In contrast to the cessation of splanchnic trapping noted 20 to 40 minutes following the injection of staphylococci, splanchnic trapping of E. coli continued unchanged for 3 to 5 hours unless the splanchnic tissues were dearly reseeding the blood stream. This resulted in the continued disappearance of E. coli over a 60 to 90 minute period, and differed from the constant bacteriemia maintained beyond 20 minutes after the injection of staphylococci.

Some of the differences in the initial clearance of these two microorganisms appeared to relate to differences in host leukocyte-bacterium relationships. In vitro studies indicated that E. coli were rapidly killed following ingestion by rabbit polymorphonuclear leukocytes. Staphylococci survive such ingestion. The injection of E. coli was followed by a prolonged granulocytopenia with evidence of sequestration of granulocytes within the pulmonary vascular bed. The injection of staphylococci was followed by a transient leukopenia, with rapid return of granulocytes to the circulation (15).

It appears probable that E. coli ingested by sequestered leukocytes are destroyed within the cell, and that leukocytes do not reenter the circulation containing living E. coli. Such intraleukocytic residence in the blood stream has been shown to be of possible importance in the maintenance of staphylococcal bacteriemia (14).

An increasing E. coli bacteriemia occurred rapidly after the initial clearance period, indicating that many sequestered bacilli remained viable. Increasing bacteriemia also occurs 3 to 5 hours after the injection of staphylococci. The bacterial or host cell mechanisms which allow this secondary resurgence of bacterial populations are currently under investigation.