Look on ebay and amazon
https://www.amazon.com/gp/product/B...rd_wg=0qcme&psc=1&refRID=V3W84S5KJRPBSDS8MRS0
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RECENT interesting findings
- Thread starter Sam_Skunkman
- Start date
Look on ebay and amazon
https://www.amazon.com/gp/product/B...rd_wg=0qcme&psc=1&refRID=V3W84S5KJRPBSDS8MRS0
Metagenomic analysis of medicinal Cannabis samples; pathogenic bacteria, toxigenic fungi, and beneficial microbes grow in culture-based yeast and mold tests.
Kevin McKernan, Jessica Spangler, Yvonne Helbert, Ryan C. Lynch , Adrian Devitt-Lee, Lei Zhang, Wendell Orphe, Jason Warner, Theodore Foss, Christopher J. Hudalla, Matthew Silva, Douglas R. Smith.
Abstract
Background: The presence of bacteria and fungi in medicinal or recreational Cannabis poses a potential threat to consumers if those microbes include pathogenic or toxigenic species. This study evaluated two widely used culture-based platforms for total yeast and mold (TYM) testing marketed by 3M Corporation and Biomérieux, in comparison with a quantitative PCR (qPCR) approach marketed by Medicinal Genomics Corporation.
Methods: A set of 15 medicinal Cannabis samples were analyzed using 3M and Biomérieux culture-based platforms and by qPCR to quantify microbial DNA. All samples were then subjected to next-generation sequencing and metagenomics analysis to enumerate the bacteria and fungi present before and after growth on culture-based media.
Results: Several pathogenic or toxigenic bacterial and fungal species were identified in proportions of >5% of classified reads on the samples, including Acinetobacter baumannii, Escherichia coli, Pseudomonas aeruginosa, Ralstonia pickettii, Salmonella enterica, Stenotrophomonas maltophilia, Aspergillus ostianus, Aspergillus sydowii, Penicillium citrinum and Penicillium steckii. Samples subjected to culture showed substantial shifts in the number and diversity of species present, including the failure of Aspergillus species to grow well on either platform. Substantial growth of Clostridium botulinum and other bacteria were frequently observed on one or both of the culture-based TYM platforms. The presence of plant growth promoting (beneficial) fungal species further influenced the differential growth of species in the microbiome of each sample.
Conclusions: These findings have important implications for the Cannabis and food safety testing industries.
http://f1000researchdata.s3.amazona...1-8940-b26c293c523f_9662_-_kevin_mckernan.pdf
Kevin McKernan, Jessica Spangler, Yvonne Helbert, Ryan C. Lynch , Adrian Devitt-Lee, Lei Zhang, Wendell Orphe, Jason Warner, Theodore Foss, Christopher J. Hudalla, Matthew Silva, Douglas R. Smith.
Abstract
Background: The presence of bacteria and fungi in medicinal or recreational Cannabis poses a potential threat to consumers if those microbes include pathogenic or toxigenic species. This study evaluated two widely used culture-based platforms for total yeast and mold (TYM) testing marketed by 3M Corporation and Biomérieux, in comparison with a quantitative PCR (qPCR) approach marketed by Medicinal Genomics Corporation.
Methods: A set of 15 medicinal Cannabis samples were analyzed using 3M and Biomérieux culture-based platforms and by qPCR to quantify microbial DNA. All samples were then subjected to next-generation sequencing and metagenomics analysis to enumerate the bacteria and fungi present before and after growth on culture-based media.
Results: Several pathogenic or toxigenic bacterial and fungal species were identified in proportions of >5% of classified reads on the samples, including Acinetobacter baumannii, Escherichia coli, Pseudomonas aeruginosa, Ralstonia pickettii, Salmonella enterica, Stenotrophomonas maltophilia, Aspergillus ostianus, Aspergillus sydowii, Penicillium citrinum and Penicillium steckii. Samples subjected to culture showed substantial shifts in the number and diversity of species present, including the failure of Aspergillus species to grow well on either platform. Substantial growth of Clostridium botulinum and other bacteria were frequently observed on one or both of the culture-based TYM platforms. The presence of plant growth promoting (beneficial) fungal species further influenced the differential growth of species in the microbiome of each sample.
Conclusions: These findings have important implications for the Cannabis and food safety testing industries.
http://f1000researchdata.s3.amazona...1-8940-b26c293c523f_9662_-_kevin_mckernan.pdf
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Bubbleblower
Member
So a change in medium could increase the incidence of fusarium from 2% to 72%, right?
Deoxynivalenol: a trigger for intestinal integrity breakdown
Deoxynivalenol: a trigger for intestinal integrity breakdown
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The mentioned "medium" isn't the medium you're using to grow your plants but what's been used to multiply the contaminating microbes on cured buds. Such a culture makes it easier to determine what's on the sample (better visibility, cheaper tests, higher sensitivity) but, as has been shown by the study, adds a strong bias because not all microbes grow equally well/fast on different growing media.
Besides, microbial contamination of pharmaceutical drugs (i.e. dried medicinal plants and products thereof, not illicit dependence causing substances) is a general problem which starts with the most simple tea like peppermint from the supermarket. Back in the day, common eye infections and similar illnesses were first treated by putting a teabag (black tea or chamomile) on the eye. Nowadays we discourage from that treatment due to the presence of too many microbes on most plant matter. Sure, the eye and more so a sick eye is very sensitive for secondary infections, but still...
pathogenic bacteria, toxigenic fungi....
They are not good....
-SamS
They are not good....
-SamS
The pathogenic fungi are nowhere near as dangerous as the mycotoxins they produce.
Blasting this shit has no effect at killing the toxins.
Moldy bud is moldy bud is deadly bud.
Fusarium produces some of the nastiest mycotoxins.
No shortcuts
Blasting this shit has no effect at killing the toxins.
Moldy bud is moldy bud is deadly bud.
Fusarium produces some of the nastiest mycotoxins.
