Enteric bacterial human pathogens, i.e., Escherichia coli, Staphylococcus aureus, Bacillus subtilis and Klebsiella pneumoniae, are the major cause of diarrheal infections in children and adults. Their structure badly affects the human immune system. It is important to explore new antibacterial agents instead of antibiotics for treatment. This project is an attempt to explain how gold nanoparticles affect these bacteria. We investigated the important role of the mean particle size, and the inhibition of a bacterium is dose-dependent. Ultra Violet (UV)-visible spectroscopy revealed the size of chemically synthesized gold nanoparticle as 6–40 nm. Atomic force microscopy (AFM) analysis confirmed the size and X-ray diffractometry (XRD) analysis determined the polycrystalline nature of gold nanoparticles. The present findings explained how gold nanoparticles lyse Gram-negative and Gram-positive bacteria.
Venomous snakes are important subjects of study in evolution, ecology, and biomedicine. Many venomous snakes have alpha-neurotoxins (α-neurotoxins) in their venom. These toxins bind the alpha-1 nicotinic acetylcholine receptor (nAChR) at the neuromuscular junction, causing paralysis and asphyxia. Several venomous snakes and their predators have evolved resistance to α-neurotoxins. The resistance is conferred by steric hindrance from N-glycosylated asparagines at amino acids 187 or 189, by an arginine at position 187 that has been hypothesized to either electrostatically repulse positively charged neurotoxins or sterically interfere with α-neurotoxin binding, or proline replacements at positions 194 or 197 of the nAChR ligand-binding domain to inhibit α-neurotoxin binding through structural changes in the receptor. Here, we analyzed this domain in 148 vertebrate species, and assessed its amino acid sequences for resistance-associated mutations. Of these sequences, 89 were sequenced de novo. We find widespread convergent evolution of the N-glycosylation form of resistance in several taxa including venomous snakes and their lizard prey, but not in the snake-eating birds studied. We also document new lineages with the arginine form of inhibition. Using an in vivo assay in four species, we provide further evidence that N-glycosylation mutations reduce the toxicity of cobra venom. The nAChR is of crucial importance for normal neuromuscular function and is highly conserved throughout the vertebrates as a result. Our research shows that the evolution of α-neurotoxins in snakes may well have prompted arms races and mutations to this ancient receptor across a wide range of sympatric vertebrates. These findings underscore the inter-connectedness of the biosphere and the ripple effects that one adaption can have across global ecosystems.
The persistence of 3 low-pathogenicity avian influenza viruses (LPAIV) (H4N6, H5N1, and H6N8) and one human influenza virus (H1N1) as well as Newcastle disease virus (NDV) and enteric cytopathogenic bovine orphan (ECBO) virus was investigated in lake sediment, duck feces, and duck meat at 30, 20, 10, and 0°C using a germ carrier technique. Virus-loaded germ carriers were incubated in each substrate, and residual infectivity of the eluted virus was quantified on cell culture after regular intervals for a maximum of 24 weeks. Data were analyzed by a linear regression model to calculate T 90 values (time required for 90% loss of virus infectivity) and estimated persistence of the viruses. In general, the persistence of all of the viruses was highest in lake sediment, followed by feces, and was the lowest in duck meat at all temperatures. For the avian influenza virus subtypes, T 90 values in sediment ranged from 5 to 11, 13 to 18, 43 to 54, and 66 to 394 days at 30, 20, 10, and 0°C, respectively, which were 2 to 5 times higher than the T 90 values of the viruses in the feces and meat. Although the individual viruses vary in tenacity, the survival time of influenza viruses was shorter than that of NDV and ECBO virus in all substrates. The results of this study suggest that lake sediment may act as a long-term source of influenza viruses in the aquatic habitat, while the viruses may remain infectious for extended periods of time in duck feces and meat at low temperatures, allowing persistence of the viruses in the environment over winter.
