Exam one: L1-L4 Flashcards

1
Q

L1:Who developed single lensed microscopes?

A

Robert Hooke and Antoni Van Leeuwenhoek

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2
Q

L1: What did Edward Jenner do?

A

reports cowpox vax against smallpox

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3
Q

L1: Florence Nightingale found:

A

hygiene is a great way to avoid infection

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4
Q

L1: Pasteur and Koch found:

A

microbes are causative agents of disease

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5
Q

L1: Hans Christian Gram did:

A

Gram Stain

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6
Q

L1: Alexander Flemming

A

Penicillin

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7
Q

L1: Chain and Florey

A

purification/production

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8
Q

L1: Avery, Macleod, McCarty

A

DNA is a transforming principle

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9
Q

L1: Watson, crick and Franklin

A

DNA structure

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10
Q

L1: Roberts

A

restriction enzymes

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11
Q

L1: Boyer and Cohen

A

recombinant DNA

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12
Q

L1: Kary Mullis

A

PCR

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13
Q

L1: morphology: how big are spheres and rods, and what microscope can you use to see them?

A

spheres are 0.2-2 µm diameter, rods are 0.2-2 µm wide. Can be seen with a light microscope

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14
Q

L1: What is the composition of a bacterial cell?

A

90% similarity to euks.
55% protein, 20% RNA, 3% DNA, 5% carb, 6% phospholipid

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15
Q

L1: What is the only envelope type found in mycoplasma?

A

cytoplasmic membrane

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16
Q

L1: What is present in the GP envelope?

A

capsule, pilli/flagella, PG, Techoic acids, cytoplasmic membrane

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17
Q

L1: What is present in the GN envelope?

A

capsule, pilli/flagella, LPS, PG, Periplasm, cytoplasmic membrane

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18
Q

L1: What part of the LPS is recognized by the immune system? What recognizes it and what does it activate?

A

lipid A tail is recognized by TLR 4 and induces immune response via Il2, Il3 and TNF-a.

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19
Q

L2: What is the origin of the normal microbiota? What is it dependent on?

A

Birth canal, is dependent on the route of delivery, who is present during birth, environment

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20
Q

L2: What factors determine the nature of the microbiota?

A

Local physiology and ecology, diet, microbial attributes, competition

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21
Q

L2: What is the microbiome of the skin?

A

Staph. epidermidis, cutibacterium

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22
Q

L2: What is the normal microbiota of the conjunctiva?

A

S. epidermidis and non-pathogenic corynebacteria

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23
Q

L2: What is the normal microbiota of the mouth?

A

s. mutans on teeth, neisseria and moraxella in throat, anaerobes and microaerophillic organisms in gingival crevice

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24
Q

L2: What is the normal microbiota of the stomach and small intestine?

A

sparsely inhabited bc too acidic

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25
Q

L2: Normal microbiota of the colon?

A

90% anaerobes: bactericides and fusobacterium
10% facultative anaerobes: E.coli, other enterobacteria

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26
Q

L2: What was found in the microbiota of breast-fed infants?

A

Increased bifidobacterium

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27
Q

L2: Normal microbiota of the nose?

A

mostly staph aureus and s. epidermidis

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28
Q

L2: Normal bacteria of the nasopharynx?

A

Similar to mouth but with strep pneumonia, neisseria meningitidis, haemophilus

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29
Q

L2: Normal microbiota of larynx, below mid ear and sinuses?

A

none, protected by mucociliary escalator

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30
Q

L2: Normal microbiota of the urinary tract?

A

scanty microbiota but contamination from perineum in first bit of urethra

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31
Q

L2: Normal Microbiota of the vagina through time?

A

Before puberty/after menopause: mixed, non-specific from skin, colon and perineum

during child bearing Yeats: lactobacillus, anaerobic GNRs, GPCs, mycoplasma, ureaplasma

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32
Q

L2: What is the role of microbiota in disease?

A

opportunists can cause disease and genetic attributes

33
Q

L2: What are the four main beneficial effects of the microbiota?

A
  1. Priming the immune system
  2. exclusionary effect as demonstrated by antibiotic treatment
  3. nutritionally via digestion, malabsorption, vitamin k
  4. normal function of organs/systems
34
Q

L3: What are the steps of patient diagnosis?

A

history, physical exam, imaging

35
Q

L3: What are the steps of specimen identification?

A

description, microscopy, culture, molecular, immune response

36
Q

L3: What do we look for in immune response of specimens?

A

cells present- WBC and where?
Immunoglobulin- Igm, igG

37
Q

L3: How do we identify etiological agents?

A

determine nature of disease, predict course and potential outcomes, tailor therapy, exclude non infectious cause of symptoms

38
Q

L3: What are sterile specimens?

A

urine and blood

39
Q

L3: What are some non-sterile specimens?

A

indirect: specimen collected through a site containing a normal microbiota
OR a site with a normal microbiota

40
Q

L3: What are the different ways we study specimens with microscopy? Type of microscopy and what to see

A

Bright field: gram stain and acid fast
dark field: thin organisms and spirochetes
fluorescence microscopy: very sensitive but artifacts can cause problems

41
Q

L3: How do we culture organisms?

A

with nutrient, selective or indicator media?

42
Q

L3: What are different incubation conditions?

A

temperatures, aerobic, microaerophillic, anaerobic, candle jar

43
Q

L3: What two important tools are required for conventional identification?

