility and resistance markers amongst Bacteroides and Prevotella to β-lactams, lincosamide and nitroimidazole from selected hospitals in Lagos, Nigeria from 1992-2011. Bacteroides, mostly B. fragilis were the sole anaerobic gram negative bacilli in peritonitis following lower abdominal surgery and bloodstream infections, while Prevotella bivia and P. melaninogenica were more frequent in periodontal abscess, pelvic inflammatory disease and chronic suppurative otitis media. The MIC range and MIC90 of the anaerobes for the antibiotics does not indicate changes in group resistance to antibiotics though isolated cases were recorded. While clear cut patterns were not established for other species, B. fragilis resistance increased for amoxicillin-clavulanic acid from 18.2% in 1992-1996 to 31.4% in 2006-2011 and from 27.3% in 1992-1996 to 34.3% in 2006-2011 for cefoxitin. In contrast, decrease susceptibility was obtained against clindamycin (54.5% in 1992-1996 to 22.9% in 2006-2011). Similarly, 22.7% of B. fragilis strains have the cepA and/or cfxA gene in 1992-1996 compared to 32.1% in 2006-2011. While not all isolates with cepA and/or cfxA genes were resistant to the β-lactams, all isolates carrying the ermF or nim genes were resistant to the lincosamide (clindamycin) or nitroimidazole (metronidazole) respectively. The presence of antibiotics resistance genes can be used in tracking resistance amongst species of Bacteroides and Prevotella. With emerging new technologies, gene screening may prove more effective and reliable for therapeutic decisions for anaerobic bacterial infections especially since the genes can be screened from the infective exudates. This will eliminate the need for culture and antibiotic susceptibility testing for this group of fastidious microorganisms.
“…Also, BFT induces the production of reactive oxygen species (ROS), DNA damage, and gut epithelial cell proliferation via the induction of spermine oxidase (SMO) and cellular inhibitor of apoptosis protein-2 (c-IAP2). 43 Figure 4 The six mechanisms involved in colon carcinogenesis by Bacteroides fragilis toxin (BFT). Colon carcinogenesis due to BFT is mediated by the induction of T-cell factor- dependent β-catenin pathway (TSF- β-catenin), cleavage of E-Cadherin, stimulation of IL-8 productionleading to the persistent proliferation of gut epithelial cells.…”
Section: Common Git Cancers Associated With Bacterial Infectionmentioning
Despite the wide medical knowledge about the direct role of many viruses in the pathogenesis of certain cancers, there is still ambiguity and hazy vision about the direct role of bacteria in cancer incidence. Understanding the role of bacteria in carcinogenesis is no longer a scientific luxury, but it has become an urgent and extremely important necessity to realize the pathogenesis of cancer caused by oncogenic bacteria as an attempt to overcome the oncogenic mechanisms exhibited by these oncogenic bacteria. This review shed the light on the indirect role of the host’s inflammatory and immunological responses in the pathogenesis of bacteria-induced cancer. Also, this review discussed the indirect role of the bacterial toxins and virulence factors in the induction of common gastrointestinal cancers, such as gallbladder cancer (GBC), colorectal cancer (CRC), and gastric cancer (GC). Finally, this review dealt with the debate about the possibility of bacterial DNA integration into the human genome and cancer incidence.
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