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This is the complete lecture note for MED614 Infectious Diseases II. You can read it online below, open it in the full viewer, or download the PDF for offline study. It pairs with the course's video lectures, so you can read and watch together.
la-NET | ONLINE LEARNING VIDEO PLATFORM FOR POST-SECONDARY & HIGHER INSTITUTION STUDENTS
la-NET | ONLINE LEARNING VIDEO PLATFORM FOR POST-SECONDARY & HIGHER INSTITUTION STUDENTS Course code: MED 614 Course title: Infectious Diseases II Course credit load: 2 Units Series 1: Host-Pathogen Interactions • Part 1.1: Principles of Host Defence o Sub Part 1.1.1: Innate immunity o Sub Part 1.1.2: Adaptive immunity o Sub Part 1.1.3: The microbiome and colonisation resistance • Part 1.2: Microbial Virulence and Pathogenicity o Sub Part 1.2.1: Mechanisms of microbial virulence o Sub Part 1.2.2: Adhesion and invasion o Sub Part 1.2.3: Microbial evasion of host defence • Part 1.3: The Host-Pathogen Relationship o Sub Part 1.3.1: Commensalism, colonisation, and infection o Sub Part 1.3.2: Factors determining disease outcome o Sub Part 1.3.3: The compromised host • Part 1.4: Principles of Diagnosis and Antimicrobial Therapy o Sub Part 1.4.1: Principles of microbiological diagnosis o Sub Part 1.4.2: Principles of antimicrobial therapy o Sub Part 1.4.3: Antimicrobial resistance Introduction This opening Series of Infectious Diseases II builds the foundational, conceptual framework the entire course rests on, working through how the human host defends itself against microbial challenge, how microorganisms in turn attempt to overcome that defence, and the genuinely wide spectrum of outcomes, from harmless colonisation to life-threatening infection, this ongoing interaction can produce.
la-NET | ONLINE LEARNING VIDEO PLATFORM FOR POST-SECONDARY & HIGHER INSTITUTION STUDENTS The aim of this Series is to equip you with an understanding of innate and adaptive immunity, the microbiome and colonisation resistance, the mechanisms of microbial virulence including adhesion, invasion, and immune evasion, the spectrum from commensalism to infection and the factors determining outcome, including the compromised host, and the principles of microbiological diagnosis, antimicrobial therapy, and antimicrobial resistance. This Series opens with the principles of host defence, moves through microbial virulence and pathogenicity and the host-pathogen relationship, and closes with principles of diagnosis and antimicrobial therapy. Series Learning Outcomes At the end of this Series, you should be able to: • SLO 1.1: describe innate and adaptive immunity • SLO 1.2: describe the microbiome and colonisation resistance • SLO 1.3: describe mechanisms of microbial virulence, including adhesion and invasion • SLO 1.4: discuss microbial evasion of host defence • SLO 1.5: describe the spectrum from commensalism to infection and the factors determining disease outcome • SLO 1.6: describe the compromised host • SLO 1.7: describe the principles of microbiological diagnosis and antimicrobial therapy • SLO 1.8: discuss antimicrobial resistance 1.1 Principles of Host Defence 1.1.1 innate immunity A genuinely rapid, non-specific first line of defence Innate immunity, the body's immediate, genuinely non-specific first line of defence, includes physical barriers such as intact skin and mucosal surfaces, chemical barriers including gastric acid and antimicrobial peptides, and cellular components, neutrophils and macrophages, capable of recognising broad, genuinely conserved microbial patterns and mounting a rapid response without requiring prior exposure to the specific organism involved. Pattern recognition receptors, including toll-like receptors, allow innate immune cells to recognise genuinely broad classes of microbial structure shared across many different pathogens,
la-NET | ONLINE LEARNING VIDEO PLATFORM FOR POST-SECONDARY & HIGHER INSTITUTION STUDENTS triggering inflammatory signalling and recruiting further immune cells to the site of infection, and this rapid, though genuinely non-specific, response provides essential early containment while the more specific adaptive response, discussed in the following sub-Part, develops. Fill in the blank: Innate immunity provides a rapid response without requiring prior ________ to the specific organism involved. 1.1.2 adaptive immunity A genuinely specific, memory-forming defence developing over days Adaptive immunity, developing over days following initial exposure, provides a genuinely highly specific response tailored to the particular pathogen encountered, mediated by B lymphocytes, producing specific antibodies, and T lymphocytes, including cytotoxic T cells directly destroying infected cells and helper T cells coordinating the broader immune response, working together to mount a genuinely targeted attack against the specific invading organism. Immunological memory, the genuinely defining feature distinguishing adaptive from innate immunity, allows a considerably faster, more effective response upon subsequent re-exposure to the same specific pathogen, and this memory-based mechanism directly underlies the principle of vaccination, deliberately generating protective immunological memory without the risk of genuine natural infection. Fill in the blank: Immunological memory allows a considerably faster, more effective response upon subsequent re-exposure to the same specific ________. 1.1.3 the microbiome and colonisation resistance The body's resident microbial community as a genuine defensive asset The microbiome, the genuinely vast community of microorganisms normally resident on and within the human body, particularly the gastrointestinal tract, provides genuine protective benefit through colonisation resistance, the normal microbiota's capacity to competitively exclude potentially pathogenic organisms from establishing themselves, whether through direct competition for nutrients and attachment sites or production of inhibitory substances. Disruption of the normal microbiome, most commonly through antibiotic therapy already introduced conceptually here and discussed further later in this Series, can genuinely reduce colonisation resistance, allowing potentially pathogenic organisms, including antibiotic-resistant organisms discussed later in this Series, or Clostridioides difficile, to establish themselves and cause genuine clinical infection where the normal, undisturbed microbiome would otherwise have prevented this.
