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PubMed1975

Cryptococcus neoformans as a cause of lytic bone lesions.

Cryptococcosis is a disseminated infection of man and animals that involves many organs, especially the central nervous system. Isolated bone involvement may cause lytic bone lesions. Diagnosis may be made by pathologic sections and culture of specimens obtained through surgical biopsy. When Cryptococcus is recovered from bone, care must be taken to study other organ systems, especially the central nervous system. Isolated bone disease without meningitis is very uncommom. Intense medical therapy is necessary for treatment of meningitis; isolated osteomyelitis may respond to surgical drainage alone.

Adult↗
PubMed1975

[Contributions to the strain-specific virulence of Cryptococcus neoformans. Animal experiments with two C. neoformans-strains isolated from bird manure. Preliminary report (author's transl)].

The results briefly presented here highlight some of the observations met with during the course of a study aimed at finding out differential pathogenic behavior of the two strains of Cryptococcus neoformans i.e. W71/A117 and W2/A94 with special reference to cryptococcoma formation. Both strains were isolated from bird excreta but differed in their gross and microscopic morphology. Groups of male albino mice NMRI were separately inoculated, intramuscularly, with a comparable dose of the two strains. All the 50 animals challenged with W71/A117 developed macroscopically distinct cryptococcoma of variable size, and fatally progressive disease, involving most of the internal organs, namely, brain, heart, lung, liver, spleen and kidneys. On the contrary, only 34 of the 50 mice infected with the strain W2/A94 showed cryptococcoma formation at the site of inoculation, which were comparatively much smaller in size and gradually diminished. None of the animals, observed over a period of 93 days, died, and showed any sign of metastasis. In another series of experiment, only one instance of mortality was observed in a group of 80 mice inoculated intraperitoneally with about 2 X 10(7) viable cells of this strain. However, the fungus could be recovered, in a majority of cases, only from the brain of animals sacrificed after one month, though most of them showed no sign of sickness. The number of mice yielding positive cultures gradually decreased, and after 87 days the fungus could not be isolated from any organ. The high morbidity and mortality in mice caused by strains W71/A117 was significantly lowered when the animals were infected intramuscularly 3 months ago with the strain W2/A94. After an observation period of 61 days, 91% of the double infected animals were still alive in comparison to 23% survival among the animals challenged with the strain W71/A117 only.

Animals↗
PubMed1992

Cryptococcus albidus isolated from pigeon excreta in Taiwan.

Cryptococcus albidus (Saito) Skinner, found frequently in the air of El-Minia, Egypt; in New Zealand and Budapest, and isolated occasionally from clinical specimens, has now been recognized as the cause of human diseases. Since isolation of this fungus from pigeon droppings has not previously been reported, this first paper reports results of its drug-susceptibility testing to gentamicin and 5-fluorocytosine, as well as its fungal cell antigenic cross reactivity with C. neoformans as detected by a Latex-Crypto-Antigen Detection System (LCAS).

Animals↗
PubMed1990

Depletion of CD4+ (L3T4+) lymphocytes in vivo impairs murine host defense to Cryptococcus neoformans.

