Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CANDIDA”

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

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

At least 1,135 records · Page 63Linked to original sources
PubMed1975

Mouth lesions in iron-deficient anemia: relationship to Candida albicans in saliva and to impairment of lymphocyte transformation.

The atrophic glossitis and angular chilosis in patients with iron-deficient anemia are associated with infection of the mouth by Candida albicans. Saliva from these patients contained more Candida and supported the growth of Candida better than did saliva from a control group. The possibility that growth of Candida may be due to impaired lymphocyte function was investigated by measuring transformation of lymphocytes stimulated with phytohemagglutinin. Transformation was depressed in iron-deficient subjects and returned to normal after correction of their iron status. The lymphocyte count in the peripheral blood was also depressed and corrected by additional iron. Impaired lymphocyte function did not explain the mouth lesions and growth of Candida in saliva since lymphocyte transformation was equally depressed in patients with and without mouth lesions. A local factor, such as an effect of lack of iron on the resident vacterial flora of the mouth, may be important.

Adolescent↗
PubMed1977

Immunodiffusion and agglutination tests for Candida in patients with neoplastic disease: inconsistent correlation of results with invasive infections.

A serological study of candidiasis was conducted with use of (1) sera sent to the laboratory by clinicians who suspected infections due to various organisms including Candida species, and (2) sera available in our serum bank from patients with candidiasis proven at autopsy and from those with documented candidemia. With this population of patients, we were able to evaluate both potential false-negative and false-positive results. Microimmunodiffusion and slide agglutination tests were used. In many cases, serial specimens were available for measurement of rises or falls in titers of agglutinating antibody. Sera from less than one-half of the patients with disseminated or invasive gastrointestinal candidiasis exhibited positive immunodiffusion reactions, titers of agglutinating antibody of greater than 1:16, or fourfold rises in titer of agglutinins. Sera from several patients with pharyngitis due to Candida and from several who were only colonized with Candida or for whom clinical or cultural evidence of candidiasis was lacking showed positive immunodiffusion reactions or agglutinin titers of greater than 1:16, and some showed fourfold rises in titer. Conversions from negative to positive immunodiffusion reactions were not consistently correlated with invasive candida infection. Using the methods described, we have not found immunodiffusion tests and titers of agglutinating antibody to be reliable indicators of invasive candida infection, since false-positive as well as false-negative reactions occur. Greater specificity for invasiveness as well as greater sensitivity in immunosuppressed patients are necessary before these tests can become important adjuncts to the evaluation of patients with suspected invasive candidiasis.

Adolescent↗
PubMed1987

Susceptibility to experimental Candida albicans urinary tract infection in the rat.

The urinary tract is resistant to ascending infection due to Candida albicans. Host and microbial factors that may alter such resistance were evaluated in the rat after inoculating C. albicans into the urinary tract. Diuresis, diabetes, candidal germ-tube formation, and vaginal Candida colonization (alone or in concert) failed to promote ascending urinary tract infection with two vaginal isolates of C. albicans capable of producing renal infection by the hematogenous route. Both germinated and ungerminated Candida adhered poorly to bladder mucosa. Unlike prior urinary tract infection due to an enterococcus that failed to agglutinate Candida in vitro, prior urinary tract infection with a mannose-binding strain of Escherichia coli that agglutinated C. albicans in vitro enhanced adherence of C. albicans to bladder mucosa and increased susceptibility to ascending C. albicans urinary tract infection. Thus, resistance to Candida ascending urinary tract infection is likely to be due to poor adherence of C. albicans to normal bladder mucosa.

Animals↗
PubMed1987

An enzyme-linked immunosorbent assay for quantifying adherence of Candida to human vascular endothelium.

Success in elucidating the pathogenesis of certain bacterial infections through studies of bacterial adherence to host cells has stimulated interest in parallel investigations of fungal adherence. Fungal adherence differs from bacterial adherence, especially when fungal coadherence (adherence of fungal cells to each other) is a factor. Using human umbilical vein endothelial cells cultured in a living monolayer in microtiter plates, we developed an ELISA to study adherence of Candida albicans to endothelial cells in the absence of yeast coadherence. A rabbit antibody to Candida detected the adherent Candida, and an alkaline phosphatase-conjugated antibody to rabbit IgG was the developing antibody. A linear relationship between the log of the optical density and the log of the number of adherent organisms was seen for wells containing 3 X 10(4)-1 X 10(6) organisms (r = .923- .965). In addition to measuring adherence of living Candida to living target cells and avoiding Candida coadherence, this assay makes it possible to investigate adherence limited to lumenal surfaces, conserves reagents, and facilitates the testing of large numbers of potential adherence modifiers.

