Week 2 - Infection and the immune response Flashcards
name the five WBCs
neutrophils, basophils, eosinophils, lymphocytes, monocytes
function of a neutrophil
as part of innate immune response they ingest and destroy invading microorganisms in tissues
function of a eosinophil
phagocytic with an affinity for antigen-antibody complexes
involved in innate and adaptive response
function of a monocyte
cytokine production - stimulated by recognition of pathogens
phagocytosis of cells
antigen presentation
form macrophages and dendritic cells
3 granulocytes
neutrophils, basophils, eosinophils - all contain granules
structure of a neutrophil
cytoplasm contains 3 types of membrane bound vesicles, secretory vesicles and granules
multi lobed nucleus (3-5)
structure of eosinophils
bilobed nucleus and contain strongly eosinophilic granules
structure of a basophil
large, intensely basophilic, cytoplasmic granules
Highly specific membrane receptors
bilobed nucleus
how does a cytotoxic T cell induce apoptosis
cell puts perforin into the cell membrane and then injects granzymes from the cell itself and these granzymes induce apoptosis
two types of t lymphocytes
helper cells (CD4+) and cytotoxic cells (CD8+)
function of b lymphocytes
produce antibodies
can become a plasma cell
macrophage function
phagocytosis of infecting microbes, antigen presentation, and general removal of dying or damaged host cells
what is the complement system
collection of plasma proteins and molecules which work together to complement killing activity of our immune system
three complement pathways
classical - activated by antigen/antibody complexes
mannose-binding lectin pathway - lectin binding to pathogen surfaces
alternative - pathogen surfaces
what does the complement pathway result in
recruitment of inflammatory cells
opsonisation of pathogens (coating surface with complement molecules)
killing of pathogens
location of adaptive response
lymphoid organs
function of primary lymphoid organs and examples
bone marrow and thymus
B lymphocytes produced and mature in bone marrow with further maturation in the spleen/lymph node
T lymphocyte precursors from bone marrow mature in the thymus
secondary lymphoid organ examples
lymph nodes and spleen
role of thymus
T cell development - precursor from bone marrow goes to the thymus to become helper or killer cells
role of lymph nodes
lymph drains from tissues
collects antigen from periphery
site of adaptive response activation
separates t and B cells in compartments (come together later)
role of spleen
filters the blood - antigens or pathogens in blood will be sieved out here
reservoir of RBCs and WBCs
collects blood-borne antigens
what is an MHC (major histocompatibility complex) antigen
molecules on the surface of the antigen presenting cell class one - presents antigen to cytotoxic cells class 2 - presents to helper cells
function of helper T cells
when they recognise antigen or pathogen they help by activating macrophage or B cell
can kill infected host cells
antibodies function
neutralises, opsonises and activates complement
Secreted into circulation by plasma cells, antibody then binds to pathogen and neutralises it and tries to eliminate it
antibodies can also coat the bacterial wall (similar to complement) or they can just activate complement
structure of antibodies
five different antibody flavours all with the same function (IgA, IgG, IgD, IgM, IgE) - all made up of a basic IgG molecule
light chain
sticky and specific to a particular antigen
function of dendritic cells
phagocytose pathogens before migrating to lymph nodes where they present antigens on their cell surface
describe the innate immune response
phagocytes identify pathogen by recognising PAMPs using PRRs - they kill pathogen and digest it down to its component proteins
phagocytes present the digested protein antigens to cells of adaptive response via MHCs
differences between innate and adaptive immune response
adaptive shows memory
innate occurs locally - adaptive occurs at lymphoid organs
innate is a fast response where as adaptive can take days/weeks
innate involves phagocytes, NK cells, dendritic cells, mast cells whereas adaptive has T cells, B cells and antigen presenting cells
how does the adaptive immune response show memory
b and T cells can create memory cells to defend against future attacks of the same pathogen - a strong and faster response would be reached next time
when is adaptive immunity triggered
when a pathogen evades the innate immune system for long enough to generate a threshold level of an antigen
steps of the adaptive response
antigen for the pathogen is taken up by an antigen presenting cell
APC travels to part of body containing immature t and B cells (eg lymph node)
Antigen is processed by the APC and is bound to MHC receptors which presents the antigen to the T cells
t cells mature and proliferate, helper T cells activate B cells which produce antibodies while killer T cells destroy pathogens that bear the antigen that was presented to them
memory t and B cells are formed after infection ends
antigen-presenting cells
dendritic cells
macrophages
B cells
how do macrophages and neutrophils recognise pathogens
receptors on cell surface such as pattern recognition receptors (PRRs) (eg. toll-like receptors) recognise components of pathogens or other components of immune system such as complement receptors and initiate phagocytosis
