1.1 GENERAL INFORMATION CONFERENCE LOCATION Hilo Hawaiian Hotel 71 Banyan Dr Hilo, HI 96720 Telephone: 808-935-9361 USA/Canada Toll Free - 1 (800) 367-5004 Fax: 1 (808) 969-6472 EMERGENCY The nearest hospital to the Hilo Hawaiian Hotel is: Hilo Medical Center 1190 Waianuenue Ave Hilo, HI 96720 Telephone: (808) 974-4700 PARKING Complimentary parking is available for IWOP-11 participants at the Hilo Hawaiian Hotel REGISTRATION AND MESSAGE BOARD The registration desk will be located in the Hilo Hawaiian Hotel Foyer, and open during the following times: Sunday, August 1, 2010; 4:00 6:00pm Monday, August 2, 2010; 7:30am 4:00pm Tuesday, August 3, 2010; 7:30 10:00am Wednesday, August 4, 2010; 7:30am 4:00pm Thursday, August 5, 2010; 7:30am 3:00pm There will be a board available for posting messages in the registration area. HELP DESK Members of the Local Arrangements Committee and the University of Hawaii at Hilo Conference Center Staff can be contacted at the Registration Desk in the Hilo Hawaii Hotel, Ground Level Foyer. SPEAKER READY ROOM The Moku Ola 1 Room will be set up for platform presentations. In an effort to provide you with the best presentation experience and ensure that your needs are met, we would like to outline the presentation review guidelines, laptop specifications, and audiovisual equipment with you. PRESENTATION REVIEW PROCESS We have created a review process to eliminate potential incompatibilities between your personal software versus the presentation software, as well as give you the opportunity to to rehearse your presentation with our audio-visual technician, Robin Black, once you arrive onsite.

2. 2 If you will be using PowerPoint for your presentations, please have a copy of your file on USB/CD-Rom upon registration in the Foyer of the ground level of the Hilo Hawaiian Hotel. Once you have registered, please make an appointment with Robin Kealoha Black, who will be reviewing all talks to ensure a smooth program. MAC Users: If you have created your presentation on a MAC, please visit our website for guidelines in order to have a successful presentation: http://uhhconferencecenter.com/av- guidelines-for-mac-users POSTER BOARDS & SESSION INFO Poster boards are 8' x 4'; each poster presentation should not be larger than 4' x 4' Poster Session A, #s 1-18; Monday, August 2, 2010; 10:30am 12:00pm Set-up: Sunday, August 1, 2010; 4:00 6:00pm Take-down: Monday, August 2, 2010; 5:00 5:30pm** Poster Session B, #s 19 38; Wednesday, August 4, 2010; 10:30 12:00pm Set-up: Monday, August 2, 2010; 5:30 6:00pm Take-down: Thursday, August 5, 2010; 3:00 4:30pm** **Please Note: Any posters left up after the designated take-down periods will be discarded. WEATHER The summer temperatures on the Big Island of Hawaii normally range from 77--80 F (25-- 26.7 C) during the day and from 61--64 F (16.1--17.8C) at night. Hilo is on the windward side of the island where rainfall may be 5--10 times higher than on the leeward side. BE PREPARED FOR ENJOYING IWOP-11 AND OTHER ACTIVITIES IN RAIN. The summer temperatures on the Big Island of Hawaii normally range from 77--80 F (25-- CURRENCY Foreign currency exchanges: Hilo Hawaiian Hotel (no currency exchange available; ATM machine in convenience store); Bank of Hawaii, Kawili Street (Yen, Euro Bank notes, Australian, Canadian, British, Hong Kong, New Zealand, Singapore); Naniloa Hotel (Yen exchange only, ATM machine available at various locations in town. 3. 3 PROGRAM SCHEDULE IN THIS BOOKLET, THE CODE INDICATED AFTER THE PRESENTATION TIME CORRELATES WITH THE CODE ASSIGNED TO EACH ABSTRACT. THE ABSTRACTS ARE FOUND AFTER THE PROGRAM SCHEDULE AND ARE ARRANGED CHRONOLOGICALLY (IN THE ORDER OF PRESENTATION) OR THE POSTERBOARD ASSIGNMENT. AN INDEX OF AUTHORS IS FOUND AT THE END OF THE BOOKLET. SUNDAY, AUGUST 1, 2010 PM 4:00 REGISTRATION OPENS FOYER, LOWER LEVEL 4:00 SET-UP OF POSTERS #1-18 LOWER LEVEL, MOKU OLA II 6:00 - 8:00 OPENING RECEPTION, WELCOME & ANNOUNCEMENTS OPEN TO ALL REGISTRANTS LOWER LEVEL [MOKU OLA BALLROOM AND GARDENS] MONDAY, AUG 2. 2010 AM 7:30 REGISTRATION FOYER, LOWER LEVEL PLATFORM SESSION I MOKU OLA I CO-CHAIRS - CCILE-MARIE ALIOUAT-DENIS, RUSSEL HAYMAN 8:00 PL1 The Biochemistry and Genetics of Mouse Resistance to Toxoplasma gondii: the Role of Immunity-Related GTPases (IRG proteins). J. P. HUNN, A. KHAMINETS, J. LILUE, B. MUELLER, N. PAPIC, N. PAWLOWSKI, T. STEINFELDT, J. C. HOWARD; Institute for Genetics, University of Cologne, Cologne, NRW, Germany. 8:20 PL2 Involvement of Integrin Alpha 2 (ITGA2) in Cryptosporidium parvum Infection. 4. 4 HAILI ZHANG, FENGGUANG GUO, GUAN ZHU; Department of Veterinary Pathobiology, Texas A&M University, TX, USA. 8:40 PL3 Lactosylceramide Mediates Pneumocystis Beta-Glucan Activation of the Human IL-23-IL-17 Axis. EVA M CARMONA, ANDREW H LIMPER. Thoracic Diseases Research Unit, Mayo Clinic, Rochester, MN, USA. 9:00 PL4 Pneumocystis carinii Lanosterol Synthase Requires Saccharomyces cerevisiae 3- Ketoreductase for Localization to Lipid Particles in Yeast. TIFFANY M. JOFFRION,1 MELANIE T. CUSHION1,2 . 1 University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA; 2 Veterans Administration Medical Center, Cincinnati, OH 45220, USA. 9:20 PL5 Characterization of Lanosterol Synthase (Erg7) from Pneumocystis jirovecii. THOMAS M. SESTERHENN,1 A. GEORGE SMULIAN,1,2 MELANIE T. CUSHION1,2 ; 1 University of Cincinnati College of Medicine, Cincinnati, OH, USA, 2 Cincinnnati Veterans Affairs Medical Center, Cincinnati, OH, USA. 9:40 PL6 Bone Marrow Failure and Immune Responses to Pulmonary Pneumocystis (PC) Infection. DAVID TAYLOR, MICHELLE WILKISON, NICOLE MEISSNER, Department of Veterinary Molecular Biology, Montana State University, Bozeman, MT 59718, USA 10:00 BREAK 10:30 POSTER SESSION A - NUMBERS 1-18 MOKU OLA II PO1 Cell Wall Assembly Components of Pneumocystis carinii Exhibit Unique Activity in Response to Alterations in Environmental Temperature. DEANNE M. HEBRINK1 , THEODORE J. KOTTOM1 , ANDREW H. LIMPER1 ; 1 Thoracic Diseases Research Unit, Mayo Clinic, Rochester, MN, USA. PO2 Influence of Climate and Ambient Air Pollutants on Pneumocystis jirovecii Pneumonia (PcP) Hospital Admission and on Antibody Responses to Major Surface Glycoprotein (Msg) in HIV-Infected Patients from San Francisco. K. DJAWE,1 L. HUANG,2 K.R. DALY,1 , L. LEVIN,1 J. KOCH1 , A. SCHWARTZMAN,2 S. FONG,2 B. ROTH,2 , A. SUBRAMANIAN,2 K. GRIECO,2 L. JARLSBERG,2 P.D. WALZER1 . 1 VAMC and U. Cincinnati, Cincinnati, OH, USA, 2 San Francisco General Hospital (SFGH) and U. California SF, San Francisco, CA, USA. PO3 Pneumocystis jirovecii Colonization in Patients Undergoing Treatment with the TNF- Antagonist Agent Infliximab. RUBN MORILLA1 , ISABEL MARTN- GARRIDO1 , GUSTAVO WISSMANN2 , VICENTE FRIAZA1 , NIEVES RESPALDIZA1 , RAFAEL TERAN1 , MARIA T. MARTINEZ-RISQUEZ1 , 5. 5 ELENA CAMPANO1 , FRANCISCO J. MEDRANO1 , CARMEN DE LA HORRA1 , JOS M. VARELA1 , JUAN POVEDANO3 , ENRIQUE J. CALDERN1 ; 1 Instituto de Biomedicina de Sevilla and CIBER de Epidemiologia y Salud Pblica. Service of Internal Medicine Virgen del Rocio University Hospital, Seville, Spain; 2 Grupo de Estudos em Pneumocystis, Servio de Infectologia, Hospital de Clnicas de Porto Alegre, Brasil; 3 Service of Rheumatology, Virgen del Roco University Hospital, Seville, Spain PO4 Dihydropteroate Synthase Mutations in Pneumocystis jirovecii Isolated from Patients with Pneumocystis Pneumonia in Brazil. GUSTAVO WISSMANN1 , ROSECLER B. MENDES1 , VICENTE FRIAZA2 , ANDR L. MLLER1 , RUBEN MORILLA2 , CARMEN DE LA HORRA2 , LUCIANO Z. GOLDANI1 , ENRIQUE J. CALDERN2 ; 1 Grupo de Estudos em Pneumocystis, Servio de Infectologia, Hospital de Clnicas de Porto Alegre, Brasil; 2 Instituto de Biomedicina de Sevilla and CIBER de Epidemiologia y Salud Pblica. Virgen del Rocio University Hospital, Seville, Spain. PO5 DHPS Mutations in Pneumocystis jirovecii Isolated from Patients with PcP in Santiago, Chile. CAROLINA A. PONCE,1 MAGALI CHABE,2 CLAUDIO GEORGE,1 ALEJANDRA CARDENAS,1 LUISA DURAN;2 JULIA GUERRERO,1 LAURENCE HUANG,3 ROBERT F. MILLER,4 SERGIO L. VARGAS1 ; 1 University of Chile School of Medicine, Santiago, Chile, 2 Institute Pasteur du Lille, France, 3 University of California San Francisco, San Francisco, CA, USA, 4 University College London, UK. PO6 Characterization of Mouse Alveolar Macrophage Binding to Pneumocystis murina Cyst and Trophic Forms. A.D. ASHBAUGH, M.J. LINKE, M.T. CUSHION; Veterans Affairs Medical Center, Cincinnati, OH, and University of Cincinnati College of Medicine, Cincinnati, OH. PO7 Human Pathogenic Microsporidia: Detection and Genotyping in HIV-positive and negative patients from Portugal. M. L. LOBO 1 , L. XIAO2 , F. ANTUNES 3 , O. MATOS1 ; 1 Instituto de Higiene e Medicina Tropical, CMDT, UNL, Lisboa, Portugal, 2 Centers for Disease Control and Prevention, Atlanta, GA, USA, 3 Hospital de Santa Maria, FM/UL, Lisboa, Portugal. PO8 QSAR Study of New Inhibitors for Pneumocystis carinii Oxidosqualene Cyclase. ALEKSEY POROLLO1 , MARGARET S. COLLINS1,2 , MELANIE T. CUSHION1,2 ; 1 University of Cincinnati College of Medicine Department of Environmental Health, Cincinnati, OH, USA; 2 University of Cincinnati Department of Internal Medicine and the Cincinnati Veterans Affairs Medical Center, Cincinnati, OH PO9 Factors Influencing the Carriage, Colonization, and Transmission of Pneumocystis carinii. K.A. LYNCH, and M.T. CUSHION, University of Cincinnati College of Medicine and the Cincinnati Veterans Affairs Medical 6. 6 Center, Cincinnati, Ohio, USA. PO10 Microscopic Studies of Anncaliia algerae-Infected Cell Cultures and Analysis of its Beta-Tubulin Gene Suggest Albendazole Sensitivity. MARIANITA SANTIANA, PETER TAKVORIAN, CYRILLA PAU, ANN CALI. Rutgers University, Newark, NJ, USA. PO11 Cryptosporidium spp. in Pet Birds in Henan, China: Prevalence and Molecular Characterizations. MENG QI,1 RONGJUN WANG,1 CHANGSHEN NING,1 LONGXIAN ZHANG,1 FUCHUN JIAN,1 YANRU SUN,1 LIHUA XIAO2 ; 1 The College of Animal Science and Veterinary Medicine, Henan Agricultural University, Zhengzhou 450002, China, 2 Division of Foodborne, Bacterial, and Mycotic Diseases, National Center for Emerging and Zoonotic Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA 30333, USA PO12 Standardization of PCR Primers for gp60-based Subtyping of Cryptosporidium hominis and Cryptosporidium parvum. SATOMI KATO, LIHUA XIAO, Atlanta Research and Education Foundation, Centers for Disease Control and Prevention. PO13 Preliminary Biochemical Data on a Type II Thioesterase from Cryptosporidium parvum (CpTEII). FENGGUANG GUO, GUAN ZHU; Department of Veterinary Pathobiology, Texas A&M University, TX, USA. PO14 Hospital-Based Monitoring of Cryptosporidium parvum, Giardia lamblia and Entamoeba histolytica in the Republic of Korea, 2004-2008. HYENG-IL CHEUN*, YI-YOUNG LIM, SHIN-HYEONG CHO, JUNG-WON JU, SANG- EUN LEE, JEONG-YEON KIM, WON-JA LEE. Division of Malaria and Parasitic Diseases, National Institute of Health, Korea Centers for Disease Control and Prevention, Seoul 122-701, Korea. PO15 Low Prevalence of Pneumocystis Pneumonia (PCP) but High Prevalence of Pneumocystis Dihydropteroate Synthase (DHPS) Gene Mutations in HIV-Infected Persons in Uganda. LAURENCE HUANG,1 STEVE M. TAYLOR,2 WILLIAM WORODRIA,3 , LEAH JARLSBERG,1 J. LUCIAN DAVIS,1 ADITHYA CATTAMANCHI,1 SAMUEL D. YOO,3 ALFRED ANDAMA,3 SASKIA DEN BOON,3 RACHEL KYEYUNE,3 STEVEN MESHNICK,2 . 