Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

micro immuno 2 > Neisseria, Haemophilus, Boretella, and Pseudomonas (2/13/2018) > Flashcards

Neisseria, Haemophilus, Boretella, and Pseudomonas (2/13/2018) Flashcards

1
Q

what is the mucus of mucosal surfaces

A

Viscous polysaccharide fluid layer and physically separates cells from luminal contents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

upper vs. lower respiratory tract

A

upper: larynx, pharynx, nasal cavity, sinus, middl ear
lower: trachea, bronchia, lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

cells of the upper female reproductive tract

A

single layer of columnar vells with tight junctions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

cells of the lower female reproductive tract

A

superficial cells terminally differentiated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

cell of the male urethral tract

A

keratinized stratied squamous cells at opening to become non-keratinzed and then eventuall psueodostratified glandular columnar along length of urethrea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

the only genus of gram negative cocci that frequently cause disease

A

neisseria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

morphology of neisseria

A 
gram negative,
diplococcci,
non-motile (twitching motility from pili)
Aerobic(but can grow anaerobically)
obligate human pathogen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

where do neisseria grow best

A

on media suppllemented with blood in the presnece of CO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

infection by Gonococci leads to

A

localized inflammation and rarely lethal, only to become serious disseminated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

where does meningococci colonize

A

nasopharynx with no local symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

3 general disease of meningococci

A

uncomplicated bacteremic process
metastatic infection of meninges
overwhelming ststem infection(circulatory collapse and disseminated intravascular coagulation (DIC))-> leads to thick blood titers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

who tends to get overhwelming systemic infection from meningococci

A

individual without IgG antibodies for the capsular polysaccharide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

capsule of meningococci

A

heavily encapsulated and produce hemolysin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

where is Gonococci found

A

cervic in women and distal urethtra in both sex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how can kids get Gonococi

A

transfer upon labor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how does gonococci attach

A

non ciliated columnar epithelium pili and surface protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

adhesins of Gonococci controlled

A

Phase variation: presence/absnse

Antigenic Variation: composition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

are men or women more often be aymptomatic caries of Gonococci

A

women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how is gonococci spread

A

multiply fast and spread in genital secretions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what does the extracellular protease of gonocci do

A

cleaves IgA1 to remove Fc-receptor end of the antibody, enabling escape from phagocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what does gonoocci do once attached to non-ciliated cels

A

cause ciliary stasis and then death of ciliated cells by LPS and peptidoglycan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

how does gonococci reach ciliated cells

A

via exocytosis because Vacuoles discarch bacteria into subepithlial connective tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

how does gonococci cause cell damage

A

NOT exotoxins, but via LPS and cell wall components (tumor necrosis factor-alpha )

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

tumor necrosis factor alpha leads to

A

sloughing of ciliated cells

non-ciliated cell lysis (leads to inflamation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Gonococcal infection of female upper reprodutive tract leads to

A

inflammation of uterus and fallopian tubes, scarring of upper tract and adjacent organs (infertility, ectopic pregnancy, pain)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

the ascent of organism into upper reproductive tract of men

A

epididymitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Disseminated gonococcal infections lead to(sprend further in the body)

A

pustular lesion of skin
inflammation of tendons and joints
suppurative arthritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Disseminated gonococcal infection results from

A

plevic inflammatory disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

the primary reservoid for meningococci

A

the human nasopharynx and also dental plaque

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

asymptomatic arriage of meningococci leads to

A

induces humoral antibody response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

how meningococci gets in the body

A

attach to nasopharyngeal epithelial cells and invade mucous membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

when do you become immune to meningococci

A

by age 20

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

how can meningococci ge in blood stream

A

deficient in complemten

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

how does meningococci attach to meninges in CNS

A

type IV pili

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what in meningococci damages hosts tissue

