Adiaspiromycosis and Emmonsia-Like Infections in Humans
To date, almost 70 human cases of pulmonary adiaspiromycosis have been reported, mostly ascribed to A. crescens (Sigler 2005, Anstead et al. 2012). The first was reported in France in 1960 (Doby-Dubois et al.
1964), presenting as a solitary human pulmonary nodule. A decade later, the first case of disseminated pulmonary disease was documented (Kodousek et al. 1971). The pathological effects of adiaspiromycosis in humans appear to depend upon adiaspore burden and host immune status, and range from asymptomatic infection which is usually selfresolving (Buyuksirin et al. 2011), through necrogranulomatous pneumonia, respiratory failure (Barbas Filho et al. 1990) and death (Peres et al. 1992). Many infections have been discovered incidentally during histopathological evaluations for other conditions (see, for example, Denson et al. 2009). The typical radiological appearance of adiaspiromycosis is of bilateral reticulonodular infiltrates (Barbas Filho et al. 1990; England and Hochholzer 1993; Denson et al. 2009) that can be mistaken for sarcoidosis, cryptococcosis and other fungal pneumonias, miliary tuberculosis or malignancy. In symptomatic patients, the disease may have a protracted, indolent course typified by fatigue, fever, weight loss, cough and dyspnoea, or a rapid acute course if initial fungal exposure was high (Barbas Filho et al. 1990; de Almeida Barbosa et al. 1997). In many symptomatic cases, infection can be linked to recent or repeated exposure to soil, nesting material or animal carcases (Barbas Filho et al. 1990; de Almeida Barbosa et al. 1997; Nuorva et al. 1997).A small number of extrapulmonary cases of human adiaspiromycosis-like infections have been reported, but in the light of recent taxonomic developments recognising several novel Emergomyces species as agents of infection in immunocompromised humans (Kenyon et al.
2014; Schwartz et al. 2015b; Dukik et al. 2017; Jiang et al. 2018), the identity of published agents needs critical re-evaluation. A case involving the appendix presumably following ingestion of the fungus was reported (Kodousek 1972). Two cases in AIDS patients ascribed to B. parvus (Emmonsia parva) (Echavarria et al. 1993; Turner et al. 1999), including a case of disseminated disease with skeletal and bone marrow involvement, likely represent cases of disseminated disease caused by an Emergomyces species. A report of an outbreak of ocular adiaspiromycosis in Brazilian children after immersion in a river (Mendes et al. 2009) almost certainly concerned an unrelated fungus.Over the last several decades, multiple reports have appeared of mostly immunocompromised patients with disseminated infections with widespread cutaneous manifestations, caused by Emmonsia-like fungi now recognised as Emergomyces species. The tissue form consists of small yeast cells rather than adiaspores. Emergomyces pasteurianus was described in 1998 from an HIV-positive Italian woman with cutaneous lesions (Drouhet et al. 1998; Gori and Drouhet 1998), with additional cases reported from Spain in a liver transplant recipient with HIV (Pelegrin et al. 2011), India in an HIV-infected man (Malik et al. 2016), China in a renal transplant patient and a steroid-treated patient (Feng et al. 2015; Tang et al. 2015), and South Africa in an HIV-infected woman (Dukik et al. 2017).
Emergomyces africanus has since emerged as a leading cause of disseminated mycoses in AIDS patients in South Africa, in which pulmonary disease was common and cutaneous involvement universal (Kenyon et al. 2014; Dukik et al. 2017). By 2015, at least 55 cases of E. africanus have been diagnosed, all occurring in patients with immuncompromising conditions (mostly advanced HIV infection) (Schwartz et al. 2015a).
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