Microbial communities living in deep aquatic sediments have adapted to survive on degraded organic matter, according to a study published in Applied and Environmental Microbiology and coauthored by professors at the University of Tennessee, Knoxville.
“There are microbes living in deep ocean sediments eating carbon, like proteins and carbohydrates, that is hundreds of years old,” said Andrew Steen, lead author of the study and assistant professor of environmental geology at UT. “However, we don’t know much about how those microbes eat that old, poor-quality food.”
Understanding how these microorganisms function on low-quality foods at a very slow pace could have future uses in biomedical applications such as a technology that could slow down cell metabolism in human organs so they can survive longer during a transplant process.
“It could also aid in preserving underground microbes that play a role in carbon sequestration, a key process in the fight against climate change,” said Steen.
To better understand how these microorganisms access this food, researchers tested different types of peptidases — digestive enzymes that work to degrade proteins — in sediment cores from the White Oak River estuary in North Carolina.
“These microbes live incredibly slow lives, with cells multiplying somewhere between every 10 years and every 10,000 years, but we aren’t sure how,” said Steen. “Our work shows that those microbes are living the same way any other microbe does, just way more slowly and with some improved ability to eat the low-quality food in their environment.”
The data collected by the researchers represented about 275 years of sediment deposition from the White Oak River estuary. Using DNA analysis of the microbes in these sediments, and by measuring peptidases, researchers evaluated how these microorganisms metabolize with little access to fresh organic matter.
Organic carbon buried in aquatic sediments is a long-term sink for atmospheric carbon dioxide, and about 40 percent of organic carbon burial occurs in estuaries and deltaic systems. Steen’s study gives insight into how these subsurface microbial communities begin the process of degrading organic carbon in such environments.
“Our study shows that, in some sense, subsurface microbes are happy to be where they are — or at least they’re well adapted to a terrible environment,” said Steen.
A pair of University of Virginia School of Medicine scientists have revealed how E. coli seeks out the most oxygen-free crevices of your colon to cause the worst infection possible. The discovery could one day let doctors prevent the infection by allowing E. coli to pass harmlessly through the body.
The new discovery shows just how the foodborne pathogen knows where and when to begin colonizing the colon on its way to making you sick. By recognizing the low-oxygen environment of the large intestine, the dangerous bacterium gives itself the best odds of establishing a robust infection — one that is punishing for the host.
“Bacterial pathogens typically colonize a specific tissue in the host. Therefore, as part of their infection strategies, bacterial pathogens precisely time deployment of proteins and toxins to these specific colonization niches in the human host. This allows the pathogens to save energy and avoid detection by our immune systems and ultimately cause disease,” said researcher Melissa Kendall, PhD, of UVA’s Department of Microbiology, Immunology and Cancer Biology. “By knowing how bacterial pathogens sense where they are in the body, we may one day be able to prevent E. coli, as well as other pathogens, from knowing where it is inside a human host and allow it to pass through the body without causing an infection.”
We’ve all seen the statistics—each year in the United States, 2 million people will get an antibiotic-resistant infection and at least 23,000 will die as a result of them. Moreover, multidrug-resistant organisms (MDROs) represent an increasing threat to global health as it’s estimated that their mortality rates will exceed those of cancer by 2050. It’s easy to see such data and focus on how to cut down the rates or how to increase antimicrobial stewardship without thinking about the perceptions or emotional impact of these infections.
How do health care workers experience MDROs? What about patients? These types of questions are rarely discussed in infection prevention or antimicrobial resistance efforts but, nonetheless, play a critical role. A new study from a research team in Germany sought to truly understand how these perceptions affect efforts such as hand hygiene, disinfection, and isolation. We all too often focus on the isolation and rapid identification of patients with MDROs but rarely discuss the social and psychological implications of such infections.
Investigators used a socio-constructivist focus and a mixed-method approach to conduct the study, which was broken into sections that included discussions, peer-assisted objective-structured clinical examination, and constructive efforts like card surveys and papers. Topics included infectious diseases and microbiology, basic hygiene procedures, communication techniques, and special protective hazardous material equipment. The research team had 51 health care workers from 13 professions across 5 hospitals participate in this training and data collection. Overall, they found that there are significant barriers both in educating clinicians and then informing patients and family members, and also in handling emotional responses in patients diagnosed and isolated with an MDRO infection.
New research led by academics at the University of Bristol Veterinary and Medical Schools used the ‘One Health’ approach to study three bacterial species in the noses of young cattle and found the carriage of the bacteria was surprisingly different. The findings which combined ideas and methods from both animal and human health research could help prevent and control respiratory diseases.
