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Microbio Lec FINAL
| Question | Answer |
|---|---|
| What is ID50? | the amount of pathogen to infect 50% of the test population |
| what's LD50? | amount of pathogen/substance to kill 50% of test population |
| exotoxins vs endotoxins | exotoxins are produced to damage host tissue to increase virulence, endotoxins are part of the LPS membrane, when dissolved they produce fever/symptoms (LipA) |
| what's virulence? | ability to rapidly cause damage |
| what's infection | invasion or colonization of the body by pathogenic organisms. |
| what's antigenic variation? | proteins on pathogen cell surface change so that immune system doesn't recognize it as the pathogen from before |
| what's a competitive inhibitor in pathogenicity? | may sit on host receptor sites to prevent pathogen from binding (like an antibody or good bacteria) |
| what are lysosomes? | suicide bags with digestive enzymes, merge with phagosomes (pouch inside a phagocytic white blood cells) that contain the pathogen to for phagolysosomes to digest the pathogen |
| four stages of phagocytosis | chemotaxis, adherence, ingestion, digestion |
| first lines of defense include | skin, tears, saliva, normal flora |
| second lines of defense include | white blood cells, inflammation, antimicrobials, lymphatic system, phagocytosis |
| chemical factors of defense in mucous membranes | lysozymes in tears that destroy peptidoglycan |
| physical factors of defense in mucous membranes | eye washing to clear it out |
| what do lymph nodes do? | filter lymph removing microorganisms, contain white blood cells, distributed through body and contain fiber to trap microorganisms |
| what is lymph made of? | interstitial fluid that's washed over cells |
| 2 characteristics of inflammation | redness, swelling |
| vasodilation does what? | result of inflammation that results in accumulation of fluid |
| what part of the brain raises body temp? | hypothalamus which dilates blood vessels |
| what are phagocytes? | white blood cells like nutrophils and monocytes/macrophages that ingest + digest pathogens |
| why are phagocytes called that? | they ingest + digest pathogens |
| macrophage vs monocyte | monocytes circulate the bloodstream, macrophages are differentiated monocytes that go to specific tissue/cells |
| portals of entry for pathogens | skin, parenteral (en cuts), mucous membranes of GI and respiratory tracts |
| why are encapsulated bacterium more virulent? | capsule resists phagocytosis like a cloak so can cause more rapid damage since not detected AND CAN EVEN REPLICATE IN PHAGOCYTES AND LYSE THE PHAGOCYTE |
| why did the vaccine where smallpox was rubbed into skin not kill? | skin is the wrong port of entry, LD50 must be lower AND the skin has a second line of defense of antigens that stop the pathogen from spreading |
| what makes a succesful pathogen? | one that doesn't kill its host before its transmitted |
| what's most bacterial damage to cells caused by? | toxins, they destroy cells or inhibit metabolic processes |
| methods of pathogens to penetrate OR evade host defenses | enzymes, capsules, cell wall components (LPS), antigenic variation |
| what are adhesins? | surface molecules on pathogens that bind to complementary proteins on host cell surface |
| what kind of bacterium have endotoxins? | gram-negative cells (LPS) |
| what's disease? | abnormal state in which part or all of the body is undergoing change in health |
| Koch's postulates: | 1) same pathogen must be present in all cases 2) pathogen must be isolated from a diseased host 3) pathogen must be inoculated into a healthy lab animal 4) pathogen must be isolated and be same as OG |
| what are reasons behind emergence of new infectious diseases? | increasing population, amount of travel + air travel, changing environments (flood, drought), pathogens crossing species barrier |
| what's a systemic infection? | microorganisms or their products are spread throughout the body by the blood or lymph. |
| mutualism is what? | symbiosis where both benefit |
| symptoms vs signs | symptoms are subjective, signs are objective and can be measured |
| acute vs chronic infections | acute develop + resolve quickly, chronic develop slowly and persist |
| subclinincal infections are what | where patient has no symptoms but are a carrier |
| Analytical vs descriptive vs experimental epidemiology | A-A group of infected are compared with healthy D-Data is collected and analyzed E-Experiments designed to test hypotheses |
| what are nosocomial infections? | health-care associated infections |
| normal microbiota are what? | microbiota that permanently colonize |
| transient microbiota are what? | persist from hours to months |
| opportunistic microbiota are what? | those that cause disease only when immunocompromised |
| what does pathogenicity refer to? | the ability to cause disease |
| what is etiology? | cause of the disease |
