As previously emphasized, a relatively small number of species are responsible for most fungal infections, but hundreds of other, normally environmental fungi increasingly cause invasive disease. Every year, the health care community is challenged by the emergence of novel pathogenic fungi. Because these new mycoses usually involve immunocompromised or debilitated patients, the reasonable assumption is that more people are becoming susceptible. However, there is growing evidence that fungi are anything but static. Over the last decades, whole-genome sequencing and other methods have revealed that fungi have multiple mechanisms for affecting rapid genetic changes. Pathogenic fungi have demonstrated impressive genetic and phenotypic plasticity. Upon the stress of confronting mammalian host defenses, the expression of hundreds of genes may be increased or downregulated. In addition to gene expression, fungi can alter ploidy and undergo chromosomal rearrangements. During infection, these “microevolutionary” changes often enhance pathogenicity, help to evade host immune responses, and lead to resistance to antifungal drugs. Two recent examples highlight this phenomenon.

In 2009, an unusual surge of cases of candidemia were reported—many patients failed to respond to antifungal chemotherapy, mortality was high, and the infecting yeast was misidentified because it was not represented in the usual clinical laboratory databases. A new pathogen had emerged, C. auris, and the situation has continued to worsen. C. auris has spread globally, and isolates are inherently resistant to the three major classes of antifungal drugs, polyenes, azoles, and echinocandins. Unlike other infectious species of Candida, C. auris in not part of the normal human microbiome, but once exposed to patients, it routinely colonizes human skin and mucosal tissue. This propensity has led to transmission by contact and nosocomial outbreaks of systemic disease. C. auris also survives for weeks on clothing, countertops, medical equipment, and other fomites. Hundreds of cases have been reported in more than 20 countries on the five major continents. It is a leading cause of candidemia in India and South Africa, and more than 250 cases have been reported in the United States. Across Europe from 2013 to 2017, there were 620 cases of C. auris causing candidemia, other clinical manifestations, or colonization. Unlike other species of Candida, C. auris can grow in high salt concentrations and at 42°C. Little is known about its origin, although it has been isolated from fish, salt water, and other environmental sites. Genotyping studies suggest that it emerged independently in four different geographic areas. It seems to have deployed multiple methods of drug resistance, which may have been spurred by exposure to antifungals in the environment. MIC assays of hundreds of isolates C. auris revealed that 90% of the isolates were resistant to fluconazole, up to 30% were resistant to amphotericin B, and ca. 2–5% were resistant to echinocandins.

For at least three decades, Emmonsia crescens has been known as an environmental, dimorphic mold and rare cause of invasive infection that is acquired by inhalation of airborne conidia; in host tissue, the fungus forms large spherical adiaspores (≤400 µm). Members of the genus Emmonsia are related phylogenetically to Blastomyces and Histoplasma. All three dimorphic pathogens have been reported from Africa (Figure 1). From 2008 to 2015, more than 50 patients in South Africa with HIV/AIDS were diagnosed with apparent Emmonsia infections. Most had pulmonary and cutaneous involvement, and despite treatment with amphotericin B, mortality was 48%. The infected tissue did not reveal large adiaspores but small ovoidal yeast cells, ca. 2.9 × 1.6 µm, and this observation signaled the emergence of a novel dimorphic pathogen, which was subsequently confirmed by DNA sequencing. This mold has been assigned a new genus and named Emergomyces africanus. As of 2017, more than 80 cases of infection with E. africanus have been reported, all in South Africa and almost exclusively in patients with HIV/ADS. Evidence suggests an environmental association with soil and infection occurring by airborne conidia. MIC data support treatment with amphotericin B, itraconazole, voriconazole, or posaconazole, but not fluconazole. Thus, a new lethal dimorphic mold has emerged in a highly restricted geographic area.

Fig1. Global distribution of endemic mycoses. Each is caused by a dimorphic environmental mold and undergoes morphogenesis within the host. (Reproduced with permission from Lee PP, Lau Y-L: Cellular and molecular defects underlying invasive fungal infections—revelations from endemic mycoses. Front Immunol 2017;8:375.)

اخر الاخبار

اخبار العتبة العباسية المقدسة

تستمر طيلة شهر رمضان.. إقامة ختمة قرآنية تعليمية في مقام الإمام المهدي (عجل الله فرجه)

في مستشفى الكفيل.. جراحة دقيقة بين الأذن والدماغ تنقذ مريضة من التهاب حاد

المجمع العلمي يُطلق مسابقة (فرسان التنزيل الفرقية الأولى) ويقيم ختمات قرآنية في محافظة المثنى

ضمن أنشطته الإنسانية.. قسم الشؤون الفكرية يفتتح البئر الـ 72 في نيجيريا

المزيد

الآخبار الصحية

دراسة تحذر من الإفراط في ممارسة الرياضة.. كيف يضر دماءك؟

الطهي بزيت الزيتون.. مضر أم مفيد؟

دماغ الرضع في خطر.. دراسة تحذر من "العدو الخفي"

التمر بالحليب عند الإفطار.. "كنز صحي" في رمضان

المزيد

الآخبار التكنلوجية

أثر نفسي غير متوقع للرياضة.. مرتبط بالغضب

القمر يواصل الانكماش.. رصد تشققات حديثة على سطحه

إطلاق أول تطبيق مراسلة "مشفّر".. ثورة في عالم الدردشة

خلل تقني يؤجّل أول رحلة مأهولة إلى القمر منذ عقود

المزيد

مواضيع ذات صلة

Pneumocystis pneumonia

Mucormycosis

Aspergillosis

Morphology and Identification of Cryptococcosis

Candidiasis

Paracoccidioidomycosis

Blastomycosis

Histoplasmosis

Coccidioidomycosis

Endemic Mycoses

Phaeohyphomycosis

Chromoblastomycosis