For the past 70 years, an­tibi­otics have given us the up­per hand against mi­cro­bial in­vaders. Now the bugs are fight­ing back. DYANI LEWIS takes a look at the next gen­er­a­tion of ‘evo­lu­tion-proof’ weapons be­ing de­vel­oped.

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AT HIS NORTH ADELAIDE PRAC­TICE, Peter-john Wormald has the un­en­vi­able job of un­block­ing the noses of peo­ple with chronic si­nusi­tis. Many of his pa­tients have spent years on an­tibi­otics that have failed to budge their in­fec­tion, pro­vid­ing the per­fect breed­ing ground for re­sis­tant su­per­bugs.

FOR FOUR OUT OF FIVE OF THEM, surgery is the an­swer. Wormald carves away in­flamed tis­sue, widens si­nus open­ings and flushes out ac­cu­mu­lated pus. For the stub­born one in five, how­ever, Wormald is con­duct­ing one of the world’s first clin­i­cal tri­als into phage ther­apy, a cen­tury-old idea that pre­dates mod­ern an­tibi­otics.

Such tri­als are des­per­ately needed. We are on the thresh­old of re­turn­ing to the dark ages that pre­ceded an­tibi­otics. In the late 19th cen­tury, tu­ber­cu­lo­sis was hu­man­ity’s great­est scourge. Robert Koch, who iden­ti­fied the causative My­cobac­terium tu­ber­cu­lo­sis, es­ti­mated that “one-sev­enth of all hu­mans die of tu­ber­cu­lo­sis”. The dis­ease is now on its way to be­com­ing un­treat­able once more. Ev­ery year, nearly half a mil­lion new cases of mul­tidrug-re­sis­tant tu­ber­cu­lo­sis (MDR-TB) oc­cur world-wide. Ex­ten­sively drug-re­sis­tant tu­ber­cu­lo­sis (XDR-TB) strains, im­per­vi­ous to the most po­tent an­tibi­otics in our ar­se­nal, have al­ready reared their head.

Even nor­mally be­nign bac­te­ria like Sta­phy­lo­coc­cus aeureus – golden staph – which harm­lessly colonises our skin and nos­trils, can cause lethal in­fec­tions if they hitch a ride into the blood­stream on a catheter or through a sur­gi­cal in­ci­sion.

In the post-an­tibi­otic era, drug-re­sis­tant strains could ren­der elec­tive surgery, like knee or hip re­place­ments, too risky. Ac­cord­ing to a 2016 re­view from Bri­tain led by econ­o­mist Jim O’neill, by 2050 drug-re­sis­tant in­fec­tions could kill 10 mil­lion peo­ple each year – higher than the toll from cancer. Our prof­li­gate use of an­tibi­otics is re­spon­si­ble. An­tibi­otics un­leash mas­sive die-offs within bac­te­rial ecosys­tems. In a text­book case of evo­lu­tion, that an­tibi­otic-laden en­vi­ron­ment se­lects for the rare bac­terium that hap­pens to have ac­quired a re­sis­tance gene. By mech­a­nisms that range from shred­ding or pump­ing out the an­tibi­otic to shield­ing vul­ner­a­ble tar­gets, re­sis­tance genes en­able bac­te­ria to dodge what­ever weapons we throw at them.

Thus armed, a sin­gle bac­te­rial cell can quickly blos­som into a re­sis­tant army of tril­lions. The re­sis­tance genes, which are car­ried on rings of DNA called plas­mids, can be shared with unrelated bac­te­ria like the lat­est piece of mal­ware. Since the first use of peni­cillin more than 70 years ago, this story has played out for ev­ery an­tibi­otic deployed. In most cases, re­sis­tance emerges within a few short years.

In 2015 a new shock emerged. Re­searchers in China re­ported find­ing E. Coli bac­te­ria in pigs, chicken and hu­mans that had ac­quired a plas­mid that made them re­sis­tant to col­istin, an an­tibi­otic of last re­sort. It’s not of­ten used in hu­mans be­cause it causes kid­ney dam­age, which is why it had re­mained ef­fec­tive. But in China, and other places, this cheap an­tibi­otic has been a main­stay of an­i­mal farm­ing. In­deed 70% of our global use of an­tibi­otics is for the pur­pose of ac­cel­er­at­ing growth in farm an­i­mals, re­duc­ing the time needed to

get them ready for mar­ket. The 2015 re­port in Lancet In­fec­tious Dis­eases made it clear that re­sis­tant bugs in farm an­i­mals could spread their mal­ware to bac­te­ria that in­fect hu­mans – till then a hy­po­thet­i­cal risk. China banned the use of col­istin in farm an­i­mals a year later.

