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Immuno practice > Unit 1 > Flashcards

Unit 1 Flashcards

0
Q

natural selection (can/cannot) be observed while it is happening

A

can

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1
Q

generation of diversity (can/cannot) be seen while it is happening

A

cannot

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2
Q

diseases in which genetic changes lead to increased pathogenicity

A

syphilis, Spanish flu

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3
Q

diseases that have lost pathogenicity

A

syphilis, scarlet fever

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4
Q

diseases in which genetic changes lead to changes in host range

A

AIDS, SARS

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5
Q

diseases in which genetic changes can lead to drug resistance

A

Staph, HIV is developing resistance to anti virals

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6
Q

clean water is associated with rarity of ___

A

cholera

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7
Q

clean air is associated with reduction in ___

A

tb

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8
Q

vaccines have helped ____ (six diseases)

A

measles, mumps, rubella
smallpox
polio
diptheria

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9
Q

recently discovered to be infectious diseases

A

stomach ulcers, cervical cancer

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10
Q

what sequence is used to determine generation of diversity

A

16s RNA

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11
Q

what is the rate of change in bacterial DNA

A

1% every 50 million years

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12
Q

bacterial DNA has this shape

A

circular

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13
Q

circles of DNA containing small numbers of genes that are not essential to the bacterium, extrachromosomal

A

plasmid

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14
Q

viruses that infect bacteria and carry a small number of genes (3 or 4) that are not essential to the bacterium, may be extrachromosomal or integrated

A

bacteriophages

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15
Q

(a lot/not a lot) of the bacterial genome has a known function

A

a lot

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16
Q

pyr- gal- amp

A

cannot make pyrimidine (lacks pyr gene)
cannot digest galactose (lacks galactose synthesis gene)
resists ampicillin (has a gene that digests ampicilin)

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17
Q

genetic basis for ID and classification of bacteria: ___ gene

A

16sRNA

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18
Q

bacterial genes with related functions all share the same regulatory elements, known as ____

A

operon

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19
Q

how is bacterial transcription regulated

A

by metabolic products or deficiencies directly (unlike eukaryotes which use a promoter)
can be positive or negative regulation

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20
Q

_____ is when bacteria in a large group express different genes than when only a small number are present

A

quorum sensing

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21
Q

Ames test

A

bacteria are used to predict if an agent could be a carcinogen

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22
Q

antibiotic resistance is usually due to:

A

acquisition of genes from some other bacteria

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23
Q

how does transformation gene exchange work

A

DNA released from a dead bacteria may be taken up non specifically by live bacteria. Could be chromosomal or plasmid DNA. May be incorporated into recipient genome by homologous recombination.

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24
Q

transformation allows the ____ gene to be transferred in S. penumonii

A

capsule

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25
Q

____ enzymes are used in genetic engineering for cutting and splicing DNA for production of new plasmids or viruses

A

restriction

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26
Q

practical uses of transformation in bacteria

A

recombinant Hep B vaccine, recombinant insulin, virus vectors for gene therapy

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27
Q

how does conjugation gene exchange work

A

F factor plasmid is injected through the male’s sex pilus, both bacteria must be alive.

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28
Q

conjugation is used to transfer ____ genes among intestinal bacteria

A

anti biotic resistance

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29
Q

F- bacteria

A

female

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30
Q

F+ bacteria

A

male, without integration

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31
Q

Hfr bacteria

A

male with integrated plasmid due to H Frequency Recombination

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32
Q

how does gene exchange occur via transduction

A

some bacteriophage (lytic phage) can infect bacteria and cause lysis, releasing DNA which can then be taken up by the bacteriophage and carried into another bacterium

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33
Q

a bacteriophage that can insert itself into the bacterial chromosome producing a prophage in the chromosome

A

lysogenic phage

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34
Q

what does a prophage do and what kind of transduction is it involved in

A

it excises itself with some adjacent bacterial DNA and which is carried out to another bacterium, specialized transduction

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35
Q

specialized transduction transfers toxins of ____ (four diseases)

A

diptheria, botulism, scarlet fever, cholera

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36
Q

non chromosomal DNA that carry genes for antibiotic resistance

A

R factors

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37
Q

regions of a bacterial chromosome that have several adjacent genes that contribute to pathogenesis of a disease

A

pathogenicity islands

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38
Q

how are pathogenicity islands transferred between bacteria

A

transformation, transduction, conjugation

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39
Q

where the bacterial genome is localized

A

nucleoid

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40
Q

what kind of ribosomes do bacteria have

A

70S

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41
Q

what is the bacteria cell wall made of

A

peptidoglycan

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42
Q

how to bacteria reproduce

A

binary fission

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43
Q

difference between gram + and -

A
  • has an LOS/LPS layer, and + has a thicker cell wall
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44
Q

steps of the gram stain

A

fix, crystal violet, iodine, decolorize, counterstain. gram + binds crystal violet permanently while gram - releases the crystal violet.