A
  • 9 log amplification
  • ability to isolate single cells on a plate
44
Q

L3: What do we look at when identify microbes?

A

gross phenotype, biochemical characteristics, antigenic structures, toxin production, nucleic acid sequences, flow on information

45
Q

L3: What is the serological detection of an infection?

A

identification of host immunoglobulins specifically recognizing antigens from pathogenic organisms

46
Q

L3: How is humoral immune response in an immunocompromised person identified?

A

IgM, clonal switching, IgG.

47
Q

L3: What happens over the Course of a primary response to an infection?

A

10 day latent period, increase in IgM before later increase in IgG, plateau phase around 15 days before decline phase.

48
Q

L3: What happens over the course of a secondary infection?

A

after second exposure, IgM increases around day 5 then decreases while IgG increases steeply and stays high past 10 day mark

49
Q

L3: When would you use a pathogen specific nucleic acid sequence?

A

When organisms are difficult or impossible to cultivate

50
Q

L3: Can a dead pathogen cause an infectious disease or pathology?

A

No, infectious agent must propagate to infect people, and dead pathogen can cause pathology bc of DNA remnants

51
Q

L3: What are some drawbacks of molecular detection?

A
  • false positive results due to contamination
    -contamination obscuring diagnosis
    -limited ability to asses pathogen properties
52
Q

L3: What are the methods of molecular detection?

A

1- PCR
2- PCR and sanger sequencing
3- next gen sequencing

53
Q

L3: What are the sequencing platform requirements?

A
  • accuracy for identification
    -informative about phylogeny
  • accurate evolutionary clock
54
Q

L3: PCR steps?

A
  • extract template
  • amplify target sequence
  • determine DNA sequence of amplicon
  • align DNA sequence with sequences obtained from phenotypically validated isolates
  • establish identification
55
Q

L3: What are some problematic situations for conventional approaches?

A
  • presence of contaminating DNA
  • polymicrobial infection
  • infection at sites with microbiota
56
Q

L3: What are the seps of next gen sequencing?

A
  1. Capture single molecule templates
  2. cluster formation
    - immobilization, 3’ extension, bridge amplification, linearization, 3’ protection, hybridization of sequencing primers
  3. simultaneous sequencing
57
Q

L4: what is a primary pathogen?

A

an organism that infects a competent host

58
Q

L4: What is an opportunistic pathogen?

A

an organism that infects a compromised host via loss of specific defense mechanisms or loss of non-specific defense

59
Q

L4: What in infection and when does it occur?

A

occurs after colonization when multiplication is sufficient to induce damage to the host

60
Q

L4: What are the 5 signs of inflammation?

A

rubor (redness), tumor(swelling), calor(warmth), dalor(pain), LOF

61
Q

L4: what is an infectious dose?

A

quantity of pathogen required to establish infection

62
Q

L4: what are key parameters of exposure?

A

proximity, time, presence/absence of barriers

63
Q

L4: what is net replication?

A

bacterial rep-bacterial death

64
Q

L4: what is a virulence determinant?

A

unique attributes that permit a microbe to successfully establish infection and cause subsequent disease

65
Q

L4: what is virulence?

A

quantitive measure of pathogenicity or likelihood of causing disease

66
Q

L4: What is infectivity?

A

quantitive mausre of pathogens ability to infect another susceptible host, aka attack rate

67
Q

L4: what is the equation for attack rate?

A

infected/#susceptible*100

68
Q

L4: what are the three keys to colonization?

A
  1. adherence via pilli
  2. motility via flagella and chemotaxis
  3. survival or fitness in an environment outside host
69
Q

L4: How do bacteria sequester iron?

A

siderophores from enteric pathogens
lactoferrin/transferrin receptors on mucosal surfaces(gonorrheaoe)

70
Q

L4: How do bacteria avoid host surveillance intracellularly?

A

-live in vacuole and modify or block phagolysosome
- break out of phagolysosome or live in cytoplasm

71
Q

L4: How do T3 secretion systems work?

A

Penetrate three barriers to release effector molecules that lead to intracellular replication

72
Q

L4: How do bacteria avoid host surveillance extracellularly?

A

-Inhibit phagocytosis via capsules, IPA proteases and binding host proteins(M-proteins)
- block complement mediated lysis
- antigenic variation

73
Q

L4: How do bacteria avoid host surveillance by altering host immune response?

A
  • exotoxin: pertussis toxin
  • endotoxin: can overstimulate host=DIC
  • antigenic variation
  • superantigens: polyclonal T-cell proliferation
74
Q

L4: What are the two types of toxins bacteria make?

A

Endotoxin and exotoxin

75
Q

L4: What are the two types of exotoxins and what does each target?

A

A catalytic subunit toxin: targets ADP ribosylates G-proteins
B membrane binding subunit: translocates A subunit into host cytoplasm
RTX: homylsins

76
Q

L4: What are the different endotoxins and what are they present in?

A

endotoxin/LPS: GN
lipoteichoic acid: GP
PG: Both GN and GP

77
Q

L4: What are the three mobile genetic elements?

A
  • carried by bacteriophages: diphtheria
  • plasmids: yersinia adhesions, invasions and effectors
  • transposons: drug resistance
78
Q

L4: How do bacteria regulate virulence determinants?

A
  1. Alter expression of determinants in response to temp, ionic conditions, oxygen concentration, pH
  2. Two component regulatory systems: R S–> S senses environmental stimuli and R is the response regulator