The following are May 2013 photo's of Cristina's EPI dog, Sadie's poo before and after treatment with Tylan for SIBO:
Sadie's poo prior to treatment with Tylan:
Sadie's poo after 1 week on Tylan:
by: Dr. Elias Westermarck
Tylosin-responsive diarrhea (TRD) is a syndrome that includes all cases in which tylosin antibiotic treatment has had a positive effect on treating dogs with intermittent or chronic diarrhea. Antibiotic treatment often leads to resolution of clinical gastrointestinal (GI) signs, and thus the term antibiotic-responsive diarrhea (ARD) was coined. Recently, trials have been published in which tylosin proved to be particularly effective in treating dogs with chronic or intermittent diarrhea, with the effect of tylosin differing from that of other antibiotics, thus indicating that the more newly established term TRD is more appropriate than ARD.
Tylosin is a macrolid, bacteriostatic antibiotic that has activity against most Gram-positive and Gram-negative cocci, Gram-positive rods and Mycoplasma. However, the Gram-negative bacteria Escherichia coli and Salmonella spp. are intrinsically tylosin-resistant. Tylosin is used only in veterinary medicine, and its most common indications are treating pigs with diarrhea or poultry with chronic respiratory diseases. Tylosin has also been used as a feed additive in food animal production, and it has been shown to increase gain and feed efficiency, especially in pigs. Debate about the mechanisms underlying tylosin-mediated growth enhancement is ongoing.
Tylosin is usually used in powder form for pigs and poultry. In Finland and in some other countries, tylosin is also available in tablet form, facilitating its use in dogs.
Our experience with tylosin is derived from numerous studies with dogs suffering from exocrine pancreatic insufficiency (EPI).These studies have clearly shown that tylosin has a favorable effect as a supportive therapy on dogs with EPI.
In Finland, tylosin has for years been the most common drug in the treatment of unspecific intermittent or chronic diarrhea in dogs. Anecdotal reports by veterinarians and dog owners reveal that many dogs with diarrhea respond well and quickly to tylosin treatment, generally within a few days of initiation of treatment. When treatment is discontinued, however, diarrhea reappears in many dogs within a matter of weeks or months. Some dogs need a treatment over very long period. Even so, the effect of controlling diarrheal signs does not appear to diminish with time, and thus there is no need to increase the dosage of the medication. No apparent tylosin-associated adverse effects have been reported.
TRD can affect dogs from all breeds and ages but is most often seen in middle-aged, large-breed dogs. The diarrea signs appear often as intermittent but progressivly become more frequent and end as persistent diarrhea. Abnormal loose fecal consistency is the predominant sign. The majority of the owners describe their dogs' feces as watery and/or mucoid indicating that TRD affects both the small and large bowel. Increased frequency of borborygmus and flatulence are also typically seen. Vomiting is occasionally seen during the diarrheal outbreaks.
In dogs with TRD the blood parameters are usually normal. Also the abnormal findings in diagnostic imaging studies and histological examination of intestinal biopsies, are only mild or completely absent.
Only a few studies on treating diarrheal signs in dogs with tylosin have been published. Van Kruiningen, (1976) reported more than 30 years ago that tylosin had a good effect in treatment of unspecific canine diarrhea. Recently, our study group performed two clinical trials to obtain more information on TRD. The first study included 14 adult pet dogs of 12 different breeds. Each dog's diet remained unchanged throughout the study. The dogs had shown chronic or intermittent diarrheal signs for a period of more than one year. Diarrhea had been successfully treated with tylosin for at least six months, and the treatment had been discontinued at least twice but the signs had always occured. When the study commenced, all dogs had been on tylosin for at least one month and were otherwise healthy. Thereafter, tylosin was discontinued and the dogs were monitored for a period of up to one month to determine whether signs of diarrhea would reappear, as suggested by the clinical history. Diarrhea reappeared in 12/14 dogs (85.7%) within 30 days. During the treatment trial diarrhea ceased with tylosin in all dogs within three days and in most dogs within 24 hours. In contrast, prednisone did not completely resolve diarrheal signs, and the probiotic Lactobacillus rhamnosus GG did not prevent the relapse of diarrhea in any of the dogs.
In the second study in an experimental dog colony, seven beagles showed signs of chronic diarrhea for at least one month. The dogs were treated with tylosin for ten days. During the treatment period the feces became significantly firmer, although they remained unacceptably loose. When the treatment was discontinued, diarrhea reappeared within three weeks. Treatment with other antibiotics (metronidazole, trimethoprim-sulfadiazine, or doxycycline) or with prednisone had almost no effect on fecal consistency, the feces remaining abnormally loose in all dogs. The diet was then changed for a ten-day period from a highly digestible moist pet food to a dry food developed for normal adult dogs. The feces again became significantly firmer, although they remained loose in some dogs. The dry food period was then extended to three months, but the fecal consistency continued to fluctuate from ideal to diarrhea. Since the consistency was not satisfactory, the dogs were treated a second time with tylosin for ten days. The feces then became normal in consistency and remained so throughout the entire three-month follow-up time. The study revealed that in the experimental dogs with chronic diarrhea the fecal consistency became significantly firmer both with tylosin treatment and with dietary modification. Neither of the treatments alone was sufficient to obtain ideal fecal consistency, but when the dogs were treated simultaneously with both regimes, permanent ideal fecal consistency was attained. The study thus indicated that tylosin and feeding regimes have synergic effects.
The etiology of TRD remains obscure. Since tylosin is an antimicrobial agent, it has been speculated that some pathogenic bacteria are likely responsible for the diarrheal signs. Based on negative culture results and ELISA tests, we have excluded such common enteropathogenic bacteria as Clostridium perfringens, Clostridium difficle, Salmonella spp., Campylobacter spp. , and Yersinia spp. as causative factors for the diarrheal signs occurring in TRD. Less well-defined species causing diarrhea in dogs, such as Plesiomonas shigelloides, Lawsoni intracellularis, and Brachyspira spp., have also been excluded.
Our ongoing studies have revealed that administration of tylosin leads to significant but transient changes in the composition of the small intestinal microflora. The results support the hypothesis that tylosin promotes the growth of beneficial commensal bacteria, while suppressing deleterious bacteria.
Besides antibacterial properties, tylosin may possess anti-inflammatory properties, contributing to its effectiveness in treating canine diarrhea. The mode of action must differ, however, from the immunomodulatory effect of prednisone because prednisone treatment did not completely resolve diarrheal signs in the same dogs that responded to tylosin.
