topic 6 Flashcards
exons
coding sections of DNA
introns
these are no coding sections of DNA
short tandem repeats
short repeated sequences of bases
there can be several hundred copies of the same STR at a single locus on both chromosomes of a homologous pair
people vary in regard to the number of these repeats at a locus of a chromosome
STRs can be used to build up a unique pattern DNA profile
as it is highly unlikely to have 2 individuals with the same combination of STRs
how is the DNA obtained
A DNA sample can be obtained from almost all biological tissue, animal or plant.
check swab, blood cells in a blood smear at scene, bone marrow in a skeleton, sperm left after a sexual assault.
The tissue sample is the physically broken down in a buffer solution containing salt and a detergent to disrupt cell membrane.
The small suspended particles, including DNA is separated from cell derbies by filtering or centrifuging.
protease enzyme are incubated with suspension to remove proteins
and the cold ethanol is added to precipitate out the DNA. then the DNA is washed in buffer solution
how do you create the DNA fragments for PCR
restriction enzymes. found naturally in bacteria to cut up invading viral DNA. the enzymes only cut DNA at specific base sequences.
if the restriction sites are either side of a short tandem repeat sequence that fragment of DNA will remain intact, but it will be cut away from the rest of the genome
if the same restriction enzyme is used to cut 2 identical DNA samples, identical STR fragments are produced
what does PCR stand for
polymerase chain reaction
what are the stages in PCR
- 95oc for 30 seconds. the DNA separates into 2 strands as hydrogen bonds between bases break.
- 55oc for 20 seconds. the primers attach at the start of the STR repeat sequence
- 70oc for 1 minute. DNA polymerase attach nucleotides are attached, extending the DNA from the primer. The STR repeated sequence and DNA adjacent is replicated.
this sequence is repeated many times in order to create millions of these STR fragments.
what needs to go into the reaction tube in PCR
- DNA polymerase. to replicate DNA
- DNA primers with fluorescent markers. attaches to the DNA and allows DNA polymerase to attach and is view-able after gel electrophoresis
- nucleotides. In order to create the New DNA.
- a sample of DNA
DNA primers
short DNA sequences complemntary to the DNA adjacent to the STR.
the DNA primers are marked with fluorescent tags.
what is gel electrophoresis
the process of separating the DNA produced by PCR according to size
stages in gel electrophoresis
- DNA fragments placed in well of agarose submerged in buffer solution in gel tank
- negative charged DNA moves towards the positive electrode. Fragments separates into invisible bands according to their size.
- transferred to nylon or nitrocellulose membrane. DNA probe binds with fragment/
- X ray film or UV light used to view DNA profile
what is DNA probe.
labelled DNA probe is a short section of DNA with a base sequence complementary to the target DNA sequence that needs to be located. the probe binds to any complementary sequences.
if probe is radioactive. X ray film is used.
if probe is fluorescent, its position on the membrane can be visualised under ultraviolet light.
one way of viewing a DNA profile produced is gel electrophoresis is by actually viewing either as an X ray film or under UV light. however there is another way to view the DNA profile…
during PCR DNA primers attach to DNA these DNA primers have fluorescent tags attached to them.
as DNA fragments with their attached fluorescent tags move through the gel they pass a laser, the dye in the tag fluoresces and the coloured light is detected.
this gives a time that it has taken for the fragment to pass through the gel. passing a separate set of fragments of a known length through gel allows the length of time for passage through the gel to be calibrated with fragment size.
the size of fragment is determined by the number of base pairs it contains.
several STR loci can be analysed at once using tags that fluoresce at different wavelengths giving different colours.
produces a digital DNA profile with a series of numbers corresponding to the number of repeated in each fragment
ways of determining time of death (4)
- body temperature
- rigour mortis
- decomposition
- forensic entomology
how does body temperature change after death
body starts to cool as soon as death occurs
it follows a sigmoid curve
initial temperature plateau for 30 minutes then falls rapidly until the same temperature as the environment
temperature decline per hour can give an estimate of time of death
factors affecting post mortem cooling (7)
- body size
- body position
- clothing
- air movement
- humidity
- hypothermia or fever
- temperature of surroundings
what is rigor mortis
after death the muscles usually total relax and then stiffen.
joints become fixed during rigor mortis and their position will depend on the body position at time of death. after a further period of time rigor mortis will pass and the muscles will relax again.
stages in rigor mortis (6)
- after death, muscle cells become starved of oxygen and oxygen dependent reactions stop.
