Busy. Please wait.

show password
Forgot Password?

Don't have an account?  Sign up 

Username is available taken
show password


Make sure to remember your password. If you forget it there is no way for StudyStack to send you a reset link. You would need to create a new account.

By signing up, I agree to StudyStack's Terms of Service and Privacy Policy.

Already a StudyStack user? Log In

Reset Password
Enter the associated with your account, and we'll email you a link to reset your password.

Remove ads
Don't know
remaining cards
To flip the current card, click it or press the Spacebar key.  To move the current card to one of the three colored boxes, click on the box.  You may also press the UP ARROW key to move the card to the "Know" box, the DOWN ARROW key to move the card to the "Don't know" box, or the RIGHT ARROW key to move the card to the Remaining box.  You may also click on the card displayed in any of the three boxes to bring that card back to the center.

Pass complete!

"Know" box contains:
Time elapsed:
restart all cards

Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.

  Normal Size     Small Size show me how


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