Information

Is there a specific word for bacterial death?


What do you call it when a bacterium dies? Cellular death is apoptosis, necrosis, and bacterial is… ? I don't simply want to write in a paper that it - well dies!


Death is appropriate. Using this word to describe both unicellular and multicellular organisms places them in the same hierarchy. This hierarchy is the domain of life.

Both prokaryotes and eukaryotes have unicellular and multicellular species.

If you choose another word for death I would suggest not using it exclusively for bacteria. If a reader finds the idea of bacterial death esoteric, they may be inspired to dig deeper into the subject. Encouraging an informed reader would seem to be an effective device in a paper for communicating scientific information.

You could qualify the word 'death' to be more precise. Senescence is the natural process of deterioration of life with age.

Google has a great tool for tracking word popularity. Here's a Google graph for 'senescence'.


Apoptosis and necrosis are only two ways by which eukaryote death is achieved. Certainly there are other ways. Say, if a tissue or organism burns, death is achieved before any nuclear changes, cell swelling or shrinking.

Same thing goes with bacteria. Death is the generic term. If you have more details, you can be more specific. In laboratories, cells die by lysis induced by the human experimenters, either by fancy P1 buffer or by the less sophisticated bleach. Sporulating bacteria autolyse the mother cells in the process of spore release. Overcrowded bacteria may decide to relieve some the pressure by having some individuals commit controlled suicide, called autolysis. For example, lytA is an autolysin stimulated by crowding in the pneumococci. The couple ccdA-ccdB sitting on the E coli plasmid F help ensure that daughter cells that did not inherit any plasmid copies commit programmed suicide. Details about these and some other described mechanisms of death in bacteria are to be found in http://www.ncbi.nlm.nih.gov/pmc/articles/PMC99002/

But if you are looking at some bacteria dying, and you have no evidence about the molecular mechanisms, death is good enough.


The word bacteriocidal is commonly used when describing agents that kill them, as opposed to agents that slow their growth which are said to be bacteriostatic.


Food poisoning

food poisoning any of a group of acute illnesses due to ingestion of contaminated food. It may result from allergy toxemia from foods, such as those inherently poisonous or those contaminated by poisons or foods containing poisons formed by bacteria or foodborne infections. Food poisoning usually causes inflammation of the gastrointestinal tract ( gastroenteritis ) this may occur suddenly, soon after the poisonous food has been eaten. The symptoms are acute, and include tenderness pain or cramps in the abdomen nausea, vomiting, or diarrhea weakness and dizziness.

The Division of Bacterial and Mycotic Diseases of the Centers for Disease Control and Prevention reports that the most commonly recognized foodborne infections are those caused by the bacteria Campylobacter, Salmonella, and Escherichia coli O157:H7. Some caliciviruses , especially the Norwalk virus , are also common causes of food poisoning. There are more than 250 known foodborne diseases.

Bacterial food poisoning may be from any of a number of different microorganisms, and includes (among other types) botulism , campylobacteriosis , Escherichia coli infection, salmonellosis , and shigellosis .

Campylobacteriosis (Campylobacter infection) is the most common foodborne illness. Contaminated or undercooked poultry or meat, unpasteurized (raw) milk, and contaminated water may cause the disease, even though this organism is commonly found in the intestinal tracts of humans and other animals without causing symptoms of illness. Symptoms of campylobacteriosis usually occur within two to ten days of ingesting the bacteria and include mild to severe diarrhea, fever, nausea, vomiting, and abdominal pain. Children, the elderly, and immunocompromised persons are particularly at risk. The bacteria is now recognized as a major contributing factor in the development of guillain-barré syndrome .

Salmonellosis (poisoning with Salmonella) is the second most common type of food poisoning. The source is usually a poultry product. Salmonella species can produce three types of illnesses: typhoid fever , gastroenteritis , and septicemia . The onset of gastroenteritis is usually 12 to 24 hours after ingestion of the contaminated food, with recovery taking from a few days to months, depending on the severity of the incident. The pathologic activity appears to be directly related to local bacterial action within the intestinal lumen and wall rather than from a toxin.

