Draw a labelled diagram of a prokaryotic cell.

Bacteria are prokaryotes that sometimes act as pathogens. Describe how the body can defend itself against pathogens.

Explain the evolution of antibiotic resistance in bacteria.

a. cell wall – uniformly thick and drawn outside the plasma membrane;
b. plasma membrane – a continuous single line;
c. cytoplasm/cytosol;
d. nucleoid/(naked) DNA – shown as a tangle of thread or irregular shape without a nuclear membrane;
e. (70S) ribosomes – drawn as a small circle or dark dot;
f. pili – hair like structures / flagellum – shown to be longer than any pili;
g. plasmid – circular ring of DNA;
h. capsule – drawn outside the cell wall;
Award [1] for each structure clearly drawn and labelled which conforms to the italicized guidelines given above.

Remember, up to TWO “quality of construction” marks per essay.

a. skin/mucus membranes act as barrier (to pathogens);
b. sebaceous glands secrete lactic acid/fatty acids/sebum / make surface of skin acidic;
c. (skin/stomach) acid prevents growth of many pathogens;
d. lysozyme in mucus can kill bacteria;
e. pathogens caught in sticky mucus and removed from body;
f. inflammatory response/inflammation can cause swelling/redness/fever (to inhibit the pathogen);
g. phagocytes/macrophages/leucocytes/white blood cells (non-specifically) identify (pathogens/bacteria/fungi/viruses) as foreign;
h. (phagocytes macrophages/leucocytes/white blood cells) ingest pathogens;
i. specific lymphocytes recognize one specific antigen;
j. (antigen-specific) lymphocytes clone themselves;
k. lymphocytes/leucocytes produce antibodies;
l. antigen-antibody complex formed and stimulates destruction of pathogen;

a. antibiotics (are chemicals) used to treat bacterial diseases;
b. within populations, bacteria vary in their (genetic) resistance to antibiotics/fitness;
c. resistance arises by (random) gene mutation;
d. when antibiotics are used antibiotic-sensitive bacteria are killed;
e. (natural) selection favours those with resistance;
f. resistant bacteria survive, reproduce and spread the gene / increase allele frequency of resistant bacteria;
g. the more an antibiotic is used, the more bacterial resistance/the larger the population of antibiotic-resistant bacteria;
h. genes can be transferred to other bacteria by plasmids;
i. doctors/vets use different antibiotics but resistance develops to these as well;
j. multiple-antibiotic resistant bacteria evolve/it becomes difficult to treat some infections;

(Plus up to [2] for quality)

Those that drew a prokaryotic cell did well but there were also quite a few eukaryotic cells as the diagram showed and labeled organelles such as mitochondria, lysosome and endoplasmic reticulum.

There were a generous number of marking points for this question. However, candidates were expected to earn some of them describing the first and second lines of defence as well as some of them from the immune response. This answer was generally done well when students weren't confused by extra material, many students had been over taught this area and confused the functions of macrophages / B cells / T cells / memory cells. Terminology and concepts found in HL were presented by students. Those were not accepted in the mark scheme as there were sufficient marks allotted to show understanding of the broad picture expected at SL. Those who used the HL material successfully generally had most of the marks in the mark scheme plus HL information. Unfortunately many got muddled as stated above.

Capable candidates answered this question very well and with clear explanation. The best responses extended their answers to include the occurrence of multiple-antibiotic resistant bacteria. Weaker and mid-range candidates mentioned that bacteria evolve to gain resistance to antibiotics but rarely that it occurs through gene mutation or suggested that mutations that give resistance occurred because bacteria required them rather than randomly. There were many vague answers as candidates seemed to have some grasp of the mechanism but difficulty explaining it.