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For MB exam
| Question | Answer |
|---|---|
| 2 Antiseptics | Detergent (SLS) Alcohol (ethanol) |
| What does a deteregents do? | an amphipathic model that breaks down membranes |
| SLS pro | good on skin and hair/living organisms |
| SLS con | does little to spores |
| What does alcohol do? | denatures lipids and proteins |
| ethanol pro | clean flat surfaces and skin. dries quickly |
| ethanol con | flammable |
| 2 Disinfectants | Phenols (lysol) Halogen (bleach |
| What does Phenol do? | Tear apart cell walls and proteins |
| Lysol pro | surface disinfection and non-critical equipment |
| Lysol con | Absorbs by porous surfaces can irritate skin!! |
| What do Halogens do? | Oxidize proteins and nucleic acids |
| Bleach pro | disinfect surfaces |
| Bleach con | toxic! Inactivated by organics |
| Chemoheterotroph | Obtains ENERGY and CARBON from organic compounds ANIMALS |
| Photoautroph | Utilizes sunlight for ENERGY and CARBON PLANTS |
| Chemoautotroph | Obtains ENERGY by oxidizing inorganic compounds, and use CO2 for carbon |
| Photoheterotroph | Uses sunlight for ENERGY, but, cannot use CO2 alone, requiring organic compounds from other organisms |
| 4 Types of T-cells? | 1. Killer T-cells (directly kills the target cell) 2. Helper T-cells (release cytokines to communicate with others) 3. Memory T-cells (long lived cells to remember) 4. Tregs (Shuts off immune system when not needed) |
| Selective Media | Only lets certain species/strains grow |
| Differential Media | Will change color depending on species grown |
| How do antibodies work? | Antibodies bind to an antigen once detected, they will then neutralize the antigen and signal other immune cells to destroy pathogen |
| How do psycrophiles adjust to their environment? | Anti-freeze proteins |
| How do halophiles adjust to their environment? | High KCl in cells to balance |
| How do thermophiles adjust to their environment? | Heat stabilizing enzymes |
| Input of glycolysis (2) | Glucose ATP |
| Output of glycolysis | Pyruvate NADH ATP |
| Intermediate step | modifies the pyruvate |
| Input of Intermediate step | Pyruvate |
| Output of Intermediate step | Acetyl-CoA CO2 NADH |
| Input of kreb cycle | Acetyle-COa |
| Output of kreb cycle | NADH FADH2 ATP CO2 |
| Metabolic Tests | Can help identity a microbe by seeing what it can catabolise (and how) Various biochemical tests can help this process Usually a special media with a color change |
| Fermentation | Do glycolysis, then stick electrons somewhere to recycle the carries Fewer ATP, but much easier |
| Electron Transport | Carriers dump off electrons that pumps protons Protons flow through ATP synthase to make ATP |
| Infectivity | How good a pathogen is at SPREADING Ex: measles vs influenza vs rabies |
| Pathogenicity | How good a pathogen is at CAUSING illness Ex: Paralytic polio vs norovirus |
| Virulence | how SEVERE is the illness Ex: Ebola vs CoV-2 vs common colds |
| 3 areas that influence the disease and goals | Etiological agent Host factors Environmental factors |
| Virulence factor: | mechanisms pathogens use to overcome host defenses Requires energy, so microbes only keep what is needed |
| 5 categories of virulence factors | 1. Toxins 2. Evasion 3. Adhesion 4. Nutrient Acquisition 5. Invasion |
| Toxins | Generate adverse functions in the host, that are beneficial to the pathogen in some way |
| Endotoxin | Piece of LPS (lipid A) released from dying Gram-bacteria Causes fever, chills, inflammation, nausea, low blood pressure |
| Exotoxins | Secreted from live bacteria, highly diverse |
| R0 | number of new cases created by a single case |
| Id50 | how many cells/virion needed to establish infection in 50% of susceptible hosts Infectivity measure Lower number is worse!!! |
| LD50 | how many cells/virions needed to kill 50% of untreated hosts pathogenicity/virulence measure |
