Lightning may become one of weather's predictors

Kate Murphy, 17 January 2017, The New York Times

Lightning’s intricate, darting dance across the sky can be mesmerising or terrifying, elegant or explosive, divine or destructive, depending on how close it is. But meteorologists have historically viewed lightning as little more than a weather byproduct. Like a rainbow, only with teeth. That view may be changing as technology has evolved to study lightning and its potential to help predict, if not drive, atmospheric events.

In 2017, two new space-based lightning sensors are set to go live, joining a growing global architecture of ground-based detection networks. “We are now in the golden age of lightning measurement and research,” said Christopher Schultz, a
meteorologist and lightning specialist at the Marshall Space Flight Centre in Huntsville, Alabama, USA.

Worldwide, thunderstorms hurl about four million lightning bolts to the ground each day. So it is not surprising that researchers have spent decades figuring out how to track and measure the phenomena, and trying to persuade funding sources that collecting data was worthwhile. “When I got started back in the 1980s, nobody cared,” said Hugh Christian, a research professor at the University of Alabama at Huntsville, USA and director of the team that developed a lightning sensor that will be attached to a truss of the International Space Station in 2017.

Locating lightning strikes
It will augment coverage provided by a geostationary satellite, known as GOES-16, that was successfully launched in November 2016. “It’s been a long road,” Christian said. “But now it’s universally accepted that lightning flash rates are correlated with storm intensification and severity.” This means the more that is known about lightning activity, it is possible to give people about the possibility of associated severe weather events like tornadoes and hail.

Experts hope to locate about 90% of lightning strikes in the Western Hemisphere, within clouds and on the ground, using detection instruments in space that work by measuring photons blinking in the clouds below and, terrestrially, by sensing radio wave disturbances.

Researchers have also discovered different and strange iterations of lightning. For example, so-called dark lightning, powerful bursts of gamma rays, can smash through the upper regions of Earth’s atmosphere and into outer space. This has implications for the functioning and longevity of satellites used for communication, military reconnaissance and GPS.

Biggest riddle
Other surprising and mysterious sorts of lightning are elves and sprites — colourful ultrafast bursts of electricity that dance above clouds into the upper atmosphere. “We’re getting pretty good at saying what lightning does, but we’re still pretty bad at saying how it does it,” Joseph Dwyer, a professor of gamma ray astronomy at the University of New Hampshire, said.

The current thinking is that ice particles in different forms within thunderstorms bump up against one another during updraughts and transfer charges. The lighter particles get positively charged and migrate to the top of the cloud, while the negatively charged, heavier particles drop to the bottom. The negative buildup at the bottom of the cloud discharges to the positively charged ground below, or upward or sideways, depending on the easiest path for release.

The same thing can happen with the accumulated positive charges if a certain threshold is met for discharge. “The problem is people have been sending up balloons and airplanes into thunderstorms for decades, and the measured electric fields are nowhere big enough to create a spark,” Joseph said. “So how does lightning get started inside thunderstorms? It’s one of the biggest mysteries in the atmospheric sciences.”

The manipulation of macrophages

Manohar G M, 17 January 2017, DHNS

In the movie Terminator 3: The Rise of Machines, the character Terminatrix (a humanoid robot) is able to manipulate cyborgs to work against humans for her own advantage. Now, scientists have discovered that some strains of bacteria could do the same to some of our cells.

Mycobacterium tuberculosis, the bacterium that causes tuberculosis, is one such. It manipulates the macrophages, a type of white blood cell that hunts and engulfs invading pathogens, to act as bacterial reservoirs and provide a survival niche. This niche not only provides the bacteria with nutrients, but also helps evade the normal immune response. In a recent study, a team of scientists from the Indian Institute of Science (IISc), Bengaluru, has explored the mechanism behind the manipulation of macrophages by this bacteria.

