Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The neurologic symptoms in human shigellosis have often been attributed to Shiga toxin, although its exact role has not been determined. By use of a [3H] thymidine-labeled HeLa cell assay, cytotoxic activity was demonstrated in stool but not cerebrospinal fluid or serum from five patients with shigellosis presenting with seizures or encephalopathy. Bacterial isolates produced 16.0-88.2 CD50 (50% cytotoxic dose) of cytotoxin/mg of protein. The toxin activity in stool and the cytotoxic activity of the isolates were not neutralized by antiserum to purified Shiga toxin. DNA hybridization studies showed that Shigella isolates from these patients lacked the structural genes for Shiga toxin. The cytotoxin produced was also distinct from Shiga-like toxins I and II. Sonicates of the Shigella strains injected intraperitoneally into mice caused lethargy and lethality. The toxin activity was heat-labile and sensitive to trypsin, indicating that its active component is protein. Ultrafiltration and gel filtration chromatography showed a molecular mass of 100-125 kDa. Thus Shiga toxin production is not essential for the development of neurologic manifestations of shigellosis; other toxic products may play a role.
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PMID:The association of Shiga toxin and other cytotoxins with the neurologic manifestations of shigellosis. 232 46

An approach for studying neurotoxicity of bacterial products is presented. Pentylenetetrazol, a convulsant drug, was injected into mice, and increased sensitivity to pentylenetetrazol was used as an indicator of neurotoxicity. The preinjection of sonicates of Shigella dysenteriae 60R or Escherichia coli H30 (producing Shiga toxin or Shiga-like toxin I, respectively) enhanced the response of mice to pentylenetetrazol within 6 h. This was indicated by a higher mean convulsion score, increased number of mice responding with convulsions, and induction of seizures in animals pretreated with a subepileptic dose of pentylenetetrazol. Preinjection of purified Shiga toxin significantly changed the response to pentylenetetrazol only when coadministered with bacterial lipopolysaccharide (LPS); mean convulsion scores were 1.6 and 0.9 for the Shiga toxin-LPS group and controls, respectively. LPS alone did not affect sensitivity to pentylenetetrazol. These results suggest that Shiga toxin and LPS together induce neurologic disorders early in the course of infection.
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PMID:An animal model for the study of neurotoxicity of bacterial products and application of the model to demonstrate that Shiga toxin and lipopolysaccharide cooperate in inducing neurologic disorders. 775

A 71-year-old woman presented with altered level of consciousness following episodes of diarrhea and abdominal pain. Shigella sonnei was later cultured from her stool. Although neurological complications, primarily seizures, have been reported sequelae in children afflicted shigellosis, there are only rare cases of encephalopathy in affected adults. A brief discussion of the neurological complications of Shigella infection and the yet undetermined role of Shiga toxin in producing neurotoxicity are presented.
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PMID:Shigella-induced encephalopathy in an adult. 892 41

Acute infectious disease presentations among many at-risk patient groups (eg, uninsured, homeless, and recent immigrants) are frequently seen in emergency departments. Therefore EDs may be useful sentinel sites for infectious disease surveillance. This article describes the background, development, and implementation of EMERGE ncy ID NET, an interdisciplinary, multicenter, ED-based network for research of emerging infectious diseases. EMERGE ncy ID NET was established in cooperation with the National Center for Infectious Diseases, Centers for Disease Control and Prevention (CDC) as part of the CDC's strategy to expand and complement existing disease detection and control activities. The network is based at 11 university-affiliated, urban hospital EDs with a combined annual patient visit census of more than 900,000. Data are collected during ED evaluation of patients with specific clinical syndromes, and are electronically stored, transferred, and analyzed at a central receiving site. Current projects include investigation of bloody diarrhea and the prevalence of Shiga toxin-producing Escherichia coli, animal exposures and rabies postexposure prophylaxis practices, seizures and prevalence of neurocysticercosis, nosocomial ED Mycobacterium tuberculosis transmission, and hospital isolation bed use for adults admitted for pneumonia or suspected tuberculosis. EMERGE ncy ID NET also was developed to be a mechanism for rapidly responding to new diseases or epidemics. Future plans include study of antimicrobial use, meningitis, and encephalitis, and consideration of other public health concerns such as injury and national and international network expansion.
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PMID:EMERGEncy ID NET: an emergency department-based emerging infections sentinel network. The EMERGEncy ID NET Study Group. 983 68

