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Toxoplasma myocarditis

a rare but serious complication in an HIV-infected late presenter

Cuervo, Guillermo; Simonetti, Antonella F.; Alegre, Oriol; Sanchez-Salado, Jose Carlos; Podzamczer, Daniel

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doi: 10.1097/QAD.0000000000001174
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A previously healthy 32-year-old man presented with a ‘flu-like’ upper respiratory infection that had progressively worsened with fatigue, cough, and dyspnea in 2 weeks. On admission, he was afebrile, with blood pressure 80/40 mmHg, basal oxygen saturation of 80%, sinus tachycardia at 150 bpm, and highly elevated cardiac troponin. The echocardiography showed an ejection fraction of 15% with predominant left ventricular failure, and urgent cardiac catheterization showed normal coronary arteries. The patient progressed to circulatory collapse with the need for inotropic support, mechanical ventilation, and mechanical circulatory support with an intraaortic balloon pump. Routine serology (pretransplant study) was positive for HIV, with a viral load of 259.564 copies/ml and severe immunosuppression (CD4+ lymphocytes 4 cells/μl). Once transferred to the coronary unit, because of multiorgan failure, the patient underwent venoarterial extracorporeal membrane oxygenation implantation.

Several serological determinations were negative, but Epstein–Barr virus (EBV) IgG, cytomegalovirus IgG, and antitoxoplasma IgG were positive, as well as blood PCR for EBV and cytomegalovirus. Because of suspected infectious myocarditis, at 48 h after admission, empirical treatment was started with ganciclovir for EBV, along with pyrimethamine and clindamycin for toxoplasma, as well as cotrimoxazole for Pneumocystis jiroveci prophylaxis. Sulfadiazine was not initially used because of severe renal impairment. Given the possibility of HIV myocarditis, antiretroviral therapy (ART) was also initiated with dolutegravir, darunavir, ritonavir, and lamivudine. Histology of the endomyocardial biopsy revealed severe active lymphocytic myocarditis and positive PCR results for EBV and Toxoplasma gondii. The patient developed pulmonary edema. Consequently, a biventricular CentriMag (Levitronix, Waltham, Massachusetts, USA) was implanted 1 week later to decompress and support both ventricles. Finally, Toxoplasma was considered to be the etiologic agent of fulminant myocarditis and ganciclovir was discontinued. Following full recovery of renal function, clindamycin was replaced by sulfadiazine. With both Bi-Ventricular Assist Device (BVAD) implantation and systemic treatment, the patient promptly recovered left ventricular function as shown on serial echocardiograms, achieving left ventricle ejection fraction of 50%. The CentriMag BVAD was removed on day 7 after implantation. Cardiac magnetic resonance showed a left ventricle ejection fraction of 51% with mild edema and delayed gadolinium enhancement (Fig. 1). The patient was discharged at day 27, fully recovered and completed 6 weeks of treatment with sulfadiazine and pyrimethamine. Follow-up at 3 months showed undetectable viral loads and 570 CD4+ lymphocytes cells/μl.

Fig. 1
Fig. 1:
Cardiac MRI (day 25 after admission).(a) Myocardial hyperintensity (myocardial-to-skeletal muscle ratio of 2) consistent with mild diffuse inflammatory edema. (b) Late enhancement sequence: altered kinetics between myocardial cavity and myocardium, suggestive of a high-extravascular component. Linear subepicardial enhancement at the lateral, medial, and basal ventricular walls.

T. gondii is a protozoan parasite of felids. The term ‘toxoplasmosis’ describes the clinical or pathologic disease caused by this parasite. Whereas the condition is usually benign in the normal host, it may have devastating consequences in immunosuppressed individuals [1]. T. gondii is the most common cause of opportunistic central nervous system infection in patients with AIDS and has been associated with a high morbidity and mortality in the past [1,2].

Nonneurologic disease, however, is rare [3]. Before highly active ART was available, a study in France (a high prevalence area for T. gondii infection) performed 182 autopsies on HIV-deceased patients and found cardiac toxoplasmosis in 21 (12%) of them. Strikingly, only three patients had no cardiac lesions associated with Toxoplasma encephalitis. Another important finding of the study was that cardiac involvement was not clinically evident premortem in most patients (n = 15; 71%) [4]. Signs and symptoms can vary. There are descriptions of cardiomegaly [5], fulminant congestive heart failure [6,7], arrhythmias [8], pericarditis [5], and chest pain mimicking myocardial infarction [9]. An etiologic diagnosis can be evident if cardiac and central nervous system involvement coexist, although diagnosis may be difficult in their absence [4]. For this reason, the cause should be actively sought in symptomatic patients [6]: the presence of T. gondii in an endomyocardial specimen should be systematically ruled out. Molecular diagnosis with PCR appears to offer greater sensitivity [10] and proved to be of great value in our patient.

The Infectious Diseases Society of America Practice Guidelines recommend sulfadiazine and pyrimethamine as the treatment of choice in patients with active toxoplasmosis. Because our patient was receiving renal replacement therapy, however, we initially preferred pyrimethamine and clindamycin [11]. Given the severity of presentation and the plausibility of HIV myocarditis, we simultaneously began ART. Immune reconstitution inflammatory syndrome was a potential concern [12], but fortunately was not a complication in our patient.

The severity of presentation also made it essential to provide aggressive supportive care. Extracorporeal membrane oxygenation proved to be remarkably as a bridge therapy, until the effectiveness of antimicrobial therapy tilted the balance favorably. This management approach has been previously reported [7].

Although cardiac toxoplasmosis is rarely diagnosed, nowadays, because of the potent ARTs available, it should be considered and promptly diagnosed if present.

Acknowledgements

Conflicts of interest

There are no conflicts of interest.

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