Radiographic manifestations of pulmonary disease in the acquired immunodeficiency syndrome (AIDS)

Radiographic manifestations of pulmonary disease in the acquired immunodeficiency syndrome (AIDS)

Radiographic Manifestations of Pulmonary Disease in the Acquired Immunodeficiency Syndrome (AIDS) By David P. Naidich, Stuart M. Garay, Barry A ...

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Radiographic Manifestations of Pulmonary Disease in the Acquired Immunodeficiency Syndrome (AIDS) By David

P. Naidich,

Stuart

M.

Garay,

Barry

A

IDS is a syndrome of truly protean manifestations, in which pulmonary abnormalities, both infectious and neoplastic, represent a major source of both morbidity and mortality (Table 1).le3 More than 50% of patients with AIDS develop pulmonary manifestations at some time in the course of their disease. At risk is a large patient population, including homsexual and bisexual men (65%), homosexual or bisexual men with a history of using IV drugs (8%), heterosexual IV drug abusers (17%), recipients of transfusions or other blood products (3%), as well as an increasing number of children born of infected mothers. Only 6% of patients have shown none of these risk factors. Clinically, these patients present with severe abnormalities of cellular and humoral immunity. Awareness of the specific types of alterations in the immune system (as discussed in the “Overview” of this Seminars) are especially important for understanding the spectrum of pulmonary diseases to which patients with AIDS are liable.4 As originally defined by the Centers for Disease Control (CDC) for the purpose of surveillance, the diagnosis of AIDS is based on the identification of a reliably diagnosed disease at least moderately predictive of cellular immune dysfunction, in the absence of an underlying cause for such immunodeficiency. The case definition has been modified to include the following diseases, either primarily or secondarily pulmonary in origin, in patients with positive serology for AIDS: (1) disseminated histoplasmosis, diag-

York,

NY

& Stratton,

I. McCauley

nosed by culture, microscopy, or rising antigen level; (2) bronchial or pulmonary candidiasis, diagnosed by microscopy or by the presence of characteristic white plaques in the bronchial mucosa (not solely by culture); (3) non-Hodgkin’s lymphoma of high grade histologic type (diffuse, undifferentiated), and of B cell or unknown immunologic phenotype; (4) Kaposi sarcoma (KS) and (5) chronic lymphoid interstitial pneumonitis (LIP) in a child under the age of 13.5 OPPORTUNISTIC

INFECTIONS

Pneumocystis carinii Pneumonia due to Pneumocystis carinii (PCP) is the most common life-threatening infection in patients with AIDS.6*7 Occurring at least once in the course of the disease in approximately 60% of patients, nearly a quarter of the initial episodes prove fatal. Table

1.

Types

and Frequency 441 Patients

Pulmonary

of Pulmonary with AIDS

Disorder

Disorders

Percent

pneumonia

373

84.6

Without coexisting infection With coexisting infection

255 118

57.8 26.8

50 37

11.3

Pneomocysris

carinii

Cytomegalovirus Mycobacterium

avium-intra-

Mycobacterium Legionella Cryptococcus

tuberculosis

Other Other pulmonary infections M avium-intracellulare

15 9

3.5 2.0

8 3

1.8 0.6

93

avium-in-

bacteria

Toxoplasmosis Kaposi Sarcoma Modified

Seminars

8.4

&/u/are

Fungi M tuberculosis Herpes simplex

Inc.

in

No. of Patients

C”S Pyogenic Legionella

0037-198X/87/2201~005$05.00/0

14

Dorothy

from

8.4 4.0

5

1.1

1

0.2

in Roantganology,

11 10

2.5 2.3

6 4 2

1.4 0.9 0.5

1

0.2 8.2

36 Murray

21.1

37 18

trace//u/are Cytomegalovirus/Cryptococ-

10016.

o 1987 by Grune

and

Cytomegalovirus CytomegaloviruslM

From the Departments of Radiology, and Pulmonary Medicine, New York University Medical Center-Bellevue Hospital, New York. David P. Naidich: Assistant Professor, Department of Radiology; Stuart M. Garay: Associate Professor, Department of Pulmonary Medicine; Barry S. Leitman: Assistant Professor, Department of Radiology; Dorothy I. McCauley: Associate Professor, Department of Radiology. Address reprint requests to D.P. Naidich, MD, Deportment of Radiology, Bellevue Hospital, 27th St and 1st Ave, New

S. Leitman,

et al’

Vol XXII,

No 1 (January).

1987:

pp 14-30

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15

Fig 1. Pneumocystis carinii pneumonia. The PA radiograph shows bilateral perihilar and basilar reticular infiltrates, without evidence of adenopathy or effusion.

