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The affix -blast means an immature cell, and -cyte indicates any cell. So how do we define if a cell is mature (-cyte) or immature (-blast)? How does this apply to odontoblasts and ameloblasts? Why are they not simply called odontocytes and amelocytes, respectively?
What are the criteria for using the affix -cyte versus -blast?
- The affix -cyte means cell;
- The affix -blast means a germ (bud) cell or a cell that produces (building) materials.
Cells are denoted as -cytes. There are many of them, e.g. melanocytes in the skin and chondrocytes in the cartillage.
Germ cells are denoted as -blasts. These cells typically are precursor cells such as the lymphoblasts that are undifferentiated precursor (stem) cells situated in the bone marrow that produce leukocytes.
Blast cells may also be cells that produce materials. Your examples are of that category; odontoblasts generate dentine, the main hard tissue of the tooth; ameloblasts deposit tooth enamel, which is the hard outermost layer of the tooth forming the surface of the crown. in that sense, also progenitor cells produce something, namely new cells. Hence, blast cells are cells with a chief building function, either materials or new cells.
There are also -clast cells - cells that destroy something. Fig. 1 below gives an overview of these cells as present in the bone, namely osteoblasts (bone builders that secrete the matrix), osteocytes (osteocytes are osteoblasts that are embedded in bone; they stop secreting matrix and only maintain it) and osteoclasts (different class of cells that mediate bone resorption).
Different cells in the bone. source: University of British Columbia
Why then do not call odontoblasts odontocytes? - Because it would mean loss of information. It would be the same as calling a car and a bike both transport vehicles. Moreover, the example in Fig.1 is quite convincing, as osteocytes and osteoblasts are considered to be different cells altogether (although the former is derived from the latter).
Microfilaments are the thinnest filaments of the organelle cytoskeleton. They are made up of linear polymers of semi units and produce force through elongation at one end fine end of the filament coupled with instant shrinkage of at the other, eventuating net movement of the overriding strands (Rao, & Maddal, 2006). They also form the tracks for the movement of the chief Myosin molecules which attach to the main microfilament and work along them (Strnad, Stumptner, Zatloukal, & Denk, 2008). Actin components are regulated by Rho family of tiny GTP-binding proteins likes of Rho itself for stress fibers or contractile acto-myosin filaments, Cdc42 for filopodia and Rac for lamellipodia.
MEISTER SHOWS THAT THE EYES HAVE IT
Can the closed eyes of an unborn baby produce messages that help normal brain development in the womb? It may seem strange to think so, but the answer is yes. MCB Professor Markus Meister made that startling discovery as a postdoc in Denis Baylor’s laboratory at Stanford, along with colleagues Rachel Wong and Carla Shatz, the current Chair of the Neurobiology Department at Harvard Medical School. The finding launched a prolific career in neurobiology. Meister has since become a leading figure in the field—a pioneer who tracks and deciphers neuronal circuits in the retina and their intimate connections with brain physiology. His studies have revealed numerous, and often surprising, aspects of the retina’s capacity to organize and process information. Due largely to his efforts, scientists now know the eyes play dynamic roles in the hardwiring of the nervous system.
Now, Meister wants to establish basic principles for neurobiology that could simplify views of the brain and its neural circuitry. How so? Meister points to molecular biology, proposing that its “fantastic success” can be attributed in part to some core principles that guide researchers in the field. “By this, I mean the idea that DNA makes RNA, and RNA makes proteins, and proteins bind to DNA, and so forth,” Meister explains. “That sort of central dogma allows people to orient their efforts . . . and to collaborate—what happens in a yeast lab might have direct consequences to what happens in a cancer lab.” By comparison, neurobiology has no central dogma, he says, and consequently, scientists in the field don’t work together as much as they could. “Researchers are split among different lines depending on what animals they work with, or what parts of the brain they’re working on,” Meister says. “So, there may be 35,000 members in the national society but only 50 or so are talking to each other at any given time.”
