Robert G. Horn

Two hundred episodes of fungemia that occurred at Memorial Sloan-Kettering Cancer Center between January 1, 1978, and June 30, 1982, are reviewed and compared with those seen from 1974 through 1977. The total number of episodes of fungemia per year increased by 30.6%, episodes per 100 new lymphoma and solid tumor patients increased by 73% and 95%, respectively, and episodes per 100 new leukemia patients decreased by 50%. Fungemia also occurred earlier during hospitalization, and embolic skin lesions were a common early sign of Candida tropicalis fungemia. Mortality was not significantly different with and without amphotericin B therapy in fungemic patients with leukemia, lymphoma, or aplastic anemia (51 of 70 vs. 21 of 24) or solid tumors (29 of 36 vs. 29 of 43); however, some patients appeared to benefit from combination therapy with amphotericin B and flucytosine. The prevalence of disseminated candidiasis at autopsy was the same in treated (11 of 15) and untreated (8 of 11) patients with leukemia, lymphoma, and aplastic anemia, but it was significantly lower in treated (none of 8) than in untreated (5 of 11) patients with solid tumors.

Abstract Highly purified lymphocytes were obtained from the lymph nodes of CFA-immune guinea pigs. Cultures of these lymphocytes did not exhibit proliferative responses upon stimulation with purified protein derivative (PPD), although they were quite responsive to stimulation with phytohemagglutinin. Addition of macrophages to these cultures resulted in marked enhancement of the PPD-induced lymphoproliferative response, but did not affect lymphocyte responsiveness to phytohemagglutinin. The ability of the purified immune lymphocytes to interact directly with soluble PPD was examined by incubating the cells for 1 hr at 37°C with various concentrations of PPD. The lymphocytes were then washed to remove unbound antigen and placed in culture. Addition of macrophages to cultures of antigen-pulsed lymphocytes did not result in the significant DNA synthesis, suggesting that the specifically immune lymphocytes were unable to bind and carry into culture sufficient antigen to allow for their subsequent activation. These results were not due to the induction of tolerance in the lymphocytes, since cultures of antigen-pulsed and untreated lymphocytes were equally responsive to continuous PPD when macrophages were added to the cultures, even when the antigen-pulsed lymphocytes had been exposed to high concentrations of PPD for 1 or 24 hr. In contrast, macrophages which were incubated for 1 hr at 37°C with a given concentration of PPD were as effective as the same concentration of PPD present continuously in macrophage-lymphocyte cultures in the induction of a lymphoproliferative response. Macrophages appear to play an obligatory role in the presentation of antigen to the immunospecific thymus-derived (T)-lymphocyte.

Neisseria gonorrhoeae are transported across the mucosa of human fallopian tubes in organ culture by mucosal cells. The steps in this process are (1) attachment of gonococci to microvilli of nonciliated cells, (2) phagocytosis of gonococci by these cells, (3) transport of phagocytic vacuoles containing gonococci to the base of the cell, and (4) exocytosis of gonococci with phagocytic vacuoles into the subepithelial tissues. In vivo gonococci in the subepithelial tissues may cause extensive local disease (e.g., salpingitis) or invade blood vessels to cause disseminated disease. Preliminary studies of human nasopharyngeal tissue in organ culture infected with Neisseria meningitidis indicate that meningococci attach to microvilli of nonciliated cells and are phagocytized by these cells. They subsequently appear in subepithelial tissues, but the route they take is not yet certain. These observations suggest that the mechanisms of attachment to and penetration of fallopian tube and nasopharyngeal mucosa by N. gonorrhoeae and N. meningitidis are similar or possibly identical.