Germs, Genes, & Civilization: How Epidemics Shaped Who We Are Today

by David P. Clark

  The empire was at a serious disadvantage compared to the nomadic barbarians. The citizens of the empire were crowded closer together into towns and cities. In addition, sewers and drains provided the rats with ideal channels of distribution within every major town. Although their assembled armies were susceptible to infection, the barbarian population was spread thinly over more rural areas. Moreover, many barbarians were nomadic, moving frequently and living in wagons or tents. These provided far less opportunity for rats than permanent towns and cities. Thus, the empire ran out of recruits, while the barbarians still had plenty of men to draw upon.

  By the time of Justinian’s death, Rome was little more than a ghost town in the middle of malaria-infected marshland. The darkness had fallen. Not until the nineteenth century would civil engineering provide hygiene as good as that of imperial Rome. Even after the empire had retreated from many outlying areas, pestilence continued to take its toll. Thus, Roman-style culture continued locally in Britain for a hundred years or more after the empire pulled out. Continuing outbreaks of bubonic plague starting in the mid–fifth century and extending over the next hundred years were a major factor in the collapse of this and other briefly lived successor cultures.

  5. Meat and vegetables

  Eating is hazardous to your health

  Smoking, drinking, eating, gambling, skiing, swimming, jogging, sitting still, playing computer games, watching TV, having sex, and taking narcotics are all hazardous to our health—although we usually are lectured only about those that aren’t respectable. Despite the exaggerations of the antismoking lobby, most deaths in industrial nations are associated with being overweight from eating too much and exercising too little. Here we worry not about overindulgence, but rather the safety of our food supply. In particular, our focus is on the contamination of food and water by microorganisms.

  Contaminated meat, especially processed meat such as sausage and hamburger, is the major cause of food poisoning in today’s industrial nations. Food poisoning is usually the result of bacteria. Although bacteria might create toxins within the food, more often the symptoms come from swallowing the bacteria themselves, which then infect the gut. Although Salmonella and E. coli are best known, several other bacteria, such as Listeria, and several viruses also contribute. Several massive recalls of frozen meat harboring E. coli O157:H7 have occurred. In 1997, the Hudson Foods plant in Columbus, Nebraska, was shut down and 25 million pounds of ground beef were recalled. This record was broken in 2002 when Pilgrim’s Pride, America’s second-largest poultry producer, recalled 27.4 million pounds of turkey and chicken products because of contamination by Listeria.

  The number of outbreaks of food poisoning has been rising recently, especially in the United States. An estimated 80 million cases of foodborne disease occur in the United States each year, although less than 1% are normally reported. With a population of around 300 million, this means that roughly one in every four people suffers food poisoning in a typical year.

  Processed meat can be safely sterilized by radiation, an approach that is widespread in Europe. A major problem in the United States is fear of radiation. Nations that do use radiation have far fewer cases of food poisoning. Another factor is the ever-increasing centralization of food processing. If one cow in a thousand carries Salmonella and the meat is sold by local butchers, only a handful of people will get sick. But if thousands of cows are processed in a central facility and their meat is mixed together in a huge vat, all of the meat becomes contaminated. A 2001 survey of ground meat (chicken, turkey, pork, and beef) in American supermarkets revealed that about 20% of the packages contained Salmonella, and over half of the bacteria were resistant to at least three antibiotics.

  Although meat still leads, vegetables and nuts are increasingly a hazard. Norovirus, Salmonella, and E. coli are all involved. Spinach carrying E. coli hit the headlines in 2006, and tomatoes or peppers with Salmonella followed in 2008. In the latter case, the FDA first blamed contaminated tomatoes for a 30-state outbreak of Salmonella Saintpaul and later shifted the guilt to Serrano peppers, thus causing widespread confusion. The origin of this Salmonella outbreak was never resolved. More than 2 million pounds of pistachios were recalled in 2008–2009 because of Salmonella contamination.

  Perhaps as much as 25% of fresh vegetables in the United States are contaminated with E. coli. Although these are mostly harmless, their natural habitat is the human intestine. Their presence shows that many fresh vegetables are contaminated by human waste. Contamination can occur during harvest or transport, or, perhaps more often, by irrigation with water that has come into contact with human waste.

  The increase in food poisoning cases led both the U.S. Department of Agriculture (USDA) and the Food and Drug Administration (FDA) to demand more regulations. In the early 1990s, government meat inspectors still examined meat by eye, and standards of hygiene continued to deteriorate. The deaths of several children in the mid-1990s triggered long-overdue technical improvements. DNA-based screening now allows rapid and accurate tracing of contaminating microorganisms. This has led to much faster intervention, to cut off contaminated food or water at their source. Coupled with improved safety procedures, this has dramatically reduced food poisoning. Between 1996 and 2004, most food-borne illnesses in the United States dropped by up to 40%, except for Salmonella. However, since 2004, there has been no significant improvement, and Salmonella infections have increased slightly. Some 5,000 Americans still die of food-borne disease each year.

  Hygiene in the home

  “The intimate connection between a woman and a broom-handle is an obvious and natural fact.”

