Journal articles: 'Cryptococcus neoformans'

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Mukherjee, Jean, Matthew D. Scharff, and Arturo Casadevall. "Cryptococcus neoformans infection can elicit protective antibodies in mice." Canadian Journal of Microbiology 40, no. 10 (October 1, 1994): 888–92. http://dx.doi.org/10.1139/m94-141.

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An IgG1 monoclonal antibody generated from a mouse infected with Cryptococcus neoformans modified the course of intravenous cryptococcal infection in A/J mice by prolonging survival and reducing lung fungal burden, brain mass, and serum polysaccharide levels. The results demonstrate that C. neoformans infection can elicit useful antibodies.Key words: Cryptococcus neoformans, monoclonal antibody, antibody immunity.

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Gaylord, Elizabeth A., Hau Lam Choy, and Tamara L. Doering. "Dangerous Liaisons: Interactions of Cryptococcus neoformans with Host Phagocytes." Pathogens 9, no. 11 (October 27, 2020): 891. http://dx.doi.org/10.3390/pathogens9110891.

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Cryptococcus neoformans is an opportunistic fungal pathogen and a leading cause of death in immunocompromised individuals. The interactions of this yeast with host phagocytes are critical to disease outcome, and C. neoformans is equipped with an array of factors to modulate these processes. Cryptococcal infection begins with the deposition of infectious particles into the lungs, where the fungal cells deploy various antiphagocytic factors to resist internalization by host cells. If the cryptococci are still engulfed, they can survive and proliferate within host cells by modulating the phagolysosome environment in which they reside. Lastly, cryptococcal cells may escape from phagocytes by host cell lysis, nonlytic exocytosis, or lateral cell-to-cell transfer. The interactions between C. neoformans and host phagocytes also influence the dissemination of this pathogen to the brain, where it may cross the blood-brain barrier and cause an often-fatal meningoencephalitis. In this review, we highlight key cryptococcal factors involved in various stages of cryptococcal-host interaction and pathogenesis.

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Lev, Sophie, Cecilia Li, Desmarini Desmarini, David Liuwantara, Tania C. Sorrell, Wayne J. Hawthorne, and Julianne T. Djordjevic. "Monitoring Glycolysis and Respiration Highlights Metabolic Inflexibility of Cryptococcus neoformans." Pathogens 9, no. 9 (August 21, 2020): 684. http://dx.doi.org/10.3390/pathogens9090684.

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Cryptococcus neoformans is a human fungal pathogen that adapts its metabolism to cope with limited oxygen availability, nutrient deprivation and host phagocytes. To gain insight into cryptococcal metabolism, we optimized a protocol for the Seahorse Analyzer, which measures extracellular acidification rate (ECAR) and oxygen consumption rate (OCR) as indications of glycolytic and respiratory activities. In doing so we achieved effective immobilization of encapsulated cryptococci, established Rotenone/Antimycin A and 2-deoxyglucose as effective inhibitors of mitochondrial respiration and glycolysis, respectively, and optimized a microscopy-based method of data normalization. We applied the protocol to monitor metabolic changes in the pathogen alone and in co-culture with human blood-derived monocytes. We also compared metabolic flux in wild-type C. neoformans, its isogenic 5-PP-IP5/IP7-deficient metabolic mutant kcs1∆, the sister species of C. neoformans, Cryptococcus deuterogattii/VGII, and two other yeasts, Saccharomyces cerevisiae and Candida albicans. Our findings show that in contrast to monocytes and C. albicans, glycolysis and respiration are tightly coupled in C. neoformans and C. deuterogattii, as no compensatory increase in glycolysis occurred following inhibition of respiration. We also demonstrate that kcs1∆ has reduced metabolic activity that correlates with reduced mitochondrial function. Metabolic inflexibility in C. neoformans is therefore consistent with its obligate aerobe status and coincides with phagocyte tolerance of ingested cryptococcal cells.

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Silva, Vanessa K. A., Robin C. May, and Marcio L. Rodrigues. "Pyrifenox, an ergosterol inhibitor, differentially affects Cryptococcus neoformans and Cryptococcus gattii." Medical Mycology 58, no. 7 (January 8, 2020): 928–37. http://dx.doi.org/10.1093/mmy/myz132.

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Abstract Cryptococcosis is a life-threatening fungal infection. New therapeutic approaches are necessary to combat cryptococcosis, as the currently available therapeutic protocols are expensive and generally result in deleterious side effects. Pyrifenox is an antifungal compound that affects phytopathogens by inhibiting the biosynthesis of ergosterol. In this study, we investigated the effects of pyrifenox on Cryptococcus neoformans and Cryptococcus gattii growth, capsule architecture and export of the major capsule component, glucuroxylomannan (GXM). Pyrifenox inhibited the growth of C. neoformans, but was significantly less effective against C. gattii. The resistance of C. gattii to pyrifenox was associated with the expression of efflux pump genes, particularly AFR1 and AFR2, since mutant cells lacking expression of these genes became sensitive to pyrifenox. Analysis of the cryptococcal capsule by India ink counterstaining, immunofluorescence, and scanning electron microscopy showed that pyrifenox affected capsular dimensions in both species. However, GXM fibers were shorter and uniformly distributed in C. neoformans, whereas in C. gattii the number of fibers was reduced. Pyrifenox-treated C. gattii developed unusually long chains of undivided cells. The secretion of GXM was markedly reduced in both species after treatment with pyrifenox. Altogether, the results indicated that pyrifenox differently affects C. neoformans and C. gattii. In addition, it highlights a potential role for pyrifenox as an inhibitor of GXM export in experimental models involving pathogenic cryptococci.

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Mylonakis, Eleftherios, Roberto Moreno, Joseph B. El Khoury, Alexander Idnurm, Joseph Heitman, Stephen B. Calderwood, Frederick M. Ausubel, and Andrew Diener. "Galleria mellonella as a Model System To Study Cryptococcus neoformans Pathogenesis." Infection and Immunity 73, no. 7 (July 2005): 3842–50. http://dx.doi.org/10.1128/iai.73.7.3842-3850.2005.

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ABSTRACT Evaluation of Cryptococcus neoformans virulence in a number of nonmammalian hosts suggests that C. neoformans is a nonspecific pathogen. We used the killing of Galleria mellonella (the greater wax moth) caterpillar by C. neoformans to develop an invertebrate host model system that can be used to study cryptococcal virulence, host immune responses to infection, and the effects of antifungal compounds. All varieties of C. neoformans killed G. mellonella. After injection into the insect hemocoel, C. neoformans proliferated and, despite successful phagocytosis by host hemocytes, killed caterpillars both at 37°C and 30°C. The rate and extent of killing depended on the cryptococcal strain and the number of fungal cells injected. The sequenced C. neoformans clinical strain H99 was the most virulent of the strains tested and killed caterpillars with inocula as low as 20 CFU/caterpillar. Several C. neoformans genes previously shown to be involved in mammalian virulence (CAP59, GPA1, RAS1, and PKA1) also played a role in G. mellonella killing. Combination antifungal therapy (amphotericin B plus flucytosine) administered before or after inoculation was more effective than monotherapy in prolonging survival and in decreasing the tissue burden of cryptococci in the hemocoel. The G. mellonella-C. neoformans pathogenicity model may be a substitute for mammalian models of infection with C. neoformans and may facilitate the in vivo study of fungal virulence and efficacy of antifungal therapies.

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Song, Ying, Yufang Qiu, Weiyou Liu, and Xiaoliang Yuan. "Research progress in immunological mechanisms of Cryptococcus." Trends in Immunotherapy 5, no. 2.1 (October 22, 2021): 72. http://dx.doi.org/10.24294/ti.v5.i2.1.1370.

