Pulmonary adiaspiromycosis: report of two cases

Santos, Vitorino Modesto dos; Fatureto, Marcelo Cunha; Saldanha, João Carlos; Adad, Sheila Jorge

doi:10.1590/s0037-86822000000500010

Cited by 10 publications

(13 citation statements)

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“…Approximately 67 probable cases of human pulmonary adiaspiromycosis due to E. crescens have been described in the literature. England and Hochholzer, in their 1993 case series and review (21), identified 46 cases; there have been 20 other cases reported since that time or that were omitted from the England and Hochholzer review (6,11,13,15,31,32,36,37,38,40,50,51,52,56,60,62) (Table 1). Adiaspiromycosis may be discovered incidentally after histopathologic exam of the lung for other conditions.…”

Section: Resultsmentioning

confidence: 99%

“…Previous cases of adiaspiromycosis have been reported from North America (Guatemala, Honduras, and the United States [Arizona, Georgia, North Carolina, New York, and Oklahoma]), South America (Argentina, Brazil, and Venezuela), and Europe (the former Czechoslovakia, France, Germany, and the former Soviet Union, Spain) (21,53). New countries from which the disease has been reported are Finland and the United Kingdom (13, 40); however, 62% of the 21 new cases from Table 1 were reported from Brazil (11,31,36,37,38,50,51,56). It is unclear if E. crescens is more common in Brazil or if this is simply reporting bias.…”

Section: Frommentioning

confidence: 99%

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Adiaspiromycosis Causing Respiratory Failure and a Review of Human Infections Due to Emmonsia and Chrysosporium spp

2012

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bWe report a case of a 27-year-old male who presented with respiratory distress that required mechanical ventilation. Transbronchial biopsy revealed adiaspores of the fungus Emmonsia crescens within granulomata, a condition known as adiaspiromycosis. The patient received amphotericin products and corticosteroids, followed by itraconazole, and made a full recovery. Emmonsia crescens is a saprobe with a wide distribution that is primarily a rodent pathogen. The clinical characteristics of the 20 cases of human pulmonary adiaspiromycosis reported since the last comprehensive case review in 1993 are described here, as well as other infections recently reported for the genus Emmonsia. Pulmonary adiaspiromycosis has been reported primarily in persons without underlying host factors and has a mild to severe course. It remains uncertain if the optimal management of severe pulmonary adiaspiromycosis is supportive or if should consist of antifungal treatment, corticosteroids, or a combination of the latter two. The classification of fungi currently in the genus Emmonsia has undergone considerable revision since their original description, including being grouped with the genus Chrysosporium at one time. Molecular genetics has clearly differentiated the genus Emmonsia from the Chrysosporium species. Nevertheless, there has been a persistent confusion in the literature regarding the clinical presentation of infection with fungi of these two genera; to clarify this matter, the reported cases of invasive Chrysosporium infections were reviewed. Invasive Chrysosporium infections typically occur in impaired hosts and can have a fatal course. Based on limited in vitro susceptibility data for Chrysosporium zonatum, amphotericin B is the most active drug, itraconazole susceptibility is strain-dependent, and fluconazole and 5-fluorocytosine are not active.A diaspiromycosis is primarily a pulmonary infection of rodents, fossorial mammals, and their predators and is caused by the soil fungi Emmonsia crescens and Emmonsia parva (17,30,35,53). It is a rare human infection. In this infection, inhaled Emmonsia conidia enlarge to form nonreplicating adiaspores. As in other mammals, the infection in humans usually involves the lungs, with only a few other cases of infection at other sites (17,30,35,53). About 70 cases of human adiaspiromycosis have been described, but much of the literature on this infection has been dispersed in less-accessible, non-English journals. Furthermore, the inconsistent nomenclature and taxonomy of Emmonsia species and their confusion with Chrysosporium species has resulted in an overall lack of consistent information on adiaspiromycosis and Chrysosporium infections. Herein, we report a case of adiaspiromycosis that resulted in respiratory failure. We also review the true cases of adiaspiromycosis that have been reported since the seminal monographs of England and Hochholzer in 1993 (21) and Sigler in 2005 (53) or omitted from those reports. Furthermore, we differentiate the cases of adiaspiromycosis from the tr...

