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1.
Int J Public Health ; 66: 634904, 2021.
Article in English | MEDLINE | ID: mdl-34335139

ABSTRACT

Objectives: We explored the association of underlying health conditions (UHC) with depression and anxiety, and examined the modification effects of suspected COVID-19 symptoms (S-COVID-19-S), health-related behaviors (HB), and preventive behaviors (PB). Methods: A cross-sectional study was conducted on 8,291 outpatients aged 18-85 years, in 18 hospitals and health centers across Vietnam from 14th February to May 31, 2020. We collected the data regarding participant's characteristics, UHC, HB, PB, depression, and anxiety. Results: People with UHC had higher odds of depression (OR = 2.11; p < 0.001) and anxiety (OR = 2.86; p < 0.001) than those without UHC. The odds of depression and anxiety were significantly higher for those with UHC and S-COVID-19-S (p < 0.001); and were significantly lower for those had UHC and interacted with "unchanged/more" physical activity (p < 0.001), or "unchanged/more" drinking (p < 0.001 for only anxiety), or "unchanged/healthier" eating (p < 0.001), and high PB score (p < 0.001), as compared to those without UHC and without S-COVID-19-S, "never/stopped/less" physical activity, drinking, "less healthy" eating, and low PB score, respectively. Conclusion: S-COVID-19-S worsen psychological health in patients with UHC. Physical activity, drinking, healthier eating, and high PB score were protective factors.


Subject(s)
Anxiety , COVID-19 , Comorbidity , Depression , Outpatients , Adolescent , Adult , Aged , Aged, 80 and over , Anxiety/epidemiology , COVID-19/epidemiology , COVID-19/prevention & control , COVID-19/psychology , Cross-Sectional Studies , Depression/epidemiology , Female , Humans , Male , Middle Aged , Outpatients/psychology , Outpatients/statistics & numerical data , Vietnam/epidemiology , Young Adult
2.
Article in English | MEDLINE | ID: mdl-34066312

ABSTRACT

BACKGROUND: The COVID-19 pandemic has been disseminating fear in the community, which has affected people's quality of life, especially those with health problems. Health literacy (HL), eHealth literacy (eHEAL), and digital healthy diet literacy (DDL) may have potential impacts on containing the pandemic and its consequences. This study aimed to examine the association between the fear of COVID-19 scale (FCoV-19S) and the health-related quality of life (HRQoL), and to examine the effect modification by HL, eHEAL, and DDL on this association. METHODS: A cross-sectional study was conducted in 11 hospitals across Vietnam from 7 April to 31 May 2020. Data were collected on 4348 outpatients, including demographic characteristics, HL, eHEAL, DDL, FCoV-19S, and HRQoL. Multiple linear regression and interaction models were used to explore associations. RESULTS: Patients with higher FCoV-19S scores had lower HRQoL scores (unstandardized coefficient, B = -0.78, p < 0.001). HL (B = 0.20, p < 0.001), eHEAL (B = 0.24, p < 0.001), and DDL (B = 0.20, p < 0.001) were positively associated with higher HRQoL scores. The negative impact of FCoV-19S on HRQoL was significantly attenuated by higher eHEAL score groups (from one standard deviation (SD) below the mean, B = -0.93, p < 0.001; to the mean, B = -0.85, p < 0.001; and one SD above the mean, B = -0.77, p < 0.001); and by higher DDL score groups (from one SD below the mean, B = -0.92, p < 0.001; to the mean, B = -0.82, p < 0.001; and one SD above the mean, B = -0.72, p < 0.001). CONCLUSIONS: eHealth literacy and digital healthy diet literacy could help to protect patients' health-related quality of life from the negative impact of the fear of COVID-19 during the pandemic.


Subject(s)
COVID-19 , Health Literacy , Telemedicine , Cross-Sectional Studies , Diet, Healthy , Fear , Hospitals , Humans , Pandemics , Quality of Life , SARS-CoV-2 , Surveys and Questionnaires , Vietnam
3.
Front Nutr ; 7: 581043, 2020.
Article in English | MEDLINE | ID: mdl-33304917

