SUMMARYThe concentrations of mannan-binding protein (MBP) in consecutive samples from 10 HIV* persons were estimated using an ELISA based on polyclonal rahbit anti-MBP. The changes in MBP with time were similar in HIV^ and HIV" persons, and did not appear to be of clinical significance. MBP was determined in a further 70 persons found HIV-1 ^ during a period af 25 years (1984)(1985)(1986). Out of the total of 80 patients, 32 have by now died from AIDS. According to the serum level of MBP the HIV-infected persons were grouped into high (>65Qng MBP/ml). intermediate (101-650 ng/ml), and low MBP (< 101 ng/ml). At the termination of the study the frequency of deaths/total in each of the groups were: high MBP, 14/39 (36%); intermediate MBP. 12/26 (46%); and low MBP, 6/14 (43%). There was no association between the MBP level of the individual and the progressive loss of CD4* T cells, and the level of MBP was not predictive for the length of time between the detection of HIV antibodies and development of AIDS, nor for the duration of AIDS before death occurred. The number of HIV ' persons without detectable MBP (10%) was significantly higher than previously reported for healthy persons (2 4%, P = 0 027). The course of HIV infection does not seem to be influenced by the level of MBP. nor does the antimicrobial activity of MBP appear to affect the progression of AIDS. Further studies are required to substantiate the significance of absenee of MBP in the susceptibility to HIV.

The effect of ciprofloxacin, lomefloxacin, fleroxacin and ofloxacin on the intracellular killing of Staphylococcus aureus in human neutrophil granulocytes was studied. Each drug was tested in concentrations of 0.25, 1, 4, 16 and 64 times the MIC and the intracellular killing was measured for up to 5 h of incubation. All four quinolones increased the intracellular killing in a concentration- and time-dependent manner. When compared at concentrations of 4 x MIC, ofloxacin increased the killing significantly more than the other quinolones. All four quinolones increased the killing significantly more than the beta-lactam dicloxacillin. All five antibiotics increased the killing significantly relative to the control without antibiotics. None of the antibiotics affected the viability of the granulocytes or their ability to generate superoxide anion. In conclusion, the quinolones increased the intracellular killing of S. aureus in neutrophil granulocytes.

The effect of dicloxacillin and fusidic acid used alone and in combination on the extracellular and intracellular killing of four isolates of Staphylococcus aureus in the presence of serum was studied. At the extracellular level, dicloxacillin (8 mg/L) had a bactericidal effect on all four isolates, whereas fusidic acid (64 mg/L) had a bacteriostatic effect on two isolates and no effect on the two other isolates. Fusidic acid significantly inhibited the extracellular bactericidal effect of dicloxacillin on two isolates. Intracellular killing was measured in human neutrophil granulocytes. Dicloxacillin (8 mg/L) significantly increased the intracellular killing of all four isolates, while fusidic acid (64 mg/L) significantly increased the intracellular killing of three isolates, but the killing was significantly lower than that of dicloxacillin. When the antibiotics were combined the intracellular killing of three of the isolates was significantly lower than that of dicloxacillin alone. The viability of the granulocytes and their ability to produce superoxide anion were not affected by the antibiotics. In conclusion, we found that the increased intracellular killing of S. aureus by dicloxacillin was inhibited by fusidic acid.