BIOLOGY, TOPIC SIX,6. Flashcards
(94 cards)
1
Q
WHAT IS A PATHOGEN?
A
A PATHOGEN IS ANY ORGANISM WHICH CAUSES DISEASE.
2
Q
INFECTIOUS DISEASES.
A
INFECTIOUS DISEASES ARE ALWAYS CAUSED BY PATHOGEBNS, WHICH CAN SPREAD FROM PERSON TO PERSON TO INFECT OTHERS.
3
Q
NON-INFECTIOUS DISEASES.
A
NON-INFECTIOUS DISEASES, SUCH AS LUNG CANCER OR DIABETES, ARE NOT CAUSED BY PATHOGENS AND TEND TO BE MORE INGLUENCED BY GENETIC OR LIFESTYLE FACTORS.
4
Q
PATHOGEN EXAMPLES.
A
PATHOGENS INCLUDE, BACTERIA, VIRUSES, PROTOCISTS AND FUNGI.
PATHOGENIC ORGANISMS.
BACTERIA,
MYOBACTERIUM TUBERCULOSIS CAUSES, TB.
VIRUS,
HIV CAUSES AIDS.
COVID-19 CAUSES CORONAVIRUS.
THE INFLUENZA VIRUS CAUSES SEASONAL FLU.
PROTOCIST,
PLASMODIUM CAUSES MALARIA.
FUNGI,
TRICHOPHYTON CAUSES ALTHLETE’S FOOT.
5
Q
BACTERIAL CELL STRUCTURE.
A
BACTERIA ARE SINGLE-CELLED PROKARYOTIC ORGANISMS WHICH CONTAIN THE FOLLOWING STRUCTURES:
CIRCULAR CHROMOSOMAL DNA.
RIBOSOMES.
CELL WALL.
PILI.
MESOSOMES.
PLASMIDS.
SLIME CAPSULE.
FLAGELLUM.
6
Q
CIRCULAR CHROMOSOMAL DNA.
A
FLOATS FREE IN THE CYTOPLASM.
7
Q
RIBOSOMES.
A
THESE ARE SMALLER THAN THOSE FOUND IN EUKARYOTIC CELLS.
70S RIBOSOMES.
8
Q
PILI.
A
PILI ARE HAIR-LIKE STRUCTURES WHICH STICK OUT FROM THE PLASMA MEMBRANE.
THEY ARE USED TO COMMUNICATE WITH OTHER CELLS, INCLUDING THE TRANSFER OF PLASMIDS BETWEEN BACTERIA.
9
Q
MESOSOMES.
A
THE MESOSOMES IS A FOLDED PORTION OF THE INNFER MEMBRANE.
WHILE SOME SCIENTISTS BELIVE THAT IT PLAYS A ROLE IN CHEMICAL REACTIONS, SUCH AS RESPIRATION, OTHER SCIENTISTS DOUBT WHETHER IT EVEN EXISTS AND THINK THAT IT MAY JUST BE AN ARTEFACT PRODUCED DURING THE PREPARATION OF BACTERIAL SAMPLES FOR MICROSCOPY.
10
Q
PLASMIDS.
A
PLASMIDS ARE SMALL, CIRCULAR RINGS OF DNA WHICH ARE SEPARATE FROM THE MAIN CHROMOSOME.
THEY HOUSE GENES WHICH ARE NOT CRUCIAL FOR SURVIVAL BUT MIGHT PROVE USEEFUL, SUCH AS ANTIBIOTIC-RESISTANCE GENES, FOR EXAMPLE.
PLASMIDS CAN REPLICATE INDEPENDENTLY FROM THE MAIN CHROMOSOMAL DNA.
11
Q
SLIME CAPSULE.
A
IN ADDITION TO A CELL WALL, SOME BACTERIA ALSO HAVE A CAPSULE WHICH IS MADE OF SLIME.
THE MAIN FUNCTION OF THE CAPSULE IS TO PROTCT THE BACTERIUM AGAINST AN IMMUNE SYSTEM ATTACK.
12
Q
FLAGELLUM.
A
ROTATES TO MOVE THE BACTERIUM.
13
Q
HIV.
A
HUMAN IMMUNODEFICENCY VIRUS, HIV.
14
Q
WHAT IS HIV?
A
HIV, IS A DEADLY VIRUS, WHICH CAN WEAKEN A PERSON’S IMMUNE SYSTEM.
15
Q
HOW DOES HIV WEAKEN AN INDIVIDUALS IMMUNE SYSTEM?
A
IT CAN WEAKEN A PERSONS’S IMMUNE SYSTEM BY DESTROYING A TYPE OF IMMUNE CELL CALLED T HELPER CELLS.
16
Q
HIV, SPREAD.
A
IT IS SPREAD THROUGH THE TRANSMISSION OF INFECTED BODILY FLUIDS. FOR EXAMPLE, DURING SEXUAL INTERCOURSE, SHARING OF NEEDLES OR BLOOD TRANSFUSION.
17
Q
OPPORTUNISTIC INFECTIONS.
A
HIV DOOES NOT KILL THE PATIENT DIRECTLY, BUT WEAKENS THE IMMUNE SYSTEM TO AN EXTENT THAT THE PATIENT IS UNABLE TO FIGHT OFF OTHER INFECTIONS WHICH NOMRALLY WOULD NOT A POSE A THREAT.
THESE ARE KNOWN AS OPPORTUNISTIC INFECTIONS.
18
Q
AIDS, STAND FOR.
