Microbiology Chapter 10 - Host-Microbe Interactions

Produce vitamins, compete with pathogens, and help immune system develop.

Pathogen = disease-causing microbe; Normal microbiota are microbes that usually don't cause disease and reside in the body.

Disruption of the normal microbiota.

A microbe that is usually harmless may cause disease in a different host. Example: Group B Strep (GBS) in newborns.

Preference of a pathogen for a specific host (or tissue).

Ability of a microbe to cause disease.

Extent of disease caused by a pathogen.

Measure of a pathogen’s contagiousness.

A pathogen's average number of secondary infections produced by an infected individual in a fully susceptible population, useful during epidemics and pandemics.

A weakened but still infectious pathogen used in vaccines, often created by growing the pathogen in cell cultures.

Infectious Dose-50; the amount of pathogen needed to establish an infection in 50% of exposed hosts.

Lethal Dose-50; amount of a toxin needed to kill 50% of affected and untreated hosts.

Molecules causing adverse host effects like tissue damage or immune suppression.

Lipid A component of Gram-negative bacteria's LPS, triggering septic shock; Often with a lower LD50.

Soluble protein toxins from Gram-positive and Gram-negative bacteria, capable of causing various effects.

Binds to host cell surface receptors, altering gene expression.

Disrupts cell membranes, causing lysis.

Enters host cells after binding to receptors.

The route a pathogen uses to enter the host.

Virulence factor that allows a pathogen to attach to host cells.

Community of microorganisms attached to a surface, often formed by adhesins.

Route a pathogen takes to leave the host.

Molecule that helps pathogens obtain iron from the host.

A metric classifying agents by risk level based on infectivity, disease severity, and transmission.

Agents posing limited risk of infection.

Infectious agents, not typically airborne.

Dangerous and incurable pathogens, not airborne or vaccine preventable.

Serious or lethal human diseases, often transmitted through the air.

Dangerous exotic pathogens, with no known cure or treatment, potentially airborne.

Procedures to minimize the spread of bloodborne pathogens, treating all patients as potential carriers.

Measures to prevent direct contact, droplet, and airborne transmission of diseases.

Generalized, non-specific immune response, a quick reaction.

Vertebrate-specific, targeted immune response, slower, and with memory.

Prevent pathogen entry; mechanical, chemical, and physical barriers.

Natural bacteria that helps optimize immune responses to pathogens.

Destroy pathogens by disrupting their plasma membranes or cell walls.

Collection of tissues filtering body fluids.

The ability of a molecule to trigger an immune response, from strongest to weakest: Proteins > Polysaccharides > Lipids > Small Molecules (Haptens).

A small molecule that cannot trigger an immune response on its own but can do so when attached to a larger carrier molecule (like a protein).

Potent T helper cell activators; they can bind to many different T cells, leading to an overactive immune response.

Immune response mediated by T cells, particularly T cytotoxic cells, to target intracellular pathogens and cancer cells.

Immune response mediated by B cells and antibodies, primarily targeting extracellular pathogens and toxins.

Process by which antigen-presenting cells (APCs) display antigens to T cells, initiating an adaptive immune response.

Engagement of T and B cell receptors by antigens, leading to cell signaling and cytokine release, initiating clonal expansion.

Rapid division and specialization of activated T and B cells into effector cells and memory cells.

The destruction of pathogens or infected cells by effector cells and the generation of memory cells for long-term immunity.

T cells develop in the bone marrow and mature in the thymus, where they undergo selection and differentiation into various subtypes.

B cells are produced and mature in the bone marrow, later differentiating into plasma cells which produce antibodies.

Directly destroys infected or cancerous cells, recognizing intracellular antigens presented by MHC I.

Coordinates the adaptive immune response by stimulating other immune cells, recognizing extracellular antigens presented by MHC II.

MHC I presents intracellular antigens to T cytotoxic cells, while MHC II presents extracellular antigens to T helper cells.

Controls the function of other immune cells, preventing excessive immune responses and autoimmune reactions.

T helper cells are essential for activating both branches of the adaptive immune system. They provide crucial support to other immune cells, leading to a robust response.

Some B cells can be activated directly by antigens without T cell help. This usually involves repetitive, non-protein antigens, such as bacterial capsule polysaccharides. However, this activation is limited in its capacity for memory.

T cells require two signals for activation: 1) interaction of the T cell receptor with the MHC-antigen complex and 2) co-stimulatory protein interactions.

When a T cell recognizes its specific antigen, it undergoes rapid proliferation, creating many identical copies of itself.

Activated T cells differentiate into various types, including memory T cells (long-term protection) and effector T cells (immediate action). T helper cells can further differentiate to become TH1 or TH2, depending on the cytokines present. These cells perform different tasks in the immune response.

T cytotoxic cells recognize infected cells by binding to MHC-I antigen complexes. They release perforins (to create pores) and granzymes (to induce apoptosis) which lead to the infected cell's death.

