Infection And Response 💘 Flashcards
What is a pathogen?
Any microorganism that causes disease
State the four main groups of pathogens and give an example of each
Bacteria e.g. Food poisoning
Virus e.g. Cold
Fungus eg athletes foot
Protist eg malaria
Describe the pathogens ‘ differences
A virus is not living
Bacteria produces toxins protist is carried by a vector
Explain how the spread of a disease can be reduced or prevented
Jabs vaccines and good hygiene by washing your hand regularly
Describe symptoms and effects of two different plant diseases
Rose black spot:black splotched on surface of leaves
Tobacco mosaic: yellowing and curling of leaves
What are the two ion deficiencies we have learnt and what effect do they have on plants?
Lack of nitrates causes stunted growth
Lack of magnesium causes chlorosis
List the main safety conditions when culturing microorganisms
Use a sterilised item to put the bacteria on the petting dish so the results are accurate
Put the Petri dish in the right temperature (25orbelow)if at 37 could cause a human pathogen
Sellotape the lid
Don’t open or have food around
Describe how you could recognise bacterial or fungal growth on a Petri dish
Smooth dots for bacteria yellowy brown colour
Furry dots or shapes for fungi could have roots coming out of it
What conditions do microorganisms need to grow
Warm moist place where there are nutrients
What is athletes foot and symptoms
It’s a rash caused by a fungus that usually appears between the toes
Affected area is red dry and flaky
Describe the life cycle of malaria
Mosquito bites infected human and picks up plasmodium which undergoes several stages of development in mosquito it then bites another human injecting plasmodium sporozoites which affect liver cells which when affected burst releasing plasmodium that infects red blood cells which then burst infecting and Mosquitos that bite the human
What are bodies first line of defences?
Skin,mucus,cilia,tears,stomach acid etc
Explain how the immune system defends against disease
The lymphocytes recognise and remember how to treat the disease as it has already treated before
Describe all the jobs of white blood cells.include phagocytosis antitoxin and antibodies in your response
There are two types of white blood cells lymphocytes make antitoxins antibodies and memory cells
Phagocytes engulf and ingest the pathogen so when your body gets that disease again it will know how to treat it
What is a vaccine
Dead weakened version of an antigen from a pathogen or microorganism in a form of a medicine
This triggers a low level immune response so your body can respond more quickly to the pathogen if infected later
How do vaccines prevent disease don’t forget to refer to next time in your answer
Because vaccines have the weakened version of the disease it won’t affect a human that much The vaccine is so the lymphocytes can learn to make antibodies for it and the phagocytes can ingest it so the next time you get that disease your white blood cells recognise ur and know how to get rid of it faster making you immune to the disease
Explain herd immunity
If there are people around you that have had a vaccine for a certain disease you still won’t get the disease because people are immune to it and can get rid of the disease so no one can pass on the disease to you
What can patients and doctors do to prevent antibiotic resistant bacteria forming
Doctors can prescribe antibiotics correctly
Patients can take the full prescribed course even if you feel better before it
What process causes bacteria to become resistant to antibiotics
Natural selection or gene mutations occur before the antibiotic is in the body bacteria without the mutation die and the others don’t
Why is a problem developing drugs that kill viruses
To reproduce viruses insert themselves into living cells so if you tried killing a virus you would be damaging your own cells which is dangerous
How would you calculate the cross sectional area in a Petri dish that has been killed by an antibiotic dish
Find the are of the circle pi x radius squared
Who discovered penicillin and how did he make his discovery
Alexander Fleming discovered penicillin by noticing that a mould with a bacteria free circle had formed on his Petri dish while studying penicillin
Describe the entire process of developing a new drug
what types of things are being tested at each stage
Include placebo double blind trial clinical toxicity efficacy and preclinical
First you do a preclinical test which is testing the drug on human cells in a lab next is the clinical test where you test it on healthy humans to test the toxicity efficacy and dose finally the drug is tested on patients sometimes control groups are given a placebo which is a no medication pill
What are monoclonal antibodies
They are antibodies that target a certain cell or chemical in or outside the body and are made in labs
What are mabs made of
Made of b lymphocytes from mice and tumour cells which then produces a hybridoma cell which can divide and make antibodies which are then cloned purified and ready to use
How do monoclonal antibodies relate to antigens
They bind to a specific cell the antibody covers the cells antigen therefore restricting the cell form getting protein which causes the cell to die
How are monoclonal antibodies used in pregnancy tests
Monoclonal antibodies bind to a hormone called hcg which is made in the early stages of pregnancy and is passed out of the body in urine
What is the independent and dependent variable
Dependent variable is the value observed by the researcher during the experiment
The independent variable influence change in the dependent variable
What are control variables
Variables that are not changed to make sure it’s a fair test
How is a control and a control variable different
A control is a second set is data which is bit affected by the substance being measured this is so you can compare the results this is different to a control variable because you are not changing the variable
What’s an interval
How much you go up on in an independent variable
How can data be more reliable
Do more repeats
Describe the effect on death rate of having only nurses working in Ward B and not doctors doctors didn’t wash hands
Lower percentage of women died
Other than improvements in hygiene, give two reasons for the low death rate from infectious diseases in modern hospitals.
