INTRODUCTION:Toxoplasma gondii is an intracellular parasite that is found worldwide. Humans are infected by consuming undercooked meat containing tissue cysts or by ingesting oocysts in food or water contaminated with feline feces. Most cases of toxoplasmosis in immunocompetent individuals are asymptomatic. However, this pathogen can cause fever, myalgias, headache, lymphadenopathy, and transaminase elevation. In immune suppressed individuals, this infection can cause severe encephalitis, hepatitis, pneumonitis and myocarditis. We present a rare case of severe acute T. gondii myocarditis in an immune competent patient.
CASE PRESENTATION:A 49 year old white male physician presents to the emergency department complaining of acute onset chest discomfort. He reports 3 days of fevers, myalgias, and nausea. His past medical history consists of viral pericarditis at age 29. He takes no prescription medications. He reports recent travel to Paris, France. On exam, he has a fever of 38.5° C. He is without lymphadenopathy or hepatosplenomegaly. His chest exam is normal. Troponin I was 0.67 ng/mL, AST 79 U/L, and ALT 100 U/L. Cardiac catheterization reveals normal coronary arteries. Echocardiogram reveals only mild diastolic dysfunction. Spiral CT shows small bilateral effusions but is without pulmonary embolism. Serum troponin level peaked at 9.25 ng/mL. Acute toxoplasma myocarditis was confirmed by an IgM titer of 3.19 IU/mL (<0.9 normal) with undetectable IgG. HIV antibody was negative. He was treated with sulfamethoxazole/trimethoprim, pyrimethamine, and leucovorin. His symptoms abated within 1 week.
DISCUSSIONS:This case represents an atypical presentation of acute Toxoplasma gondii infection. In the US, prevalence of exposure in adults is approximately 15%. However, endemic countries such as France have prevalence rates as high as 87%, with the infection acquired by ingestion of undercooked lamb or pork. Our patient reported eating undercooked lamb in Paris. By far, the majority of infected people remain asymptomatic. If symptoms develop, the usual course of disease consists of fevers, myalgias, and lymphadenopathy. Symptoms typically last for weeks to months and are self-limited. Immune suppressed individuals, on the other hand, often develop encephalitis, pneumonitis, hepatitis, and myocarditis, which are frequently fatal. It is unclear why our patient developed severe myocarditis in the presence of an intact immune system. T. gondii causes infection by two mechanisms: acute infection after initial exposure, and latent reactivation of dormant organisms. Our patient is considered an acute infection, because IgG antibodies were absent at presentation. Three months later, his IgG level was >250 IU/mL. This type of infection classically causes delayed cellular autoimmune reactions against myocardial antigens. Patients typically develop heart failure or arrhythmias from the autoimmune response rather than from cysts in cardiac tissue. Organisms are rarely recovered from cardiac biopsy. Nevertheless, reported immune competent patients with myocarditis have uniformly been treated with anti-infectives. The medical literature is overwhelmingly populated with reports of T. gondii infections in immune suppressed patients. There are few case reports documenting toxoplasma myocarditis in immune competent individuals. However, some researchers believe that many cases of non-ischemic cardiomyopathy are related to T. gondii infections and simply go unrecognized. As more and more patients become immune suppressed for various reasons, toxoplasmosis will become more common as well. Our case suggests that a high index of suspicion is needed for cases in the immune competent population.
CONCLUSION:Toxoplasma Gondii is a well described pathogen causing myocarditis principally in immune compromised patients. Even in patients with an intact immune response, toxoplasmosis should be considered in the differential diagnosis. Detailed history, physical examination, and knowledge of endemic areas can aide the practitioner in diagnosis.
DISCLOSURE:Michael Crosser, No Financial Disclosure Information; No Product/Research Disclosure Information