Bacterial gastrointestinal tract infections,all natural remedies for yeast infections,bacterial infection medication over the counter 2014 - PDF 2016

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In the present study therefore, the effects of feeding of Chikuso-1 and CO119 on bacterial flora of contents collected from various regions of gastrointestinal tract were examined in Holstein calves.
Bacterial enumerations from gastrointestinal contents: Ten gram of the gastrointestinal contents was blended with 90 mL of sterilized distilled water and serial dilutions from 10-1-10-8 were made.
Intestinal motility is the other name for the movement of intestinal muscles.
The increased sensitivity of the bowel can occur due to various problems associated with the BGA. Brain Gut Axis: Your brain is in constant contact with your gut through a highway of information. As you can see in the figure, this connection allows exchange of information between the central and gut (enteric) nervous systems.
Stress activates the Brain-Gut Axis and this activation results in release of numerous chemical mediators in the gastrointestinal tract. Lactose intolerance or lactase deficiency is another disorder that must be seriously considered when diagnosing a patient as having IBS. Dairy cows are often fed high grain diets to meet the energy demand for high milk production or simply due to a lack of forages at times.
IntroductionDairy cows are often fed high grain diets to meet the energy demand for high milk production or simply due to a lack of forages at times.
ConclusionsFeeding dairy cows diets containing high proportions of grain can lead to release of bacterial immunogens such as LPS in a large amount in the digestive tract. AcknowledgementsThe review was supported by funds from the National Key Basic Research Program of China (No. The previous researches showed that addition of two selected strains, Lactobacillus plantarum Chikuso-1 and Candida sp. Gastrointestinal contents were collected from rumen, duodenum, jejunum, ileum, cecum and colon, respectively. From each dilution, 0.05 mL of suspension was spread on Nutrient Agar (Eiken Chemical, Tokyo, Japan), de Man-Rogosa-Sharpe Agar (Becton, Dickinson and Company, Maryland, USA) and Blue Light Agar (Eiken Chemical) for enumeration of aerobic bacteria, LAB and coliform, respectively. 1b, the number of coliform in microbe-fed group seems to be smaller than that in control group in upper gastrointestinal tract such as rumen, duodenum and jejunum.
These suggest that feeding of the microbe improves bacterial flora in upper regions of gastrointestinal tract of Holstein calves.ACKNOWLEDGEMENTThis research was supported in part by Secure and Healthy Livestock Farming Project from the Ministry of Agriculture, Forestry and Fisheries of Japan (No. The gastrointestinal system moves food from the stomach into the small bowel (small intestine) and eventually into the large bowel (colon). For example irritation of nerve endings in the afferent pathway of the BGA may cause supersensitivity of the system due to release of some chemicals (cytokines and Serotonins) or the hypersensitivity could have its origin from central components of the BGA or the brain.
This is because a pain inhibitory center within the brain can suppress the sensation of pain.
This axis transfers information from brain to gastrointestinal (GI) tract or from GI tract to brain. These mediators change the sensitivity of sensory nerves, intestinal barrier integrity, intestinal immune properties, intestinal motility and many other intestinal functions. Due to the acidic environment of the stomach as well as the digestive enzymes in the small bowel, the environment of the small bowel is almost germ-free.
As a result, ruminal acidosis, especially subacute ruminal acidosis (SARA), occurs frequently in practical dairy production.
LPS can be translocated into blood due to possible alterations of permeability and injuries of the epithelial tissue of the digestive tract (particularly the lower gut). CO119 to milk replacer significantly suppressed calf diarrhea and increased the number of fecal Lactic Acid Bacteria (LAB). Aliquot of the dilution was heated in 75°C for 15 min and spread on Nutrient Agar and Clostridia Count Agar (Eiken Chemical) for enumeration of bacilli and clostridia, respectively. The first pathway of this connection is called the efferent pathway; the second one is the afferent pathway. When the bowel is irritated, these receptors convey this information to the brain through the afferent pathway of the BGA. Among a wide range of physiological effects of chemicals released from mast cells into the GI tract is an increased sensitivity of sensory terminals of the afferent BGA (BGA input). In some instances, this germ-free environment becomes populated with bacteria, which competes with the host (human) to acquire nutritious materials that are supposed to be absorbed across the wall of the small bowel. When SARA occurs, bacterial endotoxin (or lipopolysaccharide, LPS) is released in the rumen and the large intestine in a large amount. It has been recognized that the yield of harmful and toxic substances, such as lactate (particularly the D-isomer), ethanol, histamine, tyramine, tryptamine, and bacterial endotoxin (or lipopolysaccharide, LPS), in the rumen increases as a result of grain-based SARA [1, 2].
