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Hsiao-Ling Chang

Publications and source records attributed to Hsiao-Ling Chang.

5 recordsLinked to original sources

Nasopharyngeal shedding of severe acute respiratory syndrome-associated coronavirus is associated with genetic polymorphisms.

BACKGROUND: A high initial or peak severe acute respiratory syndrome (SARS)-associated coronavirus (SARS-CoV) load in nasopharyngeal specimens was shown to be associated with a high mortality rate. Because all infected individuals were devoid of preeexisting protective immunity against SARS-CoV, the biological basis for the variable virus burdens in different patients remains elusive. METHODS: The nationwide SARS database in Taiwan was analyzed, and genotyping of 281 single-nucleotide polymorphisms (SNPs) of 65 genes was performed for 94 patients with SARS, to identify SNPs for which distribution between patients with or without detectable nasopharyngeal shedding of SARS-CoV was biased. RESULTS: Titers of SARS-CoV shed in nasopharyngeal specimens varied widely, ranging from nondetectable to 10(8) SARS-CoV RNA copies/mL, and they were correlated positively with a high mortality rate (P<.0001, by trend test) and with early death (i.e., death occurring within 2 weeks of the onset of illness) (P=.0015, by trend test). Virus shedding was found to be higher among male patients (P=.0014, by multivariate logistic regression) and among older patients (P=.015, by multivariate logistic regression). Detectable nasopharyngeal shedding of SARS-CoV was associated with polymorphic alleles of interleukins 18 (P=.014) and 1A (P=.031) and a member of NF kappa B complex (reticuloendotheliosis viral oncogene homolog B [RelB]) (P=.034), all of which are proinflammatory in nature, as well as the procoagulation molecule fibrinogen-like protein 2 (P=.008). CONCLUSION: The SARS-CoV load is a determinant of clinical outcomes of SARS, and it is associated with polymorphisms of genes involved in innate immunity, which might be regulated in an age- and sex-dependent manner. The findings of the present study provided leads to genes involved in the host response to SARS-CoV infection; if substantiated with functional studies, these findings may be applicable to other newly emerged respiratory viruses (e.g., the influenza pandemic strain).

Adult↗

Hematological and biochemical factors predicting SARS fatality in Taiwan.

BACKGROUND/PURPOSE: Severe acute respiratory syndrome (SARS) has a high fatality rate worldwide. We examined the epidemiologic and clinical factors associated with death for all laboratory-confirmed SARS patients in Taiwan. METHODS: Using initial data in medical records reported by hospitals to the Center for Disease Control in Taiwan, we analyzed whether hematological, biochemical and arterial blood gas measures could predict fatality in 346 SARS patients. RESULTS: Both fatalities (n = 73; 21.1%) and survivors had elevated plasma concentration of initial C-reactive protein (CRP), but the mean CRP concentration was higher in fatalities (47.7 +/- 43.3 mg/L) than in survivors (24.6 +/- 28.2 mg/L). Initial lymphocyte counts were low in both fatalities (814 +/- 378/microL) and survivors (1019 +/- 480/microL). After controlling for age and sex, multiple logistic regression analysis showed that hematological factors significantly associated with fatality included initial neutrophil count > 7000/microL (odds ratio [OR] = 6.4), initial CRP concentration > 47.5 mg/L (OR = 5.8) and lactic acid dehydrogenase (LDH) > 593.5 IU/L (OR = 4.2). Factors significantly associated with initial CRP concentration > 47.5 mg/L included dyspnea (OR = 4.3), red blood cell count < 4.1 x 106/microL (OR = 4.3) and serum aspartate aminotransferase > 57 IU/L (OR = 3.1). CONCLUSION: Initial neutrophil count, CRP and LDH levels are important predictors of mortality from SARS.

Adult↗

SARS in Taiwan: an overview and lessons learned.

OBJECTIVES: This report aims to describe the epidemiology of severe acute respiratory syndrome (SARS) in Taiwan between March and July 2003, and to examine the public health response. METHODS: Surveillance for SARS was initiated on 14 March 2003. Response activities are described for the isolation of patients; contact tracing; quarantine of contact persons; fever screening for inbound and outbound passengers at the airport; and hospital infection control as assessed by mobile SARS containment teams. RESULTS: Between 14 March and 30 July 2003 a total of 668 probable cases of SARS were reported. Of the 668 cases, 181 (27%) were fatal. Compared to the survivors, fatal cases were more likely to be older (p < 0.001), male (p < 0.05), exposed through hospital contact (p < 0.001), and have a coexisting medical disorder (p<0.001). Between 28 March and 30 July a total of 151,270 persons were quarantined. Among them, 46 (3.0/10,000) were subsequently classified as being probable SARS cases. At the time of the mobile team assessments, 46 (53%) hospitals had implemented WHO infection control recommendations. CONCLUSIONS: In this outbreak, an emergency plan consisted of patient isolation and strict hospital infection control.

Adult↗

Transmission of the severe acute respiratory syndrome on aircraft.

BACKGROUND: The severe acute respiratory syndrome (SARS) spread rapidly around the world, largely because persons infected with the SARS-associated coronavirus (SARS-CoV) traveled on aircraft to distant cities. Although many infected persons traveled on commercial aircraft, the risk, if any, of in-flight transmission is unknown. METHODS: We attempted to interview passengers and crew members at least 10 days after they had taken one of three flights that transported a patient or patients with SARS. All index patients met the criteria of the World Health Organization for a probable case of SARS, and index or secondary cases were confirmed to be positive for SARS-CoV on reverse-transcriptase polymerase chain reaction or serologic testing. RESULTS: After one flight carrying a symptomatic person and 119 other persons, laboratory-confirmed SARS developed in 16 persons, 2 others were given diagnoses of probable SARS, and 4 were reported to have SARS but could not be interviewed. Among the 22 persons with illness, the mean time from the flight to the onset of symptoms was four days (range, two to eight), and there were no recognized exposures to patients with SARS before or after the flight. Illness in passengers was related to the physical proximity to the index patient, with illness reported in 8 of the 23 persons who were seated in the three rows in front of the index patient, as compared with 10 of the 88 persons who were seated elsewhere (relative risk, 3.1; 95 percent confidence interval, 1.4 to 6.9). In contrast, another flight carrying four symptomatic persons resulted in transmission to at most one other person, and no illness was documented in passengers on the flight that carried a person who had presymptomatic SARS. CONCLUSIONS: Transmission of SARS may occur on an aircraft when infected persons fly during the symptomatic phase of illness. Measures to reduce the risk of transmission are warranted.

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