Curious Folks Ask: 162 Real Answers on Amazing Inventions, Fascinating Products, and Medical Mysteries - Sherry Seethaler (2009)
Chapter 5. Pesky pathogens
Do you get a cold from being cold? I sat in an unheated library yesterday, and today my nose is streaming.
Modern virology textbooks reject the idea that being cold makes one catch a cold. The standard explanation of why colds are more prevalent in the winter than in the summer is that people spend more time indoors in contact with each other in the winter, which facilitates the spread of the viruses that cause colds.
Still, the folklore surrounding the relationship between cold exposure and the common cold is so longstanding and widespread that a number of researchers have considered it worthy of further exploration. Their studies suggest that Mom’s advice to “Keep warm so that you don’t catch a cold” may not have been off the mark after all.
One study of populations in seven countries in Europe, from Finland to Greece, showed that there were fewer deaths from respiratory diseases in regions where people tended to take protective measures against the cold. These included heating their homes, wearing protective clothes, and being physically active, rather than standing and shivering, when outdoors.
In the study, a given fall in temperature claimed more lives in regions with mild winters, and people in these regions were less likely to bundle up and heat their homes. For example, at the same outdoor temperature, 45 degrees Fahrenheit (7 degrees C), only 13 percent of people in Athens wore hats, whereas 72 percent of people in south Finland wore them. In addition, average living room temperatures were 4 degrees Fahrenheit (2.2 degrees C) warmer in southern Finland than in Athens.
Experimental studies on the effect of cold exposure have been mixed. One hypothesis to explain this inconsistency is that getting chilled makes a difference if a person not only has been exposed to one of the more than 200 cold viruses but also is already in the process of fighting the infection. In other words, cold exposure can turn an asymptomatic infection into full-fledged, nose-tooting misery.
Being cold may lead to the release of stress hormones, which suppress the body’s immune system. Low temperatures also cause the blood vessels in the nose and upper airways to constrict, possibly reducing the access of blood cells responsible for attacking invaders. In addition, cold air damps the action of cilia—tiny moving hairs that help eliminate contaminants in the airways.
So while doctors’ advice to wash your hands and avoid sick people will help you stay healthy, taking precautions against getting chilled may also help you fight the good fight against those insidious germs.
During cold season, we are told that antibiotics will not kill viruses and that colds are caused by a virus. What is the difference between viruses and bacteria, and why is it so hard to come up with a medicine to kill viruses?
Bacteria are single-celled organisms that contain the machinery needed to grow and replicate. Antibiotics inhibit various life processes in bacteria. Penicillin and related compounds interfere with the systems that build the cell walls of bacteria. Tetracyclines, as well as erythromycin and its relatives, block the bacterial cell’s machinery for making new proteins. Other antibiotics prevent bacteria from duplicating DNA, or from using or making essential nutrients.
Viruses are smaller than bacteria and basically consist of genetic material (RNA or DNA) packaged in a protein shell. Viruses cannot provide their own energy or replicate on their own. To reproduce, viruses must hijack the cellular machinery of another organism. Since antibiotics and antivirals must target processes that are unique to the infectious agents to avoid harming the cells of the infected organism, the simplicity of viruses means that they have fewer Achilles’ heels than bacteria. Also, viruses can hide within cells, in some cases for many years.
Thirty years ago, just three antiviral drugs were available. Genome sequencing and the study of the replication cycle of viruses have since led to major advances because antiviral drugs must be tailored to the viruses they attack. Knowledge of the structures and functions of the viral enzymes, or catalysts, guides the design of drugs that specifically block those enzymes. A similar procedure is used to develop antibiotics, although some—broad-spectrum antibiotics—are effective against a range of bacteria.
More than 40 drugs for the treatment of viral infections have now been approved, about half of which are used to treat HIV infections. One example of an antiviral medication is AZT, which inhibits an enzyme used by HIV to copy its genes into the genetic material of the cells it infects. Other antiviral medications prevent viruses from getting into cells, and still others prevent the finished virus particles from leaving cells and spreading elsewhere in the body.
Viruses and bacteria both mutate and become resistant to the drugs designed to fight them. Like the Red Queen in the sequel to Alice’s Adventures in Wonderland—running as fast as possible just to stay in place—researchers must continually develop new strategies to overcome drug resistance.
Influenza viruses are known to mutate into new, sometimes more virulent forms, which explains why some of us periodically get sick. Why is it that the same is not true for other known viruses, such as the polio and smallpox viruses?