| contamination vs infection | presence of pathogens on surface vs in tissue/body leading to infection |
| what does syndrome refer to? | group of symptoms or signs that accompany disease |
| communicable vs non-communicable diseases | those that are spread between hosts, contagious vs not transmitted like cancer |
| incidence vs prevalence | # of NEW people with disease in a specific time window vs # of ALL (ongoing and new) people infected at the time window |
| sporadic vs endemic vs epidemic vs pandemic | S-occaSional, enDemic-arounD all the time, ePidemic-many infected in short time Period, P-worlwide epidemic |
| latent infections are those that: | become something else later, like chickenpox->shingles |
| local vs systemic vs focal infectons | local stay on specific part, systemic is the full body, focal start local but spread to other parts like to other teeth |
| what do bacteremia and viremia refer to | infection caused by bacteria and viruses, respectively |
| what's toxemia | presence of toxins that cause infection |
| primary vs secondary infections | primary are the first one, secondary arise from being immunocompromised from the first |
| incubation period | no signs/symptoms |
| prodromal period | mild signs/symptoms |
| period of illness | syptoms/signs most severe |
| period of decline | syptoms/signs start to taper off |
| period of convalescence | microorganisms have reached low point and milk symptoms remain |
| reservoirs of infection | living or non living (soil, water) but have conditions for survival, replication and transmission |
| what are zoonoses | animal diseases/carriers that can be transmitted to humans |
| direct vs indirect transmission example | shaking hands vs touching door handles |
| vehicle transmission example | through another substance like water/food/blood |
| vector transmission | through a living thing |
| vector transmission methods: biological vs mechanical transmission | biological is part of life cycle is in host, mechanical is carried on thier feet/winds and is passice transport |
| R-naught represents what? | how frequently something is transmitted |
| 3 types of contact transmission | direct, indirect and droplets |
| what are fomites? | inanimate objects that carry pathogens like sheets + pens (they're a vehicle of transmission) |
| contributing factors to new disease include: | mutations, genetic recombination, inappropriate use of pesticides and antibiotics, changes to environment (organisms move to new places) |
| pathology is the study of what | disease, pathos means suffering/disease, pathogen is the cause of disease |
| how are antigens involved in immunity | some lac cell receptor antigens to viruses so the pathogen can't adhere to their cells |
| what percent of human infections involve biofilms? | 65%!! |
| how do pathogens damage host cells? | using nutrients, damage in vicinity of invasion, producing toxins that travel bloodstream and lymph nodes |
| what is hypersensitivity? | pathogenic toxins travel bloodstream and lymph nodes hyping up the body so much it damages the body - OVERREACTION |
| what are siderophores? | secreted from pathogens to steal iron from iron-transport proteins like hemoglobin |
| what are other ways pathogens steal iron? | bind directly to the hemoglobin or iron-transport proteins, or release toxins to kill host cells and scavenge iron from the dead |
| what is toxic shock syndrome | Staph a. endotoxins stimulating TONS of signals from macrophage white blood cells that tells it "I'M SUPER INFECTED LET ME DIE NOW" NOT hypersensitivity because that refers to overreactions - this is NOT an overreaction |
| what do antibiotics do to gram-negative cells? | break LPS in cell walls releasing lipid A and creating toxins until the toxins run out and pathogenic cells die |
| where are most exotoxins carried? | on plasmids since plasmids are exchanged between cells |
| what's intoxication? + example | damage is caused by toxins released by the bacteria NOT THE INFECTION; snake bite venom, or a protein synthesis inhibitor (it's damage that's not super direct) |
| neurotoxin vs cytotoxin vs aflatoxin symptoms | muscle contraction, targetes proteins, carcinogenic fungi |
| what is immunity? | how we defend against pathogens |
| what is susceptibility? | the lack of immunity |
| what is non-specific immunity + 2 lines of defense | rapid but don't remember infections, 1) physical and chemical factors in skin, normal flora, and mucous membranes, 2) white blood cells, antimicrobials |
| what is the skin made of and what does fungi produce to break it down? | keratin, keratinase |
| what are mucous membranes? | line gastrointestinal, respiratory and genitourinary tracts |
| what does the mucous membrane have that traps microorganisms? | glycoproteins that are sticky to trap them but to prevent traps from drying out so you can cough to remove them |
| chemical and physical functions of saliva | dilute microorganisms (physical) and produce amylase and lysozymes that break down bacterial cell walls (chemical) |