To Harvard via California
What principles might be applied to neurobiology? Meister’s answer to that question draws on an academic history that began in Europe. Meister was born in Germany, grew up in Italy, and then returned to Germany to attend the Technical University of Munich, where he studied physics. He stayed in Munich only three years, however, leaving in 1980 for a year at Caltech that ultimately turned into a PhD in biophysics. At Caltech, Meister studied bacterial locomotion under Howard Berg (now at MCB), who provided his 12-year-old son Henry as a collaborator. “This was when tabletop computers were just coming out,” Meister recalls. “We were working with the Apple 2 Henry knew the contents of every memory address for that machine and he was very funny. He hadn’t even gone through the voice change yet, so I had this squeaky kid telling me what to do. There was no way around him.”
In 1987, Meister left Caltech and came to Stanford for the notable postdoc that produced his groundbreaking research on the retina. That work was done using electrode arrays that Meister still uses now to probe information processing in large sets of neurons. The technology allows him to record neuronal signals in parallel, and helped identify activity patterns in the developing retina that have since been shown to be highly sophisticated. Meister says recent research indicates that interfering with this early neural activity alters hardwiring in the brain.
Meister himself, meanwhile, has turned from developmental studies towards investigations of the adult retina, which he finds more satisfying. He came to Harvard at Berg’s urging, and once here, began to focus on how the adult retina processes visual images. “I want to understand how retinal output relates to visual input,” he explains. “So, we study what neuronal computations happen in the retina and more recently, we’ve gotten into the underlying mechanisms.”
As an example of a basic principle of brain function, Meister cites a phenomenon called lateral inhibition. By this process, adjacent neurons in a circuit inhibit each other’s activity to accentuate “edges” in a given stimulus. To illustrate how this works, consider what you see around you—visual images comprise areas of contrasting light intensity, some uniformly dark, and others brighter. Through the process of lateral inhibition, a retinal neuron computes differences between the intensity in a local patch and that in the surrounding region. Neurons within uniformly intense regions send little or no output signal to the brain. Neurons located at a contrast edge, on the other hand, report large difference signals. Meister compares the process to image compression algorithms used by computers. “In storing a compressed image, the computer doesn’t write down the intensity of every pixel, it just notes changes at a contrast edge,” he explains. “The retina does the same thing: it uses lateral inhibition to emphasize changes, and that saves a lot of neural signaling. This relates to an ‘efficient coding’ hypothesis that we can apply to many areas of the brain.”
Acknowledging that biological principles should apply “in at least two places,” Meister has begun to explore how lateral inhibition discriminates among scents in the olfactory bulb—the part of the brain that processes odors. His findings show olfaction and vision share remarkable similarities: for instance, the light-sensing molecule called rhodopsin, which resides on retinal photoreceptors, is structurally nearly identical to frontline smell receptor molecules in the olfactory system. Other parallels abound, among them lateral inhibition among the output neurons of the olfactory bulb, called mitral cells. Meister suspects odors have contrast edges just as visual images do. “An animal might need to distinguish ripe from rotten fruits,” he says. “Both give off odors with similar components, and the olfactory bulb may serve to compute the differences. This ‘contrast edge’ discriminates one odor from the other and triggers a specific behavioral response: eat or don’t eat.”
Meister predicts that lateral inhibition holds true in higher neural functions, including decision making. Circuits that govern decision making likely contain pools of neurons that dictate binary reactions, such as “jump or don’t jump,” or “stay or don’t stay,” he explains. “And lateral inhibition provides a mechanism that forces these decision processes and makes them crisper,” he adds. “That way, pools of neurons that start to win out in terms of a given reaction inhibit those for the opposite reaction.”
At present, two projects play an important role in Meister’s research. One investigates how environmental features influence lateral inhibition in the retina, and how the retina in turn “selects” messages to send to the brain. His results show the retina adapts to its visual environment and maintains some flexibility in terms of its message response patterns. When these results were published last year in Nature, reporters seized on the concept of “thinking eyeballs,” an analogy Meister won’t dismiss. “This is an exciting trend that we’re following up on,” he says. “It puts a different picture on the retina—it’s not a static processing machine that images go through before they reach the brain, but a dynamic prefilter that can be adjusted according to environmental needs.”
