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Natural resistance of animals are including to amounts of mechanism in which we can enhance or strengthen their activities by using some organic / probiotic materials as following

– Physical barrier
: strengthen cell membrane and tight junction by Adimix

– Chemical barrier ; Ultracid can enhance the barrier as
: acidifier / reduce pH
: antimicrobial activity of organic acid

– Complement system
: enhance immune system and physiological function by Adimix and Activo

– Phagocytosis system ; Adimix can help to
: strengthen WBC
: enhance interleukin function

– Probiotic flora such as Toxinil, Unike , Activo can
: manipulate proper condition in GI tract to prevent bacterial colonization
: enhance non- specific immunity

Dr. Tussin Mahamongkol

Sep 05, 2015.


This Simple Difference Between Probiotics and Prebiotics

Two very popular health buzzwords unheard of of ten years ago are probiotics and prebiotics. Most of us have associated these two with benefits to our digestion, but we don’t really know much more than that.

The short version:
•  Probiotics are friendly microorganisms inhabiting our digestive tract that aid digestion and may confer additional health benefits.
•  Prebiotics are non-living, non-digestible carbs that serve as food for Probiotics.

Now the details:
Probiotics are, for the most part, bacteria that reside in our intestinal tract. Other types of probiotics are yeast. Probiotics get into our intestines from foods we eat or supplements. There are many types of probiotics, and each one behaves a bit differently in our gut. Although the term “probiotics” is relatively new, we’ve been ingesting them for thousands of years. Any food that is cultured or fermented has probiotics.

The health benefits of probiotics are potentially wide and varied, but scientists are only starting to understand the complex symbiosis between the gut, the bacteria, and the rest of our body. Some potential health benefits, aside from keeping us regular, include treatment of diarrhea, reduction of lactose intolerance, improved immune system, lower chances of colon cancer, and reduction of blood pressure and cholesterol.

By the way, when you are sick and take antibiotics, you’re killing off the germs that made you ill, but also the probiotics.

On to prebiotics. Unlike probitoics, these are not alive. Most prebiotics are some form of fiber. Our body does not digest fiber, but the bacteria in our gut, including the probiotics, digest the fiber. Feeding these helpful bacteria keeps them doing what they are supposed to do in order to help our health.

Since each of us has different bacteria swimming around in her gut, the effects of the consumption of the same exact probiotics and prebiotics may be very different. Experiment with different foods and see what works for you.

In order for the good bacteria to survive in the bowel, you need to feed them ‘prebiotic’ foods. Prebiotics are non-digestible food fibres that enable good bacteria to stick to the bowel wall and also helps to stimulate their growth.

How do they affect our health?
More and more research is pointing to the numerous benefits of incorporating prebiotics and probiotics in our diets.

“Including probiotics in the diet is one of the best ways to boost immune health and digestion, as well as supporting vitamin B12 and K production and supporting mental health,” says nutritionist .

Prebiotics on the other hand help stimulate the growth and survival of good bacteria and discourage the growth of harmful organisms.

Why it’s important to look after your gut
The digestive system is the workhorse of the body. Not only is it responsible for removing waste material from the body, it’s also responsible for the important task of breaking foods down into glucose and nutrients the body needs for energy and nourishment. The digestive system also constitutes 70 per cent of the body’s immune system which means it performs the important role of defending the body against harmful bacteria and viruses.

All signs point to a growing public interest in the possible benefits of prebiotics and probiotics in digestive health and beyond. However, science has to lead the way to ensure sound evidence is the basis for introduction of interventions for public health and new products in the marketplace. Continued research, evaluation, and public health campaigns are necessary to disseminate accurate and unbiased information.

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Saccharomyces boulardii
Scientific classification

  • Kingdom: Fungi
  • Phylum: Ascomycota
  • Subphylum: Saccharomycotina
  • Class: Saccharomycetes
  • Order: Saccharomycetales
  • Family: Saccharomycetaceae
  • Genus: Saccharomyces
  • Species: S. boulardii Binomial name

Saccharomyces boulardii
Henri Boulard
Saccharomyces boulardii is a tropical strain of yeast first isolated from lychee and mangosteen fruit in 1923 by French scientist Henri Boulard. It is related to, but distinct from, Saccharomyces cerevisiae in several taxonomic, metabolic, and genetic properties.S. boulardii is sometimes used as a probiotic with the purpose of introducing beneficial active cultures into the large and small intestine, as well as conferring protection against pathogenic microorganisms in the host.However, in immunocompromised individuals, S. boulardii has been associated with (fungemia) or localized infection, which may be fatal.
Boulard first isolated this yeast after he observed natives of Southeast Asia chewing on the skin of lychee and mangosteen in an attempt to control the symptoms of cholera. In healthy patients, S. boulardii has been shown to be non-pathogenic, non-systemic (it remains in the gastrointestinal tract rather than spreading elsewhere in the body). It grows at the unusually high temperature of 37 °C (98.6 °F).
S. boulardii is often marketed as a probiotic in a lyophilized form and is therefore often referred to as S. boulardii lyo.

