Drain outlets in patient rooms as sources for invasive fusariosis: an analysis of patients with haematological disorders.

BACKGROUND: Invasive fusariosis (IF) is a frequently fatal disease as there are few antifungals to treat it, making the prevention of IF crucial. However, fusarium infections have not been as thoroughly studied as other common pathogenic fungi such as Aspergillus or Candida. AIM: To investigate the epidemiology of IF in patients with haematological diseases in Japan and to elucidate the infectious route of fusarium infection. METHODS: We retrospectively analysed 29 IF cases in patients with haematological diseases from 2009 to 2019 in Japan. To discover the infectious source of IF, we performed an indoor environment survey targeted at indoor air and drain outlets in medical institutions and residences using culture-based and metagenomic methods. Finally, we performed aerosol- and droplet-mediated dispersion studies. FINDINGS: The epidemiological study showed that the primary pathogen of IF was Fusarium solani species complex (FSSC), and the most common species was Fusarium petroliphilum. Most patients were likely to develop IF during hospitalization. A fusarium culture was positive in 26 of 72 drain samples. Few fusarium were detected from air samples; by contrast, 29 of 108 isolates from the drain outlets were identified as fusarium. Furthermore, similar results were obtained in the metagenomic analysis. Interestingly, species belonging to FSSC were isolated from indoor drain outlets, which was similar to those of the IF patients. In the droplet-mediated dispersion study, eight to 17 colonies of fusarium were isolated. CONCLUSION: Our study indicates that causative Fusarium spp. could inhabit drain outlets in hospitals or residences, and droplet-mediated fusarium dispersion is a potential cause of IF.

Disseminated Hormographiella aspergillata infection with involvement of the lung, brain, and small intestine following allogeneic hematopoietic stem cell transplantation: case report and literature review.

Disseminated infection by Hormographiella aspergillata is extremely rare and small intestine involvement has not been reported previously. A 51-year-old man with myelodysplastic syndrome developed pneumonia after cord blood cell transplantation. Fungal growth from the biopsied lung was identified as H. aspergillata by morphology and the gene analysis. Although antifungal agents including voriconazole and liposomal amphotericin B were administered, he died of disseminated H. aspergillata infection. We review the literature and discuss the treatment and prognosis.

Pathogenicity and virulence of Candida dubliniensis: comparison with C. albicans.

Candida dubliniensis is a newly described fungus that is frequently isolated from the oral cavities of HIV-positive patients. Although extensive studies have been performed on the phylogeny of C. dubliniensis, little is known about the pathogenic ecology of this yeast. Here we examined aspects related to C. dubliniensis in comparison with those of C. albicans. When injected intravenously into mice, C. dubliniensis had a higher survival rate than C. albicans. Histopathological analysis disclosed that C. dubliniensis remained mostly in the yeast form in the infected organs, whereas C. albicans changed into the mycelial form. The host inflammatory reaction was aggressive with C. dubliniensis infection and mild with C. albicans infection. Co-culture of the yeasts with human polymorphonuclear leukocytes disclosed that C. dubliniensis is more vulnerable to the fungicidal activity of leukocytes than C. albicans. C. dubliniensis was also more susceptible to the toxic effect of hydrogen peroxide. When cultured in vitro, C. dubliniensis grew more slowly than C. albicans, but the formation of germ tubes was faster. When the fungi were cultured in RPMI 1640, a fetal bovine serum supplement suppressed the growth of C. dubliniensis but enhanced that of C. albicans. These results clearly indicated that C. dubliniensis is less virulence than C. albicans.

Atypical Cryptococcus neoformans isolate from an HIV-infected patient in Brazil.

Cryptococcus neoformans is an important fungal pathogen in immunocompromised hosts. Capsulation, urease and melanin synthesis activity of the fungus are well known virulence factors. Although artificial melanin-deficient mutants of Cr. neoformans have been investigated, the clinical mutant is rare. We found a Cr. neoformans isolate in the cerebrospinal fluid of an AIDS patient which produced a light tan colony on a caffeic acid cornmeal agar (CACA) plate. The mycological feature of the isolate was as follows; normal capsulation, defective inositol assimilation ability, serotype A; urease-positive; mating type alfa; haploid; extremely slow growth in RPMI 1640 medium, Sabouraud dextrose broth, brain heart infusion broth and yeast nitrogen base; lower production of melanin with L-DOPA substrate; and low virulence to ddY mice. We also investigated the partial DNA sequence of CNLAC1 gene between the 3085th to 3623rd base. There were many substitutions, 3 insertions and 3 deletions in the isolate compared with GenBank accession number L22866. The result indicated some functional disorder in the gene. Although the CACA plate is an excellent selective medium for Cr. neoformans, other identification methods should also be used.

Simple detection method for distinguishing dead and living yeast colonies.

A rapid and simple assay was developed for detection of yeast colonies containing dying or dead cells. Methylene blue, phloxin B, rose bengal and trypan blue at concentrations of 5-10 micromol l(-1) were shown to stain non-viable cells in colonies of Saccharomyces cerevisiae, Schizosaccharomyces pombe, Candida albicans and Filobasidium capsuligenum without staining or affecting the viability of living cells of the colonies.

Rapid, extensive and reversible vacuolation of Schizosaccharomyces pombe induced by amphotericin B.

The fission yeast Schizosaccharomyces pombe has no large vacuoles under normal growth conditions, although budding yeasts usually have large central vacuoles. The minimum inhibitory concentration of amphotericin B to S. pombe was 0.5 microgram ml-1; treatment with 0.2 microgram ml-1 for 20 min induced rapid and extensive vacuolation in S. pombe exponential phase cells. Growth rate of the cells with 0.2 microgram ml-1 amphotericin B was much reduced for 6 h, showing extensive vacuolation. Vacuolation in itself was not fatal: on removal of the drug, most cells recovered gradually and eventually multiplied.