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Microascus manginii
Microascus manginii is a filamentous fungal species in the genus Microascus.[1] It produces both sexual (teleomorph) and asexual (anamorph) reproductive stages known as M. manginii and Scopulariopsis candida, respectively.[1] Several synonyms appear in the literature because of taxonomic revisions and re-isolation of the species by different researchers.[2] M. manginii is saprotrophic and commonly inhabits soil, indoor environments and decaying plant material.[3] It is distinguishable from closely related species by its light colored and heart-shaped ascospores used for sexual reproduction.[4] Scopulariopsis candida has been identified as the cause of some invasive infections, often in immunocompromised hosts, but is not considered a common human pathogen.[5][6][7] There is concern about amphotericin B resistance in S. candida.[6] History and taxonomyThe anamorph was first documented, unintentionally, by Professor Fernand-Pierre-Joseph Guéguen in 1899[8] who mistook it for the species, Monilia candida, previously described in 1851 by Hermann Friedrich Bonorden.[9] In 1911, Jean Paul Vuillemin determined that the two taxa were distinct, noting that the taxon described by Bonorden was a yeast whereas the strain that was the subject of Guéguen's studies was filamentous and produced true conidia.[9] Vuillemin formally described the latter as S. candida.[9] At the same time, he re-described Bonordeon's yeast taxon, Monilia candida, as Monilia bonordenii.[9] Subsequent researchers described taxa that have since been reduced to synonymy with S. candida, including: S. alboflavescens in 1934, S. brevicaulis var. glabra in 1949, Chrysosporium keratinophilum var. denticola in 1969 and Basipetospora denticola in 1971.[10] The teleomorph was discovered by Auguste Loubière in 1923 and named Nephrospora manginii in honour of his mentor, Professor Louis Mangin.[11] It was later transferred to the genus Microascus by Mario Curzi in 1931.[10][2] Curzi did not provide an explanation for this transfer.[1] S. candida and M. manginii are used in the literature to describe the same species.[2] However, recent changes to the International Code of Nomenclature for algae, fungi and plants have terminated the use of dual nomenclature for fungal species with multiple forms.[12] It is not yet known which name will take priority for this fungus in the future.[12] Growth and morphologySexual formColonies of M. manginii are pale, white and rapid growing.[2][3] Growth is tolerant of cycloheximide and restricted at 37 °C.[3] The vegetative hyphae are septate and appear glassy (hyaline).[2][13] Ascomata are the sexual structures within which ascospores are produced in sacs called asci.[2] The ascomata of M. manginii are spherical, smooth-walled, dark-brown to black and 100–175 μm in size.[2][13] These fruiting bodies are also called perithecia because of their flask-like shape wherein asci grow at the base and an opening allows for the release of mature ascospores.[2][13] They are also papillate with short cone-shaped projections at the opening, sessile, and rich in carbon.[1][13] Perithecia manifest as small black dots organized in concentric rings.[13] An incubation period of over two weeks may be necessary for the production of perithecia.[13] The asci are shaped similar to an upside-down egg where the apex is broad and thicker than the base.[2][13] They are 11–16 × 8–13 μm in size and contain 8 ascospores.[1][2][13] Ascospores are nonseptate and smooth-walled.[13][4] They are characteristically uniform in heart-shape and pale, straw-colored when mature - but appear reddish-brown as a mass.[4] They each have a single inconspicuous germ pore, which is a predetermined spot in the spore cell wall where the germ tube emerges during germination.[13] Ascospores are 5–6 × 4.5–5 μm in size.[2][3][13] M. manginii is a heterothallic species and as a result, generation of sexual spores requires mating between two compatible individuals.[14] Asexual formS. candida is a hyaline mold with septate hyphae.[3][6] The white and membranous morphology of S. candida colonies differentiates it from the more common species S. brevicaulis, which is characterized by a sand-coloured and granular colonial morphology.[13] As the colony ages, it becomes slightly yellow.[1] Conidiophores are specialized hyphal stalks that have conidiogenous cells which produce conidia for asexual reproduction.[1] The Latin word for broom, scopula, was chosen as the basis of the generic name due to the broom-like appearance of the conidiophores of Scopulariopsis.[6] In S. candida, these structures are 10–20 μm in length.[1] S. candida sporulates using specialized conidiogenous cells called annellide.[1] The tip of the cell elongates and narrows each time a conidium is formed and results in a series of ring-like scars called annellations near the tip.[1] The annelloconidia are formed in dry chains that eventually break off to allow the dispersal of spores by wind.[15] They are one-celled, smooth- and thick-walled, and round but also broad-based.[13][6][10] They resemble simple yeasts.