What do we know about this virus?
BY: ALEX SHOUMATOFF
July 11, 2009. At this point, now that it has spread to virtually every corner of the globe, where it first emerged hardly matters. The priority is to save as many lives as possible. If the true Ground Zero of this pandemic is ever discovered, it probably won’t be until after it has played out, maybe by next June, if we are lucky. Then there will be time for such historical quests. The earliest confirmed case so far in from San Luis Potosi, Mexico in late February. But that is not where it started, because it was introduced, it’s where the first known transmission chains started. The index cases and first transmissions chains of HIV were identified in San Francisco’s gay community, but that it not where the first emerged. The latest thinking is that it first appeared in Gabon, and that its animal source was a chimpanzee.
Like HIV this new influenza virus is a zoonosis– a disease that many animals, including humans, can have and transmit to each other. It is assumed to have evolved in pigs and to have jumped from them to humans sometime late last year, somewhere in the world, but the smoking pigs have yet to be found. In fact, only a few thousand pigs in the world, in Canada, Argentina, Australia, have been found so far to be infected, all of them by humans. Although it is popularly called swine flu, it is a disease of Humans, and has been spreading like wildfire since the first cases were identified in April in California and Mexico. Millions of Americans have been infected. 100,000 new people are getting it every day in the UK. Dr. Keiji Fukuda, head of the World health Organization’s global influenza program, told me that in events like this a third of the population is usually infected. So we’re looking at two billion, 100 million Americans.
Such an aggressive virus, much more easily transmitted than regular, seasonal flu, has not been seen since the so-called Spanish flu pandemic of l918-9 (whose Ground Zero was actually Kansas or France) which killed anywhere from 25 to 100 million people. But this new one, which is a much-mutated descendant of the l918 virus, is not as virulent– at least not yet. Most of the cases have been mild, many have been asymptomatic, and the global death toll is at most a few thousand, fewer than the yearly fatalities from seasonal flu. The virus at this point, as one epidemiologist has put it, is “not inordinately lethal,”
But the 1918 virus was not so virulent in the spring, either, and only became deadly in October–November of l918, and the fear is that this one, which like all influenza viruses is constantly evolving new ways to evade the attempts fight it off, could do the same thing come fall, as the school year begins and the winter flu season sets in in the northern hemisphere. There are already a few dozen scattered cases around the world of resistance to oseltamivir, the most effective drug for the disease, which Roche markets with the brand name Tamiflu, and because millions have taken Tamiflu prophylactically, the resistant strains could multiply dramatically. All it would take would be a slight miscopying of its RNA, a few wrong letters, during a transmission from one person to another, to produce a mutation as lethal and unstoppable as the 1918 virus. It could happen anywhere in the world, and RNA miscopies happen routinely during the replication process of retroviruses because they don’t have DNA to recognize and fix them. This constant instability is known as antigenic drift. Or there could be a reassortment, a reshuffling of the virus’s eight genes with those of other flu strains in the same person or pig or some other animal like the fruit-eating bats that infected pig farms in Malaysia in l999 with Nipah virus, which killed 104 people. If the wrong reassortment or recombination (a reshuffling of smaller genetic segments) happened, it could become as deadly as the 1918 virus. There has been no change in its virulence so far, but no one knows what the virus is going to do. It has already shown behavior that has not been seen before and is rewriting the textbooks. It didn’t take a summer recess, and it isn’t slowed down by hot weather, the way influenza viruses are supposed to be. It isn’t following the 1918-9 pattern of having three separate waves. The progress of this pandemic is more like lots of simultaneous or overlapping waves, two or three-week local outbreaks, some in places where you would expect then and others where you would least expect them. Hopscotching hotspots in different climate and life zones, temperate, boreal, and tropical all at once. Its transmissibility is still largely a mystery. But then, this is true of the common cold. It seems almost capricious in its choice of victims, who include two Latin American presidents, a pitcher for the Texas Rangers, a flock of turkeys in Chile, 141 students at St. Francis Prep School in Queens, freckle-face Rupert Grint (who plays Ron Weasley in the Harry Potter moves, only a mild bout), and a sub-clade of duck-billed platypuses in Australia. Even the Conde Nast Building at 4 Times Square has not been spared. There have been two cases at Glamour, and one at Vogue. It’s hard to see the common thread. Like seasonal flu, it targets pregnant women, asthmatics, people with compromised immune systems and underlying conditions like asthma, emphysema, cancer, or diabetes; minorities, indigenous people, and poor people suffering from malnutrition with no access to good health care. But not the elderly; people who were around in l957 seem to have some cross-protection from the l957 Hong Kong flu pandemic. Instead, disturbingly like the 1918 virus, it also goes after perfectly healthy people in the prime of their lives, between the age of 15 and 50, whose immune systems can overreact to its invasion, causing a “cytokine storm” in the lungs so they drown in their own fluids…but not everybody in these risk groups gets it. It picks and chooses, but no one knows what its criteria are.
What is known, from the genetic sequencing of the first California and Mexican specimens that was done in April at the Centers For Disease Control in Atlanta and the National Microbiological Laboratory in Winnipeg, Canada, is that it is an H1N1 sub-type of the A type of influenza (as opposed to B or C). There are sixteen hemagglutinin (H) antigens and nine neuraminidase (N) antigens, so H1N1 is one of the 144 basic strains of A that prey on wild birds, poultry, swine, horses, dogs, cats, humans, and other mammals and jump from species to species with varying degrees of ease, sometimes causing devastating pandemics in their new hosts. The first H1N1 was the 1918 virus (although a new paper finds it was not the only H1N1 in circulation at that time). The latest thinking is that it started in birds; maybe wild migratory waterfowl defecated in a pond in Haskell, Kansas, and transmitted it to chickens, which gave it to pigs, which gave it to humans. Pigs have receptors for both bird and human viruses, so they act as intermediaries and mixing bowls, reassorting and recombining their various strains and passing them on. Very rarely is an avian virus transmitted directly to humans, although this happened in late nineties with H5N1, a chicken virus fatally infected 275-plus Asians between 2004-2007 and caused the last pandemic scare– anywhere from 5 to 150 million were expected to die– but because human-to-human transmission of an avian virus is also very difficult, died down, but is still in low-level circulation. It persists in wild migratory waterfowl, which have taken it to Europe and Africa, but so far not to the New World. H5N1 is constantly mutating and is another time bomb.
The original H1N1 killed five or six percent of the world’s population by the time its third wave petered out in 1920. The onset of the disease was very sudden. Many of its victims went to bed healthy and never woke up.
After a few weeks, it moved on, and life returned to normal. Sudden onset is a feature of this new influenza, too. On June 27, an 11-year-old girl in Sao Paolo, Brazil went to bed feeling fine, and the next morning her mother found her dead. In May my own family– we live in Montreal– was prostrated by what has all the earmarks of the pandemic virus. It passed from my three boys to my wife and completely laid them out for a week, but I didn’t get it, probably because I have l957 antibodies. By May 90 percent of the flu cases in Canada were H1N1. Ours were never diagnosed, like the overwhelming number of cases of the new flu so far, and there is no test that can retroactively confirm infection by this specific virus.
From 1920 to l957, all the annual seasonal flus were H1Nl strains, mutant offspring of the l918 virus. In l957 the seasonal H1Nl was incorporated and displaced by the Asian flu virus (an H2N2), which was displaced by the Hong Kong flu H3N2 in l968. The HlN1 lineage stopped circulating in humans until l977, when a lab contamination brought it back, giving rise to the Russian Flu. From then on the seasonal influenza virus that spreads around the globe every year has been either an H3N2 or and H1Nl. Another constantly morphing “classic swine” lineage, first identified in l930, continued to exist in pigs, and every year or two a person would get some nasty strain of it and die. There have been thirteen cases of H1N1 jumping from pigs to humans since the early nineties, but after taking their initial one or few victims, the outbreaks went nowhere. But it was only a matter of time that an H1Nl would come along with the transmissibility of the l918 virus. Especially since the pork industry is increasingly dominated by huge factory pig farms, in which tens of thousands of swine are penned together cheek by jowl in the same ventilated, fly-infested warehouse, where the possibility of transmission is greatly increased. Since the late nineties there has been a big spike in the cases of pigs co-infected with two or more varieties of flu virus.
Then in 2006 SARS (the redundantly named severe acute respiratory syndrome) broke out. It was a coronavirus that had jumped from civet cats, slinky wild felines that are a delicacy in China, probably in some local market in Guandong province. It spread to 37 countries within weeks and killed more than 700 people before it was contained, largely by the efforts of the WHO. The last case of human infection was in June 2003. But it could still be lurking in the wild civet population. In 2005 the WHO helped each of its l93 member states set up a pandemic preparedness program. By 2008 every epidemiologist, infectologist, virologist, and medical professional in the field knew we were due for a big one. There hadn’t been a big one in decades, only scares. The WHO’s world pandemic alert level was still at Phase 3, because H5N1, the wildly mutating bird flu virus, had not been contained. That was the virus that was expected to break out. But swine flu was also a possibility.
