Last October, Christina Assi, a 28-year-old photojournalist for Agence France-Presse, took a selfie against the sunset and WhatsApped it to her mother. “Be careful,” her mother replied.
Assi and some colleagues had driven to the border in southern Lebanon to cover artillery clashes between Israel and Hezbollah. Wearing protective helmets and blue flak jackets that said “PRESS” in large white letters, they set up on an exposed hill a good distance away from the smears of smoke on the horizon. Drones buzzed overhead. Suddenly, a tank shell struck right next to Assi’s position, killing her friend and colleague Issam Abdallah, a 37-year-old videographer for Reuters. The force of the impact slammed Assi into the dirt and pelted her with shrapnel.
“What happened?” she screamed. “What happened? I can’t feel my legs.” Nearly all of her right calf and half of her left calf had been blown off. Within a minute, another shell struck the Al-Jazeera car, and it erupted in gassy, billowing flames.
By the time Assi arrived at the American University of Beirut Medical Center, it was past midnight, and doctors assessed her chance of survival at 50 percent. A hospital near the border had already staked a fixator, a long metal rod with steel prongs on either end, into her leg to stabilize the bone and help control the bleeding.
Fady Haddad, the university’s head of vascular surgery, and his team painstakingly repaired and reconnected the damaged blood vessels, but 48 hours later, they had inexplicably clotted and failed. Haddad performed three more operations, but again and again the vessels failed. The reason became clear: Microbes were feasting on Assi’s necrotic flesh. Despite aggressive debridement — daily surgical scrapings of her wounds to clean out the infection — and expensive medications, the tissues in her leg grayed at the edges. The hospital’s microbiology lab identified three possible culprits: two bacteria and a fungus, a mucormycete mold. But as the infections kept worsening in spite of medication, one of Assi’s infectious-disease doctors, Souha Kanj, suspected there might be yet another fungal pathogen at play.
Kanj prescribed a second, very expensive antifungal medication and sent a culture to an Austrian lab, which two weeks later confirmed her suspicion, finding a rare strain of Aspergillus flavus. The decision to add the second medication probably helped save Assi’s life. But nothing could save her right leg: She was still in a coma when the doctors told her parents that they would need to amputate it, owing not to the initial trauma but to the aggressive, drug-resistant infections that set in afterward.
By 2050, The Lancet predicts that antimicrobial resistance will kill 8.22 million people per year, more than the number currently killed by cancer. (For context, Covid claimed an estimated three million lives during all of 2020.) And a growing body of research suggests that the 21st-century way of warfare has become a major driver of that spread. Nations of the Middle East, like Iraq, Syria, Yemen and Afghanistan, now suffer from particularly high rates of multidrug-resistant pathogens, and some of the world’s most fearsome superbugs have incubated in the region — Klebsiella pneumoniae, Pseudomonas aeruginosa, E. coli, MRSA and perhaps most notably A. baumannii, a strain of Acinetobacter that traveled home with U.S. soldiers, where it became nicknamed “Iraqibacter.”
Humans are host to more than a thousand species of bacteria, including many of the superbugs deemed critical threats by the World Health Organization. But they rarely become pathogenic in healthy people. War changes that. It deprives people of food, clean water and sanitary living conditions. When bombs and bullets fly, the resulting wounds become perforated with shrapnel, debris and soil teeming with microbes. The injured and vulnerable often wind up in close and unclean quarters — packed transport buses and boats, refugee camps, overcrowded hospitals — that allow infection to fester and spread.
As wealthier countries bomb poorer ones, devastating essential infrastructure, they have created the tragic social conditions that foster antibiotic resistance. The public-health fallout knows no borders and can carry on indefinitely, even after the bombs stop.
About a decade ago, Ghassan Abu-Sittah, a Palestinian reconstructive plastic surgeon newly arrived at the American University of Beirut, presented another new hire — Omar Dewachi, an Iraqi anthropologist and former physician — with a medical mystery that he was observing in his clinic.
Many of his patients were Iraqis, Abu-Sittah explained — men and women who traveled to Beirut for better care. And a startling number of them were suffering from infections that stubbornly failed to heal. Time and again, Abu-Sittah had to postpone reconstructive surgery. Quite a few were suffering from osteomyelitis, complicated bone infections that didn’t respond to medication; one patient, who had pus discharging from a leg fracture, had been on antibiotics for more than a year with no improvement. When civil war broke out in Syria, Abu-Sittah began seeing Syrian patients, too, and their infections were even worse. Eventually, to protect the rest of the population, the university’s immunologists began isolating all Iraqi and Syrian patients upon arrival until they could be tested for “AMR,” the medical shorthand for antimicrobial-resistant pathogens — bacteria, fungi or viruses resistant to medication.
