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

E P ID E M IO L O G Y of P S E U D O M O N A S A E R O G IN O S A :

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)