Last Updated on February 9, 2017 by Patricia Carter
Summary: Antibiotics carpet bomb the microbiome. Here’s important things to do if you must take an antibiotic as noted in this article by Dr. Robynne Chutkan, MD and gastroenterologist, see bio below. I’ve adapted the list to include the How-To-Do details. Realize that the gist of the steps below you should ALWAYS be doing, not just during times you take antibiotics. But be particularly diligent and persistent following these steps if you must take an antibiotic in order to try to counteract the antibiotics, microbiome, nuke! For even more guidance on what to do before and after taking antibiotics, Dr. Mark Hyman’s recommendations from his article, Here’s the Downside of Antibiotics Your Doctor Might Not Tell You, has been added. Last, the studies looking at antibiotics and Culturelle, VSL #3, and Saccharomyces boulardii or Florastor(®), as well as their precautions, are included.
A word of caution concerning the FODMAP and Resistant Starch prong on the below gut preservation list:
FODMAP and resistant starch are part of the preservation strategy since both build up the diversity and richness of the microbiome. This is especially important for antibiotic dosing as the antibiotics nuke the microbiome; Caution though with FODMAPs… many with gut dysfunction have a hard time eating those. If you haven’t been eating FODMAPs, start slow and see if your gut can tolerate them. The goal of the FODMAP diet is to learn your individual tolerance for FODMAPs and NOT to eliminate them from your diet. Healing the gut using healing diet tenets and lifestyle supports the microbiome and will increase what you can consume FODMAP wise!
Antibiotics, microbiome and preservation — adapted from this article by Dr. Robynne Chutkan, MD
1. Take a probiotic during and after antibiotics (continue for at least one month after finishing antibiotics). [Consume the probiotic two hours before and two hours after the antibiotic.] Probiotics containing strains of Lactobacillus and Bifidobacterium are the most useful, as well as those containing the beneficial yeast Saccharomyces boulardii. Note though that bifidobacterium, in the SCD/GAPS world, seems to be contradicted due to overgrowth concerns and here. It’s controversial however; UMass IBD-AID permits this strain; see An anti-inflammatory diet as treatment for inflammatory bowel disease: a case series report. Whole food probiotics to consider for a crowding out pathogen purpose to help preserve the beneficial microbiome constituency, are lactose-free SCD yogurt, live sauerkrauts, Kimchi, pickles, etc. such as:
If you ask your doctor about CDiff risk with the antibiotic being prescribed, often they’ll tell you it is rare (not true by the way; it’s currently an epidemic, read the post ANTIBIOTIC RESISTANCE AND MICROBIOME COMPETITIVE CROWDING OUT CONCEPTS) and then they’ll immediately prescribe Florastor(®) (which likely won’t be covered by you insurance but it costs under $20 in my area). Also concerning, only 9.6% of academic medical centers stocked Culturelle and Florastor according to this study which is detailed below. Florastor(®) is S.Boulardii, which actually is a yeast, not a bacteria. The article, Saccharomyces boulardii CNCM I-745 supports regeneration of the intestinal microbiota after diarrheic dysbiosis – a review, is extraordinarily important . It has a gut mucosal focus, and anyone thinking about taking S.boulardii should read it… more than once… to realize the potential of this yeast. This article, along with other Saccharomyces boulardii or Florastor(®) studies, is excerpted below as is information on Saccharomyces boulardii or Florastor(®) precautions.
2. Eat PREBIOTIC foods (called FODMAPs and RESISTANT STARCH) to support your gut microbes. Foods high in fiber and resistant starch feed your microbes and help to promote species diversity and richness, which can decrease dramatically after a course of antibiotics. A Convenient FODMAPs Food list from Food Washington Post and from Monash University “Low FODMAP Diet” book and app (by Sue Shepherd and Dr. Peter Gibson, MD) follows. “High” FODMAP foods promote species diversity and richness. The limits noted are threshold levels where consumption above those levels, may not be tolerable for some.