Escherichia coli O157:H7 is one of many strains of E. coli although most strains are harmless and live in the intestines of humans and other animals, this strain produces a powerful toxin and can cause severe illness. It is most frequently associated with ingestion of undercooked ground beef. Other sources of infection include contaminated sprouts, lettuce, salami, unpasteurized (raw) milk, and juice. Swimming in or drinking water contaminated with sewage can also cause infection. The most common symptoms are abdominal cramps and bloody diarrhea. It is also possible to experience nonbloody diarrhea or no symptoms. Usually there is little or no fever, and the illness may resolve in five to ten days. hemolytic uremic syndrome occurs in 2 to 7 per cent of patients.

Norwalk virus is another cause of food poisoning, usually associated with gastroenteritis . Symptoms are often mild, consisting of nausea, vomiting, diarrhea, and abdominal pain. Headache and low-grade fever may occur. The fecal-oral route via contaminated water or food is the usual method of transmission. Shellfish and salad ingredients are the foods most often implicated. Norwalk viruses are responsible for about one third of the cases of viral gastroenteritis in persons over the age of two years.

Other Poisonous Plants , Berries , and Shellfish . There are a number of poisonous berries and over 80 kinds of poisonous mushrooms. Children are frequently tempted by poisonous holly berries or the berries that grow on privet (the shrub often used for hedges). Adults often place their faith in misinformation about differences between poisonous and edible mushrooms. Although it is possible to learn to identify poisonous mushrooms and berries, it is much wiser to play safe. Children should be taught not to eat things they find in the woods or fields.

Mushroom poisoning can produce seizures, severe abdominal pain, intense thirst, nausea, vomiting, diarrhea, dimness of vision, and symptoms resembling those of alcoholic intoxication. Symptoms appear six to 15 hours after eating. Later, because of toxic injury to the liver and kidney, the person exhibits signs of hepatic and renal failure.

Mussels and clams may grow in beds contaminated by the typhoid bacillus (Salmonella typhi) or other pathogens. In addition, mussels, clams, and certain other shellfish are dangerous during warm seasons of the year, particularly in the Pacific Ocean they become poisonous as a result of feeding on microorganisms that appear in the ocean in warm weather. Paralytic shellfish poisoning is a condition characterized by paralysis of the respiratory tract. The symptoms vary there may be trembling about the lips or loss of power in the muscles of the neck. Symptoms develop quickly, within five to 30 minutes after eating.

Botulism is the most dangerous, but fortunately the rarest, type of food poisoning. Botulism-causing Clostridium botulinum bacteria and their spores are often present in the environment. The spores can be found on the surfaces of fruits and vegetables, as well as in seafood. Home-canned, low-acidic foods were once a common source for this type of poisoning. The bacteria and spores themselves are harmless the dangerous substance is the botulinum toxin produced by the bacteria when they grow. Botulism results in a descending pattern of weakness and paralysis. When it is suspected, serum, feces, and any remaining food should be tested for botulinum toxin food and fecal samples can also be cultured for Clostridium botulinum. In infant botulism, the toxin is produced when C. botulinum spores germinate in the intestines. Most cases in infants are caused by inhalation of airborne spores, but infants under one year old should not be given honey, which can contain C. botulinum spores.

Treatment . For most bacterial food poisoning, treatment is largely supportive and consists of rest, nothing by mouth until vomiting stops, medication for the diarrhea, and intravenous replacement of fluids and electrolytes as needed. While most bacterial poisonings are self-limiting, botulism must be treated promptly with antitoxin and respiratory support the greatest threat to life is respiratory failure. A large proportion of persons with botulism whose cases are misdiagnosed or treated improperly have a fatal outcome.

In general, antibiotics are not effective in treating bacterial food poisoning. However, care will be individualized to the patient dependent upon the organism causing the infection and the condition of the patient. Prevention of food poisoning by proper handwashing techniques and appropriate food handling should be emphasized.

In the United States, the Center for Food Safety and Applied Nutrition of the Food and Drug Administration has published the Foodborne Pathogenic Microorganisms and Natural Toxins Handbook, a valuable source for basic facts on this subject.