1 San Francisco, CA, USA, 2 Chapel Hill, NC, USA, 3 Kampala, Uganda. PO16 Variation in the erg11 Gene from Pneumocystis jirovecii. SCOTT P. KEELY,1 JAMES R. STRINGER,1 CARLO CONTINI,2 BETTINA LUNGREN,3 RONALD BRUBAKER4 , LAURA Q. JOHNSTON,5 EDNA S. KANESHIRO5 ; 1 Dept. Molecular Genetics, Biochemistry & Microbiology, 5 Dept. Biological Sciences, Univ. Cincinnati, Cincinnati, OH; 2 Dept. Clinical & Experimental Medicine, Univ. Ferrara, Ferrara, Italy, 3 Dept. Clinical Microbiology, Hvidovre Univ. Hospital, Hvidovre, Denmark. 4 Department of Pathology, Christ Hospital, Cincinnati, OH. 7. 7 PO17 Development of a Multilocus Sequence Typing Tool for Cryptosporidium muris and Cryptosporidium andersoni. YAOYU FENG,1 WENLI YANG,2 UNA RYAN,3 LONGXIAN ZHANG,4 MARTIN KV,5 BETISLAV KOUDELA,5 NA LI,2,6 RONALD FAYER,7 LIHUA XIAO2 ; 1 East China University of Science and Technology, Shanghai, China, 2 Centers for Disease Control and Prevention, Atlanta, GA, USA, 3 Murdoch, Western Australia, Australia, 4 Henan Agricultural University, Zhengzhou, China, 5 Academy of Sciences of the Czech Republic, esk Budjovice, Czech Republic, 6 Tongji University, Shanghai, China,7 U.S. Department of Agriculture, Beltsville, Maryland, USA. PO18 Amoebicidal and Amebastatic Activity In Vitro of the Resin of Gymnosperma glutinosum Against Acanthamoeba castellanii trophozoites. RODRIGUEZ- MONROY MA1 , PEA-JUAREZ MC2 , OMAA-MOLINA M1 , GONZALEZ- ROBLES A3 , SALAZAR-VILLATORO L3 , CANALES-MARTINEZ MM4 .1 Profesor Carrera de Medicina, U.N.A.M. F.E.S. Iztacala. 2 Profesor Carrera de Biologa, U.N.A.M. F.E.S. Iztacala. 3 Departamento de Infectmica y Patognesis Molecular, CINVESTAV, I.P.N., 4 Profesor Carrera de Medicina, U.N.A.M. F.E.S. Iztacala, Edo. Mexico. 12:00 NOON LUNCH QUEEN'S COURT PM 1:00 SYMPOSIUM "HOST RESPONSES TO IMMUNODEFICIENCY-ASSOCIATED DISEASE-CAUSING PROTISTS" MOKU OLA I 1:00 S1 Introduction CHAO-HUNG LEE, Department of Pathology & Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN, USA. 1:30 S2 Role of Host and Parasite Glycans and Glycan-Binding Proteins in Cryptosporidium-Host Cell Interactions. HONORINE D. WARD, NAJMA BHAT, ROBERTA M. CO'CONNOR, Division of Geographic Medicine and Infectious Diseases, Tufts Medical Center, Tufts University School of Medicine, Boston, MA 02111. 2:15 S3 Host Defense against Pneumocystis in Neonates: Lessons for Adults. BETH A. GARVY; Departments of Microbiology, Immunology, and Molecular Genetics and Internal Medicine Division of Infectious Diseases, University of Kentucky and VA Medical Center, Lexington, KY. 3:00 BREAK 8. 8 3:30 S4 Plasmacytoid Dendritic Cells in Aging Animals Down-Regulate Conventional Dendritic Cell Response against Encephalitozoon cuniculi Infection. JASON P GIGLEY, MAAZ SOHAIL, IMTIAZ A KHAN; Department of Microbiology, Immunology and Tropical Medicine George Washington University Medical Center, Washington DC. 4:15 S5 Toxoplasma gondii Infection and Neuropsychiatric Disease. CRAIG W. ROBERTS; Biomedical Sciences, University of Strathclyde, Glasgow, UK. 5:00 REMOVE POSTER SESSION A POSTERS 5:30 SET UP POSTER SESSION B POSTERS EVENING ORGANISM-BASED DINNERS TUESDAY, AUGUST 3, 2010 AM 7:30 REGISTRATION FOYER, LOWER LEVEL PLATFORM SESSION II MOKU OLA I CO-CHAIRS: MALCOLM FINKELMAN, BETTINA LUNDGREN 8:00 PL7 Development of a Multilocus Sequence Typing Tool for High Resolution Genotyping of Enterocytozoon bieneusi. YAOYU FENG,1 NA LI,2,3 THERESA DEAREN, MARIA LUSA LOBO4 , OLGA MATOS4 , 2 LIHUA XIAO3* ; 1 East China University of Science and Technology, Shanghai, China, 2 Centers for Disease Control and Prevention, Atlanta, GA, USA, 3 Tongji University, Shanghai, China, 1 Instituto de Higiene e Medicina Tropical, CMDT, UNL, Lisboa, Portugal. 8:20 PL8 Identification of Proteins of the Microsporidian Invasion Apparatus. KAYA GHOSH,1 , ANN CALI,2 PETER M. TAKVORIAN,2 RUTH HOGUE- ANGELLETI,3 LOUIS M. WEISS1,4 . Departments of 1 Pathology, 3 Developmental and Molecular Biology, and 4 Medicine, Albert Einstein College of Medicine, Bronx, NY 10461, 2 Department of Biological Sciences, Rutgers University, Newark, NJ 07102. 8:40 PL9 Molecular Genotyping of Viable Waterborne Protozoa. CRISTIN C. BRESCIA1 , UKO NWA3 , SHANNON M. GRIFFIN1 , MICHAEL W. WARE1 , EUNICE A.VARUGHESE1 , ANDREY I. EGOROV2 , ERIC N. VILLEGAS1,3 , 1 National Exposure Research Laboratory, 2 National Center for Environmental Assessment, US Environmental Protection Agency, Cincinnati, OH 45268, 3 Department of Biological Sciences, University of Cincinnati, Ohio 45221. 9. 9 9:00 PL10 Evolutionary Affiliation, but Metabolic Diversity between Cryptosporidium and Ascogregarina taiwanensis. GUAN ZHU,1 THOMAS J. TEMPLETON,2 SHINICHIRO ENOMOTO,3 MITCHELL S. ABRAHAMSEN,3 WEI-JUNE CHEN4 ; 1 Department of Veterinary Pathobiology, College of Veterinary Medicine & Biomedical Sciences, Texas A&M University, College Station; TX, USA, 2 Department of Microbiology and Immunology, Weill Cornell Medical College, and the Program in Immunology and Microbial Pathogenesis, Weill Graduate School of Medical Sciences of Cornell University, New York, NY, USA, 3 Department of Veterinary & Biomedical Sciences, University of Minnesota, St. Paul, MN, USA, 4 Department of Public Health and Parasitology, College of Medicine, Chang Gung University, Kwei-San, Tao- Yuan, Taiwan. 9:20 PL11 Metabolic Targets for Controlling Pneumocystis Adenosylmethionine Supply. SALIM MERALI, Department of Biochemistry, Temple University School of Medicine, Philadelphia, Pennsylvania 19140. 9:40 PL12 Pneumocystis jirovecii Multilocus Genotyping using High Throughput Methodologies for Large Scale SNPs Screening. F. ESTEVES1 , J. GASPAR2 , F. ANTUNES3 , K. MANSINHO4 and O. MATOS1 ; 1 Unidade de Protozorios Oportunistas/VIH e Outras Protozooses CMDT, Instituto de Higiene e Medicina Tropical, Universidade Nova de Lisboa, 2 Departamento de Gentica, Faculdade de Cincias Mdicas, Universidade Nova de Lisboa, 3 Clinica Universitria de Doenas Infecciosas, Faculdade de Medicina, Universidade de Lisboa, Hospital de Santa Maria, 4 Servio de Doenas Infecciosas, Hospital de Egas Moniz, Lisboa, Portugal. 10:00 FIELD TRIPS/TOURS/FREE TIME AKAKA FALLS & BOTANICAL GARDENS FIELD TRIP (w/ Lunch) HAWAII VOLCANO NATIONAL PARK FIELD TRIP (w/ Lunch) EVENING ORGANISM-BASED DINNERS WEDNESDAY, AUGUST 4, 2010 AM 7:30 REGISTRATION FOYER, LOWER LEVEL PLATFORM SESSION III MOKU OLA I CO-CHAIRS: ANN CALI, SALIM MERALI 8:00 PL13 Pseudoloma neurophilia and Pleistophora hyphessobriconis; the Causes of Two Important Microsporidial Diseases in Zebrafish, Danio rerio. MICHAEL L. KENT, JUSTIN SANDERS, VIRGINIA WATRAL, Department of Microbiology, Oregon State University, Corvallis, Oregon. 10. 10 8:20 PL14 HIV Treatment as Prevention for the Development of Protist Infections: Year 2010. JENS LUNDGREN, University of Copenhagen and State University Hospital, Panum Institute, 2200 Copenhagen N, Denmark. 8:40 PL15 An Adhesion-Induced Signaling Cascade in Pneumocystis carinii: Potential Role of the Downstream PcAce2 Transcription Factor in Cell Wall Remodeling. ANDREW H. LIMPER, THEODORE J. KOTTOM; Thoracic Diseases Research Unit, Mayo Clinic, Rochester, MN, USA. 9:00 PL16 Heterologous Systems Expressing the Recombinant Pneumocystis carinii S- Adenosyl-L-Methionine: Sterol C-24 Methyltransferase. LAURA Q. JOHNSTON, EDNA S. KANESHIRO, Dept. Biological Sciences, Univ. Cincinnati, Cincinnati, OH, USA. 9:20 PL17 Sequences of the erg11 Gene from P. jirovecii, P. carinii, P. murina and Pneumocystis from the Rhesus Macaque Monkey. SCOTT KEELY,1 JAMES R. STRINGER,1 MICHAEL J. LINKE,3 TAKAHISA FURUTA,4 EDNA S. KANESHIRO2 . 1 Dept. Molecular Genetics, Biochemistry & Microbiology, and 2 Dept. Biological Sciences, Univ. Cincinnati, Cincinnati, OH, 3 Veterans Affairs Medical Center, Cincinnati, OH, 4 Dept. Microbiology and Immunology, Institute of Medical Science, Univ. Tokyo, Tokyo, Japan. 9:40 PL18 Molecular Epidemiology of Cryptosporidium and Giardia in Children in Shanghai, China. FENG, Y.Y.1* , WANG, L2 , DUAN, L.P.2 , GOMEZ-PUERTA, L.A.2 , XIAO, L.2 *, 1 East China University of Science and Technology, Shanghai 200237, China; 2 Centers for Disease Control and Prevention, Atlanta, Georgia 30341, USA. 10:00 BREAK 10:30 POSTER SESSION B #19-36 PO19 DNA Replication Continues in Pneumocystis carinii Trophic Forms Treated with the -1,3-Glucan Synthesis Inhibitor Pneumocandin L-693,989. MICHAEL A. WYDER, LAURA Q. JOHNSTON, EDNA S. KANESHIRO, Department of Biological Sciences, University of Cincinnati, Cincinnati, OH, USA. PO20 Pneumocystis carinii Cell Wall Chitins Induce Host Lung Responses. L.R. VILLEGAS, T.J. KOTTOM, A.H. LIMPER, Thoracic Disease Research Unit, Mayo Clinic College of Medicine, Rochester, MN 55905. PO21 Alternative Activation of Alveolar Macrophages and Alteration of NFB Signaling Results in a Reduced Response to Pneumocystis Infection by Neonates. CATE KURKJIAN,1,2 MELISSA HOLLIFIELD,1,2 BRIAN S. MURPHY,1 BETH A. GARVY,1,2 . 1 Department of Microbiology, Immunology and Molecular 11. 11 Genetics and Division of Infectious Diseases, University of Kentucky, and 2 VA Medical Center, Lexington, KY. PO22 Radiation-Induced Alteration of the Cryptosporidium parvum Oocyst Proteome. SOO-UNG LEE1 , MIKYO JOUNG1 , KYOUNGJIN CHOI1 , WOO-YOON PARK2 , YOUNG-HOON JI3 , JAE-RAN YU1 . 1 Konkuk University, School of Medicine Seoul, Republic of Korea, 2 College of Medicine, Chungbuk National University, Cheongju, Republic of Korea, 3 Korea Institute of Radiological and Medical Sciences, Seoul, Republic of Korea PO23 An Approach to Investigate the Proteome of Pneumocystis carinii. VICENTE FRIAZA1 , ANNA MARTINEZ2,3 , CARMEN DE LA HORRA1 , CECILE- MARIE ALIOUAT-DENIS2,3 , NIEVES RESPALDIZA1 , ANNIE VITSE2,3 , RUBEN MORILLA1 , ELENA CAMPANO1 , EDUARDO DEI-CAS2,4 , ENRIQUE J. CALDERON1 ; 1 Instituto de Biomedicina de Sevilla and CIBER de Epidemiologia y Salud Pblica. Virgen del Rocio University Hospital, Seville, Spain, 2 Biology and Diversity of Emergent Eukaryotic Pathogens (BDEEP) (EA3609), IFR142, Institut Pasteur de Lille & 3 Department of Parasitology- Mycology, Faculty of Biological and Pharmaceutical Sciences, University of Lille Nord de France, Lille, France, 4 Department of Parasitology-Mycology, Faculty of Medicine, University of Lille Nord de France, Biology-Pathology Centre, University Hospital Center, Lille, France. PO24 Comparison of Proteomic Profiles in the Bronchoalveolar Lavage Fluid of Idiopathic Pulmonary Fibrosis Patients with and without Pneumocystis Colonization. VICENTE FRIAZA1 , CARMEN DE LA HORRA1 , RUBEN MORILLA1 , NIEVES RESPALDIZA1 , MARCO A. MONTES-CANO1 , LAURA RIVERO1 , SONIA GUTIERREZ1 , ELENA CAMPANO1 , ISABEL MARTIN- GARRIDO1 , JOSE M.VARELA1 , FRANCISCO J. MEDRANO1 , JOSE MARTIN-JUAN1 , JUAN PARRADO2 , JUAN BAUTISTA2 , ENRIQUE J. CALDERON1 ; 1 Instituto de Biomedicina de Sevilla and CIBER de Epidemiologia y Salud Pblica. Virgen del Rocio University Hospital, Seville, Spain. 