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micro immuno 2 > Mucosal surfaces, Enterobacteriacea-diarrheal diseases Salmonella and Shigella- invasive bacterial pathogens MM (2/27/18) > Flashcards

Mucosal surfaces, Enterobacteriacea-diarrheal diseases Salmonella and Shigella- invasive bacterial pathogens MM (2/27/18) Flashcards

1
Q

types of gram-negative pathogens

A

Enterobacteriaecaeae

Vibrinoaceae

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2
Q

what is mucosal surface

A

interacts with air and secretes mucus

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3
Q

defense of mucosal surface

A

innate immunity, adaptive immunity, nonspecific barriers

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4
Q

why study GI diseases

A

lots of people get it, 500,000 in hospital, 5000 deaths
$10 bill in treatment\
begin in the oral/fecal route

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5
Q

why E. Coli outbreak in germany in 2011

A

alfa sprouts

852 cases of hemolyric uremic syndrome and 32 people died

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6
Q

E. Coli in chipotle

A

53 cases, 20 hospitalization
0 death
shiga toxin

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7
Q

how gram negative mucosal pathogens leaves the feces to get to your mouth

A 
feces
food
fluid
fingers
flies
formites
fornication
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8
Q

inoculum size

A

how many needed to cause disease (some low-shigella and EHEC, EIEC, others high-ETEC, EPEC,vibrio)

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9
Q

natural barrier defences in GI

A

acidity:1-2 in stomach then 9 in Small intensine
Motility: stuff moves through Small intestine fast so bacteria can’t atach
Mucous layer and underlying glycocalyx
Tight juntion

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10
Q

where in the GI do we get lots of bacteria

A

near the end

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11
Q

what blocks infection with gram negative pathogen

A 
normal flora
natural defenses of GI
Lysozymes (doesn't work too well against gram negative though to unexposed cell wall)
Lactoferrin
Cathelicidin
Defensins
Secretory immunoglobulins
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12
Q

action of lysozyme

A

cleaves beta 1,4-glycosidic linkage between N-acetylnuramic acid and N-acetylglucosamine

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13
Q

action of lactoferrin

A

stops bacteria by sequestering iron

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14
Q

action of cathelicidin

A

disrupts bacterial membrane of Gm- and Gm+ and fungi

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15
Q

action of Defensins

A

creates pores on all microbes

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16
Q

who produced alpha-defensins

A

neutrophils and paneth cells (intestine

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17
Q

who produced beta defenisn

A

epithelial cells

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18
Q

how do bacteria overcome innate barrier defneces

A

acid resitance
Fimbriae/pili_adhere to tissue and avoid being spread
BActerial strucutre

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19
Q

what bacterial tend to be acid resitant

A

low infectious dose (Shigella and Enteroinvasive E Coli

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20
Q

What bacterial strucutres aid in overcoming pathogenic innate barrier densences

A

gram-/gram+ cell membrane sesnitive to bactericidal compounds
Cationic amino acids into cell membrane to reduce efects of cationic antimicrobial peptides
Siderophoers sequester iron

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21
Q

what immunity are macrophages part of

A

cell mediated immunity via TH1

use PAMPS

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22
Q

whta receptor is activated by gram negative bacteria

A

TLR4

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23
Q

activation of pattern recognition receptors on macrophages laed to

A

inflammatory response

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24
Q

morphology of enterobacteriaceae family

A

gram -
no spor
non acid fast
rods (coccobacilli to elongate filamentous rods)

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25
Q

growth of enterobacteriaceae family

A

faculataticve growth and visible after 12-18 hours

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26
Q

toxins on enterobacteriaceae

A

all endotoxin, some secrete exotoxin

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27
Q

cell wall components of enterobacteriaceae family

A

antignic:
o- outer antigen, LPS
k- polysaccharide capsule
H- flagella

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28
Q

source of serotypes of in bacterial species due to

A

cell surface antigens

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29
Q

where do enterobacteriaceae infections come from

A

external from environment and animal

not: salmonella ser typhi and shigella: strickly human

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30
Q

how does enterobacteriaceae cause a pathogen

A

opportunistic

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31
Q

most common infections by enterobacteriaeceae

A

UTI’s and acute diarrhea

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32
Q

what do E. Coli ferment

A

lactose

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33
Q

what do E. coli produce

A

indole

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34
Q

how to determine serotype of E. coli

A

O, K, and H antigens

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35
Q

E coli pili

A

type 1: most common, bind D mannose residues on epitheliail cells with an on/off
p pili: bind digalactoside found within urinary tract and erythrocytes
other: common to diarrheal binding to erythrocytes

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36
Q

E. coli toxins

A

alpha hemolysisn
Cytoxoic necrotizing factor
Shiga toxin

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37
Q

action of alpha-hemolysin

A

pore forming

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38
Q

action of cytoxoic necrotizing factor (CNF)

