Tag: Microbiology (Bacteriology and fungi)

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Pig-borne disease most likely jumped into humans when rearing practices changed

Almost every pig carries harmless strains of the S. suis bacterium — such strains are known as ‘commensal’ strains. However, a more virulent group of strains of the bacteria also exist, which cause disease in pigs worldwide and are a major driver of antibiotic use for prevention. Increasingly, this group of strains is also implicated in serious human diseases such as meningitis and septicaemia. In order to understand the genetic basis of disease in S. suis, an international study, led by the Bacterial Respiratory Diseases of Pigs-1 Technology (BRaDP1T) consortium, examined the genomes of 375 clinical samples from pigs and humans from the UK and Vietnam and combined these with data already published on 15 S. suis genome sequences and draft genomes from around the world. They found that the commensal strains and disease-causing strains differed genetically; in particular, the disease-causing strains have between 50 and 100 fewer genes than the commensal strains.

Dr Lucy Weinert from the Department of Veterinary Medicine at the University of Cambridge, first author of the study, says: “It seems that the loss of genes is associated with causing disease. This is something we see quite often in bacteria, but for reasons that are unclear. One possibility is that the missing genes are those that hinder the function of newly-acquired virulence factors in the genomes.” By examining the S. suis‘s ‘tree of life’ — which looks at how the bacteria have evolved over time — the researchers were able to show that the emergence of a group of strains causing meningitis in pigs and the human form of the disease dates back to the 1920s, when pig production was intensified with the introduction of wide-scale indoor rearing of meat-producing pigs in larger groups, supported by government schemes that favoured larger producers with regular throughput. However, despite having jumped the species barrier from pig to human, the bacteria do not appear to have adapted to infect humans.

“A group of more virulent strains seem to have emerged at around the time the pig industry changed, and it is these strains that mostly cause disease in pigs and humans,” says Professor Duncan Maskell, Head of the School of the Biological Sciences at Cambridge. “Human S. suis disease in the West is extremely rare, but is seen more frequently in south east Asia. It is most likely spread to humans through poor food hygiene practices or other environmental factors. This emphasises the importance of monitoring such practices and putting policies in place to reduce the risk of the spread of infections between species.”

http://www.sciencedaily.com/  Science Daily

http://www.sciencedaily.com/releases/2015/03/150331074343.htm  Original web page Science Daily

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Common bacteria on verge of becoming antibiotic-resistant superbugs

The study shows that two genes that confer resistance against a particularly strong class of antibiotics can be shared easily among a family of bacteria responsible for a significant portion of hospital-associated infections. Drug-resistant germs in the same family of bacteria recently infected several patients at two Los Angeles hospitals. The infections have been linked to medical scopes believed to have been contaminated with bacteria that can resist carbapenems, potent antibiotics that are supposed to be used only in gravely ill patients or those infected by resistant bacteria. “Carbapenems are one of our last resorts for treating bacterial infections, what we use when nothing else works,” said senior author Gautam Dantas, PhD, associate professor of pathology and immunology. “Given what we know now, I don’t think it’s overstating the case to say that for certain types of infections, we may be looking at the start of the post-antibiotic era, a time when most of the antibiotics we rely on to treat bacterial infections are no longer effective.”

Dantas and other experts recommend strictly limiting the usage of carbapenems to cases in which no other treatments can help. The study, conducted by researchers at Washington University, Barnes-Jewish Hospital and the National University of Sciences and Technology in Pakistan, is available online in Emerging Infectious Diseases. The researchers studied a family of bacteria called Enterobacteriaceae, which includes E. coli, Klebsiella pneumoniae and Enterobacter. Some strains of these bacteria do not cause illness and can help keep the body healthy. But in people with weakened immune systems, infections with carbapenem-resistant versions of these bacteria can be deadly. The Centers for Disease Control and Prevention named carbapenem-resistant Enterobacteriaceae as one of the three most urgent threats among emerging forms of antibiotic-resistant disease. Studies have shown the fatality rate for these infections is above 50 percent in patients with weakened immune systems. Two genes are primarily responsible for carbapenem-resistant versions of these disease-causing bacteria. One gene, KPC, was detected in New York in 2001 and quickly spread around most of the world, with the exception of India, Pakistan and other South Asian countries. This gene was present in the bacteria that recently contaminated medical equipment in a Los Angeles hospital where two patients died.

A second carbapenem resistance gene, NDM-1, was identified in 2006 in New Delhi, India. It was soon detected throughout South Asia, and most patients infected by bacteria with NDM-1 have had an epidemiological link to South Asian countries. Dantas and his collaborators were curious about why the two resistance genes seemed to be geographically exclusive. For the study, they compared the genomes of carbapenem-resistant bacteria isolated in the United States with those of carbapenem-resistant bacteria isolated in Pakistan. Based on the apparent geographic exclusivity of the two resistance genes, the scientists expected to find that bacteria from the two regions were genetically different. Such differences could explain why the two resistance genes weren’t intermingling. But the researchers’ results showed otherwise. The bacteria’s high genetic similarity suggests that the antibiotic resistance genes could be shared easily between bacteria from the two geographic regions. The researchers also sequenced a special portion of bacterial genetic material called plasmids. Most of a bacteria’s DNA is found in its chromosome, but bacteria also have many extra, smaller and circular bits of DNA known as plasmids that easily can pass from one bacterial strain to another. A plasmid is like a bacterial gene delivery truck; it is the primary way antibiotic resistance genes spread between bacteria.

The researchers identified a few key instances in which the plasmids carrying NDM-1 or KPC were nearly identical, meaning they easily could facilitate the spread of antibiotic resistance between disease-causing bacteria found in the United States and South Asia. Recent evidence suggests that this intermingling already may be happening in parts of China. “Our findings also suggest it’s going to get easier for strains of these bacteria that are not yet resistant to pick up a gene that lets them survive carbapenem treatment,” Dantas said. “Typically, that’s not going to be a problem for most of us, but as drug-resistant forms of Enterobacteriaceae become more widespread, the odds will increase that we’ll pass one of these superbugs on to a friend with a weakened immune system who can really be hurt by them.”

http://www.sciencedaily.com/ Science Daily

http://www.sciencedaily.com/releases/2015/03/150325210513.htm Original web page at Science Daily

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Antibiotic effectiveness imperilled as use in livestock expected to increase

Five countries — Brazil, Russia, India, China and South Africa — will experience a growth of 99 percent in antibiotic consumption, compared with an expected 13 percent growth in their human populations over the same period, the study authors report in the journal Proceedings of the National Academy of Sciences. In the United States, antibiotic consumption in animals currently represents up to 80 percent of total antimicrobial sales. Because of the incredible volume involved, this increase in antimicrobial use in animals raises serious concerns about preserving antimicrobial effectiveness in the next decades, the researchers report. Global demand for animal protein is rising dramatically, and antimicrobials are used routinely in modern animal production for disease prevention and as growth promoters. The study focused on cattle, chickens and pigs, and identified the latter two as the main contributors to antibiotic consumption.

“The discovery and development of antibiotics was a major public health revolution of the 20th century,” said senior author Ramanan Laxminarayan, a senior research scholar in the Princeton Environmental Institute. “Their effectiveness–and the lives of millions of people around the world — are now in danger due to the increasing global problem of antibiotic resistance, which is being driven by antibiotic consumption.” The study is based on a limited data set of veterinary-antimicrobials sales from 32 countries, all with developed economies. Before now there has been no quantitative measurement of global antimicrobial consumption by livestock — a critical component in assessing the potential consequences of widespread animal antibiotic use. Numerous studies have suggested links between the use of antimicrobials and antibiotic-resistant bacteria originating from livestock as well as their potential consequences for human health. Two thirds, or 66 percent, of the projected global increase in antimicrobial consumption is due to the growing number of animals raised for food production. The remaining third is attributable to a shift in farming practices, with a larger proportion of animals projected to be raised in “intensive farming systems,” or factory farms.

“For about a billion poor people, livestock are essential to survival,” said Tim Robinson, principal scientist from the International Livestock Research Institute. “They are raising their livestock in extensive, backyard systems on the whole and do not use antibiotics as growth promoters or in disease prevention. They use them when their livestock are sick and will take a disproportionately high share of the consequences as effective drugs become more costly and less available in treating their livestock and themselves when they become sick.” Having reliable global data is essential for scientists and policymakers to both measure the extent of the problem and assess potential solutions, said lead author Thomas Van Boeckel, a Fulbright research scholar in Princeton’s Department of Ecology and Evolutionary Biology.

“An important limiting factor in carrying out this first inventory of antibiotic consumption in animals was the lack of ‘modeling-ready’ data on veterinary antibiotic sales in many countries,” Van Boeckel said. “Sometimes these data are simply not collected because of lack of veterinary surveillance programs, but sometimes the barriers are more political and or legislative. With this work we hope to trigger a momentum and show how useful such data could be to inform the design of global concerted policies against antimicrobial resistance.” Antibiotic resistance is a dangerous and growing global public health threat that isn’t showing any signs of slowing down,” Laxminarayan said. “Our findings advance our understanding of the consequences of the rampant growth of livestock antibiotic use and its effects on human health–a crucial step towards addressing the problem of resistance.”

http://www.sciencedaily.com/ Science Daily

http://www.sciencedaily.com/releases/2015/03/150326162700.htm Original web page at Science Daily

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* Baboon friends swap gut germs

Baboons take turns grooming each other to make friends and cement social bonds. A new study finds that baboon friendships influence the microscopic bacteria in their guts. Previous studies have pointed to the food we eat, the drugs we take, genetics, even our house dust. Now, a new study in baboons suggests that relationships may play a role, too. The researchers studied social interactions, eating habits and bacteria in the feces of 48 wild baboons from two groups living near Mount Kilimanjaro in Kenya. Their findings appear in the March 16 issue of the journal eLife. “Poop contains a goldmine of data,” said Duke University biologist Jenny Tung, who co-authored the study. “Ninety-eight percent of the DNA in poop doesn’t come from the animal itself or the foods they eat — it’s bacterial.”

Using powerful sequencing machines to tease out each microbe’s unique genetic signature, the researchers identified the names and relative amounts of nearly 1,000 bacterial species thriving in the baboons’ bowels. The cast of characters includes relatively high levels of Firmicutes, Proteobacteria, Actinobacteria and Bacteroidetes — all of which are also commonly found in human guts. Baboons from the same troop had more similar gut microbes than baboons from different troops. The results are consistent with previous studies in humans showing that people who live together harbor similar gut germs. The connection has largely been attributed to couples and housemates eating many of the same foods in the same relative proportions, but Tung and co-author Elizabeth Archie of the University of Notre Dame and colleagues wondered if additional factors might be at play. To find out, the researchers recorded what the animals ate — a menu of grass seeds and stems, acacia seed pods, fruits and leaves.

