Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085437 (bacterial meningitis)
 4,038 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We analysed retrospectively 48 hospitalized patients with fever of unknown origin (FUO) from 1982 through 1988. The criteria of FUO were (1) temperature of more than 38.3 degrees C documented on several occasions (2) overall duration of illness more than three weeks, (3) uncertain diagnosis till one week after hospitalization. Of this group of FUO, 25 patients (52.1%) were found to have infections, 8 patients (16.7%) had collagen disorders, 7 patients (14.6%) had neoplastic disorders, 3 patients (6.3%) were crohn disease and 5 patients (10.4%) were undiagnosed. Among infectious diseases, chronic tonsillitis was the most frequent (5 patients: 20%) and they were diagnosed by the provocative examination. Non bacterial meningitis and cervical lymphadenitis were diagnosed in all 3 patients (12% in all), Adult Still's disease was found in 3 patients (37.5%) and systemic lupus erythematosus (SLE) in 2 patients (25%) in collagen disease. Immunoblastic lymphadenopathy was diagnosed in 3 patients (42.9%) of malignant diseases. Three cases of Crohn disease were revealed in all the patients of the miscellaneous group. Duration of fever was relatively short in infection diseases compared to malignant and Crohn diseases. The most common laboratory abnormality is an elevated erythrocyte sedimentation rate (89.6%). As the final diagnosis of FUO are changing with the development of diagnostic techniques, a new criteria of FUO is necessary.
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PMID:[A retrospective study of hospitalized patients with fever of unknown origin (FUO) past six years]. 235 14

Penetration of basement membrane is believed to be an essential step in the pathogenesis of bacterial meningitis. Consequently Streptococcus pneumoniae strains were tested for their ability to adhere to reconstituted basement membrane (Matrigel) and in a proceeding step penetrate this membrane by the use of surface activated plasmin. A majority of S. pneumoniae strains tested were found to adhere to reconstituted basement membrane as well as to the purified laminin component. Three out of seventeen strains also adhered to the collagen IV component. All the investigated strains also demonstrated a capacity to bind plasminogen with up to 42,000 plasminogen binding sites per bacterium as estimated by Scatchard analysis. Two strains selected for optimal adhesion and plasminogen binding were further tested for basement membrane penetration using a dual chamber model. Our data show that penetration was achieved within 3-4 h in the presence of plasminogen whereas without plasminogen no strain was able to penetrate during a 21 h incubation. The results suggest a potential role of surface associated plasminogen in bacterial penetration of basement membranes and extracellular matrix.
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PMID:Surface bound plasmin promotes migration of Streptococcus pneumoniae through reconstituted basement membranes. 1008 58

This is Part II of a 2-part paper on fever of unknown origin (FUO) in children. It examines the aetiology and management of prolonged FUO in children and the difficulties in the management of FUO in children in developing countries. Part I of this paper discussed acute FUO in children and was published in the March 2001 issue of Paediatric Drugs. Prolonged FUO is documented fever of more than 7 to 10 days which has no apparent source and no apparent diagnosis after 1 week of clinical investigations. About 34% of cases of prolonged FUO are caused by infections, with bacterial meningitis and urinary tract infection accounting for about 6.5 and 11.4%, respectively, of cases attributable to infections. Chronic infections, particularly tuberculosis and 'old' disorders such as Kawasaki disease, cat-scratch disease and Epstein-Barr virus infection presenting with 'new' manifestations, collagen-vascular diseases and neoplastic disorders are the other issues of major concern in prolonged FUO. Overall, however, there is a trend towards an increased number of undiagnosed cases. This is due to advancements in diagnostic techniques, such that illnesses which were previously common among the causes of prolonged FUO are now diagnosed earlier, before the presentation becomes that of prolonged FUO. Clinical examination supplemented with laboratory tests to screen for serious bacterial infections should be the mainstay of initial evaluation of children with prolonged FUO. Use of scanning techniques (such as computerised tomography and ultrasound) as additional supplements to this clinical examination may allow for the earlier diagnosis of causes of prolonged FUO in children such as 'occult' abdominal tumours. A common error in management of children with prolonged FUO is the failure to perform a complete history and physical examination; repeated clinical examination and continued observation are of paramount importance in the diagnosis of difficult cases. Major difficulties in the management of FUO in children in developing countries include constraints in the availability and reliability of laboratory tests, cost, misuse of antibiotics and difficulties encountered in the diagnosis of malaria and typhoid fever. Malaria and typhoid fever are major aetiological considerations in both acute and prolonged FUO in children in developing countries. The newer quinolones may hold great promise for the treatment of serious bacterial infections, including meningitis, which are associated with prolonged FUO in developing countries.
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PMID:Management of children with prolonged fever of unknown origin and difficulties in the management of fever of unknown origin in children in developing countries. 1135 97

