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Recently there has been increasing interest and research into symbiotic bacteria present in humans and human gut. I'm aware of two new discoveries:
- humans are surrounded by a unique cloud of bacteria, similar to fingerprint, useful in forensics
- human brain and cognition could be influenced by gut bacteria that produces up to 90% of serotonin and dopamine in the human body (not sure how, vagus nerve is implicated)
I've also heard that mothers pass a lot of beneficial bacteria to children during childbirth to jump start intestinal flora. Apparently this happens as the baby travels through the birth canal.
This makes me ask - do adult humans share/ pass along symbiotic or beneficial bacteria or other micro organisms?
I'm aware of viruses and diseases that can be passed via blood or be transmitted sexually, but does anything beneficial get transmitted this way?
Nonpathological bacteria Staphylococcus epidermidis on the human skin are part of normal bacterial flora that help to protect against pathogenic bacteria, such as Staphylococcus aureus. You can get "infected" by Staphylococcus epidermidis the same way as by other skin bacteria and you get a potential benefit from them. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2807625/
You can get beneficial effects from pathological bacteria passed from someone, if you you develop antibodies to them, so you can become more or less resistant to them. For example, if you are from US or Europe and travel to South Asia, you at high risk to get food poisoning from either bacteria or viruses, bot local people are at much lower risk, because they have "shared" microbes one from another.
You can get beneficial effects from probiotic supplements (live nonpathological bacteria), which prevent overgrowth of pathological bacteria in your large intestine. The bacteria in probiotics are similar than those in the human gut.
Every human has it owns unique bacterial biome, and they acquire it the day they are born. Another interesting thing is that the bacteria that each individual acquires gets much of it from there family/parents. An analogy would be portions of bacterial biomes are passed down from generation to generation although each person does generally acquire a unique set of bacteria.
Bacteria is passed throughout the population all the time generally though you only hear about the negative transfers i.e pathogens. It is hard to track what gets transferred though as most bacteria is not culturable.
The Human Biome Project has been uncovering the variety of bacterial biomes among the human population in different demographics, etc. You would probably have a fun time looking through there and uncovering some cool information.
Here's the link: The Human Biome Project
Most exchanges, aside from neo-natal transfer, are fecal-oral. Some exchanges are pneumonic, but the study of those has been limited to pathogens. I am not aware of any studies of direct epithelial contact.
In humans, the preponderance of exchanges happen early in life (neo-natal). The current school of thought is that the microbiome is established by passing through the birth canal and through breast feeding. Only Archae and bacteria have been studied up to this point, and the study of the constellation of viruses is currently being proposed.
Vanilla inhabitants: The search for associated bacteria and fungi
Last April, I ventured to Mexico as part of an international team investigating how cultivation practices influence the growth and health of the orchid Vanilla planifolia.
Vanilla planifolia produces the seedpods used to make vanilla, the spice used for flavoring desserts and beverages, and for providing wonderful aromas in candles, perfumes, and many other things. This collection trip would take me to vanilla’s native habitat of Mexico. All varieties of vanilla originated in Mexico, including those of Madagascar and Tahiti.
Tahitian vanilla is a hybrid of V. planifolia (shown) and V. odorata. Photo by H. Zell CC-BY-SA-3.0
While in Mexico, I visited three farms in the state of Veracruz and one in the state of Puebla. It was fascinating driving to these vanilla farms with my Mexican collaborators. It took us three days of traveling to complete our field collections. Each of the four farms had very different methods of growing V. planifolia. For instance, one of the farmers said he knew what his plants needed and thought growing his vanilla on concrete blocks was the best method. At another farm, the farmer brought decaying wood from a neighboring forest and used it as mulch for his vanilla plants that grew on living posts known as “tuteurs.” This was different from the other farmers who grew their vanilla on trees in the forest and wooden dead “tuteurs.”
Each of the plantations had different soil texture. At the last organic farm, the soil was compact and hard. At the farms that were in the forest, the soil appeared rich and softer. There is no way to quantify the terrestrial root growth, but I did note that the roots in the organic farms were longer and healthier, with some growing up to 4 or 5 feet when we dug the roots up from the soil.
At the Pantapec farm in the state of Puebla, Mexico, vanilla is cultivated in a highly managed environment.
By contrast, the vanilla grown at 1 de Mayo farm in the state of Veracruz, Mexico, is cultivated in a completely natural environment.
The benefits of fungi
Research on rare and endangered orchids usually focuses on finding fungi to help in the germination of orchids. We know that orchids will only germinate in nature using fungi. In addition, fungi living inside of plant leaves can benefit the plants’ health by preventing pathogens from growing. Also, bacteria living within the plants and fungi can be beneficial in the same way as the endophytic fungi. (Photo: V. planifolia tissue microscopy at 100x)
My part of the research project is to collect root samples from V. planifolia from each of these different farms to study the fungi and bacteria inhabiting this orchid. Currently, not much is known about the microbes (fungi and bacteria) that reside in orchid roots. Some fungi and bacteria can cause diseases. For example, with the appearance of a fungal pathogen such as Fusarium oxysporum, Mexican farmers can lose 67 percent of their crops when the Fusarium causes the rotting of the Vanilla’s stem and roots. On the other hand, there are beneficial fungi that inhabit roots, known as mycorrhizal fungi. These beneficial symbiotic fungi acquire mineral nutrients for the Vanilla, and sometimes receive carbon from the orchid in exchange. Although 90 percent of plant species have mycorrhizal fungi, and while we have a good understanding of mycorrhizal fungi of some of these relationships, relatively little is known about the mycorrhizal fungi of orchids, including V. planifolia. The reason for this is that isolating and growing the fungi and bacteria associated with orchid roots can be difficult, and some have never been grown outside of their host.
