Chemical control of mango anthracnose disease in Ghana

AbstractSeven different fungicides were evaluated in-vitro and in the field for their efficacy against the causal agent and incidence and severity of mango anthracnose disease in Ghana. The recommended rates of Bendazim, (Carbendazim), Funguran (Copper hydroxide), Ivory (Mancozeb), Agriette +Ivory (Fosetyl-Al +Mancozeb), Sundomil (Mancozeb+Metalaxyl), Top Cop (Copper +flowable sulphur), Mirage (Prochloraz), Bendazim+Ivory and Funguran+Ivory were mixed with potato dextrose agar (PDA) and the radial mycelial growth of the pathogen was determined on these amended media. The fungicides were applied on fruit bearing trees in a commercial farm in the Yilo Krobo District after which the disease incidence, severity and percentage of exportable fruits were determined. The results showed that the pathogen was not able to grow on PDA amended with the fungicides. In the field, Bendazim and Funguran fungicides were able to suppress the disease to a large extent resulting in the highest percentage of exportable fruits. Prochloraz solution at both ambient temperature and 53 °C were able to completely eradicate the pathogen, and prevented development of postharvest anthracnose disease symptoms.Original scientific paper. Received 30 Apr 14; revised 23 Sept 14

Pathogenicity and fungicide sensitivity of the causal agent of postharvest stem end rot disease of mango in Ghana

ABSTRACTStudies were carried out on the stem end rot disease of mango in Ghana. The incidence and severity of the disease were evaluated on mango fruits collected from major mango growing areas of Ghana. The causal agent was isolated on media and identified. The pathogenicity of the fungus and its cross-infection potential were determined on mango, avocado, papaya and banana fruits. The sensitivity of the pathogen to fungicides was determined by assessing radial mycelial growth on potato dextrose agar (PDA) amended with nine different fungicides (Bendazim, Funguran, Ivory, Topsin, Asuoku master, Kocide, Mirage, Sulphur 80 and Copper oxychloride). Stem end rot disease was prevalent in the major mango growing areas of Ghana. Two pathogens, Lasiodiplodia theobromae and Colletotrichum gloeosporioides were isolated from the disease lesions. However, only the former was able to cause stem end rot disease symptoms on the artificially inoculated fruits, confirming it as the causal agent of the disease. It was also found to be highly susceptible to Bendazim, Ivory, Topsin, Asuoku master and Mirage, whilst it was resistant to Funguran, Kocide, Sulphur 80 and Copper oxychloride.Original sciencitic paper. Received 30 Apr 15; revised 17 Oct 14

The Aetiology, Incidence and Severity of Mango Tree Decline Disease in Ghana

Mango tree decline was previously an unknown disease in Ghana. In this study, mango trees from all the major agro-ecological zones of Ghana, where mangoes are grown were surveyed for the disease incidence, severity and aetiology of a similar disease affecting the crop. Farm visits were made to some selected farms within the selected agro-ecological zones and both the local and exotic trees were inspected. The percentage of infected trees were calculated while the severity of the disease was rated on a scale of 0-5, where 0 = no symptoms and 5 = death of trees. Samples of the diseased plant parts were collected and the causal agent was isolated on media and identified. The isolated fungus was tested for its pathogenicity using mango seedlings as test crops. The disease, characterised by profuse gumming, bark cracking and die back, was found to be present in all the agro-ecological zones. The disease incidence was higher on the local variety compared to the exotic varieties. Lasiodiplodia theobromae, isolated from the diseased plant parts, was able to cause the disease on inoculated mango seedlings. The nature of the disease symptoms and its causative agent in Ghana, confirms the disease as the mango tree decline disease

Differentiation of two Botryosphaeriaceae species isolated from declining mango trees in Ghana

Lasiodiplodia theobromae is the only pathogen reported to cause mango tree decline disease in Ghana. In this study, several Botryosphaeriaceae isolates were obtained from mango tree decline disease symptoms and were identified using both phenotypic and genotypic characteristics and inoculation studies. The methods employed differentiated the isolates into two species, Lasiodiplodia theobromae and Neofussicoccum parvum. L. theobromae sporulated freely on media while N. parvum did not. Also, the species specific primer, Lt347-F/Lt347-R identified only L. theobromae while in the phylogenetic studies, L. theobromae and N. parvum clustered in different clades. L. theobromae caused dieback symptoms on inoculated mango seedlings while N. parvum did not. However, both species caused massive rot symptoms on inoculated fruits. L. theobromae was therefore confirmed as the causal agent of the tree decline disease in Ghana while N. parvum was reported for the first time as a potential pathogen of mango fruits in the country

Telomeric rather than centromeric activating KIR genes protect from cytomegalovirus infection after kidney transplantation

Cytomegalovirus (CMV) infection is a common complication after organ transplantation. Previous studies have demonstrated that activating killer-cell immunoglobulin-like receptors (KIR) may reduce the rate of CMV infection. KIR genes can be divided into haplotype A (containing a fixed set of inhibitory receptors) and haplotype B (carrying additional activating KIR genes). The KIR locus is divided into a centromeric and a telomeric portion, both of which may carry A or B haplotype motifs. We studied a cohort of 339 kidney transplant recipients to elucidate which KIR genes protect from CMV infection. CMV infection occurred in 139 patients (41%). Possession of telomeric (hazard ratio 0.64, 95% confidence interval 0.44-0.94, p = 0.02) but not centromeric (HR 0.86, 95% CI 0.60-1.23, p = 0.41) B motifs was associated with statistically significant protection from CMV infection. Due to linkage disequilibrium, we were not able to identify a single protective gene within the telomeric B complex (which may contain the KIR2DS1, KIR3DS1, KIR2DL5A and KIR2DS5 genes). The presence of known or putative ligands to activating KIR did not significantly modify the influence of telomeric B group genes. We confirm that B haplotypes protect from CMV infection after kidney transplantation and show that this arises from telomeric B haplotype genes

Algorithms for the determination of unacceptable HLA antigen mismatches in kidney transplant recipients

Transplantation and autoimmunit