{"title":"Genetic Diversity of Human Fungal Pathogens.","authors":"Jillian Freese, Sinem Beyhan","doi":"10.1007/s40588-023-00188-4","DOIUrl":"https://doi.org/10.1007/s40588-023-00188-4","url":null,"abstract":"<p><strong>Purpose of review: </strong>Fungi represent a central yet often overlooked domain of clinically relevant pathogens that have become increasingly important in human disease. With unique adaptive lifestyles that vary widely across species, human fungal pathogens show remarkable diversity in their virulence strategies. The majority of these fungal pathogens are opportunistic, primarily existing in the environment or as commensals that take advantage of immunocompromised hosts to cause disease. In addition, many fungal pathogens have evolved from non-pathogenic lifestyles. The extent of genetic diversity and heritability of virulence traits remains poorly explored in human fungal pathogens.</p><p><strong>Recent findings: </strong>Genetic variation caused by mutations, genomic rearrangements, gene gain or loss, changes in ploidy, and sexual reproduction have profound effects on genetic diversity. These mechanisms contribute to the remarkable diversity of fungal genomes and have large impacts on their prevalence in human disease, virulence, and resistance to antifungal therapies.</p><p><strong>Summary: </strong>Here, we focus on the genomic structure of the most common human fungal pathogens and the aspects of genetic variability that contribute to their dominance in human disease.</p>","PeriodicalId":45506,"journal":{"name":"Current Clinical Microbiology Reports","volume":"10 2","pages":"17-28"},"PeriodicalIF":5.2,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10310308/pdf/nihms-1910183.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10120220","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Therapeutic Strategies to Ameliorate Antibiotic Resistance and Host-Inflammation Response in Sepsis: an Innovative Approach","authors":"Parkhi Shrivastava, R. Gothalwal, P. Gandhi","doi":"10.1007/s40588-023-00194-6","DOIUrl":"https://doi.org/10.1007/s40588-023-00194-6","url":null,"abstract":"","PeriodicalId":45506,"journal":{"name":"Current Clinical Microbiology Reports","volume":"10 1","pages":"85 - 98"},"PeriodicalIF":5.2,"publicationDate":"2023-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44436177","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Zoonotic Parasites in Feral Animals Commonly Consumed in Australia — Is There a Risk?","authors":"D. Barton, Hannah Fahey, D. Jenkins, S. Shamsi","doi":"10.1007/s40588-023-00193-7","DOIUrl":"https://doi.org/10.1007/s40588-023-00193-7","url":null,"abstract":"","PeriodicalId":45506,"journal":{"name":"Current Clinical Microbiology Reports","volume":"10 1","pages":"66 - 73"},"PeriodicalIF":5.2,"publicationDate":"2023-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43769214","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Cross-kingdom Microbial Interactions Within the Oral Cavity and Their Implications for Oral Disease","authors":"G. Wijesinghe, A. Nobbs, H. Bandara","doi":"10.1007/s40588-023-00191-9","DOIUrl":"https://doi.org/10.1007/s40588-023-00191-9","url":null,"abstract":"","PeriodicalId":45506,"journal":{"name":"Current Clinical Microbiology Reports","volume":"10 1","pages":"29 - 35"},"PeriodicalIF":5.2,"publicationDate":"2023-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45838546","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The Metabolism of Susceptibility: Clearing the FoG Between Tolerance and Resistance in <i>Candida albicans</i>.","authors":"Marina Druseikis, Austin Mottola, Judith Berman","doi":"10.1007/s40588-023-00189-3","DOIUrl":"10.1007/s40588-023-00189-3","url":null,"abstract":"<p><strong>Purpose of review: </strong>Failure of antifungal treatment is alarmingly common in patients infected with <i>Candida albicans</i> isolates that test as susceptible in vitro. This means that clinical susceptibility tests have limited predictive value for treatment success. To guide the improvement of patient outcomes, we must understand the effects of environmental and metabolic states on drug responses.</p><p><strong>Recent findings: </strong>Lab conditions often deviate from host environments, and current susceptibility testing standards ignore slow-growing, tolerant phenotypes; both factors may contribute to antifungal treatment failure. Metabolomic studies reveal that strain background, nutrient availability, and drug exposure influence the metabolic state of <i>C</i>. <i>albicans</i> cells; similarly, the metabolic state influences drug susceptibility.</p><p><strong>Summary: </strong>Identifying tolerant strains in the clinic may improve patient outcomes. Studies that analyze the effects of essential but limited nutrients have the potential to improve the avoidance of persistent candidiasis and to reduce the frequency of antifungal treatment failures. Here, we highlight literature that explores the effect of drug exposure and antifungal drug resistance status on the <i>C</i>. <i>albicans</i> metabolome. Similar analyses need to be carried out relative to antifungal drug tolerance. Additionally, we focus on the biological relevance of four essential small molecules-iron, zinc, phosphate, and sphingolipids-to antifungal tolerance and resistance.</p>","PeriodicalId":45506,"journal":{"name":"Current Clinical Microbiology Reports","volume":"10 2","pages":"36-46"},"PeriodicalIF":3.1,"publicationDate":"2023-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7614596/pdf/EMS176254.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9588421","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
B. Short, A. Bakri, Abdullah Baz, Craig Williams, Jason L. Brown, G. Ramage
