Normal hosts do not present withP. aeruginosaCAP.P. aeruginosaCAP is rare, nearly always
fatal, and occurs virtually only in the setting of chronic bronchiectasis/cystic fibrosis (8,10).
With CAP, cavitation occurring after three to five days points toKlebsiella pneumoniaeas
the pathogen.K. pneumoniaeoccurs almost exclusively in patients with chronic alcoholism.
Therefore, the clinical history plus the appearance of cavitation points to the diagnosis, easily
confirmed by Gram stain/culture of the sputum/blood.K. pneumoniaeCAP often presents as
severe CAP. Acute CAP with cavitation after five to seven days is most often due to aspiration
pneumonia. Unless the aspiration is bilateral/massive or if aspiration is superimposed upon
already limited pulmonary function, such patients will not present as severe CAP (29,30,38).
These patients usually present with CAP that becomes more severe as cavitation becomes
apparent after more than one week with bilateral massive aspiration; the initial appearance of
pneumonia on CXR of severe CAP is the usual clinical presentation (8,10).
Empiric Therapy for Severe CAP
Appropriate empiric therapy depends upon identifying the most likely pathogen. The
pathogen range is predictable by host factors (8,10,39). Severe CAP may present with focal/
segmental infiltrates or bilateral interstitial infiltrates with/without accompanying hypoxemia.
The patient’s history is important in identifying previously diagnosed disorders associated
with specific immune defects. Combined with the CXR, the appearance/distribution and the
presence or absence of hypoxemia limits differential diagnostic possibilities (8,10,40,41).
An apparently normal host presenting with severe CAP with focal/segmental infiltrates
should be treated for the usual typical and atypical CAP pathogens. Appropriate empiric
therapy should be started as soon as the diagnosis of CAP is suspected (2,10,12,42–45).
Apparently, normal hosts presenting with near-normal CXR and profound hypoxemia
should be considered as having viral influenza or PCP. If severe pneumonia occurs during
influenza season, then influenza is a likely diagnostic possibility. A clue to otherwise-
unsuspected HIV is often one or more isolated cytopenias, and PCP is likely if accompanied by
an otherwise unexplained, highly elevated serum LDH. PCP is an HIV-defining illness and is
not an uncommon cause of CAP in HIV patients. Patients on steroids/immunosuppressive
therapy, and organ transplants, when present with acute CAP with focal/segmental
infiltration not accompanied by severe hypoxemia should be treated for the usual pathogens
affecting normal hosts with CAP. Empiric antibiotic therapy for CAP as in normal hosts should
be initiated even when urine/fungal pathogens are suspected while the diagnostic workup
proceeds. Because potential viral/fungal pathogens may be clinically indistinguishable, lung
biopsy usually is needed for a specific diagnosis to determine optimal specific therapy.
Immunosuppressed organ transplants presenting with bilateral symmetrical/interstitial
infiltrates may be approached as those with mild/moderate hypoxemia versus those with
severe hypoxemia. In such CAP patients, the absence of a significant diffusion defect (A–a
gradient<35) suggests pulmonary hemorrhage, pulmonary embolus, or another noninfectious
process. In those with bilateral infiltrates accompanied by a profound oxygen diffusion defect
(A–a gradient>35) viral pneumonias or PCP are the most likely diagnostic infectious
possibilities. The common noninfectious causes of bilateral pulmonary infiltrates with
hypoxemia include BOOP and ARDS (1,8,10,47,48).
The clinicians should not use the “shot gun” approach to treating severe CAP cases
based on the mistaken notion that there are many potential pathogens. The diagnostic process
based on a syndromic approach utilizing history, physical, and laboratory abnormalities,
CXR/chest CT appearance, and findings of severity of hypoxemia with limits diagnostic
possibilities. Rapid cavitation (<72 hours) with severe CAP points to MSSA/CA-MRSA CAP
superimposed on underlying influenza A pneumonia. Treat all such patients for MSSA/
CA-MRSA (10,19,35,49–58). Excluding patients with impaired CMI, severe cases of CAP with
focal/segmental defects should be treated the same way as normal hosts with antibiotics active
against typical/atypical pathogens.
Subacute/chronic CAP with focal/ segmental infiltrates (days/weeks) in patients with
decreased CMI do not present as severe CAP. Clinicians should be aware of the noninfectious
mimics of CAP both in the normal/compromised hosts. The mimics of CAP are common and
can usually be easily diagnosed on physical findings, CXR/chest CT appearance, and routine
174 Cunha