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Section: Resultsmentioning

confidence: 99%

Section: Frommentioning

confidence: 99%

Adiaspiromycosis Causing Respiratory Failure and a Review of Human Infections Due to Emmonsia and Chrysosporium spp

2012

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“…Nos trabalhos existentes, a via inalatória aparece como responsável pela infecção por Emmonsia parva var. crescens [1][2][3][4][5][6][7] . O paciente em questão adquiriu a doença ao inalar os adiásporos junto aos silos, na zona rural, desenvolvendo a forma pulmonar da doença, apesar de ser imunocompetente.…”

Section: Discussionunclassified

“…Essa resolução espontânea constitui a base do conceito atual de ser a adiaspiromicose uma doença autolimitada [2][3][4][5][6][7] . O processo inflamatório alveolar é o eixo central da morbi-mortalidade causada pela adiaspiromicose 4 .…”

Section: Discussionunclassified

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Adiaspiromicose pulmonar tratada sem antifúngicos

Silva

Liporoni

Botto

et al. 2010

Rev. Soc. Bras. Med. Trop.

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The case of a 40-year-old agricultural worker affected by pulmonary adiaspiromycosis is reported. An etiological diagnosis had been established by means of a biopsy via thoracoscopy. Treatment with corticosteroids without antifungal drugs was chosen, and the patient responded well to this, with improvements in clinical and radiological conditions three weeks after the beginning of the symptoms. O paciente referia que há duas semanas apresentava febre, cefaléia e mal estar. Uma semana antes de sua admissão, começou a manifestar tosse seca, dor torácica ventilatório dependente e dispnéia, cuja intensidade aumentou gradativamente com o passar dos dias. KeyRelatava ser tabagista há 20 anos (10 cigarros por dia). Negava etilismo e uso de medicação contínua. Em seu trabalho, entrava em contato com silos constantemente.Ao exame físico, apresentava-se em bom estado geral, subfebril (37,7ºC), corado, acianótico e anictérico. Estava taquidispnéico (32 incursões respiratórias por minuto), saturação periférica de oxigênio de 84% em ar ambiente. A ausculta pulmonar mostrava apenas roncos difusos, porém discretos. Hemodinamicamente estável. Índice de massa corpórea de 21. Sem mais alterações. O hemograma evidenciava 12.100 leucócitos, com 10.527 (87%) de neutrófilos. Série vermelha e plaquetas normais. Eletrocardiograma, função renal, eletrólitos e coagulograma sem alterações. As três amostras de bacilo álcool ácido resistente e a sorologia para HIV foram negativas.O raio-X de tórax na admissão (Figura 1) apresentava velamento heterogêneo difuso bilateral, com predomínio à direita. A tomografia de tórax (Figura 2) mostrava: opacidade mista interstício-alveolar difusa bilateral, mais acentuada a direita; discreto derrame pleural bilateral; espessamento das paredes e dilatação da luz dos brônquios peri-hilares; ausência de adenomegalia mediastinal.O paciente foi internado, recebendo 40mg por dia de prednisona, oxigênio suplementar e ampicilina/sulbactam, na dose 3g de 8/8h via endovenosa. No dia seguinte, foi submetido à biópsia pulmonar por toracotomia, devido a evolução desfavorável do caso. morte por insuficiência respiratória 2,3,4 . A resposta imunológica inicial é descrita como necrótico-exsudativa, seguindo-se por um processo natural de formação de granulomas, fibrose e cura espontânea. A formação dos granulomas isola os adiásporos e, desta forma, o diagnóstico não pode ser feito por meio da análise do escarro, mas sim por análise de cortes histológicos de tecido pulmonar. Trata-se de doença autolimitada, com melhora clínica após resolução do processo inflamatório pulmonar, no decorrer de algumas semanas 2,4-7 .

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