Topic 6: Immunity, Infection and Forensics Flashcards
what factors are used in determining time of death (TOD)
- core body temperature (measured via rectum)
- rigor mortis
- decomposition
- forensic etomology
combining these can help TOD as the changes occur in a known, specific order
how can TOD be determined using body temperature
all mammals produce heat from metabolic reactions and the human body’s core body temp is 37degreescelsius
from TOD metabolic reactions slow down and stop eventually, so body temp falls until it reaches the ambient temp aka algar mortis
a body cools following a sigmoid curve with the initial plateu lasting between 30 to 60 mins
human bodies cool at a rate of 1.5˚C to 2˚C per hour
other affecting factors(only slightly) :
- position (curled over/ spread out)
- clothing
- body mass
how is rigor mortis used to determine TOD
rigor mortis occurs when muscles stiffen after death (after totally relaxing), the joints become fixed in the position at TOD
- after death: muscle cells are starved of oxygen and oxygen dependent reactions stop
- respiration in cells becomes anaerobic, producing lactic acid
- pH of cells falls , inhibiting enzymes which inhibits anaerobic respiration
- ATP needed for muscle contraction is produced no longer, so actin + myosin can’t unbind
- proteins can no longer move over one another and shorten the muscle, fixing the muscle and joints
the smaller muscles stiffen before the larger ones and rigor mortis passes off as muscle tissue starts breaking down in the order it developed
most bodies have complete rigor mortis 6to9 hrs after death, but it will set in quicker and last for a shorter period in a high temp env. or if the person was physically active prior to death
how is extent of decomposition used to determine TOD
- over a few days - the skin turns greenish from decomposers breaking down cells and tissues
- over a few days/weeks - active bacteria causes gases like methane to form in the intestine and tissues, making the body smell and bloat. skin blisters and falls off the rest of the body
- few weeks post death - soft tissues decompose further and turn to liquid, which drains away
- over months/years - continues until only a dry skeleton remains
higher temperatures and oxygen levels allow for faster decomposition
we know the order that decomposition occurs in and can use this to determine TOD
how is succession used to determine TOD
- immediately after death conditions are move favourable for bacteria
- as bacteria decompose tissues, conditions become favourable for flies and their larvae
- when fly larvae feed on a dead body, conditions are favourable for beetles so they move in
- the dead body dries out and conditions are no longer favourable for flies so they leave and beetles remain as they can decompose the dry tissue
- when no tissues remain, conditions are no longer favourable for most organisms
this is similar to plant succession, except most early insect stay on the body as other insects colonise it
- succession is influenced by environment, there would be different findings if a body is: sealed/underground/underwater
what is the role of a forensic entomologist
they have to identify species’ of insects present on a body and what stage of it’s lifecycle it is in
how can different conditions impact forensic entomology and the life cycle of insects
- drugs present in the body
- oxygen concentration and availability
- humidity of surroundings
- temperature; higher temp increases metabolic rate which decreases the time for the life cycle to complete
what is known about insects that helps forensic entomologists determine TOD
- different insect species colonise a body at different times after death
- flies are on a body within a few hours and blowfly eggs hatch in 24hrs so, if larvae are present, they died >24hrs ago
- beetles prefer a dry body, which means the body has been there for some time already
the stage of the insect’s lifecycle can also provide clues about TOD as we know when each stage of the lifecycle will occur
outline the structure of bacteria
- cytoplasm that lacks membrane-bound organelles
- smaller ribosomes (70S)
- single circular bacterial chromosome free in the cytoplasm
- cell wall containing murein aka peptidoglycan
- cell membrane containing folds aka mesosomes
label this bacterium
label this virus
compare the structure of a virus vs bacteria
viruses have a non-cellular structure vs bacteria have a cellular structure
viruses have a protein capsid and bacterium have a polysaccharide cell wall