• High-FODMAPs protein: Legumes (chickpeas, broad beans, butter beans, kidney beans), lentils over ½ cup. Low-FODMAPs protein: Meat, fish, chicken, tofu ( I don’t recommend soy especially if you are a Westerner since many lack the microbial bacterial enzymes to properly digest soy).
• High-FODMAPs vegetables: Garlic, leeks, onions, asparagus, cabbage, brussels sprouts, beets, artichokes, sugar snap peas, peas over 1/3 cup, celery, sweet corn, mushrooms, sweet potatoes over ½ cup, cauliflower, broccoli, cooked and then cooled potatoes, spinach over 15 leaves, zucchini over ¾ cup. Low-FODMAPs vegetables: Green beans, carrots, cucumbers, lettuce, tomatoes.
• High-FODMAPs fruit and nuts: Avocados, apricots, apples, mangoes, pears, peaches, plums, pineapple over 1 slice, dates, pomegranate seeds over ½ cup, cranberries over 1 Tbsp, cherries over 3, watermelon, cashews, dried fruits, green bananas, green plantains. Pistachios, cashews and greater than 10 almonds or walnuts. Chia and flax seed both if over 1 Tbsp. Low-FODMAPs fruit and nuts: Ripe spotted bananas, oranges, grapes.
• High-FODMAPs cereals, grains, breads, pastas: Wheat products, barley, rye. Low-FODMAPs cereals, grains, breads and pastas: Gluten-free bread and pastas, oats, rice, quinoa.
• High-FODMAPs dairy products: Soft cheeses, cow’s milk, cream, ice cream, commercial yogurt, kefir (if not lactose-free). Low-FODMAPs dairy products: Lactose-free milk and yogurt, hard cheese.
• High-FODMAPs sweeteners and bakery type products: Cocoa powder and anything ending in “ol” (such as sorbitol) on the ingredient label, honey and many fruits (see above). NOTE: I don’t recommend consuming the “ol” artificial sweeteners as they were found to alter microbial metabolic pathways that are linked to host susceptibility to metabolic disease, induced dysbiosis, and glucose intolerance in healthy human subjects, see the Nature article here).
3. Drink ginger tea – it has a soothing effect on the digestive system and can help to reduce gas and bloating associated with taking an antibiotic. Tip: Thinly slice ginger root on the diagonal and freeze in single layers. It’s easy to pull out a few slices to steep in filtered water. You can do the same with turmeric root, and even add in peppermint and spearmint leaves for a even greater gut healing anti-inflammatory friendly treat.
4. Skip the acid suppression drugs. Read the post HEARTBURN DRUGS, DEMENTIA, ALZHEIMER’S RISK FOR ALL? T2D, IS IT THE CANARY IN THE COAL MINE!?! Blocking stomach acid while taking an antibiotic leaves you vulnerable to overgrowth of pathogenic bacteria like Cdiff that can lead to a serious antibiotic resistant infection. [Contact your doctor to] stop acid suppressing drugs seventy-two hours before and while taking antibiotics to allow levels of stomach acid to return to normal. In fact, acid suppression drugs can cause dysbiosis downstream (including SIBO — read the above HEARTBURN post) and hopefully, as you journey through whole, clean, low toxin, nutrient dense, and anti-inflammatory foods you’ll stop needing them entirely.
NOTE: The above antibiotic microbiome preservation section was adapted from Dr. Robynne Chutkan’s article: “5 Medications That Can Seriously Bloat You.”
Dr. Mark Hyman’s article, Here’s the Downside of Antibiotics Your Doctor Might Not Tell You, recommends the following before and after taking antibiotics. Dr. Hyman is the Medical Director at Cleveland Clinic’s Center for Functional Medicine.
- First, add in the good stuff. Eat a low-glycemic, whole-foods diet and take quality probiotics and prebiotics.
- A high-quality, multi-strain probiotic helps populate your gut with beneficial bacteria.