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45
Q

why do acid fast bacteria resist gram staining

A

mycolic acid layer

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46
Q

Gram - endotoxin

A

LPS

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47
Q

Gram + surface structure that occasionally causes septic shock

A

teichoic acids

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48
Q

slime layer for attachment, biofilms

A

glycocalyx

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49
Q

capsule achieves what for the bacteria

A

immune evasion

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50
Q

vaccines are raised against

A

the capsule

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51
Q

gram + pili

A

simple and newly discovered

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52
Q

gram - pili

A

complex, Type I attachment, variants Type 4 propulsion, Types 3 and 4 secretion

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53
Q

porin proteins are found in __ bacteria

A

gram -

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54
Q

what cleaves the peptidoglycan cell wall

A

lysozyme

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55
Q

mycobacter is acid fast ___

A

+

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56
Q

E. coli is acid fast ___

A
  • (appears blue)
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57
Q

what part of the LPS/LOS is toxic

A

the Lipid A chains

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58
Q

two types of glycocalyx

A

slime layer and capsule

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59
Q

motion of bacteria flagella

A

corkscrews, not whiplike

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60
Q

how are bacteria flagella powered

A

transmbembrane electron gradients

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61
Q

difference between eukaryotic and prokaryotic bacteria ribosomes

A

bacterial ribosomes are smaller and sediment less readily under ultracentrifugation (70S/80S)

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62
Q

chemical differences between eukaryotic and prokaryotic ribosomes are capitalized on for

A

drug targets

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63
Q

when some bacteria are nutrient depleted, they go through a multi step process to become

A

spores

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64
Q

spores can resist all cleaning except

A

autoclaving

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65
Q

with unlimited nutrients and waste removal, bacteria undergo ___ growth

A

exponential

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66
Q

pattern of bacterial growth in culture vessel

A

lag, log, stationary, death

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67
Q

facultative aerobes, obligate aerobes, and aerotolerant anaerobes have these enzymes

A

protective enzymes like catalase, oxidase, superoxide dismutase

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68
Q

how obligate anaerobes get their ATP

A

fermentation

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69
Q

bacteria that cannot ferment are ____ _____

A

obligate aerobes

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70
Q

bacteria that encode pathways for both fermentation and respiration are __ ___

A

facultative anaerobes

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71
Q

the ability of some bacteria to sense their population density and alter their genetic expression accordingly

A

quorum sensing

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72
Q

what does quorum sensing require

A

an inducer, a receptor for the inducer, and a transcriptional activator that responds to high intracellular levels of the inducer

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73
Q

examples of when bacteria use quorum sensing (two examples)

A

biofilms and coordinated expression of toxins

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74
Q

common structure of exotoxins

A

AB subunit structure. B delivers A to site of A’s toxic activity.

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75
Q

common activity for A subunit in exotoxin

A

ADP-ribosylation

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76
Q

inactivated toxoids are used for

A

vaccines

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77
Q

steps of koch’s postulates

A
  1. observe pathogen in sick animal
  2. grow pure culture of pathogen
  3. infect new animal from pure culture
  4. observe same disease in new animal
  5. obtain pure culture of same pathogen from new animal
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78
Q 
normal flora examples and where they are located 
skin:
skin:
throat:
throat:
gut:
A

S. epidermidis
C. albicans
staph and strep in throat
coliforms in gut

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79
Q

normal flora can become ___ when assumptions of commensal relationship are violated

A

opportunistic pathogens

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80
Q

normal flora that act as symbiotes and where they are found

A

lactobacillus in vagina, nutrient generating bacteria in gut

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81
Q

assumptions of commensal relationship

A

containment in appropriate compartment, immunocompetent host, balance among commensal organisms

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82
Q

commensals participate in this process that is an element of innate immunity

A

colonialization resistance

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83
Q

non pathogen ID and LD

A

very high ID and LD

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84
Q

profound toxicity may result from (3 ways)

A

superantigenicity, interference with signal transduction, depolymerization of actin

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85
Q

enterobacteriaceae is a phylogenetic grouping including foodborne members (four) and opportunistic pathogens (six)

A

Shigella, E. coli, Salmonella, Yersinia

Klebsiella, Enterobacter, Serratia, Proteus, Providencia, and Morganella

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86
Q

enterobacteriaceae are gram __ by definition

A

(-)

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87
Q

enterobacteriaceae are (sporulating/non sporulating) by definition

A

non sportulating

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88
Q

enterobacteriaceae are shaped like

A

straight rods

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89
Q

enterobacteriaceae are (aerobes, anaerobes, facultative anaerobes)

A

facultative anaerobes

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90
Q

enterobacteriaceae are catalase (+/-)

A

(+)

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91
Q

enterobacteriaceae are oxidase (+/-)

A

(-)

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92
Q

enterobacteriaceae (can/cannot) ferment glucose

A

can

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93
Q

virulence concern for enterobacteriaceae

A

promiscuous, extreme antibiotic resistance is a huge problem for the whole group

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94
Q

how to do antimicrobial sensitivity testing

A

smear an agar plate with a liquid culture of the patient isolate, place disks of various antibiotics on the plate before overnight incubation

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95
Q

results of antimicrobial sensitivity testing

A

successful plating produces a lawn of bacteria interrupted by zones of clearing around effective antibiotics. zones of clearing must be measured and compared to a table to determine which antibiotic is the most effective

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96
Q

enterobacteriaceae virulence factors in the gut

A

pili for attachment (GI and urinary tract continuously push stuff out otherwise), and T3SS (for adhesion, enterotoxins, subverting gut macrophage)

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97
Q

how enterobacteriaceae get into the gut

A

allow themselves to be sampled by M cells in Peyer’s patches, then alter local macrophages for bacterial survival and spread to the exterior surface of the gut (T3SS) OR use macrophages as Trojan Horses to gain access into the whole system (Typhoid fever) via lymph nodes

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98
Q

prevention of foodborne enterobacteriaceae

A

water treatment, handwashing, food pasteurization, cooking

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99
Q

a primarily pediatric complication caused by release of shiga toxin into the bloodstream

