Nosocomial Acinetobacter Pneumonia

The following is an abstract of the above lecture to be given at the Presidential Symposium on Wednesday 22nd November 2006 by:

Carlos M. Luna
Profesor Adjunto de Medicina Interna, Pulmonary Diseases Division, Hospital de Clínicas, Universidad de Buenos Aires, Argentina

Acinetobacter includes Gram-negative coccobacilli, strictly aerobic, nonmotile, catalase positive, and oxidase negative. A. baumannii is the main genomic species associated with outbreaks of nosocomial infection. A. baumannii became an increasingly important cause of nosocomial infections. Treatment is difficult because the organism has intrinsic and acquired resistance. In health-care settings, colonized and infected patients are the sources of infections; however, their ability to survive for prolonged periods on environmental surfaces also has contributed to protracted outbreaks in these settings. Transmission is difficult to control because Acinetobacter spp can survive for long periods of time.

In the 1970s resistance of Enterobacteriaceae was followed by the introduction of newer broad spectrum antibiotics that subsequently increased in the importance of strictly aerobic gram-negative bacilli, including Pseudomonas aeruginosa, Stenotrophomonas maltophilia, and Acinetobacter spp. Now Acinetobacter spp. became a significant colonizer and pathogen in the hospitals. Their predominant role is in nosocomial pneumonia, particularly ventilator-associated pneumonia in patients confined to hospital intensive care units (ICUs).

Microbiology

Most of Acinetobacter strains were identified as A. baumannii, particularly from respiratory tract specimens. Acinetobacters are short, plump, Gram-negative (sometimes difficult to destain) rods, pairing often occurs. Gram stain variability can be observed within a single pure culture.

Acinetobacter sp. has been isolated from various types of opportunistic infections. The incidence of Acinetobacter sp as the causative microorganism of VAP varies from one world area to other world area but even from one area in the Hospital to other area in the same Hospital.

These infections are often extremely difficult to treat because of their widespread resistance to the major groups of antibiotics. Various mechanisms of antibiotic resistance have been recognized, and combination therapy is usually required for effective treatment. Molecular identification and typing methods should form a rational scientific foundation for proper epidemiological studies of genotypically related strains involved in outbreaks.

There is an increasing role played by Acinetobacter spp. in nosocomial pneumonia in the ICU. Between 49% and 3% of included at least one Acinetobacter sp. Prior antibiotic has been found to be an independent variable associated with development of VAP by A. baumannii (OR 14, 95% CI 4.1?91, p<0.0001). The prognosis associated with this pathogen is worse than that associated with other bacteria, with the exception of P. aeruginosa. Fagon et al, confirmed in pneumonia due to Pseudomonas or Acinetobacter species, that attributable mortality was higher.

Patient characteristics likely play a major role in outcomes, include age, immunosuppression, recent surgery, acute respiratory failure, acute renal failure, septic shock and inadequacy of initial antibiotic therapy. Acinetobacter baumannii-calcoaceticus complex has become a serious nosocomial pathogen due to its persistence in the hospital environment and its broad antimicrobial resistance patterns. Prior use of imipenem induced imipenem-resistant strains and that the SOFA score at admission was the only one predictor of Hospital mortality.

Treatment of A. baumannii emphasizes the need to clearly define infection versus colonization. Agents with the most antimicrobial activity are imipenem/cilastatin, amikacin, ampicillin/ sulbactam, colistin, and tetracyclines. The role of monotherapy is unclear, but is likely adequate if the patient who does not have significant comorbidities. Resistance is increasing, and carbapenems, sulbactam, and colistin are the most sensitive agents. A. baumannii tends to cause polymicrobial colonization of the respiratory tract of patients with artificial airways. If risk of A. baumannii exists, experimental antimicrobial therapy should include a carbapenem, alone or associated to rifampin or tobramycin.

Important to the management of Acinetobacter infections is determining the source imposing infection control policies, and implementing appropriate antimicrobial use guidelines.

 

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