important but not most frequent cause of NP/HAP/VAP isP. aeruginosa, there is a tendency to
“cover” isolates cultured from respiratory secretions of intubated patients. The incorrect
clinical assumption is that the isolate in the respiratory secretions is reflective of the
pathological process in the parenchyma of the lung. Respiratory secretions and parenchyma of
the lung are rarely related and nearly always represent colonization rather than infection.
P. aeruginosaNP/VAP has a distinctive clinical presentation characterized by precipitous
clinical deterioration, cyanosis, dramatically decreased lung function, and rapid cavitation
(<72 hours) on the chest X Ray (CXR)/chest CT scan. In ventilated patients with fever and
leukocytosis with a shift to the left and pulmonary infiltrates, it is well known that the cause of
such patients’ pulmonary infiltrates is more commonly noninfectious than infectious. There
are many disorders that can present with these findings, i.e., congestive heart failure (CHF),
pulmonary hemorrhage, pulmonary drug effects, bronchiolitis obliterans organizing pneu-
monia (BOOP), adult respiratory distress syndrome (ARDS), interstitial lung disease,
lymphangitic spread of malignancies, etc. Therefore, the clinician should not conclude
pulmonary infiltrates in a febrile patient with leukocytosis, and a left shift are diagnostic of NP.
Isolates recovered from respiratory secretions in such patients should not be considered as
potential pathogen even if NP is present.P. aeruginosaNP/HAP/VAP should be considered
only if the patient has clinical presentation characteristic ofP. aeruginosapneumonia (vide
supra) whether or notP. aeruginosais cultured from respiratory secretions (7–9).
Therefore, until proven otherwise, the recovery ofP. aeruginosarespiratory secretions in a
ventilated patient with fever, leukocytosis/shift to the left, and pulmonary infiltrates should
not be considered diagnostic ofP. aeruginosa. Patients withbona fide P. aeruginosaNP/VAP
have atypical infiltrates, i.e., necrotizing pneumonia, which is responsible for the bilateral
rapid cavitary lesions seen on CXR/chest CT. The necrotic/invasive nature of this
fulminating/necrotic pneumonia is manifested by demonstrating elastin fibers using an
elastin stain in respiratory secretions. Unless occurring in the characteristic clinical context, it is
prudent not to treat possible NP/VAP based solely on respiratory secretions isolates. Since
P. aeruginosaNP/VAP is not the most frequent but is the most virulent pathogen, it is prudent
in the absence of a definitive diagnosis to empirically treat forP. aeruginosain NP/VAP
patients realizing that many such patients will, in fact, not havebona fide P. aeruginosa
NP/VAP. Given the nature/virulence ofP. aeruginosaNP/VAP, empiric coverage with an
anti-P. aeruginosaantibiotic with a low-resistance potential should be selected. For empiric
coverage whereP. aeruginosais a potential pathogen, empiric monotherapy is as efficacious as
double drug antibiotic therapy, but for provenP. aeruginosaNP/VAP, double drug therapy is
preferred.
Empiric therapy for NP/VAP is continued for two weeks. If the pulmonary infiltrates
remain unchanged after two weeks, the diagnosis of NP/VAP should be questioned and a
lung biopsy should be obtained to arrive at a definitive diagnosis (7,8).
Catheter Associated Bacteriuria (CAB)
In the urine,P. aeruginosacommonly colonizes the urine of patients with indwelling urinary
catheters, i.e., CAB. In normal hosts, CAB need not be treated since it represents colonization
and not abona fideUTI. CAB has important infection control, but not clinical importance.
Before treating CAB, it is important to remove/change the indwelling urinary catheter to avoid
trying to eradicate strains embedded in catheter biofilm. If the physician elects to treatP.
aeruginosaCAB after Foley removal/change, there are relatively few oral antibiotics available
that are effective againstP. aeruginosa(3–5).
Antibiotic Therapy of MDR P. aeruginosa Infections
To treat susceptible strains ofP. aeruginosain the CCU setting, the clinician should select an
antibiotic based upon resistance potential of the antibiotic as well as the site of infection.
Aminoglycosides concentrate the high concentration in the urine and are ideal agents to use in
P. aeruginosaurosepsis. If theP. aeruginosastrain is quinolone-sensitive, then levofloxacin is as
effective or more effective againstP. aeruginosathen ciprofloxacin. ForP. aeruginosaCAB,
single-dose amikacin therapy may be effective depending upon renal function. Alternately, the
only oral antimicrobial regularly effective against MDRP. aeruginosaCAB/UTIs is fosfomycin.
Antibiotic Therapy of MDRP. aeruginosa, K. pneumoniae, andA. baumanniiin CCU 515