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*med3* > Infectious Disease - Basics of Microbiology > Flashcards

Infectious Disease - Basics of Microbiology Flashcards

1
Q

What are the 2 types of organisms?

A

prokaryotes and eukaryotes

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2
Q

What type of organism is bacteria?

A

prokaryotes

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3
Q

what are the characteristics of prokaryotes?

A

very old form of life

no membrane bound organelles

no nucleus

nuclear material

free inside cell

bacteria are prokaryotes

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4
Q

what are the characteristics of eukaryotes?

A

more modern form of life

membrane bound organelles

nucleus

plant and animal cells

protozoa

fungi

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5
Q

What makes bacteria unique?

A

they are prokaryotes and a very old form of life

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6
Q

What color are gram positive organisms on a gram stain?

A

purple

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7
Q

What color are gram negative organisms on a gram stain?

A

red

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8
Q

what is the difference between gram positive and gram negative organisms?

A

the contents of their cell wall gram positive have a very thick cell wall allowing for it to take up the gram stain and they have lipoteichoic acids gram negative have a much thinner cell wall/periplasm and an outer membrane

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9
Q

what is unique to gram negative bacteria?

A

their outer membrane

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10
Q

what is peptidoglycan?

A

major structural component of bacterial cell walls

polymer sheets of sugars and peptides

sheets cross-linked to other sheets

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11
Q

what are peptidoglycans composed of?

A

sugars (NAG & NAM)

peptides - attach to NAM****; 3-5 aa long

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12
Q

what is the quaternary structure of peptidoglycan?

A

sugar/peptide backbone makes chains that cross link with peptide cross bridges

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13
Q

Why is peptidoglycan a target for some antibiotics?

A

human cells don’t have peptidoglycan

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14
Q

what is the difference in the peptidoglycan in gram positive vs negative?

A

gram positive = up to 40 sheets; composes 50% or more of the cell wall

gram negative = very few sheets; only 5-10% of cell wall

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15
Q

why do gram positive bugs stain purple?

A

because of the thick peptidoglycan layer in their cell wall traps the dye

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16
Q

Which bacteria have unique cell walls?

A

mycoplasma

mycobacteria

chlamydia

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17
Q

characteristics of mycoplasma

A

no cell wall does not gram stain cell membrane has sterols for extra stability

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18
Q

characteristics of mycobacteria

A

cell wall has MYCOlic acid does not gram stain well special stain used (Ziehl-Neelsen)

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19
Q

What makes the cell wall of chlamydia special?

A

lacks muramic acid

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20
Q

What are the characteristics of the cell membrane in bacteria?

A

lipoprotein bilayer electron transport and ox phos enzymes and carrier molecules (bacteria lack mitochondria)

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21
Q

what is a unique feature of gram + bacteria that drives immune rxns?

A

LTA - lipoteichoic acid

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22
Q

what is LTA?

A

major surface antigen that drives immune rxns

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23
Q

LTA has induced what abnormalities in animal studies?

A

arthritis uveitis meningeal inflammation cascades resulting in septic shock and multi organ failure

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24
Q

what does LTA induce release of?

A

cytokines

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25
Q

LTA binds _____ and activates _________.

A

antibodies; complement cascade

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26
Q

What are the 2 unique features of gram negative bacteria?

A

periplasm outer membrane

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27
Q

what is periplasm? what does it contain?

A

space btwn cell membrane and outer membrane contains many enzymes

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28
Q

What is the main factor driving an immune response for gram + bacteria?

A

LTA

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29
Q

what are the most important enzymes in the periplasm?

A

ß-lactamases - inactivates Antibiotics

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30
Q

what is special about the enzymes found in the periplasm?

A

they allow the gram neg bacteria to resist antibiotics that have a ß-lactam structure

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31
Q

what is the most important component of the outer membrane of gram neg bacteria?

A

LPS - lipopolysaccharide

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32
Q

What is a major immune trigger for gram negative bacteria?

A

LPS

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33
Q

what are the components of LPS?

A

polysaccharide lipid A O antigen

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34
Q

lipid A

A

highly toxic triggers cytokine release

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35
Q

O antigen

A

target for antibodies

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36
Q

what are bacterial capsules?

A

sticky, gelatinous layer secreted by the bacteria that helps it to attach to host cells and protects against phagocytosis

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37
Q

what are capsules composed of?

A

mainly water with some polysaccharide

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38
Q

what is the exception for bacillus anthracis capsule?

A

capsule is protein = d-glutamate

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39
Q

what is d-glutamate?

A

major virulence factor that allows unimpeded growth

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40
Q

where is d-glutamate found?

A

capsule of bacillus anthracis

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41
Q

What is the quelling rxn used for?

A

detects capsule - mainly used to detect if strep pneumonia was the cause of a bacterial lung infection

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42
Q

How is the quelling rxn performed?

A

take rabbit antiserum and add it to bacterial slide capsule swells when visualized under the microscope

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43
Q

what are the + quelling rxn encapsulated bugs?

A

strep pneumonia H. influenza N. meningitidis E. Coli Salmonella Klebsiella Group B strep (agalactiae)

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44
Q

how does the body defend itself against encapsulated bacteria?

A
  1. B-cells secrete capsular antibodies (IgG) - antibodies bind capsule to tag it for phagocytosis via Fc receptors 2. antibodies that bind to capsule can activate the complement cascade
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45
Q

what happens when the complement cascade gets activated?

A

formation of MAC –> Cell death formation of C3b –> opsonin

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46
Q

Loss of what will cause recurrent encapsulated bacterial infections?

A

loss of antibodies/b-cells or complement

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47
Q

patients without what organ are at a higher risk for infection from encapsulated bacteria?

A

spleen (i.e. sickle cell) asplenia = risk of sepsis from encapsulated bacteria; loss of splenic phagocytes

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48
Q

what is the basis for bacterial vaccines?

A

capsular polysaccharides

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49
Q

why is the polysaccharide capsule conjugated to an immune stimulator protein?

A

polysaccharides in capsule are weakly immunogenic

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50
Q

what is a glycocalyx?

A

“sugar coat” made of polysaccharides

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51
Q

what does bacteria use a glycocalyx for?

A

to adhere to surfaces (catheters)

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52
Q

what is the difference between the bacteria that use a capsule vs glycocalyx?

A

bacteria with distinct, firmly attached gelatinous layer = capsule bacteria with irregular, slimy fuzz layer = glycocalyx

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53
Q

major bacteria that uses a glycocalyx coat

A

S. epidermis - forms biofilm on catheters

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54
Q

Pili and fimbria are structurally similar to _____

A

flagella

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55
Q

what are pili/fimbria?

A

appendage/arm of bacteria, made of proteins

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56
Q

ordinary pili allows for adherence to ______

A

surfaces

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57
Q

_____ _____ attach to another bacteria for conjugation

A

sex pili

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58
Q

What is important about the pili of E. coli?

A

allows to attach in the urinary tract causing UTIs/pyelonephritis

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59
Q

what bacteria have pili with antigenic variation?

A

Neisseria Gonorrhea

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60
Q

What is antigenic variation?

A

bacteria change the makeup of the proteins of their pili

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61
Q

what are plasmids?

A

small DNA molecule within a cell, physically separated

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62
Q

What are flagella?

A

long protein arms that bacteria use to move

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63
Q

What are ribosomes?

A

site of protein synthesis

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64
Q

what are the subunits for bacterial ribosomes?

A

50S & 30S

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65
Q

Why do some antibiotics target bacterial ribosomes? (i.e. tetracyclines bind 30S subunit)

A

bacterial ribosomes differ from eukaryotic ribosomes which allows to selectively target the bacterial ribosome subunit

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66
Q

MOA aminoglycosides

A

interferes with 30S protein synthesis

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67
Q

some bacteria can enter a dormant state called _________

A

a spore “spore forming bacteria”

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68
Q

how are spores advantageous?

A

can survive a long period of starvation resistant to dehydration, heat, chemicals

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69
Q

are spores metabolically active?

A

no they are like a seed that has the potential to grow in the right conditions

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70
Q

what are the components of a spore?

A

coat - outermost cortex/core wall - innermost dipicolinic acid

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71
Q

what is the function of the spore coat?

A

impermeable to many chemicals and antibacterial agents

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72
Q

what are the spore components made out of?

A

coat = keratin-like protein cortex/core wall = peptidoglycans

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73
Q

dipicolinic acid may help with _________ __________

A

heat resistance

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74
Q

why is it difficult to kill a spore?

A

because their keratin-like coat is impermeable to many chemicals and antibacterial agents

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75
Q

what is found in large amounts within a spore?

