Immunity, Infection & Forensics Flashcards
(124 cards)
1
Q
Describe body temperature as part of forensic analysis.
A
Body cools due to lack of heat producing reactions e.g. respiration. Heat is also transferred from the body surface to the environment by radiation, conduction + water evaporation. Follows sigmoid curve. Only useful for 24 hours after death. Measured via rectum or abdominal stab.
Fever or hypothermia will affect body temperature at time of death.
Body size, position, clothing, air movement, humidity and temperature of surroundings will affect cooling of the body.
2
Q
Describe rigor mortis as part of forensic analysis.
A
Muscle cells are oxygen starved so aerobic reactions stop. Respiration becomes anaerobic and cell pH falls due to production of lactic acid. Enzyme activity is inhibited. ATP for muscle contraction is no longer produced. Bonds between muscle proteins become fixed. Proteins can no longer move over each other to shorten the muscle, fixing the muscles and joints in one position. (8-36 hrs)
Affected by:
ATP levels in muscles before death - depends on level of activity before death. Low ATP = faster rigor mortis.
Temperature - high temp = fast + short rigor mortis
Smaller muscles stiffen before larger ones as they have smaller ATP store.
Not permanent, passes after 36-48 hrs after death - enzymes (lysosomes) start to break down muscle tissue.
3
Q
Describe decomposition as part of forensic analysis.
A
Autolysis occurs when enzymes break down cells. Putrefaction is a green discoloration of the lower abdomen due to formation of sulfhaemoglobin. Darkens to red-green then to purple-black.
Gas or liquid blisters may appear.
The body bloats due to action of anaerobic bacteria which produce gases like hydrogen sulphide, methane, CO2, ammonia and hydrogen in intestines and tissues.
Rate affected by temp, injuries, clothing.
4
Q
What is forensic entomology?
A
Study of the succession of insects on the body after death.
5
Q
Describe Forensic Entomology as part of forensic analysis.
A
Records are taken about:
* The body location
* The body condition
* The location of maggots & insects on, under and around the body
Samples of each insect, maggot and larvae are collected and grown to maturity in the lab to identify each species & age determined using stage of life cycle or length of maggots. This gives information about when the eggs were laid which provides a minimum time since death.
Flies could have taken time to locate body & other factors can influence maggot growth.
The temperature of the air, ground, body and ‘maggot mass’ are measured to determine the rate of maggot development.
6
Q
Describe introns.
A
Introgenic regions, non-coding blocks.
Within introns, there are series of repeated bases - short tandem repeats.
7
Q
Define exons.
A
Expressed, coding regions.
8
Q
What can DNA profiling also be known as?
A
Genetic fingerprinting or DNA fingerprinting.
9
Q
Describe how to obtain a tissue sample/ sources of DNA.
A
Any biological tissue from plants or animals can be used. Cheek swab cells, white blood cells in a blood smear, bone marrow in a skeleton, sperm, skin, hair, saliva and sometimes fingerprints.
10
Q
Describe how to extract DNA from cells.
A
The cell membrane is disrupted in a buffer solution containing salts and detergent. The DNA is separated from the rest of the cellular components by centrifugation. The sample is incubated with proteases. The DNA is precipitated out and washed by using ice-cold ethanol.
11
Q
Describe polymerase chain reaction (PCR).
A
A sample of tissue is added to DNA polymerase, DNA primers and DNA nucleotides.
95°C the DNA separated into two strands.
55°C primers anneal at the either side of the section of DNA to be amplified.
70°C Taq polymerase binds to primer region, nucleotides are added. The STR and DNA sequence are replicated.
The cycle is repeated to make multiple copies of DNA/ amplification.
12
Q
Describe gel electrophoresis.
A
Amplified DNA is seperated into DNA fragments using restriction enzymes/ endonucleases. Load DNA onto agarose gel and add TAE buffer. An electric current is applied which causes DNA fragments to move. The fragments can be visualised using southern blotting or flourescent probes and seeing under UV light. Smaller fragments travel faster.
