Where can I get fungal extracts?

Where can I get fungal extracts?

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Does anyone know how I can get fungal extracts from fungal isolates? I have isolates in PDA slants and I'm gonna need to get their respective extracts to impregnate in sterile discs. I'm a novice in the field and all the help I can get will be greatly appreciated.

Making Agar Plates

Agar plates are the standard solid support material for growing microorganisms. Microbial growth media contains nutrients and an energy source to fuel the microbes as they grow, and agar to keep the media in a semi-solid, gel-like state.

On solid media, a single microbe will grow and divide to produce a "colony," a spot of identical descendants. Different types of microbes produce colonies with different characteristics-shape, color, texture-which help microbiologists determine if a culture is pure, or identify the types of microbes in a mixed sample.

A number of biological supply companies sell pre-made plates, but making your own is much less expensive. With a little practice, you will find that it is very easy to make your own plates, and you will have the added flexibility of being able to customize recipes to suit your needs.

Antifungal Resistance

Fungal infections that resist treatment are a challenge to the public&rsquos health.

Medical illustration of Candida spp., presented in CDC&rsquos Antibiotic Resistance Threats in the United States, 2019.

The problem

Antifungal drugs treat fungal infections by killing or stopping the growth of dangerous fungi in the body. Fungi, like bacteria, can develop antibiotic resistance, when germs like bacteria and fungi develop the ability to defeat the drugs designed to kill them. Antifungal resistance occurs when fungi no longer respond to antifungal drugs.

Only three types of antifungal drugs currently exist, so antifungal resistance can severely limit treatment options. Some types of fungi, like Candida auris, can become resistant to all three drug types. 1 Resistance is especially concerning for patients with invasive fungal infections&mdashsevere infections that affect the blood, heart, brain, eyes, or other parts of the body&mdashbecause these are serious infections that may be more difficult to treat if they are resistant and if antifungal treatment is limited. For example, bloodstream infections with the fungus Candida (a yeast) that are resistant to treatment can cause serious health problems, including disability and death.

What causes antifungal resistance?

Some species of fungi are naturally resistant to treatment with certain types of antifungal drugs. For example, the drug fluconazole does not work against infections caused by the fungus Aspergillus, a type of mold. Resistance can also develop over time when fungi are exposed to antifungal drugs. This resistance can occur when antifungal drugs are used improperly to treat sick people (e.g., when dosages are too low, or when treatment courses are not long enough), or even when antifungal drugs are used properly. 2,3 Use of fungicides in agriculture to prevent and treat fungal diseases in crops can also contribute to resistance in people exposed to those fungicides.

Some studies have indicated that antibiotics &mdashwhich include antifungal drugs&mdashmay also contribute to antifungal resistance in Candida. This resistance could occur in a variety of ways. For example, antibiotics can reduce good and bad germs in the gut, which creates favorable conditions for Candida growth. 4 It is not known if decreasing the use of all or certain antibiotics can reduce Candida infections, but appropriate use of antibiotics and antifungal drugs is one of the most important factors in fighting drug resistance.

Types of resistant fungi

Fungi that have shown resistance to antifungal drugs are Aspergillus and certain Candida species. Candida auris is a new species that is particularly resistant to antifungal drugs and can spread in healthcare settings. Learn more:


"Saccharomyces" derives from Latinized Greek and means "sugar-mold" or "sugar-fungus", saccharon (σάκχαρον) being the combining form "sugar" and myces (μύκης) being "fungus". [4] [5] cerevisiae comes from Latin and means "of beer". [6] Other names for the organism are:

  • Brewer's yeast, though other species are also used in brewing [7]
  • Ale yeast
  • Top-fermenting yeast
  • Baker's yeast[7]
  • Ragi yeast, in connection to making tapai
  • Budding yeast

This species is also the main source of nutritional yeast and yeast extract.

In the 19th century, bread bakers obtained their yeast from beer brewers, and this led to sweet-fermented breads such as the Imperial "Kaisersemmel" roll, [8] which in general lacked the sourness created by the acidification typical of Lactobacillus. However, beer brewers slowly switched from top-fermenting (S. cerevisiae) to bottom-fermenting (S. pastorianus) yeast. The Vienna Process was developed in 1846. [9] While the innovation is often popularly credited for using steam in baking ovens, leading to a different crust characteristic, it is notable for including procedures for high milling of grains (see Vienna grits [10] ), cracking them incrementally instead of mashing them with one pass as well as better processes for growing and harvesting top-fermenting yeasts, known as press-yeast. [ citation needed ]

Refinements in microbiology following the work of Louis Pasteur led to more advanced methods of culturing pure strains. In 1879, Great Britain introduced specialized growing vats for the production of S. cerevisiae, and in the United States around the turn of the century centrifuges were used for concentrating the yeast, [11] making modern commercial yeast possible, and turning yeast production into a major industrial endeavor. The slurry yeast made by small bakers and grocery shops became cream yeast, a suspension of live yeast cells in growth medium, and then compressed yeast, the fresh cake yeast that became the standard leaven for bread bakers in much of the Westernized world during the early 20th century. [ citation needed ]

During World War II, Fleischmann's developed a granulated active dry yeast for the United States armed forces, which did not require refrigeration and had a longer shelf-life and better temperature tolerance than fresh yeast it is still the standard yeast for US military recipes. The company created yeast that would rise twice as fast, cutting down on baking time. Lesaffre would later create instant yeast in the 1970s, which has gained considerable use and market share at the expense of both fresh and dry yeast in their various applications. [ citation needed ]

Ecology Edit

In nature, yeast cells are found primarily on ripe fruits such as grapes (before maturation, grapes are almost free of yeasts). [12] Since S. cerevisiae is not airborne, it requires a vector to move. [ citation needed ]

Queens of social wasps overwintering as adults (Vespa crabro and Polistes spp.) can harbor yeast cells from autumn to spring and transmit them to their progeny. [13] The intestine of Polistes dominula, a social wasp, hosts S. cerevisiae strains as well as S. cerevisiae × S. paradoxus hybrids. Stefanini et al. (2016) showed that the intestine of Polistes dominula favors the mating of S. cerevisiae strains, both among themselves and with S. paradoxus cells by providing environmental conditions prompting cell sporulation and spores germination. [14]

The optimum temperature for growth of S. cerevisiae is 30–35 °C (86–95 °F). [13]

Life cycle Edit

Two forms of yeast cells can survive and grow: haploid and diploid. The haploid cells undergo a simple lifecycle of mitosis and growth, and under conditions of high stress will, in general, die. This is the asexual form of the fungus. The diploid cells (the preferential 'form' of yeast) similarly undergo a simple lifecycle of mitosis and growth. The rate at which the mitotic cell cycle progresses often differs substantially between haploid and diploid cells. [15] Under conditions of stress, diploid cells can undergo sporulation, entering meiosis and producing four haploid spores, which can subsequently mate. This is the sexual form of the fungus. Under optimal conditions, yeast cells can double their population every 100 minutes. [16] [17] However, growth rates vary enormously both between strains and between environments. [18] Mean replicative lifespan is about 26 cell divisions. [19] [20]

In the wild, recessive deleterious mutations accumulate during long periods of asexual reproduction of diploids, and are purged during selfing: this purging has been termed "genome renewal". [21] [22]

Nutritional requirements Edit

All strains of S. cerevisiae can grow aerobically on glucose, maltose, and trehalose and fail to grow on lactose and cellobiose. However, growth on other sugars is variable. Galactose and fructose are shown to be two of the best fermenting sugars. The ability of yeasts to use different sugars can differ depending on whether they are grown aerobically or anaerobically. Some strains cannot grow anaerobically on sucrose and trehalose.

All strains can use ammonia and urea as the sole nitrogen source, but cannot use nitrate, since they lack the ability to reduce them to ammonium ions. They can also use most amino acids, small peptides, and nitrogen bases as nitrogen sources. Histidine, glycine, cystine, and lysine are, however, not readily used. S. cerevisiae does not excrete proteases, so extracellular protein cannot be metabolized.

Yeasts also have a requirement for phosphorus, which is assimilated as a dihydrogen phosphate ion, and sulfur, which can be assimilated as a sulfate ion or as organic sulfur compounds such as the amino acids methionine and cysteine. Some metals, like magnesium, iron, calcium, and zinc, are also required for good growth of the yeast.

Concerning organic requirements, most strains of S. cerevisiae require biotin. Indeed, a S. cerevisiae-based growth assay laid the foundation for the isolation, crystallisation, and later structural determination of biotin. Most strains also require pantothenate for full growth. In general, S. cerevisiae is prototrophic for vitamins.

