- Treatment outcome and factors affecting time to recovery in children with severe acute malnutrition treated at outpatient therapeutic care program. [Journal Article]
- Glob Health Action 2016.:30704.
The outpatient therapeutic care program (OTP) of children with severe acute malnutrition (SAM) has been decentralized to health post level in Ethiopia since 2008-2009. However, there is a lack of evidence regarding treatment outcomes and factors related to the duration of stay on treatment after its decentralization to health post level.This study was aimed to assess treatment outcome and factors affecting time to recovery in children with SAM treated at OTP.Health facility-based retrospective cohort study was conducted using data from 348 patient cards. The outcome variable was time to recovery. Descriptive analysis was done using percentages for categorical data and mean/median for continuous variables. A robust method of analyzing time to event data, the Cox proportional-hazard regression, was used. All statistical tests in this study are declared significant at p<0.05.89.1% of children with kwashiorkor and 69.4% of children with marasmus were recovered. Of the total children studied, 22% were readmitted cases. The median time of recovery was 35 days for children with kwashiorkor and 49 days for children with marasmus. Children older than 3 years were 33% less likely to achieve nutritional recovery [adjusted hazard ratio, AHR=0.67, 95% confidence interval, CI (0.46, 0.97)]. Similarly, marasmic children stayed longer on treatment [AHR=0.42, 95% CI (0.32, 0.56)]. However, children who gained Mid-Upper Arm Circumference (MUAC) ≥ 0.24 mm/day were 59% more likely to recover faster [AHR=1.59, 95% CI (1.23, 2.06)].Close monitoring of weight and MUAC gain to assess nutritional improvement with due emphasis given to children with lower admission weight, children of age 3 years and above and marasmic children will have a positive effect on treatment duration and outcome.
- Meta-analysis on efficacy of amoxicillin in uncomplicated severe acute malnutrition. [LETTER]
- Microb Pathog 2016 Jun 29.
- Tessaracoccus massiliensis sp. nov., a new bacterial species isolated from the human gut. [Journal Article]
- New Microbes New Infect 2016 Sep.:3-12.
A new Actinobacterium, designated Tessaracoccus massiliensis type strain SIT-7(T) (= CSUR P1301 = DSM 29060), have been isolated from a Nigerian child with kwashiorkor. It is a facultative aerobic, Gram positive, rod shaped, non spore-forming, and non motile bacterium. Here, we describe the genomic and phenotypic characteristics of this isolate. Its 3,212,234 bp long genome (1 chromosome, no plasmid) exhibits a G+C content of 67.81% and contains 3,058 protein-coding genes and 49 RNA genes.
- Anaeromassilibacillus senegalensis gen. nov., sp. nov., isolated from the gut of a child with kwashiorkor. [Journal Article]
- New Microbes New Infect 2016 Jul.:59-60.
We report the main characteristics of Anaeromassilibacillus senegalensis strain mt9(T) (= CSUR P1511) isolated from the stool of a 1-year-old kwashiorkor patient from Senegal.
- Anaerococcus rubiinfantis sp. nov., isolated from the gut microbiota of a Senegalese infant with severe acute malnutrition. [Journal Article]
- Anaerobe 2016 Aug.:85-94.
Anaerococcus rubiinfantis sp. nov. strain mt16(T) is a new species within the genus Anaerococcus, which was isolated by the culturomics approach from the gut microbiota of an infant suffering from kwashiorkor. A phenotypic, biochemical and proteomic description of this strain is hereby presented alongside a complete annotation of its genome. This strictly anaerobic species forms Gram-positive non-sporeforming cocci. The major fatty acid was hexadecanoic acid. The phylogenetic analysis of strain mt16(T) showed a 97.9% similarity level with Anaerococcus vaginalis, the closest validly published species. Its genome is 1,929,161 bp long with 29.5% G + C content and contains 1808 protein-coding genes and 56 RNA genes, among which are six rRNA genes. Genomic analysis identified 41/1864 coding genes as ORFans (2.2%) and at least 620/1808 (34.9%) orthologous proteins which are not shared with the closest phylogenetic species. We believe that the extension of the human anaerobic gut compendium by culturomics is one of the first steps that will improve the understanding of the links between the microbiome and health or disease.
