Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An 18-year-old man was admitted to Hamamatsu University Hospital on February 15, 1985, with high fever, vesicular and papular rash involving the skin and mouth, conjunctivitis, productive cough and dyspnea. A diagnosis of Stevens-Johnson syndrome was made by skin biopsy, and chest X-ray showed an infiltrate in the right lower lung filed. Despite treatment with corticosteroids and antibiotics, the mucocutaneous lesions did not heal, and the pneumonia progressed to both lung fields. Because the patient had developed dyspnea, a tracheotomy was performed, mechanical ventilatory support was instituted, and high-dose corticosteroid therapy was started. However, jaundice due to intrahepatic cholestasis, hematuria, hematochezia, sepsis, and subcutaneous and mediastinal emphysema ensued, and the patient died of respiratory failure on March 1. Postmortem examination of the lung demonstrated diffuse alveolar damage. The complement-fixation titer for Mycoplasma was 1:64, compared with a level of less than 1:4 on admission. This case was though to be one of fulminant Mycoplasma pneumoniae infection presenting with Stevens-Johnson syndrome, respiratory failure and other extra-pulmonary complications.
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PMID:[Fulminant mycoplasma pneumoniae infection presenting with Stevens-Johnson syndrome & respiratory failure]. 175 8

For years the ubiquity of Mycoplasma pulmonis in rodents overshadowed its pathogenic potential. Its etiologic significance in murine chronic respiratory disease was established only by recognition of the delicate equilibrium between organism and host. Environmental factors and genetic predisposition of the host rather than microbial virulence are the critical determinants of disease. The prevalence of M. pulmonis is undoubtedly related to the recently demonstrated in utero transmission and the ability of the organism to colonize and produce disease in the genital tract. The etiologic significance of Ureaplasma urealyticum in human genitourinary disease, like its murine counterpart, has been surrounded by controversy. Recent studies indicate that only a subgroup of colonized individuals develop clinical manifestations of disease, ranging from infertility to fetal wastage. While the natural occurrence of both respiratory and genital mycoplasmoses seriously restricts the usefulness of rats and mice for other research purposes, they represent useful models fo the study of human disease. The recognized morphologic similarities and similar natural histories of chronic bronchitis, bronchiectasis, and emphysema in humans and of M. pulmonis respiratory disease in rats and mice make the latter a particularly useful model for study of the pathogenesis of chronic pulmonary inflammation. At the same time, murine genital mycoplasmosis represents one of the few naturally occurring genital tract diseases in laboratory animals and therefore makes an attractive model for elucidating those subtle host-parasite interactions that predispose to genital disease and subsequent reproductive failure.
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PMID:Derrick Edward Award Lecture. The pathogenic potential of mycoplasmas: Mycoplasma pulmonis as a model. 698 30

In recent outbreaks of infectious bovine rhinotracheitis (IBR) in Britain a proportion of the animals affected developed a severe clinical disease characterised, at necropsy, by widespread damage to the respiratory tract. They had necrotising rhinitis, pharyngitis, laryngotracheobronchitis with extensive pseudomembrane formation and severe pneumonia with or without interstitial emphysema. Renal infarction was seen in approximatley half of the cases. The central nervous system was not affected in any of the 25 animals with severe IBR examined in this study. Tissues from the respiratory tract of 14 animals were examined for the presence of bovine herpesvirus 1 and the virus was isolated from the nasal passages of 11 and the lungs of four. Mycoplasma bovis was frequently isolated in large numbers from both the upper and lower respiratory tract.
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PMID:The pathological features of severe cases of infectious bovine rhinotracheitis. 745 96

The histologic changes in the respiratory tracts of chickens were evaluated after hatchery fumigation with 40% formaldehyde vapors and vaccination against infectious bronchitis virus with live attenuated vaccine (Massachusetts serotype). One-day-old chickens were housed in four isolation units in controlled environmental conditions, fed and watered ad libitum, and separated into four groups: 1) fumigated and vaccinated birds (FV group); 2) nonfumigated and vaccinated birds (NFV group); 3) fumigated and nonvaccinated birds (FNV group); and 4) control group (C group). All birds were tested to be free from Mycoplasma gallisepticum and Mycoplasma synoviae. After necropsy on the first, eighth, and twenty-sixth days after birth, samples from tracheal upper portion and lungs were conventionally processed for light, scanning, and transmission electron microscopy. Tissue response was monitored by microscopic examination of trachea and lung. On the first day of observation, fumigated and vaccinated birds (FV group) showed extensively damaged tracheal epithelium with exfoliated areas and some active glands with electrodense granules, and in the lung, the primary bronchi epithelium had disorganized cilia and abundant lymphocytes, with emphysematous areas in tertiary bronchus. On day 8 after vaccination, cubical and cylindrical tracheal cell proliferation was observed, and on day 26, ciliated columnar epithelium was almost regenerated with heterophil corion infiltration, and hyaline cartilage nodules appeared in parabronchi. The nonfumigated and vaccinated birds (NFV) revealed less injury on the epithelial surface and a more rapid response to epithelial regeneration than the in only fumigated animals (FNV). The control group did not show remarkable morphologic changes. Postvaccinal and fumigation effects on the upper respiratory tract were temporary, whereas in lungs, increased emphysema, cartilage nodules in the interchange zone, and general lymphocyte infiltration had caused intensive injury.
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PMID:Morphologic observations on respiratory tracts of chickens after hatchery infectious bronchitis vaccination and formaldehyde fumigation. 1100 97

