MICROPARA MIDTERM PDF

What Are Vaccines? Vaccines are substances made from germs (or parts of them) that help your body fight off diseases. The first vaccine was for smallpox, created by Edward Jenner in 1798. How Do Vaccines Work? Active Vaccination: Teaches your body to remember and fight of...

What Are Vaccines? Vaccines are substances made from germs (or parts of them) that help your body fight off diseases. The first vaccine was for smallpox, created by Edward Jenner in 1798. How Do Vaccines Work? Active Vaccination: Teaches your body to remember and fight off germs in the future. Passive Vaccination: Gives your body ready-made protection (antibodies), but it doesn’t last long. Herd Immunity: If most people in a group are vaccinated, it helps protect those who can’t get vaccinated, like babies or people with weak immune systems. Types of Vaccines Live Vaccines: Use weakened germs that can’t make you sick. They give strong, long-lasting protection (e.g., MMR for measles, mumps, and rubella). Inactivated Vaccines: Use killed germs. They’re safer for people with weak immune systems but might need more booster shots (e.g., flu shot). Toxoids: These vaccines target toxins made by germs (e.g., tetanus). You need booster shots for continued protection. Subunit Vaccines: Only use parts of germs, so they’re very safe but may need extra doses (e.g., whooping cough vaccine). DNA Vaccines: The newest type, which uses DNA to help your body create a defense. They’re still being studied. Are Vaccines Safe? Vaccines are very safe, though nothing is 100% risk-free. Any risks are usually minor and much smaller compared to the benefits of preventing serious diseases. Some myths, like the false claim that the MMR vaccine causes autism, have been proven wrong. Which Vaccines Are Available? Vaccines are available for many diseases, like COVID-19, flu, HPV, and more. Some vaccines use newer technology like mRNA vaccines (e.g., Pfizer and Moderna’s COVID-19 vaccines). Vaccines for Babies and Young Children Babies get vaccines to protect them from diseases early in life, like Hepatitis B, polio, and rotavirus. Vaccines like MMR (for measles, mumps, rubella) are given at 9-12 months and again at 4-6 years to keep children protected. COVID-19 Vaccines Moderna (mRNA-1273): mRNA Vaccine Pfizer-BioNTech (BNT162b2): mRNA Vaccine AstraZeneca (Vaxzevria): Viral Vector Vaccine Bharat Biotech (Covaxin): Inactivated Vaccine Gamaleya (Sputnik V): Viral Vector Vaccine Sinovac (CoronaVac): Inactivated Vaccine Sinopharm (BBIBP-CorV): Inactivated Vaccine Influenza Vaccines Sanofi Pasteur (Fluzone): Inactivated Vaccine AstraZeneca (FluMist Quadrivalent): Live Attenuated Vaccine Hepatitis Vaccines GlaxoSmithKline (Engerix-B): Recombinant Vaccine (Hepatitis B) GlaxoSmithKline (Havrix): Inactivated Vaccine (Hepatitis A) LG Life Sciences (Heptavax): Recombinant Vaccine (Hepatitis B) Common Vaccines for Children Merck (Gardasil 9): Recombinant Vaccine (HPV) Merck (MMR II): Live Attenuated Vaccine (Measles, Mumps, Rubella) Sanofi Pasteur (IPV): Inactivated Vaccine (Polio) Merck (Varivax): Live Attenuated Vaccine (Varicella/Chickenpox) Pfizer (Prevnar 13): Conjugate Vaccine (Pneumococcal) Sanofi Pasteur (Daptacel): Toxoid Vaccine (DTP) Sanofi Pasteur (Menactra): Conjugate Vaccine (Meningococcal) Merck (RotaTeq): Live Attenuated Vaccine (Rotavirus) Special Vaccines GlaxoSmithKline (Shingrix): Recombinant Vaccine (Shingles) Sanofi Pasteur (Dengvaxia): Live Attenuated Vaccine (Dengue) Sanofi Pasteur (IMOJEV): Live Attenuated Vaccine (Japanese Encephalitis)  Sanofi Pasteur (VERORAB): Inactivated Vaccine (Rabies) Japan BCG Lab (BCG): Live Attenuated Vaccine (Tuberculosis) EuBiologics Co. Ltd. (Euvichol-Plus): Oral Inactivated Vaccine (Cholera) Vaccine Review by Age Group: 1. Newborn Vaccines ○ BCG (Bacille Calmette-Guérin) Manufacturer: Japan BCG Laboratory Type: Live Attenuated Vaccine Age: Newborn Purpose: Protects against tuberculosis. ○ Hepatitis B (Heptavax) Manufacturer: LG Life Sciences Type: Recombinant Vaccine Age: Newborn (within 24 hours) Purpose: Protects against Hepatitis B. 2. Infant Vaccines (6-14 weeks) ○ Pentavalent (DTP-HepB-Hib) Manufacturer: Various (e.g., GlaxoSmithKline, Serum Institute) Type: Combination Vaccine (Toxoid, Recombinant, Conjugate) Age: 6, 10, 14 weeks Purpose: Protects against diphtheria, tetanus, pertussis (whooping cough), hepatitis B, and Haemophilus influenzae type B. ○ Oral Polio Vaccine (OPV) Manufacturer: Sanofi Pasteur Type: Live Attenuated Vaccine Age: 6, 10, 14 weeks Purpose: Protects against polio. ○ Inactivated Polio Vaccine (IPV) Manufacturer: Sanofi Pasteur Type: Inactivated Vaccine Age: 14 weeks Purpose: Additional protection against polio. ○ Pneumococcal Conjugate Vaccine (PCV 13) Manufacturer: Pfizer Type: Conjugate Vaccine Age: 6, 10, 14 weeks Purpose: Protects against pneumococcal infections, such as pneumonia. ○ Rotavirus (RotaTeq)  Manufacturer: Merck Type: Live Attenuated Vaccine Age: 6, 10 weeks Purpose: Protects against rotavirus, which causes severe diarrhea. 3. Vaccines for Toddlers and Older Children ○ Measles, Mumps, Rubella (MMR) Manufacturer: Merck Type: Live Attenuated Vaccine Age: 9 months, 12-15 months Purpose: Protects against measles, mumps, and rubella. ○ Japanese Encephalitis (IMOJEV) Manufacturer: Sanofi Pasteur Type: Live Attenuated Vaccine Age: 9 months Purpose: Protects against Japanese encephalitis. ○ Dengue (Dengvaxia) Manufacturer: Sanofi Pasteur Type: Live Attenuated Vaccine Age: 9 years+ (not usually given under 5 years) Purpose: Protects against dengue fever. ○ Varicella (Varivax) Manufacturer: Merck Type: Live Attenuated Vaccine Age: 12-15 months, 4-6 years Purpose: Protects against chickenpox (varicella). ○ Hepatitis A (Havrix) Manufacturer: GlaxoSmithKline Type: Inactivated Vaccine Age: 12-24 months Purpose: Protects against Hepatitis A. ○ Meningococcal (Menactra) Manufacturer: Sanofi Pasteur Type: Conjugate Vaccine Age: 9 months to 2 years Purpose: Protects against meningococcal disease, which can cause meningitis. 4. Annual or As Needed ○ Influenza (Fluzone) Manufacturer: Sanofi Pasteur  Type: Inactivated Vaccine Age: 6 months and older, given annually Purpose: Protects against influenza (flu). PPT 2 Hypersensitivity (Allergic Reactions) Hypersensitivity is an exaggerated response by the immune system, often called an allergy. The substance that triggers this reaction is called an allergen. Types of hypersensitivity reactions: ○ Type I (Anaphylactic): Quick, severe reactions like anaphylactic shock. Can be caused by allergens like peanuts or insect stings. Treated with epinephrine. ○ Type II (Cytotoxic): When antibodies attack your own cells, like in blood transfusion reactions. ○ Type III (Immune Complex): Antibody-antigen complexes can cause tissue damage, like kidney inflammation. ○ Type IV (Delayed): Delayed reactions like contact dermatitis or tissue rejection in transplants. 1. Type I (Anaphylactic) Reactions Description: This is a rapid allergic reaction, sometimes referred to as immediate hypersensitivity. It involves a fast immune response to an allergen. Mechanism: ○ When an individual is exposed to an allergen for the first time (e.g., pollen, food allergens), their body produces IgE antibodies. ○ These antibodies bind to mast cells and basophils (types of immune cells). ○ Upon second exposure to the allergen, the allergen binds to these IgE antibodies, causing the mast cells and basophils to release substances like histamine, which trigger an allergic response. Symptoms: Include swelling, redness, mucus production, difficulty breathing, itching, and in severe cases, anaphylactic shock, where blood pressure drops and the individual could die within minutes if untreated. Examples: ○ Systemic Anaphylaxis: Severe, body-wide reaction, such as from penicillin or bee stings, which requires immediate treatment with epinephrine. ○ Localized Anaphylaxis: Less severe, affecting parts of the body like the respiratory system (e.g., hay fever or asthma). Prevention: Avoiding known allergens and using desensitization therapy, which involves gradually increasing doses of the allergen to build tolerance (shifting the immune response from IgE to IgG, which does not trigger allergic reactions)​(Disorders Associated wi…). 