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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mycoplasma ovipneumoniae and Mycoplasma arginini were the species of Mollicutes most commonly isolated from 175 goats with respiratory disease in Ontario. The pathogenicity of M. ovipneumoniae, strain B321B and M. arginini, strain D53e, was assessed in goats following endobronchial inoculation. One out of three two year old goats developed fever after inoculation with a pure culture of strain B321B, and it had extensive subacute fibrinous pleuritis when necropsied three weeks later. Neither of the remaining goats had lesions in the respiratory tract. Mycoplasma ovipneumoniae was recovered from one of the animals four days after inoculation, but not at necropsy from any of the goats, at which time a marked humoral immune response with growth inhibiting antibodies was detected. In a second experiment three four to five week old goats were inoculated with the same strain and three other goats were given placebo treatment. One experimental goat developed fever and coughing, and it had extensive subacute fibrinous pleuritis in the right side and pneumonia. Another goat had focal pneumonia in the left diaphragmatic lobe. Microscopically there was subacute hyperplastic suppurative bronchiolitis, atelectasis and nonsuppurative alveolitis. The infected animals did not clear the mycoplasma and not all of them produced antibodies. Mycoplasma arginini, strain D53e, did not induce lesions in any of four goat kids within 14 days after inoculation but did cause transient elevations in rectal temperature, circulating monocytes, circulating neutrophils and blood fibrinogen. Mycoplasma arginini was infective and immunogenic for all inoculated animals and showed a particular affinity for the tonsil. Thus, this study provides the first evidence that M. ovipneumoniae is pathogenic for goats causing pneumonia and pleuritis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Experimental studies on the pathogenicity of Mycoplasma ovipneumoniae and Mycoplasma arginini for the respiratory tract of goats. 374 58

Thirty-nine foals with pneumonia were admitted to the Veterinary Medical Teaching Hospital at the University of California, Davis. Corynebacterium equi was recovered from each of them on bacteriologic culture of transtracheal aspiration specimens or lung specimens at necropsy. The foals were divided into 2 groups. Group I consisted of 20 foals that died because of C equi pneumonia and were subsequently necropsied. Group II consisted of 19 foals that were treated and discharged from the hospital. Radiography was performed on all foals. Clinical signs included increased respiratory rate, fever, cough, nasal discharge, increased bronchovesicular sounds over large airways, and wheezing over small airways. Highly significant differences were found in the mean respiratory rate (P less than 0.005) and temperature (P less than 0.001), recorded at admission, between the 2 groups; both factors were higher for group I. Hematology revealed leukocytosis with neutrophilia, monocytosis, and high plasma fibrinogen content in all foals. Significant differences were recorded in the mean total leukocyte count (P less than 0.05), mean neutrophil count (P less than 0.05), mean monocyte count (P less than 0.005), and mean fibrinogen value (P less than 0.05) between the 2 groups; values from group I were higher than those from group II. Although C equi was isolated alone from 25 of the tracheal aspirates and lung specimens, 14 cultures yielded multiple pathogens. At the time of initial examination, all foals had radiographic evidence of pneumonia. Pulmonary consolidation indicative of bronchopneumonia was identified in 31 of the 39 foals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical and radiographic findings in Corynebacterium equi pneumonia of foals. 398 94

There are approximately 20,000 excess deaths from cardiovascular disease each winter in England and Wales. The reasons for the excess have not been fully elucidated. For one year, we studied 96 men and women aged 65-74 living in their own homes in order to examine seasonal variation in plasma fibrinogen and factor VII clotting activity (FVIIc), and to investigate relationships with infection and other cardiovascular-disease risk factors. Both fibrinogen and FVIIc plasma values were greater in winter with estimated winter-summer differences (confidence intervals) of 0.13 (0.05-0.20) g/L for fibrinogen and 4.2 (1.2-7.1)% of standard for FVIIc. These differences could account for 15% and 9% increases in ischaemic heart disease risk in winter respectively. After adjustment for confounding by season, fibrinogen was strongly related to neutrophil count (p < 0.0001), C-reactive protein (p < 0.0001), alpha 1-antichymotrypsin (p < 0.0001), and self-reported cough (p < 0.0001) and coryza (p = 0.0004), but not to ambient temperature. Therefore, we suggest that seasonal variation in fibrinogen might be induced by winter respiratory infections via activation of the acute phase response. Seasonal variations in the cardiovascular risk factors fibrinogen and FVIIc provide further possible explanations for the marked seasonal variation in death from ischaemic heart disease and stroke in the elderly.
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PMID:Seasonal variations of plasma fibrinogen and factor VII activity in the elderly: winter infections and death from cardiovascular disease. 790 26