Macrophages scout for foreign pathogens, engulf them and provide us with innate immunity. However, when specific strains of mycobacterium infect these macrophages, they reprogramme these cells to act as safe havens and to obtain nourishment from them. These modified macrophages are called foamy macrophages and are found in the granulomas of the lungs of infected individuals. “Unlike other bacteria, Mycobacterium tuberculosis is not explicitly pathogenic, but it can lie dormant. Even today, it is one of the most dreaded pathogens with 6.1 million individuals newly infected with TB and 1.4 million dead due to the disease in 2015 alone,” explains Kasturi Mahadik, a research scholar at the Department of Microbiology and Cell Biology, IISc.

Molecular mechanism
The researchers have worked out the molecular mechanism involved in the generation of foamy macrophages. The elucidation of this pathway could generate new and effective targets for drug development to cure tuberculosis. The study found that the bacterium interacts with a receptor found on the membrane of macrophages called TLR2 (Toll-like receptor).

These receptors recognise foreign substances and pass on appropriate signals to the cells of the immune system through one of the signalling pathways called NOTCH1 signalling pathway. “While viruses are legendary host modifiers, bacteria have been known to manipulate the host epigenetic machinery. Host genes involved in cell cycle progression, cell ageing, survival, inflammation and immunity are important targets for such epigenetic control,” remarks Kasturi.

Signalling pathways govern basic activities of cells and coordinate cell actions by allowing them to sense or perceive changes in their microenvironment and bring about necessary changes in activities like gene expression. The signal from
outside the cells is transmitted via a chain of mediators, the end point of which may culminate in the expression of certain genes, whose products are required to
respond to the changes in the microenvironment.

Foamy macrophages contain lipid bodies that provide nutrients and anti-inflammatory mediators to help the bacteria evade our normal immune response. Genes involved in lipid biosynthesis and lipid droplet synthesis are “regulated” or “turned on” for the purpose. Conventionally, gene regulation is brought about by a protein acting as an activator or a repressor of gene function.

Condensing or relaxing
The study found that either condensing or relaxing a chromosome regulates the genes required for the generation of foamy macrophages. Genes reside on chromosomes, and when chromosomes tightly coil up, they are not free to be transcribed and are therefore switched off. On the other hand, a relaxed and free chromosome can be bound by positive activators, which assist in gene expression and can be switched on.

The DNA in the chromosome is wound around proteins called histones. Action of methylase enzyme at certain places on histones leads to tightening of chromosomes and silencing of the genes, while actions of a demethylase enzyme can remove the methyl groups on the histones and relax the chromosome for gene expression.

Another important aspect that the study found is the role of a demethylase enzyme, namely JMJD3 (Jumonji Domain containing protein), that is responsible for demethylating histones that results in the expression of the above mentioned genes.

JMJD3 is repressed by a complex of proteins and one of them, called MINT/spen, was not found to be produced in foamy macrophages. Thus, this allows the JMJD3 to express the genes involved in foamy macrophage development.

This research is a key insight that could drive the direction for drug development against TB. “Study of factors leading to reactivation from latent TB into active TB could be vital to completely eradicate the disease. Knowledge of mycobacteria governed epigenomics would also aid the understanding of pathologies associated with the disease progression. Further, mycobacterial infection results in a predisposition to several other infections and it would be fascinating to note the impact of epigenetic factors during co-infections,” signs off Kasturi.

(The author is with Gubbi Labs, a Bengaluru-based research collective)

Radio bursts traced to faraway galaxy

Dennis Overbye, 17 January 2017, The New York Times

Astronomers have traced a series of brief, enigmatic bursts of radio waves to a galaxy far, far away and indeed a long time ago — some three billion years or so. But as much as you might be hoping or dreading it to be true, this is probably not E.T.

“We’ve joked about spaceship battles and death stars blowing up, but we think we can explain it with ordinary physics,” said Shami Chatterjee, a Cornell University astronomer. Shami is the lead author of a paper published in Nature this month that details the search for the source of the radio waves known as “fast radio bursts,” — intense pulses of radiation from the sky lasting only a few milliseconds.

These have been disappointing times for those yearning for some alien direction from Out There. Last summer, Russian astronomers reported that they had recorded a promising-sounding signal from a star in the Hercules constellation, but they dismissed it when it became public as a freak bit of random radio noise, the astrophysical equivalent of a cosmic butt dial. More recently, searches for radio signals from a set of stars with anomalous spectral features and another star known as Tabby’s Star that has shown suspicious variations in its light seem to have come up empty.

