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I have read that fungi cannot live without air. Does a couple of minutes in a swimming pool full of chlorinated water kill them as it would a mammal? I've never heard this suggested. Will they survive by enjoying trapped air? Or by "holding their breath" for a long time?
There is a lot of anecdotal evidence that frequent visits to the pool help with fungal infections. Surely, someone from the scientific community must have noticed too, right? So why don't we frequently hear people suggesting to go swimming to treat these infections?
Because scientific results suggest the opposite!
Incidence of occult athlete's foot in swimmers
In our results, 22 swimmers had positive cultures (15%), 8 of these cases had no lesions (36%). They included 7 infections with Trichophyton mentagrophytes (87.5%) and one with T. rubrum (12.5%). We observed one case with a dual infection. Only one sample from the inanimate environment was positive. This study showed a significant incidence of occult athlete's foot in swimmers. To control this endemic problem, adequate preventive measures must be taken.
Foot Infections in Swimming Baths
A 10% random sample of all bathers at a public swimming bath were examined for tinea pedis and verruca.
The overall incidence of tinea pedis was 8·5% and of verruca 4·8%. The incidence of tinea pedis in 205 male adults was 21·5%, in 288 boys 6·3%, in 60 adult females 3·3%, and in 220 girls 0·9%. The incidence of verruca in juveniles ranged from 4·2% in boys to 10·5% in girls.
It was clear that both infections spread within the baths, and since a relatively small proportion of users admitted to taking precautions to avoid contracting or developing infections it seems advisable that more publicity about recommendations on foot care should be provided.
Onychomycosis in Icelandic Swimmers
The prevalence of culture-positive onychomycosis was 15% in women and 26% in men. Our results suggest that onychomycosis of the toenails is at least 3 times more prevalent in swimmers than in the rest of the population.
Does this mean that not only is going to the swimming pool not a cure of fungal infections, but it is actually the cause? Well, maybe not. While the articles show that there is a larger incidence of fungal infections among swimmers, they only show correlation, not causality. People who partake in sports activities have a bigger chance of having these infections than the general public. These are also the people who are more likely to go swimming.
To settle the matter for good, we need an article named "Prevalence of fungal infections among occasionally swimming couch potatoes" :-)
Why does programmed cell death, or apoptosis, occur? Does it take place among bacteria and fungi or only in the cells of higher organisms?
"In short, the question of why programmed cell death occurs should be subdivided into two related questions: Why are cells that die by programmed cell death generated? and Why do these cells die instead of surviving?
"The answer to the first of these questions depends on the cell being considered. For example, some cells are generated in excess and only those that become properly functional survive (as happens in parts of the nervous system). In some cases, the mechanism that generates cells that are needed also fortuitously generates unneeded ones as well (as happens in the immune system). And some cells that die are needed, but only transiently.
"Cells die either because they are harmful or because it takes less energy to kill them than to maintain them. At present, programmed cell death--as it is described based on the morphology of apoptosis and the biochemistry that involves a specific family of protein-cleaving enzymes--has been demonstrated to occur only in animals, although it remains possible that bacteria, fungi and plants use similar processes to eliminate unwanted cells."
Michael Hengartner, senior staff investigator at Cold Spring Harbor Laboratory, offered a more extensive investigation of the question:
"Let's start with the first part of the question: Why does programmed cell death occur? There are several reasons: it gets rid of cells that are not needed, in the way or potentially dangerous to the rest of the organism.
"Cells that are not needed may never have had a function. In other cases, they may have lost their function, or they may have competed and lost out to other cells. In some organisms, especially lower species, there are cells that die off very soon after they are born. There is no clear reason why they ever existed. These cells are probably evolutionary relics that were useful in the past, but no longer serve any valuable function. For an example of cells that lose their function, consider the cells in the tail of the tadpole, which become superfluous when the animal develops into a frog.
"An instance of cellular competition occurs in the developing human brain. The brain makes many more neurons than we need, probably because the body does not 'know' how many neurons will suffice and because wiring together an intricate structure such as the brain is not easy. For example, many neurons will fail to reach their targets--their axons may take a wrong turn or may terminate prematurely. These strays that fail to establish a proper connection will die. Death here functions as a built-in error-correcting mechanism.
"More generally, building a complex organism like a human being is like creating an intricate sculpture. Cell division forms the clay, whereas cell death sculpts the clay into the desired form. Consider human hands, which start out as paddlelike structures. Fingers develop in the paddles, but then the cells in the tissue between the fingers must die for a proper hand to form.
"One of the most fascinating reasons for cell death is to get rid of dangerous cells, those that could be harmful to the rest of the organism. One might say that the cells kill themselves for the greater good. They could be mutants that would become cancerous--apoptosis is therefore very important in the formation (or nonformation) of cancer. Also, positive and negative selection occur among the cells of the immune system. Cells that recognize 'self' (that is, ones that would attack the organism's own cells) are instructed to die during this process. Finally, cells that are infected by a virus can sometimes recognize the infection and kill themselves before the virus has time to replicate and spread to other cells.
"Programmed cell death, in the sense of suicide deliberately induced by the organism, certainly does occur in multicellular plants and fungi whether it occurs through the same molecular mechanism as the one found in metazoans (multicellular animals) remains to be determined. Cell death is common among plants, especially among the higher plants. The xylem in trees, through which water rises to the leaves, consists of spaces left by dead cells. Cell death occurs very visibly when deciduous trees drop their leaves in the fall. (Incidentally, this is where the name 'apoptosis' comes from: it is the Greek word for the falling of leaves from trees, as well as the losing of hair from balding men--which incidentally is also thought to involve apoptosis!) Plant cells cannot move, so plants use a slash-and-burn technique to cope with infection: all the cells in an infected area may kill themselves to halt the spread of the disease.
"Is there programmed cell death among single-celled organisms? The answer gets caught up in a question of semantics between a cell choosing to die and being forced to die. But some forms of programmed death are found in unicellular organisms, including bacteria. The death of the mother cell during sporulation, the process in which spores are created, could be considered a kind of programmed cell death. Certain parasites, such as trypanosomes (which cause malaria), change form to elude the immune response from their host the laggards who o fail to undergo the change will die off in a kind of cellular altruism.
"Another parallel example occurs among slime molds, such as Dictyostelium discoideum, a species at the interface between unicellular and multicellular organisms. These animals spend most of their lives as unicellular amoebae. But, when starved, the cells aggregate and meld into a single 'slug' that migrates and eventually forms a funguslike structure, consisting of a stalk topped by a ball of spores. The spores disperse in search of a more hospitable environment. The stalk cells do not reproduce, so in a sense they sacrifice themselves. In most single-celled organisms (particularly bacteria), it is not clear whether cell death follows the same pattern or biomolecular mechanisms as the apoptosis that occurs in higher organisms.
"One highly unusual form of cell death occurs in cells infected by certain plasmid viruses that instruct the host cell to create two chemicals: a long-lived toxin and an unstable antidote. During replication, about 1 percent of the cells lose the parasitic plasmid in their DNA the daughter cells still contain the toxin but can no longer manufacture the antidote, so they die. This is a rare instance of cellular murder rather than suicide.
