Age distribution of dengue cases in southern Vietnam from 2000 to 2015.

BACKGROUND: Dengue is the most common vector-borne viral infection. In recent times, an increase in the age of cases with clinical dengue has been reported in the national surveillance system and published literature of Vietnam. This change not only alter the risk of transmission and disease burden in different populations but also will impact for prevention and control strategies. A retrospective study was conducted from 2000 to 2015 in 19 provinces of southern Vietnam to describe the changes in age distribution of dengue cases and circulating serotypes. METHODOLOGY/PRINCIPAL FINDINGS: The study is a time trend analysis of the data aggregated from the database of dengue surveillance system. The database consisted of clinically diagnosed and laboratory-confirmed cases of dengue in southern Vietnam from 2000 to 2015. In the study period, the mean age of dengue cases increased from 12.2 ± 8.8 years old (y/o) to 16.8 ± 13.3 y/o between 2000 and 2015. Majority of severe cases were observed in the age group of 5-9 y/o and 10-14 y/o. Overall, the mortality and case fatality rates (CFR) were lowest during 2010 to 2015, and all four serotypes of dengue were observed. CONCLUSIONS/SIGNIFICANCE: With the exception of severe form, the age distribution of clinical cases of dengue appears to be shifting towards older age groups. An increase in the mean age of clinical cases of dengue has been observed in southern Vietnam over the past decade, and the highest incidence was observed in age group of 5-14 y/o. All serotypes of dengue were in circulation.

Impact of Antimicrobial Stewardship Program on Vancomycin Usage: Costs and Outcomes at Hospital for Tropical Diseases in Ho Chi Minh City, Vietnam.

BACKGROUND: Nowadays, with the emergence of vancomycin-resistant strains, the clinical use of vancomycin has been followed closely by applying the antimicrobial stewardship program (ASP) to enhance effectiveness in treatment and reduce cost burden for patients. METHODS: A descriptive cross-sectional study at the Hospital for Tropical Diseases was conducted to assess the inpatient status assigned to intravenous vancomycin and factors associated with the cost of treatment during two periods of implementing ASP, which were i) from April 1, 2016 to March 31, 2018 (previous ASP-pASP) and ii) from June 1, 2018 to March 31, 2020 (new ASP-nASP). RESULTS: Among 1375 patients who met the sampling criteria, there were 601 and 774 patients in pASP and nASP, respectively. The rate of no improvement/mortality in the pASP was higher than that in nASP (37.10% vs 25.98%, p <0.05). The proportion of patients with two or more infection episodes in nASP is lower than that in pASP (9.83% vs 18.64%, p<0.05). Besides, nASP has higher length of therapy (LOT) and higher day of therapy (DOT). The average treatment cost in the pASP is higher than that in the nASP, 1891.22 (95% CI, 1713.46-2068.98) USD vs 1775.55 (95% CI, 1576.22-1974.88) USD. There are seven factors (p<0.05) that associate with the total cost of treatment (age, number of infection episodes, length of stay, discharge status, clinical department, LOT, DOT) in pASP. On the other hand, the nASP has five factors (p<0.001), in which the log(LOT) and age are not as statistically significant (p=0.5127 and 0.3852, respectively) as in the pASP model. CONCLUSION: The implementation and improvement of the ASP at the Hospital for Tropical Diseases have initially shown benefits for patients using intravenous vancomycin. Specifically, the ASP helps to reduce treatment costs, improve patient outcomes, reduce length of stay and decrease the average daily dose of vancomycin.

Structural basis for distinct inflammasome complex assembly by human NLRP1 and CARD8.

Nod-like receptor (NLR) proteins activate pyroptotic cell death and IL-1 driven inflammation by assembling and activating the inflammasome complex. Closely related sensor proteins NLRP1 and CARD8 undergo unique auto-proteolysis-dependent activation and are implicated in auto-inflammatory diseases; however, their mechanisms of activation are not understood. Here we report the structural basis of how the activating domains (FIINDUPA-CARD) of NLRP1 and CARD8 self-oligomerize to assemble distinct inflammasome complexes. Recombinant FIINDUPA-CARD of NLRP1 forms a two-layered filament, with an inner core of oligomerized CARD surrounded by an outer ring of FIINDUPA. Biochemically, self-assembled NLRP1-CARD filaments are sufficient to drive ASC speck formation in cultured human cells-a process that is greatly enhanced by NLRP1-FIINDUPA which forms oligomers in vitro. The cryo-EM structures of NLRP1-CARD and CARD8-CARD filaments, solved here at 3.7 Å, uncover unique structural features that enable NLRP1 and CARD8 to discriminate between ASC and pro-caspase-1. In summary, our findings provide structural insight into the mechanisms of activation for human NLRP1 and CARD8 and reveal how highly specific signaling can be achieved by heterotypic CARD interactions within the inflammasome complexes.