pathogens Flashcards
what are some host factors that predispose to opportunistic factors
- local (5)
- systemic (9)
Local
- anatomical defects (eg broken skin
- surgical/other wounds
- burns
- catheterisation (bladder, IV)
- foreign bodies in general = niches for bacteria, decrease number required to get infection
systemic
- extremes of age
- leucopenia
- malignancy
- malnutrition
- diabetes
- liver disease
- certain disease (HIV, measles)
- treatment with anitmicrobials (c. difficile, thrush)
- primary immunodeficiency
pseudomonas
- gram stain
- motility
- aerobic/non aerobe
- fermenters?
- spores?
- catalase, oxidase tests
how is it divided into species? and subtypes?
G- rod
motile
aerobes (or facultative anaerobe)
non-fermenting
non-sporing
catalase +
oxidase +
produce pyocyanin (turqoise pus)
divided into species by biochem tests
- subtypes of p. aeruginosa by serotype/biotype
can do pulsed-field gel electrophoresis on genomic DNA to trace outbreaks
why are pseudomonas so ubiquitous
low nutritional requirements
intrinsically resistant to many commonly used antibiotics + weak disinfectants
readily acquires resistance form other bacteria
what are the species of Pseudomonas (and related genera)
- why are they important
Ps. aeruginosa* - ubiquitous saprophyte, important opp pathogen
Burkholderia cepacia* - opp pathogen
Stenotrophomonas maltophilia* - opp pathogen
Burkholderia pseudomallei - causes melioidosis
- = colonise resp tract of cystic fibrosis patients
which infections is ps aeruginosa most commonly associated wtih?
common nocosomial pathogen
previous: burns, febrile neutropenia
major problem in cystic fibrosis
superficial infections
skin: wound infection, otitis externa, folliculitis (eg from hot tubs)
eye: keratitis, corneal ulcer, deep infection -> blindness
deep + systemic
pulmonary: nocosomial pneumnia, chronic infection in CF patiets
other
- uti
- endocarditis
- osteomyelitis
- septicaemia
=> in immunocompromised
Ps aeruginosa pathogenesis
- adhesion and invasion
- spread and multiplication
- tissue damage
adheres weakly to intact epithelium (flagella, pilli, LPS)
invasion - doesn’t invade skin unless v large numbers
- once adherent - bacteria produce biofilm
(capsule helps adherence + biofilm production)
spread facilitated by
- reduced PMNs
- flagella
- exoenzymes )act on pulmonary tissue + surfactant
- exotoxins - inhibit phagocytosis
tissue damage
- type 3 secreted proteins
- other exotoxins + enzymes
how does ps. aeruginosa adhere to epithelium?
flagella
pili
LPS
LPS core binds to CFTR (CF transmembrane conductance reg.)
- in healthy - macrophages come along and clean
- in CF - CFTR is abnormal - don’t actually bind -> hang around in airways and create biofilm
pseudomonas control
can’t be eradicated => management is directed towards prevention
- ↓risk of susceptible patients by suitable management of burns, neutropenia, catheters, ventilators
- be alert, treat early
- hand hygiene
- lifelong monitoring + treatment of CF patients
how does ps. aeruginosa cause tissue damage?
type 3 secreted proteisn
= exoenzymes S,T,U,Y
= act on various host cell targets - interfere with phagocytosis
- enhance cytokine production
Exotoxin A - block protein synthesis
LasA and LasB - proteases, act together as elastase
Phospholipase - damages cell membranes, degrades surfactant
how does ps aeruginosa change its properties in biofilms?
change gene transcription
non-motile
more capsule material => mucoid (biofilm production)
more adherent
less invasive
shorter LPS (no O-antigen)
slower growth
increase resistance to Ab (slow growth, more stuff on outside)
(this helps them get established in CF patients)
how do biofilms form in pseudomonas?
is a cycle
- sit on surface, respond to environmental signals
have bacterial “cross-talk” = quorum sensing
- communicate with ech other and change their form
bacteria that form biofilms
pseudomonas
s. epidermidis
what happens with pseudomonas in patients with cystic fibrosis?
defect in CFTR
- abnormal ion transport
- thicker mucus
- impaired mucociliary function
pseudomonas + staph aren’t inhibited by high salt concentration
biofilm - resist mechanical removal; are less visible to innate imm system
are less virulent in the biofilm -> persist