Cyanobacteria are a group of photosynthetic bacteria, some of which are nitrogen-fixing, that live in a wide variety of moist soils and water either freely or in a symbiotic relationship with plants or lichen-forming fungi (as in the lichen genus Peltigera).  They range from unicellular to filamentous and include colonial species. Colonies may form filaments, sheets, or even hollow spheres. Some filamentous species can differentiate into several different cell types: vegetative cells – the normal, photosynthetic cells that are formed under favorable growing conditions akinetes – climate-resistant spores that may form when environmental conditions become harsh and thick-walled heterocysts – which contain the enzyme nitrogenase, vital for nitrogen fixation    in an anaerobic environment due to its sensitivity to oxygen. 
Nitrogen fixation Edit
Some cyanobacteria can fix atmospheric nitrogen in anaerobic conditions by means of specialized cells called heterocysts.   Heterocysts may also form under the appropriate environmental conditions (anoxic) when fixed nitrogen is scarce. Heterocyst-forming species are specialized for nitrogen fixation and are able to fix nitrogen gas into ammonia ( NH
3 ), nitrites (NO −
2 ) or nitrates (NO −
3 ), which can be absorbed by plants and converted to protein and nucleic acids (atmospheric nitrogen is not bioavailable to plants, except for those having endosymbiotic nitrogen-fixing bacteria, especially the family Fabaceae, among others).
Free-living cyanobacteria are present in the water of rice paddies, and cyanobacteria can be found growing as epiphytes on the surfaces of the green alga, Chara, where they may fix nitrogen.  Cyanobacteria such as Anabaena (a symbiont of the aquatic fern Azolla) can provide rice plantations with biofertilizer. 
Many cyanobacteria form motile filaments of cells, called hormogonia, that travel away from the main biomass to bud and form new colonies elsewhere.   The cells in a hormogonium are often thinner than in the vegetative state, and the cells on either end of the motile chain may be tapered. To break away from the parent colony, a hormogonium often must tear apart a weaker cell in a filament, called a necridium.
Each individual cell (each single cyanobacterium) typically has a thick, gelatinous cell wall.  They lack flagella, but hormogonia of some species can move about by gliding along surfaces.  Many of the multicellular filamentous forms of Oscillatoria are capable of a waving motion the filament oscillates back and forth. In water columns, some cyanobacteria float by forming gas vesicles, as in archaea.  These vesicles are not organelles as such. They are not bounded by lipid membranes but by a protein sheath.
Cyanobacteria can be found in almost every terrestrial and aquatic habitat – oceans, fresh water, damp soil, temporarily moistened rocks in deserts, bare rock and soil, and even Antarctic rocks. They can occur as planktonic cells or form phototrophic biofilms. They are found in endolithic ecosystems.  A few are endosymbionts in lichens, plants, various protists, or sponges and provide energy for the host. Some live in the fur of sloths, providing a form of camouflage. 
Aquatic cyanobacteria are known for their extensive and highly visible blooms that can form in both freshwater and marine environments. The blooms can have the appearance of blue-green paint or scum. These blooms can be toxic, and frequently lead to the closure of recreational waters when spotted. Marine bacteriophages are significant parasites of unicellular marine cyanobacteria. 
Cyanobacterial growth is favored in ponds and lakes where waters are calm and have little turbulent mixing.  Their life cycles are disrupted when the water naturally or artificially mixes from churning currents caused by the flowing water of streams or the churning water of fountains. For this reason blooms of cyanobacteria seldom occur in rivers unless the water is flowing slowly. Growth is also favored at higher temperatures which enable Microcystis species to outcompete diatoms and green algae, and potentially allow development of toxins. 
Based on environmental trends, models and observations suggest cyanobacteria will likely increase their dominance in aquatic environments. This can lead to serious consequences, particularly the contamination of sources of drinking water. Researchers including Linda Lawton at Robert Gordon University, have developed techniques to study these.  Cyanobacteria can interfere with water treatment in various ways, primarily by plugging filters (often large beds of sand and similar media) and by producing cyanotoxins, which have the potential to cause serious illness if consumed. Consequences may also lie within fisheries and waste management practices. Anthropogenic eutrophication, rising temperatures, vertical stratification and increased atmospheric carbon dioxide are contributors to cyanobacteria increasing dominance of aquatic ecosystems. 
Cyanobacteria have been found to play an important role in terrestrial habitats. It has been widely reported that cyanobacteria soil crusts help to stabilize soil to prevent erosion and retain water.  An example of a cyanobacterial species that does so is Microcoleus vaginatus. M. vaginatus stabilizes soil using a polysaccharide sheath that binds to sand particles and absorbs water. 
Some of these organisms contribute significantly to global ecology and the oxygen cycle. The tiny marine cyanobacterium Prochlorococcus was discovered in 1986 and accounts for more than half of the photosynthesis of the open ocean.  Circadian rhythms were once thought to only exist in eukaryotic cells but many cyanobacteria display a bacterial circadian rhythm.
"Cyanobacteria are arguably the most successful group of microorganisms on earth. They are the most genetically diverse they occupy a broad range of habitats across all latitudes, widespread in freshwater, marine, and terrestrial ecosystems, and they are found in the most extreme niches such as hot springs, salt works, and hypersaline bays. Photoautotrophic, oxygen-producing cyanobacteria created the conditions in the planet's early atmosphere that directed the evolution of aerobic metabolism and eukaryotic photosynthesis. Cyanobacteria fulfill vital ecological functions in the world's oceans, being important contributors to global carbon and nitrogen budgets." – Stewart and Falconer 
Cyanobacteria have several unique features. As the endosymbiotic plastids are endosymbiotic cyanobacteria, they share these features insofar as they have not lost them.
Carbon fixation Edit
Cyanobacteria use the energy of sunlight to drive photosynthesis, a process where the energy of light is used to synthesize organic compounds from carbon dioxide. Because they are aquatic organisms, they typically employ several strategies which are collectively known as a "carbon concentrating mechanism" to aid in the acquisition of inorganic carbon ( CO
2 or bicarbonate). Among the more specific strategies is the widespread prevalence of the bacterial microcompartments known as carboxysomes.  These icosahedral structures are composed of hexameric shell proteins that assemble into cage-like structures that can be several hundreds of nanometers in diameter. It is believed that these structures tether the CO
2 -fixing enzyme, RuBisCO, to the interior of the shell, as well as the enzyme carbonic anhydrase, using metabolic channeling to enhance the local CO
2 concentrations and thus increase the efficiency of the RuBisCO enzyme. 
Electron transport Edit
In contrast to purple bacteria and other bacteria performing anoxygenic photosynthesis, thylakoid membranes of cyanobacteria are not continuous with the plasma membrane but are separate compartments.  The photosynthetic machinery is embedded in the thylakoid membranes, with phycobilisomes acting as light-harvesting antennae attached to the membrane, giving the green pigmentation observed (with wavelengths from 450 nm to 660 nm) in most cyanobacteria. 