In another pending project, Meister collaborates with Alan Litke from the University of California at Santa Cruz on efforts to create a “wireless rat.” With this project, he and his colleague will affix wireless transmitters directly to rat neurons, allowing them to monitor brain function among free ranging, unanaesthetized animals. “Increasing evidence shows that what we observe in the anaesthetized brain is a pale shadow of what the brain does when it’s fully engaged,” Meister says.
Meister credits his Harvard collaborators with helping to keep his research on track. Colleagues in psychology, he says, keep him focused on what animals do with their nervous systems while Harvard physicists provide input on neuronal modeling. Meanwhile, neurobiology offers Meister a broad expanse of uncharted territory, in which—he suggests—many of the simplest questions remain unanswered.
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How Plague Works
If you've ever watched "Monty Python and the Holy Grail," chances are you have a clear mental image of what a plague-stricken village looks like. It's dirty – even squalid – and its inhabitants are similarly filthy. There's also one resident with a very particular occupation. He wheels a cart through town, calling, "Bring out your dead!" The other villagers are all too willing to comply, and some even want to add their still-living relatives to the cart.
The scene is meant to be funny, but in many ways, it's not too far off the mark. Plague is a real disease, and for much of human history, outbreaks have sparked desperate attempts to stop its spread. During past plague pandemics, some communities persecuted and executed minorities believed to be responsible for the illness. Officials also sealed infected people and their families inside their homes. People under such quarantines had no way of working or buying food, and starvation was a real possibility. Death tolls were so high that bodies had to be carted away and buried together in mass graves. Because of the sheer number of deaths in England, there is less genetic diversity there today than there was in the 11th century [source: New Scientist].
Body collectors and grimy villages may seem like things of the past, especially in affluent parts of the world. But in some countries, including Vietnam and India, people can still remember the most recent plague epidemics. In several parts of the world, plague is endemic – it exists all the time, but not necessarily in epidemic proportions. Today, people can contract plague in major cities as well as in more remote areas. There are a few hundred to a few thousand new cases around the world every year.
Plague is an infectious disease caused by a bacterium called Yersinia pestis. It spreads throughout animal populations, including humans, through the bites of infected fleas. These fleas often feed on rats, which is why large numbers of dead rats are a sign of an impending epidemic. The most well-known form of plague, bubonic plague, is named for the painfully swollen lymph nodes, or buboes, that the disease causes.
In this article, we'll explore how Yersinia pestis lives, reproduces and creates infections. We'll also look at plague's symptoms and how doctors can treat it. Let's begin by examining plague's history and some of the controversies behind the epidemics that have been attributed to it.
Today, some of the illnesses that cause the most alarm are newly discovered, deadly diseases, usually spread by viruses. Scientists isolated avian flu H5N1 in 1996. Person-to-person spread is rare, but the virus has a mortality rate of about 60 percent in humans. A virus also causes Ebola, identified in 1976. Ebola has an average mortality rate of 50 percent. The first known case of HIV was reported in the 1950s. Scientists isolated the virus responsible in the 1980s. The mortality rates for this disease dropped from 16.3 per 100,000 in 1998 to just 3.7 per 100,000 in the U.S. in 2017, thanks to the availability of drugs to treat it.
In 202, the novel coronavirus (COVID-19) outbreak quickly caused a worldwide pandemic, shuttering schools, churches, businesses and society in general in an effort to limit spread of the damaging respiratory illness. The severe social distancing was forced due to the fact that the airborne COVID-19 is exceptionally contagious, and also because many people don't show symptoms at all, so they can easily and unknowingly transmit the disease to others.
People have reacted to the appearance of each of these diseases with fear and dread. A major outbreak of plague today would spark a similar reaction. But unlike many of today's newsmakers, plague comes from an old bacterium rather than a new virus. Researchers believe that Yersinia pestis diverged from the less-lethal Yersinia pseudotuberculosis about 20,000 years ago [source: Huang]. Some believe that plague lived in rats before humans existed. Descriptions of a disease resembling plague also appear in ancient texts, including the Christian Bible.