Escherichia coli NU14, a cystitis isolate used to study the pathogenesis of cystitis and to develop a FimH (type 1 fimbrial adhesin) vaccine, was assessed for extended virulence genotype, phylogenetic background, and FimH sequence and binding phenotype(s). NU14 exhibited the same virulence genotype and was derived from the same (meningitis- and cystitis-associated) subclone of E. coli O18:K1:H7 as the archetypal neonatal bacterial meningitis (NBM) isolate RS218. NU14 also displayed the same Ser62Ala FimH polymorphism as did NBM isolates RS218 and IHE3034-conferring both collagen binding and a distinct monomannose binding capability (which characterizes uropathogenic but not commensal E. coli and dramatically increases adherence to uroepithelial cells). These findings establish that strain NU14 exhibits numerous urovirulence-associated traits and derives from the single most prevalent clonal group in acute cystitis. They provide further evidence of clonal and pathotypic similarities between cystitis and NBM isolates of E. coli O18:K1:H7.
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PMID:Clonal and pathotypic analysis of archetypal Escherichia coli cystitis isolate NU14. 1174 Jul 31

The role of infectious and inflammatory causes of stroke is much more significant in children than in adults. Conversely, that of atherosclerotic disease, ischaemic heart disease and hypertensive haemorrhages has a lesser prominence in children. Bacterial meningitis caused by Streptococcus pneumoniae, Haemophilus influenzae, or Neiserria meningitidis has been known to cause stroke in children. The mechanism appears to be the spread of meningeal inflammation to involve the walls of intracranial vessels, resulting in arterial thrombosis with ischaemia or rupture with haemorrhage. Other infections caused by atypical bacterial agents such as Mycoplasma tuberculosis and viral agents such as varicella-zoster virus have also been well documented as causes of stroke. Non-infectious, inflammatory causes of stroke, such as collagen vascular disease and primary angiitis of the central nervous system, have been reported in children as well as adults. In this review, we will focus on recent advances in the field of childhood stroke caused by infectious and inflammatory disorders.
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PMID:Infectious and inflammatory disorders of the circulatory system and stroke in childhood. 1192 29

In this study we aimed to investigate the findings in patients with adult-onset Still's disease (AOSD) admitted with fever of unknown origin (FUO) during the last 18 years in our unit, in order to discover the ratio of such patients to all patients with FUO during the same period, and to determine the clinical features of AOSD in FUO. The number and the aetiologies of the patients with FUO diagnosed between 1984 and 2001, and the clinical features of those with AOSD, were taken from the patient files. The diagnosis of AOSD was reanalysed according to the diagnostic criteria of Cush et al. [11]. The presumed diagnoses before a diagnosis of AOSD was established were also noted. The chi(2) and Fisher's exact tests were used for statistical analysis. We studied 130 patients with a diagnosis of FUO, 36 (28%) of whom had collagen vascular diseases. Of these 36 patients, 20 (56%, 12 female, 8 male, mean age 34 years, range 16-65) had AOSD. Clinical and laboratory findings were as follows: fever (100%), arthralgia (90%), rash (85%), sore throat (75%), arthritis (65%), myalgia (60%), splenomegaly (40%), hepatomegaly (25%), lymphadenopathy (15%), anaemia (65%), neutrophilic leukocytosis (90%), increased erythrocyte sedimentation rate (100%), elevated transaminase levels (65%), a negative RF (100%), and a negative FANA (80%). Antibiotics had been prescribed in 18 (90%) of cases. The presumed infectious diagnoses were streptococcal tonsillitis/pharyngitis (50%), infective endocarditis (four patients), sepsis (two patients) and acute bacterial meningitis (two patients). The presumed non-infectious diagnoses were acute rheumatic fever (three patients), seronegative rheumatoid arthritis (two patients) and polymyositis (two patients). Sixteen patients were followed for a mean duration of 30 months (range 2-59). A remission was obtained with indomethacin in three cases (19%), and with prednisolone in the remainder. Relapse was detected in three cases (19%). AOSD is one of the most frequent aetiologies of FUO. During the diagnostic course of a patient with FUO, a maculopapular rash and/or arthralgia and/or sore throat should raise the suspicion of AOSD. Because the disease has heterogeneous clinical findings, certain bacterial infections (e.g. streptococcal pharyngitis and sepsis) are generally considered and the prescribing of antibiotics is common.
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PMID:Fever of unknown origin: a review of 20 patients with adult-onset Still's disease. 1274 Jun 70