While most of the high-energy electrons derived from water are used by the cyanobacterial cells for their own needs, a fraction of these electrons may be donated to the external environment via electrogenic activity. 
Respiration in cyanobacteria can occur in the thylakoid membrane alongside photosynthesis,  with their photosynthetic electron transport sharing the same compartment as the components of respiratory electron transport. While the goal of photosynthesis is to store energy by building carbohydrates from CO2, respiration is the reverse of this, with carbohydrates turned back into CO2 accompanying energy release.
Cyanobacteria appear to separate these two processes with their plasma membrane containing only components of the respiratory chain, while the thylakoid membrane hosts an interlinked respiratory and photosynthetic electron transport chain.  Cyanobacteria use electrons from succinate dehydrogenase rather than from NADPH for respiration. 
Cyanobacteria only respire during the night (or in the dark) because the facilities used for electron transport are used in reverse for photosynthesis while in the light. 
Electron transport chain Edit
Many cyanobacteria are able to reduce nitrogen and carbon dioxide under aerobic conditions, a fact that may be responsible for their evolutionary and ecological success. The water-oxidizing photosynthesis is accomplished by coupling the activity of photosystem (PS) II and I (Z-scheme). In contrast to green sulfur bacteria which only use one photosystem, the use of water as an electron donor is energetically demanding, requiring two photosystems. 
Attached to the thylakoid membrane, phycobilisomes act as light-harvesting antennae for the photosystems.  The phycobilisome components (phycobiliproteins) are responsible for the blue-green pigmentation of most cyanobacteria.  The variations on this theme are due mainly to carotenoids and phycoerythrins that give the cells their red-brownish coloration. In some cyanobacteria, the color of light influences the composition of the phycobilisomes.   In green light, the cells accumulate more phycoerythrin, whereas in red light they produce more phycocyanin. Thus, the bacteria appear green in red light and red in green light.  This process of complementary chromatic adaptation is a way for the cells to maximize the use of available light for photosynthesis.
A few genera lack phycobilisomes and have chlorophyll b instead (Prochloron, Prochlorococcus, Prochlorothrix). These were originally grouped together as the prochlorophytes or chloroxybacteria, but appear to have developed in several different lines of cyanobacteria. For this reason, they are now considered as part of the cyanobacterial group.  
In general, photosynthesis in cyanobacteria uses water as an electron donor and produces oxygen as a byproduct, though some may also use hydrogen sulfide  a process which occurs among other photosynthetic bacteria such as the purple sulfur bacteria.
Carbon dioxide is reduced to form carbohydrates via the Calvin cycle.  The large amounts of oxygen in the atmosphere are considered to have been first created by the activities of ancient cyanobacteria.  They are often found as symbionts with a number of other groups of organisms such as fungi (lichens), corals, pteridophytes (Azolla), angiosperms (Gunnera), etc. 
There are some groups capable of heterotrophic growth,  while others are parasitic, causing diseases in invertebrates or algae (e.g., the black band disease).   
Primary chloroplasts are cell organelles found in some eukaryotic lineages, where they are specialized in performing photosynthesis. They are considered to have evolved from endosymbiotic cyanobacteria.   After some years of debate,  it is now generally accepted that the three major groups of primary endosymbiotic eukaryotes (i.e. green plants, red algae and glaucophytes) form one large monophyletic group called Archaeplastida, which evolved after one unique endosymbiotic event.    
The morphological similarity between chloroplasts and cyanobacteria was first reported by German botanist Andreas Franz Wilhelm Schimper in the 19th century  Chloroplasts are only found in plants and algae,  thus paving the way for Russian biologist Konstantin Mereschkowski to suggest the symbiogenic origin of the plastid in 1905.  Lynn Margulis brought this hypothesis back to attention more than 60 years later  but the idea did not become fully accepted until supplementary data started to accumulate. The cyanobacterial origin of plastids is now supported by various pieces of phylogenetic,    genomic,  biochemical   and structural evidence.  The description of another independent and more recent primary endosymbiosis event between a cyanobacterium and a separate eukaryote lineage (the rhizarian Paulinella chromatophora) also gives credibility to the endosymbiotic origin of the plastids. 
In addition to this primary endosymbiosis, many eukaryotic lineages have been subject to secondary or even tertiary endosymbiotic events, that is the "Matryoshka-like" engulfment by a eukaryote of another plastid-bearing eukaryote.  
Within this evolutionary context, it is noteworthy that, as far as we can tell, oxygenic photosynthesis only evolved once (in prokaryotic cyanobacteria), and all photosynthetic eukaryotes (including all plants and algae) have acquired this ability from them. In other words, all the oxygen that makes the atmosphere breathable for aerobic organisms originally comes from cyanobacteria or their later descendants. 
Cyanobacteria are challenged by environmental stresses and internally generated reactive oxygen species that cause DNA damage. Cyanobacteria possess numerous E. coli-like DNA repair genes.  Several DNA repair genes are highly conserved in cyanobacteria, even in small genomes, suggesting that core DNA repair processes such as recombinational repair, nucleotide excision repair and methyl-directed DNA mismatch repair are common among cyanobacteria. 
Cyanobacteria are capable of natural genetic transformation.    Natural genetic transformation is the genetic alteration of a cell resulting from the direct uptake and incorporation of exogenous DNA from its surroundings. For bacterial transformation to take place, the recipient bacteria must be in a state of competence, which may occur in nature as a response to conditions such as starvation, high cell density or exposure to DNA damaging agents. In chromosomal transformation, homologous transforming DNA can be integrated into the recipient genome by homologous recombination, and this process appears to be an adaptation for repairing DNA damage. 
Historically, bacteria were first classified as plants constituting the class Schizomycetes, which along with the Schizophyceae (blue-green algae/Cyanobacteria) formed the phylum Schizophyta,  then in the phylum Monera in the kingdom Protista by Haeckel in 1866, comprising Protogens, Protamaeba, Vampyrella, Protomonae, and Vibrio, but not Nostoc and other cyanobacteria, which were classified with algae,  later reclassified as the Prokaryotes by Chatton. 
The cyanobacteria were traditionally classified by morphology into five sections, referred to by the numerals I–V. The first three – Chroococcales, Pleurocapsales, and Oscillatoriales – are not supported by phylogenetic studies. The latter two – Nostocales and Stigonematales – are monophyletic, and make up the heterocystous cyanobacteria.  
The members of Chroococales are unicellular and usually aggregate in colonies. The classic taxonomic criterion has been the cell morphology and the plane of cell division. In Pleurocapsales, the cells have the ability to form internal spores (baeocytes). The rest of the sections include filamentous species. In Oscillatoriales, the cells are uniseriately arranged and do not form specialized cells (akinetes and heterocysts).  In Nostocales and Stigonematales, the cells have the ability to develop heterocysts in certain conditions. Stigonematales, unlike Nostocales, include species with truly branched trichomes. 