The sequencing of the California and Mexico sequences reveals that two of its genes are avian, one is human, and three are swine, all which have been circulating in pigs in North America since the late l990s, and the last two are a Eurasian swine strain which has not been seen in H1N1s in humans or North American pigs before. It is the first quadruple reassortment, the most cosmopolitan concoction, in the annals of influenza virology. One scientist described it to me as a “collaborative effort”– one more reason why the attempt to nail down where it emerged is an exercise in futility: which of its four components are you talking about, and how far back do you want to go (The first influenza viruses are thought to have appeared about 200 years ago, in birds, so ultimately they are all bird viruses.) The three North American components of this pandemic virus are known quantities, but how this new Eurasian component got into the mix is another mystery. The best guess is that a human got it from a pig in Asia and flew to North America and infected some pigs there, who reassorted it with the three other strains they already had, and that the new, highly transmissible concoction jumped back to humans sometime at the end of last year. This timeline can “be inferred from plotting how many changes it would have undergone in a year to take it back to when it was just a pig virus,” Dr. Michael Shaw, a microbiologist at the CDC who has been working on influenza viruses since l975, told me. “But this assumes that the rate is constant, and when a virus in in a new host, it adapts and the rate of change changes,” he cautioned. I asked if it could have reassorted in a human, not a pig, and Dr. Shaw said, “It’s possible, but it’s hard to imagine it didn’t come from pigs at some point. The reagents that picked it up were ones we created for swine viruses. They are one of the first things we try because of the random swine cases that pop up.”
So there is a lot of conjecture about the actual process, but a pig somewhere is the most likely source.
The WHO’s Dr. Fukuda told me that “historically, these new viruses have usually come from southeast Asia, where people, pigs, and poultry have traditionally lived in close proximity, on different floors of the same house, for centuries, and there is a reservoir of viruses in birds, bats, civet cats, and other wild animals in the nearby rain forest. But with the mobility and facility of exchange in the modern world, it could have happened anywhere– maybe even on a factory pig farm in Iowa.”
This is where things stood on July 11– there were many more uncertainties than certainties, more questions than answers– when Dr. Margaret Chan, the WHO’s directorgeneral, raised the global pandemic alert to Phase 6, the highest level. There is always the possibility that the virus could mutate into a weaker form and fade away, but the consensus in the scientific community, at least of the dozens of scientists I have talked to, is that such a fortunate outcome is unlikely, it isn’t going to be like the millennium bug, where nothing happened, given the fact that it has overrun the planet in only six weeks, racing through populations that have no immunity to it. The good thing is that it is having such an easy time of it that it is under no pressure to mutate.
Few doubted that there was going to be a big surge of infections in the fall. But would it be like 1918, 1957, or 1968– the least severe of the 20th-century flu pandemics, which claimed a million, lives? Or would it be something completely new and different? This is what Dr. Fukuda thought. “The world is not the same as it was fifty or a hundred years ago,” he pointed out. “There are many more of us, and we are more urbanized, which makes us more vulnerable to pandemic viruses. Places that took a year for the l918 virus to get to now can be reached in a day.” In 2008 the 190 contracting states of the ICAO, the International Civil Aviation Organization, reported that 2,271,000,000 passengers traveled by, so as with AIDS, the main vector of this disease is the airplane. “But we also have antibiotics, and most of the deaths in the Great Flu were from bacterial pneumonia, complications of viral pneumonia that are now treatable, and we have Tamiflu and ventilators, and soon we will have a vaccine, and our communications systems have taken a quantum leap. Thanks to the Internet, news of a local outbreak can be transmitted around the world instantaneously, so our ability to monitor the course of the pandemic and any change the virus might undergo, and to contain it is much greater.”
Because of these reasons, most of the scientists I talked to had a “gut feeling,” as one of them put it, that this pandemic was going to be more like l957, which took two million lives. Even that relatively moderate scenario would be overwhelming to existing health systems everywhere. But nobody really knew. As Rear-Admiral Dr. Ann Schuchat, the director of the CDC’s Center For Immunization and Respiratory Diseases reminded a packed press conference of reporters clamoring for black-and-white, 24-hour news-cycle answers that she and no one else could give, “the virus is running the show,” and Dr. Joe Bresee of its Influenza Division cautions, “there are a lot of moving parts in this.” As Darwin asserted 150 years ago, evolution is not foreseeable.
The projections as of August 12, based on its progress so far, are that, even without any change in the virulence of the virus. The USA could be looking at tens of millions of illnesses, hundreds of thousands of hospitalizations, and tens of thousands of deaths this winter. The average seasonal flu season sees 200,000 hospitalizations and 36,000 deaths. Or worse: 40% of the USA could be infected, and there could be hundreds of thousands of deaths.
The only thing that can be done now is to try to monitor what the virus is doing—a task made even more daunting since the testing of all but the most severe cases was suspended in early July. The focus is now on tracking syndrome-like patterns: if there is a sudden cluster of severe respiratory illness in a hospital or a community, it could mean the virus is doing something, and that is where the containment effort has to be directed.
All eyes were on the southern hemisphere– Latin America, Australia, South Africa– where it was winter and the pandemic was in full swing. A lot of deaths were being reported, particularly in Argentina. What was happening in these countries offered the best clues to what the North might expect in the fall, so at the end of July I embarked on a sixteen-day tour of Mexico, Argentina, and Brazil to find out what the virus had been up to.
July 29. We are cruising through a majestic high desert, headed for the mythical Ground Zero of the pandemic, a pueblo in the state of Vera Cruz called La Gloria. In late March and early April almost of a third of La Gloria’s 3000 residents were smitten with severe flu symptoms. One of them, a five-old-boy with slick-backed hair named Edgar Hernandez, who fell ill on April 2, was declared Patient Zero, the earliest confirmed case in the world (which was not true, the earliest cases, the index cases, were from California: a 10 year old boy in San Diego county, who fell ill on March 30, and a nine-year-old girl in Imperial County, California on March 28). The media picked up on the appealing narrative and Edgar became an international celebrity. Even CNN’s Dr. Sanjay Gupta paid the kid a visit. Edgar’s nasopharyngeal swab had been among those sent to Winnipeg, which reported on the 23rd that he and the others had been infected by the new strain of H1N1 swine influenza virus that the CDC had just isolated and sequenced from the two California cases. The swine label brought immediate suspicion on the 16 factory pig farms in the Perote Valley, whose Lagunas or waste ponds, their local opponents had already been complaining, contained all kinds of pathogens that were fouling the air and the groundwater. The farms belong to Granjas Carroll, a Mexican subsidiary of Virginia-based Smithfield Foods, the world’s largest pork producer and processor. The operation of the Perote farms, where 950,000 pigs are being fattened, is highly mechanized. They employ only a handful of local people. So the people of the Perote Valley’s environment was being ruined to line the pockets of the gringos, and they were getting nothing out of it except this terrible new influenza. The outbreak was a windfall for the activistas, who were trying it Granja Carroll from putting in three more farms near La Gloria.
And it was a plausible theory. This novel H1N1 has been found in human feces, and pigs regularly pick up influenza viruses in the dropping of migratory birds and poultry, or it could have been transmitted to one of the workers. Smithfield’s lagoons are notoriously leaky. In l997 the company was fined a record $12.6 million by the EPA for a total of 6,900 violations of the Clean Water act, including a massive spill from a huge waste pond on one of its Virginia farms into the Pagan River, which runs into Chesapeake Bay. Millions of fish were killed, holes were eaten into their flesh by a ghastly dinoflaggelate in the pig waste called Pfisteria piscida, suffered neurological impairment and were unable to remember how to get home. 100 pathogens have been found in pig waste. According to Jeff Stietz’s 2006 exposé of Smithfield’s practices in Rolling Stone, “a single lagoon releases millions of bacteria in a day.” The company’s farmers in Iowa spray dry powdered pig shit up into the air so the wind will blow it off the property. The people local who breathe it suffer from “bronchitis, asthma, heart palpitations, headaches, diarrhea, nosebleeds, and brain damage.”
Smithfield also has factory farms in China and regularly ships breeding pigs from the States to its international partners. The North American components could have gotten to China in one of them (they were identified in pigs in Hong Kong in January 2008), and mixed with the Eurasian swine component in the swine there, and somebody at Smithfield could have been asymptomatically infected with the new reassortment and then visited the farms in the Perote valley, and the virus could have gotten to La Gloria in one of the workers or in the air. Granja Carroll, however, claims it has tested its pigs, and none of them have the virus. Who did the testing, and how conscientiously, though, and whether the results were independently verified, is another question. It would be a mistake to diminish the horror of these operations– one blogger, J.A. Ginzburg, describes them as “agriculture on steroids.” The pigs are “so shot up with drugs and chemicals that their immune systems are damaged and they fall prey to microbes, parasites, and fungi. They live in a state of dying until they are slaughtered.” But is Smithfield implicated? Are the smoking pigs on one of its farms here? Preliminary investigations by the local health authorities concluded “the disease vector was a type of fly that reproduces in pig waste and that the outbreak was linked to the pig farms.”
In Mexico City two days ago, I heard a completely different etiological narrative from Dr. Malachias Lopez Cervantes, an infectious-disease specialist at UNAM, the National University. The pandemic started in California.
The two children who fell ill in late March had no connection to each other, to Mexicans, or swine. After Winnipeg announced that the Mexico specimens they had been sent were the same virus, the CDC said that the California cases were linked to the Mexican outbreak. So a number was done on Mexico. The virus became known as Mexican swine flu, even though its scientific name was A/California (H1N1), and it should have beencalled by scientific convention California swine flu.
The tag was unfortunate for Mexico, which is heavily dependent on tourism. Within days of the CDC’s April 21 announcement, seven airlines suspended their flights to Mexico, bookings were canceled, and four cruise lines were bypassing their usual Mexican ports of call. Spring break in Cancun was a total bust, and by the last week in June tourism revenue nationwide was down 43%. It was also unfortunate for innocent pigs the world over. 350,000 swine in Egypt, and the only pig in Afghanistan, were slaughtered, and swine don’t have the virus (except for a few thousand in Argentina and Australia. The Canadian ones were culled). We do. It was also a disaster for the pork industry, even though you can’t get the virus from processed pig meat. Smithfield’s stock took a dive. By April 27 Russia and China had slapped bans on pork products from the United States and Mexico, and six other countries followed suit. China quarantined 71 Mexicans in the country even though they showed no sign of being infected. It shows you how important words can be.