Unexpected discovery?
So at least for now, the skies appear to be bereft of intelligence. But the new results from the fast radio burster, known as 121102 — after November 2, 2012, the date it was first observed — need not discourage any aficionados of cosmic mystery. Most likely, Shami said in a telephone interview, the bursts could be caused by weird reactions between a neutron star — the dense spinning magnet left behind by a supernova explosion — and the debris from that explosion.

Or perhaps from some unexpected quirk of a supermassive black hole in the centre of the galaxy, a dwarf assemblage of stars some three billion light-years away in the constellation Auriga. There are problems with both explanations, however, he added.
Fast radio bursts have led astronomers on a merry chase ever since they were
discovered in 2007 in data recorded earlier by the Parkes radio telescope in Australia. Because they are so short and until recently have never been seen to repeat, these phantoms have been hard for astronomers to study. Usually, astronomers notice them after the fact. Moreover, radio telescopes have poor angular resolution, making it impossible to determine exactly what star or distant galaxy they came from.

The radio emissions themselves, Shami said, resemble the blasts from pulsars — the spinning neutron stars that emit clocklike pulses of radiation and whose discovery in 1968 did indeed elicit speculation about little green men. But the radio waves arrive on Earth dispersed or spread out in time by wavelength, which implies that they have travelled from far outside our galaxy.

That great distance also implies that they are enormously more powerful than pulsars in our galaxy, adding to the mystery of what they are and raising the question of why they are not seen within our own galaxy, the Milky Way. In all, 18 of the fast bursters have been spotted since they were first recognised in 2007 — a small number. If extrapolated to the whole sky, that means 5,000 to 10,000 of these flashes should happen every day.

Where are they? Lacking much evidence to the contrary, astronomers theorised that the bursts resulted from apocalyptic events like collisions of neutron stars. At one point, Shami said, there were more theoretical models of the bursts than observed bursts. “Many things go bang,” he explained.

The big break came in 2012 when the burst known as 121102 repeated itself. Subsequent observing campaigns with the Very Large Array of telescopes in New Mexico and the Arecibo radio telescope in Puerto Rico, USA recorded a total of nine bursts over 83 hours of observing time and a terabyte of data during a six-month period in 2016. That meant that whatever was causing 121102, at least, was not destroying it. “We definitely know, for this one case anyway, the radio burst is not cataclysmic,” Shami said.

In addition, papers also have been submitted to the Astrophysical Journal Letters by two other groups led by Shriharsh Tendulkar of McGill University, Canada and by Benito Marcote of the Joint Institute for VLBI in Europe, in Dwingeloo, the Netherlands.

Massive stars
Following up on the Very Large Array observations, Benito’s team on the European VLBI network was able to pinpoint the location of the burst to a faint dwarf galaxy in the Auriga constellation. Shriharsh and his colleagues then used the eight-metre Gemini North telescope on Mauna Kea in Hawaii to observe the galaxy and measure its distance. That distance, three billion light-years, confirmed the original supposition that the fast bursts come from far, far away. “The host galaxy is puny,” Shriharsh said during the news conference in Grapevine. That dwarf galaxy is only a hundredth of the mass of the Milky Way.

If this burster, 121102, is indeed typical of the bunch, the astronomers said, this might be a clue. Such galaxies are typically home to some of the most violent events in the universe, Shami said, things that go seriously boom in the night like certain kinds of gamma-ray bursts and superluminous supernova explosions that result in extremely magnetic pulsars known as magnetars.

These are the signatures of massive stars, of the deaths of massive stars, he said. But this only raises more questions. “The only one that repeats is from three billion light-years,” Shami mused. “Where are all the nearby ones?” he asked, noting that they should be even brighter, saturating our radio receivers. “It’s very curious,” he said.