Un­til re­cently, we’ve man­aged to out­ma­noeu­vre dis­ease-caus­ing bac­te­ria. When one an­tibi­otic suc­cumbed to re­sis­tance, there was an­other pop­ping out of the pipe­line. Over the past few decades, how­ever, the steady flow has dried to a trickle.

Phar­ma­ceu­ti­cal mak­ers see lit­tle profit in the costly de­vel­op­ment of new an­tibi­otics. That’s be­cause, at least in the near fu­ture, the ma­jor­ity of in­fec­tions will still be treat­able by avail­able low-cost an­tibi­otics. That leaves a rel­a­tively small mar­ket for the new drug. “For a phar­ma­ceu­ti­cal com­pany, the eco­nomics just don’t make any sense,” says chemist Mark Blaskovich from the Univer­sity of Queens­land. “Why would you in­vest in some­thing where it’s a sin­gle two-week course and you’re cured, as op­posed to an on­go­ing ther­apy [like new treat­ments for cancer] cost­ing thou­sands, or hun­dreds of thou­sands, of dol­lars a year.”

Ac­cord­ing to a re­cent re­port from the Pew Char­i­ta­ble Trust, just 40 an­tibi­otics are chug­ging along the drug de­vel­op­ment pipe­line, com­pared to sev­eral hun­dred drugs for cancer. To make mat­ters worse, bac­te­ria are in­creas­ingly arm­ing them­selves with mul­ti­ple re­sis­tance mech­a­nisms. When it comes to treat­ing gon­or­rhoea and tu­ber­cu­lo­sis, for ex­am­ple, doc­tors now have few drugs that still work.

While health au­thor­i­ties like the World Health Or­gan­i­sa­tion ex­hort the com­mu­nity to limit their use of an­tibi­otics to slow the spread of re­sis­tant bac­te­ria, it won’t elim­i­nate the hordes of re­sis­tant mi­crobes al­ready in our midst.

In 2014, at the time of an­nounc­ing the O’neill-led re­view, then Bri­tish prime min­is­ter David Cameron warned: “If we fail to act, we are look­ing at an al­most un­think­able sce­nario where an­tibi­otics no longer work and we are cast back into the dark ages of medicine.”.

Now we are “be­yond a tip­ping point”, ac­cord­ing to Michael Gillings, a mi­cro­bi­ol­o­gist at Mac­quarie Univer­sity, Syd­ney. “It might have been pos­si­ble to stop this 40 to 50 years ago,” he says, “now we have the prob­lem for­ever.”

AS AN­TIBI­OTIC af­ter an­tibi­otic in­vari­ably fails, sci­en­tists are search­ing for al­ter­na­tive weapons.

One of those weapons was dis­cov­ered amid the fog of World War I. In the sum­mer of 1915, an out­break of se­vere haem­or­rhagic dysen­tery raged through the ranks of French sol­diers sta­tioned at Maisons-laf­fitte on the out­skirts of Paris. Sev­eral of the sol­diers were hos­pi­talised, and French-cana­dian mi­cro­bi­ol­o­gist Félix d’hérelle, work­ing at the In­sti­tut Pas­teur in Paris, was sent to in­ves­ti­gate. He dis­cov­ered that stool sam­ples from the sol­diers not only con­tained the dysen­tery-caus­ing bac­terium Shigella but also the an­ti­dote – “un mi­crobe in­vis­i­ble” which, when added to Shigella in a dish, killed it.

Across the chan­nel, Bri­tish mi­cro­bi­ol­o­gist Fred­er­ick Twort had also stum­bled across bac­te­ri­akilling agents in his cul­ture dishes. Both turned out to be bac­te­rio­phages, or ‘phages’ for short. These ‘bac­te­ria eaters’ are viruses that specif­i­cally in­fect and kill bac­te­ria, much as the flu virus in­fects our own cells.

It was d’hérelle that first had the idea of har­ness­ing phages as a clin­i­cal treat­ment. In 1919, he un­leashed his poo-de­rived con­coc­tion on a small group of Parisian chil­dren with dysen­tery. The trial was a suc­cess, and phage ther­apy quickly gained the at­ten­tion of the med­i­cal com­mu­nity. By the 1940s, how­ever, it had all but been aban­doned in the West in favour of the new­fan­gled – and less finicky – an­tibi­otics.

