theatlantic--2020-05-26--America’s Never-Ending Battle Against Flesh-Eating Worms

The Florida Keys are a place where deer stand next to children at school-bus stops .
They lounge on lawns .
They eat snacks right out of people ’ s hands .
So when the deer began acting strangely in the summer of 2016 , the people of the Keys noticed .
Bucks started swinging their heads erratically , as if trying to shake something loose .
Then wounds opened on their heads—big , gaping wounds that exposed white slabs of bone .
Something was eating the deer alive .
Traveling the world to see microbes , plants , and @ @ @ @ @ @ @ , deserts , the icy poles—and wherever else they may be .
Read more That something , lab tests would later confirm , was the New World screwworm , a parasite supposed to have been eradicated from the United States half a century ago .
No one in the Keys had ever seen it .
If you had asked an old-time Florida rancher though , he might have told you boyhood stories of similarly disfigured and dying cattle .
In those days , screwworms found their way into cattle through any opening in @ @ @ @ @ @ @ newborn calves , scratches from barbed wire , even a tick bite .
Then they feasted .
Screwworms once killed millions of dollars ’ worth of cattle a year in the southern U.S. Their range extended from Florida to California , and they infected any living , warm-blooded animal : not only cattle but deer , squirrels , pets , and even the occasional human .
In fact , the screwworm ’ s scientific name is C. hominivorax or “ man eater ” —so named after a horrific outbreak among prisoners on Devil @ @ @ @ @ @ @ French penal colony in South America .
For untold millennia , screwworms were a grisly fact of life in the Americas .
In the 1950s , however , U.S. ranchers began to envision a new status quo .
They dared to dream of an entire country free of screwworms .
At their urging , the United States Department of Agriculture undertook what would ultimately become an immense , multidecade effort to wipe out the screwworms , first in the U.S. and then in Mexico and Central America—all the way down to the narrow @ @ @ @ @ @ @ of Panama .
The eradication was a resounding success .
But the story does not end there .
Containing a disease is one thing .
Keeping it contained is another thing entirely , as the coronavirus pandemic is now so dramatically demonstrating .
To get the screwworms out , the USDA to this day maintains an international screwworm barrier along the Panama-Colombia border .
The barrier is an invisible one , and it is kept in place by constant human effort .
Every week , planes drop 14.7 million sterilized screwworms over the @ @ @ @ @ @ @ A screwworm-rearing plant operates 24/7 in Panama .
Inspectors cover thousands of square miles by motorcycle , boat , and horseback , searching for stray screwworm infections north of the border .
The slightest oversight could undo all the work that came before .
The insect is relentless in its search for hosts .
Those who fight it must be relentless too .
This past August , I went to Panama to meet the people who maintain the screwworm barrier .
The Keys outbreak was long over by then , quelled within months @ @ @ @ @ @ @ Panama .
As startling as it was to Floridians , it had been just a small , gruesome blip in the history of the screwworm .
A transcontinental screwworm barrier has been in place for 50 years—longer than many of the people who now maintain it have been alive .
They work for a joint commission of Panama ’ s agricultural department and the USDA known as COPEG , or the Comisión Panamá–Estados Unidos para la Erradicación y Prevención del Gusano Barrenador del Ganado .
The day before I landed at Tocumen International @ @ @ @ @ @ @ taken off and released their precious loads of screwworms over the Panama-Colombia border .
More screwworm flights were scheduled for the next day , a Wednesday , and Thursday and Saturday and Monday and so on and on .
“ We will be here for a long time , ” a COPEG staff member in Panama told me with evident pride .
“ We should be here for the next 100 years.
” In the early days of the eradication effort , USDA scientists were not so certain of success—or longevity .
They @ @ @ @ @ @ @ because they didn ’ t have enough funding .
In press interviews , they worried about what laughingstocks they ’ d be if their “ idiotic insect-sex scheme ” failed and , God forbid , became an extremely mockable symbol of government waste .
Read : Decapitated worms get better , see again The man who came up with the scheme , and believed in it most passionately , was Edward F. Knipling , a USDA entomologist who , in the 1930s , spent long hours watching screwworms mate .
As a boy @ @ @ @ @ @ @ insect pests on his family ’ s Texas farm .
“ Every plant that we grew , ” he later said , “ there was some type of insect that was causing damage.
” Screwworms infected the farm ’ s cows and pigs , and Knipling remembered them as one of the worst pests .
He had to climb into the hog pens to smear medicine on the wounds of uncooperative sows .
“ That was a very unpleasant task , ” he recalled some eight decades later , in an interview shortly @ @ @ @ @ @ @ actually flies , with big red eyes and metallic blue-green bodies .
After mating , the females lay their eggs in open wounds , and the resulting larvae eat through a ring of surrounding flesh .
Once sufficiently engorged , the larvae drop off the wounds to pupate , emerging as a new generation of flies .
As Knipling watched screwworms churn through their life cycle in his government laboratory , he made an observation whose importance he could intuit but not yet put to use : Female screwworms mate only once in @ @ @ @ @ @ @ screwworm mates with a sterile male , she will never have any offspring .
So if the environment could somehow be saturated with sterile males , Knipling surmised , screwworms would very quickly mate themselves out of existence .
But Knipling did not know how to sterilize male screwworms .
In any case , the U.S. was entering World War II , and his expertise was needed elsewhere .
Knipling was reassigned to a lab in Florida , where his team perfected incredibly effective pesticides such as DDT that protected troops from insect-borne @ @ @ @ @ @ @ the war , but it would later devastate the environment from overuse .
This experience shaped the rest of Knipling ’ s career .
He devoted himself to sterilizing insects , a way to control pests without pesticides .
After the war , Knipling went back to studying screwworms with his fellow entomologist Raymond Bushland .
Scientists now knew , from the horrific consequences of atomic bombs dropped on Japan , that high doses of radiation damage human tissue and cells .
When a colleague introduced Knipling to research on the sterilization of @ @ @ @ @ @ @ : Could radiation sterilize screwworms too ?
The entomologists managed to get access to an X-ray machine at a nearby military hospital where one of Bushland ’ s old Army buddies worked .
Every Thursday afternoon , Knipling and Bushland put their screwworms through the X-ray machine , experimenting with different developmental stages and radiation levels .
They needed screwworms that were damaged enough to be sterile but not so damaged that they could not attract a mate in the wild .
The best time to irradiate , the two found , was @ @ @ @ @ @ @ stage , when the adult fly ’ s ovaries and testes were developing and thus most sensitive to radiation .
The radiation worked .
These screwworms indeed turned sterile , but Knipling and Bushland still needed to prove that irradiated males could actually mate with fertile females in the field .
In 1951 , a USDA team began releasing sterile male screwworms on Sanibel Island off the coast of Florida .
The screwworms persisted , so the team in turn persisted , releasing sterile males on the island for two more years .
@ @ @ @ @ @ @ The team thought that fertile males were probably flying over from the mainland .
So in 1954 , the scientists tried again on a more remote island : Curaçao in the Dutch Caribbean .
This time , they succeeded .
Screwworms disappeared from the island within months .
From here , a quietly audacious project to reengineer the environment for livestock got underway , ultimately changing the lives of cattle , deer , and humans throughout the North American continent .
When the Florida Cattlemen ’ s Association caught wind of the success @ @ @ @ @ @ @ potential closer to home .
The group lobbied state and federal officials for a bigger undertaking .
And in 1957 , the USDA began a campaign to wipe out the flesh-eating parasites east of the Mississippi River .
When that succeeded two years later , ranchers in Texas , Louisiana , New Mexico , Arizona , and California started clamoring for their own eradication program .
Screwworms were so widespread in those states that they had shaped cowboy culture : Long days of “ riding the range , ” for example , were @ @ @ @ @ @ @ .
For the USDA , though , the West proved a challenge on a different scale .
The screwworm-eradication program had to build a new plant in Mission , Texas , to produce as many as 200 million sterile flies each week .
Because screwworms prefer to eat living flesh , feeding the plant ’ s flies was a grisly logistical puzzle .
Initially , USDA scientists gave the screwworms a mixture of warm ground beef and blood , but beef was expensive .
At various times , they substituted cheaper meats such @ @ @ @ @ @ @ cow lung , and even nutria—an invasive rodent that was then taking over Louisiana .
By 1962 , the flies at the Mission plant were consuming 240,000 pounds of meat and 10,000 gallons of whole blood every week .
In the earliest days of sterile-screwworm testing , the flies stank so badly that airlines refused to ship them .
Workers learned to spray the boxes with cologne .
The Mission plant closed in 1981 , when screwworm rearing moved to Mexico and then later to Panama .
Today , the screwworm-production facility in @ @ @ @ @ @ @ plantation , about 20 miles east of the country ’ s capital .
The roof is painted a smooth mint green , and the facility is the program ’ s most modern yet .
But screwworms still have primordial urges : They still have to feed on animal remnants .
So when I stepped inside the facility last August , the first thing I noticed was the smell—foul , with a metallic tang .
My brain involuntarily matched it to bloody tampon .
Screwworms are no longer given raw meat , but their @ @ @ @ @ @ @ in other ways .
The current diet is a more economical mix of powdered blood , milk , and egg—reconstituted and then thickened with cellulose into a dark-brown sludge .
I watched workers pipe it into trays , the diet gushing like sewage .
The rearing facility itself is a windowless maze of concrete .
Each room is maintained at a prescribed temperature and humidity , optimized for a particular stage of screwworm development .
The larvae , for example , hatch in a room heated to 102 degrees Fahrenheit , which mimics @ @ @ @ @ @ @ .
Once hatched , they are wheeled to cooler rooms , where they crawl out of their food and become pupae .
My glasses fogged up multiple times as we moved through rooms hot and cold , dry and humid , following the screwworm ’ s life cycle .
In the 102-degree hatching room , staff pulled out a tray of food to show me a “ feeding pocket.
