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Chlamydia pneumoniae is a common cause of respiratory infection. It has also been shown to be associated with coronary heart disease. Two proteins that have been reported to be recognized frequently during human infection are proteins having molecular masses of 43 and 53 kDa. In order to develop a useful alternative serological test to the microimmunofluorescence (micro-IF) assay, recombinant 43-kDa and 53-kDa chlamydia-specific proteins were evaluated in dot blot and/or for comparison to the standard micro-IF test. Primers for amplification were derived from genome sequence information for two C. pneumoniae genes (CPn0809 and CPn0980) encoding 53-kDa proteins and four C. pneumoniae genes (CPn0562, CPn0927, CPn0928, and Cpn0929) encoding 43-kDa proteins of unknown function, which were Chlamydia specific and not found in Chlamydia trachomatis . The 53-kDa protein product of CPn0809 or the N-terminal 18-kDa portion had better specificity than any of the 43-kDa recombinants but was much less sensitive than micro-IF. In contrast, the 53-kDa protein encoded by CPn0980 was recognized by 11 of 12 (92%) acute-phase sera, 35 of 46 (76%) chronic sera, 0 of 12 micro-IF-negative sera ( C. pneumoniae and C. trachomatis negative), and 1 of 12 (8%) C. pneumoniae negative, C. trachomatis positive sera. Thus, it appears that the 53-kDa protein encoded by CPn0980 has potential use for serodiagnosis of C. pneumoniae infection.

OBJECTIVE: To report a case of phenytoin toxicity successfully treated with multiple-dose activated charcoal. CASE SUMMARY: A 36-year-old man was first admitted with chronic phenytoin toxicity secondary to hepatitis and was treated symptomatically. His serum phenytoin concentration was 149.8 μmol/L on admission and decreased slowly over his 6-day hospitalization to 134.8 μmol/L. Upon readmission approximately 24 hours later, his phenytoin concentration was 186.7 μmol/L. Because of acute phenytoin toxicity, he was treated with multiple-dose activated charcoal. His phenytoin concentration after four doses of activated charcoal returned to the therapeutic range within 36 hours and his symptoms abated quickly, thus decreasing his hospital stay. DISCUSSION: The exact mechanism of action of multiple-dose activated charcoal to decrease serum phenytoin concentrations is unknown. Several mechanisms of action have been reported in the literature and are discussed. CONCLUSIONS: Multiple-dose activated charcoal was used successfully in treating acute phenytoin toxicity in our patient. Based on his previous admission for chronic phenytoin toxicity, his hospital stay was reduced by three days. The use of multiple-dose activated charcoal in acute phenytoin toxicity has potential therapeutic and financial implications.