A
ACQUIRED IMMUNODEFICENCY SYNDROME, AIDS.
19
Q
ZTHE DEVELOPMENT OF AIDS.
A
WHEN THE PATIENT’S IMMUNE SYSTEM HAS WEAKEND TO A PARTICULARLY LOW LEVEL, THIS IS SEEN BY A LOW T HELPER CELL COUNT IN HOSPITAL BLOOD TESTS, THE PATIENT HAS DEVELOPED A DISEASE CALLED AIDS.
20
Q
WHAT IS AIDS?
A
AIDS IS A DISEASE.
21
Q
THE LATENCY PERIOD.
A
THE TIME BETWEEN INITIAL INFECTION AND THE ONSET OF AIDS SYMPTOMS, THE LATENCY PERIOD, VARIES GREATLY BETWEEN INDIVIDUALS BUT IT IS USUALLY AROUND TEN,10, YEARS.
22
Q
THE LENGTH OF THE LATENCY PERIOD, DEPENDANT ON.
A
THE LENGTH OF THE LATENCY PERIOD DEPENDS ON THE INDIVIDUAL’S AGE, STRENGTH OF THEIR IMMUNE SYSTEM AND ACCESS TO HEALTHCARE.
23
Q
THE STAGES OF THE SYMPTOMS OF AIDS.
A
THE PERSON WILL FIRST DEVELOP LESS SERIOUS, MINOR INFECTIONS WHICH WILL GRADUALLY BECOME MORE AND MORE SEVERE.
AS THE PATIENT’S BODY TRIES TO FIGHT OFF MORE INFECTIONS, THE LOWER THEIR T CELL LEVELS DROP.
EVENTUALLY THEIR IMMUNE SYSTEM WILL BE SO WEAK THAT THEY WILL DIE OF AN OPPORTUNISTIC INFECTION BECAUSE THEY DO NOT HAVE ENOUGH IMMUNE CELLS TO DEFEND THEMSELVES.
24
Q
HIV STRUCTURE.
A
THE HIV VIRUS CONSISTS OF A CORE OF RNA AND ENZYMES, REVERSE TRANSCRIPTASE AND INTERASE, WHICH ARE ENCLOSED IN A PROTIEN COAT CALLED A CAPSID.
SURROUNDING THE CAPSID IS AN OUTER LAYER CALLED THE ENVELOPE WHICH CONTAINS ATTACHMENT PROIENS, THESE PROTIENS ARE CRUCAL FOR THE VIRUS TO ENTER THE HOST CELL.
THE ACT LIKE LITTLE KEYS TO ACCESS OUR CELLS.
25
HIV REPLICATION.
IF A PERSON WITH HIV EXCHANES BODILY FLUIDS WITH ANOTHER PERSONS, HIV CAN INFECT THE SECON INDIVIDUAL AND WILL BE PRESENT IN THEIR BLOODSTREAM.
THE HIV VIRUD USES ITS ATTACHMENT PROTIENS TO ENTER HUMAN IMMUNE CELLS, SPECIFICALLY THE HELPER T CELL, BY BINDING TO RECEPTORS ON THE T CELL.
THE CAPSID IS RELEASED INTO THE CELL, WHERE IS BREALS APART TO RELEASE RNA AND ENZYMES.
THE ENZYME REVERSE TRANSCRIPTASE CONVERTS THE RNA INTO DNA.
THE SIGLE-STRANDED DNA IN CONVERTED TO DOUBLE-STRANDED DNA WHICH THE ENZYME INTEGRASE CAN INSERT THE DNA OF THE T CELL.
THE T CELL NOW HAS 'INSTRUCTIONS", GENES, TO PRODUCE VIRAL PROTIENS.
THE VIRAL DNA IS TRANSCRIBED AND TRANSLATED AND THE VIRAL PROTIENS ARE USED TO BUILD NEW VIRUS PARTICLES, WHICH MOVE OUT OF THE T CELL AND INFECT OTHER CELLS.
26
TB, STAND FOR.
TUBERCULOSIS, TB.
27
TUBERCULOSIS, CAUSES.
TUBERCULOSIS, TB, IS CAUSED BY BACTERIUM CALLED MYOBACTERIUM TUBERCULOSIS.
28
TUBERCULOSIS, SPREAD.
IT IS SPREAD THROUGH LIPID DROPLETS. FOR EXAMPLE WHEN AN INFECTED PERSON SNEEZES OR COUGHS.
THE LIPIS DROPLETS ARE INHALED BY ANOTHER PERSON, CAUSING THE BACTERIA TO MOVE INTO THE LUNGS.
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TUBERCULOSIS, ONCE THE BACTERIA IS IN THE LUNGS.
ONCE THEY ARE IN THE LUNGS, THE BACTERIA ARE ENGULFED BY A TYPE OF WHIT BLOOD CELL CALLKED A PHAGOCYTE.
PHAGOCYTES USUALLY WORK BY DIGESTING AND KILLING THE PATHOGEN, BUT MYOBACTERIUM TUBERCULOSIS IS ABLE TO DISRUPT THIS PROCESS.
THE BACTERIA ARE ABLE TO SURVIVE AND REPLICATE FROM INSIDE PHAGOCYTES.
30
TUBERCULOSIS SYMPTOMS AND INFECTION.
THE TIME BETWEEN INFECTION WITH MYOBACTERIUM TUBERCULOSIS AND THE ONSET OF SYMPTOMS CAN VARY BETWEEN INDIVIDUALS, THE LATENCY PERIOD BETWEEN A FEW WEEKS AND MANY YEARS.
