Bio diseases .pdf

60. Pathogen: A pathogen is any microorganism that can cause disease, including bacteria, viruses, fungi, and protozoa. They invade the host, multiply, and trigger an immune response. 61. Causes of Disease: ​ Viruses – Infect host cells and hijack their machinery to reproduce (e.g., HIV). ​...

60. Pathogen: A pathogen is any microorganism that can cause disease, including bacteria, viruses, fungi, and protozoa. They invade the host, multiply, and trigger an immune response. 61. Causes of Disease: ​ Viruses – Infect host cells and hijack their machinery to reproduce (e.g., HIV). ​ Bacteria – Release toxins or damage tissues (e.g., Mycobacterium tuberculosis). ​ Protozoans – Single-celled parasites that invade tissues (e.g., Plasmodium spp. causing malaria). ​ Fungi – Cause infections by breaking down tissues (e.g., Candida causing thrush). 62. Examples of Diseases: ​ AIDS (Virus – HIV) ○​ Symptoms: Weak immune system, frequent infections, weight loss. ○​ Transmission: Bodily fluids (blood, semen, vaginal fluids, breast milk). ○​ Treatment: Antiretroviral therapy (ART). ○​ Long-term effects: Leads to AIDS, increasing vulnerability to infections and cancer. ​ Tuberculosis (Bacterium – Mycobacterium tuberculosis) ○​ Symptoms: Persistent cough, weight loss, night sweats, fever. ○​ Transmission: Airborne droplets. ○​ Treatment: Long-term antibiotics (e.g., rifampicin, isoniazid). ○​ Long-term effects: Can cause lung damage or spread to other organs. ​ Malaria (Protozoan – Plasmodium spp.) ○​ Symptoms: Cyclical fever, chills, sweating, headaches. ○​ Transmission: Anopheles mosquito bites. ○​ Treatment: Antimalarial drugs (e.g., chloroquine, artemisinin-based therapy). ○​ Long-term effects: Can lead to anemia, organ damage, or death. ​ Athlete’s Foot (Fungus – Trichophyton) ○​ Symptoms: Itchy, flaky skin between toes. ○​ Transmission: Contact with infected surfaces. ○​ Treatment: Antifungal creams or powders. ○​ Long-term effects: Chronic infection if untreated. General Defense System 63. Skin as a Barrier: ​ Sebum – Oily secretion that inhibits microbial growth. ​ Exfoliation – Constant shedding of skin removes pathogens. ​ Scab formation – Prevents microbial entry after injury. 64. Blood Clotting & Hemophilia:  ​ Blood clotting prevents infection by sealing wounds. ​ Hemophilia is a disorder where blood doesn’t clot properly, increasing infection risk. 65. Barriers to Pathogens: ​ Physical: Skin, mucus, cilia in the respiratory tract. ​ Chemical: Stomach acid, lysozymes in tears and saliva. ​ Biological: Beneficial gut bacteria outcompeting harmful microbes. 66. Non-Specific Responses: ​ Phagocytosis: White blood cells engulf pathogens. ​ Lysosomes & Lysosomal Enzymes: Break down the pathogen inside phagocytes. ​ Mast Cells & Histamine: Trigger inflammation by increasing blood flow and permeability. 67. Cause of Swelling, Redness, and Heat in Infections: ​ Swelling (Edema) – Histamine causes fluid leakage from blood vessels. ​ Redness (Erythema) – Increased blood flow to the area. ​ Heat – More blood in the area raises the temperature, limiting pathogen replication. 68. Edward Jenner’s Work: ​ Developed the first smallpox vaccine in 1796 using cowpox. ​ Proved that exposure to a milder virus could confer immunity. 69. Ethical Issues in Jenner’s Research: ​ Experimented on an 8-year-old boy (James Phipps) without consent. ​ Would be considered unethical today due to lack of informed consent. 70. Differences Between Non-Specific and Specific Immunity: ​ Non-Specific (Innate): General defenses (e.g., skin, phagocytosis, inflammation). ​ Specific (Adaptive): Targets particular pathogens (e.g., antibodies, memory cells). Specific Defense System 71. Antigen & Antibody: ​ Antigen: A foreign molecule (usually a protein) that triggers an immune response. ​ Antibody: A Y-shaped protein produced by B cells that binds to specific antigens. 72. Antibody Structure (Diagram Needed): ​ Constant region: Determines antibody class. ​ Variable region: Binds to specific antigens. ​ Disulfide bridges: Hold the structure together.  ​ Hinge region: Provides flexibility. ​ Light & heavy chains: Form the antibody. 73. How Phagocytes Recognize ‘Self’ and ‘Non-Self’: ​ They detect MHC (Major Histocompatibility Complex) markers. ​ ‘Non-self’ cells have foreign antigens, triggering phagocytosis. 74. Autoimmune Disorders: ​ Occur when the immune system attacks the body’s own cells. ​ Caused by failure in self-recognition. 75. Examples of Autoimmune Diseases: ​ Type 1 Diabetes – Immune system attacks insulin-producing pancreatic cells. ​ Rheumatoid Arthritis – Immune system targets joint linings, causing inflammation. Adaptive (Specific) Immune Response 76. Differences Between Humoral (Antibody) and Cellular Responses The humoral immune response is mediated by B cells and involves antibody production, while the cellular immune response is mediated by T cells and directly targets infected or abnormal cells. ​ Humoral (Antibody-Mediated) Response: ○​ Activated by extracellular pathogens (e.g., bacteria, viruses in the bloodstream). ○​ B cells recognize antigens and produce antibodies that neutralize pathogens. ○​ Memory B cells ensure faster responses in future infections. ​ Cellular (Cell-Mediated) Response: ○​ Activated by intracellular pathogens (e.g., viruses inside cells, cancer cells). ○​ T cells (especially cytotoxic T cells) kill infected cells. ○​ Helper T cells release cytokines to activate other immune cells. 77. Antigen-Antibody Complex Formation ​ An antigen is a foreign molecule that triggers an immune response. ​ Antibodies (produced by B cells) have specific binding sites that recognize and attach to antigens. ​ This forms an antigen-antibody complex, which marks the pathogen for destruction via phagocytosis or neutralization. 78. Different Antibody Types (Immunoglobulins: IgG, IgM, etc.) ​ IgG – Most abundant, provides long-term immunity, crosses the placenta. ​ IgM – First antibody produced during an infection, forms pentamers.  ​ IgA – Found in mucosal secretions (e.g., tears, saliva, breast milk). ​ IgE – Involved in allergic reactions, binds to mast cells. ​ IgD – Helps in B cell activation, function still not fully understood. 79. Major Histocompatibility Complex (MHC) and Its Role in Infection Control ​ MHC proteins are found on cell surfaces and present antigens to immune cells. ​ MHC I (on all nucleated cells) presents intracellular antigens (e.g., viral proteins) to cytotoxic T cells. ​ MHC II (on antigen-presenting cells like macrophages) presents extracellular antigens to helper T cells, triggering antibody production. 80-81. Role of Interleukin-1 (IL-1) and Interleukin-2 (IL-2) in Immunity ​ IL-1 is secreted by macrophages to stimulate helper T cells and induce fever (inflammation). ​ IL-2 is secreted by activated helper T cells to stimulate B and T cell proliferation. ​ In the humoral response, IL-2 helps activate B cells to produce antibodies. ​ In the cellular response, IL-2 promotes cytotoxic T cell activation and expansion. 82. Differences Between B Cells and T Cells Feature B Cells T Cells Origin Bone marrow Bone marrow (mature in thymus) Role Produce antibodies Destroy infected cells, activate B cells Response Humoral (antibody-mediated) Cellular (cell-mediated) Type Activation By free-floating antigens By antigen-presenting cells (MHC) 83. Roles of Different Immune Cells ​ B cells – Produce antibodies and differentiate into memory or plasma cells. ​ Helper T cells (CD4+ T cells) – Activate B cells, cytotoxic T cells, and macrophages. ​ Cytotoxic T cells (CD8+ T cells) – Destroy virus-infected or cancerous cells. ​ Memory T cells – Provide long-term immunity by remembering past infections. ​ Suppressor T cells (Regulatory T cells) – Prevent excessive immune responses to avoid autoimmune diseases. 84. Primary vs. Secondary Immune Response & Role of Memory Cells ​ Primary Response (first exposure) ○​ Slow (~5-10 days to produce antibodies). ○​ Involves naive B and T cells. ○​ Low antibody levels, short-lived response. ​ Secondary Response (subsequent exposure) ○​ Faster (~1-3 days) and stronger due to memory cells. ○​ Produces more antibodies for longer periods. ○​ Prevents reinfection or reduces severity of disease. 