A case of Fusobacterium necrophorum sepsis (Lemierre's syndrome) with pulmonary septic emboli and liver abscess

Lemierre’s syndrome is an uncommon and potentially fatal complication of oropharyngeal and facial infections. It involves an associated septic thrombophlebitis, bacteremia, and septic emboli. Traditionally, compromise of the internal jugular vein has been described in conjunction with an infection caused by anaerobes, especially, Fusobacterium necrophorum. In recent years, however, variant forms have been appearing, including other vessel compromise and other etiologic agents. We present the case of Lemierre’s syndrome in a 31-year-old male with facial vein thrombosis, septic emboli to the lungs, and bacteremia caused by methicillin-resistant Staphylococcus aureus. We hope that this case will raise awareness about variant presentations and promote a timely diagnosis and appropriate treatment of this potentially fatal infection.

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Fusobacterium necrophorum subsp. necrophorum Liver Abscess with Pylephlebitis: An Abdominal Variant of Lemierre’s Syndrome

Case Reports in Infectious Diseases ◽

10.1155/2020/9237267 ◽

2020 ◽

Vol 2020 ◽

pp. 1-6

Author(s):

Natasa Radovanovic ◽

Igor Dumic ◽

Mladjen Veselinovic ◽

Susanne Burger ◽

Tamara Milovanovic ◽

...

Keyword(s):

Portal Vein ◽

Liver Abscess ◽

Treatment Strategy ◽

Clinical Presentation ◽

Fusobacterium Necrophorum ◽

Significant Morbidity ◽

Lemierre’S Syndrome ◽

Vein Thrombosis ◽

Source Of Infection ◽

Lemierre's Syndrome

Liver abscess associated with suppurative portal vein thrombosis (pylephlebitis) secondary to Fusobacterium necrophorum has been rarely reported. It is considered to be an abdominal variant of Lemierre’s syndrome associated with significant morbidity and mortality. We report a case of 69-year-old man who developed liver abscess and pylephlebitis due to F. necrophorum with an unclear source of infection. We discuss the pathogenesis, diagnosis, and treatment strategy for this entity, with a review of previously published cases of pyelephlebitis due to F. necrophorum in regard to their clinical presentation and outcome.

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Lemierre’s syndrome as a consequence of acute supraglottitis

The Journal of Laryngology & Otology ◽

10.1258/0022215021910375 ◽

2002 ◽

Vol 116 (3) ◽

pp. 216-218 ◽

Cited By ~ 5

Author(s):

Andrew Hope ◽

Nigel Bleach ◽

Sabour Ghiacy

Keyword(s):

Computed Tomography ◽

Jugular Vein ◽

Fusobacterium Necrophorum ◽

Lemierre’S Syndrome ◽

Jugular Vein Thrombosis ◽

Vein Thrombosis ◽

Intravenous Antibiotics ◽

Intracranial Thrombosis ◽

Internal Jugular Vein Thrombosis ◽

Lemierre's Syndrome

Lemierre’s syndrome comprises internal jugular vein thrombosis following oropharyngeal sepsis and is a rare and serious condition. It is most commonly caused by the anaerobe Fusobacterium necrophorum and typically presents as metastatic sepsis to the lungs and joints. Thrombosis is demonstrated by computed tomography (CT) of the neck, and it is routinely treated with intravenous antibiotics and anti-coagulation.We describe a case of Lemierre’s syndrome following acute supraglottitis. The clinical features were of retrograde intracranial thrombosis, rather than the more usual metastatic sepsis.

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The Forgotten Disease: A Case of Lemierre’s Syndrome with Distal Extremity Involvement

Case Reports in Infectious Diseases ◽

10.1155/2020/4346937 ◽

2020 ◽

Vol 2020 ◽

pp. 1-4

Author(s):

John Gaskill ◽

Michael Aronson

Keyword(s):

Care Center ◽

Tertiary Care ◽

Rare Condition ◽

Fusobacterium Necrophorum ◽

Lemierre’S Syndrome ◽

Intravenous Antibiotics ◽

Adjacent Structures ◽

Oropharyngeal Infection ◽

Fluid Collections ◽

Lemierre's Syndrome

Once coined the “Forgotten Disease,” Lemierre’s syndrome is a rare condition that results from oropharyngeal infection with the gram-negative, anaerobic Fusobacterium necrophorum. The typical progression of illness involves spread to adjacent structures such as the internal jugular vein with resulting thrombophlebitis. Septic emboli to distant sites are also a common sequela. Here, we present a case of Lemierre’s syndrome in a 20-year-old, otherwise healthy, male. The patient presented with fever, sore throat, and dysphagia. Imaging revealed peritonsillar multiloculated fluid collections and necrotizing pneumonia with multiple pulmonary abscesses. The patient’s hospital course was complicated by the development of necrotizing fasciitis in his right lower leg, which required incision and drainage with surgical washout. In addition to systemic intravenous antibiotics and anticoagulation, he underwent multiple thoracentesis procedures. The patient was ultimately transferred to a tertiary care center due to persistent fevers and lung abscesses. This case highlights the challenges of initial diagnosis, as well as the treatment choices faced by the attending physicians.