A

Lipooligosaccharides, eliciting host inflammatory response, hemorrhaging of blood into skin and mucous membranes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

how does meningococcus survive in the blood

A

serum antibody recognition and evasion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

target for serum antibodies recognition of meningococcus

A

LPS (LOS), protein I on the Outer membrane and other proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

how are meningococcus different from on eanothe

A

devided via their group specific capsular polysaccharide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

how does meningococcus evade

A

alter LPS with host derived N-acetylneuraminic acid (sialic acid) the surface component of RBC
LOS is similar to antigens in human erythrocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Meningococcus Dissemination into intravascular coagulation(DIC) is due to

A

ability to survive in bloodstream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

DIC of Meningococcus leads to

A

skin manifestation
meningitis
shock
death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

how does Body respond to LOS

A

TNF-alpha

IL-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

the more the body responds to LOS, the greater:

A

damage and risk of death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

how to treat neisseria

A

resist penicillin, tearacyclin and other antibiotics

use antimicrobial chemoprophylaxis of close contacts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

how does neisseria resist penicillin

A

plasmid encoded beta-lactamase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

where does resitance to etracyclin come from

A

streptococcal dervied

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

types of meningococci vaccines

A

quadrivalent (MPSV4)-derived against capsular polysaccharide from 4 serotypes
tetravalent (MCV4)-polysaccharide protein conjugate(for young chidlren

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

why are vaccines to gonococci difficult to preoduce

A

antigenic and phase variation

protective intraceullar components

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

how to stop the spread of gonococci

A

condom
partner notification
early diagnosis and tratment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

the ability to turn on and off certain genes

A

phase variation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

how does N. Gonorrhoeae survive

A

by phase variation

antigenic variation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

changes in composition or structure of molecules

A

antigenic variation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

phase variation

A

changing what is expressed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

why use antigenic variation over phase variation

A

the protein being altered is critcal for survival

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

morphology of Haemophilus sp.

A

small gram negative coccobacilli, aerobic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

where do you find Haemophilus sp.

A

upper respiratory tract of most children and adults

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

types of strains of Haemophilus

A

encapsulated and non-typable(no capsule)

58
Q

how doe Haemophilus attach

A

via type IV pili and outer membrane proteins

59
Q

what is needed for H influenzae to grow

A

Hemin (x factor)

NAD+ ( V factor)

60
Q

where does H influenzae get X and V facor

A

lysed blood (choclate agar( not whole blood)

61
Q

what does Haemophilus grow

A

needs only NAD+ so blood agar

62
Q

types of typeable H influenzae strains

A

7( all have distinct capsular polysaccharides

63
Q

diseases by H influenzae

A 
Meningitis (type B)
Ottis (non type)
Sinusitis (non type)
Epiglottitis ( B)
Tracheobronchitis (Non)
Bacteremia (B)
Pneumonia (NON)
64
Q

most virulent Haemophilus

A

H. Influenzae type b

65
Q

what does H. influenzae type b (Hib) cause

A

bacteremia (bloodstream) and meningitis in children younger than 2

66
Q

non-typeable strains of haemophilus (NTHI) cause what

A

respiratory tract disease in infacts, childre, and immunocompromised adults

67
Q

the predominant bacterial pathogen of otitis media

A

H. influenzae

68
Q

H.. parainfluenzae can cause

A

pneumonia or bacteria endocarditis

69
Q

H. ducreyi can cause

A

chancroid(STD)

70
Q

H. aphrophilus is

A

a normal flora of mouth and can occasionally cause bacteral endocarditis

71
Q

H. aegyptius can cause

A

conjuctivites and brazilian purpurix fever

72
Q

what i the capsule of capsulated H.

A

polyribosyl ribital phosphate

73
Q

roll of polyribosyl Ribitol phosphate in H.

A

restance to phgocytosis (as long as no antibody present)

74
Q

Virulence Factors for H.

A

Polyribosyl Ribitol phosphate Capsule
Endotoxin
IgA1 protease
Pili and OM proteins

75
Q

what does the Hib vaccine go after

A

the capsule

76
Q

roll of pili and OM proteins on typeable and non-typable H.