At each farm, I wanted to sample five individual plants of V. planifolia. Additionally, because of the lifestyle of this orchid, I also wanted to sample the above-ground roots (epiphytic) and the below-ground (terrestrial) roots in the soil. Using either a scissors or a scalpel, I cut small root samples and placed them into Ziploc bags. The vanilla plants are very precious to the farmers, and so a few were initially uncomfortable with our cutting off pieces, but ultimately they were very accommodating.
Epiphytic or terrestrial?
Typically, vanilla grows as a vine, with two types of roots: epiphytic roots (those that wrap around trees or other structures) and terrestrial (soil) roots. This is referred to as hemiepiphytic, because it starts in the ground and grows upward onto the tree’s bark. Many research papers suggest that epiphytic roots do not harbor many fungi, because these roots can photosynthesize, and do not need mutualistic fungus partners.
Back here at the Chicago Botanic Garden, I am in the process of evaluating the microbial community that lives in the root samples I collected. We are using a new technique called high-throughput sequencing that will enable me to evaluate the entire fungal and bacterial community within the orchid’s roots by using their DNA as a way to fingerprint the individual species of microbes. We are not certain how many species of fungi and bacteria we will find, but we predict that this method will give us a good picture of the fungal and bacterial community in these roots and if these communities differ among the different farming techniques. These data will be used to better understand how epiphytic orchids utilize mycorrhizal fungi and refine the best conditions to grow vanilla and prevent diseases in the plants.
This research trip was a delight, not only because of the samples that I collected, but also because I could learn more about how vanilla is grown and used. The farmers showed us how they cure and prepare the vanilla by fermenting it in the sun and before drying it thoroughly. I also tasted homemade “vanilla moonshine,” generously offered by the farmer’s wife. When visiting Papantla, I learned about the Aztec myth that explained how forbidden love created the sacred vanilla orchid. And of course, I was elated because I usually spend the majority of my research time in the lab. And here I was in the tropics, after spending the previous months facing the bitter Chicago 2014 winter.
The human microbiome Me, myself, us
WHAT’S a man? Or, indeed, a woman? Biologically, the answer might seem obvious. A human being is an individual who has grown from a fertilised egg which contained genes from both father and mother. A growing band of biologists, however, think this definition incomplete. They see people not just as individuals, but also as ecosystems. In their view, the descendant of the fertilised egg is merely one component of the system. The others are trillions of bacteria, each equally an individual, which are found in a person’s gut, his mouth, his scalp, his skin and all of the crevices and orifices that subtend from his body’s surface.
A healthy adult human harbours some 100 trillion bacteria in his gut alone. That is ten times as many bacterial cells as he has cells descended from the sperm and egg of his parents. These bugs, moreover, are diverse. Egg and sperm provide about 23,000 different genes. The microbiome, as the body’s commensal bacteria are collectively known, is reckoned to have around 3m. Admittedly, many of those millions are variations on common themes, but equally many are not, and even the number of those that are adds something to the body’s genetic mix.
And it really is a system, for evolution has aligned the interests of host and bugs. In exchange for raw materials and shelter the microbes that live in and on people feed and protect their hosts, and are thus integral to that host’s well-being. Neither wishes the other harm. In bad times, though, this alignment of interest can break down. Then, the microbiome may misbehave in ways which cause disease.
That bacteria can cause disease is no revelation. But the diseases in question are. Often, they are not acute infections of the sort 20th-century medicine has been so good at dealing with (and which have coloured doctors’ views of bacteria in ways that have made medical science slow to appreciate the richness and relevance of people’s microbial ecosystems). They are, rather, the chronic illnesses that are now, at least in the rich world, the main focus of medical attention. For, from obesity and diabetes, via heart disease, asthma and multiple sclerosis, to neurological conditions such as autism, the microbiome seems to play a crucial role.
A bug’s life
One way to think of the microbiome is as an additional human organ, albeit a rather peculiar one. It weighs as much as many organs (about a kilogram, or a bit more than two pounds). And although it is not a distinct structure in the way that a heart or a liver is distinct, an organ does not have to have form and shape to be real. The immune system, for example, consists of cells scattered all around the body but it has the salient feature of an organ, namely that it is an organised system of cells.
The microbiome, too, is organised. Biology recognises about 100 large groups of bacteria, known as phyla, that each have a different repertoire of biochemical capabilities. Human microbiomes are dominated by just four of these phyla: the Actinobacteria, Bacteroidetes, Firmicutes and Proteobacteria. Clearly, living inside a human being is a specialised existence that is appropriate only to certain types of bug.
Specialised but not monotonous. Just as ecosystems such as forests, grasslands and coral reefs differ from place to place, so it is with microbiomes. Those of children in Malawi and rural Venezuela, for instance, contain more riboflavin-producing bugs than do those of North Americans. They are also better at extracting nutrition from mother’s milk because they turn out lots of an enzyme known as glycoside hydrolase. This converts carbohydrates called glycans, of which milk has many, into usable sugars.
That detail is significant. Glycans are indigestible by any enzyme encoded in the 23,000 human genes. Only bacterial enzymes can do the job. Yet natural selection has stuffed milk full of them—a nice example of co-evolution at work.
This early nutritional role, moreover, is magnified throughout life. Like the glycans in milk, a lot of carbohydrates would be indigestible if all the digestive system had to work with were the enzymes that it makes for itself. The far larger genome of the microbiome has correspondingly greater capabilities, and complex carbohydrates are no match for it. They are relentlessly chewed up and their remains spat out as small fatty-acid molecules, particularly formic acid, acetic acid and butyric acid, that can pass through the gut wall into the bloodstream—whence they are fed into biochemical pathways that either liberate energy from them (10-15% of the energy used by an average adult is generated this way) or lay them down as fat.
