Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The radiological changes in two cases of inhalation anthrax are correlated with pathological findings. The earliest radiological sign was widening of the mediastinum, followed by prominent lung markings with peribronchial infiltration due to pulmonary oedema and haemorrhage. Associated pleural effusions are common, and non-specific super-imposed pulmonary infiltration may also be present. Inhalation anthrax must be considered in any case of mediastinal widening in a patient coming in contact with imported animal products or with livestock in endemic areas.
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PMID:Radiological changes in inhalation anthrax. A report of radiological and pathological correlation in two cases. 81 21

In experimental anthrax intoxication, a highly important stage of its pathogenesis consists in microcirculatory disturbances with the phenomena of blood sludge, accompanied by the increased permeability of blood vessels not only for plasma, but also for red blood cells. These disturbances result in perivascular hemorrhages, hemorrhagic infiltrations, edema and cavitary transudates. Pulmonary edema and, as a consequence, the accumulation of fluid in pulmonary alveoli and the respiratory tract are of particular importance and, probably, can be considered the basic cause of the ensuing acute and fatal asphyxia. Such vascular and pulmonary insufficiency is accompanied by a decrease in the content of macroergic compounds (and in particular ATP), the characteristic deformation of red blood cells and disturbances in their oxygen transport function, which is linked with the decreased content of 2,3-diphosphoglycerate.
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PMID:[Experimental characteristics of anthrax intoxication]. 244 50

Widespread vaccination has largely eliminated anthrax in Europe (the last case was reported in France in 1972) but the disease remains endemic in many developing countries. The usual cutaneous presentation (malignant pustules) is much more familiar than the various visceral manifestations including digestive tract, pulmonary or meningeal signs. We report a case of a 33-year-old immigrant living in France who was hospitalized for asthenia, dyspnoea, mucopurulant expectoration and moderate diarrhoea 3 days after a 3-month stay in Senegal and Gambia. The temperature was 39 degrees C at admission and blood pressure 110/70 mmHg. Crepitants were heard at the base of the right lung and the rest of the physical examination was normal. Blood was drawn for culture. Laboratory tests and the chest X-ray led to the diagnosis of pneumopathy and a treatment of amoxicillin and clavulanic acid was given with oxygenotherapy. The patient's temperature returned to normal but over the next 48 hours the dyspnoea worsened together with the black diarrhoea. The abdomen was painful. There were no skin lesions. The chest X-ray revealed an extension of the bilateral pulmonary images and bilateral pleural effusion. Laboratory tests revealed thrombopenia (platelet count 38,000/mm3) hyperleukocytosis (WBC 48,000/mm3) and haemolysis (Hb 4 milligrams). The diagnosis was made on the basis of the initial blood cultures which were positive for Bacillus anthracis. All other samples were negative, including HIV serology. Despite adapted antibiotic therapy (penicillin G, 8MU/day, was initiated on day 2), multiple organ failure occurred with septic shock and pulmonary oedema. The patient died in the intensive care unit on day 7. Fatal outcome due to anthrax is described in 25% of the visceral forms but reaches 100% in cases of septicaemia. The haemolysis observed in this case is not mentioned in the classical descriptions of anthrax. When treating septic syndromes in patients who have returned from endemic zones, clinicians should entertain the diagnosis of anthrax since the risk of fatal outcome is increased greatly in case of delayed diagnosis.
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PMID:[Visceral form of human anthrax imported from Africa]. 802 24

We describe the 11th case of bioterrorism-related inhalational anthrax reported in the United States. The presenting clinical features of this 94-year-old woman were subtle and nondistinctive. The diagnosis was recognized because blood cultures were obtained prior to administration of antibiotics, emphasizing the importance of this diagnostic test in evaluating ill patients who have been exposed to Bacillus anthracis. The patient's clinical course was characterized by progression of respiratory insufficiency, pleural effusions and pulmonary edema, and, ultimately, death. Although her B anthracis bacteremia was rapidly sterilized after initiation of antibiotic therapy, viable B anthracis was present in postmortem mediastinal lymph node specimens. The source of exposure to B anthracis in this patient is not known. Exposure to mail that was cross-contaminated as it passed through postal facilities contaminated with B anthracis spores is one hypothesis under investigation.
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PMID:Fatal inhalational anthrax in a 94-year-old Connecticut woman. 1185 84