No shortcuts
Mmmm... was think i burned the shit out of this toxicogenic funghi and pathogenic
bacteria with decarboxilation...
but a analyise brings that all samples bring to 5% of this pathogens,
maybe terpenes can deactivate those pathogenic bacteries and funghi cause
for now long time i use BHO and nothing happends...,hmmm...
hope i dont die cause i have a plan to survive...
bacteria with decarboxilation...
but a analyise brings that all samples bring to 5% of this pathogens,
maybe terpenes can deactivate those pathogenic bacteries and funghi cause
for now long time i use BHO and nothing happends...,hmmm...
hope i dont die cause i have a plan to survive...
BHO is one of the best extraction methods regarding avoiding toxins because only a very few are enough lipophilic to be extracted with butane.
High temperatures (somewhere between 150 and 250°C) certainly kills all pathogens and inactivates many toxins but by far not all.
Smoking or eating pathogenic fungi and bacteria is, with a few exceptions like enterobacteria, E. coli, P. aeruginosa, or salmonellae, usually only dangerous for people with a suppressed immune system (cancer, asthma, aids) or who already suffer from severe infections.
Fortunately, rather fresh and halfway properly dried plant material which isn't covered with dirt and grime contains in most cases only trace amounts of mycotoxins. Fungi start producing that stuff when running out of food in order to fight competition. Oxygen free storage (anaerobic bacteria) would be a different pair of shoes but that is something most only try for fun.
High temperatures (somewhere between 150 and 250°C) certainly kills all pathogens and inactivates many toxins but by far not all.
Smoking or eating pathogenic fungi and bacteria is, with a few exceptions like enterobacteria, E. coli, P. aeruginosa, or salmonellae, usually only dangerous for people with a suppressed immune system (cancer, asthma, aids) or who already suffer from severe infections.
Fortunately, rather fresh and halfway properly dried plant material which isn't covered with dirt and grime contains in most cases only trace amounts of mycotoxins. Fungi start producing that stuff when running out of food in order to fight competition. Oxygen free storage (anaerobic bacteria) would be a different pair of shoes but that is something most only try for fun.
More then 20 years old but still gold:
http://www.internationalhempassociation.org/jiha/iha01205.html
Microbiological contaminants of marijuana
J. M. McPartland
Use of marijuana as a medicament is on the rise. Many medical marijuana users have a suppressed immune system, owing to their disease or treatment. Herbal marijuana, whether field grown or hydroponically cultivated, contains many microorganisms. Many of these organisms may pose a threat to immunosuppressed individuals. The microflora of marijuana is well described in the literature. Similarly, the microflora that cause opportunistic infections in AIDS patients is well documented. These separate literatures are correlated with commentary, and methods for detecting and eliminating microbial contaminants are discussed.
Introduction
Marijuana is classified as a Schedule I drug "having no medical use, with a high potential for abuse" by the US Drug Enforcement Administration. Nevertheless, a handful of US citizens are permitted use of government-supplied "medical marijuana" for a variety of ailments (Bowersox 1992). Additionally, a large clinical trial utilizing marijuana in AIDS patients has been approved in San Francisco (Doblin 1994).
Doblin and Kleiman (1991) document the widespread illicit use of marijuana for medical purposes. Nearly half of the oncologists polled by Doblin and Kleiman recommended that their patients experiment with marijuana as a medicine. Many of these patients, however, are immuno-suppressed, making them very susceptible to opportunistic bacteria and fungi. Since hundreds of bacteria and fungi are associated with the cultivation of marijuana (McPartland 1991), possible microbiological hazards need to be assessed.
A majority of the organisms associated with marijuana are strictly plant pathogens. They cannot infect healthy humans. But a subset of opportunistic plant pathogens are associated with "post-harvest" or "storage" decay of marijuana. These organisms may infect immuno-compromised individuals and become opportunistic human pathogens. Additionally, many opportunist organisms on plants produce dangerous toxins and/or elicit allergenic reactions when inhaled.
Lastly, a handful of strictly human pathogens have been isolated from marijuana, as contaminants. These agents are highly infectious, and some also exude toxins.
http://www.internationalhempassociation.org/jiha/iha01205.html
Microbiological contaminants of marijuana
J. M. McPartland
Use of marijuana as a medicament is on the rise. Many medical marijuana users have a suppressed immune system, owing to their disease or treatment. Herbal marijuana, whether field grown or hydroponically cultivated, contains many microorganisms. Many of these organisms may pose a threat to immunosuppressed individuals. The microflora of marijuana is well described in the literature. Similarly, the microflora that cause opportunistic infections in AIDS patients is well documented. These separate literatures are correlated with commentary, and methods for detecting and eliminating microbial contaminants are discussed.
Introduction
Marijuana is classified as a Schedule I drug "having no medical use, with a high potential for abuse" by the US Drug Enforcement Administration. Nevertheless, a handful of US citizens are permitted use of government-supplied "medical marijuana" for a variety of ailments (Bowersox 1992). Additionally, a large clinical trial utilizing marijuana in AIDS patients has been approved in San Francisco (Doblin 1994).
Doblin and Kleiman (1991) document the widespread illicit use of marijuana for medical purposes. Nearly half of the oncologists polled by Doblin and Kleiman recommended that their patients experiment with marijuana as a medicine. Many of these patients, however, are immuno-suppressed, making them very susceptible to opportunistic bacteria and fungi. Since hundreds of bacteria and fungi are associated with the cultivation of marijuana (McPartland 1991), possible microbiological hazards need to be assessed.
A majority of the organisms associated with marijuana are strictly plant pathogens. They cannot infect healthy humans. But a subset of opportunistic plant pathogens are associated with "post-harvest" or "storage" decay of marijuana. These organisms may infect immuno-compromised individuals and become opportunistic human pathogens. Additionally, many opportunist organisms on plants produce dangerous toxins and/or elicit allergenic reactions when inhaled.
Lastly, a handful of strictly human pathogens have been isolated from marijuana, as contaminants. These agents are highly infectious, and some also exude toxins.
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Look this one Sam..
