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Radiology > CHEST
Histoplasmosis, Thoracic
Article Last Updated: Aug 15, 2007
AUTHOR AND EDITOR INFORMATION
Section 1 of 12  
Author: Fahad M Alhameed, MD, AmBIM, FCCP, FRCPC, Deputy Chairman of Intensive Care Department, Consultant Critical Care and Pulmonary Medicine, Department of Intensive Care and Pulmonary Medicine, King Khalid National Guard Hospital, Jeddah, Saudi Arabia
Fahad M Alhameed is a member of the following medical societies: American College of Chest Physicians, American Thoracic Society, Canadian Medical Association, and Royal College of Physicians and Surgeons of Canada
Coauthor(s):
Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St. Boniface General Hospital;
Bruce Maycher, MD, Director of Pulmonary Radiology, St Boniface General Hospital; Associate Professor, Department of Radiology, University of Manitoba
Editors: Satinder P Singh, MD, Associate Professor of Radiology, Director of Cardiac CT, Director of Combined Cardiopulmonary and Abdominal Radiology, Department of Radiology, University of Alabama at Birmingham; Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand; Eric J Stern, MD, Professor of Radiology, Adjunct Professor of Medicine, Adjunct Professor of Medical Education and Biomedical Informatics, University of Washington School of Medicine; Director of Thoracic Imaging, Harborview Medical Center; Associate Medical Staff, Seattle Cancer Care Alliance; Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute; Barry H Gross, MD, Professor, Department of Radiology, University of Michigan Medical School; Professor, University of Michigan Cancer Center
Author and Editor Disclosure
Synonyms and related keywords:
Histoplasma capsulatum, pulmonary histoplasmosis, histoplasmoma, disseminated histoplasmosis
Background
Histoplasmosis is the most common of the endemic mycoses and a major cause of morbidity and mortality in patients living in endemic areas. Histoplasma capsulatum first was described in 1905 by Samuel Darling, a US Army pathologist stationed in Panama. Darling examined visceral tissues and bone marrow from a young man from Martinique whose death originally was attributed to miliary tuberculosis. The organism initially was described as protozoal. Because it lacked a kinetoplast, Darling assumed that it was a different species of Leishmania. He termed it H capsulatum. In 1912, after reviewing tissue specimens, da Rocha-Lima suggested that the organism resembled a yeast rather than a protozoan. H capsulatum has since been found worldwide. In the United States, histoplasmosis is highly prevalent in the Ohio and Mississippi River valleys.
Pathophysiology
The respiratory tract is considered the portal of entry for H capsulatum in most patients. Cellular immunity plays the primary role in defense against the organism. After conidia have been inhaled and settle into the alveoli, they bind to the CD2/CD18 family of integrins and are engulfed by both neutrophils and macrophages but not killed. In the macrophages, conidia transform into yeast within the pulmonary parenchyma; the yeast migrates, presumably intracellularly, to local draining lymph nodes and, subsequently, to distant organs rich in mononuclear phagocytes, such as the liver and spleen. The transition from the mycelial to the yeast phase is one of the most critical determinants for establishing infection. Cellular immunity to Histoplasma develops within 2 weeks of exposure. These defense mechanisms are sufficient to control the infection in immunocompetent subjects, explaining the subclinical or self-limited course characteristic of acute histoplasmosis. Yeast grows more rapidly within macrophages from HIV-infected individuals or within macrophages infected in vitro with a macrophage-tropic strain of HIV. Among T-cell populations, CD4 cells are vitally important, as demonstrated by Gomez when mice deficient in CD4 cells died when challenged with a sublethal inoculum of yeast. The hallmark of tissue response to this fungus is the development of caseating and/or noncaseating granulomas in which calcium may be deposited. Granulomas consist of an admixture of mononuclear phagocytes and lymphocytes, principally T cells. The putative function of the granuloma is to contain fungal growth. Progressive clinically evident dissemination occurs primarily in patients with underlying immunosuppressive disorders, those at the extreme ranges of age, and/or in patients who have experienced an unusually heavy exposure.
Frequency
United States
The infection is most common in the southeastern, mid-Atlantic, and central states and in the Ohio and Mississippi River valleys.
