Clinical profile of patients with post-caesarean wound infection: experience of Patan Hospital, Nepal

Introduction: Would infection following caesarean delivery adds physical, psychological, and health burden to individual and health care system. This hospital based study aim to determine the rate of infection, the risk factors, pathogens and antibiotic sensitivity. Method: A prospective study was carried out to analyze the wound infection in women following caesarean delivery in the Department of Obstetrics and Gynecology, Patan Hospital, Nepal, between January 2018 to December 2018. The study was approved from the institutional review committee. Clinicodemographic data during perinatal period of caesarean delivery were descriptive analyzed in relation to wound infection. Result: Wound infection occurred in 102 (3.1%)of 3285 caesarean section (of total 7131 deliveries during the study period. The caesarean SSI rate was 3.1%, all were incisional SSI (84 superficial and 18 deep) and there were no organ-space SSI. Majority (81.3%) SSI cases were detected in emergency LSCS. Coagulase Negative Staphylococci was the most common organism isolated from wound swab. Routine postoperative antibiotics did not have a major impact in reducing wound infection rate. Multiple per vaginal examinations, prolonged rupture of membrane and staples for skin closure were more commonly associated with SSI. Conclusion: Reduction in caesarean rate is the major key factor for decreasing the post caesarean wound infection. Protocol should be developed and strictly implemented by all the health care professionals in order to minimize and prevent the infection rate after caesarean section. Keyword: Caesarean section, surgical site infection (SSI), wound infectio

Evidence of experimental vertical transmission of emerging novel ECSA genotype of Chikungunya Virus in Aedes aegypti.

BACKGROUND: Chikungunya virus (CHIKV) has emerged as one of the most important arboviruses of public health significance in the past decade. The virus is mainly maintained through human-mosquito-human cycle. Other routes of transmission and the mechanism of maintenance of the virus in nature are not clearly known. Vertical transmission may be a mechanism of sustaining the virus during inter-epidemic periods. Laboratory experiments were conducted to determine whether Aedes aegypti, a principal vector, is capable of vertically transmitting CHIKV or not. METHODOLOGY/PRINCIPAL FINDINGS: Female Ae. aegypti were orally infected with a novel ECSA genotype of CHIKV in the 2nd gonotrophic cycle. On day 10 post infection, a non-infectious blood meal was provided to obtain another cycle of eggs. Larvae and adults developed from the eggs obtained following both infectious and non-infectious blood meal were tested for the presence of CHIKV specific RNA through real time RT-PCR. The results revealed that the larvae and adults developed from eggs derived from the infectious blood meal (2nd gonotrophic cycle) were negative for CHIKV RNA. However, the larvae and adults developed after subsequent non-infectious blood meal (3rd gonotrophic cycle) were positive with minimum filial infection rates of 28.2 (1∶35.5) and 20.2 (1∶49.5) respectively. CONCLUSION/SIGNIFICANCE: This study is the first to confirm experimental vertical transmission of emerging novel ECSA genotype of CHIKV in Ae. aegypti from India, indicating the possibilities of occurrence of this phenomenon in nature. This evidence may have important consequence for survival of CHIKV during adverse climatic conditions and inter-epidemic periods

Vertical transmission of Chikungunya virus in <i>Ae. aegypti</i> as determined by measuring log₁₀ RNA copies/pool of larvae and adults by real time RT-PCR.

<p>Horizontal line represent mean value for each group. Asterisks are indicating significant differences between the two groups (**p<0.01).</p

Molecular epidemiology and complete genome characterization of H1N1pdm virus from India.

BACKGROUND: Influenza A virus is one of world's major uncontrolled pathogen, causing seasonal epidemic as well as global pandemic. This was evidenced by recent emergence and continued prevalent 2009 swine origin pandemic H1N1 Influenza A virus, provoking first true pandemic in the past 40 years. In the course of its evolution, the virus acquired many mutations and multiple unidentified molecular determinants are likely responsible for the ability of the 2009 H1N1 virus to cause increased disease severity in humans. Availability of limited data on complete genome hampers the continuous monitoring of this type of events. Outbreaks with considerable morbidity and mortality have been reported from all parts of the country. METHODS/RESULTS: Considering a large number of clinical cases of infection complete genome based sequence characterization of Indian H1N1pdm virus and their phylogenetic analysis with respect to circulating global viruses was undertaken, to reveal the phylodynamic pattern of H1N1pdm virus in India from 2009-2011. The Clade VII was observed as a major circulating clade in phylogenetic analysis. Selection pressure analysis revealed 18 positively selected sites in major surface proteins of H1N1pdm virus. CONCLUSIONS: This study clearly revealed that clade VII has been identified as recent circulating clade in India as well globally. Few clade VII specific well identified markers undergone positive selection during virus evolution. Continuous monitoring of the H1N1pdm virus is warranted to track of the virus evolution and further transmission. This study will serve as a baseline data for future surveillance and also for development of suitable therapeutics

Details of positive cases for H1N1pdm virus during investigation of suspected samples from 2010–2011.

<p>Details of positive cases for H1N1pdm virus during investigation of suspected samples from 2010–2011.</p

Phylogenetic tree of concatenated whole genome of representative global H1N1pdm viruses including four Indian viruses sequenced in this study generated by Bayesian method.

<p>Each strain is abbreviated with virus subtype, country of origin, strain name and year of isolation in parenthesis. Scale bar indicates number of nucleotide substitutions per site. The Indian isolates sequenced in this study are highlighted in different font in clade VII. Other Indian isolates are highlighted by solid diamond in respective clades. Each clade is defined by long branch and nodes supported by high Bayesian posterior probability (BPP) values (100%).</p

Details of the genome sequences of the H1N1pdm virus isolates retrieved and investigated in the whole genome and complete HA gene based phylogenetic analysis in this study.

<p>Note: The isolates in bold font are sequenced in this study.</p

Confirmation of H1N1pdm virus.

<p>(<b>A</b>) Microscopic photograph of healthy and Influenza A (H1N1pdm) virus infected Madin Darby Canine Kidney Cells. (<b>B</b>) Immunofluorescence assay. (<b>C</b>) Haemagglutination assay. (<b>D</b>) WHO CDC Real-Time PCR amplification. Real time amplification curve of positive clinical samples showing amplification of all four probes.</p

(A) Monthly trend of pandemic influenza A H1N1 and seasonal flu reported from September 2010 to December 2011.

<p>(B) Age and sex wise distribution of the influenza A H1N1 2010–2011 suspected ILI cases.</p

Description of major/important non-conservative and clade specific amino acid substitutions among the four Indian H1N1pdm virus (sequenced in this study) compared to prototype H1N1pdm strain (California/04/2009) and other Indian (A/Pune/NIV6447/2009) virus strain (sequenced previously).

<p>Note: Major non conservative changes involving basic to acidic amino acid are written in bold font and also underlined; The hydrophobic to hydrophilic amino acid substitutions and vice-versa are written in bold font. The substitutions involving charged residues to uncharged residues; cyclic to acyclic and vice versa are written in italics. The clade specific substitutions (NP:V100I; NA:V106I; NS1:I123V; HA:S220T, I338V) are written in normal font.</p>*<p>The residue position for the HA is the numbering considered inclusive of signal peptide.</p