2 Departamento de Bioqumica y Biologa Molecular, Universidad de Sevilla, Seville, Spain. PO25 Association of Idiopathic Pulmonary Fibrosis Severity and Pneumocystis jirovecii Colonization. NIEVES RESPALDIZA1 , ISABEL MARTIN-GARRIDO1 , EDUARDO MARQUEZ-MARTIN2 , VICENTE FRIAZA1 , SONIA GUTIERREZ1 , RUBEN MORILLA1 , LAURA RIVERO1 , ELENA CAMPANO1 , RAFAEL TERAN1 , MARCO A. MONTES-CANO1 , JOSE M.VARELA1 , FRANCISCO J. MEDRANO1 , JOSE MARTIN-JUAN2 , CARMEN DE LA HORRA1 , ENRIQUE J. CALDERON1 ; 1 Instituto de Biomedicina de Sevilla and CIBER de Epidemiologia y Salud Pblic; 2 Servicio de Neumologa, Virgen del Rocio University Hospital, Seville, Spain. PO26 Treatment of Pneumocystis carinii with Sodium Nitrite in Suspension or Biofilm Cultures Dramatically Reduces Viability. M.T. CUSHION1,2 , M.S. COLLINS1,2 , 12. 12 D.J. HASSETT3 ; 1 University of Cincinnati College of Medicine, Department of Internal Medicine; 2 Cincinnati Veterans Affairs Medical Center, Cincinnati, Ohio; 3 University of Cincinnati College of Medicine, Department of Molecular Genetics, Biochemistry and Microbiology, Cincinnati, OH PO27 The Effect of Oxygen on Viability, Sterol Uptake, and Transcriptional Responses in Pneumocystis carinii. TIFFANY M. JOFFRION,1,* MARGARET S. COLLINS,1 MELANIE T. CUSHION1,2 . 1 University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA; 2 Veterans Administration Medical Center, Cincinnati, OH 45220, USA. PO28 Morphometrics of Assemblages of Giardia duodenalis Cysts from the Feces of Dogs and Cats. HEEJEONG YOUN,1 DWIGHT D. BOWMAN,2 STEPHANIE B. YAGER,2 BRITTA A. OKYERE,2 BO LI,2 DAVID KYUHYUNG KANG,2 MARISSA KARPOFF,2 HYUN JI KIM,2 HUSSNI O. MOHAMMED,2 ARACELI LUCIO-FORSTER,2 JANICE L. LIOTTA.2 1 College of Veterinary Medicine, Seoul National University, Seoul, Korea; 2 Department of Microbiology & Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY, USA. PO29 Use of the Luna Stain Allows Specific, Rapid and Unequivocal Detection of Pseudoloma neurophilia Spores in Formalin Fixed Zebrafish Tissue Sections. TRACY S. PETERSON, MICHAEL L. KENT, Department of Microbiology, Oregon State University, Corvallis, Oregon. PO30 Seroprevalence and in vitro Isolation of Toxoplasma gondii from Chronically Infected Pigeons in Portugal. HELGA WAAP1 , RITA CARDOSO2,3 , HELENA NGELO4 , ANABELA VILARES4 , HELDER CORTES5 , JOS MEIRELES3 , ALEXANDRE LEITO2 ; 1 Instituto Nacional de Recursos Biolgicos-LNIV, Lisbon, Portugal, 2 Instituto de Investigao Cientfica e Tropical, CIISA, Lisbon, Portugal, 3 Faculdade de Medicina Veterinria, CIISA, Lisbon, Portugal, 4 Instituto Nacional de Sade Dr. Ricardo Jorge, Lisbon, Portugal, 5 Laboratrio de Parasitologia Victor Caeiro (ICAAM) Universidade de vora, Portugal. PO31 Prevalence, Genetic Characteristics, and Zoonotic Potential of Cryptosporidium in Farm Rabbits in China. KE SHI1 , FUCHUAN JIAN1 , CHAOCHAO LV1 , CHANGSHEN NING1 , LONGXIAN ZHANG1, 2, 3 *, XUPENG REN1 , THERESA K. DEAREN2 , NA LI2 , MENG QI1 , LIHUA XIAO2 *; 1 College of Animal Science and Veterinary Medicine, Henan Agricultural University, Zhengzhou 450002, P. R. China, 2 Atlanta Research and Education Foundation, 1670 Clairmont Road, Decatur, GA 30033, USA, 3 Division of Foodborne, Bacterial and Mycotic Diseases, National Center for Emerging and Zoonotic Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA 30333, USA. PO32 Cryptosporidium parvum Induces an Invasive Intestinal Adenocarcinoma in 13. 13 Immunosupressed Hosts. GABRIELA CERTAD,1 SADIA BENAMROUZ- HAMRAOUI,1, 2 KARINE GUYOT,1 ANTHONY MOURAY,3 THIERRY CHASSAT,3 BAPTISTE DELAIRE,4 VALERIE CONSEIL,2 EDUARDO DEI- CAS,1, 5 COLETTE CREUSY,4 ; 1 BDPEE-EA3609- Biologie et Diversit des Pathognes Eucaryotes Emergents, IFR142-Institut Pasteur de Lille France, 2 Laboratoire Environnement et Sant, FLST, Universit Catholique de Lille, Universit Lille Nord-de-France, 3 Plateau dExprimentation Animale, Institut Pasteur de Lille, France, 4 Service dAnatomie et Cytologie Pathologiques, Groupe Hospitalier de lUniversit Catholique de Lille, France, 5 Service dParasitologie- Mycologie, CHRU de Lille, Universit Lille Nord-de-France, France. PO33 Distribution of Pneumocystis Colonization in the Human Lung. SHEILA SIVAM,1 FRANK C. SCIURBA,1 LORRIE LUCHT,1 YINGZE ZHANG,1 STEVEN R. DUNCAN,1 KAREN A NORRIS,2 ALISON MORRIS1,2 . 1 Department of Medicine, 2 Department. of Immunology, University of Pittsburgh, Pittsburgh, Pennsylvania. PO34 Isolation and Biological Characterization of Free-Living Amoeba Isolated from Clinical Cases of Amoebic Keratitis, Contact Lenses and Lens Solutions. MARITZA OMAA-MOLINA1 , REN MNDEZ-CRUZ1 , ARTURO GONZLEZ-ROBLES2 , MARCO RODRGUEZ-MONROY1 , ELIZABETH RAMREZ-FLORES1 , MA. DOLORES HERNNDEZ-MARTNEZ1 , MA. ESTHER INIESTRA-SOLRZANO1 , ALEXANDER BERNAL-ESCOBAR1 . 1 School of Superior Studies Iztacala, UNAM. Los Reyes Iztacala, Tlalnepantla, Mexico State, Mexico. 2 Department of Infectomic and Molecular Pathogenesis Center for Research and Advanced Studies, Mexico City, Mexico. PO35 Pneumocystis jirovecii Colonization in Elderly Adults Admitted to the Hospital with Community-Acquired Pneumonia in Santiago, Chile. MARILZ HERNANDEZ, PATRICIA PIZARRO, ANDREA ARAYA, REBECA BUSTAMANTE, CAROLINA A. PONCE, SERGIO L. VARGAS. University of Chile School of Medicine, Santiago, Chile. PO36 Molecular Epidemiology of Cryptosporidium in HIV Patients in Henan, China. LING WANG,1,2 XUDONG ZHAO,3 HONGWEI ZHANG,3 LONGXIAN ZHANG,4 LIHUA XIAO,2 YAOYU FENG1 ; 1 East China University of Science and Technology, Shanghai, China, 2 Centers for Disease Control and Prevention, Atlanta, Georgia, USA, 3 Henan Provincial Center for Disease Control and Prevention, Zhengzhou, China, 4 Henan Agricultural University, Zhengzhou, China. 12:00 LUNCH QUEEN'S COURT 14. 14 PM PLATFORM SESSION IV MOKU OLA I CO-CHAIRS: SATOMI KATO, EVA CARMONA 1:00 PL19 Development of a Multiplex-PCR/Single Base Extension Methodology for Pneumocystis jirovecii Genotyping. F. ESTEVES1 , J. GASPAR2 , F. ANTUNES3 , K. MANSINHO4 and O. MATOS1 ; 1 Unidade de Protozorios Oportunistas/VIH e Outras Protozooses CMDT, Instituto de Higiene e Medicina Tropical, Universidade Nova de Lisboa, 2 Departamento de Gentica, Faculdade de Cincias Mdicas, Universidade Nova de Lisboa, 3 Clinica Universitria de Doenas Infecciosas, Faculdade de Medicina, Universidade de Lisboa, Hospital de Santa Maria, 4 Servio de Doenas Infecciosas, Hospital de Egas Moniz, Lisboa, Portugal. 1:20 PL20 Propylene Glycol Induces Pseudocyst Formation in Acanthamoeba spp. JARMILA KLIESCIKOVA, EVA HORACKOVA, EVA NOHYNKOVA, Department of Tropical Medicine, 1st Medical Faculty, Charles University in Prague and Faculty Hospital Bulovka, 128 00 Prague 2, Czech Republic. 1:40 PL21 Autophagy-Related Processes in Toxoplasma gondii. DEBASISH GHOSH, JULIA WALTON, ANTHONY P. SINAI*. Department of Microbiology, Immunology and Molecular Genetics, University of Kentucky College of Medicine, 800 Rose St. Lexington, KY 40536. 2:00 ROUND TABLE DISCUSSION I "FUTURE OF FUNDING FOR OPPORTUNISTIC PROTIST RESEARCH" MOKU OLA I CO-CHAIRS: ANTHONY SINAI; MELANIE T. CUSHION 3:00 BREAK PLATFORM SESSION V MOKU OLA I CO-CHAIRS: NICOLE MEISSNER, SCOTT KEELY 3:30 PL22 Evaluating the Effects of Chemical Sanitizers and UV Irradiation on Toxoplasma gondii Oocyst Viability. MICHAEL W. WARE,1 SWINBURNE A. J. AUGUSTINE,1 DAVID O. ERISMAN,1 LEAH FOHL VILLEGAS,1 MARY JEAN SEE,2 SAMUEL L. HAYES,3 LARRY WYMER,1 H. D. ALAN LINDQUIST,4 FRANK W. SCHAEFER III,4 J. P. DUBEY,5 ERIC N. VILLEGAS1,2* ; 1 National Exposure Research Laboratory, 3 National Risk Management Research Laboratory, 4 National Homeland Security Research Center, U.S. Environmental Protection Agency, Cincinnati, OH 45268; 2 Department of Biological Sciences, University of Cincinnati, Cincinnati, OH 15. 15 45220; 5 Animal Parasitic Disease Laboratory, Agricultural Research Service, U.S. Department of Agriculture, Beltsville, MD, 20705 3:50 PL23 Identification of the Microsporidium Anncaliia algerae as the Causative Agent of a Human Vocal Cord Infection. ANN CALI,1 RONALD NEAFIE,2 LOUIS M. WEISS,3 KAYA GHOSH,4 RACHNA GUPTA,5 REBECCA B. VERGARA,6 PETER M. TAKVORIAN,1,3 . 1 Department of Biological Sciences, Rutgers University, Newark, NJ 07102, 2 American International Pathology Laboratories, Silver Spring, MD 20910, 3 Department of Pathology, Division of Parasitology and Tropical Medicine, Albert Einstein College of Medicine, Bronx, NY 10461, 4 Department of Microbiology and Immunolgy, Albert Einstein College of Medicine, Bronx, NY 10461, 5 ID Care, 105 Raider Blvd. Suite 101, Hillsborough, NJ 08844, 6 Department of Pathology, Newton Memorial Hospital, Newton NJ 07860 . 4:10 PL24 Wildtype CD4 T Cells have Increased Bcl2 Expression in Response to Pneumocystis Infection. MICHAEL M. OPATA, MELISSA L. HOLLIFIELD, BETH A. GARVY; Department of Microbiology, Immunology and Molecular Genetics, University of Kentucky College of Medicine and VA Medical Center, Lexington, KY 40536 USA. 4:30 PL25 Diagnosis and Age Distribution of Primary Infection by Pneumocystis jirovecii: A Study on Autopsied Lungs. SERGIO L. VARGAS1 ; CAROLINA .A. PONCE1 ; J. ASTORGA3, M. GALLO2 ; MAGALI CHABE3 ; ISABELLE DURAND- JOLY3 , EL MOUKHTAR ALIOUAT3 , EDUARDO DEI CAS3 . 1 Biomedical Sciences Institute, University of Chile School of Medicine, 2 Servicio Mdico Legal, Santiago, Chile and, 3 Pasteur Institute of Lille, France. 4:50 PL26 Genetic Mapping of Virulence Genes of Cryptosporidium hominis. NA LI,1,2,3 LIHUA XIAO,1 VITALIANO A. CAMA,1 YNES ORTEGA,4 ROBERT H. GILMAN,5 YAOYU FENG6 ; 1 Centers for Disease Control and Prevention, Atlanta, GA, USA, 2 Atlanta Research and Education Foundation, Atlanta, GA, USA, 3 Tongji University, Shanghai, China, 4 University of Georgia, Griffin, GA, USA, 5 Johns Hopkins University, Baltimore, MD, USA, 6 East China University of Science and Technology, Shanghai, China. 6:00 INTERNATIONAL DINNER W/ ENTERTAINMENT MOKU OLA BALLROOM AND GARDENS THURSDAY, AUGUST 5, 2010 AM 7:30 REGISTRATION FOYER, LOWER LEVEL 16. 16 PLATFORM SESSION VI MOKU OLA I CO-CHAIRS: SHEILA SIVAM, GUAN ZHU 8:00 PL27 Pneumocystis (13)--D-Glucan (BG): Role in Diagnosis and Potential Contribution to Pathophysiology. MALCOLM A. FINKELMAN; Associates of Cape Cod, Inc., Falmouth, MA, USA 8:20 PL28 The Biochemistry and Genetics of Mouse Resistance to Toxoplasma gondii: the Role of Immunity-Related GTPases (IRG proteins). J. P. HUNN, A. KHAMINETS, J. LILUE, B. MUELLER, N. PAPIC, N. PAWLOWSKI, T. STEINFELDT, J. C. HOWARD; Institute for Genetics, University of Cologne, Cologne, NRW, Germany. 8:40 PL29 Acanthamoeba culbertsoni Elicits Soluble Factors that Exert Anti-Microglial Cell Activity. FRANCINE MARCIANO-CABRAL, JENICA L. HARRISON, GABRIELA A. FERREIRA, ERINN S. RABORN, AUDREY D. LAFRENAYE, GUY A. CABRAL; Virginia Commonwealth University, School of Medicine, Richmond, VA, USA 9:00 PL30 Functional Complementation of Saccharomyces cerevisiae erg11 Deletion Mutant by the Pneumocystis carinii erg11 cDNA and Comprehensive Identification of >20 Sterols in Wild Type and Transformed Yeast Cells. STEPHENSON W. NKININ,1 JAMES R. STRINGER,2 SCOTT KEELY,2 KENNETH D.R. SETCHELL,3 JOS-LUIS GINER,4 EDNA S. KANESHIRO1 . 