Neisseria, Haemophilus, Boretella, and Pseudomonas (2/13/2018) Flashcards
what is the mucus of mucosal surfaces
Viscous polysaccharide fluid layer and physically separates cells from luminal contents
upper vs. lower respiratory tract
upper: larynx, pharynx, nasal cavity, sinus, middl ear
lower: trachea, bronchia, lungs
cells of the upper female reproductive tract
single layer of columnar vells with tight junctions
cells of the lower female reproductive tract
superficial cells terminally differentiated
cell of the male urethral tract
keratinized stratied squamous cells at opening to become non-keratinzed and then eventuall psueodostratified glandular columnar along length of urethrea
the only genus of gram negative cocci that frequently cause disease
neisseria
morphology of neisseria
gram negative, diplococcci, non-motile (twitching motility from pili) Aerobic(but can grow anaerobically) obligate human pathogen
where do neisseria grow best
on media suppllemented with blood in the presnece of CO2
infection by Gonococci leads to
localized inflammation and rarely lethal, only to become serious disseminated
where does meningococci colonize
nasopharynx with no local symptoms
3 general disease of meningococci
uncomplicated bacteremic process
metastatic infection of meninges
overwhelming ststem infection(circulatory collapse and disseminated intravascular coagulation (DIC))-> leads to thick blood titers
who tends to get overhwelming systemic infection from meningococci
individual without IgG antibodies for the capsular polysaccharide
capsule of meningococci
heavily encapsulated and produce hemolysin
where is Gonococci found
cervic in women and distal urethtra in both sex
how can kids get Gonococi
transfer upon labor
how does gonococci attach
non ciliated columnar epithelium pili and surface protein
adhesins of Gonococci controlled
Phase variation: presence/absnse
Antigenic Variation: composition
are men or women more often be aymptomatic caries of Gonococci
women
how is gonococci spread
multiply fast and spread in genital secretions
what does the extracellular protease of gonocci do
cleaves IgA1 to remove Fc-receptor end of the antibody, enabling escape from phagocytosis
what does gonoocci do once attached to non-ciliated cels
cause ciliary stasis and then death of ciliated cells by LPS and peptidoglycan
how does gonococci reach ciliated cells
via exocytosis because Vacuoles discarch bacteria into subepithlial connective tissue
how does gonococci cause cell damage
NOT exotoxins, but via LPS and cell wall components (tumor necrosis factor-alpha )
tumor necrosis factor alpha leads to
sloughing of ciliated cells
non-ciliated cell lysis (leads to inflamation)
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)
the ascent of organism into upper reproductive tract of men
epididymitis
Disseminated gonococcal infections lead to(sprend further in the body)
pustular lesion of skin
inflammation of tendons and joints
suppurative arthritis
Disseminated gonococcal infection results from
plevic inflammatory disease
the primary reservoid for meningococci
the human nasopharynx and also dental plaque
asymptomatic arriage of meningococci leads to
induces humoral antibody response
how meningococci gets in the body
attach to nasopharyngeal epithelial cells and invade mucous membrane
when do you become immune to meningococci
by age 20
how can meningococci ge in blood stream
deficient in complemten
how does meningococci attach to meninges in CNS
type IV pili
what in meningococci damages hosts tissue
Lipooligosaccharides, eliciting host inflammatory response, hemorrhaging of blood into skin and mucous membranes
how does meningococcus survive in the blood
serum antibody recognition and evasion
target for serum antibodies recognition of meningococcus
LPS (LOS), protein I on the Outer membrane and other proteins
how are meningococcus different from on eanothe
devided via their group specific capsular polysaccharide
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
Meningococcus Dissemination into intravascular coagulation(DIC) is due to
ability to survive in bloodstream
DIC of Meningococcus leads to
skin manifestation
meningitis
shock
death
how does Body respond to LOS
TNF-alpha
IL-1
the more the body responds to LOS, the greater:
damage and risk of death
how to treat neisseria
resist penicillin, tearacyclin and other antibiotics
use antimicrobial chemoprophylaxis of close contacts
how does neisseria resist penicillin
plasmid encoded beta-lactamase
where does resitance to etracyclin come from
streptococcal dervied
types of meningococci vaccines
quadrivalent (MPSV4)-derived against capsular polysaccharide from 4 serotypes
tetravalent (MCV4)-polysaccharide protein conjugate(for young chidlren
why are vaccines to gonococci difficult to preoduce
antigenic and phase variation
protective intraceullar components
how to stop the spread of gonococci
condom
partner notification
early diagnosis and tratment
the ability to turn on and off certain genes
phase variation
how does N. Gonorrhoeae survive
by phase variation
antigenic variation
changes in composition or structure of molecules
antigenic variation
phase variation
changing what is expressed
why use antigenic variation over phase variation
the protein being altered is critcal for survival
morphology of Haemophilus sp.
