Topic GuideAcute Pulmonary Infections

Bacterial Pneumonias• Klebsiella (Friedländer's) Pneumonia• Streptococcus pyogenes Pneumonia• Pseudomonas Pneumonia

Viral, Mycoplasmal, and Rickettsial Pneumonias• Chlamydia trachomatis Pneumonia

Other Infections• Pulmonary Cystic Fibrosis (Mucoviscidosis)

Topic GuidePulmonary Tuberculosis• General Considerations• Primary Pulmonary Tuberculosis• Postprimary (Reinfection, Reactivation) Tuberculosis• Bronchiectasis• Unusual Radiographic Manifestations of Pulmonary Tuberculosis• Tuberculosis in the Immunosuppressed Patient• Tuberculoma• Healing of Pulmonary Tuberculosis• Complications of Reinfection Pulmonary Tuberculosis• Hematogenous Tuberculosis• Miliary Pulmonary Tuberculosis• Subacute and Chronic Hematogenous Pulmonary Dissemination• Atypical Mycobacteria• Surgical Measures in Pulmonary Tuberculosis• Complicating Aspergillomas

Topic Guide• Actinomycosis• Nocardiosis

Mycotic Diseases of the Lung• Coccidioidomycosis• Histoplasmosis• Cryptococcosis• North American Blastomycosis• South American Blastomycosis (Paracoccidioidomycosis)• Pulmonary Aspergillosis• Moniliasis (Candidiasis)• Geotrichosis• Other Mycoses

Topic GuideDiseases of Spirochetal Origin• Syphilis• Leptospirosis

Protozoan Diseases• Amebiasis• Toxoplasmosis

Platyhelminth (Flatworm) Infestation• Echinococcosis (Hydatid Disease)• Cysticercosis• Paragonimiasis• Schistosomiasis

Nemathelminth (Roundworm) Infestation

Tropical Eosinophilia

ACUTE PULMONARY INFECTIONSType Organism Characeristics Roentgen Pattern

Lobar (alveolar, air-space) pneumonia

Streptococcus pneumoniae pneumonia.

Periphery of the lung via the airways.

Alveolar transudation (edema) is followed by migration of leukocytes into the alveolar fluid.

“Lobar “is a misnomer in most cases.

peripheral homogeneous (consolidation) opacity spreads toward the hilum and tends to cross segmental lines.

Alveolar pneumonia is not necessarily confined to a lobe, nor does it involve an entire lobe in many instances.

Bronchopneumonia (lobular pneumonia).

staphylococcal infection of the lung.

Originates in the airways and spreads to peribronchial alveoli.

Confined by interlobular septa.

patchy disease causing poorly defined opacitiesa variety of roentgen patterns may result, including a confluent consolidation resembling lobar (alveolar) pneumonia.

Acute interstitial pneumonia

virus or a mycoplasma

Interstitial involvement is masked by alveolar exudate

alveolar consolidation, if present, is not usually as confluent or as dense as in lobar or lobular pneumonia

Mixed pneumonia

This is a combination of lobar, bronchopneumonia, and interstitial pneumonia

Bacterial PneumoniasPneumococcal Pneumonia

• S. pneumoniae – caused by types 1, 3, 4, 5, 7, 8, 9, or 12.– Type 8 is the most common. – Type 14 causes pneumonia in children but rarely in adults. – The mortality rate for pneumonia caused by type 3 is higher than for the others.

• “lobar” pneumonia• generally more severe in those with alcoholism, neoplastic disease,

chronic pulmonary disease, or altered immunity. • lower lobes and posterior segments of upper lobes are most commonly

involved. • The onset is sudden• gross pathologic changes are evident early in the disease• roentgen findings can be observed within 6 to 12 hours after onset of

symptoms.

Pneumococcal Pneumonia• Involvement usually begins

peripherally and spreads centripetally with homogeneous involvement that may cross segmental boundaries.

• Consolidation: homogeneous density.

• An entire lobe may be affected; more commonly only one or a few segments are involved.

• Density usually extends to the pleural surface.

• A peripheral, nonsegmental, sublobar consolidation is seen when peripheral spread across segmental boundaries occurs.

Lobar pneumonia in the right middle lobe. Note the homogeneous opacity clearly defined by the secondary fissure in the frontal projection ( A) and by the major fissure as well as the secondary fissure in the lateral view ( B).

Pneumococcal Pneumonia• all of the elements in the

diseased lobe except the larger bronchi may be affected, resulting in almost complete airlessness.

• Larger bronchi: seen as air-containing, radiolucent tubes within the otherwise homogeneous density, the “air bronchogram.”

• Pleural involvement: elevation of the hemidiaphragm on the affected side.

• Pleural fluid: sufficient to obscure the depth of the costophrenic sulcus.

• Opacity caused by this disease can be differentiated from that produced by atelectasis.

Right-upper-lobe pneumococcal pneumonia. A: Roentgenogram obtained the day after onset of symptoms shows the disease clearly defined by the minor fissure. Consolidation is not complete. B: Three days later, there is complete consolidation of the right upper lobe. The upper-lobe volume is slightly reduced, but there is no significant collapse.

Pneumococcal PneumoniaThe spherical pattern (round pneumonia) often reported in children is a form in which the well-circumscribed spherical consolidation may simulate a pulmonary or paramediastinal mass.

Frontal view of the chest shows a rounded soft-tissue density in the posterolateral aspects of both lower lobes with mild bilateral hilar prominence.

Pneumococcal Pneumonia

In patients with emphysema, radiolucent blebs surrounded by consolidation may simulate cavities. In some patients, the distribution of the disease is somewhat patchy or lobular, simulating the distribution in bronchopneumonia.

Bronchopneumonia• usually occurs as a complication of various debilitating diseases, often at the extremes of life. • It is most commonly found in the very young or very old who are afflicted with another disease. • The infection is often mixed, so that several pathogenic bacteria can be isolated from the sputum. • The disease originates in numerous adjacent areas of the lung, resulting in scattered foci of inflammation that vary in

size and shape but produce enough density to be visible on the film. • The inflammatory disease does not cross septal boundaries. Therefore, the pattern of disease is discontinuous or

patchy.• The pneumonic consolidation causes densities of varying sizes that are usually rather small and poorly defined and may

be described as mottled. • The location is usually basal, but disease may occur anywhere in the lung.• It often occurs as a complication of another pulmonary disease, which may obscure the pneumonia or vice versa. • It is particularly difficult to define and diagnose when it occurs as a complication in cardiac failure with pulmonary

congestion and edema, which also cause basal opacity. • It is also difficult to differentiate from other acute or subacute pulmonary diseases such as adult respiratory distress

syndrome (ARDS). • Occasionally, the process is extremely widespread and simulates miliary pulmonary disease, with small, poorly defined

nodules scattered uniformly throughout both lungs. • In contrast to alveolar pneumonia, bronchopneumonia originates in the bronchial airways and involves the surrounding

parenchyma. • As indicated, it may become confluent and then resemble alveolar pneumonia. • It should be remembered that neoplasms can be masked by patchy focal pneumonia, and if clinical symptoms persist

unduly, progress roentgenograms as well as cytologic studies should be recommended.

Bronchopneumonia

Note that the widespread, mottled opacity is more severe on the left than on the right. The disease is very extensive.

Aspiration Pneumonia• Aspiration pneumonia is usually a mixed bacterial infection caused by aspiration of foreign material into

the bronchial tree. The causes are numerous and range from aspiration of vomitus by a postsurgical or semicomatose patient to aspiration as a result of paresis or paralysis of the pharyngeal muscles.

• Tracheoesophageal fistula, gastroesophageal reflux, and various other esophageal lesions can also cause aspiration pneumonitis. Gram-negative organisms included in the aspirate may produce pneumonia followed by necrosis and abscess formation.130 This complication is discussed in the section on lung abscess.

• The radiographic findings vary with the extent of disease and its location. The right lower and middle lobes are most frequently affected, but involvement of the left lower lobe is not unusual. Irregular, poorly defined areas of increased density are seen and may be extensive ( Fig. 24-4). Early in the disease these densities are focal, but later they may become conglomerate. In some instances the disease is acute and clears rapidly as the patient recovers from the condition that produced the aspiration. In other instances the pneumonia results from a chronic disease, and repeated aspiration leads to chronic basal pneumonitis, which causes patchy or linear basal opacity (Fig. 24-5 and Fig. 24-6). Aspiration of acid-containing gastric contents (Mendelson's syndrome), can produce a chemical pneumonitis causing pulmonary edema, often in a dependent portion of one or both lungs. The appearance is similar to basal pulmonary edema of other causes. The roentgen findings are therefore varied, and it may not be possible to differentiate this basal inflammatory disease from other nonspecific basal pneumonia or from the chronic pneumonia associated with bronchiectasis. However, correlation of the history with clinical and roentgen findings usually leads to the proper diagnosis.

Aspiration pneumoniaNote the scattered patchy opacities in the lower half of the left lung and a similar but less extensive change at the right base. This was an acute process that cleared quickly on treatment.

Chronic aspiration pneumoniaThe pneumonia in the parahilar areas and at the right base is somewhat more clearly defined and stringy than the acute process. This patient had partial esophageal obstruction and had aspirated intermittently for several months.

Chronic Recurrent AspirationA and B: Computed tomographic findings in a patient with chronic recurrent aspiration. Multifocal, patchy air-space disease is present bilaterally with a tree-in-bud pattern seen in the periphery of the lungs where aspirated material has become inspissated in bronchioles. Note also the dilated esophagus with retained contrast material within the lumen.

Pneumonia in Children• Differences in response to pulmonary infection in infants and young children, compared with

older children and adults, are probably based on anatomic and immunologic factors.9,64 Airways are small, soft, and easily collapsible; resultant air trapping with overinflation can be found in a variety of infections in the first 12 to 18 months of life. In the newborn period, B streptococcal pneumonia causes an appearance similar to that of hyaline membrane disease. In fetal aspiration syndrome, rapid roentgenographic changes result as the aspirated material is cleared and overinflation disappears.

• Staphylococcal pneumonia has a very rapid course, with early development (within hours) of effusion, empyema, and bronchopleural fistula with pyopneumothorax or lung abscess.90 Pneumatoceles are very common as the pneumonia clears.

• Upper-airway infection may be associated with pulmonary disease, so a chest roentgenogram may be the initial study. When lungs are hypoaerated or edematous, obstruction due to epiglottitis should be suspected.

• It is very important to correlate the roentgen findings with clinical signs and symptoms. For example, Chlamydia trachomatis causes conjunctivitis in neonates and may produce pneumonia which is interstitial, scattered, and bilateral and is associated with overinflation of the lungs. Cough is often the only symptom, so a chest film showing these findings in a neonate with conjunctivitis should suggest the diagnosis. 113

Klebsiella (Friedländer's) Pneumonia

• Klebsiella pneumonia is a confluent alveolar type of pneumonia caused by Klebsiella pneumoniae. The disease occurs most frequently in elderly and debilitated patients. The onset is usually sudden, and the illness is often fatal within a few days. It may begin as bronchopneumonia manifested by patchy areas of opacity, usually in one or both upper lobes, but spreads rapidly to become confluent. It may involve an entire lobe. The involved lobe tends to increase in volume, resulting in convexity of the adjacent interlobar fissure. Extensive destruction of tissues leads to abscess formation in many of these patients, and the abscess cavities are typically thin walled, if a wall can be demonstrated ( Fig. 24-7). Often, the confluent pneumonia surrounding the cavity obscures its actual wall. At times the necrosis is extensive and extremely large cavitation results when the necrotic material sloughs out. Pleural effusion is common, and empyema often follows the effusion. In the more chronic form, the disease tends to be patchier, the cavitation is smaller, and the lesions may closely simulate those of TB. Pneumatoceles may occasionally occur during resolution of Klebsiella pneumonia.

Klebsiella pneumonia

A: The disease is extensive, with evidence of cavitation in which there are masses of dense necrotic material. B: Ten days later, considerable advance of the disease is evident.

• The diagnosis should be suspected when a rapidly progressing confluent pneumonia is observed in one or both upper lobes, resulting in increased lung volume, in which cavitation forms quickly. When the disease progresses more slowly, it is often less confluent, and its distribution in one or both upper lobes plus the presence of cavities often leads to a mistaken diagnosis of TB. Bacteriologic studies are then needed for differentiation. In patients who survive, a considerable amount of fibrosis may result, leading to contraction of the lobe with secondary changes in the thorax resulting from the loss of lung volume. In this respect, the disease may resemble chronic TB.

• Enterobacter and Serratia are similar gram-negative bacteria that cause pneumonia infrequently. The most common of these is Serratia marcescens, which usually causes either a focal pneumonia or a diffuse process that may involve several lobes. Pleural effusion is common. Both Enterobacter and Serratia are usually found in debilitated hospitalized patients, often in association with other organisms as a cause for pulmonary infection. As an opportunistic pathogen in immunosuppressed patients, Serratia may produce a necrotizing bronchopneumonia but usually does not cause a frank lung abscess .

Rapid progression of gram-negative pneumonia from right-upper-lobe consolidation ( A) to extensive cavitation (B and C) in 10 days

Staphylococcal Pneumonia• Pneumonia caused by Staphylococcus aureus may be primary in the lungs or secondary to a primary

staphylococcal infection elsewhere in the body. In the secondary type, there is hematogenous spread of the organism, whereas in the primary type the pulmonary spread is usually bronchogenic. The disease usually occurs in debilitated adults and in infants during the first year of life, and recurrent staphylococcal infections are common in patients who use intravenous drugs and those with AIDS. The onset of the illness is usually abrupt, with severe prostration. Death may occur within 24 to 48 hours. Because some of the many areas of involvement occur adjacent to the pleura, it is common to have pleural infection with empyema and bronchopleural fistula.

• In children, the roentgen findings are rather characteristic and consist of dense areas of pulmonary involvement that may be segmental and local or diffuse. Consolidation rapidly spreads to involve a whole lobe (confluent bronchopneumonia); bronchi are usually obscured by exudate, so an air bronchogram is not ordinarily seen. Pleural effusion, empyema, and pneumothorax are common, and pneumatoceles are often noted. Abscess formation may also occur, and coalescence of small abscesses is frequent. A pneumatocele is distinguished from an abscess by its thin wall and rapid change in size. The pathogenesis of pneumatoceles is not known with certainty. The most popular theory hypothesizes that a check-valve obstruction develops between the lumen of a small bronchus and the adjacent interstitium. Multiple pneumatoceles may develop, usually in the first week of the disease, and they may become very large. Accumulation of fluid with air–fluid levels is common during the active phase of pneumonia. Pneumatoceles may persist for months but usually disappear completely ( Fig. 24-9). In adults the findings are not as characteristic. Pneumothorax and pneumatocele are less common but do occur, and pleural effusion and empyema are not as common as in children, with the exception of patients with AIDS and intravenous drug users. Abscesses are slightly more common than in children and tend to coalesce ( Fig. 24-10).

• The disease is usually bilateral, may be diffuse and somewhat nodular, but is seldom lobar in distribution.

Staphylococcal pneumonia in the left lower lobe resulting in the formation of a pneumatocele. A: Note the homogeneous opacity at the left base, indicating rather extensive pneumonia. There is a radiolucent area surmounting a fluid level. The pulmonary alveolar disease surrounding the pneumatocele makes it impossible to determine the thickness of the wall. B: The inflammatory disease has cleared almost completely, leaving the thin-walled, cyst-like pneumatocele. This film was obtained 1 month after that shown in A. C: The pneumatocele is no longer visible on this film obtained 3 months after the initial examination.

Staphylococcal pneumonia

There is extensive disease in the left lower lobe, in which numerous small, rounded, lucent areas represent small pneumatoceles or abscesses.

• Pleural effusion, often resulting in empyema, occurs in about one half of the patients. Rapid change and lack of correlation between severity of clinical symptoms and roentgen findings are often observed. Resolution is usually slow in both children and adults. When the disease is hematogenous, septic emboli may cause multiple small abscesses and widespread, small foci of pneumonia.

Streptococcus pyogenes Pneumonia

• Pneumonia caused by S. pyogenes (Lancefield group A, hemolytic streptococcus) usually occurs after such acute infectious diseases as measles and influenza. This disease is now rare. It is roentgenographically similar to staphylococcal pneumonia in the frequency of pleural involvement, including empyema if antibiotic therapy is not initiated promptly. The pulmonary involvement has a tendency to be more diffuse and interstitial in type than in staphylococcal pneumonia, with fine opacities radiating outward to the periphery from the hila. The combination of rapidly developing, hazy, nodular opacities in an acutely ill patient with subsequent cavitation in many of the areas is highly characteristic of either staphylococcal or streptococcal pneumonia, with the former more likely. S. pyogenes infections usually do not cause pneumatoceles.

Tularemic Pneumonia• Tularemia is an infectious disease caused by Francisella tularensis, a small gram-negative

bacillus. It is a disease of small animals and may spread to humans directly from the animals.127 The most common mode of infection is through the skin of hunters who dress small game. The infection may also be transmitted by means of tick bites as well as the bites of horse and deer flies. Pulmonary involvement in the form of pneumonia resulting from this organism is present in approximately 50% of humans affected. The roentgen findings are not characteristic, but some authors have reported a high incidence of oval lesions resembling an abscess without cavitation. However, others have indicated a great variability in pulmonary findings. 91 The infection may produce unilateral or bilateral pulmonary inflammatory disease, which is usually poorly circumscribed. Occasionally, the distribution is lobar, resulting in consolidation of an entire lobe. The infection is commonly a basal one, and there is usually more disease on one side than the other, so that it is asymmetrical when bilateral. A small amount of pleural effusion is not uncommon, 26 and hilar lymph-node enlargement is also present in many instances. The time required for resolution varies widely. In some patients complete clearing may occur within 7 to 10 days, and in others the disease may persist for 6 weeks. Because the roentgen picture is not characteristic, the diagnosis must be confirmed by laboratory methods. The organisms are difficult to isolate from the sputum, but if the disease is suspected, its presence can be proved by means of agglutination tests.

Brucellosis Pneumonia• Brucellosis in humans in the United States is usually caused by Brucella

suis. Pulmonary involvement is rare, and symptoms are usually mild.41,103 The roentgen findings are varied. Strands of opacity that radiate outward from the hila are often associated with hilar adenopathy and may be bilateral. Pleural involvement with effusion is occasionally encountered. In other instances, widespread miliary disease that resembles miliary bronchopneumonia is found. Solitary, circumscribed pulmonary nodules have also been described. The pulmonary roentgen changes appear quickly but tend to persist for long periods with very slow resolution. The diagnosis cannot be made on roentgen examination but must depend on the results of bacteriologic studies, agglutination, and skin tests. Calcifications in the spleen that have a typical appearance may be a clue to the diagnosis in the patient with the appropriate exposure history.

Pertussis Pneumonia• Whooping cough is usually caused by Bordetella pertussis. The organism

may also cause pneumonia, an unusual but not rare complication. The pulmonary disease begins in the paroxysmal stage of whooping cough and extends into the resolution phase. It is usually found in children but may occur in adolescents and adults.

• The pulmonary disease tends to be central, with radiating parabronchial strands of opacity. The radiographic findings resulting from this distribution of disease consist of blurring of the cardiac margins and an irregular appearance termed the “shaggy heart” pattern. There may also be some subsegmental areas of consolidation as well as scattered areas of atelectasis, presumably caused by mucus plugs, particularly in older children and adults. In some instances, the pneumonia may be caused by other organisms complicating whooping cough, a widespread bronchopneumonia.

Pseudomonas Pneumonia• There is an increasing incidence of pneumonia caused by Pseudomonas aeruginosa, a gram-

negative bacillus. Cases usually occur among hospitalized patients and are often related to the use of antibiotics, steroids, and immunosuppressive and cytotoxic drugs. There is evidence that positive-pressure breathing apparatus, 57 suction and nebulizing devices, and tracheostomies are major factors in the development of this disease. P. aeruginosa is a water-associated organism found in many environmental sources, both in the hospital and outside it. 117 The causative organism is extremely difficult to eradicate once pulmonary disease is established.

• Several roentgen patterns of pulmonary involvement have been described: (1) bilateral pneumonic consolidation, with early patchy, scattered disease progressing and coalescing to involvement of the major portions of both lungs; (2) extensive bilateral pneumonic consolidation with abscess formation (abscesses may be multiple and small or few and large); (3) diffuse nodular or patchy densities with or without abscess formation; and (4) unilateral pneumonia, similar to the coalescent bilateral pneumonia. Many species of Pseudomonas are angioinvasive. Pathologic specimens show that bacterial colonies actually invade pulmonary blood vessels and cause a vasculitis and thrombotic occlusion. This predisposes areas of Pseudomonas pneumonia to undergo necrotic infarction, and lung cavitation is a prominent feature of many Pseudomonas infections.29 Therefore, almost any pattern may occur, so the radiographic findings are not diagnostic ( Fig. 24-11). Pleural effusion may occur, but it is not a prominent feature of the disease. There is evidence that the presence of P. aeruginosa in the sputum of patients with chronic lung disease indicates underlying bronchiectasis.