” When screwworms eat , they like to pack themselves tightly together like cigarettes in a carton , their mouths shoved down into the @ @ @ @ @ @ @ the air .
I had come across pictures of feeding pockets in animals ’ open wounds before .
Now I forced myself to look at the writhing brown mass , imagining this protein sludge to be flesh yielding to thousands of relentless mouths .
“ For me , beautiful , ” said Sabina Barrios , the head of screwworm production , gesturing at the feeding pocket .
What she saw were healthy screwworms that would grow big and fat .
In a few days , they would turn into pupae , also big @ @ @ @ @ @ @ with radioactive cobalt 60 .
And a couple of days after that , they would emerge as flies , vigorous and ready to mate .
A hundred and fifteen people work to keep the plant operating 24 hours a day , every day , to produce 20 million of these flies a week .
COPEG does more than produce sterile flies .
It also runs a network of screwworm-inspection posts and offices that reaches into the most remote parts of the country .
Early the next morning , I set out for the @ @ @ @ @ @ @ least populated province , with Pamela Phillips and John Welch .
Both are scientists who have spent decades working on screwworm eradication ; Phillips is now COPEG ’ s technical director , and Welch is its former technical director and current screwworm-program liaison .
Phillips and Welch work for COPEG through the USDA , and they had to inform the U.S. embassy that they were going to the Darién .
We also had to avoid “ red zones , ” areas in the province that the U.S. government considers too risky for its @ @ @ @ @ @ @ COPEG ’ s Panamanian inspectors still work in those parts . )
FARC guerrillas used to roam the Darién , and drugs from South America still pass through here on their way north .
Welch is a bearded Texan with no fewer than two screwworm tattoos .
He learned to speak Spanish after joining the program in 1984 , and despite his very American accent , he launched into easy jokes with everyone we met .
He hired Phillips to analyze satellite imagery for screwworm habitats in 1994 .
After 25 years of @ @ @ @ @ @ @ of an old married couple .
“ I ’ m biologically 67 , ” Welch told me .
“ Mentally , still a teenager , ” Phillips added .
As scientists , they have both found in screwworms a formidable intellectual challenge .
As nature lovers , they enjoy the opportunities for travel that come with the job too .
Read : Why Italians are growing apples for wild bears Welch may be an adolescent at heart , but his back doesn ’ t handle these trips as well as it used to @ @ @ @ @ @ @ so festooned with potholes that Phillips had to frequently swerve into the opposite lane to avoid them .
When we crossed into the province , we stopped at a checkpoint to show our passports to the Senafront , Panama ’ s border police .
COPEG has a checkpoint here too , mere feet away—but for animals .
Cattle leaving the Darién are unloaded one by one and inspected for wounds , which are painted with a blue-green anti-parasite medication to kill any screwworms .
Not too far past this checkpoint , the highway @ @ @ @ @ @ @ only way to travel farther is by river .
We , along with several Panamanian staff , put all our things in waterproof trash bags and got into a small COPEG boat .
We arrived first in the town of Garachiné , a small collection of mostly cinder-block houses , then climbed into a COPEG pickup to jostle along the uneven dirt road to the smaller town of Sambu .
During the hour-long drive , we passed more horses and riders than cars .
Butterflies erupted by the road in regular bursts .
@ @ @ @ @ @ @ wild than it used to be .
What was once rainforest and swamp is now pastureland .
“ People bring cattle here to fatten them up , ” Phillips said .
Cattle ranching has been expanding in the Darién , and COPEG inspectors must travel down ever more roads and rivers to visit ever more farms .
At a farm between Garachiné and Sambu , a farmer greeted us with his infant boy in tow , having recognized the COPEG logo—a retro-looking atomic fly—on our car .
Inspectors stop by regularly to check @ @ @ @ @ @ @ , reminding them to be vigilant of screwworms .
A COPEG veterinarian , Manuel Sánchez , showed me the handwritten log recording several years of visits to this farm .
Staff members visit the highest-risk farms in this region at least once a month , medium-risk farms every four months , and the rest once a year .
The small COPEG outpost in this zone is responsible for a total of 224 farms .
There are 12 other COPEG field posts like it in the Darién .
We were late leaving Garachiné , @ @ @ @ @ @ @ to move through the area ’ s shallow rivers and estuaries was on its way out .
If the tide got too low , we would have to spend the night in Garachiné , where the COPEG office keeps a stack of old mattresses handy for stranded employees .
We decided that the few hundred feet of mud and shallow water that separated us from the boat were traversable .
But the mud gave way like quicksand , swallowing our feet whole .
I pulled out my left leg , then my right @ @ @ @ @ @ @ .
Phillips almost lost her shoe .
We eventually made it to the boat , wet and oozing mud .
When the USDA began expanding the screwworm program into Central America , it dispatched scientists to all sorts of remote places .
They collected new screwworm strains , studied the habitat in each country , and when screwworms were thought to be eradicated from a region , verified that they were gone .
The work took Welch to Mexico , Panama , Costa Rica , Belize , Guatemala , Honduras , Nicaragua , @ @ @ @ @ @ @ , Uruguay , Jamaica , Aruba , and Cuba ’ s Guantánamo Bay .
He and his colleagues hiked up and down mountains , sometimes in pouring rain , to check traps baited with a chemical attractant called Swormlure .
On easier days , they sat for hours next to rotting liver , waiting for its odor to attract live screwworms .
Sometimes they slept in cars and on hut floors .
Sometimes they camped , falling asleep to the sounds of wind and water .
The U.S. government ’ s decision to @ @ @ @ @ @ @ about money .
Protecting American livestock by dropping sterile flies over the narrow 50-mile Isthmus of Panama is cheaper than maintaining a barrier , even a virtual one , along the 2,000-mile U.S.-Mexico border .
The U.S. had officially declared victory over the screwworm in 1966 , but the barrier of sterile flies it established on the U.S.-Mexico border quickly proved ineffective .
Ranchers in the U.S. Southwest continued to see outbreaks .
With Mexico ’ s cooperation , the eradication front moved south to the Isthmus of Tehuantepec , where Mexico narrows @ @ @ @ @ @ @ split the bill based on the value of the livestock that would benefit in each country : 80 percent U.S. , 20 percent Mexico .
In 1985 , USDA scientists proposed moving the barrier south again—to the even narrower Isthmus of Panama , where it would be cheaper to maintain .
But it would require convincing the governments of seven more countries to agree to—and help pay for—screwworm eradication .
The late 1980s were turbulent times for Central America .
Both state-sponsored and guerrilla attacks on civilians were widespread .
Other parts of @ @ @ @ @ @ @ region as part of Cold War politics .
“ A lot of people speculated I was with the CIA , ” says John Wyss , a retired USDA scientist and administrator who spent long periods in Central America working on the screwworm program ’ s expansion .
Negotiations between USDA officials and their Central American colleagues took place against a backdrop of violence .
Another USDA scientist , in his memoir , recalled negotiating with Honduran government officials about screwworms—only to learn two weeks later that the building where they had met had @ @ @ @ @ @ @ did have enthusiastic local allies , Wyss told me : Livestock owners in every country loved the idea .
The negotiations went slowly , but by 1994 , all of the countries had signed cooperative agreements with the U.S .
In 2000 , when Central American eradication was in its final phases , Wyss wrote a paper touting the program ’ s political achievements .
“ There is one tool that has played an important role since the beginning of the screwworm eradication program , one that is frequently overlooked or not even @ @ @ @ @ @ @ This tool is the cooperative agreement.
” These agreements outline , in bureaucratic detail , how salaries will be paid , how property will be managed , and how the agreement itself will be amended .
Panama was declared free of screwworm in 2006 , and the sterile-insect barrier was erected .
COPEG is now jointly headed by two director generals : Vanessa Dellis for the U.S. and Enrique Samudio for Panama .
The screwworm program costs $ 15 million a year , a small fraction of the estimated $ 796 million a @ @ @ @ @ @ @ ( That estimate , from 1996 , is equivalent to $ 1.3 billion in today ’ s dollars . )
Still , the program is constantly looking for ways to cut costs .
At the production facility , Phillips showed me prototypes of small , climate-controlled rearing cabinets , which could eliminate the need to heat or cool entire rooms .
Biologists are also developing a genetically modified male-only strain of screwworms , which would require fewer flies to be raised and released .
A cheaper program is a more sustainable one , @ @ @ @ @ @ @ years , the success of screwworm eradication has inspired scientists to apply the sterile-insect technique to other agricultural pests such as the Mexican fruit fly , the Mediterraean fruit fly , and the pink bollworm .
These programs have had varying degrees of success in the U.S. , but none has expanded as widely as the screwworm effort .
Screwworm infections , meanwhile , are still endemic in livestock and wildlife south of the sterile-insect barrier .
South American countries , such as Uruguay , have at times inquired about eradicating the parasite @ @ @ @ @ @ @ it alone makes little sense , given the porousness of national borders .
And getting the entire South American continent on board is so colossal a financial and diplomatic undertaking that it hardly seems possible .
I wondered about this when I was in Panama , and I ’ ve been wondering about it now , while I ’ m confined to my apartment .
Today , the world is struggling to contain a pestilence of a very different kind .
Nations are closing their borders to fend for themselves , and the @ @ @ @ @ @ @ in global leadership .
Containment is about science , yes , but it ’ s also about politics .
Screwworm eradication worked only because it had support from both .
Read : When conservationists kill lots ( and lots ) of animals In late 2016 , when screwworms showed up in the Florida Keys , experts immediately suspected that they had come from Cuba .
The U.S.-led eradication program had never reached the island—the two countries weren ’ t exactly on good terms in the ’ 80s and ’ 90s—so screwworms continued to @ @ @ @ @ @ @ Cuban screwworm experts still had to deal with the pests the old-fashioned way , by treating infections as they arose .
