Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022568 (keratitis)
 5,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Between 1996 and 2005 the carcasses of 355 harbour seals originating from the coast of Schleswig-Holstein, Germany, were investigated for pathological changes. The animals were collected before (n=280) and after (n=75) the second phocine distemper virus (PDV) epizootic in 2002. The seals were either found dead or were killed due to severe illness. Necropsy was performed in each case, in addition to histopathological, immunohistochemical, microbiological and parasitological examinations. Throughout the period of study, the respiratory and alimentary tracts were the organ systems most consistently affected by pathological change. The most common cause of death was bronchopneumonia caused by parasitic and/or bacterial infection of the lung. Less frequently identified changes included: trauma, gastroenteritis, uterine torsion or dystocia, polyarthritis/polymyositis, intestinal torsion, septicaemia, dermatitis, and keratitis. The most frequent causes of bronchopneumonia, gastroenteritis, polyarthritis, dermatitis and septicaemia were infections with alpha/beta-haemolytic streptococci, Escherichia coli and Clostridium perfringens. A number of changes were more frequently identified after 2002. These included the presence of parasites in the lung, stomach and intestine; bronchopneumonia, gastritis, enteritis, septicaemia and perinatal death. The increased prevalence of these changes may have been related to the preceding PDV epidemic.
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PMID:Pathological findings in harbour seals (Phoca vitulina): 1996-2005. 1762 67

A 35-year-old man with severe eczematous dermatitis and recurrent staphylococcal skin infections, some of which required hospitalization, is presented. Other medical concerns include recurrent oral staphylococcal infections, otitis media, ocular herpes simplex virus keratitis, asthma, steroid-induced gastritis, steroid-induced cataracts, recurrent upper respiratory infections, and acute pharyngitis. Past medical history includes retained dentition of six primary teeth, two episodes of childhood pneumonia that required hospitalization, and three wrist and ankle fractures. Laboratory data showed an eosinophil count of 2,400 cells/ml; the highest IgE level was 17,028 IU/mL. Considering the clinical and laboratory findings, the diagnosis of hyperimmunoglobulin E syndrome was made. DNA sequencing showed a novel signal transducer and activator of transcription 3 (STAT3) gene mutation within intron 12, specifically adenine to cytosine, two base pairs upstream of exon 13.
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PMID:Hyperimmunoglobulin E syndrome with a novel STAT3 mutation. 1989 24