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Microbiology
Celebration 4 Material
| Term | Definition |
|---|---|
| Antibiotic drugs tend to exhibit a ______ of activity. | Spectrum |
| Broad-spectrum antibacterial drugs | Broad range of microbes are affected by the antimicrobial |
| Narrow-spectrum antibacterial drugs | Is what is wanted, only a few microbes are affected |
| Antimicrobial drugs must exhibit ______. | Selective toxicity |
| Selective toxicity | Ability of a drug to kill/inhibit a pathogen while damaging the host as little as possible |
| Therapeutic dose | Want a small amount of this. Concentration of drug needed for it to bring about change |
| Toxic dose | Want a large number. How much drug it takes for it to be toxic to the host |
| Therapeutic index | Ratio of toxic dose to therapeutic dose |
| Bactericidal drugs usually effect the bacteria's: | Cell wall synthesis (blocks peptidoglycan production), plasma membrane, and nucleic acids |
| Bacteriostatic drugs usually effect the bacteria's: | Protein synthesis and folic acid synthesis (is a part of enzymes) |
| B-lactam (beta lactam) | Targets the pathogen's cell wall and its transpeptidation, is most common structural component in most antibiotics. |
| Transpeptidation | Generation of peptidoglycan layer that is disrupted by beta lactam |
| Some antibiotics disrupt protein synthesis/translation, commonly through interactions with the ________. Name the antibiotics. | Ribosome. Tetracydine, isoniazid, erythromycin, certrixone, chloramphenicol. |
| Trimethoprim | Antibiotic that disrupts folic acid synthesis |
| What compounds interfere with DNA gyrase, have what affects does this produce? | Quinolones and rifamycins. Prevents supercoiling and packaging of DNA in bacterial cell |
| Sulfa drugs | Sulfanilamide and trimethoprim, disrupts folic acid synthesis |
| Isoniazid | Affects only mycobacterium, interferes with mycolic acid synthesis |
| Daptomycin | Affects gram positive bacterial infections by forming pores in plasma membrane |
| Plantensimycin | Broad-spectrum antibiotic effective against MRSA and vancomycin resistant enterococci. Affects synthesis of lipids for membrane. |
| Factors that influence antimicrobial drugs | 1. Ability of drug to reach site of infection 2. Susceptibility of pathogen to drug 3. Ability of drug to reach concentrations in body that exceed MIC of pathogen |
| Kirby-Bauer Disk Diffusion Test | Disks dunked in specific drugs are put onto inoculated plate of microbe. Establishes concentration gradient and zone of inhibition. |
| Minimum inhibitory concentration (MIC) | |
| Minimum lethal concentration (MLC) | |
| Mechanisms of drug resistance: | 1. Target modification (changes shape of targeted areas so it doesn't attach anymore) 2. Inactivating antibiotic (B-lactimases) 3. Interference with porins to downregulate or increase efflux using pumps 4. Target bypass, adapts a new way to do things |
| Mechanisms of resistance transfer: | 1. Conjugation- modified pili pokes hole in another bacteria to transfer DNA 2. Transformation- brining in DNA from outside environment 3. Transduction- transfer of DNA via viral delivery (bacteriophage) |
| Causes of antimicrobial resistance: | Antimicrobials in animal feed gets into meat, into food supply via manure. Unregulated antibiotic prescription in developing countries. Healthcare centers are perfect place for them to thrive (many drugs, many pathogens, many transmission opportunities) |
| Reservoirs | Animate/inanimate habitat where pathogens are naturally found |
| Sources | Thing that disseminates infection agent from reservoir to new hosts. |
| Communicable disease | Transmit human-human, may need a vector/fomite |
| Contagious disease | Easily transmitted from one host to next, DIRECTLY human-human |
| Infectious disease | Illness caused by pathogens. Pathogen replicates, causes infection w/ symptoms, and can be one of six categories (like true pathogen, opportunistic, source, reservoirs, communicable...) |
| Fomite | Inanimate object |
| Vector | Insects |
| Biological vector | Life cycle of pathogen needs insect (pathogen replicates in insect before transmission) |
| Mechanical vector | Insect is just moving pathogen from reservoir to host. |
| Endemic | Present in a given population at a given rate. (malaria, in some parts of Africa but not Norway) |
| Outbreak | Where the cases of disease are greater than expected in an area |
| Epidemic | Outbreak occurs over a larger geographic area (food borne disease shipped all over America) |
| Pandemic | Entire world is affected highly by pathogen (COVID-19, Spanish flu) |
| Common source infections | Usually from water or food, looks like acute infection curve |
| Host-to-host infections | Slow, progressive rise and a gradual decline |
| Signs | Objective things (fever, BP, rash) |