International
H capsulatum is endemic in areas of North and Latin America but can be found throughout the world. The conditions that favor the growth of this fungus in soil typically are found in the temperate zone between latitudes 45° north and 30° south. Factors accounting for its geographic distribution include humid environmental conditions and acidic permeable soil. The organism commonly is found in bird and bat droppings, most often where guano is decaying and mixed with soil.
Mortality/Morbidity
Only 5% of infected individuals develop symptomatic disease after a low-level exposure to Histoplasma. The estimated incidence of histoplasmosis is 1 per 2000 persons. After 2 Indianapolis epidemics, progressive disseminated histoplasmosis (PDH) developed in 8% of clinically recognized cases of histoplasmosis. In the 2 epidemics, the primary risk factors for this manifestation of histoplasmosis were age greater than 54 years and immunosuppression. Among patients with AIDS, the incidence may approach 25%. When the condition is not treated, mortality is almost 100%. Before effective antifungal agents were introduced, most children died within 5-6 weeks of symptom onset.
Race
In histoplasmosis, unlike coccidioidomycosis, no differences are known in susceptibility or resistance to infection among racial or ethnic groups.
Sex
Male-to-female ratio is approximately 4:1. The higher frequency in men probably is correlated to a higher incidence of smoking.
Age
Clinical disease more commonly occurs in older persons and those younger than 2 years.
Clinical Details
The clinical spectrum of the disease depends on the extent of exposure, age, presence of underlying lung disease, general immune status, and specific immunity to H capsulatum. Lungs are the most common organs involved. Infections can be classified as follows: - Pulmonary histoplasmosis
- Acute asymptomatic pulmonary histoplasmosis: This is the most common manifestation that occurs following histoplasmosis infection (>90%). This type commonly occurs in individuals with normal immunity residing in endemic areas. Patients have positive skin-test results, but most have normal chest radiographs and negative serology-test results.
- Acute symptomatic pulmonary histoplasmosis: This is a benign, self-limited illness characterized by symptoms of fever, chills, headache, cough, and retrosternal or pleuritic chest pain. Malaise, weakness, fatigue, and myalgia are observed in a distinctly smaller percentage of patients. Symptoms commonly are mistaken for a flulike illness; however, coryza and sore throat are not typical symptoms of histoplasmosis and suggest alternative diagnoses. Physical examination usually is unremarkable except for fever. Rales and, rarely, hepatosplenomegaly may be detected . Symptoms typically develop 2-4 weeks after infection, depending on the intensity of exposure and immunity status of the patient, and typically resolve within several weeks.
- Acute reinfection pulmonary histoplasmosis: This is not uncommon in those residing in endemic areas and subject to reexposure. The duration of illness is often shorter than it is in primary infection. The characteristic chest radiograph shows numerous small nodules diffusely scattered throughout both lung fields.
- Chronic pulmonary histoplasmosis: This occurs in patients with underlying lung disease, especially chronic obstructive pulmonary disease (COPD). Affected patients develop a productive cough, dyspnea, chest pain, fatigue, fever, and sweats and have fibrotic apical lesions with cavitation on chest radiographs or CT. The clinical and radiographic findings resemble those seen in reactivation tuberculosis; the 2 syndromes often are confused, and incorrect diagnoses have resulted in inappropriate treatment.
- Progressive disseminated histoplasmosis (PDH): It occurs in immunodeficient patients with defective T-cell immunity (patients with AIDS or hematologic malignancies [eg, Hodgkin and non-Hodgkin lymphoma] or those taking immunosuppressive medications). Patients at the extreme of ages also are at risk for disseminated disease. PDH can develop upon reexposure to a large inoculum of the fungus or upon reactivation of dormant endogenous foci. Most cases are believed to arise from endogenous reactivation, because the disease develops in those who reside in remote endemic areas. Fever and malaise are the 2 most common manifestations, followed by weight loss, cough, and diarrhea. Patients can develop hepatosplenomegaly, lytic bone lesions, skin lesions, peripheral lymphadenopathy, prostatitis, or epididymitis.
