Bio CH 5-11
Bio CH 5-11
Bio CH 5-11
• M phase (mitosis) ③
① prophase
② metaphase ④
③ anaphase
④ telophase
• Cytokinesis
In DNA: In RNA:
Deoxyribose sugar Ribose sugar
• Adenine • Adenine Purines & Pyramidines
• cytosine • cytosine
• guanine • guanine The nitrogenous base molecules that are
• thymine • uracil found in the nucleotides of DNA (A, T, C, G)
and RNA (A, U, C, G) occur in two structural
Double-stranded Single-stranded forms: purines and pyrimidines.
(Double helix)
The bases adenine and guanine are
* A phosphodiester bond lies between purines – they have a double ring
the carbon number 3 of the sugar in structure.
one nucleotide and carbon number 5 The bases cytosine, thymine and uracil
the of next sugar of the next are pyrimidines – they have a single ring
nucleotide. structure.
The structure of DNA
. made of two polynucleotide chains.
. chains coil around to form a double
helix.
. The chains run in opposite directions -
they are antiparallel.
. Each strand is made of a phosphate
sugar backbone and bases.
. Adenine (A) always pairs with thymine (T).
. Guanine (G) always pairs with cytosine (C).
(The complementary base pairs)
. A links with T by 2 hydrogen bonds; G
links with C by 3 hydrogen bonds.
. The distance between the two backbones
① DNA double helix unwinds, the hydrogen
is constant and three rings wide.
bond is broken, and the two strands are
. The phosphate group and deoxyribose
separate.
sugar are arranged alternatively.
② Activated deoxyribonucleotides will form
The structure of RNA hydrogen bonds with complementary base
• Made of single polynucleotide strand. pairs.
. Adenine (A) always pairs with uracil (U). -Every strand will act as a template and a
. Guanine (G) always pairs with cytosine (C). new strand forms accordingly.
. The phosphate group and ribose sugar ③ DNA polymerase will catalyse the
are arranged alternatively. formation of phosphordieter bonds
between adjacent deoxyribonucleotides.
DNA replication -A new complementary strand is formed.
Occurs in the nucleus during S phase of
interphase; requires ATP.
Enzymes needed
• Helicase: to break H bonds to separate 2
DNA strands.
• DNA polymerase: to synthesise a new
strand of DNA, to catalyst the formation
of phosphodiester bond (inserts
nucleotides).
• DNA ligase: to join DNA fragments
together, to catalyse the formation of
phosphodiester bonds.
* DNA polymerase only works in the 5' to The genetic code
3' direction, this means that DNA
• it is a three-leer code, each sequence of
polymerase is only able to add
three bases codes for one amino acid.
nucleotides starting from the 3' end of
•These triplets are known as codons.
the new strand.
• some of these triplets of bases code for
. The leading is strand replicated
start and stop signals.
continuously in the 3' to 5' direction.
• the code is universal; each triplet codes
. The second strand which is called the
for the same amino acid in all living things.
lagging strand is replicated
• There are four bases so there are 64
discontinuously in the 5' to 3' direction.
dierent triplets possible yet there are
→ this means it is replicated in short only 20 amino acids that commonly occur
sections forming Okazaki fragments. in biological proteins. This results in multiple
• the Okazaki fragments are joined codons coding for the same amino acids
together with DNA ligase. thus the code is said to be degenerate.
Protein Synthesis
Protein synthesis is the process in which
polypeptide chains are synthesised from
DNA in the ribosomes.
Transcription Translation
① DNA molecule unwinds( the hydrogen ① RNA binds to the ribosome
bonds between the complementary base ② tRNA carries a specific amino acid to
pairs break); when the 2 strands are the ribosome, tRNA binds to the large
separate, free activated ribonucleotides subunit of the ribosome, this tRNA has
bases will form hydrogen bonds with specific anti codon for a specific amino
complementary bases on the DNA acid. The anti codon of tRNA is
strand. (Only one strand acts as a complementary to the codon on mRNA;
template; it can be called a template they will form temporary hydrogen bonds
strand or a transcribed strand). with their complementary bases.