Clinical differences are apparent with PCP in patients with AIDS, compared with patients with other immunodeficiencies.8 In AIDS patients, the diagnosis requires a higher than usual degree of clinical suspicion. The patient frequently presents subacutely with fever, cough, and dyspnea,

Pneumocystis Fig 2. nantly by foamy exudates methanamine stain.)

cerinii pneumonia. in the alveoli

for as long as 2 weeks. Although laboratory studies often reveal lymphopenia and abnormalities in gas exchange, these findings are nonspecific. When compared with the pre-AIDS era, drug therapy in AIDS is accompanied by an unusually high frequency of adverse reactions.

Histologic section from e transbronchiel (curved arrows) within which individual

biopsy. round

PCP cysts

is characterized can be identified.

predomi(Silver

16

Trimethoprim-sulfamethoxazole may cause leukopenia, diffuse erythematous skin rash (including Stevens-Johnson syndrome), hepatotoxicity, thrombocytopenia, azotemia, and drug fever in up to 65% of patients. Similar problems, including hypoglycemia, orthostatic hypotension, and azotemia also occur with greater than expected frequency following administration of pentamidine. As will be discussed, these differences in clinical presentation and course have significant implications for the interpretation of radiographic findings in patients suspected of having AIDS. The radiographic manifestations of PCP have been widely reviewed. 9-” Typically, PCP causes

NAIDICH

ET AL

bilateral perihilar or basilar reticular or reticulonodular infiltrates that rapidly progress in three to five days to diffuse air-space consolidation involving almost the entire lung (Fig 1). Despite its pathologic designation as an interstitial pneumonitis, the hallmark of PCP is the presence of organisms within intraalveolar exudates, using appropriate stains such as silver methanamine (Fig 2). It is probable that most changes recognized initially radiographically are mainly a consequence of air-space disease (Fig 3). No significant statistical differences have been noted in the spectrum of radiographic findings in AIDS patients from those with other immunode-

rl

Fig 3. Pneumocystis carinii pneumonia. (A) Note the diffusely symmetrical reticular infiltrates with early focal coalescence. (6) CT section 1.5-cm thick through the midlung demonstrates a predominately reticular appearance sparing the lung periphery, especially posteriorly.

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ficiencies8 Atypical patterns, including a normal chest radiograph, are seen in non-AIDS patients,‘-” but are probably more common in AIDS. In a review of 30 cases of PCP diagnosed in the pre-AIDS era, Doppman et al’* reported a 56% incidence of atypical radiographic findings,

Fig 4. Pneumocystis carinii pneumonia. and El PA and lateral chest radiographs asymmetric pulmonav consolidation, cially prominent in the right lower lobe. bronchial biopsy documented PCP.

(A show espaTrans-

17

including unilateral distribution, lobar involvement, nodularity, abscess formation with cavitation, and linear atelectasis. A similar spectrum of radiographic changes has been noted in patients with AIDS, including asymmetrical pulmonary disease (Fig 4), and

18

predominantly upper lobe involvement, simulating tuberculosis (Fig 5).13-” Of particular interest is the presence of cystic parenchymal changes complicating an otherwise unremarkable case of PCP (Fig 6).‘* These cysts pose a risk of spontaneous pneumothorax. While enlarged hilar and mediastinal nodes, as well as pleural effusions have been documented in PCP, in our experience these findings are much more suggestive of associated tuberculosis, KS or lymphoma. Radiographic clearing of PCP can usually be demonstrated 2 weeks following initiation of therapy.6 This is not significantly different from the time interval previously established for other

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immunosuppressed populations.8 In a small percentage of cases, radiographic and pathologic evidence of residual disease persists, sometimes organisms on associated with Pneumocystis bronchial lavage or biopsy.‘9*20 That PCP itself may cause fibrosis, and not associated antibiotic or oxygen therapy, has recently been documented by Schinella et al.2’ Unfortunately, despite a good initial response, relapse and recurrence are frequent, occurring in approximately 30% within 6 to 8 months. In a high percentage of patients, respiratory failure indistinguishable from other forms of the adult respiratory disease syndrome (ARDS) develops (Fig 7). For those patients requiring endotracheal intubation and

Fig 5. fneumocystis carinii pneumonia. (A) PA radiograph shows, bilateral lung disease restricted to the apices. initially suggestive of mycobacterial infection. (6) CT through the left lung apex shows sharply demarcated parenchymal consolidation associated with air bronchograms and discrete cavities. Transbronchial biopsy showed PCP. Cultures for tuberculosis all proved negative.