In fact, Dr. Lopez maintained, the virus was in California before it ever got to Mexico, and was taken over the border by migrant crop pickers returning from the Imperial Valley to the state of San Luis Potosi for the Christmas holidays. That was where the first outbreak in Mexico, and the pandemic’s first fatalities (the California children recovered) happened. From San Luis the disease spread down into Mexico City, a seething conurbation of 20 million with terrible air pollution and when I lived there twenty years ago “fecal storms” wafting from the outlying shantytowns, from which it was said you could get hepatitis and amoebic dysentery. By mid-March the city’s hospitals began to see a four-fold increase in patients with ARDS, acute respiratory distress syndrome. Half of the people in La Gloria work in Mexico City during the week, Dr. Lopez went on, and some of them must have brought the virus back with them to the pueblo, which sits at 9,000 feet. At this altitude all kinds of respiratory viruses are in circulation. The people in the village had been complaining of flu symptoms since January, but this could have been from other viruses and bacteria, or the new H1N1 could have arrived much earlier.
The Ministry of Health first thought the La Gloria outbreak must be an unusually nasty and contagious variety of the regular seasonal flu. It wasn’t until April 25th that President Calderón announced that a new pandemic virus was on the loose in the republic, and declared a national emergency. All normal activities of the society were suspended until the Ministry of Health figured out what was going on and what to do. On April 16th, when the presence of the new virus was still not known, President Obama made a state visit to Mexico, was given a tour of the magnificent Museum of Anthropology and Archaeology by its director, who died of fulminating pneumonia a week later. Luckily, Obama didn’t get it. “Can you imagine, we almost bumped off Obama!” a friend in Mexico City exclaimed.
The problem with the Mexican not-us narrative is that there should be cases in the Imperial Valley in December, January, or February, but there aren’t. Which doesn’t mean some won’t surface. The true Ground Zero could be San Luis Potosi. Maybe that’s where the smoking pigs are. Granjas Caroll has farms there, too.
The majestic desert plain, cut with deep snaking arroyos and spattered with old volcanoes, and the occasional Douglas pine forest, gives way to malpais, black-lava badlands in which tall yucca-like isotes have sprouted. We pass a man on a burro with a boy clinging to him. To the east the snow-covered cone of the Pico de Orizaba, the highest peak in Mexico, soars to 18,490 feet. It hasn’t done anything since 1657, but much of central Mexico is actively volcanic. Its history is punctuated with portentous eruptions. Two hours after President Calderón announced the national emergency, an earthquake measuring 8.5 on the Richter scale, whose epicenter was in nearby Morelos, shook Mexico City.
Living in such an uncertain landscape, knowing that at any moment your world could crumble and turn upside down must have an effect on your psyche. You would develop the ability to accept whatever happens. Maybe that’s why Mexicans are so famous for being un-phased and fatalistic.
On the flight down I sat next to a young woman from San Luis Potosi who was studying to be an ICU ventilator technician, a career choice she had made before the pandemic. “We are more used to sickness and death than you Americans,” she told me. “You think have conquered them, but of course you haven’t.”
There’s a lot of social turbulence in Mexico at the moment as well. The government is fighting almost a civil war with the narcotrafficantes. The three main cartels of have 150,000 men armed with Uzis among them. Alvaro Mayorga, the sterling 24-year-old from Guadalajara who has been setting my itinerary and appointments and is sitting in back, has heard the government has made a secret alliance with one of the cartels to get rid of the others. But PAN, the party in power, is suffering a crisis in confidence. It just took a beating in the by-elections. The 450,000 bureaucrats in the government are consuming 90% of the federal budget. Corruption is institutionalized.
“So all things considered, the government’s rapid response was truly impressive,” I say. This is because, as I have been discovering, there is a small community of dedicated, highly trained epidemiologists, infectologists, microbiologists, and medical professionals in the country, and the Ministry of Health is constant communication with the CDC.
After the usual run-around (not that the people we stop and ask don’t know where it is, but they don’t know how to explain how to get there; there’s still a lot of ignorance in the countryside), we find the road to La Gloria at the second ranchito on the road from Tatlalco to Los Altos. It is eight kilometers long. We have been hearing that the flamboyant governor of Vera Cruz, Fidel Herrera Beltran, is planning to pave it and make La Gloria a new tourist destination, capitalizing on its sudden new fame as Ground Zero, and was going to put a statue of little Edgar in the main square. But the road is already paved, and not recently. Only in the last kilometer, zipping past scrawny little milpa (corn) fields and wastelands full of white-flowering chicalote, do we encounter fresh pavement. Then there is a detour around an arroyo where a bridge is being built and we reach the pueblo, which has a classic Latin American timelessness like the town where nothing ever happens in A Hundred Years of Solitude.”In a village like this, half the people aren’t talking to each other,” Alvaro says. Apparently there is a lot of envy of Edgar and his family, because the villagers think that every time a reporter or film crew arrives to interview him, the Hernandezes get money.
Some of the villagers are claiming that they got sick before he did. So the Hernandezes are not doing any more press. They just want to be left alone.
Heading up the freshly paved main drag, we run into a crew– Radio Vera Cruz. They are filming Edgar’s older brother Fernando for a segment in the evening news about La Gloria becoming the new tourist destination. Edgar is standing in the doorway of his house. I have no interest in bothering the kid and his family.
The broadcaster, a vivacious, buxom blonde in a baseball cap whose name is Billie J. Parker, tells me she is descended from Quanah Parker, the last Commanche chief. She
wants to interview me in front of the statue of Edgar. This is starting to get surreal. Edgar, she tells me as we walk to the central plaza, has become a niño milagroso, one of the hundreds of local wonderworkers in Mexico, to whom the faithful make prayers an offerings and pilgrimages. “On my father’s ranch in Guadalajara, we pray for rain to Santo Santiago,” Alvaro tells me. Edgar, Billie J. goes on, “is el niño que se curo. People with respiratory problems from all over the world will be coming to get cured by him. He’s already been on in Russia, China, and Japan.” In the plaza there is there are two men from a German public station, who have chartered a big bus from a Mexican production company. And this is three months after the outbreak. The theory that La Gloria is Ground Zero has been discredited, but they’re still coming. The statue of Edgar is on its pedestal, but covered with a black plastic garbage bag. The governor will come and unveil it when the paving of the road is finished, que falta poco, Billie J. says, there only a little bit left to go.
Later in the day, I meet the governor in his mansion in Xalapa, the state capital. He explains that he got the idea for the statue form the famous statue in Brussels of Manneken Pis, the Pissing Boy, whose urine was believed to be curative during the Black Plague in the Middle Ages. But in his statue Edgar is just standing there, and the governor’s intention was only to commemorate his survival.
Many of the news stories on La Gloria are by reporters who have clearly never set foot in the place and have run with the Smithfield narrative. La Gloria “lies in the shadow of a massive USA-owned pig farm.” (The Daily Mail). “Hundreds’ of [Edgar’s] neighbors, who live among pig-breeding farms, complaining about the stench of the waste, fearing air and water contamination, were suffering flu-like systems.” (The San Jose Mercury). In fact, the nearest farm is eight kilometers further down the road, in the ranchito of Xaltepec. In the beginning Smithfield gave tours to journalists, but the press was so bad it stopped and now it has imposed a media blackout on all sixteen of its farms in the Perote Valley. So we aren’t going to be able to get in there, which I’m perfectly happy with. The last thing I want to do to get the virus and become a carrier. But I do need to check out the farm’s Laguna? It is covered or open to the elements, in which case fecal particles containing the virus could be picked up by the wind, which is strong and constant around here. This is one of the ways a lethal new reassortment could get back into the human population, so I have to see how these operations handle their waste.
No one from La Gloria will take us to the farm because being a gringo, I could be a Smithfield operative and not who I say I am, and the activistas, whom the local people are behind have been getting threatening phone calls and harassed the federales. So there is no choice but to head out to Xaltepec on our own. It’s too bad there is so much distrust in Mexico, I say to Jesus, our driver, and he says, “It’s necessary. People have to be cautious, because they have been enganados so many times.”
Alvaro and I sneak around to the back of the farm and see that there is a concrete lined waste basin covered with black plastic, but there is a pipe from it emptying into an open area the size of a football field which is four-fifths dry, but the other fifth is a standing pool of water, so pathogens could become airborne. It’s not bio secure.
Yesterday at UNAM, Dr. Magdalena Escorcia, a veterinarian in the commercial bird department, assured me, “The conditions for viral transmission between birds, pigs, and humans do not exist in Mexico. Our poultry is kept away from the wild birds. The big chicken farms are between the migratory corridors, and they are kept away from the pig farms, and both are kept away from large concentrations of people. We have systems all over the country that impedes these contacts every since the l994-5 H5N2 outbreak, which came from wild birds and which we controlled by quarantining the farms and sacrificing about a million chickens.
“With this H1N1,” she contended, “it is not a swine virus, it’s a human virus. Up to now, there is no evidence anywhere in the world that pigs infected humans. But there is evidence that humans infected pigs.”
The CDC’s Dr. Shaw would agree with her. He says, “Swine-like is more like it. It’s like viruses we have seen in pigs. It’s not something we know was in pigs. It really doesn’t have any close relative.”