A

dipicolinic acid

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76
Q

what are the major spore forming bacteria? (5)

A

Bacillus anthracis Bacillus cereus Clostridium perfringens Clostridium tetani Clostridium botulinum

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77
Q

what are the 3 methods used to identify bacteria?

A

shape color after staining special tests

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78
Q

what are the 3 common bacterial shapes?

A

cocci - sphere bacilli - rod coccobacillus - mixture

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79
Q

what are the patterns seen for cocci?

A

diplococci - pairs streptococci - chains staphylococci - bunches/clusters

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80
Q

why/how do streptococci form chains?

A

each new bacteria forms away from the older bacteria so that you get them forming away from each other to get these long curved chains

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81
Q

most cocci are gram ____

A

positive

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82
Q

what are the 2 main gram positive cocci?

A

streptococcus and staphylococcus

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83
Q

what are the gram negative cocci bacteria?

A

Neisseria (meningitidis/gonorrhea) Moraxella catarrhalis

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84
Q

rods are also called what?

A

bacilli

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85
Q

most rods and coccobacillus are gram _____

A

negative

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86
Q

what are the few gram positive rods?

A

Corynebacterium (diphtheria) Clostridium Listeria Bacillus (anthrax, cereus)

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87
Q

what are some other less common bacteria shapes?

A

branching/filamentous spirochetes vibrio

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88
Q

Main bacteria that have a branching/filamentous shape

A

actinomycetes nocardia

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89
Q

Branching/filamentous bacteria look like _____

A

fungi

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90
Q

what are the main spirochetes?

A

Treponema (syphilis) Borrelia (Lyme disease) Leptospira (leptospirosis)

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91
Q

what 2 bacteria are described as being pleomorphic and an obligate intracellular pathogen?

A

Rickettsia Chlamydia

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92
Q

What are pleomorphic bacteria?

A

bacteria that can take on many shapes

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93
Q

What are the common bacterial stains?

A

gram stain Giemsa Ziehl-Neelsen Silver India ink - crypto coccus (fungi)

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94
Q

what are the simple stains used to visualize bacteria?

A

methylene blue safranin crystal violet

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95
Q

what are the steps of a gram stain?

A

fixation crystal violet iodine (all bacteria look purple) decolorization - gram Positive are Purple safranin - gram Positive still Purple, gram negative are red/pink

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96
Q

what color is gram positive on a gram stain? why?

A

Positive = Purple they retain crystal violet in cell walls to look purple

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97
Q

what color is gram negative on gram stain? why?

A

red = do not retain crystal violet in cell walls - take up safranin counter stain

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98
Q

why is gram positive purple?

A

thick cell wall of peptidoglycan in gram positive bacteria

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99
Q

What bugs do not gram stain well?

A

treponema (syphilis) - too thin to see mycobacteria (tuberculosis) - mycolic acids in cell wall mycoplasma - no cell wall intracellular bacteria

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100
Q

what are the main intracellular bacteria?

A

Rickettsia - obligate intracellular Chlamydia - obligate intracellular; no muramic acid cell wall Legionella - mostly intracellular

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101
Q

what is the stain used for mycobacteria called?

A

acid fast

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102
Q

what is muramic acid?

A

1 of the 2 components of peptidoglycan

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103
Q

What is the Giemsa stain?

A

mixture of methylene blue, eosin, and Azure B

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104
Q

How does the Giemsa stain work?

A

enters cells and stains nucleic acids

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105
Q

What is the Giemsa stain used for?

A

protozoa - plasmodium & trypanosomes intracellular bugs -chlamydia, rickettsia, borrelia (sometimes intracellular)

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106
Q

Giemsa stain is used for what purpose?

A

to get inside the cells

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107
Q

What is the Ziehl-Neelsen stain?

A

acid-fast stain used to detect mycobacterium (esp. TB), nocardia

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108
Q

What is carbolfuschin?

A

used in the acid-fast stain to visualize mycobacterium (esp. TB) also used for nocardia

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109
Q

How does the acid fast stain work?

A

carbolfuschin stains everything purple then acid solvent is used to decolorize anything that is not an acid fast bug

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110
Q

The silver stain is used for what 3 organisms?

A

Pneumocystis pneumonia (HIV/AIDS) Legionella H. Pylori

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111
Q

contaminated water w/ outbreaks in nursing homes is characteristic of what bacteria?

A

Legionella

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112
Q

Gastric ulcers are caused by what bacteria?

A

H. Pylori

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113
Q

What stain is used for fungi and yeast?

A

india ink

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114
Q

what is different about India ink?

A

it is a negative stain, meaning it makes the background very dark not the organisms and the unstained organisms stand out in contrast to the dark background

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115
Q

India ink is used primarily to detect what bacteria?

A

cryptococcus neoformans

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116
Q

When stained with India ink, what pattern will you see if the is cryptococcus neoformans present?

A

the large polysaccharide capsule creates halos

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117
Q

what is cryptococcus neoformans?

A

a fungi that exists as a yeast

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118
Q

What special color is associated with each of the following bacteria? staph aureus pseudomonas aeruginosa serrate actinomyces

A

staph aureus - golden, yellow pseudomonas aeruginosa - blue-green (pyocyanin) serrate - red actinomyces - yellow-orange

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119
Q

when actinomyces “Cement” together what are they called?

A

sulfur granules

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120
Q

what does “aureus” mean?

A

gold

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121
Q

growth plates generally use what substance?

A

agar

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122
Q

what is needed for a growth plate?

A

agar in Petri dish nutrients added to support growth - sugar, water, salts, amino acids

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123
Q

what is agar?

A

semi-solid substance made from seaweed

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124
Q

why is agar used on growth plates?

A

because bacteria usually don’t consume/decompose it so it will be there indefinitely to grow on top of

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125
Q

what are the two types of culture media?

A

non-selective & selective

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126
Q

what are non-selective culture media’s used for?

A

general purpose, can grow many bugs

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127
Q

nutrient agar is what type of culture media?

A

non-selective

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128
Q

what is the most commonly used non-selective media?

A

blood agar

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129
Q

which type of culture media contain toxic substances?

A

selective culture media

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130
Q

What grows on Thayer-Martin media?

A

Neisseria

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131
Q

what is a disadvantage to using selective media?

A

contains toxic substances

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132
Q

what does it mean for a culture medium to be enriched?

A

special nutrients added so many bugs will grow

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133
Q

what does it mean for a culture medium to be differential?

A

different bugs grow with different patterns

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134
Q

What is blood agar enriched with?

A

sheeps blood

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135
Q

Why is blood agar considered a differential medium?

A

because some use alpha hemolysis and some use beta hemolysis

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136
Q

what type of culture media is blood agar?

A

enriched - blood differential - hemolytic patterns

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137
Q

what type of culture media is eosin methylene blue?

A

selective - only gram neg. differential - lactose fermenters

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138
Q

what do fastidious bacteria require?

A

special nutrients, won’t grow on standard media

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139
Q

what are 2 important fastidious bacteria?

A

H. Influenza Legionella

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140
Q

what type of culture media is blood agar?

A

contain mammalian blood - usually 5% sheep blood non-selective enriched - blood differential - hemolysis pattern

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141
Q

What hemolysis patterns are seen on blood agar?

A

alpha, beta, gamma

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142
Q

why is there a zone a white around the beta hemolytic bacteria?

A

because they are completely hemolyzing all the blood cells that are around them

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143
Q

What are the different patterns of hemolysis on blood agar?

A

beta = lysis alpha = partial gamma = no lysis

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144
Q

why is blood agar so useful for identifying bacteria?

A

because it distinguishes a lot of different kinds of streptococcus

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145
Q

most gram positive bacteria are of what shape?

A

cocci

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146
Q

cocci are split into what 2 groups?

A

catalase (+) clusters - staph catalase (-) chains - strep

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147
Q

How do you distinguish between different types of strep?

A

see hemolysis pattern on blood agar

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148
Q

What strep are beta hemolytic?

A

s. progenies (group A) s. agalactiae (group B)

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149
Q

what strep are alpha hemolytic?

A

s. pneumonia s. viridans

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150
Q

what strep are gamma hemolytic?

A

enterococcus (group D) s. bovis

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151
Q

what gram negative rod is beta hemolytic?

A

pseudomonas

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152
Q

what is unique about pseudomonas beta hemolysis?

A

it produces greenish-metallic appearing colonies

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153
Q

what pigments are produced my pseudomonas creating the unique color on blood agar?

A

pyoverdin and pyocyanin (blue)

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154
Q

what staph is beta hemolytic?

A

staph aureus

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155
Q

what is chocolate agar?