small gram negative coccobacilli, aerobic
where do you find Haemophilus sp.
upper respiratory tract of most children and adults
types of strains of Haemophilus
encapsulated and non-typable(no capsule)
how doe Haemophilus attach
via type IV pili and outer membrane proteins
what is needed for H influenzae to grow
Hemin (x factor)
NAD+ ( V factor)
where does H influenzae get X and V facor
lysed blood (choclate agar( not whole blood)
what does Haemophilus grow
needs only NAD+ so blood agar
types of typeable H influenzae strains
7( all have distinct capsular polysaccharides
diseases by H influenzae
Meningitis (type B) Ottis (non type) Sinusitis (non type) Epiglottitis ( B) Tracheobronchitis (Non) Bacteremia (B) Pneumonia (NON)
most virulent Haemophilus
H. Influenzae type b
what does H. influenzae type b (Hib) cause
bacteremia (bloodstream) and meningitis in children younger than 2
non-typeable strains of haemophilus (NTHI) cause what
respiratory tract disease in infacts, childre, and immunocompromised adults
the predominant bacterial pathogen of otitis media
H. influenzae
H.. parainfluenzae can cause
pneumonia or bacteria endocarditis
H. ducreyi can cause
chancroid(STD)
H. aphrophilus is
a normal flora of mouth and can occasionally cause bacteral endocarditis
H. aegyptius can cause
conjuctivites and brazilian purpurix fever
what i the capsule of capsulated H.
polyribosyl ribital phosphate
roll of polyribosyl Ribitol phosphate in H.
restance to phgocytosis (as long as no antibody present)
Virulence Factors for H.
Polyribosyl Ribitol phosphate Capsule
Endotoxin
IgA1 protease
Pili and OM proteins
what does the Hib vaccine go after
the capsule
roll of pili and OM proteins on typeable and non-typable H.
adherence to mucosal
involved in twitching motility and biofilm
where do NTHI form biofims
human airways
can the body mount a quick response against capsules it has already seen
yes
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)
how to attack unencapsulated strains of H.
must develop novel surface targets
what do H. influenzae and non-typeable isolates produce to resist penicillin and ampicillin
Beta-lactamse
how to kill H. influenzae and NTHI
chloramphenicol
also use 3rd gen cephalosporins (ceftriaxone or cefotaxime)
benifit of 3rd gen cephalosporins
penetrate meninges welll and corotcosteriods reduce complications
why decrease the amount of biofilm is good
decrease resistance to antimicrobials
antigens used for development of vaccine for unencapsulated H.
