Estimate Of People Who Are Affected By The Common Cold
  In this extensive article providing an overview of why and how of an estimate of people who are affected by the common cold globally since 1910.The first appearance of the disease was unremarkable: It was a mild but highly contagious flu no different from the types in normal, recurring epidemics. In March 1918 a few small outbreaks appeared on opposite sides of the world—at Army camps in the United States, where war mobilization was under way, and in China. By April United States troops had carried the disease to France; at the end of the month flu swept into Spain, proving especially potent there; by May, when the contagion finally began to subside in the United States, flu was rampant everywhere on the Continent.
Normal life in some countries came to a virtual standstill. In the space of one month, for example, 53,000 Swiss took to their beds. At midsummer, half of the population of Chungking, in China, was down with flu. The Great War was affected (pages 124-135). So many infantrymen were sick in the German camps along the Marne that General Erich von Ludendorff despaired of mounting an offensive. Still the disease’s deadly potential remained hidden. Most flu victims recovered normally, and medical authorities assumed that the pandemic would soon end.
But in late August, 1918, a new, far more virulent, version of flu suddenly sprang out simultaneously in Boston, in Brest, France, and in Freetown, Sierra Leone—three Atlantic ports actively engaged in the transshipment of men to the European war zone. Within days, the new sickness struck down thousands of soldiers, sailors and civilians, prostrating half of the men in some Army units. This was at best a skeletal estimate of people who are affected by the common cold.
This second wave of influenza had an alarming tendency to give way to pneumonia, often causing breathing difficulties and death within a day. Treatment was fruitless. “On admission most of the early cases were blue as huckleberries. Most of them died. Nearly all were coughing up liquid blood,” one doctor wrote. “We had to stand by helpless except for what temporary relief we could give.” Most frightening of all, mortality was highest not among the elderly’ the primary victims of most flu epidemics, but among young adults in the prime of life.
Cities from Chicago to Calcutta mobilized for the battle against flu. Theaters and churches were closed by government proclamation and the public was urged to get plenty of bed rest, eat regularly and “beware of persons shaking hands.” New York’s Commissioner of Health made sneezing and coughing in public p1ac.a punishable offense, subject to fine or jailing; he also called for “spotless Sundays” and advised young couples who could not refrain from kissing to do so through handkerchiefs. San Francisco required its citizens to wear face masks in all public buildings— prompting the police to complain that robbers, thus disguised, were more brazen than ever. In every major American metropolis, several hospitals were devoted solely to the care in isolation of flu victims.
Still the toll of sick and dead continued to climb. In the United States alone, 500,000 people died—one person in every 200. In isolated settlements in Alaska, where the Eskimos had had no previous exposure to influenza, casualties soared as high as 100 per cent; in Samoa 25 per cent of the population died.
Closing in on the cause
When the pandemic ended in the spring of 1919 medical authorities were still unsure what had caused it, why it subsided or how they could prevent another one. Again scientists found Pfeiffer’s bacillus in flu victims, but the bacteria still did not always cause flu in healthy volunteers.
Equally baffling, scientists were unable to prove that influenza was caused by a virus. Monkeys, rabbits and other animals were inoculated with filtered throat washings from flu patients, yet they failed to get the disease. Even when, in a risky and heroic experiment, scientists filtered sputum and juices from the lungs of dead flu victims and inoculated human volunteers with the filtrate, illness rarely appeared. (Medical historians theorize that these experiments—which should have worked—failed for one of three reasons: because the dead flu victims were no longer shedding infectious virus particles, because the crude filters available in 1918 held back virus particles along with bacteria, or because the volunteers already had antibodies to the flu.) As late as 1922, Robert Donaldson of St. George’s Hospital Medical School in London wrote that ‘‘there is not the slightest shred of evidence that the disease is due to a so-called filter-passing virus.” The mystery seemed insoluble.
Research on the basic nature of viruses progressed rapidly, however. Soon after the War, virologists turned to animal experiments, which often give conflicting results because of the presence of antibodies or bacterial disease. To surmount these obstacles, scientists devised methods of sustaining live animal tissue in the laboratory—bits of nerve fiber, rabbit cornea, chicken kidney and many other tissues—by bathing them periodically in nutrients. These procedures allowed brief cultivation of animal viruses, but the cultures were constantly plagued by bacterial contamination. To keep ahead of the invading bacteria, researchers in the era before antibiotics had to transfer each culture to a fresh test tube every few days—a process that discouraged the growth of most viruses as well.
