Chlamydia Trachomatis Strains and Virulence: Rethinking Links to Infection Prevalence and Disease Severity
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B DAMB 721 Microbiology Final Exam B 100 points December 11, 2006 Your name (Print Clearly): _____________________________________________ I. Matching: The questions below consist of headings followed by a list of phrases. For each phrase select the heading that best describes that phrase. The headings may be used once, more than once or not at all. Mark the answer in Part 2 of your answer sheet. 1. capsid 7. CD4 2. Chlamydia pneumoniae 8. Enterococcus faecalis 3. oncogenic 9. hyaluronidase 4. pyruvate 10. interferon 5. Koplik’s spot 11. hydrophilic viruses 6. congenital Treponema pallidum 12. Streptococcus pyogenes 1. “spreading factor” produced by members of the staphylococci, streptococci and clostridia 2. viral protein coat 3. central intermediate in bacterial fermentation 4. persistant endodontic infections 5. a cause of atypical pneumonia 6. nonspecific defense against viral infection 7. has a rudimentary life cycle 8. HIV receptor 9. Hutchinson’s Triad 10. measles 11. resistant to disinfection 12. β-hemolytic, bacitracin sensitive, cause of suppurative pharyngitis 2 Matching (Continued): The questions below consist of diseases followed by a list of etiologic agents. Match each disease with the etiologic agent. Continue using Part 2 of your answer sheet. 1. dysentery 6. Legionnaire’s 2. botulism 7. gas gangrene 3. cholera 8. tuberculosis 4. diphtheria 9. necrotizing fascitis 5. enteric fever 10. pneumoniae/meningitis 13. Clostridium botulinum 14. Vibrio cholera 15. Mycobacterium bovis 16. Shigella species 17. Streptococcus pneumoniae 18. Clostridium perfringens 19. Salmonella typhi 20. Streptococcus pyogenes 3 II. Multiple Choice: Choose the ONE BEST answer. Mark the correct answer on Part 1 of the answer sheet. -
Compendium of Measures to Control Chlamydia Psittaci Infection Among
Compendium of Measures to Control Chlamydia psittaci Infection Among Humans (Psittacosis) and Pet Birds (Avian Chlamydiosis), 2017 Author(s): Gary Balsamo, DVM, MPH&TMCo-chair Angela M. Maxted, DVM, MS, PhD, Dipl ACVPM Joanne W. Midla, VMD, MPH, Dipl ACVPM Julia M. Murphy, DVM, MS, Dipl ACVPMCo-chair Ron Wohrle, DVM Thomas M. Edling, DVM, MSpVM, MPH (Pet Industry Joint Advisory Council) Pilar H. Fish, DVM (American Association of Zoo Veterinarians) Keven Flammer, DVM, Dipl ABVP (Avian) (Association of Avian Veterinarians) Denise Hyde, PharmD, RP Preeta K. Kutty, MD, MPH Miwako Kobayashi, MD, MPH Bettina Helm, DVM, MPH Brit Oiulfstad, DVM, MPH (Council of State and Territorial Epidemiologists) Branson W. Ritchie, DVM, MS, PhD, Dipl ABVP, Dipl ECZM (Avian) Mary Grace Stobierski, DVM, MPH, Dipl ACVPM (American Veterinary Medical Association Council on Public Health and Regulatory Veterinary Medicine) Karen Ehnert, and DVM, MPVM, Dipl ACVPM (American Veterinary Medical Association Council on Public Health and Regulatory Veterinary Medicine) Thomas N. Tully JrDVM, MS, Dipl ABVP (Avian), Dipl ECZM (Avian) (Association of Avian Veterinarians) Source: Journal of Avian Medicine and Surgery, 31(3):262-282. Published By: Association of Avian Veterinarians https://doi.org/10.1647/217-265 URL: http://www.bioone.org/doi/full/10.1647/217-265 BioOne (www.bioone.org) is a nonprofit, online aggregation of core research in the biological, ecological, and environmental sciences. BioOne provides a sustainable online platform for over 170 journals and books published by nonprofit societies, associations, museums, institutions, and presses. Your use of this PDF, the BioOne Web site, and all posted and associated content indicates your acceptance of BioOne’s Terms of Use, available at www.bioone.org/page/terms_of_use. -
2012 Case Definitions Infectious Disease
Arizona Department of Health Services Case Definitions for Reportable Communicable Morbidities 2012 TABLE OF CONTENTS Definition of Terms Used in Case Classification .......................................................................................................... 6 Definition of Bi-national Case ............................................................................................................................................. 7 ------------------------------------------------------------------------------------------------------- ............................................... 7 AMEBIASIS ............................................................................................................................................................................. 8 ANTHRAX (β) ......................................................................................................................................................................... 9 ASEPTIC MENINGITIS (viral) ......................................................................................................................................... 11 BASIDIOBOLOMYCOSIS ................................................................................................................................................. 12 BOTULISM, FOODBORNE (β) ....................................................................................................................................... 13 BOTULISM, INFANT (β) ................................................................................................................................................... -
