Rajni Gaind

Dr. Rajni Gaind


Research Focus & Metrics

Academic Career Length

18Years (2009-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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21 January 2020 in Monaldi Archives for Chest Disease
Verified
Journal Article
Open access
PDF file
NGNitesh Gupta
Nitesh Gupta
SASumita Agrawal
Sumita Agrawal
PIPranav Ish
Pranav Ish
SMSuruchi Mishra
Suruchi Mishra
RGRajni Gaind
Rajni Gaind
*G*Safdarjung Hospital COVID 2019 working group
*Safdarjung Hospital COVID 2019 working group
COVID-19 has now become a pandemic. It has spread from Wuhan, China, in December 2019 to a large number of countries within three months. The objective of this work is to report the initial experience with epidemiologic and clinical features, as well as with the management of COVID-19 patients in India. This is a descriptive case series of the first 21 COVID-19 infected patients confirmed with polymerase chain reaction (PCR) and admitted to a tertiary care centre in India from 01.02.2020 to 19.03.2020. Clinical, laboratory, and radiologic data were collected, including age, sex, nationality, travel history, symptoms, duration of stay, and comorbidities. The mean age of the population was 40.3 years with a male preponderance. Thirteen (62%) patients had recent travel history outside India in the previous 30 days, two thirds of whom had travelled to Italy. The most common symptoms were fever and cough (42.9%) followed by sore throat, headache and breathlessness. Vital and laboratory parameters were preserved in all patients and none of them required ventilatory support. Among the first 21 patients diagnosed with COVID-19 infection in India, the typical clinical presentation consisted in a mild upper respiratory tract infection predominantly affecting the young male population. One patient required supplemental oxygen. All patients recovered with no residual symptoms. *The Safdarjung Hospital COVID 2019 working group: Nitesh Gupta, Sumita Agrawal, Pranav Ish, Suruchi Mishra, Rajni Gaind, Ganapathy Usha, Balvinder Singh, Manas Kamal Sen, Shibdas Chakrabarti (Consultant and Head, Pulmonary Medicine); NK Gupta (Professor, Pulmonary medicine); Dipak Bhattacharya (Consultant, Pulmonary medicine); Rohit Kumar (Assistant Professor, Pulmonary Medicine); Siddharth R. Yadav (Assistant Professor, Pulmonary Medicine); Rushika Saksena (Specialist, Microbiology); Rojaleen Das (Assistant Professor,Microbiology); Vikramjeet Dutta (Assistant Professor, Microbiology); Anupam Kr Anveshi (Senior Resident, Microbiology); Santvana Kohli (Assistant Professor, Anaesthesiology); Naveen KV (Assistant Professor, Anaesthesiology); Amandeep Jaswal (Assistant Professor, Anaesthesiology).

25 May 2012 in Virology Journal
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Journal Article
Open access
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JSJatin Shrinet
Jatin Shrinet
SJShanu Jain
Shanu Jain
ASAnil Sharma
Anil Sharma
SSShashi Shekhar Singh
Shashi Shekhar Singh
KMKalika Mathur
Kalika Mathur
SSSujatha Sunil
Sujatha Sunil
Background: Chikungunya (CHIK) is currently endemic in South and Central India and exist as co-infections with dengue in Northern India. In 2010, New Delhi witnessed an outbreak of CHIK in the months October-December. This was the first incidence of a dominant CHIK outbreak in Delhi and prompted us to characterize the Delhi virus strains. We have also investigated the evolution of CHIK spread in India. Findings: Clinical samples were subjected to RT-PCR to detect CHIK viral RNA. The PCR amplified products were sequenced and the resulting sequences were genetically analyzed. Phylogenetic analysis based on partial sequences of the structural proteins E1 and E2 revealed that the viruses in the latest outbreak exhibited ECSA lineage. Two novel mutations, E1 K211E and E2 V264A were observed in all Delhi isolates. In addition, CHIKV sequences from eight states in India were analyzed along with Delhi sequences to map the genetic diversity of CHIKV within the country. Estimates of average evolutionary divergence within states showed varying divergence among the sequences both within the states and between the states. We identified distinct molecular signatures of the different genotypes of CHIKV revealing emergence of a new signature in the New Delhi clade. Statistical analyses and construction of evolutionary path of the virus within the country revealed gradual spread of one specific strain all over the country. Conclusion: This study has identified unique mutations in the E1 and E2 genes and has revealed the presence of ancestral CHIKV population with maximum diversity circulating in Maharashtra. The study has further revealed the trend of CHIK spread in India since its first report in 1963 and its subsequent reappearance in 2005.

1 March 2019 in Microbial Pathogenesis
Verified
Journal Article
Closed access
MJManisha Jain
Manisha Jain
ASAmit Sharma
Amit Sharma
MSM.K. Sen
M.K. Sen
VRVandana Rani
Vandana Rani
RGRajni Gaind
Rajni Gaind
JSJ.C. Suri
J.C. Suri

