**Note: articles and references are below…scroll down!**Current Events in Evolution! Name: _______________________

Honors Biology

Instructions1. Choose the topic that interests you most:

Evolution of Bedbugs Evolution of Antibiotic Resistance Evolution of Lactose Intolerance Evolution of Sickle Cell Heterozygote Carriers Antibiotic Use in Livestock Feedlots

2. You may work alone, in pairs, or groups of 3 (no more than 3)

3. Read the articles and sources provided, and use your knowledge of evolution from class to create a creative mini-presentation on your current event for the class tomorrow. Your presentation will be in the form of a…(one of the following)

poem song/rap comic strip poster with diagram or flow chart

** You have the entire class period today to plan your presentation. ** Each presentation should begin with a 3 minute introduction/explanation of your topic.** The creative presentation (poem, song, comic strip, etc.) should be 5 minutes long.

Assessment:o Group

Accuracy of content Use of relevant terms and explanations of concepts that relate to our study of evolution Brief oral summary of the topic before your creative presentation Overall effort

o Individual Active participation Good use of class time

You will turn in this sheet tomorrow when you do your presentation.

Bedbugs Finding a Way into New York’s SchoolsBy GEOFFREY DECKERPublished: September 24, 2010 NY Times

Having invaded New York City’s bedrooms, retail stores, movie theaters and offices, bedbugs are now showing up with growing frequency in another place: public schools.

Brooklyn Transition Center, a public high school in Bedford-Stuyvesant, is among the New York City schools where bed bugs have turned up, staff members said. There were 1,019 confirmed cases of bedbugs in the 2009-10 school year — an 88 percent increase from the previous school year, according to Education Department records.

So far this month, the city’s 311 help line has received 22 calls about bedbugs in schools, its records show. It is unclear whether additional cases were reported by other means.

School officials declined to provide the full number of confirmed cases since classes started on Sept. 8. But the Education Department spokeswoman, Marge Feinberg, said there had been no instances of city schools being closed because of bedbugs. “Each confirmed case is dealt with expeditiously,” she said.

At the Brooklyn Transition Center, a public high school in Bedford-Stuyvesant where middle-school students from the Beginning with Children Charter School also study, a Police Department school security officer and three teachers said Friday that there had been multiple instances of bedbugs since the beginning of the school year. “We really need somebody to come clean it up,” said a teacher who was in front the school building, on Ellery Street, about 2 p.m.

“It was a problem last spring and we thought it would be gone this year, but it’s still a problem,” said the teacher, who spoke on the condition of anonymity and was eventually asked by a security guard to end the interview. Ms. Feinberg said the school’s principal, Valerie Miller, told her that bedbugs had been found in the school twice this month, and that the two classrooms involved had been treated. Ms. Feinberg said that Ms. Miller told her, “There were no instances where it was widespread.”

Ms. Miller also told her that parents of children in the affected classrooms were notified, Ms. Feinberg said. Bedbugs feed on humans, but do not transmit disease. Still, now that they are showing up in the schools, they are

joining lice as a scourge of families that include young students. While schools are not considered ideal feeding spots for the nocturnal parasites, classrooms could be serving as a transportation hub to and from homes, further fanning a citywide resurgence of the pests, experts say. And it could get worse in the months ahead.

“What we’ve found is that they crop up during winter time, on heavy clothing, like jackets,” Ms. Feinberg said. Mike Orlino of Superior Pest Elimination, a company based on Staten Island that has contracted with the Education

Department since 2004, said the company had seen a huge increase in cases. It treated 29 schools for bedbugs last year, he said.

Schools in Brooklyn and Queens, the city’s most populous boroughs, had the most confirmed cases last year, Ms. Feinberg said. Brooklyn reported 439 cases, and Queens reported 327.

Ms. Feinberg would not say how many schools were affected and declined to name schools other than Brooklyn Transition where bedbugs were discovered.

City officials have started to track the problem more closely, said Nick Sbordone, a spokesman for the city’s Department of Information Technology and Telecommunications. Since the city started counting 311 calls related to bedbugs, in March, operators have received 121 calls about bedbugs in schools, including the calls since the current school year started, he said.

This month the city updated its nine-page “Bedbug Kit,” which outlines ways to detect and deal with the insects, Ms. Feinberg said. The manual includes a letter school administrators can use to notify parents whenever bedbugs are found in a school.

Gov. David A. Paterson signed a law last month that requires schools in large districts to notify parents of any infestation. The law does not take effect until July.

Ms. Feinberg said, “We go above and beyond the legal requirement.” She added that “currently just the parents of students who are affected” must be notified. The union representing teachers acknowledged the difficult circumstances schools face, but called on officials to research safer, more effective methods of eradicating the bugs.

“Our school communities need to be able to count on more support from governmental agencies as well as legislation to address this increasing problem,” said Richard Riley, a United Federation of Teachers spokesman.

Correction: October 8, 2010

An article on Sept. 25 about bed bugs in the city’s public schools misstated the timeframe during which a Staten Island company, Superior Pest Elimination, began working for the city’s Department of Education. It started work in 2004, not in the 1990s.

Bed bugs bite back thanks to evolutionSeptember 2010

Cimex lectularius, the bed bug

Bed bugs might sound like an old-fashioned problem, but now they are back — and with a vengeance. Fifty years ago, the blood-sucking pests were nearly eradicated in the United States thanks in part to the use of pesticides like DDT. Today, they are creeping over sheets — and tormenting hapless sleepers — across the country. New York was recently declared America's most bed-bug-infested city: Times Square movie theatre, the Empire State Building, and the offices of a major fashion magazine — not to mention the homes of 11,000 New Yorkers who filed official complaints about the vermin last year — have all housed these itchiest of bedfellows. And the Big Apple is not alone in its disturbed slumber. This summer, the Centers for Disease Control and Prevention (CDC) and the Environmental Protection Agency (EPA) issued a joint statement on the resurgence of bed bugs throughout the country. Wherever you live — whether that's Los Angeles or Louisville — bed bugs may soon be coming to a mattress near you!