And even they agreed that their island was the likely source of the Keys outbreak .
“ We asked them what did they think , and they laughed and said , ‘ What do you think ?
We ’ re right here , ’ ” Welch recalled .
That Cuban and U.S. entomologists could talk to one another at all was new .
For decades , USDA employees were prohibited from communicating @ @ @ @ @ @ @ they attended the same international screwworm meetings .
Then , in late 2014 , President Barack Obama relaxed U.S. restrictions on trade with Cuba and relations started to thaw .
So even when DNA tests were ultimately inconclusive about the origin of the Keys outbreak , scientists in both countries began to talk about implementing an eradication program in Cuba , and a Cuban scientist traveled to Panama to visit the COPEG production plant .
But in August 2017 , strange stories started to circulate about American diplomats in Cuba .
They were @ @ @ @ @ @ @ “ sonic attacks.
” In response , the U.S. withdrew its nonessential staff from the country and expelled two Cuban diplomats .
Cuban scientists stopped replying to the Americans ’ emails about screwworms .
On my last full day in Panama , I woke up before dawn to head to the airport , where I would board a small turboprop plane loaded with 2.1 million sterilized screwworms .
I had wandered the airport ’ s passenger terminals with my carry-on just a few days earlier , but now I was whisked into a @ @ @ @ @ @ @ was COPEG ’ s dispersal center .
Four days a week , a white van that workers call the “ Pupamobile ” drops off coolers of sterilized pupae .
The center then bursts into activity .
A repurposed industrial pill-counting machine spits out 450 milliliters of pupae at a time onto aluminum trays , which are then stacked about 50 deep .
Two days later , the adult emerge as flies .
They are moved into a cold room , where they enter a dormant state ; the sluggish flies are then loaded @ @ @ @ @ @ @ onto the plane .
I was there on Monday , which meant that two flights were scheduled that morning .
The planes are used military aircraft , each customized with a continuously rotating dispersal machine that spits flies out of the plane ’ s belly at an adjustable rate per nautical mile .
( In the old days , a technician threw out small cardboard boxes of flies by hand , but the boxes sometimes didn ’ t break open on impact and the flies died inside . )
The dispersal machine is @ @ @ @ @ @ @ ’ t wake until they hit warm outside air .
A few , however , always manage to escape into the cockpit .
One of the pilots came over to introduce himself as Michael Jackson .
( Yes , he explained , his father was a big fan . )
Jackson used to do medical evacuations , but he had switched to more regularly scheduled screwworm-dispersal flights , and I would be flying with him that morning .
I climbed into his plane and noticed , with slight hesitation , that the only @ @ @ @ @ @ @ in the cockpit .
He nodded .
I was to sit there .
As usual , a technician sat next to the screwworm box in the back , logging temperatures and confirming the dispersal machine ’ s proper function .
By the time we took off , at 6:50 a.m. , the sun had burned off some of the clouds .
“ You are so lucky .
We have good weather today , ” Jackson said .
Good weather meant good visibility .
I watched as the sea of rust-red roofs around Panama @ @ @ @ @ @ @ of the Darién .
I had never before flown so close to the ground : When we passed over towns where field inspectors had recently found screwworm infections , we dipped to just 1,500 feet to make sure the sterile flies would not be blown off course on their journey back to earth .
We were low enough to pick out individual cattle , scattered like grains of rice on a green plain .
Read : The mystery of the disappearing seabird The wildlife were not as easy to spot from the plane @ @ @ @ @ @ @ altered by our flight .
Welch had told me that howler monkeys in Panama sometimes fell from trees after screwworms ate out their eyes .
That doesn ’ t happen anymore .
Jaguars , sloths , tapirs , horses , coyotes , buffalo , rabbits , and squirrels up and down the North American continent are now spared from screwworms too .
In the U.S. , the main ecological consequence of eradication has been a dramatic increase in the wild-deer population , which once fluctuated with screwworm numbers .
The parasite used to @ @ @ @ @ @ @ , whose unhealed belly buttons were open wounds .
In the Keys , the recent screwworm outbreak became obvious during mating season , when males began fighting one another with their antlers .
Their small , usually harmless nicks and cuts turned large and horrific once screwworms invaded them .
When the plane reached the Colombian border , Jackson notified air traffic control and continued on for 20 nautical miles .
Every month , the program asks Colombia for permission to release screwworms within its borders , hoping to create a screwworm-free buffer @ @ @ @ @ @ @ We looped over the Darién and this thin slice of Colombia several times in four hours , until the plane had dispersed all 2.1 million flies onboard .
The dispersal machine whirred behind us , spinning at its preset speed , pushing out clumps of flies at its preset rate .
Screwworms that had spent their entire life crammed in a factory would now wake to find themselves falling thousands of feet through thin air .
They would land , and then they would mate .
That ’ s what their evolutionary instincts @ @ @ @ @ @ @ ’ s what the humans who sterilized them want them to do .
During the final hour of the flight , I looked intently out the window , hoping for a last glimpse of all the places I had been .
We flew over the potholed highway into the Darién .
We flew over the yellow ribbons of river that led to Sambu and Garachiné .
We flew over COPEG ’ s production plant , with millions of screwworms feeding beneath its unmistakable green roof .
The next day , I would fly @ @ @ @ @ @ @ on a jetliner bound for America—where USDA-graded steaks sit on supermarket shelves , where deer leap across the landscape , and where the efforts of a distant group of people keep us safely ignorant of screwworms .

The Florida Keys are a place where deer stand next to children at school-bus stops. They lounge on lawns. They eat snacks right out of people’s hands. So when the deer began acting strangely in the summer of 2016, the people of the Keys noticed. Bucks started swinging their heads erratically, as if trying to shake something loose.
Then wounds opened on their heads—big, gaping wounds that exposed white slabs of bone. Something was eating the deer alive.
That something, lab tests would later confirm, was the New World screwworm, a parasite supposed to have been eradicated from the United States half a century ago. No one in the Keys had ever seen it. If you had asked an old-time Florida rancher though, he might have told you boyhood stories of similarly disfigured and dying cattle. In those days, screwworms found their way into cattle through any opening in the skin: the belly buttons of newborn calves, scratches from barbed wire, even a tick bite. Then they feasted.
Screwworms once killed millions of dollars’ worth of cattle a year in the southern U.S. Their range extended from Florida to California, and they infected any living, warm-blooded animal: not only cattle but deer, squirrels, pets, and even the occasional human. In fact, the screwworm’s scientific name is C. hominivorax or “man eater”—so named after a horrific outbreak among prisoners on Devil’s Island, an infamous 19th-century French penal colony in South America.
For untold millennia, screwworms were a grisly fact of life in the Americas. In the 1950s, however, U.S. ranchers began to envision a new status quo. They dared to dream of an entire country free of screwworms. At their urging, the United States Department of Agriculture undertook what would ultimately become an immense, multidecade effort to wipe out the screwworms, first in the U.S. and then in Mexico and Central America—all the way down to the narrow strip of land that is the Isthmus of Panama. The eradication was a resounding success. But the story does not end there. Containing a disease is one thing. Keeping it contained is another thing entirely, as the coronavirus pandemic is now so dramatically demonstrating.
Read: The ‘golden death’ bacterium found in a rotten apple
To get the screwworms out, the USDA to this day maintains an international screwworm barrier along the Panama-Colombia border. The barrier is an invisible one, and it is kept in place by constant human effort. Every week, planes drop 14.7 million sterilized screwworms over the rainforest that divides the two countries. A screwworm-rearing plant operates 24/7 in Panama. Inspectors cover thousands of square miles by motorcycle, boat, and horseback, searching for stray screwworm infections north of the border. The slightest oversight could undo all the work that came before.
The insect is relentless in its search for hosts. Those who fight it must be relentless too.
This past August, I went to Panama to meet the people who maintain the screwworm barrier. The Keys outbreak was long over by then, quelled within months by the release of sterile screwworms from Panama. As startling as it was to Floridians, it had been just a small, gruesome blip in the history of the screwworm.
A transcontinental screwworm barrier has been in place for 50 years—longer than many of the people who now maintain it have been alive. They work for a joint commission of Panama’s agricultural department and the USDA known as COPEG, or the Comisión Panamá–Estados Unidos para la Erradicación y Prevención del Gusano Barrenador del Ganado. The day before I landed at Tocumen International Airport, two small COPEG planes had taken off and released their precious loads of screwworms over the Panama-Colombia border.
More screwworm flights were scheduled for the next day, a Wednesday, and Thursday and Saturday and Monday and so on and on. “We will be here for a long time,” a COPEG staff member in Panama told me with evident pride. “We should be here for the next 100 years.”
In the early days of the eradication effort, USDA scientists were not so certain of success—or longevity. They had to bootleg money from other programs because they didn’t have enough funding. In press interviews, they worried about what laughingstocks they’d be if their “idiotic insect-sex scheme” failed and, God forbid, became an extremely mockable symbol of government waste.
Read: Decapitated worms get better, see again
The man who came up with the scheme, and believed in it most passionately, was Edward F. Knipling, a USDA entomologist who, in the 1930s, spent long hours watching screwworms mate. As a boy, he had waged constant war against insect pests on his family’s Texas farm. “Every plant that we grew,” he later said, “there was some type of insect that was causing damage.” Screwworms infected the farm’s cows and pigs, and Knipling remembered them as one of the worst pests. He had to climb into the hog pens to smear medicine on the wounds of uncooperative sows. “That was a very unpleasant task,” he recalled some eight decades later, in an interview shortly before he died.
Adult screwworms are actually flies, with big red eyes and metallic blue-green bodies. After mating, the females lay their eggs in open wounds, and the resulting larvae eat through a ring of surrounding flesh. Once sufficiently engorged, the larvae drop off the wounds to pupate, emerging as a new generation of flies. As Knipling watched screwworms churn through their life cycle in his government laboratory, he made an observation whose importance he could intuit but not yet put to use: Female screwworms mate only once in their entire life. If a female screwworm mates with a sterile male, she will never have any offspring. So if the environment could somehow be saturated with sterile males, Knipling surmised, screwworms would very quickly mate themselves out of existence.