A

variant of blood agar contains RBCs that are lysed by heating contains NAD (factor V) & hemming (factor X)

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156
Q

what bacteria is chocolate agar used to identify?

A

H. Influenzae *** very important to know

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157
Q

Why is H. Influenzae considered a fastidious organism?

A

Because it needs factor V (NAD) and factor X (hemin)

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158
Q

In what scenario would H. Influenzae grow on bood agar?

A

If s. Aureus is present

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159
Q

Where does the NAD needed for chocolate agar come from?

A

Inside RBCs

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160
Q

What is thayer-martin media selective for?

A

Neisseria (think M looks like N)

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161
Q

When testing for Neisseria why is it important to have a media that is selective?

A

Neisseria often come from sites with lots of other flora (throat, genitalia)

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162
Q

How is Thayer-martin media selective for neisseria?

A

It is enriched with vancomycin, colistin (polymyxin), & nystatin

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163
Q

What are the actions of vancomycin, colistin (polymyxin), & nystatin?

A

Vancomycin - kills most gram positive organisms Colistin - kills most gram negatives (except Neisseria) Nystatin - kills fungi

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164
Q

What agar is selective for Bordetella pertussis?

A

Bordet-Gengou Agar Aka Potato Agar

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165
Q

What does Bordetella pertussis cause? Why is it so rare?

A

Whooping cough; vaccines

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166
Q

Why is Bordet-Gengou agar aka potato agar?

A

Prepared from potatoes - high in starch which is favorable to pertussis bacteria

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167
Q

What 2 media are used to detect Corynebacterium diphtheriae?

A

Loffler’s media - selective Tellurite media - differential

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168
Q

What is another name for Tellurite media?

A

Cysteine-Tellurite agar

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169
Q

What does C. Diphtheriae look like on tellurite media?

A

C. Diphtheriae reduces K+ tellurite to tellurium producing gray-black colored colonies

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170
Q

What media is special for mycobacterium tuberculosis?

A

Lowenstein-jensen agar

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171
Q

What is lowenstein-jensen agar enriched with?

A

Eggs Flour Glycerol Salt

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172
Q

what stain is used for M. tuberculosis?

A

Ziehl-Neelsen stain (acid-fast)

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173
Q

why is it important to treat suspected patients for tb before lab cultures come back?

A

because M. tuberculosis is slow growing, it can take several weeks for visible colonies to appear

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174
Q

what is Eatons agar used to detect?

A

mycoplasma pneumonia

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175
Q

why its mycoplasma unique?

A

no cell wall - poorly visualized with gram stain

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176
Q

what is Eatons media enriched with to grow m. pneumonia?

A

cholesterol

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177
Q

why is m. pneumonia considered fastidious?

A

because it requires cholesterol to grow

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178
Q

why is Eatons agar rarely used in the modern era?

A

because it takes days to weeks to grow

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179
Q

how is mycoplasma pneumonia diagnosed?

A

serology (antibody testing) PCR (bacterial DNA) Cold agglutinins (IM antibodies)

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180
Q

What is MacConkey’s agar selective for ?

A

gram negative bacteria

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181
Q

how is MacConkey’s selective for gram negative?

A

contains bile salts as inhibitors of gram positive bacteria growth

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182
Q

how is MacConkey’s differential for lactose fermenters?

A

lactose fermenters produce an acid that turns the agar pink; non-lactose fermenters are colorless

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183
Q

what shapes are gram negative bacteria categorized into?

A

diplococci coccbacillus rods comma (oxidase +)

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184
Q

what does sorbitol MacConkey agar detect?

A

E. coli O157:H7 strains (shiga-like toxin)

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185
Q

How does E. coli O157:H7 look on sorbitol MacConkey agar compared to other E. coli?

A

O157:H7 cannot ferment sorbitol and other E. coli can O157:H7 grows colorlessly and other E. coli produce pink colonies

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186
Q

buffered charcoal yeast extract is used to detect what bacteria?

A

Legionella (only 1 L in name - charcoaL)

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187
Q

why is it important to culture legionella?

A

can contaminate water supplies and cause an outbreak

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188
Q

what is another way to test for legionella?

A

urinary antigen test - only works for a “type 1 infection” (negative result is not definitive)

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189
Q

what is Sabouraud’s agar selective for?

A

fungi

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190
Q

what inhibits bacterial growth in sabouraud’s agar?

A

acid or antibiotics

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191
Q

If something is growing on Sabourauds agar what are they trying to tell you?

A

that it’s a fungi

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192
Q

what are the 4 different bacterial growth environments?

A

obligate anaerobes - no O2 obligate aerobes - O2 only facultative anaerobes - both intracellular

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193
Q

what are the 2 biochemical methods used to generate ATP inside cells?

A

respiration fermentation

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194
Q

how does respiration produce ATP?

A

ETC requires O2 ***

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195
Q

how does fermentation produce ATP?

A

sugars –> acids does NOT require O2****

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196
Q

Does respiration or fermentation make more ATP?

A

respiration

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197
Q

what 2 enzymes present in aerobic organisms allows then to survive in environments with a lot of O2?

A

superoxide dismutase & catalase

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198
Q

what does superoxide dismutase do?

A

catalyzes superoxide (O2-) radical to O2 od hydrogen peroxide

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199
Q

what does catalase do?

A

converts hydrogen peroxide (H2O2) to oxygen and water

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200
Q

why do obligate aerobes need O2 to generate ATP?

A

because O2 is the final electron acceptor during respiration

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201
Q

what 3 bacteria are the main obligate aerobes?

A

pseudomonas aeruginosa mycobacterium tuberculosis nocardia (opportunistic infections)

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202
Q

what is the benefit of being an obligate aerobe?

A

can make a lot of ATP

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203
Q

obligate anaerobic bacteria are common among the normal flora or what?

A

gut and mouth

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204
Q

obligate anaerobes _____ (do/do not) cause communicable diseases?

A

do not

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205
Q

obligate anaerobes often live near ______ surfaces

A

mucosal

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206
Q

99% of fecal flora are obligate _______

A

anaerobes

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207
Q

when will an obligate anaerobe cause infection?

A

when the surface breaks down i.e. abscesses

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208
Q

what type of antibiotic will not work on anaerobes and why?

A

aminOglycosides require O2

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209
Q

what method do obligate anaerobes use to make ATP?

A

fermentation

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210
Q

what are the byproducts of fermentation?

A

gases - CO2 & H2 short chain FA’s - acetic acid, isobutyric acid etc. causes a foul smell that you get from pustules

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211
Q

3 main obligate anaerobes

A

actinomyces - gums, dental abscess bacteroides - abdominal abscess clostridium

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212
Q

what are the 3 types of clostridium?

A

botulinum perfringens tetani

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213
Q

what are two key anaerobic infections?

A

abdominal abscesses/perforations aspiration pneumonia

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214
Q

What anaerobic bacteria is the cause of abdominal abscesses/perforations?

A

Bacteroides fragilis

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215
Q

what is the treatment for b. fragilis?

A

metronidazole w/ gram neg. agent

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216
Q

b. fragilis _____(is/is not) resistant to many antibiotics

A

is

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217
Q

what happens in aspiration pneumonia?

A

when you aspirate vomit, mouth anaerobes enter the lungs

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218
Q

what 3 bacteria commonly cause aspiration pneumonia?

A

peptostreptococcus fusobacterium prevotella

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219
Q

what is the treatment for aspiration pneumonia?

A

clindamycin

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220
Q

what antibiotic is used on anaerobic infections above the diaphragm?

A

clindamycin (lungs)

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221
Q

what antibiotic is used on anaerobic infections below the diaphragm?

A

metronidazole (abscesses/perforations)

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222
Q

what are facultative anaerobes?

A

can live w/o O2 but use it when it’s available

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223
Q

what type of organism can perform respiration and fermentation?

A

facultative anaerobe

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224
Q

what is the Pasteur effect?

A

if a facultative anaerobe is in an environment with O2, fermentation is inhibited

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225
Q

what 3 common bacteria are facultative anaerobes?

A

staph strep E.coli

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226
Q

How do obligate intracellular bacteria get ATP?

A

depend on host cell

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227
Q

how come obligate intracellular bacteria do not gram stain well?

A

because they live inside other cells so it is difficult to get them on a slide

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228
Q

what are 3 disadvantages of intracellular bacteria

A

cannot synthesize their own ATP do not gram stain well difficult to grow - need cell culture

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229
Q

what are the 2 most important obligate intracellular bacteria to know?

A

Rickettsia Chlamydia

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230
Q

What does Rickettsia cause and how is it Dx’d?

A

Rocky Mountain spotted fever Dx’d clinically or w/ Ab tests

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231
Q

How is Chlamydia Dx’d?