Where's the evolution? What's to be done if you wind up the unhappy bunkmate to a nest of these pests? In the past, the answer was simply to spray with a pesticide. Unfortunately, that response is less effective than it used to be — not because the pesticides used today are weak — but because bed bugs have evolved resistance to the most commonly used chemicals. Pyrethrums, which are both toxic and repellent to insects, are currently the top choice for bed bug infestations. This class of chemicals includes pyrethrins, which are extracted from chrysanthemum plants, and pyrethroids, the synthetic versions of those chemicals. The evolution of pyrethrin in plants in the first place probably resulted from natural selection for plants better able to avoid being eaten by insects. We humans have simply co-opted the plants' chemicals defenses to deal with our own insect problems. Pyrethrums are especially useful to us because they generally have a stronger effect on bugs than on mammals, making them relatively safe for use in homes.

Pyrethrums work by attacking the nervous system. Insects (and humans) have tiny pores in the membranes of their nerve cells that can be opened to allow sodium into the cells, triggering a nerve impulse. Pyrethrums muck up the nervous system by binding to the sodium pores, locking them in the open position. This allows sodium to pour into the cell continuously, causing the nerve to fire repeatedly and eventually leading to paralysis. Mammals and insects inherited similar nerve cells from our common ancestor — meaning that the human nervous system is also vulnerable to pyrethrums. However, pyrethrums are relatively safe for us because, in comparison to insects, our bodies have more effective ways to break the compounds down before they can do major damage.

So, how do resistant bed bugs survive pyrethrum spraying? Biologists have actually figured out exactly which mutations are responsible for many cases of resistance. For example, changing just two of the 2000 amino acids that make up part of the sodium pore is enough to make an insect 250 times more resistant to a commonly used pyrethroid. These mutations may change the pore so that the insecticide can no longer bind to it effectively and/or may change the way the pore responds when the insecticide binds.

Such mutations arise randomly and are favored when a population of organisms winds up in an environment in which the mutations happen to be useful — in this case a bed sprayed with pyrethrum. In that situation, if some (or even just one) of the insects carry the resistance mutations, those insects will be better able to survive and reproduce and will wind up passing the mutation on to their offspring. As this process continues through several generations, the population may evolve such that every individual carries the resistance mutations — an outcome which is great for the bugs but immensely frustrating for the human occupants of the bed!

The key to this process of natural selection is having the right genetic variation in the insect population. If the population doesn't happen to carry any of the advantageous resistance mutations, the pyrethrum treatment will wipe out

the bed bug population. It might seem then, that resistant populations should be rare — after all, how many bed bug populations are likely to be lucky enough to carry just the right mutations to survive pyrethrum spraying? A lot, it turns out. Here's why. Bed bug populations have been primed with the right sort of genetic variation by their evolutionary history — a history which includes extensive exposure to a different insecticide, DDT. Like pyrethrums, DDT kills insects by acting on the sodium pores in their nerve cells — and it just so happens that many of the same mutations that protect an insect against DDT also happen to protect it from pyrethrums. When DDT was first introduced, such mutations were probably extremely rare. However, with the widespread use of DDT in the 1950s and 60s, such mutations became much more common among bed bugs through the process of natural selection. Though DDT is rarely used today because of its environmental effects, these mutations have stuck around and are still present in modern bed bug populations. Because of the action of natural selection in the past (favoring resistance to DDT), many bed bug populations today are primed with the right sort of genetic variation to evolve resistance to pyrethrums rapidly.

And evolve rapidly they have! In the last decade, resistance to pyrethrums among bed bugs has become a major problem in the U.S. and may help explain why the pests are crawling into bed next to more and more of us. The map below shows how prevalent just two of the mutations conferring resistance have become. The pace at which widespread resistance has evolved suggests that relying on chemicals alone to control bed bug infestations is not enough — and may even encourage the evolution of more resistant populations. Instead, the CDC and the EPA recommend a more integrated approach, one that incorporates pesticides, along with other techniques to which resistance is unlikely to evolve: heat treatment (temperatures between 113 and 120°F can kill the bugs), vacuuming, removing clutter, and sealing cracks and crevices. The rapid evolution of insecticide resistance in these pests has made it harder — but not impossible — to kick them out of bed for good!

Sources:http://www.nytimes.com/2010/09/25/nyregion/25bedbugs.html?_r=1&scp=3&sq=bed%20bugs&st=csehttp://evolution.berkeley.edu/evolibrary/news/100901_bedbugshttp://www.awitness.org/column/principles_evolution.html

Livestock kick a drug habitSeptember 2005, updated August 2009

"Just say no to drugs" was the message sent to chicken farmers in July

of 2005 when the FDA banned the use of the antibiotic Baytril in poultry production. Citing concerns for human health, the FDA will no longer allow poultry producers to give their chickens, turkeys, and ducks Baytril-laced water to treat and prevent respiratory infections in the birds. That move reinforced the actions of McDonald's, Wendy's, and other fast food giants that have, in recent years, refused to buy chicken treated with Baytril and other selected drugs. Even the pork industry is getting in on the act. In August, Smithfield Foods Inc., the company likely to have supplied that glazed ham for your Sunday supper, announced that it would stop treating its pigs with selected antibiotics for growth-promotion purposes.

Where's the evolution?But how does using an antibiotic on chickens and pigs affect human health, and what does this all have to do with evolution? At issue is the evolution of antibiotic resistant bacteria.

When a farmer treats a chicken flock with the antibiotic Baytril, it kills most of the bacteria responsible for the respiratory infection — but it also kills many of the campylobacter bacteria that naturally live in the chickens' guts. Ever take an antibiotic for strep throat and wind up with an upset stomach? You've done the same thing — killed most of your naturally-occurring gut bacteria!