The fat of the land
This role in nutrition points to one way in which an off-kilter microbiome can affect its host: what feeds a body can also overfeed or underfeed it. One of the first analyses of such an effect was Jeffrey Gordon’s work on bacteria and obesity. In 2006 Dr Gordon, who works at the Washington University School of Medicine, in St Louis, Missouri, published a study that looked at the mixture of bacteria in the guts of fat and thin Americans. Fat people, he discovered, had more Firmicutes and fewer Bacteroidetes than thin ones. And if dieting made a fat person thin, his bacterial flora changed to match.
Experiments on mice suggest this is not just a question of the bacteria responding to altered circumstances. They actually assist the process of slimming by suppressing production of a hormone that facilitates the storage of fat, and of an enzyme that stops fat being burned. This may help explain an otherwise weird observation from agriculture, which is that adding antibiotics to cattle feed helps fatten beasts up—though cattle treated in this way put on muscle mass as well as fat.
Having shown that gut bacteria are involved in obesity, Dr Gordon wondered if the converse was true. In a study he conducted in Malawi, he revealed at a meeting last year, he found that it is. Having the wrong sort of bacteria can cause malnutrition, too.
To show this, he and his team looked at 317 pairs of twins (some fraternal, some identical). In 43% of these pairs, both members were well nourished. In 7% both were malnourished. Crucially, though, in 50% of them one twin was well nourished and one malnourished.
As in the case of overweight and slim Westerners, the well-nourished and malnourished twins had different microbiomes. The bugs in the malnourished children lacked both the ability to synthesise vitamins and the ability to digest complex carbohydrates. And when Dr Gordon transplanted some of the microbiomes into specially prepared mice which had, up until that point, had sterile guts, the bacteria induced the same results in the rodents as had appeared in the people they were taken from. Thus it would seem bacteria might cause malnutrition even in someone whose diet would otherwise be sufficient to sustain him.
If that is true (and the human studies to prove the point have yet to be done) it is an extraordinary result. Some malnutrition, obviously, is caused by an inadequate diet. But in the case of twins, their diet can be assumed to be the same and therefore, in the case of the discordant twins, to be adequate. It might thus be possible to treat quite a lot of malnutrition by rejigging a sufferer’s gut bacteria.
Even more surprising than the microbiome’s contribution to diseases of nutrition, though, is its apparent contribution to heart disease, diabetes, multiple sclerosis and many other disorders.
The link with heart disease is twofold: an observation in people, and an experiment on mice. The observation in people was made by Jeremy Nicholson of Imperial College, London. Dr Nicholson, who studies the links between metabolic products and disease, has shown that the amount of formic acid in someone’s urine is inversely related to his blood pressure—a risk factor for cardiac problems. The connection appears to be an effect that formic acid has on the kidneys: it acts as a signalling molecule, changing the amount of salt they absorb back into the body from blood plasma that is destined to become urine. Since the predominant source of formic acid is the gut microbiome, Dr Nicholson thinks the mix of bacteria there is a factor in heart disease.
Stanley Hazen of the Cleveland Clinic in Ohio has come up with a second way that the microbiome can affect the heart. He and his colleagues worked with mice specially bred to be susceptible to hardening of the arteries. They found that killing off the microbiome in these mice, using antibiotics, significantly reduced their atherosclerosis—though why this should be so remains obscure.
The link with diabetes was noticed in morbidly obese people who had opted for a procedure known as Roux-en-Y, which short-circuits the small intestine and thus reduces the amount of food the body can absorb. Such people are almost always diabetic. As a treatment for obesity, Roux-en-Y is effective. As a treatment for diabetes, it is extraordinary. In 80% of cases the condition vanishes within days. Experiments conducted on mice by Dr Nicholson and his colleagues show that Roux-en-Y causes the composition of the gut microbiome to change. Dr Nicholson thinks this explains the sudden disappearance of diabetes.
The diabetes in question is known as type-2. It is caused by the insensitivity of body cells to insulin, a hormone that regulates the level of blood sugar. Insulin sensitivity is part of a complex and imperfectly understood web of molecular signals. Dr Nicholson suspects, though he cannot yet prove, that some crucial part of this web is regulated by the microbiome in a way similar to the role played by formic acid in the case of high blood pressure. The intestinal bypass, by disrupting the microbiome, resets the signal, and the diabetes vanishes.
Besides heart disease and type-2 diabetes, Dr Nicholson also thinks several autoimmune diseases, in which the body’s immune system attacks healthy cells, involve the microbiome. A lot of immune-system cells live in the gut wall, where they have the unenviable task of distinguishing friendly bacteria from hostile ones. They do so on the basis of molecules (generally proteins or carbohydrates) on the bacteria’s surfaces. Occasionally a resemblance between a suspicious-looking bacterial marker and one from a human cell leads the immune system to attack that cell type, too. As with many of the links between the microbiome and ill health, it is not clear whether this is just bad luck or reflects circumstances in which the interests of some set of bugs in the microbiome diverge from those of the ecosystem as a whole.
Autoimmune diseases linked by Dr Nicholson to the microbiome include type-1 diabetes (caused not by insulin resistance, but by the autoimmune destruction of insulin-secreting cells), asthma, eczema and multiple sclerosis. Again, the details are obscure, but in each case some component of the microbiome seems to be confusing the immune system, to the detriment of body cells elsewhere.
