Background: The extensive misuse of antibiotics has increased cross-resistance to macrolide–lincosamide–streptogramin B (MLSB) antibiotics among Staphylococci. Objectives: The study aimed to investigate the distribution of MLSB resistance phenotypes and their encoding genes among Staphylococci isolated from the Intensive Care Units of Assiut University Hospitals. Methodology: A total of 243 nosocomial staphylococcal isolates were collected. MLSB phenotypes were assessed by double disc diffusion method (D test) and the encoding genes (ermA, ermB, ermC, msrA, mphC and lnuA) were detected by PCR. Results: Of all isolates, 93.8% were resistant to erythromycin. MLSB resistance phenotypes detected were the constitutive phenotype (cMLSB) (56.8%), macrolide/macrolide–streptogramin B resistance (M/MSB) (24.7%) and the inducible resistance (iMLSB) (12.3%). The most prevalent MLSB resistance genes were ermC in the cMLSB, msrA in the M/MSB and ermC and msrA in the iMLSB phenotype isolates. The most common gene combinations were either the msrA with erm genes or with both erm and mphC genes. Most of the strains harboring these combinations were of the cMLSB phenotype. The coexistence of the 4 gene groups was detected in 3.8% of the isolates; all of them were of the constitutive phenotype. Conclusion: A high percentage of erythromycin resistance and an alarming percentage of iMLSB phenotype were detected among our isolates. Routine D- test is mandatory to discover the inducible phenotype prone to acquire clindamycin resistance especially in patients with life threatening infections.

Background: The extensive misuse of antibiotics has increased cross-resistance to macrolide–lincosamide–streptogramin B (MLSB) antibiotics among Staphylococci. Objectives: The study aimed to investigate the distribution of MLSB resistance phenotypes and their encoding genes among Staphylococci isolated from the Intensive Care Units of Assiut University Hospitals. Methodology: A total of 243 nosocomial staphylococcal isolates were collected. MLSB phenotypes were assessed by double disc diffusion method (D test) and the encoding genes (ermA, ermB, ermC, msrA, mphC and lnuA) were detected by PCR. Results: Of all isolates, 93.8% were resistant to erythromycin. MLSB resistance phenotypes detected were the constitutive phenotype (cMLSB) (56.8%), macrolide/macrolide–streptogramin B resistance (M/MSB) (24.7%) and the inducible resistance (iMLSB) (12.3%). The most prevalent MLSB resistance genes were ermC in the cMLSB, msrA in the M/MSB and ermC and msrA in the iMLSB phenotype isolates. The most common gene combinations were either the msrA with erm genes or with both erm and mphC genes. Most of the strains harboring these combinations were of the cMLSB phenotype. The coexistence of the 4 gene groups was detected in 3.8% of the isolates; all of them were of the constitutive phenotype. Conclusion: A high percentage of erythromycin resistance and an alarming percentage of iMLSB phenotype were detected among our isolates. Routine D- test is mandatory to discover the inducible phenotype prone to acquire clindamycin resistance especially in patients with life threatening infections.

Background: The extensive misuse of antibiotics has increased cross-resistance to macrolide–lincosamide–streptogramin B (MLSB) antibiotics among Staphylococci. Objectives: The study aimed to investigate the distribution of MLSB resistance phenotypes and their encoding genes among Staphylococci isolated from the Intensive Care Units of Assiut University Hospitals. Methodology: A total of 243 nosocomial staphylococcal isolates were collected. MLSB phenotypes were assessed by double disc diffusion method (D test) and the encoding genes (ermA, ermB, ermC, msrA, mphC and lnuA) were detected by PCR. Results: Of all isolates, 93.8% were resistant to erythromycin. MLSB resistance phenotypes detected were the constitutive phenotype (cMLSB) (56.8%), macrolide/macrolide–streptogramin B resistance (M/MSB) (24.7%) and the inducible resistance (iMLSB) (12.3%). The most prevalent MLSB resistance genes were ermC in the cMLSB, msrA in the M/MSB and ermC and msrA in the iMLSB phenotype isolates. The most common gene combinations were either the msrA with erm genes or with both erm and mphC genes. Most of the strains harboring these combinations were of the cMLSB phenotype. The coexistence of the 4 gene groups was detected in 3.8% of the isolates; all of them were of the constitutive phenotype. Conclusion: A high percentage of erythromycin resistance and an alarming percentage of iMLSB phenotype were detected among our isolates. Routine D- test is mandatory to discover the inducible phenotype prone to acquire clindamycin resistance especially in patients with life threatening infections.

