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From my basic understanding, antibiotics kill living things, bacteria for example.
Do the antibiotics consumed by a human-being distinguish between what they kill? Or do they just kill every bacteria they find? And if that's the case, which bacteria do antibiotics find or do they find all bacteria in a human's body? Again, if that is the case, does that mean that after taking antibiotics for a certain time that the human body is free of all bacteria?
There are several reasons why this might not be true, as Alexander has discussed. An antibiotic often has a molecular target that isn't present in all bacteria, it's extremely hard to get antibiotics to certain parts of your body, and some bacteria will be defended against a antibiotic attack by biofilms, resistance mechanisms, and sheer statistical probability.
That is not to say that many don't die. Indeed, one of the major causes of Clostridium difficile infection is that antibiotics kill most of your gut bacteria, allowing the somewhat better protected C. diff to proliferate, start producing toxins, and send you to the hospital with symptoms ranging from diarrhea to perforated colon and worse. That disease is a direct consequence of "Antibiotics kill some but not all bacteria in you".
Just a quick answer: No, there is no way to kill all bacteria in your body once they are there. The only way to keep a person sterile is to prevent any bacteria entering the guts during and all time after the birth. Look for gnotobiology and gnotobionts to learn more about these organisms (including humans).
Here are some reasons why:
Most antibiotics have selective action on certain type of bacteria. This is due to the mechanisms involved in their action, permeability through the bacterial wall, their effective concentrations etc. Even broad-spectrum antibiotics have selective action. None is universal (and it is hardly possible to create those).
Antibiotics can't reach all the places in your body. Many bacteria either create some barrier against the immune response or the body eventually builds one. In the worst cases the whole bacterial infection is isolated and petrified (calcifications), as it is the case for tuberculosis and so-called Gohn's complex in lungs.
As long as you are not isolated from the society and secluded into a sterile box you will have a steady contact with millions of bacteria which re-invade your skin and guts. There is no way you can stop it and your gut flora will beging to restore spontaneously.
Antibiotic resistance: How do antibiotics kill bacteria?
This is a multi-part series on antibiotic resistance in bacteria.
Eventually, we'll reach the ways in which bacteria develop antibiotic resistance, but before we get there, we'll spend a little more time on antibiotics themselves.
What have we learned so far?
1. Antibiotics are natural products, made by bacteria and some fungi. We have also learned about the difference between antibiotics and synthetic drugs. There isn't always a clear distinction since chemical groups can be added to antibiotics, making them partly synthetic and partly natural.
2. Antibiotics are a chemically diverse group of compounds. Antibiotics are not DNA. Neither are they proteins, although some antibiotics contain amino acids, which are the building blocks of proteins. In a way, antibiotics are kind of luxury molecules, since they aren't essential for life.
Bacteria don't even make them until the population reaches a certain density and phase of growth. Even though we can describe all antibiotics with a single word, there is no single description that does justice to these fascinating compounds.
We can group antibiotics into classes, either by chemical similarity - peptide antibiotics all contain amino acids held together by peptide bonds, ß-lactams all have a ß lactam ring - by the range of organisms they can kill - broad spectrum antibiotics kill a wide variety of bacteria, where narrow spectrum antibiotics have more specific targets or by the metabolic pathway that they target.
Perhaps the easiest way to categorize antibiotics is by the organisms that produce them. Even there, antibiotics defy easy groupings. The majority are made by denizens of the dirt, but both fungi and bacteria get into the act.
But what do antibiotics do?
How do they fulfill their role as agents of warfare? They do kill bacteria - but how? In a bacterial population, do all members get killed? Unfortunately, no, many antibiotics work by preventing bacterial growth. This means that most antibiotics only kill growing bacteria.
They keep bacteria from getting bigger?
No. When we talk about animals, plants, or people growing, we're really describing individual organisms getting larger. But, when we talk about bacterial growth, we're referring to the size of a bacterial population and not just the size of a cell.
In order for bacteria to grow, then, they need to make all the parts necessary for building new bacterial cells. DNA must be copied. New RNA, ribosomes, and proteins must be made. Cell walls must be built. Membranes have to be synthesized. And, then, of course the cells must divide. Many, if not most, antibiotics act by inhibiting the events necessary for bacterial growth. Some inhibit DNA replication, some, transcription, some antibiotics prevent bacteria from making proteins, some prevent the synthesis of cell walls, and so on. In general, antibiotics keep bacteria from building the parts that are needed for growth.
There are some antibiotics that act by attacking plasma membranes. Most antibiotics, though, work by holding bacterial populations in check until the immune system can take over. This also brings us, to our first mechanism of antibiotic resistance.
Persistance is resistance.
If bacteria need to grow in order to be killed by antibiotics, then bacteria, can escape from antibiotics, by NOT growing or by growing very slowly. This phenomenon has been observed with biofilms (colonies of bacteria living on a surface) (1), E. coli in urinary tract infections (2), and most notably in the slow growing bacteria, that cause tuberculosis, Mycobacterium tuberculosis, and leprosy, Mycobacterium leprae (3).
It seems funny to think that not growing can be a mechanism for survival. But if you're a bacteria, and you can hang around long enough in an inactive, non-growing state, enventually your human host will stop taking antibiotics, they will disappear from your environment and you can go back to growing.
1. P.S. Stewart 2002. "Mechanisms of antibiotic resistance in bacterial biofilms." Int J Med Microbiol. 292(2):107-13.
2. Trülzsch K, Hoffmann H, Keller C, Schubert S, Bader L, Heesemann J, Roggenkamp A. 2003. "Highly Resistant Metabolically Deficient Dwarf Mutant of Escherichia coli Is the Cause of a Chronic Urinary Tract Infection." J Clin Microbiol. 41(12): 5689-5694.
3. Gomez JE, McKinney JD. 2004. Tuberculosis (Edinb). 84(1-2):29-44.
Other articles in this series:
1. A primer on antibiotic resistance: an introduction to the question of antibiotic resistance.
2. Natural vs. synthetic drugs: what is the difference between an antibiotics and synthetic drugs?
3. How do antibiotics kill bacteria? a general discussion of the pathways where antibiotics can act and one characteristic that helps some bacteria survive.
4. Are antibiotics really only made by bacteria and fungi? It depends on what you'd like to call them.
5. The Five paths to antibiotic resistance: a quick summary
If a human takes antibiotics are all bacteria in the body killed? - Biology
13a. Infectious Disease
In the previous chapter, we learned about the ways that our bodies protect us against pathogens. In this chapter, we discuss the most important categories of pathogens, the disease-causing organisms introduced in the previous chapter. We explore how they cause harm, how they are transmitted from person to person, and how they are studied so that steps may be taken to hold them in check.
As indicated in the previous chapter, pathogens are disease-causing organisms. There are different types of pathogens and a wide range of differences within each type. As a result, each pathogen has specific effects on the body, and some pathogens are a greater menace than others. In this chapter, we look at bacteria, viruses, protozoans, fungi, parasitic worms, and prions. We consider the general means these different types of pathogens use to attack the body and cause symptoms. Keep in mind, however, as we do so, that some of the symptoms are caused not by the pathogen itself but by the immune responses our body uses to protect us (Chapter 13).
Virulence is the relative ability of a pathogen to cause disease. Some factors contributing to this ability are how easily the pathogen invades tissues and the degree and type of damage it does to body cells. An organism that always causes disease—the typhoid bacterium, for instance—is highly virulent. On the other hand, the yeast Candida albicans, which sometimes causes disease, is moderately virulent.
Bacterial cells differ greatly from the cells that make up our bodies. Recall from Chapter 3 that our bodies are made up of eukaryotic cells that contain a nucleus and membrane-bound organelles. Bacteria, in contrast, are prokaryotes, which means they lack a nucleus and other membrane-bound organelles. Nearly all bacteria have a semirigid cell wall composed of a strong mesh of peptidoglycan, a type of polymer consisting of sugars and amino acids. The cell wall endows most types of bacteria with one of three common shapes: a sphere (a spherical bacterium is called a coccus) that can occur singly, in pairs, or in chains a rod (bacillus) that usually occurs singly or a spiral or corkscrew shape (spirilla) (Figure 13a.1).