They also noted when the baboons in each group hung out in close proximity to each other without physical contact, and measured how often they groomed each other. They found that, in both groups, baboons who groomed each other more often shared more similar sets of gut microbes. How friendly two baboons were to each other was a better predictor of how alike their gut bacterial communities were than whether they merely hung out in the same places, were related, or what they ate.

How fecal bacteria find their way from a baboon’s colon to her fur and from there to another baboon’s gut is unclear, but the researchers have a few ideas. “When baboons groom each other they’re combing through each other’s fur for parasites, dirt, dead skin. Sometimes they pull things off and put them in their mouths,” Archie said. “Males and females also spend a lot of time grooming close to the genital area during estrous,” Tung said. Hugging and cuddling and other forms of physical contact could play a role in allowing people to swap gut germs, too, the researchers say, especially after touching surfaces such as bathroom sinks and toilet handles. “This is another way that social relationships can influence your health,” Archie said. “Not only are relationships important for the transmission of harmful bacteria like the ones that cause pneumonia or strep throat, but they’re important for the transmission of microbes that are harmless or potentially good for you, too.”

http://www.sciencedaily.com/  Science Daily

http://www.sciencedaily.com/releases/2015/03/150316160714.htm  Original web page at Science Daily

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Red deer as maintenance host for bovine tuberculosis, Alpine region

To estimate the prevalence of bovine tuberculosis in the Alpine region, we studied the epidemiology of Mycobacterium caprae in wildlife during the 2009–2012 hunting seasons. Free-ranging red deer (Cervus elaphus) were a maintenance host in a hot-spot area, mainly located in Austria. Bovine tuberculosis has one of the broadest host ranges of any known zoonotic pathogens. In addition to cattle, bovine tuberculosis affects many wild animal populations in North America, Europe, Africa, Asia, and New Zealand. Under certain conditions, wildlife play a role as reservoir and source of infection for domestic animals. Mycobacterium caprae has been isolated from cattle, domestic goats, domestic pigs, red deer (Cervus elaphus), and wild boar. Evidence is increasing that M. caprae is emerging in free-ranging red deer and cattle in the Alps.

To estimate the prevalence of bovine tuberculosis (which is caused by M. bovis and M. caprae) in wildlife in the Alps, we investigated 1,655 hunted red deer of both sexes and different ages in Austria, Germany, Switzerland (including the Principality of Liechtenstein), and Italy. The deer were hunted specifically for the study by trained hunters. A sampling/hunting plan was calculated in advance that indicated the number of animals needed in each sampling region to calculate prevalence estimates; the number was based on the red deer density of a region. The numbers of animals killed and sampled during 3 consecutive hunting seasons (2009–10, 2010–11, and 2011–12) coordinated nearly perfectly with the sampling plan that had been developed for each sampling area.

After pathomorphologic examination of carcasses (from Germany, Austria, Italy, Swiss Tessin) or samples (from Swiss St. Gall, Swiss Grisons, and Liechtenstein), we conducted microbiological analysis from sample material. Sample material included both medial retropharyngeal lymph nodes and tracheobronchial, mediastinal, and mesenteric lymph nodes and any other tissue with macroscopically visible lesions. For bacteriologic cultivation the sample material was homogenized by using the IKA Ultra Turaxx Tube Drive System (Staufen, Germany), decontaminated with 1% N-acetyl-L-cystein solution and neutralized in phosphate buffer (pH 6.8) as recommended by the World Organisation for Animal Health. After sedimentation, inoculation was performed on 2 growth media: Stonebrink including PACT (polymyxin B, amphotericin B, carbenicillin, and trimethoprim) and Lowenstein-Jensen with glycerin and PACT (Heipha Diagnostika, Eppelheim, Germany). After 12 weeks’ incubation, a total of 82 bacterial cultures from 59 hunted red deer from Austria, Germany, and Italy were isolated. All isolates were identified as M. caprae whether by reversed line blotting (Geno Type MTBC, HAIN Lifescience, Nehren, Germany) or by restriction fragment length polymorphism PCR of the gyrB gene, as previously described.

http://wwwnc.cdc.gov/eid/  Emerging Infectious Diseases

http://wwwnc.cdc.gov/eid/article/21/3/14-1119_article  Original web page at Emerging Infectious Diseases

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Amphibian chytrid fungus reaches Madagascar

The chytrid fungus, which is fatal to amphibians, has been detected in Madagascar for the first time. This means that the chytridiomycosis pandemic, which has been largely responsible for the decimation of the salamander, frog and toad populations in the USA, Central America and Australia, has now reached a biodiversity hotspot. The island in the Indian Ocean is home to around 290 species of amphibians that are not found anywhere else in the world. Another 200 frog species that have not yet been classified are also thought to live on the island. Researchers from the Helmholtz Centre for Environmental Research (UFZ) and TU Braunschweig, together with international colleagues, are therefore proposing an emergency plan. This includes monitoring the spread of the pathogenic fungus, building amphibian breeding stations and developing probiotic treatments, say the scientists, writing in Scientific Reports, the acclaimed open-access journal from the publishers of Nature. The entire amphibian class is currently afflicted by a global pandemic that is accelerating extinction at an alarming rate.

Although habitat loss caused by human activity still constitutes the main threat to amphibian populations, habitat protection no longer provides any guarantee of amphibian survival. Infectious diseases are now threatening even seemingly secluded habitats. The most devastating of the known amphibian diseases is chytridiomycosis, which is caused by a deadly chytrid fungus (Batrachochytrium dendrobatidis, or Bd). The fungus attacks the skin, which is particularly important in amphibians because they breathe through it. A large number of species have already been lost in this way — particularly in tropical Central America, where two-thirds of the colourful harlequin frog species have already been decimated across their entire area of distribution. Bd has now been identified in over 500 amphibian species, 200 of which have seen a significant decline in numbers. The pathogen is therefore classified worldwide as one of the greatest threats to biodiversity. Until now, however, a few islands like Madagascar were thought not to have been affected. The last series of tests from 2005 to 2010 found no trace of the pathogenic fungus there. However, an analysis of the latest series of tests shows that the chytrid fungus also poses a threat to amphibians in Madagascar. “This is sad news for amphibian-lovers around the world,” says Dr Dirk Schmeller of the UFZ, who was involved in analysing the samples. “Firstly, it means that an island that is home to a particularly high number of amphibian species is now at risk. Several hundred species live only on this island. And, secondly, if the pathogen has managed to reach such a secluded island, it can and will occur everywhere. “For the study that has just been published, the research team analysed samples from over 4000 amphibians from 50 locations in Madagascar taken since 2005.

Samples from four species of Madagascan frog (Mantidactylus sp.) taken in 2010, and from one Mascarene frog (Ptychadena mascareniensis) taken in 2011 from the remote Makay massif tested positive for the fungus. In samples from 2013 and 2014 the pathogen was found in five different regions. Prof. Miguel Vences from TU Braunschweig says, “The chytrid fungus was found in all four families of the indigenous Madagascan frogs, which means it has the potential to infect diverse species. This is a shock!” The study also shows that the disease affects amphibians at medium to high altitudes, which ties in with observations from other parts of the world, where the effects of the amphibian epidemic have been felt primarily in the mountains. The fact that the fungus has been identified in a very remote part of the island has puzzled the researchers. There is some hope that it may prove to be a previously undiscovered, native strain of the pathogen, which may have existed in the region for some time and have gone undetected because of a lack of samples. In this case, Madagascar’s amphibians may have developed resistance to it. However, further research is needed to confirm this hypothesis before the all-clear can be given. It is also possible that the fungus was brought to the island in crustaceans or the Asian common toad (Duttaphrynus melanostictus), carried in by migratory birds or humans. “Luckily, there have not yet been any dramatic declines in amphibian populations in Madagascar,” Dirk Schmeller reports. “However, the pathogen appears to be more widespread in some places than others. Madagascar may have several strains of the pathogen, maybe even the global, hypervirulent strain.

This shows how important it is to be able to isolate the pathogen and analyse it genetically, which is something we haven’t yet succeeded in doing.” At the same time, the researchers recommend continuing with the monitoring programme across the entire country to observe the spread of the disease. The scientists also suggest setting up extra breeding stations for key species, in addition to the two centres already being built, to act as arks, so that enough amphibians could be bred to recolonise the habitats in a crisis. “We are also hopeful that we may be able to suppress the growth of the Bd pathogen with the help of skin bacteria,” says Miguel Vences. “It might then be possible to use these bacteria as a kind of probiotic skin ointment in the future.” A high diversity of microbial communities in the water could also reduce the potential for infection, according to earlier investigations conducted by UFZ researchers and published in Current Biology. The outbreak of amphibian chytridiomycosis in Madagascar puts an additional seven per cent of the world’s amphibian species at risk, according to figures from the Amphibian Survival Alliance (ASA). “The decline in Madagascan amphibians is not just a concern for herpetologists and frog researchers,” says Dr Franco Andreone from the International Union for Conservation of Nature (IUCN), who is one of the study authors. “It would be a great loss for the entire world.” In the coming months, the scientists therefore plan to work with the government to draw up an emergency plan to prevent this scenario.

http://www.sciencedaily.com/ Science Daily

http://www.sciencedaily.com/releases/2015/02/150226122443.htm Original web page at Science Daily

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Spillover of Mycobacterium bovis from wildlife to livestock, South Africa

Bovine tuberculosis is an infectious disease caused by Mycobacterium bovis. The wide host range of the pathogen comprises humans and domestic and wild animals. Great strides in controlling bovine tuberculosis have drastically reduced its prevalence in livestock and humans, particularly in industrialized countries. However, in developing countries in southern Africa and elsewhere, bovine tuberculosis remains a challenge to animal health because of a total or partial lack of bovine tuberculosis control, limited by a lack of funds.

The control and/or elimination of bovine tuberculosis in both developing and industrialized countries can be complicated by wildlife reservoirs of the disease, which pose a threat of re-infection in livestock. In sub-Saharan Africa, particularly South Africa and Uganda, African buffalos (Syncerus caffer) serve as wildlife reservoirs of bovine tuberculosis; in Zambia, lechwe antelopes (Kobus leche Kafuensis) have been identified as wildlife reservoirs. New reports have suggested greater kudu (Tragelaphus strepsiceros) and common warthog (Phacochoerus africanus) as potential wildlife reservoirs of bovine tuberculosis.

