DOCSLIB.ORG

Investigating the Function of the Mold Specific Gene <I>M46</I>

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Investigating the Function of the Mold Specific Gene <I>M46</I> The University of Southern Mississippi The Aquila Digital Community Dissertations Spring 5-2013 Investigating the Function of the Mold Specific Gene M46, in the Pathogenic Dimorphic Fungus Histoplasma capsulatum Davida LaShaundra Crossley University of Southern Mississippi Follow this and additional works at: https://aquila.usm.edu/dissertations Part of the Biology Commons, and the Ornithology Commons Recommended Citation Crossley, Davida LaShaundra, "Investigating the Function of the Mold Specific Gene M46, in the Pathogenic Dimorphic Fungus Histoplasma capsulatum" (2013). Dissertations. 741. https://aquila.usm.edu/dissertations/741 This Dissertation is brought to you for free and open access by The Aquila Digital Community. It has been accepted for inclusion in Dissertations by an authorized administrator of The Aquila Digital Community. For more information, please contact [email protected]. The University of Southern Mississippi INVESTIGATING THE FUNCTION OF THE MOLD SPECIFIC GENE M46, IN THE PATHOGENIC DIMORPHIC FUNGUS HISTOPLASMA CAPSULATUM by Davida LaShaundra Crossley Abstract of a Dissertation Submitted to the Graduate School of The University of Southern Mississippi in Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy May 2013 ABSTRACT INVESTIGATING THE FUNCTION OF THE MOLD SPECIFIC GENE M46, IN THE PATHOGENIC DIMORPHIC FUNGUS HISTOPLASMA CAPSULATUM by Davida LaShaundra Crossley May 2013 Histoplasma capsulatum (Hc) is a dimorphic fungus that is the etiologic agent for the respiratory infection histoplasmosis. The fungus is found in the environment in contaminated soils of birds and bat excreta as a multi-cellular saprophytic mold. Once the soil is disturbed, spores are released and are inhaled into the lungs. In the lungs, the fungus converts to uni-cellular parasitic yeast (Maresca & Kobayashi, 1989). The conversion from mold to yeast is a requirement for pathogenesis. Previously, several mold specific genes have been isolated by our laboratory from a subtracted cDNA library. One such gene, is M46. M46 is a single copy gene and has a predicted protein size of 8.5 kDa. Northern blot analysis of M46 in four major Hc strains, revealed that M46 is not expressed in yeast. The gene is expressed in mold for strains G186AS and Downs, but is silent in strains G184AS and G217B. These findings suggest that M46 may not be involved in dimorphism. According to NCBI Genbank, M46 does not have a homolog, and therefore the function is unknown. Several experiments were conducted to gather more information about possible functions of M46. Over expression of M46 in the yeast did not induce filamentous growth. Examination of a M46 knock out mutant constructed by allelic replacement, with confocal microscopy, scanning electron microscopy (SEM), and transmission electron microscopy (TEM), did not reveal any ii significant structural changes. Therefore, M46 may not be involved in maintaining the mold and yeast morphology. Growth curve studies of the M46 knockout and wild type strains, revealed that M46 is not involved in maintaining the normal growth rate in mold and yeast. Parallel comparison of gene expression of the M46 knockout and wild type strain via RNA sequencing, suggest that the function of M46 may be correlated with drug resistance and iron and sugar transport. iii COPYRIGHT BY DAVIDA LASHAUNDRA CROSSLEY 2013 The University of Southern Mississippi INVESTIGATING THE FUNCTION OF THE MOLD SPECIFIC GENE M46 IN THE PATHOGENIC DIMORPHIC FUNGUS HISTOPLASMA CAPSULATUM by Davida LaShaundra Crossley A Dissertation Submitted to the Graduate School of The University of Southern Mississippi in Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy Approved: Glenmore Shearer, Jr. Director Mohamed Elasri Anthony Bell Yan Lin Guo Susan A. Siltanen Dean of the Graduate School May 2013 ACKNOWLEDGMENT This has been such an amazing long adventure. “Exploring where no man has ever gone before,” as Dr. Shearer would say. I am blessed to be able to have the opportunity to broaden my knowledge by exploring science. This has laid the foundation for the beginning of a new life for me, in which I may broaden and increase the knowledge of many others. To Dr. Shearer, I