As a result, immune responses are caused by circulating LPS, which include increases in the concentrations of neutrophils and the acute phase proteins in the bloodstream. It remains unknown however, whether feeding of the microbe could affect bacterial flora in the specific areas of gastrointestinal tract in host animals. The first site of control is located in the intestine and is called the enteric nervous system.
The brain also can control the functions of the GI tract, such as digestion, secretion, absorption and movement of the bowel through the efferent pathways of the BGA. The increased activity of the afferent sensory nerves could result in increased BGA activity which in turn results in increased output of this system in the form of increased discharge of the efferent nerves of the BGA. The intestines of babies typically have a strong capacity to digest this milk sugar. The bacteria also make a variety of toxins and irritants that can result in bowel inflammation and irritation, creating symptoms of diarrhea, bloating and abdominal pain. Many other bacterial immunogens may also be released in the digestive tract following feeding dairy cows diets containing high proportions of grain. Other immunogenic virulence factors such as fimbrial adhesins, heat-stable and heat-labile toxins, and inflammatory peptides are also released in the digestive tract due to disturbance in microbial ecology [2].
Changes in blood concentrations of metabolites and minerals were also observed, which indicates metabolic alterations occur following the entry of endotoxin into blood.
In the present study, the effects of feeding of Chikuso-1 and CO119 (microbe-fed) on bacterial flora of various gastrointestinal regions were examined in Holstein calves. The second site of control is located in the brain, and is part of the central nervous system.


Food stimuli usually cause symptoms by affecting the afferent pathways while psychological stimuli do it through affecting the efferent pathways of BGA.
The increased discharge of the efferent nerves of the BGA translates into an increase in the release of mast cell mediators.
LPS can be translocated into the bloodstream across the epithelium of the digestive tract, especially the lower tract, due to possible alterations of permeability and injuries of the epithelial tissue. Among those harmful and toxic substances, the bacterial endotoxin LPS has received a lot of attention because LPS potentially causes systemic immune responses and metabolic changes in the body. The bacterial immunogens can also lead to reduced supply of nutrients for synthesis of milk components and depressed functions of the epithelial cells in the mammary gland. Gastrointestinal contents of control and microbe-fed calves were collected from rumen, duodenum, jejunum, ileum, cecum and colon, respectively and immediately inoculated on the selective agar media for LAB, coliform, aerobic bacteria, bacilli and clostridia for bacterial enumeration.
These two regulatory systems are closely linked through a highway of nerves and the whole system is called the Brain Gut Axis (BGA).
This may result in increased pain sensation with minimal irritant stimuli (hyperalgesia).
Recently, there are several reports that claim that a significant group of IBS patients have bacterial overgrowth as the cause of their symptoms.
However, the other immunogens of bacterial origin induced by feeding high grain diets are attracting attention. The immune responses and metabolic alterations caused by circulating bacterial immunogens will exert an effect on milk production. Immune responses are subsequently caused by circulating LPS, and the systemic effects include increases in concentrations of neutrophils and the acute phase proteins such as serum amyloid-A (SAA), haptoglobin (Hp), LPS binding protein (LBP), and C-reactive protein (CRP) in blood.
This paper reviews the yield and translocation of LPS as well as other bacterial immunogens in the digestive tract and the immune responses and metabolic alterations caused by LPS in dairy cows fed diets containing high portions of grain. Results have shown that increases in concentrations of ruminal LPS and plasma acute phase proteins (CRP, SAA, and LBP) are associated with declines in milk fat content, milk fat yield, 3.5% fat-corrected milk yield, as well as milk energy efficiency.