In the case of multiple sclerosis, a confirmatory study was published last year by Kerstin Berer and her colleagues at the Max Planck Institute for Immunobiology and Epigenetics in Freiburg, Germany. They showed, again in mice, that gut bacteria are indeed involved in triggering the reaction that causes the body’s immune system to turn against certain nerve cells and strip away their insulation in precisely the way that leads to multiple sclerosis.
These and other examples of microbiomes going awry raise an intriguing question. If gut bacteria are making you ill, can swapping them make you healthy? The yogurt industry has been saying so loudly for many years: “Top up your good bacteria!” one advert enjoins. The implication is that an external dose of suitable species acts as a tonic to health.
A question of culture
Clinical trials have indeed shown that probiotics (a mixture of bacteria found, for example, in yogurt) ease the symptoms of people with irritable-bowel syndrome, who often have slightly abnormal gut microbiomes. Whether they can cause a beneficial shift in other people is not known. A paper published last year by Dr Gordon’s group reported that in healthy identical twins the microbiome is unaffected by yogurt when one twin was asked to eat yogurt regularly for a couple of months while his sibling did not, no change in the microbiome was seen.
Yogurts are limited in the range of bacteria they can transmit. Another intervention, though, allows entire bacterial ecosystems to be transferred from one gut to another. This is the transplanting of a small amount of faeces. Mark Mellow of the Baptist Medical Centre in Oklahoma City uses such faecal transplants to treat infections of Clostridium difficile, a bug that causes severe diarrhoea and other symptoms, particularly among patients already in hospital.
According to America’s Centres for Disease Control and Prevention, C. difficile kills 14,000 people a year in America alone. The reason is that many strains are resistant to common antibiotics. That requires wheeling out the heavy artillery of the field, drugs such as vancomycin and metronidazole. These also kill most of the patient’s gut microbiome. If they do this while not killing off the C. difficile, it can return with a vengeance.
Dr Mellow has found that treating patients with an enema containing faeces from a healthy individual often does the trick. The new bugs multiply rapidly and take over the lower intestine, driving C. difficile away. Last year he and his colleagues announced they had performed this procedure on 77 patients in five hospitals, with an initial success rate of 91%. Moreover, when the seven who did not respond were given a second course of treatment, six were cured. Though faecal transplantation for C. difficile has still to undergo a formal clinical trial, with a proper control group, it looks a promising (and cheap) answer to a serious threat.
Perhaps the most striking claim, however, for links between the microbiome and human health has to do with the brain. It has been known for a long time that people with autism generally have intestinal problems as well, and that these are often coupled with abnormal microbiomes. In particular, their guts are rich in species of Clostridia. This may be crucial to their condition.
A well functioning microbiome is not one without internal conflicts—there is competition in every ecosystem, even stable, productive ones. Clostridia kill bacteria competing for their niches with chemicals called phenols (carbolic acid, the first antiseptic, is one such). But phenols are poisonous to human cells, too, and thus have to be neutralised. This is done by adding sulphate to them. So having too many Clostridia, producing too many phenols, will deplete the body’s reserves of sulphur. And sulphur is needed for other things—including brain development. If an unusual microbiome leads to the gut needing extra sulphur, the brain may pay the price by developing abnormally.
Whether this actually is a cause of autism is, as yet, unproven. But it is telling that many autistic people have a genetic defect which interferes with their sulphur metabolism. The Clostridia in their guts could thus be pushing them over the edge.
The microbiome, made much easier to study by new DNA-sequencing technology (which lets you distinguish between bugs without having to grow them on Petri dishes), is thus a trendy area of science. That, in itself, brings risks. It is possible that long-term neglect of the microbes within is being replaced by excessive respect, and that some of the medical importance now being imputed to the microbiome may prove misplaced.
Whether or not that is true, though, there is no doubt that the microbiome does feed people, does help keep their metabolisms ticking over correctly and has at least some, and maybe many, ways of causing harm. And it may do one other thing: it may link the generations in previously unsuspected ways.
A lot of the medical conditions the microbiome is being implicated in are puzzling. They seem to run in families, but no one can track down the genes involved. This may be because the effects are subtly spread between many different genes. But it may also be that some—maybe a fair few—of those genes are not to be found in the human genome at all.
Though less reliably so than the genes in egg and sperm, microbiomes, too, can be inherited. Many bugs are picked up directly from the mother at birth. Others arrive shortly afterwards from the immediate environment. It is possible, therefore, that apparently genetic diseases whose causative genes cannot be located really are heritable, but that the genes which cause them are bacterial.
This is of more than merely intellectual interest. Known genetic diseases are often hard to treat and always incurable. The best that can be hoped for is a course of drugs for life. But the microbiome is medically accessible and manipulable in a way that the human genome is not. It can be modified, both with antibiotics and with transplants. If the microbiome does turn out to be as important as current research is hinting, then a whole new approach to treatment beckons.
This article appeared in the Science & technology section of the print edition under the headline "Me, myself, us"
Bacteria vs. Virus
Bacteria and viruses are different types of pathogens, organisms that can cause disease. Bacteria are larger than viruses and are capable of reproducing on their own. Viruses are much smaller than bacteria and cannot reproduce on their own. Instead, viruses reproduce by infecting a host and using the host's DNA repair and replication systems to make copies of itself.
The symptoms of a bacterial or viral infection depend on the area of the body that is affected. Sometimes the symptoms of the two can be very similar. For example, runny nose, cough, headache, and fatigue can occur with the common cold (virus) and with a sinus infection (bacteria). A doctor may use the presence of other symptoms (such as fever or body aches), the length of the illness, and certain lab tests to determine if an illness is due to a virus, bacteria, or some other pathogen or disease process.
