In protected soil environments, near water sources, that are disturbed either naturally or by human activity, P. brasiliensis has been epidemiologically observed (although not isolated). A known animal carrier is the armadillo. In the natural environment, the fungi are found as filamentous structures, and they develop infectious spores known as conidia.Human to human transmission has never been proven. Mechanism
Primary infection, although poorly understood due to lack of data, is thought to occur through inhalation of the conidia through the respiratory tract, after inhaling fungal conidia produced by the mycelial form of P. brasiliensis. This occurs predominantly in childhood and young adulthood, after exposure to agricultural activity. Infection may occur through direct skin inoculation, although this is rare.After inhalation into the alveoli, there is rapid multiplication of the organism in the lung tissue, sometimes spreading via the venous and lymphatic systems. Approximately 2% of people develop clinical features after the initial asymptomatic infection.The type of immune response determines the clinical manifestation of the infection, with children and HIV co-infected individuals most commonly developing the acute/subacute disseminated disease. Most of those infected develop a Type 1 T-cell (Th1) mediated immune response, resulting in fibrosing alveolitis and compact granuloma formation that control fungal replication, and latent or asymptomatic infection. It then is thought to remain dormant in residual lung lesions and mediastinal lymph nodes. A deficient Th1 cell response results in the severe forms of the disease.
An epidemic outbreak has never been observed. It has the highest prevalence of all systemic mycoses (fungal infections) in the area. As many as 75% of people in endemic areas have been estimated to be infected with the asymptomatic form (up to 10 million people), with 2% developing clinically significant disease. Morbidity and mortality is strongly associated with patients socioeconomic background, with most adult patients being male agricultural workers. Other risk factors include smoking, alcohol use, HIV co-infection or other immunosuppression. 80% of reported cases are in Brazil, in the southeast, midwest, and south, spreading in the 1990s to the Amazon area. Most of the remaining infections are in Argentina, Colombia and Venezuela. Most epidemiological reports have focused on P. brasliensis, with P. lutzii epidemiology poorly understood as of 2015.Rising cases have been linked to agriculturalization and deforestation in Brazil, urbanisation to peripheral city areas with poor infrastructure, as well as increased soil and air humidity. One Brazilian indigenous tribe, the Surui, after changing from subsistence agriculture to coffee farming showed higher infection rates than surrounding tribes.There have also been reports in non-endemic areas with the rise of eco-tourism, in the United States, Europe and Japan. All reported cases were returned travellers from endemic regions. History
Lutz-Splendore-de Almeida disease is named for the physicians Adolfo Lutz, Alfonso Splendor (1871–1953), an Italo-Brazilian Parasitologist and Floriano Paulo de Almeida (1898–1977), a Brazilian Pathologist specializing in Pathologic Mycology (Study of Infectious Fungi), who first characterized the disease in Brazil in the early 20th century.