Here's the problem: not all of the campylobacter are killed, and the few that survive probably carry a mutation that makes them resistant to Baytril. These resistant campylobacter then pass that mutation on to their offspring as they multiply. Hence, natural selection causes the evolution of Baytril-resistant campylobacter bacteria. If campylobacter get into your body (perhaps through contaminated chicken meat), you may wind up with food-poisoning. With normal campylobacter, you could just take the antibiotic Cipro to clear up the infection — but since Baytril and Cipro are similar antibiotics, Baytril-resistant bacteria are also likely to be Cipro-resistant...and, voila, you end up with a terrible case of food-poisoning and no useful drug to treat it.

The potential ramifications become even more frightening when you consider the fact that bacteria have the unusual ability to pass genes back and forth between species in a process called horizontal transfer. Cipro is one of the few antibiotics used to fight the anthrax bacterium. If a campylobacter passed its Cipro-resistance gene on to an anthrax bacterium, we could end up facing a frightening "super-bug."

The evolution of antibiotic resistant bacteria is a serious concern — and it is not just limited to Baytril. Many human antibiotics have sister-drugs that are freely used on livestock in copious amounts. The presence of these antibiotics sets the stage for the evolution of resistant bacteria in any environment: in the animals themselves or in the soil and water contaminated by the antibiotic.

News update, August 2009 In 2005, the FDA banned the preventative use of the antibiotic Baytril in poultry production. This move was

aimed at slowing the evolution of drug resistant bacteria that threaten human health. Exposure to Baytril is likely to select for strains of bacteria resistant to the critical human antibiotic Cipro. However, since this first step, the FDA has taken no further action curbing the use of other antibiotics in livestock — though tens of millions of pounds of these drugs are used on U.S. livestock and tens of thousands of people die as the result of antibiotic resistant infections each

year. Now, Congress and the Administration may be picking up where the FDA left off. In March of this year, a bill to

limit the use of antibiotics in livestock feed was introduced in the House of Representatives. And in July, the Principal Deputy Commissioner of Food and Drugs came out in favor of the new legislation — which would phase out the preventative use of medically important antibiotics in livestock and require that new animal antibiotics be evaluated against the same criteria. Under the new legislation, the drugs could still be used to treat sick animals. If the bill goes into effect, it would recognize the evolutionary consequences of our actions and, in so doing, help modern medicine fight the battle against drug resistant pathogens.

Pathogens in Our PorkBy NICHOLAS D. KRISTOFPublished: March 15, 2009

“We don’t add antibiotics to baby food and Cocoa Puffs so that children get fewer ear infections. That’s because we understand that the overuse of antibiotics is already creating “superbugs” resistant to medication.

Yet we continue to allow agribusiness companies to add antibiotics to animal feed so that piglets stay healthy and don’t get ear infections. Seventy percent of all antibiotics in the United States go to healthy livestock, according to a careful study by the Union of Concerned Scientists — and that’s one reason we’re seeing the rise of pathogens that defy antibiotics.

These dangerous pathogens are now even in our food supply. Five out of 90 samples of retail pork in Louisiana tested positive for MRSA — an antibiotic-resistant staph infection — according to a peer-reviewed study published in Applied and Environmental Microbiology last year. And a recent study of retail meats in the Washington, D.C., area found MRSA in one pork sample, out of 300, according to Jianghong Meng, the University of Maryland scholar who conducted the study.

Regardless of whether the bacteria came from the pigs or from humans who handled the meat, the results should sound an alarm bell, for MRSA already kills more than 18,000 Americans annually, more than AIDS does.

MRSA (pronounced “mersa”) stands for methicillin-resistant Staphylococcus aureus. People often get it from hospitals, but as I wrote in my last column, a new strain called ST398 is emerging and seems to find a reservoir in modern hog farms. Research by Peter Davies of the University of Minnesota suggests that 25 percent to 39 percent of American hogs carry MRSA.

Public health experts worry that pigs could pass on the infection by direct contact with their handlers, through their wastes leaking into ground water (one study has already found antibiotic-resistant bacteria entering ground water from hog farms), or through their meat, though there has been no proven case of someone getting it from eating pork. Thorough cooking will kill the bacteria, but people often use the same knife to cut raw meat and then to chop vegetables. Or they plop a pork chop on a plate, cook it and then contaminate it by putting it back on the original plate.

Yet the central problem here isn’t pigs, it’s humans. Unlike Europe and even South Korea, the United States still bows to agribusiness interests by permitting the nontherapeutic use of antibiotics in animal feed. That’s unconscionable.

The peer-reviewed Medical Clinics of North America concluded last year that antibiotics in livestock feed were “a major component” in the rise in antibiotic resistance. The article said that more antibiotics were fed to animals in North Carolina alone than were administered to the nation’s entire human population.

“We don’t give antibiotics to healthy humans,” said Robert Martin, who led a Pew Commission on industrial farming that examined antibiotic use. “So why give them to healthy animals just so we can keep them in crowded and unsanitary conditions?”

The answer is simple: politics…..”

Meat Farmers Brace for Limits on AntibioticsBy ERIK ECKHOLMPublished: September 15, 2010

RALSTON, Iowa -- Piglets hop, scurry and squeal their way to the far corner of the pen, eyeing an approaching human. ''It shows that they're healthy animals,'' Craig Rowles, the owner of a large pork farm here, said with pride.

Mr. Rowles says he keeps his pigs fit by feeding them antibiotics for weeks after weaning, to ward off possible illness in that vulnerable period. And for months after that, he administers an antibiotic that promotes faster growth with less feed.

Dispensing antibiotics to healthy animals is routine on the large, concentrated farms that now dominate American agriculture. But the practice is increasingly condemned by medical experts who say it contributes to a growing scourge of modern medicine: the emergence of antibiotic-resistant bacteria, including dangerous E. coli strains that account for millions of bladder infections each year, as well as resistant types of salmonella and other microbes.

Now, after decades of debate, the Food and Drug Administration appears poised to issue its strongest guidelines on animal antibiotics yet, intended to reduce what it calls a clear risk to human health. The guidelines, which are voluntary and will not have the binding force of regulations, would end farm uses of the drugs simply to promote faster animal growth and call for tighter oversight by veterinarians.