Medical uses
There are numerous randomized, double-blind placebo-controlled studies showing the efficacy of S. boulardii in the treatment and prevention of gastrointestinal disorders.

Acute diarrhea
Two studies each showed a significant reduction in the symptoms of acute gastroenteritis in children, versus placebo, by measuring frequency of bowel movements and other criteria. Children over three months are recommended to take two doses of 250 mg a day (BID) for five days to treat acute diarrhea. Children under three months are recommended to take half a 250 mg capsule or sachet twice daily for five days.

A prospective placebo-controlled study found a significant reduction in symptoms of diarrhea in adults as well taking 250 mg of S. boulardii twice a day for five days or until symptoms are relieved.

Recurrent Clostridium difficile infection
Administration of two 500 mg doses per day of S. boulardii when given with one of two antibiotics (vancomycin or metronidazole) was found to significantly reduce the rate of recurrent Clostridium difficile (pseudomembranous colitis) infection. No significant benefit was found for prevention of an initial episode of Clostridium difficile-associated disease.

Irritable bowel syndrome
A prospective placebo-controlled study found patients with diarrhea-predominant irritable bowel syndrome (IBS) had a significant reduction on the number and consistency of bowel movements. Another study in 2011 did not find any change in bowel frequency.

Inflammatory bowel disease
Further benefits to inflammatory bowel disease (IBD) patients have been suggested in the prevention of relapse in Crohn’s disease patients currently in remission[14] and benefits to ulcerative colitis patients currently presenting with moderate symptoms. The recommended dosage is three 250 mg[dubious – discuss] capsules a day (TID).[citation needed]

Travelers’ diarrhea
Austrian vacationers taking S. boulardii traveling around the world were found to have significantly fewer occurrences of travelers’ diarrhea than those taking placebo.A meta-analysis of twelve studies from 1977 to 2005 investigating the efficacy of probiotics found them to be safe and effective for the treatment of travelers’ diarrhea, having a pooled relative risk of 0.85 with respect to placebo (between 0.79 and 0.91 with 95% confidence). Three of four studies concerning S. boulardii found it to be an effective treatment. The recommended dosage is one 250 mg[dubious – discuss] capsule or sachet per day (QD).[citation needed]

Antibiotic-associated diarrhea
There is evidence for its use in the prophylactic (preventative) treatment of antibiotic-associated diarrhea (AAD) in adults. There is further evidence for its use to prevent antibiotic-associated diarrhea in children

HIV/AIDS-associated diarrhea
S. boulardii has been shown to significantly increase the recovery rate of stage IV AIDS patients suffering from diarrhea versus placebo. On average, patients receiving S. boulardii gained weight while the placebo group lost weight over the 18 month trial. There were no reported adverse reaction observed in these immunocompromised patients.

Mechanisms of action

Antitoxin effects
S. boulardii secretes a 54 kDa protease, in vivo. This protease has been shown to both degrade toxins A and B, secreted from Clostridium difficile, and inhibit their binding to receptors along the brush border. This leads to a reduction in the enterotoxinic and cytotoxic effects of C. difficile infection.[21]

Antimicrobial effects
Escherichia coli and Salmonella typhimurium, two pathogenic bacteria often associated with acute infectious diarrhea, were shown to strongly adhere to mannose on the surface of S. boulardii via lectin receptors (adhesins). Once the invading microbe is bound to S. boulardii, it is prevented from attaching to the brush border; it is then eliminated from the body during the next bowel movement.[22]

Trophic effects on enterocytes
The hypersecretion of water and electrolytes (including chloride ions), caused by cholera toxin during a Vibrio cholerae infection, can be reduced significantly with the introduction of S. boulardii. A 120 kDa protease secreted by S. boulardii has been observed to have an effect on enterocytes lining the large and small intestinal tract–inhibiting the stimulation of adenylate cyclase, which led to the reduction in enterocytic cyclic adenosine monophosphate (cAMP) production and chloride secretion.

During an E. coli infection, myosin light chain (MLC) is phosphorylated leading to the degradation of the tight junctions between intestinal mucosa enterocytes. S. boulardii has been shown to prevent this phosphorylation, leading to a reduction in mucosal permeability and thus a decrease in the translocation of the pathogenic bacteria.
Polyamines (spermidine and spermine) have been observed to be released from S. boulardii in the rat ileum. Polyamines have been theorized to stimulate the maturation and turnover of small intestine enterocytes.[25]

Anti-inflammatory effects
Interleukin 8 (IL-8) is a proinflammatory cytokine secreted during an E. coli infection in the gut. S. boulardii has been shown to decrease the secretion of IL-8 during an E.