M. bovis is endemic in buffaloes and has spilled into other wildlife species, particularly in the Kruger National Park (KNP) and adjacent game reserves that form part of the Greater Kruger National Park Complex (GKNPC) in South Africa. Except for data from sporadic regulatory bovine tuberculosis surveillance activities in cattle adjacent to the GKNPC, no data exist on the transmission of bovine tuberculosis from the GKNPC, where it is endemic, into livestock in neighboring communities. Because of the potentially negative implications of livestock–wildlife interactions on livestock and human health, the presence and role of zoonotic diseases in these communities needs to be investigated.

We report on an investigation into the status and genotype of bovine tuberculosis in livestock in rural communities bordering the bovine tuberculosis–endemic GKNPC. The study was conducted in a rural community under the Mnisi Tribal Authority. The community is situated in Mpumalanga Province, South Africa, and borders the GKNPC in the west and 1 private game reserve. We constructed maps for this study using ArcGIS version 10.2 (http://www.arcgis.com). The KNP and private game reserves are fenced and have buffer zones established by double fencing.

http://wwwnc.cdc.gov/eid/ Emerging Infectious Diseases

http://wwwnc.cdc.gov/eid/article/21/3/13-1690_article Original web page at Emerging Infectious Diseases

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Mycobacterium bovis infection in humans and cats in same household, Texas, USA, 2012

Mycobacterium bovis infection of cats is exceedingly rare in regions where bovine tuberculosis is not endemic. We describe the diagnosis and clinical management of pulmonary M. bovis infection in 2 indoor-housed cats and their association with at least 1 M. bovis–infected human in Texas, USA, in September 2012.

Tuberculosis in humans and animals results from infection by bacilli within the Mycobacterium tuberculosis complex. Despite ≈99.95% genome sequence identity, M. bovis and M. tuberculosis exhibit distinct differences in host adaptation and susceptibility. M. bovis is the primary causative agent of bovine tuberculosis and infects a wider range of hosts than M. tuberculosis. In domestic cats, tuberculosis is caused primarily by infection with M. bovis or M. microti ; M. tuberculosis infection is less common. Before implementation of bovine tuberculosis control programs and wide-scale pasteurization of milk, alimentary tract disease was the most common form of tuberculosis in cats; today, lymphadenopathy and cutaneous forms are more common. Diagnosis is based on clinical examination, imaging, biopsy with histopathologic examination, culture of aspirates or tissues, and specific immune-based blood assays. Intradermal skin tests are generally unreliable for diagnosing tuberculosis in cats. Client history is critical for determining the possibility for exposure of the cat to the pathogen, and zoonotic aspects should be considered.

We describe the diagnosis and clinical management of pulmonary M. bovis infection in 2 indoor-housed cats and their association with at least 1 M. bovis–infected human in Texas, USA. In September 2012, a 5-year-old female domestic cat (cat Y) was seen by a veterinarian for dyspnea, tachypnea, hyporexia, and lethargy. She lived indoors with 4 other cats and their female owner. The vague history provided by cat Y’s owner indicated that, ≈11 months earlier, her husband had died of tuberculosis only 6 weeks after diagnosis and initiation of directly observed antimycobacterial therapy. At the time the husband’s tuberculosis was diagnosed, the woman was Mantoux-test negative; ≈2 months after his death, she converted to skin-test positive but had normal findings on thoracic radiographs. She was subsequently treated with antimycobacterial drugs. The woman also reported that, in June 2012, another cat in the household was euthanized after clinical signs developed that were similar to those of cat Y; no necropsy was performed. Additional pertinent history included relocation of the deceased husband from Mexico to Texas 15 years earlier, frequent contact with recent immigrants from Central America and Mexico, and consumption of unpasteurized Mexican cheeses.

Read more : http://wwwnc.cdc.gov/eid/article/21/3/14-0715_article

http://wwwnc.cdc.gov/eid/ Emerging Infectious Disease

http://wwwnc.cdc.gov/eid/article/21/3/14-0715_article Original web page at Emerging Infectious diseases

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* Mothers can pass traits to offspring through bacteria’s DNA, mouse study shows

A new study in mice by researchers at Washington University School of Medicine in St. Louis has shown that the DNA of bacteria that live in the body can pass a trait to offspring in a way similar to the parents’ own DNA. According to the authors, the discovery means scientists need to consider a significant new factor — the DNA of microbes passed from mother to child — in their efforts to understand how genes influence illness and health. The study appeared online Feb. 16 in Nature. “We have kept bacteria on one side of a line separating the factors that shape our development — the environmental side of that line, not the genetic side,” said co-senior author Herbert W. Virgin IV, MD, PhD. “But our results show bacteria stepping over the line. This suggests we may need to substantially expand our thinking about their contributions, and perhaps the contributions of other microorganisms, to genetics and heredity.”

Bacteria are most familiar through their roles in harmful infections. But scientists have realized that such bacteria are only a tiny fraction of the bacterial communities that live in and on our bodies. Most bacteria are commensal, which means they do not cause harm and often confer benefits. Commensal bacteria influence traits such as weight and behavior. But until now, researchers thought the bacteria that exerted these effects were acquired during a person’s life. The study is the first to show that bacterial DNA can pass from parent to offspring in a manner that affects specific traits such as immunity and inflammation. The researchers linked commensal bacteria in mice to the animals’ susceptibility to a gut injury. Mice with certain inherited bacteria are susceptible to the injury, which is caused by exposure to a chemical. Female mice pass the bacteria to their offspring, making them vulnerable to the injury. Others carrying different bacteria are less susceptible.

In the short term, the findings may help scientists eliminate a significant “bug” in studies of genetically engineered mice. In several fields of research, scientists have been confronted intermittently with the sudden, unexplained appearance of new or altered traits in mice. The traits often spread from one mouse habitat to the next, suggesting a spreading microbial infection is responsible. But the traits also consistently pass from mother to offspring, suggesting a genetic cause. Thaddeus Stappenbeck, MD, PhD, a professor of pathology and immunology, and co-senior author Virgin, the Edward Mallinckrodt Professor of Pathology and head of the Department of Pathology and Immunology, encountered this problem in their studies of inflammatory bowel diseases, such as Crohn’s disease and ulcerative colitis. They were surprised to find that roughly half their mice had low levels in the gut of IgA, an antibody linked to these disorders. IgA helps defend the body against harmful invaders. It is commonly present in mucus made by the body in areas where the exterior world encounters the body’s interior, such as the eyes, nose, throat and gut. When the scientists housed mice with low levels of the antibody with mice that had high levels of the antibody, all of the mice ended up with low antibody levels in a few weeks. When they bred the mice, the offspring whose mothers had low levels of the antibody also had low levels.

Eventually, the scientists learned that one of the culprits likely responsible for the spread of low antibody levels is a bacterium called Sutterella. This bacterium and others found in the low-IgA mice could explain both ways that decreased antibody levels were spreading: Mice that were housed together acquired low antibody levels through normal spread of the bacteria, and mouse mothers passed the same bacteria to their descendants. The latter explanation involves a major change in thinking because it suggests that traits affected by bacteria can pass from mothers to their offspring in the same manner as traits affected by mouse DNA. To prove that this change in antibody levels represented a significant change in the mice that could be thought of as a trait, the researchers fed the mice a chemical they use to characterize the gut’s response to injury as part of their studies of inflammatory bowel diseases. In mice with low levels of the antibody, the compound caused much more damage. “The implications for mouse experiments are profound and could help us cut through some persistent sources of confusion,” Stappenbeck said. “When we study mice, we have to account for the possibility that inherited bacteria and their genes could be influencing the trait we’re trying to learn about.” According to Stappenbeck, one way to do this will be to stop housing experimental and control mice in separate colonies. This would help ensure that any inherited microbes that influence a trait of interest are present in both groups. In the long term, Virgin expects the expanded model of heredity to produce a more complicated but also much more insightful picture of how human, bacterial and viral genes influence human health.

http://www.sciencedaily.com/ Science Daily

http://www.sciencedaily.com/releases/2015/02/150216125425.htm Original web page at Science Daily

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Lyme disease costs up to $1. 3 billion per year to treat, study finds

Lyme disease, transmitted by a bite from a tick infected by the Borrelia burgdorferi bacteria, had long been considered easy to treat, usually requiring a single doctor’s visit and a few weeks of antibiotics for most people. But new research from the Johns Hopkins Bloomberg School of Public Health suggests that a prolonged illness associated with the disease is more widespread and serious in some patients than previously understood. With an estimated 240,000 to 440,000 new cases of the tick-borne illness diagnosed every year, the researchers found that Lyme disease costs the U.S. health care system between $712 million and $1.3 billion a year — or nearly $3,000 per patient on average — in return doctor visits and testing, likely to investigate the cause of some patients’ lingering symptoms of fatigue, musculoskeletal pain and memory problems. These visits come after patients have finished their original course of antibiotics. Some doctors call those persistent symptoms post-treatment Lyme disease syndrome (PTLDS); others call it chronic Lyme disease. Still others attribute the complaints of fatigue, headaches and memory problems to the hum of daily life, the aches and pains that come with aging.

At the core of the controversy is whether PTLDS can be a severe and chronic condition that requires more than reassurance and symptomatic therapy. While a blood test can confirm Lyme disease, there is no definitive test for PTLDS and there are no approved or proven treatments. It’s a controversial topic in medicine, the Hopkins researchers say. A report on the findings is published online Feb. 4 in the journal PLOS ONE. “Our study looks at the actual costs of treating patients in the year following their Lyme diagnosis,” says study author Emily Adrion, MSc, a PhD candidate in the Department of Health Policy and Management at the Johns Hopkins Bloomberg School of Public Health. “Regardless of what you call it, our data show that many people who have been diagnosed with Lyme disease are in fact going back to the doctor complaining of persistent symptoms, getting multiple tests and being retreated. They cost the health care system about $1 billion a year and it is clear that we need effective, cost-effective and compassionate management of these patients to improve their outcomes even if we don’t know what to call the disease.” Adrion and her colleagues looked at medical claims data from approximately 47 million people enrolled in a wide range of commercial health insurance plans in the United States between 2006 and 2010. The researchers ended up analyzing 52,795 cases of Lyme disease patients under the age of 65 who had been treated with antibiotics within 30 days of a Lyme disease test order and/or Lyme disease diagnosis.