On top of being old, plague is virulent or highly infective. It generally gets the credit for three major pandemics, or massively widespread epidemics:
- Justinian's Plague lasted from 542-546. It claimed about 100 million victims in Europe, Asia and Africa.
- The Black Death moved across Europe in the 1300s, killing about a third of the continent's population. In total, there were about 50 million deaths in Europe, Asia and Africa.
- The Third Pandemic started in Canton and Hong Kong during the late 1800s. Ships carried the illness to five continents. Thirteen million people died in India alone [source: WHO].
An infamous epidemic, the Great Plague of London, took place during the 16th century. The Great Plague killed up to a fifth of London's population, but the disease did not spread around the world. In other words, it didn't escalate from an epidemic to a pandemic.
During each of these epidemics, no one knew what caused the disease or how it spread. During the Black Death, for example, many blamed the illness on toxic miasmas, so people focused on keeping bad air away. Plague doctors, who usually had little to no medical training, wore masks stuffed with herbs to filter the air. In some cities, people blamed dogs and cats for the illness. The resulting slaughter of rats' natural predators may have encouraged the spread of the disease. In Rome, on the other hand, a large population of feral cats may have provided people with additional protection. A study of tree rings released in 2015 also suggests that, before the disease spread to Europe, the initial Asian reservoir for plague-carrying fleas may have been gerbils rather than rats.
Historical records describe a number of different symptoms during these and other outbreaks. These include rashes, nausea, sensitivity to light, diarrhea and coughing. Swollen, painful buboes appear consistently in most accounts. This is one of the reasons why plague takes the blame for so many pandemics.
The idea that bubonic plague was behind these pandemics has become part of the conventional wisdom – it's something everyone knows. However, some researchers have doubts. Next, we'll take a look at the bacterium behind plague and why some scientists believe it didn't cause the Black Death.
During the Great Plague of London, a tailor in Eyam, Derbyshire received a flea-infested shipment of cloth. Soon thereafter, people started getting sick. Under the advice of the town's rector, Eyam's residents decided to isolate themselves. As a result, the disease didn't spread beyond the town. Learn more about the Eyam plague at the Eyam Museum.
In 1894, researchers made a major breakthrough in plague research. Two doctors, Alexandre Yersin and Kitasato Shibasuburo, each realized that the bacterium Yersinia pestis causes plague. In 1898, another doctor, Paul-Louis Simond, discovered that fleas carry the disease from rats to people. These discoveries took place during the Third Pandemic, and they established a direct link between plague and that particular outbreak. This made it seem likely that plague had also been at the root of the Black Death, the Great Plague of London, Justinian's plague and other outbreaks.
However, the doctors practicing during the earliest pandemics didn't have the tools they needed to accurately diagnose diseases. The microscope and the idea that germs cause disease came around during the 16th century, long after many epidemics ended. There were also no accurate, standardized recordkeeping methods during most plague pandemics. For these reasons, there's not a lot of concrete evidence to prove plague was behind it all. One French team claimed to have found Yersinia pestis DNA in tooth pulp from plague-era mass graves, but other researchers haven't been able to duplicate these results.
Researchers also note a few reasons why plague may not have been the real culprit. Some claim that historical literature doesn't mention a die-off of rats, which typically happens before a plague epidemic. Others say the opposite. Some scientists claim the Black Death and other epidemics spread too far and too quickly for fleas and rats to have been the carriers.
Alternate theories for the disease behind the Black Plague and other epidemics are anthrax and a hemorrhagic virus like Ebola. Circumstantial evidence supports each of these theories. The epidemics started suddenly and seemed to end spontaneously, which is typical of some viral outbreaks. In the years before the Great Plague of London in particular, people started to rely on domestic cows for red meat instead of wild game. This made it more likely for cattle-borne anthrax to infect people. However, there's no clear indication of a massive cow die-off before the Great Plague.