13
Q
What are the 4 shapes of bacteria?
A
- cocci
- vibrios
- bacilli
- spirilla
14
Q
What are the 2 types of bacteria?
A
- Gram positive bacteria
- Gram negative bacteria
15
Q
What is lipopolysaccharide (LPS)?
A
Important outer membrane component of gram negative bacteria.
16
Q
How does LPS affect staining of bacteria?
A
LPS is an endotoxin: it blocks antibiotics, dyes and detergents so it protects the thin inner membrane and cell wall of gram negative bacteria. Makes them resistant to pencilin and lysosome.
Gram negative bacteria reject stain so remain pink.
Gram positive bacteria take up stain so turn purple.
17
Q
Give the name for asexual bacteria reproduction.
A
Binary fission
18
Q
Describe binary fission.
A
- Bacteria reaches a certain size
- DNA is replicated
- Old cell wall begins to break down around middle of cell
- DNA is associated with cell membrane. Cell pinches together forming a septum
- Two new identical daughter cells are formed. Plasmids often divide at the same time
- time between the divisions is the Generation Time
19
Q
What are the 3 forms of bacterial sexual reproduction?
A
- Transformation
- Transduction
- Conjugation
Horizontal gene transfer
20
Q
Describe Transformation
A
A short piece of DNA is released by a donor (which does not need to be alive) or the DNA is in the ‘environment’. This is actively taken up by the recipients. The new DNA replaces a similar piece of DNA in the recipient.
21
Q
Describe Transduction
A
A small amount of DNA is transferred from one bacterium to another by a bacteriophage.
22
Q
Describe Conjugation
A
Plasmid DNA is transferred from one bacterium to another by direct contact. The donor cells (F+) produces a sex pilus. A cytoplasmic bridge is created to the recipient cell (F-). DNA is transferred through the pilus.
23
Q
What are viruses?
A
Small organic particles with a structure that is quite different from that of bacteria and much simpler.
24
Q
What do viruses consist of?
A
They consist of a strand of nucleic acid (DNA or RNA) enclosed within a protein coat (capsid). Viral DNA can be single or double stranded.
25
Describe viral replication
1. Virus attaches to host cell
2. Virus inserts nucleic acid
3. Viral nucleic acids replicate
4. Viral protein coats synthesised
5. New virus particles formed
6. Virus particles released due to cell lysis
26
Describe the conseqence of viral replication cell lysis to host cell.
It kills the host cells and it results in cell contents e.g. enzymes and other chemicals being released damaging neighbouring cells. This can result in the disease symptoms produced by the viral infection.
27
Describe the viral envelope.
Some viruses have an outer envelope taken from the host cell's surface membrane, contains lipids and proteins. It also has glycoproteins from the virus itself which are antigens - helps virus attach to cell and penetrate the surface membrane.
28
What are the two pathways for viral reproduction.
* Lytic pathway
* Lysogenic pathway
29
Describe the lytic pathway.
* Viral genetic material is replicated independently of the host DNA straight after entering the host cell.
* Mature viruses are made by the host cell
* Cell bursts and releases large numbers of new virus particles
* These go on to invade other host cells
* The virus is said to be virulent (disease causing)
30
Describe the lysogenic pathway.
* Viruses are non-virulent when they first get into the host cell
* They insert their DNA into the host DNA so it is replicated every time the host cell divides
* No mRNA is produced from viral DNA because one of the viral genes causes the production of a repressor protein.
* This makes it impossible to translate the rest of the viral genetic material.
* The virus remains dormant and becomes lytic and therefore virulent under the right conditions.
31
Give the 4 major entry routes of pathogens into the body.
1. Cuts in the skin
2. Through the digestive system via contaminated food or drink
3. Through the respiratory system by being inhaled
4. Through other mucosal surfaces e.g. inside of nose, mouth, genitals.
32
List the 6 major transmission routes of pathogens into the body.