Most taxa included in the phylum or division Cyanobacteria have not yet been validly published under The International Code of Nomenclature of Prokaryotes (ICNP) except:
- The classes Chroobacteria, Hormogoneae, and Gloeobacteria
- The orders Chroococcales, Gloeobacterales, Nostocales, Oscillatoriales, Pleurocapsales, and Stigonematales
- The families Prochloraceae and Prochlorotrichaceae
- The genera Halospirulina, Planktothricoides, Prochlorococcus, Prochloron, and Prochlorothrix
Formerly, some bacteria, like Beggiatoa, were thought to be colorless Cyanobacteria. 
Stromatolites are layered biochemical accretionary structures formed in shallow water by the trapping, binding, and cementation of sedimentary grains by biofilms (microbial mats) of microorganisms, especially cyanobacteria. 
During the Precambrian, stromatolite communities of microorganisms grew in most marine and non-marine environments in the photic zone. After the Cambrian explosion of marine animals, grazing on the stromatolite mats by herbivores greatly reduced the occurrence of the stromatolites in marine environments. Since then, they are found mostly in hypersaline conditions where grazing invertebrates cannot live (e.g. Shark Bay, Western Australia). Stromatolites provide ancient records of life on Earth by fossil remains which date from 3.5 Ga ago.  As of 2010 [update] the oldest undisputed evidence of cyanobacteria is from 2.1 Ga ago, but there is some evidence for them as far back as 2.7 Ga ago. Oxygen concentrations in the atmosphere remained around or below 1% of today's level until 2.4 Ga ago (the Great Oxygenation Event). The rise in oxygen may have caused a fall in the concentration of atmospheric methane, and triggered the Huronian glaciation from around 2.4 to 2.1 Ga ago. In this way, cyanobacteria may have killed off much of the other bacteria of the time. 
Oncolites are sedimentary structures composed of oncoids, which are layered structures formed by cyanobacterial growth. Oncolites are similar to stromatolites, but instead of forming columns, they form approximately spherical structures that were not attached to the underlying substrate as they formed.  The oncoids often form around a central nucleus, such as a shell fragment,  and a calcium carbonate structure is deposited by encrusting microbes. Oncolites are indicators of warm waters in the photic zone, but are also known in contemporary freshwater environments.  These structures rarely exceed 10 cm in diameter.
One former classification scheme of cyanobacterial fossils divided them into the porostromata and the spongiostromata. These are now recognized as form taxa and considered taxonomically obsolete however, some authors have advocated for the terms remaining informally to describe form and structure of bacterial fossils. 
The unicellular cyanobacterium Synechocystis sp. PCC6803 was the third prokaryote and first photosynthetic organism whose genome was completely sequenced.  It continues to be an important model organism.  Cyanothece ATCC 51142 is an important diazotrophic model organism. The smallest genomes have been found in Prochlorococcus spp. (1.7 Mb)   and the largest in Nostoc punctiforme (9 Mb).  Those of Calothrix spp. are estimated at 12–15 Mb,  as large as yeast.
Recent research has suggested the potential application of cyanobacteria to the generation of renewable energy by directly converting sunlight into electricity. Internal photosynthetic pathways can be coupled to chemical mediators that transfer electrons to external electrodes.  In the shorter term, efforts are underway to commercialize algae-based fuels such as diesel, gasoline, and jet fuel.   
Researchers from a company called Algenol have cultured genetically modified cyanobacteria in sea water inside a clear plastic enclosure so they first make sugar (pyruvate) from CO
2 and the water via photosynthesis. Then, the bacteria secrete ethanol from the cell into the salt water. As the day progresses, and the solar radiation intensifies, ethanol concentrations build up and the ethanol itself evaporates onto the roof of the enclosure. As the sun recedes, evaporated ethanol and water condense into droplets, which run along the plastic walls and into ethanol collectors, from where it is extracted from the enclosure with the water and ethanol separated outside the enclosure. As of March 2013, Algenol was claiming to have tested its technology in Florida and to have achieved yields of 9,000 US gallons per acre per year.  This could potentially meet US demands for ethanol in gasoline in 2025, assuming a B30 blend, from an area of around half the size of California's San Bernardino County, requiring less than one-tenth of the area than ethanol from other biomass, such as corn, and only very limited amounts of fresh water. 
Cyanobacteria may possess the ability to produce substances that could one day serve as anti-inflammatory agents and combat bacterial infections in humans.  Cyanobacteria's photosynthetic output of sugar and oxygen has been demonstrated to have therapeutic value in rats with heart attacks. 
Spirulina's extracted blue color is used as a natural food coloring. 
Possible use off-Earth, e.g. Mars Edit
Researchers from several space agencies argue that cyanobacteria could be used for producing goods for human consumption in future manned outposts on Mars, by transforming materials available on this planet. 
Some cyanobacteria can produce neurotoxins, cytotoxins, endotoxins, and hepatotoxins (e.g., the microcystin-producing bacteria genus microcystis), which are collectively known as cyanotoxins.
Specific toxins include anatoxin-a, guanitoxin, aplysiatoxin, cyanopeptolin, cylindrospermopsin, domoic acid, nodularin R (from Nodularia), neosaxitoxin, and saxitoxin. Cyanobacteria reproduce explosively under certain conditions. This results in algal blooms which can become harmful to other species and pose a danger to humans and animals if the cyanobacteria involved produce toxins. Several cases of human poisoning have been documented, but a lack of knowledge prevents an accurate assessment of the risks.    
Recent studies suggest that significant exposure to high levels of cyanobacteria producing toxins such as BMAA can cause amyotrophic lateral sclerosis (ALS). People living within half a mile of cyanobacterially contaminated lakes have had a 2.3 times greater risk of developing ALS than the rest of the population people around New Hampshire's Lake Mascoma had an up to 25 times greater risk of ALS than the expected incidence.  BMAA from desert crusts found throughout Qatar might have contributed to higher rates of ALS in Gulf War veterans.  
Several chemicals can eliminate cyanobacterial blooms from smaller water-based systems such as swimming pools. They include calcium hypochlorite, copper sulphate, cupricide, and simazine.  The calcium hypochlorite amount needed varies depending on the cyanobacteria bloom, and treatment is needed periodically. According to the Department of Agriculture Australia, a rate of 12 g of 70% material in 1000 l of water is often effective to treat a bloom.  Copper sulfate is also used commonly, but no longer recommended by the Australian Department of Agriculture, as it kills livestock, crustaceans, and fish.  Cupricide is a chelated copper product that eliminates blooms with lower toxicity risks than copper sulfate. Dosage recommendations vary from 190 ml to 4.8 l per 1000 m 2 .  Ferric alum treatments at the rate of 50 mg/l will reduce algae blooms.   Simazine, which is also a herbicide, will continue to kill blooms for several days after an application. Simazine is marketed at different strengths (25, 50, and 90%), the recommended amount needed for one cubic meter of water per product is 25% product 8 ml 50% product 4 ml or 90% product 2.2 ml. 
Some cyanobacteria are sold as food, notably Arthrospira platensis (Spirulina) and others (Aphanizomenon flos-aquae) . 