- Prebiotics, a form of soluble fiber, which also helps feed good bugs, which can be found in onions, garlic, resistant starch, sweet potatoes, dandelion greens and jicama.
- Resistant Starch. I like to supplement with my favorite resistant starch found in Bob’s Red Mill Unmodified Potato Starch. I suggest adding about 1 teaspoon to a glass of water. Unlike regular starch, your small intestine doesn’t absorb potato starch. Instead, your gut bacteria process it, creating molecules that help balance blood sugar and healthy gut flora. In other words, when you consume resistant starch, it “resists” digestion and does not spike blood sugar or insulin.
- Then, focus on gut repair – especially after you’re finished using antibiotics. Utilize gut-healing nutrients including L-glutamine, omega-3 fats, vitamin A and zinc to repair your gut lining so it can resume its normal, natural functions. The use of digestive enzymes can help you digest your food better.
- That’s it … pretty simple but with amazing results. If you’ve ever used antibiotics, did you use prebiotics, probiotics, healing foods, or other nutrients to help recover?
Culturelle, VSL #3, and Saccharomyces boulardii or Florastor(®) related studies
- Prevention of Clostridium difficile infection with Saccharomyces boulardii: A systematic review, 2009 — note this is an early study, certainly before realization of microbiome awareness.
Conclusion: There may be some benefit in using S boulardii for treatment and secondary prevention in patients experiencing recurrent CDI in conjunction with a particular concurrent antibiotic treatment. Because only a small number of studies address the primary prevention of CDI, more research is required before any changes in practice can be recommended with regard to using S boulardii prophylactically. The risks of administering S boulardii seem to be minimal compared with placebo, but because of case reports of potential morbidity secondary to serious fungemia, the use of this yeast agent should be considered on a case-by-case basis.
- Saccharomyces boulardii CNCM I-745 supports regeneration of the intestinal microbiota after diarrheic dysbiosis – a review, 2015. This is an extraordinarily important article with a gut mucosal focus, and anyone thinking about taking S.boulardii should read it… more than once… to realize the potential of this yeast. See below for the many conditions associated with gut dysbiosis.
Its action is based on multiple mechanisms, including immunological effects, pathogen-binding and antitoxinic effects, as well as effects on digestive enzymes… Correlated with these effects, but also due to its inherent properties, S. boulardii is able to create a favorable growth environment for the beneficial intestinal microbiota, while constituting extra protection to the host mucus layer and mucosa…Several human studies as well as animal models demonstrate that treatment with S. boulardii in dysbiosis leads to the faster reestablishment of a healthy microbiome. The most relevant effects of S. boulardii on the fecal composition include an increase of short chain fatty acid-producing bacteria (along with a rise in short chain fatty acids), especially of Lachnospiraceae and Ruminococcaceae, as well as an increase in Bacteroidaceae and Prevotellaceae.
