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)

Community-acquired pneumonia (CAP) is a major cause of morbidity and mortality in elderly patients. Therefore, efforts to optimize the healthcare process for patients with CAP are warranted. An organized approach to management is likely to improve clinical results. Assessing the severity of CAP is crucial to predicting outcome, deciding the site of care, and selecting appropriate empirical therapy. Unfortunately, current prognostic scoring systems for CAP such as CURB-65 (confusion, uraemia, respiratory rate, low blood pressure and 65 years of age) or the Pneumonia Severity Index have not been validated specifically in older adults, in whom assessment of mortality risk alone might not be adequate for predicting outcomes. Obtaining a microbial diagnosis remains problematic and may be particularly challenging in frail elderly persons, who may have greater difficulties producing sputum. Effective empirical treatment involves selection of a regimen with a spectrum of activity that includes the causative pathogen. Although most cases of CAP are probably caused by a single pathogen, dual and multiple infections are increasingly being reported. Streptococcus pneumoniae remains the overriding aetiological agent, particularly in very elderly people. However, respiratory viruses and 'atypical' organisms such as Chlamydia pneumoniae are being described with increasing frequency in old patients, and aspiration pneumonia should also be taken into consideration, particularly in very elderly subjects and those with dementia. Age >65 years is a well established risk factor for infection with drug-resistant S. pneumoniae. Clinicians should be aware of additional risk factors for acquiring less common pathogens or antibacterial-resistant organisms that may suggest that additions or modifications to the basic empirical regimen are warranted. In addition to administration of antibacterials, appropriate supportive therapy, covering management of severe sepsis and septic shock, respiratory failure, as well as management of any decompensated underlying disease, may be critical to improving outcomes in elderly patients with CAP. Immunization with pneumococcal and influenza vaccines has also been demonstrated to be beneficial in numerous large studies. There is good evidence that implementation of guidelines leads to improvement in clinical outcomes in elderly patients with CAP, including a reduction in mortality. Protocols should address a comprehensive set of elements in the process of care and should periodically be evaluated to measure their effects on clinically relevant outcomes. Assessment of functional clinical outcome variables, in addition to survival, is strongly recommended for this population.
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PMID:Improving outcomes of elderly patients with community-acquired pneumonia. 1858 47

Hypercytokinemia is gaining recognition as the mechanism of fatality from influenza. No work to date has addressed the role of high mobility group box 1 protein (HMGB1) in influenza, the parallel being that in other severe proinflammatory cytokine syndromes (e.g., sepsis and malaria) levels of circulating HMGB1 are elevated and may correlate with death. Using a commercially available ELISA for HMGB1, we found that HMGB1 was not increased in the plasma of influenza virus-infected mice (A/Japan/305/57) on day 7 post infection, about the time of peak mortality, and peak levels of HMGB1 in the plasma did not occur until relatively late in infection, on day 9 post infection. In keeping with the late peak of HMGB1 being unassociated with mortality, administration of ethyl pyruvate, which inhibits active secretion but not passive release of HMGB1, to influenza virus-infected mice, did not affect their survival. Further work is required to determine whether influenza virus infection induces passive release of HMGB1, and whether HMGB1 neutralization with a specific Ab would improve survival.
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PMID:Systemic release of high mobility group box 1 protein during severe murine influenza. 1860

Experimental endotoxemia as a model of the initial septic response affects the autonomic nervous system with profound cardiovascular sequelae. Whether the postsynaptic sympathoneural activity to the muscle vascular bed is altered in the early septic phase remains to be determined. The present study aimed to elucidate the early effects of LPS on muscle sympathetic nerve activity (MSNA) and cardiovascular regulation in healthy humans. Young, healthy volunteers randomly received either an LPS bolus (4 ng/kg body wt, n = 11) or placebo (saline; n = 7). Experimental baroreflex assessment (baseline measurements followed by infusion of vasoactive drugs nitroprusside/phenylephrine) was done prior to and 90 min following LPS or placebo challenge. MSNA, heart rate, blood pressure, and blood levels of catecholamines, TNF-alpha and IL-6 were measured sequentially. Endotoxin but not placebo-induced flu-like symptoms and elevated cytokine levels. In contrast to placebo, LPS significantly suppressed MSNA burst frequency 90 min after injection [mean +/- SE: 12.1 +/- 2.9 vs. 27.5 +/- 3.3 burst/min (post- vs. pre-LPS); P < 0.005] but increased heart rate [78.4 +/- 3.1 vs. 60.6 +/- 2.0 beats/min (post- vs. pre-LPS); P < 0.001]. Baseline blood pressure was not altered, but baroreflex testing demonstrated a blunted MSNA response and uncoupling of heart rate modulation to blood pressure changes in the endotoxin group. We conclude that endotoxin challenge in healthy humans has rapid suppressive effects on postsynaptic sympathetic nerve activity to the muscle vascular bed and alters baroreflex function which may contribute to the untoward cardiovascular effects of sepsis.
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PMID:Endotoxemia causes central downregulation of sympathetic vasomotor tone in healthy humans. 1863 46

