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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The first Scandinavian cases of Zellweger syndrome (ZS) are described. A brother and sister, children of first cousins, had the typical clinical symptoms and pathological findings. Extensive metabolic studies in the boy were negative. Pipecolic acid in the urine was not elevated. Both children died at 14 weeks of age. Two months earlier the girl had suffered severe intestinal bleeding. Both had pneumocystic carinii pneumonia at autopsy although no evidence of immune deficiency had been found in the boy. The girl had used up her visible iron depots while the boy still had abundant but probably physiologic amounts of hemosiderin in the RES. Most of the cerebral abnormalities are unspecfic and possibly related to anoxia or other causes of delayed maturation. The white matter abnormalities in ZS patients may only be quantitatively different from the common "fatty metamorphosis" in infants. Previously reported ultrastructural abnormalities (absence of peroxisomes and very sparse smooth endoplasmic reticulum, as well as mitochondrial abnormalities) which are possibly unique for ZS, are confirmed. It is stressed that these were seen despite phenobarbital treatment which normally stimulates the formation of smooth endoplasmic reticulum.
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PMID:The Zellweger syndrome: subcellular pathology, neuropathology, and the demonstration of pneumocystis carinii pneumonitis in two siblings. 30 90

Open lung biopsies from three patients with Legionnaires' disease were examined by light and transmission electron microscopy. The patients had serious underlying disease. All developed a rapidly progressive pneumonia unresponsive to penicillin, oxacillin, and gentamicin. One patient, who received erythromycin, survived. Light microscopy in all three showed severe acute bronchopneumonia. The Legionnaires' disease bacterium was seen in tissue sections and confirmed by direct immunofluorescence. Transmission electron microscopy showed numerous rod-shaped intracellular organisms that were morphologically similar to other gram-negative bacteria and the Rickettsieae. They were within phagolysosomes, free in the cytoplasm, and rarely within structures resembling dilated rough endoplasmic reticulum. Lung tissue changes included marked detachment and necrosis of alveolar pneumocytes, septal and alveolar exudate with lysis, and prominent endothelial cell swelling and degeneration. Capillary and epithelial basement membranes were consistently intact, suggesting that the tissue changes are potentially capable of reverting to normal structure and function.
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PMID:Ultrastructure of lung in Legionnaires' disease. Observations of three biopsies done during the Vermont epidemic. 43 34

Neuroepithelial cells (NEC) and neuroepithelial bodies (NEB) were found in the lungs of rats among cells of the alveolar epithelium. The peculiar features of NEC structure included microvilli with microfibrils penetrating deep into the cytoplasm, and a complicated structure of the endoplasmic reticulum: reticulum membrane complex. NEC's are arrayed on the alveolar basal membrane singly, in pairs and in larger numbers forming NEB. The latter consist of cells differing in shape, size, and ultrastructure. Most of them have no microvilli with microfibrils inside. In chronic pneumonia NEC's occur more frequently, the ultrastructure of most cells being well-developed.
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PMID:[Ultrastructure of the neuroepithelial cells of the respiratory portion of the lungs in experimental inflammatory diseases of the lungs]. 57 7

Morphological studies of aortic fatty dots and streaks, and the adjacent normally appearing intima, in a 5 3/4-year-old boy who died of pneumonia, showed several hitherto unreported features. In lesions, lipid vacuoles and/or other cytoplasmic "inclusions" (ultrastructurally considered to present complex forms of lipids) were present on occasion in the endothelium but consistently involved the (intimal) smooth muscle cells (SMC). Similar changes were present in the adjacent intima, but were here less prominent and "tapered off" distally. A moderate number of macrophages also contained cytoplasmic lipids but such cells entirely free of lipid inclusions were observed, too. Most surprisingly, dilated and many cisternae of rough-surfaced endoplasmic reticulum (ER) in the SMC of lesions were associated spatially with cytoplasmic droplets and other forms of lipids. The results of these studies question the generally accepted central role of macrophages as being primarily involved in the pathogenesis of tissue changes in Tangier disease. It is possible that in view of the absence or paucity of high-density lipoproteins (HDL) and alterations of (their) apo A-I and apo A-II (as well as of other lipids), the arterial SMC may be in some way involved in the metabolism of the above substances in this disorder. Support of this tentative (and highly speculative) assumption must await further work utilizing tissues and cells other than those containing macrophages and other derivatives of reticulo-endothelial system.
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PMID:Aortic features in Tangier disease and pathogenetic considerations--Part I. Fatty dots and streaks. 138 Apr 64