31
TUBERCULOSIS SYMTPTOMS.
INITIAL SYMPTOMS INCLUDE A COUGH AND FEVER WHICH IS CAUSED BY INFLIMATION OF THE LUNGS.
THE LUNGS BECOME PROGRESSIVELY MORE DAMAGED, LEADING TO RESPITORY FAILURE AND SOMETIMES DEATH. IT CAN ALSO SPREAS TO OTHER PARTS OF THE BODY, SUCH AS THE KIDNEYS AND THE BRAIN.
32
TUBERCULOSIS SYMPTOMS, NOT APPEARING IMMEDIATELY.
OFTEN THE SYMPTOMS OF TUBERCULOSIS DO NOT APPEAR IMMEDIATELY.
OUR BODY IS ABLE TO SEAL OFF INFECTED PHAGOCYTES INSIDE STRUCTURES WITHIN OUR LUNGS CALLED TUBERCLES.
THE BACTERIA WITHIN THE TUBERCLES LIE DORMANT FOR A PERIOD OF TIME UP TO A FEW YEARS.
THE BACTERIA THEN BECOME REACTIVATED, REACTIVATION CAN BE STIMULATED BY A WEAKENED IMMUNE SYSTEM, FOR EXAMPLE DUE TO AIDS.
33
DEFENSIVE BARRIERS.
OUR BODIES HAVE SEVERAL DEFENSIVE BARRIERS TO PREVENT US BECOMING INFECTED BY PATHOGENS.
34
BODY CAVITIES.
OUR BODY CAVITIES, SUCH AS EYES, NOSE, MOUTH, GENITALS, ARE LINED WIT A MUCUS MEMBRANE, WHICH CONTAINS AN ENZYME CALLED LYSOZYME.
LYSOZYME KILLS BACTERIA BY DAMAGING THEIR CELL WALLS, CAUSING THEM TO BURST OPEN.
35
SKIN.
OUR SKIN ACTS AS A PHYSICAL BARRIER TO STOP PATHOGENS FROM GETTIGN INSIDE OF US.
IF OUR SKIN IS CUT OR WOUNDED, OUR BLOOD QUICKLY CLOTS TO MINIMISE THE ENTRY OF PATHOGENS.
36
TRACHEA.
THE TRACHEA, WINDPIPE, CONTAINS GOBLET CELLS WHICH SECRETE MUCUS.
PATHOGENS THAT WE INHALE BECOME TRAPPED IN THE MUCUIS, WHICH IS SWEPT TOWARDS THE STOMACH BY THE ACTION OF CILIATED EPITHELIAL CELLS.
37
STOMACH.
OUR STOMACH CONTAISN GASTRIC JUICES WHICH ARE HIGHLY ACIDIC, THEESE WILL DENATURE PROTIENS AND KILL ANY PATHOGENS THAT HAVE BEEN INGESTED IN OUR FOOD AND DRINKS.
38
INTESTINES.
THE INSIDES OF OUR INTESTINES AND THE SURFACE OF OUR SKIN ARE COVERED IN HARMLESS BACTERIA WHICH WILL COMPETE WITH ANY PATHOGENIC ORGANISMS AND REDUCE THEIR ABILITY TO GROW.
39
NON-SPECIFIC IMMUNE RESPONSE.
THE NON-SPECIFIC IMMUNE RESPONSE IS OUR IMMEDIATE REPSONSE TO INFECTION AND IS CARRIED OUT IN EXACTLY THE SAME WAY REGARDLESS OF THE PATHOGEN, IT IS NOT SPECFIC TO A PARTICULAR PATHOGEN.
THE NON-SPECIFIC IMMUNE REPSONSE INVOLVES INFLAMMATION, THE PRODUCTION OF INTERFERONS AND PHAGOCYTOSIS.
40
INFLIMMATION.
THE PROTIENS WHICH ARE FOUND ON THE SURFACE OF A PATHOGEN, ANTIGENS, ARE DETECTED BY OUR IMMUNE SYSTEM.
IMMUNE CELLS RELEASE MOLECULES TO STIMULATE VASODILATION, THE WIDENING OF BLOOD VESSELS, AND TO MAKE BLOOD VESSELS MORE PERMEABLE.
THIS MEANS THAT MORE IMMUNE CELLS CAN ARRIVE AT THE SITE OF INFECTION BY MOVING OUT OF THE BLOODSTREAM AND INTO THE INFECTED TISSUE.
THE INCREASED BLOOD FLOW IS WHY AN INFLAMES PART OF YOUR BODY LOOKS RED OR SWOLLEN.
41
PRODUCION OF INTEFERONS.
IF THE PATHOGEN WHICH HAS INFECTED YOU IS A VIRUS, YOUR BODY CELLS THAT HAVE BEEN INVADED BY THE VIRUS WILL START TO MANUFACTURE ANTI-VIRAL PROTIENS CALLED INTERFERONS.
THEY SLOW DOEN VIRAL REPLICATION IN THREE,3, DIFFERENT WAYS:
STIMULATE INFLIMATION TO BRING MORE IMMUNE CELLS TO THE SITE OF INFECTION.
INHIBIT THE TRANSLATION OF VIRAL PROTIENS TO REDUCE VIRAL REPLICATION.
ACTIVATE T KILLER CELLS TO DESTROY INFECTED CELLS.
42
PHAGOCYTES.