So why is this disease called swine flu then? “Because it’s a mistake.” Who started calling it that? The Health Minister, Jose Angel Cordoba [he was following the CDC’s description]. And we weren’t allowed to correct the mistake, because we weren’t allowed to say anything. But if you think of the human genome, it has the information of worms and flies. But this does not mean we are worms or flies. It means that we have a common ancestor way back. The same with this virus; if it has porcine information, it doesn’t mean it came from a pig.” So there is a huge misconception? “Yes. I was one of the first to start correcting; it’s not swine flu. [The WHO stopped calling it that on April 30 and switched to the more neutral H1N1 Influenza A, while the CDC adopted “the novel H1N1,” but the damage was already done.] If it were because of pigs our veterinarians and scientists would have been infected long ago. [Not if the pigs weren’t in Mexico)]. But the media still insists on calling it swine flu.”
Calderón and Obama both declared a national emergency on April 26. The Ministry of Health did not give out any information for the first three days, and forbad the scientists at the hospitals and the university to speak to the press. The media filled the void with sensational rumors, which created panic and a run on Tamiflu and masks.
Alvaro happened to be in Mexico City and he stayed holed up in an apartment with some friends for the three days, “then we said, let’s go out and see if it’s real, if we can get it. A lot of people thought it was a ruse by the government to distract the population from the real problems.” The streets were deserted. Instead of the usual throngs, only the occasional masked person hurried by. Soldiers were passing out masks at metro entrances. Calderon had ordered 4 million tababocas to be distributed free in the federal district. Within twenty-four hour the pharmacies were cleaned out of Tamiflu and alcohol gel. A black market arose, and the police began to ticket vendors who were selling them at forty times their usual price. After four days the Ministry realized it had to tell the people what it knew, and lifted the media blackout. It also requisitioned all the Tamiflu in the country, which was a good thing, because it discouraged prophylactic taking of the drug, which would have facilitated the proliferation of resistant strains. The five-day Holy Week holiday was extended to ten. Everyone was to stay at home, and if they had to go out, to practice social distancing, to remain at least six feet apart from each other- a tall order in this congested city where five million ride the metro every day— and to refrain from greeting each other with the traditional hugs and kisses. Restaurants were forbidden to seat customers and were only allowed to do take out and delivery, cinemas, nightclubs, gyms, bars were shut down, concerts were canceled, football games continued to be played, but in empty stadiums, most churches stopped having mass and urged their congregations to stay home and listen to the services on the radio. The padres who still gave Holy Communion wore rubber gloves and put the wafers in the hands of the supplicants, whose mouth were masked. After a week, the restaurants were allowed to have customers again, but the maître d’s all had masks,” Alvaro recalled. “Frezas, preppie girls, began to venture into the malls again, with masks decorated with diamonds and glitter and pig noses. Some even covered the grills of their cars with supersized tapabocas.”
I catch the Minister of Health, Dr. Jose Angel Cordoba, as he is preparing to take off with the president for a Latin American summit in Costa Rica. All the presidents and their health ministers are attending. The main topic will be of course the pandemic. And Mexico, being the first country to be hit and having responded on the whole so admirably, will be the star. After the summit, Jorge Arias, Costa Rica’s Nobel prizewinning president, will himself come down with a mild case and be quarantined for a week.
What is the virus doing now? I ask. Dr. Cordoba says the central Mexican outbreak is over. Seasonal flu has returned as the main virus in circulation. But there is a serious outbreak in the south, in Chiapas and the Yucatan, where it is a hundred degrees. This baffles everyone. Influenza viruses are supposed to be suppressed by hot weather. What does it mean? “We don’t know,” he tells me. A gastroenterologist trained in France, he has a calm, reassuring manner and talks to you as of you were a patient. “But from the beginning it has some characteristics that permit it to be different from the seasonal virus. Of the 21,000 confirmed influenza cases since April, 16,000 are the novel H1N1, and 5000 are seasonal. But the season of the seasonal is strange. It is strange that both viruses are in circulation at this time of year. Most flu cases happen in the winter. From December on influenza viruses circulate easily.”
I spoke to half a dozen other scientists about the Chiapas-Yucatan outbreak, which is very important to understand. They all had different theories. Is the virus more heattolerant because its two avian genes make it reproduce most efficiently at 41 degrees, the body temperature of a bird? Could viruses in general evolving more heat-tolerance, as the biosphere is heating up? Could this H1N1 be some kind of a new designer virus created by global warming? A lot of other pathogens are being unleashed by climate change. (The WHO’s Dr. Chan specializes in this issue.) Or is this not really new behavior? What did the original H1N1 do in the summer of 1918? What did it do in Africa? We don’t know.
The seasonal virus usually dies down by the following summer because most people by then have antigens against it. But this virus is racing through virgin populations that have no defenses against it. Most of the people in southern Mexico are poor, malnourished Indians, riddled with intestinal worms and other parasites, with no access to decent health care. Indigenous people have little resistance to exotic influenza or cold viruses. The Great Flu of l919 wiped out entire communities in northern Canada.
Before that, the Americas were largely depopulated by the common cold. The aborigines in Australia are being hit hard, and by June 10th the remote first-nations community of St. Theresa Point in Manitoba had 200 cases, a tenth of its population. The 27 most severe ones were airlifted to Winnipeg, 500 miles away.
Arguing against giving too much import to the health status and possible genetic susceptibility of southern Mexicans is the fact that the flu is also raging through summer camps in North Canada, where the campers are mainly well-nourished white kids without parasites or weakened immune systems.
Dr. Patricia Volkow Fernandez, the chief of infectology at the national cancer hospital in Tlalpan, has just returned from a week in Chiapas with several of her nurses.
We speak in her tiny office. The corridors of the hospitals are full of poor, uncomplaining men and women and children with shaved heads, sitting against the walls, waiting patiently to be seen. “This hospital is always crowded,” Dr. Volkow says. She is a passionately caring woman, the granddaughter of Leon Trotsky, the Bolshevik revolutionary, who was assassinated with an ice ax sunk into his brain in nearby Coyoacan in 1940. The health system in Chiapas is completely overwhelmed, she tells me. It’s not like like up here. There’s a huge lack of machines and trained people, and there are so many pregnant women, and they are the ones it attacks first and hardest.
“This is a very crowded city, and people cough and sneeze and spit without any precautions,” Dr. Volkow goes on. “We were trying to teach people how to cough even before this epidemic. Hand-to-and transmission is impossible to control. Somebody gives you a hundred-peso bill that somebody sneezed on; you grip a handle in the metro. My husband, Rogelio Peress-Padilla, is the director of INER, the national referral hospital for respiratory diseases, so we lived through the whole thing. It started in San Luis Potosi.
The earliest cases in Mexico City were in late February. I had three patients, brothers who had come from McAllen, Texas four days before, and the son of one of them. They fell ill on March 11. By mid-March there were four times more cases of severe pneumonia at INER than the year before. The first case of severe flu that I saw was my own sixteen-year-old daughter. She fell ill on March 12, as did half her classroom. We started her on the antiviral amantadine but it didn’t do any good. She tested positive for seasonal flu with the rapid test. We didn’t know that this H1Nl would also give a positive result, because we didn’t even know it existed. But we knew something was wrong. I was absolutely astonished by her case. She could have died. It progressed to the point where it was no longer in our hands. After six days she developed ARDS because of the inflammation from the augmented infection process. She had high fever and was dehydrated. We put her in a private hospital and under IV and antibiotic she recovered in two days. She was never ventilated, but I toured the ICU at INER and there were children and all these healthy young people on ventilators. I was shivering. I was never so much shocked, except when AIDS broke out. At that moment I thought, this is a tsunami. And it was only the beginning.”
“In the three hospitals in the south there are six of us who all went to medical school together and have known each other for years and we were in constant touch. ‘How many ventilators do you still have?’ ‘When do you start the Tamiflu?’ Do you know what the most important machine in this outbreak was? The cellphone.”
At his home in Cuernavaca, I ask Dr. Carlos Arias, a microbiologist at UNAM, “What is the importance of viruses in the scheme of things, anyway? Do they ever do anything positive?” And he says, “There’s a huge ongoing debate about whether viruses are living things. It depends on how you define life. But they are unquestionably the optimized machines for replication. They trick the cells of their host to do what they want, and what they want is the optimized parasitization. They need a living organism to multiply, and when they infect people, it doesn’t give us an advantage. It’s always bad news. HIV is very smart because it makes its host last twenty-thirty years. It’s advantageous for the virus that its stays alive as long as possible.”
I put the same question to Dr. Escorcia, and she said, “Viruses are part of evolution. The first living thing was an RNA-type virus, if you accept that viruses are alive. When a diabetic’s feet gets gangrene and are threatened with amputation, there is a certain bacteriophage virus that is injected. Gangrene is a bacterial infection. But in nature, viruses are generally prejudicativos; they have a deleterious effect on their hosts. They don’t want their hosts to die for their own survival, but they aren’t very smart, and sometimes they forget.”
Like the 1918 HlN1, which killed 100 million of its human hosts.
Saturday night I get together with old friends. One of them, a drole British expat, muses, “Maybe this pandemic isn’t such a bad thing. After all, it’s not as if there is a shortage of us.”
Paco, waxing eloquent after a few whiskeys, tells me, “I was in England yesterday and they already have 100,000 cases day. But they’re prepared. We’re just praying it won’t come back to us. We’re already pre-doomed. We don’t need any extras. Who knows the damage global warming is going to do, or whether the financial fuck-up will lead to global depression. And now this pandemic. How do you see the future?”
Then he offers his own theory: “You know what? A Mexican fucked a pig in America. That’s how it started.”
August 2. I fly down to Buenos Aires, where it is the middle of winter. Argentina has just surpassed Mexico in fatalities and moved up to the number two spot, although it has 40 million people, and Mexico100 million. Argentina’s health-care system is on a par with Mexico’s, but the government is dysfunctional and the country is a basket case. 40% of its citizens now live below the poverty line, which is defined as a family of four having less than $111 a month.
