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PubMedDate not supplied

Meningitis caused by Cryptococcus neoformans var. gattii and var. neoformans in Papua New Guinea.

Eleven cases of cryptococcal meningitis were diagnosed and biotyped from September 1991 to August 1992 in Papua New Guinea (PNG). Seven isolates were Cryptococcus neoformans var. gattii from paediatric and adult patients, one with diabetes mellitus and 4 were C. neoformans var. neoformans from adults, of whom 2 had human immunodeficiency virus type 1 (HIV-1) infection, and one each had tuberculosis and Plasmodium vivax malaria. Significant clinical findings were headache, fever, meningism, vomiting, photophobia, papilloedema and cranial nerve lesions. Five patients (45.5%) died; 3 of these were adults with var. gattii and 2 were men with both var. neoformans and HIV-1 infections. This prospective tropical study documents the emergence of C. neoformans var. neoformans in patients with HIV-1 infection in a country where previously var. gattii had predominated in the immunocompetent. There has been no earlier report of cryptococcosis in an HIV-1 seropositive patient in PNG. Despite presumed exposure to both varieties of C. neoformans, var. gattii infections had been most frequent. As HIV-1 spreads, the proportion of hosts infected with var. neoformans may rise. The course of meningitis caused by the 2 varieties of C. neoformans may differ, with mortality in the tropics remaining particularly high. In PNG the environmental source of C. neoformans remains elusive.

Adolescent↗
PubMed1998

Antigen-induced protective and nonprotective cell-mediated immune components against Cryptococcus neoformans.

Mice immunized with two different cryptococcal antigen preparations, one a soluble culture filtrate antigen (CneF) in complete Freund's adjuvant (CFA) and the other heat-killed Cryptococcus neoformans cells (HKC), develop two different profiles of activated T cells. CneF-CFA induces CD4+ T cells responsible for delayed-type hypersensitivity (DTH) reactivity and for amplification of the anticryptococcal DTH response, whereas HKC induce CD4+ and CD8+ T cells involved in anticryptococcal DTH reactivity and activated T cells which directly kill C. neoformans cells. The main purpose of this study was to assess the level of protection afforded by each of the two different T-cell profiles against challenge with viable C. neoformans cells, thereby identifying which activated T-cell profile provides better protection. CBA/J mice immunized with CneF-CFA had significantly better protective responses, based on better clearance of C. neoformans from tissues, on longer survival times, and on fewer and smaller lesions in the brain, than HKC-immunized mice or control mice similarly infected with C. neoformans. Both immunization protocols induced an anticryptococcal DTH response, but neither induced serum antibodies to glucuronoxylmannan, so the protection observed in the CneF-CFA immunized mice was due to the activated T-cell profile induced by that protocol. HKC-immunized mice, which displayed no greater protection than controls, did not have the amplifier cells. Based on our findings, we propose that the protective anticryptococcal T cells are the CD4+ T cells which have been shown to be responsible for DTH reactivity and/or the CD4+ T cells which amplify the DTH response and which have been previously shown to produce high levels of gamma interferon and interleukin 2. Our results imply that there are protective and nonprotective cell-mediated immune responses and highlight the complexity of the immune response to C. neoformans antigens.

Animals↗
PubMed2001

Activation of Valpha14(+) natural killer T cells by alpha-galactosylceramide results in development of Th1 response and local host resistance in mice infected with Cryptococcus neoformans.

We examined the effect of alpha-galactosylceramide (alpha-GalCer) on the synthesis of gamma interferon (IFN-gamma) and local resistance in mice infected intravenously with Cryptococcus neoformans. The level of IFN-gamma in serum increased on day 3, reached a peak level on day 7, and decreased to the basal level on day 14 postinfection in mice treated with alpha-GalCer, while in vehicle-treated mice, no increase was detected at any time points except for a small increase on day 7. Such effects were not observed in NKT-KO mice. In CD4KO mice, minor synthesis of IFN-gamma was detected on day 3 in sera but was completely abolished by day 7. The alpha-GalCer-induced IFN-gamma production on day 3 was partially reduced in mice depleted of NK cells by treatment with anti-asialo-GM(1) antibody (Ab). Spleen cells obtained from infected and alpha-GalCer-treated mice on day 7 produced a large amount of IFN-gamma upon restimulation with live organisms, while only a marginal level of production was detected in splenocytes from infected and vehicle-treated mice. Such effects were abolished in CD4KO and NKT-KO mice. Finally, the fungal loads in the lungs and spleen on days 7 and 14 were significantly reduced in alpha-GalCer-treated mice compared to those in control mice. In NKT-KO mice, local resistance elicited by alpha-GalCer was completely abolished, although no obvious exacerbation of infection was detected. Furthermore, treatment with anti-IFN-gamma monoclonal Ab mostly abrogated the protective effect of this agent. Thus, our results indicated that activation of Valpha14(+) NKT cells resulted in an increased Th1 response and local resistance to C. neoformans through production of IFN-gamma.