Mating Edit

Yeast has two mating types, a and α (alpha), which show primitive aspects of sex differentiation. [23] As in many other eukaryotes, mating leads to genetic recombination, i.e. production of novel combinations of chromosomes. Two haploid yeast cells of opposite mating type can mate to form diploid cells that can either sporulate to form another generation of haploid cells or continue to exist as diploid cells. Mating has been exploited by biologists as a tool to combine genes, plasmids, or proteins at will. [ citation needed ]

The mating pathway employs a G protein-coupled receptor, G protein, RGS protein, and three-tiered MAPK signaling cascade that is homologous to those found in humans. This feature has been exploited by biologists to investigate basic mechanisms of signal transduction and desensitization. [ citation needed ]

Cell cycle Edit

Growth in yeast is synchronised with the growth of the bud, which reaches the size of the mature cell by the time it separates from the parent cell. In well nourished, rapidly growing yeast cultures, all the cells have buds, since bud formation occupies the whole cell cycle. Both mother and daughter cells can initiate bud formation before cell separation has occurred. In yeast cultures growing more slowly, cells lacking buds can be seen, and bud formation only occupies a part of the cell cycle. [ citation needed ]

Cytokinesis Edit

Cytokinesis enables budding yeast Saccharomyces cerevisiae to divide into two daughter cells. S. cerevisiae forms a bud which can grow throughout its cell cycle and later leaves its mother cell when mitosis has completed. [24]

S. cerevisiae is relevant to cell cycle studies because it divides asymmetrically by using a polarized cell to make two daughters with different fates and sizes. Similarly, stem cells use asymmetric division for self-renewal and differentiation. [25]

Timing Edit

For many cells, M phase does not happen until S phase is complete. However, for entry into mitosis in S. cerevisiae this is not true. Cytokinesis begins with the budding process in late G1 and is not completed until about halfway through the next cycle. The assembly of the spindle can happen before S phase has finished duplicating the chromosomes. [24] Additionally, there is a lack of clearly defined G2 in between M and S. Thus, there is a lack of extensive regulation present in higher eukaryotes. [24]

When the daughter emerges, the daughter is two-thirds the size of the mother. [26] Throughout the process, the mother displays little to no change in size. [27] The RAM pathway is activated in the daughter cell immediately after cytokinesis is complete. This pathway makes sure that the daughter has separated properly. [26]

Actomyosin ring and primary septum formation Edit

Two interdependent events drive cytokinesis in S. cerevisiae. The first event is contractile actomyosin ring (AMR) constriction and the second event is formation of the primary septum (PS), a chitinous cell wall structure that can only be formed during cytokinesis. The PS resembles in animals the process of extracellular matrix remodeling. [26] When the AMR constricts, the PS begins to grow. Disrupting AMR misorients the PS, suggesting that both have a dependent role. Additionally, disrupting the PS also leads to disruptions in the AMR, suggesting both the actomyosin ring and primary septum have an interdependent relationship. [28] [27]

The AMR, which is attached to the cell membrane facing the cytosol, consists of actin and myosin II molecules that coordinate the cells to split. [24] The ring is thought to play an important role in ingression of the plasma membrane as a contractile force. [ citation needed ]

Proper coordination and correct positional assembly of the contractile ring depends on septins, which is the precursor to the septum ring. These GTPases assemble complexes with other proteins. The septins form a ring at the site where the bud will be created during late G1. They help promote the formation of the actin-myosin ring, although this mechanism is unknown. It is suggested they help provide structural support for other necessary cytokinesis processes. [24] After a bud emerges, the septin ring forms an hourglass. The septin hourglass and the myosin ring together are the beginning of the future division site. [ citation needed ]

The septin and AMR complex progress to form the primary septum consisting of glucans and other chitinous molecules sent by vesicles from the Golgi body. [29] After AMR constriction is complete, two secondary septums are formed by glucans. How the AMR ring dissembles remains poorly unknown. [25]

Microtubules do not play as significant a role in cytokinesis compared to the AMR and septum. Disruption of microtubules did not significantly impair polarized growth. [30] Thus, the AMR and septum formation are the major drivers of cytokinesis. [ citation needed ]

Differences from fission yeast Edit
  • Budding yeast form a bud from the mother cell. This bud grows during the cell cycle and detaches fission yeast divide by forming a cell wall [24]
  • Cytokinesis begins at G1 for budding yeast, while cytokinesis begins at G2 for fission yeast. Fission yeast “select” the midpoint, whereas budding yeast “select” a bud site [31]
  • During early anaphase the actomyosin ring and septum continues to develop in budding yeast, in fission yeast during metaphase-anaphase the actomyosin ring begins to develop [31]

Model organism Edit

When researchers look for an organism to use in their studies, they look for several traits. Among these are size, generation time, accessibility, manipulation, genetics, conservation of mechanisms, and potential economic benefit. The yeast species S. pombe and S. cerevisiae are both well studied these two species diverged approximately 600 to 300 million years ago , and are significant tools in the study of DNA damage and repair mechanisms. [32]

S. cerevisiae has developed as a model organism because it scores favorably on a number of these criteria.

  • As a single-cell organism, S. cerevisiae is small with a short generation time (doubling time 1.25–2 hours [33] at 30 °C or 86 °F) and can be easily cultured. These are all positive characteristics in that they allow for the swift production and maintenance of multiple specimen lines at low cost.
  • S. cerevisiae divides with meiosis, allowing it to be a candidate for sexual genetics research.
  • S. cerevisiae can be transformed allowing for either the addition of new genes or deletion through homologous recombination. Furthermore, the ability to grow S. cerevisiae as a haploid simplifies the creation of gene knockout strains.
  • As a eukaryote, S. cerevisiae shares the complex internal cell structure of plants and animals without the high percentage of non-coding DNA that can confound research in higher eukaryotes.
  • S. cerevisiae research is a strong economic driver, at least initially, as a result of its established use in industry.

In the study of aging Edit

For more than five decades S. cerevisiae has been studied as a model organism to better understand aging and has contributed to the identification of more mammalian genes affecting aging than any other model organism. [34] Some of the topics studied using yeast are calorie restriction, as well as in genes and cellular pathways involved in senescence. The two most common methods of measuring aging in yeast are Replicative Life Span (RLS), which measures the number of times a cell divides, and Chronological Life Span (CLS), which measures how long a cell can survive in a non-dividing stasis state. [34] Limiting the amount of glucose or amino acids in the growth medium has been shown to increase RLS and CLS in yeast as well as other organisms. [35] At first, this was thought to increase RLS by up-regulating the sir2 enzyme, however it was later discovered that this effect is independent of sir2. Over-expression of the genes sir2 and fob1 has been shown to increase RLS by preventing the accumulation of extrachromosomal rDNA circles, which are thought to be one of the causes of senescence in yeast. [35] The effects of dietary restriction may be the result of a decreased signaling in the TOR cellular pathway. [34] This pathway modulates the cell's response to nutrients, and mutations that decrease TOR activity were found to increase CLS and RLS. [34] [35] This has also been shown to be the case in other animals. [34] [35] A yeast mutant lacking the genes sch9 and ras2 has recently been shown to have a tenfold increase in chronological lifespan under conditions of calorie restriction and is the largest increase achieved in any organism. [36] [37]

Mother cells give rise to progeny buds by mitotic divisions, but undergo replicative aging over successive generations and ultimately die. However, when a mother cell undergoes meiosis and gametogenesis, lifespan is reset. [38] The replicative potential of gametes (spores) formed by aged cells is the same as gametes formed by young cells, indicating that age-associated damage is removed by meiosis from aged mother cells. This observation suggests that during meiosis removal of age-associated damages leads to rejuvenation. However, the nature of these damages remains to be established.

During starvation of non-replicating S. cerevisiae cells, reactive oxygen species increase leading to the accumulation of DNA damages such as apurinic/apyrimidinic sites and double-strand breaks. [39] Also in non-replicating cells the ability to repair endogenous double-strand breaks declines during chronological aging. [40]

Meiosis, recombination and DNA repair Edit

S. cerevisiae reproduces by mitosis as diploid cells when nutrients are abundant. However, when starved, these cells undergo meiosis to form haploid spores. [41]

Evidence from studies of S. cerevisiae bear on the adaptive function of meiosis and recombination. Mutations defective in genes essential for meiotic and mitotic recombination in S. cerevisiae cause increased sensitivity to radiation or DNA damaging chemicals. [42] [43] For instance, gene rad52 is required for both meiotic recombination [44] and mitotic recombination. [45] Rad52 mutants have increased sensitivity to killing by X-rays, Methyl methanesulfonate and the DNA cross-linking agent 8-methoxypsoralen-plus-UVA, and show reduced meiotic recombination. [43] [44] [46] These findings suggest that recombination repair during meiosis and mitosis is needed for repair of the different damages caused by these agents.

Ruderfer et al. [42] (2006) analyzed the ancestry of natural S. cerevisiae strains and concluded that outcrossing occurs only about once every 50,000 cell divisions. Thus, it appears that in nature, mating is likely most often between closely related yeast cells. Mating occurs when haploid cells of opposite mating type MATa and MATα come into contact. Ruderfer et al. [42] pointed out that such contacts are frequent between closely related yeast cells for two reasons. The first is that cells of opposite mating type are present together in the same ascus, the sac that contains the cells directly produced by a single meiosis, and these cells can mate with each other. The second reason is that haploid cells of one mating type, upon cell division, often produce cells of the opposite mating type with which they can mate. The relative rarity in nature of meiotic events that result from outcrossing is inconsistent with the idea that production of genetic variation is the main selective force maintaining meiosis in this organism. However, this finding is consistent with the alternative idea that the main selective force maintaining meiosis is enhanced recombinational repair of DNA damage, [47] since this benefit is realized during each meiosis, whether or not out-crossing occurs.