T cell-mediated immunity has been shown to play an important role in the host defense to Cryptococcus neoformans. Infections due to C. neoformans are increased in patients with AIDS who are deficient in the CD4+ subset of T lymphocytes. Thus, the effect of CD4+ (L3T4+) lymphocyte depletion on murine host defenses to C. neoformans was studied. The mAb GK 1.5 was administered to mice, and CD4+ T lymphocyte depletion was confirmed by the analysis of T cell subsets in blood, spleen, lymph node, and lung. Evidence of a functional defect was confirmed by demonstrating that the splenocytes of treated mice were unable to proliferate in response to class II incompatible spleen cells. Furthermore, delayed type hypersensitivity to C. neoformans was abrogated by CD4+ lymphocyte depletion. Mice depleted of CD4+ lymphocytes were inoculated with a virulent strain of C. neoformans by the i.v. or the intratracheal route. After i.v. inoculation of C. neoformans, the survival of mice depleted of CD4+ lymphocytes was reduced (27.8 +/- 1.8 vs 36.0 +/- 3.1 days, p less than 0.04). After intratracheal inoculation, C. neoformans disseminated from the lung to extrapulmonary organs. Dissemination occurred earlier in mice depleted of CD4+ lymphocytes compared to mice that received control antibody, and the burden of C. neoformans in extrapulmonary organs was greater in mice depleted of CD4+ lymphocytes than control mice. Surprisingly, there was no increase in the burden of C. neoformans in the lungs of CD4+ lymphocyte-depleted mice. Survival of mice inoculated with C. neoformans and depleted of CD4+ lymphocytes was reduced compared to control mice and was related to the increased rate of accumulation of organisms in the brains of treated mice. The mean survival of GK 1.5-treated mice was 34.1 +/- 0.9 days compared to control mice with a mean survival of 40.6 +/- 9 days (p less than 0.001). These data suggest that CD4+ lymphocytes play a prominent role in the host defense of infections due to C. neoformans, that CD4+ lymphocytes are required in extrapulmonary organs for optimal clearance of C. neoformans and that CD4+ lymphocytes are critical for survival of mice infected with C. neoformans.

Animals↗
PubMed1988

Induction of antigen-specific suppression by circulating Cryptococcus neoformans antigen.

Immunoaffinity chromatography of sera from mice infected with Cryptococcus neoformans (Inf-MS) on a column with rabbit anti-cryptococcal antibody as the ligand resulted in the adsorption of the component(s) that induce suppression of the cryptococcal delayed-type hypersensitivity (DTH) response. In contrast, immunoaffinity chromatography of Inf-MS on columns coupled with cryptococcal antigen or goat anti-mouse IgM, IgG, and IgA did not adsorb the suppressive component(s). Quantification of cryptococcal antigen and anti-cryptococcal antibody in Inf-MS and column fractions established a direct correlation between cryptococcal antigen levels and suppressive activity; no correlation was observed between anti-cryptococcal antibody levels and suppressive activity. The suppression induced by Inf-MS was shown to be specific in that suppressive sera did not affect the induction of DTH responses to Listeria monocytogenes or dinitrofluorobenzene. These collective results provide evidence that cryptococcal antigen is the component in Inf-MS that induces antigen-specific suppression of the cell-mediated immune response to C. neoformans.

Animals↗
PubMed1989

Fungicidal activity of IFN-gamma-activated macrophages. Extracellular killing of Cryptococcus neoformans.

Cryptococcus neoformans is an encapsulated yeast-form fungus which causes pulmonary and meningeal infections preferentially in the immunocompromised host. It is thought that cell-mediated immunity is important for acquired resistance against cryptococcosis with activated macrophages as the final effector cells. However, specific polysaccharides in the capsule of C. neoformans protect the fungus from adherence to phagocytes and from subsequent phagocytosis. We have studied extracellular killing of C. neoformans by IFN-gamma-activated macrophages and their products. Murine bone marrow-derived macrophages stimulated with rIFN-gamma for 24 h were able to effectively suppress the growth of C. neoformans and the effect of IFN-gamma was augmented by LPS. Killing of C. neoformans was also achieved by cell-free supernatants from bone marrow-derived macrophages stimulated with IFN-gamma plus LPS. Our results indicate that killing of C. neoformans by activated macrophages is independent from toxic oxygen radicals and mediated by secreted protein(s) of apparent molecular mass of 15 and 30 kDa. These findings indicate that activated macrophages play a major role in host defense, although the fungus resists phagocytosis and remains in the extracellular milieu.

Animals↗
PubMed1989

Paradoxical role of capsule in murine bronchoalveolar macrophage-mediated killing of Cryptococcus neoformans.