would like to give many thanks for allowing me to be a student in your lab and for the many conversations that has challenged my way of thinking. I would also like to thank my lab colleagues, Melissa Adams, Lacey Howard, and Logan Blancett for the countless advice and mental support for when our projects were just not moving for us. Big thanks to Hana Ali, Rupesh Patel, Danielle Williamson, and Erin Smith for the tremendous hours of help and support throughout the years. Dr. Gordon Cannon, Dr. Mohamed Elasri, Dr.Yan Lin Guo, and Dr. Anthony Bell, you were all great committee members and your advice was of such tremendous help. I would also like to thank Dr. Shahid Karim and his lab for advice and for emergency supplies throughout the day, and Dr. Kenneth Curry and his lab for advice and help with experiments. To my family, I would like to thank my dad Michael Crossley, Sr, and my mother Barbara Crossley, for many years of support mentally and financially. You were always there for me, and there is no way that I could possibly pay you back for all your love. I hope in exchange that I have made you proud. I would like to dedicate this iv dissertation to my mother and father, as well as the late Mrs. Idell Smith. To Idell, I know that you will not be able to see me graduate, but I know that you are watching me from above, and you will be there in spirit. Thank you so much and I love you all. v TABLE OF CONTENTS ABSTRACT……………………………………………………………………………..ii ACKNOWLEDGMENTS……………………………………………………….……...iv LIST OF TABLES…………………………...……...……………………...…….…...viii LIST OF ILLUSTRATIONS……………...………………………...……..……..….....ix CHAPTER I. INTRODUCTION…………………………………….……………….…1 II. BACKGROUND AND LITERATURE REVIEW..…………………….4 Histoplasma capsulatum (Hc) History HistoplasmosisTreatment and Diagnosis Mold and Yeast Morphotype Virulence in Hc Strains and Varients Molecular Challenges Approaches to Identify Phase Specific Genes Examples of Phase Specific Genes III. GENERAL MATERIAL AND METHODOLOGY……………...….…16 Experimental Strains and Growth Conditions RNA and DNA Purifications Transformations Genetic Manipulation Procedures Blotting Techniques Microscopy Preparations RNA Sequencing IV. CHARACTERIZATION OF M46………………………………………27 M46 Sequence Analysis Genomic Copy Number of M46 Northern Blot Analysis of M46 in Four Major Hc Strains NCBI GENBANK M46 Homologs vi V. OVER EXPRESION OF M46 IN YEAST…………………………….…32 Northern Blot Confirmation of M46 Over Expression Phenotype of M46 Over Expression in Yeast VI. GENOMIC DISRUPTION OF M46……………………………….....….36 Construction of Genomic Replacement Plasmid M46 Genomic Replacement Map Confirmation of M46 Knock out Phenotype Observation Growth Curve Analysis VIII. VII. RNA SEQUENCING……………...…………...…………………..…….49 FPKM Scatter Plot of M46 Knock out vs Wild type Northern Blot Confirmation of DGE Results Celelsu Gene Ontology Analysis of M46 Knock out Strain VIII. DISCUSSION………………………..…………………………….....….59 Confirmation of General Characterization of M46 Rapid Methods for Determining the Function of M46 M46 Knock out Confirmation Morphological and Growth Studies RNA Sequencing APPENDIX…………………………………………...……………………..…………74 REFERENCES….…………………….…………………………......…………...….....77 vii LIST OF TABLES Table 1. NCBI Blast Homologs of M46………….……………………..……………....31 2. RNA Sequencing Analysis of Genes with Undetectable Read………………..54 viii LIST OF ILLUSTRATIONS Figure 1. M46 Genomic and Putative Protein Sequence. ………..…………….……..….28 2. Genomic Copy Number of M46……………………………..…………………29 3. Northern blot Analysis of M46 in Four Major Hc strains………………...……30 4. Over Expression Plasmid of M46………….…………………………………...33 5. Northern Blot of M46 Over Expression in the Yeast Phase…………....………34 6. M46 Over Expression in Yeast Grown in Liquid HMM Media…......................35 7. M46 Over Expression in Yeast Grown on HMM Solid Media…….…..……....35 8. Construction of Replacement Plasmid pUDCg::hph……………………….......37 9. The Genomic Replacement Map of M46…………………..………..………....39 10. Confirmation of M46 Knock out via PCR………………………………….…..40 11. Confirmation of M46 Knock out via Southern Blot Analysis………………….41 12. Confirmation of M46 Knock out via Northern Blot Analysis………….………41 13. Phenotype of M46 Knock out and Wild type in Liquid Media.……….....…… 43 14. Phenotype of M46 Knock out and Wild type on Solid Media…………………44 22. Phe 15. Phenotype of M46 Knockout and Wild type Yeast using SEM…………..