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MIP 351 > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

upper respiratory track

A

s. pneumoniae
h. influenza

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2
Q

lower respiratory track bronchitis and pneumonia

A

s. pneumoniae
h. influenza
maybe mycoplasma pneumoniae

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3
Q

lower respiratory track atypical pneumonia

A

legionella pneumophila
chlamydia pneumophilia

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4
Q

tuberculosis

A

mycobacterium tuberculosis

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5
Q

what types of airway immune cells are there & functions

A

alveolar macrophages (M1 proinflammatory, M2 anti-inflammatory) — M1 main players
dendritic cells sample antigens
Tregs reduce activation of CD4 T cells
Mucosal Associated Invariant T cells (early immune responses)

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6
Q

a gram negative bacillus facultative intercellular pathogen
one flagella, motile, strict aerobe
uses amino acids (not sugars) as main carbon source and energy

(serotyoes 1 and 6 most frequently isolated)

A

legionella pneumophilia

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7
Q

can be aerosolized and spread through air conditioning systems (not spread person to person)

A

l. pneumophila

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8
Q

forms biofilms in water, expresses flagellum when reaching stationary phase (less oxygen/nutrients)

A

l. pneumophila

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9
Q

list 2-3 mechanisms this pathogen can use to protect itself from destruction by the immune system

A

intracellular living (avoids MAC killing & neutralization/aggregation by antibodies)

inhibition of phage some lysosome fusion

mechanism to escape the cell

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10
Q

Type IV membrane protein, MOMP

A

adhesion factors

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11
Q

effectors inhibit phage some lysosome fusion and high jack host ribosomes for nutrients

A

survival and replication

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12
Q

phosphatase, lipase, nuclease

A

kills host cells, extracellular enzymes that aid in dissemination

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13
Q

how does MOMP use opsonization to its advantage

A

C3b binds MOMP, alveolar macrophages engulph

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14
Q

other than human cells, what can l. pneumophila survive in

A

protozoa

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15
Q

what are two types of legionellosis

A

pontiac fever (flu-like less severe) and legionnaires’ disease

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16
Q

diagnosing legionnaires disease

A

urinary At test (usually serotype 1 but can test positive for up to a year)

culture of respiratory samples (L-cysteine and iron media), slow growing

immunoassays to detect Ab or Ag (usually epidemiological investigations)

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17
Q

why should l. pneumophila not be treated with beta lactams

A

many strains produce beta lactamases, but macrolides and fluoroquinolones should work

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18
Q

gram positive diplococcus alpha hemolytic catalase negative

gram negative coccobacillus non-hemolytic catalase positive

A

s. pneumoniae

h. influenza

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19
Q

similarities between s. pneumoniae and h. influenza

A

capsules (used for typing and vaccines)
can pick up DNA from environment (naturally transformable)

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20
Q

MAC complex is only relevant for what kind of bacteria

A

gram negative (inserted into outer membrane)

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21
Q

a polysaccharide capsule, adhesins (pili, chlorine binding proteins), and mucus degrading enzymes are virulence factors of what cell envelope

A

s. pneumoniae

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22
Q

how does natural competency work in s. pneumoniae

A

stationary phase/quorum sensing, produces lysin to kill neighboring cells

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23
Q

pore forming toxin released after autolysis, damages epithelium, released after phagolysosome fusion, pro inflammatory/leads to increased transmission shedding in nasal and respirator

A

pneumolysin

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24
Q

difference between septicemia and meningitis

A

into blood vs into brain

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25
Q

what do non type able h. influenzae lack

A

a capsule

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26
Q

LOS (shorter sugars that LPS), type IV fimbriae, adhesins, IgA protease, protein 5 (inhibits complement cascade)

A

virulence factors of h. influenzae

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27
Q

what does capsule protect against

A

MAC formation and competent cascade (opsonization)

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28
Q

binds C4b and blocks formation of C3 convertase, hides from PRRs and TLRs using sialic acid

A

LOS

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29
Q

explain phase variation

A

methylation of dna alters gene expression

upregulate to increase attachment/adherence

downregulate when exposed to immune system to hide

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30
Q

how are s. pneumoniae and h. influenzae transmitted

A

human to human
co colonize with other pathogens

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31
Q

common s. pneumoniae and h. influenzae diseases

A

sinusitis
otitis media (ear)
lower respiratory track infections (children and older adults)

invasive: meningitis and bacteremia/sepsis

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32
Q

Type B h. influenzae vs. other types

A

invasive (capsulated) vs. non-invasive

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33
Q

diagnosis of s. pneumoniae

A

gram stain of sputum cfs blood
partial (alpha) hemolysis on blood agar
optochin disc sensitivity