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719A Rare Variant of Lemierre's Syndrome – Fusobacterium necrophorum Sepsis from Gynecological Origin

Open Forum Infectious Diseases ◽

10.1093/ofid/ofu052.427 ◽

2014 ◽

Vol 1 (suppl_1) ◽

pp. S203-S203

Author(s):

Shivani Garg ◽

Jorge Mora ◽

Glenn Eiger

Keyword(s):

Rare Variant ◽

Fusobacterium Necrophorum ◽

Lemierre’S Syndrome ◽

Lemierre's Syndrome

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Human Infection withFusobacterium necrophorumwithout Jugular Venous Thrombosis: A Varied Presentation of Lemierre’s Syndrome

Case Reports in Infectious Diseases ◽

10.1155/2017/5358095 ◽

2017 ◽

Vol 2017 ◽

pp. 1-3

Author(s):

Muhammad Asim Rana ◽

Yashwant Kumar ◽

Abdullah Ali Lashari ◽

Ahmed F. Mady

Keyword(s):

Nerve Palsy ◽

Jugular Vein ◽

Kidney Injury ◽

Severe Pneumonia ◽

Fusobacterium Necrophorum ◽

Human Infection ◽

Upper Respiratory Tract ◽

Lemierre’S Syndrome ◽

Upper Respiratory ◽

Lemierre's Syndrome

Lemierre’s syndrome is also known as postangina septicemia, which is commonly caused byFusobacterium necrophorumalso known as Necrobacillus and also by other microorganisms likeStaphylococcus,Streptococcus,Peptostreptococcus, andBacteroides. Though the disease starts as an upper respiratory tract infection, it may spread and cause thrombophlebitis of the internal jugular vein. It may present itself through cranial nerve palsy or sepsis involving distant organs like the lungs or bones. It is also known as forgotten disease because of its rarity.Fusobacterium necrophorumusually causes infection in animals and rarely affects humans. We hereby present a case of Necrobacillus infection which did not cause any thrombophlebitis but resulted in severe pneumonia and acute kidney injury, leading to respiratory failure and requiring mechanical ventilation.

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Activation of the Contact System at the Surface of Fusobacterium necrophorum Represents a Possible Virulence Mechanism in Lemièrre's Syndrome

Infection and Immunity ◽

10.1128/iai.05264-11 ◽

2011 ◽

Vol 79 (8) ◽

pp. 3284-3290 ◽

Cited By ~ 19

Author(s):

Karin Holm ◽

Inga-Maria Frick ◽

Lars Björck ◽

Magnus Rasmussen

Keyword(s):

Specific Interaction ◽

Fusobacterium Necrophorum ◽

Pulmonary Involvement ◽

Surface Proteins ◽

Contact System ◽

Central Component ◽

Contact Activation ◽

Lemierre’S Syndrome ◽

Content Type ◽

Lemierre's Syndrome

ABSTRACTFusobacterium necrophorumcauses Lemièrre's syndrome, a serious disease with septic thrombophlebitis of the internal jugular vein, pulmonary involvement, and systemic inflammation. The contact system is a link between inflammation and coagulation, and contact activation by the bacteria could therefore contribute to the abnormal coagulation and inflammation seen in patients with Lemièrre's syndrome. In this study,F. necrophorumwas found to bind radiolabeled high-molecular-weight kininogen (HK), a central component of the contact system. Binding was inhibited by the addition of unlabeled HK and domain D5 of HK but not other components of the contact system, indicating a specific interaction mediated through the D5 region. Binding of HK was significantly reduced after pretreatment of the bacteria with trypsin, suggesting that surface proteins are involved in HK binding. Incubation of the bacteria with human plasma resulted in an HK breakdown pattern suggestive of bradykinin release, and bradykinin was also detected in the supernatant. In addition, we show that factor XI (FXI), another component of the contact system, binds toF. necrophorumand that the bound FXI reconstitutes the activated partial thromboplastin time of FXI-deficient plasma. Thrombin activity was detected at the surface of the bacteria following incubation with plasma, indicating that the intrinsic pathway of coagulation is activated at the surface. This activity was completely blocked by inhibitors of the contact system. The combined results show that the contact system is activated at the surface ofF. necrophorum, suggesting a pathogenic role for this system in Lemièrre's syndrome.

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Lemierre’s Syndrome: A Neglected Disease with Classical Features

Case Reports in Medicine ◽

10.1155/2015/846715 ◽

2015 ◽

Vol 2015 ◽

pp. 1-4 ◽

Cited By ~ 2

Author(s):

Andreas V. Hadjinicolaou ◽

Yiannis Philippou

Keyword(s):

Jugular Vein ◽

Fusobacterium Necrophorum ◽

Blood Cultures ◽

Inotropic Support ◽

Lemierre’S Syndrome ◽

Jugular Vein Thrombosis ◽

Intensive Care Admission ◽

Vein Thrombosis ◽

History Of ◽

Lemierre's Syndrome

We report the case of a previously healthy, immunocompetent 23-year-old male who presented to the Emergency Department with general malaise, difficulty in breathing, fever, and chest pain. He reported a two-week history of progressively worsening sore throat that he presumed to be a viral infection and thus initially neglected. However, when his condition deteriorated, he was admitted to hospital acutely unwell and in respiratory distress. He quickly developed septic shock requiring intensive care admission for inotropic support. Ultrasound and CT imaging revealed internal jugular vein thrombosis with associated septic emboli reaching the lungs to form bilateral cavitations and consequently pleural effusions. Blood cultures were positive forFusobacterium necrophorum. Based on these findings, a diagnosis of Lemierre’s syndrome was made. The patient was treated with appropriate antibiotics and anticoagulation and gradually recovered. He was discharged 20 days after admission with advice to complete a six-week course of antibiotics.

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