The pathogenicity and pathogenesis of Lelystad virus was studied in six 6-day-old SPF piglets. A third passage of the agent was propagated on porcine alveolar macrophages and intranasally inoculated into pigs. Pigs were killed at hours 24, 48, 60, and 72, and on days 6 and 8 after inoculation. From day 2 on pigs developed diffuse interstitial pneumonia with focal areas of catarrhal pneumonia, and from this day on splenic red pulp macrophages were enlarged and vacuolated. Lelystad virus was re-isolated from the lungs of infected pigs from day 2 after inoculation. Lelystad virus antigens were detected by immunohistochemical techniques in bronchiolar epithelium and alveolar cells, and in spleen cells of infected pigs from day 2 after inoculation. Ultrastructural examination of tissues by electron microscopy revealed degenerating alveolar macrophages and epithelial cells in lungs and nasal mucosa, with excessive vacuolation of the endoplasmic reticulum. Although the respiratory tract seems to be the target organ for this virus, macrophages in other organs, such as the spleen, can also be infected. This preference for macrophages may impair immunological defences.
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PMID:Pathological, ultrastructural, and immunohistochemical changes caused by Lelystad virus in experimentally induced infections of mystery swine disease (synonym: porcine epidemic abortion and respiratory syndrome (PEARS)). 194 40

Forty-six human temporal bones from 24 individuals were removed at autopsy and prepared for electron microscopy. The adequacy of histologic preservation was evaluated by light and electron microscopy. Characteristic autolytic changes included vacuolization of afferent neurons and neural poles of inner and outer hair cells, lysis of limiting membranes of hair and supporting cells, swelling of endoplasmic reticulum, and dissolution of mitochondrial cristae. The rate of autolysis varied significantly within cellular components of the inner ear. The neural poles of hair cells demonstrated more rapid autolysis than apical poles and nerve terminals showed more autolysis than myelinated nerve fibers. Postmortem time and the cause of death affected the adequacy of histologic preservation. Fixation in patients dying of pneumonia, hypoxia, head injury, or malignancy tended to be poor, whereas the fixation achieved in patients dying of cardiac disease with postmortem time of under 140 minutes was generally good.
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PMID:A study of postmortem autolysis in the human organ of Corti. 390 Jan 49

The ultrastructure of three human lymphoblastoid B cell lines, Raji, RPMI 4098, and WIL-2, was analyzed after the cells were incubated with tunicamycin, and antibiotic that selectively inhibits N-linked glycosylation of macromolecules. After a 24-hour exposure to 1.0 microgram/ml of tunicamycin, the lymphocytes lose their microvilli and become smooth spheres or develop a few blebs. Also, the cells show a dilation of the endoplasmic reticulum and an increase in myelin figures resulting from intracellular membrane accumulation, possibly lysosomal in origin. These ultrastructural alterations are similar to those observed in Tay-Sachs, Fabrey's, and Gaucher's diseases, Type II pneumocytes in viral pneumonitis, certain lysosomal storage diseases, and in aging fibroblasts. Therefore, tunicamycin-treated cells may be a useful model in the correlation of altered ultrastructural pattern in membrane flow with the etiology of certain diseases.
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PMID:Ultrastructural alterations in human lymphoblastoid B cell lines treated with tunicamycin. 697 75

We have described the ultrastructural morphology of splenic and pulmonary exudates from guinea pigs infected intranasally and intraperitoneally by Legionella pneumophila. Legionella pneumophila produced pneumonia and splenitis by both routes of inoculation. The microbe was also disseminated to other organs. Within neutrophils, Legionella pneumophila typically displayed degenerating forms, suggesting that this intracellular environment is somewhat hostile to the bacterium. By contrast, macrophages tended to contain intact forms, located within organelles morphologically identical with rough endoplasmic reticulum. Some bacteria were replicating at this site. In macrophages containing greater than 25 microbes per section, Legionella pneumophila was usually dispersed within the cytoplasm outside of organelles, and many of the heavily infected macrophages exhibited ultrastructural features of injury. Neutrophils phagocytosed Legionella pneumophila, but we found no ultrastructural evidence of either ingestion of Legionella pneumophila by macrophages or of localization of the microbe to primary or secondary phagosomes of macrophages. Our findings support the contention that Legionella pneumophila is an intracellular parasite of macrophages. The homing of Legionella pneumophila to cytoplasmic organelles morphologically indistinguishable from rough endoplasmic reticulum has no bacteriologic parallel. It remains to be determined how Legionella pneumophila enters this organelle, whether this structure is, in fact, functional rough endoplasmic reticulum and whether this site is actively involved in replication of the bacterium. The animal models used herein seem suitable for further delineation of these questions.
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PMID:Electron microscopic examination of the inflammatory response to Legionella pneumophila in guinea pigs. 705 88