② RNA polymerase will catalyse the ③ A second tRNA molecule with a specific
formation of phosphodiester bonds amino acid binds to the next codon on
between the activated ribonucleotides; it mRNA, those 2 tRNA's will hold the amino
catalyses the formation of primary RNA acids in place side by side for peptide
from DNA. bond to form.
③ the RNA molecule leaves the DNA and ④ Peptidyl transferase in the ribosome
the DNA rewinds and form hydrogen catalyses the formation of peptide bonds.
bonds again. ⑤ the ribosome moves along mRNA one
→ the RNA formed is primary RNA and codon at a time, the direction of this
contains non-coding sequence that must movement is from 5' to 3’.
be removed before it leaves the nucleus.
④ In RNA splicing the non-coding
sequence called introns are going to be
removed and the coding sequence called
exons are going to be joined together to
form matured messenger RNA.
⑤ the mRNA leaves the nucleus through
nuclear pores to the ribosomes.
From triplets to codons to Missene:
anticodons to polypeptide • the base pair changes, and introduces
a new amino acid to the polypeptide
• Triplets are 3 bases on the DNA; each chain.
triplet codes for a specific amino acid.
• (T,A,C) is the start codon on the DNA. -
't b
G
• (A,T,C) (A,T,T) (A,C,T) are the 3 stop triplets (G,T,G) codes for (His) and
G T T
(G,T,T) codes for (Gln).
on the DNA. -
→ when the RNA reaches the stop codon,
it will transcribe it and leave.
• the start codon on the RNA is (A,U,G). Nonsense:
• The stop codons on the RNA can be: • the base pair changes, and it introduces
(U,A,G) (U,A,A) (U,G,A). an early stop codon in mRNA; this results in
pre mature ending, creating a short
DNA polypeptide chain.
Accgc
at
-
I
A C G
.
....
31 -
② The stem
• The vascular tissues are in bundles,
and The bundles are peripheral.
③ The leaf
• The vascular tissues are peripheral,
xylem is facing the upper epidermis.
Structure of xylem
• Xylem vessel transports water and • from cortex cell to endodermis:
minerals from roots to shoots. ~ The endodermis has suberised cells.
~ suberin is a chemical substance that
• Xylem tissue is made up of: is hydrophobic, it accumulates in
- xylem vessel endodermis cell walls.
- tracheids
- parenchyma
- sclerenchyma
Xylem vessel elements:
• Dead and hollow, reduces resistance
to the flow of water.
• No organelles, to provide maximum
space and minimum resistance.
• Thick cell walls + lignified, prevents
the inward collapse of xylem vessel.
• Pith, allow the lateral movement of
water.
• Large lumen, reduces resistance to
the flow of water.
• Lack of end walls, reduces
resistance to the flow of water.
Movement of water
• from soil to root hair cell: ~ partial suberisation:
~ soil has a higher water potential 1- band of Suberin forms
than the cytoplasm. 2- only apoplast pathway blocked
~ the water moves down the water 3- only symplast pathway available
potential gradient, from soil to root
hair cell by osmosis. ~ complete suberisation:
1- cell wall will be completely filled with
• from root hair cell to context cell: Suberin blocking both symplast and
~ root hair cell has higher water apoplast pathway.
potential than the cortex cell.
~ water moves down the water
potential gradient, it can move by • This arrangement is thought to:
apoplast or symplast pathway. ~ give plants control over what mineral
ions can pass into xylem vessels.
~ may help with root pressure.
• from endodermis to xylem: • when water reaches xylem vessel it will
~ by diusion. leave through diusion.
• when water is moving from xylem to
• what helps water move up the xylem mesophyll it can use apoplast and
vessel: symplast pathway.
