Histoplasmosis is a dimorphic fungus most commonly found in soil along river valleys. The organism is endemic to the Ohio and Mississippi river valleys. Bird or bat droppings are the media for its growth. The organism exists as mycelia in the environment and is inhaled into the lungs where it reaches the alveoli. Once at body temperature the organism converts to the more familiar yeast phase. In the normal host the yeast organisms are engulfed by macrophages where they proliferate until the host develops specific cellular immunity and delayed hypersensitivity which requires 12-14 days. During the interval the infected macrophages migrate to regional lymph nodes where there is commonly dissemination to the reticulo-endothelial system. Once delayed hypersensitivity develops the infection is controlled. Eventually there is calcification at the initial site of infection and within the involved lymph nodes. There are 3 forms of infection:
1- Primary Disease:
The vast majority of individuals with normal immunity who develop histoplasmosis experience a clinically unrecognized infection. Chest radiographs in these patients are usually performed at some point after the infection, and the most frequently encountered abnormality is a solitary, well marginated, pulmonary nodule. Symptomatic patients develop a benign, self limited illness characterized by mild, generally non-productive cough to flu-like symptoms. The CXR is normal in 40 to 70% of cases. In symptomatic patients the most common radiographic finding is a single area or multiple patchy areas of consolidation and adenopathy which can progress to form a solitary or multiple pulmonary nodule(s) (histoplasmoma). A miliary pattern can be seen. The lesions heal with calcification (granulomas). Some nodules may continue to slowly enlarge (doubling time 14-113 months) because of continued elaboration of collagen at the peripheral of the lesion- possibly a response to leakage of H. capsulatum antigen.
Immune compromised patients are still at risk for H. capsulatum infection. The CXR may be normal in up to 50% of cases. The most common radiographic finding is a diffuse miliary pattern. HRCT will also demonstrate a diffuse pattern of 1 to 3 mm nodules and there is frequently associated hilar or mediastinal adenopathy.
2- Chronic Pulmonary Histoplasmosis:
Chronic disease occurs almost entirely in patients with pre-existing COPD. Patients complain of malaise, cough, and night sweats. Spores are deposited within bullae where they stimulate the development of fluid within the cavity. The disease generally involves the upper lobes (apical-posterior segments). Segmental airspace opacities are seen and abut the pleural surface. Cavitation (similar to TB) with considerable fibrosis is seen as the disease progresses.
3- Disseminated Disease:
Disseminated histoplasmosis is a systemic illness that affects multiple organ systems. It occurs in immunocompromised patients with defective T-cell immunity (due to lymphoreticular malignancy, cytotoxic agents, corticosteroids, or HIV. Patients at the extremes of age are also at risk for disseminated disease. Symptoms include fever, weight loss, cough, and dyspnea. The infection may represent progression of a primary histoplasmosis infection or reactivation of a previously dormant infection. Patients can develop a raised skin lesion, lytic bony lesions, hepatosplenomegaly, peripheral lymphadenopathy, or epididymitis/prostatitis. A normal CXR is seen in about 30% of non-HIV immune compromised patients. Diffuse, small (under 3mm), nodular opacities are the most common radiographic feature. Linear and irregular opacities are the next most common finding. Focal air space opacity is seen infrequently (about 10% of cases) and adenopathy is rare. The adrenals are also involved in a majority of cases.
Complications of Hisplasmosis Infection:
2- Mediastinal Granuloma
3- Fibrosing Mediastinitis
CXR: The chest radiograph may appear normal, reveal a non-specific widening of the mediastinum, or may demonstrate the presence of a lobulated mediastinal/hilar mass. Hilar and/or mediastinal adenopathy are also commonly seen. Calcification within the mediastinum or hila can be seen in up to 86% of patients. Bronchial obstruction can result in pulmonary infiltrates due to atelectasis or infection. Pulmonary venous obstruction manifests with localized pulmonary venous hypertension: peribronchial cuffing, septal thickening, and localized edema. Vascular compression can result in infarction which can also produce peripheral wedge-shaped radiographic opacities. The presence of a dilated left superior intercostal vein (aortic nipple) can occur in association with superior vena caval obstruction. The extent of mediastinal involvement is frequently underestimated on the CXR.
CT: On CT, calcification of the mediastinal mass/adenopathy is common and is seen in up to 85% of cases. Other CT findings include an infiltrative hilar/mediastinal mass, tracheobronchial narrowing, pulmonary vessel entrapment, SVC obstruction, and pulmonary infiltrates (due to bronchial obstruction with atelectasis, or pulmonary infarction due to vascular entrapment). Differential considerations include infiltrative malignancy (lung cancer, lymphoma, or mediastinal desmoid tumor).
MR: T1 images typically demonstrate a heterogeneous, infiltrating intermediate signal mass. The T2 signal appearance is more variable- with both regions of increased and decreased signal. Heterogeneous enhancement of the mass can be seen following the administration of gadolinium.
Radionuclide studies are able to show abnormalities in perfusion or ventilation secondary to vascular or airway narrowing. In one reported case of FDG PET imaging, fibrosing mediastinitis appeared predominantly as a hypometabolic mass which contained foci of increased metabolic activity.