Some microalgae contain substances of high biological value, such as polyunsaturated fatty acids, amino acids, proteins, pigments, antioxidants, vitamins, and minerals.  Edible blue-green algae reduce the production of pro-inflammatory cytokines by inhibiting NF-κB pathway in macrophages and splenocytes.  Sulfate polysaccharides exhibit immunomodulatory, antitumor, antithrombotic, anticoagulant, anti-mutagenic, anti-inflammatory, antimicrobial, and even antiviral activity against HIV, herpes, and hepatitis. 
Cyanobacteria activity turns Coatepeque Caldera lake a turquoise color
Cyanobacterial bloom near Fiji
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This article incorporates text available under the CC BY 2.5 license.
Why It’s Time to Stop Punishing Our Soils with Fertilizers
Researcher Rick Haney travels the U.S. preaching the benefits of healthy soils. In a Yale Environment 360 interview, he talks about the folly of pursuing ever-greater crop yields using fertilizers and other chemicals and how farmland can by restored through natural methods.
The soil health movement has been in the news lately, and among its leading proponents is U.S. Department of Agriculture (USDA) researcher Rick Haney. In a world where government agencies and agribusiness have long pursued the holy grail of maximum crop yield, Haney preaches a different message: The quest for ever-greater productivity — using fertilizers, herbicides, pesticides, and whatever other chemicals are at hand — is killing our soil and threatening our farms.
Soil researcher Rick Haney of the U.S. Department of Agriculture USDA
Haney, who works with the USDA’s Agriculture Research Service in Texas, conducts online seminars and travels the country teaching farmers how to create healthy soil. His message is simple: Although the United States has some of the richest soils in the world, decades of agricultural abuse have taken their toll, depleting the dirt of essential nutrients and killing off bacteria and fungi that create organic material essential to plants. “Our mindset nowadays is that if you don’t put down fertilizer, nothing grows,” says Haney, who has developed a well-known method for testing soil health. “But that’s just not true, and it never has been.”
In an interview with Yale Environment 360, Haney describes how research is validating the value of natural methods such as plowing less, growing cover crops, and using biological controls to keep pests in check. In the face of a proposed 21 percent cut in the USDA’s budget by the Trump administration, Haney also stressed the importance of unbiased, government studies in a field where research is often dominated by the very corporations that benefit from overuse of fertilizers and chemicals. “We need more independent research,” Haney maintains. “We are only at the tip of the iceberg in terms of what we understand about how soil functions and its biology.”
Yale Environment 360: You’ve been working with farmers to improve their soil?
Rick Haney: That’s right. We know that over the past 50 years the levels of organic matter — it is kind of a standard test for soil in terms of its health and fertility — have been going way down. That’s alarming. We see organic matter levels in some fields of 1 percent or less. Whereas you can go to a pasture sitting right next to it where organics levels are 5 percent or 6 percent. So that is how drastically we have altered these systems. We are destroying the organic matter in the soil, and we’ve got to bring that back to sustain life on this planet.
The good news is that soil will come back if you give it a chance. It is very robust and resilient. It’s not like we have destroyed it to the point where it can’t be fixed. The soil health movement is trying to bring those organic levels back up and get soil to a higher functioning state.
e360: What has caused this decline in soil quality?
Haney: We see that when there is a lot of tillage, no cover crops, a system of high intensity [chemical-dependent] farming, that the soil just doesn’t function properly. The biology is not doing much. It’s not performing as we need it to. We are essentially destroying the functionality of soil, so that you have to feed it more and more synthetic fertilizers just to keep growing this crop.
e360: So it’s like a drug addict who needs a bigger and bigger fix each year?
Haney: That’s correct. It’s true that we are seeing that our yields have come up a lot in the last 50 years, but it is taking more and more external inputs to keep it going. And that’s not sustainable, it’s not going to work in the long run.
e360: Farmers say they need the fertilizer because the soil is depleted.
Haney: We were applying fertilizers and getting these big yields, so that system seemed to be working — until we began seeing, for example, the dead zone in the Gulf of Mexico [created by algal blooms triggered by high nitrogen levels from fertilizer], and we started wondering if this was really working right. Are we putting on too much fertilizer? And the answer is, “Yes we are.” It’s like instead of feeding your children a balanced diet, let’s just feed them vitamins. That’s not going to work, is it?
Our mindset nowadays is that if you don’t put down fertilizer, nothing grows. But that’s just not true, and it never has been. The biggest issue with all this is that we keep wanting to get higher and higher yields. But the reality is that you are shooting yourself in the foot doing that.
e360: How so?
Haney: Well, if we are going to overproduce corn, wheat, soy, sorghum — look at the price. Why is the price low? Right now, these guys are planting corn around here, and I’ve talked to several of them who tell me that they won’t be making any profit this year. They are looking at a loss. It’s just crazy. If you are going to overproduce your product, the price drops. So what are we doing?
We had a guy I talked to last week who said, “If I adopt these soil health principles, my yields will fall.” And I said, “Yeah, I hope so, I hope everyone’s yields fall.” There’s just this mindset that we’ve got to increase the yields, increase the yields, increase the yields. You can’t keep doing that.
e360: So you’re saying that this obsession with increasing yields has been destructive to the farmer’s bottom line and ultimately destructive to the soil that farming depends on?
Haney: Absolutely. Let’s produce an adequate amount of these commodities, but not too much. That way the price will come up and farmers can actually make a profit doing this. Farmers have such slim margins on their profits. So if we can make them more efficient with their fertilizer use and still produce the same amount of crop, that is a win for everybody. Let’s get that soil back to a healthier state where we don’t need to put so much fertilizer on and begin to work with nature instead of against it.
e360: What about pesticides — do they harm the biological activity in the soil?
Haney: Yes, it’s like chemotherapy for cancer: It’s not targeted, it just kills everything. Something similar happens in the soil when we use fungicides and pesticides. Pesticides kill the good bugs as well as the bad bugs. Fungicides kill all the fungi in the soil, including the helpful ones. But fungi are absolutely essential. We need to bring the fungi back, not kill them off. If you go into a forest, which contains some of the most fertile soils you will ever see, peel the leaf matter back and you will see fungi everywhere.
e360: Our efforts to control nature often backfire.
Haney: Our approach is to manipulate what’s happening out there by plowing and adding lots of chemicals. Nature is always going to win in the end. We can come up with these things to kill this weed or this insect, but eventually you need to come up with something different because nature is going to find a way around that. Look at the resistance that weeds are developing to Roundup [the herbicide glyphosate] now.
The usual program is, “Let’s kill everything and grow what we want,” instead of, “Let’s grow a lot of different things to help grow what we want more efficiently.” That’s a very different mindset. We need to work with the natural system instead of trying to fight against it.
e360: Does too much fertilizer also disturb the biology of the soil?
Haney: I believe it does. We see that. In those fields the microbe activity is low, organic matter is low. There has been some research showing that these high nitrogen inputs are destroying the carbon in the soil. Because the microbes use up the extra nitrogen and then they really tear the carbon out, creating lots of C02, rather than sequestering it in the soil. So there is evidence that excessive nitrogen actually causes more carbon to leave the system. Whereas we need more carbon in the soil rather than less.
e360: The Paris Climate Accord called for an increase of carbon in the soils by 0.4 percent a year. So how do we do that?