1- cohesion and adhesion properties of *NOTE: xylem vessel elements are
water. elongated cells that are joined end to
2- root pressure (passage cells). end to form a continuous xylem vessel.
3- transpiration pull.
Structure of phloem
• phloem tissue transports water and Movement in phloem
assimilates (sucrose & amino acids)
Translocation: the transport of assimilates
dissolved in water from sources to sinks.
from source to sink and requires ATP.
• phloem tissue is made up of: * sucrose moves in both apoplast &
- phloem sieve tube element symplast by diusion until it reaches
- companion cells companion cells.
The sucrose loading mechanism
By apoplast: ~ since the sieve tubes have
• companion cells pump hydrogen ions membranes this results the increase
out of the cytoplasm via a proton pump in hydrostatic pressure in sieve tube.
and into their cell wall. (Active process)
→ this leads to higher proton Near the sink:
concentration in cell wall than the • The sink cells are using up/storing the
cytoplasm. sucrose, this leads to lower
• this creates a proton concentration concentration in the sink compared to
gradient that is used by co-transporters sieve tube.
to move protons & sucrose. → this leads to sucrose moving from
companion cell to sink cell by apoplast
~ protons: will move back into the
& symplast pathways (diusion)
companion cell cytoplasm down The
• when sucrose leaves the sieve tube it
concentration gradient by facilitated
lowers the concentration of sucrose
diusion through the sucrose co-
transporter. → thus leading to higher water
~ sucrose: is transported through the potential in the sieve tube.
sucrose co-transporter from the cell → as a result water moves out of the
wall to cytoplasm by secondary active sieve tube by osmosis, the hydrostatic
transport. (against concentration pressure decreases in sieve tube.
gradient)
sucrose is loaded into phloem sieve
tube by diusion from cytoplasm of
companion cell through
plasmodesmata.
Mass flow
Near the source:
• The sucrose is actively loaded from
companion cell to phloem sieve tube
→ this increases the concentration
of sucrose in the sieve tube so
decreases the water potential in the
sieve tube.
→ as a result of the decreased
water potential, water will move *NOTE: The phloem sap will move from
from the near xylem vessel into the the area of high hydrostatic pressure to
sieve tube by osmosis. area of lower hydrostatic pressure.
The mammalian circulatory system 3 layers in arteries and veins
In one complete circuit of the body ① Tunica intima ( endothelium):
blood passes through the heart twice. • elastic fibres
. one cell thick layer of squamous
It consists of:
epithelial cells
• The heart
• The blood vessels ② Tunica media:
• The blood • collagen
• smooth muscle
• elastic fibres
③ Tunica externa:
• collagen
• elastic fibre
Blood vessels
Arteries: closer to the heart.
Structure:
• oval shape
• the tunica media is thick → withstand
the high pressure of blood.
• narrow lumen → ensures blood
remains at high pressure, which also
providing resistance to blood flow to
Pulmonary circulation: allow gas exchange as blood passes.
Movement of blood from heart to lung • collagen: helps the artery withstand
and back to heart. pressure.
Systematic circulation: • elastic fibre: allow vessel to stretch
Movement of blood from heart to the and recoil to with stand pressure and
rest of body and back to heart. help smoothing out pulsatile flow.
• smooth muscle: contract and relax to
Artery: transport blood away from maintain blood flow and control the
the heart at high pressures; arterioles amount of blood reaching the tissues.
are smaller arteries. Contract: lumen of artery gets smaller
Capillary: smallest & thinnest blood (vasoconstriction) → reduces blood
vessel to allow exchange of substances. flow.
Relax: lumen of artery gets wider
Vein: returns low pressure blood back
to the heart; venule’s are smaller (vasodilation) → increase blood flow.
veins.
Muscular arteries:
- the further away from the heart
the more muscular the arteries will
become.
Function: - maintain blood flow by
vasoconstriction & vasodilation.