Genome sequencing Edit

S. cerevisiae was the first eukaryotic genome to be completely sequenced. [48] The genome sequence was released to the public domain on April 24, 1996. Since then, regular updates have been maintained at the Saccharomyces Genome Database. This database is a highly annotated and cross-referenced database for yeast researchers. Another important S. cerevisiae database is maintained by the Munich Information Center for Protein Sequences (MIPS). The S. cerevisiae genome is composed of about 12,156,677 base pairs and 6,275 genes, compactly organized on 16 chromosomes. [48] Only about 5,800 of these genes are believed to be functional. It is estimated at least 31% of yeast genes have homologs in the human genome. [49] Yeast genes are classified using gene symbols (such as sch9) or systematic names. In the latter case the 16 chromosomes of yeast are represented by the letters A to P, then the gene is further classified by a sequence number on the left or right arm of the chromosome, and a letter showing which of the two DNA strands contains its coding sequence. [50]

Systematic gene names for Baker's yeast
Example gene name YGL118W
Y the Y to show this is a yeast gene
G chromosome on which the gene is located
L left or right arm of the chromosome
118 sequence number of the gene/ORF on this arm, starting at the centromere
W whether the coding sequence is on the Watson or Crick strand

  • YBR134C (aka SUP45 encoding eRF1, a translation termination factor) is located on the right arm of chromosome 2 and is the 134th open reading frame (ORF) on that arm, starting from the centromere. The coding sequence is on the Crick strand of the DNA.
  • YDL102W (aka POL3 encoding a subunit of DNA polymerase delta) is located on the left arm of chromosome 4 it is the 102nd ORF from the centromere and codes from the Watson strand of the DNA.

Gene function and interactions Edit

The availability of the S. cerevisiae genome sequence and a set of deletion mutants covering 90% of the yeast genome [51] has further enhanced the power of S. cerevisiae as a model for understanding the regulation of eukaryotic cells. A project underway to analyze the genetic interactions of all double-deletion mutants through synthetic genetic array analysis will take this research one step further. The goal is to form a functional map of the cell's processes.

As of 2010 [update] a model of genetic interactions is most comprehensive yet to be constructed, containing "the interaction profiles for

75% of all genes in the Budding yeast". [52] This model was made from 5.4 million two-gene comparisons in which a double gene knockout for each combination of the genes studied was performed. The effect of the double knockout on the fitness of the cell was compared to the expected fitness. Expected fitness is determined from the sum of the results on fitness of single-gene knockouts for each compared gene. When there is a change in fitness from what is expected, the genes are presumed to interact with each other. This was tested by comparing the results to what was previously known. For example, the genes Par32, Ecm30, and Ubp15 had similar interaction profiles to genes involved in the Gap1-sorting module cellular process. Consistent with the results, these genes, when knocked out, disrupted that process, confirming that they are part of it. [52]

From this, 170,000 gene interactions were found and genes with similar interaction patterns were grouped together. Genes with similar genetic interaction profiles tend to be part of the same pathway or biological process. [53] This information was used to construct a global network of gene interactions organized by function. This network can be used to predict the function of uncharacterized genes based on the functions of genes they are grouped with. [52]

Other tools in yeast research Edit

Approaches that can be applied in many different fields of biological and medicinal science have been developed by yeast scientists. These include yeast two-hybrid for studying protein interactions and tetrad analysis. Other resources, include a gene deletion library including

4,700 viable haploid single gene deletion strains. A GFP fusion strain library used to study protein localisation and a TAP tag library used to purify protein from yeast cell extracts. [ citation needed ]

Stanford University's yeast deletion project created knockout mutations of every gene in the S. cerevisiae genome to determine their function. [54]

Synthetic yeast genome project Edit

The international Synthetic Yeast Genome Project (Sc2.0 or Saccharomyces cerevisiae version 2.0) aims to build an entirely designer, customizable, synthetic S. cerevisiae genome from scratch that is more stable than the wild type. In the synthetic genome all transposons, repetitive elements and many introns are removed, all UAG stop codons are replaced with UAA, and transfer RNA genes are moved to a novel neochromosome. As of March 2017 [update] , 6 of the 16 chromosomes have been synthesized and tested. No significant fitness defects have been found. [55]

Astrobiology Edit

Among other microorganisms, a sample of living S. cerevisiae was included in the Living Interplanetary Flight Experiment, which would have completed a three-year interplanetary round-trip in a small capsule aboard the Russian Fobos-Grunt spacecraft, launched in late 2011. [56] [57] The goal was to test whether selected organisms could survive a few years in deep space by flying them through interplanetary space. The experiment would have tested one aspect of transpermia, the hypothesis that life could survive space travel, if protected inside rocks blasted by impact off one planet to land on another. [56] [57] [58] Fobos-Grunt's mission ended unsuccessfully, however, when it failed to escape low Earth orbit. The spacecraft along with its instruments fell into the Pacific Ocean in an uncontrolled re-entry on January 15, 2012. The next planned exposure mission in deep space using S. cerevisiae is BioSentinel. (see: List of microorganisms tested in outer space)

Brewing Edit

Saccharomyces cerevisiae is used in brewing beer, when it is sometimes called a top-fermenting or top-cropping yeast. It is so called because during the fermentation process its hydrophobic surface causes the flocs to adhere to CO2 and rise to the top of the fermentation vessel. Top-fermenting yeasts are fermented at higher temperatures than the lager yeast Saccharomyces pastorianus, and the resulting beers have a different flavor than the same beverage fermented with a lager yeast. "Fruity esters" may be formed if the yeast undergoes temperatures near 21 °C (70 °F), or if the fermentation temperature of the beverage fluctuates during the process. Lager yeast normally ferments at a temperature of approximately 5 °C (41 °F), where Saccharomyces cerevisiae becomes dormant. A variant yeast known as Saccharomyces cerevisiae var. diastaticus is a beer spoiler which can cause secondary fermentations in packaged products. [59]

In May 2013, the Oregon legislature made S. cerevisiae the official state microbe in recognition of the impact craft beer brewing has had on the state economy and the state's identity. [60]

Baking Edit

S. cerevisiae is used in baking the carbon dioxide generated by the fermentation is used as a leavening agent in bread and other baked goods. Historically, this use was closely linked to the brewing industry's use of yeast, as bakers took or bought the barm or yeast-filled foam from brewing ale from the brewers (producing the barm cake) today, brewing and baking yeast strains are somewhat different.

Nutritional yeast Edit

Saccharomyces cerevisiae is the main source of nutritional yeast, which is sold commercially as a food product. It is popular with vegans and vegetarians as an ingredient in cheese substitutes, or as a general food additive as a source of vitamins and minerals, especially amino acids and B-complex vitamins.

Uses in aquaria Edit

Owing to the high cost of commercial CO2 cylinder systems, CO2 injection by yeast is one of the most popular DIY approaches followed by aquaculturists for providing CO2 to underwater aquatic plants. The yeast culture is, in general, maintained in plastic bottles, and typical systems provide one bubble every 3–7 seconds. Various approaches have been devised to allow proper absorption of the gas into the water. [61]

Saccharomyces cerevisiae is used as a probiotic in humans and animals. Especially, a strain Saccharomyces cerevisiae var. boulardii is industrially manufactured and clinically used as a medication.

Several clinical and experimental studies have shown that Saccharomyces cerevisiae var. boulardii is, to lesser or greater extent, useful for prevention or treatment of several gastrointestinal diseases. [62] Moderate quality evidence shown Saccharomyces cerevisiae var. boulardii to reduce risk of antibiotic-associated diarrhea both in adults [63] [62] [64] and in children [63] [62] and to reduce risk of adverse effects of Helicobacter pylori eradication therapy. [65] [62] [64] Also some limited evidence support efficacy of Saccharomyces cerevisiae var. boulardii in prevention (but not treatment) of traveler's diarrhea [62] [64] and, at least as an adjunct medication, in treatment of acute diarrhea in adults and children and of persistent diarrhea in children. [62] It may also reduce symptoms of allergic rhinitis. [66]

Administration of S. cerevisiae var. boulardii is considered generally safe. [64] In clinical trials it was well tolerated by patients, and adverse effects rate was similar to that in control groups (i. e. groups with placebo or no treatment). [63] No case of S. cerevisiae var. boulardii fungemia has been reported during clinical trials. [64]

In clinical practice, however, cases of fungemia, caused by Saccharomyces cerevisiae var. boulardii are reported. [64] [62] Patients with compromised immunity or those with central vascular catheters are at special risk. Some researchers have recommended not to use Saccharomyces cerevisiae var. boulardii for treatment of such patients. [64] Others suggest only that caution must be exercised with its use in risk group patients. [62]

Saccharomyces cerevisiae is proven to be an opportunistic human pathogen, though of relatively low virulence. [67] Despite widespread use of this microorganism at home and in industry, contact with it very rarely leads to infection. [68] Saccharomyces cerevisiae was found in the skin, oral cavity, oropharinx, duodenal mucosa, digestive tract, and vagina of healthy humans [69] (one review found it to be reported for 6% of samples from human intestine [70] ). Some specialists consider S. cerevisiae to be a part of the normal microbiota of the gastrointestinal tract, the respiratory tract, and the vagina of humans, [71] while others believe that the species cannot be called a true commensal because it originates in food. [70] [72] Presence of S. cerevisiae in the human digestive system may be rather transient [72] for example, experiments show that in the case of oral administration to healthy individuals it is eliminated from the intestine within 5 days after the end of administration. [70] [68]

