Autoimmune allergic reaction causing myopericarditis following vaccination is extremely rare and, in this regard, much attention has been paid to smallpox vaccine.¹ Halsell et al.,² reported 18 cases of probable myopericarditis in 230,734 primary vaccines after smallpox vaccination (an incidence of 7.8 per 100,000 over 30 days). No cases of myopericarditis following smallpox vaccination were reported among 95,622 vaccines who were previously vaccinated. A causal relationship was supported by the close temporal clustering (7-19 days; mean, 10.5 days following vaccination) and wide temporal distribution, occurrence in only primary vaccinees, and lack of evidence for alternative etiologies associated with myopericarditis.²

The meningococci causing primary meningococcal pericarditis (PMP) are usually of serotype C (88% of cases in one series) or, less commonly, serotypes B or W135.³ PMP is a purulent pericarditis caused by N. meningitidis, with no evidence of previous meningococcemia or meningitis, with development of cardiac tamponade in many cases. Evaluation of PMP versus viral pericarditis is important since the former usually requires pericardial drainage in addition to antibiotics.

Perimyocarditis is an acute inflammation of the pericardium and the underlying myocardium resulting in myocellular damage. It can be considered an acute pericarditis with elevated cardiac biomarkers. Although cardiac biomarkers were elevated in our patient, the echocardiography showed normal myocardium and normal wall motion.

PMP is a rare form, usually presented as acute purulent pericarditis, that is complicated by cardiac tamponade and requires pericardial drainage. PMP is typically caused by Neisseria meningitidis of serotype C, or, less commonly, B or W135. In general, meningococcal myopericarditis is categorized into three etiologies; primary meningococcal disease, secondary disease due to disseminated meningococcemia, and reactive meningococcal pericarditis (RMP), an immunologic complication.⁴ Because of the negative history of infection, the exposure to meningococcal conjugate vaccine (groups A, C, W-135 and Y) five days prior to the onset of symptoms, and negative serology for infectious and autoimmune diseases, we concluded that pericarditis was reactive rather than a result of direct infection of the myocardium, and a combination of acetylsalicylic acid and colchicine was initiated.

Many case reports of RMP following meningococcal infection have been reported, but no case report of RMP following meningococcal vaccination has been published. RMP is a rare condition and may be more severe than purulent pericarditis; cardiac tamponade is relatively common, requiring high doses of steroids and/or pericardiocentesis. RMP is usually seen 6-15 days after the onset of illness and is characterized by a type III hypersensitivity reaction, either against the specific serotype of the N. meningitidis or against a newly antigenic, damaged pericardial tissue because of molecular mimicry with microbial antigens. Contrary to purulent pericarditis, RMP represents a late complication and there have been many reported cases of RMP post-meningococcal infection in global literature since 1969 ( Table 2 ).^{5 - 10} Severe disease, age (adults and young teenagers), and serogroup C seem to predispose to post-infectious, immune-related complications including arthritis, vasculitis, pleuritis, and pericarditis.^{7 - 9} Recently, much attention has been given to smallpox vaccine due to its association with myocarditis.¹ There is one reported case of myocarditis that developed hours after diphtheria, tetanus, and acellular pertussis (DTaP) vaccination in a 3-month-old infant,¹¹ and another case of myocarditis after tetanus vaccination in a 14-year-old child.¹² In line with these observations, our patient was a young adult, presenting in poor clinical condition, elevated inflammatory markers suggestive of severe disease, and responsive to anti-inflammatory drugs without antibiotics. We considered the diagnosis of reactive pericarditis rather than myopericarditis due to normal echocardiography and a conservative course of management. The clinical data presented in the case report support the etiologic relationship between meningococcal vaccination and pericarditis. It may be an association, or even a causative relationship. Taking the risk of myocardial biopsy in consideration, histopathological diagnosis of the myocardial biopsy will show diffuse inflammation and will not specify the exact meningococcal etiology.

Table 2

Reference	Patient age/y	Time of pericarditis diagnosis	Neisseria meningitidis serogroup	Clinical presentation	Therapy
Chiappini 5	10	7 d	C	Meningitis	Prednisone + Aspirin
El Bashir 6	13	7 d	C	Meningitis	Dexamethasone + Ibuprofen, later diclofenac sodium
Dupont7	14	3 d	C	Meningitis	ASA
Stephani 8	14	9 d	C	Meningitis, endophthalmitis	Prednisone + Antibiotics
Fuglsang Hansen 9	N/A	11 d	N/A	Meningitis	Steroid + Pericardiocentesis
Akinosoglou K 10	28	N/A	B	Meningococcemia and acute abdominal pain	Steroid + Antibiotics

y: years; d: days; CSF, cerebrospinal fluid; ASA, acetylsalicylic acid; NSAID, non-steroid anti-inflammatory drug; N/A: not available; Limited data due to language constrains (Danish, German).

Further observations and studies are needed to support this case report to prove a causative role of meningococcal vaccine in pericarditis.

Patients who have chest complaints after vaccination should be evaluated for post-vaccine pericarditis and myocarditis. High clinical suspicion, careful examination and close observation may be required so that atypical presentation and manifestations are not overlooked. Endomyocardial biopsy specimens might help to determine the relative causative role of vaccine in the development of myocarditis. In our case, the mild illness, uncomplicated course, and good response to treatment deferred the need for biopsy. To our knowledge, there is no case report of reactive pericarditis following meningococcal vaccination.