Dolores Ferradas, my fixer, picks me up at the airport.
A woman in her forties, she has a trenchant sense of humor. “La presidente is not going to see you,” she reports. I was hoping to get an interview with Christina Fernandes Kirchner, whose government is really being run by her husband, Nestor Kirchner, the former president. “Not even her cabinet and staff can get in to see her. She’s busy with herself: the hairdresser, the decorator. She doesn’t care what people think.”
We visit with Guillermo Lobo, who is the Anderson Cooper of Argentina, at the Channel 13 news studio. “When the news about la gripe a came in April, we were not surprised, because we were all sick,” Lobo, a handsome, compassionate man in his thirties, tells. “We were already having a dengue fever epidemic, which the government was doing nothing about. There was no spraying campaign.
“The president was bleeding power,” he continues, “so she called the December parliamentary elections six months early, for June 26. Her approach to the pandemic was to deny that it existed until after the election, so that the government wouldn’t look weak and incompetent. The only step she took was to ban flights from Mexico, which was useless, because our first case, in April, a few days after the outbreak in Mexico was announced, was a lawyer in Puerto Madrin, down in Patagonia, who had been in the States, and the first case in Buenos Aires was a girl who had just been in Disneyworld.
Within hours half her school came down with it, and the school was closed, but all the schools should have been closed right away, and this didn’t happen for eight weeks until after the elections. So many children were infected Christiana’s health minister Graciela Ocaña wanted to declare a state of national emergency but Christina wouldn’t let her do it, so Graciela quit. Graciela wasn’t a doctor, and was also having trouble with the labor union that underwrites health care, whose leader is close to Kirchner, so she was overwhelmed and unable to do anything.”
The pandemic was peaking just as the elections were held. As the disease spread, mass panic and the self-preservation instinct took over, much as Albert Camus depicts in his 1947 masterpiece, The Plague, about a little city in Algeria that is struck by bubonic plague. In the first weeks, the hospitals of Buenos Aires were overwhelmed by the worried well, which made it harder to treat the ones who were really ill. Then as people began to realize that the hospitals were a good place to get the disease, they began to stay away, and only the really ill came. A bus coming from Chile, where there were more reported cases (a function mainly of the fact that Chile was doing a better job of keeping track of them), was stoned because it was believed to have an infected passenger. The rich flew to Montevideo and cleaned Uruguay out of Tamiflu and masks. People desisted from kiss-kiss greetings, and no longer shared their mate gourds, although they continued to drink the soothing national beverage. But as in Mexico, and in The Plague, the doctors and health-care professionals, largely left to their own devices and getting contradictory information from the various authorities and experts, did not abandon their posts, and found out what do from word of mouth and the WHO and CDC Web sites and acted heroically.
“It was very hard to be a reporter,” Guillermo recalls. “The government was saying tudo tranquilo, and Dr. Chan was saying there was a pandemic. Officialdom and the opposition were both using the Pandemic as propaganda, and the principle victim was information.”
Until the election, Guillermo was the main source of reliable information, Dolores says. “The people believed him more than the government. Listening to him explaining things objectively me feel less worried. He said the t.v. And the press had to take the role of the government because it was not communicating how to proceed. A lot of people didn’t think it was very serious. Boca Junior, one of the big soccer teams, started calling themselves La Gripe A, and telling its opponents they better wear masks.”
Blogs were putting out all kinds of misinformation. One conspiracy theory, which I had already heard in Mexico, accuses the pharmaceutical giant Roche, which makes Tamiflu, of deliberately unleashing the virus so it could make a killing. 80% of the ingredients of Tamiflu come from the Chinese anise tree, and none other than Donald Rumsfeld owns ninety percent of global anise production. Rumsfeld was Ford’s secretary of defense during the l976 Fort Dix H1N1 outbreak, when a vaccine was rushed into production and given to 40 million people and 400 people got Gillian Barr syndrome from it. The following year he became the CEO of Senale, the biotech that gave us NutraSweet, Dramamine, and the first oral contraceptive, and in l984 of Giliad, which developed Tamiflu, so he knew how much money there is to be made in pandemics. And this vaccine is the biggest bonanza in pharmaceutical history. Its manufacturers stand to make billions, and if there is a mutation that takes off fast enough, it may not even work. “After the elections,” continues Guillermo, “it was completely different. The government started doing what it should have done in May and June. The new minister got the support and funding that Graciela had been unable to. Schools were closed. We just had our annual rural in Buenos Aires, a major agricultural exhibition, but there were no pigs.”
Now the epicenter of the pandemic has moved north, to the province of Santa Fe. The city of Rosario is being hammered. “If you take reasonable precautions, you’re not going to get it in Buenos Aires,” Dolores assures me.
Buenos Aires still has its Old World charm. The porteños are still elegant. The men dress like English country gentlemen fifty years ago, in tweed jackets with a white kerchief in the breast pocket and club ties and dark pants and shoes. But now there are homeless camps in the median strip of the Avenida 9 de Julio. “We have no middle class any more,” Dolores laments. “Only the very rich and the very poor.”
What happened? I ask, and she explains, “In 20001 the rich class got financially sick and the poor got even sicker and the most important organ, the preoccupation for many of us, is in your pocket. People are getting more stressed and having more heart attacks. There is a pandemic of psychological and neurological disease and it will get worse, and if this is happening to the wealthy imagine for the people who live in extreme conditions. Financial breakdown provokes health breakdown and family breakdown. ‘My father is without work, I don’t respect him.’ The economic crash has had a lot worse impact on the society than the influenza impact. The last few presidents stole a lot of money. That is why we are having this problem.”
This jibes with what Dr. Fukuda told me: “What is interesting about Argentina is how the pandemic brings out the sociopolitical weakness. It’s pretty Severely impacted, which shows that beyond the health impact there is a general impact on social functioning. Countries can be impacted by an event like this in a lot of different ways. During the avian flu outbreak, books were written that made it almost Technicolor and graphically emphasized some aspects. That was good for getting attention, but in a lot of ways the more interesting and important story is the issues that come into play for countries, communities, or at the global level. A lot of subtle and important things go on in terms of the political impact on the economy. Some of them help us get these diseases under control and others, like trade restrictions and the inability to travel, act as barriers. These outbreaks set things loose in a certain way. A whole group of things happen during an event like this.”
I meet with the new Minister of Health, Dr. Juan Luis Manzur, who is a down-toearth surgeon and good people. Even Dolores says he has cintura. Dr. Manzur tells me the good news: Dr. Ian Lipkin, a microbiologist at Columbia University has sequenced eleven samples from Argentina report and there are no significant differences in the virus.
But this raises the question why are so many more dying here, if the health system is as good as Mexico’s. The same question was raised about the Mexican outbreak. Were Mexicans having more severe responses due to, it was variously proposed, HIV, or being immune-compromised by a heavy lode of other infections, or could it be the altitude? But there is no evidence for any of the three. Dr. Hector Hugo Schwab, the health secretary of the outlying municipality of Malvinas, suggests that Argentines, being mainly of Spanish and Italian descent, could have a greater susceptibility than the more north- European population of North America. “We’ll know, he tells me, when Spain, Italy, and the rest of the Mediterranean basin are hit in the coming weeks.” But it could be simply that fifteen million are living in poverty, malnourished, in poor health and with poor access to health care, and that the government did nothing for the first eight weeks. More than one doctor will tell me that the delay in implementing containment and mitigation measures (and the president still hasn’t declared a national health emergency) and the confused information about what to do if you got sick, were responsible for unnecessary and avoidable loss of life. “No one deserves to die of this, especially pregnant women and children,” I will hear from Dr. Monica Foccoli of the Hospital Das Clinicas, where 140 were admitted, 15 put on ventilators, and three died, two of them with confirmed infection. Chile, which has the highest standard of living in Latin America and a president who is a doctor herself and an excellent health-care system and responded to its outbreak even more impressively than Mexico, has had, as of September 14, only 104 confirmed deaths, as opposed to Argentina’s 466, plus another 300 suspected. I have a round-table at the intendencia of Malvinas with Dr. Schwab, the intendente (mayor) Jésus Cariglino, and several men his administration.
“We are critical of how so many things were badly managed,” the mayor tells me. “The denial, the style of the government communicating with the people. The messages were confused about swine flu. If you have fever and other symptoms, stay home. In fact they needed to be seen if they were very sick. Only give Tamiflu to the ones who were hospitalized. But anybody who is very sick should get it within 48 hours, and 25% of our outpatients had serious lung problems. Some were coming in already inflamed by the cytokine storm. Others had acute renal insufficiency and needed dialysis; you can have multiple organ problems from swine flu. Ten percent needed to be put on ventilators, and of them 90% died. We have 16 confirmed fatalities in the intendencia for the two months, but we suspect the final number was more than 120. We are working on our death register. There were 300 fatalities in one month, a 25% increase from last year, and 120 were unusual. This means that the national figures are grossly underestimated.”
We proceed to the Dr. Federico Abete Trauma Hospital, a modern, state-of-the-art facility, Argentina’s showcase hospital, which is Cariglino’s brainchild. “Fourteen years ago I realized that the paradigm had to be changed to a system that can answer to the needs of the nation. We started working with cancer patients and developing gynecological relationships with women for the whole nine months. Then we realized the need for an inclusive, specialized trauma hospital that would cover all the catastrophes that could befall our 400,000 constituents. Car accidents, big fires, seasonal flu complications. Abete has 120 ICU beds and 100 ventilators, two Da Vinci robots to help with surgery. The equipment is very new and sophisticated. I had to fight everybody to get this hospital. The medical corporations, the trade unions, the medical college, and a little, too, the political population. They were scared of change.” When the virus came in May, Abete was chosen as the hospital of referral for H1N1 cases from all over the country. “Abete is the only hospital in the world that is exclusively dedicated to swine flu,” Dr. Schwab tells me. “We do our own testing and are getting a $200,000 sequencing machine so we can tell if there are any mutations. Bird flu could still come in the next five years, and global warming is pushing dengue and yellow fever south, into our municipio, so the need for this facility is not going to go away.”