In the for­mer East­ern bloc, phage ther­apy is alive and kick­ing. Spe­cial­ist in­sti­tutes in Ge­or­gia and Poland have carved out a niche sup­ply­ing per­son­alised phage reme­dies for stub­born bac­te­rial in­fec­tions. Now, in the face of fail­ing an­tibi­otics, re­searchers in Western coun­tries are fol­low­ing their lead.

Nev­er­the­less, rig­or­ous clin­i­cal trial data re­mains sparse. Re­searchers like Wormald, who also leads oto­laryn­gol­ogy head and neck surgery at Adelaide and Flin­ders univer­si­ties, are now play­ing catch-up to test whether phage ther­apy is as ef­fec­tive as its pro­po­nents have long sug­gested.

Twice a day for two weeks, nine of his pa­tients flush out their si­nuses with a briny so­lu­tion con­tain­ing phages that kill golden staph, the most com­mon cul­prit in chronic si­nusi­tis. This usu­ally harm­less mi­crobe lives on most peo­ple’s skin and nos­trils, but can over­run nasal cav­i­ties, wounds or sur­gi­cal in­ci­sions when a per­son’s im­mune sys­tem is at a low ebb or the mi­cro­bial ecosys­tem has been thrown out of whack with an­tibi­otics. At the end of the two weeks, Wormald sees mod­est im­prove­ment. Three months on, the re­sults are dra­matic. “They are ab­so­lutely 100%,” he says. The likely ex­pla­na­tion is that phages stay on the job: as long as there are bac­te­ria, they hang around and at­tack.

Wormald uses a cock­tail of four dif­fer­ent phages that to­gether kill about 95% of golden staph strains cir­cu­lat­ing in the hu­man pop­u­la­tion. Other cock­tails – such as one used to treat leg ul­cers – also com­bine phages to tar­get sev­eral dif­fer­ent bac­te­rial species at once. Cock­tails guard not only against treat­ment fail­ure but against re­sis­tance, says Wormald: “While [the bac­te­ria] might try to be­come re­sis­tant to one strain of the phage, they’re likely to be ham­mered by the oth­ers.”

In an­other re­cent trial conducted at wound cen­tres in the US state of Wash­ing­ton, phages were dabbed onto the gan­grenous toes of six peo­ple with di­a­betes. It was a last-ditch at­tempt to spare their toes. In all cases the phage prepa­ra­tion – ob­tained from the Ge­orge Eli­ava In­sti­tute in Tbil­isi, Ge­or­gia – did the trick.

Even more promis­ing, re­searchers in the US an­nounced in April 2017 the suc­cess­ful de­ploy­ment of phages to treat a man on the brink of death due to a mul­tidrug-re­sis­tant Acine­to­bac­ter bau­man­nii in­fec­tion. The phages were in­tro­duced via ca­theters into the man’s ab­dom­i­nal cav­ity, and in­jected in­tra­venously. It is the first re­port of phage ther­apy thwart­ing a sys­temic in­fec­tion with no ap­par­ent side-ef­fects; the caveat is it was a sin­gle case and is yet to be pub­lished in the peer­re­viewed lit­er­a­ture.

Like guided mis­siles, phages tar­get en­emy bac­te­ria with great pre­ci­sion. In prin­ci­ple that makes them safe – both for us and for the le­gions of ben­e­fi­cial mi­crobes that in­habit our bod­ies. “They have a very low po­ten­tial to do harm,” says phage re­searcher Steve Abedon of Ohio State Univer­sity.

As phage ther­apy be­comes more wide­spread, will phage-re­sis­tant bac­te­ria emerge? Yes, but un­like the arms race be­tween bac­te­ria and an­tibi­otics, which re­quires hu­mans to keep up­grad­ing their weaponry to stay in the game, phages do it by them­selves. As bac­te­ria evolve re­sis­tance to the phages that prey on them, phages evolve new ways to tar­get them.

Also, when it comes to new phage va­ri­eties, na­ture has been prodi­gious. Phages are the most abun­dant life form on the planet and they are ev­ery­where. A drop of sea­wa­ter, a smear of poo, a clump of dirt – all teem with a mul­ti­tude of phage types. This makes for an es­sen­tially lim­it­less pool from which to fish for new weaponry. In the­ory, for ev­ery both­er­some bac­terium there should be a phage to prey on it.

