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Micro > Lecture 8 and 9 > Flashcards

Lecture 8 and 9 Flashcards

1
Q

Stain and shape of Enterobacteriaceae organisms

A

GramNeg
Rods
All have capsule (very large in Klebsiella)

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2
Q

O2 requirement of enterobacteriaceae

A

Facultatively anaerobic

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3
Q

How do enterobateriaceae move

A

Either peritrichous flagella or are nonmotile

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4
Q

O-antigens are what?

A

Part of LPS

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5
Q

H antigens are what?

A

Flagella

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6
Q

K/Vi antigens are what?

A

Capsular type

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7
Q

What is the main cause of foodborne illnesses?

A

Bacteria

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8
Q

What tests can you use for enterobacteriaceae

A

IMViC

Carbohydrate metabolism

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9
Q

What is IMViC

A

A test to identify a type of bacteria from the coliform group

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10
Q

What is enterotube?

A

A test tube to identify different enterobacteriaceae

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11
Q

What is unique about gut bacteria and how sense hormones?

A

They can response to stress-induced hormones levels (tells them this is a good time to attack)

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12
Q

Why do bacteria often go undetected in the body?

A

Many can block signaling pathways that would signal their presence

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13
Q

What is unique about pathogenic E. coli?

A

They never enter the cell but they produce protein that can facilitate entry of other bacteria and survival in a cell

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14
Q

What are the three diseases associated with E. coli?

A

Enteric
UTI
Sepsis/meningitis

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15
Q

What antigens are present on enterobacteriaceae

A

O
H
K/Vi

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16
Q

How can you detect E. coli in the lab?

A

All lac+
Copious acid production
Detected by green metallic sheen on EMB agar

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17
Q

What type of E. coli causes UTIs?

A

Uropathogenic E. coli

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18
Q

What type of E. coli causes sepsis and meningitis?

A

Meningitis associated E. coli

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19
Q

Why is E. coli the most common cause of UTI?

A

Proximity of anus to urethra

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20
Q

Uropathogenic E. coli interact with blood how?

A

Have “P” pilus will faciliates blood cell binding

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21
Q

How many types of diarrhea are caused by E. coli?

A

5

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22
Q

EPEC (EPEC) do what?

A

Bundle in the intestine against microvilli

Inhibit water uptake

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23
Q

EPEC stands for?

A

Enteropathogenic E. coli

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24
Q

Who can get EPEC?

A

Young children

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25
Q

Symptoms of EPEC

A

Watery, self-limiting diarrhea

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26
Q

ETEC stands for?

A

Enterotoxigenic E. coli “Montezuma’s Revenge”

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27
Q

ETEC symptoms

A

Watery diarrhea
Increased gut motility
Cramps

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28
Q

ETEC are found were?

A

Have CFA adhesion pili and stick to brush-border

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29
Q

ETEC produces what?

A

2 LT toxins (AB toxins like cholera)
STa toxin (activates cGMP production and water secretion)
STb toxin

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30
Q

EHEC stands for?

A

Enterohemorrhagic E. Coli (157:H7)

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31
Q

EHEC symptoms

A

Blood diarrhea without fever (hemorrhagic colitis)

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32
Q

What toxins does EHEC produce

A

Verotoxin (ABt-protein synthesis inhibitor-aquired by phage conversion)

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33
Q

EHEC can cause what symptoms outside of the GI tract?

A

Hemolytic-Uremic syndrome

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34
Q

What is hemolytic uremic syndrome?

A

Uremia and organ failure due to damage of glomerular endothelium

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35
Q

EIEC stands for what?

A

Enteroinvasive E. Colic

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36
Q

What is EIEC indistinguishable from?

A

Shigella dysenteriae type I

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37
Q

Symptoms of EIEC?

A

Blood in diarrhea

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38
Q

What type of E. coli should you not treat with antibiotics and why?

A

EHEC

The bacteria end up producing more toxin in response to Abx

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39
Q

How can EIEC invade and colonize?