Background: The extensive misuse of antibiotics has increased cross-resistance to macrolide–lincosamide–streptogramin B (MLSB) antibiotics among Staphylococci. Objectives: The study aimed to investigate the distribution of MLSB resistance phenotypes and their encoding genes among Staphylococci isolated from the Intensive Care Units of Assiut University Hospitals. Methodology: A total of 243 nosocomial staphylococcal isolates were collected. MLSB phenotypes were assessed by double disc diffusion method (D test) and the encoding genes (ermA, ermB, ermC, msrA, mphC and lnuA) were detected by PCR. Results: Of all isolates, 93.8% were resistant to erythromycin. MLSB resistance phenotypes detected were the constitutive phenotype (cMLSB) (56.8%), macrolide/macrolide–streptogramin B resistance (M/MSB) (24.7%) and the inducible resistance (iMLSB) (12.3%). The most prevalent MLSB resistance genes were ermC in the cMLSB, msrA in the M/MSB and ermC and msrA in the iMLSB phenotype isolates. The most common gene combinations were either the msrA with erm genes or with both erm and mphC genes. Most of the strains harboring these combinations were of the cMLSB phenotype. The coexistence of the 4 gene groups was detected in 3.8% of the isolates; all of them were of the constitutive phenotype. Conclusion: A high percentage of erythromycin resistance and an alarming percentage of iMLSB phenotype were detected among our isolates. Routine D- test is mandatory to discover the inducible phenotype prone to acquire clindamycin resistance especially in patients with life threatening infections.

Background: An increasing pattern of fluoroquinolone resistance (FQR) among bacterial pathogens has been described worldwide. In this study, we compared the patterns of genetic mechanisms that confer FQR for Escherichia coli and Klebsiella pneumoniae isolated from the Assiut University Hospitals in Egypt. Methods: Eighty-seven clinical E. coli and K. pneumoniae isolates were tested for mutations in gyrA, gyrB, parC, and parE genes by polymerase chain reaction (PCR) amplification and DNA sequencing. The presence of plasmid-mediated quinolone resistance (PMQR) genes qnrA, qnrB, qnrS, aac(6¢)-Ib, qepA was screened by PCR and characterized by conjugation. Correlations between different FQR mechanisms and ciprofloxacin minimal inhibitory concentration (MIC) levels were determined. Results: A higher number of quinolone resistance-determining region (QRDR) mutations was detected in E. coli, while the number of PMQR determinants was significantly higher in K. pneumoniae. However, K. pneumoniae showed stronger correlations than E. coli between MIC levels and number of mutations in the QRDR per isolate (rs = 0.8, p 0.0001 and rs = 0.7, p 0.0001, respectively) as well as between MIC levels and number of plasmids (rs = 0.4, p = 0.005 and rs = 0.3, p = 0.02, respectively). Conclusions: Although we observed a prevalence of chromosomal mutations for E. coli and the presence of plasmid-encoded genes for K. pneumoniae that resulted in FQR phenotype, high levels of FQR appeared to occur as a result of gradual accumulation of mutations in QRDR for both bacteria. To our best of knowledge, this is the first study to report and compare the correlation between FQ MIC levels and different genetic mechanisms for FQR in Enterobacteriaceae.

