Host-Microbe Interactions, Pathogenesis, and Immunity: Microbiology Study Notes

Study Guide - Smart Notes

Tailored notes based on your materials, expanded with key definitions, examples, and context.

Host-Microbe Interactions and Pathogenesis

Overview of Host-Microbe Interactions

Host-microbe interactions refer to the dynamic relationships between microorganisms and their human hosts. These interactions can be beneficial, neutral, or harmful, and are central to understanding infectious disease and immunity.

Mutualistic Relationship: Both host and microbe benefit (e.g., gut microbiota aiding digestion).
Commensal Relationship: Microbe benefits, host is unaffected (e.g., skin microbiota).
Parasitic Relationship: Microbe benefits at the host's expense, often causing disease.

Example: Lactobacillus in the vagina helps maintain pH and prevent infections (mutualism).

Microbiota and Disease

Normal microbiota are essential for health, but disruptions can lead to disease. Antibiotic therapy, dysbiosis, and genetic factors can influence susceptibility to infection.

Immune System Development: Microbiota help train the immune system.
Antibiotic Therapy: Can disrupt microbiota, leading to overgrowth of pathogens.
Dysbiosis: Imbalance in microbiota linked to inflammatory diseases.
Genetic Factors: Host genetics affect susceptibility to pathogens.

Pathogenesis: Steps in Infectious Disease

Stages of Pathogenesis

Pathogenesis is the process by which microbes cause disease. It involves several key steps:

Entry into Host: Pathogens must enter the host through portals of entry (skin, respiratory tract, GI tract, urogenital tract).
Adherence to Host Tissues: Pathogens use adhesins (cell wall components, pili, capsules) to attach to host cells.
Invasion and Evasion: Pathogens invade tissues and evade immune defenses (e.g., hiding from phagocytosis).
Replication: Pathogens replicate while avoiding immune detection.
Transmission: Pathogens exit the host via portals of exit (respiratory droplets, feces, urine, blood).

Portals of Entry and Exit

Portals of entry are anatomical sites where pathogens gain access to the host. Portals of exit are routes by which pathogens leave the host to infect new individuals.

Entry: Skin, respiratory tract, GI tract, urogenital tract.
Exit: Respiratory droplets, feces, urine, blood, skin.

Virulence Factors and Toxins

Virulence Factors

Virulence factors are molecules produced by pathogens that enhance their ability to cause disease. These include adhesins, toxins, enzymes, and mechanisms for immune evasion.

Adhesins: Allow attachment to host cells.
Toxins: Damage host tissues and disrupt normal function.
Immune Evasion: Capsule formation, antigenic variation, hiding within host cells.

Endotoxins vs. Exotoxins

Endotoxins and exotoxins are two major classes of bacterial toxins. They differ in structure, source, and effects.

Property	Endotoxin	Exotoxin
Made by	Gram-negative bacteria	Gram-positive and Gram-negative bacteria
Released from	Cell wall when bacteria die	Actively secreted
Fever	Common	Rare
Can be neutralized by vaccines	No	Yes
Toxicity level	Lower (high LD50)	Higher (low LD50)

Additional info: LD50 refers to the lethal dose required to kill 50% of a test population.

Immune System: Innate and Adaptive Immunity

Innate Immunity

Innate immunity is the body's first line of defense, providing rapid, non-specific protection against pathogens. It includes physical barriers, chemical defenses, and cellular responses.

Physical Barriers: Skin, mucous membranes.
Chemical Barriers: Lysozyme in tears, stomach acid.
Cellular Defenses: Neutrophils, macrophages, natural killer cells.

First-Line Defenses

Mechanical Barriers: Skin, mucous membranes, cilia.
Chemical Barriers: Lysozyme, acidic pH.
Physical Barriers: Structures that block pathogen entry.

Second-Line Defenses

Molecular Defenses: Cytokines, complement system.
Cellular Defenses: Phagocytic cells (neutrophils, macrophages).