The diagnostic protocol used for dogs with chronic diarrhea by the Faculty of Veterinary Medicine, University of Helsinki, is represented in Figure 1. In patients with chronic diarrhea, every effort should be made to achieve a diagnosis to enable a specific therapy. Unfortunately, this is not always possible in which case empirical therapeutic trials are used in the workup of these patients. There are conflicting opinions about how long an empirical therapy should be attempted. We recommend ten days if a dog has chronic diarrhea or if the interval between intermittent diarrheal episodes is only a few days. If signs of diarrhea disappear or are relieved during this period, the treatment should be continued another 2-6 weeks. When the interval between episodes of intermittent diarrhea is long, i.e. more than one week, the length of the empirical treatment period should be prolonged. The workup protocol displayed in Figure 1 for patients with chronic or intermittent diarrhea is applicable to most veterinary practices. It is also useful regardless of whether the clinical signs are typical of large- or small-intestine disease. The prevalence of diseases that can simultaneously affect the small and large intestines is high.
The initial evaluation (A) comprises obtaining a thorough case history (A1), conducting a physical examination (A2), and taking the basic laboratory tests, including a complete blood count, a serum chemistry profile, and measurement of serum concentrations of trypsin-like immunoreactivity (TLI) (A3). According to the initial examination, the patients are then divided into two groups. The first group includes patients showing clinical abnormalities in addition to diarrhea (Group B), while the second group shows no obvious abnormalities other than diarrhea (Group C).
Patients with obvious abnormalities (B) suffering from systemic disorders with secondary diarrhea (B1a), such as hepatic failure, renal failure, hypoadrenocorticism, and EPI (B1b), should be identified before starting trial therapies. Also if hypoproteinemia (B1c), melena and/or anemia (B1d), or abnormal palpation findings (B1e) are found, the reason for these abnormalities should be examined.
Dogs with diarrhea but no other abnormalities (C) are treated orally with fenbendazol 50 mg/kg for three days (C1) to rule out endoparasites as the causative factor for GI signs.
Food is probably the most common cause of diarrhea (C2), and adverse food reaction should always be excluded before empirical treatment trials with different drugs are initiated. Opinions vary widely about how the diet should be changed for a dietary treatment trial. Unfortunately, current recommendations are largely based on anecdotal evidence rather than on controlled trials. The most common recommendation is to use a diet with novel protein and carbohydrate sources, with the former restricted to a single animal source.
If modifying the feeding regime fails to produce a satisfactory fecal consistency, the next step is to treat the dog with tylosin 25 mg/kg BW q24h (C3). Dogs responding to tylosin treatment will usually do so within 3-5 days, and diarrhea will remain absent as long as treatment continues. In many dogs, diarrhea will reappear within some weeks upon discontinuation of treatment. If diarrheal signs reappear, the dog owner should change the dog's diet once again to make sure that the feeding regime is not involved in the etiology of the signs. If diarrheal signs continue, tylosin treatment is re-initiated. The effect of tylosin does not appear to diminish even in dogs that have been treated for years. The dose of tylosin for long-term use should be tapered to the lowest possible dose that controls clinical signs. Many dogs need only half of the recommended dose.
Although no adverse effects during tylosin treatment have been reported, efforts should be made to reduce the use of tylosin. This is because our recently conducted studies have indicated that tylosin causes wide resistance to antibiotics in the intestine (unpublished results). Certain probiotic lactic acid bacteria (LAB) have been shown to be effective in the prevention and treatment of a variety of diarrheal disorders in humans and in experimental mouse models. Hopefully in the future a probiotic LAB can be used instead of tylosin to treat or prevent chronic diarrhea in dogs with TRD.
With dogs not responding positively to dietary modification or tylosin treatment diagnostic imaging studies (D) should be performed and the workup continued as displayed in Figure 1.
Figure 1. Diagnostic approach to dogs presenting with chronic diarrhea at the Veterinary School in Helsinki, Finland. (click on figure to enlarge)
1. Westermarck E, Skrzypczak T, Harmoinen J, Steiner JM, Ruaux C, Williams DA, Eerola E, Sundbäck P, Rinkinen M. Tylosin-responsive chronic diarrhea in dogs. J Vet Intern Med 2005;19:177-186.
2. Westermarck E, Frias R, Skrzypczak T. Effect of diet and tylosin on chronic diarrhea in beagles. J Vet Intern Med 2005;19:822-827.
3. Westermarck E, Wiberg M. Exocrine pancreatic insufficiency in dogs. Vet Clin Small Anim 2003; 33: 1165-1179.
4. Van Kruiningen HJ. Clinical efficacy of tylosin in canine inflammatory bowel disease. J Am Anim Hosp Assoc 1976;12:498-501.
** For EPI dogs with SIBO the current "general" recommendation (in the USA) is a 30-45 day course of Tylan (first choice) to treat SIBO / ARD /TRD **
(previously recommended dose) Tylan Dosage for Dogs (administer twice daily with food) ....with 100g Tylan powder
30 lbs - 1/8 tsp
60 lb - 1/4 tsp
90 lb - 3/8 tsp
120 lb - 1/2 tsp
The new recommendation is Tylosin (25 mg/kg BID for 6 weeks)
For those interested in ordering Tylan in capsules, you can request to have this done at a "compounding pharmacy" in your area. To find a compounding pharmacy in your area (in the USA) please click on this "Pharmacy Compounding Accredited Board" link which lists them according to state: http://www.pcab.info/find-a-pharmacy.shtml
Encapsulating powder yourself is also an option. For examples of encapsulating machines see this forum thread: http://www.epi4dogs.com/apps/forums/topics/show/4148905-capsule-production-lab
Read more: Metronidazole Dose for Dogs | eHow.com http://www.ehow.com/about_5471971_metronidazole-dose-dogs.html#ixzz1aOG5iDPw
Metronidazole (Flagyl) Dosage for Dogs (administer twice daily with food) Vets usually recommend dosing dogs with 15 mg of metronidazole per kilo weight (2.2 lbs.) of the animal twice a day. This means that a 40-pound dog will can take 250mg of Metronidazole (technically 272 mg) twice a day with food 12 hours apart
INTERNATIONAL WEIGHT CONVERSION
Given any weight in kg, multiply by 2.2 to convert to pounds. To convert pounds to kilograms, divide by 2.2 (or multiply by 0.454, which is almost the same thing)
medical shorthand indicating the dosage frequency....for example, 'q' in front of a number means "every" so many hours or days. 'q8h' means every 8 hours; 'q3d' would mean every 3 days. Frequency can also be expressed as the number of times per 24 hour day that a drug should be given: 's.i.d' means once a day; 'b.i.d.' means twice a day; 't.i.d.' means three times a day; and so on. So you can see that 't.i.d' and 'q8h' mean nearly the same thing.
Drug doses are usually expressed in relation to the weight of the patient. Thus, a dose rate of 10 mg/kg means giving 10 milligrams of drug for each kilogram of the patient's body weight. Divide by 2.2 to get the dose per pound of body weight, and you would get 4.54 mg per pound. For some drugs you might round that up to 5 mg/lb (really equivalent to 11 mg/kg). At 10 mg/kg a 20 kg (44 pound) animal would get 200 mg of drug. A 30 kg (66 pound) animal would get 300 mg; and so on....