Under certain circumstances, such as degraded immunity, Saccharomyces cerevisiae can cause infection in humans. [68] [67] Studies show that it causes 0.45-1.06% of the cases of yeast-induced vaginitis. In some cases, women suffering from S. cerevisiae-induced vaginal infection were intimate partners of bakers, and the strain was found to be the same that their partners used for baking. As of 1999, no cases of S. cerevisiae-induced vaginitis in women, who worked in bakeries themselves, were reported in scientific literature. Some cases were linked by researchers to the use of the yeast in home baking. [67] Cases of infection of oral cavity and pharynx caused by S. cerevisiae are also known. [67]

Invasive and systemic infections Edit

Occasionally Saccharomyces cerevisiae causes invasive infections (i. e. gets into the bloodstream or other normally sterile body fluid or into a deep site tissue, such as lungs, liver or spleen) that can go systemic (involve multiple organs). Such conditions are life-threatening. [67] [72] More than 30% cases of S. cerevisiae invasive infections lead to death even if treated. [72] S. cerevisiae invasive infections, however, are much rarer than invasive infections caused by Candida albicans [67] [73] even in patients weakened by cancer. [73] S. cerevisiae causes 1% to 3.6% nosocomial cases of fungemia. [72] A comprehensive review of S. cerevisiae invasive infection cases found all patients to have at least one predisposing condition. [72]

Saccharomyces cerevisiae may enter the bloodstream or get to other deep sites of the body by translocation from oral or enteral mucosa or through contamination of intravascular catheters (e. g. central venous catheters). [71] Intravascular catheters, antibiotic therapy and compromised immunity are major predisposing factors for S. cerevisiae invasive infection. [72]

A number of cases of fungemia were caused by intentional ingestion of living S. cerevisiae cultures for dietary or therapeutic reasons, including use of Saccharomyces boulardii (a strain of S. cerevisiae which is used as a probiotic for treatment of certain forms of diarrhea). [67] [72] Saccharomices boulardii causes about 40% cases of invasive Saccharomyces infections [72] and is more likely (in comparison to other S. cerevisiae strains) to cause invasive infection in humans without general problems with immunity, [72] though such adverse effect is very rare relative to Saccharomices boulardii therapeutic administration. [74]

S. boulardii may contaminate intravascular catheters through hands of medical personnel involved in administering probiotic preparations of S. boulardii to patients. [72]

Systemic infection usually occurs in patients who have their immunity compromised due to severe illness (HIV/AIDS, leukemia, other forms of cancer) or certain medical procedures (bone marrow transplantation, abdominal surgery). [67]

A case was reported when a nodule was surgically excised from a lung of a man employed in baking business, and examination of the tissue revealed presence of Saccharomyces cerevisiae. Inhalation of dry baking yeast powder is supposed to be the source of infection in this case. [75] [72]

Virulence of different strains Edit

Not all strains of Saccharomyces cerevisiae are equally virulent towards humans. Most environmental strains are not capable of growing at temperatures above 35 °C (i. e. at temperatures of living body of humans and other mammalian). Virulent strains, however, are capable of growing at least above 37 °C and often up to 39 °C (rarely up to 42 °C). [69] Some industrial strains are also capable of growing above 37 °C. [67] European Food Safety Authority (as of 2017) requires that all S. cerevisiae strains capable of growth above 37 °C that are added to the food or feed chain in viable form must, as to be qualified presumably safe, show no resistance to antimycotic drugs used for treatment of yeast infections. [76]

The ability to grow at elevated temperatures is an important factor for strain's virulence but not the sole one. [69]

Endophytic Fungi as a New Source of Antirheumatoid Metabolites

4 Higher Fungi as Source of Antiinflammatory

Medicinal mushrooms (MM) can be defined as macroscopic fungi that are used in the form of extracts or powder for prevention, alleviation, or healing of multiple diseases, and/or in balancing a healthy diet. There are more than 130 medicinal functions produced by MMs and fungi. 53 The mushrooms possess a high protein content (20%–30% of dry matter), and all the essential amino acids are presented. They are rich in chitin as a source of dietary fiber and have high vitamin B content. The mushrooms are low in total fat but with a high proportion of unsaturated fatty acids, and have no cholesterols. They have been used not only as a source of delicious foodstuffs and food-flavoring substances, but as medicinal resources as well. The medicinal properties of mushrooms have been confirmed through an intensive research conducted worldwide. 54 Mushrooms possess immense nutritional and medicinal biocomponents that substantiate their usage in maintaining global public health. It was shown that they constitute a rich source of bioactive compounds exhibiting antitumor, hypocholesterolemic, immunosuppressive, antioxidant, antimicrobial, and antiinflammatory properties. These compounds are polysaccharides, complexes (polysaccharide-protein and polysaccharide-peptide), ribonucleases, proteases, and lectins.

Other mushroom compounds of therapeutic interest are the secondary metabolites, especially some low molecular weight compounds such as lactones, terpenoids, and alkaloids, antibiotics with different chemical groups, and metal chelating agents. 55,56 Many species of mushrooms are used in traditional medicine, but the following are the most valuable: Ganoderma lucidum, Lentinus edodes, Trametes versicolor, Schizophyllum commune, Flammulina velutipes, Pleurotus ostreatus, Agaricus bisporus, A. brasiliensis, Tricholoma matsutake, Auricularia auricula, Grifola frondosa, Cordyceps sinensis, Coprinus comatus, Inonotus obliquus, Phellinus linteus, Laetiporus sulphureus, and Hericium erinaceus. These and other species are referred to as “medicinal mushrooms” due to their long history of medical use. The biologically active compounds and extracts from this species exhibit a broad spectrum of pharmacological activities, 57–66


An ergot kernel, called a sclerotium, develops when a spore of fungal species of the genus Claviceps infects a floret of flowering grass or cereal. The infection process mimics a pollen grain growing into an ovary during fertilization. Infection requires that the fungal spore have access to the stigma consequently, plants infected by Claviceps are mainly outcrossing species with open flowers, such as rye (Secale cereale) and ryegrasses (genus Lolium). The proliferating fungal mycelium then destroys the plant ovary and connects with the vascular bundle originally intended for seed nutrition. The first stage of ergot infection manifests itself as a white soft tissue (known as sphacelia) producing sugary honeydew, which often drops out of the infected grass florets. This honeydew contains millions of asexual spores (conidia), which insects disperse to other florets. Later, the sphacelia convert into a hard dry sclerotium inside the husk of the floret. At this stage, alkaloids and lipids accumulate in the sclerotium.

Claviceps species from tropic and subtropic regions produce macro- and microconidia in their honeydew. Macroconidia differ in shape and size between the species, whereas microconidia are rather uniform, oval to globose (5×3μm). Macroconidia are able to produce secondary conidia. A germ tube emerges from a macroconidium through the surface of a honeydew drop and a secondary conidium of an oval to pearlike shape is formed, to which the contents of the original macroconidium migrates. Secondary conidia form a white, frost-like surface on honeydew drops and spread via the wind. No such process occurs in Claviceps purpurea, Claviceps grohii, Claviceps nigricans, and Claviceps zizaniae, all from northern temperate regions.

When a mature sclerotium drops to the ground, the fungus remains dormant until proper conditions (such as the onset of spring or a rain period) trigger its fruiting phase. It germinates, forming one or several fruiting bodies with heads and stipes, variously coloured (resembling a tiny mushroom). In the head, threadlike sexual spores form, which are ejected simultaneously when suitable grass hosts are flowering. Ergot infection causes a reduction in the yield and quality of grain and hay, and if livestock eat infected grain or hay it may cause a disease called ergotism.

Black and protruding sclerotia of C. purpurea are well known. However, many tropical ergots have brown or greyish sclerotia, mimicking the shape of the host seed. For this reason, the infection is often overlooked.

Insects, including flies and moths, carry conidia of Claviceps species, but it is unknown whether insects play a role in spreading the fungus from infected to healthy plants. [7]

The evolution of plant parasitism in the Clavicipitaceae dates back at least 100 million years, to the early-mid Cretaceous. An amber fossil discovered in 2014 preserves a grass spikelet and an ergot-like parasitic fungus. The fossil shows that the original hosts of the Clavicipitaceae could have been grasses. The discovery also establishes a minimum time for the conceivable presence of psychotropic compounds in fungi. [8] [9] Several evolutionary processes have acted to diversify the array of ergot alkaloids produced by fungi these differences in enzyme activities are evident at the levels of substrate specificity (LpsA), product specification (EasA, CloA) or both (EasG and possibly CloA). [10] The "old yellow enzyme", EasA, presents an outstanding example. This enzyme catalyzes reduction of the C8=C9 double-bond in chanoclavine I, but EasA isoforms differ in whether they subsequently catalyze reoxidation of C8–C9 after rotation. [10] This difference distinguishes most Clavicipitaceae from Trichocomaceae, but in Clavicipitaceae it is also the key difference dividing the branch of classical ergot alkaloids from dihydroergot alkaloids, the latter often being preferred for pharmaceuticals due to their relatively few side effects. [10]

The ergot sclerotium contains high concentrations (up to 2% of dry mass) of the alkaloid ergotamine, a complex molecule consisting of a tripeptide-derived cyclol-lactam ring connected via amide linkage to a lysergic acid (ergoline) moiety, and other alkaloids of the ergoline group that are biosynthesized by the fungus. [11] Ergot alkaloids have a wide range of biological activities including effects on circulation and neurotransmission. [12]

Ergot alkaloids are classified as:

Ergotism is the name for sometimes severe pathological syndromes affecting humans or other animals that have ingested plant material containing ergot alkaloid, such as ergot-contaminated grains. The Hospital Brothers of St. Anthony, an order of monks established in 1095, specialized in treating ergotism victims [14] with balms containing tranquilizing and circulation-stimulating plant extracts. The common name for ergotism is "St. Anthony's Fire", [14] in reference to this order of monks and the severe burning sensations in the limbs which was one of the symptoms. [15] There are two types of ergotism, the first is characterized by muscle spasms, fever and hallucinations and the victims may appear dazed, be unable to speak, become manic, or have other forms of paralysis or tremors, and suffer from hallucinations and other distorted perceptions. [16] This is caused by serotonergic stimulation of the central nervous system by some of the alkaloids. [16] The second type of ergotism is marked by violent burning, absent peripheral pulses and shooting pain of the poorly vascularized distal organs, such as the fingers and toes, [16] and are caused by effects of ergot alkaloids on the vascular system due to vasoconstriction, sometimes leading to gangrene and loss of limbs due to severely restricted blood circulation.

