Plagues and Pestilence Final – Flashcards
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| symbiosis |
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| relationships between one organism and another |
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| mutualism |
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| relationship in which both partners benefit |
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| commensalism |
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| relationship in which one partner benefits and the other is unaffected |
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| parasitism |
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| relationship in which one partner benefits and the other is harmed |
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| normal microbiota |
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| microorganisms found on the body of a healthy individual. protect against harmful microbiota and stimulate immune system |
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| pathogen |
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| an organism that causes disease in an otherwise healthy person |
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| virulence |
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| quantitative term referring to a pathogen's disease causing ability |
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| opportunist |
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| infection |
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| when colonized organisms have a parasitic relationship with their host |
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| disease |
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| an infection that causes characteristic signs and symptoms |
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| primary infection |
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| initial disease that may cause the host to be prone to other diseases |
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| secondary infection |
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| additional infection resulting from primary infection |
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| communicable disease |
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| A disease that can be transferred from person to person |
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| infectious dose |
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| incubation period |
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| time between introduction of organism to onset of symptoms |
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| phase of illness |
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| follows incubation; individual experiences symptoms of disease |
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| convalescence |
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| recuperation and recovery; infection may still spread |
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| acute disease |
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| rapid onset, lasts short time |
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| chronic disease |
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| symptoms develop slowly and persist |
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| localized disease |
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| infection limited to small area |
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| latent disease |
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| never really goes away, becomes reactive |
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| systemic disease |
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| agent has disseminated or spread throughout the body |
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| viremia |
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| viruses circulating in blood |
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| septicemia |
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| acute life threatening illness caused by infectious agents circulating in blood |
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| toxemia |
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| toxins circulating in blood |
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| Koch's postulate |
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•The microbe must be present in every case of disease •Must be pure culture from diseased host •Same disease must be produced in susceptible experimental host •Must be recovered from experimental host |
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| Molecular Koch's postulates |
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–Virulence factor—gene or products should be found in pathogenic strain –Introduction of cloned virulence gene should change non-pathogenic strain to pathogenic strain and disrupting virulence gene should reduce pathogenicity –Virulence genes must be expressed during disease –Antibodies and immune cells against virulence gene should be protective |
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| Mechanism of pathogenicity |
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| mechanism used to overcome immune response |
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| how does ingesting toxins cause disease? |
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| foodborne intoxication |
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| how does colonization on surface of host followed by toxin production lead to disease? |
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| organism multiplies on host surface then interferes with cell function |
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| how does invasion of host tissues cause disease? |
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| microbes penetrate barriers and multiply in tissues; generally can avoid macrophages |
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| how does invasion of host tissues followed by production of toxins cause disease? |
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| penetration of host barriers with addition of toxin production |
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| what kind of virus is HIV? |
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| ribonucleic acid virus; can only be seen by electron microscope |
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| retrovirus |
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| RNA virus that is replicated in the host cell via enzyme reverse transcriptase to produce DNA from an RNA genome |
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| HIV target |
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| T4 cells |
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| B cells antibodies against HIV |
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| cannot act upon virus hidden in T lymphocytes |
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| what causes death in HIV patients |
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| opportunistic infection |
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| why is it difficult to develop vaccines against hiv? |
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| rapid rate of mutation |
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| AZT |
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| Azidothymidine, inhibits multipication |
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| origin of HIV I |
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| many places/spreads rapidly (hiv IA or IB) |
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| origins of HIV II |
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| west Africa |
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| HIV O |
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| Cameroon and Gabon (has not spread much) |
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| social and global effects of HIV |
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| reduces life expectancy, cripples life expectancy |
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| causative agent of sleeping sickness |
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| trypanosoma (highly pathogenic, death in 4 to 6 months) |
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| winterbottom's sign |
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| swelling of cervical lymphnodes |
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| vector that transmits sleeping sickness to humans |
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| tsetse fly |
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| why is sleeping sickness hard to control |
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| hard to control tsetse fly; treatment requires toxic drugs given intravenously |
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| drugs for sleeping sickness |
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| pentamidine, suramin, and melarsopol |
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| causative agent of river blindness |
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| onchocerca volculus (worm common in Africa) |
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| vector of river blindness worm |
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| transmitted by black fly simulium damnosum |
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| microfilaria |
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| juvenile stages of river blindness worm |
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| how does microfilaria cause blindness in sleeping sickness patients? |
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| microfilaria migrate into eyes invading cornea and retina. body's inflammatory response causes partial loss of vision |
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| what is the proof that guinea worm disease was around in ancient egypt? |
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| calcified worms in mummies |
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| how do humans become infected by guinea worm? |
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| juvenile worms ingested by small shrimp called water flea, humans drink raw contaminated water w/ flea in it |
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| what is the role of stomach gastric juice in the development of guinea worm? |
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| gastric juices digest water fleas, freeing the worms |
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| how is guinea worm currently treated? |
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| no drug treatment is available for this infection. the only treatment is by extracting worms or surgery |
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| focus of guinea worm eradication program |
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| sanitation (passing water through filters) |
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| adherence |
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| first step in colonization and infection, pathogen attaches to host cells to avoid being removed |
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| colonization |
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| establishment to a site of reproduction of microbes on an entity, not necessarily resorting in tissue invasion |
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| type III secretion systems |
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| mechanisms by which bacterial pathogens transfer gene products directly into host cells |
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| toxin |
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| poisonous chemical substance |
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| endotoxin |
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| lipopolysaccharide component of the outer membrane of a gram negative bacteria |
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| exotoxin |
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| toxic protein produced by a microorganism (often simply referred to as a toxin) |
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| neurotoxins |
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| damage to nervous system, major symptom is paralysis |
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| enterotoxin |
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| damages intestines and tissues of digestive tract |
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| cytotoxins |
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| damage to variety of cells; interference with cell function |
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| first antibiotic |
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| discovered the first antibiotic salvarsan |
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| chemotherapeutic agent |
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| chemical used as a therapeutic mediacation |
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| antimicrobial drug or agent |
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| chemical used to treat microbial infection |
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| semisynthetic |
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| antibiotics chemically altered to add new characteristic |
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| antibiotic |
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| chemical produced by molds or bacteria that kills or inhibits growth of microorganisms |
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| broad spectrum antimicrobials |
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| inhibits or kills wide range of organisms |
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| narrow spectrum antimicrobials |
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| inhibit or kill limited range of bacteria |
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| synergistic |
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| agents acting together to produce a greater effect than produced individually |
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| antagonistic |
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| antimicrobial therapy, combination where the actions of one interferes with the actions of the other |
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| additive |
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| combination is neither synergistic or antagonistic |
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| adverse effects of antimicrobial agents |
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| allergic reactions, toxic effects (aplastic anemia), supression of the normal microbiota |
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| minimum inhibitory concentration |
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| lowest concentration of a specific antimicrobial drug needed to prevent the growth of a bacterial strain in vitro |
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| minimum bactericidal concentration |
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| lowest concentration of a specific antimicrobial drug that kills 99.9% of cells of a given strain of bacterial in vitro |