The data were compared to nearly 264,000 other similar people with no evidence of Lyme disease exposure. The researchers found that, on average, people with Lyme disease cost the system $2,968 more than matched controls. They had 87 percent more visits to the doctor and 71 percent more visits to the emergency room within the year following diagnosis. Those with Lyme disease were nearly five times more likely to have any PTLDS-related diagnosis — fatigue, nerve pain, joint pain, cognitive troubles — within that year and were 5.5 times more likely to have a diagnosis of debility and excessive fatigue. Among those with Lyme disease, having one or more PTLDS-related diagnosis was associated with $3,798 more in health care costs as compared to those with no post-treatment symptoms.

Lyme disease is named after the town in Connecticut where it was first recognized in 1975. It now hits its peak in June and July and is found from Maine to Virginia along the East Coast of the United States. The tick causes a skin reaction that resembles a bulls-eye or spider bite. If left untreated, Lyme disease may lead to neurologic and rheumatic symptoms weeks or months later. Treatment with the antibiotic doxycycline is associated with a more rapid resolution of early signs of infection and prevention of the majority of later symptoms, the researchers say. Still, some patients report symptoms lasting for weeks, months or years beyond completion of the original antibiotic regimen. There is no approved therapy for these patients and the magnitude of the problem in the U.S. population has never been systematically studied. The Centers for Disease Control and Prevention estimates 10 to 20 percent of those treated for Lyme disease with the recommended two-to-four week course of antibiotics continue to have symptoms. But, in the new study, the researchers found that more than 63 percent of those treated for Lyme disease had at least one PTLDS-related diagnosis — a rate 36 percentage points higher than those who did not have Lyme disease. The study’s lead author John Aucott, MD, an assistant professor of rheumatology at the Johns Hopkins University School of Medicine, says it does no good to keep debating the existence of long-term problems related to Lyme disease while people are suffering a debilitating illness. And he says that increasing awareness of potential complications is crucial to avoid misdiagnosis and unnecessary medical testing. “These patients are lost,” he says. “No one really knows what to do with them. It’s a challenge, but the first thing we need to do is recognize this is a problem. There’s not a magic pill. These patients already got the magic pill and it didn’t work.”

http://www.sciencedaily.com/ Science Daily

http://www.sciencedaily.com/releases/2015/02/150205095049.htm Original web page at Science Daily

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GM microbes created that can’t escape the lab

Critics of genetic engineering have long worried about the risk of modified organisms escaping into the environment. A biological-containment strategy described this week in Nature, has the potential to put some of those fears to rest and to pave the way for greater use of engineered organisms in areas such as agriculture, medicine and environmental clean-up. Two US teams have produced genetically modified (GM) bacteria that depend on a protein building block — an amino acid — that does not occur in nature. The bacteria thrive in the laboratory, growing robustly as long as the unnatural amino acid is included in their diet. But several experiments involving 100 billion or more cells and lasting up to 20 days did not reveal a single microbe capable of surviving in the absence of the artificial supplement. “Our strains, to the extent that we can test them, won’t escape,” says Dan Mandell, a synthetic biologist at Harvard Medical School in Boston, Massachusetts, and an author on one of the two studies describing the strategy. The microbes also do not swap their engineered DNA with natural counterparts because they no longer speak life’s shared biochemical language. “Establishing safety and security from the get-go will really enable broad and open use of engineered organisms,” says Farren Isaacs, a synthetic biologist at Yale University in New Haven, Connecticut, who led the other study.

Biocontainment could provide added safety in the biological production of drugs or fuels, where microbes can be kept separate from their surroundings. But the modified bacteria could also permit controlled release into the human body or the environment. “Containment might no longer be of the physical kind,” says Tom Ellis, a synthetic biologist at Imperial College London who was not involved in the research. The new technique originated in the laboratory of George Church, a geneticist at Harvard Medical School. Two years ago, Church and his team (which included Isaacs) reported the synthesis of a strain of Escherichia coli that had a reprogrammed genetic code. Instead of recognizing a particular DNA triplet known as the amber stop codon as an order to terminate protein synthesis, the recoded bacterium read the same instruction as a directive to incorporate a new kind of amino acid into its proteins. Church and Isaacs have independently made this engineered microbe reliant on unnatural amino acids. The Isaacs team used genomic sequencing to identify sites in essential bacterial proteins where the microbes could incorporate synthetic amino acids without affecting overall function, whereas Church’s group started with the protein structures and added elements to help integrate and accommodate the artificial amino acids.

These organisms are also more resistant to viruses than their natural counter­parts because of the mismatch between the genetic code of the virus and that of its host. Looking ahead, Church and his team are working to co-opt seven different codons, instead of just one. “That would be more than enough to be resistant to all viruses and to create a lot of opportunity for safety,” Church says. Isaacs has also developed a different safeguarding system, in which E. coli can grow only in environments containing synthetic chemicals needed for gene expression. He described the work this month in Nucleic Acids Research. Another research team led by Jef Boeke at the New York University Langone Medical Center and Patrick Yizhi Cai at the University of Edinburgh, UK, has been working on a similar strategy in yeast. Commonly used in industry and biotechnology, yeast has its genetic mater­ial packaged in chromosomes similarly to animals and plants rather than bacteria. “That’s a strategy that is going to be more easily adaptable to other organisms beyond E. coli,” says Isaacs. His team is now engineering a bacterium that is dependent on synthetic chemicals as well as on artificial protein building blocks. “I think ultimate solutions for robust biocontainment will involve multiple approaches that are deployed at the same time in a single organism,” he says. Such a beast will present a real challenge for regulators, says Todd Kuiken, senior research associate for the Science and Technology Innovation Program at the Woodrow Wilson International Center for Scholars in Washington DC. “What we’re now starting to talk about is a really, completely synthetic organism,” Kuiken says. “How do you evaluate that once you put it out into the field?”

Nature 517, 423 (22 January 2015) doi:10.1038/517423a

http://www.nature.com/news/index.html  Nature

http://www.nature.com/news/gm-microbes-created-that-can-t-escape-the-lab-1.16758  Original web page at Nature

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* Antibiotics, bacteria, resistance genes found in dust from feedlots

After testing dust in the air near cattle feedlots in the Southern High Plains, researchers at The Institute of Environmental and Human Health at Texas Tech University found evidence of antibiotics, feedlot-derived bacteria and DNA sequences that encode for antibiotic resistance.
The study was published online in the National Institutes of Environmental Science’s peer-reviewed journal, Environmental Health Perspectives. The research was funded through a grant from Texas Tech’s College of Arts and Sciences. It is the first study documenting aerial transmission of antibiotic resistance from an open-air farm setting. Phil Smith, an associate professor of terrestrial ecotoxicology at the institute, said that while scientists couldn’t assess if the amounts of these materials were dangerous to human health, it helped explain a previously uncharacterized pathway by which antibiotic-resistant bacteria could travel long distances into places inhabited by humans.

The findings come weeks after a report commissioned by British Prime Minister David Cameron concluded that failure to battle drug-resistant infections and their causes could result in 10 million extra deaths a year by 2050 at a cost of $100 trillion to the global economy. “You can look in the news, and people are raising red flags about antibiotic resistance all the time,” Smith said. “Microbes are pretty promiscuous with their genetic information, and they share it across species fairly easily. We know it’s there. We know what causes it, but we don’t have a really good handle on how it’s transmitted and how it moves in the environment. This is an attempt to provide better clarity on that issue. “Everyone is fairly certain antibiotic resistance comes from extensive use of antibiotics in animal-based agriculture. About 70 percent of all antibiotics used are for animal agricultural purposes. Overuse contributes to antibiotic resistance. But how does it happen? How does it get from where the drugs are used into the human environment and natural environment?”

Smith said scientists collected air samples upwind and downwind of each feedlot. After analysis, they found greater amounts of bacteria, antibiotics and DNA sequences responsible for antibiotic resistance downwind of the feedlots compared to upwind, which helped scientists determine the source of the materials they found. Because the antibiotics are present on the particulate matter with bacteria, the selective pressure for bacteria to retain their resistance remains during their flight, said Greg Mayer, an associate professor of molecular toxicology at the institute. With wind blowing regularly on the Southern High Plains, the antibiotics and bacteria can travel on the dust and particulate matter far from the original starting point at the feedlot. Add the infamous West Texas dust storms into the picture, and these materials have the potential to travel hundreds of miles into cities and towns and possibly around the globe.

“I think implications for the spread of some feedlot-derived, antibiotic-resistant bacteria into urban areas is paramount to the research,” Mayer said. “Now, we haven’t yet taken samples from an urban area to determine whether bacteria from that particulate matter originated from feedlots or whether it still has antibiotic resistant bacteria on it. However, this study is proof of the principle that antibiotic-resistant bacteria could plausibly travel through the air. “Further studies are now needed to show where the particulate matter is traveling and what is happening to its passengers when it gets there.”

http://www.sciencedaily.com/ Science Daily

http://www.sciencedaily.com/releases/2015/01/150122114357.htm Original web page at Science Daily

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New salmonella serotype discovered

The latest honor to come Lubbock’s way may not sound good at first, but when realizing it’s a breakthrough in biological sciences, it will become something to brag about. Marie Bugarel, a research assistant professor at Texas Tech University’s Department of Animal and Food Sciences in the College of Agricultural Sciences and Natural Resources, has discovered a new serotype of the salmonella bacteria. The new serotype was confirmed by the Pasteur Institute in Paris, the international reference center for salmonella. Because convention calls for a new serotype to be named after the city in which it is discovered, this one will be called Salmonella Lubbock (officially Salmonella enterica subsp. enterica Lubbock). “More important than the name, however, is that this discovery illustrates there is more that needs to be discovered about salmonella and how it interacts with cattle populations,” said Guy Loneragan, a professor of food safety and public health who, along with Kendra Nightingale, are Bugarel’s mentors at Texas Tech. “With this understanding will come awareness of how to intervene to break the ecological cycle and reduce salmonella in animals and in beef, pork and chicken products.” Bugarel, who came to Texas Tech with an extensive background in salmonella research, has worked on developing new tools to detect salmonella, new approaches to distinguish serotypes and ways to understand salmonella’s biology. Her work has led to a patent application that has been licensed to a high-tech biosciences research company. Her invention means it is now possible to simultaneously detect and distinguish specific strains of salmonella by targeting a specific combination of DNA. That will allow for early detection in food while also identifying whether or belongs to a highly pathogenic strain.