* Inhalation
* Direct Contact
* Inoculation
* Vectors
* Ingestion
* Fomites
33
Describe inhalation as a transmission route.
Breathing in of lipid droplets containing the pathogen which were previously expelled from a respiratory tract (e.g. by cough/ sneeze).
34
Describe direct contact as a transmission route.
Can occur from sharing needles, unprotected sex, direct blood-to-blood transfer through cuts and grazes, maternal transmission from mother to unborn child in breast milk.
35
Describe inoculation as a transmission route.
Pathogens enter the body directly through a break in the skin e.g. dog bite, tattooing, infected needle.
36
Describe vectors as a transmission route.
A living organism that transmits infection from one host to another e.g. mosquito's - malaria.
37
Describe ingestion as a transmisssion route.
Consuming contaminated food or drink leads to vomiting and diarrhoea. Greatest risk from raw/ undercooked food.
38
Describe fomites as a transmission route.
Inanimate objects that carry pathogens from one host to another. e.g. hospital bedding, towels.
39
Describe the skin as a barrier from infection.
Contains the tough protein keratin, however the skin can be breached by wounds. Blood clotting prevents this. Skin flora outcompetes and prevents colonisation by other bacteria.
40
Describe the mucosal membranes as a barrier from infection.
Line the airways and the gut. The mucus traps microbes and other particles. Beating cilia carry the mucus up to the throat to be swallowed. Secretions from eyes & nose contain the enzyme lysozyme that breaks down bacterial cell walls causing them to burst.
41
Describe stomach acid as a barrier to infection.
Contains hydrochloric acid, giving a pH of less than 2.0. This kills most bacteria that enter with food or drink. This is also the optimum pH for the digestive enzyme pepsin.
42
Describe the gut flora as a barrier to infection.
Beneficial bacteria found in both intestines. We have a mutualistic relationship with them. They aid digestion and outcompete pathogenic bacteria for food and space - competitively exclude pathogenic bacteria. The bacteria also secrete chemicals (lactic acid) to aid the defence against pathogens.
43
What 2 things can happen when bacteria get into the body?
1. They grow in a localised area
2. Get into the blood supply and get carried around the body
44
How do bacteria make people unwell?
Through the toxins bacteria produce either as by-products of their metabolism or part of their parasitic lifestyle to incapacitate their host or its immune response.
45
2 types of toxins?
* Endotoxins
* Exotoxins
46
Describe endotoxins.
* Lipopolysaccahride part of outer layer of gram negative bacteria. Released on the death of bacteria.
* Rarely fatal
* Tend to cause symptoms such as fever, vomiting and diarrhoea
* The symptoms can indirectly lead to death e.g. by dehydration
47
Describe exotoxins.
* Soluble proteins
* Produced and released into the body by bacteria as they metabolise and reproduce. Stronger ability to trigger an immune response
* Rarely cause fever
* Responsible for some of the most dangerous and fatal bacterial diseases
48
Describe what is meant by the non-specific immune response and its purpose.
* Response that is effective against wide range of infectious agents/ pathogens
* Does not involve recognition of pathogen
* Does not react to specific antigens (memory cells not present)
To destroy, prevent the multiplication and spread of invading pathogens.
49
Give the 4 main processes of the non-specific immune response.
1. Lysozyme action (secretions in the mouth, eyes, nose)
2. Inflammation (release of histamine)
3. Interferon (anti-microbial proteins)
4. Phagocytosis
50
What is the purpose of inflammation?
To destroy the cause of infection and remove it and its products from the body. If this fails to limit the spread of infection, widepsread infection leading to septic shock (sepsis) occurs.
51
Describe inflammation/ inflammatory response.
1. Damage/ infection causes damaged mast cells and basophils to release histamine in response to the recognition of antigens on the surface of a pathogen.