Use of terpenes for the treatment of digestive tract infections
WO 2002056879 A1
The prevention and treatment of digestive tract infections in humans and animals by orally administering a single terpene, a terpene mixture or a liposome-terpene (s) composition before or after the onset of a gastro-intestinal infection is described. Such infections may include traveller's diarrhea, ulcers, anthrax and other bacterial and parasitical infections.
The present invention relates to the treatment of microbial infections, especially the prevention and treatment of digestive tract infections in humans and animals, by orally administering a single terpene, a terpene mixture or a liposome-terpene (s) composition before or after the onset of the infection.
Digestive tract infections are mainly caused by pathogenic and opportunistic microorganisms and toxins produced by them. These illnesses are present in all types of animals and humans .
Diseases caused by organisms pathogenic to humans and animals are very common and encompass a range from the trivial to the lethal . With the arrival of the so-called 'antibiotic age' following World War II, it was hoped that the scourge of infection would be I largely controlled on a permanent basis. However, this has not proved to be the case and in recent years many formerly useful prior art anti-bacterials have become ineffective as resistance has emerged. In the case of fungal infections the armamentarium has always been limited and the need remains for additional and more effective treatments .
In recent years, a number of particularly difficult problems have emerged and these have engaged considerable public concern. For instance, the rapidly rising prevalence of multiply resistant Staphylococcus aure s (MRSA) in hospitals in Western countries which has led to many deaths and, to all intents and purposes, only Vancomycin now stands as a fall-back treatment. Another example is outbreaks of severe E. coli infection, such as that in Scotland in the late nineteen-nineties which killed over 150 people. In the case of E. coli, there are particular problems in respect of treatment in that, even if the organism is killed quickly, the patient may die as the result of endotoxins being released from the organism if it is lysed as a result of anti-microbial attack.
Not all the mechanisms governing the emergence of resistance to anti-bacterials are understood but sufficient is known to suggest strongly that whilst a fairly simple game of molecular roulette will produce new anti-bacterials, any such product will not remain free of resistance for long. Thus, it would appear that any solution to this apparently intractable problem of reduced effectiveness in anti-bacterials would need to be radically different to those employed in the prior art.
Recently with the scare of bio-terrorism there has been an increased concern with pathogens that can produce deadly outbreaks . This is the case with anthrax. Anthrax is considered a potential agent for use in biological warfare. Anthrax is an acute infectious disease caused by the spore-forming bacteria Bacillus anthracis . Anthrax is primarily a disease of domesticated and wild animals, particularly herbivorous animals . Humans become infected with anthrax by handling products from infected animals or by inhaling anthrax spores from contaminated animal products. Anthrax can also be spread by eating undercooked meat from infected animals. Anthrax infection can occur in three forms: cutaneous, inhalation, and gastrointestinal. The most common form is the cutaneous anthrax infection, which occurs when bacteria enter a cut or abrasion on the skin. This infection begins as a raised itchy bump that develops into a vesicle and then a painless ulcer, usually 1-3 cm in diameter, with a characteristic black necrotic area in the center. About 20% of untreated cases of cutaneous anthrax result in death. Deaths may be prevented with prompt antimicrobial treatment. The inhalation form has early symptom similar to a common cold which progressively results in severe breathing problems . This type of anthrax is usually fatal. The intestinal form is characterized by an acute inflammation of the intestinal tract. The initial signs are nausea, loss of appetite, vomiting, and fever followed by abdominal pain, vomiting of blood and severe diarrhea. Intestinal anthrax results in death in 25% to 60% of cases. Anthrax is treated with antimicrobials and can be prevented with vaccination. The Department of Defense in the USA has a mandatory anthrax vaccination of all active military personnel.
Another digestive infection in humans is traveller's diarrhea, which affects over seven million visitors to high-risk tropical and semitropical areas every year. Others suggest that the incidence of traveller's diarrhea is 15 - 56% among international travelers. Approximately 1% of the sufferers are hospitalized, at least 20% are confined to bed for a day and nearly 40% have to change plans in their travel itinerary.
Traveler's diarrhea, defined as the passage of more than 3 unformed stools in a 24-hour period, is a self-limiting illness lasting 3 - 5 days. The illness may be presented either as (1) acute watery diarrhea (2) diarrhea with blood (dysentery) or (3) chronic diarrhea, often with clinical nutrient malabsorption. Several factors contribute to the development of diarrhea in travelers, including personal (age, socioeconomic status, body weight, preexisting gastrointestinal illnesses) , behavioral (mode of travel, standard of accommodation, eating in public places, dietary errors) and travel related (destination, duration of stay, country of origin, season) . Approximately 85% of lithe diarrheas among international travelers are produced by bacterial enteropathogens . These pathogens are usually acquired through ingestion of fecally contaminated food or water. Sometimes dirty hands or insects are the vectors of fecal contamination. Cooked food is safe to consume as long as the temperature at the interior of the food reaches 160°F or more. An undercooked hamburger is risky food, because ground meat can become contaminated at the processing plant and during preparation.
The common pathogens that produce traveler's diarrhea include Clostridium difficile, Yersenia enteroli tica, Shxgella sp . , Campylobacter sp . , Salmonella sp . , ETEC (enterotoxigenic) and EAEC (enteroaggregative) Escherichia coli . Traveler's diarrhea produced by Shxgella sp. or Salmonella sp . tend to cause a more severe and longer lasting disease than that caused by the most common cause, enterotoxigenic E. coli (ETEC) . Campylobacter jejuni is a relativelly common cause of traveler's diarrhea especially in the winter. Viruses such as rotavirus, cytomegalovirus and Norwalk agent are less common causes.
There are several groups of pathogenic Ξ. coli . They include Enterotoxigenic (ETEC) , which produce a range of toxins, heat-stable or heat-labile in nature. ETEC is the most common cause of diarrhoea disease in children in the developing world; it also causes many travelers ' diarrhoea cases .
Verocytotoxic E. coli (VTEC) strains produce toxins that destroy the gut ucosa and can cause kidney damage; E. coli 0157 H:7 is the most publicised example of this type.
Enteropathogenic E. coli (EPEC) do not appear to produce toxins but may attach the microvilli, this group often causes infection in babies and young children.
