Exam Review (Lessons 5,6,7,8)

LESSON 5 - CHAPTER 9: Biological Safety Levels = Different biological safety levels (BSL) exist for handling microbes based on their potential risk  BSL-1: Basic precautions; non-pathogenic microbes. BSL-2: Enhanced precautions; moderate-risk pathogens. BSL-3: High-risk pathogens; lab equipped with controlled access. BSL-4: Extreme pathogens; isolated, specialized facilities. What are fomites  Inanimate objects that can harbor and transmit infectious agents. Ex: Doorknobs, toys, or towels. 2 Factors Deciding Cleanliness Level  (1) Application for which the item will be used (2) Level of resistance to antimicrobial treatment by potential pathogens. Compare Disinfectants, Antiseptics, & Sterilant  disinfectant = Reduces or destroys microbial load of an inanimate item through application of heat or antimicrobial chemicals. Common Application: cleaning surfaces like lab benches, clinical surfaces, and bathrooms. Ex: chlorine bleach or products containing chlorine. Antiseptics = Reduces microbial load on skin or tissue through application of an antimicrobial chemical. Common Application: Cleaning skin broken due to injury; cleaning skin before surgery. Ex: isopropyl alcohol, hydrogen peroxide. Sterilant = Agents that kill all forms of microbial life, including endospores, vegetative cells, and viruses from an inanimate item. Common Application: Preparation of surgical equipment and of needles used for infection. Ex: Pressurized steam (autoclave), chemicals, radiation. Principles of controlling the presence of microorganisms through Sterilization and Disinfectant  Sterilization: Complete elimination of all microorganisms through autoclaving, incineration, and chemical means. Disinfection: Reduction of pathogenic microorganisms; methods include heat, chemicals, and irradiation. Phenol Coefficient = Used to evaluate the potency of disinfectants compared to phenol; higher coefficients indicate greater effectiveness. Ex: a chemical agent with a phenol coefficient greater than 1.0 is more effective than phenol, such as chloramine. Test Methods  Disk-Diffusion Method: Evaluates effectiveness of chemical by measuring zones of inhibition around antimicrobial disks. Use-Dilution Method: Determines the minimum concentration of disinfectant needed to kill a test organism. In-Use Method: Assessment of effectiveness in clinical settings; ensures practical application outcomes. CHAPTER 10: Bacteriostatic vs. Bactericidal  Bacteriostatic Inhibits bacterial growth but does not kill bacteria; often used when the immune system can clear the infection. Bactericidal: Kills bacteria, crucial in severe infections (e.g. immunocompromised patients) when immediate bacterial elimination is necessary. Broad-Spectrum vs. Narrow-Spectrum Drugs  Broad-Spectrum: Effective against a wide range of bacteria; used as empiric therapy while awaiting lab identification. Helpful for polymicrobial infections and prophylaxis during surgery. However, they can disrupt normal microbiota, increasing the risk of superinfection. Ex: tetracycline (broad-spectrum, against both gram-positive and gram-negative bacteria). Narrow-Spectrum: Targets specific bacteria. Best used when the pathogen is identified to reduce collateral damage to normal microbiota. Ex: Penicillin (narrow spectrum, primarily against gram-positive). Superinfections = Secondary infections that occur during or after treatment with antibiotics due to disturbance of normal flora. 6 Modes of Action (Antibacterial drugs)  (1) Inhibit Cell Wall Biosynthesis: Target Peptidoglycan subunits and Penicillin-binding proteins (2) Inhibit biosynthesis: Target 50S and 30S ribosomal subunit (3) Disrupt Membrane: Target Lipopolysaccharide, inner and outer membranes. (4) Inhibit Nucleic Acid Synthesis: Target RNA and DNA (5) Antimetabolites: Target Folic acid synthesis enzyme and Mycolic acid synthesis enzyme. (6) Mycobacterial adenosine triphosphate (ATP) synthase inhibitor: target mycobacterial ATP synthase. Selectivity for Bacterial Cells  Bacterial cells have unique structures (like peptidoglycan) that are not present in human cells, allowing