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PubMedDate not supplied

Co-infection by Cryptococcus neoformans and Mycobacterium avium intracellulare in AIDS.

In the observation of various opportunistic pathogens in HIV-positive persons, co-infection by Cryptococcus neoformans together with Mycobacterium avium intracellulare was found if there was a CD4 lymphocyte count as low as 3-20 microl. In 1540 HIV-positive patients under treatment at a Berlin hospital (Auguste-Viktoria-Krankenhaus) during 1985-1994, all AIDS-relevant diseases were examined in a multivariate analysis as variables of influence on the manifestation of a systemic Mycobacterium avium complex (MAC) infection. The analysis involved data on 36 cases of cryptococcosis and 202 cases with a typical clinical course in whom MAC had been detected at sterile body sites. As significant and independent factors of influence, the following were identified: C. neoformans infection, wasting syndrome, lower age, low CD4 lymphocyte count and preceding Pneumocystis carinii pneumonia (PcP) prophylaxis. Cryptococcosis ranged first with an odds ratio of 2.75. The concomitant manifestation of cryptococcosis and systemic MAC infection in six patients is shown. Because both opportunists, C. neoformans and avian mycobacteria, may have their common habitat in droppings of defined species of pet birds, a common source of infection deserves further clinical and epidemiological attention.

Journal Article↗
PubMed1997

Expression of cytokines and inducible nitric oxide synthase mRNA in the lungs of mice infected with Cryptococcus neoformans: effects of interleukin-12.

We have recently established a murine model of pulmonary and disseminated infection with a highly virulent strain of Cryptococcus neoformans and demonstrated that administration of interleukin-12 (IL-12) protected the animals against infection. In this study, we extended these studies by investigating the host defense mechanisms. In particular, we examined the expression of mRNA for helper T-cell 1 (Th1) cytokines (IL-2, lymphotoxin, and gamma interferon [IFN-gamma]), Th2 cytokines (IL-4, -6, and -10), macrophage-derived cytokines (tumor necrosis factor alpha [TNF-alpha], IL-1beta, transforming growth factor beta [TGF-beta, IL-12p40, and IFN-gamma-inducing factor [IGIF]), and inducible nitric oxide synthase (iNOS) in the lungs on days 1, 3, 7, and 14 after infection and following treatment with IL-12. There was little or no expression of mRNAs for Th1 cytokines, TNF-alpha, IL-12p40, IGIF, and iNOS in the infected mice, but expression increased markedly after treatment with IL-12. In contrast, the mRNAs for Th2 cytokines, IL-1beta, and TGF-beta were detected at considerable levels during the early stages of infection, and, interestingly, expression was not suppressed by IL-12 but rather augmented, particularly during the late stage. Similar results were also obtained for IFN-gamma, IL-4, IL-10, and TNF-alpha measured in the lung homogenates by enzyme-linked immunosorbent assay. These results suggest that the predominance of expression of Th2 cytokines and TGF-beta over Th1 cytokines, TNF-alpha, IL-12p40, IGIF, and iNOS is associated with severe lethal infection in mice and that administration of IL-12 protects infected animals by stimulating Th1 cytokines.

Animals↗
PubMed1988

Simultaneous infection with Cryptococcus neoformans and Legionella pneumophila. In vivo expression of common defects in cell-mediated immunity.

We describe 3 patients with simultaneous infection by Cryptococcus neoformans and Legionella pneumophila. Legionnaires' disease (pneumonia) occurred shortly after onset of cryptococcal meningitis in a cardiac transplant patient receiving ciclosporin, a second patient with chronic lymphocytic leukemia and a third patient with Hodgkin's disease and autoimmune hemolytic anemia. Defects in cell-mediated immunity have been identified in patients with hematologic malignancies and in those who have received organ transplants. Clinical and experimental data suggest that the primary host defense mechanism against cryptococcal and Legionella infection involves cell-mediated immunity. Thus, the simultaneous occurrence of cryptococcal and L. pneumophila infection in these 3 patients supports experimental studies which have demonstrated common host defense mechanisms against both pathogens.

