Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Cryptococcus”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 217 records · Page 12Linked to original sources
PubMed1975

Relationship between polyene resistance and sterol compositions in Cryptococcus neoformans.

Six mutants of Cryptococcus neoformans resistant to nystatin and pimaricin and three mutants resistant to amphotericin B were isolated by ultraviolet irradiation techniques from two wild-type strains. The major sterols of the wild-type strains were Delta(7)-ergosten-3beta-ol and ergosterol. All six mutants resistant to nystatin and pimaricin showed either loss of ergosterol and concurrent production of Delta(7, 22)-ergostadien-3beta-ol and Delta(7)-ergosten-3beta-ol, or loss of both the wild-type sterols, with production of Delta(8(9))-ergosten-3beta-ol and Delta(5, 8(9), 22)-ergostatrien-3beta-ol. The mutants producing Delta(7, 22)-ergostadien-3beta-ol and Delta(7)-ergosten-3beta-ol showed relatively low levels of resistance to nystatin and pimaricin, whereas the mutants producing Delta(8(9))-ergosten-3beta-ol and Delta(5, 8(0), 22)-ergostatrien-3beta-ol showed a high level of resistance to either drug. Although highly resistant to amphotericin B, however, the three mutants produced sterol compositions identical to those of the wild types, indicating that the strains acquired resistance other than by alteration of the membrane sterols. The mutants producing Delta(8(9)) and Delta(5, 8(9), 22) sterols were not virulent for mice, showed reduced growth rates at 25 C, and failed to grow at 37 C. The other mutants showed a slightly reduced rate of growth both at 25 and 37 C, and the virulence in mice was slightly reduced in comparison with that of the wild types. These comparisons were on gross observations and were not statistically analyzed.

Animals↗
PubMed1981

Particle size of airborn Cryptococcus neoformans in a tower.

Nearly 10(6) cells of Cryptococcus neoformans were cultured per g of pigeon droppings in a vacant tower. The air in the tower contained an average of 45 viable cells of C. neoformans per 100 liters: 60% of the cells were less than 4.7 micron in diameter. It is estimated that a human exposed to this atmosphere for 1 h would have 41 cells of c. neoformans deposited in the lungs. Sweeping resulted in the aerosolization of large numbers of cells of C. neoformans from 4.7 to 11 micron in diameter, the number of cells less than 4.7 micron remained relatively constant. One minute after sweeping, 4.4% of viable airborne cells of C. neoformans were less than 1.1 micron in diameter. We believe that this is the first report of isolating such small cells of C. neoformans from a natural site.

Aerosols↗
PubMed1972

Production of diagnostic pigment by phenoloxidase activity of cryptococcus neoformans.

Cryptococcus neoformans produces brown pigmented colonies when grown on agar media made from an extract of potatoes and carrots, broad beans (Vicia faba), or Guizotia abyssinica seeds. Since other yeasts do not produce the pigment, these media are useful as differential isolation media for C. neoformans. Similar specific pigment was produced by C. neoformans on chemically defined agar media which contained six different substrates of phenoloxidase (o-diphenol: oxygen oxidoreductase EC 1.10.3.1) an enzyme which catalyses the oxidation of o-diphenols to melanin. Substrates were incorporated singly into the media and included L-3, 4-dihydroxyphenylalanine (L-DOPA), chlorogenic acid, protocatechuic acid, catechol, norepinephrine, and 3-hydroxytyramine hydrochloride (dopamine). No pigment was produced on media without substrate. Phenoloxidase activity in (NH(4))(2)SO(4) precipitates of C. neoformans cell-free extract was assayed by measuring increases in absorbance at 480 nm produced in solutions of L-DOPA. This reaction showed oxygen uptake and was effectively inhibited by copper chelators, but not by catalase. The enzyme also oxidized the five other substrates which induced pigment formation. Electron micrographs of cells incubated in L-DOPA showed deposition of the pigment in the cell wall.

Agar↗
PubMed1973

Cryptococcus neoformans of unusual morphology.