Influenza viruses do evolve particularly quickly. Vaccine strains used against influenza must be changed at least every two to three years, because the proteins on the virus surface keep changing, thereby disguising it from the immune system. Vaccines against polio and many other human viruses have been stable for decades.
Part of what determines how fast a virus mutates is the type of genetic material it uses. Some viruses have genomes consisting of DNA. A chemically similar molecule, RNA, serves as the genetic material for other viruses. Another type of virus, the retrovirus, has RNA as its genetic material but copies RNA into DNA within an infected cell.
As a general rule, DNA viruses mutate more slowly than retroviruses, which mutate more slowly than RNA viruses. The fastest-mutating RNA virus has a mutation rate about 100,000 times faster than the slowest-mutating DNA virus. This range reflects the accuracy and proofreading ability of the machinery used to copy the different types of genetic material.
The genome of the variola (smallpox) virus is DNA, and a comparison of 45 virus samples from around the world during the 30 years prior to the eradication of smallpox revealed little sequence diversity. Yet genetic spellchecking is not the whole story, because polio, measles, and influenza are all caused by RNA viruses.
The mutation rate in viruses is also influenced by their generation time, genomic architecture (how the DNA or RNA is folded and whether it is single- or double-stranded), viral and host enzymes, and opportunities for virus particles to exchange genetic material with one another.
Yet higher mutation rates do not always enhance evolution. In an experiment in which the mutation rate of poliovirus was artificially increased by a factor of 10, the production of the virus decreased 1,000-fold, probably the result of an error catastrophe. In fact, increasing mutation rates to a lethal level is the mechanism of some antiviral drugs, such as ribavirin, a treatment for hepatitis C.
Therefore, mutation rate is insufficient to explain why influenza is a master of disguise compared to other RNA viruses, and the specific constraint on the evolution of surface protein variation remains a mystery.
Are any viruses nonpathogenic and used by our bodies, much like a lot of bacteria help us digest our food and so on?
“Bacteria are our friends” claims an adorably nerdy T-shirt sported by some biologists. Those who would roll their eyes at what they view to be a fashion faux pas have undoubtedly at least heard of beneficial bacteria. Ongoing research shows that our microscopic buddies do even more for us than we once thought. Related research suggests that viruses may also merit their own fan club.
About 1,000 species of normal, or commensal, bacteria inhabit our bodies. In total, we are lugging around a few pounds of bacteria. These bacterial cells, which are smaller than our own cells, significantly outnumber the human cells in our bodies. The highest concentration of bacteria is found in our intestines, especially the colon, and bacteria comprise approximately 60 percent of the solids in feces.
Commensal bacteria synthesize important nutrients and digest various compounds. Laboratory animals raised under sterile conditions retain water in their intestines because they lack bacteria that break down mucus. These animals also have altered immune systems.
Commensal bacteria stimulate the developing immune system but also help it develop regulatory mechanisms that prevent it from overreacting and causing chronic inflammation. Furthermore, they provide a physical barrier against disease-causing organisms, which may invade after treatment with antibiotics inadvertently wipes out our bacterial friends.
Viruses must hijack the machinery in a host organism’s cells to replicate. The hijacked cell may be killed, or at least prevented from carrying out its normal function. This is not a very happy state of affairs, unless the cells the virus infects are themselves dangerous invaders. This is the case with some bacteriophages (phages)—tiny viruses that infect bacteria.
Recent evidence suggests that phage predation on the bacteria that cause cholera—a waterborne diarrhea disease—can explain why most cholera epidemics tend to be self-limiting. A study found that as the cholera bacteria spread, the phages that prey on them became more abundant in the environment and in stool samples of those infected with cholera, until the epidemic rapidly collapsed.
Phage therapy has also been used successfully to treat diseases. Some researchers have hypothesized that phages play a normal role in regulating the ecosystem of bacteria in our bodies, and that they may contribute to our immune defenses to other viruses and even cancer.
Maybe T-shirts saying “Viruses are our friends” are about to come into vogue. If they do, you read it here first.
Why do we ache when we get sick with a cold or the flu?
The warfare used by our bodies against an invading virus, rather than damage from the virus itself, causes symptoms of the common cold and the flu. In response to infection, white blood cells release chemicals to communicate with other cells. These chemical messages amplify the triggering event (detection of a virus) and activate whole-body defense responses.
