Types of pathogens
Bacteria |
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. |
Viruses |
Non-living infectious agents. Rapidly reproduce. Pathogenic, attack other organisms (bacteriophages attack bacteria). |
Protoctista (protista) |
Eukaryotic organism |
Fungi |
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. |
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
Disease |
Type of pathogen |
Symptoms |
Bacterial meningitis |
Gram neg. bacterium |
Fever, drowsiness, light sensitivity, vomiting... |
Tuberculosis (TB) |
Gram pos. bacterium |
Weight loss, fever, chest pain, coughing... |
HIV / AIDS |
Virus |
Fever, sore throat, rash, muscle pain... |
Influenza |
Virus |
Fever, headache, dry cough, cold symptoms... |
Athlete's foot |
Fungus |
Itchy red rash between toes, flaky dry skin. |
Ringworm |
Fungus |
Silvery ring-like rash. |
Malaria |
Protist |
Fever, sweats, vomiting, diarrhoea... |
Plant diseases
Disease |
Type of pathogen |
Symptoms |
Black sigatoka (bananas) |
Fungus |
Premature ripening, brown + shriveled leaves. |
Tobacco Mosaic Virus (TMV) (tomatoes, cucumbers...) |
Virus |
Stunting, leaf curling, yellowing plant... |
Ring rot (potatoes, tomatoes...) |
Gram pos. bacterium |
Vascular wilt, discolouration and loss of texture... |
Potato / tomato blight |
Protist |
Shrivel + turn brown, fine white fungal growth around lesions... |
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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 |
Anti-oomycetes |
e.g. glucanases (enzyme which breaks down glucans) |
General toxins |
e.g. chemicals broken down into cyanide |
Insecticides |
e.g. caffeine, pyrethrins (in chrysanthemums, act as insect neurotoxins) |
Physical defenses in plants
Physical defenses |
Waxy cuticle, cell wall... |
Callose |
Block sieve plates, thicken walls... |
Non-specific animal defences
Keeping the pathogens out |
Skin |
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 |
Fevers |
Cytokines stimulate hypothalamus to increase temperature. |
Cytokines |
Cell-signalling molecules. |
Opsonins e.g. immunoglobin G and M (IgG / IgM) |
Bind to + tag path. Phagocytes = opsonin-binding receptors. |
Phagocytosis |
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 |
Phagocytosis
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). |
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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.
PRIMARY IMMUNE RESPONSE:
B plasma cells - Produce antibodies, act as opsonins (label cells) or as agglutinins.
SECONDARY IMMUNE RESPONSE:
B memory cells - Stay in the blood. If infected again, will divide into plasma cells.
Autoimmune diseases
Diseases |
Part affected |
Treatment |
Rheumatoid arthritis |
Joints |
No cure, anti-inflam. drugs and steroids... |
Lupus |
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
Pharmogenetics |
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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