Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We presented atypical manifestations in tuberculous meningitis (TbM) and herpes simplex encephalitis (HSE), lymphocytic dominant cerebrospinal fluid pleocytosis in bacterial meningitis, and a hitherto easily overlooked critical illness polyneuropathy (CIP) associated with sepsis. 1) We presented 2 TbM patients with atypical manifestations. One patient was a 25-year-old man who exhibited polymorphonuclear (PMN) dominant pleocytosis in CSF throughout his clinical course. He died the next day after a CSF culture yielded the growth of tuberculous bacilli, before receiving appropriate anti-TBM therapy. This was a rare TbM example of persistent PMN dominant CSF pleocytosis. The other patient was a 39-year-old woman whose CSF pleocytosis changed from lymphocytic dominant to PMN dominant about 1 month after the initiation of antituberculous chemotherapy. This CSF change was followed by multiple cerebral infarcts due to vauculitis caused by TbM. Administration of prednisolone caused marked improvement of the patient's symptomatology. Tuberculomas appeared transiently during anti-TbM therapy, consistent with paradoxical progression of tuberculoma. 2) A few patients with HSE may show atypical CSF findings such as PMN dominant pleocytosis, absence of pleocytosis, and low sugar value. Our national survey of HSE patients showed following percentages of these atypical findings: PMN dominant pleocytosis observed in 10% of the patients in the early stage and at the time of exacerbation, no pleocytosis in 0.9% (1 patient), and low sugar value in 4%. 3) Bacterial meningitis typically causes PMN dominant CSF pleocytosis. However, Listeria meningitis (LM) may cause lymphocytic dominant pleocytosis in 30% of the patients, particularly in elderly ones. We showed one such 69-year-old patient with persistent lymphocytic dominant CSF pleocytosis throughout the clinical course. 4) CIP, septic encephalopathy and critical illness myopathy are 3 major complications associated with sepsis. CIP is a frequent cause of neuromuscular weakness due to axonal dysfunction, which occurs to critically ill patients with sepsis, particularly when multiple organ dysfunctions are present. We showed our CIP patient associated with acute bacterial endocarditis and multiple organ failure. We should bear in mind these atypical manifestations, and frequent and important complications associated with sepsis such as CIP, to provide appropriate management to patients with neuro-infection and sepsis.
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PMID:[Neuro-infections to be borne in mind]. 1223 30

An obstetrician examined records of all maternal deaths that occurred in the Chatinkha Maternity Wing of Queen Elizabeth Central Hospital in Blantyre, Malawi, during 1989-1990. None of the deaths were caused by conditions unrelated to pregnancy. In 1989 there were 78 maternal deaths out of 14,272 live births (a maternal mortality ratio of 546/100,000 live births). In 1990 there were 73 maternal deaths out of 14,281 live births (a maternal mortality ratio of 511/100,000 live births). In each year, 37 women died directly from complications of pregnancy, delivery, or their management. In 1989, the leading cause of maternal death was postabortal sepsis (15 cases), followed by obstructed labor (8 cases) and puerperal sepsis (6 cases). In 1990, the leading causes were puerperal sepsis (13 cases) and postabortal sepsis (10 cases). The number of HIV-seropositive women among direct maternal deaths was 8 for both years. In 1990, the cesarean section rate was 6.5%. Women who had undergone a cesarean section faced a risk of puerperal sepsis-related death 8.5 times greater than that of women who had delivered vaginally. The 1990 mortality rate among induced abortion cases may have been as high as 8%. There were 41 and 36 indirect maternal deaths in 1989 and 1990, respectively. The leading causes of indirect maternal death were fever (8 cases) and bacterial meningitis (5 cases). The cause could not be determined in 15 cases. By 1990, the leading causes of indirect maternal death were bacterial meningitis (8 cases) and AIDS (6 cases). 5 of the 8 bacterial meningitis cases tested positive for HIV. The 4 patients with tuberculosis and 3 patients with septicemia were HIV positive. 41% and 56% of maternal deaths in 1989 and 1990, respectively, were avoidable. When one excluded uncertain avoidable factors, 21% and 45% of maternal deaths could not be avoided. The leading avoidable factors were deficient hospital care (18 cases), patient's delay (12 cases), and illegal abortion (10 cases) in 1989; they were patient's delay (10 cases) and illegal abortion (8 cases) in 1990.
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PMID:Maternal mortality at Queen Elizabeth Central Hospital, 1989 to 1990. 1231 71

