An 85-year-old diabetic male patient, who never drank alcohol, was diagnosed with T2DM 20 years ago; he was managed with diet control and oral hypoglycemics. However, he was shifted to insulin therapy over the last five years to improve glycemic control. He had a long history of renal stone formation. His family gave a history of epilepsy for the past three years, and he was given Levetiracetam 1000 mg for six months that was reduced to 500 mg for six more months. He was then maintained on Gabapentin 400 mg twice daily until now. He is a mild smoker. In the last three years, he experienced marked constipation that could last a few days. In addition, he was always on multi-vitamin, multi-mineral and Cod-liver oil food supplements.
One week before admission, due to his wife's sickness (she took care of him) his condition worsened due to a change in diet and therapy incompliance. Initially, he started to experience dizziness and an altered mental state. Then, his condition gradually deteriorated and he had urinary and fecal incontinence, agitation, insulting and threatening others, refusing help, and refusing to shower and change his spoiled clothes. However, they did not give a history of seizure attacks during that period.
After one week, his wife recovered and started to take care of him. She noticed that his urine was milky and his mental state significantly deteriorated. On November 2, 2019, the family transferred him to El-Rehab-2 Private Hospital (Assiut, Egypt), where he was admitted to the Department of Internal Medicine. On examination at admission, he was confused, disoriented to time, place and person, dizzy and dehydrated. His vital signs were stable, his weight was 60 kg and height was 170 cm, but no recent weight loss was revealed from his clinical history. Abdominal examination showed mild tenderness over the supra-pubic area, the chest and heart examination was unremarkable. Abdominal ultrasonography of the kidneys, urinary tract and liver was unremarkable. A complete laboratory work up was done including blood and urine ethanol, urinalysis, urine culture and sensitivity. The major finding was hyperglycemia with fair glycemic control as indicated from HbA1c <=7.6%, high blood and urinary ethanol content (measured by enzymatic colorimetric kit, cat#TBS2090; Tribioscience, Palo Alto, CA, USA - lower detection limit of 0.1 mg/dL). Complete blood count revealed mild normocytic-normochromic anemia with relative/absolute monocytosis ( Table 1). The mid-stream fresh sample of urine was cloudy, positive for ethanol (= 580 mg/dL), acidic (pH 5.5), negative for proteins, highly positive for glucose (+++), and mildly positive for ketones (+) and lactate (+) tested by urinary dip strips. The urine showed pus cells (55/HPF) and a few red blood cells (5/HPF). Numerous budding large yeast cells (nearly 1/4 of pus cell size) were easily identified upon direct examination of a wet mount of the sample sediment between slide and cover on a phase contrast microscope.  
Culture of the fresh mid-stream urine sample on Sabouraud Dextrose Agar at 37  C for 24 hours revealed Candida sp . colonies. Subculturing, to ensure purity and optimal growth, with chloramphenicol, confirmed the presence of large white, round, curved, soft and smooth to wrinkle colonies with a characteristic yeast odor ( Figure 1A). Examination of air-dried fixed smears stained with Gram's stain under a light microscope using 100x oil immersion objective showed gram positive budding yeast cells indicative of Candida albicans that was confirmed by positive germ tube formation by germ tube test ( Figure 1B). Briefly, one colony was emulsified in human serum and incubated at 37  C for two hours. Five or more germ tubes (short and aseptate germinating hyphae)/HPF were observed in a wet mount preparation. Disk diffusion antifungal susceptibility testing was conducted using C. albicans ATCC 90028 as a standard control strain. An inoculum from a 48-hour old culture with ~1 - 5 x 10 6 CFU/mL was plated on the dry surface of Mueller-Hinton agar supplemented with 2% glucose and 0.5 mug/mL methylene blue. After 3-5 minutes, the antifungal disks for Fluconazole (25 mug), Itraconazole (8 mug), Nystatin (100 U), and Amphotericin B (10 mug) were applied with gentle pressure (Rev.7/03.12.2012; Liofilchem   S.r.l., Italy). After 24 hours of aerobic incubation at 35  C, the diameter of the growth inhibition zone was manually measured for comparison of the antifungal sensitivity that turned highest with Itraconazole followed by Nystatin, Amphotericin B then the least effective was Fluconazole ( Figure 1C).  
Insulin Glargine 40 IU SC daily with Insulin Aspart SC six hourly was administered with dose adjustment according to sliding scale, along with normal saline (0.9%) I/V infused. I/V antifungal, Amphotericin B (Fungizone), 40 mg/day for five days as a five hour I/V infusion was administered.
At the end of the five day treatment period, these interventions led to rapid improvement in the short-term glycemic control marker and the patient regained his consciousness, was cooperative and oriented to time and place. Furthermore, his urine became normal, free from the yeast and no more ethanol was detectable in the urine or blood.