PHAGOCYTES ARE A TYPE OF WHITE BLOOD CELL WHICH CAN DESTROY PATHOGENS, TYPES OF PHAGOCYTE INCLUDE MACROPHAGES, MONOCYTES AND NEUTROPHILS.
43
PHAGOCYTOSIS.
THEY FIRST DETECT THE PRESENCE OF THE PATHOGEN WHEN RECEPTORS ON ITS SURFACE BIND TO ANTIGENS ON THE PATHOGEN.
THE PHAGOCYTE THEN WRAPS ITS CYTOPLASM AROUND THE PATHOGEN AND ENGULFS IT.
THE PATHOGEN IS CONTAINED WITHIN A TYPE OF VESCILE CALLED A PHAGOSOME.
ANOTHER TYPE OF VESICLE, CALLED A LYSOSOME, WHICH CONTAISN DIGESTIVE ENZYMES, LYSOZYMES WILL FUSE WITH THE PHAGOSOME TO FORM A PHAGOLYSOSOME.
LYSOZYMES DIGEST THE PATHOGEN AND DESTROY IT.
THE DIGESTED PATHOGEN WILL BE REMOVED FROM THE PHAGOCYTE BY EXOCYTOSIS, BUT THEY WILL KEEP SOME ANTIGEN MOLECULES TO PRESENT ON THE SURFACE OF THEIR CELLS, THIS SERVES TO ALERT OTHER CELLS OF THE IMMUNE SYSTEM TO THE PRESENCE OF A FOREIGN ANTIGEN.
THE PHAGOCYTE IS NOW REFERRED TO AS AN ANTIGEN-PRESENTING CELL.
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SPECIFIC IMMUNE RESPONSE.
THE SPECIFIC IMMUNE RESPONSE HAPPEND AFTER THE NON-SPECIFIC RESPOINSE AND IS AN ATTACK AIMED AT A PARTICULAR ANTIGEN.
IT INVOLVES THE ACTIVATION OF TWO,2, TYPES OF IMMUNE CELLS:
T LYMPHOCYTES,
AND B LYMPHOCYTES.
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WHAT ARE T LYMPHOCYTES?
T LYMPHOCYTES ARE WHITE BLOOD CELLS WHICH CONTAISN RECEPTORS ON THEIR CELL SURFACE.
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T LYMPHOCYTES, DIFFERENCES BETWEEN THEM.
DIFFERENT T CELLS HAVE DIFFERENT SHAPED RECEPTORS ON THEIR SURFACE, SO THEY WILL BIND TO A DIFFERENT-SHAPED ANTIGEN.
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T LYMPHOCYTE RESPONSE.
WEHN A PARTICULAR T CELL BINDS TO A COMPLIMENTARY ANTIGEN, THE T CELL WILL BECOME ACTIVATED, THIS IS CALLED CLONAL SELECTION.
ONCE IT IS ACTIVATED, THE T CELL DIVIDES BY MITOSIS TO PRODUCE CLONES OF ITSELF, THIS IS CALLED CLONAL EXPANSION.
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T HELPER CELLS.
T HELPER CELLS RELEASE CHEMICALS, THEY RELEASE A TYPE OF CYTOKINE CALLED INTERLEUKINS, TO ACTIVATE B LYMPHOCYTES.
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T KILLER CELLS.
T KILLER CELLS DESTROY ANY CELLS WHICH HAVE BEEN INFECTED WITH THE PATHOGEN.
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T REGULATORY CELLS.
T REGULATORY CELLS SUPRESS OTHER IMMUNE CELLS AND PREVENT THEM FROM ATTACKING OUR OWN, HOST, CELLS.
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T MEMORY CELLS.
T MEMORY CELLS REMAIN IN THE BLOOD STREAM IN LOW LEVELS IN CASE REINFECTION OCCURS.
IF THE ANTIGEN IS DETECTED AGAIN AT A LATER DATE, THEY WILL DIVIDE INTO T HELPER, T KILLER AND T REGULATORY CELLS.
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B CELLS, ACTIVATED.
B CELLS ARE ACTIVATED WHEN CHEMICALS ARE RELEASED FROM T HELPER CELLS.
THEY ARE ALSO ACTIVATED WHEN THE ANTIBODY MOLECULES ON THEIR SURFACE BIND TO A COMPLIMENTARY ANTIGEN.
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B CELLS, DIFFERENCES.
DIFFERENT B CELLS HAVE DIFFERENT SHAPED ANTIBODIES ON THEIR SURFACE, SO ONLY THE B CELLS WITH THE CORRECT-SHAPED ANTIBODIES WILL BE ACTIVATED.
54
B LYMPHOCYTE RESPONSE.
ONCE THEY ARE ACTIVATED, THE B CELLS DIVIDE BY MITOSIS AND DIFFERENTIATE INTO TWO,2, KINDS OF CELLS, PLASMA CELLS AND MEMORY CELLS.
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PLASMA CELLS.
PLASMA CELLS CAN PRODUCE ANTIBODIES WITH A COMPLIMENTARY SHAPE TO THE ANTIGEN.
56
MEMORY CELLS.
MEMORY CELLS REMAIN IN THE BLOODSTREAM IN LOW LEVELS IN CASE REINFECTION OCCURS.
IF THE ANTIGEN IS DETECTED AGAIN AT A LATE DATE, THEY WILL QUICKLY DIVIDE INTO PLASMA CELLS.
57
ANTIBODIES STRUCTURE.