| Symptoms | Subjective things (pain, fatigue, chills, headache) |
| Disease curve stages | 1. Incubation period- time between infection and development of early symptoms 2. Prodromal phase- early symptoms 3. Acute phase- signs occur, best rate of infection to others if communicable 4. Period of decline 5.Convalescent phase |
| Epidemiology | Study of the occurrence distribution and determinants of disease in a population |
| Public health | Health of a given population as a whole |
| Major goals of epidemiology | 1. Monitor public health (incidence and prevalence) 2. Respond to outbreaks (determine cause) 3. Prepare for future outbreaks (risk factors, control measures) |
| Incidence | Number of new cases/time |
| Prevalence | Total number of cases in population/time (morbidity/time) |
| Morbidity | Disease burden of a population |
| Mortality | How many die of disease |
| Agencies involved in public health | WHO and CDC |
| John Snow | Founder of epidemiology (w/ cholera and Broad Street pump) |
| Evidence of epidemic | Where cases occur, where cases don't occur |
| Environmental factors in epidemiological triangle | Climate, geographic location, availability of transmitting vector, food source |
| Host factors in epidemiological triangle | General health, sex, lifestyle, age, ethnicity, occupation |
| Etiological factors in epidemiological triangle | Fungi, bacteria, virus, parasite, or prion |
| Population | Any defined group of people |
| Disability-Adjusted Life Year (DALY) | Measures disease burden in terms of lost years of life due to disease, disability due to disease, and premature death |
| Herd immunity | Resistance of a group to infection due to immunity of a high proportion of a group |
| Basic reproduction number (R0) | Number of expected secondary causes of a given disease from each single case (w/ no herd immunity) |
| Notifiable diseases | When you test positive the doctor must notify the government of it so they can track outbreaks and inform the public |
| Since the 1970s at least ____ never-before-described human diseases have been identified. | 40 |
| What factors contribute to the increase of emerging and reemerging diseases? | Vector's spread for emerging, vaccination for reemerging diseases |
| Healthcare-acquired infections (HAIs) | Infections due to a hospital stay. 5-10% of all acute care patents contract at least 1 HAI during stay. 1 in 31 hospitalized people. |
| Bioterrisism | 2001 anthrax to government officials |
| U.S. Biological Weapons Defense Initiative | Classifies pathogens and restricts who can work with them (A, B, C). Also has warehouses throughout U.S. to stockpile vaccines and medical equipment, more biodefense research, training "first responders" |
| USBWDI Classification A | Pathogens with high risk to be used in terror (anthrax, botulism, small pox) |
| USBWDI Classification B | Pathogens with moderate risk to be used in terror |
| USBWDI Classification C | Pathogens with lower risks for terror, would need engineering to be weaponized |
| Innate immunity | Immediate response in all eukaryotes. General response to broad range of pathogens. Primary effectors: phagocytes (dendritic cells, neutrophils, and macrophages) |
| Immunity | Ability of organism to resist infection |
| Adaptive immunity | 4-7 days to work, only in vertebrates. Tailors response to specific antigens and remembers them to amplify response to next exposure. Primary effectors: Lymphocytes (B lymphocytes and T lymphocytes) |
| A _____ collection of microbes fine tune our immune system to fight pathogens while training it to _____ nonpathogens, food, and self-tissues. | Wide, tolerate |
| Hygiene hypothesis | With everyone being cleaner there is less exposure to diverse microbes when growing up, leading to a less regulated immune system and more autoimmune diseases |
| Studies of germ-free animals has shown: | That they are affected by hygiene hypothesis |
| Mechanical barriers | First-line defense of flushing, rinsing, and trapping actions. Ex: tears and mucus |
| Physical barriers | First-line defense of structural blockade to entry Ex: skin |
| Chemical barriers | First-line defense of molecules that directly attack microbes or generate environment that limits their survival. Ex: lysosomes, AMPs, stomach acid |
| Antimicrobial peptides (AMPs) | Proteins that destroy a wide spectrum of viruses, parasites, bacteria, and fungi by stimulating leukocytes and directly targeting pathogens. |
| Lymphatic system | Second line of defense that is a separated circulatory system that drains lymph from extravascular tissues. |
| Lymph nodes | Contains high concentrations of immune system cells |
| Mucosa-associated lymphoid tissues (MALT) | A more diffused area that samples the area to see if there is an issue. Adenoids and tonsils |
| Secondary lymphoid tissue | Lymph nodes and MALTs and spleen filter lymph and sample body sites for antigens |