Although people with bacterial meningitis lack adequate protective antibody against the invading pathogen, most do not have an underlying immunodeficiency. Certain comorbid conditions increase the risk for development of bacterial sepsis and meningitis. In addition, certain congenital complement deficiencies, defects of antibody production, or asplenia may be first recognized by the occurrence of bacterial meningitis, particularly when it occurs in infants or young children. Deficiencies of the terminal components of complement (C5-C9) or properdin have been associated with recurrent or invasive neisserial infections, and asplenia, agammaglobulinemia, and deficiencies of the early components of complement (e.g., C1-C3) are associated with risks of infections caused by Streptococcus pneumoniae, Haemophilus influenzae, and meningococci. The presence of congenital or acquired immunodeficiencies should be considered in persons who present with bacterial meningitis on the basis of the etiology, clinical epidemiology, and presence of other risk factors.
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PMID:Indications for the immunological evaluation of patients with meningitis. 1252 51

Matrix metalloproteinase-9 (MMP-9) appears to contribute to blood-brain barrier damage and neuronal injury in bacterial meningitis. To further explore the function of MMP-9 in meningeal inflammation, we injected 10(4) colony forming units (CFU) of a Streptoccocus pneumoniae type 3 strain into the right forebrain of MMP-9 deficient mice (MMP-9(-/-), n=16) and wild-type controls (129 x B6, n=15). The clinical course of the disease, leukocyte recruitment into the subarachnoid space and bacterial titers in the brain did not differ. Yet, clearance of the bacteria from blood (log CFU/ml 4.7 [3.8/5.4] vs. 3.6 [3.0/4.0]; P=0.005) and spleen homogenates (log CFU/ml 5.3 [4.8/5.5] vs. 4.0 [2.8/4.7]; P=0.01) was reduced in MMP-9 deficient mice. A reduced systemic bacterial clearance of MMP-9(-/-) mice was confirmed in experimental S. pneumoniae peritonitis/sepsis. This implies a compromised systemic, but not intracerebral host response against S. pneumoniae in MMP-9 deficiency.
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PMID:Matrix metalloproteinase-9 deficiency impairs host defense mechanisms against Streptococcus pneumoniae in a mouse model of bacterial meningitis. 1258 31

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

In spite of the progress in antibiotic therapy and immunoprophylaxis Neisseria meningitidis remains one of the major causes of meningitis and sepsis burdened by high mortality. In this paper characteristics of N. meningitidis and in particular its epidemiology, virulence factors, antibiotic therapy and resistance mechanisms, immuno- and chemoprophylaxis, are discussed. Data from the National Reference Centre for Bacterial Meningitis are also presented. These data indicate that this pathogen is the most common laboratory confirmed bacterial etiologic agent of community-acquired meningitis in Poland.
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PMID:[Epidemiology and therapy of infections caused by Neisseria meningitidis]. 1496 44

Neisseria meningitidis is a leading cause of bacterial meningitis and sepsis in the US, Europe and in many other parts of the world, including parts of sub-Saharan Africa (known as the African 'meningitis belt'). There are > 500000 cases of meningococcal disease annually with an estimated death toll of 135000 worldwide. Approximately 10 - 15 % of survivors experience significant morbidity in the form of neurological sequelae, including hearing loss, speech disorders, loss of limbs, mental retardation and paralysis. Disease is usually caused by N. meningitidis serogroups A, B, C, Y or W-135. Prevention of meningococcal disease includes isolation, chemoprophylaxis and vaccination with available polysaccharide vaccines. However, the polysaccharide meningococcal vaccines (i.e., A and C; A, C and W-135; or A, C, Y and W-135) initially developed in the 1970s are generally poorly immunogenic in children or require repeated doses and do not produce long-lasting immunity. Conjugate vaccine technology has been very successfully used in childhood vaccines for the prevention of other bacterial meningitis pathogens, including vaccines against Haemophilus influenzae serotype b (Hib) and more recently, the seven- and nine-valent conjugate pneumococcal vaccines. Newly released meningococcal conjugate vaccines against N. meningitidis serogroup C have been highly efficacious in young children and adolescents, with minimal side effects. Conjugate vaccines targeting other important meningococcal serogroups (e.g., N. meningitidis serogroup A, responsible for the large pandemic outbreaks and the majority of disease in sub-Saharan Africa and serogroups Y and W-135) are under development and together with the serogroup C conjugates, have the potential to significantly impact worldwide sporadic and epidemic meningococcal disease. The search for an effective serogroup B meningococcal vaccine remains elusive. This manuscript reviews the conjugate meningococcal vaccines and their potential for meningococcal disease prevention.
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PMID:Meningococcal conjugate vaccines. 1510 68