A

DNA testing

232
Q

what are facultative intracellular bacteria?

A

they can live inside other cells if they need to

233
Q

what bacteria are facultative intracellular?

A

mycobacterium legionella salmonella neisseria listeria brucella francisella yersinia pestis

234
Q

what facultative intracellular bacteria use macrophages?

A

mycobacterium legionella listeria brucella francisella yersinia pestis

235
Q

besides macrophages, what cell does listeria use? what about brucella?

A

listeria - monocytes brucella - neutrophils

236
Q

what facultative intracellular bacteria uses intestinal cells?

A

salmonella

237
Q

what facultative intracellular bacteria uses urethral epithelial cells?

A

neisseria

238
Q

what does the bacterial growth curve look like in the lag phase?

A

its a flat line because the bacteria are not dividing

239
Q

what happens in the growth phase of the bacterial growth curve?

A

aka exponential phase/log phase bacteria have started to multiply

240
Q

what is the generation/doubling time in reference to the bacterial growth curve?

A

time it takes for the # of cells to double

241
Q

during what phase of the bacterial growth curve do antibiotics have their greatest effect?

A

growth phase

242
Q

what happens in the stationary phase of the bacterial growth curve?

A

bacteria are continuing to grow but they are also starting to die bc there is a lack of nutrients amt of death = amp of growth total # of bacteria doesn’t change

243
Q

what does the stationary phase look like on the bacterial growth curve?

A

flat line amt of death = amt of growth

244
Q

what happens during the death phase of the bacterial growth curve?

A

the number of bacteria dying exceeds the number that are growing and the number of bacteria decreases and the growth curve shows a downhill slope

245
Q

what is so important about bacterial gene transfer?

A

key for evolution of antibiotic resistance

246
Q

why would antibiotics stop working leading to development of antibiotic resistance?

A

the bacteria have evolved and now have genetic resistance to a given antibiotic

247
Q

what are the 3 key mechanisms by which which bacteria transfer genes?

A

transformation conjugation transduction

248
Q

what is the easiest method of bacterial gene transfer?

A

bacterial transformation

249
Q

what is bacterial transformation?

A

direct uptake of DNA from the surrounding environment allows fo evolution of DNA over time

250
Q

what mechanism is used when transferring genes to introduce them to bacteria for replication?

A

bacterial transformation

251
Q

what is bacterial conjugation’?

A

when one bacteria cell directly transfers genetic information to another cell using an appendage called a pilus

252
Q

what are sex pili?

A

what bacterial cells use to transfer genetic info during conjugation

253
Q

How is the DNA transferring in bacterial conjugation?

A

via plasmids

254
Q

what are plasmids?

A

small DNA molecules within a cell that are physically separated from chromosomal DNA

255
Q

plasmids can replicate _____

A

independently

256
Q

what can the genes found in plasmids code for?

A

antibiotic resistance toxins

257
Q

how is it proven that conjugation takes place between two bacteria?

A

transformation vs. conjugation experiment where 2 different strains that require 2 different amino acids for growth were put together w/ DNAase and they grew proves that genetic material must have been transferred through conjugation bc the DNAase destroyed any leaked DNA

258
Q

what do high frequency strains of bacteria do?

A

they take plasmids and incorporate it into their DNA

259
Q

Why are high frequency strains of bacteria important?

A

because when they conjugate with a bacteria that doesn’t have the plasmid they tend to transfer their entire genome along with the plasmid

260
Q

what are high frequency strains used for?

A

gene mapping

261
Q

What is the site of origin of genetic transfer for high frequency strains?

A

plasmid

262
Q

What is Lancefield grouping?

A

system to classify streptococci based on C carbohydrates in the cell wall that allow agglutination with particular antisera

263
Q

Lancefield Group A

A

Strep pyogenes

264
Q

Lancefield Group B

A

Strep agalactiae

265
Q

Lancefield Group D

A

enterococcus

266
Q

what are the hemolysis patterns seen on blood agar?

A

β = lysis - will have a white ring around the bacteria because of hemolysis α = partial γ = no lysis

267
Q

what is the catalase test used for?

A

to differentiate staph from strep

268
Q

what are the gram + rods?

A

clostridium corynebacterium listeria bacillus

269
Q

what are the gram + cocci and how do you distinguish them?

A
  1. catalase (+) staph 2. coagulase (+) S. aureus 3. novobiocin sensitive - S. epidermidis 4. novobiocin resistant - S. saprophyticus 1. catalase (-) strep 2. blood agar hemolysis β –> bacitracin test α –> optochin test γ –> bile-esculin agar bacitracin sensitive - S. pyogenes (group A) bacitracin resistant - S. agalactiae (group B) optochin sensitive - S. pneumonia optochin resistant - S. viridans bile & NaCl - enterococcus bile only - Strep. bovis
270
Q

what is the algorithm for gram positive bacteria?

A
272
Q

what 2 gram positive bacteria resemble fungi?

A

actinomycesnocardia

273
Q

what gram positive bacteria is catalase +, coagulase +?

A

staph aureus

274
Q

strep grows in ______

A

chains

275
Q

staph grows in _____

A

clusters

276
Q

What system classifies only streptococci?

A

lancefield grouping

277
Q

what are the different forms of cocci?

A

diplococci - pairsstreptococci - chainsstaphylococci - clusters

278
Q

what is the catalase test?

A

differentiates staph from strepH2O2 on slide + bacteria–> bubbles = catalase +

279
Q

what does the catalase enzyme do?

A

produced by bacteria that use oxygenbreaks down H2O2 into H2O and O2 = bubbles

280
Q

how do you know that staph is aerobic?

A

because it has catalase and only organisms that use oxygen will have catalase

281
Q

what is chronic granulomatous disease?

A

loss of function of NADPH oxidase - phagocytes cannot generate H2O2 to kill bacteria

282
Q

what is the importance of NADPH oxidase?

A

respiratory burst - phagocytes use NADPH oxidase to generate H2O2 from O2

283
Q

how come people with CGD can still clear catalase negative infections?

A

catalase negative bacteria generate their own H2O2 which the phagocytes use for respiratory burst despite the loss of functions of NADPH oxidase

284
Q

what 5 organisms cause almost all CGD infections?

A

staph aureus*pseudomonasserratianocardiaaspergillus*all catalase +

285
Q

why do ppl with CGG get recurrent catalase + bacterial infections?

A

no NADPH oxidase = no H2O2 = no resp. burst = recurrent infections

286
Q

what is the coagulase test used for?

A

differentiates staph aureus from other staph

287
Q

how is the coagulase test done?

A

add rabbit plasma to tube with bacteriacoagulase causes fibrin clots (clumping)clumping = coagulase +no clumping = coagulase negative

288
Q

what is the novobiocin sensitivity test used for?

A

differentiates S. saprophyticus from S. epidermidis

289
Q

how is the novobiocin sensitivity test done?

A

plate bacteria on agar with novobiocin “disk”measure clearance zone around diskresistant = growth near edge of disksensitive = large zone of clearance around disk

290
Q

what is the bacitracin sensitivity test used for?

A

differentiates group A strep from group B strep

291
Q

what does bacitracin interfere with?

A

peptidoglycan synthesis

292
Q

how is the bacitracin sensitivity test done?

A

plate bacteria on agar with bacitracin disk and measure the clearance zone

293
Q

how do all antibiotic sensitivity tests work?

A

plate bacteria with antibiotic disk and measure the zone of clearance around the diskresistant = no zonesensitive = large zone

294
Q

what is the optochin sensitivity test used for?

A

differentiate S. pneumonia from S. viridans strep

295
Q

what bacteria is optochin sensitive?

A

S. pneumonia

296
Q

ethylhydrocupreine

A

optochin

297
Q

what is bile-esculin agar selective for?

A

group D strep - enterococcus and strep bovismedia turns dark brown/black

298
Q

why does bile-esculin agar only grow group D strep?

A

bile salts inhibit most gram positive bacteria but group D strep can hydrolyze esculin and the media will turn brown/black

299
Q

how can you differentiate the 2 group D strep?

A

NaCl media - differentiates enterococcus from non-enterococcus group D bacteria

300
Q

how does NaCl media differentiate enterococcus?

A

enterococcus is salt tolerant and can grow in high salt concentrations so if the bacteria grows on NaCl you know its enterococcus and if not it is strep bovis

301
Q

what is mannitol salt agar (MSA) used for?

A

differentiates staph species

302
Q

what is used in MSA to differentiate staph?

A

high [salt] + mannitol + pH indicator (phenol red)mannitol fermenters make acid –> phenol red turns yellow

303
Q

what color is s. aureus on MSA?