A

Has invasive colonization factors (Ipas) produced from a shigella plasmid

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40
Q

EAEC stands for what?

A

Enteroaggregative E. Coli

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41
Q

EAEC symptoms

A

Noninflammatory pediatric diarrhea in developing countries

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42
Q

How does EAEC stick?

A

Aggregative pili form infective foci in intestine

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43
Q

Who is susceptible to E. coli meningitis

A

Neonates

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44
Q

Why can E. coli cause meningitis in neonates?

A

Has a K1 capsule which mimics NCAM receptor (which makes it hard to target)

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45
Q

Meningitis associated E. Coli is similar to what?

A

N. meningitidis B capsular antigen

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46
Q

Salmonella will have what common lab findings?

A

Lac-

H2s+

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47
Q

All salmonella belong to what species?

A

S. enterica

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48
Q

What two types of salmonella need to be considered separately?

A

S. typhi
S. paratyphi
These penetrate intestinal epithelium

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49
Q

What diseases are caused by salmonellsa?

A

Typhoid fever
Bacteremia/Septicemia
Enterocolitis/Gastroenteritis

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50
Q

What organism causes typhoid fever?

A

S. typhi

S. paratyphi

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51
Q

How does S. typhi reach blood stream?

A

Through intestinal mucosa

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52
Q

Where does S. typhi disseminate once in the blood?

A

Via macrophages to liver, spleen,, gallbladder

53
Q

How does typhoid fever kill you

A

Intestinal hemorrhage

54
Q

What type of salmonella causes bacteremia/septicemia?

A

S. Cholerasuis

55
Q

What type of PT typically gets bacterermia/septicemia from S. cholerasuis?

A

Immuncompromised

56
Q

What type of salmonella causes enterocolitis/gastroenteritis?

A

S. Enteriditis

57
Q

What are symptoms of S. enteriditis?

A

N/V/D
Fever
Typically self-limiting
Can colonize the gallbladder and shed for weeks

58
Q

What is a common source for S. enteriditis?

A

Eggs and poultry

Fecal-oral route

59
Q

How does S. enteriditis cause illness?

A

Binds to invades gut epithelium
Can reach blood stream
Produce cytotoxic enterotoxin
Typhoid toxin enters host cells (ADP ribosylates a G protein and damages DNA)

60
Q

Lab results for shigella?

A

Lac -

H2S -

61
Q

Where is the only place shigella typically attacks?

A

GI

62
Q

What are symptoms of shigella?

A

Fever and watery diarrhea for 2 days
Then, 2 days of blood and mucousy stool
Dehydration may be lethal

63
Q

Shigella transmission

A

4 Fs

64
Q

How does shigella cause illness?

A

Phagocytosed by M cells and given to macrophages
Lyse phagolysosome and replicate in cytoplasm
Release IL-1 and permeabilize cell junction
Spread by actin tails
Has shigella enterotoxin

65
Q

How does Yersinia adhere?

A

YadA

66
Q

What specific antigens does yersinia have and why are they significant?

A

V and W

Allows for intracellular growth

67
Q

What bug causes “plague”

A

Yersinia pestis

68
Q

Symptoms of yersinia pestis?

A

Malaise, headache, vomiting

Painful buboes in groin or other lymph nodes

69
Q

What is a secondary infection from yersinia pestis?

A

Septicemia (may be primary or secondary to bubonic)

70
Q

What is the third type of infection from yersinia pestis?

A

Pneumonic
Cough with blood tinged sputum
100% fatal in 24 hours

71
Q

Why can fleas spread yersinia pestis?

A

Ymt phospholipase also the bug to live in a flea

72
Q

How does yersinia pestis cause illness?

A

Genes turn on at 37° C
Type III inserts toxic Yops into host
Inhibits MAP kinase

73
Q

When yersinia pestis inhibits MAP Kinase what subsequent pathways are effected?

A

Cytokine production
Cell replication
Prevents phagocytosis
Inhibits platelet aggregation

74
Q

What is Tx for yersinia pestis PT if asymptomatic?