But Knipling did not know how to sterilize male screwworms. In any case, the U.S. was entering World War II, and his expertise was needed elsewhere. Knipling was reassigned to a lab in Florida, where his team perfected incredibly effective pesticides such as DDT that protected troops from insect-borne diseases. DDT helped the U.S. win the war, but it would later devastate the environment from overuse. This experience shaped the rest of Knipling’s career. He devoted himself to sterilizing insects, a way to control pests without pesticides.
After the war, Knipling went back to studying screwworms with his fellow entomologist Raymond Bushland. Scientists now knew, from the horrific consequences of atomic bombs dropped on Japan, that high doses of radiation damage human tissue and cells. When a colleague introduced Knipling to research on the sterilization of other flies by radiation, he wondered: Could radiation sterilize screwworms too?
Read: Nuclear tests marked life on earth with a radioactive spike
The entomologists managed to get access to an X-ray machine at a nearby military hospital where one of Bushland’s old Army buddies worked. Every Thursday afternoon, Knipling and Bushland put their screwworms through the X-ray machine, experimenting with different developmental stages and radiation levels. They needed screwworms that were damaged enough to be sterile but not so damaged that they could not attract a mate in the wild. The best time to irradiate, the two found, was 5.5 to 5.7 days into the pupal stage, when the adult fly’s ovaries and testes were developing and thus most sensitive to radiation.
The radiation worked. These screwworms indeed turned sterile, but Knipling and Bushland still needed to prove that irradiated males could actually mate with fertile females in the field. In 1951, a USDA team began releasing sterile male screwworms on Sanibel Island off the coast of Florida. The screwworms persisted, so the team in turn persisted, releasing sterile males on the island for two more years. It still didn’t work. The team thought that fertile males were probably flying over from the mainland. So in 1954, the scientists tried again on a more remote island: Curaçao in the Dutch Caribbean. This time, they succeeded. Screwworms disappeared from the island within months.
From here, a quietly audacious project to reengineer the environment for livestock got underway, ultimately changing the lives of cattle, deer, and humans throughout the North American continent.
When the Florida Cattlemen’s Association caught wind of the success on Curaçao, it immediately recognized the potential closer to home. The group lobbied state and federal officials for a bigger undertaking. And in 1957, the USDA began a campaign to wipe out the flesh-eating parasites east of the Mississippi River. When that succeeded two years later, ranchers in Texas, Louisiana, New Mexico, Arizona, and California started clamoring for their own eradication program. Screwworms were so widespread in those states that they had shaped cowboy culture: Long days of “riding the range,” for example, were dedicated to finding signs of screwworm infection.
For the USDA, though, the West proved a challenge on a different scale. The screwworm-eradication program had to build a new plant in Mission, Texas, to produce as many as 200 million sterile flies each week. Because screwworms prefer to eat living flesh, feeding the plant’s flies was a grisly logistical puzzle. Initially, USDA scientists gave the screwworms a mixture of warm ground beef and blood, but beef was expensive. At various times, they substituted cheaper meats such as horse, whale, pig or cow lung, and even nutria—an invasive rodent that was then taking over Louisiana. By 1962, the flies at the Mission plant were consuming 240,000 pounds of meat and 10,000 gallons of whole blood every week. In the earliest days of sterile-screwworm testing, the flies stank so badly that airlines refused to ship them. Workers learned to spray the boxes with cologne.
The Mission plant closed in 1981, when screwworm rearing moved to Mexico and then later to Panama. Today, the screwworm-production facility in Panama is located on an old sugarcane plantation, about 20 miles east of the country’s capital. The roof is painted a smooth mint green, and the facility is the program’s most modern yet. But screwworms still have primordial urges: They still have to feed on animal remnants. So when I stepped inside the facility last August, the first thing I noticed was the smell—foul, with a metallic tang. My brain involuntarily matched it to bloody tampon.
Screwworms are no longer given raw meat, but their keepers make sure they get animal protein in other ways. The current diet is a more economical mix of powdered blood, milk, and egg—reconstituted and then thickened with cellulose into a dark-brown sludge. I watched workers pipe it into trays, the diet gushing like sewage.
The rearing facility itself is a windowless maze of concrete. Each room is maintained at a prescribed temperature and humidity, optimized for a particular stage of screwworm development. The larvae, for example, hatch in a room heated to 102 degrees Fahrenheit, which mimics the body temperature of an infected animal. Once hatched, they are wheeled to cooler rooms, where they crawl out of their food and become pupae. My glasses fogged up multiple times as we moved through rooms hot and cold, dry and humid, following the screwworm’s life cycle.
In the 102-degree hatching room, staff pulled out a tray of food to show me a “feeding pocket.” When screwworms eat, they like to pack themselves tightly together like cigarettes in a carton, their mouths shoved down into the food and their white tails wriggling in the air. I had come across pictures of feeding pockets in animals’ open wounds before. Now I forced myself to look at the writhing brown mass, imagining this protein sludge to be flesh yielding to thousands of relentless mouths.
“For me, beautiful,” said Sabina Barrios, the head of screwworm production, gesturing at the feeding pocket. What she saw were healthy screwworms that would grow big and fat. In a few days, they would turn into pupae, also big and fat, that could be sterilized with radioactive cobalt 60. And a couple of days after that, they would emerge as flies, vigorous and ready to mate. A hundred and fifteen people work to keep the plant operating 24 hours a day, every day, to produce 20 million of these flies a week.
COPEG does more than produce sterile flies. It also runs a network of screwworm-inspection posts and offices that reaches into the most remote parts of the country. Early the next morning, I set out for the Darién, Panama’s easternmost and least populated province, with Pamela Phillips and John Welch. Both are scientists who have spent decades working on screwworm eradication; Phillips is now COPEG’s technical director, and Welch is its former technical director and current screwworm-program liaison.
Phillips and Welch work for COPEG through the USDA, and they had to inform the U.S. embassy that they were going to the Darién. We also had to avoid “red zones,” areas in the province that the U.S. government considers too risky for its employees to enter at all. (COPEG’s Panamanian inspectors still work in those parts.) FARC guerrillas used to roam the Darién, and drugs from South America still pass through here on their way north.
Welch is a bearded Texan with no fewer than two screwworm tattoos. He learned to speak Spanish after joining the program in 1984, and despite his very American accent, he launched into easy jokes with everyone we met. He hired Phillips to analyze satellite imagery for screwworm habitats in 1994. After 25 years of working together, their dynamic resembles that of an old married couple. “I’m biologically 67,” Welch told me. “Mentally, still a teenager,” Phillips added. As scientists, they have both found in screwworms a formidable intellectual challenge. As nature lovers, they enjoy the opportunities for travel that come with the job too.
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Welch may be an adolescent at heart, but his back doesn’t handle these trips as well as it used to. The road to the Darién is so festooned with potholes that Phillips had to frequently swerve into the opposite lane to avoid them. When we crossed into the province, we stopped at a checkpoint to show our passports to the Senafront, Panama’s border police. COPEG has a checkpoint here too, mere feet away—but for animals. Cattle leaving the Darién are unloaded one by one and inspected for wounds, which are painted with a blue-green anti-parasite medication to kill any screwworms.
Not too far past this checkpoint, the highway in the Darién simply ends. The only way to travel farther is by river. We, along with several Panamanian staff, put all our things in waterproof trash bags and got into a small COPEG boat. We arrived first in the town of Garachiné, a small collection of mostly cinder-block houses, then climbed into a COPEG pickup to jostle along the uneven dirt road to the smaller town of Sambu. During the hour-long drive, we passed more horses and riders than cars. Butterflies erupted by the road in regular bursts. But the land here is far less wild than it used to be. What was once rainforest and swamp is now pastureland. “People bring cattle here to fatten them up,” Phillips said.
Cattle ranching has been expanding in the Darién, and COPEG inspectors must travel down ever more roads and rivers to visit ever more farms. At a farm between Garachiné and Sambu, a farmer greeted us with his infant boy in tow, having recognized the COPEG logo—a retro-looking atomic fly—on our car. Inspectors stop by regularly to check the animals and chat with the farmers, reminding them to be vigilant of screwworms. A COPEG veterinarian, Manuel Sánchez, showed me the handwritten log recording several years of visits to this farm. Staff members visit the highest-risk farms in this region at least once a month, medium-risk farms every four months, and the rest once a year. The small COPEG outpost in this zone is responsible for a total of 224 farms. There are 12 other COPEG field posts like it in the Darién.
We were late leaving Garachiné, and the high tide that allows boats to move through the area’s shallow rivers and estuaries was on its way out. If the tide got too low, we would have to spend the night in Garachiné, where the COPEG office keeps a stack of old mattresses handy for stranded employees. We decided that the few hundred feet of mud and shallow water that separated us from the boat were traversable. But the mud gave way like quicksand, swallowing our feet whole. I pulled out my left leg, then my right leg, and then my left again. Phillips almost lost her shoe. We eventually made it to the boat, wet and oozing mud.
When the USDA began expanding the screwworm program into Central America, it dispatched scientists to all sorts of remote places. They collected new screwworm strains, studied the habitat in each country, and when screwworms were thought to be eradicated from a region, verified that they were gone. The work took Welch to Mexico, Panama, Costa Rica, Belize, Guatemala, Honduras, Nicaragua, the Dominican Republic, Colombia, Argentina, Uruguay, Jamaica, Aruba, and Cuba’s Guantánamo Bay. He and his colleagues hiked up and down mountains, sometimes in pouring rain, to check traps baited with a chemical attractant called Swormlure. On easier days, they sat for hours next to rotting liver, waiting for its odor to attract live screwworms. Sometimes they slept in cars and on hut floors. Sometimes they camped, falling asleep to the sounds of wind and water.