la-NET | ONLINE LEARNING VIDEO PLATFORM FOR POST-SECONDARY & HIGHER INSTITUTION STUDENTS Fill in the blank: Colonisation resistance is the normal microbiota's capacity to competitively exclude potentially ________ organisms. Figure 1.1: A labelled diagram comparing innate and adaptive immune response timelines and characteristics. Pilot questions 1.1 1. Describe the components of innate immunity. (Linked to SLO 1.1) 2. Describe pattern recognition receptors. (Linked to SLO 1.1) 3. Describe the roles of B lymphocytes and T lymphocytes in adaptive immunity. (Linked to SLO 1.1) 4. Explain immunological memory and its relevance to vaccination. (Linked to SLO 1.1) 5. Describe colonisation resistance. (Linked to SLO 1.2)
la-NET | ONLINE LEARNING VIDEO PLATFORM FOR POST-SECONDARY & HIGHER INSTITUTION STUDENTS 1.2 Microbial Virulence and Pathogenicity 1.2.1 mechanisms of microbial virulence The genuine tools a pathogen uses to cause disease Virulence factors, genuinely specific molecular tools a microorganism possesses enabling it to cause disease, include toxins, directly damaging host tissue or disrupting normal cellular function, enzymes, facilitating tissue invasion or degrading host defensive molecules, and capsules, physically resisting phagocytosis by host immune cells, and the specific combination of virulence factors a given organism possesses directly determines its genuine disease-causing potential. Pathogenicity, an organism's genuine capacity to cause disease, varies considerably across different microorganisms, from genuinely obligate pathogens causing disease in essentially every host they infect, to opportunistic pathogens, causing disease only in a genuinely compromised host, a distinction with direct relevance to the compromised host discussion later in this Series, illustrating how genuinely context-dependent the outcome of host-pathogen interaction can be. Fill in the blank: Capsules physically resist ________ by host immune cells. 1.2.2 adhesion and invasion The genuinely essential first steps of establishing infection Adhesion, a microorganism's genuine capacity to attach to host cells or tissue surfaces, typically mediated by specific surface structures including pili and adhesins binding to specific host cell receptors, represents a genuinely essential first step in establishing infection, since organisms unable to adhere are typically cleared by normal host mechanical defences, including mucociliary clearance already introduced in relation to innate immunity. Invasion, a microorganism's genuine capacity to penetrate host epithelial barriers and disseminate to deeper tissue, whether through direct cellular invasion or exploitation of normal host transport mechanisms, follows successful adhesion in genuinely pathogenic organisms, and understanding this specific, sequential adhesion-then-invasion process directly informs both diagnostic sampling strategy and, in some cases, specific therapeutic approaches targeting these particular steps. Fill in the blank: Adhesion is typically mediated by specific surface structures including pili and adhesins binding to specific host cell ________.
la-NET | ONLINE LEARNING VIDEO PLATFORM FOR POST-SECONDARY & HIGHER INSTITUTION STUDENTS 1.2.3 microbial evasion of host defence A genuine evolutionary arms race between pathogen and host Microorganisms employ genuinely diverse strategies to evade host defence, including antigenic variation, altering surface antigens to avoid recognition by existing immune memory, direct interference with phagocytic killing mechanisms, and, in some cases, genuine intracellular survival, hiding within host cells to avoid extracellular immune surveillance entirely, each strategy directly countering a genuinely specific component of the host defence system already discussed earlier in this Series. This genuine evolutionary arms race between host defence and microbial evasion strategy directly explains why certain infections, despite an apparently intact host immune system, can genuinely persist or recur, and understanding the specific evasion mechanism a given pathogen employs directly informs both the expected natural history of infection and, in some cases, the specific therapeutic or preventive approach most likely to succeed against it. Fill in the blank: Antigenic variation involves altering surface antigens to avoid recognition by existing immune ________. Table 1.1: Comparing microbial virulence mechanisms Mechanism Genuine function Example Toxin production Direct tissue damage or cellular disruption Exotoxin release Capsule formation Resistance to phagocytosis Encapsulated bacteria Antigenic variation Evasion of existing immune memory Surface antigen alteration Pilot questions 1.2 1. Describe virulence factors and give examples. (Linked to SLO 1.3) 2. Distinguish obligate from opportunistic pathogens. (Linked to SLO 1.3) 3. Describe adhesion as a
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