Controversy surrounds these pandemics, but not everyone thinks plague wasn't the cause. As mentioned earlier, some epidemiologists claim that plague could have spread from person to person via the human flea, Pulex irritans. In this case, rats wouldn't need to carry the fleas from place to place – humans would have done all the carrying for them. Another theory is that a different type of plague infection, pneumonic plague, was responsible.
Plague is a vector-borne illness, meaning it requires a living host to carry it from one animal to another. Most of the time, a specific species of flea – Xenopsylla cheopis – is the vector. Also known as the Oriental rat flea, Xenopsylla cheopsis prefers to feed on rats and other rodents, which can carry plague.
The Oriental rat flea has a physical trait that makes it very efficient at transmitting plague. Its digestive system can become blocked by a large mass of plague bacteria. When a blocked flea bites a host, it often regurgitates plague-infected blood back into the wound. Fleas that aren't prone to blockage, like the human flea, may still transmit plague by carrying bacteria on their mouthparts.
After the infected flea bites the host, the bacteria suppress the body's natural inflammatory response. They also use proteins to protect themselves from the immune system. For these reasons, it's not immediately obvious that anything is wrong.
The bacteria hitch a ride into the nearest lymph node, using white blood cells to carry them. Once the bacteria reach a lymph node, they multiply. Due to the overwhelming presence of bacteria and the endotoxins in their cell walls, the lymph node begins to swell. In a few days, the node becomes a painful, egg-sized bubo. The body's natural immune defenses kick in, causing a high fever in an attempt to kill the bacteria. Chills, muscle pain and weakness are also common.
If the infected flea bites the victim on the hand or arm, the bubo forms in the axillary lymph nodes under the arm. If it bites the foot or leg, the bubo forms in the inguinal lymph nodes in the groin. A bite to the head causes a bubo in the maxillary lymph nodes in the neck and jaw. If a flea bites the victim's torso, the bubo can form in the abdominal cavity, where doctors may not detect them.
Unless multiple plague-carrying fleas bite a person, bubonic plague generally causes only one bubo. Sometimes, it may cause a few buboes in the same cluster of lymph nodes. This is one of the reasons why some researchers doubt that bubonic plague was the culprit behind the Black Death and other pandemics. Some historical accounts describe victims as covered in buboes, which doesn't generally happen with bubonic plague.
Like the idea that plague was behind the Black Death, the theory that "Ring around the Rosie" is about plague has become part of the conventional wisdom. However, some researchers doubt that the rhyme has anything to do with plague. Although the words can be interpreted as describing the symptoms and outcome of plague infection, the rhyme didn't appear in print until the 1800s. See "Ring Around the Rosie" at Snopes.com to learn more.
Septicemic and Pneumonic Plague
In addition to being virulent, plague is adaptable. It can live in the bodies of rodents, cats, fleas and humans. Plague can also cause different symptoms depending on how it enters a person's body. These abilities all come from the bacterium's DNA, which carries all the instructions it needs to multiply and make people sick.
Sometimes, plague-infected material enters the body through broken skin. For example, someone might touch infected blood while skinning a dead rodent. This can lead to septicemic plague, which does not always produce buboes. Plague bacteria and toxins in the blood overwhelm the body's immune defenses. This causes a high fever, abdominal pain and exhaustion. If left untreated, or if the immune system is irreparably damaged, septicemic plague leads to multiple organ failure and death. Septicemic plague can also occur as a complication of bubonic plague.
If someone inhales droplets of moisture containing plague bacteria, the result can be primary pneumonic plague. This can happen when an infected person coughs or sneezes. Cats can contract pneumonic plague, and they can transmit the disease to humans when they cough or sneeze. As with septicemic plague, pneumonic plague can be a complication of bubonic plague – in this case, it is known as secondary pneumonic plague. Pneumonic plague causes the typical symptoms of pneumonia, including high fever and a cough that produces bloody sputum.