Nicholas Bakalar and Kenneth Chang Jan 24 , 2017, The New York Times

Absolutely every bit of our galaxy

Absolutely every bit of our galaxy

Astronomers have arrived at what they believe to be the most accurate measure yet of the mass of the Milky Way: about 4.8 x 10(11) times the mass of the sun, or ‘solar masses’, to use a standard unit of mass in astronomy. This comes to about 9.5 x 10(41) kg — that is, 95 followed by 40 zeros. The number, of course, is inexact, as obviously no direct measure of all the billions of stars and other objects in the Milky Way could be taken.

But in a paper to be published in The Astrophysical Journal, scientists used methods of measurement that involve complex mathematical and statistical techniques called hierarchical Bayesian analysis, as well as direct measurements of the velocity of globular clusters, the tightly packed spherical groups of 10,000 to 1,00,000 old stars that move through the galaxy. Just as the mass of the sun can be calculated by measuring its gravitational pull on Earth, the mass of the Milky Way can be calculated by measuring its gravitational pull on the globular clusters.

The estimate includes everything within 125 kiloparsecs of the centre of the galaxy — that is, within 3.9 x 10(18) km. And ‘everything’ is not just stars: There are planets, moons, gases, dust and other objects, not to mention the immense amount of dark matter. It cannot be detected directly, but its mass can be inferred from its gravitational effect on other objects.

“The biggest thing is that we’re including measurement uncertainties that are carried through the analysis,” said the lead author, Gwendolyn M Eadie, a doctoral candidate at McMaster University in Hamilton, Ontario, Canada. “So we have a good handle on the uncertainty in our mass estimate. The low end is 4.0 x 10(11) solar masses, and the high end is 5.8 x 10(11).”

Gwendolyn said that the findings were important from an astronomer’s perspective. “The methods we’ve developed could be important in other studies that do other kinds of research,” she said. “These methods have been used in other fields, but they’re starting to become more useful in astronomy now that we have computers that can do these complex calculations.” What does it mean for the rest of us? “It just satisfies curiosity about the world we live in,” she said.

When Venus smiled for a few days

For a few days, Venus smiled — sideways. When Japan’s Akatsuki spacecraft pulled into orbit around Venus in December 2015 and turned on its instruments, it almost immediately discovered a bow-shape feature in the atmosphere stretching 6,000 miles, almost pole to pole — a sideways smile.

More remarkably, while Venus’ winds blow at speeds up to 250 mph and clouds whip around the planet every four days, this gargantuan sideways smile did not move, but remained fixed above the ground for four days. Because of Akatsuki’s large looping orbit, the spacecraft could not make more observations for a month.

When the spacecraft looked at the same region again, the smile had disappeared. Except for a few brief glimmers in April and May last year, the smile has not returned. In a recent paper published in the journal Nature Geoscience, scientists working on the mission describe their observations in detail and suggest it was a “gravity wave” — a disturbance in the winds caused by the underlying topography that propagated upward. The bow-shape arc appeared above Aphrodite Terra, a highland region about the size of Africa that rises up to three miles from the surface.

Scientists working on data from the European Space Agency’s Venus Express reported finding a similar disturbance in the atmosphere. The authors of the new paper said that numerical simulations provided preliminary support for the idea, but that they still could not explain how the gravity wave forms and propagates in the lower atmosphere. Or why the prominent smile was seen in December 2015 and not since. Scientists also cannot yet answer the big question Akatsuki was sent to investigate: Why do the winds blow so fast on Venus to begin with?

A cure for neglected tropical diseases

Siddharth Kankaria Jan 24 , 2017

How many tropical diseases do you know of? Malaria, dengue and sleeping sickness immediately come to mind. Maybe leprosy, if you think hard enough. But, many of us may not have heard of Cutaneous Leishmaniasis, a less dangerous but a much more prevalent cousin of kala azar (black fever). Cutaneous Leishmaniasis (CL) is caused by the protozoan Leishmania, which are transmitted by the bite of infected female sandflies. 