ANTIBODIES HAVE A QUATERNARY STRUCTURE MADE UP OF FOUR,4, POLYPEPTIDE CHAINS, TWO,2, HEAVY CHAINS AND TWO,2, LIGHT CHAINS, HELD TOGETHER DISULFIDE BRIDGES.
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VARIABLE REGION.
ANTIBODIES ARE COMPOSED OF A VARIABLE REGION, WHICH IS DIFFERENT IN DIFFERENT ANTIBODIES, WHERE THE ANTIGEN-BINDING SITE IS LOCATED.
THE ANTIGEN BINDING SITE HAS A COMPLIMENTARY SHAPE TO THE ANTIGEN WHICH MAKES IT SPECIFIC TO THAT PARTICULAR ANTIGEN.
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CONSTANT REGION.
ANTIBODIES ALSO HAVE THE CONSTANT REGION WHICH IS THE SAME FOR ALL ANTIBODIES.
THE CONSTANT REGION CONTAINS ANOTHER BINDING SITE WHICH ALLOWS THE ANTIBODY TO BIND TO IMMUNE SYSTEM CELLS, SUCH AS B CELLS OR PHAGOCYTES.
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HINGE REGION.
IN BETWEEN THE VARIABLE REGION AND THE CONSTANT REGION IS THE HINGE REGION WHICH PROVIDES THE ANTIBODY WITH FLEXIBILITY.
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HOW DO ANTIBODIES WORK?
ANTIBODIES WORK TO DESTROY PATHOGENS IN THREE,3, DIFFERENT WAYS.
AGGLUTINATION,
NEUTRALISING TOXINS,
AND BLOCKING ACCESS TO HUMAN CELLS.
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AGGLUTINATION.
ANTIBODIES EACH CONTAIN TWO,2, ANTIGEN-BINDING SITES WHICH MEANS THAT THEY CAN BIND TO TWO,2, PATHOGENS AT THE SAME TIME.
THIS CAUSES PATHOGENS TO BECOME CLUMPED TOGETHER.
PHAGOCYTES CAN THEN ENGULF AND DIGEST LOST OF PATHOGENS AT THE SAME TIME, WHICH MAKE PHAGOCYTOSIS MORE EFFICENT.
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NEUTRALISING TOXINS.
CERTAIN PATHOGENS, SUCH AS BACTERIA, MAKE US FEL ILL BY RELEASING TOXINS.
ANTIBODIES CAN BIND TO TOXINS WHICH RENDERS THEM HARMLESS, IT NEUTRALISES THEM.
THE ANTIBODY-TOXIN COMPLES CAN THEN BE DESTROYED BY PHAGOCYTES.
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BLOCKING ACCESS TO HUMAN CELLS.
PATHOGENS ENTER HOST CELLS WHEN THEIR ANTIGENS BIND TO RECEPTOR MOLECULES ON HOST CELLS, LIKE A KEY OPENING A LOCK.
WHEN ANTIBODIES BIND TO ANTIGENS, IT PREVENTS THE ANTIGEN FROM FITTING IN THE RECEPTOR WHICH MEANS IT CAN NOT GET INSIDE THE CELL.
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MEMBRANE BOUND OR SECRETED ANTIBODIES.
ANTIBODIES CAN EITHER BE MEMBRANE-BOUND, FOEEXAMPLE FOUND ON THE SURFACE OF B CELLS, OR SECRETED BY PLASMA CELLS AND FLOAT FREELY IN THE BLOODSTREAM.
66
THE HEAVY CHAINS, MEMBRANE-BOUND ANTIBODIES.
THE HEAVY CHAINS OF MEMBRANE-BOUND ANTIBODIES CONTAIN AN EXTRA REGION WHICH ENABLES ATTACHMENT TO THE CELL MEMBRANE.
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THE PRIMARY IMMUNE RESPONSE.
THE PRIMARY IMMUNE RESPIONSE OCCURS WHEN YOU ARE INFECTED WITH A PATHOGEN FOR THE FIRST TIME.
IT IS COMPOSED OF THE NON-SPECIFIC AND THE SPECIFIC IMMUNE RESPONSE.
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THE PRIMARY IMMUNE RESPONSE, SPEED.
THIS PROCESS IS SLOW BECAUSE IT TAKES TIME FOR THE CORRECT B CELL TO BE ACTIVATED, CLONAL SECTION, AND DIVIDE INTO LOTS OF PLASMA CELLS, CLONAL EXPANSION, IN ORDER TO PRODUCE ANTIBODIES WITH A COMPLIMENTARY SHAPE TO THE ANTIGEN.
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PRIMARY IMMUNE RESPONSE, SYMPTOMS.
THE INFECTED PERSON WILL EXPERIENCE SYMPTOMS WHILE THE T AND B CEELLS MOUNT AN IMMUNE RESPONSE.
AS PART OF THE PRIMARY RESPONSE, BOTH T AND B CELLS PRODUCE MEMORY CELLS.
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THE SECONDARY IMMUNE RESPONSE.
IF YOU ARE RE-INFECTED WITH THE SAME PATHOGEN IN THE FUTURE, THE T AND B MEMORY CELLS WILL RECOGNISE THE ANTIGEN AND START DIVIDING.
T MEMORY CELLS WILL DIVIDE INTO THE CORRECT TYPE OF T KILLER CELL TO KILL ANY CELLS THAT ARE INFECTED WITH THE PATHOGEN.
B MEMORY CELLS WILL DIVIDE INTO PLASMA CELLS TO PRODUCE A LARGE NUMBER OF ANTIBODIES WHICH IS COMPLIMENTARY TO THE ANTIGEN MOLECULES ON THE PATHOGEN.