- Malnutrition-associated liver steatosis and ATP depletion is caused by peroxisomal and mitochondrial dysfunction. [JOURNAL ARTICLE]
- J Hepatol 2016 Jun 13.
Severe malnutrition in young children is associated with signs of hepatic dysfunction such as steatosis and hypoalbuminemia, but its etiology is unknown. Peroxisomes and mitochondria play key roles in various hepatic metabolic functions including lipid metabolism and energy production. To investigate the involvement of these organelles in the mechanisms underlying malnutrition-induced hepatic dysfunction we developed a rat model of malnutrition.Weanling rats were placed on a low protein or control diet (5% or 20% of calories from protein, respectively) for four weeks. Peroxisomal and mitochondrial structural features were characterized using immunofluorescene and electron microscopy. Mitochondrial function was assessed using high-resolution respirometry. A novel targeted quantitative proteomics method was applied to analyze 47 mitochondrial proteins involved in oxidative phosphorylation, tricarboxylic acid cycle and fatty acid β-oxidation pathways.Low protein diet-fed rats developed hypoalbuminemia and hepatic steatosis, consistent with the human phenotype. Hepatic peroxisome content was decreased and metabolomic analysis indicated peroxisomal dysfunction. This was followed by changes in mitochondrial ultrastructure and increased mitochondrial content. Mitochondrial function was impaired due to multiple defects affecting respiratory chain complex I and IV, pyruvate uptake and several β-oxidation enzymes, leading to strongly reduced hepatic ATP levels. Fenofibrate supplementation restored hepatic peroxisome abundance and increased mitochondrial β-oxidation capacity, resulting in reduced steatosis and normalization of ATP and plasma albumin levels.Malnutrition leads to severe impairments in hepatic peroxisomal and mitochondrial function, and hepatic metabolic dysfunction. We discuss the potential future implications of our findings for the clinical management of malnourished children.Severe malnutrition in children is associated with metabolic disturbances that are poorly understood. In order to study this further, we developed a malnutrition animal model and found that severe malnutrition leads to an impaired function of liver mitochondria which are essential for energy production and a loss ofperoxisomes, which areimportant for normal liver metabolic function.
- Daily co-trimoxazole prophylaxis to prevent mortality in children with complicated severe acute malnutrition: a multicentre, double-blind, randomised placebo-controlled trial. [Journal Article]
- Lancet Glob Health 2016 Jul; 4(7):e464-73.
Children with complicated severe acute malnutrition (SAM) have a greatly increased risk of mortality from infections while in hospital and after discharge. In HIV-infected children, mortality and admission to hospital are prevented by daily co-trimoxazole prophylaxis, despite locally reported bacterial resistance to co-trimoxazole. We aimed to assess the efficacy of daily co-trimoxazole prophylaxis on survival in children without HIV being treated for complicated SAM.We did a multicentre, double-blind, randomised, placebo-controlled study in four hospitals in Kenya (two rural hospitals in Kilifi and Malindi, and two urban hospitals in Mombasa and Nairobi) with children aged 60 days to 59 months without HIV admitted to hospital and diagnosed with SAM. We randomly assigned eligible participants (1:1) to 6 months of either daily oral co-trimoxazole prophylaxis (given as water-dispersible tablets; 120 mg per day for age <6 months, 240 mg per day for age 6 months to 5 years) or matching placebo. Assignment was done with computer-generated randomisation in permuted blocks of 20, stratified by centre and age younger or older than 6 months. Treatment allocation was concealed in opaque, sealed envelopes and patients, their families, and all trial staff were masked