Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We reviewed retrospectively the clinical records, autopsy protocols and central nervous system tissue sections of 50 patients who underwent orthotopic liver transplantation for end-stage liver disease between 12/83 and 8/93. The postoperative survival period ranged from hours (6), weeks (17), months (17), to years (10). All patients received immunosuppressive drugs from the immediate postoperative period to the time of their death (cyclosporine, steroids; occasionally azathioprine, OKT3, FK506). Nineteen patients had neurological manifestations (hepatic encephalopathy) prior to surgery. Post-transplant neurologic signs and symptoms included: hepatic encephalopathy/altered mental status (11), focal or generalized seizures (9) and stroke (2). In the majority of cases (37) the cause of death was septicemia and/or bleeding diathesis. The neuropathologic findings present in 36 patients could be classified into 3 distinct categories: metabolic disorders: hepatic/anoxic encephalopathy, central pontine myelinolysis (15); cerebrovascular disease: subarachnoid and/or intracerebral hemorrhage, bland or hemorrhagic infarction (23); and infection: bacterial meningitis/cerebritis, multifocal fungal microabscesses, presumptive viral meningitis/encephalomyelitis (10). In conclusion, 72% of 50 patients who came to autopsy after liver transplantation were found to have neuropathologic abnormalities; these abnormalities were predominantly infections and vascular diseases.
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PMID:Neuropathology of liver transplantation. 760 96

Outbreaks of neonatal multifocal encephalomalacia with sepsis have been reported among flocks of very young chicks in Belgium, Scotland, and the United States. The purposes of the present study were to describe intralesional bacterial cocci in chicks with this type of encephalomalacia and to determine its incidence during 1991-95, and to determine the importance of this lesion with respect to the frequency of all other brain lesions/ diseases during the same time period. All laboratory records of broiler chickens examined at the Georgia Poultry Laboratory from Jan. 1, 1991, through Dec. 31, 1995, where the histopathologic diagnoses included the letter string *encephal* were retrieved for further study. The leading etiology for brain disease was nutritional encephalomalacia (57%), followed by neonatal encephalomalacia (22%), septic meningoencephalitis (16%), and Marek's disease (14%), in turn followed by nonpurulent encephalitis (7%), avian encephalomyelitis (3%), and mycotic meningoencephalitis (3%). Diagnosis of neonatal multifocal encephalomalacia with sepsis in the brains of Georgia chicks is a perennial one. Microscopically, the condition is characterized by mild to maximal multifocal locally extensive fibrin thrombosis of blood capillaries, and necrosis (encephalomalacia, malacia) of surrounding zones of brain stem and/or cerebral hemisphere neuropile. In 44% of cases of neonatal encephalomalacia fibrin thrombosis of blood capillaries was accompanied by intralesional gram-positive coccoid bacteria that were most abundant in medium- and small-sized arterioles or venules. Only gram-positive coccoid bacteria are found in cases of neonatal encephalomalacia (P < 0.05), and only gram-negative rod-shaped bacteria are found in cases of septic meningoencephalitis (P < 0.05). Therefore, bacterial culture and routine light microscopic histopathology are sufficient for diagnosing the condition when the differential diagnosis for neurologic disease in chicks includes neonatal encephalomalacia.
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PMID:Neonatal multifocal encephalomalacia and other lesions in the brains of Georgia chicks: 1991-95. 898 Aug 22

Tyrosine kinase blockers from the AG 126/AG-556 tyrphostin family are shown to inhibit the lipopolysaccharide (LPS)-induced production of tumor necrosis factor alpha (TNFalpha), nitric oxide (NO), and prostaglandin E2 (PGE2) in primary rat astrocytes cultures. The tyrphostin AG-556 which was previously shown to be effective against sepsis in mice and dogs also show excellent efficacy in inhibiting experimental autoimmune encephalomyelitis (EAE) in mice. AG-556 does not block the activation of JNK/SAPK and of p38/HOG and therefore seems to act at a target down stream to these kinases which is activated in stress or at a target on an obligatory parallel pathway. These findings together with previous results showing inhibition of sepsis in mice and dogs suggest that protein tyrosine kinase (PTK) blockers of the AG-556 family may be considered in the management of human autoimmune disorders such as multiple sclerosis (MS).
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PMID:Suppression of experimental autoimmune encephalomyelitis by tyrphostin AG-556. 987 84