FIGURE 13a.1. Bacteria have three basic shapes: (a) spherical (coccus), (b) rod-shaped (bacillus), and (c) corkscrew-shaped (spirilla). All bacteria are prokaryotic cells, meaning they lack a nucleus and membrane-bound organelles.
· Vaccinations have helped eliminate certain infectious diseases.
Bacteria can reproduce rapidly. This rapid growth rate is a matter of concern because the greater the number of bacteria, the greater harm they can potentially do. Rapid reproduction is possible because bacteria reproduce asexually in a type of cell division called binary fission, in which the bacterial genetic material (DNA) is copied, the cell is pinched in half, and each new cell contains a complete copy of the original genetic material. Under ideal conditions, certain bacteria can divide every 20 minutes. Thus, if every descendant lived, a single bacterium could result in a massive infection of trillions of bacteria within 24 hours. If a percentage of the descendant bacteria die before dividing, the population of bacteria will begin to grow more slowly than does a population in which all descendants survive, but the populations will eventually have the same growth rate.
Bacteria have defenses or other adaptive mechanisms that affect their virulence. Some bacteria have long, whiplike structures called flagella that allow them to move and spread through tissues to new areas where they can cause infection. Bacteria may also have filaments, called pili, that help them attach to the cells they are attacking. Outside the bacterial cell, there is often a capsule that provides a means of adhering to a surface and prevents scavenger cells of the immune system (phagocytes see Chapter 13) from engulfing them.
Bacterial enzymes and toxins . Destructive enzymes and toxins (poisons) are among the offensive mechanisms that certain bacteria use to spread and to attack. Some of these bacteria secrete enzymes that directly damage tissue and cause lesions, allowing the bacteria to push through tissues like a bulldozer. An example is Clostridium, the bacterium that causes gas gangrene, a condition in which tissue dies because its blood supply is shut off. The bacterium secretes an enzyme that dissolves the material holding muscle cells together, permitting the bacteria to spread with ease. When this bacterium digests muscle cells for energy, a gas is produced that presses against blood vessels and shuts off the blood supply. In addition, Clostridium causes anemia by secreting an enzyme that bursts red blood cells.
Most bacteria, however, do their damage by releasing toxins (poisons) into the bloodstream or the surrounding tissues. If the toxins enter the bloodstream, they can be carried throughout the body and disturb body functions.
The disease symptoms depend on which body tissues are affected by the toxin. Thus, the bacteria that cause various types of food poisoning have different effects. Staphylococcus is often found contaminating poultry, meat and meat products, and creamy foods such as pudding or salad dressing. These bacteria multiply when food is undercooked or unrefrigerated. The toxins they produce stimulate cells in the immune system to release chemicals that result in inflammation, vomiting, and diarrhea. Another type of food poisoning is caused by Salmonella, often encountered in undercooked contaminated chicken or eggs. In this case, the toxin causes changes in the permeability of intestinal cells, leading to diarrhea and vomiting. One type of Escherichia coli (E. coli) food poisoning is often caused by contaminated meat, particularly ground meat. Besides vomiting and diarrhea, E. coli toxin can cause kidney failure in children and the elderly. The toxin that causes botulism, a type of food poisoning often brought on by eating improperly canned food, is one of the most toxic substances known. Produced by the bacterium Clostridium botulinum, it interferes with nerve functioning, especially motor nerves that cause muscle contraction. Death occurs because muscle paralysis prevents breathing. If enough of it is consumed, this toxin is almost always fatal.
Beneficial bacteria . Many bacteria are beneficial. For instance, certain bacteria are important in food production, especially of dairy products such as cheese and yogurt. Other bacteria are important in the environment, serving as decomposers or driving the cycling of nitrogen, carbon, and phosphorus between organisms and the environment (see Chapter 23). Yet other bacteria are important in genetic engineering (see Chapter 21). Some bacteria are normal residents in the body that keep potentially harmful microorganisms in check.
Antibiotics . Fortunately, bacteria can be killed. As we learned in Chapter 13, the human body has its own array of defenses against foreign invaders. But when the body needs outside help, we can call on antibiotics, chemicals that inhibit the growth of microorganisms. Antibiotics work to reduce the number of bacteria or slow the growth rate of the population, allowing time for body defenses to conquer the bacteria. Some antibiotics kill bacteria directly by preventing the synthesis of bacterial cell walls, causing them to burst. Recall that our body cells lack cell walls (see Chapter 3). Thus, our cells are unaffected by antibiotics that target cell walls. Some antibiotics block protein synthesis by bacteria but do so without interfering with cell protein synthesis in human body cells. This selective action is possible because the structure of ribosomes, the organelles on which proteins are synthesized, is slightly different in bacteria and humans.
When antibiotics were introduced during the 1940s, they were considered to be miracle drugs. For the first time, there was a cure for devastating bacterial diseases such as pneumonia, bacterial meningitis, tuberculosis, and cholera. Today, there are more than 160 antibiotics. These lifesaving drugs have become so commonplace that we take them for granted.
Unfortunately, antibiotics are losing their power. Infections that were once easy to cure with antibiotics can now turn deadly as bacteria gain resistance to the drugs. Several bacterial species capable of causing life-threatening illnesses have produced strains that are resistant to every antibiotic available today.1
Contradictory as it may seem, the use of antibiotics can actually increase antibiotic resistance in a strain of bacteria. When a strain of bacteria is exposed to an antibiotic, the bacteria that are susceptible die. The more resistant bacteria may survive and multiply. If the bacteria are exposed to the antibiotic again, the selection process is repeated. With each exposure to the drug, the resistant bacteria gain a stronger foothold. Making matters worse, antibiotics kill beneficial bacteria along with the harmful ones. Normally, the beneficial bacterial strains help keep the harmful strains in check. Loss of the "good" bacteria can allow the harmful ones to dominate.
The overuse and misuse of antibiotics are largely to blame for the resistance problem. An example of overuse is when physicians prescribe antibiotics for illnesses that are viral, such as a cold or flu. This is overuse antibiotics have no effect on viruses, so they are unnecessary for treating such illnesses. Patients misuse antibiotics when they stop taking their medicine as soon as they feel better instead of completing the full course of treatment. By stopping too early, they may be leaving the bacteria with greater resistance alive. Hospitals use antibiotics heavily, so it is not surprising that they are breeding grounds for antibiotic-resistant bacteria. The resistant bacteria survive, outgrow susceptible strains, and spread from person to person. Indeed, most infections by antibiotic-resistant bacteria occur in hospitals. An example is Staphylococcus aureus, which can cause many types of infections, including blood poisoning, pneumonia, skin infections, heart infections, and nervous system infections. The strain of S. aureus called MRSA (methicillin- resistant Staphylococcus aureus), is actually resistant to many antibiotics. For many years, MRSA existed only in hospitals, but it is now found in the community at large. For a time, vancomycin was the only antibiotic that remained effective against MRSA. Unfortunately, a vancomycin-resistant S. aureus (VRSA) has arisen. An antibiotic-resistant strain of another bacterium, Clostridium difficile (C. diff), is more dangerous than other strains, because it produces more toxin. Outbreaks of C. difficile are spreading in hospitals, because antibiotics are used heavily there. Hospital-acquired C. difficile infections cause 18,000 to 20,000 deaths a year in the United States.
More than 40% (by mass) of the antibiotics used in the United States are given to livestock to promote growth and ensure health. Farmers also spray crops with antibiotics to control or prevent bacterial infections in the crops. These practices also contribute to antibiotic resistance.