The present results suggest that feeding of Chikuso-1 and CO119 improves bacterial flora on rumen and upper small intestine in the gastrointestinal tract of Holstein calves. These problems are especially likely to occur when a large amount of this type of sugar is consumed. The review is based on studies carried out with dairy cows although studies involving beef cattle are also cited where data on dairy cows are lacking.Lipopolysaccharide and Other Bacterial Immunogens Released in the Rumen and the Large IntestineIt is widely accepted that free ruminal LPS concentrations increase after grain engorgement, especially during experimentally-induced SARA. Emotions, feelings, and stress can modify the function of this inhibitory center and it is not surprising that psychological well-being has an important impact on the magnitude and severity of the perceived pain. Undigested sugar will eventually be consumed by bacteria in the large bowel and produce several gases. Blood glucose and nonesterified fatty acid concentrations are enhanced accompanying an increase of blood LPS after increasing the amount of grain in the diet, which adversely affects feed intake of dairy cows.
Thus is short answer the effect of stress can persist even in the absence of initiating factors. One such gas is hydrogen, which is used to diagnose this problem with a Breath Test. As the proportions of grain in the diet increase, patterns of plasma I?-hydoxybutyric acid, cholesterol, and minerals (Ca, Fe, and Zn) are also perturbed. Symptoms of IBS are common among people with lactose intolerance, particularly distension and gas following consumption of dairy products. They also found feeding grain to cows not adapted to grain resulted in higher free ruminal endotoxin, and the endotoxin concentration in the rumen increased by 15 to 18 times within 12 hours after SARA was induced by feeding grain.
It has been demonstrated that increases in concentrations of ruminal LPS and plasma acute phase proteins (CRP, SAA, and LBP) are associated with declines in milk fat content, milk fat yield, 3.5% fat-corrected milk yield, as well as milk energy efficiency.
A decline in ruminal pH during SARA causes death and cell lysis of Gram-negative bacteria, resulting in an increase in free ruminal LPS concentration [1a€“3]. However, rapid growth of Gram-negative bacteria can also result in the shedding of LPS in the rumen [1, 10].
LPS released during growth of bacteria may account for as much as 60% of that released in the rumen [11]. It was reported that the autolysis of Fibrobacter succinogen during rapid growth was 10 times higher than that during the stationary phase [12].
It is possible that a certain range of ruminal pH after grain engorgement is conducive to bacteria rapid growth, which leads to an increase in free ruminal LPS concentration. It was shown that high-grain diets which were normally associated with SARA resulted in much higher numbers of E.
It is suggested that the increased shedding of LPS during the early hours postfeeding is due to rapid growth of Gram-negative bacteria, and the later release of LPS is because of bacterial cell lysis as a result of the lower pH in the rumen.LPS may also be produced in other parts of the gastrointestinal tract. During grain-based SARA, more starch may enter the lower digestive tract including the ileum and the large intestine where the metabolite profile may resemble that in the rumen and LPS may be produced in a significant amount. They pointed out feeding forage pellets did not increase the content of starch in the diet. Therefore, the increase in cecum LPS could be attributed to more starch entering the lower gut rather than the acidic disturbance in the lower gut.The starch entering the lower gut may be conducive to the growth of Gram-negative bacteria, which may result in an increase in LPS as described above.
Grain feeding (90% grain in the diet) increased the numbers of anaerobic bacteria in the colon by 1000-fold.It is also worth mentioning that other immunogenic virulence factors may be produced by pathogenic E.
For example, ruminants, especially cattle, are the major reservoir of Shiga toxin-producing E. Even healthy cattle can shed a significant amount of STEC which has led to frequent infections in humans around the world [16].Translocation of the Bacterial Immunogens in the Digestive TractEndotoxin produced in the digestive tract can be translocated into the bloodstream, thus the concentration of blood LPS increases [4, 17]. It was also observed in other studies that SARA led to a rise of blood LPS concentrations [18, 19]. Although there is a general agreement that LPS translocation into blood occurs as a result of grain-induced SARA, the translocation sites remain unknown. There is no direct evidence that free ruminal LPS during grain-induced SARA is translocated across the rumen wall into circulating blood. Rumen epithelium has a multilayer structure whose tight junctions are located in the middle layers, stratum grannulosum, and spinosum [20]. Although the external layer of rumen epithelium has no tight junctions, it may have up to 15 cell layers, which can limit the permeability of LPS, a large molecule [21]. Studies were conducted to investigate ruminal absorption of endotoxin in steers by administering 51Cr-labeled E.