A

yellowmannitol fermenter = acid = phenol red turns yellowmost other staph do not ferment mannitol

304
Q

what are the shapes of gram negative bacteria?

A

diplococcicoccobacillusrodscomma shape

305
Q

what are the gram negative coccobacillus?

A

haemophilus influenzapasteurellabordetella pertussisbrucellayersinia pestis

306
Q

what are the gram negative diplococci?

A

Neisseria meningitidis (maltose fermenter)Neisseria gonorrhea (non-maltose fermenter)

307
Q

gram negative rods can be further divided into what?

A

lactose fermenter & lactose non-fermenter

308
Q

what gram negative rods are “fast” lactose fermenters?

A

klebsiellaE. coliEnterobacter

309
Q

what gram negative rods are “slow” lactose fermenters?

A

citrobacterserratia

310
Q

what gram negative rods are oxidase (+) lactose non-fermenters?

A

pseudomonasH. pylori

311
Q

what gram negative rods are oxidase (-) lactose non-fermenters?

A

shigellasalmonellaproteus

312
Q

what are the comma shape gram negative bacteria?

A

campylobacter (grows in warm temps 42ºC)vibrio (grows in alkaline environments)

313
Q

which neisseria species can metabolize maltose?

A

meningitidis

314
Q

what agar is used to test for lactose fermentation?

A

MacConkey’s

315
Q

how is MacConkey’s agar selective for gram negative bacteria?

A

contains bile salts to inhibit the growth of gram positive bacteria

316
Q

what color will gram negative bacteria that can ferment lactose be when placed on MacConkey’s agar?

A

pinklactose fermentation produces acid turning the agar pinknon-lactose fermenters are colorless

317
Q

what are “slow” fermenters?

A

citrobacter and serratia can initially appear as non-lactose fermenting due to slow growth, longer incubation will show growth and turn media pink

318
Q

the oxidase test is for what enzyme?

A

cytochrome oxidase

319
Q

how does the oxidase test work?

A

bacterial colonies on paper discs w/ indicator that will change color in the presence of oxidase

320
Q

what are the 2 groups of oxidase + gram negative bacteria?

A

lactose non-fermenting rodscomma shaped

321
Q

how can you differentiate oxidase negative gram negative rods?

A

hydrogen sulfide testing (H2S)

322
Q

what bacteria are distinguished using H2S?

A

salmonella and proteus produce H2Sshigella does NOT produce H2S

323
Q

what test is used to look for production of hydrogen sulfide?

A

triple sugar iron (TSI) testorganisms that produce H2S will turn TSI media black

324
Q

what are virulence factors?

A

bacterial features that allow evasion of host defensesprotein AIgA proteaseM protein

325
Q

what is protein A?

A

key virulence factor for staph Aureuspart of the peptidoglycan cell wallinhibits phagocytosis

326
Q

how does protein A help the bacteria evade the immune system?

A

inhibits phagocytosis by binding Fc of IgG preventing opsonization and phagocytosis by macrophages and prevents complement activation

327
Q

what is IgA protease?

A

enzymes that cleave IgA, allows for colonization of mucosal surfaces

328
Q

IgA is important for what?

A

mucosal infections (GI, Resp)

329
Q

IgA protease is an important virulence factor for what bacteria?

A

s. pneumoniah. influenzaneisseria gonorrhoeae & meningitidis

330
Q

what helps s. pneumonia get into the respiratory tract?

A

IgA protease

331
Q

What is the M protein?

A

surface molecule of group A strep (s. pyogenes)

332
Q

how does the M protein work?

A

prevents phagocytosis by interfering with the complement system:binds to factor H (protects our own cells from complement activation)breaks down C3-convertase, prevents opsonization by C3b

333
Q

M protein causes the Sx seen in what illnesses?

A

strep throatrheumatic fever

334
Q

what is thought to be the bases of rheumatic heart disease?

A

M protein shares properties with myosin-> autoimmune damage to the heart in pts that have had a bacterial infection w/ s. pyogenes

335
Q

what are the post-strep complications that M protein is responsible for?

A

rheumatic heart diseaseglomerulonephritis*different subtypes of M protein

336
Q

endotoxin vs. exotoxin

A

endotoxin - component of the outer cell membrane of gram neg. bugsexotoxin - proteins synthesized by some bacteria

337
Q

endotoxins are found only in gram ______ bacteria

A

negativegram positive bacteria do not have an outer cell membrane

338
Q

LPS

A

lipopolysaccharidewhat makes up endotoxin

339
Q

how is endotoxin released into the tissues?

A

when the cell dies

340
Q

what is an important distinction regarding how bacterial toxins get into the blood?

A

endotoxin - cell dies and releases contents - NOT SECRETEDexotoxin - secreted

341
Q

what are bacterial toxins made of?

A

endo - fat/sugarexo - protein

342
Q

what key features do all endotoxins have?

A

Lipid A coreO antigen

343
Q

what does lipid A do?

A

responsible for most of the toxicitytrigger the immune system and the secretion of cytokines causing hypoTN/edema etc.

344
Q

O antigen

A

terminal end sugars that vary among bacterial strainsdo not cause disease by themselvestarget for the immune system, part of the way immune system targets and kills the endotoxin

345
Q

how come people with gram neg. infections can get very sick?

A

endotoxin can lead to fever and shock by triggering the release of TNF and IL-1 which are key immune components of sepsis and shock

346
Q

what 2 cytokines are important components of sepsis and septic shock?

A

TNFIL-1

347
Q

why can’t you vaccinate against endotoxin?

A

because it generates a weak Ab response

348
Q

endotoxin is heat _______

A

stable - can tolerate high temps

349
Q

what are the 3 ways that endotoxin/LPS can activate the immune system?

A

macrophagescomplementtissue factor

350
Q

how does LPS activate macrophages?

A

binds to receptor CD14 aka endotoxin receptor

351
Q

once macrophages are activated by LPS what do they secrete?

A

IL-1: feverTNF: fever & hypoTNNO: hypoTN

352
Q

what happens when LPS activates the complement system?

A

C3a and C5a get released

353
Q

how will a patient present with a gram neg. infection that has activated complement via LPS?

A

C3a: hypoTN & edemaC5a: neutrophils chemotaxis & edema

354
Q

what are anaphylatoxins?

A

toxins that cause anaphylaxiscomplement proteins C3a and C5a

355
Q

C3a

A

hypoTNedema

356
Q

C5a

A

neutrophil chemotaxisedema

357
Q

How does endotoxin cause coagulation problems and DIC?

A

endotoxin directly activates TF (tissue factor) leading to coagulation problems and DIC

358
Q

what is lipooligosaccharide?

A

LOSmake up endotoxin of some gram neg. bacteria (non-enteric)

359
Q

what is the most important example of a gram neg. bacteria whose endotoxin is made up of LOS? how is this different than LPS?

A

N. meningitidislacks O-antigen

360
Q

what are the systemic reactions a person can develop from endotoxin?

A

meningococcemiagram (-) sepsis

361
Q

how do you get meningococcemia?

A

N. meningitidis gets in the bloodstream and causes hypoTN and go into shock because of the endotoxin LOS

362
Q

how do you get gram negative sepsis?

A

bacteria in blood streami.e. - bacteria (E.coli) in bloodstream from a UTIendotoxin causes shock

363
Q

what are exotoxins?

A

proteins that are secreted by bacteria to cause disease Sx

364
Q

what is the structure of exotoxins?

A

two component “A-B” polypeptideA = active = toxicB = binding = binds to cell surface

365
Q

what are the different categories of exotoxins?

A

protein synthesis inhibitorsincrease fluid secretion (diarrhea)inhibit phagocytosisinhibit neurotransmitter release (botulinum)lyse cell membranessuperantigens

366
Q

Which bacteria produce exotoxins that inhibit protein synthesis?

A

Corynebacterium diphtheriaPseudomonas aeruginosaShigellaEnterohemorrhagic E. Coli (EHEC)

367
Q

what 2 exotoxins work by ADP ribosylation?

A

Diphtheria toxinExotoxin A (pseudomonas aeruginosa)

368
Q

Corynebacterium diphtheria exotoxin

A

diphtheria toxin

369
Q

pseudomonas aeruginosa exotoxin

A

exotoxin A

370
Q

How do diphtheria toxin and exotoxin A inhibit protein synthesis?

A

ADP ribosylationaddition of ADP-ribose to proteins makes them dysfunctional

371
Q

What are the S/Sx of diphtheria?

A

sore throat with membraneswollen nodes

372
Q

how does the diphtheria toxin work?

A

Inactivates EF-2 (elongation factor 2) which is necessary for protein synthesisLETHAL TOXIN****

373
Q

How did diphtheria become largely eradicated?