RADIOGRAPHIC

Fig 6. nia proven tic changes

MANIFESTATIONS

IN AIDS

fneumocystis carinii pnea on biopsy with extensive in both upper lung fields.

mechanically approximates Mycohacterial

19

mloCYS-

assisted ventilation, 90%~.637~22

the mortality

Infections

Infection with Mycobacterium tuberculosis occurs in approximately 10% of AIDS patients.3.4.7 Frequently, the infection may precede the diagnosis of AIDS, sometimes by several months. M tuberculosis may be more common in IV drug abusers and in Haitians than in homosexual or bisexual men. Although evidence suggests reactivation as the primary mechanism of

infection,23 chest radiographs usually show a pattern more consistent with primary infection, including hilar and mediastinal adenopathy and noncavitary pulmonary infiltrates distributed equally in both the upper and lower lung fields (Fig 8).24 There is a consistent lack of apical or cavitary disease. The diagnosis is generally made from sputum culture; histologic examination usually does not reveal acid-fast organisms, or granulomas. In nearly 50% of cases, M tuhcrculosis can be obtained from at least one extrapulmonary site. Therapy is conventional (isoniazid

Fig 7. Pneumocystis carinii plicated by ARDS. PA radiographs air space disease in a patient failure, indistinguishable from ARDS.

pneumonia comshows diffuse with respiratory other forms of

NAlDlCH

Fig 8. Mycobacterium losis. Diffuse mediastinal adenopathy is associated defined nodular densities lungs.

and rifampin), and unlike many other infections in AIDS patients, there is generally a good clinical response. Mycobacterium avium-intracellulare (MAI) infection in AIDS patients is also frequent, occurring in up to 20% of cases, and varies considerably from its manifestations in nonimmunocompromised patients.25 In the normal host, MA1 is primarily a pulmonary process, characterized by slowly progressing focal lesions with frequent cavitation, usually in emphysematous patients between 50 to 60 years of age. On the contrary, in AIDS, MA1 is usually widely disseminated at the time of diagnosis.26 Although chest radiographic findings may be present, including mediastinal and hilar lymphadenopathy, diffuse patchy alveolar infiltrates, pulmonary nodules, and even miliary disease, the most important clinical involvement is often nonpulmonary. MA1 is often diagnosed from lymph nodes, liver, bone marrow, stool, blood, or urine even when the chest radiograph is norma1.26*27 Unlike in M tuberculosis infection, no therapeutic regimen has been efficacious. Ansamycin, a rifampin derivative, and clofazamine have in vitro effect and are usually administered with at least two other antituberculous drugs.

Cytomegalovirus

ET AL

tubsrcuand hiler with illin both

Infection

While cytomegalovirus (CMV) is the most frequent infectious organism found in autopsied AIDS patients, the clinical significance of this finding is unclear.28 Although frequently recovered from bronchoscopic lavage specimens, evidence of disease requires histologic demonstration of typical viral inclusion bodies. Radiographically, CMV pneumonia is associated with bilateral infiltrates usually indistinguishable from those caused by PCP (Figs 1 and 2). Small diffuse nodulation, miliary or larger, may occur. Dissemination to other viscera may take place,

Fig 9. Cryptococcus radiograph was interpreted through the upper lobes on the right.

neoformans pneumonia. The PA as normal. This CT section demonstrates a cavitated nodule

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21

Miliary histoplasmosis. (A) PA radiograph. Diffuse miliary disease is present along with ill-defined infiltrates in Fig 10. lung fields. (B) CT section through the midlung fields reveals innumerable small nodules with early confluence both upper This appearance is nonspecific. In drug addicts, miliary nodules may be the result of foreign body apparent nc rar the right hilum. Disseminated histoplasmosis was documented by both transbronchial biopsy and bone marrow biopsy or other gra anulomas. and culture

22

especially terminally. Infarction and necrosis of the adrenal glands may be noted. At present there is no effective treatment for CMV pneumonia. Fungus Infection