selective targeting. Differences in Modes of Action of drugs that target fungi, protozoa, Helminths, & viruses  fungi: Often target ergosterol in cell membranes. Protozoa: Interfere with metabolic pathways unique to protozoans. Helminths: Block neuronal transmission causing starvation, paralysis, and death of the worm. Viruses: Often inhibit viral replication processes. Ex: Neuraminidase inhibitors (e.g., Tamiflu) prevent influenza viruses from being released, reducing symptoms and illness duration. Challenges for Selective Drug Development  Fungi and protozoa are eukaryotic; therefore, they share more characteristics with human cells, making selective targeting difficult, particularly for HIV infections due to its rapid mutation rate and integration into host cells. Concept of Drug Resistance  Occurs when microorganisms evolve mechanisms to withstand the effects of drugs. Contributing factors: Overuse of antibiotics, incomplete treatments, and using broad-spectrum treatments when not needed. How can Microorganisms Development or Acquire drug resistance?  Microbes can gain resistance through mutations, gene transfer, or exposure to sub-therapeutic concentrations of drugs. Mechanisms of Drug Resistance  Enzymatic modification of drug, modification of drug targets, and efflux pumps. Superbug = Refers to highly resistant bacteria, such as MRSA or XDR-TB. Testing the Effectiveness of Antimicrobials  Kirby-Bauer Disk Diffusion Test = Assesses susceptibility by measuring growth of inhibition zone around drug-impregnated disks; larger clear zones indicate greater susceptibility. Minimal Inhibitory Concentration (MIC) = Lowest concentration of drugs preventing visible growth; informs therapeutic decisions. Inhibits visible growth, observed as turbidity (cloudiness). Minimal Bactericidal Concentration (MBC): Lowest concentration killing >99.99% of the starting inoculum; indicates toxicity and efficacy. No visible growth. Methods for Discovery of new Antimicrobial Agents  High-throughput screening, combinatorial chemistry, exploration of environmental niches, development of inhibitors of resistance mechanisms, & inhibitors of virulence factors. Challenges in Development: Rapid mutation rates in pathogens and the economic burden of developing new antimicrobials hinder discovery efforts. LESSON 6 - CHAPTER 11: Characteristics of an infection  Infection = A state where pathogens invade the body and multiply. Sign: Objective and measurable evidence of disease observable by a clinician (e.g., high blood pressure, fever). Symptom: Subjective evidence of disease reported by the patient, but not clinically confirmed or objectively measured (e.g., pain, fatigue, nausea). Sign vs. Symptom: Signs are measurable; symptoms are subjective (experienced). Syndrome = A group of signs and symptoms that occur together and characterize a particular abnormality (e.g. “-emia” = of the blood or “pathy” = disease). Types of Diseases  Communicable Disease: Can be transmitted from one host to another (e.g., influenza or tonsillitis). Noncommunicable Disease: Not spread from person to person (e.g., tetanus caused by Clostridium tetani). Contagious Disease: A communicable disease that spreads easily (e.g., measles). Noncontagious Disease: Cannot be transmitted (e.g., tetanus). Noninfectious Disease: Not caused by pathogens, often related to genetic factors, the environment, or immune system dysfunction. (e.g., sickle cell anemia). Types of Infectious Diseases  Iatrogenic Diseases: Caused by medical treatment or diagnostic procedures (e.g., infections from surgery). Nosocomial Diseases: Acquired in healthcare settings (e.g., MRSA). Zoonotic Diseases: Transmitted from animals to humans (e.g., rabies). 