A

DPT vaccine (diphtheria-pertussis-tetanus)

374
Q

how does diphtheria toxin inactivate EF-2?

A

toxin stimulates a reaction so that NAD will be converted to nicotinamide and an ADP ribosyl group will be transferred to EF-2 resulting in no protein synthesisLETHAL TOXIN****only takes a small amount of toxin to completely shut down protein synthesis

375
Q

what types of infection does pseudomonas aeruginosa cause?

A

skinsepsispneumonia

376
Q

what is the mechanism for exotoxin A

A

same as diphtheria toxinexotoxin A ADP ribosylates EF-2 = no protein synthesis

377
Q

Shigella exotoxin

A

shiga toxin

378
Q

what does shigella cause?

A

infectious diarrhea

379
Q

how does shiga toxin halt protein synthesis?

A

binds to 60S ribosome in cells and removes a specific adenine residue from rRNA in the 60S ribosomal subunit

380
Q

What is the main way that shigella can cause illness?

A

invasion of GI mucosal cells is the main cause of disease

381
Q

Do all strains of shigella produce the shiga toxin?

A

No, there are non-toxigenic strains that still cause significant disease by invading the GI mucosal cells

382
Q

How does shigella mainly cause disease?

A

invasion of GI mucosal cellsshiga toxin causes disease but not the main mechanismall strains of shigella cause disease this way, it is known because of the non-toxigenic strains that still cause significant disease

383
Q

Enterohemorrhagic E. Coli (EHEC) exotoxin

A

shiga-like toxin

384
Q

what is the mechanism of shiga-like toxin?

A

same as shiga toxinbinds to 60S ribosome in cells and removes a specific adenine residue from rRNA in the 60S ribosomal subunit

385
Q

what does EHEC cause?

A

bloody diarrhea

386
Q

what is the classic serotype of E. coli?

A

O157:H7 - causes EHEC

387
Q

How does E. Coli O157:H7 cause disease?

A

do not invade host cellsattach to intestinal epithelial cells and secrete proteins into host cells & toxin effects

388
Q

What is the difference in mechanisms between shigella and EHEC?

A

shigella causes disease mainly by bacteria invading GI mucosal cellsEHEC causes disease mainly by the shiga-like toxin (inflammation) it produces because it is not invasive

389
Q

Shiga and shiga-like toxin can lead to what?

A

cytokine release –> systemic circulation –> hemolytic uremic syndrome (HUS)

390
Q

what is one of the worst complications of EHEC?

A

HUS - acute Renal failure, hemolytic anemia

391
Q

What bacteria produce exotoxins that increase fluid secretion?

A

Enterotoxigenic E. coli (ETEC)Bacillus anthracis (anthrax)Vibrio cholera

392
Q

How is fluid secretion in the GI tract regulated?

A

CFTR - cystic fibrosis regulator proteinGs protein in GI tract stimulates AC to increase cAMP which activates CFTR to secrete more Cl-cells in the GI tract secrete chlorideamount of Cl- secreted = amt of water in GI tract

393
Q

How do toxins increase Cl- secretion to cause diarrhea?

A

activate Gs or AC => CFTR secretes more Cl- => more H2O in GI tract => diarrhea

394
Q

ETEC exotoxins

A

LT - heat labile toxinST - heat stable toxindifferentiated by heat stability

395
Q

how does ETEC heat labile toxin work to increase fluid secretion?

A

activates adenylyl cyclase => increase cAMP => increase water in gut => diarrhea

396
Q

how does ETEC heat stable toxin work to increase fluid secretion?

A

activates guanylyl cyclase => increase cGMP => stimulate Cl- secretion => inhibit NaCl absorption => increase water in gut => diarrhea (watery)

397
Q

What 3 proteins does bacillus anthracis make?

A

PA - protective AgLF - lethal factorEF - edema factoronly cause toxicity in pairs

398
Q

Edema toxin is made up of what 2 proteins produced by bacillus anthracis? how does it work to increase fluid secretion?

A

PA + EFmimics adenylyl cyclase

399
Q

where are the main sites of disease for anthrax?

A

skin - most commonlungs - necrotizing pneumoniaGI - ulcers

400
Q

What is important about the skin and GI lesions caused by anthrax?

A

they have an edematous border that may be cause by edema factornecrotic looking lesions surrounded by an area of swollen skin tissue caused by edema factor and increased fluid secretion related to the exotoxin

401
Q

How does cholera toxin increase fluid secretion?

A

permanently activates Gs => increase cAMP

402
Q

what does cholera toxin cause?

A

voluminous “rice-water” diarrhea

403
Q

where is cholera commonly found?

A

areas without clean water

404
Q

What ends up causing death in people with cholera?

A

profound dehydrationelectrolyte lossesshock

405
Q

what is the mainstay of treatment for cholera?

A

aggressive volume repletionthe body will clear the infection in time but you have to give enough fluids to compensate for the loss caused by the cholera toxin until the body eliminates it

406
Q

what toxin inhibits phagocytosis?

A

pertussis toxin secreted by Bordetella pertussis

407
Q

What does pertussis toxin cause?

A

whooping cough

408
Q

how does pertussis toxin inhibit phagocytosis?

A

inhibits Gi proteins - inhibiting the inhibitor = over activation of AC which increases cAMP in neutrophils causing impaired recruitment of neutrophils to control infection

409
Q

what bacteria produce neurotoxins?

A

Clostridium tetaniClostridium botulinum

410
Q

clostridium tetani and botulinum toxins work by disruption of what?

A

SNARE proteins - vesicles can’t release their neurotransmitter

411
Q

what do SNARE proteins do?

A

allows vesicles in the neuron to “dock” and unload their neurotransmitter

412
Q

Clostridium tetani exotoxin

A

tetanospasmin

413
Q

How does tetanospasmin work?

A

works on inhibitory interneurons in the spinal cord called Renshaw cells inhibiting the inhibitory cells causes overactive neurological activity = muscle ridigity

414
Q

what does Tetanus cause?

A

rigid paralysis

415
Q

how does botulinum toxin work?

A

prevents Ach release at NMJ => no muscle contraction => muscle flaccidity

416
Q

what does botulinum toxin cause?

A

flaccid paralysis

417
Q

what bacteria produce exotoxins that lyse cell membranes?

A

Clostridium perfringensStrep pyogenes

418
Q

what does clostridium perfringens cause when infecting wounds?

A

gas gangrene

419
Q

clostridium perfringens exotoxin

A

α-toxin

420
Q

what is alpha toxin?

A

phospholipase C enzyme that degrades phosphatidylcholine and sphingomyelin

421
Q

what does alpha toxin cause?

A

myonecrosis - muscle breakdowndecline in muscle blood flow => occlusive plugs (platelets, leukocytes, fibrin) => low oxygen environment => C. perfringens thrives (anaerobic)

422
Q

how does alpha toxin cause disease?

A

lysing cell membranes and allowing the degradation of muscle cells to occur

423
Q

strep pyogenes causes what?

A

strep throat which can lead to sequelae like rheumatic fever and glomerulonephritis

424
Q

strep pyogenes exotoxin

A

streptolysin O aka cytolysin because it lyses cells

425
Q

strep pyogenes will show what kind of hemolysis?

A

β hemolysis from streptolysin O or streptolysin S toxin

426
Q

what are ASO antibodies used for?

A

anti-streptolysin Oelevated following strep infectioncan be useful in suspected rheumatic heart disease or post-strep glomerulonephritis to see if they have ever had strep throat

427
Q

how are toxins used as a basis for many vaccines?

A

turn the toxin into a toxoid - an inactivated bacterial toxinused to prevent diphtheria and tetanus

428
Q

What is in the DTaP combined immunization?

A

diphtheria toxoidtetanus toxoid”acellular” pertussis - inactivated toxin plus some bacterial elements

429
Q

what toxins are plasmid-encoded?

A

E. coli heat labile toxin

430
Q

what toxins are bacteriophage-encoded?

A

***corynebacterium diphtheriastrep pyogenes erythrogenicE. coli shiga-like toxinbotulinum toxincholera toxinbacteriophage gives bacteria DNA and allows them to acquire a new ability to synthesize exotoxins

431
Q

what are superantigens?

A

exotoxins that activate a massive number of T-cells

432
Q

how are superantigens different from regular antigens?

A

a normal Ag is processed and presented by an APC on MHC to trigger a T-cell receptor and activation of a single T-cella superAg is NOT processed, it directly connects the MHC complex to the TCR and triggers many T cells to be activated

433
Q

what cytokines are released in large amounts from superantigens?

A

IFN-γ and IL-2 causing massive vasodilation and shock

434
Q

what bacteria can synthesize toxins that act as superantigens?