- Respiration in the cells becomes anaerobic and produces lactic acid
- the pH of the cell falls, inhibiting enzymes and thus inhibiting anaerobic respiration.
- The ATP needed for muscle contraction is no longer produced. as a result, bonds between the muscle proteins become fixed.
- the proteins can no loner move over one another to shorten the muscle, fixing the muscle and joints.
- after a whole muscle tissue starts to break down and rigor mortis passes
Rigor mortis starts with smalled muscles stiffening before larger ones.
stages of decomposition
- autolysis
- putrefaction
- bloated
- dry body
autolysis
the first stage of decomposition
when the body own enzymes, from the digestive tract and lysosomes breaks down cells
bacteria from the gut and gaseous exchange system rapidly invade the tissues after death, releasing enzymes that result in decomposition. the loss of oxygen in the tissues favours the growth of anaerobic bacteria
putrefaction
second stage of decomposition
greenish discoloration of the skin of lower abdomen
due to formation of sulphaemoglobin in the blood
as it spreads across the body skin will darken to reddish-green and then turn a purple black in colour.
gas or liquid blisters may appear on the skin.
bloated
the 3rd stage of decomposition bloating of body due to gas production increased action of bacteria produce gases including hydrogen sulphide, methane, Carbon dioxide, ammonia and hydrogen. these form in the intestines and tissues. body will smell and become bloated. with further decomposing will deflate
dry body
the 4th and final stage in decomposition
the body deflates and fluids associated with putrefaction drains away.
soft tissues dry out and shrink
how does environmental temperature affect rate of decomposition
- low temperature slows down decomposition
- warm temperatures speeds it up
- intense heat denatures enzymes involved in autolysis delaying decay
ways of identifying a body (3)
- finger prints
- dental records
- DNA profile
forensic entomology
the study of organisms on a decaying body to estimate time since death
succession in corpses first wave
organisms present - bluebottles - green bottles - house fly - cow face fly state of body: fresh
succession in corpses second wave
state of body
bloated by gases.
species present
- flesh flies
succession in corpses third wave
state of body active decomposition (fatty acids have turned to a waxy substance) species present - beetle larvae - tabby moth maggot
succession in corpses fourth wave
state of body active decomposition (fermentation) species present - cheese skipper - lesser house fly
what is succession in corpses
as one organism feeds on a decomposing body, conditions change in such a way that it becomes attractive to another group of organisms.
as corpse continues to change, it attracts different organisms that feed on it until only the skeleton remains
forensic entomologists use the predictable sequence of organisms that feed on a decomposing body to determine time of death
decomposition role in the carbon cycle
a corpse is a great source of energy for decomposes
carbon dioxide is released into the atmosphere by respiring decomposes
this recycles the carbon back into a form that can be used in photosynthesis to synthesis more organic molecules.
what are the differences between bacteria and viruses
bacteria contain cell surface membrane, cytoplasm, cell wall, ribosomes, plasmids and sometimes mesosomes, flagellum and pilli.
viruses contain no cell wall, cell surface membrane, cytoplasm or organelles. nucleic acid enclosed in protein coat
bacteria have circular strand of DNA as the genetic material.
viruses have DNA or RNA as genetic material
bacteria can live independently.
Viruses must have a living organisms as host
bacteria’s average diameter is 0.5 - 5 um.
viruses 20- 40 nm wide range of sizes and shapes
bacteria often have mucus based outer capsule.
virus may have outer membrane of host cell surface membrane, but containing glycoproteins from the virus
features of virus
10 -100 times smaller than bacteria have no cell wall or ribosomes not a living cell nucleic acid DNA or RNA present infects plants, animals and bacteria can reproduce with host cell a sexual reproduction
what do viruses consist of
a strand of nucleic acid (RNA /DNA) enclosed within a protein coat
the DNA can be single or double stranded
some have outer envelope taken from the host cell’s surface membrane. the envelope contains lipids, proteins and glycoproteins from virus itself and act as antigens
how do viruses invade cells and reproduce (6 steps)
- virus attaches to host cell
- virus inserts nucleic acid
- viral DNA is incorporated into the human DNA
- viral DNA is replicated
- viral protein coat is synthesised
- new virus particles are formed
- virus particles released due to cell lysis
characteristics of gram positive bacteria
- peptidoglycan cell wall
- takes up violet stain but not safranin
- deep purple colour after staining
- eukayotic cell
- nucleus surrounded by envelope
- mitochondria
- large ribosomes
- contains cytoskeleton
- several long strands of DNA associated with histones
- sometimes contain cillia and flagella.