5 periods of disease  (1) Incubation Period; Pathogen multiplies; no signs or symptoms. (2) Prodromal Period; General symptoms (fever, pain) appear. (3) Period of Illness; Peak severity of signs and symptoms. (4) Period of Decline; Symptoms fade as pathogens decrease; risk of secondary infections may rise. (5) Period of Convalescence; Recovery occurs, but some damage may remain. Pathogenicity  The ability of a microorganism to cause disease, and the degree to which an organism is pathogenic is called virulence. Difference between ID50 and LD50  ID50 (Median Infectious Dose): The number of microorganisms needed to cause an active infection in 50% of inoculated animals. LD50 (Median Lethal Dose): The number of microorganisms needed to kill 50% of hosts. Significant for determining virulence. Types of Pathogens  Primary Pathogens: Cause disease in healthy individuals (e.g., tuberculosis). Opportunistic Pathogens: Cause disease when the host's defenses are down (e.g., Candida in immunocompromised patients). Stages of Pathogenesis  Exposure: Encounter with pathogens through skin or mucous membranes. Not all contacts cause infection. Adhesion: Pathogens attach to host cells using adhesion factors, enhanced by biofilms. Invasion: Pathogens spread in the body, damaging tissues and evading immune responses. Intracellular pathogens enter host cells. Infection: Pathogen multiplication leads to infections classified as: Local: Confined to one area (e.g., boils) Focal: Spreads to secondary sites (e.g., gum to bloodstream). Systemic: Widespread (e.g., chickenpox). Portals of entry  Sites where pathogens enter the body. Ex: mucous membranes of the respiratory tract, gastrointestinal tract, and the genitourinary tract. How do virulence factors contribute to signs and symptoms of infectious disease  virulence factors = Unique features produced by individual pathogens affecting disease severity. Impact of Gene Inactivation: If the genes encoding virulence factors are inactivated, virulence in the pathogen is diminished. Endotoxins vs. Exotoxins  Endotoxins: Found on the outer membrane of gram-negative bacteria; trigger inflammatory responses (e.g., lipopolysaccharides from E. coli). Exotoxins: Proteins produced by gram-positive (mainly) and gram-negative bacteria; often highly toxic (e.g., diphtheria toxin). Types of exotoxins  Intracellular Targeting Toxins: Comprise of two types: A-B toxins - A for action; B for binding (e.g. diphtheria toxin). Membrane-Disrupting Toxins: Damage host cell membranes (e.g., hemolysins). Superantigens: Trigger excessive immune response (e.g., toxic shock syndrome toxin). Virulence factors for Immune Evasion  Capsules: make it difficult for immune cells to attach to the bacteria and engulf them. Proteases: pathogens produce this to protect themselves against phagocytosis. Fimbriae: Aid in adhesion and inhibit phagocytosis. Mycolic Acid: Provides resistance against immune mechanisms in phagolysosomes. Coagulase: exploits that natural mechanism of blood clotting to evade the immune system. Kinases: Break down fibrin clots, allowing pathogens to escape and spread. Antigenic Variation: Alters surface proteins to avoid detection by the immune system. Viral Adhesion and Antigenic Variation  Adhesion: viruses adhere to host cells using viral proteins to facilitate attachment. Ex: hemagglutinin in influenza. Antigenic Variation: Viruses change surface proteins to evade immunity; Drift Minor changes due to mutations; Shift: Major changes from gene reassortment during co-infections (e.g., influenza). CHAPTER 12: Prevalence vs. Incidence  Prevalence = Total number of cases of a disease in a population at a given time. Incidence = Number of new cases of a disease occurring in a specific time period. Morbidity vs. Mortality  Morbidity: Refers to the presence of disease or the adverse effects of disease; Morbidity Rate: Rate of disease in a population. Mortality: Refers to death caused by a disease; Mortality Rate: Rate of death in a population. Types of Diseases  Sporadic Disease: Occurs occasionally (e.g. tetanus, rabies, plague). Endemic Disease: Constantly present in a population within a particular geographic region (e.g., malaria in certain regions like Brazil). Epidemic Disease: Sudden increase in cases in a specific area (e.g. influenza; with rising cases during winter in northern hemisphere). Pandemic Disease: Worldwide spread (e.g., COVID-19, HIV/AIDS). Epidemiology and Public Health  Epidemiology = It’s the study of how infectious diseases spread geographically and over