Cancer is among the leading causes of death globally. Despite advances in cancer research, a full understanding of the exact cause has not been established. Recent data have shown that the microbiome has an important relationship with cancer on various levels, including cancer pathogenesis, diagnosis and prognosis, and treatment. Since most studies have focused only on the role of bacteria in this process, in this article we review the role of fungi—another important group of the microbiome, the totality of which is referred to as the “mycobiome”—in the development of cancer and how it can impact responses to anticancer medications. Furthermore, we provide recent evidence that shows how the different microbial communities interact and affect each other at gastrointestinal and non-gastrointestinal sites, including the skin, thereby emphasizing the importance of investigating the microbiome beyond bacteria.
Background:The frequency of nosocomial yeast infections has increased dramatically in the recent years. They are considered an important cause of morbidity and mortality in immunocompromised cancer patients. The majority of yeast infections are caused by Candida species. However, species like Trichosporon and Rhodotorula should be considered as possible infectious agents as well.Objectives: This study aimed at determining the prevalence of yeast species, their distribution among patients and the antifungal susceptibility profile at Oncology Center, Mansoura, Egypt.Methods: From December 2016 till November 2017, cancer patients who developed infective episodes two days or more following hospital admission were included in the study. Clinical samples were collected according to the site of infection using standard sterile procedures. Blood samples were cultured using the BACT-ALERT system. Fungal identification and susceptibility testing were performed by Vitek 2 system. Results:Eighty-seven fungal strains were obtained from our patients. A higher isolation rate was observed in urine samples (47.1%) followed by oropharyngeal (24.1%) and blood (21.8%) samples. The majority of the yeast species were Candida albicans (40.2%), C. tropicalis (14.9%), C. parapsilosis (9.2%), C. famata (6.9%) and C. guilliermondii (6.9%). Out of the 87 samples, 8 (9.2%) were resistant to fluconazole, 7 (8.0%) were resistant to flucytosine, 5 (5.7%) were resistant to voriconazole and amphotericin B, and no sample was resistant to caspofungin or micafungin. Conclusions:Vitek 2 system offers a novel method for the early identification and susceptibility testing of different yeast species. It helps to minimize the risk for emergence of resistant species and reduce mortality rates, particularly in cancer patients.
Background: Recently, an increasing number of resistant-to-terbinafine dermatophytosis cases have been reported. Thus, identifying an alternative antifungal agent that possesses a broad-spectrum activity, including against resistant strains, is needed. Methods: In this study, we compared the antifungal activity of efinaconazole to fluconazole, itraconazole, and terbinafine against clinical isolates of dermatophyte, Candida, and molds using in vitro assays. The minimum inhibitory concentration (MIC) and minimum fungicidal concentration (MFC) of each antifungal was quantified and compared. Both susceptible and resistant clinical isolates of Trichophyton mentagrophytes (n=16), T. rubrum (n=43), T. tonsurans (n=18), T. violaceum (n=4), Candida albicans (n=55), C. auris (n=30), Fusarium sp., Scedosporium sp., and Scopulariopsis sp. (n=15 for each) were tested. Results: Our data shows that efinaconazole was the most active antifungal, compared to the other agents tested, against dermatophytes with MIC50 and MIC90 (Concentration that inhibited 50% and 90% of strains tested, respectively) values of 0.002 and 0.03 μg/ml, respectively. Fluconazole, itraconazole and terbinafine showed MIC50 and MIC90 values of 1 and 8 μg/ml, 0.03 and 0.25 μg/ml, and 0.031 and 16 μg/ml, respectively. Against Candida isolates, efinaconazole MIC50 and MIC90 values were 0.016 and 0.25 μg/ml, respectively, whereas fluconazole, itraconazole and terbinafine had MIC50 and the MIC90 values of 1 and 16 μg/ml, 0.25 and 0.5 μg/ml, and 2 and 8 μg/ml, respectively. Against various mold species, efinaconazole MIC values ranged from 0.016 and 2 μg/ml, compared to 0.5 to greater than 64 μg/ml for the comparators. Conclusions: efinaconazole showed superior potent activity against a broad panel of susceptible and resistant dermatophyte, Candida, and mold isolates.