One chemical that plays a dominant role is bradykinin, which is a peptide, or small protein. It causes aches by stimulating sensory nerves. Other chemicals, including histamine and prostaglandins, may sensitize nerve endings to bradykinin. Bradykinin also causes other symptoms. When administered into the noses of healthy volunteers, it causes a runny, congested nose and throat irritation.
These symptoms make us feel miserable, but they ultimately help us get well. For example, fever facilitates the destruction of viruses and bacteria. Even cold-blooded lizards move to warmer places when they have an infection, and if prevented from warming their bodies above their usual temperature, they are more likely to die from the infection.
Similarly, that annoying stuffy nose may inhibit virus replication by raising the temperature of the nasal passages. Viruses that cause upper-airway infections generally propagate best at temperatures a few degrees below body temperature—conditions found in nasal passages cooled by inhaled air, but not in a congested airway.
Aches and fatigue also serve an adaptive purpose by making us rest, thereby directing more of our resources toward fighting infection (and making us feel less guilty about curling up in bed with a cup of cocoa and a good book).
You stated previously, “Fever facilitates the destruction of viruses and bacteria.” Then why do we take medication to lower the body’s temperature when we have a fever? Once our body temperature has been lowered (from the meds), is our body still fighting the invaders?
Most cold and flu medications are designed to relieve the symptoms of the illness so that we can function better, but they do not cure the viral infection. Fever-reducing drugs—collectively known as antipyretics—seem to be effective at reducing the mental dysfunction sometimes observed in patients with fever. Most antipyretics are also analgesics, or painkillers.
Fever increases metabolic demands and may stress a patient. Fever has also been associated with seizures in children. However, despite the widespread use of antipyretics, these drugs have failed to prevent fever-associated seizures in experimental studies.
Our bodies are still fighting the infection when we take antipyretics, but some studies have shown that taking antipyretics may slightly worsen symptoms or prolong illness. For example, patients infected with rhinovirus (which causes the common cold) who were treated with aspirin or acetaminophen had worse nasal congestion and produced virus particles longer than patients who were not treated with antipyretics.
Healthy as a dog
My dog never gets ill, yet everyone in my house gets colds, flu, etc. From what I have witnessed, humans seem to be the most disease-prone of any species on the planet. What is the reason for this?
Your dog is probably healthier because he is exposed to fewer other dogs than humans are exposed to other humans. Humans and dogs are susceptible to many of the same types of diseases, including parasitic, viral, and bacterial infections. Canine infectious respiratory disease, or “kennel cough,” is a significant problem in boarding facilities and other densely housed dog populations.
Infectious disease is also a problem in livestock, especially animals raised in crowded conditions. Just as history is full of examples of human populations that succumbed to diseases carried by explorers and colonists, domestic and wild-animal populations also have suffered after exposure to foreign germs.
Children in daycare have a higher incidence of colds than children without extensive contact with other children outside the home. We develop immunity as we get older; preschoolers have about six to ten colds per year compared to two to four in adults. However, immunity usually protects only against repeat infections with the same virus, and at least 200 known viruses cause colds.
Keep off the grass
I am concerned about bodily fluids released onto the increasingly popular synthetic playing fields during practices and sporting events. What are schools/colleges/stadiums doing to minimize the growth of potentially dangerous bacteria within the 3-D realm of the turf material?
Bacteria and viruses last a disturbingly long time on various types of surfaces. Studies of disease-causing bacteria and viruses have shown that many species survive days, weeks, months, or even years. Most survive longest under cool, humid conditions.
Synthetic turf has gotten a bad rap from reports that athletes who train mostly on synthetic fields may be at a greater risk of skin infections than athletes who train on grass fields. For example, during one season, five of 58 players on the St. Louis Rams football team got methicillin-resistant Staphylococcus aureus (MRSA) skin infections. Some opposing players developed MRSA infections after playing the Rams on their artificial turf.
Scientists from the Centers for Disease Control and Prevention (CDC) investigated the outbreak of MRSA among Rams players and opponents but did not find any MRSA on the artificial turf. Of course, this is like searching for a needle in a haystack, so it does not prove that the bacteria are absent. But the general consensus is that the turf is not the most likely source of the bacteria that caused the outbreak.
Instead, the CDC concluded that artificial turf can increase athletes’ susceptibility to skin infections because falls on artificial turf often lead to “turf burns.” Turf burns are especially common on older-model fields like the one the Rams played on, which lack a cushioning rubber/sand base. The raw skin of a turf burn provides an easy entry point for bacteria.