1 Dept. Biological Sciences, and 2 Dept. Molecular Genetics, Biochemistry & Microbiology, University of Cincinnati, Cincinnati, OH; 3 Dept. Pediatrics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, 4 Dept. Chemistry, SUNY-ESF, Syracuse, NY, USA. 9:20 PL31 Effect of Calmodulin on Phagocytic Activity of Alveolar Macrophages during Pneumocystis Pneumonia. CHUNG-PING LIAO, JINGHONG WANG, PAMELA J. DURANT, CHAO-HUNG LEE,* Department of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA 9:40 BREAK PLATFORM SESSION VII MOKU OLA I CO-CHAIRS: LAURENCE HUANG, TIFFANY JOFFRION 10:10 PL32 MicrosporidiaDB a New Integrated Genomic Resource. LOUIS M. WEISS,1,2 OMAR S. HARB,3 DAVID S. ROOS3 for the EuPathDB Team 3,4 . Departments of 1 Pathology and 2 Medicine, Albert Einstein College of Medicine, Bronx, NY, 10461; 3 Department of Biology, University of Pennsylvania, Philadelphia, PA, 17. 17 19104., 4 Department of Genetics, University of Georgia, Athens, GA, 30602. 10:30 PL33 Adherence and Internalization of Cryptosporidium parvum Oocysts Associated with Fresh Produce. RONALD FAYER, DUMITRU MACARICIN, GARY BAUCHAN, MONICA SANTIN-DURAN; USDA, Agricultural Research Service, Beltsville, Maryland, USA. 10:50 PL34 Blastocystis hominis Induces Increased Permeability of HT-29 Polarized Monolayers and Resists Phagocytosis by Macrophages. LUIZ BERMUDEZ,1,2 VIRGINIA WATRAL,2 BRITTANY MORGAN,2 SASHA ROSE,1 MICHAEL KENT 2,1 , 1 Department of Biomedical Sciences, College of Veterinary Medicine, Oregon State University, Corvallis OR, 97331, 2 Department of Microbiology, Oregon State University, Corvallis OR, 97331 11:10 ROUND TABLE DISCUSSION II "NOMENCLATURE: HOW SHOULD WE ABBREVIATE GENES, CDNA, GENE PRODUCTS, ETC. IN OPPORTUNISTIC PROTIST PUBLICATIONS?. WHAT ARE BEING USED AND CAN WE ACHIEVE UNIFORMITY?" CHAIR: ANDREW LIMPER, LOUIS WEISS DISCUSSANTS: MELANIE T. CUSHION, LIHUA XIAO 12:00 NOON LUNCH QUEEN'S COURT PM PLATFORM SESSION VIII MOKU OLA 1 CO-CHAIRS: YAOYU FENG, ERIC VILLEGAS 1:00 PL35 -Microsporidia Spore Adherence in a Mouse Animal Model. CORY A. LEONARD, J. RUSSELL HAYMAN; East Tennessee State University, James H. Quilllen College of Medicine, Johnson City, TN. 1:20 PL36 Transcriptomic Approaches to Study Stage-Specific Genes of Pneumocystis carinii. ANNA MARTINEZ,1 MAGALI CHABE,1 MELANIE CUSHION,2 CHRISTINE HUBANS,3 DAVID HOT,4 EDUARDO DEI-CAS,5 EL MOUKHTAR ALIOUAT,1 CECILE-MARIE ALIOUAT-DENIS,1 ; 1 BDEEP- EA3609-Laboratoire de Parasitologie-Mycologie, Facult de Pharmacie de Lille, Universit Lille Nord-de-France & IFR142-Institut Pasteur de Lille, France, 2 University of Cincinnati College of Medicine, Dept of Internal Medicine, Division of Infectious Diseases, Cincinnati Veterans Administration Medical Center, Cincinnati, Ohio, USA, 3 Genoscreen Company, Campus de lInstitut Pasteur de Lille, France, 4 TAG Transcriptomics and Applied Genomics 18. 18 UMR8161, Institut Pasteur de Lille, France, 5 BDEEP-EA3609-IFR142-Institut Pasteur de Lille & Service de Parasitologie-Mycologie, CHRU de Lille, Universit Lille Nord-de-France, France. 1:40 PL37 Pneumocystis S-Adenosylmethionine Transport. OSCAR PEREZ-LEAL,1 CAMILO MONCADA,1 ALLEN B. CLARKSON,2 SALIM MERALI1 , 1 Department of Biochemistry, Temple University School of Medicine, Philadelphia, Pennsylvania 19140 and 2 Department of Medical Parasitology, New York University School of Medicine, New York, New York 10016. 2:00 PL38 Pneumocystis Occurrence in Wild Rodents from South East Asia. MAGALI CHABE,1 VINCENT HERBRETEAU,2 JEAN-PIERRE HUGOT,3 YANNICK CHAVAL,4 EDUARDO DEI-CAS,5 SERGE MORAND6 ; 1 BDEEP-EA3609- Laboratoire de Parasitologie-Mycologie, Facult de Pharmacie de Lille, Universit Lille Nord-de-France & IFR142-Institut Pasteur de Lille, France, 2 Cemagref, UMR TETIS, Montpellier, France & IRD, UR178, Mahidol University, Nakhon Pathom, Thailand, 3 OSEB, UMR 5202 CNRS, Musum National dHistoire Naturelle, Paris, France, 4 Centre de Biologie et de Gestion des Populations (CBGP), Campus International de Baillarguet, Montferrier sur Lez, France, 5 BDEEP-EA3609-IFR142-Institut Pasteur de Lille & Service de Parasitologie-Mycologie, CHRU de Lille, Universit Lille Nord-de-France, France, 6 Institut des Sciences de l'Evolution CNRS-UM2, Universit Montpellier 2, France. 2:20 PL39 Yeast Proteome Substrate Microarrays Provide Novel Insights into Pneumocystis carinii PcCbk1 and PcSte20 Signaling Biology. THEODORE J. KOTTOM1 , ANDREW H. LIMPER1 ; 1 Thoracic Diseases Research Unit, Mayo Clinic, Rochester, MN, USA. 2:40 CLOSING COMMENTS Looking to the Future - LOUIS WEISS 3:00 BREAK 3:00-4:30 POSTER SESSION B TAKE DOWN MOKU OLA II 19. 19 ABSTRACTS PL1 The Biochemistry and Genetics of Mouse Resistance to Toxoplasma gondii: the Role of Immunity-Related GTPases (IRG proteins). J. P. HUNN, A. KHAMINETS, J. LILUE, B. MUELLER, N. PAPIC, N. PAWLOWSKI, T.STEINFELDT, J. C. HOWARD; Institute for Genetics, University of Cologne, Cologne, NRW, Germany. Toxoplasma gondii strains differ greatly in their virulence for mice. Relatively avirulent strains are confronted by the interferon-g- inducible IRG proteins that accumulate on the cytosolic face of the parasitophorous vacuole (1). These vesiculate and ultimately rupture the vacuolar membrane, leading to the death of the parasite (1, 2). This confrontation attenuates the infection and enables the parasite to effect the bradyzoite transition and encystment without prejudice to the host. Loss of IRG proteins by genomic disruption disturbs this equilibrium and greatly enhances the virulence of genetically avirulent strains (3). Virulent strains, by contrast, resist the initial loading of IRG proteins onto the parasitophorous vacuole and replicate uncontrollably (4, 5). The IRG proteins are large, self-activating GTPases with dynamin- like features. Their function depends on a dynamic control system, exercised by three regulatory members of the family acting as guanine nucleotide dissociation inhibitors, that maintains the effector IRG proteins in the inactive GDP-bound (6). This control is released upon infection with avirulent strains by the formation of the parasitophorous vacuole membrane (PVM) on which effector IRG proteins rapidly accumulate in the GTP- bound active form (7). It follows that IRG proteins should be the targets for virulence factors derived from T. gondii, and we will present evidence that virulent strains can inactivate IRG proteins. We will also put the dynamic relationship between genetically variable T. gondii strains and mice into an ecological context and show that there is a corresponding polymorphic variation in the IRG resistance proteins, enabling certain wild mouse IRG genotypes to resist virulent T. gondii strains. We argue that resistance to T. gondii is largely driving the recent evolution of the IRG system in the mouse (8). References: (1) Martens et al, 2005. PLoS Pathogens 1(3):e24 (73); (2) Zhao, YO et al, 2009. PLoS Pathog 5(2): e1000288; (3) Taylor, GA et al, 2007 Microbes Infect. 9:1644; (4) Zhao, YO et al, 2009. Memorias do Instituto Oswaldo Cruz. 104(2):234-40; (5) Khaminets, A et al, 2010, Cellular Microbiology, Epub ahead of print, PMID: 20109161; (6) Hunn, JP et al, 2008, EMBO Journal, 27(19):2495-509; (7) Papic, N et al, 2008 J. Biological Chemistry 283(46):32143- 51; (8) Hunn, JP and Howard, JC, 2010 PLoS Pathogens, in press. PL2 Involvement of Integrin Alpha 2 (ITGA2) in Cryptosporidium parvum Infection. HAILI ZHANG, FENGGUANG GUO, GUAN ZHU; Department of Veterinary Pathobiology, Texas A&M University, TX, USA. Cryptosporidium parvum interacts with host cell membrane during invasion and development. However, very little is known on the host cell membrane proteins that interact with C. parvum. We have previously observed from our microarray and qRT-PCR date that gene expression profiles of several extracellular membrane (ECM) proteins 20. 20 changed upon C. parvum infection, such as some host cell integrin subunits. For example, the expression of integrin A2 (ITGA2) was increased by ~40% upon C. parvum infection, implying that integrins might be involved in interacting with parasite. To further test the hypothesis, we generated several stable ITGA2 knockdown lines of HCT-8 cells using plasmid-based RNA interference technology. We observed constant ~20% reduction of parasite invasion in the ITGA2-knockdown cells in comparison with controls. Furthermore, parasite invasion was also decreased by 20-30% in HCT-8 cell treated with ITGA2-specific antibodies. These observations suggest that human ITGA2, and probably other integrin subunits might participate in interacting with C. parvum. PL3 Lactosylceramide Mediates Pneumocystis Beta-Glucan Activation of the Human IL- 23-IL-17 Axis. EVA M CARMONA, ANDREW H LIMPER. Thoracic Diseases Research Unit, Mayo Clinic, Rochester, MN, USA. Respiratory failure in Pneumocystis pneumonia is believed to be due largely to an exaggerated host inflammatory response to the organism rather than to the organism burden itself. Prior data from our laboratory demonstrated that dendritic cells (DC) play an important role orchestrating this inflammatory response. In particular, stimulation of DC by Pneumocystis beta-glucans (PCBG) induced a cytokine environment rich in IL-1 that favored a Th1 phenotype with subsequent IFN- production. Recent data have revealed that fungal pathogens are also potent inducers of Th17 cells. Moreover, IL-17R deficient mice have poor defense against some fungal infections. Therefore, this study was designed to investigate whether PCBG-stimulated-DCs participate in Th17 differentiation and to study the molecular mechanisms that mediate this process. In addition, we investigated the role of lactosylceramide; a glycosphingolipid important in PC based inflammation, in modulating this axis. Methods: Human DCs derived from peripheral blood monocytes were stimulated with PCBG prior to co- culture with nave CD4 cells. Cytokine secretion important for Th17 differentiation was measured by ELISA in the supernatant of these cells. NF-B activation was also analyzed in nuclear and cytosolic extracts after stimulation with PCBG. A lactosylceramide inhibitor, PDMP, was used to study the role of glycosphingolipids as costimulatory molecule in PCBG induced IL- 23- IL7 axis. Results: We observed that PCBG activates the IL-23-IL-17 axis. Secondly, PCBG induces activation of both the classical and the alternative pathways of NF- B in DC. We further demonstrated that PDMP decreases IL-23 production through NF-B. Conclusions: These findings provide evidence that PCBG matured-DC elicits activation of the IL-23-IL-17 pathway though activation of both the classical and the alternative pathways of NF-B. Our data also indicates that lactosylceramide is crucial for activation of this pathway. Further investigations are needed, but these studies provide further evidence of lactosylceramide as new tool to modulate the inflammatory response induced by PCBG in the immunocompromised host. PL4 Pneumocystis carinii Lanosterol Synthase Requires Saccharomyces cerevisiae 3- Ketoreductase for Localization to Lipid Particles in Yeast. TIFFANY M. JOFFRION,1 MELANIE T. CUSHION1,2 . 