Bugs: GI Bacteria Flashcards

(126 cards)

1
Q

two serogroups of vibrio cholerae that harbor cholera toxin

A

O1, O139

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2
Q

what makes O1 and O139 serogroups of vibrio cholerae pathogenic

A

bacteriophage CTXɸ

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3
Q

function of bacteriophage CTXɸ

A

cholera toxin

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4
Q

reservoir of vibrio cholerae

A

shellfish, humans

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5
Q

transmission of vibrio cholerae

A

contaminated foods, fecal-oral route

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6
Q

clinical presentation of vibrio cholerae

A

cholera
- watery (secretory) diarrhea (rice-water stool)
- no fever (non-invasive)
- dehydration

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7
Q

complications of vibrio cholerae

A

aspiration pneumonia, cholera sicca

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8
Q

anatomical location of vibrio cholerae

A

small intestine

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9
Q

virulence factor of vibrio cholerae

A
  • type IV toxin co-regulated pilus (TCP)
  • cholera toxin: activates stimulatory G protein complex by ADP-ribosylation –> activates adenylyl cyclase –> increases cAMP –> opens CFTR –> Cl- efflux –> H2O efflux
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10
Q

lab tests of vibrio cholerae

A

Gram negative, oxidase positive, single polar flagellum, TCBS agar yellow

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11
Q

shape of vibrio cholerae

A

comma-shaped, bacillus

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12
Q

transmission of clostridium perfringens

A

contaminated meats that have not been properly stored/reheated

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13
Q

clinical presentation of clostridium perfringens

A

food poisoning
- watery diarrhea (lasts ~24 hours)
- no fever (non-invasive)

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14
Q

anatomical location of clostridium perfringens

A

small intestine

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15
Q

how does clostridium perfringens develop in food

A

germinates in certain foods at < 140°F –> enables high number of bacteria to form

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16
Q

virulence factor of clostridium perfringens

A

C. perfringens toxin (CPE): binds host claudin –> forms pores –> calcium influx –> cell death

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17
Q

lab tests of clostridium perfringens

A

Gram positive, anaerobe, double zone of hemolysis on blood agar

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18
Q

shape of clostridium perfringens

A

bacillus

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19
Q

transmission of ETEC

A

fecal-oral route

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20
Q

geography and population of ETEC

A

travelers to endemic regions (south/southeast asia, africa, south/central america, mexico)

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21
Q

clinical presentation of ETEC

A

Traveler’s diarrhea
- watery diarrhea
- no fever (non-invasive)
- dehydration

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22
Q

anatomical location of ETEC

A

small intestine

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23
Q

virulence factors of ETEC

A

use colonizing factors; enterotoxins: heat-stable toxin (binds and activates guanylyl cyclase C –> increases cGMP –> stimulates ion secretion –> H2O efflux), heat-labile toxin (similar to cholera toxin)

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24
Q

lab tests of ETEC

A

Gram negative, oxidase negative, MR positive, indole positive, urease negative, ferments lactose

