Micro Final Study Guide PDF

Innate Immunity and First Line of Defense First Line of Defense: Physical Barriers: Skin, mucous membranes, and cilia in the respiratory tract that trap and remove pathogens. Chemical Factors: Lysozyme: Found in tears, saliva, and sweat, it breaks down bacterial cell walls. Acidity: Low pH of stoma...

Innate Immunity and First Line of Defense First Line of Defense: Physical Barriers: Skin, mucous membranes, and cilia in the respiratory tract that trap and remove pathogens. Chemical Factors: Lysozyme: Found in tears, saliva, and sweat, it breaks down bacterial cell walls. Acidity: Low pH of stomach acid and skin inhibits microbial growth. Sebum: Creates a protective film on the skin. Second Line of Defense: Involves internal processes such as inflammation, fever, phagocytosis, and the complement system. Components of the Innate Immune System Formed Elements in the Blood: Erythrocytes (RBCs): Transport oxygen. Leukocytes (WBCs): Include neutrophils, monocytes/macrophages, eosinophils, basophils, and lymphocytes. Platelets: Involved in clotting and inflammation. Phagocytosis: Steps: Chemotaxis: Movement of phagocytes toward pathogens. Adherence: Binding of phagocyte receptors to pathogen molecules. Ingestion: Pathogen engulfed into a phagosome. Digestion: Fusion of phagosome with lysosome to form a phagolysosome, where enzymes break down the pathogen. Inflammation: Signs: Redness, heat, swelling, pain. Stages: Vasodilation and increased permeability: Allows immune cells to reach the site. Phagocyte migration: Neutrophils and monocytes arrive. Tissue repair: Regeneration and resolution of inflammation. Fever: Caused by pyrogens resetting the hypothalamus to a higher temperature. Enhances immune response and inhibits pathogen replication. Complement System: Consists of proteins (C1–C9). Functions include: Opsonization (C3b): Enhances phagocytosis. Membrane attack complex (C5b-C9): Creates pores in pathogens, leading to lysis. Inflammation (C3a, C5a): Attracts immune cells to the infection site. Interferons (IFNs): Proteins produced by virus-infected cells that inhibit viral replication in neighboring cells. Iron-Binding Proteins: Examples: Transferrin, lactoferrin. Bind free iron, limiting availability to pathogens. Antimicrobial Peptides (AMPs): Small proteins that destroy pathogens by disrupting membranes or interfering with DNA/RNA. Adaptive Immunity Humoral vs. Cellular Immunity: Humoral: Mediated by B cells and antibodies targeting extracellular pathogens. Cellular: Mediated by T cells targeting intracellular pathogens. Antibody Structure and Function: Structure: Y-shaped molecule with variable and constant regions. Function: Neutralization, opsonization, agglutination, and activation of the complement system. Immunoglobulin Classes: IgG: Most abundant, crosses placenta. IgA: Found in mucosal areas and secretions. IgM: First produced during infection. IgE: Involved in allergic reactions. IgD: Function unclear, found on immature B cells. B Cells and Clonal Selection: B cells recognize specific antigens and proliferate into plasma cells (antibody production) and memory cells. Antibody Mechanisms: Agglutination: Clumping of antigens. Opsonization: Enhanced phagocytosis. Neutralization: Blocking pathogen interaction with host cells. Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC): Killing by NK cells, macrophages. T Cells: CD4+ T Cells (Helper T Cells): Activate B cells and cytotoxic T cells. CD8+ T Cells (Cytotoxic T Cells): Kill infected or cancerous cells. Antigen-Presenting Cells (APCs): Examples: Dendritic cells, macrophages. Present antigens on MHC molecules to T cells. MHC Molecules: MHC I: Found on all nucleated cells, presents endogenous antigens to CD8+ T cells. MHC II: Found on APCs, presents exogenous antigens to CD4+ T cells. Cytokines: Signaling proteins regulating immune responses. Types of Adaptive Immunity: Natural Active: Infection. Artificial Active: Vaccination. Natural Passive: Antibodies from mother to fetus. Artificial Passive: Antibody injection. Diagnostic Tests and Reactions (Chapters 18–19 Part A) Precipitation Reactions: Occur when soluble antigens react with antibodies to form insoluble complexes. Used to detect small quantities of antigens or antibodies. Agglutination Reactions: Clumping of particles (e.g., RBCs or latex beads) coated with antigens or antibodies. Used in blood typing and diagnosis of infections. Immunofluorescence Reactions: Use fluorescent-labeled antibodies to detect specific antigens. Direct method: Detects antigen. Indirect method: Detects antibodies bound to antigens. Neutralization Reactions: Antibodies block pathogen/toxin activity. Used in virus detection and toxin neutralization. Pregnancy Test: Detects human chorionic gonadotropin (hCG) in urine via antibodies. ELISA