“This is like a real-life ER or Dr. House,” Graciela Bonfioli, Abete’s medical director, tells me. “At the peak, 90% of our respirators were in use. Now it’s bajo. There are no adults, only a few in the pediatric ICU”
A seventh-month-old boy named Roman, who has been in the PICU ward for 45 days, is co-infected with both porcino and rsv, syncytial virus, one of the hundred or so viruses and microbes that can cause respiratory complications. He has had a tracheotomy and is hooked up to a ventilator through a hole in his throat. “We almost lost him,” the young doctor on duty, Gustavo Laprotta, tells me. “After weeks on the ventilator, his upper airway got inflamed, so we had to do the tracheotomy. We were really worried, because this child’s case was really bad. But he has turned the corner. The ventilator is giving some support, but the strength of his breathing is almost entirely Roman’s. If all is okay, he’ll be out in a week. 50% percent of our children, ten out of twenty, have been co-infected with other viruses or bacteria, and of them sixteen survived. When it was clear that Roman was going to make it, we opened a bottle of champagne and had a party.” Roman is alert and sucking a pacifier and looks ready to make up for lost time.
Roman’s father, Claudio Camargo, a 29-year-old construction workers, is at his bedside. Roman is his third child. He and his wife take turns being with the infant. Claudio doesn’t know how his son got the virus. Maybe the neighbors, maybe the school his brother and sister go to, maybe the hospital he went to before for bronchitis.
We proceed to the genetics lab, where a young technician with a prosthetic right hand is performing the rapid real-life test on some samples. First the RNA is extracted with several chemical agents, and then it is put into 96 well plates. “We get four reactions for every patient,” he explains. “ We see the reading on a computer screen. “This one is co-infected with the novel H1N1 and this year’s seasonal virus.” What? I ask in alarm.
This is one way the virus could get nastier, if it reassorts or recombines in the wrong way with A Brisbane. “25% of our samples are co-infected,” the technician tells me.
I e-mail several scientists and they say this couldn’t be true. And it’s isn’t, fortunately, I find out from Dr. Elsa Baumeister, the senior geneticist at the Malbran National Microbiological Institute, the central testing facility for the whole country. The technician is misinterpreting the four parameters of the test. But he needs to be straightened out. Dr. Baumeister tells me that Dr. Lipkin has sequences samples from the beginning and middle of the outbreak, and to be absolutely sure there are no changes, samples from the end are still being done, and the entire genome of two isolates, one from a severe case, and another from a mild one, has to be sequenced. She says that at the height of the outbreak, for a whole month, up to early July 1200 samples a day were coming in for testing. Now it’s down to 100. “There were sensational stories in the papers that if you had seasonal flu and got swine, you were dead, and this caused panic. Everybody was giving his opinion.”
Dr. Baumeister is right: co-infection would still need to produce a deleterious reassortment to be a problem, and it’s hypothetical because there isn’t any co-infection, in Argentina or anywhere. Maybe there are some barriers between A Brisbane and the pandemic H1N1 because they are circulating together in many places the scariest situation in Argentina is the two farms with infected pigs. Their names are a closely guarded secret, but I have a press clip that tells the highway and what kilometer one of the farms is on, so late one day Dolores and I drive out to the wet pampa of Canuelas and it is right where the paper said it was. Good information for a change.
The piggeries are right off the roads, and in the twilight we meet a woman on a motorcycle who is going home for the day. She works in the maternity, taking care of the 800 piglets. There are 600 mothers here, and 1600 weaned pigs and 3000 gordos are a kilometer up the road. “The pigs started coughing,” the woman tells us. “But this is common at this time of year.” A pig’s cough sounds almost like a dog’ bark and can be heard from a hundred yards away. “In winter the temperature is lower, and the fans are used less, so there is less ventilation and the pigs get mycoplasma [walking pneumonia in people]. A veterinarian analyzed one the pig’s lungs and the person at the lab who did the tests was infected with la gripe A and we were told he might have sneezed over the lung sample and contaminated it. Then SENASA [the Servicio Nacional de Sanidad y Qualidad Agroalimentario] came and swabbed all the pigs and they were all negative.”
What do you do with the excrement? I ask. “Some of it is thrown away in the countryside, and some of it is put in holes with water and bacteria is added to degrade it. The Lagunas are open but they are controlled by Secretario del Medio Ambiente.”
Next afternoon, I get the timeline on the farm outbreak from SENASA’s National Director, Dr. Jorge Horacio Dillon. “On 15/6 some the pigs started showing the symptoms in the brochure. On the 17th more pigs got sick and the owner got worried because the symptoms were different from the seven other respiratory diseases that pigs can get in Argentina. The next day five to seven samples, necropsies from the sick pigs, were sent to INTA, the National Institute of Agricultural Technology, where they were analyzed in the laboratory to see if they had one of the habitual respiratory diseases. On the 19th INTA pathologist send the samples to SENASA, and we diagnosed that it’s a virus A. On the 23rd the samples were sent to Malbran for more detailed diagnosis. On 6/24 Malbran confirmed that the samples were positive for the new HlN1. The decision was made not to cull the pigs because by then they had recovered, and there was no reason to destroy the business.
“We went to the farm and found two of the employees with flu symptoms, but they weren’t severe enough to go to the doctor so they never suspected that it was la gripe A. This farm had no ingresso of new animals for six months, so pigs did not introduce the virus. Our hypothesis that it was the couple who lived on the farm who infected them is waiting to be confirmed by their samples, which are at Malbran.”
How many pigs were infected? “27% of them, 1632 of the 6104. We reported it to the OIE [the International Organization of Epizootes (diseases that spread in animals)]. It was not possible to isolate the animals. When we arrived at the establishment on the 24th the sickness was not present. The animals were well.”
Dr. Dillon shows me SENASA’s latest software, which enables him to zoom in on the farm in Canuelas and see what other operations are in a thirteen-kilometer radius. “We have a database of 260,00 establishments and 400,000 producers,” he tells me proudly.
We know how many animals each has and can track their movements to the slaughterhouses and from farm to farm and what the sanitary conditions are.” The farm is the only piggery in the area; chicken farms surround it. Not good. The conditions are present for a nasty avian co-infection. But Dr. Dillon points out that none of the chicken farms and within a kilometer of the piggery. “The only way avian virus could be transmitted to a pig,” he assures me, “is if the infected chicken’s excrement volatizes, and these influenza viruses are very labile [weak]. They only live a few hours outside their host, so the window for one of these volatized viruses to be windblown into the nostrils of a pig is very small.”
“Every morning a woman has been sweeping pigeon shit off the steps of my hotel,” I tell Dr. Dillon, “and I’ve been reading up on all these viruses that jump readily from birds to mammals and seem to have the run of the animal kingdom, and I’m getting a little paranoid. What about dogs and cats? Can they get this flu? “There are no reports of sick dogs or cats, but they could be carriers,” he says. “What about palomas [pigeons]?
Could they transmit bird flu? “It could be possible, but it would be very difficult, and even more difficult person to person.” Then he gets philosophical. “In this life you have to die of something. But for now there is no avian flu in any of the Americas. Not the H5N1 that killed many in Asia, at least. But in life everything comes sooner or later.
Viruses, like everything, are fluid. They can change their behavior, and this one seems to be doing so.”
What Dr. Dillon does not tell us is that the pigs infected one of SENASA’s veterinarians. This disturbing piece of information I learn from Dr. José La Torre, the country’s top animal virologist, whose office is out in La Matanza, the grim suburb of Buenos Aires where the slaughterhouses are. This is the first and only confirmed case of pigs giving the virus to humans. The good news is that the veterinarian’s infection was mild. The virus apparently didn’t reassort in the pigs. This is an important point: even if there is co-infection and cross-species transmission, it doesn’t mean that anything nasty is going to happen. But what Dr. Las Torre tells me is not exactly reassuring.
“The only predictability of this virus is that it’s unpredictable. In math, two and two is always four, but in biology it is four sometimes. Where is the origin of all these damn viruses? Their natural reservoirs are the wild birds. Goose, ducks, cormorants. The viruses are not virulent for these populations. The wild birds are infected but not sickened. How they transmit the viruses to humans and other populations is in their migratory corridors. They make contact with bridge birds, ones that live between the natural environment and the homes of people. Not only chickens but also garden birds like English sparrow and pigeons. And the bridge birds can get sick. A paper was just published about the first case in Argentina of H1N1 in the Tinamou, wild flightless birds of the pampa. “In Argentina there is more severe disease and mortality. But the virus itself is no more virulent than the California or Mexico ones. The viruses and the host cause the pathology.
You see wild birds that are infected but not sick. Swine are very susceptible to H1N1, but their disease is mild. These influenza viruses have a wide host range.” I have just been reading about Hendra virus, which broke out in a suburb of Brisbane and killed 19 horses and their trainer, and 1000-kilometer north two horses and their owner over August-September 1994. The source of this equine virus, its natural reservoir, seem to have been fruit bats, as with the Malaysian Nipah swine virus, to which it is closely related.