B cell activation in a T cell-dependent manner requires two signals: 1) the B cell receptor binding to extracellular antigen and 2) co-stimulatory proteins interacting, often involving cytokine release from a T helper cell.

Activated B cells proliferate into numerous clones, all recognizing the same epitope. These clones differentiate into plasma cells (antibody production) and memory B cells (long-term immunity).

Antibodies are proteins secreted by plasma cells. They bind to specific antigens that triggered the B cell's activation.

There are five major antibody isotypes: IgG, IgA, IgM, IgE, and IgD, each with unique characteristics and functions. IgG is the most abundant, crosses the placenta, and provides long-lasting immunity. IgM is produced early in infection.

The ability of the immune system to mount a faster and more effective response to pathogens encountered before.

During primary exposure, IgM is produced first, followed by IgG. In a secondary response, memory cells quickly produce high levels of high-affinity IgG, with only a small amount of IgM.

Serological testing measures antibody titers in a person's blood to determine if they have been exposed to a specific pathogen or have been vaccinated.

Convalescent plasma is plasma from recovered patients. It contains antibodies against a specific pathogen and can be used to provide passive immunity for currently infected individuals.

Humoral immunity refers to immunity mediated by antibodies in the bloodstream. The four types are: natural active, artificial active, natural passive, and artificial passive immunity.

Cells that engulf and destroy foreign invaders, such as bacteria and viruses. These include macrophages, neutrophils, and dendritic cells.

Cells that capture and present antigens to T cells, initiating an adaptive immune response. Dendritic cells are the most important type.

The first leukocytes to arrive at a site of injury. They release antimicrobial peptides (AMPs) to fight infection.

Granulocytes that target parasites. They release enzymes and toxins stored in their granules.

Granulocytes packed with defense molecules, including histamine, which contribute to allergies and fighting parasites.

Similar to basophils, they play a role in allergies and fighting parasites, releasing histamine and other inflammatory mediators.

Large, circulating leukocytes that mature into macrophages once they enter tissues.

Large phagocytic cells that can be fixed (residing in specific tissues) or wandering (roaming around) to engulf and destroy invaders.

White blood cells responsible for adaptive immunity. They recognize specific antigens and coordinate a tailored immune response.

Lymphocytes that provide innate immune protection against viruses, bacteria, parasites, and even tumor cells.

Signaling proteins that allow cells to communicate with each other. They regulate and coordinate immune responses.

A type of cytokine that attracts white blood cells to areas where they are needed, like a battleground.

Proteins like transferrin and lactoferrin that bind iron, making it unavailable to pathogens, which need iron for growth.

Organic molecules produced by some pathogens to snatch iron from our iron-binding proteins, allowing them to thrive.

Bacteria that break down red blood cells (RBCs) to access the iron-rich hemoglobin within, overcoming our iron-binding defenses.

A complex system of over 30 proteins that work together in a cascade to enhance the immune response.

There are three pathways: the classical (triggered by antibodies), alternative (activated directly by pathogens), and lectin pathway (activated by mannose-binding lectin).

The complement system is tightly regulated to prevent self-damage. This is achieved through self-destruct mechanisms and regulators that shut down the cascade after a threat passes.

The localized response to tissue injury, characterized by redness, pain, heat, and swelling. It serves to protect, fight infection, and initiate tissue repair.

The first stage, characterized by vasodilation (blood vessel widening) and increased vessel permeability, allowing fluid to leak into the tissues.

Molecules released during inflammation that contribute to vasodilation, increased vessel permeability, and attracting immune cells.

The second stage, where white blood cells are recruited to the site of injury by chemoattractants.

The final stage, where inflammation subsides, swelling decreases, and tissue repair begins.

The formation of new blood vessels, which occurs during the resolution phase of inflammation to provide nutrients and oxygen for tissue repair.

A collection of dead tissue cells and white blood cells that accumulates in the resolution phase of inflammation at a wound.

An abnormally high systemic body temperature triggered by pyrogens (fever-inducing substances), which act on the hypothalamus.

Substances like bacterial endotoxins that trigger fever by acting on the hypothalamus.

Fever increases antiviral effects of interferons, enhances phagocyte efficiency, promotes leukocyte production, limits microbial growth, and can promote tissue repair.

Any substance that is foreign to the body and can trigger an immune response. Most antigens are proteins or polysaccharides from bacteria, viruses, fungi, protists, or cancer cells.

The specific part of an antigen that is recognized by antibodies or T cell receptors.

Proteins produced by B cells that specifically bind to antigens, neutralizing their effects and marking them for destruction.

A small molecule that is not immunogenic on its own but can become immunogenic when bound to a larger carrier molecule.

A type of antigen that activates a large number of T cells, leading to a massive immune response that can be harmful.

A microbe capable of causing disease.