Introduction to Bacteriology

Bacteria are single-celled microorganisms that lack a nuclear membrane, are metabolically active and divide by binary fission. Medically they are a major cause of disease. Superficially, bacteria appear to be relatively simple forms of life in fact, they are sophisticated and highly adaptable. Many bacteria multiply at rapid rates, and different species can utilize an enormous variety of hydrocarbon substrates, including phenol, rubber, and petroleum. These organisms exist widely in both parasitic and free-living forms. Because they are ubiquitous and have a remarkable capacity to adapt to changing environments by selection of spontaneous mutants, the importance of bacteria in every field of medicine cannot be overstated.

The discipline of bacteriology evolved from the need of physicians to test and apply the germ theory of disease and from economic concerns relating to the spoilage of foods and wine. The initial advances in pathogenic bacteriology were derived from the identification and characterization of bacteria associated with specific diseases. During this period, great emphasis was placed on applying Koch's postulates to test proposed cause-and-effect relationships between bacteria and specific diseases. Today, most bacterial diseases of humans and their etiologic agents have been identified, although important variants continue to evolve and sometimes emerge, e.g., Legionnaire's Disease, tuberculosis and toxic shock syndrome.

Major advances in bacteriology over the last century resulted in the development of many effective vaccines (e.g., pneumococcal polysaccharide vaccine, diphtheria toxoid, and tetanus toxoid) as well as of other vaccines (e.g., cholera, typhoid, and plague vaccines) that are less effective or have side effects. Another major advance was the discovery of antibiotics. These antimicrobial substances have not eradicated bacterial diseases, but they are powerful therapeutic tools. Their efficacy is reduced by the emergence of antibiotic resistant bacteria (now an important medical management problem) In reality, improvements in sanitation and water purification have a greater effect on the incidence of bacterial infections in a community than does the availability of antibiotics or bacterial vaccines. Nevertheless, many and serious bacterial diseases remain.

Most diseases now known to have a bacteriologic etiology have been recognized for hundreds of years. Some were described as contagious in the writings of the ancient Chinese, centuries prior to the first descriptions of bacteria by Anton van Leeuwenhoek in 1677. There remain a few diseases (such as chronic ulcerative colitis) that are thought by some investigators to be caused by bacteria but for which no pathogen has been identified. Occasionally, a previously unrecognized diseases is associated with a new group of bacteria. An example is Legionnaire's disease, an acute respiratory infection caused by the previously unrecognized genus, Legionella. Also, a newly recognized pathogen, Helicobacter, plays an important role in peptic disease. Another important example, in understanding the etiologies of venereal diseases, was the association of at least 50 percent of the cases of urethritis in male patients with Ureaplasma urealyticum or Chlamydia trachomatis.

Recombinant bacteria produced by genetic engineering are enormously useful in bacteriologic research and are being employed to manufacture scarce biomolecules (e.g. interferons) needed for research and patient care. The antibiotic resistance genes, while a problem to the physician, paradoxically are indispensable markers in performing genetic engineering. Genetic probes and the polymerase chain reaction (PCR) are useful in the rapid identification of microbial pathogens in patient specimens. Genetic manipulation of pathogenic bacteria continues to be indispensable in defining virulence mechanisms. As more protective protein antigens are identified, cloned, and sequenced, recombinant bacterial vaccines will be constructed that should be much better than the ones presently available. In this regard, a recombinant-based and safer pertussis vaccine is already available in some European countries. Also, direct DNA vaccines hold considerable promise.

In developed countries, 90 percent of documented infections in hospitalized patients are caused by bacteria. These cases probably reflect only a small percentage of the actual number of bacterial infections occurring in the general population, and usually represent the most severe cases. In developing countries, a variety of bacterial infections often exert a devastating effect on the health of the inhabitants. Malnutrition, parasitic infections, and poor sanitation are a few of the factors contributing to the increased susceptibility of these individuals to bacterial pathogens. The World Health Organization has estimated that each year, 3 million people die of tuberculosis, 0.5 million die of pertussis, and 25,000 die of typhoid. Diarrheal diseases, many of which are bacterial, are the second leading cause of death in the world (after cardiovascular diseases), killing 5 million people annually.