to treatment assignment. Children were given recommended medical care and feeding, and followed up for 12 months. The primary endpoint was mortality, assessed each month for the first 6 months, then every 2 months for the second 6 months. Secondary endpoints were nutritional recovery, readmission to hospital, and illness episodes treated as an outpatient. Analysis was by intention to treat. This trial was registered at ClinicalTrials.gov, number NCT00934492.Between Nov 20, 2009, and March 14, 2013, we recruited and assigned 1778 eligible children to treatment (887 to co-trimoxazole prophylaxis and 891 to placebo). Median age was 11 months (IQR 7-16 months), 306 (17%) were younger than 6 months, 300 (17%) had oedematous malnutrition (kwashiorkor), and 1221 (69%) were stunted (length-for-age Z score <-2). During 1527 child-years of observation, 122 (14%) of 887 children in the co-trimoxazole group died, compared with 135 (15%) of 891 in the placebo group (unadjusted hazard ratio [HR] 0·90, 95% CI 0·71-1·16, p=0·429; 16·0 vs 17·7 events per 100 child-years observed (CYO); difference -1·7 events per 100 CYO, 95% CI -5·8 to 2·4]). In the first 6 months of the study (while participants received study medication), 63 suspected grade 3 or 4 associated adverse events were recorded among 57 (3%) children; 31 (2%) in the co-trimoxazole group and 32 (2%) in the placebo group (incidence rate ratio 0·98, 95% CI 0·58-1·65). The most common adverse events of these grades were urticarial rash (grade 3, equally common in both groups), neutropenia (grade 4, more common in the co-trimoxazole group), and anaemia (both grades equally common in both groups). One child in the placebo group had fatal toxic epidermal necrolysis with concurrent Pseudomonas aeruginosa bacteraemia.Daily co-trimoxazole prophylaxis did not reduce mortality in children with complicated SAM without HIV. Other strategies need to be tested in clinical trials to reduce deaths in this population.Wellcome Trust, UK.
- Noncontiguous finished genome sequence and description of Bacillus andreraoultii strain SIT1(T) sp. nov. [Journal Article]
- New Microbes New Infect 2016 Mar.:25-35.
Bacillus andreraoultii strain SIT1(T) (= CSUR P1162 = DSM 29078) is the type strain of B. andreraoultii sp. nov. This bacterium was isolated from the stool of a 2-year-old Nigerian boy with a severe form of kwashiorkor. Bacillus andreraoultii is an aerobic, Gram-positive rod. We describe here the features of this bacterium, together with the complete genome sequencing and annotation. The 4 092 130 bp long genome contains 3718 protein-coding and 116 RNA genes.
- Genome sequence and description of Desnuesiella massiliensis gen. nov., sp. nov. a new member of family Clostridiaceae. [Journal Article]
- New Microbes New Infect 2016 May.:84-90.
Desnuesiella massiliensis, strain MT10(T) gen. nov., sp. nov. is a newly proposed genus within the family Clostridiaceae, isolated from the digestive microbiota of a child suffering from kwashiorkor. Desnuesiella massiliensis is a facultatively anaerobic, Gram-positive rod. Here we describe the features of this organism, together with the complete genome sequence and annotation. The 5 503 196-bp long genome (one chromosome but no plasmid) contains 5227 protein-coding and 81 RNA genes, including 14 rRNA genes.
- Bacillus niameyensis sp. nov., a new bacterial species isolated from human gut. [Journal Article]
- New Microbes New Infect 2015 Nov.:61-9.
Bacillus niameyensis sp. nov. strain SIT3(T) (= CSUR P1266 = DSM 29725) is the type strain of B. niameyensis sp. nov. This Gram-positive strain was isolated from the digestive flora of a child with kwashiorkor and is a facultative anaerobic rod and a member of the Bacillaceae family. This organism is hereby described alongside its complete genome sequence and annotation. The 4 286 116 bp long genome (one chromosome but no plasmid) contains 4130 protein-coding and 66 RNA genes including five rRNA genes.