What can you do to slow the spread of drug-resistant bacteria? Use antibiotics responsibly. Do not insist on a prescription for antibiotics against your doctor's advice. Take antibiotics exactly as prescribed, and be sure to complete the recommended treatment. Also, reduce your risk of getting an infection that might require antibiotic treatment by washing your hands frequently, rinsing fruits and vegetables before eating them, and cooking meat thoroughly.
Viruses are responsible for many human illnesses. Some viral diseases, such as the common cold, are usually not very serious. Other viral diseases, such as yellow fever, can be deadly.
Most biologists do not consider a virus to be a living organism because, on its own, it cannot perform any life processes (see Chapter 1 for a review on the basic characteristics of life). To copy itself, a virus must enter a host cell. The virus exploits the host cell's nutrients and metabolic machinery to make copies of itself that then infect other host cells.
Viruses are much smaller than bacteria. A virus consists of a strand or strands of genetic material, either DNA or RNA, surrounded by a coat of protein, called a capsid (Figure 13a.2). The genetic material carries the instructions for making new viral proteins. Some of these proteins become structural parts of the new viruses. Some of them serve as enzymes that help carry out biochemical functions important to the virus. Some are regulatory proteins, such as the proteins that trigger specific viral genes to become active under certain sets of conditions or the proteins that convert the host cell into a virus-producing factory.
FIGURE 13a.2. (a) The structure of a typical virus. A coat, called a capsid, made of protein surrounds a core of genetic information made of DNA or RNA. Some viruses have an outer membranous layer, called the envelope, from which glycoproteins project. (b) Steps in viral replication.
Which part of a virus would have to change for it to be able to infect a new type of tissue?
The glycoprotein on its surface. It is the fit between the glycoprotein and the host cell receptor that determines whether the virus can infect the cell.
Some viruses have an envelope, an outer membranous layer studded with glycoproteins. In some viruses, the envelope is actually a bit of plasma membrane from the previous host cell that became wrapped around the virus as it left the host cell. The envelope of certain other viruses—those in the herpes family, for instance—comes from a previous host cell's nuclear membrane. In any case, the virus produces the glycoproteins on the envelope. Some glycoproteins are important for attachment of the virus to the host cell.
A virus can replicate (make copies of itself) only when its genetic material is inside a host cell. Figure 13a.2 illustrates the general steps in the replication of viruses that infect animal cells:
1. Attachment. The virus gains entry by binding to a receptor (a protein or other molecule of a certain configuration) on the host cell surface. Such binding is possible because the viral surface has molecules of a specific shape (glycoproteins or capsids) that fit the host's receptors. The host cell receptors play a role in normal cell functioning. However, a molecule on the surface of the virus has a shape that is similar to the chemical that would normally bind to the receptor. Viruses generally attack only certain kinds of cells in certain species, because a particular virus can infect only cells bearing a receptor the virus can bind to. For example, the virus that causes the common cold infects only cells in the respiratory system, and the virus that causes hepatitis infects only liver cells.
2. Penetration. After a virus has bound to a receptor on a host cell, the entire virus enters the host cell, often by phagocytosis by the host cell. Once inside, the virus loses its capsid, leaving only its genetic material intact.
3. Production of viral genetic information and proteins. Viral genes then direct the host cell machinery to make thousands of copies of viral DNA or RNA. Next, viral genes direct the synthesis of viral proteins, including coat proteins and enzymes.
4. Assembly of new viruses. Copies of the viral DNA (or RNA) and viral proteins then assemble to form new viruses.
5. Release. Some viruses leave the cell through budding, or shedding. In this process, the newly formed viruses push through the host cell's plasma membrane and become wrapped in this membrane, which forms an envelope. Budding need not kill the host cell. Other virus types do not acquire an envelope, but rather cause the host cell membrane to rupture, releasing the newly formed viruses and killing the host cell.
Viruses can cause disease in several ways, as summarized in Table 13a.1. Some viruses cause disease when they kill the host cells or cause the cells to malfunction. The host cell dies when viruses leave it so rapidly that it lyses (bursts). In such cases, disease symptoms will depend on which cells are killed. However, if viruses are shed slowly, the host cell may remain alive and continue to produce new viruses. Slow shedding causes persistent infections that can last a long time. Some viruses can produce latent infections, in which the viral genes remain in the host cell for an extended period without harming the cell. At any time, however, the virus can begin replicating and cause cell death as new viruses are released.
TABLE 13a.1. Possible Effects of Animal Virus on Cells
An example of a virus that can act in all of these ways is the herpes simplex virus that causes fever blisters ("cold sores") on the mouth. The virus is spread by contact (discussed shortly) and enters the epithelial cells of the mouth, where it actively replicates. Rapid shedding kills the host cells, causing fever blisters. Slow shedding may not cause outward signs of infection, but the virus can still be transmitted. When the blisters are gone, the virus remains in a latent form within nerve cells without causing symptoms. However, stress can activate the virus. It then follows nerves to the skin and begins actively replicating, causing new blisters in the same region of the mouth.
Certain viruses can also cause cancer. Some do this when they insert themselves into the host chromosome near a cancer- causing gene and, in so doing, alter the functioning of that gene. Still other viruses bring cancer-causing genes with them into the host cell.
Unfortunately, viruses are not as easy to destroy as bacteria. One reason is the difficulty of attacking viruses inside their host cells without killing the host cell itself. Most attempts to develop antiviral drugs have failed for this reason. Nonetheless, some drugs are now available to slow viral growth, and others are being developed. Most of the antiviral drugs available today, including those against the herpes virus and HIV, work by blocking one of the steps necessary for viral replication. As mentioned in Chapter 13, interferons are proteins produced by virus-infected cells that protect neighboring cells from all strains of viruses. Interferons are not as useful as originally hoped, but they have been used for certain viral infections, including hepatitis C and the human papillomavirus that causes genital warts.
Because of these obstacles to treatment, the best way to fight viral infections is to prevent them with vaccines (discussed in Chapter 13).
How does the structure and replication cycle of viruses explain why antibiotics are not effective against viral diseases?
Protozoans are single-celled eukaryotic organisms with a well- defined nucleus. They can cause disease by producing toxins or by releasing enzymes that prevent host cells from functioning normally. Protozoans are responsible for many diseases, including malaria, sleeping sickness, amebic dysentery, and giardiasis. Giardiasis is a diarrheal disease that can last for weeks. There are frequent outbreaks of giardiasis in the United States, most of them resulting from water supplies contaminated with human or animal feces. Even clear and seemingly clean lakes and streams in the wilderness can contain Giardia (Figure 13a.3). Fortunately, drugs are available to treat protozoan infections. Some of these drugs work by preventing protozoans from synthesizing proteins.
FIGURE 13a.3. Giardia is a protozoan that is commonly found in lakes and streams used as sources of drinking water, even those in pristine areas. It causes severe diarrhea that lasts for weeks and can be especially dangerous for children.
Like the protozoans, fungi are also eukaryotic organisms with a well-defined nucleus in their cells. Some fungi exist as single cells. Others are organized into simple multicellular forms, with not much difference among the cells. There are more than 100,000 species of fungi, but fewer than 0.1% cause human ailments. Fungi obtain food by infiltrating the bodies of other organisms—dead or alive—secreting enzymes to digest the food, and absorbing the resulting nutrients. If the fungus is growing in or on a human, body cells of the human are digested, causing disease symptoms. Some fungi cause serious lung infections, such as histoplasmosis and coccidioidomycosis. Other, less-threatening fungal infections occur on the skin and include athlete's foot and ringworm. Most fungal infections can be cured. Fungal cell membranes have a slightly different composition from those of human cells. As a result, the membrane is a point of vulnerability. Some antifungal drugs work by altering the permeability of the fungal cell membrane. Others interfere with membrane synthesis by fungal cells. Fungal infections of the skin, hair, and nails can be combated with a drug that prevents the fungal cells from dividing.