A

hemolytic uremic syndrome

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100
Q

patients positive for this antigen may develop reactive arthritis after an infection by Shigella, Salmonella, Yersinia, campylobacter, or chlamydia

A

Human Leukocyte Antigen

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101
Q

major opportunistic nosocomial pathogens that rarely cause symptoms in previously healthy people

A

ICU bugs: Klebsiella, Enterobacter, Serratia, Proteus, Providencia, Morganella

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102
Q

how to prevent spread of ICU bugs

A

switching of IV lines and catheters, ICU and patient scrubdowns, minimization of hospital stays

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103
Q

obligate anaerobes derive all their ATP from ____

A

fermentation

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104
Q

products of fermentation

A

organic acids, alcohols, solvents

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105
Q

enzymes necessary to grow in an oxygen atmosphere

A

catalase, superoxide dismutase, peroxidase

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106
Q

two sources of anaerobic pathogens

A

normal flora that escape their proper compartment and form an abscess at a new site OR soil organisms that enter the body through wounds or consumption

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107
Q

consumption of vacuum packed food causes ingestion of

A

anaerobic pathogens

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108
Q

culture of anaerobes requires:

A

anoxic conditions-growth and handling
reducing agents and tightly stoppered in fully filled container-liquid
agar plates incubated in an anaerobic jar
anaerobic glovebox

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109
Q

how to identify unknown anaerobes

A

gram stain, gas chromatography of fermentation products

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110
Q

major pathogenic anaerobes (three)

A

Clostridium, GNAB, actinomyces

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111
Q

Gram + anaerobic pathogens

A

Clostridium and Actinomyces

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112
Q

normal flora anaerobic pathogens

A

GNAB, actinomyces, C. difficile

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113
Q

type of anaerobic pathogen from soil

A

Clostridium (minus C. difficile)

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114
Q

anaerobic pathogens from the soil use ___ ability to jump into humans

A

spore forming

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115
Q

how is anaerobic virulence determined

A

exotoxin expression

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116
Q

anaerobic pathogen diseases that result from neurotoxin expression

A

tetanus and botulism

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117
Q

anaerobic pathogen diseases that depend on tissue-degrading enzymes

A

gas gangrene and abscess formation

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118
Q

abscess disease treatment begins with ______

A

surgery (draining, debriding)

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119
Q

toxigenic disease treatment begins with ___

A

antitoxin

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120
Q

anaerobic infection treatment concludes with ____

A

antibiotics

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121
Q

there are cases of C. difficile infections being passed between two hospital patients who were both examined by the same colonoscope–how?

A

C. difficile forms spores and colonoscopes cannot be auto claved

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122
Q

some foodborne Clostridium infections can be treated without antibiotics–how?

A

because exotoxins. Botulism can be caused by ingestion of C. botulinum toxin without any live Clostridia being present (or not able to colonize gut). These intoxications can be treated with antitoxin and do not require antibiotics.

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123
Q

why do anaerobes grow slowly in culture

A

their metabolism is inefficient

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124
Q

abscesses fill with:

A

bacteria and dead neutrophils

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125
Q

what does a test tube culture look like if it is growing a strict aerobe

A

growth just at top

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126
Q

what does a test tube culture look like if it is growing a strict anaerobe

A

growth only at bottom

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127
Q

what does a test tube culture look like if it is growing facultative anaerobe

A

growth throughout

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128
Q

how does gas chromatography work to identify anaerobes

A

either extracts from culture or pus sample are run against control mixes of several acids

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129
Q

penicillin G, cefoxitin, chloramphenicol, clindamycin, metronidazole

A

antibiotics for anaerobic bacteria

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130
Q

shape of pathogenic anaerobes

A

rods

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131
Q

anaerobic bacteria that form spores

A

clostridium and some GNAB

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132
Q

TB has been a major human disease for ___ years

A

5000

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133
Q

eradication of TB seemed possible until__

A

AIDS

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134
Q

implications of slow growing mycobacteria

A

delays in vitro culture results, defeats some antibiotics

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135
Q

mycobacteria gram stain result

A

poor gram staining because of mycolic acid cell wall structure

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136
Q

acid fast result for mycobacteria

A

(+)

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137
Q

how does TB get to the CNS

A

hematogenous spread

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138
Q

how does TB get to the GI tract

A

swallowing infected sputum

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139
Q

how does an immunocompetent person react to TB infection

A

strong CMI response, can hold infection latent for decades

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140
Q

how does hematogenous spread of infection occur

A

intracellular infection of naive macrophages (Trojan Horse)

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141
Q

response in immunocompetent host to TB in macrophages

A

CD8 cells kill infected macrophages and establish granulomas in which infection is contained

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142
Q

extrapulmonary manifestations of TB are ___ and are usually a sign of ___

A

scrofula in neck, genitourinary, CNS (meningitis or abscess), skeletal
reactivation

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143
Q

response to pediatric TB

A

trace source (it was recently acquired) and watch for miliary and meningitis (lethal pediatric infections)

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144
Q

TB infection protocol: determine exposure by __ and/or __, perform __ ___ ___ as soon as cultures grow