S. boulardii is absent from the natural gut microbiota. If administered, it achieves steady-state concentrations in the colon within 3 days and is cleared from the stools 2–5 days after discontinuation.56,57 In mice, S. boulardii reached 107 colony forming units (CFU)/g of feces in a steady state, when 5×108 CFU was administered daily. When the administration was stopped, the yeast still numbered 7.3×106 CFU/g 3 days later, but was undetectable after 1 week.58
Compared with bacterial probiotics, the yeast cells of S. boulardii have the following advantages: they are antibiotic resistant due to their fungal nature, and they do not exchange DNA, eg, resistance genes with bacteria.53
Prebiotic effect. The cell wall material of S. boulardii is composed of glucans, mannoproteins, and chitin, which serve as excellent substrates for microbial fermentation, especially for various SCFA producers. This helps explain the increase in butyrate and other SCFA produced within the colon after S. boulardii administration.95,96
Elimination of bacterial toxins, pathogen binding, and growth inhibition of microbial pathogens. S. boulardii produces factors that neutralize bacterial toxins and modulate host cell signaling pathways implicated in proinflammatory response during bacterial infection.53 For example, S. boulardii releases a protease that cleaves C. difficile toxins;101 also, S. boulardii can inactivate cholera toxin102 and dephosphorylate lipopolysaccharides from Escherichia coli O55B5.103
In addition, a direct binding to some pathogens is possible: strains of E. coli, Salmonella typhimurium, and S. typhi adhere to the surface of S. boulardii, thus preventing adhesion to and invasion of the host.104–106 Moreover, S. boulardii can inhibit the growth of a number of microbial pathogens like S. typhimurium107and C. albicans.108
Physical barrier effect and colonization resistance. The presence of an intact mucus layer is pivotal to the protection of the intestinal mucosa against bacterial infiltration.15 It can be hypothesized that the sticky outer mucus surface offers the opportunity for S. boulardii to grow and build protective interlaced layers, making it even more difficult for pathogenic strains to reach the mucosa.19
In the healthy situation, commensals have been shown to limit pathogen colonization by competing for metabolites, thereby leading to “colonization resistance.”109 Similarly, S. boulardii – by its mere presence and/or its metabolic activity – may hinder potentially harmful bacteria from occupying a niche at the exposed mucosa. At the same time, S. boulardii itself is not competitive enough to keep this position for long, once habitual/essential bacteria regenerate. Yet its makeshift function may give the host further opportunities to rebuild the mucus layer by reducing the pressure from the potentially harmful microbiota. Studies are needed to verify this hypothesis.
Although the use of S. cerevisiae (eg, S. boulardii CNCM I-745) is considered safe, an increased number of S. cerevisiae infections (fungemia) have been observed in critically ill and/or immunocompromised patients.59 Interestingly, virulence seems to be associated with an enhanced tolerance to oxidative stress 60 as well as increased copy numbers of genes of the purine nucleotide synthesis pathway, which in turn increase survival rates in the bloodstream of the host.61 However, in order to cause fungemia, S. cerevisiae first needs to cross the intestinal barrier and reach the bloodstream in sufficient numbers.
- Efficacy and safety of the probiotic Saccharomyces boulardii for the prevention and therapy of gastrointestinal disorders, 2012 which discusses:
Clinical efficacy of Saccharomyces boulardii as a probiotic in acute gastrointestinal conditions: Antibiotic-associated diarrhea, Clostridium difficile infection, Helicobacter pylori infection, and Acute, persistent, enteral nutrition-related feeding, and travelers diarrhea.
Clinical efficacy of Saccharomyces boulardii as a probiotic in chronic diseases (IBD, IBS, Parasitic, HIV diarrhea)
- Probiotics and the gut microbiota in intestinal health and disease, 2016. S. boulardii, but not the Gram-positive probiotics LGG and L. plantarum, have been reported to protect against the development of C. difficile-associated diarrhea and prevent disease recurrence.96 Although controversial,97treatment with S. boulardii seems to be particularly effective for secondary prevention of disease in specific patient populations at risk for recurrent C. difficile infection.98
- Probiotics for the treatment of Clostridium difficile associated disease. This 2013 review paper updated the current and potential future role of probiotics forClostridium difficile-associated disease.
- Survey and Systematic Literature Review of Probiotics Stocked in Academic Medical Centers within the United States, 2013. The study was a systematic search of medical centers which evaluated Culturelle, Florastor, Lactinex, and VSL #3. Of those 4 probiotics, none were supported by a strong evidence base. However, the results suggested that both Culturelle and Florastor appear to be supported by more evidence compared to other probiotics. Excerpts focusing on Florastor:
Although no probiotics were supported by a strong evidence base, both Culturelle and Florastor appear to be supported by more evidence compared to Lactinex and VSL #3, which had low/no evidence to moderate evidence base for all of the indications identified. Only 27.2% and 9.6% of academic medical centers stocked Culturelle and Florastor, respectively, whereas 51% of academic medical centers stocked at least 1 probiotic that was supported by low/no evidence. These results suggest that a majority of academic medical centers stock a probiotic that lacks a reliable evidence base.