Chlamydia Cell Biology and Pathogenesis
HHS Public Access Author manuscript Author ManuscriptAuthor Manuscript Author Nat Rev Manuscript Author Microbiol. Author Manuscript Author manuscript; available in PMC 2016 June 01. Published in final edited form as: Nat Rev Microbiol. 2016 June ; 14(6): 385–400. doi:10.1038/nrmicro.2016.30. Chlamydia cell biology and pathogenesis Cherilyn Elwell, Kathleen Mirrashidi, and Joanne Engel Departments of Medicine, Microbiology and Immunology, University of California, San Francisco, California 94143, USA Abstract Chlamydia spp. are important causes of human disease for which no effective vaccine exists. These obligate intracellular pathogens replicate in a specialized membrane compartment and use a large arsenal of secreted effectors to survive in the hostile intracellular environment of the host. In this Review, we summarize the progress in decoding the interactions between Chlamydia spp. and their hosts that has been made possible by recent technological advances in chlamydial proteomics and genetics. The field is now poised to decipher the molecular mechanisms that underlie the intimate interactions between Chlamydia spp. and their hosts, which will open up many exciting avenues of research for these medically important pathogens. Chlamydiae are Gram-negative, obligate intracellular pathogens and symbionts of diverse 1 organisms, ranging from humans to amoebae . The best-studied group in the Chlamydiae phylum is the Chlamydiaceae family, which comprises 11 species that are pathogenic to 1 humans or animals . Some species that are pathogenic to animals, such as the avian 1 2 pathogen Chlamydia psittaci, can be transmitted to humans , . The mouse pathogen 3 Chlamydia muridarum is a useful model of genital tract infections . Chlamydia trachomatis and Chlamydia pneumoniae, the major species that infect humans, are responsible for a wide 2 4 range of diseases , and will be the focus of this Review. -
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. -
Chlamydia Trachomatis Infection Is Driven by Nonprotective Immune Cells That Are Distinct from Protective Populations
Pathology after Chlamydia trachomatis infection is driven by nonprotective immune cells that are distinct from protective populations Rebeccah S. Lijeka,b,1, Jennifer D. Helblea, Andrew J. Olivea,c, Kyra W. Seigerb, and Michael N. Starnbacha,1 aDepartment of Microbiology and Immunobiology, Harvard Medical School, Boston, MA 02115; bDepartment of Biological Sciences, Mount Holyoke College, South Hadley, MA 01075; and cDepartment of Microbiology and Physiological Systems, University of Massachusetts Medical School, Worcester, MA 01605 Edited by Rafi Ahmed, Emory University, Atlanta, GA, and approved December 27, 2017 (received for review June 23, 2017) Infection with Chlamydia trachomatis drives severe mucosal immu- sequence identity, Chlamydia muridarum, the extent to which the nopathology; however, the immune responses that are required for molecular pathogenesis of C. muridarum represents that of Ct is mediating pathology vs. protection are not well understood. Here, unknown (6). Ct serovar L2 (Ct L2) is capable of infecting the we employed a mouse model to identify immune responses re- mouse upper genital tract when inoculated across the cervix into quired for C. trachomatis-induced upper genital tract pathology the uterus (7, 8) but it does not induce robust immunopathology. and to determine whether these responses are also required for This is consistent with the human disease phenotype caused by Ct L2, bacterial clearance. In mice as in humans, immunopathology was which disseminates to the lymph nodes causing lymphogranuloma characterized by extravasation of leukocytes into the upper genital venereum (LGV) and is not a major cause of mucosal immunopa- thology in the female upper genital tract (uterus and ovaries). tract that occluded luminal spaces in the uterus and ovaries. -
Product Description EN Bactoreal® Kit Chlamydiaceae
Product Description BactoReal® Kit Chlamydiaceae For research only, not for diagnostic use BactoReal® Kit Chlamydiaceae Order no. Reactions Pathogen Internal positive control DVEB03113 100 FAM channel Cy5 channel DVEB03153 50 FAM channel Cy5 channel DVEB03111 100 FAM channel VIC/HEX channel DVEB03151 50 FAM channel VIC/HEX channel Kit contents: Detection assay for Chlamydia and Chlamydophila species Detection assay for internal positive control (control of amplification) DNA reaction mix (contains uracil-N glycosylase, UNG) Positive control for Chlamydiaceae Water Background: The Chlamydiaceae family currently includes two genera and one candidate genus: genus Chlamydia (including the species Chlamydia muridarum, Chlamydia suis, Chlamydia trachomatis), genus Chlamydophila (including the species Chlamydophila