In her research for Salmonella Lubbock, the impetus was to reduce salmonella in food and improve public health. She focused on providing solutions to control salmonella in cattle population, which led to a better understanding of the biological makeup of salmonella itself, including its genetic makeup. Through this approach, Bugarel discovered the new strain never before described. The long-held standard way of distinguishing one strain of salmonella from another is called serotyping and is based on the molecules on the surface of the bacterium. Each serotype has its own pattern of molecules, called antigens, and the collection of molecules provides a unique molecular appearance. These antigens interact with certain antibodies found in specifically prepared serum, thus providing the serotype. It is similar to how blood typing is performed. “This discovery reinforces my feeling that the microbiological flora present in cattle in the United States harbors a singularity, which is an additional justification of the research we are doing in the International Center for Food Industry Excellence (ICFIE) laboratories at Texas Tech,” Bugarel said. “Additional research will be performed to better describe the characteristics of this atypical bacterial flora and, more specifically, of the Lubbock serotype.”

With this discovery, Loneragan believes between 20 and 30 percent of two current strains, Salmonella Montevideo and Salmonella Mbandaka, will be reclassified as Salmonella Lubbock. The algorithm used in serotyping has some stopping points, but Bugarel discovered a need to go a step further to get the correct strain name. Therefore some of those strains called Montevideo and Mbandaka are now Salmonella Lubbock. Some of the strains of Salmonella Lubbock fall into the category of serotype patterns that are more broadly resistant to many families of antibiotics, furthering the need for more research on the subject. Human susceptibility to the Lubbock strains remains unknown. “We will continue to develop methods to detect, identify and control the presence of pathogenic microorganisms in food products in order to improve food safety and public health,” Bugarel said. “Kendra and I have been honored to serve as Marie’s mentors,” Loneragan said. “But now, the growth in Marie’s expertise means that she is becoming the mentor to us. Many students, and the citizens of the United States in general and Texas in particular, are benefitting from her commitment to research excellence at Texas Tech. We are very lucky to have her.”

http://www.sciencedaily.com/ Science Daily

http://www.sciencedaily.com/releases/2015/01/150116143835.htm Original web page at Science Daily

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* Testing for Bovine Tuberculosis is more effective than badger culls at controlling the disease

Modelling produced by researchers at Queen Mary University of London (QMUL) has found that the only effective potential Bovine Tuberculosis (TB) control strategies are badger culling, cattle testing, controlling cattle movement, and ceasing the practice of housing farm cattle together during winter. The modelling found that in a region containing about 1.5m cows of which 3000 to 15,000 might have TB, badger culling could account for a reduction of 12 in the number of infected cattle. While reducing the testing interval by one month could reduce the number of those infected by 193. The model showed that regular and frequent testing of cattle could eventually lead to the eradication of the disease, whether or not badgers were culled and despite the current test being at most 80% accurate. Badger culling alone, however did not lead to TB eradication in the study and is therefore unlikely to be a successful control strategy. The model also suggested that housing cattle in large sheds over winter could potentially double the number of infected animals in a herd, as under such conditions there is a much greater chance of TB being passed between cows. This is the first large-scale model of TB in cattle and badgers that included the possibility of the infection being passed in both directions between the two species. The model successfully mimicked the changing patterns of TB in the UK, including the changes seen after TB controls were reduced during the foot-and-mouth epidemic of 2002. Researchers Dr Aristides Moustakas and Professor Matthew Evans, of QMUL’s School of Biological and Chemical Sciences, used state-of-the-art computer modelling to understand how the interaction of different factors impacted on infection rates. Such factors included the movement and life-cycles of badgers and cattle; how cattle are moved and housed; how frequently cattle are tested, different types of badger culling; and the infection rates between animals. The research is published online in Stochastic Environmental Research and Risk Assessment. Professor Matthew Evans, Professor of Ecology at QMUL, said: “Of the available Bovine Tuberculosis control strategies we believe that how frequently cattle are tested and whether or not farms utilise winter housing have the most significant effect on the number of infected cattle.” “TB is a complex disease and modelling it is difficult but we’ve successfully used our model to replicate real world situations and are confident that it can be used to predict the effects of various changes in the way we tackle the disease.” “Our modelling provides compelling evidence, for those charged with controlling Bovine TB, that investment in increasing the frequency of cattle testing is a far more effective strategy than badger culling.”

http://www.sciencedaily.com/  Science Daily

http://www.sciencedaily.com/releases/2015/01/150114072705.htm Original web page at Science Daily

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Streptococcus equi subsp. zooepidemicus infections associated with guinea pigs

Streptococcus equi subsp. zooepidemicus is a known zoonotic pathogen. In this public health investigation conducted in Virginia, USA, in 2013, we identified a probable family cluster of S. zooepidemicus cases linked epidemiologically and genetically to infected guinea pigs. S. zooepidemicus infections should be considered in patients who have severe clinical illness and report guinea pig exposure. Streptococcus equi subsp. zooepidemicus is a facultative pathogen affecting animals and humans. Infections have occurred in horses, pigs, ruminants, guinea pigs, monkeys, cats, and dogs. Zoonotic transmission of S. zooepidemicus is rare and is usually associated with drinking unpasteurized milk or through contact with horses by persons who usually have underlying health conditions. Few if any human case-patients with S. zooepidemicus infection have documented guinea pig exposure even though S. zooepidemicus infections have been described in guinea pigs since 1907. This case report describes 1 probable and 1 confirmed human case of severe S. zooepidemicus infection and the laboratory methods used to link human and guinea pig isolates. S. zooepidemicus infection should be considered in patients who have purulent wounds or systemic symptoms of infection who have had known contact with guinea pigs or their environment. Likewise, patients whose specimen cultures reveal S. equi or further test results show S. zooepidemicus should be questioned about guinea pig exposure as well as exposure to other animals associated with this pathogen: horses, pigs, ruminants, monkeys, cats, and dogs.

http://wwwnc.cdc.gov/eid/  Emerging Infectious Diseases

http://wwwnc.cdc.gov/eid/article/21/1/14-0640_article  Original web page at Emerging Infectious Diseases

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Species of bird ‘paints’ its own eggs with bacteria to protect embryo

Through an experiment published in the Journal of Animal Ecology, scientists from several research groups precluded several female hoophoes from impregnating their eggs with this substance, which they produce themselves inside the so-called uropygial gland. The research groups involved in this project were the following: Animal Behaviour and Ecology, Microorganism-Produced Antagonistic Substances, both from the UGR, and Evolutive Ecology and the Behaviour and Conservation groups from the Dry Areas Experimental Station (Almería, CSIC). By doing so they confirmed that the amount of pathogen bacteria that could be found inside the eggs which failed to hatch was higher in those nests in which they had experimentally precluded the females from using their secretion than in those where they were allowed to use this substance. They concluded that this secretion provides a barrier for the entry of pathogens towards the interior of the egg. On the other hand, not just the secretion as a whole, but particularly the bacteria that did produce bacteriocins (small antimicrobial proteins) in that secretion, the enterococci, are beneficial for the developing embryos, since successful hatches were directly related to the amount of these enterococci in the egg shells and in the secretions of the females. The more enterococci they had, the higher the rate in their successful hatching. As UGR zoology professor, Manuel Martín-Vivaldi, one of the authors of this research underlines, during the last few years the field of evolutive ecology has acknowledged “the important role played by bacteria, not just as infectious agents capable of producing diseases, but also as allies of animals and other living creatures in their struggle against disease, due to their extraordinary capacity to synthesise compounds with antimicrobial properties” In the case of the hoophoe’s uropygical gland, scientists have confirmed that its components are very different from those of other birds. This is to a large extent due to the action of the bacteria present in this particular gland. This research has also revealed that hoophoes have developed an exceptional property in their eggs — which has not so far been found in any other species of bird. This consists in the presence in the surface of many small depressions that do not completely penetrate the shell, and whose function appears to be the retention of this bacteria-carrying secretion that covers the egg. “With this experiment, we have been able to establish that if the females can use their secretion, towards the end of the incubation period, those tiny craters are full of a substance saturated with bacteria. If we preclude the use of this secretion, these tiny craters appear empty towards the end of the hatching process,” said professors Martín-Vivaldi. These results prove that in this particular species of bird, “its reproductive strategy has evolved hand in hand with the use of bacteria which may be beneficial for the production of antimicrobial substances, which they cultivate in their gland and then apply upon eggs which are particularly endowed to retain them” These scientists are currently working to determine the specific composition of the bacterial community within the gland, how these symbionts are acquired, and the types of antimicrobial compounds which synthesize these bacteria, capable of protecting the embryos which are undergoing development.

http://www.sciencedaily.com/  Science Daily

http://www.sciencedaily.com/releases/2015/01/150113090420.htm   Original web page at Science Daily

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Genome sequencing traces MRSA spread in high transmission setting

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Guts of obese dogs look similar to those of obese people

Obese people have a less diverse array of bacteria living in their guts than do thin people—and the same holds true for dogs. In a new study, researchers fed seven beagles unrestricted amounts of food for 6 months, during which each dog gained an average of 4.93 kilograms—about 67% of their initial average weight of 7.37 kilograms. The investigators fed another seven beagles controlled food portions, and, as expected, this group did not gain weight. When the researchers examined the fecal samples collected from both groups after 6 months, they found that the guts of obese beagles contained a smaller diversity of bacteria than those of the other dogs. What’s more, microbes from the phylum Firmicutes were the predominant group in the lean dogs, whereas Gram-negative bacteria called Proteobacteria were prevalent in the obese group, the team reported online this month in the Journal of Veterinary Internal Medicine. The researchers speculate that an abundance of Proteobacteria may lead to an increase in lipopolysaccharide, a major component of the cell wall of Gram-negative bacteria, which has been linked to weight gain in mice. More research is needed to examine what role gut bacteria may play in the development of obesity, however, the authors say.

http://www.sciencemag.org/ Science Magazine

http://news.sciencemag.org health/2014/11/guts-obese-dogs-look-similar-those-obese-people?rss=1  Original web page at Science Magazine

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Vegetable oil ingredient key to destroying gastric disease bacteria

The bacterium Helicobacter pylori is strongly associated with gastric ulcers and cancer. To combat the infection, researchers at University of California, San Diego School of Medicine and Jacobs School of Engineering developed LipoLLA, a therapeutic nanoparticle that contains linolenic acid, a component in vegetable oils. In mice, LipoLLA was safe and more effective against H. pylori infection than standard antibiotic treatments. The results are published online Nov. 24 in the Proceedings of the National Academy of Sciences.

