Burkholderia pseudomallei lectins: occurrence and expression.

Lectins, also known as sugar binding proteins, play an essential role in the initiation of bacterial infections and biofilm production. To date, several lectins of Gram-negative bacteria such as Pseudomonas aeruginosa, Burkholderia cenocepacia, Ralstonia solanacearum and Chromobacterium violaceum have been identified. There are no published reports on the presence of lectins in Burkholderia pseudomallei, the causative agent of melioidosis. The aim of this study was to identify possible lectin genes of B. pseudomallei and generate recombinant proteins for assessment of hemagglutinating activity. Seven hypothetical lectins of B. pseudomallei were retrieved from the UniProt database. Four lectin domains, i.e., ricin B, C-type, H-type and Bulb-type lectins were identified. In silico analysis using a ligand binding site prediction server (3DLigandSite) predicted the presence of Nacetylglucosamine and calcium binding sites in two C-type lectins. Four recombinant proteins with the molecular weights of 11.7, 30.2, 36.2 and 46.4 kDa were expressed from the cloned genes; however none of them expressed any hemagglutinating activity. Further characterization of B. pseudomallei lectins may be able to provide insights into bacterial-host interaction that are required to initiate infections.

Burkholderia pseudomallei lectins: occurrence and expression

Lectins, also known as sugar binding proteins, play an essential role in the initiation of bacterial infections and biofilm production. To date, several lectins of Gram-negative bacteria such as Pseudomonas aeruginosa, Burkholderia cenocepacia, Ralstonia solanacearum and Chromobacterium violaceum have been identified. There are no published reports on the presence of lectins in Burkholderia pseudomallei, the causative agent of melioidosis. The aim of this study was to identify possible lectin genes of B. pseudomallei and generate recombinant proteins for assessment of hemagglutinating activity. Seven hypothetical lectins of B. pseudomallei were retrieved from the UniProt database. Four lectin domains, i.e., ricin B, C-type, H-type and Bulb-type lectins were identified. In silico analysis using a ligand binding site prediction server (3DLigandSite) predicted the presence of Nacetylglucosamine and calcium binding sites in two C-type lectins. Four recombinant proteins with the molecular weights of 11.7, 30.2, 36.2 and 46.4 kDa were expressed from the cloned genes; however none of them expressed any hemagglutinating activity. Further characterization of B. pseudomallei lectins may be able to provide insights into bacterial-host interaction that are required to initiate infections.

Colonial morphotypes and biofilm forming ability of Burkholderia pseudomallei.

Burkholderia pseudomallei the causative agent of melioidosis, is being increasingly recognized as an important cause of morbidity and mortality in South East Asia. Biofilm formation of B. pseudomallei may be responsible for dormancy, latency and relapse of melioidosis. Based on the colonial morphology of the bacteria on B. pseudomallei selective agar medium, seven distinct morphotypes were identified. This study was conducted to assess the in vitro biofilm produced by B. pseudomallei and to investigate possible correlation between B. pseudomallei morphotypes with biofilm forming abilities of the isolates. Using a standard biofilm crystal violet staining assay, comparison was made between the biofilm forming ability of 76 isolates of B. pseudomallei and Burkholderia thailandensis ATCC 700388. Amongst the blood isolates, 30.2% were considered as high biofilm producers and 27.9% were low producers, 33.3% of the pus isolates were considered as high and 16% low biofilm producers. Most of the isolates were identified as morphotype group 1 which displayed a rough centre with irregular circumference on the agar medium. However, we did not find any correlation of B. pseudomallei morphotypes with biofilm forming abilities (p > 0.05). Additional studies are needed to identify internal and external factors which contribute to the high and low biofilm formation of B. pseudomallei.

Stroke disease management--a framework for comprehensive stroke care.

Disease management is an approach to patient care that coordinates medical resources for the patient across the entire healthcare delivery system throughout the lifetime of the patient with the disease. Stroke is suitable for disease management as it is a well-known disease with a high prevalence, high cost, variable practice pattern, poor clinical outcome, and managed by a non-integrated healthcare system. It has measurable and actionable outcomes, with available local expertise and support of the Ministry of Health. Developing the programme requires a multidisciplinary team, baseline data on target populations and healthcare services, identification of core components, collaboration with key stakeholders, development of evidence-based clinical practice guidelines and carepaths, institution of care coordinators, use of information technology and continuous quality improvement to produce an effective plan. Core components include public education, risk factor screening and management, primary care and specialist clinics, acute stroke units, inpatient and outpatient rehabilitation facilities, and supportive community services including medical, nursing, therapy, home help and support groups for patients and carers. The family physician plays a key role. Coordination of services is best done by a network of hospital and community-based care managers, and is enhanced by a coordinating call centre. Continuous quality improvement is required, with audit of processes and outcomes, facilitated by a disease registry. Pitfalls include inappropriate exclusion of deserving patients, misuse, loss of physician and patient independence, over-estimation of benefits, and care fragmentation. Collaboration and cooperative among all parties will help ensure a successful and sustainable programme.