A

TST and/or IGRA, antibiotic resistance testing

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145
Q

directly observed therapy for TB

A

4+ drug therapy featuring isoniazid, isolate patient for first two weeks

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146
Q

TB vaccine

A

BCG, used abroad, not cost effective here

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147
Q

best way to reduce TB

A

good diet and housing

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148
Q

atypical mycobacteria are ____ acquired and do not cause ___

A

environmentally, leprosy/TB

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149
Q

atypical mycobacteria infection in an immunocompetent adult is usually _____

A

cutaneous

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150
Q

atypical mycobacteria infection in a child is usually ___

A

scrofula

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151
Q

immunosuppressed hosts of atypical mycobacteria may exhibit:

A

TB like symptoms (particularly from M. kansasii or MAI/C

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152
Q

atypical mycobacteria infections are (easy/difficult) to treat

A

difficult, require multiple antibiotics

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153
Q

M. leprae challenge

A

no in vitro culture system

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154
Q

M. leprae has a (long/short) incubation period

A

long, doesn’t transmit easily

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155
Q

Tuberculoid leprosy

A

PPD+, paucibacillary, vigorous CMI both contains infection and damages nerves

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156
Q

Lepromatous Leprosy

A

multibacillary, weak CMI, extensive cutaneous symptoms, PPD-

157
Q

Lepromin PPD tests:

A

anti-leprosy response and position on the tuberculoid-lepromatous spectrum, does NOT test exposure

158
Q

treatment for leprosy

A

2 years dapsone+rifampin

159
Q

CMI stands for

A

cell mediated immune response

160
Q

CMI response to TB infection

A

terminates the unimpeded growth of the M. tuberculosis 2-3 weeks after initial infection

161
Q

miliary TB

A

more likely to develop right after primary infection, less likely as a reactivation. hematogenous spread of TB through body, many tiny noncalcified foci of infection appear like millet seeds in lung on chest x ray

162
Q

M tuberculosis diagnosis-TB meningitis

A

Brudzinski’s neck sign (lay child flat, pull up head, knees come up as well)

163
Q

MAI, MAC

A

M avium and M intracellulare, very difficult to distinguish

164
Q

result of MAI/MAC

A

pulmonary disease indistinguishable from TB in severely immunocompromised patients, environmentally widespread, found in soil and water
highly drug resistant

165
Q

transmission methods of spirochetes

A

sexual, vector-borne, environmental

166
Q

action of spirochetes

A

cross quickly into bloodstream causing immediate bacterermia and eventual multi-organ infections. some cross the blood-brain barrier leading to meningitis and other CNS symptoms

167
Q

why no vaccines for spirochetes?

A

virulence factors are primarily for immune evasion, not very antigenic to start with and may immunomodulate the host to further decrease the response.

168
Q

why is diagnosis of spirochete infection challenging?

A

disease proceeds in phases which may be separate by months or years (need for meticulous history!), treponema are too small to see by standard microscopy, Lyme has no clear and quick lab test

169
Q

eye exams can be useful to diagnosis of ___ infections

A

spirochete

170
Q

antibiotic resistance is/is not a problem for spirochete infections

A

is not

171
Q

spirochete reaction to treatment

A

Jarisch-Herxheimer

172
Q

stages of syphilis

A

painless chancre, rash with flu (meningitis possible), latency or dangerous cardiac or CNS involvement (gummas possible)

173
Q

congenital syphilis

A

devastating but preventable with prenatal care

174
Q

Lyme disease requires ___ ___ to transmit (amount of time)

A

24 hours

175
Q

prevention of lyme

A

prompt removal of ticks with gloves, tweezers, possible doxycycline

176
Q

three phases of Lyme disease

A

skin infection, immune/neurological issues, chronic lyme with more severe immune, neuro-, fibromyalgia

177
Q

antibiotic treatment for lyme

A

may take a month but no more than that

Jarisch-Herxheimer reaction may help to confirm diagnosis

178
Q

vibrio shape

A

curved rods

179
Q

vibrio gram stain

A

gram -

180
Q

where do vibrios reside

A

oceans

181
Q

what disease do vibrios cause

A

fecal-oral gastroenteritis

182
Q

H pylori causes

A

peptic ulcers

183
Q

vibrios may infect wounds contaminated by

A

seawater, ocean debris

184
Q

gastroenteritis and peptic ulcers require that the vibrios have __ ___ factors

A

GI virulence factors

185
Q

most pathogenic strains of V cholerae

A

contain O1 genetic marker of colonization by lysogenic bacteriophage that carries virulence factors

186
Q

how is V cholerae transmitted

A

fecal oral

187
Q

how does V cholerae infect the host

A

usually killed by stomach acid

if it survives, secretes mucinase to attach to and colonize the intestine

188
Q

after colonizing the intestine, V cholerae secretes

A

choleragen

189
Q

choleragen is

A

an AB subunit enterotoxin that interferes with signal transduction

190
Q

choleragen causes

A

massive watery diarrhea

191
Q

main problems to treat with cholera

A

dehydration and electrolyte imbalance

192
Q

Campylobacter jejuni carries:

A

GI virulence factors like pili that allow it to establish a locus of infection in the intestine

193
Q

characteristics of syphilitic meningitis

A

low inflammation, may not express Brudzinski’s signs

194
Q

gummas

A

gummatous syphilis: granulomatous lesions with rubbery, necrotic center (primarily liver, bones, testes)

195
Q

cardiovascular syphilis

A

aneurysm of ascending aorta caused by chronic inflammation of vasa vasorum

196
Q

Argyll Robertson pupil

A

hallmark of neurosyphilis

one or both pupils fail to respond to light but does constrict to focus on a near object

197
Q

major intracellular pathogens (there are a lot, like ten)