characteristics of gram negative bacteria
- liposaccharid layer outside peptidoglycan cell wall
- does not take up crystal violet. takes up safarin
- pink colour
- prokayrotic cell
- does not contain nucleus, mitochondria or cytoskeleton small 20nm ribosomes
- circular DNA with no histones
- some have flagella.
symptoms of HIV / AIDS
viral disease
HIV - human immunodeficiency virus
initial symptoms are fevers, headaches, tiredness, swollen glands or no symptoms at all
after 12 weeks HIV antibodies appear in the blood
all symptoms disappear for years but eventually patients will suffer weight loss, fatigue, diarrhoea, night sweats and infections such as thrush. this is full blown AIDs
dementia, cancer and opportunistic infections such as TB take hold
what is AIDs
acquired immune deficiency syndrome
is caused by infection of HIV
symptoms of AIDs are those of opportunistic infections such as TB
HIV is a envelope virus. the lipid envelope is formed from the host cell membrane sticking through the envelope are viral glycoproteins
how is HIV transferred
- HIV is found in the blood, vaginal secretions and semen
transmitted by direct blood / body fluid transfer through cuts
needle sharing, unprotected sex
maternal transmission from mother to unbron child or in breast milk.
what are the phases of HIV infection / AIDs
- acute phase
- chronic phase
- Disease phase
acute phase of HIV infection
HIV antibodies appear in blood 3-12 weeks after initial infection
sweats, fever, headache, sore throat, swollen lymph nodes or no symptoms at all.
there is rapid replication of virus and loss of T helper cells
after a few weeks infected T helper cells are recognised by T killer cells and destroyed reducing rate of viral replication
chronic phase of HIV infection / AIDs
second phase
also called latent stage
virus continues to reproduce rapidly but numbers are kept in check by the immune system
no symptoms but increasing tendency to suffer colds or other infections slow to rid of
dormant diseases like TB or shingles can reactivate
this phase can last for a long time with correct lifestyle and drug treatment
disease phase of HIV infection / AIDs
increased viral load and declining T helper cells indicates the onset of AIDs
low number of T helper cells leaves immune system vulnerable
high risk of infection by opportunistic such as pneumonia and TB
significant weight lost, dementia and tumours such as kaposisarcoma
antigens
any molecule the body recognises as not being of its own self.
what is the difference between non specific immune response and specific immune response
non specific immune response helps to destroy any invading pathogen whereas specific immunity is always directed at a specific pathogen.
what are the no specific responses to infection
- lysozyme
- inflammation
- phagocytosis
- lymph system
- interferon
lysozyme
is an enzyme that kills bacteria by breaking down their cell wall.
it is found in tears, saliva and nasal secretions
protects the body from harmful bacteria in the air we breath in or the food that we eat.
inflammation
inflammatory response
damaged white blood cells and mast cells release histamine which causes arterioles to dilate increasing blood flow and capillary permeability causing leakage
plasma fluid, white blood cells and antibodies leaks into tissues causing oedema
infecting bacteria are now attacked by intact white blood cells.
types of white blood cells (3)
- neutrophils
- lymphocytes
- monocytes (which produce macrophages)
neutrophils
type of white blood cell
makes up 70%
leave blood capillaries by squeezing between the cells of capillary walls.
Ingest and destroy bacteria.
80 million produced every minute (more during infection)
only last a few days
lymphocytes
type of white blood cell
makes up 24%
2 types:
- B cells and T cells
involved in the immune response including antibody production and immunity
some cells last only a few days, others can survive for years
defend against specific diseases. specific immune system
monocytes
type of white blood cell
makes up 4%
circulate in the blood for a day or 2 before they move into the tissue by squeezing between the cells of the capillary walls.
here they become macrophages and engulf bacteria, foreign matter and cell debris.
numerous in the lungs, liver, kidneys, spleen and lymph nodes.
what are phagocytes
phagocytes are white blood cells that engulf bacteria and other foreign matter in the blood and tissues.
include both neutrophils and macrophages (from monocytes)
phagocytosis
- chemicals released by bacteria and the cells damaged at the site of infection attract phagocyte white cells
- neutrophils arrive first followed by macrophages.