We investigated a T-cell activation deficiency in a 3-month-old boy with protracted diarrhea, serious cytomegalovirus pneumonia, and a family history (in a brother) of cytomegalovirus infection and toxoplasmosis. In spite of detection of normal number of peripheral lymphocytes, T cells did not proliferate after activation by anti-CD3 and anti-CD2 antibodies, although proliferation induced by antigens was detectable. We sought to determine the origin of this defect as it potentially represented a valuable tool to analyze T-cell physiology. T-cell activation by anti-CD3 antibody or phytohemagglutinin (PHA) led to reduced interleukin-2 (IL-2) production and abnormal nuclear factor-activated T cell (NF-AT; a complex regulating the IL-2 gene transcription) binding activity to a specific oligonucleotide. T-cell proliferation was restored by IL-2. Early events of T-cell activation, such as anti-CD3 antibody-induced cellular protein tyrosine phosphorylation, p59fyn and p56lck kinase activities, and phosphoinositide turnover, were found to be normal. In contrast, anti-CD3 antibody-induced Ca2+ flux was grossly abnormal. Release from endoplasmic reticulum stores was detectable as tested in the presence of anti-CD3 antibody or thapsigargin after cell membrane depolarization in a K+ rich medium, whereas extracellular entry of Ca2+ was defective. The latter abnormality was not secondary to defective K+ channel function, which was found to be normal. A similar defect was found in other hematopoietic cell lineages and in fibroblasts as evaluated by both cytometry and digital video imaging experiments at a single-cell level. This primary T-cell immunodeficiency appears, thus, to be due to defective Ca2+ entry through the plasma membrane. The same abnormality did not alter B-cell proliferation, platelet function, and polymorphonuclear neutrophil (PMN) function. Elucidation of the mechanism underlying this defect would help to understand the physiology of Ca2+ mobilization in T cells.
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PMID:A primary T-cell immunodeficiency associated with defective transmembrane calcium influx. 753 12

The adenovirus type 2 (Ad2) early region 3 (E3) codes for a 19-kDa glycoprotein (gp19) that associates with the class I major histocompatibility (MHC) heavy chain in the endoplasmic reticulum (ER) and prevents the transport of class I MHC protein products to the cell surface. It has been shown previously in tissue culture that this reduction in class I MHC expression allows infected cells to escape detection by class I MHC restricted CD8+ cytotoxic T-lymphocytes (CTL). We now report the results of studies on the effects of Ad2/gp19 expression on virulence in vivo. Since we wanted to isolate the effect of Ad2/gp19 from the effects of other Ad E3 region gene products and human Ads do not replicate in the mouse, we cloned the Ad2/gp19 open reading frame (ORF) into the HindIII C region of WR vaccinia virus (VV). Two VV recombinants were constructed by inserting the Ad2/gp19 ORF in either an expressing (V-e19(+)) or a non-expressing (V-e19(-)) orientation under control of the VV P7.5 promoter. The V-e19(+)recombinant expressed Ad2/gp19 in infected tissue and could be co-precipitated with an antibody to the class I MHC antigen Kd. However, intracerebral or intranasal infections of BALB/c (H-2d), BALB.G (H-2g), or C3H (H-2k) mice showed that Ad2/gp19 expression by V-e19(+) had no significant effect either on viral lethality or on its ability to replicate in vivo when compared to V-e19(-). Furthermore, the nature of the CD8+ CTL response to a V-e19(+)-induced pneumonia in (H-2d) mice was unchanged by Ad2/gp19 expression. Modulating the CD8+ CTL response, by interfering with infected target presentation, may not be important in the control of VV replication or virulence in vivo when other aspects of the immune response to viral infection are not altered. However, the two VV recombinants V-e19(+) and V-e19(-) were both equally attenuated (10-fold) when compared to wild-type VV. This attenuation, which has been reported previously for an intracerebral infection, is believed to be caused by the disruption of a 37-kDa ORF in the VV HindIII C region. Interestingly, our studies showed that the attenuation is not accompanied by a reduction in viral titers in infected tissue.
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PMID:Association of vaccinia virus-expressed adenovirus E3-19K glycoprotein with class I MHC and its effects on virulence in a murine pneumonia model. 817 41


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