The agency's final version is expected within months, and comes at a time when animal confinement methods, safety monitoring and other aspects of so-called factory farming are also under sharp attack. The federal proposal has struck a nerve among major livestock producers, who argue that a direct link between farms and human illness has not been proved. The producers are vigorously opposing it even as many medical and health experts call it too timid.

Scores of scientific groups, including the American Medical Association and the Infectious Diseases Society of America, are calling for even stronger action that would bar most uses of key antibiotics in healthy animals, including use for disease prevention, as with Mr. Rowles's piglets. Such a bill is gaining traction in Congress.

''Is producing the cheapest food in the world our only goal?'' asked Dr. Gail R. Hansen, a veterinarian and senior officer of the Pew Charitable Trusts, which has campaigned for new limits on farm antibiotics. ''Those who say there is no evidence of risk are discounting 40 years of science. To wait until there's nothing we can do about it doesn't seem like the wisest course.''

With the backing of some leading veterinary scientists, farmers assert that the risks are remote and are outweighed by improved animal health and lower food costs. ''There is no conclusive scientific evidence that antibiotics used in food animals have a significant impact on the effectiveness of antibiotics in people,'' the National Pork Producers Council said.

But leading medical experts say the threat is real and growing. Proponents of strong controls note that the European Union barred most nontreatment uses of antibiotics in 2006 and that farmers there have adapted without major costs. Following a similar path in the United States, they argue, would have barely perceptible effects on consumer prices.

Resistance can evolve whenever drugs are used against bacteria or other microbes because substrains that are less susceptible to the treatment will survive and multiply.

Drug use in humans, including overuse and misapplication, clearly accounts for a large share of the surge in antibiotic resistant infections, a huge problem in hospitals in particular. Yet biologists and infectious disease specialists say there is also enormous circumstantial and genetic evidence that antibiotics in farming are adding to the threat.

Livestock and poultry have been identified as the most likely sources of drug-resistant strains of microbes like salmonella and campylobacter that have caused outbreaks of severe intestinal illness in people and of E. coli strains that cause serious bladder, blood and other infections. (Resistant strains have not been implicated in the recent outbreak of salmonella contamination in eggs.)

In a letter to Congress in July, Dr. Thomas R. Frieden, director of the Centers for Disease Control and Prevention, cited ''compelling evidence'' of a ''clear link between antibiotic use in animals and antibiotic resistance in humans.''

As drug-resistant strains of microbes evolve on the farms, they are passed along in meat sold in grocery stores. They can infect people as they handle the uncooked product or when eating, if cooking is not thorough. The dangerous strains can also enter the environment via manure or the clothes of farm workers.

Genetic studies of drug-resistant E. coli strains found on poultry and beef in grocery stores and strains in sick patients have found them to be virtually identical, and further evidence also indicated that the resistant microbes evolved on farms and were transferred to consumers, said Dr. James R. Johnson, an infectious-disease expert at the University of Minnesota. Hospitals now find that up to 30 percent of urinary infections do not respond to the front-line treatments, ciprofloxacin and the drug known as Bactrim or Septra, and that resistance to key newer antibiotics is also emerging. E. coli is also implicated in serious blood, brain and other infections.

''For those of us in the public health community, the evidence is unambiguously clear,'' Dr. Johnson said. ''Most of the E. coli resistance in humans can be traced to food-animal sources.''

The proposed Food and Drug Administration guidelines focus on the use of antibiotics to speed growth. Just how antibiotics have this effect, which has been known for decades, is unclear, but scientists suspect that the drugs improve the absorption of nutrients as they prevent low-grade disease.

Mr. Rowles, the proprietor of Elite Pork and a trained veterinarian himself, estimates that by feeding his pigs an antibiotic in their final months he is saving $1 to $3 per animal in feed costs. For the consumer, this is negligible, but from his perspective it looms larger because, he said, in good years his net profit is only $7 to $10 per animal.

More contentious is the routine use of antibiotics to prevent disease, as Mr. Rowles and other pork producers do with newly weaned pigs.

Dr. James McKean, an extension veterinarian at Iowa State University, said experience in Denmark, Europe's leading pork producer, showed that ending the practice would result in more illness, suffering and death among pigs, and cause a jump in antibiotic treatments of actual disease.

Dr. McKean estimated that a ban on most nontreatment uses of antibiotics would raise the cost of pork by 5 cents a pound.

Others counter that farmers in Denmark have learned to hold down illness in young pigs by extending the weaning period, altering feeds and providing more space and veterinary scrutiny of the animals. Some of the drugs used in prevention by farmers like Mr. Rowles would also be permitted under the measure before Congress because they are not used in human medicine.

''In the end, the producers will do what is right,'' Mr. Rowles said. ''We will make sure we deliver a product that meets the needs of consumers.''

''My only concern is that we make decisions in a scientific fashion, not a political fashion,'' he said. PHOTOS: Piglets at Elite Pork near Ralston, Iowa, are raised on a diet heavy with antibiotics. The purpose is both to

ward off diseases and to promote faster growth.; Excenel RTU antibiotic at Elite Pork.; Craig Rowles, the owner of Elite Pork, last month. He says that by feeding his pigs an antibiotic he saves $1 to $3 per animal in feed costs. (A14); A sow feeding her young at Elite Pork. ''In the end, the producers will do what is right,'' said Craig Rowles, Elite's owner.; The nurseries at Elite Pork near Ralston, Iowa, are home to hundreds of piglets fed a diet rich in antibiotics. (PHOTOGRAPHS BY BRIAN C. FRANK FOR THE NEW YORK TIMES) (A21)

Correction: September 21, 2010, Tuesday This article has been revised to reflect the following correction: An article on Wednesday about the use of

antibiotics in livestock may have left the incorrect impression about the effect of a proposal under consideration by the Food and Drug Administration. While the guidelines that the agency is expected to issue, seeking to end the use of antibiotics to promote growth in healthy animals, are indeed its strongest yet, they are voluntary and will not have the binding force of regulations. And an accompanying picture caption referred imprecisely to an injectable antibiotic, Excenel RTU. Excenel is used in the treatment of swine disease, but it is not used to prevent disease or promote faster growth in pigs and thus would not fall under the F.D.A.'s proposed guidelines.

