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Postgraduate Education Corner: PULMONARY AND CRITICAL CARE PEARLS |

A 49-Year-Old Man With Chest Pain and Fever After Returning From FranceAdult Man With Chest Pain and Fever FREE TO VIEW

Kyle R. Brownback, MD; Michael S. Crosser, MD; Steven Q. Simpson, MD
Author and Funding Information

From the Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of Kansas Medical Center, Kansas City, KS.

Correspondence to: Kyle R. Brownback, MD, Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of Kansas Medical Center, 3901 Rainbow Blvd, Kansas City, KS 66160; e-mail: kylebrownback@gmail.com


Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


© 2012 American College of Chest Physicians


Chest. 2012;141(6):1618-1621. doi:10.1378/chest.11-2085
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A 49-year-old man presented to the ED complaining of acute onset of chest discomfort. The patient described the pain as being substernal in location, pressure like in character, and radiating to the jaw. He also reported mild shortness of breath. He described a cough productive of clear sputum, fever, chills, nausea, and generalized myalgias that had begun 4 days previously. The patient had taken antacids at home with some improvement, although the pain quickly returned and led him to present to the ED for evaluation.

The patient’s medical history was significant for an episode of pericarditis 25 years previously, and he was taking no medications on admission. The patient had no family history of coronary artery disease. He had never used tobacco products, drank alcohol only occasionally, was employed at this medical center as a pulmonologist (and is a coauthor of this article). The patient had been in Paris, France, 2 weeks previously, during which time he consumed medium-rare prepared lamb.

Physical Examination

On arrival at the ED, the patient was afebrile, with a heart rate of 98 beats/min, BP of 106/59 mm Hg, a respiratory rate of 12 breaths/min, and an oxygen saturation of 97% on room air. He was alert, oriented, and in moderate distress secondary to chest discomfort. Examination of head, eyes, ears, nose, and throat; chest; heart; and extremities revealed the following: ropharynx clear with no jugular venous distention; breath sounds clear to auscultation bilaterally; cardiac regular rate and rhythm with an S3 gallop; and no clubbing, cyanosis, or edema. The remainder of the physical examination was normal.

Laboratory Findings

Hemoglobin level was 14.6 g/dL, WBC count was 6,700/μL, and platelets were 139,000/μL. Sodium level was 134 mM, potassium level was 3.6 mM, bicarbonate level was 24 mM, BUN level was 16 mg/dL, and creatinine level was 1.2 mg/dL. Total bilirubin was 0.5 mg/dL, aspartate aminotransferase was 50 u/L, alanine aminotransferase was 72 u/L, and D-dimer was normal. His myoglobin was normal at 48 ng/mL, although the troponin was slightly elevated at 0.67 ng/mL. The patient’s ECG showed a normal sinus rhythm with a normal axis and 1 mm of ST-segment elevation in leads V2 and V3 (Fig 1). His chest radiograph showed a normal cardiac and mediastinal silhouette with clear lung fields. A CT chest scan showed no evidence of a pulmonary embolism, and he had mild dependent pulmonary vascular congestion with small bilateral pleural effusions.

Figure Jump LinkFigure 1. The patient’s ECG on admission reveals 1 mm of ST-segment elevation in leads V2 and V3.Grahic Jump Location

An echocardiogram was performed, showing normal left ventricular systolic function with an ejection fraction of 60%, no wall motion abnormalities, normal valvular structures, normal pulmonary artery pressures, and no evidence of a pericardial effusion. The patient subsequently went to left-sided heart catheterization, which revealed normal caliber of all of the coronary arteries without any areas of stenosis.

The patient was discharged home later that day but presented again to the ED the following day with a fever of 38.5°C, further elevation of his troponin to 7.54 ng/mL, and recurrence of chest pain.

What is the diagnosis?
Diagnosis: Acute Toxoplasma gondii myocarditis

Toxoplasma gondii is an obligate intracellular protozoan that may take many different forms, including the oocyst, the tachyzoite, and the bradyzoite. Felines are the definitive hosts of Toxoplasma gondii, and their digestive tract is the site of replication and production of oocysts. During acute infection, these oocysts are shed in the feces of the cat and may be transmitted to other mammals upon ingestion, which gives rise to the tachyzoite stage. The tachyzoite is the rapidly replicating stage of the protozoa; upon replication, the tachyzoite may disseminate throughout the body of the host. Tachyzoites will initiate a strong inflammatory reaction and, under pressure from the host immune system, may form bradyzoites that exist as cysts in the skeletal muscle. The bradyzoites may be released from the cysts and transform back into tachyzoites in the setting of the consumption of undercooked meat from an intermediate host, such as pork or lamb. It is important to recognize that the prevalence of Toxoplasma gondii in retail meats in the United States is much lower than it is in Europe, and the majority of the meat that is involved in the United States is pork. One European study found that the principal risk factor for acute infection with Toxoplasma gondii in immunocompetent individuals was consumption of undercooked beef or lamb.