Adhesiveness↗
PubMed1991

Candida albicans stimulates endothelial cell eicosanoid production.

The response of human umbilical vein endothelial cells to invasion by Candida species was examined in vitro. Live Candida albicans caused significant endothelial release of eicosanoids, mainly prostaglandins. Since prostaglandin I2 (PGI2) is an important prostaglandin produced by endothelial cells, factors influencing its release were studied. The ability of different strains and species of Candida to induce endothelial PGI2 release was closely related to their capacity to injure the endothelium (r = .99). C. albicans was the only species tested that either stimulated PGI2 release or damaged the endothelial cells; only this organism possessed detectable phospholipase activity. Candida glabrata and Candida tropicalis had no phospholipase activity and neither increased PGI2 release nor caused significant endothelial damage. Close proximity with germinated C. albicans was required for endothelial injury and PGI2 release. The ability of C. albicans to stimulate endothelial cells may have important implications in regulating neutrophil activities against organisms that interact with endothelial cells.

Arachidonic Acid↗
PubMed1994

High prevalence of antifungal resistance in Candida spp. from patients with AIDS.

Three hundred and forty-eight isolates of Candida spp. from patients treated at a regional infectious diseases unit for AIDS, immunocompromised patients admitted to the Hope Hospital and isolates referred from around the North West of England were tested for their in-vitro susceptibility to amphotericin B, fluconazole and flucytosine using standardized methods. Candida albicans comprised 73% of isolates, Candida glabrata 10% and Candida parapsilosis 7%. Ninety-six percent of isolates were susceptible to amphotericin B and resistance to > or = 12.5 mg/L fluconazole was found in 61 (17.5%) of the 348 isolates tested. Among isolates from patients with AIDS the incidence of fluconazole resistance was 33% whereas in other patients the incidence was only 11%. Flucytosine resistance was seen in only 12 (3.4%) isolates, 11 of which were C. albicans and in 6.5% of isolates from patients with AIDS. Resistance to fluconazole and flucytosine is now sufficiently prevalent among Candida spp. isolated from patients with AIDS to warrant routine susceptibility testing of yeast isolates.

AIDS-Related Opportunistic Infections↗
PubMed1998

Multi-centre evaluation of the Etest method for antifungal drug susceptibility testing of Candida spp. and Cryptococcus neoformans. BSAC Working Party on Antifungal Chemotherapy.

Ten laboratories tested 18 isolates of Candida spp. and two of Cryptococcus neoformans against amphotericin B, flucytosine, fluconazole and itraconazole on two occasions by the Etest method. Two individuals read each set of results. Of the 18 isolates of Candida spp., five were duplicated, but the participants were not told this. In 40 of the 60 drug-organism combinations studied, at least 80% of the Etest MICs fell within a five-concentration range corresponding to the modal MIC +/- 1 log2 dilution. In five combinations, >50% of the Etest MICs fell outside this five-concentration range. In 17 (85%) of the 20 drug-organism combinations tested in duplicate, at least 80% of the paired Etest results fell within two concentrations of each other (corresponding to one log2 dilution). Overall, 88.5% of the paired Etest results for amphotericin B agreed to within two concentrations, as did 94% of results for flucytosine, 92% for fluconazole and 79% for itraconazole. The broth microdilution MICs of the four antifungal agents for the 15 isolates were measured on five occasions in the Mycology Reference Laboratory, Bristol. In each case, the results fell within a three log2 concentration range. In 24 (40%) of the 60 drug-organism combinations tested, at least 80% of the Etest results fell within the broth microdilution test MIC range, but 27 (45%) showed <50% exact agreement. In 33 (73%) of 45 drug-organism combinations involving flucytosine, fluconazole or itraconazole, at least 80% of the Etest results fell within the same class (susceptible, resistant, or susceptible dependent upon dose) as the broth microdilution results. With fluconazole, the Etest method misclassified three susceptible isolates of Candida spp. as resistant in 1.5-15% of tests. With itraconazole, the Etest misclassified seven susceptible isolates of Candida spp. as resistant in 5-62.5% of tests. The Etest also misclassified both C. neoformans isolates as resistant to flucytosine, fluconazole and itraconazole in 7.5-65% of tests. Our results suggest that the Etest is suitable for routine use with Candida spp. and amphotericin B or flucytosine. It is less reliable for the azoles, and isolates that appear to demonstrate acquired resistance should be retested with well-established reference methods.