Dr. La Torre speaks contemptuously of “the psychosis of masks and alcohol gal. Soap and water is just as good, and the mask is useless, because the virus can get in through the conjunctiva of your eyes. When I was a student, years ago, there was a photograph in my microbiology textbook of the virus-filled vapor cloud of a sneeze, which was called the pfleuger. The pfleuger, strobelit against a black background, was ovoid and about a square meter and was spewing out of the nose of a man with a moustache whose face was shot in profile. There are hundreds of thousands of viruses in the pfleuger, and all it takes is for one of them to find a point of entry.”
Dr. Pedro Cahn, who pioneered Argentina’s treatment of its AIDS patients and spends his mornings at the public Hospital Fernandes, treating poor walk-ins, tells me “massive disturbance of natural systems will only promote more viruses emerging. What we are doing to the nature is not costless. Yes it’s very nice to have efficient ways of producing food, like the boom in soy production. But when you have a lot of farms and are burning trees, you are changing the environment so that it is more favorable to the emergence and spread of viruses.” In Southeast Asia and the Amazon, soy farmers and local homesteaders are relentlessly chipping away at the last rain forests, and this is where many of these viruses are lurking, waiting for new hosts to invade. So if this pandemic doesn’t turn into Armageddon, some other one is bound to sooner or later, and each exercise in preparedness will make us readier when the Big One comes.
August 8. I was planning to proceed to Chile, but the outbreak there has peaked. I was going to down to Puerto Mont, a small city in the south where the Chilean outbreak was focused. It is being held out as the model for pandemic preparedness. Tudo Latin American needs to take a page from Chile’s book. Chile has the highest standard of living in Latin America and the population is more German. They’re more organized and have the Protestant work ethic, while here, Dolores says, “we do it the Latin way: everything is last-minute and disorganized.” It doesn’t look like the Argentina going to have the vaccine this year. If the virus returns with a vengeance, millions could die before it is available. But maybe the big second wave won’t come until the spring, when its winter returns. Who knows? Everything is out of whack with this pandemic. The immediate concern is the return of dengue, which is already taking it toll in the northern provinces.
Now the gripe A is spreading up into Paraguay and southern Brazil. Brazil is where the action is. There is new concern about the virus that killed with eleven-year-old Laguna girl in Sao Paulo. The fact that she went to bed fine and died in her herself, is scarily like the pathology of the 1918 virus. Two scientists at the Instituto Adolfo Lutz isolated and sequenced the sample of a 26-year- old man who had recently been in Mexico and had a mild case, and they reported that it was a new strain. The CDC rejected the report, saying that there weren’t enough changes to call it a new strain, but by then the press had picked up on the report and was saying that there was a virulent new strain in Sao Paolo. But then more of the genome was released on Gen Bank, and an American virologist I had been e-mailing with said there was a polymorphism in the PB1 gene that made it more like the 1918 virus “and likely contributed to the rapid spread of cases and deaths in the area.” It is a “poster child” for the dreaded mutation.
I change my flight from Santiago to Sao Paulo.
On the plane I flip through Veja, Brazil’s Newsweek, and there is a photo of a bubbly fourteen-year-old-girl who was flying home to Rio from Disneyworld and came down with fulminating pneumonia and was let off in Panama City where they failed to diagnose it properly and give her Tamiflu and she died. The title of the story is, “She never came back.”
The Estado do Sao Paulo reports that 8.3 percent of the world’s deaths from a gripe suina are from Brazil. Sao Paulo has 69. My taxi man, a laid-back obese guy says “This is much less than are killed by assaltantes, or in car accidents, or by the regular flu, so I’m not losing sleep over it.”
I go to the Instituto Adolfo Lutz, and sit down with Drs. Cecilia Luis Santos and Teresina Maria Paiva, who co-authored the paper on the Sao Paulo 1454, the sample Cecilia isolated and Teresina sequenced. Teresina is talkative and does all the talking.
Cecilia remains silent except when she agrees with Teresa that what my American source told me is complete nonsense. “Our virus is not a poster child,” Teresina says. “We can’t say that, no one can say that. It has a few small changes, but a vaccine for A California would still be protectivo. We saw polymorphisms, the normal drift in all retroviruses, and what happened was that an American reporter translated one word wrong in the communiqué of the Sao Paulo ministry of health wrote that we had found a de novo mutation, that would kill many people, and this brought us a lot of problems. It was very embarrassing and distracting– we’ve had 12,000 samples to analyze since April, but our colleagues at the ÇDC assured me that this happens all the time with the press, and not to worry about it. None of the changes in this virus changes the amino acids’ ability to function. It’s dangerous to make such an assertion about the polymorfismo this man has found. A polymorfimso alters a few sequences, but it has no effect.” So it’s a false alarm. “There are lineages or optimists and pessimists, too,” Teresina says. “We are optimists. We are not terroristas.”
Teresina tells me that the Laguna girl came from a middle-class family. “The Father is a teacher, and she was studying English. They live in Osasco, out by the airport. The girl had been playing with her three-year-old sister in the park then she sat with her parents on their bed and went to bed. She was coughing a little and had some fever. At 5:30 in the morning her mother found her dead. Her skin had turned blue. We first thought it was the seasonal H1N1, which killed a 3 year old in Ribeiro Preto and two people in Santa Catarina last year. Last year’s strain was muito perigroso.”
The virus may not be more virulent, but it is taking a heavy toll in Brazil. As of September 5, there have been 657 confirmed fatalities, which puts it the number one spot, above the USA.
September 10th. I fly down to Atlanta and spend the talking to the scientists at the CDC. I already met several of them at an all-day Flu Summit at the Nation Institute of Health in Bethesda, Maryland on
July 9. They looked very smart in their black naval uniforms and racks of ribbons and gold-striped sleeves with the caduceus of the Public Health Service. The secretaries of health and human welfare, homeland security, and education, Kathleen Sibelius, Janet Napolitano, and Arne Duncan, gave strong speeches, President Obama video-conferenced from Italy his gratitude to the great work everybody was doing. It was a full day of one high-powered, articulate speaker after another giving his perspective on the pandemic.
There weren’t a lot of media. The event was more an opportunity for people in different fields, involved in different aspects of the pandemic, to share their experiences and get to know each other. I left the summit prouder to be American than I had been in a while, with the feeling that the situation is in the hands of extremely competent, caring people, who are doing everything humanly, possible. But still there were anxieties at the summit about if there is a big surge in the fall no city has enough ventilators or ICU beds to handle it, and whether the vaccine will be out in time.
The CDC complex is an exquisitely understated piece of modern architecture with military accents.
There is an installation of bloated armchairs, symbolizing America’s obesity epidemic, in the exhibition space. Obesity is the latest H1N1 risk factor to be added to the list, and there is a lot it in Atlanta, and a lot of infection at the moment. The school year starts early in the Southeast on August 10th, it’s getting nailed.
I go over the outstanding questions. The central etiological one is where are the smoking pigs? Which ties in to the whole question of the swine designation. Dr. Michael Shaw explains, “The 1918 HlN1 established two lineages, one in humans and the other in pigs. Occasionally there were jumps, but they were different enough that a flu immunologist knows what you mean when you say swine flu. It means where you see it the most, to distinguished it from avian, human, or equine. It doesn’t mean it came immediately from swine, but that it is closely related to viruses circulating in swine for years and years. We’ve been seeing these triple assortments in pigs more than a decade.”
But can’t reassortment happen in people, too? I ask, and Dr. Shaw says, “Yes. A few years ago we had an H1N2 that was a reassortment of seasonal H1N1 and an H3N2 in the USA for about a year. They do pop up, but fortunately most of them don’t work. But with this pandemic virus, it would to imagine that pigs were not involved at some point. But maybe a long time ago. Look at measles, which came from rinderpest, which the first domesticated animals got from wildebeest.”
Dr. Nancy Cox, the director of the Influenza Division and one of world’s foremost authorities on flu viruses, explained, “we could identify from the California sequences that it was something similar to what has been circulating in pigs, that we were detecting in humans. From the very beginning we looked for a pig connection but couldn’t find one.”
Dr. Caroline Bridges has been working on the numerous other H1N1’s that circulate in pigs and occasionally jump to humans, sometimes with fatal consequences. “Up to the late nineties, pigs were mainly infected by the classic swine H1N1, which remained relatively stable. But then there was a huge change in the diversity of pig flus [coinciding with huge factory farms taking over the pork industry, which, it has been proposed, has accelerated pig-virus evolution.] We started to see 2s, 3s, and 4s, and triple assortments. The problem is that there is no national swine virus surveillance program, so we don’t really know what they have and what new reassortments they may be coming up with.”
The first pigs with the pandemic virus were found in Alberta at the beginning of May. A carpenter on the farm who had just been in Mexico was the probable source. The pigs were culled, and, Dr. Bridges continued, “When that herd didn’t get to market, nobody wanted to test their pigs at all. There was a tremendous disincentive for testing, and what little testing is done in the USA came to a halt, even though there is no scientific reason for thinking that once the animals recover— and pig flu cases are usually mild– they can’t be processed. While the big industrial farms are generally bio secure, the smaller operations and backyard herds aren’t. So the lack of surveillance in pigs is a vulnerability in our pandemic preparedness, and the pork industry needs to know what strains are circulating in its pigs so it can develop vaccines for them. Flu delays pigs’ weight gain.”
As for the other issue, the Mexican label, Dr. Cox tells me the earliest confirmed case is now a mild one in late February from San Luis Potosi, so the Mexican not-us narrative has a timeline problem.
The earliest American case is a month later. “If the USA were the true source, we would see a different spread pattern, and we would have picked up earlier cases in California, because our flu surveillance systems also register mild cases.” This is because the USA is a rich country, Dr. Shaw explained, while countries like Mexico and Argentina, which are more concerned with things like dengue and malaria than mild flu, was only picking up the severe cases, so it’s numbers are skewed, because they’re only getting the tip of the iceberg. While the only cases in the USA were still just the two in California, Mexico was already in the throes of a much more severe outbreak than anyone realized.”