Enteroinvasive E. coli (EIEC) attaches to the mucosal lining of the large intestine and invade the cells, causing tissue destruction and inflammation. EIEC are usually food borne pathogens and are an important cause of disease in areas of poor hygiene.
The severity of the disease symptoms are dependent on the strain encountered and the underlying health of the individual. EIEC and VTEC strains can cause very serious disease ( aemorrhagic colitis and renal failure) and require hospitalisation. Milder cases are usually treated by fluid and electrolyte replacement and rest.
The use of antibiotics limits the course of diarrhea to a little over a day compared with an average of over 3 - 5 days when diarrhea remains untreated. The widespread resistance of the traditional antimicrobial agent, Trimethoprim plus sulfamethoxazole (TMP/SMX) , and fluoroquinolones are the main reasons of concern about the continuous use of antimicrobials for the treatment of traveler's diarrhea (Dupont et al, 1998). The extensive use of antibiotics can also lead to overgrowth syndromes, Candida vagini tis can occur, the overgrowth of Clostridium difficile due to less competitive environment in the gastrointestinal tract can also result in diarrhea.
Short-term travelers that have experience diarrhea do not develop protection, since it requires continued exposure to enteropathogens to develop immunological protection against traveler's diarrhea. Vaccination is a promising option, but vaccines against all enteropathogens that cause traveler's diarrhea have not been developed. Other protection methods to treat traveler's diarrhea are: the use of nonabsorbed antimicrobials, which have fewer side effects and should be safer to use in children and pregnant women in whom quinolones are contraindicated; antisecretory and antimotility agent (loperamide) ; the use of attapulgite, a hydrated aluminum silicate clay preparation; and probiotics i.e. lactobacillus, which appear to be useful in the prevention or treatment of travelers diarrhea. In all cases the restoration of water and electrolyte balance is necessary. The following table shows the current treatments for Traveler's Diarrhea:
Figure imgf000009_0001
Ericsson, Charles (1998)
In humans and animals, peptic ulcers are open sores produced by a bacteria. These open sores can be present on the entire gastro-intestinal tract, mainly esophagus, stomach and proximal part of the small intestine. There is evidence that support the role of H. pylori as the etiologic agent of chronic gastritis and peptic ulcer. H. pylori , a gram-negative, microaerophilic spiral bacteria is the major cause of gastro-duodenal disease, including chronic gastritis, gastric and duodenal ulcers and gastric neoplasia. Greater than 50% of North American adults over 50 years of age are infected with H. pylori . In contrast, in some developing and newly industrialized countries virtually all adults are infected. In developing countries almost all children are infected by age 10, whereas in developed countries only the children of lower socioecono ic levels are infected. H. pylori is characterized by very high urease activity that may be associated with virulence, in the absence of urea H. pylori is sensitive to acidic pH. Urease activity may be an important colonization and survival factor by generating ammonia in the immediate bacterial microenvironment . H. pylori has been classified as a type 1 carcinogen by the World Health Organization because of the danger of persistent infection with the bacterium causing gastric cancer. H. pylori infection is of extreme importance in the causation of peptic ulcer disease. By initiating a gastritis or dyspeptic symptoms, it can predispose to subsequent episode of either gastric lymphoma or stomach cancer.
The eradication of H. pylori has been obtained with combination therapy, triple therapy using bismuth plus two antibiotics (metronidazole and either amoxicillin or tetracycline has been effective) . Problems due to development of antimicrobial resistant and side effects (diarrhea, nausea, abdominal pain and others) may explain why the use of antibiotics has not become a preferred treatment for gastritis and peptic ulcers due to H. pylori .
Antibacterial treatment of H. pylori is difficult because of the habitat occupied by the organism below the layer of the mucus adherent to the gastric mucosa. Access of antibacterial agents to this site is limited from the lumen of the stomach and also from the gastric blood supply.
The use of medium chain fatty acids and medium chain triglycerides has been shown to inhibit the growth of H. pylori in vitro. The mechanism by which they exert antibacterial effect is thought to involve: 1) damage to the bacterial outer membrane leading the increase membrane fluidity and permeability, 2) Incorporation of these fatty acids, making the bacterial membrane unstable, 3) Production of peroxides due to oxidation of fatty acids.
The mode of transmission of H. pylori in humans is still poorly understood. There are reports of detection of this microorganism in the oral cavity and in the feces . If H. pylori is harvested in the oral cavity or bowel, these might represent important reservoir for the reinfection and transmission with consequences from treatment. One vector for the transmission of H. pylori are flies, they can carry viable H. pylori in their external surf ces and alimentary tracts .
In animals, the presence of scours in calves is of economic importance. It is estimated that the death lost of calves less than 6 months of age is approximately 2.5% or over 100,000 a year. Most of the mortality and morbidity of the calves are due to infectious diseases, mainly scours. More than 90% of scours in calves is produced by E. coli and Salmonella . Clostridia has proved to be fatal in the majority of cases. There are preventive methods like (I) vaccination of the mothers in order to passively transfer antibodies in colostrum; (2) the use of immunological supplements for milk replacers; (3) the use of probiotics to create a gastro-intestinal healthy environment (4) changes in calf management. None of these protective measures are 100% effective.
Another animal of economic importance is swine. The incidence of diarrhea in neonates and weaned piglets is very high. Again, E. coli and Salmonella are the main microorganisms involved in diarrhea in swine. There are losses in the nursery while piglets are still lactating and after weaning. There are similar preventive methods as in calves. One of the preferred methods is segregated early weaning (SEW) . The basis of early weaning is that the earlier piglets are weaned from the sow the less are the chances of crossover diseases between sow and piglets. This method requires the use of antibiotics.
In both cases, calf and piglet scours, the preferred method of treatment is antibiotics. The European Community has banned the use of 5 antibiotics and in the Unites States the FDA is banning the use of fluoroquinolone in animals due to the development of Campylobacter resistant to this antibiotic. Bacteria resistance has encouraged the development of antibiotic- alternative products.