viruses have one type of nucleic acid vs bacteria have two
outline the carbon cycle
- CO2 is converted into to carbon compounds in plant tissues via photosynthesis
- C is passed onto animals when the eat plants
- C is passed on to decomposers when they eat dead organic matter
- C is returned to the atmosphere as CO2 via respiration of living organisms
- if dead organic matter isn’t decomposed, the C compounds can be turned into fossil fuels and burnt to release CO2 via combustion
what effects can higher temperatures have on a lifecycle (eg. of a fly)
higher temps increase metabolic rate because enzymes are working more optimally, shortening the lifecycle
this could be more detailed/improved
compare plant and animal succession
Plant:
much larger timescale
species are replaced over time
reach a climax community
animal:
early insects often stay as others colonise the body
no climax community
define antibiotic
a chemical that kills or inhibits the growth of microorganisms
can be bactericidal or bacteriostatic
define bactericidal antibiotic
a chemical that kills/destroys bacteria
define bacteriostatic antibiotic
chemicals that prevent the multiplication of bacteria, so there is no cell division; the host’s own immune system can then destroy the pathogens
what is the actual mechanism of an antibiotic
- some inhibit enzymes needed to make chemical bond in bacterial cell walls. this prevents proper growth of the bacteria and can also lead to cell death, because the weakened cell wall can’t take the pressure as water moves via osmosis into the cell causing lysis
- some inhibit protein production by binding to bacterial ribosomes as the cell can no longer make proteins, it can’t make enzymes needed to carry out metabolic processes for growth and development
why do antibiotics only affect bacteria
mammalian cells don’t have cell walls, they have different enzymes and have different (larger) ribosomes
viruses don’t have enzymes or ribosomes (they use the host cell’s)
how does PCR work and why is it used in DNA profiling
PCR = polymer chain reaction
it amplifies the section of DNA so that it can be studied
- A reaction mixture is set up by mixing the DNA sample, primers, free nucleotides and
DNA polymerase. - The mixture is then heated to 95 degrees to break the hydrogen bonds, separating the two strands
- The mixture is then cooled to 50-65, so that the primers can anneal the strands
- Temperature is increased to 72 degrees as this is the optimum temperature for DNA polymerase (<3 bc doesn’t denature at high temps)
DNA polymerase lines up free DNA nucleotides alongside each template strand and complementary base pairing results in the forming of complementary strands - 2 new copies of the fragment DNA have formed, completing one PCR cycle. The cycle then repeats and the amount of DNA doubles each time
what are the elements of making a DNA profile
- extract the DNA
- amplify sample using PCR
- cut up the DNA using restriction enzymes, making fragments of different lengths
- separate and visualise the fragments using gel electrophoresis
- compare these with a reference point
outline gel electrophoresis
restriction enzymes are used to fragment the DNA
- fragmented DNA is placed into wells into an agarose gel plate, which is then covered in an electricity conducting buffer solution
- an electrical current is passed across the gel; as DNA fragments are charged negatively, they move to the cathode at the far end of the gel
- shorter DNA fragments will move faster and therefore further, whilst the longer ones do the opposite
- stain it (eg. methylene blue)
the gel is then viewed under UV light where the fragments will appear as bands
define pathogen
a microorganism that has the potential to cause disease
define infection
the invasion and multiplication of pathogenic microbes in an individual or population; always communicable
do not always result in disease
define disease
when the infection causes damage to the individuals vital function or systems
outline the entry routes of pathogens
broken skin: direct access to tissues and bloodstream
through the digestive system: via contaminated food or drink
through the respiratory system: inhalation
through mucosal surfaces: eg. inside of nose/mouth/genitals
outline the barriers to prevent infection
stomach acid: pathogens that you eat or drink will mostly be killed by stomach acid, the survivors may pass into the intestines where they can invade cells of the gut wall and cause disease