Parasitic worms are multicellular animals that benefit from a close, prolonged relationship with their hosts while harming, but usually not killing, their hosts. They include flukes, tapeworms, and roundworms, such as hookworms and pinworms. They can cause illness by releasing toxins into the bloodstream, feeding off blood, or competing for food with the host. Parasitic worms cause many serious human diseases, including ascariasis, schistosomiasis, and trichinosis.
Ascariasis is caused by a large roundworm, Ascaris, that is about the size of an earthworm. People become infected with Ascaris when they consume food or drink contaminated with Ascaris eggs. The eggs develop into larvae (immature worms) in the person's intestine. The larvae then penetrate the intestinal wall, enter the bloodstream, and travel to the lungs. After developing further, the worms are coughed up and swallowed, thus returning to the intestine. Within 2 to 3 months, they mature into male and female worms, which live for about 2 years. During those years, female worms can produce more than 200,000 eggs a day.
As much as 25% of the world population is infected with Ascaris, particularly in tropical regions. Up to 50% of the children in some parts of the United States (mostly rural areas in the Southeast) are infected. Many people with ascariasis have no symptoms. However, the worms can cause lung damage and severe malnutrition. When many worms are present, they can block or perforate the intestines, leading to death.
Prions (pree'-ons) are infectious particles of proteins—or, more simply, infectious proteins. They are misfolded versions of a harmless protein normally found on the surface of nerve cells. If a prion is present, it somehow causes the host protein to change its shape to the abnormal form. Prions cause a group of diseases called transmissible spongiform encephalopathies (TSEs), which are associated with degeneration of the brain. The misshapen proteins clump together and accumulate in the nerve tissue of the brain. These clumps of prions may damage the plasma membrane or interfere with molecular traffic. Spongelike holes develop in the brain, causing death.
Transmissible spongiform encephalopathies are progressive and fatal. Prions cannot be destroyed by heat, ultraviolet light, or most chemical agents. Currently, there is no treatment for any disease they cause. Several of the TSEs are animal infections, notably mad cow disease, scrapie in sheep, and chronic wasting disease (CWD), which affects deer and elk.
Prions also cause a human neurological disorder called Creutzfeldt-Jakob disease (CJD). Indeed, the prion responsible for mad cow disease is thought to cause one form of CJD. The incubation period for CJD can be months to decades. Symptoms include sensory and psychiatric problems. Once the symptoms begin, death usually occurs within a year.
How does an animal become infected with prions? In the case of mad cow disease, it appears that cattle become infected when they eat prions in contaminated food. For example, prions have been passed along in the protein supplements fed to cattle to increase their growth and milk production. Those protein supplements had been prepared from the carcasses of animals considered unfit for human consumption, a practice banned in the United States in 1997. A broader ruling prohibiting the use of any high-risk animal parts in any animal feed went into effect in 2009. Any protein supplements prepared from animals infected with mad cow disease would have contained prions. The prions pass through the intestinal wall, enter the lymphatic system, and are then transported by nerves to the brain and spinal cord. In contrast, CWD can apparently be spread by animal-to-animal contact, including contact with body fluids such as urine or feces from infected animals. Scientists also think that the prions responsible for CWD may remain in the soil or water for years. As a result, healthy animals may become infected from living in a region previously occupied by diseased animals. Humans can become infected with prions by eating contaminated substances, through tissue transplant, or through contaminated surgical instruments.
Mad cow disease is spread in cattle when they consume contaminated food. There are laws to prevent feeding cattle food that might be contaminated. When violations of the laws occur, who should be held responsible: the food manufacturers or the farmers?
Spread of a Disease
Obviously, you catch a disease when the pathogen enters your body. But how do diseases travel from person to person or enter the body in the first place? The answer to this question varies with the type of pathogen.
• Direct contact. One means of transmission is direct contact of an infected person with an uninfected person, as might occur when shaking hands, hugging and kissing, or being sexually intimate. For example, sexually transmitted diseases (STDs) including chlamydia, gonorrhea, syphilis, genital herpes, and HPV are spread when a susceptible body surface touches an infected body surface (see Chapter 17a). The organisms that cause STDs generally cannot remain alive outside the body for very long, so direct intimate contact is necessary. A few disease-causing organisms—HIV and the bacterium that causes syphilis, for instance—can spread across the placenta from a pregnant woman to her growing fetus.
• Indirect contact. Indirect contact, the transfer from one person to another without their touching, can spread other diseases. Most respiratory infections, including the common cold, are spread by indirect contact (see Chapter 14). When an infected person coughs or sneezes, airborne droplets of moisture full of pathogens are carried through the air (Figure 13a.4). The infected droplets may be inhaled or land on nearby surfaces. When another person touches an affected surface, the organisms are transmitted. In this way, droplet infection spreads pathogens on contaminated inanimate objects, including doorknobs, drinking glasses, and eating utensils.
FIGURE 13a.4. Pathogens can be spread through the air in droplets of moisture when an infected person sneezes or coughs.
• Contaminated food or water. Certain diseases are transmitted in contaminated food or water. You have read that spoiled food can cause food poisoning. Another disease transmitted by food or water is hepatitis A, an inflammation of the liver caused by a certain virus. Legionella, the bacterium that causes a severe respiratory infection known as Legionnaires' disease, is a common inhabitant of the water in condensers of large air conditioners and cooling towers. The disease-causing bacteria are spread through tiny airborne water droplets. Coliform bacteria come from the intestines of humans and are, therefore, an indicator of fecal contamination of water. Their numbers are monitored in drinking and swimming water. To be safe, drinking water should not have any coliform bacteria.
• Animal vectors. Another means of transmission is by vector, an animal that carries a disease from one host to another. The most common vector-borne disease in the United States is Lyme disease. It is caused by a bacterium transmitted by the deer tick (the vector), which is about the size of the head of a pin (Figure 13a.5). The tick larva picks up the infectious agent when it bites and sucks blood from an infected animal. When the tick subsequently feeds on a human or other mammalian host, the bacteria gradually move from the tick's gut to its salivary glands and then are passed to its victim. The incubation period, during which there are no symptoms, can be as long as 6 to 8 weeks. Early symptoms include a headache, backache, chills, and fever. Often, a rash resembling a bull's eye develops, with an intense red center and border. Over a period of weeks, the circle increases in diameter. Weeks to months later, unless the disease is treated promptly, pain, swelling, and arthritis may develop. Cardiovascular and nervous system problems may follow the arthritis.
FIGURE 13a.5. A tiny tick, the deer tick, is a vector that transmits the bacterium responsible for Lyme disease. One characteristic sign of Lyme disease is a red bull’s-eye rash surrounding the tick bite. The rash gradually increases in diameter.
Mosquitoes transmit the West Nile virus, which can cause both meningitis (inflammation of the meninges, the protective coverings of the central nervous system) and encephalitis (brain inflammation Figure 13a.6).
FIGURE 13a.6. Mosquitoes are the vector that transmits West Nile virus.
The first reported cases of West Nile virus in North America were in New York City in 1999. Since then, the disease has spread to nearly every state. The virus can infect certain vertebrates, including humans, horses, birds, and occasionally dogs and cats. Testing mosquitoes and dead birds, especially crows and starlings, for the virus is one way to track its spread. Because the symptoms are similar to those of the flu—fever, headache, and muscle and joint pain—many people who become infected are unaware of it—and most infected people under the age of 50 have few symptoms or none at all. However, older people have weaker immune systems. If they become infected, they are more likely to develop meningitis or encephalitis, either of which can cause brain damage, paralysis, or death.
You can protect yourself from West Nile virus and other mosquito-borne viral infections such as Eastern equine encephalitis by avoiding wet and humid places that harbor mosquitoes. If you must enter an area where mosquitoes are likely to be, wear light-colored clothing that covers your body, and use insect repellent.
Infectious Diseases as a Continued Threat
An epidemic is a large-scale outbreak of an infectious disease. The most notorious epidemics—bubonic plague, cholera, diphtheria, and smallpox—have happened in the distant past, although new outbreaks may occur sporadically. However, outbreaks of serious new diseases continue to present problems. We discuss some of these modern-day plagues elsewhere in the text.