We encountered a 63-year-old man whose dry cough due to interstitial pneumonia had been successfully with an anti-thrombin drug, argatroban, which was given to treat exacerbated Buerger's disease. We therefore prospectively evaluated fibrinogen, fibrin-degradating product D-dimer, thrombin anti-thrombin III complex, and plasmin anti-plasmin complex in patients with interstitisal lung diseases. In a preliminary study, we found that some patients actually had elevated levels of these markers. These findings suggested that increased coagulability was involved in the pathophysiology of interstitial pneumonia. In this study, we measured the levels of serum-soluble thrombomodulin as a marker of endothelial cell damages that lead to hemostasis. We found that serum levels of thrombomodulin were high in about 35% of patients with sarcoidosis, interstitial pneumonia associated with collagen diseases, or idiopathic interstitial pneumonia. Furthermore, these levels decreased as the patients' conditions improved. Although further evaluation is needed, these results suggest that endothelial cell damage and hemostasis are involved in the pathophysiology of interstitial pneumonia.
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PMID:[Evaluation of serum thrombomodulin in patients with interstitial pneumonia]. 784 12

Little is known of the inflammatory characteristics of acute infections of the respiratory tract caused by virus and unusual bacteria such as Chlamydia pneumoniae. A case is reported in whom inflammatory indices in sputum were used to investigate, for the first time, the airway inflammation during an episode of acute bronchitis caused by C pneumoniae. The patient presented with a dry cough of five days duration. C pneumoniae was identified by polymerase chain reaction (PCR) in a nasopharyngeal swab collected on day 5. Virological studies were negative. Clinical and inflammatory indices in induced sputum were measured on days 6, 8, and 11. The cough cleared spontaneously by day 11. Forced expiratory volume in one second was normal throughout. Sputum findings identified intense airway inflammation characterised by increased total cell and lymphocyte counts followed by an increase in neutrophils and a decrease in the CD4/CD8 ratio, activation of CD8 lymphocytes, and exudation as indicated by an increase in fluid phase fibrinogen. These observations suggest that sputum might be useful to monitor an inflammatory/immune response of the airway in acute infections.
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PMID:Markers of inflammation in induced sputum in acute bronchitis caused by Chlamydia pneumoniae. 940 85

Co-administration of antihypertensive drug therapy and hormonal replacement therapy (HRT) is frequent in postmenopausal women but it is not known whether HRT interacts with concomitant antihypertensive therapy. The present study was designed to investigate efficacy and safety of the ACE inhibitor moexipril in comparison to placebo in hypertensive, postmenopausal women on HRT. After a 4-week placebo run-in phase, 95 postmenopausal women (35-74 years of age) who had a sitting diastolic blood pressure (BP) of 95-114 mm Hg and were treated with HRT were randomised to a 12-week treatment with moexipril 15 mg or placebo. Efficacy and safety were assessed by measuring changes in sitting BP and metabolic parameters associated with cardiovascular disease including triglycerides, total cholesterol, HDL, LDL, total cholesterol/HDL ratio and glucose. Adverse events were recorded continuously. After 12 weeks of treatment, moexipril 15 mg was significantly more effective in reducing sitting systolic and diastolic BP from baseline than placebo (-12.2/-9.9 mm Hg vs -1.6/-4.3 mm Hg, P < 0.001). Metabolic parameters were not affected by treatment with moexipril: mean levels of triglycerides, total cholesterol, HDL, LDL, total cholesterol/HDL ratio and glucose remained unchanged throughout the study. Fibrinogen, an independent cardiovascular risk factor, increased after placebo (+35.0 mg/dl) and decreased after treatment with moexipril (-33.6 mg/dl), the difference, however, was not statistically significant. Moexipril was well-tolerated by postmenopausal women using HRT. The most frequent adverse events included headache (21.3%), cough (12.8%) and rhinitis (10.6%) and there were no significant differences in the number and severity of adverse events between the moexipril and placebo groups. This study indicates that moexipril is effective and well tolerated in the treatment of hypertensive, postmenopausal women and can safely be co-administered to HRT.
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PMID:Co-administration of an ACE-inhibitor (moexipril) and hormonal replacement therapy in postmenopausal women. 1037 52