Pseudomonas pneumonia in a patient with chronic debilitating disease. A: Initial examination reveals bilateral diffuse disease at the right medial base and in the left parahilar area. B: One week later, note the mass-like opacity in the left midlung and more patchy disease in the right midlung and medial base. There is nothing characteristic about the disease pattern, as is often the case. C: Diffuse hematogenous dissemination in another patient. Note scattered, poorly defined disease, largely basal.

• Although most Pseudomonas infections occur in debilitated or hospitalized patients, they can occur in otherwise healthy persons. Serious, even fatal, Pseudomonas pneumonias have been associated with use of home and motel whirlpool spas and jacuzzis, presumably because of inhalation of large numbers of aerosolized bacteria from contaminated units into the lungs. 68,117

• Melioidosis, which is caused by infection with P. pseudomallei, is endemic in the tropics, chiefly in India, Burma, Sri Lanka, and South America. Since the Vietnam

• War, sporadic cases have been reported in the United States, chiefly in Vietnam veterans. 19 The infection may be acute or chronic. The acute form is more common and is characterized by indistinct nodular disease that is often widely scattered but tends to involve the upper lobes. The nodules coalesce and cavitate in a high percentage of cases. The chronic form simulates pulmonary TB, because the nodules often involve the upper lobes and frequently cavitate. Hilar adenopathy is uncommon, and pleural effusion is rare.

• Occasionally, pulmonary cavitation appears acutely years after the initial infection, so it should be suspected when a parenchymal cavity appears in an apparently healthy patient who was in an endemic area some years earlier.

Anaerobic Bacterial Pneumonias• Several anaerobic organisms may cause pulmonary infection. They include, among

others, Bacteroides fragilis, Bacteroides melaninogenicus, and Bacteroides oralis; members of the genera Fusobacterium, Clostridium, and Eubacterium; and the gram-positive cocci of the genera Peptostreptococcus and Peptococcus. Most of the infections are caused by several organisms, because many are caused by aspiration of oral secretions, particularly in patients with poor oral hygiene. They may also occur in diabetic patients, those with malignant disease, and immunosuppressed patients. An alveolar type of pneumonia, which may be extensive, is usually produced. The right lower lobe is the most common site, but frequently more than one lobe is involved. About one half of patients have pulmonary disease only, about one fourth have pleural and parenchymal disease, and the remainder have only the pleura involved, usually with empyema. Abscess formation and necrotizing pneumonia are common complications. Abscess occurs in more than 50% of patients with pulmonary disease. Bronchopleural fistula may also complicate the disease.

• Anaerobic bacteria therefore are a prominent cause of aspiration pneumonia, lung abscess, necrotizing pneumonia, and empyema. The mortality rate is high in these patients, many of whom have depressed immune responses or leukopenia.13

Other Bacterial Pneumonias• Pneumonia caused by infection with Proteus vulgaris is largely basal, may be alveolar or lobular in distribution, and

tends to produce cavitation. It may cause a decrease in volume of the involved lung. Rarely, Escherichia coli causes pneumonia, which is usually multilobar and basal. Pneumatoceles are occasionally seen in this infection, and the alveolar pneumonia caused by this organism rarely results in massive cavitation. Pleural effusion is common.

• Pneumonic involvement may occur in typhoid fever, usually as a bronchopneumonia with cavitation, pleural effusion, or empyema. Salmonella organisms other than Salmonella typhosa may produce a similar pattern in the lung. An acute miliary pattern has also been described in salmonella bacteremia. 42 Hemophilus influenzae, type B, is a rare cause of pneumonia9 that is being seen increasingly in HIV-positive patients as a cause of pneumonia.

• In adults, these infections appear as acute lobular lower-lobe pneumonia or as a more confluent lobar alveolar process. The latter is somewhat more common.

• Pneumatoceles are rare but have been reported. Patients with alcoholism, who are immunocompromised, or who are undergoing chemotherapy are at risk. In infants, pleural effusion and empyema are common in addition to extensive alveolar disease. The latter may be a patchy, segmental type of density, but a variety of manifestations have been described, including reticular or linear, nodular, reticulonodular, ground-glass, and honeycomb patterns. Pleural effusion is fairly common and may be complicated by empyema. Cavitation is rare; roentgenographic findings clear slowly.

• Pulmonary involvement also occurs in patients with anthrax or bubonic plague. In anthrax pneumonia, there is often substantial mediastinal lymph node enlargement, pleural effusion, and sometimes intrapulmonary hemorrhage in addition to extensive pulmonary disease. Plague can often involve the lung. 5 In secondary pneumonic plague, bilateral small densities are the most common early manifestation. The disease may spread to involve much of the lungs with a dense alveolar process, which is often fatal. Rarely, the pattern is that of bilateral extensive mottled densities, which resemble the pattern of ARDS. This pattern reflects intravascular coagulopathy in some instances.

Legionnaires' Disease• Legionnaires' disease, which affected almost 200 people at the Legionnaires' Convention in Philadelphia in July 1976, is

caused by the aerobic, gram-negative bacillus Legionella pneumophila.27 Since this original description, 34 Legionella species and 52 serogroups have been isolated, with about half proving pathogenic to humans. The bacteria is associated with water reservoirs, including air-conditioning cooling towers. 116 Clinically, the acute disease is characterized by a high fever, chills, and a nonproductive cough, often associated with chest pain, malaise, muscle and abdominal pain, headaches, and gastrointestinal symptoms. Hyponatremia and elevated creatine phosphokinase are two abnormal laboratory results that can occur with Legionnaires' disease but are not often present in patients with other community-acquired pneumonias.116 Since the outbreak in Philadelphia, many sporadic and local outbreaks throughout the United States have been reported.

• Predisposing factors include smoking, alcoholism, diabetes, heart disease, and immunosuppression.• Roentgen findings are largely those of an alveolar pneumonic process that is bilateral in about one half of the reported

cases ( Fig. 24-12). There tends to be lower-lobe predominance. The alveolar disease may have a lobar or lobular distribution. At times, the alveolar process appears as a large, very poorly marginated, generally round or oval opacity. Some of these are central and some peripheral; they may be unilateral or bilateral. The round lesions appear to be somewhat more common than any other roentgen manifestation. The round, mass-like lesions often progress rapidly to involve an entire lobe. Early in the disease there may be patchy, ill-defined opacities that in many cases progress to a lobar pattern. One patient has been reported in whom there was virtually universal involvement of both lungs by an alveolar process in which air bronchograms were very prominent. Cavitation, presumably a result of necrotizing pneumonia, has been reported in several patients, most of whom were immunosuppressed. One patient has been reported in whom pneumatocele formation and spontaneous pneumothorax were manifest.

• Pleural effusion may occur, but its incidence is difficult to evaluate because many of the patients have complicating renal or cardiovascular disease. Resolution is usually slow and lags behind clinical improvement. An interstitial pattern may appear during resolution.

Legionella pneumonia in a patient with acquired immunodeficiency syndrome. A: Initial film shows bilateral upper-lobe disease, which appears to present a mixed interstitial and alveolar pattern. B: Two and one-half weeks later, there is extensive bilateral disease which appears to be in a largely alveolar pattern. This disease is more diffuse and less mass-like than the original descriptions.

• It is evident that there is a wide variety of roentgen patterns in this disease, so the diagnosis cannot be made on the basis of chest roentgenograms. However, the disease should be suspected in a patient with atypical pneumonia in whom roentgenograms show unilateral or bilateral, large, poorly marginated, rounded alveolar opacities that progress rapidly to involve one or more entire lobes.

• The Pittsburgh pneumonia agent (Tatlockia micdadei, Legionella micdadei) was described in 1979. It is a gram-negative, weakly acid-fast bacillus that appears to be identical to the Tatlock organism isolated 37 years earlier. It has been recognized as a disease seen mainly in renal transplantation patients and others treated with high-dose corticosteroid therapy. However, it has also been reported 94 in patients who were not immunosuppressed. Radiographic findings are those of an alveolar type of pneumonia, usually in one lobe, either segmental or subsegmental and nodular in appearance. In the compromised patient, it spreads very rapidly and occasionally cavitates. Pleural effusion is found in about 30% of patients. The organism is similar to L. pneumophila, and the two diseases are found simultaneously in a few patients. The diagnosis is made by lung biopsy.

Hospital-Acquired (Nosocomial) Pneumonias

• Hospital-acquired pneumonias are important because the impaired resistance of the hospital patients renders them very susceptible to gram-negative bacilli such as P. aeruginosa, E. coli, and other Enterobacter species. Outbreaks of Staphylococcus, Klebsiella, Proteus, and other pneumonias have also been reported.

• Furthermore, the wide use of antibiotics has resulted in resistant pathogens that may also cause pneumonia. The lungs are involved in 10% to 30% of infections acquired in hospitals. In this patient population, mortality may be very high and every precaution must be taken to avoid contamination of respiratory therapy equipment, anesthesia machines, air-conditioners, and other devices used in patient care. Pseudomonas infection is particularly common in this group of patients, is very difficult to treat, and has a high mortality rate despite treatment with various combinations of antibiotics. Nosocomial pneumonia should be considered when a hospitalized patient develops leukocytosis, cough, or fever. In this situation, any new or increasing pulmonary opacity may represent pneumonia. There are no specific patterns for the various organisms involved, so the radiologist's role is to note the disease and suggest the possibility of pneumonia.

Viral, Mycoplasmal, and Rickettsial Pneumonias

Mycoplasmal Pneumonia• Mycoplasma pneumoniae (the Eaton agent) pneumonia is responsible for a significant percentage of

primary atypical pneumonia in children and young adults (15% to 20% or more). It probably accounts for almost 50% of pneumonias found in children younger than 16 years of age. The remainder of patients with primary pneumonia have disease caused by adenovirus, parainfluenza virus, respiratory syncytial virus, and probably other viruses. In many patients, the cause is not determined. Cold agglutinins are found in the serum of 50% to 60% of patients with Mycoplasma pneumonia. A titer of 1:32 or higher is considered positive and is usually found 10 to 14 days after onset of the symptoms. A high titer is usually present. Mycoplasmal pneumonia tends to occur in epidemics, as well as sporadically, so it is difficult to obtain meaningful figures as to relative frequency. The disease usually occurs in young, healthy adults. It is acute, mild, and self-limited in most instances but may be severe with widespread pulmonary disease. Occasional fatalities have been reported. The inflammatory exudate is sometimes more interstitial than in the bacterial pneumonias, but alveolar exudate, which contains fewer cells and more fluid than in the bacterial type, is also present. The onset of symptoms is gradual, and there is often a delay in the appearance of visible pulmonary density on roentgen examination for 2 or 3 days. Putman and colleagues 108 described two groups of patients with different clinical and radiographic findings. One group with acute chest pain, cough, and fever developed segmental or lobar air-space disease. The other group had a more chronic course, were afebrile, and had no cough or chest pain. They developed interstitial changes and a reticulonodular or mixed pattern of focal air-space and interstitial disease. Others have noted less relation between symptoms and anatomic distribution.

• Roentgen findings reflect the anatomic changes. Recognizable forms can be divided into several types:

1. Peribronchial or interstitial type. The findings in the peribronchial type consist of streaky densities extending outward from the hilum following the pattern of the vascular markings, limited to a single segment or affecting one or several lobes. Alveolar exudate may produce scattered patchy density as well as the linear shadows.2. Bronchopneumonic type. The roentgen findings are similar to those described for bronchopneumonia and may be just as widespread. Opacities that are usually poorly defined and scattered may be noted in any lobe or segment and may be bilateral.3. Segmental and lobar types. The findings are those of homogeneous density representing consolidation in a segment, several segments, or a lobe. Single-lobe involvement occurs in almost 50% of patients. Air bronchograms may be present. The appearance of the consolidation is similar to that found in S. pneumoniae lobar pneumonia. Pleural effusion occurs in about 20% of patients with this type of disease and is rare in the interstitial type.4. Diffuse type. A bilateral reticulonodular pattern throughout both lungs. Pleural effusion is rare.

• One or more of these gross anatomic types of the disease may be present in a single patient. There is a tendency for the disease to clear in one area and spread in another, often in the opposite lung. Atelectasis may be produced by bronchial obstruction and is frequently lobular and focal in type. Occasionally, a pneumatocele may result from check-valve obstruction and must be differentiated from lung abscess (see Fig. 24-7). Resolution is usually slow, and it is common to see persistent pulmonary lesions for a week or longer after the clinical findings have disappeared. Occasionally, the delay is considerably greater. Mycoplasmal pneumonia cannot be differentiated from viral infections of the lung, and when the distribution is segmental or lobar it is similar to bacterial pneumonia ( Fig. 24-13, Fig. 24-14 Fig. 24-15).

Viral pneumonia

A: Extensive interstitial disease is seen throughout the entire right lung, with similar but much less marked change on the left. B: Diffuse involvement, which appears to be mainly interstitial, is confined largely to the right upper lobe in another patient.

Viral pneumonia

In these two patients, the disease is largely alveolar in type, being rather diffuse in the patient shown in A and localized into an irregular, mass-like lesion in the patient shown in B.

Mycoplasmal pneumonia

A: The air bronchogram denotes alveolar disease, but there also appears to be some interstitial change in the upper central lung. B: Alveolar pneumonia, which is probably subsegmental, is noted in the left lower lobe.

• In the differential diagnosis, there are findings that help to differentiate mycoplasmal from bacterial pneumonia. They consist of the lack of pleural involvement, manifested by absence of elevation of the diaphragm and absence of pleural fluid in most cases. The delay in appearance of pulmonary disease after clinical onset is also helpful. The tendency to clear in one area and spread in another is more common in this disease than in bacterial pneumonia. Bilateral involvement is probably more common than in bacterial pneumonias, with disease often in one lower lobe and the opposite upper or middle lobe. However, because the roentgen pattern may vary widely, the diagnosis must be substantiated by clinical and laboratory findings ( Fig. 24-16).

Viral pneumonia simulating minimal tuberculosis. A: Note the disease in the right subclavicular area. B: Close-up view shows the disease in the first anterior interspace. C: Roentgenogram of the same area shown in B, obtained 2 weeks later, shows complete clearing of the disease.

Adenovirus Pneumonia• There are 28 types of the adenovirus, which is a common cause of upper

respiratory disease and may cause pneumonia, often in epidemics. The disease is usually more severe in infants and young children than in adults. The most common roentgenographic pattern is that of a widely scattered patchy or confluent disease, usually in a peribronchial distribution. Slow resolution is usually noted, with residual bronchiectasis in some children and obliterative bronchiolitis and other chronic lung disease in others. This virus also causes acute bronchiolitis with overinflation in infants and can cause unilateral hyperlucent lung (Swyer-James syndrome).

• Bronchiolitis can also be caused by other viruses such as the respiratory syncytial virus, rhinovirus, influenza virus, and parainfluenza virus, usually in children. It is unusual in adults and is rarely diagnosed. Although pulmonary involvement may be extensive, the acute illness may not be severe, particularly in adults.

Other Viral Pneumonias• Several viruses are capable of causing pneumonia, often in epidemics. 24 A number of new viral diseases, including Ebola fever and

Hantavirus pulmonary syndrome, have emerged in recent years as life-threatening epidemics. 14 The roentgenographic findings of most viral pneumonias are similar to those described for mycoplasmal pneumonia, so the cause cannot be established on the basis of these findings alone. In some epidemics, the pericardium is involved, leading to effusion, often associated with pleural effusion as well. Often the virus is not definitely identified in these patients and the diagnosis is based on clinical findings. The disease usually is not as prolonged or severe as mycoplasmal pneumonia.

• Epidemic influenza, which is a viral disease, may be associated with virus infection of the pulmonary parenchyma in addition to involvement of the tracheobronchial tree. Roentgen signs are variable, with findings often bilateral and extensive. Especially in severe epidemics of the past, the pneumonia was often of the interstitial type with hazy, strand-like densities radiating outward from the hila. These result in a coarse appearance of the bronchovascular pattern and irregular hilar thickening.

• In other patients, segmental or lobar consolidation may be present; it may be bilateral. A diffuse, patchy pattern resembling pulmonary edema has also been described. Pleural effusion is rare in uncomplicated influenza pneumonia. The diagnosis is often made from clinical findings during an epidemic. The roentgen changes are then largely confirmatory, but radiographic examination is useful to observe the course of the pulmonary parenchymal disease. A complicating staphylococcal pneumonia may also occur, particularly in epidemics in which influenza is severe. Most fatalities are caused by this complication.

• Herpes simplex pneumonia may occur in neonates and immunocompromised hosts. It is a severe, often fatal disease in neonates, with an initial interstitial pattern progressing to coalescent air-space densities and a diffuse alveolar “white-out” of both lungs in the fatal cases. The pathology is that of a necrotizing hemorrhagic pneumonia. The disease is usually widely disseminated in these neonates.

• Pneumonia associated with chickenpox (varicella) is believed by some to be viral in origin and has been reported occasionally. It usually occurs in adults with severe chickenpox. Roentgen findings consist of widespread, poorly defined, patchy or nodular densities associated with an increase in parahilar markings and occasionally enlargement of the hilar nodes ( Fig. 24-17). Densities are most marked in the parahilar areas and at the bases. Individual nodules are generally round but are poorly defined peripherally. There is often considerable change in the roentgen findings from day to day, because the densities are transitory. Clearing is usually slow, however. In patients with fatal disease, pulmonary involvement may be virtually total, with little if any visible aerated lung. In rare instances, scattered small calcifications result from varicella pneumonia in adults. No hilar node calcification is observed. It is entirely possible for bacterial pneumonia to appear in patients with these various viral diseases and there is no way to differentiate the cause on chest radiographs.

Varicella Pneumonia

Varicella pneumonia in an adult. Soft, rounded nodular opacities are noted bilaterally.

• Measles (rubeola) is occasionally associated with pneumonia caused by the virus. 110 Pneumonia caused by other organisms sometimes complicates measles, however, so roentgen differentiation is not possible. The measles virus causes reticuloendothelial involvement resulting in hilar and mediastinal adenopathy. The virus may also involve the lung to produce an interstitial process that is manifested as a widespread reticular type of reaction, with predilection for the bases.

• Consolidation of lung with varying degrees of atelectasis most probably represents a complicating bacterial pneumonia.• Atypical measles pneumonia occurs in adolescents and young adults after previous “incomplete” immunity conferred by killed

rubeola virus vaccine. It is probably a hypersensitivity response in incompletely immunized patients. The pneumonia is usually segmental and bilateral but may involve most or all of a lobe. Other patterns include “round” pneumonia, diffuse perihilar opacity, and multiple nodules. Pleural effusion and hilar adenopathy occur in about one third of patients. Usually the patients have the skin eruption of measles. The acute pneumonia usually clears promptly, but rarely a nodule persists for 1 to 2 years. 83

• Pneumonic involvement may occur with several other viral diseases, including smallpox, lymphocytic choriomeningitis, and cytoplasmic inclusion disease in infants and children. There is nothing characteristic about the roentgen appearance of the pneumonia associated with these diseases except that the pneumonia is usually bilateral and often extensive. Cytomegalovirus infection is the most common viral infection in immunosuppressed patients. In patients having cytomegalovirus disease, nodules have been reported involving the outer one third of the lungs. Lung biopsy may be necessary to establish the diagnosis.

• Hantavirus caused an outbreak of a new fatal pneumonia in young, otherwise healthy persons living in the southwestern United States in 1993. Since then, an increasing number of cases have been identified outside of that area as well. The virus is spread by rodents; inhalation of aerosolized, virus-infected rodent droppings is the mode of transmission to humans. Patients present with a prodrome of fever and flu-like symptoms, followed by cough, increasing dyspnea, and rapid progression to fulminant pulmonary failure, which is often fatal. 58,61 The chest film often shows bilateral, interstitial edema with rapid progression to a picture of noncardiogenic pulmonary edema with bilateral air-space disease and normal heart size. Widespread increased capillary permeability within the lungs is believed to be the cause of the roentgenographic findings and rapid development of pulmonary edema in infected patients. Copious secretions may be noted on bronchoscopy or on suctioning.58 Pleural effusions are common.61

Psittacosis (Ornithosis)• Psittacosis, or ornithosis, caused by Chlamydia psittaci, is primarily a

disease of birds and is transmitted to humans by members of the parrot family. 125 It is also found in other domesticated and wild birds and may be transmitted to humans by them. The disease may be unilateral or bilateral, focal or multifocal, resembling lobular pneumonia. This results in a roentgen pattern of patchy consolidation that may be relatively focal or bilateral and widely scattered. A reticular pattern (interstitial) has also been reported. Enlargement of hilar nodes may also be present. Pleural involvement is uncommon. The roentgen changes tend to persist for a long time (6 to 9 weeks) after the initial symptoms. The diagnosis is confirmed by serologic and bacteriologic studies but can be suspected when this type of disease is seen in a patient who has had contact with birds.