skin: keratin is a physical barrier, blood clots to stop entering after damage
gut and skin flora: flora compete with pathogens for nutrients and space, limiting the no. of pathogens living in the gut/on the skin to make it harder for them to infect the body
- gut flora secrete chemicals to destroy pathogens
lysozyme: mucosal surfaces (eyes/mouth/nose) produce secretions (tears/saliva/mucus)
they all contain lysozyme, an enzyme that kills bacteria by damaging cell wals
outline direct vs indirect methods of disease transmission
direct: physical contact/oral transmission/droplet infection/spores
indirect: vectors (when the pathogen reaches the host via other organisms)
what are some social factors affecting transmission
- poor ventilation
- poor health
- homelessness; often aren’t registered with a dr either
- overcrowding
- poor diet
- poor health ie. autoimmune disorders
explain inflammation’s role in the non-specific immune response
- the infection site becomes red, warm swollen and painful
- mast cells (immune system cells) recognise foreign antigens on the pathogen or just broken skin and release histamine
- histamine stimulates vasodilation and increased capillary permeability around the site
increased blood flow brings loads of immune system cells
increased permeability allows these cells to moves out of the blood vessels and into the infected tissue, it is also what lets blood plasma enter the tissues and create swelling
immune system cells then begin destroying the pathogen
explain the role of interferons in the non-specific immune response
virus-infected cells produce interferons (anti-viral proteins) that prevent the viruses spreading to uninfected cells
how:
- inhibit the production of viral proteins to prevent viral replication
- activate cells involved in the specific immune response to kill infected cells
- activate other mechanism of the non-specific immune response eg. promoting inflammation to bring immune system cells to infection site
explain the role of phagocytosis and lysozyme action in the non-specific immune response
- phagocyte recognises the antigens of a pathogen
- phagocytes cytoplasm moves round the pathogen, engulfing it
- pathogen is now contained in a phagocytic vacuole in the cytoplasm of the phagocyte
- a lysosome fuses with the phagocytic vacuole and the enzymes break the pathogen down
- the phagocyte presents the pathogens antigens. It sticks the antigens on it’s surface to activate other immune cells
so it’s aka ‘antigen-presenting cell’
what are lymphocytes
white blood cells that help to defend against specific diseases, they circulate in the blood and lymph, gathering in large numbers at an infection site
what are B cells
cell that secrete antibodies in response to antigens, antibodies can also be bound to the cell surface membrane of the B cell
formed in the bone marrow
what are T cells
a type of white blood cell; lymphocytes
produced in the bone marrow, but mature in the thymus
have specific antigen receptors on their cell surface membranes that bind only to antigens with the complementary shape
what do T helper cells do
release cytokines that will:
- stimulate B cells to divide and become capable of antibody production
- stimulate T killer cell division
- enhance phagocyte division
what are T killer cells
destroy cells with antigens on their cell surface membranes recognised as non-self, including body cells infected with pathogens (intracellular bacteria/viruses)
what are T memory cells
remain for months/years, allow immune system to quickly respond to a second infection by the same antigen
what are B effector cells
they differentiate into plasma cells which release antibodies
what are B memory cells
remain for months/years, allow immune system to quickly respond to a second infection by the same antigen
outline the humoral response
- complementary amtibody receptors on surface of B cells bind to non-self antigens
- B cell becomes an antigen-presenting cell, antigen is presented on an MHC protein
- B cell is activated by a T helper cell’s cytokines that stimulate cell division and differentiation
- B cells divide by mitosis to produce effector cells and B memory cells
- effector cells become plasma cells (that last for a few days), antibodies released by plasma cells mark bacteria for destruction by macrophages
outline the activation of T cells
- CD4 receptors on a T cell are specific to different antigens, when a receptor meets a complementary antigen on an antigen presenting cell (eg. phagocyte), it binds