Adult↗
PubMed2005

Disseminated Cryptococcus neoformans in a cirrhotic patient.

Disseminated cryptococcal infection often occurs in the setting of an immuncompromised patient. We report a case of disseminated Cryptococcus neoformans in a cirrhotic patient, referred for Orthotopic Liver Transplantation evaluation due to acute hepatic decompensation.

Cryptococcosis↗
PubMed1987

Role of natural killer cells in resistance to Cryptococcus neoformans infections in mice.

Previous studies have suggested a possible role for natural killer (NK) cells in resistance to some fungal infections, including Cryptococcus neoformans infections. The role of NK cells in early clearance of C neoformans from tissues and in long-term survival was studied in mice following intravenous inoculations of the organism. Mice treated with anti-asialo GM1 antiserum to temporarily reduce NK activity demonstrated an increase in colony-forming units (CFU) of C neoformans in the lung 24 hours after an intravenous inoculation of the organism. CFU in liver, spleen, kidney, and brain were not different in anti-asialo GM1 antiserum-treated versus control mice. An NK-specific reagent, anti-NK 1.1 monoclonal antibody, was used to deplete mice of NK cells in vivo for at least 14 days without affecting other natural defenses. The number of C neoformans retained in the lungs 24 hours after inoculation of the organism was significantly greater in NK cell-depleted mice than in controls, although CFU in other organs were unaffected. Following the intravenous inoculation of C neoformans, the survival of anti-NK 1.1-treated mice was not different from control mice. The effect of NK cell activity on resistance to C neoformans was also determined after an intratracheal inoculation of the organism. Mice pretreated with anti-NK 1.1 demonstrated no increases in CFU in the lungs, spleen, or brain as compared with controls. These data indicate that NK cells can play a role in vivo in early resistance against C neoformans if the organism is delivered via the intravenous route. However, NK cells do not play a role in either determining survival after an intravenous inoculation nor in resistance during an infection acquired via the respiratory tract.

Animals↗
PubMedDate not supplied

[Pleural empyema caused by Cryptococcus neoformans in a patient with liver cirrhosis].

Gram negative infections, particularly by E. coli, are usually observed in cirrhotic patients while infections by Cryptococcus neoformans are commonly found in immunosuppressed patients. The case of a cirrhotic patient with hepatitis C virus infection who developed pleural infection by C. neoformans is presented. No disease other than cirrhosis was observed in the patient. The treatment with oral fluconazole was initiated with good clinical response and infection cure. The efficacy of fluconazole in infections by this microorganism has been reported in other cases, mainly in patients with acquired immunodeficiency syndrome. The fact that the patient may be a liver transplant candidate, given the hepatic cirrhosis, leads to speculation as to the need for chronic treatment with fluconazole to avoid reactivation of C. neoformans on initiation of pharmacologic immunosuppression.

Administration, Oral↗
PubMed1968

Modified Littman oxgall agar to isolate Cryptococcus neoformans.

Littman Oxgall Agar was modified by adding an extract of Guizotia abyssinica seeds with a water diluent for rehydration. In this medium, colonies of Cryptococcus neoformans became brown, but the color failed to develop in eight other yeasts and yeast phases of diphasic organisms. The depression of saprophytic fungi noted on Littman Oxgall Agar was not lost in the modification.

Blastomyces↗
PubMed1978

In Vitro and In Vivo Activity of a Synthetic Halogenated Quinoline Against Cryptococcus neoformans.

The minimum inhibitory concentrations of a halogenated quinoline, 3-amino-7-chloro-3,4-dihydro-1-hydroxycarbostyril (CBS), against nine clinical strains of Cryptococcus neoformans were determined by in vitro testing. The CBS was fungistatic at a minimum concentration of 0.2 mug/ml at 48 h for several strains. In vivo toxicity studies were carried out in mice. Mice were also infected with C. neoformans strain Price and injected with various concentrations of CBS. Mean life expectancy of treated groups of animals was increased over infected untreated controls.

Journal Article↗
PubMed1993

A T cell-independent protective host response against Cryptococcus neoformans expressed at the primary site of infection in the lung.