Many bacterial diseases can be viewed as a failure of the bacterium to adapt, since a well-adapted parasite ideally thrives in its host without causing significant damage. Relatively nonvirulent (i.e., well-adapted) microorganisms can cause disease under special conditions - for example, if they are present in unusually large numbers, if the host's defenses are impaired, (e.g., AIDS and chemotherapy) or if anaerobic conditions exist. Pathogenic bacteria constitute only a small proportion of bacterial species many nonpathogenic bacteria are beneficial to humans (i.e. intestinal flora produce vitamin K) and participate in essential processes such as nitrogen fixation, waste breakdown, food production, drug preparation, and environmental bioremediation. This textbook emphasizes bacteria that have direct medical relevance.

In recent years, medical scientists have concentrated on the study of pathogenic mechanisms and host defenses. Understanding host-parasite relationships involving specific pathogens requires familiarity with the fundamental characteristics of the bacterium, the host, and their interactions. Therefore, this section first presents with the basic concepts of the immune response, bacterial structure, taxonomy, metabolism, and genetics. Subsequent chapters emphasize normal relationships among bacteria on external surfaces mechanisms by which microorganisms damage the host host defense mechanisms source and distribution of pathogens (epidemiology) principles of diagnosis and mechanisms of action of antimicrobial drugs. These chapters provide the basis for the next chapters devoted to specific bacterial pathogens and the diseases they cause. The bacteria in these chapters are grouped on the basis of physical, chemical, and biologic characteristics. These similarities do not necessarily indicate that their diseases are similar widely divergent diseases may be caused by bacteria in the same group.


Anthrax

Infectious Agent: Bacteria, Bacillus anthracis
Symptoms: respiratory failure, flu-like symptoms,
Transmission/Vector: infected meat
Prevention: Vaccines can be given to at-risk populations (military), avoid contact with infected persons or animals
Additional Notes: Anthrax spores can survive for long periods, making anthrax an possible pathogen for bioterrorism (anthrax can be mailed in envelopes). There are also gastrointestinal and cutaneous forms of infection.


Is there a specific term for imbuing abstract concepts with 'agency'?

I'm a biologist, and when we give scientific presentations it is often convenient to talk about evolution in the context of it trying to 'achieve something', like it has conscious 'agency'. We of course know that this isn't the case, it's just an easy way to frame a point.

The bacteria is trying to become more resistant to antibiotics.

So my question is: is there a specific word for giving abstract concepts (e.g. evolution) an agency?

The only one that springs to mind is personification, but to my mind that only applies if you are giving the subject people-like traits?


4. Climate Change

Despite what some governments might think, climate change has emerged as one of the most pressing issues of our time. Scientists have measured the chemical signal from greenhouse gases and determined that it's a direct result of human industrial activity.

Climate change is one of the most pressing issues of our time.

The battle against climate change seems daunting. First, scientists must convince the general public — especially legislators — that the phenomenon exists. Then, there's the huge task of identifying possible solutions.

With global consequences, climate change scientist is a job that's not likely to end within our lifetimes, meaning there's plenty of room for new environmental specialists.


