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Hematoporphyrin derivative (Hpd) localizes selectively in malignant and rapidly metabolizing tissues and undergoes a cytotoxic reaction when exposed to light of a specific wavelength. Hpd has been studied extensively with regard to the diagnosis and treatment of tumors but not with regard to bactericidal activity. This investigation assessed the effect of light-activated Hpd on various microorganisms, on human polymorphonuclear leukocytes, and on the interactions of polymorphonuclear leukocytes and bacteria. Light-activated Hpd was 99.9% bactericidal against Staphylococcus aureus, Streptococcus faecalis, Bacteroides fragilis, Streptococcus M-G intermedius, Streptococcus mutans, Peptostreptococcus anaerobius, Peptococcus magnus, and Clostridium perfringens, but did not affect Escherichia coli, Pseudomonas aeruginosa, or Candida albicans. Photoactivation of Hpd rendered 98% of polymorphonuclear leukocytes inviable. Combinations of light-activated Hpd and polymorphonuclear leukocytes had a 4-log (99.99%) bactericidal effect on both intra- and extracellular S. aureus. The ability of Hpd to localize in inflammatory tissues may have therapeutic applications in the treatment of abscesses.

The diagnosis of severe progressive cutaneous protothecosis in a 34-year-old woman was made by skin biopsy and culture. Analysis of host defense mechanisms revealed a persistent defect in the ability of the patient's PMN to kill the infecting organism. Specific IgG and IgE antibody was demonstrated. Serum levels of complement and immunoglobulins were normal or elevated. The patient was not anergic and peripheral blood lymphocytes responded to nonspecific mitogens. Treatment with amphotericin B and tetracycline resulted in resolution of skin lesions and negative cultures.

Administration of corticosteroids, aspirin, or indomethacin induces marked inhibition of adherence of polymorphonuclear leukocytes (PMNLs) in vitro. The effects of three newer nonsteroidal anti-inflammatory agents on PMNL adherence were defined. Adherence of PMNLs after passage through a nylon-wool column was measured in normal volunteers who had ingested a single tablet of 300 mg of ibuprofen, 300 mg of fenoprofen, or 200 mg of sulindac. Adherence was significantly decreased from baseline at 4 hr after ibuprofen or fenoprofen was taken, remained suppressed at 24 hr, and returned to normal at 48 hr. Sulindac mildly inhibited PMNL adherence 48 hr after drug ingestion. Inhibition of adherence with ibuprofen and fenoprofen also occurred after incubation of control PMNLs with plasma specimens from volunteers 4 and 24 hr after drug administration, a result suggesting a partially plasma-mediated factor. Zymosan-induced augmented adherence was also inhibited by pretreatment in vitro with ibuprofen at a concentration of 25 micrograms/ml and fenoprofen at 50 micrograms/ml.

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