  —Suellen Hoy, Chasing Dirt

  The great age of hygiene lasted from roughly 1850 to 1950. The front-line troops in the battle for cleanliness were mostly women. Since the 1950s, women have gradually abandoned the home and ventured forth to find external employment. Hygiene standards in the home have inevitably relaxed. Houses are cleaned less often, laundry is done less often, and both are done less thoroughly. Despite the outbreaks in fast-food restaurants that hit the headlines, most foodborne disease actually occurs in the home and goes unreported.

  In England, about 1,000 outbreaks of Salmonella per year are serious enough to be officially recorded. About 80% to 90% of these involve household exposure and affect only one or two people. The major sources of contamination are sponges and dishrags, which spread bacteria over countertops, dishes, and hands. Bacteria die off in a few hours when surfaces are dry, but they can survive for days or weeks in damp or moist surroundings. Zap your wet sponge or damp dishcloth in the microwave oven for a couple minutes if you want to sterilize it.

  About 25% of Americans don’t bother to clean their cutting boards after hacking up raw meat or chicken. Vegetables or bread sliced on the same board then pick up bacteria. A few years back, housewives were told that plastic countertops and cutting boards are safer because their smooth surfaces allow them to be wiped clean more thoroughly than wood. No one bothered to do the experiment, however, and the opposite was proven true: Wooden cutting boards are safer than plastic ones. First, plastic might look smooth to you, but on a microscopic scale, it is covered with hills and valleys where bacteria can hide. Second, many wooden boards contain phenolic compounds that are toxic to bacteria. Third, as wooden boards dry in the air, they tend to suck bacteria on their surfaces into pores in the wood. The bacteria might survive, but they become trapped and cannot get back to the surface.

  Cannibalism is hazardous to your health

  Cannibalism undeniably shortens your life expectancy if you are on the menu. But what if you’re the cannibal? Eating people should be highly nutritious—after all, the human body contains all needed nutrients. True enough—if the victim was well fed. But even so, there’s a snag. You are more likely to catch some nasty infection from eating another human than from gulping down part of a pig or sheep. Cannibalism is relatively rare among animals, too, and part of the reason is the same; carnivores are
more likely to be infected by a disease lurking in a close relative than by a disease that infects another species.

  The most spectacular disease spread by cannibalism is kuru, which used to be endemic among the Fore tribe of New Guinea. Kuru is passed on by eating the brains of previous victims. The Fore did not eat their enemies, but they practiced ritual cannibalism of their own deceased kin. Women had the honor of preparing the brains of dead relatives and taking part in their ritual consumption. Consequently, 90% of the victims were women and the younger children who helped them. Kuru develops very slowly, and it can take 10 to 20 years for symptoms to appear. First comes severe headaches. Difficulty in walking and neural degeneration follow, with death resulting in one to two years. No one born to the Fore since 1959, when cannibalism stopped, has developed kuru.

  Most diseases result from microorganisms that contain their own genes as DNA or RNA. However, kuru and related weird diseases of the nervous system have infectious agents that contain no DNA or RNA. Instead, infection results from rogue proteins known as prions. This protein is actually coded for by a gene belonging to the victim. This gene normally produces a protein that is found on the surface of nerve cells, especially in the brain. Stanley Prusiner, who won the 1997 Nobel Prize for discovering prions, was ridiculed for a decade by those who refused to believe that a lone protein could cause an infection.

  The critical property of the prion protein is that it has two alternative structures. These differ only in the way the protein folds. Occasionally, the properly folded form rearranges to produce the rogue form of the protein, which somehow cripples nerve cells and leads to their death. When a rogue prion protein enters a healthy nerve cell, it binds to its normal relatives and incites them to refold into the incorrect shape. After most of the prion proteins convert to the bad form, the nerve cells die. Patches of neighboring cells die, leaving holes in the brain like those in Swiss cheese. Prion disease is known as spongiform encephalopathy because the brain decays into a spongy mass. If the defective prions manage to establish themselves, the disease might progress slowly but is ultimately fatal.

  Because the prion is coded by one of the victim’s own genes, it can cause spontaneous, inherited, or infectious disease. There is a very low chance that a prion somewhere in the brain might spontaneously flip-flop into the bad form. This happens in about one person in a million. In inherited prion disease, a defect in the prion gene generates a mutant prion protein that changes into the rogue form more frequently. Infectious prion disease happens when the victim consumes prions that are already in the rogue conformation.

  Many details of prion disease are still mysterious. The extremely low frequency of infection and the long period before symptoms appear make study difficult.

  Mad cow disease in England

  Scrapie of sheep was the first prion disease identified, in 1738. Infected sheep behave strangely and scrape themselves against trees and fences, damaging their fleece and skin. Scrapie is transmitted when the remains of dead sheep contaminate pasture. Infection of new victims by prions is difficult, and only certain genetic breeds of sheep are susceptible.