Dr Shailza Singh and her team from the National Centre for Cell Science (NCCS), Pune, have been studying this disease extensively for years. In a recent collaborative study with Dr Sudipta Basu and his team from the Indian Institute of Science Education and Research (IISER), Pune, the researchers have discovered a new lead compound to help combat this neglected tropical disease. Often called white leprosy, CL is known to cause skin lesions and ulcers on exposed parts of the body, while often leaving behind life-long scars and severe disabilities. According to statistics released by the World Health Organisation, around 0.9 to 1.3 million new cases of Leishmaniasis surface every year, leading to up to 20,000 to 30,000 deaths annually. Conventional methods of treating CL include administration of antimony-based compounds or oral, topical or liposomal preparations of anti-fungal compounds. However, these approaches have increasingly been proven ineffective, insufficient or too expensive to use.

The problem of causative protozoans becoming resistant to most anti-leishmanial drugs further exacerbates the situation. Thus, it has become paramount to identify new compounds that could be used to treat leishmaniasis. Several natural compounds such as alkaloids, phenolic compounds, terpenes and saponins are known to have anti-leishmanial properties. Recent studies have found a class of anti-fungal compounds called ‘coumarins’ that possess anti-protozoal properties.

Testing therapeutic efficacy
In order to take this lead forward, researchers from NCCS, comprehensively surveyed several coumarin derivatives for their therapeutic efficacy against leishmaniasis, and in this pursuit, also collaborated with the team at IISER Pune. “Our goal was to explore the possibility of using coumarin derivatives as anti-leishmanial agents. Towards this, we have designed a set of coumarin derivatives using computer aided drug designing, which could serve as probable drug candidates for the treatment of leishmaniasis,” explains Dr Shailza.

The research team’s initial screening of coumarin derivatives led to the identification of some 1000-odd compounds, which were ultimately narrowed down to five promising drug candidates, based on various judging criteria like their three-dimensional shape, size, and chemical properties. After this, the scientists wanted to test these five drug candidates for their biological activity and compatibility. They performed various microbiological experiments in this regard, and arrived at one of the compounds which showed the best anti-leishmanial properties, nicknamed ‘C2’ (compound 2). C2 was shown to cause a reduction in size and mobility of the parasitic protozoan cells, which are known to cause leishmaniasis. In addition, C2 was also shown to attenuate these protozoal cells’ ability to infect macrophages, a specialised infection-fighting cell found in the immune system of higher animals.

Further, in order to check the effect of C2 on lesions manifested during Leishmaniasis, the scientists took experimental mice infected with cutaneous leishmaniasis lesions, and then treated them with oral doses of C2. To their surprise, the leishmanial lesions in mice reduced in size by almost 50%. It was thus evident that C2 exhibited the highest anti-leishmanial properties amongst the shortlisted drug candidates both in vitro and in vivo. In order to further enhance the solubility of C2 inside the body, the scientists designed a tiny nanometre scale drug carrier made up of lipids. This lipid-based drug carrier ensures that the drug is released in a much more sustained and prolonged fashion inside the body.

Effective strategy
In further experiments with protozoan cell cultures of Leishmania, the scientists used these lipid-based drug carriers to deliver C2 inside the Leishmania cells. Their results successfully demonstrated that a sustained release of C2 within these Leishmania cells triggered them to commit cellular suicide. Such instances of cellular suicide are generally characterised by an observable decrease in the integrity of mitochondrial membranes and can be quantified using mitochondrial dyes.

This cellular suicide in Leishmania cells can be viewed as an instance of programmed cell death triggered by toxic external factors — the compound C2 in this case. Such a targeted killing of protozoal cells could be a very effective strategy of combating the spread of leishmaniasis infections within the host. Backed by these conclusive results, the researchers now feel that C2 could serve as a promising drug candidate, which, with further modification and development, can be converted into a potent anti-leishmanial compound.

(The author is with Gubbi Labs, a Bengaluru-based research collective)

Shedding light on the human genome

Natalie Angier Jan 24 , 2017 The New York Times

They said it was their family curse: a rare congenital deformity called syndactyly, in which the thumb and index finger are fused together on one or both hands. Ten members of the extended clan were affected, and with each new birth, they told Dr Stefan Mundlos of the Max Planck Institute for Molecular Genetics, Germany the first question was always: “How are the baby’s hands? Are they normal?” The family, under promise of anonymity, is taking part in a study by Stefan and his colleagues of the origin and development of limb malformations. And while the researchers cannot yet offer a way to prevent syndactyly, or to entirely correct it through surgery, Stefan has sought to replace the notion of a family curse with “a rational answer for their condition,” he said.

