Case Presentation: A healthy 19-year-old female presented to the emergency department with 6 days of progressively worsening fever, chills, body aches, sore throat, and a negative outpatient work-up for COVID, influenza, RSV, strep, and monospot. She appeared in acute respiratory distress, reporting new pleuritic chest pain, trismus, severe right neck pain, and tender lymphadenopathy. Her vital signs revealed hypotension, hypoxia, and tachycardia. Labs showed elevated lactate (2.4 mmol/L), neutrophilic leukocytosis (11,900/uL with 10% bands), thrombocytopenia (34,000/uL), elevated NT-proBNP (1,303 pg/mL), and acute kidney injury. Imaging revealed bilateral multifocal consolidations on CT chest, consistent with septic emboli, and a CT neck showed patent veins without necrotizing infection. CT maxillofacial did not show odontogenic or sinus disease. A transthoracic echocardiogram showed no vegetations but identified a right-to-left shunt. She was started on broad-spectrum antibiotics, received 5 L of IV fluids, and was admitted to the ICU for septic shock and acute hypoxic respiratory failure (pO2 55). Norepinephrine was used for 9 hours, and high-flow nasal cannula for 4 hours. On hospital day 2, blood cultures grew gram-negative bacilli, and infectious disease consultation suggested Fusobacterium necrophorum bacteremia, though repeat Doppler ultrasound showed patent neck veins. By hospital day 4, with increased fever and submandibular swelling, a CT angiogram showed a phlegmon and sub-occlusive thrombus in the right internal jugular vein (IJV). F. necrophorum was confirmed on blood cultures, and the diagnosis of Lemierre’s syndrome was made. Her antibiotic regimen was narrowed to ampicillin-sulbactam. On hospital day 5, an MRI showed intracranial extension of the infection, correlating with decreased right-sided hearing. She was switched to ceftriaxone and metronidazole for improved intracranial penetration, and therapeutic low-molecular-weight heparin was initiated due to an expanding thrombus and her cardiac shunt. On hospital day 8, the patient developed chest pain and dyspnea; CT chest showed left-sided pleural fluid and loculation, consistent with an empyema. A chest tube was placed with minimal drainage, and two doses of tissue plasminogen activator (5 mg) were used to encourage drainage. By hospital day 13, the patient showed significant clinical improvement, with a repeat CT chest showing decreased pleural fluid. The chest tube was removed, and antibiotics were narrowed to metronidazole monotherapy. She was discharged on hospital day 15 with instructions to continue antibiotics and anticoagulation for a 4-week total duration.
Discussion: Lemierre’s syndrome, often caused by F. necrophorum, typically follows an odontogenic infection and presents with sepsis after recent sore throat, IJV thrombosis, and septic emboli to end organs. This patient exhibited pulmonary septic emboli despite a lack of initial IJV thrombosis on imaging, with IJV thrombophlebitis and intracranial extension emerging later in the disease. The patient improved clinically after antibiotics, chest tube placement, and anticoagulation therapy.
Conclusions: Though rare, Lemierre’s syndrome should be suspected in young patients with fulminant sepsis and septic emboli, even in the absence of IJV thrombosis on imaging. Anticoagulation, though not standard for this condition, may be beneficial when there is evidence of an enlarging thrombus with potential intracranial extension.