1 University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA; 2 Veterans Administration Medical Center, Cincinnati, OH 45220, USA. Organisms in the genus Pneumocystis are ubiquitous, opportunistic fungi capable of 21. 21 causing a lethal pneumonia in immunocompromised mammalian hosts. Pneumocystis spp. are unique members of the fungal kingdom due to the absence of ergosterol in their cellular membranes. Although thought to obtain cholesterol by scavenging, transcriptional analyses indicate that Pneumocystis carinii encodes gene homologs involved in sterol biosynthesis. To better understand the sterol pathway in these uncultivable fungi, yeast deletion strains were used to interrogate the function and localization of P. carinii lanosterol synthase (ERG7) to lipid particles, which requires a 3- ketoreductase (ERG27) in yeast. Expression of PcErg7p in an ERG7 null mutant of the yeast Saccharomyces cerevisiae did not alter its growth rate and produced functional lanosterol synthase, as evidenced by the presence of lanosterol detected by gas chromatographic analysis in levels comparable to that produced by the yeast enzyme. Western blotting revealed that like the S. cerevisiae Erg7p, the PcErg7p localized to lipid particles in yeast with a functional ERG27p, but this trafficking was interrupted in an ERG27 deletion strain. In P. carinii, the presence of PcErg7p in apparent lipid particles was detected by fluorescence microscopy. By using the yeast heterologous system, we show for the first time that the P. carinii lanosterol synthase localizes to lipid particles and that this targeting requires the 3-ketoreductase encoded by ERG27. Moreover, the yeast heterologous system should be a useful tool for further analysis of the P. carinii sterol pathway. PL5 Characterization of Lanosterol Synthase (Erg7) from Pneumocystis jirovecii. THOMAS M. SESTERHENN,1 A. GEORGE SMULIAN,1,2 MELANIE T. CUSHION1,2 ; 1 University of Cincinnati College of Medicine, Cincinnati, OH, USA, 2 Cincinnnati Veterans Affairs Medical Center, Cincinnati, OH, USA. Although the introduction of HAART has resulted in a marked reduction of Pneumocystis pneumonia (PCP) in AIDS patients, mortality remains at the same rate today as it was in the pre-HAART era (10- 15%). The rate is even higher in non-AIDS patients. There is a critical need for new therapeutic options for PCP due to problems of toxicity with current drugs and the potential of emerging resistance to standard therapies. One proposed target for an alternate Pneumocystis therapy is the sterol biosynthesis pathway. This pathway produces sterol components essential for viability in these organisms. One enzyme in the pathway, Erg7, is responsible for the production of lanosterol, the first sterol intermediate of the mammalian and fungal sterol biosynthesis pathways. Recent studies in our laboratory using a combined in silico discovery platform and in vitro screening system have identified potential inhibitors to the P. carinii Erg7p (PcErg7). Although drug responses in animal models have been reflective of activity in humans, it would be desirable to screen these putative scaffolds against the P. jirovecii Erg7 (PjErg7). To that end, portions of a putative PjErg7 gene were amplified by PCR from clinical isolates using degenerate primers based on the sequence of Erg7 from P. carinii and several other closely related fungi. The putative PjErg7 sequence was found to have a high homology to PcErg7. Additionally, in silico analysis showed a number of consistencies between the two genes, including conserved catalytic domains and predicted trans-membrane regions. Previous studies by our lab and others have established a set of tools that provided evidence for the function and localization of the PcErg7. We propose to apply these tools to the putative PjErg7 to see if there is correlation between the function and localization of PjErg7 and PcErg7. [Supported by the National Institutes 22. 22 of Health NIAID N01AI-25467, R01 AI050450 and R01AI44651; and the Department of Veterans Affairs] PL6 Bone Marrow Failure and Immune Responses to Pulmonary Pneumocystis (PC) Infection. DAVID TAYLOR, MICHELLE WILKISON, NICOLE MEISSNER, Department of Veterinary Molecular Biology, Montana State University, Bozeman, MT 59718, USA. We recently demonstrated in a mouse model that lack of type I IFN-signaling in lymphocyte competent mice (IFNAR-/- mice) results in bone marrow (BM) depression, lymphocyte-deficiency ( RAG-/- mice) does not significantly affect hematopoiesis. However, lack of both lymphocytes and IFNAR (IFrag-/- mice) results in BM failure due to apoptosis of all lineages following Pneumocystis (PC) lung infection. Infection with other fungal pathogens such as Cryptococcus did not induce BM failure. BM failure following PC infection was also associated with loss of bone mass. Here we further examined mechanisms involved in the induction of BM failure in our system. We found that lack of IFNAR-signaling during PC lung infection resulted in increased oxidative stress in BM cells and increased osteoclast activity, as measured by TRAP assay. Increased total Caspase activity in BM cells correlated with cell loss. Extensive kinetic studies revealed that signals at day 7 post infection appeared critical in determining the outcome of disease. Quantitative RT-PCR at day 7 demonstrated excessive up-regulation of iNOS in BM cells from IFrag-/- mice compared to RAG-/- mice, significantly reduced expression of OPG, a decoy receptor for the apoptosis-inducing cytokine TRAIL and the osteoclast-differentiation factor RANKL, and down-regulation of the anti- apoptotic factor Bcl10, Bcl2, Birc2 (IAP) and others. Caspase 8 activity, as the initiator caspase for the extrinsic pathway of apoptosis, was induced in BM cells of both IFrag-/- and RAG-/- mice following PC lung infection. However, only in IFrag-/- mice was the executioner caspase 3 also induced which is followed by apoptosis. Conclusion: We propose that lack of type-I-IFN-signaling negatively affects the regulation of oxidative stress, decoy mechanisms for TRAIL and RANKL in BM cells as well as anti-apoptotic mechanisms. This may have accelerated BM cell death following systemic responses to PC lung infection resulting in BM failure due to excessive induction of Capase activity via the extrinsic pathway of apoptosis. Support: RO1HL090488 and COBRE 2P20RR020185- 06 PO1 Cell Wall Assembly Components of Pneumocystis carinii Exhibit Unique Activity in Response to Alterations in Environmental Temperature. DEANNE M. HEBRINK1 , THEODORE J. KOTTOM1 , ANDREW H. LIMPER1 ; 1 Thoracic Diseases Research Unit, Mayo Clinic, Rochester, MN, USA. Pneumocystis carinii is an opportunistic organism that causes pneumonia in immune- compromised hosts. Recent studies in our lab have reported interesting responses in P. carinii life cycle proteins to alterations in environmental temperature (Burgess et al., Am J Resp Cell Molec Biol 2009). The purpose of this study was to investigate the effects of variations in environmental temperature the organism may encounter on components of the cell-wall assembly machinery such as 1,3- -glucan synthase, which is involved in synthesizing the main structural component of the cell wall, namely 1,3--glucan. The activity of the 1,3--glucan synthase enzyme was determined at incubation temperatures ranging from 4o C to 45o C by measuring 23. 23 incorporation of [14 C]-uridine 5- diphosphoglucose (UDP-glucose), the substrate for the enzyme into insoluble carbohydrate. Interestingly, these experiments revealed the enzyme is most active at temperatures between 4o C and 25o C and dramatically lower at physiologically relevant temperatures such as 37o C. Real-time PCR data further confirmed a similar temperature response at the transcript level for PcGsc-1 with greater RNA expression at 4o C and 10o C compared to physiological temperatures. RNA expression for transcripts that encode other proteins involved in cell-wall biogenesis such as PcCdc42, PcMsg1, and PcKre6 also have higher RNA expression at sub- physiological temperatures while RNA expression for other regulatory genes including PcCdc13 and PCFlo8 do not seem to be influenced by changes in environmental temperature. Lastly, future aims will determine whether environmental temperature has any effect on the overall metabolic activity of P. carinii by measuring cellular ATP production in Pneumocystis after short-term culture at these temperatures. These studies suggest that temperatures more typically found outside of the mammalian host are more conducive to processes involved in cell-wall assembly and provide interesting insights into the life cycle of P. carinii. PO2 Influence of Climate and Ambient Air Pollutants on Pneumocystis jirovecii Pneumonia (PcP) Hospital Admission and on Antibody Responses to Major Surface Glycoprotein (Msg) in HIV-Infected Patients from San Francisco. K. DJAWE, MS1 , L. HUANG, MD2 , K.R. DALY, PHD1 , L. LEVIN, PHD1 , J. KOCH1 , A. SCHWARTZMAN, BS2 , S. FONG, BA2 , B. ROTH, MPH2 , A. SUBRAMANIAN, MD2 , K. GRIECO, DO2 , L. JARLSBERG, BA2 , P.D. WALZER, MD, MSC1 . 1 VAMC and U. Cincinnati, Cincinnati, OH, United States, 2 San Francisco General Hospital (SFGH) and U. California SF, San Francisco, CA, United States. Background: Pneumocystis jirovecii pneumonia (PcP) is an important opportunistic infection in immunocompromised patients. The influence of seasonality on this fungal infection is not well established. Furthermore, the influence of ambient air pollutants on PcP incidence is unknown. The Major Surface Glycoprotein (Msg) is a crucial protein complex in Pneumocystis pathogenicity and is involved in host-organism interaction. Different risk factors have been associated with antibody responses to recombinant Msg fragments, but the influence of climate and air pollutants on antibody responses to Msg fragments is unknown. Objectives: The objectives of this study are to determine the influence of climate and ambient air pollutants on PcP incidence and on antibody responses to Pneumocystis Msg recombinant fragments. Methods: From January 1, 2000 to December 31, 2008, 140 HIV+ patients were admitted at San Francisco General Hospital (SFGH) with confirmed PcP. Daily climate data from San Francisco were collected from the California Irrigation Management Information System (CIMIS) website, and daily pollutants data were collected from San Francisco EPA website. Logistic regression was used to determine the risk of PcP associated with different environmental parameters at the time of hospital admission and at different lag times (29-31 days and 59-61 days before admission). Tobit regression was used to estimate the effect of climate and air pollutants on antibody responses to the Msg fragments. Results: We found that PcP hospital admission was associated with higher temperature and higher ozone levels, but only the effect of temperature was significant (P = 0.02). In contrast, lower humidity, rainfall, CO, NO2 and SO2 was insignificantly associated with an increase in PcP admission. 24. 