Dengue is the most rapidly spreading viral disease transmitted by the bite of infected Aedes mosquitos. The pathogenesis of dengue is still unclear; although host immune responses and virus serotypes have been proposed to contribute to disease severity. In this study, we examined the circulating dengue virus (DENV) and measured plasma levels of inflammatory mediators. Ninety-eight patients during a dengue outbreak in eastern India in 2016 were included in the study. The presence of DENV was demonstrated by detecting NS1 antigen; IgM capture ELISA and serotypes were discriminated by type-specific RT-PCR and/or sequencing. Plasma samples were assayed for 41-plex cytokine/chemokines using multiplex Luminex assay. Eighty-five (87%) samples were positive by NS1/IgM capture ELISA/RT-PCR. All four serotypes of DENV were detected in this outbreak, with DENV-2 as the predominant type, seen in 55% of cases. Mixed infections were seen in 39% of subjects. Among the host inflammatory biomarkers, GM-CSF, IFN-γ, IL-10, IL-15, IL-8, MCP-1, IL-6, MIP-1β, and TNF-α levels were significantly increased in dengue with and without warning signs, in severe dengue patients in comparison to healthy controls. Four cytokines IFN-γ, GM-CSF, IL-10, and MIP-1β correlated significantly with disease severity and could serve as potential predictor for disease severity. Information on the host biomarkers and the dengue serotype may help guide in optimizing effective intervention strategies.

Many viruses target host cell mitochondria to create a microenvironment conducive to viral dissemination. Dengue virus also exploits host cell mitochondria to facilitate its viral life cycle.

Introduction: Neonatal Septicemia is an important cause of morbidity and mortality. As infections due to ESBL producing K. pneumoniae & E. coli are on the rise, the present study was carried out in the NICU of KIMS, Narketpally, with an aim to identify any environmental sources & the mode of transmission over a period of 3 years from August 2006 to July 2009. Materials and Methods: A total of 264 neonates admitted with clinical features suggestive of septicemia in the NICU were studied by blood culture and CRP estimation. Antibiotic susceptibility pattern was determined. ESBL detection was done by double disc synergy test. Environmental samples from various sites (Incubators, phototherapy units, suction apparatus, trolley, door, floor, work surfaces) were collected using sterile swabs every month and processed simultaneously. Results: Of the 264 blood cultures, 197 (75%) showed bacterial growth. K. pneumoniae, 64 (32.7%) was the commonest organism followed by E. coli 55 (28%), S. aureus 31 (16%), Pseudomonas aeruginosa 28 (14%), Acinetobacter 13 (7%), and Coagulase negative Staphylococci 6 (2.8%) respectively. K. pneumoniae & E. coli were isolated from various environmental sites at least on one occasion and consistently from phototherapy units, door & floor of the NICU. The similarity between antibiograms of ESBL producing strains of K. pneumoniae & E. coli isolates from neonates and environment of NICU were statistically significant (P < 0.05). Conclusion: Wide spread use of third generation cephalosporins as a preemptive antibiotic for suspected cases of septicemia have contributed to the emergence of ESBL producing K. pneumoniae & E. coli in addition to other risk factors, both of which have extensively colonized the environment of the NICU. Repeated isolation of these two organisms from the NICU environment proves that some of the neonatal infections may be from the environment itself. Transmission can be stopped by maintaining the sterility of the NICU & hand hygiene among the mothers and health care workers.

Background. Dengue is the most rapidly spreading viral disease transmitted by the bite of infected Aedes mosquitos. Pathogenesis of dengue is still unclear; although host genetic factors, immune responses and virus serotypes have been proposed to contribute to disease severity. The development of high-throughput methods have allowed to scale up capabilities of identifying the key markers of inflammation. Since NS1 protein of dengue virus has been reported to activate immune cells towards enhanced inflammation through TLR2, we examined the role of a polymorphism, a 23bp deletion in 5'UTR region of TLR2 gene in patients with dengue (with and without warning signs) and correlated with plasma levels of inflammatory mediators with disease severity and viral serotypes. Methods: Eighty nine patients classified as per WHO 2009 criteria during dengue outbreak in Odisha, India in 2016 were included in the current study. Presence of dengue virus (DENV) was demonstrated by detecting NS1 antigen, IgM capture ELISA and serotypes in circulation were discriminated by type-specific RT-PCR and/or sequencing. Sixty-one confirmed dengue cases were typed for TLR2 indel polymorphism and compared with 485 disease free controls. Plasma samples were assayed for 41-plex cytokine/ chemokines using Luminex bead based immunoassay. Results: Presence of 23bp deletion allele of TLR2 gene was significantly more in patients with severe dengue in comparison to dengue fever cases (p= 0.03; Odds ratio 4.05) although the frequency of insertion (Ins) allele of TLR2 was comparable in healthy controls and dengue cases (82.4 and 87.9 % respectively). Seventy-three (82%) samples were found to be positive by NS1/ IgM capture ELISA/ RT-PCR. DENV-2 was predominant (58%) during the outbreak. Among the host inflammatory biomarkers 9 molecules were significantly altered in dengue patients when compared to healthy controls. The increased levels of IFN-γ, GM-CSF, IL-10, IL-1Rα and MIP-1β correlated significantly with severe dengue. Conclusions:The frequency of 23bp Indel mutation of TLR2 was comparable between healthy controls and dengue fever (with and without warning signs), suggesting that this indel mutation does not contribute significantly to susceptibility/ resistance to dengue; however, del allele of TLR2 gene was significantly more associated in patients with severe dengue symptoms when compared to dengue fever cases. INTRODUCTIONDengue virus transmitted by Aedes mosquito, is an increasing global problem, with an estimate of 390 million infections per year and about 3.6 billion people at risk to dengue. India alone contributed to 34% of the total global infections (Bhatt et al 2013). Infection with the dengue virus (DENV) resulted with a spectrum of clinical manifestations ranging from asymptomatic infection, self-limiting, dengue fever (DF) with or without warning signs or to life threatening severe There are four antigenically related but distinct serotypes of this virus, described as DENV-1, DENV-2, DENV-3, and DENV-4. The dengue virus is a positive ...

Background Acute encephalitis syndrome (AES) is a major public health concern in India, causing febrile illness principally associated with viral infection. Bacteria-like scrub typhus and leptospirosis also cause acute febrile illness. Therefore, this study was conceived to address the possible etiological agents contributing to sporadic AES in a tertiary care center in Odisha, India. Method This was a prospective hospital-based study that enrolled 92 consecutive patients with clinically diagnosed AES whose blood/cerebrospinal fluid samples were tested for IgM antibodies to dengue, Japanese encephalitis (JE), herpes simplex virus (HSV), Epstein-Barr virus (EBV), leptospirosis and scrub typhus. Results Viral antibodies to dengue were detected in three (3.26%) cases, HSV1 in four (4.34%) and HSV2 in three (3.26%) cases. Significantly, antibodies to EBV in 22 (23.591%) and to JE in 27 (29.34%) cases were detected. Notably, 30 (32.60%) and 11(12.0%) of patients had IgM antibodies to leptospirosis and scrub typhus, respectively. Conclusion This observation indicates an association of leptospirosis and scrub typhus infection in sporadic cases of AES, besides other viruses.