A

Neisseria, Enterics (Shigella, E. coli, Salmonella, Yersinia), Mycobacter, some bacilli, Legionella, Listeria, Rickettsial, Chlamydia, some fungal infections (Histoplasma, Cryptococcus), ALL viruses

198
Q

strategies for intracellular survival

A

escape the endosome, subvert the endosome, survive endolysosomal fusion

199
Q

facultative intracellular pathogens

A

can divide independently on agar plates but enter host cells as part of their pathogenesis (Neisseria, Enterics, Mycobacter, bacilli, Legionella)

200
Q

obligate intracellular pathogens

A

Rickettsial, Chlamydia–require host cell resources to multiply

201
Q

how are obligate intracellular pathogens grown in lab

A

tissue cultures like viruses

202
Q

how intracellular pathogens use human macrophages

A

for transport around the body and to evade humoral and surface-innate immunity (actin based cell-cell spread)

203
Q

how intracellular pathogens use T3SS

A

enhance phagocytosis by the target cell type or alter the endosome so lysosomes fail to fuse it

204
Q

antibiotics used to treat intracellular infections

A

tetracyclines (contraindicated in pregnancy)

must cross human cell membrane easily and remain active or activatable after doing so

205
Q

facultative intracellular bacterium that causes gastroenteritis when it contaminates cold-stored pre-prepared foods

A

Listeria monocytogenes

206
Q

how does Listeria monocytogenes infect its host

A

after endocytosis, it escapes the endosome and uses actin-based motility to spread between cells (ActA virulence factor)

207
Q

Listeria monocytogenes can cause what in immunosuppressed? and will complicate what?

A

dangerous disease such as meningitis

pregnancy (no deli meat or cheese)

208
Q

Chlamydia obligate intracellular replication strategy and how they enter cells

A

tiny, infectious, rugged elementary bodies which “unpack” into larger, delicate reticulate bodies after cell penetration. They carry a T3SS for entry

209
Q

Chlamydia infection carries a risk of:

A

Reactive Arthritis sequel

210
Q

difficulties in diagnosing chlamydia

A

may hide behind other STD on exam

211
Q

common problem with chlamydia

A

reinfection from partner

212
Q

chlamydia ____ bodies are small, infectious, have a rigid outer membrane, are rugged, bind to receptors on epithelium of lung or mucous membrane

A

elementary

213
Q

chlamydia ____ bodies are the non infectious intracellular form, metabolically active, replicating, synthesizes own DNA RNA and proteins, requires ATP from host cell, fragile Gram - membrane

A

reticulate

214
Q

Listeria shape and gram stain

A

small gram + rod

215
Q

Listeria motility

A

tumbling by temperature sensitive flagella

216
Q

Listeria hemolysis

A

beta hemolytic

217
Q

structural virulence factors for Staph

A

Protein A, capsule, coagulase

218
Q

a basic component of understanding the prevention and control of infection

A

Chain of Infection

219
Q

how HAI’s (hospital acquired infections) occur

A

direct contact with infecting agent from an infected or colonized individual carried from one person to another by health care workers
indirect contact via contaminated equipment or other inanimate objects
respiratory transmission (airborne or droplet)

220
Q

how the infecting agent leaves the reservoir host

A

portal of exit

221
Q

isolation/cohorting of infected individuals in the hospital (does/does not) help to eliminate the source of the infectious agent

A

does help

222
Q

standard precautions for healthcare workers

A

clean hands when entering and leaving the patient’s room, cover mouth and nose with arm or tissue when coughing or sneezing, wear gown and glove if soiling is likely, wear mask and eye protection if splashing with body fluids likely

223
Q

diseases that can be suspended in the air and travel via air currents

A

TB, chickenpox, shingles, measles, pandemic influenza

224
Q

airborne infection precautions

A

N95 mask and gown, private negative pressure room, patients wear surgical masks if leaving room

225
Q

examples of diseases spread by droplets

A

bacterial meningitis, seasonal flu, pertussis, mumps

226
Q

precautions used for droplet diseases

A

surgical mask and gown, frequent hand washing

227
Q

used for patients known or suspected to be infected or colonized with epidemiologically important microorganisms (MRSA, VRE, resistant acinetobacter, ESBL gram negatives)

A

contact precautions

228
Q

examples of contact precautions

A

gowns, alcohol based hand washing products

229
Q

diseases for which you should use Contact PLUS Precautions

A

C diff, acute diarrhea with a likely infectious cause or in adult with recent history of antibiotic use, Norovirus/Rotavirus, enteric infections (including Campylobacter, Cryptosporidium, Salmonella, Shigella, Escherichia coli)

230
Q

what are the Contact PLUS Precautions

A

hand washing with soap and water, room disinfected with bleach

231
Q

a method to prevent a patient in a compromised health situation (patient in chemo) from being contaminated by other people or objects

A

Reverse (Protective) Isolation

232
Q

what to wear for reverse isolation

A

gown, surgical mask, gloves

233
Q

most resistant infectious agent to antiseptics and disinfectants

A

bacterial spores

234
Q

infectious agents with low resistance to disinfection and antisepsis

A

HIV- lipid viruses

235
Q

describes process that destroys or eliminates all forms of microbial life and is carried out in healthcare facilities by physical or chemical methods

A

sterilization

236
Q

living tissues (can/cannot) be sterilized

A

cannot

237
Q

describes a process that eliminates many or all pathogenic microorganisms except bacterial spores on inanimate objects