The results showed no absorption either through lymph (the thoracic duct) or blood (the portal vein) occurred in any of the steers, whether forage-fed (100% alfalfa hay diet), grain-fed (92% concentrate diet based on sorghum grain), or ruminally acidotic. Therefore, it seems the ruminal epithelium is impermeable to endotoxin at the physiological state unless the rumen epithelial structure is disrupted to a greater extent. Epithelium in the intestines is of a monolayer structure with tight junctions at the apical pole of the cells. However, since the rumen is an immense LPS source, LPS entering the intestines may not be completely detoxified in the duodenum and may be translocated into circulation across the intestines.
In addition, a source of LPS which is translocated into blood circulation may be produced originally in the lower gut.
The bypass starch which reaches the ileum and large intestine may result in a change of microbiota there and thus the release of LPS in a manner described previously for the rumen. In fact, many forms of starch can pass through the pregastric stomach (rumen) to the intestines [28]. However, in their study an alfalfa-pellet induced SARA challenge did not increase cecum LPS release compared with control because feeding forage pellets did not increase the content of starch in the diet. Although free rumen LPS concentration increased by 3.5-fold, this increase was not accompanied by increases in LPS and the acute phase proteins such as LPS binding protein (LPB), serum amyloid-A (SAA), and haptoglobin (Hp) in peripheral circulation. They suggested that LPS translocation across rumen epithelium did not occur, neither did the translocation across intestinal epithelium. The reason could be that either LPS produced in the rumen during SARA failed to penetrate the rumen wall, or feeding alfalfa pellets did not increase additional starch flow to the intestines to modify the profile of bacterial communities of the lower gut. Collectively, LPS can be produced in the lower gut following feeding a high grain diet, thus it may disrupt the barrier function of monolayer epithelial structure of the intestines as described above. Although an in vitro study with an Ussing chamber system demonstrates that LPS goes through the colon of ruminant animals [22], in vivo studies are warranted to verify that the barrier failure and subsequent LPS translocation occur in the lower gut after a grain-based challenge.The Immune Response to the Bacterial ImmunogensAfter LPS is translocated into the blood stream, immune responses are subsequently caused by circulating LPS [31], and the systemic effects include an increase in the blood concentrations of neutrophils [3] and the acute phase proteins, such as SAA, Hp, and LPB [4]. The increase of acute phase proteins in the systemic circulation is a non-specific acute phase response activated by endotoxin. The translocation of LPS into the systemic circulation stimulates the release of proinflammatory cytokines such as interleukin-1 (IL-1), IL-6, and tumor necrosis factor-I± (TNF-I±) by mononuclear phagocytes, and these mediators in turn result in enhanced secretion of acute phase proteins from hepatocytes [32].When the proportion of concentrate in steer diets was enhanced from 0% to 76%, ruminal LPS concentrations were continually increasing, and the acute phase proteins (SAA and Hp) in plasma also kept rising [9].
Many studies have confirmed that increases in ruminal LPS content result in a rise of the acute phase proteins such as SAA [5, 6, 33], LBP [6, 21], and C-reactive protein (CRP) [6, 33] in blood of dairy cows. Therefore, the circulating LPS resulting from feeding increasing proportions of grain to dairy cows can lead to proinflammatory reactions, and in turn milk production in dairy cows can be adversely affected. It was demonstrated that increases in concentrations of ruminal LPS and plasma acute phase proteins (CRP, SAA, and LBP) were associated with declines in milk fat content, milk fat yield, 3.5% fat-corrected milk yield, as well as milk energy efficiency [33]. Other immunogenic virulence factors in the digestive tract following feeding a high grain diet may have contributed to the inflammation which has been observed in many studies on grain-induced SARA in dairy cattle.
