Edexcel Categories Archives: Add Topic 6

4.6.18 How an ‘evolutionary race’ exists between pathogens and drug developers

The evolutionary arms race between bacteria and drug developers is, at the moment, tipped against humans. There are over 100 different types of antibiotic and in the 40years since their development 4 species of  bacterium have developed resistance against all  of    them.

E.g. Methicillin Resistant Staphyloccus Aureus (MRSA) has been named the Superbug, because we have do drugs left that can kill it.

Unless drug developers discover another branch of antibiotics we’re not currently using (i.e. another way of targeting prokaryotic structures without damaging eukaryotic ones) there may well be a global pandemic of resistant bacteria.

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4.6.17 Why antibiotic resistance in bacteria is an increasing problem

Bacteria are becoming resistant to antibiotics. Bacteria develop resistance  through mutation. A bacteria can mutate and develop resistance by;


  1. Having an enzyme that breaks the antibiotic down


  1. Having a protein which pumps antibiotic out of the cell


  1. Mutating the structure of the bacterium so that the antibiotic no longer works This problem is very serious. Bacteria become resistant because;
  2. Bacteria mutate very easily. One in every million bacteria contains a mutation. That might sound like a small amount, but consider that one E coli bacterium can reproduce to form a colony of 2 million bacteria in two hours. Over weeks, months and years that’s a lot of mutations, some of which will be beneficial


  1. Bacteria reproduce very quickly (they divide every 20min) so a bacterium with a beneficial mutation will spread quickly


  1. Bacteria have the ability to pass copies of plasmids from one to another (conjugation). So a mutation in one bacterium can quickly be copied to others, even others in different


  1. The use of antibiotics speeds the rise of immunity. If a bacterial population is continually exposed to antibiotic all bacteria will die. As soon as a bacterium mutates the rest of the bacteria will be killed off by the latest dose of antibiotic; now the field is open for the mutated bacterium to grow without


  1. Humans have been reckless with use of antibiotics. They are often given to people who don’t need them (i.e. they have viral infections) or to people who don’t bother to complete the course of
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4.6.16 How to investigate the effect of different antibiotics on bacteria

The effectiveness of antibiotics can be measured using a disc diffusion technique.


  1. A bacterial lawn is grown on an agar plate (either by spreading the bacteria over the plate, or by using a pour plate).


  1. A disc of blotting paper is soaked in antibiotic of known concentration and placed in the centre of the


  1. A clear circle of dead bacteria will form around the disc


  1. The diameter / radius of the circle of dead bacteria is proportional to the effectiveness of the antibiotic
  2. This can be compared to other antibiotics, as long as the same concentration of antibiotic is used. In addition, one can also compare the effectiveness of an antibiotic with a disinfectant or sanitiser (e.g. Phenol coefficient)
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4.6.15 Bacteriostatic and bacteriocidal antibiotics

Antibiotics work by targeting prokaryotic features not found in eukaryotic cells, e.g. penicillin targets the cell wall and breaks it down. Penicillin can be taken in large doses by humans because it has no effect on our cells (we have no cell walls).


Bacteriostatic antibiotics stop bacteria reproducing, they do not kill bacteria


Bacteriocidal antibiotics kill bacteria

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4.6.14 How ‘the evolutionary race’ between pathogens and their hosts has resulted in sophisticated invasion mechanisms

We have evolved a very effective immune system, consisting of barriers, non-speficif  defence mechanisms and specific ones. If we’re so good at fighting infections, why do we  still get ill?


Answer: pathogens are evolving as well. So how has TB evolved to beat us?

  1. It is spread by droplet infection, which is the most effective method of infection


  1. It specifically targets epithelial cells, which means that, when inhaled, it is exactly where it wants to be


  1. It does not kill immediately. This means that it has a large window of opportunity to spread to others


  1. It has a very thick waxy cell wall, which means it is partially protected against lysozyme


  1. It can survive inside macrophages and lie dormant until the immune system is weakened, when it can re-infect.

So how has HIV evolved to beat us?


  1. It weakens the immune system to increase its chance of survival


  1. It stays in the body for years, so it can spread


  1. It specifically targets Helper T cells


  1. It is spread by sexual contact, so it is easily spread
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4.6.13 How individuals may develop immunity

Both T and B Cells differentiate into Memory Cells, which remain in our lymph nodes and wait until we are re-exposed to the same pathogen.


When the Memory B cell is activated by the old antigen it makes large quantities on  antibody quickly and kills the pathogen before it can infect us properly. The memory cells provide active immunity.


When we are exposed to a new antigen it takes us about a week to be able to make new antibody. However, a second exposure to antigen produces a much faster response, and several orders of magnitude higher levels of antibody are produced.


Plasma B cells make lots of antibody on re- exposure

Without immunity the level of antibody produced by plasma cells is much less

Passive Immunity is immunity to a pathogen without Memory cells. It can occur through antibody injection or from drinking breast milk (breast milk contains high [antibody])

Active Natural Immunity – the process above

Passive Natural Immunity – beastfeeding (antibody in milk)

Artificial Active Immunity – vaccination

Artificial Passive Immunity – antibody injection

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4.6.12 The major routes pathogens may take in entering the body and the role of barriers in protecting the body from infection

Barrier Mechanisms include;

Skin, Stomach Acid, Normal Flora, Epithelial cells.

