The world of Danish children’s television is not for the prudish. Kids who turn on the tube in Denmark might be greeted by gratuitous flatulence, cursing, casual nudity, or cross-dressing puppets. One show centers on a pipe-smoking pirate who wallops ninjas and flirts with Satanism. In another, an audience of 11-to-13-year-olds asks probing questions about the bodies of adults who disrobe before them. As Christian Groes, an anthropologist at Denmark’s Roskilde University, told me, Danish children’s television is not unlike an LSD trip: “Everything is possible in that universe,” he said, loosely quoting a friend, “and people won’t complain about it.” But people did complain when the Danes debuted a kids’ animated series in January featuring a protagonist with an absurdly long, prehensile penis. The show, which is produced by DR, the same Danish production company responsible for the pirate and strip-down shows, was written for 4-to-8-year-olds. It centers on the eponymous John Dillermand, a mustachioed claymation character whose last name translates roughly to “penis man.” (In Danish, diller is a silly, cheeky bit of phallic slang, the equivalent of pee-pee, willy, or weiner in English.) Gifted, or perhaps cursed, with a retractable phallus that seems capable of extending at least 20 times the length of his body, Dillermand must navigate life alongside his über-ostentatious junk, which at times has a mind of its own. His schlong graffities walls, digs up gardens, lassos a moving caravan, and even coils itself into a bobbing, seaworthy boat—not always with Dillermand’s permission. Scandalized viewers criticized Dillermand as inappropriate, tone-deaf, and a jarring choice on the heels of the country’s growing #MeToo movement. But the series’s creators, and many bemused fans, defended it as a subversive comedy that has served up opportunities for parents to have frank and unsqueamish conversations about anatomy with their kids. “The series is about being true to one’s self,” Morten Skov Hansen, the head of DR Ramasjang, the company’s kids’ channel, told me in an email. “It’s as desexualized as it can possibly get.” While I don’t speak Danish, the tone of John Dillermand is not easily lost in translation: The show isn’t about sex. It’s about taking responsibility for your actions, and the awkward realities of inhabiting a human body. But in every minute of the Dillermand jaunt, there’s also a reminder that male bodies are still allowed freedoms that female ones are not. John Dillermand is, in some ways, a throwback to the man-children who have dominated kids’ TV across continents and decades. Dillermand, who is middle-aged, lives with his remarkably spry great-grandmother (oldemor, in Danish), and retains the worldview of a young boy. He is clad inexplicably in a red-and-white striped swimsuit (which graciously accommodates his elongating appendage, because a nude penis would have been a bridge too far), and occasionally a pom-pommed beanie. A character reminiscent of Mr. Bean or Inspector Gadget, he lacks street smarts and maturity, and innocently sees the world as his playground. Were Dillermand typically endowed, he might be merely bumbling or pitiable. But his giant penis—billed in the show’s theme song as the largest in the world—won’t allow him to languish in anonymity. A manifestation of his id, his pecker acts of its own accord. It’s sassy. It’s hedonistic. It’s got an appetite (for food, mostly), and isn’t afraid to buck social norms to sate it. This tension between man and member drives the show’s zany plot. After Dillermand’s penis plucks an ice-cream cone from a child’s hand and flings it onto a stoplight, Dillermand must redirect traffic and set the situation right. When the diller nearly drowns several kids, John wrangles it into a makeshift propeller to airlift the children to safety. Dillermand’s penis wields weapons with abandon—a dagger, a chain saw, a rifle. It provokes animals and bullies children. It steals. It commits acts of violence. It even terrifies Santa Claus (who mistakes the penis for a snake) so badly that he tumbles down a chimney and injures himself. Dillermand has enough self-awareness to occasionally bemoan the shenanigans of his wayward penis, pulling his hat over his face and groaning, “Ugh, that dumb diller.” It’s often Oldemor who must remind her man-child great-grandson to pak den væk—put it away!—when Dillermand’s diller runs amok. “What will the neighbors think?” she screeches. But Dillermand always comes through in the end, picking up a lesson or two about conscientiousness along the way. In the months since its premiere, John Dillermand has accumulated a veritable cavalry of tiny fans. Anne Sofie Pleidrup, who lives with her husband, her son, 6, and her daughter, 7, in Denmark, told me that her entire family has been enjoying the show. Both her children are creeping up to the age when anatomical differences are starting to fascinate them, and she was delighted that “they found the same punch lines funny.” Dillermand embodies a child’s view of the human body: strange, impossible, invincible, hilarious. He validates the idea that the diller is okay for kids to discuss. Children have parroted the show’s theme song to their parents, requested Dillermand-themed cakes, and packed superlong penises onto snowmen. “It’s removing some of the stigma about talking about a penis—it’s just a body part,” Eileen Crehan, a sex-education researcher at Tufts University, told me. With a squint, one could imagine Dillermand’s genitals as an extra-long arm or leg. By Danish standards, Dillermand is actually “fairly mild,” Andreas Lieberoth, an educational psychologist at Aarhus University, told me. He and many other experts I spoke with shrugged the series off as no big deal—just the latest in a long line of edgy or bodily brazen Danish shows. The show's success could also be read as a testament to Denmark’s progressive approach to sexuality and autonomy in general. Sex education has been a requirement in Danish elementary schools since 1970 (a year after the country became the world’s first Western nation to legalize pornographic imagery). It's hard to imagine Dillermand sitting well in countries with a more fraught approach to sex, such as the United States, where “we sexualize everything,” Hilary Reno, a sexual-health expert at Washington University in St. Louis, told me. But in Denmark—where people boast of their frisind, a free-spirited, open-minded approach to life—kids begin discussing love, sexuality, relationships, and consent as early as kindergarten, learning while young that their bodies are things to be acknowledged, not repressed. Perhaps in this context, a penis does not have to be a sexual device—especially when viewed through the eyes of a 4-year-old. “It’s a good message for bodies in general,” Kathryn Macapagal, a sexual-health researcher and clinical psychologist at Northwestern University, told me. “Your body gets you into trouble, but it can also do lots of amazing things.” Dillermand himself learns this lesson: After trying to barter his penis away at a flea market, he ultimately accepts and embraces his misbehaving pecker, hijinks and all. Yet despite its candy striping, John Dillermand’s penis is, in the end, still a penis. The diller acts as if morally bankrupt; it is recklessness incarnate. It threatens, perhaps even overtly, to absolve men of responsibility. “To me, this penis is out of control,” Crehan said. Despite its lighthearted tone, John Dillermand—a show about men, dreamed up by men—reinforces the bottom line about male sexuality: It’s so uncontrollable, it can demand its own television series. Some of the trouble can be traced back to the pure creep factor of the main character. Dillermand, despite his apparent age, is jobless and friendless. He piddles the day away on the front lawn, playing pranks or practicing badminton with his only willing athletic partner, who is—surprise!—his own penis. While Oldemor urges him to rub elbows with doctors and lawyers, Dillermand manages to befriend only a lonely young boy, with whom he filches candy from a shop. And Dillermand himself is not completely sexless. In one episode, he nurses an obvious crush on his thankfully age-appropriate neighbor Yvonne. His penis, by and large, behaves itself. But the character’s desires evoke the discomfiting possibility of an unwelcome advance nonetheless. Groes, the gender scholar, worries that the diller’s presence is so commanding that it actually distracts from the rest of the show’s content. When Groes’s 8-year-old son watched the show, “he didn’t get it,” Groes told me. “Because the attention was on something else, which was funnier, stranger, and weirder.” At its worst, Dillermand, inadvertently or not, threatens to reinforce the same “locker-room tendencies” the Western world has hoped to move away from, Groes told me. “It’s probably the most classic stereotype you can come up with: a man having certain abilities because he has a big penis.” Dillermand’s life revolves around the power of his appendage. The show ultimately glorifies the consequences of an uninhibited penis, rather than grappling with them. Dillermand’s predicament, Groes said, is a “classic macho claim: ‘I can’t control my penis.’” DR, the company behind the show, has argued that Dillermand and his penis could have "easily" been swapped out for a female-bodied character. And yet, on one point, every person I spoke with agreed: Reimagined with a biologically female lead, John Dillermand would not have worked. Even in Denmark, vaginas and vulvas aren’t considered innocent or endearing enough to delight young minds. Diller jokes are embedded in the cultural zeitgeist; the word itself is emblematic of contrarian playfulness and parody. But the Danes I talked with told me that the impish female counterpart of the word diller does not exist. “There is still shame with talking about women’s genitalia in public spaces,” Crehan said. An especially large vagina might be labeled as a signal of looseness and corruption—a dangerous “weapon” used to exert undue influence over others. The idea of a massive, magical vulva taking the place of Dillermand’s penis is difficult to even envision. In the days after the show premiered, the Danish internet overflowed with memes flaunting female versions of Dillermand, some sporting the appropriately gigantic genital accoutrement, or a tangle of unspooling breasts. But “would people receive it the same way with a vulva or vagina reaching out to grab a kid’s ice-cream cone? I don’t think so,” Macapagal told me. From there, the possibilities start to spiral: Would Carol’s clitoris have been celebrated for taming a lion? Would audiences have laughed to see Vicky’s vulva stabbed, smashed, or electrocuted? This imbalance is a reminder of the dominance of masculinity, Groes said. Although the sexuality of the penis can be toggled on and off, female genitalia occupy a cultural space with decidedly less dynamic range. The sexuality of women is still taboo enough that it is most easily ignored; when it is offered a modest fraction of the spotlight typically reserved for men, it is excoriated for its audacity. While the nuanced lore of the penis thrives, female genitals are struggling to shed their “hypersexualized” identity, says Rachel Hardeman, a reproductive-health-equity researcher at the University of Minnesota. In John Dillermand, the female presence is so starkly absent that one cannot help but confront the reasons it has been erased. The show isn’t uncomfortable because it’s so radical to make a children’s series about a penis, but because it’s decidedly not. from https://ift.tt/3ktRIz7 Check out http://natthash.tumblr.com