A number of new antimicrobial agents have been licensed in the last years, most prominently a number of new antiviral and antimycotic agents. The development of new antibacterial agents has slowed down, new agents are mainly targeted at a small but rapidly growing number of patients infected with bacteria resistant to the current antibiotics. The rates of resistance against antibiotics are rapidly rising, especially for gram-positive cocci and, in addition, for gram-negative nosocomial agents. Rising rates of resistances are further present in chronic viral infections, e. g., HIV infection. Instruments to monitor and minimize the rates of resistances are necessary. Important changes are to be found in a number of infectious complications. For patients with sepsis a new therapeutic principle, drocretogrin, has been found to reduce mortality. Additionally, low-dose corticosteroids in selected patients, close control of blood sugar and other interventions have shown to be effective. Corticosteroids have proven to be effective as well in the reduction of complications in adults with bacterial meningitis, most pronounced in pneumococcal meningitis. With new drugs licensed for the treatment of malaria and changes in the epidemiology, the guidelines for therapy and prevention have been reformulated.
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PMID:[Infectious diseases-Part II: New agents, resistances, and treatment strategies]. 1514 88

The complement C5 deficiency is a recessive autosomal defect associated with recurrent infectious episodes, generally caused by Gram-negative micro-organisms. To date, only two mutations responsible for C5 deficiency have been characterized, both in heterozygosis. In this paper, we evaluate by immunochemical methods the C5 deficiency in a six-member family, in which one member suffered from meningococcal sepsis and several pneumonia episodes; and a second one with two bacterial meningitis episodes and frequent tonsillitis, pneumonia and herpetic episodes. We also characterize the molecular basis of this deficiency. No C5 protein was found in the serum from three of the children. They were found to be homozygous for a double mutation in the exon 40 of the C5 gene. The parents and the other children have half-normal levels of C5, and they were heterozygotes for the double mutation. This mutation modifies the reading frame, leading to a premature stop codon, and the resulting protein lacks 50 amino acids. As a result, homozygotes and heterozygotes have a total or a partial C5 deficiency respectively. This is the first report of a whole molecular characterization of C5 deficiency.
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PMID:C5 complement deficiency in a Spanish family. Molecular characterization of the double mutation responsible for the defect. 1548 49

Recent aspects of pathogen determination and therapeutic management are reviewed based on a clinical analysis of 50 of our adult patients with bacterial meningitis (BM). The sensitivity for detecting pathogens using gram-stained smears and cultures of CSF was high in untreated patients, but low in patients previously treated with antibiotics. Latex agglutination for antibodies of pathogens is rapid and has a potential for determining pathogens in partially treated meningitis. The PCR also has a potential for determining pathogens in pre-treated, culture-negative cases and for detecting whether the bacterial pathogen is resistant or sensitive to antibiotics. The initial empiric regimen of antibiotics has been modified with elevation in the detection rate of drug-resistant bacilli. The proportion of patients undergoing treatment with VCM and/or Carbapenems has recently increased at our department. A combination of dexamethasone under administration of antibiotics has also been established as effective in adult BM. On admission, some patients are difficult to diagnose as BM rather than herpes simplex encephalitis (HSVE). A serum CRP value of >2.0 mg/dl proved useful for such different diagnosis in our patients. The predictors of a poor outcome based on multivariate logistic analysis in our BM patients were level of unconsciousness and sepsis.
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PMID:[Bacterial meningitis: determination of pathogens and therapeutic management]. 1565 10


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