Seven studies out of the 24 RCTs identified were related to Florastor use (Table A2). Of those studies, 1 was related to the use of Florastor for rotaviral diarrhea, 4 for antibiotic-associated diarrhea, and 2 for CDD recurrence. The risk of bias in these studies ranged from low to high. While 29% of the studies were found to have a low risk of bias, 57% had an unknown risk of bias, and 14% had a high risk of bias.22–28
A majority (57%) of the evidence identified evaluated the use of Florastor in antibiotic- associated diarrhea. Three (75%) of these studies showed a statistically significant benefit for decreasing the incidence of antibiotic-associated diarrhea, while 1 (25%) did not report a statistically significant benefit. Additionally, 1 (25%) study showed a statistically significant benefit for decreasing hospitalization duration, 1 (25%) showed no benefit, and 2 (50%) studies did not evaluate duration of hospitalization.23–26Overall, Florastor had a moderate evidence base for antibiotic-associated diarrhea.
Of the 2 RCTs identified regarding the use of Florastor for Clostridium difficile–associated disease (CDD) recurrence, 1 study showed a statistically significant benefit for decreasing the incidence of CDD recurrence in patients with recurrent CDD, while that same study found no benefit in those with an initial CDD. The other study showed no benefit for the use of Florastor in CDD recurrence in patients who received vancomycin or metronidazole.27,28 Overall, Florastor had a moderate evidence base for CDD recurrence.
There was 1 RCT identified for the use of Florastor in rotaviral diarrhea. This RCT showed a statistically significant benefit for decreasing the incidence and duration of rotaviral diarrhea. Overall, Florastor had a moderate evidence base for rotaviral diarrhea.22
- Bacterial counts from five over-the-counter probiotics: are you getting what you paid for?, 2014. Florastor(®) packaging did not state an expected concentration and was found to have 9.2 × 10(9)-1.3 × 10(10) CFU/g
Florastor(®) Precautions
The article, Efficacy and safety of the probiotic Saccharomyces boulardii for the prevention and therapy of gastrointestinal disorders notes that caution should be taken when using S.boularii in patients with risk factors for adverse events, such as immunocompromised patients. That is concerning since actually a lot of folks take immuno-suppression drugs. Some studies such as this, discuss the risk as “reports of fungemia in both immunocompromised and immunocompetent patients. The reports also suggest increased risk for fungemia in patients with central venous catheters and the critically ill (6). These patients, however, are at higher risk of developing CDI and its associated complications. Therefore, this patient population may benefit from preventive therapy.” Check with your doctor if there are other patient circumstances with increased risk. There are also special precautionary situations noted on the Florastor website FAQ: Do not use Florastor if you are currently using a central line or port. Central lines include short- and long-term central venous catheters (CVCs) and peripherally inserted central catheters (PICCs). Do not use Florastor if you are allergic to any of its components (especially yeast).
Dr. Chutkan’s bio, Gastroenterologist and Wellness Expert:
A member of the faculty at Georgetown Hospital since 1997, Dr Chutkan founded the Digestive Center for Women (DCW) in 2004, an integrative gastroenterology practice that includes nutritional therapy, stress reducing techniques such as meditation, biofeedback and counseling, as well as gastrointestinal procedures like endoscopy, colonoscopy, and video capsule endoscopy. In addition to digestive disorders in women, her clinical areas of interest include alterations in gut bacteria (dysbiosis), inflammatory bowel diseases, irritable bowel syndrome, and food as medicine. She is a recognized leader in gastroenterology both nationally and internationally and Washingtonian magazine has consistently named her one of the top doctors in her field. Board certified in Gastroenterology, Dr Chutkan serves on numerous committees and boards and is actively involved in patient and physician education. She is a past Governing Board member of the American Society for Gastrointestinal Endoscopy (ASGE) and former Chair of their Training Committee and Public Relations Committee. She is the author of the bestselling book Gutbliss, and the newly released The Microbiome Solution, and has lectured extensively throughout the United States and Europe. Mount Sinai Hospital, GI fellowship, Columbia College of Physicians & Surgeons, MD, Yale University, BS.