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Whether infection of Cryptococcus causes disease in host or not depends on the virulence of the pathogen and the immune defense ability of the host. Cryptococcus neoformans (C. neoformans) mainly causes opportunistic infections in the immunocompromised or immunodeficient patients. In contrast, Cryptococcus gattii (C. gattii) mainly attacks the immunocompetent individuals. On the one hand, the host immune cells can eliminate the invasive Cryptococcus through a complex immune mechanism; on the other hand, Cryptococcus can evade the clearance of host immune cells by adopting various strategies (immune escape). This review mainly focuses on the pathogenic mechanism of Cryptococcus, and the host’s immune defense mechanism against cryptococcal infection.

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King, John W. "Cryptococcus neoformans." Emerging Infectious Diseases 14, no. 5 (May 2008): 762. http://dx.doi.org/10.3201/eid1405.0508.

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Warnock, David W. "Cryptococcus neoformans." Journal of Antimicrobial Chemotherapy 44, no. 1 (July 1999): 139. http://dx.doi.org/10.1093/jac/44.1.139.

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Mayer, François L., and James W. Kronstad. "Cryptococcus neoformans." Trends in Microbiology 28, no. 2 (February 2020): 163–64. http://dx.doi.org/10.1016/j.tim.2019.10.003.

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Rocco, Mark La. "Cryptococcus neoformans." Clinical Microbiology Newsletter 14, no. 23 (December 1992): 177–81. http://dx.doi.org/10.1016/0196-4399(92)90044-a.

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Heung, Lena J., and Tobias M. Hohl. "DAP12 Inhibits Pulmonary Immune Responses to Cryptococcus neoformans." Infection and Immunity 84, no. 6 (April 11, 2016): 1879–86. http://dx.doi.org/10.1128/iai.00222-16.

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Cryptococcus neoformansis an opportunistic fungal pathogen that is inhaled into the lungs and can lead to life-threatening meningoencephalitis in immunocompromised patients. Currently, the molecular mechanisms that regulate the mammalian immune response to respiratory cryptococcal challenge remain poorly defined. DAP12, a signaling adapter for multiple pattern recognition receptors in myeloid and natural killer (NK) cells, has been shown to play both activating and inhibitory roles during lung infections by different bacteria and fungi. In this study, we demonstrate that DAP12 plays an important inhibitory role in the immune response toC. neoformans. Infectious outcomes in DAP12−/−mice, including survival and lung fungal burden, are significantly improved compared to those in C57BL/6 wild-type (WT) mice. We find that eosinophils and macrophages are decreased while NK cells are increased in the lungs of infected DAP12−/−mice. In contrast to WT NK cells, DAP12−/−NK cells are able to repressC. neoformansgrowthin vitro. Additionally, DAP12−/−macrophages are more highly activated than WT macrophages, with increased production of tumor necrosis factor (TNF) and CCL5/RANTES and more efficient uptake and killing ofC. neoformans. These findings suggest that DAP12 acts as a brake on the pulmonary immune response toC. neoformansby promoting pulmonary eosinophilia and by inhibiting the activation and antifungal activities of effector cells, including NK cells and macrophages.

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Monari, Claudia, Thomas R. Kozel, Francesco Bistoni, and Anna Vecchiarelli. "Modulation of C5aR Expression on Human Neutrophils by Encapsulated and Acapsular Cryptococcus neoformans." Infection and Immunity 70, no. 7 (July 2002): 3363–70. http://dx.doi.org/10.1128/iai.70.7.3363-3370.2002.

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ABSTRACT Cryptococcus neoformans and cryptococcal surface polysaccharides influenced C5aR expression on human polymorphonuclear neutrophils (PMN). Encapsulated and acapsular strains produced dramatically different effects. Treatment of PMN with acapsular cryptococci up-regulated C5aR expression; whereas treatment with encapsulated cells suppressed C5aR expression. Glucuronoxylomannan (GXM), the principal constituent of the cryptococcal capsule, was responsible for such inhibition. Increased C5aR expression following treatment with acapsular cryptococci was accompanied by increased binding of C5a to PMN, increased superoxide production in response to stimulation with C5a, and an increased chemotactic response to C5a. Conversely, decreased C5aR expression following treatment with encapsulated cryptococci or acapsular cryptococci that had been pretreated with GXM was accompanied by decreased binding of C5a to PMN and a decreased chemotactic response to C5a. Our results raise the possibility that the down-regulation of C5aR expression by encapsulated cryptococci might alter PMN function at the site of cryptococcal infection.

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Diniz-Lima, Israel, Leonardo Marques da Fonseca, Elias Barbosa da Silva-Junior, Joyce Cristina Guimarães-de-Oliveira, Leonardo Freire-de-Lima, Danielle Oliveira Nascimento, Alexandre Morrot, et al. "Cryptococcus: History, Epidemiology and Immune Evasion." Applied Sciences 12, no. 14 (July 13, 2022): 7086. http://dx.doi.org/10.3390/app12147086.

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Cryptococcosis is a disease caused by the pathogenic fungi Cryptococcus neoformans and Cryptococcus gattii, both environmental fungi that cause severe pneumonia and may even lead to cryptococcal meningoencephalitis. Although C. neoformans affects more fragile individuals, such as immunocompromised hosts through opportunistic infections, C. gattii causes a serious indiscriminate primary infection in immunocompetent individuals. Typically seen in tropical and subtropical environments, C. gattii has increased its endemic area over recent years, largely due to climatic factors that favor contagion in warmer climates. It is important to point out that not only C. gattii, but the Cryptococcus species complex produces a polysaccharidic capsule with immunomodulatory properties, enabling the pathogenic species of Cryptococccus to subvert the host immune response during the establishment of cryptococcosis, facilitating its dissemination in the infected organism. C. gattii causes a more severe and difficult-to-treat infection, with few antifungals eliciting an effective response during chronic treatment. Much of the immunopathology of this cryptococcosis is still poorly understood, with most studies focusing on cryptococcosis caused by the species C. neoformans. C. gattii became more important in the epidemiological scenario with the outbreaks in the Pacific Northwest of the United States, which resulted in phylogenetic studies of the virulent variant responsible for the severe infection in the region. Since then, the study of cryptococcosis caused by C. gattii has helped researchers understand the immunopathological aspects of different variants of this pathogen.

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van de Wetering, J. K., F. E. J. Coenjaerts, A. B. Vaandrager, L. M. G. van Golde, and J. J. Batenburg. "Aggregation of Cryptococcus neoformans by Surfactant Protein D Is Inhibited by Its Capsular Component Glucuronoxylomannan." Infection and Immunity 72, no. 1 (January 2004): 145–53. http://dx.doi.org/10.1128/iai.72.1.145-153.2004.

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ABSTRACT Cryptococcus neoformans is an opportunistic pathogen invading the immunocompromised host. Infection starts with the inhalation of acapsular or sparsely encapsulated cells, after which capsule synthesis is initiated. The capsule is the main virulence factor of this yeast-like fungus. Pulmonary surfactant protein D (SP-D) is an important component of the local innate defense system. In the present study, interactions of SP-D with intact C. neoformans cells and their isolated capsular components were investigated. Although encapsulated cryptococci were bound, SP-D showed the highest affinity for acapsular C. neoformans. Only acapsular cryptococci were aggregated by SP-D. Furthermore, the cryptococcal capsular components glucuronoxylomannan (GXM) and mannoprotein 1 (MP1) were bound with relatively high affinity, in contrast to GalXM and MP2. Binding as well as aggregation of acapsular C. neoformans by SP-D could be inhibited by GXM in concentrations that are likely to be present in the lung after infection, suggesting that not only the capsule hampers SP-D function within the innate defense system of the lung but also the secreted capsular component GXM.