Compared with the incidence of other opportunistic infections, fungal pneumonias are unusual, occurring in ~5% of AIDS patients.4*6T7 They usually are disseminated. Cryptococcus neoformans is the most common organism, found usually in association with brain or meningeal involvement.29 In the noncompromised host, cryptococcal infection is often associated with peripheral pulmonary nodules, whereas in the immunocompromised patient, it demonstrates a wider variety of radiographic abnormalities.30 These include single or multiple nodules that may progress to confluence or cavitation, segmental consolidation, or bilateral foci of bronchopneumonia. Thoracic manifestations may be exceedingly subtle (Fig 9). C neoformans may be recovered from bronchoalveolar lavage fluid. Histologic confirmation is sometimes possible via transbronchial or open lung biopsy. As noted previously, disseminated Histoplasma capsulatum infection is considered diagnostic of AIDS in a patient who has a positive AIDS serology. The occurrence of histoplasmosis is greatest in those who live or originate in endemic regions. Like patients with MAI, chest radiographs may be normal in patients with disseminated histoplasmosis, documented by culture of blood or bone marrow. Associated infections, including PCP, esophageal candidiasis, recurrent mucocutaneous herpes simplex, and disseminated MA1 are common. Chest radiographs may reveal infiltrates, or less commonly, evidence of miliary disease (Fig 1O).3’ Lung biopsy is usually diagnostic, although care must be exercised not to mistake the typical configuration of H capsulatum for cysts of P carinii. Unlike cryptococcal infection, treatment for disseminated histoplasmosis with amphotericin B may be ineffective. In addition to C neoformans and H capsulaturn, a variety of other fungi may be found in aspatients with AIDS, including Nocardia teroides, Coccidioides immitis, as well as Candida and Aspergillus. Each may result in radiographically discernible pulmonary disease.

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ET AL

Nocardiosis most commonly presents as a unilateral segmental or lobar cavitary infiltrate, often associated with mycobacterial disease (Fig 11). Coccidiomycosis occurs in AIDS patients living in endemic areas. Radiographically, it typically causes single or multiple, thin-walled cavities. These may be indistinguishable from those caused by other infections, including PCP (Fig 12). The diagnosis is generally made on biopsy, which discloses characteristic thick-walled spherules when stained with periodic acid-Schiff stain. Aspergillosis, especially the invasive form, is rare among AIDS patients, although a form of pseudomembranous necrotizing bronchial aspergillosis has been described.32 Aspergillus may be found as a saprophyte that colonizes previously formed cavities associated with some other pulmonary infection (Fig 13). Bacterial

Infection

Although initially thought to be rare, the incidence of bacterial infections of the lung in patients with AIDS is increasing.33 Streptococcus pneumoniae and Hemophilus influenzae are most commonly cited as causing focal parenchyma1 disease; other bacteria, including Legionella pneumoniae have been demonstrated, alone (Fig 14) or in association with other infections, notably PCP.34 Most bacterial infections respond to

Fig 11. Nocardia asteroides infection. There ara focal cavitary infiltrates in the left apex and right base. Note the absence of effusion or edenopathy. The diagnosis was confirmed by transbronchial biopsy of the right lower lobe.

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23

Fig 13. Pneumocystis cariniihlycobacterium tubercuIosidAspergillus fumigstus: PA radiograph. There is an irregular cavity in the right upper lobe within which there is a well-defined filling defect. There were faint bilateral perihilar infiltrates es well. Transbronchial biopsy confirmed all three diagnoses. The cavity is of uncertain age.

Coccidiomycosis/pneumocystis pneumonia. Fig 12. The right lung shows a well-defined, thin-walled cavity in the right lower lobe, associated with faintly visible perihilar infiltrates. Transbronchial biopsy end levage revealed Pneumocystis. Repeat biopsy specifically directed to the region of the cavity demonstrated coccidiomycosis.

appropriate antibiotic therapy, hence the need for prompt and accurate diagnosis. While focal consolidation occasionally may be caused by PCP, this finding should raise a suspicion of bacterial infection, including staphycococcal or gram-negative pneumonia. Rarely, infection with other pulmonary pathogens, including toxoplasma, cryptosporidia, adenovirus, and varicella virus, may occur. The diagnosis almost always depends on histologic or microbacteriologic confirmation, often in a patient with extrathoracic disease. KAPOSI

Pulmonary involvement occurs in approximately 20% of patients with epidemic KS. It may be clinically indistinguishable from opportunistic infections. In the pre-AIDS era, chest radiographic signs of KS included hilar and mediastinal adenopathy, nodular infiltrates, and pleural effusions. These findings have been reported in AIDS-related KS. However, a diffuse pattern indistinguishable from that of PCP is common.35-37 The parenchyma1 disease most often appears as bilateral fluffy nodular infiltrates (Fig 15). Unilateral disease or

SARCOMA

Approximately 25% of AIDS patients have ~s.4.W The classic form of KS usually affects older males of either Jewish or Italian ancestory. In contrast, patients with AIDS develop an epidemic form of KS that bears a striking resemblance to certain forms of the diseasenoted in Africans. In AIDS, KS is a multicentric process that frequently involves lymph nodesand viscera, especially the GI tract.35,36

Fig 14. Legionella pneumonia. There dation of the right upper lobe. The diagnosis by direct fluorescent antibody stains.