The immunomodulator Linomide (roquinimex) ameliorates the development of numerous inflammatory and immunological diseases, including sepsis, arthritis, and encephalomyelitis. However, the mechanism underlying this protective effect of Linomide remains unclear. In this study, we wanted to evaluate the effect of Linomide treatment on the different steps in the extravasation process of leukocytes stimulated by tumor necrosis factor alpha (TNF-alpha) in vivo. For this purpose, we used intravital microscopy in the mouse cremaster muscle microcirculation. We found that pretreatment with Linomide dose-dependently (3-300 mg/kg) reduced TNF-alpha-induced leukocyte adhesion and tissue recruitment. Notably, at 300 mg/kg response to TNF-alpha was nearly abolished, i.e. leukocyte adhesion was decreased by 83% and recruitment by 86%. In fact, the anti-inflammatory effect of this dose of Linomide corresponded in magnitude to the potency of 10 mg/kg of dexamethasone. Moreover, administration of Linomide did not alter the systemic leukocyte counts. On the other hand, 1-10 mg/kg of dexamethasone decreased the circulating number of mononuclear leukocytes by 77%. Taken together, our novel findings demonstrate that Linomide is a potent inhibitor of leukocyte adhesion and recruitment in cytokine-activated tissues. These data may help explain the documented protection provided by Linomide in inflammatory diseases characterized by cytokine and leukocyte accumulation.
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PMID:Linomide abolishes leukocyte adhesion and extravascular recruitment induced by tumor necrosis factor alpha in vivo. 1107 99

Enteroviruses are a common cause of childhood infections, from hand, foot and mouth disease, to lethal brainstem encephalitis. Enterovirus 71 was first isolated in 1969. Brainstem encephalomyelitis and pulmonary oedema are postulated to be causally related and have been found to be a common feature of fatal enterovirus 71 cases. A fatal case of enterovirus 71 infection in a 2-year-old, previously healthy boy is reported. He presented to the Department of Paediatrics with clinical features of sepsis within 3 days of onset of fever. A few minutes after injection of midazolam, fentanyl and vecuronium for intubation, cardiac arrest developed and was not amenable to various treatment modalities. Pulmonary haemorrhage and oedema were noted during intubation, and postmortem examination confirmed the presence of brainstem encephalomyelitis.
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PMID:First fatal case of enterovirus 71 infection in Hong Kong. 1151 56

Nitric oxide (NO) plays an important regulatory/modulatory role in a variety of inflammatory conditions. NO is a small, short-lived molecule that is released from a variety of cells in response to homeostatic and pathologic stimuli. It may act as a vasodilator and a platelet inhibitor and may interfere with adhesion molecules to prevent neutrophil adhesion. NO release may also lead to the formation of highly reactive species such as peroxynitrite and stable nitrosothiols and may cause mitochondrial damage and nitration of protein tyrosine residues. In addition, NO inhibits cell proliferation via inhibition of polyamine synthesis and cell uptake and may well act as a 'brake' on the proliferative response following cytokine exposure. All three isoforms of nitric oxide synthases are found in the kidney during inflammation. The site of NO release impacts significantly on its net function and structural impact. NO plays a protective role in many forms of immune injury, such as nephrotoxic serum-induced glomerulonephritis, autoimmune tubular interstitital nephritis, and experimental allergic encephalomyelitis. NO overproduction in sepsis, after cytokine exposure, inducible NO synthase transcription, and local inflammation can autoinhibit endothelial NO synthase, leading to selective renal and mesenteric vasoconstriction.
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PMID:Role of nitric oxide in inflammatory conditions. 1196 94

Between one-third and one-half of all cases of sepsis are known to be caused by gram-positive microorganisms through the cell wall component, e.g. lipoteichoic acid (LTA). Gram-positive bacteria are also known to induce encephalomyelitis and meningeal inflammation, and enhance the production of nitric oxide (NO) via expression of inducible nitric oxide synthase (iNOS) in murine tissue macrophages. It remains to be explored if LTA could activate microglia considered to be resident brain macrophages. We report here that LTA derived from gram-positive bacteria (Staphylococcus aureus) significantly induces NO release and iNOS expression in primary microglia. LTA-induced NO accumulation was detected at 2 h in microglial culture and was significantly attenuated by pretreatment with anti-CD14, complement receptor type 3 (CR3) or scavenger receptor (SR) antibodies. LTA activated mitogen-activated protein kinases (MAPKs) such as extracellular signal-regulated kinase, p38 MAPK or c-Jun N-terminal kinase in cultured microglia. LTA-elicited microglial NO production was also drastically suppressed by SB203580 (p38 MAPK inhibitor) or pyrrolidine dithiocarbamate (an inhibitor of nuclear factor kappaB), indicating that p38 MAPK and nuclear factor kappaB were involved in microglial NO release after LTA challenge. These results suggest that gram-positive bacterial product such as LTA can activate microglia to release NO via the signal transduction pathway involving multiple LTA receptors (e.g. CD14, CR3 or SR), p38 MAPK and nuclear factor kappaB. The in vivo study further confirmed that administered intracerebrally LTA induced considerable noticeable iNOS, phospho-IkappaB and phospho-p38 MAPK expression in microglia/macrophages.
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PMID:Signal transduction pathways of nitric oxide release in primary microglial culture challenged with gram-positive bacterial constituent, lipoteichoic acid. 1587 5