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Holcomb, Zachary E., Julie M. Steinbrink, Aimee K. Zaas, Marisol Betancourt, Jennifer L. Tenor, Dena L. Toffaletti, J. Andrew Alspaugh, John R. Perfect, and Micah T. McClain. "Transcriptional Profiles Elucidate Differential Host Responses to Infection with Cryptococcus neoformans and Cryptococcus gattii." Journal of Fungi 8, no. 5 (April 22, 2022): 430. http://dx.doi.org/10.3390/jof8050430.

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Many aspects of the host response to invasive cryptococcal infections remain poorly understood. In order to explore the pathobiology of infection with common clinical strains, we infected BALB/cJ mice with Cryptococcus neoformans, Cryptococcus gattii, or sham control, and assayed host transcriptomic responses in peripheral blood. Infection with C. neoformans resulted in markedly greater fungal burden in the CNS than C. gattii, as well as slightly higher fungal burden in the lungs. A total of 389 genes were significantly differentially expressed in response to C. neoformans infection, which mainly clustered into pathways driving immune function, including complement activation and TH2-skewed immune responses. C. neoformans infection demonstrated dramatic up-regulation of complement-driven genes and greater up-regulation of alternatively activated macrophage activity than seen with C gattii. A 27-gene classifier was built, capable of distinguishing cryptococcal infection from animals with bacterial infection due to Staphylococcus aureus with 94% sensitivity and 89% specificity. Top genes from the murine classifiers were also differentially expressed in human PBMCs following infection, suggesting cross-species relevance of these findings. The host response, as manifested in transcriptional profiles, informs our understanding of the pathophysiology of cryptococcal infection and demonstrates promise for contributing to development of novel diagnostic approaches.

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Hidore, M. R., and J. W. Murphy. "Natural cellular resistance of beige mice against Cryptococcus neoformans." Journal of Immunology 137, no. 11 (December 1, 1986): 3624–31. http://dx.doi.org/10.4049/jimmunol.137.11.3624.

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Abstract 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)

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Etoughe, FN, M. Raiteb, YB Komba, F. Ihhibane, R. Moutai, and N. Tassi. "Les infections à Cryptococcus neoformans chez les patients infectés par le VIH : à propos de 27 cas." Revue Malienne d'Infectiologie et de Microbiologie 15, no. 1 (May 14, 2020): 2–9. http://dx.doi.org/10.53597/remim.v15i1.1560.

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But du travail : Décrire les profils épidémiologiques, clinico-paracliniques, thérapeutiques et évolutifs des patients infectés par le VIH qui ont présenté une infection à Cryptococcus neoformans. Matériel et méthode : Étude rétrospective portant sur les dossiers de 27 patients infectés par le VIH suivis au Service des Maladies Infectieuses du CHU Mohamed VI et hospitalisés pour une infection à Cryptococcus neoformans entre janvier 2007 et juillet 2018. Résultats : La prévalence était de 3,37 %. L'âge moyen des patients était de 39,22 ans [19-64] avec une prédominance masculine (21 hommes, 77,7 %). La cryptococcose était révélatrice de l'infection à VIH chez 16 patients (60%). La localisation neuroméningée était présente chez 25 patients (92,6%). Les céphalées dominaient le tableau clinique chez 23 patients (85 %). L'examen à l'encre de chine a permis d'isoler le Cryptococcus neoformans que dans le LCR chez 21 patients (78%) et la culture chez 22 patients (81,5%). Le bilan d'extension montrait des hémocultures positives à Cryptococcus neoformans chez 7 patients (26%). Le taux moyen des lymphocytes CD4 était 56 cellules /mm3. Onze patients (41%) ont été traités par l'association Amphotéricine B + Fluconazole et 16 patients (59%) par Fluconazole en monothérapie. L'évolution était favorable chez 22 patients (81,5%) Conclusion : La fréquence et la gravité de l'infection à Cryptococcus neoformans chez les patients infectés par le VIH implique un dépistage même en absence de signes cliniques en cas d'immunodépression profonde.

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Han, Lian-Tao, Lei Wu, and Tong-Bao Liu. "A Predicted Mannoprotein Cmp1 Regulates Fungal Virulence in Cryptococcus neoformans." Pathogens 9, no. 11 (October 24, 2020): 881. http://dx.doi.org/10.3390/pathogens9110881.

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The capsule of the fungal pathogen Cryptococcus neoformans consists of glucuronoxylomannan (GXM), glucuronoxylomannogalactan (GXMGal), and mannoproteins (MPs). MPs are a kind of glycoproteins with low content but high immunogenicity, which can stimulate the immune protection of the host. However, there is not much information about the role of mannoproteins in virulence of the human fungal pathogen C. neoformans. In this study, we reported the identification and functional analysis of a predicted mannoprotein Cmp1 that regulates fungal virulence in C. neoformans. Gene expression pattern analysis indicates that the CMP1 gene was ubiquitously expressed at all stages of cryptococcal development. Subcellular localization analysis indicated that Cmp1 was localized in the cytoplasm of cryptococcal cells. Disruption or overexpression of CMP1 results in impairing capsule formation in Cryptococcus, but it does not affect the melanin production and sensitivity under various stress conditions, nor does it affect the sexual reproduction process of Cryptococcus. Survival assay showed that the pathogenicity of the cmp1Δ mutant or the CMP1 overexpression strain was significantly attenuated in a murine inhalation model of cryptococcosis. In conclusion, our findings implied that the mannoprotein Cmp1 is required for the virulence of C. neoformans.

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Conn, Brittney N., and Karen L. Wozniak. "Innate Pulmonary Phagocytes and Their Interactions with Pathogenic Cryptococcus Species." Journal of Fungi 9, no. 6 (May 27, 2023): 617. http://dx.doi.org/10.3390/jof9060617.

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Cryptococcus neoformans is an opportunistic fungal pathogen that causes over 180,000 annual deaths in HIV/AIDS patients. Innate phagocytes in the lungs, such as dendritic cells (DCs) and macrophages, are the first cells to interact with the pathogen. Neutrophils, another innate phagocyte, are recruited to the lungs during cryptococcal infection. These innate cells are involved in early detection of C. neoformans, as well as the removal and clearance of cryptococcal infections. However, C. neoformans has developed ways to interfere with these processes, allowing for the evasion of the host’s innate immune system. Additionally, the innate immune cells have the ability to aid in cryptococcal pathogenesis. This review discusses recent literature on the interactions of innate pulmonary phagocytes with C. neoformans.

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Voelz, Kerstin, David A. Lammas, and Robin C. May. "Cytokine Signaling Regulates the Outcome of Intracellular Macrophage Parasitism by Cryptococcus neoformans." Infection and Immunity 77, no. 8 (June 1, 2009): 3450–57. http://dx.doi.org/10.1128/iai.00297-09.

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ABSTRACT The pathogenic yeast Cryptococcus neoformans and C. gattii commonly cause severe infections of the central nervous system in patients with impaired immunity but also increasingly in immunocompetent individuals. Cryptococcus is phagocytosed by macrophages but can then survive and proliferate within the phagosomes of these infected host cells. Moreover, Cryptococcus is able to escape into the extracellular environment via a recently discovered nonlytic mechanism (termed expulsion or extrusion). Although it is well established that the host's cytokine profile dramatically affects the outcome of cryptococcal disease, the molecular basis for this effect is unclear. Here, we report a systematic analysis of the influence of Th1, Th2, and Th17 cytokines on the outcome of the interaction between macrophages and cryptococci. We show that Th1 and Th17 cytokines activate, whereas Th2 cytokines inhibit, anticryptococcal functions. Intracellular yeast proliferation and cryptococcal expulsion rates were significantly lower after treatment with the Th1 cytokines gamma interferon and tumor necrosis factor alpha and the Th17 cytokine interleukin-17 (IL-17). Interestingly, however, the Th2 cytokines IL-4 and IL-13 significantly increased intracellular yeast proliferation while reducing the occurrence of pathogen expulsion. These results help explain the observed poor prognosis associated with the Th2 cytokine profile (e.g., in human immunodeficiency virus-infected patients).