Chlamydia trachomatis Pneumonia

• There have been several reports on the radiographic findings in C. trachomatis pneumonia in infants younger than 6 months of age, and this organism has been reported as the causative agent in a distinctive pneumonia in this group. Radkowski and associates 113 reported on 125 patients observed over a period of 3½ years.

• Although the x-ray findings are not diagnostic, most patients have hyperinflation plus a variety of patterns of bilateral disease, including relatively minimal interstitial disease, areas of atelectasis, patchy coalescent pneumonia involving small volumes of lung, and rare pleural effusion. 126 The clinical signs and symptoms are relatively few, so the chest findings on radiography are those of more disease than would be expected. The infants are afebrile but have a cough, conjunctivitis, and elevated serum immunoglobulins.

• In adults there are streaky opacities, usually bilateral, with associated atelectasis but rarely pneumonic consolidation. 30

Rickettsial Pneumonias• Q Fever. Q fever is caused by a rickettsia, an intracellular parasite considered to be

intermediate between bacteria and viruses. The causative organism is Coxiella burnetii. The roentgen findings consist of a subsegmental, segmental, or lobar consolidation varying from a patchy nonhomogeneous shadow to frank air-space opacity in the area of involvement. Hilar node involvement and small focal lesions are uncommon. There appears to be a difference between sporadic and epidemic disease.41 Round pneumonia, sometimes multiple, is common in the epidemic group but less so in sporadic cases. Pleural involvement is rare in epidemic disease and occurs in approximately one third of the sporadic cases. This is manifested by a small amount of pleural fluid. The roentgen findings usually appear within 48 hours of onset of disease and resolve rather slowly, so that the pulmonary consolidation persists longer than in pneumococcal pneumonia. This disease does not exhibit the migratory type of change often found in viral pneumonia. As in other pneumonias, the diagnosis depends on correlation of clinical, roentgen, and serologic findings.

• Other Rickettsial Pneumonias. Pulmonary involvement has been reported occasionally in patients with other rickettsial diseases such as Rocky Mountain spotted fever and typhus, when severe. The roentgen findings are not characteristic in these diseases, but the opacities usually are scattered and produce disseminated shadows on the chest roentgenogram.

Other Infections: Lung Abscess• When an acute suppurative pulmonary infectious process breaks down to form a cavity, regardless of size, it is termed lung abscess. Most lung

abscesses are bronchogenic in origin and result from aspiration of foreign material after dental operations, surgery of the respiratory tract and elsewhere, and various conditions that produce unconsciousness. This type of abscess may also be secondary to stasis of secretions from various causes (e.g., bronchogenic carcinoma) or other endobronchial obstructions that result in incomplete drainage of a bronchus. As indicated, anaerobic organisms are often the cause of lung abscess. Hematogenous lung abscess, which is usually produced by staphylococcus and occasionally by streptococcus, has been discussed in a previous section, as has the abscess formation in pneumonia produced by Klebsiella. Cavitation occurs in approximately 5% of patients with pulmonary infarction and, when infected, an abscess is formed.

• Because lung abscess is, in many instances, the result of aspiration of foreign material, it is usually found in areas of the lung that are dependent at the time of aspiration. The posterior segment of the upper lobe is the most common site, and the right side is affected more than the left. The next most common sites are the superior segments of the lower lobes, because these segments are dependent when the patient is supine. The basal segments of the lower lobes are also commonly involved, and abscess can occur in any segment of any lobe. The lesion is peripheral in relation to the bronchopulmonary segment involved, but on the frontal roentgenogram it may project in a central position. The pleura adjacent to the abscess is usually involved, so there may be pleural effusion.

• The early roentgen finding is consolidation that produces an opacity which is usually confined to one pulmonary segment. Characteristically, the lesion has an opaque center with a hazy and poorly defined periphery and is often roughly spherical in shape. When bronchial communication is established, the fluid contents of the cavity are replaced, at least in part, by air, and the radiolucent abscess cavity appears within the area of disease. It is usually incompletely drained, so that an air–fluid level can be outlined within it. In these cases the fluid produces, in the dependent portion, homogeneous opacity that blends with the wall of the cavity. Drainage of the abscess may vary, so that at times it may contain more or less air. When the necrotic lung tissue has not sloughed completely, it is common to observe a crescent-shaped radiolucency caused by air in the superior aspect of the partially formed cavity. In some patients, several small cavities may appear within the area and remain as separate lesions or coalesce to form one or more larger cavities. These may be well outlined on the routine frontal and lateral roentgenogram, but small cavities can be hidden by the surrounding pneumonic consolidation. When cavitation is suspected, computed tomography (CT) may be indicated, because it can reveal lesions not seen on plain films. CT also aids in localizing and in defining the inner and outer walls of the abscess cavity and may identify complications such as rupture of the cavity into a bronchus or into the pleural space ( Fig. 24-18). In acute lung abscess the outer wall is usually poorly defined. As the abscess becomes more chronic, its wall thickens and the external surface is more sharply marginated. Complications are much less common now than before the use of antibacterial drugs, but empyema and spread of the infection locally or by aspiration of pus from the abscess into a more dependent portion of the lung may occur. CT occasionally may be necessary to differentiate lung abscess from empyema and may also be useful to guide percutaneous catheter drainage.

Acute lung abscess

A: Note the irregular radiolucency in the right subclavicular area, in which there is a fluid level. There is a smaller cavity in the plane of the third anterior rib. B: Tomogram of the upper cavity, which lies posteriorly. The wall is difficult to define, and a considerable amount of inflammatory disease is present adjacent to the cavity. C: The smaller cavity is faintly defined on this tomogram. Its medial wall is visualized, whereas the inflammatory disease laterally produces homogeneous density, making the wall indistinct.

• Differential diagnosis depends on the stage of disease when the roentgenogram is obtained. In the early stage, before excavation and communication with a bronchus have occurred, the process cannot be differentiated from that of a segmental pneumonia. However, excavation usually occurs early, and the abscess cavity can then be seen on the roentgenogram if the examination is made with the patient upright. The clinical findings of cough with profuse, foul-smelling sputum shortly after the onset of the acute process strongly suggest lung abscess. If the cavity is not visible on a plain film, CT is indicated. Chronic lung abscess must be differentiated from cavitary TB, the fungal infections that produce cavitation, infected lung cyst, and bronchogenic carcinoma in which the central portion of the lesion has sloughed. This differentiation can be very difficult to make roentgenographically, and examination of the sputum for bacteria and fungi along with appropriate cultures is used to confirm the diagnosis. Cytologic study of the sputum and bronchial aspirates is also indicated in patients with chronic abscesses, particularly in smokers older than 40 years of age, because of the high incidence of bronchogenic carcinoma.

Middle Lobe Syndrome

• The term middle lobe syndrome, commonly used in the past, is not used frequently now. It refers to recurrent pneumonitis and atelectasis in the middle lobe caused by present or previous obstruction of the bronchus to this lobe. 31 The middle lobe bronchus arises approximately 2 cm below the origin of the upper lobe bronchus and is relatively pliable, and there are nodes adjacent to it that may produce compression of the bronchus when they become enlarged. When compression is sufficient to cause partial obstruction, infection can result. The obstruction may persist or decrease, leading to atelectasis, bronchiectasis, and chronic pneumonitis or to temporary resolution of the process. Endobronchial disease at the site of the lymph-node compression may result in gradually increasing stenosis of the middle lobe bronchus. The roentgen findings in the lung are somewhat varied, depending on the relative amount of pneumonitis and atelectasis. The lobe is usually decreased in size. This results in downward displacement of the secondary interlobar fissure and an increase in opacity below and lateral to the right hilum. The opacity is sometimes difficult to see in the posteroanterior roentgenogram, although it may cause blurring of the right cardiac margin. It usually can be readily outlined on the lateral film. Then the middle lobe is clearly defined as a wedge-shaped or triangular area of opacity sharply bounded above and below by normally aerated lung. The apex of the triangle is at the hilum and the base is at the anterior inferior thoracic wall. When the lobe is not clearly defined in either projection, it may be seen in an anteroposterior lordotic view. When bronchiectasis is marked, the dilated bronchi may be visible as air-filled tubular structures within the consolidated lung. The hilar nodes producing the obstruction may contain calcium. The relationship of these nodes to the middle lobe bronchus can be determined accurately by means of CT.

• Collateral ventilation of the middle lobe appears to be relatively ineffective, compared with that of the other lobes. This may account for the persistent collapse of the middle lobe in this syndrome.

• Because bronchogenic carcinoma can cause similar findings, bronchoscopy, with biopsy or even surgical exploration, may be required to make the diagnosis in this type of disease (Fig. 24-19 and Fig. 24-20).

• Surgical removal is the usual treatment, because the bronchial changes are generally irreversible by the time the syndrome is recognized. Furthermore, there is a high incidence of bronchogenic carcinoma in patients with recurrent or persistent middle lobe infection and atelectasis.

Middle lobe syndrome

A: Note the contracted middle lobe below the right hilum, which obscures the central portion of the right atrial silhouette. B: The lateral view shows the contracted middle lobe (arrows). C: The bronchogram shows obstruction (arrow) of the middle-lobe bronchus. The upper- and lower-lobe bronchi are partially filled.

Acute pneumonia in the right middle lobe. A: Hazy alveolar disease below the right hilum at the medial base blurs the right cardiac margin in this area. B: In the lateral view, the disease is clearly defined. It lies in the right middle lobe.

Pulmonary Cystic Fibrosis (Mucoviscidosis)

• Cystic fibrosis is the term used to describe the generalized process of which fibrocystic disease of the pancreas is the most commonly recognized finding. It is a congenital disease, transmitted as an autosomal recessive trait, in which there is an abnormality involving the salivary, mucous, and sweat glands. There also may be an abnormality of mucociliary transport. Sodium and chloride levels in the sweat are elevated, so the diagnosis can be confirmed by a positive sweat test (a finding of more than 50 mEq of chloride per liter of sweat) and by demonstration of decreased amounts of pancreatic enzymes in duodenal contents. This disease is discussed here because a major pulmonary manifestation is one of repeated airway and parenchymal infections. Thick, tenacious mucus tends to obstruct the smaller airways.

• Pulmonary manifestations vary in degree but are almost invariably present if the child lives long enough to develop them.• The earliest roentgen change in fibrocystic disease is hyperinflation, which is diffuse and symmetrical. 59 This is often difficult to

recognize in children, but films exposed in inspiration and expiration may indicate the distended state of the lungs. The degree of obstruction tends to increase to a different extent in various segments, so that small areas of opacity resulting from focal atelectasis are visible as the disease progresses. These patients experience repeated pulmonary infection, so findings of pneumonia are superimposed. The infection is usually widespread and peribronchial in distribution, which leads to a rather irregular, stringy accentuation of peribronchial markings extending outward from the hila on both sides. This is often associated with areas of poorly defined, hazy opacity caused by

• focal areas of pneumonitis. Segmental or lobar collapse may also occur, and the repeated infection leads to a considerable amount of fibrosis and often to bronchiectasis. Bronchial walls are thickened. This is manifested by the presence of parallel lines, which represent bronchial walls seen in profile, or thick circles when the thickened bronchial walls are viewed in cross-section. When bronchiectasis is severe, cyst-like structures are visible, usually in the central and upper lungs.

• The fibrosis and inflammatory disease produce irregular stringy and patchy shadows. The lung between the consolidated areas is emphysematous, giving a characteristic roentgenographic picture in far advanced disease ( Fig. 24-21). It is often possible to suspect the presence of cystic fibrosis early in the disease when hyperinflation, which may often be associated with small areas of focal atelectasis that are somewhat irregular in distribution, is noted in the infant. Allergic bronchopulmonary aspergillosis (ABPA), to which patients with cystic fibrosis are susceptible, 70 may be a complicating factor and is said to be present in 10% of patients. It is probably an important factor in clinical deterioration when it complicates cystic fibrosis. ABPA is discussed in the section on fungal chest infections.

Cystic fibrosis of the pancreas with chronic pulmonary disease. There is extensive involvement throughout both lungs. Rounded and oval radiolucencies represent thick-walled bronchi, some of which are dilated, indicating bronchiectasis. There also is evidence of some overinflation, bilateral hilar adenopathy, and patchy alveolar disease.

• An increasing number of patients live into adult life, and in these young adults there is often a rather characteristic radiographic appearance. The disease usually involves the upper lobes with a combination of patchy, linear, and nodular densities interspersed with radiolucent areas. In one study bronchiectasis was observed in 90%; hyperinflation in 76%, particularly in the lower lobes; and cyst-like air spaces in 24%. 36 There was an increase in hilar size in 74%. Parenchymal disease was more prominent in the upper and central lung in 70% ( Fig. 24-22); in the remainder, involvement was general. Mucus plugs with atelectasis were observed mainly in the upper lobes. In this study, 30 of 39 patients observed for 1 year or longer showed progression of the pulmonary disease on chest films. In chronic cases, architectural distortion develops, with upper-lobe hilar retraction. Rarely, lung abscess may develop. Hypertrophic pulmonary osteoarthropathy has been reported in adults with cystic fibrosis. Chronic obstructive pulmonary disease (COPD) is a major cause of disability in adults with cystic fibrosis. Infections with S. aureus or P. aeruginosa and cor pulmonale are common causes of death. Adult patients with end-stage cystic fibrosis are now being treated successfully with bilateral lung transplantation.

Cystic fibrosis in the adult. A: In this 28-year-old with cystic fibrosis who is not acutely ill, there is upper-lobe predominance, particularly on the right, but disease is rather general. B: Nine months later, much of the acute disease has cleared, but thick-walled, dilated bronchi are more clearly defined; upper and central predominance is again noted.

Chronic Granulomatous Disease of Childhood

• Chronic granulomatous disease of childhood is another genetically determined disorder in which pulmonary infections begin early in life and persist or recur at intervals.131 Their leukocytes phagocytize bacteria normally but do not destroy them properly. Lobar and lobular pneumonia may occur in these patients, complicated by lung abscess and empyema. The organisms usually involved are staphylococci, Klebsiella, E. coli, S. marcescens, Nocardia, and fungi (see Fig. 24-48).

• The major features of the infections are hilar adenopathy and recurrent pneumonia, which often does not clear completely and may go on to abscess formation. In some patients, the pneumonia resolves slowly and may become clearly defined, with sharp borders and homogeneous density. It is then termed encapsulated pneumonia.

Nocardia infection complicating chronic granulomatous disease of childhood. Computed tomogram shows multiple cavitary masses and nodules caused by disseminated infection.

PULMONARY TUBERCULOSIS: General Considerations

• The incidence of pulmonary TB in the United States decreased from 53 cases per 100,000 in 1953 to 9.4 cases per 100,000 in 1984. 123,129,129A After 1984, this steady decline in the incidence of the disease stopped, and in 1986 there was a 2.6% increase in reported cases that persisted through 1988. Increasing numbers of cases were being reported in patients with HIV infection, persons immigrating from countries were TB is endemic, the homeless, the jobless, intravenous drug users, prison inmates, and residents of nursing homes. These factors, combined with unsupervised and inadequate or noncompliant drug therapy, have led to a resurgence of multiple-drug-resistant cases as well. 17,98,123,129A These ominous trends stimulated renewed efforts in this country to curb the infection. New federal funding for TB control clinics to improve case findings and reinstitute the practice of direct observation of patient treatment appears to have reversed the trend. 123 Overall, new cases of TB in this country decreased to 8.7 per 100,000 in 1995. Nevertheless, incidence rates are much higher in some HIV-infected populations on the east coast. 85,123 Worldwide, the epidemic of TB goes virtually unabated, with an estimated 7.6 million new cases occurring in developing countries each year. As many as 3 million people die annually from TB worldwide. 20,123 Therefore, on all fronts, the disease is still of considerable social and economic importance.

• Mycobacterium tuberculosis is an aerobic bacillus that stains acid-fast red with carbol-fuchsin. 35 Most infections occur when aerosolized droplets containing the organism are inhaled into the lungs and deposited in the middle and lower lobes. 35 An initial focus of infection develops in the lung and subsequently spreads to regional lymph nodes. Further dissemination occurs via lymphohematogenous routes to other parts of the lungs, especially lung apices, and to extrapulmonary sites.

• The tubercle bacillus injures the tissues, resulting in an alveolar exudate termed tuberculous pneumonia. The disease may advance rapidly and cause a poorly defined pulmonary shadow of varying size and density. This is usually homogeneous when the lesion is small. If the process is halted by means of antibacterial drugs before caseation necrosis occurs, complete clearing of the process can occur. A chest roentgenogram does not permit a positive diagnosis of exudative TB, but the findings may be typical enough that the diagnosis of an exudative type of lesion can be suggested. Subsequent complete clearing then tends to substantiate the impression.

• In the majority of cases, however, primary TB remains clinically silent. Host defenses temporarily contain the infection by forming granulomas or tubercles consisting of epithelioid cells, lymphocytes, and Langhans' giant cells that wall off the bacilli. This corresponds to the development of delayed hypersensitivity to TB antigens that occurs around 1 to 3 weeks after inoculation. 35,96,134 By 3 weeks, a tuberculin skin test (PPD) is usually positive. 134 The tubercles that form may coalesce to form larger nodules that are visible as oval or rounded opacities on the chest radiograph. Tubercles may continue to enlarge and undergo central caseation necrosis, or they may heal with fibrosis and calcification. 10,96,106 Viable bacilli often survive within dormant tubercles, only to become reactivated at a later date to cause postprimary (reactivation) TB. When liquefaction occurs in the areas of caseous necrosis, infected material is extruded into an adjacent bronchus, leaving a tuberculous cavity behind and spreading the infection endobronchially to other parts of the lung.

• Clinically active TB develops in only about 5% to 10% of exposed people. This most often occurs as reactivation of dormant infection sometime in the future, but it may occur as progression of primary infection or as uncontrolled dissemination if host defenses fail. 35,134 Dissemination of the tubercle bacillus is of three types: bronchogenic, hematogenous, and lymphangitic. Bronchogenic dissemination occurs when exudate from a cavity or small area of caseation drains into a bronchus and is aspirated into previously uninfected areas, either on the same or on the opposite side. This type of spread occurs frequently after bleeding and when there is a cavity emptying into a bronchus. Hematogenous dissemination leads to miliary TB and to extrapulmonary lesions throughout the body. Acute massive hematogenous spread causes miliary TB, whereas chronic spread in smaller amounts usually results in the chronic extrapulmonary foci. Lymphangitic dissemination is common in primary infection. It is responsible for involvement with subsequent enlargement of hilar and mediastinal nodes that is often seen in children. In adults, hilar and mediastinal adenopathy can be seen in both primary infection and reactivation. 11,52,71,78 On contrast-enhanced CT scans, tuberculous lymph nodes typically demonstrate low-attenuation, necrotic centers with rim enhancement. 7,11,52

• The reaction to M. tuberculosis depends on the presence or absence of immunity to tuberculoprotein. In persons having no tissue hypersensitivity or immunity, primary TB results. In those with immunity produced by previous infection or bacille Calmette-Guérin (BCG) vaccination, reactivation (reinfection) disease may develop.*

Primary Pulmonary Tuberculosis• Primary, or first-infection, TB occurs when the living tubercle bacilli produce a local inflammatory process

in the lung in a patient who has not been previously infected and therefore is not sensitized to the tuberculoprotein. This form usually occurs in children. 124 The disease remains often undetected because there are few clinical symptoms. If a roentgenogram is obtained in the early phase, the disease resembles any other segmental pneumonic process in that it is a poorly defined opacity, usually limited to a relatively small subsegment. In some patients, the diseased area is larger, with one or several segments or an entire lobe involved. In susceptible persons (e.g., blacks, poorly-nourished children), the disease may be more widespread and may occasionally cavitate; pneumatoceles may occur. 124 The lymphangitic spread of the disease to the hilar and paratracheal nodes results in enlargement, which may be recognizable roentgenographically. At times adenopathy can be massive. The changes produced in the lymphatics may occasionally be sufficient to appear as streaks of increased opacity between the primary pneumonic disease and the hilum. If serial films are obtained, slow resolution will be noted over 6 months to 1 year. At times the original lesion disappears so completely that it cannot be recognized on later roentgenograms, but there is often a small nodule that later may become calcified. The calcification within the hilar nodes and the parenchymal calcification then remain as the only residues of primary TB. This combination of primary parenchymal opacity plus regional node calcification is termed a primary complex or primary Ranke complex, and the parenchymal nodule is called a Ghon tubercle. The diagnosis cannot be made on roentgen study alone, but in many patients the appearance is so typical that the diagnosis is relatively certain. Progress roentgenograms tend to substantiate the conclusion, and the tuberculin skin test can be used to confirm it (Fig. 24-23). As a rule, the calcifications secondary to histoplasmosis are larger than those in TB.