The athletes themselves are the most likely source of the bacteria, which spread through skin-to-skin contact. Close to one-third of people carry Staphylococcus aureus on their skin or in their noses, and about 1 percent of people carry the MRSA strain that resists the class of antibiotics that has traditionally been used to treat Staphylococcus aureus infections. MRSA was mostly unknown outside the hospital setting until the late 1990s, but it has become increasingly common in the community since then.
Antibacterial sprays can be applied to artificial turf, but no research has been conducted on their effectiveness in preventing disease. To prevent skin infections, the CDC recommends showering after working out, keeping wounds covered, and avoiding the sharing of personal items such as towels and razors.
Why is it so difficult to find a cure for AIDS?
Drug and vaccine development is complicated because HIV—the immunodeficiency virus that causes AIDS—is a “moving target.” HIV mutates frequently, resulting in different genetic variants of HIV being prevalent in different populations and even multiple variants within an infected individual.
The first HIV drug was introduced in 1987 with much excitement, but HIV resistance soon arose. Now more than 20 HIV drugs have been approved by the U.S. Food and Drug Administration. An increased understanding of HIV has made it possible to design drugs that interfere with different stages of the virus’s life cycle.
HIV multiplies in certain cells of the immune system, destroying them in the process. The virus recognizes a cell, binds to it, fuses with it, and injects its genetic material into the cell. HIV is a retrovirus—its genetic material is RNA, from which the virus’s reverse transcriptase enzyme produces DNA. Viral DNA is then integrated into the host cell’s DNA. This enables HIV to exploit the cell’s machinery to make more viral RNA and viral proteins, which are packaged into new virus particles.
Current HIV treatments usually combine multiple drugs. For example, one or more drugs that block reverse transcriptase may be combined with a protease inhibitor—a drug that interferes with the processing steps necessary to make mature viral proteins. Since these drugs work in different ways, the virus would need to develop multiple mutations to resist all of them.
Determining the genetic makeup of the HIV infecting a patient has also become a part of standard care. The information is used to help predict what drugs are likely to be effective against the variants of HIV that infect the patient, and what drugs are likely to fail because of resistance. When necessary, treatment regimens can be altered to keep up with an evolving virus.
HIV drugs can have serious side effects, and patients have difficulty staying on complicated regimens, requiring them to take multiple pills each day. In addition, HIV can lie dormant in cells for many years, making it difficult to completely eradicate. Still, in the developed world, these therapies have led to a drastic improvement in the prognosis for HIV-infected patients.
Sadly, progress has been much slower in the developing world. Cost is one complication. Treatment of one HIV patient in the Unites States runs approximately $20,000 per year. Another is that patients often lack access to medical experts who can monitor and respond to drug resistance and side effects.
I have heard that there is a way to treat hepatitis C infections that is more effective than the conventional treatment. What is this cure called, and what does it consist of?
The World Health Organization estimates that approximately 3 percent of the world population has been infected with the hepatitis C virus (HCV), which can be transmitted by sharing needles, sexually, and through blood transfusions received before donors were screened for HCV (1992 in the United States). In about one-quarter of cases, the infection clears up on its own. Of those who remain chronically infected, a subset will develop cirrhosis of the liver. HCV infection is the most frequent reason for liver transplantation.
Current treatment for chronic HCV infection is a combination of ribavirin and interferon, usually administered for several months. These medicines are effective for just over half of patients. They are more effective with some strains of HCV than others. The treatment also has a number of side effects and is unsuitable for patients with certain health conditions.
Other treatments are under development, including small molecules designed to block different steps in the viral replication process. Unfortunately, the virus quickly evolves resistance to these drugs, but drug cocktails that contain a variety of replication blockers may ultimately prove effective.
A plethora of alternative treatments for HCV are being promoted. Surveys of HCV patients in the United States reveal that about 40 percent of them take alternative medicines for HCV, mostly herbal products, often in addition to conventional treatment.
Because these herbal preparations have not been rigorously tested and are not regulated by the Food and Drug Administration, conventional medical professionals are concerned about their safety and value. In a review of the management of HCV published in 2006 in the journal Gastroenterology, the American Gastroenterological Association concluded that alternative therapies do not have a role in the treatment of hepatitis C.