what is a toll-like receptor and what does it do
recognises conserved patterns on pathogens and within pathogens
number of different ones but they all recognise PAMPs
when the receptor recognises the PAMP it initiates an inflammatory response
examples of when an inflammatory response causes more harm than the agent itself may have produced
allergies, autoimmune diseases and chronic inflammatory conditions
clinical features of inflammation
redness (rubor) – small blood vessel dilation
heat (calor) – increased blood flow to vasodilation and fever
swelling (tumor) – fluid in extracellular matrix
pain (dolor) – stretching of tissue due to oedema, mediators such as bradykinin and serotonin stimulate pain receptors
loss of function (function laesa) – movement inhibited by pain and severe swelling immobilises area
process of acute inflammation
vasoconstriction to minimise blood loss
vasodilation
increased vascular permeability as a direct result of the realise of histamine from mast cells
increased blood flow and vascular permeability can dilute toxins and bacterial products at site of injury/infection - these also are associated with an influx of phagocytes at site
when may chronic inflammation occur
when acute inflammation is unable to clear an infectious pathogen
also maybe be involved in the progression of degenerative neurological diseases, heart disease and metastatic cancer
how do neutrophils and macrophages respond to pathogens
during phagocytosis, pathogens are engulfed into a plasma membrane-derived vacuole called a phagosome where there are destructive enzymes to kill
role of lymphatic capillaries
absorb excess fluid and return it to the great vessels at the root of the neck
smallest lymphatic vessel
role of lymphatic vessels
remove excess fluid from tissues of the body
where are lymphatic vessels found
throughout body apart from central nervous system and eyes
very little found in bones
where does the lymph of the lower body return to
thoracic duct
where does the lymph from lower body go after the thoracic duct
makes its way up the chest, behind oesophagus and passes into the place for the left internal jugular vein, meets the subclavian vein and enters bloodstream
how is the flow of lymph controlled
when you breathe in, pressure falls in the thorax and rises in the abdomen and that encourages the fluid to go into thoracic duct
valves in lymphatic vessels prevent back flow
when muscles contract, the tissues press on the lymphatic vessels which moves fluid along
where does the lymph of the upper body (head, right side of chest, neck and each upper limb) go
local lymphatic ducts take lymph to the union of the internal jugular vein
lymphodema
damaged lymphatic vessels do not repair well and so fluid cannot drain away causing swelling
cause of secondary lymphoma
develops in people who previously had a normal lymphatic system that has become damaged
cause of primary lymphodema
mutations in the genes responsible for the development of the lymphatic system - fluid does not drain properly - often runs in families
how can cancer treatment cause lymphodema
lymph glands are removed and radiotherapy can damage vessels and lead to lymphodema
how is lymph cleaned in the lymphatic vessels
filters called lymph nodes filter out bacteria, tumour cells etc. - sometimes not all tumour cells are filtered leading to metastasis
what are the principle lymph nodes and where are they located
Axillary lymph nodes – under the arm
Cervical lymph nodes – neck region
Supraclavicular lymph nodes – along the clavicle (collar bone)
Mesenteric lymph nodes – lower abdomen
Mediastinal lymph nodes – behind the sternum
Inguinal lymph nodes – upper thigh region
what is lymph
water, proteins, salts, lipids, white blood cells, and other substances that must be returned to the blood
clinical features of lymphodema
Swelling of part or all of your arm or leg, including fingers or toes
A feeling of heaviness or tightness
Restricted range of motion
Aching or discomfort
Recurring infections
Hardening and thickening of the skin (fibrosis)
how does lymphatic fluid build up in tissue
from the hydrostatic pressure and osmotic pressure exerted on the capillaries - pushes the fluid out between gaps in endothelial cells
or from protein leakage
microbiology
study of microorganisms and their relationship with humans
cellular microorganisms
bacteria, fungi, protozoa/other parasites
acellular microorganisms
viruses, prions
describe a prokaryote
no membrane bound nucleus transcription/translation coupled single, circular chromosomal DNA additional DNA carried in plasmids 70S ribosome made up of 30S and 50S subunits
describe a eukaryote
DNA on chromosomes in membrane-bound nucleus
transcription and translation are compartmentalised
cytoplasm is rich in membrane-bound organelles
80S ribosomes
classes of bacteria
gram-positive
gram-negative
gram-variable
gram-stain unreliable
process of gram staining bacteria
bacteria is fixed to slide
slide is flooded with crystal violet and iodine
an acid toner or alcohol based agent decolourises the gram negative
counterstained with an agent such as safranin so we can see bacteria under microscope (stains gram -ve pink)
colours of the bacteria in each step of gram staining
blue/purple when stained with crystal violet
iodine stains purple
gram -ve is decolourised by an agent such as acid toner