A case of primary cryptococcosis of the lungs was caused by an isolate of Cryptococcus neoformans that assumes a giant form in tissue but which has a normal appearance on artificial culture. Electron microscopy revealed gross enlargement of the capsule and plasma membranes in the tissue form.

Biopsy↗
PubMed1975

Phagocytosis of Cryptococcus neoformans by alveolar macrophages.

Guinea pig pulmonary macrophages phagocytized but did not kill nonencapsulated cells of Cryptococcus neoformans. The phagocytic process was inhibited by cryptococcal capsular polysaccharide. Pulmonary macrophages, activated by preinjecting heat-killed bacteria into intact animals, did not kill the engulfed yeast cells. Labeled cells of C. neoformans were neither killed nor cleared from guinea pig lungs 6 h postexposure. The results of our experiments indicate that during the first few hours after the lung is exposed to the infectious particle of C. neoformans the pulmonary macrophage does not function primarily to kill engulfed yeast cells. We believe that a rapid yet transient acute inflammatory response probably plays a major role in this process during the first few hours after C. neoformans enters the lung.

Acid Phosphatase↗
PubMed1976

Nature of the effector cells responsible for antibody-dependent cell-mediated killing of Cryptococcus neoformans.

Studies were performed to identify the types of human peripheral blood leukocytes capable of killing Cryptococcus neoformans in the presence of anticryptococcal antibody in vitro. A total of 24.1 +/- 2.7% (mean +/- standard error of the mean of four experiments) of the original cryptococcal inoculum survived in a mixed mononuclear, cell preparation (approximately 30% monocytes) after 4 h of incubation at 37 degrees C with rabbit anticryptococcal antibody. When phagocytic cells were removed, there was 36.4 +/- 4.6% survival in six experiments, compared with 52.8% survival in the presence of purified granulocytes (mean of two experiments) and 96.9 +/- 1% survival in the presence of purified T cells. There was never any significant killing in control mixtures that contained leukocytes with normal rabbit serum nor in those that contained anticryptococcal antibody without effector leukocytes. Significant antibody-dependent fungicidal activity was seen with ratios of effector to target cells as low as 6.25:1. These observations indicate that multiple types of peripheral blood leukocytes, excluding T cells, are capable of antibody-dependent fungicidal activity.

Antibodies, Fungal↗
PubMed1977

Capsule size of Cryptococcus neoformans: control and relationship to virulence.

Capsule size of five isolates of Cryptococcus neoformans was controlled by cultivation in media containing varying amounts of sugar. High concentrations of sugar (e.g., 16%) suppressed encapsulation whereas low concentrations (e.g., 1%) allowed maximal encapsulation. Suppression of capsule size was attributed at least in part to the increased osmolarity of the medium because a medium with low sugar concentration but having high osmolarity (by virtue of added sodium chloride) also produced cells having small capsules. The extent of control was more marked with certain of the isolates than with others. Mice were intravenously inoculated with cells of a single isolate cultivated so as to have either small or large capsules, and virulence was measured by comparing death rates. Results indicate that virulence after such an inoculation is a constant characteristic of an isolate and is not affected by size of the capsule of the cells in the inoculum.

Cryptococcus↗
PubMed1977

Non-encapsulated variant of Cryptococcus neoformans. II. Surface receptors for cryptococcal polysaccharide and their role in inhibition of phagocytosis by polysaccharide.

The binding of cryptococcal polysaccharide to a non-encapsulated strain of Cryptococcus neoformans was studied. Binding of purified polysaccharide to the yeast was determined by inhibition of phagocytosis and by indirect immunofluorescence techniques. The ability of cryptococcal polysaccharide to prevent phagocytosis of the non-encapsulated strain appears to be directly related to adherence of polysaccharide to the yeast via specific receptors on the cell surface. Addition of varying doses of cryptococcal polysaccharide to non-encapsulated yeast cells inhibited phagocytosis only at polysaccharide concentrations at which the polysaccharide could be demonstrated on the yeast surface by immunofluorescence. Macrophages treated with cryptococcal polysaccharide had no detectable amounts of cryptococcal polysaccharide adherent to their surface, and they had a normal ability to phagocytize the yeast. Kinetic studies showed that inhibition of phagocytosis is directly related to the presence of cryptococcal polysaccharide at the yeast surface rather than to some indirect effect by the polysaccharide on serum components necessary for phagocytosis. Purified polysaccharide from C. neoformans serotypes A, B, C, and D bound to the yeast, but type III pneumococcal polysaccharide did not inhibit phagocytosis of the nonencapsulated yeast. Cryptococcal polysaccharide did not bind to cells of Candida albicans, C. pseudotropicalis, Torulopsis sp., Rhodotorula sp., or Saccharomyces cerevisiae.