Vaccines
Better knowledge on immunity
Infectious
Describes a pathogen that can easily be transmitted or an infected person who can pass on a disease
Vector
An animal that spreads a communicable disease e.g. Mosquitos for malaria
Antibiotic
Group of medicines discovered by Alexander Fleming that kills bacteria and fungi but not viruses
Chitin
Polymer made of sugars which forms cell walls of fungi and the exoskeletons of insects
Branching filaments of fungus that spread out
Hyphae
Malaria
A communicable disease caused by a protist transmitted in mosquitoes which attacks red blood cells
Insecticide
A chemical that kills insects
Lysozymes
Antibacterial enzymes in tears to prevent eye infections
Cilia
Tiny hair like projections from ciliated cells that waft mucus out the gas exchange system
A protein on the surface of a pathogen that your antibodies recognise as foreign
Antigen
Antitoxin
Protein produced by body to neutralise harmful toxins produced by pathogens
Antiseptic
Substance applied to skin or another surface to destroy pathogens
Anaesthetic
Drug which stops all pain sensations and can be local or general
How effective a drug is
Efficacy
Double blind trials
Medical experiment in which both doctors and patients don’t know who has been given the drug or the placebo
Placebo
Medicine with only psychological effects and no drugs inside it to actually help you
Phagocytes
Type of white cell that engulf pathogens
Lymphocytes
Type of white blood cell that produces antibodies
Y shaped proteins produces by the immune system that helps stop intruders harming the body
Antibodies
Complement system
Multi catalytic system compromising multiple proteins with enzymic activity
Activation of complement cascade stimulated by some pathogens regulating acute inflammation
Pathogens coated for recognition opsonisation
Terminal components may kill pathogens via membrane lysis
Inflammatory response
Pathogen binds to complement c3 initiating complement cascade
Release of histamine and chemoattractants
Increased permeability of vessels leads to oedema altered adhesive ness of endothelium allows cell migration
Phagocyte recognises opsonised pathogens
Innate immunity
Quick Recognises foreign pathogens No memory Antigen non specific Macrophages and phagocytosis and inflammatory response
Adaptive immunity
Takes days to develop
Antigen specific
Generates memory
Results in immunity
Prions
Small infectious particles
Helminths
Worm parasites
Infection via larvae and eggs
Theee types tape worm flukes and roundworms
Primary vs secondary lymphoid tissues
Primary is sites where lymphocytes differentiate t lymphocytes in thymus b lymphocytes in bone marrow
Secondary are specialised sites for turning on the acquired immune response such as lymph nodes spleen MALT GALT NALT etc
Non hematopoetic stromal cells help organise lt architecture
Lymphatic
Form from joining lymph capillaries superficial lymphatic flow to superficial veins
Flow into lymph nodes in axillary (armpit) inguinal (groin) or cervical (neck) areas where they drain into deep lymphatics which follow main vessels
Spleen
Largest lymphoid organ
Directs immune responses to antigens in the flood and is important for clearance of affected blood cells
Hyposlenism predisposes to infection and a sign or presence of nuclear fragments in rbcs in peripheral blood
Splemagaly common in chronic disease
Innate defences
Phagocytes activate NADPH oxidase causing respiratory burst releasing toxic oxygen radicals which damage microbrial membranes and ctivste microbicidal enzymes found in granules
Neutrophil catch bacteria using NETS which contain chromatin granule proteins and enzymes to degrade pathogen virulence factors
Cytokines and chemokines
Hormones of immune system which allow communication
Referred to as interleukins
Small molecular weight chemotactic cytokines known as chemokines
Usually short lasting
Can be co regulated and help define cell subsets eg Th 1 and Th2 CD4+ lymphocytes
Five types of antibodies
Ig G A M E D
G has 4 subclasses 1,2,3,4 with decreasing order of abundance
A has two subclasses 1 and 2
A and G also have polymorphic variants called allotypes
Antibodies diversity is due to
Encoded by multiple gene segments
Germ line diversity
Combinations and junctional diversity (somatic recombination)
Somatic hyper mutation
Somatic hypermutation introduces random changes to antibody binding site directed by activation induced deaminade AID which binds to specific hotspots. Affects affinity so there’s selection mechanisms to generate higher affinity clones
Immune cells and epitomes
B cells use antibodies to recognize ‘conformational epitotes’