- Miliary pulmonary histoplasmosis: This is a special presentation that follows a more intense exposure. Patients often develop reticulonodular or miliary pulmonary infiltrates (a scenario that resembles miliary tuberculosis) and may progress to respiratory failure or extrapulmonary PDH (see Images 6-7).
- Nonpulmonary histoplasmosis
- Pericarditis occurs in 5-10% of symptomatic cases of acute histoplasmosis; it is caused by an immunologic reaction to histoplasmosis in the adjacent mediastinal lymph nodes.
- Rheumatologic syndromes, such as arthralgias, erythema nodosum, and erythema multiforme, are present in approximately 6% of patients, most of whom are women. In some patients, this manifestation of histoplasmosis may be the presenting complaint. Frank arthritis is distinctly uncommon.
- Sarcoidosis-like syndrome is so termed because distinguishing between histoplasmosis and sarcoidosis can be difficult. The 2 disorders may demonstrate similar histopathologic features, and serum angiotensin-converting enzyme levels are elevated in both. Therefore, for patients presenting with mediastinal or hilar lymphadenopathy and residing, or having recently resided, in an endemic region, it is critically important to consider histoplasmosis in the differential diagnosis.
- African histoplasmosis
- H capsulatum var duboisii is a variant that is primarily seen in Africa; however, a few cases have been reported in the United States and Chile. The yeast form of H capsulatum var duboisii typically is much larger, with a diameter as great as 15 µm, and has a thicker wall.
- The clinical picture associated with infection by H capsulatum var duboisii is distinctly different from that associated with H capsulatum var capsulatum.
- Most frequently, the skin and skeleton are affected by this pathogen. Skin ulcers, nodules, and psoriasis-like lesions are common. Osteolytic bone lesions are noted in as many as 50% of patients. The skull and ribs are the bones affected most often, followed by the vertebrae. The organism produces granulomatous inflammation within bone. Pulmonary involvement is uncommon, even in the presence of dissemination.
Complications of histoplasmosis infection
- Mediastinal granuloma: Mediastinal granuloma is an uncommon late sequela of mediastinal adenitis and is characterized by massive enlargement of the mediastinal lymph nodes, which become encapsulated and caseous centrally. A consequence of enlarged nodes is the creation of sinuses or fistulas between the airways and the pericardium or esophagus. There is no associated fibrotic reaction. Extrinsic compression of the trachea can cause respiratory distress, especially in young children, and prolonged obstruction can cause bronchiectasis or bronchial stenosis.
- Fibrosing mediastinitis: Fibrosing mediastinitis represents an excessive fibrotic response to a prior episode of histoplasmosis in which almost all mediastinal structures can be involved. It is postulated to occur as a result of leakage of antigen from caseous nodes into the mediastinum, which stimulates an abnormal immunologic/inflammatory response leading ultimately to fibrosis. The fibrosis can constrict or obstruct mediastinal structures such as the superior vena cava (SVC), pulmonary arteries or veins, the bronchi, and the esophagus. Affected patients usually are young and can be asymptomatic. However, symptoms commonly develop gradually as the mediastinal structures are obliterated, causing cough, dyspnea, SVC syndrome, dysphagia, hemoptysis, and hoarseness. It is associated with higher morbidity and mortality and is less amenable to treatment.
- Broncholithiasis: When lymph nodes and pulmonary granulomas calcify, they can erode into the adjacent bronchi, causing hemoptysis and/or obstruction. Patients can expectorate rocklike particles of tissue, which can result in recurrent and severe hemoptysis, bronchial obstruction, or tracheoesophageal fistula.
- Cavitary pulmonary histoplasmosis: Patients can develop progressive upper lobe infiltrates with cavitation, which indicates disease progression. Men older than 50 years with preexisting chronic lung disease (usually emphysema) constitute the highest proportion of patients. This disease is unusual in patients younger than 40 years (<5% of all cases).