Animals↗
PubMed1984

Infection with Cryptococcus neoformans var. gattii leading to a pulmonary cryptococcoma and meningitis.

A patient who lived in Ohio, U.S.A., developed a large pulmonary cryptococcoma and meningitis as the result of infection with Cryptococcus neoformans var. gattii, an organism of subtropical and tropical distribution. He had no obvious predisposing illness or condition associated with increased susceptibility to cryptococcosis. Although he was found to have cutaneous anergy, his lymphocytes showed significant transformation responses in vitro when cultured both with mitogens and with killed cryptococci. The meningitis responded to intrathecal amphotericin B. The cryptococcoma, however, did not resolve in response to vigorous antifungal therapy during a period of more than 4 months. Eventually, the cryptococcoma was surgically removed. This case is unusual both for the finding of C. neoformans var. gattii outside its apparent endemic area as well as for the clinical features of the disease.

Adult↗
PubMed1997

Effect of serum IgG1 to Cryptococcus neoformans glucuronoxylomannan on murine pulmonary infection.

Little is known about the role of Ab in protection against pulmonary fungal pathogens. The ability of murine IgG1 mAb 2H1 to modify pulmonary Cryptococcus neoformans infection was investigated in intratracheal infection. mAb 2H1 binds C. neoformans glucuronoxylomannan. mAb 2H1 was given to A/JCr mice 24 h before infection. Two C. neoformans strains were studied: ATCC 24067 (serotype D) and 62070 (serotype A). Fungal burden was determined by CFU 14 days after infection for both strains, and at 2 h, 24 h, 48 h, 7 days, and 28 days after infection for strain 24067. On day 14, mAb 2H1 treatment reduced CFU in the lung, brain, and liver for strain 62070 infection. Minor reductions in lung CFU followed infection with strain 24067 in mAb 2H1-treated mice, despite prolonged survival. The limited ability of mAb 2H1 to reduce lung CFU may reflect rapid phagocytosis of yeast by alveolar macrophages, seen by electron microscopy 2 h after infection, regardless of whether mice had received mAb. Alveolar macrophages phagocytosed and reduced C. neoformans CFU in vitro only in the presence of mAb 2H1. Differences were apparent in phagocytosis and in vitro killing between strains 24067 and 62070. Serum IgG1 modified the course of pulmonary infection in mice by prolonging survival, reducing CFU, and reducing tissue glucuronoxylomannan Ag. mAb administration was associated with enhanced granulomatous inflammation, but did not prevent infection or dissemination. Despite incomplete protection by serum Ab against pulmonary infection, our results provide encouragement for continued vaccine development.

Animals↗
PubMed1985

Comparison of Media for the Isolation of Cryptococcus neoformans.

Four media, Staib's Guizotia abyssinica, trypan blue, and Staib's with 2 and 10 mg of methyl violet per liter, were compared for the selective and differential isolation of Cryptococcus neoformans from environmental samples. Trypan blue medium allowed for the differentiation of C. neoformans colonies from Candida albicans colonies several days earlier than did Staib's medium. The addition of methyl violet to Staib's medium was found to be inhibitory to some strains of all species tested. Diphenyl in Staib's medium inhibited the growth of 30 strains of C. neoformans and C. albicans.

Journal Article↗
PubMedDate not supplied

Cytologic diagnosis of Cryptococcus neoformans in HIV-positive patients.

OBJECTIVE: To present experience with the cytologic diagnosis of pulmonary cryptococcosis in bronchial washings and bronchoalveolar lavage in human immunodeficiency virus (HIV)-positive patients in Thailand. STUDY DESIGN: The study group consisted of 54 HIV-positive patients admitted to the Faculty of Medicine, Srinagarind Hospital, during the period January 1992-June 1994. Bronchial washing and bronchoalveolar lavage specimens were studied for Cryptococcus neoformans by routine Papanicolaou and special staining methods. RESULTS: The Cryptococcus organism, an encapsulated yeast with a clear halo on Papanicolaou-stained smears, was found both extracellularly and in histiocytes in 4 of 54 (7.4%) cases. A definitive diagnosis was confirmed by positive staining of the capsular mucopolysaccharides with periodic acid-Schiff and Mayer's mucicarmine stain and of the cell wall with methenamine silver. Lung biopsy was performed in one case and revealed cryptococcosis. CONCLUSION: This study underscores the usefulness of cytologic screening in the detection of this opportunistic pulmonary infection. The cytopathologist and cytotechnologist should be alert for the presence of Cryptococcus in cytologic specimens from HIV-positive patients.

