microbiology final studying

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microbiology final studying
2013-12-09 01:00:13

microbiology terms and concepts ch. 30, 31, and 33
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  1. virulence factors
    • invasiveness
    • infectivity
    • toxigenicity
  2. invasiveness
    motility, flagella
  3. infectivity
    • adherence (adhesion proteins and pilli)
    • capsules
  4. pathogenic potential (Toxigenicity)
    secretion of toxins
  5. host parasite relationship factors
    • number of organisms present
    • degree of virulence
    • host defenses or degree of resistance
  6. Primary vs opportunistic
    • Primary - usually causes disease
    • Opportunistic - isn't in the right place, or over grows, if considerations are right.
  7. zoonoses
    the transfer of disease between species
  8. equation for infection
  9. steps to disease
    • 1) maintain a reservoir
    • 2) transport to host
    • 3) adhere to, colonize, and/or invade host
    • 4) evasion of host defenses
    • 5) multiple or complete the life cycles on or in host
    • 6) damage host
  10. 1) maintain a reservoir
    humans, animals, and environment
  11. 2) transport to host
    direct and indirect contact

    • Indirect: vehicles (soil, food, and water),
    • arthropods, and fomites
  12. 3) attachment and colonization
    pilli, fimbrae, capsule and slim layer, and s layer

    also charged molecules hanging outside of the cell, help it adhere
  13. 4) Evasion
    • prevention of fusion process
    • secretion of pore forming proteins (to colaspe lysome)
    • evading the complement system (moditification of proteins)
    • antigen variation, a race to out modify the immune system
  14. active vs passive invasion
    active - secretion of an enzyme tobreak down host's barrier. 

    passive - through a scrap or puncture by an arthropod.
  15. pathogenicity islands
    genes that cause pathology

    genes that encode the virulence factors
  16. endotoxins vs exotoxins
    endotoxins -  usually gram negative, toxins are in cell wall

    Exotoxins - secreted proteins ofter gram postive, some of the most potent toxins.
  17. Name the four types of exotoxins
    • 1) AB exotoxins (B binds) (Not all AB are type 2)
    • 2) Specific host site bonding (many are AB)
    • 3) membrane disrupting exotoxins (pore forming or degrade membrane)
    • 4) superantigens (overactivates the immune system)
  18. three types examples of host site specific.
    • 1) neurotoxins (neurvous system, Botulism, tetanus)
    • 2) enterotoxins, (vibrocholerae cholera)
    • 3) cytotoxins (cell death, diphtheria, AB, no ribosomal created protein)
  19. membrane disrupting exotoxins, two types
    • 1) pore forming exotoxins
    •      hemolysins from streptococcus and s. Aureus.

    • 2) Phospholipases
    •      causes necrosis of tissues
    •      Gangrene is caused by clostridium profrengenes
  20. superantigens
    the over reaction of the immune system

    a toxins triggers the t-cell response without the antigen presenting cell (APC)

    toxic shock syndrome (icky tampon!)
  21. endotoxins
    lipopolysaccharides (LPS) - lipid A portion of the LPS causes the disease

    • t-cell binds to the lipid A portion
    • not as potent as exotoxins, yes.
  22. describe chemotherapeutic agents and what are they selectively toxic to?
    they are used to treat disease.  They are selectively toxic to 16S Ribosomal DNA in prokaryotes, we have 18S rDNA
  23. When and to what gram type of cell is penicillin most effective?
    Gram positive in the log phase.
  24. What is streptomyocin effective against?
    Turbcurlosis (TB), kills more microbes.  Targets SS ribosomes.
  25. Why is penicillin ineffective against TB?
    thick mycolic acid, stains g(+), but more like gram (-)
  26. general characteristics of antibiotics
    • selective toxicity
    • therapeutic index

    (toxic dose)/(therapeutic does) = TI
  27. level of antimicrobial activity
    • 1) minimal inhibitory concentration (MIC)
    •      where no growth was seen
    • 2) minimal lethal concentration (MLC)
    •      Where subculture does not grow
  28. Four different ways of detecting antimicrobial activity
    • 1) Dilution susceptibility test
    •        Different concentrations of the drug in the media, differentiates the MIC from the MLC

    • 2) Disk diffusion test (Zone of inhibition)
    •           Cannot compare Zone of inhibition directly across different antibiotics)

    • 3) Kirby-Bauer method
    •            Standardized method that compares disk diffusion to the degree of microbial resistance.

