DOCSLIB.ORG

Chapter 13 Topics

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Chapter 13 Topics Chapter 13 Human Host Topics • Acquire resident flora - Human Host • New born exposure - how do we - Progress of an Infection acquire our normal flora? - Epidemiology Acquire resident flora Acquire resident flora • The human body supports a wide range • Beneficial outcome of habitats – Provide nutrients (Vit K) – temperature, pH, nutrient, oxygen tension – Microbial antagonism • Wide range of microbes can inhabit – Development of immune system • Resident flora or microflora • Adverse effects – Microbes (from bacteria to sometimes – Escape immune system viruses) that inhabit but do not harm the – Multiply and disrupt tissue oportunistic! host Association between microbes and humans 1 New born exposure Progress of an Infection • Mother’s birth canal • Pathogenicity • Mother’s breast milk • Portals of entry • Bottle-feeding • Attachment • People • Surviving host defenses • Causing disease • Process of infections and disease • Portals of exit Pathogens : any organism Contamination : microorganisms capable of causing disease present on or in host Infection : multiplication of Pathogenicity : capacity to microorganisms on or in hosts produce disease Disease : disturbance in health status of host Virulence : degree or intensity of disease True pathogen Opportunistic pathogen • Cause disease in immune • Cause disease in compromised host healthy individuals • Gain access (injury) to sterile • Associated with a specific and regions recognizable disease • Examples: – Pseudomonas aeruginosa • Examples: – Staphylococcus epidermidis – Staphylococcus aureus • – E. coli 2 Opportunistic Infections: pathogens Factors that predispose a person to infections that do not cause disease under normal circumstances but under the right conditions…….can cause disease 1)Failure of host defense mechanisms – immunocompromised patients 2)Organisms at unusual sites in body 3)Disturbances in normal microflora – super-infections Virulence Portals of entry • Virulence factors (Any characteristic or • Most pathogens have specific portals on structure) entry…..and EXIT! – Ability to establish itself in the host – Skin – Gastrointestinal tract – Cause damage – Respiratory tract – Often associated with toxins – Urogenital – Placenta – Inoculum size Skin Gastrointestinal tract • Staphylococcus aureus • Salmonella, Shigella, Vibrio – Boils • Viruses – polio, hepatitis A • Protozoan – Giardia lamblia • Enter via ingestion or the anal route 3 Urogenital Respiratory tract • Numerous sexual transmitted diseases • Streptococcus pneumoniae (STDs) • Virus – human papillomavirus – Sore throat, meningitis – Genital warts • Fungi – Cryptococcus • Protozoan – Trichomonas – pneumonia – trichomoniasis • Bacteria – Neisseria gonorrhoeae – Gonorrhea • Acquire by intercourse or intimate contact Placenta • Some bacteria can penetrate the placenta barrier – Syphilis spirochete • Birth canal – Herpes simplex virus – Remember the STORCH test? 4 Portal of exit Inoculum size • Enables pathogen to spread to other hosts • Infectious dose (ID) – Respiratory – minimum number of bacteria – Salivary required to cause disease – Skin – Fecal – Low ID = high virulence – Urogenital – Blood • Persistence Mechanisms of adhesion by pathogens Attachment • Adhesion –Binding between specific molecules on both the host and pathogen • Structures –Capsules –Pili or fimbriae –Hooks or Teeth!! Causing disease Surviving host defenses • Virulence factors • Anti-phagocytic factors – Exoenzymes – Capsule – Toxins • Prevent phagocytosis – Capsule – Leukocidins • Occurrence of infection • Toxic to phagocytes - WBCs • Signs and symptoms – Some microbes survive inside phagocytes Mycobacterium tuberculosis 5 Bacterial toxins Bacteria produce toxins – • Exotoxins Endotoxins- part of the cell wall of gram-negative bacteria and are released when cells die - LPS – Gram positive and Gram negative cells – Excreted (ex. Hemolysins) Exotoxins - produced by and released from bacteria - botulinum toxin - on the other hand toxins can be – Highly toxic in small amounts used to treat disease - • Endotoxins Called neurotoxins if affect neural tissue – Gram negative cells – Membrane