Generally, secondary pneumonic plague is not as contagious as the primary variety. This is because people who contract primary pneumonic plague tend to be healthy and active when they become infected. They can produce a cough that's strong enough to propel infected droplets of moisture through the air. Victims of secondary pneumonic plague, however, are usually very sick by the time the infection reaches their lungs. They can't always cough forcefully enough to expel infected particles into the air. Either way, without antibiotic treatment, pneumonic plague is almost always fatal.
Pneumonic plague is the least common form of plague, but it's the one most likely to be used as a biological weapon. This is because pneumonic plague is highly contagious, highly lethal and easy to spread. In the past, other forms of plague have also been used as weapons. According to some accounts, the Black Death started after invading forces tossed plague-ridden bodies over the walls of a besieged city. The Japanese military also reportedly dropped bombs containing infected fleas over mainland China during World War II [source: PBS].
In addition to causing pneumonic and septicemic plague, Yersinia pestis can infect other parts of the body when it comes into contact with them. If blood carries plague to the cerebrospinal fluid that surrounds the brain and spinal cord, the result can be plague meningitis. Plague can also infect the tissues of the throat, causing plague pharyngitis.
Before the discovery of antibiotics, all of these forms of plague could be fatal. But today, prompt treatment, particularly in cases of bubonic plague, makes survival much more likely. In spite of these advances, plague still thrives in many parts of the world.
Long before the development of microscopes and antibiotics, many cultures associated outbreaks of plague with rats – specifically, dead rats. This is because plague is an enzootic disease, or a disease that lives primarily in nonhuman animals. The animals that typically carry plague include prairie dogs, voles, wild gerbils and other rodents. Rats, however, are the most common.
When plague-infected rats die, their fleas look for new hosts. Fleas generally prefer to feed off of specific animals, but they will turn to other food sources when necessary. So when an outbreak of plague kills lots of rats, their fleas jump to the nearest source of blood. When people are that source, plague becomes an epizootic disease, or a disease that jumps from animals to humans. Many epizootic diseases, including avian flu, are particularly lethal to humans, who have no natural resistance.
The concept of natural resistance may be behind sudden plague outbreaks as well. When most of the rats in a particular area die of plague, the ones that survive have natural immunity. They pass this immunity to their offspring, but it becomes diluted over several generations. The rats lacking immunity then die of plague, which is usually present in the rodent population. A few rats survive, and the cycle begins again.
The fact that rats are a natural reservoir of plague is one of the reasons why the disease is less common today. In many industrialized nations, particularly in affluent areas, rats are not as common as they were before and during the Middle Ages. Better standards of living and better hygiene practices have cut down on the rat population, and with fewer rats come a smaller disease reservoir.
But the natural rat reservoir is also why plague still exists. In impoverished areas and developing nations, rats can still be prevalent. Exterminating the entire species would be almost impossible and would also affect the rest of the ecosystem.
In agricultural societies, people tend to live and work near fields and storage buildings where rats live. In addition, a mild climate and lots of sandy soil are ideal for the development of the rats' fleas. Places with both of these qualities tend to be prone to plague. Examples of such locations are the American southwest, as well as parts of South America, Africa and Asia. The three countries where the disease endures most significantly are Peru, Madagascar and the Democratic Republic of Congo. Although the Black Death and other epidemics had an enormous impact on Europe, plague is not common there today [source: WHO].
Human behavior can also affect plague outbreaks. For example, in 1989, stored food from an unusually large harvest in Botswana led to a higher-than-normal rat population. Fleas from these rats made their way to people, and plague began to spread. In Mozambique, the practice of catching and skinning rats leads to plague infections in women and children [source: Munyinyewa].
For all of these reasons, public health officials still have to focus on preventing plague and on improved tests and treatments.
Treating and Preventing Plague
Bubonic plague has a distinctive set of symptoms, but it can sometimes be difficult to diagnose. Without a visible bubo, the first symptoms simply resemble the flu. If buboes form in the abdomen, a doctor might mistake bubonic plague for appendicitis. There are also other illnesses that can cause painfully swollen lymph nodes. These include cat-scratch fever and mononucleosis. Even anthrax, which starts with similar flu-like symptoms, can provoke swelling in the lymph nodes.
