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论文范文
1. Introduction R. typhi, previously known as R. mooseri, belongs to the typhus group of rickettsiae (together with R. prowazekii which causes epidemic typhus) [1–3]. The main vector is the rat flea Xenopsylla cheopis, although other arthropods, such as the cat flea Ctenocephalides felis, have been implicated in the life cycle of R. typhi [1–3]. Humans are considered accidental hosts, primarily contaminated by inoculation of the rickettsiae through a fleabite site on their skin [2, 3]. Although history of a fleabite is not usually recalled, humans are typically infected in areas where close contact with animals and their fleas are most likely to occur [4]. Murine typhus is an endemic infection in tropical and subtropical seaboard regions throughout the world, including the Mediterranean [2]. In Greece, the disease was first described in 1932 [5]. Since then, endemic cases have been reported on the Greek islands of Euboea and Crete [5]. Here, we present a case of severe murine typhus presenting as acalculous cholecystitis in an otherwise healthy man. 2. Case Presentation A 54-year-old Caucasian male was referred from Kasos island to the infectious diseases unit of our hospital with a 10-day history of fever, throbbing frontal headache, chills, and malaise. The patient was already receiving amoxicillin-clavulanate for suspected sinusitis, without apparent improvement. He lived in a rural area, worked as a cafeteria owner, and had frequent contact with animals (pigs and chicken) and bees. His past medical history was significant only for heterozygous β-thalassemia. Upon presentation, the patient appeared ill, with a temperature of 38°C, resting blood pressure 110/55 mmHg, heart rate 85 beats per minute, respiratory rate 18 breaths per minute, and oxygen saturation 93% on room air. Auscultation revealed mildly prolonged expiration with no additional sounds, while mild right upper quadrant (RUQ) tenderness was noted. A rash was difficult to detect due to his dark complexion. The remainder of the examination was normal. There was evidence of lymphopenia (1 × 109/L, reference range [RR] 1.5–3.6 × 109/L), mild anemia (hemoglobin, 12.3 g/dL [RR 14–18 g/dL]; MCV, 62.9 fl [RR 80–99 fl]), and thrombocytopenia (131 × 109/L [RR 150–450 × 109/L]). In the peripheral blood smear, Howell-Jolly bodies were observed. Additional workup revealed mild hyponatremia (130 mEq/L [RR 135–145 mEq/L]), mild elevation of alanine aminotransferase (ALT, 51 U/L [RR 8–40 U/L]), aspartate aminotransferase (AST, 60 U/L [RR 8–40 U/L]), lactate dehydrogenase (LDH, 379 U/L [RR 80–230 U/L]), and a high C-reactive protein (13.2 mg/dL, normal < 0.8 mg/dL). Urine testing showed mild proteinuria, red blood cells (6/HPF), white blood cells (9/HPF), and a bland urine sediment. Arterial blood gas analysis on ambient air showed mild hypoxemia (pH 7.44, PaO2 70 mmHg, and PaCO2 33 mmHg), but no abnormalities were apparent on chest X-ray. The patient was placed off the antibiotics that he was taking, blood and urine cultures were drawn, and serology was obtained for viral infections (HIV, hepatitis B and C viruses, CMV, and EBV) and zoonoses (Brucella spp., Rickettsia spp., Coxiella burnetii, Leishmania spp., and leptospirosis) because of his epidemiological history. On the second day of hospitalization, while still febrile, the patient developed acute RUQ pain, with elevation of liver enzymes (ALT 61 U/L; AST 89 U/L; LDH 535 U/L). Abdominal ultrasound revealed thickened gallbladder wall with a layered appearance and mild pericholecystic fluid (Figure 1), while a positive ultrasonographic Murphy’s sign was induced by the ultrasound probe. Subsequently, the patient was started on ceftriaxone plus metronidazole. On day 3, indirect immunofluorescence (IFA) obtained on admission revealed a high titer for R. typhi (IgM 1 : 800, IgG negative), while the remaining workup was negative, including serology for other rickettsiae. Therefore, doxycycline 100 mg twice per day was added and ceftriaxone with metronidazole was stopped. ![]() |
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