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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