Fulminant Community-Acquired Acinetobacter baumannii Pneumonia as a Distinct Clinical Syndrome: Treatment

Twelve patients (92%) had a fulminant course presenting with septic shock and respiratory failure, and 11 patients (85%) needed ventilator support and were treated in an ICU. All patients had positive blood culture results. A high mortality rate (62%) was again observed. The mortality rate reported in our study (57.8%) and previous studies among patients with CAP-AB was comparable to those reported for patients with severe CAP due to S pneumoniae (40 to 75%), Legionella pneumophila (33 to 56%), or Staphylococcus aureus (72 to 100%) in the Nottingham series. Some findings that are not present in our series are the absence of pleural effusion and cavitation seen on the CXR. comments

Our study found that the following factors were associated with higher mortality in the CAP-AB group: AB bacteremia; platelet count of < 120 X 109 cells/L; pH < 7.35 on presentation; and the presence of DIC. In contrast to the study by Anstey et al, our study showed that survival among CAP-AB patients was not improved with appropriate empirical antibiotics treatment. It appears that AB triggers severe systemic inflammatory response syndrome very early on in the course of CAP-AB, together with septic shock, DIC, and ARDS. Antibiotic therapy and supportive treatment are therefore often unable to salvage the patients with CAP-AB. In the study by Chen et al, four of the five patients who survived the infection were treated with a combination of a third-generation cephalosporin and an aminoglycoside. In our study, although a trend to better survival was noted in patients treated with this combination vs treatment with other antibiotics, no statistical significance was detected.
AB was recognized as a hospital-acquired pathogen, especially in patients with VAP. HAP-AB is regarded as a heterogeneous disorder, and the prognosis usually depends on the underlying condition but not on the acquisition of AB infection itself. On the contrary, CAP-AB seems to be a distinct clinical syndrome. The question of why CAP-AB is more fulminant than HAP-AB, when they are both caused by the same organism, is intriguing. A few postulates are possible.

This entry was posted in Pulmonary Function and tagged Acinetobacter baumannii, community-acquired pneumonia, hospital-acquired pneumonia.