Infections with the encapsulated fungus Cryptococcus neoformans are usually acquired via inhalation, and the presence of a capsule has been identified as a virulence factor. Therefore, we studied murine bronchoalveolar macrophage (BAM)-mediated killing and phagocytosis of encapsulated and acapsular strains of C. neoformans. After 2 h, BAM killed encapsulated strains CN52 and MP415 more readily than acapsular strains CN602 and CAP67 (54.9 and 36.2% vs 26.1 and 6.7%, respectively, p less than 0.001). Pre-incubating CN602 with purified capsular polysaccharide increased killing to 42.7% (p = 0.04). Significantly greater killing of the encapsulated strains also occurred in vivo. BAM-mediated killing of CN52 appeared to proceed by non-oxidative mechanisms, as BAM released minimal amounts of H2O2 after stimulation with CN52, and killing was not reduced by inhibitors or scavengers of the respiratory burst. The association between encapsulation and susceptibility to BAM fungicidal effects was not attributable to differences in yeast ingestion. Using the same low ratio of organisms to BAM as in the killing assay, greater than 95% of both CN52 and CN602 were phagocytosed. However, BAM phagocytosed significantly greater numbers of acapsular CN602 when incubated with a higher inoculum. Phagocytosis and killing of CN52 and CN602 required fresh serum as a source of C. Phagocytosis of CN52, but not CN602, was profoundly inhibited if BAM were plated on surfaces coated with mAb against the C3bR (CR1). mAb against the iC3b receptor (CR3) did not affect phagocytosis of either strain. These data demonstrate the innate ability of BAM to preferentially kill, by apparently non-oxidative mechanisms, an encapsulated as opposed to acapsular organism. Inasmuch as different receptors appear involved in phagocytosis of encapsulated versus acapsular C. neoformans, the disparity in killing may result from the greater ability of receptors mediating uptake of encapsulated organisms to trigger the antimicrobial armamentarium of the BAM.

Administration, Intranasal↗
PubMed1989

Phagocytosis of Cryptococcus neoformans by rat alveolar macrophages.

A radiolabeling method was developed to investigate the interaction in vitro between Cryptococcus neoformans and Lewis rat alveolar macrophages (AM phi). AM phi were harvested by lung lavage, monolayers of adherent cells were established in wells of microtiter plates and [51Cr]-labeled yeast cells were added to the monolayers. After removal of extracellular yeasts, the adherent radioactivity associated with the AM phi was directly proportional both to the number of yeasts added and to the number of yeasts per AM phi as determined by microscopic examination of Giemsa-stained monolayers. Phagocytosis (attachment and/or ingestion) of radiolabeled C. neoformans by AM phi was a sensitive, quantitative and reproducible assay for the evaluation of the AM phi-C. neoformans interaction. AM phi were able to phagocytose encapsulated strains of C. neoformans. The extent of phagocytosis was inversely related to the capsule size. Normal rat serum (NRS) was an excellent source of opsonins for the ingestion. Inactivation of serum complement or depletion of C3 by affinity chromatography removed most of the opsonic activity of NRS. Specific antibodies against C. neoformans did not increase phagocytosis.

Agglutination Tests↗
PubMed1989

Killing of Cryptococcus neoformans by rat alveolar macrophages.

The addition of [51Cr]-labeled yeast cells of Cryptococcus neoformans to monolayers of Lewis rat alveolar macrophages (AM phi) provided a sensitive and reproducible in vitro assay of phagocytosis. AM phi and yeast cells were incubated in 10% (v:v) normal rat serum for 1 h, non-AM phi associated yeast cells were removed and the AM phi-associated radioactivity (phagocytosis) determined. Replicate wells were replenished with fresh medium and reincubated. At different times, yeast-AM phi monolayers were treated with a non-cryptococcocidal mixture of DNAse and sodium deoxycholate to release the yeast cells from the AM phi. The fate of the yeast cells was critically evaluated by [51Cr]-release and viable plate counts. Killing was detected by plate counts within an hour following phagocytosis and did not increase significantly during the next 5 h. Strains of C. neoformans with small, medium, or large capsules varied in their susceptibility to killing from 10% to 95% but susceptibility to killing was not directly related to capsule size and the extent of phagocytosis. Release of 51Cr did not correlate with viability as determined by culture. The 51Cr was associated with two pools in the yeast cells; one, representing 15-20% of the radiolabel, was easily released and was probably bound to low molecular weight compounds in the cytoplasm. The majority of label was tightly bound to the particulate alkali-soluble cell wall fraction.