is dense consoliwas confirmed

24

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ET AL

Fig 15. Kaposi sarcoma. (A) Ill-defined bilateral nodular densities are present. (B) CT shows the poorly marginated parenchymal opacities scattered throughout the lungs, a nonspecific appearance. Open lung biopsy revealed KS.

even a normal chest radiograph have been reported. Pleural effusions occur in approximately 30% of patients and may be unilateral or bilateral (Fig 16) .35236*37 The diagnosis of KS is difficult. The pleural effusions are typically exudative and serosanguinous. Cytologic examination of pleural fluid is not diagnostic, nor is pleural biopsy. Fiberoptic bronchoscopy may provide a tentative diagnosis by allowing visualization of endobronchial tumors. These appear as multiple red or violaceous lesions that are slightly raised and vascu-

lar. The diagnosis is difficult to confirm with transbronchial biopsy as there are no specific or unequivocal cytologic markers.38 Histologically, the tumor consists of loosely aggregated spindle cells often containing atypical nuclei and occasional mitoses, which tend to surround small bronchi and blood vessels within the interstitium. Vascular slits and hemosiderin deposits are characteristically present (Fig 17). Pulmonary involvement tends to be focal, relatively acellular, and is generally randomly scattered throughout the pulmonary parenchyma,

RADIOGRAPHIC

Fig chymal pleural KS.

MANIFESTATIONS

16. Kapoei sarcoma. infiltrate is associated effusion. Open lung

IN AIDS

25

A widespread parenwith a moderate right biopsy demonstrated

making the diagnosis problematic, even with open lung biopsy, Histologic confirmation is warranted, despite the progressive nature of pulmonary KS, because palliation has been reported with combination chemotherapy. LYMPHOPROLIFERATIVE

DISEASES

Lvmphocytic Interstitial Pneumonitis Lymphocytic interstitial pneumonitis (LIP) is a diffuse pulmonary disorder characterized by

the interstitial accumulation of mature lymphocytes, plasma cells, and reticuloendothelial cells. Frequently idiopathic, LIP is also associated with a wide variety of immunologic disorders, such as Sjiigren syndrome, systemic lupus erythematosis, myasthenia gravis, pernicious anemia, and chronic active hepatitis. LIP is now considered diagnostic of AIDS when confirmed histologically in a child under 13 years of age.’ While much less common, presentation in adults with AIDS has been documented.39 Clinically

Fig 17. Kaposi sarcoma. Histologic section from an open lung biopsy showing the characteristic features. The tumor consists of loosely aggregated spindle cells (straight arrow), often containing atypical nuclei and occasional mitoses, which tend to surround small bronchi and blood vassals. Vascular slits and hemosidarin deposits are characteristically present as well (curved arrows). The diagnosis may be difficult to establish via transbronchial biopsy as crush artifacts, hemorrhage, granulation tissue, and fibrosis may mimic KS.

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Fig 18. Lymphocytic interstitial pneumonitis. There is subtle increase in linear parenchymal markings bilaterally; a nodular density is present in the right upper lobe. Open lung biopsy documented LIP.

and radiographically, LIP may be indistinguishable from opportunistic infections (Fig 18). Diagnosis requires open lung biopsy, which reveals diffuse infiltration of the alveolar septa and peribronchial areas with a variable admixture of inflammatory cells, frequently with nodular aggregates of lymphoid cells with germinal centers. Clinical response is variable, but improvement may occur following appropriate immunosuppressive therapy. AIDS-Related

Lymphoma

Primary CNS lymphoma and other undifferentiated lymphomas are now recognized by the CDC as critera for the diagnosis of AIDS.’ Most are non-Hodgkin’s lymphomas of B cell phenotype, although an increased incidence of all lymphomas, including Hodgkin’s disease has been noted. Similar to lymphomas that arise in patients immunosuppressed from other causes, such as renal transplant recipients, AIDS-related lymphomas have a tendency to be highly aggressive neoplasms with poorly differentiated histologic subtypes and a poor prognosis. Typically, the disease is in an advanced stage at the time of diagnosis. In most series, a significant percentage of AIDS-related lymphomas are extranodal in distribution.40,4’V42 Pathologically, involvement is most frequently noted in the CNS, the GI system, and the liver, spleen, and bone marrow. Thoracic involvement is relatively rare and often

difficult to document.43 Mediastinal and hilar lymphadenopathy may be absent (Fig 19). In a series of 70 patients reported by Marchevsky et a1,44only two patients had documented pulmonary lymphoma; both showed bilateral changes, and one case had a left pleural effusion. DIAGNOSIS

