The Role of Maize Tassels in Amelioration of Heavy Metals from Contaminated Soils and its Effects on Vegetables.

Vegetables depend on water as solvent for their growth and have greater potential of accumulating in their edible parts heavy metals which are dangerous to human health.  Maize tassel was applied to soil to determine its role in removal of heavy metals such as Manganese (Mn), Iron (Fe), Cadmium (Cd) and Zinc (Zn) from the contaminated soil with cabbage as the test crop. The average mean concentration of the heavy metals after twenty one and fifty one days were; Mn (0.402 mg/kg and 7.427 mg/kg), Fe (0.894 mg/kg and 4.838 mg/kg) and Zn (0.155 mg/kg and 1.073 mg/kg) respectively. The concentration of cadmium in the wastewater sample used was 0.680mg/l, and its concentrations in tap water (<0.002mg/l), in soil (<0.002mg/kg) were below the detection limit. The enrichment factor for Mn, Fe and Zn in soil treated with maize tassel (T1) are 9.73, 10.70 and 5.23 respectively, whereas treatment without (T2) are 1.05, 1.86 and 4.52 respectively. The high enrichment of T1 is attributed to the availability of the active site within the tassel absorbent. Keywords: Heavy metals, maize tassel, contaminated soil, wastewater

The use of maize tassel as an agricultural by-product to ameliorate heavy metals in contaminated groundwater

The presence of heavy metals in drinking water usually tends to pose some adverse effects to the consumers. It is in the light of this that maize tassel which is usually an agricultural by product was used to remove mercury arsenic, manganese and lead from contaminated water. Maize tassel was milled into fine powder. A laboratory simulated contamination of the above mentioned metals was prepared to a concentration of 2.000  mg/L. Groundwater contaminated samples were also obtained and run through 20.0g of the powdered maize tassel at specific time steps of 0, 15, 30, 45 and 60 minutes respectively. The water that drained out of the tassel was then analyzed for the amount of metals remaining in it using Shimadzu Atomic Absorption Spectrophotometer model AA6300. The concentrations of arsenic, manganese lead and mercury in the laboratory  simulated solution after it had passed through the maize tassel for a period of 60 minutes was 0.001 mg/L, 0.005 mg/L, 0.203 mg/L and 0.020 mg/L respectively. The concentrations of arsenic, manganese, lead and mercury in the contaminated groundwater after passing through the tassel  was 0.0005 mg/L, 0.0021 mg/L, 0.050 mg/L and 0.025 mg/L respectively

Secondary bacterial infections of buruli ulcer lesions before and after chemotherapy with streptomycin and rifampicin

Buruli ulcer (BU), caused by Mycobacterium ulcerans is a chronic necrotizing skin disease. It usually starts with a subcutaneous nodule or plaque containing large clusters of extracellular acid-fast bacilli. Surrounding tissue is destroyed by the cytotoxic macrolide toxin mycolactone produced by microcolonies of M. ulcerans. Skin covering the destroyed subcutaneous fat and soft tissue may eventually break down leading to the formation of large ulcers that progress, if untreated, over months and years. Here we have analyzed the bacterial flora of BU lesions of three different groups of patients before, during and after daily treatment with streptomycin and rifampicin for eight weeks (SR8) and determined drug resistance of the bacteria isolated from the lesions. Before SR8 treatment, more than 60% of the examined BU lesions were infected with other bacteria, with Staphylococcus aureus and Pseudomonas aeruginosa being the most prominent ones. During treatment, 65% of all lesions were still infected, mainly with P. aeruginosa. After completion of SR8 treatment, still more than 75% of lesions clinically suspected to be infected were microbiologically confirmed as infected, mainly with P. aeruginosa or Proteus miriabilis. Drug susceptibility tests revealed especially for S. aureus a high frequency of resistance to the first line drugs used in Ghana. Our results show that secondary infection of BU lesions is common. This could lead to delayed healing and should therefore be further investigated

Genomic Diversity and Evolution of Mycobacterium ulcerans Revealed by Next-Generation Sequencing

Mycobacterium ulcerans is the causative agent of Buruli ulcer, the third most common mycobacterial disease after tuberculosis and leprosy. It is an emerging infectious disease that afflicts mainly children and youths in West Africa. Little is known about the evolution and transmission mode of M. ulcerans, partially due to the lack of known genetic polymorphisms among isolates, limiting the application of genetic epidemiology. To systematically profile single nucleotide polymorphisms (SNPs), we sequenced the genomes of three M. ulcerans strains using 454 and Solexa technologies. Comparison with the reference genome of the Ghanaian classical lineage isolate Agy99 revealed 26,564 SNPs in a Japanese strain representing the ancestral lineage. Only 173 SNPs were found when comparing Agy99 with two other Ghanaian isolates, which belong to the two other types previously distinguished in Ghana by variable number tandem repeat typing. We further analyzed a collection of Ghanaian strains using the SNPs discovered. With 68 SNP loci, we were able to differentiate 54 strains into 13 distinct SNP haplotypes. The average SNP nucleotide diversity was low (average 0.06–0.09 across 68 SNP loci), and 96% of the SNP locus pairs were in complete linkage disequilibrium. We estimated that the divergence of the M. ulcerans Ghanaian clade from the Japanese strain occurred 394 to 529 thousand years ago. The Ghanaian subtypes diverged about 1000 to 3000 years ago, or even much more recently, because we found evidence that they evolved significantly faster than average. Our results offer significant insight into the evolution of M. ulcerans and provide a comprehensive report on genetic diversity within a highly clonal M. ulcerans population from a Buruli ulcer endemic region, which can facilitate further epidemiological studies of this pathogen through the development of high-resolution tools

Laboratory diagnosis of Buruli ulcer : challenges and future perspectives

Current options to control Buruli ulcer (BU) are limited, as no effective vaccine is available and knowledge on transmission mechanisms of the causative agent, Mycobacterium ulcerans, is incomplete. Early case detection and rapid initiation of treatment are key elements to prevent the development of large, disfiguring ulcers often associated with permanent physical disability and stigma. BU has been reported from 34 countries, with the greatest disease burden in West Africa and steadily increasing case numbers in south-eastern Australia. The disease can present in a variety of clinical manifestations, including relatively unspecific, painless nodules, plaques, and edema, which may eventually progress to chronic, ulcerative lesions. The clinical diagnosis of BU is therefore complicated by a broad differential diagnosis, particularly in tropical areas, where the prevalence of other skin conditions with a similar appearance is high. With the introduction of combination antibiotic therapy, replacing excision surgery as the standard treatment for BU, pre-treatment confirmation of the clinical diagnosis has further gained in importance to avoid the redundant use of anti-mycobacterial drugs. At present, available confirmatory diagnostic tests either lack sufficient sensitivity/specificity or are centralized and thus often not accessible to patients living in remote, rural areas of Africa. In recognition of this disparity, WHO and other stakeholders have called for new diagnostic tools for BU that can be applied at district hospitals or primary healthcare facilities. This chapter highlights challenges, advances and future prospects for the necessary decentralization of the diagnosis of BU