| what's body odor? | bacteria that live on skin decomposing dead skin cells |
| how do normal microbiota help? | compete with possible pathogens for nutrients and produce substances that are harmful to pathogens |
| what are the 3 components of blood? | 1) cells + cell fragments, 2) plasma where #1 is suspended in, 3) serum which produces antibodies and is the liquid that remains after plasma is clotted |
| what do red blood cells do? | transport O2 and CO2 |
| what are components of white blood cells innate immune system? | neutrophils and monocytes (that also mature into macrophages to perform phagocytosis after differentiation) |
| what % of white blood cells are neutrophils vs monocytes? | 60-70% vs 3-8%!! |
| what is the component of the adaptive immune system? | lymphocytes that learn to recognize invaders |
| how does the lymphatic system work? | blood is carried by capillaries to bathe all cells, blood plasma coats cells (interstitial fluid/I.F.), I.F. is then drained into lymph capillaries and filtered through lymph nodes which carry defnse cells that eliminate infectious agents |
| what is the lymphatic system composed of? | lymph (interstitial fluid washed over cells), lymphatic vessels (where liquid travels), lymphoid tissue (lymph nodes and spleen that filter interstitial fluid and monitor blood, respectively) |
| direction of filtration in lymphatic system | interstitial fluid->lymph capillaries and vessels->lymph nodes->ducts->blood plasma |
| where are lymph nodes and what do they have? | neck, armpits and groin and are sites of T and B-cell activation, part of adaptive immunity to destroy cells |
| what are reticular fibers? | fibers in lymph nodes that physically trap microorganisms |
| what are monocytes and where are they located? | in blood vessels and they squeeze through endothelial cells to assist injured tissue |
| what happens at initial stages of infection? | neutrophils increase concentration and macrophages clean up cell debris |
| what is a DWC? | Differential White Cell count to detect the increased concentration of neutrophils in body due to initial stage of infection |
| what is the residual body in phagocytosis? | indegistible pathogenic/toxin material |
| what is inflammation and what line of defense? | redness, pain, heat, swelling and sometimes seizure and is part of the second line of defense (remember, white blood cells are 2nd) |
| 3 goals of inflammation: | 1) destroy/remove damgaged tissue/cells, 2) confine area of damage, 3) repair/replace damaged tissue/cells |
| 3 stages of inflammation: | 1) vasodilation from histamines that allow neutrophils and macrophages to rush to the area leading to overlapping epithelial cells to spread apart, leaking, 2) phagocyte migration and phagocytosis, 3) tissue repair like pus/scabs |
| what is pus made of? | phagocytes that have engulfed microorganisms, digested them and DIED!! |
| what are CAM and what do they do? | Cellular Adhesion Molecules go to the site of inflammation and help white blood cells adhere to blood vessels and migrate into infected tissue! |
| what do aspirin and ibuprofen do? | reduce prostaglandins (chemical signals) given off by dying cells, so these meds reduce pain and inflammation |
| minimum inhibitory concentration | lowest concentration of a chemical (antibiotic) that prevents bacterial or fungal growth...helps us understand effectiveness of antimicrobial agents |
| what are substances that are antibody generators/elicit an antibody? | antigens |
| where are B-cells derived from? and is it humoral or cell-mediated immunity? | bone marrow, humoral immunity (think humoral refers to bones) |
| where are T-cells derived from? and is it humoral or cell-mediated immunity? | thymus (t for thymus like actually) and cell-mediated immunity since they act on intracellular pathogens |
| do antibodies have the same basic structure? | yes, they vary only in the antigen-binding site region |
| what's an epitope? | region on an antigen that's recognized by antibodies, binds to the paratope on antibodies (each antibody has the same paratope [para the pathogen]) |
| what are cytokines? | produced by T-cells and are chemical messengers that kill infected lymphocytes |
| what is immunity? | ability of an organism to defend itself against infectious agents and other foreign substances |
| what's adaptive immunity? | targets specific pathogens using specialized defenses |
| what's active immunity? | when your body ACTIVELY makes antibodies |
| what's passive immunity? | when your body is given immunity, made by someone else |
| describe natural active immunity | when body makes antibodies in response to antigens |
| describe artificial active immunity | when body makes antibodies through mimicked infections i.e. vaccines think of it like a trial run |
| describe natural passive immunity | like newborns in breastmilk |
| describe artificial passive immunity | antibody injection |