| Primary lymphoid tissue | thymus and bone marrow. Site of production and maturation of leukocytes |
| Blood | Mostly eukaryocytes, with leukocytes |
| Hematopoiesis | Differentiation of stem cells into RBC or WBC |
| Cytokines | Chemical messenger cells use to communicate with each other |
| Chemokines | Type of cytokine that tells cells to group (recruit) together and induces differential gene expression. Too much=anaphalactic shock |
| Plasma | Liquid of blood without cells |
| Serum | Liquid of blood without clotting factors |
| What are the major cell types found in normal human blood? | 1. RBC 2. Leukocytes 3. Lymphocytes 4. Neutrophils 5. Monocytes |
| Hematopoietic stem cell | Cell in bone marrow that divides into myeloid precursor or lymphoid precursor |
| Monocyte | Makes dendritic cells and macrophages. Formed from myeloid precursor |
| What types of cells are antigen presentation cells? | Dendritic cells and macrophages |
| Phagocytic cells | Dendritic cells, macrophages, neutrophils, eosinophils |
| Granulocytes | Neutrophils, eosinophils, basophils, and mast cells. All made from myeloid precursor |
| Cells for inflammatory response | Basophils and mast cells |
| Lymphoid precursor | Forms B-cell, T-cell, and NK cells |
| Cell-mediated immunity (kills infected host cells) | NK cells and T cells |
| Cells in innate immunity | Dendritic cells, macrophages, granulocytes, and NK cells |
| Cells in adaptive immunity | T cells and plasma cell (from B cells) |
| Plasma cell | Formed from B cell to serve as antibody-mediated immunity |
| B cell | Has antigens on surface, can be activated to be a plasma cell by T helper cells. Produces antibodies. |
| Neutrophils | Highly phagocytic, fights many invaders especially bacteria and viruses. Mostly in circualtory system |
| Eosinophils | Moderately phagocytic, attacks allergens and parasites |
| Basophils | Attacks allergens and parasites that are too big to phagocytize (like parasitic worms) |
| Mast cells | Moderately phagocytic attacking bacteria, allergens and parasites. Resides in tissues (mucosal membranes) and releases histamine to cause inflammation and eye watering. |
| Macrophages | Highly phagocytic, can be fixed or wandering, activates adaptive immune responses. |
| Dendritic cells | Highly phagocytic; activates adaptive immune response |
| NK cells | Innate immunity to viruses, bacteria, parasites, and tumer cells. Finds them as they don't present MHC I and presents stress protein. Releases granules into diseased cell with perforin and granzymes to cause apoptosis. |
| Perforin | Released by NK cells, pokes holes in diseased host so that it lyses |
| Granzymes | Released by NK cells to cause apoptosis |
| Molecules released by leukocytes into local environment | 1. Cytokines to signal something is wrong and cause fever and inflammation 2. Iron-binding proteins to limit iron to be used by bacteria 3. Complementary proteins for inflammation and tags targets for death 4. |
| Signaling proteins that allow cells to _______ with each other, _____ and ______ immune actions. | Communicate, initiating, coordinating |
| Interleukins (ILs) | Stimulates hematopoiesis, fever, inflammation, and apoptosis |
| Interferons (IFNs) | Signal when pathogens (especially viruses) or tumor cells are detached. Can also recruit. |
| Hematopoiesis | Differentiation of stem cells into red or WBCs |
| Amount of freely available iron in circulation and within our tissues is well _____ the necessary amount microbes require for survival. | Below |
| Siderophores | Bacteria makes these to steal iron from host iron-binding proteins to being back to bacteria |
| Hemolytic bacteria | Collects hemoglobin from host red blood cells and lyses them to steal iron to use. |
| Classical pathway | Complement proteins activated when antibodies bind to pathogens, has multiple steps |
| C3 | Complementary protein that binds to pathogen |
| Alternative pathway | Complementary proteins activated by directly interacting with protein |
| Lectin pathway | Complementary proteins activated when mannose-binding lectin (MBL) binds to pathogen (to its carbohydrates) |
| All three complement protein pathways have these 3 outcomes: | 1. Opsonization 2. Cytolysis 3. Inflammation |
| Opsonization | C3b tags pathogen for phagocytosis |
| Cytolysis | C5b and others make membrane attack complex, allowing water and ions to rush in and lyse pathogen |
| Inflammation | C5a and C3a recruit leukocytes from blood into tissue, leukocytes release chemicals for imflammation |
| Three main goals of inflammation: | 1. Recruits immune defenses to injured tissues 2. Limit spread of infectious agents 3. Delivers oxygen, nutrients, and chemical factors essential for tissue recovery |