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SECONDARY IMMUNE RESPONSE, SPEED.
THE SECONDARY IMMUNE RESPONSE IS MUCH QUICKER THAN THE PRIMARY IMMUNE RESPONSE.
IT HAPPENS SO QUICKLY THAT THE PATHOGEN IS SUPRESSED BEFORE YOU ARE ABLE TO EXPERIENCE SYMPTOMS, YOU ARE IMMUNE TO THE PATHOGEN.
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ACTIVE IMMUNITY.
ACTIVE IMMUNITY OCCURS WHEN YOUR BODY MAKES ITS OWN ANTIBODIES AFTER BEING STIMULATED BY AN ANTIGEN.
THIS PROCESS CAN BE NATURAL, FOR EXAMPLE IF YOU CATCH A COLD, YOUR BODY WILL MAKE ITS OWN ANTIBODIES AGAINST THE COMMON COILD OR VIRUS, OR IT CAN BE ARTIFICIAL, FOR EXAMPLE IF YOU ARE VACCINATED WITH A HARMLESS FORM OF AN ANTIGEN.
ACTIVE IMMUNITY LASTS LONGER THAN PASSIVE IMMUNITY SINCE MEMORY CELLS WILL REMAIN IN THE BODY FOR YEARS BUT IT TAKES TIME TO DEVELOP.
PASSIVE IMMUNITY PROVIDES IMMEDIATE PROTECTION AGAINST PATHOGENS BUT IS SHORT-LIVED.
ANTIBODIES THAT ARE TRANSFERRED FROM MOTHER TO CHILD DURING BREASTFEEDING ONLY REMAIN IN THE BODY FOR ABOUT EIGHTEEN,18, MONTHS.
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PASSIVE IMMUNITY.
PASSIVE IMMUNITY OCCURS WHEN YOU ARE GIVEN READY-MADE ANTIBODIES THAT HAVE BEEN PRODUCED BY ANOTHER ORGANISMN.
THIS PROCESS CAN BE NATURAL, FOR EXAMPLE WHEN BABIES RECIEVE FROM THEIR MOTHER WHEN THEY BREASTFEED, OR ARTIFICIAL, FOR EXAMPLE ANTBOFTY INJECTIONS CAN BE GIVEN FOR SOME DISEASES, THS IS BEING TESTED AS A TREATMENT FOR EBOLA.
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VACCINES, CONTAINS.
VACCINES CONTAIN A DEAD OR WEAKENED FORM OF A PATHOGEN WHICH IS INJECTED INTO THE BLOODSTREAM.
SOMETIMES VACCINES CONTAIN JUST THE ANTIGEN PROTIENS WITHOUT THE REST OF THE PATHOGEN.
OTHER VACCINES MIGHT CONTAIN A VARIETY OF DIFFERENT ANTIGENS TO PROTECT AGAINST DIFFERENT STRAINS OF PATHOGENS WHICH VARY IN SHAPE OF THE PROTIENS ON THEIR CELL SURFACE MEMBRANES, ANTIGENIC VARIATION.
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VACCINES, FUNCTION.
THE INJECTION OF WEAKENED ANTIGENS STIMULATES A PRIMARY IMMUNE RESPONSE AND THE PRODUCTION OF MEMORY T CELLS AND MEMORY B CELLS, RESULTING IN IMMUNITY WITHOUT BECOMING ILL FROM THE DISEASE.
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EVOLUTIONARY RACE.
OUR IMMUEN SYSTEM HAS EVOLVED TO INNCREASE OUR DEFENCE AGAINST PATHOGENS.
AS THIS HAS HAPPENED, PATHOGENS HAVE ALSO EVOLVED TO BECOME BETTER AT INFECTING US.
THIS IS KNOWN AS AN EVOLUTIONARY RACE.
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ANTIBIOTICS, ROLE.
ANTIBIOTICS ARE SUBSTANCES WHICH PREVENT THE GROWTH OF BACTERIA.
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HOW MANY DIFFERENT TYPES OF ANTIBIOTICS ARE THERE?
THERE ARE TWO,2, DIFFERENT TYPES OF ANTIBIOTICS, BACTERICIDAL AND BACTERIOSTATIC.
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BACTERICIDAL.
BACTERICIDAL ANTIBIOTICS KILL BACTERIA AND CELLS.
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BACTERIOSTATIC.
BACTERIOSTATIC ANTIBIOTIC WHICH INHIBIT THE GROWTH OF BACTERIA.
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ANTIBIOTICS, DAMAGING THE CELL WALL.
ANTIBIOTICS CAN PREVENT BONDS FORMING BETWEEN MUREIN, PEPTIDOGLYCAN, MOLECULES WHICH MAKE UP THE CELL WALL.
THIS WEAKENS THE CELL WALL AND PREVENTS BACTERIAL CELLS FROM GROWING PROPERLY.
IF WATER, H2O, ENTERS THE BACTERIAL CELL BY OSMOSIS, THE WEAKENED CELL WALL CANNOT WITHSTAND THE INCREASED HYDROSTATIC PRESSUE AND CAN BURST, LYSIS, KILLING THE BACTERIA.
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PREVENTING PROTIEN SYNTHESIS.
ANTIBIOTIC MOLECULES BIND TO BACTERIAL RIBOSOMES AND PREVENT THEM FROM CARRYING OUT TRANSLATION.
THIS PREVENTS THE SYNTHESIS OF ENZYMES, WHICH ARE PROTIENS, WHICH CATALYSE IMPORTANT METABOLIC REACTIONS.