A

staph aureus - toxic schock syndrome toxin (TSST-1)strep pyogenes - pyrogenic exotoxin A or C

435
Q

what bacteria can cause toxic shock syndrome?

A

staph >> strep

436
Q

what is toxic shock syndrome? initial Sx?

A

the body’s reaction to a superantigenfevershock (hypoTN)diffuse red rash (looks like sunburn)diarrhea - unique for TSS

437
Q

why is TSS more common with staph?

A

staph normally present in the vagina can cause TSS after having a tampon in

438
Q

what is strep TSS associated with?

A

necrotizing fasciitis

439
Q

how doe TSS progress?

A

after weeks - desquamation of palms and solesmulti-organ system failure

440
Q

how can you differentiate between TSS and sepsis?

A

diffuse sunburn type rashpresence of diarrhea

441
Q

women using tamponssurgical wound with packing

A

staph + packing = TSSclassic scenarios for toxic shock syndrome

442
Q

what do all clostridia have in common?

A

all form sporesall obligate anaerobesall form toxins(tetani, botulinum, perfringens, difficile)

443
Q

Where are c. tetani spores found and how does this relate to how they enter the body?

A

found in the soilenter body through penetrating injury - barefoot on rusty nail or splinter

444
Q

how does c. tetani cause disease?

A

spores from soil enter the body through an open wound –> spores germinate into bacteria –> tetanospasmin is produced –> travels to sp. c. –> blocks glycine and GABA release by inhibitory neurons (renshaw cells)inhibit the inhibitor –> overactive

445
Q

what are renshaw cells?

A

inhibitory spinal cord interneurons

446
Q

what type of paralysis does c. tetani cause?

A

spastic

447
Q

classic Sx for tetanus

A

lockjaw = trismusRisus sardonicus - forced grin d/t spastic facial muscles (evil smile)

448
Q

What is the treatment for tetanus?

A

wound debridementmetronidazoletetanus immune globulin - binds circulating toxinBenzo’s or neuromuscular blockers until toxin wears off

449
Q

is there a vaccine for tetanus?

A

yes, DTaP. toxoid vaccine

450
Q

botulinum produces heat-______ spores

A

resistantcan survive up to 100ºc – cook your food!!

451
Q

how does botulinum cause disease?

A

works at NMJ preventing Ach release = no muscle contractions = floppy baby syndrome (flaccid paralysis)

452
Q

some variants of ______ toxin are carried by bacteriophages

A

botulinumDNA not found in the bacteria itself but found in a virus that infects the bacteria and delivers the ability to synthesize toxin

453
Q

3 types of botulism

A

foodinfantwound

454
Q

how do adults get botulism?

A

ingestion of toxin from undercooked food, canned food**multiple sick adults after a meal

455
Q

how do infants get botulism?

A

ingestion of spores –> growth in intestine**contaminated honey

456
Q

why should you worry about botulism in canned food?

A

anaerobic environment promotes growth

457
Q

what is the incubation period for botulism before Sx present?

A

12-48 hrs

458
Q

what are the Sx of botulism?

A

3 D’s:DiplopiaDysphagiaDysphonia

459
Q

Dx of botulism

A

often clinical, but spores and toxins can sometimes be detected in stool

460
Q

Tx of botulism

A

antitoxin - blocks circulating toxin –> cannot block toxin already in nerves (like tetanus) –> supportive care –> toxin washout

461
Q

where is c. perfringens found?

A

soil

462
Q

what does c. perfringens do?

A

infects dirty wounds (soil) –> gas gangrenecauses food poisoning

463
Q

what is gas gangrene?

A

aka clostridial myonecrosistraumatic wound compromises the vasculature creating a favorable environment for anaerobic growth (w/o good blood supply –> less O2 –> anaerobic growth

464
Q

what toxin is produced by c. perfringens that is involved in the pathogenesis of clostridial myonecrosis?

A

α-toxin

465
Q

what does the α-toxin produced by c. perfringens do?

A

destroys muscle tissue and causes hemolysis = favorable anaerobic environmentlecithinase - degrades phospholipids in cell membranes helping it to break down muscle tissue and cause hemolysis

466
Q

what is lecithinase

A

(α-toxin)phospholipase that acts on lecithin

467
Q

S/Sx gas gangrene

A

severe pain at injury site within 24 hoursskin tense and tendersystemic toxicity - fever, hypoTN, shock

468
Q

Dx gas gangrene

A

gas at injury site on imaginingcrepitus

469
Q

Tx gas gangrene

A

surgical debridementbroad spectrum antibiotics

470
Q

C. perfringens food poisoning pathogenesis

A

undercooked meats –> ingest spores –> produce enterotoxin –> LATE ONSET watery diarrhea

471
Q

how long after ingestion of c. perfringens spores will you see watery diarrhea?

A

8-22 hrs, late onset

472
Q

what is special about the watery diarrhea that c. perfringens causes?

A

LATE ONSET b/c spores have to germinate and produce toxin

473
Q

what is the difference between food poisoning caused by c. perfringens, S. aureus, and B. cereus

A

c. perfringens causes a late onset watery diarrhea b/c of spore ingestionS. aureus and B. cereus cause early onset watery diarrhea from ingestion of preformed toxin

474
Q

How does GI flora help defend ingestion of c. diff?

A

normal GI flora prevent overgrowth of c. diff

475
Q

what does c. diff cause?

A

antibiotic-associated colitis

476
Q

antibiotic-associated colitis

A

antibiotics alter normal gut flora, creating a favorable environment for c. diff

477
Q

what population commonly gets antibiotic-associated colitis?

A

hospitalized patients on antibiotics –> exposed to c. diff

478
Q

what are the toxins ordered by c. diff?

A

Toxin A: enterotoxin –> watery diarrheaToxin B: cytotoxin –> cell necrosis/fibrin deposition***Toxin B stronger

479
Q

is c. diff invasive?

A

no, disease caused by toxins A/B

480
Q

how do the toxins of c. diff cause disease?

A

toxins bind GI cells and are internalized –> destroy cytoskeleton of GI cells –> pseudomembrane of the colon

481
Q

what does c. diff colitis cause?

A

massive watery diarrhea **look for recent antibiotic use

482
Q

what will you see on endoscopy in c. diff colitis?

A

pseudomembrane formation = white-yellow plaquesmucosal ulcerations, fibrin, inflammatory cells

483
Q

Dx c. diff colitis

A

stool detection of Toxin A and B

484
Q

c. diff colitis aka

A

pseudomembranous colitis

485
Q

Tx c. diff colitis

A

metronidazoleORAL vancomycin

486
Q

Tx for severe, recurrent c. diff colitis infections

A

surgerystool transplant - introduce stool with healthy bacteria

487
Q

what is metronidazole used to Tx?

A

anaerobes below the diaphragm

488
Q

why is oral vancomycin rarely used and why is it used to Tx c. diff colitis?

A

it is poorly absorbed but in c. diff this is good so that it stays in the colon and kills the c. diff bacteria

489
Q

what are the special features of corynebacterium diphtheria?

A

produces exotoxinunique lab diagnostic techniques

490
Q

how does the diphtheria exotoxin cause disease?

A

β-prophage (lysogenic phage) –> incorporates DNA into bacteria –> synthesis of exotoxin –> inactivates EF-2 (necessary for tln)

491
Q

diphtheria exotoxin is synthesized and secreted from DNA that ______ part of the bacterial genome

A

is not

492
Q

what carries the DNA for diphtheria exotoxin?

A

a phage called β-prophage = lysogenic phage

493
Q

how does diphtheria exotoxin inactivate EF-2?

A

Adp-Ribosylation of EF-2 —> no protein synthesis

494
Q

what are the characteristics of corynebacterium?

A

gram + rodscurved”Chinese character” distribution

495
Q

In order to culture corynebacterium, what special medium is used?

A

Loeffler’s or Tinsdale (tellurite plate)

496
Q

corynebacterium will grow _______ on tinsdale media and ________ on loeffler’s media

A

black coloniesmetachromatic (blue/red) granules

497
Q

Dx corynebacterium

A

Elek test for toxin detection

498
Q

how does the Elek test work?

A

plate unknown bacteria on agar plate w/ diphtheria antitoxin-impregnated filter paper underneathif unknown bacteria secretes diphtheria toxin you can visualize precipitation @ 45º angles

499
Q

Sx of diphtheria

A

sore throat, fever, LADgray-white membrane in pharynx

500
Q

why is diphtheria a serious illness?

A

b/c absorption/dissemination of toxin can cause:myocarditis = heart failure, arrhythmias, heart blockCNS disease = neuropathiesrenal disease = renal failure

501
Q

how do children often die from diphtheria?