The neurotropic activities of the ergot alkaloids may also cause hallucinations and attendant irrational behaviour, convulsions, and even death. [11] [12] Other symptoms include strong uterine contractions, nausea, seizures, high fever, vomiting, loss of muscle strength and unconsciousness. Since the Middle Ages, controlled doses of ergot were used to induce abortions and to stop maternal bleeding after childbirth. [17] Klotz offers a detailed overview of the toxicities in mammalian livestock, stating that the activities are attributable to antagonism or agonism of neurotransmitters, including dopamine, serotonin and norepinephrine. As well, he shares that the adrenergic blockage by ergopeptines (e.g., ergovaline or ergotamine) leads to potent and long-term vasoconstriction, and can result in reduced blood flow resulting in intense burning pain (St. Anthony's fire), edema, cyanosis, dry gangrene and even loss of hooves in cattle or limbs in humans. Reduced prolactin due to ergot alkaloid activity on dopamine receptors in the pituitary is also common in livestock. Reduced serum prolactin is associated with various reproductive problems in cattle, and especially in horses, including agalactia and poor conception, and late-term losses of foals and sometimes mares due to dystocia and thickened placentas. [10] Although both gangrenous and convulsive symptoms are seen in naturally occurring ergotism resulting from the ingestion of fungus infected rye, only gangrenous ergotism has been reported following the excessive ingestion of ergotamine tartrate. [18] Ergot extract has been used in pharmaceutical preparations, including ergot alkaloids in products such as Cafergot (containing caffeine and ergotamine [17] or ergoline) to treat migraine headaches, and ergometrine, used to induce uterine contractions and to control bleeding after childbirth. [19] Clinical ergotism as seen today results almost exclusively from the excessive intake of ergotamine tartrate in the treatment of migraine headache. [18]

In addition to ergot alkaloids, Claviceps paspali also produces tremorgens (paspalitrem) causing "paspalum staggers" in cattle. [20] The fungi of the genera Penicillium and Aspergillus also produce ergot alkaloids, notably some isolates of the human pathogen Aspergillus fumigatus, [21] and have been isolated from plants in the family Convolvulaceae, of which morning glory is best known. The causative agents of most ergot poisonings are the ergot alkaloid class of fungal metabolites, though some ergot fungi produce distantly related indole-diterpene alkaloids that are tremorgenic. [10]

Ergot does not contain lysergic acid diethylamide (LSD) but instead contains lysergic acid as well as its precursor, [22] ergotamine. Lysergic acid is a precursor for the synthesis of LSD. Their realized and hypothesized medicinal uses have encouraged intensive research since the 1950s culminating on the one hand in development of drugs both legal (e.g., bromocriptine) and illegal (e.g., lysergic acid diethylamide= LSD), and on the other hand in extensive knowledge of the enzymes, genetics, and diversity of ergot alkaloid biosynthetic pathways. [10]

The January 4, 2007 issue of the New England Journal of Medicine includes a paper that documents a British study of more than 11,000 Parkinson's disease patients. The study found that two ergot-derived drugs, pergolide and cabergoline, commonly used to treat Parkinson's Disease may increase the risk of leaky heart valves by up to 700%. [23]

Ergotism is the earliest recorded example of mycotoxicosis, or poisoning caused by toxic molds. [24] Early references to ergot poisoning (ergotism) date back as far as 600 BC, an Assyrian tablet referred to it as a 'noxious pustule in the ear of grain'. [25] In 350 BC, the Parsees described 'noxious grasses that cause pregnant women to drop the womb and die in childbed'. [25] In ancient Syria, ergot was called 'Daughter of Blood'. [26] Radulf Glaber described an ailment he called 'hidden fire' or ignus ocultus, in which a burning of the limb is followed by its separation from the body, often consuming the victim in one night. [26] In 1588, Johannes Thallius wrote that it is called 'Mother of Rye', or rockenmutter, and is used to halt bleeding. [26]

Human poisoning due to the consumption of rye bread made from ergot-infected grain was common in Europe in the Middle Ages. The first mention of a plague of gangrenous ergotism in Europe comes from Germany in 857, following this France and Scandinavia experienced similar outbreaks [27] England is noticeably absent from the historical regions affected by ergotism as their main source of food was wheat, which is resistant to ergot fungi. [26] In 944, a massive outbreak of ergotism caused 40,000 deaths in the regions of Aquitaine, Limousin, Perigord, and Angoumois in France. [24] In Hesse in 1596, Wendelin Thelius was one of the first to attribute ergotism poisoning to grain. [27] In 1778, S. Tessier, observing a huge epidemic in Sologne, France in which more than 8,000 people died, recommended drainage of fields, compulsory cleaning of grain, and the substitution of potatoes for affected grain. [27]

Saint Anthony's fire and the Antonites Edit

In 1722, the Russian Tsar Peter the Great was thwarted in his campaign against the Ottoman Empire as his army, traveling down the Terek steppe, were struck by ergotism and were forced to retreat in order to find edible grains. A diary entry from the time describes that as soon as people ate the poisoned bread they became dizzy, with such strong nerve contractions that those who did not die on the first day found their hands and feet falling off, akin to frostbite. [28] The epidemic was known as Saint Anthony's fire, [14] or ignis sacer, and some historical events, such as the Great Fear in France during the French Revolution have been linked to ergot poisoning. [29] Saint Anthony was a 3rd Century Egyptian ascetic who lived by the Red Sea and was known for long fasting in which he confronted terrible visions and temptations sent from the Devil. [27] He was credited by two noblemen for assisting them in recovery from the disease they subsequently founded the Order of St. Anthony in honor of him. [26] Anthony was a popular subject for art in the Middle Ages and his symbol is a large blue "T" sewn onto the shoulder of the order's monks, symbolizing the crutch used by the ill and injured. [30]

The Order of St. Anthony, who were also known as Antonites, grew quickly and hospitals spread through France, Germany, and Scandinavia and gained wealth and power as grateful patrons bestowed money and charitable goods to the hospitals. [26] By the end of the Middle Ages, there were 396 settlements and 372 hospitals owned by the order [30] and pilgrimages to such hospitals became popular as well as the donation of limbs lost to ergotism, which were displayed near shrines to the saint. [26] These hagiotherapeutic centers were the first specialized European medical welfare systems and the friars of the order were knowledgeable about treatment of ergotism and the horrifying effects of the poison. [30] The sufferers would receive ergot-free meals, wines containing vasodilating and analgesic herbs, and applications of Antonites-balsalm, which was the first transdermal therapeutic system (TTS) in medical history. [25] Their medical recipes have been lost to time, though some recorded treatments still remain. [30] After 1130 AD, the monks were no longer permitted to perform operations, and so barber surgeons were employed to remove gangrenous limbs and treat open sores. [30] Three barbers founded a hospital in Memmingen in 1214 and accepted those who were afflicted with the gangrenous form of ergotism. Patients were fed and housed with the more able-bodied individuals acting as orderlies and assistants. Patients with the convulsive form of ergotism, or ergotismus convulsivus, were welcomed for only nine days before they were asked to leave as convulsive ergotism was seen as less detrimental. Though the sufferers often experienced irreversible effects, they most often returned to their families and resumed their livelihoods. [30]

An important aspect to the Order of St. Anthony's treatment practices was the exclusion of rye bread and other ergot-containing edibles, which halted the progression of ergotism. [26] There was no known cure for ergotism itself, however there was treatment of the symptoms, which often included blood constriction, nervous disorder, and/or hallucinations if the sufferer survived the initial poisoning, his limbs would often fall off and he or she would continue to improve in health if they halted consumption of ergot. [27] The trunk of the body remained relatively untouched by the disease until its final stages and the victims, not understanding the cause of their ailment, would continue to imbibe ergot-laden food for weeks until the condition reached their digestive system. [30] It is believed that the peasantry and children were most susceptible to ergotism, though the wealthy were afflicted as well, as at times entire villages relied on tainted crops for sustenance and during times of famine, ergotism reached into every house. [25] Ergot fungus is impervious to heat and water, thus it was most often baked into bread through rye flour though other grasses can be infected, it was uncommon in Medieval Europe to consume grasses other than rye. [26] The physiological effects of ergot depended upon the concentration and combinations of the ingested ergot metabolites, as well as the age and nutritional status of the afflicted individual. [28] The Antonites began to decline after physicians discovered the genesis of ergotism and recommended methods for removing the sclerotium from the rye crops. In 1776, the cloisters of the Antonites were incorporated into the Maltese Knights Hospitaller, losing much of their medical histories in the process and losing the ergotism cures and recipes due to lack of use and lack of preservation. [30]