Background: An increasing pattern of fluoroquinolone resistance (FQR) among bacterial pathogens has been described worldwide. In this study, we compared the patterns of genetic mechanisms that confer FQR for Escherichia coli and Klebsiella pneumoniae isolated from the Assiut University Hospitals in Egypt. Methods: Eighty-seven clinical E. coli and K. pneumoniae isolates were tested for mutations in gyrA, gyrB, parC, and parE genes by polymerase chain reaction (PCR) amplification and DNA sequencing. The presence of plasmid-mediated quinolone resistance (PMQR) genes qnrA, qnrB, qnrS, aac(6¢)-Ib, qepA was screened by PCR and characterized by conjugation. Correlations between different FQR mechanisms and ciprofloxacin minimal inhibitory concentration (MIC) levels were determined. Results: A higher number of quinolone resistance-determining region (QRDR) mutations was detected in E. coli, while the number of PMQR determinants was significantly higher in K. pneumoniae. However, K. pneumoniae showed stronger correlations than E. coli between MIC levels and number of mutations in the QRDR per isolate (rs = 0.8, p 0.0001 and rs = 0.7, p 0.0001, respectively) as well as between MIC levels and number of plasmids (rs = 0.4, p = 0.005 and rs = 0.3, p = 0.02, respectively). Conclusions: Although we observed a prevalence of chromosomal mutations for E. coli and the presence of plasmid-encoded genes for K. pneumoniae that resulted in FQR phenotype, high levels of FQR appeared to occur as a result of gradual accumulation of mutations in QRDR for both bacteria. To our best of knowledge, this is the first study to report and compare the correlation between FQ MIC levels and different genetic mechanisms for FQR in Enterobacteriaceae.

Background: An increasing pattern of fluoroquinolone resistance (FQR) among bacterial pathogens has been described worldwide. In this study, we compared the patterns of genetic mechanisms that confer FQR for Escherichia coli and Klebsiella pneumoniae isolated from the Assiut University Hospitals in Egypt. Methods: Eighty-seven clinical E. coli and K. pneumoniae isolates were tested for mutations in gyrA, gyrB, parC, and parE genes by polymerase chain reaction (PCR) amplification and DNA sequencing. The presence of plasmid-mediated quinolone resistance (PMQR) genes qnrA, qnrB, qnrS, aac(6¢)-Ib, qepA was screened by PCR and characterized by conjugation. Correlations between different FQR mechanisms and ciprofloxacin minimal inhibitory concentration (MIC) levels were determined. Results: A higher number of quinolone resistance-determining region (QRDR) mutations was detected in E. coli, while the number of PMQR determinants was significantly higher in K. pneumoniae. However, K. pneumoniae showed stronger correlations than E. coli between MIC levels and number of mutations in the QRDR per isolate (rs = 0.8, p 0.0001 and rs = 0.7, p 0.0001, respectively) as well as between MIC levels and number of plasmids (rs = 0.4, p = 0.005 and rs = 0.3, p = 0.02, respectively). Conclusions: Although we observed a prevalence of chromosomal mutations for E. coli and the presence of plasmid-encoded genes for K. pneumoniae that resulted in FQR phenotype, high levels of FQR appeared to occur as a result of gradual accumulation of mutations in QRDR for both bacteria. To our best of knowledge, this is the first study to report and compare the correlation between FQ MIC levels and different genetic mechanisms for FQR in Enterobacteriaceae.