A

Tetracycline

75
Q

Tx for y. pestis if symptomatic?

A

Streptomycin

76
Q

Y. enterocolitica Sx?

A

Enterocolitis with intestinal abscesses
Severe bloody diarrhea with cramping and fever
Lasts longer
Mesenteric adenitis
Spread in feces (common in cattle and hog reservoirs)

77
Q

Y. enterocolitica Tx?

A

Ampicillin

78
Q

What enterobacteraceae is only a respiratory bug?

A

Klebsiella pneumoniae

79
Q

K. granulomatis symtoms

A

This is an enterobacteriaeceae but is an STD

Genital infection that can mimic syphilis

80
Q

What enterobacteriaceae is commonly associated with UTI

A

Proteus mirabilis, Proteus vulgaris

Urease production can result in bladder stones

81
Q

Proteus mirabilis, Proteus vulgaris on agar

A

Swarming motility

82
Q

Serratia marcescens causes what in whom?

A

Pneumonia, bacteremia, endocarditis in immunocompromised PTs

83
Q

What is the new goal of treating enterobacteriaceae?

A

Return normal mucous production

MUC2 inhibits inflammatory and is carbon source for normal flora

84
Q

Vibrio shape and stain

A

Gram neg. comma shaped rod
polar flagellum
2 circular chromosomes

85
Q

Vibrio environment

A

Alkalophiles

86
Q

Where do V. cholera live?

A

Copods in ocean

87
Q

V. cholera antigens?

A

H antigens

O antigens

88
Q

What is the most common form of v cholera now?

A

O1 El Tor Inaba

89
Q

O1 El Tor Inaba produces?

A

Hemolysin

90
Q

Why is O1 El Tor Inaba bad?

A

Polymyxin resistanct

91
Q

How many organisms for V cholera to infect?

A

10^6

92
Q

Who is more susceptible to cholera infections?

A

Antacid users

93
Q

V. cholera Sx

A

N/V loose stools
“rice water stools”
No pain

94
Q

How does V cholera cause infection?

A

Fibriae bind to gut epithelium
Toxin from PAI island on Chrom 1
Regulated by ToxR (activated by appropriate temp, acidity,…)

95
Q

V. Cholera AB toxin mechanism

A

B binds as pentramer to receptor ganglioside Gm1
ADP ribosylates Gs Protein
Increase cAMP ion secretion into gut
Water follows

96
Q

V. cholera Tx

A

Rehydration and electrolytes

Doxy can limit shedding but not stop symptoms (azithro if pregnant)

97
Q

V. parahemolyticus symptoms

A

-12-24 hr incubation, then nausea, vomiting, watery to bloody
diarrhea, with or without gastroenteritis -self limiting, resolves in 1-4 days

98
Q

V. parahemolyticus pathogenesis

A

-biofilms, T3SS and T6SS, hemolytic/cytotoxic enterotoxin

99
Q

V. parahemolyticus control

A

-rehydration and electrolyte replacement, Doxycycline if necessary

100
Q

V. vulnificus symptoms

A 
very rapid (hours) cellulitis and necrosis

101
Q

V. vulnificus cause

A

-infected wounds from handling contaminated seafood (esp shellfish)
-bacteremia from eating raw oysters (always from contaminated seawater)
eventual liver damage (alcoholic predisposition): 50% fatal

102
Q

V. vulnificus pathogenesis

A

-antiphagocytic capsule contributes to virulence -necrotizing cytotoxin

103
Q

V. vulnificus control

A

-Doxycycline right away! (Cipro if pregnant) -takes 18 hours to get a positive culture; too late

104
Q

Campylobacter shape and stain

A

Gram neg curved, helical, or gull-winged, polar flagella (sometimes bipolar)

