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*
Distinguish between bacteriostatic
& bactericidal antibiotics
Describe how to investigate the
effect of different antibiotics on
bacteria
*
One of the best examples of natural selection &
Adaptation is the evolution of genetic resistance in
pathogens.
Pathogenic bacteria rapidly develops resistance to
antibiotics.
This results in an evolutionary race between the bacteria
& humans, in which the participants are engaged in a
continuous struggle against each other with no long term
*
*
An antibiotic is given for the treatment of an
infection or a disease caused by bacteria.
Antibiotics target microorganisms such as
bacteria, fungi & parasites. However, they are
not effective against viruses.
*
It was thought that the battle against disease
would be won with the use of antibiotics
But….
Bacteria that cause disease rapidly develop
resistance to antibiotics
As quickly as we evolve mechanisms to
combat pathogens, they evolve new methods
of overcoming our immune system.
*
Mutations cause resistance to antibiotics:
The bacteria may produce an enzyme that
enable the cell to break down the antibiotic
They may change the structure of it’s protein so
antibiotics no longer have an effect
It might code for a protein pump that removed
the antibiotic from the bacterial cell.
Genes for
antibiotic
resistance
may be
transferred to
other non-
resistant
bacteria by
conjugation,
transformatio
n or
transduction.
*
*
The presence of antibiotics produces a selection
pressure
Those bacteria which does not have the gene for the
resistance are selected against & are likely to be
destroyed
Those with the gene are selected for, they survive,
grow & reproduce.
The gene frequency for resistance increases within
the population
*
*
Transformation
The problem further continues as bacteria transfers
resistant genes between species. They spread by;
Bacteria take up fragments of DNA from a lysed
bacterial cell & incorporates to its own DNA.
*
Transduction
Bacteriophages (viruses which target bacteria) can pick up
bacterial genes by accident & transfer these genes to other
*
Conjugation
Genes for resistance are commonly kept on bacterial plasmids.
Bacteria can share plasmids through conjugation. It forms
cytoplasmic bridges (pili) between their cytoplasms. Once the
pili is formed, plasmids are replicated & one copy of the
plasmid passes from one bacteria to another via the pili.
*
*
Antibiotic
A used
Antibiotic
B used
Antibiotic
C used
Bacteria are now
resistant to
Antibiotic A, B & C
X Y Z
Bacterialpopulation
Time
X- Antibiotic A kills the non resistant
bacteria. The survivors are mutant
bacteria which are resistant to antibiotic
A. These resistant ones are now selected
by nature to survive &  in no., as they
cannot be killed by antibiotic A
Y- Antibiotic B kills the bacteria that are non
resistant to antibiotic B, but does not kill all the
bacteria. The survivors are mutant bacteria
which are resistant to Antibiotic A & B. the
resistant ones are selected by nature to survive
&  in no. as they cannot be killed by both
antibiotic A & B. The survivors are mutant
bacteria which now have genes for resistance
to antibiotic A & B.
Z- exposure to antibiotic C will now select & favor the
survival of mutant bacteria which have genes for
resistance to antibiotic A, B & C. These are called as
superbugs or multiple drug resistant bacteria. They
are commonly found in hospitals, where many
antibiotics are frequently used. Thus, natural
selection is responsible for the  in abundance of
resistant bacteria.
*
1. Bactericidal: antibiotics destroy bacteria. E.g.
Penicillin is a bactericidal.
2. Bacteriostatic: antibiotics prevent the multiplication of
the bacteria. The hosts own immune system then
destroy the bacteria
 Inhibition of bacterial cell wall synthesis
 Disruption of the cell membrane causing changes
in permeability
 Inhibition of nucleic acid synthesis & replication
 Inhibition of protein synthesis
 Inhibition of specific enzymes found in bacterial
cell wall

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Investigating Bacteriostatic & Bactericidal Antibiotics