This study investigated the clinical manifestations and outcomes of central nervous system (CNS) infection by enteroviruses. Cases with CNS involvement among all enterovirus-culture-positive cases from January 1995 to June 2003 were retrospectively reviewed. Among 1028 enterovirus-culture-positive cases, there were 333 cases involving the CNS. Of these, the ratio of male to female subjects was 1.78, and the mean (+/- standard deviation) age was 6.83 +/- 5.9 years; 21 were premature neonates, and 10 failed to thrive. Disease entities included 282 cases of aseptic meningitis (84.7%), 44 cases of encephalitis (13.2%), and 7 cases of encephalomyelitis/polio-like syndrome (2.1%). Of these cases, 97.9% (326/333) had fever with peak body temperature at 38.9 degrees C, 85% had headache and vomiting, 70% had meningeal signs, 64% had neck stiffness, 16.6% (55/333) had change of consciousness, 5.4% (18/333) had seizures and 5.2% (17/333) had myoclonic jerks. Mannitol was administered in 77.2% of patients (257/333), along with intravenous immunoglobulin in 6.6% (22/333). Twelve cases received ventilator support. One patient died of hand-foot-and-mouth disease, encephalitis plus cardiopulmonary failure, and 2 premature neonates died of hepatic failure, disseminated intravascular coagulation, sepsis-like syndrome and myocarditis. Eighteen had neurologic sequelae, including 7 with limb weakness, 5 with epilepsy, 2 with sixth cranial nerve palsy, 3 with cerebral palsy, 4 with psychomotor retardation, 2 with spasticity, and 1 with hearing loss. Factors associated with unfavorable outcomes (death or sequelae) included younger age (p=0.0003), higher peak white blood cell count (WBC) [p=0.0009] and skin rash (p=0.005). Younger age and higher peak WBC were poor prognostic factors of severe enterovirus CNS infection. Death was related to neonatal enterovirus infection and enterovirus 71 infection in young children.
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PMID:Clinical features and factors of unfavorable outcomes for non-polio enterovirus infection of the central nervous system in northern Taiwan, 1994-2003. 1634 42

Melioidosis which is infection with Burkholderia pseudomallei, is an important cause of sepsis in India, southeast Asia and northern Australia. Mortality is high and treatment is problematic. Neurological melioidosis is unusual but meningoencephalitis, encephalomyelitis and brain microabscess can occur Dural sinus thrombosis is not an uncommon cerebrovascular disorder with various etiologies. Hypercoagulable state, pregnancy, dehydration, certain blood dyscrasia and contraceptive pills are common causes however meningitis and local head & neck infections may lead to this condition. Dural sinus thrombosis complicating septicemic melioidosis has never been reported. The authors report a 42-year-old Thai man suffering from septicemic melioidosis with dural sinus thrombosis. He had high fever, headache, left hemiparesis, focal seizure and increased intracranial pressure. Diabetes and mild alcoholic cirrhosis were diagnosed in this admission. CT scan, MRI brain and MRV revealed superior saggital sinus thrombosis with complicating venous infarction over right posterior parietal lobe. Hemoculture demonstrated Burkholderia pseudomallei and CSF was acellular Investigations for causes of dural sinus thrombosis were all negative. This patient gradually improved after treatment with ceftazidime, antiepileptic drug and heparin without clinical recurrence. Neuromelioidosis is a rare syndrome that may present as brain abscess, encephalitis or meningoencephalitis. The authors report dural sinus thrombosis associated with septicemic melioidosis. The authors' hypothesis of venous thrombosis in the presented case is sepsis induced hypercoagulable state. Physicians should be aware of cerebral venous thrombosis in case of suspicious melioidosis with neurological involvement. Prompt treatment with intravenous heparin and antibiotic is potentially effective.
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PMID:Dural sinus thrombosis in melioidosis: the first case report. 1657 13

Reduced level of consciousness is a common clinical finding in acutely sick patients. In the majority of cases a cause for the encephalopathy is readily identifiable,whilst in a minority the aetiology is more difficult to ascertain. Frequently the onset of encephalopathy is associated with, or follows, infection. The mechanisms through which infection leads to encephalopathy are diverse. They range from direct microbial invasion of the brain or its supporting structures, to remote, infection-triggered mechanisms such as acute disseminated encephalomyelitis. Most common however, is the encephalopathy caused through a remote effect of systemic sepsis-septic encephalopathy. This article discusses the clinical presentation and underlying pathogeneses of the acute encephalopathies associated with infection, aiming to aid both their recognition and treatment.
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PMID:Infection-associated encephalopathies: their investigation, diagnosis, and treatment. 1671


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