- bacterium with antigen on surface is engulfed by neutrophil or macrophage
- the phagocyte encloses the bacterium inside a vacuole
- lysosomes fuse with vacuole releasing enzymes that destroy foreign material
- residual body is discharged
- phagocyte removes antigens on bacteria surface and places on own membrane becoming an APC
lymphatic system
- tissue fluid drains into lymphatic vessels
- the fluid / lymph flows along and passes through lymph nodes eventually returning to the blood via lymphatic and thematic ducts
- as lymph passes through lymph nodes any pathogens present attract lymphocytes and macrophages which destroy the microbes.
interferon
provides non specific defence against viruses
viruses infected cells produce this protein which diffuses to surrounding cells preventing viruses from multiplying
it inhibits viral protein synthesis to limit the formation of new virus particles
which cells are involved in the specific immune response / cell mediated
lymphocytes
defend the body against specific diseases.
T helper and T killer cells
B cells
B lymphocytes
B lyphocyte cells are produced and mature in bone marrow.
Each B cell has one specific type of antigen receptor on its surface. The B cell is activated when its receptor binds to an antigen with the complementary shape
once activated B cells turn into B effector cells / plasma cells
each B cell binds to only one specific antigen.
antibodies
are special protein molecules of a class known as immunoglobulins.
antibodies bind to to the antigens on the microbe cell surface membrane.
they act as labels, allowing phagocytes to recognise and destroy the cell.
produced by B effector cells / plasma cells
made of 4 amino acids chains. the amino acid sequences and hence shape of the binding site is different in each type of antibody.
antibodies have 2 antigen binding sites.
polypeptide chains held together by disulfide bonds
features and functions of antibodies
- opsonisation: particles are coated with antibodies, marking them for phagocytes.
- precipitation. soluble toxins are made insoluble and inactive
- agglutination: microorganisms are clumped together for easier phagocytosis
- lysis. breaking open of bacterial cells.
T lymphocyte production (6)
- immature T cells produced by division of stem cells in bone marrow
- immature T cells move to the thymus via the blood
- T cells mature in the thymus
- Mature T cells leave the thymus in the blood and move to lymph nodes and the spleen
- as lymph fluid passes through a lymph node, T cells are activated by any pathogens present
- as blood passes through the spleen, T cells are activated by any pathogens present
what are the 2 types of T lymphocytes
- T helper cells.
- T killer cells.
function of T helper cells
stimulate B cells to divide into plasma cells. by producing cytokines
enhance the activity of phagocytosis
stimulate T killer cells to divide by producing cytokines.
function of T Killer cells
destroys any cell with non self antigens on their surface membrane
including infected body cells and transplant tissue
does this by lysis of cell membrane
activation of T helper cells (4)
- macrophage engufs bacterium with antigens on surface.
- macrophage presents antigens on its surface and becomes and antigen presenting cell (APC)
- T helper cells with complementary CD4 receptors bind to APC. activating the T helper cell
- T helper cell then divides ( proliferates) to produce
clone of T memory cells
clone of active T helper cells
T memory cells remain in body for months - years. this means upon second infection the immune system can respond more quickly.
clonal selection of B cells (5)
- antigen binds to B cell with complementary receptor becoming APC
- active T helper cell with complementary receptor binds to APC and produces cytokines (proteins) that stimulate the B cell to divide
- the B cell divides (proliferate) to give B memory and B effector cells
- B effector cells differentiate to produce plasma cells which release antibodies.