Humans may become infected with toxoplasmosis via the ingestion of cysts in undercooked meats or the consumption of water or food containing oocysts excreted in the feces of infected felines. The incubation period ranges from 10 to 23 days. In the immunocompromised patient, toxoplasmosis can present as a life-threatening illness, although in these individuals the infection almost always represents a reactivation of a latent infection. Toxoplasmosis primarily presents with CNS manifestations in the immunocompromised, although it may also present with pneumonitis, chorioretinitis, or as multiorgan failure and shock. In contrast, the majority of primary toxoplasmosis infections in those with intact immune systems are unrecognized, but they may feature isolated cervical lymphadenopathy.

Myocarditis is defined as inflammation of the myocardium, and typical causes include infections, toxicity from drugs or medications, and systemic diseases. The clinical presentation is variable, from asymptomatic patients with ECG abnormalities to patients with fulminant heart failure and severe ventricular dysfunction. Acute myocarditis may also mimic acute myocardial infarction, via both chest pain and acute ST-segment elevations. Although endomyocardial biopsy is the gold standard for diagnosis, it is limited by its invasiveness and poor sensitivity. Cardiac biomarkers, including creatine kinase and troponin T, may be elevated in acute myocarditis and support a diagnosis in the correct clinical scenario.

Toxoplasmosis has been reported as a cause of myocarditis in both immunocompromised and immunocompetent patients. The clinical presentations of toxoplasmosis involving the heart include ventricular tachycardia, chronic constrictive pericarditis, congestive heart failure, sudden cardiac death, and, with this report, chest pain. Treatment of toxoplasmosis in patients who are immunocompetent is usually not necessary and is recommended only when there is evidence of damage to vital organs. Typical treatment regimens include sulfadiazine with pyrimethamine and folinic acid, although azithromycin, clindamycin, or atovaquone may be substituted for sulfadiazine.

With regard to the toxoplasmosis-specific immunoglobulin levels in patients who are immunocompetent, an elevation in the IgA and IgM levels are seen in the first few weeks after infection. The IgA and IgM levels peak approximately 1 month after the infection, falling to nondetectable levels over the next 6 to 9 months. IgG levels generally begin to increase only after 1 to 2 months following infection, reaching their peak 6 to 9 months later.

Clinical Course

The patient presented with acute myocarditis following a large inoculum of Toxoplasma gondii from infected, undercooked lamb in a region with a high prevalence of infection in the food supply. His presentation mimicked an acute myocardial infarction, causing chest pain, elevated cardiac biomarkers, and ECG changes, without associated heart failure. The patient’s toxoplasmosis IgM titer was 3.19 IU/mL (normal <0.9 IU/mL), with a negative toxoplasmosis IgG, consistent with an acute toxoplasmosis infection. He was treated with trimethoprim-sulfamethoxazole, folinic acid, and pyrimethamine and had complete clinical recovery without subsequent relapse and with his ECG changes resolved. At 3-month follow-up, his IgG titer was >250 IU/mL.

  1. Toxoplasmosis infection is typically asymptomatic in patients who are immunocompetent, whereas it may present as a life-threatening illness with reactivation in the patient who is immunocompromised.

  2. Typical causes of myocarditis include infection, systemic diseases, and drugs. Typical infectious causes include viruses, bacteria, protozoa, and parasites.

  3. Treatment of toxoplasmosis infection in patients who are immunocompetent with signs of vital organ damage includes pyrimethamine with sulfadiazine and folinic acid.

Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Dubey JP, Miller NL, Frenkel JK. TheToxoplasma gondiioocyst from cat feces. J Exp Med. 1970;1324:636-662. [CrossRef] [PubMed]
 
Frenkel JK.Hammond DM, Long PL. Toxoplasmosis: parasite life cycle pathology and immunology. The Coccidia. 1973; Baltimore, MD University Park Press:343-410
 
Dec GW Jr, Waldman H, Southern J, Fallon JT, Hutter AM Jr, Palacios I. Viral myocarditis mimicking acute myocardial infarction. J Am Coll Cardiol. 1992;201:85-89. [CrossRef] [PubMed]
 