The U.S. government’s decision to eradicate screwworms in Central America was ultimately about money. Protecting American livestock by dropping sterile flies over the narrow 50-mile Isthmus of Panama is cheaper than maintaining a barrier, even a virtual one, along the 2,000-mile U.S.-Mexico border.
The U.S. had officially declared victory over the screwworm in 1966, but the barrier of sterile flies it established on the U.S.-Mexico border quickly proved ineffective. Ranchers in the U.S. Southwest continued to see outbreaks. With Mexico’s cooperation, the eradication front moved south to the Isthmus of Tehuantepec, where Mexico narrows to 120 miles. The two countries split the bill based on the value of the livestock that would benefit in each country: 80 percent U.S., 20 percent Mexico.
In 1985, USDA scientists proposed moving the barrier south again—to the even narrower Isthmus of Panama, where it would be cheaper to maintain. But it would require convincing the governments of seven more countries to agree to—and help pay for—screwworm eradication.
The late 1980s were turbulent times for Central America. Both state-sponsored and guerrilla attacks on civilians were widespread. Other parts of the U.S. government were intervening in the region as part of Cold War politics. “A lot of people speculated I was with the CIA,” says John Wyss, a retired USDA scientist and administrator who spent long periods in Central America working on the screwworm program’s expansion. Negotiations between USDA officials and their Central American colleagues took place against a backdrop of violence. Another USDA scientist, in his memoir, recalled negotiating with Honduran government officials about screwworms—only to learn two weeks later that the building where they had met had been blown up.
Read: Death-cap mushrooms are spreading across North America
The eradication effort did have enthusiastic local allies, Wyss told me: Livestock owners in every country loved the idea. The negotiations went slowly, but by 1994, all of the countries had signed cooperative agreements with the U.S.
In 2000, when Central American eradication was in its final phases, Wyss wrote a paper touting the program’s political achievements. “There is one tool that has played an important role since the beginning of the screwworm eradication program, one that is frequently overlooked or not even mentioned,” he wrote. “This tool is the cooperative agreement.” These agreements outline, in bureaucratic detail, how salaries will be paid, how property will be managed, and how the agreement itself will be amended. Panama was declared free of screwworm in 2006, and the sterile-insect barrier was erected. COPEG is now jointly headed by two director generals: Vanessa Dellis for the U.S. and Enrique Samudio for Panama.
The screwworm program costs $15 million a year, a small fraction of the estimated $796 million a year that it saves American farmers. (That estimate, from 1996, is equivalent to $1.3 billion in today’s dollars.) Still, the program is constantly looking for ways to cut costs. At the production facility, Phillips showed me prototypes of small, climate-controlled rearing cabinets, which could eliminate the need to heat or cool entire rooms. Biologists are also developing a genetically modified male-only strain of screwworms, which would require fewer flies to be raised and released. A cheaper program is a more sustainable one, and sustainability is essential.
Cornelia Li
Over the years, the success of screwworm eradication has inspired scientists to apply the sterile-insect technique to other agricultural pests such as the Mexican fruit fly, the Mediterraean fruit fly, and the pink bollworm. These programs have had varying degrees of success in the U.S., but none has expanded as widely as the screwworm effort. Screwworm infections, meanwhile, are still endemic in livestock and wildlife south of the sterile-insect barrier. South American countries, such as Uruguay, have at times inquired about eradicating the parasite. But for any country to go it alone makes little sense, given the porousness of national borders. And getting the entire South American continent on board is so colossal a financial and diplomatic undertaking that it hardly seems possible.
I wondered about this when I was in Panama, and I’ve been wondering about it now, while I’m confined to my apartment. Today, the world is struggling to contain a pestilence of a very different kind. Nations are closing their borders to fend for themselves, and the U.S. is entirely absent from its role in global leadership. Containment is about science, yes, but it’s also about politics. Screwworm eradication worked only because it had support from both.
Read: When conservationists kill lots (and lots) of animals
In late 2016, when screwworms showed up in the Florida Keys, experts immediately suspected that they had come from Cuba. The U.S.-led eradication program had never reached the island—the two countries weren’t exactly on good terms in the ’80s and ’90s—so screwworms continued to prosper 90 miles from the Keys. Cuban screwworm experts still had to deal with the pests the old-fashioned way, by treating infections as they arose. And even they agreed that their island was the likely source of the Keys outbreak. “We asked them what did they think, and they laughed and said, ‘What do you think? We’re right here,’” Welch recalled.
That Cuban and U.S. entomologists could talk to one another at all was new. For decades, USDA employees were prohibited from communicating with their Cuban counterparts, even when they attended the same international screwworm meetings. Then, in late 2014, President Barack Obama relaxed U.S. restrictions on trade with Cuba and relations started to thaw. So even when DNA tests were ultimately inconclusive about the origin of the Keys outbreak, scientists in both countries began to talk about implementing an eradication program in Cuba, and a Cuban scientist traveled to Panama to visit the COPEG production plant.
But in August 2017, strange stories started to circulate about American diplomats in Cuba. They were falling ill, from mysterious and unconfirmed “sonic attacks.” In response, the U.S. withdrew its nonessential staff from the country and expelled two Cuban diplomats. Cuban scientists stopped replying to the Americans’ emails about screwworms.
On my last full day in Panama, I woke up before dawn to head to the airport, where I would board a small turboprop plane loaded with 2.1 million sterilized screwworms. I had wandered the airport’s passenger terminals with my carry-on just a few days earlier, but now I was whisked into a wing closed to commercial passengers. This was COPEG’s dispersal center.
Four days a week, a white van that workers call the “Pupamobile” drops off coolers of sterilized pupae. The center then bursts into activity. A repurposed industrial pill-counting machine spits out 450 milliliters of pupae at a time onto aluminum trays, which are then stacked about 50 deep. Two days later, the adult emerge as flies. They are moved into a cold room, where they enter a dormant state; the sluggish flies are then loaded into a washing-machine-size metal box and loaded onto the plane.
I was there on Monday, which meant that two flights were scheduled that morning. The planes are used military aircraft, each customized with a continuously rotating dispersal machine that spits flies out of the plane’s belly at an adjustable rate per nautical mile. (In the old days, a technician threw out small cardboard boxes of flies by hand, but the boxes sometimes didn’t break open on impact and the flies died inside.) The dispersal machine is kept cold, so the flies won’t wake until they hit warm outside air. A few, however, always manage to escape into the cockpit.
One of the pilots came over to introduce himself as Michael Jackson. (Yes, he explained, his father was a big fan.) Jackson used to do medical evacuations, but he had switched to more regularly scheduled screwworm-dispersal flights, and I would be flying with him that morning. I climbed into his plane and noticed, with slight hesitation, that the only open seat was the co-pilot’s in the cockpit. He nodded. I was to sit there. As usual, a technician sat next to the screwworm box in the back, logging temperatures and confirming the dispersal machine’s proper function.
By the time we took off, at 6:50 a.m., the sun had burned off some of the clouds. “You are so lucky. We have good weather today,” Jackson said. Good weather meant good visibility. I watched as the sea of rust-red roofs around Panama City gave way to the emerald lushness of the Darién. I had never before flown so close to the ground: When we passed over towns where field inspectors had recently found screwworm infections, we dipped to just 1,500 feet to make sure the sterile flies would not be blown off course on their journey back to earth. We were low enough to pick out individual cattle, scattered like grains of rice on a green plain.
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The wildlife were not as easy to spot from the plane, but their lives would also be altered by our flight. Welch had told me that howler monkeys in Panama sometimes fell from trees after screwworms ate out their eyes. That doesn’t happen anymore. Jaguars, sloths, tapirs, horses, coyotes, buffalo, rabbits, and squirrels up and down the North American continent are now spared from screwworms too. In the U.S., the main ecological consequence of eradication has been a dramatic increase in the wild-deer population, which once fluctuated with screwworm numbers. The parasite used to kill a large proportion of newborn fawns, whose unhealed belly buttons were open wounds. In the Keys, the recent screwworm outbreak became obvious during mating season, when males began fighting one another with their antlers. Their small, usually harmless nicks and cuts turned large and horrific once screwworms invaded them.
When the plane reached the Colombian border, Jackson notified air traffic control and continued on for 20 nautical miles. Every month, the program asks Colombia for permission to release screwworms within its borders, hoping to create a screwworm-free buffer zone that reinforces the continental barrier. We looped over the Darién and this thin slice of Colombia several times in four hours, until the plane had dispersed all 2.1 million flies onboard. The dispersal machine whirred behind us, spinning at its preset speed, pushing out clumps of flies at its preset rate. Screwworms that had spent their entire life crammed in a factory would now wake to find themselves falling thousands of feet through thin air. They would land, and then they would mate. That’s what their evolutionary instincts have primed them to do; that’s what the humans who sterilized them want them to do.
During the final hour of the flight, I looked intently out the window, hoping for a last glimpse of all the places I had been. We flew over the potholed highway into the Darién. We flew over the yellow ribbons of river that led to Sambu and Garachiné. We flew over COPEG’s production plant, with millions of screwworms feeding beneath its unmistakable green roof. The next day, I would fly through the same airspace, this time on a jetliner bound for America—where USDA-graded steaks sit on supermarket shelves, where deer leap across the landscape, and where the efforts of a distant group of people keep us safely ignorant of screwworms.


theatlantic--2020-03-20--Why the Coronavirus Has Been So Successful

During a cytokine storm , the immune system isn ’ t just going berserk but is also generally off its game , attacking at will without hitting the right targets .
When this happens , people become more susceptible to infectious bacteria .
The storms can also affect other organs besides the lungs , especially if people already have chronic diseases .