2. Histamine causes the vasodilation of **arterioles** nearby so increases blood flow to the area.
3. Histamine also causes the capillaries to increase their permeability so vessels leak.
4. So plasma fluid, white blood cells and antibodies leak from the blood to site of infection - oedema.
5. WBC begin to destroy pathogen.
6. Interleukin is released from WBC and attracts more phagocytic cells to site of infection.
7. Neutrophils can destroy bacteria.
8. Monocytes will move into site and differentiate into macrophages which engulf dead neutrohils, bacteria, cell debris.
9. Pus will collect at the site (made up of dead WBC)
10. The pus will break down and be absorbed by the surrounding tissue.
52
What is histamine?
An amine which is involved in inflammatory response to infection.
53
What is interleukin?
Protein which regulates inflammation.
54
Describe the appearance of inflammation.
* Red
* Swollen (oedema)
* Painful
* Warm
55
Describe lysozyme action.
An antibacterial enzyme that degrades the peptidoglycan found in bacterial cell walls causing cells to swell and burst. Found in tears, nasal secretion and saliva.
56
Describe the action of Interferon.
Provides defence against viruses (but also some bacteria and protozoa).
Released from infected cells. It binds to surrounding cell surface receptors preventing viral protein synthesis and therefore replication of new viral particles. So virus cannot infect more cells.
57
Describe phagocytosis.
1. Bacterium binds to receptors on macrophage surface and psueodpodia surround the bacterium
2. Bacterium is engulfed by macrophage into a phagosome.
3. Lysosome containing digestive enzymes binds to phagosome forming phagolysosome.
4. Bacterium is digested
5. A small vacuole containing some fragments of the bacterium buds off from the phagolysosome
6. Phagolysosome fuses with cell surface membrane and contents are released by exocytosis. Within the small vacuole, a bacterial fragment is bound to an MHC protein.
7. Vacuole fuses with cell curface membrane and bacterial fragment is presented on the macrophage cell membrane as an antigen.
8. Macrophage has now bcome an APC - specific immune response can now begin.
58
Describe the white blood cells
White blood cells also known as leucocytes.
Neutrophils -> for non specific:
* 70% of WBCs
* Ingest and destroy bacteria (5-20 in phagocytosis)
* Last only a few days
Lymphocytes -> specific:
* 2 types - T cells and B cells
* B cells produce antibodies
* Some last few days, others years
Monocytes & Macrophages -> both
* Monocytes circulate in the blood and move into tissue and differentiate into macrophages
* Macrophages engulf bacteria, foreign matter and cell debris in phagocytosis. Macrophages will present antigen to lymphocytes.
Eosinophils & Basophils
* Granular cytoplasm
* Basophils produce histamine
59
What does APC represent?
Antigen-presenting cell
60
What does MHC represent?
Major Histocompability protein
61
Name the 2 types of specific immune response.
* cell-mediated
* humoral
62
Give the 4 characteristics of specific immune response.
1. It can distinguish self from non-self
2. It is specific
3. It is diverse - can recognise many different antigens
4. It has immunological memory (memory cells)
63
What is an antigen?
A molecule (usually protein or polysaccharide) found on the surface of cells or particles. It is recognised by immune system cells as non-self and activates/initiates an immune response.
64
What happens to a macrophage at the end of phagocytosis?
Macrophage is now an APC (antigen presenting cell).
65
Describe the primary immune response.
Occurs when the body meets a specific pathogen for the first time.
The Humoral Response:
* T helper and T memory cells are created
* B effector cells and B memory cells are created
* B effector cells differentiate into plasma cells to produce antibodies
The Cell Mediated Response:
* T killer cells are involved
66
Describe how a T helper cell is activated.
* A T helper cell with complementary CD4 receptors binds to the antigen/MHC complex on the macrophage APC. The T helper cell becomes activated.
* The activated T helper cell divides/proliferates by mitosis to form clones of active T helper cells.
* Active T helper cells also differentiate and divide to form T memory cells. These remain dormant until they are used in the secondary immune response when the antigen is encountered again.