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Editor’s Note: The Atlantic is making vital coverage of the coronavirus available to all readers. Find the collection here. Every day, more than 1 million American deltoids are being loaded with a vaccine. The ensuing immune response has proved to be extremely effective—essentially perfect—at preventing severe cases of COVID-19. And now, with yet another highly effective vaccine on the verge of approval, that pace should further accelerate in the weeks to come. This is creating a legion of people who no longer need to fear getting sick, and are desperate to return to “normal” life. Yet the messaging on whether they might still carry and spread the disease—and thus whether it’s really safe for them to resume their unmasked, un-distanced lives—has been oblique. Anthony Fauci said last week on CNN that “it is conceivable, maybe likely,” that vaccinated people can get infected with the coronavirus and then spread it to someone else, and that more will be known about this likelihood “in some time, as we do some follow-up studies.” CDC Director Rochelle Walensky had been no more definitive on Meet the Press a few days before, where she told the host, “We don’t have a lot of data yet to inform exactly the question that you’re asking.” At this point in the pandemic, with deliverance in sight for so many people, the vagueness can justifiably be maddening. For a year now, the public-health message has been to wait. First we waited until it was safe to go outside. Then we waited for vaccines to be developed, tested, and approved. Now people are being asked to wait their turn to get vaccinated; then to wait a few more weeks until they’ve received their second dose; and then two weeks more to make sure that their immune responses have fully kicked in. And finally, when all that waiting is done, we’re supposed to wait for “some time” more? The experts urging patience are, of course, correct. There are myriad details of physiology and molecular immunology that remain to be understood, and we do not know how quickly transmission rates will drop as large numbers of people get vaccinated. At an individual level, though, the proper advice on what constitutes safe behavior does not depend on any scientific study whose results are pending. It depends on what’s happening in the world around us. As you’ve heard ad nauseam by now, the SARS-CoV-2 vaccines were developed at record speed. They were created in the heat of an emergency, while thousands of people were dying every day, as a way to stop the carnage. They are proving remarkably effective at this. The vaccines were never expected to block infection by the virus altogether, explains Stephen Thomas, the chief of the infectious-disease division at SUNY Upstate and the coordinating principal investigator for the Phase 3 Pfizer-BioNTech vaccine clinical trial. “I don’t really think that’s feasible or plausible,” he told me. Most vaccines work by training the body to prevent a virus from replicating to such a degree that a person gets sick. They don’t typically prevent a person from getting infected; they simply make that infection less consequential, and enable the body to clear it more quickly. If a vaccine could reliably prevent future infections from ever taking hold, it would provide what’s known as “sterilizing immunity,” Syra Madad, an epidemiologist at NYC Health + Hospitals, told me. This is an uncommon occurrence. The measles vaccine is often cited as an exception, but she says that there is no reason to expect the COVID-19 vaccines to fall into this rare category. Indeed, there is no obvious mechanism by which they could. “To generate sterilizing immunity in a mucosal space using a vaccine that’s injected into your muscle is extremely difficult,” Angela Rasmussen, a virologist at Georgetown University, told me. She said that early evidence in rhesus macaques has suggested that the AstraZeneca vaccine could provide sterilizing protection, but only when administered as a nasal spray. Other researchers have begun to work on nasally delivered vaccines that could theoretically serve to coat our mucous membranes with antiviral armor, though there is no certainty that this approach would be effective at preventing severe disease. So it’s safe to assume that the current batch of COVID-19 vaccines won’t stop viral transmission outright. But it’s also safe to assume that they will reduce that transmission to some extent, because they impede viral replication. “It is highly plausible that a vaccine that prevents disease by lowering the amount of virus in a person could also lower that person’s ability to infect others through the same mechanism,” Thomas said. The tricky part is determining the degree to which this happens. “No definitive clinical trial can give you this evidence,” Rasmussen said. The trials were really designed for speed and safety, so the researchers were most concerned with looking for symptomatic COVID-19 or adverse reactions, not asymptomatic infections. To know how often vaccinated people were asymptomatically carrying the virus, researchers would have had to test each of the tens of thousands of people in their clinical trials as frequently as possible. Some ongoing trials have taken to swabbing the noses of vaccinated people occasionally, and this could add insight into how common it is for people to carry the virus after vaccination. Early evidence from Johnson & Johnson’s clinical trial, for example, suggests a significant reduction in transmission after vaccination, though this remains to be verified. Still, occasional testing is bound to miss cases of infection, and finding some virus in some noses doesn’t tell us how infectious the owners of those noses might be—or whether they’re infectious at all. The only way to answer this question for certain would be to run a “challenge” trial in which vaccinated and unvaccinated people were deliberately exposed to the virus under similar conditions, and then tested to see what percentage of them got infected. That’s just step one. Then the vaccinated-but-infected people would need to hang out with a bunch of unvaccinated people to see if they got infected, and at what rate. This is not going to happen. Challenge trials are ethical minefields in normal times; at this point, any study that involves withholding a vaccine from a control group would be difficult to justify. More trial data are expected over the next few months, and these may help narrow our uncertainty. It would certainly be useful to get a better sense of whether the risk of catching COVID-19 from your grandmother, for example, drops by something like 90 percent once she’s vaccinated, or whether it’s closer to 10 percent—but that number isn’t going to be exact, and it won’t be static, either. Even if we could somehow run the sort of challenge trial described above, whatever value it produced could change as new variants of the virus take hold, and it might well vary across regions with different patterns of prior infection, behavioral norms, local weather, and other variables we don’t even know to look for. All of this is academic. Whatever trial data might arrive in the coming months won’t change the practical advice: As long as a lot of virus is still circulating in a community and many people remain unvaccinated, the mere fact that some have protection will not mean that it’s responsible for them to forgo precautions and do whatever they like. A different kind of data, though, will offer that reassurance and certainty. This is what we’re really waiting on. “We will absolutely get to a point when we can say that vaccinated people don’t need to wear masks,” Madad said, but that will be driven largely by changes in the number of cases, and in the vaccination rate. The sooner we can drive the former down and the latter up, the sooner normalcy returns. As populations draw closer to herd immunity, the chance of a vaccinated person both carrying the virus and coming into close contact with a nonimmune person will become so low that the guidelines will change. But as long as the virus remains omnipresent, the risk of getting infected (and transmitting) the virus after being vaccinated remains too high to countenance. This message need not be seen as pessimistic or ambiguous. It tells us very clearly that our social lives can resume, but only when the whole community is ready. The turning point does not arrive for individuals, one by one, as soon as they’ve been vaccinated; it comes for all of us at once, when a population becomes immune. How quickly this occurs depends on how reliably those vaccines reduce transmission. But it will primarily be a function of how quickly people get access to vaccines, how much immunity already exists in a population, and how much attention is given to basic preventive measures that should never go away, such as well-ventilated workspaces and responsible sick-leave policies. Much of this is in our hands now. We are not waiting on a clinical study; we are waiting on one another. from https://ift.tt/3bLwsRJ Check out http://natthash.tumblr.com The call came in at 7:42:02 p.m. on March 21, 2019. A man in his early 60s had just sat down to dinner with his daughter and her boyfriend at an otherwise empty North Brooklyn restaurant, when he suddenly slumped in his chair. The daughter shouted at a hostess to call 911. Within seconds—by precisely 7:42:16, according to my review of the incident—a New York City Fire Department emergency-response unit had acknowledged the assignment, and would arrive on the scene some two and a half minutes later. In the meantime, a dispatcher stayed on the line. “Is this for you, or someone else?” the dispatcher asked the hostess. “For someone else,” the hostess replied. “Is the person breathing?” the dispatcher asked. Confusion. Was the man having a seizure? Before long, it was established that he was not seizing and was unconscious. He had no discernible pulse. The dispatcher instructed the daughter and boyfriend, both in their 30s, to ease the man down to the hardwood floor, belly-up, and expose his chest. The event was one of the more than 350,000 out-of-hospital cardiac arrests that occur annually in the United States. They are a leading cause of death, and only about one in 10 victims survives. Without early 911 access and cardiopulmonary resuscitation (CPR)—the first two links, followed by early defibrillation, in the out-of-hospital “chain of survival”—death is certain. Over-the-phone CPR instruction by a dispatcher, also known as telephone CPR or T-CPR, can enable a caller to become a lay rescuer, and by doing so make the difference between life and death. Early CPR performed by a lay rescuer is associated with a roughly twofold increase in the chances of survival. However, T-CPR is not as widespread as most 911 callers might expect. I would know. The boyfriend in this story? That’s me. The man was my girlfriend’s dad, Todd. For him to have a shot at survival, either my partner or I would need to intervene. I was about to perform CPR on my future father-in-law. Many dispatchers are trained to recognize signs of cardiac arrest from an oral description and then direct callers to begin CPR—even callers who might be in shock, as my partner and I were. But there is no universal requirement for dispatchers to do this. Few of the dispatch centers that have implemented T-CPR protocols deliver instructions consistently, and fewer still have strict quality-improvement measures in place. On the night of Todd’s cardiac arrest, I was fortunate that my hands were guided by the right dispatcher. According to Robert Fazzino, a paramedic and the FDNY medical-affairs representative who procured our incident report, the hostess handed the cordless phone to my partner, Lex, who then handed it to me. Kneeling over Todd’s tensed body, I wedged the receiver between my right ear and shoulder. The dispatcher told me to interlock my hands—one atop the other, at the midpoint of the nipple line—and get ready to start pumping up and down, hard and fast. The clock was ticking. This wasn’t the first time I’d been involved in an emergency that required CPR. When I was a teenage pool lifeguard, a 74-year-old swimmer fell unconscious one summer afternoon. After I pulled her out of the water, five other guards and I performed CPR on her for several long minutes until paramedics arrived. She died days later. Now here I was again, face-to-face with someone clinging to life—only this time, it was a loved one, and my training was rusty. In my lifeguarding days, I was regularly drilled on the CPR procedures for infants, children, and adults. Was it 15 compressions to two breaths for an adult? Or 30 to two? I was blanking. “What are the ratios?” I blurted out. The dispatcher, realizing I was at least somewhat CPR conversant, seized the moment. No breaths necessary, he said. “Just stay on my count.” That’s exactly what I did, according to the call audio. I counted aloud with the dispatcher, using my upper-body weight to press down on Todd’s sternum, before releasing: down and release, down and release. One and two and three and four and five and six … Time slowed. I closed my eyes. Don’t stop, I thought. After what felt like an eternity, I heard sirens approaching. “The public assumes that if they call 911 and someone’s in cardiac arrest that they’re going to get [CPR] instructions,” says Michael Kurz, a University of Alabama cardiologist and the volunteer chair of the American Heart Association’s T-CPR Task Force. “That’s not the case. It is the minority of cardiac arrests that receive that instruction.” If I’ve learned anything in the weeks and months I’ve spent reconstructing the events of that evening, and researching the availability of T-CPR nationwide, it’s that we were very, very lucky. Dial 911 to report a cardiac arrest, and depending on where you are—a big city, a rural town, or somewhere in between—you may be told to wait until help arrives, to stand idle as your loved one’s fate hangs in the balance. Why didn't that happen to us? One day in August 1974, a panicked mother called the fire department in Phoenix, Arizona. A dispatcher listened as the woman explained that she and her husband had just pulled their 2-year-old son from the family swimming pool, and that the toddler was turning purple. “He’s not breathing!” she shouted. “I want you to stay on the line,” the dispatcher said, noting the caller’s address. “I have a medic that is going to give you some help while I send someone.” The phone was passed to a department paramedic, Bill Toon, who had just clocked in. As Toon wrote in Principles of Emergency Medical Dispatch years later, the department’s single paramedic unit was far enough away that the odds of it arriving in time to help were slim. “The dispatchers had little or no training in this area at this point in time,” he added. Toon took it upon himself to assist the family until the paramedic unit arrived. “I began to give the caller a crash course in CPR because the only real chance the child had of surviving was with his family doing the saving,” Toon wrote. After about a minute of over-the-phone instructions, Toon heard the toddler start to cry—a relief, because if he could cry, he could breathe. “That was a pretty sweet sound for everyone involved,” Toon recalled. The three-minute, eight-second call was a signal moment in the emerging field of pre-arrival instruction and T-CPR. Toon’s ad hoc actions were remarkable because T-CPR protocols did not yet exist, making the episode’s recording an instant historical artifact. As Audrey Fraizer wrote in The Journal of Emergency Dispatch in 2019, word of the event made the national rounds and, as she later told me, helped in the push to standardize care in emergency dispatching. By the early 1980s, the emergency medical system in King County, Washington, had become the first to implement a T-CPR script for dispatchers fielding cardiac-arrest calls. In the time since, T-CPR’s spread has been significant, albeit somewhat haphazard. A 2015 evidence review conducted by the American Heart Association suggested that, despite “rapid and widespread adoption,” dispatcher CPR instruction “does not lead to more successful resuscitations or improved survival.” But in Arizona, the birthplace of the practice, out-of-hospital cardiac-arrest victims who were provided with T-CPR were almost 65 percent more likely to survive than those who didn’t receive T-CPR, according to a February 2020 AHA T-CPR policy statement. Those who survived were also far less likely to have suffered brain damage. Eight states—Indiana, Kentucky, Louisiana, Maryland, Tennessee, Virginia, West Virginia, and Wisconsin—currently require emergency dispatchers to provide T-CPR. But other states and jurisdictions—Arizona and New York among them—do not. The dispatchers in these states, says April Heinze of the National Emergency Number Association (NENA), a nonprofit that works to standardize 911 services, are going to send help, but until the ambulance arrives they may not be able to assist callers much. To be sure, about one-third of the emergency dispatch centers in the U.S.