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34
Q

h. influenza diagnosis methods

A

gram stain of sputum/CSF/blood
cannot differentiate between other h
grows in chocolate agar (not blood)
need V factor for species ID

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35
Q

why can h. influenza grow with s. aureus

A

needs V factor and X factor that s. aureus can produce by lysing red blood cells

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36
Q

more diagnosis of s. pneumoniae

A

pcr for pneumolysin gene
lateral flow for capsular antigen (not children)
bile solubility testing/dissolves colonies
quellung test = swollen capsule

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37
Q

gram negative, no peptidoglycan, small bacteria, cholesterol and long chain fatty acids for growth, obligate pathogen

A

mycoplasma pneumoniae

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38
Q

how is m. pneumoniae transmitted

A

person to person vis respiratory droplets, s. pneumoniae and h. influenza two other CAP along with this pathogen

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39
Q

is it common to have invasive m. pneumoniae infections

A

no (upper or lower)
tracheobronchitis, pharyngitis

“walking pneumonia” slow progression of symptoms to high fever and persistent cough

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40
Q

apical organelle, CARDS toxin, production of peroxides, intracellular survival, and molecular mimicry are all virulence factors of what

A

m. pneumoniae

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41
Q

complex structure surrounded by P proteins adhesins, involved in attachment and gliding motility

A

apical organelle

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42
Q

what happens with P1 and P30 proteins

A

high similarity to host, antibodies can cause damage to host (molecular mimicry)

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43
Q

what are host receptors for m. pneumoniae made from

A

sialic acid

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44
Q

immunogenic toxin, modulates host cells to cause hyper inflammatory state (adds ADP), can cause cell death (creates vacuoles inside cell)

A

CARDS toxin

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45
Q

is m. pneumoniae more of an intracellular or extracellular pathogen

A

more extracellular but can be intracellular, inside cell protects against phagocytosis and antibiotics

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46
Q

list ways m. pneumoniae can cause direct damage to host

A

adhesins/membrane fusion damage, disturbance of metabolisms/nutrient depletion, toxin damage

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47
Q

how to diagnose m. pneumoniae

A

molecular tests (preferred), serological (ElISA, IFA, LAT), culture (not usual/may take weeks for positive culture), drug testing/typing/PPLO agar in specialized lab (need microscope to visualize)

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48
Q

antibiotics to treat m. pneumoniae

A

macrolides, tetracyclines (older children and adults), fluoroquinoloes

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49
Q

acid fast positive, gram variable bacilli, no spores/exotoxins, aerobic, non-motile, facultative intracellular, slow-growing

A

mycobacterium tuberculosis

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50
Q

why is m. tuberculosis a risk 3 pathogen

A

highly contagious
low infectious dose
no effective vaccine
hard to treat

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51
Q

what intrinsic mechanisms of resistance does m. tuberculosis have

A

thick peptidoglycan layer
thick mycolic acid/lipid layer

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52
Q

transmission of m. tuberculosis

A

indirect person to person (airborne aerosol particles)

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53
Q

“containment phase”
no overt signs of disease
no transmission
dormant m. tuberculosis in granulosas

A

latent tuberculosis

54
Q

LAM, fibronectin binding proteins, PDIM, type 7secretion system, survival under hypoxia conditions are all virulence factors of what

A

m. tuberculosis

55
Q

how to diagnose tb

A

tuberculin skin test (TST), interferon-gamma release assays (IGRAs)

(measure ability of immune system to recognize and respond to mycobacteria antigens)

56
Q

culture of slow growing bacteria (solid or liquid media)
acid fast and aura,une microscopy
Pert (qPCR that detects rig resistance)

A

diagnostic methods for tb

57
Q

treatment of tb

A

isoniazid (adverse reactions are common)
rifampin, pyrazinamide, ethambutol

58
Q

why can’t TB be treated with just one antibiotic?

A
  • need to prevent selection of antibiotic resistant strains
  • bacteria replicate slowly
  • bacteria replicate inside macrophages
59
Q

what is drug resistance mostly due to in m. tuberculosis

A

mutations (HGT not described)

60
Q

drug resistance multiple (MDR) vs. extensively (XDR)

A
  • isoniazid and rif
  • fluoroquinolones and injectable drug
61
Q

E. coli
Shigella
Smonella
Campylobacter
Yersinia
Aeromonas
C. difficile

A

invasive bacteria

62
Q

E. coli
clostridium
perfringens
Vibrio cholera
bacillus cereus

A

toxic bacteria

63
Q

gram positive bacillus, obligate anaerobe, motile, spore-forming

A

c diff

64
Q

flagellum, type IV pili, fibronectin binding protein, toxins, biofilms, spores are all virulence factors of what