Clostridial Clostridium perfringens types A and C and Clostridium difficile are the principal enteric clostridial pathogens of swine. History, clinical signs of disease, and gross and microscopic findings form the basis for a presumptive diagnosis of C. perfringens type-C enteritis. Confirmation is based on isolation of large numbers of type-C C. perfringens and/or detection of beta toxin in intestinal contents.

Diagnosis of C. perfringens type-A infection, however, remains controversial, mostly because the condition has not been well defined and because type-A organisms and their most important major (alpha) toxin can be found in intestinal contents of healthy and diseased pigs. Isolation of large numbers of C. perfringens type A from intestinal contents, in the absence of other enteric pathogens, is the most reliable criterion on which to base a diagnosis. Recently, beta2 (CPB2) toxinproducing C. perfringens type A has been linked to disease in piglets and other animals. However, implication of CPB2 in pathogenesis of porcine infections is based principally on isolation of C. perfringens carrying cpb2, the gene encoding CPB2, and the specific role of CPB2 in enteric disease of pigs remains to be fully defined. Clostridium difficile can also be a normal inhabitant of the intestine of healthy pigs, and diagnosis of enteric infection with this microorganism is based on detection of its toxins in feces or intestinal contents.

Clinical signs of disease and lesions. Clinical disease can be peracute, acute, or chronic, with signs of the acute and peracute conditions including intense abdominal pain, depression, and bloody diarrhea (Fig. 1), which begins 8 to 22 hours after exposure to C. perfringens type C. Sow feces contains small numbers of type-C organisms, and these multiply rapidly in the small intestine of piglets, out-competing other bacteria and becoming the dominant organisms in the population. The course of the disease is usually 24 or fewer hours in 1- to 2-day-old piglets, but chronic disease (usually in older animals) can persist for 1 or 2 weeks, and is characterized by persistent diarrhea without blood, and dehydration.33 Marked anal hyperemia can be observed just before death in acute and chronic forms.
Clostridium perfringens type A resembles type C in culture, but it produces CPA and not CPB . Also, many strains of C. perfringens type A produce CPB2, and recent information suggests a role for this toxin in porcine clostridial enteritis, as nearly all type-A strains isolated from pigs with this condition produce CPB2. Clinical signs of type-A enteritis have been reproduced by oral inoculation with pure cultures and culture supernatants of C. perfringens type A. Type-A disease develops during the first week of life, and sows are the likely source of infection. However, diagnosis is complicated by the fact that differentiation between normal flora and disease-causing strains is not possible, and it may be that under appropriate conditions, any strain of C. perfringens type A can cause disease.

Thus, discussion of the epidemiology of type-A enteric infections is highly speculative. The exception to this statement is the relatively new information indicating that most strains from disease cases are CPB2 positive.
Clostridium perfringens is an inefficient sporulator, but spores are nonetheless likely to be important in maintaining the organism in the environment. The organism can also be isolated from pig feed.

Penicillin, Ampicillin, Tylosin, Lincomycin.

Dr. Tussin Mahamongkol

Antibiotic growth promoter (AGP) is a specific kind of antibiotics mixed in animal feeds resulting to bacteriostatic or/ and bactericidal effects in animals that leads to prevention of bacterial infections , losses of sickness and mortality and also increase of productive performance as well.

By trend of global bans of AGPs’ usages, we need products to replace AGPs. One of them is organic acid. Organic acids have been used for decades in commercial compound feeds, mostly for feed preservation, for which formic and propionic acids are particularly effective. In EU, these two organic acids and several others (lactic, citric, fumaric and sorbic acids) and their salts (e.g., calcium formate, calcium propionate) are used under classification ‘feed preservatives’. One such organic acid salt is also approved for use as a zootechnical additive (product that formerly includes antibiotics and other growth promoters) for enhancing performance in pigs.

Experience has shown that acidifiers are the most reliable product group of non – antibiotic growth promoters available in Europe and can also be used safely and effectively with other additives. The main mode of action of organic acids is through their antimicrobial effects, the magnitude of which is dependent on the chemical properties of the individual acid or acid salt.

