P1.027: Possible contribution of Mycoplasma pneumoniae infection to a brain abscess caused by Fusobacterium necrophorum

Introduction: The number of reported cases of Lemierre syndrome, commonly caused by Fusobacterium necrophorum, has been increasing over the past several decades. Besides, there were a few reports of infections with Mycoplasma pneumoniae in the setting of Lemierre syndrome. We report a case of a brain abscess caused by Fusobacterium necrophorum, in which Mycoplasma pneumoniae and Paenibacillus barengoltzii were also identified.

Case Description: An adolescent male presented to the emergency department for fevers, seizures, and altered mental status. He had symptoms of sinusitis for the last previous weeks and was prescribed a course of amoxicillin/clavulanate. A brain computed tomography scan was performed revealing a 3.3 cm right frontal lobe abscess with surrounding vasogenic edema. He was intubated and admitted to the pediatric intensive care unit and was given appropriate antibiotics. A stereotactic bifrontal craniotomy with irrigation was performed by neurosurgery to drain the abscess. Respiratory infectious disease PCR (Polymerase Chain Reaction) panel identified Mycoplasma pneumoniae. Abscess fluid culture revealed Fusobacterium necrophorum and later grew Paenibacillus barengoltzii. The patient did not have any residual neurological deficits but has been admitted to the hospital twice for seizure-like activity over the six months after his discharge.

Discussion: A literature review was performed. There were four reported cases of Lemierre syndrome due to Fusobacterium necrophorum in which Mycoplasma pneumoniae was identified. Moreover, Mycoplasma pneumoniae was found to be the cause of a cerebellopontine angle abscess in a single reported case, as evidenced by a positive 16S ribosomal DNA (Deoxyribonucleic Acid) PCR in the abscess fluid. In a quality assessment involving 10 cases with limb defects and burn wounds, Mycoplasma spp. and Mycoplasma salivarium were isolated by molecular methods in one patient. There were no reported cases involving Paenibacillus barengoltzii in association with brain abscesses in humans and/or in association with Mycoplasma pneumoniae or Fusobacterium necrophorum infections. It is unclear whether the presence of Mycoplasma pneumoniae in our case and the above cases is a result of coinfection with Fusobacterium necrophorum or a mere coincidence of both infections occurring simultaneously. However, the increasing reports of the above may hint to possible coinfection and/or superinfection relationships of those two bacteria. The growth of Paenibacillus barengoltzii in our case is important to note but is of unknown significance at this time.

Conclusion: Considering the increasing number of reports of Mycoplasma pneumoniae infections/colonizations in the setting of Lemierre Syndrome, further research may be needed to elucidate the reality of this relationship between these two bacteria. While the significance of this finding is uncertain, the growth of Paenibacillus barengoltzii from the brain abscess culture in our case is a previously unreported finding.