So maybe the smoking pigs are in San Luis Potosi. I would start looking on the Granja Caroll farms there.
A week later, I ask the CDC’s director, Dr. Thomas Frieden, the CDC’s director, how this pandemic is different from the three twentieth-century ones? And he tells me, “Whatever I say, can only be said with the caveat so far, cuz it ain’t over yet, and we don’t know what will be happening. Compared to the l918 pandemic, so far this one is not more deadly than the routine flu virus. There a new article that finds similarities to 1957, which had a mild spring wave, and kept having sporadic local outbreaks over the summer, then after the school kids came back, there was a second, bigger wave that was still mild, then in January a third, deadlier wave that hit the elderly– which this one is not yet doing.” Dr. Cox had been telling about this third wave, at the beginning of l958. “By then people were not interested. They thought it was gone and didn’t get the vaccine, which was late coming to some places, and then you saw a wave of elderly affected and quite a number of deaths that could have been prevented. So if something like that happens, we may have to change our immunization strategy. And a new co-infection with H3N2, a seasonal strain, has just turned up in Cairo. That could make the elderly more susceptible, so we’re monitoring what the virus is doing in Egypt very closely.”
“So far there hasn’t been any more virulent mutation,” Dr. Frieden continues, “but only time will tell what will happen going forward. It shows you the value of the lab work here. We are getting new samples from all over the world on a daily basis. I was New York City’s health commissioner this spring, and it was a really challenging situation. The city had probably 800,000 cases. Things that were completely unheard of happened, like 100 kids with flu coming into the school nurse’s office in the same morning. People were going into the hospitals with symptoms they wouldn’t have been worried about if they hadn’t heard of swine flu.
“Is there going to be huge second wave? No one knows. Which means two things, 1) we have to monitor intensively what the virus is doing and 2) be ready to pivot. And there is every reason to get vaccinated. So far it’s an excellent match with the circulating strains.”
The good news is that forty million doses will be available in the USA by mid-October, some sooner for people in the highest risk groups like pregnant women, 1 to 15 years olds, and the country’s eleven million health workers. And only one shot will be needed. But the antigens take 21 days to become effective. Canadians won’t get their vaccine till November, and the poorer countries not for months. On September 17 President Obama pledged ten percent of America’s supply to the poorer countries, and Australia, Brazil, France, Italy, New Zealand, Switzerland, and the UK followed suit. Dr. Cox tells me, “What we learned from the southern hemisphere’s winter wave is that the same age and risk groups were affected in terms of infection, hospitalization, and deaths that we saw in the spring, and this consistency helped drive our guidelines for vaccination prioritization. We were watching closely what happened in August in the temperate regions of Brazil and Australia, and the virus didn’t mutate. If there is a sudden change in its pathology, if the attack rate of the elderly, says, were to suddenly spike somewhere, that’s something we would have to be all over.”
But there were ways in which virus behaved differently in Mexico, I point, like the big outbreak in Chiapas and the Yucatan at the height of summer, and Dr. Cox says, “We need to study the heat stability of this virus. The lipid in the viral membranes of seasonal strains melts at high temperature, and this makes them unstable. We need to look at this one’s membranes.
“One of the worse-case scenarios is if the pandemic virus co-infects with H5N1, and there is a new reassortment that gets the virulence of the avian strain but retains its human transmissibility. There have been plenty of chances for this to happen, but it hasn’t. There’s no sign of it anywhere.”
Another worry is that a lethal reassortment could result from co-infection with the seasonal H1N1. Or if it picks up A Brisbane’s N, it could get Tamiflu resistance. There are scattered reports of Tamiflu resistance– in Hong Kong, Denmark, mostly recently a summer girls’ camp in North Carolina. Roche, which stands to lose a bundle if one of the resistant mutations takes off, said on September 11 that there are still only 23 cases worldwide. If Tamiflu becomes ineffective, that will leave another drug, Relenza, as the first line of defense. But Relenza is taken as a spray and only protects your airways, and the disease can attack your liver, kidneys, and other organs. Dr. Shaw explains that “you can see a mutation pop up and never seen it again, or you can see one that confers some advantage, and a small group develops.” So far, knock on wood; none of the resistant mutations have been transmitted to other people.
The other parts of the genome that the CDC’s microbiologists are watching carefully are the PB1 cleavage site, whose PB1-F2 protein could cause death in its host cells were it to be expressed, which could be triggered by a point mutation. The expression of its PB1-F2 protein is what made the 1918 virus so lethal.
Also position 627 of the PB2 gene, and the receptor-binding site on the Ha. And other changes that haven’t been envisioned. How can the CDC keep on top of something that could happen anywhere in the world? For one thing, by being in constant touch with the NIH’s Genbank, where as of August 26 detailed genetic information on more than 1400 viruses in 30 countries was posted, and with the WHO’s surveillance teams, and with Canada’s crack Global Health Intelligence Network, which picked up the first clue of the SARS outbreak in Guangdong in November, 2002.
The nerve center of the CDC’s surveillance operation is its Emergency Operations Room, which is like a war room. It has 232 work stations, each with a computer and a phone, that are manned 24/7 365 days a year by 15 to 27 teams in three rotating eighthours shifts, Mark Channer, the emergency operations specialist who gives me the tour, tells me. Specialist Channer is a stark black man who was previously in army operations, and he has the military fondness of numbers and initials, spit out with high –decibel precision. The EOR is 24,000 square feet.
It was started after the anthrax bioterrorist scare following 9/11, and kept growing as the bird flu and SARS outbreaks came. It is part of the prodigious growth that America’s whole security system has experienced in the last eights.
“The EOR operates under the incident management system, which is based on the incident command system,” Specialist Channer continues. “Everything builds around the science and expands or contracts as needed. There is no set Maginot Line.
All the templates are national response frameworks used throughout the USA and by every federal agency, including FEMA and Homeland Security. From the time H1N1 appeared in Mexico we’ve been frozen in pandemic preparedness phase. But we’re monitoring everything: hurricane response, the Olympics, the Superbowl, the national conventions.
The bioterrorism watch team is working round the clock. We’re doing global disease detection on H5N1. It’s one of the DCIR’s, the director’s critical information requirements. The DCIR’s are up on a big screen. There’s a rickettsia (Rocky Mountain spotted fever) outbreak in Mexico, the salmonella outbreak last year that was first blamed on tomatoes, then peppers (also from Mexico, that hotbed of pathogenicity) is under control, but not entirely over. “Other watch teams are monitoring Internet and news sources, open sources like CNN.”
“What if they’re wrong?” I ask. “On open source is just a hint,” explains Specialist Channer. “It needs to be confirmed by the SME’s.” The subject matter experts.
“Any disease that’s out there can be in the USA in matter of hours. We have to identify it, contain it, treat it, and eradicate it if we can’t mitigate it. Just because H1N1 is going doesn’t mean we aren’t monitoring multiple other things.”
The commanding officer of the EOR is Rear Admiral Stephen Redd, who is a mildmannered epidemiologist, not the General Patten type. It he who has to make the call if the shit hits the fan. “The five teams answer to me,” he explains. “They are 1) the lab folks, who do EPI surveillance and disease and virus characterization and are looking for mutations, and 2) community mitigation. (Like teaching school kids the “Dracula Sneeze,” to expel their pleuger into their raised forearm.) 3) The vaccine task force 4) Medical care and countermeasures. 5) State and local coordination.
And all five requires quick, precise, non-alarming risk communication, which the CDC is excellent. Everything from the MMWR, the Morbidity and Mortality Weekly Report, which is a must-read for the medical profession, to Facebook and Twitter to reach the teens and twenty-something who have the greatest risk of succumbing to a cytokine storm.
“We were not expecting this one to be recognized here,” Dr. Redd continues. “We thought it would be somewhere like Asia and that we would have more time. We had a few mild cases, and at the same time there was a severe outbreak in Mexico, so from the beginning we understood this was not going to be as clear as we would like and we would have to live with it.”
“Do you have a work-up of the different scenarios and responses that you can share?” The best publically modeling is actually in the President’s Council of Advisors on Science and Technology’s August 7 Report to the President on USA Preparations for 2009-H1N1 Influenza. It has some scary projections, too scary in the opinion of some CDC personnel.
“What if say a little town in the Florida panhandle suddenly got a cluster of fulminating pneumonia. Can you walk me through how you would handle it.”
“In the first place, we have to be invited,” Dr. Redd explains. “The state health department moves in first, and if they can’t identify what it is they send samples to us, and we can sequence them in four hours.”
“But that could take a few weeks,” I say, recalling that the California kids were swabbed on March 28 and 30, and the sequencing wasn’t finished until the 15th of April.
“What if people in this town are dying in their sleep? Do you quarantine it? Implement a cordon sanitaire where no one can go in or out?” The Plague scenario.
Dr. Frieden told me that “quarantine is not usually an effective strategy in influenza pandemics because there are many patients without symptoms, and the virus could have already escaped before you implement it.”
So this is not looking good. How can we be sure that some random human fuck-up or failure to act along the line, which is bound to happen won’t enable a lethal mutation to get the jump on us.
As Dr. Bridges put it, “To quote a Nobel Prize winner, which one I no longer remember, ‘It’s our wits versus the virus’s genes,’ and we are clearly not winning.”
I think what she, and Drs. Frieden and Redd, were implying is that containment of a lethal mutation may not be possible, any more than it has been possible to contain the virus in its present form. Look at how quickly SARS tore through three emergency rooms in Toronto in early 2003.
But let’s not freak out, either. As Dr. Bresee said, “There are a lot of moving parts in this.”
When was there ever any certainty?