Abu-Sittah had assembled some remarkable data: roughly 70 percent of his patients from Iraq and almost 80 percent from Syria had infections that were resistant to multiple drugs. What was driving this startling rise in resistance?
As the two men discussed this question over coffee, Dewachi’s first thought was sanctions. He had grown up in Baghdad and did his residency at Baghdad Hospital during the devastating embargo that the United Nations Security Council placed on Iraq in 1990, after it invaded Kuwait. The sanctions lasted nearly 13 years. Baghdad Hospital, once the medical crown jewel of the Middle East, could no longer acquire cleaning supplies, surgical gloves, ventilators or medication, and the quality of care crumbled. As stocks of the proper drugs dwindled, Dewachi and other health care professionals were forced to trade medicines with one another out of the trunks of their cars, an act punishable by death under the dictatorship. Antibiotics in particular were in short supply; patients often couldn’t finish the recommended course, or they were forced to take second-rate ones manufactured with lower concentrations of active ingredients than claimed on their labels. The suboptimal dosing killed some bacteria, but not all, increasing the likelihood of resistance.
This was especially a problem when patients were housed in groups, as they were in the English-style, open-ward system of Baghdad Hospital. Nurses and doctors moved quickly among patients without changing their smocks and other personal protective equipment, which were in limited supply. Infection spread easily, especially among the immunocompromised or malnourished, conditions all too common during those desperate times. Vaccines were scarce and seldom prioritized. Patient mortality was high.
Frustrated with their inability to care for patients properly, many doctors fled, paying smugglers for fake passports and other travel documents. Dewachi made that decision himself at age 25, in 1998, walking out of Baghdad Hospital at the end of his shift, never to return. After passing through Jordan with a single suitcase, he settled in Beirut, working under the table as an emergency-room and operating-room physician, without the prohibitively expensive medical licensing required of foreigners wishing to practice in Lebanon. After a year, he took leave to get a master’s degree in public health at the American University of Beirut, and so began his second flight, from medicine to anthropology. Three weeks before 9/11, he arrived in the United States to start a doctoral program in anthropology at Harvard, studying the impact of war and sanctions on Iraq’s health care system. He joined the American University of Beirut as an assistant professor in 2011. Three days after he arrived, a street vendor self-immolated in Tunis, sparking the Arab Spring. To think through the emerging upheaval in the Middle East, Dewachi founded a health-and-society working group, and it was at one of the first meetings that he met Abu-Sittah.
Abu-Sittah never lived in Iraq, but he witnessed the medical crisis there as part of a public-health delegation. A Palestinian born in Kuwait, he emigrated to Britain in 1988, at age 18, to attend medical school in Glasgow. Just after the Persian Gulf war, in 1991, he traveled throughout Iraq with a Harvard team studying infant mortality and nutritional status and saw firsthand how this so-called clean war with fewer civilian casualties was made more lethal by other means: infrastructure collapse — the decimation of electricity plants, generators, sewage and water-treatment plants. Most infant mortality was diarrheal, caused by unsanitary water. In Diyala, northeast of Baghdad, he witnessed sewage being pumped into the river.
“If you dismantle the health infrastructure of urban life, you can take more lives than bombs could ever do,” Abu-Sittah told me.
As Dewachi and Abu-Sittah continued to meet and discuss antimicrobial resistance, Abu-Sittah brought up a possible link between AMR and war that medicine, to his knowledge, had not considered. Maybe, Abu-Sittah theorized, resistance accelerated because of how bombs had changed. In the Iran-Iraq war during the 1980s, both sides deployed conventional bombs encased in steel. But in the Persian Gulf and Iraq wars, the Americans had used extremely heavy bombs, weighing up to 30,000 pounds, encased in heavy metals like cobalt and tungsten. Might these heavy metals be causing genetic changes in the bacteria, driving them to evolve into antibiotic-resistant strains?
