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Objective:To assess facility readiness and identify barriers to the facility-based management of childhood severe acute malnutrition (SAM) in public healthcare settings.Design:Qualitative methods were applied to assess readiness and identify different perspectives on barriers to the facility-based management of children with SAM. Data collection was done using in-depth interviews, key informant interviews, exit interviews and pre-tested observation tools.Settings:Two tertiary care and four district hospitals in Rangpur and Sylhet Divisions of Bangladesh.Participants:Healthcare professionals and caregivers of children with SAM.Results:Anthropometric tools, glucometer, medicines, F-75, F-100 and national guidelines for facility-based management of childhood SAM were found unavailable in some of the hospitals. Sitting and sleeping arrangements for the caregivers were absent in all of the chosen facilities. We identified a combination of health system and contextual barriers that inhibited the facility-based management of SAM. The health system barriers include inadequate manpower, rapid turnover of staff, increased workload, lack of training and lack of adherence to management protocol. The major facility barriers were insufficient space and unavailability of required equipment, medicines and foods for hospitalised children with SAM. The reluctance of caregivers to complete the treatment regimen, their insufficient knowledge regarding proper feeding, increased number of attendants and poverty of parents were the principal contextual barriers.Conclusions:The study findings provide insights on barriers that are curbing the facility-based management of SAM and emphasise policy efforts to develop feasible interventions to reduce the barriers and ensure the preparedness of the facilities for effective service delivery.

Background: Severe acute malnutrition (SAM) contributes to a substantial number of child deaths globally per year. The mortality rates can be lowered markedly if guideline-based management protocol is properly followed. However, case-fatality rates in resource-poor centers remain high even after introducing the guidelines. Perhaps, the lack of adequate knowledge leading to inappropriate management by the health care providers is responsible for such burden. Objective: We aimed to evaluate health care providers’ knowledge, attitude, and practice regarding the facility-based management of children with SAM in Bangladesh. Methods: This was a qualitative study where data were collected cross-sectionally from 4 district and 2 tertiary care hospitals. Twenty-six semi-structured in-depth interviews were conducted among the doctors and nurses involved in inpatient care of SAM. Twenty-eight hours of observation were done in each facility to obtain information regarding the management practices. Results: The doctors had substantial knowledge in managing children with SAM in the facilities. However, knowledge of nurses was found suboptimal when evaluated based on the national guideline. Both doctors and nurses demonstrated favorable attitude toward management of childhood SAM. Identification of SAM at the facilities was poor due to lack of practice in relation to anthropometric measurements. In addition, improper practices related to blood glucose testing, dehydration monitoring, essential micronutrient administration, and follow-up of children with SAM were observed. Conclusion: The study results underscore the importance of taking appropriate measures to enhance knowledge and ensure proper practice in relation to inpatient care of children with SAM according to the national guideline in Bangladesh.

Disrupted development of the gut microbiota is a contributing cause of childhood malnutrition. Bifidobacterium longum subspecies infantis is a prominent early colonizer of the infant gut that consumes human milk oligosaccharides (HMOs). We found that the absolute abundance of Bifidobacterium infantis is lower in 3- to 24-month-old Bangladeshi infants with severe acute malnutrition (SAM) compared to their healthy age-matched counterparts. A single-blind, placebo-controlled trial (SYNERGIE) was conducted in 2- to 6-month-old Bangladeshi infants with SAM. A commercial U.S. donor–derived B. infantis strain (EVC001) was administered daily with or without the HMO lacto- N -neotetraose for 28 days. This intervention increased fecal B. infantis abundance in infants with SAM, although to levels still 10- to 100-fold lower than in untreated healthy controls. EVC001 treatment promoted weight gain that was associated with reduced intestinal inflammation markers in infants with SAM. We cultured fecal B. infantis strains from Bangladeshi infants and colonized gnotobiotic mice with these cultured strains. The gnotobiotic mice were fed a diet representative of that consumed by 6-month-old Bangladeshi infants, with or without HMO supplementation. One B. infantis strain, Bg_2D9, expressing two gene clusters involved in uptake and utilization of N -glycans and plant-derived polysaccharides, exhibited superior fitness over EVC001. The fitness advantage of Bg_2D9 was confirmed in a gnotobiotic mouse model of mother-to-infant gut microbiota transmission where dams received a pretreatment fecal community from a SAM infant in the SYNERGIE trial. Whether Bg_2D9 is superior to EVC001 for treating malnourished infants who consume a diet with limited breastmilk requires further clinical testing.

Dysregulations in the mammalian target of rapamycin (mTOR) pathway are associated with several human anomalies. We aimed to elucidate possible implications for potential aberrations in the mTOR pathway with childhood malnutrition. We analyzed the activity of phospho-mTORC1 and the expressions of several mTOR pathway genes, namely: MTOR, TSC1, LAMTOR2, RPS6K1 and RICTOR from peripheral blood mononuclear cells isolated from venous blood of children suffering from different forms of malnutrition and compared them with those from healthy children. Significant reduction in the phosphorylation of mTORC1 was noted, as well as a decrease in expression of LAMTOR2 gene and increase in TSC1 gene expression were observed between malnourished children in comparison to the healthy children. The deregulation in the activity of the TSC1 and LAMTOR2 gene was significantly associated with all forms of childhood malnutrition. Our findings provide key insights into possible down-modulation in the overall activity of the mTOR pathway in childhood malnutrition. Further studies focusing on the analysis of a multitude of components involved in the mTOR pathway both at the gene and protein expression levels are required for conclusive evidence for the aforementioned proposition. publishedVersion