In health through awareness,
Last updated: February 9, 2017 at 7:30 am to add Dr. Mark Hyman’s recommendations for what to do before and after taking antibiotics, excerpted from his article, Here’s the Downside of Antibiotics Your Doctor Might Not Tell You.
Prior update Oct 11, 2016 added clarification in the FODMAP section that “”High” FODMAP foods promote species diversity and richness. The limits noted are threshold levels where consumption above those levels, may not be tolerable for some.” Prior updates updated the title to “What to do if taking ANTIBIOTICS, MICROBIOME”. Prior title was “Antibiotics, Microbiome, and Preservation”. The visual readout compatibility of excerpted studies was also updated.
The Best Way To Take Probiotics When You’re On Antibiotics, July 2019, Vincent Pedre,
https://www.mindbodygreen.com/articles/how-and-when-to-take-probiotics-when-taking-antibiotics
You’ll take this S. boulardii (2 capsules with every a tibiotic dose) + 100 billion CFU probiotic regimen throughout the course of your antibiotic treatment. Then, once you’re done with your antibiotic course, you’ll continue the same regimen for one to two months to help your gut continue to recover.
2017 DCD, Antibiotic Prescribing and Use, https://www.cdc.gov/antibiotic-use/
[Johnson et al 2012] Probiotics for the prevention of Clostridium difficile-associated diarrhea: a systematic review and meta-analysis, https://www.ncbi.nlm.nih.gov/pubmed/23362517
Download fulltext at: https://www.researchgate.net/publication/235383789_Probiotics_for_the_prevention_of_Clostridium_difficile-associated_diarrhea_A_systematic_review_and_meta-analysis
An article discussing the study is: Cochrane, The use of probiotics to prevent Clostridium difficile diarrhea associated with antibiotic use https://www.cochrane.org/CD006095/IBD_use-probiotics-prevent-clostridium-difficile-diarrhea-associated-antibiotic-use
What did the researchers investigate? The researchers investigated whether probiotics prevent CDAD in adults and children receiving antibiotic therapy and whether probiotics causes any harms (side effects). The researchers searched the medical literature extensively up to 21 March 2017.
What did the researchers find? This review includes 39 randomized trials with a total of 9955 participants. Thirty-one studies (8672 participants) assessed the effectiveness of probiotics for preventing CDAD among participants taking antibiotics. Our results suggest that when probiotics are given with antibiotics the risk of developing CDAD is reduced by 60% on average. Among trials enrolling participants at high risk of developing CDAD (> 5%), the potential benefit of probiotics is more pronounced with a 70% risk reduction on average. Side effects were assessed in 32 studies (8305 participants) and our results suggest that taking probiotics does not increase the risk of developing side effects. The most common side effects reported in these studies include abdominal cramping, nausea, fever, soft stools, flatulence, and taste disturbance. The short-term use of probiotics appears to be safe and effective when used along with antibiotics in patients who are not immunocompromised or severely debilitated. Despite the need for further research, hospitalized patients, particularly those at high risk of CDAD, should be informed of the potential benefits and harms of probiotics.
From the study:
Conclusion: Moderate-quality evidence suggests that probiotic
prophylaxis results in a large reduction in CDAD without an increase in clinically important adverse events. Moderate-quality evidence supports a large protective effect of probiotics in preventing CDAD. Given the low
cost of probiotics and the moderate-quality evidence suggesting the absence of important adverse effects, there seems little reason not to encourage the use of probiotics in patients receiving antibiotics who are at appreciable risk for CDAD.