associated Called enterotoxins if affect digestive system • Lipopolysaccharide (LPS) Toxoids are inactivated exotoxins that are – Fever associated inactivated and used to stimulate an immune response - tetanus toxoid Bacteria release substances that damage host tissues Hemolysins - lyse red cells Leukocidins - kill white blood cells Coagulase - accelerates clotting Streptokinase - digests clots and enables bacteria to spread Hyaluronidase - digests hyaluronic acid, a glue- like substance that holds the cells together in tissues and allows the organism to penetrate to deeper tissue Endotoxins 6 Differential characteristics of bacterial Process of infections and exotoxins and endotoxins disease • Stages of Disease – Incubation – Prodromal – Invasive – Decline – Convalescence • Signs and symptoms Stages in course of infectious disease Signs and symptoms • Signs - objective evidence of disease based on observation • Symptoms – subjective evidence of disease based on the patient • Syndrome – sign and symptoms defined a particular disease Persistence • Latency – Viral • Herpes virus – Bacterial • Tuberculosis • Sequelae – long-term damage to tissues or organs Meningitis deafness 7 Epidemiology Epidemiology • The study of disease in populations – Statistics – Prevalence – total numbers of cases in – Strategies the population at any given time – Reservoir – Incidence – Number of new cases over – Carriers a defined period of time – Vectors • Center for Disease Control and – Acquisition and transmission Prevention (CDC) – Nosocomial – Koch’s postulates Statistical data can be represented graphically, and can be used to predict trends Patterns of infectious disease occurrence Reservoirs Two types of vectors • Site at which the organism remains and can potentially infect. • A) Living Reservoirs – Humans Carriers – Animals Zoonosis • B) Non-living Reservoirs – Soil – Water 8 Vectors Nonliving Reservoirs • Biological – Participates in the pathogen’s life cycle • Soil – Infected with the pathogen – Transmit bacteria, protozoa, helminths, – Transmit by bites, defecation fungi • Mechanical – Transmit spores, cysts, ova, larvae – Not part of pathogen’s life cycle • Water – similar to soil – Not infected with the pathogen Acquisition and Kinds of diseases transmission Infectious disease - caused by infectious agent Noninfectious disease - caused by some • Communicable other factor - for example a poison • Non-communicable Communicable or contagious disease - • Patterns of transmission measles, hepatitis, TB Non-communicable disease - cannot be spread from host to host - food poisoning Communicable Non-communicable • Infected host transmits an • Host acquires infectious agent infectious agent to another host – From self (compromised • Receiving host must become individual)- microflora infected – Nonliving reservoir – soil – cannot be spread from host to host!!! 9 Patterns of transmission Horizontal • Horizontal • Disease is spread through a • Vertical population from one infected • Contact - Direct person to another • Indirect Contact – Kissing, sneezing The Anatomy of a Sneeze Vertical • The disease is transmitted from parent to offspring – Ovum, sperm, placenta, milk - remember that milk also provides protection to newborn Indirect Contact Transmission • Food, water, and biological products • Direct - Kissing, sex (blood, serum, tissue), • Fomite (door knobs, toilet seats, etc.) • Droplets - Talking • Air • Vertical – Mother to fetus – Droplet nuclei (dried microscopic residue) – Aerosols (dust or moisture particles) • Vector - 10 Summary of how communicable infectious diseases are acquired Nosocomial infections • Infectious diseases that are acquired or developed from a hospital stay – Urinary tract infections – Respiratory infections – Surgical incisions Over 70% of all Nosocomial Hospital infections are caused by biofilms Most common nosocomial infections Infectious disease is due to host- microbe interaction that results in some type of insult to the host. However, the microbe is usually just trying to perpetuate itself however it can. Many diseases can be prevented. Some diseases can be cured, but not all. Then the host- microbe relationship is successful for the microbe and failing for the host. 11.