Ascitic Fluid↗
PubMed1977

Cryptococcus neoformans: size range of infectious particles from aerosolized soil.

Although cryptococcosis is characterized as a chronic central nervous system disease, it is generally accepted that the lungs are the primary portal of entry for the etiological agent. Despite this, there is a distinct lack of evidence that viable airborne particles of Cryptococcus neoformans are small enough to reach the alveoli. Two encapsulated strains and one nonencapsulated strain of C. neoformans were inoculated into 250-g quantities of sterile soil. Throughout the 0 to 12 weeks of incubation, this soil was aerosolized in a sealed chamber with a Waring blender. Samples of the resultant dust cloud were taken with an Anderson air sampler from which the numbers and sizes of viable airborne particles were determined. Of the viable organisms aspirated into the air sampler, 15% were 0.65 to 2 micron in diameter. As incubation time in soil increased, the size of the particles decreased, and increased numbers of C. neoformans cells 0.65 to 2 micron in diameter were isolated. The presence of viable cells less than 2 micron in soil aerosols indicated that, under certain conditions in nature, C. neoformans cells exist in sizes that are capable of deep lung deposition.

Aerosols↗
PubMed1977

Immune response to Cryptococcus neoformans soluble polysaccharide: immunological unresponsiveness.

Mice injected with 100 to 800 microgram of Cryptococcus neoformans soluble polysaccharide showed a reduced ability to produce antibody after a challenge immunization with polysaccharide emulsified in Freund incomplete adjuvant. These animals were considered immunologically unresponsive. Animals given an initial injection of 25 or 50 microgram of polysaccharide responded to a challenge immunization in the same manner as control animals. Reversion of unresponsive mice to antibody production without further antigenic stimulation did not occur during a 12-week experimental period. These animals exhibited a partial response to challenge immunization 8 weeks after induction of unresponsiveness, and they were fully responsive to challenge immunization at 12 weeks. Animals given a single dose of 0.1, 0.4, or 1.6 microgram of polysaccharide produced a marked anamnestic response after challenge immunization. Repeated injections of subimmunogenic doses of polysaccharide did not produce a marked anamnestic response and would induce unresponsiveness only when the cumulative dose reached 100 to 400 microgram of polysaccharide, suggesting that injected cryptococcal polysaccharide might be sequestered in some manner until an amount of antigen sufficient for induction of unresponsiveness is accumulated. This possibility was confirmed by immunofluorescence studies that revealed a long-term deposition of polysaccharide in the tubular epithelial cells of the kidney.

Animals↗
PubMed1978

Cryptococcus neoformans: pseudohyphal forms surviving culture with Acanthamoeba polyphaga.

During experiments on the gastrointestinal tract as a possible portal of entry for Cryptococcus neoformans, we occasionally observed the free-living amoeba, Acanthamoeba polyphaga, growing in the presence of C. neoformans cultured from mouse feces. Examination of the amoebic trophozoites revealed that they were engorged with yeast cells. Over a period of 2 to 3 weeks of incubation, the amoebae apparently killed most of the yeast cells. Some of the surviving C. neoformans cells formed atypical colonies which contained pseudohyphae. Seven other strains have since been cultured with this amoeba. Pseudohyphal forms were found among the surviving colonies in all strains tested. Virulence studies were performed on one randomly selected pseudohyphal isolate from each of the eight strains of C. neoformans. Pseudohyphal isolates from seven of the eight strains failed to kill mice 30 days after intracranial inoculation. The potential role of soil amoebae in the control of C. neoformans in nature is discussed.