- the T cell is now activated and divides via mitosis to create clones
- during mitosis there is also some differentiation to form T killer cells amd T memory cells
outline the cell mediated response
- T helper cell releases cytokines to stimulate cell division, T killer cell with a receptor complementary to the antigen binds to the infected body cell
- T killer cells divide by mitosis to produce clones of active T killer cells and memory cells
- T killer cells release proteins (perforin) that create pores in the membrane of the infected cell
- water and ions flow into the cell, causing lysis. pathogens are released and labelled by antibodies
how does our body prevent attack from our own immune system
membrane proteins on cell surface identify the cells and so avoid destruction, any non-self calls will be destroyed by apoptosis (programmed cell death)
what are autoimmune diseases
where the body identifies self cells as non-self and targets these for destruction
eg. auto-destruction of insulin-secreting cells in the pancreas, leading to type 1 diabetes
outline the secondary immune response
compare the primary and secondary immune responses
T and B memory cells remain from the primary immune response
this allows the secondary response to be much faster and stronger, often allowing the elimination of the pathogen before the infected person can show symptoms
same:
- both produce antibodies
- both start with a non-specific immune response
- both give rise to memory cells
different:
- 2nd is stronger than 1st
- 2nd is when pt is more likely not to have symptoms
- 2nd is when plasma cells multiply faster
how many wood could a woodchuck chuck if a woodchuck could chuck wood
3
what is HIV
human immunodeficiency virus - it infects and destroys T helper cells, this impacts the immune response hugely because T helper cells activate other immune system cells
also enters phagocytes, part of the non-specific response
spread through: infected bodily fluids, a host is infected when the fluids contact mucosal surfaces/damaged tissue
how does HIV replicate
- GP120 (glycoprotein) on HIV attaches to CD4 receptor on the cell membrane of the host T helper cell
- viral envelope fuses with T cell and the capsid is released into the cell, where it uncoats and releases the RNA into the cell’s cytoplasm
- inside the cell, reverse transcriptase is used to make a complementary strand of DNA from the viral RNA template
- double-strand DNA is made from this and inserted into the human DNA
- host cell enzymes are used to make viral proteins from the viral DNA within the human DNA
- the viral proteins are assembled into new viruses which bud from the cell, going on to infect other cells
how does HIV go on to AIDS and what are AIDS symptoms as it progresses
acquired immune deficiency syndrome - where the immune system deteriorates and eventually fails
HIV becomes AIDS when - symptoms of a failing immune system appear and T helper cell counts drop between a certain level
- people with AIDS develop opportunistic infections
HIV –> AIDS without treatment is approx. 10 years
- initial AIDS symptoms: minor mucous membrane infections and recurring respiratory infection because of below average T helper cell no.
- further decrease is T helper cell number as AIDs progresses; susceptible to more serious infections eg. chronic diarrhoea/TB
- late stages of AIDS, v low T helper cell no. and suffer from a range of v serious infections like toxoplasmosis of brain/cadidiasis of respiratory system
the infections are the fatal part
treated with antiretroviral medication
outline the onset of tuberculosis
caused by mycobacterium tuberculosis
its airborne and contained in droplets in the air
- the bacteria is inhaled, where phagocytes take up the bacteria
- the bacteria survives and replicates in the phagocytes, the infected phagocytes are sealed off in tubercles in the lungs so most people don’t immediately develop TB
- the dormant bacteria may later on be reactivate and overcome the immune system, causing TB
more likely in those with weakened immune system eg. people with AIDS
infection –> development can be weeks to years
it then progresses:
- initial TB symptoms; fever, general weakness, sever coughing, due to lung inflammation
- as it progresses, lungs are damaged and if left untreated it can cause respiratory failure, which can lead to death
- TB can spread from lungs to brain, kidneys etc. if left can lead to organ failure –> death
yes or no?