time, aiming to understand and control outbreaks. Role of Public Health Organizations: Monitor health trends, implement disease prevention strategies. Notifiable Diseases (or reportable diseases): Diseases that must be reported to public health authorities (e.g., HIV, measles, West Nile virus infections). Pioneers of Epidemiology  John Snow: Father of epidemiology; identified cholera source in London (1854) via contaminated water. Stopped outbreak by removing a contaminated water pump. Florence Nightingale. Documented soldier deaths in the Crimean War, revealing preventable diseases led to most fatalities. Influenced military healthcare improvements. Joseph Lister: Introduced several disinfection protocols that lowered post-surgical infection rates (e.g. carbolic acid for disinfection). Types of Epidemiological Studies  Observational: Data collected without manipulation; includes descriptive and analytical studies. Strengths: Easier to conduct, identifies associations; ethical for studying outbreaks. Limitations: Cannot establish causality; potential confounding factors. Experimental: Involves manipulation of subjects to assess treatment effects. Strengths: Stronger evidence for cause-effect relationships; can incorporate Koch’s postulates. Limitations: More complex, ethical challenges. Comparison of the studies  Koch’s Postulates: Only experimental designs can apply these postulates for causation. Evidence Strength: Experimental studies provide the most robust evidence for disease etiology. Types of disease transmissions  Living Reservoirs = Organisms that harbor pathogens, facilitating transmission to hosts. Ex: Humans and animals. Nonliving reservoirs = Environmental sites harboring pathogens. Ex: Soil and water. Carriers = Individuals transmitting pathogens without symptoms. Ex: Passive Carrier and Active carrier. Modes of transmissions  Contact Transmission: Direct or indirect contact; Direct: transmission of pathogens that occurs through physical contact (e.g. kissing, touching, sexual intercourse). Indirect: inanimate objects (fomites) that facilitate the indirect transmission of pathogens. (e.g. contaminated doorknobs, towels, and syringes). Vector Transmission: animals (typically arthropods) carrying disease that can be transmitted. Mechanical vector: carries a pathogen on its body from one host to another (e.g. houseflies transferring bacteria from garbage to food). Biological vector: carries a pathogen from one host to another after becoming infected itself (e.g. infected mosquito bites uninfected person). Vehicle Transmission: transmission of pathogens through vehicles (e.g. food, water, air). What are Nosocomial Infections  also called healthcare-associated infections (HAIs). Infections acquired in health-care facilities. Higher rates due to compromised host factors and invasive procedures. International Public Health Entities  World Health Organization (WHO): Coordinates international health activities, provides guidance. Such as monitoring and reporting infectious diseases and developing and implementing strategies for their control and prevention. Emerging vs. Reemerging Infectious Diseases  Emerging Infectious Diseases: New diseases appearing in populations (e.g., Ebola). Reemerging Infectious Diseases: Diseases that have declined but are now increasing (e.g., tuberculosis and malaria).

LESSON 7 – CHAPTER 13: Why are physical defenses called Innate “Nonspecific”  they do not target any specific pathogen; rather, they defend against a wide range of potential pathogens. Why are physical defenses called “Innate” Nonspecific  they are build-in mechanisms of the human organism. Physical Barriers  Skin: Thick outer layer preventing pathogen entry. Mucous Membranes: Release mucus that traps pathogens. Endothelia: Tightly packed cells providing an effective frontline barrier against invaders. Mechanical Defenses  Role: Compete with pathogens for resources and produce substances harmful to pathogens. Ex: In the vagina, resident microbiota compete with opportunistic pathogens like Candida, limiting nutrient availability and inhibiting Candida growth to prevent