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Intro Micro Flashcards

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1
Q

Cryptococcus neoformans

A

Only encapsulated yeast

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2
Q

LPS

A

Found in G-ve outer membrane layer (aka endotoxin)

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3
Q

G+ve acids in PG layer

A

Teichoic acid and Lipoteichoic acid

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4
Q

Peptidoglycan (PG)

A

Aka cell wall, thick in G+ve and thin in G-ve; cross-linked NAM and NAG chains
*important target for antibiotics

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5
Q

Gram Staining

A
  1. Crystal violet (stains cell wall)
  2. Iodine (shrinks cell wall)
  3. Decolouriser (removes crystal violet from G-ve cell walls
  4. Safranin (stains cell wall of G-ve pink)
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6
Q

G-ve PG linkage

A

Peptide bond linkage, LPS in outer leaflet, portions in outer membrane (diffusion of specific low molecular weight hydrophilic compounds)

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7
Q

LPS (endotoxin)

A

Lipid A - anchors the LPS in the phospholipid layer and is assoc w/ the sx’s of toxic shock
- LPS is physical barrier to protect the G-ve bacteria

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8
Q

Porins

A

Water-filled open channels that allow passive diffusion of molecules and blocks entry of harmful substances; contributes to abx resistance by G-ve bacteria

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9
Q

G-ve

A

2 layers, LPS/lipoprotein/PG, thin cell wall (PG), periplasmic space, outer membrane, porins, less permeable and more resistant to abx

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10
Q

G+ve

A

1 layer, PG/Teichoic/Lipoteichoic acids, thick cell wall (PG), more permeable and less resistant to abx

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11
Q

Acid Fast Stain

A

used when specimen can’t be stained w/ Gram Stain

  1. Carbol fuschin
  2. Heat 🔥
  3. Decolourise
  4. Methylene Blue
    * stains Mycobacterium and Nocardia
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12
Q

Endospore Stain

A
  1. Malachite green
  2. Steam bath
  3. Water rinse
  4. Safranin (same as last step in Gram Stain)
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13
Q

Endospore

A

Resistant to heat and radiation, keratin-like coat responsible for resistance to chemicals

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14
Q

Capsule

A
  • aka “K antigen”
  • strongly attached/difficult to remove, highly organized, antiphagocytic (important for virulence), protection against dehydration and facilitate attachment to surfaces
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15
Q

Slime Layer

A

Loosely attached/easily removed, unorganized, protection against dehydration and facilitate attachment to surfaces

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16
Q

Flagella

A

Aka “H antigen”

  • cocci are rarely motile they just drift in fluids
  • motility is key for bacteria causing UTIs, motility is turned on or off in response to the env
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17
Q

Endoflagellum

A

Corkscrew motility, “spirochetes” (Borrelia burgdorferi - Lime Dz, Treponema pallidum - Syphilis)

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18
Q

KOH prep

A
  1. 10% KOH
  2. Heat 🔥
  3. Keratin dissolves
  4. Fungal cells visible
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19
Q

Mycoplasmas

A

Atypical bacteria, can’t be gram stained bc no PG cell wall, sterols present in outer cytoplasmic membrane to provide rigidity, capable of independent growth
E.g. - mycoplasma pneumoniae

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20
Q

Actinomycetales

A

Aerobic: mycobacterium (tuberculosis, leprae, marinum) and Nocardia
Anaerobic: actinomyces

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21
Q

Mycobacterium

A 
Mycolic acids (lipids) in CW forming a "waxy" outer coat, slow growth, limited penetration of nutrients; arabinogalactan links mycolic acids to PG
E.g. - Mycobacterium tuberculosis
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22
Q

Chlamydia

A

Unusual lifecycle w/ 2 developmental forms:

  • elementary bodies (EB): infections form
  • reticulate bodies (RB): replicating form
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23
Q

Chlamydia and Rickettsia

A

Can’t survive outside of host cell, can’t be cultured on laboratory medium

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24
Q

Fungi

A

Ergosterol in phospholipid bilayer (target for antifungals), nuclear dsDNA circular, 80S ribosome, diploid gene structure
Cell wall: chitin - made of B(1,4)-linkage of NAGs

