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 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Severe Acute Respiratory Syndrome (SARS) epidemic illustrated the crucial role of infection surveillance and control measures in the combat of any highly transmissible disease. We conducted an interview survey of 121 medical staff 145 doctors, 46 staff nurses and 30 medical assistants) in a state hospital in Malaysia three months after the end of SARS epidemic (from October to December 2003). Staff was grouped according to those directly involved in the care of suspected SARS patients [S+ group n=41] and those who were not [S- group; n=80]. On hand washing following sneezing, coughing and touching patients, the proportions of medical staff that reported an increase after the SARS crisis were 22.3%, 16.5% and 45.5% respectively. On wearing masks, gloves, and aprons when meeting potentially infectious patients, the proportions that reported an increase were 39.7%, 47.1% and 32.2% respectively. Significantly more staff in S+ than S- group reported these increases. Sixty percent of staff was aware of changes in hospital infection control policies after SARS; 93.4% was aware of notifying procedures, and 81.8% was aware of whom to notify in the hospital. Regarding infection isolation ward, Infectious Control Nurse and Infection Control Committee Chairman in the hospital, the proportions of staff that could correctly name them were 39.7%, 38.3% and 15.7% respectively. Significantly more in S+ than S- group could do so. However, more than half the staff claimed ignorance on the knowledge of infection isolation ward (56.2%), Infection Control Nurse (57.9%) and Chairman (65.3%). Our findings demonstrated that SARS crisis had some positive impact on the infection control practices and awareness of medical staff especially on those with direct SARS involvement. Implications for future control of infectious diseases are obvious.
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PMID:Change in infection control practices and awareness of hospital medical staff in the aftermath of SARS. 1588 69

Severe acute respiratory syndrome (SARS) is a newly emerged infectious disease that has caught the medical profession by surprise in 2003. The major clinical features include persistent fever, chills/rigor, myalgia, malaise, dry cough, headache and dyspnoea but diarrhea occurs in 40-70% of patients after hospital admission. Respiratory failure is the major complication of SARS; at least half of the patients require supplemental oxygen during the acute phase whereas about 20% of patients progress to acute respiratory distress syndrome requiring invasive mechanical ventilatory support. In contrast, the severity is generally mild in infected young children. Due to our limited understanding of this new disease, treatment of SARS was empirical in 2003. Protease inhibitor (Lopinavir/ritonavir) in combination with ribavirin may play a role as antiviral therapy in the early phase whereas nelfinavir is a promising alternative. The role of interferon and systemic steroid in preventing immune-mediated lung injury deserves further investigation. In addition, other anti-viral treatment, RNA interference, monoclonal antibody, synthetic peptides, and vaccines are being developed. Rapid diagnosis, early isolation, and good infection control measures are important in preventing spread of the infection.
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PMID:An overview on severe acute respiratory syndrome (SARS). 1631 5

Severe acute respiratory syndrome (SARS) is a recently discovered viral disease, characterized by fever, cough, acute fibrinous pneumonia and high infectivity. Specific pathogen-free (SPF) chickens were immunized with inactivated SARS coronavirus and their eggs were harvested at regular intervals. Yolk immunoglobulin (IgY) was extracted using the water dilution method, followed by further purification on a Sephadex G-75 column. SDS-polyacrylamide gel electrophoresis (SDS-PAGE), Western blot and neutralization test results showed that the IgY obtained was of a high purity and had a strong reactive activity with a neutralization titer of 1:640. Lyophilization and stability tests showed that lyophilized anti-SARS coronavirus IgY had promising physical properties, with no significant reduction in reactive activity and good thermal stability. All these data suggest that the anti-SARS coronavirus IgY could be a new useful biological product for specific antiviral therapy against SARS.
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PMID:Preparation and evaluation of anti-SARS coronavirus IgY from yolks of immunized SPF chickens. 1632 77

The clinical presentation of SARS is nonspecific and diagnostic tests do not provide accurate results early in the disease course. Initial diagnosis remains reliant on clinical assessment. To identify features of the clinical assessment that are useful in SARS diagnosis, the exposure status and the prevalence and timing of symptoms, signs, laboratory and radiographic findings were determined for all adult patients admitted with suspected SARS during the Toronto SARS outbreak. Findings were compared between patients with laboratory-confirmed SARS and those in whom SARS was excluded by laboratory or public health investigation. Of 364 cases, 273 (75%) had confirmed SARS, 30 (8%) were excluded, and 61 (17%) remained indeterminate. Among confirmed cases, exposure occurred in the healthcare environment (80%) or in the households of affected patients (17%); community or travel-related cases were rare (<3%). Fever occurred in 97% of patients by the time of admission. Respiratory findings including cough, dyspnea and pulmonary infiltrates evolved later and were present in only 59, 37 and 68% of patients, respectively, at admission. Direct exposure, fever on the first day of illness, and elevated temperature, pulmonary infiltrates, lymphopenia and thrombocytopenia at admission were associated with confirmed cases. Rhinorrhea, sore throat, and an elevated neutrophil count at admission were associated with excluded cases. In the absence of fever or significant exposure, SARS is unlikely. Other clinical, laboratory and radiographic findings further raise or lower the likelihood of SARS and provide a rational basis for estimating the likelihood of SARS and directing initial management.
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PMID:Early diagnosis of SARS: lessons from the Toronto SARS outbreak. 1658 72