Convulsions and encephalopathy are common complications of Shiga toxin (Stx)-producing Shigella and enterohemorrhagic Escherichia coli infections. In previous studies, we demonstrated that Stx and lipopolysaccharide (LPS) act in concert to enhance mice sensitivity to pentylenetetrazole (PTZ)-induced seizures via mechanisms involving tumor necrosis factor alpha (TNFalpha), interleukinl beta and nitric oxide. To further elucidate the role of the host response in Shigella-related seizures, we studied the ability of Shigella dysenteriae and its products to modulate seizures in C3H/HeJ (lps(d/d)) and in C3H/HeN (lps(n/n) mice. Injection of S. dysenteriae 60R sonicate elevated plasma TNFalpha and enhanced the convulsive response to PTZ in both mouse strains. Induced TNFalpha levels were markedly lower in LPS-hyporesponsive C3H/HeJ mice than in LPS- responsive C3H/HeN mice: 7.4 ng/ml vs 44 ng/ml (induced by 4LD50). Accordingly, a higher dose of S. dysenteriae sonicate was needed to sensitize the C3H/HeJ mice to seizures. Stx or LPS alone did not enhance seizures in either strain. Stx together with LPS enhanced seizures in LPS-responsive mice, but not in LPS-hyporesponsive mice in which they induced only a minor elevation in TNFalpha levels (1.5 ng/ml). As compared to LPS-responsive mice, the LPS-hyporesponsive mice were less susceptible to the lethal effects of Shigella sonicate and were resistant to the lethal effect of purified Stx with LPS. These results demonstrate the crucial role of the host response with regard to the sensitivity to to LPS, and specifically TNFalpha production, in Shigella lethality and Shigella-related seizures.
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PMID:Enhancement of pentylenetetrazole-induced seizures by Shigella dysenteriae in LPS-resistant C3H/HeJ mice: role of the host response. 1200 30

Various drugs have been associated with the development of thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS). Among the biologic agents, alpha-interferon therapy, used for treatment of hepatitis B and chronic myelogenous leukemia, has been associated with TTP in a few recent reports. The authors report the first case of TTP/HUS occurring in a metastatic melanoma patient receiving treatment with high-dose interleukin-2 (IL-2). A 57-year-old patient with malignant melanoma presented with seizures 3 days after completing the first week of high-dose IL-2, and the characteristic hematologic picture revealed TTP/HUS. This occurrence is unlikely to be explained by the association with malignant melanoma, which was not presenting with widespread visceral disease at the time of the occurrence, or by the use of other medications. Similar cytokine release profiles are encountered in TTP, HUS caused by Shiga toxin-1, HUS caused by E. coli O157, after IL-2 or IL-2-containing biochemotherapy, as well as in TTP caused by interferon-alpha. This cytokine profile could reflect a common cause, or just the presence of similar pathways involved.
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PMID:Thrombotic thrombocytopenic purpura/hemolytic uremic syndrome associated with high-dose interleukin-2 for the treatment of metastatic melanoma. 1572 58

During one year from November 2002 to October 2003, 810 patients with epilepsy were examined in Shiga Medical Center for Children, and 186 patients (23%) were over 18 years old. Among them, 162 adult patients (male; 52%, female; 48%) were regularly examined at the outpatient-clinic. Seizures persisted in 56% of these adult patients. Over 80% of the patients were classified as symptomatic epilepsy. Seventy-eight percent of the cases were combined with physical or mental disability. Six percent of the patients had psychological disorders and 11% of the patients had internal diseases. Fifteen percent of the patients had jobs, 4% were married, and 8% had driver's licenses. Seventy percent of the patients were not independent because of their handicap. In our children's hospital, adult patients with epilepsy are increasing, and a countermeasure is necessary. It is important to join networks between regional adult hospitals and clinics. On the other hand, pediatric neurologists must study psychological and internal diseases, management of women with epilepsy, and employment and driving in patients with epilepsy.
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PMID:[Treatment of adult patients with epilepsy in the children's hospital]. 1591 37