……45 16. Phenotype of M46 Knockout and Wild type Mold using SEM……………..….45 17. Phenotype of M46 Knockout and Wild type Yeast using TEM…......................46 25. Phenotype of M46 knockout vs Wild type mold transmission e 18. Phenotype of M46 Knock out and Wild type Mold using TEM...……………. 46 19. Growth Curve of M46 Knock out and Wild type Yeast………….….................47 20. Growth Curve of M46 Knock out and Wild type Mold…..................................48 ix 21. RPKM 1,000 Scatter Plot of M46 Knock out and Wild type…………...…..….50 22. RPKM 5,000 Scatter Plot of M46 Knock out and Wild type ……..…..……….51 23. RPKM 10,000 Scatter Plot of M46 Knock out and Wild type …………….......52 24. RPKM 20,000 Scatter Plot of M46 Knock out and Wild type………….….......53 25. Northern blot Analysis of RNA seq Confirmation……………….………...….54 26. M46 Knock out Cellular Component Ontology Report………………..............56
Load more

Recommended publications
  • Turning on Virulence: Mechanisms That Underpin the Morphologic Transition and Pathogenicity of Blastomyces
    Virulence ISSN: 2150-5594 (Print) 2150-5608 (Online) Journal homepage: http://www.tandfonline.com/loi/kvir20 Turning on Virulence: Mechanisms that underpin the Morphologic Transition and Pathogenicity of Blastomyces Joseph A. McBride, Gregory M. Gauthier & Bruce S. Klein To cite this article: Joseph A. McBride, Gregory M. Gauthier & Bruce S. Klein (2018): Turning on Virulence: Mechanisms that underpin the Morphologic Transition and Pathogenicity of Blastomyces, Virulence, DOI: 10.1080/21505594.2018.1449506 To link to this article: https://doi.org/10.1080/21505594.2018.1449506 © 2018 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group© Joseph A. McBride, Gregory M. Gauthier and Bruce S. Klein Accepted author version posted online: 13 Mar 2018. Submit your article to this journal Article views: 15 View related articles View Crossmark data Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=kvir20 Publisher: Taylor & Francis Journal: Virulence DOI: https://doi.org/10.1080/21505594.2018.1449506 Turning on Virulence: Mechanisms that underpin the Morphologic Transition and Pathogenicity of Blastomyces Joseph A. McBride, MDa,b,d, Gregory M. Gauthier, MDa,d, and Bruce S. Klein, MDa,b,c a Division of Infectious Disease, Department of Medicine, University of Wisconsin School of Medicine and Public Health, 600 Highland Avenue, Madison, WI 53792, USA; b Division of Infectious Disease, Department of Pediatrics, University of Wisconsin School of Medicine and Public Health, 1675 Highland Avenue, Madison, WI 53792, USA; c Department of Medical Microbiology and Immunology, University of Wisconsin School of Medicine and Public Health, 1550 Linden Drive, Madison, WI 53706, USA.
    [Show full text]
  • 1 Recurrent Loss of Abaa, a Master Regulator of Asexual Development in Filamentous Fungi
    bioRxiv preprint doi: https://doi.org/10.1101/829465; this version posted November 4, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC 4.0 International license. 1 Recurrent loss of abaA, a master regulator of asexual development in filamentous fungi, 2 correlates with changes in genomic and morphological traits 3 4 Matthew E. Meada,*, Alexander T. Borowskya,b,*, Bastian Joehnkc, Jacob L. Steenwyka, Xing- 5 Xing Shena, Anita Silc, and Antonis Rokasa,# 6 7 aDepartment of Biological Sciences, Vanderbilt University, Nashville, Tennessee, USA 8 bCurrent Address: Department of Botany and Plant Sciences, University of California Riverside, 9 Riverside, California, USA 10 cDepartment of Microbiology and Immunology, University of California San Francisco, San 11 Francisco, California, USA 12 13 Short Title: Recurrent loss of abaA across Eurotiomycetes 14 #Address correspondence to Antonis Rokas, [email protected] 15 16 *These authors contributed equally to this work 17 18 19 Keywords: Fungal asexual development, abaA, evolution, developmental evolution, 20 morphology, binding site, Histoplasma capsulatum, regulatory rewiring, gene regulatory 21 network, evo-devo 22 1 bioRxiv preprint doi: https://doi.org/10.1101/829465; this version posted November 4, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC 4.0 International license. 23 Abstract 24 Gene regulatory networks (GRNs) drive developmental and cellular differentiation, and variation 25 in their architectures gives rise to morphological diversity.