AIDS-Related Opportunistic Infections↗
PubMed1996

Resistance to Cryptococcus neoformans is associated with an inflammatory response to Toxoplasma gondii in the central nervous system of mice.

We have studied the resistance of Toxoplasma gondii-infected mice to subsequent infection with Cryptococcus neoformans. Mice infected with the moderately virulent ME49 strain of T. gondii are resistant to proliferation of yeast cells in their brains after intravenous inoculation of the serotype A C. neoformans strain 184. The resistance serves to limit proliferation of yeast cells that colonize the brain. Maximal levels of resistance correlate not with maximal systemic specific anti-Toxoplasma resistance but rather with high levels of inflammatory response, presumably to parasites released from cysts in the brain. Resistance is localized, as mice infected with ME49 show only limited resistance in their lungs after intratracheal instillation of yeast cells, but there is substantial protection against development of cerebral cryptococcosis.

Animals↗
PubMed2005

CpG oligodeoxynucleotides promote the host protective response against infection with Cryptococcus neoformans through induction of interferon-gamma production by CD4+ T cells.

In the present study, we elucidated the effect of synthetic CpG-containing oligodeoxynucleotides (ODN) on pulmonary and disseminated infection caused by Cryptococcus neoformans. CDF-1 mice were inoculated intratracheally with a highly virulent strain of this pathogen, which resulted in massive bacterial growth in the lung, dissemination to the brain and death. Administration of CpG-ODN promoted the clearance of C. neoformans in the lungs, decreased their dissemination to brain and prolonged the survival of infected mice. These effects correlated well with the enhanced production of interleukin (IL)-12 and interferon (IFN)-gamma and attenuated secretion of IL-4 in bronchoalveolar lavage fluids (BALF) and promoted development of Th1 cells, as indicated by the increased production of IFN-gamma by paratracheal lymph node cells upon restimulation with cryptococcal antigens. The IFN-gamma synthesis in BALF was inhibited by depletion of CD8(+) and CD4(+) T cells on days 7 and 14 after infection, respectively, but not by depletion of NK and gammadelta T cells. Consistent with these data, intracellular expression of IFN-gamma was detected predominantly in CD8(+) and CD4(+) T cells in the lung on days 7 and 14, respectively. The protective effect of CpG-ODN, as shown by the prolonged survival, was completely and partially inhibited by depletion of CD4(+) or CD8(+) T cells, respectively, but not by depletion of other cells. Finally, TNF-alpha was markedly induced by CpG-ODN, and the protective effect of this agent was strongly inhibited by neutralizing anti-TNF-alpha MoAb. Our results indicate that CpG-ODN alters the Th1-Th2 cytokine balance and promotes host resistance against infection with C. neoformans.

Animals↗
PubMed1990

Passive immunization against Cryptococcus neoformans with an isotype-switch family of monoclonal antibodies reactive with cryptococcal polysaccharide.

The in vivo properties of an immunoglobulin isotype-switch family of monoclonal antibodies specific for the polysaccharide capsule of Cryptococcus neoformans were examined in a murine model of cryptococcosis. Subclass-switch variants were isolated by sequential sublining of an immunoglobulin G subclass 1 (IgG1)-secreting cell line. Antibodies of the IgG1, IgG2a, and IgG2b isotypes with identical reactivities with cryptococcal polysaccharide were prepared. The antibodies had the distinct biological properties associated with the heavy chains of each respective isotype. The antibodies were used prophylactically or therapeutically in an attempt to alter the course of cryptococcal infection in mice. Survival of mice and a tissue census of the numbers of viable cryptococci in the lung, spleen, and brain were used as indicators of efficacy. Passive immunization with the IgG2a and IgG2b antibodies effected a reduction in the numbers of cryptococci in lung and spleen. Passive immunization with the IgG1 antibody was markedly less effective. Passive immunization had little or no effect on the numbers of cryptococci in brain tissue, regardless of the immunoglobulin isotype. Despite apparent efficacy with regard to reduction in the numbers of yeast cells in the lung and spleen, the results showed no improvement in survival from murine cryptococcosis. Our results indicate that passive immunization produces a modest effect on the course of murine cryptococcosis in tissues other than brain. However, under the experimental conditions used, such treatment does not have a measurable impact on the ultimate outcome of the infection.

Animals↗