Test 4 – Microbiology – Flashcards
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| pathology |
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| the study of disease |
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| etiology |
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| the study of the cause of disease |
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| pathogenesis |
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| the development of disease (steps) |
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| infection |
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| colonization of the body by pathogens |
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| disease |
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| an abnormal state in which the body is not functioning normally |
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| transient microbiota |
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| may be present for days, weeks, or months |
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| normal microbiota |
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| permanently colonize the host |
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| normal microbiota protects the host by |
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| occupying niches that pathogens might occupy, producing acids (change pH), and producing bacteriocins |
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| bacteriocins |
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| chemical warfare packages that keep number of competing bacteria down |
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| microbial antagonism |
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| a competition between microbes |
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| microbial antagonism example |
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| the growth of the normal microbiota prevents/inhibits the growth of harmful microbes that usually cause disease |
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| types of colonization of bacteria |
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| transient microbiota, normal microbiota, microbial antagonism |
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| symbiosis |
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| the relationship between normal microbiota and the host |
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| commensalism |
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| one organism benefits and the other is unaffected ex: corneum bacteria |
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| mutualism |
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| both organisms benefit ex: e.coli intestine *probiotics* |
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| parasitism |
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| one organism benefits at the expense of the other ex: disease causing baceria detrimental to host |
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| opportunisitic pathogens |
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| beneficial but moves to other parts of body and causes disease there; an organism takes advantage of their environment ex: AIDS & pneumonia |
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| Koch's postulates |
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| are used to prove the cause of an infectious disease. some can cause several disease conditions, some are only in humans. |
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| exception to Koch's postualtes |
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| mutations, most bacteria cannot be grown in pur culture, same disease can be cause by a number of different pathogens, etc. |
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| Koch's postulate #1 |
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| the same pathogen must be present in every case of the disease |
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| Koch's postulate #2 |
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| the pathogen must be isolated from the diseases host and grown in pure culture |
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| Koch's postulate #3 |
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| the pathogen from the pure culture must cause the disease when it is inoculated into a healthy, susceptible subject |
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| Koch's postulate #4 |
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| the pathogen must be isolated from the inoculated animal and must be shown to be the original subject then compared to pathogen grown in pure culture |
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| symptom |
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| a change in body function hat is felt by a patient as a result of disease. qualitative. |
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| sign |
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| a change in a body that can be measure or observed as a result of disease. quantitative. |
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| syndrome |
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| a specific group of signs and symptoms that accompany a disease |
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| epidemiology part 1 |
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| the study of how diseases are transmitted and where and when diseases occur |
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| communicable disease |
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| a disease that is spread from one host to another |
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| contagious disease |
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| a disease that is easily spread from one host to another |
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| noncommunicable disease |
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| a disease that is not transmitted from one host to another |
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| incidence |
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| fraction of a population that contracts a disease during a specific time |
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| prevalence |
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| fraction of a population having a specific disease at a given time |
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| sporadic disease |
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| disease that occurs occasionally in a population |
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| endemic disease |
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| disease constantly present in a population |
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| epidemic disease |
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| disease acquired by many hosts in a given area in a short time |
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| pandemic disease |
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| worldwide epidemic |
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| acute disease |
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| symptoms develop rapidly. short ex: influenza |
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| chronic disease |
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| disease develops slowly. longer. symptoms less severe than acute symptoms ex: mono, hep b, tb |
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| subacute disease |
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| symptoms between acute and chronic. gray are |
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| latent disease |
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| disease with a period of no symptoms when the causative agent is inactive ex: shingles |
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| herd immunity |
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| immunity in most of a population. important in vaccinations |
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| local infection |
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| pathogens are limited to a small area of the body ex: boils |
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| systemic infection |
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| an infection throughout the body ex: measles |
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| focal infection |
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| systemic infection that began as a local infection |
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| sepsis |
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| toxic inflammatory condition arising from the spread of microbes, or their toxins, from a focus of infection |
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| septicemia |
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| blood poisoning |
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| bacteremia |
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| bacteria in the blood |
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| toxemia |
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| toxins in the blood |
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| viremia |
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| viruses in the blood |
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| predisposing factors |
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| gender, inherited traits, climate and weather, nutrition, fatigue, age, lifestyle, chemotherapy, emotional disturbances |