Load more

Recommended publications
  • Genetic Engineering and Sustainable Crop Disease Management: Opportunities for Case-By-Case Decision-Making
    sustainability Review Genetic Engineering and Sustainable Crop Disease Management: Opportunities for Case-by-Case Decision-Making Paul Vincelli Department of Plant Pathology, 207 Plant Science Building, College of Agriculture, Food and Environment, University of Kentucky, Lexington, KY 40546, USA; [email protected] Academic Editor: Sean Clark Received: 22 March 2016; Accepted: 13 May 2016; Published: 20 May 2016 Abstract: Genetic engineering (GE) offers an expanding array of strategies for enhancing disease resistance of crop plants in sustainable ways, including the potential for reduced pesticide usage. Certain GE applications involve transgenesis, in some cases creating a metabolic pathway novel to the GE crop. In other cases, only cisgenessis is employed. In yet other cases, engineered genetic changes can be so minimal as to be indistinguishable from natural mutations. Thus, GE crops vary substantially and should be evaluated for risks, benefits, and social considerations on a case-by-case basis. Deployment of GE traits should be with an eye towards long-term sustainability; several options are discussed. Selected risks and concerns of GE are also considered, along with genome editing, a technology that greatly expands the capacity of molecular biologists to make more precise and targeted genetic edits. While GE is merely a suite of tools to supplement other breeding techniques, if wisely used, certain GE tools and applications can contribute to sustainability goals. Keywords: biotechnology; GMO (genetically modified organism) 1. Introduction and Background Disease management practices can contribute to sustainability by protecting crop yields, maintaining and improving profitability for crop producers, reducing losses along the distribution chain, and reducing the negative environmental impacts of diseases and their management.
    [Show full text]
  • Zoonotic Diseases Fact Sheet
    ZOONOTIC DISEASES FACT SHEET s e ion ecie s n t n p is ms n e e s tio s g s m to a a o u t Rang s p t tme to e th n s n m c a s a ra y a re ho Di P Ge Ho T S Incub F T P Brucella (B. Infected animals Skin or mucous membrane High and protracted (extended) fever. 1-15 weeks Most commonly Antibiotic melitensis, B. (swine, cattle, goats, contact with infected Infection affects bone, heart, reported U.S. combination: abortus, B. suis, B. sheep, dogs) animals, their blood, tissue, gallbladder, kidney, spleen, and laboratory-associated streptomycina, Brucellosis* Bacteria canis ) and other body fluids causes highly disseminated lesions bacterial infection in tetracycline, and and abscess man sulfonamides Salmonella (S. Domestic (dogs, cats, Direct contact as well as Mild gastroenteritiis (diarrhea) to high 6 hours to 3 Fatality rate of 5-10% Antibiotic cholera-suis, S. monkeys, rodents, indirect consumption fever, severe headache, and spleen days combination: enteriditis, S. labor-atory rodents, (eggs, food vehicles using enlargement. May lead to focal chloramphenicol, typhymurium, S. rep-tiles [especially eggs, etc.). Human to infection in any organ or tissue of the neomycin, ampicillin Salmonellosis Bacteria typhi) turtles], chickens and human transmission also body) fish) and herd animals possible (cattle, chickens, pigs) All Shigella species Captive non-human Oral-fecal route Ranges from asymptomatic carrier to Varies by Highly infective. Low Intravenous fluids primates severe bacillary dysentery with high species. 16 number of organisms and electrolytes, fevers, weakness, severe abdominal hours to 7 capable of causing Antibiotics: ampicillin, cramps, prostration, edema of the days.