Dewachi realized that they needed to do some real research. As a first step, Abu-Sittah introduced him to a colleague at the American University of Beirut Medical Center, an infectious-disease doctor named Abdul Rahman Bizri. Bizri said the hospital was especially vexed by a bacterium called A. baumannii — the entire region was. The microbe was lazy, and wasn’t generally harmful unless a person had a weakened immune system. But in the vulnerable, it could infect the bloodstream, urinary tract, lungs and any other soft tissue, including the brain. It also had a huge adaptive advantage: It could easily acquire genes of resistance.
A. baumannii emerged as a global threat in the 2000s, during the U.S.-led wars and occupations, attracting attention because it killed wounded U.S. soldiers who most likely acquired it from field clinics or hospitals at some point during their evacuations. The Walter Reed Army Institute of Research gathered data from facilities where soldiers returning from Iraq and Afghanistan were treated; in 2003, 12 percent of the Acinetobacter infections they tracked were resistant to a key antibiotic called imipenem, but by 2015 — though the total number of infections was significantly lower — the rate of resistance had risen to 99.2 percent. The microbe tended to stick around hospitals and was difficult to eradicate. “It’s like the ISIS of bacteria,” Bizri joked to Dewachi. “The West can’t defeat it.”
There’s a colonial trope in which invading forces blame their struggles on the dirtiness of the people and the places that they have invaded. Dewachi had every right to be offended by the “Iraqibacter” nickname, but when he heard it, “a lightbulb turned on,” he told me. “Like, ‘The anthropologist just found the treasure.’”
What actually offended him wasn’t the name, but the sloppiness of the scientific explanation for it. What was Iraqi about Iraqibacter? Rumors among American soldiers had turned it into an almost mythical problem, imagining that the insurgents were rubbing bombs with the flesh of dead animals. Dewachi scoured the medical literature and news. “We’re now facing a new enemy invader emerging from Iraq,” Neil deGrasse Tyson said on the PBS show “Nova.” “These guys can survive for weeks at a time without food or water. We don’t know how to fight them, but we’ve got to find out. Guns and tanks won’t help us here.” Tyson added: “What we really need is a good biologist.”
“No, man,” Dewachi thought to himself. “What you need is a good anthropologist.” Only an anthropologist, he realized, could get at the confluence of social, historical and medical factors driving AMR.
And so Dewachi and Abu-Sittah began meeting weekly to discuss these issues. Doctors and microbiologists are often focused on narrow research questions around which they can design experiments to definitively answer them. That’s essential to scientific progress, but it can result in fragmented literature and intellectual silos.
To pull together experts from many different disciplines, Dewachi and Abu-Sittah founded a conflict-medicine research group based at the university, and in 2018, Dewachi and some others organized a research retreat for microbiologists, historians of science, anthropologists, clinicians and public-health experts studying war injuries. Over several days, sitting by a lake at the Brocher Foundation in Switzerland, the team sought to pin down why conflict drives antimicrobial resistance. A medical anthropologist pointed to agricultural literature describing how heavy metals from battery plants and fertilizers were correlated with increasing AMR. A microbiologist who worked in Beirut half a century ago said that the first outbreak of A. baumannii in Lebanon was actually during the war in the 1980s.
Over the course of the week, it really hit home for everyone that there wasn’t one single cause driving AMR. War created the perfect convergence, a toxic biosphere for the acceleration of resistance.
It was by mere chance that Alexander Fleming discovered what would become the first industrially produced antibiotic. He was growing staph cultures in 1928 when a mold contaminated one of his plates, creating a clear nimbus where none of the cloudy staph could grow. Fleming tested the mold and found it wasn’t harmful to animals. He understood its therapeutic potential immediately, but he spent the next decade trying to get chemists interested in figuring out how to concentrate it for medical use. He had pretty much given up by the time a small group of Oxford chemists solved the problem in 1939. By 1945, penicillin was in mass production, and the drug was administered to the Allied forces, preventing and curing wound infections as well as treating syphilis, gonorrhea and other G.I. scourges.
But that same year, in his acceptance speech for the Nobel Prize, Fleming was already warning against antibiotic resistance. He told a hypothetical story of a man with a sore throat who stops taking penicillin once he feels better, which breeds a resistant bug that kills his wife. “Moral: If you use penicillin, use enough,” Fleming said.
