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Biology A level - Communicable Diseases Cheat Sheet by

This is a cheat sheet for A level OCR Gateway biology, Chapter 12 from Module 4. Specification reference: 4.1.1

Types of pathogens

Prokar­yotes. Classified by shape and cell walls (gram positive / negative bacteria). Gram positive bacteria (e.g. MRSA) look purple after staining, gram negative (e.g. E.coli) looks red.
Non-living infectious agents. Rapidly reproduce. Pathog­enic, attack other organisms (bacte­rio­phages attack bacteria).
Protoc­tista (protista)
Eukaryotic organism

Viral infection

1. Attachment of virus.
2. Virus implants DNA (viral nucleic acid) in host cell.
3. Cell replicates viral nucleic acid.
4. Synthesis of viral proteins.
5. Assembly of virus particles.
6. Virus leaves cell. Lysis of host cell.

Viral infection diagram

Transm­ission of animal pathogens

Physical contact e.g. HIV, bacterial meningitis
Direct contact, increased risk if overcr­owding, poor hygiene...
Droplet infection e.g. influenza, TB
Indirect contact, increased risk if overcr­owding, poor ventil­ati­on...
Vectors e.g. malaria, bubonic plague, rabies
Indirect contact, increased risk if poor waste disposal (breeding ground for vectors), climate change...
Fomites e.g. athlete's foot, gas gangrene
Infected surfaces, indirect contact, increased risk if living in unclean condit­ions...
Digestion e.g. cholera, food poisoning
DIirect contact, increased risk if sewage water, poor diet / nutrit­ion...
Innocu­lation e.g. malaria, rabies
Direct contact, increased risk if sharing needles...

Animal diseases

Type of pathogen
Bacterial meningitis
Gram neg. bacterium
Fever, drowsi­ness, light sensit­ivity, vomiti­ng...
Tuberc­ulosis (TB)
Gram pos. bacterium
Weight loss, fever, chest pain, coughi­ng...
Fever, sore throat, rash, muscle pain...
Fever, headache, dry cough, cold sympto­ms...
Athlete's foot
Itchy red rash between toes, flaky dry skin.
Silvery ring-like rash.
Fever, sweats, vomiting, diarrh­oea...

Plant diseases

Type of pathogen
Black sigatoka (bananas)
Premature ripening, brown + shriveled leaves.
Tobacco Mosaic Virus (TMV) (tomatoes, cucumb­ers...)
Stunting, leaf curling, yellowing plant...
Ring rot (potatoes, tomato­es...)
Gram pos. bacterium
Vascular wilt, discol­our­ation and loss of texture...
Potato / tomato blight
Shrivel + turn brown, fine white fungal growth around lesions...

Recogn­ising attack on plants

Molecules from pathogen / products from pathogenic enzymes recognised by cell by receptors in membrane.
Signalling molecules alert nucleus to attack.
Defensive molecules directly attack
AND / OR defensive chemicals alert other cells through plasmo­desmata
AND / OR strengthen cell walls with callose and lignin
Callose - polysa­cch­aride (beta 1,3 and beta 1,6 glycosidic bonds).
- can block plasmo­desmata
- can thicken infected cell walls
- seals sieve plates in phloem to isolate cell

Chemical defenses in plants

Insect repellent
e.g. pine resin, citronella
Antiba­cterial compound
e.g. phenols (antis­ept­ics), antiba­cterial gossypol (in cotton), defensins (plant protein which disrupts bacterial / fungal mambranes)
Antifungal compounds
e.g. chitinase, saponins, antifungal gossypol, phenols
e.g. glucanases (enzyme which breaks down glucans)
General toxins
e.g. chemicals broken down into cyanide
e.g. caffeine, pyrethrins (in chrysa­nth­emums, act as insect neurot­oxins)

Physical defenses in plants

Physical defenses
Waxy cuticle, cell wall...
Block sieve plates, thicken walls...