TREATMENT (by Dr. Jorg Steiner - May 2010)
HOW I TREAT - SMALL INTESTINAL DYSBACTERIOSIS
Jörg M. Steiner, Dr.med.vet., PhD, DACVIM, DECVIM-CA
College Station, Texas, USA
Oxytetracycline (10-20 mg/kg BID to TID for 4-6 weeks) used to be the therapy of choice. Unfortunately, oxytetracycline for oral use has become largely unavailable. Tylosin (25 mg/kg BID for 6 weeks) is the new antibiotic agent of choice. Other antibiotics, such as metronidazole can also be used. Some dogs respond to therapy rapidly and do not have a recurrence. However, other dogs do not respond to antibiotic therapy alone. If there is no marked improvement after 2 weeks of appropriate antibiotic therapy further work-up is necessary. Some dogs may respond to therapy with a complete resolution of clinical signs but may have a recurrence of clinical signs as soon as antibiotic therapy is discontinued. These patients require further diagnostic work-up. In some of these patients a specific underlying cause of the dysbiosis can be identified and treated accordingly. However, in some dogs no specific cause can be identified and prolonged, maybe even life-long, antimicrobial therapy is required.
If serum cobalamin concentration is decreased below the lower limit of the reference range
cobalamin should be supplemented parenterally.
Probiotics have garnered a lot of interest in both human and veterinary medicine. Initially, probiotics were mostly embraced by holistic physicians and veterinarians and the expectations for probiotics were dramatic, with probiotics being hypothesized to be of benefit in disorders ranging from stress to gastrointestinal health, weight management, and even the prevention of cancer. These unrealistic expectations have been replaced with well-defined requirements for probiotics and controlled studies of their beneficial effects.
The three key requirements for a probiotic for use in dogs are:
1) the probiotic must be safe;
2) the probiotic must be stable; and
3) the probiotic must be efficacious.
In a recent study, 8 veterinary and 5 human probiotics were evaluated and only 2 of the 13 products contained the strains and concentrations of those strains indicated on the label.2 Several of the products contained bacterial species that could potentially act as pathogens. Thus, in order to ensure safety, the probiotic product should adhere to strict production and storage requirements. The probiotic also must be stable throughout transport and storage until the product is being administered by the pet-owner. In order to ensure that a certain number of colonies are administered to the patient, the colonies in the product should neither proliferate nor die.
Finally, a probiotic must be efficacious. In order to be efficacious, the bacteria must reach the intestinal lumen. This requires that the bacterial species being used in the formulation are both acid- and bile-acidresistant. Also, the bacterial species of the probiotic preparation should adhere to the intestinal mucosa to prolong the time of interaction. Finally, the presence of the probiotic species must have beneficial effects in the host. Several controlled studies have been conducted in dogs that also show that certain probiotics carry health benefits in dogs with gastrointestinal disorders.
Prebiotics are substances that preferentially support the resident bacterial ecosystem of the
intestine. Basically, prebiotics are non-digestible food components (dietary fibre) that are being
fermented by intestinal bacteria. This can lead to normalization of the intestinal microbiota. In a
recent study the use of fructooligosaccharides (FOS) in the diet showed a lasting advantageous
effect.1 While this has not been evaluated as of yet, other prebiotics, such as inulin or beet-pulp
may also prove to be beneficial.
SIBO or ARD: What's in a Name?
The upper small intestine is supposed to be relatively sterile, and increased numbers of bacteria have been incriminated as a cause of intestinal dysfunction. This process has been called "small intestinal bacterial overgrowth" (SIBO), and is likely to occur secondary to partial obstructions, blind loops and exocrine pancreatic insufficiency (EPI), when bacteria can accumulate and ferment undigested food. Yet an idiopathic form of SIBO has been claimed in large breed dogs, especially young German shepherd dogs. The belief now is that true overgrowth does not exist in this syndrome, and that a more accurate term is "antibiotic-responsive diarrhea" (ARD) because it is characterized by the positive response to antibiotic therapy.
It is agreed that in all monogastric species, including dogs and cats, bacterial numbers in the intestine gradually increase towards the ileocolic valve, with the colon containing approximately 1013 organisms per gram of feces. The composition of the flora as well as numbers also changes along the tract, with a progressively increasing proportion of gram-negative and obligate anaerobic bacteria. Yet the assumption that the proximal small intestine in dogs is virtually sterile has been extrapolated from human gastroenterology. The numerical cut-off for normality of 1 x 105 colony forming units per milliliter (cfu/mL) total bacterial numbers or 1 x 104 cfu/mL anaerobes was based inappropriately on the numbers found in the human small intestine. While this is not quite as erroneous as believing that counting bacterial numbers in feces is representative of the situation in the small intestine, it has focused our attention on the wrong etiology.
Initially these cut-off numbers were considered valid because they matched results that were obtained by a methodology that was unfortunately flawed: duodenal juice samples were placed in transport medium and posted to a laboratory for enumeration, and undoubtedly, the number of viable organisms initially present were underestimated. Other workers then struggled to confirm this cut-off, with numbers up to 1 x 109 cfu/mL being reported in clinically healthy dogs. Yet when bacterial numbers in the duodenum of cats were first reported as up to 1 x 109 cfu/ml it was assumed that this was because cats were different, and that their carnivorous diet encouraged the growth of anaerobes, especially Clostridia, rather than the fact that the numbers actually reflected the true situation more closely because of better technique.
The technique of culturing and counting the numbers of organisms in the duodenum has been considered the ‘gold standard’ for diagnosing SIBO, but is actually technically demanding and prone to significant error.
Collection of duodenal juice is difficult, because in the anesthetized patient there is often very little fluid present endoscopically. The duodenum is a relatively smooth tube in dogs and cats, in contrast to the human duodenum where annular folds trap pockets of fluid. So at times when a lot of fluid is found, it seems most likely that this is recently secreted gastric, pancreatic or biliary fluid, and therefore not truly representative. It is also not uncommon to suck up tissue and blood when trying to collect juice, but the alternatives of flushing with sterile saline or trying to culture adherent bacteria from endoscopic biopsy specimens are also flawed if it is the absolute numbers of bacteria in the juice that are important. And even when a representative juice sample is obtained, unless it is collected and transported under anaerobic conditions for immediate plating-out many organisms, especially anaerobes, will die. Furthermore, counting is done manually on serial dilutions of samples and requires excellent microbiological technique. Finally, recent molecular techniques analyzing 16S bacterial rRNA in duodenal juice has identified a large number of organisms that are unculturable by conventional techniques.
In summary, the technique of bacterial quantitation of duodenal juice is so difficult and prone to error, not to mention labor-intensive and expensive, that it is not a technique that should be contemplated in practice.
