No abstract

Foot-and-mouth disease (FMD) is endemic in Bangladesh, and the implementation of a control programme for this disease is at an early stage, according to the FAO- and OIE-proposed Progressive Control Pathway for FMD (PCP-FMD) Roadmap. To develop an effective control programme, understanding of foot-and-mouth disease virus (FMDV) serotypes, even subtypes within the serotypes is essential. The present investigation aims at viral VP1 coding region sequence-based analysis of FMD samples collected from 34 FMD outbreaks during 2012-2016 in Bangladesh. Foot-and-mouth disease virus (FMDV) serotype O was responsible for 82% of the outbreaks in Bangladesh, showing its dominance over serotype A and Asia1. The VP1 phylogeny revealed the emergence of two novel sublineages of serotype O, named as Ind2001BD1 and Ind2001BD2, within the Ind2001 lineage along with the circulation of Ind2001d sublineage in Bangladesh, which was further supported by the multidimensional scaling with distinct clusters for each sublineage. The novel sublineages had evident genetic variability with other established sublineages within Ind2001 lineage. Ten mutations with three or more amino acid variations were detected within B-C loop, G-H loop and C-terminal region of the VP1 protein of FMDV serotype O viruses isolated exclusively from Bangladesh. Furthermore, two amino acid substitutions at positions 197 and 198 within the VP1 C-terminal region are unique to the novel sublineages. The existence of widespread genetic variations among circulatory FMDV serotype O viruses makes the FMD control programme complex in Bangladesh. Adequate epidemiological data, disease reporting, animal movement control, appropriate vaccination and above all stringent policies of the government are necessary to combat FMD in Bangladesh.

Arsenic (As) contaminated soils are enriched with arsenotrophic bacteria. The present study analyzes the microbiome and arsenotrophic genes-from As affected soil samples of Bhanga, Charvadrason and Sadarpur of Faridpur district in Bangladesh in summer (SFDSL1, 2, 3) and in winter (WFDSL1, 2, 3). Total As content of the soils was within the range of 3.24–17.8 mg/kg as per atomic absorption spectroscopy. The aioA gene, conferring arsenite [As (III)] oxidation, was retrieved from the soil sample, WFDSL-2, reported with As concentration of 4.9 mg/kg. Phylogenetic analysis revealed that the aioA genes of soil WFDSL-2 were distributed among four major phylogenetic lineages comprised of α, β, γ Proteobacteria and Archaea with a dominance of β Proteobacteria (56.67 %). An attempt to enrich As (III) metabolizing bacteria resulted 53 isolates. ARDRA (amplified ribosomal DNA restriction analysis) followed by 16S rRNA gene sequencing of the 53 soil isolates revealed that they belong to six genera; Pseudomonas spp., Bacillus spp., Brevibacillus spp., Delftia spp., Wohlfahrtiimonas spp. and Dietzia spp. From five different genera, isolates Delftia sp. A2i, Pseudomonas sp. A3i, W. chitiniclastica H3f, Dietzia sp. H2f, Bacillus sp. H2k contained arsB gene and showed arsenite tolerance up-to 27 mM. Phenotypic As (III) oxidation potential was also confirmed with the isolates of each genus and isolate Brevibacillus sp. A1a showed significant As (III) transforming potential of 0.2425 mM per hour. The genetic information of bacterial arsenotrophy and arsenite oxidation added scientific information about the possible bioremediation potential of the soil isolates in Bangladesh.Electronic supplementary materialThe online version of this article (doi:10.1186/s13568-016-0193-0) contains supplementary material, which is available to authorized users.

Leigh syndrome (LS) is a rare, inherited neurometabolic disorder that presents with bilateral brain lesions caused by defects in the mitochondrial respiratory chain and associated nuclear-encoded proteins. We generated human induced pluripotent stem cells (iPSCs) from three LS patient-derived fibroblast lines. Using whole-exome and mitochondrial sequencing, we identified unreported mutations in pyruvate dehydrogenase (GM0372, PDH; GM13411, MT-ATP6/PDH) and dihydrolipoyl dehydrogenase (GM01503, DLD). These LS patient-derived iPSC lines were viable and capable of differentiating into progenitor populations, but we identified several abnormalities in three-dimensional differentiation models of brain development. LS patient-derived cerebral organoids showed defects in neural epithelial bud generation, size and cortical architecture at 100 days. The double mutant MT-ATP6/PDH line produced organoid neural precursor cells with abnormal mitochondrial morphology, characterized by fragmentation and disorganization, and showed an increased generation of astrocytes. These studies aim to provide a comprehensive phenotypic characterization of available patient-derived cell lines that can be used to study Leigh syndrome.

