Candida Cell Wall Research Articles

Intermittent ketoconazole therapy of chronic mucocutaneous candidiasis in childhood.

We report the clinical and laboratory findings in two children with chronic mucocutaneous candidiasis (CMC) treated successfully with intermittent long-term ketoconazole therapy. Both had chronic infection of the nails, skin and mucous membranes with positive cultures for candida. Both were resistant to multiple local and systemic antifungal agents. After institution of ketoconazole therapy there was a dramatic improvement with clearing of the oral (one week), skin (two months) and nail lesions (5 months). After 8 months the drug was stopped and clinical remission persisted for 10 and 7 months respectively. Relapse of oral candidiasis was treated with a short course of ketoconazole (4-16 weeks) leading to complete healing of the lesions. Clinical improvement was not related to an amelioration in lymphocyte transformation. There was no change in the progressive deterioration of the lymphocyte responses to candida antigen which was probably due to persisting candida cell wall components (e.g. mannan).

Role of Candida albicans in Granulomatous II. In Vivo Degradation of C. albicans in Hepatic Macrophages of Mice

Hepatic granulomas were induced in mice by injection of blastospores, cell walls, and glucan of Candida albicans. Granulomatous reactions in liver tissue initially multiplied but later decreased. A dose-response relationship was apparent with up to 3 mg of inoculum. Shortly after injection of C. albicans spores, fungal elements appeared in liver macrophages and were detectable in granuloma and Kupffer cells for 20 days. Gram-stain, periodic acid-Schiff (PAS), and immunofluorescence reactions soon vanished, and the organisms could no longer be seen. Glucan of C. albicans, which lacked PAS and immunofluorescence reactivity, proved active in initiation of granulomas. Degradation of phagocytized spores of C. albicans, reductions of cytoplasm, and cell wall deformation and collapse support the premise that loss of PAS and immunofluorescence reactivity was caused by enzymatic breakdown of candida cell wall mannan in macrophages. We conclude that C. albicans can induce granulomatous reactions in mouse liver when the glucan that forms the cell wall matrix in Candida persists in identifiable residues.

Candida albicansand the fungicidal activity of the blood

Experiments on the killing of the young synchronous blastospores of C. albicans in blood from normal subjects and diabetic patients are described. With inocula of between 10 and 100 young blastospores about 75% of the inoculum was killed in 5 hr., and as the concentration of the inoculum was increased an increase in the percentage survival occurred. The killing of propagules with hyphal lengths up to 200 μ was within the same range as that for small blastospores. The capacity of the blood to kill propagules with hyphal lengths greater than 200 μ rapidly decreased with increasing length of the hyphae. Visual observations on the phagocytosis of C. albicans by polymorphonuclear leucocytes are described.It is shown that over 90% of suspensions of synchronous blastospores are killed by the leucocytes in autologous plasma, but when the plasma is treated with zymosan or Candida cell wall antigens less than 50% of the inoculum is killed. Adsorbtion of serum with a C. albicans somatic antigen had little effect on ...

Polysaccharide Antigens of Candida Cell Wall

Summary Immunochemical studies of Candida cell wall have established that the mannan is the major antigen. There at least two serologic groups within C. albicans; group A mannan contains all the determinants present in group B plus additional determinants. C. tropicalis mannan is antigenically very similar to C. albicans group A mannan. Cross-reactions of anti-C. albicans group A serum with several mannose-containing fungal polysaccharides were studied.