T cell-independent host resistance expressed against a primary lung infection with Cryptococcus neoformans was investigated. Following intratracheal inoculation of the yeast, BALB/cBy scid/scid mice or CD4+ plus CD8+ T cell-depleted BALB/cBy mice developed a primary lung infection that remained stable for several weeks before progressing and disseminating to kill the host. By contrast, normal BALB/cBy hosts resolved the infection after 4 to 8 weeks. Thy+ CD4- CD8- cells were found to accumulate in the pulmonary alveoli of infected scid/scid or normal mice. Depletion of these cells caused the infection to progress more rapidly and resulted 4 weeks later in a 30- to 70-fold increase in yeast numbers in the lungs and dissemination to extrapulmonary sites. Cytofluorometric studies revealed that the Thy+ CD4- CD8- cells responsible were negative for the CD3 T cell marker. A small percentage of these Thy+ CD3- cells expressed asialo-Gm1, but treatment with asialo-Gm1 antibody did not have the same infection-enhancing effect as Thy-1 monoclonal antibody treatment. Further experiments revealed that Thy-1 monoclonal antibody treatment had no effect on the establishment of infectious foci in the brain or liver following intravenous inoculation of the yeast. The data point to the existence of an early resistance mechanism for which Thy+ CD3- CD4- CD8- cells are essential. This mechanism of host defense, while insufficient for complete protection, may be capable of delaying the development of cryptococcal meningoencephalitis by restricting the growth of the yeast at primary sites of infection in the lungs, even in immunodeficient mice.

Animals↗
PubMed1993

Differential host susceptibility to intracerebral infections with Candida albicans and Cryptococcus neoformans.

To investigate the immune defense mechanisms employed against fungi in the brain, mice were experimentally infected by intracerebral inoculation of Candida albicans or Cryptococcus neoformans. Parameters such as median survival time and numbers of yeast cells in the brains were assessed for naive and immunomodulated mice. We found that no mice survived either C. albicans or C. neoformans challenge at doses of > or = 10(6) yeast cells per mouse. However, when the inoculum size was decreased (< or = 10(5) yeast cells per mouse), C. albicans was no longer lethal (100% survival), whereas 100 and 70% of the mice still succumbed to challenge doses of 10(4) and 10(3) C. neoformans yeast cells, respectively. Pharmacological manipulation and transfer experiments revealed that the myelomonocytic compartment had a minor role against C. neoformans but was deeply involved in the control of intracerebral C. albicans infection. By counting the number of yeast cells in the brains of naive and immunomodulated animals, we established that, unlike C. albicans, C. neoformans remained essentially in the brain, where massive colonization and damage occurred whether naive or immunomodulated defense mechanisms were employed by the host. Overall, these data suggest that the differential role of the myelomonocytic compartment, together with the diverse tropisms of the two fungi, can explain the different development and outcome of intracerebral C. albicans and C. neoformans infections.

Animals↗
PubMed1971

Ultrastructural characteristics of Coccidioides immitis, a morphological variant of Cryptococcus neoformans and Podosypha ravenelii.

Electron microscopic examination of Coccidioides immitis revealed dense septum-associated bodies, characteristic of Ascomycetes. Similar examinations of a filamentous variant of Cryptococcus neoformans failed to clarify the taxonomic position of this yeast but did not exclude the possibility that this organism is a heterobasidiomycete. Septal pores were not seen in either organism.

Basidiomycota↗
PubMed2004

Paradoxical inflammatory reaction during treatment of Cryptococcus neoformans var. gattii meningitis in an HIV-seronegative woman.

A human immunodeficiency virus (HIV)-seronegative woman was admitted to the hospital with postpartum onset Cryptococcus neoformans var. gattii meningitis and markedly increased intracranial pressure. A poor initial response to antifungal therapy was followed, 2 months after hospital admission, by severe acute meningeal and cerebral inflammation and clearance of yeast cells from cerebrospinal fluid. This first reported case of paradoxical inflammatory reaction to C. neoformans illustrates important aspects of the host-pathogen interaction and highlights possible effects of immunomodulatory therapies.

