A disease caused by the fungus Histoplasmacapsulatum. Most people with histoplasmosis have no symptoms. However, it can cause acute or chronic lung disease and progressive disseminated histoplasmosis, which affects a number of organs. Infants, young children, and older persons’particularly those with chronic lung disease’are at increased risk for severe disease. Disseminated histoplasmosis is most frequently seen in people with cancer or AIDS. The acute respiratory disease of histoplasmosis is characterized by respiratory symptoms, a general ill feeling, fever, chest pains, and a dry or nonproductive cough. Distinct patterns may be seen on a chest x-ray. Chronic lung disease related to histoplasmosis resembles tuberculosis and can worsen over months or years. The disseminated form is fatal unless treated. Mild cases resolve without treatment. Severe cases of acute histoplasmosis and all cases of chronic and disseminated histoplasmosis are treated with antifungal medications, usually for life in those with compromised immune systems.
Histoplasmosis is caused by the reproductive cells (spores) of the fungus Histoplasmacapsulatum. The spores are extremely light and float into the air when dirt or other contaminated material is disturbed.
Even if you’ve had histoplasmosis in the past, you can still get the infection again. However, if you contract histoplasmosis again, the illness will likely be milder than the initial infection.
The histoplasmosis fungus thrives in damp soil that’s rich in organic material, especially the droppings from birds and bats. For that reason, it’s particularly common in chicken and pigeon coops, old barns, caves and parks. Histoplasmosis isn’t contagious, so it can’t be spread from person to person.
H capsulatum in the saprobic state grows in the mycelial form. Macroconidia and microconidia are produced on the hyphae of mycelium and are converted to the yeast form under temperature-controlled regulation. The aerosolization of conidia and mycelial fragments from contaminated soil results in alveolar deposition via inhalation.
The host defense includes the fungistatic properties of neutrophils and macrophages. T lymphocytes are crucial in limiting the extent of infection. Susceptibility to dissemination is increased markedly with impaired cellular host defenses.
Conversion from the mycelial to the pathogenic yeast form occurs intracellularly. After phagocytosis by macrophages, the yeast replicates in approximately 15-18 hours. Despite fusion with lysosomes, multiplication continues within the phagosomes. Proposed theories suggest that the yeasts may produce proteins that inhibit the activity of lysosomal proteases.
As the host immunity response develops, yeast growth ceases within 1-2 weeks after exposure. Cytokines systemically activate the fungistatic activity of macrophages against intracellular yeasts. With further maturation of the cell-mediated response, delayed-type hypersensitivity to histoplasmal antigens occurs (3-6 wk after exposure). Approximately 85-90% of individuals who are immunocompetent produce a positive response to skin antigen test for Histoplasmaspecies. Over weeks to months, the inflammatory response produces calcified fibrinous granulomas with areas of caseous necrosis.
Clinical manifestations of histoplasmosis appear with continued exposure to large inocula. The initial pulmonary infection may disseminate systemically, with hematogenous spread, and produce extrapulmonary manifestations. Hematogenous spread to regional lymph nodes may occur through the lymphatics or the liver and spleen. Progressive disseminated histoplasmosis is rare in adult hosts who are immunocompetent. Systemic spread usually occurs in patients with impaired cellular immunity and typically involves the CNS, liver, spleen, and rheumatologic, ocular, and hematologic systems.
Several types of histoplasmosis exist. The mildest form produces no signs or symptoms, but severe infections can be life-threatening. When signs and symptoms do occur, they usually appear three to 17 days after exposure and may include:
- Muscle aches
- Dry cough
- Chest discomfort
In some people, histoplasmosis can also produce joint pain and a rash. People who have an underlying lung disease, such as emphysema, may develop a chronic form of histoplasmosis.
Symptoms of chronic histoplasmosis may include weight loss and a cough that brings up blood. The symptoms of chronic histoplasmosis sometimes can mimic those of tuberculosis.
The most severe variety of histoplasmosis occurs primarily in infants and in people with compromised immune systems. Called disseminated histoplasmosis, this variety can affect nearly any part of your body, including your mouth, liver, central nervous system, skin and adrenal glands. If untreated, disseminated histoplasmosis is usually fatal.
Endemic mycoses can be challenging to diagnose and accurate interpretation of laboratory data is important to ensure the most appropriate treatment for the patients. Although the definitive diagnosis of histoplasmosis (HP), one of the most frequent endemic mycoses in the world, is achieved by direct diagnosis performed by micro and/or macroscopic observation of Histoplasmacapsulatum (H. capsulatum), serologic evidence of this fungal infection is important since the isolation of the etiologic agents is time-consuming and insensitive. A variety of immunoassays have been used to detect specific antibodies to H. capsulatum. The most applied technique for antibody detection is immunodiffusion with sensitivity between 70 to 100 % and specificity of 100%, depending on the clinical form. The complement fixation (CF) test, a methodology extensively used on the past, is less specific (60 to 90%). Detecting fungal antigens by immunoassays is valuable in immunocompromised individuals where such assays achieve positive predictive values of 96–98%. Most current tests in diagnostic laboratories still utilize unpurified antigenic complexes from either whole fungal cells or their culture filtrates. Emphasis has shifted, however, to clinical immunoassays using highly purified and well-characterized antigens including recombinant antigens. In this paper, we review the current conventional diagnostic tools, such as complement fixation and immunodiffusion, outline the development of novel diagnostic reagents and methods, and discuss their relative merits and disadvantages to the immunodiagnostic of this mycosis.
Treatment usually isn’t necessary if you have a mild case of histoplasmosis. But if your symptoms are severe or if you have the chronic or disseminated forms of the disease, you’ll likely need treatment with one or more antifungal drugs. Some of these medications come in pill form, but the strongest varieties are administered intravenously.