A host of new antibiotics were identified in the decades after Fleming’s discovery: streptomycin, which treated tuberculosis, as well as tetracyclines, vancomycin, ampicillin, methicillin, cephalosporins and quinolones — a series of discoveries that did as much as anything else to double human life expectancy over the course of the 20th century. But by the end of the 1970s, the financial incentives of the pharmaceutical industry began to shift, given the outsize profits to be reaped not from one-time cures but from “drugs for life” that patients take for decades — e.g., statins for high cholesterol. Moreover, in the 1980s, safety standards increased and regulatory processes grew longer and more expensive, changes that further discouraged pharmaceutical companies from developing antibiotics. On average, the W.H.O. says, it takes 10 to 15 years for an antibiotic candidate to be developed and tested, and only a tiny fraction of those in development will ever reach patients.
Today, Dewachi and his colleagues are using microbiology not to invent new antibiotics but to understand the process by which war undermines them. At the end of June, I visited the lab of Antoine Abou Fayad at the American University of Beirut, who joined the conflict-medicine research group in 2017. Since then, the questions that Dewachi and Abu-Sittah posed to him about heavy metals and AMR have become his major area of focus, and his lab’s findings have been published in The Lancet and Nature.
Abou Fayad is a 38-year-old man with hooded eyes and a youthful cowlick. In a sterile, white-and-gray room with fluorescent lighting, he put on latex gloves, opened the CryoCube, a thick freezer set at minus 80 degrees Celsius, and pulled out a small rectangular box caked in ice with 96 small vials of A. baumannii. There were more than 22,000 samples of bacteria in his lab, a veritable library of infection. More samples, like those from Christina Assi’s injuries, were being sent to him daily from American University of Beirut Medical Center and other hospitals throughout the region.
Resistant bacteria are classified in three ways, Abou Fayad said, approaching a whiteboard and scribbling abbreviations: multidrug resistant (MDR), meaning resistant to at least three classes of antibiotics; extensively drug resistant (XDR), meaning resistant to all classes but two (generally colistin and tigecycline); and pan-drug resistant (PDR), meaning they’re basically resistant to everything. When Abou Fayad first arrived in 2017, he explained, “I used to get one sample a month” of PDR bacteria. “Now, we get one sample a day.” Acinetobacters account for 20 percent of intensive-care-unit infections globally, and almost all of them are pan-drug resistant.
Abou Fayad thinks the estimate of eight million AMR-related deaths by 2050 is far too low, mostly because there are very few new antibiotics in the pipeline. Moreover, safety standards have increased since the golden age of antibiotic discovery. If all the clinically utilized antibiotics were resubmitted to the F.D.A. today, Abou Fayad says, few would be approved; most are nephrotoxic, meaning harmful to the kidneys. “Colistin: nephrotoxic,” he said. “Tetracycline family: nephrotoxic. Ciprofloxacin has been associated with neural side effects in a number of patients. We’re not just talking one or two.”
Abou Fayad rummaged around his lab counters and plucked out some large vials containing bullets and shrapnel. He directed our attention to his lab’s research assistant, Aya Taleb, who was masked and pipetting nutrients into one such vial, in which Acinetobacter was growing on an M4 casing — one of many that the Lebanese Army had fired into sandbags on Abou Fayad’s behalf, so he could study the effect of their heavy metals on bacteria.
Many heavy metals are naturally antibacterial; copper, for example, is sometimes used to coat surfaces in operating rooms for that reason. Abou Fayad and Taleb began with an Acinetobacter control strain that was sensitive to all antibiotics. Every few weeks, Taleb cultures an agar, a petri dish with nourishment, with the microbe growing in the vial to see how sensitive it is to antibiotics. To ensure objectivity, they were blinding the metal content of each vial — though a few metals had clearly outed themselves, like the copper that was oxidizing and leaching dark green into its liquid.
The results won’t be finalized or peer-reviewed for another year, but what Abou Fayad said he was witnessing was striking. The Acinetobacter was absorbing small particles of heavy metals and then developing a gene that constructed a pump within the bacteria — an e-flux pump — that evacuated the heavy metals. Because heavy metals and antibiotics resemble one another, that same pump worked to expel antibiotics. In other words, the microbe was learning how to flush out toxins. And then it was sharing its recipe with similar bacteria.
Many of the places that now need quality antibiotics are receiving sham versions that are less than full strength. Abou Fayad pulled out a bin of Syrian antibiotics. When tested in the lab, not one of them measured the concentration on its packaging. “If they say 500 milligrams, they’re probably 100 milligrams,” Abou Fayad said.