Cattle, like humans, harbour a wide range of bacteria in their noses, microbes which are normally present and probably necessary for health like those that live in the gut. However, some species of these bacteria do cause serious illness at times, particularly when infection becomes established in the lower respiratory tract within the lungs.
In an open access paper published in Scientific Reports today [Friday 16 August], the researchers investigated the patterns of acquiring and clearing these microbes in healthy young cattle, which have not previously been studied in detail.
The research team took nasal swabs at intervals during the first year of life, to detect their presence and measure their abundance using a DNA-detection technique called quantitative polymerase chain reaction (qPCR) that targeted genes found in three bacterial species well-known for their ability to cause respiratory disease in cattle: Histophilus somni, Mannheimia haemolytica and Pasteurella multocida.
The evolution of more severe infections is not necessarily driven by bacteria multiplying faster, new research shows.
Humans and animals can develop resistance to harmful bacteria (pathogens) over time or with antibiotics or vaccines, and it is usually assumed that pathogens respond by multiplying faster.
But the new study — led by the University of Exeter — shows pathogen virulence and replication rates can evolve separately.
The authors believe that, once resistance spreads in host species, virulence may be driven by other means such as by manipulating host immune systems.
The research examined the spread of bacteria called Mycoplasma gallisepticum among house finches — a rare example of a well-studied host-bacteria evolution where humans have not intervened with antibiotics or vaccines.
“We actually have a very poor understanding of how pathogens evolve in response to natural host resistance,” said Dr Camille Bonneaud, of the Centre of Ecology and Conservation on Exeter’s Penryn Campus in Cornwall.
“This is because there are very few systems in the wild that have been monitored in sufficient detail, without being subjected to human intervention.
“We typically assume that pathogens respond to host resistance (including to vaccines) by increasing their rate of replication, allowing them to transmit faster to other hosts before they are cleared by their current host.
“However, our study shows that pathogens can evolve to become more virulent without increasing their rate of replication.
“We hypothesise that the increase in virulence that we observed in this study was driven by an improved ability of the pathogen to manipulate the host immune system in order to generate the symptoms necessary for its transmission.”
The authors say this could lead to new approaches for tackling pathogens.
For example, if trying to kill the pathogen inevitably leads to more virulent infections, it might be worth trying to slow down pathogen evolution by combining treatments that both eliminate the pathogen and prevent it manipulating host immune systems.
Some populations of house finches have been exposed to Mycoplasma gallisepticum for more than 20 years, while others have not — and have therefore not developed resistance.
In the study, carried out in Arizona and supported by Arizona State University and Auburn University, 57 finches from previously unexposed populations were exposed to the pathogen.
The findings show virulence has increased consistently over more than 150,000 bacterial generations since outbreak (1994 to 2015).
By contrast, while replication rates increased from outbreak to the initial spread of resistance (1994 to 2004), no further increases have occurred subsequently (2007 to 2015).
Canadian Journal of Microbiology
Probiotics have become one of the potential solutions to global restriction on antibiotic use in food animal production. Bacillus species have been attractive probiotics partially due to their long-term stability during storage. In this study, 200 endospore-forming bacteria isolates were recovered from sourdough and the gastrointestinal tract (GIT) of young broiler chicks. Based on the production of a series of exoenzymes and survivability under stress conditions similar to those in the poultry GIT, 42 isolates were selected and identified by 16S rRNA gene sequencing. Seven strains with a profile of high enzymatic activities were further evaluated for sporulation efficiency, biofilm formation, compatibility among themselves (Bacillus spp.), and antagonistic effects against three bacteria pathogenic to poultry and humans: Enterococcus cecorum, Salmonella enterica, and Shiga-toxin-producing Escherichia coli. The strains from sourdough were identified as Bacillus amyloliquefaciens whereas the ones from the chicks’ GIT were Bacillus subtilis. These strains demonstrated remarkable potential as probiotics for poultry.
Posted in Bacillus, Salmonella, Uncategorized
RASFF – aflatoxins (B1 = 45; Tot. = 49.2 µg/kg – ppb) in pistachios in shell from Iran in Germany
RASFF – foodborne outbreak caused by Listeria monocytogenes (>1.5x10E4 CFU/g) in chilled roast pork (carne mechada) from Spain in Spain
Posted in food bourne outbreak, food contamination, food death, Food Hygiene, Food Illness, Food Inspections, Food Micro Blog, Food Microbiology, Food Microbiology Blog, Food Pathogen, food recall, Food Safety, Food Safety Alert, Food Testing, Listeria, Listeria monocytogenes, listeriosis, Uncategorized
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