Definition

Hypersensitivity reaction to Aspergillus spores with mucoid impaction.

Epidemiology

Most common bronchopulmonary mycosis in humans Affects younger adults (ages 20–40; women slightly more often than men) Atopic patients with bronchial asthma or in the setting of cystic fibrosis (occurs in 10% of cystic fibrosis patients, 1–2% of asthma patients).

Etiology, pathophysiology, pathogenesis

Type I or III hypersensitivity reaction in the bronchial system and the adjacent lung tissue Leads to cystic-varicose bronchiectasis.

Imaging Signs

Modality of choice

CT is preferable to plain radiography.

Radiographic and CT findings

Linear shadow bands bifurcate to form V- or Y–shaped figures (bronchoceles, i.e., cystic mucus-filled bronchiectatic areas); there may be fluid shadows Mucus obstruction causes atelectasis Transient eosinophilic infiltrates Predilection for the proximal bronchial areas, and the upper and middle lung fields.

Pathognomonic findings

Bifurcating linear shadow bands “Finger in glove” and “toothpaste” shadows.

Clinical Aspects

Typical presentation

Chronic recurrent asthma Cough with viscous sputum Hemoptysis Eosinophilia Hyphae in the sputum Antigen reaction.

Therapeutic options

Steroids.

Course and prognosis

Variable Recurrent allergic bronchopulmonary aspergillosis leads to central bronchiectasis and fibrosis in the upper field.

What does the clinician want to know?

Suspected diagnosis.

Differential Diagnosis

Fig. 7.1 Allergic bronchopulmonary aspergillosis in a 10-year-old girl with cystic fibrosis. The plain chest radiograph shows pronounced bronchial walls in the perihilar region and in the lower lung fields with faint bronchiectasis in the right middle lung field. Findings in the left upper lung field include an area of opacity that appears to “branch” peripherally. A similar, round pleural opacity is also seen nearby. These findings correspond to confluent areas of tubular impaction in allergic bronchopulmonary aspergillosis.

Tips and Pitfalls

Findings are nonspecific.

Selected References

Franquet T et al. Spectrum of pulmonary aspergillosis: histologic, clinical, and radiologic findings. Radiographics 2001; 21: 825–837

Johkoh T et al. Eosinophilic lung diseases: diagnostic accuracy of thin section CT in 111 patients. Radiology 2000; 216: 773–780

Ward S et al. Accuracy of CT in the diagnosis of allergic bronchopulmonary aspergillosis in asthmatic patients. AJR Am J Roentgenol 1999; 173: 937–942

Definition

Immune reaction of the alveoli and bronchioles to inhalation of toxic substances Synonym: Organic dust toxic syndrome.

Epidemiology

Typical constellations are named after the specific type of exposure Farmer’s lung (thermophilic actinomycetes) Pigeon breeder’s lung (proteins) Ventilator pneumonitis or Monday morning fever (heat tolerant bacteria), etc.

Etiology, pathophysiology, pathogenesis

Allergic granulomatous reaction (bronchiolitis and alveolitis) Inhalation of animal proteins, pathogenic microorganisms, spores, mineral oils, chemical organic substances (measuring 1–5 µm) Prerequisite is an individual predisposition In the acute stage there is bronchiolitis with proliferation of alveolar cells Subacute stage involves development of interstitial granulomas The chronic stage includes development of interstitial fibrosis, honeycomb lung, and cysts.

Imaging Signs

Modality of choice

CT.

Radiographic findings

Findings are usually normal in the acute and subacute stages Rarely, there will be discrete ground-glass opacities or nodular and reticulonodular changes The chronic stage includes fibrosis predominantly in the middle field that spares the costophrenic angle.

CT findings

– Acute and subacute stages: Disseminated, ill-defined centrilobular nodules that can resemble ground-glass lesions Diffuse or nodular ground-glass opacity Predominantly in the middle and lower lung fields.

– Chronic stage: Honeycomb fibrosis, cystic changes, traction bronchiectasis, and volume loss No pleural or subpleural involvement No lymphadenopathy.

Pathognomonic findings

In the subacute phase these include diffuse and nodular ground-glass opacities, ill-defined centrilobular nodules (acinar nodules), predominantly in the middle and lower lung fields Later findings include fibrotic changes, acinar nodules, and ground-glass opacities.

Clinical Aspects

Typical presentation

The acute stage (4–8 hours after exposure) is characterized by flulike symptoms, nonproductive cough with dyspnea, resolving within 1–2 weeks The subacute chronic stage manifests as recurrent, episodic, and progressive shortness of breath (a sign of restrictive and obstructive pulmonary dysfunction).

Fig. 7.2 Acute stage of extrinsic allergic alveolitis in a 45-year-old woman.

a The plain chest radiograph shows no abnormal findings.

b CT shows ground-glass opacification uniformly involving all lung segments.

