We have discussed allergic bronchopulmonary mycosis already in the previous chapter; therefore, we will briefly recall the main aspects, as this is necessary for differential diagnosis.

In most patients, a type I immune reaction with IgE antibodies is produced, causing a similar clinical presentation as in allergic asthma. Patients cannot cough up mucus; however, hyperreactivity of the airways is much less pronounced as in asthma. Dyspnea in mucoid impaction is predominantly induced by obstruction of the airways by thick mucus plugs [6]. The disease presents as an eosinophilic bronchitis with extreme hyperplasia of goblet cells in the mucosa and the bronchial glands. Hyperplasia of the smooth muscle layer is common (Fig. 10.1). Silver impregnation stains, such as Grocott methenamine, can highlight the causing fungal remnants. On bronchoscopy these mucus casts can be completely removed from the bronchial tree by sucking up with the bronchoscope. This is almost diagnostic for mucoid impaction and in addition relives symptoms of the patient.

The second form of ABPM is bronchocentric granulomatosis. This is a combined immune reaction toward fungal proteins with an IgE-based antibody reaction and a granulomatous type IV reaction. The disease presents with necrotizing bronchitis/bronchiolitis with peribronchiolar extension of the inflammatory infiltrates. Within the bronchiolar walls, epithelioid cell granulomas and/or palisading histiocytic granulomas are found. In addition there is usually a dense infiltrate of eosinophils (Fig. 10.2). In full-blown disease, the necrosis might outline the bronchial tree like a cast formed by necrotic debris. In the lumina remnants of organisms might be demonstrated using silver impregnation or other special stains. In this classic variant, BCG is induced by an allergic reaction against different types of fungi, most often members of the Aspergillus family. However, AFS and GMS stains should always be performed to exclude mycobacteria, especially when the inflammatory infiltrates contain predominantly neutrophils. The clinical information about positive allergy tests might be helpful. In rare cases bronchocentric, necrotizing granulomatosis might also be seen in the setting of Wegener’s disease [7]. Therefore ANCA tests can be helpful in this differential diagnosis.

In rare cases ABPM can present as eosinophilic pneumonia (Fig. 10.3). This is very similar to chronic eosinophilic pneumonia, which will be discussed below.

Bronchial asthma has already been discussed in airway diseases so the reader is referred to Chap. 6; drug allergies have been discussed in the previous chapter.

Eosinophilic pneumonias can present as acute or chronic eosinophilic pneumonia.

On CT/HRCT EP present focal densities, sometimes with ground-glass pattern; in other cases, there might be densities fluctuating over time within different lung lobes (Fig. 10.4). There is no specific feature, which might differentiate EP from other pneumonias. Clinically EP present with a sudden onset of cough, fever usually of 1 week duration, myalgia and chest pain, and dyspnea. Spontaneous resolution does occur in some cases; in others clinical symptoms worsen rapidly. Most often patients present without blood eosinophilia. In some progressive cases, patients can die with respiratory failure.

In acute as well as chronic eosinophilic pneumonia, parasitic infection is the most common cause. Eosinophilic pneumonia can also be seen in vasculitis, especially eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome), in drug reactions, in exogenous vapor inhalation, in hypereosinophilic syndrome, and in allergic fungal reactions; finally in some cases, no underlying etiology can be detected, leaving this EP as idiopathic.

Macroscopically on gross sections, there are grayish-red consolidations, not otherwise specific.

The most prominent feature is a dense infiltration of the lung by eosinophils, although macrophages can sometimes be present in substantial number (Fig. 10.5). Eosinophilia can be also seen in bronchoalveolar lavage; the percentage is usually above 25 %. Fibrosis, sometimes presenting as organizing pneumonia, can be seen in chronic eosinophilic pneumonia (Figs. 10.6 and 10.7). Peripheral blood eosinophilia may or may not be present. Eosinophils are directly responsible of tissue damage or at least are part of the process.