There is this review article which is very detailed:
Sulfur Cycling and the Intestinal Microbiome
"Approximately 20% of methionine and 25% of cysteine supplied in the diet is metabolized in the gastrointestinal tract [34], and, due to the high metabolic activity of the intestinal ecosystem, the concentration of free methionine and cysteine in the colon is extremely low [35]."
"About 25% of the transsulfuration reactions in the human occur in the intestinal mucosa [36] and, if homocysteine accumulates, there is a dysfunction in patients leading to inflammatory intestinal disease [36, 37]."
"Endogenous sulfur-containing compounds present in the intestinal ecosystem includes sulfated bile, chondroitin sulfate, heparin and sulfomucins [31, 69, 70]."
"SRB [sulfate-reducing bactaeria] become established in individuals at a very early age and persist in the gut throughout their life [29]."
"In terms of oxygen tension, the intestinal tract is interesting in that it has an aerobic periphery maintained by intestinal epithelial cells and an anaerobic lumen resulting from high bacterial metabolic activity. The large intestine is covered by a dense mucous layer which contains few bacterial cells and a loose mucous layer which is highly populated by foraging bacteria [104]. The inner mucous layer contains a variety of antibacterial compounds produced by intestinal cells and serves to protect the intestinal cells. Various bacteria are attached to the outer mucous layer forming a biofilm which excludes pathogens and promotes fermentative bacteria to convert mucin glycans to butyrate which is important energy source for the colonocytes."
"As H2S diffuses from the lumen to the colonocytes, low levels of hydrogen sulfide stimulate oxygen consumption by mitochondrial respiration but at >20 microM H2S, mitochondrial cytochrome oxidase in colonocytes is inhibited [105]. Initially, hydrogen sulfide binds to the cytochrome oxidase with one molecule of H2S binding to oxidized Fe in heme a3 and another molecule of H2S binding to a reduced CuB binuclear center of cytochrome oxidase."
"Intestinal anaerobic bacteria ferment carbohydrates and dietary materials to produce propionic, acetic and butyric acids with butyric acid serving as an important energy source for colonic epithelial cells. While the concentration of hydrogen sulfide in the intestinal lumen would be in the range of 0.1–0.5 mM, hydrogen sulfide at 2 mM was found to prevent oxidation of butyric acid in the distal and ascending regions of the colon by inhibiting acyl-CoA dehydrogenase [106]. This depriving of colonic cells of energy may be important in the pathogenesis of ulcerative colitis, a disease of the large bowel, without affecting the small bowel because epithelial cells of the small bowel do not use butyric acid but instead use glucose and glucosamine for energy [11]."
"There is evidence that H2S is a bacterial cytoprotectant molecule against antimicrobials and oxidative stress. Documentation that H2S could increase resistance of Escherichia coli to antibiotics was first documented over 40 years ago [128]. Given the widespread use of antibiotics in the medical, agricultural, and food industries, microbes capable of H2S production could potentially have a large impact. Our group has found that, after administering a broad-spectrum antibiotic cocktail to mice (adapted from Chen et al., [129]), there was a bloom of sulfate-reducing bacteria 7–14 days after the cessation of antibiotic treatment (our unpublished data)."
"Shatalin et al. [130] found that bacteria exposed to hydrogen peroxide or ampicillin that were lacking H2S enzymes had more DNA breaks than cells capable of producing H2S, or had exogenous H2S supplementation, suggesting that H2S protects chromosomal DNA. Superoxide dismutase and catalase both function to partition reactive oxygen species for cellular protection. H2S has been shown to enhance the activity of both catalase and superoxide dismutase [133], and also to prevent reactions that produce reactive oxygen species [134]."
"Glutathione is the primary defense against oxidative damage to intestinal cells."
"It has been proposed that a common mechanism of bactericidal antibiotic action occurs by hydroxyl radicals being generated in microbes regardless of drug–target interaction [138]. There is evidence that H2S could protect microbes from bactericidal antibiotics through scavenging of reactive oxygen species or by induction of the glutathione cascade [139, 140]. However, that theory was challenged by subsequent studies that showed that reactive oxygen species do not play a role in the bactericidal activity by antibiotics [141, 142]. In this scenario, H2S must protect bacteria from bactericidal antibiotics through a mechanism not related to oxidative stress. Due to the substantial evidence that H2S acts as a cytoprotectant for bacterial cells in the presence of antimicrobials, it is imperative for future studies to look into routes of H2S production inhibition or H2S inactivation to improve the efficacy of antibiotics."
"There are several bacterial processes that may result in production of H2S in the colon (Fig. 6). The anaerobic dissimilatory SRB produce hydrogen sulfide from inorganic sulfate and sulfated compounds supplied in the diet. An important source of endogenous sulfate is the enzymatic removal of sulfate from sulfated mucin. Hydrogen sulfide is also produced by bacterial metabolism of sulfur-containing amino acids and especially cysteine. Hydrogen sulfide diffuses to the intestinal cells where a significant quantity of H2S is oxidized by colonocytes to thiosulfate and tetrathionate. Bacterial and intestinal cells involved in the degradation of tetrathionate and thiosulfate results in the release of hydrogen sulfide. In many instances, sulfite produced from thiosulfate dehydrogenase is also reduced to hydrogen sulfide."
"It has been reported that, when using human fecal materials, sulfated mucin, cysteine, taurine and other sulfur- containing endogenous compounds produce hydrogen sulfide at a faster rate than the reduction of sulfate [43]. Some H2S is released by flatulence and feces, while a significant quantity of H2S is oxidized by colonocytes to thiosulfate and tetrathionate. The presence of thiosulfate in portal blood [43, 144] suggests that the amount of recycled H2S could be significant. Near the intestinal wall, the environment is micro-aerophilic and H2S could signal facultative bacteria to produce cytochrome oxidases that are not inhibited by H2S."
If you happen to read it in details, you'll notice that the idea of avoiding most food sources of sulfur possible in attempt to solve this issue goes down the drain because even if you fasted, there are still bile compounds and mucusal lining that will keep a steady supply for them.
Like it was mentioned, the cancer therapists seemed to have dealt with this problem often.
I lied elsewhere, there's more from Gerson:
"Now about three or four months ago a case came to Philadelphia. She told me when her son and brother brought her in that she had suffered from cancer of the rectum. At first the doctors didn't want to operate, then they couldn't. It was too late. Then she spent a half at the Hoxey Clinic, and then she came home with a liver full of cancer and hard as a board. I told her son and brother that this was too much, it wouldn't go. Take her home and make her comfortable. But they insisted I must try. And I did. And she is doing well! She can eat and drink, and anterior part of her liver is a scar, hard as though it were calcified. Probably there is enough liver left. The son asked when they took her home after eight weeks, "You see, why didn't you want to take her?" At least for four weeks, every two hours and sometimes even every hour, she took enemas twice a day! She had so much gas and eliminated such large amounts of evil-smelling masses. When she left, we had to paint the room. It couldn't be washed off the paint."
In extreme cases, if you were to avoid something, it must be animal proteids for a while since they are the major source of sulfur in people's diets. Some inevitably escapes digestion and considering their high sulfur content, this small portion can be a lot for someone with an infection.
Metchnikoff observed that animals that feed on corpses don't have problems with putrefaction (!) because their intestines move fast enough. Which is why the focus should be on vigorous activity and robust immunity.
Sometimes nutrients only work when given in conjuction and when you manage to get a break from at least part of chronic poisoning (through frequent enemas for example).