- B memory cells remain for months - years in the body enabling an individual to respond more quickly upon second infection.
under the influence of cytokines, the B cells divide (proliferate) to produce 2 cones of cells:
- B effector cells
these differentiate to produce plasma cells, which release antibodies into the blood and lymph. these plasma cells are relatively short lived, lasting only a few days - B memory cells
like T memory cells, these cells are long lived . they remain for months - years in the body, enabling an individual to respond more quickly to the same antigen in the future.
primary immune response
the first time a B cell comes across a non self antigen that is complementary to its cell surface receptor, the production of sufficient antibody producing cells by clonal selection takes about 10 -17 days. during this time it takes to produce antibodies, the person is likely to suffer the symptoms of infection.
memory cells produced after first exposure to antigens
the role of T killer cells
- cell infected with bacterium becomes APC
- T killer cells with complemntary receptor binds to APC
- T helper cell makes cytokines which stimulate T cells to divide to produce
- Memory T killer cells
- Active T killer cells - active T killer cells bind to infected cells presenting antigens (APC)
- T killer cell releases chemicals that causes pores to form in the infected cell, causing lysis. the infected cell dies and the bacterium is expelled where it can be labelled by antibodies from B cells as targets for destruction by macrophages.
secondary immune response
if infected by the same bacterium or virus again, the immune system responds much faster.
involves memory cells and only takes about 2-7 days.
the B memory cells produced in the primary response can differentiate (proliferate) immediately to produce plasma cells and release antibodies.
there is a greater production of antibodies and the response lasts longer.
the invading viruses or bacteria are often destroyed so rapidly that the person is unaware of any symptoms. so the person is said to be immune
what are the benefits of a secondary response
- much shorter lag period as more of the specific lymphocytes already in circulation
- more rapid production of effector cells
- much greater production of antibodies or T killer cells.
apoptosis
programmed cell death
how do we avoid attack by our own immune system
some of the membrane proteins on the surface of our own cells mark the cell as self.
they allow us to distinguish between our own cells and those of foreign invaders.
there are hundreds of alleles for these proteins, so the combination of proteins on our cell surfaces is unique to each individual and is not found on the cells of anyone else.
when B and T cells mature any lymphocytes for self membrane proteins are destroyed by apoptosis leaving only lymphocytes with receptors for foreign non self antigens.
on occasions particular cells may alter so they become foreign and are destroyed by the immune system
what is tuberculosis
bacterial disease
at first infection no symptoms tubercles form in the lungs due to the inflammatory response of a person’s immune system.
some bacteria survive in tubercles lie dormant.
lung tissue is slowly destroyed causing breathing problems.
serious cough, weight loss, appetite loss, fever.
TB targets cells in immune system can invade glands and central nervous system
how is TB transmitted
- droplet infection: droplets of mucus and saliva can remain suspended for several hours in poorly ventilated areas. TB can also survive as dust from dried droplets
- close contact with infected person
- poor health
- poor diet
- overcrowded living conditions.
primary infection by TB
- TB bacteria are inhaled and lodge in the lungs were they start to multiply
- causes an inflammatory response. macrophages engluf bacteria. mass of tissue granoloma forms which are anaerobic for TB an contain dead bacteria and macrophages. called tubercles
after 3-8 weeks infection is controlled and lungs heal
however TB can survive inside macrophages as thick waxy cell wall is hard to break down
they can also target other immune cells suppress T cells reducing antibody production and attack T killer cells.
active tuberculosis
either the immune system cannot contain the disease when it first arrives. or old infection may break out if the immune system is no longer working properly
80% active TB is a reactivation of previous cases.
- reduced activity of the immune system can be caused by old or young age, malnutrition, poor living conditions or AIDS.
- bacteria multiply rapidly creating cavities in lung tissue
- coughing up blood, shortness of breath, loss of appetite, weight loss, fever and extreme fatigue
- The lung damage will eventually kill the sufferer
HIV directly targets white blood cells and reduces a patients ability to fight any infection, TB can kill a person with AIDs.
symptoms of active TB
- coughing: patient may cough up blood
- shortness of breath
- loss of appetite and weight loss
- fever and extreme fatigue
fever
- part of the inflammatory response
- caused by substances released from neutrophils and macrophages
these chemicals effect they hypothalamus setting core body temperature higher.
effectors act to raise temperature
enhances immune function of phagocytosis.
bacteria / viruses may reproduce more slowly
temperature above 40oc denatures enzymes and 42 -43oc is life threatening.
TB will stop reproducing above 42oc
glandular TB
TB bacteria can infect bones, lymph nodes and the centrral nervous system.
usually follow initial pulmonary infections
glandular TB main symptom is enlarged lymph nodes near neck and armpits and sometimes in the chest but these can only be seen on X ray.
Asian people are more likely to get glandular TB.