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Franco, Débora Quioqueti de Souza, Gabriela Bócoli Martins de Oliveira, Ana Carolina de Souza Luiz, Lucas Bessa, Poliana Silva Beker dos Reis, and Lídia Hilderbrand Pulz. "Pneumonia e leptomeningite criptocócica em felino: relato de caso." Revista de Educação Continuada em Medicina Veterinária e Zootecnia do CRMV-SP 17, no. 2 (August 5, 2019): 14–22. http://dx.doi.org/10.36440/recmvz.v17i2.37917.

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A criptococose é uma doença fúngica infecciosa, tegumentar e/ou sistêmica, crônica, de distribuição global, causada por levedura sapróbia do gênero Cryptococcus que pode infectar humanos, animais silvestres e mamíferos domésticos, especialmente felinos domésticos. Duas espécies estão mais diretamente envolvidas com a doença: o Cryptococcus neoformans e o Cryptococus gattii, porém pacientes imunocomprometidos têm, como principal causador, o Cryptococcus neoformans. Todavia, O Cryptococcus gattii, além de afetar hospedeiros imunossuprimidos, também pode causar a doença em indivíduos imunocompetentes. Este relato apresenta os achados clínicos e o diagnóstico firmado com o exame histopatológico de um caso de pneumonia e leptomeningite criptocócica em um felino, macho, sem raça definida, de cinco anos de idade, atendido no Hospital Veterinário “Dr. Vicente Borelli” – do Centro Universitário da Fundação de Ensino Octávio Bastos (Unifeob).

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Steen, B. R., S. Zuyderduyn, D. L. Toffaletti, M. Marra, S. J. M. Jones, J. R. Perfect, and J. Kronstad. "Cryptococcus neoformans Gene Expression during Experimental Cryptococcal Meningitis." Eukaryotic Cell 2, no. 6 (December 2003): 1336–49. http://dx.doi.org/10.1128/ec.2.6.1336-1349.2003.

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ABSTRACT Cryptococcus neoformans, an encapsulated basidiomycete fungus of medical importance, is capable of crossing the blood-brain barrier and causing meningitis in both immunocompetent and immunocompromised individuals. To gain insight into the adaptation of the fungus to the host central nervous system (CNS), serial analysis of gene expression (SAGE) was used to characterize the gene expression profile of C. neoformans cells recovered from the CNS of infected rabbits. A SAGE library was constructed, and 49,048 tags were sequenced; 16,207 of these tags were found to represent unique sequences or tag families. Of the 304 most-abundant tags, 164 were assigned to a putative gene for subsequent functional grouping. The results (as determined according to the number of tags that identified genes encoding proteins required for these functions) indicated that the C. neoformans cells were actively engaged in protein synthesis, protein degradation, stress response, small-molecule transport, and signaling. In addition, a high level of energy requirement of the fungal cells was suggested by a large number of tags that matched putative genes for energy production. Taken together, these findings provide the first insight into the transcriptional adaptation of C. neoformans to the host environment and identify the set of fungal genes most highly expressed during cerebrospinal fluid infection.

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Poley, Marian, Richard Koubek, Leonard Walsh, and Brian McGillen. "Cryptococcal Meningitis in an Apparent Immunocompetent Patient." Journal of Investigative Medicine High Impact Case Reports 7 (January 2019): 232470961983457. http://dx.doi.org/10.1177/2324709619834578.

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Cryptococcal meningitis is an uncommon and severe infection that tends to affect immunocompromised hosts worldwide and in the United States. Annually it is estimated that there are 200 000 cases of cryptococcal meningitis, with the most recent estimate of 3400 cases per year in the United States alone. However, despite the low incidence, 1-year mortality is estimated at 20% to 30% even with long-term consolidation antifungal therapy. A 37-year-old man presented to the emergency department with headaches, dysarthria, hallucinations, and acute worsening of altered mental status, and he was found to have increased intracranial pressure, cerebrospinal fluid leukocytosis, and few encapsulated yeasts consistent with Cryptococcus neoformans meningitis in addition to radiologic evidence consistent with a cryptococcoma of the lungs. This report highlights the occurrence of Cryptococcus neoformans meningitis in a presumed immunocompetent host. The clinician should be aware of sources of minor immunosuppression, as they may contribute to development of Cryptococcus neoformans meningitis. Mortality in this condition remains high due to subacute presentations and delayed diagnosis in non-immunocompromised patients.

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Paterson, D. "Cryptococcus neoformans infection." Liver Transplantation 8, no. 9 (September 2002): 846–47. http://dx.doi.org/10.1053/jlts.2002.32261.

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Recio, Raul, and Ana Perez-Ayala. "Cryptococcus neoformans Meningoencephalitis." New England Journal of Medicine 379, no. 3 (July 19, 2018): 281. http://dx.doi.org/10.1056/nejmicm1801051.

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Mustiani, Siti Nabila, Yunan Jiwintarum, and Yudha Anggit Jiwantoro. "Studi Jamur Cryptococcus Neoformans Penyebab Kriptokokosis pada Kotoran Burung, Tanah, dan Udara di Pasar Burung Lingkungan Sindu dengan Media Potato Dextrose Agar (PDA)." JURNAL KESEHATAN POLTEKKES KEMENKES RI PANGKALPINANG 7, no. 1 (October 17, 2019): 30. http://dx.doi.org/10.32922/jkp.v7i1.82.

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Cryptococcus neoformans adalah jamur patogen oportunistik penyebab kriptokokosis, yaitu mikosis yang berpotensi mematikan pada manusia. Jamur ini banyak terdapat pada lingkungan yang tercemar kotoran burung seperti pasar burung. Salah satu pasar burung yang keadaan lingkungannya mendukung untuk pertumbuhan Cryptococcus neoformans adalah pasar burung Lingkungan Sindu, namun belum pernah diteliti tentang adanya jamur Cryptococcus neoformans di lingkungan tersebut. Penelitian ini bertujuan untuk mengetahui studi jamur Cryptococcus neoformans penyebab kriptokokosis pada kotoran burung, tanah, dan udara di pasar burung Lingkungan Sindu dengan media Potato Dextrose Agar (PDA). Penelitian ini menggunakan metode observasional deskriptif dengan total 12 sampel yang diambil dari 4 area di pasar burung Lingkungan Sindu. Data yang dikumpulkan berupa hasil identifikasi makroskopis dan mikroskopis koloni yang tumbuh pada media PDA. Hasil identifikasi menunjukkan bahwa Cryptococcus neoformans terdapat pada 2 sampel dari 4 sampel kotoran burung, 1 sampel dari 4 sampel udara, dan tidak terdapat pada sampel tanah. Hal ini menunjukkan bahwa jamur Cryptococcus neoformans ditemukan paling banyak pada sampel kotoran burung yaitu 50%, kemudian pada sampel udara yaitu 25%, sementara pada sampel tanah tidak ditemukan jamur Cryptococcus neoformans (0%).

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Pal, M. "Cryptococcus neoformans var. neoformans and Munia Birds Cryptococcus neofovmans var. neoformans bei Prachtfinken." Mycoses 32, no. 5 (April 24, 2009): 250–52. http://dx.doi.org/10.1111/j.1439-0507.1989.tb02242.x.

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Alobaidi, Demah, Abdullahi Elsheikh Mahgoub, Ghassan Bachuwa, and Danielle Osterholzer. "Cryptococcus neoformans var. grubii septic arthritis in an immunocompromised patient on haemodialysis with history of splenectomy and sarcoidosis." BMJ Case Reports 15, no. 7 (July 2022): e248217. http://dx.doi.org/10.1136/bcr-2021-248217.