    [Show full text]
  • Vesicular Transport in Histoplasma Capsulatum: an Effective Mechanism for Trans-Cell Wall Transfer of Proteins and Lipids in Ascomycetes
    Cellular Microbiology (2008) 10(8), 1695–1710 doi:10.1111/j.1462-5822.2008.01160.x First published online 5 May 2008 Vesicular transport in Histoplasma capsulatum: an effective mechanism for trans-cell wall transfer of proteins and lipids in ascomycetes Priscila Costa Albuquerque,1,2,3 by additional ascomycetes. The vesicles from H. cap- Ernesto S. Nakayasu,4 Marcio L. Rodrigues,5 sulatum react with immune serum from patients Susana Frases,2 Arturo Casadevall,2,3 with histoplasmosis, providing an association of the Rosely M. Zancope-Oliveira,1 Igor C. Almeida4 and vesicular products with pathogenesis. The findings Joshua D. Nosanchuk2,3* support the proposal that vesicular secretion is a 1Instituto de Pesquisa Clinica Evandro Chagas, general mechanism in fungi for the transport of Fundação Oswaldo Cruz, RJ Brazil. macromolecules related to virulence and that this 2Department of Microbiology and Immunology, Division process could be a target for novel therapeutics. of Infectious Diseases, Albert Einstein College of Medicine, Yeshiva University, New York, NY, USA. Introduction 3Department of Medicine, Albert Einstein College of Medicine, Yeshiva University, New York, NY, USA. Histoplasma capsulatum, a dimorphic fungus of the 4Department of Biological Sciences, The Border phylum Ascomycota, is a major human pathogen with Biomedical Research Center, University of Texas at El a worldwide distribution (Kauffman, 2007). The fungus Paso, El Paso, TX, USA. usually causes a mild, often asymptomatic, respiratory 5Instituto de Microbiologia Professor Paulo de Góes, illness, but infection may progress to life-threatening sys- Universidade Federal do Rio de Janeiro, RJ Brazil. temic disease, particularly in immunocompromised indi- viduals, infants or the elderly.
    [Show full text]
  • 2 the Numbers Behind Mushroom Biodiversity
    15 2 The Numbers Behind Mushroom Biodiversity Anabela Martins Polytechnic Institute of Bragança, School of Agriculture (IPB-ESA), Portugal 2.1 ­Origin and Diversity of Fungi Fungi are difficult to preserve and fossilize and due to the poor preservation of most fungal structures, it has been difficult to interpret the fossil record of fungi. Hyphae, the vegetative bodies of fungi, bear few distinctive morphological characteristicss, and organisms as diverse as cyanobacteria, eukaryotic algal groups, and oomycetes can easily be mistaken for them (Taylor & Taylor 1993). Fossils provide minimum ages for divergences and genetic lineages can be much older than even the oldest fossil representative found. According to Berbee and Taylor (2010), molecular clocks (conversion of molecular changes into geological time) calibrated by fossils are the only available tools to estimate timing of evolutionary events in fossil‐poor groups, such as fungi. The arbuscular mycorrhizal symbiotic fungi from the division Glomeromycota, gen- erally accepted as the phylogenetic sister clade to the Ascomycota and Basidiomycota, have left the most ancient fossils in the Rhynie Chert of Aberdeenshire in the north of Scotland (400 million years old). The Glomeromycota and several other fungi have been found associated with the preserved tissues of early vascular plants (Taylor et al. 2004a). Fossil spores from these shallow marine sediments from the Ordovician that closely resemble Glomeromycota spores and finely branched hyphae arbuscules within plant cells were clearly preserved in cells of stems of a 400 Ma primitive land plant, Aglaophyton, from Rhynie chert 455–460 Ma in age (Redecker et al. 2000; Remy et al. 1994) and from roots from the Triassic (250–199 Ma) (Berbee & Taylor 2010; Stubblefield et al.
