If there are mouth ulcers or skin lesions, the disease is likely to be widespread.Two presentations are known, firstly the acute or subacute form, which predominantly affects children and young adults, and the chronic form, predominantly affecting adult men. Most cases are infected before age 20, although symptoms may present many years later. Juvenile (acute/subacute) form
The juvenile, acute form is characterised by symptoms, such as fever, weight loss and feeling unwell together with enlarged lymph nodes and enlargement of the liver and spleen. This form is most often disseminated, with symptoms manifesting depending on the organs involved. Skin and mucous membrane lesions are often present, and bone involvement may occur in severe cases. This acute, severe presentation may mimic tuberculosis, lymphoma or leukaemia. Adult (chronic) form
The chronic form presents months to years after the initial infection occurs and most frequently presents with dry cough and shortness of breath. Other symptoms include excess salivation, difficulty swallowing, and difficulties with voice control. Upper respiratory tract mucosal lesions may be present, as well as increased mucus production and coughing up blood. Both pulmonary and extrapulmonary involvement is common.Up to 70% of cases have mucosal involvement, with lesions often found in the mouth, oropharynx, larynx, and palate. Classic lesions are superficial painful granular ulcers, with small spots of bleeding. Cause
Paracoccidioidomycosis is caused by two species of fungi that can exist as a mold or yeast depending on temperature, P. brasiliensis and P. lutzii.
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.