Elastic arteries:
- the closer to the heart the
more elastic the arteries will
become. Veins: capillaries join together to form
Function: venules which join to form veins.
- withstand pressure and Structure:
smooth out the pulsatile flow.
• large lumen - reduces friction which
otherwise would slow down blood
movement.
• thinner walls - blood flowing through
veins is under very low pressure.
• no distinct shape
• contains valves - prevents backflow of
blood; allow blood moving toward the
heart and closes pathway when blood
travels in opposite direction.
• skeletal muscles - when these muscles
Capillaries: branched arterioles into contract, they squeeze inwards on the
smaller blood vessels (5-10 µm). veins temporarily raising the pressure
• made of squamous epithelial cells. within them.
Features:
• one cell thick → short diusion
distance.
• small gaps between the cells in the
walls of capillary → more diusion.
• have large surface area → more
diusion. ( decreases the blood
pressure)
• small lumen diameter → slow down
blood → more diusion.
Tissue fluid Lymph vessels
• A fluid that bathes the cells in the • Lymph vessels go in parallel with
tissues, it's the real medium for veins, they end in the vein very close
exchange of waste & nutrients. to the heart.
→ formed from the plasma that • Large molecules that are not able to
leaks from the gaps of capillary. pass through the capillary wall enter
the lymphatic system as lymph.
• The movement of lymph within is
gonna be by the contraction of
muscles, any backflow is prevented
by values.
• Around the intestine there are a lot
of lymph vessels to transport lipids.
• Lymph nodes: are check points that
has lymphocytes in them (their
receptors detect antigen).
• If a tumor forms and pushes
At the arterial end of capillary: against lymph vessel it will block it
• there is a high concentration of causing oedema.
solute in the capillary, as a result we
have a solute concentration gradient - 90% of tissue fluid will return through
this causes the water to move into veins, the other 10% will return as
the capillary (down the water lymph through lymph vessel.
potential gradient).
• the hydrostatic pressure within the Blood
capillary is high relatively, as a result
we have a hydrostatic pressure
gradient this causes the water to
move out of the capillary.
• AS a result of both forces the net
movement of water is gonna be out
of the capillary.
At the venous end of capillary:
• the hydrostatic pressure within
the capillary is low, but the solute
concentration is high.
• As a result, the net movement of
water is gonna be into the
capillary.
Cells of the blood Lymphocytes: a type of phagocyte.
Neutrophil: a type of phagocyte. → B-lymphocytes: produce antibodies,
Function: phagocytosis they mature in bone narrow.
- it accumulates in the site of infection → T-lymphocytes: (killer or helper)
to fight the infection by phagocytosis. doesn't produce antibodies, they
→ phagocytosis have receptors on mature in thymus gland ( that is near
their plasma membrane that helps the heart).
identify cell and non-cell antigen. Structure: big round nucleus that
Structure: multi-lobed nucleus and has occupies most of the cell and doesn't
granular cytoplasm (contains have granules.
lysozomes).
4O2 + Hb Hb4O2
The molecular level shows the
cooperative binding:
• The binding of the first oxygen
molecule changes the (3D) shape of
haemoglobin, making it easier for each
successive oxygen molecule to bind.
The physiological level: (Describe &
explain the graph) shows the binding
and dissociation of haemoglobin:
• At the respiring tissue we have low
partial pressure of oxygen and the
ainity of haemoglobin towards * The higher the partial pressure of
oxygen is at its lowest, the oxygen the faster the reaction.
haemoglobin dissociates from oxygen
that is binded to. Q/ Why is the line not linear?
• At the lung we have high partial • Because haemoglobin has ainity
pressure of oxygen and the ainity towards the oxygen, this ainity
of haemoglobin towards oxygen is at increases as the partial pressure
its highest so oxygen binds to increases.
hemoglobin easily. • When the first oxygen binds to
• At medium partial pressure of haemoglobin it changes the shape
oxygen, oxygen binds more easily to making it easier for second, third and
haemoglobin and saturation fourth oxygen to bind to it.
increases quickly; at this point on the
graph a small increase in partial
pressure of oxygen causes a large
increase in haemoglobin saturation.