—approximately 2,000—provide some sort of medical advice via telephone, helping bystanders assist someone who is choking, seizing, or even giving birth. Of those, “many do so without being required by law,” Heinze told me last spring. In her home state of Michigan, she added, more than 70 percent of dispatch centers provide these services, despite no mandate to do so. “Many others probably also do telephone CPR just because they know that’s the right thing to do,” Heinze, a former longtime 911 dispatcher, said. Only recently has there been a proper drive, spearheaded largely by the AHA, to integrate T-CPR into the national 911 system, which itself dates back to only the late 1960s. “The push for telephone CPR just happened within the last year or two,” Heinze told me. “Legislation is very slow. It doesn’t happen overnight.” That at least eight states have T-CPR-specific legislation on the books, well, “I think that’s actually pretty good, to be honest with you.” Still, nearly 50 years since Bill Toon’s impromptu T-CPR guidance, fewer than half of those who experience cardiac arrest outside of a hospital in America receive bystander CPR. Lay-rescuer rates are especially low in minority communities, due to both a lower overall availability of T-CPR and a widespread fear that involvement with a 911 call will lead to encounters with police or immigration authorities. The main obstacle to scaling up T-CPR, however, remains the patchwork nature of 911 itself. Though the national system is coordinated by the Federal Communications Commission, 32 states have adopted “home rule,” meaning that 911 and other services fall under local or regional control. As a result, implementing universal, consistent T-CPR programs is slowed by funding and staffing shortages and communication problems. The AHA has argued that T-CPR is overwhelmingly cost-effective compared with other measures designed to reduce the time to first chest compression. Yet states and localities have limited budgets for new emergency-services initiatives. And 911 dispatchers, who are in short supply nationwide, were overburdened even before the start of the coronavirus pandemic. They are at the crux of a tightly choreographed feat of adrenaline, transportation, and communication; a high-stress job performed on marathon shifts, with varying degrees of training, and for low pay. Given the existing demands on dispatchers, who are disproportionately women, some are understandably wary of being held accountable for negative outcomes. “If anything goes wrong,” Heinze said, “the liability then falls more on the dispatcher than it does on the organization.” Complicating matters is the fact that none of the nearly 6,000 emergency dispatch centers in the U.S. operates in exactly the same way. So when a 911 call from one area is routed to a dispatch center in the next town over—a not-uncommon occurrence—a caller may be transferred from a dispatcher trained in T-CPR to one who is not. And by the time responders arrive, it could be too late for someone like Todd in the throes of cardiac arrest. Even when a bystander is lucky enough to connect with the right dispatcher, there are many points when things can go wrong. The reality is that not all bystanders can or will act. Some simply aren’t physically capable of doing so. CPR requires two hands and has been compared to shoveling snow or walking through sand; one must push down 2.5 inches on the victim’s chest 100 to 120 times a minute in order to generate enough cardiac output. “It’s very tiring,” Fazzino, the FDNY liaison, explained. Others might be concerned about infection risk, a worry inflamed by the coronavirus pandemic. Still others might be hesitant to perform CPR for fear of inadvertently causing physical harm, or of interfering with what they believe fate has decided for the victim. To avoid these pitfalls in the course of T-CPR, dispatchers such as Adolfo Bonafoux don’t ask many questions once they’ve established that someone is calling on behalf of a person who is not breathing. “I will tell you what to do,” says Bonafoux, who fields emergency medical calls at the heavily fortified, Bronx-based PSAC II, one of New York City’s two public-safety answering centers. By not asking questions or for a caller’s permission, “it takes the option away from you,” Bonafoux explained to me. “You’re more willing to act and follow my direction. Because if I give you the choice, you’re gonna stop and think. You’re gonna start to weigh all the variables. And that time is very valuable.” Bonafoux is a former U.S. Army medic with 20 years of emergency-medical-service experience. He joined the FDNY in 2007, first as a paramedic and then, after being injured in the field, as a dispatcher. (He has formal training in, among other things, T-CPR protocols, a requirement instituted by the department’s medical directors.) Technically, he’s what’s known as an ARD, or assignment-receiving dispatcher. He isn’t the first person a caller talks to—that would be a police dispatcher, who discerns whether the caller needs to speak with the police, the fire department, or emergency medical services, and notes the caller’s location. Bonafoux receives the medical calls transferred from that police dispatcher, and handles the pre-arrival medical portion of the relay. “My philosophy is if you’re not willing to do it, you’re going to stop me,” Bonafoux said. “Obviously I can’t force anybody over the phone to do anything. So I take an aggressive stance. A lot of times people, in a pressure situation, they’ll just do. They won’t hesitate, they won’t think about it, they’ll just do.” Following Todd’s accident, I suspected that simply asking “What are the ratios?” had indicated to our dispatcher that I was familiar with CPR. And because of that baseline, it didn’t take much to get me to go. Bonafoux later confirmed that hunch. He was the voice on the other end of the line, who walked us out of the depths of what Lex and I have taken to calling the Bad Night. “Muscle memory,” he said. “Once you have done it before, you remember it. Your brain starts remembering it. Your body remembers how to do it. That all contributed to the success of your father-in-law.” The first responders, a paramedic team, arrived on the scene at 7:44:55 p.m., followed by the engine company, an FDNY lieutenant, and basic and advanced life-support units. “From the time that the call comes in to the time that somebody is actually standing there, a professional provider, is [about] four minutes,” Fazzino told me over the phone, as he paged through our case file. The “real magic,” he said, is in that response time. I remember a paramedic from the first unit crouching beside me, slinging a life-support bag off her shoulder and asking how long I’d been going at it, before relieving me. “Would you have guessed that was, you know, two and a half minutes of CPR you did?” Fazzino asked. “You get that serious fight-or-flight adrenaline rush. Your sense is enhanced. It becomes very surreal.” What felt like an eternity was really 150 seconds. By 8 p.m., Todd had been shocked seven times with a portable defibrillator—typical, Fazzino said, for ventricular fibrillation, the kind of electrical disturbance of the heart that Todd experienced. Responders, now numbering at least a half-dozen, ran Todd’s electrocardiogram. That included the multiple defibrillation attempts, medications administered, and intubation. Start to finish, the event clocked in at about 35 minutes, on par for this type of resuscitative effort in the field. Total call duration, including the T-CPR? Six minutes. By 8:20 p.m., Todd was loaded into an ambulance. Lex and I got into a second ambulance, which followed closely as our caravan sped toward NYU Langone, the nearest hospital, about 10 minutes away. Port Authority officials temporarily halted Queens-Midtown tunnel traffic to allow us to slip through. I remember the lights streaking past our windows. Todd was shocked an eighth time after being reeled into the emergency room. A long night was still ahead of us. But he now had a pulse—a testament to the help we’d gotten in those crucial first moments. Without T-CPR, “God forbid, what could have happened to your father-in-law?” asked Democratic Representative Norma Torres of California. “You wouldn’t have had somebody talking you through that.” Torres, a former 911 operator in Los Angeles, is the lead sponsor of the 911 SAVES Act, a bipartisan bill that aims to reclassify 911 operators and other public-safety telecommunicators as “protective service occupations” under the Office of Management and Budget’s Standard Occupational Classification System. As it stands, dispatchers like Bonafoux are classified more as office secretaries. Torres wants to change that federal labor designation—with no disrespect to secretarial workers, she said—to encourage states to recognize dispatchers as crucial workers, recognition that in some states could exempt them from government furlough. Without dispatchers, Torres said, “we can’t get the help that we need.” A recently formed NENA-AHA working group, meanwhile, is focused on further standardizing T-CPR. (The AHA, for its part, has also launched Don’t Die of Doubt, a campaign to address the “alarming drop” since the start of the pandemic in 911 calls and ER visits by people needing urgent medical care after a stroke or heart attack.) But it would seem that scaling up T-CPR is as much about recognizing and supporting dispatchers as it is training lay people in CPR, something Lex and I have undertaken in the aftermath of our experience. Here’s what I do know: The FDNY location from which the responding units were dispatched, is mere blocks from the restaurant. NYU Langone happens to be one of the country’s top cardiac-care hospitals, too. Not only did I have the advantages of previous CPR training and Bonafoux’s experienced help, but we were in the right place at the right moment. Both luck and privilege—our well-appointed location, my previous training—were on my family’s side. But the further I dig into the night of March 21, 2019, the clearer it becomes that I won’t ever be able to fully account for what transpired. I’d been on the fence about joining Lex and Todd for dinner, but made the last-minute decision to go. What if I hadn’t? It’s also entirely possible that, had Lex not immediately cried out for someone to call 911, kick-starting the “chain of survival,” this story would have a much different finale. I asked Fazzino how many out-of-hospital cardiac arrests were reported in New York City in 2019, and of those patients, how many survived until either emergency services arrived or they reached a hospital. He couldn’t say for sure, but noted that the “vast majority” of patients behind such emergency requests that come into the city’s two call centers ultimately do not make it. Of the minority of people who do survive, how many of them get to go home? That number, Fazzino said, is even smaller. Todd did what many people have not, “which is to cross the line and then come back to tell the story about it.” The first night at the hospital, Todd was put into therapeutic hypothermia—“on ice,” the doctors called it—in an attempt to redirect blood from the rest of his body to his brain. We were told he would stay in this medically induced coma for up to 72 hours. The next morning, less than 18 hours after his heart gave out, he woke up on his own. I can still see the look of surprise and excitement on the attending nurse’s face. “Who did the bystander CPR?” one of his doctors asked. Lex pointed at me. “Well done.” The following evening, in a quiet moment in a hospital lounge, Lex and I decided to get married. Todd was able to come to the wedding, three months later. “By the way,” he said, shortly before being discharged. “Thanks.” from https://ift.tt/3qZTHOd Check out http://natthash.tumblr.com Editor’s Note: The Atlantic is making vital coverage of the coronavirus available to all readers. Find the collection here. All major indicators of COVID-19 transmission in the United States continued to fall this week. Nationally, cases have been falling for six weeks, hospitalizations have been dropping sharply for five weeks, and deaths have been declining for four weeks. The average number of people in the hospital with COVID-19 this week was just under the average we saw during the high points of the April