HIV-infected patients suffer from a variety of lung infections and neoplasms. Several factors are crucial in making the correct diagnosis. The CD4 count is a measure of a patient’s immune status and is predictive of which pulmonary manifestation will be encountered (Table 6.1). For example, cytomegalovirus (CMV) infections are encountered in patients
with CD4 counts under 20 cells/mm³, whereas Nocardia pneumonia and Kaposi sarcoma are encountered when the count is less than 200 cells/mm³ (4).

Patient demographics also help to determine likely pulmonary manifestations (Table 6.1). Intravenous drug abusers are more likely to suffer infections such as Staphylococcus aureus pneumonia, septic emboli, and tuberculosis (5), whereas CMV infections are more frequent in patients infected by HIV through sexual contact (6).

Prophylactic antimicrobial therapy decreases the likelihood of infection with drug-susceptible organisms (4) but may delay diagnosis by interfering with blood and sputum culture results (7). Integration of the radiographic appearance with demographic data, laboratory results, and clinical presentation is necessary to reach a reasonable differential diagnosis (8).

AIDS patients have altered B-cell function and are therefore susceptible to severe infections by encapsulated bacteria, such as Streptococcus pneumoniae and Hemophilus influenza, with any CD4 count (9). As the CD4 count falls, the susceptibility to bacterial infection increases (10). The introduction of Pneumocystis carinii pneumonia (PCP) prophylaxis has increased the incidence of bacterial pneumonia relative to that of PCP (10). Intravenous drug abusers are at greater risk to develop S. aureus pneumonia, septic emboli, and empyema (5).

Bacterial pneumonia typically presents with segmental or lobar airspace disease. In patients with AIDS there is a higher incidence of multilobar pneumonia (4) and of rapid progression and cavitation (7) (Fig. 6.1) than in non-immunocompromised hosts. Pyogenic airway disease with bronchitis, bronchiolitis, and bronchiectasis is common in HIV-infected
patients with normal CD4 counts. The radiographic findings are subtle and include bronchial wall thickening on the CXR and tree-in-bud opacities, bronchiectasis, bronchial wall thickening, and mucoid impactions on HRCT (11).

Fungal pneumonia is uncommon in AIDS patients because neutrophil activity is preserved. Patients receiving antiviral therapy that induces granulocytopenia are susceptible to fungal infections (7) (Fig. 6.5). The common pathogens causing fungal pneumonia are Cryptococcus and Aspergillus. Cryptococcus is a fungus that commonly causes meningitis. The radiographic features of Cryptococcus pneumonia include nodular interstitial infiltrates, solitary or multiple pulmonary nodules or masses that may cavitate, pleural effusions, and lymph node enlargement (20). The radiographic appearance of Aspergillus is discussed later in this chapter (Fig. 6.6).

P. carinii is a unicellular organism that behaves like a protozoan but is classified as a fungus (21). The organism cannot be grown in cultures, and therefore the diagnosis is based on visualizing the organism (or its cyst) in special stains preformed on sputum or bronchoalveolar lavage fluid. PCP can occur at any level of immunosuppression, but it becomes common when CD4 counts are at or below 200 cells/mm³. Despite the use of effective prophylactic therapy and the resultant decline in PCP, it remains the most common opportunistic pulmonary infection in AIDS. Approximately 70% of AIDS patients will suffer at least one PCP infection during the course of their disease. It is more common in homosexual and male patients (21,22). PCP in AIDS patients is insidious and presents with nonproductive cough, dyspnea, low-grade fever, and malaise (8).

The radiologic manifestations of PCP are varied. In most cases it presents as bilateral, diffuse, symmetric parenchymal abnormality with a perihilar and basilar predominance (Fig. 6.7). Early findings are often subtle, and the CXR is normal or nearly normal in anywhere from 10% to as many as 39% of patients (8). Infection may appear as interstitial granular or reticular opacities or as airspace disease. Without treatment PCP often progresses to confluent airspace disease (22,23). Upper lobe disease is classically seen in patients receiving aerosolized prophylactic pentamidine therapy (23). Radiographic improvement is expected within 10 days of appropriate treatment, although there is usually initial radiographic worsening due to capillary leak. Atypical manifestations are encountered in approximately 5% and include isolated lobar disease, focal parenchymal opacities, nodules and masses, a miliary pattern, endobronchial lesions, and pleural effusions (23).

AIDS patients may present with cystic lesions (Fig. 6.8), thin or thick walled, regular or irregular in shape, that may be surrounded by GGOs (Fig. 6.9), indicating inflammatory pneumonitis. This form of disease is termed cystic PCP and is rare in non-AIDS patients (21,23). The cystic lesions show a predilection for the lung apices and subpleural
areas, and patients present with spontaneous pneumothorax in 6% to 7% of cases (Fig. 6.10). The pneumothoraces are frequently bilateral, associated with a higher mortality rate of 33% to 57%, and not always responsive to standard chest tube placement (21).

Chest CT and HRCT are helpful for the patient with a nonspecific clinical presentation and normal or near normal CXR or when PCP relapse is suspected in the presence of an abnormal CXR from a previous episode of infection (21). At HRCT, PCP manifests as GGOs that may be diffuse and homogeneous or patchy and geographic in distribution, often in the perihilar lungs (7,21). GGO is attributed to accumulation of fluid, organisms, and debris within the alveoli and is considered highly suggestive of P. carinii infection in the setting of HIV infection (Figs. 6.6, 6.9, and 6.10). HRCT may show thickening of interlobular septa secondary to edema and cellular infiltration and may delineate the extent and distribution of cyst formation and changes of interstitial fibrosis secondary to chronic PCP. CT findings may suggest an alternative diagnosis, an additional diagnosis along with PCP (Fig. 6.6), or another pathogen and may help to direct a biopsy.