Recently Simmons et al. reported a new mechanism for SARS virus entry into target cells, where MDL28170 was identified as an efficient inhibitor of CTSL-meditated substrate cleavage with IC(50) of 2.5 nmol/l. Based on the molecule fingerprint searching method, 11 natural molecules were found in the Traditional Chinese Medicines Database (TCMD). Molecular simulation indicates that the MOL376 (a compound derived from a Chinese medicine herb with the therapeutic efficacy on the human body such as relieving cough, removing the phlegm, and relieving asthma) has not only the highest binding energy with the receptor but also the good match in geometric conformation. It was observed through docking studies that the van der Waals interactions made substantial contributions to the affinity, and that the receptor active pocket was too large for MDL21870 but more suitable for MOL736. Accordingly, MOL736 might possibly become a promising lead compound for CTSL inhibition for SARS therapy.
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PMID:Virtual screening for finding natural inhibitor against cathepsin-L for SARS therapy. 1699 15

SARS coronavirus (SARS-CoV) emerged in 2002 as an important cause of severe lower respiratory tract infection in humans and in vitro models of the lung are needed to elucidate cellular targets and the consequences of viral infection. The severe and sudden onset of symptoms, resulting in an atypical pneumonia with dry cough and persistent high fever in cases of severe acute respiratory virus brought to light the importance of coronaviruses as potentially lethal human pathogens and the identification of several zoonotic reservoirs has made the reemergence of new strains and future epidemics all the more possible. In this chapter, we describe the pathology of SARS-CoV infection in humans and explore the use of two models of the human conducting airway to develop a better understanding of the replication and pathogenesis of SARS-CoV in relevant in vitro systems. The first culture model is a human bronchial epithelial cell line Calu-3 that can be inoculated by viruses either as a non-polarized monolayer of cells or polarized cells with tight junctions and microvilli. The second model system, derived from primary cells isolated from human airway epithelium and grown on Transwells, form a pseudostratified mucociliary epithelium that recapitulates the morphological and physiological features of the human conducting airway in vivo. Experimental results using these lung epithelial cell models demonstrate that in contrast to the pathology reported in late stage cases SARS-CoV replicates to high titers in epithelial cells of the conducting airway. The SARS-CoV receptor, human angiotensin 1 converting enzyme 2 (hACE2), was detected exclusively on the apical surface of cells in polarized Calu-3 cells and human airway epithelial cultures (HAE), indicating that hACE2 was accessible by SARS-CoV after lumenal airway delivery. Furthermore, in HAE, hACE2 was exclusively localized to ciliated airway epithelial cells. In support of the hACE2 localization data, the most productive route of inoculation and progeny virion egress in both polarized Calu-3 and ciliated cells of HAE was the apical surface suggesting mechanisms to release large quantities of virus into the lumen of the human lung. Preincubation of the apical surface of cultures with antisera directed against hACE2 reduced viral titers by two logs while antisera against DC-SIGN/DC-SIGNR did not reduce viral replication levels suggesting that hACE2 is the primary receptor for entry of SARS-CoV into the ciliated cells of HAE cultures. To assess infectivity in ciliated airway cultures derived from susceptible animal species we generated a recombinant SARS-CoV by deletion of open reading frame 7a/7b (ORF 7a/7b) and insertion of the green fluorescent protein (GFP) resulting in SARS-CoV GFP. SARS-CoV GFP replicated to similar titers as wild type viruses in Vero E6, MA104, and CaCo2 cells. In addition, SARS-CoV replication in airway epithelial cultures generated from Golden Syrian hamster tracheas reached similar titers to the human cultures by 72 h post-infection. Efficient SARS-CoV infection of ciliated cell-types in HAE provides a useful in vitro model of human lung origin to study characteristics of SARS-CoV replication and pathogenesis.
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PMID:SARS-CoV replication and pathogenesis in an in vitro model of the human conducting airway epithelium. 1745 29