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Bio 142 1st Edition Exam 3 Study Guide The Immune System What is the immune system The immune system is the body s defense against invaders and malfunctioning cells What are the three levels of the immune system 1 o Physical and chemical barrier to entry 2 o Innate immune response This is the general immune response against all invaders At this point the specific invader doesn t matter and won t be recognized 3 o Adaptive immune response The immune system learns over time as it is confronted with various invaders It can now attack specifically for a certain invader and quicker What makes up the first line of defense The first line of defense is the physical and chemical barriers of the body This includes Skin o Skin physically prevents invaders from entering the body Mucous o Mucous is in the nasal passage and traps microbes This explains why when you consistently touch your mouth or nose during cold season you will more than likely get sick Normal bacterial and fungal flora can out compete invaders Whether you like it or not there are millions of micro bacteria on your body These keep you safe from invaders Sweat o Our sweat is acidic with a pH of 3 5 The sweat itself can kill of bacteria and invaders as well as cool down the body Stomach acid o In the odd instance that we ingest an invader the acidity of the stomach pH near 1 kills invaders What makes up the second line of defense The second line of defense is the innate immune response This is the body s first attempt to respond to invaders Once again the immune system does not recognize a specific invader at this point Instead the immune system recognizes molecules found on microbes that are not associated with the body s own cells This is when it attacks This is does not improve with repeated exposure to microbes What are the specific cells found in the second line of defense There specific cells found within the second line of defense Leukocytes o These are white blood cells They leave the blood and go into the tissues to attack Within the leukocytes there are other specific cells Neutrophil These are a common phagocyte leukocyte that makes up 70 of all leukocytes Their sole purpose is to hunt down and neutralize invaders They do this by engulfing intruders This is known as phagocytosis or the cells eating other cells These specific cells will arrive first but die quickly Eosinophil These cells target parasites nematodes and release enzymes to destroy invaders They DO NOT use phagocytosis Natural Killer cells o These cells target abnormal cells or cancerous cells and virus infected cells They recognize abnormal cells via antigens and release chemical that causes apoptosis Apoptosis is cell death via cell lysis They do not target specific antigens or microbes just all abnormal cells Basophil o These cells work with mast cells and gather at the site to release compounds and do not actually attack the invader These include histamine and prostaglandins Histamine is an organic compound that dilates capillaries Prostaglandins are a group of lipid compounds that promote blood flow Both of these compounds speed up the response time from other leukocytes Monocytes o These are also known as macrophages They also do not attack the invader and instead migrate to the site of infection through the blood At the site they engulf the invader but do not destroy it Rather the cell presents the invader to the adaptive immune response Dendritic Cells o These cells often line organs and bind to small invaders They then relocate these invaders to the lymph system where the invaders are presented to the adaptive immune response Complement Proteins o These proteins are produced in the liver and found in the blood They remain inactive until they are triggered by a microbe They then flag the invaders which attract macrophages The flagging triggers a lysis of gram negative bacteria These proteins also trigger inflammation Inflammation is when blood vessels dilate and become more permeable This allows more blood to flow thus speeding up the reaction time for defense cells and proteins What is the inflammatory response The inflammatory response is the body s permeability to allow defenses to leave the bloodstream and defend the affected tissues This results in the coordinated response to infection or physical injury What cells are included in the inflammatory system Mast cells and basophils o These remain in the damaged area and release histamine and prostaglandins Neutrophils monocytes and complement proteins o They clean up the infected area There are some leukocytes that release pyrogen which leads to an increase in the body s temperature This is a fever When is inflammation bad If the all clear isn t sent from the signaling pathway to shut off inflammation the immune response may go overboard If sent overboard some healthy tissue may be destroyed from the inflammatory response What makes up the third line of defense Certain cells are specifically made for specific functions in identifying invaders and protecting the body in future attacks Lymphocytes o These cells are also a type of leukocyte and are the cornerstone of the adaptive immune response o On all cells there are structures called antigens These structures can be potentially investigated by the body s defense cells The body recognizes its own cells when normal and foreign cells are outsiders Even on a transplanted organ the body recognizes the foreign antigens and will attack it Abnormal cells are also attacked after the antigens are investigated Antigen presentation All nucleated cells have Major Histocompatibility Complex MHC proteins on their surfaces These are a platform where the body s cells attach from their own cytoplasm This attachment is called an antigen Example dendritic cell that engulfs a microbe The dendritic cell breaks down the microbe and places part of the invader on its cell surface via MHC The cell is then recognized by lymphocytes and the invaders are targeted for termination What are the different lymphocytes B cells o These lymphocytes have a specific type of B Cell Receptor on their surfaces They circulate around blood and lymph nodes looking for invaders via antigens After they have contacted a specific invader they sensitize Sensitize is complex but it alerts the attention of Helper T Cells The Helper T Cells then activate the B Cell o Now active sensitized B Cells can produce plasma cells These plasma cells create antibodies and memory B Cells The memory B


Examples of Chemiluminescent Reactions

The luminol reaction is a classic chemistry demonstration of chemiluminescence. In this reaction, luminol reacts with hydrogen peroxide to release blue light. The amount of light released by the reaction is low unless a small amount of suitable catalyst is added. Typically, the catalyst is a small amount of iron or copper.

The reaction is:

C8H7N3O2 (luminol) + H2O2 (hydrogen peroxide) → 3-APA (vibronic excited state) → 3-APA (decayed to a lower energy level) + light

Where 3-APA is 3-Aminopthalalate.

Note there is no difference in the chemical formula of the transition state, only the energy level of the electrons. Because iron is one of the metal ions that catalyzes the reaction, the luminol reaction can be used to detect blood. Iron from hemoglobin causes the chemical mixture to glow brightly.