A

adherence to mucosal

involved in twitching motility and biofilm

77
Q

where do NTHI form biofims

A

human airways

78
Q

can the body mount a quick response against capsules it has already seen

A

yes

79
Q

how do we immunize infants

A

use PRP-conjugated diphtheria tocoid(pure wasnt strong enough to cause ann immune response, so they conjugated it with something worse)

80
Q

how to attack unencapsulated strains of H.

A

must develop novel surface targets

81
Q

what do H. influenzae and non-typeable isolates produce to resist penicillin and ampicillin

A

Beta-lactamse

82
Q

how to kill H. influenzae and NTHI

A

chloramphenicol

also use 3rd gen cephalosporins (ceftriaxone or cefotaxime)

83
Q

benifit of 3rd gen cephalosporins

A

penetrate meninges welll and corotcosteriods reduce complications

84
Q

why decrease the amount of biofilm is good

A

decrease resistance to antimicrobials

85
Q

antigens used for development of vaccine for unencapsulated H.

A

OM proteins and Type IV pili

86
Q

morphology of Bordetella

A

small gram negative coccobacilli
aerobic (microaerophilic)
slow grow

87
Q

where do we find bordetella

A

uper respiratory tract of adults in humans

88
Q

what carries and spreads bordetella

A

old adults

89
Q

what does bordetella cause

A

pertussis “Whooping Cough”

90
Q

what does bordetella attach to

A

ciliated epithelial cells

91
Q

Virulence factors of Bordetella

A

Filamentous Hemagglutinin (FHA)
Fimbreiae and pertactin
Pertussis toxin

92
Q

roll of filamentous hemagglutinin (FHA)

A

binds to host amino acid

93
Q

roll of fimbriae and pertactin in Bordetella

A

adherence to mucosal surfaces

94
Q

roll of pertussis toxin

A

paralyzes cilia

induces

95
Q

does bordetella invade epithelial cells

A

no, but they have been found inside alveolar macrophages

tend to just sit on the mucous

96
Q

stages of pertussis

A

7-10 day incubation
catarrhal: 1-2 weeks
Paroxysmal: 1-6 weeks
Convalescent:2-3 weeks

97
Q

symtomes of the Catarrhal stage

A

Cold like symptons

increasing cough severity

98
Q

symptoes of parozysmal stage

A

paroxysms(rapid coughs)

vomiting and exhaustions common

99
Q

symptomes ofthe convalescent stage

A

recoverey

subsequent infection can re-exacerbate paroxysms

100
Q

first vaccine for pertussis

A

whole cell that gave little protection after 5-10 days

101
Q

modern pertussis vaccine

A

Acellular, made of purified inactive cellular components, with multiple compositions based on age group

102
Q

when is DTAP vs Tdap done

A

DTaP: infants
Tdap: 10+ Year old

103
Q

morphology of Pseudomonas aeruginosa

A

gram negative bacillus (rod)
motile with one or several flagella and polar pili
aerobic (but some grow anaerobical by nitrate respiration)

104
Q

where is pseudomonas aeruginosa found

A

soil and water, ubiquitous

105
Q

what do pseudomonas aeruginosa produce

A

produce water soluble pigments as antibacterials
pyocyanin: blue-green
pyoverdin (green)
Fluorescein (yellow)

106
Q

what do pseudomonas aeruginosa smell like

A

fruity or grapelike (in colonies or bear wounds)

107
Q

growth needs of pseudomonas aeruginosa

A

grow fast
are robust
with minimal nutritional requirement (need only acetate and ammonia as carbon and nitrogen sources)-found in petroleum and toxic waste
can live in hand cream, soap, and dilute antiseptics

108
Q

can pseudomonas aeruginosa do fermentation

A

no

109
Q

Persistence Virulence Factors for Pseudomonas aeruginosa

A 
Mucoid polysacharide capsule (alginate)
siderophores
elastase
exotoxin a
phospholipase C
110
Q

Dissemination Virulence Factors for Pseudomonas Aeruginosa

A 
Toxin A
Collagenase
Elastase
Exoenzymes
Flagella
heat stable hemolysin
Tissue damage by proteasea and toxins
111
Q

action of siderophores (iron binding compounds)