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25
Q

Yeast

A

Unicellular fungi that does not grow as hyphae

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26
Q

Mycelium

A

Mat of interwoven hyphae, can be septate or non-septate

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27
Q

Hyphae Tip Extension

A

Growth/extension of hyphae occurs continuously at tips

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28
Q

Hyphae

A

Threadlike, branching, cylindrical tubules composed of fungal cell attached end to end, grow by extending in length from tips

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29
Q

Dimorphism fungi

A

Can grow as either yeast or mold, depending on environmental conditions and temp (usually yeast @ body temps)

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30
Q

Pseudohyphae

A

buds grow but don’t detach; visible constriction, lack permanence/differentiation/true branches/arthrospores and chlamydospores
- e.g. Candida infections

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31
Q

Catalase test

A
  1. Loop of H2O2 onto slide
  2. Mix loop of single colony
  3. If “fizzing” then it is +
    (+ Staphylococcus, - Streptococcus)
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32
Q

Saprophytic fungi

A

Obtain nutrients and energy from dead or decaying organic material (occasionally human tissue)

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33
Q

Superantigens

A

Aka exotoxins, cause activation/proliferation of CD4+ T-cells
E.g. - S. aureus

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34
Q

Cytokine Storm

A

Viral infection causing massive release of IL-1, IL-6, TNF-a
E.g. - SARS (IFN type I release)

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35
Q

Enterotoxins

A

Released from the microbe, so a form of exotoxins

E.g. - anthrax lethal toxin, shiga toxin, cholera toxin

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36
Q

Herx Reaction

A

Cause: rapid release of LPS endotoxin from killing bacteria too fast w/ anti-microbial tx
ROS: fever, chills, HA, hypotension, can cause death
*resembles bacterial sepsis

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37
Q

PANDAS

A

Pediatric Autoimune Neuropsychiuatric Disorders Assoc w/ Streptococcal infections
*Sydenham’s chorea

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38
Q

Asplenic Pt’s

A

Susceptibility: encapsulated organisms usually cleared through opsoinzation w/ Abs
E.g. - pneumococcal, meningococcal, and Haemophilus influenzae
*highest risk is w/in first 2 yrs s/p splenectomy

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39
Q

Direct Transmission

A

Sexual; skin-skin (MRSA), animal bites, droplets (Pertussis)

*e.g. - Gonorrhea (sexual; humans), Tetanus (soil), Rabies (animals)

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40
Q

Indirect Transmission

A

Vehicles, vectors, airborne/aerosols

*e.g. - Dengue (mosquito-human), West Nile (mosquitoes-birds)

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41
Q

Airborn Transmission

A 
Droplet nuclei are suspended in the air for a long period of time; droplet nuclei = dried residue < 5 micrometers 
E.g. - measles
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42
Q

Vehicles

A

Food, water, blood (biological stuff), fomites (inanimate objects like door handles/clothing)
- can passively carry or provide growth environment for pathogen and its products

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43
Q

Propogative

A

Multiplies but no change/development

E.g. - bacteria

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44
Q

Cyclopropogative

A

Multiplies AND changes/develops

E.g. - Protozoa

45
Q

Cyclodevelopmental

A

Develops but does NOT multiply
E.g. - most nematodes and trematodes
*1 larvae = 1 adult

46
Q

Sanitation

A

Reduce #s to acceptable public health level

47
Q

Sterilization

A

Destruction of all micro organisms

48
Q

Disinfectant

A

Sterilization/sanitation used only on inanimate objects

*e.g. - bleach would only be used as disinfectant

49
Q

Antiseptic

A

Sanitation/sterilization used on living tissue

50
Q

Most resistant microorganisms

A
  1. Prions
  2. Endospores
  3. Mycobacteria
  4. Small naked viruses
    * (G-ve are more resistant than G+ve)
51
Q

Virulence

A

Damage in a susceptible host due to host-microbe interaction

*(what microbe is doing and how host is responding)

