Infections

Chp 7

pathogens

disease causing agents such as bacterium or virus

bacteria

prokaryote, simple unicellular organism. majority non-pathogenic, live in skin and alimentary canal. some are pathogens

bacteria structure

dna floats freely/form of circular plasmids, no membrane bound organelles, slime layer, capsule, flagella

virus

infectious agent, non living, infect living cells to reproduce (cells become damaged or die)

virus structure

dna/rna coated by protein, some have external lipid envelope

bacteriophages

viruses that multiply in bacteria cells, causing their death

process of viral replication

virus binds to receptor on cell, rna enters cell, makes dna copy of its rna, virus dna integrates with cell dna in nucleus, new viral rna produced which leaves the cell

transmission of pathogens

contact (direct or indirect), ingestion, body fluids, droplets, airborne transmission (remain viable after exhaled droplets evaporate), vectors (mosquitoes, ticks, mice)

external defences (non specific)

skin (bacteria, sebum and sweat kill and prevent pathogen growth), mucous membranes (digestive, urinary and reproductive tracts), hairs, cilia, acids (stomach, vagina, urine, sweat), lysozyme (enzyme that kills bacteria, in saliva, sweat, tears), cerumen (ear wax), movement of fluid

protective reflexes

sneezing, coughing, vomiting, diarrhoea

phagocytes (and types)

leucocytes that engulf and digest pathogens and cell debris by phagocytosis. monocytes, macrophages, neutrophils, dendritic cells

phagocytosis

phagocyte moves to pathogen, changes shape, enclosing it. lysosomes release enzymes that destroy the pathogen. harmless particles released from phagocyte

monocytes

phagocyte in the blood that moves into infected tissues to differentiate into macrophages

macrophages

phagocyte from monocytes. either move through tissue or fixed in one place to consume pathogens

neutrophils

granulated leucocyte, most abundant, short lifespan, making up most of the pus formed

dendritic cells

projections from cytoplasm, antigen-presenting cells, able to detect engulf and process pathogens

inflammation purpose

reduce spread of pathogens and kill them, remove damaged tissue and cell debris, begin repair of damaged tissue

signs of inflammation

redness, swelling, heat, pain

inflammatory response

damage causes mast cells to release histamine, heparin, other chemicals into tissue fluid. histamine increases blood flow to tissue from vasodilation. heparin prevents clotting. other chemicals attract phagocytes. abnormal conditions stimulate pain receptors. phagocytes die, form pus. repair of damaged tissue

histamine

released by mast cells in inflammatory response. increases blood flow via vasodilation, walls of capillaries become permeable, more fluid moves into tissue. causes heat, redness, swelling

heparin

released by mast cells in inflammatory response. prevents clotting. a clot of fluid forms around damaged area, slows spread of pathogen

fever

elevation of body temperature, due to resetting of body’s set point by pyrogens

fever steps

pyrogens released by leucocytes, act on hypothalamus to raise body’s set point. hypothalamus detects body’s temp is lower than new set point, shivering and vasoconstriction to raise temp. fever breaks, lowers set point to normal, vasodilation and sweating

fever benefits

high temps inhibit growth of pathogens, increase rates of reaction and repair, interferons work more quickly inhibit viral replication

lymphatic system

lymph nodes trap pathogens in network of fibres, macrophages engulf them

B-cells (+ maturation)

lymphocyte produced in bone marrow. mature in bone marrow, then goes into lymphoid tissue

T-cells (+ maturation)

lymphocyte produced in bone marrow. mature in thymus, then goes into lymphoid tissue

antibody mediated immunity (humoral response)

production of antibodies by B-cells, which circulate the body attacking pathogens

cell-mediated response

T-cells cause formation of lymphocytes that destroy pathogens

antigen

substances capable of producing immune response, self or non-self antigens

antibodies (immunoglobins)

protein produced by plasma cells (B-cells) in response to non-self antigens. combines with specific antigen to form antigen-antibody complex

classes of antibodies

IgM, IgA, IgD, IgG, IgE

antigen-presenting cells (+ examples)

detect presence of non-self antigen, engulf and digest pathogen, produce small fragments that move to cell surface to present antigen to lymphocytes. dendritic cells, macrophages, B-cells

antibody-mediated immunity steps

antigen activates B-cells, which digest it and present it. activates T-cells to release cytokines, cause B-cells to enlarge and divide. clone cells formed become plasma cells, some memory cells. plasma cells secrete specific antibody to attack antigen which travel through fluid to reach invasion site.

plasma cells

secrete antibodies in humoral response

memory cells

allow for rapid response if exposed to antigen again

primary response

first exposure to antigen. takes several days to build up antibodies

secondary response

second exposure to same antigen. immune response faster due to memory cells recognising antigen, plasma cells able to form rapidly

how antibodies work

antibody-antigen complex. prevent entry or reacting with cells, agglutination, coating pathogens so easier consume by phagocytes

killer T-cell

move to infection site, attach to invading cell and secrete chemical to destroy antigen

helper T-cell

both humoral and cellular immunity. bind to antigen on antigen-presenting cells, stimulate secretion of cytokines

cytokines stimulates:

attract lymphocytes intensifies response, attracts macrophages to destroy antigens, intensifies phagocytic activity, promote action of killer T-cells

suppressor T-cells

act when immune activity excessive, when infection has been dealt with. release substances to inhibit T and B-cell activity

cell-mediated immunity steps

T-cells activated by antigen-presenting cells, enlarge and divide. clone cells formed become memory cells, most develop further into different T-cell types (killer, helper, suppressor)

immunity

resistance to infection by pathogens. natural or artificial

passive immunity

receives antibodies from someone else, short lived. naturally- baby via placenta. artificially- injected with antibodies to fight infection

active immunity

body exposed to antigen and produces antibodies, lasts longer due to memory cells. natural- having disease and recovering. artificial- injected with antigens of infection

immunisation

programming immune system so body can respond rapidly to pathogens

vaccinations

artificial introduction of antigens of the pathogen

living attenuated vaccine

living weakened pathogen of reduced virulence

inactivated vaccine

dead pathogens, shorter lasting

toxoid vaccines

toxins produced by bacteria made inactive (toxoids)

sub-unit vaccine

fragment of organism used

vaccination schedule

start at 2 months. boosters to stimulate secondary response for longer lasting antibodies and more memory cells

herd immunity

large percentage of people immune in population, less chances of transmitting the disease

considerations of vaccines

allergic reaction, ethical concerns- animal testing and use, religious beliefs

antibiotics (+ types)

fight infections, especially of bacteria. bactericidal antibiotics- destroy cell wall or membrane. bacteriostatic antibiotics- stop reproduction

antivirals

treat viral infections, harder to develop as virus invade cell, killing virus kills the cell