The scientists have traced the family’s limb anomaly to a novel class of genetic defects unlike any seen before, a finding with profound implications for understanding a raft of heretofore mysterious diseases. The mutations affect a newly discovered design feature of the DNA molecule called topologically associating domains, or TADs. It turns out that the vast informational expanse of the genome is divvied up into a series of manageable, parochial and law-abiding neighbourhoods with strict nucleic partitions between them — each one a TAD.

Folding protocol
By studying TADs, researchers hope to better fathom the deep structure of the human genome, in real time and three dimensions, and to determine how a quivering, mucilaginous string of some three billion chemical subunits that would measure more than six-feet long if stretched out nonetheless can be coiled and compressed down to four-10,000ths of an inch, the width of a cell nucleus.

“DNA is a superlong molecule packed into a very small space, and it’s clear that it’s not packed randomly,” Stefan said. “It follows a very intricate and controlled packing mechanism, and TADs are a major part of the folding protocol.” For much of the past 50 years, genetic research has focused on DNA as a kind of computer code, a sequence of genetic “letters” that inscribe instructions for piecing together amino acids into proteins, which in turn do the work of keeping us alive.

Most of the genetic diseases deciphered to date have been linked to mishaps in one or another protein recipe. Scanning the DNA of patients with Duchenne muscular dystrophy, for example, scientists have identified telltale glitches in the gene that encodes dystrophin, a protein critical to muscle stability. The mutant product that results soon shatters into neurotoxic shards.

Yet, researchers soon realised there was much more to the genome than the protein codes it enfolded. “We were caught up in the idea of genetic information being linear and one-dimensional,” said Job Dekker, a biologist at the University of Massachusetts Medical School, USA. For one thing, as the sequencing of the complete human genome revealed, the portions devoted to specifying the components of hemoglobin, collagen, pepsin and other proteins account for just a tiny fraction of the whole, maybe three per cent of human DNA’s three billion chemical bases. And there was the restless physicality of the genome, the way it arranged itself during cell division into 23 spindly pairs of chromosomes that could be stained and studied under a microscope, and then somehow, when cell replication was through, merged back together into a baffling, ever-wriggling ball of chromatin — DNA wrapped in a protective packaging of histone proteins.

Through chromosome conformation studies and related research, scientists have discovered the genome is organised into about 2,000 jurisdictions. As with city neighbourhoods, TADs come in a range of sizes, from tiny walkable zones a few dozen DNA subunits long to TADs that sprawl over tens of thousands of bases and you’re better off taking the subway. TAD borders serve as folding instructions for DNA.

Different domains
TAD boundaries also dictate the rules of genetic engagement. Scientists have long known that protein codes are controlled by an assortment of genetic switches and enhancers — noncoding sequences designed to flick protein production on, pump it into high gear and muzzle it back down again. The new research indicates that switches and enhancers act only on those genes, those protein codes, stationed within their own precincts. “Genes and regulatory elements are like people,” Job said. “They care about and communicate with those in their own domain, and they ignore everything else.”

What exactly do these boundaries consist of? Scientists are not entirely sure, but preliminary results indicate that the boundaries are DNA sequences that attract the attention of sticky, roughly circular proteins called cohesin and CTCF, which adhere thickly to the boundary sequences like insulating tape. Between those boundary points, those clusters of insulating proteins, the chromatin strand can loop up and over like the ribbon in a birthday bow, allowing genetic elements distributed along the ribbon to touch and interact with one another. But the insulating proteins constrain the movement of each chromatin ribbon, said Richard A Young of the Whitehead Institute for Biomedical Research, USA, and keep it from getting entangled with neighbouring loops — and the genes and regulatory elements located thereon.

The best evidence for the importance of TADs is to see what happens when they break down. Researchers have lately linked a number of disorders to a loss of boundaries between genomic domains, including cancers of the colon, esophagus, brain and blood. In such cases, scientists have failed to find mutations in any of the protein-coding sequences commonly associated with the malignancies, but instead identified DNA damage that appeared to shuffle around or eliminate TAD boundaries. As a result, enhancers from neighbouring estates suddenly had access to genes they were not meant to activate.