A

c diff

65
Q

what does the type IV pilus promote

A

biofilm formation

66
Q

toxins A and B are needed to cause infection, internalized, acidification what ultimately happens

A

breakdown of tight junctions and apoptosis

67
Q

how is c diff transmitted

A

endogenous (previously existing but gut overrun when normal flora are lost)

exogenous (normal flora are lost and c diff are introduced (exposure to spores)

68
Q

excessive diarrhea
abdominal cramping
fever
white plaques on colon (dead epithelial and immune cells)
can progress to toxic mega colon, septic shock

A

pseuomembranous colitis

69
Q

how to diagnose c diff

A

molecular tests, gram stains, enzyme immunoassay, colonoscopy

70
Q

how to treat c diff

A

stop current antibiotic treatment
vancomycin or fidaxomicin
surgical management
fecal microbiota transplant

71
Q

enteric gram negative bacillus, facultative anaerobe, motile, ferments lactose, toxigenic and facultative intracellular pathogens

A

e. coli

72
Q

what is the most common cause of sepsis/CA-UTIs and HA-UTIs and most important cause of gastroenteritis

A

pathogenic e coli

73
Q

what does ETEC, EPEC, EAEC, EIEC, EHEC stand for

A

toxigenic, pathogenic, aggregative, invasive, hemorrhagic

74
Q

mostly acquired through HGT, endotoxin (LPS), capsule, flagella, siderophores (iron) are general virulence factors of what bacteria

A

e. coli

75
Q

colonization factor antigen (fiambriae/attachment), toxins (heat stable Sta and STb —> watery diarrhea)

A

EnteroToxigenic

76
Q

EAF (adherence factor BFP & LEE type three secretion system)

A

EnteroPathogenic

77
Q

AAF (adherence fimbriae), stacked-brick configuration, cytotoxins and enterotoxins (shortening microvilli, cytokine release/neutrophil recruitment)

A

EnteroAggregative

78
Q

plasmid encoded invasion genes (plnv), t3ss, ONLY intracellular pathogen

A

EnteroInvasive

79
Q

shiga-toxin, causes colitis/bloody diarrhea, type 3 secretion system, pathology similar to EPEC

A

EnteroHemorragic

80
Q

what type of toxin is a shiga toxin

A

AB/can allow dissemination to other organs

81
Q

what is usually travelers diarrhea: watery vomiting cramps nausea

A

ETEC

82
Q

which e. coli binds and destroys microvilli

A

EPEC

83
Q

along with ETEC, what other strain is involved in travelers diarrhea

A

EAEC

84
Q

what is the most common e. coli strain in developing countries

A

EHEC

85
Q

kidney disease with fragmented red blood cells, reduced platelet count, acute renal failure

A

hemolytic uremic syndrome (HUS)

86
Q

shiga toxin 2 most commonly responsible for causing what

A

HUS

87
Q

acquired through ingestion of contaminated food or water, person to person possible, animal reservoirs, carriers possible

A

epidemiology of e. coli

88
Q

immunoassay to detect ST/PCR for ST; PCR for LEE; PCR for AAC plasmid; PCR for genes modulating invasion

A

ETEC; EPEC; EAEC; EIEC

89
Q

in the highest incidence of renal failure in children, what do latex agglutination tests and immunoassays detect

A

O and H antigens; shiga toxin or toxin genes

90
Q

how to treat e. coli infections

A

fluids, no antibiotics, dialysis/renal failure, no vaccine

91
Q

Gram-negative curved rods, motile, facultative anaerobes, can form biofilms, mostly halophilic/halotolerant

A

vibrio spp

92
Q

difference between v. cholera/v. parahaemolyticus and v. vulnificus

A

gastroenteritis vs additionally septicemia and wound infections

93
Q

water is inanimate reservoir (free living/biofilms/associated with shellfish and filter feeders), estuary or sea water, humans living reservoir through water/food contamination fecal oral route

A

v. cholerae

94
Q

no human to human transmission, acid sensitive bacteria (reduced gastric acid leads to increased susceptibility), asymptomatic carriage in endemic areas is common

A

v. cholerae

95
Q

what is serotyping determined by for v. cholerae

A

the O antigen

96
Q

what cholera pandemic are we currently in

A

7th

97
Q

what case fatality ratio needs to be exceeded to be considered a pandemic

A

1%

98
Q

List 4 reasons why cholera has resurfaced in parts of the world

A
  • conflict/war
  • climate change
  • insecurity/poverty
  • COVID19 (resources diverted to the pandemic)
99
Q

AB cholera toxin (Ctx), Toxin Co-regulated pilus (TCP), acquired by HGT from a bacteriophage and regulated by a virulence regulon