Bubonic plague is a dangerous disease if left untreated. Without medical attention, pneumonic and septicemic plague are almost always fatal, and they don't generally form the buboes that can make plague easier to detect. Therefore, doctors do more than just look for buboes when making a diagnosis. They also ask about exposure to rats and other rodents, particularly in plague-prone areas. The final diagnosis often comes from examining smears of bodily fluids through a microscope. In cases of suspected bubonic plague, fluid drawn from the bubo is usually the best option, since it tends to include lots of bacteria. Doctors can also examine blood, sputum and Cerebrospinal fluid.
Without treatment, bubonic plague is up to 60 percent fatal, and pneumonic plague is almost always fatal. With prompt antibiotic treatment – within 24 hours of showing symptoms – the mortality rate drops significantly. For this reason, researchers at the Institut Pasteur have developed a new, faster test. The test uses a dipstick rather than microscopes and slides. Instead of looking for bacteria, it detects the presence of a specific molecule that is part of Yersinia pestis' cell wall. The test can confirm a diagnosis in about 15 minutes. [sources: BBC, Stephenson].
Effective treatment of plague requires antibiotics. Streptomycin is used most often, but tetracycline and gentamicin can work as well. Sometimes, doctors will prescribe antibiotics to family members or people who have been bitten by fleas in plague-prone parts of the world. Doctors may also isolate the infected person, particularly if he has contracted pneumonic plague.
Symptoms generally improve within a few days of treatment, but buboes can take weeks to return to normal. However, a drug-resistant form of the disease has emerged in Mozambique. Exactly how this strain will affect public health remains to be seen.
Since plague is a dangerous disease, doctors generally have to report suspected cases to the proper authorities. In the United States, the doctor has to notify local and state health departments. The U.S. Centers for Disease Control (CDC) confirms the diagnosis and informs the World Health Organization (WHO). In a case of biological warfare, all of these agencies would be involved in the response. Likely tactics would include quarantines and preventive doses of antibiotics, particularly in cases of pneumonic plague.
Health officials work to prevent future plague outbreaks by educating people about the disease. Officials also monitor the number of suspected cases and rat populations. For example, great gerbils living in Kazakhstan can carry plague. When these gerbils reach a certain population density, plague usually breaks out in humans two years later.
Plague can seem like a distant possibility to people who live in clean homes with few rodents nearby. However, experts disagree about whether another plague pandemic is possible. Some feel that improvements in hygiene, medical care and pest control make a worldwide outbreak almost impossible. Others believe that plague's exceptional virulence and its ability to become airborne in pneumonic cases will transcend any human efforts into stopping its spread.
Antibiotics are typically used to treat bacterial infections. However, in recent years, improper and unnecessary use of antibiotics has promoted the spread of several strains of antibiotic-resistant bacteria.
In cases of antibiotic resistance, the infectious bacteria are no longer susceptible to previously effective antibiotics. According to the CDC, at least 2 million people in the U.S. are infected with antibiotic-resistant bacteria every year, leading to the death of at least 23,000 people.
"Pretty much any infection you can think of now has been identified as being associated with some level of resistance," said Dr. Christopher Crnich, an infectious disease physician and hospital epidemiologist at the University of Wisconsin Hospitals and Madison Veterans Affairs Hospital. "There's very few infections that we now treat where infections caused by resistant bacteria is not a clinical concern."
MRSA, for example, is one of the more notorious antibiotic-resistant bacterial strains it resists methicillin and other antibiotics used to treat Staphylococcus infections, which are acquired primarily through skin contact. MRSA infections occur in health-care settings such as hospitals and nursing homes, where it can lead to pneumonia or bloodstream infections. MRSA also spreads in the community, especially in situations where there is a lot of exposed skin, other physical contact, and the use of shared equipment &mdash for example, among athletes, in tattoo parlors, and in day care facilities and schools. Community-acquired MRSA most often causes serious skin infections.
An important facet of combating antibiotic resistance is to be careful about their use. "It's so important for us to use antibiotics intelligently," Crnich told LiveScience. "You only want to use an antibiotic when you have a clear-cut bacterial infection."
