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V.N-immunology
| Term | Definition |
|---|---|
| Macro-parasites | Worms |
| Micro-parasites | -Protozoa -Fungi -Bacteria -Viruses |
| Variance in Susceptibility | Sick cell anaemia -Mutation -2 Copies of Gene is Fatal -1 Copy makes red blood cells much less susceptible to Malaria Parasites |
| Immune System is seen as a castell Why is this? | -Physical/Physiological Barriers -Innate Immunity -Specific Adaptive/Acquired Immunity |
| Barriers and Portal of Entry | -Lungs-Cilia and Mucus -Gut -Mucus, Acid and Bacteria |
| Lysozyme | -Enzyme that attacks component of bacteria cell walls -Breaks up 'Lyses' Bacteria -Present in tears, saliva and other secretions |
| Transferrins | -Used in Iron Metabolism -Bind Tightly to iron -Present in plasma, milk (Lactoferrin) and other fluids |
| Lactoferrin | -In milk -Lowers 'free' iron concentration limiting ability of bacteria to multiply |
| Innate Immune Responses | -Next line of defence-"Guards on Parapet" -DO NOT require prior exposure to Agent -Operate before other immune responses -Operate closely with other mech responding to injury -Hope invading org(Pathogen)posses Recognition -Acute Phase |
| Innate Immune Responses | -Overlap with mech that sense tissue damage |
| Pathogen Associated Mol. | -Lipopolysaccharide-Signif. comp. of walls of gram negative bacteria -Bacterial DNA -Double Stranded RNA- only exists in Viruses |
| Innate Immune Mechanisms | -Complement -Phagocytes -Neutrophils & Macrophages -Natural Killer Cells |
| Phagocytes (2) | -Neutrophils -Macrophages |
| Complement (Inserting Tube) | -Use Circulating, preformed Elements (C1,C2,C3, etc) -Components can split (e.g. C3 into C3a,C3b) Subunits are active -Presence of Pathogen Alters Balance, Driving Formation of C3b-Complement Activation -Leads to Formation of 'holes' in Bact Cell |
| Phagocytsis | -Phagocyte recognizes Bacterium (Chemotaxis) -Adherence Through PAMP Recognition -Memb Activation through 'Donger' signal -Initiation of Phagocytosis -Phagosome formation -Fusion of Granules -Killing and Digesting -Release of waste products |
| Phagocytes 1-Macrophages | -Produced in Bone marrow before circulating in blood as MONOCYTES -Settle in tissues as MACROPHAGES -Present in tissue before pathogen arrives and recruited in response |
| Phagocytes 2-Neutrophils | -Produced in Bone Marrow -Commonest white blood cell in circulation -Only Recruited in Tissue in response to Pathogen -Functions as Phagocyte -Also generates 'Reactive' mol. in a Respiratory burst (Absces) |
| Eosinophil | -Worm invader Neutrophils will be replaced by Eosinophils -Generate Respiratory Burst -NOT Phagocytes (Worm To Big) -Stick to surface of worm and attack with Lethal Agents -Large No. generates greener pus |
| Natural killer Cells | -Markers Inhibit NK cells -Target cells and bring about its destruction (Apoptosis) |
| Apoptosis | -Programmed cell death |
| Specific Adaptive Immunity -2 Main Effector Branches | -Next Line of Defence -Also known as ACQUIRES IMMUNITY -Only produced in response to invader 1) Humoral Immunity (Anitbody) 2) Cell Mediated Immunity |
| Specific Adaptive Immunity | -Pathogen mol. act as ANTIGENS |
| Antigens | -Stimulate Lymphocytes to produce antibodies -Recycles to cell surface bound to a host mol (MHC1 or 2) |
| Antibody | - =Immunoglobulin (Ig) |
| 2 Main Types of Lymphocytes | 1) B Lymphocytes 2) T Lymphocytes |
| B-Lymphocytes | -Produce Antibody |
| T-Cells (Lymphocytes) | -Important in process of producing antibodies |
| MHC 1 | -Function to present antigens, self-molecules |
| MHC 2 | -Found On Specialized Antigen Presenting Cells e.g Macrophages, dendritic cells |
| Dendritic Cell | -Antigen Presenting Cell |
| Antibody Types (5) | 1) IgA 2) IgD 3) IgE 4) IgG 5) IgM |
| IgA | -Secreted Across Epithelia - N.B in Mucosal Defence-Gut, Respir Tract, Urogenital Tract |
| IgD | -Stays bound to B-Cells Membrane -Functions as Antigen Receptor |
| IgG | -Major Circulating Antibody -Stays in blood, Released into tissue by Inflammation |
| IgM | -1st Antibody Type Produced in Most Instances -Initially Memb. bound, later released -Up to 10 binding sites therefore very 'Sticky' |