Then there was the issue of antibiotic dumping, an example of good intentions gone awry. “This happens in conflict quite a lot,” Abou Fayad said. A pharmaceutical company or nonprofit will donate a big batch of an antibiotic that’s near its expiration date — like meropenem, a very serious, intravenous carbapenem that should be reserved as a last-resort medication. “They start to distribute it like bonbons. Everybody will be on meropenem, even if you’re not sick,” Abou Fayad said, because everyone wants to use the drug before it expires.
In terms of driving resistance, this is like striking a match in a gas station. Bacteria are everywhere in our bodies; antibiotics select for resistance. With the more sensitive bacteria wiped out, there’s nothing to keep the resistant bacteria in check, allowing them to gain ground and ultimately enter the environment in higher proportions.
“We don’t have a proper sewage system” in Lebanon, Abou Fayad said. “Somebody poops in the south” — and whether it’s in the water or the food, “you can taste it in the north.”
When I met Dewachi in Beirut, he had food poisoning. He refused antibiotics — on principle. His mother chided him, asking what kind of doctor would deny himself treatment. We were flying to Baghdad in a few days, and I asked what he planned to do.
Drink water, eat simple foods and let it pass, he said.
The world was catching up to Dewachi: The W.H.O., which now sees antimicrobial resistance as one of the leading global health threats, had become concerned with the role of war in its rise. Since 2017, in an effort to get better data on AMR, the organization has helped Ukraine increase its number of microbiology laboratories from four to more than 100. The University of Baghdad College of Medicine had been collecting data since 2014, and the country’s Ministry of Health began collecting AMR data in collaboration with the W.H.O. in 2018.
But during my time in Baghdad, I understood why the acceleration of resistance was an anthropological question, not just a medical or scientific one. Global health workers were afraid to speak to me, worried about crossing the Iraqi Ministry of Health, for complex political reasons. Which is why ethnographic research in pharmacies and hospitals was so critical.
Fortunately, Dewachi was feeling better by the time we ran into Mohammed Maaroof, a doctor in the Specialized Burns Hospital in Baghdad’s Medical City. Maaroof said that he first encountered A. baumannii more than a decade ago in patients referred to him by the U.S. military hospital in the Green Zone. Now he sees it constantly. Burn victims are especially vulnerable to bacterial infection, because burns obliterate the body’s barrier against the environment, allowing all of the bacteria that naturally colonize the skin into the soft tissues of the body. The ubiquity of burns in war injuries makes infection all but inevitable.
Dewachi underscored how sanctions exacerbated the distortions of the dictatorship, stripping the hospital system of resources, destroying morale and undermining scientific practices. One Iraqi medical-school professor — who asked not to be named for fear of professional reprisal — told me that under the dictatorship, if evidence-based medicine called for a drug that was unavailable, doctors often felt pressured to offer a poor substitute, without being able to acknowledge that it was the incorrect treatment. Some even went so far as to parrot the state’s rhetoric, setting themselves up in opposition to a corrupt global scientific consensus: “We are Iraqis. We are the sons of Babylon and Sumeria. And for sure we are better than others.”
Dewachi believes that even decades after Saddam’s fall and the end of the U.S. occupation, the medical culture has not entirely reset — many younger doctors in Iraq told him that they struggle to implement infection-prevention-and-control procedures under their managers, older, jaded doctors who say it is impossible given the heavy workload and limited resources. For this reason, the medical-school professor has helped lead training workshops on AMR stewardship. The first point he wanted doctors to understand: that it’s OK to say, “I don’t know.”
Hospital systems in developing countries can be a nexus of spread, by drawing the sick closely together. Jamal Abed Kadhim, a microbiologist and the head of infection prevention and control at the Ministry of Health, told me that there were far too few hospitals to serve Iraq’s patients; whenever an AMR outbreak happened, he hoped that it was in a hospital that had science-minded staff members he could trust.
I asked Kadhim what he made of the term “Iraqibacter.” “Americans are afraid of Iraqis,” he said. “They think of us like killers in the movie ‘The Purge.’”
Perhaps the best way to think about “Iraqibacter” is that it emerged not from Iraq per se but from the privations of war. In war, wounded patients may receive antibiotics prophylactically while they await diagnosis, if precise diagnosis is even possible. Doctors, overburdened with pressing crises, are otherwise scarce or prohibitively expensive, leading civilians to skip doctor visits altogether and go directly to pharmacies. In Iraq, such practices have become an entrenched culture. Technically, Iraq has prohibited the sale of antibiotics without a prescription since 1970, but the law has not been enforced. “This is what war does,” Dewachi told me later. “It creates medical cultures that are very difficult to change.”