Emerging Diseases and Reemerging Diseases
An emerging disease is a disease with clinically distinct symptoms whose incidence has increased, particularly over the last two decades. Among these diseases are HIV, SARS, H1H5 influenza, and H1N1 influenza. Other diseases have reemerged that were thought to have been conquered. A reemerging disease is a disease that has reappeared after a decline in incidence. For example, due to new drug-resistant strains of bacteria, tuberculosis is once again a global problem. We consider three factors that play important roles in the emergence and reemergence of disease.
1. Development of new organisms that can infect humans and of drug-resistant organisms. Most of the time, a pathogen infects only one type or a few types of organisms. Mutations are changes in genetic information that occur randomly. Some mutations allow the pathogen to "jump species" from its original host and infect another type of organism. Recall that a virus can penetrate a cell only if the virus has the appropriate molecule on its surface—one that will fit into a receptor on the host cell. Another mechanism that could allow an animal virus to infect humans is mixing of genetic information of an animal virus and a human virus, which might occur if both viruses infected the same cell. This is how the H1N1 virus that causes swine flu developed. A person passed human influenza A viruses to a pig with influenza A. When the viruses infect the same cell, pieces of the viruses' genetic material get mixed and create a new strain of virus.
Pathogens can also undergo changes in their response to drugs. We have seen that certain bacteria have acquired resistance to antibiotics, for example. As a result, some diseases that were once easily cured by antibiotics are now much more difficult to treat.
Improper antibiotic treatment during the reemergence of tuberculosis (TB) has led to antibiotic-resistant strains of TB that, in turn, make TB more difficult to treat. Infections with multi-drug-resistant strains of Mycobacterium tuberculosis, the bacterium that causes TB, are increasing at an alarming rate. The World Health Organization coined a new term to describe drug resistance in a new strain of the tuberculosis bacterium—XDR, which stands for extensively drug resistant. The new XDR strain causes a tuberculosis infection that is nearly impossible to treat.
2. Environmental change. Changes in local climate—the annual amount of rainfall and the average temperature—can affect the distribution of organisms and change the size of the geographical region where certain organisms can live. Global warming makes the redistribution of pathogens a growing concern.
3. Population growth. Another important factor in the emergence or reemergence of diseases is the increase of the human population in association with the development and growth of cities. Swelling human populations in cities cause people to move out of the city into surrounding areas, creating suburbs. If the surrounding areas were previously undeveloped, the move brings more people into contact with animals and insects that might carry infectious organisms. Indeed, wild animals serve as reservoirs for more than a hundred species of pathogens that can affect humans. The development of suburbs also destroys populations of predators, such as foxes and bobcats. In some regions of New York, the loss of predators has led to an increase in numbers of tick-carrying mice and an increase in the incidence of Lyme disease.
Population density and mobility also enable infectious diseases to spread more easily today than in the past. Densely populated cities allow diseases to begin spreading quickly, and air travel enables them to spread over great distances, (Figure 13a.7).
FIGURE 13a.7. Air travel is one reason that new diseases can spread rapidly.
Global Trends in Emerging Infectious Diseases
Emerging infectious diseases are a concern because of economic costs and public health issues. These diseases are not evenly distributed throughout the world. The most important factors determining where new infectious disease will emerge are (1) the rate of human population growth and the density of the human population, and (2) the number of species of wild mammals. Most pathogens responsible for emerging infectious diseases are spread to humans by animals—wildlife, pets and livestock, and vectors. As we have seen, the development of drug resistance in some pathogens has also led to emergent infectious diseases.
Epidemiology is the study of patterns of disease, including rate of occurrence, distribution, and control. Most diseases can be described as having one of the following four patterns:
• Sporadic diseases occur only occasionally at unpredictable intervals. They affect a few people within a restricted area.
• Endemic diseases are always present in a population and pose little threat. The common cold provides an example.
• An epidemic disease occurs suddenly and spreads rapidly to many people. Outbreaks of smallpox and cholera are examples of epidemics.
• A pandemic is a global outbreak of disease. HIV/AIDS is considered to be a pandemic.
Epidemiologists are "disease detectives" who try to determine why a disease is triggered at a particular time and place. The first step in answering this question is to verify that there is indeed a disease outbreak, defined as more than the expected number of cases of individuals with similar symptoms in a given area. Next, epidemiologists try to identify the cause of the disease whether it can be transmitted to other people and, if it can be, how the disease is transmitted. To identify the cause of an infectious disease, epidemiologists try to isolate the same infectious agent from all people showing symptoms of the condition. They also try to identify factors—including age, sex, race, personal habits, and geographic location—shared by people with symptoms of the condition. These factors might provide a clue as to whether the condition can be transmitted and how.
In this chapter, we considered infectious disease—the pathogens that cause them, the methods by which they spread, reasons for emerging and reemerging diseases, and the epidemiologists that track the causes. In the next chapter we examine the respiratory system, which brings life-giving oxygen into the body and rids the body of carbon dioxide.
1 Bacteria resistant to all antibiotics available today include some strains of Staphylococcus aureus (skin infection, pneumonia), Mycobacterium tuberculosis (tuberculosis), Enterococcus faecalis (intestinal infections), and Pseudomonas aeruginosa (many types of infections).
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Kill a bacterium.jpg
Bacteria, however, are able to develop strategies to avoid antibiotic assassination.
Viva la resistance!
Bacteria can escape destruction in a number of ways.
Bacteria can pre-emptively sabotage the antibiotic by cutting it to pieces.
Bacteria can also avoid detection by disguising themselves. Antibiotics target a precise component of the bacterial cell a lock which exactly matches their deadly key. However, bacteria can subtly alter the shape of this lock so the key cannot fit, thus rendering it useless.
For most antibiotics to work they have to first get inside the bacteria: they must pass through the cell wall and cell membrane. Some bacteria change their membrane so it acts like chemical waterproofing and the antibiotic cannot penetrate it.
Even if the antibiotic gets inside, the bacteria can simply pump it back out. This is done by proteins known as efflux pumps. And as Hendrik van Veen who studies this process at the University of Cambridge put it: “These efflux pumps are in the membrane and have binding sites that basically suck up antibiotics from the membrane and then throw it out”
Where does resistance come from?
Resistance mechanisms are produced by changes to the bacteria’s DNA. DNA is a set of instructions which tell a cell, human or bacterial, what proteins to make. Each protein is a machine which accomplishes a task. For instance the protein Aquaporin is a tunnel that allows water to get into a cell. These instructions are written in a language of four letters, A, T, G and C.
When cells divide they produce two copies of the DNA so both cells have the instructions they need. This copying produces some spelling mistakes, a G misprinted as a C. Many spelling mistakes do nothing a sentence still makes sense even if one letter is wrong as seeen here.
Occasionally typos can do a lot of damage, like printing “Tigers, None” as opposed to “Tigers, Nine” when trying to provide a warning about entering a dangerous area. Bacteria with these harmful typos die off.
Some typos, however, are beneficial: “let them eat cakes” is better than “let them eat rakes”. It is possible that one of more typos will allow bacteria to survive an antibiotic. This is known as resistance. Other bacteria are killed by the antibiotic so only the resistant remain and grow quickly since the competition is removed. To make things worse, from our point of view, bacteria can share their resistance strategies.
Bacteria can contain structures called plasmids. Plasmids are individual books containing, among other things, resistance recipes. Bacteria produce copies of these books and give them to each other, a natural form of peer to peer sharing. Resistance on plasmids can be spread from bacteria to bacteria so resistance does not have to be developed afresh each time, it can be borrowed.
Resistance is an example of evolution. But how are bacteria evolving to deal with antibiotics so quickly, a mere ninety years since we started using them?