A

compete with transferrin for iron
leads to increased production of elastase and exotoxin A
this daages tissues or creates conditions that make iron more accessible

112
Q

action of phospholipase C

A

hydrolyzes phospholipids in eukaryotic membrane as a usable phosphate

113
Q

where we may encounter pseudomonas

A

vegies and plants
water taps, drains, wet surface (otitis externa -swimmer’s ear)
hot tubs

114
Q

what kind of pathogen is Pseudomonas

A

Opportunistic pathogen(doesn’t bind well to healthy epithelium and needs large numbers to get far)

115
Q

after pseudomonas enters the body, it spreads via

A

avoiding phagocytosis and successful adherence to a surface

116
Q

how does pseudomonas bind to epithelium

A

flagella and pili interactions with glycolipid on host cells and Toll like Recetpors

117
Q

is pseudomonas found in hospital infections

A

yes

118
Q

parts of LPS

A

adhesion
Lipid A=endotoxin
core oligosaccharide
Long O-antigen side chains

119
Q

role of lipid A in LPS

A

interact with host TLR4 to initiate inflammatory response

120
Q

role of core oligosaccharide in LPS

A

interacts with CFTR (ATP binding cassette transporter, cystic fibrosis transmembrane conductance regulator) for bacterial internalization and initaion of immune resitanec

121
Q

roll of Long O-antigen side chains

A

Responsible for resistance to human serum, antibiotics, detergents

122
Q

roll of exotoxins of pseudomonas

A

cause local inflammation

exotoxin A; kill host cells via ADP ribosylation of EF-2

123
Q

regulation of exotoxins

A

tightly

124
Q

what are multifucntional enzymes

A

(proteases): elastase, LasA

125
Q

action of Elastatse

A

cleaves elastin and collagen - direct tissue damage
Cleaves proteinase inhibitors
Cleaves immune system components

126
Q

action of LasA

A

serine protease that works with elastase to degrade elastin

127
Q

what kind of secretion of Pseudomonas have

A

Type III (directly transfers virulence into host cells)

128
Q

type III secretion resembles

A

Flagella

129
Q

what does type III secretion from pseudomonas target

A

specific proteins on host cells

130
Q

what causes pseudomonas to do type III secretion

A

host cell contact, low Ca

131
Q

main causes of death due to cystic fibrosis

A

Pseudomonas infections because it can adhear well now

132
Q

what causes Cystic Fibrosis

A

A defect in the CFTR(Cystic Fibrosis transmembrane conductance regulator) protein located on chromosome 7

133
Q

CFTR may cause what

A

decreased sialylation of surface glycolipids- P. aeruginosa binds to these
dehydration of respiratory secretions
mucoid exopolysaccharide (alginate) shields organism from immune syste,however, these produce less protease and toxins

134
Q

why can P. Aeruginosa so easily sit in the lungs and create chronic infections

A

biofilms

135
Q

how does Pseudomonas mediate Sepsis

A

LPS, specifically lipid A moiety, ltimtaely triggering Tumor necrosis factor
this leads to stimulation of macrophages to produce interleukin-1beta

136
Q

overresponding of immune system.
sever systemic illness marked by hemodnamic derangements and organ malfunction brought about by the interaction of certain micobial products with host reticuloendothelial cells

A

sepsis

137
Q

sepsis eventually leads to

A

Multi-organ dysfunction syndrom

138
Q

reuslt of Multi-organ dysfunction syndrome

A

high cardiac output, low blood pressure

Districube shock

139
Q

Requirements for sepsis

A

large pop of infecting organizing
presence of bacterial products that stimulate release of host cytokines
Widespread dissemination of microbial products to hosts’s reitculoenothelal system

140
Q

mortality of sepsis depends on

A 
nature and severity of infection
host defesnse state
promptness and efficacy of treatment
neutropenic patients: 50-70% mortality
Pseudomonas endocarditis: 50% mortality
Sepsis that reach shock stage: >50%
141
Q

treating sepsis

A

easy to identify and culture, but depends on location (some places have different resistance)

micro immuno 2 (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions