Fig. 6.36 A-G. Histoplasmosis capsulati (due to H. capsulatum var. capsulatum). A The right upper lung of a patient with miliary histoplasmosis: the tiny nodules cannot be accurately distinguished from miliary tuberculosis and many other miliary patterns. B Disseminated acute histoplasmosis in a 10- year-old child. C Chronic histoplasmosis causing fibrosis, with cavitation in the right upper lobe. There are calcified hilar nodes. Radiologically (and clinically) this is indistinguishable from tuberculosis, but both Histoplasma capsulatum var. capsulatum and Aspergillus were recovered from this lung. D Bilateral apical fibrosis from histoplasmosis, again indistinguishable from tuberculosis. E, F The characteristic pattern of calcified healed disseminated histoplasmosis. There may be no clinical evidence and the patient may be unaware of having been infected. G A histoplasmona in the left lower lobe of an asymptomatic patient. There is central calcification. Histoplasmomas have no diagnositc characteristics and only the histology will establish the diagnosis.

Imaging Diagnosis

The imaging pattern of histoplasmosis capsulati is so similar to tuberculosis that there is a temptation to refer the reader to Chap. 5. As with tuberculosis, there are acute primary patterns, a chronic reactivation form, a disseminated form and the end results when healed (Fig. 6.36).

Many patients with a positive histoplasmin skin test have multiple calcified nodules in the lung parenchyma, usually in the periphery, and also in the hilar nodes. These are usually incidental findings on a radiograph taken for some other reason. Skin tests sometimes may help to distinguish histoplasmosis from tuberculosis. In a few patients there will be a pulmonary nodule, usually solitary and peripheral (subpleural), well defined, and from a few millimeters to, more commonly, several centimeters across. Some of these nodules slowly enlarge (rather like a tuberculoma): CT scanning is useful to identify calcification, but when seen in older patients this does not always exclude carcinoma. Needle biopsy may be required or even removal of a nodule, particularly when there are several nodules resembling metastases. Even when the needle biopsy shows there is no malignancy, routine follow-up chest imaging to assess any change in the size of any particular nodule may be advisable.

Asymptomatic but enlarged lymph nodes can be calcified, and "eggshell" calcification is a common pattern in histoplasmosis. When the enlarged nodes are not calcified, histoplasmosis cannot be distinguished from any other cause of lymphadenopathy. Pressure from large infected lymph nodes can erode the walls of the bronchi and result in broncholithiasis or, if the nodules are sufficiently large, cause pressure constriction and obstruction: some of the pulmonary radiographic changes may be the result of this. In the more acute primary infection, there will be a "primary complex" with peripheral lung consolidation of varying density and often with associated lymphadenopathy. Parenchymal pneumonic changes may be fleeting, resembling an eosinophilic pneumonia. There is little relationship between the severity of the radiographic changes and the clinical illness. The latter may be mild, even when chest radiographs suggest an extensive process. As the lungs clear, commonly there may be small residual calcified foci. The lymphadenopathy subsides also, but not necessarily in step with the pulmonary improvement.

Acute histoplasmosis is the result of heavy exposure and inhalation, such as may happen when an individual has entered a cave and been the first to disturb accumulated bat droppings. The result can be a severe and often overwhelming illness, causing acute dyspnea, high fever, and fatigue. This is a very dramatic event: in many countries when an important person, such as a king or a priest, has been buried deeply within a cave or in a large, partially closed building, a "curse" is placed on those who may enter and desecrate this sacred resting place. Anyone who ventures to go in search of treasure may develop acute histoplasmosis, which is often fatal in its own right, but especially hazardous for those who believe that they are victims of the supernatural!

In some patients with acute lung infections, the imaging pattern is disseminated miliary nodulation, with lymphadenopathy. These patients are often severely ill, but if they survive and healing occurs, there will be calcified granulomas spread in a "snow storm" pattern throughout both lungs. Such numerous calcified miliary foci are very rarely the result of tuberculosis (but may follow chickenpox pneumonia, especially in adults).

Chronic pulmonary histoplasmosis is almost always superimposed on previous extensive lung disease (e. g., chronic obstructive pulmonary disease and emphysema). Chest radiographs show bullae in the upper lobe, often with contained fluid. The yeast grows in them and eventually spills throughout the bronchial tree, causing pneumonia in different segments of the lungs. This chronic form results in local necrosis, vascular occlusion, and fibrosis. It has been postulated that this is more of an antigen-antibody reaction, rather than the result of the infection. Chronic histoplasmosis is episodic, with symptoms waxing and waning over months, with hemoptysis and shortness of breath often changing but almost always with gradual progression. On imaging, the lung changes can be segmental or lobar, or peripheral opacities. Cavities often become thickwalled but, nevertheless, may continue to enlarge and spread in the adjacent lung. Overall the result is pulmonary fibrosis, very similar to chronic tuberculosis and radiographically indistinguishable (Fig. 6.36 C, D). Other fungal infections, such as aspergillosis, are liable to develop within the damaged lung. At any time this apparently chronic but suppressed histoplasmosis can break down and become more acute.

Fibrosis of the mediastinum is another complication of histoplasmosis which can compress or displace the vena cava, the pulmonary vessels, the trachea and bronchi, and even the esophagus. In endemic areas, histoplasmosis capsulati is probably the commonest cause of mediastinal fibrosis.