In October 1983, the National Heart, Lung and Blood Institute (NHLBI) convened a workshop in order to assess the diagnosis and treatment of pulmonary complications in AIDS patients.3 Of a total of 1,067 patients with the diagnosis of AIDS evaluated by the six participating medical centers, 441 patients (41%) were found to have pulmonary disorders (Table 1). In order to facilitate diagnostic evaluation, the following guidelines were adopted by the NHLBl workshop, which with only minor variations are still widely accepted: While other procedures have been proposed as alternate methods for identifying opportunistic infections, including sputum induction, and even transthoracic needle biopsy, symptomatic patients with diffuse abnormalities noted on chest roentgenograms should have diagnostic fiberoptic bronchoscopy (FOB) .45,46Whenever possible, this should include both bronchoalveolar lavage (BAL) and transbronchial biopsy (TBB), preferably in combination. As reported by Broaddus et a14’ in their series of 276 bronchoscopic examina-

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Fig 19. Non-Hodgkin’s tymphoma confirmed by open lung biopsy. (A) There is a well-defined mass near the right hilum. (6) CT section through the midlung field demonstrates the mass in the superior segment of the right lower lobe. No other abnormalities were present.

Pneumocytis carinii pneumonia: gallium Fig 20. scintigraphy. Gallium scan of the thorax obtained at the time of a normal chest radiograph shows considerable activity throughout both lungs. Proved by BAL. (Courtesy of Dr Howard Banner, Department of Nuclear Medicine, Bellevue Hospital. New York City.)

27

tions performed on 171 patients with known or suspected AIDS, BAL and TBB proved to have sensitivities of 86% and 87%, respectively, in the detection of all pathogens combined.47 When BAL and TBB were combined, the yield for all pathogens was 98%; the sensitivity for P carinii alone was 100%. Follow-up in all negative cases of at least 3 weeks duration failed to detect any additional false negative results. When symptomatic, patients with negative chest radiographs should be further evaluated with gallium scintigraphy. Several reports have documented the utility of gallium scanning in the detection of PCP, with sensitivities ranging from 95% to 1oo%.48z49Unfortunately, the specificity of a positive gallium scan is significantly lower, usually around 50%. Diffuse activity is most commonly seen with PCP, although it may also result from other infections or inflammatory conditions (Fig 20); focal uptake, especially when corresponding to regional lymph nodes, suggests mycobacterial infection (Fig 2 l), or much less commonly lymphoma, while focal parenchymal uptake usually correlates with bacterial infection. At present, positive scans still require histologic or microbiologic corroboration before the institution of potentially toxic drug therapy. In light of these recommendations. and based on our own experience, the following interpretative guidelines are suggested: (1) There are no pathognomonic radiographic abnormalities or lung disease in AIDS; histologic or bacteriologic confirmation needs to be

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28

ET AL

Fig 21. Mycobacterium tuberculosis: gallium scintigraphy. (A) PA radiograph shows focal mediastinal and hilar adenopathy, especially on the left side. (B) Gallium scan demonstrates focal nodal accumulation in the mediastinum and left hilum, as well as the left supraclavicular space. Although nonspecific. nodal accumulation is suggestive of mycobacterial infection or. less commonly, lymphoma. Uptake of this type is unusual in patients with KS. (Courtesy of Dr Howard Banner, Department of Nuclear Medicine, Bellevue Hospital, New York City.)

obtained whenever possible in order to facilitate appropriate therapy and limit unnecessary adverse drug reactions. (2) Opportunistic infection and neoplasm may be present despite a normal appearing chest radiograph. When symptomatic, such patients should be further evaluated with a gallium scan. (3) Mediastinal and hilar adenopathy should always be interpreted as indicative of serious intrathoracic disease. Adenopathy should not be interpreted as a manifestation of the diffuse lymphadenopathy syndrome, or AIDS-related complex (ARC). In our experience, adenopathy is an unusual manifestation of PCP, and instead is most frequently caused by mycobacterial infection, lymphoma, or KS. Similar diagnostic considerations apply to the identification of pleural disease.

(4) Although focal parenchymal disease may be a manifestation of PCP, the increasing incidence of serious bacterial infections in patients with AIDS justifies an aggressive diagnostic approach in order to identify treatable infections. Despite obvious limitations, accurate interpretation of radiographic findings can play an important role in the overall work-up and management of patients suspected of having AIDS. It is to be expected that familiarity with the wide range of clinical and radiographic manifestations of this syndrome will be increasingly important. ACKNOWLEDGMENT We wish to acknowledge the invaluable contribution of Jane Crafts in the preparation and review of this manuscript.