Even ignoring the problems of methodology, is there any evidence that a true increase in bacterial numbers, ie, SIBO, can exist? In humans with blind intestinal loops constructed by radical bypass surgery, there is good evidence for numbers as high as 1012 cfu/mL, and clinical consequences (eg, diarrhea, raised serum folate, low serum cobalamin) are well documented. Similar overgrowth is seen when strictures (benign or neoplastic) prevent passage of ingesta. Blind loops are very uncommon in small animal gastroenterology but overgrowth probably occurs when partial obstructions in dogs and cats cause luminal contents to stagnate. Antibiotic-responsive diarrhea can be seen with a focal annular adenocarcinoma when the limited extent of the tumor would not be expected to compromise the residual intestine’s ability to compensate. Overgrowth has also been described in 100% of dogs with EPI, although these results were still based on quantitative duodenal juice culture. However, the lack of antibacterial pancreatic secretions and the presence of undigested food seem logical reasons for SIBO to develop, and the requirement for antibiotics in some patients with EPI before an optimal response to enzyme replacement support the idea of secondary SIBO.
There is general agreement that SIBO can occur secondary to blind loops, partial obstruction and EPI. The controversy exists concerning the syndrome seen in large breed dogs, previously termed idiopathic SIBO.
It has become evident that there is a great variation in bacterial numbers between individuals and even within individual patients on a daily basis. The influence of coprophagy on duodenal bacterial numbers has also largely been ignored.
But even if we could rely on duodenal juice culture for reliable results, the finding of similar numbers in clinically healthy dogs questions the relevance of absolute numbers. It has been suggested that it is the type of flora and/or how the host and flora interact that are more important than numbers. Indeed, dogs treated successfully with antibiotics do not necessarily show a decrease in duodenal bacterial numbers. Established reference ranges in cats are set higher, and idiopathic SIBO is not recognized. Hence idiopathic SIBO is probably a misnomer, although there are clearly dogs with diarrhea that respond to antibiotics.
Although we cannot confirm idiopathic SIBO by bacterial numbers, a characteristic syndrome is recognized in dogs, where no underlying cause for gastrointestinal signs can be found but the signs are controlled by antibiotics. It therefore seems more logical to refer to this syndrome as antibiotic-responsive diarrhea (ARD), because that is what it truly is, whilst the evidence for true SIBO is lacking. It is likely that the syndromes of ARD and SIBO are not strictly identical: some cases of ARD may actually have a specific but undiagnosed infection. However, the term ARD is more appropriate than idiopathic SIBO as we cannot reliably count bacterial numbers but we can see a response to antibiotics.
The causes of idiopathic / ARD are uncertain, but IgA deficiency is one potential mechanism that has been studied. Confusing reports concerning serum IgA concentrations in German shepherds are probably irrelevant, as it is the mucosal secretion of IgA that is clinically important. However, conflicting studies about whether fecal IgA deficiency exists have also been published. Recently four allotypes (A–D) of the canine IgHA gene, encoding IgA heavy chains with potentially different functionality, have been found in dogs. All German shepherds studied so far are variant C and no association between variant and disease has yet been shown.
Molecular studies have also suggested that ARD is associated with increases in pro-inflammatory cytokine mRNA expression yet without histologic evidence of inflammation. This has lead to the hypothesis that SIBO is a precursor of inflammatory bowel disease (IBD), although this remains supposition. Indeed quantification of cytokine mRNA expression by real-time RT-PCR, has cast doubt on those earlier, semi-quantitative studies.
The development of diarrhea is believed to be related to a number of mechanisms:
The syndrome originally termed idiopathic SIBO is characteristically a problem of young, large-breed dogs, especially German shepherds. It is not recognized in small dogs or aged dogs. It has also never been definitively identified in cats, although the efficacy of metronidazole in mild cases of IBD has never been fully explained. Chronic or recurrent diarrhea is typical, but some dogs show colitis-like signs. Most dogs are polyphagic and often coprophagic, but anorexia is sometimes seen and may be related to acquired cobalamin deficiency. Weight loss and/or stunting are seen in more severely affected dogs.
The diagnosis of SIBO is difficult as quantitative duodenal juice culture is flawed. In contrast, ARD is readily defined by the response to antibiotic, and the recent reports of tylosin-responsive diarrhea, are probably no more than another manifestation of ARD or an undiagnosed infection.
There have been attempts to find indirect tests for SIBO but none have been shown to be reliable markers of antibiotic responsiveness.
Historically SIBO was first identified in a group of dogs with chronic diarrhea all showing increased folate and decreased cobalamin serum concentrations. This resembled the pattern seen in humans with blind intestinal loops. All of the dogs were subsequently found to have increased bacterial numbers, and a specificity of 100% was claimed. However, further studies showed that this pattern of folate/cobalamin was only present in 5% of dogs with culture-proven SIBO. Thus with such a poor sensitivity, folate and cobalamin cannot be used to diagnose SIBO, although a low serum cobalamin does have a value as an indication to treat.
Intestinal bacteria are the sole source of breath hydrogen. Theoretically SIBO should cause increased breath hydrogen or at least an early peak of hydrogen excretion following ingestion of carbohydrate. Unfortunately the technique is technically demanding, and other causes of carbohydrate malabsorption and increased intestinal transit rate will cause similar abnormal results.
Intestinal bacteria can deconjugate bile salts, which are absorbed but then are poorly extracted by the liver and are therefore measurable in serum. Theoretically SIBO should cause increased serum unconjugated bile acids (SUCA). Unfortunately, SUCA concentrations fluctuate significantly after a meal, and since Lactobacilli are one of the major organisms able to deconjugate bile acids their relevance to disease is questionable.
The treatment of secondary SIBO depends first on treating any underlying cause, such as EPI. Idiopathic SIBO/ARD is treated simply by antibiotics. Oxytetracycline is the first choice in the UK but metronidazole, tylosin or amoxicillin may be equally effective. A response should be seen within 7 to 10 days and, if positive, antibiotics should be continued for up to 6 weeks. Some cases never relapse on cessation of treatment, others relapse months later and require a second course of antibiotics. But typically, dogs relapse within days of treatment finishing. In these cases an underlying cause should again be looked for, but ultimately repeated courses or continuous antibiotic therapy may be required. Surprisingly, it may be possible to reduce the dose and dosage interval. Whilst this is not considered best practice for antibiotic usage, and resistance is likely to develop, in reality it works.
Adjunctive therapy may be helpful, and mild cases may be controlled by diet alone. A highly digestible, low fat diet seems beneficial, but the inclusion of prebiotics such as fructo-oligosaccharides are logical although not yet proven. This syndrome is also a potential target for probiotic therapy. Acquired cobalamin deficiency should be treated with parenteral vitamin B12.