“Current H. pylori treatments are facing a major challenge — antibiotic resistance,” said Liangfang Zhang, PhD, professor in the UC San Diego Moores Cancer Center and Department of Nanoengineering. “Our goal was to develop a nanotherapeutic that can tolerate the harsh gastric environment, kill H. pylori and avoid resistance.” Zhang and Marygorret Obonyo, PhD, assistant professor in the Moores Cancer Center and Department of Medicine, are co-senior authors of the study. LipoLLA is a lipid (fat) particle that contains linolenic acid. When LipoLLA encounters H. pylori, it fuses with the bacterial membrane. Then the particle’s linolenic acid payload spills out, disrupting the membrane and killing the bacteria. Zhang, Obonyo and their team labeled LipoLLA particles with fluorescent markers, fed them to mice and watched as the particles distributed themselves in the stomach lining — and stayed there. After treatment, they measured bacterial load in the stomach and markers of inflammation. Compared to standard antibiotic therapies, LipoLLA was more effective at getting rid of H. pylori. What’s more, LipoLLA was not toxic to the mice and the bacteria did not develop resistance to the therapy. “This is the first step to verify that we can make this therapeutic nanoparticle and demonstrate that it works to reduce H. pylori colonization. We’re now working to further enhance the particle, making it more stable and more effective,” Zhang said.

http://www.sciencedaily.com/ Science Daily

http://www.sciencedaily.com/releases/2014/11/141125124802.htm Original web page at Science Daily

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* Vultures evolved an extreme gut to cope with disgusting dietary habits

How is it that vultures can live on a diet of carrion that would at least lead to severe food-poisoning, and more likely kill most other animals? This is the key question behind a recent collaboration between a team of international researchers from Denmark’s Centre for GeoGenetics and Biological Institute at the University of Copenhagen, Aarhus University, the Technical University of Denmark, Copenhagen Zoo and the Smithsonian Institution in the USA. An “acidic” answer to this question is now published in the scientific journal Nature Communications. When vultures eat lunch they happily strip the rotting carcasses they find back to the bone. And if, however, the animal’s hide is too tough to easily pierce with their beak, they don’t hesitate to enter it using other routes, among them the back entrance — so to speak: via the anus. Although their diet of meat that is both rotting and liberally contaminated with feces would likely kill most other animals, they are apparently immune to the cocktail of deadly microbes within their dinner such as Clostridia, Fuso- and Anthrax-bacteria. “To investigate vultures’ ability to survive eating this putrid cocktail, we generated DNA profiles from the community of bacteria living on the face and gut of 50 vultures from the USA. Our findings enable us to reconstruct both the similarities, and differences, between the bacteria found in turkey vultures and black vultures, distributed widely in the Western Hemisphere. Apparently something radical happens to the bacteria ingested during passage through their digestive system,” says Lars Hestbjerg Hansen, a professor at Aarhus University who together with PhD-student Michael Roggenbuck lead the study while he was at the University of Copenhagen. On average, the facial skin of vultures contained DNA from 528 different types of micro-organisms, whereas DNA from only 76 types of micro-organisms were found in the gut. Michael Roggenbuck explains: “Our results show there has been strong adaptation in vultures when it comes to dealing with the toxic bacteria they digest. On one hand vultures have developed an extremely tough digestive system, which simply acts to destroy the majority of the dangerous bacteria they ingest. On the other hand, vultures also appear to have developed a tolerance towards some of the deadly bacteria — species that would kill other animals actively seem to flourish in the vulture lower intestine.”

These observations raise the question as to whether the Clostridia and Fusobacteria in the gut simply out-compete the other bacteria but don’t confer any benefit to the vulture, or in contrast, if their presence actually confers dietary advantages for the vultures. The team’s results suggest that it’s probably a bit of both — while other microorganisms are likely out-competed by the surviving bacteria, the vultures also receive a steady stream of important nutrients when the bacteria break down the carrion. Of broader significance, Gary Graves of the Smithsonian Institution’s National Museum of Natural History observed: “The avian microbiome is terra incognita but it is not unreasonable to suppose that the relationship between birds and their microbes has been as important in avian evolution as the development of powered flight and song.”

http://www.sciencedaily.com/ Science Daily

http://www.sciencedaily.com/releases/2014/11/141125111814.htm Original web page at Science Daily

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Microbiome science threatened by contamination

DNA contamination is ubiquitous in laboratory equipment commonly used to analyse the microbes that inhabit the human body. This contamination could seriously undermine cutting-edge work to understand the ‘microbiome’. The body’s microorganisms have long been known to play crucial roles both in sickness and in health, and the increasing ease of genetic sequencing has revolutionized their study. But newcomers to the field may be mistaking experimental contamination for breakthroughs, warns Alan Walker, a microbiologist at the University of Aberdeen, UK. “If you look back in the literature, there’s been stuff about contamination in reagents going back decades.” But, he adds, “as microbiota research has boomed, there have been a lot of people drawn into the field who aren’t aware of this literature”. In one of the first systematic investigations of the problem, Walker and his colleagues have shown that two commonly used sequencing techniques (known as 16S rRNA and whole-genome shotgun metagenomics) can lead to genuine results being “effectively swamped” by contamination. The team used the two techniques — and off-the-shelf DNA-extraction kits — to sequence a pure culture of the bacterium Salmonella bongori as well as a series of diluted versions. To ensure that the results would not be affected by conditions at one particular lab, they conducted the experiments at three different institutions. In all cases, contamination increased with each dilution, and quickly drowned out the original Salmonella signal. The researchers published their results in BMC Biology on 12 November. The team traced at least part of the contamination to the DNA-extraction kits used in the experiments. The kits are not sold as sterile, Walker points out, and part of the problem is researchers assuming that they are. He told Nature that people working with samples that contain a large number of microbes — such as faecal samples — will probably not have problems, because the original signal is strong enough to overcome the contamination. But microbiome researchers are increasingly working with samples with low microbial biomass, including material from spinal fluid, blood and the lungs. Researchers in Walker’s lab routinely run controls alongside their samples, to detect contamination. Walker says that they have detected strains of microbes in their controls that other studies have reported as actual findings. “We haven’t challenged anyone directly,” he says. “We hope the message will stand for itself. We’re trying to nip it in the bud now before it becomes more of an issue.” The paper adds to concerns in the scientific community that sequencing technology has developed so fast that in some cases it has outpaced scientists’ ability to use it. In a paper published last month in PLOS ONE, biologist Richard Lusk of the University of Michigan in Ann Arbor analysed data from four independent sequencing experiments, looking for potential contamination. He found DNA from a wide variety of species, with dilute samples more likely to suffer problems. “Both my paper and this paper came to essentially the same conclusion,” says Lusk — namely, that it is necessary to run blank controls alongside a sample. “However, if that sample is really dilute, and the species you think might be a contaminant is infrequent, that’s always going to be really hard,” he says.

He adds that it is especially useful that Walker and his colleagues were able to trace so much variation to DNA-extraction kits, and that this should help researchers to design better experiments in future. Stratec Molecular, a biomedical company in Birkenfeld, Germany, that manufactures one of the kits in question, said in a statement that its product was designed for use with stool samples, not with diluted bacterial cultures as in Walker’s study. The company added, “The PSP Spin Stool DNA Plus Kit is neither marketed as sterile nor as DNA-free. Therefore, a certain degree of contaminating material cannot be excluded. Any contamination may indeed be detected through off-label-use application as in the present study.” Another manufacturer, Qiagen of Hilden, Germany, also stressed that its kit was “not designed to be DNA-free or to be used in low-biomass applications”. It added, “We welcome this research and believe that it will help to drive awareness of the importance of additional experimental controls in deep sequencing and low-biomass applications.” Stratec recommends the use of controls to deal with potential contamination. The company says that it has looked into producing DNA-free kits, and concluded that although it is technically feasible, they would probably be too expensive to produce. In the meantime, the warning from experts in the field is caveat experimenter. “This is a problem that has been known in the field for quite some time,” Peer Bork, head of bioinformatics at the European Molecular Biology Laboratory in Heidelberg, Germany, told Nature. “It’s only a part of a much bigger problem as it is not only the kits, but also sampling, DNA extraction in general, library preparation, sequencing, processing et cetera.”

Nature doi:10.1038/nature.2014.16327

http://www.nature.com/news/index.html  Nature

http://www.nature.com/news/microbiome-science-threatened-by-contamination-1.16327  Original web page at Nature

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Genomic definition of hypervirulent and multidrug-resistant Klebsiella pneumoniae clonal groups

Multidrug-resistant and highly virulent Klebsiella pneumoniae isolates are emerging, but the clonal groups (CGs) corresponding to these high-risk strains have remained imprecisely defined. We aimed to identify K. pneumoniae CGs on the basis of genome-wide sequence variation and to provide a simple bioinformatics tool to extract virulence and resistance gene data from genomic data. We sequenced 48 K. pneumoniae isolates, mostly of serotypes K1 and K2, and compared the genomes with 119 publicly available genomes. A total of 694 highly conserved genes were included in a core-genome multilocus sequence typing scheme, and cluster analysis of the data enabled precise definition of globally distributed hypervirulent and multidrug-resistant CGs. In addition, we created a freely accessible database, BIGSdb-Kp, to enable rapid extraction of medically and epidemiologically relevant information from genomic sequences of K. pneumoniae. Although drug-resistant and virulent K. pneumoniae populations were largely nonoverlapping, isolates with combined virulence and resistance features were detected.

