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Paracoccidioidomycosis
Published in Rebecca A. Cox, Immunology of the Fungal Diseases, 2020
Beatriz Jimenez-Finkel, Angela Restrepo-Moreno
Paracoccidioidomycosis is a chronic granulomatous disease, characterized by a primary pulmonary infection, and by dissemination to mucosal surfaces, skin, reticuloendothelial system, and adrenals.1 The disease is geographically restricted to certain areas of Central and South America. The etiologic agent Paracoccidioides brasiliensis is a dimorphic fungus which has an exogenous habitat.1,2
Terbinafine
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
Terbinafine is fungicidal against Histoplasma capsulatum and Blastomyces dermatitidis (Shadomy et al., 1985). It is also active against Paracoccidioides brasiliensis isolates in vitro (Hahn et al., 2002). In addition, in a case report by Ollague et al. (2000) terbinafine was successful in the treatment of paracoccidioidomycosis.
Granulomas and Granulomatous Inflammation
Published in Philip T. Cagle, Timothy C. Allen, Mary Beth Beasley, Diagnostic Pulmonary Pathology, 2008
Coccidioides immitis is found in southern parts of North America, and Central and South America. It is characterized by large sporangia, 30 to 60 μmin diameter; the endospores are each 1 to 5 μm. They can be identified in H&E-stained sections; however, they are also stained by GMS and PAS. The sporangia can be found within giant cells or free within necrosis. Paracoccidioides brasiliensis—found in South America—is characterized by multiple buds growing out of one organism. The single fungus is 5 to 15 μm in diameter, but with budding may approach 20 to 40 μm. The fungus is uninucleate, and the buds are of varying size and shape. The organisms can be demonstrated by H&E, PAS, and GMS stains (Fig. 14).
Inhaled antifungal therapy: benefits, challenges, and clinical applications
Published in Expert Opinion on Drug Delivery, 2022
The incidence of fungal infections has increased substantially over the past two decades. Currently, over 300 million people are afflicted with a serious fungal infection and the annual mortality associated with fungal infections is more than 1.6 million worldwide [1]. For pulmonary mycoses, invasive forms are associated with high morbidity and mortality rates [2]. Those who are non-immunocompetent or have impaired lung function such as patients who suffer from Coronavirus disease 2019 (COVID19), influenza, human immunodeficiency virus/acquired immune deficiency syndrome (HIV/AIDS), tuberculosis (TB), cancers, chronic obstructive pulmonary disease (COPD), and asthma are at high risk of fungal infection [3,4]. The primary cause of pulmonary fungal infections consists of several fungal species including Aspergillus spp., Mucor spp., Fusarium spp., Scedosporium spp., Blastomyces dermatitidis, Coccidioides spp., Cryptococcus spp., Histoplasma spp., Paracoccidioides brasiliensis, and Pneumocystis jirovecii [5–7]. This review will largely focus on cases of Aspergillus spp.
Endemic mycoses: epidemiology and diagnostic strategies
Published in Expert Review of Anti-infective Therapy, 2020
Andrés Tirado-Sánchez, Gloria M. González, Alexandro Bonifaz
This disease often presents an acute course and is caused by dimorphic fungi, Paracoccidioides brasiliensis, and less frequently Paracoccidioides lutzii, both belonging to the order Onygenales [52]. Other cryptic species include P. americana, P. restrepiensis, and P. venezuelensis [53]. PCM is less frequent than HPL; however, it has increased in recent years. PCM is commonly reported in South American countries: Brazil is most frequent; however, it has also been reported in minor proportions in Argentina, Colombia, Paraguay, Ecuador, Peru, Venezuela, and Mexico [54]. The etiological agent is found in acid soil, contaminated with plant detritus (coffee and sugar cane). The climate of fungus predilection is tropical and humid regions. The disease occurs in all age groups, although it predominates among men (farmers and outdoor workers) of the third and fourth decade of life [54,55]. Children are rarely affected [54]. Infection is often asymptomatic; the clinical expression of PCM depends on three factors: inoculum amount, agent virulence, and host immune response, as occurs in HPL [54]. Clinical manifestations may be acute (affecting children and young adults) or chronic (affecting older adults) [56].
Immunosuppression in the Management of Presumed Non-infective Uveitis; Are We Sure What We are Treating? Notes on the Antimicrobial Properties of the Systemic Immunosuppressants
Published in Ocular Immunology and Inflammation, 2020
Ciclosporin A (CsA, cyclosporine) is a cyclic peptide originally isolated from a newly-discovered fungus (Tolypocladium inflatum) in 1971, during investigations at Sandoz into potential new antibiotics. Initially, CsA was found to be active only against Neurospora crassa (an Ascomycete mould, not known to be pathogenic in humans and coincidentally, widely used as a laboratory organism in fungal genetics studies) and Rhodotorula rubra,(an environmentally widespread Basidiomycete yeast which can be a human pathogen in the immunosuppressed). No antibacterial activity was discovered. However, later it was discovered that calcineurin is necessary for Cryptococcus neoformans metabolism at human body temperature, and subsequently that both CsA and FK506 were effective antifungals against this organism.16 It transpires that calcineurin inhibition is the mechanism of both T-cell immunosuppression and most antifungal activity.17 Ciclosporin is now also known to be active against Paracoccidioides brasiliensis in a murine model.18