Fig. 7.3 Severe fibrosis of the lung within the framework of an extrinsic allergic alveolitis in a 60-year-old man (bird-keeper). Fibrosis with cystic parenchym alterations. Traction bronchiectasy, widening of the central tracheobronchial system and decreased lung volume, encapsulated pneumothorax on the right.

History (antigen exposure and time-dependent symptoms), specifically immunoglobulin G (IgG) antibodies, radiographic findings, decreased pO₂ Diagnosis is confirmed by bronchoalveolar lavage and by bronchial provocation testing where indicated.

Therapeutic options

Prophylaxis against exposure Steroids.

Course and prognosis

Variable Prognosis is good with prompt diagnosis and prophylaxis against exposure.

What does the clinician want to know?

Extent of organ manifestation Disease activity Course under therapy.

Differential Diagnosis

Tips and Pitfalls

The acute stage is often misdiagnosed as a flulike infection The chronic stage is indistinguishable from other chronic inflammatory pulmonary disorders.

Selected References

Lynch DA et al. Can CT distinguish hypersensitivity pneumonitis from idiopathic pulmonary fibrosis? AJR Am J Roentgenol 1995; 165: 807–811

Matar LD, McAdams HP, Sporn TA. Hypersensitivity pneumonitis. AJR Am J Roentgenol 2000; 174: 1061–1066

Sennekamp J, Müller-Wening D. [Exogen-allergische Alveolitis.] Pneumologe 2006; 3: 461–470 [In German]

Definition

A group of etiologically and clinically heterogeneous disorders with tissue eosinophilia and usually but not invariably blood eosinophilia—Loeffler infiltrate Acute eosinophilic pneumonia Chronic eosinophilic pneumonia Idiopathic hypereosinophilic syndrome.

Epidemiology

Chronic eosinophilic pneumonia is often associated with atopic disorders (especially asthma) Women are affected twice as often as men Peak occurrence at age 30–40 years Hypereosinophilia syndrome is more common in men than women by a ratio of 7: 1.

Etiology, pathophysiology, pathogenesis

Etiology is either unclear or reactive secondary to drugs, parasites (ascarids, amebas), fungi, etc. Morphologic findings include edema, and alveolar and interstitial eosinophilic infiltrates.

Imaging Signs

Modality of choice

CT is usually preferable to plain radiography.

Radiographic and CT findings

– Loeffler syndrome: Ill-defined transient or migrating nonsegmental infiltrates CT shows ground-glass or denser foci with halos.

– Acute eosinophilic pneumonia: Bilateral reticular and nodular nonsegmental opacities CT shows ground-glass opacities.

– Chronic eosinophilic pneumonia: Homogeneous peripheral subpleural shadows (“negative image” of the edema) persisting for months, bilateral in 50% of cases, nonsegmental, predilection for the upper lobe, air bronchogram may be present Resolves leaving bandlike densities parallel to the pleura CT allows better evaluation of the characteristic topology.

– Idiopathic hypereosinophilic syndrome: Loeffler-like picturebut persistent, due at least partially to cardiac involvement Pleural effusion occurs in 50% of cases.

Pathognomonic findings

– Acute eosinophilic pneumonia: Edemalike infiltrates.

– Chronic eosinophilic pneumonia: Peripheral subpleural shadows (“negative image” of the edema) which resolve leaving bandlike densities parallel to the pleura.

– Loeffler syndrome: Transient infiltrates with halo.

– Idiopathic hypereosinophilic syndrome: Nodular infiltrates with halo.

Clinical Aspects

Typical presentation

– Loeffler syndrome: Minimally symptomatic.

– Acute eosinophilic pneumonia: Fever Dyspnea Myalgia Malaise Blood eosinophilia is not invariably present.

Fig. 7.4 Eosinophilic pneumonia in a 54-year-old man.

a The plain chest radiograph shows partially fine nodular and partially streaky reticular shadowing bilaterally and primarily in the basal region.

b Similar changes seen on CT, except that the nodular opacities appear as focal ground-glass opacities.

Fig. 7.5 Eosinophilic pneumonia in a 34-year-old man. The plain chest radiographs and CT show patchy, minimally dense infiltrates with pleural involvement in both upper lobes.

– Idiopathic hypereosinophilic syndrome: Long history Severe eosinophilia Involves multiple organ systems (heart more than lung).

Therapeutic options

Simple pulmonary eosinophilia usually resolves spontaneously Corticosteroids are indicated in the other idiopathic eosinophilic disorders.

Course and prognosis

Simple pulmonary eosinophilia has a good prognosis even without treatment Acute and chronic eosinophilic pneumonia and hypereosinophilic syndrome have a good prognosis with steroid therapy Recurrence is rare in acute eosinophilic pneumonia but common in chronic eosinophilic pneumonia.

What does the clinician want to know?