Adiaspiromycosis: Description, Causes and Risk Factors:
A rare pulmonary mycosis of humans and of rodents and other animals that dig in soil or are aquatic, caused by the fungus.
Adiaspiromycosis is a pulmonary fungal infection of worldwide distribution which affects lower order mammals and, rarely, humans. The causative agents are two variants of the saprophytic soil mould Emmonsia parva (Chrysosporium parvum). Adiaspiromycosis was first discovered in rodents from Transcaucasia (Russia),' and its worldwide distribution in various mammal species was subsequently established. The first case of Adiaspiromycosis in a human was diagnosed in France in 1964, since when a total of 46 cases of adiaspiromycosis have been reported from France, the Czech Republic, Germany, Spain, Latin America, and the USA. The causative fungi are presently considered to constitute the genus Emmonsia, with a single species E parva. This species is divided into two varieties-namely, Eparva var. parva and Eparva var. crescens. Recent synonyms include Chrysosporium parvum. Only E parva crescens has been reported to be present in humans. The taxonomy of the Chrysosporiumrelated fungi, which include numerous human pathogens, such as Blastomyces, Histoplasma
, and Trichophyton species, may be revised in the light of DNA sequencing.
The term adiaspiromycosis derives from the conidia of this fungus, the adiaconidia, which exhibit the unique property of progressive enlargement, without replication, at elevated temperature (37 C). An inhaled conidium 2-4 µm in diameter, can grow to 200-400 µm or more, which results in a million fold expansion of its volume. The pulmonary lesions produced by the enlarging conidia consist of discrete or confluent fibrotic granulomas, each containing one or more spherical, thick-walled adiaconidia that, when mature, are just large enough to be seen with the unaided eye.
Proliferation or replication of the adiaconidia does not occur in human tissues. The granulomas therefore maintain a bronchiolocentric pattern of distribution indicative of an inhalational portal of entry, and secondary dissemination within or beyond the lungs does not appear to happen, despite an unconvincing claim to the contrary. Symptomatic disease has been attributed to inflammation and fibrosis associated with the granulomatous inflammatory reaction, and to displacement and compression of terminal airways and alveoli by massive numbers of progressively enlarging but sterile adiaconidia.
Because adiaspiromycosis occurs so infrequently in humans, little clinical experience with it has accumulated. The Czechoslovakian workers have proposed a clinicopathologic classification based upon the density of granulomas found in the lungs. Solitary adiaspiromycotic granuloma is an incidental finding in lung tissue removed for another reason; patients with this form of the disease have no symptoms or radiographic abnormalities attributable to the fungal infection. Disseminated granulomatous pulmonary adiaspiromycosis is a localized or diffuse bilateral pulmonary disease
that has a finely nodular or reticulonodular radiographic pattern; only those patients with the densest most severe bilateral involvement have had symptoms, which include fever, cough, and progressive dyspnea. No more than half a dozen symptomatic patients have been described.
The disease can be localized andsymptom-less, or disseminated, occasionallysevere, or even fatal.The severity and extent ofthe disease in the lungs depends on the amountof the dust-borne conidia inhaled.
Diagnosis of adiaspiromycosis is difficult because the fungus is not easily cultured and there are not yet any reliable serological tests. The gold standard remains histological examination of a biopsy. Pathologists must then recognize large spherules with a trilamellar wall that can be surrounded by granulomas with or without necrosis or fibrosis. In latter chronic stages, the fungus may take on different sizes, thereby resembling other fungi or inhaled pollen grains or even helminths, according to some authors. The diagnosis is usually established by lung biopsy.
A therapeutic strategy for adiaspiromycosis has not been yet clearly established. Most of the time, patients with disseminated adiaspiromycosis have recovered without treatment. The ability to control such rare infections is largely dependent on the diagnosis of the etiological agents.
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