On Baghdad’s Al-Kindi Street, there are countless pharmacies, brightly lit with clean white floors. I walked into one and asked the pharmacist for ciprofloxacin, an antibiotic on the World Health Organization’s watch list because of its relatively high risk of selecting bacterial resistance. The pharmacist handed it to me without asking anything about my condition; he didn’t even specify how many days I should take the course.
“Wars can kill thousands, but bacteria kills millions,” Osama Zuhair Salman, the technical director of Baghdad Teaching Hospital, told me. Not only is bacteria developing antimicrobial resistance much faster than humans are developing antibiotics, but climate change is expanding the range of resistant pathogens, and globalization makes spread inevitable. As a medical resident in 2016, Salman watched a cousin suddenly lose a newborn to AMR, a baby whose conception had taken 10 years and countless rounds of IVF. That moved Salman to take part in efforts to implement strict infection-prevention protocols.
“The world is a small village,” he said. “The infection that happens in Delhi can have consequences in America and vice versa. So, your measures, however perfect they are, they are useless if they are not applied in all of the world at the same time.”
At Baghdad Hospital, we could see the challenges Iraq’s largest medical institution was confronting in its most vulnerable patients. The neonatal intensive-care unit for babies presumed to have infections appeared absolutely sterile: white walls, linoleum floors, bright, full-spectrum lights. Six premature babies were encased in their own incubators while the heart monitors and IV drips emitted an eerie, asynchronous house music.
A tiny baby, purple, with legs that were basically just bones, had a feeding tube secured to her mouth by two bands of gauze crisscrossed around her head, X-ing out her face. Another baby, perfectly plump with jet-black hair, was asleep, head resting on little hand, neck scrunched back, eyes closed, but face straining to look all the way up.
Doctors had drawn blood from all six newborns to test for antimicrobial resistance. Two results weren’t in yet, and three had tested negative, but Ahmed Mustafa, a young pediatrician at the unit, suspected that all were positive, based on the failure of the babies to recover. The one confirmed positive was the baby with jet-black hair, his scrunched neck a symptom of meningitis. The tissues surrounding his brain and spinal cord were inflamed by a resistant A. baumannii infection. He was being treated intravenously with colistin, which was nephrotoxic, meaning it could cause his kidneys to fail. As his warm belly rose and fell, toxins washed through his system, potentially leaving lasting neurological damage.
Nearly every weekend, health workers test the neonatal intensive-care unit for pathogens, swabbing the babies, incubators and surfaces, and very often they find something lingering, often A. baumannii. Ideally, the unit would close for sterilization during a major outbreak, but there are too many babies with life-threatening infections to ever shut down the I.C.U. Resistant A. baumannii is endemic throughout much of the Middle East, and so the babies and those trying to save them must trade risks — medical attention in exchange for possible exposure to a potentially lethal infection.
During the first 43 days of the war in Gaza, Ghassan Abu-Sittah volunteered as a reconstructive surgeon. By the second week, he said, there were 6,500 wounded in Gaza, with only 2,500 hospital beds available. Patients with burns and crushed limbs and dirty blast injuries with complicated constellations of shrapnel shared mattresses and crowded into the hospital halls. At the end of October, Abu-Sittah decided to swab eight consecutive patients that came to him from other hospitals. Seven of the eight were infected with multi-drug-resistant bacteria. Later in the fall of 2023, he said, less than half of those who needed antibiotics in Gaza could get them; many were taking only partial treatments.
By November 2023, the sort of testing Abu-Sittah did in October was inconceivable. Gaza had run out of lab supplies, not to mention more basic items like disinfectant. There were too many critically injured patients to afford the time for data-gathering and research. Precise diagnosis of infections was a luxury, requiring resources that were unavailable. Even if doctors in Gaza wished to outsource lab testing, Israel wouldn’t let samples out of the region.
Israel also wasn’t letting many critical medical supplies in, on the grounds that they might be repurposed for military use. Israel’s list of restricted items is known as the “dual use” list and includes anesthesia machines, crutches, generators, X-ray machines, oxygen concentrators, water-test kits and detergent. “If we want to achieve our war goals, we give the minimal aid,” Prime Minister Benjamin Netanyahu of Israel said in a news conference in January.