what are the elements of the non-specific immune response
- inflammation
- interferons
- phagocytosis
what is the role of a primer in PCR
they anneal to complementary bases at either end of the DNA strand to be amplified, forming sites on the DNA that DNA polymerase can bind to
what are the uses of PCR
- identifying pathogens/ diagnosing infections
- amplifying crime scene DNA for profiling
- amplifying DNA samples for paternity testing
- amplifying DNA when testing for genetic conditions
what is a retrovirus
a virus that can make DNA from RNA and utilises reverse transcriptase
outline and explain the structure of an antibody
made or 4 polypeptide chains, 2 heavy and 2 light
each chain has a variable and constant region
- variable region: forms antigen binding sites, the shape of that region is complementary to a specific antigen
- constant region: allows binding to receptors on immune system cell (same in all antibodies)
- hinge region: allows flexibility when antibody binds to antigen
disulphide bridges hold together the polypeptide chains
how do antibodies help to clear an infection, 3 key characteristics
- agglutinating pathogens: 1 antibody has 2 binding sites so 2 pathogens can be bound to 1 antibody
Pathogens are tightly clumped so cannot exchange food/oxygen/minerals with their surroundings, so metabolic process stop and the cells die
phagocytes then bind to the antibodies and phagocytose lots of pathogens at once - neutralising toxins: antibodies bind to pathogen produced toxins, preventing them from affecting human cells
- preventing pathogen binding to human cells: when antibodies bind to antigens on pathogens they may block cell surface receptors needed to bind to host cells
what are the types of antibodies
- membrane-bound, attached to B cell via extra protein section on heavy chain
- secreted, not attached to anything
both are coded for by a single gene, copied into mRNA during transcription
how is mRNA modified before translation
- genes have sections that don’t code for amino acids (introns) and sections that do (exons)
this is in eukaryotes not prokaryotes - in transcription, introns and exons are both copied into mRNA, the mRNA with both is called pre-mRNA
- introns are removed by splicing, the exons are joined which forms mRNA strands, occurs in nucleus and is a post-transcriptional change
alternative splicing - sometimes done and is when some exons are removed with the introns, forming different mRNA strands
So, >1 amino acid sequence (and therefore protein) can form from 1 gene
what is active immunity
when your immune system makes it’s’ own antibodies after being stimulated by an antigen
long-term, slow protection
natural - becoming immune after catching a disease
artificial - becoming immune after a vaccine
what is passive immunity
when you’re given antibodies made by another organism
short-term, immediate protection
natural - baby becomes immune due to mother’s antibodies, via placenta and breast milk
artificial - becoming immune after being injected with antibodies
what are the evasion mechanisms of HIV
- reduces number of immune system cells in the body, reducing the chance of it’s detection
- antigenic variation: high rate of mutation in genes coding for antigen proteins, forms new strains so primary response needed for each strain
- disrupts antigen presentation in infected cells, preventing them being recognised and killed
what are the evasion mechanisms of Mycobacterium tuberculosis
- when inside phagocytes, the bacterium has a waxy cell wall and prevents lysosomes from fusing with phagocytes backless so bacteria within tubercules can’t be destroyed
- disrupts antigen presentation in infected cells, preventing them being recognised and killed
infection control practices in hospitals
- doctors and nurses not to wear ties/long sleeve
- use of disposable bedding
- hand washing with antibacterial soap
- separating highly contagious infected patients
what are vaccines and how do they work
vaccine contains antigens that are intentionally put into the body to induce artificial active immunity
Vaccines can contain dead or weakened pathogens, less harmful strains of a pathogen, antigens alone, or a piece of genetic material that codes for the antigens
can be administered orally or by injection
they allow for a strong secondary response when the pathogen actually enters the body
give an example of a post-transcriptional change
splicing of mRNA
how do decomposes work
they break down organic material and respire, releasing CO2 into the atmosphere
how is decomposition rate affected by temp
increasing it to optimal increased enzyme activity
increased temp increased growth rate of bacteria/fungi/decomposers
what are the changes in the body in the first week acts death
body temp falls
rigor mortis
breakdown of tissues by enzymes
bloating and discolouration
why does invading bacteria not survive in the stomach
the pH is too low for most bacterial enzymes to function
how could a bacterial molecule trigger a specific immune response
phagocytes engulf the bacterial molecule and become an APC
T helper cells with complementary CD4 receptors bind to the APC
cytokine is released which causes B cell cloning and B effected cell formation
plasma cells produce antibodies
what is meant by Q10 temperature coefficient
the ratio of the rate of an enzyme reaction taking place at temperatures different by 10 degrees
outline the activation of the specific immune response
- receptors on T cells bind to specific antigens on APC’s like phagocytes
- this activates the cell and it divides
- b-cells are activated when they bind to antigens and form an antigen-antibody complex
- this and cytokines cause activation and division