The oldest profession
“Antibiotic resistance is probably as old as the bacteria themselves.” states UCL’s Adam Roberts. Antibiotic resistant bacteria have been found trapped in 1000-year-old Incan mummies, imprisoned in 30,000 year old permafrost and in a New Mexico cave which had been isolated from the outside world for four million years.
The reason for this is that the vast majority of our antibiotics were first produced by soil bacteria, or fungi, to kill of other bacteria. Bacteria which produce antibiotics themselves need to be resistant for their own protection. Once antibiotics are present in the environment any other resistant bacteria will gain a massive advantage.
Anywhere bacteria are found there is likely to be antibiotics and resistance. Roberts swabbed the Naked Scientists’ offices and found two interesting bacterial species. One displayed resistance to four different types of antibiotics and another was producing an antibiotic that killed drug resistant E. coli.
Antibiotic resistance is only useful if antibiotics are present. Absent antibiotics means that a bacterium is just wasting energy fighting what is not there. Resistance is evolved away when no longer useful, however in our modern world antibiotics are ever present.
A modern problem
The world has been flooded with human produced antibiotics creating conditions in which resistance is always useful, and several practices are leading to higher levels of resistance.
Antibiotics are prescribed to many of us when we’re ill. Ideally they wipe out non-resistant bacteria and any resistant bacteria are gobbled up by the immune system. Problems occur when people do not take antibiotics correctly.
If treatment is stopped early, non-resistant bacteria remain and overwork the immune system allowing resistant individuals to slip through and cause future infections.
Sometimes the wrong antibiotic is prescribed. Treating a bacterium with an antibiotic it is resistant to does not cure the infection and, therefore, boosts the total amount of antibiotic in circulation, increasing the pressure for resistance to occur.
Antibiotic levels are also increased when people pressure their doctors into prescribing antibiotics for viral infections, e.g. colds. Antibiotics here will do nothing to eradicate the viruses and unused antibiotics get excreted in the patient’s urine. This introduces antibiotics into the sewer bacteria encouraging them to develop resistance. People also use antibiotics prescribed for their friends or purchase them on the internet. However, one of the biggest causes of resistance doesn’t come from humans…
80% of antibiotics sold in the United States are used on livestock. This is to increase growth since animals do not then devote energy to their immune systems. Antibiotics then enter the environment through animal urine. With the human population rising, along with our demand for cheap meat, this practice is only likely to increase.
Human and animal use provides constant but low-dose exposure to antibiotics. If antibiotics were encountered only as acute high doses then bacteria would be killed before they could divide and produce resistance. Low doses mean that bacteria are not killed outright (only slowed) so resistance has time to evolve.
Through our continued use of antibiotics, bacteria are fast becoming resistant to the full spectrum of chemical agents which humans have developed. New antibiotics, ones with no resistance, are hard to grow.
In 2015 scientists from Northeastern University in the USA discovered the first new antibiotic for nearly 30 years.
Making new antibiotics is extremely difficult. The first step is discovering the new antibiotic. To look for a new antibiotic, you first must grow the bacteria or mould you are interested in and see if it produces any antibiotic reaction. 99% of bacteria cannot be grown in the lab, we cannot (at present) replicate their natural environment.
The Northeastern team overcame this by using a device known as an iChip. Bacteria are enclosed in the iChip before being put into the ground meaning that soil nutrients reach the bacteria mirroring its native ecosystem. Using this method the bacterium Eleftheria terrae was cultured, for first time, and found to produce a substance named Teixobactin which has antibiotic properties against Staphylococcus aureus (the SA of MRSA)
Before Teixobactin can be utilised in the clinic, it needs to go through rigorous clinical trials and its production scaled up to industrial levels. The Tufts Centre for the Study of Drug Development estimates the cost of making a new drug is $2.558 billion. For drug development to be economically viable the company developing that drug has to make a profit.
This return is expected for cholesterol lowering drugs which are prescribed by doctors in large numbers. The is not true for new antibiotics. To prevent resistance any new antibiotic will become a medicine of last resort and only used for infections that are resistant to other antibiotics. It would take an astronomically long time for a pharmaceutical company to make their money back.
It may be in the future that governments offer incentives to cover the cost of new drug manufacture since antibiotics do not fit the standard “big pharma” company policy.
Whilst we wait for Teixobactin, it may be time for humans to use bacteria’s natural enemies against them.
The enemy of my enemy is my friend
When you get infected by a virus the outcome is a cold. Bacteria can get colds too. Viruses which prey on bacteria are known as bacteriophages. A bacteriophage sticks to a target bacterium and injects its genetic material. This material instructs the bacteria to make more bacteriophages until they burst out killing the bacterium the newly produced viruses repeat the process.
University of Leicester’s Martha Clokie is using bacteriophages to treat the common hospital acquired infection Clostridium difficile (C. diff). Clokie has found a cocktail of four viruses which kill 90% of C. diff strains found in hospitals. What benefits do viruses have over antibiotics?
“One is the fact that they’re so specific. If you’ve got that hospital superbug, C. diff, and I give you a set of viruses, I will just remove that one species, not the others” says Clokie. Antibiotics act like a fire bomb indiscriminately killing all bacteria (including good bacteria) which live in our stomachs. This is why you may have an upset stomach after ingesting antibiotics. Bacteriophages are sharp shooters and only eliminate one specific bacteria. Bacteriophages cannot infect humans.
C. diff produces a thick sticky sheet known as a biofilm which antibiotics cannot penetrate protecting the bacteria. Bacteriophages pierce through this layer making C. diff more susceptible to antibiotics, allowing the use of antibiotics they were previously resistant to.
How long until viruses are the cure?
“I’m working with my collaborators at the University of Loughborough and we’ve shown that we can encapsulate these viruses into a pH-sensitive polymer so we can take them the same as you take an antibiotic.” explains Clokie. The pH-sensitive polymer is a capsule that allows the viruses to be taken as a pill and survive the acidic stomach.
Using viruses to cure infections was used in the former Soviet Union. During the cold war Russian scientists were isolated from Western developments in antibiotics, so they developed alternative measures. In Georgia, bacteriophages are approved by the country’s health authorities.
If viruses do not rush into save us how worried should we be?
In 2014 the British government commissioned a review on antibiotic resistance. The report estimated that 700,000 people annually are dying due to infections caused by resistant bacteria. This number is set to rise to 10 million deaths a year by 2050 if steps are not taken. At present cancer kills 8.2 million people a year.
The cost to the world from now until 2050 by antibiotics is estimated at $100 trillion.
These statistics threaten a return to the dark ages by which patients can no longer be given antibiotics before surgery or cancer patients (whose immune systems are blitzed by treatment) can no longer rely on chemical protection.
What can be done?
Antibiotic use must be controlled. Lord O’Neill, who chaired the review, has called on modern governments not to allow the prescription of antibiotics until the infection has been scanned for resistance, so that only the correct antibiotic is prescribed.
There must be global agreement on the reduction of antibiotics in farming.
Research into new antibiotics must be funded in a manner which is cost-effective. Research must also continue into alternative options such as bacteriophages and new vaccines which prevent us getting the initial infection, reducing antibiotic demand.
Modern sewer systems reduced the death total from infectious diseases in the western world before antibiotics. Developing countries will need similar improvements in waste management to help curb deaths and prevent infections.
Lastly, members of the general public can help by never demanding antibiotics for a cold, taking antibiotics as directed and by washing their hands when entering and exiting GP surgeries and hospitals.
Antibiotic resistance is a real concern, one that if left unchecked could send humanity spiralling back to the middle ages. It is one, however, that is potentially solvable if allocated the correct amount of time, resources and education. Only time will tell which direction humanity will take.
Short Essay on Antibiotics
The term antibiotic was de­rived from antibiosis, a phenomenon of antagonism of one organism by another. Antibiosis has been observed by many scientific workers dealing with microorganisms growing on plates (petridishes), but the credit of discovering and exploiting the product (antibiotic) for useful purpose goes to Alexander Fleming (1928). While working in a hospital laboratory in London, he found that in a plate containing Staphylococcus aureus, a contaminating fungus (Penicillium notatum) inhibited bacterial growth. The substance produced by the mold was named penicillin.