Amoeba↗
PubMed1978

Phagocytosis of Cryptococcus neoformans by normal and thioglycolate-activated macrophages.

Phagocytosis of Cryptococcus neoformans by normal and thioglycolate-activated mouse peritoneal macrophages was studied. Thioglycolate-activated macrophages exhibited a lower percent phagocytosis than did normal macrophages. Differences in phagocytosis could not be attributed to differences in macrophage viability, minor variations in the concentration of adherent macrophages, or a general depression in activated macrophage phagocytosis. Thioglycolate-activated macrophages required heat-labile opsonins for optimal phagocytosis of non-encapsulated cryptococci, whereas nonactivated macrophages did not require heat-labile opsonins for phagocytosis of the yeast. Both types of macrophages exhibited similar sensitivity to the phagocytosis-inhibiting properties of cryptococcal polysaccharide. The results show that depletion of heat-labile opsonins from serum or inactivation of yeast-bound, heat-labile opsonins by polysaccharide cannot account for the phagocytosis-inhibiting properties of cryptococcal polysaccharide.

Animals↗
PubMed1978

Delayed-type hypersensitivity responses in infected mice elicited by cytoplasmic fractions of Cryptococcus neoformans.

Four subcellular fractions of Cryptococcus neoformans prepared by differential centrifugation of disrupted whole yeast and a 3-day culture filtrate were examined for their ability to elicit delayed-type hypersensitivity in sensitized animals. The methods used to detect sensitization were (i) the footpad swelling test and inhibition of peritoneal macrophage migration in mice and (ii) skin testing in guinea pigs. Two entities, the post-mitochondrial supernatant and the culture filtrate, showed considerable activity in the footpad test, with 26- and 30-microliter 24-h swellings, respectively, at 6 weeks after infection. With the latter there was interference from a strong antibody-mediated 4-h skin reaction. The post-mitochondrial supernatant produced strong delayed-type hypersensitivity in guinea pigs at a dose of 69 microgram, and there was no demonstrable cross-reactivity in animals sensitized with heterologous fungi. The footpad swelling in mice correlated well with the macrophage migration inhibition test, with 71% inhibition in mice infected subcutaneously with C. neoformans at 6 weeks. However, mice infected intravenously developed poorer cell-mediated immunity than the subcutaneously infected mice. The post-mitochondrial supernatant was found to contain detectable amounts of cryptococcal capsular polysaccharide.

Animals↗
PubMed1979

Kinetics of lymphocyte transformation in mice immunized with viable avirulent forms of Cryptococcus neoformans.

A murine model was developed to study the cell-mediated immune response of mice immunized with one of two live, avirulent forms of Cryptococcus neoformans: a nonencapsulated mutant and a thinly encapsulated pseudohyphal variant. A lymphocyte transformation assay was used to evaluate the cellular response of control and sensitized spleen cells after in vitro incubation with three merthiolate-killed whole-cell antigens of C. neoformans. An antigen-to-spleen cell ratio of 10:1 and 5 days of incubation of antigen-spleen cell mixtures were established as optimal conditions for maximum lymphocyte transformation. Maximum responses occurred from 2 to 3 weeks after the last of eight weekly intraperitoneal inoculations of C. neoformans. This assay provided an accurate, reproducible method of studying cell-mediated immunity to C. neoformans, and applications to the study of cryptococcal pathogenesis are proposed.

Animals↗
PubMed1979

Opsonization of Cryptococcus neoformans by human immunoglobulin G: role of immunoglobulin G in phagocytosis by macrophages.