Sources: http://evolution.berkeley.edu/evolibrary/news/050915_baytrilhttp://www.nytimes.com/glogin?URI=http://www.nytimes.com/2009/03/15/opinion/15kristof.html&OQ=_rQ3D2&OP=5f4e6c57Q2FQ5CoQ3BRQ5CfXQ5Ez.XXTQ26Q5CQ26rrQ3EQ5CrPQ5CQ3A-Q5CXet7tX7Q5CQ3A-h.tzTXWQ258TQ3C0http://query.nytimes.com/gst/fullpage.html?res=9905EFDA143AF936A2575AC0A9669D8B63&pagewanted=2

Evolution of Antibiotic Resistance:When a sick person takes antibiotics, the drugs begin to kill off the bacteria. But if treatment stops prematurely, it

leaves some microbes alive -- the ones with mutations that make them resistant to the drugs. As these survivors multiply, they pass along their protective mutations to all their descendants. In this way, the bacteria evolves into a new drug-resistant strain.

Forty or fifty years ago, thanks to antibiotics, scientists thought medicine had all but eradicated infectious agents as a major health threat. Instead, the past two decades have seen an alarming resurgence of infectious diseases and the appearance of new ones.

Today, the AIDS virus, tuberculosis, malaria, diarrheal diseases and other infectious agents pose far greater hazards to human existence than any other creatures.

This upsurge of infectious disease is a problem we have unwittingly created for ourselves. The rise of rapid, frequent, and relatively cheap international travel allows diseases to leap from continent to continent. Inadequate sanitation and lack of clean drinking water are another factor. A third is the "antibiotic paradox" -- the overuse of the "miracle drugs" to the point that they lose their potency.

Whenever antibiotics wage war on microorganisms, a few of the enemy are able to survive the drug. Because microbes are always mutating, some random mutation eventually will protect against the drug. Antibiotics used only when needed and as directed usually overwhelm the bugs. Too much antibiotic use selects for more resistant mutants. When patients cut short the full course of drugs, the resistant strains have a chance to multiply and spread.

In some countries, such as the United States, patients expect and demand antibiotics from doctors, even in situations where they are inappropriate or ineffective. Our immune systems will cure many minor bacterial infections on their own, if given the chance, and antibiotics have no effect on viral infections at all. Every time antibiotics are used unnecessarily, they add to the selective pressure we are putting on microbes to evolve resistance. Then, when we really need antibiotics, they are less effective.

While drug companies race to develop new antibiotics that kill resistant microbes, scientists are urging patients and doctors to limit antibiotic use.

That means not asking for penicillin when all you have is a cold, since colds are caused by viruses that are not affected at all by antibiotics. It means taking all the pills that are prescribed, even if you're feeling better. Physicians have to resist prescribing the strongest and most broadly effective drugs unless the disease absolutely requires it. If society adopts these measures rigorously, the drugs may regain at least some of their lost "miracle" powers.

The Escape of the Pathogens: An Evolutionary Arms Race (1 of 2)Human populations are constantly locked in evolutionary arms races with pathogens that

invade our bodies. We must recognize that these pathogens (such as the flu virus shown at right) are continuously evolving entities in order to develop better ways to fight them and control their evolution.

An ounce of prevention...every year?Recently, the mayor of New York City called upon citizens to get a head start on one

particular evolutionary arms race: “I urge older New Yorkers and others at risk to protect themselves from flu and pneumonia through a simple and proven ounce of prevention: immunizations. The time to get immunized is now, before the peak of the flu season.”1

Many of those New Yorkers had already gotten flu shots the year before and the year before that, but, perhaps strangely, they were being asked to get yet another immunization. Why do we need a new flu shot every year? Can’t modern medicine invent just one vaccine that would do the trick?

Flu viruses evolve rapidly.As they circulate through populations around the world and switch hosts, flu viruses change so much that our vaccines are rendered obsolete every year. The flu is a problem for which a solution must be redesigned and rebuilt every year, like a bridge that gets washed away every flood season. Only by understanding the flu as an evolving entity can we understand why our solution to the problem must change every year.

The Escape of the Pathogens: An Evolutionary Arms Race (2 of 2)Every day we come into contact with millions of bacteria and viruses. Some are harmful and others are beneficial,

while the rest have no apparent effect on our health. When harmful microorganisms enter our bodies, a battle ensues.Rapid reproduction and natural selection

Because bacteria and viruses reproduce rapidly, they evolve rapidly. These short generation times—some bacteria have a generation time of just 15 minutes—mean that natural selection acts quickly. In each pathogen generation, new mutations and gene combinations are generated that then pass through the selective filter of our drugs and immune response. Over the course of many pathogen generations (a small fraction of a single human lifetime), they adapt to our defenses, evolving right out from under our attempts to rid ourselves of them.

Applying our knowledge of evolutionBut that doesn’t mean that we should stop trying to win these battles. By understanding these pathogens as evolving entities, subject to the same processes of evolution that we can study in fruit flies or the fossil record, we may be able to identify ways to slow their progress.

Sources: http://evolution.berkeley.edu/evosite/relevance/IApathogens2.shtmlhttp://www.pbs.org/wgbh/evolution/library/10/4/l_104_03.html

Got lactase?April 2007

In the US and many other countries, we've certainly "got milk," but not everyone can enjoy it. For around 10% of Americans, 10% of Africa's Tutsi tribe, 50% of Spanish and French people, and 99% of Chinese, a tall cold glass of milk means an upset stomach and other unpleasant digestive side effects. In fact, most adults in the world are lactose intolerant and cannot digest lactose, the primary sugar in milk. And yet, regardless of our ancestry, most of us began our lives happily drinking milk from a bottle or breast — so what happened in the intervening time? Why do so many babies enjoy lactose and so many adults avoid it?