Preferred Examination
Diagnostic modalities include cultures, fungal stains of tissue or body fluids, and tests for antibodies and antigens. Each test has limitations that must be recognized to be used correctly. The success rates vary considerably and often are correlated with the number of specimens collected, the source of the specimen, and the burden of infection. Antigen detection Antigen is detected in as many as 90% of patients with PDH, 40% with cavitary disease, and 20% with acute pulmonary histoplasmosis. Histoplasma glycoprotein antigen can be detected in the urine of 90% of patients with disseminated infection and in 75% of those with diffuse acute pulmonary histoplasmosis. The sensitivity of antigen detection is lower in serum than in urine, and the highest diagnostic yield can be achieved by testing both specimens. The test has excellent usefulness for monitoring relapses of PDH, especially in patients with immunosuppression. Antigen detection is much more sensitive than serology for identifying relapses and has been applied successfully to cerebrospinal fluid in patients with meningitis. Antigen levels fall with successful therapy and increase with relapse. The specificity of this test also is relatively good; however, in patients infected with Blastomyces dermatitidis, Paracoccidioides brasiliensis, or Penicillium marneffei, a high degree of cross-reactivity exists in the enzyme-linked immunosorbent assay urine antigen test. Serology Serologic tests are positive in approximately 80% of patients with disseminated histoplasmosis, 90% of patients with acute pulmonary histoplasmosis, and almost 100% of patients with chronic pulmonary histoplasmosis. A high serum concentration of antibodies develops within 8 weeks of exposure in most patients and then declines to low or undetectable levels over a 2- to 5-year period. The complement fixation test is more sensitive than the immunodiffusion test. Complement fixation titers of 1:32 or higher are highly suggestive of acute infection. False-positive results may occur in blastomycosis, coccidioidomycosis, candidiasis, and aspergillosis. Fungal cultures Cultures provide the strongest proof for histoplasmosis but are limited by low sensitivity (10-15%) in self-limited infections and by delayed growth (2-4 wk). In patients with disseminated disease, the highest yield is from bone marrow or blood cultures, which are positive in more than 75% of patients. The organisms can be found in sputum or bronchoscopy specimens in 60-85% of patients with cavitary histoplasmosis. Cultures usually are negative in patients with mild acute pulmonary, pericardial, or rheumatologic manifestations. Fungal staining Fungal staining permits rapid diagnosis but with a lower sensitivity than culture or antigen detection. Bone marrow, cerebrospinal fluid, and bronchoalveolar lavage are associated with the highest yields (see Images 1-2). Fungal staining of lung or mediastinal lymph node tissue permits rapid diagnosis of histoplasmosis but has a lower sensitivity than culture or antigen detection. Polymerase chain reaction techniques are in development and may assist in the correct diagnosis of H capsulatum infections in patients in whom morphology is inconclusive and cultures are negative. Histologically, noncaseating granulomas are commonly seen (see Image 3). Skin test Skin tests rarely are helpful. Radiologic modalities Radiographic findings primarily depend on the type of presentations and the immune status of the host. Although chest radiographic findings are normal in most patients, it is the first radiologic modality performed. The most common abnormal radiographic findings consist of single or multiple poorly defined areas of airspace consolidation, frequently in the lower lobes. With time, these opacities are cleared and form a nodule that can later calcify.
Blastomycosis, Thoracic
Coccidioidomycosis, Thoracic
Sarcoidosis, Thoracic
Other Problems to Be Considered
Blastomycosis
Coccidioidomycosis
Mycobacterium tuberculosis
Nonmycobacterial tuberculosis
Miliary tuberculosis
Lymphoma
HIV
Sarcoidosis
Findings
Radiographic findings depend primarily on the type of presentations and the immune status of the host.
- Chest radiographic findings are normal in most patients. A solitary pulmonary nodule is a frequent finding on chest radiographs of the patient with asymptomatic primary infection. These nodules vary from a few millimeters to several centimeters. Most of these nodules have well-defined margins and central, laminar, or diffuse calcification patterns. Interestingly, some nodules can slowly enlarge because of continued elaboration of collagen at the periphery of the lesion and, thus, can be difficult to distinguish from malignancy.
- As many as 10-25% of patients with asymptomatic infection develop single or multiple poorly defined areas of airspace consolidation and/or nodules, with or without hilar lymph node enlargement. Enlarged lymph nodes often are seen after an asymptomatic infection. Adenopathy is frequently seen with lung parenchymal abnormalities and often contains calcification. This calcification occasionally may be seen on CT only. Patients with noncalcified mediastinal adenopathy need to be distinguished from sarcoidosis, lymphoma, and metastases. Enlarged lymph nodes can cause significant bronchial or tracheal compression or obstruction and may cause esophageal obstruction. Atelectasis, collapse, and obstructive pneumonitis can develop as a consequence of airway obstruction.