That said, it hasn’t all been smooth sail­ing for the phage field. The largest ran­domised clin­i­cal trial of phage ther­apy to date – car­ried out in 2016 in Bangladesh with 100 chil­dren suf­fer­ing di­ar­rhea – was

Three months on, the re­sults are dra­matic: “They are ab­so­lutely 100%.” The likely ex­pla­na­tion is that phages stay on the job: as long as there are bac­te­ria, the phages hang around and at­tack.

a fail­ure, with the phage cock­tail pro­vid­ing no ben­e­fit. There were, how­ever, mit­i­gat­ing fac­tors. The phages only tar­geted Escherichia coli (E. coli) and it turned out that more than a third of the chil­dren weren’t in­fected with this bac­terium. For the rest of the chil­dren, the phage dose was too low to be ef­fec­tive. What­ever the rea­son for the trial’s fail­ure, the re­sults played to the per­cep­tion of phages as a finicky ther­apy that won’t eas­ily re­place an­tibi­otic pills.

Phage ther­apy faces other hur­dles. One is find­ing com­mer­cial back­ers. “They’re the most ubiq­ui­tous bi­o­log­i­cal en­tity on Earth,” says Abedon, “so they’re just free for the tak­ing.” This makes them unattrac­tive to phar­ma­ceu­ti­cal com­pa­nies. With­out in­vest­ment to cover the cost of con­duct­ing ex­pen­sive clin­i­cal tri­als, phage ther­apy will strug­gle to be­come any­thing more than a niche treat­ment.

Vin­cent Fis­chetti, a phage re­searcher at Rock­e­feller Univer­sity, New York, also pre­dicts “an up­hill bat­tle” in gain­ing reg­u­la­tory ap­proval. Reg­u­la­tors favour wellde­fined sin­gle-mol­e­cule drugs. A com­plex cock­tail of viruses could prove chal­leng­ing, he says.

Once ap­proved, the ef­fec­tive­ness of phage for­mu­la­tions would also need to be care­fully mon­i­tored and mod­i­fied in step with the march of bac­te­rial evo­lu­tion. This is sim­i­lar to the an­nual re­vamp that the flu vac­cine gets – and why you need a fresh jab each year – but it’s an­other mark against phages, po­ten­tially mak­ing them less at­trac­tive to in­vestors. IF PHAGES THEM­SELVES are too messy, Fis­chetti has an­other so­lu­tion: com­man­deer their weaponry. Once phages home in on their tar­get, they act like hy­po­der­mic sy­ringes, in­ject­ing their ge­netic blue­print into their bac­te­rial host. Within min­utes that blue­print is di­rect­ing the as­sem­bly of dozens of new phage prog­eny. To break out, they drill holes in the tough outer wall of the bac­te­rial cell by de­ploy­ing deadly en­zymes called lysins. These lysins them­selves are be­ing de­vel­oped as sin­gle-mol­e­cule patentable drugs, closer to what phar­ma­ceu­ti­cal com­pa­nies and reg­u­la­tory agen­cies are ac­cus­tomed to.

Lysins also have the ad­van­tage over phages – and tra­di­tional an­tibi­otics – of be­ing ex­tremely ef­fi­cient killers. In 2001, Fis­chetti’s team showed that, within sec­onds, a pu­ri­fied phage lysin oblit­er­ated 15 dif­fer­ent strains of the pneu­mo­nia-caus­ing bac­te­ria Strep­to­coc­cus pneu­mo­niae in test tubes but were less deadly to­wards harm­less throat bac­te­ria.

Their abil­ity to specif­i­cally tar­get bac­te­ria is not as finely honed as that of phages, but is su­pe­rior to an­tibi­otics. For in­stance, Fishcetti says it is pos­si­ble to di­rect spe­cific lysins to wipe out all strep­to­cocci, or all staphy­lo­cocci, or all pneu­mo­cocci. Nor do lysins just work in test tubes; they have res­cued mice from death by mul­tidrug-re­sis­tant golden staph in­fec­tions.

In 2016, Fis­chetti and col­leagues un­ex­pect­edly found that lysins could even chase down and kill Strep­to­coc­cus pyo­genes, the bac­terium re­spon­si­ble for “strep throat”. The pyo­genes hide away in­side throat cells, where an­tibi­otics are un­able to reach them, mak­ing strep throat highly re­sis­tant to treat­ment. Re­mark­ably the lysin did not harm the throat cells.

“Lysins are right up there as prob­a­bly the best chance of killing or­gan­isms at least as well as cur­rent an­tibi­otics,” Fis­chetti says.