and July hospitalization surges. States and territories reported 14,463 COVID-19 deaths in the past seven days, the first weekly total under 15,000 we’ve seen so far in 2021. The decline in cases and deaths appears to have slowed this week. After so many weeks of very rapid improvements in reported cases and deaths, a slowing of those declines was inevitable. But we don’t think that a true plateau is the only or even likeliest explanation for what we’re seeing this week. Instead, we think we’re once again seeing the equivalent of a holiday-reporting effect. Two confounding events that occurred last week—Presidents’ Day and the beginning of a major winter storm that knocked out power for millions of Americans—resulted in slowdowns in case reporting. As we’ve seen with other holidays and storms, these kinds of disruptions produce a predictable series of reporting artifacts: first an artificial drop, then an artificial rise. We should always look for confounding factors before interpreting the data as suggesting a change in the direction of the pandemic—and in this week’s data, we found them. Artificially low numbers from last week’s disruptions make this week’s case and death declines look smaller by contrast, and make the daily numbers look as though they’re reversing direction, especially as backlogs roll in. The death-reporting process was also affected by the federal holiday and the storm, producing similar artifacts in the data. Even hospitalization numbers appear to have wobbled in a similar way, probably as a result of both small reductions in reporting and small reductions in the number of people who sought care at hospitals over the three-day weekend and during major regional storms. [Read: A simple rule of thumb for knowing when the pandemic is over] We’ve also seen large numbers of deaths from much earlier periods reported this month, including a backlog of more than 1,500 deaths in Indiana reported on February 4, nearly 4,500 old but previously unreported deaths in Ohio reported from February 11 to 13, plus a smaller addition of deaths in Virginia (total size still unknown), which the state notes is due to processing death certificates from the postholiday (January) surge. This brings us to a crucial point that news summaries frequently get wrong: The deaths that states and territories report on a given day do not represent people who died on that day. Reported deaths lag behind cases by two to three weeks on average, and many reported deaths actually took place substantially earlier. When reported cases rose during previous surges, deaths lagged weeks behind. The same is true now, as cases decline. Why this matters: We have every reason to believe that far fewer people actually died of COVID-19 this week than in previous weeks, because cases and hospitalizations continue to drop. But we won’t see those smaller death numbers for weeks to come—probably for more than two or three weeks, as previously overwhelmed public-health officials are able to catch up on processing death certificates. The backlogs in reported deaths have also affected our numbers for nursing homes and other long-term-care facilities: Indiana added 659 historical resident deaths and one staff death to its cumulative total for the week ending February 17, and Ohio added 1,150 historical resident deaths. We can chart a national trajectory of deaths in long-term-care facilities despite these and other recent large additions by working with the data from the 52 jurisdictions that have not included major backlogs or reassignments in recent months. The resulting visualization is an incomplete representation of deaths in LTC facilities in absolute numbers, but it allows us to understand the national trend: Weekly deaths in long-term-care facilities continue to decline. If we view deaths in long-term-care facilities in these 52 jurisdictions as a share of COVID-19 deaths in the U.S., we see that the percentage of the country’s COVID-19 deaths that are occurring in these facilities also continues to decline. The New York Times also recently analyzed trends in nursing-home cases and deaths in relation to national case and death figures. [Read: The last days of loneliness ] When our project ceases data compilation on March 7, the only comparable, public federal data set will be the CDC/Centers for Medicare and Medicaid Services data set on COVID-19—which is only partially comparable, as it includes only nursing homes and not other long-term-care facilities, such as assisted-living and independent-living facilities. These nursing-home data have been reported weekly by facilities to CMS since May 17 through the CDC’s National Healthcare Safety Network. Cases and deaths are reported as cumulative and weekly totals, and some facilities include cumulative data dating back to January 1, 2020. We’ll be writing more about that in next week’s additions to our series of trainings on federal COVID-19 data. Although COVID-19 has disproportionately harmed Black, Latino, and Indigenous people in many areas of the U.S., it appears that vaccinations are not being proportionately administered to many of these communities. The Verge visualized vaccine administration in Chicago, New York City, and Washington, D.C., and found substantial mismatches between areas with the highest case or death rates and areas with the highest vaccine administration. A Los Angeles Times investigation likewise found that the areas hardest hit by COVID-19 in and around Los Angeles currently have the lowest vaccination rates. Inequities in vaccine distribution and administration result from many factors, including inaccessible systems, state-level decisions, fixed age cutoffs, and problems with people actively circumventing the processes established. Federal vaccine data include race and ethnicity for slightly more than half of all reported doses, but aren’t broken down by state and don’t allow for crucial age-race cross-comparison. Data from the 40 states that publicly report race and ethnicity data for vaccinations, compiled by KFF and others, track vaccinations by race and ethnicity, but most states do not include age breakdowns, and some are missing race and ethnicity data for more than 30 percent of vaccinations. Reporting at the metro level and rough analysis within states have given us plentiful warning that vaccine rollouts are currently missing many of the communities at the greatest risk from COVID-19. Without better data about who has been vaccinated across all U.S. jurisdictions, we will not be able to identify and address the full range of inequities in the rollout. Mandy Brown, Artis Curiskis, Alice Goldfarb, Erin Kissane, Kara Oehler, Jessica Malaty Rivera, and Peter Walker contributed to this report. from https://ift.tt/3bDQNbE Check out http://natthash.tumblr.com On this episode of the podcast Social Distance, listeners with mild COVID-19 cases call in with their questions. James Hamblin explains why he thinks the summer could be wonderful. And Maeve Higgins shares nun news from Ireland. Listen to their conversation here: Subscribe to Social Distance to receive new episodes as soon as they’re published. What follows is a transcript of the episode, edited and condensed for clarity: Maeve Higgins: I’ve been dying to tell you about the latest Irish news. Ireland is under pretty severe lockdown at the moment. You’re not allowed to move from county to county. But some nuns put this video online of them performing an exorcism in Dublin, and they’re not from Dublin. James Hamblin: Oh, and you’re not allowed to … do exorcisms outside of your locality? Higgins: I mean, you’re allowed to, but you’re just not allowed to break COVID guidelines to go and do an exorcism. Hamblin: What happened to them? Are they in trouble? Higgins: Nothing’s happened to them. The government was already keeping an eye on them. It’s just these two nuns. They’re in a group called the Carmelite Sisters of the Holy Face of Jesus. And they got in trouble just before the Christmas holidays too, because they were selling potions online, so the nuns were, like, known to the authorities and then they broke the COVID rules and came and did an exorcism. Hamblin: Speaking of religion and COVID, when we talk about people forgoing vaccines, religious exemptions have been a huge thing here in the United States for kids going to school unvaccinated. I’m foreseeing some pretty big debates in the coming months and maybe years about requirements for vaccination and religious beliefs. There’s going to be a lot to unpack there. Higgins: There is. And Jim, I read your piece about how a COVID-vaccinated summer could be wonderful. And I want to ask you about population-level immunity. You wrote that “no other country has endured so much death and illness. But for all the failures that led to this point, the U.S. does finally seem to be experiencing some protective effects of population-level immunity.” Could you tell me more about that? Hamblin: The numbers in the U.S. look really promising. Cases are going down really quickly and deaths are plummeting because, among those cases, the high-risk people are being vaccinated or have been vaccinated. Add to that the effects of places that have already been hit really hard, where the virus seemed to be kind of burning out, at least temporarily, on its own. And you’ve got warm weather on the horizon where people could be outside. It’s a coalescing moment, and I don’t know that it’ll last, but things are looking really promising for the summer. And I’ve been trying to deal with how you genuinely let yourself be pulled forward by the hope and joy in being able to do things that we couldn’t do for a long time, while not getting complacent and declaring things “over” or repeating the same mistakes we’ve been making for the last year. Higgins: So many people are still catching and experiencing COVID. And we get so many brilliant messages from listeners, so I thought it could be really fun to hear from them today. Hamblin: Yeah, that would be great. Honestly, the voicemails we get are my favorite part of this whole podcast. Higgins: The first caller is a 68-year-old in central Pennsylvania. His name is Patrick. And he recently got a mild COVID case and wanted to talk about his immunity—and if and when he needs to schedule a vaccination appointment. Hamblin: Hello, Patrick. How are you feeling? Patrick: Not too bad, actually. I had a fairly mild run of this, and the only symptom left over is sort of a foggy-headed lightness. I can give you a pretty concise timeline [of my illness]. In the vaccine rollout here in this area, my wife was entitled to a first shot. She got her first Moderna shot on January 23 and showed her first symptoms of COVID on the 29th. On the 31st, she tested positive and went through a 10-day period where she had mild symptoms. I tested twice negative during that period. On the 13th of February, I started showing symptoms and tested positive on the 14th. Higgins: You tested positive on Valentine’s Day? Patrick: I did. Higgins: And you got it from your wife? Patrick: (Laughs.) I did. Higgins: Patrick, I’m sorry. What a gift. Hamblin: Well, I’m glad you’re both doing okay now. I hope things continue to improve for you. And so you’re specifically wondering about vaccination now, after having gone through this? Patrick: Yes. For both of us. My wife’s already had her first shot. She’s due for her second. Should she get it? And I actually have an appointment scheduled for March 3 that I haven’t canceled yet. And I’ve heard several things from primary-care doctors. And I’m just curious to see what your take is. Hamblin: Well, I never want to contradict anyone’s own doctor, because everyone has unique considerations. What’s the gist of what you’re hearing? Patrick: [That I should wait] three months. And the reason given to me is: “because you would have the immunity, and that is the current guideline.” So at least part of that answer has to do with current distribution protocol, I suppose. Hamblin: So with a lot of diseases, you don’t want to get vaccinated right after you’ve had it, because there can be an increased rate of side effects. If you already have high levels of this acute immune reaction going on, and then you get vaccinated, your body could react more strongly than it would otherwise. We don’t know a lot yet about how that would work with this vaccine, because it’s so new, and I think it’s very reasonable to wait that amount of time. I doubt that it would be a high-risk thing to go ahead and get it. But I also would expect that you have enough protection, having just been sick, that it would be almost impossible for you to get a serious bout of COVID in that time. You are protected, essentially, at least from severe disease. So I don’t think you can go wrong by waiting that period. I certainly wouldn’t wait a year. I wouldn’t expect the immunity that you’re going to have after this infection lasts extremely long or is going to be 100 percent. We’re not seeing people have reinfection cases really shortly after being sick, so I think that should be reassuring. Patrick: What about my wife’s case of getting a second shot? Hamblin: People seem to be pretty well protected after the first dose. The second dose is yet another exposure to this spike protein, which you just naturally got. They’re not exactly comparable, but I expect the effect is similar. It’s like your immune system is doing push ups: Is it better if you do 10 or 20? Sure, do 20 if that makes you stronger, but 10 also is nice. I wish I could be more definitive here. And if there were a serious risk in either direction, I would definitely tell you. But I don’t see one. Patrick: Thank you both for doing this. I’ve followed this podcast since the beginning, and