In some rare cases .... some dogs "may" have an adverse reaction to Metronidazole... especially if used long-term. The treatment is to stop the Metronidazole immediately.... but Valium may also be used as an antidote to Metronidazole poisoning. The following is an actual example of an Metronidazole poisoning with an EPI dog:
Dave & Linda, owners of Sasha
Our GSD, Sasha, was taking Metronidazole and was on her third round. I let her outside in the late evening to do her business before bedtime. Walking back to the house, she began to stumble and stagger, barely making it up the back porch steps. The best way to describe her walk was as if she were in a drunken stupor. Then when she came inside, she threw up four times. The fact that she had a hard time standing and walking really scared us, so my husband took her to an emergency vet center since it was already 10 p.m. After racking up a $1258 bill there, we received a call at 8 a.m. (Sasha was left there overnight) the next morning informing us our dog was getting worse, now not being able to stand at all and her eyeballs were rolling around in her head. They suggested we come pick her up and take her to another hospital to see a neurologist. Our poor Sasha had to be rolled out on a gourney and lifted and put in the back seat of our car.
After the 25 mile drive to the other hospital, techs lifted Sash out of our car and carried her in on a stretcher! She laid sideways on a mat on the floor as her eyes continued to roll in her head. It was heartbreaking, and we thought for sure we would lose her. The neurologist suspected Metronidazole toxicity but said he wanted to rule out a brain tumor or spinal infection so told us he wanted to perform an MRI on her head and do a spinal tap. We agreed to this but are always hesitant about anesthesia, especially with a dog in this condition.
This is where we made another costly mistake. In retrospect, looking up the side effects of Metronidazole, a rare side effect is built-up toxicity from it, of which Sasha had the exact symptoms - vomiting, unable to walk or stand, disorientation, the eyes rolling. Time and Valium is the antidote.
The MRI and spinal tap came back normal. so the vet started Sasha on Valium, and within 24 hours she made a remarkable improvement. We picked her up the next day and could not believe that was the same very sick dog we left there, as she waked right up to us with her tail wagging!
This was a $3,900 lesson. My point is if your pet is on Metronidazole and you notice any side effects that affect the central nervous system, Stop the metro immediately. Go to your vet for the Valium. We could have saved a lot of money if we would have gone this route at first. If after a day of the Valium there was no improvement, then the MRI and spinal tap would have been needed.
Hope our story helps someone. These scary and horrible side effects from the Metronidazole are rare, but they do happen, so be mindful of them if you pet is on this medication. I am also happy to add that Sasha doesn't appear to have any residual effects and was totally back to her normal self within a few days.
SIBO "Small Intestinal Bacterial Overgrowth"
The proximal small intestine normally contains few bacteria.In small intestinal bacterial overgrowth (SIBO) there is proliferation of abnormal numbers of bacteria in the lumen of the upper small intestine. The definition of what is considered an abnormal number of bacteria in the dog is still under discussion. It is classically stated that in normal household pet dogs no more than 104 to 105 bacteria per mL of juice are present in the lumen of the upper small intestine. Although recent reviews have questioned the accuracy of this upper limit of normal, some of the reported variation may reflect inclusion of dogs not from household environments rather than pet dogs. However, it is generally accepted that species normally present in the proximal small intestine of dogs include E. coli, enterococci and lactobacilli, and that obligate anaerobic species are rare. In dogs with SIBO there are not only increased numbers of intraluminal bacteria, but the composition of the flora also changes to a predominantly anaerobic one, resembling that of the colon.
SIBO in the dog has been infrequently reported, probably because of the difficulty in establishing the diagnosis, and initial descriptions were limited to its occurrence in German Shepherd Dogs. However, in recent years it has been described as a common finding in dogs with chronic small intestinal disease, either as a cause or a consequence of their disease. This condition in the dog has been controversial because of difficulties in defining its aetiology and pathogenesis. There have been suggestions that it be renamed antibiotic-responsive diarrhoea (ARD) until more is known about its aetiopathogenesis. However, this does not apply to all cases since it is not always associated with diarrhoea; indeed, weight loss alone can be the only presenting sign.
Accumulated data on clinical cases indicate that SIBO should be considered an important emerging syndrome that may occur in many breeds of dog. It typically presents in young animals as chronic intermittent small bowel diarrhoea, which may be accompanied by loss of body weight or failure to gain weight. Clinical signs are variable and some animals may only exhibit weight loss, while others may have intermittent vomiting or signs suggestive of mild colitis.
SIBO may develop if the normal host defence mechanisms, such as gastric acid secretion, intestinal peristalsis, the ileocaecal valve, intestinal immunoglobulin secretion, and mucus barrier are impaired. In people, SIBO is usually associated with intestinal stasis (blind loop syndrome). Small intestinal dysmotility, as evidenced by reduced migrating motor complex activity, is probably responsible for the prevalence of SIBO in elderly human patients. In dogs, there is rarely evidence for stasis, and the cause of SIBO is often unknown. A naturally developing enteropathy associated with SIBO was first described in German Shepherd Dogs, and it has been postulated that this is related to an apparent relative deficiency of IgA in this breed. SIBO may also develop secondary to exocrine pancreatic insufficiency, and has been reported in asymptomatic laboratory Beagles. We have documented SIBO by culture of duodenal juice in over half of dogs with chronic intestinal disease; dogs of many breeds are affected, although there is a predominance of German Shepherd Dogs. Serum IgA levels in these dogs have been variable. Predisposing conditions usually cannot be identified, although it remains important to rule out causes of intestinal stasis, such as neoplasia and intussusception. Increased numbers of pathogenic E. coli have been demonstrated in the duodenal juice of these dogs, and these may also play a role in the development of this condition. SIBO may furthermore be a secondary complication of many intestinal diseases due to altered intestinal motility and/or local immunity; in addition, malabsorption of nutrients may cause an environment favourable for bacterial proliferation. Conversely, bacterial antigens gaining access to the lamina propria also may cause an inflammatory reaction, although this tends to be milder.
Bacteria or their secreted products can directly damage the mucosa or indirectly impair absorption by competing for nutrients and by changing intraluminal factors such as the concentration of conjugated bile acids. This results in diarrhoea and steatorrhoea, competition with the host for nutrients, and weight loss. Enterocyte damage is often not visible on light microscopy, but may be demonstrated using biochemical or ultrastructural studies, or by measurement of intestinal permeability. Increased mucosal production of interleukin-6, a cytokine that plays a central role in the regulation of inflammatory and immune reactions, has been demonstrated in people with SIBO, suggesting heightened mucosal immune activity.
The species of bacteria in duodenal juice of dogs with SIBO varies markedly, with coliforms, staphylococci, enterococci, and Clostridium and Bacteroides spp predominating. Anaerobic overgrowth is most common, found in approximately 70% of dogs with SIBO. This is of clinical significance, since anaerobic bacteria have a much greater potential to damage the intestinal brush borderand cause malabsorption; in addition, anaerobes, especially Bacteroides, are the major cause of bile salt deconjugation resulting in fat malabsorption and steatorrhoea.
