The pathogenesis of dengue virus infection is attributed to complex interplay between virus, host genes and host immune response. Host factors such as antibody-dependent enhancement (ADE), memory cross-reactive T cells, anti-DENV NS1 antibodies, autoimmunity as well as genetic factors are major determinants of disease susceptibility. NS1 protein and anti-DENV NS1 antibodies were believed to be responsible for pathogenesis of severe dengue. The cytokine response of cross-reactive CD4+ T cells might be altered by the sequential infection with different DENV serotypes, leading to further elevation of pro-inflammatory cytokines contributing a detrimental immune response. Fcγ receptor-mediated antibody-dependent enhancement (ADE) results in release of cytokines from immune cells leading to vascular endothelial cell dysfunction and increased vascular permeability. Genomic variation of dengue virus and subgenomic flavivirus RNA (sfRNA) suppressing host immune response are viral determinants of disease severity. Dengue infection can lead to the generation of autoantibodies against DENV NS1antigen, DENV prM, and E proteins, which can cross-react with several self-antigens such as plasminogen, integrin, and platelet cells. Apart from viral factors, several host genetic factors and gene polymorphisms also have a role to play in pathogenesis of DENV infection. This review article highlights the various factors responsible for the pathogenesis of dengue and also highlights the recent advances in the field related to biomarkers which can be used in future for predicting severe disease outcome.

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The prevalence of multidrug resistance among enterococci was found to be 63%, the resistance being more common in Enterococcus faecium as compared to Enterococcus faecalis. The study highlights the emergence and increased prevalence of multidrug resistant enterococci which pose a serious therapeutic challenge.

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The emergence of resistance to multiple antimicrobial agents in Gram-negative bacteria is a significant threat to public health, as it restricts the armamentarium of the clinician against these infections. The aim of this study was to determine the burden of extensively drug-resistant (XDR) and pandrug-resistant (PDR) Gram-negative bacteria at a tertiary-care centre. Antimicrobial susceptibility testing of 1240 clinical isolates of Gram-negative bacteria obtained from various clinical samples during the study period was carried out by the Kirby-Bauer disc diffusion method. Minimum inhibitory concentration of all antibiotics including tigecycline and colistin was determined by Vitek-2 automated susceptibility testing system. Out of 1240 isolates of Gram-negative bacteria, 112 isolates (9%) were resistant to all the antibiotics tested by Kirby-Bauer disc diffusion method. This finding was corroborated by Vitek-2. In addition, Vitek-2 found that 67 isolates were resistant to all antibiotics except tigecycline and colistin. A total of 30 isolates were susceptible to only colistin, and four isolates were susceptible to only tigecycline. It was also found that six isolates (excluding five isolates of Proteus spp.) were resistant to both colistin and tigecycline. Thus, 101 (8.1%) out of 1240 isolates were XDR and 11 isolates (0.9%) were PDR. The findings of this study reveal increased burden of XDR and PDR Gram-negative bacteria in our centre. It also highlights the widespread dissemination of these bacteria in the community. This situation warrants the regular surveillance of antimicrobial resistance of Gram-negative bacteria and implementation of an efficient infection control program.