Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023241 (Legionella)
6,990 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The risk of opportunistic infection in the renal transplant patient is due to an interaction between two major factors: the epidemiologic exposures (particularly within the hospital environment) and the net state of immunosuppression. The net state of immunosuppression is determined by the nature, dose, and duration of the immunosuppressive therapy being administered; the presence or absence of granulocytopenia and technical factors that could compromise the primary mucocutaneous barriers to infection; such metabolic factors as uremia, hyperglycemia, and the state of nutrition; and, finally, the immunomodulating effects of such viruses as CMV, the hepatitis viruses, and HIV. The major types of opportunistic infection to which the renal transplant patient is susceptible are the following: the viruses of the herpes group and papovaviruses; bacteria such as L monocytogenes, N asteroides, and Legionella; such fungi as Candida, Aspergillus, C neoformans, and the Mucoraceae; and protozoans such as P carinii, S stercoralis, and T gondii.
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PMID:Opportunistic infections in renal allograft recipients. 305 19

A 2 yo male child ingested approximately 15 ml of a Gun Blue solution containing selenious acid, nitric acid and copper nitrate. He was immediately given milk and vomited spontaneously blood-stained food with a garlic smell. He was admitted to our Centre less than 3 hr following ingestion. An esophago-gastroscopy showed a second degree burn of both esophagus and stomach. He became comatose and had to be ventilated mechanically. Metabolic acidosis, leucocytosis, hyperglycemia and hemoconcentration were also observed. During the following day he developed a severe intestinal distension, a cardiomyopathy (CPK = 1,302, cardiac arrhythmia), and moderate hepatic, renal and pulmonary dysfunctions. Plasma selenium concentration was 285 micrograms/L and the maximum urinary concentration was 28,459 micrograms/L. After 4 days, his condition had improved considerably and he was about to be extubated when he suddenly developed acute respiratory distress. A similar episode occurred 24 hr later. His lung function progressively deteriorated; later he required the use of an extracorporeal membrane lung. Legionella dumofii was found the causative agent. He died 17 d after ingestion despite aggressive treatment. Acute selenious acid poisoning and its relation to Legionnaire's disease is discussed.
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PMID:Acute poisoning by selenious acid. 408 70