abortus, Chlamydophila caviae Chlamydophila felis, Chlamydia pecorum, Chlamydophila pneumoniae, Chlamydophila psittaci), and candidatus Clavochlamydia. All Chlamydiaceae are obligate intracellular Gram-negative bacteria that cause diseases in humans and animals worldwide. Description: BactoReal® Kit Chlamydiaceae is based on the amplification and detection of the 23S rRNA gene of C. muridarum, C. suis, C. trachomatis, C. abortus, C. caviae, C. felis, C. pecorum, C. pneumoniae and C. psittaci using real-time PCR. It allows the rapid and sensitive detection of the 23S rRNA gene of Chlamydiaceae from DNA samples purified from different sample material (e.g. with the QIAamp DNA Mini Kit). For subtyping please contact ingenetix. PCR-platforms: BactoReal® Kit Chlamydiaceae is developed and validated for the ABI PRISM® 7500 instrument (Life Technologies), LightCycler® 480 (Roche) and Mx3005P® QPCR System (Agilent), but is also suitable for other real-time PCR instruments. Sensitivity and specificity: BactoReal® Kit Chlamydiaceae detects at least 10 copies/reaction. -
Leptospirosis: a Waterborne Zoonotic Disease of Global Importance
August 2006 volume 22 number 08 Leptospirosis: A waterborne zoonotic disease of global importance INTRODUCTION syndrome has two phases: a septicemic and an immune phase (Levett, 2005). Leptospirosis is considered one of the most common zoonotic diseases It is in the immune phase that organ-specific damage and more severe illness globally. In the United States, outbreaks are increasingly being reported is seen. See text box for more information on the two phases. The typical among those participating in recreational water activities (Centers for Disease presenting signs of leptospirosis in humans are fever, headache, chills, con- Control and Prevention [CDC], 1996, 1998, and 2001) and sporadic cases are junctival suffusion, and myalgia (particularly in calf and lumbar areas) often underdiagnosed. With the onset of warm temperatures, increased (Heymann, 2004). Less common signs include a biphasic fever, meningitis, outdoor activities, and travel, Georgia may expect to see more leptospirosis photosensitivity, rash, and hepatic or renal failure. cases. DIAGNOSIS OF LEPTOSPIROSIS Leptospirosis is a zoonosis caused by infection with the bacterium Leptospira Detecting serum antibodies against leptospira interrogans. The disease occurs worldwide, but it is most common in temper- • Microscopic Agglutination Titers (MAT) ate regions in the late summer and early fall and in tropical regions during o Paired serum samples which show a four-fold rise in rainy seasons. It is not surprising that Hawaii has the highest incidence of titer confirm the diagnosis; a single high titer in a per- leptospirosis in the United States (Levett, 2005). The reservoir of pathogenic son clinically suspected to have leptospirosis is highly leptospires is the renal tubules of wild and domestic animals. -
Gonorrhea, Chlamydia, and Syphilis
2019 GONORRHEA, CHLAMYDIA, AND SYPHILIS AND CHLAMYDIA, GONORRHEA, Dedication TAG would like to thank the National Coalition of STD Directors for funding and input on the report. THE PIPELINE REPORT Pipeline for Gonorrhea, Chlamydia, and Syphilis By Jeremiah Johnson Introduction The current toolbox for addressing gonorrhea, chlamydia, and syphilis is inadequate. At a time where all three epidemics are dramatically expanding in locations all around the globe, including record-breaking rates of new infections in the United States, stakeholders must make do with old tools, inadequate systems for addressing sexual health, and a sparse research pipeline of new treatment, prevention, and diagnostic options. Lack of investment in sexual health research has left the field with inadequate prevention options, and limited access to infrastructure for testing and treatment have allowed sexually transmitted infections (STIs) to flourish. The consequences of this underinvestment are large: according to the World Health Organization (WHO), in 2012 there were an estimated 357 million new infections (roughly 1 million per day) of the four curable STIs: gonorrhea, chlamydia, syphilis, and trichomoniasis.1 In the United States, the three reportable STIs that are the focus of this report—gonorrhea, chlamydia, and syphilis—are growing at record paces. In 2017, a total of 30,644 cases of primary and secondary (P&S) syphilis—the most infectious stages of the disease—were reported in the United States. Since reaching a historic low in 2000 and 2001, the rate of P&S syphilis has increased almost every year, increasing 10.5% during 2016–2017. Also in 2017, 555,608 cases of gonorrhea were reported to the U.S. -
Evaluating Alternative Hypotheses to Explain the Downward Trend in the Indices of the COVID-19 Pandemic Death Rate