Reproduction in prokaryotes is asexual and usually takes place by binary fission. Recall that the DNA of a prokaryote exists as a single, circular chromosome. Prokaryotes do not undergo mitosis. Rather the chromosome is replicated and the two resulting copies separate from one another due to the growth of the cell. The prokaryote, now enlarged, is pinched inward at its equator and the two resulting cells, which are clones, separate. Binary fission does not provide an opportunity for genetic recombination or genetic diversity, but prokaryotes can share genes by three other mechanisms.
In transformation, the prokaryote takes in DNA found in its environment that is shed by other prokaryotes. If a nonpathogenic bacterium takes up DNA for a toxin gene from a pathogen and incorporates the new DNA into its own chromosome, it too may become pathogenic. In transduction, bacteriophages, the viruses that infect bacteria, sometimes also move short pieces of chromosomal DNA from one bacterium to another. Transduction results in a recombinant organism. Archaea are not affected by bacteriophages but instead have their own viruses that translocate genetic material from one individual to another. In conjugation, DNA is transferred from one prokaryote to another by means of a pilus, which brings the organisms into contact with one another. The DNA transferred can be in the form of a plasmid, a small circular piece of extrachromosomal DNA, or as a hybrid, containing both plasmid and chromosomal DNA. These three processes of DNA exchange are shown in Figure 2.
Reproduction can be very rapid: a few minutes for some species. This short generation time coupled with mechanisms of genetic recombination and high rates of mutation result in the rapid evolution of prokaryotes, allowing them to respond to environmental changes (such as the introduction of an antibiotic) very quickly.
Figure 2. Gene transfer mechanisms in prokaryotes. There are three mechanisms by which prokaryotes can exchange DNA. In (a) transformation, the cell takes up prokaryotic DNA directly from the environment. The DNA may remain separate as plasmid DNA or be incorporated into the host genome. In (b) transduction, a bacteriophage injects DNA into the cell that contains a small fragment of DNA from a different prokaryote. In (c) conjugation, DNA is transferred from one cell to another via a mating bridge, or pilus, that connects the two cells after the sex pilus draws the two bacteria close enough to form the bridge.
The Evolution of Prokaryotes
How do scientists answer questions about the evolution of prokaryotes? Unlike with animals, artifacts in the fossil record of prokaryotes offer very little information. Fossils of ancient prokaryotes look like tiny bubbles in rock. Some scientists turn to genetics and to the principle of the molecular clock, which holds that the more recently two species have diverged, the more similar their genes (and thus proteins) will be. Conversely, species that diverged long ago will have more genes that are dissimilar.
Scientists at the NASA Astrobiology Institute and at the European Molecular Biology Laboratory collaborated to analyze the molecular evolution of 32 specific proteins common to 72 species of prokaryotes. 2 The model they derived from their data indicates that three important groups of bacteria—Actinobacteria, Deinococcus, and Cyanobacteria (collectively called Terrabacteria by the authors)—were the first to colonize land. Actinobacteria are a group of very common Gram-positive bacteria that produce branched structures like fungal mycelia, and include species important in decomposition of organic wastes. You will recall that Deinococcus is a genus of bacterium that is highly resistant to ionizing radiation. It has a thick peptidoglycan layer in addition to a second external membrane, so it has features of both Gram-positive and Gram-negative bacteria.
Cyanobacteria are photosynthesizers, and were probably responsible for the production of oxygen on the ancient earth. The timelines of divergence suggest that bacteria (members of the domain Bacteria) diverged from common ancestral species between 2.5 and 3.2 billion years ago, whereas the Archaea diverged earlier: between 3.1 and 4.1 billion years ago. Eukarya later diverged from the archaean line. The work further suggests that stromatolites that formed prior to the advent of cyanobacteria (about 2.6 billion years ago) photosynthesized in an anoxic environment and that because of the modifications of the Terrabacteria for land (resistance to drying and the possession of compounds that protect the organism from excess light), photosynthesis using oxygen may be closely linked to adaptations to survive on land.
In Summary: The Prokaryotic Cell
Prokaryotes (domains Archaea and Bacteria) are single-celled organisms lacking a nucleus. They have a single piece of circular DNA in the nucleoid area of the cell. Most prokaryotes have a cell wall that lies outside the boundary of the plasma membrane. Some prokaryotes may have additional structures such as a capsule, flagella, and pili.
The bacterial cell
All living organisms on Earth are made up of one of two basic types of cells: eukaryotic cells, in which the genetic material is enclosed within a nuclear membrane, or prokaryotic cells, in which the genetic material is not separated from the rest of the cell. Traditionally, all prokaryotic cells were called bacteria and were classified in the prokaryotic kingdom Monera. However, their classification as Monera, equivalent in taxonomy to the other kingdoms—Plantae, Animalia, Fungi, and Protista—understated the remarkable genetic and metabolic diversity exhibited by prokaryotic cells relative to eukaryotic cells. In the late 1970s American microbiologist Carl Woese pioneered a major change in classification by placing all organisms into three domains—Eukarya, Bacteria (originally called Eubacteria), and Archaea (originally called Archaebacteria)—to reflect the three ancient lines of evolution. The prokaryotic organisms that were formerly known as bacteria were then divided into two of these domains, Bacteria and Archaea. Bacteria and Archaea are superficially similar for example, they do not have intracellular organelles, and they have circular DNA. However, they are fundamentally distinct, and their separation is based on the genetic evidence for their ancient and separate evolutionary lineages, as well as fundamental differences in their chemistry and physiology. Members of these two prokaryotic domains are as different from one another as they are from eukaryotic cells.