Primary tuberculosis

A: The primary disease is noted in the left upper lung, largely in the plane of the second anterior interspace. It consists of poorly defined opacity in the parenchyma, accompanied by enlarged hilar nodes. B: In a roentgenogram obtained 1 month later, there is a clearly defined strand of opacity extending into the area of the previous disease. The enlarged nodes have regressed.

The primary pulmonary parenchymal focus is usually solitary but may be multiple. There are several variations from the typical findings described. In some patients, the primary parenchymal opacity is so small as to be invisible on a roentgenogram, whereas lymph node enlargement in the hilum in the same patient may beconsiderable. Distribution in the lungs is random, so that lower-lobe disease is at least as common as upper-lobe disease. The lower-lobe lesions usually do not cause atelectasis in children, so they often escape notice. In some cases, no visible hilar node enlargement is demonstrated.

Tuberculous Pleural Effusion• Occasionally, the first manifestations of TB are pleural effusion and pleural

disease, which may hide the parenchymal disease. As a part of the primary disease, pleural effusion is more common in adults than in children. The figures vary, but about 10% of children and 30% of adults with primary TB have pleural effusion, usually unilateral and on the side of the parenchymal disease. In some reports, the incidence of effusion is considerably higher.

• Tuberculous pleurisy develops when subpleural foci of infection rupture into the pleural space. It can occur at any time during the course of TB, but it most commonly occurs 3 to 7 months after the initial exposure. 35,51,96 Diagnosis is frequently very difficult, because the tubercle bacillus rarely can be cultured from the pleural fluid.

• Often a pleural biopsy is required to confirm the diagnosis. 96• Pleural effusions in primary TB usually clear completely in a month or two without

treatment. Occasionally, the effusion persists, leaving a residual sac of fluid often encased in thickened pleura. Eventually, some of these pleural residues may calcify peripherally or centrally and form long-term sequelae of fibrothorax.

Atelectasis• A major cause of the opacity that is sometimes associated with primary TB in

children is now known to be atelectasis, which usually results from compression of an upper-lobe bronchus by the large hilar nodes. Complete occlusion may occur when there is an added factor of bronchial infection or edema. The atelectasis may appear and disappear from time to time, producing opacity and decreased volume of the involved lobe or segment when present. If the atelectasis persists despite treatment with antituberculosis drugs, it usually indicates bronchostenosis. Surgical removal of the involved lobe may then become necessary. The more usual course, however, is for the atelectasis to clear as the inflammatory process subsides in the nodes and in the bronchial wall. Therefore, roentgen findings vary in these patients. They consist of the hilar node enlargement plus varying amounts of opacity in the involved lobe, depending on the amount of atelectasis present in addition to the actual tuberculous disease. The parenchymal opacity often remains after the atelectasis clears ( Fig. 24-24). Bronchiectasis may also result as a complication of this type of disease.

Primary tuberculosis with atelectasis. A: Note the homogeneous opacity in the right upper lobe. The minor fissure is greatly elevated, indicating a considerable amount of atelectasis. B: In a roentgenogram obtained 5 weeks later, the upper lobe has expanded. Residual pulmonary disease is present above the right hilum; right upper hilar nodes are enlarged.

Progression

• The usual course of primary TB is slow resolution, which may occur in 3 to 9 months. Progressive primary TB may occur in several situations. It is most common in infants younger than 1 year of age, in patients using corticosteroids, and in other susceptible patients (often with other chronic illness). The pulmonary involvement increases; often cavitation occurs, with subsequent bronchogenic spread or pleural involvement with effusion and/or empyema and occasionally with bronchopleural fistula.

Tuberculous Pericarditis

• Tuberculous pericarditis usually is caused by rupture of a caseous mediastinal node into the pericardium. This may cause acute tamponade, making immediate pericardiocentesis imperative. In other cases, a more gradual accumulation of pericardial fluid is associated with tuberculous pericarditis. The size of the cardiac shadow increases, and the presence of fluid can usually be determined by echocardiography. One, now rare, cause of calcific constrictive pericarditis is prior tuberculous pericarditis.

Hematogenous Dissemination and Miliary Tuberculosis

• Widespread hematogenous dissemination of TB as the result of primary infection is uncommon but is a very serious complication because it may lead to miliary TB and to involvement of many extrapulmonary structures, including the meninges. This complication usually occurs in infants younger than 2 years of age and is much less common in older children. It usually develops within 6 months of the initial primary infection.

Other Complications

• Occasionally the hilar or paratracheal lymph nodes may become so large that they extend into the adjacent pulmonary parenchyma and may require surgical removal.

• Bronchoesophageal fistula has also been reported, when caseating nodal disease extends into the esophagus and into a bronchus.

Primary Tuberculosis in the Adult• Unusual pulmonary manifestations of TB have been reported because of

decreased exposure in childhood and development of the primary form of the disease in many adults.18,102 There is more lower-lobe disease in adults. Equal incidence or slight predominance of lower- and middle-lobe disease has been reported. 134 Choyke and associates23 reported a 40% incidence of lower-lobe disease and a 58% incidence of upper-lobe disease in one series of 103 adults. Cavitation was present in 8%, which is higher rate than that reported in children. Pleural effusion was present in about 30%, also more common than in children. On the other hand, adenopathy occurred in only about 10%, almost half in the right paratracheal nodes. Others have reported a higher incidence of adenopathy. All of the patients with adenopathy had parenchymal disease demonstrated on chest roentgenography. In this series, about 15% of the patients were immunocompromised, so that TB can be an opportunistic infection. ARDS occurred as a complication of miliary TB in four patients. This is a particularly difficult situation, and prompt antituberculosis drug therapy may be life-saving.

Postprimary (Reinfection, Reactivation) Tuberculosis

• Reinfection or reactivation TB occurs when tubercle bacilli produce pulmonary inflammatory disease in a person who was previously sensitized to tuberculin. Unlike primary TB, this condition tends to be progressive, leading to symptomatic pulmonary disease unless treated. Lymph node involvement is much less common than in primary disease. The disease has a considerable tendency to localize in the upper lobes. There is no certain way to distinguish between the two types on roentgen study, however.

Early Reinfection Tuberculosis• The upper lobes are the most common site, and the parenchymal disease is most often found in

the apical and posterior segments of the upper lobe. The right side is affected somewhat more frequently than the left. However, it is not uncommon to see the initial opacity in the superior segment of the lower lobe on either side. The basal segments of the lower lobe are not often the site of the original disease in reactivation pulmonary TB. The disease is asymptomatic in its early stages, and a chest roentgenogram often indicates a lesion before the onset of subjective symptoms and before physical findings can be elicited on examination of the chest. As far as the roentgen findings are concerned, there is nothing characteristic about early tuberculous disease except its location in the upper lobe, which is usually fairly peripheral in relation to the hilum. Characteristically the disease appears as an area of mottled opacity that varies considerably in size, and the limits of the lesion are usually poorly circumscribed. The hazy character and poor definition of the lesions suggest a pneumonic or exudative process, in contrast to the more clearly defined, strand-like character of chronic fibrotic disease. It is not uncommon for this disease to be obscured to a greater or lesser extent by the clavicle or by one of the upper ribs and thus escape attention unless the roentgenogram is examined carefully ( Fig. 24-25, Fig. 24-26, and Fig. 24-27). In other patients the disease may be undetected until it is well advanced, so it is not unusual to find extensive disease with cavitation and bronchogenic spread to the opposite lung or the lower lobe of the same lung. In others, the initial chest roentgenogram reveals a large area of segmental or lobar consolidation representing tuberculous pneumonia.

Minimal pulmonary tuberculosis in the right upper lobe. Note the hazy, poorly defined opacity in the first anterior interspace laterally, immediately below the clavicle. Some disease was also concealed by the clavicle. Compare this area with the same area on the patient's left side, which is normal. B: Somewhat more extensive disease is present in the right upper lobe in the supraclavicular area, in the first anterior interspace, and medial to the first rib. Some of the disease is obscured by the clavicle. The left side is normal.

Minimal tuberculosis in the left apex. The disease is clearly defined in the supraclavicular area. It contains some calcium. There were also several calcified nodes in the left hilum, some of which are shown here. Note the minimal amount of pleural thickening lateral to the pulmonary disease.

Minimal tuberculosis. A: The disease is rather poorly defined, largely in the lateral aspect of the second anterior interspace. B: Close-up view of the upper-right lung shows the hazy opacity to better advantage. Its haziness and poor definition are compatible with active disease.

• At times the disease appears as a relatively clearly defined linear opacity, resembling a fibrotic scar. However, it must be remembered that TB cannot be classified as inactive on the basis of a single study. Because there is a wide variation in susceptibility, the virulence and number of organisms, and the gross pathologic response to the disease, it is not surprising that roentgen study of TB should demonstrate a wide variation in the appearance of the disease. 134 In some patients the location and appearance of the initial tuberculous process are characteristic enough for the radiologist to make a presumptive diagnosis of pulmonary TB, but this should always be confirmed by bacteriologic study of sputum or of specimens obtained during fiberoptic bronchoscopy.

• Recently, a number of articles have reported on the characteristic findings of pulmonary TB on CT and high-resolution CT (HRCT) ( Fig. 24-28 and Fig. 24-29). HRCT has been shown to be more sensitive than chest radiography for detecting early active disease. 53,56,63,67,71,72,73 and 73A,89,95,100,101 HRCT findings of postprimary TB include 2- to 4-mm centrilobular nodules or branching structures (the “tree-in-bud” sign); cavities; bronchiectasis; lobular consolidation; ground-glass opacities; and small (6 to 10 mm), nodular opacities. These often, although not invariably, are seen in cases of active pulmonary TB. The tree-in-bud pattern is typical of endobronchial spread of TB but again is not specific for TB and can be seen in other disease processes such as diffuse panbronchiolitis, acute bronchitis/pneumonia caused by other infections, aspiration pneumonia, and bronchiectasis of any cause with mucoid impaction. 2,7,53 The tree-in-bud sign, however, is one of the earliest

• HRCT findings of bronchogenic spread of TB. On histopathology, this sign corresponds to impaction of caseous material within dilated, small distal bronchioles including the terminal bronchioles, the respiratory bronchioles, and the alveolar ducts. 54

A and B: Computed tomographic findings of active tuberculosis. Multiple foci of patchy disease are noted bilaterally, characterized by larger nodular opacities (arrows) and surrounding areas of tree-in-bud formations ( arrowheads).

A: Chest film taken at presentation of a 34-year-old man with a history of tuberculosis shows left pleural fibrosis and scattered nodular opacities in both apices and in the left lower lung. B and C: Computed tomography more clearly demonstrates the presence of open cavities in both apices and multiple areas of bronchogenic spread of tuberculosis to the left and right upper lobes, lingula, and left lower lobe. Left pleural fibrosis and bilateral calcified hilar nodes are also present.

• CT findings associated with cases of inactive or stable TB include fibrotic irregular lines, parenchymal bands, calcified nodules and calcified adenopathy, architectural distortion of the bronchovascular bundles, bronchiectasis, and pericicatricial emphysema. 53,56,63,67,71,72 and 73,89,95,100,101 As with chest radiographs, disease inactivity can not be determined solely on the basis of CT findings on a single CT examination but requires confirmation of negative sputum cultures and serial examinations over time.

• CT findings of primary TB include lobar consolidation with hilar or mediastinal adenopathy. With intravenous contrast enhancement, tuberculous adenopathy typically shows rim enhancement with low-density, necrotic centers.54,72 Areas of lung consolidation may show cavitation. 72

Bronchogenic Spread of Tuberculosis

• When enough necrosis is produced by the action of the tubercle bacillus, a cavity is formed and the necrotic material is extruded through a bronchus. The cavity appears on the roentgenogram as a rounded or oval area of radiolucency, usually surrounded by a moderately thick wall and often by a considerable amount of disease in the same area. Exudate from this cavity can be expectorated, or it may be aspirated, resulting in bronchogenic spread of infection to other parts of the same lung or to the opposite lung. New foci of infection are then set up that in turn may undergo eventual cavitation. Small foci of tuberculous pneumonia are started by these bronchogenic aspirates. All of these lesions may heal, go on to caseation and cavitation, or become productive lesions resulting in the formation of a considerable amount of granulation tissue and eventual fibrosis. The fibrosis may be extensive, leading to a considerable loss in lung volume and tracheobronchial distortion.

• Bronchogenic spread of TB results in a characteristic appearance on CT. In addition to the tree-in-bud sign, CT may demonstrate patchy areas of air-space disease consisting of poorly defined nodular opacities measuring 3 to 10 mm in diameter (see Fig. 24-28 and Fig. 24-29).37,67,96 Typically, these areas of involvement are widely scattered in different parts of the lung. An open cavity in the same or opposite lung is often identified. The nodular opacities of bronchogenic spread are less uniform, less well marginated, larger, and less evenly distributed than the smaller (1 to 3 mm), discrete nodules of miliary TB. 67,96 Not surprisingly, CT often reveals more extensive bronchogenic spread of TB than is appreciated on the chest radiograph (see Fig. 24-29).67,96

Cavitation• The presence of cavitation in a patient with pulmonary TB is common and is often readily detected roentgenographically

because the cavity is large enough to produce a distinct round or oval radiolucency with a moderately thick wall. If there is uncertainty about the presence of a cavity, CT should be used to confirm or exclude its presence (see Fig. 24-29). CT is very valuable in detection of cavitary disease and is more reliable than chest radiography.

• As with other aspects of tuberculous disease, there is wide variation in the appearance of tuberculous excavation from one patient to the next. The cavitations appear as radiolucent areas that vary widely in size but are generally round or oval. The inner wall of a cavity may be smooth or irregular ( Fig. 24-30). The walls are usually moderately thick except in tension cavities, which become fairly large and may exhibit thin walls. A tension cavity develops because a check-valve type of obstruction of the bronchus leading to it allows air to enter the cavity more freely than it can escape. This type of cavity may disappear very quickly after treatment is instituted, because the bronchial obstruction that contributed to its size may be relieved quickly and permit the cavity to collapse. Thick-walled cavities, on the other hand, often show little tendency to close, or they may close or decrease in size very slowly when treated. Although not as common as in lung abscess, fluid can occasionally be present in a tuberculous cavity, so fluid levels can be demonstrated on horizontal-beam roentgenograms or CT. Air–fluid levels, however, may also be an indication of superimposed bacterial or fungal infection in a chronic tuberculous cavity. 35,67,96 In general, the walls of the cavities decrease in thickness and become less distinct as the disease regresses under treatment. Fibrosis, with contraction of the previously involved lung, and emphysema may result in production of irregular or oval radiolucencies that simulate cavities very closely. In these instances it is often difficult and sometimes impossible to differentiate a thin-walled cavity from an area of emphysema unless the disease has been well documented by repeated roentgenograms during its course. In these patients, CT is often of considerable value.

• If cavitation or extensive disease has occurred in a lobe or segment, fibrosis is a part of the healing process and results in volume loss, often with bronchial, hilar, and mediastinal distortion.

• Tuberculous disease activity can not be determined on the basis of radiographic or CT appearance of the cavity alone, and diagnosis must be made from results of sputum cultures and serial imaging analysis. 35,67,96 Even chronic cavities can continue to discharge viable bacilli.

Advanced bilateral pulmonary tuberculosis. A: Note the large apical cavity on the right in the supraclavicular area. The disease is extensive in the upper half of both lungs, and several suspicious radiolucent areas are noted on the left. B and C: In tomograms of the patient shown in A, the apical cavity on the right, some shift of the trachea to the right, and several small cavities on the left are evident.

Bronchiectasis

• Endobronchial involvement in pulmonary TB is very common and leads to bronchiectasis in many instances. The presence of bronchiectasis in patients with TB can often be diagnosed or at least suspected on routine roentgenograms, because the thick-walled bronchi filled with air stand out in contrast to the diseased lung surrounding them. In other cases, particularly in less extensive disease, the diagnosis can be made with a high degree of certainty on CT. If the extent of bronchiectasis is to be determined before surgical removal, bronchography or, more commonly, CT is used to make this assessment. Bronchiectasis in patients with pulmonary TB may be saccular or cylindrical and is found in the lobe or segment involved by the disease. Occasionally, it is detected in an area where there is no obvious parenchymal involvement. Presumably, the bronchiectasis was caused by tuberculous disease which has resolved to the point where no roentgen evidence of parenchymal involvement remains. For this reason, many investigators consider that CT or bronchography is indicated before segmental surgery is undertaken in patients with pulmonary TB. Because antituberculosis drug therapy is very effective, surgery is now limited to the occasional patient with severe bronchiectasis, hemorrhage, or repeated infection localized to the site of earlier TB. There is some difference in the appearance of bronchiectasis in TB compared with that caused by other conditions. In TB there is often peripheral obliteration and more fibrosis with greater distortion of bronchi ( Fig. 24-31).

• Bronchiectasis in tuberculosis (TB). A: Note the dilation of the upper-lobe bronchi, which are also crowded in a patient who had previous extensive TB of the right upper lobe. There is very little alveolar filling, and the distal ends of the bronchi are obstructed. The latter finding is characteristic of TB. B: Bronchogram of a patient with far-advanced TB of long duration. The right upper lobe is contracted, and there is extensive saccular bronchiectasis, bronchial distortion, and failure of parenchymal filling.

Bronchiectasis in tuberculosis (TB). A: Note the dilation of the upper-lobe bronchi, which are also crowded in a patient who had previous extensive TB of the right upper lobe. There is very little alveolar filling, and the distal ends of the bronchi are obstructed. The latter finding is characteristic of TB. B: Bronchogram of a patient with far-advanced TB of long duration. The right upper lobe is contracted, and there is extensive saccular bronchiectasis, bronchial distortion, and failure of parenchymal filling.

Unusual Radiographic Manifestations of Pulmonary Tuberculosis

In addition to the unusual distribution and other differences described in adults with primary TB, several other possible findings should be mentioned:1. Multiple bilateral large pulmonary nodules.2. Multiple small, scattered, cavitary foci that resemble hematogenous staphylococcal abscesses. These lesions remain unchanged and can therefore be differentiated from acute staphylococcal disease, which changes rather rapidly.3. Pulmonary gangrene resulting from TB. The patients are very ill and this disease is often fatal. A large, homogeneous, lobar alveolar process is observed to increase in density; the lobe increases in volume, and cavitation appears with a large intracavity mass of necrotic tissue, similar to that sometimes observed in Klebsiella pneumonia.624. Rasmussen aneurysm, a rare pseudoaneurysm caused by erosion of a peripheral pulmonary artery branch within a tuberculous cavity. It can simulate a mass within a cavity. Complications include formation of an arteriovenous fistula, rupture with hemoptysis, and sometimes exsanguination. These aneurysms can be treated by embolization to occlude the involved pulmonary artery branch.5. A nonspecific severe, widespread interstitial pattern throughout both lungs. This occurs in middle-aged and elderly patients with emphysema. The patients are not very ill, and there is no radiologic change over many months. Diagnosis is usually made by open lung biopsy. Response to good antituberculosis drug therapy is very slow. Pneumothorax may complicate this unusual form of TB. 102

Tuberculosis in the Immunosuppressed Patient

• The cell-mediated immune response (T lymphocytes) is largely involved in the destruction of tubercle bacilli. There are several situations in which cell-mediated immunity is depressed.93 They include acquired immunodeficiency syndrome (AIDS) (see Chapter 25),104A aging, starvation, chronic illness, alcoholism, cancer, sarcoidosis, silicosis, pregnancy, radiation, and drugs such as corticosteroids, immunosuppressive drugs, and cytotoxic drugs used in cancer chemotherapy. Patients with these conditions are at risk if exposed to the organism. The highest incidence appears to be in elderly persons, debilitated persons, and patients with AIDS, chronic diseases, or malignancy. Although TB is difficult to manage in patients with silicosis, the incidence of TB in patients with silicosis is decreasing. Whether this will remain true in the future is not certain, since the incidence of TB may be increasing.

• The radiographic appearance of TB depends on the level of immunosuppression. It is similar to that in other patients except when T-cell depression becomes significant. Then the disease is likely to progress more rapidly, to become far advanced, and to develop miliary spread. This can occur in primary as well as in reactivation TB.