T cells use T cell receptors to recognize linear epitotes
Epitotes are segments of amino acids
MHC cells take up broken down peptide antigens and take them to surface of phagocytosis cells for receptors to bind
MHC class one
One heavy chain
Expressed on all uncleared cells
Carry peptides generated in cytosol or endoplasmic reticulum
Present peptides to CD8+ T cells
Surveillance for virus infection and altered self
Class two MHC
Has two heavy chains On specialised antigen presenting cells Carry peptides generated in endosomal compartments Present peptides to CD4+ cells Surveillance for exogenous pathogens
Affinity vs avidity
Affinity is strength of interaction between receptor and ligand
Avidity is combined strength of interactions
Valency
How many interactions that contribute to avidity
Fab and fc
Fab is fragment antigen binding site (light chain and variable region)
Fc is fragment crystallisable which dictates consequences of binding (heavy chain)
Examples of each antibody
M- activates complement system
A- transports across epithelium
G- diffusion into extra cellular sites opoinisation, activated complement system, stuck to blood
E-stuck to tissues, sensitization of mast cells
Many phenotypic molecules are called
T cells develop under
Cluster of differentiation
Transcription factors
Sometimes T cells stop working
Senescent T cells enter terminal differentiation state and doing excessive cell replication associated with irreversible cycle arrest and telomere shortening
Anergic T cells
Unresponsive state induced by suboptimal stimulation (signal one without 2/3) at time of priming by antigen
Exhausted T cells
Overstimulation bia signal 1 and 3 causing hierarchal loss of effector functions and memory T cell property and by expression of multiple inhibitory receptors
Three signals required (along with antigen) for T cell activation and differentiation
Signal one is TCR engagement is the antigen present?
Signal two is costimulation is the antigen meaningful?
Signal three is cytokines what type of T cell should I become to respond correctly
Polycythemia
Primary secondary
Relative
Excess red blood cells
Causes dizziness headaches red face breathing difficulties itchiness etc
Primary due to genetic problems ( eg due to high working EPO or JAK 2)
Secondary is due to conditions that promote RBC development eg epo secreting tumors
Relative when blood cells normal but reduced plasma volume
Type one hypersensitivity
IgE
Soluble antigen
Causes mast cell activation
Eg asthma anaphylaxis
Type two hypersensitivity
IgG Cell or matrix associated antigen Cell surface receptors Complement Antibody alters signalling Eg some drug allergies eg penicillin
Type three hypersensitivity
IgG
Soluble antigen
Complement phagocytes
Eg serum sickness
Type four hypersensitivity
TH1 cells > soluble antigen > macrophage activation eg tuberculin
TH2> soluble antigen> eosinophil activation> eg chronic asthma
CT2 > cell associated antigen> cytotoxicity> eg contact dermatitis
Example of primary immunodeficiency
Chronic granulomatous disease
Affects how phagocytes kill pathogens
Recessive sec linked
Symptoms include impetigo skin and rectal abscesses recurrent pneumonia granulomas etc
Secondary immunodeficiency
HIV Three stages third one is aids Normal cd4 count is 500-1500 Do Elisa test to identify it Affects immune system
Therapeutic interventions for autoimmune disease
Cytokines therapy
Reduce lymphocyte activation by interfering with signaling pathways eg steroids blocking cell surface receptors
Killing the cells causing the disease eg anti B cell antibodies rituximab
Pneumonia’s for hypersensitivity
ABCD
ALLERGY ANTIBODY COMPLEXES DELAYED
ACID
AKKEGY CYTOTOXIC IMMUNE COMPLEX DELAYED
Immediate reaction
HEC
Release of mast cell mediators:
Histamine causes smooth muscle contraction promoting edema and acts as chemoattractant to other wbcs
Cytokines induce inflammation
Enzymes eg Tryptase activate complement
Immediate reaction TLP
TH2 cytokines- IL4 activates TH2 cells IL 3&5 induce eosinophil activation
Leukitrines cause bronchial and guy contraction and chemotaxis of eosinophils and neutrophils
Prostaglandins cause vasodilation increased vascular permeability and bronchial and gut contraction
Late response
Causes migration of leukocytes especially eosinophils which release peroxidase and other mediators causing further tissue damage
Type three hypersensitivity reason
Due to infectious and environmental agents
Normally removed by complement constantly which causes tissue damage
Deposited in kidneys blood vessels and joints causing immune response