Symptomatic SIBO typically presents in young animals as chronic intermittent small bowel diarrhoea, which may be accompanied by loss of body weight or failure to gain weight. Diarrhoea often has been present since puppyhood, and gradually worsens. Some dogs also may have signs of a mild colitis, due to colonic irritation by bacterial metabolites, and these dogs may be erroneously diagnosed as having primary colitis. Weight loss may be severe, and is in some dogs the only sign. Appetite is often reduced. Vomiting is not typically associated with bacterial overgrowth; its presence suggests concurrent inflammatory bowel disease. Some dogs with SIBO are presented because of excessive intestinal gas.
CBC and biochemical profile should be performed to rule out systemic disease. Faeces should be examined for parasites and cultured for enteric pathogens. Abdominal radiography and especially ultrasound can be helpful to rule out partial obstruction, particularly in young (intussusception) or older (neoplasia) animals. Subsequently, exocrine pancreatic insufficiency (EPI) should be ruled out by assay of serum TLI activity.
Serum folate and cobalamin
Assays of serum folate and cobalamin appear to be the most helpful aids to the diagnosis of SIBO in the dog for use in general practice, although they have poor sensitivity (i.e., many affected dogs do not have abnormal test results). Normal serum vitamin concentrations do not exclude the possibility of SIBO, because alterations depend on the type and numbers of organisms present, the severity of any secondary mucosal damage that may interfere with folate absorption despite high intraluminal concentration, and depletion of body stores. If pancreatic function is normal (i.e., serum TLI is normal) then finding a decreased serum cobalamin concentration or increased serum folate is supportive of SIBO. If both of these are found together, SIBO is extremely likely; however, this combination occurs infrequently. High serum folate may also be a consequence of high folate intake, such as a high-folate diet or coprophagia. Demonstration of low serum cobalamin is the more useful finding, since it is less influenced by diet and coprophagia and appears to relate more to the severity of clinical disease
Measurement of intestinal permeability is a sensitive tool for the detection of mucosal damage, but it does not tell you about the underlying cause. However, these tests are useful to detect and assess the severity of mucosal damage in dogs with overgrowth. Increased intestinal permeability can be demonstrated using a differential sugar absorption test in 50-60% of clinical cases with SIBO, even when there are no histologic abnormalities. In addition, changes in intestinal permeability following antibiotics may be used to monitor response to treatment. Normalization of intestinal permeability following antibiotic therapy suggests successful treatment, and antibiotics may be discontinued. Antibiotics possibly should be continued longer if permeability remains high despite apparent response to treatment; in addition, other causes of intestinal disease should be suspected and investigated (e.g., dietary sensitivity). Persistent high permeability in dogs with a poor clinical response should prompt one to look for underlying disease, such as a primary inflammatory bowel disease.
Breath hydrogen testing
Breath tests measure the breath excretion of CO2 or hydrogen (H2) produced by intraluminal bacterial metabolism of an administered substrate. They appear to be the one of the most sensitive and specific tests available for the diagnosis of SIBO, although they are not yet technically feasible in most veterinary practices. The H2 breath test has been used most often in both human and veterinary medicine. It has been used not only for diagnosis of SIBO but also for detection of carbohydrate malassimilation and measurement of oro-caecal transit time. The time after ingestion of the test substrate at which increased breath H2 concentrations are first detected is used to distinguish between SIBO and carbohydrate malabsorption. In SIBO, elevated breath H2 concentrations occur within 1 to 2 hours after ingestion of the test substrate. An H2 breath test using a multiple sugar solution has been used successfully for detection of SIBO in dogs and has the advantage that it simultaneously allows for quantification of intestinal permeability. A limitation of breath H2 tests in people is that 15-20% of the human population have intestinal flora that does not produce hydrogen, and therefore cannot demonstrate a positive test result if bacterial overgrowth develops. The same probably applies to the dog, since there are significant numbers of dogs with culture-proven overgrowth but persistently negative breath tests.
The H2 breath test is more sensitive than serum folate and cobalamin assay, and has been useful to identify cases of SIBO with a falsely negative duodenal juice culture. A positive breath H2 test is very suggestive of SIBO, and there is no need to culture duodenal juice in these cases. However, a negative test does not rule it out, and culture of duodenal juice remains necessary in these patients.
Culture of duodenal juice
Definitive diagnosis of SIBO is based on results of microbiologic culture of duodenal juice, obtained usually at endoscopy or alternatively via intra-operative permucosal aspiration. Juice culture is still the gold standard for the diagnosis of SIBO, but it is technically difficult, time-consuming and expensive, and it may still not identify all cases of SIBO (for example when this is in the more distal portions of the small intestine or in isolated pockets). However, intestinal biopsies can be taken at the same time as the juice collection, and these are useful to rule out primary mucosal disease as the cause of malabsorption. Duodenal biopsy in SIBO is often normal. Over 75% of clinical cases with SIBO will have no histologic abnormalities, whereas mild to moderate lymphocytic infiltrates occur in up to 25%. Mild lymphocytic-plasmacytic enteritis can occur as a consequence of SIBO, and may resolve following appropriate antibiotic treatment.
Duodenal bacterial counts may be influenced by environmental factors, such as housing conditions (kennelled dogs tend to have higher bacterial numbers, perhaps associated with coprophagia) and infective load (such as endoparasites and naturally occurring enteropathogens in hot climates). This should be taken into account when defining bacterial levels deemed diagnostic of bacterial overgrowth.
Bacterial deconjugation of bile salts may result in increased serum concentrations of unconjugated bile acids. Unlike the conjugated bile acids normally present in the small intestinal lumen, these unconjugated bile acids (UBA) diffuse across the intestinal mucosa into the blood. Dogs with SIBO have been shown to have significantly higher serum concentrations of UBA. This test has also proven useful to identify dogs with culture proven SIBO that did not have abnormal serum vitamin concentrations. Until now, this test was technically too complicated for routine use, but new developments should lead to this becoming more available in the near future. It may therefore become a useful addition to the battery of diagnostic tests required to diagnose SIBO.
Response to treatment with antibiotics may also help in the tentative diagnosis of SIBO. However, lack of response does not rule it out, since prolonged treatment may be required in some dogs before clinical improvement is manifest.
SIBO can be a subclinical intestinal abnormality, as has been reported in man, German Shepherd dogs and laboratory Beagles. Development of clinical signs in these individuals probably depends on the nature of the bacterial population (for instance, colonization with anaerobes is more likely to result in signs) and the effect of the overgrowth flora on the local immune system. These patients may be identified on basis of abnormalities in serum folate and/or cobalamin concentrations, a positive hydrogen breath test, or by culture of duodenal juice aspirated in the course of other investigations. Treatment is not required as long as they are asymptomatic; however, they are at risk for developing signs once the delicate balance in their intestinal ecosystem is disturbed. Progressive decreases in serum cobalamin concentration in dogs with asymptomatic SIBO often precede development of clinical signs.