Test: Enzyme-Linked Immunosorbent Assay detects antigens or antibodies. High sensitivity, used for HIV, hepatitis, and COVID-19. Antibody Titer and Seroconversion: Titer: The concentration of antibodies in serum. Seroconversion: Transition from antibody-negative to antibody-positive status. Hypersensitivity Reactions and Immune Disorders Types of Hypersensitivity: Type I (Immediate): Allergies, mediated by IgE and mast cells releasing histamine. Type II (Cytotoxic): Involves IgG or IgM binding to cells, leading to lysis (e.g., Rh incompatibility). Type III (Immune Complex): Antigen-antibody complexes deposit in tissues, causing inflammation. Type IV (Delayed): Mediated by T cells, takes 24–48 hours (e.g., contact dermatitis). ABO Blood Group System: Based on A, B antigens on RBCs. Incompatible transfusions cause hemolysis. Rh Factor & Hemolytic Disease of the Newborn: Rh incompatibility during pregnancy can cause fetal anemia. Autoimmune Diseases: Examples: Rheumatoid arthritis, lupus. Typically involve Type II, III, or IV hypersensitivity. Human Leukocyte Antigen (HLA): HLA genes encode MHC molecules, essential for tissue compatibility. Transplant Rejection: Mediated by the recipient's immune response to donor MHC molecules. Immune System and Cancer: Immune cells like cytotoxic T cells and NK cells target tumor cells. HIV/AIDS Portals of Entry/Transmission: Blood, sexual contact, vertical transmission (mother to child). Worldwide rates vary, with highest prevalence in Sub-Saharan Africa. Pathogenicity: Targets CD4+ T cells, weakening the immune system. Viral Structure: Enveloped RNA virus, contains reverse transcriptase, integrase, and protease. Viral Replication: Attachment: Binds CD4 receptor and co-receptors (CCR5 or CXCR4). Entry: Fusion of viral envelope with cell membrane. Reverse Transcription: RNA converted to DNA by reverse transcriptase. Integration: Viral DNA integrates into the host genome via integrase. Assembly and Release: New virions are assembled and released. Progression of HIV Infection: Acute Phase: Flu-like symptoms, high viral load. Chronic Phase: Asymptomatic period, gradual CD4+ T cell decline. AIDS: Severe immunosuppression, opportunistic infections. Treatment: Antiretroviral therapy (ART) targets various stages of viral replication. Vaccination: No effective vaccine currently, though research is ongoing. Fungal and Protozoan Diseases Fungal Structures: Septate Hyphae: Hyphae with cross-walls. Aerial Hyphae: Grow above the surface and produce spores. Vegetative Hyphae: Grow within the substrate to absorb nutrients. Life Cycle of Fungi: Asexual Reproduction: Spore formation via mitosis. Sexual Reproduction: Fusion of haploid nuclei to form a diploid zygote. Fungal Diseases: Examples: Candidiasis, histoplasmosis, and ringworm. Malaria: Replication: Plasmodium sporozoites infect liver cells, form merozoites, which infect RBCs. Cyclical fever results from synchronized RBC lysis. Euglena: A flagellated protozoan capable of photosynthesis and heterotrophic feeding. Protozoa and Sexual Reproduction: Protozoa reproduce sexually via gamete fusion or conjugation. Let me know if you'd like more details on specific sections! Chapter 19 Part B: HIV Portals of Entry/Transmission Including Worldwide Rates Transmission: Blood (e.g., transfusions, needle sharing). Sexual contact (vaginal, anal, oral). Mother-to-child (vertical transmission during pregnancy, birth, or breastfeeding). Worldwide, the highest prevalence is in Sub-Saharan Africa. Rates have decreased globally due to prevention efforts but remain significant in vulnerable populations. Pathogenicity HIV targets the immune system, particularly CD4+ T cells, macrophages, and dendritic cells. Leads to progressive immune suppression. Results in opportunistic infections and AIDS (Acquired Immunodeficiency Syndrome). Viral Structure Enveloped virus with a lipid bilayer. Two single strands of RNA. Enzymes: Reverse Transcriptase, Integrase, and Protease. Surface glycoproteins (gp120 and gp41) for host cell attachment. Viral Replication Attachment: gp120 binds to CD4 receptors and co-receptors (CCR5 or CXCR4) on host cells. Entry: Virus fuses with the host membrane, releasing RNA into the cytoplasm. Reverse Transcription: Viral RNA is converted into complementary DNA (cDNA) by reverse transcriptase. Integration: Viral DNA is integrated into the host genome via integrase, forming a provirus. Transcription and Translation: Host machinery produces viral proteins and RNA. Assembly and Budding: New virions are assembled and released, using protease to process proteins. Progression of HIV Infection and Phases Acute Phase: High viral load, flu-like symptoms, rapid CD4 decline. Chronic Phase (Clinical Latency): Asymptomatic or mild symptoms. Slow but steady loss of CD4 cells. AIDS: CD4+ T cell count