Neisseria, Haemophilus, Boretella, and Pseudomonas (2/13/2018) Flashcards
(141 cards)
1
Q
what is the mucus of mucosal surfaces
A
Viscous polysaccharide fluid layer and physically separates cells from luminal contents
2
Q
upper vs. lower respiratory tract
A
upper: larynx, pharynx, nasal cavity, sinus, middl ear
lower: trachea, bronchia, lungs
3
Q
cells of the upper female reproductive tract
A
single layer of columnar vells with tight junctions
4
Q
cells of the lower female reproductive tract
A
superficial cells terminally differentiated
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
6
Q
the only genus of gram negative cocci that frequently cause disease
A
neisseria
7
Q
morphology of neisseria
A
gram negative, diplococcci, non-motile (twitching motility from pili) Aerobic(but can grow anaerobically) obligate human pathogen
8
Q
where do neisseria grow best
A
on media suppllemented with blood in the presnece of CO2
9
Q
infection by Gonococci leads to
A
localized inflammation and rarely lethal, only to become serious disseminated
10
Q
where does meningococci colonize
A
nasopharynx with no local symptoms
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
12
Q
who tends to get overhwelming systemic infection from meningococci
A
individual without IgG antibodies for the capsular polysaccharide
13
Q
capsule of meningococci
A
heavily encapsulated and produce hemolysin
14
Q
where is Gonococci found
A
cervic in women and distal urethtra in both sex
15
Q
how can kids get Gonococi
A
transfer upon labor
16
Q
how does gonococci attach
A
non ciliated columnar epithelium pili and surface protein
17
Q
adhesins of Gonococci controlled
A
Phase variation: presence/absnse
Antigenic Variation: composition
18
Q
are men or women more often be aymptomatic caries of Gonococci
A
women
19
Q
how is gonococci spread
A
multiply fast and spread in genital secretions
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
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
22
Q
how does gonococci reach ciliated cells
A
via exocytosis because Vacuoles discarch bacteria into subepithlial connective tissue
23
Q
how does gonococci cause cell damage
A
NOT exotoxins, but via LPS and cell wall components (tumor necrosis factor-alpha )
24
Q
tumor necrosis factor alpha leads to
A
sloughing of ciliated cells
non-ciliated cell lysis (leads to inflamation)
25
Gonococcal infection of female upper reprodutive tract leads to
inflammation of uterus and fallopian tubes, scarring of upper tract and adjacent organs (infertility, ectopic pregnancy, pain)
26
the ascent of organism into upper reproductive tract of men
epididymitis
27
Disseminated gonococcal infections lead to(sprend further in the body)
pustular lesion of skin
inflammation of tendons and joints
suppurative arthritis
28
Disseminated gonococcal infection results from
plevic inflammatory disease
29
the primary reservoid for meningococci
the human nasopharynx and also dental plaque
30
asymptomatic arriage of meningococci leads to
induces humoral antibody response
31
how meningococci gets in the body
attach to nasopharyngeal epithelial cells and invade mucous membrane
32
when do you become immune to meningococci
by age 20
33
how can meningococci ge in blood stream
deficient in complemten
34
how does meningococci attach to meninges in CNS
type IV pili
35
what in meningococci damages hosts tissue
Lipooligosaccharides, eliciting host inflammatory response, hemorrhaging of blood into skin and mucous membranes
36
how does meningococcus survive in the blood
serum antibody recognition and evasion
37
target for serum antibodies recognition of meningococcus
LPS (LOS), protein I on the Outer membrane and other proteins
38
how are meningococcus different from on eanothe
devided via their group specific capsular polysaccharide
39
how does meningococcus evade
alter LPS with host derived N-acetylneuraminic acid (sialic acid) the surface component of RBC
LOS is similar to antigens in human erythrocytes
40
Meningococcus Dissemination into intravascular coagulation(DIC) is due to
ability to survive in bloodstream
41
DIC of Meningococcus leads to
skin manifestation
meningitis
shock
death
42
how does Body respond to LOS
TNF-alpha
| IL-1
43
the more the body responds to LOS, the greater:
damage and risk of death
44
how to treat neisseria
resist penicillin, tearacyclin and other antibiotics
| use antimicrobial chemoprophylaxis of close contacts
45
how does neisseria resist penicillin
plasmid encoded beta-lactamase
46
where does resitance to etracyclin come from
streptococcal dervied
47
types of meningococci vaccines
quadrivalent (MPSV4)-derived against capsular polysaccharide from 4 serotypes
tetravalent (MCV4)-polysaccharide protein conjugate(for young chidlren
48
why are vaccines to gonococci difficult to preoduce
antigenic and phase variation
| protective intraceullar components
49
how to stop the spread of gonococci
condom
partner notification
early diagnosis and tratment
50
the ability to turn on and off certain genes
phase variation
51
how does N. Gonorrhoeae survive
by phase variation
| antigenic variation
52
changes in composition or structure of molecules
antigenic variation
53
phase variation
changing what is expressed
54
why use antigenic variation over phase variation
the protein being altered is critcal for survival
55
morphology of Haemophilus sp.
