Myocarditis by Toxoplasma gondii in an immunocompetent young man

We present the case of a 15-year-old male patient, with no relevant previous medical history, who came to Accident & Emergency reporting oppressive, non-radiating chest pain associated with dyspnoea lasting approximately one hour, within the previous 24 h. He reported no associated sweating or dizziness, or palpitations, but he had had a fever in the previous few days. On examination: BP 100/54 mmHg; HR 100 bpm; afebrile; SatO₂ 98%; heart sounds were of tachycardia without murmurs; and the rest of the examination was unremarkable.

A series of electrocardiograms (ECG) showed diffuse concave ST-segment elevation, more marked in the lateral and inferior leads. Laboratory tests showed elevated troponin I (8.66 mg/dl). The rest of the laboratory tests, chest X-ray and transthoracic echocardiogram were normal. Cardiac magnetic resonance imaging (cardiac MRI) was performed; the study met two diagnostic criteria (Lake Louise) for myocarditis by cardiac MRI: hyperintensity on the T2-STIR sequence associated with oedema, with late enhancement with a lateral subepicardial pattern consistent with hyperintense segments on T2-STIR. Both ventricles had normal segmental and overall contractility, with a left ventricular ejection fraction of 56% (Fig. 1A). The patient was diagnosed with myopericarditis and admitted to cardiology for seven days. He made good progress on treatment with non-steroidal anti-inflammatory drugs (NSAIDs) and cardiac MRI in six months was recommended.

Figure 1.

Cardiac magnetic resonance imaging study. A. Enhanced sequences (short-tau-inversion recovery [STIR]) revealed myocardial oedema in the lateral-apical aspect (arrowheads). B,C. In the later study after the intravenous administration of contrast, gadolinium uptake was observed with a subepicardial and lateral intramyocardial distribution (arrows).

Ten days after being discharged, the patient consulted with painless occipital and right retroauricular lymphadenopathy, 1–1.5 cm in size and adhered to deep planes. He had not had any fever or other symptoms of infection. He only reported having had contact with cats and a canary. Multiple serology was performed for viruses (CMV, EBV, HIV, HBV, HAV, ECV, rubella), syphilis and toxoplasma, as well as an immunological study. He was diagnosed with acute toxoplasmosis (IgG 1,100 IU/ml and IgM 28.65 IU/ml) and no treatment was prescribed, as he was asymptomatic.

Six months later, the patient attended the cardiology clinic for review after having had a follow-up cardiac MRI. The new cardiac MRI once again showed findings consistent with myocarditis with oedema and late enhancement, with a similar distribution to the previous scan (Fig. 1B, C). The Infectious Diseases Unit was consulted about the case and it was decided to request repeat serology for toxoplasma. This came back positive: IgG 2.16 IU/ml and IgM 3.33 IU/ml. PCR for toxoplasma was also requested from the reference laboratory, with negative results.

It was decided to treat with pyrimethamine 50 mg/12 h loading doses followed by 25 mg/12 h, sulfadiazine 500 mg, two/6 h for four weeks and calcium folinate 15 mg/24 h. From a cardiological standpoint, the patient was asymptomatic at all times, except for self-limiting episodes of palpitations, for which he received treatment with carvedilol 6.25 mg/12 h. At the next follow-up cardiac MRI four months later, the patient showed no signs of myopericarditis.

Acute Toxoplasma gondii infection in immunocompetent patients is asymptomatic in most cases, but they may occasionally develop fever, lymphadenopathy and asthenia.¹ However, there are very few cases published in the literature of T. gondii myocarditis in non-immunocompromised patients.² The clinical manifestations associated with myocarditis are fever, dyspnoea, chest pain, lymphadenopathy and myalgia.^3,4 In our case, the patient had a primary infection due to T. gondii, which we decided not to treat as he was immunocompetent and practically asymptomatic, despite the fact that the onset was with acute myopericarditis. At subsequent check-ups, he was diagnosed with subacute myocarditis, so due to the persistence of disease, we decided he required treatment, and this then resolved the condition.

In the published cases of myopericarditis in immunocompetent patients, the treatment is not clear, and although most authors decide to give specific treatment, as in our case,^4–8 there are reports of cure with no treatment.^9,10 Although it been described, the persistence of myocarditis six months after diagnosis of the acute infection is also unusual.⁵

Routine serology testing is not usually performed in myopericarditis, as it has low diagnostic yield and rarely changes patient management. However, repeat cardiac MRI is recommended in the follow-up of these patients, as the persistence of inflammatory activity is not a common finding and should prompt us to seek an aetiological diagnosis and specific treatment.

Funding

The authors received no funding for the writing or publication of the manuscript.

Conflicts of interest

The authors declare that they have no conflicts of interest.