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| stages of disease |
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| incubation, prodromal, illness, decline, convalescence |
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| incubation period |
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| between initial infection and appearance of signs or symptoms |
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| prodromal period |
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| mild, early symptoms |
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| period of illness |
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| most severe, overt signs and symptoms, usually when most deaths occur |
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| period of decline |
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| symptoms decrease and getting better but susceptible to secondary infections by opportunistic pathogens |
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| period of convalescence |
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| regain strength and body returns to normal |
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| reservoirs of infection |
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| continual sources of infection ex: human, animal, nonliving |
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| human reservoir |
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| only effect humans-must reside in patients. carriers may have inapparent infections of latent disease. ex: AIDS, gonorrhea |
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| animal reservoir |
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| live in animals. some zoonoses may be transmitted to humans ex: rabies, lyme disease |
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| nonliving reservoir |
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| found in soil, air, water. ex: botulism, tetanus |
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| 3 ways disease spreads |
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| contact, vehicle, vectors |
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| direct contact |
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| close associations with people ex: kissing, touching |
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| indirect contact |
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| through inaminate objects ex: tissues |
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| inanimate objects are called |
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| fomites |
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| droplet contact |
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| coughing, sneezing, talking |
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| vehicle transmission |
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| inanimate reservoirs, fomites are not reservoirs they are just a mediator |
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| vectors transmission |
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| usually arthoropods ex: fleas, ticks, etc. |
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| vector mechanical transmission |
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| fly walking on a hamburger and don't know where it has been before |
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| vector biological transmission |
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| pathogen reproduces within the vector ex: rocky mountain spotted fever |
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| nosocomial infections are acquired |
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| as a result of a hospital stay. affect 5-15% of all hospital patients |
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| 3 factors that cause nosocomial infecitons |
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| people, compromise of immune systems, improper sterilization of equipment or techniques |
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| nosocomial infections target |
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| burn, surgery, and suppressed immune system patients |
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| nosocomial infections are most often caused by |
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| opportunistic pathogens. normal microbiota getting in wher eit shouldn't be |
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| Centers for Disease Control and Prevention (CDC) |
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| collects and analyzes epidemiological information in the US. Hospitals mandated to report disease. |
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| descriptive epidemiology |
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| collect and analyze data to back track to source of disease |
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| analytical epidemiology |
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| compare diseased group to healthy group-stats |
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| experimental epidemiology |
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| controlled experiments using scientific method |
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| John Snow |
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| mapped the occurrence of cholera in London |
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| Ignaz Semmelweis |
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| showed that handwashing decreased the incidence of puerperal fever |
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| Florence Nightingale |
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| showed that improved sanitation decreased the incidence of epidemic typhus |
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| case reporting |
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| health care workers report specified disease to local, state, and national offices |
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| nationally notifiable diseases |
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| physicians are required to report occurence |
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| mucous membrane portal of entry |
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| respiratory, gastrointestinal, genitourinary, eye |
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| skin portal of entry |
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| sebaceous and sweat glands, hair follicles |
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| parenteral route portal of entry |
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| puncutre in skin |
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| placental portal of entry |
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| mother to unborn child |
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| preferred portal of entry |
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| most pathogens have and if come in a different way it won't do anything or will be mild |
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| plague and anthrax |
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| have multiple portals of entry |
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| ID50 |
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| infectious dose, how many present needed to get 50% of sample population sick. varies with portal of entry. |
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| LD50 |
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| lethal dose, how much is needed to kill 50% of same population. varies by toxin. |
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| adherence |
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| when a pathogen binds to a cell |
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| adherence can be located |
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| on glycocallyx, fimbrae, pili, flagell |
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| what adheres to surface of cell |
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| ligands or biofilms |
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| pathogens penetrate host defenses by |
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| capsules, cell wall components, enzymes, antigenic variation, penetration into the host cell cytoskeleton |
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| penetrate host defense: capsules |
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| make pathogen "invisible" to host defenses; prevent phagocytosis |
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| penetrate host defense: cell wall components |
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| "invisible", proteins that trick cell into thinking it is something good is coming |
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| proteins in cell wall components |
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| M proteins, Opa proteins, mycolic acids (waxy) |
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| penetrate host defense: enzymes |
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| wall-off infection-dissolve blood clots, "liquefies" cells, dissolve connective tissue. IgA antibodies, IgA protease |
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| IgA antibodies and protease |
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| anti: keep pathogens from attaching to mucousal membranes. protease: destroy IgA-produced by pathogens |
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| penetrate host defense: antigenic variation |