For example, a variety of virulence factors that have the potential to cause inflammation are produced by Escherichia coli spp., as well as other members of the Enterobacteriacae [34]. These virulence factors include fimbrial adhesins, heat-stable and heat-labile toxins, and inflammatory peptides. For example, low ruminal and intestinal pH due to high grain feeding increases the risk of shedding enterohemorrhagic E. Blood glucose was enhanced accompanying an increase of blood LPS during a grain-based SARA challenge [4]. In fact, many studies showed feed intake decreased following occurrence of SARA [37a€“39], and reduced feed intake is a consistent sign of SARA in both dairy cows [2, 40, 41] and beef cattle [42, 43]. It can be seen that raising barley grain proportion from 0 to 15% did not affect feed intake, whereas feed intake was reduced significantly after barley proportions reached 30 and 45%. The barley proportions and DM contents in the diets of the aforementioned two studies were different, which might serve as an explanation for the differences in DM intake between the two studies.The lower feed intake cannot be simply attributed to increases in blood glucose and NEFA after increasing grain amount in the diet.
Feeding dairy cows high-grain diets rich in rapidly fermentable carbohydrates will lead to increased yield of volatile fatty acids, especially propionate in the rumen, and its absorption into the bloodstream [44]. The absorption of propionate into blood circulation or its effects on rumen receptors may result in decreased feed intake in cows fed high grain diets [6].
In addition, deceased feed intake with increasing the amount of grain in the diet may be due to enhanced release of endotoxin and other bacterial immunogens in the digestive tract and their translocation into blood. Increased endotoxin concentrations in the bloodstream will lead to release of cytokines such as IL-1, IL-6, and TNF-I± due to activation of macrophages [32], and IL-1 and TNF-I± can suppress feed intake in different species [45].After increasing the proportions of grain in the diet, diurnal patterns of plasma I?-hydoxybutyric acid, cholesterol, and minerals (Ca, Fe, Zn, and Cu) were perturbed [36, 46].
When dairy cows were fed diets containing barley grain at 0, 15, 30 and 45% (DM basis), plasma I?-hydoxybutyric acid and cholesterol concentrations decreased with increasing barley proportions in the diet [36]. Increasing the amount of barley grain in the diet was also associated with quadratic responses of plasma Ca, Fe and Zn concentrations [46].
Their study revealed that the increase in rumen endotoxin in response to high grain diet, and the resulting increases in plasma SAA and CRP, were strongly correlated with fluctuations of plasma minerals [46].
The changes in plasma concentrations of metabolites and minerals as a result of increasing grain amount in the diet may have an effect on the health and productivity of dairy cows. A detailed discussion on this issue is beyond the scope of this paper, and a review paper published recently by Ametaj et al. The redirection or repartition of nutrient use in addition to a low nutrient supply due to depressed low feed intake will decrease nutrient flow to the mammary gland.
Furthermore, when endotoxin and other immunogens are transported to the mammary gland through blood circulation, metabolism in this tissue can be affected. On the one hand, the bacterial immunogens that enter the mammary tissue will elicit a local immune response, and more nutrients or precursors of milk components will be directed to support immune response processes including the synthesis of immune molecules. The repartition of precursor use will lead to less precursors being used for synthesizing milk components, resulting in reduced synthesis of milk components. On the other hand, the bacterial immunogens entering the mammary tissue may directly exert harmful effects on the mammary epithelial cells, which may lead to depressed functions and proliferation of the epithelial cells and increased cell apoptosis. Pieces of evidence pinpoint the suppressive effects of LPS on key enzymes, such as fatty acid synthetase and acetyl-CoA carboxylase which are related to de novo fatty acid synthesis [48, 49] in the mammary tissue and down-regulation of the activity of lipoprotein lipase [50] which is involved in the uptake of fatty acids for incorporation into milk fat [51].
Moreover, LPS in the mammary tissue will activate neutrophils and activated neutrophils are able to produce a large quantity of bactericidal molecules such as reactive oxygen species that have been associated with tissue damage. It was demonstrated in vitro that activated blood neutrophils had a cytotoxic effect on bovine mammary epithelial cells [52] potentially through the release of reactive oxygen species such as hydroxyl radicals [53].



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