Several years later Florey, Chain and Heatley of the Oxford University were successful in isolating penicillin from the culture filtrate of the fungus. It was found to produce miraculous results in curing infections caused by staphylococci and other Gram-positive cocci and was acclaimed as a “wonder drug”. In 1946, Waksman and his collaborators of the Rutgevs University in the USA reported another important antibiotic, streptomycin, produced by an actinomycetes, Streptomyces griseus, effective against tuber­culosis.
Since then, systematic search of antibiotic-producing organisms isolated from thousands of soil samples collected from different parts of world has yielded several thousand antibiotics. However, major­ity of them were found to be unsuitable for application to humans because of toxicity. The rest of them have been found to be clinically useful. Most of these antibiotics are produced by actinomycetes belong­ing to a single genus, Streptomyces, and comparatively few from fungi.
All antibiotics are secondary metabolites of the producing organisms which means that these sub­stances are not essential for their growth. In the natural environment, an antibiotic — if produced at all— probably serves as an agent helping the producer to compete with other organisms for food and space. In culture, antibiotics are produced only when active growth has ceased.
Like other chemotherapeutants, an ideal antibiotic is one which attacks exclusively the pathogens without causing damage to the host. The attack on the pathogens may result in inhibition of growth without killing the pathogen. In that case, the antibiotic is said to have a bacteriostatic effect.
If the target pathogen is killed, the antibiotic effect is called bactericidal. Some antibiotics exert the killing effect by lysis of the affected bacteria. In that case, the effect is known as bacteriolytic. These properties are characteristics of the antibiotics, rather than that of target cells.
However, all antibiotics are not effective on all bacteria. The range of different types of bacteria that can be inhibited, killed or lysed by an antibiotic substance determines its antibiotic spectrum. Generally, the bacteria are divided into two groups — Gram-positive and Gram-negative when an antibiotic shows antibacterial activity against both groups it is said to have a broad-spectrum.
An antibiotic which can be administered through oral route, rather than by intramuscular injection is considered as more desirable. It should also be quickly absorbed to attain an effective concentration in blood, and excreted without leaving undesirable side effects. Obviously, an oral antibiotic should not be inactivated in the acidic gastric juice.
Another desirable property of an antibiotic is its ability to with­stand the inactivating enzymes secreted by other bacteria. For example, many bacteria can produce an enzyme, penicillinase which causes hydrolysis of the 3-lactam ring of penicillins, leading to formation of an inactive product, called penicilloic acid. Bacteria also produce similar other enzymes resulting in inactivation of several other antibiotics. Such bacteria become resistant to the antibiotics by virtue of such inactivating enzymes.
The natural antibiotics, i.e. those produced by different organisms, sometimes do not possess all the desirable properties. They have to be chemically modified to give these properties. Such modified antibiotics are called semi-synthetic ones.
Large number of semi-synthetic derivatives of penicillins and cephalosporin are now available which are resistant to the β-lactamase and are able to resist acidic pH of the gastric juice. Also, chemical modifications have added activity against a broader spectrum of bacteria.
Some representative antibiotics and the producing organisms are listed in Table 11.1:
The Full Course – A Bacteria Infection
Imagine that you are sick with a bacterial infection. Your doctor prescribes an antibiotic to be taken every day for eight days.
Coloured beads represent the harmful bacteria that are in your body:
Disease-Causing Bacteria Represented By
Least resistant bacteria green disks
Resistant bacteria blue disks
Extremely resistant bacteria orange disks
Each time you toss a number cube, it is time to take the antibiotic.
The number on the number cube tells you what to do.
1.Work in pairs for this activity. Begin with 20 beads: 13 green, 6 blue, and 1 orange. These beads represent the harmful bacteria living in your body before you begin to take the antibiotic. Set the extra bead aside for now.
2.It is time to take your antibiotic. Toss a number cube and follow the directions in the Number Cube Key below.
3.The bacteria are reproducing all of the time. If one or more bacteria of a particular type are still alive in your body, add 1 bead of that colour to your population.
For example, if you have resistant (blue) and extremely resistant (orange) bacteria in your body, add 1 blue bead and 1 orange bead to your population.
4.Record the number of each type of bacteria in your body in Table 1, “Number of Harmful Bacteria inYour Body” below.
5.Repeat Steps 2-4 until you have completed Table 1.
6.Use your data in Table 1 to graph the population for each type of bacteria. Plot the total number of bacteria vs number of days in MS Excel or Numbers. Use different coloured lines to represent each type of bacteria, and create a key accordingly.
Table 1: Number of Harmful Bacteria in Your Body
Least Resistant Bacteria (green)
Resistant Bacteria (blue)
Extremely Resistant Bacteria (orange)
1. Did the antibiotic help you to completely kill all of the harmful bacteria living in your body? Explain.
No, the antibiotic did not help me to completely kill all of the harmful bacteria living in my body. The least resistant bacteria was killed first, leaving the most resistant bacteria behind to multiply, reproduce and grow in its numbers.
- Imagine infecting someone else immediately after catching the infection (before you started taking the antibiotic). With what type of bacteria would you be most likely to infect them?
I would be most likely to infect them with the least resistant bacteria.
- Imagine infecting someone else near the end of your antibiotic course. With what type of bacteria would you be most likely to infect them?
I would be most likely to infect them with the most resistant bacteria.
- Suppose most infected people stopped taking the antibiotic when they begun to feel better. (For example, conside the point in the simulation when there were only three harmful bacteria left.) What do you predict might happen to an antibiotic’s ability to kill the harmful bacteria if the infection returns? Explain your reasoning.
The antibiotic’s ability to kill the harmful bacteria if the infection returns will be weaker now, because the antibiotic did not fully kill/wipe out all the
bacteria in the body the first time round. The bacteria in the body would then multiply and reproduce, this time, becoming more resistant to the
antibiotic, all because the person stopped taking the antibiotics when they just begun to feel better.
Changing human lifestyles and societal norms are impacting the human microbiome and contributing to poorer health in the population. 1 The use of antimicrobials, especially antibiotics, diminishes variation in the microbiome 2 and contributes to the spread of antimicrobial resistance (AMR), one of the biggest public health threats facing the world. 3 Microbiome research and medicine continues to expand, including personalized probiotics and prebiotics, personalized diets and faecal microbiota transplantation (FMT). 4
Public knowledge and attitudes around the role of the microbiome in health and wellbeing has not yet been investigated, and there may be potential to improve appropriate use of antimicrobials and other lifestyle behaviours through education on the microbiome. UK household surveys across the last decade suggest a continued misunderstanding of the effect of antibiotics and hygiene on the microbiome and immune system. 5 , 6 Current antimicrobial stewardship (AMS) campaigns and education of the public, including children, 7–11 do not feature messages on the adverse effect of antimicrobials on the microbiome. It is unclear how microbiome information through media, products (such as dietary supplements), and advertisements are affecting public behaviour and attitudes, if at all.