small gram negative coccobacilli, aerobic
56
where do you find Haemophilus sp.
upper respiratory tract of most children and adults
57
types of strains of Haemophilus
encapsulated and non-typable(no capsule)
58
how doe Haemophilus attach
via type IV pili and outer membrane proteins
59
what is needed for H influenzae to grow
Hemin (x factor)
| NAD+ ( V factor)
60
where does H influenzae get X and V facor
lysed blood (choclate agar( not whole blood)
61
what does Haemophilus grow
needs only NAD+ so blood agar
62
types of typeable H influenzae strains
7( all have distinct capsular polysaccharides
63
diseases by H influenzae
```
Meningitis (type B)
Ottis (non type)
Sinusitis (non type)
Epiglottitis ( B)
Tracheobronchitis (Non)
Bacteremia (B)
Pneumonia (NON)
```
64
most virulent Haemophilus
H. Influenzae type b
65
what does H. influenzae type b (Hib) cause
bacteremia (bloodstream) and meningitis in children younger than 2
66
non-typeable strains of haemophilus (NTHI) cause what
respiratory tract disease in infacts, childre, and immunocompromised adults
67
the predominant bacterial pathogen of otitis media
H. influenzae
68
H.. parainfluenzae can cause
pneumonia or bacteria endocarditis
69
H. ducreyi can cause
chancroid(STD)
70
H. aphrophilus is
a normal flora of mouth and can occasionally cause bacteral endocarditis
71
H. aegyptius can cause
conjuctivites and brazilian purpurix fever
72
what i the capsule of capsulated H.
polyribosyl ribital phosphate
73
roll of polyribosyl Ribitol phosphate in H.
restance to phgocytosis (as long as no antibody present)
74
Virulence Factors for H.
Polyribosyl Ribitol phosphate Capsule
Endotoxin
IgA1 protease
Pili and OM proteins
75
what does the Hib vaccine go after
the capsule
76
roll of pili and OM proteins on typeable and non-typable H.
adherence to mucosal
| involved in twitching motility and biofilm
77
where do NTHI form biofims
human airways
78
can the body mount a quick response against capsules it has already seen
yes
79
how do we immunize infants
use PRP-conjugated diphtheria tocoid(pure wasnt strong enough to cause ann immune response, so they conjugated it with something worse)
80
how to attack unencapsulated strains of H.
must develop novel surface targets
81
what do H. influenzae and non-typeable isolates produce to resist penicillin and ampicillin
Beta-lactamse
82
how to kill H. influenzae and NTHI
chloramphenicol
| also use 3rd gen cephalosporins (ceftriaxone or cefotaxime)
83
benifit of 3rd gen cephalosporins
penetrate meninges welll and corotcosteriods reduce complications
84
why decrease the amount of biofilm is good
decrease resistance to antimicrobials
85
antigens used for development of vaccine for unencapsulated H.