Amphotericin B↗
PubMed1999

A comparative evaluation of Etest and broth microdilution methods for fluconazole and itraconazole susceptibility testing of Candida spp.

The Etest strip is a promising tool of broad application in clinical microbiology. The method provides MIC readings and is easier to perform than broth microdilution. We carried out a study to compare the MICs of fluconazole and itraconazole obtained by the Etest with those obtained by broth microdilution, performed according to the guidelines of the NCCLS document M27-A, with 402 clinical isolates (360 Candida albicans, 17 Candida tropicalis, nine Candida krusei, nine Candida glabrata and seven Candida parapsilosis) and seven control isolates. The agreement between MICs by the two methods (at +/- 2 dilutions) was 74.5% for fluconazole and 61.4% for itraconazole. These results suggest that further development is necessary to standardize the medium and incubation conditions before introduction of the Etest as a routine method in the clinical microbiology laboratory for fluconazole and itraconazole susceptibility testing.

AIDS-Related Opportunistic Infections↗
PubMed2001

HWY-289, a novel semi-synthetic protoberberine derivative with multiple target sites in Candida albicans.

The antifungal properties of 515 synthetic and semi-synthetic protoberberines were investigated. HWY-289 was chosen for further study because it exhibited the most significant anti-Candida activity (MICs were 1.56 mg/L for Candida albicans and Candida krusei; 6.25 mg/L for Candida guilliermondii) but did not demonstrate toxicity in rats. HWY-289 inhibited the incorporation of L-[methyl-(14)C]methionine into the C-24 of ergosterol in whole cells of C. albicans (IC(50) 20 microM). However, HWY-289 (100 microM) had no effect on mammalian cholesterol biosynthesis in rat microsomes while miconazole (100 microM) was a potent inhibitor of cholesterol biosynthesis under identical assay conditions. A second major target site for HWY-289 was identified that involves cell wall biosynthesis in C. albicans. HWY-289 was a potent inhibitor of the chitin synthase isozymes CaCHS1 and CaCHS2, with IC(50) values of 22 microM for each enzyme. The effect was highly specific in that HWY-289 had no significant effect on C. albicans CaCHS3 (IC(50) > 200 microM). Thus, HWY-289 compared favourably with well-established antifungal agents as an inhibitor of the growth of Candida species in vitro, and may have considerable potential as a new class of antifungal agent that lacks toxic side effects in the human host.

Antifungal Agents↗
PubMed1994

Candida antigen titer is a marker of neutrophil dysfunction after severe injury.

UNLABELLED: Trauma patients with positive Candida antigen titers have high mortality rates. Death is the result of sepsis and multi-organ system failure. Considerations of host immunity to Candida led us to concurrently study the function of neutrophils (PMNs) from severely injured adults with positive titers (n = 20), patients with negative titers matched for age, sex, and injury (n = 20), and volunteers (n = 20). Anticandidal PMN function was determined using a 3H-glucose incorporation assay. RESULTS are expressed as mean percentage of growth inhibition +/- SEM. RESULTS: PMN, from all groups inhibited Candida growth, although PMNs from titer-positive patients demonstrated less growth inhibition. In vitro cytokines granulocyte macrophage-colony stimulating factor [(GM-CSF), interferon-gamma (IFN-gamma), and interleukin 8 (IL-8)] improved function of PMNs from each group and corrected the impaired anticandidal function of PMNs from titer-positive patients, with GM-CSF being most effective. CONCLUSIONS: Seriously injured patients with positive Candida antigen titers have PMNs with impaired anticandidal function, which can be restored by cytokines. These findings begin to explain why seriously injured patients with positive Candida antigen titers have increased mortality and to offer hope of therapeutic intervention.

Adult↗
PubMed1994

Monocytes overcome lymphocyte dysfunction in injured adults with elevated Candida antigen titers.

OBJECTIVE: Severely injured adults with elevated Candida antigen titers have increased mortality from sepsis, in part because of known neutrophil (PMN) dysfunction. Since PMN function is modulated by monocytes and lymphocytes, this study was undertaken to determine the ability of monocytes and lymphocytes isolated from injured adults with elevated Candida antigen titers to activate the anticandidal function of normal PMNs. METHODS: Lymphocytes with or without monocytes, isolated from 18 injured adults with elevated titers, were cultured in the presence or absence of heat-killed Candida albicans for 48 hours. Culture supernatants were harvested, diluted 1:40, 1:160, and 1:640, and tested for the ability to stimulate the anticandidal function of normal PMNs using an 3H-glucose incorporation assay. Monocytes and lymphocytes isolated from nine volunteers were studied for comparison. RESULTS: Supernatants of lymphocytes from healthy volunteers that were cultured with heat-killed C. albicans significantly augmented normal PMN anticandidal function. Supernatants of lymphocytes from injured adults with elevated titers that were cultured with heat-killed C. albicans did not significantly augment normal PMN anticandidal function. Supernatants of monocytes or lymphocytes from both groups of patients were able to upregulate PMN anticandidal function. CONCLUSIONS: Lymphocytes from injured adults with elevated Candida antigen titers are defective in their ability to stimulate PMN anticandidal function. Monocytes from these patients can respond to Candida exposure and overcome the lymphocyte functional defect seen in injured patients with elevated titers.

Adult↗
PubMed2005

Treatment of Candida infection: a view from the trenches!

PURPOSE OF REVIEW: To provide an overview of the treatment of Candida infections from the perspective of the infectious disease clinician in the community. An insight is given into relevant issues as they apply to clinical practice. As community hospitals strive to provide state-of-the-art medical care to critically ill patients, effective infection control programs and the infectious disease consultation availability become indispensable. RECENT FINDINGS: Candida infections rank as the fourth most common cause of nosocomial bloodstream infections. Although C. albicans remains the most common pathogen, emerging trends in invasive candidiasis are notable for a dramatic increase in infections due to non-albicans Candida species, reflecting changes in clinical practice. These trends affect our practice because infections with non-albicans species raise concerns for inherent decreased antifungal susceptibility, ultimately impacting our preventive, empirical and therapeutic approaches. It seems inevitable for most acutely ill patients today to be admitted to the intensive care unit, thus increasing their risk for nosocomial infections. In addition, cost containment efforts may force patients receiving intravenous therapy into less supervised environments, potentially increasing their risk for candidemia. SUMMARY: Potentially fatal Candida infections are commonplace in seriously ill hospitalized patients. The infectious disease physician is challenged to develop expertise in using the newly introduced antifungal agents, applying evidence-based guidelines developed from quality randomized clinical trials. The infectious disease specialist is called to play a multidisciplinary role formulating infection control policies, developing drug formularies, educating the staff and treating the sickest patients. Infection surveillance in local communities coupled with available antifungal agents may improve our management of Candida infections.

Antifungal Agents↗
PubMed1991

Phylogenetic analysis of five medically important Candida species as deduced on the basis of small ribosomal subunit RNA sequences.

The classification of species belonging to the genus Candida Berkhout is problematic. Therefore, we have determined the small ribosomal subunit RNA (srRNA) sequences of the type strains of three human pathogenic Candida species; Candida krusei, C. lusitaniae and C. tropicalis. The srRNA sequences were aligned with published eukaryotic srRNA sequences and evolutionary trees were inferred using a matrix optimization method. An evolutionary tree comprising all available eukaryotic srRNA sequences, including two other pathogenic Candida species, C. albicans and C. glabrata, showed that the yeasts diverge rather late in the course of eukaryote evolution, namely at the same depth as green plants, ciliates and some smaller taxa. The cluster of the higher fungi consists of 10 ascomycetes and ascomycete-like species with the first branches leading to Neurospora crassa, Pneumocystis carinii, Candida lusitaniae and C. krusei, in that order. Next there is a dichotomous divergence leading to a group consisting of Torulaspora delbrueckii, Saccharomyces cerevisiae, C. glabrata and Kluyveromyces lactis and a smaller group comprising C. tropicalis and C. albicans. The divergence pattern obtained on the basis of srRNA sequence data is also compared to various other chemotaxonomic data.

Base Sequence↗
PubMed1998

Interactions between Candida species and platelets.