Bacillus anthracis infections are frequently associated with severe and often irreversible hypotensive shock despite appropriate antibiotics and aggressive hemodynamic and pulmonary support. Based on the observations that the anthrax secreted proteins-protective antigen (PA), lethal factor (LF), and edema factor (EF) also produce shock and mortality in animal models, we chose to characterize further the clinical chemistries and microscopic pathology of toxin treated rats. Groups of three male Sprague Dawley rats received bolus intravenous infusions of PA/LF, PA/EF, LF, or EF alone and blood samples and tissues were collected and assayed for chemistries and tissue pathology. In PA/LF and PA/EF treated animals but not other groups, chemistries showed transaminasemia and elevated lactate dehydrogenase. PA/LF treated animals alone showed elevated hemoglobin and hematocrits; PA/EF treated animals alone showed lymphopenia. Pathology was remarkable for pulmonary edema in PA/LF treated rat lungs and pulmonary hemorrhage in PA/EF treated rat lungs. These results are consistent with our and others' previous findings that the morbidity and mortality associated with anthrax are not cytokine-mediated but due to a direct effect of the toxins on the cardiovascular system along with toxin-specific alterations in blood counts. PA/LF pathology matches that seen with acute cardiac failure, and PA/EF pathology coincides with direct vascular endothelial injury. These observations provide a rational basis for drug interventions to reduce the effect of these toxins on the heart and blood vessels.
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PMID:Anthrax toxin-induced shock in rats is associated with pulmonary edema and hemorrhage. 1822 26

A major virulence factor of Bacillus anthracis is the anthrax Lethal Toxin (LeTx), a bipartite toxin composed of Protective Antigen and Lethal Factor. Systemic administration of LeTx to laboratory animals leads to death associated with vascular leakage and pulmonary edema. In this study, we investigated whether systemic exposure of mice to LeTx would induce gene expression changes associated with vascular/capillary leakage in lung tissue. We observed enhanced susceptibility of A/J mice to death by systemic LeTx administration compared to the C57BL/6 strain. LeTx-induced groups of both up- and down-regulated genes were observed in mouse lungs 6 h after systemic administration of wild type toxin compared to lungs of mice exposed to an inactive mutant form of the toxin. Lungs of the less susceptible C57BL/6 strain showed 80% fewer differentially expressed genes compared to lungs of the more sensitive A/J strain. Expression of genes known to regulate vascular permeability was modulated by LeTx in the lungs of the more susceptible A/J strain. Unexpectedly, the largest set of genes with altered expression was immune specific, characterized by the up-regulation of lymphoid genes and the down-regulation of myeloid genes. Transcripts encoding neutrophil chemoattractants, modulators of tumor regulation and angiogenesis were also differentially expressed in both mouse strains. These studies provide new directions for the investigation of vascular leakage and pulmonary edema induced by anthrax LeTx.
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PMID:Anthrax lethal toxin-induced gene expression changes in mouse lung. 2203 74

Anthrax is associated with severe vascular leak, which is caused by the bacterial lethal toxin (LeTx). Pleural effusions and pulmonary edema that occur in anthrax are believed to reflect endothelial injury caused by the anthrax toxin. Since vascular leak can also be observed consistently in rats injected intravenously with LeTx, the latter might present a simple physiologically relevant animal model of acute lung injury (ALI). Such a model could be utilized in evaluating and developing better treatment for ALI or acute respiratory distress syndrome (ARDS), as other available rodent models do not consistently produce the endothelial permeability that is a major component of ARDS. The biological activity of LeTx resides in the lethal factor metalloprotease that specifically degrades MAP kinase kinases (MKKs). Recently, we showed that LeTx inactivation of p38 MAP kinase signaling via degradation of MKK3 in pulmonary vascular endothelial cells can be linked to compromise of the endothelial permeability barrier. LeTx effects were linked specifically to blocking activation of p38 substrate and MAP kinase-activated protein kinase 2 (MAPKAPK2 or MK2) and phosphorylation of the latter's substrate, heat shock protein 27 (HSP27). We have now designed a peptide that directly and specifically activates MK2, causing HSP27 phosphorylation in cells and in vivo. The MK2-activating peptide (MK2-AP) also blocks the effects of LeTx on endothelial barriers in cultured cells and reduces LeTx-induced pulmonary vascular leak in rats. Hence, MK2-AP has the therapeutic potential to counteract anthrax or pulmonary edema and vascular leak due to other causes.
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PMID:Anthrax lethal toxin-induced lung injury and treatment by activating MK2. 2606 27