it’s been quite helpful. Hamblin: That’s great to hear. It’s been a pleasure to do. And it’s great to hear from you. Higgins: Okay, Jim, now we’re going to hear from Camie in Idaho. Hamblin: Hi, Camie. How are you feeling? Camie: As well as can be expected, I guess, under the circumstances. I definitely don’t have it as bad as many people have had it. So we feel very blessed. My husband was in quarantine for 10 days. I’m actually in quarantine for 21 days because of underlying health conditions. My doctor just wants to be on the very safe side, which I appreciate. And that started me thinking that, when we’re done with this, what does that mean? Should we be just disinfecting when we recover, just like with any cold or flu? How much of this is sticking to surfaces, and what exactly do we have to clean? It made me think also about when the cruise ships came back and they were finding active, live coronavirus weeks and weeks after. Hamblin: Are there other people in your household? Camie: No, it’s just my husband and I, but we have a new grandbaby. We want to go see her, and I don’t want to inadvertently infect her when we go see her eventually. Hamblin: Absolutely. This has been a point of a lot of confusion over the course of the pandemic. I and most other people making recommendations this time last year were much more about surfaces, about hand hygiene, about sterilizing high-touch surfaces. And then, over the course of the year, it’s really turned out that the virus doesn’t linger very long on surfaces. And when it does, it doesn’t seem to happen in infectious doses. You’re just very unlikely to get enough of a viable virus onto your hand after you touch something and then touch your face and infect yourself. There are other infections that certainly work that way. But just because you are able to detect some RNA of that virus on, say, a cruise-ship doorknob or something, that doesn’t mean that someone who touched that would get sick. It’s kind of a fine distinction, but we had to play it safe at the time. So we sort of overestimated that and didn’t pay enough attention to air. It seems like surface transmission can happen from touching something, but it would have to be within a very short period. Say, someone came into your office right after you’ve been working at a desk for eight hours and then for some reason had to put their face onto your desk. Briefly touching a handrail as you went down a staircase and then someone coming by an hour later and using that same handrail—that seems like as close to a zero percent possibility as possible. And so the time period in which the virus is persisting on surfaces at all is short enough that once you and your husband are clear of needing to quarantine, the surfaces in your house should not be expected to contain any lingering virus. Camie: Should we stay away from the grandbaby, even after my 21 days of quarantining? Hamblin: If you’re going to see people, stay outdoors, wear a mask, don’t have prolonged close contact unless this person is in your tight bubble and you’re all being really vigilant. But no, there’s no reason to expect that you’re at any increased risk of infecting other people in that period. Higgins: Camie, thanks so much. And I hope you just feel 100 percent really soon. Camie: Thank you so much. I so appreciate your help. Wonderful to talk with you. from https://ift.tt/3koPBg8 Check out http://natthash.tumblr.com The past 11 months have been a crash course in a million concepts that you probably wish you knew a whole lot less about. Particle filtration. Ventilation. Epidemiological variables. And, perhaps above all else, interdependence. In forming quarantine bubbles, in donning protective gear just to buy groceries, in boiling our days down to only our most essential interactions, people around the world have been shown exactly how linked their lives and health are. Now, as COVID-19 vaccines rewrite the rules of pandemic life once more, we are due for a new lesson in how each person’s well-being is inextricably tangled with others’. This odd (and hopefully brief) chapter in which some Americans are fully vaccinated, but not enough of us to shield the wider population against the coronavirus’s spread, brings with it a whole new set of practical and ethical questions. If I’m vaccinated, can I travel freely? Can two vaccinated people from different households eat lunch together? If your parents are vaccinated but you’re not, can you see them inside? What if only one of them got both shots? What if one of them is a nurse on a COVID-19 ward? After asking four experts what the vaccinated can do in as many ways as I could come up with, I’m sorry to report that there are no one-size-fits-all guides to what new freedoms the newly vaccinated should enjoy. Still, there is one principle—if not a black-and-white rule—that can help both the vaccinated and the unvaccinated navigate our once again unfamiliar world: When deciding what you can and can’t do, you should think less about your own vaccination status, and more about whether your neighbors, family, grocery clerks, delivery drivers, and friends are still vulnerable to the virus. The COVID-19 vaccines are fantastic. The shots that are currently available are tremendously effective at protecting the people who get them from severe illness, hospitalization, and death—all the things we want to avoid if we have any hope of fully reopening society. Even so, advice on what people can do once vaccinated gets complicated. Those who are vaccinated can still be infected by, and test positive for, SARS-CoV-2; they’re just way, way less likely to get sick as a result. The sticky element is whether not-sick-but-still-infected vaccinated people can spread the virus to others and get them sick. So far, the early data have been promising, showing that the vaccines stop at least some transmission, but the matter is not scientifically settled. [Read: The one area where the U.S. COVID-19 strategy seems to be working] This leaves us in an awkward situation. Getting vaccinated means that your choices no longer endanger you much, but they still might make you a risk to everyone else. To put this in more concrete terms: If a vaccinated person goes out to eat, they can’t yet be sure that they’re not carrying the virus and spreading it to their unvaccinated fellow diners and the restaurant staff, or that they won’t pick up the virus at the restaurant and bring it home to their unvaccinated family. So, first, a very broad guideline for navigating a world in which vaccinations are rising and infections are dropping: Whether you’re vaccinated or not, how much you can safely branch out in your activities and social life depends on the baseline level of virus in your community. You can imagine that, in pandemic life, each of us has been dealt a certain number of risk points that we can spend on seeing friends outside, going to work, sending the kids to day care, and so on. If you or someone you live with is especially vulnerable to the virus, you might choose to spend fewer points by getting groceries delivered; if you live alone in an area where very few people are sick, you might choose to spend more points by forming a bubble with friends. The vaccine delivers you a huge number of bonus points, if you’re lucky enough to get one. And when spread of the virus is low, everyone gets more points. Saskia Popescu, an infectious-disease epidemiologist at George Mason University, told me that everyone, vaccinated or not, should try to keep track of three metrics in your area: The number of new daily cases per 100,000 people, the rate at which people transmit the virus to one another, and the rate at which people test positive for the virus. Popescu said that there are no magic numbers that would immediately bring the country back to pre-COVID life, but she’ll feel better about reopening when we hit daily case rates of just one to two per 100,000, transmission rates of .5 or less, and test-positivity rates at or below 2 percent. (As of last week, no U.S. state had reached the trifecta, and the country as a whole is still far from it.) Many local public-health departments regularly provide these numbers. [Read: A simple rule of thumb for knowing when the pandemic is over] You might be tempted to factor vaccination rates into your safety equation too, but Whitney Robinson, an epidemiologist at the University of North Carolina, told me that those numbers shouldn’t be anyone’s main safety indicator. That’s because vaccine distribution so far has been concentrated in particular social networks (for instance, health-care workers) and demographic groups (notably the white and wealthy), so an entire community won’t necessarily reap the benefits that a local vaccination rate of 15, or even 50, percent might imply. Knowing the overall risk of infection in your area is at least a first step toward making better decisions about whether you should host that birthday party or take Grandpa out to lunch. Even for people who are vaccinated, all of the public-health experts I spoke with emphasized, it’s still important to not throw caution to the wind. If vaccinated people flock to indoor restaurants or go unmasked in a crowd, they’re not just risking infecting others if they can indeed spread the virus, Popescu said. They’re contributing to a sense that life as we knew it before March 2020 is back, despite the fact that more than 65,000 people are still contracting the virus each day. Simply returning to our old habits would be deadly. That doesn’t mean that any loosening up is off the table for the vaccinated. Far from it—plenty of public-health experts have argued that vaccinated people safely seeing relatives or returning to the office can benefit everyone, because seeing how much the shot improves life will persuade more people to take it. Downplaying the vaccines’ success could discourage people from getting them, because if it won’t change their lives, they have no incentive. The best way forward for us all is for vaccinated people to spend their extra risk points in ways that don’t put unvaccinated people in danger. As you consider whether you should do things that you wouldn’t have done before the vaccine, think creatively about how you can make those things safer for everyone involved. “Grandparents really want to be able to go hug their grandchildren,” Tara Kirk Sell, a senior scholar at the Johns Hopkins Center for Health Security, told me. “I don’t have a problem with that.” But consider asking Grandma and Grandpa to wear masks during that hug, or meet you outside, or avoid sleeping over. Throughout the pandemic, we’ve developed an arsenal of strategies to make particular settings and activities safer. The vaccine is an extra-strong weapon against transmission that some people can deploy, but that doesn’t mean they need to discard all of the other ones to use it. [Julia Marcus: Vaccinated people are going to hug each other] How many of those methods you choose should depend on how many vulnerable people you regularly come into contact with. A vaccinated oncologist who lives with her immunocompromised sister is going to behave differently from a vaccinated retiree who lives alone. That said, there are plenty of settings, such as restaurants and stores, where you don’t know or can’t control how many vulnerable people are around you. For that reason, small private gatherings where you can adjust your anti-spread tactics to accommodate everyone’s risk factors are a safer first step toward normalcy than activities such as concerts, indoor dining, or big weddings. Travel in small groups might be a nearer goal, too: Popescu said she hopes that by the end of the year, she can take a vacation in another state with her husband without worrying that she’s “being a bad steward of public health.” Playing it safe, even as you loosen up a little, is the best way to ensure that someday, you will again live in a world with bars and birthday parties and movie theaters. It’s also the best way to keep yourself from getting sick with COVID-19 in the future—regardless of whether you’re already vaccinated. No one knows exactly how long you’ll be protected against serious illness if you get a vaccine (or were previously infected), simply because no one has been vaccinated for more than seven months yet. Given what we do know so far, the most likely way for a vaccinated person to get seriously ill from the coronavirus would be if they encounter a variant that the vaccine they received doesn’t effectively protect against. Such variants are much more likely to emerge if the virus is allowed to rage in particular places or groups before the overwhelming majority of the world’s people can be vaccinated. As Gregg Gonsalves, an epidemiologist at the Yale School of Public Health, put it, “In the context of epidemiology, we’re all in the same boat.” from https://ift.tt/2ZSZ31L Check out http://natthash.tumblr.com On its face, reinfection appears to be a straightforward term. It is literally “infection, again”—a recovered person’s second dalliance with the same microbe. Long written into the scientific literature of infectious disease, it is a familiar word, innocuous enough: a microbial echo, an immunological encore act. But thanks to the pandemic, reinfection has become a semantic and scientific mess. Newly saddled with the baggage of COVID-19, reinfection has taken on a more terrifying aspect, raising the specter of never-ending cycles of disease. It has sat at the center of debates over testing, immunity, and vaccines; its meaning muddled by ominous headlines, it has become wildly misunderstood. When I ask immunologists about reinfection in the context of the coronavirus, many sigh. I don’t blame them. At the heart of