GCSE Biology Disease & immunity revision

A communicable disease is one that can pass from an infected host to another organism. The agents that cause it are pathogens — tiny organisms or particles from four groups: viruses, bacteria, protists and fungi. Every pathogen must get into a host, reproduce there, and reach new hosts, and exam questions like you to link the type of pathogen to the damage it does.

Pathogens travel between hosts by a few standard routes. Direct contact (touching an infected person, sexual contact, exchange of body fluids), water (drinking or washing in contaminated water), air (droplets from coughs and sneezes that are breathed in) and vectors — organisms such as mosquitoes that carry pathogens between hosts without falling ill themselves. The route matters because it tells you the control: clean water stops waterborne spread, barriers stop contact spread, and netting or insecticides stop vectors.

Measles is a viral disease that spreads in droplets expelled in coughs and sneezes. It causes fever and a red skin rash. Most people recover, but measles can be fatal if complications develop — the virus can cause infections of the lungs (pneumonia) or the brain (encephalitis). There is no specific treatment, so control relies on the MMR vaccination keeping coverage high.

HIV is spread by sexual contact or by the exchange of body fluids such as blood — for example when drug users share needles. It begins with a mild, flu-like illness. The virus then hides inside the immune system, attacking immune cells so the body can no longer defend itself against other infections or cancers; at this late stage the infection is described as AIDS. Antiretroviral drugs stop the virus replicating inside the cells, so a person who takes them as prescribed can live many years with an undetectable viral load and normal life expectancy.

Tobacco mosaic virus (TMV) attacks plants, not people. It causes a mosaic pattern of discolouration on leaves because it damages chloroplasts. With fewer working chloroplasts the leaf cannot photosynthesise properly, so the plant is stunted and yields fall. There is no cure, so growers rely on resistant strains, field hygiene and removing infected plants.

Salmonella bacteria are spread through food prepared in unhygienic conditions or eaten undercooked, especially poultry and eggs. The bacteria secrete toxins that cause fever, abdominal cramps, vomiting and diarrhoea. Control in the UK includes vaccinating poultry against salmonella, thorough cooking and kitchen hygiene — the vaccination works because vaccinated birds do not carry the bacteria into the food chain.

Gonorrhoea is a sexually transmitted bacterial disease. Symptoms include a thick yellow or green discharge from the vagina or penis and pain on urinating. It was once easily treated with penicillin, but strains resistant to penicillin are now common, so other antibiotics are used. Prevention is by barrier contraception such as condoms and by testing and treating partners.

Both diseases show the two big bacterial themes: toxins cause the damage, and antibiotic resistance changes the treatment. Those threads continue in the antibiotics section below.

Malaria is caused by a protist parasite. The protist is picked up by a mosquito when it feeds on an infected person and is injected into the next person the mosquito bites — the mosquito is the vector, and it does not get the disease itself. The parasite infects red blood cells, and the disease causes recurring episodes of fever; severe cases can be fatal. Antimalarial drugs can treat the infection or be taken to reduce risk, and spread is controlled by stopping mosquitoes breeding, sleeping under insecticide-treated nets and killing adults with insecticides. No widely used vaccine exists, so prevention is everything.

Rose black spot is a fungal disease of roses. It produces purple or black spots on the leaves, which often turn yellow and fall early. With damaged leaves the plant photosynthesises less, so growth and flowering suffer. Spores spread in wind or water splash, so control means removing and destroying affected leaves and treating with fungicides.

The body’s first line of defence works on every pathogen the same way — that is why it is called nonspecific. Each barrier has a place and a mechanism, and GCSE answers score by naming both.

If a pathogen breaches these barriers and enters the blood, the immune system takes over — and that response is specific to the invader.

Every cell has molecules on its surface called antigens. Your immune system recognises your own antigens; a pathogen’s antigens are foreign, and it is their shape that the immune response locks on to. Two white blood cell types run the show.

Phagocytes travel in the blood and engulf and digest pathogens — a process called phagocytosis. This response is fast but not picky. Lymphocytes are the specialists: when they meet a foreign antigen, they produce antibodies — proteins whose shape is complementary to that specific antigen. Antibodies stick to the pathogen, tagging it for destruction and helping phagocytes find it. Lymphocytes also release antitoxins, which bind to toxins and neutralise them.