22 February 2021 in Frontiers in Microbiology
Verified
Journal Article
Open access
MAMudsser Azam
Mudsser Azam
RGRajni Gaind
Rajni Gaind
GYGulshan Yadav
Gulshan Yadav
ASAmit Sharma
Amit Sharma
KUKirti Upmanyu
Kirti Upmanyu
RSRuchi Singh
Ruchi Singh
Background: The resistance to colistin and carbapenems in Klebsiella pneumoniae infections have been associated with increased morbidity and mortality worldwide. A retrospective observational study was conducted to determine the prevalence and molecular events contributing to colistin resistance.Methods: Clinical samples were screened for colistin resistance and underlying mechanisms were studied by PCR-based amplification and sequence analysis of genes of two-component regulatory system (phoPQ and pmrAB), regulatory transmembrane protein-coding mgrB, and mobilized colistin resistance genes (mcr-1-8). Gene expression of pmrC and pmrK was analyzed by qRT-PCR, and the genetic relationship was assessed by MLST. The putative effect of amino-acid substitutions was predicted by a combination of bioinformatics tools.Results: Of 335 Klebsiella spp. screened, 11 (3.2%) were identified as colistin-resistant (MIC range, 8 to >128 μg/ml). K. pneumoniae isolates belonged to clonal complex-11 (CC11) with sequence types (STs): 14, 16, 43, 54, 147 and 395, whereby four isolates conferred three novel STs (3986, 3987 and 3988) profiles. Sequence analysis revealed non-synonymous potentially deleterious mutations in phoP (T151A), phoQ (del87–90, del263–264, L30Q, and A351D), pmrA (G53S), pmrB (D150V, T157P, L237R, G250C, A252G, R315P, and Q331H), and mgrB (C28G) genes. The mgrB gene in three strains was disrupted by insertion sequences encoding IS1-like and IS5/IS1182 family-like transposase genes. All 11 isolates showed an elevation in the transcription level of pmrC gene. Mobilized colistin-resistance (mcr) genes were not detected. All but one of the colistin-resistant isolates was also resistant to carbapenems; β-lactamase genes blaNDM-1-like, blaOXA-48-like, and blaCTX-M-like were detected in eight, five, and nine isolates, respectively.Conclusion: All the studied colistin- and carbapenem-resistant K. pneumoniae isolates were genetically distinct, and various mechanisms of colistin resistance were detected, indicating its spontaneous emergence in this bacterial species.

8 July 2016 in BMC Microbiology
Verified
Journal Article
Open access
PDF file
GMGajanand Mittal
Gajanand Mittal
RGRajni Gaind
Rajni Gaind
Deepak KumarDeepak Kumar
Deepak Kumar
GKGaurav Kaushik
Gaurav Kaushik
KGKunj Bihari Gupta
Kunj Bihari Gupta
MDMonorama Deb
Monorama Deb
Resistance amongst the commensal flora is a serious threat because a very highly populated ecosystem like the gut, may at a later stage, be a source of extra intestinal infections, resistant strains may spread to other host or transfer genetic resistance element to other members of micro-biota including pathogens. This study was carried out to assess fecal colonization by carbapenemase producing Enterobacteriaceae (CPE) and associated risk factors among 100 patients admitted to intensive care unit (ICU). The phenotypic and molecular characterizations of CPE were also included. Colonization with CPE was observed in 6.6 % (8/122) controls. Among ICU patients, fecal carriage of CPE was significantly higher on day 4 (D4) (22 %) as compared to day 1 (D1) (11 %) (p value 0.002). The carbapenemase genes detected included OXA- 48, 181, KPC and NDM-1 with NDM-1 being the predominant carbapenemase in both ICU D1 and D4. Among the 50 CPE isolates, 8 (16 %) were susceptible to meropenem and imipenem (Minimum inhibitory concentration; MIC ≤ 1 mg/L) and all were susceptible to colistin (MIC range 0.125 - 1 mg/L) and tigecycline (MIC range 0.06- 1.5 mg/L). The risk factors associated with CPE carriage were duration of ICU stay, use of ventilator and aminoglycosides. Prior colonization with CPE could result in their influx and spread in ICU, challenging infection control measures. Exposure to ICU further increases risk of colonization with diverse carbapenemase-producing Enterobacteriaceae. Gut colonization with these strains may be a source of endogenous infection and horizontal transfer of these genes in future.

4 August 2017 in New Microbes and New Infections
Verified
Journal Article
Open access
NKN. Kaur
N. Kaur
JJJ. Jain
J. Jain
AKA. Kumar
A. Kumar
MNM. Narang
M. Narang
MZM.K. Zakaria
M.K. Zakaria
SSSujatha Sunil
Sujatha Sunil
Chikungunya fever is a major public health issue in India affecting billions. After 2010, the infection was in a decline until in 2016, when a massive outbreak affected the country. In this report, we present serologic and molecular investigations of 600 patient samples for chikungunya and dengue viruses along with clinical and comorbidity features. We recruited 600 patients during this outbreak and evaluated them for chikungunya and dengue virus antibodies and virus RNA through IgM, NS1 antigen and quantitative real-time PCR (qPCR). We further evaluated Zika virus RNA by qPCR. Additionally, we documented all clinical and comorbid features that were observed during the outbreak in the hospital. We report a total incidence rate of 58% of chikungunya during the outbreak in our hospital. Within the recruited patients, 70% of the patients were positive for chikungunya virus IgM whereas 24.17% were positive by qPCR. None of the samples was positive for Zika virus RNA. Additionally, coinfection of dengue and chikungunya was seen in 25.33% of patients. Analysis of clinical features revealed that 97% of patients had restricted movements of the joints with other features like swelling, itching and rashes of varying severity observed. Twelve patients presented with comorbid conditions, and two fatalities occurred among these comorbid patients. The high incidence of coinfection in the current outbreak warrants implementation of routine testing of both chikungunya and dengue virus in suspected patients for better patient management. The post–acute phase complications reported in the hospitals require in-depth studies to understand the actual impact of the current outbreak.