Haney: We hear a lot about the need to plant trees, to not cut the rainforests and that’s all important. But we have this huge resource — all over the world — of dirt that is sitting there with nothing on it. When we plant plants on it, it starts sucking carbon out of the air and putting it in the soil. That’s what the natural process is.
We should never have soil bare — ever. Right now, farmers leave their fields bare for much of the year. If they would only plant a diverse, multi-species cover crop, just think of the carbon that we could sequester out of the atmosphere and put into the soil on the 150 million acres of corn and wheat land in this country. We could pull a phenomenal amount of carbon back into the soil, which is where it is supposed to be.
e360: Cover crops also do a lot to return nutrients to the soil. Legumes, for example, enrich the soil with nitrogen.
Haney: That’s right, and carbon, too. This is something farmers were forced to do before they had fertilizers. When I did my Ph.D. dissertation, I referenced a lot of papers from the 1910s, ’20s and ’30s. They were already studying the biological components of soil, and they knew how important it was. And then synthetic fertilizers came along, and we just forgot about all that, we just ignored it.
Currently we have this conservation reserve system where we pay farmers to take their fields out of production. We should be planting these with cover crops after the harvest and letting them grow until everything freezes and over-winters. And you could have contracts where you let other farmers graze that land, because when you get the cover crops in there and the animals back in the system, now you are reproducing the Midwest when it was still a prairie and the buffalo were there. If you bring animals in, it really boosts the health of the soil.
e360: You helped to develop a new way to test soil. Why was that needed?
Haney: Until now, we weren’t testing for the right components. We were basically ignoring the biological contributions to nitrogen and phosphate, for example. The estimates that you see in the literature are that one gram of dirt can contain 6 to 10 million organisms. Without them, nothing would grow. The microorganisms are after carbon. And the plant roots will leak out carbon compounds that attract the microorganisms. In exchange, the microbes break down organic matter in the soil, which delivers nitrogen and phosphate in a form that the plant can use. So there is this beautiful nutrient cycle around the plant root. And that is something that we have tried to reproduce in the lab with our new testing method.
We dry the soils and then re-wet them and we measure the amount of C02 [a product of bacterial activity] coming out of the soil in 24 hours. The amount of C02 is directly proportional to how healthy that soil is. It’s amazingly simple.
e360: When farmers see the low levels of biological functioning in their soil, they may be inspired to practice some of the healthy techniques that you have been talking about?
Haney: Our job is to give farmers the confidence to make these changes. We say, “Try this out on 100 acres. I’m not saying do this on all your 2,000 acres. Use baby steps. And if it works for you, adopt it.” We’ve had guys who tell me, “You saved me $60,000 in fertilizer costs last year. “And my response to that is, “No, you saved the money because you chose to trust the data.” We get those calls a lot. Those guys are shocked.
e360: They see quick results?
Haney: Not always. The soil health movement is just getting started and people are saying that within two or three years you’re going to transform your soil. Well, I say it took 50 years to basically destroy it, so it is going to take more than two or three years to build it back. So we need to be in this for the long haul. But the direction is clear.
e360: Where do we go from here?
Haney: We need more independent research. We are only at the tip of the iceberg in terms of what we understand about how soil functions and its biology. We are at the beginning, and anyone who tells you that they know what is going on in soil is either lying or trying to sell you something. It’s mind-bogglingly complex to understand all the interactions, because it’s a dynamic living system.
e360: The new administration has threatened huge cuts in science research budgets in many agencies. Do you expect your program to be affected?
Haney: My research budget has been cut, cut, and cut. I’m not saying that the government needs to throw an enormous amount of money at us. But give us enough to function properly. We can’t have private industry doing all the research. Government needs to fill in the gaps, because you can’t guarantee that industry-funded research is unbiased.
e360: The agricultural industry has a vested interest in selling these pesticides and fertilizers. They are not likely to fund research into methods that use less of that stuff.
Haney: That’s right. My concern is, we’re not really very forward-thinking in politics these days. It’s all instant gratification. No long-term policy goals. That’s not smart. That’s not how our Founding Fathers thought. They looked way down the road. What happened to that?
Richard Schiffman reports on the environment and health for a variety of publications that include The New York Times, Scientific American, the Atlantic and Yale Environment 360. His latest book is a collection of nature-inspired poems entitled "What the Dust Doesn't Know." More about Richard Schiffman →
Scientists seek a deeper understanding of how silver kills bacteria
Silver’s popularity as a bacteria killer has led to companies embedding tiny, nano-sized silver particles in running shirts, underwear, socks, shoe insoles, food cutting boards, toothbrushes and an expanding array of other "antibacterial" consumer goods. But there is concern that these growing non-medical applications could lead to some bacterial strains becoming resistant to silver and other antimicrobial metals, says Natalie Gugala, a PhD student in Ray Turner’s lab at the University of Calgary. Credit: Riley Brandt, University of Calgary
Silver has been used for centuries as an antimicrobial to kill harmful bacteria. Ancient civilizations applied the metal to open wounds. Ship captains tossed silver coins into storage barrels to keep drinking water fresh.
In hospitals today, silver is used in bandages to treat burn victims, destroy pathogenic microbes on catheters, and combat dangerous "superbugs" that have grown resistant to traditional antibiotic drugs.
But the molecular mechanisms of how silver kills bacteria, and how resistance to silver develops in these microorganisms, are not fully understood. Now a new study, led by Faculty of Science biological scientists at the University of Calgary, helps enhance understanding of silver's antibacterial properties.
The research team performed a chemical genetic screen on a "library" of 4,000 mutant strains of the bacterium Escherichia coli (E. coli), in which a unique gene in each strain has been "knocked out," or deleted.
The team identified the genes in all these strains that showed either resistance or sensitivity when exposed to silver—producing the first genetic map of the genes that contribute to either silver resistance or toxicity in E. coli.
"Our study is the first of its kind to evaluate the genetic response in cells allowed to grow in the presence of silver, and thus provide a list of genes for resistance and toxicity, and map them to biological processes," says Dr. Raymond Turner, PhD, professor of biochemistry in the Department of Biological Sciences.
Study pinpoints new genes and molecular mechanisms involved in silver toxicity
Natalie Gugala, a PhD student of Turner's, mapped all 225 genes that were either resistant or sensitive to their corresponding biological pathways. These cellular mechanisms included transporting metals through the cell wall, energy producing, regulating the cell, and other processes.
"We've shown that there are many different genes that are likely affected and several different pathways," says Gugala, lead author of the team's scientific paper.
"It is likely that silver acts in multiple ways on bacteria," says Dr. Gordon Chua, PhD, associate professor of integrative cell biology in the Department of Biological Sciences. "Our study identified new genes and molecular mechanisms involved in silver toxicity as well as resistance."
The team's paper, "Using a Chemical Genetic Screen to Enhance Our Understanding of the Antibacterial Properties of Silver," is published in the journal Genes.
The important role of molecules in our health
E. coli is just one of many microorganisms that can cause illness and life-threatening infections. Many bacteria and other microbes are becoming increasingly resistant to traditional antibiotics.