We found that 20 randomized trials testing the effect
of probiotics (Bifidobacterium, Lactobacillus, Saccharomyces,
or Streptococcus species) in patients receiving antibiotics
showed a large relative risk reduction in the incidence of
CDAD (relative risk, 0.34 [CI, 0.24 to 0.49]). Of the 20
trials, 19 were blinded (Figure), and results were robust to
sensitivity analyses of worst-plausible-case assumptions regarding missing outcome data. Our judgment is that the
evidence warrants moderate confidence in this large relative
risk reduction (Table 2).
Data Synthesis: Twenty trials including 3818 participants met the
eligibility criteria. Probiotics reduced the incidence of CDAD by
66% (pooled relative risk, 0.34 [95% CI, 0.24 to 0.49]; I
2 0%).
In a population with a 5% incidence of antibiotic-associated CDAD
(median control group risk), probiotic prophylaxis would prevent 33
episodes (CI, 25 to 38 episodes) per 1000 persons. Of probiotictreated patients, 9.3% experienced adverse events, compared with
12.6% of control patients (relative risk, 0.82 [CI, 0.65 to 1.05];
I2 17%).
Clostridium difficile infection: risk with broad-spectrum antibiotics, NICE 2015, https://www.nice.org.uk/advice/esmpb1/chapter/Full-evidence-summary-medicines-and-prescribing-briefing
C. difficile may be found in the gut of people with no symptoms: up to 3% of healthy adults, 7% of residents in long‑term care facilities, 14−20% of older people on hospital wards and about 66% of healthy children aged under 2 years.
Although no particular antibiotics can be ruled out, those most commonly implicated in C. difficile infection are clindamycin, cephalosporins (in particular second‑ and third‑generation cephalosporins), quinolones, co‑amoxiclav and aminopenicillins (for example, ampicillin and amoxicillin, which may be related to their volume of use rather than being ‘high risk’) (NICE clinical knowledge summary: diarrhoea – antibiotic associated). Compared with narrow‑spectrum antibiotics, broad‑spectrum antibiotics are more likely to significantly change the gut flora, potentially allowing other bacteria, such as C. difficile, to become established.
Which Antibiotics Are Most Associated with Causing Clostridium difficile Diarrhea? 2017, https://www.pharmacytimes.com/contributor/sean-kane-pharmd/2017/03/which-antibiotics-are-most-associated-with-causing-clostridium-difficile-diarrhea
Antibiotic Classes with Highest Risk of C difficile (odds ratio 5 or more)
Without a doubt, clindamycin carries the highest risk of C difficile infection with an odds ratio of about 17-20 compared to no antibiotic exposure.3-5 Fluoroquinolones, cephalosporins, aztreonam, and carbapenems carry a fairly high risk, all of which being associated with an odds ratio of approximately 5 compared to no antibiotic exposure.
Antibiotic Classes with Moderate Risk of C difficile (odds ratio 1 to 5)
Macrolides, sulfonamides/trimethoprim, and penicillins are associated with a moderate risk of C difficile infection with odds ratios between about 1.8 and 3.3.3-5 Within this group, penicillins are generally associated with a slightly higher risk (odds ratio about 50% higher) compared to macrolides and sulfonamides/trimethoprim.
Clinical Implications of C difficile Risk Data
On the basis of the available data, clindamycin should absolutely be avoided among patients who are at risk for C difficile infection, particularly in elderly patients and those with frequent antibiotic exposure or hospitalizations. Given the available data, it’s clear that clindamycin is a well-deserving candidate of its boxed warning specifically for C difficile risk.6
[Zmora et al 2018] Personalized Gut Mucosal Colonization Resistance to Empiric Probiotics Is Associated with Unique Host and Microbiome Features
Highlights
•The murine & human gut mucosal microbiome only partially correlates with stool
•Mice feature an indigenous-microbiome driven colonization resistance to probiotics
•Humans feature a person-specific gut mucosal colonization resistance to probiotics (persisters and resisters)
•Probiotic colonization is predictable by pre-treatment microbiome & host features (algorithm developed predicts persisters and resisters)
[Suez et al 2018] Post-Antibiotic Gut Mucosal Microbiome Reconstitution Is Impaired by Probiotics and Improved by Autologous FMT
Highlights
• Murine gut mucosal probiotic colonization is only mildly enhanced by antibiotics
• Human gut mucosal probiotic colonization is significantly enhanced by antibiotics
• Post antibiotics, probiotics delay gut microbiome and transcriptome reconstitution
• In contrast, aFMT restores mucosal microbiome and gut transcriptome reconstitution
S.boulardii and antibiotics.