    [Show full text]
  • The Resistance to Host Antimicrobial Peptides in Infections Caused by Daptomycin-Resistant Staphylococcus Aureus
    antibiotics Communication The Resistance to Host Antimicrobial Peptides in Infections Caused by Daptomycin-Resistant Staphylococcus aureus Md Saruar Bhuiyan 1,† , Jhih-Hang Jiang 1,† , Xenia Kostoulias 1, Ravali Theegala 1, Graham J. Lieschke 2 and Anton Y. Peleg 1,3,* 1 Infection and Immunity Program, Monash Biomedicine Discovery Institute, Department of Microbiology, Monash University, Clayton, VIC 3800, Australia; [email protected] (M.S.B.); [email protected] (J.-H.J.); [email protected] (X.K.); [email protected] (R.T.) 2 Australian Regenerative Medicine Institute, Monash University, Clayton, VIC 3800, Australia; [email protected] 3 Department of Infectious Diseases, The Alfred Hospital and Central Clinical School, Monash University, Melbourne, VIC 3004, Australia * Correspondence: [email protected] † These authors contributed equally to this work. Abstract: Daptomycin is an important antibiotic for the treatment of infections caused by Staphylococcus aureus. The emergence of daptomycin resistance in S. aureus is associated with treatment failure and persistent infections with poor clinical outcomes. Here, we investigated host innate immune responses against clinically derived, daptomycin-resistant (DAP-R) and -susceptible S. aureus paired isolates using a zebrafish infection model. We showed that the control of DAP-R S. aureus infections was attenuated in vivo due to cross-resistance to host cationic antimicrobial Citation: Bhuiyan, M.S.; Jiang, J.-H.; peptides. These data provide mechanistic understanding into persistent infections caused by DAP-R Kostoulias, X.; Theegala, R.; Lieschke, S. aureus and provide crucial insights into the adaptive evolution of this troublesome pathogen. G.J.; Peleg, A.Y. The Resistance to Host Antimicrobial Peptides in Keywords: S.
    [Show full text]
  • 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.
    [Show full text]
  • 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).
    [Show full text]
  • Chapter 2 Disease and Disease Transmission
    DISEASE AND DISEASE TRANSMISSION Chapter 2 Disease and disease transmission An enormous variety of organisms exist, including some which can survive and even develop in the body of people or animals. If the organism can cause infection, it is an infectious agent. In this manual infectious agents which cause infection and illness are called pathogens. Diseases caused by pathogens, or the toxins they produce, are communicable or infectious diseases (45). In this manual these will be called disease and infection. This chapter presents the transmission cycle of disease with its different elements, and categorises the different infections related to WES. 2.1 Introduction to the transmission cycle of disease To be able to persist or live on, pathogens must be able to leave an infected host, survive transmission in the environment, enter a susceptible person or animal, and develop and/or multiply in the newly infected host. The transmission of pathogens from current to future host follows a repeating cycle. This cycle can be simple, with a direct transmission from current to future host, or complex, where transmission occurs through (multiple) intermediate hosts or vectors. This cycle is called the transmission cycle of disease, or transmission cycle. The transmission cycle has different elements: The pathogen: the organism causing the infection The host: the infected person or animal ‘carrying’ the pathogen The exit: the method the pathogen uses to leave the body of the host Transmission: how the pathogen is transferred from host to susceptible person or animal, which can include developmental stages in the environment, in intermediate hosts, or in vectors 7 CONTROLLING AND PREVENTING DISEASE The environment: the environment in which transmission of the pathogen takes place.
    [Show full text]
  • STD (Sexually Transmitted Disease) Or STI (Sexually Transmitted Infection): Should We Choose? Janet Byron Anderson, Phd
    STD (sexually transmitted disease) or STI (sexually transmitted infection): Should we choose? Janet Byron Anderson, PhD 1. Clinical foundation of the problem Another surprise: Documented incidence had shown Each of the terms—“sexual(ly)”, “transmitted”, “disease”, that the two routes of sexual transmission were male-to- and “infection”—is problematic independently, as this female and male-to-male. However, on 15 July 2016 the study will show. Moreover, co-occurring variants, used CDC reported the first case of suspected female-to-male as synonyms in English medical articles worldwide, ag- sexual transmission in New York City [4]. Since 2008, gravate the problem. The purpose of this study is to pro- then, the Zika virus has shown that it is now sexually pose a single term that can stimulate discussion about transmissible. “Transmissible” denotes a potential, and is whether the co-occurring variants are clinically and lin- distinct from “transmitted”, which denotes a reality. guistically justifiable—especially now, when STDs/STIs To say that Zika has proved to be transmissible through have become a global health problem, and public health sexual contact means that it can be transmitted through agencies in every country are scrambling to educate their sex but that it need not be (Zika remains a chiefly vec- citizens. [Until the presentation advances to the point tor-borne disease). However, cases reported since 2008 where the question posed in the title can be definitively document the reality of transmittedness through sexual answered, I’ll use the expression “STD/STI” or the terms contact. “illness(es)” and “condition(s)”.] The predisposing epidemiologic context will first be clar- This carefully differentiated language is used by the ified, for it sheds light on two of the problematic terms: European Centre for Disease Prevention and Control chiefly “transmitted” but also “sexual(ly)”.