52
Q

Pathogenicity

A

Ability to cause damage and infection, must look at virulence factors to determine pathogenicity

53
Q

Acute Infection

A

Incubation and prodrome shorter, more severe symptoms than persistent

54
Q

Persistent Infection

A

Longer incubation, prodrome and duration of symptoms (less severe sx’s than acute infection)
*takes body a long time to get rid of the infection

55
Q

Prodromal

A

Nonspecific symptoms that are too vague to be able to diagnose what organism is infecting

56
Q

Chronic Persistent Infection

A

Long duration, develops slowly, shedding continues
*more about the physical process
E.g. - typhoid fever, leprosy, syphilis

57
Q

Latent Persistent Infections

A

Genome maintained in host in absence of microbial replication
E.g. - TB

58
Q

Intoxication

A

Ingest food or something with toxin in it

59
Q

Infection

A

Ingest bacterium that is actively releasing a toxin

60
Q

Class I Toxins

A

Membrane acting/bind to host cell surface

61
Q

Class II Toxins

A

Membrane damaging

62
Q

Class III Toxins

A

Intracellular toxin

63
Q

Tetanus Toxin

A

Producer: Clostridium tetani
Effect: Zn2+ dependent protease that inhibits neurotransmission at inhibitory synapses
ROS: spastic paralysis

64
Q

Pertussis Toxin

A

Producer: Bordetella pertussis
Effect: ADP-ribosylation of G proteins, blocks inhibition of adenylate cyclase
ROS: cough

65
Q

Toxic Shock Syndrome Toxin

A

Producer: S. aureus
Effect: acts on vascular system causing inflammation
ROS: fever and shock

66
Q

Pyogenic Exotoxins

A

Producer: Streptococcus pyogenes
Effect: localized erythematous rxn

67
Q

Hyaluronidase

A

Breaks down hyaluronic acid in CT and allows the microbe to be able to spread

68
Q

Catalase

A

Breakdown H2O2

69
Q

Urease

A

Inactivate urea to make an acidic environment more alkaline

e.g. - H. pylori

70
Q

Coagulase

A

Converts fibrinogen to fibrin in order to form clots

71
Q

Neuraminidase

A

Degrade sialic acid

- Why?

72
Q

Vibrio cholerae Infectious Dose

A 
Water = 10^4 - 10^6
Food = 10^2 - 10^4
73
Q

Mycobacterium tuberculosis Infectious Dose

A

10 bacilli

74
Q

Staph aureus Incubation Period

A

2-4 hours

*infectious dose impacts incubation period

75
Q

Tetanus Incubation Period

A

4 days to weeks

*infectious dose impacts incubation period

76
Q

Plasmodium (malaria) Incubation Period

A

7-30 days

*infectious dose impacts incubation period

77
Q

Ways microorganisms survive transmission?

A

Cyst, endospore, vectors, etc.

78
Q

Disinfectants useful against bacterial spores?

A

Hydrogen Peroxide, Formaldehyde, Chlorine

79
Q

Site of entry?

A

usually the same as the site of exit

Pertussis - respiratory, salmonella - GI, gonorrhea - GU, trachomatis - eyes, S. Aureus - skin

80
Q

True infections

A

Don’t require pre-existing host compromise aka can infect uncompromised host, sometimes the exposure is due to accidental contact
(*true pathogens can also be opportunistic)

81
Q

Opportunistic Infection

A

Always requires pre-existing host compromise aka cannot infect uncompromised host, usually exposure is due to accidental contact
*opportunistic pathogens are mostly opportunistic

82
Q

Components of Exotoxins?

A

A - for Active (enzymatic)

B - for Binding (G proteins etc.)

