Reversible neutrophil defect in patients with bacterial endocarditis.
The bactericidal capacities of neutrophilic polymorphonuclear neukocytes (PMN) from five untreated adults with bacterial endocarditis (BE), eight untreated patients with other forms of acute bacterial infection (ABI), and fourteen drug-free uniinfected normal subjects (NS) were compared with a new technique that uses five increasing bacteria-to-neutrophil ratios ranging from 1.25 to 100 Staphylococcus aureus per neutrophil. PMN from uninfected NS or untreated patients with ABI demonstrated a similar and reproducible ability to kill increasing numbers of S. aureus in 8 per cent normal serum. In contrast, the bactericidal activities of the PMN from untreated patients with BE were significantly depressed and the defect was more apparent at high ratios. Neutrophils from some of these individuals had decreased bactericidal action only at high ratios, indicating a quantitative type of neutrophil defect. There was no morphologic deficiency in the uptake of bacteria by BE neutrophils and comparable rates of glucose [-1-14C] oxidation were found in BE and control neutrophils stimulated with various ratios of heat-killed bacteria. Therefore, the observed abnormality appeared to be that of intracellular killing rather than of ingestion. The proportions of bacteria killed by the MN of untreated patients with BE improved after antibiotic treatment and became equal to those of NS or untreated ABI patients. This rapid return to normal bactericidal function by the PMN during treatment indicates that the prior deficiency was an acquired consequence of the infectious process of BE.
D000328:Adult; D000900:Anti-Bacterial Agents / Q000494:pharmacology; D001424:Bacterial Infections / Q000097:blood; D001681:Biological Assay; D001770:Blood Bactericidal Activity / Q000187:drug effects; D001786:Blood Glucose / Q000378:metabolism; D004697:Endocarditis, Bacterial / Q000097:blood* / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000378:metabolism* / Q000502:physiology; D010084:Oxidation-Reduction; D013211:Staphylococcus aureus / Q000378:metabolism
D000900:Anti-Bacterial Agents; D001786:Blood Glucose