ABSTRACT

Background: The COVID-19 pandemic causes a huge burden for affected countries. Several public health interventions were applied to contain the infection. However, the pandemic itself and the lockdown measure negatively influence people's lifestyles and psychological health. Purpose: To explore determinants of healthy dietary intake and depression, and examine the interaction between healthy dietary intake and COVID-19 lockdown on depression. Methods: A cross-sectional study was conducted at 18 hospitals and health centers from February 14 to May 31, 2020. Data of 8,291 outpatients were collected including patients' characteristics, clinical parameters, health literacy, healthy dietary intake (using the healthy eating score, HES), other health-related behaviors, and depression (using the patient health questionnaire, PHQ). Depression was defined as PHQ score ≥ 10. Results: Protective factors of healthy dietary intake and depression were higher education, better medication payment ability, higher social status, more physical activity, and higher health literacy, whereas older age, ever married, own business or other types of occupation, lockdown, suspected COVID-19 symptoms, and comorbidity were associated with lower HES scores and a higher depression likelihood. Besides, overweight/obesity and alcohol drinking were associated with lower HES scores. As compared with patients not under lockdown and with lowest HES score, those who were under lockdown and with lowest HES score had 10.6 times higher depression likelihood (odds ratio, OR, 10.60; 95% CI 6.88, 16.32; p < 0.001), whereas people with higher HES score had 15% lower depression likelihood (OR 0.85; 95% CI 0.82, 0.89; p < 0.001). Conclusions: Healthy dietary intake and depression were determined by several sociodemographic, clinical, and behavioral factors. Lockdown measure affects people's dietary intake behavior and depression. Importantly, healthy dietary intake potentially modifies the negative effect of lockdown on depression.

4.
Sci Transl Med ; 8(357): 357ra124, 2016 09 21.
Article in English | MEDLINE | ID: mdl-27655850

ABSTRACT

New therapeutic approaches are urgently needed to improve survival outcomes for patients with necrotizing pneumonia caused by Staphylococcus aureus One such approach is adjunctive treatment with intravenous immunoglobulin (IVIG), but clinical practice guidelines offer conflicting recommendations. In a preclinical rabbit model, prophylaxis with IVIG conferred protection against necrotizing pneumonia caused by five different epidemic strains of community-associated methicillin-resistant S. aureus (MRSA) as well as a widespread strain of hospital-associated MRSA. Treatment with IVIG, either alone or in combination with vancomycin or linezolid, improved survival outcomes in this rabbit model. Two specific IVIG antibodies that neutralized the toxic effects of α-hemolysin (Hla) and Panton-Valentine leukocidin (PVL) conferred protection against necrotizing pneumonia in the rabbit model. This mechanism of action of IVIG was uncovered by analyzing loss-of-function mutant bacterial strains containing deletions in 17 genes encoding staphylococcal exotoxins, which revealed only Hla and PVL as having an impact on necrotizing pneumonia. These results demonstrate the potential clinical utility of IVIG in the treatment of severe pneumonia induced by S. aureus.


Subject(s)
Immunoglobulins, Intravenous/therapeutic use , Methicillin-Resistant Staphylococcus aureus/physiology , Pneumonia, Necrotizing/drug therapy , Pneumonia, Necrotizing/microbiology , Acute Lung Injury/drug therapy , Acute Lung Injury/microbiology , Acute Lung Injury/pathology , Animals , Antibiotic Prophylaxis , Antibodies, Neutralizing/immunology , Bacterial Toxins/immunology , Disease Models, Animal , Exotoxins/immunology , Hemolysin Proteins/immunology , Humans , Leukocidins/immunology , Linezolid/pharmacology , Linezolid/therapeutic use , Methicillin-Resistant Staphylococcus aureus/immunology , Rabbits , Vancomycin/pharmacology , Vancomycin/therapeutic use
5.
mBio ; 6(1): e02272-14, 2015 Feb 17.
Article in English | MEDLINE | ID: mdl-25691592