any conversation about reinfection is a largely unsolved mystery: whether COVID-19 survivors are truly safe from the coronavirus. Last summer, a cluster of apparent cases of reinfection seemed to hint that the virus was stronger than the body’s ability to protect against it—that reinfection, though uncommon, could be chalked up to a failure of the body’s defenses. But infection is a two-player game, and a change in either contender can affect the dynamics of a second confrontation. On occasion, the body’s immune strongholds might weaken and crack. Or a microbe might alter its surface until it’s unrecognizable to the host that once fought it off—even if the original defenses raised against the bug are still standing tall. These latter cases might be described less strictly as reinfection than as, well, another infection. As the coronavirus continues to mutate—a process hastened by the sheer number of hosts that the virus has found around the globe—cases such as these might soon become our startling reality. Already, researchers have identified several instances in which new variants have set up shop in COVID-19 survivors. Experts haven’t yet settled on common terms to describe these incidents, or distinguish them from cases in which people’s immune defenses have simply dropped. But untangling how and why the coronavirus reestablishes itself in certain people is essential to preventing that from happening. Understanding reinfection will affect how we develop vaccines and treatments, and monitor the virus’s movements in the future. It could help us figure out how durable immunity to the coronavirus truly is, and the limits of the virus’s capacity to change. To understand reinfection, it’s helpful to first get a grip on plain old infection. As Brianne Barker, an immunologist at Drew University, explains it, infection fundamentally represents an interaction between a microbe and a host: The bug establishes itself in a living home, where it can reproduce. Some infections are noisy. They come with the signs and symptoms of illness, either because the pathogen is causing a ruckus, or because the body has grown cantankerous in its effort to evict an unwelcome tenant. Other microbes are silent houseguests, so unobtrusive that we don’t even notice them. Coronavirus infections seem capable of running the gamut. A person’s infection status can’t tell you whether they can spread the microbe, either. “You can be infected without being infectious,” Katia Koelle, a virologist at Emory University, told me. The same rules of the road apply to reinfection. A repeat infection won’t necessarily come with the same symptoms, or the same level of contagiousness. In the most classical portrait of reinfection, the microbe is effectively identical; your body, with its memory of the bug, is not. That probably means you’re not “completely susceptible again,” says Angela Rasmussen, a virologist affiliated with Georgetown University. Typically, a person’s second rendezvous with a pathogen will be much milder, and pose less of a transmission threat. Immune cells are able to mount faster and stronger attacks; occasionally, these quick-draw assaults are so powerful that the microbe is purged before it gets a second shot at infection. Other times, immune responses are too weak or sluggish to forestall infection entirely, but still strong enough to exterminate the interloper before it causes symptoms. Most people “have probably been reinfected with lots of viruses in their lives and not known it, because they didn’t get sick,” Barker told me. Repeat tussles with the same pathogen can also come with perks. Immune cells glean more intel on invaders each time they meet them, and strengthen their skills for future bouts. That’s textbook immunology: a body learning from experience. [Read: Immunology is where intuition goes to die.] In some cases, the immune system can be prone to amnesia. The body’s memory of the measles virus (or the measles vaccine), for instance, seems to last decades, perhaps an entire lifetime. But the mumps virus appears to make less of a lasting impression. Researchers aren’t sure why some microbes are more memorable than others, but there are hints. The nature of the initial encounter can influence the immune system’s later reactions. More severe sickness, for example, sometimes goads the body into taking a threat more seriously and locking away information about it long term. (Very severe disease, however, can so thoroughly overwhelm the body that the immune system doesn’t form a good memory of the virus.) Certain bugs might also directly interfere with immune cells’ long-term memory. And factors such as age or biological sex can affect the potency of immune responses as well. Against respiratory viruses such as the new coronavirus, “people generally have a very strong immune response,” Koelle said. With only about a year’s worth of data, scientists can’t yet confidently forecast how long that protection will last—but a growing body of evidence suggests some serious staying power. Last summer, researchers in Hong Kong reported the world’s first confirmed coronavirus reinfection, roughly five months after the patient’s initial illness. But his first case had been mild, and his second was symptomless, a fairly unsurprising, perhaps even comforting, trajectory. At the time, many experts floated the notion that the man had not mounted a good enough immune response the first time around—that his body had, on some level, failed him. Since then, dozens of similar cases of milder reinfections have been conclusively documented, and more are suspected. But consider the other party in this fight. Although the coronavirus mutates more slowly than other respiratory viruses, it still evolves dizzyingly fast. No single genetic change can turn a virus invisible to an entire immune system, but successive shifts in the virus’s appearance can chip away at its familiarity. Subsequent infections under these circumstances are less about the body forgetting, and more about the virus disguising itself—the difference between a robbery abetted by a faulty security system, and one that succeeds because the burglar was in costume. “From the body’s perspective, that can be a whole different bug,” C. Brandon Ogbunu, a disease ecologist and computational biologist at Yale, told me. Eventually, every evolving virus may change enough that a new infection is no longer a reinfection, but a separate, related one: a sororal infection, or an epi-infection. [Read: The body is far from helpless against coronavirus variants.] These evasion tactics seem to play a role in enabling coronaviruses that cause common colds to infiltrate the human population on a regular basis, says Jesse Bloom, an evolutionary biologist and virologist at the University of Washington. In December, Bloom’s team posted a preprint study detailing the intricate arms race between human and microbe: Antibodies that could successfully squelch one version of a common-cold coronavirus stick around in people for years, but struggle to extinguish its genetically rejiggered descendants. “It makes perfect sense—it’s what viruses do,” Oliver Fregoso, a virologist at UCLA, says. “Viruses are going to evolve in a way that [allows] them to continue infecting. Otherwise, they go extinct.” No part of reinfection is cut-and-dried. Every infection, foreign or familiar, to some extent, reflects the push and pull between immunity and viral evolution—both of which can make a once-familiar foe appear foreign. Unfortunately, “it’s hard to parse out how much is due to you, as the patient, versus the characteristics of the virus,” Bloom says. The majority of people infected by the coronavirus don’t get the chance to measure their immune response, or genetically sequence the virus infecting them, which would be a surefire way to tell whether the pathogen has morphed into something new. But the more we understand about how these dynamics work, the better equipped we’ll be to tinker with them—and give our own bodies the edge. “We have to be able to explain when things don’t go right,” Ogbunu said. Scientists might be able to more effectively tailor treatments, some perhaps more suited to people with weaker immune systems, others hyper-focused on foiling certain variants of the virus. The same intel could inform the production and distribution of vaccines, which could be reformulated to get ahead of new variants. Understanding the root of most coronavirus reinfections is about prioritizing what’s in our pandemic playbook: shoring up our defense, or hitting the virus hard with the best offense we’ve got. Sarah Cobey, an immunologist at the University of Chicago, says the past year hasn’t shaken her faith in the human immune system. Some rare individuals have gotten very ill the second time they’ve been infected, a few even sicker than the first. But failed or aberrant immunity to the coronavirus is unlikely to be the norm. Most of the reinfections we document going forward will probably involve the virus adopting a new and foreign guise, Cobey says, rather than “something really weird happening with immune memory.” [Read: A simple rule of thumb for knowing when the pandemic is over.] In many ways, the virus-shift version of repeat infections is the easier one. It’s expected and trackable, with testing and genomic surveillance; it’s haltable, with measures that keep the virus from spreading and lingering in hosts. Encouragingly, none of the variants yet seems capable of completely eluding a typical immune response to the OG coronavirus or an OG-based vaccine—which is also very good news. It’s a hint that, by and large, our immune systems are working as they should. The shots we’ve developed to protect us from the coronavirus will still dial down our risks of getting seriously sick with COVID-19; vaccine makers will update their recipes to account for the variants. People who are hit naturally with one variant, then another, will probably experience gentler symptoms the second time, if they feel ill at all. (Frequent, symptomatic reinfections with the same variant, by contrast, would forecast a less rosy future.) The coronavirus is very likely here to stay, even after the pandemic officially ends. The virus will continue to have opportunities to evolve; in its myriad forms, it will cross paths with many of us again and again. “Reinfections are probably something we’re going to have to get used to,” Barker said. But virus and human will grow accustomed to each other, reaching something of a détente; immunity will, over time, build like a seawall. Actualizing that reality will require vigilance on our behalf, too. If repeat infections tell us anything, it’s that the less the virus mutates, the longer we’ll be able to protect ourselves against it. Viruses can’t replicate and evolve when they’re starved of hosts, and we’ve long known how to best cut the conduits they travel. To ensure our future, we might be wise to learn from our past. Perhaps our immune systems—and the virus—can relate. from https://ift.tt/3bznx5H Check out http://natthash.tumblr.com Editor’s Note: The Atlantic is making vital coverage of the coronavirus available to all readers. Find the collection here. In the middle of January, the deadliest month of the pandemic, one day after inauguration, the Biden administration put out a comprehensive national strategy for “beating COVID-19.” The 200-page document includes many useful goals, such as “Restore trust with the American people” and “Mount a safe, effective, and comprehensive vaccination campaign.” But nowhere does it give a quantitative threshold for when it will be time to say, “Okay, done—we’ve beaten the pandemic.” A month later, it’s time to get specific. The facts are undeniable: The seven-day average of new cases in the United States has fallen by 74 percent since their January peak, hospitalizations have gone down by 58 percent, and deaths have dropped by 42 percent. Meanwhile, more than 60 million doses of vaccine have gone into American arms. At some point—maybe even some point relatively soon—the remaining emergency measures that were introduced in March 2020 will come to an end. But when, exactly, should that happen? The problem is that the “end of the pandemic” means different things in different contexts. The World Health Organization first declared a “public health emergency of international concern” on January 30, 2020, holding off on labeling it a “pandemic” until March 11. The imposition (and rescinding) of these labels is a judgment made by WHO leadership, and one that can reflect murky, tactical considerations. Regardless of what WHO decides (and when) In the meantime, national governments—and individual states within the U.S.