As Willie set off at a run for the office, Tom admonished the chicks, rubbing them with his fingers. “Little chicks, I’ll say a prayer for you,” he said. “At this rate, you’re gonna have to make up for our lack of Easter egg sales this year.”
Tom sneezed loudly.
“Bless me!” he groaned, wiping his nose with the back of a hand that still clutched a turkey chick. “Dang, that sun is bright!”
But the sun, however, was shining at his back.
That morning, on the outskirts of Kansas City alone, nearly a dozen veterinarians were dragged out of bed by workers in the poultry industry.
Around the tenth of April, by the slimmest of chances, it had arrived.
“False fowl plague?”
The vet’s eyes opened wide when he heard the news from that same poultry worker. “Are you talking about Newcastle disease? That’s absurd. Every poultry worker I know mixes Newcastle vaccine with their birds’ drinking water. What’s that? A new strain, you say?”
After hanging up, the vet hurriedly dialed the number of the Livestock Vaccine Research Center, sliding an arm into his shirtsleeve as he did so.
Li Xulao lived in a lonely village in China’s rice belt, not far from Yancheng city in Jiangsu Province. Although this retired farmer was over eighty years old now—even he didn’t know his exact age—he was still an early riser. Because he had grown weak and hard of hearing in his advancing years, Li Xulao spent most of his time just sitting near the door of his house, so as not to get in the way of his son, his daughter-in-law, and his grandson, who was a member of the village’s district council. Between those times when he nodded off, he would smoke—it was his only pleasure. That day, on the morning of the eleventh of April, he got up while it was still dark outside and offered up a votive light at the memorial tablet of his ancestors. When he was finished, he lit his pipe with the candle, went to the door, and sat down. When the eastern sky at last began to take on a whitish hue, a deep, milky fog rose amid the belt of rice paddies all around him, obscuring the neighborhood farmhouses and the willow trees, making them as black and indistinct as brushstrokes of India ink.
Spring is here, Li Xulao thought as he slowly breathed in the smoke from his long khsier pipe. You feel mighty grateful for spring when you’re old. When you’re old, even the summers are chilly, but from here on, it ought to get better and better and better.
The old man refilled his pipe and stroked his thin, sparse beard with a slightly trembling hand.
The world is getting better and better too. My grandson brags about it too much, but even so things have gotten so we can even survive famines without too much suffering. There are no wars now either. Bit by bit, the world is getting better. I hope I can live long enough to see my great-grandson’s face …
That was when the old man noticed something white moving down the small creek just in front of him. It was part of a network of streams that flowed among the rice paddies in the area. The water flowed so slowly that it was hard to tell if it was moving at all, but the white thing was floating along with what current there was.
“What’s that?” he said to himself.
The old man might have been hard of hearing, but his vision was fairly sharp. He was about to start smoking that second pinch of tobacco when he stopped his hand and strained his eyes. Right beside the thing drifting in the creek was another, identical, white thing. They formed a pair, approaching from out of the fog, moving forward together. Moments later, more white objects just like them began to appear, one after another, from beneath that pall of fog. The old man stood up suddenly. The khsier pipe fell from his hands and made a loud crack against the ground. The old man looked around at the fog in every direction and tottered back into the house. He bowed down before the altar and broke into bitter tears.
“Father, what’s happening?”
His daughter-in-law had heard his cries and was now getting up out of bed, wiping the sleep from her eyes. “What’s the matter? Are you all right?”
“Something terrible is going to happen,” the old man said between childlike wails. “Some terrible, terrible thing is going to happen. I wanted to live a little longer, to see this world get a little better. I wanted to eat some more good things, soft enough for an old man’s teeth. I wanted to see my grandson take a bride, to see the face of my great-grandchild. But it’s all over now. Something terrible is going to happen. I know.”
“Are you all right?” said another voice. His grandson had gotten out of bed and come into the room to take his turn asking the question.
“The ducks are all dead. They came floating down the stream.” The old man pointed outside. Still crying, he said, “I know. This is a sign that something terrible is happening. Even worse than those Riben ping invaders from Japan who took away my other children. I’m telling you, I know …”
The old man’s grandson, who had quickly gotten into his work clothes, rushed outside. Almost right away, he came running back in. “It’s true! Father, there’s a big stir over at Zhang Si’s place too, and at Wong’s. We’ve been hit too!”
“All of them?” said the old man’s son, who had also gotten out of bed.
“More than half are alive, but they all look sick.”
“I wonder why?” Li Xulao’s son tilted his head. “They were fine yesterday.”
“At any rate, I’m heading to the committee meeting. I’ll come right back afterward—you’d better hurry up and isolate the sick ducks.”
“Something terrible is going to happen,” the old man wept, his voice growing all the louder. “This is a sign. I know.”
“It is not a sign,” said his grandson, with eyes glinting. “It must be another plot of the American Empire. Surely you’ve heard how they used airplanes to drop infected insects and rats everywhere during the Korean War. There were a lot of contagious microbes spread around near Beijing. In Liaodong and Liaoxi a lot of people died of anthrax in their lungs.”
