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Strickland, T.

Publications and source records attributed to Strickland, T..

5 recordsLinked to original sources

Management factors influence Salmonella persistence in reused poultry litter over three successive flocks

Salmonella infections are a leading cause of bacterial food-borne illness worldwide. Infections are highly associated with the consumption of contaminated food, and in particular, chicken meat. Understanding how management practices and environmental factors influence Salmonella populations in broiler chicken production may aid in reducing the risk of food-borne illness in humans. Utilizing whole genome sequencing with antimicrobial and heavy metal resistance, virulence factor and plasmid identification, we have characterized the genetic diversity of Salmonella enterica isolates (n = 55) obtained from broiler chicken litter. S. enterica isolates were recovered from the litter of broiler chickens over three consecutive flocks in four broiler houses on a single integrated farm in Georgia, USA. The chickens were raised under a newly adopted "No Antibiotics Ever" program and copper sulfate was administered via drinking water. In-silico serovar prediction identified three S. enterica serovars: Enteritidis (n = 12), Kentucky (n = 40) and Senftenberg (n = 3). Antimicrobial susceptibility testing revealed that only one S. Kentucky isolate was resistant to streptomycin, while the remaining isolates were susceptible to all antibiotics tested. Metal resistance operons, including copper and silver, were identified chromosomally and on plasmids in serovar Senftenberg and Kentucky isolates, respectively. Serovar Kentucky isolates harboring metal resistance operons were the only Salmonella isolates recovered from the litter of third flock cohort. These results suggest the addition of copper sulfate to drinking water may have selected for S. Kentucky isolates harboring plasmid-borne copper resistance genes and may explain their persistence in litter from flock to flock. ImportanceSalmonella foodborne illnesses are the leading cause of hospitalizations and deaths, resulting in a high economic burden on the healthcare system. Globally, chicken meat is one of the highest consumed meats and is a predominant source of foodborne illness. The severity of Salmonella infections depends on the presence of antimicrobial resistance genes and virulence factors. While there are many studies which have investigated Salmonella strains isolated from post-harvest chicken samples, there is a gap in our understanding of the prevalence and persistence of Salmonella in pre-harvest and in particular their makeup of antibiotic resistance genes, virulence factors and metal resistance genes. The objective of this study was to determine how on-farm management practices and environmental factors influence Salmonella persistence, as well as the antimicrobial resistance genes and virulence factors they harbor. In this study we demonstrate that broiler chickens raised without antibiotics are less likely to harbor antibiotic resistance, however the practice of adding acidified copper sulfate to drinking water may select for strains carrying metal resistant genes.

genomics↗

Broiler house environment and litter management practices impose selective pressures on antimicrobial resistance genes and virulence factors of Campylobacter

Campylobacter infections are a leading cause of bacterial diarrhea in humans globally. Infections are due to consumption of contaminated food products and are highly associated with chicken meat, with chickens being an important reservoir for Campylobacter. Here, we characterized the genetic diversity of Campylobacter species detected in broiler chicken litter over three consecutive flocks and determined their antimicrobial resistance and virulence factor profiles. Antimicrobial susceptibility testing and whole genome sequencing were performed on Campylobacter jejuni (n = 39) and Campylobacter coli (n = 5) isolates. All C. jejuni isolates were susceptible to all antibiotics tested while C. coli (n =4) were resistant to only tetracycline and harbored the tetracycline-resistant ribosomal protection protein (TetO). Virulence factors differed within and across grow houses but were explained by the isolates flock cohort, species and multilocus sequence type. Virulence factors involved in the ability to invade and colonize host tissues and evade host defenses were absent from flock cohort 3 C. jejuni isolates as compared to flock 1 and 2 isolates. Our results show that virulence factors and antimicrobial resistance genes differed by the isolates multilocus sequence type and by the flock cohort they were present in. These data suggest that the house environment and litter management practices performed imposed selective pressures on antimicrobial resistance genes and virulence factors. In particular, the absence of key virulence factors within the final flock cohort 3 isolates suggests litter reuse selected for Campylobacter strains that are less likely to colonize the chicken host. ImportanceCampylobacter is a leading cause of foodborne illness in the United States due to the consumption of contaminated food products or from mishandling of food products, often associated with chicken meat. Campylobacter is common in the microbiota of avian and mammalian gut; however, the acquisition of antimicrobial resistance genes and virulence factors may result in strains that pose a significant threat to public health. Although there are studies that have investigated the genetic diversity of Campylobacter strains isolated from post-harvest chicken samples, there is limited data on the genome characteristics of isolates recovered from pre-harvest broiler production. In this study, we show that Campylobacter jejuni and Campylobacter coli that differ in their carriage of antimicrobial resistance and virulence factors may differ in their ability to evade host defense mechanisms and colonize the gut of chickens and humans. Furthermore, we found that differences in virulence factor profiles were explained by the species of Campylobacter and its multilocus sequence type.