We report a case of hepatitis C virus-associated glomerulonephropathy presenting with MPO-ANCA-positive, rapidly progressive glomerulonephritis(RPGN). A 60-year-old woman was admitted to our hospital for evaluation of RPGN. Laboratory evaluation revealed microhematuria, proteinuria(800 mg/day), anemia, renal failure(blood urea nitrogen 27 mg/dl, serum creatinine 2.2 mg/dl), cryoglobulinemia, hypocomplementemia, positive MPO-ANCA(232 EU), and hepatitis C virus infection(GOT 58 IU/l, GPT 38IU/l, HCV-RNA(PCR) 1,200 kcopy/ml, serotype 1). After admission, the patient's renal function and anemia deteriorated rapidly, then prednisolone(30 mg/day) was started. After treatment her renal function gradually improved, then a renal and liver biopsy was performed. The renal biopsy revealed six sclerosing fibrous crescentic glomeruli in twelve glomeruli. Immunofluorescent examination revealed granular deposits of IgG, C3, and fibrinogen along the glomerular basement membrane and mesangial matrix. The pathogenesis of RPGN in this case may relate to the deposition of immune complexes in the glomeruli because immunofluorescent examination was revealed to be the immune-complex type, but not pauci immune type nephritis. Liver histology revealed chronic active hepatitis with mild piecemeal necrosis and did not reveal vasculitis. Although her renal function was improved after treatment with prednisolone, she suffered from pulmonary manifestations(dry cough etc.) on the 120th hospital day. Suddenly she died because of pulmonary hemorrhage on the 180th hospital day. These findings suggest that various HCV-induced immunological abnormalities, such as positive MPO-ANCA, cryoglobulinemia and hypocomplementemia, play an important role in the pathogenesis of this RPGN, although we could not demonstrate deposition within glomeruli of immune complexes containing HCV. The effect of interferon therapy on such immunological abnormalities remains to be documented. Since interferon is known to have immunomodulatory effects, we selected corticosteroid therapy. Future studies need to focus on the optimal treatment strategy for hepatitis C virus-associated glomerulonephritis.
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PMID:[A case of hepatitis C virus-associated glomerulonephropathy presenting with MPO-ANCA-positive rapidly progressive glomerulonephritis]. 1089 95

A 91-year-old man was admitted with colliquative diarrhea, anorexia and weight loss. He had a history of healed tuberculosis, hypertension and atherosclerotic abdominal aortic aneurysms. On admission, shortness of breath without cough, exertional dyspnea, and ascites were also noticed. His chest X-ray and CT showed almost normal findings in the lung fields except for calcified old pleurisy. Since laboratory tests revealed thrombocytopenia, low fibrinogen, and increased CA19-9. DIC induced by an unknown cancer was diagnosed. He died on the eighth day due to progressive respiratory failure which did not respond to oxygen therapy. Autopsy revealed that he had a poorly differentiated adenocarcinoma in the cecum complicated with pulmonary lymphangitis carcinomatosa. Lymphangitis should be considered in the case of unexplained progressive respiratory failure developing in patient with cancer, even in the absence of X-ray findings.
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PMID:[A very elderly autopsy case of cecal cancer with pulmonary lymphangitis carcinomatosa]. 1103 30

Work in swine confinement buildings leads to an inflammatory response and may be associated with increased levels of acute phase proteins. We compared the inflammatory response of a control group of young former farm workers with age-matched former farm workers who had previously developed the lower airway symptoms of wheeze, cough, tightness of the chest during work in swine confinement buildings, and because of these symptoms had stopped work. Both groups were subjected to an experimental exposure in a swine confinement building for 3 hours. Complement activation and acute phase proteins were measured in blood samples and broncho-alveolar lavage. Plasma C3d levels correlated with respirable dust, significantly so for individual cases and for the whole cohort. Plasma C3, fibrinogen and alpha (1) -acid glycoprotein peaked 1 and 6 h after exposure start, mannan-binding lectin, C-reactive protein and alpha(1)-antitrypsin peaked after 2 h. Surfactant protein D (SP-D) and alpha (2) -macroglobulin were downregulated. In lavage, only SP-D, alpha (2)-macroglobulin and fibronectin were detected. FEV(1), FVC, TLC and FEV(25-75) did not vary during exposure. There was complement activation in response to respiratory dust, more so amongst cases than in the control group. Acute exposure, with work related levels of organic dust containing endotoxin, leads to a weak systemic inflammatory response.
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PMID:Plasma C3d levels of young farmers correlate with respirable dust exposure levels during normal work in swine confinement buildings. 1285 33

A 7-year-old Thoroughbred gelding was admitted to Equine Hospital, Korea Racing Association for evaluation and treatment of colic. Based on the size and duration of the large colonic and cecal impaction, a routine ventral midline celiotomy and large colon enterotomy were performed to relieve the impaction. Six days following surgery the gelding exhibited signs of lethargy, fever, inappetence and diarrhea. Eleven days following surgery, the jugular veins showed a marked thrombophlebitis. On the sixteenth day of hospitalization the gelding died suddenly. Upon physical examination, the horse was febrile, tachycardic and tachypnoeic. Thoracic excursion appeared to be increased; however, no abnormal lung sounds were detected. No cough or nasal discharge was present. Hematology revealed neutrophilic leukocytosis. Serum biochemistry was normal but plasma fibrinogen increased. In necropsy, fibrinopurulent fluid was present in the thoracic cavity. There were firm adhesions between visceral pleura and thoracic wall. White, mixed and red thrombi were formed in both jugular veins from the insertion point of IV catheter. Histopathological examination showed fibrinopurulent inflammation and vascular thrombosis in the lung. The pleura showed edematous thickening and severe congestion. The clinicopathological and pathological findings suggest that septic thrombi associated with septic thrombophlebitis metastasized into the pulmonary circulation and were entrapped in the pulmonary parenchyma and provoked pleuropneumonia.
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PMID:A hematogenic pleuropneumonia caused by postoperative septic thrombophlebitis in a Thoroughbred gelding. 1502 89


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