This might explain why some COVID-19 patients end up with complications such as heart problems and secondary infections .
But why do some people with COVID-19 get incredibly sick , while others escape with mild or nonexistent symptoms @ @ @ @ @ @ @ people are at risk of more severe infections possibly because their immune system can ’ t mount an effective initial defense , while children are less affected because their immune system is less likely to progress to a cytokine storm .
But other factors—a person ’ s genes , the vagaries of their immune system , the amount of virus they ’ re exposed to , the other microbes in their bodies—might play a role too .
In general , “ it ’ s a mystery why some people have mild disease , @ @ @ @ @ @ @ ” Iwasaki says .
Coronaviruses , much like influenza , tend to be winter viruses .
In cold and dry air , the thin layers of liquid that coat our lungs and airways become even thinner , and the beating hairs that rest in those layers struggle to evict viruses and other foreign particles .
Dry air also seems to dampen some aspects of the immune response to those trapped viruses .
In the heat and humidity of summer , both trends reverse , and respiratory viruses struggle to get a foothold .
@ @ @ @ @ @ @ during the pandemic Unfortunately , that might not matter for the COVID-19 pandemic .
At the moment , the virus is tearing through a world of immunologically naive people , and that vulnerability is likely to swamp any seasonal variations .
After all , the new virus is transmitting readily in countries like Singapore ( which is in the tropics ) and Australia ( which is still in summer ) .
And one recent modeling study concluded that “ SARS-CoV-2 can proliferate at any time of year.
” “ I don ’ t @ @ @ @ @ @ @ the weather is going to have the effect that people hope it will , ” Gralinski says .
“ It may knock things down a little , but there ’ s so much person-to-person transmission going on that it may take more than that.
” Unless people can slow the spread of the virus by sticking to physical-distancing recommendations , the summer alone won ’ t save us .
“ The scary part is we don ’ t even know how many people get normal coronaviruses every year , ” Frieman says .
@ @ @ @ @ @ @ surveillance networks for coronaviruses like [ we do for ] flu .
We don ’ t know why they go away in the winter , or where they go .
We don ’ t know how these viruses mutate year on year.
” Until now , research has been slow .
Ironically , a triennial conference in which the world ’ s coronavirus experts would have met in a small Dutch village in May has been postponed because of the coronavirus pandemic .
“ If we don ’ t learn from this pandemic @ @ @ @ @ @ @ more , then we ’ re very , very bad at this , ” Frieman says .

We’ve known about SARS-CoV-2 for only three months, but scientists can make some educated guesses about where it came from and why it’s behaving in such an extreme way.
One of the few mercies during this crisis is that, by their nature, individual coronaviruses are easily destroyed. Each virus particle consists of a small set of genes, enclosed by a sphere of fatty lipid molecules, and because lipid shells are easily torn apart by soap, 20 seconds of thorough hand-washing can take one down. Lipid shells are also vulnerable to the elements; a recent study shows that the new coronavirus, SARS-CoV-2, survives for no more than a day on cardboard, and about two to three days on steel and plastic. These viruses don’t endure in the world. They need bodies.
But much about coronaviruses is still unclear. Susan Weiss, of the University of Pennsylvania, has been studying them for about 40 years. She says that in the early days, only a few dozen scientists shared her interest—and those numbers swelled only slightly after the SARS epidemic of 2002. “Until then people looked at us as a backward field with not a lot of importance to human health,” she says. But with the emergence of SARS-CoV-2—the cause of the COVID-19 disease—no one is likely to repeat that mistake again.
To be clear, SARS-CoV-2 is not the flu. It causes a disease with different symptoms, spreads and kills more readily, and belongs to a completely different family of viruses. This family, the coronaviruses, includes just six other members that infect humans. Four of them—OC43, HKU1, NL63, and 229E—have been gently annoying humans for more than a century, causing a third of common colds. The other two—MERS and SARS (or “SARS-classic,” as some virologists have started calling it)—both cause far more severe disease. Why was this seventh coronavirus the one to go pandemic? Suddenly, what we do know about coronaviruses becomes a matter of international concern.
Read: What will you do if you start coughing?
The structure of the virus provides some clues about its success. In shape, it’s essentially a spiky ball. Those spikes recognize and stick to a protein called ACE2, which is found on the surface of our cells: This is the first step to an infection. The exact contours of SARS-CoV-2’s spikes allow it to stick far more strongly to ACE2 than SARS-classic did, and “it’s likely that this is really crucial for person-to-person transmission,” says Angela Rasmussen of Columbia University. In general terms, the tighter the bond, the less virus required to start an infection.
There’s another important feature. Coronavirus spikes consist of two connected halves, and the spike activates when those halves are separated; only then can the virus enter a host cell. In SARS-classic, this separation happens with some difficulty. But in SARS-CoV-2, the bridge that connects the two halves can be easily cut by an enzyme called furin, which is made by human cells and—crucially—is found across many tissues. “This is probably important for some of the really unusual things we see in this virus,” says Kristian Andersen of Scripps Research Translational Institute.
For example, most respiratory viruses tend to infect either the upper or lower airways. In general, an upper-respiratory infection spreads more easily, but tends to be milder, while a lower-respiratory infection is harder to transmit, but is more severe. SARS-CoV-2 seems to infect both upper and lower airways, perhaps because it can exploit the ubiquitous furin. This double whammy could also conceivably explain why the virus can spread between people before symptoms show up—a trait that has made it so difficult to control. Perhaps it transmits while still confined to the upper airways, before making its way deeper and causing severe symptoms. All of this is plausible but totally hypothetical; the virus was only discovered in January, and most of its biology is still a mystery.
Read: Should you take Advil for COVID-19?
The new virus certainly seems to be effective at infecting humans, despite its animal origins. The closest wild relative of SARS-CoV-2 is found in bats, which suggests it originated in a bat, then jumped to humans either directly or through another species. (Another coronavirus found in wild pangolins also resembles SARS-CoV-2, but only in the small part of the spike that recognizes ACE2; the two viruses are otherwise dissimilar, and pangolins are unlikely to be the original reservoir of the new virus.) When SARS-classic first made this leap, a brief period of mutation was necessary for it to recognize ACE2 well. But SARS-CoV-2 could do that from day one. “It had already found its best way of being a [human] virus,” says Matthew Frieman of the University of Maryland School of Medicine.
This uncanny fit will doubtlessly encourage conspiracy theorists: What are the odds that a random bat virus had exactly the right combination of traits to effectively infect human cells from the get-go, and then jump into an unsuspecting person? “Very low,” Andersen says, “but there are millions or billions of these viruses out there. These viruses are so prevalent that things that are really unlikely to happen sometimes do.”
Since the start of the pandemic, the virus hasn’t changed in any obviously important ways. It’s mutating in the way that all viruses do. But of the 100-plus mutations that have been documented, none has risen to dominance, which suggests that none is especially important. “The virus has been remarkably stable given how much transmission we’ve seen,” says Lisa Gralinski of the University of North Carolina. “That makes sense, because there’s no evolutionary pressure on the virus to transmit better. It’s doing a great job of spreading around the world right now.”
Read: The U.K.’s coronavirus “herd immunity” debacle
There’s one possible exception. A few SARS-CoV-2 viruses that were isolated from Singaporean COVID-19 patients are missing a stretch of genes that also disappeared from SARS-classic during the late stages of its epidemic. This change was thought to make the original virus less virulent, but it’s far too early to know whether the same applies to the new one. Indeed, why some coronaviruses are deadly and some are not is unclear. “There’s really no understanding at all of why SARS or SARS-CoV-2 are so bad but OC43 just gives you a runny nose,” Frieman says.
Researchers can, however, offer a preliminary account of what the new coronavirus does to the people it infects. Once in the body, it likely attacks the ACE2-bearing cells that line our airways. Dying cells slough away, filling the airways with junk and carrying the virus deeper into the body, down toward the lungs. As the infection progresses, the lungs clog with dead cells and fluid, making breathing more difficult. (The virus might also be able to infect ACE2-bearing cells in other organs, including the gut and blood vessels.)
The immune system fights back and attacks the virus; this is what causes inflammation and fever. But in extreme cases, the immune system goes berserk, causing more damage than the actual virus. For example, blood vessels might open up to allow defensive cells to reach the site of an infection; that’s great, but if the vessels become too leaky, the lungs fill even more with fluid. These damaging overreactions are called cytokine storms. They were historically responsible for many deaths during the 1918 flu pandemic, H5N1 bird flu outbreaks, and the 2003 SARS outbreak. And they’re probably behind the most severe cases of COVID-19. “These viruses need time to adapt to a human host,” says Akiko Iwasaki of the Yale School of Medicine. “When they’re first trying us out, they don’t know what they’re doing, and they tend to elicit these responses.”
Read: We were warned
During a cytokine storm, the immune system isn’t just going berserk but is also generally off its game, attacking at will without hitting the right targets. When this happens, people become more susceptible to infectious bacteria. The storms can also affect other organs besides the lungs, especially if people already have chronic diseases. This might explain why some COVID-19 patients end up with complications such as heart problems and secondary infections.
But why do some people with COVID-19 get incredibly sick, while others escape with mild or nonexistent symptoms? Age is a factor. Elderly people are at risk of more severe infections possibly because their immune system can’t mount an effective initial defense, while children are less affected because their immune system is less likely to progress to a cytokine storm. But other factors—a person’s genes, the vagaries of their immune system, the amount of virus they’re exposed to, the other microbes in their bodies—might play a role too. In general, “it’s a mystery why some people have mild disease, even within the same age group,” Iwasaki says.
Coronaviruses, much like influenza, tend to be winter viruses. In cold and dry air, the thin layers of liquid that coat our lungs and airways become even thinner, and the beating hairs that rest in those layers struggle to evict viruses and other foreign particles. Dry air also seems to dampen some aspects of the immune response to those trapped viruses. In the heat and humidity of summer, both trends reverse, and respiratory viruses struggle to get a foothold.
