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. Author manuscript; available in PMC: 2021 Jun 1.
Published in final edited form as: Clin Res Hepatol Gastroenterol. 2019 Oct 10;44(3):e59–e60. doi: 10.1016/j.clinre.2019.09.001

Pyogenic liver abscesses from Fusobacterium nucleatum in an immunocompetent host

Kanupriya Soni a, Zachary Fricker b, Michelle Theresa Long b,*
PMCID: PMC7145721  NIHMSID: NIHMS1060672  PMID: 31607642

A previously healthy 43-year-old man was admitted with sepsis and acute, severe right upper quadrant (RUQ) pain. The pain was pleuritic and alleviated when supine. Two weeks prior he had a fever (101F), myalgia, and malaise. Six days prior to the onset of symptoms, he participated in a 10-mile endurance event with military-style obstacles on converted farm land, during which he unintentionally ingested muddy water. He also had small abrasions on his knees at the time.

Physical exam was notable for low-grade fever (99.1F), tachycardia (118 bpm), and moderate RUQ tenderness. Laboratory studies were notable for neutrophilic leukocytosis (18.3K/uL with 85% neutrophils), elevated alkaline phosphatase (185U/L) and INR (1.39) with normal serum aminotransferases and bilirubin. Abdominal ultrasound and computed tomography scan identified greater than 10 hypoattenuating hepatic lesions with thickened walls and peripheral enhancement. The largest lesion measured 8 × 4 × 6 cm. Mild splenomegaly and portal vein dilation were also present.

The main differential diagnosis of multiple hepatic lesions includes malignancy (primary hepatic and metastatic), benign lesions (e.g., hemangioma, adenoma), and infection [1]. Common pathogens include anaerobic, Gram negative (e.g., Escherchia coli, Klebsiella penumonia), and Gram positive organisms (e.g., Staphlococcal and Streptococcal species) [2]. Other etiologies include fungi (e.g., Histoplasma, Aspergillus, Candida) and parasites (e.g., Entamoeba histolytica, Echinococcal species) [3]. Pyogenic liver abscesses may be secondary to biliary disease, trauma, or spread hematogenously via the portal or hepatic veins [4]. Here, evaluation included HIV Ag/Ab, Histoplasma urine-antigen, Echinococcus-Ab, Entamoeba Histolytica IgG-Ab, Leptospira-Ab, as well as bacterial and fungal blood culture and stool ova and parasite exam. All of the above tests were negative.

Aspiration of hepatic abscesses yielded approximately 200 cc of thick, purulent fluid and culture grew Fusobacterium nucleatum. The patient received intravenous penicillin for six weeks with resolution of symptoms and normalization of laboratory values. Dental evaluation and colonoscopy performed to assess for a source of infection were unremarkable. Subsequent MRI showed resolution of the liver abscesses, splenomegaly, and portal and splenic vein dilation suggesting resolving portal hypertension secondary to mass effect from abscesses.

Fusobacterium nucleatum is an anaerobic Gram-negative bacillus associated with a variety of infections such as Lemierre’s Syndrome. Risk factors for pyogenic liver abscess include diabetes mellitus or other immunocompromised such as malignancy, and dental manipulation [1,5]. Severe complications are possible, with reported 5% in-hospital mortality [2].The incidence of Fusobacterium-related infection is 3.6 per 100,000 people [2]. It is a common cause of liver abscess in feedlot cattle due to ruminal acidosis [6]. Limited available data suggest zoonotic infection is possible via animal bites or other contact of bodily fluids with open sores or mucous membranes [7,8]. Fusobacterium may survive in soil up to 18 weeks. [9]. Here, we present a case of multiple pyogenic liver abscesses from Fusobacterium nucleatum in an immunocompetent host without oropharyngeal or colonic pathology. The patient had a potential exposure to the pathogen through swallowing muddy water or through contact of skin breaks with contaminated soil while participating in an endurance event on a manure-contaminated field.

Acknowledgments

Funding

Dr. Long is supported in part by the National Institute of Diabetes and Digestive and Kidney Diseases K23 DK113252, the Boston University School of Medicine Department of Medicine Career Investment Award and the Boston University Clinical Translational Science Institute UL1 TR001430.

Footnotes

Disclosure of interest

The authors declare that they have no competing interest.

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