24 Only lower lag humidity 29-31 days was significantly associated with an increase in PcP admission (P = 0.01). None of the parameters had a lag 59-61 days significant effect on PcP. We also found significant seasonal variations in antibody responses to MsgA, the amino terminus fragment (P = 0.01), but not to MsgC, the carboxyl terminus fragment. Both temperature and CO levels had significant effects on antibody responses to MsgA, but only humidity had a significant effect on antibody responses to MsgC when controlling for CD4 cell counts. Conclusion: Thus, climate and ambient air pollutants have complex effects on the occurrence of, and antibody responses to PcP, in San Francisco. Further investigation of these factors should help in understanding of the epidemiologic features of PcP. PO3 Pneumocystis jirovecii Colonization in Patients Undergoing Treatment with the TNF- Antagonist Agent Infliximab. RUBN MORILLA1 , ISABEL MARTN- GARRIDO1 , GUSTAVO WISSMANN2 , VICENTE FRIAZA1 , NIEVES RESPALDIZA1 , RAFAEL TERAN1 , MARIA T. MARTINEZ-RISQUEZ1 , ELENA CAMPANO1 , FRANCISCO J. MEDRANO1 , CARMEN DE LA HORRA1 , JOS M. VARELA1 , JUAN POVEDANO3 , ENRIQUE J. CALDERN1 ; 1 Instituto de Biomedicina de Sevilla and CIBER de Epidemiologia y Salud Pblica. Service of Internal Medicine Virgen del Rocio University Hospital, Seville, Spain; 2 Grupo de Estudos em Pneumocystis, Servio de Infectologia, Hospital de Clnicas de Porto Alegre, Brasil; 3 Service of Rheumatology, Virgen del Roco University Hospital, Seville, Spain. Infliximab, a chimeric anti-tumor necrosis factor (TNF)- monoclonal antibody, has become an established effective therapy for inflammatory rheumatic disease. However, TNF- is a critical factor in host defense and the suppression of its biological activity may be associated with the increased risk of opportunistic infections. The frequent use of infliximab in clinical practice has identified Pneumocystis jirovecii pneumonia (PcP) as a serious complication. Individuals colonized with Pneumocystis may be at high risk of development of PcP when they have undergone immunosuppressive therapies. Hence, we addressed the question of the frequency of Pneumocystis colonization among patients treated with infliximab. We examined 125 oropharyngeal washes (OW) collected from 78 individuals with rheumatoid arthritis, 30 with ankylosing spondylitis and 17 with psoriatic arthritis. Half of them had undergone infliximab therapy. Using a real- time polymerase chain reaction assay based on the amplification of the large subunit of mitochondrial DNA (mtLSU rDNA) of Pneumocystis, P. jirovecii colonization was detected in 32 (25,6%) patients. Colonization was associated with use of corticosteroid and methotrexate, but only duration of infliximab therapy was significantly and independently associated with Pneumocystis colonization in a multivariate regression model. There is a high rate of P. jirovecii colonization among patients with rheumatologic diseases treated with infliximab. The identification of patients colonized by P. jirovecii before starting the treatment with infliximab using noninvasive samples as OWs could be a strategy for PcP prevention that warrants further investigation for its validation. PO4 Dihydropteroate Synthase Mutations in Pneumocystis jirovecii Isolated from Patients with Pneumocystis Pneumonia in Brazil. GUSTAVO WISSMANN1 , ROSECLER B. MENDES1 , VICENTE FRIAZA2 , ANDR L. MLLER1 , RUBEN 25. 25 MORILLA2 , CARMEN DE LA HORRA2 , LUCIANO Z. GOLDANI1 , ENRIQUE J. CALDERN2 ; 1 Grupo de Estudos em Pneumocystis, Servio de Infectologia, Hospital de Clnicas de Porto Alegre, Brasil; 2 Instituto de Biomedicina de Sevilla and CIBER de Epidemiologia y Salud Pblica. Virgen del Rocio University Hospital, Seville, Spain. Pneumocystis pneumonia (PcP) is a common opportunistic infection causing morbidity and mortality in immunocompromised patients, particularly in HIV-infected individuals. A combination of trimethoprim (TMP) and sulfamethoxazole (SMX) is the first choice for both prophylaxis and treatment of PcP. Several studies have showed an association between the failure of sulfa prophylaxis and the presence of mutations in P. jirovecii dihydropteroate synthase (DHPS) gene, especially at nucleotide positions 165 and 171 which entail an amino acid change at positions 55 and 57. Bronchoalveolar lavage samples were obtained from 11 PcP patients from January to September 2007 at the Hospital de Clnicas de Porto Alegre, Brazil. The DNA was extracted using a commercial kit (Qiagen, Hilden, Germany). A touchdown PCR using the primers DHPS-3 (5-GCG CCT ACA CAT ATT ATG GCC ATT TTA AAT C-3) and DHPS-4 (5-GGA ACT TTC AAC TTG GCA ACC AC-3) was used to amplify the DHPS gene. DHPS polymorphisms, at codons 55 and 57, were detected by using AccI and HaeIII restriction enzymes. The P. jirovecii DHPS gene was amplified successfully in samples from 9 of 11 patients (82%). DHPS wild type 55/Thr, 57/Pro were detected in 7 patients, and mutations were obtained in two patients (one had a single mutation 55/Thr, 57/Ser and the other had a double mutation 55/Ala, 57/Ser). The absence of P. jirovecii DHPS mutations was reported from Brazilian PcP patients during 1997-2004. The present study could detect mutant genotypes in samples collected during 2007 in Brazil. As PcP is a common opportunistic infection in patients with AIDS in developing countries, it will be important to monitor the prevalence of P. jirovecii DNA mutations related to resistance to sulfa-drugs in these countries. PO5 DHPS Mutations in Pneumocystis jirovecii Isolated from Patients with PcP in Santiago, Chile. CAROLINA A. PONCE,1 MAGALI CHABE,2 CLAUDIO GEORGE,1 ALEJANDRA CARDENAS,1 LUISA DURAN;2 JULIA GUERRERO,1 LAURENCE HUANG,3 ROBERT F. MILLER,4 SERGIO L. VARGAS1 ; 1 University of Chile School of Medicine, Santiago, Chile, 2 Institute Pasteur du Lille, France, 3 University of California San Francisco, San Francisco, CA, USA, 4 University College London, UK. Trimethoprim-sulfamethoxazole (TMP- SMZ) is the mainstay of therapy and prophylaxis for P. jirovecii pneumonia (PcP). Concern about emerging resistance has been raised because mutations in the fas gene coding for the dihydropteroate synthase (DHPS) enzyme, a target for sulfa drugs, has been described in 4-81% of P. jirovecii isolates in different parts of the world. P. jirovecii isolates from 94 patients (median age, 39 years; range, 5-82 years) whose respiratory samples were referred to our laboratory in Santiago, Chile for diagnostic analysis between 2002 2010, and confirmed as PcP by Gomori-Grocott stain and fluorescent-labeled monoclonal antibody stain or PCR, were evaluated for mutations at positions 165 and 171 using Touch Down PCR with primers DHPS-3 and DHPS-4 and restriction enzymes Accl and Hae lll for RFLP-PCR analyses. Mutations were classified according to the pattern of band polymorphisms visualized by UV in 2% agarose gel with ethidium bromide. Fas gene 26. 26 polymorphisms were detected in 43 (45.7%) of the 94 patients. Five (5.3%) were found to have a single mutation at position 165; one (1.1%) had a single mutation at position 171. Fifteen (16.0%) had double mutations at positions 165 and 171. Twelve (12.8%) patients were found to have co-infections with wild type and a mutation at position 165; and 10 (10.6%) had wild type plus double mutations. DHPS mutations are frequent in Chile and their relationship with clinical outcome of PcP needs to be explored especially since TMP-SMZ is the only therapeutic option in our country. [Fondecyt 1060750] PO6 Characterization of Mouse Alveolar Macrophage Binding to Pneumocystis murina Cyst and Trophic Forms. A.D. ASHBAUGH, M.J. LINKE, M.T. CUSHION; Veterans Affairs Medical Center, Cincinnati, OH, and University of Cincinnati College of Medicine, Cincinnati, OH. Alveolar macrophages are the primary phagocytic cells in the lung and are the principal effector cells involved in clearance of Pneumocystis infection. Several alveolar macrophage receptors have been shown to be involved in Pneumocystis binding and uptake facilitated by Pneumocystis glycoproteins and -1,3-D-glucan. However, it is unknown whether all life cycle forms of Pneumocystis are bound and taken up by alveolar macrophages and if so, whether different receptors are used for each form. Echinocandin treatment (ECH) of Pneumocystis-infected mice has been shown to shift the population to one made up of almost exclusively trophic forms. The ECH mouse model was used to interrogate the binding and phagocytosis of P. murina by alveolar macrophages. Alveolar macrophages from mouse lungs were adhered to 10 well glass slides at a concentration of 104 macrophages/well. Fluorescently labeled mixed populations of P. murina from control mice or enriched trophic populations from ECH mice were added to the macrophages, incubated and attachment assessed by fluorescent microscopy. Results were expressed as the percentage of alveolar macrophages with at least one 1 attached organism. Preliminary data showed binding averages of 55% (36% cysts and 19% trophs) and 49% (33% cysts and 16% trophs) when P. murina concentrations of 4 x 105 and 2 x 105 organisms/well were used, respectively. When the ECH P. murina were used at the same concentrations, the binding averages were reduced to 36% (5% cysts and 31% trophs) and 31% (5% cysts and 26% trophs) respectively. This data suggests a higher affinity of cyst binding to alveolar macrophages than trophs due to their more complex surface antigen profile. Further experiments are needed to better understand the fate of each life cycle form in alveolar macrophage mediated clearance. PO7 Human Pathogenic Microsporidia: Detection and Genotyping in HIV-positive and negative patients from Portugal. M. L. LOBO 1 , L. XIAO2 , F. ANTUNES 3 , O. MATOS1 ; 1 Instituto de Higiene e Medicina Tropical, CMDT, UNL, Lisboa, Portugal, 2 Centers for Disease Control and Prevention, Atlanta, GA, USA, 3 Hospital de Santa Maria, FM/UL, Lisboa, Portugal. Most cases of microsporidiosis are associated with severe depletion of the patients immune system. The main goal of this study was to provide information on the occurrence of microsporidia involved in humans in Portugal, and evaluate their public health importance. Stool from 856 children and adults (561 HIV-positive, 255 HIV- negative, 29 persons with undetermined HIV 27. 