Background: An increasing pattern of fluoroquinolone resistance (FQR) among bacterial pathogens has been described worldwide. In this study, we compared the patterns of genetic mechanisms that confer FQR for Escherichia coli and Klebsiella pneumoniae isolated from the Assiut University Hospitals in Egypt. Methods: Eighty-seven clinical E. coli and K. pneumoniae isolates were tested for mutations in gyrA, gyrB, parC, and parE genes by polymerase chain reaction (PCR) amplification and DNA sequencing. The presence of plasmid-mediated quinolone resistance (PMQR) genes qnrA, qnrB, qnrS, aac(6¢)-Ib, qepA was screened by PCR and characterized by conjugation. Correlations between different FQR mechanisms and ciprofloxacin minimal inhibitory concentration (MIC) levels were determined. Results: A higher number of quinolone resistance-determining region (QRDR) mutations was detected in E. coli, while the number of PMQR determinants was significantly higher in K. pneumoniae. However, K. pneumoniae showed stronger correlations than E. coli between MIC levels and number of mutations in the QRDR per isolate (rs = 0.8, p 0.0001 and rs = 0.7, p 0.0001, respectively) as well as between MIC levels and number of plasmids (rs = 0.4, p = 0.005 and rs = 0.3, p = 0.02, respectively). Conclusions: Although we observed a prevalence of chromosomal mutations for E. coli and the presence of plasmid-encoded genes for K. pneumoniae that resulted in FQR phenotype, high levels of FQR appeared to occur as a result of gradual accumulation of mutations in QRDR for both bacteria. To our best of knowledge, this is the first study to report and compare the correlation between FQ MIC levels and different genetic mechanisms for FQR in Enterobacteriaceae.

Background and aim: Varicocele is one of the most common causes of male infertility. Leptin that has a role in sperm motility may have a role of varicocele. We aimed to study the effect of varicocelectomy on the serum and seminal leptin in patients with asthenozoospermia and the correlation between leptin levels, sperm parameters and varicocele grade. Methods: Thirty-six male patients with varicocele having isolated asthenozoospermia were included in this study. Thirty normal fertile controls were included. Semen analysis, serum and seminal leptin measurements were performed for all participants at baseline and for patients three months after varicocelectomy. Microsurgical varicocelectomy has been performed for patients. Results: Seminal and serum leptin levels were significantly higher in patients than controls. Seminal leptin was positively correlated with varicocele grade (r = 0.357, p  .05) while no correlation was found between serum leptin varicocele grade (r = 0.056, p = .37). Both seminal and serum leptin were inversely correlated with sperm motility (r = −0.92 and r = −0.87, p  .001; respectively). Seminal and serum leptin were significantly improved after varicocelectomy. Conclusion: Varicocele is associated with higher levels of seminal and serum leptin especially in higher grads and this was correlated with negative effects on sperm motility. Leptin levels were significantly decreased after repair.

AIM: To evaluate the effect (clinically, histopathologically and immunohistochemically) and safety of a single intra-pterygium injection of bevacizumab. METHODS: Prospective interventional study comprised 40 eyes of 40 patients with primary fleshy pterygia who attended the Outpatient Clinic of Department of Ophthalmology, Assiut University Hospitals, Egypt from May 2015 to May 2016. Patients were randomly classified into 2 groups: the first group received a single intralesional injection of bevacizumab (Avastin; Genentech, San Francisco, CA, USA); the second group comprised patients who did not receive subconjunctival bevacizumab. Excision of pterygium and conjunctival auto graft was done in both groups. The excised pterygium tissues were subjected to histopathological and immunohistochemical evaluation. RESULTS: The study comprised 40 eyes of 40 patients (33 men, 7 women) of age range from 31-58y. The study group included 22 eyes. The control group included 18 eyes. A decrease in the vascularity of the pterygium was noted in all injected cases. The mean vessel count was higher in non-injected pterygia than that in injected pterygia and the difference was statistically significant (P=0.001). Also, the mean vessel count in both groups was significantly higher than normal conjunctive (P=0.005 and 0.001). A statistically significant difference in vascular endothelial growth factor (VEGF) expression between injected and non-injected cases was detected in the epithelial, stromal and endothelial cells (P=0.0001, 0.016, 0.014). No serious intraoperative complications occurred in both groups. CONCLUSION: The use of single intra lesional injection of Avastin in pterygium decreased vascularity and decreased VEGF expression in injected pterygium after one month. Our study proved the effect of single intra lesional injection of Avastin on pterygium. Further studies may enable limiting the need for surgery and improve quality of life for patients with pterygia.