| Vascular changes in early inflammation | First phase of inflammation. Vasoactive molecules from epithelium and leukocytes induce blood vessel dilation to increase blood flow and vessel permeability to allow swelling as plasma leaks and leukocytes go to site. |
| Leukocyte recruitment | Second phase of inflammation. Leukocytes go through margination and diapedesis to leave blood and go into tissue |
| Resolution | Third phase of inflammation. As threat passes blood vessels go back to normal, leukocytes go through apoptosis, healing begins and fluid goes to lymphatic capillaries |
| Three benefits of fever: | 1. Enhances antiviral effects of interferons 2. Increases phagocyte efficiency and leukocyte production 3. Limits growth of certain pathogens |
| Fever | Signaled by hypothalamus that makes body's thermostat to set above 98.6 degrees F in response to infection. Tylenol and ibuprophen |
| Margination | When leukocytes roll towards the margins (sides) of blood vessel walls in preparation to cross into tissue |
| Diapedesis | When leukocytes squeeze to fit across the walls of blood vessels to get into tissues |
| Primary cells for adaptive immune response | Phagocytes and lymphocytes |
| Two branches of adaptive immune system | 1. Cellular response (T-cell mediated) 2. Humoral response (antibody mediated) |
| Receptor of T/B cells | All over T/B cells, all recognize a singular, same kind of cell via its molecular patterns. |
| Specificity | Lymphocytes have surface receptors that interact with individual antigens (specifical molecular components of target cell) |
| Specificity of antigen-antibody reaction is dependent on: | Interaction between specific receptor and the antigen that will make a immune response when they bind together |
| Substances that induce an immune response are called | Antigens |
| Epitope | A distinct portion of an antigen that interacts with the antibody (binds to its antigen-binding site). Also called antigenic determinent |
| Biomolecules from most immunogenic (ability to generate immune response) to least: | Proteins (have lots of binding sites) -> polysaccharides -> lipids -> small molecules |
| The first antigen exposure induces | Multiplication of antigen reactive cells, resulting in multiple copies/clones. |
| Antigen presenting cell (APC) | Dendritic cells and macrophages, presents antigen to T cell in cellular response of adaptive immunity |
| Cellular response | 1. APC presents antigen to T cell 2. T cell is activated, releases cytokines, also interacts with B cells to stimulate humoral response 3. Proliferation 4. Differentiation of T cells to memory and T effector 5. Eliminates antigen |
| Humoral response | 1. Antigen binds to B cell 2. B cell activates, w/ T cell fully stimulating it. Cytokines released 3. Proliferation 4. Differentiation to plasma cells or memory B cell 5. Eliminates antigen |
| Proliferation | Clonal expansion of T/B cells after they are activated, so that they can differentiate into memory or effector cells. |
| T cytotoxic cell (Tc cell) | Destroys infected cells, cancer cells. and transplanted tissues. Has CD8 |
| T helper cells (Th cell) | Releases cytokines that can stimulate/suppress other white blood cells. Coordinates adaptive immune response (talks to Tc cells and B cells). Has CD4 |
| How to tell T cells apart | Presence of clusters of differentiation (CD) proteins. |
| Th 1 | Subclass of Th cell that stimulates T cytotoxic cells (promotes cellular response). Also produces cytokines for NK and macrophages |
| Th 2 | Subclass of Th cell that stimulates B cells (promotes humoral response) |
| T regulatory cells | Subclass of Th cell that decreases immune response once threat has passed |
| How body screens T cells | Occurs in thymus. Recognize MHC? N->die Y-> Can be self-reactive? Y->die N-> Live |
| How body screens B cells | In bone marrow. Can make antibodies to self-antigens? Y-> die N-> live |
| MHC I (Major histocompatibility complex I) | Displays proteins inappropriate for inside host (like viral proteins, shows something is wrong). Is in every cell that is NOT erythrocytes or cells that have MHC II |
| MHC II | Antigen presenting cells (monocytes, dendritic cells, macrophages, B-cells) |
| Steps to present intracellular antigens to T cytotoxic cells | 1. Intracellular antigen is broken into fragments by cell's proteasome 2. Fragments transported to ER by protein 3. Protein fragments associate with MHC I in ER 4. MHC I-antigen complexes make way to cell surface to be displayed to Tc cells |
| Process of MHC II presenting extracellular antigens to Th cells | 1.Antigen presenting cell takes up extracellular antigens by phagocytosis 2. Vesicle-antigen fuses w/ lysosome (phagolysosome), breaks down antigen, and MHC II fuses with it 3. Pieces of antigen associate with MHC II 4. Complex goes to surface-> Th |