IF THESE METABOLIC REACTIONS DO NOT TAKE PLACE, THE BACTERIAL CELL CANNOT GROW AND REPRODUCE PROPERLY.
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ANTIBIOTICS, EUKARYOTIC CELLS.
ANTIBIOTICS HAVE NO EFFECT ON EUKARYOTIC CELLS, SUCH AS HUMA CELLS, SINCE EUKARYOTIC CELLS DO NOT HAVE A CELL WALL AND THEIR RIBOSOMES ARE A DIFFERENT SIZE, WHICH MEANS THAT ANTIBIOTICS CANNOT BIND TO THEM.
SIMILARLY, ANTIBIOTICS HAVE NO EFFECT ON VIRUSES BECAUSE THEY DO NOT POSSE EITHER A CELL WALL OR RIBOSOMES.
THIS IS WHY IS WOULD BE POINTLESS PRESCRIBING ANTIBIOTICS FOR A VIRAL INFECTION, SUCH AS MEASELS OR THE FLU.
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HOSPITAL ACQUIRED INFECTIONS.
HOSPITAL ACQUIRED INFECTIONS, HAIs, ARE INFECTIONS WHICH ARE TRANSMITTED IN HOSPITAL.
THEY SPREAD AS A RESULT OF POOR HYGINE AND CAN SPREAD EASILY BECAUSE PATIENTS HAVE WEAKEND IMMUNE SYSTEMS.
THE SPREAD OF HOSPITAL ACUIRED INFECTIONS CAN BE PREVENETED BY GOOD HYGIENE PRACTICES, SUCH AS HAND WASHING AND STERILISING SURGICAL EQUIPMENT.
INFECTIONS CAUSED BY ANTIBIOTIC-RESISTANT BACTERIA SUCH AS MRSA ARE PARTICULARLY DANGEROUS FORMS OF HOSPITAL ACQUIRED INFECTIONS BECAUSE THEY CANNOT BE TREATED BE TREATED BY ANTIBIOTICS.
THE ROTATED USE OF DIFFERENT ANTIBIOTICS.
TAKING THE FULL COURSE OF ANTIBIOTICS.
AVOIDING OVERUSE OF ANTIBIOTICS, SUCH AS FOR MINOR INFECTIONS OR VIRAL DISEASES.
TO PREVENT ANTIBIOTIC RESISTANCE.
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BACTERIA AND FUNGI.
MICRORGANISMS SUCH AS BACTERIA AND FUNGI ARE ABLE TO FEED OFF AND DECOMPOSE DEAD ORGANIC MATTER, THEY DO THIS BY SECRETING DIGESTIVE ENZYMES ONTO THE ORGANISMS.
THEY DIGEST THE TISSUE OF THE DEAD ORGANISMS INTO SMALLER MOLECULES, SUCH AS GLUCOSE WHICH IS CONVERTED INTO CARBON DIOXIDE, CO2, THROUGH RESPIRATION.
METHANE IS ALSO RELEASED FROM MICROBRIAL DECOMPOSITION.
THEY PLAY A VERY IMPORTANT ROLE IN THE CARBON CYCLE BY UNLOCKING THE CARBON WITHIN GLUCOSE AND OTHER BIOLOGICAL MOLECULES AND RELEASING IT INTO THE ATMOSPHERE AS CARBON DIOXIDE, CO2, GAS.
THE CARBON CAN THEN BE ABSORBED BY PLANTS, CONVERTED INTO GLUCOSE BY PHOTOSYNTHESIS AND USED TO BUILD BIOLOGICAL MATERIAL IN LIVING ORGANISMS.
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EXTENT OF BODY DECOMPISITION.
As soon as a living organism dies, microorganisms will release digestive enzymes which will begin to break down the body tissues into smaller molecules. Depending on the extent of bodily decomposition, a rough TOD can be calculated. However, abiotic conditions such as oxygen availability and environmental temperature will affect how fast microbial decomposition occurs, so this also needs to be factored in. Here’s a rough outline of the stages of decomposition and how these relate to the time of death of a corpse:
From a few hours to a few days - the skin beings to turn green as cells and tissues begin to be broken down
From a few days to a few weeks - methane is given off and the body becomes bloated; skin starts to fall off
After several weeks - tissues liquefy and leak outside of the body
From a few months to a few years - the body tissues have been completely broken down and only a the bones remain
After several decades - the bones disintegrate and nothing remains of the body.
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FORENSIS ENTOMOLOGY.
Forensic entomology is the study of the insects feeding and living off a corpse. Depending on the species that is present (and the stage of the life cycle it is in), a time of death can be estimated.
From a few hours - flies are the first insects to appear on the body (blowflies then flesh flies). They will start to lay eggs which take about 24 hours to hatch. This means that if larvae are found on the body, we know that the TOD was less than 24 hours ago.
The next insect to colonise is beetles, which eat decomposed body fat.
A type of moth known as the pyralid moth will appear at a similar time to beetles. They will feed on liquefied parts of the corpse as well as any clothes the body may be wearing.
The next insect to appear is one called the cheese skipper which appears once the body’s proteins have been digested. They feed off digested food molecules and can also feed on any food present in the digestive system which has not been fully digested.
One of the last insects to appear is the burying beetle, which mostly eats dead flesh.
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STAGE OF SUCCESSION.