Non-sp­ecific animal defences

Keeping the pathogens out
Physical barrier, healthy microo­rga­nisms to outcompete pathogens, sebum secretion.
Mucous membranes
Contains phagoc­ytes.
Tears / urine / acid in stomach
Contain lysozymes.
Coughing / sneezing
Ejects pathog­en-­con­taining mucus.
Vomiting / diarrhoea
Expel pathog­en-­con­taining gut contents.
Inflam­matory response
Localised response to pathogen charac­terised by pain / heat / redness / swelling (separate block).
Blood clotting
Cascade reaction (seaprate block).
Destroying pathogens
Cytokines stimulate hypoth­alamus to increase temper­ature.
Cell-s­ign­alling molecules.
Opsonins e.g. immuno­globin G and M (IgG / IgM)
Bind to + tag path. Phagocytes = opsoni­n-b­inding receptors.
Phagocytes = neutro­phils and macrop­hages (separate block).

Inflam­matory response and blood clotting

Inflam­matory response
Mast cells released, release histamines and cytokines. Histamines --> make blood vessels dilate (heat and redness) + blood vessels walls become more leaky --> blood plasma is forced out and becomes tissue fluid (swelling and pain). Cytokines --> attract phagoc­ytes.
Blood clotting
Damaged tissue --> acivates platelets --> thromb­opl­astin released. Thromb­opl­astin + Ca2+ = prothr­ombin --> thrombin --> catalyses fibrinogen --> fibrin --> blood clot


Phagocytes attracted by chemicals produced by path.
Phagocyte recognises path. as non-self.
Phagocyte engulfs path. --> phagosome.
Lysozymes combines with phagosome --> phagol­yso­some.
Digested path. absorbed, antigen combines with MHC to form MHC complex.
Phagocyte + MHC complex = antige­n-p­res­enting cell (APC).

Antibody structure

Variable region - Changes in every antibody and is comple­mentary to antigen.
Agglut­ination - Antigens bind to multiple pathogens to clump them together.
Neutra­lis­ation - Stop pathogens entering host cell OR act as antito­xins.

Cell mediated immunity - specific response

T lympho­cytes respond to changed cells.
An APC is formed (phago­cytosis by macrop­hages). T helpers bind to presented antigens.
T helper carrying the correct antibody is activated and divides by mitosis (clonal expansion).
T cells can then take one of four paths:
- Develop into T memory cells
- Produce interl­eukins to trigger phagoc­ytosis
- Produce interl­eukins to trigger B cell division
- Develop into T killer cells
T helper cell - Produce interl­eukins, stimulate B cells and antibody production and attract other T cells and antibo­dies.
T killer cell - Kill pathogen - produce perforin which make holes in pathogen membrane.
T memory cell - Immuno­logical memory, remain in blood for a long time. Second infection = rapid division of T killer cells.
T regulator cells - Prevent autoimmune response, repress immune system after pathogen has been destroyed.

Humoral immunity - specific response

Activated T helper cells bind to B lympho­cytes presenting the correct antigen (clonal selection) and activates it with interl­eukins.
B cells can then become one of two things:
- Become a B plasma cell.
- Become a B memory cell.
B lympho­cytes / cells - APCs, respond to antigens and APCs.
B plasma cells - Produce antibo­dies, act as opsonins (label cells) or as agglut­inins.
B memory cells - Stay in the blood. If infected again, will divide into plasma cells.

Autoimmune diseases

Part affected
Rheumatoid arthritis
No cure, anti-i­nflam. drugs and steroi­ds...
Skin, joints and organs
No cure, anti-i­nflam. drugs, steroi­ds...
Type 1 diabetes
Insuli­n-s­ecr­eting parts of pancreas
Insulin inject­ions, pancreas transp­lant...

Natural v. artifi­cial, active v. passive immunity

Natural active
Secondary immune response (memory T and B cells).
Natural passive
Antibodies cross from placenta / mothers' milk.
Artificial active
Body simulated to make own antibodies (e.g. injection of weakened / dead path., isolated antige­ns...)
Artificial passive
Antibodies made in other animal, collected and injected.

Drug design of the future

Person­alised meds, genotype and drugs interact.
Synthetic biology
Develop bacteria to produce otherwise rare drugs, GM mammals and nanotech.

Antibiotic dilemma

Antibi­otics = selective toxins, harm bacteria but not human cells.
Random mutation in bacteria could lead to antibiotic resistance --> whole population / species develops with trait (bacteria reproduce rapidly therefore antibi­oti­c-r­esi­stant generation arrives quickly).
Specific example - MRSA

Research - computer models, deep sea microo­rga­nis­ms...
Bacterial resistance building faster than antibi­otics are developed.


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