The presence of unvaccinated free-roaming dogs (FRD) amidst human settlements is a major contributor to the high incidence of rabies in countries such as India, where the disease is endemic. Estimating FRD population size is crucial to the planning and evaluation of interventions, such as mass immunisation against rabies. Enumeration techniques for FRD are resource intensive and can vary from simple direct counts to statistically complex capture-recapture techniques primarily developed for ecological studies. In this study we compared eight capture-recapture enumeration methods (Lincoln–Petersen’s index, Chapman’s correction estimate, Beck’s method, Schumacher-Eschmeyer method, Regression method, Mark-resight logit normal method, Huggin’s closed capture models and Application SuperDuplicates on-line tool) using direct count data collected from Shirsuphal village of Baramati town in Western India, to recommend a method which yields a reasonably accurate count to use for effective vaccination coverage against rabies with minimal resource inputs. A total of 263 unique dogs were sighted at least once over 6 observation occasions with no new dogs sighted on the 7th occasion. Besides this direct count, the methods that do not account for individual heterogeneity yielded population estimates in the range of 248–270, which likely underestimate the real FRD population size. Higher estimates were obtained using the Huggin’s Mh-Jackknife (437 ± 33), Huggin’s Mth-Chao (391 ± 26), Huggin’s Mh-Chao (385 ± 30), models and Application “SuperDuplicates” tool (392 ± 20) and were considered more robust. When the sampling effort was reduced to only two surveys, the Application SuperDuplicates online tool gave the closest estimate of 349 ± 36, which is 74% of the estimated highest population of free-roaming dogs in Shirsuphal village. This method may thus be considered the most reliable method for estimating the FRD population with minimal inputs (two surveys conducted on consecutive days).

The growing worldwide challenge of cirrhosis and hepatocellular carcinoma due to increasing prevalence of excessive alcohol consumption, viral hepatitis, obesity, and the metabolic syndrome has sparked interest in stem cell-like liver progenitor cells (LPCs) as potential candidates for cell therapy and tissue engineering, as an alternative approach to whole organ transplantation. However, LPCs always proliferate in chronic liver diseases with a predisposition to cancer; they have been suggested to play major roles in driving fibrosis, disease progression, and may even represent tumor-initiating cells. Hence, a greater understanding of the factors that govern their activation, communication with other hepatic cell types, and bipotential differentiation as opposed to their potential transformation is needed before their therapeutic potential can be harnessed.

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Staphylococcus aureus in biofilms is highly resistant to the treatment with antibiotics, to which the planktonic cells are susceptible. This is likely to be due to the biofilm creating a protective barrier that prevents antibiotics from accessing the live pathogens buried in the biofilm. S. aureus biofilms consist of an extracellular matrix comprising, but not limited to, extracellular bacterial DNA (eDNA) and poly-β-1, 6-N-acetyl-d-glucosamine (PNAG). Our study revealed that despite inferiority of dispersin B (an enzyme that degrades PNAG) to DNase I that cleaves eDNA, in dispersing the biofilm of S. aureus, both enzymes were equally efficient in enhancing the antibacterial efficiency of tobramycin, a relatively narrow-spectrum antibiotic against infections caused by gram-positive and gram-negative pathogens, including S. aureus, used in this investigation. However, a combination of these two biofilm-degrading enzymes was found to be significantly less effective in enhancing the antimicrobial efficacy of tobramycin than the individual application of the enzymes. These findings indicate that combinations of different biofilm-degrading enzymes may compromise the antimicrobial efficacy of antibiotics and need to be carefully assessed in vitro before being used for treating medical devices or in pharmaceutical formulations for use in the treatment of chronic ear or respiratory infections.

BackgroundBiofilm formation by Staphylococcus aureus is an important virulence attribute because of its potential to induce persistent antibiotic resistance, retard phagocytosis and either attenuate or promote inflammation, depending upon the disease syndrome, in vivo. This study was undertaken to evaluate the potential significance of strength of biofilm formation by clinical bovine mastitis-associated S. aureus in mammary tissue damage by using a mouse mastitis model.MethodsTwo S. aureus strains of the same capsular phenotype with different biofilm forming strengths were used to non-invasively infect mammary glands of lactating mice. Biofilm forming potential of these strains were determined by tissue culture plate method, ica typing and virulence gene profile per detection by PCR. Delivery of the infectious dose of S. aureus was directly through the teat lactiferous duct without invasive scraping of the teat surface. Both bacteriological and histological methods were used for analysis of mammary gland pathology of mice post-infection.ResultsHistopathological analysis of the infected mammary glands revealed that mice inoculated with the strong biofilm forming S. aureus strain produced marked acute mastitic lesions, showing profuse infiltration predominantly with neutrophils, with evidence of necrosis in the affected mammary glands. In contrast, the damage was significantly less severe in mammary glands of mice infected with the weak biofilm-forming S. aureus strain. Although both IL-1β and TNF-α inflammatory biomarkers were produced in infected mice, level of TNF-α produced was significantly higher (p<0.05) in mice inoculated with strong biofilm forming S. aureus than the weak biofilm forming strain.ConclusionThis finding suggests an important role of TNF-α in mammary gland pathology post-infection with strong biofilm-forming S. aureus in the acute mouse mastitis model, and offers an opportunity for the development of novel strategies for reduction of mammary tissue damage, with or without use of antimicrobials and/or anti-inflammatory compounds for the treatment of bovine mastitis.