27 status, and 9 with other immunosuppressions) with gastrointestinal complains, urine from 50 patients (40 HIV-positive and 10 HIV- negative), and pulmonary specimens from 200 patients (150 HIV-positive and 50 HIV- negative) were analysed for the presence of microsporidia by PCR. The presence of Enterocytozoon bieneusi and the Vittaforma- like parasite were detected in 6.3% (54/856) and 6.8% (58/856) of stool samples, respectively. A statistically significant association was observed between microsporidia infection and age; children were at a significantly higher risk of infection than adults. Encephalitozoon intestinalis was identified in 2% (1/50) of urine samples. Encephalitozoon cuniculi and Vittaforma-like parasite were each identified in 0.5% (1/200) of the pulmonary specimens studied. Genotyping analysis confirmed the presence of pathogenic microsporidia in Portuguese patients. Data from the study showcase the harmful role of microsporidia in susceptible populations. (Supported in part by Associao para a Investigao e Desenvolvimento da Faculdade de Medicina de Lisboa. ML Lobo is supported by PhD grant-SFRH/BD/34674/2007-FCT) PO8 QSAR Study of New Inhibitors for Pneumocystis carinii Oxidosqualene Cyclase. ALEKSEY POROLLO1 , MARGARET S. COLLINS1,2 , MELANIE T. CUSHION1,2 ; 1 University of Cincinnati College of Medicine Department of Environmental Health, Cincinnati, OH, USA; 2 University of Cincinnati Department of Internal Medicine and the Cincinnati Veterans Affairs Medical Center, Cincinnati, OH Pneumocystis pneumonia (PcP) remains a significant opportunistic infection in patients with compromised immune systems. The limited repertoire of treatment alternatives and emerging resistance to the standard anti-PcP therapies drives the search for new chemotherapeutic agents. In this work, we focused on the oxidosqualene cyclase (OSC) enzyme in the sterol biosynthesis pathway using Pneumocystis carinii (Pc) as a model organism. In contrast to the efforts to identify specific inhibitors for its active site, we evaluated another structural cavity as an alternative target. This structural site is involved in OSC enzymatic function and contains amino acids conserved among the fungi. Using large scale virtual screening, three new classes of inhibitors for OSC were identified. An array of compounds, derivatives of these classes, was experimentally validated using an in vitro drug screening system for Pc. A cytotoxicity assay to determine potential toxicity was conducted using the mammalian cell lines, A549 (human) and L2 (rat). Here, we report results of the in vitro assays and corresponding observed quantitative structure- activity relationships (QSAR). Of 35 total compounds evaluated, 3 compounds were found to show marked anti-Pc activity, 4 and 12 with moderate and slight activity, respectively. The active compounds exhibit various levels of cytotoxicity, including 2 inhibitors of the desired efficacy with 1:10 activity/toxicity ratio. [Supported by the Midwest Center for Emerging Pathogens, Cincinnati OH; National Institute of Environmental Sciences NIEHS P30- ES006096; National Institutes of Health NIAID N01AI-25467, R01 AI050450 and R01AI44651; and the Department of Veterans Affairs]. PO9 Factors Influencing the Carriage, Colonization, and Transmission of Pneumocystis carinii. K.A. LYNCH, and M.T. CUSHION, University of Cincinnati College of Medicine and the Cincinnati 28. 28 Veterans Affairs Medical Center, Cincinnati, Ohio, USA. Studies suggest that Pneumocystis can exist with little consequence to hosts with intact immune systems, although the length of resident time within the lung is not known nor the host factors that may influence colonization in hosts with intact immune systems. Likewise, the widespread prevalence of Pneumocystis in these immune competent (IC) populations suggests an efficient mechanism of transmission. In the present study we evaluated the effects of gender and age of IC rats on length of P. carinii (Pc) colonization and ability to transmit the infection. In the 1st study, the period of carriage of Pc in IC male and female rats at different ages (weanling, juvenile, adult) was determined after intra-tracheal inoculation of 2 x 107 Pc followed by PCR with Rc1 and Rc2 primers of oral swabs taken for up to 1 year. Once the rats had 3 consecutive negative oral swabs they were sacrificed and their lung tissue was processed and verified for lack of Pc by PCR. Time to clearance ranged from 169 d to 190 d with no significant differences among the groups, although weanling and juvenile females trended towards earlier clearance than males. In the 2nd study, adult IC male and female rats were inoculated as above, and immunosuppressed at 2-, 4- and 6 months post inoculation to determine whether Pc were infective to the host after short to long periods of carriage. Rats immunosuppressed after 2 months of carriage produced significantly more infections in 5/8 (female) and 6/8 (male) rats than rats after 4-6 months of carriage (0-2 rats per group), without difference between genders. In the 3rd study, the influence of age on the transmission in IC rats was evaluated. IC intra-tracheally inoculated donor weanling, juvenile and adult female rats were housed with age-matched uninoculated IC female recipients for a total of 14 pairs. Oral swabs were taken on a daily basis up until 14 days of exposure. Seven matched pairs in each group that were positive by 7-days exposure were removed, separated, and immunosuppressed. The remaining 7 pairs were co-housed for 14 days, separated and immunosuppressed. Juvenile rats were the first to become positive for Pc with all 7 of the early group turning positive in 2 days. Weanlings took an average of 7 days of exposure and adults 9 days of exposure. However, resultant infections were generally higher in the adult recipients. Interestingly, with 1 exception, the recipient rats had higher burdens than the donor rats. Under the conditions described here, gender does not appear to play a role in clearance of Pc in IC rats. IC rats infected with Pc were efficient in transmitting the infection to IC recipients, but the time in which Pc in IC rats that could produce an active infection was limited to less than 4 months, suggesting there is a constant circulation of Pc in IC populations. [Supported by National Institutes of Health NIAID N01AI-25467, R01 AI050450 and R01AI44651 and by the Medical Research Service, Department of Veterans Affairs] PO10 Microscopic Studies of Anncaliia algerae- Infected Cell Cultures and Analysis of its Beta-Tubulin Gene Suggest Albendazole Sensitivity. MARIANITA SANTIANA, PETER TAKVORIAN, CYRILLA PAU, ANN CALI. Rutgers University, Newark, NJ, USA. The microsporidium, Anncaliia algerae (Brachiola algerae), is an obligate intracellular parasite. It has been identified as an opportunistic human pathogen but treatment has not been evaluated for infection with this organism. Albendazole has been the medication of choice used to treat other microsporidial infections affecting humans, with varying results. We have studied various parameters of albendazole treatment during infection in rabbit kidney cells and have found 29. 29 that treatment causes abnormalities to the structure of the intracellular stages of the parasite. Sustained albendazole treatment also has an attenuating effect on infection, inhibiting up to 98% of spore production, but release from treatment re-establishes the infection without new exposure to the parasite. In addition, we also performed an analysis of the beta-tubulin gene sequence and found that 5 of the 6 specific amino acids, which are highly suggestive of benzimidazole sensitivity, are conserved among Anncaliia algerae and other organisms sensitive to albendazole. Results from this study give an insight to a possible long-term treatment for Anncaliia algerae infections that can be affordable and widely available. PO11 Cryptosporidium spp. in Pet Birds in Henan, China: Prevalence and Molecular Characterizations. MENG QI,1 RONGJUN WANG,1 CHANGSHEN NING,1 LONGXIAN ZHANG,1 FUCHUN JIAN,1 YANRU SUN,1 LIHUA XIAO2 ; 1 The College of Animal Science and Veterinary Medicine, Henan Agricultural University, Zhengzhou 450002, China, 2 Division of Foodborne, Bacterial, and Mycotic Diseases, National Center for Emerging and Zoonotic Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA 30333, USA To characterize the prevalence of Cryptosporidium species/genotypes in pet birds in Henan, China, 434 fecal samples were acquired from 14 families of birds in pet shops. The overall prevalence of Cryptopsoridium was 8.1% (35/434) by the Sheathers sugar flotation technique. The Cryptosporidium-positive samples were analyzed by DNA sequence analysis of the small subunit (SSU) rRNA gene. Three Cryptosporidium species and two genotypes were identified, including C. baileyi (18/35 or 51.4%) in five red-billed leiothrixes (Leiothrix lutea), four white Java sparrows (Padda oryzivora), four common mynas (Acridotheres tristis), two zebra finches (Taeniopygiagutttata), a crested Lark (Galerida cristata), a Gouldian finch (Chloebia gouldiae), and a black-billed magpie (Pica pica); Cryptosporidium meleagridis (3/35 or 8.6%) in a Bohemian waxwing (Bombycilla garrulus), a Rufous turtle dove (Streptopelia orientalis), and a fan- tailed pigeon (Columba livia); Cryptosporidium galli (5/35 or 14.3%) in four Bohemian waxwings (Bombycilla garrulus) and a silver-eared Mesia (Leiothrix argentauris); Cryptosporidium avian genotype III (3/35 or 8.6%) in two cockatiels (Nymphicus hollandicus) and a red-billed blue magpie (Urocissa erythrorhyncha); and Cryptosporidium avian genotype V (6/35 or 17.1%) in six cockatiels (Nymphicus hollandicus). Among the pet birds, 12 species represented new hosts for Cryptosporidum infecitons. This is the first report of cryptosporidiosis in pet birds in China. PO12 Standardization of PCR Primers for gp60-based Subtyping of Cryptosporidium hominis and Cryptosporidium parvum. SATOMI KATO, LIHUA XIAO, Atlanta Research and Education Foundation, Centers for Disease Control and Prevention. The 60 kDa glycoprotein (gp60 or cpgp15/45) gene has been widely used for subtyping human-pathogenic Cryptosporidium spp. However, there are no standardized primers for PCR analysis and poor PCR sensitivity has been a major issue associated with the gp60 subtyping. In this study, we assessed the specificity and sensitivity of 43 published primers. Primers with narrow specificity were eliminated based on sequence polymorphism in the primer region identified 30. 