Another good example of chemical luminescence is the reaction that occurs in glow sticks. The color of the glow stick results from a fluorescent dye (a fluorophore), which absorbs the light from chemiluminescence and releases it as another color.

Chemiluminescence doesn't only occur in liquids. For example, the green glow of white phosphorus in damp air is a gas-phase reaction between vaporized phosphorus and oxygen.


Peptidoglycan - The bacterial wonder wall

Quick, can you describe your grandparents? Staphylococcus aureus, or the Golden Staph, can and it is a single cell. If you couldn't you should visit them more often. In any case, a very cool paper came out recently but before we can get there we need to begin by going backwards to explain a very important bacterial structure called peptidoglycan.

Peptidoglycan is a polymer of amino acids (hence the peptido-) and sugars (hence the –glycan) that makes up the cell wall of all bacteria. This structure is so fundamental to bacterial life that major functional division of bacterial species is based on the structure of this peptidoglycan layer, which can be exploited by a special staining protocol.

Yeah, I've used this before but its still works. Credit: Me.

Back in 1884 a guy named Gram developed a staining technique to visualise bacterial samples (now called a Gram stain). It was really important because, as the story goes, pneumonia was a big problem at the time and there were three causes unknown (later identified as viral pneumonia) and two types of bacterial pneumonia caused by either Streptococcus pneumoniae or Klebsiella pneumoniae. Importantly pneumonia caused by Streptococcus is more contagious and develops faster than pneumonia caused by Klebsiella, which tends to only affect the immuno-compromised. Gram’s stain, which was fast and definitive, allowed for the three different types of pneumonia patient to be grouped together, reducing spread and therefore preventing disease.

Gram Stain of mixed cultures of S. aureus (purple) and E. coli (red). Credit: Wikimedia.

So how did Gram’s stain work? Because of the peptidoglycan layer. The thickened peptidoglycan layer in Gram positive cells allows them to retain the stain (hence remaining ‘stain positive’ or ‘Gram positive) where as the thin layer seen in Gram negative cells cannot prevent the stain from leeching out (hence stain and Gram negative). Of course Gram himself didn’t know this but his stain was a success and it was 1884 so give him a break.

Pretty simple picture but everything is colour coded. Credit: Wikimedia.

Peptidoglycan is also vitally important for the way antibiotics work. The role of a bacterial cell wall is defensive. The wall is there for the same reason our skin is on us, to keep the insides in and the outsides out and it does this by physically limiting the size and shape of the cell. In the microbial world one of the most important forces changing cell size and shape is, believe it or not, water.

A bacterial cell is a little salty bubble generally existing in a less salty environment. The problem lies in that the less salty environment wants to even out all the salt concentrations so water would rush into the cell to dilute its saltiness until it matches that of the environment, or until it bursts and kills the cell. This process is given the name osmosis. The role of peptidoglycan is to act as a physical barrier to the cell taking on to much water and killing itself. Its like trying to inflate a balloon inside a small box, once a certain amount of air goes in the box pushes back on the expanding balloon and no more air can be pushed into the balloon.

But suppose we could break this peptidoglycan wall, that would result in the bacterium losing this protective layer and becoming vulnerable to osmosis causing the cell pop. Wouldn’t that be a great antibiotic?

Turns out it is a great antibiotic, penicillin. Penicillin works by inhibiting the repair of the peptidoglycan layer, therefore damage compounds and the peptidoglycan is compromised causing it to become susceptible to osmotic lysis.

This also explains why penicillin and its derivative are more effective against Gram positive cells. With its peptidoglycan layer hidden beneath an outer lipid membrane it is harder for the penicillin to reach the peptidoglycan where it has activity whereas Gram positive cell walls leave the peptidoglycan exposed.

Penicillin is so good at killing bacteria that bacteria have had to evolve a way around it. They do this in two ways, they either destroy the penicillin itself or they change the target of penicillin to something penicillin can’t recognise. Either way our use of penicillin, and our exploitation of this peptidoglycan wall triggered an arms race with the microbial world so that they could protect the precious peptidoglycan.

I mentioned at the top that S. aureus knows what is grandparent looked like and that this was related to peptidoglycan and this comes back to how this bacteria determines how it will divide.