Caucasians are more likely to get pulmonary TB
how is TB diagnosed
- skin and blood tests
tuberculin is injected under the skin if the skin becomes inflamed this is a +ve result as antibodies cause inflammation indicating TB antigens present. Test can give a negative if the person has latent TB. false positive if a person has had the TB vaccination. - Identification of bacteria:
sample cultured and stained. only some types of bacteria take up certain stains - chest X-rays
discover the extent of damage and see spread
tuberculin
the name given to extracts from several species of mycobacteria and is usually composed of a mixture of purified proteins
mycobacteria
genus of bacteria that TB bacterium belongs to
M. tuberculosis
Mycobacteria turberculosis
structure of HIV virus
- 2 copies of mRNA
- viral protein. e.g reverse transcriptase and integrase
- capsid containing mRNA and viral proteins made up of protein units
- layer of viral protein
- then the HIV envolope derived from the host cell made up of
1. lipid bilayer
2. glycoprotein
how does HIV invade T helper cells
- glycoproteins molecules called gp120 which are located on the virus surface, bind to the CD4 receptors on the surface of the T helper cells.
- The envelope surrounding the virus fuses with the T helper cell membrane, enabling the virus RNA to enter the cell.
- macrophages also have CD4 receptors so the virus can also infect the
how does HIV hijack the T cells protein synthesis
once inside the host T helper cell, the virus needs to make the host cell replicate new virus components.
- Reverse transcriptase is en enzyme used by the virus to revers normal transciption and to manufacturer DNA from the RNA template.
- once the HIV DNA strand is produced, it is integrated into the host’s DNA by another HIV enzyme, integrase.
- once the HIV genome is integrated into the host cell’s genome, it can be transcribed and translated to produce new virus protein.
retroviruses contain
RNA and reverse transcriptase
mRNA splicing
between transcription and translation, messenger RNA is often edited.
the non coding introns are removed and the remaining sequences are spliced together and will be expressed, are exons.
this means that several proteins can be formed from 1 length of mRNA spliced in different ways.
one gene –> several related proteins
how do virus particles exit the host cell
new viral proteins, glycoproteins and nuclear material are assembled into a new virus
the new virus buds of T cell taking some of the cell surface membrane as their envolope.
this causes lysis of the host cell killing it
summarised process of how HIV viruses destroys T helper cells
- HIV surface proteins bind to cell receptors (CD4).
- virus envelope fuses with cell surface membrane
- virus reverse transcriptases copies virus RNA into virus DNA
- intergrase inserts virus DNA into host DNA
- translation of virus envelope proteins
- transport of virus envelope proteins
- virus envelope proteins incorporated into the cell membrane
- Translation of other virus proteins
- new virus assembled
- virus particle budding of cell becomes wrapped in cell membrane, forming the virus envelope.
what type of cells does HIV invade
T helper cells
also macrophages as they also contain CD4 receptors
how are T helper cell loss in AIDs and how does this effect the rest of the immune system
T helper cells are killed by lysis as new viruses bud and leave infected cells.
these infected cells are killed by T killer cells
as the no. of viruses increases the no. of host T helper cells decreases
the loss of T helper cells means that macrophages, B cells and T killer cells are not successfully activated and so do not function properly leading to immune system becoming deficient.
drugs used to treat AIDs / HIV are called
antiretroviral Drugs
what are the 2 types of drugs used to treat HIV / AIDs
- reverse trasncriptase inhibitors
- protease inhibitors
also have intergrase inhibitors and fusion inhibitors
how do reverse transcriptase inhibitors work?
treating HIV
anti retroviral drugs
prevent viral RNA from making DNA for integration into host’s genome by inhibiting enzyme reverse transcropase
how do protease inhibitors work?
treating HIV
Antiretroviral drug
inhibit the protease that catalyses the cutting of larger proteins into small polypeptides for use in the construction of new viruses.
how do we prevent the entry of pathogens
- the skin
- mucous membranes
- stomach acid
- gut flora
- eyes
how do the eyes prevent pathogen entry
tears contain enzyme lysozyme which helps to digest microbes
how does the respiratory tract prevent pathogen entry
contains a mucus membrane which traps bacteria.