infections. Enzymatic Protection in Body fluids  Lactoperoxidase: An enzyme in saliva and mucus that produces antimicrobial compounds to inhibit microbial growth and maintain oral health by targeting bacteria. Lysozyme: An antibacterial enzyme in saliva, tears, and mucus that cleaves bacterial cell walls, particularly effective against gram-positive bacteria, leading to their destruction. Lactoferrin: Found in tears, saliva, and mucus; it binds iron to limit its availability to microbes, reducing bacterial and fungal growth. Functions of Key chemical defenses  Antimicrobial Peptides (AMPs): Kill bacteria by attaching membranes or interfering with cells functions. Complement Components: Opsonization of pathogens to aid phagocytosis, chemoattractant for phagocytes, proinflammatory anaphylatoxins. Cytokines: alert cells to viral infections, induce apoptosis in infected cells, and activate immune defenses. Acute-phase Proteins: inhibit the growth of bacteria and assist in the trapping and killing of bacteria. Stimulating Inflammation/Fever example  Cytokines can lead to fever, enhancing metabolic rates to fight infection. Components of Blood  Red Blood Cells (erythrocytes) = Transport oxygen. White Blood Cells (leukocytes) = Immune function. Platelets (thrombocytes) = Blood clotting. Which blood components innate the immune system components  Neutrophils, Monocytes, Eosinophils: Key WBC in innate immunity. Process of Hematopoiesis  Formation of blood elements occurring in bone marrow with neutrophils being the most common. Granulocytes vs. Agranulocytes  Granulocytes: Neutrophils, eosinophils, basophils; involved in inflammation. Distinguished by the number of lobes in their nuclei and the straining properties of their granules. Agranulocytes: Monocytes, lymphocytes; involved in adaptive immunity. Leukocytes Mechanisms for Pathogen Recognition  PAMPs (Pathogen-Associated Molecular Patterns): Recognized by immune cells. Ex: nucleic acids such as viral DNA or RNA. PRRs (Pattern Recognition Receptors): Detect PAMPs; include TLRs (Toll-Like Receptors). Can be found on the plasma membrane or in internal phagosomes. Process of Phagocytosis  phagocytes whose main function is to seek, ingest, and kill pathogens. Stages: the engulfment of a pathogen, the formation of a phagosome, the digestion of the pathogenic particle in the phagolysosome, and the expulsion of undigested materials from the cell. What happens to Cellular Remains during Phagocytosis  Debris can be presented as antigens on cell surfaces to alert adaptive immunity. Signs of inflammation  Erythema (Redness): Increased blood flow to the injured site due to vasodilation from histamine release. Edema (Swelling): Increased vascular permeability allows fluid, proteins, and immune cells to enter the tissue. Heat: Increased blood flow raises the temperature at the injury site. Pain: Stimulation of nerve pain receptors in the tissue due to inflammatory events. Altered Function: Reduced function of the affected area due to pain and swelling. Explanation of Fever  Fever is a systemic response, usually triggered by pyrogens that raise the hypothalamic set point. It enhances immune functions while inhibiting pathogen growth. Advantages and disadvantages posed by inflammatory responses  Advantages: Recruitment of immune cells, dilution of toxins and pathogens, initiation of repair mechanisms. Risks: tissue damage, chronic inflammation. Ex: Tuberculosis. Definitions regarding Specific Adaptive Immunity  Memory: Ability to quickly respond to pathogens to which it has previously been exposed. Ex: After recovering from chickenpox, the body retains memory of the varicella-zoster virus, enabling specific protection against future exposures. Primary Response: Initial response to a pathogen or vaccine, slower and less effective. Ex: contracting chickenpox for the first time, triggering a primary immune response as the body produces antibodies. Secondary Response: Faster, more effective due to memory cells. Ex: after exposure to chickenpox, if the person contracts the virus again, memory cells allow for a faster and more effective response. Humoral