Terpenes are widespread in nature, mainly in plants as constituents of essential oils. Their building block is the hydrocarbon isoprene (C5H8)n. Terpenes have been found to be effective and nontoxic dietary antitumor agents which act through a variety of mechanisms of action (Crowell and Gould, 1994 and Crowell et al, 1996). Terpenes, i.e. geraniol, tocotrienol, perillyl alcohol, b-ionone and d-limonene, suppress hepatic HMG-COA reductase activity, a rate limiting step in cholesterol synthesis, and modestly lower cholesterol levels in animals (Elson arid Yu, 1994) . D-limonene and geraniol reduced mammary tumors (Elegbede et al, 1984 and 1986 and Karlson et al, 1996) and suppressed the growth of transplanted tumors (Yu et al, 1995) . Terpenes have also been found to inhibit the in-vitro growth of bacteria and fungi (Chaumont and Leger, 1992, Moleyar and Narasimham, 1992 and Pattnaik, et al, 1997) and some internal and external parasites (Hooser, et al, 1986) . Geraniol was found to inhibit growth of Candida albicans and Saccharomyces cerevisiae strains by enhancing the rate of potassium leakage and disrupting membrane fluidity (Bard, et al, 1988) . B-ionone has antifungal activity which was determined by inhibition of spore germination, and growth inhibition in agar (Mikhlin et al, 1983 and Salt et al, 1986) . Teprenone (geranylgeranylacetone) has an antibacterial effect on H. pylori (Ishii, 1993) . Solutions of 11 different terpenes were effective in inhibiting the growth of pathogenic bacteria in in-vitro tests; levels ranging between 100 ppm and 1000 ppm were effective. The terpenes were diluted in water with 1% polysorbate 20 (Kim et al, 1995) . Diterpenes, i.e. trichorabdal A (from R. Trichocarpa) has shown a very strong antibacterial effect against H. pylori (Kadota, et al, 1997) .
Rosanol a commercial product with 1% rose oil has been shown to inhibit the growth of several bacteria (Pseudomona, Staphylococus , E. coli and Hpylori) . Geraniol is the active component (75%) of rose oil. Rose oil and geraniol at a concentration of 2 mg/litre inhibited the growth of H pylori in vitro. Some extracts from herbal medicines have been shown to have an inhibitory effect on H. pylori , the most effective being decursinol angelate, decursin, magnolol, berberine, cinnamic acid, decursinol and gallic acid (Bae, et al 1998) . Extracts from cashew apple, anacardic acid and (E) -2-hexenal, have shown bactericidal effect against H. pylori . There may be different modes of action of terpenes against H. pylori . They could (1) interfere with the phospholipid bilayer of the cell membrane (2) impair a variety of enzyme systems (HMG-reductase) and (3) destroy or inactivate genetic material.
SUMMARY OF THE INVENTION
Prevention and treatment of digestive tract infections by orally administering a biocidal terpene, a biocidal terpene mixture or a liposome-terpene (s) composition before of after the onset of the infection.
Use of terpenes for the treatment of digestive tract infections
WO 2002056879 A1
The prevention and treatment of digestive tract infections in humans and animals by orally administering a single terpene, a terpene mixture or a liposome-terpene (s) composition before or after the onset of a gastro-intestinal infection is described. Such infections may include traveller's diarrhea, ulcers, anthrax and other bacterial and parasitical infections.
The present invention relates to the treatment of microbial infections, especially the prevention and treatment of digestive tract infections in humans and animals, by orally administering a single terpene, a terpene mixture or a liposome-terpene (s) composition before or after the onset of the infection.
Digestive tract infections are mainly caused by pathogenic and opportunistic microorganisms and toxins produced by them. These illnesses are present in all types of animals and humans .
Diseases caused by organisms pathogenic to humans and animals are very common and encompass a range from the trivial to the lethal . With the arrival of the so-called 'antibiotic age' following World War II, it was hoped that the scourge of infection would be I largely controlled on a permanent basis. However, this has not proved to be the case and in recent years many formerly useful prior art anti-bacterials have become ineffective as resistance has emerged. In the case of fungal infections the armamentarium has always been limited and the need remains for additional and more effective treatments .
In recent years, a number of particularly difficult problems have emerged and these have engaged considerable public concern. For instance, the rapidly rising prevalence of multiply resistant Staphylococcus aure s (MRSA) in hospitals in Western countries which has led to many deaths and, to all intents and purposes, only Vancomycin now stands as a fall-back treatment. Another example is outbreaks of severe E. coli infection, such as that in Scotland in the late nineteen-nineties which killed over 150 people. In the case of E. coli, there are particular problems in respect of treatment in that, even if the organism is killed quickly, the patient may die as the result of endotoxins being released from the organism if it is lysed as a result of anti-microbial attack.
Not all the mechanisms governing the emergence of resistance to anti-bacterials are understood but sufficient is known to suggest strongly that whilst a fairly simple game of molecular roulette will produce new anti-bacterials, any such product will not remain free of resistance for long. Thus, it would appear that any solution to this apparently intractable problem of reduced effectiveness in anti-bacterials would need to be radically different to those employed in the prior art.
Recently with the scare of bio-terrorism there has been an increased concern with pathogens that can produce deadly outbreaks . This is the case with anthrax. Anthrax is considered a potential agent for use in biological warfare. Anthrax is an acute infectious disease caused by the spore-forming bacteria Bacillus anthracis . Anthrax is primarily a disease of domesticated and wild animals, particularly herbivorous animals . Humans become infected with anthrax by handling products from infected animals or by inhaling anthrax spores from contaminated animal products. Anthrax can also be spread by eating undercooked meat from infected animals. Anthrax infection can occur in three forms: cutaneous, inhalation, and gastrointestinal. The most common form is the cutaneous anthrax infection, which occurs when bacteria enter a cut or abrasion on the skin. This infection begins as a raised itchy bump that develops into a vesicle and then a painless ulcer, usually 1-3 cm in diameter, with a characteristic black necrotic area in the center. About 20% of untreated cases of cutaneous anthrax result in death. Deaths may be prevented with prompt antimicrobial treatment. The inhalation form has early symptom similar to a common cold which progressively results in severe breathing problems . This type of anthrax is usually fatal. The intestinal form is characterized by an acute inflammation of the intestinal tract. The initial signs are nausea, loss of appetite, vomiting, and fever followed by abdominal pain, vomiting of blood and severe diarrhea. Intestinal anthrax results in death in 25% to 60% of cases. Anthrax is treated with antimicrobials and can be prevented with vaccination. The Department of Defense in the USA has a mandatory anthrax vaccination of all active military personnel.