Read: How you should get food during the pandemic
Unfortunately, that might not matter for the COVID-19 pandemic. At the moment, the virus is tearing through a world of immunologically naive people, and that vulnerability is likely to swamp any seasonal variations. After all, the new virus is transmitting readily in countries like Singapore (which is in the tropics) and Australia (which is still in summer). And one recent modeling study concluded that “SARS-CoV-2 can proliferate at any time of year.” “I don’t have an immense amount of confidence that the weather is going to have the effect that people hope it will,” Gralinski says. “It may knock things down a little, but there’s so much person-to-person transmission going on that it may take more than that.” Unless people can slow the spread of the virus by sticking to physical-distancing recommendations, the summer alone won’t save us.
“The scary part is we don’t even know how many people get normal coronaviruses every year,” Frieman says. “We don’t have any surveillance networks for coronaviruses like [we do for] flu. We don’t know why they go away in the winter, or where they go. We don’t know how these viruses mutate year on year.” Until now, research has been slow. Ironically, a triennial conference in which the world’s coronavirus experts would have met in a small Dutch village in May has been postponed because of the coronavirus pandemic.
“If we don’t learn from this pandemic that we need to understand these viruses more, then we’re very, very bad at this,” Frieman says.


Jeffrey Goldberg

The senator from California seems like the obvious choice to be Joe Biden ’ s running mate .
So why is she keeping mum about her thinking ?
A few weeks ago , an adviser to Kamala Harris called me to talk through some polling data .
“ We understand that Joe Biden ’ s the nominee , but the party is so much different than a septuagenarian white male , ” the adviser said .
“ Kamala Harris is more symbolic of that changing America—America coming together—than some of the other potential candidates ” for vice president .
The @ @ @ @ @ @ @ because , officially , Harris is pretending that she ’ s not campaigning to be Biden ’ s running mate .
In public , Harris has repeatedly insisted that she ’ s not talking about or thinking about her prospects of being picked .
But judging from my conversations with people around Harris , she and her team use her prospects to book events and television hits that aim to show she ’ s neither overeager nor overambitious .
She and her team are avoiding situations that could create stumbles .
They ’ @ @ @ @ @ @ @ background , and the force of her personality propel her .
They ’ re picking specific moments for her to grab attention on the Senate floor or send a calibrated tweet .
They ’ re tuning out political reporters who are stuck on their couches , looking to drum up content during the pandemic .
They ’ re trying to ease concerns in Biden ’ s orbit that if she ’ s picked and they win , she ’ ll start running for president the morning after the inauguration .
They want her @ @ @ @ @ @ @ be the Democratic nominee in 2024 .

More +
He joined The Atlantic in 2007 as a national correspondent and in 2016 was named the magazine’s 15th editor in chief. During his editorship, The Atlantic has set new audience and subscription records, and won its first-ever Pulitzer Prizes. In 2022, The Atlantic received the National Magazine Award for General Excellence from the American Society of Magazine Editors, the top award in the industry. In 2020, Goldberg was named editor of the year by Adweek, which also named The Atlantic magazine of the year.
Before joining The Atlantic, Goldberg served as the Middle East correspondent, and then the Washington correspondent, for The New Yorker. Earlier in his career, he was a writer for The New York Times Magazine, where he wrote 15 cover stories. He began his career as a police reporter for The Washington Post. Goldberg is the author of Prisoners: A Story of Friendship and Terror. A former fellow of the American Academy in Berlin, he also served as a public-policy scholar at the Woodrow Wilson International Center for Scholars, and as the distinguished visiting fellow at the Carnegie Endowment for International Peace. Goldberg is the recipient of numerous awards, including the National Magazine Award for reporting, the Daniel Pearl Award for reporting, the Overseas Press Club Award for human-rights reporting, and the International Consortium of Investigative Journalists Prize for best investigative reporting.


theatlantic--2020-04-21--Why Some People Get Sicker Than Others

Why Some People Get Sicker Than Others

Read : The best hopes for a coronavirus drug COVID-19 is , in many ways , proving to be a disease of uncertainty .
According to a new study from Italy , some 43 percent of people with the virus have no symptoms .
Among those who do develop symptoms , it is common to feel sick in uncomfortable but familiar ways—congestion , fever , aches , and general malaise .
Many people start to feel a little bit better .
Then , for many , comes a dramatic tipping point .
“ Some people really fall off the cliff @ @ @ @ @ @ @ good predictors of who it ’ s going to happen to , ” Stephen Thomas , the chair of infectious diseases at Upstate University Hospital , told me .
Those people will become short of breath , their heart racing and mind detached from reality .
They experience organ failure and spend weeks in the ICU , if they survive at all .
Meanwhile , many others simply keep feeling better and eventually totally recover .
Kola ’ s friend Karan Mahajan , an author based in Providence , Rhode Island , contracted @ @ @ @ @ @ @ she did .
In stark contrast to Kola , he said , “ My case ended up feeling like a mild flu that lasted for two weeks .
And then it faded after that.
” Listen to James Hamblin interview Kola and Mahajan on an episode of Social Distance , The Atlantic ’ s podcast about life in the pandemic : Apple Podcasts or Spotify ( How to Listen ) “ There ’ s a big difference in how people handle this virus , ” says Robert Murphy , a professor of medicine @ @ @ @ @ @ @ Global Communicable Diseases at Northwestern University .
“ It ’ s very unusual .
None of this variability really fits with any other diseases we ’ re used to dealing with.
” This degree of uncertainty has less to do with the virus itself than how our bodies respond to it .
As Murphy puts it , when doctors see this sort of variation in disease severity , “ that ’ s not the virus ; that ’ s the host.
” Since the beginning of the pandemic , people around the world @ @ @ @ @ @ @ chronically ill people are most likely to die from COVID-19 .
But that is far from a complete picture of who is at risk of life-threatening disease .
Understanding exactly how and why some people get so sick while others feel almost nothing will be the key to treatment .
Read : The pandemic is turning the world upside down Hope has been put in drugs that attempt to slow the replication of the virus—those currently in clinical trials like remdesivir , ivermectin , and hydroxychloroquine .
But with the flu and most @ @ @ @ @ @ @ often effective only early in the disease .
Once the virus has spread widely within our body , our own immune system becomes the thing that more urgently threatens to kill us .
That response can not be fully controlled .
But it can be modulated and improved .
One of the common , perplexing experiences of COVID-19 is the loss of smell—and , then , taste .
“ Eating pizza was like eating cardboard , ” Mahajan told me .
Any common cold that causes congestion can alter these sensations to some @ @ @ @ @ @ @ taste and smell is happening with coronavirus infections even in the absence of other symptoms .

The COVID-19 crash comes suddenly. In early March, the 37-year-old writer F. T. Kola began to feel mildly ill, with a fever and body aches. To be safe, she isolated herself at home in San Francisco. Life continued apace for a week, until one day she tried to load her dishwasher and felt strangely exhausted.
Her doctor recommended that she go to Stanford University’s drive-through coronavirus testing site. “I remember waiting in my car, and the doctors in their intense [protective equipment] coming towards me like a scene out of Contagion,” she told me when we spoke for The Atlantic’s podcast Social Distance. “I felt like I was a biohazard—and I was.” The doctors stuck a long swab into the back of her nose and sent her home to await results.
Lying in bed that night, she began to shake, overtaken by the most intense chills of her life. “My teeth were chattering so hard that I was really afraid they would break,” she said. Then she started to hallucinate. “I thought I was holding a very big spoon for some reason, and I kept thinking, Where am I going to put my spoon down?”
An ambulance raced her to the hospital, where she spent three days in the ICU, before being moved to a newly created coronavirus-only ward. Sometimes she barely felt sick at all, and other times she felt on the verge of death. But after two weeks in the hospital, she walked out. Now, as the death toll from the coronavirus has climbed to more than 150,000 people globally, Kola has flashes of guilt and disbelief: “Why did my lungs make it through this? Why did I go home? Why am I okay now?”
Read: The best hopes for a coronavirus drug
COVID-19 is, in many ways, proving to be a disease of uncertainty. According to a new study from Italy, some 43 percent of people with the virus have no symptoms. Among those who do develop symptoms, it is common to feel sick in uncomfortable but familiar ways—congestion, fever, aches, and general malaise. Many people start to feel a little bit better. Then, for many, comes a dramatic tipping point. “Some people really fall off the cliff, and we don’t have good predictors of who it’s going to happen to,” Stephen Thomas, the chair of infectious diseases at Upstate University Hospital, told me. Those people will become short of breath, their heart racing and mind detached from reality. They experience organ failure and spend weeks in the ICU, if they survive at all.
Meanwhile, many others simply keep feeling better and eventually totally recover. Kola’s friend Karan Mahajan, an author based in Providence, Rhode Island, contracted the virus at almost the same time she did. In stark contrast to Kola, he said, “My case ended up feeling like a mild flu that lasted for two weeks. And then it faded after that.”
Related Podcast
Listen to James Hamblin interview Kola and Mahajan on an episode of Social Distance, The Atlantic’s podcast about life in the pandemic:
Apple Podcasts or Spotify (How to Listen)
“There’s a big difference in how people handle this virus,” says Robert Murphy, a professor of medicine and the director of the Center for Global Communicable Diseases at Northwestern University. “It’s very unusual. None of this variability really fits with any other diseases we’re used to dealing with.”
This degree of uncertainty has less to do with the virus itself than how our bodies respond to it. As Murphy puts it, when doctors see this sort of variation in disease severity, “that’s not the virus; that’s the host.” Since the beginning of the pandemic, people around the world have heard the message that older and chronically ill people are most likely to die from COVID-19. But that is far from a complete picture of who is at risk of life-threatening disease. Understanding exactly how and why some people get so sick while others feel almost nothing will be the key to treatment.
