The lung in tropical eosinophilia compared to that in pulmonary hypertension. Fine structural basis of respiratory disability.
Light and electronmicroscopic changes in lung biopsies were studied in six patients with tropical pulmonary eosinophilia, aged 20 to 37 years, of varying duration, and with severe haematologic (blood eosinophil count of 3,600 to 18,200 per mm3), and respiratory changes. On light microscopy the main pathologic reaction consisted of large mononuclear cells and eosinophils in and around the alveoli and blood vessels, and proliferated reticulin. Fine structural changes probably being described for the first time, included the presence of many alveolar macrophages characterised by abundant cytoplasm, irregular or stunted microvilli, increased phagolysosomes with ingested debris, and depletion of other organelles. Eosinophils bearing typical old and young granules, were encountered in and around the alveoli and blood vessels in all case, and collagenosis around alveolar cells in a few. Subacute pneumonitis producing compression and disorganisation of alveoli and blood vessels, and lack of normal apposition of air and blood spaces, appear responsible for the respiratory disability. The detection of mycobacteria, cocci or chlamydia-like bodies in two specimens and of intranuclear virus-like particles in another, could either indicate secondary infection or have an immunogenic significance, in the absence of detection of filarial elements in any of the specimens. Lung biopsies from two additional patients (aged 13 & 32) who had mitral stenosis probably due to rheumatic heart disease, and secondary pulmonary hypertension, were studied as "control" specimens. Both at light and electronmicroscopy these specimens did not show any eosinophils or neutrophils, and fewer macrophages in the lung parenchyma. In contrast to tropical eosinophilia and, as expected, there was considerably more fibrosis of the lung parenchyma, especially in the alveolar subepithelial region and in the vessel walls. This, together with fibroblasts full of endoplasmic cisterns, noted particularly in the younger patient with shorter duration, probably represented an earlier change in this condition.
Manghani
D K
DK
Department of Neuropathology and applied Biology, Bombay Hospital, India.
Dastur
D K
DK
Udwadia
F E
FE
D000293:Adolescent; D000328:Adult; D001706:Biopsy; D004804:Eosinophils / Q000473:pathology / Q000648:ultrastructure; D005260:Female; D006801:Humans; D006976:Hypertension, Pulmonary / Q000473:pathology*; D008168:Lung / Q000473:pathology / Q000648:ultrastructure*; D016676:Macrophages, Alveolar / Q000648:ultrastructure; D008297:Male; D008854:Microscopy, Electron; D008871:Microvilli / Q000648:ultrastructure; D011650:Pulmonary Alveoli / Q000473:pathology / Q000648:ultrastructure; D011657:Pulmonary Eosinophilia / Q000473:pathology*; D011658:Pulmonary Fibrosis / Q000473:pathology