Lysins are not only po­tent an­timi­cro­bials; they also have a rep­u­ta­tion for be­ing evo­lu­tion-proof. That’s be­cause lysins tar­get pep­ti­do­gly­can, a fun­da­men­tal build­ing block of the bac­te­rial cell wall. Any tweak­ing of these build­ing blocks to evade lysins would likely be deadly to the cell, too. “Lysins have evolved to tar­get sub­strates that the bac­te­ria can’t change very eas­ily,” Fis­chetti ex­plains. Of course, he and oth­ers aren’t tak­ing any chances. They look all the time, he says, and haven’t found one or­gan­ism that’s re­sis­tant to lysin.

De­spite the im­pres­sive re­sults com­ing out of pre­clin­i­cal tri­als, progress to­wards hu­man tri­als of lysins has been slug­gish. That’s about to change. Fis­chetti has been work­ing with the com­pany Con­tra­fect on a lysin treat­ment for golden staph blood in­fec­tions. A phase II clin­i­cal trial will kick off mid-2017, fol­low­ing on from a suc­cess­ful phase I safety trial that ended in 2016. Fis­chetti ex­presses con­fi­dence that the trial, which will take about two years to com­plete, will be a suc­cess: “From what I see in an­i­mal stud­ies and [other] ex­per­i­ments, it works ev­ery time.”

ONE OF THE REA­SONS that su­per­bugs emerge is be­cause an­tibi­otics are so deadly. In the wake of the mi­cro­bial holo­caust, re­sis­tant or­gan­isms thrive. Roy Robins-browne at Mel­bourne’s Do­herty In­sti­tute thinks there’s a bet­ter way to treat the trou­ble­some bac­te­ria that cause in­fec­tions. In­stead of try­ing to kill them, just de­fang them.

In 2013, Robins-browne and his team un­veiled re­gacin, a mol­e­cule that ef­fec­tively de­fangs the deadly di­ar­rhoea-caus­ing en­teropathogenic E. coli (EPEC). Re­gacin, turns off the “vir­u­lence” genes that make this bac­te­ria such a bad ass, pre­vent­ing them from set­ting up camp in the in­tes­tine and pump­ing out poi­sonous tox­ins. In mice, re­gacin works against an Epec-like mouse pathogen. So far, Robins-browne hasn’t found any re­gacin-re­sis­tant mu­tants. In hu­mans, he says, us­ing a drug like re­gacin could turn the deadly EPEC back into a harm­less strain of E. coli, with­out fear of re­sis­tance emerg­ing. But Robins-browne is yet to find back­ing from the phar­ma­ceu­ti­cal in­dus­try to de­velop the drug fur­ther. “You can ar­gue till you’re blue in the face about how this doesn’t select for re­sis­tance,” he says, “but they don’t be­lieve you.”

While Robins-browne’s strat­egy is to dis­arm bac­te­ria, there is an­other way of curb­ing their ag­gres­sion: make them think they don’t have the num­bers to mount a suc­cess­ful at­tack.

Some bac­te­ria have a clever way of sens­ing the size of their ranks. Known as “quo­rum sens­ing”, re­searchers first stum­bled on this phe­nom­e­non in the 1960s in an un­likely place: the bob­tail squid. It needs cam­ou­flage from preda­tors be­low that can see it sil­hou­et­ted against the light. The squid solves that prob­lem by virtue of a light or­gan on its un­der­belly that houses lu­mi­nes­cent bac­te­ria. These mi­cro­bial light bulbs glow only once they reach a thresh­old pop­u­la­tion. The bac­te­ria ‘ping’ each other with a protein that lets the oth­ers know they are there. The more ‘pings’, the greater their num­ber. When there are enough ‘pings’, the whole group turns on its bi­o­lu­mi­nes­cence.

Re­searchers sub­se­quently dis­cov­ered quo­rum sens­ing can be used for more ag­gres­sive pur­poses. Dis­ease-caus­ing bac­te­ria use it to co­or­di­nate a suc­cess­ful in­va­sion. As soon as there’s a ‘quo­rum’, they pump out tox­ins and tis­sue-di­gest­ing en­zymes. In about two-thirds of in­fec­tions, the bac­te­ria also hun­ker down into re­silient, slime-shrouded biofilms that pro­tect them against the im­mune sys­tem and an­tibi­otics.

It wasn’t long be­fore sci­en­tists were look­ing for ways to si­lence this mi­cro­bial chat­ter. Drugs that do this are called quo­rum quenchers. “Quo­rum sens­ing in­hi­bi­tion jams the com­mu­ni­ca­tion lines,” ex­plains

mi­cro­bi­ol­o­gist Tom Coenye from the Univer­sity of Gent in Bel­gium.