A

disinfection

238
Q

the reduction of microorganisms on living tissue/skin

A

antisepsis

239
Q

antiseptics (do/do not) kill spores

A

do not

240
Q

critical items require what level of cleaning

A

sterilization via physical methods

241
Q

examples of critical items

A

items that enter normally sterile parts of the body such as surgical instruments, implants, and invasive monitoring device

242
Q

level of cleaning used for semicritical items

A

high level disinfectant

243
Q

examples of semi critical items

A

items that come into contact with mucous membranes or nonintact skin (respiratory therapy and anesthesia equipment, some endoscopes, laryngoscope blades, diaphragm fitting rings)

244
Q

how non critical items should be cleaned

A

alcohols, phenolics, halogens, quaternary ammonium compounds

245
Q

examples of non critical items

A

bedpans, blood pressure cuffs, crutches, computers

246
Q

most widely used method for sterilizing inanimate objects

A

auto claving

247
Q

benefits of auto claving

A

short processing time, highly effective

248
Q

sterilization method used for products that contain petroleum based liquids

A

dry heat sterilization

249
Q

used for products that may rust or corrode with moisture

A

dry heat sterilization

250
Q

how irradiation sterilization works

A

high energy gamma rays penetrate throughout product resulting in damage to nucleic acid

251
Q

items for which irradiation sterilization is used

A

single use medical supplies-syringes, implants, catheters, IV sets, surgical gloves, gauze

252
Q

when would filtration be used for sterilization

A

liquids that contain protein or other delicate compounds that may be destroyed by heat or radiation

253
Q

disadvantage of ethylene oxide gas sterilization

A

highly flammable and potentially explosive

254
Q

plasma sterilization is often used for items such as

A

endoscopes (high penetration of medical lumens)

255
Q

benefits of plasma sterilization

A

rapid turnaround, small enough to place next to where procedure is being performed

256
Q

compounds active against viruses (hepatitis, HIV)

A

chlorine

257
Q

compounds with broad antimicrobial spectra including, at higher concentrations, bacterial spores and M tuberculosis

A

chlorine

258
Q

used for antisepsis of skin, mucous membranes, wound sites

A

iodophores (complexes of iodine with detergents)

259
Q

used as a surgical scrub and for the treatment and prevention of infections in wounds, ulcers, cuts, and burns

A

betadine (iodine compound)

260
Q

used for general skin cleansing, surgical scrub, pre operative skin prep, can be used for showering before surgery

A

chlorhexidine

261
Q

compound with a strong bacteriostatic action against many gram positive organisms (including staph)

A

phenolics/phisohex

262
Q

powerful surfactants with built in detergent activity (do not work on endospores, M tuberculosis, non enveloped viruses)

A

Quaternary ammonium compounds

263
Q

metals used to control bacterial growth

A

silver and copper

264
Q

five strep species

A

Group A, Group B, pneumococci, viridans strep, enterococci

265
Q

three staph species

A

S aureus, S epidermidis, S saphrophyticus

266
Q

two Neisseria species

A

N meningitidis, N gonnorhoeae

267
Q

gram - cocci

A

Neisseria

268
Q

gram + cocci

A

staph and strep

269
Q

maltose fermenters in Neisseria

A

N meningitidis

270
Q

Neisseria that do not ferment maltose

A

N gonnorrhoeae

271
Q

catalase positive, gram + cocci

A

staph

272
Q

catalase -, gram + cocci

A

strep

273
Q

coagulase + staph

A

S aureus

274
Q

two species of coagulase - staph

A

S epidermidis and S saprophyticus

275
Q

Novobiocin sensitive, coagulase - staph

A

S epidermidis

276
Q

Novobiocin resistant, coagulase - staph

A

S saprophyticus

277
Q

two species of alpha hemolytic strep

A

S pneumoniae, Viridans group

278
Q

two species of Beta hemolytic strep

A

Group A, Group B

279
Q

two species of Gamma hemolytic strep

A

Group D: E faecalis, S bovis

280
Q

alpha hemolytic strep sensitive to optochin (bile salts)

A

S pneumoniae

281
Q

alpha hemolytic strep resistant to bile salt optochin

A

Viridans group

282
Q

members of the Viridans group

A

S sanguis, S mutans

283
Q

beta hemolytic strep sensitive to bacitracin

A

Group A (S pyrogenes)

284
Q

beta hemolytic strep resistant to bacitracin

A

Group B (S agalactiae)

285
Q

gamma hemolytic strep that grows in NaCl

A

E faecalis

286
Q

gamma hemolytic strep that does not grow in NaCl

A

S bovis

287
Q

appearance of Staph growths

A

grow in clumps, cocci

288
Q

hemolysis of S aureus

A

Beta

289
Q

color of S aureus colonies

A

gold

290
Q

what allows subtyping of S aureus

A

different bacteriophages affect different strains

291
Q

what does Protein A do (S aureus virulence factor)

A

binds immunoglobins

292
Q

what does the capsule do

A

inhibits phagocytosis

293
Q

S aureus toxins

A

coagulase, Protein A, enterotoxin, exfoliatin, Leukocidin, TSS toxin

294
Q

common S aureus presentation

A

abscesses

295
Q

reservoir and transmission of S aureus

A

30% of ppl carry S aureus in nose/skin

transmission by direct contact or by fomites

296
Q

hemolysis of S epidermidis

A

non hemolytic

297
Q

where is S epidermidis found

A

normal flora of skin and mucous membrane of many people

298
Q

typical infection sites for S epidermidis

A

piercings, catheters, IV lines, shunts

because it attaches to nylon and plastic readily

299
Q

hemolysis of S saprophyticus

A

non hemolytic

300
Q

what infection does S saprophyticus cause

A

UTIs in women (but not main cause)