Adolescent↗
PubMed1998

IL-5 is required for eosinophil recruitment, crystal deposition, and mononuclear cell recruitment during a pulmonary Cryptococcus neoformans infection in genetically susceptible mice (C57BL/6).

CBA/J (highly resistant), BALB/c (moderately resistant), and C57BL/6 (susceptible) mice displayed three resistance patterns following intratracheal inoculation of Cryptococcus neoformans 52. The inability to clear the infection correlated with the duration of the eosinophil infiltrate in the lungs. The role of IL-5 in promoting the pulmonary eosinophilia and subsequent inflammatory damage in susceptible C57BL/6 mice was investigated. C57BL/6 mice developed a chronic alveolar, peribronchiolar, and perivascular eosinophilia following C. neoformans infection. This resulted in the accumulation of intracellular Charcot-Leyden-like crystals in alveolar macrophages by wk 4 and the extracellular deposition of these crystals in the bronchioles with associated destruction of airway epithelium by wk 6. IL-5 mRNA was expressed in the lungs, and injections of anti-IL-5 mAb prevented eosinophil recruitment and crystal deposition but did not alter cryptococcal clearance. Depletion of CD4+ T cells (but not CD8+) ablated IL-5 production by lung leukocytes in vitro and eosinophil recruitment in vivo. Neutralization of IL-5 also inhibited the recruitment of macrophages, CD8+ T lymphocytes, and B lymphocytes by 47 to 57%. Anti-IL-5 mAb inhibited CD4+ T lymphocyte recruitment by 30% but did not affect neutrophil recruitment. Thus, the development of a chronic eosinophil infiltrate in the lungs of C. neoformans-infected C57BL/6 mice is a nonprotective immune response that causes significant lung pathology. Furthermore, IL-5 promotes the recruitment and activation of eosinophils, resulting in the recruitment of additional macrophages and lymphocytes into the lungs.

Animals↗
PubMed1979

Pulmonary infection with capsule-deficient cryptococcus neoformans.

A case of bilateral lobar pneumonia due to Crytococcus neoformans is presented. The capsule-deficient fungal organisms within tissue were suggestive of Histoplasma capsulatum. Cultures grew Cryptococcus neoformans and there was cryptococcal antigen in the serum. Pulmonary cryptococcosis and the occurrence of unencapsulated cryptococci are reviewed. The important role both culture and the latex agglutination test for cryptococcal antigen play in the differential diagnosis of systemic fungal infections with over-lapping histopathology are discussed.

Adult↗
PubMed2005

Cryptococcus neoformans meningitis at 2 hospitals in Washington, D.C.: adherence of health care providers to published practice guidelines for the management of cryptococcal disease.

Meningitis due to Cryptococcus neoformans may be associated with elevated intracranial pressure (ICP), but management of this complication is often overlooked. We retrospectively analyzed 39 consecutive patients with cases of culture-proven, community-acquired meningitis and ascertained adherence to Infectious Diseases Society of America (IDSA) practice guidelines for management of cryptococcal meningitis. Of these 39 patients, 26 (67%) had infection due to C. neoformans. Cerebrospinal fluid opening pressure had been measured for 13 (50%) of these 26 patients, and major deviations from the guidelines with respect to ICP management were observed in the care of 14 (54%). Seven (50%) of these 14 patients developed neuropathies during therapy, compared with 1 of the 5 patients whose care had minor or no deviations from the guidelines (P=.024). Major departures from the IDSA guidelines for management of ICP due to C. neoformans meningitis are common and can be associated with neurological injury during therapy.

Antifungal Agents↗
PubMed1996

Intravascular granuloma induced by intravenous inoculation of Cryptococcus neoformans.

In rodents an intravenous administration of viable Cryptococcus (C.) neoformans cells frequently resulted in attachment of intravascular cryptococcal granulomas to inner walls of the large to medium-sized veins of various organs, including the lungs, liver and spleen. In order to elucidate the pathogenesis of granulomatous changes, the cells composing the intravascular granulomas were observed by electron microscopic peroxidase (PO) cytochemistry. The granuloma composing cells could be divided into the following four types according to the pattern of endogenous peroxidase activity: exudate macrophage (M phi, type I), PO-negative M phi (type II), resident M phi (type III) and other inflammatory cells (type IV). In the intravenous granulomas of the lung, the percentages of composed cells were 39.0% for type I, 57.9% for type II, 0% for type III and 3.1% for type IV. By contrast, in the interstitial granulomas in the lung, type III M phi s, possibly derived from alveolar M phi s, played a significant role in granuloma formation. This may indicate that the intravascular granuloma is almost composed of macrophages derived from monocytes rather than alveolar macrophages. The expression of ICAM-1 on endothelia of the pulmonary veins was examined by immunoelectron microscopy. An immunogold labeling index was significantly augmented on the surface of endothelia in response to intravenous challenge of C. neoformans. The intravascular granuloma demonstrates that the monocytes develop into the granuloma-composing macrophages and suppress the cryptococcal activities even in the peripheral blood resulting in an assistance of endothelial functions.

Animals↗
PubMed1990

Cell-wall glucans of Cryptococcus neoformans Cap 67.

Purified cell walls derived from Cryptococcus neofromans Cap 67, an acapsular mutant, consisted of 86% Glc and 7.3% GlcNAc. The integrity of the cell walls was disrupted in three successive extractions with 60% 4-methylmorpholine N-oxide (4-MMNO) at 120 degrees. Four 4-MMNO-soluble D-glucopyranans were isolated. Released within 0.5 h was water-insoluble Gi-1, followed by two water-soluble Gs fractions and water-insoluble Gi-2 over 17.5 h. A 4-MMNO-insoluble residue, containing 27% of GlcNAc, was also isolated. Gi-1 and Gi-2 were isolated as precipitates during dialysis of 4-MMNO extracts and were each reduced with NaBH4 to permit their investigation in alkaline solution. Gs-1 and Gs-2 were separated by ion-exchange chromatography of the water-soluble fractions. The structures of the D-glucopyranans were determined by 13C-n.m.r. spectroscopy and by g.l.c.-mass spectrometry of their per-O-methylated derivatives. Gi-1 was a (1----3)-alpha-D-glucopyranan (97%) with some (1----4)-D-glucosidic linkages (3%) and no chain-branching. Gs-1 and Gs-2 were (1----6)-beta-D-glucopyranans branched at O-3 (10-12%) with beta-D-Glcp-(1----3)-beta-D-Glcp side chains. Gs-2 may have approximately 2% more chain branching than Gs-1. Gi-2 was a D-glucopyranan with 80% of its structure like that of Gi-1, and 20% like that of Gs-1 and -2; the water-insolubility of Gi-2 suggests that these structures were covalently linked. Almost identical D-glucopyranans were obtained from aged cultures that had thickened walls (as observed by electron microscopy).

Cell Wall↗
PubMed1970

In Vivo Susceptibility of Cryptococcus neoformans to Hamycin, Amphotericin B, and 5-Fluorocytosine.

Previous investigations have shown that hamycin is 5 to 10 times more active in vitro than amphotericin B against Cryptococcus neoformans, whereas 5-fluorocytosine is approximately 15 times less active. Present studies are concerned with a comparison of these drugs in vivo. Three strains of C. neoformans which varied in both their virulence for mice and their susceptibilities to the antifungal agents were studied. Acute experimental infections were established in mice by using inocula containing approximately 4 x 10(6) cells. The mice were treated by gastric intubation for 28 days; daily dosages of the three drugs ranged from 12.5 to 250 mg/kg. The polyenes were suspended in 5% dimethyl sulfoxide, whereas 5-fluorocytosine was suspended in saline. Amphotericin B was the most effective drug, with almost complete absence of toxic deaths in control mice and increased survival in mice infected with two of the three strains and treated with 25 mg/kg per day or more. 5-Fluorocytosine was nontoxic but provided protection against only one strain. Hamycin was both the least effective and the most toxic compound, providing only slight protection at doses of 12.5 or 25 mg/kg per day and causing toxic deaths in over 50% of uninfected mice at doses above 25 mg/kg per day.

Journal Article↗