Prokaryotic cells (i.e., Bacteria and Archaea) are fundamentally different from the eukaryotic cells that constitute other forms of life. Prokaryotic cells are defined by a much simpler design than is found in eukaryotic cells. The most-apparent simplification is the lack of intracellular organelles, which are features characteristic of eukaryotic cells. Organelles are discrete membrane-enclosed structures that are contained in the cytoplasm and include the nucleus, where genetic information is retained, copied, and expressed the mitochondria and chloroplasts, where chemical or light energy is converted into metabolic energy the lysosome, where ingested proteins are digested and other nutrients are made available and the endoplasmic reticulum and the Golgi apparatus, where the proteins that are synthesized by and released from the cell are assembled, modified, and exported. All of the activities performed by organelles also take place in bacteria, but they are not carried out by specialized structures. In addition, prokaryotic cells are usually much smaller than eukaryotic cells. The small size, simple design, and broad metabolic capabilities of bacteria allow them to grow and divide very rapidly and to inhabit and flourish in almost any environment.
Prokaryotic and eukaryotic cells differ in many other ways, including lipid composition, structure of key metabolic enzymes, responses to antibiotics and toxins, and the mechanism of expression of genetic information. Eukaryotic organisms contain multiple linear chromosomes with genes that are much larger than they need to be to encode the synthesis of proteins. Substantial portions of the ribonucleic acid (RNA) copy of the genetic information (deoxyribonucleic acid, or DNA) are discarded, and the remaining messenger RNA (mRNA) is substantially modified before it is translated into protein. In contrast, bacteria have one circular chromosome that contains all of their genetic information, and their mRNAs are exact copies of their genes and are not modified.
What are the gut microbiota and human microbiome?
The human body is host to trillions of microbes, or bacteria. Some of these are useful, and some are harmful.
Some scientists have estimated that there are 10 times more microbial cells in the body than there are human cells, while others say that the ratio may be closer to 1:1.
Recent scientific advances in genetics mean that humans know a lot more about the microbes in the body.
Many countries have invested a lot in researching the interactions within the human body’s ecosystem and their relevance to health and disease.
The two terms microbiota and microbiome are often used to mean the same thing and are used interchangeably. This article will explain the differences between them and how both are being used and research in modern medicine.
Share on Pinterest The gut microbiota is with humans from birth and affects function throughout the body.
The human microbiota consists of a wide variety of bacteria, viruses, fungi, and other single-celled animals that live in the body.
The microbiome is the name given to all of the genes inside these microbial cells.
Every human being harbors anywhere between 10 trillion and 100 trillion microbial cells in a symbiotic relationship. This benefits both the microbes and their hosts, as long as the body is in a healthy state. Estimates vary, but there could be over 1,000 different species of microorganism making up the human microbiota.
There are plenty of projects trying to decode the human genome by sequencing all human genes. In a similar way, the microbiome has been subject to intensive efforts to unravel all its genetic information.
The following video about the human ecosystem, produced by the Genetic Science Learning Center of the University of Utah, Salt Lake City, will help create a picture of this delicate but vital relationship.
It is a good introduction to the range of habitats for different types of microbe in the body, including the differences between the dry environment of the forearm and the wet and oily environment of the armpit.
The microbes in the body are so small that they make up only about 2 to 3 percent of the total weight of the human body, despite outnumbering the cells.[S2]
A 2012 study published in Nature by the Human Microbiome Project Consortium found the following:
- Samples of mouth and stool microbial communities are particularly diverse
- In contrast, samples from vaginal sites show particularly simple microbial communities.
The study demonstrated the great diversity of the human microbiome across a large group of healthy Western people but poses questions for further research. How do microbial populations within each of us vary across a lifetime, and are patterns of colonization by beneficial microbes the same as those shown by disease-causing microbes?
The gut microbiota used to be called the microflora of the gut.
Around this time, in 1996, Dr. Rodney Berg, of Louisiana State University’s Microbiology and Immunology department, wrote about the gut microbiota, summing up its “profound” importance.
“ The indigenous gastrointestinal tract microflora has profound effects on the anatomical, physiological, and immunological development of the host,” Dr. Berg wrote, in a paper published in Trends in Microbiology.
“The indigenous microflora stimulates the host immune system to respond more quickly to pathogen challenge and, through bacterial antagonism, inhibits colonization of the GI tract by overt exogenous pathogens.”
This symbiotic relationship benefits humans, and the presence of this normal flora includes microorganisms that are so present in the environment that they can be found in practically all animals from the same habitat.
However, these native microbes also include harmful bacteria that can overcome the body’s defenses that separate them from vital systems and organs. Examples include
In summary, there are beneficial bacteria in the gut, and there are harmful bacteria that can cross into wider systems and can cause local infections of the GI tract. These infections include food poisoning and other GI diseases that result in diarrhea and vomiting.
The gut microbiota contains over 3 million genes, making it 150 times more genetically varied than the human body.
The gut microbiota of each individual is unique. It can heavily contribute to how a person fights disease, digests food, and even their mood and psychological processes.
Microorganisms have evolved alongside humans and form an integral part of life, carrying out a range of vital functions.
They are implicated in both health and disease, and research has found links between bacterial populations, whether normal or disturbed, and the following diseases:
The human microbiome has an influence on the following four broad areas of importance to health:
As well as absorbing energy from food, gut microbes are essential to helping humans take in nutrients. Gut bacteria help us break down complex molecules in meats and vegetables, for example. Without the aid of gut bacteria, plant cellulose is indigestible.
Gut microbes may also use their metabolic activities influence food cravings and feelings of being full.
The diversity of the microbiota is related to the diversity of the diet. Younger adults trying out a wide variety of foods display a more varied gut microbiota than adults who follow a distinct dietary pattern.
From the moment an animal is born, they start building their microbiome. Humans acquire their first microbes from the entrance of their mother’s cervix on arrival into the world.