Evaluating alternative hypotheses to explain the downward trend in the indices of the COVID-19 pandemic death rate Sonali Shinde1, Pratima Ranade1 and Milind Watve2 1 Department of Biodiversity, Abasaheb Garware College, Pune, Pune, Maharashtra, India 2 Independent Researcher, Pune, Maharashtra, India ABSTRACT Background: In the ongoing Covid-19 pandemic, in the global data on the case fatality ratio (CFR) and other indices reflecting death rate, there is a consistent downward trend from mid-April to mid-November. The downward trend can be an illusion caused by biases and limitations of data or it could faithfully reflect a declining death rate. A variety of explanations for this trend are possible, but a systematic analysis of the testable predictions of the alternative hypotheses has not yet been attempted. Methodology: We state six testable alternative hypotheses, analyze their testable predictions using public domain data and evaluate their relative contributions to the downward trend. Results: We show that a decline in the death rate is real; changing age structure of the infected population and evolution of the virus towards reduced virulence are the most supported hypotheses and together contribute to major part of the trend. The testable predictions from other explanations including altered testing efficiency, time lag, improved treatment protocols and herd immunity are not consistently supported, or do not appear to make a major contribution to this trend although they may influence some other patterns of the epidemic. Conclusion: The fatality of the infection showed a robust declining time trend between mid April to mid November. Changing age class of the infected and Submitted 7 December 2020 Accepted 3 March 2021 decreasing virulence of the pathogen were found to be the strongest contributors to Published 20 April 2021 the trend. -
Metabolic Sensor Governing Bacterial Virulence in Staphylococcus Aureus
Metabolic sensor governing bacterial virulence in PNAS PLUS Staphylococcus aureus Yue Dinga, Xing Liub, Feifei Chena, Hongxia Dia, Bin Xua, Lu Zhouc, Xin Dengd,e, Min Wuf, Cai-Guang Yangb,1, and Lefu Lana,1 aDepartment of Molecular Pharmacology and bChinese Academy of Sciences Key Laboratory of Receptor Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China; cDepartment of Medicinal Chemistry, School of Pharmacy, Fudan University, Shanghai 201203, China; dDepartment of Chemistry and eInstitute for Biophysical Dynamics, The University of Chicago, Chicago, IL 60637; and fDepartment of Basic Sciences University of North Dakota School of Medicine and Health Sciences, Grand Forks, ND 58203 Edited by Richard P. Novick, New York University School of Medicine, New York, NY, and approved October 14, 2014 (received for review June 13, 2014) An effective metabolism is essential to all living organisms, in- To survive and replicate efficiently in the host, S. aureus has cluding the important human pathogen Staphylococcus aureus.To developed exquisite mechanisms for scavenging nutrients and establish successful infection, S. aureus must scavenge nutrients adjusting its metabolism to maintain growth while also coping with and coordinate its metabolism for proliferation. Meanwhile, it also stress (6, 11). On the other hand, S. aureus produces a wide array must produce an array of virulence factors to interfere with host of virulence factors to evade host immune defenses and to derive defenses. However, the ways in which S. aureus ties its metabolic nutrition either parasitically or destructively from the host during state to its virulence regulation remain largely unknown. Here we infections (6). -
Assessing Lyme Disease Relevant Antibiotics Through Gut Bacteroides Panels
Assessing Lyme Disease Relevant Antibiotics through Gut Bacteroides Panels by Sohum Sheth Abstract: Lyme borreliosis is the most prevalent vector-borne disease in the United States caused by the transmission of bacteria Borrelia burgdorferi harbored by the Ixodus scapularis ticks (Sharma, Brown, Matluck, Hu, & Lewis, 2015). Antibiotics currently used to treat Lyme disease include oral doxycycline, amoxicillin, and ce!riaxone. Although the current treatment is e"ective in most cases, there is need for the development of new antibiotics against Lyme disease, as the treatment does not work in 10-20% of the population for unknown reasons (X. Wu et al., 2018). Use of antibiotics in the treatment of various diseases such as Lyme disease is essential; however, the downside is the development of resistance and possibly deleterious e"ects on the human gut microbiota composition. Like other organs in the body, gut microbiota play an essential role in the health and disease state of the body (Ianiro, Tilg, & Gasbarrini, 2016). Of importance in the microbiome is the genus Bacteroides, which accounts for roughly one-third of gut microbiome composition (H. M. Wexler, 2007). $e purpose of this study is to investigate how antibiotics currently used for the treatment of Lyme disease in%uences the Bacteroides cultures in vitro and compare it with a new antibiotic (antibiotic X) identi&ed in the laboratory to be e"ective against B. burgdorferi. Using microdilution broth assay, minimum inhibitory concentration (MIC) was tested against nine di"erent strains of Bacteroides. Results showed that antibiotic X has a higher MIC against Bacteroides when compared to amoxicillin, ce!riaxone, and doxycycline, making it a promising new drug for further investigation and in vivo studies.