Case Presentation: The patient is a 31 year old male with a medical history of HIV on antiretroviral therapy who was seen in the emergency department for chest pain and dyspnea, then discharged after a negative cardiac workup. He re-presented two days later with worsening chest tightness, dyspnea, and vomiting. On examination, the patient was tachycardic with an audible friction rub. Workup revealed white blood cell count of 18,500 cells/mm3, HIV viral load 77 copies, absolute CD4 count 77, and diffuse ST elevation on electrocardiogram. He was admitted for presumed viral pericarditis and started on fluids and corticosteroids. Transthoracic echocardiogram was notable for a left ventricular ejection fraction of 45% and a moderate sized pericardial effusion measuring 2.32 centimeters without tamponade. Blood cultures identified Neisseria meningitidis, prompting pericardiocentesis with evacuation of 335 milliliters of fluid. A pericardial drain was placed via fluoroscopic guidance with rapid symptomatic improvement. Pericardial fluid studies were consistent with gross purulence, and cultures identified the same organism. Lumbar puncture was not suggestive of meningitis, and cerebrospinal fluid cultures had no growth. Repeat echocardiogram demonstrated improvement of his effusion and he was discharged with 4 weeks of intravenous ceftriaxone. At outpatient follow-up he was asymptomatic.
Discussion: Purulent pericarditis is a complication of bacterial pericarditis with a mortality rate of 40% even in those who are treated, often with post-mortem diagnosis (1). Neisseria meningitidis is a less common causative organism of purulent pericarditis and is typically early sequelae at the onset of meningococcemia or meningitis (2-3). Meningococcal pericarditis is classified as disseminated disease with pericarditis, reactive pericarditis, or primary pericarditis (PMP) in the absence of meningeal invasion or disseminated disease (4). PMP is rare and typically progresses rapidly into tamponade (3, 4). As PMP occurs in the absence of meningitis, the diagnosis is elusive. This can lead to delays in treatment and inappropriate initial treatment as high doses of ceftriaxone or benzylpenicillin are required for bactericidal activity, which is not included in the typical therapy for pericarditis. Though pericardial disease is one of the most common cardiac complications of HIV (5), PMP in an HIV positive patient is not reported in the literature. In this case an HIV-positive male presented with PMP without signs of invasive meningococcal disease. Interestingly, this patient did not have tamponade or hemodynamic collapse that is typical for PMP (3). The patient’s immunocompromised HIV status and thus inability to mount an appropriate immune response could have contributed to his milder presentation. Our case also highlights the value of blood cultures to aid in the diagnosis of a pericardial effusion, as well as pericardiocentesis as both a diagnostic and therapeutic intervention in the setting of an invasive pyogenic pathogen. It is important to consider PMP in individuals at risk for N. meningitidis including students, military recruits, unvaccinated, and immunocompromised patients.
Conclusions: Primary meningococcal pericarditis is an uncommon presentation of Neisseria meningitidis and is a diagnostic challenge due to nonspecific symptoms. Though it typically presents with tamponade and hemodynamic compromise, it may present differently in those who are immunocompromised as seen in this case.