The team's research fits well with the Faculty of Science's Grand Challenges. Specifically, "Personalized Health at the Molecular Level" prioritizes research aimed at minimizing antibiotic resistance, and understanding the role molecules have in our health.
"We need to understand how silver works if we're going to continue using it and before we develop more silver-based antimicrobials," Turner says.
Along with antibiotics: custom-designed metal antimicrobials
Determining at the molecular level how silver and other metals, such as copper and gallium, are able to kill bacteria could lead to improved medical therapies. Some research shows adding a metal to a traditional antibiotic that doesn't work anymore makes the drug effective again, Turner notes. "I foresee us using custom-designed metal antimicrobials along with antibiotics.
"This personalized health approach, using studies like ours, leads to identifying a set of marker genes that could be used to select specific metal-antimicrobial therapies tailored to combat bacterial infections in individual patients," he adds.
Silver's popularity as a bacteria killer has led to companies embedding tiny, nano-sized silver particles in running shirts, underwear, socks, shoe insoles, food cutting boards, toothbrushes and an expanding array of other "antibacterial" consumer goods.
But there is concern that these growing non-medical applications could lead to some bacterial strains becoming resistant to silver and other antimicrobial metals—as some bacteria have done with traditional antibiotics. "We need to be sure that we're using these metals in the appropriate setting," Gugala says. "If we know how they work, we might be able to better prevent their inappropriate use."
Robotics helped screen bacteria
The team performed their chemical genetic screen using a robot, designed for automated handling and processing of high-density bacterial colony plates, in Chua's laboratory.
Researchers then used "colony-scoring" software to measure the differences in growth and size of each plate's bacterial colony. E. coli strains with genes deleted involved in producing sensitivity, or toxicity, to silver grew larger colonies. Strains with genes deleted involved with resistance grew smaller colonies.
The team used a novel chronic, non-lethal exposure approach compared with most previous research, which exposed bacteria to acute, lethal dosages of silver to determine toxicity only.
Kate Chatfield-Reed, then a PhD student of Chua's, helped "normalize," or standardize, the data to identify strains showing statistically significant changes in growth rate when exposed to silver, compared with untreated control plates.
Why don't sea slugs and sea snails melt in salt water?
land snails and slugs melt when you put salt on them, how can similar creatures live in salt water? What's the difference?
When you salt a slug you create a difference in the salt content in their cells and the outside environment. This causes the water in their cells to diffuse towards the higher concentration of salt outside. This makes it look like they are melting.
The difference is there is a balance between the salt inside a sea slug and its marine environment. If you removed it from the water and doused it in salt, its likely they would also easily dehydrate as they lack a more robust barrier to direct contact with the salt.
Marine gastropods have internal osmolarity equivalent, or just about, to the ambient osmolarity of those salts. Terrestrial gastropods are similar, but aren't completely adapted like marine gastropods are, for submersion in saline water.
They are, however, the same in that pouring salt on them would have the same effect. When you pour pure salt on a slug, it's essentially 100% salt externally. Marine gastropods live in saltwater that is around 35 psu (formerly ppt), which is 3.5% concentration. That is the biggest difference in this scenario.
Why doesn't submersion in water kill fungi? - Biology
Control of Microbial Growth (page 1)
In the 19th century, surgery was risky and dangerous, and patients undergoing even the most routine operations were at very high risk of infection. This was so because surgery was not performed under aseptic conditions. The operating room, the surgeon's hands, and the surgical instruments were laden with microbes, which caused high levels of infection and mortality.
Surgeons in the mid-1800s often operated wearing their street clothes, without washing their hands. They frequently used ordinary sewing thread to suture wounds, and stuck the needles in the lapels of their frock coats in between patients. Surgical dressings were often made up of surplus cotton or jute from the floors of cotton mills. It was against this background that French scientist Louis Pasteur demonstrated that invisible microbes caused disease.
Pasteur's work influenced the English surgeon Joseph Lister, who applied Pasteur's germ theory of disease to surgery, thus founding modern antiseptic surgery. To disinfect, Lister used a solution of carbolic acid (phenol), which was sprayed around the operating room by a handheld sprayer.
19th Century surgery using Lister's carbolic acid sprayer.
It was clear that Lister's techniques were effective in increasing the rates of surviving surgery, but his theories were controversial because many 19th century surgeons were unwilling to accept something they could not see. Also, perhaps another reason that surgeons were slow to pick up on Lister's methods was the fact that during surgery they were required to breathe an irritating aerosol of phenol.
Control of Microbial Growth
The control of microbial growth is necessary in many practical situations, and significant advances in agriculture, medicine, and food science have been made through study of this area of microbiology.
"Control of microbial growth", as used here, means to inhibit or prevent growth of microorganisms. This control is affected in two basic ways: (1) by killing microorganisms or (2) by inhibiting the growth of microorganisms. Control of growth usually involves the use of physical or chemical agents which either kill or prevent the growth of microorganisms. Agents which kill cells are called cidal agents agents which inhibit the growth of cells (without killing them) are referred to as static agents. Thus, the term bactericidal refers to killing bacteria, and bacteriostatic refers to inhibiting the growth of bacterial cells. A bactericide kills bacteria, a fungicide kills fungi, and so on.
In microbiology, sterilization refers to the complete destruction or elimination of all viable organisms in or on a substance being sterilized. There are no degrees of sterilization: an object or substance is either sterile or not. Sterilization procedures involve the use of heat, radiation or chemicals, or physical removal of cells.
Methods of Sterilization
Heat : most important and widely used. For sterilization one must consider the type of heat, and most importantly, the time of application and temperature to ensure destruction of all microorganisms. Endospores of bacteria are considered the most thermoduric of all cells so their destruction guarantees sterility.
Incineration: burns organisms and physically destroys them. Used for needles, inoculating wires, glassware, etc. and objects not destroyed in the incineration process.
Boiling: 100 o for 30 minutes. Kills everything except some endospores. To kill endospores, and therefore sterilize a solution, very long (>6 hours) boiling, or intermittent boiling is required (See Table 1 below).
Autoclaving (steam under pressure or pressure cooker)
Autoclaving is the most effective and most efficient means of sterilization. All autoclaves operate on a time/temperature relationship. These two variables are extremely important. Higher temperatures ensure more rapid killing. The usual standard temperature/pressure employed is 121ºC/15 psi for 15 minutes. Longer times are needed for larger loads, large volumes of liquid, and more dense materials. Autoclaving is ideal for sterilizing biohazardous waste, surgical dressings, glassware, many types of microbiologic media, liquids, and many other things. However, certain items, such as plastics and certain medical instruments (e.g. fiber-optic endoscopes), cannot withstand autoclaving and should be sterilized with chemical or gas sterilants. When proper conditions and time are employed, no living organisms will survive a trip through an autoclave.
Schematic diagram of a laboratory autoclave in use to sterilize microbiological culture medium. Sterilization of microbiological culture media is is often carried out with the autoclave. When microbiological media are prepared, they must be sterilized and rendered free of microbial contamination from air, glassware, hands, etc. The sterilization process is a 100% kill, and guarantees that the medium will stay sterile unless exposed to contaminants.