{"title":"There Is More to Wounds than Bacteria: Fungal Biofilms in Chronic Wounds","authors":"B. Short, A. Bakri, Abdullah Baz, Craig Williams, Jason L. Brown, G. Ramage","doi":"10.1007/s40588-022-00187-x","DOIUrl":"https://doi.org/10.1007/s40588-022-00187-x","url":null,"abstract":"","PeriodicalId":45506,"journal":{"name":"Current Clinical Microbiology Reports","volume":"10 1","pages":"9-16"},"PeriodicalIF":5.2,"publicationDate":"2023-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45986847","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Ubiquitin-Mediated Regulation of Autophagy During Viral Infection.","authors":"Joydeep Nag, Janvi Patel, Shashank Tripathi","doi":"10.1007/s40588-022-00186-y","DOIUrl":"https://doi.org/10.1007/s40588-022-00186-y","url":null,"abstract":"<p><strong>Purpose of review: </strong>Virus infections skew the host autophagic response to meet their replication and transmission demands by tapping into the critical host regulatory mechanisms that control the autophagic flux. This review is a compendium of previous reports highlighting the mechanisms that viruses adapt to hijack the host ubiquitination machinery to repurpose autophagy for their sustenance.</p><p><strong>Recent findings: </strong>Emerging evidence suggests a critical role of host ubiquitin machinery in the manifestation of the antiviral or proviral functions of autophagy. Lately, more emphasis has been laid to identify specific host E3 ubiquitin ligases, their targets (viral or host), and characterizing corresponding ubiquitin linkages by biochemical or genome-wide genetic screening approaches.</p><p><strong>Summary: </strong>Here, we highlight how viruses ingeniously engage and subvert the host ubiquitin-autophagy system to promote virus replication and antagonize intracellular innate immune responses.</p>","PeriodicalId":45506,"journal":{"name":"Current Clinical Microbiology Reports","volume":"10 1","pages":"1-8"},"PeriodicalIF":5.2,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9839220/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10606007","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The Role of Host and Fungal Factors in the Commensal-to-Pathogen Transition of <i>Candida albicans</i>.","authors":"Ilse D Jacobsen","doi":"10.1007/s40588-023-00190-w","DOIUrl":"https://doi.org/10.1007/s40588-023-00190-w","url":null,"abstract":"<p><strong>Abstract: </strong></p><p><strong>Purpose of review: </strong>The fungus <i>Candida albicans</i> has evolved to live in close association with warm-blooded hosts and is found frequently on mucosal surfaces of healthy humans. As an opportunistic pathogen, <i>C. albicans</i> can also cause mucosal and disseminated infections (candidiasis). This review describes the features that differentiate the fungus in the commensal <i>versus</i> pathogenic state and the main factors underlying <i>C. albicans</i> commensal-to-pathogen transition.</p><p><strong>Recent findings: </strong>Adhesion, invasion, and tissue damage are critical steps in the infection process. Especially invasion and damage require transcriptional and morphological changes that differentiate <i>C. albicans</i> in the pathogenic from the commensal state. While the commensal-to-pathogen transition has some conserved causes and features in the oral cavity, the female urogenital tract, and the gut, site-specific differences have been identified in recent years.</p><p><strong>Summary: </strong>This review highlights how specific factors in the different mucosal niches affect development of candidiasis. Recent evidence suggests that colonization of the gut is not only a risk factor for systemic candidiasis but might also provide beneficial effects to the host.</p>","PeriodicalId":45506,"journal":{"name":"Current Clinical Microbiology Reports","volume":"10 2","pages":"55-65"},"PeriodicalIF":5.2,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10154278/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9431485","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Shadab Farhadi Cheshmeh Morvari, Bethany L McCann, Elaine M Bignell
{"title":"Conserved and Divergent Features of pH Sensing in Major Fungal Pathogens.","authors":"Shadab Farhadi Cheshmeh Morvari, Bethany L McCann, Elaine M Bignell","doi":"10.1007/s40588-023-00195-5","DOIUrl":"10.1007/s40588-023-00195-5","url":null,"abstract":"<p><strong>Purpose of review: </strong>For human fungal pathogens, sensory perception of extracellular pH is essential for colonisation of mammalian tissues and immune evasion. The molecular complexes that perceive and transmit the fungal pH signal are membrane-proximal and essential for virulence and are therefore of interest as novel antifungal drug targets. Intriguingly, the sensory machinery has evolved divergently in different fungal pathogens, yet spatial co-ordination of cellular components is conserved.</p><p><strong>Recent findings: </strong>The recent discovery of a novel pH sensor in the basidiomycete pathogen <i>Cryptococcus neformans</i> highlights that, although the molecular conservation of fungal pH sensors is evolutionarily restricted, their subcellular localisation and coupling to essential components of the cellular ESCRT machinery are consistent features of the cellular pH sensing and adaptation mechanism. In both basidiomycetes and ascomycetes, the lipid composition of the plasma membrane to which pH sensing complexes are localised appears to have pivotal functional importance. Endocytosis of pH-sensing complexes occurs in multiple fungal species, but its relevance for signal transduction appears not to be universal.</p><p><strong>Summary: </strong>Our overview of current understanding highlights conserved and divergent mechanisms of the pH sensing machinery in model and pathogenic fungal species, as well as important unanswered questions that must be addressed to inform the future study of such sensing mechanisms and to devise therapeutic strategies for manipulating them.</p>","PeriodicalId":45506,"journal":{"name":"Current Clinical Microbiology Reports","volume":"10 3","pages":"120-130"},"PeriodicalIF":3.1,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10421798/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10053874","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}