Klebsiella pneumoniae is a frequent cause of nosocomial infections and has also emerged as an agent of severe community-acquired infections, including pyogenic liver abscess, pneumonia, and meningitis. The rise of antimicrobial drug resistance in K. pneumoniae, a member of the ESKAPE group (Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa, and Enterobacter species) of bacterial pathogens, raises serious therapeutic challenges. Most multidrug-resistant (MDR) K. pneumoniae isolates, which produce extended-spectrum β-lactamases (ESBLs) and/or carbapenemases in combination with quinolone and aminoglycoside resistance, belong to particular clones. Invasive community-acquired isolates are predominantly of capsular serotypes K1 and K2 and appear to differ in clonal background from MDR isolates (7–11). Controlling the emergence of these 2 types of high-risk clones and mitigating the alarming prospect of strains that would combine high virulence with multidrug resistance requires a precise definition of clonal groups (CGs) and rapid identification of their medically relevant features. K. pneumoniae clones have been recognized so far by using multilocus sequence typing (MLST) based on 7 housekeeping genes. However, MLST fails to draw clear discontinuities between CGs. Rapid, high-throughput sequencing promises to revolutionize medical microbiology and molecular epidemiology by improving discriminatory power and providing access to the resistome and virulome of clinical isolates. However, it remains challenging to extract medically relevant information from genome sequences in a timely manner. The objectives of this work were to delineate precisely, based on genome-wide genotyping, CGs corresponding to highly virulent and MDR K. pneumoniae isolates; extract the antimicrobial drug resistance and virulence-associated genomic features of those CGs by using a rapid and simple bioinformatics tool; and detect potential dual-risk isolates carrying virulence and resistance genes.

http://wwwnc.cdc.gov/eid/  Emerging Infectious Diseases

http://wwwnc.cdc.gov/eid/article/20/11/14-0206_article  Original web page at Emerging Infectious Diseases

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Fungus from Asia threatens European salamanders

North American salamanders and newts are safe for now, but epidemic could spread through pet trade. The North American eastern newt (Nothophthalmus viridescens) could be at risk from an imported fungus. In 2010, a fungus started killing massive numbers of fire salamanders in the Netherlands. Biologists have now discovered that the disease comes from Asia — and that for salamanders elsewhere, it is likely a death sentence. When the Dutch fire salamanders (Salamandra salamandra) started dying out, conservationists collected all the healthy-looking ones they could find in the wild. They gathered about 39 animals, and began keeping them in captivity — but those salamanders started dying, too. Tests for one suspected cause, ranavirus, came back negative. So did tests for a fungus called Batrachochytrium dendrobatidis (Bd), which has been devastating amphibian populations around the world, driving some to extinction. But when An Martel, a veterinary surgeon at Ghent University in Belgium, and her team examined the animals with a microscope, they saw telltale strands of fungus woven into the salamanders’ skin. It turned out to be a new killer fungus, a cousin of Bd that the team named Batrachochytrium salamandrivorans. Now, the researchers report in Science that salamander or newt species in Europe and North America are vulnerable to it. “First we were very happy because it is very exciting to detect a novel species of fungus,” says Martel. “But then it was scary.” By 2013, only 4% of the Dutch fire salamander population was still alive. And there are no natural barriers to prevent the Dutch outbreak and two new outbreaks Belgium from spreading to the rest of Europe. To predict the impact of the fungus, Martel’s team exposed 10 species of frog and toad, 24 species of salamander and newt, and 1 species of wormlike caecilian to spores of the fungus. The fungus attacked only salamanders and newts — and of 44 individual European salamanders infected, 41 died. Next, the researchers tested more than 5,000 individual amphibians from around the world for traces of the fungus. They found B. salamandrivorans in animals from Thailand, Vietnam and Japan — but these amphibians did not seem to be ill, suggesting that they have evolved some defences. It is likely that the outbreaks in Europe began with imported Asian salamanders. The team did not detect the fungus in any North American samples. But Jodi Rowley, an amphibian biologist at the Australian Museum Research Institute in Sydney, says that does not mean the fungus is not a threat to those species. “I would be very surprised if it wasn’t already in America, at least within the pet trade, given the volume of trade of pet salamanders,” she says. “There needs to be increased testing of amphibians as they come in through the borders.” Lobbying for this testing is a passion of Karen Lips, a conservation biologist at the University of Maryland in College   Park who has studied Bd since 1997, and is a co-author of the latest study. “Here in the US, we have no way to require any testing or surveillance of wildlife imports that may be bringing pathogens and parasites,” she says, adding that three bills currently in Congress would call for increased surveillance — but that they are “just sitting there” without any action to turn them into law. “We can take all the things we learned from Bd and do a much better job,” says Lips. But her hopes are tempered by experience. She has seen Bd drive dozens of frog species to extinction in the Americas.  “There is a voice in the back of my head that says don’t get your hopes up so high,” she says. “How good are we at keeping things out, even little microbes? We couldn’t even keep out Ebola.” Nature doi:10.1038/nature.2014.16249

http://www.nature.com/news/index.html  Nature

http://www.nature.com/news/fungus-from-asia-threatens-european-salamanders-1.16249  Original web page at Nature

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Scientific breakthrough will help design antibiotics of the future

Researchers at the University of Bristol focused on the role of enzymes in the bacteria, which split the structure of the antibiotic and stop it working, making the bacteria resistant. The new findings, published in Chemical Communications, show that it is possible to test how enzymes react to certain antibiotics. It is hoped this insight will help scientists to develop new antibiotics with a much lower risk of resistance, and to choose the best medicines for specific outbreaks.

Using a Nobel Prize-winning technique called QM/MM — quantum mechanics/molecular mechanics simulations – the Bristol research team was able to gain a molecular-level insight into how enzymes called ‘beta-lactamases’ react to antibiotics. Researchers specifically want to understand the growing resistance to carbapenems, which are known as the ‘last resort’ antibiotics for many bacterial infections. Resistance to carbapenems makes some bacterial infections untreatable, resulting in minor infections becoming very dangerous and potentially deadly. The QM/MM simulations revealed that the most important step in the whole process is when the enzyme ‘spits out’ the broken down antibiotic. If this happens quickly, then the enzyme is able to go on chewing up antibiotics and the bacterium is resistant. If it happens slowly, then the enzyme gets ‘clogged up’ and can’t break down any more antibiotics, so the bacterium is more likely to die. The rate of this ‘spitting out’ depends on the height of the energy barrier for the reaction — if the barrier is high, it happens slowly; if it’s low, it happens much more quickly.

Professor Adrian Mulholland, from Bristol University’s School of Chemistry, said: “We’ve shown that we can use computer simulations to identify which enzymes break down and spit out carbapenems quickly and those that do it only slowly. “This means that these simulations can be used in future to test enzymes and predict and understand resistance. We hope that this will identify how they act against different drugs – a useful tool in developing new antibiotics and helping to choose which drugs might be best for treating a particular outbreak.”

http://www.sciencedaily.com/  Science Daily

http://www.sciencedaily.com/releases/2014/10/141017101337.htm  Original web page at Science Daily

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Evolution of extreme parasites explained by scientists

Extreme adaptations of species often cause such significant changes that their evolutionary history is difficult to reconstruct. Zoologists at the University of Basel in Switzerland have now discovered a new parasite species that represents the missing link between fungi and an extreme group of parasites. Researchers are now able to understand for the first time the evolution of these parasites, causing disease in humans and animals. The study has been published in the latest issue of the scientific journal Proceedings of the National Academy of Sciences (PNAS).

Parasites use their hosts to simplify their own lives. In order to do so, they evolved features that are so extreme that it is often impossible to compare them to other species. The evolution of these extreme adaptations is often impossible to reconstruct. The research group lead by Prof. Dieter Ebert from the Department of Environmental Science at the University of Basel has now discovered the missing link that explains how this large group of extreme parasites, the microsporidia, has evolved. The team was supported in their efforts by scientists from Sweden and the U.S.

Microsporidia are a large group of extreme parasites that invade humans and animals and cause great damage for health care systems and in agriculture; over 1,200 species are known. They live inside their host’s cells and have highly specialized features: They are only able to reproduce inside the host’s cells, they have the smallest known genome of all organisms with a cell nucleus (eukaryotes) and they posses no mitochondria of their own (the cell’s power plant). In addition, they developed a specialized infection apparatus, the polar tube, which they use to insert themselves into the cells of their host. Due to their phenomenal high molecular evolution rate, genome analysis has so far been rather unsuccessful: their great genomic divergence from all other known organisms further complicates the study of their evolutionary lineage.

The team of zoologists lead by Prof. Dieter Ebert has been studying the evolution of microsporidia for years. When they discovered a new parasite in water fleas a couple of years ago, they classified this undescribed species as a microsporidium, mostly because it possessed the unique harpoon-like infection apparatus (the polar-tube), one of the hallmarks of microsporidia. The analysis of the entire genome had several surprises in store for them: it resembles more that of a fungus than of a microsporidium and also has a mitochondrial genome. The new species, now named Mitosporidium daphniae, thus represents the missing link between fungi and microsporidia.

With the help of scientists in Sweden and the U.S., the Basel researchers rewrote the evolutionary history of microsporidia. First, they showed that the new species derives from the ancestors of all known microsporidians and further, that the microsporidians derive from the most ancient fungi; thus its exact place in the tree of life has finally been found. Further research confirms that the new species does in fact have a microsporidic, intracellular and parasitic lifestyle, but that its genome is rather atypical for a microsporidium. It resembles much more the genome of their fungal ancestors. The scientists thus conclude that the microsporidia adopted intracellular parasitism first and only later changed their genome significantly. These genetic adaptations include the loss of mitochondria, as well as extreme metabolic and genomic simplification. “Our results are not only a milestone for the research on microsporidia, but they are also of great interest to the study of parasite-specific adaptations in evolution in general,” explains Ebert the findings.

http://www.sciencedaily.com/  Science Daily

http://www.sciencedaily.com/releases/2014/10/141013190427.htm  Original web page at Science Daily

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* Manure fertilizer increases antibiotic resistance

Pseudomonas bacteria in soil benefit from manure fertilizer treatments. Treating dairy cows and other farm animals with antibiotics and then laying their manure in soil can cause the bacteria in the dirt to grow resistant to the drugs. But a study now suggests that the manure itself could be contributing to resistance, even when it comes from cows that are free of antibiotics. The mechanism at work is not yet clear, but the finding — published on 6 October in Proceedings of the National Academy of Sciences — suggests a complex link between antibiotic use in agriculture and resistance in human pathogens. Many bacteria in the environment naturally carry antibiotic-resistance genes, probably as defence against the antibiotics produced by some soil fungi and bacteria. Laboratory-made versions of these antibiotics are used to treat infection in humans and animals, and to promote growth in livestock. Because manure itself is known to change the composition of bacterial communities in soil, a team led by microbiologist Jo Handelsman, then at Yale University in New Haven, Connecticut, decided to examine whether it also affects drug resistance. The team treated soil samples with either a nitrogen-based fertilizer or with manure from cows that had never been fed antibiotics. The researchers examined soil bacteria sampled before and after the treatment, searching for genes that encode enzymes called β-lactamases, which break down a class of antibiotic that includes penicillin. Two weeks after treatment, the soil spread with manure contained significantly higher numbers of bacteria producing β-lactamases than did soil treated with only the nitrogen-based fertilizer. By tracing genetic markers in the resistant bacteria, the researchers found that these bacteria came from the soil rather than from the manure, suggesting that the manure treatment had helped these natural bacteria to grow by feeding them or eliminating their competitors. The manure was particularly beneficial for Pseudomonas species, which are common in human infections. But it is unclear how manure creates a better environment for antibiotic-resistant bacteria. Handelsman — now associate director for science at the White House Office of Science and Technology Policy — and her colleagues suggest that certain nutrients or heavy metals in the manure could be responsible, because bacteria with β-lactamases are also more likely to be resistant to metals. The authors say that they plan to test this in the future.

