Questions on pathogens and non-specific defences

Question 1

Describe the stages of phagocytosis, in order, from the phagocyte approaching a bacterium to the display of its antigens.

Accepted Answer

B1 the phagocyte moves towards the bacterium along a concentration gradient of chemicals released by the pathogen or by damaged tissue, which is chemotaxis B1 receptors on the phagocyte's cell-surface membrane attach to antigens on the bacterium's surface B1 the membrane folds around the bacterium and the edges fuse, enclosing it in a vesicle called a phagosome B1 lysosomes move to the phagosome and fuse with it, emptying hydrolytic enzymes inside, and those enzymes hydrolyse the bacterium B1 the phagocyte moves some of the bacterium's antigens to its own cell-surface membrane and displays them, becoming an antigen-presenting cell

Question 2

Describe the transmission, mode of infection and pathogenic effect of the stem rust fungus, Puccinia graminis, on wheat.

Accepted Answer

B1 spores are released from pustules on infected plants and carried by the wind, over long distances, to other wheat plants B1 a spore germinates on the stem or leaf in a film of water, and the germ tube grows to a stoma and enters through it B1 hyphae grow between the host cells and haustoria push into living cells and absorb sugars and other nutrients B1 less sugar reaches the grain, so the grains are small and shrivelled and yield falls, and the infected tissue photosynthesises less B1 pustules rupture the epidermis so more water is lost, and weakened stems break or fall over

Question 3

Compare physical barriers with chemical barriers as defences against infection, using a named example of each.

Accepted Answer

B1 both act against any pathogen without recognising which one it is, and both act at the same speed on every exposure B1 a physical barrier blocks or removes pathogens, whereas a chemical barrier destroys them B1 a named physical barrier with how it works, for example skin, which is dry, dead and keratinised, or mucus which traps particles while cilia sweep it to the throat B1 a named chemical barrier with how it works, for example stomach acid near pH 2, which denatures the enzymes and other proteins of swallowed bacteria, or lysozyme, which hydrolyses bacterial cell walls

Question 4

A drug prevents lysosomes from fusing with phagosomes inside a phagocyte. Suggest how this would affect a patient's response to a bacterial infection.

Accepted Answer

B1 bacteria are still engulfed, because chemotaxis, attachment and the forming of the phagosome are unaffected B1 hydrolytic enzymes are not emptied into the phagosome, so the bacteria are not hydrolysed and may survive inside the phagocyte B1 fewer antigens become available to be moved to the phagocyte's cell-surface membrane, so antigen presentation is reduced B1 the specific response is therefore slow to begin, since clonal selection cannot start until antigen is presented, and the infection is likely to be more severe and to last longer

Question 5

Explain how cholera toxin causes the severe diarrhoea seen in cholera.

Accepted Answer

B1 cholera toxin binds to cells lining the small intestine and raises the level of the messenger molecule cyclic AMP inside them B1 this holds open a chloride channel, so chloride ions flow out of the cells through it into the lumen of the gut B1 this lowers the water potential of the gut lumen below that of the epithelial cells and the tissue fluid behind them A1 water then moves out of the cells and into the lumen down a water potential gradient by osmosis, producing large volumes of watery diarrhoea

Question 6

A virus enters a host cell, replicates and is released. Explain how the virus uses the host cell to produce new virus particles, and explain how the release of those particles usually affects the host cell.

Accepted Answer

B1 the virus's nucleic acid is transcribed and translated using the host cell's own ribosomes, enzymes and nucleotides, since a virus has no metabolism of its own B1 hundreds of new virus particles are assembled inside the host cell using these host resources B1 many viruses are released by bursting the cell open, which is lysis and destroys the host cell A1 other viruses, HIV among them, bud out through the cell surface membrane instead, so the infected cell declines more gradually rather than bursting at once

Question 7

A cell lining the airway is infected by influenza virus and secretes interferon. Explain how this reduces the spread of the virus to other cells in the tissue.