the mucus is then swallowed and passed into the digestive system
how does the Gastrointestinal tract prevent pathogen entry
stomach acid. helps to destroy microbes which are eaten
gut bacteria
compete with pathogens for food and space. they competitively exclude them. these bacteria also excrete lactic acid which deters pathogens.
how does the skin prevent pathogen entry
- skin is a tough barrier which only allows pathogens to enter if cut
skin flora: own microbes out compete pathogens
sebum made by skin also kills microbes
active immunity
the body cells involved
passive immunity
protection developed in other individuals
natural immunity
the normal body response to infection
artificial immunity
medical procedure
passive natural immunity
immunity by naturally obtaining antibodies.
antibodies cross placenta to protect fetus as immune system develops
breast milk, especially colostrum also contains antibodies protecting a young infant as they build their immune system
passive artificial immunity
artificially receiving antibodies
when an injection contains antibodies, usually from the blood of animals following exposure to an antigen; injecting these antibodies will neutralise the antigen, but will not provide long term protection
active natural immunity
active- body cells involved
normal response to foreign antigen
active artificial immunity
vaccines use antigens from pathogens in a harmless form to cause a primary response
upon infection of the active pathogen there will be a secondary response and they will not become ill
vaccines may contain
- attenuated viruses. these viruses have been weakened so they are harmless
- Killed bacteria.
- A toxin that has been altered into a harmless form.
- An antigen bearing fragment of the pathogen.
herd immunity
vaccinations for infectious diseases protect the individual as well as the community.
when enough people are immunised, the disease is less likely to be transferred from 1 person to another and so there is less disease in the community as a whole.
this means anyone who did not respond to the vaccine or cannot have the vaccine is protected.
can you be vaccinated for TB or HIV
there is no current vaccination against AIDS
but the BCG vaccine against TB has been widely used in the UK
are vaccinations dangerous?
No.
after vaccination the person may suffer mild soreness at the site of the injection or general feeling of being unwell.
research studies have indicated very occasionally more serious and long term damage to certain vaccines some of which have been withdrawn.
the balance of risk and benefit is crucial.
although the whooping cough vaccine on very rare occasions can cause brain damage, a child actually contracting whooping cough is more at risk of brain damage and death.
what are antibiotics
antibiotic is a chemical substance produced by a microorganism, which has the capacity to inhibit the growth and even to destroy bacteria and other microorganisms in dilute solutions.
what are the 2 types of antibiotics
- bactericidal
- bacteriostatic
bactericidal antibiotics
these antibiotics destroy bacteria
bacteriostatic antibiotics
these antibiotics prevent the multiplication of the bacteria
allowing time for the host immune system to destroy the pathogens
how discovered the first antibiotic
fleming
discovered penicillin
what are the different ways in which antibiotics work? (5)
- inhibition of specific enzymes found in bacterial cell but not in host
- inhibiting bacterial cell wall synthesis leading to lysis
- inhibiting of nucleic acid synthesis, replication and transcription preventing cell division and enzyme synthesis
- disruption of cell membrane changing the permeability leading to lysis
- inhibition of protein synthesis enzymes and other essential proteins not produced.
why do bacterial populations evolve so quickly
- bacteria reproduce very fast
- bacterial population sizes are usually in billions. very large so no. of cells contain mutations is vast
- some of these random mutations will be advantageous.
- antibiotics provide a strong selection pressure
conjugation
process of horizontal evolution by bacteria
2 cells fuse one strand of plasmid DNA transfers between conjugating bacteria
each bacterium replicates strand to make complete strand of DNA
horizontal evolution
were genes is passed from one bacterium to another.
conjugation
how can we prevent antibiotic resistance and hospital acquired infections
- antibiotics should only be used when needed
- patients should complete treatments to ensure all bacteria are destroyed
- infection control should be used in hospitals to prevent bacteria from spreading
how is TB treated
antibiotics
active TB bacteria can be killed by antibiotics
a combination of 4 given for 2 months with 2 continued for a further 4 months usually works.
procedure for investigating the effectiveness of antibiotics
- a sterile nutrient agar plate seeded with suitable bacteria
- apply antibiotics to a sterile filter paper disc. then lay on the bacterial lawn using sterile forceps
- seal petri dish allowing for gas exchange
- incubate below 30 oc for 24 hours
- look for zone of inhibition around discs the larger the area the better the antibiotic
antiseptic technique should be used.