Reporting in the journal Science, Richard and his colleagues described a case of leukemia in which a binding site for insulator proteins had been altered not far from a gene called TAL1, which if improperly activated is known to cause leukemia. Now that researchers know what to look for, he said, TAD disruptions may prove to be a common cause of cancer. The same may be true of developmental disorders — like syndactyly.

The spectre of superbugs

Sabrina Tavernise & Denise Grady June 07, 2016, The New York Times

Military researchers in the US have identified the first patient in the United States to be infected with bacteria that are resistant to an antibiotic that was the last resort against drug-resistant germs. The patient is well now, but the case raises the spectre of superbugs that could cause untreatable infections, because the bacteria can easily transmit their resistance to other germs that are already resistant to additional antibiotics. The resistance can spread because it arises from loose genetic material that bacteria typically share with one another.

“Think of a puzzle,” said Dr Beth Bell, of the Centers for Disease Control and Prevention, USA. “You need lots of different pieces to get a result that is resistant to everything. This is the last piece of that puzzle, unfortunately, in the United States. We have that genetic element that would allow for bacteria that are resistant to every antibiotic.”

The bacteria are resistant to a drug called colistin, an old antibiotic that in the United States is held in reserve to treat especially dangerous infections that are resistant to a class of drugs called carbapenems. If carbapenem-resistant bacteria, called CRE, also pick up resistance to colistin, they will be unstoppable. “This is huge,” said Dr Lance Price, a researcher at George Washington University. “We are one step away from CRE strains that cannot be treated with antibiotics. We now have all the pieces in place for it to be untreatable.”

The gene for resistance to colistin was first found in China, where the drug is used in pig and poultry farming. Researchers reported its discovery there in November. It has also been found in the intestine of one pig in the United States. CRE is still relatively rare, causing just 600 deaths a year, but by 2013, researchers had identified it in healthcare facilities in 44 states. Dr Thomas R Frieden, director of the Centers for Disease Control and Prevention. often calls it the “nightmare superbug,” because it is resistant to all but one antibiotic — colistin.

“We risk being in a post-antiobiotic world,” Dr Thomas said. “That wouldn’t just be urinary tract infections or pneumonia — that could be for the 6,00,000 patients a year who need cancer treatment.” He added, “The medicine cabinet is empty for some patients.”

The colistin resistance in the United States came to light when a 49-year-old woman, who Dr Beth said was “connected ...to the military,” was treated for a urinary infection at a military clinic in Pennsylvania. Because her urine culture had unusual results, the sample was sent to the Walter Reed National Military Medical Center, which identified the drug resistance. The bacteria, though resistant to colistin and some other antibiotics, were not resistant to carbapenems. Doctors there published a report on the case in a medical journal.

Sample analysis
Patrick McGann, a scientist at the Walter Reed Army Institute of Research and lead author of the paper, said researchers had only started analysing samples a few weeks ago. They tested samples from 6 patients, and one of them was the woman’s. Dr Beth said researchers did not know how the patient contracted the resistant bacteria. The microbes have been found in people in Asia and Europe, but the patient had not traveled during the past 5 months. It is possible that she contracted the bacteria from food, or from contact with someone else who was infected, Dr Beth said. Public health workers will interview the woman and will probably test her family members and other close contacts for the bacteria, she said.

Infectious disease doctors have long warned that overuse of antibiotics in people and in animals put human health at risk by reducing the power of the drugs, some of modern medicine’s most prized jewels. About 2 million Americans fall ill from antibiotic-resistant bacteria every year and at least 23,000 die from those infections.

The CRE germs usually strike people receiving medical care in hospitals or nursing homes, including patients on breathing machines or dependent on catheters. Healthy people are rarely, if ever, affected.

But the bugs attack broadly, and the infections they cause are not limited to people with severely compromised immune systems. CRE was believed to be the cause of infections from improperly cleaned medical scopes that led to the death of 2 people at Ronald Reagan UCLA Medical Center in California last year.