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A male adult in his mid-40s with end-stage renal disease (ESRD) on haemodialysis, with history of splenectomy and sarcoidosis, developed septic arthritis of the knee. Excision and drainage was performed and empiric antibiotics were initiated. Cultures were initially negative without clinical improvement. Eventually, the aerobic synovial fluid culture grew Cryptococcus neoformans (formerly Cryptococcus neoformans var. grubii). The patient was treated with liposomal amphotericin B and then switched to fluconazole until the infection resolved. This case highlights the less well-recognised association between cryptococcal arthritis and immunodeficiency states like ESRD, splenectomy and sarcoidosis.

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Gupta, Munesh K., Ragini Tilak, Namrata Pal, Ashish Kumar Singh, Jaya Chakravarty, and Bhupendra Kumar. "Cryptococcus neoformans var. grubii: The In Vitro Antifungal Susceptibility Pattern in Addition to the Quantification of Phospholipase and Proteinase Enzymatic Activities." Avicenna Journal of Clinical Microbiology and Infection 10, no. 1 (March 29, 2023): 32–37. http://dx.doi.org/10.34172/ajcmi.2023.3367.

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Background: Cryptococcal meningoencephalitis is a life-threatening fungal infection in human immunodeficiency virus (HIV)-infected patients. Cryptococcus neoformans var. grubii and neoformans are the causative agents that usually respond well to fluconazole and amphotericin B. However, resistance/ non-responding cryptococcal meningitis cases to fluconazole and amphotericin B have been reported globally. Methods: The causative Cryptococcus was identified by phenotypic and singleplex polymerase chain reaction (PCR) targeting the putative sugar transporter (STR1) gene. In addition, the phospholipase and proteinase enzymatic activities of the isolates were determined by the plate method using egg yolk agar and bovine serum albumin agar plates, respectively. Finally, the in-vitro minimal inhibitory concentration (MIC) of fluconazole, voriconazole, and amphotericin B against isolated C. neoformans strains was determined by the broth microdilution method. Results: A total of 50 C. neoformans strains were isolated from the cerebrospinal fluid of HIV-infected patients, which were further identified as variety grubii by simplex polymerase chain reaction (PCR). All the isolated strains producing phospholipase and proteinase enzymes were determined by the calculation of Pz, a ratio of colony diameter and diameter of colony plus the precipitation zone. A comparative high proteinase enzyme activity was observed, and these strains produced medium to high phospholipase (mean Pz 0.3720±0.082, range 0.23-0.56) and proteinase activity (Mean Pz 0.3069±0.086, range 0.012- 0.54). A varied antifungal MIC was detected, and voriconazole had the lowest MIC50 and MIC90 (0.03 & 0.06 µg/mL) in comparison to fluconazole and amphotericin B. Conclusion: Cryptococcus neoformans var. grubii is the commonest cause of cryptococcal meningoencephalitis in HIV-infected patients. The isolates had varied extracellular hydrolytic enzyme activities. The emergence of C. neoformans strains with higher fluconazole MIC (≥4 mcg/mL) could have resulted in treatment failure.

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Kobayashi, Cláudia Castelo Branco Artiaga, Lúcia Kioko Hasimoto e. Souza, Orionalda de Fátima Lisboa Fernandes, Sula Cristina Assis de Brito, Ana Cláudia Silva, Efigênia Dantas de Sousa, and Maria do Rosário Rodrigues Silva. "Characterization of Cryptococcus neoformans isolated from urban environmental sources in Goiânia, Goiás State, Brazil." Revista do Instituto de Medicina Tropical de São Paulo 47, no. 4 (August 2005): 203–7. http://dx.doi.org/10.1590/s0036-46652005000400005.

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Cryptococcus neoformans is an opportunistic fungal pathogen that causes meningoencephalitis as the most frequent clinical presentation in immunocompromised patients, mainly in people infected by HIV. This fungus is an environmental encapsulated yeast, commonly found in soil enriched with avian droppings and plant material. A total of 290 samples of pigeon and the other avian droppings, soil, ornamental trees and vegetable material associated with Eucalyptus trees were collected to study environmental sources of Cryptococcus species in Goiânia, Goiás State. The determination of varieties, serotypes and the susceptibility in vitro to fluconazole, itraconazole and amphotericin B of C. neoformans isolates were performed. C. neoformans var. grubii (serotype A) was found in 20.3% (36/177) of pigeon dropping samples and in 14.3% (5/35) of samples of Eucalyptus. None of the environmental isolates of C. neoformans showed in vitro resistance to three antifungal agents. The knowledge of major route for human cryptococcal infection (inhalation of infectious particles from saprophytic sources) and a total of 60 C. neoformans isolates obtained from AIDS patients with cryptococcal meningitis between October 2001 and April 2002 justify the study of the habitats of these yeasts as probable sources of cryptococcosis in this city.

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Zhao, Youbao, Jianfeng Lin, Yumeng Fan, and Xiaorong Lin. "Life Cycle ofCryptococcus neoformans." Annual Review of Microbiology 73, no. 1 (September 8, 2019): 17–42. http://dx.doi.org/10.1146/annurev-micro-020518-120210.

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Cryptococcus neoformans is a ubiquitous environmental fungus and an opportunistic pathogen that causes fatal cryptococcal meningitis. Advances in genomics, genetics, and cellular and molecular biology of C. neoformans have dramatically improved our understanding of this important pathogen, rendering it a model organism to study eukaryotic biology and microbial pathogenesis. In light of recent progress, we describe in this review the life cycle of C. neoformans with a special emphasis on the regulation of the yeast-to-hypha transition and different modes of sexual reproduction, in addition to the impacts of the life cycle on cryptococcal populations and pathogenesis.

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Dominic, RM Saldanha, H. V. Prashanth, Shalini Shenoy, and Shrikala Baliga. "Diagnostic Value of Latex Agglutination in Cryptococcal Meningitis." Journal of Laboratory Physicians 1, no. 02 (July 2009): 067–68. http://dx.doi.org/10.4103/0974-2727.59702.

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ABSTRACT Background: Cryptococcus neoformans is the most common fungal pathogen to infect the central nervous system, and an effective diagnostic method is therefore necessary for the early diagnosis of cryptococcal meningitis. Aim: The efficacy of India ink preparation, cerebrospinal fluid (CSF) culture and CSF cryptococcal antigen detection by the latex agglutination test for diagnosis of cryptococcal meningitis are compared to determine the most efficient test. Materials and Methods: Two hundred CSF samples from human immunodeficiency virus - positive patients suspected to be suffering from meningitis were screened for Cryptococcus neoformans. Results: Latex agglutination for cryptococcal antigen detection was found to be more sensitive compared to India ink staining and CSF culture. Conclusion: Antigen detection by latex agglutination proved to be both sensitive and specific method for the diagnosis of cryptococcal meningitis. Rapid, early diagnosis of infection by detection of cryptococcal antigen by latex agglutination may alter the prognosis for these patients.

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Salkowski, Cindy A., and Edward Balish. "Susceptibility of congenitally immunodeficient mice to a nonencapsulated strain of Cryptococcus neoformans." Canadian Journal of Microbiology 37, no. 11 (November 1, 1991): 834–39. http://dx.doi.org/10.1139/m91-144.

