Pulmonary damage by Vibrio vulnificus cytolysin

In the July 1996 issue of Infection and Immunity, Park et al. reported pulmonary changes which appear to be caused by Vibrio vulnificus cytolysin (3). According to these investigators, severe edema and neutrophilic infiltration of perivascular tissue were observed in the lungs of mice after intravenous administration of 8 hemolytic units of the cytolysin (3). To the best of my knowledge however, it is not yet certain whether the pathological changes observed in mice also occur in humans during illness caused by the bacterium. Although the presence of pulmonary infiltrates in the chest radiographs of patients with V. vulnificus septicemia has previously been reported, pathological findings in the lungs were not described in these cases (2). A review of the literature has shown the presence of pulmonary edema and/or intraalveolar hemorrhage in patients with V. vulnificus infections (1, 4, 5). No perivascular edema and/or neutrophilic infiltration, however, was documented in such cases. Pulmonary edema is a pathological process different from perivascular edema in that proteinaceous fluid accumulates in alveolar spaces and not in perivascular tissue. Although the exact cause of the difference in pulmonary pathologies of V. vulnificus infection between humans and animals remains unknown, one possibility is that the aforementioned difference represents different stages of the same process. Another possibility is that the difference in the dose of the toxin in animal experiments and human diseases is the cause of the aforementioned difference in pulmonary pathologies. Alternatively, either certain factors other than cytolysin may play a crucial role in the pathogenesis of pulmonary lesions in human illness or the reactions of humans to the cytolysin are different from those of mice. I would like to know whether Dr. Park et al. know of any human cases that show changes similar to those observed in their experiments and whether they could observe any intraalveolar hemorrhage and/or edema in the lung tissues of the mice during their experimental studies. Since the pathophysiology of V. vulnificus infection still remains enigmatic, the opinion of Dr. Park et al. on this issue would be greatly appreciated.