    [Show full text]
  • Studies of Staphylococcal Infections. I. Virulence of Staphy- Lococci and Characteristics of Infections in Embryonated Eggs * WILLIAM R
    Journal of Clinical Investigation Vol. 43, No. 11, 1964 Studies of Staphylococcal Infections. I. Virulence of Staphy- lococci and Characteristics of Infections in Embryonated Eggs * WILLIAM R. MCCABE t (From the Research Laboratory, West Side Veterans Administration Hospital, and the Department of Medicine, Research and Educational Hospitals, University of Illinois College of Medicine, Chicago, Ill.) Many of the determinants of the pathogenesis niques still require relatively large numbers of and course of staphylococcal infections remain staphylococci to produce infection (19). Fatal imprecisely defined (1, 2) despite their increas- systemic infections have been equally difficult to ing importance (3-10). Experimental infections produce in animals and have necessitated the in- in suitable laboratory animals have been of con- jection of 107 to 109 bacteria (20-23). A few siderable assistance in clarifying the role of host strains of staphylococci have been found that are defense mechanisms and specific bacterial virulence capable of producing lethal systemic infections factors with a variety of other infectious agents. with inocula of from 102 to 103 bacteria (24) and A sensitive experimental model would be of value have excited considerable interest (25-27). The in defining the importance of these factors in virulence of these strains apparently results from staphylococcal infections, but both humans and an unusual antigenic variation (27, 28) which, the usual laboratory animals are relatively re- despite its interest, is of doubtful significance in sistant. Extremely large numbers of staphylo- human staphylococcal infection, since such strains cocci are required to produce either local or sys- have been isolated only rarely from clinical in- temic infections experimentally.
    [Show full text]
  • Virulence During Newcastle Disease Viruses Cross Species Adaptation
    viruses Review Virulence during Newcastle Disease Viruses Cross Species Adaptation Claudio L. Afonso Base2bio, LLC, Oshkosh, WI 54905, USA; [email protected]; Tel.: +1-800-817-7160 Abstract: The hypothesis that host adaptation in virulent Newcastle disease viruses (NDV) has been accompanied by virulence modulation is reviewed here. Historical records, experimental data, and phylogenetic analyses from available GenBank sequences suggest that currently circulating NDVs emerged in the 1920–19400s from low virulence viruses by mutation at the fusion protein cleavage site. These viruses later gave rise to multiple virulent genotypes by modulating virulence in opposite directions. Phylogenetic and pathotyping studies demonstrate that older virulent NDVs further evolved into chicken-adapted genotypes by increasing virulence (velogenic-viscerotropic pathotypes with intracerebral pathogenicity indexes [ICPIs] of 1.6 to 2), or into cormorant-adapted NDVs by moderating virulence (velogenic–neurotropic pathotypes with ICPIs of 1.4 to 1.6), or into pigeon-adapted viruses by further attenuating virulence (mesogenic pathotypes with ICPIs of 0.9 to 1.4). Pathogenesis and transmission experiments on adult chickens demonstrate that chicken-adapted velogenic-viscerotropic viruses are more capable of causing disease than older velogenic-neurotropic viruses. Currently circulating velogenic–viscerotropic viruses are also more capable of replicating and of being transmitted in naïve chickens than viruses from cormorants and pigeons. These evolutionary virulence changes are consistent with theories that predict that virulence may evolve in many directions in order to achieve maximum fitness, as determined by genetic and ecologic constraints. Keywords: NDV; evolution; virulence; host adaptation Citation: Afonso, C.L. Virulence during Newcastle Disease Viruses Cross Species Adaptation.