Another digestive infection in humans is traveller's diarrhea, which affects over seven million visitors to high-risk tropical and semitropical areas every year. Others suggest that the incidence of traveller's diarrhea is 15 - 56% among international travelers. Approximately 1% of the sufferers are hospitalized, at least 20% are confined to bed for a day and nearly 40% have to change plans in their travel itinerary.
Traveler's diarrhea, defined as the passage of more than 3 unformed stools in a 24-hour period, is a self-limiting illness lasting 3 - 5 days. The illness may be presented either as (1) acute watery diarrhea (2) diarrhea with blood (dysentery) or (3) chronic diarrhea, often with clinical nutrient malabsorption. Several factors contribute to the development of diarrhea in travelers, including personal (age, socioeconomic status, body weight, preexisting gastrointestinal illnesses) , behavioral (mode of travel, standard of accommodation, eating in public places, dietary errors) and travel related (destination, duration of stay, country of origin, season) . Approximately 85% of lithe diarrheas among international travelers are produced by bacterial enteropathogens . These pathogens are usually acquired through ingestion of fecally contaminated food or water. Sometimes dirty hands or insects are the vectors of fecal contamination. Cooked food is safe to consume as long as the temperature at the interior of the food reaches 160°F or more. An undercooked hamburger is risky food, because ground meat can become contaminated at the processing plant and during preparation.
The common pathogens that produce traveler's diarrhea include Clostridium difficile, Yersenia enteroli tica, Shxgella sp . , Campylobacter sp . , Salmonella sp . , ETEC (enterotoxigenic) and EAEC (enteroaggregative) Escherichia coli . Traveler's diarrhea produced by Shxgella sp. or Salmonella sp . tend to cause a more severe and longer lasting disease than that caused by the most common cause, enterotoxigenic E. coli (ETEC) . Campylobacter jejuni is a relativelly common cause of traveler's diarrhea especially in the winter. Viruses such as rotavirus, cytomegalovirus and Norwalk agent are less common causes.
There are several groups of pathogenic Ξ. coli . They include Enterotoxigenic (ETEC) , which produce a range of toxins, heat-stable or heat-labile in nature. ETEC is the most common cause of diarrhoea disease in children in the developing world; it also causes many travelers ' diarrhoea cases .
Verocytotoxic E. coli (VTEC) strains produce toxins that destroy the gut ucosa and can cause kidney damage; E. coli 0157 H:7 is the most publicised example of this type.
Enteropathogenic E. coli (EPEC) do not appear to produce toxins but may attach the microvilli, this group often causes infection in babies and young children.
Enteroinvasive E. coli (EIEC) attaches to the mucosal lining of the large intestine and invade the cells, causing tissue destruction and inflammation. EIEC are usually food borne pathogens and are an important cause of disease in areas of poor hygiene.
The severity of the disease symptoms are dependent on the strain encountered and the underlying health of the individual. EIEC and VTEC strains can cause very serious disease ( aemorrhagic colitis and renal failure) and require hospitalisation. Milder cases are usually treated by fluid and electrolyte replacement and rest.
The use of antibiotics limits the course of diarrhea to a little over a day compared with an average of over 3 - 5 days when diarrhea remains untreated. The widespread resistance of the traditional antimicrobial agent, Trimethoprim plus sulfamethoxazole (TMP/SMX) , and fluoroquinolones are the main reasons of concern about the continuous use of antimicrobials for the treatment of traveler's diarrhea (Dupont et al, 1998). The extensive use of antibiotics can also lead to overgrowth syndromes, Candida vagini tis can occur, the overgrowth of Clostridium difficile due to less competitive environment in the gastrointestinal tract can also result in diarrhea.
Short-term travelers that have experience diarrhea do not develop protection, since it requires continued exposure to enteropathogens to develop immunological protection against traveler's diarrhea. Vaccination is a promising option, but vaccines against all enteropathogens that cause traveler's diarrhea have not been developed. Other protection methods to treat traveler's diarrhea are: the use of nonabsorbed antimicrobials, which have fewer side effects and should be safer to use in children and pregnant women in whom quinolones are contraindicated; antisecretory and antimotility agent (loperamide) ; the use of attapulgite, a hydrated aluminum silicate clay preparation; and probiotics i.e. lactobacillus, which appear to be useful in the prevention or treatment of travelers diarrhea. In all cases the restoration of water and electrolyte balance is necessary. The following table shows the current treatments for Traveler's Diarrhea:
Figure imgf000009_0001
Ericsson, Charles (1998)
In humans and animals, peptic ulcers are open sores produced by a bacteria. These open sores can be present on the entire gastro-intestinal tract, mainly esophagus, stomach and proximal part of the small intestine. There is evidence that support the role of H. pylori as the etiologic agent of chronic gastritis and peptic ulcer. H. pylori , a gram-negative, microaerophilic spiral bacteria is the major cause of gastro-duodenal disease, including chronic gastritis, gastric and duodenal ulcers and gastric neoplasia. Greater than 50% of North American adults over 50 years of age are infected with H. pylori . In contrast, in some developing and newly industrialized countries virtually all adults are infected. In developing countries almost all children are infected by age 10, whereas in developed countries only the children of lower socioecono ic levels are infected. H. pylori is characterized by very high urease activity that may be associated with virulence, in the absence of urea H. pylori is sensitive to acidic pH. Urease activity may be an important colonization and survival factor by generating ammonia in the immediate bacterial microenvironment . H. pylori has been classified as a type 1 carcinogen by the World Health Organization because of the danger of persistent infection with the bacterium causing gastric cancer. H. pylori infection is of extreme importance in the causation of peptic ulcer disease. By initiating a gastritis or dyspeptic symptoms, it can predispose to subsequent episode of either gastric lymphoma or stomach cancer.
