disease🦠 Flashcards
in phagocytosis, when the bacteria is engulfed, how are its antigens removed for APC
in the phagosome the bacteria is partly broken down by lysozyme so antigens still whole
how are correct t helper cells selected
receptors on plasma membrane of t helper cell are complementary to antigen
explain importance of b memory cells in immunity
- produced in primary immune response
- remain in body
- produce secondary immune response
- quickly before symptoms occur
- divide into plasma cells
- to rapidly produce antibodies
- long term immunity
describe the action of phagocytic cells at site of infection
- pathogen recognised as foreign
- binds to antigen
- phagocytosis/ pathogen engulfed
- forming phagosome
- lysosomes fuse to phagosome forming phagolysosome
- release enzymes to digest pathogen
where are b and t lymphocytes made and where do they mature
b lymphocytes- made in bone marrow, mature in bone marrow
t lymphocytes- made in bone marrow, mature in thymus gland
describe the changes that occur to t lymphocytes during an immune response. explain the roles of t lymphocytes in fighting a pathogen
- t cell with complementary receptors to antigen is selected for
- by clonal selection
- this t cell undergoes clonal expansion
- t helper cells release cytokines
- to stimulate b cells to differentiate into plasma cells
- to stimulate macrophages to carry out phagocytosis more actively
- t killer cells kill infected host cells
- secrete enzymes
- t memory cells stay in body to provide long term immunity
- secondary immune response if reinfected, rapid response
- active immunity
-cell mediated response
what is parasite
- lives in host
- gains nutrients from host
- at expense of host
how does plasmodium bypass human primary defence
- mosquito feeds on blood
- breaks skin so cannot act as barrier
why is malaria common in tropical areas
suitable climate for mosquito
why are erythrocytes that contain plasmodium more likely to be engulfed by phagocytes than healthy erythrocytes
different chemicals that attract phagocytes are released from infected erythrocytes
describe how structure of antibody allows them to perform function
- 4 polypeptides 2 light chains 2 heavy chains
- variable region allows binding to antigen
- 2 variable regions allow binding of more than one antigen
- variable region on different antibodies allows specificity to different antigens
- constant region allows binding to phagocytes
- hinge region allows flexibility
- disulfide bonds hold polypeptides together
how do antibodies neutralise
- prevent binding to host cell
- block antigen of pathogen
- bind to toxins
explain agglutination of antibodies
- clump together many pathogens
- so phagocyte can engulf many pathogens at once
- clump too large to enter host cell
why is saying that bacteria are immune to antibiotics incorrect
- do not have immune system
- resistant
- bacteria are unicellular
why are phagocytes described as the secondary defence
-involved after pathogen has entered body
why are phagocytes considered non specific
-able to digest many different pathogens
how do phagocytes pass from blood into tissue fluid
- lobed nucleus so cell can change shape
- can move through pores in capillary walls
- histamine makes capillary walls leaky
infective agent that causes tuberculosis
M.tuberculosis
how does tuberculosis pathogen spread
- droplets
- cough
- inhaled by individuals
factors that increase TB infection
- overcrowding
- poor diet
- homelessness
- not vaccinated due to no access
how does mosquito transmit malaria to human
- mosquito is vector
- plasmodium present in mosquito saliva
- infected mosquito bites human
- plasmodium passes from saliva to blood
which lymphocytes secrete substances to kill infected cells
-T
which lymphocytes activate other lymphocytes
T
why is influenza vaccine changed every year
- different antigen shape
- mutates
- antibody produced needs to match new strain
difference between primary and secondary immune response
- secondary starts earlier
- secondary more rapid
- secondary produces more antibodies
role of memory cells
- recognise pathogen
- produce clones
- B memory cells divide into plasma cells which produce antibodies
- T memory cells differentiate into T killer cells which kill infected host cells
- pathogen killed before symptoms
drug which inhibits viral enzyme that allows it to leave host cell- how does drug reduce spread of virus
- virus cannot leave host cell
- fewer viruses produced
- cannot infect other cells
why would drug researchers focus on plants used in traditional medicine
- already identified medicinal properties
- reduces time in finding active chemicals
- reduces cost
how does reverse transcriptase allow virus to take over cell
converts rna into dna
- reverse transcriptase in nucleus
- viral DNA inserted into host DNA
- so viral RNA is transcribed
- to code for viral proteins
how do cytokines stimulate specific groups of B cells to divide
- cytokine has specific shape
- cytokine is complementary to receptor on b cell
- cytokine binds to receptor
- activates clonal expansion
primary defence
- skin prevents entry of pathogens
- tears kill bacteria
- mucus traps pathogens
how is vaccination active
body produces antibodies and lymphocytes are activated
why do you need different vaccines for different pathogens
- each pathogen has different antigen
- antigens have specific shape
- antibodies are complementary to antigen
- different antibody needed for each pathogen
difference in primary and secondary immune response
primary is slower due to clonal selection and expansion
secondary is quicker due to memory cells
what type of pathogen is ring rot
bacteria
what type of pathogen is potato blight
protoctist
what type of pathogen is black sigatoka
fungi
what type of pathogen is ring worm
fungi
passive plant defences against pathogens
- bark
- casparian strip
- tannins (enzyme inhibitor on surface)
- waxy cuticle
- cellulose cell wall
- resin in bark
- toxic compounds
active plant defences against pathogens
- hypersensitivity (rapid death of tissue surrounding infection)
- release of callose and lignin, deposited between plasma membrane and cell wall forms barrier
- callose helps narrow plasmodesmata
- sieve plates blocked with callose
- callose grows into xylem
cell signalling in plant defence
- pathogens break down cell wall with cellulase
- molecules produced in this breakdown act as cell signalling molecules and trigger receptors
- triggering of receptors cause release of phytoalexins
- plants under attack secrete ethene from leaves
- ethene vaporises and stimulates other leaves and plants to react
- salicylic acid migrates to uninfected area
- then activates defence mechanism
- systemic acquired resistance
role of phytoalexins
- disrupt pathogen metabolism
- delay pathogen reproduction
- disrupt bacteria plasma membrane
- stimulate release of chitinases
meningitis pathogen name
N. meningitidis
direct vs indirect transmission
direct- from host to host
indirect- by a vector
second line of defence in humans
- phagocytosis
- blood clotting
- inflammation
- wound repair
describe blood clotting
- platelets come into contact with collagen from wall
- platelets stick together to form temporary plug
- platelets release thromboplastin which converts prothrombin in thrombin
- thrombin converts fibrinogen into fibrin
- fibrin forms mesh which traps blood cells to form clot
what happens in inflammation
- increased blood flow and phagocytes move into tissue
- mast cells secrete histamine
- histamine causes vasodilation, leaky capillaries, phagocytes leave blood, release of cytokines
what is chemotaxis
neutrophils attracted to site of infection by chemical stimuli
what are macrophages
- larger than neutrophils
- travel in blood as monocytes and settle in tissues as macrophages
- become APC
what is opsonisation
antibody binds to pathogen to make it easily identifiable to phagocytes
types of vaccine
live attenuated and inactivated