Treatment with neoadjuvant chemotherapy (NAC) in muscle invasive bladder cancer (MIBC) is associated with clinical benefit in urothelial carcinoma. While extensive research evaluating role of tumor mutational expression profiles and clinicopathologic factors into chemoresponse has been published, the role of gut microbiome (GM) in bladder cancer in chemoresponse has not been thoroughly evaluated. A working knowledge of the microbiome and its effect on all forms of cancer therapy in BC is critical. Here we examine gut microbiome of bladder cancer patients undergoing NAC. Overall, there was no significant difference in alpha and beta diversity by responder status. However, analysis of fecal microbiome samples showed that a higher abundance of Bacteroides within both institutional cohorts during NAC was associated with residual disease at the time of radical cystectomy regardless of chemotherapy regimen. Group community analysis revealed presence of favorable microbial subtypes in complete responders. Finally, fecal microbial composition outperformed clinical variables in prediction of complete response (AUC 0.88 vs AUC 0.50), however, no single microbial species could be regarded as a fully consistent biomarker. Microbiome-based community signature as compared to single microbial species is more likely to be associated as the link between bacterial composition and NAC response.
Background and Aim: Pseudomonas aeruginosa (P. aeruginosa) is an important causative organism of burn infection. Several virulence factors are implicated in P. aeruginosa colonization and invasion, making P. aeruginosa infection's outcome worse. Type III secretion system (T3SS) effector proteins are among these virulence factors. The present study evaluated the frequency of genes encoding T3SS effectors as a virulence determinant in P. aeruginosa isolates from burn patients.Materials and Methods: Wound swabs were collected from burn patients admitted to the Plastic and Reconstructive Surgery Center, Mansoura University, Egypt, and identified by different microbiological testing methods. The modified Kirby Bauer's disc diffusion method was used to test the antibiotic susceptibility of P. aeruginosa isolates against different antibiotics. Prevalence and the presence of exo genes that encode type T3SS proteins (exoS, exoT, exoU, and exoY) in P. aeruginosa isolates were evaluated by the multiplex PCR. Chi-square and Fisher's test were used for statistical analysis.Results: A total of 45 P. aeruginosa isolates were identified from 101 burn patients, including 27 males and 18 females, with a mean age of 15.78±2.65 years old. P. aeruginosa isolates were mostly susceptible to piperacillin/tazobactam and imipenem (73.33 and 62.22%), respectively; while the lowest susceptibility rates were in ceftazidime (4.44%), Tobramycin (4.44%), and ceftriaxone (6.67%). The exoY and exoT genes were detected in 100% of the P. aeruginosa isolates, while 62.22% and 42.22% of clinical isolates harbored exoS and exoU genes, respectively. Conclusion:This study established a correlation between T3SS proteins, particularly exoS and exoU genes and antimicrobial resistance in P. aeruginosa isolates from burn infection.
Background and Objectives: The global spread of carbapenem resistance and the resulting increase in mortality forced the World Health Organization (WHO) to claim carbapenem-resistant enterobacteriaceae (CRE) as global priority pathogens. Our study aimed to determine the prevalence of carbapenemase-encoding genes and major plasmid incompatibility groups among Gram-negative hospital-based isolates in Egypt. Material and Methods: This cross-sectional study was carried out at Mansoura University Hospitals over 12 months, from January to December 2019. All the isolates were tested for carbapenem resistance. The selected isolates were screened by conventional polymerase chain reaction (PCR) for the presence of carbapenemase genes, namely blaKPC, blaIMP, blaVIM, and blaNDM-1. PCR-based plasmid replicon typing was performed using the commercial PBRT kit. Results: Out of 150 isolates, only 30 (20.0%) demonstrated carbapenem resistance. Klebsiella pneumoniae was the most resistant of all isolated bacteria, and blaNDM was the predominant carbapenemases gene, while the most prevalent plasmid replicons were the F replicon combination (FIA, FIB, and FII) and A/C. Plasmids were detected only in Klebsiella pneumoniae, Escherichia coli, Enterobacter cloacae, and Pseudomonas aeruginosa. Remarkably, we found a statistically significant association between carbapenemase genes and plasmid replicons, including blaNDM, IncA/C, and IncX. Conclusions: Our study demonstrated an alarming rise of plasmid-mediated carbapenem-resistant bacteria in our locality. The coexistence of resistance genes and plasmids highlights the importance of a targeted antibiotic surveillance program and the development of alternative therapeutic options at the local and international levels. Based on our results, we suggest a large-scale study with more Enterobacteriaceae isolates, testing other carbapenemase-encoding genes, and comparing the replicon typing method with other plasmid detection methods. We also recommend a national action plan to control the irrational use of antibiotics in Egypt.
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