The eradication of H. pylori has been obtained with combination therapy, triple therapy using bismuth plus two antibiotics (metronidazole and either amoxicillin or tetracycline has been effective) . Problems due to development of antimicrobial resistant and side effects (diarrhea, nausea, abdominal pain and others) may explain why the use of antibiotics has not become a preferred treatment for gastritis and peptic ulcers due to H. pylori .
Antibacterial treatment of H. pylori is difficult because of the habitat occupied by the organism below the layer of the mucus adherent to the gastric mucosa. Access of antibacterial agents to this site is limited from the lumen of the stomach and also from the gastric blood supply.
The use of medium chain fatty acids and medium chain triglycerides has been shown to inhibit the growth of H. pylori in vitro. The mechanism by which they exert antibacterial effect is thought to involve: 1) damage to the bacterial outer membrane leading the increase membrane fluidity and permeability, 2) Incorporation of these fatty acids, making the bacterial membrane unstable, 3) Production of peroxides due to oxidation of fatty acids.
The mode of transmission of H. pylori in humans is still poorly understood. There are reports of detection of this microorganism in the oral cavity and in the feces . If H. pylori is harvested in the oral cavity or bowel, these might represent important reservoir for the reinfection and transmission with consequences from treatment. One vector for the transmission of H. pylori are flies, they can carry viable H. pylori in their external surf ces and alimentary tracts .
In animals, the presence of scours in calves is of economic importance. It is estimated that the death lost of calves less than 6 months of age is approximately 2.5% or over 100,000 a year. Most of the mortality and morbidity of the calves are due to infectious diseases, mainly scours. More than 90% of scours in calves is produced by E. coli and Salmonella . Clostridia has proved to be fatal in the majority of cases. There are preventive methods like (I) vaccination of the mothers in order to passively transfer antibodies in colostrum; (2) the use of immunological supplements for milk replacers; (3) the use of probiotics to create a gastro-intestinal healthy environment (4) changes in calf management. None of these protective measures are 100% effective.
Another animal of economic importance is swine. The incidence of diarrhea in neonates and weaned piglets is very high. Again, E. coli and Salmonella are the main microorganisms involved in diarrhea in swine. There are losses in the nursery while piglets are still lactating and after weaning. There are similar preventive methods as in calves. One of the preferred methods is segregated early weaning (SEW) . The basis of early weaning is that the earlier piglets are weaned from the sow the less are the chances of crossover diseases between sow and piglets. This method requires the use of antibiotics.
In both cases, calf and piglet scours, the preferred method of treatment is antibiotics. The European Community has banned the use of 5 antibiotics and in the Unites States the FDA is banning the use of fluoroquinolone in animals due to the development of Campylobacter resistant to this antibiotic. Bacteria resistance has encouraged the development of antibiotic- alternative products.
Terpenes are widespread in nature, mainly in plants as constituents of essential oils. Their building block is the hydrocarbon isoprene (C5H8)n. Terpenes have been found to be effective and nontoxic dietary antitumor agents which act through a variety of mechanisms of action (Crowell and Gould, 1994 and Crowell et al, 1996). Terpenes, i.e. geraniol, tocotrienol, perillyl alcohol, b-ionone and d-limonene, suppress hepatic HMG-COA reductase activity, a rate limiting step in cholesterol synthesis, and modestly lower cholesterol levels in animals (Elson arid Yu, 1994) . D-limonene and geraniol reduced mammary tumors (Elegbede et al, 1984 and 1986 and Karlson et al, 1996) and suppressed the growth of transplanted tumors (Yu et al, 1995) . Terpenes have also been found to inhibit the in-vitro growth of bacteria and fungi (Chaumont and Leger, 1992, Moleyar and Narasimham, 1992 and Pattnaik, et al, 1997) and some internal and external parasites (Hooser, et al, 1986) . Geraniol was found to inhibit growth of Candida albicans and Saccharomyces cerevisiae strains by enhancing the rate of potassium leakage and disrupting membrane fluidity (Bard, et al, 1988) . B-ionone has antifungal activity which was determined by inhibition of spore germination, and growth inhibition in agar (Mikhlin et al, 1983 and Salt et al, 1986) . Teprenone (geranylgeranylacetone) has an antibacterial effect on H. pylori (Ishii, 1993) . Solutions of 11 different terpenes were effective in inhibiting the growth of pathogenic bacteria in in-vitro tests; levels ranging between 100 ppm and 1000 ppm were effective. The terpenes were diluted in water with 1% polysorbate 20 (Kim et al, 1995) . Diterpenes, i.e. trichorabdal A (from R. Trichocarpa) has shown a very strong antibacterial effect against H. pylori (Kadota, et al, 1997) .
Rosanol a commercial product with 1% rose oil has been shown to inhibit the growth of several bacteria (Pseudomona, Staphylococus , E. coli and Hpylori) . Geraniol is the active component (75%) of rose oil. Rose oil and geraniol at a concentration of 2 mg/litre inhibited the growth of H pylori in vitro. Some extracts from herbal medicines have been shown to have an inhibitory effect on H. pylori , the most effective being decursinol angelate, decursin, magnolol, berberine, cinnamic acid, decursinol and gallic acid (Bae, et al 1998) . Extracts from cashew apple, anacardic acid and (E) -2-hexenal, have shown bactericidal effect against H. pylori . There may be different modes of action of terpenes against H. pylori . They could (1) interfere with the phospholipid bilayer of the cell membrane (2) impair a variety of enzyme systems (HMG-reductase) and (3) destroy or inactivate genetic material.
SUMMARY OF THE INVENTION
Prevention and treatment of digestive tract infections by orally administering a biocidal terpene, a biocidal terpene mixture or a liposome-terpene (s) composition before of after the onset of the infection.
Bubbleblower
Member
But it is, if you actually read the study you'll find they use the term “platform”, I used the term medium to put it in a broader perspective;
"all sources of microbial inputs, including below ground compartments should be considered important for optimal Cannabis growth and consumer safety."