Leukocytes and Their Functions

Leukocyte	Function	Associated Conditions
Neutrophils	Phagocytosis, acute infection	Bacterial infection
Eosinophils	Fight parasites, allergies	Parasitic infection, allergy
Basophils	Release histamine	Allergic reactions
Monocytes	Phagocytosis, become macrophages	Chronic infection/inflammation
Lymphocytes	Adaptive immunity	Viral infection

Cytokines

Cytokines are signaling proteins that regulate immune responses. Interferons (IFN-α, IFN-β) are produced by virus-infected cells to alert neighboring cells.

Type	Function
Interleukins (IL)	Regulate growth and differentiation of immune cells
Interferons (IFN)	Antiviral responses
Tumor Necrosis Factor (TNF)	Promotes inflammation

Inflammation and Fever

Inflammation is a protective response to infection or injury, characterized by redness, heat, swelling, pain, and loss of function. Fever is a systemic response that enhances immune efficiency.

Cardinal Signs of Inflammation: Redness, heat, swelling, pain, loss of function.
Fever: Increases phagocyte efficiency, inhibits pathogen growth.

Equation:

Adaptive Immunity

Features of Adaptive Immunity

Adaptive immunity is specific, develops over time, and provides long-lasting protection. It involves T cells and B cells, which recognize and eliminate specific antigens.

Cellular Immunity: T cells (helper and cytotoxic) target infected cells.
Humoral Immunity: B cells produce antibodies to neutralize pathogens.

Comparison of Innate and Adaptive Immunity

Feature	Innate Immunity	Adaptive Immunity
Response Time	Immediate	4-7 days
Specificity	Non-specific	Specific
Memory	No	Yes

Steps in Adaptive Immune Response

Antigen Presentation: Antigen-presenting cells (APCs) display antigens to T cells.
Lymphocyte Activation: T and B cells are activated by antigen recognition.
Lymphocyte Proliferation and Differentiation: Activated cells multiply and specialize.
Antigen Elimination and Memory: Effector cells eliminate antigens; memory cells ensure rapid response upon re-exposure.

Self-Tolerance Screening

T cells and B cells are screened for self-tolerance to prevent autoimmune reactions. Cells that react to self-antigens undergo apoptosis.

Antibodies and Immunoglobulins

IgG: Most abundant, crosses placenta, activates complement.
IgA: Found in secretions (tears, saliva, mucus).
IgM: First produced in response to antigen.
IgE: Involved in allergies and parasitic infections.

Immunological Memory

Memory cells allow for a faster and stronger response upon re-exposure to an antigen. The secondary immune response is more efficient due to the presence of memory cells.

Primary Response: Slower, produces IgM first, then IgG.
Secondary Response: Rapid, produces high-affinity IgG.

Biosafety and Precautions

Biosafety Levels

Biosafety levels (BSL) define laboratory practices and containment measures for handling infectious agents.

Level	PPE Required	Examples
BSL-1	Standard precautions	Non-pathogenic E. coli
BSL-2	Lab coats, gloves, eye protection	Staphylococcus aureus
BSL-3	Respirators, biosafety cabinets	Mycobacterium tuberculosis
BSL-4	Full-body suits, positive pressure	Ebola virus

Types of Precautions

Contact Precautions: Prevent transmission via direct contact.
Droplet Precautions: Prevent transmission via respiratory droplets.
Airborne Precautions: Prevent transmission via airborne particles.

Lymphatic System and Immune Surveillance

Lymphatic System Overview

The lymphatic system transports lymph, filters pathogens, and supports immune cell maturation.

Primary Lymphoid Tissues: Thymus (T cell maturation), bone marrow (B cell maturation).
Secondary Lymphoid Tissues: Lymph nodes, spleen, MALT, GALT.

Functions of Lymphatic System

Transport and Filtration: Lymph vessels transport and filter lymph.
Immune Surveillance: Lymph nodes screen for pathogens.

Summary

This study guide covers the essential concepts of host-microbe interactions, pathogenesis, innate and adaptive immunity, virulence factors, biosafety, and the lymphatic system. Understanding these topics is fundamental for success in college-level microbiology.