http://www.nature.com/news/index.html  Nature

http://www.nature.com/news/manure-fertilizer-increases-antibiotic-resistance-1.16081  Original web page at Nature

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Pneumonia bacterium leaves tiny lesions in the heart

The long-observed association between pneumonia and heart failure now has more physical evidence, thanks to research in the School of Medicine at The University of Texas Health Science Center at San Antonio. The researchers found proof that Streptococcus pneumoniae, the leading cause of community-acquired pneumonia, actually physically damages the heart. The bacterium leaves tiny lesions that researchers detected in mouse, rhesus macaque and human autopsy tissue samples. “If you have had severe pneumonia, this finding suggests your heart might be permanently scarred,” said study senior author Carlos Orihuela, Ph.D., associate professor of microbiology and immunology at the UT Health Science Center San Antonio. It’s not yet known whether the small lesions contribute to increased risk of death in humans or if the scarring that occurs afterward is permanent, ultimately diminishing cardiac function in individuals who have recovered from a severe infectious disease episode. The team will study the long-term ramifications in non-human primates at the Texas Biomedical Research Institute’s Southwest National Primate Research Center. Streptococcus pneumoniae in the blood invaded the heart and formed lesions in the myocardium, the muscular middle layer of the heart wall, the researchers showed. The team identified mechanisms by which the bacterium is able to spread across endothelial cells in cardiac blood vessels to travel to and infect the heart. “Fortunately, we have a candidate vaccine that can protect against this,” Dr. Orihuela said. The Health Science Center, St. Jude’s Children’s Research Hospital in Memphis, Tenn., and the University of Oklahoma have claimed intellectual property protection on the vaccine project. The candidate vaccine acts to stop both the movement of the infection into the heart and the toxin that kills heart muscle cells called cardiomyocytes. The vaccine protected immunized animals against cardiac lesion formation, the study showed. Study limitations included the small sample size of human tissues analyzed, the researchers noted. The American Heart Association and the National Institutes of Health funded the project. The journal PLoS Pathogen published the study online Sept. 18.

http://www.sciencedaily.com/  Science Daily

http://www.sciencedaily.com/releases/2014/09/140925132557.htm  Original web page at Science Daily

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Targeting protein-making machinery to stop harmful bacteria

One challenge in killing off harmful bacteria is that many of them develop a resistance to antibiotics. Researchers at the University of Rochester are targeting the formation of the protein-making machinery in those cells as a possible alternate way to stop the bacteria. And Professor of Biology Gloria Culver has, for the first time, isolated the middle-steps in the process that creates that machinery — called the ribosomes. “No one had a clear understanding of what happened inside an intact bacterial cell,” said Culver, “And without that understanding, it would not be possible to block ribosome formation as a new means of stopping bacterial growth.” Since proteins are essential for life, organisms would die-off if not allowed to manufacture proteins. Culver’s work has been published in Nature Structural and Molecular Biology. Ribosomes are made of ribonucleic acid (RNA) and protein molecules that fit together like pieces of a puzzle. In order for the puzzle to work, the strands of RNA molecules need to be pared down to the right size. This multi-step process happens very quickly, making it difficult to capture a piece of ribosomal RNA in one of the intermediate states. Culver and graduate student Neha Gupta have managed to do just that by using genetic tags as markers inside E. coli cells. By attaching the tags to non-functional regions of the uncut RNA, the researchers were able to isolate the immature RNA strands during the various stages of processing. On analyzing the intermediate fragments, Culver and Gupta found that ribosomal RNA does not follow a single sequential series of steps. While there appears to be an early common step, some of the intermediate RNA strands had started losing fragments from one side, while other intermediate RNAs at a similar stage were being cleaved from the other side. The different pathways of processing the RNA take place simultaneously among the various molecules, resulting in RNA strands being able to fit together with protein molecules to form fully-developed ribosomes. Targeting ribosomes to kill drug-resistant bacteria is nothing new, except, in the past, scientists focused on mature ribosomes. While a range of antibiotics were developed to attack the ribosomes, the microbes eventually became resistant to those drugs. While Culver’s work creates new possibilities for stopping super-bugs, a great deal of work remains to be done. “If bacterial cells have more than one way to make ribosomes, blocking just one pathway may not be enough to kill them.” said Culver. “But our discoveries suggest that there is at least one common step that could be exploited to one day help scientists prevent the ribosomes from developing, which would kill off the bacteria.”

http://www.sciencedaily.com/  Science Daily

http://www.sciencedaily.com/releases/2014/09/140907181202.htm  Original web page at Science Daily

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Bacteria harbor secret weapons against antibiotics

The ability of pathogenic bacteria to evolve resistance to antibiotic drugs poses a growing threat to human health worldwide. And scientists have now discovered that some of our microscopic enemies may be even craftier than we suspected, using hidden genetic changes to promote rapid evolution under stress and developing antibiotic resistance in more ways than previously thought. The results appear in a new paper in the journal Biomicrofluidics, from AIP Publishing. In the paper, researchers from Princeton University in New Jersey describe how they observed two similar strains of E.coli bacteria quickly developing similar levels of antibiotic resistance using surprisingly different genetic mutations. Developing different solutions to the same problem shows the bacteria have a diverse arsenal of genetic “weapons” they can develop to fight antibiotics, potentially making them more versatile and difficult to defeat. “Bacteria are clever — they have hidden ways to respond to stress that involve re-sculpting their genomes,” said Robert Austin, a biophysicist at Princeton who led the research team. Realizing how effectively bacteria can survive drugs is a sobering thought, Austin said. “It teaches us that antibiotics have to be used much more carefully than they have been up to this point,” he said. Austin and his colleagues specialize in developing unique, fluid-filled microstructures to test theories of bacterial evolution. Instead of using test tubes or Petri dishes — uniform environments that, Austin notes, exist only in the “ivied halls of academia” — the researchers build devices that they believe better mimic natural ecological niches. The team uses a custom-made microfluidic device that contains approximately 1,000 connected microhabitats in which populations of bacteria grow. The device generates complex gradients of food and antibiotic drugs similar to what might be found in natural bacterial habitats like the gut or other compartments inside a human body. “In complex environments the emergence of resistance can be far more rapid and profound than would be expected from test tube experiments,” Austin said.

From previous experiments with the complex microfabricated devices, the researchers knew that some ordinary, “wild-type” strains of E.coli bacteria quickly evolved antibiotic resistance. They wondered if a mutant strain called GASP, which reproduces more quickly with limited nutrients than the wild type, would develop the same type of antibiotic resistance when exposed to the same drug. By sequencing the genomes of wild type and GASP bacterial colonies that has been exposed to the antibiotic ciprofloxacin (Cipro), the researchers found different genetic mutations could lead to similar levels of antibiotic resistance. For example, two different mutant strains emerged: one of the antibiotic-resistant GASP strains evolved in such a way that it no longer needed to make biofilms in order to survive stress. It did so by “borrowing” a piece of leftover DNA from a virus that infects bacteria. The other strain did not do this excision, indicating that in evolution the strains can hedge their bets. Viruses routinely inject their own DNA into bacteria and sometimes DNA sequences remain that no longer seem to have any function in terms of viral replication. Under normal circumstances the leftover DNA may neither help nor hinder the bacteria, but in times of stress the bacteria can use the new DNA to rapidly evolve antibiotic resistant mutations. The results demonstrate the subtlety and diversity of the tools that bacteria have to fight stress, said Austin. He wonders whether our remaining effective methods for killing bacteria, such as using ethanol to disinfect surfaces, are also vulnerable, and his team plans to test whether bacteria in their devices can evolve ethanol resistance.

http://www.sciencedaily.com/ Science Daily

http://www.sciencedaily.com/releases/2014/09/140909113225.htm  Original web page at Science Daily

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A gut microbe that stops food allergies

A class of bacteria commonly found in the guts of people—and rodents—appears to keep mice safe from food allergies, a study suggests. The same bacteria are among those reduced by antibiotic use in early childhood. The research fits neatly into an emerging paradigm that helps explain a recent alarming increase in food allergies and other conditions, such as obesity and autoimmune disease, and hints at strategies to reverse the trend. Food allergies have increased about 50% in children since 1997. There are various theories explaining why. One is that the 21st century lifestyle, which includes a diet very different from our ancestors’, lots of antibiotic use, and even a rise in cesarean section deliveries, has profoundly changed the makeup of microbes in the gut of many people in developed countries. For example, the average child in the United States has taken three courses of antibiotics by the time he or she is 2 years old, says Martin Blaser, an infectious disease specialist and microbiologist at New York University in New York City. Cathryn Nagler, an immunologist at the University of Chicago in Illinois, has spent years probing links between the immune system, intestinal bacteria, and the onset of allergies. Back in 2004, she and her colleagues reported that wiping out gut bacteria in mice led to food allergies. Since then, Nagler has continued trying to understand which bacteria offer allergy protection and how they accomplish that. In one of the latest efforts, Nagler’s team first confirmed that mice given antibiotics early in life were far more susceptible to peanut sensitization, a model of human peanut allergy. Then, they introduced a solution containing Clostridia, a common class of bacteria that’s naturally found in the mammalian gut, into the rodents’ mouths and stomachs. The animals’ food allergen sensitization disappeared, the team reports online today in the Proceedings of the National Academy of Sciences. When the scientists instead introduced another common kind of healthy bacteria, called Bacteroides, into similarly allergy-prone mice, they didn’t see the same effect. Studying the rodents more carefully, the researchers determined that Clostridia were having a surprising effect on the mouse gut: Acting through certain immune cells, the bacteria helped keep peanut proteins that can cause allergic reactions out of the bloodstream. “The bacteria are maintaining the integrity of the intestinal barrier,” Nagler says.

The research “opens up new territory,” Blaser says. It “extends the frontier of how the microbiome is involved” in immune responses and the roles played by specific bacteria. (Blaser’s group reported earlier this month in Cell that giving mice penicillin soon after birth changed their gut microbiome and made them much more likely to be obese as adults.) Nagler and her university have filed for a patent application on the new findings. The ultimate goal is to “interrupt [the allergy] process by manipulating the microbiota,” she says—a probiotic consisting of Clostridia could be a new allergy therapy, for example. Nagler knows of none on the market yet, and they would need testing in people before becoming a treatment of choice.

http://www.sciencemag.org/  Science Magazine

http://news.sciencemag.org/biology/2014/08/gut-microbe-stops-food-allergies?rss=1  Original web page at Science Magazine