safranin stains -ve pink whereas gram +ve will stay purple
difference between gram -ve and gram +ve bacteria
gram positive have a thick peptidoglycan layer in their cell wall where as gram negative have a reduce peptidoglycan layer surrounded by an outer membrane that includes lipopolysaccharides and lipoproteins
how are gram-stain unreliable bacteria detected
very small bacteria with an atypical life cycle, atypical structure or without a complex cell wall cannot be detected by gram staining so other methods such as PCR can be used
different shapes of bacteria
cocci, diplococcic, bacilli (rod), coccobacilli and spirochetes
structure of bacteria
capsule - tough polysaccharide layer that prevents it from being englufed
flagellum - allows movement through propulsion
chromosome (DNA) is loosely organised in cytoplasm
mesosomes - infolding that create a layer surface area for respiration
plasmids - short pieces of circular DNA that replicate independently
pili - hair-like and are present on surface of bacteria tp help bacteria help to each other or other structures
colonisation
successful immigration where a population becomes integrated into a local community - spread to a new area but does not cause harm
sterile body sites
blood, tissues, CNS, lower respiratory tract, organ systems , sinuses, inner and middle ear, renal system down to posterior uretha, female reproductive tract down to cervix, eye
non sterile body sites
nose, throat, large intestine, vagina, uretha, skin, mouth
virulence factors
mechanisms that the bacteria use to cause damage and problems for human host
three main classes of parasites in humans
protozoa, helminths and ectoparasites
opportunistic infection
infections that occur more often or are more severe in people with weakened immune systems than in people with healthy immune systems
nosocomial infection
hospital acquired infections
locations for bacteria to enter the body
skin with cut or tear, the mouth, nose, respiratory tract, ears, eyes, urogenital tract, anus, GI tract
can enter bloodstream or peritoneum through a break in the normal barrier
what are toxins
bacterial products that directly harm tissue or trigger destructive biological activities
endotoxins
bacterial toxins consisting of lipids that are located within cell wall of gram negative bacteria
exotoxins
toxic substances secreted by bacteria and released outside of cell
common pathogens and their infection
streptococcus pneumoniae - pneumonia
staphylococcus aureus - cellulitis, septic arthritis and osteomyelitis
normal flora
microorganism’s living on body but not causing disease
course of bacterial infection
Penetration - break in epithelium, pili adhere to surfaces
Colonisation - uses nutrients from environment, replicates
Tissue destruction - releases degradative enzymes, release toxins (either endo or exo) -
Body response - WBCs and antibodies respond, pus formed from dead neutrophils
infection control precautions
hand washing, PPE, environmental cleaning, injury prevention
care with body fluids, broken skin and mucous membranes
breaking chain of infection
three stages of sepsis
sepsis
severe sepsis - sepsis with evidence of organ hypoperfusion (inadequate delivery of oxygen and nutrients)
septic shock - severe sepsis with hypotension (low bp) despite fluid resuscitation or vasopressor/inotropic support
cause of ebola and route of transmission
caused by a virus which lives in bats and is transmitted by body fluid
affects of ebola on body
virus triggers a hemorrhagic fever
blood vessels burst causing internal bleeding
routes for intervention of ebola
vaccine
antibody based therapies
drugs with antibodies that bind to virus
transmission of Zika virus
mosquitoes
can also enter through pregnant mother and can cause babies to be born with microcephaly
symptoms and affects of Zika virus
asymptomatic in some, flu symptoms in others
may later in life develop into Guillian-bare syndrome which breaks down parts of the nervous system
affects of malaria on body
parasites first invade liver then turn into another form and escape into red blood cells – parasites erupt out of red blood cells every few days resulting in a fever – repeats
In falciparum Malaria, the parasites make the red blood cells sticky, and that’s to stop them getting recognised in your spleen - can then get caught in blood vessels and if this prevents oxygen getting to brain it can cause cerebral malaria and death
chagas disease transmission
triatomine bug sucks your blood while you’re asleep and leaves their faeces (parasite located in here) on you which causes you to itch - end up rubbing parasite into your lips allowing it to enter
affects of chagas disease
acute response then a 15 year ish phase of no symptoms - after this period you may die of a massive heart attack of hugely expanded oesophagus or colon bc parasites have stayed there
preventing cholera
purify water - boil or filter
avoid salad and any food that may have been washed
vaccine
affects of cholera
gets into intestine and causes a leakage of body fluids into the intestine and very serious diarrhoea - can dehydrate very quickly
cause of cholera
bacterial disease spread through contaminated water
common gram +ve cocci
staphylococcus aureus
streptococcus pneumoniae
what type of bacteria are listeria monocytogenes and corynebacterium diphtheriae
gram +ve rods
common gram -ve cocci
neisseria meningiditis
common gram -ve rods
e.coli