TreatmentAn attempt should be made to identify and correct an underlying cause, such as partial obstruction due to intussusception, tumours or foreign bodies. Detection of dysmotility is more difficult and often not feasible; however, motility modifying agents such as cisapride or low-dose erythromycin may empirically be used in refractory patients. In many dogs with SIBO a cause cannot be found, and long-term oral antibiotic treatment is required. Oxytetracycline (10-20 mg/kg TID for 28 days) is used initially, and may need to be continued for extended periods if clinical signs recur on withdrawal of medication. Its mechanism of action may involve more than just pure antibacterial action (e.g., direct influence on the mucosa), although this is not certain. Metronidazole (10-20 mg/kg TID) and tylosin (20 mg/kg BID) are good alternative choices and are used if dogs fail to respond to oxytetracycline. Broad-spectrum bactericidal antibiotics tend to be less effective.
Dietary management with a low fat diet may also be valuable, because this can minimize the secretory diarrhoea, which is a consequence of bacterial metabolism of fatty acids and bile salts. Since intestinal permeability is often increased in SIBO, a restricted antigen diet may be of value to reduce the incidence of secondary dietary sensitivities. Dietary supplementation with fructo-oligosaccharides has been suggested as a means of modifying bacterial counts in the small intestine in German Shepherd Dogs with asymptomatic naturally occurring bacterial overgrowth. However, since these compounds are more likely to affect the large rather than the small intestine, further studies in clinical cases are required to assess the efficacy of prebiotics in the management of canine SIBO.
Probiotics are a mixture of non-pathogenic bacteria, often containing Lactobacillus, which can change intestinal pathobiology by preventing enteric infections, modifying metabolic actions of intestinal bacteria, and promoting nutrition. They also may promote local mucosal and systemic immune response. Probiotics are extensively used in large animals, and have also been advocated as a means of modulating gut flora in people with gastrointestinal disease.
Parenteral cobalamin (e.g., 500µg/month for 6 months) may help dogs with apparent cobalamin deficiency. It may have to be given more frequently if serum cobalamin levels remain subnormal. Persistently low serum cobalamin levels are often associated with a poor clinical response to treatment.
Prolonged antibiotic therapy is often required in treatment of dogs with idiopathic SIBO, and serial measurement of intestinal permeability and breath H2 testing are helpful in monitoring response to treatment. Some dogs with SIBO relapse as soon after antibiotics are discontinued. In these patients long-term antibiotic treatment will be required, but empiric reduction of the dose to well below the recommended level may be effective in controlling signs.
In dogs with moderate to marked inflammatory bowel disease, corticosteroids should be added to the treatment regimen if response to antibiotics alone is inadequate. Corticosteroids are not recommended in the initial treatment of dogs with lymphocytic/plasmacytic enteritis and SIBO because in our experience they appear to worsen clinical signs associated with SIBO.
Chronic SIBO may cause permanent functional damage to the intestinal mucosa. This may explain the poor response to treatment of some dogs, and also the need for indefinite dietary management with controlled diets after apparent successful antibiotic therapy in some dogs with chronic SIBO.
1. 1.Rutgers HC, Batt RM, Elwood CM, Lamport A. Small intestinal bacterial overgrowth in dogs with chronic intestinal disease. J Am Vet Med Assoc 1995;206:187-19
2. 2.Rutgers HC, Batt RM, Proud FJ, et al. Intestinal permeability and function in dogs with small intestinal bacterial overgrowth. J Sm Anim Pract 1996;37:428-434
3. 3.Bissett SA, Guilford WG, Spohr A. Breath hydrogen testing in small animal practice. Comp Cont Educ 1997;19:916-931
4. Ludlow CL, Davenport DJ. Small intestinal bacterial overgrowth. In: Bonagura JD, ed. Current Veterinary Therapy XIII. Philadelphia, WB Saunders, 1999: 637-641
5. Melgarejo T, Williams DA, O'Connell NC, Setchell KD. Serum unconjugated bile acids as a test for intestinal bacterial overgrowth in dogs. Dig Dis Sci 2000; 45:407-414
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Roger M Batt
Masterfoods, Mars Inc.
Waltham-on-the-Wolds, Leicestershire, UK
Roger Batt qualified as a veterinarian from Bristol University in 1972 and obtained his PhD at the Royal Postgraduate Medical School in London. In 1980 he moved to the University of Liverpool where he established a comparative gastroenterology research group. In 1990 he was appointed Professor of Veterinary Medicine at the Royal Veterinary College in London. In 1998 he moved to the Waltham Centre for Pet Nutrition to become Head of Research and in 2001 was given the status of Visiting Professor at the University of Bristol.
His research has focused on gastrointestinal disease in specific breeds of dog. He has over 300 publications, and for his research has received a 1989 Ralston Purina Award from the American Veterinary Medical Association, the 1990 Walter-Frei Prize from the University of Zurich, the 1991 Woodrow Award from the British Small Animal Veterinary Association, and the 1997 Oscar W. Schalm Award from Davis, University of California. In 1993 he became the first President of the European Society of Comparative Gastroenterology.
F.P. Gaschen Email: firstname.lastname@example.org
In humans small intestinal bacterial overgrowth (SIBO) is most frequently a secondary phenomenon associated to anatomical abnormalities that facilitate migration of large intestinal bacteria towards the small intestine or preventing the normal bacterial clearance, or to functional problems associated with disturbed intestinal motility. Multifactorial causes have also been reported (eg, immunodeficiency, etc.).
In dogs, secondary proliferations have been described in association with gastric and intestinal surgery or with exocrine pancreatic insufficiency. However, the existence of a primary, idiopathic SIBO is subject to controversy, although the syndrome has been the object of numerous scientific publications during the 1980s and 1990s. The diagnosis and definition of SIBO are complicated. The recognized diagnostic gold standard is anaerobic and aerobic bacteriologic culture of intestinal juice. The method is work intensive and requires the immediate proximity of an adequately equipped bacteriologic laboratory since numerous bacteria do not survive snap freezing. Previously, concentrations of more than 105 colony forming units (CFU)/mL intestinal juice were considered diagnostic of SIBO. Currently, it is believed that small intestinal bacterial concentrations up to 107 CFU/mL may be physiological in dogs.
In a recent publication, intestinal juice was cultivated in dogs with chronic enteropathies. The bacterial concentrations detected in the small intestinal juice of dogs which later responded to antibiotics (antibiotic responsive diarrhea or ARD) were not higher than those found in the dogs that did not respond to antibiotics. The etiology of ARD is not known, a bacterial infection with unidentified bacteria cannot be ruled out. The work intensive procedure of quantitative small intestinal bacterial culture is of questionable value in the diagnosis of chronic canine enteropathies. Other less complicated and less accurate diagnostic methods are available to detect bacterial proliferation in the small intestine. Serum folic acid levels may increase in dogs with SIBO because numerous bacteria synthesize folic acid. On the other hand, serum vitamin B12 (cobalamine) concentration is often decreased in association with intestinal malabsorption. However, these parameters cannot distinguish dogs that will respond to antibiotic treatment from those who will not. Bile acids are produced in the liver and conjugated to proteins before they are excreted in the biliary tree and undergo enterohepatic circulation. Some of the bacteria involved in SIBO are able to deconjugate these bile acids in the intestinal lumen. Serum concentrations of deconjugated bile acids are used in human medicine in the diagnosis of SIBO; however, they have proven useless in dogs.
