Rapidly Fatal Bacteremia Caused byShigella sonneiwithout Preceding Gastrointestinal Symptoms in an Adult Patient with Lung Cancer

To the Editor—Shigella sonnei is a rare cause of fatal bacteremia in adult patients [1–5]. We describe an unusual case of a patient with S. sonnei bacteremia who presented with adult respiratory distress syndrome and multiorgan failure that led to rapidly fatal outcome. A 62-year-old man with underlying diabetes mellitus, hypertension, and hy pertriglycemia visited our hospital after experiencing shortness of breath and palpitation for 3 weeks. He was a merchant and lived in Indonesia. He visited a local hospital in Indonesia and received a diagnosis of hepatomegaly and multiple hepatic nodules. Neither cardiovascular abnormalities nor evidence of acute coronary syndrome were noted. Seven days prior to admission to our hospital, he visited a regional hospital in Taiwan. Computed tomography disclosed a hilar mass in the right mediastinum and several nodules in the right lower lung field and the liver. Transcutaneous biopsy of the hepatic tumor revealed small cell lung cancer. He was transferred to our hospital to receive chemotherapy for lung cancer with liver metastasis. On initial examination, he was aware and alert but appeared to be chronically ill. He was afebrile (body temperature, 36.3°C), had a pulse rate of 101 beats per min, and had a respiratory rate of 20 breaths per min. Icteric sclerae and hepatomegaly were noted. His white blood cell count was 4920 cells/µL, his hemoglobin level was 11.5 g/dL, and his platelet count was 129,000 cells/µL. Biochemical examinations revealed a bilirubin level (total/direct) of 17.8/11.2 mg/dL, an alanine aminotransferase level of 363 mg/dL, an aspartate aminotransferase level of 359 mg/dL, and a serum creatinine level of 1.8 mg/dL. Chest radiography disclosed a right hilar mass and a small amount of pleural effusion. Chemotherapy with cisplatin (70 mg once per day) and etoposide (100 mg once per day) was initiated. Chest tightness developed on the second day after treatment initiation. Electrocardiography revealed inverted T waves over the precordial leads (V4 to V6), elevated creatine kinase levels (579 U/L; reference range, 38–160 U/L), and an elevated creatine kinase-muscle-brain fraction (186.5 U/L; reference range, <16 U/L). A diagnosis of non-ST-segment elevation myocardial infarction was made, and the patient was transferred to the intensive care unit for further treatment. Ten hours later, a high spiking fever (temperature, 40°C) and loss of consciousness occurred. Profound shock with systolic blood pressure of 80 mm Hg also developed (baseline systolic blood pressure was <160 mm Hg), and the inotropic agents norepinephrine and dopamine were administered. Piperacillin-tazobactam (3000 mg of piperacillin plus 375 mg of tazobactam every 6 h) was administered empirically. Persistent high spiking fever, leukopenia (white blood cell count, 880 cells/µL), anuria, and adult respiratory distress syndrome developed rapidly. Rapid deterioration of liver function (alanine aminotransferase level, 5727 mg/dL; aspartate aminotransferase level, 25,615 mg/dL) and renal function (blood urea nitrogen level, 90.9 mg/mL; serum creatinine level, 3.9 mg/dL) were also noted. Shock and adult respiratory distress syndrome progressed, and the patient died 26 h after the first episode of spiking fever. The patient's fibrinogen level was 322.3 mg/dL (reference range, 163.5–362.7 mg/dL), his fibrinogen degradation production level was 10 µg/mL (reference level, <4.1 µg/mL), and his D-dimer level was 2.4 µg/mL (reference level, <2.09 µg/dL), indicating the possible presence of disseminated intravascular coagulopathy. No gastrointestinal symptoms, such as diarrhea, nausea, vomiting, or abdominal pain, were noted before or after the febrile episode. Two sets of blood cultures (Bactec 9240; Becton Dickinson) both yielded S. sonnei growth on the day after the patient's death. The isolate was identified to the species level with use of conventional biochemical methods, serogrouping, and 3 commercial identification systems: the Vitek Gram Negative Identification Card (identity probability, 99%), the API 20E (identity, 99%; T value, 0.92; bioMérieux), and the Phoenix System (confidence value, 99%; NMIC/ID-4; Becton Dickinson). The isolate was susceptible to ampicillin (minimum inhibitory concentration [MIC], ⩽4 µg/mL), ciprofloxacin (MIC, ⩽0.5 µg/mL), piperacillin-tazobactam (MICs, ⩽4 and ⩽4 µg/mL), and cefotaxime (MIC, ⩽1 µg/mL) but resistant to trimethoprim-sulfamethoxazole, as determined by the Phoenix System. Stool cultures were not performed because of a lack of diarrhea during hospitalization. Shigella species often cause diarrhea or gastrointestinal inflammation in humans and are rarely associated with bacteremia [1, 2]. Children are more susceptible than adults, and the most common causative organism is Shigella flexneri [1, 2]. Among the 9 reported cases of S. sonnei bacteremia [1, 3–10], all patients had preceding diarrhea (88.9%) or abdominal pain (11.1%). In contrast, our patient did not present with any symptom or sign that suggested preceding gastrointestinal infection. Two of the 9 reported patients with S. sonnei bacteremia died, but neither of these deaths was directly associated with sepsis due to Shigella species. Our patient died during the bacteremic stage of S. sonnei infection because of complications of sepsis and multiorgan failure, despite receiving piperacillin-tazobactam, which has been shown to have good in vitro activity against S. sonnei. The patient's poor underlying condition (lung cancer and myocardial infarction) probably contributed to the rapidly fatal outcome. In summary, we report a rapidly fatal case of S. sonnei bacteremia without any associated gastrointestinal symptoms. In immunocompromised hosts, S. sonnei should be included in the list of etiologies associated with severe sepsis and disastrous complications, even in the absence of preceding gastrointestinal diseases. Potential conflicts of interest. All authors: no conflicts.