[6] Annelloconidia are hyaline and 6–8 × 5–6 μm in size.[13][6] The smooth hyaline annelloconidia can also distinguish S. candida from S. brevicaulis, which has conidia that are rough-walled, truncate and covered in tiny, thorny outgrowths.[13] Isolates of S. candida can produce sterile perithecia-like structures.[14] PhysiologyThe optimal growth temperature range for S. candida is 24–30 °C (75–86 °F), with a minimum of 5 °C and maximum 37 °C.[3] It is a keratinophilic species which may contribute to its role in nail infections.[16] It grows well on protein-rich surfaces and is able to digest α-keratins.[16] In vitro study of antifungal susceptibilities reports S. candida as relatively more resistant to the antifungal drug amphotericin B, and susceptible to Itraconazole and miconazole.[6] Habitat and ecologyM. manginii is a saprobic fungus.[17] It has a worldwide distribution.[17] It is often isolated from decaying plant material, soil and indoor environments, but also human skin and nails, dust, chicken litter, atmosphere, book paper and cheese, among other locations.[3] Contaminated dust, soil and air samples are often found in North America and Europe.[10] In Portugal, S. candida was identified as the most prevalent fungal species contaminating the air of three poultry slaughterhouses in 2016.[18] Contamination with fungal pathogens was found on equipment used in physiotherapy clinics in Brazil, specifically electrodes and ultrasound transducers,[19] S. candida was found on several contact electrodes.[19] PathogenicityInvasive fungal infections are becoming increasingly common in patients who are immunocompromised.[5] M. manginii and S. candida are not traditionally recognized as common human pathogens.[20] However, they were identified as opportunistic human and plant pathogens in a few reported cases.[21] Other Scopulariopsis species have been associated with nail infection and keratitis (S. brevicaulis), and brain abscess and hypersensitivity pneumonitis (S. brumptii).[6] A case of disseminated infection caused by Scopulariopsis species in a 17-year old patient with chronic myelogenous leukemia was described in 1987.[5] After receiving an allogenic bone marrow transplantation for cancer treatment, the patient complained of recurrent fever, nosebleeds, and abnormal sensations of the nose.[5] Amphotericin B therapy was administered but symptoms persisted.[5] Within two months of transplant, the patient experienced a short period of improvement followed by rapid deterioration and death.[5] The autopsy discovered Scopulariopsis species in the lungs, blood, brain and nasal septum, and exhibited high resistance to amphotericin B in vitro.[5] In 1989, the species responsible for the disseminated infection was identified as S. candida.[7] S. candida was identified as the cause of invasive sinusitis in a 12-year old girl undergoing treatment for non-Hodgkin's lymphoma in 1992.[6] This is the second reported case of invasive sinus disease caused by Scopulariopsis species and only reported case due to S. candida.[6] The patient was immunocompromised at the time of fungal infection due to ongoing cancer treatment.[6] The clinical presentation resembled an infection by fungi in the order Mucorales, and involved myalgia, cheek swelling and tenderness, a week-long fever, and extensive necrosis of maxillary sinuses.[6] As a result, the presumed diagnosis was mucormycosis until further examination of patient specimens showed abundant growth of a powdery, tan mold that was distinguished as S. candida by several features (e.g., septate hyphae, round and smooth conidia, broom-shaped conidiophores).[6] The patient immediately received surgical drainage and debridement of damaged tissue, and amphotericin B to treat the fungal infection.[6] Subsequent identification of S. candida as the cause of disease prompted administration of additional antifungal medication, Itraconazole, to address potential amphotericin B resistance.[6] The patient was cured of invasive sinusitis with no signs of progressive sinus disease.[6] This marked the first successful treatment of an invasive infection caused by Scopulariopsis species in an immunocompromised host.[6] Immunosuppression was suspected to play a role in the ability of S. candida to cause invasive infection.[6] The most significant contributor to managing the disease was likely strengthening the patient's immune system by suspending chemotherapy and administrating granulocyte colony-stimulating factor.[6] S. candida and M. manginii have been identified in cases of onychomycoses.[2] They mainly cause tissue damage to the big toe and rarely other nails.[16] Common symptoms include difficulty walking while wearing shoes, thickening and discolouration of nails, and deformation of nails.[15] The infection often begins at the lateral edge of the nail instead of the proximal edge.[16] Patients are typically middle-aged or older.[15] The mechanism of these infections is not well-characterized.[15] In addition, the published cases of onychomycoses caused by these species are not all reliable.[16] References
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