Lactose is broken down by a protein called lactase, which acts as a pair of molecular scissors, snipping the lactose molecule in two. Anyone who drank milk as a baby carries a working version of the gene that codes for lactase. In lactose tolerant individuals, that gene keeps working into adulthood, producing the protein that digests lactose and makes eating ice cream a pleasant experience. But in people who are lactose intolerant, that lactase gene is switched off after weaning. Now, new research reveals that the Stone Age ancestors of European dairy-lovers probably couldn't digest milk either. So how did they get from bellyaches to milk mustaches? The answer is an evolutionary story that takes us from the milkmaids of the Alps to the Maasai herdsmen of Africa.

Prevalance of lactose tolerance and reliance on dairy products vary throughout the world.

Where's the evolution?Mutations that keep the lactase gene permanently switched on are common among modern Europeans — but not among their ancestors. In March 2007, a team of German and British researchers announced that they went looking for that mutation in the 7000-year-old fossils of ancient Europeans and came up empty-handed. The researchers managed to extract the length of DNA corresponding to the lactose tolerance mutation from eight Neolithic human fossils and one Mesolithic fossil, but those DNA sequences did not carry the telltale mutation. The results suggest that as late as 5000 BC most ancient Europeans could not have digested milk as adults — and that they only later evolved into milk-drinking societies.

Today, the ability to digest milk as an adult seems like a clear benefit, but that wasn't always the case. Lactose tolerance is only advantageous in environments and cultures where humans have access to domesticated dairy animals. Multiple lines of evidence from human genetics, cattle genetics, and archaeological records suggest that Middle Eastern and North Africans populations domesticated cattle between 7500 and 9000 years ago, and that these animals were later brought into Europe. In that cow-friendly environment, being able to drink milk directly (instead of having to process it into lower-lactose cheese) would have been advantageous, providing additional sustenance and, during droughts, a source of water. The lactose tolerance mutation arose randomly (as all mutations do), but once it arose, it had a distinct advantage in these populations. Natural selection would have favored individuals carrying the lactose tolerance mutation, spreading it through ancient European populations that depended on dairying. Many thousands of years later, we see the indirect (but delicious) effects of this mutation's success in European cuisines: oozing French cheeses, Swiss milk chocolate, and creamy Italian gelatos.

How do we know?How did Sarah Tishkoff's team identify the African lactose tolerance mutations and show that they had been

advantageous? To identify the mutations, the team collected DNA samples from African participants and tested those same individuals for lactose tolerance. They looked for mutations in the DNA samples that always showed up in lactose tolerant individuals but weren't found in lactose intolerant individuals. To double check that the candidate mutations they'd

identified weren't red herrings, the team then did Petri-dish-style experiments, which helped show that those signature mutations were likely to keep the lactase gene turned on.

To show that the mutations were advantageous, the team looked for evidence of what geneticists call a "selective sweep" — the rapid spread of an advantageous mutation through a population that simultaneously spreads the DNA sequences adjacent to the new mutation. To understand how selective sweeps work, consider this hypothetical example. Imagine that a new advantageous mutation occurs on Chromosome 4, right next to, say, a gene coding for bushy eyebrows and a gene coding for black hair. In genetic terms, we would say that the mutation and those genes are "linked" — that is, they are close together on the same chromosome. The new mutation is so advantageous that its carrier leaves lots of offspring — many of whom carry the mutation and the other linked genes. As natural selection spreads this mutation, it tends to bring along nearby gene versions (bushy eyebrows, black hair). Those neutral gene versions can hitchhike their way to high frequency along with an advantageous mutation if they are very closely linked — so a large portion of the population might wind up carrying the genes for black hair and bushy eyebrows, even though these traits are not particularly advantageous. Of course, over time recombination tends to break down the associations between nearby genes, but in a selective sweep, the mutation spreads so rapidly that recombination doesn't have time to break the genetic alliance up much. The faster the sweep, the less the alliance can be broken up, and the slower the sweep, the more the alliance can be broken up.

Tishkoff's team studied their DNA samples to see how much of the genetic sequences surrounding the lactose tolerance mutations had been swept to high frequency along with the advantageous mutations. A surprisingly large portion of the chromosome seems to have escaped the dissociating effects of recombination and "come along for the ride" offered by lactose tolerance. Based on these studies, Tishkoff's team estimates that the most successful of the African lactose tolerance mutations arose within the last 7000 years and quickly spread through dairying populations.

Surprisingly, with respect to dairying, human populations on separate continents seem to have led parallel lives — or rather, followed parallel evolutionary trajectories. Recent evidence suggests that cattle may have been domesticated independently in several places, including Africa. As African populations began herding cattle, lactose tolerance became an advantageous trait. The stage was set, in Africa too, for the spread of a lactose tolerance mutation. In January 2007, an international team of researchers led by geneticist Sarah Tishkoff announced that they had uncovered the genetic roots of Africans' lactose tolerance. Just as in Europe, on this continent, mutations (in this case, probably three) randomly arose, and these happened to have the effect of keeping the lactase gene switched on. And just as in Europe, these mutations were favored by natural selection and quickly spread through dairy-dependent populations.

A Maasai warrior donates blood for a DNA sample.

While this discovery answers many questions, it also highlights new mysteries. For example, Tishkoff's team discovered that in the Hadza population (a group of Tanzanian hunter-gatherers), around 50% are lactose tolerant — a percentage usually indicative of a dairy-dependent society. And yet, as far as is known, the Hadza have never had much to do with cattle or relied on milk in their diets — so what explains their lactose tolerance? Are they the long lost descendents of a group of cattle herders? Has the tribe changed its basic mode of making a living? Or could the lactose tolerance mutation provide some other yet-to-be-discovered advantage, beyond allowing adults to drink milk?

Whatever the answers such spin-off questions, research into the evolutionary origins of lactose tolerance has already clearly illuminated some fascinating aspects of human evolutionary history. Perhaps most intriguingly, the convergent evolution of African and European populations in relation to cattle domestication reveals that shared aspects of human culture across different ethnic groups affects our evolution in similar ways. Regardless of skin color or geography —

whether dealing with Stone Age Europeans, Swiss milk maids, Maasai warriors, or modern hunter-gatherers — evolution plays by the same rules.