Abu-Sittah began going to the supermarket across the street from Al-Shifa hospital several times a week, in order to concoct his own disinfectant with vinegar, saline and dishwashing soap, a wartime trick he learned from another physician he met in Beirut. One of Abu-Sittah’s patients was a 9-year-old girl whose body was studded with gravel and dirt and shards of metal. He and other surgeons took her to the operating room every 24 to 36 hours to debride her wounds. After the second surgery, the hospital ran out of anesthetic. At one point, terrified of the pain, she skipped a debridement. By morning, her dressings were soaked with pus and green discharge, and her temperature had spiked.
Abu-Sittah told her father that unless her wounds were cleaned, she would succumb to sepsis and be dead by the end of that week. Abu-Sittah took her to the operating room and scrubbed her with his vinegar disinfectant. She screamed continuously as tears rolled down her father’s face. It was one of the darkest moments of Abu-Sittah’s life.
By November, patients with dirty wounds and dead tissue were waiting up to two or three weeks for their first debridement — something that typically should happen within 24 hours of injury. By Dec. 7, 20 out of 22 hospitals in northern Gaza identified by CNN had been damaged or destroyed, and 14 had been directly hit, including Al-Shifa. By Dec. 21, a W.H.O. official said that no hospitals were functioning in northern Gaza and described one recently disabled facility as a “place where people are waiting to die.”
“You have 100,000 wounded, most of whom haven’t received proper treatment,” Abu-Sittah told me this summer. “Many are malnourished and combating infection. Their open wounds act like petri dishes.” Even before the war, 34 percent of Gazan hospitals had resistant bacteria in their water. Now, water-treatment and sewage-treatment plants have been destroyed, with supply reduced by 94 percent. Oxfam concluded that “Israel has systematically weaponized water” in Gaza; Israel has also cut off electricity for more than a year. Biological waste isn’t incinerated; it’s buried or flushed, pouring back into the community. Thousands of bodies are decaying under more than 40 million tons of urban rubble, with asbestos and heavy metals that cause bacterial mutation. Every time it rains, carcasses and debris leach into the ground and infiltrate the groundwater. Mysterious skin infections are raging through the population. Polio has re-emerged for the first time in 25 years and left a 10-month-old baby partially paralyzed.
“Water currents in the East Mediterranean travel up from Alexandria past Gaza,” Abu-Sittah said, up “to Syria, to Greece, Italy.” His point was that the infections of war can’t be contained to war zones: “Everything that reaches the sea is going to reach the Earth.”
At the end of May, a 5-year-old Gazan boy named Adam Afana arrived in Beirut for medical care, the first to receive treatment under a fund established by Abu-Sittah and his colleagues. Adam’s arm was nearly severed at the elbow when an Israeli missile hit his grandmother’s house. His sister was instantly killed and his brother and mother seriously injured; his father, who was loaded into an ambulance alongside Adam, died later. The family was treated at Al-Shifa hospital, in Gaza, until the hospital was hit by Israeli forces. They eventually fled to Egypt, where Adam was diagnosed with osteomyelitis, a serious bone infection. Doctors wished to amputate his arm, but his uncle refused, signing a waiver accepting responsibility for the decision.
When Dewachi and I met Adam, this summer in Beirut, he had been on a daily drip of IV antibiotics for a month. He sauntered into the living room of the apartment where he was being hosted, demanding Pringles, which he carried in his right hand, his left arm hanging at an unnatural angle, like a boomerang, at his side. He wore a mischievous smile and ears that he was still growing into.
His mother was in critical condition in Egypt, and he avoided talking about her. They would be apart for at least six months. Antoine Abou Fayad investigated the infection in Adam’s arm: It was Acidocella facilis, a rare, “extremophile” bacterium — meaning one that thrives in the most punishing climates and temperatures — and an unusual challenge for doctors to treat.
“This is the dark poetics of it,” Dewachi told me. World War II, he pointed out, is what gave the world penicillin, but now the 21st century’s brutal modes of conflict have brought all our means of fighting infection to the breaking point. The innovations of war, such as they are, have outpaced those of medicine, which has brought us to a grim possibility: Born in war, antibiotics now risk becoming another of its casualties.
Enri Canaj is a photographer from Albania. His first monograph is titled “Say Goodbye Before You Leave.” He is a member of Magnum Photos.
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