| IgE | -Activates other cells especially Mast Cells -Shown to be N.B in rejection of larger parasites (Worms) -N.B in allergic disease |
| Antibody Functions (3) | 1) Neutralisation 2) Agglutination (Coagulation) 3) Opsonisation |
| 1) Neutralisation | -Prevents viral entry into cells -Deactivates Toxins |
| 2) Agglutination (Coagulation) | -Makes bacteria clump together and therefore easier for phagocytes to eliminate (IgM is very good at this) |
| 3) Opsonisation | -Enhances the process of phagocytosis |
| Neutralisation | -Viral Molecule binds to cell receptor facilitating entry into the cell - Antibody binds to viral mol and prevents it binding to cell receptor, thereby preventing entry into the cell |
| Opsonization | 1-Antibody Binding to Bacterium 2-Antibody-coated bacterium binds to Fc receptors on cell surface 3-Macrophage Memb Surrounds Bacterium |
| Lysosome | -Is a cell organelle that contains "Lytic" Products |
| Antibody Functions | 1) Complement Activation -Improved complement Function 2) Activation of cells such as mast cells, eosinophils and macrophages |
| Blood Groups | -Group A -Group B -Group AB -Group O |
| Blood Group- A | -Antibodies Present= Anti-B -Antigens Present= A antigen |
| Blood Group- B | -Antibodies Present= Anti-A -Antigen Present= B antigen |
| Blood Group- AB (Universal Acceptor) | -Antibodies Present= NONE -Antigens Present= A & B antigens |
| Blood Group- O (Universal Donor) Given in emergency when cant test! | -Antibodies Present= Anti-A and Anti-B -Antigens Present= NONE |
| Blood Transfusions | -Can get away with any blood for cat first time but might not work the second time |
| Transfusion In Cats | -AB cats have no antibodies so can get blood from any animal -Transfusing A blood into a B cat results in rapid destruction of donated type A blood -Transfusion of Type B Blood into A cats produces milder clinical signs half-life of 21 days |
| 1)Haemolytic Disease of Newborn (Neonatal) | -Occurs when a mother produces antibodies against the blood group antigens of their young -Exposure in pregnancy or prior to transfusion |
| 2)Haemolytic Disease of Newborn (Neonatal) | -Antibodies cross Placenta or are ingested in colostral milk and attack RBC before or just after the animal is born -Potential Problem in Cats, horses, pigs |
| Blood Groups and Parentage | -Prior to DNA testing, blood types used to be used to confirm parents |
| T-Cells (2) | 1- T Helper Cells 2- Cytotoxic T cells |
| 1-T Helper Cells | -Help direct immune response/ Activate B-cells |
| 2-Cytotoxic T Cells | --Capable of killing -Virally infected cells -Cells with bacteria -Tumour Cells --Cell-Mediated Immunity |
| Cytokines | -Signaling Mol. release by immune cells(especially T-Cells) -Stimulate other immune processes -can Bias immune response according to need -Interleukins (IL-2, IL-5) -Interferons (Gamma-, beta-interferons) |
| Immunity & Inflammation | -Any Injury can cause inflammation -If Sterile, Immune mechanisms stay quiet -In presence of pathogens, initial inflammation (Acute) dominated by Neutrophils (innate immunity) -Pathg N.C quickly, inflammation persists-becom chronic-Lymphocytes appear |
| Sickness Behavior | -Fever -Anorexia (Reduced Appetite) -Depression |
| Process Of Sickness Behaviour Acute Phase Response | -Tied to many of the innate responses |
| Process Of Sickness Behaviour Passive Response to infection | -Debilitation and physical weekness |
| Process Of Sickness Behaviour Adaptive Response-Motivated behavior? | -Innate highly conserved behavior -"Choices" are made -Tied to innate immune mechanisms-Acute phase response |
| Fever | -Raised set point for thermoregulation -Inc. Metabolic Rate (13% for each Degree) -Posture to minimize heat loss |
| Anorexia | -Motivation to feed is reduced -Motivation to rest is increased -If immune response is not rapidly effective anorexia continues and compromises host wellbeing and survival |
| Immunopathology | -Where damaged caused by immune response is greater than harm caused by invading organism -Parasite itself does not cause much damage -The host's response to parasite causes the damage |
| Immune Evasion | -Antigenic shift in viruses -Herpes viruses can prevent antigen presentation by MHC on infected cells -High lipid Content of Mycobacteria wall means they can be phagocytosed but not broken down -Pathogens release immune modifying factors -Wall off |