A specific mechanism used by a pathogen to overcome host defenses.

A pathogen's preference for a specific host or tissue within a host.

Virulence factors harm the host directly by damaging cells or indirectly by provoking dangerous immune responses.

Previously unknown or rare pathogens that have recently begun to cause disease.

An enzyme secreted by pathogens to break down host tissues and invade deeper.

The damage caused by pathogens to host cells, ranging from mild to severe.

A strategy used by pathogens to evade the immune system by altering their surface molecules.

A system classifying infectious agents based on their risk to humans, ranging from BSL-1 (minimal risk) to BSL-4 (highly dangerous).

Proteins that directly target pathogens to disrupt their cell membranes or walls.

White blood cells with granules in their cytoplasm that are visible under a microscope.

White blood cells that lack granules in their cytoplasm.

A test that measures the different types of white blood cells in the blood, which can indicate a disease.

Lymphocytes are white blood cells involved in adaptive immunity. The main types are B cells, T cells, and NK cells.

B cells and T cells are the only lymphocytes involved in adaptive immunity.

Signaling proteins that allow cells to communicate with each other. They regulate and coordinate immune responses.

An exaggerated, overactive response by the immune system involving excessive cytokine production. It can be dangerous, leading to tissue damage.

Cytokines that attract white blood cells to areas where they are needed, like a battleground.

Iron-binding proteins like transferrin and lactoferrin bind iron, making it unavailable to pathogens that need iron for their growth.

Some pathogens produce siderophores, molecules that snatch iron from our iron-binding proteins, or they break down red blood cells to access the iron-rich hemoglobin.

A complex system of over 30 proteins that work together in a cascade to enhance the immune response.

The classical pathway is triggered by antibodies, the alternative pathway activates directly by interacting with the invading agent, and the lectin pathway is activated when mannose-binding lectin binds to sugars on the microbe's surface.

Regulating the complement system is crucial to prevent self-damage. Without regulation, the cascade could continue unchecked, leading to harmful inflammation.

The cardinal signs of inflammation are redness, pain, localized heat, and swelling.

A collection of dead tissue cells and white blood cells that forms in the late resolution phase of inflammation.

An abnormally high systemic body temperature triggered by pyrogens (fever-inducing substances), which act on the hypothalamus.

Some B cells can be activated directly by antigens without T cell help. This is usually limited to repetitive non-protein antigens, like bacterial capsule polysaccharides.

T cells require two signals for activation: 1) interaction of the T cell receptor with the MHC-antigen complex, and 2) co-stimulatory protein interactions.

Activated T cells differentiate into memory T cells for long-term protection, and effector T cells for immediate action.

T cytotoxic cells kill infected or cancerous cells by recognizing intracellular antigens presented by MHC I.

T cytotoxic cells release perforins to create pores in target cells and granzymes to induce apoptosis.

B cells require two signals for activation in a T cell-dependent manner: 1) the B cell receptor binding to extracellular antigen and 2) co-stimulatory proteins interacting, often involving cytokine release from a T helper cell.

B cell clones differentiate into plasma cells (antibody production) and memory B cells (long-term immunity).

Antibodies are proteins secreted by plasma cells. They bind to specific antigens that triggered the B cell's activation, neutralizing them and marking them for destruction.

IgM is produced early in infection, while IgG is the most abundant and provides longer-lasting immunity.

Convalescent plasma is plasma from recovered patients, containing antibodies against a specific pathogen. This is a passive immunity treatment for infected individuals.

Many emerging pathogens have expanded their host or tissue range, meaning they can now infect humans, sometimes even targeting specific tissues within the body.

Normal microbiota are microbes that usually don't cause disease and reside in our body, while pathogens are disease-causing microbes.

Pathogenicity is the ability of a microbe to cause disease, while virulence measures the degree or extent of disease caused by a pathogen.

The amount of pathogen needed to establish an infection in 50% of exposed hosts.

The amount of toxin needed to kill 50% of affected and untreated hosts.

The complement system is powerful but needs to be tightly regulated to prevent damage to our own tissues. Uncontrolled activation can lead to inflammation and autoimmune diseases.

Redness (rubor), swelling (tumor), heat (calor), and pain (dolor). These are caused by the body's response to injury or infection, involving vasodilation, increased vessel permeability, and the recruitment of immune cells.

Angiogenesis is the formation of new blood vessels. It occurs in the resolution phase of inflammation to provide nutrients and oxygen for tissue repair.

Pus is a yellowish-white fluid that accumulates in the resolution phase of inflammation. It consists mainly of dead white blood cells, bacteria, and other debris.

Fever is an abnormally high systemic body temperature triggered by pyrogens (fever-inducing substances). It is a systemic response to infection and can enhance the immune system's ability to fight pathogens by increasing antiviral effects, enhancing phagocyte efficiency, promoting leukocyte production, and limiting the growth of some pathogens.