373 research outputs found

    Understanding the Genetics of Clubroot Resistance for Effectively Controlling this Disease in Brassica Species

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    Clubroot disease is one of the most serious diseases of Brassica species, which is caused by soil-borne pathogen Plasmodiophora brassicae Woronin. Clubroot disease has a long history on vegetable crops belonging to the Brassica species; most recently, this disease is also invading rapeseed/canola crop around the globe. The clubroot disease causes significant yield and quality losses in highly infected fields. Clubroot pathogens invade into the host plant roots and infect root tissues with the formation of abnormal clubs, named as galls, which results in incompetent plant roots to intake water and nutrients and eventually dead plants. As it is a soil-borne disease and accomplishes its disease cycle in two different phases and both phases are highly efficient to damage root system as well as to release more inoculum, there are many challenges to control this disease through chemical and other cultural practices. In general, clubroot disease can be effectively managed by developing resistant cultivars. In this chapter, various resistance sources of clubroot disease in different Brassica species have been discussed with potential applications in canola/rapeseed breeding programs worldwide. Importance of gene mapping and molecular marker development efforts by different research studies for clubroot in B. rapa, B. oleracea, and B. napus has been stressed. Transcriptomic and metabolomic changes occurring during host–pathogen interactions are also covered in this chapter, which would enhance our understanding and utilization of clubroot resistance in Brassica species

    Major role of pKpQIL-like plasmids in the early dissemination of KPC-type carbapenemases in the UK

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    Objectives: KPC-producing Enterobacteriaceae were first seen in the UK in 2003 and have been increasingly reported since 2010, largely owing to an ongoing outbreak in North-West England. We examined the role of clonal spread and plasmid transmission in their emergence. Methods: Isolates comprised KPC-positive Klebsiella pneumoniae (n=33), Escherichia coli (n=7) and Enterobacter spp. (n=4) referred to the national reference laboratory between 2008 and 2010 from 17 UK centres, including three in North-West England. Isolates were typed by MLST. Plasmids were transferred by electroporation and characterised by PCR or sequencing. PCR screening assays were developed to distinguish plasmid pKpQIL variants. Results: The K. pneumoniae isolates included 10 STs, of which three belonged to clonal group (CG) 258. CG258 (n=19) isolates were detected in 13 centres but accounted for only 7/19 (36.8%) of those from North-West England. Most KPC-producers (37/44, 84.1%), including 16/19 CG258 K. pneumoniae carried blaKPC on IncFIIK2 plasmids. Sequencing of a subset of these plasmids (n=11) revealed similarities with published pKpQIL. One variant, pKpQIL-UK - identified in K. pneumoniae CG258 (n=5) and ST468 (n=1) isolates from distinct centres - had only a few nucleotide changes from classical pKpQIL, whereas pKpQIL-D1 (n=1) and pKpQIL-D2 (n=4), from isolates of various species in the North-West, harboured large variations reflecting replacement of the partitioning and replication functions and potentially thereby facilitating spread. PCR revealed that 36/37 (97.3%) IncFIIK2-type plasmids in KPC-positive isolates had pKpQIL markers. Conclusions: pKpQIL-like plasmids played a major role in the early dissemination of KPC enzymes in the UK

    Prevalence and correlates of cardiometabolic multimorbidity among hypertensive individuals: A cross-sectional study in rural South Asia—Bangladesh, Pakistan and Sri Lanka

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    Objective: To determinate the prevalence and correlates of cardiometabolic multimorbidity (CMM), and their cross-country variation among individuals with hypertension residing in rural communities in South Asia.Design: A cross-sectional study.Setting: Rural communities in Bangladesh, Pakistan and Sri Lanka.Participants: A total of 2288 individuals with hypertension aged ≥40 years from the ongoing Control of Blood Pressure and Risk Attenuation- Bangladesh, Pakistan and Sri Lanka clinical trial.Main outcome measures: CMM was defined as the presence of ≥2 of the conditions: diabetes, chronic kidney disease, heart disease and stroke. Logistic regression was done to evaluate the correlates of CMM.Results: About 25.4% (95% CI 23.6% to 27.2%) of the hypertensive individuals had CMM. Factors positively associated with CMM included residing in Bangladesh (OR 3.42, 95% CI 2.52 to 4.65) or Sri Lankan (3.73, 95% CI 2.48 to 5.61) versus in Pakistan, advancing age (2.33, 95% CI 1.59 to 3.40 for 70 years and over vs 40-49 years), higher waist circumference (2.15, 95% CI 1.42 to 3.25) for Q2-Q3 and 2.14, 95% CI 1.50 to 3.06 for Q3 and above), statin use (2.43, 95% CI 1.84 to 3.22), and higher levels of triglyceride (1.01, 95% CI 1.01 to 1.02 per 5 mg/dL increase). A lower odds of CMM was associated with being physically active (0.75, 95% CI 0.57 to 0.97). A weak inverted J-shaped association between International Wealth Index and CMM was found (p for non-linear=0.058), suggesting higher risk in the middle than higher or lower socioeconomic strata.Conclusions: CMM is highly prevalent in rural South Asians affecting one in four individuals with hypertension. There is an urgent need for strategies to concomitantly manage hypertension, cardiometabolic comorbid conditions and associated determinants in South Asia
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