Carbon dioxide: only aects the • At each partial pressure of oxygen,
ainity of haemoglobin towards the hemoglobin is less saturated than
oxygen (it doesn't bind to haemoglobin. it would be at a low partial pressure
• The eect of partial pressure of of carbon dioxide.
carbon dioxide on the ainity of
haemoglobin towards oxygen is called
the Bohr eect or Bohr shi.
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Infectious diseases
• diseases caused by an organisms
known as pathogens.
• called communicable diseases as
they are passed from infected to
uninfected people (transmissible). Communicable diseases:
• caused by direct or indirect spread
of pathogens from a person or ting
to another.
Distribution of disease:
Transmission of cholera: • It is diicult to prevent and control
• caused by bacterium vibrio cholera cholera because of:
• comma-shaped, has flagella, motile. • the fast-growing cities in developing
• spread by the faecal-oral route it is countries not having the appropriate
a water-borne and food-borne infrastructure.
disease. • humanitarian cities (eg. Displacement
of people due to wars) which can
→ the disease occurs where people cause the destruction of sanitation
do not have access to proper infrastructure and for the provision
sanitation (clean water) and of poor sanitation facilities in
uncontaminated food. overcrowded temporary housing.
• infected people eggiest large • the use of raw human sewage to
numbers of the bacteria in their irritate crops.
faeces → if these faeces • prevention of cholera:
contaminate the water supply, then • sewage treatment.
the bacteria are transmied to • the provision of clean, piped water
uninfected people. that has been chlorinated to kill
Eects: bacteria.
• if bacteria is not killed by stomach • vaccination programs in areas
acid, bacteria reaches the small where cholera is endemic.
intestine.
• bacteria secretes choleragen toxin, • Cholera can be controlled by:
toxin binds to complementary • access to oral rehydration therapy.
receptor on intestinal epithelial cells • monitoring programmes by WHO.
and enters via endocytosis. • using antibiotics in severe cases.
• disrupts function of intestine
epithelial lining. Diagnosis: microscopical analysis of
• loss of chloride ions and sodium ions faeces.
from epithelial cells.
• water potential decreases, water
moves out from blood down water
potential gradient by osmosis through
partially permeable membrane.
Symptoms:
• vomiting
• low blood pressure
• diarrhea
• rapid weight loss
Transmission of malaria: Treating Malaria:
• caused by one of four species of • anti -malarial drugs (eg quinine,
the protoctist plasmodium. chloroquine).
• Chloroquine inhibits protein synthesis
• plasmodium is most motile during and prevents parasite from spreading
initial infective stages. within the body it is also used as a
prophylactic (preventative) drug,
• these protocists are transmied to stopping an infection occurring if a
humans by an insect vector: person is bien by an infected
mosquito.
• Female Anopheles mosquitoes feed • prophylactic drugs are taken before,
on human blood to obtain the protein during and aer visiting an area
they need to develop their eggs. where malaria is endemic.
• Combination therapy: where multiple
• if the person they bite is infected drugs are used at the same time →
with plasmodium, the mosquito will used to prevent drug-resistance.
take up some of the pathogen with
the blood meal. Prevention of Malaria:
• Use prophylactic/preventive drugs.
• when feeding on the next human, • reduce number of mosquitoes
plasmodium pass from the mosquito (spray insecticide, spread oil over
to the new humans blood. water surface to prevent mosquito
breeding).
• Malaria may also be transmied • avoid being bien by mosquitoes
during blood transfusion and when (sleep beneath mosquito nets and
unsterile needles are re-used. use insect repellent.
• plasmodium can also pass from
mother to child across the placenta.