"soil is undoubtedly the most important factor..for determining what microbes are present."
Understanding cultivarspecificity and soil determinants of the cannabis microbiome
They destroy your resistance;
“DON disintegrates a human Caco-2 cell monolayer within <1 h after exposure to concentrations as low as 1.39uM.”
QFT.
Fusarium, which produces deoxynivalenol (DON) is the biggest problem and IMO the main cause of CHS.
This post explains how (and solves the mystery why only people younger than 50 suffer from it).
Yes, they can, they are the key for preventing these things, the plants defense system.
People only started getting sick from weed after we started converting terpenes to THC with all our special fertilizers.
We know this thanks to our "Drugs Informatie en Monitoring Systeem" that has been tracking this since 1976.
We never had any cannabis related health problems untill 2001 when these fertilizers became popular.
The Effect of Nitrogen Fertilization on Fusarium Head Blight development and Deoxynivalenol Contamination in Wheat
Mmmm... was think i burned the shit out of this toxicogenic funghi and pathogenic
bacteria with decarboxilation...
but a analyise brings that all samples bring to 5% of this pathogens,
maybe terpenes can deactivate those pathogenic bacteries and funghi cause
for now long time i use BHO and nothing happends...,hmmm...
hope i dont die cause i have a plan to survive...
Sory, but trying to read this hurts my brain.
Not sure if you're trying to say its ok to process moldy weed....but its not ok and in fact super dangerous
Please show us the peer-reviewed science that shows that BHO kills/inactivated mycotoxins, especially those from Fusarium Oxysporum.
No you get wrong Thcvhunter,
first of all i never claimed i used moldy buds for making BHO...
that will be stupid to do and am awared of a danger that
moldy buds brings for health..
thing is that all samples that they tested haved this pathogens,
so normal non-moldy buds still brings pathogens inside self,
that claims Sams link and that is what i commented in mine previous post.
Hope this clears a bit for you...
Kind regards
Effect of medical cannabis on thermal quantitative measurements of pain in patients with Parkinson’s disease
A. Shohet, A. Khlebtovsky, N. Roizen, Y. Roditi, R. Djaldetti
2016 EJP doi:10.1002/ejp.942
Abstract
Background: Cannabis can alleviate pain of various etiologies. This study assessed the effect of cannabis on motor symptoms and pain parameters in patients with Parkinson’s disease (PD).
Methods: Twenty patients with PD who were licensed to use cannabis underwent evaluation before and 30 min after cannabis consumption and again after long-term use. Motor function was assessed with the Unified PD Rating scale (UPDRS) by two raters, one blinded. Pain was assessed with the Pain Rating Index (PRI) and Visual Analogue Scale
(VAS) of the short-form McGill Pain Questionnaire. Thermal quantitative sensory testing (QST) was performed in 18 patients. The two consecutive QST measurements were validated in 12 cannabis-naıve patients with PD.
Results: There was a significant decrease from baseline to 30 min after cannabis consumption in mean motor UPDRS score (38.1 18 to 30.4 15.6, p < 0.0001), total PRI (27 13.5 to 9.7 11, p = 0.001), and VAS score (6.4 2.8 to 3.6 3.1, p = 0.0005). Mean cold pain threshold decreased significantly in the more affected limb, but only after exclusion of two patients who consumed cannabis by vaporizer rather than smoking (19.5 5.2 to 15.6 8.7 °C, p = 0.02). After longterm (median 14 weeks) exposure, mean heat pain threshold decreased significantly in the more affected limb in all treated patients (43.6 3.5 to 40.9 3.3 °C, p = 0.05) and in cannabis smokers (43.7 3.6 to 40.3 2.5 °C, p = 0.008).
Conclusions: Cannabis improved motor scores and pain symptoms in PD patients, together with a dissociate effect on heat and cold pain thresholds. Peripheral and central pathways are probably modulated by cannabis.
Significance: Quantitative sensory test results are significantly altered following cannabis consumption in patients with PD. Cannabis probably acts on pain in PD via peripheral and central pathways.
A. Shohet, A. Khlebtovsky, N. Roizen, Y. Roditi, R. Djaldetti
2016 EJP doi:10.1002/ejp.942
Abstract
Background: Cannabis can alleviate pain of various etiologies. This study assessed the effect of cannabis on motor symptoms and pain parameters in patients with Parkinson’s disease (PD).
Methods: Twenty patients with PD who were licensed to use cannabis underwent evaluation before and 30 min after cannabis consumption and again after long-term use. Motor function was assessed with the Unified PD Rating scale (UPDRS) by two raters, one blinded. Pain was assessed with the Pain Rating Index (PRI) and Visual Analogue Scale
(VAS) of the short-form McGill Pain Questionnaire. Thermal quantitative sensory testing (QST) was performed in 18 patients. The two consecutive QST measurements were validated in 12 cannabis-naıve patients with PD.
Results: There was a significant decrease from baseline to 30 min after cannabis consumption in mean motor UPDRS score (38.1 18 to 30.4 15.6, p < 0.0001), total PRI (27 13.5 to 9.7 11, p = 0.001), and VAS score (6.4 2.8 to 3.6 3.1, p = 0.0005). Mean cold pain threshold decreased significantly in the more affected limb, but only after exclusion of two patients who consumed cannabis by vaporizer rather than smoking (19.5 5.2 to 15.6 8.7 °C, p = 0.02). After longterm (median 14 weeks) exposure, mean heat pain threshold decreased significantly in the more affected limb in all treated patients (43.6 3.5 to 40.9 3.3 °C, p = 0.05) and in cannabis smokers (43.7 3.6 to 40.3 2.5 °C, p = 0.008).
Conclusions: Cannabis improved motor scores and pain symptoms in PD patients, together with a dissociate effect on heat and cold pain thresholds. Peripheral and central pathways are probably modulated by cannabis.
Significance: Quantitative sensory test results are significantly altered following cannabis consumption in patients with PD. Cannabis probably acts on pain in PD via peripheral and central pathways.