  Mad cow disease broke out in England in 1985 and has since killed more than 150,000 cattle. Even more were destroyed to halt its spread. Before 1985, the disease was unknown. Mad cow disease is not “natural,” because cows are not naturally carnivorous. However, to avoid waste, animal remains (including the brains) were ground up and added to animal feed—a mind is a terrible thing to waste. Because sheep remains were fed to cows, the emergence of mad cow disease was originally blamed on sheep with scrapie. However, people in England have eaten sheep with scrapie since the 1700s without noticeable ill effects. Nor have other domestic animals caught scrapie, despite sharing the same fields. Experiments confirmed that sheep prions do not infect cows.

  It is now thought that a random flip-flop event converted a normal prion into a rogue prion inside a cow’s brain somewhere in England in the late 1970s. The rogue cow prions were recycled by feeding animal remains and eventually spread, causing an epidemic. The kuru epidemic in New Guinea presumably occurred the same way. A prion spontaneously misfolded in a member of the tribe a few generations ago, and the disease then spread by cannibalism.

  In the last half-century, four outbreaks of prion disease have occurred among farmed mink in Wisconsin. These mink are often fed on “downer cattle,” animals that fall down and die out on the range and thus cannot (legally) be fed to humans. Assuming that all four outbreaks were due to cattle with bovine spongiform encephalopathy (BSE, the official name for “mad cow disease”), and knowing the total number of downer cattle fed to mink during this period, probably about 1 in 28,000 had BSE. Taking into account the total number of cows in Wisconsin, this implies that 1 in every 980,000 suffers spontaneous BSE. This is essentially the same rate as for humans with spontaneous prion disease.

  If all animals suffer spontaneous prion misfolding at about the same rate, why has mad cow disease not appeared in the United States or other industrial nations that recycle animal remains into feed? One major reason might be that England is much more densely populated, by both people and domestic animals, than the United States. Consequently, animal byproducts were more intensively recycled. Alternatively, the British BSE outbreak might have been triggered by a rare mutation that yielded an unusually infectious and virulent form of BSE.

  Why did the epidemic start when it did? During the 1980s, several changes took place in the British rendering industry that processed animal remains. A new American process was introduced that used lower temperatures, and solvent extraction was abandoned. Solvents had been used to remove animal fat as tallow. When new regulations for using flammable solvents were introduced, most rendering plants just gave up solvent extraction rather than buy expensive new machinery. During the 1980s, the addition of meat and bone meal to cattle feed rose from 1% to 12%. This was partly due to the increased cost of imported fishmeal and soybean meal, due, in turn, to a drop in value of the pound.

  Experiments suggest that the previous process was not hot enough to inactivate the prions anyway. On the other hand, prions are protected by animal fat, so the combination of high temperature and fat removal might have made the earlier process safer. Perhaps, then, the mad cow epidemic was triggered by the solvent safety legislation. Or maybe it merely resulted from the increased use of rendered products.

  The political response

  Political responses to health issues can be divided into those that are ideological and those that are nonpartisan and show that our leaders can nobly rise above mere party lines. When a new problem arises in society, especially a novel health issue, the response of the political establishment is pretty much as follows:

  1. The problem does not exist.

  2. The problem is extremely rare and, in any case, is declining. There are more important things to worry about.

  3. The problem has been highly exaggerated by irresponsible activists and popular journalists.

  4. There is a serious problem, and we have been doing everything possible to deal with it from the very beginning.

  Both the American response to the AIDS crisis and the British response to mad cow disease followed these stages. Consider the British government’s statements on what it preferred to refer to as BSE:

  “Nobody need be worried about BSE in this country or anywhere else.”—John Gummer, U.K. Agriculture Minister, 1990

  “There is a continued downturn in incidence of BSE.”—Angela Browning, Junior Agriculture Minister, 1995

  In 1995, replying to a mother whose daughter had died of BSE, John Major, the prime minister, wrote, “I should make it clear that humans do not get mad cow disease.” The deliberate lying finally stopped on March 20, 1996, when Stephen Dorrell, Secretary of Health, admitted in parliament that BSE had infected humans who had eaten beef. By May 1996, BSE had affected 160,000 cattle on more than 30,000 English farms.

  After mad cow disease broke out in England, the recycl
ing of animal remains in feed was prohibited and infected herds were destroyed. British beef was banned from many other nations, despite the British government’s campaign of secrecy.

  Mad cow disease has recently regained attention because a handful of cattle in the United States have been diagnosed positive. Consequently, several countries have instituted restrictions on the import of American beef.

  Mad cow disease in humans

  When prions are subverted into changing shape, they fold to mimic the prion that triggers the disease. When rogue cow prions infect humans, the misfolded prions are characteristic of mad cow disease. In humans with spontaneous prion disease or kuru, the detailed shape of the misfolded prions is different. This is because the incoming prions form a template upon which healthy prions aggregate after refolding into the rogue conformation.

  Calculations based on the history and age distribution of BSE in humans since the outbreak started suggest an average incubation period of about 17 years. The total number of cases expected is estimated to be 200 to 300. These estimates are much lower than many earlier and overly emotional predictions and reflect the extremely low infectivity of prions when crossing the boundary from one species to another.