A rare case of cardiac and ophthalmic manifestations of meningococcal septicemia

Acute pericarditis is usually a self-limiting disorder that commonly occurs due to viral etiology or unexplained causes. Meningococcal pericarditis (MP) is a remarkably uncommon clinical entity that manifests as a complication during the acute or convalescent phase of meningococcal meningitis. However, its occurrence within the context of meningococcal septicemia has also been documented. We report a rare case of a previously healthy male patient who developed both acute pericarditis and uveitis as a presentation of meningococcal septicemia, with no characteristic skin rashes or meningeal signs.

A 45-year-old man with no prior medical history presented to the emergency department reporting a two-day history of sharp, retrosternal chest pain at rest. The pain worsened with deep inspiration and assuming a supine position, but improved when sitting upright. Additionally, he experienced fever (38 °C), sore throat, pronounced fatigue, myalgia, and blurred vision in his right eye. Upon admission, the patient was febrile yet alert, with vital signs within normal limits. Notably, there was an absence of skin rashes and peripheral edema. Examination revealed conjunctival injection and corneal haze in the right eye. Visual acuity was significantly reduced, as he was unable to recognize faces at a distance of one meter (Figure 1A). Heart and lung sounds were unremarkable. His blood pressure was 95/60 mmHg (1 mmHg=0.133 kPa), and heart rate of 110 beats /min, irregular. Respiratory rate was 18 breaths/min, and oxygen saturation (SaO₂) was 95%.

Figure 1.

The clinical manifestations, electrocardiogram, imaging results and sequencing results of our patient. A: a photo of the right eye of the patient depicting a red and hazy cornea (a red arrow); B: electrocardiogram at presentation revealed an atrial fibrillation; C: electrocardiogram recorded by the ambulance two days before admission revealed ST elevation in multiple leads consistent with acute pericarditis; D: transthoracic echocardiography (subcoastal view) demonstrating extensive circumferential pericardial effusion along the lateral and posterior left ventricular walls, and right ventricle with a widest diameter of 1.7 cm (red arrow); E: whole genome sequencing of Neisseria meningitidis showing the serogroup W sequence type 11 (cc11), Nm6 strain.

Electrocardiography (ECG) revealed newly diagnosed atrial fibrillation (Figure 1B). Notably, an ECG obtained two days prior in an ambulatory setting demonstrated ST-segment elevation in multiple leads, suggestive of acute pericarditis (Figure 1C). Laboratory investigations revealed elevated troponin I levels (5.4 ng/mL; reference range: 0–0.35 ng/mL) and a marked systemic inflammatory response (SIR). This included a significantly elevated C-reactive protein (CRP) of 401.68 mg/L, leukocytosis of 12.2×10⁹/L with a neutrophilic predominance (76%), and a markedly elevated procalcitonin (PCT) level of 26.33 ng/mL (reference range: 0.00–0.50 ng/mL). Transthoracic echocardiography (TTE) demonstrated findings consistent with myopericarditis, including a reduced left ventricular ejection fraction (LVEF) of 48% and significant pericardial effusion (echo-free space in the pericardial sac up to 15 mm). Notably, there was no evidence of cardiac tamponade (Figure 1D). Initial management included a daily dose of 1,600 mg ibuprofen. Given the high suspicion for a bacterial etiology based on the pronounced SIR, blood cultures were obtained, and empiric broad-spectrum intravenous (IV) antibiotic therapy was initiated with ceftaroline (1.2 g/d) and moxifloxacin (400 mg/d). Gram stainning of the positive blood cultures revealed Gram-negative diplococci, with subsequent growth observed within 24 h. Bacterial identification using a latex agglutination test detected antigens of Neisseria meningitidis serogroup Y/W 135. This diagnosis of meningococcemia was further confirmed by matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry. Whole genome sequencing performed on the isolated bacteria identified Neisseria meningitidis serogroup W sequence type 11 (cc11), Nm6 strain (Miseq Illumina platform) (Figure 1E). Lumbar puncture revealed normal cerebrospinal fluid (CSF) with no evidence of meningitis. Additionally, computed tomography (CT) scans of the brain and chest, along with magnetic resonance imaging (MRI) of the brain, were unremarkable. Ophthalmological evaluation confirmed infectious uveitis, and endophthalmitis was suspected. Consequently, topical dexamethasone and moxifloxacin eye drops were initiated.

Antibiotic susceptibility testing demonstrated bacterial sensitivity to ceftriaxone and meropenem. Consequently, antibiotic therapy was de-escalated, with ceftaroline being replaced by intravenous ceftriaxone. Considering the localization of the infection within the pericardial cavity, an extended four-week course of antibacterial therapy was administered. This resulted in significant clinical improvement. PCT and leukocyte levels normalized (0.04 ng/mL and 5.3×10⁹/L, respectively). CRP remained mildly elevated at 18 mg/L. Repeated blood cultures were negative. Repeated TTE revealed recovered left ventricular systolic function, with LVEF improving to 62%. No evidence of hypo- or akinetic segments was observed. However, a significant pericardial effusion persisted. The echo-free space measured 1.8 cm along the lateral and posterior left ventricular walls, and 1.3 cm along the right atrium. The effusion contained echogenic fibrinous strands, although there were no signs of cardiac tamponade. Despite high-dose ibuprofen (1,600 mg/d), the pericardial effusion remained. Therefore, anti-inflammatory treatment was augmented with colchicine (0.5 mg twice daily). The patient was discharged with a recommendation for close follow-up.