—have to make their own determinations about when and how to reopen their schools and loosen their restrictions on businesses. I reached out to prominent public-health experts to find out which epidemiological criteria ought to be met before these kinds of steps are taken. The most obvious interpretation of “beating COVID-19” would be that transmission of the coronavirus has stopped, a scenario some public-health experts have hashtagged #ZeroCOVID. But the experts I spoke with all agreed that this won’t happen in the U.S. in the foreseeable future. “This would require very high levels of vaccination coverage,” said Celine Gounder, an infectious-disease specialist at NYU who served on Joe Biden’s coronavirus task force during the transition. The U.S. may never reach vaccination rates of 75 to 85 percent, the experts said. [Read: The good news of COVID-19 is sticking for now] “The question is not when do we eliminate the virus in the country,” said Paul Offit, the director of the Vaccine Education Center and an expert in virology and immunology at the Children’s Hospital of Philadelphia. Rather, it’s when do we have the virus sufficiently under control. “We’ll have a much, much lower case count, hospitalization count, death count,” Offit said. “What is that number that people are comfortable with?” In his view, “the doors will open” when the country gets to fewer than 5,000 new cases a day, and fewer than 100 deaths. That latter threshold, of 100 COVID-19 deaths a day, was repeated by other experts, following the logic that it approximates the nation’s average death toll from influenza. In most recent years, the flu has killed 20,000 to 50,000 Americans annually, which averages out to 55 to 140 deaths a day, said Joseph Eisenberg, an epidemiologist at the University of Michigan. “This risk was largely considered acceptable by the public,” Eisenberg said. Monica Gandhi, an infectious-disease specialist at UC San Francisco, made a similar calculation. “The end to the emergency portion of the pandemic in the United States should be heralded completely by the curtailing of severe illness, hospitalizations, and deaths from COVID-19,” she said. “Fewer than 100 deaths a day—to mirror the typical mortality of influenza in the U.S. over a typical year—is an appropriate goal.” The “flu test” proposed here is not a perfect apples-to-apples comparison. Deaths attributed to COVID-19 are directly reported to public-health authorities, while the mortality numbers from seasonal flu are CDC estimates based on national surveillance data that have been fed into statistical models. But researchers believe that the straightforward counts of influenza deaths—just 3,448 to 15,620 in recent years—are substantially too low; while direct counts of COVID-19 deaths are likely to be more accurate. One big reason: Far more COVID-19 tests are done in a single day than flu tests in an entire year, and flu tests have a greater tendency to return false negatives. In any case, we are nowhere near 100 COVID-19 deaths a day. Since last spring, no state has reported fewer than 474 deaths a day, as measured by a rolling seven-day average at the COVID Tracking Project at The Atlantic. Right now, the country as a whole is still reporting close to 2,000 deaths a day, and just two weeks ago that number was more than 3,000. So, if we’re going by the flu test, we still have a very long way to go. [Read: The most likely timeline for life to return to normal] Some experts were even more conservative. Crystal Watson, a health-security scholar at Johns Hopkins University, suggested a threshold of 0.5 newly diagnosed cases per 100,000 people every day, and a test-positivity rate of less than 1 percent. That would translate to fewer than 2,000 cases a day in the U.S., compared with the current 60,000 or more. We’d also want to log at least one month of normal hospital operations without staff or equipment shortages, she said. While every proposed threshold remains far below what we’re seeing right now, the researchers I spoke with believe that if vaccine uptake is high enough, those numbers can be reached. Watson suggested a target of 80 percent coverage for populations older than 65, and 70 to 80 percent for everyone else. For the latter, “perhaps 60 percent is more realistic,” she said. So far, no state has reached those vaccination levels in any population. It is possible, however, that in specific, high-risk subpopulations, targeted efforts could drive vaccination rates to very high levels. Our best example is in long-term-care facilities, which have been linked to 35 percent of total COVID-19 deaths in the U.S. The federal government’s vaccine rollout made residents and staff in these facilities a priority and provided specific funds and operational help to vaccinate these people beginning in December. At the COVID Tracking Project, we’ve seen the share of deaths attributed to long-term-care facilities drop by more than half over the past six weeks, which suggests the vaccines are working. The large number of Americans who’ve already been infected will also be crucial for reaching transmission-slowing levels of immunity. The CDC estimates that more than 83 million Americans have been infected with COVID-19, far more than the official, confirmed case total of 28 million. Forty-four million Americans have received at least one dose of a vaccine. Even assuming some overlap between the previously infected and the vaccinated, perhaps 100 to 120 million Americans have some level of immunity. That’s roughly one-third of the population. It could take months for the size of this group to reach a point where the number of COVID-19 deaths a day falls below 100. Until then, we’ll be confronted with a different sort of risk: that, for some, the pandemic feels like it’s over long before it actually is. Just as the country has never taken a unified approach to battling COVID-19, we may very well end up without a unified approach to deciding when it ends. That’s why public-health experts are desperately urging Americans to hold firm even as the pandemic seems to be receding. “We’re lifting mitigation measures too soon,” warned Gounder, the infectious-disease specialist at NYU. “We’re taking our foot off the brake before putting the car into park.” If enough people ignore that message and decide the pandemic is over for them, it may very well put off the moment when we can say that the pandemic is over for everyone. from https://ift.tt/3qT48De Check out http://natthash.tumblr.com The American government’s COVID-19 response has been a disaster, right? The United States strategy is a four-alarm dumpster fire, sent from hell to remind Americans to never again elect a president who describes the scientific method as “Now they have it, they have studied it, they know very much.” When people needed coronavirus guidance, U.S. leaders had none. Government officials told people not to wear masks, oh wait, to definitely wear masks—oh wait, there actually aren’t any masks. Kindergartners went to internet school for a year because America simply refused to get a clue. In many, many ways, the U.S. pandemic response has been exactly as bad, confusing, and deadly as it has seemed. Vaccination is the exception. On that front, it turns out that America did, in the end, “know very much.” Especially when compared with Europe’s, the U.S.’s vaccination rollout isn’t a tortilla-wrapped turd—it looks almost like a success. It’s true that Israel, which benefited from its countrywide electronic medical-record system and its decision to buy lots of vaccine doses relative to its population, has the U.S. beat. The United Arab Emirates is also lapping much of the world, immunizing people of all ages using China’s vaccine. The United Kingdom, which authorized the Pfizer-BioNTech shot in December, before any other Western nation, is performing especially well relative to the rest of the globe. The U.K.’s apparent lead over the U.S. is at least in part due to its decision to start mass vaccinations by giving the first dose of the two-dose regimen to as many people as possible, a strategy called “First Doses First.” But despite lost doses and frustrating vaccine websites, the U.S. is vaccinating its residents faster than any member of the European Union—which may be surprising, given that so many European health-care systems are touted as being more efficient than America’s. As of this writing, the U.S. has vaccinated 15.9 people out of every 100, while Germany has vaccinated just five, France has reached four, and Croatia less than three. The U.S. government, finally, appears to have done something right. Still, this story is more about the foibles of the European Union than the triumph of the United States. The EU worried that if it left each of its member countries to acquire vaccines for itself, smaller and poorer nations wouldn’t be able to buy enough. European leaders bet that, by negotiating for vaccines as a bloc, they could match America’s purchasing power. The U.S. pursued vaccine procurement through Operation Warp Speed, a massive new public-private partnership. But the EU opted to handle negotiations through its executive branch, the European Commission. And unfortunately for Europeans, the commission wasn’t very good at its assigned task. It turns out that a deliberative body built for leisurely trade negotiations doesn’t move quickly during a public-health crisis. “The commission has gone from procuring printer paper to procuring this astonishingly large set of vaccines,” says Scott Greer, a health-policy professor at the University of Michigan. The Trump administration’s Operation Warp Speed didn’t worry about the cost of the vaccines or whether the vaccine companies could be held liable for side effects. The Europeans focused on trying to get a low price for the vaccines, and on making sure the vaccine companies could be sued if the vaccines caused problems. The U.S. threw money at the problem, flooding vaccine makers with billions of dollars in subsidies to increase the speed of vaccine testing and manufacturing. Unlike the EU, the U.S. and the U.K. bought millions of doses of various vaccine candidates last summer, without knowing which ones would be effective. “The U.S. and the U.K. locked in their supplies before they knew the vaccine was going to work,” Lawrence Gostin, a professor of global-health law at Georgetown University, told me. “The EU was more risk-averse.” The FDA was also faster to approve the vaccines than its European counterpart, the European Medicines Agency, which wanted to be extra sure that the vaccines were safe. The U.K. and the U.S. made deals with vaccine companies much earlier than the EU did, putting the EU weeks, if not months, behind. The EU is “a tanker,” not “a speedboat,” European Commission President Ursula von der Leyen said recently. Once it finally approved the vaccines, the EU realized that it had bought too few doses. In July, the U.S. ordered 600 million doses of the Pfizer vaccine. The EU put in its order four months later—for half as many doses, The Guardian reported. “More [vaccines] could have been ordered, and faster,” German Health Minister Jens Spahn admitted earlier this month. And when vaccine makers in Europe had manufacturing issues in late January, Europe’s vaccine shortage intensified, causing clinics from Madrid to Paris to Lisbon to cancel vaccination appointments. U.S. vaccine manufacturers, meanwhile, have kept up with demand better than those in China or even Canada, Bloomberg’s Noah Smith points out. The U.S. has problems with anti-vaccine sentiment. But getting shots into the arms of hesitant Europeans has proved even trickier. For a continent often stereotyped as sophisticated and progressive, Europe has a shockingly high rate of vaccine aversion. Only 36 percent of Western Europeans “strongly agree” that vaccines are safe, compared with 48 percent of North Americans. One in three French people disagree that vaccines are safe, the highest percentage in the world, according to the Wellcome Trust, and a recent poll found that only 40 percent of French people want the COVID-19 vaccine. French women might not get fat, but they also don’t get vaccinated—a major barrier to reaching herd immunity on the Continent. Although Operation Warp Speed was successful, at least in comparison with Europe’s efforts, part of its victory came down to luck. If the vaccines that the U.S. scooped up so many doses of, by Moderna and Pfizer, had failed clinical trials, “the U.S. would look extraordinarily stupid right now,” Greer says. And the U.S. has also made plenty of mistakes. Some experts say, for instance, that the FDA should approve the AstraZeneca vaccine, which has already been given the green light by the U.K. and even the cautious EU. Vaccine distribution is still profoundly unequal, with many vaccine hubs being placed in wealthier areas and requiring reliable transportation. Many Black Americans, who have been disproportionately affected by COVID-19, have spent weeks trying and failing to get vaccine appointments for their elderly relatives. Europe may catch up to the U.S. in vaccinations, once its supply of vaccines starts to flow. The U.K.’s example suggests that it’s wise to distribute the vaccine through the doctors and nurses who generally vaccinate people against the flu and other bugs. “The British, after a record of unremitting incompetence during this pandemic, finally had the good idea of asking the National Health Service to do the vaccines,” Greer says. For COVID-19, a disease in which so much hinges on preexisting risk factors, getting people vaccinated through their regular doctors is smart. “The National Health Service knows you, and it knows your risk,” Greer says. But the U.S. doesn’t have a National Health Service, and its underfunded public-health departments are already struggling to keep up with lockdowns, contact tracing, and vaccinating. It’s not clear whether the American vaccine story will look as positive after the very old and the very motivated have been vaccinated, and the people remaining are those who don’t have a doctor, don’t trust their doctor, or can’t get to the doctor. Either way, the debate over which rich country’s vaccination program worked best “is going to be of academic interest [only] by the end of 2021,” Greer says, because people in those countries who want the vaccine will likely have received one by then. In 2022, few will remember whether Estonia or Croatia vaccinated its population faster. The lessons of the U.S. and EU vaccine rollouts may fade into irrelevance—until the next pandemic. from https://ift.tt/3qHRyXf Check out http://natthash.tumblr.com A few years ago, when I still had confidence in our modern ability to fight viruses, I pored over a photo essay