ARD may affect young dogs. German shepherd dogs may be predisposed to that disease due to a disorder in the production of immunoglobulin A (IgA). In a case study from Finland, middle-aged large breed dogs were affected with ARD and only responded to tylosin. Clinical signs associated with ARD may vary considerably: chronic recurring, mostly small intestinal diarrhea is frequent (although large intestinal signs may also occur). Additionally, dogs with ARD may show borborygmus, flatulence, dysorexia and weight loss.
What are the implications of these findings for clinical practice? Even though the very existence of canine idiopathic SIBO is questioned, a number of dogs with chronic enteropathies do respond favorably to antibiotic treatment. This suggests that imbalances of the small intestinal bacterial flora could play an important role in the pathogenesis of IBD. This is why a global and systematic approach is necessary in dogs with chronic recurring diarrhea. Diseases known to cause secondary SIBO such as exocrine pancreatic insufficiency must be ruled out. Once identifiable causes of chronic enteropathies have been excluded, the remaining differential diagnoses include food intolerance or allergy, ARD and IBD. A pragmatic approach according to the severity of clinical signs is recommended. In mild cases, changing to a "hypoallergenic" diet is recommended. If this approach fails after 3 to 4 weeks, oral antimicrobial treatment with metronidazole (10–20 mg/kg BID), tylosine (10–20 mg/kg once daily or BID) or tetracycline (10–20 mg/kg TID) should be considered. Interestingly these three substances may have immunomodulating or even antiinflammatory effects in addition to their antimicrobial properties. In the more severe cases or in dogs that do not respond to the above treatment, additional exams must be recommended (abdominal ultrasound, endoscopy of the digestive tract with sampling of mucosal biopsies, etc.).
ScienceDaily (Jan. 21, 2010) — Bacteria that produce compounds to reduce inflammation and strengthen host defences could be used to treat inflammatory bowel disease (IBD). Such probiotic microbes could be the most successful treatment for IBD to date, as explained in a review published in the February issue of the Journal of Medical Microbiology.
IBD is inflammation of the gastro-intestinal tract that causes severe watery and bloody diarrhoea and abdominal pain. It is an emerging disease that affects 20 out of 100,000 genetically susceptible people in Europe and North America. The most common manifestations of IBD are Crohn's disease and ulcerative colitis. While the exact causes are unclear, IBD is known to be the result of an overactive immune response that is linked to an imbalance of the normal types of bacteria found in the gut.
Several recent studies have identified butyric acid as a potential therapeutic agent for IBD. Some gut bacteria produce butyric acid naturally in the intestines, but in IBD patients some of these strains are heavily depleted. Trials in mice have shown that injecting one such strain Faecalibacterium prausnitzii into the digestive tract is effective at restoring normal levels of gut bacteria and treating the symptoms of IBD. In addition, novel identified butyrate-producing strains, such as Butyricicoccus pullicaecorum, have been shown to exert similar effects.
Butyric acid has well-known anti-inflammatory effects and is able to strengthen intestinal wall cells -- making it an ideal therapeutic agent against IBD. In addition to butyric acid, it is hypothesized that strains such as F. prausnitzii and B.pullicaecorum secrete other anti-inflammatory compounds that may enhance the therapeutic effect.
Prof. Filip Van Immerseel, a medical microbiologist from Ghent University in Belgium said that a new treatment for IBD would be welcomed. "Conventional drug therapy has limited effectiveness and considerable side effects. Probiotics are live bacterial supplements or food ingredients, which when taken in sufficient numbers confer health benefits to the host," he said. Previous trials of probiotics to treat IBD using mainly lactic acid bacteria have given mixed results. "Now we realise that lactic acid is used for growth by a certain population of bacteria that produce butyric acid, which could explain why some of the older studies had a positive outcome. Recent trials focussing on butyric acid-producing bacterial strains have been extremely promising and could lead to a new treatment for IBD."
Developing an effective probiotic treatment for IBD will not be easy, however. "As butyric acid-producing bacteria are naturally depleted in IBD patients, we will need to identify strains that are able to colonize the gut without being outcompeted. Many bacterial species produce butyric acid and possibly other anti-inflammatory molecules so it's a case of finding which is the most robust under these conditions," said Prof. Van Immerseel.
Editor's Note: This article is not intended to provide medical advice, diagnosis or treatment.
The following is a list of "some" probiotics that have been used successfully with EPI dogs.... HOWEVER.... please note that not all probiotics will have the same result with every dog.... effectiveness depends on each individual dog's gut flora.... and unfortunately, they can vary dramatically from one dog to another.
What we at epi4dogs found what works best is to "try" a probiotic...... start with 1/2 the recommended dose and work up to a full dose within a week or two ... some dogs will have loose stools from the probiotic.. so you need to start slow. ALWAYS give probiotics 2-4 hours away from any antibiotic given. If your dog seems to be extra sensitive and not able to handle any of the suggested canine probiotic..... then start with a single strain "Acidophulis" (you can use human grade Acidophulis).... this particular probiotic strain seems to be tolerable by most all dogs....
Some of the Probiotic products used are as follows:
A general guideline to reading "poo"
(re-printed with permission from a Pancreatitis group)
Yellow or greenish stool -- indicates rapid transit (small bowel).
Black, Tarry stool -- indicates bleeding in the upper digestive tract.
Bloody stool -- red blood or clots indicate bleeding in the colon.
Pasty, light-colored stool -- indicates lack of bile (liver disease).
Large, gray, rancid-smelling stool -- indicates inadequate digestion or absorption (malabsorption syndrome).
Watery stool -- indicates small bowel wall irritation (toxins and severe infections).
Foamy stool -- suggests a bacterial infection.
Greasy stool -- often with oil on the air around the anus: indicates malabsorption.
Excessive mucus -- a glistening or jelly like appearance: indicates colonic origin.
(the more watery the stool, the greater the odor)
Food like or smelling like sour milk -- suggests both rapid transit and malabsorption.
Putrid smelling -- suggests an intestinal infection.
Several in an hour, each small, with straining -- suggests colitis
Three or four times a day each large -- suggests malabsorption or small bowel disorder.
Condition of Dog
Weight loss, malnutrition -- suggests small bowel disorder.
Normal appetite, minimal weight loss -- suggests large bowel disorder.
Vomiting - small bowel origin, except for colitis.