    [Show full text]
  • New Histoplasma Diagnostic Assays Designed Via Whole Genome Comparisons
    Journal of Fungi Article New Histoplasma Diagnostic Assays Designed via Whole Genome Comparisons Juan E. Gallo 1,2,3, Isaura Torres 1,3 , Oscar M. Gómez 1,3 , Lavanya Rishishwar 4,5,6, Fredrik Vannberg 4, I. King Jordan 4,5,6 , Juan G. McEwen 1,7 and Oliver K. Clay 1,8,* 1 Cellular and Molecular Biology Unit, Corporación para Investigaciones Biológicas (CIB), Medellín 05534, Colombia; [email protected] (J.E.G.); [email protected] (I.T.); [email protected] (O.M.G.); [email protected] (J.G.M.) 2 Doctoral Program in Biomedical Sciences, Universidad del Rosario, Bogotá 111221, Colombia 3 GenomaCES, Universidad CES, Medellin 050021, Colombia 4 School of Biological Sciences, Georgia Institute of Technology, Atlanta, GA 30332, USA; [email protected] (L.R.); [email protected] (F.V.); [email protected] (I.K.J.) 5 Applied Bioinformatics Laboratory, Atlanta, GA 30332, USA 6 PanAmerican Bioinformatics Institute, Cali, Valle del Cauca 760043, Colombia 7 School of Medicine, Universidad de Antioquia, Medellín 050010, Colombia 8 Translational Microbiology and Emerging Diseases (MICROS), School of Medicine and Health Sciences, Universidad del Rosario, Bogotá 111221, Colombia * Correspondence: [email protected] Abstract: Histoplasmosis is a systemic fungal disease caused by the pathogen Histoplasma spp. that results in significant morbidity and mortality in persons with HIV/AIDS and can also affect immuno- competent individuals. Although some PCR and antigen-detection assays have been developed, Citation: Gallo, J.E.; Torres, I.; conventional diagnosis has largely relied on culture, which can take weeks. Our aim was to provide Gómez, O.M.; Rishishwar, L.; a proof of principle for rationally designing and standardizing PCR assays based on Histoplasma- Vannberg, F.; Jordan, I.K.; McEwen, specific genomic sequences.
    [Show full text]
  • Novel Taxa of Thermally Dimorphic Systemic Pathogens in the Ajellomycetaceae (Onygenales)
    Novel taxa of thermally dimorphic systemic pathogens in the Ajellomycetaceae (Onygenales) 1,2 1,2,3 1,4 5 Mean K2P distance of each window Proportion of zero non−conspecific1,6 K2P distances 1,6 1,6 1,2 Mean K2P distance of each window Proportion of zero non−conspecific K2P distances Mean K2P distance of each window Proportion of zero non−conspecific K2P distances Karolina Dukik , Yanping Jiang , Peiying Feng , Lynne Sigler , J. Benjamin0.13 Stielow , Joanna Freeke , Azadeh Jamalian , Sybren de Hoog Mean K2P distance of each window Proportion of zero non−conspecific K2P distances 1.0 0.45 Mean K2P distance of each window Proportion of zero non−conspecific K2P distances 0.6 0.12 0.20 0.8 0.25 1.0 0.04 0.20 0.35 0.11 0.4 0.15 0.6 0.20 0.8 Distance 0.15 Proportion 0.10 Mean K2P distance of each window Proportion of zero non−conspecific K2P distances Mean K2P distance of each window Proportion of zeroDistance non−conspecific K2P distances 0.10 0.16 Distance 0.2 0.4 Proportion Proportion 0.25 0.15 0.6 Mean K2P distance of each window0.02 Proportion of zero non−conspecific K2P distances 0.10 0.09 Mean K2P distance of each window Proportion of zero non−conspecific K2PMean distances K2P distance of each window ProportionMean of K2P zero distance non−conspecific of each window K2P distances Proportion of zero non−conspecific K2P distances Distance 1.0 0.2 Distance 0.05 Proportion 0.10 Mean K2P distance of each window Proportion of zero non−conspecific K2P distances 0.4 0.45 Mean K2P distance of each window Proportion Proportion of zero non−conspecific
    [Show full text]
  • Coccidioidomycosis and Histoplasmosis in Equines: an Overview to Support the Accurate Diagnosis