vs. Cellular Immunity  Humoral: mechanisms of adaptive specific immunity that involve B cells and antibody production. Cellular: Mediated by T cells; targets infected or defective cells. Antigens vs. Epitopes  Antigens: Molecules that elicit immune response. Antigens are unique to a specific pathogen, whereas PAMPs are found on numerous pathogens. Epitopes: Specific parts (exposed regions of the surface) of antigens recognized by immune receptors. Structures and Functions of Antibodies  Antibody (also called immunoglobulins): are glycoproteins that are present in both the blood and tissue fluids. Binding Site: The y-shaped arms of an antibody are known as the “fab region” which is the fragment of antigen binding. Classes of Antibodies: IgG, IgM, IgA, IgE, IgD with distinct functions. Comparison of MHC Molecule Structures  MHC Class I: Present on all nucleated cells; recognize CD8+ T cells. MHC Class II: Present on macrophages, dendritic cells, and B cells; recognize CD4+ T cells. Structures: MHC I: formed by domains α1 and α2; MHC II: formed by domains α1 and β1. Antigen-Presenting Cells  Dendritic cells, macrophages, B cells processing and presenting antigens via MHC molecules. Antigen Processing and Presenting with MHC I and MHC II  MHC I: Proteins in the cytoplasm are degraded by proteasomes; Peptides bind to MHC I and are presented on the cell surface; If infected, pathogen-specific peptides signal CD8 T cells for destruction. MHC II: APCs recognize and internalize pathogens via phagocytosis; Pathogen proteins are degraded in phagolysosomes; Selected immunogenic peptides bind to MHC II and are presented to CD4 T cells. Similarities and Differences in MHC structures  Similar: Both MHC pathways present antigens to T cells for immune response. Different: cell type and Antigen source. T-cell Maturation  Occurs in the thymus, where T cells undergo selection for functionality and self-tolerance. Classes of Cells  Helper T Cells (CD4+): Activate other immune cells. Orchestrate humoral and cellular immunity; involved in the activation of macrophages and NK cells. Cytotoxic T Cells (CD8+): Directly kill infected cells; destroy cells infected with intracellular pathogens. Superantigens Effect on T-cell activation  Superantigens activate T cells by binding to both MHC II on APCs and the TCR β chain, bypassing specific recognition. This triggers excessive cytokine release, causing a cytokine storm that can lead to severe inflammation, shock, and multi-organ failure. Ex: Staphylococcal enterotoxin produced by Staphylococcus aureus. Often results in toxic shock syndrome. B Cell production and maturation  B cells originate from hematopoietic stem cells in the bone marrow and mature there. Positive and negative selection occurs to ensure functional and non-self-reactive receptors. Naïve mature B-cells then migrate to the spleen for final maturation. B-cel receptors vs. T-cell receptors  BCRs (IgD and IgM) can bind free antigens, whereas TCRs recognize antigens only presented by MHC molecules. B-cell Activation Types  T-dependent: Requires help from T cells; stronger response. T-independent: Direct activation; weaker response. Primary vs Secondary Antibody Responses  Primary is slow and produces IgM; Secondary is rapid, stronger, predominantly IgG. Types of Artificial Immunity  Include active immunity (vaccination) and passive immunity (antibody transfer). Variolation vs. Vaccination  Variolation vs Vaccination  Variolation: Inoculation with smallpox material aimed to induce a mild case for immunity. Risks included severe infections and outbreaks due to contagion. (uses live pathogens). Vaccination: Introduces cowpox to induce immunity against smallpox, developed by Jenner. It is safer than variolation with much lower risks of severe infection. (uses weakened or inactive forms). Types of Vaccines  Live-attenuated; weakened strain of whole pathogen. inactivated; whole pathogen killed or inactivated with heat, chemicals, or radiation. subunit vaccines; immunogenic antigens. toxoid; inactivated bacterial toxin. conjugate; capsule polysaccharide conjugated to protein. mRNA vaccines (excluded in