PEDIATRICS Vol. 102 No. 1 Supplement July 1998, pp. 210-213

COMMENTARY:
Pseudomonas aeruginosa Infection as a Complication of Therapy in Pancreatic Fibrosis (Mucoviscidosis), by Sterling D. Garrard, et al, Pediatrics, 1951;8:482

Received Mar 19, 1998; accepted Mar 19, 1998.

From the Department of Pediatrics, Children's Hospital Medical Center, Seattle, Washington.

This landmark article represents the first report of Pseudomonas aeruginosa as a significant clinical pathogen in patients with cystic fibrosis (CF). The authors summarize the case histories of four consecutive patients with CF admitted to a Chicago pediatric teaching hospital. In all four, P aeruginosa was the predominant organism cultured from tracheobronchial secretions. The histories were remarkably similar. The patients (two male, two female) were very young, ranging from 14 months to 5 years of age, and had previously been diagnosed with "pancreatic fibrosis" based on the absence of pancreatic digestive enzymes. The four patients had received pancreatic enzyme replacement (pancreatin) and prolonged antibiotics prophylaxis. The antibiotic regimens consisted of a variety of oral antibiotics, including sulfonamides, penicillin, aureomycin, and zephiran, as well as aerosol polymixin, prescribed as treatments for Staphylococcus aureus tracheobronchial infections.

The patients presented with acute respiratory distress and were diagnosed as having diffuse bronchopneumonia based on physical examination and chest radiography. Treatment consisted of intramuscular streptomycin (or terramycin) and penicillin. Repeated bronchial lavage was attempted to clear airway secretions. The two female patients did not respond to therapy and died within hours. The two males responded briefly, but subsequently died at 8 weeks and 1 year after initial culture of P aeruginosa. Similar postmortem findings in all patients included pancreatic fibrosis, suppurative bronchitis, multiple pulmonary abscesses, and bronchiectasis.

In their discussion, the authors emphasize several salient features of CF pulmonary disease. First, they raise the potential role of prolonged antimicrobial therapy in altering tracheobronchial flora. S aureus, the predominant pathogen in all initial descriptions of the illness, was being eliminated by antistaphylococcal antibiotic therapy. In its place, was emerging P aeruginosa. This phenomenon of shifting bacterial flora had been reported recently in other illnesses, but not in CF. Second, the authors address the importance of P aeruginosa as an emerging opportunistic infection in the tracheobronchial tree, noting rapid development of antibiotic resistance attributable to its ability to "develop genetic mutations" and alter its "morphologic appearance". Third and most important, the authors challenge the pediatric community to "critically examine" the clinical recommendation for prolonged antibiotic prophylaxis. Realizing the effectiveness of this regimen against S aureus, they suggested that physicians also weigh the risk of emergence of resistant strains of P aeruginosa. They recommended, "Effective antibiotics should be employed judiciously and changed when specifically indicated based upon cultures of tracheobronchial secretions. To minimize the appearance of resistant strains, combinations of two antibiotics having different mechanisms of action are desirable."

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