    Journal of Equine Veterinary Science 40 (2016) 62–73 Contents lists available at ScienceDirect Journal of Equine Veterinary Science journal homepage: www.j-evs.com Review Article Coccidioidomycosis and Histoplasmosis in Equines: An Overview to Support the Accurate Diagnosis Raimunda Sâmia Nogueira Brilhante a,*, Paula Vago Bittencourt b, Rita Amanda Chaves Lima a, Débora Castelo-Branco a, Jonathas Sales Oliveira a, Adriana Pinheiro b, Rossana Cordeiro a, Zoilo Pires Camargo c, José Júlio Costa Sidrim a, Marcos Fábio Gadelha Rocha a,b a Department of Pathology and Legal Medicine, School of Medicine, Specialized Medical Mycology Center, Postgraduate Program in Medical Microbiology, Federal University of Ceará, Fortaleza, Ceará, Brazil b School of Veterinary, Postgraduate Program in Veterinary Science, State University of Ceará, Fortaleza, Ceará, Brazil c Department of Microbiology, Immunology and Parasitology, São Paulo Federal University, São Paulo, Brazil article info abstract Article history: Fungal infections of the respiratory tract of horses are not as frequent as those of bacterial Received 15 September 2015 and viral origin, often leading to worsening of clinical conditions due to misdiagnosis and Received in revised form 9 February 2016 incorrect treatment. Coccidioidomycosis and histoplasmosis are systemic mycoses caused Accepted 9 February 2016 by the dimorphic fungi Coccidioides spp. and Histoplasma capsulatum, respectively, which Available online 21 February 2016 affect humans and a variety of other animals, including equines. These systemic mycoses of chronic and progressive nature can exhibit clinical manifestations similar to other Keywords: microbial infections. Thus, this article broadly discusses the epidemiology, etiology, viru- Coccidioidomycosis Histoplasmosis lence, pathogenesis, clinical presentation, treatment, and diagnostic strategies of coccidi- Equines oidomycosis and histoplasmosis, to support accurate diagnosis.
    [Show full text]
  • Product Sheet Info
    Product Information Sheet for NR-44360 Histoplasma capsulatum, Strain 7090 Citation: Acknowledgment for publications should read “The following Catalog No. NR-44360 reagent was obtained through BEI Resources, NIAID, NIH: Histoplasma capsulatum, Strain 7090, NR-44360.” This reagent is the tangible property of the U.S. Government. Biosafety Level: 3 For research use only. Not for human use. Appropriate safety procedures should always be used with this material. Laboratory safety is discussed in the following Contributor and Manufacturer: publication: U.S. Department of Health and Human Services, Primavera Alvarado, Ph.D., Laboratorio de Micología, Instituto Public Health Service, Centers for Disease Control and de Biomedicina, Caracas, Venezuela Prevention, and National Institutes of Health. Biosafety in Microbiological and Biomedical Laboratories. 5th ed. Product Description: Washington, DC: U.S. Government Printing Office, 2009; see Classification: Ajellomycetaceae, Histoplasma www.cdc.gov/biosafety/publications/bmbl5/index.htm. Species: Histoplasma capsulatum (also referred to as Ajellomyces capsulatus and Emmonsiella capsulata) Disclaimers: Strain: 7090 You are authorized to use this product for research use only. It Original Source: Histoplasma capsulatum (H. capsulatum), is not intended for human use. strain 7090 was isolated in 2000 from a 25-year-old male patient with cutaneous histoplasmosis and history of HIV Use of this product is subject to the terms and conditions of the infection in Caracas, Venezuela.1 BEI Resources Material Transfer Agreement (MTA). The MTA Comment: H. capsulatum, strain 7090 was deposited as a is available on our Web site at www.beiresources.org. pathogenic strain, which was confirmed in mice.1 While BEI Resources uses reasonable efforts to include Histoplasma capsulatum is a thermally dimorphic accurate and up-to-date information on this product sheet, environmental fungus that inhabits soil.