OM proteins and Type IV pili
morphology of Bordetella
small gram negative coccobacilli
aerobic (microaerophilic)
slow grow
where do we find bordetella
uper respiratory tract of adults in humans
what carries and spreads bordetella
old adults
what does bordetella cause
pertussis “Whooping Cough”
what does bordetella attach to
ciliated epithelial cells
Virulence factors of Bordetella
Filamentous Hemagglutinin (FHA)
Fimbreiae and pertactin
Pertussis toxin
roll of filamentous hemagglutinin (FHA)
binds to host amino acid
roll of fimbriae and pertactin in Bordetella
adherence to mucosal surfaces
roll of pertussis toxin
paralyzes cilia
induces
does bordetella invade epithelial cells
no, but they have been found inside alveolar macrophages
tend to just sit on the mucous
stages of pertussis
7-10 day incubation
catarrhal: 1-2 weeks
Paroxysmal: 1-6 weeks
Convalescent:2-3 weeks
symtomes of the Catarrhal stage
Cold like symptons
increasing cough severity
symptoes of parozysmal stage
paroxysms(rapid coughs)
vomiting and exhaustions common
symptomes ofthe convalescent stage
recoverey
subsequent infection can re-exacerbate paroxysms
first vaccine for pertussis
whole cell that gave little protection after 5-10 days
modern pertussis vaccine
Acellular, made of purified inactive cellular components, with multiple compositions based on age group
when is DTAP vs Tdap done
DTaP: infants
Tdap: 10+ Year old
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)
where is pseudomonas aeruginosa found
soil and water, ubiquitous
what do pseudomonas aeruginosa produce
produce water soluble pigments as antibacterials
pyocyanin: blue-green
pyoverdin (green)
Fluorescein (yellow)
what do pseudomonas aeruginosa smell like
fruity or grapelike (in colonies or bear wounds)
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
can pseudomonas aeruginosa do fermentation
no
Persistence Virulence Factors for Pseudomonas aeruginosa
Mucoid polysacharide capsule (alginate) siderophores elastase exotoxin a phospholipase C
Dissemination Virulence Factors for Pseudomonas Aeruginosa
Toxin A Collagenase Elastase Exoenzymes Flagella heat stable hemolysin Tissue damage by proteasea and toxins
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
action of phospholipase C
hydrolyzes phospholipids in eukaryotic membrane as a usable phosphate
where we may encounter pseudomonas
vegies and plants
water taps, drains, wet surface (otitis externa -swimmer’s ear)
hot tubs
what kind of pathogen is Pseudomonas
Opportunistic pathogen(doesn’t bind well to healthy epithelium and needs large numbers to get far)
after pseudomonas enters the body, it spreads via
avoiding phagocytosis and successful adherence to a surface
how does pseudomonas bind to epithelium
flagella and pili interactions with glycolipid on host cells and Toll like Recetpors
is pseudomonas found in hospital infections
yes
parts of LPS
adhesion
Lipid A=endotoxin
core oligosaccharide
Long O-antigen side chains
role of lipid A in LPS
interact with host TLR4 to initiate inflammatory response
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
roll of Long O-antigen side chains
Responsible for resistance to human serum, antibiotics, detergents
roll of exotoxins of pseudomonas
cause local inflammation
exotoxin A; kill host cells via ADP ribosylation of EF-2
regulation of exotoxins
tightly
what are multifucntional enzymes
(proteases): elastase, LasA
action of Elastatse
cleaves elastin and collagen - direct tissue damage
Cleaves proteinase inhibitors
Cleaves immune system components
action of LasA
serine protease that works with elastase to degrade elastin
what kind of secretion of Pseudomonas have
Type III (directly transfers virulence into host cells)
type III secretion resembles
Flagella
what does type III secretion from pseudomonas target
specific proteins on host cells
what causes pseudomonas to do type III secretion
host cell contact, low Ca
main causes of death due to cystic fibrosis
Pseudomonas infections because it can adhear well now
what causes Cystic Fibrosis
A defect in the CFTR(Cystic Fibrosis transmembrane conductance regulator) protein located on chromosome 7
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
why can P. Aeruginosa so easily sit in the lungs and create chronic infections
biofilms
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
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
sepsis eventually leads to
Multi-organ dysfunction syndrom
reuslt of Multi-organ dysfunction syndrome
high cardiac output, low blood pressure
Districube shock
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
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%
treating sepsis
easy to identify and culture, but depends on location (some places have different resistance)