Usage in gynaecology and obstetrics Edit

Midwives and very few doctors in Europe have used extracts from ergot for centuries:

  1. In a Nürnberg manuscript of 1474 powdered ergot was prescribed together with Laurel-fruits and rhizomes of Salomon's seals to cure »permutter« or »heffmutter«, that means pain in the lower abdomen caused by the »uprising of the womb« [31]
  2. In a printed book of 1582 the German physician Adam Lonicer wrote, that three sclerotia of ergot, used several times a day, were used by midwives as a good remedy in case of the »uprising and pain of the womb« (»auffſteigen vnd wehethumb der mutter«) [32] wrote in 1586, that sclerotia of ergot held under the tongue, would stop bleeding [33]

To prove that ergot is a harmless sort of grain, in 1774 the French pharmacist Antoine-Augustin Parmentier edited a letter he had received from Madame Dupile, a midwife of Chaumont-en-Vexin. She had told him that if uterine contractions were too weak in the expulsion stage of childbirth, she and her mother gave peeled ergot in an amount of the filling of a thimble solved in water, wine or broth. The administration of ergot was followed by a mild childbirth within 15 minutes. [34] The French physician Jean-Baptiste Desgranges (1751–1831) published in 1818, that in 1777 he had met midwives in Lyon, who successfully treated feeble uterine contractions by administering the powder of ergot. Desgranges joined this remedy into his therapeutic arsenal. From 1777 to 1804 he was successful in alleviating childbirth for more than twenty women by the administration of the powder of ergot. He never saw any side-effect of this treatment. [35]

In 1807 Dr. John Stearns of Saratoga County wrote to a friend, that he had used over several years a »pulvis parturiens« with complete success in patients with »lingering parturitation«. This »pulvis parturiens« consisted of ergot, that he called a »spurious groth of rye«. He boiled »half a drachm« (ca. 2g) of that powder in half a pint of water and gave one third every twenty minutes, till the pains commenced. [36] In 1813 Dr. Oliver Prescott (1762–1827) of Newburyport published a dissertation "on the natural history and medical effects of the secale cornutum," in which he described and analysed the experience he had gathered over five years while using ergot in cases of poor uterine action in the second stage of labour in childbirth. [37]

The 1836 Dispensatory of the United States recommended »to a woman in labour fifteen or twenty grains [ca. 1 to 1,3g] of ergot in powder to be repeated every twenty minutes, till its peculiar effects are experienced, or till the amount of a drachm [ca. 3,9g] has been taken«. [38]

In 1837 the French Codex Pharmacopee Francaise required ergot to be kept in all pharmacies. [39]

Low to very low evidence from clinical trials suggests that prophylactic use of ergot alkaloids, administered by intravenous (IV) or intramuscular (IM) in the third stage of labor, may reduce blood loss and may reduce the risk of moderate to severe hemorrhage following delivery, however this medication may also be associated with higher blood pressure and higher pain. [40] It is not clear of oral ergo alkaloids are beneficial or harmful as they have not been well studied. [40] A 2018 Cochrane Systematic Review concluded that other medications such as oxytocin, syntometrine and prostaglandins, may be preferred over ergot alkaloids. [40]

Though ergot was known to cause abortions in cattle and humans, it was not a recognized use for it as abortion was illegal in most countries, thus evidence for its use in abortion is unknown. [24] Most often, ergot was used to speed the process of parturition or delivery, and was not used for the purpose of halting postpartum bleeding, which is a concern of childbirth. [27] However, until anesthesia became available, there was no antidote or way of controlling the effects of ergot. So if the fetus did not move as expected, the drug could cause the uterus to mold itself around the child, rupturing the uterus and killing the child. David Hosack, an American physician, noted the large number of stillbirths resulting from ergot use and stated that rather than pulvis ad partum, it should be called pulvis ad mortem. [27] He began advocating for its use to halt postpartum bleeding. Eventually, doctors determined that the use of ergot in childbirth without an antidote was too dangerous. They ultimately restricted its use to expelling the placenta or stopping hemorrhage. Not only did it constrict the uterus, ergot had the ability to increase or decrease blood pressure, induce hypothermia and emesis, and influence pituitary hormone secretions. [24] In 1926, Swiss psychiatrist Hans Maier suggested to use ergotamine for the treatment of vascular headaches of the migraine type. [16]

In the 1930s, abortifacient drugs were marketed to women by various companies under various names such as Molex pills and Cote pills. Since birth control devices and abortifacients were illegal to market and sell at the time, they were offered to women who were "delayed". The recommended dosage was seven grains of ergotin a day. According to the United States Federal Trade Commission (FTC) [41] these pills contained ergotin, aloes, Black Hellebore, and other substances. The efficacy and safety of these pills are unknown. The FTC deemed them unsafe and ineffective and demanded that they cease and desist selling the product. Currently, over a thousand compounds have been derived from ergot ingredients. [16]

Speculated cause of hysterics and hallucinations Edit

It has been posited that Kykeon, the beverage consumed by participants in the ancient Greek Eleusinian Mysteries cult, might have been based on hallucinogens from ergotamine, a precursor to the potent hallucinogen lysergic acid diethylamide (LSD), and ergonovine. [42] [16] [43]

An article appearing in the July 23, 1881 edition of Scientific American entitled "A New Exhilarating Substance" denotes cases of euphoria upon consuming tincture of ergot of rye, particularly when mixed with phosphate of soda and sweetened water. In rainy years, it was thought rye bread exceeded 5% ergot. [44]

British author John Grigsby contends that the presence of ergot in the stomachs of some of the so-called 'bog-bodies' (Iron Age human remains from peat bogs Northeast Europe, such as the Tollund Man) is indicative of use of Claviceps purpurea in ritual drinks in a prehistoric fertility cult akin to the Greek Eleusinian Mysteries. In his 2005 book Beowulf and Grendel, he argues that the Anglo-Saxon poem Beowulf is based on a memory of the quelling of this fertility cult by followers of Odin. He writes that Beowulf, which he translates as barley-wolf, suggests a connection to ergot which in German was known as the 'tooth of the wolf'. [45]

Linnda R. Caporael posited in 1976 that the hysterical symptoms of young women that had spurred the Salem witch trials had been the result of consuming ergot-tainted rye. [46] However, Nicholas P. Spanos and Jack Gottlieb, after a review of the historical and medical evidence, later disputed her conclusions. [47] Other authors have likewise cast doubt on ergotism as the cause of the Salem witch trials. [48]

Mankind has known about Claviceps purpurea for a long time, and its appearance has been linked to extremely cold winters that were followed by rainy summers. [ citation needed ]

The sclerotial stage of C. purpurea conspicuous on the heads of ryes and other such grains is known as ergot. Favorable temperatures for growth are in the range of 18–30 °C. Temperatures above 37 °C cause rapid germination of conidia. [ citation needed ] Sunlight has a chromogenic effect on the mycelium, with intense coloration. [ citation needed ] Cereal mashes and sprouted rye are suitable substrates for growth of the fungus in the laboratory. [ citation needed ]

Claviceps africana infects sorghum. In sorghum and pearl millet, ergot became a problem when growers adopted hybrid technology, which increased host susceptibility. [16] It only infects unfertilized ovaries, so self-pollination and fertilization can decrease the presence of the disease, but male-sterile lines are extremely vulnerable to infection. [ citation needed ] Symptoms of infection by C. africana include the secretion of honeydew (a fluid with high concentrates of sugar and conidia), which attracts insects like flies, beetles, and wasps that feed on it. This helps spread the fungus to uninfected plants.

In Sorghum this honeydew can be spotted coming out of head flowers. A whitish sticky substance can also be observed on leaves and on the ground. [49]

C. africana caused ergot disease that caused a famine in 1903-1906 in Northern Cameroon, West Africa, and also occurs in eastern and southern Africa, especially Zimbabwe and South Africa. Male sterile sorghums (also referred to as A-lines) are especially susceptible to infection, as first recognized in the 1960s, and massive losses in seed yield have been noted. Infection is associated with cold night temperatures that are below 12 °C occurring two to three weeks before flowering. [ citation needed ]

Sorghum ergot caused by Claviceps africana Frederickson, Mantle and De Milliano is widespread in all sorghum growing areas, whereas the species was formerly restricted to Africa and Asia where it was first recorded more than 90 years ago, it has been spreading rapidly and by the mid-1990s it reached Brazil, South Africa, and Australia. By 1997, the disease had spread to most South American countries and the Caribbean including Mexico, and by 1997 had reached Texas in the United States. [16]

Management Edit

Partners of the CABI-led programme, Plantwise including the Ministry of Agriculture and Livestock in Zambia have several recommendations for managing the spread of ergot, these include planting tolerant varieties, disk fields after harvest to prevent sorghum ratoon and volunteer plants from developing, remove any infected plants, and carrying out 3 year crop rotations with legumes. [49]

Claviceps paspali infects wild grasses and could be found on the common grass Paspalum. Like the C. africana, C. paspali also secretes honeydew which is consumed by bees. The bees then create a honey called fic'e (Paraguayan Makai Indian language), which is infused with secretions from the plants and has a pungent aroma. If consumed in high amounts, the honey can cause drunkenness, dizziness and even death. [50]

This article incorporates text from a free content work. Licensed under CC-BY-SA License statement/permission on Wikimedia Commons. Text taken from PMDG: Ergot sugary disease in sorghum, Chanda Bwalya, CABI. To learn how to add open license text to Wikipedia articles, please see this how-to page. For information on reusing text from Wikipedia, please see the terms of use.