Other researchers (see reviews of alternative treatments for HCV infections in Antiviral Therapy, volume 12, page 285, and Journal of Hepatology, volume 40, page 491) are less dismissive and call for large-scale, properly designed clinical trials on these herbal products to help people make informed decisions about them. The National Institutes of Health recently began a clinical trial on the most popular herbal treatment for HCV, Silybum marianum—milk thistle. Glycyrrhizin—an extract of licorice root—and extracts of bovine thymic gland have shown mildly promising results. To learn more about HCV clinical trials, visit http://www.clinicaltrials.gov.
With the demise of SureBeam, are there any other players left for the possible irradiation of incoming products from Mexico or other countries? Many of us thought that irradiation would provide protection against coliforms and salmonella, which frequently occur on produce and other foodstuffs.
The now-bankrupt company SureBeam produced electron beam food irradiation systems. Two alternative methods exist for the irradiation of food: gamma rays and X-rays. Gamma rays are produced by radioactive cobalt. X-rays and electron beams are generated electrically, which allows them to be switched on and off. Despite this advantage, irradiation with gamma rays is generally the preferred method because X-rays are more expensive to produce, and electron beams do not penetrate deeply into food.
At low doses, irradiation kills insects, delays fruit ripening, and prevents vegetables from sprouting. At medium doses, it reduces disease-causing microbes as well as bacteria, molds, and yeast that cause food spoilage. Hospitals use irradiation at higher doses to sterilize meals for patients who have weak immune systems. NASA has also used irradiation at high doses to sterilize meat for astronauts. Irradiation works by damaging DNA, which interferes with cellular processes and cell division.
In 1963 the U.S. Food and Drug Administration first approved irradiation to rid wheat, wheat flour, and potatoes of insects. Since the mid-1980s the FDA has approved irradiation of spices, meat, and fresh fruit and vegetables. Currently only 10 percent of herbs and spices and less than 1 percent of meat and produce are irradiated in the United States.
Opposition, rather than lack of technology, has slowed the implementation of irradiation. One set of arguments concerns the safety and nutritional quality of irradiated food. Like any method of food preservation and preparation, irradiation results in small losses of nutrients. Irradiation also results in the formation of 2-alkylcyclobutanones—chemicals that are unique to irradiated foods. The World Health Organization and other public health agencies have reviewed the scientific studies and concluded that irradiated foods are safe.
Others oppose additional processing of food and express concern that irradiation makes it possible to cover up unsanitary food handling, especially fecal contamination. Avoiding fecal contamination is critical for preventing food-borne viral diseases because the small size of viruses makes them resistant to irradiation at doses approved for foods. Bacterial spores—the dense, hardy, hibernation state of bacteria—are also resistant to irradiation. Therefore, irradiation can be an additional food safety tool, not a cure-all.
I read that it took three years to create in 2002 the first virus made from scratch with commercially available ingredients. Does this mean that we can “create life” now?
A paper published in the journal Science in August 2002 describes the creation of poliovirus from scratch based on its genetic blueprint. The researchers first synthesized a string of approximately 7,500 nucleotides (the chemical building blocks of RNA and DNA) according to the known genetic sequence of poliovirus. They then added the virus’s synthesized genome to a solution containing enzymes (catalysts) and amino acids (building blocks of protein). This step permitted the appropriate virus proteins to be synthesized.
To prove that the newly created virus worked, the researchers injected it into mice. As expected for the virus that causes polio, the mice became paralyzed.
About a year later, another group synthesized a virus in just two weeks, surprisingly fast compared to the three years it took to make the first virus from scratch. Still, both viruses have relatively small genomes compared to other viruses. Synthesizing a genome gets more complex as the number of nucleotides that need to be linked increases.
Whether or not we can now create life depends on your definition of life, a topic that has given rise to much philosophical pondering. Some scientists do not consider a virus to be “alive” because viruses cannot reproduce on their own. They exploit the machinery of the cell they infect to make it churn out new virus particles. Other scientists consider viruses to be alive because they contain sufficient genetic information for self-existence.
On the other hand, bacteria are certainly alive, but no one has made bacteria from scratch yet. Building bacteria has two major complications. First, bacteria have larger genomes than viruses. Second, while the simplest viruses consist of a string of nucleotides surrounded by a few proteins, bacteria are cells with complicated component parts that have specialized functions. So human-created bacteria remain in the realm of science fiction for now.
Why are scientists unable to create life?