Reduced vascular endothelial growth factor (VEGF) has been reported in bronchoalveolar lavage fluid and lungs of severe emphysema patients. Airway epithelial cells (AEC) are exposed to various environmental insults like cigarette smoke and bacterial infections, but their direct effect on VEGF production in well-differentiated primary human AEC remains unclear. The current authors determined the effect of cigarette smoke extract (CSE) alone and in combination with Mycoplasma pneumoniae (Mp) on VEGF production in well-differentiated primary normal human bronchial epithelial (NHBE) and small airway epithelial cells (SAEC) in air-liquid interface cultures. Secretion and expression of VEGF were determined by ELISA and real-time RT-PCR, respectively. Cell growth, apoptosis, extracellular signal-regulated kinase (ERK)1/2 and protein kinase (PK)C signalling pathways were evaluated to further dissect VEGF regulation under CSE treatment. CSE significantly reduced VEGF secretion in NHBE and SAEC. In SAEC, Mp alone significantly increased the VEGF, while the presence of CSE attenuated Mp-induced VEGF production. While ERK inhibitor reduced VEGF secretion only in NHBE, a PKC inhibitor significantly decreased VEGF secretion in both NHBE and SAEC. In conclusion, direct cigarette smoke extract exposure significantly reduced vascular endothelial growth factor production in well-differentiated primary human airway epithelial cells, in part through modifying extracellular signal-regulated kinase 1/2 and protein kinase C signalling pathways.
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PMID:Cigarette smoke extract reduces VEGF in primary human airway epithelial cells. 1912 86

Swyer-James Macleod syndrome is a rare disorder that leads to recurrent respiratory infections. The fibrosis and obstruction of the terminal and respiratory bronchioles, likely caused by respiratory infections in early childhood, prevents normal development of the alveolar bud. Organisms that have been associated with this syndrome include adenovirus, measles, bordetella pertussis, mycobacterium spp, influenza A and mycoplasma. The syndrome is an acquired cause of unilateral emphysema. The diagnosis of the syndrome can be made in infancy or early childhood, but in asymptomatic individuals can be delayed until adulthood and rarely in the elderly. Chest radiographs and computed tomographic (CT) scan can confirm the diagnosis and exclude other possibilities. A case of Swyer- James Macleod syndrome diagnosed at age 63 in a patient with recurrent respiratory infections and a history of childhood pertussis is presented.
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PMID:A 63-year-old man with recurrent pulmonary infections: a case of Swyer-James Macleod syndrome. 2129 92

A 7-year-old girl presented with subcutaneous emphysema, pneumomediastinum (PM), pneumoretroperitoneum, and pneumothorax caused by Mycoplasma pneumoniae (MP). The patient had been treated with clarithromycin for pneumonia at another hospital; however, her condition deteriorated and complications developed. Soon after admission to our hospital, we started the patient on minocycline and prednisolone, and the complications improved promptly. Laboratory data showed serum ferritin and urinary beta-2-microglobulin levels were greatly elevated. We therefore speculated that the patient might have underlying hypercytokinemia. Prednisolone is an effective treatment for hypercytokinemia. We therefore recommend prednisolone treatment for cases of severe M. pneumoniae pneumonia that do not respond to antimicrobial agents.
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PMID:A 7-year-old girl with subcutaneous emphysema, pneumomediastinum, pneumothorax, and pneumoretroperitoneum caused by Mycoplasma pneumoniae pneumonia. 2190 97

Feline polycystic kidney disease (PKD) is an inherited disorder caused by the mutation of PKD1 gene that eventually lead to the development of chronic kidney disease. The latter condition causes hypertension and eventually progress into congestive heart failure. Feline parvovirus (FPV) is a highly contagious and often fatal disease infecting cats and other members of Felidae. An 8-month-old female domestic shorthair cat was presented with complaint of wound dehiscence a day after ovarian hysterectomy procedure. The wound at the suture site appeared necrotic, purulent with foul smell. The cat was found to have diarrhoea during the fixation of suture breakdown and, later, was tested positive with parvovirus infection. Complete blood count revealed anaemia, neutrophilia, lymphopenia and thrombocytosis. Biochemistry profiles showed hypoproteinaemia and elevated of urea and creatinine. The cat was hospitalised, and symptomatic treatments were given. During hospitalisation, the cat showed symptoms of polydipsia and polyuria and found dead 2 days later. Post-mortem findings demonstrated the cat had oral ulceration, thoracic effusion, fibrinopleuropneumonia, pericardial effusion, left ventricular hypertrophy and right ventricular dilation, chronic passive liver congestion, mesenteric lymphadenomegaly, intestinal haemorrhage, adrenomegaly and polycystic kidney. Histopathological evaluation revealed fibrinous pleuropneumonia, pulmonary atelectasis, emphysema and oedema, hypertrophic cardiomyopathy, hepatic necrosis, splenic necrosis, intestinal necrosis, renal necrosis and renal polycystic. Staphylococcus aureus and Escherichia coli were isolated from bronchus swab and intestinal segment, respectively. Polymerase chain reaction (PCR) revealed parvovirus infection. The cat was definitely diagnosed with polycystic kidney disease concurrent with parvoviral and secondary bacterial infections.
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PMID:Polycystic kidney disease concurrent with feline parvovirus and bacterial infections in domestic shorthair cat: a case report. 3301 78