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The susceptibility of congenitally immunodeficient mice to a nonencapsulated strain of Cryptococcus neoformans (strain M7) was evaluated. Gnotobiotic mice with defined congenital defects in innate immunity (beige) or cell-mediated immunity (athymic) or with combined defects in innate and cellular immunity (beige athymic) were i.v. challenged with C. neoformans M7. The nonencapsulated strain of C. neoformans produced a persistant low-grade infection in the brains of all immunodeficient and immunocompetent mice used in this study. Immunocompetent mice (nu/+;bg/+) and immunodeficient bg/bg mice readily cleared nonencapsulated cryptococci from their kidneys, liver, lungs, and spleen. In contrast to nu/+ mice, nu/nu mice had a reduced capacity to clear nonencapsulated cryptococci from their kidneys and liver after i.v. challenge. Both bg/bg–nu/nu and bg/bg–nu/+ mice developed a low-grade infection in their kidneys, liver, lungs, and spleen, which was maintained throughout the 21-day study. Persistent infections were not due to reversion to an encapsulated state. These data indicate that a capsule may not always be necessary for C. neoformans to survive, in vivo, in tissues of immunodeficient and immunocompetent mice. Key words: Cryptococcus neoformans, capsule, immunodeficient mice.

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Islam, Jemima, Mir Wasim Ali, Sabyasachi Chowdhury, Soumyadip Rakshit, Md Karimulla Mondal, Anup Kumar Datta, Kokila Banerjee, and Soumitra Ghosh. "Disseminated Cryptococcosis in an Immunocompetent Patient: A Case Study." Asian Journal of Research in Infectious Diseases 14, no. 2 (August 7, 2023): 52–59. http://dx.doi.org/10.9734/ajrid/2023/v14i2288.

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Cryptococcosis is the fungal infection caused by the yeast that belongs to the cryptococcus species which is divided into two broad categories, Cryptococcus neoformans and Cryptococcus gattii. Cryptococcosis is the opportunistic infection in the immunocompromised individual, particularly in HIV infected individual. In immunocompetent individuals, there may be serological evidence of cryptococcal infection, but cryptococcal disease is very rare in the absence of impaired immunity. Here we are reporting a case of disseminated cryptococcosis (multiple cold abscesses, sacroiliitis and asymptomatic pulmonary nodules) in an immunocompetent patient, which was initially thought to be mycobacterium tuberculosis infection.

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Favalessa, Olivia Cometti, Luciano Correa Ribeiro, Tomoko Tadano, Cor Jesus Fernandes Fontes, Flávio Basili Dias, Bruno Pereira Albuquerque Coelho, and Rosane Christine Hahn. "Primeira descrição da caracterização fenotípica e susceptibilidade in vitro a drogas de leveduras do gênero Cryptococcus spp isoladas de pacientes HIV positivos e negativos, Estado de Mato Grosso." Revista da Sociedade Brasileira de Medicina Tropical 42, no. 6 (December 2009): 661–65. http://dx.doi.org/10.1590/s0037-86822009000600010.

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Foram avaliados 37 isolados de 10 pacientes HIV negativos e 26 positivos, em Mato Grosso. Exame direto, cultura e quimiotipagem de espécies foram realizados. Cetoconazol, itraconazol, voriconazol, fluconazol e anfotericina B foram avaliados. Foram identificadas 37 leveduras do gênero Cryptococcus spp sendo 26 de pacientes HIV- positivos (25 Cryptococcus neoformans e um Cryptococcus gattii) e 10 de HIV- negativos (cinco Cryptococcus neoformans e cinco Cryptococcus gattii). Considerando isolados clínicos (Cryptococcus neoformans) de HIV positivos observou-se resistência (8% e 8,7%) e susceptibilidade dose-dependência (20% e 17,4%) para fluconazol e itraconazol respectivamente. Para isolados de Cryptococcus neoformans oriundos de pacientes HIV negativos, observou-se susceptibilidade dose-dependência (40%) ao fluconazol. Os isolados de Cryptococcus gattii provenientes de pacientes HIV- negativos mostraram-se susceptíveis a todos os antifúngicos, exceto um isolado de Cryptococcus gattii que foi susceptível dose-dependente ao fluconazol (20%). O isolado proveniente do paciente HIV- positivo demonstrou resistência ao fluconazol (CIM > 256µg/mL) e itraconazol (CIM=3µg/mL).

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Jassem, Inaam K., Sudad J. Mohammed, Tawfeq W. Tawfeq, and Jassem M. Karhoot. "Cryptococcus neoformans Isolated from burn Patients in Burn Hospital in Baghdad." Journal of the Faculty of Medicine Baghdad 55, no. 4 (January 2, 2014): 362–464. http://dx.doi.org/10.32007/jfacmedbagdad.554586.

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Background: wound infections are associated with increased morbidity and mortality. Etiologic agents of wound infections vary with geographical location Patients and Methods: All burn patients admitted to Specialized Burn Hospital from November 2011 to May 2012. Once fungal infection was suspected clinically, swabs were harvested for the culture of yeast. The sensitivities of the identified yeast were determined and the positive samples and cases were analyzed.Objective: This study presents Cryptococcus neoformans and their Characteristics identified from burn patients at a major Iraqi Specialized Burn Hospital. Result: The most predominant yeast isolates was Candida species which represented (56.94%), followed by Cryptococcus species (27.77%) . Twenty fungal cultures were positive for Cryptococcus species. Cryptococcus neoformanus was recorded higher percentages 8 (11.11%) follows by Cryptococcus laurentii 6 (8.33%), Cryptococcus albidus 4 (5.55%) and Cryptococcus humicola 2 ( 2.77%). Conclusion: Cryptococcus species isolated from burn patient in a Burn Hospital in Baghdad were identified.

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Castle, Sherry A., Elizabeth A. Owuor, Stephanie H. Thompson, Michelle R. Garnsey, J. Stacey Klutts, Tamara L. Doering, and Steven B. Levery. "β1,2-Xylosyltransferase Cxt1p Is Solely Responsible for Xylose Incorporation into Cryptococcus neoformans Glycosphingolipids." Eukaryotic Cell 7, no. 9 (August 1, 2008): 1611–15. http://dx.doi.org/10.1128/ec.00458-07.

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ABSTRACT The Manα1,3(Xylβ1,2)Manα structural motif is common to both capsular polysaccharides of Cryptococcus neoformans and to cryptococcal glycosphingolipids. Comparative analysis of glycosphingolipid structural profiles in wild-type and mutant strains showed that the Xylβ1,2-transferase (Cxt1p) that participates in capsular polysaccharide biosynthesis is also the sole transferase responsible for adding xylose to C. neoformans glycosphingolipids.

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Scott, Keela, Caitlyn Smith, Daniel Walker, and Belinder Fender. "Cryptococcal Meningitis in an Immunocompetent Male: Case Report." RRNMF Neuromuscular Journal 4, no. 2 (June 19, 2023): 7–9. http://dx.doi.org/10.17161/rrnmf.v4i2.18989.

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Cryptococcal meningitis is a life-threatening condition caused by an invasive, opportunistic, encapsulated saprophytic fungus, either Cryptococcus neoformans or Cryptococcus gattii most often in immunocompromised patients, especially those with human immunodeficiency virus (HIV). Overwhelming invasive infection of immunocompetent patients is rather uncommon, and diagnosis is often challenging due to a more indolent course. We present a case of cryptococcal meningitis (CM) in a 72-year-old immunocompetent male following a recent motor vehicle accident.

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Kretschmer, Matthias, Joyce Wang, and James W. Kronstad. "Peroxisomal and Mitochondrial β-Oxidation Pathways Influence the Virulence of the Pathogenic Fungus Cryptococcus neoformans." Eukaryotic Cell 11, no. 8 (June 15, 2012): 1042–54. http://dx.doi.org/10.1128/ec.00128-12.