Tuberculoma• The term tuberculoma refers to the round, focal, tuberculous lesion that may be solitary or multiple. There are many

inflammatory nodules in which tubercle bacilli cannot be found. The histopathologic findings are nonspecific. They are termed chronic nonspecific granuloma and cannot be differentiated from tuberculoma by roentgenographic methods. The tuberculous nodules vary in size from a few millimeters to 5 or 6 cm but usually range from 1 to 3 cm. They may or may not contain calcium and usually contain caseous debris. Small flecks of calcium may be scattered in the lesion, and in some instances calcium may form a more or less complete shell or ring in or near the outer wall of the nodule. Several concentric rings of calcium or an eccentric or central nidus of calcium may be present. The pathogenesis is varied, and the nodule may represent either primary or reinfection disease. Sometimes the nodule results when a cavity is sealed by obstruction of its draining bronchus. It may also be a residual localized area of caseation that persists when the remainder of the primary disease clears. It is not unusual to see a few tiny satellite nodules or poorly defined areas of opacity in the vicinity of a tuberculoma. All of these lesions are potentially dangerous, because they may contain viable tubercle bacilli for long periods and may break down at any time with resultant dissemination of the disease. They may remain constant in size or grow very slowly over a period of years.

• The roentgen finding is that of a round parenchymal nodule. If concentric rings of calcium are visible, the lesion is almost certainly a tuberculoma or other chronic inflammatory granuloma (Fig. 24-32). If no calcium is demonstrated on the routine roentgen study of the chest, CT is indicated. Calcium can often be seen on CT when its presence is not detected on the preliminary film. If no calcification is found, differentiation of the tuberculoma or other infectious granuloma from bronchogenic carcinoma, other lung tumors, or solitary pulmonary metastasis may be impossible. Recent preliminary studies by Swenson and others suggest that small noncalcified nodules that fail to show significant contrast enhancement on dynamic serial CT scanning while intravenous contrast is being administered are likely to be benign. 129A In the patient with a small, solitary nodule that is not clearly benign, resection must be considered, unless previous films from 2 or 3 years ago indicate that the lesion has been present for a long time and is unchanged. Transbronchial or percutaneous needle biopsy may clearly demonstrate granulomatous disease. If there is doubt or if malignancy is found, resection is necessary.

TuberculomaNote the dense, calcified nodule in the right midlung. Some disease is also noted lateral to it and above it in the lateral aspect of the second anterior interspace. Some calcified hilar nodes are noted bilaterally.

Healing of Pulmonary Tuberculosis• In general, pulmonary TB heals slowly, so that it is possible by serial roentgenography to follow the

gross anatomic changes in the disease. Differences can be noted in the manner of healing, which depends on the type of involvement and the susceptibility of the tubercle bacilli to the antituberculosis drugs as well as on the response of the patient. Complete resolution often occurs in some areas. It is a common observation that complete resolution occurs and is most striking in patients with relatively acute disease in which the process is presumed to be largely exudative ( Fig. 24-33). This accounts for the decreased thickness of the walls of cavities that is often noted in patients undergoing treatment. The exudative portion of the process making up the cavitary wall resolves, resulting in a decrease in thickness. In patients in whom the disease has progressed to the point of necrosis, complete resolution is not possible. In these patients, fibrosis with contraction of the scars results in shrinkage in the volume of the involved lobe or segment and sometimes a decrease in the size of the hemithorax. The mediastinal structures are retracted to the side of involvement. The hilum is elevated in upper-lobe disease, and sometimes the hemidiaphragm is raised. The lesions that contain granulation tissue as well as caseation, and are often noted as poorly defined nodules, show gradual reduction in size. The individual nodules tend to become more clearly defined on the roentgenogram, evidently also because of contraction and fibrosis. This type of lesion often is the site of calcium deposition and in some instances becomes densely calcified with the passage of time. Many of the lesions contain central areas of necrosis in which viable organisms can be found after long periods of apparent inactivity. In summary, as visualized roentgenographically, there is considerable difference in the healing process from one patient to another, but it is unusual to see the disease disappear entirely ( Fig. 24-34).

Far-advanced bilateral pulmonary tuberculosis, showing the regression resulting from treatment with antituberculosis drugs. A: Note the extensive bilateral disease. B: Study made 9 months later shows great improvement. The remaining disease consists largely of fibrous strands with a few nodules in each lung.

Far-advanced pulmonary tuberculosis. A: Initial film shows the bilateral disease. A large cavity in the right apex is rather poorly defined on this film. B: Nine months later, the right lung shows the result of treatment. The large apical cavity is more clearly defined. The upper lobe is contracted, but much of the exudative disease has cleared. C: Sixteen months after the initial examination, most of the residual disease has been resected and now the findings are those of surgical scarring in the right second anterior interspace and in the left subclavicular area.

• CT is very helpful in demonstrating nodular residuals that cannot be clearly defined on routine chest roentgenography. Examination of surgical specimens has demonstrated that it is very difficult to be certain on roentgen examination that no residual disease is present.

• Roentgenographic changes observed during the healing process have very little prognostic value. Studies have shown that it is not necessary to take routine follow-up roentgenograms when a patient undergoing treatment has no clinical signs to warrant concern. After treatment, chest radiographic study is necessary if symptoms recur. When examining a patient with residuals of TB, it is imperative to compare the earliest available chest film with the current one, because changes are subtle and gradual and may be overlooked if only the most recent film is used for comparison.

Complications of Reinfection Pulmonary Tuberculosis: Pleural Effusion and Empyema

• Because pulmonary TB is a peripheral lesion, pleural involvement is common ( Fig. 24-35); effusion may be found in patients without an obvious pulmonary lesion. In some instances the opacity produced by the fluid obscures the parenchymal disease. In others, pleural effusion is the only roentgen manifestation and, even when the fluid has been removed or absorbed, no definite pulmonary parenchymal focus is roentgenographically visible. In some patients the fluid disappears spontaneously or can be successfully aspirated, and in others tuberculous empyema results. Occasionally, the pleural space may be involved by secondary infection. The tuberculous empyema is similar to empyema of nonspecific origin in its roentgen appearance. It is usually loculated and may become very large. If it is present and undrained for a long time, calcification may occur, producing marked radiographic opacity outlining the wall. Bronchopleural fistula may also occur, with drainage of all or part of the contents of the empyema and entrance of air into it. Pleurocutaneous fistula and bronchopleurocutaneous fistula are rare complications of chronic TB. In some patients with tuberculous pleural disease, considerable fibrosis in the pleural space results in marked pleural thickening and constriction of the adjacent lung or of the entire hemithorax if the disease is extensive, so-called fibrothorax. Calcification may then occur in or adjacent to either the visceral or parietal pleura or both.

• Occasionally, an empyema develops years after the initial pleural infection and should be suspected if the volume of the fibrothorax increases. The presence of fluid within the pleural space or between the layers of fibrothorax can be detected by ultrasonography in most instances; CT may also be useful in this situation, particularly if ultrasonography is equivocal. If the pleural infection remains active, chest wall extension of the empyema may develop; this is called empyema necessitatis.

Pulmonary tuberculosis, showing the development of pleural effusion. A: Bilateral tuberculosis of the upper lobe is manifested by opacity that is rather homogeneous and more intense on the right than on the left. There is no evidence of pleural fluid on the right, and there was none on the left. B: Four weeks later, a large pleural effusion on the right is evident. Note that the parenchymal disease has regressed slightly owing to treatment during the interval.

Bronchostenosis

• Narrowing of a bronchus may result from pressure of an enlarged lymph node that is involved by TB. This is usually found in children with primary TB. It is also caused by endobronchial inflammation and granuloma formation or fibrosis in the postprimary or reinfection form of the disease. Roentgen findings are not evident until the obstruction is sufficient to cause either atelectasis or obstructive overinflation. Broncho stenosis may also result in repeated nonspecific infections distal to the narrow bronchus. Complete bronchial occlusion as the result of tuberculous fibrosis rarely may be the cause of mucoid impaction.

Broncholithiasis

• Occasionally, a calcified node adjacent to a bronchus erodes into the bronchus and the calcified material from the node is extruded into the bronchus, producing a broncholith. This may cause very few symptoms or on rare occasions it may result in bronchogenic spread of tuberculous disease or hemorrhage. The calcification may also cause bronchial obstruction with overinflation or atelectasis. This complication may also occur in patients with calcified nodes caused by lesions other than pulmonary TB. Radiographic findings vary with the situation. The calcified nodes are often visible, and their relationship to the bronchus can best be determined by

• CT (Fig. 24-36).

Computed tomogram demonstrates a broncholith protruding into airway of the bronchus intermedius near the take-off of the middle-lobe and lower-lobe bronchi.

Tuberculous Pneumothorax

• When pneumothorax complicates pulmonary TB, it creates the hazard of widespread pleural involvement leading to tuberculous empyema and bronchopleural fistula.

• This is because the pneumothorax often results from rupture of a caseous subpleural focus into the pleural space in advanced disease. It is also possible for a small subpleural bleb to rupture, leading to a simple pneumothorax that resolves quickly without further complication. The roentgen appearance is similar to that noted in pneumothorax from other causes, but the tuberculous disease is visible and a considerable amount of adhesive pleuritis may result in irregular or loculated pneumothorax. This is an uncommon complication of TB.

Dissemination to Other Organs

• Patients with pulmonary TB occasionally develop disease in other organs and systems such as the larynx, ileum and cecum, urogenital organs, and skeletal system.

• Gastrointestinal disease and laryngeal disease are frequently the result of contact with sputum and only rarely indicate a hematogenous spread. On the other hand, renal TB or skeletal involvement indicates hematogenous or lymphangitic spread. These lesions are discussed by organ or system in the appropriate chapters.

Hematogenous Tuberculosis• Hematogenous pulmonary TB includes several types of disease. When the

organisms enter the blood stream, it is possible to get hematogenous involvement of numerous other organs and systems. The actual mode of dissemination is difficult to determine in any specific instance, but dissemination may occur by way of the lymphatics and enter the bloodstream through the thoracic duct, by direct rupture of a caseous focus into a vessel, or by formation of a subintimal tubercle that serves as a source of organisms. The invasion of the bloodstream may occur in any stage of TB. When hematogenous dissemination develops, numerous factors have a bearing on the resultant disease, including the age of the patient, the number and virulence of the organisms entering the bloodstream, the individual and racial susceptibility, the general health of the patient, and the patient's state of allergy and immunity at the time of the invasion. Prompt treatment with antibacterial drugs usually alters the disease considerably in a favorable manner.

Miliary Pulmonary Tuberculosis• Two clinical types of miliary TB are recognized—acute miliary TB and subacute or chronic miliary

pulmonary dissemination. Miliary dissemination can occur at any time after the primary infection.35 Acute miliary TB follows massive bloodstream invasion and produces a severe acute illness, frequently with fatal termination before the use of antituberculosis drugs. In infants and children it may result by spread from a primary site and produces severe clinical manifestations. It usually occurs in malnourished or chronically ill infants, who are unusually susceptible. In most children, however, the number of organisms is small and host resistance sufficient to prevent miliary spread of the disease, so there are no clinical manifestations. In adults, particularly in the older age group, the disease may be insidious and extremely difficult to recognize. Findings on chest roentgenograms depend on the size and number of miliary tubercles. The actual nodules visualized on a roentgenogram are the result of superimposition of many small parenchymal lesions that create sufficient opacity to be recognized as a small nodule. In the typical patient the appearance is that of a fine granularity or tiny nodulation scattered uniformly throughout both lungs. At times the lesions are rather clearly defined as innumerable fine nodules, each sharply delineated; in other patients they are less sharply outlined, with hazy margins ( Fig. 24-37 and Fig. 24-38). In some patients with miliary pulmonary TB, no lesions can be seen on the initial chest film, but in most instances a classic miliary pattern develops during the course of the disease. 39

• Because miliary disease in adults can take up to 6 weeks to become apparent on chest radiographs, 6,43,47,96 CT may be helpful in detecting the disease earlier. In cases of miliary TB, CT demonstrates innumerable 1- to 3-mm, discrete nodules randomly distributed throughout the lungs 72 (Fig. 24-39).

Miliary tuberculosis. Close-up view of the right upper lung in a patient with miliary tuberculosis shows the numerous small opacities along with a smallincrease in interstitial markings.

Posteroanterior (A) and lateral (B) views showing miliary tuberculosis. Note the extensive miliary nodules, more dense and clearly defined than those in FIG. 24-37. The patient had weight loss, fever, and a cough.

A and B: Miliary tuberculosis. Computed tomography demonstrates widely disseminated tiny nodules of uniform size and uniform distribution.

• Some findings may suggest TB on the initial chest radiograph, however. Pleural involvement is common, resulting in unilateral or bilateral pleural effusion that varies considerably in amount. Rarely, recurrent pneumothorax complicates the disease. The cause is not certain, but subpleural caseating nodules may rupture into the pleural space in some instances. The individual lesions are largely exudative, and when treatment with antibacterial drugs is effective, the widely scattered foci usually disappear completely. They do not result in scattered pulmonary calcifications.

• The differential diagnosis of miliary TB is often difficult from a roentgen standpoint because numerous other diseases produce widespread scattered and miliary type of nodulation in both lungs. Correlation of clinical and roentgen findings is very important in all instances. Several acute processes cannot be differentiated from miliary TB on a single chest roentgenogram. Miliary bronchopneumonia, which may be of viral or bacterial origin, and bronchiolitis in children that results in widespread miliary nodulation may closely resemble miliary TB. In other diseases such as sarcoidosis, the pneumoconioses, and miliary pulmonary carcinomatosis, the history and clinical course usually permit differentiation. Several additional conditions can produce acute, diffuse miliary lesions in the lung. They include other bacterial infections such as staphylococcal and streptococcal pneumonia, viral and rickettsial infections such as chickenpox and Q fever, mycotic infections such as histoplasmosis and blastomycosis, and parasitic infestations such as schistosomiasis. Also included are the noninfectious diseases, acute berylliosis, miliary hemorrhages, and acute, diffuse, interstitial fibrosis as described by Hamman and Rich. It is therefore evident that the roentgen findings must be correlated with the results of clinical and laboratory examinations. In some instances, serial roentgenograms, spaced over a period of days or weeks, are helpful in establishing the diagnosis.

• In the immunocompromised patient and the infant with acute febrile illness and miliary pulmonary disease, and in difficult cases in elderly patients, lung biopsy to get a prompt diagnosis may be indicated, since a delay in treatment could be fatal.

Subacute and Chronic Hematogenous Pulmonary Dissemination

• Subacute and chronic hematogenous pulmonary dissemination is a somewhat different clinical entity from acute miliary TB in that it is often asymptomatic. Repeated small episodes may occur, so that lesions, although widespread and distributed rather uniformly throughout both lungs, are likely to be somewhat more variable in size than in the acute miliary process. When this type of dissemination is extensive, the roentgen findings are similar to those in the acute type of miliary TB, but there is considerable difference in the clinical course. In other instances the hematogenous pulmonary dissemination may be relatively localized, producing small, poorly defined, rounded or oval areas of density in a segment or lobe. Some of these nodules may regress, and others may coalesce to form larger nodules; these may heal in a manner similar to that described for reinfection TB. In patients with far-advanced pulmonary TB and a considerable amount of cavitation, there may be hematogenous spread to the lower lobes or to the opposite lung, resulting in scattered lesions that cannot be differentiated from the secondary lesions produced by bronchogenic spread of the disease.

Atypical Mycobacteria

• Some Mycobacteria species that can cause pulmonary disease that is similar to TB caused by M. tuberculosis but slightly different from the standpoint of roentgen findings. These mycobacteria have been classified according to growth characteristics when exposed to light into four groups 133:

• Group I. Photochromogens: M. kansasii, M. marinum, and M. simiae• Group II. Scotochromogens: M. scrofulaceum, M. szulgai, and M. gordonae• Group III. Nonphotochromogens: M. avium-intracellulare (Fig. 24-40), M.

nonchromogenicum, M. terrae, M. novum, M. triviale, M. xenopi, M. malmoense, and M. ulcerans

• Group IV. The rapid growers: M. fortuitum, and M. chelonei• The clinical and radiologic aspects have been discussed at length by

Wolinsky, 132 Woodring and Vandiviere, 133 and others.3,25,107,121 The most important of these pulmonary pathogens are M. avium-intracellulare, M. xenopi (particularly in Ontario121) (Fig. 24-41), and M. kansasii.

A and B: Atypical mycobacterial infection caused by Mycobacterium avium-intracellulare in a middle-aged white woman with chronic cough. Computed tomogram shows focal bronchiectasis and some surrounding inflammatory disease in the left lung apex and a cluster of nodular opacities and tree-in-bud pattern in the lateral aspect of the right upper lobe. Calcified granulomas are noted in the right hilum. Group

Atypical mycobacterial infection caused by Mycobacterium xenopi. A: A large cavity with an air–fluid level is present in the right upper lobe, and a calcified granuloma is noted in the left lower lung. B and C: Computed tomogram demonstrates a thick, irregular, walled cavity with air–fluid–debris level. Bronchiectasis in noted medial to the cavity, and one of the dilated bronchi communicates with the cavity ( C).

M. avium-intracellulare (M. avium complex) infections appear to be increasing, particularly in persons with decreased cellular immunity or chronic lung disease, but also in those without predisposing cause. The radiologic features are slightly different from those of M. tuberculosis and show the following contrasts:• 1. There is an increase in cavitation in relation to the amount of lung involved.• 2. Thin-walled cavities without much surrounding disease are seen; cavities may be small. However, in general, cavities caused by

atypical mycobacteria are• indistinguishable from those caused by M. tuberculosis.3,25,84• 3. Spread is more often contiguous than bronchogenic.• 4. The anterior segment of the upper lobe appears to be involved more frequently than in M. tuberculosis.• 5. There is marked pleural thickening over the involved areas of lung.• 6. There is more involvement of apical and anterior segments of the upper lobes.• 7. Clustered opacities around irregular translucent areas with radiating line shadows are seen; opacities resembling tumors

occasionally occur.• 8. Disease is usually unilateral even when far advanced.• 9. It is usually found in older age groups.• 10. Pleural effusion is uncommon and small in amount.• 11. Adenopathy is uncommon.• 12. Disease is often extensive when first discovered.• 13. There is a marked predominance of whites to blacks (10:1).• Although these findings differ somewhat from those in TB, the variety of findings in M. tuberculosis infections is such that

roentgenographic differentiation cannot be made. At times atypical mycobacterial infection can be suggested, however. These atypical organisms usually do not respond well to antituberculosis drug therapy. M. avium complex appears to be particularly difficult to control; surgical removal of residual disease may be necessary and should perhaps be considered after antituberculosis therapy.

Surgical Measures in Pulmonary Tuberculosis

• Despite the undoubted value of the various antibacterial drugs now available for the treatment of TB, in some patients cavities fail to close or tubercle bacilli continue

• to be discharged in pulmonary secretions. Tuberculous bronchiectasis may cause repeated hemorrhage, may cause repeated nonspecific infections, or may harbor an

• aspergilloma, which can also cause bleeding and be difficult to eradicate. These patients then become possible candidates for surgery, which is usually a resection of

• the residual disease. The roentgen findings after pulmonary resection for TB are similar to those described in Chapter 31.

• Before effective drugs were available, thoracoplasty and plombage were used in an attempt to close cavities and promote healing. Thoracoplasty is used very rarely

• today, and plombage is no longer used. Older patients who have had these procedures may be examined by means of chest films, so examples of patients who have

• undergone these procedures are included ( Fig. 24-42 and Fig. 24-43).

Left thoracoplasty. This surgical procedure, which was used extensively before the advent of antituberculosis drugs, is employed rarely at present. There has been extensive resection of the upper seven ribs on the left, compressing the left upper lung. Regeneration of the ribs has formed a solid bony plate along the upper lateral chest wall. The scoliosis is a common result of thoracoplasty.

Lucite-ball plombage. Although this procedure has been abandoned, occasionally patients are observed with the rounded lucencies representing Lucite balls, usually at the apex of one hemithorax, as in this patient.

Complicating Aspergillomas

• Chronic tuberculous cavities may remain open long after sterilization and become colonized by Aspergillus organisms that develop into fungus balls or aspergillomas11

ACTINOMYCOSIS• Actinomycosis in humans is caused most commonly by an anaerobic organism, Actinomyces israelii. This organism occurs as a

filamentous, gram-positive, non–acid-fast, rod-shaped bacterial form in the mouth and as a mycelial form in infected tissues. 69 Other actinomycetes can cause human infection, including A. bovis, A. naeslundii, A. ericksonii, A. meyeri, and A. propionicus. The organisms are now established as bacteria, but roentgen and clinical findings are often similar to those of mycotic infections in that they produce chronic suppurative infections. 69,122 The disease may affect any part of the body but is found most frequently in and about the jaw (the cervicofacial form of the infection). There is also an abdominopelvic form, often associated with appendiceal surgery or use of intrauterine devices, and a thoracic form of the infection.4,69 Pulmonary infection is said to occur in approximately 15% of patients with the disease. However, in recent years, the incidence of pulmonary involvement has declined considerably; the classic empyema with chest wall sinus tracts and pulmonary parenchymal disease is rarely seen and is avoided by timely antibiotic therapy. Occasionally, however, it is still encountered as a complication of thoracic surgery or in debilitated patients such as alcoholics or those with COPD.69 This form of the disease is characterized by its tendency to produce suppurative sinus tracts and its ability to cross tissue planes that provide a barrier to the usual infections. Drainage from actinomycosis sinus tracts demonstrates sulfur granules, a hallmark of the infection. 4,69

• The roentgen findings vary greatly. The disease may be unilateral or bilateral but tends to be unilateral unless widely disseminated. It produces a dense, confluent opacity in the affected lung, usually in a lower lobe peripherally, in which cavitation may be present ( Fig. 24-44 and Fig. 24-45). The cavity may persist after treatment as a thin-walled, cystic shadow. In the classic chest wall disease, pleural involvement results in varying amounts of pleural thickening and fluid. Infection of the chest wall causes soft-tissue swelling and may cause periosteal reaction and/or destruction of ribs with sinus tract formation. This is characteristic of advanced disease, which is now observed infrequently. The parenchymal involvement may resemble acute alveolar pneumonia in some instances. In other cases, the disease is manifested as a local, mass-like opacity resembling bronchogenic carcinoma. Another roentgen pattern is that of a fan-shaped consolidation near the hilum or radiating from the hilum into the superior segment of the lower lobe. Rarely, hematogenous spread from a focal area of disease results in a miliary pulmonary pattern.