A

myocarditis and heart failure

502
Q

you can vaccinate for diphtheria with a _____ vaccine

A

toxoid

503
Q

Tx for acute diphtheria infection

A

penicillindiphtheria antitoxin (passive immunization)diphtheria toxoid (active immunization)

504
Q

listeria is found in _____

A

soil

505
Q

what is unique about how listeria moves?

A

tumbling motilitymoves inside cells from cell to cell to avoid extracellular responsetakes over host cell machinery and polymerizes actin to move, generating “actin rockets”

506
Q

what type of organism is listeria?

A

facultative intracellular

507
Q

what population is susceptible to listeria?

A

people with poor cell-mediate immunity:neonatesHIVorgan transplant

508
Q

how is listeria ingested in adults?

A

contaminated food: likes cold tempundercooked meat, unwashed vegetables****unpasteurized cheese/milk

509
Q

how do neonates get infected with listeria?

A

transplacental or vaginal transmission

510
Q

what does listeria cause?

A

gastroenteritis - N/V/D, self-limitedmeningitis

511
Q

bacteremia will be present in the ______ if a pregnant woman is infected with listeria

A

3rd trimester

512
Q

listeria in pregnancy will present as…

A

flu-like illness - fever/chills

513
Q

is listeria infection in pregnancy serious?

A

no - often resolves spontaneously and rarely caused fetal demise/newborn infection

514
Q

listeria can cause meningitis in what 2 populations and why

A

elderly and newborns both have poor cell-mediated immunity

515
Q

what is granulomatosis infantiseptica?

A

infection of a baby from mom in pregnancy = severe in utero infection from listeria

516
Q

S/Sx granulomatosis infantiseptica

A

baby develops disseminated abscesses and/or granulomasskin lesions - papules/ulcersmost babies stillborn or die soon after birth

517
Q

what organs are involved in granulomatosis infantiseptica

A

liverspleenlungskidneysbrain

518
Q

what is the distinctive inflammatory pattern seen in the placenta with babies who have granulomatosis infantiseptica

A

chorioamnionitis - inflammation of the chorionvillitis - inflammation of the villiabscess formation

519
Q

mom w/ flu-like illness in 3rd trimester and miscarries

A

granulomatous infantiseptica from listeria

520
Q

what does bacillus anthracis cause?

A

anthrax - skin or pulmonary diseaselargely eradicatedweapon of bioterrorism

521
Q

what does bacillus cereus cause?

A

food poisoning

522
Q

why is bacillus anthracis used as a weapon of bioterrorism?

A

spores can be released into a populated area and cause widespread disease

523
Q

bacillus anthracis is the only bacteria with a ________ capsule

A

polypeptide

524
Q

most bacteria have a ______ capsule

A

polysaccharide

525
Q

b. anthracis capsule contains _____

A

D-glutamate

526
Q

how does a polypeptide capsule benefit b. anthracis?

A

D-glutamate limits/prevents phagocytosis

527
Q

b. anthracis is found in ____

A

soil

528
Q

what animals are susceptible to b. anthracis? as a result, what occupation is at risk?

A

cattlesheephorsesfarmers

529
Q

spores from _____ can be used as bioterrorism weapon

A

b. anthracis

530
Q

what toxins does b. anthracis produce?

A

edema toxinlethal toxin

531
Q

how does edema toxin cause disease?

A

edema factor activates AC –> increases cAMP –> fluid secretion

532
Q

what are the active components of the toxins produced by b. anthracis?

A

edema factorlethal factor

533
Q

how does lethal toxin cause disease?

A

lethal factor is a protease that inhibits cell signaling and causes apoptosis

534
Q

how does b. anthracis cause cutaneous disease?

A

spores enter skin through cut/abrasion –> bacteria vegetate and grow –> PAINLESS black ulcers surrounded by edemacan progress to bacteremia and death

535
Q

in anthrax cutaneous disease, what causes the edema seen surrounding each ulcer formed?

A

edema factor

536
Q

what is the treatment for anthrax cutaneous disease?

A

ciprofloxacindoxycyclineclindamycin

537
Q

in b. anthracis cutaneous disease, ulcers are formed surround by edema. what causes this edema?

A

edema factor

538
Q

what form of anthrax is most dangerous?

A

pulmonary disease

539
Q

woolsorters’ disease

A

anthrax pulmonary disease

540
Q

how does anthrax cause woolsorters’ disease?

A

inhalation of spores into lungs –> flu Sx that rapidly progress

541
Q

where did woolsorters’ disease get it’s name?

A

ppl that work on wool from farm animals would inhale the spores and become sick

542
Q

in woolsorters’ disease, what do the flu Sx rapidly progress to?

A

pulmonary hemorrhagemediastinitisshockdeath

543
Q

classic finding of pulmonary anthrax on CXR

A

widened mediastinum from mediastinitis

544
Q

treatment for pulmonary anthrax

A

difficult to treat = multi-drug regimenantitoxin

545
Q

what is the classic cause for a widened mediastinum? How can you distinguish this cause from pulmonary anthrax?

A

aortic dissectionpulmonary anthrax = flu Sx & possible anthrax exposure

546
Q

what does b. cereus cause?

A

food poisoning from enterotoxins

547
Q

what organism is classically ingested from undercooked/reheated rice?

A

b. cereus

548
Q

reheated rice syndrome

A

b. cereus food poisoning

549
Q

pathogenesis of b. cereus food poisoning

A

bacteria in uncooked rice –> heat-resistant spores survive cooking –> cooked rice at room temp allows bacteria to multiply –> direct ingestion of enterotoxin

550
Q

what are the 2 types of b. cereus food poisoning?

A

emetic = vomit no diarrheadiarrheal = diarrhea no vomit

551
Q

pathogenesis of b. cereus emetic food poisoning

A

direct ingestion of toxin: Cereulide –> abdominal cramps, N/V w/o diarrhea

552
Q

how long after ingestion of b. cereus will Sx of emetic food poisoning develop? how does this compare to the diarrheal type?

A

emetic = 1-5 hrsdiarrheal = 8-16

553
Q

b. cereus emetic food poisoning classically occurs in what type of food?

A

rice dishes

554
Q

Sx of b. cereus diarrheal food poisoning will show _______ after ingestion

A

8-16 hours

555
Q

Sx of b. cereus diarrheal food poisoning

A

abdominal crampsdiarrheaNO VOMITING

556
Q

the toxins that cause b. cereus diarrheal food poisoning are heat ____

A

labile - destroyed by heat - COOK FOOD

557
Q

how can you reduce risk of illness w. b. cereus diarrheal food poisoning?

A

cook food thoroughly

558
Q

what foods are commonly associated with b. cereus diarrheal food poisoning?

A

meatvegetablessauces

559
Q

where is actinomyces found normally?

A

oral florafemale genital tract

560
Q

does actinomyces like O2?

A

no it is an anaerobe

561
Q

why was actinomyces first considered a fungi?

A

because it clusters into long filaments resembling fungiclassified as branching filamentous

562
Q

what does actinomyces cause?

A

head/neck abscesses (normal oral flora, gets into soft tissue => abscess)IUD infections in women

563
Q

what procedure is actinomyces infection usually preceded by? how will they present?

A

dental work/orofacial traumafacial mass present on examoften yellow center (suffer granules)often draining puss

564
Q

what is the treatment for actinomyces abscesses?

A

penicillindrainage

565
Q

what shape is nocardia?

A

branching filamentous (like actinomyces), resembles fungi

566
Q

what other bacteria besides mycobacteria is acid-fast?

A

nocardia

567
Q

what does nocardia produce that is used for identification?

A

urease

568
Q

does nocardia like O2?

A

yes - obligate aerobeloves lungs = pulmonary infection

569
Q

nocardia is found in ____ but it can be ingested by ______

A

soilinhalation

570
Q

nocardia is a very rare cause of infection but it can potentially cause what 2 illnesses?

A

pneumoniaskin infection

571
Q

the infection that nocardia causes is dependent on what factor?

A

immune system functionimmunocompromised = pneumoniaimmunocompetent = skin infection

572
Q

how does nocardia cause pneumonia?

A

inhalation of bacteria in immunocompromised patients (HIV/AIDS)

573
Q

immunocompromised patientbranchingacid-fast

A

classic nocardia infection scenario

574
Q

nocardia skin infection often invades the skin during what 2 activities? why?

A

gardeningfarmingfound in soil

575
Q

nocardia in immunocompetent patients causes what?

A

skin infection

576
Q

DOC for nocardia

A

TMP-SMX aka bactrim

*med3* (21 decks)

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