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Pathogens_2024_Sintchenko.pdf

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Pathogens Presented by Prof Vitali Sintchenko Faculty of Medicine and Health Originally developed by Dr Christina Adler Faculty of Medicine and Health The University of Sydney Page 1 Host – microbe interactions The University of Sydney Page 2 Learning objectives...

Pathogens Presented by Prof Vitali Sintchenko Faculty of Medicine and Health Originally developed by Dr Christina Adler Faculty of Medicine and Health The University of Sydney Page 1 Host – microbe interactions The University of Sydney Page 2 Learning objectives Define the terms pathogens, opportunistic pathogen, acute infection, persistence and chronicity Describe the stages of infection with a pathogen Know routes of transmission of microorganism Detail the conditions under which an opportunistic pathogen can cause an infection The University of Sydney Page 3 Pathogens The University of Sydney Page 4 Infection and pathogenicity Infection: Disease/no disease Pathogenicity: Ability of pathogen to cause disease Infectious disease: Change in health state of host from carrying out normal activities Virulence: degree of harm inflicted on host by microorganism Opportunistic pathogen: cause infection away from typical niche or different environment The University of Sydney Page 5 Virulence Virulence: degree of harm inflicted on host by microorganism Virulence factors: physical or chemical characteristics of a pathogen which contributes to the disease-causing proces Pathogenicity islands: a group of genes encoding for virulence factors that can be transferred from bacteria-to- bacteria The University of Sydney Page 6 Pattern of infection – Incubation period: no signs/symptoms – Prodromal stage: onset of symptoms, unclear diagnosis – Illness period: Severe, characteristic signs/symptoms – Recovery/convalescence The University of Sydney Page 7 Questions 1. At which stage during infection would you likely be infectious? A. Incubation period B. Prodromal stage C. Illness period D. Recovery The University of Sydney Page 8 Stages of infection Infection is a competition Host is a source of nutrients for resources and energy Pathogen develops mechanisms to access and exploit host 1. Transmission 2. Adherence 3. Invasion 4. Surviving – Evasion of host defenses 5. Damaging host The University of Sydney Page 9 1. Transmission Direct – Physical contact – Airborne, under 1m – Vector: insects, ticks, bats – Vertical contact: mum to baby Indirect – Contact – Food/water/ blood products – Airborne, longer distance The University of Sydney Page 10 Question 1. An individual with COVID-19 touches a door handle. A second person later touches the same door handle and contracts COVID-19. What type of transmission of a virus would this be? A. Direct – physical contact B. Direct – airborne C. Indirect – physical contact D. Indirect – airborne The University of Sydney Page 11 2. Adherence First step in infective process is adherence and invasion Entry site: skin, oral, gut, respiratory tract and eyes Non-specific Specific – Adhesins: pili, fimbriae, capsules The University of Sydney Page 12 3. Invasion – attack strategies – Actively or passively penetrate mucous membrane or epithelium – Active invasion and spread: enzyme production, and microbial toxins – Inhibition of phagocytosis – Bacteremia: enters blood – Septicemia: infection disease in blood The University of Sydney Page 13 4. Surviving – evasion of host defenses Pathogen to overcome innate/adaptive immune systems Overcome resident microbiota Protection strategies: – Hiding (within a capsule, in biofilms, inside phagocytes) – Capsule (Streptococcoccus pneumoniae) – Intracellular pathogens (Mycobacterium tuberculosis, Chlamydia…) – Camouflage or molecular ‘mimicry’ (coating with host macromolecules e.g. immunoglobulins) – Streptococci produce enzyme streptokinase that effectively coats the bacteria with host protein called plasmin – Immune evasion (antigenic variation) The University of Sydney Page 14 Acute and chronic infections Acute infection An infection (usually primary) characterised by sudden onset, rapid progression, and often with severe systemic symptoms Chronic infection Characterized by the continued presence of infectious agent following the primary infection and may include chronic or recurrent disease (i.e. reactivation) The University of Sydney Page 15 5. Damage to host/Virulence Virulence: magnitude of harm Types of virulence factors Virulence factors: increase – Rapid replication virulence – Integration of pathogen Pathogenicity Islands genome into host to alter function – Use of toxins Exotoxins: Gram +ve, heat sensitive, travel in host Endotoxins: LPS on Gram – ve, heat stable, fever, shock The University of Sydney Page 16 Propensity for causing disease – Simple ‘hit-and-run’ infections (e.g. pertussis, influenza) vs long- term ‘co-existence and subversion’ (e.g. tuberculosis, herpes) – Strict pathogens – Positive culture is always associated with disease – Example: Mycobacterium tuberculosis – Opportunistic pathogens – Positive culture is NOT always associated with disease – Typically members of the normal microbial flora – Cause disease when introduced to unprotected sites (blood, tissues) or when immune system is defective – Example: Candida albicans The University of Sydney Page 17 Opportunistic infections Weakened immune system Example: frequent antibiotic usage – Oral thrush – Candida albicans Different niche Example: Bacterial endocarditis – Streptococcus viridans – Oral commensal – Previous rheumatic heat disease – Infection of damaged heart valves The University of Sydney Page 18 Rate of infection Influenced by virulence and host defenses ID50 = # micro-organisms required to cause disease in 50% of inoculated hosts The University of Sydney Page 19 Questions 1. Which of the following would be the best description of the disease process in periodontal disease? A. Dysbiosis of commensals B. Infection cause by an opportunistic pathogen C. Infection caused by a highly virulent pathogen 2. Opportunistic infection caused by Candida albicans is an example of a: A. Local infection B. Infection that has spread to another niche C. Caused by endotoxins The University of Sydney Page 20 COMMONWEALTH OF AUSTRALIA Copyright Regulation WARNING This material has been reproduced and communicated to you by or on behalf of the University of Sydney pursuant to Part VB of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act. The University of Sydney Page 21

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