30 with an alignment of nucleotide sequences from major subtype families of C. hominis and C. parvum. Based on this, 10 forward and 9 reverse primers were further evaluated using DNA preparations of major subtype families of C. hominis (Ia, Ib, Id, and Ie) and C. parvum (IIa, IIc, and IId) and real-time PCR. Three outer primer combinations, gp15ATG/HW4, HW3/HW4, and S60.ATGF/gp15extR, and two inner primer combinations, AL3532/LX0375 and AL3532/AL3535, produced better amplifications. These primers were able to amplify DNA of all major subtype families of C. hominis and C. parvum. Based on amplification efficiency in real-time PCR, the combination of S60.ATGF/gp15extR in primary PCR and AL3532/AL3535 in secondary PCR was selected. The use of standardized gp60 primers should improve the gp60-based subtyping and promote its use in molecular epidemiologic investigations of cryptosporidiosis. PO13 Preliminary Biochemical Data on a Type II Thioesterase from Cryptosporidium parvum (CpTEII). FENGGUANG GUO, GUAN ZHU; Department of Veterinary Pathobiology, Texas A&M University, TX, USA. The genome of Cryptosporidium parvum encodes a type II thioesterase (TEII) ortholog. This is unique to Cryptosporidium as TEII is absent in other apicomplexans. To understand its potential role in the parasite, we cloned the CpTEII gene and expressed its product as maltose-binding protein (MBP)-fused protein for biochemical analysis. We have tested its activity towards acyl-CoAs with various chain lengths (C4 to C24) and discovered that CpTEII is only able to hydrolyze C6- to C12-length acyl-CoAs. It displays the highest activity towards decanoyl CoA. The preliminary biochemical data is in line with our hypothesis that CpTEII might play a similar role as in bacteria, i.e., the removal of aberrant acyl chains from polyketide synthases (PKSs). We are currently studying its activity towards acyl-acyl carrier protein (ACP) derived from C. parvum fatty acid synthase (CpFAS1) and polyketide synthase(CpPKS1) to further delineate the potential involvement of CpTEII in the fatty acid/polyketide synthesis in the parasite. PO14 Hospital-Based Monitoring of Cryptosporidium parvum, Giardia lamblia and Entamoeba histolytica in the Republic of Korea, 2004-2008. HYENG-IL CHEUN*, YI-YOUNG LIM, SHIN- HYEONG CHO, JUNG-WON JU, SANG- EUN LEE, JEONG-YEON KIM, WON-JA LEE. Division of Malaria and Parasitic Diseases, National Institute of Health, Korea Centers for Disease Control and Prevention, Seoul 122-701, Korea. Infectious status of Cryptosporidium parvum, Giardia lamblia and Entamoeba histolytica as water- and food-borne parasite was investigated in hospital-based diarrheal patients in the Republic of Korea from 2004 to 2008. A total of 104,483 stool samples were collected from the across nation in 106 hospitals. Infections in different age groups, gender and seasonal distribution was analyzed. Fecal samples that were positive for C. parvum, G. lamblia and E. histolytica were 0.5, 0.5 and 0.3%, respectively. There was not significant difference by gender for C. parvum (P = 0.3748), G. lamblia (P = 0.1796) and E. histolytica (P = 0.8362). If those over 60- years old was taken as the reference group, positivity of 2-9 years olds (P = 0.0019) was significantly higher in C. parvum, however all age group were lower than the over-60 age group with respect to infection with G. lamblia and E. histolytica. Analyses of infections during certain years showed that C. 31. 31 parvum and E. histolytica infections were highest during the 2004-2005 period, however G. lamblia infections were significantly lower during 2004-2005 compared to other years. Analyses of seasonality, C. parvum and G. lamblia infections peaked during March and September, and E. histolytica infections peaked in June. Information on hospital-based protozoa in terms of patient gender, age, and seasonal patterns would improve diarrheal medical care, reduce the burden of acute gastrointestinal infections and help the development of control strategies for diarrheal diseases in the Republic of Korea. PO15 Low Prevalence of Pneumocystis Pneumonia (PCP) but High Prevalence of Pneumocystis Dihydropteroate Synthase (DHPS) Gene Mutations in HIV-Infected Persons in Uganda. LAURENCE HUANG, MD1 , STEVE M. TAYLOR, MD, MPH2 , WILLIAM WORODRIA, MBCHB, MMED3 , LEAH JARLSBERG, BA1 , J. LUCIAN DAVIS, MD1 , ADITHYA CATTAMANCHI, MD1 , SAMUEL D. YOO, MD3 , ALFRED ANDAMA, BS3 , SASKIA DEN BOON, PHD3 , RACHEL KYEYUNE, MBCHB3 , STEVEN MESHNICK, MD, PHD2 . 1 San Francisco, CA, USA, 2 Chapel Hill, NC, USA, 3 Kampala, Uganda. Rationale: PcP was the most frequent cause of pneumonia in hospitalized HIV-infected persons in Uganda who had negative sputum acid fast bacillus (AFB) smears and underwent bronchoscopy, accounting for 39% (32 of 83) of cases [Worodria 2003]. Although trimethoprim-sulfamethoxazole (TMP-SMX) is effective in preventing PcP, its use has been associated with the presence of DHPS mutations and putative TMP-SMX drug resistance. As TMP-SMX use has increased in Uganda, the current prevalence of PcP and DHPS mutations are unclear. Objectives: 1. To determine the prevalence of PcP in hospitalized HIV-infected persons with suspected pneumonia and negative sputum AFB smears. 2. To determine the prevalence of DHPS mutations in persons with PcP. Methods: We enrolled consecutive HIV- infected adults with cough >2 weeks and suspected pneumonia who were admitted to Mulago Hospital in Kampala, Uganda between September 2007 and July 2008. Patients underwent standardized evaluation including sputum x2 sent for AFB smear and bronchoscopy with bronchoalveolar lavage (BAL) if AFB smears were negative. BAL specimens were examined for PcP at Mulago using a modified Giemsa stain and also sent to the University of North Carolina for polymerase chain reaction (PCR) and DNA sequencing at the DHPS locus. Results: Pneumocystis was identified microscopically in 7 of 133 (5.3%) BAL specimens. Overall, persons with PcP had a lower median CD4+ T-cell count (10 cells/ul vs. 86 cells/ul, P = 0.01) and tended to be less likely to have received PcP prophylaxis or antiretroviral therapy than persons without PcP. There was 100% concordance between modified Giemsa microscopy and PCR. DHPS PCR was positive in all 6 of the PcP microscopy- positive BAL specimens tested and negative in all 124 of the PcP microscopy-negative specimens tested. All 6 PCR-positive BAL specimens contained Pneumocystis DHPS mutations; the most frequent DHPS genotype was GT3 (Thr55/Ser57), seen in 4 of the 6 cases. Conclusions: The prevalence of PcP in hospitalized HIV-infected adults undergoing bronchoscopy at Mulago Hospital is low and has decreased compared to an earlier study (October 1999 through February 2000) conducted prior to the widespread use of TMP-SMX for PcP prophylaxis in Uganda. The prevalence of Pneumocystis DHPS mutations is high. Interestingly, the most frequent DHPS genotype (GT3) reported in this study is rarely reported in the US and has 32. 32 been associated with the use of sulfadoxine (plus pyrimethamine) rather than sulfamethoxazole (TMP-SMX). This raises the question of whether sulfa drugs used for indications other than PcP prophylaxis such as malaria treatment may also be associated with the presence of PcP that contains DHPS mutations. PO16 Variation in the erg11 Gene from Pneumocystis jirovecii. SCOTT P. KEELY,1 JAMES R. STRINGER,1 CARLO CONTINI,2 BETTINA LUNGREN,3 RONALD BRUBAKER4 , LAURA Q. JOHNSTON,5 EDNA S. KANESHIRO5 ; 1 Dept. Molecular Genetics, Biochemistry & Microbiology, 5 Dept. Biological Sciences, Univ. Cincinnati, Cincinnati, OH; 2 Dept. Clinical & Experimental Medicine, Univ. Ferrara, Ferrara, Italy, 3 Dept. Clinical Microbiology, Hvidovre Univ. Hospital, Hvidovre, Denmark. 4 Department of Pathology, Christ Hospital, Cincinnati, OH. The erg11 gene codes for sterol 14- demethylase (14DM), a key enzyme in sterol biosynthesis and the target for triazole antimycotic drugs. Two sterol composition phenotypes have been described in patients with pneumonia caused by P. jirovecii; one phenotype has a much higher amount of lanosterol derivatives (C31 and C32 sterols) dominated by pneumocysterol. Most of the Pneumocystis-distinct sterols in this phenotype were those with a methyl group present at the C-14 position of the sterol nucleus suggesting that the P. jirovecii present might lack 14DM activity. To gain insight into whether the apparent lack of 14DM activity might be due to mutation of the erg11 gene, we have analyzed a 1,000-bp segment of this 1,800-bp gene in nine specimens of P. jirovecii (from the USA, Italy and Denmark). Thus far, two alleles of the erg11 gene have been observed: allele 1 with G at position 238 and allele 2 with A at this nucleotide position. All three specimens from Italy had allele 2, two of which were shown to contain high proportions of pneumocysterol. The other specimens analyzed had allele 1. The two alleles differ at a single site that is located in an apparent intron. Sequencing of the entire erg11 gene from these and additional samples is in progress [Supported in part by NIH grant RO1 AI064084]. PO17 Development of a Multilocus Sequence Typing Tool for Cryptosporidium muris and Cryptosporidium andersoni. YAOYU FENG,1 WENLI YANG,2 UNA RYAN,3 LONGXIAN ZHANG,4 MARTIN KV,5 BETISLAV KOUDELA,5 NA LI,2,6 RONALD FAYER,7 LIHUA XIAO2 ; 1 East China University of Science and Technology, Shanghai, China, 2 Centers for Disease Control and Prevention, Atlanta, GA, USA, 3 Murdoch, Western Australia, Australia, 4 Henan Agricultural University, Zhengzhou, China, 5 Academy of Sciences of the Czech Republic, esk Budjovice, Czech Republic, 6 Tongji University, Shanghai, China,7 U.S. Department of Agriculture, Beltsville, Maryland, USA. Although genotyping tools have been developed and widely used in the characterization of the transmission of intestinal Cryptosporidium spp., they are not available for C. muris and C. andersoni, two most common gastric Cryptosporidium spp. of mammals. In this study, we screened the C. muris whole genome sequencing data for microsatellite and minisatellite sequences. Among the 13 potential loci (six microsatellite and seven minisatellite loci) evaluated by PCR and DNA sequencing, four were eventually chosen. DNA sequence analyses of 27 C. muris and 17 C. andersoni DNA preparations showed the presence of 5-10 subtypes of C. 33. 33 muris and 1-4 subtypes of C. andersoni at each locus. Altogether, 11 C. muris and seven C. andersoni multilocus sequence typing (MLST) subtypes were detected among the 16 C. muris and 12 C. andersoni specimens successfully sequenced at all four genetic loci. In all analyses, the C. muris isolate (TS03) originated from an East African mole rat (Tachyoryctes splendens) differed significantly from other C. muris isolates, approaching the extent of genetic differences between C. muris and C. andersoni. Thus, a MLST technique was developed for high resolution typing of C. muris and C. andersoni. It should be useful in the characterization of the population genetics and transmission of gastric Cryptosporidium spp. PO18 Amoebicidal and Amebastatic Activity In Vitro of the Resin of Gymnosperma glutinosum Against Acanthamoeba castellanii trophozoites. RODRIGUEZ- MONROY MA1 , PEA-JUAREZ MC2 , OMAA-MOLINA M1 , GONZALEZ- ROBLES A3 , SALAZAR-VILLATORO L3 , CANALES-MARTINEZ MM4 .1 Profesor Carrera de Medicina, U.N.A.M. F.E.S. Iztacala. 2 Profesor Carrera de Biologa, U.N.A.M. F.E.S. Iztacala. 3 Departamento de Infectmica y Patognesis Molecular, CINVESTAV, I.P.N., 4 Profesor Carrera de Medicina, U.N.A.M. F.E.S. Iztacala, Edo. Mexico. We investigated the in vitro activity of the resin of Gymnosperma glutinosum (a plant that belongs to the Asteraceae family, considered one of the most important families of plants in traditional medicine in Mexico) on Acanthamoeba castellanii trophozoites. We measured the effects on cell viability by the reduction of tetrazolium salts (MTT protocol), in an attempt to identify other useful agents that can be used against Acanthamoeba sp. Strains of Acanthamoeba sp. constitute a factor contributing to the occurrence of chronic granulomatous amoebic encephalitis, keratitis, pneumonia, as well as inflammations of other organs. Treatment of these diseases is very difficult and not always effective. A majority of these infections have been fatal. The aim of this study was to investigate and evaluate the in vitro effect of the resin of Gymnosperma glutinosum on the growth of A. castellanii tro