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| pathogen alters its antigens and is unaffected by the antibodies produced. activating alternate genes. |
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| penetrate host defense: penetration into the host cell cytoskeleton |
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| modify cytoskeleton of cell, trick actin/cytoskeleton to bring pathogen into the cell |
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| pathogens damage host cells by |
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| using the host's nutrients, direct damage to the vicinity of invasion, production of toxins |
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| pathogens damage host cells: using the host's nutrients |
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| strip away iron from host cell to make available for pathogen causing damage |
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| pathogens damage host cells: direct damage |
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| replication of virus will cause cell to rupture |
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| pathogens damage host cells: production of toxins |
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| waste products are toxic to cells; poisons produced by pathogen. poisons=toxins |
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| endotoxins |
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| components of gram negative bacteria cell walls. cell divides or dies and they are released, making you sick and seems to get worse, but really getting better because the toxin is just being released but not reproduced. |
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| exotoxins |
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| produced by cell and released. actual exotoxins cause signs and symptoms of diseases |
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| portals of exit |
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| respiratory tract, gastrointestinal tract, genitourinary tract, skin, blood |
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| ancient times: honey |
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| egyptians were using honey on wounds. now know it has hydrogen peroxide |
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| ancient times: moldy bread |
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| pushing against skin infections |
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| ancient times: potions |
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| people patenting these and would give to children, would actually make them die because so potent and contained opium. |
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| chemotherapy |
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| the idea of using chemicals to treat disease |
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| antimicrobial drugs |
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| paul elrich. drugs inhibit/interfere with growth of microbes but do not harm the host. led to discovery of sulfa drugs |
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| antibiotic |
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| substances produced by microbes in small amounts that inhibit the growth of other microbes |
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| sulfa drugs |
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| used in world war II with great success and led to increased interest in antibiotics |
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| antibiotics in nature |
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| easy to discover and see but have no clinical use |
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| 1940 oxford |
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| clinical trials in US for penicillin bfound moldy cantelope in Peoria, Illinois a new strain that produced enough penicillin to start clinical trials |
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| narrow-spectrum drug |
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| only affect a select group of microbes |
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| broad-spectrum drug |
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| effect a more diverse range of microbes |
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| hard to find drugs to fight |
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| protozoans, viruses, and tapeworms. viruses use the machinery of host cells so take a risk of killing host cells. |
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| when using broad-spectrum drugs |
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| make sure you don't mess with normal microbiota or you leave open for opportunistic pathogens to enter |
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| super infection |
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| normal microbiota produces excessively due to use of antibiotics |
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| 2 types of action of antimicrobial drugs |
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| bacteriostatic and bactercidal |
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| bactericidal |
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| kill the target organism ex: amino glycides, penicillins, etc. |
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| bacteriostatic |
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| inhibit growth/delay bacter growth and replication ex: tetracycline |
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| basic actions of antimicrobial drugs: inhibit cell wall synthesis |
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| blacking cross links between disaccharides = lysis |
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| basic actions of antimicrobial drugs: inhibition of protein synthesis |
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| change shape of mRNA, ribosomes |
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| basic actions of antimicrobial drugs: inhibition of nucleic acid replication and transcription |
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| block normal growth of cell |
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| basic actions of antimicrobial drugs: injury to plasma membrane |
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| liquify plasma membranes-use as topical ointments to keep local |
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| basic actions of antimicrobial drugs: inhibition of synthesis of essential metabolites |
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| competitive inhibition of enzymatic bacteria. bind to active site of enzymes. |
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| disk-diffusion method |
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| used in lab |
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| E test |
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| estimation minimum inhibitory concentration. strips have gradient of concentration |
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| broth dilution test |
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| look for presence or absence of growth, minimum bactericidal concentration. figures out doses. + and - controls. |
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| 4 mechanisms of resistance |
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| blocking entry, inactivating enzymes, alteration of target molecule, efflux of antibiotic |
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| mechanisms of resistance: blocking entry |
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| cell wall blocks entry |
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| mechanisms of resistance: inactivating enzymes |
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| using enzymes to inactivate target molecule |
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| mechanisms of resistance: alteration of target molecule |
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| target site/molecule is altered so antibiotic can't fit |
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| mechanisms of resistance: efflux of antibiotic |
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| pump out of the cell if have enough through efflux |
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| bacteria become resistant to anitbiotics by |
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| mutation and horizontal gene transfer |
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| can expect that each bacteria colony has |
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| some cells that are mutated |
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| antibiotic misuse |
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| misuse of antibiotics selects for resistance mutants. |
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| synergism |
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| occurs when the effect of two drugs together is greater than the effect of either alone |
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| antagonism |
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| occurs when the effect of two drugs together is less than the effect of either alone |
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| other places for microbial agents |
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| quorum sensing, RNA interference, chemicals already present in plants and animals. animals ex: frogs produce hundreds of peptides on skin that have microbial features |