Accepted Answer

B1 interferon is a protein that diffuses from the infected cell and binds to receptors on the cell-surface membranes of neighbouring cells B1 binding switches on genes in those cells, putting them into an antiviral state B1 the proteins made inhibit protein synthesis at the ribosomes, or activate an enzyme that hydrolyses viral RNA B1 a virus entering one of those cells cannot be replicated, because it depends on the host cell's ribosomes and enzymes to make new virus particles

Question 8

Staphylococcus species produce exotoxins and Salmonella species produce endotoxins. Compare exotoxins with endotoxins.

Accepted Answer

B1 an exotoxin is a protein, whereas an endotoxin is a lipopolysaccharide that forms part of the outer membrane of the bacterial cell wall B1 an exotoxin is secreted by living bacteria, whereas an endotoxin is released mainly when the bacteria die and their walls break down B1 exotoxins are made by Gram-positive and Gram-negative bacteria, whereas endotoxins come only from Gram-negative bacteria such as Salmonella B1 an exotoxin acts on a specific target and is potent in small amounts, whereas an endotoxin causes general effects such as fever and inflammation through the host's response

Question 9

Explain why an antibiotic that cures tuberculosis has no effect whatever on influenza.

Accepted Answer

B1 tuberculosis is caused by a bacterium while influenza is caused by a virus B1 antibiotics work by disrupting structures or processes that bacteria have and human cells do not, such as the peptidoglycan cell wall or the 70S ribosomes B1 a virus has no cell wall, no ribosomes and no metabolism of its own, so there is nothing for the drug to disrupt

Question 10

Explain how inflammation at the site of an infection helps the body to clear the pathogen.

Accepted Answer

B1 mast cells in the damaged tissue release histamine B1 histamine dilates the arterioles and makes capillary walls more permeable, so more blood arrives and more tissue fluid leaks out into the tissue B1 that tissue fluid carries antibodies into the infected tissue, and cytokines attract phagocytes, which leave the capillaries and move to the site

Question 11

Oral rehydration solution, a drink of water, salts and glucose, does nothing whatever to the cholera bacterium, yet it keeps most cholera patients alive. Suggest why.

Accepted Answer

B1 the damage in cholera is done by a toxin rather than by the bacterium itself: the toxin holds open the chloride channels of the cells lining the small intestine, so chloride ions pour into the lumen B1 water follows the chloride into the lumen by osmosis, and the diarrhoea can remove several litres a day, so what kills is dehydration, the loss of water and salts, which the solution replaces by mouth A1 the bacterium does not destroy the host's cells the way a virus does by lysis, so a patient whose water and salts are kept replaced survives while the body's defences clear the infection

Question 12

Bacteria in a deep wound release tetanus toxin, which travels to the spinal cord. There it stops certain neurones releasing a transmitter that normally inhibits motor neurones, making them less likely to fire. Suggest how the toxin causes the sustained muscle spasms of tetanus.

Accepted Answer

B1 without that inhibition, the motor neurones fire impulses far more often, even continuously B1 so acetylcholine is released at the neuromuscular junctions almost without pause, and the muscle fibres are stimulated again and again B1 the muscle contracts and cannot relax, producing sustained spasms

Question 13

Much of the lung damage seen in tuberculosis is caused by the body's own inflammatory response rather than by a toxin the bacterium releases. Explain how this happens.

Accepted Answer

B1 Mycobacterium tuberculosis survives inside the very macrophages that engulf it, rather than being destroyed by them B1 the host's immune system responds with a sustained inflammatory response that walls the infected cells off into masses called granulomas A1 it is this ongoing walling-off response, rather than a released toxin, that causes much of the tissue damage seen in the lungs

Question 14

Compare a neutrophil with a macrophage as phagocytes, referring to how long-lived each is and what each does after it has engulfed a pathogen.