| 2 types of immune responses in adaptive immunity | humoral (free-floating made by bone marrow, antibodies made by B cells), cell-mediated (intracellular, thymus, cytokines by T cells) |
| B cells can become two cell types; name and describe them | plasma: produce antibodies, memory: persist post-infection so body has quicker response |
| T cells can become two cell types; name and describe them | T helper cells: release cytokines to call forth B-cells to produce antibodies, Cytotoxic T Lymphocytes: Kill infected cells by inducing apoptosis (cell suicide) |
| what are antigens? | substances that elicit antibody response (stands for ANTIbody GENerators |
| are antigens always pathogenic? | anything non-self, not always pathogenic includes pollen |
| what's a hapten | molecules that are physically too small to generate antibodies so scientists conjugate them for vaccine usage so their large enough to be recognized by immune system |
| what is the FC region on antibodies and what does it do? | Fragment that can Crystalize and be stuck on surface of a cell (otherwise it's free floating) |
| what is Ig, what does it stand for and how many classes? | Antibodies, Immunglobulin, 5: IgG, IgM, IgA, IgD, IgE |
| What does IgG do? | Good mom, passes placental barrier |
| What does IgM do? | M-ega first reponder that shows up first, part of initial immune response and can later differentiate into memory B cells too |
| What does IgA do? | in sAliva, binds to pathogens preventing pathogens from binding to host cells |
| What does IgD do? | Dexter likes Blood; B-cell memory cells and also connects to IgM since those are first responders |
| What does IgE do? | Eh-chu histamines from allergies |
| why are B cells called that? | they were isolated from the Bursa of Fabricius, an organ in birds |
| what are B cells matured from and do B cells have different antibodies? | stem cells, and yes there are 5 different Ig classes |
| 5 results of Ag-Ab binding: | 1) agglutination, 2) opsonization, 3) neutralization, 4) cytotoxicity, 5) activation of complement |
| what is agglutination? | antibodies have paratopes that bind to epitopes on pathogens, one on each side of Y on antibody, and they can cluster |
| what is opsonization? | pathogens are marked by a protein, opsinin, for phagoyctes to target for phagocytosis |
| what is neutralization? | bacteria is coated with antibodies that prevents proteins on pathogen surface from binding with protein receptors on host cells |
| what is cytotoxicity? | antibodies attach to pathogen and use macrophages and other white blood cells to kill it - antibodies attach to flag natural killer cells and macrophages |
| what is activation of complement? | uses proteins suspended in blood created by the liver to cause cell inflammation and lysis in infected host cells - antibodies binding to pathogen that leads to cell lysis |
| T cell travel arrows | Bone marrow->Thymus (To maTure)->lymphoid tissue (lymph nodes and spleen) |
| Do B AND T cells use antibodies? | NO! B cells have 5 antibody Immunoglobulin classes, T cells produce cytokines that BRING FORTH B-cells to produce antibodies |
| Does HIV use B or T cells? | T cells, since they're intracellular and bind to cell receptor proteins in cytokines IRONIC ASF |
| what are Cytotoxic T Lymphocytes/CD8 T cells? | Cells that have cell receptors that recognize antigens on virus-infected cells to flag them for T cells that release the perforin protein to poke holes in infected cell then releases granxymes to induce apoptosis |
| What do Natural Killer cells do? | work on tumor cells by either initiating apoptosis or puncturing holes in cells; they can detect cells that have become factories for tumor cells as well! |
| Three types of lymphocytes: | B-cells, T-cells, and Natural Killer Cells |
| what's an antibody titer? | blood is drawn out and amount of anitbodies in serum is measured (again, serum is the 3rd component of blood); if you've been exposed to antibodies whether naturally, artificially, pasively or actively, they'll show up in your blood |
| difference between antibody timeline in active vs passive immunity | active immunity (through antigen experience OR vaccines) will persist in body post-infection, passive immunity (through mother's breastmilk OR antibody injection) will last in system for 3 weeks then the body recognizes them as foreign and degrades them |
| primary vs secondary response in immunological memory | primary response is first contact with antigen on pathogen, secondary response is like prior approval to neutralize the specific antigen so the response time is WAAAY faster |
| why is frequent exposure to allergens bad? | first time body is interpreting it and then targets it, second and more times it's developed a secondary response so can lead to airway blockage faster |
| non-specific vs innate vs adaptive immunity | skin+microbiota, neutrophils+macrophages, B+T cells |
Created by:
AKDakd