**2.8 Parasites**

*Dirofilaria* is one of the most common parasites that lead to the granulomatous inflammation in lungs. This nematode infects dogs more commonly, but the disease can also occur in humans, as the infection is transmitted through an insect bite; the larva enters the right heart and into the pulmonary arteries during embolism, causing thrombosis of the latter with an infarct-like necrosis development (**Figure 14**). In one-third of the cases, granulomas are formed in the adjacent lung

#### **Figure 13.**

*Perivascular foreign-body granuloma (talcosis) in a case of pneucystic pneumonia in a drug abuser. H&E in bright field versus polarization.*

**Figure 14.** Dirofilaria *larva in the pulmonary artery, infiltration of plasma cells and eosinophils. H&E.*

tissue, necrotizing or non-necrotizing vasculitis is observed in half of the cases, and two-thirds of the cases demonstrate eosinophilic infiltration [18].

#### **2.9 Tuberculosis**

Tuberculosis is caused by members of the *Mycobacterium tuberculosis* family, namely, *M. tuberculosis, M. bovis,* and *M. africanum*, which belong to the group of rapidly growing mycobacteria. The virulence of these microorganisms varies from moderate to highly virulent strains. Changes observed in the lungs in tuberculosis patients can be very diverse ranging from common necrotizing granulomas, miliary necrotizing granulomas to non-necrotizing granulomas, tuberculoma, and healed

**59**

**Figure 15.**

*periphery. H&E.*

*Pathology of Sarcoidosis and Differential Diagnostics of other Granulomatous Diseases*

fibrosus granulomas, all of these depend on the virulence on the one hand and the immune defense status on the other (**Figure 15**) [19]. Granulomas in tuberculosis usually have a bronchiolocentric localization, but it should be kept in mind that this could be the case in any infectious granulomatosis and even in sarcoidosis. Histological features in tuberculosis are indistinguishable from those in nontuberculous granulomatosis. This was confirmed in a study by Corpe and Stergus, in which 27 pathologists, specializing in the mycobacterial disease diagnostics, were asked to evaluate 25 histological slides without information about culture-confirmed infection. In most cases, it was not possible to distinguish between tuberculosis and mycobacteriosis [20]. Thus, the tuberculosis diagnosis **should be based** on the identification and subsequent determination of the type of *Mycobacterium*.

*Tuberculous necrotizing granuloma with lymphocytes, histiocytes, and giant multinucleated Langhans at the* 

Non-tuberculosis mycobacteriosis is an inflammation caused by mycobacteria not belonging to the *Mycobacterium tuberculosis* family; those are *M. avium, M. fortuitum, M. gordonae, M. kansasii, M. xenopi*, and *M. marinum*, also designated as MAC complex. Unlike *Mycobacterium tuberculosis*, these mycobacteria can be detected intracellularly in macrophages (histiocytes), and they can be numerous in immunocompromised individuals. The diagnosis is made based on acid-fast stain, cultural or molecular biological tests. As mentioned above, the histological changes are often similar to those in tuberculosis. Non-necrotizing granulomas, histiocytic granulomas, and granulomas consisting of foamy and granular macrophages containing mycobacteria can also be detected. Solovieva et al. have described the

• tuberculous granuloma—epithelioid cell tissue, variable number of Langhans

• a reactive, necrotizing multibacillarity—weak inflammatory response, abun-

following spectrum of histological changes in mycobacteriosis:

cells and the necrosis intensity, few mycobacteria;

dance of mycobacteria in the necrosis area;

*DOI: http://dx.doi.org/10.5772/intechopen.90693*

**2.10 Non-tuberculosis mycobacteriosis**

*Pathology of Sarcoidosis and Differential Diagnostics of other Granulomatous Diseases DOI: http://dx.doi.org/10.5772/intechopen.90693*

#### **Figure 15.**

*Sarcoidosis and Granulomatosis - Diagnosis and Management*

tissue, necrotizing or non-necrotizing vasculitis is observed in half of the cases, and

*Perivascular foreign-body granuloma (talcosis) in a case of pneucystic pneumonia in a drug abuser. H&E in* 

Tuberculosis is caused by members of the *Mycobacterium tuberculosis* family, namely, *M. tuberculosis, M. bovis,* and *M. africanum*, which belong to the group of rapidly growing mycobacteria. The virulence of these microorganisms varies from moderate to highly virulent strains. Changes observed in the lungs in tuberculosis patients can be very diverse ranging from common necrotizing granulomas, miliary necrotizing granulomas to non-necrotizing granulomas, tuberculoma, and healed

two-thirds of the cases demonstrate eosinophilic infiltration [18].

Dirofilaria *larva in the pulmonary artery, infiltration of plasma cells and eosinophils. H&E.*

**58**

**2.9 Tuberculosis**

**Figure 14.**

**Figure 13.**

*bright field versus polarization.*

*Tuberculous necrotizing granuloma with lymphocytes, histiocytes, and giant multinucleated Langhans at the periphery. H&E.*

fibrosus granulomas, all of these depend on the virulence on the one hand and the immune defense status on the other (**Figure 15**) [19]. Granulomas in tuberculosis usually have a bronchiolocentric localization, but it should be kept in mind that this could be the case in any infectious granulomatosis and even in sarcoidosis. Histological features in tuberculosis are indistinguishable from those in nontuberculous granulomatosis. This was confirmed in a study by Corpe and Stergus, in which 27 pathologists, specializing in the mycobacterial disease diagnostics, were asked to evaluate 25 histological slides without information about culture-confirmed infection. In most cases, it was not possible to distinguish between tuberculosis and mycobacteriosis [20]. Thus, the tuberculosis diagnosis **should be based** on the identification and subsequent determination of the type of *Mycobacterium*.