Animals↗
PubMed1989

5-Fluorocytosine resistance in clinical isolates of Cryptococcus neoformans.

Thirty six clinical isolates of Cryptococcus neoformans were tested for their susceptibility to 5-fluorocytosine and amphotericin B by the determination of minimum inhibitory concentrations and minimum fungicidal concentrations. 22.2% of the isolates were resistant to 5-fluorocytosine and 36.1% indicated 5-fluorocytosine tolerance. All strains were sensitive to amphotericin B.

Amphotericin B↗
PubMed1988

Enhanced binding of capsular polysaccharides of Cryptococcus neoformans to polystyrene microtitration plates for enzyme-linked immunosorbent assay.

A sensitive enzyme-linked immunosorbent assay (ELISA) to measure antibodies against capsular polysaccharide was developed, based on the enhanced binding of polysaccharide to polystyrene microtitration plates. The wells of the microtitration plate were primed with an adipic acid dihydrazide derivative of bovine serum albumin (AH-BSA) (100 micrograms/mL, 0.01 M NaPO4-0.14 M NaCl, pH 7.2 (PBS]. Capsular polysaccharide, the glucuronoxylomannan of Cryptococcus neoformans serotype A, was oxidized with NaIO4 for 5 min; the reaction was then quenched with ethylene glycol. The partially oxidized polysaccharide was dialyzed vs. PBS, and its concentration was adjusted to 50 micrograms/mL with PBS. This solution (100 microL/well) was covalently bound to the AH-BSA primed microtitration plates through formation of a Schiff base between the hydrazide group on the AH-BSA and the aldehyde groups on the polysaccharide. Antimouse IgG-alkaline phosphatase conjugate was used in an indirect ELISA to measure captured murine monoclonal antibodies directed against glucuronoxylomannan. Mean absorbances, after 15 min, were 0.13 in negative control wells, and greater than 0.7 in test wells. No intermediate steps were required to block nonspecific binding of antibody.

Antibodies↗
PubMed1988

In vitro susceptibility of Cryptococcus neoformans isolates from patients with acquired immunodeficiency syndrome.

Cryptococcus neoformans strains from 26 individual patients with acquired immunodeficiency syndrome (AIDS) and three isolates from patients without AIDS were tested for their susceptibility to amphotericin B, flucytosine, ketoconazole, and miconazole nitrate. Ninety percent of the C neoformans isolates from patients with AIDS were inhibited by drug concentrations within achievable serum levels. The minimum fungicidal concentration of the four tested antifungal agents, however, exceeded obtainable cerebrospinal fluid levels.

Acquired Immunodeficiency Syndrome↗
PubMed1988

C1q enhances the phagocytosis of Cryptococcus neoformans blastospores by human monocytes.

We investigated whether C1q, a subunit of the first component of C, could modulate human peripheral blood monocyte-mediated phagocytosis of Cryptococcus neoformans (CN). Adherence of monocytes to C1q-coated surfaces induced a significant enhancement of ingestion of CN blastospores that had been opsonized with specific anticapsular IgG (IgG-CN). Additionally, C1q enhanced the monocyte-mediated phagocytosis of CN opsonized with C (CN-absorbed, nonimmune, normal human serum; C-CN). Ingestion of IgG- and C-CN by control and C1q-stimulated monocytes was maximal by 1 h of incubation. The monocyte-mediated enhancement of phagocytosis caused by C1q was paralleled by a proportionate increase in fungicidal activity, an effect which was maximal by 3 h of incubation. Human serum albumin-adherent, control monocytes exhibited only a low level of killing after 3 h of incubation. C1q enhancement was blocked by preincubation of the surfaces with a goat, polyclonal F(ab')2 anti-C1q. This study describes a new cellular function for the cell surface C1q receptor: the enhancement of phagocytosis of a pathogenic organism by monocytes.