OM proteins and Type IV pili
86
morphology of Bordetella
small gram negative coccobacilli
aerobic (microaerophilic)
slow grow
87
where do we find bordetella
uper respiratory tract of adults in humans
88
what carries and spreads bordetella
old adults
89
what does bordetella cause
pertussis "Whooping Cough"
90
what does bordetella attach to
ciliated epithelial cells
91
Virulence factors of Bordetella
Filamentous Hemagglutinin (FHA)
Fimbreiae and pertactin
Pertussis toxin
92
roll of filamentous hemagglutinin (FHA)
binds to host amino acid
93
roll of fimbriae and pertactin in Bordetella
adherence to mucosal surfaces
94
roll of pertussis toxin
paralyzes cilia
| induces
95
does bordetella invade epithelial cells
no, but they have been found inside alveolar macrophages
| tend to just sit on the mucous
96
stages of pertussis
7-10 day incubation
catarrhal: 1-2 weeks
Paroxysmal: 1-6 weeks
Convalescent:2-3 weeks
97
symtomes of the Catarrhal stage
Cold like symptons
| increasing cough severity
98
symptoes of parozysmal stage
paroxysms(rapid coughs)
| vomiting and exhaustions common
99
symptomes ofthe convalescent stage
recoverey
| subsequent infection can re-exacerbate paroxysms
100
first vaccine for pertussis
whole cell that gave little protection after 5-10 days
101
modern pertussis vaccine
Acellular, made of purified inactive cellular components, with multiple compositions based on age group
102
when is DTAP vs Tdap done
DTaP: infants
Tdap: 10+ Year old
103
morphology of Pseudomonas aeruginosa
gram negative bacillus (rod)
motile with one or several flagella and polar pili
aerobic (but some grow anaerobical by nitrate respiration)
104
where is pseudomonas aeruginosa found
soil and water, ubiquitous
105
what do pseudomonas aeruginosa produce
produce water soluble pigments as antibacterials
pyocyanin: blue-green
pyoverdin (green)
Fluorescein (yellow)
106
what do pseudomonas aeruginosa smell like
fruity or grapelike (in colonies or bear wounds)
107
growth needs of pseudomonas aeruginosa
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
can pseudomonas aeruginosa do fermentation
no
109
Persistence Virulence Factors for Pseudomonas aeruginosa
```
Mucoid polysacharide capsule (alginate)
siderophores
elastase
exotoxin a
phospholipase C
```
110
Dissemination Virulence Factors for Pseudomonas Aeruginosa
```
Toxin A
Collagenase
Elastase
Exoenzymes
Flagella
heat stable hemolysin
Tissue damage by proteasea and toxins
```
111
action of siderophores (iron binding compounds)
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
action of phospholipase C
hydrolyzes phospholipids in eukaryotic membrane as a usable phosphate
113
where we may encounter pseudomonas
vegies and plants
water taps, drains, wet surface (otitis externa -swimmer's ear)
hot tubs
114
what kind of pathogen is Pseudomonas
Opportunistic pathogen(doesn't bind well to healthy epithelium and needs large numbers to get far)
115
after pseudomonas enters the body, it spreads via
avoiding phagocytosis and successful adherence to a surface
116
how does pseudomonas bind to epithelium
flagella and pili interactions with glycolipid on host cells and Toll like Recetpors
117
is pseudomonas found in hospital infections
yes
118
parts of LPS
adhesion
Lipid A=endotoxin
core oligosaccharide
Long O-antigen side chains
119
role of lipid A in LPS
interact with host TLR4 to initiate inflammatory response
120
role of core oligosaccharide in LPS
interacts with CFTR (ATP binding cassette transporter, cystic fibrosis transmembrane conductance regulator) for bacterial internalization and initaion of immune resitanec
121
roll of Long O-antigen side chains
Responsible for resistance to human serum, antibiotics, detergents
122
roll of exotoxins of pseudomonas
cause local inflammation
| exotoxin A; kill host cells via ADP ribosylation of EF-2
123
regulation of exotoxins
tightly
124
what are multifucntional enzymes
(proteases): elastase, LasA
125
action of Elastatse
cleaves elastin and collagen - direct tissue damage
Cleaves proteinase inhibitors
Cleaves immune system components
126
action of LasA
serine protease that works with elastase to degrade elastin
127
what kind of secretion of Pseudomonas have
Type III (directly transfers virulence into host cells)
128
type III secretion resembles
Flagella
129
what does type III secretion from pseudomonas target
specific proteins on host cells
130
what causes pseudomonas to do type III secretion
host cell contact, low Ca
131
main causes of death due to cystic fibrosis
Pseudomonas infections because it can adhear well now
132
what causes Cystic Fibrosis
A defect in the CFTR(Cystic Fibrosis transmembrane conductance regulator) protein located on chromosome 7
133
CFTR may cause what
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
why can P. Aeruginosa so easily sit in the lungs and create chronic infections
biofilms
135
how does Pseudomonas mediate Sepsis
LPS, specifically lipid A moiety, ltimtaely triggering Tumor necrosis factor
this leads to stimulation of macrophages to produce interleukin-1beta
136
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
sepsis
137
sepsis eventually leads to
Multi-organ dysfunction syndrom
138
reuslt of Multi-organ dysfunction syndrome
high cardiac output, low blood pressure
| Districube shock
139
Requirements for sepsis
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
mortality of sepsis depends on
```
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
treating sepsis
easy to identify and culture, but depends on location (some places have different resistance)