Candida spp. are able to cause disseminated disease in immunocompromised patients. This study examined the interactions of Candida spp. with platelets, complement and polymorphonuclear leucocytes (PMNLs). With the exception of C. albicans, all other Candida spp., including a C. albicans strain previously classified as C. stellatoidia, aggregated human platelets at a ratio of yeast cells: platelets of 1:80. Usually, those species and strains that aggregated platelets were either killed or prevented from growing in platelet-rich plasma indicating that the aggregation released microbicidal or microbistatic substances that were active against Candida spp. All Candida spp. were resistant to attack by complement in 50% serum. However, all species activated complement as determined by the presence of C3 fragments on their surface, in particular a 195-kDa fragment corresponding to C3c, two fragments at 67 and 40 kDa corresponding to iC3b, and a 33-kDa fragment corresponding to C3d. When strains were tested for their ability to stimulate the release of pro-inflammatory substances from platelets and PMNLs, it was found that most strains stimulated PMNLs to release interleukin(IL)-8 but not IL-1beta or leucotriene B4. The ability of C. albicans to evade complement-mediated killing and not to aggregate platelets may contribute to the survival of this species in the blood during vascular infections.

Anticoagulants↗
PubMed1994

Suppression of anti-Candida activity of murine and human neutrophils by glucocorticoids.

Effects of glucocorticoid (GC) compounds on inhibitory activity of neutrophils to mycelial growth of Candida albicans were examined by in vitro crystal violet staining method with 14 hr coculture. Both GC hormones (hydrocortisone > or = 6 x 10(-7) M and corticosterone > or = 10(-6)M) and anti-inflammatory GC agents (prednisolone > or = 10(-7) M and dexamethasone > or = 10(-8) M) significantly suppressed anti-Candida activity of murine casein-induced neutrophils. Anti-Candida activity of human neutrophils prepared from peripheral blood was also suppressed by hydrocortisone (> or = 6 x 10(-7) M). These GC compounds did not affect the Candida growth in the absence of neutrophils. Steroidal compounds without anti-inflammatory activity, cholesterol, cholic acid, aldosterone did not suppress neutrophil activity. These results suggest that GCs at their physiological or clinical concentration may suppress anti-Candida activity of neutrophils in vivo.

Aldosterone↗
PubMed1990

Characterization of Candida albicans epidermolytic proteases and their role in yeast-cell adherence to keratinocytes.

Epidermolytic proteases were partially purified from six strains of Candida albicans, four of which were isolated from patients with cutaneous diseases. Two of the strains exhibited a unique time-course of enzyme production compared to that previously reported, with detectable epidermolytic protease levels being significantly delayed. All epidermolytic proteases had pH and temperature optima of 4-4.5 and 35-37 degrees C, respectively. These conditions are consistent with the microenvironment of human skin, a habitat where an epidermolytic protease would appear to be an important advantage to the yeast. Candida epidermolytic proteases were more active against a substrate of normal human epidermis than that obtained from psoriatic patients. When human epidermis replaced bovine serum albumin as the protein source within the culture medium, the epidermolytic activity of the resultant enzyme was reduced by 9 and 25% for normal and psoriatic epidermis substrates, respectively. The proteases were found to contain major protein bands at 42 and 66 kDa. The ability of these same Candida strains to adhere to human epidermal cells was studied and found to be optimal at 35-37 degrees C within neutral pH values. Pepstatin, bovine brain gangliosides, and convalescent human serum all interfered with the adherence of the yeast to epidermal cells. A higher yeast-epidermal-cell adherence for Candida was demonstrated on normal rather than psoriatic epidermal cells, and after treating the cells with partially purified Candida protease.

Adult↗
PubMed1996

Coaggregation of Candida albicans with oral Actinomyces species.

Eight strains of Actinomyces were examined for their ability to coaggregate in vitro with four strains of Candida albicans. The Actinomyces coaggregated to various degrees with all of the Candida strains. Exposure of the Candida but not the Actinomyces to heat, trypsin, proteinase K, amphotericin B or trichodermin abolished coaggregation. All sugars tested did not inhibit any of the reactions. All coaggregating pairs were disaggregated by the addition of SDS, but nonionic detergents had no effect. The addition of urea or EDTA completely reversed coaggregation. Actinomyces strains were sensitive to periodate oxidation, whereas the Candida strains were unaffected. These data suggest that the coaggregations involve a protein on the Candida surface that may interact with carbohydrates or carbohydrate-containing molecules on the surface of the Actinomyces. These observations expand the known range of intergeneric coaggregations occurring between human oral microbes and indicate that coaggregation of C. albicans and Actinomyces may be an important factor in oral colonization by this yeast.

Actinomyces↗