Case report

A 32-year-old previously healthy male presented with a 5-day history of progressive fatigue, myalgia, anorexia, headache, and intermittent high fevers, followed by nausea and a retrosternal burning sensation. He denied upper respiratory symptoms, sore throat, cough, diarrhea, or abdominal pain. He specifically denied anorectal pain, tenesmus, rectal discharge, or rectal bleeding, and digital rectal examination and perianal inspection were unremarkable. He had no relevant medical history and no regular medications. He is a man who has sex with men (MSM), recorded as a potentially relevant epidemiologic factor; he had no recent travel, animal exposures, or wilderness activities. HIV, hepatitis A, B, and C serologies, and syphilis testing (RPR) were negative or nonreactive. Atypical pathogen serologies obtained during the fever work-up (Mycoplasma pneumoniae IgM, cytomegalovirus IgM, and Epstein–Barr virus viral capsid antigen IgM) were also negative; Chlamydia pneumoniae IgG was mildly elevated (13.83; reference < 9.0) with a negative IgM, a pattern consistent with prior rather than acute infection.

On arrival, he was critically ill: temperature 39.5°C, blood pressure 81/44 mmHg, heart rate 113 bpm. Laboratory findings revealed an elevated C-reactive protein (21.25 mg/dL [212.5 mg/L]), elevated lactate (23.5 mg/dL [2.6 mmol/L]), leukocytosis (11.2 × 103/μL [11.2 × 109/L]) with 91% neutrophils, and severe thrombocytopenia (platelets 14 × 103/μL [14 × 109/L]). Coagulation studies showed markedly elevated D-dimer (4825 ng/mL FEU [4.83 mg/L FEU]), elevated fibrinogen (682 mg/dL [6.82 g/L]), and a positive lupus anticoagulant (dilute Russell's viper venom time [dRVVT] normalized ratio 1.29; reference < 1.21). Hepatic dysfunction was evidenced by hyperbilirubinemia (total bilirubin 6.44 mg/dL [110.1 μmol/L]; direct 4.98 mg/dL [85.2 μmol/L]), with mildly elevated aminotransferases (AST 48 U/L; ALT 75 U/L) and a normal alkaline phosphatase (109 U/L). Additional findings included hyperglycemia (glucose 124 mg/dL [6.9 mmol/L]), mildly elevated creatinine (1.19 mg/dL [105.2 μmol/L]) with a blood urea nitrogen of 10 mg/dL [3.6 mmol/L urea], hyponatremia (sodium 128 mmol/L), and hypokalemia (potassium 3.1 mmol/L).

Chest radiograph demonstrated bilateral basal infiltrates and opacities (Fig. 1). Contrast-enhanced CT of the chest, abdomen, and pelvis identified a 1.5-cm hypodense hepatic dome collection consistent with pyogenic liver abscess with regional hepatic vein thrombophlebitis and bilateral multifocal peripheral wedge-shaped pulmonary nodules consistent with septic emboli (Fig. 2). The hepatic vein finding was characterized by wall thickening and enhancement with internal low density consistent with infected thrombus, without imaging features of bland thrombosis such as an extensive thrombus burden, venous obstruction, or a hepatic perfusion abnormality (Fig. 3). Importantly, the same study demonstrated a patent portal and superior mesenteric venous system without intraluminal thrombus, periportal inflammatory change, or gas, and no rectal, sigmoid, or colonic wall thickening, pericolic fat stranding, perirectal fluid, or intra-abdominal or pelvic collection. Echocardiography revealed right ventricular volume overload, mild pulmonary hypertension, and an engorged inferior vena cava without valvular vegetations. Otolaryngologic evaluation, including bedside pharyngolaryngoscopy, excluded an oropharyngeal or deep neck source, and no F. necrophorum was identified from a pharyngeal source, effectively excluding classic Lemierre's syndrome; dedicated imaging of the internal jugular veins was not performed, and the venous findings in this case were characterized on abdominal CT alone.

Figure 1: Chest radiograph demonstrating bilateral basal infiltrates and opacities corresponding to the septic pulmonary emboli demonstrated on chest CT (Fig. 2A).

Figure 2: Axial chest and abdominal CT: (A) multiple bilateral peripheral wedge-shaped pulmonary nodules, a pattern characteristic of septic emboli; (B) small right pleural effusion; (C) ring-enhancing hypodense lesion in hepatic segment 8 (S8) dome, consistent with a pyogenic abscess.

Figure 3: Coronal abdominal CT demonstrating the hepatic S8 dome abscess (arrowhead) with adjacent hepatic vein thrombophlebitis (arrow), identified by wall thickening and enhancement of the hepatic vein with internal low density, findings supporting infected (septic) thrombus rather than bland thrombosis, which would instead show an extensive thrombus burden, venous obstruction, or a hepatic perfusion abnormality, none of which were present on this study.

Empiric intravenous meropenem and doxycycline were initiated on admission for broad-spectrum coverage of mixed aerobic and anaerobic pathogens. Two blood culture bottles (aerobic and anaerobic) were collected in the emergency department; the anaerobic bottle grew a gram-negative bacillus after approximately 24 hours, subsequently identified as F. necrophorum. Susceptibility testing showed the isolate was sensitive to clindamycin, cefmetazole, metronidazole, penicillin, ampicillin/sulbactam, piperacillin/tazobactam, meropenem, and doxycycline. Bone marrow biopsy was performed given the severity of thrombocytopenia to exclude a primary hematologic process; it demonstrated reactive myeloid hyperplasia, consistent with a consumptive peripheral etiology rather than primary marrow pathology. On day 5, once the organism and its pan-susceptible profile were confirmed, therapy was de-escalated from meropenem and doxycycline to piperacillin/tazobactam and metronidazole. Percutaneous drainage was deferred given the small lesion size and rapid clinical response. Platelets rose from 14 × 103/μL on admission to 95 × 103/μL by day 5 and normalized at 393 × 103/μL by discharge. Inflammatory markers and bilirubin resolved in parallel. Follow-up ultrasound on day 7 confirmed complete hepatic lesion resolution, and the patient was discharged on day 12 on oral metronidazole 250 mg four times daily for 7 days and moxifloxacin 400 mg once daily for 14 days. Because contrast-enhanced abdominal and pelvic imaging had already excluded bowel or rectal wall thickening and an intra-abdominal or pelvic abscess, and the patient had no abdominal or anorectal symptoms, melena, or hematochezia, endoscopic evaluation was not pursued. At two-week infectious disease follow-up, there were no new events; a right lower lung lesion tracked on serial chest radiographs had subsided, and follow-up abdominal imaging confirmed a resolved liver abscess with stable hepatic vein thrombophlebitis and no new emboli. The patient had a full recovery with no complications or sequelae at this follow-up point.