“Something terrible is going to happen,” the old man said, his sobs growing louder. “We’d finally made a lasting peace in this world, but now something awful is going to happen again.”
The old man’s grandson charged out of the house like a bullet. The others hurried outside to see about the ducks, and when he was alone in the dim house the old man crouched down before the votive light, twisting and turning his body as he cried on and on in a voice that sounded ready to expire at any moment.
It was three days later that a new strain of contagious poultry disease bore down ferociously on Japan’s chicken belt in Kyushu.
In barely a single week’s time—from the start of the second week of April until the weekend—it became clear that this “Tibetan flu” (named for the region where the first outbreak took place) was going to be a serious worldwide problem. This was clear from the moment people became aware of the flu strain’s abnormally short incubation period and of the extremely high level of communicability that resulted from it. From February through the middle of March, the outbreaks had expanded at a comparatively leisurely tempo, but as soon as April arrived the rate of infection skyrocketed.
For microorganisms with such simple bodily structures as viruses to undergo sudden, striking changes in transmissibility in the midst of such an epidemic was as extreme a scenario as might be imagined—but it was not outside the realm of possibility. This is because of the phenomenon of so-called “subcultural change,” an example of which is how an utterly normal type of influenza virus turned into the A1 epidemic in the years between 1945 and 1949. This virus, to which almost no one in the world had any immunity at the time, first caused a series of localized outbreaks that began all over Europe but were small enough in scale that they were hardly viewed as problematic. In 1948 and 1949, however, a major epidemic exploded across first central Europe, and then, in 1950 and 1951, throughout the Scandinavian north and England. It was believed that this had happened because the A1 virus had at first been insufficiently adapted to the human body, but as the
number of infections increased, its compatibility with its host likewise improved, at last resulting in that explosive spike in the rate of infections.
For similar reasons, the Tibetan flu became a worldwide problem during that two-week period in the first half of April. During that time, the epidemic reached Ankara, Turkey, in the west, and in the east spread beyond Singapore, all the way to Hong Kong. By the time these outbreaks had become apparent, the Tibetan flu virus had already been carried to nearly all parts of the world by swift international transport and had planted its seeds everywhere.
Reports from a school in Bombay made it known that the incubation period was so brief that if a single member of a given group came down with it in the morning, nearly every member of that group would be exhibiting symptoms of influenza by evening. That meant that the incubation period wasn’t much longer than a scant ten hours! Up until that time, the shortest reported incubation had been only twenty-four hours, during that great pandemic of 1918–19. Most strains of influenza have an incubation period of forty-eight hours.
This extremely short incubation period alone was sufficient to show how powerful the virus’s reproductive ability was, which in turn demonstrated how aggressively communicable it was. And that meant …
This was an entirely new strain—utterly unlike any of the various types of influenza that caused outbreaks large and small almost every year. It was a new virus, against which human beings had almost nothing in the way of immunological defense.
When newspaper headlines announced an OUTBREAK OF NEW INFLUENZA, uncomfortable memories surfaced in the hearts of many who remembered the two prior pandemics of the twentieth century. The first had been the so-called Spanish flu, which had broken out in 1918—the same year that the First World War had drawn to a close—and it ravaged the entire planet. The second pandemic—the Asian flu—was fresher in people’s memories. Caused by the influenza A2 virus, it had started in 1957 and continued into the following year, traveling all around the globe. By this time, few people remained who remembered the horrors of the Spanish flu, and those who had only memories of the Asian flu—with its high rate of morbidity but relatively low number of fatalities—saw this as a rather gloomy development to be sure, but hardly a cause for alarm.
It was during this period, however, that the medical community received two deeply disturbing reports.
The first came from Italy’s Consiglio Nazionale delle Ricerche, where this Tibetan flu virus had first been isolated. It said that while this new strain’s virulence rivaled that of the 1918 Spanish flu, it was an entirely new genus that they had dubbed “Invfluenzavirus A-Minus.”
The second report stated that at around the same time that this Tibetan flu had first appeared, an entirely new, extremely virulent form of Newcastle disease (also known as false fowl plague) had broken out and started spreading worldwide. The virus that caused Newcastle disease was part of the same myxovirus group that included influenza. Intensely communicable, with a high rate of mortality that ranged from twenty to one hundred percent, this disease also rendered hens incapable of laying eggs almost as soon as they contracted it. What now left the doctors speechless was that this poultry disease, which had started popping up here and there with the onset of spring, was beginning to show signs of spreading worldwide, overlapping with last winter’s worldwide mumps epidemic. The egg prices that normally came down somewhat in the spring were instead skyrocketing. And that was hardly the worst of it. A hurried accounting of reports that had come in from poultry farms sent involuntary shudders down the spines of disease prevention officials—the number of fertilized eggs that died in the incubators had begun to climb precipitously in the middle of March.
What did all of this mean?
The answer was simple. The millions of fertilized eggs that were desperately needed in order to make a vaccine for this new type of influenza were about to become very hard to get.
As he peered into his microscope, Professor Kaji of Osaka University’s Research Institute for Microbial Diseases muttered, “This is bad. This is very, very bad.”