The inflammatory response of host endothelial cells is included in the development of vascular damage observed in enterohemorrhagic Escherichia coli (EHEC) infection, resulting in hemolytic uremic syndrome (HUS). The response to a non-conventional treatment for a group of D+ HUS (diarrhea positive HUS) patients, with clinical hemodynamic parameters of septic shock was evaluated in this prospective study (1999-2003). Twelve children 2.8 +/- 0.6 years old, with D+ HUS produced by E. coli infection with serological evidence of Shiga toxin, presenting severe unstable hemodynamic parameters and neurological dysfunction at onset, were studied. The protocol included fresh frozen plasma infusions, methylprednisolone pulses (10mg/k/day) for three consecutive days and plasma exchange for five days, starting after admission to the intensive care unit (ICU). The twelve patients with increased pediatric risk of mortality (PRISM) score: 18 +/- 2 after admission to intensive care unit (ICU), required dialysis for 17.4 +/- 4 days, mechanical ventilator assistance for 10 +/- 1 days and early inotropic drugs support for 10.5 +/- 1 days. Neurological dysfunction included generalized tonic-clonic seizures lasting for 5.4 +/- 1 days, n:8. Focal seizures were present in the remaining patients. Dilated cardiomyopathy was present in 6 children. Eight children suffered hemorrhagic colitis. Nine patients survived. Within one year of the injury, neurological sequelae, Glasgow outcome scale (GOS) 3 and 4, were present in two patients, chronic renal failure in one patient. We suggest that early introduction of this protocol could benefit D+ HUS patients with hemodynamic instability and neurological dysfunction at onset. Further studies are likely to elucidate the mechanisms involved in this early adverse clinical presentation of D+ HUS patients.
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PMID:Postdiarrheal Shiga toxin-mediated hemolytic uremic syndrome similar to septic shock. 1629 34

Hemolytic uremic syndrome is caused primarily by Shiga toxin-producing Escherichia coli O157:H7. The most common cause of acute renal failure in children, hemolytic uremic syndrome also can occur in adults. Characteristic features of the syndrome are microangiopathic anemia, thrombotic thrombocytopenia, and renal failure. Although the presentation of this syndrome is diverse, the classic prodromal illness is bloody diarrhea following ingestion of hamburger meat contaminated with E. coli O157:H7, the most common mode of infection in the United States. Children with hemolytic uremic syndrome generally present with gastroenteritis complaints (e.g., abdominal pain or tenderness, nausea or vomiting, fever, anemia); affected adults may be asymptomatic. Complications from hemolytic uremic syndrome can include intussusception, chronic renal failure, and seizures in severe cases. Because an incubation period of approximately one week occurs between the start of diarrhea and the onset of hemolytic uremic syndrome, physicians should maintain a high index of suspicion; early laboratory testing is important to diagnose and manage this syndrome. Obtaining a complete blood count and stool culture and performing Shiga toxin testing are the first of a series of tests that may help diagnose hemolytic uremic syndrome.
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PMID:Hemolytic uremic syndrome: an emerging health risk. 1700 34

Shiga toxin (Stx) from enterohemorrhagic Escherichia coli (STEC) is the main cause of hemorrhagic colitis which may derive to hemolytic-uremic syndrome (HUS). HUS is characterized by acute renal failure, thrombocytopenia and microangiopathic hemolytic anemia. Mortality in the acute stage has been lower than 5% of total affected argentine children with endemic HUS. Common signs of severe CNS involvement leading to death included seizures, alteration of consciousness, hemiparesis, visual disturbances, and brainstem symptoms. The main purpose of the present work was to study the direct involvement of Stx2 in brain cells by intracerebroventricular (i.c.v.) administration of Stx2. Immunodetection of Stx2 was confirmed by immunoelectron cytochemistry in different subsets and compartments of affected caudate putamen cells of corpus striatum. Transmission electron microscopy (TEM) studies revealed apoptotic neurons, glial ultrastructural alterations and demyelinated fibers. The i.c.v. microinfusion was applied for the first time in rats to demonstrate the direct action of Stx2 in neurons and glial cells. The toxin may affect brain neuroglial cells without the involvement of proinflammatory or systemic neurotoxic elements.
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PMID:Intracerebroventricular administration of Shiga toxin type 2 induces striatal neuronal death and glial alterations: an ultrastructural study. 1761 Aug 52


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