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ABSTRACTAn understanding of the connections between metabolism and elaboration of virulence factors during host colonization by the human-pathogenic fungusCryptococcus neoformansis important for developing antifungal therapies. Lipids are abundant in host tissues, and fungal pathogens in the phylum basidiomycota possess both peroxisomal and mitochondrial β-oxidation pathways to utilize this potential carbon source. In addition, lipids are important signaling molecules in both fungi and mammals. In this report, we demonstrate that defects in the peroxisomal and mitochondrial β-oxidation pathways influence the growth ofC. neoformanson fatty acids as well as the virulence of the fungus in a mouse inhalation model of cryptococcosis. Disease attenuation may be due to the cumulative influence of altered carbon source acquisition or processing, interference with secretion, changes in cell wall integrity, and an observed defect in capsule production for the peroxisomal mutant. Altered capsule elaboration in the context of a β-oxidation defect was unexpected but is particularly important because this trait is a major virulence factor forC. neoformans. Additionally, analysis of mutants in the peroxisomal pathway revealed a growth-promoting activity forC. neoformans, and subsequent work identified oleic acid and biotin as candidates for such factors. Overall, this study reveals that β-oxidation influences virulence inC. neoformansby multiple mechanisms that likely include contributions to carbon source acquisition and virulence factor elaboration.

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Voelz, Kerstin, and Robin C. May. "Cryptococcal Interactions with the Host Immune System." Eukaryotic Cell 9, no. 6 (April 9, 2010): 835–46. http://dx.doi.org/10.1128/ec.00039-10.

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ABSTRACT Opportunistic pathogens have become of increasing medical importance over the last decade due to the AIDS pandemic. Not only is cryptococcosis the fourth-most-common fatal infectious disease in sub-Saharan Africa, but also Cryptococcus is an emerging pathogen of immunocompetent individuals. The interaction between Cryptococcus and the host's immune system is a major determinant for the outcome of disease. Despite initial infection in early childhood with Cryptococcus neoformans and frequent exposure to C. neoformans within the environment, immunocompetent individuals are generally able to contain the fungus or maintain the yeast in a latent state. However, immune deficiencies lead to disseminating infections that are uniformly fatal without rapid clinical intervention. This review will discuss the innate and adaptive immune responses to Cryptococcus and cryptococcal strategies to evade the host's defense mechanisms. It will also address the importance of these strategies in pathogenesis and the potential of immunotherapy in cryptococcosis treatment.

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Santangelo, Rosemary, Hans Zoellner, Tania Sorrell, Christabel Wilson, Christine Donald, Julianne Djordjevic, Yi Shounan, and Lesley Wright. "Role of Extracellular Phospholipases and Mononuclear Phagocytes in Dissemination of Cryptococcosis in a Murine Model." Infection and Immunity 72, no. 4 (April 2004): 2229–39. http://dx.doi.org/10.1128/iai.72.4.2229-2239.2004.

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ABSTRACT Secreted phospholipase B (PLB) activity promotes the survival and replication of Cryptococcus neoformans in macrophages in vitro. We therefore investigated the role of mononuclear phagocytes and cryptococcal PLB in the dissemination of infection in a mouse model, using C. neoformans var. grubii wild-type strain H99, a PLB1 deletion mutant (Δplb1), and a reconstituted strain (Δplb1rec ). PLB facilitated the entry of endotracheally administered cryptococci into lung IM. PLB was also required for lymphatic spread from the lung to regional lymph nodes and for entry into the blood. Langhans-type giant cells containing budding cryptococci were seen free in the lymphatic sinuses of hilar nodes of H99- and Δplb1rec -infected mice, suggesting that they may have a role in the dissemination of cryptococcal infection. The transfer of infected lung macrophages to recipient mice by tail vein injections demonstrated that these cells can facilitate hematogenous dissemination of cryptococci to the brain, independent of cryptococcal PLB secretion. PLB activities of cryptococci isolated from lung macrophages or infected brains were not persistently increased. We conclude that mononuclear phagocytes are a vehicle for cryptococcal dissemination and that PLB activity is necessary for the initiation of interstitial pulmonary infections and for dissemination from the lung via the lymphatics and blood. PLB is not, however, essential for the establishment of neurological infections when cryptococci are presented within, or after passage through, mononuclear phagocytes.

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Khanal, Basudha, S. K. Sharma, and M. Deb. "CRYPTOCOCCAL MENINGITIS IN A NON-AIDS PATIENT." Journal of Nepal Medical Association 41, no. 142 (January 1, 2003): 323–25. http://dx.doi.org/10.31729/jnma.759.

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Cryptococcal meningitis that occurred in a patient with no obviouspredisposing factor is reported. The necessity to identify this entity in thecases of chronic meningitis is discussed.ABSTRACTKey Words: Meningitis, Cryptococcus neoformans

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de Oliveira, Haroldo C., Rafael F. Castelli, Flavia C. G. Reis, Juliana Rizzo, and Marcio L. Rodrigues. "Pathogenic Delivery: The Biological Roles of Cryptococcal Extracellular Vesicles." Pathogens 9, no. 9 (September 16, 2020): 754. http://dx.doi.org/10.3390/pathogens9090754.

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Extracellular vesicles (EVs) are produced by all domains of life. In fungi, these structures were first described in Cryptococcus neoformans and, since then, they were characterized in several pathogenic and non-pathogenic fungal species. Cryptococcal EVs participate in the export of virulence factors that directly impact the Cryptococcus–host interaction. Our knowledge of the biogenesis and pathogenic roles of Cryptococcus EVs is still limited, but recent methodological and scientific advances have improved our understanding of how cryptococcal EVs participate in both physiological and pathogenic events. In this review, we will discuss the importance of cryptococcal EVs, including early historical studies suggesting their existence in Cryptococcus, their putative mechanisms of biogenesis, methods of isolation, and possible roles in the interaction with host cells.

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Martinez, Luis R., and Arturo Casadevall. "Susceptibility of Cryptococcus neoformans Biofilms to Antifungal Agents In Vitro." Antimicrobial Agents and Chemotherapy 50, no. 3 (March 2006): 1021–33. http://dx.doi.org/10.1128/aac.50.3.1021-1033.2006.

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ABSTRACT Microbial biofilms contribute to virulence and resistance to antibiotics by shielding microbial cells from host defenses and antimicrobial drugs, respectively. Cryptococcus neoformans was demonstrated to form biofilms in polystyrene microtiter plates. The numbers of CFU of disaggregated biofilms, 2,3-bis(2-methoxy-4-nitro-5-sulfophenyl)-5-[(phenylamino)carbonyl]-2H-tetrazolium hydroxide reduction, and light and confocal microscopy were used to measure the fungal mass, the metabolic activity, and the appearance of C. neoformans biofilms, respectively. Biofilm development by C. neoformans followed a standard sequence of events: fungal surface attachment, microcolony formation, and matrix production. The susceptibilities of C. neoformans cells of the biofilm and planktonic phenotypes to four antifungal agents were examined. The exposure of C. neoformans cells or preformed cryptococcal biofilms to fluconazole or voriconazole did not result in yeast growth inhibition and did not affect the metabolic activities of the biofilms, respectively. In contrast, both C. neoformans cells and preformed biofilms were susceptible to amphotericin B and caspofungin. However, C. neoformans biofilms were significantly more resistant to amphotericin B and caspofungin than planktonic cells, and their susceptibilities to these drugs were further reduced if cryptococcal cells contained melanin. A spot enzyme-linked immunosorbent assay and light and confocal microscopy were used to investigate how antifungal drugs affected C. neoformans biofilm formation. The mechanism by which amphotericin B and caspofungin interfered with C. neoformans biofilm formation involved capsular polysaccharide release and adherence. Our results suggest that biofilm formation may diminish the efficacies of some antifungal drugs during cryptococcal infection.

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Chen, Sunxiao, Hongli Yan, Lei Zhang, Wei Kong, Yi Sun, Weiwei Zhang, Yan Chen, and Anmei Deng. "Cryptococcus Neoformans Infection and Immune Cell Regulation in Human Monocytes." Cellular Physiology and Biochemistry 37, no. 2 (2015): 537–47. http://dx.doi.org/10.1159/000430375.