To stop the spread of Tibetan flu, universities and laboratories throughout Japan were working frantically on a vaccine for the influenza A-Minus virus. But more than actually working on the vaccine itself, they had been reduced to sending research staff out to secure the fertilized eggs needed to do the work. Throughout the latter half of April, shipments of chicken eggs had plummeted to two thirds of what they had been, and with the spread of Newcastle disease, further declines were expected. Already, eggs were selling for forty yen apiece on the retail market. In the poultry industry, one dealer after another was going bankrupt, watching helplessly as entire flocks were wiped out in a matter of days. The government announced that they were considering importing eggs from abroad, but already Newcastle disease had appeared in Europe and America, and with the entire world in a scramble to deal with the influenza, a ruckus over imports hardly seemed to be in the cards. On top of this, with the “new strain” of Newcastle disease, hens didn’t just stop laying eggs; many of the females thought to have acquired immunity either laid mostly dead eggs or eggs that died around the fourth day thanks to incipient infections.
Viruses, unlike bacteria, cannot reproduce outside of living cells, so unless the cells of a living embryo were present inside a developing egg—a fertilized one that had been incubating for around ten days—it was utterly impossible to grow a culture of the influenza virus inside an egg.
In a desperate effort to keep the work of producing a vaccine going, microbiologists joined forces with Health and Welfare–related offices to scrounge for duck and quail eggs. At the same time, research continued into whether or not there was anything besides the chicken egg that could function as a unit for the mass-production of viral cultures. As for growing cultures in tissue samples, it was also possible to use living human or animal cells grown in culture solution. Cells from the kidneys of monkeys were frequently used for tissue culturing, though they were hard to handle, and there was not sufficient time to gather enough to produce millions of doses of vaccine.
In the midst of such a furor, Professor Kaji was attempting to isolate the Tibetan flu virus from the lung tissues of the first person in Osaka to have died of it. The victim was a forty-two-year-old man. Three days after contracting influenza, he had developed a violent, suffocative bronchitis and exhibited symptoms of pneumonia to go along with it. At last he had died, despite his doctor’s treatment and the medical regimen administered. The rate of death from Tibetan flu was unusually high, especially in Asia, and reports had even come in from some places telling of victims who had died without becoming aware of any symptoms, so Professor Kaji had focused his attention on the first person to die of an A-Minus-type infection in Osaka. He had been a salaryman in robust health with no particular problems in any of his organs. The tissue sample from his lungs was first liquefied and then run through a super-centrifuge, to which a microbe filtration device was attached to screen out the assorted germs. The filtered, germless fluid was then transferred to a culture of cells from the kidney of a Japanese macaque that were being grown in culture solution at thirty-nine degrees Centigrade. Forty-eight hours later, human blood would be used to check for corpuscular agglutination. If the influenza virus had grown inside the living cells to surpass a density of one million virions per milliliter, a phenomenon called a “crosslinking reaction” would occur, and the corpuscles would agglutinate. By diluting the culture solution in many gradual stages and studying the degree to which the blood cells were caused to agglutinate each time, it was possible to learn the number of virus particles present. After that, the culture would be mixed with antibodies for the A-Minus type, obtained from the lymph of house mice that had been infected beforehand—to observe the neutralization effect. Prior to that, however, at the stage of estimating viral density by way of the corpuscular agglutination reaction, the professor had tried adding drops of blood not only to the culture solution, but also to the live
r cells themselves. As soon as he peered into his microscope to look at that fluid, those muttered words had escaped from the professor’s mouth.
“This is bad!”
A part-time lab assistant—a young coed who had just started medical school—turned around to look at him. “What’s wrong?”
“I’m seeing corpuscular adhesion.”
The apple-cheeked woman peeked at what he was doing from over his shoulder. “What does that mean?” she asked. “Flu viruses always make blood condense, right?”
“This isn’t simple condensation. It’s adhesion. Have a look. You see? The corpuscles are being adsorbed onto the surface of the kidney cells.”
“No kidding,” the med student said, fascinated, as she looked through the eyepiece of the microscope.
“So basically,” Professor Kaji said, “what we’ve got here is an influenza A-Minus virus with characteristics of the HA type.”
“The HA type?” she said, her voice rising half an octave. “Is there such a thing?”
“You’ve never heard of it? It’s the contagion that causes a bug called parainfluenza. Tohoku University first discovered a strain of its virus group in 1953. It’s the one that’s also been called ‘Sendai virus’ and ‘influenza D.’ ”
“Influenza D?” Her eyes widened at that. “Flu just has the A and B types, doesn’t it?”
Professor Kaji stared for a moment at the face of this young student—if she were any younger, he thought she’d probably reek of baby formula—and then just shook his head and resignedly began to speak. “Now, see here. Just because it’s called influenza, it doesn’t mean there are only two kinds. What we usually call influenza actually comes in three types: A, B, and C.”
“Well, I didn’t know about C.”
“That’s because it never causes any major epidemics. It’s constantly going around here and there, but most people have antibodies for it, so it doesn’t get far. Even within the influenza A species, there are various types of flus, flus that people get, that horses get, that pigs get, that ducks get, et cetera et cetera.”
Virus: The Day of Resurrection Page 9