85. Role of Plasma and Memory Cells in Secondary Response ​ Plasma cells – Produce large amounts of antibodies. ​ Memory cells – Quickly recognize and respond to previously encountered antigens, reducing the lag phase. 86. Clonal Selection & Expansion Theory ​ Clonal Selection: A specific B or T cell is selected when it encounters its matching antigen. ​ Clonal Expansion: The selected cell proliferates rapidly, forming plasma (or cytotoxic) and memory cells. ​ This ensures a targeted and effective immune response. 87. Antigenic Variability and Its Impact on Immunity ​ Some pathogens (e.g., influenza virus, HIV) mutate rapidly, changing their surface antigens. ​ This antigenic drift (small changes) or antigenic shift (major changes) allows them to evade immune detection. ​ Frequent mutations require updated vaccines (e.g., annual flu vaccines). 88. Role of Vaccines in Protection ​ Vaccines expose the immune system to weakened, inactivated, or fragmentary forms of a pathogen. ​ This triggers memory cell formation, providing immunity without causing the disease. ​ Examples: ○​ Live attenuated vaccines – Weakened but active (e.g., MMR, polio). ○​ Inactivated vaccines – Killed pathogens (e.g., Hepatitis A). ○​ Subunit vaccines – Only specific antigens used (e.g., HPV, pertussis). 89. Different Methods of Vaccine Manufacture ​ Live attenuated vaccines – Grown in a lab and weakened (e.g., measles, rubella). ​ Inactivated vaccines – Heat or chemicals used to kill the pathogen (e.g., rabies). ​ Toxoid vaccines – Inactivated bacterial toxins used (e.g., tetanus). ​ Recombinant DNA vaccines – Engineered proteins stimulate immunity (e.g., HPV).  ​ mRNA vaccines – Encode a viral protein that the body produces temporarily. 90. How mRNA Vaccines Work and Their Benefits ​ mRNA vaccines (e.g., Pfizer-BioNTech, Moderna COVID-19 vaccines) deliver genetic instructions for cells to produce a harmless version of the pathogen’s spike protein. ​ The immune system then recognizes the protein and builds antibodies against it. ​ Advantages: ○​ No need for live viruses. ○​ Faster production. ○​ Can be modified quickly for new variants. Herd Immunity & Vaccines 91. Herd Immunity (Population Immunity) ​ Herd immunity occurs when a large portion of a population becomes immune to a disease (through vaccination or previous infection), reducing its spread. ​ This protects vulnerable individuals (e.g., infants, immunocompromised people) who cannot be vaccinated. ​ Examples: ○​ Measles: Highly contagious (R₀ ~12-18); requires ~95% vaccination for herd immunity. ○​ Whooping cough (pertussis): Requires high vaccination rates, but waning immunity means booster shots are necessary. 92. The Discredited MMR-Autism Link ​ A 1998 study falsely claimed a link between the MMR vaccine (measles, mumps, rubella) and autism. ​ This study has been completely debunked, and the author lost his medical license. ​ Numerous studies have confirmed no connection between vaccines and autism. Disease Outbreaks & Containment 93. Course of Disease Outbreaks Outbreaks typically follow a pattern: 1.​ Introduction – First cases appear, often due to a new pathogen or increased exposure. 2.​ Growth (Exponential Phase) – Cases increase rapidly as transmission occurs. 3.​ Peak – Infection rate reaches maximum before interventions take effect. 4.​ Decline – Immunity, vaccination, or control measures reduce cases. 5.​ Endemic or Eradication – Disease stabilizes at a low level or disappears. 94. Methods to Contain Disease Outbreaks ​ Quarantine & Isolation – Restricting movement of infected individuals. ​ Vaccination – Preventing future infections. ​ Hygiene Measures – Handwashing, mask-wearing, sanitation. ​ Contact Tracing – Identifying and isolating potential cases. ​ Public Health Campaigns – Educating communities on prevention. 