OPPORTUNISTIC INFECTIONS: NECROTIZING PNEUMONIAS

G POS STAPH AUREUS

GENERAL:
Imp Staph: aureus, epidermidis, saprophyticus
G Pos cocci form clumps/ clusters
VIRULENCE:
Many cell surface PRO; multifactorial
disease
Staph Aureus 1:10 infxns
Cell-Associated Virulence:
o 1. capsule
o 2. PRO A: (bind Fc empnt lgG); stop phagocytosis &
complement activation
o 3. Clumping Factor: binds fibrinogen fibrin bacterial
aggregation Extracellular Enzymes:
o 1. coagulase: prothrombin staphylothrombin fibrin
formation = clotting! o
2. hyaluronidase/nucleases/lipases
o 3. catalase: stops MPO system; inhibit phagocytosis
o 4. staphylokinase: dissolves fibrin clots o 5. PCNases: when
inappropriate therapy Toxins:
o Exfoliative/TSST-1 /Enterotoxins = release of cytokines
o Cytotoxins lyse many cells
o Panton-Valentine Leukocidin (PVL): leuko destruction/tissue
necrosis

Severe necrotic hemorrhagic pneumonia

(immuno-comp, kids)

Previously healthy lungs + predisposing viral

infxn

Community acquired!

EPIDEMIOLOGY of STAPH AUREUS:

Nml flora: anterior nares/perineum/skin (shed from here)
Trans: close contact/ ingested in food/fomites
Asympomatic carriers
PATHOLOGY/DISEASE of STAPH AUREUS:
Lots of ways to enter = ultimate opportunist
Affects any body site (skin, deep tissues, wounds, etc)
RESPIRATORY INFXNS due to STAPH AUREUS:
Inhalation Pneumonia
o Community acquired after influenza (varied severity )
Aspiration Pneumonia:
o Hospital-acquired after intubation
Hematogenous Pneumonia:
o From thrombus or vegetation
o Empyema, pulmonary infxn (common cause)
PREDISPOSING FACTORS:

Chemotaxis, opsonization, staphylocida! (DM decompensation) defects,

presence of foreign body
DX:
Clinical: (nothing unique or radiologic!!!)
o Helpful!: Predisposing factors, poor response pnemococcal
pneumo, rapid cavitation bronchopneumonia, lots of
pulmonary consolidation, empyema

Lab: G stain, direct specimen, need colonies (blood), catalase?,

coagulase?, beta-hemolytic on BAP, facultative halophile MSA yellow
TX:
Hospital strains resistant to AB! Need antimicrobial suscep testing
o MRSA (methiciliin resis); hospital & community w/PVL o VISA
(vanco intermediate resistant) o VRSA (vanco resistant: van A
operon)
PREVENTION:
Candidate
Vaccines:
o
1. NABI Pharm (failed clinical trials)
o
2. Inhibitex (veronate. aurexis)
Non-immunc based:

Good hygiene, prophylaxis for surg. hand washing

G NEG PSEUDOMONAS AERUGINOSA

GENERAL:
G Neg aerobic bacillus
Used in bioremediation of petrochem waste materials
Degrades materials w'ith C, H, O, N (or combo)
Pyoverdin (green pigmnt) & pyocyanin (blue pigmnt)
VIRULENCE:
I. pyocyanin: ROS production

2. exotoxin A. A-B toxin, same mech diphtheria toxin, ciliastasis,

immunosuppressor
3. elastases (LasA/LasB): elastolytic
4. alginate: slime layer/biofllm, inhibit muco escalator, glycocalyx
5. pili: attachment
6. LPS: endotoxin activity
EPIDEMIOLOGY of PSEUDOMONAS AEROGINOSA:

widespread in environment
carried on skin/feces
nml flora & opportunistic flora in hospital
Trans: sinks, fomites, plants, fruits, hands, etc
PATHOLOGY/DISEASE of PSEUDOMONAS AEROGINOSA:
Not super virulent
Needs significant break in host defense
Compromised hosts only
INFXNS (non-pneumonia):
UTI. pneumonia, eye, ear, skin
2nd leading cause infection in bum patients
common cause of death in CF
RESPIRATORY INFXNS due to PSEUDOMONAS AEROGINOSA:
Primary
o Inhalation therapy with nebulization
Secondary
o Immunosuppression/ host compromise o
Associated with bacteremia (IV drug use)
Clinically:
o Nml Pts: toxicity, cyanosis, empyema o CF: chronic/recurrent.
confined to respiratory tract, bilateral w/residual damage
DX:
Need to isolate & ID in lab!
Grow in lots of different media
Blue-green water soluble pigment highly characteristic
IX:
MDR common; need susceptibility tests!
Hard to clear, relapse common
Systemic inxn needs combos for synergism
NO broad spectrum Ab (suppress nml flora)