Lactose IntoleranceThe best documented differences in nutritional adaptation relates to milk sugar, or lactose , which is commonly

found in uncooked dairy products. Most human adults have moderate to severe difficulty in digesting lactose. They experience bloating, stomach cramps, belching, flatulence, and even diarrhea when they drink milk. Not surprisingly, this commonly results in the exclusion of dairy products from their diet. This problem is most often due to an inability to produce sufficient amounts of the enzyme lactase , which breaks down lactose in the small intestine to aid its absorption into the blood stream. Those who have this problem are said to be lactose intolerant due to their lactase deficiency.

The ability to produce lactase is genetically controlled. The gene that codes for it (LCD) is on chromosome 2. The vast majority of babies throughout the world can digest their mother's milk. However, there is a decline in lactase production as people grow older. This decline usually begins by two years of age, which is shortly after the time when babies are weaned in most societies. For some people, the reduction in lactase production does not start to occur until they are around twenty. More rarely, lactase continues to be produced at sufficient levels to consume milk throughout life.

Lactose intolerance is at its highest frequency in some parts of Africa, East Asia, and among Native Americans (as shown in the table below). Northern Europeans generally have the lowest frequency of this dietary problem.

POPULATION LACTOSE

INTOLERANT ADULTS

U.S. European Americans 2-19 % Latinos (Hispanic

Americans) 52 %

African Americans 70-77 % Native Americans 95 % Asian Americans 95-100 % Mexico 83 % Europe Sweden 4 % Switzerland 12 % Spain 15 % Finland 18 % Estonia 28 % England 32 % Hungary 37 % Greece 88 % Jordan 79 % Africa Southern Sudan (cattle

herders) 17 %

Ibo and Yoruba (Nigeria) 99 %

Asia Japan 90 % Thailand 99 % Australia (Aborigines) 85 %

Source: Robert D. McCracken, "Lactase Deficiency: An Example of Dietary Evolution,"Current Anthropology 12 (Oct.-Dec. 1971, pp. 479-517) and Norman Kretchner, "Lactoseand Lactase," Scientific American 277 (Oct. 1972, pp. 71-78)

Given this distribution pattern of lactose intolerance, it is not surprising that dairy products are popular among most Europeans but are rarely found in Asian, Native American, and most African cuisines (except among cattle herders in East Africa). In the majority of non-European populations, fresh milk is considered an unpleasant substance to be

consumed only as a last resort. It is now clear that lactose tolerant Europeans are atypical for humanity and for the entire animal kingdom. Evolutionary Significance of Lactose Tolerance

The common ability of people in Europe and some other areas of the world to continue producing lactase as adults is very likely a relatively recent evolutionary development. Prior to the domestication of cattle, sheep, goats, and horses after about 9000 years ago, milk was most likely only consumed by babies and very young children. That milk was human milk. Dairy products such as cow's milk, yoghurt, and cheese did not exist. When nutrient rich nonhuman milk became widely available in pastoralist societies, the rare genetic variations that allowed some adults to easily digest lactose were selected for and this trait became more common. In other words, natural selection shifted to favor lactose tolerant people, resulting in the progressive evolution of the gene pools of these populations. Support for this hypothesis was provided in 2007 by Joachim Burger and his team of researchers at the University of Mainz in Germany. Their analysis of DNA in bones from 10 Central and Eastern European human skeletons dated between 3,800 and 6,000 years ago showed that the allele that allows lactose tolerance in adulthood was not yet present despite the fact that these populations apparently had been raising milk producing farm animals for hundreds or even thousands of years. Sarah Tishkoff from the University of Maryland also reported in 2007 that the mutations among East Africans that keep the lactase gene permanently turned on are different from those of Europeans who share this trait. Her genetic studies among 43 East African ethnic groups also suggests that 3 different mutations resulting in lactose tolerance in Africa arose 2,700-6,800 years ago.

Sources:http://evolution.berkeley.edu/evolibrary/news/070401_lactosehttp://anthro.palomar.edu/adapt/adapt_5.htm

“An example of nature selecting against both homozygotes was found in Central Africa. This is an area in which malaria has long been a serious problem. While 10% of the world's human population is infected by malaria, 90% of the cases are in sub-Saharan Africa. It is the major cause of death there. Children and pregnant women are especially vulnerable. An African child dies of malaria every 30 seconds on average. Malaria is caused by several related parasitic microorganisms (plasmodia ) that feed on red blood cells. The microorganisms are transmitted from person to person by mosquitoes when they suck blood from their victims. People who produce normal red cells are good hosts and easily get the disease, which is debilitating and ultimately often results in death.

There is a high frequency of an inherited condition known as sickle-cell trait in African malarial zones. Homozygous recessive sicklers (aa) have resistance to falciparum malaria because their misshapen, deflated red cells are poor hosts. Unfortunately, these individuals usually die in childhood from bacterial infections made worse by weakened immune systems and sickle-cell anemia . About 100,000 people around the world succumb to such sickle-cell related health problems every year. However, that is far fewer than the1,500,000 who die from malaria.

People who are heterozygous (Aa) for sickle-cell trait also have moderately good resistance to malaria because some of their red cells are misshapen and deflated, but they rarely develop the severe life threatening anemia and related problems typical of homozygous (aa) sicklers. Those who are homozygous dominant (AA) produce normal red blood cells, which makes them excellent hosts for malaria. Therefore, in falciparum malarial environments, nature selects for heterozygous sicklers. At the same time, it selects against homozygous sicklers and people who produce normal red blood cells.

Normal human red cells Deflated red cells from human with sickle-cell

anemia

The sickling allele was not produced by natural selection. It apparently pops up periodically as a random mutation. Unless it is selected for, its frequency remains very low within a population's gene pool because it results in a selective disadvantage for those who inherit it. The presence of widespread falciparum malaria changes the situation. The otherwise harmful sickling allele provides an advantage for heterozygous individuals.

