What recovery looks like: response and remission

What is the difference between responding to treatment and becoming durably symptom-free? In this chapter you will learn to recognise the two stages of recovery — response and remission — and how your diary shows you where you stand.

Response: when your body begins to react

Response^[G] is the first tangible sign that treatment is working. It does not happen from one moment to the next, and it is not necessarily dramatic — often it is more of a quiet, gradual easing. The most telling sign is the fall in the daily stool count: what used to be frequent, urgent passing many times a day begins to thin out. In parallel, the consistency of the stool also changes — from watery, formless stool it gradually becomes more formed, closer to normal. The bloating and cramps ease too, and often some appetite and energy return.

It is important that response is not yet the end of the road. At this point your body has set off in the right direction, but the process is fragile: the freshly engrafting gut flora is still building, and the pathogen has not yet been pushed back for good. So you must not stop the course at the first signs of response, or "let loose" with your old habits. Response is rather an encouraging milestone: it says you are on the right track, and it is worth continuing exactly as you agreed with your doctor.

The best tool for measuring response is not your feeling, but your diary. A single good day is not yet a trend; but the direction looking back over seven days reveals a great deal. If the stool count is heading down, the Bristol value^[G] is approaching the 3–4 target band, and bloody stool disappears, then the numbers are clearly speaking of response.

Remission: durable freedom from symptoms

Remission^[G] is the destination the whole programme is about: durable freedom from symptoms. Here the complaints not only ease but disappear — passing stool becomes regular and normal, the Bristol value stays steadily in the 3–4 band, there is no bloating, cramping or bloody stool, and this state holds not for a day or two, but durably. Remission is not a single "cured" moment, but a stable, reliable everyday normal that gives back your sense of security.

What distinguishes true remission from a passing good spell is durability. In a recurrent Clostridioides difficile infection the symptoms could ease temporarily before too, only to return — which is why remission is always proven by time. If freedom from symptoms holds for weeks while the dose gradually falls, that is a strong sign of an engrafted, working gut flora^[G]: your own system is now keeping the pathogen in check on its own.

This does not mean that reaching remission is the end of everything. The remainder of the programme is precisely about how to keep this state — by carrying the taper through, by reinforcing your lifestyle, and by knowing the signs of relapse. Remission, then, is not the finish line, but a stable foundation on which you build durable health.

🍽️ Eating during these days

During the days of response and remission, the task of eating is to reinforce and make durable the colonisation resistance that lies behind lasting freedom from symptoms. As the symptoms ease, the goal is no longer to firm up the stool, but to feed the engrafting flora and make it more diverse. The concrete eating task for the three days: keep the familiar morning intake on an empty stomach with plenty of water, continue fluid replacement even if the symptoms are improving, and every day work the day's plant into at least one meal.

For these days (64–66), the Plant Calendar (Appendix F) brings three fermented plant foods: kimchi (64), miso (65) and tempeh (66). These bring live microbial cultures and further plant variety into the diet — exactly when the engrafting gut flora is building its diversity. In the second half of the programme (about days 61–90) the goal is to maintain full diversity and fermentable fibre sources: the more kinds of plant fibre pass across your plate, the more kinds of beneficial bacteria you feed, and the more short-chain fatty acids (including butyrate) are produced, which support the gut barrier and colonisation resistance. A diverse, stable flora is the foundation of resilience — this is what makes the pathogen's return difficult. Introduce fermented foods in small portions, and if you do not tolerate one of them, leave it out and come back to it later.

References

[7] van Nood E, Vrieze A, Nieuwdorp M et al. Duodenal infusion of donor feces for recurrent Clostridium difficile. N Engl J Med. 2013. Link

Open-label RCT in patients with recurrent C. difficile infection comparing duodenal donor faeces infusion (after short vancomycin + bowel lavage) with standard 14-day vancomycin, with or without bowel lavage. The primary endpoint was diarrhoea resolution without relapse at 10 weeks. The trial was stopped early at interim analysis: 13/16 patients (81\%) in the FMT arm achieved resolution after a single infusion, substantially exceeding both vancomycin arms. Establishes FMT as superior to antibiotic monotherapy for recurrent CDI and provides the landmark evidence base for FMT clinical translation.

[357] Lewis SJ, Heaton KW. Stool form scale as a useful guide to intestinal transit time. Scand J Gastroenterol. 1997. Link

The authors evaluated the responsiveness of the Bristol Stool Form Scale to changes in whole-gut transit time (WGTT). Sixty-six volunteers had WGTT measured with radiopaque markers and recorded stool form on a 7-point scale and defecation frequency; measurements were repeated under senna and loperamide. Baseline WGTT correlated with frequency (r=0.35, P=0.005) and stool output (r=-0.41, P=0.001), and best with stool form (r=-0.54, P<0.001). Senna (n=44) shortened WGTT and increased frequency, form score and output (all P<0.001); loperamide (n=43) lengthened WGTT and reduced frequency, form score and output (all P<0.001). The Bristol scale is a valid surrogate for intestinal transit time and is responsive to pharmacological alteration.

[365] Reed AD, Theriot CM. Contribution of Inhibitory Metabolites and Competition for Nutrients to Colonization Resistance against Clostridioides difficile by Commensal Clostridium. Microorganisms. 2021. Link

This review examines how commensal Clostridium species mediate colonization resistance against C. difficile. Commensal Clostridia modify primary bile acids into secondary bile acids that suppress C. difficile spore germination and vegetative outgrowth. They additionally produce antimicrobial peptides and short-chain fatty acids that directly inhibit C. difficile and compete for limiting nutrients such as proline, important for C. difficile growth via Stickland fermentation. Loss of commensal Clostridia after broad-spectrum antibiotics is a key mechanistic step toward CDI susceptibility. The authors argue that restoring defined Clostridium consortia is a rational, mechanism-driven alternative to FMT for preventing recurrent CDI.

[369] Weingarden A, González A, Vázquez-Baeza Y, Weiss S, Humphry G, Berg-Lyons D, Knights D, Unno T, Bobr A, Kang J, Khoruts A, Knight R, Sadowsky MJ. Dynamic changes in short- and long-term bacterial composition following fecal microbiota transplantation for recurrent Clostridium difficile infection. Microbiome. 2015. Link

This study tracked fecal microbiota dynamics in four patients with multiply recurrent, antibiotic-refractory C. difficile infection treated with FMT, sampling daily up to 28 days and weekly up to 84 days post-FMT (with sampling out to 151 days). 16S rRNA gene profiling was compared to Human Microbiome Project body-site references. Pre-FMT samples were markedly dysbiotic. FMT produced a rapid normalization of fecal community composition toward a healthy donor-like state within days, and this normalization was largely sustained over months. Time-course visualization highlighted both rapid early shifts and longer-term stabilization. The findings document the kinetics of FMT-driven microbiota recovery in refractory CDI and support its durability.