The type of organism which can be found on a body change over time - this is known as succession. It is similar to plant succession except that most of the early insects, such as flies and beetles, will remain on the body even as new insect species arrive. The stage of succession will be affected by things such as the location of a body - different stages of succession will be seen depending on whether the body is in open air or submerged in water. Succession of a body happens in the following stages:
Bacteria are the first type of organism present on the human body - immediately after death the conditions in a dead body are most favourable to bacteria
As bacteria decompose and digest body tissues, the conditions become more favourable for flies. The flies will lay eggs in the body which will hatch into larvae.
The fly larvae break down tissues of the corpse further, resulting in conditions which are suitable for beetles.
The body begins to dry out, which results in flies leaving the body as they prefer more moist environments. Beetles remain on the body since they can digest dry tissue.
When the body has been fully decomposed, there is no material for the insects to feed on so any remaining insects will leave.
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BODY TEMPERATURE.
Respiration inside of our cells generates heat as a by-product, maintaining our body temperature at 37oC. When somebody dies, chemical reactions such as respiration stop and their body temperature goes down. Body temperature decreases until there is no difference between the temperature of the body and its surroundings. This reduction in body temperature is known as algor mortis.
Since body temperature decreases at a rate of 1.5oC to 2.0oC each hour after death, the TOD can be calculated by recording the temperature of the corpse. For example, if the temperature of the body is 30oC, we know that it must have been dead for around 3.5 - 4.5 hours. Factors such as the weather, the amount of clothing and the amount of body fat on a person can influence the rate of cooling, so this needs to be taken into account when estimating TOD.
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DEGREE OF MUSCLE CONTRACTION.
Approximately 4-6 hours after death, the body will begin to stiffen in a process called rigor mortis. This happens because oxygen is no longer available since the person has stopped breathing. This means that the muscle cells can no longer respire aerobically so they carry out anaerobic respiration instead, resulting in an accumulation of lactic acid. Lactic acid causes a drop in pH which causes enzymes (such as ATP synthase) to denature. When ATP synthase loses the shape of its active site, it can no longer produce ATP for muscle contraction, resulting in muscle fibres becoming fixed in position and the body stiffens.
Rigor mortis begins with the smaller muscles in the head and ends with the largest muscles in the lower part of the body. By 12-18 hours after death, every muscle in the body will have stiffened. By determining which muscles have undergone rigor mortis, the forensic scientist can calculate an approximate TOD. Factors such as the degree of muscle development and temperature will affect the rate of rigor mortis.
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DNS PROFILING.
DNA profiling is a technique which can be used to analyse a sample of DNA (e.g. one found at a crime scene) and compare it to DNA samples taken from the suspects.
The DNA sample will be collected (this is usually blood, saliva or semen) and amplified using PCR.
The PCR products are separated using gel electrophoresis, which separates the DNA fragments according to length.
The gel is visualised using UV light and the banding patterns from the suspect’s DNA can be compared with that found at the crime scene.
The same technique can also be used to identify genetic relationships between people (as in paternity testing) or to determine evolutionary relationships between organisms.
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POLYMERASE CHAIN REACTION, PCR.
PCR is a technique used to amplify fragments of DNA. This is important because the DNA sample collected at a crime scene doesn’t contain enough material for accurate analysis. Before PCR is carried out, you need to prepare a mixture containing the following:
DNA sample
Free DNA nucleotides
Primers (these are short pieces of DNA which bind to the beginning of the DNA fragment and initiate replication)
The enzyme DNA polymerase which has been extracted from thermophilic (heat-loving) bacteria.
PCR is then carried out in the following stages:
Separation of the DNA strands - the mixture is heated to 95 Degrees C which causes hydrogen bonds between the DNA strands to break.
Annealing of the primer - the mixture is then cooled to around 60 Degrees C which allows the primer to anneal to the DNA.
Free DNA Nucleotides Align According To Base Pairing Rules.
DNA synthesis - The temperature is increased to 72 Degrees C which is the optimum temperature for DNA polymerase. DNA polymerase forms a new DNA strand from catalysing the formation of phosphodiester bonds between the free DNA nucleotides which align along the DNA template strand by complementary base pairing rules.
Around 30-40 cycles of PCR are carried out, which generates millions of DNA fragments. Each PCR cycle doubles the amount of DNA, so huge numbers of DNA fragments can be quickly generated.
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FLUORESCENT TAGS.
So that the DNA can be visualised, we add a fluorescent molecule which binds to the DNA and makes it visible when exposed to UV light.
A common fluorescent tag is ethidium bromide, which inserts itself between the DNA bases and gives off fluorescence under UV light.
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ELECTROPHORESIS.
Once the DNA fragments have been amplified and stained with a fluorescent dye, they need to be separated.
This is done using gel electrophoresis, which separates the DNA strands according to length.
It works because DNA is negatively charged, which means it will move towards a positive charge when placed in an electric field.
Shorter DNA fragments travel through the gel more quickly, which means they will travel a longer distance than the larger DNA fragments, so shorter DNA fragments are closer to the Anode.
Gel electrophoresis is carried out in the following steps:
An agarose gel is prepared which contains a row of wells at the top of the gel. The gel is placed into a tank containing buffer solution which is able to conduct electricity.
The DNA sample is mixed with a loading dye - this turns the DNA mixture a dark colour and helps you see what you’re doing. A fixed volume of the DNA samples are pipetted into the wells.
An electrical current is passed through the gel and the DNA will begin to move towards the bottom of the gel (towards the anode).
Once the dye has reached the bottom, the electricity is turned off and the banding pattern is visualised under UV light.