Symptoms:
• fever. • muscle pain
• anaemia • shivering
• Nausea • sweating
• Headaches. • Enlarged spleen
Diagnosis:
• Microscopical analysis of blood
• din stick test for malaria
antigen in blood.
HIV/AIDS • the virus show no symptoms and
• human immunodeficiency virus is a people do not know they are infected
retrovirus ( its genetic material is because the virus can change its
RNA). surface protein, making it diicult for
• the virus is not transmied by a the human immune system to recognize
vector and it is unable to survive it and for a vaccine to be developed.
outside of human body. Opportunistic infections: an infection
• the virus is spread by intimate caused by pathogens that take
human contact and can only be advantage of a host with weekend
transmied by direct exchange of immune system (Eg. Oral thrush,
body fluids. pneumonia, tuberculosis,malaria,…).
* AIDS is a collection of these
Transmission of HIV/AIDS: opportunistic diseases associated with
• sexual intercourse immunodeficiency caused by HIV
• blood donation infection.
• sharing of needles used by
intravenous drug users. • preventing the transmission of HIV:
• from mother to child across the • HIV-positive mothers and their babies
placenta. can be treated with drugs.
• mixing of blood between mother • Blood donations can be screened for
and child during birth. HIV and heat-treated to kill any viruses.
• from mother to child through • condoms, femidoms and dental dams
breast milk. can be used.
• intravenous drug users encouraged
Eects: hot to share needles.
• when the virus is activated, HIV Controlling HIV can occur by:
infects cells of the immune system, • contact tracing
called helper T-cells. • screening blood donations
• this destroys helper T cells causes • public health measures widespread
their number to decrease, as a result HIV testing of the population and
body is unable its to defend self education programs.
against infection. • using anti-retroviral drugs
• this allows a range of pathogens to
cause a variety of opportunistic • The socio-economic status of a person
infections. with HIV can determine how it is controlled.
For example, HIV-positive mothers are
Symptoms: advised not to breaseed in high-income
• flu-like symptoms then symptomless countries, however, in low- and middle-
(since virus can stay dormant for income countries breaseeding oers
years). protection against other diseases.
Tuberculosis Symptoms:
• caused by mycobacterium • racking cough • sweating
tuberculosis, mycobacterium bovis. • coughing blood • weight loss
• M. Tuberculosis causes TB in humans. • chest pain • loss of appetite
• M. Bovis causes TB in cows, humans • fever • shortness of breath
and other mammals.
Diagnosis:
Transmission of mycobacterium • X-ray
tuberculosis: • microscopical examination of sputum
• pathogen is in air borne droplets (mucus and pus) for bacteria.
• when infected people with the active
form of the disease cough or sneeze, Treatment of tuberculosis:
the M. Tuberculosis bacteria enters • long treatment time because
the air in tiny droplets of liquid. bacteria is slow growing and not very
• tuberculosis is transmied when responsive to drugs.
uninflected people then inhale these • combination therapy (use multiple
droplets. antibiotics).
• DOTS (direct observation treatment,
short course) makes sure patient take
Transmission of mycobacterium bovis: medicine regularly and reduce spread
• it occurs in cale, but is spread to of drug resistance.
humans through contaminated meat
an unpasteurised milk. Prevention of tuberculosis:
• use of BCG vaccine ( the only vaccine
for TB.
Eects:
• the vaccine protects up to 70-80%. Of
• site of primary infection= lungs.
those who receive it, although its
• secondary infections in lymph
eectiveness decreases with age
modes, bones and gut
unless the person is exposed to TB.
• slow infection- many infections are
• isolate patients which are in
controlled by immune system and
infectious stages.
people don't suer symptoms,
• contact tracing and TB screening for
cannot pass on the disease.
early detection to prevent spread.
• bacteria maybe activated aer
• Routinely testing cale for TB, and
many years when immune system
destroying those that test positive.
weakened by other infections.
