We investigated the drug susceptibility pattern of Streptococcus pneumoniae and viridans streptococci from pediatric sinusitis that were obtained from October 1995 to June 1996. The results are summarized as follows;
1. The frequency of detection of penicillin (PC)-intermediate S. pneumoniae (PISP)+PC-resistant S. pneumoniae (PRSP) was 49.6% in the 188 strains obtained, and that of PISP was high. The MIC distribution of drug susceptibility of cefditoren for PISP+PRSP was the lowest.
2. The serovariants or serogroups of PSSP were widely distributed many serovariants, but those of PISP+PRSP were almost 19, 23 and 6 type.
3. The frequency of detection of macrolides (MLs)-resistance of both PSSP and PISP+PRSP was high. And that of MLs-constitutive-resistant strains of PSSP and that of MLs-induced resistant strains of PISP+PRSP were high.
4. The frequency of detection of multiple drug-resistant strains of Streptococcus oralis and Streptococcus mitis was high. The drug susceptibility patterns of those organisms were similar to that of S. pneumoniae.

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We determined the minimal inhibitory concentrations (MIC) of four aminoglycoside antibiotics including arbekacin (ABK), tobramycin (TOB), isepamicin (ISP) and amikacin (AMK) against 123 strains clinically isolated of Pseudomonas aeruginosa. The results are as follows.
(1) The MIC₅₀ of TOB, which was the lowest, was 3.13μg/ml. Next was, that of ABK, 6.25μg/ml. Those of ISP and ABK were 12.5μg/ml.
(2) In the determination of sensitivity percent using the breakpoint MIC, that of TOB, the highest, was 47.2%, while those of the other three aminoglycosides were almost equal (6.5-8.9%).
(3) On analysis of correlgram of MICs between ABK and the other three aminoglycosides, the strains for which the MIC ABK was ≥25μg/ml, showed high cross resistance.
These findings can be summarized as follows; the activity of ABK against P. aeruginosa is inferior to that of TOB, but equal to that of ISP and AMK.

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The in vitro inhibitory effect of purified camellia oil was tested with 14 Staphylococcus aureus strains isolated from patients with atopic dermatitis by the method previously reported. Purified camellia oil was demonstrated to have a potent inhibitory effect on the growth of 7 of 8 drug-sensitive strains and 2 of 6 drug-resistant strains with 45.7% to 93.9% inhibition. There was no inhibition of one sensitive strain and 2 drug-resistant strains. However, growth of these 2 drug-resistant strains was accelerated by addition of purified camellia oil. No significant relationship was observed between the inhibitory effect of purified camellia oil and coagulase type or phage type. These findings suggest that the inhibitory effect of purified camellia oil may explain the susceptibility of S. aureus to drugs. Further studies are required to establish whether these inhibitory effects play a role in vivo.

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We obtained Pseudomonas aeruginosa strain R 1 from P. aeruginosa PAO 1 grown on an agar plate containing ofloxacin (OFLX) and cefsulodin (CFS). The sensitivity P. aeruginosa R 1 was altered to become more resistant to chloramphenicol (CP), tetracycline (TC), quinolones and β-lactam antibiotics than P. aeruginosa PAO 1, the parent strain. We studied bactericidal activities when TC, CP, ceftadidime (CAZ), sulbactam/cefoperazone (SBT/CPZ) were combined with fosfomycin (FOM). The combination of FOM with CAZ, SBT/CPZ or β-lactam antibiotics, had a synergistic effect, but TC and CP which are also pumped-out by efflux proteins were not affected. More CPZ accumulated in the periplasm of P. aeruginosa R 1 treated with FOM than in the untreated bacteria. It was concluded that FOM synergistically potentiated the bactericidal activity of β-lactam antibiotics against Na1B type P. aeruginosa with the efflux proteins.

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