An autoclave for use in a laboratory or hospital setting.
Why is an autoclave such an effective sterilizer? The autoclave is a large pressure cooker it operates by using steam under pressure as the sterilizing agent. High pressures enable steam to reach high temperatures, thus increasing its heat content and killing power. Most of the heating power of steam comes from its latent heat of vaporization. This is the amount of heat required to convert boiling water to steam. This amount of heat is large compared to that required to make water hot. For example, it takes 80 calories to make 1 liter of water boil, but 540 calories to convert that boiling water to steam. Therefore, steam at 100º C has almost seven times more heat than boiling water.
Moist heat is thought to kill microorganisms by causing denaturation of essential proteins. Death rate is directly proportional to the concentration of microorganisms at any given time. The time required to kill a known population of microorganisms in a specific suspension at a particular temperature is referred to as thermal death time (TDT) . Increasing the temperature decreases TDT, and lowering the temperature increases TDT. Processes conducted at high temperatures for short periods of time are preferred over lower temperatures for longer times.
Pick the right water
It turns out that using the right kind of water makes a difference in a water bath. Tap water is not right because of the dissolved ions. Using tap water can cause scaly buildup at the least and even chlorinedriven corrosion in some cases.
Some scientists use water from a lab purification unit. Surely, that is a good choice, right? Not necessarily, because even that water can corrode stainless steel. Some lab purification units include a salt back flush that can leave sodium ions in the water, and that&rsquos what corrodes the stainless steel. That kind of water could even put pits in a water bath&rsquos surface.
Instead, the best choice is just distilled or deionized water. That should be exactly what a water bath needs, but there&rsquos more.
Just adding the right water can extend the life of a water bath and keep it from looking flaky and fouled up on the surface, but that won&rsquot be enough to back off the lagoon syndrome. For that, adding a commercial algicide or biocide can do the trick.
Other Important Factors to Consider
What is antifungal soap?
An antifungal soap is a type of soap that contains one or more ingredients that can kill and wash away bacteria and fungi. These usually have antibacterial and disinfectant properties to effectively get rid of fungi.
They should also have soothing ingredients that can help treat infected skin. Many people who are unfortunate to catch these infections end up with dry, flaky, itchy skin, so trying to tame the irritation is key.
Because of the dryness and scaliness of many fungal infections, antifungal soap is ideally moisturizing. Rich oils and butter can help make the skin soft and supple again post-infection. They also double as soothing ingredients because they are emollients that can coat the infected skin, providing relief at least temporarily.
How does antifungal soap work?
Active ingredients that can kill fungus work directly on the infected surface. They kill any leftover colonies that have begun developing on the skin to ensure that the infection doesn’t spread or worsen. They also wash away any impurities like dirt or sweat, because these can further irritate the infected skin.
If the soap has soothing ingredients, they help the skin’s surface become less inflamed and irritated. Many soaps provide immediate relief because of ingredients like tea tree oil or vegetable glycerin.
Who is this kind of soap for?
Anyone can be unlucky to contract a fungal infection if they’re not careful. Therefore, it’s a soap that can be used by people of all ages and skin types.
However, they are especially useful for active people—mostly the athletes, sports enthusiasts, and gym buffs. Some fungal infections start when we sweat too much and cause dampness and humidity in certain parts of the body. That is exactly what happens in athlete’s foot (foot sweat) and jock itch (sweat near the genitals and inner thighs).
By using antifungal soap regularly, people who sweat a lot can avoid contracting fungal infections that are difficult to manage.
What are the different types of antifungal soaps?
Most antifungal soaps fall under two main categories: bar soaps and liquid body washes. Most antifungal ingredients can be found in either of the formats. While both can be very effective for killing fungus, each type has its pros and cons.
Bar soaps are easier to use because all you need to do is rub it all over your body, paying special attention to infected areas. However, they run out way faster because they can melt easily, especially when the bar soap is made mostly of organic and essential oils.
Liquid soaps, on the other hand, are easier to share with other members of the house. That’s because sharing a dispenser is way more hygienic than sharing a bar of soap that everyone rubs around their body. The downside is that liquid soaps are less portable because they come in huge bottles.
Why do you need an antifungal body wash?
When you have a fungal infection, the doctor will most likely prescribe you with medicine, whether oral or topical. However, sometimes these treatments are not enough. Your skin will still feel overly dry, and you’re still vulnerable to rashes, scaling, and small lesions.
An antifungal soap or body wash can help out with that. Showering with these is a great way to provide immediate relief, which oral drugs can’t promise. An antifungal soap works directly on the infected skin, washing away any new fungus or bacteria. It can also get rid of product buildup from topical creams and powders applied throughout the day.
How do antibiotics kill bacterial cells but not human cells?
In order to be useful in treating human infections, antibiotics must selectively target bacteria for eradication and not the cells of its human host. Indeed, modern antibiotics act either on processes that are unique to bacteria--such as the synthesis of cell walls or folic acid--or on bacterium-specific targets within processes that are common to both bacterium and human cells, including protein or DNA replication. Following are some examples.
Most bacteria produce a cell wall that is composed partly of a macromolecule called peptidoglycan, itself made up of amino sugars and short peptides. Human cells do not make or need peptidoglycan. Penicillin, one of the first antibiotics to be used widely, prevents the final cross-linking step, or transpeptidation, in assembly of this macromolecule. The result is a very fragile cell wall that bursts, killing the bacterium. No harm comes to the human host because penicillin does not inhibit any biochemical process that goes on within us.
Bacteria can also be selectively eradicated by targeting their metabolic pathways. Sulfonamides, such as sulfamethoxazole, are similar in structure to para-aminobenzoic acid, a compound critical for synthesis of folic acid. All cells require folic acid and it can diffuse easily into human cells. But the vitamin cannot enter bacterial cells and thus bacteria must make their own. The sulfa drugs such as sulfonamides inhibit a critical enzyme--dihydropteroate synthase--in this process. Once the process is stopped, the bacteria can no longer grow.
Another kind of antibiotic--tetracycline--also inhibits bacterial growth by stopping protein synthesis. Both bacteria and humans carry out protein synthesis on structures called ribosomes. Tetracycline can cross the membranes of bacteria and accumulate in high concentrations in the cytoplasm. Tetracycline then binds to a single site on the ribosome--the 30S (smaller) ribosomal subunit--and blocks a key RNA interaction, which shuts off the lengthening protein chain. In human cells, however, tetracycline does not accumulate in sufficient concentrations to stop protein synthesis.
Similarly, DNA replication must occur in both bacteria and human cells. The process is sufficiently different in each that antibiotics such as ciprofloxacin--a fluoroquinolone notable for its activity against the anthrax bacillus--can specifically target an enzyme called DNA gyrase in bacteria. This enzyme relaxes tightly wound chromosomal DNA, thereby allowing DNA replication to proceed. But this antibiotic does not affect the DNA gyrases of humans and thus, again, bacteria die while the host remains unharmed.
Many other compounds can kill both bacterial and human cells. It is the selective action of antibiotics against bacteria that make them useful in the treatment of infections while at the same time allowing the host to live another day.