A

A-B toxin that produces G proteins (disrupt intraceullar signalling)

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39
Q

action of shiga toxin(Stx)

A

A-B toxin that blocks pr synth by ribosomal modification

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40
Q

pathogenic E coli

A 
UropathogenicE. coli (UPEC)
EnterotoxigenicE. coli (ETEC)
EnteropathogenicE. coli (EPEC)
EnteroinvasiveE. coli (EIEC)
EnterohemorrhagicE. coli (EHEC)
EnteroaggregativeE. coli (EAEC)
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41
Q

Enteropathogenic E. Coli (EPEC) causes

A

common causative agenet of nursery outbreaks in developing coutnries

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42
Q

adult inoculum of Enteropathogenic E. Coli (EPEC)

A

10^8 to 10^10 CFU

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43
Q

how does Enteropathogenic E. Coli (EPEC) attach to distal small intestinal enterocytes

A

bundle-forming pili (Bfp)

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44
Q

how does Enteropathogenic E. Coli (EPEC) inject into host cell

A

Type III secretion system to inject over 30 E. Coli secretion proteins(not toxin though)

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45
Q

how does Enteropathogenic E. Coli (EPEC) formation of attaching and effacing (A/E) lesion

A

Intimin-Tir interaction

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46
Q

how do we think Enteropathogenic E. Coli (EPEC) cause diarrheal disease

A

effacement of the microvilli and disruption of tight junctions

47
Q

where does Enterohemorrhhagic E. Coli (EHEC) occur

A

developed countries

48
Q

source of Enterohemorrhhagic E. Coli (EHEC)

A

animal products, unpasteurized juice, fresh veggies

49
Q

inoculum of Enterohemorrhhagic E. Coli (EHEC)

A

100 CFU

50
Q

what genes does Enterohemorrhhagic E. Coli (EHEC)

A

similar to EPEC (eae genes)

51
Q

what toxin does Enterohemorrhhagic E. Coli (EHEC) produce

A

toxin the leads to hemolytic uremic syndrome (bloody diarrhea)

52
Q

most notorious Enterohemorrhhagic E. Coli (EHEC)

A

E. coli O157:H7

53
Q

primary reservoid of Enterohemorrhhagic E. Coli (EHEC)

A

cattle

54
Q

how does Enterohemorrhhagic E. Coli (EHEC) cause problems

A

causes attaching effacing lesion in colon via long polar fimbriae leading to A/E lesion similar to EPEC
Shiga toxin: hemorrhagic colitis, Hemolytic uremic syndrome

55
Q

what does Enterohemorrhhagic E. Coli (EHEC) act on

A

shiga toxinthe blood vessels under the epithelial cells of the villus

56
Q

what does Enteroinvase E coli (EIEC) cause

A

similar to shigella, mild version of shigellosis

57
Q

who gets Enteroinvase E coli (EIEC)

A

children under 5 in developing countires

58
Q

where is Enteroinvase E coli (EIEC) found

A

contaminated food and water

humans the only reservoid

59
Q

what does Enteroaggregative E. coli (EAEC) cause?

A

watery diarrhea that last longer than 14 days

60
Q

how does Enteroaggregative E. coli (EAEC) do to cause problems

A

tight adherence to epithelial cells in a stacked brick pattern

61
Q

symptoms of intestinal E. Coli infections

A 
usually a couple days after inoculation and self limiting
Except::
EAEC: can last for weeks
EPEC: can be chronic
EHEC and EIEC: bloody diarhhea
62
Q

diagnosis of E. Coli mediated disease

A

not best to use culture because we have it in our bottle as part of the flora
assays available to detect toxins/genes with virulences
Screening tests

63
Q

why not do assays

A

healthy people can test positive

Expensive

64
Q

how to do a screening test for O157:H7

A

grown on MacConkey agar supplemented with sorbital (not lactose). cannot ferment sorbital so colonies will have no color

65
Q

how to treat diarrheal disease

A

supportive therapy, keep hydrated

66
Q

treating hemorrhagic colitis/HUS

A

hemodialysis/hemapheresis

67
Q

why not use antimotility agenst on diarrheal disease

A

because it keeps the bacteria from leaving

68
Q

what is shigella

A

specialized E coli

69
Q

antigens of shigella

A

O and K, but no H (O is main)