Photosynthesis, Cellular Respiration, & Fermentation

You've already learned a little bit about photosynthesis thanks to our study of plant cells. You learned that photosynthesis happens in the chloroplasts that are found only in plant cells. Let's think about what else you've already learned.

You've already learned that there are two basic types of organisms when it comes to food: producers and consumers. Producers are able to make their own food. Consumers get the food they need by eating other organisms. You learned that only plants are producers, and that they make their own food by combining water (H2O), carbon dioxide (CO2) and energy from the sun to produce sugar (C6H12O6) and oxygen (O2). This process, you learned, is called photosynthesis. In the process of making sugar, plant cells also lock some of the energy they collected from sunlight into the sugar molecule.

Okay, great. So how do cells (remember, both plant and animal cells need energy, and neither can directly use the energy provided by the sun) get the energy out of the sugar molecule? They do it with a process called cellular respiration. In cellular respiration, cells use oxygen to break the sugar molecule. That releases the energy which is then transferred to an ATP (adenosine triphosphate) molecule. ATP is the fuel that cells need for energy. And where does cellular respiration happen? As you've learned, it happens in those handy mitochondria.

So really, you already know all the basics. There are just a few details that you need to learn, and they are covered in Section 1 of Chapter 5 in your textbook and, of course, right here. Let's start with photosynthesis


If you were to look at plant cells under a microscope and compare them to animal cells, there are two things that you would notice immediately. First, you would notice the cell wall that surrounds the plant cell. You would notice it the same way that Robert Hooke noticed it. The second thing you would notice is that a plant cell is green and an animal cell is basically clear. If you were looking at a relatively large plant cell, and you were using a microscope like the ones we have at school, you would notice that not the entire plant cell was green. Instead, you would notice that there were large green objects inside of the plant cell. These large green objects, of course, are chloroplasts. And the reason that they are green is because they contain a green pigment called chlorophyll.

Have a look at this illustration from your book:

Do you notice how the chemical formula that defines photosynthesis looks a little different from the way you originally learned it? Instead of CO2 + H2O + light it shows 6CO2 + 6H2O + light. That's because chemical equations, just like math equations, have to balance. The original formula takes one carbon atom (that's how many carbon atoms are in CO2), 2 hydrogen atoms (that's how many hydrogen atoms there are in H2O), and 3 oxygen atoms (2 that are in CO2 and one that is in H2O) and turns it into glucose (which contains 6 carbon atoms, 12 hydrogen atoms, and 6 oxygen atoms) and an oxygen molecule (O2, which contains 2 oxygen atoms). That just doesn't add up! You can't magically turn 1 carbon atom from CO2 into 6 carbon atoms in C6H12O6. But if you do the math with the formula in the illustration above, you'll see that the number of atoms of carbon, oxygen, and hydrogen on both sides of the equation are correct. You will get way more practice balancing chemical equations when you study chemistry in 8th grade science.

Cellular Respiration

It is tempting to think of cellular respiration as the opposite of photosynthesis. If you look at the illustration from our book, below, you'll see why:

Do you see the way the chemical formula for cellular respiration is the reverse of the chemical formula for photosynthesis? The only real difference is that in one, the energy is sunlight and in the second, the energy is the ATP molecule. It's that reversal that makes many people think of photosynthesis and cellular respiration as being opposites. They are not! Rather, they are complementary to one another. Without photosynthesis, there would be no sugar, without which there could be no cellular respiration. On the other hand, cellular respiration produces the H2O and CO2 that are needed for photosynthesis. It's really important for you to remember that cellular respiration in eukaryotic cells takes place in the mitochondria. Both animal cells and plant cells depend on cellular respiration for their energy needs, because both animal cells and plant cells need ATP. Plant cells may be able to use the energy from the sun to make sugar, but they can't use the sun's energy as fuel. They need ATP the same way that animal cells do, and ATP can only be formed through cellular respiration. The illustration below from your book shows the way that photosynthesis and cellular respiration complement each other.

Do you see what I don't like about this illustration? Is it clear from this illustration that plant cells also have mitochondria? Not clear enough, in my opinion! So remember! Plant cells have mitochondria, too!


What happens when there is not enough oxygen to keep the cellular respiration reaction alive? Your book makes it seem like the answer is very simple. Let's start with the simple answer in your book. If there is not enough oxygen for cells to perform cellular respiration, they resort to another method of producing energy called fermentation. They still break down the sugar molecule to release the energy so that it can be transferred to an ATP molecule, but they do it without oxygen. In cellular respiration, CO2 and H2O are produced along with the energy. In fermentation, CO2 and something called lactic acid are produced. Just like your book explains, you've probably experienced fermentation yourself when you've had to run the Wednesday mile and you've really pushed yourself to get a good grade. You know that burning or stinging sensation that you feel in your muscles when you push yourself running? That's caused by a buildup of lactic acid in your muscles. No matter how hard your lungs and heart work to get oxygen to the cells in your leg muscles, they still aren't getting enough to produce all the energy they need through cellular respiration. So, they are forced to switch to fermentation, and lactic acid is produced.

There are some organisms that get all of their energy needs from fermentation. One common example is yeast. Yup. That same stuff that you drop into the bread maker. You should have noticed that there were lots of bubbles in the tubes containing the yeast and sugar water in our classroom. You've already seen live yeast cells in class that I projected from a microscope to the screen. A few classes got lucky and were able to see some yeast cells that were in the process of reproducing. I know you're going to be happy to hear this: yeast cells reproduce by budding! Just when you thought it was safe to forget all about budding and the pain it has caused you on past tests, it's back!

So how does yeast make bread rise? It's pretty simple, really. Bread is made mostly of flour. You probably already know that bread is "carbs", or carbohydrates. Do you remember what carbohydrates are? That's right, they are just long strings of sugar molecules. Yeast uses those sugar molecules to get the energy it needs, and in the process it creates CO2. That CO2 makes bubbles inside of the bread dough, and those bubbles make the dough get larger, or rise.

There is another way that fermentation caused by yeast is important. Grape juice also contains a lot of sugar. When yeast is added to grape juice, it uses the sugar for energy. Yes, it produces CO2, but it also produces alcohol. That's how grape juice is turned into wine!

The Global Warming Connection

Remember An Inconvenient Truth, the Al Gore documentary movie? One of the scenes in the movie showed the earth at night as photographed from space. Vice President Gore said that the large red areas were forests burning. There are plenty of naturally-occurring forest fires, but humans purposely set forests ablaze, too. In Brasil, for example, parts of the rainforest are burned to create more land for crops and housing. Think about what this means for global warming.

Global warming is caused by too much carbon dioxide in the atmosphere. The carbon dioxide acts as a blanket. When sunlight hits the earth, it can't radiate back into space because of the carbon dioxide and other greenhouse gases that are present in the atmosphere. So, the earth gets hotter.

Burning forests is a double-whammy. First, removing trees means that they aren't there anymore to convert carbon dioxide into sugar and oxygen. Second, when we burn the trees, we are releasing all of the carbon dioxide that they have collected. When mitochondria combine glucose with oxygen to produce energy, they are "burning" the sugar through a process called oxidation. There are many examples of oxidation in real life. When a nail gets rusty, that's oxidation. And, of course, when something burns, that's oxidation, too. The only difference between rusting, burning, and the way that mitochondria release the energy from a glucose molecule is the speed of the reaction. Rusting is very slow oxidation and burning is very fast oxidation. So burning the sugar in the trees is just a very fast version of what mitochondria do: the sugar releases carbon dioxide and energy in the form of heat. Some trees have been alive for hundreds or even thousands of years! So when we burn them, we are releasing hundreds or thousands of years worth of "captured" carbon dioxide.

That's it, folks. If you can remember the chemical formula for both photosynthesis and cellular respiration, if you can explain how the two processes complement one another, and if you can explain what happens when there is not enough oxygen for cellular respiration, then you've learned what you need to have learned.

These videos will help you to understand photosynthesis and cellular respiration. Don't be afraid of the complicated scientific vocabulary! You will understand more than you think if you just stop once in a while and try to make a connection between what is going on in the video and what you have already learned.

What happens during a fungal culture test?

Fungi can occur in different places in the body. Fungal culture tests are performed where fungi is likely to be present. The most common types of fungal tests and their uses are listed below.