    [Show full text]
  • Genome Analysis Reveals Evolutionary Mechanisms of Adaptation In
    www.nature.com/scientificreports OPEN Genome analysis reveals evolutionary mechanisms of adaptation in systemic dimorphic Received: 16 October 2017 Accepted: 1 March 2018 fungi Published: xx xx xxxx José F. Muñoz 1, Juan G. McEwen2,3, Oliver K. Clay3,4 & Christina A. Cuomo 1 Dimorphic fungal pathogens cause a signifcant human disease burden and unlike most fungal pathogens afect immunocompetent hosts. To examine the origin of virulence of these fungal pathogens, we compared genomes of classic systemic, opportunistic, and non-pathogenic species, including Emmonsia and two basal branching, non-pathogenic species in the Ajellomycetaceae, Helicocarpus griseus and Polytolypa hystricis. We found that gene families related to plant degradation, secondary metabolites synthesis, and amino acid and lipid metabolism are retained in H. griseus and P. hystricis. While genes involved in the virulence of dimorphic pathogenic fungi are conserved in saprophytes, changes in the copy number of proteases, kinases and transcription factors in systemic dimorphic relative to non-dimorphic species may have aided the evolution of specialized gene regulatory programs to rapidly adapt to higher temperatures and new nutritional environments. Notably, both of the basal branching, non-pathogenic species appear homothallic, with both mating type locus idiomorphs fused at a single locus, whereas all related pathogenic species are heterothallic. These diferences revealed that independent changes in nutrient acquisition capacity have occurred in the Onygenaceae and Ajellomycetaceae, and underlie how the dimorphic pathogens have adapted to the human host and decreased their capacity for growth in environmental niches. Among millions of ubiquitous fungal species that pose no threat to humans, a small number of species cause dev- astating diseases in immunocompetent individuals.
    [Show full text]
  • The Global Epidemiology of Emerging Histoplasma Species in Recent Years
    available online at www.studiesinmycology.org STUDIES IN MYCOLOGY ▪: 100095 (2020). The global epidemiology of emerging Histoplasma species in recent years Anderson Messias Rodrigues1*, Mathew A. Beale2, Ferry Hagen3,4,5, Matthew C. Fisher6, Paula Portella Della Terra1, Sybren de Hoog3, Raimunda S^amia Nogueira Brilhante7, Rossana de Aguiar Cordeiro7, Debora de Souza Collares Maia Castelo-Branco7, Marcos Fabio Gadelha Rocha8, Jose Júlio Costa Sidrim7, and Zoilo Pires de Camargo1* 1Laboratory of Emerging Fungal Pathogens, Department of Microbiology, Immunology and Parasitology, Federal University of S~ao Paulo, S~ao Paulo, 04023-062, Brazil; 2Parasites and Microbes Programme, Wellcome Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridge, CB10 1SA, UK; 3Westerdijk Fungal Biodiversity Institute, Utrecht, The Netherlands; 4Department of Medical Microbiology, University Medical Center Utrecht, Utrecht, The Netherlands; 5Laboratory of Medical Mycology, Jining No. 1 People's Hospital, Jining, Shandong, People's Republic of China; 6MRC Centre for Global Infectious Disease Analysis, School of Public Health, Imperial College London, London, UK; 7Specialized Medical Mycology Center, Postgraduate Program in Medical Microbiology, Federal University of Ceara, Fortaleza, Ceara, Brazil; 8Postgraduate Program in Veterinary Science, State University of Ceara, Fortaleza, Ceara, Brazil *Correspondence: Anderson Messias Rodrigues, [email protected]; Zoilo Pires de Camargo, [email protected] Abstract: Histoplasmosis is a serious infectious disease in humans caused by Histoplasma spp. (Onygenales), whose natural reservoirs are thought to be soil enriched with bird and bat guano. The true global burden of histoplasmosis is underestimated and frequently the pulmonary manifestations are misdiagnosed as tuberculosis. Molecular data on epidemiology of Histoplasma are still scarce, even though there is increasing recognition of histoplasmosis in recent years in areas distant from the traditional endemic regions in the Americas.