The UK 5 year action plan for AMR highlights the important role of children and adolescents and aims to improve education so that young people leave school with the knowledge and skills to prevent infection and emergence of AMR. 12 Adolescents are a neglected demographic for behaviour change towards antibiotics this is concerning as European population surveys and UK household surveys continually show adolescents to have the poorest knowledge of appropriate antibiotic use. 5 , 6 , 13–16 Qualitative research grounded in behavioural theory is needed to understand how to best intervene to improve behaviour. One qualitative study with English adolescents (16–18 years) found lack of concern for antibiotic resistance, and potentially damaging beliefs about antibiotic use. 17 Furthermore, Eley et al. 18 found English school students (7–16 years) lacked knowledge of the effects of antibiotics on beneficial bacteria in the body. Adolescents are a key demographic for education around improved diet as their fruit and vegetable intake is very low 19 therefore behaviour change interventions around the microbiome have the potential to impact multiple areas of public health to benefit adolescents. Adolescents may be exposed to information on the microbiome in schools as well as through media and adverts and full-time education offers opportunity for improved health education, especially with statutory health education introduced in England in 2020. 20
Behavioural models provide a theoretical lens for researchers to explore facilitators and barriers to desirable behaviours and identify where intervention can effect change. 21 The Theoretical Domains Framework (TDF) was developed to understand implementation of evidence-based practice and behaviour change in healthcare professionals through amalgamating 33 theories into 14 domains to explain influencers of behaviour. 22–24 It is often used in health research with patients, the public and young people. 22 , 25 The TDF fits into the COM-B model, which is at the centre of the behaviour change wheel. COM-B looks at behaviour in terms of Capability, Opportunity and Motivation and is often used in conjunction with the TDF for intervention design. 21
This study aimed to investigate 14–18-year-old adolescents’ knowledge and attitudes towards the human microbiome and antibiotic resistance and explore educators’ capability, motivation and opportunity to embed microbiome teaching in English schools.
Do antibiotics kill good bacteria?
Karen - A lot of antibiotics prescribed are indiscriminate and they will kill our good bacteria as well as the targeted bacteria that they want to kill. They do destroy your gut bacteria and that's sometimes why, when you take a course of antibiotics, you get an upset stomach, diarrhoea et cetera. The best way to try and avoid that is to take some of these probiotic yogurts whilst you're taking the course of antibiotics and possibly for a week or so afterwards. Just to give your own bacteria a chance to recover because although a certain number of your own bacteria will get killed, and that can cause the upset stomach, there are still enough left there that they will regenerate once the antibiotic pressure is removed. Chris - It's often said that the spectrum of bugs that you have in your intestines is more unique to you than your own fingerprint is. So if antibiotics wipe out some of those bacteria, can you actually get back the very ones you had before or do you end up substituting some that are vaguely right, but they're not exactly what you had previously? Karen - Generally, they do all come back because if you imagine the surface of the gut is like your fingers. There are deep crypts and everything is in there, so the bacteria find hiding places away from the antibiotics. So generally, most of them come back again. There are certain bacteria that seem to be particularly susceptible and can get lost. One of them for example is a species called oxalobacter and if you don't have oxalobacter, you're more likely to get kidney stones. Oxalobacter can be eliminated forever with certain antibiotics.
What are antibiotics and how do they work?
Any substance that inhibits the growth and replication of a bacterium or kills it outright can be called an antibiotic. Antibiotics are a type of antimicrobial designed to target bacterial infections within (or on) the body. This makes antibiotics subtly different from the other main kinds of antimicrobials widely used today:
- Antiseptics are used to sterilise surfaces of living tissue when the risk of infection is high, such as during surgery.
- Disinfectants are non-selective antimicrobials, killing a wide range of micro-organisms including bacteria. They are used on non-living surfaces, for example in hospitals.
Of course, bacteria are not the only microbes that can be harmful to us. Fungi and viruses can also be a danger to humans, and they are targeted by antifungals and antivirals, respectively. Only substances that target bacteria are called antibiotics, while the name antimicrobial is an umbrella term for anything that inhibits or kills microbial cells including antibiotics, antifungals, antivirals and chemicals such as antiseptics.
Most antibiotics used today are produced in laboratories, but they are often based on compounds scientists have found in nature. Some microbes, for example, produce substances specifically to kill other nearby bacteria in order to gain an advantage when competing for food, water or other limited resources. However, some microbes only produce antibiotics in the laboratory
How do antibiotics work?
Antibiotics are used to treat bacterial infections. Some are highly specialised and are only effective against certain bacteria. Others, known as broad-spectrum antibiotics, attack a wide range of bacteria, including ones that are beneficial to us.
There are two main ways in which antibiotics target bacteria. They either prevent the reproduction of bacteria, or they kill the bacteria, for example by stopping the mechanism responsible for building their cell walls.
Why are antibiotics important?
The introduction of antibiotics into medicine revolutionised the way infectious diseases were treated. Between 1945 and 1972, average human life expectancy jumped by eight years, with antibiotics used to treat infections that were previously likely to kill patients. Today, antibiotics are one of the most common classes of drugs used in medicine and make possible many of the complex surgeries that have become routine around the world.
If we ran out of effective antibiotics, modern medicine would be set back by decades. Relatively minor surgeries, such as appendectomies, could become life threatening, as they were before antibiotics became widely available. Antibiotics are sometimes used in a limited numbers of patients before surgery to ensure that patients do not contract any infections from bacteria entering open cuts. Without this precaution, the risk of blood poisoning would become much higher, and many of the more complex surgeries doctors now perform may not be possible.
In this article, we’ll discuss 11 of nature’s most useful antibiotics.
1. Garlic & Onion
Garlic and onion share common medicinal properties. Both also contain natural antifungal, antibacterial, and anti-cancer agents. According to the journal publication Pharmacognosy Reviews, “At the time when antibiotics and other pharmacy products did not exist, a bulb of garlic itself represented a whole pharmacy industry due to the broad spectrum of effects.”
2. Ginger Root
Ginger, an incredibly versatile plant, can be eaten fresh, powdered, or dried as a spice. You can also consume it as an extract, oil, capsule, lozenge, or tincture. Ginger helps relieve nausea, loss of appetite, and motion sickness. As an antibiotic, ginger acts as a potent anti-inflammatory and a decent general-purpose pain reliever.
3. Coconut Oil
Speaking of versatile, consider coconut – or in this case, coconut oil. A natural antibiotic, it helps cure coughs, candida, inflammation, and even warts. Due to its antimicrobial properties, coconut oil can also prevent harmful pathogens from entering your digestive system. Coconut oil is also a good antibiotic because of its antiviral and antifungal properties.
4. Apple Cider Vinegar
You might consider Apple Cider Vinegar (ACV) the most popular item on this list – and for a good reason. Containing acetic acid, ACV is one potent anti-inflammatory. It helps reduce the symptoms of many conditions, including acne, arthritis, and gout. Besides helping ease pain, ACV also provides a good dose of probiotics.
Winnie The Pooh’s favorite food also happens to be an excellent antibacterial. Honey contains hydrogen peroxide, the stuff our parents loved to splash on our cuts (to our dismay!). Also related, research shows that common honey kills over 60 different types of bacteria. Additionally, honey serves as an excellent alternative treatment for wound care.
6. Grapefruit Seed Extract
The use of grapefruit seed extract goes all the way back to the 16 th century. At this time, it treated infections of the gastrointestinal (GI) tract. Besides its natural antibacterial properties, GSE helps boost circulation, reduce joint inflammation, and protect our skin from UV damage.
7. Oil of Oregano
Oil of oregano has anti-inflammatory, antiviral, and antifungal properties. If added to nature’s medicine cabinet, “Triple-O” can treat the common cold, infections, and parasites. Taking oil of oregano as a supplement may help protect the skin against harmful bacteria.
Massive research efforts are underway to discover the relatively newfound medical properties of cloves. A particular area of interest to scientists is using the spice to maintain and improve oral health. Studies show that cloves effectively kill off bacteria, gingivitis, and plaque, which may help reduce inflammation of the gums. In one study, a homemade mouth rinse consisting of clove, basil, and tea tree oil killed a greater number of oral bacteria than store-bought mouth rinse!
Thyme, an essential oil, is commonly used in many commercial household cleaners – that’s how powerful this stuff is. Health-wise, thyme is a natural antiseptic and antimicrobial agent. It can even be used to prevent skin conditions such as acne and eczema. Because of its potency, thyme should be diluted with coconut or olive oil before applying to the skin.
A member of the sunflower family, echinacea flower works as one of the best natural antibiotics for the common cold. Studies show that using supplements of the flower can reduce the severity of cold symptoms by up to 50 percent. Other natural antibiotic uses include: ear infections, athlete’s foot, sinus infections, and hay fever.