67
Describe how a B cell is activated.
* An antigen on a bacterium binds to a complementary shaped receptor on the B cell.
* The B cell engulfs the bacterium and carries out antigen processing and presentation. Antigen is bound to an MHC protein. The B cell has now become an antigen-presenting cell (APC).
* An activated T helper cell binds with its CD4 receptors to the antigen/MHC complex on the B cell. The activated T helper cell releases cytokines, which activates the B cell and stimulates it to divide by mitosis. This is known as clonal selection.
* Some active B cell clones differentiate and divide to form B memory cells. These remain dormant until they are used in the secondary immune response when the antigen is encountered again.
68
Describe antibody production from B cells.
* Other active B cell clones become B effector cells.
* B effector cells differentiate into plasma cells.
* Plasma cells produce and secrete antibodies. The binding region of the antibody is the same complementary shape as the receptor on the B cell which bound the original antigen.
69
What type of protein are antibodies?
Immunoglobulin, a form of globular protein.
70
Describe the main role of antibodies.
Antibodies bind to the complementary antigen on the surface of the pathogen. This is known as opsonisation. They cause pathogens to agglutinate (clump together) which helps prevent their spread throughout the body.
71
Describe how antibodies enhance the process of phagocytosis by macrophages.
1. The constant region of the antibody binds to the antibody receptor on the surface of a macrophage.
2. The macrophage engulfs the antibodies and pathogens into a vacuole. An increased number of pathogens are engulfed in the same period of time – this enhances phagocytosis.
3. Lysosomes fuse with the vacuole, releasing their digestive enzymes that destroy the pathogen.
72
What is the humoral response?
The activation of T helper cells and B cells, followed by the production of antibodies in the bloodstream.
73
Describe how a T killer cell is activated.
* A bacterium or virus with antigens on its surface infects a host body cell.
* The host cell carries out antigen processing and presentation. Antigen is bound to an MHC protein. The host cell has now become an APC.
* T killer cell with a complementary receptor binds to the antigen/MHC complex. In the presence of cytokines released from active T helper cells, the T killer cell will be activated and stimulated to divide by mitosis.
* Some active T killer cell clones differentiate and divide to form T killer memory cells. These remain dormant until they are used in the secondary immune response when the antigen is encountered again.
* Population of active T killer cell clones created.
* Active T killer cells bind to other infected host cells which are presenting antigen (APCs)
* Active T killer cell releases enzymes (**perforins**) that create pores in the infected host cell membrane. Water and ions enter the cell, causing cell lysis (it swells and bursts) destroying the host cell. Any live pathogens with the host cell are released. Antibodies bind to the antigen on the pathogen surface (opsonisation) for destruction by macrophages in phagocytosis.
74
What is the role of macrophages following host cell destruction by T killer cells?
They carry out phagocytosis of agglutinated pathogen (pathogen clumped together by antibodies) following cell lysis and the host cell debris.
75
What is the cell mediated response?
The activation of T killer cells, followed by the lysis of infected host cells.
76
Describe Active Natural Immunity.
An individual mounts a specific primary immune response after naturally contracting a pathogen and creates antibodies and memory cells (long term protection).
Example: A child is exposed to the chicken pox virus for the first time.
77
Describe Passive Natural Immunity
Antibodies from one individual are passed to a second individual in a natural process. (short term protection).
Example: Antibodies have passed from mother to baby via the placenta or breast milk.
78
Describe Passive Artificial Immunity.
Antibodies from one individual are passed to another individual via an injection to provide immediate protection. (short term protection)
Example: Antibodies are injected into an individual infected with Ebola after being removed from another person who has survived and created them in a primary immune response to Ebola.
79
Describe Active Artifical Immunity.
A form of the pathogen is injected into the individual who then mounts a specific primary immune response to create antibodies and memory cells (long term protection).
Example: An attenuated form of the measles virus is injected.