Without these early microbial guests, adaptive immunity would not exist. This is a vital defensive mechanism that learns how to respond to microbes after encountering them. This allows for a quicker and more effective response to disease-causing organisms.
Rodents that are completely clean of microorganisms show a range of pathological effects, and an underdeveloped immune system is among them.
The microbiota also relates to autoimmune conditions and allergies, which can be more likely to develop when exposure to microbes is disturbed early on.
The microbiota can affect the brain, which is also involved in digestion. Some have even called the gut microbiota a “second brain.”
Small molecules released by the activity of gut bacteria trigger the response of nerves in the gastrointestinal tract.
Researchers have also observed links between the gut microbiome and psychological disorders, such as depression and autistic spectrum disorder (ASD).
Bacterial populations in the gastrointestinal system have provided insights into gut conditions, including inflammatory bowel diseases (IBD), such as Crohn’s disease and ulcerative colitis. Low microbial diversity in the gut has been linked to IBD as well as obesity and type 2 diabetes.
The status of the gut microbiota has been linked to metabolic syndrome. Changing the diet by including prebiotics, probiotics, and other supplements has reduced these risk factors.
Gut microbes and their genetics affect energy balance, brain development, and cognitive function. Research is ongoing on exactly how this occurs and ways this relationship can be used for human benefit.
Disturbing the microbiota with antibiotics can lead to disease, including infections that become resistant to an antibiotic.
The microbiota also plays an important role in resisting intestinal overgrowth of externally introduced populations that would otherwise cause disease – the “good” bacteria compete with the “bad,” with some even releasing anti-inflammatory compounds.
The human microbiome: why our microbes could be key to our health
Both inside and out, our bodies harbour a huge array of micro-organisms. While bacteria are the biggest players, we also host single-celled organisms known as archaea, as well as fungi, viruses and other microbes – including viruses that attack bacteria. Together these are dubbed the human microbiota. Your body’s microbiome is all the genes your microbiota contains, however colloquially the two terms are often used interchangeably.
Hang on, aren’t microbes supposed to be dangerous?
It’s a bit of a spectrum: some are pathogens, but others only become harmful if they get in the wrong place or boom in number, and some are very useful to the body – such as by helping to break down the array of sugars found in human breast milk. “These sugars are not broken down by the infant,” said Prof John Cryan, a neuropharmacologist and microbiome expert from University College Cork. Instead, microbes in the baby’s gut do the job.
Other key roles of our microbes include programming the immune system, providing nutrients for our cells and preventing colonisation by harmful bacteria and viruses.
Where do my gut microbes come from? Do I just pick them up from my surroundings?
Partly. But it is more complicated than that. “It is still a little bit controversial but for the most part it is thought that we are sterile when we are in utero, and as we are being born, as we emerge through the birth canal from our mums, we get this handover bacteria,” said Cryan. “It is like a gulp at birth. Those bacteria are really important for starting the whole process.”
Cryan notes that during pregnancy a mother’s microbiome shifts, apparently to an optimum mix for offspring. “If you are not born by vaginal delivery, but are born by [caesarean] section, things start off being different,” he said. Indeed, studies have suggested that these differences could be one of the reasons why babies born by caesarean section have a higher risk of conditions including asthma and type 1 diabetes. That said, doctors have cautioned parents against attempting to seed babies born by caesarean section with vaginal bacteria.
Our gut microbiome changes quickly over our first year or two, shaped by microbes in breast milk, the environment and other factors, and stabilises by the time we are about three years old. But our environment, our long-term diet, stress and the drugs we take, such as antibiotics, continue to play a role as we age, meaning our microbiome can change throughout our life.
It seems like microbes are everywhere – how many are we talking about?
The figure that has been bandied out since the 1970s is that microbes outnumber our own cells by about 10 to one. But a study from 2016 suggests that in fact microbial cells and human cells coexist in somewhere around a 1.3 to one ratio – suggesting they only slightly outnumber our own cells, although that doesn’t count viruses and viral particles.
Does this mean I am not human?
Some say we should be seen as a holobiont, a term that reflects the intimate, co-dependent relationship humans have with microbes. “I tell this joke that the next time someone goes to the bathroom and they get rid of some of their microbes they are becoming more human,” said Cryan.
But Ellen Clarke, a philosopher of biology at the University of Leeds, is not convinced. “It all depends on what you mean by ‘human’ in the first place,” she said. “If you think that a human is a collection of cells that all share copies of the same chromosomes, then it is shocking to be told that our bodies contain cells with bacterial DNA.”
But as Clarke points out, human cells don’t just contain chromosomes, but also carry DNA within our cellular powerhouses, mitochondria, which are evolutionary descendants of bacteria. Our genome also contains stretches of genetic material called transposons that, at least in some cases, are thought to have been introduced long ago by viruses. “I prefer to define a human in evolutionary terms, and if we do this then mitochondria are parts of a human, and so are transposons, but gut microbes are not, and neither are prosthetic limbs nor unborn foetuses,” said Clarke, pointing out that microbes can escape the body and live without us.
Are microbes the same in my gut as on my skin?
No, different parts of the body – the skin, vagina, gut – all have very different, distinct communities of microbes. While gut microbes have gained a lot of attention, microbes elsewhere are also important: in recent studies, scientists have found that bacteria commonly found on the skin might help to protect against skin cancer.
Microbiomes also differ from person to person. “When you look at the overall active microbiomes between two healthy people, even if they are living in the same city, you see a tremendous amount of disagreement in their microbiome,” said Rob Knight, professor of paediatrics, computer science and engineering at the University of California San Diego and an expert on the human microbiome.
Variability in the gut microbiome, Knight notes, helps to explain why people respond differently to the same foods. “Whether tomatoes are good or bad for you, whether rice is good for you or worse for you than ice cream and so on is explained by your microbiome,” he said.