2. Type II (Cytotoxic) Reactions Description: In Type II hypersensitivity, the immune system attacks the body's own cells that it mistakenly identifies as foreign. Mechanism: ○ This reaction involves IgG or IgM antibodies, which bind to antigens on the surface of the body’s own cells (such as red blood cells). ○ The antigen-antibody complexes activate complement proteins, which leads to the destruction of the target cells, a process called cell lysis. Symptoms: Depending on the specific reaction, symptoms can include destruction of blood cells or tissue damage. Examples: ○ ABO Blood Group Incompatibility: If someone receives the wrong type of blood during a transfusion (e.g., Type A blood given to a person with Type B blood), the body’s antibodies attack the donor red blood cells. ○ Hemolytic Disease of the Newborn (Rh Incompatibility): Occurs when an Rh-negative mother carries an Rh-positive baby. The mother’s body may produce antibodies that attack the baby’s red blood cells during subsequent pregnancies. ○ Drug-Induced Reactions: Certain drugs can bind to red blood cells and make them targets for destruction by the immune system​(Disorders Associated wi…). 3. Type III (Immune Complex) Reactions Description: In Type III hypersensitivity, antigen-antibody complexes (immune complexes) form in the blood and deposit in various tissues, leading to inflammation and tissue damage. Mechanism: ○ These immune complexes form when antibodies bind to soluble antigens in the bloodstream. ○ Normally, these complexes are removed, but in certain cases, they get deposited in tissues such as the kidneys, joints, or blood vessels. ○ The deposited complexes activate complement, leading to inflammation and tissue damage. Symptoms: Symptoms depend on where the immune complexes are deposited. In the kidneys, it can cause nephritis (kidney inflammation); in the joints, it can lead to arthritis. Examples:  ○ Glomerulonephritis: A kidney disorder that develops after an infection, where immune complexes get trapped in the kidney, leading to inflammation and damage. ○ Rheumatoid Arthritis: Immune complexes form in the joints, leading to chronic inflammation and joint damage. ○ Systemic Lupus Erythematosus (SLE): A chronic autoimmune disease where immune complexes can damage many parts of the body, including the skin, kidneys, and joints​(Disorders Associated wi…). 4. Type IV (Delayed Cell-Mediated) Reactions Description: Type IV hypersensitivity is also called delayed hypersensitivity because it takes 24-48 hours for symptoms to appear after exposure to the antigen. Mechanism: ○ Instead of antibodies, this type of reaction involves T cells. ○ Upon first exposure to the antigen, T cells are sensitized and develop into memory T cells. ○ When the individual is exposed again, these memory T cells activate and recruit other immune cells (like cytotoxic T lymphocytes and macrophages) to the site of the antigen, leading to an immune response. ○ This immune response can cause inflammation and tissue damage. Symptoms: Delayed inflammation and tissue damage that occurs days after exposure. Examples: ○ Tuberculosis (TB) Skin Test: A small amount of TB antigen is injected under the skin. If the person has been exposed to TB before, a delayed reaction occurs with swelling and redness at the site after 48 hours. ○ Contact Dermatitis: A skin reaction (like a rash) that occurs after contact with substances such as poison ivy, latex, or certain metals (e.g., nickel). ○ Tissue Rejection: In organ transplants, T cells attack the transplanted tissue as foreign, leading to transplant rejection​(Disorders Associated wi…)​(Disorders Associated wi…). Summary of Key Points: Type I: Immediate, driven by IgE antibodies and involves allergic reactions such as anaphylaxis. Type II: Cytotoxic, involves IgG/IgM antibodies attacking cells, often seen in blood transfusions and Rh incompatibility. Type III: Immune complex-mediated, where antibody-antigen complexes deposit in tissues and cause inflammation.  