Mutations in subunits of the mitochondrial NADH dehydrogenase cause mitochondrial complex I deficiency, a group of severe neurological diseases that can result in death in infancy. The pathogenesis of complex I deficiency remain poorly understood, and as a result there are currently no available treatments. To better understand the underlying mechanisms, we modelled complex I deficiency in Drosophila using knockdown of the mitochondrial complex I subunit ND-75 (NDUFS1) specifically in neurons. Neuronal complex I deficiency causes locomotor defects, seizures and reduced lifespan. At the cellular level, complex I deficiency does not affect ATP levels but leads to mitochondrial morphology defects, reduced endoplasmic reticulum-mitochondria contacts and activation of the endoplasmic reticulum unfolded protein response (UPR) in neurons. Multi-omic analysis shows that complex I deficiency dramatically perturbs mitochondrial metabolism in the brain. We find that expression of the yeast non-proton translocating NADH dehydrogenase NDI1, which reinstates mitochondrial NADH oxidation but not ATP production, restores levels of several key metabolites in the brain in complex I deficiency. Remarkably, NDI1 expression also reinstates endoplasmic reticulum-mitochondria contacts, prevents UPR activation and rescues the behavioural and lifespan phenotypes caused by complex I deficiency. Together, these data show that metabolic disruption due to loss of neuronal NADH dehydrogenase activity cause UPR activation and drive pathogenesis in complex I deficiency.

Mitochondria, special double-membraned intracellular compartments or ‘organelles’, are popularly known as the ‘powerhouses of the cell’, as they generate the bulk of ATP used to fuel cellular biochemical reactions. Mitochondria are also well known for generating metabolites for the synthesis of macromolecules (e.g., carbohydrates, proteins, lipids and nucleic acids). In the mid-1990s, new evidence suggesting that mitochondria, beyond their canonical roles in bioenergetics and biosynthesis, can act as signalling organelles began to emerge, bringing a dramatic shift in our view of mitochondria’s roles in controlling cell function. Over the next two and half decades, works from multiple groups have demonstrated how mitochondrial signalling can dictate diverse physiological and pathophysiological outcomes. In this article, we will briefly discuss different mechanisms by which mitochondria can communicate with cytosol and other organelles to regulate cell fate and function and exert paracrine effects. Our molecular understanding of mitochondrial communication with the rest of the cell, i.e. mitochondrial signalling, could reveal new therapeutic strategies to improve health and ameliorate diseases.

Aging in mammals leads to reduction in genes encoding the 45-subunit mitochondrial electron transport chain complex I. It has been hypothesized that normal aging and age-related diseases such as Parkinson’s disease are in part due to modest decrease in expression of mitochondrial complex I subunits. By contrast, diminishing expression of mitochondrial complex I genes in lower organisms increases lifespan. Furthermore, metformin, a putative complex I inhibitor, increases healthspan in mice and humans. In the present study, we investigated whether loss of one allele of Ndufs2, the catalytic subunit of mitochondrial complex I, impacts healthspan and lifespan in mice. Our results indicate that Ndufs2 hemizygous mice (Ndufs2+/−) show no overt impairment in aging-related motor function, learning, tissue histology, organismal metabolism, or sensitivity to metformin in a C57BL6/J background. Despite a significant reduction of Ndufs2 mRNA, the mice do not demonstrate a significant decrease in complex I function. However, there are detectable transcriptomic changes in individual cell types and tissues due to loss of one allele of Ndufs2. Our data indicate that a 50% decline in mRNA of the core mitochondrial complex I subunit Ndufs2 is neither beneficial nor detrimental to healthspan.

Foodborne pathogens are affecting public health globally. Street foods being an important part in daily life of urban people are considered as a major source of foodborne pathogens. The major sources of street food contamination are water and the unhygienic condition of the vendors and food preparing places. This study was carried out to assess the load of antibiotic resistant enteric bacteria in the hands of street food vendors. A total of 20 street food vendors were selected from various locations in the Dhaka University campus and their hands were rinsed with 500 mL normal saline. Most of the samples contained high total viable counts, total coliforms count and total fecal coliforms count. A total of 25 selective colonies were identified as enteric bacteria including E. coli, Klebsiella spp. and Acinetobacter spp. by biochemical tests and 16S rDNA sequencing. All these isolates showed high antibacterial resistance against Amoxacilin (64%) and most of them showed sensitivity against Ciprofloxacin (76%) and Azithromycin (72%). This study revealed that the hand hygiene of street vendors is very poor and may have serious implications for public health due to possible contamination of food. This study, therefore, suggests proper training and education of street food vendors in order to improve their knowledge of personal hygiene and sanitation. Bangladesh J Microbiol, Volume 34 Number 1 June 2017, pp 33-38