REFERENCES 1. Centers for Disease Control: Pneumocystis pneumonia-Los Angeles. MMWR 1981;30:250-252 2. Centers for Disease Control: Kaposi’s sarcoma and pneumocystis pneumonia among homosexual men-New York City and California. MMWR 1981;30:305-308 3. Murray JF, Felton CP, Garay SM, et al: Pulmonary

complications of the acquired immunodeficiency syndrome. N Engl JMed 1984;310:1682-1688 4. Hopewell PC, Lute JM: Pulmonary involvement in the acquired immunodeficiency syndrome. Chest 1985,87:104112 5. Centers for Disease Control: Revision of the case defini-

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tion of acquired immunodeficiency syndrome for national reporting-United States. Ann Intern Med 1985;103:402-403 6. Garay SM. Belenko M, Schwiep F, et al: The initial episode of pneumocystis carinii pneumonia in the acquired immunodeticiency syndrome. Chest (in press) 7. Stover DE, White DA, Roman0 PA, et al: Spectrum of pulmonary diseases associated with the acquired immunodeficlency syndrome. Am J Med 1985;78:429-437 8. Kovacs JA, Hiemenz JW, Macher AM: Pneumocystis carinii pneumonia. A comparison between patients with the acquired immunodeficiency syndrome and patients with other immunodeficiencies. Ann Intern Med I984;100:663671 9. Forrest JV: Radiographic findings in pneumocystis carinii pneumonia. Radiology 1972;103:539-544 IO. Dee P, Winn W. McKee K: Pneumocystis carinii infection of the lung: Radiologic and pathologic correlation. AJR i 979; I32:741-746 I I. Siegel R, Wolson AH: The radiographic manifestations of chronic pneumocystis carinii pneumonia. AJR 1977;128:150-152 12. Doppman JL. Geelhoed GW, De Vita VT: Atypical radiographic features in pneumocystis carinii pneumonia. Radiology 1975;l 14~39-44 13. McCauley DI, Naidich DP, Leitman BS, et al: Radiographic patterns of opportunistic lung infections and Kaposi sarcoma in homosexual men. AJR 1982;139:653-658 14. Gamsu G, Hecht ST, Birnberg FA, et al: Pneumocystis carinii pneumonia in homosexual men. AJR 1982; I39:647 -65 I 15. Cohen BA, Pomeranz S, Rabinowitz JG, et al: Pulmonary complications of AIDS: Radiologic features. AJR 1984; 143: I 15-l 22 16. Goodman PC. Broaddus VC, Hopewell PC. Chest radiographic patterns in the acquired immunodeficiency syndrome. Am Rev Respir Dis 1984;129:36 17. Milligan SA, Stulbarg MS, Gamsu G, et al: Pneumocyslis carinii pneumonia radiographically stimulating tuberculosis. Am Rev Respir Dis 1985;132:1 124-I 126 18. Goodman PC, Daley C, Minagi H: Spontaneous pneumothorax in AIDS patients with pneumocystis carinii pneumona. AJR 1986;147:29-31 19. DeLorenzo LJ, Maguire GP, Wormser GP, et al: Persistence of pneumocystis carinii pneumonia in the acquired immunodeficiency syndrome. Evaluation of therapy by follow-up transbronchial lung biopsy. Chest 1985;88:7982 20. Shelhamer JH, Ognibene FP, Macher AM, et al: Persistence of Pneumocystis carinii in lung tissue of acquired immunodeficiency syndrome patients treated for pneumocystis pneumonia. Am Rev Respir Dis 1984;130:1 161-l 165 21. Schinella RA, Clancey C, Fazzini E, et al: Pneumocystis carinii as a cause of pulmonary fibrosis. Am Rev Respir Dis 1986;133:180 (abstr) 22. Rosen MJ, Cucco RA, Teirstein AS: Outcome of intensive care in patients with the acquired immunodeticiency syndrome. J Intens Care Med 1986;1:55-60 23. Pitchenik AE, Cole C, Russell BW, et al: Tuberculosis, atypical mycobacteriosis, and the acquired immunodeficiency syndrome among Haitian and non-Haitian patients in South Florida. Ann fnfern Med 1984;101:641-646