- In acute symptomatic pulmonary histoplasmosis, radiographic findings include areas of airspace parenchymal consolidation that involve more than one segment or lobe, simulating acute bacterial pneumonia.
- Pleural effusions are seen in a minority of patients with acute pulmonary histoplasmosis, and organisms rarely are isolated from pleural fluid.
- After heavy exposure, radiographs can show widely disseminated, diffuse, fairly discrete nodular shadows throughout the lungs (with individual lesions measuring 1-10 mm in diameter), termed miliary histoplasmosis (see Images 4-5), a scenario similar to miliary tuberculosis (see Images 6-7). The infiltrates clear within 2-8 months; however, lesions may fibrose and calcify or persist for many years.
- Lung cavitation usually is noted in persons with underlying obstructive lung disease, and it is similar to chronic active tuberculosis, with predominantly upper lobe disease characterized by fibrosis, necrosis, cavitation, and granulomatous inflammation.
Findings
CT scanning in patients with histoplasmosis is helpful in detecting calcification in a lung nodule (histoplasmoma) and evaluating patients with fibrosing mediastinitis and broncholithiasis. CT is more sensitive in detecting subtle calcification in a nodule and can identify other smaller nodules that are not seen on chest radiographs (see Image 13).
- CT is very useful in the evaluation of patients with suspected fibrosing mediastinitis. CT can define the extent of the fibrous mass in the mediastinum/hilum and demonstrate its obstructing effect on SVC, pulmonary vessels, esophagus, trachea, or bronchi. Venous collaterals can be seen, indicative of long-standing venous occlusion. Stippled or dense calcification within the mass is present in most of these patients with fibrosing mediastinitis and easily can be seen on CT (see Image 9).
- Serial CT scans can identify progression of the fibrosis and assess the indications for surgery.
- CT is superior to MRI in demonstrating calcification.
In a retrospective review of the radiographic findings of fibrosing mediastinitis (FM) in 33 patients on various imaging studies, including chest radiographs, CT scans, MRI examinations, esophagrams, ventilation perfusion scans, angiograms, and venograms, Sherrick et al reported the following1:
- Bronchial narrowing in 11 patients (33%)
- Pulmonary artery obstruction/narrowing in 6 patients (18%)
- Esophageal narrowing in 3 patients (9%)
- SVC obstruction/narrowing in 13 patients (39%)
Two distinctly different radiographic patterns were identified, including a localized pattern seen in 27 patients (82%) that frequently contained calcification and a diffuse pattern seen in 6 patients (18%) that did not contain calcification. The localized pattern most likely was a result of histoplasmosis and did not show radiographic evidence of improvement with steroid therapy. More likely, the diffuse pattern was truly idiopathic or of a noninfectious etiology. Several patients with the diffuse pattern showed radiographic evidence of improvement with steroid therapy. In patients without calcification or with progressive radiographic findings, it is advisable to obtain tissue specimens for definitive diagnosis. CT nicely demonstrates the abnormalities associated with broncholithiasis. It can both identify calcified lymph nodes not visible on chest radiographs and show their relation to the affected airway. Soft-tissue mass is not associated with broncholithiasis; if found, it should lead to consideration of other diseases, such as lung cancer engulfing a calcified node.
Findings
MRI is comparable to CT in defining the extent of hilar or mediastinal lymphadenopathy. The primary advantage of MRI is its ability to diagnose vascular obstruction without the need for intravenous contrast material, especially in patients with renal failure. However, CT is superior to MRI in demonstrating calcification. The adenopathy associated with fibrosing mediastinitis demonstrates relatively low signal intensity on T2-weighted images.
Findings
Ultrasound (US) has a limited role in diagnosing histoplasmosis; however, US helps define hepatomegaly or splenomegaly. US also assesses the extent of pleural and pericardial effusions, cardiac tamponade, calcification of the pericardium, or constrictive pericarditis.
