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Trichosporon
Published in Rossana de Aguiar Cordeiro, Pocket Guide to Mycological Diagnosis, 2019
João Nobrega de Almeida Júnior
An in-house real-time PCR assay designed with T. asahii-specific primers/probe has been shown to detect T. asahii DNA in blood samples of trichosporonosis patients, with higher sensitivity than the polysaccharide antigen assay for Cryptococcus (Mekha et al., 2007).
Epidemiology of fungal infections: What, where, and when
Published in Mahmoud A. Ghannoum, John R. Perfect, Antifungal Therapy, 2019
Frederic Lamoth, Sylvia F. Costa, Barbara D. Alexander
Trichosporon spp., saprophytic yeasts usually found in the soil, can be cultured from human skin, stool, and urine. These organisms have been implicated as the etiologic agent of white piedra, an infection of the distal end of the hair shaft, as well as causing cutaneous infections in immunocompetent patients [476–478]. In immunosuppressed patients, particularly in those with underlying malignancy, it has been implicated as the cause of fungemia, renal insufficiency, pulmonary infiltrates, cutaneous lesions, chorioretinitis, and chronic hepatic trichosporonosis [479–488]. An increasing incidence of trichosporonosis has been reported over the last decade [489,490]. Increasing use of echinocandins, to which Trichosporon spp. are intrinsically resistant, may be involved in this changing epidemiology. A recent review of 203 cases of invasive trichosporonosis reported in the literature since 1994 shows that the disease affects mainly patients with hematologic cancers (39%), especially those with neutropenia [490]. Other populations at risk include patients with other immunosuppressive conditions and newborns (21% and 12% of cases, respectively). T. asahii was the most frequent pathogenic agent (46.7% of cases), followed by T. inkin and T. mucoides/dermatis. Fongemia was present in 74% of cases. Other affected organs were skin, lung, liver/spleen, intestinal tract, brain and eye.
Amphotericin B Deoxycholate
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Neil R. H. Stone, Tihana Bicanic
Trichosporon asahii is considered resistant. AMB was not effective in the persistently neutropenic rabbit model of disseminated trichosporonosis (Walsh et al., 1992). This may be due to the lack of activity of AMB on Trichosporon biofilms, as has been observed in vitro (Iturrieta-González et al., 2014).
Promethazine inhibits efflux, enhances antifungal susceptibility and disrupts biofilm structure and functioning in Trichosporon
Published in Biofouling, 2023
Ana Luiza Ribeiro Aguiar, Bruno Nascimento da Silva, Nicole de Mello Fiallos, Lívia Maria Galdino Pereira, Maria Laína Silva, Pedro Freitas Santos Manzi de Souza, Fernando Victor Monteiro Portela, José Júlio Costa Sidrim, Marcos Fábio Gadelha Rocha, Débora Souza Collares Maia Castelo-Branco, Rossana de Aguiar Cordeiro
Invasive fungal infections affect more than 2 million people worldwide annually (Brown et al. 2012), being associated with high mortality and morbidity rates (Rauseo et al. 2020; Rodrigues and Nosanchuk 2020). Trichosporon spp. are yeast-like fungi, opportunistic pathogens known to cause superficial infections, such as white piedra, onychomycosis and tinea pedis (Colombo et al. 2011; Singh et al. 2019). Furthermore, Trichosporon species have been recognized as emerging agents of systemic infections (Guo et al. 2019; Singh et al. 2019; Ramírez and Moncada 2020). Risk factors for Trichosporon systemic infections include HIV infection, organ transplantation, diabetes, use of immunosuppressive agents and neutropenia (Li et al. 2020). Invasive trichosporonosis has been reported as the second most common yeast infection in patients with hematological malignancies, with mortality rates to up 90% (Colombo et al. 2011; Foster et al. 2018; Kourti and Roilides 2022).
Inhibitory effect of a lipopeptide biosurfactant produced by Bacillus subtilis on planktonic and sessile cells of Trichosporon spp.
Published in Biofouling, 2018
Rossana de Aguiar Cordeiro, Ewerton Weslley Caracas Cedro, Ana Raquel Colares Andrade, Rosana Serpa, Antonio José de Jesus Evangelista, Jonathas Sales de Oliveira, Vandbergue Santos Pereira, Lucas Pereira Alencar, Patrícia Bruna Leite Mendes, Bárbara Cibelle Soares Farias, Vânia Maria Maciel Melo, Zoilo Pires de Camargo, Débora de Souza Collares Maia Castelo-Branco, Raimunda Sâmia Nogueira Brilhante, José Júlio Costa Sidrim, Marcos Fábio Gadelha Rocha
Invasive trichosporonosis is frequently associated with fungal colonization of catheters (Chagas-Neto et al. 2009; Ruan et al. 2009; Liao et al. 2015). Trichosporon biofilms are formed after attachment of planktonic cells to these abiotic surfaces, which leads to the formation of well-structured communities that are resistant to antifungals and host immune response (Chagas-Neto et al. 2008; Colombo et al. 2011; Liao et al. 2015). Biofilm-mediated invasive infections are difficult to eradicate and may lead to persistent and/or recurrent infections (Colombo et al. 2011; Ramage et al. 2012; Liao et al. 2015). In vivo studies have shown that Trichosporon biofilms tolerate very high concentrations (>1,000 μg ml−1) of amphotericin B, caspofungin and azoles (Di Bonaventura et al. 2006; Iturrieta-González et al.2014; Cordeiro et al. 2015). Based on the pronounced resistance of these communities to antifungal agents, the search for anti-biofilm molecules is justified.
Heterologous extracellular DNA facilitates the development of Trichosporon asahii and T. inkin biofilms and enhances their tolerance to antifungals
Published in Biofouling, 2022
Lívia Maria Galdino Pereira, Ana Raquel Colares de Andrade, Fernando Victor Monteiro Portela, Ana Luiza Ribeiro Aguiar, Bruno Nascimento da Silva, Santiago Gonçalves Bezerra Moura, Mariana Lara Mendes Pergentino, Marcos Fábio Gadelha Rocha, José Júlio da Costa Sidrim, Débora de Souza Collares Maia Castelo Branco, Rossana de Aguiar Cordeiro
Invasive trichosporonosis are opportunistic infections that occur in immunocompromised patients, mainly those with hematological malignancies (Ramírez and Moncada 2020). Clinical evidences suggest that these infections may be mediated by biofilms formed on implanted medical devices (Iturrieta-Gonzalez et al. 2014; Bongomin et al. 2019), which hinders the eradication of the infectious process and may lead to high mortality rates (Sugimoto et al. 2018).