80
Define attenuated.
Living pathogen but cannot produce disease.
81
Describe vaccines.
Contains one or more antigens that are also found on the pathogen or the toxin. Does not protect against contracting the pathogen.
82
Describe attenuated virus vaccines.
Weakened viruses that are harmless (non-pathogenic) and less virulent. They will reproduce very slowly but not result in symptoms in the host.
83
Describe killed bacteria vaccines.
The bacteria have been killed by chemicals, heat or radiation.
84
Describe harmless toxin vaccines.
Inactivated toxic compound that causes the illness rather than the microorganism that produces it.
85
Describe antigen-bearing fragment vaccines.
A newer form of vaccine. It can consist of a surface protein of the microorganism i.e. glycoprotein or capsid fragment.
86
What is ‘herd immunity’?
When enough people in a population are successfully vaccinated and immunised, the pathogen is less likely to be transferred from one person to another. This reduces the incidence of the disease in the community and protects those not able to be vaccinated.
87
What are adjuvants?
Additives in vaccines to increase inflammatory response so there is a more effective immune response.
88
Contrast the primary and secondary immune response.
secondary response (compared to primary response):
* Faster rate of antibody production.
* Shorter time lag between exposure & antibody production.
* Higher concentration of antibodies.
* Antibody level remains higher after the secondary response
* Pathogen usually destroyed before any symptoms.
89
Compare passive and active immunity.
* Both involve antibodies
* Both can be natural or artificial
90
Contrast passive and active immunity.
**Passive**:
* no memory cells & antibodies not replaced when broken down = short-term
* immediate
* antibodies from external source
* direct contact with antigen not necessary
**Active**:
* memory cells produced = long-term
* time lag
* lymphocytes produce antibodies
* direct contact with antigen necessary
91
State the meaning of the term bacterial infection.
Bacteria are inside the cells
92
How does mycobacterium tuberculosis cause disease/ primary infection with TB?
* Bacteria inhaled in water droplets and lodge in lungs and bacteria start to multiply triggering an inflammatory response
* Bacteria are engulfed by a macrophage but resist digestion due to their thick waxy cell walls.
* The bacteria lie dormant in macrophages and a mass of tissue (granuloma or tubercle) forms
* Tubercle, is anaerobic and contains dormant bacteria and macrophages
* As the macrophages are unable to present antigen the immune system is suppressed.
* The person has no signs or symptoms of the disease and are said to have latent TB.
93
Describe Mycobacterium tuberculosis.
* Has thick and waxy cell walls to resist digestion from macrophages.
* Requires O2 to survive so most bacteria die inside tubercles.
* Can lie dormant for many years.
94
Describe the primary stage of infection with TB (latent TB).
* Droplet infection - entry toute = repiratory tract, inhaled from infected person
* May last several months/ years - no symptoms
* Not infectious
95
Describe the active TB/ secondary phase.
The bacteria multiply rapidly and destroy the lung tissue, creating holes or cavities. Reduced gas exchange and breathing problems. The bacteria are able to leave the tubercles and potentially spread around the body. Occurs when the patient’s immune system is weakened/ suppressed. This could be due to age (very young or very old), malnutrition, poor living conditions, other infections e.g. HIV or number of bacteria is too high.
96
Describe the sequence of symptoms that result in the death of a person infected with Mycobacterium tuberculosis (TB).
Coughing (sometimes with blood), shortness of breath/ breathing problems, loss of appetite, weight loss, fever, extreme fatigue, TB causes suppression of immune system can results in opportunistic infections... Leads to death.
97
What is glandular TB?
The bacteria move to infect other parts of the body e.g. blood, lymph nodes and central nervous system. Lymph nodes in the neck or armpits can enlarge.
98
State the ways in which TB can be diagnosed.
Skin (injecting a small amount of tuberculin) and blood tests, identification of bacteria in sputum, chest X-rays to identify tubercles.