Skin adaptions for defence

The skin is made from 2 layers

  • Outer epidermis layer
  • Inner dermis layer

The epidermis provides a physical barrier to invading pathogens. There are 2 layers in the epidermis;

  • Outer cornified layer, composed of compacted dead dry cells filled with indigestible keratin protein (which also forms nails and hair)


  • Inner Malpighian layer, site of rapid mitosis and


The skin also has chemical defence mechanisms;


  • sweat & sebaceous glands secrete sebum, which is an oil with pH 3 – 5. This makes the skin acidic


  • sebaceous glands also secrete the enzyme lysozyme, which is a natural antibiotic. Lysozyme destroys bacterial cell

Stomach Acid

Is made from HCl at pH 1 – 2. it is a very effective barrier.

Normal Flora

The skin, respiratory tract and gut are covered with commensual bacteria, which are part of the normal flora of the body. Commensual bacteria are adapted to live the environment of the skin and the gut and the and compete with invading pathogens for the limited supply of nutrients.

Epithelial call adaptions for defence

  1. Epithelial cells are closely packed & connected by tight junctions forming a continuous impermeable layer


  1. Epithelial cells have cilia, which form a direct physical barrier preventing pathogen attachment


  1. Cilia ‘beat’ in waves, which helps clear bacteria out of the lungs and into the throat, where they are swallowed. Ingested bacteria are quickly killed by the low stomach pH and digestive proteases. Cilia also beat in the GI


  1. Epithelial cells secrete mucus, which is trapped by cilia. Mucus also directly prevents pathogen attachment


  1. Mucus contains lysozyme


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4.6.11 How an infectious disease can interfere with the body’s negative feedback mechanisms for the thermoregulation

Homeostasis is the maintenance of the body’s internal environment. This is carefully controlled by a series of systems, which aim to keep conditions at a stable controlled level.

Body Tempereature

Body temperature is carefully regulated to maintain a steady 37.5˚C, which is the optimum temperature for human enzymes. Sensors (thermoreceptors) in the hypothalamus continually monitor blood temperature and activate warming / cooling processes to keep  the temperature as stable as possible.

Tuberculosis bacterium (Mycobacterium tuberculosis) causes fever.

How does fever work?

All white blood cells communicate with each other and the rest of the immune system using a class of hormones called cytokines. The cytokines have hundreds of different roles and many more are yet to be discovered. One class of cytokine is the hormone interleukin,  which causes fever.


Fever can be induced by many factors. The general class of hormones that lead to fever are called pyrogens (interleukin is a natural pyrogen). However, bacterial toxins, viral proteins and substances produced by necrotic tissue may also trigger fever.


Pyrogens travel in the blood to the hypothalamus in the brain. They bind to receptors there and trigger a complex set of reactions that lead to the production of PGE2 hormone, which


elevates the thermoregulatory set point, i.e. it re-sets the body’s natural thermostat to a higher temperature.


The hypothalamus now thinks body temperature is too low and triggers a system of responses which aim to generate heat (thermogenesis) and raise body temperature. These mechanisms include; shivering, increased muscle tone, vasoconstriction and the production of thyroxine hormone (which makes respiration less efficient, therefore producing more heat).


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4.6.9 The roles of B cells and T cells in the body’s immune responce

There are two different types of Immune Response; A Cell-mediated Immune Response

B             Antibody-mediated Immune Response.




Cell-Mediated Immune Responce

  1. Competent T Cells recognise a specific foreign antigen using its T cell receptor.


  1. Activated T Cell undergoes rapid mitosis forming a large number of identical clone T


  1. Cloned T Cells differentiate into Killer, Helper, Memory or Suppressor T


  1. Killer and Helper Cells migrate to the site of infection


Killer T Cells: attach to the infected / foreign cell and release the enzyme Perforin, which makes holes in the pathogen’s cell membrane causing it to die


Helper T Cells: stimulate B cells to start producing antibody and attract macrophages to the site of infection

Memory T Cells: remain in the lymph nodes. They will respond rapidly if the same pathogen invades the body again, because they have the right T cell receptor to recognise the pathogen. This means that the body can mount an immune response before infection becomes serious


Suppresor T Cells: stop the immune reaction after about a week


AntiBody-Mediated Immune Responce:

  1. B cells are recognise a specific foreign antigen using the antibody molecules on their surface. B cells can also be activated by macrophages & Helper T cells. When a macrophage digests a pathogenic cell antigens from the cell membrane get stuck in the macrophage’s membrane; any B Cells which come into contact with the antigen will then be activated


  1. The activated B cell undergoes rapid mitosis and lots of clone B cells are produced


  1. Cloned B Cells differentiate into either Plasma or Memory cells

Plasma Cells

  1. Plasma cells antibody, which is specific for one antigen only
  2. Antibody is transported via the lymph to the site of infection
  3. Antibody attaches to the specific antigen
  4. An antigen-antibody complex is formed

Memory Cells

Memory Cells continue to secrete antibody for many years, so that if the body is infected by the same pathogen the Memory B cells can produce an instant supply of antibody before the infection becomes serious.


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