    [Show full text]
  • Sexually Transmitted Infections Treatment Guidelines, 2021
    Morbidity and Mortality Weekly Report Recommendations and Reports / Vol. 70 / No. 4 July 23, 2021 Sexually Transmitted Infections Treatment Guidelines, 2021 U.S. Department of Health and Human Services Centers for Disease Control and Prevention Recommendations and Reports CONTENTS Introduction ............................................................................................................1 Methods ....................................................................................................................1 Clinical Prevention Guidance ............................................................................2 STI Detection Among Special Populations ............................................... 11 HIV Infection ......................................................................................................... 24 Diseases Characterized by Genital, Anal, or Perianal Ulcers ............... 27 Syphilis ................................................................................................................... 39 Management of Persons Who Have a History of Penicillin Allergy .. 56 Diseases Characterized by Urethritis and Cervicitis ............................... 60 Chlamydial Infections ....................................................................................... 65 Gonococcal Infections ...................................................................................... 71 Mycoplasma genitalium .................................................................................... 80 Diseases Characterized
    [Show full text]
  • Transmission of SARS-Cov-2: Implications for Infection Prevention Precautions
    Transmission of SARS-CoV-2: implications for infection prevention precautions Scientific brief 9 July 2020 This document is an update to the scientific brief published on 29 March 2020 entitled “Modes of transmission of virus causing COVID-19: implications for infection prevention and control (IPC) precaution recommendations” and includes new scientific evidence available on transmission of SARS-CoV-2, the virus that causes COVID-19. Overview This scientific brief provides an overview of the modes of transmission of SARS-CoV-2, what is known about when infected people transmit the virus, and the implications for infection prevention and control precautions within and outside health facilities. This scientific brief is not a systematic review. Rather, it reflects the consolidation of rapid reviews of publications in peer-reviewed journals and of non-peer-reviewed manuscripts on pre-print servers, undertaken by WHO and partners. Preprint findings should be interpreted with caution in the absence of peer review. This brief is also informed by several discussions via teleconferences with the WHO Health Emergencies Programme ad hoc Experts Advisory Panel for IPC Preparedness, Readiness and Response to COVID-19, the WHO ad hoc COVID-19 IPC Guidance Development Group (COVID-19 IPC GDG), and by review of external experts with relevant technical backgrounds. The overarching aim of the global Strategic Preparedness and Response Plan for COVID-19(1) is to control COVID-19 by suppressing transmission of the virus and preventing associated illness and death. Current evidence suggests that SARS-CoV-2, the virus that causes COVID-19, is predominantly spread from person-to-person.
    [Show full text]
  • Virulence of Japanese Encephalitis Virus Genotypes I and III, Taiwan
    Virulence of Japanese Encephalitis Virus Genotypes I and III, Taiwan Yi-Chin Fan,1 Jen-Wei Lin,1 Shu-Ying Liao, within a year (8,9), which provided an excellent opportu- Jo-Mei Chen, Yi-Ying Chen, Hsien-Chung Chiu, nity to study the transmission dynamics and pathogenicity Chen-Chang Shih, Chi-Ming Chen, of these 2 JEV genotypes. Ruey-Yi Chang, Chwan-Chuen King, A mouse model showed that the pathogenic potential Wei-June Chen, Yi-Ting Ko, Chao-Chin Chang, is similar among different JEV genotypes (10). However, Shyan-Song Chiou the pathogenic difference between GI and GIII virus infec- tions among humans remains unclear. Endy et al. report- The virulence of genotype I (GI) Japanese encephalitis vi- ed that the proportion of asymptomatic infected persons rus (JEV) is under debate. We investigated differences in among total infected persons (asymptomatic ratio) is an the virulence of GI and GIII JEV by calculating asymptomat- excellent indicator for estimating virulence or pathogenic- ic ratios based on serologic studies during GI- and GIII-JEV endemic periods. The results suggested equal virulence of ity of dengue virus infections among humans (11). We used GI and GIII JEV among humans. the asymptomatic ratio method for a study to determine if GI JEV is associated with lower virulence than GIII JEV among humans in Taiwan. apanese encephalitis virus (JEV), a mosquitoborne Jflavivirus, causes Japanese encephalitis (JE). This virus The Study has been reported in Southeast Asia and Western Pacific re- JEVs were identified in 6 locations in Taiwan during 1994– gions since it emerged during the 1870s in Japan (1).
    [Show full text]