• When the combination of pulmonary disease and chest wall involvement with empyema and sinus tracts is present, actinomycosis may be strongly suspected. However, it must be differentiated by bacteriologic examination from TB, chronic fungal infections, Nocardia, and tumors.

ActinomycosisThe dense, confluent consolidation in the left lower lung obscures the left hemidiaphragm and left lower cardiac border. The patient also had a chest wall mass and sinus tracts typical of this disease.

A and B: Actinomycosis infection of the chest wall. Computed tomogram shows a chronic draining sinus tract that can be traced from the skin surface into the abdomen, through the diaphragm, and into the right pleural space.

• CT findings of thoracic actinomycosis include air-space consolidation with adjacent pleural thickening. Hilar or mediastinal lymph nodes (usually measuring less than 2 to 2.5 cm) are seen in 75% of patients on CT. Like adenopathy, cavitation and microabscesses are appreciated more often on CT than on conventional plain films in this infection.4,69 With chest wall invasion, inflammatory chest wall masses, abscesses, and sinus tracts may be identified on CT. 4 MRI is probably superior to CT in demonstrating the extent of soft-tissue infection and sinus tract formation, since both of these demonstrate high signal intensity on T2-weighted images. CT, however, is better for demonstrating rib and bone destruction and periostitis. Traditional sinograms with contrast injection of sinus tracts may also be needed to follow the course of these sinuses. Infections and sinus tracts have been known to communicate to the pleural space, to the chest wall, to the mediastinum, and through the diaphragm (Fig. 24-45).69

NOCARDIOSIS

• Nocardia asteroides is the most common of several species of Nocardia that can cause disease. It is an aerobic, gram-positive, filamentous, beaded acid-fast bacterium. It is recognized increasingly as an opportunistic infection in patients with underlying chronic debilitating disease or immunodeficiency, particularly in those who have undergone therapy with immunosuppressive or cytotoxic agents or steroids, including patients with cancer, organ transplants, diabetes mellitus, or chronic liver disease. Patients with congenital immune deficiencies and those with AIDS are also at risk. 16,112 In nocardiosis, pulmonary roentgen findings are varied. They may be similar to those of actinomycosis, mycosis, or TB and consist of homogeneous segmental or lobar air-space consolidation; or they may consist of one or more discrete nodules or rounded opacities. Cavitation is common. 16,44 Pleural involvement with empyema and chest wall invasion can also occur with Nocardia, and extrapulmonary dissemination to the central nervous system, cutaneous sites, and elsewhere have been reported ( Fig. 24-46, Fig. 24-47 and Fig. 24-48).16 The disease is frequently bilateral. It crosses fissures and anatomic barriers if not properly treated, but not as frequently as actinomycosis.

• On CT, the most common finding is one or more nodules or mass-like opacities which may or may not undergo cavitation. When compared with conventional radiography, CT shows more nodules and is better for characterizing the extent of disease (see Fig. 24-48).16 CT is also useful for localizing lesions when aspiration or biopsy is needed for diagnosis. This is often required, because isolation of Nocardia from sputum is difficult owing to the organism's slow growth and prolonged incubation period of up to 5 weeks. 16 The diagnosis is often elusive until material for histologic study is obtained by aspiration lung biopsy, transbronchial aspiration, bronchial brushing, or open lung biopsy.

• Pulmonary nocardiosis can present as an acute pneumonia, as a subacute process, or as a chronic indolent infection with prominent constitutional symptoms of fever, weight loss, and malaise.16 The roentgen alterations in the lungs persist for long periods, frequently with little change unless the patient is treated with appropriate antibiotics. It is not unusual for the disease to run a protracted course with very little variation in the appearance of the pulmonary lesions and very few symptoms.

• Pleural involvement with empyema and extension to involve the ribs with production of chest wall abscess is not as common as in actinomycosis but can be seen with nocardiosis. Occasionally, Nocardia may involve the skin when inoculated in a traumatic event. Then, extremely rarely, it may spread through the bloodstream to the lungs to produce disseminated pulmonary disease. Mediastinitis with adenopathy and obstruction of the superior vena cava has been reported. Nocardiosis is one of the few benign diseases that can cause obstruction of the superior vena cava. 104 In addition to differentiation of this disease from TB, the other chronic infectious lesions of the lungs must be included in the differential diagnosis. Identification of the causative agent is necessary to confirm the diagnosis.

Nocardiosis. A: This film shows a small amount of poorly defined opacity at the right base just above the diaphragm. B: Roentgenogram obtained 9 months later shows extensive progression of the disease with large, poorly defined nodular and patchy opacity in both lungs. A large homogeneous consolidation in which there is a cavity (arrow) is seen in the right upper lobe. There has been open drainage of the pleural space in the right upper anterolateral chest wall.

Necrotizing cavitary pneumonia caused by Nocardia infection

MYCOTIC DISEASES OF THE LUNG

• Mycotic diseases of the lung are caused by a variety of organisms, many of which are capable of producing acute lung disease (e.g., pneumonia, lung nodules), chronic stable or slowly progressive lung disease, or disseminated multiorgan infection. 86 Some fungal species are saprophytes or are of very low virulence, but in compromised hosts they may produce life-threatening acute pneumonia. The diseases must be differentiated from each other, from pulmonary TB, and occasionally from lung tumor. The ultimate diagnosis depends on demonstration of the causative agent in bronchial secretions or in sections of the lung. In some instances studies based on immunologic reactions are sufficient. These consist of skin tests, agglutination, complement fixation, and precipitation reactions. 119

• The gross anatomic changes in pulmonary disease produced by these varied organisms may be similar. On the basis of roentgen examination it is often possible to indicate only that the lesion is a chronic inflammatory disease of unknown origin. At other times it is possible to make the diagnosis with a considerable degree of accuracy on the basis of clinical findings correlated with roentgen manifestations.

Coccidioidomycosis• Coccidioidomycosis is caused by the fungus Coccidioides immitis.28 It is an endemic pulmonary disease occurring in the arid southwestern part of the United States, particularly

in the San Joaquin valley in California and in southern Arizona. Primary pulmonary coccidioidomycosis is usually asymptomatic and is discovered incidentally on a chest film (60%). There may be calcified granulomas in the lung or hilar nodes; in other cases, there may be a focus of pulmonary fibrosis or pleural thickening, and in some there may be no recognizable residual. If a chest film is obtained during the asymptomatic acute phase, a focus of alveolar pneumonia may be observed. The primary or initial infection may also produce an acute pneumonia associated with symptoms of an acute pulmonary disease, including fever, malaise, headache, and cough. Erythema nodosum is a common clinical manifestation during the acute febrile illness, and in the San Joaquin valley this clinical syndrome is known as valley fever. Erythema nodosum is often associated with arthralgias and occurs at about the time the reaction to the coccidioidin skin test becomes positive. It may be the only symptom and indicates a good prognosis. Before this time, some patients (about 10%) develop a toxic erythema, usually in the first few days of illness. The rash is a diffuse, fine, macular erythematous reaction covering the trunk and extremities and usually occurs in children with the disease.

• Roentgen findings in symptomatic primary disease are those of air-space pneumonia, which results in homogeneous opacity that is poorly circumscribed and may be segmental or lobar. It tends to involve the lower lobes and may be associated with some atelectasis. In other patients, there is patchy central disease that tends to resolve quickly (in 1 to 2 weeks). Pleural involvement is found in about 20%, usually manifested by a minimal effusion. The hilar nodes are enlarged in about 20% of these patients, usually on the side of the alveolar disease. The roentgen findings in this type of involvement simulate those of other acute, atypical pneumonias. The pneumonia of coccidioidomycosis may be localized to one segment, but wider dissemination has also been reported, with multiple areas of pneumonic consolidation.

• Occasionally, the adenopathy in the hilar and mediastinal nodes is the predominant feature, and in these patients there may or may not be evidence of pulmonary parenchymal involvement. Multiple nodular parenchymal lesions have also been reported but are not as common as the more localized pneumonitis. Cavitation within the area of disease is not uncommon. The cavities are usually small and may disappear quickly in the primary type of infection. Occasionally, small pleural effusion is the only evidence of the disease noted on the chest roentgenogram. Although effusion occurs in about 20% of patients with coccidioidomycosis, pleuritic chest pain has been reported in 70%. Massive effusion is rare and may result from direct spread of pulmonary disease across the pleural space.

• Persistent pulmonary coccidioidomycosis is found in about 5% of patients. It is a much more significant type of disease and may be fatal. In these patients, coccidioidal pneumonia may persist for months, with large areas of dense consolidation clearing very slowly. The patients are often very sick with persistent fever, prostration, chest pain, productive cough, and occasional hemoptysis. This type of the disease usually occurs in susceptible patients and occasionally in immunosuppressed patients. Cavitation, either thick- or thin-walled, may also occur and may be chronic. Bronchiectasis and bronchial stenosis are uncommon. 87

• A more benign type of residual or persistent pulmonary coccidioidomycosis results when the acute primary disease subsides without much dissemination. The primary disease may clear completely, but when there is residual disease, it usually assumes one of three general radiographic types: cavitation; nodules, which may be single or multiple; or pulmonary opacity, which may be relatively focal and occur in a single area or in several areas. The residual type of cavitation in this form of coccidioidomycosis often is thin-walled and may remain unchanged in size and shape for years. There usually is some fibrotic disease in the area of cavitation, but this is not always true.

• Studies of many patients have shown that the thin-walled cavity that was originally thought to be characteristic of the disease occurs in only 50% to 60% of patients, and the remaining cavities have relatively thick walls. Spontaneous closure of cavities occurs in about one half of the patients. Most of the cavities are single and in the upper lung, and more than half are 4 cm or less in diameter. Cavitation may be complicated by secondary infection, including formation of Aspergillus fungus balls, pyopneumothorax when the cavity is subpleural in location, or pulmonary hemorrhage, which usually is not significant. These complications are uncommon. Cavitation in coccidioidomycosis must be differentiated from that in pulmonary TB and other mycotic infections. This usually is not possible on roentgen evidence alone, but as a general rule the residual cavity in coccidioidomycosis has less pulmonary disease around it than is seen in untreated pulmonary TB, because bronchogenic spread is much less common. This finding is important in the differential diagnosis of untreated patients with chronic pulmonary disease in whom there is persistent cavitation (Fig. 24-49).

• Rarely, a pulmonary mycetoma (fungus ball) may be caused by C. immitis.109 Arthrospores and spherules may be present along with hyphae of the mycelial phase in a pulmonary cavity. The appearance is similar to that of an aspergilloma, a much more common cause of fungus ball.

• The nodular residuals of coccidioidomycosis vary considerably in size and number. They may or may not contain calcium. When single, they must be differentiated from those of other diseases that cause solitary pulmonary nodulation, including primary bronchogenic tumor. When multiple, the lesions must be distinguished from other mycotic disease and from pulmonary TB. These differentiations are not possible on roentgen examination and must be based on skin tests with coccidioidin and serologic studies. The infiltrative fibrotic type of residual disease is similar to the fibrotic residues of numerous other inflammations, so there is nothing in the roentgenogram to indicate the nature of the original disease. Pleural thickening and effusion are occasionally noted as the end results of this disease, but there is nothing characteristic about these findings. Cavities are often peripheral and tend to rupture into the pleural space, resulting in empyema. Occasionally, they cause spontaneous pneumothorax.

• Disseminated coccidioidomycosis occurs rarely when the initial infection fails to become localized. This is very uncommon in whites, but members of dark-skinned races are more susceptible. Clinically, dissemination is a continuation and progression of the primary infection, is often manifested by exacerbation of symptoms, and may result in acute respiratory failure. Occasionally, an acute form of the disease may progress rapidly and disseminate widely. Although the miliary spread usually occurs early in the disease, it is sometimes a late complication of chronic pulmonary or extrapulmonary forms. Radiographic findings vary considerably, from universal hematogenous spread of disease resembling miliary TB to local spread confined to the lungs. There is often bronchogenic dissemination to the opposite lung or other lobes, which results in scattered involvement of varying extent. Large cavities may appear, along with pleural involvement leading to empyema. Associated with the extensive pulmonary opacities in this form of the disease, there is often spread to abdominal viscera, the skeletal system, lymph nodes, and sometimes the brain and meninges. The disseminated type of involvement is usually lethal.

Coccidioidomycosis. A: Note the cavity in the left subclavicular area. The elongated cavity has a moderately thick wall, but there is very little parenchymal disease around it. B: One year later, the cavity is larger, the wall is thinner, and again very little other parenchymal disease is observed.

• Rarely, a pulmonary mycetoma (fungus ball) may be caused by C. immitis.109 Arthrospores and spherules may be present along with hyphae of the mycelial phase in a

• pulmonary cavity. The appearance is similar to that of an aspergilloma, a much more common cause of fungus ball.• The nodular residuals of coccidioidomycosis vary considerably in size and number. They may or may not contain calcium. When single, they must be differentiated• from those of other diseases that cause solitary pulmonary nodulation, including primary bronchogenic tumor. When multiple, the lesions must be distinguished

from• other mycotic disease and from pulmonary TB. These differentiations are not possible on roentgen examination and must be based on skin tests with coccidioidin

and• serologic studies. The infiltrative fibrotic type of residual disease is similar to the fibrotic residues of numerous other inflammations, so there is nothing in the• roentgenogram to indicate the nature of the original disease. Pleural thickening and effusion are occasionally noted as the end results of this disease, but there is• nothing characteristic about these findings. Cavities are often peripheral and tend to rupture into the pleural space, resulting in empyema. Occasionally, they cause• spontaneous pneumothorax.• Disseminated coccidioidomycosis occurs rarely when the initial infection fails to become localized. This is very uncommon in whites, but members of dark-skinned• races are more susceptible. Clinically, dissemination is a continuation and progression of the primary infection, is often manifested by exacerbation of symptoms,

and• may result in acute respiratory failure. Occasionally, an acute form of the disease may progress rapidly and disseminate widely. Although the miliary spread usually• occurs early in the disease, it is sometimes a late complication of chronic pulmonary or extrapulmonary forms. Radiographic findings vary considerably, from

universal• hematogenous spread of disease resembling miliary TB to local spread confined to the lungs. There is often bronchogenic dissemination to the opposite lung or

other• lobes, which results in scattered involvement of varying extent. Large cavities may appear, along with pleural involvement leading to empyema. Associated with

the• extensive pulmonary opacities in this form of the disease, there is often spread to abdominal viscera, the skeletal system, lymph nodes, and sometimes the brain

and• meninges. The disseminated type of involvement is usually lethal.

Histoplasmosis• Histoplasmosis is caused by the fungus Histoplasma capsulatum.40 It was originally thought to be a rare and fatal

disease, but it is now known that the disseminated• form, which may be fatal, is only one of several types of the disease. The primary form is much more common and is by

far the most common fungal disease in the• United States. It is endemic in the Mississippi, St. Lawrence, and Ohio river valleys and along the Appalachian

Mountains. 86 In many areas, histoplasmin skin• sensitivity indicating previous infection is almost universal in young adult lifetime residents. The disease is less common

elsewhere in the United States but is found in• almost all states, as well as in Mexico and Panama.• The primary form of histoplasmosis, a localized pneumonic disease, is usually relatively benign and passes unnoticed in

most instances (95%). The roentgen changes• found in acute benign disease are varied, with single or multiple areas of pneumonic consolidation. The disease cannot

be distinguished from primary TB• roentgenographically. It is often segmental in distribution and may be accompanied by hilar node enlargement. The

hilar node involvement may be more prominent• than the parenchymal disease in some subjects (Fig. 24-50), particularly children. In addition to the localized

pneumonic consolidation, there is a more disseminated• form, which often occurs in local epidemics. Poorly defined, patchy or nodular lesions are scattered throughout both

lungs ( Fig. 24-51 and Fig. 24-52). Later they• become more clearly defined, round nodules varying in size up to 1 cm. With healing, some of the nodules may

disappear completely, whereas others may gradually• decrease in size and become calcified ( Fig. 24-53). Calcification often occurs in the involved hilar nodes as well.

• Histoplasmosis is the most common cause of broncholithiasis, which is produced when a calcified node erodes into a bronchus. Studies of large groups of people in

• endemic areas have shown that, as a general rule, the amount of calcification in parenchymal nodules and in hilar nodes is greater in histoplasmosis than in TB. The

• primary form of the disease may clear and leave no pulmonary residuals that can be recognized on roentgenograms. In other cases, a solitary calcified parenchymal

• nodule with or without calcified hilar nodes may be present ( Fig. 24-54). Caseous lymphadenitis is common during the primary infection ( Fig. 24-55; see Fig. 24-52).

• Cyst-like lesions may develop in the mediastinum and become very large when liquefaction occurs in enlarged coalescent nodes. These lesions can measure 10 cm

• or more in diameter and may be asymptomatic. Air–fluid levels can develop within them when there is communication with the bronchial tree or lung. Remnants of

• lymph node tissue may be observed in these cyst-like lesions, which tends to confirm the impression that they represent excavated lymph nodes. Miliary parenchymal

• calcifications scattered throughout the lungs and large “mulberry” calcified hilar nodes are usually associated with histoplasmin sensitivity rather than tuberculin

• sensitivity.

• Symptomatic primary infection is usually found in infants and young children. In contrast to patients with the more benign common form, these patients usually have a cough and are often febrile for a few days, or occasionally for 2 to 3 weeks or longer. Roentgen findings consist of hilar and mediastinal adenopathy with a focal opacity representing air-space disease in the lung. Nodes may calcify and occasionally may obstruct a bronchus or rupture into it.

• The acute epidemic form of histoplasmosis reported in several localities in the endemic regions probably represents a heavy exposure that results in more pulmonary parenchymal involvement than in the usual primary form of the disease. Extensive bilateral lobular or nodular air-space disease may involve both lungs, and sometimes a miliary spread throughout both lungs is observed. The residuals are similar to those of the benign primary form, except that there may be more scattered, calcific, parenchymal foci in the severe acute epidemic form. It appears that reinfection may produce the acute, chronic, or disseminated form of histoplasmosis.

• Disseminated histoplasmosis is a progressive disease with dissemination not only to the lungs but also to other organs, including the bone marrow. The course may be extremely rapid and fulminating or slowly progressive, leading to cachexia and anemia. It usually occurs in infants, in patients with compromised cellular immunity, or in those who have been immunosuppressed. Marked variation has been found in the roentgen manifestations of disseminated pulmonary histoplasmosis, ranging from widespread granular nodulations throughout both lungs (the most common finding) to a lobar type of pneumonic consolidation. Scattered involvement simulating other types of pneumonia may also be noted, and occasionally there is massive pleural effusion. In infants younger than 1 year of age the acute disseminated form is often fatal; hepatosplenomegaly is common in addition to the extensive pulmonary involvement.

• There is an intermediate form of histoplasmosis that results in chronic active fibrocavitary pulmonary disease resembling reinfection TB clinically and radiographically.

• Cavitation along with local ill-defined opacities and nodulation similar to that seen in chronic pulmonary TB is often found. Pleural involvement, fibrosis, and contraction of the involved lobe or segment with alteration in the size of the thorax and mediastinal deviation may also be produced ( Fig. 24-56). Histoplasmosis involving hilar nodes adjacent to bronchi may cause collapse of the middle lobe (middle lobe syndrome) or of other pulmonary segments. It may also be the cause of broncholithiasis. In patients with chronic active pulmonary histoplasmosis, the apical posterior segments are involved and cavitation is common, often persisting for long periods. These persistent cavities often enlarge gradually and may become very large. Disease in the adjacent lung is common, and fibrosis may become extensive.

Histoplasmosis. The parenchymal disease is minor and consists of a small amount of patchy opacity above the right hilum; there is bilateral hilar nodeenlargement, more on the right than on the left.