70
Q

do shigella invade cells

A

yes, and multiple within epithelial cells

71
Q

what toxin does shigella produce

A

shiga toxin

72
Q

4 types of shigella

A
  • Shigelladysenteriae(serogroup A) –Type 1 causes most severe disease
  • Shigellaflexneri(serogroup B) –Most common
  • Shigellaboydii(serogroup C)
  • Shigellasonnei(serogroup D) –Most common
  • Subgroups found within each of these.
73
Q

who does shigellosis infect

A

strictly human (150 million cases) and 600k global deaths per year

74
Q

how id shigellosis spread

A

food.water contamination by humans

75
Q

incidence and prevalence of shigellosis is related to whay

A

personal and community sanitiation, so wars enable outbreak

76
Q

inoculum of shigellosis

A

as little as 10 organisms

77
Q

what does shigellosis resist

A

acid resistant

78
Q

pathogensis of shigella

A

infect M cells via invasion plasmid antigenin colon and pyers patch
enter macrophage, and lyse phagosome, killing macrophage
enters in the lamina propria to infect the basal part of enterocyte using invastion plasmid antigens (IpaA and IpaD) using type 3 secretion
uses actin fillaments to move around into new cells
eveutally killls epitehlial cells

79
Q

shigella infection cycle is like

A

Listeria monocytogenes

80
Q

diseases of shigella

A

ulcer develops when invaded cells die and foll off

Diarrhead as response of inflammatory response

81
Q

what do ulcers do for shigella

A

allow shigela to reach lamina propria

82
Q

what kind of diarrhea is a reuslt of shigella

A

classic dysentery - small volume diarrhea, leukocytes, and RBC’s

83
Q

Shigella dysenteriae type 1 mortality rate

A

high mortality even with adults, alwaus have shiga toxin

84
Q

shigella dysenteriae type 1 results in

A

kills intestinal epithelial and endothelial cells
Disrupts Na absorption
Toxin can be systemic

85
Q

immunologic protection of shigella

A

does produce immunological protection, but no cross protection

86
Q

diagnosis of shigella

A

stool culture, O antigen aglutination tests to determine serotype

87
Q

how to treat diseases by shigella

A

self limiting, but antibiotics like ciproflaxacin and azithromycin can shorten illness time

88
Q

vaccine for shigella

A

no, but in the works

89
Q

two types of salmonella

A

S. bongori

S. enterica

90
Q

medicall important infections arise from what salmonella

A

S. enterica

91
Q

subspecies of S. enterica

A

multiple: medicall importatn belong to the enterica subspecies

92
Q

naming salmonella species

A

diff subspecies have different disease
go by species name, subspecies, then serotype
but sorten to jus first part of species name, then serotype

93
Q

salmonella enterica gastroenteritis occures where and why

A

industrialized nation and improper food handling, food born, eggs and poltry

94
Q

inoculum range of salmonella enterica gastroenteritis

A

200-10^6, due to acid amount

95
Q

symptoms of salmonella enterica gastroenteritis

A

abdominal pain, nausea, vomiting, and diarrhea

96
Q

how long does salmonella stay in yo

A

recover after 3-4 days, but cary for 20 weeks (5% OF PATIENTS)

97
Q

how to get salmonella

A

fecal (human or animal)– oral transmission

98
Q

acid sensitivey of salmonella vs shigellae

A

more acid sensitive than shigellae

99
Q

low pH causes salmonella to do what

A

express 40 PR found on pathogenicity islands on large virulence plasmds

100
Q

where does salmonella infections colonize

A

small intestine

101
Q

how does sallmonella infect

A
  1. Organism makes contact with M cell (likely via Type 1 pili) and injects effector molecules into cell with Type III secretion system.
  2. These events induce surface “ruffles” and uptake of the organisms (microbe-directed phagocytosis).
  3. Multiplies and remains within cell vesicles for many hours (unlike Shigella).
  4. Organisms released to lamina propria, inflammatory response is activated, ingested by phagocytes, then kills phagocyte.
  5. Macs engulf most, but some escape to cause a transient bacteremia
    - -the typhoid serovarswill survive and grow within the macrophages
102
Q

why does Salmonella typhi cause

A

no animal reservoid, sticktly human

but also asymptomatic carriers

103
Q

salmonella typhi carries have what colonized in them

A

gall bladders, and organisms can be cultured from their feces

104
Q

typhi can surive how long in the macrophage

A

long time due to inhibiting oxidative burst

105
Q

how does salmonella typhi enter the lymph

A

via macrophage via mesenteric lymph nodes, spleen, liver, bone marrow, then blood

106
Q

whay of typhi causes fever

A

endotoxin

107
Q

how long can typhi fever last

A

weeks if untreated

108
Q

prolonged infected by typhi results in

A

perforated bowel

109
Q

immunity of salmonella

A

Humoral (Th2 and cell-mediated (Th1)

110
Q

what does salmonella do with host response to survive long

A

exploit host response

111
Q

how to identity salmonella

A

culture from stool or blood, identify O serogroup

112
Q

how to treat gastroenteritis from salmonella

A

fluid/electrolyte replacement

(antibioitcs for severe cases cuz it can increase the duration of infection and the incidence of the carrier state

113
Q

how to treat typhoid fever

A

antibiotics such as ciproflaxacin in the first line

micro immuno 2 (8 decks)

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