The ultimate solution was deceptively simple. In 1928 Dr. Ernest W. Good pasture and Alice M. Woodruff, two Vanderbilt University scientists, managed—after hundreds of false starts—to grow the fowl-pox virus in nature’s own sterile incubators, fertilized chicken eggs. Furthermore, they passed the virus from egg to egg and then returned it to live chickens, conclusively proving the existence of viral disease in animals. They later showed that fertilized eggs—a cheap convenient laboratory medium—could sustain variety human viruses as well.
The final clue in the case of the missing flu virus came from a physician, but from an astute veterinarian. During 1918 pandemic J. S. Koen, an Iowa inspector for the U.S. Bureau of Animal Industry, noted a pig disease that resembled Spanish flu. Despite considerable opposition from farmers, who feared that consumers would avoid pork, Koen maintained that the swine disease was connected to human influenza. In 1919 he wrote: “I believe I have as much to support this diagnosis in pigs as the physicians have to support a similar diagnosis in man. The similarity of the epidemic among people and the epidemic among pigs was so close, the reports so frequent, that an outbreak in the family would be followed immediately by an outbreak among the hogs, and vice versa, as to present a most striking coincidence if not suggesting a close relation between the two conditions. It looked like ‘flu,’ and until proved it was not ‘flu,’ I shall stand by that diagnosis.”
In 1928 Koen’s conviction prohibited a team of government veterinarians to instill mucus from sick pigs into the noses of healthy ones, which promptly got sick. However, when the veterinarians tried to transmit the disease with filtered mucus, the experiment failed—presumably because the filters were defective. The virus hypothesis remained unproved.
But Richard Shope, a brilliant young pathologist at The Rockefeller Institute for Comparative Pathology in Princeton, New Jersey, was intrigued by the experiments. He visited pig farmers in the Midwest, learning that swine influenza still occurred there every autumn. And in late 1928 Shope repeated the government experiment, this time with the institute‘s excellent equipment. The filtered fluid consistently produced disease, proving that pig influenza, at least, was caused by a virus.
But the cause of human flu remained elusive. During a 1933 influenza epidemic in England a team of British researchers, Wilson Smith, Christopher Andrewes and P. P. Laidlaw, injected filtrates of human throat washings into various animals. Nothing happened, because (it is now known) the scientists did not try nasal administration, the only practical route for influenza experiments. A few weeks later, however, the virologists learned from the Wellcome Laboratories in London that some ferrets used there in research.
One canine distemper seemed to have caught flu accidentally; Andrewes himself had just contracted influenza so Smith inoculated healthy ferrets with filtrate from his colleague’s throat washings, this time using the nasal as Shope had done.
On the day that Andrewes returned to work, the inoculate ferrets developed sneezing, fever and nasal discharge— classic signs of animal influenza. The British team fin had proved that human flu was caused by a virus. Only 1 did they learn that their experiment began with a fortuitous fluke: The ferret illness that had initially been report them by the Wellcome Laboratories turned out to be car distemper after all. The final step in the experiment revealed that ferret influenza was the same as human influenza—was equally lucky. Three years later, while a searcher was examining an inoculated ferret, the animal sneezed in his face—and the scientist contracted influenza. The proof was complete.
Now research accelerated rapidly. Smith, drawing on Good pasture’s work, successfully cultivated the flu virus chicken eggs. Then Wendell M. Stanley, a 31-year- chemist at The Rockefeller Institute, crystallized proof that viruses are a transition form between the living the nonliving. They are inanimate chemical compounds more than submicroscopic cells, for only chemicals can be crystals. Yet they possess the power to reproduce the selves, as only living things can. British bacteriologist V ham Elford accurately measured the sizes of different ruses, filtering them through very thin membranes, e graded according to its pore size. And finally, in 1939, G man virologists using a new invention, the electron microscope, were able to clearly see the ghostly particles that they had studied blindly for so long.
Scientists eventually discovered that human influenza was caused by not just one virus, but three different type of viruses, labeled A, B and C. Type A, the virus that initially isolated by the British researchers, is the most common type and by far the most important. It is responsible I most flu epidemics and most flu-related deaths in adults Type B also causes epidemics, though less frequently than it occurs primarily in school-age children. Type C is relatively inconsequential; it erupts only occasionally and then as a very mild infection. |