A recent paper in Nature Communications by Prof. Simon Foster’s group (Turner et al., 2010, see below) has shown that the Golden Staph has detectable ridges in its peptidoglycan structure, a kind of pie crust that can be found in a very specific pattern. They found that one ridge was equatorial (whole rib), a second ridge bisected only one hemisphere (half rib) and a third ridge perpendicularly bisected one half of the previously bisected hemisphere (quarter rib).

Its been known for some time that Staphylococcus forms in bunches, in fact it name comes from the Greek word for grapes, and even more recently it has been observed that staphylococcal cell division takes place in a very specific order. The first division is within the x-axis, the second within the y-axis then the third in the z-axis before repeating itself. Each cell division takes place within a new plane and at right angles to the last cell division.

My own rendering of S. aureus division patterns. Each division numbered in order and it should be obvious that Ƈ' and Ɗ' are the same stage in a repeating cycle. Credit: Me.

What Prof. Foster and his group have shown is that the pie-crusts or peptidoglycan ribs mark the site of peptidoglycan synthesis during Staphylococcal cell division and because of the way each cell divides it retains the information of the two previous divisions, its parental and grand-parental divisions! Furthermore, this observation indicates this process is not random and so probably driven by the peptidoglycan itself.

Peptidoglycan is a wonderful substance. Without it bacteria would be vulnerable to death by water, we wouldn’t be able to quickly, easily or cheaply tell them apart and we would be without penicillin, possibly the second greatest biomedical innovation after vaccines. Now it seems that peptidoglycan can control the site of cell division, in S. aureus anyway, indicating there might be more to discover about this bacterial wonderwall.

Turner, R., Ratcliffe, E., Wheeler, R., Golestanian, R., Hobbs, J., & Foster, S. (2010). Peptidoglycan architecture can specify division planes in Staphylococcus aureus Nature Communications, 1 (3), 1-9 DOI: 10.1038/ncomms1025

van Heijenoort J (2001). Formation of the glycan chains in the synthesis of bacterial peptidoglycan. Glycobiology, 11 (3) PMID: 11320055

The views expressed are those of the author(s) and are not necessarily those of Scientific American.

ABOUT THE AUTHOR(S)

Dr James Byrne has a PhD in Microbiology and works as a science communicator at the Royal Institution of Australia (RiAus), Australia's unique national science hub, which showcases the importance of science in everyday life.


What Plants and Foods Are GMOs?

There are only a few types of transgenic, or “genetically modified,” plants that have been approved for commercial production in the United States. The table below shows those different plants and what genetic traits in the plants have been added or changed by scientists. These plants have one or more of the following traits modified by genetic engineering.

Controlling nearby weeds is important for healthy growth of soybeans. Click for more detail.

Herbicide Resistance – Herbicides are chemicals used to kill weeds. On large farms that use herbicides, these chemicals can leak into the environment or they can stick to the crops, ending up in your food in small amounts. If farmers could use less toxic chemicals to kill weeds, it would be safer for people eating the crops and for the environment. Many transgenic plants have a gene added making them resistant to a specific, low-toxicity herbicide. This allows farmers to use herbicides that do less harm to the environment and people.

Pest Resistance – Some plants have been modified to have a bacterial gene. This bacterial gene makes a protein which kills only certain types of insects that harm plants. The protein is not toxic to people or to other insects or animals, but it protects the plants from that specific pest.Because of this, farmers do not have to use toxic pesticides on these plants.

Many papayas can catch ringspot virus. Click for more detail.

Virus Resistance – Did you know that plants can get sick from viruses? These viruses do not make people sick, but they can damage crops. Genes have been added to some plants so they won't catch these specific viruses.

Changed Metabolism – Genes have also been added to plants to change the types of sugars or fats that a plant makes. This can be used to make the plant safer to eat. Some of these genes make the plant less likely to get bruised or damaged during shipping which means less food gets thrown in the trash.

This table shows types of transgenic plants that are grown on farms. Click for more information.

Knowing the type of genetically modified crops that we can grow, we can think more about whether growing them is safe and whether it benefits farmers.

Additional images via Wikimedia Commons. Potato image by Agricultural Research Service.