Introduction to Infectious Diseases

Vocabulary flashcards covering key terms from the lecture notes.

Antimicrobial stewardship

Coordinated program to optimize antimicrobial use to improve patient outcomes, minimize resistance, and reduce costs.

Pharmacist role in ID

Pharmacist activities in ID, including confirming antibiotic regimens (dose, route, frequency, duration), checking interactions and allergies, counseling, and participating in stewardship.

Human microbiota

Community of microorganisms that colonize the human body from birth, outnumbering human cells about 10:1.

Colonization resistance

Microbiota-mediated protection that prevents establishment and overgrowth of invading pathogens.

Infectious disease

Disorder resulting from a microbe interacting with the host, causing damage and clinical signs/symptoms.

Pathogen

A microorganism capable of causing disease.

Virulence

A quantitative measure of the pathogenicity or likelihood of causing disease.

Virulence factors

Properties that enable a pathogen to establish infection (e.g., adherence factors, toxins, enzymes, biofilm).

Opportunistic pathogen

Microbe that causes disease primarily in hosts with compromised defenses.

Endogenous reservoir

Reservoir that is part of the host’s own normal flora (e.g., intestinal microbiota).

Exogenous reservoir

Reservoir outside the host, such as other people, animals, environment, or objects.

Mode of transmission

Pathway by which a pathogen moves from reservoir to host, direct or indirect.

Direct transmission

Direct transfer of a pathogen through contact or droplets from one person to another.

Indirect transmission

Transmission via vectors or inanimate objects (fomites), food, water, or surfaces.

Portal of entry

Site by which a pathogen enters the host (e.g., respiratory, GI, GU, skin).

Physical barriers

External barriers like skin and mucous membranes that prevent entry.

Chemical barriers

Chemical defenses such as low pH and lysozymes that inhibit microbes.

Inflammation

Non-specific host response to infection or injury to kill pathogens and repair tissue.

Fever

Raised body temperature as part of the host’s defense, can inhibit pathogens and boost immunity.

Innate immunity

Immediate, non-specific defense including barriers, phagocytes, NK cells, receptors, cytokines, and complement.

Adaptive immunity

Specific immune response with memory, including humoral (B cells/antibodies) and cellular (T cells) components.

Phagocytosis

Engulfment and digestion of pathogens by phagocytes (macrophages, neutrophils, dendritic cells).

Dendritic cells

Antigen-presenting phagocytes that activate T lymphocytes and bridge innate and adaptive immunity.

Monocytes

Circulating white blood cells that mature into tissue macrophages and participate in phagocytosis.

Neutrophils

Most abundant leukocytes; first responders in bacterial infections; destroy pathogens in vesicles.

Eosinophils

Leukocytes that fight parasites and participate in allergic responses.

Basophils

Leukocytes involved in allergic reactions; release histamine upon activation.

CD4 helper T cells

T lymphocytes that activate other immune cells, including B cells and CD8+ T cells.

CD8 cytotoxic T cells

T lymphocytes that destroy infected host cells presenting the same antigen.

B-lymphocytes

B cells that produce antibodies and differentiate into plasma cells.

Immunoglobulins

Antibodies; five classes (IgM, IgG, IgA, IgD, IgE) with distinct roles in immunity.

IgM

First circulating antibody to appear; pentamer; activates complement; does not cross placenta.

IgG

Most abundant antibody; crosses placenta; mediates opsonization and complement activation.

IgA

Antibody in mucosal secretions; protects mucosal surfaces; present in secretions and breast milk.

IgD

Antibody primarily on B cell surfaces; aids activation; does not cross placenta.

IgE

Antibody bound to mast cells/basophils; mediates allergic reactions and anaphylaxis.

Left shift

Increase in immature neutrophils (bands) in blood, indicating acute infection.

Lag phase

Initial period after exposure when bacteria adapt and prepare to grow but do not divide.

Log phase

Exponential growth phase where bacteria divide rapidly.

Stationary phase

Phase where growth slows due to nutrient depletion and waste buildup.