Swapping genes between species has been possible for over 30 years, but building a living cell remains a holy grail for biologists. By assembling a cell from small molecules, they would gain valuable knowledge of cellular function, just as engineers gain a better understanding of how a machine works by constructing it than by merely studying it.
Biologists have synthesized small viruses, but viruses are basically strands of genetic material—RNA or DNA—packaged with a few proteins. Many scientists do not consider them alive because they must exploit the cellular machinery of a host organism to reproduce.
On the other hand, even the simplest bacterial cell has complex component parts that allow it to take in food, eliminate waste, replicate genetic material, build proteins, and repair and expand the cell membrane. Building all of these parts from scratch is technically challenging.
Progress is being made. It is now possible to build cell-like compartments that can produce protein. A published blueprint details the genes and component parts predicted to be sufficient to assemble a minimal cell that can survive under controlled laboratory conditions. Also, recent research has shown that it is possible to remove and replace the entire genome of a bacterial cell.
Efforts are under way to synthesize a minimal genome and place it in a bacterial cell that has had its own genetic material removed. The result would not be a completely synthetic organism. Still, it would be an intermediate step that would reveal whether researchers have identified all the genes necessary for life. Many researchers are optimistic that a fully synthetic cell is not far off.
I was bitten by a tick at the base of Palomar Mountain near San Diego. The tick was on me for about one to two hours. I never got a rash. Is Lyme disease present in that area?
Lyme disease is spread via the bite of a tick infected with Borrelia burgdorferi bacteria. The first symptom, experienced by about 80 percent of those infected with Lyme disease, is a red rash around and expanding out from the bite. The rash generally occurs within a week or two of infection and may be accompanied by fatigue, headache, joint pain, and muscle aches. If it’s left untreated, more severe symptoms can develop, including swelling in one or more joints, facial nerve palsy, and inflammation of the brain. Lyme disease can be treated with antibiotics.
Prompt removal of a tick reduces your chances of being infected, because it usually takes more than one day of the tick’s sucking your blood for the bacteria to be transmitted to you. Unfortunately, nymphal (young) ticks are as small as a poppy seed, and you may not even notice having been bitten.
Lyme disease occurs across North America, Europe, and northern Asia. In the United States, about 20,000 cases are reported each year, according to the CDC. The disease is found across the United States, including Southern California, but more than 90 percent of reported cases are in the Northeast, plus Wisconsin and Minnesota.
Lizards may be a part of the explanation for the relative scarcity of Lyme disease in the western United States. When ticks feed on the blood of the western fence lizard, one of the most common lizards in California and surrounding areas, the ticks can be cleansed of the Lyme bacterium by a protein in the lizards’ blood. Feeding on eastern fence lizards has also been shown to clear the Lyme pathogen from ticks, but eastern fence lizards are less important hosts for ticks than are their cousins in the west.
The CDC website is a good source of additional information on Lyme disease: http://www.cdc.gov/ncidod/dvbid/lyme/.
What is mononucleosis, and what causes it?
Mononucleosis is an infectious disease with a triad of symptoms: fever, sore throat, and swollen lymph glands. It is caused by the Epstein-Barr virus (EBV), which belongs to a family of viruses that includes the virus that causes herpes. EBV is transmitted via saliva.
According to the CDC, EBV is one of the most common human viruses. The CDC estimates that up to 95 percent of adults have been infected with EBV by age 40. Infection with EBV often occurs in childhood (when the inadvertent sharing of drool among peers is not uncommon).
When infection with EBV occurs in childhood, symptoms usually are nonexistent or very mild. However, between one-third and one-half of EBV infections occurring during adolescence or young adulthood result in mononucleosis. Mononucleosis is most common in 15- to 17-year-olds, but it can occur at any age.
Most patients recover from mononucleosis within a month without medication. In rare cases, complications may include blood disorders, heart problems, neurological disorders, or rupture of the spleen.
Does putting all the dishes together in the sink (rather than running water and washing each dish individually) spread more germs than kill them? Use more water? Use more soap?
One study showed that people use between 6 and 30 gallons of water to hand-wash a load of dishes. Filling the sink with water and not letting the water run continuously used the least water. Hand-washing used more water on average (16 gallons) than a dishwasher (11 gallons). However, 60 percent of dishwasher users pre-rinse their dishes, which sends another 20 gallons down the drain. Soap use likely parallels water use.