    • 4) Epsilemeter test
    •             intersection of elliptical zone of inhibition with strips that indicate MIC (tear shape of inhibition, the microbes are sad and crying) 

    "Death to the Microbes!!" Andrea, otherwise a cheerful person, but not to bad microbes.
  29. Mechanisms of action for microbial drugs
    • 1)  Inhibitors of cell wall synthesis
    • 2)  Nucleic acid synthesis
    • 3)  Metabolic antagonists
    • 4)  Protein synthesis inhibitor
  30. 1) Inhibitors of cell wall synthesis
    • Penicillin
    •      inhibits transpeptidase
    •      competitive inhibitor
    • Semisynthetic Penicillin
    •      broader spectrum
    •      different side groups
    • Cephalosporins
    •      used by most patients that are allergic to penicillin, structually and functionally similar
    • Vancomycin
    •       Targets tetrapeptide linkages by physically binding to aminoacids and sterically blocking the glycosidic linkage and the peptidase.
  31. 2)  Protein synthesis inhibitors
    • aminoglycoside antibiotics
    •      cause misreading of mRNA by binding to the 30s ribosomal subunit, this is bacteriosidal
    • Tetracyclines
    •      reversibly binds to the 30s ribsomal subunit.  Inhibits binding of the aminoacyl-tRNA, bacteriostatic
    • Macrolide
    •      inhibits translocation of tRNA by binding to the 23s rRNA of the 50s ribosomal subunit, somewhat bacteriostaic
    • chloramphenicol
    •       inhibits peptidyl transferase reaction on 50s ribosomal subunit, bacteriostatic
  32. 3) metabolic antagonists
    bind to essential enzymes for metabolic processes by competively inhibiting use of metabolites by key enzymes

    • 1) Sulfonamides
    •          sulfur drugs, an analog for PABA (p-aminobenzoic acid) precurser to make folic acid
    • 2) Trimethoprim
    •          Interferes with folic acid as well, it is a synthetic antibiotic
  33. 4)  Nucleic acid synthesis inhibition
    higher side effects, blocks either DNA replication or DNA transcription

    • Quinolones
    •           bacteriosidal, targets gyrase, which is a topoisomerase
  34. influencing factors of antimicrobial drugs
    • Susceptibilty of pathogen to drug
    • abiltiy of drug to reach:
    •      the site of infection
    •      Concentration in body that exceed pathogen MIC

    Where + how + frequency of admin = speed of metabolism
  35. drug resistance
    • resistance can be transmitted
    • mechanism is not confined to a single drug class
    • resistant mutants arise spontaneously and are selected for
    • Superbugs are resistant to multiple antibiotics
  36. mechanisms of resistance
    • 1) altered antibiotic target - mutation
    • 2) antibiotic resistant genes (pick up plasmids)
    • 3) antibiotic degrading enzyme
    • 4) Antibiotic altering enzyme
    • 5) Make pump to get out of cell
  37. Origin and transmission of drug resistance
    • 1) bacterial chromosomes
    • 2) plasmids
    • 3) transposons/integrons
  38. Epidemiology of Disease
    • Monitor public health data
    • Respond to disease outbreak
    • Investigate emerging and reemerging diseases

    MMWR-Morbidity mortality weekly report
  39. Types of disease
    • Sporadic-occurs occasionally at irregular intervals
    • Endemic-steady low level frequency at moderately regular intercal maintained
    • Epidemic-sudden increase in frequency above expected number
    • Pandemic-increase in disease occurrence within large population over wide region (usually worldwide)
  40. Incidence versus prevalence
    Morbidity versus mortality
    Signs vs symptoms
    #new vs #new+ongoing

    #infected vs # deaths

    Objective vs subjective changes
  41. Course of infectious diseases
    • 1) incubation period
    • 2) prodromal stage
    • 3) Illness
    • 4) Convalescence
  42. Surveillance methods
    • Review of death certificates
    • field investigation of epidemics
    • investigation of actual cases
  43. Remote Sensing and Geographic Information Systems
    • RS-gathering of digital images of Earth's surface
    • GIS-data management systen organizes/displays digital map data
  44. Inf. Dis, Epi,
    • Tries to determine:
    •     Causative agent
    •     source and or reservoir of agent
    •     mechanism of transmission
    •     host/environmental factors facilitating development of disease
    •     best control methods
    • Correlation with single causative agent
  45. Types of epidemics
    • Common source epidemic (food/water)
    • Propagated epidemic (like strep throat)
  46. Herd Immunity
    Resistance of population to infection/spread based on immunizations ~70% optimal
  47. Infectious disease cycle
    • 1) Pathogen
    •          Koch's Postulates
    • 2) Source/Reservoir
    •          S-Source of transmission to host
    •           R-Normal location of pathogen
    • 3) Transmission to host
    •          Airborne, contact, vehicle, vector-borne
    • 4) Susceptibility of host
    • 5) Exit from host
  48. Transmission to host
    • Airborne-Indirect (>1 meter) Direct (<1 meter)
    • Contact-Direct (physical interaction), Indirect (intermediate usually inanimate-fomites), Droplet(large particles)
    • Vehicle-Inanimate objects sometimes single vehicle pathogen to multiple hosts
    • Vector-External (mechanical transmission-passive carriage of pathogen  on body of vector and no growth of pathogen during transmission), Internal (carried within vector 1-harborage transmission: pathogen does not undergo changes within vector, 2-Biological transmission: pathogen undergoes changes within vector)