301
Q

a method based on antisera to carbohydrate antigens of the cell wall used to classify strep

A

Lancefield group

302
Q

appearance of pneumococci

A

diplococci

303
Q

Lancefield classification of pneumococci

A

no Lancefield group

304
Q

pneumococci virulence factors

A

no toxins. polysaccharide capsule is both antigen and virulence factor which prevents phagocytosis and stimulates the opsonizing antibody

305
Q

reservoir of pneumococci

A

found in throat of 5-50% of people

306
Q

Lancefield classification of Viridans group

A

none

307
Q

viridans group virulence factors

A

enzymes that metabolize extracellular polysaccharides, acids

308
Q

reservoir of viridans group

A

normal flora of mouth in all people

309
Q

Group A strep virulence factors

A

pili encoded by a pathogenicity island, numerous toxins

310
Q

diagnostically useful hemolysin for Group A strep

A

IgM antibody from Streptolysin O

311
Q

reservoir of Group A strep

A

found in pharynx and skin of 10% of ppl

312
Q

beta hemolytic strep, resistant to bacitrain, positive in CAMP test

A

Group B strep

313
Q

main virulence factor of Group B strep

A

capsule

314
Q

reservoir and transmission of Group B strep

A

found in genital tract of 25% of women

can be transmitted to baby at or before birth

315
Q

non hemolytic strep, bile resistant

A

Group D

316
Q

non hemolytic strep, no Lancefield group, obligate anaerobes, found in abscesses that contain a complex mix of microorganisms, not primary pathogens

A

Peptostreptococcus

317
Q

reservoir or peptostreptococcus

A

normal flora of mouth, respiratory tract, female genital tract, bowel

318
Q

gram -, diplococci, require chocolate agar

A

Neisseria

319
Q

what does heating the chocolate agar achieve

A

inactivates fatty acids

320
Q

endotoxin in Neisseria

A

LOS membrane

321
Q

helps Neisseria attach to surfaces

A

IgA protease

322
Q

transmission of N meningitidis

A

droplets

323
Q

virulence factor of N meningitidis

A

polysaccharide capsule

324
Q

N gonorrhoeae virulence factor

A

pili allow attachment

325
Q

transmission of N gonorrhoeae

A

sexual or neonatal

326
Q

The application of knowledge of the organisms most likely to cause infection in a given clinical setting and its most likely susceptible antibiotic

A

empiric therapy

327
Q

what should you perform on recovered isolates of microorganisms before treating someone with an infection and why

A

antimicrobial susceptibility testing (AST) because different organisms vary in their susceptibility to antimicrobial agents

328
Q

vancomycin should be used for treatment of gram (+/-) bacterial infections

A

gram +, because it cannot penetrate the outer membrane of gram - bacteria

329
Q

Group A strep (S pyogenes) remain universally susceptible to what antibiotic

A

penicillin

330
Q

series of factors to consider for optimal choice of antimicrobial agent

A

age, history of previous adverse reactions to antimicrobial agent, pregnancy, renal and hepatic function, site of infection

331
Q

stomach pH varies with age. The pH of gastric secretions is (higher/lower) in young children.

A

higher pH, less acidic. Also less acidic in older people.

332
Q

implication of a longer half life for an antibiotic

A

increase the time between doses

333
Q

______: encompasses all the ways that the body manipulates a drug, including absorption, distribution, metabolism, and excretion

A

pharmacokinetics

334
Q

_____: describes the biochemical and physiologic effects of the drug and its mechanism of action on the bacteria

A

pharmacodynamics

335
Q

antimicrobial agents that inhibit the growth and/or reproduction of the infecting agent but fail to actually kill the agent

A

bacteriostatic

336
Q

examples of bacteriostatics

A

macrolids (erythromycin), clindamycin, sulfamethoxazole, trimethoprim, tetracyclines, and chloramphenicol

337
Q

examples of bacteriocidals

A

Beta lactam antibiotics (penicillins and cephalosporins), vancomycin, aminoglycosides (gentamycin), and fluoroquinolones (ciprofloxacin)

338
Q

antimicrobials may be ___ at low concentrations but ____at high concentrations

A

bacteriostatic, bacteriocidal

339
Q

the inhibitory concentration used to quantitate the activity of an agent against an organism

A

Minimum Inhibitory Concentration (MIC)

340
Q

examples of broad spectrum antibiotics

A

carbapenems, extended spectrum cephalosporins, beta lactam/beta lactam inhibitor combinations, newer fluoroquinolones

341
Q

examples of narrow spectrum antibiotics

A

older penicillins, macrolides, vancomycin (only gram +)