textbook). Advantages and Disadvantages to vaccines  Varies by type regarding efficacy, side effects, and immune response. LESSON 8 – CHAPTER 15: Type I Hypersensitivity (Immediate hypersensitivity)  Mechanism: allergen-specific IgE antibodies bind to mast cells via their Fc receptor. When the specific allergen binds to the IgE, cross-linking of IgE induces degranulation of mast cells. Examples: Allergies (hay fever, asthma, anaphylaxis, hives). Antigen Form: soluble antigen. Immune reactant: IgE. Type II Hypersensitivity (Cytotoxic hypersensitivity)  Mechanism: IgG or IgM antibody binds to cellular antigen, leading to complement activation and cell lysis. IgG can also mediate ADCC with cytotoxic T cells, natural killer cells, macrophages, and neutrophils. Examples: Hemolytic disease of the newborn (HDN), Hemolytic transfusion reactions (HTR). Antigen form: cell-bound antigen. Immune reactant: IgG or IgM. Type III Hypersensitivity (Immune complex-mediated)  Mechanism: Antigen-antibody complexes are deposited in tissues. Complement activation provides inflammatory mediators and recruits neutrophils. Enzymes released from neutrophils damage tissue. Examples: Systemic lupus erythematosus, rheumatoid arthritis. Antigen form: soluble antigen. Immune reactant: IgG and IgM. Type IV Hypersensitivity (Delayed type hypersensitivity)  Mechanism: T_H1 cells secrete cytokines, which activate macrophages and cytotoxic T cells. Examples: Contact dermatitis, type I diabetes mellitus, multiple sclerosis. Antigen form: soluble or cell-bound antigen. Immune reactant: T cells. Medically Significant Aspects  Type I is often allergic reactions; Type II involves cytotoxic reactions; Type III involves immune-complex diseases; Type IV involves delayed immune responses Autoimmune Diseases: Type II and Type III hypersensitivities can be classified as autoimmune disorders. ABO Blood Groups  A, B, AB, O classifications are based on the presence or absence of antigens on red blood cells. Universal Donor Type: Type O (no antigens). Universal Acceptor Type: Type AB (both A and B antigens present, no antibodies against A or B). Immunological reactions may occur when incompatible blood types are mixed, leading to transfusion reactions. Rh Factors  Presence (+) or absence (-) of RhD protein on red blood cells; important in determining compatibility for blood transfusions and pregnancy complications (Rh incompatibility). Development of Autoimmune Diseases  The immune system mistakenly attacks self-antigens, leading to tissue damage. This happens because there is a loss of immune tolerance, and the mechanism responsible for autoimmune diseases include type II, III, and IV hypersensitivity reactions. Known causes include genetic predisposition, environmental triggers (infections, chemicals), and hormonal influences. Organ-Specific Autoimmune Diseases vs. Systemic Autoimmune Diseases  Organ -specific: Examples: celiac disease, Graves disease, Hashimoto thyroiditis, type I diabetes mellitus, and Addison disease Potential treatments: Insulin therapy for diabetes, thyroid hormone replacement for Hashimoto's. Systemic: Examples: multiple sclerosis, myasthenia gravis, psoriasis, rheumatoid arthritis, and systemic lupus erythematosus. Treatments may include immunosuppressants, corticosteroids, and symptom management. Adaptive Immune Response to Tumors  The immune system can recognize cancer cells due to abnormal proteins or antigens (tumor antigens) expressed on their surfaces. Cancer cells can suppress immune responses, making it challenging for the immune system to eliminate them. Tumor Vaccines  Preventative Cancer Vaccines: HPV vaccines for cervical cancer, Hepatitis B vaccine for liver cancer. Therapeutic Cancer Vaccines: Sipuleucel-T for prostate cancer, and T-VEC (for melanoma) stimulate the immune system to target existing tumors. Risks and Benefits to Tumor Vaccines  Risks: Potential adverse effects, variable effectiveness, and limited application as many therapeutic vaccines are experimental. Benefits: Tumor vaccines can enhance the immune response against cancer cells and prevent cancer from viral infections.