J Antimicrob Chemother 1999; 41(Suppl. A): 170.
Department of Bacteriology, Faculty of Medicine Juntendo University, 2-1-1 Hongo, Bunkyo-ku, 113-8421, Tokyo, Japan. longzhu@med.juntendo.ac.jp
We have experienced a fatal case of postoperative toxic shock syndrome (TSS) caused by a highly virulent methicillin-resistant Staphylococcus aureus (MRSA) strain, designated Sak-1, which was characteristic in its increased production of toxic shock syndrome toxin 1 (TSST-1) in human whole blood (about 30-fold greater amount as produced in Todd Hewitt broth). This augmenting effect of human blood on TSST-1 production was also observed with horse blood, but not with sheep blood. Fresh human serum was also effective but sera of commercially available mammalian species tested were not as effective. Sak-1 also produced high amount of TSST-1 in the circulating blood of mice experimentally infected with the strain. To investigate the overall prevalence of such strains among Japanese MRSA clinical isolates, TSST-1 as well as enterotoxin production was assayed with 541 clinical Staphylococcus aureus (S. aureus) strains isolated all over Japan between 1981~2 and 1992~6. Among the isolates in 1981~2, only 5.06% of MRSA produced TSST-1. In contrast, 79.66% of MRSA strains produced TSST-1, and most of them(77.3%) co-produced enterotoxin C as Sak-1 did. The effect of blood on the production of TSST-1 was tested with each of 157 TSST-1 producing MRSA strains. When cultured in blood, 29.65% of the strains (including Sak-1) produced an increased amount of TSST-1 (Type I), while the 70.35% produced less amount of TSST-1 (Type II) as compared in Todd Hewitt broth. The mechanism underlying the blood-induction of TSST-1 and its correlation with severity of TSS still remain unclear at this moment. For the treatment of such a fulminante MRSA infection case some supportive therapy such as g-glubulin infusion with a high toxin-neutralizing activity may be useful. This possibility is now under investigation in our laboratory.