Read: The pandemic is turning the world upside down
Hope has been put in drugs that attempt to slow the replication of the virus—those currently in clinical trials like remdesivir, ivermectin, and hydroxychloroquine. But with the flu and most other viral diseases, antiviral medications are often effective only early in the disease. Once the virus has spread widely within our body, our own immune system becomes the thing that more urgently threatens to kill us. That response cannot be fully controlled. But it can be modulated and improved.
One of the common, perplexing experiences of COVID-19 is the loss of smell—and, then, taste. “Eating pizza was like eating cardboard,” Mahajan told me. Any common cold that causes congestion can alter these sensations to some degree. But a near-total breakdown of taste and smell is happening with coronavirus infections even in the absence of other symptoms.
Jonathan Aviv, an ear, nose, and throat doctor based in New York, told me he has seen a surge in young people coming to him with a sudden inability to taste. He’s unsure what to tell them about what’s going on. “The non-scary scenario is that the inflammatory effect of the infection is temporarily altering the function of the olfactory nerve,” he said. “The scarier possibility is that the virus is attacking the nerve itself.” Viruses that attack nerves can cause long-term impairment, and could affect other parts of the nervous system. The coronavirus has already been reported to precipitate inflammation in the brain that leads to permanent damage.
Though SARS-CoV-2 (the new coronavirus) isn’t reported to invade the brain and spine directly, its predecessor SARS-CoV seems to have that capacity. If nerve cells are spared by the new virus, they would be among the few that are. When the coronavirus attaches to cells, it hooks on and breaks through, then starts to replicate. It does so especially well in the cells of the nasopharynx and down into the lungs, but is also known to act on the cells of the liver, bowels, and heart. The virus spreads around the body for days or weeks in a sort of stealth mode, taking over host cells while evading the immune response. It can take a week or two for the body to fully recognize the extent to which it has been overwhelmed. At this point, its reaction is often not calm and measured. The immune system goes into a hyperreactive state, pulling all available alarms to mobilize the body’s defense mechanisms. This is when people suddenly crash.
Read: My whole household has COVID-19
Bootsie Plunkett, a 61-year-old retiree in New Jersey with diabetes and lupus, described it to me as suffocating. We met in February, taping a TV show, and she was her typically ebullient self. A few weeks later, she developed a fever. It lasted for about two weeks, as did the body aches. She stayed at home with what she presumed was COVID-19. Then, as if out of nowhere, she was gasping for air. Her husband raced her to the hospital, and she began to slump over in the front seat. When they made it to the hospital, her blood-oxygen level was just 79 percent, well below the point when people typically require aggressive breathing support.
Such a quick decline—especially in the later stages of an infectious disease—seems to result from the immune response suddenly kicking into overdrive. The condition tends to be dire. Half of the patients with COVID-19 who end up in the intensive-care unit at New York–Presbyterian Hospital stay for 20 days, according to Pamela Sutton-Wallace, the regional chief operating officer. (In normal times, the national average is 3.3 days). Many of these patients arrive at the hospital in near-critical condition, with their blood tests showing soaring levels of inflammatory markers. One that seems to be especially predictive of a person’s fate is a protein known as D-dimer. Doctors in Wuhan, China, where the coronavirus outbreak was first reported, have found that a fourfold increase in D-dimer is a strong predictor of mortality, suggesting in a recent paper that the test “could be an early and helpful marker” of who is entering the dangerous phases.
These and other markers are often signs of a highly fatal immune-system process known as a cytokine storm, explains Randy Cron, the director of rheumatology at Children’s of Alabama, in Birmingham. A cytokine is a short-lived signaling molecule that the body can release to activate inflammation in an attempt to contain and eradicate a virus. In a cytokine storm, the immune system floods the body with these molecules, essentially sounding a fire alarm that continues even after the firefighters and ambulances have arrived.
At this point, the priority for doctors shifts from hoping that a person’s immune system can fight off the virus to trying to tamp down the immune response so it doesn’t kill the person or cause permanent organ damage. As Cron puts it, “If you see a cytokine storm, you have to treat it.” But treating any infection by impeding the immune system is always treacherous. It is never ideal to let up on a virus that can directly kill our cells. The challenge is striking a balance where neither the cytokine storm nor the infection runs rampant.
Cron and other researchers believe such a balance is possible. Cytokine storms are not unique to COVID-19. The same basic process happens in response to other viruses, such as dengue and Ebola, as well as influenza and other coronaviruses. It is life-threatening and difficult to treat, but not beyond the potential for mitigation.
At Johns Hopkins University, the biomedical engineer Joshua Vogelstein and his colleagues have been trying to identify patterns among people who have survived cytokine storms and people who haven’t. One correlation the team noticed was that people taking the drug tamsulosin (sold as Flomax, to treat urinary retention) seemed to fare well. Vogelstein is unsure why. Cytokine storms do trigger the release of hormones such as dopamine and adrenaline, which tamsulosin can partially block. The team is launching a clinical trial to see if the approach is of any help.
One of the more promising approaches is blocking cytokines themselves—once they’ve already been released into the blood. A popular target is one type of cytokine known as interleukin-6 (IL-6), which is known to peak at the height of respiratory failure. Benjamin Lebwohl, director of research at Columbia University’s Celiac Disease Center, says that people with immune conditions like celiac and inflammatory bowel disease may be at higher risk of severe cases of COVID-19. But he’s hopeful that medications that inhibit IL-6 or other cytokines could pare back the unhelpful responses while leaving others intact. Other researchers have seen promising preliminary results, and clinical trials are ongoing.
Read: The best hopes for a coronavirus drug
If interleukin inhibitors end up playing a significant role in treating very sick people, though, we would run out. These medicines (which go by names such as tocilizumab and ruxolitinib, reading like a good draw in Scrabble) fall into a class known as “biologics.” They are traditionally used in rare cases and tend to be very expensive, sometimes costing people with immune conditions about $18,000 a year. Based on price and the short supply, Cron says, “my guess is we’re going to rely on corticosteroids at the end of the day. Because it’s what we have.”
That is a controversial opinion. Corticosteroids (colloquially known as “steroids,” though they are of the adrenal rather than reproductive sort), can act as an emergency brake on the immune system. Their broad, sweeping action means that steroids involve more side effects than targeting one specific cytokine. Typically, a person on steroids has a higher risk of contracting another dangerous infection, and early evidence on the utility of steroids in treating COVID-19, in studies from the outbreak in China, was mixed. But some doctors are now using them to good effect. Last week, the Infectious Diseases Society of America issued guidelines on steroids, recommending them in the context of a clinical trial when the disease reaches the level of acute respiratory distress. They may have helped Plunkett, the 61-year-old from New Jersey. After three days on corticosteroids, she left the ICU—without ever being intubated.
Deciding on the precise method of modulating the immune response—the exact drug, dose, and timing—is ideally informed by carefully monitoring patients before they are critically ill. People at risk of a storm could be monitored closely throughout their illness, and offered treatment immediately when signs begin to show. That could mean detecting the markers in a person’s blood before the process sends her into hallucinations—before her oxygen level fell at all.
In typical circumstances in the United States and other industrialized nations, patients would be urged to go to the hospital sooner rather than later. But right now, to avoid catastrophic strain on an already overburdened health-care system, people are told to avoid the hospital until they feel short of breath. For those who do become critically ill and arrive at the ER in respiratory failure, health-care workers are then behind the ball. Given those circumstances, the daily basics of maintaining overall health and the best possible immune response become especially important.
The official line from the White House Coronavirus Task Force has been that “high-risk” people are older and those with chronic medical conditions, such as obesity and diabetes. But that has proven to be a limited approximation of who will bear the burden of this disease most severely. Last week, the Centers for Disease Control and Prevention released its first official report on who has been hospitalized for COVID-19. It found that Latinos and African Americans have died at significantly higher rates than white Americans. In Chicago, more than half of the people who have tested positive, and nearly 60 percent of those who have died, were African American. They make up less than one-third of the city’s population. Similar patterns are playing out across the country: Rates of death and severe disease are several times higher among racial minorities and people of low socioeconomic status.
Read: What the racial data show
These disparities are beginning to be acknowledged at high levels, but often as though they are just another one of the mysteries of the coronavirus. At a White House briefing last week, Vice President Mike Pence said his team was looking into “the unique impact that we’re seeing reported on African Americans from the coronavirus.” Anthony Fauci, the director of the National Institute of Allergy and Infectious Diseases, has noted that “we are not going to solve the issues of health disparities this month or next month. This is something we should commit ourselves for years to do.”
While America’s deepest health disparities absolutely would require generations to undo, the country still could address many gaps right now. Variation in immune responses between people is due to much more than age or chronic disease. The immune system is a function of the communities that brought us up and the environments with which we interact every day. Its foundation is laid by genetics and early-life exposure to the world around us—from the food we eat to the air we breathe. Its response varies on the basis of income, housing, jobs, and access to health care.
The people who get the most severely sick from COVID-19 will sometimes be unpredictable, but in many cases, they will not. They will be the same people who get sick from most every other cause. Cytokines like IL-6 can be elevated by a single night of bad sleep. Over the course of a lifetime, the effects of daily and hourly stressors accumulate. Ultimately, people who are unable to take time off of work when sick—or who don’t have a comfortable and quiet home, or who lack access to good food and clean air—are likely to bear the burden of severe disease.
Much is yet unknown about specific cytokines and their roles in disease. But the likelihood of disease in general is not so mysterious. Often, it’s a matter of what societies choose to tolerate. America has empty hotels while people sleep in parking lots. We are destroying food while people go hungry. We are allowing individuals to endure the physiological stresses of financial catastrophe while bailing out corporations. With the coronavirus, we do not have vulnerable populations so much as we have vulnerabilities as a population. Our immune system is not strong.