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exam 4
chapter 15.2
| Question | Answer |
|---|---|
| Set of standards that must be met to demonstrate that X pathogen causes X disease | koch's postulates |
| when was it developed? | 1884, still used today |
| 1st postulate | the suspected pathogen must be found in every case of disease and not be found in healthy individuals |
| 2nd postulate | the suspected pathogen can be isolated and grown in pure culture |
| 3rd postulate | a healthy test subject infected with the suspected pathogen must develop the same signs and symptoms of disease as aseen in postulate 1 |
| 4th postuate | the pathogen must be re-isolated from the new host and must be identical to the pathogen from postulate 2 |
| koch's wrong assumptions | pathogens are found only in disease individuals, all subjects are equally susceptible to infection, all pathogens can be grown in a culture |
| what is the name of the improved postualtes? | molecular koch's postulates |
| how did the postulates imporve? | with molecular methodologies, overcame some of koch;s limitations, identifies genes instead of pathogen |
| molecular koch's postualtes 1. | the phenotype should be associated only with pathogenic strains of a species ex:EHEC causes intestinal inflimmation where as nonpathogenic strands of e.coli does not |
| molecular postulates 2 | inactivation of the suspected gene(s) associated with pathogenicity should result in a measurable loss pf pathogenicity; ex: when a gene is EHEC in inavtivated, it reduces its abilty to cause disease |
| molecular postulate 3 | reversion of the inactive gene should restore the disease phenotype ex: when gene is coded back in for toxin, it causes disease |
| current limitations of koch | genetic manipulation of some organisms isnt possible iwth current techniques, some diseases do not have suitable animal models |
| definition of pathogenicity | ability of pathogen to cause disease |
| definition of virulence | degree of pathogenicity, continuum, ex: anthracis is highly virulent, rhinovirus is low virulent |
| virulence curve | virulence that is modeled in a controlled experiment |
| median infectious dose | number of pathogens required to INFECT 50%of those inncolucated |
| median lethal dose | number of pathogens required to KILL 50%of those infected |
| primary pathogen | cause disease in a host regardless of host's resident microbiota or immune system, ex:enterohemmorhagic e. coli (shiga toxin) |
| opportunistis pathogen | can only cause disease in situations that compromise the host's defenses, like protective barriers, immune system, or normal microbiota, ex: candida albicans with disrupted microbiota, can cause UTI caused by e.coli |
| what can effect susceptibility to disease | drugs, resident microbiota, genetics, and age can all influence susceptibility to disease |
| 5 stages of pathogenecity/infection | exposure to host, adhesion, invasion, infection, and transmission |
| exposure, or contact can occur by | pathogens being exposed to portals of entry ti begin adhesion, mucosa entry is worse (example: uninary, gastro, and respitory) pathogen is usually suited for portal |
| parental route | goes through a break in the skin |
| TORCH are pathogens that | cross the placenta barrier as portal of entry |
| adhesion factors | adhesins and biofilm |
| adhesins are | molecule/structures that bind to certain host receptors |
| biofilms are | production of community glycocalyx |
| invasion occurs when | colonization is established |
| pathogens produce toxins to | allow further colonization into the body.tissue and protection from immune system |
| virulence helps with | the degree of invasion example: Heliobacter pylori urease production to neutralize stomach acid |
| intracellular pathogens invade by | endocytosis and envasion of homt immune defenses |
| invasion mechanisms are | effector protiens secreted to trigger entry membran ruffling (exL slmonella and shigella) |
| another invasion mechanism is | surface protiens allow for binding to host cell (trojan horse approach) |
| some pathogens are able to survive | phagolysosomes within WBCs (listeria, monoctogenes, and mycobacterium tuberculosis |
| multiplication leads to | established host infection |
| local type of infection | small area of the body |
| focal infection | pathogen or toxin spreads to secondary location |
| systematic infection | occurs throughout body (ex: septicemia), focal: blood |
| primary infections can lead to | seconday infection of different pathogen ex: HIV lowers immune system and opens doors for yeast and others, rhinoviruses can lead to bacterial pneumonia |
| portal of exit | where the pathogen exits to transmit to a new host |
Created by:
olivemaryjo
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