342
Q

natural antibiotics have ___ toxicity and ___ effectiveness

A

high, low

343
Q

synthetic antibiotics have __ toxicity and __ effectiveness

A

low, high

344
Q

five main mechanisms of antibiotics

A 
interfere with cell wall synthesis
interfere with protein synthesis
interfere with cytoplasmic membrane function
interfere with nucleic acid synthesis
interfere with metabolic pathway
345
Q

why use cell wall synthesis as a target of antibiotics

A

because humans don’t have a cell wall

346
Q

why use protein synthesis as a target of antibiotic action

A

because humans and bacteria have different ribosomes

347
Q

the beta lactams

A

penicillins, cephalosporins, carbapenems, monobactams

348
Q

antibiotics that interfere with cell wall synthesis

A

beta lactams, vancomycin, bacitracin

349
Q

antibiotics that act on the cell membrane

A

polymyxins

350
Q

antibiotics that interfere with folate synthesis

A

sulfonamides, trimethoprim

351
Q

antibiotics that interfere with nucleic acid synthesis

A

DNA Gyrase-quinolones

RNA Polymerase-Rifampin

352
Q

antibiotics that interfere with ribosomes

A

macrolides, clindamycin, linezolid, chlamphenicol, strepogramins, tetracyclines, aminoglycosides

353
Q

mechanism of action of antibiotics that inhibit cell wall synthesis

A

inhibit cross linking between peptide chains

354
Q

the cross linking of peptide chains in the cell wall is catalyzed by a series of transpeptidase enzymes referred to as:

A

penicillin binding proteins (PBPs)

355
Q

features of beta lactams

A

house with attached garage, can give very high doses, binds at the active site of the transpeptidase enzyme, bacteriocidal, irreversible

356
Q

four main beta lactam classes:

A

penicillins, cephalosporins, monobactams, carbapenems

357
Q

how does MRSA become resistant to beta lactams

A

by modifying the PBP

358
Q

how does the beta lactam bind to the PBP

A

it is a structural analog for the catalytic site

359
Q

as you increase from 1st generation to 4th generation of cephalosporins, what increases?

A

resistance to enzymes that destroy that antibiotic

360
Q

monobactams are active against gram (+/-) bacilli

A

gram -

361
Q

use carbapenems for:

A

bacteria that won’t be affected by penicillin or cephalosporin

362
Q

glycopeptides (vancomycin) are effective against gram (+/-) and have this mechanism of action

A

gram +

(not gram - because of LPS)bind to aa residues thus preventing the cross linking of the peptidoglycan sheets

363
Q

how does fosfomycin work

A

inhibits phosphoenel pyruvate, halting muramic acid synthesis

364
Q

when should you use fosfomycin

A

treating UTIs, one megadose

365
Q

three mechanisms of action when inhibiting protein synthesis

A

act on large ribosomal subunit
act on small ribosomal subunit
block elongation process of assembling polypeptide

366
Q

risk with using aminoglycosides

A

very close therapeutic to toxic index

367
Q

the innate ability of a bacterial species to resist activity of a particular antimicrobial agent through its inherent functional or structural characteristics

A

intrinsic/natural resistance

368
Q

gram negative bacteria have intrinsic resistance to what type of antibiotics

A

vancomycin

369
Q

enterococci have intrinsic resistance to all

A

cephalosporins

370
Q

antibiotic resistance that occurs due to chromosomal mutation

A

mutational resistance

371
Q

resistance that occurs when a particular microorganism obtains the ability to resist the activity of a particular antimicrobial agent to which it was previously suscepitible. this occurs through _______

A

acquired, horizontal gene transfer

372
Q

four major mechanisms of antibiotic resistance

A

enzymatic inactivation, decreased permeability, efflux, alteration of target site (this is what MRSA uses, alters PBP)

373
Q

what is an ESBL and what are the most common producers of ESBLs

A

extended spectrum B-lactamases: enzymes that mediate resistance to extended spectrum cephalosporins but do not affect carbepenems

produced by Gram (-)

374
Q

the action of a beta lactamase inhibitor

A

irreversibly bind to enzyme so the enzyme is taken out of the system, allowing the antibiotic to work

375
Q

example of a beta lactamase inhibitor

A

clavulanate (used with amoxicillin)

376
Q

what do beta lactamases do

A

they inactivate beta lactam antibiotics by splitting the amide bond of the beta lactam (attached garage) ring

377
Q

three types of beta lactamases

A
  1. ESBLs (cephalosporins are useless, use carbepenems, produced by Gram -)
  2. amp c beta lactamases (resistance to penicillin)
  3. carbepenemases (largest antibiotic resistance spectrum-super bugs)
378
Q

what antibiotic do you use against MRSA

A

vancomycin

379
Q

producing decoy D-ala residues at the cell surface confer resistance to which antiobiotic

A

vancomycin

380
Q

advantages of Gram staining

A

simple, reliable, gives preliminary information

381
Q

advantages of culture methods to determine cause of infection

A

can identify bacteria more specifically

382
Q

disadvantages of culture method to identify bacterial cause of infection

A

slower turnaround

383
Q

advantages of bacterial antigen testing

A

rapidly performed, relatively inexpensive

384
Q

disadvantages of bacterial antigen testing

A

some assays have poor sensitivity and there is limited availability of some assays

385
Q

direct antigen testing and detection from clinical specimens have which advantages

A

relatively inexpensive, easy to perform, rapid turnaround time

386
Q

the gram stain does not differentiate between:

A

normal flora from pathogenic bacteria

387
Q

an advantage of the molecular methods of infectious agent detection over the traditional methods

A

more rapid identification of fastidious or slow growing organisms is possible

388
Q

disadvantage of the molecular methods used to identify an infectious agent

A

detect live AND dead nucleic acids

389
Q

IgM response is:

A

immediate

390
Q

IgG response is:

A

long lasting

391
Q

higher dilution is consistent with ____ level (higher/lower) level of antibody in patient serum

A

higher

Immuno practice (3 decks)

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