Skin or nail scraping

  • Used to diagnose superficial skin or nail infections
  • Test procedure:
    • Your health care provider will use a special tool to take a small sample of your skin or nails
    • Used to diagnose yeast infections in your mouth or vagina. It may also be used to diagnose certain skin infections.
    • Test procedure:
      • Your health care provider will use a special swab to gather tissue or fluid from mouth, vagina, or from an open wound
      • Used to detect the presence of fungi in the blood. Blood tests are often used to diagnose more serious fungal infections.
      • Test procedure:
        • A health care professional will need a blood sample. The sample is most often taken from a vein in your arm.
        • Used to diagnose more serious infections and sometimes to help diagnose a vaginal yeast infection
        • Test procedure:
          • You will provide a sterile sample of urine in a container, as instructed by your health care provider.

          Sputum Culture

          Sputum is a thick mucus that is coughed up from the lungs. It is different from spit or saliva.

          • Used to help diagnose fungal infections in the lungs
          • Test procedure:
            • You may be asked to cough up sputum into a special container as instructed by your provider

            After your sample is collected, it will be sent to a lab for analysis. You may not get your results right away. Your fungal culture needs to have enough fungi for your health care provider to make a diagnosis. While many types of fungi grow within a day or two, others can take a few weeks. The amount of time depends on the type of infection you have.

            Five Steps to Treating Candida Overgrowth, Naturally

            Most naturopaths will tell you that they spend a great deal of their time with patients treating yeast overgrowth, also called candidiasis, and the persistent physical and psychological symptoms that come along with it. I'm certainly no exception. A day does not go by when I don't have a handful of people coming in with one or more of the telltale signs. Candida albicans is a naturally occurring, and usually benign yeast, that grows in the gastrointestinal tract. When it over-proliferates in the body, though, the symptoms can be debilitating:

            • Painful and persistent gas and bloating
            • Recurrent yeast infections in women
            • Constipation, or diarrhea
            • Migraines
            • Weight gain
            • Depression and brain fog
            • Skin issues like eczema and acne
            • Food sensitivities
            • Fibromyalgia or chronic fatigue syndrome

            As I've written about before, the microbiome of the gut is a delicate garden and it is easily tipped into yeast overgrowth. There are several causes. In my practice, the number one contributing factor is prolonged use of antibiotics. Others include: birth control, decreased digestive function, stress, and impaired immunity. In many of my patients, I see candidiasis leading to, or running tandem with, small intestinal bacterial overgrowth (SIBO), leaky gut syndrome, irritable bowel syndrome, and food sensitivities.

            My patient Anne was a poster child for candida overgrowth. A landscape architect in her late 30s, she spoke softly and deliberately when describing her symptoms to me: itchy ears, gassy and bloated all the time, painful periods, deep fatigue, achy knees, and a recent diagnosis of acne rosacea. She had the white coating of thrush at the back of her throat and yeast infections three or four times each year for the last three years. When I asked her about antibiotic use she described two years of chronic sinus infections during which she'd been taking antibiotics nearly the entire time. She also had a long history of birth control use: 12 years, although she'd stopped a few years prior.

            In a case like Anne's, I don't necessarily even need to run diagnostics to confirm what I already know. But I typically spot candidiasis one of two ways: with a questionnaire or with a comprehensive digestive stool analysis (CDSA). Oftentimes, doctors will diagnose candida overgrowth based just on symptoms and physical exam results.

            Anne's CDSA came back with huge numbers of Candida albicans, loads of bad bacteria as well as poor markers of digestion and absorption so her candidiasis had so disrupted her the microflora that she was progressing into SIBO and leaky gut syndrome.

            Treatment for my patients that show up positive for candidiasis is in five steps: starve the yeast, kill it off, repopulate the gut, support the body's ability to detoxify and--so important--ensure that the patient is able to emotionally cope with all the physical effects of detoxing from candidiasis.

            With Anne, we did the following:

            1. Starve the yeast: This is the first step and we do this with diet. First, no sugar, which will feed the candida. No fruit in the first two weeks of treatment, then fruit is limited to two low-glycemic choices. No milk, which has the sugar lactose that tends to promote yeast overgrowth and in some cases, because milk can contain antibiotics, can promote overgrowth. No yeast-containing foods such as alcohol, peanuts, melons are recommended. Remove food sensitivities: By removing foods a patient is sensitive to (through testing, or an elimination diet), the gastrointestinal tract is better able to repair.

            2. Kill the critters: This is can be a months-long process. Each month, I switch the protocol. Potentent antifungal herbs that I use: berberine, grapefruit seed extract, olive lea f-- there are many that are valuable. These are always combined with caprylic acid, which is also excellent at breaking down candida.

            3. Repopulate the gut: It's essential to put good bugs into the gut to crowd out the bad ones sacchromyces boulardii is particularly good at this. I have people rotate probiotics monthly. Probiotics also encourage proper bowel movements if you're not pooping properly, the body will recirculate yeast and that's the last thing you want. Other things that ensure elimination: flaxseeds, psyllium and chia seeds mixed in salads and smoothies. Fermented foods are great for repopulating the gut with good bacteria: kimchi, sauerkraut, kefir, yogurt and coconut water are my patients' favorites.

            4. Support the detox process: Enhanced liver function is imperative at this time. The liver is the body's oil filter and when you get rid of Candida, it has to function optimally to help the body rid itself of the yeast. Too, candida has been shown to damage the liver. My favorite approach to liver support is biotherapeutic drainage, but I also use milk thistle and things like molybdenum.

            5. Emotional healing: It is so important to take it easy while going through this process. The feared die-off reaction can amplify the symptoms of Candida for a short period of time and this can be upsetting and debilitating. I happily spend a lot of time supporting my patients through this phase. I often recommend constitutional homeopathic remedies, which are excellent at rebalancing and supporting the body's overall vitality during this time of cleansing.

            With Anne, it took us about six months to go through this process but at the end she was symptom-free: No more itching or aching, she could eat without fear of immediately bloating up with gas, her skin was clear and her periods were starting to regulate. She no longer suffered from deep fatigue all day. Some people take longer to heal from yeast overgrowth, and some take a much shorter period of time. Lots of factors determine how long it takes: the strength of the immune system, the degree of stress in one's life (both environmental and emotional), the health of the individual organs being treated and, of course, a patient's attitude towards his or her healing goes a long way toward hurting or helping the healing process. As with all natural medicine cures, it's not always a linear progression but the result is that, as in Anne's case, the problem is gone for good.

            If you're struggling with similar symptoms, a naturopathic doctor who can focus on creating ultimate health through the use of natural therapeutics is what your gut just may need. If you want to schedule an appointment with Dr. Maura Henninger, click here. Become a fan of Dr. Maura on Facebook, connect with her on LinkedIn and follow her on Twitter.

            Autoclaving Dry Yeast Extract Powder - (Nov/06/2007 )

            Is it possible to efficiently autoclave a decent amount of yeast extract powder (500g) in a beaker?

            Or will this not become fully sterilized due to heat transfer properties? Or will it become one big giant clump or something?

            I have a non-sterile 100L fermentation vessel, but I am trying to limit what type of contaminants I am throwing in. So autoclaving the additions may help a bit.

            I would not recommend autoclaving dry yeast powder.
            Firstly an autoclave uses steam to sterile. Thus, the dry yeast powder will become wet/watery yeast powder after the autoclaving. Secondly powders do not readily sterile as they need to be in contact with steam. Something the centre of a powder does not experience easily.

            It would be better to autoclave a solution of yeast powder. However do not make it too concentrated as you will experience significate millard reaction and caramelisation. Both of which reduce the availability of free reducing sugars (glucose, fructose) and the millard reaction has a significate impact on free amino acids, removing as much as half of the free amino acid contant.

            Actually, better to just make up a litre of yeast extract with sterile distilled water and filter sterile the lot. (the bottle in use is pre autoclaved.)

            Hmm.. since you have 100L fermenter, might you also have a gamma steriliser? That works great on powders.

            I would not recommend autoclaving dry yeast powder.
            Firstly an autoclave uses steam to sterile. Thus, the dry yeast powder will become wet/watery yeast powder after the autoclaving. Secondly powders do not readily sterile as they need to be in contact with steam. Something the centre of a powder does not experience easily.

            It would be better to autoclave a solution of yeast powder. However do not make it too concentrated as you will experience significate millard reaction and caramelisation. Both of which reduce the availability of free reducing sugars (glucose, fructose) and the millard reaction has a significate impact on free amino acids, removing as much as half of the free amino acid contant.

            Actually, better to just make up a litre of yeast extract with sterile distilled water and filter sterile the lot. (the bottle in use is pre autoclaved.)

            Hmm.. since you have 100L fermenter, might you also have a gamma steriliser? That works great on powders.

            i did some research on the mallaird reaction and it says its the reaction between a reducing sugar and amino acids? the only things I autoclave at high concentrations are pure tryptone and yeast, and sometimes a mixture of both. There arent any reducing sugars in either. are there?

            there are sugars in yeast extract (total carbohydrate 163mg/g) and a little bit in caesin tryptone (total carbohydrate 4.3mg/g). And consider that the tryptone was made by treatment with HCl and yeast extract by autolysis and concentration of the soluble portion of the lysate. there is a good chance that all the carbohydrate in trytone consist of simple sugars and a proportion of the carbohydrate are free and small sugar moietoes. Really large complex sugars would probably be preferentially spun down.

            And finally there is thermal lysis to consider in regards to the sugars when confronted with an autoclave.

            Watch the video: Acne Vulgaris and Extracting large Whiteheads - Part 1 (August 2022).