A

virulence mechanisms of V. cholera

100
Q

for v. cholera infections mucus, bile salts, and osmolarity will stimulate what

A

production of Toxr regulon gene expression (production of Ctx toxin)

101
Q

what does the type 2 section system secrete in v. cholera infections

A

GpbA adhesins (water biofilm and copepod/epithelial cell attachment), HapA protease (gain nutrients, break down mucus/remove sialic acid, cleaves A unit of toxin, degrades adhesin)

102
Q

what does the A subunit of the cholera toxin ultimately cause

A

increased cAMP, which causes reflux of ions and watery diarrhea

103
Q

Endotoxin, T6ss, and capsule are all other virulence factors of v. cholera — what does the T6ss do?

A

inject damaging effector proteins in host cell and gut normal flora

104
Q

asymptomatic or self-limited, abrupt onset of white diarrhea and vomiting, death due to dehydration, electrolyte imbalance, shock, cardiac arrest, or renal failure

A

symptoms of cholera

105
Q

how does TCBS media work

A

thiosulfate and sodium citrate inhibits growth of enterobacteria, sucrose fermentation turns media yellow

106
Q

what color does v. cholera turn on TCBS media

A

yellow

107
Q

how to treat cholera

A

rehydration, antibiotics not recommended (only in pregnant/immune compromised cases)

108
Q

sari filtration and solar water disinfection are two ways of preventing what

A

cholera transmission or at least reducing it

109
Q

vaxchora, dukoral, and sanchol/euvichol-plus are what

A

vaccines for cholerae

110
Q

gram negative (helical or spiral), motile, urease positive, microaerophilic, slow grower (up to 10 days)

A

h. pylori

111
Q

gastritis, peptic ulcers, cancer, transmitted person to person through contaminated food or water

A

h. pylori

112
Q

outer membrane proteins, ureas, type 4 secretion system (CagA and Pg fragments modulate apoptosis of host cell), VacA toxin, flagellum are all virulence factors of what

A

h. pylori

113
Q

increases the pH around the bacterium, produces a,momia which is toxic and disrupts tight junction integrity, produces CO2

A

urease

114
Q

A T5SS autotransporter delivered toxin, present in all strains, pore-forming cytotoxin (allows for nutrient release from cell)

A

VacA

115
Q

where is the VacA toxin located

A

the cytoplasm

116
Q

Secreted by T4ss, an oncoprotein, short term exposure leads to apoptosis, long term leads to apoptosis resistant cells from h. pylori infection

A

CagA

117
Q

how is h. pylori diagnosed

A

noninvasive (stool antigen test, urea breast test, serology to detect IgG

invasive (endoscopy/stomach tissue biopsy — histology staining, culture, rapid urease testing) needed for antibiotic susceptibility testing

118
Q

what does a urea breath test detect

A

CO2

119
Q

how is h. pylori treated

A

amoxicillin and clarithromycin (plus protein pump inhibitor)

check for eradication

120
Q

enteric gram negative bacillus, facultative intracellular pathogens, facultative anaerobes, motile, do not ferment lactose

A

salmonella enterica

121
Q

what are the effector proteins secreted by T3ss with salmonella enterica that facilitate endocytosis and polymerize host cell actin

ENTRY

A

SPI-1

122
Q

what is the s. enterica T3ss that injects effector proteins into endocytic vacuole to prevent phagosome/lysosome fusion

SURVIVAL

A

SPI-2

123
Q

gastroenteritis or enteric fever (the latter is systemic and is limited to humans)

A

salmonellosis

124
Q

eating raw or undercooked food, incubating 6-48 hours, may be asymptomatic to diarrhea and fever, usually self-limiting

A

non-typhiodal salmonella gastroenteritis

125
Q

what is associated with the typhoidal systemic disease

A

dissemination to liver, spleen, and lymph nodes

126
Q

systemic disease that initially does not trigger inflammatory response (GI tract to blood back to GI tract)

A

typhoid fever

127
Q

what are rose spots

A

spots on upper chest and abdomen that are not contagious and don’t itch before typhoid fever

128
Q

Tyhoidal toxin is made up of what

A

AB: B binds host receptor
A has two parts
CdtB = DNAse — cell cycle arrest, nuclear swelling
PltA = changes gene expression in host

129
Q

what diagnostic test must be carried out to diagnose typhoidal salmonella infection

A

culture

130
Q

what is the treatment for salmonella

A

none for gastroenteritis

antibiotic treatment prolonged for typhoid fever

131
Q

TCV, Ty21a, and ViPS are all vaccines for what

A

typhoid fever

132
Q

what is the age cutoff for unonjugated polysaccharide vaccines

A

2 years old

MIP 351 (3 decks)

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