Micro-nano patterns created directly over solid surfaces to combat microbial activity help in preventing hospital-acquired infections. This Letter is focused on defining surface topologies by laser patterning over solid surfaces. Studies on designing surface topologies and bacterial culture have been carried out and the feasibility of micro scale features in restricting bacterial growth has been investigated. The effects of the engineered roughness index and contact angle are discussed. Contact angle measurement over patterned surfaces using a novel computer vision-based technique is demonstrated and the effect of contact angle on bacterial adhesion has been presented. The results obtained show that the designed micro scale geometries can effectively reduce the growth of bacteria on the said surfaces.

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The host-parasite interaction is a complex molecular cross-talk, where the parasite employs a repertoire of surface and secretory effector molecules for host cell manipulation and successful parasitism. The current study identifies an Amastine like Surface Protein (ALSP), expressed in abundant amount in the intracellular amastigotes form of Leishmania donovani, the causative agent of visceral leishmaniasis. Characterization and subcellular localization of the protein indicates its stage specific presence in the cytosol of the amastigotes. MALDI-TOF MS analysis reveals its molecular mass to be 10.147 kDa. The trypsin digested purified native protein shows 100% identity with the leishmanial ALSP through MALDI-TOF-MS-MS peptide analysis. Prediction of its presence and expression was done by immunolocalization and transcript level observations. Based on in-silico study, ALSP has been hypothesized to serve as a source of energy for the intracellular parasite during parasitism by conversion of triglycerides into glycerol and fatty acid, assigning a role in virulence through triglyceride lipase activity. The intracellular survival of the parasite with the intervention of the target protein may help in harnessing the candidate molecule, as an appealing target for design of novel chemotherapeutics against visceral leishmaniasis in future.

Leishmania establishes a successful parasitism by evading both oxidative and non-oxidative killing pathways, and its drug resistance against the currently available therapeutics demands for a safe and cheap drug. Since the parasite synthesizes ergosterol instead of cholesterol, using the same biochemical pathway and enzymes, an inhibitor of HMG-CoA-Reductase, Lovastatin, has been tried for its anti-Leishmanial effect. Lovastatin, being an inhibitor of HMG-CoA-Reductase, inhibits infection by cholesterol depletion, while chromium chloride complexes, at their higher concentrations, are reported to exhibit cytotoxicity. In intracellular amastigotes, cytotoxicity has been checked by assessing various manifestation of cell death, viz. DNA fragmentation, AnnexinV-FITC binding and JC-1 fluorescence ratio. Release of hydrogen peroxide (HPO) and nitric oxide (NO) has been assessed in live cell. Lovastatin and CrCl3.6H2O in combination has appeared to be ineffective on promastigotes but has induced cytotoxic effect on the intracellular amastigotes through up-regulation of cellular signalling mechanisms. CrCl .6H2O stimulates generation of NO, leading to reduction of the number of intracellular amastigote, while Lovastatin shows HPO-mediated killing of the same, keeping the host cell unaffected. This novel therapeutic approach, involving two known safe compounds in suboptimal doses, may resolve human visceral Leishmaniasis.