Type IV: Delayed T-cell-mediated, where T cells trigger immune responses after 24-48 hours, leading to conditions like contact dermatitis and transplant rejection. 2.Autoimmune Diseases Autoimmune diseases occur when the immune system mistakenly attacks the body’s own tissues. Examples include: Multiple Sclerosis: Attacks nerve cells, leading to muscle weakness. Type 1 Diabetes: Destroys insulin-producing cells in the pancreas. 3. Reactions to Transplants Transplanted organs or tissues can be rejected by the body, as the immune system sees them as foreign. Immunosuppressive drugs (like Cyclosporine) are often used to prevent rejection. 4. The Immune System and Cancer The immune system helps fight cancer by recognizing and destroying abnormal cells. Some cancer cells can escape detection or grow too fast for the immune system to handle. 5. Immunotherapy for Cancer Immunotherapy uses the immune system to attack cancer cells, offering a targeted treatment that avoids harming healthy cells. Approaches include: Dendritic cell therapy: Activates cancer-fighting cells. Immunotoxins: Combines toxins and antibodies to target cancer cells specifically. 6. Cancer Vaccines Therapeutic vaccines: Used to treat existing cancers by stimulating the immune system to attack cancer cells. Prophylactic vaccines: Prevent cancer by targeting viruses that cause cancer, like Hepatitis B (linked to liver cancer) and HPV (linked to cervical cancer). 7. Immunodeficiencies Immunodeficiencies occur when the immune system is too weak to defend the body properly. Types: Congenital: Present from birth (e.g., DiGeorge’s syndrome, which affects the thymus gland). Acquired: Caused by external factors like HIV or certain cancers. Ppt 3 Adaptive Immunity Adaptive immunity is a defense mechanism that targets specific pathogens and remembers them for a faster response in the future. Unlike innate immunity, which reacts the same way to any invader, adaptive immunity customizes its response and gets stronger upon repeated exposure. Key Components of Adaptive Immunity: 1. Humoral Immunity (Antibody-Mediated): ○ Involves B cells that produce antibodies to neutralize pathogens circulating outside cells, such as bacteria. 2. Cellular Immunity (Cell-Mediated): ○ Involves T cells that directly attack infected cells or manage other immune cells to clear out intracellular pathogens, like viruses. B Cells and Antibodies (Humoral Immunity) Antigens are substances (often part of pathogens) that stimulate an immune response. Antibodies (or Immunoglobulins, Ig) are Y-shaped proteins produced by B cells to target antigens. Antibody Classes: IgG: Most common; protects blood and tissues. IgM: First responder in blood; short-lived. IgA: Found in mucous; prevents pathogens from attaching to surfaces. IgD: Involved in starting immune responses. IgE: Involved in allergies and defense against parasites. How Antibodies Work: Agglutination: Clumps pathogens together for easier elimination. Opsonization: Marks pathogens for destruction by immune cells. Neutralization: Blocks pathogen entry into cells. Activation of Complement: Helps to destroy pathogens directly. T Cells and Cellular Immunity T Helper Cells (CD4+): Activate other immune cells using chemical signals called cytokines. Cytotoxic T Cells (CD8+): Destroy infected cells by inducing programmed cell death (apoptosis). T Cell Activation Process: 1. Antigen-Presenting Cells (APCs), like dendritic cells, display pathogen fragments to T cells. 2. T Helper Cells release cytokines to recruit and activate immune cells. 3. Cytotoxic T Cells kill infected or abnormal cells. Immune Memory The adaptive immune system creates memory cells that "remember" specific pathogens. ○ Primary Response: Slow and weak, occurring on first exposure.  ○ Secondary Response: Faster and stronger due to memory cells from prior exposure. Types of Adaptive Immunity 1. Naturally Acquired Active Immunity: From infection. 2. Naturally Acquired Passive Immunity: From mother to baby. 3. Artificially Acquired Active Immunity: Through vaccination. 4. Artificially Acquired Passive Immunity: From antibody injections. Dual Nature of Adaptive Immunity Adaptive immunity has two main branches, each targeting different kinds of threats: 1. Humoral Immunity (Antibody-Mediated): ○ Deals with pathogens circulating outside cells, such as bacteria or viruses in the bloodstream. ○ B cells are the primary players here, as they produce antibodies to target and neutralize these pathogens. 2. Cellular Immunity (Cell-Mediated): ○ Targets pathogens inside cells (like viruses within infected cells) that antibodies cannot reach. ○ T cells are responsible for directly attacking infected cells or helping other immune cells to eliminate the invader. Humoral Immunity Function: Primarily involves antibodies produced by B cells to fight off extracellular pathogens. B Cells: When they encounter an antigen, they can produce antibodies to target the antigen. Pathway: Humoral immunity is especially useful for defending against pathogens in body fluids (e.g., blood, lymph). Activation of B Cells B cells become active in two steps:  1. Antigen Binding: B cells have specific receptors that allow them to bind to a specific antigen (foreign substance). 2. Helper T Cell Activation: Often, B cells need help from T helper (TH) cells. When a B cell presents the antigen to a TH cell, the TH cell releases cytokines (chemical signals) that fully activate the B cell. Once activated, the B cell undergoes clonal expansion, creating two types of cells: Plasma Cells: Produce antibodies that circulate to fight off the pathogen. Memory B Cells: Remain in the body long-term and quickly respond if the same pathogen is encountered again. Antigen–Antibody Binding When antibodies (produced by B cells) bind to antigens, several reactions can take place, helping the body to eliminate the pathogen: 1. Agglutination: Antibodies clump antigens together, making it easier for immune cells to clear them. 2. Opsonization: Antibodies coat the pathogen, marking it for easier ingestion and destruction by immune cells. 3. Neutralization: Antibodies block harmful parts of pathogens or toxins, preventing them from entering and damaging cells. 4. Complement Activation: Antibodies activate a group of proteins (the complement system) that assists in destroying pathogens. 5. Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC): This method uses antibodies to target large pathogens, which immune cells then attack from the outside. The Results of Antibody Binding The interactions between antibodies and antigens help eliminate pathogens in multiple ways: Agglutination and Opsonization help immune cells detect and ingest pathogens. Neutralization prevents pathogens from attaching to host cells. Complement Activation and ADCC lead to the direct killing of pathogens or infected cells. Extracellular Killing Some immune responses target pathogens too large for phagocytosis, such as parasitic worms. Eosinophils: These cells release toxic compounds around the parasite, attacking it externally. Natural Killer (NK) Cells: NK cells are nonspecific immune cells that can recognize and kill infected or abnormal cells (like tumor cells) by inducing apoptosis (programmed cell death). They target any cell not showing “self” markers. Immunological Memory After the immune system fights off an infection, it retains a “memory” of the pathogen: 1. Primary Response: The first encounter with a pathogen triggers a slower, less intense response, as B and T cells work to identify and fight the pathogen. 