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          Atypical Fibroxanthoma

 
 

                

Infections are a common cause of granulomatous lung disease. 

 

Granulomas may present as a nodular mass of the lung but may be spread diffusely through the lung.

Infectious agents causing granulomatous lung diseases are as follows:

Mycobacteria:                            

Mycobacterium Tuberculosis

Atypical Mycobacterial Infection

Fungi:

Histoplasmosis (Histoplasma Capsulatum)

Coccidioidomycosis

Cryptococcus

Blastomycosis

Filamentous bacteria:                 

Actinomycosis

Nocardiosis

Other Organism:

Pneumocystis Carinii

 

Certain features may be present which support a diagnosis of infection:

 

 - Most important feature is necrosis, but less so if the "necrosis" is no more than some degenerative change in collagen.

 

- If the necrotic center contains neutrophils, the index of suspicion for infection should be especially high .

 

Pathologists should search for fungal infection.

 

- Most necrotizing granulomas are related to infection.

 

- Special Stains:   In a few cases the organisms may be visible on the H & E stained section. Special stains like Ziehl - Neelsen (ZN) stain for microbacteria  and  Grocott’s  Methenamine Silver (GMS) stain for fungi.

 

Grocott’s  Methenamine Silver (GMS):   Advantage and disadvantage of GMS:  GMS is much more reliable than PAS for staining fungi.   Black/lung debris/pigment are usually distinguishable by being more heterogenous than fungal spores and may confuse the picture on the GMS. In this case    PAS is helpful.

 

- Tissue necrosis and a vasculitis are commonly seen in infections. [Differential diagnosis:-  Pulmonary angiitis / granulomatosis (Wegener’s granulomatosis etc ] . Such vasculitis is usually non-necrotising, showing mural/intimal infiltration by lymphocytes and other mononuclear cells.

 

- In Chronic Granulomatous Disease, an inherited group of conditions characterized by abnormal phagocytic cell function, necrotizing granulomas occur with a number of infectious pathogens.

- Microorganisms are generally found most frequently in an extracellular location within the debris of the necrotic granuloma center, and not in the cellular rim.

- In mycobacterial infection, microorganisms may be relatively few and far between, requiring thorough searching of one or two adequately stained sections. Despite the higher index of suspicion and endless staining/searching  nothing may be found.

- A significant proportion of infectious granulomas (proven some other way), and almost one third of radiographically solitary granulomatous lesions, will be negative on special staining.

Therefore a lack of organisms does not exclude an infectious etiology.

In such circumstances, the pathologist can  describe the lesion, and convey the suspicion, but indicate the lack of stainable microorganisms.

- If granulomatous inflammation, especially in association with  necrosis, is found in an otherwise typical nodular fibrous lesion of silicosis , the index of suspicion of a complicating mycobacterial infection should be very high.

- Obviously, in any case, if fresh material is available (Autopsy,/Open/ Thoracoscopic lung biopsy) , and the possibility of infection is suspected , tissue should be sent for microbiological examination for appropriate culture.

Serology, particularly in some of the fungal infections, may also provide useful information.

Visit:

Pathological Diagnosis of Granulomatous Lung Diseases

Non-necrotising Granulomatous Inflammation of the lung

An approach to Histopathological Examination of Pulmonary Granulomatous Inflammation

              

Differential diagnosis and etiology of epitheloid cell granulomatosis of the lung.Verh Dtsch Ges Pathol. 2000;84:118-28.

Our knowledge on epithelioid cell granulomatosis of the lung has been extended in recent years. New entities have been added, like zirconiosis, others like tuberculosis, mycobacteriosis and sarcoidosis have gained new interest, because molecular techniques allowed new insight into their pathogenesis and a more rapid and species-specific diagnosis. Experimental work in addition has added a lot of information about the network of cytokines and other inflammatory mediators responsible for granuloma formation, however, our knowledge of this network is still incomplete. Three types of agents are now known to cause epitheloid cell granulomas: infectious organisms (bacteria, fungi, and parasites), products of plants and animals (pollen, sporangia, proteins), and metallic compounds. In addition there is still a group of epithelioid cell granulomatoses with unknown etiology. Sarcoidosis, one of these granulomatosis, has recently elicited an old controversy: By molecular techniques Mycobacteria and Corynebacterium acnes have been identified in sarcoid granulomas and a link to the aetiology of sarcoidosis has been proposed. If these bacteria induce some cases of sarcoidosis by an allergic mechanism, has still to be proven.

Anatomopathology of pulmonary granulomatoses.Rev Pneumol Clin. 1993;49(6):263-7.

Pulmonary granulomatosis are lung diseases due to inflammatory lesions with characteristic histiocyte reactions seen in granulomas often composed of epithelioid and giant cell formations. There are a number of pathological entities depending upon whether the aetiology is infectious or immunologic. The pathologist is asked to determine the type of reaction and to identify the greatest number of elements possible for the aetiologic diagnosis.

Pulmonary sarcoidosis: a mimic of respiratory infection.Semin Respir Infect. 1995 Sep;10(3):176-86.

Sarcoidosis is an idiopathic multisystem disorder with several clinical and roentgenographic features suggestive of respiratory infection. In the absence of infection, it is characterized by the microscopic presence of noncaseating epithelioid granuloma in affected tissues. When present, constitutional symptoms, fever, coughing, and exertional dyspnea usually develop insidiously, although occasionally Lofgren's syndrome--the triad of bilateral hilar adenopathy, erythema nodosum and polyarticular arthritis--may herald the onset of acute disease. Pulmonary involvement is the roentgenographic hallmark of sarcoidosis; bilateral hilar adenopathy is the most common manifestation. However, parenchymal infiltrates and pleural effusion may occur. Although numerous bacterial and fungal organisms may mimic the clinical and roentgenographic features of sarcoidosis, tuberculosis and fungal infections associated with granulomatous inflammation are the infectious processes most apt to cause diagnostic confusion. Several diagnostic clues are available to the clinician confronted with the consideration of sarcoidosis. Roentgenographic staging of the disorder (stage 0, normal radiograph; stage I, isolated bilateral hilar adenopathy; stage II, hilar adenopathy and parenchymal involvement; stage III, isolated parenchymal involvement; and stage IV, parenchymal fibrosis) provides a framework on which a differential diagnosis of likely infectious agents may be constructed and a history of travel to regions of endemic fungal infection may further narrow the differential diagnosis. An unexplained exudative lymphocytic pleural effusion or CD-4 lymphocyte predominance in bronchoalveolar lavage (BAL) fluid may also suggest a diagnosis of sarcoidosis. However, the definitive diagnosis of sarcoidosis is dependent upon the histological demonstration of noncaseating granuloma and the exclusion of infection in the appropriate clinical and roentgeno- graphic setting.

                   

 
 October 2009 
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