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25
shape of ETEC
bacillus
26
transmission of EPEC
fecal-oral route
27
main population affected by EPEC
pediatric
28
clinical presentation of EPEC
pediatric diarrhea - watery diarrhea - no fever (non-invasive)
29
anatomical location of EPEC
small intestine
30
virulence factor of EPEC
- BfpA (bundle-forming pili) --> secretes T3SS proteins (Tir, Map) --> change host cytoskeleton and promote pedestal formation --> disrupts brush border microvilli --> loss of absorptive surfaces (attaching and effacing behavior) - Tir: forms tight associations with formed pedestal - MAP: disrupts mitochondrial function
31
lab tests of EPEC
Gram negative, oxidase negative, MR positive, indole positive, urease negative, ferments lactose (differentiated from other E. coli by NAAT for the bfpa gene)
32
shape of EPEC
bacillus
33
transmission of EAEC
fecal-oral route
34
geography and population affected by EAEC
children of endemic regions
35
clinical presentation of EAEC
- acute/chronic watery diarrhea - no fever (non-invasive) - diarrhea may be mucoid (b/c of Pet toxin)
36
complications of EAEC
growth retardation (due to chronic diarrhea and malnutrition)
37
anatomical location of EAEC
terminal ileum, large intestine
38
virulence factor of EAEC
- AAF (aggregative adherence fimbriae) and dispersin protein: attachment - Pet (plasmid-encoded toxin): cleaves spectrin/fodrin --> exfoliation of mucoid - EAST (enteroaggregative heat-stable enterotoxin): similar to ETEC heat -stable toxin - biofilms: contribute to persistence
39
lab tests of EAEC
heterogenous collection; Gram negative, oxidase negative, MR positive, indole positive, urease negative, ferments lactose, stacked-brick appearance
40
shape of EAEC
bacillus
41
bacteria that cause watery diarrhea
vibrio cholerae, clostridium perfringens, ETEC, EPEC, EAEC
42
important strain of EHEC
O157:H7
43
transmission of EHEC O157:H7
outbreaks; contaminated meats and vegetables, items that have come into contact with contaminated fecal matter (usually from cows)
44
risk factors of EHEC
children < 5 y.o. and elderly
45
clinical presentation of EHEC
hemorrhagic colitis - inflammatory diarrhea - watery --> bloody diarrhea - no fever (non-invasive)
46
complications of EHEC
severe dehydration, hemolytic uremic syndrome in children
47
anatomical location of EHEC
large intestine
48
virulence factor of EHEC
- shiga toxin (removes an adenine nucleobase from the 28S rRNA of the 60S ribosomal subunit --> inhibits protein synthesis and kills cells --> contributes to blood in diarrhea) - pedestal formation (like EPEC)
49
lab tests of EHEC
Gram negative, oxidase negative, MR positive, Indole positive, urease negative, ferments lactose O157:H7 clear on SMAC agar (does not ferment sorbitol) NAAT for stx genes immunoassay for Stx proteins
50
shape of EHEC
bacillus
51
geography of EIEC
very rare in US; outbreaks can occur
52
transmission of EIEC
fecal-oral route
53
clinical presentation of EIEC
mild bacillary dysentery - diarrhea - fever! (invasion) - pus and blood in stool - dehydration
54
anatomical location of EIEC
large intestine
55
virulence factor of EIEC
similar to Shigella flexneri
56
lab tests of EIEC
Gram negative, oxidase negative, MR positive, Indole positive, urease negative, ferments lactose (must differentiate from Shigella)
57
shape of EIEC
bacillus
58
geography of Shigella spp.
S. dysenteriae and S. boydii: rare in US S. sonnei: most common in US
59
transmission of Shigella spp.
fecal-oral route
60
risk factors of Shigella spp.
crowded living situations, MSM
61
unique characteristic of Shigella flexneri
lacks the shiga toxin (similar to EIEC)
62
clinical presentation of Shigella spp
shigellosis (bacillary dysentery) - inflammatory diarrhea - fever! (invasion) shigella dysenteriae: most severe form of shigellosis (carries shiga toxin)
63
clinical presentation of Shigella dysenteriae
severe bacillary dysentery - inflammatory diarrhea - watery --> grossly bloody diarrhea - mucus, pus, and blood in stool - fever! (invasion)
64
complications of Shigella dysenteriae
toxic megacolon, obstruction, bacteremia, HUS
65
anatomical location of Shigella dysenteriae
large intestine
66
pathogenesis of Shigella spp.
enter M cells of large intestine --> enter macrophages and colonic epithelial cells on basal laminal side --> secretes T3SS proteins (IpaA, IpaB, IpaC) to escape phagosome and replicate within cytoplasm --> actin tail polymerization --> propels bacteria into adjacent cells
67
virulence factor of Shigella spp.
shiga toxin (sometimes present; removes an adenine nucleobase from the 28S rRNA of the 60S ribosomal subunit --> inhibits protein synthesis and kills cells --> contributes to blood in diarrhea)
68
lab tests of Shigella spp.
Gram negative, do not ferment lactose, do not produce H2S, non-motile, oxidase negative, white colonies on HE agar
69
shape of Shigella spp.
bacillus
70
reservoir of Salmonella typhi
humans (only infects humans)
71
transmission of Salmonella typhi
fecal-oral route
72
risk factors of Salmonella typhi
international travel
73
clinical presentation of Salmonella enterica serovar typhi
typhoid fever (enteric fever) - high fever - constipation - rose spots
74
complications of Salmonella enterica serovar typhi
septicemia, ileal perforation
75
anatomical location of Salmonella enterica serovar typhi
liver, spleen, bone marrow
76
unique characteristics of Salmonella enterica serovar typhi
bacteria is shed by diarrhea every few weeks chronic colonization in gallbladder
77
pathogenesis of Salmonella spp.
enters epithelial cells and M cells from apical side --> enter macrophages and intestinal epithelial cells on basal laminal side --> spreads systemically --> 1st T3SS facilitates entry (membrane ruffling) --> 2nd T3SS forms salmonella containing vacuole (SCV)