Matrix metalloproteinases (MMPs) and TNF-alpha converting enzyme (TACE) contribute to the pathophysiology of bacterial meningitis. To date, MMP-inhibitors studied in models of meningitis were compromised by their hydrophobic nature. We investigated the pharmacokinetics and the effect of TNF484, a water-soluble hydroxamate-based inhibitor of MMP and TACE, on disease parameters and brain damage in a neonatal rat model of pneumococcal meningitis. At 1 mg/kg q6h TNF484 reduced soluble TNF-alpha and the collagen degradation product hydroxyproline in the cerebrospinal fluid. Clinically, TNF484 attenuated the incidence of seizures and was neuroprotective in the cortex. Water-soluble MMP-inhibitors may hold promise in the therapy of bacterial meningitis.
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PMID:In pneumococcal meningitis a novel water-soluble inhibitor of matrix metalloproteinases and TNF-alpha converting enzyme attenuates seizures and injury of the cerebral cortex. 1514 98

The meninges comprise the dura mater and the leptomeninges (arachnoid and pia mater). Dura forms an outer endosteal layer related to the bones of the skull and spine and an inner layer closely applied to the arachnoid mater. Leptomeninges have multiple functions and anatomical relationships. The outer parietal layer of arachnoid is impermeable to CSF due to tight intercellular junctions; elsewhere leptomeningeal cells form demosomes and gap junctions. Trabeculae of leptomeninges compartmentalize the subarachnoid space and join the pia to arachnoid mater. In bacterial meningitis leptomeningeal cells secrete cytokines. Pia mater is reflected from the surface of the brain and spinal cord onto arteries and veins, thus separating the subarachnoid space from the brain and cord. A sheath of leptomeninges accompanies arteries into the brain and is related to the pathways for the drainage of interstitial fluid that play a role in inflammatory responses in the brain and appear to be blocked by amyloid-beta in Alzheimer's disease. Specialised leptomeningeal cells in the stroma of the choroid plexus form collagen whorls that become calcified with age. Leptomeningeal cells also form channels in the core and apical cap of arachnoid granulations for the drainage of CSF into venous sinuses. In the spine, leptomeninges form highly perforated intermediate sheets of arachnoid and delicate ligaments that compartmentalize the subarachnoid space; dentate ligaments anchor subpial collagen to the dura mater and stabilize the spinal cord. Despite the multiple anatomical arrangements and physiological functions, leptomeningeal cells retain many histological features that are similar from site to site.
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PMID:Microscopic morphology and histology of the human meninges. 1594 78

Adverse outcome in bacterial meningitis is associated with the breakdown of the blood-brain barrier (BBB). Matrix-metalloproteinases (MMPs) facilitate this process by degradation of components of the BBB. This in turn results in acute complications of bacterial meningitis including edema formation, increased intracranial pressure and subsequent ischemia. We determined the parenchymal balance of MMP-9 and TIMP-1 (tissue inhibitor of MMP) and the structural integrity of the BBB in relation to cortical damage in an infant rat model of pneumococcal meningitis. The data demonstrate that the extent of cortical damage is significantly associated with parenchymal gelatinolytic activity and collagen type IV degradation. The increased gelatinolysis was found to be associated with a brain parenchymal imbalance of MMP-9/TIMP-1. These findings provide support to the concept that MMPs mediated disruption of the BBB contributes to the pathogenesis of bacterial meningitis and that protection of the vascular unit may have neuroprotective potential.
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PMID:In bacterial meningitis cortical brain damage is associated with changes in parenchymal MMP-9/TIMP-1 ratio and increased collagen type IV degradation. 1625 22

This report describes a 38-year-old man with osteogenesis imperfecta who died of a ruptured cerebral artery aneurysm and bacterial meningitis. He had multiple long bone fractures in the past, and approximately 4 months before death, he had surgery to relieve symptoms of basilar impression. The surgery was complicated by a postoperative wound infection. For the next 4 months, he had intermittent headaches and vomiting. He was found dead in his bed at home. At autopsy, he had a ruptured anterior communicating artery aneurysm and bacterial meningitis. Cerebrospinal fluid and blood cultures had growth of Staphylococcus aureus. Osteogenesis imperfecta is a disorder of type I collagen. Type I collagen is present in many tissues, including blood vessels. The etiology of cerebral artery aneurysm formation is multifactorial. Some patients with cerebral artery aneurysms have been shown to have abnormalities in type III collagen. There has not been a reported relationship made between abnormalities in type I collagen and aneurysms. Meningitis can also result in cerebral artery aneurysms, but they are usually due to Aspergillus or Mycobacterium species. The case we report is unique; cerebral artery aneurysm formation may have been due to osteogenesis imperfecta and/or bacterial meningitis.
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PMID:Ruptured cerebral artery aneurysm and bacterial meningitis in a man with osteogenesis imperfecta. 1673 28


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