Selection favoring the sickling allele is an example of biocultural evolution . Human culture altered the environment, which resulted in factors that were advantageous to both the malarial microorganisms and the mosquitoes that transmit them between people. The sequence of events apparently began about 2000 years ago with the introduction into Africa of Southeast Asian root and tree crops that were adapted to the humid tropics. This resulted in an agricultural revolution and a subsequent human population explosion in sub-Saharan Africa. Slash-and-burn forest clearance for preparing agricultural fields altered the natural environment in a way that selected for the Gambiae group of anopheles mosquitoes that are largely responsible for spreading malaria. At the same time, the progressively increased density of humans made it easier for mosquitoes to find hosts and to inadvertently spread malaria. The more people who acquired malaria, the more likely it was for mosquitoes to transmit the malaria plasmodia to new hosts. Subsequently, the sickling allele became increasingly valuable as a population defense against the devastating effects of malaria. This natural selection by malaria in sub-Saharan Africa was not so complete as to result in a balanced polymorphism in just one generation. In fact, after nearly 2,000 years of selecting for the sickle-cell allele, it is not often found to be above 20% in any major African population.

Sickle-cell trait is very rare in North America with a single exception--African Americans. One in 12 of them carry the allele for sickle-cell trait and about 80,000 have sickle-cell anemia or other related clinical symptoms. One in 375 African American children is homozygous recessive for it. This is not surprising because most African Americans have ancestors who came from the malarial zones of West and Central Africa” (O’Neil 2010).”

Source: http://anthro.palomar.edu/synthetic/synth_4.htm

Sickle Cell Anemia and Genetics: Background InformationGenetics of Sickle Cell Anemia

“Sickle cell anemia was the first genetic disease to be characterized at the molecular level. The mutation responsible for sickle cell anemia is smallójust ONE nucleotide of DNA out of the three billion in each human cell. Yet it is enough to change the chemical properties of hemoglobin, the iron and protein complex that carries oxygen within red blood cells.

There are approximately 280 million hemoglobin molecules in each red blood cell (RBC). The protein portion of hemoglobin consists of four globin subunits: two alpha (a) and two beta (b). These two types of subunits are encoded by the a and b globin genes, respectively. While the binding of oxygen actually occurs at the iron sites, all four globin chains must work together in order for the process to function well.

Sickle cell anemia, also known as sickle cell disease, is caused by a point mutation in the b globin gene. As a result of this mutation, valine (a non-polar amino acid) is inserted into the b globin chain instead of glutamic acid (an electrically charged amino acid). The mutation causes the RBCs to become stiff and sometimes sickle-shaped when they release their load of oxygen. The sickle cell mutation produces a "sticky" patch on the surface of the b chains when they are not complexed with oxygen. Because other molecules of sickle cell hemoglobin also develop the sticky patch, they adhere to each other and polymerize into long fibers that distort the RBC into a sickle shape.

The sickled cells tend to get stuck in narrow blood vessels, blocking the flow of blood. As a result, those with the disease suffer painful "crises" in their joints and bones. They may also suffer strokes, blindness, or damage to the lungs, kidneys, or heart. They must often be hospitalized for blood transfusions and are at risk for a life-threatening complication called acute chest syndrome. Although many sufferers of sickle cell disease die before the age of 20, modern medical treatments can sometimes prolong these individualsí lives into their 40s and 50s.

There are two b globin alleles important for the inheritance of sickle cell anemia: A and S. Individuals with two normal A alleles (AA) have normal hemoglobin, and therefore normal RBCs. Those with two mutant S alleles (SS) develop sickle cell anemia. Those who are heterozygous for the sickle cell allele (AS) produce both normal and abnormal hemoglobin. Heterozygous individuals are usually healthy, but they may suffer some symptoms of sickle cell anemia under conditions of low blood oxygen, such as high elevation. Heterozygous (AS) individuals are said to be "carriers" of the sickle cell trait. Because both forms of hemoglobin are made in heterozygotes, the A and S alleles are codominant.

About 2.5 million African-Americans (1 in 12) are carriers (AS) of the sickle cell trait. People who are carriers may not even be aware that they are carrying the S allele!

Sickle Cell Anemia and MalariaIn the United States, about 1 in 500 African-Americans develops sickle cell anemia. In Africa, about 1 in 100 individuals develops the disease. Why is the frequency of a potentially fatal disease so much higher in Africa?

The answer is related to another potentially fatal disease, malaria. Malaria is characterized by chills and fever, vomiting, and severe headaches. Anemia and death may result. Malaria is caused by a protozoan parasite (Plasmodium) that is transmitted to humans by the Anopheles mosquito. When malarial parasites invade the bloodstream, the red cells that contain defective hemoglobin become sickled and die, trapping the parasites inside them and reducing infection.

Compared to AS heterozygotes, people with the AA genotype (normal hemoglobin) have a greater risk of dying from malaria. Death of AA homozygotes results in removal of A alleles from the gene pool. Individuals with the AS genotype do not develop sickle cell anemia and have less chance of contracting malaria. They are able to survive and reproduce in malaria-infected regions. Therefore, BOTH the A and S alleles of these people remain in the population. SS homozygotes have sickle cell anemia, which usually results in early death. In this way, S alleles are removed from the gene pool.

In a region where malaria is prevalent, the S allele confers a survival advantage on people who have one copy of the allele, and the otherwise harmful S allele is therefore maintained in the population at a relatively high frequency.

The frequency of the S allele in malaria-infected regions of Africa is 16%. The sickle cell allele is also widespread in the Mediterranean and other areas where malaria is or used to be a major threat to life. In contrast, the S allele frequency is only 4% in the United States, where malaria has been virtually eliminated. Malaria was once common in the United States, but effective mosquito control caused the number of cases to drop. Recently, however, there has been an increase in the number of malarial cases because of increased travel, immigration, and resistance to medication. In Southern California there was a 1986 outbreak of nearly 30 cases of malaria transmitted by local mosquitos!” (UW 2010)

Source: http://chroma.gs.washington.edu/outreach/genetics/sickle/sickle-back.html