Either method of hand-washing dishes has avoidable food safety pitfalls. Leaving dirty dishes to soak for a long time can allow bacteria to multiply. Sponges, cloths, and towels can harbor bacteria and should be changed often. Also, the Food and Drug Administration recommends that cutting boards used to cut raw meat be sanitized at a high temperature in a dishwasher or rinsed with a diluted solution of chlorine bleach.
The government says that the cow suffering from mad cow disease was found before it got into the food chain. However, did the disease strike the cow just before it was sent to slaughter, so that it was a “downed” animal, or was the disease developing for some time and could have entered the food chain if the cow was not a “downer”? Testing every cow, as they do in Japan, sounds like the best way to protect the beef we eat.
The cow, the second confirmed U.S. case of mad cow disease, or bovine spongiform encephalopathy (BSE), was a downer—too sickly to walk. Since inability to walk is a symptom of advanced BSE, the U.S. Department of Agriculture targets downer cattle in its surveillance program, which tests about 1,000 cattle per day.
The USDA also bans downer cattle from the human food chain. (The cow in question was destined for pet food.) However, cattle can be infected with BSE long before they show any symptoms. In fact, the USDA has speculated that the 12-year-old cow may have become infected with BSE before the 1997 ban on feeding rendered meat and bonemeal to cows.
Stanley Prusiner, who won a Nobel Prize for discovering the cause of BSE and related diseases, argues that all slaughtered cattle should be tested for BSE. He thinks this is important for consumer safety and to provide insight into BSE—for example, to determine if new strains of the disease arise.
The USDA opposes universal testing. It even blocked one meatpacking company, Kansas-based Creekstone Farms, from testing every cow it slaughtered, which it wanted to do to maintain its beef exports to Japan. The USDA believed that permitting Creekstone to run its own tests would set an expensive precedent and force all meatpackers to do the same.
At $30 per animal, it would cost more than a billion dollars to test the 35 million cattle slaughtered annually in the United States. Universal testing would raise beef prices by approximately 5 cents per pound, a price most consumers would probably pay willingly if it ensured safety.
However, the USDA argues that it is not appropriate to test all cattle, because most cattle in this country are slaughtered between 18 and 20 months of age, and BSE is usually undetectable before 30 months.
In any case, new slaughtering practices, banning downer cattle, and increased surveillance mean that our beef is safer than it was back when our regulatory agencies did not believe BSE had reached American shores.
What is the latest research about how prions make cows or people mad?
Prions are proteins believed to cause mad cow disease (BSE) and its human equivalent, variant Creutzfeldt-Jakob disease (vCJD), as well as a number of other so-called prion diseases.
When it was initially proposed, the protein-only hypothesis—the idea that a protein on its own could cause disease—was considered preposterous, because a protein cannot replicate itself. Other disease-causing agents, including bacteria and viruses, have a genetic blueprint—DNA or RNA—which permits them to churn out copies of themselves.
Even after the 1997 Nobel Prize in Physiology or Medicine was awarded to Stanley Prusiner for research on prions as disease-causing agents, many scientists continued to believe that prion diseases were caused by an as-yet-undiscovered virus. Part of the continuing skepticism about the protein-only hypothesis resulted from scientists’ inability to perform a key experiment: synthesize prion protein from scratch and show that this protein could cause neurological disease in animals.
Researchers had purified prions from the brain tissue of infected animals and had shown that they caused disease, but critics argued that the “purified” protein might not be completely free of DNA or RNA. The key experiment of synthesizing prions and showing that they can cause disease was finally done, and its publication, in Science in August 2004, silenced most of the skeptics.
As for how prions cause disease, scientists believe it has to do with protein folding. Prions, like other proteins, can bend into more than one shape. Prions in one shape are harmless, but in the other (infectious) shape they end up clumping together and damaging nerve cells. The word “spongiform” in BSE describes what the brain looks like (spongy) after prions wreak havoc.
In humans, and probably all vertebrates, normal prions are concentrated in the central nervous system. Their function is unknown, but one recent study suggests they may play a role in memory. Whatever their usual function, scientists think that when infectious prions come into contact with normal prions, they force the normal prions to refold into the infectious form. This sets up a chain reaction of refolding prions in the nervous system.
Many questions about prion diseases remain unanswered. Researchers are still trying to determine the length of time between consumption of infectious prions and the onset of symptoms of vCJD, what exactly happens in the body during that time, and what quantity of infectious prions is needed to cause illness. Another mystery is why prion diseases, including BSE, chronic wasting disease in deer and elk, and scrapie in sheep, differ in how easily they spread.