• pasteurizing milk (kills any TB-
• the incubation period is few weeks
causing bacteria present in the milk).
to few years.
• Ensuring meat is cooked properly.
Antibiotics • penicillin is only eective against
• a substance derived from a living bacteria that are still growing.
organism that is capable of killing or • penicillin is not eective against all
inhibiting the growth of a bacteria because the bacteria may have:
microorganism without harming the 1- thick cell walls which reduce
infected organism. permeability.
2- enzymes which breakdown penicillin.
How do antibiotics work? • penicillin and other antibiotics do not
• inhibit bacterial cell wall synthesis aect viruses as they do not have cells
• inhibit activity of specific (or cell walls), When virus replicates, uses
membrane protein/ glycoprotein → the host cells mechanism for tranelation
blocking binding to cell. and translocation, so not even these
• block specific enzyme action. processes can be targeted as antibiotics
• inhibit protein synthesis and nucleic do not bind to the proteins that hot cells
acid synthesis. uses in these processes.
How penicillin aects bacteria? Antibiotic resistance
In the absence of penicillin:
• bacterial cell wall is made up of • when antibiotics are no longer
peptidoglycan. eective against bacteria, antibiotic
• these peptidoglycan molecules are resistance can be spread from
held together by cross-links that form bacteria to bacteria.
between them. Caused by:
• when bacteria cells grow, it secretes • random mutation in bacteria so
autolysins enzymes that create small when bacteria is treated with
holes in the bacterial cell wall, these antibiotic it won't die, the bacteria
allow the bacterial cell wall to stretch, can continue to reproduce with less
with new peptidoglycan molecules competition from non-resistance
then joining up via cross-links. bacteria.
In the presence of penicillin: • antibiotic resistance gene is passed
• pencilin stops these cross-links to the next generation and other
forming by inhibiting the enzymes bacteria.
that catalyse their formation. • This is evolution by natural selection.
• However, the autolysins keep creating • Some pathogenic bacteria have
holes in the bacterial cell walls, new become resistant to penicillin as they
peptidoglycan formed but cannot link have acquired genes that code for
up making the cell wall weaker. the production of the enzyme β-
• cell walls unable to with stand turgor lactamase (also known as
pressure, when water moves in by penicillinase), which breaks down
osmosis, bacteria bursts and dies. penicillin.
Bacteria can spread antibiotic Causes of antibiotic resistance:
resistance genes using: • due to patients not completing the
• vertical transmission → Bacteria course of antibiotics given.
reproduce a sexually by binary • treatment may not be completed
fission (the DNA of the bacterial so some susceptible bacteria
chromosome is replicated and the survives.
bacterial cell divides in two, with each • Bacteria replicates and have
daughter cell receiving a copy of the increased chance of mutation/
chromosome). becoming resistant.
• due to overuse of antibiotics in
• Horizontal transmission → the
situations where they were not
plasmids are frequently transferred
necessary.
between bacteria, this occurs during
• incorrect use of antibiotics.
conjugation (when a thin tube forms
between two bacteria to allow the Consequences of antibiotic resistance:
exchange of DNA). • Bacteria can carry several antibiotic
• In this way, a bacterium containing resistance genes.
a mutant gene that gives it antibiotic • develop multiple resistance.
resistance could pass this gene on to • become a "super bug".
other bacteria (even those from a • cannot be killed/ inhibited by common
dierent species). This is how antibiotics.
‘superbugs’ with multiple resistance
have developed. Ways to prevent antibiotic resistance:
• avoiding the overuse of antibiotics.
• antibiotics not being used in non-
serious infections and viral infections.
• finishing the entire course.
• use antibiotic specific to the infection
instead of using wide-spectrum
antibiotics.
• changing the type of antibiotics
prescribed for certain diseases.
• more tightly control on industries.
Steps:
1) Inject mice with an antigen that
stimulates the production of
antibody-producing plasma cells.