Severe acute respiratory syndrome (SARS) is a recently emerged infectious disease with significant morbidity and mortality. An epidemic in 2003 affected 8,098 patients in 29 countries with 774 deaths. The aetiological agent is a new coronavirus spread by droplet transmission. Clinical and general laboratory manifestations included fever, chills, rigor, myalgia, malaise, diarrhoea, cough, dyspnoea, pneumonia, lymphopenia, neutrophilia, thrombocytopenia, and elevated serum lactate dehydrogenase (LD), alanine aminotransferase (ALT) and creatine kinase (CK) activities. Treatment has been empirical; initial potent antibiotic cover, followed by simultaneous ribavirin and corticosteroids, with or without pulse high-dose methylprednisolone, have been used. The postulated disease progression comprises (1) active viral infection, (2) hyperactive immune response, and (3) recovery or pulmonary destruction and death. We investigated serum LD isoenzymes and blood lymphocyte subsets of SARS patients, and found LD1 activity as the best biochemical prognostic indicator for death, while CD3+, CD4+, CD8+ and natural killer cell counts were promising predictors for intensive care unit (ICU) admission. Plasma cytokine and chemokine profiles showed markedly elevated Th1 cytokine interferon (IFN)-gamma, inflammatory cytokines interleukin (IL)-1beta, IL-6 and IL-12, neutrophil chemokine IL-8, monocyte chemoattractant protein-1 (MCP-1), and Th1 chemokine IFN-gamma-inducible protein-10 (IP-10) for at least two weeks after disease onset, but there was no significant elevation of inflammatory cytokine tumor necrosis factor (TNF)-alpha and anti-inflammatory cytokine IL-10. Corticosteroid reduced IL-8, MCP-1 and IP-10 concentrations from 5-8 days after treatment. Measurement of biochemical markers of bone metabolism demonstrated significant but transient increase in bone resorption from Day 28-44 after onset of fever, when pulse steroid was most frequently given. With tapering down of steroid therapy, there was a decrease in bone resorption marker together with an increase in bone formation markers round Day 50, suggesting that some of the bone loss might be reversed. Our research studies on the chemical pathology and clinical immunology of SARS should have implications for the pathophysiology and therapy of this potentially lethal infection.
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PMID:Severe acute respiratory syndrome: clinical and laboratory manifestations. 1845 12

Febrile Respiratory Illness (FRI) is defined as a new or worsening episode of either cough or shortness of breath, presenting with fever (temperature 38 degrees C or higher) or chills in the previous 24 hours. Some FRI could cause large outbreaks of potentially life-threatening diseases (multi- or extensively drug resistant MTB, SARS, pandemic influenza) if not adequately controlled. Emergency Departments (EDs) are preferential sites of disease transmission because of the presence of both infectious and susceptible patients in the same space, the lack of rapid isolation of infectious patients, and the frequent and close contacts among patients and HCWs often not protected by PPE. The management of risk of FRI transmission is thus extremely important in EDs, where all procedures of infection control should be in place and continually monitored and assessed. In this article the main procedures for the management of risk of FRI transmission in EDs are described and discussed.
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PMID:Risk management of febrile respiratory illness in emergency departments. 1862 80

Acute respiratory distress syndrome (ARDS) caused by mycoplasmas is very rare. This report describes a severe case of atypical pneumonia due to M. pneumoniae in a formerly healthy young woman who developed high grade fever and cough leading to severe disseminated lung disease and finally to fatal ARDS. This case came into picture when killer atypical pneumonia, namely, SARS (severe acute respiratory syndrome), spread very fast from South-Asian countries to the rest of the world. Moreover, the clinical presentation and radiologic features of SARS bear resemblance to the syndrome of atypical pneumonia, which lead us to investigate this case into detail. We suggest that M. pneumoniae infections should be included in the differential diagnosis of pathogens causing ARDS, establishing an early diagnosis may have important therapeutic implications.
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PMID:A fulminant case of acute respiratory distress syndrome associated with Mycoplasma pneumoniae infection. 2069 25

Even though coronavirus infection of humans is not normally associated with severe diseases, the identification of the coronavirus responsible for the outbreak of severe acute respiratory syndrome showed that highly pathogenic coronaviruses can enter the human population. Shortly thereafter, in Holland in 2004, another novel human coronavirus (HCoV-NL63) was isolated from a seven-month old infant suffering from respiratory symptoms. This virus has subsequently been identified in various countries, indicating a worldwide distribution. HCoV-NL63 has been shown to infect mainly children and the immunocommpromised, who presented with either mild upper respiratory symptoms (cough, fever and rhinorrhoea) or more serious lower respiratory tract involvement such as bronchiolitis and croup, which was observed mainly in younger children. In fact, HCoV-NL63 is the aetiological agent for up to 10% of all respiratory diseases. This review summarizes recent findings of human coronavirus HCoV-NL63 infections, including isolation and identification, phylogeny and taxonomy, genome structure and transcriptional regulation, transmission and pathogenesis, and detection and diagnosis.
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PMID:Understanding Human Coronavirus HCoV-NL63. 2070 Mar 97


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