If we contrast GFS with BFS, one of the key differences is the clinical manifestation of alcohol toxicity, as discussed earlier. A BFS patient, even with substantial ethanol in the bladder, would not have alcohol in their bloodstream and would not manifest symptoms of intoxication; thus, BFS patients can be asymptomatic and go unnoticed. In contrast, a GFS patient can develop alcohol intoxication spontaneously even without any alcohol ingestion, potentially resulting in adverse legal consequences such as DUI [
26‐
31]. They may fail abstinence monitoring. The GFS patients may be symptomatic and thus seek medical treatment.
Both BFS and GFS are triggered by deranged microbiota within the hollow organs, leading to ethanol fermentation due to the overgrowth of fermenting yeast within the bladder and gut. To our knowledge, BFS appears to happen exclusively in the case of poorly controlled diabetes and resulting hyperglycosuria [
2]. BFS should be caused by Crabtree-positive yeast, such as
C. glabrata. On the other hand, GFS cases have typically been reported in patients with underlying medical conditions causing gut dysbioses, such as Crohn’s disease with strictures, short gut syndrome after surgery, or previous antibiotic use [
27,
32‐
35]. A significant amount of ethanol is produced within the gut lumen, especially after consuming carbohydrate-rich food, causing alcohol intoxication in GFS patients [
26,
27,
36]. The causative agents in most GFS cases are fermenting yeast, but high-alcohol-producing
Klebsiella pneumoniae (K. pneumoniae) was recently identified as a causative microorganism of antifungal-resistant GFS [
37,
38]. The partial pressure of oxygen within the gut lumen is less than 1 mm Hg [
39], much lower than that of the bladder lumen. This near-anoxic environment should allow Crabtree-positive yeast (e.g.,
C. glabrata, S. cerevisiae), Crabtree-negative yeast (e.g.,
C. albicans), and facultative anaerobes (e.g.,
K. pneumoniae) to perform anaerobic fermentation within the gut lumen [
27,
35‐
37,
40‐
42].