Adjuvants, Immunologic↗
PubMed1987

Ultrastructure of the mitotic apparatus in Cryptococcus neoformans.

Mitosis in Cryptococcus neoformans was examined by electron microscopy. Observation of serial sections showed that the separation of chromosomes occurred in the karyokinetic nucleus in the bud, that the microtubule organizing center (MTOC) was composed of two globular elements and a bridged middle piece, and that the nuclear envelope of the karyokinetic nucleus was partially destroyed during mitosis. These findings are similar to those reported in the heterobasidiomycetous yeasts. In addition, some of the prophase cells showed extension of the karyokinetic nucleus into the bud unaccompanied by the MTOC and swelling of the middle piece of the MTOC.

Anaphase↗
PubMed1987

Extracellular iron chelation in Cryptococcus neoformans.

Low-iron minimal medium supported growth of Cryptococcus neoformans but spent medium contained no hydroxamates, organic acids or other iron chelators. Exogenous deferoxamine stimulated growth in extreme iron-limitation, while neither organic acids nor quartersaturated transferrins were stimulatory. These results suggest two iron uptake mechanisms, one dependent upon exogenous hydroxamate, the other hydroxamate-independent.

Cryptococcus↗
PubMed1986

Thermal death potentiation by amphotericin B in Cryptococcus neoformans and its dependence on pre-incubation temperature.

Thermal death of Cryptococcus neoformans in the presence of amphotericin B was strongly dependent upon the temperature of pre-incubation. The entropy coefficient, that is, the increase in entropy of activation of thermal death per square unit concentration of the drug in the medium, was 35 times higher after pre-incubation at 25 degrees C than at 39 degrees C. This means that C. neoformans cells grown at lower temperatures were much more sensitive to the temperature-dependent fungicidal effect of amphotericin B.

Amphotericin B↗
PubMed1986

Natural cellular resistance of beige mice against Cryptococcus neoformans.

Previous reports have demonstrated that natural killer (NK) cells are capable of inhibiting the growth of Cryptococcus neoformans in vitro, and recent studies indicate that adoptively transferred NK cell-enriched spleen cell populations enhance clearance of cryptococci from the tissues of cyclophosphamide-pretreated recipients. The primary objective of these studies was to confirm that NK cells participate in early clearance of C. neoformans in vivo. Secondarily, the anti-cryptococcal activities of polymorphonuclear leukocytes and macrophages were examined. Seven-week-old C57BL/6 bg/+ mice, which have normal levels of NK cell activity, were compared with their bg/bg littermates, which have impaired NK cell function. One and 3 days after injecting both groups of mice i.v. with 2 X 10(4) cryptococci, we assessed the NK cell activities in spleens, lungs, and livers and clearance of the organism from corresponding tissues as determined by the mean log10 numbers of cryptococcal colony-forming units (CFU) per organ. Three days postinfection, the mean numbers of cryptococcal CFU in lungs and spleens of bg/+ mice were significantly lower than in the corresponding organs of bg/bg mice. NK cell activities in spleens and lungs of bg/+ mice were significantly higher than were the NK cell activities in similar cell populations from bg/bg mice. In contrast, the mean numbers of cryptococcal CFU in livers of the two groups of animals were nearly equivalent, a situation not unexpected, since liver NK cell activities were extremely low and similar in both groups of animals. Although these data indicated a correlation between early clearance of cryptococci from tissues and levels of NK cell activities in the corresponding tissues, it was also possible that differences in phagocytic cell function between the bg/+ and bg/bg animals could account for the observed differences in clearance of cryptococci from the tissues. Therefore, phagocytic cells from the two groups of animals were compared with respect to their abilities to phagocytize and inhibit the growth of cryptococci and to their abilities to respond to chemotactic stimuli in vivo. Peritoneal PMNL from bg/+ and bg/bg mice were similar in their abilities to phagocytize and inhibit the growth of cryptococci, as well as in their chemotactic responses to viable cryptococci or sodium caseinate. In addition, there were no differences in splenic macrophage functions between the two groups of mice.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