Defenses against candida infections

Abstract

We have been particularly interested in matching underlying disease to type of superinfection. It has been stated that leukopenia is associated with Candida superinfection; however, this author does not believe there is evidence that people who have disease induced neutropenia acquire systemic candidiasis. Those acquiring candidiasis generally have had a variety of treatments and neutropenia may be one of the resulting effects; but I know of no epidemiologic data showing that untreated people with any disease which is associated with profound neutropenia have an increased incidence of disseminated infection from Candida or from species of Aspergillus or Mucor. The only two infections that are known to occur with increased frequency in untreated Hodgkin’s disease are tuberculosis and cryptococcosis. For these infections, the evidence seems reasonably good, but the data are less secure for listeriosis, toxoplasmosis, salmonellosis and nocardiosis, since these infections have all been described primarily after the patients with Hodgkin’s disease were under anti tumor therapy. We talk about the susceptibility of patients with, for example, Hodgkin’s disease to acquire superinfections; but often it is not the underlying disease, but their disease, plus what we’ve done to them that makes them susceptible to certain superinfections. Dr. Donald Armstrong (an earlier author in this series) and I examined his experience at Memorial Hospital in New York City; we found that ‘about one half the people acquiring listeria infections in that hospital had low lymphocyte counts before they developed listeriosis.’ This is of interest since Tripathy and Mackanessz6”’ indicate that if the host wishes to handle listeria most effectively a committed lymphocyte and a macrophage that understands the information that it gets from the lymphocytes are necessary. Consequently, the half of the patients at Memorial Hospital who lack the normal number of lymphocytes may have had increased susceptibility to listeriosis because of this. In addition, the patients at Memorial Hospital generally manifested immunoglobulin G deficiency. A study by Njoku-obi and Osebold” indicates that optimal host defense against listeric infections requires not only committed lymphocytes and informed macrophages but also circulating immunoglobulins; in some way that is not clear, these immunoglobulins help in phagocytosis and also in intracellular destruction of the opsonized organisms. Here again, susceptibility to the listeric infection appears to be predicated upon underlying lymphocytic malignancy plus host modification by therapy. In the leukemic patient, the organisms causing most of the trouble among the fungi are species of Candida. Why are such patients inordinately susceptible to these particular yeasts? The data suggest that antibiotics, steroids, anti leukemia agents, neutropenia and direct access for the organism to the blood stream all act in concert to promote Candida. In this regard, the evidence is beginning to accumulate that the scalp vein needle is less dangerous than the intravenous catheter by about ten-fold in terms of the proclivity for superinfections.’ A prospective study by Curry and Quie’ on the use of hyperalimentation by intravenous catheter showed that 27% of individuals so treated developed bacteremia or fungemia,