- Read more about the life history and ecology of bacteria from the University of California, Berkeley.
- Watch: Bacteria: Energy Producers of the Future? From the National Science Foundation.
- Learn how bakers and their bread are a microbial match, from NPR.
This article was updated on Apr. 25, 2019, by Live Science Contributor Rachel Ross.
Dr. Lai: We can make vats of the 4 RNA letters. Scientists can just affix one letter after another until they have the entire long string of letters. As soon as the genetic sequence of the coronavirus was released back in January, we had the ability to make this vaccine, which we started immediately.
Now, naked RNA is not very stable, and it’s not going to just magically get translated into proteins. It has to be in a cell’s cytoplasm to work. With injections, most of the vaccine liquid is going into the space between cells, not into cells. The vaccine still has to be “taken in” by the cells. So scientists developed nanotechnology (very tiny) lipid (fat/oil) micelles (balls) to enclose the mRNA. If you recall from biology class, our cells have a lipid membrane. These lipid nanoparticles merge with our cell membranes and release the mRNA into the cytoplasm where they can be translated into spike proteins. (Envision two blobs of oil merging in a pot of water.) Scientists have only started to work with this type of technology for vaccine development in the past few years.
Side note: Nanotechnology just refers to anything that’s tiny. It has nothing to do with microchips. There is technology in the word because making things tiny requires advanced machines. It’s not a nano Wi-Fi RFID Bluetooth tracking system. It’s just tiny oily bubbles holding long mRNA molecules and a few proteins.
As I mentioned earlier, mRNA isn’t super stable. Plus, cells don’t automatically translate all mRNA into proteins repeatedly until the mRNA disintegrates. We don’t want to waste the vaccine mRNA. We really want the cells that take up the vaccine to translate as many copies of the spike protein as possible so our immune system has plenty of enemy spike proteins to train against. The vaccine manufacturers use proprietary tricks to make the mRNA more appealing and more stable (called adjuvants). We probably won’t get that trade secret even during the FDA hearings. So that’s another unknown in my mind. We don’t know much about the adjuvants in the vaccines. But it wouldn’t be anything elaborate, and it is unlikely to cause problems. The nanoparticle lipids (totally benign fats) seem to be more reactogenic than the adjuvants.
The mRNA vaccine ingredients include the mRNA inside of a fat blob along with some company proprietary adjuvants. We won’t know every last ingredient in the vaccines, but based on what we know about the production, there are no parts of fetuses, mercury, thimerosal, or tracking devices. To summarize, although the Pfizer and Moderna vaccines don’t have any long term safety data, the statistics are really quite favorable. I would definitely get either vaccine, based on what I know at this time.
Peer review information Nature Structural & Molecular Biology thanks Binks Wattenberg, Ming Zhou, and the other, anonymous, reviewer(s) for their contribution to the peer review of this work. Florian Ullrich and Anke Sparmann were the primary editors on this article and managed its editorial process and peer review in collaboration with the rest of the editorial team.
Publisher’s note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
What is meant by fixing the smear?
The preparation of a smear is required for many laboratory procedures, including the Gram-stain. The purpose of making a smear is to fix the bacteria onto the slide and to prevent the sample from being lost during a staining procedure.
Beside above, what is fixing in microbiology? Fixation is process by which the internal & external structures of cells & microorganisms are preserved & fixed. It inactivates enzymes that might disrupt cell morphology & toughens cell structures so that they don't change during staining & observation.
One may also ask, what are the two methods of fixing a smear?
Answer: The two methods of fixing a smear are heat fixing and chemical fixing. Heat fixing is performed by passing the dry smear through the Bunsen burner several times. Chemical fixing is done by covering the smear with 95% methyl alcohol.
What are two reasons for heat fixing a smear?
The dry smear is heated on a hot plate or passed through a flame several times to heat fix it. Heat fixing denatures bacterial enzymes, preventing them from digesting cell parts, which causes the cell to break, a process called autolysis. The heat also enhances the adherence of bacterial cells to the slide.