| Role of Tc cells in adaptive immune response | Interferons attract activated Tc cells, cytokines from Tc attract NK cells and macrophages, Tc releases perforins and granzymes to kill cell |
| Gene shuffling | A random process that gives rise to receptors on T and B cells that could bind to normal body cells. Are why they are screened |
| Process of T-dependent antigens activating B cells | 1. Extracellular antigen binds to B cell receptor 2. Antigen enters cell (endocytosis), is processed so epitopes are displayed on surface by MHC II 3. MCH II-antigen on B cell binds to Th 1 cell that recognizes epitope 4. Cytokines are released |
| T-independent activation | Multiple BCRs on a given B cell directly bind to the antigen. A polysaccharide holds the antigens that will bind to the B cell. |
| Immunoglobulins | (Ig) also called antibodies, secreted by plasma cells |
| Three ways antibodies elicit a response | 1. Neutralize antigens 2. Activate complement protein (causes cytolysis, opsonization, inflammation) 3. Increases phagocytosis (antibodies will precipitate, agglutinate, or opsonization the bacteria to do this) |
| Light chain | The variable area of immunoglobulins |
| Heavy chain | The area of immunoglobulins that is not variable |
| Five major classes (isotypes) of antibodies/Igs | IgG, IgA, IgM, IgE, IgD (G A M E D) |
| IgA | In plasma cells around tissues that produce fluid |
| IgM | Aggregates together in 5s to be attached using 1 or more joining (J) chains for maximum binding capability |
| IgE | In serum and is antibody that binds to eosinophils and mast cells (deals with allergic responses) |
| IgD | In serum with no known function |
| IgG | Most common antibody, is the primary effector |
| Antibody graph on initial antigen exposure (primary antibody response) | IgM first, then IgG. Both are low and similar concentrations, just at different times |
| Antibody graph on later antigen exposures (secondary antibody response) | High concentration of IgG with a lower concentration of IgM at the same time |
| Active immunity | The one benefitting from the antibodies is the one who made them |
| Passive immunity | The one benefiting from antibodies did not make them. No long term immunity (as no memory cells) |
| Natural active immunity | Immunity from previous infection |
| Natural passive immunity | Antibodies passing across placenta from mother to baby |
| Artificial active immunity | Vaccination triggers immune response |
| Artificial passive immunity | Antivenom neutralizes toxins |
| Vaccine | Deliberate exposure to an antigen |
| Live attenuated vaccine | Live but weakened virus. Gold standard type that makes strong immune response and causes lifelong immunity. May have issues with immunocompromised |
| Inactivated vaccine | Has entire virus particles that are dead/inactivated. Safter but needs boosters |
| Replicating Viral Vector vaccine | Alters low-pathogenic virus into viral vectors that will produce same proteins as disease-causing virus. Makes strong immune response but may not work if host is already immune to low-pathogenic virus |
| Non-replicating viral vector vaccine | Like replicating viral vector but doesn't replicate in body. Improved safety and efficacy but needs high doses to get immunity |
| DNA vaccine | Takes genes that produce same antigenic proteins as virus. Easy to make and produce but sometimes host will integrate it instead of fighting it |
| RNA vaccine | Uses piece of mRNA to produce same antigenic proteins as virus. Takes away risk of integration but may trigger unintended immune responses. |
| Subunit vaccine | Uses antigenic proteins from virus without genetic material. Safer than genetic material but needs multiple doses and adjuvants to produce a stronger immune response |
| Macrolides | Antibiotic class that inhibits protein synthesis |
| Interleukin 1 | Fever |
| Interleukin -12 | cell differentiation |
| Interleukin -10 | anti-inflammation |
| Interleukin 4 | B-cell response |
| Interleukin 2 | T-cell responses |
| Cephalosporins | Antibiotic class that inhibit cell wall synthesis |
| MALT | Antibiotic class that inhibit protein synthesis. Macrolides Aminoglycosides Lincosamides Tetracyclines |
| Aminoglycosides | Antibiotic class that inhibits protein synthesis |
| Tetracyclines | Antibiotic class that inhibits protein synthesis |
| Penicillins | Antibiotic class that inhibits cell wall synthesis |
| SulFOnamides | Antibiotic class that inhibits FOlate synthesis |
| FluoroQUINolones | Antibiotic class that inhibits DNA replication (QUINtuplets) |
| Carbapenems | Antibiotic class that inhibit cell wall synthesis |
| Lincosamides | Antibiotic class that inhibits protein synthesis |
| Glycopeptides | Antibiotic class that inhibits cell wall synthesis |
| Phenicol | Antibiotic class that inhibits protein synthesis |
| Rifamycin | Antibiotic class that inhibits RNA polymerase |
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