Porter SB, Sande MA. Toxoplasmosis of the central nervous system in the acquired immunodeficiency syndrome. N Engl J Med. 1992;32723:1643-1648. [CrossRef] [PubMed]
 
Luft BJ, Hafner R, Korzun AH, et al. Toxoplasmic encephalitis in patients with the acquired immunodeficiency syndrome. Members of the ACTG 077p/ANRS 009 Study Team. N Engl J Med. 1993;32914:995-1000. [CrossRef] [PubMed]
 
Gorgievski-Hrisoho M, Germann D, Matter L. Diagnostic implications of kinetics of immunoglobulin M and A antibody responses toToxoplasma gondiiJ Clin Microbiol. 1996;346:1506-1511. [PubMed]
 
Lauer B, Niederau C, Kühl U, et al. Cardiac troponin T in patients with clinically suspected myocarditis. J Am Coll Cardiol. 1997;305:1354-1359. [CrossRef] [PubMed]
 
Cook AJC, Gilbert RE, Buffolano W, et al. European Research Network on Congenital Toxoplasmosis Sources of toxoplasma infection in pregnant women: European multicentre case-control study. BMJ. 2000;3217254:142-147. [CrossRef] [PubMed]
 
Dubey JP, Hill DE, Jones JL, et al. Prevalence of viableToxoplasma gondiiin beef, chicken, and pork from retail meat stores in the United States: risk assessment to consumers. J Parasitol. 2005;915:1082-1093. [CrossRef] [PubMed]
 
Eza DE, Lucas SB. Fulminant toxoplasmosis causing fatal pneumonitis and myocarditis. HIV Med. 2006;76:415-420. [CrossRef] [PubMed]
 
Pergola G, Cascone A, Russo M. Acute pericarditis and myocarditis byToxoplasma gondiiin an immunocompetent young man: a case report. Infez Med. 2010;181:48-52. [PubMed]
 

Figures

Figure Jump LinkFigure 1. The patient’s ECG on admission reveals 1 mm of ST-segment elevation in leads V2 and V3.Grahic Jump Location

Tables

Suggested Readings

Dubey JP, Miller NL, Frenkel JK. TheToxoplasma gondiioocyst from cat feces. J Exp Med. 1970;1324:636-662. [CrossRef] [PubMed]
 
Frenkel JK.Hammond DM, Long PL. Toxoplasmosis: parasite life cycle pathology and immunology. The Coccidia. 1973; Baltimore, MD University Park Press:343-410
 
Dec GW Jr, Waldman H, Southern J, Fallon JT, Hutter AM Jr, Palacios I. Viral myocarditis mimicking acute myocardial infarction. J Am Coll Cardiol. 1992;201:85-89. [CrossRef] [PubMed]
 
Porter SB, Sande MA. Toxoplasmosis of the central nervous system in the acquired immunodeficiency syndrome. N Engl J Med. 1992;32723:1643-1648. [CrossRef] [PubMed]
 
Luft BJ, Hafner R, Korzun AH, et al. Toxoplasmic encephalitis in patients with the acquired immunodeficiency syndrome. Members of the ACTG 077p/ANRS 009 Study Team. N Engl J Med. 1993;32914:995-1000. [CrossRef] [PubMed]
 
Gorgievski-Hrisoho M, Germann D, Matter L. Diagnostic implications of kinetics of immunoglobulin M and A antibody responses toToxoplasma gondiiJ Clin Microbiol. 1996;346:1506-1511. [PubMed]
 
Lauer B, Niederau C, Kühl U, et al. Cardiac troponin T in patients with clinically suspected myocarditis. J Am Coll Cardiol. 1997;305:1354-1359. [CrossRef] [PubMed]
 
Cook AJC, Gilbert RE, Buffolano W, et al. European Research Network on Congenital Toxoplasmosis Sources of toxoplasma infection in pregnant women: European multicentre case-control study. BMJ. 2000;3217254:142-147. [CrossRef] [PubMed]
 
Dubey JP, Hill DE, Jones JL, et al. Prevalence of viableToxoplasma gondiiin beef, chicken, and pork from retail meat stores in the United States: risk assessment to consumers. J Parasitol. 2005;915:1082-1093. [CrossRef] [PubMed]
 
Eza DE, Lucas SB. Fulminant toxoplasmosis causing fatal pneumonitis and myocarditis. HIV Med. 2006;76:415-420. [CrossRef] [PubMed]
 
Pergola G, Cascone A, Russo M. Acute pericarditis and myocarditis byToxoplasma gondiiin an immunocompetent young man: a case report. Infez Med. 2010;181:48-52. [PubMed]
 
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