[Kabbani et al 2017] Prospective randomized controlled study on the effects of Saccharomyces boulardii CNCM I-745 and amoxicillin-clavulanate or the combination on the gut microbiota of healthy volunteers
Antibiotic treatment is associated with marked microbiota changes with both reductions and increases in different genera. S. boulardii treatment can mitigate some antibiotic-induced microbiota changes (dysbiosis) and can also reduce antibiotic-associated diarrhea.
Healthy subjects were randomized to one of 4 study groups: SB for 14 days, Amoxicillin-Clavulanate (AC) for 7 days, SB plus AC, Control (no treatment). Participants gave stool samples and completed gastro-intestinal symptom questionnaires. Microbiota changes in stool specimens were analyzed using 16s rRNA gene pyrosequencing (bTEFAP).
1. Subjects treated by S boulardii + AC had fewer adverse events and tolerated the study regimen better than those receiving the AC alone.
2. Control subjects had a stable microbiota throughout the study period.
2. Significant microbiota changes were noted in the AC alone group during antibiotic treatment. AC associated changes included reduced prevalence of the genus Roseburia and increases in Escherichia, Parabacteroides, and Enterobacter. Microbiota alterations reverted toward baseline, but were not yet completely restored 2 weeks after antibiotherapy.
4. No significant shifts in bacterial genera were noted in the SB alone group.
5. Adding SB to AC led to less pronounced microbiota shifts including less overgrowth of Escherichia and to a reduction in antibiotic-associated diarrhea scores.
Infectious Diseases / Bacteria / Viruses
Immune System / Vaccines
Pharmacy / Pharmacist
Public Health
One course of antibiotics disrupts gut microbiome for a year, 2015, http://www.medicalnewstoday.com/articles/302179.php
Antibiotics and microbiome: Microbiome diversity in feces was significantly reduced for up to 4 months in participants taking clindamycin and up to 12 months in those taking ciprofloxacin.
Amoxicillin had no significant effect on microbiome diversity in either the gut or oral cavity, but it was associated with the greatest number of antibiotic-resistant genes.
The microorganisms in participants’ feces were severely affected by most antibiotics for months. In particular, researchers saw a decline in the abundance of health-associated species that produce butyrate, a substance that inhibits inflammation, cancer formation and stress in the gut. The drugs were found to enrich genes associated with antibiotic resistance and to severely affect microbial diversity in the gut for months after exposure. By contrast, microorganisms in the oral cavity and saliva showed signs of recovery in as little as a few weeks after drug exposure.
“Antibiotics should only be used when really, really necessary. Even a single antibiotic treatment in healthy individuals contributes to the risk of resistance development and leads to long-lasting detrimental shifts in the gut microbiome. Certainly we cannot live or survive without antibiotics; that’s out of the question. But there are situations when we should not use them, like when there are no evidence-based reasons.”
Probiotics in the prevention of antibiotic-associated diarrhoea and Clostridium difficile infection, 2011 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3105609/
Antibiotics and probiotics: L. rhamnosus GG, S. boulardii and two mixtures, one containing L. casei DN-114 001 and the other Lactobacillus acidophilus CL1285, all have good evidence of efficacy in preventing AAD in clinical trials, but evidence of feasibility and efficacy in routine practice is required. The evidence for prevention and treatment of CDAD is currently equivocal. There may be other strains that have equal or better efficacy and research is required to establish which strains are the best to use.