Accepted Answer

B1 neutrophils are short-lived and arrive first at a site of infection, whereas macrophages are larger and live for longer B1 large numbers of neutrophils die in the process of phagocytosis, and their dead bodies are what makes up pus, whereas macrophages usually survive engulfing a pathogen A1 macrophages, but not neutrophils, present antigens from the pathogen on their own cell-surface membrane, linking the non-specific response to the specific one

Question 15

Antibodies and complement proteins can coat a pathogen before a phagocyte engulfs it. Explain how this coating, called an opsonin, makes phagocytosis more effective.

Accepted Answer

B1 receptors on the phagocyte's cell-surface membrane can grip the antibody or complement coating a pathogen, as well as recognising patterns on the pathogen's own surface B1 this gives the phagocyte an additional, firmer hold on the pathogen than binding directly to the pathogen's own surface alone would give A1 opsonisation therefore speeds up attachment and increases the chance that the pathogen is engulfed

Question 16

A fever raises body temperature by a few degrees. A bacterium that infects humans grows fastest at 37 °C and more slowly at 40 °C. Suggest why the bacterium grows more slowly at 40 °C, and suggest why a body temperature above about 41 °C is dangerous to the patient.

Accepted Answer

B1 40 °C is above the optimum of some of the bacterium's enzymes, so bonds holding their tertiary structure break and the shape of the active site changes B1 fewer enzyme-substrate complexes form, so the bacterium's metabolic reactions slow and it grows and divides more slowly B1 the patient's own enzymes and other proteins also begin to denature at such temperatures, disrupting metabolism, especially in the brain

Question 17

A patient prescribed a broad-spectrum antibiotic for a bacterial infection develops digestive upset during the course of treatment. Suggest why.

Accepted Answer

B1 resident microbiota in the gut normally provide a biological, competitive defence by occupying space and using resources that would otherwise be available to pathogens B1 a broad-spectrum antibiotic kills bacteria generally, including a good many of the resident gut microbiota, not only the pathogen being treated A1 with the resident microbiota reduced, the balance of the gut is disturbed, which is what produces the digestive upset

Question 18

The table shows the usual time between eating contaminated food and the first symptoms for two causes of food poisoning. Suggest an explanation for the difference, in terms of the type of toxin each produces.

Accepted Answer

B1 Staphylococcus produces an exotoxin, which it secretes into the food while growing in it before the food is eaten B1 the toxin is already present when the food is eaten, so it acts at once without the bacteria needing to grow in the gut B1 Salmonella produces endotoxin, which is part of its wall, so the bacteria must first multiply and invade the gut lining and be killed before enough endotoxin is released to cause symptoms

Question 19

A race of stem rust called Ug99 was identified in Uganda in 1999. It can infect wheat varieties carrying the resistance gene Sr31, which most other races cannot. Explain how Ug99 could have spread once wheat carrying Sr31 was widely grown.

Accepted Answer

B1 a mutation in the fungus produced a variant that the Sr31 resistance did not recognise or stop B1 on fields of Sr31 wheat that variant could infect plants and reproduce while other races could not, so it was selected B1 it produced large numbers of spores which were carried by the wind to other fields and regions, so its frequency in the fungus population increased

Question 20

Give one named human disease caused by a bacterium and one named human disease caused by a protoctistan.

Accepted Answer

B1 a bacterial disease named, for example tuberculosis caused by Mycobacterium tuberculosis, or cholera caused by Vibrio cholerae B1 a protoctistan disease named, for example malaria caused by Plasmodium

Question 21

Interferon is classed as part of the non-specific response to infection. Explain why.

Accepted Answer

B1 it is released in response to infection by many different viruses, and the antiviral state it produces acts against any virus B1 it does not recognise or bind a particular antigen, and it is produced at the same speed on every infection, with no memory

Cause of food poisoning	Usual time from eating to first symptoms
Staphylococcus aureus	A few hours
Salmonella species	12 hours to 3 days