Hemoglobin level was primarily associated with iron status in these Indian toddlers; however, maternal hemoglobin level, family wealth, and food insecurity were also important factors. Strategies for minimizing childhood anemia must include optimized iron intake but should simultaneously address maternal anemia, poverty, and food insecurity.
Background
The molecular structure of circulating enteric fever pathogens was studied using hospital-based genomic surveillance in a tertiary care referral centre in South India as a first genomic surveillance study, to our knowledge, of blood culture-confirmed enteric fever in the region.
Methods
Blood culture surveillance was conducted at St John’s Medical College Hospital, Bengaluru, between July 2016 and June 2017. The bacterial isolates collected were linked to demographic variables of patients and subjected to WGS. The resulting pathogen genomic data were also globally contextualized to gauge possible phylogeographical patterns.
Results
Hospital-based genomic surveillance for enteric fever in Bengaluru, India, identified 101 Salmonella enterica Typhi and 14 S. Paratyphi A in a 1 year period. Ninety-six percent of isolates displayed non-susceptibility to fluoroquinolones. WGS showed the dominant pathogen was S. Typhi genotype 4.3.1.2 (H58 lineage II). A fluoroquinolone-resistant triple-mutant clone of S. Typhi 4.3.1.2 previously associated with gatifloxacin treatment failure in Nepal was implicated in 18% of enteric fever cases, indicating ongoing inter-regional circulation.
Conclusions
Enteric fever in South India continues to be a major public health issue and is strongly associated with antimicrobial resistance. Robust microbiological surveillance is necessary to direct appropriate treatment and preventive strategies. Of particular concern is the emergence and expansion of the highly fluoroquinolone-resistant triple-mutant S. Typhi clone and its ongoing inter- and intra-country transmission in South Asia, which highlights the need for regional coordination of intervention strategies, including vaccination and longer-term strategies such as improvements to support hygiene and sanitation.
This study aimed to determine the antibiotic susceptibility pattern of Staphylococcus aureus (SA) and the circulating clones in Bangalore, India. Susceptibility testing was performed for all cases of SA infections in a tertiary-care hospital. Panton-Valentine leucocidin (PVL) encoding genes were detected, and sequence type and spa type were determined. Out of the 92 collected strains, 52.2% were methicillin-resistant SA (MRSA), isolated from community-acquired (CA) infections in 60.4% and hospital-acquired (HA) infections in 39.6%. S. aureus isolates were also highly resistant to erythromycin (54.3%) and ciprofloxacin (70.6%) in methicillin-susceptible SA (MSSA) and MRSA, as well as in CA and HA infections. MRSA were found to be significantly more resistant to gentamicin (p <0.001), cotrimoxazole (p <0.001) and ciprofloxacin (p 0.001) than MSSA, but no significant difference was observed between CA- and HA-SA. ST217 appeared as a new emerging and prevalent clone, but ST772 remained the predominant clone, all being PVL-positive isolates. Our study points out the high prevalence of MRSA, even in the community, and the worrying increase of resistance to ciprofloxacin and erythromycin among CA-MSSA. Emergence of clone ST217 is reported for the first time in India.
These findings suggest that the burden of rickettsial infection among children in India is high, with a substantially high complication rate. Rickettsial-specific ELISA tests can help in early diagnosis and early institution of appropriate treatment that may prevent life-threatening complications.
Introduction
– An unprecedented rise in number of COVID-19 associated mucormycosis (CAM) cases has been reported in India. Myriad hyptheses are proposed for the outbreak. We recently reported uncontrolled diabetes and inappropriate steroid therapy as significant risk factors for the outbreak. However, Mucorales contamination of hospital environment was not studied. We, therefore, planned this multi-centre study across India to determine possible Mucorales contamination of hospital environment during the outbreak.
Methods
Eleven hospitals from four zones of India representing high to low incidence for mucormycosis cases were included in the study. Samples from a variety of equipment used by the patients and ambient air were collected during May 19, 2021 through August 25, 2021.
Results
None of the hospital equipment sampled was contaminated with Mucorales. However, Mucorales were isolated from 11.1% air-conditioning vents and 1.7% of patients’ used masks. Other fungi were isolated from 18% hospital equipment and surfaces, and 8.1% used masks. Mucorales grew from 21.7% indoor and 53.8% outdoor air samples. Spore counts of Mucorales in air were significantly higher in the hospitals of North and South zones compared to West and East zones (
P
< 0.0001). Among Mucorales isolated from the environment
Rhizopus
spp. were the commonest genus.
Conclusion
– We found contamination of air-conditioning vents and hospital air by Mucorales. Presence of Mucorales in these areas demands regular surveillance and improvement of hospital environment, as contamination may contribute to healthcare associated mucormycosis outbreaks, especially among immunocompromised patients.
Concanavalin-A (Con-A) hepatitis is regarded as a T cell-mediated model of acute liver injury. Mincle is a C-type lectin receptor (CLR) that is critical in the immune response to mycobacteria and fungi, but does not have a well-defined role in pre-clinical models of non-pathogen mediated inflammation. Since Mincle can ligate the cell death ligand SAP130, we postulated that Mincle signaling drives intrahepatic inflammation and liver injury in Con-A hepatitis. Acute liver injury was assessed in the murine Con-A hepatitis model using C57BL/6, Mincle−/−, and Dectin-1−/− mice. The role of C/EBPβ and HIF-1α signaling was assessed using selective inhibitors. We found that Mincle was highly expressed in hepatic innate inflammatory cells and endothelial cells in both mice and humans. Furthermore, sterile Mincle ligands and Mincle signaling intermediates were increased in the murine liver in Con-A hepatitis. Most significantly, Mincle deletion or blockade protected against Con-A hepatitis whereas Mincle ligation exacerbated disease. Bone marrow chimeric and adoptive transfer experiments suggested that Mincle signaling in infiltrating myeloid cells dictates disease phenotype. Conversely, signaling via other CLRs did not alter disease course. Mechanistically, we found that Mincle blockade decreased the NF-κβ related signaling intermediates, C/EBPβ and HIF-1α, both of which are necessary in macrophage-mediated inflammatory responses. Accordingly, Mincle deletion lowered production of nitrites in Con-A hepatitis and inhibition of both C/EBPβ and HIF1-α reduced the severity of liver disease. Our work implicates a novel innate immune driver of Con-A hepatitis and, more broadly, suggests a potential role for Mincle in diseases governed by sterile inflammation.
Due to a high level of antimicrobial resistance amongst the pathogens causing UTI in India, it is cautious to advise or modify therapy, as far as possible, after culture and sensitivity testing have been performed. Regional surveillance programs are warranted for the development of national UTI guidelines.
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