  • 1. * Distinguish between bacteriostatic & bactericidal antibiotics Describe how to investigate the effect of different antibiotics on bacteria
  • 2. * One of the best examples of natural selection & Adaptation is the evolution of genetic resistance in pathogens. Pathogenic bacteria rapidly develops resistance to antibiotics. This results in an evolutionary race between the bacteria & humans, in which the participants are engaged in a continuous struggle against each other with no long term
  • 3. *
  • 4. * An antibiotic is given for the treatment of an infection or a disease caused by bacteria. Antibiotics target microorganisms such as bacteria, fungi & parasites. However, they are not effective against viruses.
  • 5. * It was thought that the battle against disease would be won with the use of antibiotics But…. Bacteria that cause disease rapidly develop resistance to antibiotics As quickly as we evolve mechanisms to combat pathogens, they evolve new methods of overcoming our immune system.
  • 6. * Mutations cause resistance to antibiotics: The bacteria may produce an enzyme that enable the cell to break down the antibiotic They may change the structure of it’s protein so antibiotics no longer have an effect It might code for a protein pump that removed the antibiotic from the bacterial cell. Genes for antibiotic resistance may be transferred to other non- resistant bacteria by conjugation, transformatio n or transduction.
  • 7. *
  • 8. * The presence of antibiotics produces a selection pressure Those bacteria which does not have the gene for the resistance are selected against & are likely to be destroyed Those with the gene are selected for, they survive, grow & reproduce. The gene frequency for resistance increases within the population
  • 9. *
  • 10. * Transformation The problem further continues as bacteria transfers resistant genes between species. They spread by; Bacteria take up fragments of DNA from a lysed bacterial cell & incorporates to its own DNA.
  • 11. * Transduction Bacteriophages (viruses which target bacteria) can pick up bacterial genes by accident & transfer these genes to other
  • 12. * Conjugation Genes for resistance are commonly kept on bacterial plasmids. Bacteria can share plasmids through conjugation. It forms cytoplasmic bridges (pili) between their cytoplasms. Once the pili is formed, plasmids are replicated & one copy of the plasmid passes from one bacteria to another via the pili.
  • 13. *
  • 14. * Antibiotic A used Antibiotic B used Antibiotic C used Bacteria are now resistant to Antibiotic A, B & C X Y Z Bacterialpopulation Time X- Antibiotic A kills the non resistant bacteria. The survivors are mutant bacteria which are resistant to antibiotic A. These resistant ones are now selected by nature to survive &  in no., as they cannot be killed by antibiotic A Y- Antibiotic B kills the bacteria that are non resistant to antibiotic B, but does not kill all the bacteria. The survivors are mutant bacteria which are resistant to Antibiotic A & B. the resistant ones are selected by nature to survive &  in no. as they cannot be killed by both antibiotic A & B. The survivors are mutant bacteria which now have genes for resistance to antibiotic A & B. Z- exposure to antibiotic C will now select & favor the survival of mutant bacteria which have genes for resistance to antibiotic A, B & C. These are called as superbugs or multiple drug resistant bacteria. They are commonly found in hospitals, where many antibiotics are frequently used. Thus, natural selection is responsible for the  in abundance of resistant bacteria.
  • 15. * 1. Bactericidal: antibiotics destroy bacteria. E.g. Penicillin is a bactericidal. 2. Bacteriostatic: antibiotics prevent the multiplication of the bacteria. The hosts own immune system then destroy the bacteria
  • 16.  Inhibition of bacterial cell wall synthesis  Disruption of the cell membrane causing changes in permeability  Inhibition of nucleic acid synthesis & replication  Inhibition of protein synthesis  Inhibition of specific enzymes found in bacterial cell wall

Editor's Notes

  1. More than 3000 years ago, the Egyptians, Chinese & central Americans Indians used mold to treat rashes & infected wounds. They did not understand what caused the diseases or how the mold help to treat them, in same cases they believed that mold drove evil sprits that caused the disease. In 1928, Alexandra Fleming was working in a hospital in London, he was studying bacterium staphylococcus aureus. One day he spot a green growing on his agar plates. He noticed that there was a clear area ……
  2. Why do some microorganisms make antibiotics? Antibiotics help microorganisms to compete in the envt. …….but produce large quantities as they r ageing,,,,shud be produced when they r young, if for that reason….
  3. Bacteria mutate frequently. Every now & again one of the mutation is beneficial. The problem Is that these resistant bacteria are selected for through the use of antibiotics. This comp kills everything apart from the resistant bacterium, so its free to preproduce without any competition.
  4. Unfortunately this is half of the problem
  5. The economic implication of drug resistance is immense. In 1992, the treatment of non-resistant Tb cost $12,000 & the treatment of multiple-drug resistant TB cost $180,000. it is estimated that till date more than 5 million tons of antibiotics have been used on humans & domestic animals, thus exerting massive selection on the world's bacteria, resulting in resistance. The pharmaceutical companies makes immense profit, but humans are at risk.
  6. Bactericidal drugs are those that kill target organisms.  Bacteriostatic drugs inhibit or delay bacterial growth and replication.
  7. There are 5 common prokaryotic cellular processes which antibiotic target; Inhibition of CW synthesis: binds to proteins in the CW, prevent development of the peptidoglycan layer of CW – bacteria cant grow properly eventually causing lysis . Disruption of CM: binds to the cell membrane & alter its structure, making it more permeable– leads to lysis & cell death --- can affect the host cell to some extent & are only used as last resort against heavily resistant bacteria. DNA replication inhibitors: stop DNA coiling during binary fission,,, meaning bacteria cannot replicate DNA & cannot reproduce. Inhibition of protein synthesis: binds to 70s ribosomes & inhibit protein synthesis.