The incidence of acute pericarditis in individuals with meningococcal infection has yet to be established. Retrospective analyses suggest a pericardial involvement rate of 0.3%–5.1% in patients with meningococcal meningitis, with even a lower rate reported in meningococcemia cases. Finkelstein et al[1] proposed a classification system for MP, differentiating three distinct types: disseminated meningococcal disease with pericarditis (DMP), isolated MP (IMP), and reactive MP (RMP). These types are distinguished by symptom onset timing, pathophysiology, pericardial fluid characteristics, and the potential for tamponade development. DMP manifests early, typically within the first seven days of infection, in patients with overt meningococcal disease. This is attributed to direct bacterial invasion of the pericardium by Neisseria meningitidis.[1] IMP is unique in its early presentation of pericardial fluid accumulation and its high propensity for cardiac tamponade (approximately 75% of cases) during the initial stages of meningococcemia. In contrast, RMP arises much later, often after initiating antibiotic therapy, as an immunological response to the bacteria. IMP is specifically characterized by fluid accumulation in the pericardial sac early in the disease course or meningococcemia leading to cardiac tamponades in approximately 75% of cases.

We report the case of a 45-year-old man who presented with classic symptoms of acute pericarditis. Initially, viral etiology was suspected to be the most common cause of acute pericardial injury. However, persistent symptoms of systemic inflammation with a severe inflammatory response in laboratory tests, including positive PCT, did not fit the initial diagnosis of viral pericarditis and facilitated the identification of another etiology. Detection of Gram-negative diplococci in a blood culture was unexpected, as no signs of meningitis were present. Lumbar puncture was also unremarkable. According to the clinical presentation and disease course in patients with Neisseria meningitidis serogroups W sequence type 11 (cc11), Nm6 strain in blood, the conclusion was made that the patient has IMP. However, pericardiocentesis was not performed for technical reasons, and pericardial effusion was not studied. It is worth noting that patients with Neisseria meningitidis serogroup W135 are likely to have extra meningeal involvemen.[2] Given that the patient complained of a sore throat and had no evidence of pneumonia on lung CT, we assumed that the entry route for meningococcemia (Neisseria meningitidis) was nasopharyngeal mucosa.

IMP is also responsive to antibiotics. The prognosis is generally good if antibacterial therapy is initiated early. In our patient, antibacterial treatment with ceftaroline and moxifloxacin was initiated immediately after blood culture. According to the observational data, Gram-positive organisms caused approximately 40% to 45% of all cases of purulent pericarditis. Therefore, ceftaroline was chosen as an empirical antibacterial therapy considering its prominent activity against staphylococci (including methicillin-resistant Staphylococcus aureus [MRSA]) and streptococci. Upon receiving the antibiotic susceptibility data ceftaroline was changed to IV ceftriaxone. Moxifloxacin was added due to its lipophilicity, which provides moxifloxacin with a large volume of distribution (2.2 L/kg) and increases concentrations in a difficult-to-reach focus of infection (pericarditis, endophthalmitis). Our patient responded well to antibacterial therapy. Symptoms resolved, and laboratory markers of inflammation normalized. However, moderate pericardial effusion remained despite the high dose of nonsteroidal anti-inflammatory drugs (NSAIDs) requiring enhancement of anti-inflammatory treatment with colchicine.

Another rare manifestation of the patient’s meningococcal infection was infectious uveitis and endophthalmitis. Ophthalmic complications in meningococcal infections, ranging from conjunctival infection to severe endophthalmitis, are uncommon.[3] While eye involvement typically arises as a complication of meningitis, isolated cases of meningococcal endophthalmitis (ME) have been documented.[3] ME is a sight-threatening condition, with vision loss and retinal detachment occurring in up to 75% of patients regardless of antibiotic therapy. Treatment for ME includes local administration of third-generation cephalosporins, delivered topically, intravitruly, or subconjunctially. The efficacy of topical corticosteroids remains controversial. Despite prompt administration of topical and systemic antibiotics during hospitalization, our patient did not experience significant visual improvement. Follow-up ophthalmological assessment revealed visual acuity (visus) of 0.01 in the right eye, along with fibrin strand formation in the vitreous cavity.

This case underscores the importance for clinicians to maintain a high suspicion for rare extra-meningeal manifestations of meningococcal infection, extending beyond the classic presentations. A pronounced SIR in patients presenting with acute pericarditis should prompt a thorough investigation to rule out bacterial etiologies, including Neisseria meningitidis.

In conclusion, this case report describes an atypical presentation of meningococcemia, characterized by concurrent acute myopericarditis and meningococcal uveitis. Notably, these manifestations emerged in the absence of the classic clinical features typically associated with meningococcal disease.