Why has the microbiome become such a hot topic for research?
Over recent years the gut microbiome in particular has been linked to a plethora of diseases and conditions, from diabetes to autism and anxiety to obesity.
The gut microbiome has also been linked to how individuals respond to certain drugs, including how cancer patients respond to chemotherapy, and it has even, tentatively, been suggested that it could be linked with how well we sleep.
Meanwhile, a range of studies have raised the importance of other aspects of our microbiome, including that the vaginal microbiome is important in whether an HIV-prevention drug applied to the vagina is effective.
How infectious bacteria can produce genetic variants among sibling cells
In human reproduction, the genes of the mother and father are combined and mixed in countless variations. Their offspring can differ significantly from one another. However, bacteria multiply by simple cell division, so that the two daughter cells carry the same genetic material as the mother cell. A research team led by Dr. Simon Heilbronner from the Interfaculty Institute for Microbiology and Infection Medicine at the University of Tübingen and the German Center for Infection Research has recently discovered how infectious bacteria can produce genetic variants among sibling cells. Certain sections of the genetic material are doubled or multiplied. This gives the bacteria new capabilities that make it possible for them to influence the immune system of the host in their favour. The results of this study, published in the journal Nature Communications, provide important information on how pathogens develop and adapt in their battle against the human immune system.
If bacteria multiply by simple division, clones are created. The cells all have the same genetic composition and the same properties. "However, the bacteria must remain flexible, because their environmental conditions are constantly changing. This is particularly true of pathogens that are struggling with the human immune system and need to deal with any antibiotics that may be administered if they are to survive," says Dr. Heilbronner. His team has shown how the bacterial pathogen Staphylococcus aureus causes inflammation, and how variants develop if gene exchange with other bacterial communities is not possible.
Accordion genes expand the possibilities
"We found that in Staphylococcus aureus, some parts of the genetic material may be available in the form of several exact copies. The number of such copies varies greatly between closely related bacteria," according to Dr. Heilbronner. Genetic mechanisms during cell division result in duplicates being able to multiply in the genetic material of the bacteria. "They can expand and shorten again, like an accordion. This results in a variety of daughter cells with different properties in the course of a few generations." Expanded genetic material leads to stronger protein production by the bacterial cell. "For example, if these proteins transport antibiotics out of the cell or influence the immune system, the bacteria may improve their chances of survival," according to the researcher.
The Tübingen researchers have now shown that such genetic processes occur frequently in Staphylococcus aureus. "Administration of antibiotics can strengthen them. The pathogens now have better ways to respond to human immune cells." The team believes that these processes are important in the evolution of pathogens that are successful and therefore dangerous for humans. The team's findings will be used in the development of new forms of treatment by the Tübingen Cluster of Excellence "Controlling Microbes to Fight Infections."
Homology to known virus types
This is the big one. On finding any potentially "new" virus from a human population, the first thing researchers will do is compare its sequence with known families of virus. Nowadays this takes about two seconds. An alien-made and controlled super-virus is likely to be very different to any naturally occuring virus family. What will happen:
virologists are surprised,
Depending on how much advanced improvements/controls the aliens have built into their virus, its discovery could hit the field of virology from so far out in left field that the discoverers get accused of faking it, cheating etc. All the attention would only encourage us to look further into where this virus came from.
So, to play it very safe, aliens should restrict themselves to using an already-existing virus family such as SARS, and applying only a few point mutations.
Would that be enough to dramatically increase the human death rate? We don't know. But remember, in a farm or a forest somewhere, Mother Nature herself is putting those same mutations into SARS right now.
Nothing is impossible. Science will never definitively prove anything (nor does it have to). However, it can bring up some very solid evidence to support or refute the hypothesis that it is a man made virus.
There is a big difference between how man-made products work and how evolved products work. The man made product has a purpose, and it is tailored to that purpose. Any purposeful construction quickly reveals that it had a purpose.
Evolved products are typically spaghetti code, taking advantage of whatever could be found at the time. A gene for the eyeball is good for the liver? Great! Upregulate it and start churning out liver enzymes! However, this makes the product of such evolution notoriously difficult to predict. It's hard to look at a genome and say "this make a Monkey" or "this causes hemorrhagic fever." If a product is man-made, that unpredictability gets in the way of achieving the man-made purpose. We typically design structures which can be analyzed to prove that they work.
A great example is Stuxnet, the virus that hit the Iranian nuclear refinement centrifuges. After we analyzed the code for Stuxnet, it was very clear that it had exactly one target. A particular model of controller by a particular company was targeted, and the damage done was extremely targeted to the devices being controlled. Nobody who saw the disassembled code for Stuxnet could disagree on what its purpose was.
Let's contrast this with an evolved example: sickle cell anemia (SCA). SCA is a debilitating disease buried in our genetic code. You'd think we'd have evolved away from such a useless bit of code, but we haven't. It's not obvious why until you look at the entire ecosystem and find malaria. Malaria is a major killer in many parts of the world, and it turns out that if you have just one set of SCA genes, rather than the 2 required to get the disease, you gain resistance against malaria.
Both of these are examples of a very focused goal, but the results differ greatly. When you disassemble Stuxnet, it's very clear what it was intended to do. When you disassemble the genes for SCA, there's no obvious way to tell that it's a solution to malaria. The body simply found some genes that did the job, and ran with them. Without malaria, it's just a message without a context. With man-made things, the context is always visible.
You might be able to cover your tracks a bit by "evolving" a virus artificially in a computer. However, you would still likely do it fast enough that there would be telltale signs of order, signs of trying to accomplish an objective.