    [Show full text]
  • Descriptions of Medical Fungi
    DESCRIPTIONS OF MEDICAL FUNGI THIRD EDITION (revised November 2016) SARAH KIDD1,3, CATRIONA HALLIDAY2, HELEN ALEXIOU1 and DAVID ELLIS1,3 1NaTIONal MycOlOgy REfERENcE cENTRE Sa PaTHOlOgy, aDElaIDE, SOUTH aUSTRalIa 2clINIcal MycOlOgy REfERENcE labORatory cENTRE fOR INfEcTIOUS DISEaSES aND MIcRObIOlOgy labORatory SERvIcES, PaTHOlOgy WEST, IcPMR, WESTMEaD HOSPITal, WESTMEaD, NEW SOUTH WalES 3 DEPaRTMENT Of MOlEcUlaR & cEllUlaR bIOlOgy ScHOOl Of bIOlOgIcal ScIENcES UNIvERSITy Of aDElaIDE, aDElaIDE aUSTRalIa 2016 We thank Pfizera ustralia for an unrestricted educational grant to the australian and New Zealand Mycology Interest group to cover the cost of the printing. Published by the authors contact: Dr. Sarah E. Kidd Head, National Mycology Reference centre Microbiology & Infectious Diseases Sa Pathology frome Rd, adelaide, Sa 5000 Email: [email protected] Phone: (08) 8222 3571 fax: (08) 8222 3543 www.mycology.adelaide.edu.au © copyright 2016 The National Library of Australia Cataloguing-in-Publication entry: creator: Kidd, Sarah, author. Title: Descriptions of medical fungi / Sarah Kidd, catriona Halliday, Helen alexiou, David Ellis. Edition: Third edition. ISbN: 9780646951294 (paperback). Notes: Includes bibliographical references and index. Subjects: fungi--Indexes. Mycology--Indexes. Other creators/contributors: Halliday, catriona l., author. Alexiou, Helen, author. Ellis, David (David H.), author. Dewey Number: 579.5 Printed in adelaide by Newstyle Printing 41 Manchester Street Mile End, South australia 5031 front cover: Cryptococcus neoformans, and montages including Syncephalastrum, Scedosporium, Aspergillus, Rhizopus, Microsporum, Purpureocillium, Paecilomyces and Trichophyton. back cover: the colours of Trichophyton spp. Descriptions of Medical Fungi iii PREFACE The first edition of this book entitled Descriptions of Medical QaP fungi was published in 1992 by David Ellis, Steve Davis, Helen alexiou, Tania Pfeiffer and Zabeta Manatakis.
    [Show full text]
  • Epizootic Lymphangitis Is a Debilitating Fungal Disease, Caused by Some Isolates Lymphangitis of Histoplasma Capsulatum, Which Mainly Occurs in Equids
    Epizootic Importance Epizootic lymphangitis is a debilitating fungal disease, caused by some isolates Lymphangitis of Histoplasma capsulatum, which mainly occurs in equids. Its most common form is an ulcerative, suppurative, spreading dermatitis and lymphangitis; however, some Pseudoglanders, animals can develop lesions in other organs, particularly the respiratory tract or eye. Pseudofarcy, Epizootic lymphangitis spreads most readily where large numbers of animals are assembled, and it was a serious problem during the early twentieth century when large Equine Histoplasmosis, numbers of horses were stabled together. This disease has now become uncommon in Histoplasmosis Farciminosi, most countries, though it can still be a significant concern in some areas. Most recent African Farcy, descriptions are from Ethiopia, where equids are widely employed as work animals, Equine Blastomycosis, epizootic lymphangitis is common, and effective treatment can be unaffordable, Equine Cryptococcosis leading to uncontrolled spread of the organism and significant economic losses. Rare clinical cases that appear to be caused by the same organism have also been reported sporadically in other species such as dogs, cats and badgers. Some of these cases were Last Updated: December 2019 recognized in countries thought to be free of epizootic lymphangitis. Etiology Epizootic lymphangitis results from infection by a dimorphic fungus, Histoplasma capsulatum, which exists as a yeast in animal tissues and a saprophytic mycelium (mold) in the environment. This organism is a member of the family Ajellomycetaceae and order Onygenales. Its teleomorph stage is called Ajellomyces capsulatus. Traditionally, H capsulatum has been divided into three subspecies: H. capsulatum var. capsulatum, which causes most cases of histoplasmosis, especially in the Americas; H.
    [Show full text]