Numerous trials have demonstrated their mode and magnitude of action and have established effective doses for piglets, fattening pigs and sows. The use of formic acid and its double potassium salt in particular have been the subject of intense investigation, with the result that we now know its dose – dependent effect on growth performance and feed conversion in pigs under a range of different environmental conditions and feed formulations. Its main mode of action is its antimicrobial effect, which makes it comparable with antibiotic growth promoters; however organic acids also reduce pH in stomach, which optimizes condition for pepsin activity and increases the digestibility of nitrogen, phosphorus and several minerals. This is not only beneficial in sparing nutrients but also prevents losses that might otherwise contribute to environmental pollution. More recently, the use of acids in general and diformates in particular has spread to the poultry and aquaculture industries. Its performance – enhacing effects in poultry and fish are documented. With a growth – promoting effect similar to that of AGPs switching growth promoters to organic acids, especially potassium diformate, can be achieved without detriment to profitability.

Organic acids in pig diets.
Addition of organic acids to feed combat susceptible microorganisms, including pathogenic bacteria and some fungi, which would otherwise cause spoilage and reduce its nutritive value by metabolizing the starch and protein therein.

In pig diets, organic acids and their salts also take effect in GI tract, mainly in the proximal part – the stomach and small intestine. Firstly, organic acids lower the pH of the stomach content, which can be especially beneficial at weaning, when the gastric acid secretion capacity of the animal’s stomach is often insufficiently developed. Although pH reduction can inhibit pathogen growth and optimize pepsin activity, pH alone does not account for the numerous benefits reported when organic acids are included in diets for pigs. Inorganic acids such as hydrochloric and phosphoric acid (both of which reduce stomach pH), do not improve growth rate or feed conversion of pigs in vivo. Supplementation of diets with organic acids reduces the pH in the stomach, especially in weaning pigs, where it stimulates the conversion of inactive pepsinogen to active pepsin. This may improve protein digestibility and decrease the rate of gastric emptying. Organic acids also stimulate exocrine pancreatic secretion of enzymes and bicarbonate, thus assisting protein and fat digestion.
Furthermore, organic acid anions can complex with calcium, phosphorus, magnesium and zinc, improving the digestion of these minerals and reducing the excretion of supplemental minerals and nitrogen. This is particularly useful from the perspective of the European pig production systems, which have come under scrutiny from legislators because of their emissions into environment. The bacteriostatic or bactericidal effects of organic acid anions also take effect in the proximal GI tract. Here, the differential inhibition of pathogens compared to beneficial bacteria such as Lactobacilli and Bifidobacteria improve the microbial load (Eubiosis)in the tract, preventing post – weaning diarrhea. As several studies have shown that the bactericidal effect of organic acids persists in the absence of a significant decrease in pH, they are useful in combating bacterial pathogens in grower – finisher pigs and sows.

Other studies have demonstrated that adding organic acids in diets for pigs stimulates secretion of pancreatic enzymes – especially butyrates and propionates – may influence gut morphology and intermediary metabolism via metabolic enzyme activity. Butyric acid for instance is the main energy source for the epithelial cells of the large intestine and is considered to be effective for promoting thr epithelial growth.

Organic acids in poultry diets
One of the first reports of improved broiler performance when diets were supplemented with single acid was for formic acid (Vogt et al., 1981). Subsequently, Izat et al. (1990a) reported reduced levels of Salmonella spp. in carcass and caecal samples after including calcium formate in broiler diets. Izat et al. (1990b) showed that buffered propionic acid could be used to counteract pathogenic microflora in the intestine of broiler chickens, which result in a significant reduction in carcass contamination with E. coli and Salmonella spp.

The use of pure formic acid in breeder diets reduced the contamination of tray liners and hatchery waste with S.enteritidis (Humphrey and Lanning. 1988). Hinton and Linton (1988) studied salmonella infections in broilers using a mixture of formic and propionic acids. They demonstrated that 0.6 % of this organic acid blend was effective in preventing intestinal colonization with Salmonella spp. from contaminated feeds.

Improvements in broiler performance and hygiene in response to organic acids are often reported. However, an important limitation is that organic acids are rapidly metabolized in the foregut (crop and gizzard) which will reduce their impact on growth performance. Double salts of organic acids such as potassium diformate and sodium diformate, which reach the small intestine have been shown to have a significant impact. Furthermore, diformates reduced number of pathogenic bacteria (Salmonella, Campylobacter and Enterobacter)in broiler chickens and increase number of Lactobacilli and Bifidobacteria (Luckstadt and Theobald. 2009). Mickkelsen et al. (2009) showed that 0.45% potassium diformate reduced mortality caused by necrotic enteritis (Clostridium perfringens).

The mode of action of acidifiers in poultry is mainly antimicrobial, whereas in pigs, a key activity is reduction of stomach pH. Other trials have shown improved health status in chickens as demonstrated by improved gut microflora (lower Enterobacteria numbers and high Lactobacilli and Bifidobacteria counts).

Dr. Tussin Mahamongkol

Sep 05, 2015.