Findings
Angiography can be helpful in demonstrating some conditions associated with histoplasmosis (eg, superior vena cava obstruction) and in detecting when great vessels are involved in fibrosing mediastinitis.
Medical/Legal Pitfalls
- Failure to maintain a high index of suspicion may result in misdiagnosis or delay in diagnosis.
- Failure to carefully review the patient's occupation, travel history, and region of habitation may result in misdiagnosis.
- Failure to ask for the type of culture specific to an organism may delay diagnosis.
- Failure to consider histoplasmosis because of a normal chest radiograph may delay diagnosis.
We thank Sean Tsuyuki, MD, for his contributions to this article.
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Thoracic histoplasmosis. Gomori methenamine silver staining performed on lung tissue shows the yeast phase of histoplasmosis. |
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Thoracic histoplasmosis. Another image of yeast phase of histoplasmosis. |
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Thoracic histoplasmosis. A transbronchial biopsy was performed. Pathologic examination of the specimen revealed multiple noncaseating granulomas present diffusely (same patient as in Image 1). |
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Thoracic histoplasmosis. A 36-year-old man developed progressive cough, fever, and dyspnea. Chest radiograph shows multiple diffuse tiny but discrete pulmonary nodules. This miliary pattern can be seen in miliary tuberculosis, histoplasmosis, blastomycosis, silicosis, berylliosis, miliary sarcoidosis, and metastatic malignancy. |
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Thoracic histoplasmosis. This is a lateral view of the same patient as in Image 4. |
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Thoracic histoplasmosis. High-resolution CT of the chest confirms chest radiographic findings and nicely shows the tightly formed micronodules in both upper lobes. |
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Thoracic histoplasmosis. CT image at the lung bases confirms the diffuse nature of the disease (a miliary form of disseminated pulmonary histoplasmosis [DPH]). |
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Thoracic histoplasmosis. Chest radiograph demonstrates a lobulated soft-tissue mass in the right paratracheal region, with an enlarged and dense right hilum, suggesting lymphadenopathy. The radiographic differential diagnosis for these findings includes lung cancer, primary tuberculosis, histoplasmosis in endemic areas, lymphoma, and (less likely) sarcoidosis (due to its asymmetric nature of nodal enlargement). Further workup revealed that this patient had a sarcoid-type reaction to histoplasmosis. |
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| Media file 9:
Thoracic histoplasmosis. Noncontrast chest CT image of the same patient as in Image 7 shows multiple enlarged lower paratracheal lymph nodes (arrows). There is a vague airspace opacity in the right upper lobe, as well. |
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Thoracic histoplasmosis. Fibrosing mediastinitis is a rare but well-known clinical manifestation of histoplasmosis. Contrast enhanced chest CT at the level of the aortic arch in a patient with histoplasmosis and fibrosing mediastinitis shows an ill-defined soft-tissue mass encasing and narrowing the trachea. The superior vena cava is also significantly narrowed (arrowhead). |
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Thoracic histoplasmosis. A chest radiograph in a 44-year-old man originally referred to an oncologist for left lung nodule considered to be a neoplasm. Review of the chest radiograph reveals a well-circumscribed dense calcified nodule in the left lower lobe (arrow) consistent with a healed calcified granuloma. Subsequent history revealed extensive travel to the histoplasma endemic areas. The antibody testing showed H and M precipitins by immunodiffusion test. |
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Thoracic histoplasmosis. A close-up of the left lower lobe nodule is shown here. |
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Thoracic histoplasmosis. Lung windows of the chest CT of the same patient as in Images 11 and 12 confirm a well-defined granuloma that was calcified on soft-tissue windows (not shown). Additionally, there were many other nodules in both lungs that were not seen on the chest radiograph. |
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Thoracic histoplasmosis. A case of histoplasmoma in another patient showing 2 well-defined left upper lobe nodules confirmed by needle biopsy. In cases with noncalcified nodules, resection or percutaneous needle biopsy is occasionally required to establish the benign etiology of the lesion, as in this case. |
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Thoracic histoplasmosis. A close-up view of the histoplasmoma (same patient as in Image 14). |
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Histoplasmosis, Thoracic excerpt Article Last Updated: Aug 15, 2007
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