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variably sized spherules measuring 50 to 100 microns contain numerous refractile endospores
from 2 to 5 microns in size. The inflammatory response is poor. Occasionally, persons taking
anabolic steroids or corticosteroids can develop disseminated coccidioidomycosis almost
identical to that seen in AIDS.[483]
TOXOPLASMOSIS.-- In AIDS, toxoplasmosis is usually associated with disseminated
infection and secondary pulmonary involvement. The most common clinical finding is a cough,
either productive or non-productive. An abnormal chest roentgenogram marked by bilateral
interstitial infiltrates may appear in only half of cases. Diagnosis can be made by
bronchoalveolar lavage in most cases.[477]
Histologically, there may be focal necrosis with vague granuloma formation and/or
diffuse interstitial mixed inflammatory cell infiltrates with alveolar lining cell hyperplasia.
Diagnosis depends upon finding Toxoplasma gondii pseudocysts filled with bradyzoites, but
these are infrequent--even in severe infections. Free tachyzoites are small and difficult to
distinguish from debris or cell fragments with hematoxylin-eosin staining. T gondii pseudocysts
must be distinguished from cytomegalovirus cells lacking a visible nucleus but containing
intracytoplasmic virions. Cytomegalovirus tends to have a thinner wall, and the cytoplasmic
basophilic bodies of CMV are coarser than bradyzoites.[475]
ASPERGILLOSIS.-- Pulmonary aspergillosis does not occur commonly with AIDS, but
may appear late in the course when the CD4 lymphocyte count is <100/µL. Aspergillosis may
often occur in association with other infections such as cytomegalovirus and P jiroveci (carinii)
(in over half of cases), bacterial, or fungal pneumonias. Over 80% of cases are accompanied by
neutropenia (which can complicate antiretroviral therapy). In 15% of cases there is a history of
corticosteroid therapy or broad-spectrum antibiotic therapy.[622,623] Marijuana smoking may
also be a risk because marijuana is an excellent fungal growth medium.
The major clinical findings with pulmonary aspergillosis in AIDS are fever, cough, and
dyspnea in over half of cases. Other findings may include pleuritic chest pain, malaise, and
weight loss. The two clinical patterns of pulmonary aspergillosis in AIDS are: (1) acute invasive
pulmonary aspergillosis with prolonged cough and fever, and (2) obstructing-bronchial
aspergillosis with dyspnea, cough (sometimes productive of bronchial casts containing the fungal
hyphae), and chest pain. Dissemination of infection occurs in a few cases, with the central
nervous system, kidney, and heart most likely to be affected. Bronchoalveolar lavage may yield
a diagnosis in 67% of cases, though finding Aspergillus in BAL specimens does not always
indicate a true infection, but rather upper respiratory tract colonization. A transbronchial biopsy
is diagnostic in 27% of cases.[622,623] A serum galactomannan assay can be helpful in
diagnosing invasive aspergillosis, but there is cross-reactivity with other fungi.[624]
Radiographically, there may be unilateral or bilateral infiltrates with angioinvasion and
thick-walled, .cavitary, upper lobe disease that may be complicated by hemoptysis. On
computed tomographic scans, parenchymal nodules with surrounding peripheral halo of ground
glass attenuation and variable cavitation from focal infarction may be seen. An uncommon
variant known as obstructing bronchial aspergillosis may produce bilateral diffuse lower lobe
consolidation on chest radiograph because of post-obstructive atelectasis. Airway impaction
produces a “finger-in-glove” pattern.[607]
Histologically, the hyphae of Aspergillus are best identified in bronchoalveolar lavage
specimens, but they can also be readily identified in biopsied tissues. The lungs grossly may