of the 1918 flu pandemic. How quaint, I remember thinking, as I looked at people bundled up for outdoor classes and court and church. How primitive their technology, those nurses in gauze masks. How little did I know. I felt secure, foolishly, in our 100 additional years of innovation. But it would soon become clear that our full-body hazmat suits and negative-pressure rooms and HEPA filters mattered little to Americans who couldn’t find N95 masks. In our quest for perfect solutions, we’d forgotten an extremely obvious and simple one: fresh air. A colleague joked, at one point, that things would have gone better in the pandemic if we still believed in miasma theory. Miasma theory—discredited, of course, by the rise of germ theory—held that disease came from “bad air” emanating from decomposing matter and filth. This idea peaked in the 19th century, when doctors, architects, and one particularly influential nurse, Florence Nightingale, became fixated on ventilation’s importance for health. It manifested in the physical layout of buildings: windows, many of them, but also towers erected for the sole purpose of ventilation and elaborate ductwork to move contaminated air outdoors. Historic buildings still bear the vestigial mark of these public-health strategies, long after the scientific thinking has moved on. The obsession with ventilation—and miasma theory in general—was indeed wrong when it came to pathogens such as cholera and yellow fever that we now know spread through other means (water and mosquitoes, respectively). But it did make sense for the diseases that invisibly stalked people through 19th-century air: measles, tuberculosis, smallpox, influenza—all much diminished as threats in the 21st century. “We’ve gotten so good at preventing so many diseases, there’s been a loss of knowledge and a loss of experience,” Jeanne Kisacky, the author of Rise of the Modern Hospital, says. Science is not a simple linear march toward progress; it also forgets. Today, amid a pandemic caused by a novel airborne virus, these old ideas about ventilation are returning. But getting enough schools and businesses on board has been difficult. Fixing the air inside modern buildings, where many windows don’t or barely open, means fighting against the very nature of hermetically sealed modern buildings. They were not built to deal with airborne threats. Nineteenth-century hospitals were. That era saw the rise of well-ventilated “Nightingale pavilions,” named after Florence Nightingale, who popularized the design in her 1859 book, Notes on Hospitals. As a nurse in the Crimean War, she saw 10 times more soldiers die of disease than of battle wounds. Nightingale began a massive hygiene campaign in the overcrowded hospitals, and she collected statistics, which she presented in pioneering infographics. Chief among her concerns was air. Notes even laid out exact proportions for 20-patient pavilions that could allow 1,600 cubic feet of air per bed. Each pavilion was a separate wing, radiating from a central corridor. And it had large windows that faced each other, which allowed a cross breeze to blow between the beds. The windows stayed open no matter the weather. There were stories, Kisacky told me, of hospitals in winter where “the patients are closing the windows, and the nurses are opening them. And the doctors come and knock the glass out to make sure they stay open.” In some pavilions, a central fireplace heated the room, so that contaminated air rose out of the ward via the chimney effect. That heat might have been nice in the winter but “they would run fires in the fireplaces in August to keep the air moving,” Kisacky said. “You wouldn’t want to be the patient in the bed closest to that.” The pavilion-plan hospitals formalized the fear of “bad air” in hospital design, but the idea is much older. The Greek physician Hippocrates warned in the fifth century B.C. that bad air was the cause of pestilence. People in the Middle Ages believed some version of this too. The word miasma, which dates to the 17th century, comes from the ancient Greek for “pollution.” In the 19th century, the fear of outbreaks fueled new sanitation campaigns to rid cities of miasma. Homes needed ventilation as well. In Victorian England, reformers successfully fought a window tax that penalized large windows, says Henrik Schoenefeldt, an architectural historian at the University of Kent. Bigger windows meant better ventilation. One doctor, Schoenefeldt told me, even railed against small windows as a “crime” that was killing people. When I was Zooming with another historian of architecture, Harriet Richardson Blakeman of Edinburgh College, she pointed her webcam up toward the ceiling. Above the door was a grate, which ventilated the room that had become her office in her Victorian-era home. (Blakeman thinks the grate may have actually been added some decades after the house was first built, as ventilation continued to be a concern.) The massive growth of cities in the 19th century also sparked the creation of bigger and more elaborate public buildings, which meant the creation of bigger and more elaborate ventilation systems in new museums, prisons, and courthouses. “There are new types of buildings being invented to respond to urbanization,” Alistair Fair, an architectural historian also at Edinburgh College, says. This was a time of innovation in ventilation too. In these complicated buildings, simple windows and chimneys would no longer do. Instead, intake vents were installed, as were ducts that wove through the walls and floors. A famous example is the Palace of Westminster, in London, whose construction began in 1840. The building’s architect consulted with a doctor, David Boswell Reid, and Reid suggested extensive revisions to the architectural plan to improve ventilation. The two iconic towers of Westminster—the Victoria Tower and the one that holds Big Ben—are both also ventilation towers that helped draw warm, stale air out of the buildings. Reid further insisted on an expensive third tower, the Central Tower, for the sole purpose of ventilation. The ventilation system as a whole, which also included mechanical fans, valves, and a series of air chambers in the basement, accounted for a quarter of the building’s costs. Physically, too, “that system, when it was completed, took up about a quarter of the entire building,” said Schoenefeldt, who has extensively studied historical ventilation in Westminster. The system’s physical remnants are still in the building, now unused. Even in the 19th century, the building’s ventilation did not always work as designed—Reid was a doctor, not an engineer, after all—but the principles of his designs were influential. “The Palace of Westminster was, at the time, the technologically most sophisticated building constructed in Europe,” Schoenefeldt told me. Its ventilation system inspired those in the era’s new museums, concert halls, and courthouses. By the late 19th century, scientists were developing the beginnings of germ theory. John Snow had drawn his famous map of a cholera outbreak, which he traced to a single water pump. Louis Pasteur had shown that organisms cannot spontaneously generate in sterilized broth. And Robert Koch had identified the microorganisms that cause tuberculosis, cholera, and anthrax. But germ theory did not immediately do away with the importance of fresh air. “Early understandings of the germ, which emphasized its ubiquitous presence in air and water and its hardiness outside the body, neatly harmonized with already accepted modes of protection,” Nancy Tomes, a science historian at Stony Brook University, writes in The Gospel of Germs. The shift, like most paradigm shifts in science, was gradual. For hospitals, the pavilion style continued into the 1930s, Annmarie Adams, an architectural historian at McGill University, told me. The 1918 flu pandemic struck at a time when germ theory was taking hold but people still recognized the importance of air. Even in modern hospitals today, where hand-washing and disinfection are paramount, the flow of air remains tightly controlled. Infectious patients are put in negative-pressure rooms, which contaminated air cannot escape. Immunocompromised patients are put in positive-pressure rooms, where contaminated air cannot enter. If anything, the flow of air is controlled in ever more sophisticated ways. Outside hospitals, though, the menace of “bad air” has faded away. Airborne diseases simply don’t exist the way they did 100 years ago, Tomes says. Measles and smallpox have been vanquished through vaccines. Tuberculosis is treatable with antibiotics. The common remaining airborne pathogens are the cold and flu, diseases taken so unseriously that you might be docked for missing school or work on account of them. Without deadly airborne pathogens in the literal air we breathe, we’ve lost an intuitive sense of their invisible danger. And we’ve lost the relatively simple ways of mitigating that danger. Fresh air became less important; homes and workplaces were sealed up for energy efficiency. Imagine, Tomes said to me, a sci-fi movie featuring a scary new virus. You would probably picture people protecting themselves with space suits and respirators. “Nobody ever goes to open a window,” she said. Who would have thought that the key to fighting this novel coronavirus would be as simple as fresh air? Only everyone 100 years ago. Before COVID-19 hit last year, Linsey Marr, an environmental engineer at Virginia Tech, was one of the few scientists already studying airborne transmission of viruses. She told me she would read medical textbooks that claimed pathogen-laden droplets from our mouths fell to the ground within six feet. Until recently, however, scientists couldn’t measure what remained airborne, because they had no way of collecting delicate live viruses from the air. There were other signs the textbooks were off, though: Marr knew, based on simple calculations she did with her undergrad students, that droplets of a certain size could linger midair. And papers going back decades suggested that common respiratory ailments such as the flu were indeed airborne, which official medical sources kept downplaying. “I just kind of figured, well, maybe 30 years from now, people will look back at these papers, mine and other people’s, and realize, ‘Oh yeah,’” she said. “Finally there’ll be enough evidence showing that these diseases are really transmitted by breathing in virus from the air.” Then a mysterious new respiratory virus began sickening people in China at the end of 2019. Scientists quickly identified it as a novel coronavirus, but it took several more months for health agencies to acknowledge that COVID-19 spreads through air—a blip in the normally glacial pace of science but a long time in an emergency when cases are growing exponentially. Experts were initially reluctant to label the virus “airborne,” because they typically used that term to describe pathogens that linger infectiously in the air for hours, such as measles. The coronavirus doesn’t seem to last as long, but it can still transmit through the air when people talk and breathe. The smoking gun, in Marr’s view, was a study that found live viruses lingering in the air seven to 16 feet away from patients. Super-spreader events and asymptomatic spread—when people aren’t coughing or sneezing—offer additional circumstantial evidence, she said, that the virus is spreading via small aerosoles from breathing and talking. In July, she was one of 239 experts who signed an open letter to the World Health Organization outlining the evidence for airborne transmission. The WHO eventually acknowledged airborne transmission, as did the CDC, finally, in October. In retrospect, it’s remarkable how long it took to say what should be intuitive: A virus that infects the respiratory system spreads through air. “It seems like it would be obvious, right?” Marr said. A 19th-century doctor, who didn’t even know what viruses were, might have thought so too. Still, early advice that focused on hand-washing and sanitizing surfaces has stuck, as evidenced by the hygiene theater that continues to pervade public spaces. Genuine confusion exists about the changing scientific consensus, but so does inertia. Wiping surfaces and erecting plexiglass barriers is easier than installing expensive air filters or, God forbid, reconfiguring a hermetically sealed building’s entire ventilation system. Even the CDC’s school-reopening guidelines, released just this month, said little about ventilation. Like so many viruses before it, the coronavirus is likely to be tamed by vaccines. Perhaps soon, ventilation won’t matter again. But COVID-19 is a humbling reminder of the value of lost knowledge. I’m writing this now at my desk, which is in front of a radiator, which is in front of a window. For apartment buildings like mine, built in the early 20th century, this is by design. The radiator runs too hot, so that residents can keep the window open for ventilation. (I am indeed too hot. The window is open.) This quirk of old building design went viral months ago in a collective aha moment. This thing that never made sense actually makes sense! Like many old buildings, my apartment has pipes that somehow always need to be repaired. I remember going downstairs one day to find a giant trench dug out in the lobby, where a steam radiator had exploded. And in the past year of working from home, I have cursed the lack of central AC and the overwhelming heat of the radiators. But the window is open today. The air is good. This is a building designed in a time of airborne pathogens. from https://ift.tt/3aFVFxn Check out http://natthash.tumblr.com |
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