Disseminated pulmonary histoplasmosis. Note the small, poorly defined nodules scattered throughout the left lung. The patient had been ill for several weeks.

A and B: Histoplasmosis. Computed tomogram shows a cavitating nodule in the right upper lobe and mediastinal adenopathy caused by histoplasmosis infection.

Histoplasmosis. Examples of calcified pulmonary nodules. A: The nodules seen here are rather uniform in size, and all are calcified. B: Fewer nodules but less calcification and more variation in size are noted in this patient.

Histoplasmosis. There is a solitary, partially calcified parenchymal nodule in the right upper lung with several partially calcified right hilar nodes. The left hilum is also prominent; enlarged nodes appear there.

Histoplasmosis. There are enlarged nodes in the left hilum and some parenchymal disease in the lung lateral to the hilum, which appears somewhat nodular. No other disease was observed.

Histoplasmosis. Note the conglomerate disease in the central and basal lung. There is also some pleural thickening and a small amount of fluid. No definite hilar enlargement is present. This is the same patient whose roentgenogram, obtained 5 years before this study, is shown in FIG. 24-55. Slow progression of disease as illustrated here is unusual in our experience.

• Mediastinal involvement by histoplasmosis can result in fibrosing mediastinitis, a progressive fibrotic process that entraps, encases, and narrows mediastinal

• structures such as the superior vena cava, the pulmonary arteries and veins, and the central airways ( Fig. 24-57).79,86 The fibrosis may be either localized

• (mediastinal granuloma) or diffuse (fibrosing mediastinitis). 45 The primary disease may have been asymptomatic, but the resultant fibrosing mediastinitis can produce

• pulmonary arterial and venous obstruction, central lymphatic obstruction, pericardial involvement, and esophageal involvement in addition to superior vena caval

• obstruction. Most cases of fibrosing mediastinitis are now thought to be caused by an abnormal, hyper-reactive fibrotic response to H. capsulatum antigens.45,86 Viable

• fungal organisms are rarely recovered or grown from mediastinal tissue samples obtained from patients with fibrosing mediastinitis. 45 Both CT and MRI can be used to

• evaluate the extent of mediastinal fibrosis more effectively than conventional chest films. On MRI, fibrosing mediastinitis appears as abnormal soft tissue infiltrating

• the mediastinum with relatively low signal intensity on all pulse sequences ( Fig. 24-57). On CT, calcifications within the infiltrating soft tissue may help differentiate

• this condition from infiltrating lymphoma or carcinoma.86 Effective therapy for fibrosing mediastinitis does not exist, and surgical palliation is of limited or no value.

• Rarely, calcification of the pericardium may result from Histoplasma pericarditis.

Evaluation of fibrosing mediastinitis by magnetic resonance imaging. T1-weighted coronal ( A) and axial (B) and T2-weighted axial (C) images show low-signal-intensity fibrotic material encasing the airways and obliterating the right pulmonary artery.

• In some cases, the sole manifestation of disease is a solitary pulmonary nodule, the histoplasmoma. This lesion may be associated with calcified hilar nodes, and

• there may be a few satellite nodules in the lung. Calcification may or may not be present in the lesion, which varies from 1 to 3 cm or more in diameter. The

• calcification may be laminated, annular, solid, or stippled, and it may be central with a laminated or annular peripheral ring. The vast majority remain stable for years,

• but occasionally a slow increase in size is observed, suggesting that some histoplasmomas contain viable organisms although most lesions are quiescent. Skin

• testing, complement-fixation studies, and mycologic studies are required to differentiate this disease from pulmonary TB; occasionally, both diseases are present in

• the same patient. When the nodule does not contain calcium, it cannot be differentiated from neoplasm on chest radiography, tomography, or CT; in such cases,

• biopsy may be necessary.

Cryptococcosis• Cryptococcosis (torulosis) is caused by Cryptococcus neoformans. Pulmonary lesions have been reported in increasing numbers of patients with and without• involvement of the central nervous system. As in other chronic pulmonary infections, several forms of pulmonary involvement are found and the diagnosis

cannot be• made from roentgenograms alone.32,60 Three general types of radiographic change have been described. The first is a fairly well circumscribed, round mass

or nodule• usually occurring in the lower half of either lung, which must be differentiated from neoplasm and from other chronic pulmonary granulomas. They tend to

be• peripheral and may become large (up to 10 cm in diameter). At times, multiple, closely grouped, mass-like densities may be observed. The second form is a• pneumonic type of lesion consisting of a somewhat irregular opacity more likely to appear in the lower than in the upper lobe. It represents granulomatous

disease. 32• This type of disease may be extensive but usually is confined to one segment or lobe and often is associated with lymph node enlargement; cavitation is rare.

This is• the most common form. The third type is a widespread miliary variety of nodulation, often found in conjunction with severe central nervous system infection.

This type• of disease is frequently found as an opportunistic infection associated with such chronic processes as Hodgkin's disease, leukemia, and lymphoma; in patients

who• have received steroid or antibiotic therapy; or as a complication of AIDS. Cavitation may occur in this form; pleural involvement with effusion may be present

but is• uncommon. Often the diagnosis is not made until autopsy in patients having disseminated disease.• In seven patients with AIDS complicated by cryptococcosis, Miller and associates 92 found that hilar or mediastinal adenopathy and interstitial pulmonary

disease,• alone or in combination, were the most common findings on chest films. They believe that the interstitial process is a manifestation of disseminated disease

and its• presence should initiate a search for silent cryptococcal meningitis. Although the diagnosis cannot be made on the basis of roentgenographic findings, the• combination of signs of meningeal irritation and pulmonary lesions resembling those described is suggestive. When the disease is confined to the lung in a• noncompromised host, spontaneous resolution without treatment occurs in most cases.

North American Blastomycosis• North American blastomycosis is caused by the yeast-like fungus Blastomyces dermatitidis. Although much less common than

histoplasmosis, it occurs in• approximately the same geographic areas of the United States but extends more eastward and northward. There are two general types,

cutaneous and disseminated.• In the disseminated form, the portal of entry is usually the respiratory tract, and 95% of the patients have some form of pulmonary

involvement. The roentgen findings• in pulmonary disease produced by this organism are not diagnostic and are related to the clinical form of the disease. 111 In the acute form,

there are four major• roentgenographic patterns. (1) Air-space involvement causing a patchy segmental or lobar consolidation is present in most patients. There

are often several foci of• disease, and involvement may be multilobar. The disease is usually located in the upper lung. In this type, resolution usually takes place

slowly and may require• several months. Cavitation may complicate this acute form. (2) A large, round, tumor-like mass or masses may be present and may cavitate.

(3) An extensive• reticulonodular or miliary interstitial pattern may be present. (4) A severe form of acute disease may occur in which there is bilateral

exudate with the distribution• resembling that of pulmonary alveolar edema. The onset is rapid, and the condition is very toxic in these patients. Several patients have

developed ARDS as a result• of this severe disease; this combination is usually fatal.• The chronic form of the blastomycosis in the upper lobe resembles pulmonary TB. In the most common form, there is a fibronodular

appearance consisting of• pulmonary nodules and linear fibrotic strands ( Fig. 24-58, Fig. 24-59, and Fig. 24-60). Only slightly less common is cavitary upper-lobe

disease in which the walls are• moderately thick and smooth. Much less common is a mass-like appearance, which can closely resemble bronchogenic carcinoma ( Fig. 24-

60). The disease may• extend to the pleura, cross interlobar fissures, invade the chest wall, and cause rib destruction, but not as frequently as actinomycosis.

North American blastomycosis. Note the extensive disease in the right parahilar and medial basal areas as well as in the central and right lung laterally. Adjacent to the dense homogeneous involvement, several scattered, poorly defined nodules are observed. Roentgenographic findings in this disease are nonspecific.

North American blastomycosis. Numerous disseminated nodules, ranging up to 1 cm or more in diameter, are observed. On the right, either dense disease overlies the hilum or adenopathy is present, but no adenopathy is noted on the left.

Blastomycosis. Chest film (A) and computed tomogram (B) show a large, mass-like consolidation in the left upper lobe plus multiple nodules in the opposite lung. The mass-like appearance of these opacities could be mistaken for a lung neoplasm with metastases.

• Chest radiographic findings in 63 patients reported by Sheflin and colleagues 120 showed single upper-lobe involvement in 27 patients and multilobar disease in 21. In

• nine patients, the major abnormality was a pulmonary mass. Pleural effusion and/or adenopathy (hilar or mediastinal) was present in 20%. Cavitation was found in 23

• patients. Five patients had diffuse disease, and only one had a miliary type of disease.• Blastomycosis is unusual in children except in small epidemics, which have been

reported on several occasions. Children develop alveolar disease, with multiple• small, thin-walled cavities in about 25% of cases. Hilar adenopathy may also be

present, and pleural effusion is not unusual. If children develop the disseminated• form, it may be fulminant with a high mortality rate. Because these changes are

similar to those noted in pulmonary TB, mycotic infections, and other chronic• inflammatory diseases as well as neoplasm, the diagnosis must be based on mycologic

studies.

South American Blastomycosis (Paracoccidioidomycosis)

• This disease, caused by Blastomyces brasiliensis, is found most commonly in Brazil but has also been reported in the other South American countries. Pulmonary

• involvement is said to occur in 80% of patients with the visceral type of disease. The portal of entry may be the intestinal tract in this disease; the pulmonary lesions

• are secondary and are widespread and nodular in type, often associated with hilar adenopathy. The disease may also manifest as a cavitary pulmonary mass. 1

• Destructive bone lesions are common in the disseminated form.

Pulmonary Aspergillosis• Aspergillus species are ubiquitous and cause a wide spectrum of pulmonary diseases. These include

asymptomatic saprophytic colonization of the airways or• pre-existing cavities (aspergillomas), ABPA, semi-invasive (chronic necrotizing) aspergillosis, and

invasive pulmonary aspergillosis. 38 Aspergillus infections have also• been categorized as primary or secondary. Most often, Aspergillus infection is a secondary process in

patients who have been treated with antibiotics and in those• with debilitating disease. However, it occurs rarely as a primary disease in otherwise healthy persons.• Two clinical and roentgen types of the primary disease have been described. The first is an acute

bronchopneumonic form with scattered multiple areas of pneumonic• consolidation, some of which break down to form cavities. This disease may progress with severe

invasive destructive pulmonary disease eventually leading to death.• The invasive form is usually seen in infants. There is often enough hilar node enlargement to be

recognized as such on the roentgenograms. The second type of• primary disease is more chronic and milder. Irregular and rounded nodular opacities closely

resembling those seen in pulmonary TB are present. The clinical course• of this disease is less severe than that of TB; the diagnosis must be made on the basis of

identification of the organism in the sputum, often with some reservation• because the organism is so commonly found there.

Secondary Aspergillosis• Secondary aspergillosis is found in three classic forms, the aspergilloma

(mycetoma or fungus ball), ABPA, and a severe life-threatening form (invasive pulmonary

• aspergillosis), which usually is found in patients with severe immunosuppression and neutropenia from aplasia-producing cytotoxic drugs, steroids, or other

• immunosuppressive agents. More recently, a more indolent form of Aspergillus infection has been recognized. Semi-invasive aspergillosis or chronic necrotizing

• aspergillosis is less aggressive than invasive pulmonary aspergillosis and occurs in milder forms of immunosuppression, often in patients who have underlying lung

• disease (i.e., patients with alcoholism, chronic debilitating disease, COPD, sarcoidosis). 38

Invasive Pulmonary Aspergillosis• Invasive pulmonary aspergillosis can develop in immunocompromised patients and, rarely, in

immunocompetent patients. Patients with acute leukemia and• granulocytopenia are particularly susceptible. Occasionally it occurs as a complication of

influenza-like viral infections in the noncompromised host. It may be• associated with other infections; mucormycosis appears to be the most common of these.77• The radiographic changes are quite variable. Air-space disease in the form of “round” pneumonia

resembling a poorly defined mass, single or multiple, seems to be a• common finding. Many of these lesions eventually cavitate, and some are probably hemorrhagic

pulmonary infarcts ( Fig. 24-61). The latter results when the organism• invades and obstructs a branch of the pulmonary artery. Some of the cavitations exhibit an air-

crescent sign, caused by a mass within the cavity, that does not move• with a change in the position of the patient and probably represents necrotic tissue in an area of

infarction. A diffuse bronchopneumonia pattern may develop at any• time. This may progress to extensive bilateral pulmonary involvement. Chest wall invasion can

occur, with bone destruction, but is not common. If this is complicated• by empyema, the prognosis is poor. Rarely, a miliary spread throughout the lung is observed. In

these patients the prognosis is also poor, and the immediate cause of• death may be aspergillosis. Because the or

A and B: Computed tomographic (CT) scans of a 22-year-old man with acute myelogenous leukemia undergoing chemotherapy and severely neutropenic with fever. CT demonstrates the typical features of invasive pulmonary aspergillosis in this patient population. Two inflammatory masses are seen, each with a surrounding CT halo of ground-glass opacity around the denser center of the mass. Invasive pulmonary aspergillosis invades pulmonary blood vessels, causing hemorrhagic infarction, and the CT halo corresponds to hemorrhage and edema around the focus of fungal infection.

• The CT appearance of invasive pulmonary aspergillosis can be quite characteristic early in the course of the infection ( Fig. 24-61). CT may show one or more nodules

• or masses with the CT halo sign, a surrounding zone of ground-glass opacity which results from pulmonary hemorrhage around the focus of infection and infarction

• caused by the angioinvasive aspergillus organism. 66 This is a feature of early invasive pulmonary aspergillosis and precedes cavitation of the nodules on plain films

• or CT. CT is more accurate than chest radiography in detecting early lesions of invasive pulmonary aspergillosis. The use of CT in the evaluation of the neutropenic

• patient is discussed in Chapter 25.• Sometimes the invasive form of the infection invades the airways rather than the blood

vessels. This has been called invasive aspergillosis of the airways or• necrotizing aspergillus tracheobronchitis. Like the angioinvasive form of the infection, the

invasive airway disease occurs usually in severely immunocompromised• patients, but it is much less common than the angioinvasive form. CT findings may include

lobar consolidation, peribronchial consolidation, centrilobular nodules,• tree-in-bud opacities, and, less commonly, diffuse bronchiectasis indicative of an infectious

bronchitis and bronchiolitis. 80

Semi-invasive or Chronic Necrotizing Pulmonary Aspergillosis

• This form of the infection usually occurs in patients with milder forms of immunosuppression, often in conjunction with underlying lung disease. Among those at risk

• are patients with sarcoid, diabetes mellitus, COPD, alcoholism, or malnutrition ( Fig. 24-62). Corticosteroid therapy and prior radiation treatment are also predisposing

• factors.38 As the name implies, semi-invasive aspergillosis is more indolent and chronic than invasive pulmonary aspergillosis. It typically is more localized, usually

• begins in an upper lobe or lung apex, and slowly progresses. Its appearance often mimics that of reactivation TB. 38 Consolidation and then cavitation gradually

• progress over the course of weeks to months. Exuberant adjacent pleural reaction is a common associated feature, and infection may extend to chest wall or

• mediastinal invasion38

A and B: Semi-invasive pulmonary aspergillosis. This elderly man with chronic obstructive pulmonary disease developed a progressive right-upper-lobe pneumonia as the result of aspergillus infection. Computed tomography nicely demonstrates the patient's extensive emphysema and the extent of the necrotizing pneumonia.

Mycetoma (Aspergilloma)• The aspergilloma (mycetoma) or fungus ball consists of a localized round or ovoid mass made up of Aspergillus hyphae

(the mycelial form), blood, cellular debris,• fibrin, and mucus that occupies a cavity slightly larger than the mass. This is a saprophytic, noninvasive colonization of a

pre-existing cavity by Aspergillus• organisms.38 The cavities and fungus balls are usually found in the upper lobe, probably because the primary disease

that causes the underlying cavity, commonly TB• or sarcoidosis, occurs in the upper lobe. A thin, radiolucent rim is observed surrounding the mass. This is caused by air

in the space between the thin cavity wall and• the mass and is referred to as the air-crescent sign or Monod's sign. 38 Air-crescent formation is also seen in invasive

pulmonary aspergillosis, but the pathophysiology• is different: in the invasive form, pulmonary infarction and cavitation are caused by the invasive fungal infection, but in

the noninvasive aspergilloma the intracavitary• mass usually moves within the cavity. This can be demonstrated on CT by imaging in the supine and prone positions. CT

is often helpful in detecting and diagnosing• mycetomas, particularly when there is extensive underlying lung disease that makes the plain film difficult to interpret (

Fig. 24-63). Calcification may occur within the• mass and may be extensive. Hemorrhage is common, often recurrent, and can be severe and life-threatening. There

may be no other symptoms, or the patient may• have mild constitutional symptoms of weight loss and fatigue.• Rarely, other organisms can form fungus balls. Candida species, C. immitis, Monosporium, Sporotrichum, and

Trichophyton species, among others, have been• implicated.38 About 10% of mycetomas undergo spontaneous lysis.

A and B: Aspergilloma. This 37-year-old Tibetan monk had a history of surgery in the right lung apex for tuberculosis. A small residual apical space remained after surgery, and years later a fungus ball developed within it.

Allergic (Hypersensitivity) Bronchopulmonary Aspergillosis

• ABPA is seen in patients with chronic bronchial asthma and is caused by a hypersensitivity reaction to antigens of species of the genus Aspergillus, chiefly

• Aspergillus fumigatus.81 Both type I and type III hypersensitivity reactions are present in this disorder. Serum immunoglobulin E is elevated, and immunoglobulin G

• precipitins to Aspergillus antigens are present. The presence of peripheral blood and often lung-tissue eosinophilia is characteristic, as is positive immediate skin-test

• reactivity to Aspergillus antigens.38,129 The organisms colonize the airways and are sometimes found in the sputum during an initial asthmatic attack or early in the

• course of bronchial asthma. The patients usually have wheezing, fever, cough, and mucopurulent sputum, often with expectoration of mucus plugs. A history of

• asthma refractory to standard bronchodilator treatments is often elicited.• The roentgenographic findings can be divided into transient and permanent shadows 65 (Fig. 24-64). Transient shadows

are of several types. (1) Homogeneous• consolidation may be present and may be large or small without loss of volume. These lesions may be massive, often are

multiple, and tend to be central in location.• (2) A nonhomogeneous shadow or patchy consolidation may be present. (3) Small, circular, or nodular shadows may be

present. (4) Transient atelectasis of a• segment, lobe, or lung may be present. (5) Band-like and gloved-finger shadows 2 to 3 cm long and 5 to 8 mm wide may

be present; at times they have a rounded• end, caused by mucoid impaction. (6) Two parallel hairline shadows may be present, with a radiolucent zone between the

lines representing a normal bronchus (tram• line). (7) A well-outlined, circular (ring) shadow with a diameter of 2 to 3 cm, also representing a bronchus, may be

present.

A–C: Allergic bronchopulmonary aspergillosis (ABPA). Roentgenographic and computed tomographic (CT) images demonstrate central bronchiectasis, a characteristic feature of ABPA. The CT also shows some mucoid impaction in the left lower lobe ( B).

• The permanent shadows include the following: (1) parallel lines similar to tram lines but with a width larger than that of a normal bronchus; (2) hairline ring shadow 1

• to 2 cm in diameter; (3) decreased volume but with aeration in the segment or lobe involved; (4) narrowing or loss of vascular shadows; and (5) long-line shadows.