The first encounter is slow: the body needs days to make enough antibodies, which is why you feel ill. Some lymphocytes stay behind as memory cells, holding the antibody blueprint. If the same pathogen returns, memory cells produce antibodies far faster and in far greater amounts, so the pathogen is destroyed before you feel anything. That is immunity.

A vaccination introduces small quantities of dead or inactive pathogens (or their antigens). The antigens still trigger lymphocytes, so antibodies are made — but because the pathogen is dead or inactive, there is nothing to cause disease. Memory lymphocytes remain, so a real infection meets a fast, massive antibody response and is beaten before symptoms develop. The person is immune.

Vaccination protects more than the vaccinated. If a large majority of a population is immune, the pathogen can rarely find a susceptible host, its chain of spread breaks down and even unvaccinated people are largely protected — herd immunity. This is how vaccination programmes prevent epidemics and have made diseases such as smallpox disappear.

Vaccines have advantages: they have controlled or wiped out deadly diseases, and they protect people who cannot be vaccinated through herd immunity. They have disadvantages to evaluate too: a vaccine does not always give everyone immunity, some cause mild reactions such as swelling or a slight fever, and a very small number of individuals may have more serious side effects — the benefits and risks must be weighed on data, not anecdotes.

Antibiotics — penicillin is the classic — cure bacterial infections. They kill bacteria or stop them growing, while leaving body cells unharmed. Different antibiotics work on different bacteria, so doctors match the drug to the infection. Crucially, antibiotics do nothing against viruses: viruses reproduce inside your cells, hidden away where an antibiotic cannot reach them without damaging your own cells. That is why a cold or flu gets rest and symptom relief, not antibiotics.

Within any bacterial population, mutations arise randomly. One mutation can make a bacterium immune to a given antibiotic. When the antibiotic is used, the susceptible bacteria die but the resistant ones survive, find the space free, and reproduce — a textbook demonstration of natural selection. Repeated or unnecessary courses speed this up. MRSA, a strain of *Staphylococcus aureus* resistant to many antibiotics, is the famous hospital example.

Slowing resistance needs action on all sides: doctors prescribe antibiotics only when necessary and appropriate, never for viral infections; patients complete the prescribed course so every susceptible bacterium is killed; antibiotics are restricted in animal feed; and pharmaceutical research hunts for new antibiotics. These strategies are all applications of evolution — which is why resistance questions in the exam often credit a natural-selection chain.

A final distinction to keep sharp: painkillers and most other medicines treat the symptoms — they block pain, lower fever, ease inflammation — but they do not kill pathogens. Antibiotics (for bacteria) are the class that actually remedies an infection.

Many drugs began life as plant or microbial extracts. Digitalis, a heart drug, comes from foxgloves; aspirin was developed from a compound in willow bark; and penicillin was discovered by Alexander Fleming in 1928 when the *Penicillium* mould killed bacteria in one of his culture plates. Modern drugs are usually synthesised in the lab, but the starting molecule is often still a natural compound — and newly discovered organisms remain a source of candidates.

Before a candidate drug touches a patient it goes through preclinical testing: first on cells and tissues, then on live animals, looking for efficacy (does it work?), toxicity (what harm does it do?) and dosage (what concentration gives benefit with acceptable risk?).

1. 1Clinical trials — healthy volunteers

   The drug is first given to healthy volunteers at a low dose to check safety and find how the body handles it.

2. 2Clinical trials — patients

   Then patients receive the drug, with doses increased gradually to find the optimum dose — effective, with side effects that are acceptable.

3. 3Placebo and blind designs

   Patients are split into groups; one receives the drug, the other a placebo that looks identical but contains no drug. In double-blind trials neither patients nor doctors know who got which until the end, so neither expectation bias nor accidental influence can skew the results.

4. 4Peer review and licensing

   Results are checked by peer review before publication, and regulators license the drug only if the evidence shows it works and is safe enough.