2. Secondary Response: Upon re-exposure to the same pathogen, memory cells quickly react, leading to a faster and stronger immune response. Innate Immunity Overview The Concept of Immunity Immunity refers to the body’s ability to fight off diseases caused by pathogens (such as bacteria or viruses). There are two types of immunity: 1. Innate Immunity: The body’s immediate, general defense mechanism. It fights off pathogens without targeting specific ones. 2. Adaptive Immunity: A specialized defense system that develops over time and targets specific pathogens. Host Defenses (Image 1) There are three main lines of defense in the body: 1. First Line of Defense: Physical barriers like skin, mucous membranes, and normal microbiota. 2. Second Line of Defense: Cells like phagocytes and processes like inflammation, fever, and antimicrobial substances. 3. Third Line of Defense: T cells, B cells, and antibodies, which form part of adaptive immunity. First Line of Defense: Physical Factors Skin: The outer layer of the skin is a tough barrier that sheds regularly, preventing microbes from entering. Mucous Membranes: These membranes produce mucus, a sticky substance that traps microbes and prevents them from entering the body. Other defense mechanisms include tears, saliva, urine, and vomiting, which physically remove microbes from the body. First Line of Defense: Chemical Factors Sebum: An oily substance on the skin that lowers pH, preventing the growth of many microbes. Lysozyme: An enzyme found in sweat, tears, and saliva that breaks down bacterial cell walls. Low pH: Stomach acid (pH 1.2-3) and vaginal secretions (pH 3-5) kill or inhibit the growth of many pathogens. Normal Microbiota The beneficial bacteria that live in and on our bodies. These compete with pathogens for space and resources, preventing harmful microbes from growing. Second Line of Defense (Image 2) If microbes penetrate the first defense layer, the body activates the second line of defense: Phagocytic cells (like neutrophils and macrophages) that eat up harmful pathogens. Inflammation: Swelling and redness to trap and fight off infections. Fever: Increases the body’s temperature to kill or slow down pathogens. Antimicrobial substances: Chemicals that destroy microbes or stop their growth. White Blood Cells (WBCs) and their Functions (Image 3) Different types of WBCs play key roles in innate immunity:  Neutrophils: Attack bacteria and are active during the early stages of infection. Basophils: Release histamine, a chemical that promotes inflammation. Eosinophils: Target large parasites and release toxins to destroy them. Monocytes: When they move into tissue, they become macrophages, which engulf and digest pathogens. Dendritic Cells: Capture microbes and activate the adaptive immune system. Phagocytosis (Image 4) Phagocytosis is the process by which immune cells, like neutrophils and macrophages, engulf and destroy pathogens. The steps include: 1. Chemotaxis: The immune cells are attracted to the microbes. 2. Adherence: The immune cells attach to the microbes. 3. Ingestion: The microbes are engulfed into the immune cell. 4. Digestion: The microbes are broken down by enzymes inside the immune cell. Inflammation (Image 5) Inflammation is the body’s response to injury or infection. Vasodilation: Blood vessels widen to increase blood flow to the infected area, causing redness and heat. Phagocytes move to the area to destroy invading microbes. As phagocytes kill microbes, they sometimes die, forming pus. Fever A fever is an elevated body temperature in response to infection. Benefits: Fever increases white blood cell activity and speeds up tissue repair. Risks: High fevers can be dangerous, leading to seizures, delirium, or even death. Antimicrobial Substances 1. Complement System: A set of proteins that help destroy microbes by: ○ Cytolysis: Breaking down bacterial cells. ○ Enhancing phagocytosis: Making it easier for immune cells to engulf microbes. ○ Triggering inflammation: To recruit more immune cells. 2. Interferons: Proteins that protect uninfected cells from viral infections by stopping viral replication. 3. Antimicrobial Peptides: Small proteins that kill microbes by disrupting their cell membranes.