ABSTRACT

UNLABELLED: Staphylococcus aureus is a Gram-positive, commensal bacterium known to asymptomatically colonize the human skin, nares, and gastrointestinal tract. Colonized individuals are at increased risk for developing S. aureus infections, which range from mild skin and soft tissue infections to more severe diseases, such as endocarditis, bacteremia, sepsis, and osteomyelitis. Different virulence factors are required for S. aureus to infect different body sites. In this study, virulence gene expression was analyzed in two S. aureus isolates during nasal colonization, bacteremia and in the heart during sepsis. These models were chosen to represent the stepwise progression of S. aureus from an asymptomatic colonizer to an invasive pathogen. Expression of 23 putative S. aureus virulence determinants, representing protein and carbohydrate adhesins, secreted toxins, and proteins involved in metal cation acquisition and immune evasion were analyzed. Consistent upregulation of sdrC, fnbA, fhuD, sstD, and hla was observed in the shift between colonization and invasive pathogen, suggesting a prominent role for these genes in staphylococcal pathogenesis. Finally, gene expression data were correlated to the roles of the genes in pathogenesis by using knockout mutants in the animal models. These results provide insights into how S. aureus modifies virulence gene expression between commensal and invasive pathogens. IMPORTANCE: Many bacteria, such as Staphylococcus aureus, asymptomatically colonize human skin and nasal passages but can also cause invasive diseases, such as bacteremia, pneumonia, sepsis, and osteomyelitis. The goal of this study was to analyze differences in the expression of selected S. aureus genes during a commensal lifestyle and as an invasive pathogen to gain insight into the commensal-to-pathogen transition and how a bacterial pathogen adapts to different environments within a host (e.g., from nasal colonization to invasive pathogen). The gene expression data were also used to select genes for which to construct knockout mutants to assess the role of several proteins in nasal colonization and lethal bacteremia. These results not only provide insight into the factors involved in S. aureus disease pathogenesis but also provide potential therapeutic targets.


Subject(s)
Carrier State/microbiology , Gene Expression Regulation, Bacterial , Osteomyelitis/microbiology , Sepsis/microbiology , Staphylococcal Infections/microbiology , Staphylococcus aureus/physiology , Virulence Factors/biosynthesis , Animals , Disease Models, Animal , Gene Expression Profiling , Gene Knockout Techniques , Mice, Inbred BALB C , Sigmodontinae , Staphylococcus aureus/genetics , Staphylococcus aureus/isolation & purification , Staphylococcus aureus/pathogenicity , Virulence , Virulence Factors/genetics
6.
J Infect Dis ; 209(10): 1533-41, 2014 May 15.
Article in English | MEDLINE | ID: mdl-24280367

ABSTRACT

BACKGROUND: Detailed knowledge on protein repertoire of a pathogen during host infection is needed for both developing a better understanding of the pathogenesis and defining potential therapeutic targets. Such data, however, have been missing for Staphylococcus aureus, a major human pathogen. METHODS: We determined the surface proteome of methicillin-resistant S. aureus (MRSA) clone usa300 derived directly from murine systemic infectiON. RESULTS: The majority of the in vivo-expressed surface-associated proteins were lipoproteins involved in nutrient acquisition, especially uptake of metal ions. Enzyme-linked immunosorbent assay (ELISA) of convalescent human serum samples revealed that proteins that were highly produced during murine experimental infection were also produced during natural human infection. We found that among the 7 highly abundant lipoproteins only MntC, which is the manganese-binding protein of the MntABC system, was essential for MRSA virulence during murine systemic infection. Moreover, we show that MntA and MntB are equally important for MRSA virulence. CONCLUSIONS: Besides providing experimental evidence that MntABC might be a potential therapeutic target for the development of antibiotics, our in vivo proteomics data will serve as a valuable basis for defining potential antigen combinations for multicomponent vaccines.


Subject(s)
Anti-Bacterial Agents/pharmacology , Bacterial Proteins/metabolism , Gene Expression Regulation, Bacterial/physiology , Methicillin-Resistant Staphylococcus aureus/drug effects , Methicillin-Resistant Staphylococcus aureus/metabolism , Proteomics , Animals , Bacterial Proteins/genetics , Enzyme-Linked Immunosorbent Assay/methods , Humans , Kidney/microbiology , Lipoproteins/genetics , Lipoproteins/metabolism , Membrane Proteins/genetics , Membrane Proteins/metabolism , Methicillin-Resistant Staphylococcus aureus/pathogenicity , Mice , Serum/immunology , Staphylococcal Infections/immunology , Staphylococcal Infections/microbiology , Staphylococcal Infections/prevention & control , Staphylococcal Vaccines/immunology , Virulence
7.
Clin Infect Dis ; 55(6): 781-8, 2012 Sep.
Article in English | MEDLINE | ID: mdl-22670044