95. How Vaccines & Boosters Are Made ​ Vaccines are developed using inactivated, weakened, or genetic material from pathogens. ​ Boosters are additional doses to reinforce immunity when it wanes over time. Types of Immunity 96. Active vs. Passive Immunity Type Description Examples Active Immune system produces its own Natural infection, vaccines (e.g., MMR) Immunity antibodies after infection or vaccination Passive Antibodies are transferred from Maternal antibodies (breast milk), Immunity another source antibody injections (e.g., snake antivenom) 97. Natural vs. Induced Immunity Type Description Examples Natural Immunity acquired through natural Recovering from chickenpox, Immunity infection or maternal transfer maternal antibodies Induced Immunity gained via medical intervention Vaccination, monoclonal Immunity antibody therapy Monoclonal Antibodies & Immune Disorders 98. Monoclonal Antibodies ​ Monoclonal antibodies are lab-engineered antibodies that bind to specific targets. ​ Used in cancer treatment (e.g., Herceptin for breast cancer), autoimmune diseases, and COVID-19 therapies. 99. Immune System Problems: Allergies & Organ Rejection ​ Allergies – Overreaction of the immune system to harmless substances (e.g., pollen, food). ​ Transplant Rejection – Immune system attacks transplanted organs because they are recognized as "non-self". 100. Importance of Blood Groups in Transfusions ​ Blood groups (A, B, AB, O) determine compatibility for transfusions. ​ Incompatible transfusions can cause hemolysis (red blood cell destruction), leading to severe reactions. Antibiotics & Resistance 101. What Is an Antibiotic? ​ Antibiotics are substances that kill or inhibit bacterial growth. ​ Not effective against viruses (e.g., colds, flu). 102. How Antibiotics Work ​ Penicillin – Inhibits bacterial cell wall synthesis. ​ Tetracyclines – Block protein synthesis. ​ Quinolones – Disrupt bacterial DNA replication. 103. Development of Antibiotics ​ First antibiotic (penicillin) discovered by Alexander Fleming (1928). ​ Modern antibiotics are chemically modified for effectiveness. 104. Antibiotic Resistance ​ Overuse & misuse of antibiotics lead to resistant bacteria (e.g., MRSA). ​ Mechanisms of Resistance: ○​ Producing enzymes that deactivate antibiotics. ○​ Modifying target sites to prevent antibiotic binding. ○​ Increasing efflux pumps to remove antibiotics. Epidemiology & Disease Patterns 105-107. Observing Patterns in Disease Outbreaks ​ Epidemiologists analyze how diseases spread, peak, and decline. ​ Flu outbreaks in schools and measles in London follow similar cycles: ○​ High contact rates → rapid spread. ○​ Immunity or intervention → decline in cases. 108. What Is Epidemiology? ​ Study of disease distribution and factors influencing outbreaks. 109. Types of Data Collected by Epidemiologists ​ Incidence & prevalence (number of cases). ​ Transmission routes (e.g., airborne, direct contact). ​ Risk factors (e.g., age, geography). 110. John Snow & the Broad Street Cholera Epidemic ​ Identified contaminated water as the source of cholera in London (1854). ​ Removed the Broad Street pump handle, stopping the outbreak. 111. The SIR Model for Disease Spread ​ SIR Model (Susceptible-Infected-Recovered): ○​ S – Susceptible people at risk. ○​ I – Infected individuals spreading disease. ○​ R – Recovered individuals who are immune. 112-113. R₀ (Basic Reproduction Number) & Its Role in SIR Model ​ R₀ (R-naught): Average number of secondary infections from one case. ○​ R₀ < 1: Disease dies out. ○​ R₀ > 1: Disease spreads. ​ Measles R₀ ≈ 12-18 (highly contagious). ​ COVID-19 (original strain) R₀ ≈ 2.5-3 (varies by variant). COVID-19 & Public Health Measures 114. Public Health Measures Observed During COVID-19 ​ Lockdowns – Restricted movement to reduce spread. ​ Social Distancing – Kept people apart to slow transmission. ​ Mask-Wearing – Reduced respiratory droplet spread.  ​ Hand Hygiene – Frequent washing/sanitizing. ​ Vaccination Programs – Mass immunization efforts. 115. Why COVID-19 Measures Were Instigated ​ Flattening the curve – Slowing infection rates to prevent healthcare collapse. ​ Reducing severe cases & deaths – Protecting vulnerable populations. ​ Preventing mutation risks – Slower spread means fewer new variants. 