99
How do TB bacteria affect immune system?
Bacteria can suppress T cells, reduces antibody production by reducing cytokine production so less active B cells, less plasma cells, less antibodies and less attack by T Killer cells.
100
Why do bacteria evolve so quickly?
1. Fats generation time , faster reproductive rate
2. Bacterial populations are very large: very large gene pool - many mutations in DNA.
3. Some random mutations will be advantageous: may allow the bacterial cell to use a different food resource, reproduce more quickly, infect other cells more quickly, produce advantageous symptoms in the host for their transmission i.e. coughing or sneezing.
Those bacteria with a new advantageous allele are more likely to survive, reproduce and spread from cell to cell and host to host.
101
What is an antibiotic?
A chemical substance, produced by microorganisms, which has the capacity to inhibit the multiplication/replication, or even destroy bacteria within a patient. Works by principle of selective toxicity.
102
Describe how antibiotics work.
* slowing bacterial cell growth/reproduction so fewer cells produced,
* giving more time for immune system to respond,
* by clonal expansion of B cells, antibody production,
* and by phagocytosis (macrophages engulf + digest bacteria)
103
Outline how antibiotics can disrupt bacterial cell growth and division
1. Inhibition of bacterial cell wall synthesis: If a weak wall forms, this can lead to cell lysis.
2. Disruption of the cell membrane: This can cause changes in permeability that can lead to cell lysis.
3. Inhibition of nucleic acid synthesis, replication and transcription: This can prevent cell division (binary fission) and/or synthesis of enzymes.
4. Inhibition of protein synthesis: Enzymes and other essential proteins are not produced.
5. Inhibition of specific bacterial enzymes: this would inhibit bacterial cell processes but not those of the host.
104
Name the two types of antibiotic and describe how they work.
Bactericidal: Antibiotic that destroys/kills bacteria. Can cause the cell to lyse.
Bacteriostatic: Antibiotic that inhibits the multiplication/replication (NOT growth) of bacteria. The host’s own immune system can then destroy the bacterial population.
105
Describe Broad Spectrum and Narrow Spectrum Antibiotics
Broad Spectrum Antibiotics:
* Destroy a wide range of harmful bacteria and pathogens
* Also destroy neutral and ‘good’ bacteria (gut flora)
Narrow Spectrum Antibiotics
* Targets one or two specific pathogens
106
What factors influence the effectiveness of any antibiotic?
* Its concentration
* How quickly it reaches the infected tissue and how quickly it is excreted
* The pH of the local environment where the antibiotic is working
* Whether the host cell or the pathogen destroys the antibiotic
* The susceptibility of the pathogen to the antibiotic (if it is resistant)
107
Describe the difference between disinfectants and antiseptics.
* Disinfectants kill bacteria from the area/ instrument - reduces likelihood of bacteria being transferred.
* Antispetics applied to skin and wounds to kill bacteria to reduce chance of infection of wound.
108
Why are bacteria becoming resistant to antibiotics?
The presence of an antibiotic/ immune system provides a selection pressure for the bacteria. There is some naturally occurring genetic variation in the bacterial population. A random mutation created a new allele for resistance. Those which possess an advantageous allele for resistance are more likely to survive and reproduce. The advantageous allele may be for a new enzyme that can breakdown/destroy the antibiotic, a cell membrane protein that pumps out the antibiotic or for a new metabolic pathway that bypasses the reactions inhibited by the antibiotic. The frequency of the allele in the bacterial population will increase. The allele can be passed via vertical evolution to ‘offspring’ and/or horizontal evolution to other bacteria of the same or different species via conjugation.
109
Give two examples of multi-drug resistant bacteria.
Mycobacterium tuberculosis (TB) and methicillin-resistant Staphylococcus aureus (MRSA).
110
Outline the measures hospitals use in controlling the development of multi-drug resistant bacteria and their spread.
