Fusobacterium necrophorum causes a range of mild to life threatening infections and there is uncertainty in terms of diagnosis and treatment due to the lack of knowledge on their pathogenic mechanisms. This study characterised genomes of F. necrophorum to compare their virulence factors and investigate potential infection markers. 27 isolates of F. necrophorum from patients with pharyngotonsillitis were subjected to whole genome sequencing and compared with 42 genomes published in the NCBI database. Phylogenomics, pangemome, pan-GWAS and virulome were analysed to study strain variations with reference to virulence factors. Core genome based phylogenomic tree exhibited three clades of which Clade A belonged to F. necrophorum subsp necrophorum, clades B and C were F. necrophorum subsp funduliforme. Pan-GWAS and Pan-Virulome suggest some marker genes associated with clinical sources of isolation that needs further validation. Our study highlights some interesting features of the pathogenesis of F. necrophorum infections. Although the animal isolate genomes had some marker genes, the genomes of human isolates did not exhibit clear correlation to their clinical sources of isolation. This prompts to think of other mechanisms such as co-infections or host factors that can be involved in the pathogenesis.

UNASSIGNED: Lemierre\'s syndrome is typically caused by Fusobacterium necrophorum where an oropharyngeal infection is followed by septic internal jugular vein thrombophlebitis with subsequent septic embolization. Yet, the pathogenesis of septic thrombophlebitis, differences dependent on the presence of jugular vein thrombosis, and the role of anticoagulant therapy are insufficiently understood.
UNASSIGNED: Patients with invasive infection with F. necrophorum and Lemierre\'s syndrome who had been investigated for jugular vein thrombosis were included from a previous population-based observational study in Sweden. Medical records were reviewed and compared in patients with and without jugular vein thrombosis. Then, patients with jugular vein thrombosis were compared by exposure to therapeutic, prophylactic, or no anticoagulation. Outcomes examined were thrombosis progression, early or late peripheral septic complications, chronic major sequelae, 30-day mortality, and major bleeding.
UNASSIGNED: Fifty-one of 82 (62%) radiologically investigated patients with Lemierre\'s syndrome had jugular vein thrombosis. Patients with jugular vein thrombosis had lower platelet levels (median, 76 vs 112 ×109/L; P = .04) on presentation and more days to defervesence (12 vs 7 days; P = .03) yet similar rates of major sequelae and 30-day mortality. No significant differences in outcomes were seen between patients with jugular vein thrombosis exposed to therapeutic, prophylactic, or no anticoagulation therapy, yet study outcomes were rare.
UNASSIGNED: Patients with Lemierre\'s syndrome with jugular vein thrombosis were more severely affected, yet had similar prognosis. Most patients with jugular vein thrombosis recovered well without therapeutic anticoagulation therapy, though adverse events were similarly rare in anticoagulated patients. The observational design and rarity of study outcomes require cautious interpretation.

OBJECTIVE: Lemierre\'s syndrome (LS) is a rare condition that typically starts with a bacterial oropharyngeal infection complicated by a thrombophlebitis of the internal jugular vein and septic emboli to the lungs or other organs. The most common organism isolated is Fusobacterium necrophorum, although other causative organisms are isolated in rare cases.
METHODS: We discuss a case of LS in a 44-year-old, previously healthy man presenting with an oropharyngeal infection. F. necrophorum was isolated from blood cultures and Computed tomography of the chest demonstrated septic emboli in the lungs. Magnetic resonance imaging showed a thrombophlebitis of the sigmoid and transverse vein with continuity to the internal jugular vein.
METHODS: Case report and literature review.
RESULTS: F. necrophorum isolates show in vitro susceptibility to metronidazole, clindamycin, beta-lactam/beta-lactamase inhibitor combinations and carbapenems with no signs of resistance or reduced sensitivity. Anticoagulation is believed to play a favourable role in recovery of the disease because of the potential for faster resolution of thrombophlebitis and bacteraemia. Conflicting results exist in literature with many studies or reviews indicating a favourable outcome both with and without anticoagulation. Anticoagulation for LS consists in most cases of Warfarin or Low molecular weight heparins, with the last being the first choice in children. Indications for the use of anticoagulation in literature are significant clot burden, complication of septic emboli, arterial ischemic stroke, poor response to antibiotics, thrombophilia and cerebral infarction.
CONCLUSIONS: Antibiotics are considered the mainstay of treatment, although statistically valid trials to evaluate optimal treatment regimens have not yet been conducted due to the low incidence of the infection. The use of anticoagulation in LS is still heavily debated as a result of conflicting results in literature. Due to the disease\'s low incidence, statistically valid trials that evaluate anticoagulation are lacking. Further prospective and randomized research is needed to establish the benefit of anticoagulation in the treatment of LS.