ABSTRACT

BACKGROUND: Since its emergence in 2000, epidemic spread of the methicillin-resistant Staphylococcus aureus (MRSA) clone USA300 has led to a high burden of skin and soft tissue infections (SSTIs) in the United States, yet its impact on MRSA bloodstream infections (BSIs) is poorly characterized. METHODS: To assess clonality of the MRSA isolates causing SSTI and BSI during the epidemic period, a stratified, random sample of 1350 unique infection isolates (from a total of 7252) recovered at the Community Health Network of San Francisco from 2000 to 2008 were selected for genotyping. Risk factors and outcomes for 549 BSI cases caused by the USA300 epidemic clone and non-USA300 MRSA clones were assessed by retrospective review of patient medical records. RESULTS: From 2000 to 2008, secular trends of USA300 SSTI and USA300 BSI were strongly correlated (Pearson r = 0.953). USA300 accounted for 55% (304/549) of BSIs as it was the predominant MRSA clone that caused community-associated (115/160), healthcare-associated community-onset (125/207), and hospital-onset (64/182) BSIs. Length of hospitalization after BSI diagnosis and mortality rates for USA300 and non-USA300 were similar. Two independent risk factors for USA300 BSI were identified: concurrent SSTI (adjusted relative risk, 1.4 [95% confidence interval {CI}, 1.2-1.6]) and anti-MRSA antimicrobial use in the preceding 30 days (0.7 [95% CI, .6-.8]). Isolates from concurrent SSTI were indistinguishable genotypically from the USA300 isolates that caused BSI. CONCLUSIONS: USA300 SSTIs serve as a source for BSI. Strategies to control the USA300 SSTI epidemic may lessen the severity of the concurrent USA300 BSI epidemic.


Subject(s)
Bacteremia/epidemiology , Community-Acquired Infections/epidemiology , Epidemics , Methicillin-Resistant Staphylococcus aureus/isolation & purification , Soft Tissue Infections/epidemiology , Staphylococcal Skin Infections/epidemiology , Adolescent , Adult , Aged , Aged, 80 and over , Bacteremia/microbiology , Child, Preschool , Community-Acquired Infections/microbiology , Female , Humans , Male , Methicillin-Resistant Staphylococcus aureus/classification , Methicillin-Resistant Staphylococcus aureus/genetics , Middle Aged , Molecular Typing , Retrospective Studies , San Francisco/epidemiology , Soft Tissue Infections/microbiology , Staphylococcal Skin Infections/microbiology , Young Adult
8.
Proc Natl Acad Sci U S A ; 107(12): 5587-92, 2010 Mar 23.
Article in English | MEDLINE | ID: mdl-20231457

ABSTRACT

Community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) is epidemic in the United States, even rivaling HIV/AIDS in its public health impact. The pandemic clone USA300, like other CA-MRSA strains, expresses Panton-Valentine leukocidin (PVL), a pore-forming toxin that targets polymorphonuclear leukocytes (PMNs). PVL is thought to play a key role in the pathogenesis of necrotizing pneumonia, but data from rodent infection models are inconclusive. Rodent PMNs are less susceptible than human PMNs to PVL-induced cytolysis, whereas rabbit PMNs, like those of humans, are highly susceptible to PVL-induced cytolysis. This difference in target cell susceptibility could affect results of experimental models. Therefore, we developed a rabbit model of necrotizing pneumonia to compare the virulence of a USA300 wild-type strain with that of isogenic PVL-deletion mutant and -complemented strains. PVL enhanced the capacity of USA300 to cause severe lung necrosis, pulmonary edema, alveolar hemorrhage, hemoptysis, and death, hallmark clinical features of fatal human necrotizing pneumonia. Purified PVL instilled directly into the lung caused lung inflammation and injury by recruiting and lysing PMNs, which damage the lung by releasing cytotoxic granule contents. These findings provide insights into the mechanism of PVL-induced lung injury and inflammation and demonstrate the utility of the rabbit for studying PVL-mediated pathogenesis.


Subject(s)
Acute Lung Injury/etiology , Bacterial Toxins/toxicity , Exotoxins/toxicity , Leukocidins/toxicity , Methicillin-Resistant Staphylococcus aureus/pathogenicity , Neutrophils/drug effects , Neutrophils/physiology , Pneumonia, Staphylococcal/etiology , Acute Lung Injury/microbiology , Acute Lung Injury/pathology , Animals , Bacterial Toxins/genetics , Disease Models, Animal , Exotoxins/genetics , Gene Deletion , Genes, Bacterial , Genetic Complementation Test , Humans , In Vitro Techniques , Leukocidins/genetics , Methicillin-Resistant Staphylococcus aureus/genetics , Neutrophils/pathology , Pneumonia, Staphylococcal/microbiology , Pneumonia, Staphylococcal/pathology , Rabbits , Virulence/genetics
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