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24. Pitchenik AE, Rubinson HA: The radiographic appearance of tuberculosis in patients with the acquired immune deficiency syndrome (AIDS) and pre-AIDS. Am Rev Respir 1985;131:393-396 25. Marinelli DL, Albelda SM, Williams TM, et al: Nontuberculous mycobacterial infection in AIDS: Clinical. pathologic, and radiographic features. Radiokg-v 1986; I60:77-82 26. Macher AM, Kovacs JA, Vee G, et al: Bacteremia due to Mycobacterium avium-intracellulare in the acquired immunodeficiency syndrome. Ann intern Med 198X:99:782 785 27. Hulnick DH, Megibow AJ, Naidich DP, et al: CT in abdominal tuberculosis. Radiology I985;157: I99- 204 28. Niedt GW, Schinella RA: Acquired immunodeficiency syndrome: Clinicopathologic study of $6 patients. Arch Path01 Lab Med 1985;109:127--734 29. Zuger A, Louie E, Holzman RS, et al: C’ryptococcal disease in patients with the acquired immunodeticiency syndrome. Ann Intern Med 1986;104:234-240 30. Khoury MB, Goodwin JD, Ravin CE. et al: Thoracic cryptococcosis: Immunologic competence and radiologic appearance. AJR 1984: I41 :893-896 3 I Wheat LJ, Slama TG, Zeckel ML. Histoplasmosis in the acquired immune deficiency syndrome 4m J Med 1985;78:203~210 32. Pervez NK, Kleinerman J, Kattan M, et al: Pseudomembranous necrotizing bronchial aspergillosis. .&I Rev RespirDis 1985;131:961-963 33. Polsky B. Gold JWM, Whimbey E. et al: Bacterial pneumonia in patients with the acquired immunodeticiency syndrome. Ann /ntern Med 1986; IO4:38-4 I 34. SimberkofJ MS, Sadr WE, Rahal Jr JJ: Streptococcus pneumoniae infections and bacteremia in patients with acquired immune deficiency syndrome, with report of a pneumococcal vaccine failure. Am Rev Rrspir Dis 1984: 130:1174-1176 35. Garay SM. Belenko M. Fazzini E. et al: Pulmonary manifestations of Kaposi’s sarcoma. Chest (in press) 36. Ognibene FP, Steis RG, Macher Am, et ;II: Kaposi’s sarcoma causing pulmonary infiltrates and respiratory failure in the acquired immunodeticiency syndrome. Ann Intern Med 1985:102:471-475 37. Meduri DE, Stover M, Lee AJ. CI al: Pulmonary Kaposi sarcoma in the acquired immune deficiency syndrome: Pathological and clinical manifestationa Am Rev. RespDis 1985;131:75 (abstr) 38. Lau KY, Av J, Rubin A, et al: Letter to the Editor: Kaposi’s sarcoma of the tracheobronchial [rec. Chesr 1986;89: 158-l 59 39. Solal-Celigny P, Couderc LJ, Herman D, ot al: Lymphoid interstitial pneumonitis in acquired immunodeficiency syndrome-related complex. Am Rev Rrspir Di.\ 1985; 131:956&960 40. loachim HL, Cooper MC, Hellman CC: Lymphomas in men in high risk for acquired immune deficiency syndrome (AIDS). Cancer 1985;56:2831-2842 41. Nyberg DA, Jeffrey Jr RB. Federle MP. et al: AIDSrelated lymphomas: Evaluation by abdominal CT. Radio1og.v 1986;159:59--63 42. Zeigler JL. Beckstead JA, Volberdinp PA. et al:

30 Non-Hodgkin’s lymphoma in 90 homosexual men: Relation to generalized lymphadenopathy and the acquired immunodeficiency syndrome. N Engl J Med 1984;311:565-570 43. Stern RG, Gamsu G, Golden JA, et al: Intrathoracic adenopathy: Differential feature of AIDS and diffuse lymphadenopathy syndrome. AJR 1984;142:689-692 44. Marchevsky A, Rosen MJ, Chrystal G, et al: Pulmonary complications of the acquired immunodeficiency syndrome: A clinicopathologic study of 70 cases. Hum Pathol 1985;16:659-670 45. Bigby TD, Margolskee D, Curtis JL, et al: The usefulness of induced sputum in the diagnosis of pneumocystis carinii pneumonia in patients with the acquired immunodeficiency syndrome. Am Rev Respir Dis 1986; 133:5 15-5 18 46. Blumenfied W, Wagar E, Hadley WK: Use of the

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transbronchial biopsy for diagnosis of opportunistic pulmonary infections in acquired immunodeficiency syndrome (AIDS). Am JClin Path01 1984;31:1-5 47. Broaddus C, Dake MD, Stulbarg MS, et al: Bronchoalveolar lavage and transbronchial biopsy for the diagnosis of pulmonary infections in the acquired immunodeficiency syndrome. Ann Intern Med 1985;102:747-752 48. Tuazon CU, Delaney MD, Simon GL, et al: Utility of gallium scintigraphy and bronchial washings in the diagnosis and treatment of pneumocystis carinii pneumonia in patients with the acquired immune deficiency syndrome. Am Rev Respir Dis 1985;132:1087-1092 49. Kramer EL, Sanger JJ, Garay SM, et al: Chest gallium scans in patients with acquired immunodeficiency syndrome. Submitted for publication, July 1986