78
lab tests of Salmonella spp.
Gram negative, does not ferment lactose, motile, produces H2S, black colonies on HE agar Widel test for serology
79
shape of Salmonella spp.
bacillus
80
transmission of Salmonella enterica serovar Enteritidis
fecal-oral route, contact with animals, contaminated food
81
risk factors of Salmonella enterica serovar Enteritidis
children, elderly
82
clinical presentation of Salmonella enterica serovar Enteritidis
gastroenteritis (caused by nontyphoidal salmonella) - inflammatory diarrhea - fever! (invasion) - water --> bloody diarrhea
83
complications of Salmonella enterica serovar Enteritidis
bacteremia, reactive arthritis, osteomyelitis in pts w/ sickle cell anemia or thalassemia
84
anatomical location of Salmonella enterica serovar Enteritidis
small intestine
85
geography of Yersinia spp.
northern states
86
transmission of Yersinia spp.
direct animal contact, ingestion of contaminated products (dairy)
87
risk factor of Yersinia spp.
individuals with iron metabolism issues
88
clinical presentation of Yersinia spp.
yersiniosis - inflammatory diarrhea - fever (invasion) - pharyngitis - vomiting - pseudoappendicitis - blood and pus in stool in children
89
complications of Yersinia spp.
septicemia, erythema nodosum, reactive arthritis
90
anatomical location of Yersinia spp.
terminal ileum
91
virulence factor of Yersinia spp.
T3SS in macrophage; enterotoxin
92
lab tests of Yersinia spp.
Gram negative, do not ferment lactose, do not produce H2S, oxidase negative, motility at room temp but not at body temp, bipolar staining on gram stain
93
shape of Yersinia spp.
bacillus
94
transmission of campylobacter jejuni
poultry, contaminated water, unpasteurized raw milk
95
clinical presentation of campylobacter jejuni
campylobacteriosis - inflammatory diarrhea - fever (invasion) - mucus, pus, blood in stool - may mimic appendicitis
96
complications of campylobacter jejuni
reactive arthritis, Guillain-Barré syndrome
97
anatomical location of campylobacter jejuni
terminal ileum, large intestine
98
virulence factor of campylobacter jejuni
- CadF: adherence to intesinal epithelium - CDT (cytolethal distending toxin) --> host cell death --> release of IL-8
99
lab tests of campylobacter jejuni
Gram negative, single polar flagellum, rapid darting motility, oxidase positive, grows at 42°C, prefers higher levels of CO2 for growth, growth on Skirrow agar
100
shape of campylobacter jejuni
curved, S-shaped bacillus
101
transmission of listeria monocytogenes
undercooked processed meat, contaminated dairy products and vegetables, transplacental (refrigeration does not prevent growth of organism)
102
risk factors of listeria monocytogenes
pregnant women, fetuses, neonates, elderly, immunocompromised
103
clinical presentation of listeria monocytogenes
listeriosis - watery, inflammatory diarrhea - fever (invasion) - vomiting - blood in stool is uncommon - systemic in immunocompromised pts
104
anatomical location of listeria monocytogenes
small intestine
105
virulence factor of listeria monocytogenes
- internalin proteins: enable attachment - listeriolysin O: used to escape host phagosome and suppresses T cell activation - ActA: coordinates assembly of actin filaments; allows propulsion into next cell - macrophage carries bacteria to other parts of host in disseminated disease
106
lab tests of listeria monocytogenes
Gram positive, beta-hemolytic, catalase positive, exhibits tumbling motility, umbrella-like growth in stab motility agar, grow at low temps (4°C)
107
shape of listeria monocytogenes
coccobacillus
108
transmission of clostridioides difficile
fecal-oral route
109
clinical association of clostridioides difficile
antibiotic use (e.g., clindamycin, cephalosporin, ampicillin)
110
risk factors of clostridioides difficile
hospitalized elderly (nosocomial)
111
clinical presentation of clostridioides difficile
C. difficile-associated diarrhea (pseudomembranous colitis) - inflammatory diarrhea - low-grade fever (non-invasive) - blood and pus in stool (in severe disease) - recurrence can occur
112
anatomical location of clostridioides difficile
large intestine
113
virulence factor of clostridioides difficile
- can only establish infection after antibiotic usage and clearance of commensal intestinal bacteria - Tcd A/B exotoxins (glucosylate host cellular GTPases --> increase permeability of tight junctions --> inflammation)
114
lab tests of clostridioides difficile
Gram positive, obligate anaerobe, forms sub-terminal spores Tcd toxin detected by NAAT Tcd protein detected by immunoassay
115
shape of clostridiodes difficile
bacillus
116
epidemiological association of bacillus cereus
meats, vegetables
117
clinical presentation of bacillus cereus
- rice and water diarrheal disease (infection) - emetic disease (intoxication)
118
anatomical location of bacillus cereus
intestine
119
virulence factor of bacillus cereus
enterotoxins: heat-stable emetic toxin, heat-labile enterotoxin
120
lab tests of bacillus cereus
catalase positive, beta-hemolytic, motile, lecithinase positive, spore-forming
121
shape of bacillus cereus
bacillus
122
clinical presentation of staphylococcus aureus
toxin-mediated food poisoning, emesis
123
virulence factor of staphylococcus aureus
heat-stable superantigens (cause PMN infiltration, brush border loss in jejunum, mast cell activation --> emesis and diarrhea)
124
lab tests of staphylococcus aureus
Gram positive, catalase positive, coagulase positive, beta-hemolytic
125
bacteria that cause inflammatory diarrhea
EHEC, EIEC, Shigella spp., Salmonella spp., Yersinia spp., campylobacter jejuni, listeria monocytogenes, clostridioides difficile
126
bacteria that cause emesis
bacillus cereus, staphylococcus aureus