Community-acquired pneumonia (CAP) and sepsis are important causes of morbidity and mortality. We describe the development of two molecular assays for the detection of 11 common viral and bacterial agents of CAP and sepsis: influenza virus A, influenza virus B, respiratory syncytial virus A (RSV A), RSV B, Mycoplasma pneumoniae, Chlamydophila pneumoniae, Legionella pneumophila, Legionella micdadei, Bordetella pertussis, Staphylococcus aureus, and Streptococcus pneumoniae. Further, we report the prevalence of carriage of these pathogens in respiratory, skin, and serum specimens from 243 asymptomatic children and adults. The detection of pathogens was done using both a manual enzyme hybridization assay and an automated electronic microarray following reverse transcription and PCR amplification. The analytical sensitivities ranged between 0.01 and 100 50% tissue culture infective doses, cells, or CFU per ml for both detection methods. Analytical specificity testing demonstrated no significant cross-reactivity among 19 other common respiratory organisms. One hundred spiked "surrogate" clinical specimens were all correctly identified with 100% specificity (95% confidence interval, 100%). Overall, 28 (21.7%) of 129 nasopharyngeal specimens, 11 of 100 skin specimens, and 2 of 100 serum specimens from asymptomatic subjects tested positive for one or more pathogens, with S. pneumoniae and S. aureus giving 89% of the positive results. Our data suggest that asymptomatic carriage makes the use of molecular assays problematic for the detection of S. pneumoniae or S. aureus in upper respiratory tract secretions; however, the specimens tested showed virtually no carriage of the other nine viral and bacterial pathogens, and the detection of these pathogens should not be a significant diagnostic problem. In addition, slightly less sensitive molecular assays may have better correlation with clinical disease in the case of CAP.
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PMID:Detection of 11 common viral and bacterial pathogens causing community-acquired pneumonia or sepsis in asymptomatic patients by using a multiplex reverse transcription-PCR assay with manual (enzyme hybridization) or automated (electronic microarray) detection. 1865 Mar 51

Over last decade problem of infectious diseases in Poland remains stable with trends of decreasing incidence of most reported infectious diseases. In particular there was observed decrease in incidence of tuberculosis and foodborne infections causes by Salmonella sp. On the other hand it was observed increase of reported foodborne infections caused by Campylobacter and Yersinia as well and viral ones caused by noroviruses and rotaviruses. Despite marked increase of diagnosed and reported cases sensitivity of reporting of those infections remains unacceptably low. Reported incidence of HIV infections remains relatively stable over last years. But increased fraction of heterosexually transmitted cases points to the problem of increased incidence out of so called "risk groups" among the general population. It was also noted worrisome increase of incidence of syphilis. The highest incidence was noted regarding influenza and other upper respiratory tract infections. Low level of vaccinations against influenza remains the problem which requires continuous health promotion efforts. The best epidemiological situation was observed among vaccine preventable diseases, which reflects effectiveness of vaccination program. Though widening of our program into several important infections included in vaccination programs of other EU countries would be needed in oncoming years. Infectious diseases caused 0.70% of deaths. Mortality from infectious diseases was 6.8/100,000 and was significantly higher among men (8.8) then among women. (5.0). In urban settings mortality from infectious diseases was higher (7.4/100,000) then in the country (5.8). In particular districts (voivodeships) mortality indices remained in the range of 5.2 (podlaskie) to 9.7 (slaskie). The highest number of deaths was caused by sepsis (41.1%, without neonatal sepsis).
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PMID:[Infectious diseases in Poland in 2006]. 1880 59

Infections of the respiratory system are responsible for the majority of hospitalizations and deaths in pediatric patients in developing countries. We selected 177 necropsies of pediatric patients who died as a result of serious respiratory infections. The histopathological findings and epidemiological data were reviewed, and lung tissue samples were separated for immunohistochemistry testing. Conventional immunohistochemistry techniques were used to detect viral antigens in formalin-fixed, paraffin-embedded (FF-PE) lung tissue samples using a pool of monoclonal antibodies against respiratory viruses (respiratory syncytial virus, influenza A and B, adenovirus, and parainfluenza 1, 2, and 3 viruses) as primary antibodies. The histopathological findings were classified into bronchopneumonia (BCP) and interstitial pneumonitis (IP) patterns. The immunohistochemistry results were compared with histopathological patterns and epidemiological data. Positive results for viruses were found in 34% and 62.5% of the BCP and IP cases, respectively. Males and infants below 1 year of age were more frequent in the group that had positive results for viruses. Acute enteritis was the main cause of hospitalization and sepsis the most frequent cause of death in this group. A clear seasonal distribution was observed, with the majority of cases occurring in the 2nd and 3rd trimesters (autumn and winter) of each year in the period studied. Immunohistochemistry is an affordable and easy-to-perform method for viral-antigen detection in FF-PE tissue samples. Although BCP is a classic histopathological pattern found in bacterial infections, it is possible that children with serious respiratory infections had concomitant viral and bacterial infections, regardless of their previous immunologic state.
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PMID:Respiratory viruses in pediatric necropsies: an immunohistochemical study. 1901 65