116. Efficacy of COVID-19 Public Health Measures The effectiveness of public health measures during COVID-19 varied based on implementation and adherence. ​ Lockdowns & Social Distancing → Reduced transmission but had economic and mental health impacts. ​ Mask-Wearing → Effective in limiting airborne spread, especially indoors. ​ Vaccination Campaigns → Significantly reduced severe illness and mortality. ​ Hand Hygiene & Surface Cleaning → Less effective than initially thought but still contributed to reducing overall infections. ​ Testing & Contact Tracing → Helped control outbreaks but was overwhelmed in some regions. ​ Border Controls & Travel Restrictions → Delayed spread but could not prevent introduction of variants. Overall, countries that implemented strict and early measures had lower mortality rates (e.g., New Zealand, Taiwan), while those with delayed or inconsistent policies faced worse outcomes (e.g., U.S., Brazil). Flattening the Curve 117. Meaning & Importance of Flattening the Curve ​ Flattening the curve refers to reducing the rate of infection so that the healthcare system does not become overwhelmed. ​ Instead of a sharp spike in cases leading to hospital overcrowding, the goal was to spread infections over time. ​ This allowed hospitals to manage patient loads, ensure availability of ventilators, and prevent excessive deaths. Key Strategies: 1.​ Social distancing 2.​ Mask mandates 3.​ Remote work and school closures 4.​ Vaccination Huge efforts were invested in this because overwhelmed hospitals lead to higher death rates, delayed non-COVID treatments, and collapse of healthcare systems (e.g., in Italy during early 2020). SIR Model & Disease Spread 118. How SIR Models Work The SIR model is a mathematical framework for predicting disease spread. ​ S (Susceptible) – People who can catch the disease. ​ I (Infectious) – People who have the disease and can spread it. ​ R (Recovered/Removed) – People who are immune or dead (no longer spreading infection). Formula & Flow: 1.​ S → I: People become infected based on contact rates. 2.​ I → R: Infected people recover or die at a certain rate. 3.​ Reduction in S leads to a decline in I as herd immunity develops. Example: If COVID-19 has an R₀ = 3, then one person infects 3 others, and the model predicts how fast cases rise and fall. Variations of the SIR Model 119. Adjusted SIR Models The basic SIR model assumes all individuals are equally likely to be infected, but real-world outbreaks involve complexities. Common Variations: 1.​ SEIR Model: ○​ Adds E (Exposed) category for those infected but not yet infectious (incubation period). ○​ Useful for diseases like COVID-19, which has a 2-14 day incubation. 2.​ SIRS Model: ○​ Allows recovered individuals to become susceptible again (e.g., flu, where immunity wanes). 3.​ Age-Structured Models: ○​ Accounts for differences in transmission across age groups (e.g., COVID-19 affected elderly more severely). 4.​ Spatial Models: ○​ Includes geographic movement, useful for tracking global pandemics. These variations make models more accurate for policy-making. Zoonotic Diseases 120. What Are Zoonotic Diseases? ​ Zoonoses are diseases that originate in animals and jump to humans. ​ 60% of human infectious diseases are zoonotic (Wellcome Institute). ​ Spread via direct contact, consumption, or vectors (e.g., mosquitoes, ticks). Example: Rabies ​ Cause: Rabies virus (transmitted via bites from infected animals, e.g., dogs, bats). ​ Symptoms: Fever, aggression, paralysis, fear of water, fatal without treatment. ​ Treatment: Post-exposure prophylaxis (PEP) vaccine if given before symptoms appear. ​ Prevention: Vaccinating pets, avoiding wild animals, quick wound cleaning. Other Examples: ​ COVID-19 (bats → humans via an intermediary host) ​ Ebola (fruit bats → primates → humans) ​ Avian flu (birds → humans) Understanding zoonotic diseases is key to preventing future pandemics (e.g., better regulation of wildlife trade, improved surveillance).