• Most patients progress to varying degrees of pulmonary overinflation, some develop areas of fibrosis, and others have small areas of atelectasis (segmental or less)

• that may persist. Pleural effusion is rare but may appear. Bronchocentric granulomatosis with severe bronchial necrosis and granuloma formation appears to be a

• variant. The toothpaste and gloved-finger shadows represent mucus plugs or impactions in most instances. Occasionally, mucoid impaction may occur in asthmatics

• without aspergillosis. The tram-line shadows represent bronchi that are normal in diameter, whereas parallel-line shadows represent bronchi that are increased in

• diameter. The ring shadow represents a dilated bronchus observed on end. The latter two findings indicate bronchiectasis, which is usually central and becomes• permanent if the patient is not treated promptly. Long-line shadows probably represent a wall of a bulla in some instances and pleura in others. The diagnosis is

made• on the basis of a history of bronchial asthma, the presence of eosinophilia, and the changing roentgenographic pattern of the lungs as described. This disease

usually• responds quickly to corticosteroid therapy.• The CT hallmark of ABPA is prominent, central or proximal bronchiectasis. Central bronchiectasis is so characteristic that if it is identified on CT in a patient with• asthma or wheezing, the diagnosis of ABPA should be suggested. Areas of mucous plugging are very apparent on CT as well (see Fig. 24-64).• In addition to asthmatics, patients with cystic fibrosis are susceptible. The complication of bronchopulmonary aspergillosis appears to be a major factor when

these• patients deteriorate rapidly, so prompt treatment is important. If it is important to outline the bronchi for detection of bronchiectasis as well as extent of the

pulmonary• involvement, CT is very helpful in evaluation of this disease. Bronchial wall thickening and bronchiectasis are usually clearly defined.• Bronchocentric granulomatosis is now thought to represent a variant of ABPA in which a more localized Aspergillus infection produces granulomatous

inflammation• and disruption centered on the bronchioles. It occurs in young asthma patients. 129

Moniliasis (Candidiasis)• Candida (Monilia) albicans is a yeast-like organism, frequently present in the normal mouth, that is usually

saprophytic but occasionally mildly pathogenic for humans.• Because the organism is often present in normal people, it is difficult to document this disease. The literature is

very confusing, and many reported cases are probably• examples of other diseases. However, most investigators agree that Monilia can produce bronchopulmonary

disease, particularly in elderly or debilitated persons,• immunocompromised hosts, and infants. It is therefore an opportunistic organism that can produce disseminated

fatal disease in susceptible subjects. Roentgen• findings consist of a rather fine, mottled type of nodulation ranging from 2 mm to 1 cm in diameter associated

with some prominence of pulmonary markings or, more• commonly, segmental homogeneous consolidation. It can also produce a diffuse bronchopneumonia pattern that

may be bilateral.• Segmental or lobar air-space pneumonia has also been described. In infants, it can be a fatal disease, with

progressive alveolar consolidation and occasional• cavitation. It also can be widely disseminated to other organs as well as the lungs. Cavitation, with or without a

mycetoma, is rare but is simulated when the disease• involves an area of lung in which there are pre-existing emphysematous bullae. There may be some enlargement

of the hilar nodes. As with the other fungal diseases,• the diagnosis must rest on identification of the organism. Bronchial secretions should be examined, rather than

sputum, because the organism is a normal inhabitant• of the mouth.

Geotrichosis• Geotrichum candidum is a fungus frequently found in the mouth and gastrointestinal

tract of healthy subjects; it occasionally becomes pathogenic and causes• pulmonary as well as skin and mucous membrane infection. Pulmonary

manifestations of geotrichosis are not characteristic. Irregular, patchy densities are noted,

• often in the upper lungs. Cavitation may develop, the cavities having rather thin walls. Enlargement of the hilar nodes is frequent. The disease may closely resemble

• pulmonary TB (Fig. 24-65). Geotrichum has a tendency to produce an opportunistic type of pulmonary disease in severely debilitated or immunosuppressed patients.

• In these patients, bronchopulmonary involvement is often extensive, with air-space disease resembling extensive bronchopneumonia; often the infection is fatal.

• Endobronchial disease, with positive sputum cultures and no pulmonary involvement visible on chest films, may also occur in these patients. The diagnosis is based

• on a positive skin test plus demonstration of the organism on repeated sputum examination. Other fungal infections and TB must be excluded by appropriate studies,

• because, as in moniliasis, the organism may be saprophytic rather than pathogenic.

Geotrichosis. Note the nodular disease in the left upper portion of the lung, which resembles pulmonary tuberculosis. Since the disease progressed slowly, resection was done, proving it to be geotrichosis.

Other MycosesSporotrichosis

• Sporotrichosis, produced by Sporotrichum schenckii, usually involves the skin, mucous membranes, and lymphatics. Rarely, pulmonary infection is the primary

• manifestation of the disease, presumably caused by inhalation of spores. Most reported cases have been in the Mississippi and Missouri river valleys. 105 Of all

• reported cases, 40% have been in alcoholics. There is nothing characteristic about the pneumonia it produces. 88 However, cavitation, which may be bilateral, is often

• observed, usually in upper lobes. The pulmonary infection may be local, indolent, and granulomatous and resemble chronic pulmonary TB, or it may be suppurative

• and produce foci of bronchopneumonia. Scattered hematogenous small-nodular disease is rare, but hilar adenopathy is common. S. schenckii is sometimes found as

• a secondary invader in patients with chronic pulmonary TB.

Penicilliosis

• Fungi of the genus Penicillium are capable of producing a pulmonary infection known as penicilliosis. This disease is very rare. The fungus can cause lung abscess

• that cannot be distinguished from cavitation produced by other organisms; there are no roentgen signs that would lead to the specific diagnosis.

Mucormycosis (Phycomycosis)

• Mucor is a genus of fungus that is widely distributed in nature and not usually pathogenic to humans. Along with Absidia and Rhizopus, it is a member of the class

• Phycomycetes. Several cases of severe disseminated infection caused by this fungus have been reported in diabetics ( Fig. 24-66). This infection is also found in

• patients with other underlying debilitating disease, such as leukemia or lymphoma, and in immunosuppressed patients. It is an opportunistic organism found most

• often in patients with hematologic disorders. In some of these, a widespread, rapidly fatal confluent pneumonia that may cavitate is present. Like invasive pulmonary

• aspergillosis, mucormycosis is angioinvasive. The hyphae tend to invade and occlude vessels, and the resultant infarction leads to the cavitation. The chest film and

• CT findings may therefore resemble those of invasive pulmonary aspergillosis. In some instances, mucormycosis may be the cause of a solitary pulmonary nodule.

Mucormycosis infection in a diabetic patient. A large thick walled cavity is present in the right midlung and a second mass in the right lung apex.

DISEASES OF SPIROCHETAL ORIGIN

Syphilis• Involvement of the lungs in syphilis is very rare, but when it does occur it may simulate other chronic pulmonary diseases

symptomatically and radiographically. The diagnosis depends on exclusion of other diseases and on laboratory studies as well as response to antiluetic therapy.

• Three radiographic types of pulmonary involvement have been described. (1) Interstitial fibrosis may occur, resulting in linear opacities radiating into the lungs from the hila. (2) A large, solitary mass (gumma) may be present. It may be clearly circumscribed and resemble pulmonary tumor. Because some irregular inflammatory disease may surround it, the lesion can simulate other types of inflammatory disease. 50 (3) Chronic lobar pneumonia may occur with fibrosis and decreased size of the diseased lobe. This type resembles chronic pulmonary TB. Another chest film finding in patients with syphilitic aortitis is the presence of extensive calcifications in the wall of a dilated ascending aorta, with ascending aortic disease occurring out of proportion to, or in the absence of, calcification involving the descending aorta.

• However, radiographic findings are not diagnostic, so serologic and histologic studies are necessary.

Leptospirosis• Leptospirosis is produced by a group of spirochetes called Leptospira. Four of more than 100 serogroups cause most of the disease

in humans. Several clinical forms have been described, and pulmonary involvement (in 20%) is only a part of widespread disease in most instances. Occasionally, hemorrhagic pneumonitis is an early or striking manifestation.74

• Three general types have been described. The most common (57% of 58 patients in one study 55) consists of widely disseminated small areas of air-space consolidation representing hemorrhage and edema. The individual lesions are poorly defined, with hazy nodules that resemble other acute, disseminated pulmonary inflammations. A second type of leptospirosis (16%) is characterized by a large confluent area of consolidation similar to that found in lobar or segmental pneumonia.

• A third type (27%) consists of small, patchy densities that resemble bronchopneumonia or a more linear interstitial type of disease, such as is noted in virus pneumonitis. Im and colleagues55 describe this type as having a diffuse ground-glass appearance. Pleural effusion, often large, is common. Because the “pneumonia” is hemorrhage, it usually resolves within 2 weeks in patients who survive. The diagnosis cannot be made on the basis of roentgen findings and depends on bacteriologic studies.

PROTOZOAN DISEASES• Amebiasis• Amebic infection of the thorax is usually secondary to gastrointestinal involvement, which follows the ingestion of the cysts of Entamoeba histolytica. It often is• associated with hepatic amebiasis. Rarely (fewer than 5% of cases), amebic lung abscess or ameboma is found without other signs or symptoms of amebiasis.• The roentgen signs are somewhat different in the two types of disease. In the pulmonary disease without hepatic abscess, parenchymal consolidation, often• complicated by abscess, develops well above the diaphragm. The abscess is similar to that produced by other organisms. When an abscess evacuates into a• bronchus, an air–fluid level can be demonstrated in upright views. The abscess cavity may become very large, and associated pleural effusion is not uncommon.• When an ameboma without cavitation is present, it resembles any other lung mass and must be differentiated from other inflammatory masses and from tumor.• When the pulmonary disease or pleural disease is secondary to hepatic involvement, the appearance is somewhat more characteristic. The hepatic abscess causes• elevation of the diaphragm, and fluid in the right pleural space is common. The lower and middle lobes adjacent to the diaphragm are involved by a confluent• pneumonia in which cavitation may occur. In some instances the infection is confined to the pleural space, in which case an amebic empyema is formed; this is often• loculated at the base. In other instances, there is a combination of pleural and pulmonary involvement, with empyema and lung abscess. An amebic lung abscess may• rupture into a bronchus and drain spontaneously. Empyema must be drained if it does not rupture into the lung and drain spontaneously. Rarely, hepatic amebic• abscess may extend into the pericardium, resulting in amebic pericarditis. The diagnosis is confirmed by the presence of E. histolytica in the sputum or in the pleural• fluid.• Toxoplasmosis• Toxoplasmosis is caused by the protozoan parasite Toxoplasma gondii. The organism has an affinity for the central nervous system, the eyes, and the lungs. There is• an infantile form of the disease in which it is not uncommon to find cerebral involvement, beginning in utero, resulting in scattered intracranial calcifications in the• newborn. The disease behaves differently in the adult and involves the lungs primarily, rather than the central nervous system. The roentgen findings in the lungs are• similar to those noted in bronchopneumonia or viral pneumonia, namely air-space disease, often with some interstitial involvement. Enlargement of the hilar nodes is• frequently associated with the pulmonary involvement. Miliary dissemination produces opacities not unlike those noted in other acute miliary infections. If the disease• becomes chronic, it may result in scattered areas of fibrosis and in scattered nodules, some or all of which may become calcified.• Toxoplasmosis can also be an opportunistic disease involving the central nervous system and the lungs. Radiographic changes in the lung are variable. Widely• scattered, small, nodular or miliary densities have been described as the most common manifestation. In other cases there is focal air-space disease bilaterally, and• changes simulating interstitial pulmonary edema have also been described. The diagnosis can be made by serologic tests.

PLATYHELMINTH (FLATWORM) INFESTATION

• Echinococcosis (Hydatid Disease)• The small tapeworm, Echinococcus granulosus, is found in the intestinal tract of dogs. Its larval form is the cause of hydatid cysts. The ova are ingested

by humans• and migrate to the liver or lungs, where they produce a round or oval density that may become massive ( Fig. 24-67). Since the cyst is readily molded

as it grows, the• shape varies depending on its relation to the bony thorax. It appears on the roentgenogram as a round or oval, clearly defined, dense mass that may

produce some• adjacent atelectasis. A change in shape may be noted at fluoroscopy and with change in position of the patient. A wall, the pericyst, is formed and is

composed of an• external capsule produced by the host tissue. The hydatid cyst itself has a double wall composed of a thick outer membrane (the exocyst) and a thin

inner wall of• germinal cells (the endocyst). The cyst may rupture into a bronchus and empty part of its contents, in which case an air–fluid level is noted. This

indicates separation• of the cyst from the host tissue capsule (pericyst). When this is observed, the roentgenographic diagnosis can be made with reasonable certainty. The

collapsed cyst• wall may float on the fluid surface and be outlined by air above it on an upright film (the water-lily, camalote, or iceberg sign). 15 This is virtually

pathognomonic of• hydatid disease.• Rarely, rupture of the pericyst or host capsule leaves air between it and the exocyst. The crescent or meniscus sign, representing radiolucent air

between the cyst and• the host, may then be observed; it is a distinctive roentgen sign of hydatid cyst. Pulmonary cyst walls rarely calcify, in contrast to the hepatic lesions, in

which• calcification is common. When the cyst ruptures, there is a possibility of spread to other parts of the lung, giving rise to multiple, small daughter cysts.

Occasionally,• many small cysts are scattered throughout the lungs. Rarely, the cysts form in the pleural space or rupture into the pleural space and cause pleural

effusion. When• calcified hydatid cysts are present in the liver and a pulmonary cyst is detected, the diagnosis can be made with a considerable degree of accuracy.

114

Echinococcal disease. A: Computed tomogram (CT) through the abdomen demonstrates a large cyst with daughter cysts in the liver. Infection has broken out through the liver capsule and transgressed the diaphragm; pockets of infection are present in the right lung base. B: A more superior CT slice demonstrates a nodule in the right lung apex caused by dissemination of the infection to the lungs.

Cysticercosis• Occasionally, humans develop autoinfection when they ingest eggs of

the pork tapeworm, Taenia solium. The eggs emerge as oncospheres in the gastrointestinal

• tract, enter the bloodstream, and are carried to various organs and tissues where they metamorphose into cysticerci. The cysticerci may be found scattered widely

• throughout the tissues, including the lungs, where they produce scattered, soft-tissue nodular densities. When the tapeworms die, calcification occurs and multiple

• oval or spindle-shaped calcifications measuring about 3 by 10 mm can then be noted, scattered in the lungs and in other tissues as well. The disease, cysticercosis, is

• very rare in the United States but common in Africa, China, and India.

Paragonimiasis• The lung fluke Paragonimus westermani is distributed widely in the Far East, particularly Korea, Taiwan, and Indonesia; in Africa; and in parts of South• America.12,22,99,128 Humans are infested by eating undercooked crayfish or crabs or drinking infested water. The larval forms are liberated in the jejunum

and migrate• through the diaphragm and pleural space into the lung, where they mature into adult flukes, usually in the lower lobes. The disease is mild and seldom fatal

but does• produce symptoms in some patients. Hemoptysis is a frequent symptom of infestation, along with cough productive of brown or rusty sputum and chest pain.

In about• one third of those infested, the organism causes an ill-defined consolidation in the lower lung in the form of a hazy shadow of low, uneven density. In about

another• third, the density is more homogeneous, is more clearly defined, and may appear lobulated. Thin-walled, cyst-like cavitations may develop within the area of• consolidation. Often the cavities are multiple and have a bubble-like appearance. In some patients, the disease is manifested by linear streaks that appear

within a• shadow of low-density consolidation. The involved area does not usually occupy a very large volume of the lung and may be unilateral or bilateral. The basal

and• peripheral midzone pulmonary disease is often not very conspicuous because of the small volume of lung involved and the low density of the disease, which

may• disappear completely. Pleural thickening in the interlobar fissures is also observed, and fleeting densities thought to represent Löffler's pneumonia often

accompany• the disease. Dense linear opacities are caused by burrows of the organism, which can be demonstrated by bronchography to be independent of bronchi. The

burrows• probably communicate with the cavities. Pleural effusion is common (in about 50%) and may be the only manifestation of the disease in some patients.• Reports differ somewhat as to incidence of various findings. Suwanik and Harinsuta 128 found the following: (1) ring-like, cystic cavities with crescent-shaped

opacity• along one side ranging from 6 mm to 4 or 5 cm in 82%; (2) poorly defined nodular opacities up to 3 or 4 cm, usually basal or peripheral, in 48%; (3) linear

shadows at• bases, usually associated with ring-like shadows, in 21%; and (4) pleural thickening in 21%.• Calcification may develop, probably in dead parasites. Complications include empyema, bronchopleural fistula, and pulmonary cavitation. Ova may be found

in the• pleural fluid and in the sputum during the periods of hemoptysis. The disease may persist for many years.

Schistosomiasis• Schistosomiasis is caused by three blood flukes of the genus Schistosoma, S. mansoni, S. japonicum, and S. haematobium. It is

common in many parts of the world,• including Africa, Asia, and Puerto Rico, but is rarely if ever acquired in the United States. Pulmonary disease is usually caused

by S. mansoni or S. japonicum.• Several types of pulmonary reaction to the infestation may occur. As the larval forms pass through the lungs, an apparent

allergic response produces transient mottled• densities. Roentgen findings in this acute form consist of transient interstitial opacities, usually a fine nodular pattern that may

resemble miliary TB but clears• spontaneously without treatment.• Ova reach the lungs from the veins of the bladder, intestine, and liver. They may implant in or around pulmonary arterioles,

producing a necrotizing arteritis and• intra-arterial and periarterial granulomas, which result in a chronic pulmonary disease. Either of these granulomas may

obstruct the vessel. The organisms rarely• cause multiple arteriovenous fistulae.• Roentgen findings in the chronic form consist of central enlargement of pulmonary arteries secondary to pulmonary

hypertension and evidence of cor pulmonale,• which occurs in only 5% of patients with pulmonary disease. 82 More commonly, a diffuse, fine, reticular pattern is observed.

At times, the appearance is more nodular,• as reaction to the ova produces local densities in the interstitial tissue of the lung. The multiple arteriovenous fistulae caused

by the necrotizing arteritis result in• cyanosis with very little change noted on roentgenograms; this is a rare phenomenon. Occasionally, a circumscribed nodule is

produced by a granulomatous mass• surrounding an adult worm.21

NEMATHELMINTH (ROUNDWORM) INFESTATION

• Several roundworms cause pulmonary symptoms and transitory roentgen changes in the lungs as the larvae are carried to the lungs through the veins or lymphatics.

• As the larvae emerge from the alveolar capillaries into the bronchial tree, they produce an allergic response, usually accompanied by eosinophilia. A combination of

• edema and hemorrhage causes radiographic findings of patchy areas of poorly defined opacity scattered throughout the lungs. The changes are transitory, and their

• extent is related to the severity of the infestation. The following roundworms are among those causing such a reaction: Ascaris lumbricoides, Strongyloides stercoralis,

• Ancylostoma duodenale, and Necator americanus (hookworm). Ascariasis is often the cause of a Löffler's pneumonia, which changes rapidly and usually clears in

• about 10 days. Opportunistic pulmonary strongyloidiasis has been reported in compromised hosts, and it can be fatal. 49 However, it responds to treatment with

• antihelminthic agents if recognized soon enough. The usual pulmonary reaction to Strongyloides is similar to the reaction to Ascaris. In the opportunistic form, a

• variety of lung manifestations have been described, including miliary, lobular, and lobar patterns. Cavitation or pleural effusion is rare.• Filariasis caused by infestation with Filaria or Wuchereria bancrofti, Wuchereria malayi, or Loa loa is probably the cause of tropical eosinophilia

(see next section).• Dirofilaria immitis (dog heartworm) may also cause pulmonary disease in humans.75,76 Typically, it produces a solitary pulmonary nodule, often

peripheral, without• calcification and with a slightly irregular appearance. At first the small area of consolidation may be poorly defined; it then tends to decrease in

size over a few weeks• or months, after which it becomes more clearly defined. Rarely, multiple nodules are observed that may resemble pulmonary metastases. They

produce no symptoms.• Histologic examination of tissue is required to differentiate the nodule from tumor. Trichinella spiralis larvae usually produce no pulmonary

reaction as they pass• through the pulmonary circulation. In roundworm infestation, the diagnosis is made by discovery of the larvae or mature worm in a stool

specimen.

TROPICAL EOSINOPHILIA

• Tropical eosinophilia or pulmonary eosinophilosis is manifested by symptoms of cough, fever, lassitude, wheezing, chest pain, and sometimes dyspnea and weight

• loss associated with an elevation of the leukocyte count. Eosinophilia is extreme (usually more than 3,000 eosinophils per cubic millimeter of blood) and persists for

• weeks. Most reported cases originated in India, Indonesia, Sri Lanka, Pakistan, Southeast Asia, North Africa, and some areas of South America. A few cases have

• been reported in the United States and elsewhere throughout the world, primarily in persons who had traveled to an endemic area. Some cases have been reported in

• persons who had lived in India but had been away more than a year before the onset of symptoms. The disease is mild and self-limited, but relapses may occur. Most

• cases are definitely caused by filarial infestation, usually by W. bancrofti, and the disease usually responds well to diethylcarbamazine, a drug effective in filariasis. 97

• In other cases, the cause cannot be established.• Roentgen findings are of several types. The most common appearance is that of increased pulmonary markings

extending out from the hila, associated with mottled• parenchymal disease that is rather general in distribution. The hilar nodes may be enlarged. Next in frequency is the

addition of areas of patchy pneumonitis to the• small mottled densities. Increased markings alone are almost as common, and extensive scattered involvement by a

pneumonia-like process is noted occasionally.• The apices are usually spared. CT findings may resemble those of miliary TB or hypersensitivity pneumonitis. On HRCT,

small, centrilobular, rounded, nodular• opacities may be seen through the lung fields ( Fig. 24-68).

Tropical eosinophilia in a 22-year-old man from India with fever. High-resolution computed tomography demonstrates poorly defined centrilobular, nodular opacities resulting from infection by the filarial organism Wuchereria bancrofti, which causes a type of hypersensitivity reaction in the lung. Findings mimic those ofmiliary tuberculosis.