Influenza A viruses causes a variety of illnesses in humans. The most common infection, seasonal influenza, is usually a mild, self-limited febrile syndrome, but it can be more severe in infants, the elderly, and immunodeficient persons, in whom it can progress to severe viral pneumonitis or be complicated by bacterial superinfection, leading to pneumonia and sepsis. Seasonal influenza also occasionally results in neurologic complications. Rarely, viruses that have spread from wild birds to domestic poultry can infect humans; such "avian influenza" can range in severity from mild conjunctivitis through the rapidly lethal disease seen in persons infected with the H5N1 virus that first emerged in Hong Kong in 1997. To develop effective therapies for this wide range of diseases, it is essential to have laboratory animal models that replicate the major features of illness in humans. This review describes models currently in use for elucidating influenza pathogenesis and evaluating new therapeutic agents.
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PMID:Animal models for the study of influenza pathogenesis and therapy. 1917 18

A prospective epidemiological study was conducted to evaluate the incidence of febrile cough episodes among adult Muslims travelling from Marseille to Saudi Arabia during the Hajj pilgrimage and to assess if use of statin had an influence on this incidence. In total, 580 individuals were presented with a questionnaire. A significant proportion of individuals had chronic medical disorders, e.g. diabetes mellitus (132, 22.8%) and hypertension (147, 25.3%). Pilgrims had a low level of education and a low employment rate. Sixty (10.3%) were treated with statins for hypercholesterolemia. Four hundred and fourty-seven pilgrims were presented a questionnaire on returning home. A total of 74 travellers (16.6%) experienced fever during their stay in Saudi Arabia (67 attended a doctor) and 271 (60.6%) had cough (259 attended a doctor); 70 travellers with cough were febrile (25.9%). Seventy per cent of the travellers who suffered cough episodes developed their first symptoms within 3 days, suggesting a human to human transmission of the responsible pathogen, with short incubation time as evidenced by a bimodal distribution of cough in two peaks at a 24 h interval. None of demographical and socioeconomic characteristics, underlying diseases or vaccination against influenza significantly affected the occurrence of cough. Diabetes correlated with an increased risk of febrile cough (OR = 2.02 (1.05-3.89)) as well as unemployment (OR = 2.22 (0.91-5.53)). Use of statins had no significant influence on the occurrence of cough and/or fever during the pilgrimage. This result suggests that while treatment with a statin has been demonstrated to reduce the mortality from severe sepsis associated with respiratory tract infections, it probably does not play a role in the outcome of regular febrile cough episodes as observed in the cohort studied here.
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PMID:Incidence of Hajj-associated febrile cough episodes among French pilgrims: a prospective cohort study on the influence of statin use and risk factors. 1941 5

Meticillin-resistant Staphylococcus aureus (MRSA), usually known as a nosocomial pathogen, has emerged as the predominant cause of skin and soft-tissue infections in many communities. Concurrent with the emergence of community-acquired MRSA (CA-MRSA), there have been increasing numbers of reports of community-acquired necrotising pneumonia in young patients and others without the classic health-care-associated risk factors. Community-onset necrotising pneumonia due to CA-MRSA is now recognised as an emerging clinical entity with distinctive clinical features and substantial morbidity and mortality. A viral prodrome (eg, influenza or influenza-like illness) followed by acute onset of shortness of breath, sepsis, and haemoptysis is the most frequent clinical presentation. The best treatment of this partly toxin-mediated disease has not been clearly defined. Whereas cases of CA-MRSA pneumonia have now been reported from almost every continent, the overall burden of disease of this emerging syndrome remains incompletely described. We report two related cases of community-onset pneumonia due to the MRSA USA300 genotype and review the literature regarding the emergence of CA-MRSA pneumonia.
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PMID:Emergence of community-acquired meticillin-resistant Staphylococcus aureus strain USA300 as a cause of necrotising community-onset pneumonia. 1946 78

The activity of innate immunity is not simply dictated by the presence of an antigen but also by the balance between negative regulatory and immune potentiator pathways. Even in the absence of antigen, innate immunity can 'inflame' if negative regulators are absent. This resting state is adaptable and dictated by environmental influences, host genetics and past infection history. A return to homoeostasis post inflammation may therefore not leave the tissue in an identical state to that prior to the inflammatory event. This adaptability makes us all unique and also explains the variable outcome experienced by a diverse population to the same inflammatory stimulus. Using murine models we have identified that influenza virus causes a long-term modification of the lung microenvironment by a de-sensitization to bacterial products and an increase in the myeloid negative regulator CD200R (CD200 receptor). These two events prevent subsequent inflammatory damage while the lung is healing, but also they may predispose to bacterial colonization of the lower respiratory tract should regulatory mechanisms overshoot. In the extreme, this leads to bacterial pneumonia, sepsis and death. A deeper understanding of the consequences arising from innate immune cell alteration during influenza infection and the subsequent development of bacterial complications has important implications for future drug development.
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PMID:The innate immune rheostat: influence on lung inflammatory disease and secondary bacterial pneumonia. 1961 99


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