| Who has PRRs? | Immune cells AND non-immune cells |
| 3 Molecular Defenses | 1. PRRs of MAMPs 2. Iron sequestion 3. Complement |
| How do PRRs work | host proteins, recognize MAMPs and induce some response |
| PRR activation | - Direct antimicrobial activity - Transcription/translation of cytokines |
| Cytokine types | 1. Chemokines- attractants for immune cells 2. Interferons- Induce antiviral transcriptional state |
| How does iron sequestion work? | Some immune proteins sequester (take) iron to starve pathogens, but some pathogens can get around this Because iron is a heavily limited nutrient of the body!! |
| Effects of complement | 1. Osponization 2. Lysis 3. Induce inflammation |
| Cellular Defense components | 1. Phagocytes 2. Dendritic cells 3. Mast cells, basophils NEUTROPHILS |
| Granulocytes | Use granules full of AMPs |
| Granulocyte examples | Eosinophils Basophils Mast cells NEUTROPHILS |
| Neutrophils | Main innate cel!! Secrete AMPs Alarm sounders Eat pathogens (phagocytosis) |
| Agranulocyte examples They are no granules, mostly just phagocytosis | 1. Dendritic cells (phagocytosis) 2. Monocytes (can be macrophages) |
| 3 Steps of inflammation | 1. Vascular change 2. Leukocyte recruitment 3. Resolution |
| Vascular change | Vasodilation to increase blood flow to deliver nutrients and immune cells to tissue |
| Leukocyte recruitment | The chemokines attract leukocytes to infections Marginatin Diapedesis |
| Margination | Slowing of leukocytes in blood |
| Diapedesis | Slipping through vessel walls |
| Resolution | After clearance, new cytolines slow immunity to induce healing factors!!! Btw pus is the dead immune cells :( |
| Pyrogen | induces cytokines (like IL-1 and IFNa) to cause fever • Communicates with hypothalamus |
| Low grade fever | is protective 37.5-38.3 needed |
| High fever | 40.5 |
| Fatal fever | 43 |
| Class 1 MHC | presents internal antigens On almost all cells Communicates to cytotoxic T cells |
| Class 2 MHC | presents external antigens Only on antigen presenting cells (APCs) Communicates to helper T cells |
| APCs include | 1. Macrophages 2. Dendritic cells 3. B cells |
| Humoral immunity | B-cell mediated Outside cells |
| Cellular immunity | T-cell mediated Inside cells |
| Cellular response (T cells) 4 steps | 1. Antigen presentation 2. Activation 3. Differentiation and Proliferation 4. Effector function |
| Step 1: Antigen presentation | APC presents antigens, then travels to the lymph node |
| Step 2: Activation | If a T cells binds a matching antigen on an APC, it receives signals to activate |
| Superantigens: | bacterial toxins that mess this up • Activate T cells without proper antigen presentation |
| Step 3: Differentiation and Proliferation | T cells make lots of clonal copies Differentiate into helper subtypes and memory subtypes Determined by cytokines from APC |
| Step 4: Effector Function | Cytotoxic cells circulate, looking for matching antigen When found, kill that cell! |
| Perforin | Poke holes |
| Grazymes | induce death |
| Humoral response (B cells) 4 steps | 1. Antigen presentation 2. Activation 3. Differentiation and Proliferation 4. Effector function |
| Step 1: Antigen presentation | B cells directly interact with external antigens with BCR Internalize antigen, present on MHC II |
| Step 2: Activation | B cell is activated, either: By a helper T cell recognizing antigen and MHC 2 By a large antigen with many identical epitopes |
| Step 3: Proliferation and Differentiation | B cells make lots of clonal copies Become either: Plasma cells: make TONS of antibodies Memory B cells: long lived, faster secondary response |
| Step 4: Effector Function | Plasma cells secrete tons and tons of antibodies • Soluble B cell receptor • Y-shaped • Also called immunoglobulins (Igs) |
| Antibody Functions (3) | Neutralization Activate complement Osponization |
Created by:
liladdoyle