* Monitors use of antibiotics - only uses when necessary
* Monitoring levels of drug resistant infections
* Educating patients about importance of taking the full course of antibiotics
* Screening and isolation of suspected infected patients
* Regular deep cleaning and changing of bedding
* Washing bedding at higher temperature to kill bacteria
* Hospitals changing code of practice to ensure stricter hygiene practices
* Wearing specific suitable clothing for doctors and nurses
* Antiseptic solutions readily available to reduce infections
111
Describe how HIV invades T helper cell.
Glycoprotein molecules on the surface of HIV called gp120 bind to CD4 receptors on the surface of T helper cells. The HIV envelope fuses with the T helper cell surface membrane and the HIV capsid enters the cell. The capsid releases the RNA genome, reverse transcriptase and integrase into the cytoplasm.
112
Why can HIV also infect macrophages?
Macrophages have CD4 receptors
113
Describe what happens after HIV has entered the T helper cell.
Formation of viral DNA from viral RNA using reverse transcriptase by reverse transcription. The new DNA is integrated into the host cell’s genome using the enzyme integrase. The viral genome can now be transcribed and translated to produce new viral RNA and proteins
114
How does HIV destroy T helper cells?
HIV DNA becomes incoporated into the DNA of T helper cell. Many HIV particles are made. Many HIV viruses bud out of the T helper cell taking some host cell surface membrane to form their envelope. T helper cells is killed cell lysis as their cell membrane is destroyed.
Infected T helper cells will also be destroyed by T killer cells.
115
What is the consequence of HIV on the immune system?
As the number of virus particles increase the number of T helper cells decreases, reducing cytokines. Macrophages, B cells and T killer cells are unable to be activated successfully and the immune system becomes deficient. Vulnerable to secondary and opportunistic infections.
116
What determines the speed of the development of AIDS?
Many factors are involved – the health of the host before infection, their genetic resistance to infection, the quality of their immune response to infection, their lifestyle, their nutritional status, the availability of drug treatment, other infections.
117
Describe the acute phase in AIDS.
Person may experience fever, sweats, headache, sore throat and swollen lymph glands. HIV antibodies appear in the blood after 3–12 weeks (once detected the individual is said to be HIV positive). There is a rapid replication of new virus particles and loss of T helper cells. After a few weeks, infected T helper cells are targeted by T killer cells and destroyed. This greatly reduces the rate of viral replication, but does not totally eliminate it.
118
Describe the chronic/ latent phase in AIDS.
Can last 20 years. The virus replicates rapidly, but the immune system keeps numbers in check. There may be no symptoms apart from more colds and minor infections. TB and shingles can reactivate. HIV positive individuals are infectious.
119
Describe the disease phase in AIDS.
Eventually an increased viral load and significant reduction in T helper cell count indicates the onset of AIDS. The immune system is now vulnerable to opportunistic infections such as TB and pneumonia. Karposi’s sarcoma (type of skin cancer) can develop. There is also significant weight loss and sometimes the development of dementia. The development of these symptoms leads to death.
120
What are the drugs used to treat an HIV infection collectively known as?
Antiretroviral drugs
121
Describe the drugs used to treat HIV and how they work.
* Reverse transcriptase inhibitors – prevent viral RNA from making DNA
* Protease inhibitors – inhibit the proteases that catalyse the cutting of larger proteins into small polypeptides for use in the construction of new viruses.
* Integrase inhibitors - prevent viral DNA from intergating into host DNA preventing latency
122
Why are the drugs given in combination?
HIV can develop resistance to anti-HIV drugs so drugs given in combiation to target and destroy many different strains of HIV.
123
Explain why antibiotics are not used to treat viral infections.
Antibiotics target organelles/ structures found in bacteria so viruses are unaffected by the antibiotics.
124
Describe how one gene can give rise to more than one protein.
Splicing removes introns from pre-mRNA. Alternative splicing also removes exons not needed. So mRNA produced is different so translation of the mRNA gives a different amino acid sequence so a different protein is produced.