| Where do all these cells come from? | -Bone Marrow |
| B-Cells are derived from? | Bone Marrow |
| T-Cells are Derived from? | Thymus |
| Immunodeficiency | -Foetus only develops a working immune system later in pregnancy -Genetic Defects in immune function -Could be deficient in T & B Cell Function |
| Acquired Immunodeficiency | -Starvation-Especially low protein diets -"side effect" of disease -"side Effect" of Drug -to prevent rejection of transplant -Corticosteroid Therapy -Toxicity of bone marrow -Due to infection |
| Immunisation (2) | 1)Active 2)Passive |
| 1) Passive Immunisation | -Transfer of antibodies from mother to offspring -In Utero -In Colostral Milk -Anti-venoms -Tetanus antitoxin |
| 2) Active Immunisation | =Vaccination |
| Principle of Vaccination | -Requires exposure to pathogen or antigen without causing disease -Stimulate appropriate immune response (Antibody and cell-mediated immunity) |
| Vaccination | -Killed Org. generally stimulates as strong an immune response and a live one -Live org. can be used if not going to cause disease and a better cell-mediated immunity |
| 2 Components of Vaccinology | -Strength of immune response straight after vaccination (Ability to stop pathogen) -Duration of immunity post-vaccination-Memory Cells |
| Duration of Immunity- Might need to | Boost |
| Vaccine Failure | No vaccine 100% -Wrong strain -Overwheling infective dose -Rapid decline of response -Maternally derived antibody -Poor Responders Misuse of Vaccine -Wrongly manufactured or stored -Out of date -Wrong injection site |
| Maternally derived antibody | -Vaccinating the young animal when passively transferred antibodies still present =Enough Antibody to 'block' vaccine =But not enough to protect anst viral exp -Greater problem with killed vaccines |
| Poor responders | -The average animal versus an animal at the lower end of response |
| Adjuvants | -Non-infectious material included in vaccine -Boosts immunity by=Promoting innate immunity =which reinforces response -Many killed vaccines included aluminum salts |
| Example of vaccine | -Tetanus Toxoid =Deactivated toxin =Commonly used in horses and humans |
| Kitten Vaccines | -1st Dose at 6,8-9 or 12 weeks (12 months) of age -Core Vaccine boosters every 3 years |
| Puppy Vaccines | -1st dose at 6,8 or 12 weeks of age -Newer vaccines give at least years protection |
| Vaccine to stimulate maternal antibody | -Active immunization of mother-antibodies in colostrum transfer to calf (passive) and prevent disease |
| BCG | -Given to Humans to prevent Tuberculosis |
| Why have some vaccines been so poor? | -Vaccines for disease that ordinarily provoke a good, solid immunity tend to work well -Vaccines against disease where natural immunity is very poor (TB) or develops only slowly (Helminths) have worked less well |
| Vaccines Needed | -Better TB Vaccine -Malaria -Hiv |
| Vaccine Risks | -No therapy is without risk! -For serious, life-threatening diseases -Over-vaccination |
| Over-Vaccination | -Poor knowledge of how long immune response stimulated by vaccines |
| Allergic Disease | -Inappropriate response to something that would not expect to react against -Antigen=Allergen -Immediate Reaction or Delayed (over days) |
| Role of Mast Cells and IgE | -Mast cells are immune cells that reside in tissue -N.B. role in rejection of helminth parasites -Critical role of IgE along mast cells -Mast Cells Release histamine |
| Anaphylaxis | -Due to Bees and Wasps -Due to widespread Mast cell activation Respiratory Problems -Anaphylactic shock |
| Atopy | -(genetic) predisposition to mount excessive IgE response -Atopic Dermatitis -Asthma |
| Asthma | -Immediate response to allergens=Mast cells -Delayed and prolonged damage to airways-eosinophils |
| Autoimmune Disease | -Inappropriate expression of immune response to 'self' -Diabetes |
| Hygiene Hypothesis | -Disease increase as standard of living increases -When hygiene standards are high, immune system has little to do -Rather than stay quiet-Inapp Activation occurs |
Created by:
Melissa Jones
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