Ranaviruses infect fish, amphibians, and reptiles. The present study was conducted to compare the persistence of amphibian and reptilian ranaviruses in a pond habitat. The 4 viruses used in this study included 2 amphibian ranaviruses, Frog virus 3 (FV3, the type species of the genus Ranavirus) and an isolate from a frog, and 2 ranaviruses of reptilian origin (from a tortoise and from a gecko). A sandwich germ-carrier technique was used to study the persistence of these viruses in sterile and unsterile pond water (PW) and soil obtained from the bank of a pond. For each virus, virus-loaded carriers were placed in each of the 3 substrates, incubated at 4 and 20°C, and titrated at regular intervals. Serial data were analyzed using a linear regression model to calculate T-90 values (time required for 90% reduction in the virus titer). Resistance of the viruses to drying was also studied. All 4 viruses were resistant to drying. At 20°C, T-90 values of the viruses were 22 to 31 d in sterile PW and 22 to 34 d in unsterile PW. Inactivation of all 4 viruses in soil at this temperature appeared to be non-linear. T-90 values at 4°C were 102 to 182 d in sterile PW, 58 to 72 d in unsterile PW, and 30 to 48 d in soil. Viral persistence was highest in the sterile PW, followed by the unsterile PW, and was lowest in soil. There were no significant differences in the survival times between the amphibian and reptilian viruses. The results of the present study suggest that ranaviruses can survive for long periods of time in pond habitats at low temperatures. KEY WORDS: Ranaviruses · Pond water · Persistence · Soil Resale or republication not permitted without written consent of the publisherDis Aquat Org 98: [177][178][179][180][181][182][183][184] 2012 transmitted to healthy salamanders after putting them in the water where infected salamanders were previously kept, even after passing the water through 0.45 µm pore size filters. In one transmission study, it has been observed that salamanders acquired infection after water-bath exposure to ATVcontaminated water and also transferred the infection to other healthy individuals (Brunner et al. 2007). The exposure of Rana sylvatica tadpoles to sediments collected from a pond where a ranavirus die-off had occurred resulted in the development of infection in the exposed individuals (Harp & Petranka 2006). Similarly, experimentally inoculated moist sediments also transmitted ATV infection and caused mortality in larval salamanders (Brunner et al. 2007). These studies indicate that in a small pond habitat, contaminated water and soil can be a potential source of virus transmission to susceptible animals.There is scarcity of data on the environmental persistence of iridoviruses infecting reptiles and amphibians. One report shows that the infectivity of ATV-contaminated water was lost after a 2 wk incubation at 25°C (Jancovich et al. 1997). Langdon (1989) observed that a fish ranavirus, closely related to amphibian ranaviruses, can survive for 97 d in water at 15°C. A comparison ...
We describe a clonal outbreak of quinolone-resistant Haemophilus influenzae (QRHI) from an affiliated long-term care facility (LTCF-A); the outbreak was associated with the clinical use of levofloxacin, which was determined to be a risk factor for acquisition of QRHI. The minimum inhibitory concentration to which 90% of isolates were susceptible (MIC90), as determined by broth microdilution, was >4 microg/mL for levofloxacin, >2 microg/mL for moxifloxacin, >2 microg/mL for gatifloxacin, and 8 microg/mL for gemifloxacin. The MIC90, as determined by Etest (AB Biodisk), was >32 microg/mL for levofloxacin, ciprofloxacin, moxifloxacin, and gatifloxacin. Having been a resident at LTCF-A and having chronic obstructive pulmonary disease were significant risk factors for acquisition of QRHI at our 500-bed hospital (New York Hospital Queens). All QRHI isolates were found to be genetically related by pulsed-field gel electrophoresis, were nontypeable, were susceptible to ceftriaxone and azithromycin, and were negative for beta -lactamase production. Emphasis on patient contact and respiratory isolation and placing colonized or infected patients in cohorts yielded a marked reduction in the prevalence of QRHI at LTCF-A.
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