A 40-year-old Japanese woman was admitted to our hospital after a 5-day history of yellowish vaginal discharge, and 3-day history of fever, shaking chills, and appetite loss. She did not have any relevant past medical history and had not been prescribed any medications, including antibiotics. She had never been abroad and had not had any raw foods in the previous month. Her last menstrual period had finished 2 weeks before the day of hospital admission.
At first, we diagnosed severe bacterial colitis and hypovolemic shock and started large volumes of hydration, dopamine infusion, and intravenous ciprofloxacin (300 mg, 2 times daily). However, her vital signs did not recover. On day 2, we learned that she had begun menstruating 4 days prior to admission, and that she kept a tampon inserted 3 days until the day of admission. Additional testing of her vaginal discharge showed the following; polymorphonuclear leukocytes 2+, and Nugent score, 1. We suspected TSS or septic shock of unknown origin and changed the antibiotics to vancomycin (1 g, 2 times daily, intravenously), clindamycin (600 mg, 4 times daily, intravenously), and meropenem (500 mg, 4 times daily, intravenously). On day 4, community-acquired S. aureus was detected from the tampon and vaginal discharge and her vital signs gradually recovered enough to stop the dopamine infusion, and her diarrhoea stopped. Two sets of blood culture and urine culture were negative. We diagnosed staphylococcal TSS owing to tampon use, discontinued meropenem on day 11, and continued antibiotic treatment with the combination of vancomycin and clindamycin for 14 days. On day 14, the patient was found to have peeling skin at the end of her fingers (Fig. 1). The patient was discharged on day 18, without any damage to her organs or deterioration in activities of daily living.
Her vital signs on the day of admission were as follows: blood pressure, 86/49 mmHg; heart rate, 121 beats per minute; body temperature, 39.8  C; respiratory rate, 36 breaths per minute; and peripheral capillary oxygen saturation level on room air, 96%. She was alert and physical examination showed generalized rash on her hand and neck. Results of cardiovascular, respiratory, and abdominal examinations were normal, except tenderness on the right costal-vertebral angle. Laboratory data revealed WBC of 19,200/mul, CRP level of 14.5 mg/dL, BUN level of 28.4 mg/dL, s-Cre level of 1.7 mg/dL, serum total protein level of 6.0 g/dL, serum albumin level of 3.3 g/dL, and procalcitonin level of 5.4 ng/mL. Results of liver function tests were normal except for an LDH level of 328 IU/L. Urine dipstick examination revealed 3+ protein and 2+ occult blood. A microscopic examination detected 5 to 10 RBCs per high-power field and more than 100 WBCs per high-power field. Testing of her vaginal discharge showed the following: polymorphonuclear leukocytes, 4+; and Nugent score, 4. Gram stain of both urine and vaginal discharge showed clustered gram-positive cocci.
At first, we diagnosed severe urinary tract infection and septic shock. We started large volumes of hydration, dopamine infusion, and intravenous ampicillin (2 g, 3 times daily) and gentamicin (120 mg, once daily). However, her vital signs did not recover and she experienced diarrhoea. On day 2, S. aureus was detected from urine and vaginal discharge. We suspected staphylococcal TSS or septic shock of unknown origin, and changed the antibiotics to vancomycin (1 g, 2 times daily, intravenously), clindamycin (600 mg, 4 times daily, intravenously), and meropenem (1 g, 3 times daily, intravenously) for covering enteric bacteria and anaerobes like Bacteroides spp. On day 3, community-acquired S. aureus was detected from both urine and vaginal discharge, and she recovered adequately enough to discontinue dopamine and large volumes of hydration. Two sets of blood cultures were negative. Gynaecological examination revealed narrowing of the vaginal opening caused by vulvar lichen sclerosus, a chronic and progressive dermatologic disorder of genital skin that can cause vulvar pruritus, dysuria, and sexual dysfunction due to cleft narrowing. We diagnosed staphylococcal TSS caused by vaginitis and discontinued meropenem on day 9 and continued vancomycin in combination with clindamycin for 14 days. On day 14, we noted peeling skin at the end of her fingers (Fig. 2). The patient showed full recovery and was discharged on day 17.
The following 13 antimicrobials were tested: ampicillin, cefazolin, imipenem, gentamicin, gentamicin, erythromycin, clindamycin, telithromycin, levofloxacin, minocycline, vancomycin, teicoplanin, arbekacin, and trimethoprim/sulfamethoxazole. According to M100-S20, published by the Clinical and Laboratory Standards Institute, the isolates from Case 1 and Case 2 were resistant to ampicillin, cefazolin, imipenem, and gentamicin, but were susceptible to erythromycin, clindamycin, and minocycline. The 2 isolates were tested for genes encoding selected exotoxins including TSST-1, exfoliative toxins A and B (ETA and ETB), staphylococcal enterotoxins A to E (entA, entB, entC, entD, and entE), and Panton-Valentine leukocidin (PVL) by multiplex real-time polymerase chain reaction (PCR) analysis. Both isolates contained genes encoding for the toxins ETA, ETB, and TSST-1, but were negative for other exotoxins, including PVL. The isolates were also typed to determine their staphylococcal cassette chromosome mec (SCCmec) type by multiplex PCR targeting the cassette chromosome recombinases (ccr) and mec gene complex. Both isolates were identified as the group ST8-MRSA with SCCmec type IV, which has recently been one of a major genotype in the community in Japan.