105
Q

Campylobacter oxygen requirement

A

Microaerophile

106
Q

C. jejuni temperature

A

42° C

107
Q

C. fetus temp

A

25° C

108
Q

C. jejuni

A

-disease of the large intestine
-presents as abdominal pain (gastroenteritis), with cramps, fever,
very bloody diarrhea (sometimes blood red) (= invasive organism) -self-limiting within a week or so in typical pts.
-may invade the bloodstream and cause enteric fever in immunocomp. -sequela
-1-4 weeks after C. jejuni infection, patients (~1/2000) can develop Guillain-Barré syndrome (demyelinating neural disease, progressive flaccid paralysis) – molecular mimicry: autoantibodies to GM1 gangliosides

109
Q

C. jejuni sources?

A

-a zoonosis (50-100% of chickens and turkeys in US infected) -human acquisition
-fecal-oral route
-consumption of contaminated poultry or milk -incidence peaks in the summer
most common in infants and young adults

110
Q

C. jejuni pathogenesis

A
  • produces an inflammatory enterotoxin

- C. jejuni bacteremia indicates an invasive potential

111
Q

C. jejuni control

A
  • rehydration therapy to treat diarrhea

- tetracycline, quinolones or clarithromycin for systemic infections

112
Q

C. fetus clinical

A

-usually causes systemic infections, septicemia (rarely diarrhea) -spontaneous abortions in cattle

113
Q

C. fetus epidemilogy

A
  • zoonosis (cattle)

- humans acquire from eating contaminated undercooked beef -elderly, ill, and immunosuppressed especially susceptible

114
Q

C. fetus pathogenesis

A

-major virulence factor is an S-layer protein that inhibits complement fixation by C3b; less opsonization = less phagocytosis

115
Q

C. fetus control

A

-tetracyclines, macrolides and quinolones

116
Q

Helicobacter pylori shape and stain

A

Gram neg spirillum

117
Q

H. pylori oxygen

A

Microaerophile

118
Q

H. pylori lab

A

-oxidase+, catalase+

119
Q

H. pylori produces what?

A

produces HUGE amounts of urease (urease test positive in minutes to hours)

120
Q

H pylori lives where?

A

not invasive; colonizes gastric mucosa, esp. antrum (Lewis blood group adhesin)

121
Q

H. pylori leads to what?

A

stimulates gastrin production, which stimulates acid production in the fundus

122
Q

H. pylori diagnosis

A
  • serologic test (but antibodies remain after eradication)
  • gram stain / culture of gastric biopsy
  • urea breath test: 14C-urea is fed, detection of 14CO2 in breath is diagnostic of urease activity in stomach
123
Q

Who should possibly have H. pylori and not know it

A

Be aware of the potential for gastritis caused by H. pylori in GERD patients being treated long-term with Proton pump inhibitors, which mask the H. pylori infection

124
Q

Why do people with type O blood have more H. pylori?

A

Binds to Lewis antigen (antigen if you are O blood type)

125
Q

H. pylori pathogenesis

A

H. pylori bind to base of gastric mucosal cells where pH is 7.4, rather than the pH 2 conditions of the apical border
huge amounts of urease buffer pH by forming NH3 from urea
-produce a vacuolating toxin VacA
-activated by stomach acid
-binds to sphingomyelin “lipid rafts” in gastric epithelial cells -insert into cell as selective anion channel
-cause extensive vacuolation of epithelial cells and release of urea,
also inhibition of antigen presentation pathways and T cells

126
Q

What is the only one of four virulence factors in H. pylori that causes symptoms?

A

CagA
ulcer-assoc. strains produce a cytotoxin, CagA -secreted by T4SS
- induces apoptosis in host cells
- potential oncoprotein
- Production of both virulence factors is enhanced by salt

127
Q

H. pylori control

A

Treat ulcer with bismuth subsalicylate

  • Treat infection with tetracycline or macrolide + metronidazole
  • Treat acid with PPI
  • recovery from ulcer only occurs if infection treated, too (bicarbonate only allows H. pylori to spread)
128
Q

How can you differentiate E. coli from salmonella?

A

No vomiting with E. coli

Micro (13 decks)

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