genetics↗

A role for myeloid miR-155 in regulating hypoxia induced seizures in neonatal C57BL/J6 mice

Hypoxic ischaemic injury (HIE) in the neonatal brain has significant consequences on neurodevelopment and increases the occurrence of neurological deficits in infants. HIE is also a leading cause of neonatal seizures. Therapeutic options for the treatment of HIE are very limited. Hypoxia-ischemia directly damages brain tissue in a primary-wave of injury which activates a cascade of events triggering local and systemic inflammatory responses, driven by the innate immune system, which contribute to a significant secondary-wave of injury taking place as early as 6 hours post-hypoxia-ischaemia. Levels of the well documented inflammatory microRNA, miR-155 are elevated in rodent seizure and epilepsy models. Here, we assessed the impact of, miR-155 deletion in myeloid cells, on regulating inflammation and seizure severity in a preclinical model of neonatal hypoxia-induced seizures (Hypoxia-Sz). Wildtype miR-155 (miR-155+/+LysMCre) mice were compared to a mouse line in which miR-155 was deleted in myeloid cells (miR-155fl/fl LysMCre). We demonstrate significant upregulation of miR-155 target genes, brain-derived neurotrophic factor (bdnf), arginase-2 (arg-2), ship-1 and socs-1 in miR-155fl/fl LysMCre mice compared to controls at various time points following Hypoxia-Sz. Conversely, we report decreased mRNA levels of pro-inflammatory cytokines IL-1{beta} and IL-6 and lower protein levels of IL-1{beta} in miR-155fl/fl LysMCre mice as compared to WTs. Myeloid miR-155 deletion significantly reduced behavioural seizure severity score, reduced electrographically (EEG) measured seizure frequency and seizure burden as compared to mice to wildtypes, suggesting miR-155 regulation of seizure occurrence in this model. Behavioural tests for motor functions at 5 weeks post Hypoxia-Sz demonstrated differences between genotypes. Excitingly this work highlights that inhibition of miR-155, specifically in myeloid cells, may hold therapeutic benefit for both seizures and comorbidities associated with hypoxic brain injury.

neuroscience↗

Open spaced ridged hydrogel scaffolds containing TiSAMP surface chemistry promotes regeneration and recovery following spinal cord injury.

The spinal cord has poor ability to regenerate after injury, which may be due to cell loss, cyst formation, inflammation, and scarring. A promising approach to treat spinal cord injury (SCI) is the use of biomaterials. We have developed a novel hydrogel scaffold fabricated from oligo(poly(ethylene glycol) fumarate) (OPF) as a 0.08 mm thick sheet containing polymer ridges and a cell-attractive surface chemistry on the other side. When the cells are cultured on OPF with the chemical patterning, the cells attach, align, and deposit ECM along the direction of the pattern. Animals implanted with the rolled scaffold sheets had greater hindlimb recovery compared to the multichannel scaffold control, likely due to the greater number of axons growing across. Inflammation, scarring, and ECM deposits were equal across conditions. Overall, the results suggest that the scaffold sheets promote axon outgrowth that can be guided across the scaffold, thereby promoting hindlimb recovery.

neuroscience↗

Newly regenerated axons through a cell-containing biomaterial scaffold promote reorganization of spinal circuitry and restoration of motor functions with epidural electrical stimulation.

We report the effect of newly regenerated neural fibers via bioengineered scaffold on reorganization of spinal circuitry and restoration of motor functions with electrical epidural stimulation (EES) after spinal transection (ST). Restoration across multiple modalities was evaluated for 7 weeks after ST with implanted scaffold seeded with Schwann cells, producing neurotrophic factors and with rapamycin microspheres. Gradual improvement in EES-facilitated stepping was observed in animals with scaffolds, although, no significant difference in stepping ability was found between groups without EES. Similar number of regenerated axons through the scaffolds was found in rats with and without EES-enabled training. Re-transection through the scaffold at week 6, reduced EES-enabled motor function, remaining higher compared to rats without scaffolds. The combination of scaffolds and EES-enabled training demonstrated synaptic changes below the injury. These findings indicate that sub-functional connectivity with regenerated across injury fibers can reorganize of sub-lesional circuitry, facilitating motor functions recovery with EES.

neuroscience↗