83
Q

Adhesion of Microbes

A

Nonspecific or specific, can involve specialized (e.g. - pili/fimbriae) or non-specialized structures (e.g. - capsule)
Role: prevent removal

84
Q

Adhesins

A

Ligands that help indicate tissue tropism, component on bacterial cell used for attachment to a tissue, cell or surface
(Fimbriae/pili, TA and LTA in G+ve, LPS in G-ve)

85
Q

Receptors

A

Indicates tissue tropism, host cell molecule that bacterial adhesins attach to

86
Q

Tropism of Streptococcus mutants

A

Bacterial adhesin: cell-bound protein

Location of relevant host cell receptor: pellicle of tooth

87
Q

Tropism of uropathogenic E. coli

A

Bacterial adhesin: Type I or P fimbriae

Location of relevant host cell receptor: GU epithelium

88
Q

Biofilm Formation

A

Attachment to surface, replication and microbe production of sticky expolymeric substance (EPS) coating
*default mode of growth for microbes

89
Q

Advantages of Biofilm Formation

A
  1. Better resistance to antimicrobial agents
  2. Resists host immune response
  3. Acts as reservoir
90
Q

Acquisition of Iron by microbes

A
  1. Surface receptors binding to iron containing compounds (OMPs of Neisseria)
  2. Produce siderophores to chelate iron (E. coli and K. pneumoniae)
  3. Reduction of Fe3+ in protein complex to Fe+ which releases gather iron by changing the affinity of the chelator (L. monocytogenes)
91
Q

Siderophore

A

Synthesis is triggered by iron limitation conditions, has high affinity for iron, siderophore-iron complexes are taken up by surface siderophore receptors and transported into the microbe

92
Q

Iron in the body? (Susceptibility)

A

Enhanced susceptibility (bc microorganisms need it and if you have a lot of it they’ll chill and take your iron)

93
Q

Intracellular Phase for Growth

A

Obligate - Chlamydia trachomatis
Facultative - Salmonella
Not necessary - Vibrio cholerae

94
Q

Streptokinase/Staphylokinase (“invasins”)

A

Converts plasminogen to plasmin (protease), used by host to dissolve fibrin clots
*in absence of streptokinase there is an abscess formed by fibrin barrier, with presence of streptokinase the fibrin barrier is broken down by plasmin enabling spread

95
Q

Virulence: exotoxins

A

Cell damage and release of nutrients; evasion of host immune system

96
Q

Virulence: Biofilm Formation

A

Evasion of host immune system; resistance to chemicals

97
Q

Virulence: Ag variation

A

Evade host immune system

98
Q

Virulence: Secreted Toxins

A

Release of nutrients; breakdown of tissue barriers; evasion of host immune system

99
Q

Virulence: Dimorphism

A

Able to adapt to body environment

100
Q

Virulence: Survival at 37C

A

Adaptation to body environment

101
Q

Virulence: Attachment

A

Prevents removal

102
Q

Virulence: Degradative Enzymes

A

Breakdown of tissue barriers; release of nutrients

103
Q

Chediak-Hegashi Syndrome

A

Can’t traffic the engulfed microorganism to be destroyed

104
Q

Chronic Granulomatous Dz

A

Mechanism: impaired NADPH oxidase function, pathogens are phagocytosis but not digested
ROS: infections w/ S. areus, Aspergillis and Candida

105
Q

Leukocyte Adhesion Deficiency (LAD)

A

Defect: CD18
Mechanism: neutrophils and other cells cannot emigrate through the vessel wall to infected site
ROS: delayed separation of umbilical cord
Tx: BMT

106
Q

Duncan Syndrome

A

*X-linked
Mechanism: functional suppression of T cells that renders them incapable of killing EBV infected B cells
ROS: no major sx’s until they get EBV

107
Q

Wiskott-Aldrich Syndrome

A

ROS: pyogenic infections, eczema and thrombocytopenia (leads to patechiae)

108
Q

Encapsulated Organisms (capsule is #1 virulence factor)

A

Some Killers Have Pretty Nice Slimy Capsules

  • Strep pneumo
  • Klebsiella
  • H.influenzae
  • Pseudomonas
  • Neisseria meningiditis
  • Salmonella
  • Cryptococcus neoformans
109
Q

Silent Subclinical Viruses?

A

CMV and EBV, causes life-long infection

Microbiology (14 decks)

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