This tricks the bac­te­ria into act­ing as if they don’t have the num­bers to mount an of­fen­sive or build a biofilm. That makes it eas­ier for the im­mune sys­tem – or an­tibi­otics – to come in and counter the would-be in­vaders.

Dozens of quo­rum quenchers have been iden­ti­fied. In petri dishes, Coenye has found, they pre­vent bac­te­ria from build­ing biofilm fortresses. In mice, quo­rum quenchers have re­duced the sever­ity of Pseu­domonas aerogi­nosa lung in­fec­tions.

But quo­rum quenchers have their lim­i­ta­tions. Most peo­ple seek treat­ment when their in­fec­tions are well and truly es­tab­lished – too late for quo­rum quenchers to work. Their role, there­fore, will be in pre­vent­ing the spread of in­fec­tions in the first place.

One no­to­ri­ous source of drug-re­sis­tant in­fec­tion in hos­pi­tals is via med­i­cal de­vices such as ca­theters or re­place­ment joints. That’s why He­len Black­well, a chemist at the Univer­sity of Wis­con­sin, is de­vel­op­ing ways of im­preg­nat­ing ca­theters and re­place­ment hips with chem­i­cals that act as quo­rum quenchers. Pre­vent­ing post-op­er­a­tive in­fec­tions could help elim­i­nate the need for an­tibi­otics and re­duce the chance for re­sis­tance to evolve and spread.

Mean­while, Coenye is hop­ing quo­rum quenchers will make cur­rent an­tibi­otic ther­a­pies more ef­fec­tive. His work on hamameli­tan­nin – a nat­u­rally oc­cur­ring quo­rum quencher found in the bark of witch hazel – makes golden staph biofilms more sus­cep­ti­ble to an­tibi­otics.

The up­shot would be that an­tibi­otics could be used at lower doses and for shorter du­ra­tions, re­duc­ing the chance of an­tibi­otic re­sis­tance and ex­tend­ing the use­ful life of the an­tibi­otics we cur­rently rely on. WITH DEATHS FROM drug-re­sis­tant in­fec­tions now es­ti­mated at 700,000 a year glob­ally, there’s no doubt our seven-decade dream run with an­tibi­otics is draw­ing to a close.

Recog­nis­ing the dan­gers, gov­ern­ments and phar­ma­ceu­ti­cal com­pa­nies are be­gin­ning to re­spond. In 2016, nearly 100 phar­ma­ceu­ti­cal com­pa­nies pledged to work with gov­ern­ments to rein­vig­o­rate the an­timi­cro­bial de­vel­op­ment pipe­line.

Over­all sci­en­tists are think­ing broadly. In ad­di­tion to phages, lysins, quo­rum quenchers and vir­u­lence dis­rup­tors, the war chest in­cludes pro­bi­otic cap­sules packed with ben­e­fi­cial bac­te­ria to edge out trou­ble­mak­ers, as well as vac­cines and drugs such as host de­fence pep­tides that ramp up the body’s own nat­u­ral de­fences.

For now this is an arms race that we are los­ing. To buy time, our best bet is to rob re­sis­tant bac­te­ria of their evo­lu­tion­ary ad­van­tage by min­imis­ing the use of an­tibi­otics.

With suf­fi­cient in­vest­ment in re­search and de­vel­op­ment, the next gen­er­a­tion of smart weapons will hope­fully be ready be­fore an­tibi­otics are ren­dered use­less. If the re­searchers are right, our new weapons should pro­tect us a lot longer than 70 years.

DYANI LEWIS is a free­lance sci­ence jour­nal­ist based in Ho­bart, Aus­tralia.

IMAGES 01 Erax­ion / Dreamstime 02 Photo Sci­ence Li­brary 03 Peter-john Wormald 04 Ami Images / Getty Images 05 Eli­ava In­sti­tute

Sage of phage: Felix d’herelle first had the idea of har­ness­ing phage to treat in­fec­tion in 1915. 02

Cut­ting- edge: Sur­geon Peter-john Wormald, cen­tre, cur­rently re­lies on surgery to help pa­tients whose in­fected si­nuses fail to re­spond to an­tibi­otic treat­ment. He hopes phage ther­apy will pro­vide a bet­ter, less in­tru­sive op­tion.

05 Weapons against su­per­bugs: am­pules of clin­i­cal- grade phage from the Eli­ava In­sti­tute in Ge­or­gia.

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