The role of immunoglobulin G (IgG) as an opsonin in phagocytosis of Cryptococcus neoformans by macrophages was investigated. Labeling with 125I showed that IgG isolated from normal human serum bound to non-encapsulated C. neoformans. Furthermore, IgG-opsonized cryptococci were agglutinated by anti-serum to IgG heavy chains, indicating that normal human serum contains antibody that will bind to the yeast surface. The IgG isolated from normal serum accounted for all opsonizing activity found in normal human serum, since differences were not noted between the opsonizing activities of whole serum, heat-inactivated serum and purified IgG when these opsonins were compared at equivalent concentrations of IgG. Phagocytosis of IgG-opsonized cryptococci was inhibited by anti-macrophage IgG, a reagent known to block Fc-mediated attachment and ingestion, and by pepsin digestion of opsonizing IgG. Thus, IgG opsonization is an Fc-dependent process. Opsonizing IgG appears to play its major role during the attachment phase of phagocytosis, since antimacrophage IgG blocked attachment of cryptococci to macrophages but could not block ingestion of IgG-opsonized cryptococci that had been allowed to attach to macrophages. Ingestion of opsonized cryptococci was not blocked by 2-deoxy-D-glucose, a reagent known to block Fc-mediated ingestion, thus confirming that IgG has a primary role in attachment and suggesting that ingestion is mediated by a process that is not Fc dependent.

Agglutination↗
PubMed1979

Opsonization of Cryptococcus neoformans by human immunoglobulin G: masking of immunoglobulin G by cryptococcal polysaccharide.

Previous studies have shown that attachment of non-encapsulated cryptococci to macrophages is highly dependent on opsonizing immunoglobulin G (IgG) and that cryptococcal polysaccharide inhibits the attachment phase of phagocytosis. We investigated various mechanisms by which cryptococcal polysaccharide might interfere with the opsonizing action of IgG. Cryptococcal polysaccharide did not appreciably prevent binding of opsonizing IgG to the yeast. Furthermore, cryptococcal polysaccharide acted as a noncompetitive inhibitor with respect to the opsonizing action of IgG. These experiments suggested that cell wall-bound IgG is masked in some manner such that it is unable to participate in Fc-mediated phagocytosis. This appeared to be the case, since cryptococcal polysaccharode inhibited agglutination of IgG-opsonized yeast cells by antiserum to IgG. There was good dose-response correlation between the amount of polysaccharide needed to inhibit phagocytosis of non-encapsulated Cryptococcus neoformans and the amount of polysaccharide needed to prevent agglutination of IgG-opsonized cryptococci by antiserum to IgG. The ability of cryptococcal polysaccharide to prevent agglutination of IgG-opsonized cryptococci by antiserum to IgG was lost if dextran, a substance known to enhance agglutination of several particles, was incorporated into the medium.

Agglutination↗
PubMed1979

Chemotaxigenesis and activation of the alternative complement pathway by encapsulated and non-encapsulated Cryptococcus neoformans.

In the presence of serum, whole cells of encapsulated and non-encapsulated Cryptococcus neoformans generated a chemotactic response by neutrophils. Heat inactivation of serum ablated all chemotactic activity. Cryptococcal polysaccharide was not chemotaxigenic. Assays for alternative complement pathway activation such as depletion of alternative complement pathway factor B or electrophoretic conversion of factor B closely paralleled chemotaxis assays. Cells of encapsulated and non-encapsulated C. neoformans activated the alternative complement pathway, whereas cryptococcal polysaccharide was inactive. Failure of the capsular material to activate the alternative pathway was not due to serotype specificity because polysaccharide of several serotypes failed to achieve activation. The results suggest that chemotaxigenesis and alternative complement pathway activation are functions of the yeast cell wall. The results support our proposal that the cryptococcal capsul does not prevent potential opsonins from reaching binding and activation sites at the yeast cell wall or the release of biologically active soluble cleavage products into the surrounding medium; however, cell wall-bound cleavage products remain bound to the cell wall beneath the capsule. Therefore, they are unable to participate as opsonins in phagocytosis.

Animals↗
PubMed1980

Isolation and characterization of arginine auxotrophs of Cryptococcus neoformans.

Arginine auxotrophs were isolated in both mating types of Cryptococcus neoformans. In both mutants, the auxotrophy was due to the lack of active argininosuccinate lyase. The virulence in mice of the mutants was compared with that of the wild type. One auxotroph displayed a loss of virulence which appeared to be related to the presence of another mutation, one which prevented normal cell separation after budding. The other auxotroph had reduced virulence compared with the wild type, but a variant isolated from it by mouse passage had virulence equivalent to that of the wild type while maintaining the auxotrophic requirements.

Animals↗