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Background/Aims: Cryptococcus neoformans infections are becoming increasingly prevalent and remain a life-threatening clinical issue in immune-compromised hosts. The microorganism evades a variety of endogenous anti-fungal mechanims of host immune cells. The signaling pathways in human immune cells that become activated in response to Cryptococcus neoformans infection have yet to be fully characterized. Methods: Human monocytes were incubated with Cryptococcus neoformans, and the whole transcriptome of monocytes was sequenced before and after exposure to Cryptococcus neoformans using mass parallel sequencing techniques. Based on the genes that demonstrated altered expression patterns, we performed GO and KEGG enrichment analysis to further characterize the pathways involved in monocyte activation by Cryptococcus neoformans. Results: We found that immune and inflammatory responses, as well as chemotaxis, were the most heavily activated cellular events. Specifically, the toll-like receptor, tumor necrosis factor, NF-kB and Jak-STAT pathways were the most active pathways in response to Cryptococcus neoformans infection. The sequencing data of selected genes from the transcriptome analysis were further validated by real-time polymerase chain reactions. Conclusion: Taken together, our study is the first characterization of the transcriptome alterations in human immune cells upon C. neoformans infection, providing additional information that may be helpful in discovering novel anti-fungal targets.

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Perfect, J. R., G. M. Cox, R. K. Dodge, and W. A. Schell. "In vitro and in vivo efficacies of the azole SCH56592 against Cryptococcus neoformans." Antimicrobial Agents and Chemotherapy 40, no. 8 (August 1996): 1910–13. http://dx.doi.org/10.1128/aac.40.8.1910.

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Multiple isolates of Cryptococcus neoformans were tested to compare the in vitro activity of a new triazole, SCH56592, with those of amphotericin B, fluconazole, and itraconazole, MICs of each drug were determined, and minimum fungicidal concentrations of SCH56592 and amphotericin B were measured. MICs of SCH56592 were lower than those of amphotericin B and fluconazole but not those of itraconazole. Minimum fungicidal concentrations of SCH56592 were lower than those of amphotericin B. SCH56592 in the presence of human serum produces an in vitro fungicidal effect for Cryptococcus neoformans. The data indicate that SCH56592 might exert fungicidal as well as inhibitory properties in vivo. On the basis of these results, SCH56592 was evaluated with a rabbit model of experimental cryptococcal meningitis; SCH56592 treatment was compared with treatment with fluconazole. Despite no detectable drug concentrations in the cerebrospinal fluid, the activity of SCH56592 against C. neoformans infection was equivalent to that of fluconazole. SCH56592 has potent in vitro activity against C. neoformans and compares favorably to treatment with fluconazole for a central nervous system infection. SCH56592 should be studied for use in humans with cryptococcal infections.

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Franzot, Sarah P., Ira F. Salkin, and Arturo Casadevall. "Cryptococcus neoformans var.grubii: Separate Varietal Status for Cryptococcus neoformans Serotype A Isolates." Journal of Clinical Microbiology 37, no. 3 (1999): 838–40. http://dx.doi.org/10.1128/jcm.37.3.838-840.1999.

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Cryptococcus neoformans var. neoformanspresently includes isolates which have been determined by the immunologic reactivity of their capsular polysaccharides to be serotype A and those which have been determined to be serotype D. However, recent analyses of the URA5 sequences and DNA fingerprinting patterns suggest significant genetic differences between the two serotypes. Therefore, we propose to recognize these genotypic distinctions, as well as previously reported phenotypic differences, by restricting C. neoformans var. neoformans to isolates which are serotype D and describing a new variety, C. neoformans var. grubii, for serotype A isolates.

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Lee, S. C., D. W. Dickson, C. F. Brosnan, and A. Casadevall. "Human astrocytes inhibit Cryptococcus neoformans growth by a nitric oxide-mediated mechanism." Journal of Experimental Medicine 180, no. 1 (July 1, 1994): 365–69. http://dx.doi.org/10.1084/jem.180.1.365.

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Cryptococcus neoformans is an opportunistic fungus that causes life-threatening meningoencephalitis in 5-10% of patients with acquired immune deficiency syndrome. Cryptococcal meningoencephalitis is characterized by a lymphohistiocytic infiltrate, accumulation of encapsulated forms of C. neoformans, and varying degrees of glial reaction. Little is known about the contribution of endogenous central nervous system cells to the pathogenesis of cryptococcal infections. In this study, we investigated the role of astrocytes as potential effector cells against C. neoformans. Primary cultures of human fetal astrocytes, activated with interleukin 1 beta plus interferon gamma inhibited the growth of C. neoformans. The inhibition of C. neoformans growth was paralleled by production of nitrite, and reversed by the inhibitors of nitric oxide (NO.) synthase, NG-methyl-mono-arginine and NG-nitro-arginine methyl ester. The results suggest a novel function for human astrocytes in host defence and provide a precedent for the use of NO. as an antimicrobial effector molecule by human cells.

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Okudo, Jerome, Valerie F. Civelli, Vishal K. Narang, Royce H. Johnson, Nadir Khan, Brittany Andruszko, and Arash Heidari. "A Rare Case of Cryptococcus gattii Meningitis in Advanced HIV Disease, Sagittal Thrombosis, and Immune Reconstitution Syndrome, Resolved With Isavuconazonium." Journal of Investigative Medicine High Impact Case Reports 8 (January 2020): 232470962095988. http://dx.doi.org/10.1177/2324709620959880.

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Cryptococcus gattii is a species that has received more recognition in the recent past as distinct from Cryptococcus neoformans. C gattii is known to cause meningeal disease in both immunocompetent and immunosuppressed hosts. Patients may be clinically asymptomatic until immunosuppressive conditions occur such as corticosteroid treatment or an HIV infection. HIV-associated cryptococcal infections are most often due to C neoformans. C gattii is found in a minority. Speciation and subtyping of Cryptococcus are not always accomplished. In many parts of the world, there is no availability for speciation of Cryptococcus. Travel history may provide a clue to the most probable species. This case demonstrates a case of C gattii meningitis with a multiplicity of complications. These include advanced HIV disease secondary to nonadherence, immune reconstitution inflammatory syndrome, and superior sagittal sinus thrombosis. The patient represented diagnostic and therapeutic dilemmas over time. Headache was the primary symptom in cryptococcal meningitis, immune reconstitution inflammatory syndrome, and superior sagittal sinus thrombosis. All are discussed in detail as potential etiologies for the primary disease. Isavuconazonium is a relatively new broad-spectrum antifungal azole that was used as salvage therapy.

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Machado, Clenise Canello, Aline Almeida Amaral, and Luiz Carlos Severo. "Cryptococcus neoformans var. neoformans isolado do solo." Revista do Instituto de Medicina Tropical de São Paulo 35, no. 1 (February 1993): 77–79. http://dx.doi.org/10.1590/s0036-46651993000100011.

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Na tentativa de identificar a possível fonte de infecção, inquiriu-se, na história epidemiológica de 42 pacientes portadores de criptococose, o contato com pombos. Informações compatíveis com nicho ecológico do Cryptococcus neoformans foram positivas em 16. Foram colhidas 59 amostras de solo contendo fezes de pombos, penas e material orgânico. O C. neoformans foi detectado em 4. Uma das amostras era originada da capital e três do interior do estado. O sorotipo A do C. neoformans isolado de um liquor coincidiu com o sorotipo da amostra isolada do centro de Porto Alegre, local apontado pelo paciente como possível fonte de infecção, caracterizando caso de Cryptococcus neoformans var. neoformans.

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Journal articles on the topic 'Cryptococcus neoformans'

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