Echoviruses Workup

  • Author: Mary T Busowski, MD; Chief Editor: Burke A Cunha, MD   more...
 
Updated: Aug 18, 2011
 

Laboratory Studies

  • Viral isolation through cell culture: Until recently, echoviral infections were diagnosed via isolation of the virus in cell culture. The diagnosis can be proven by isolating the virus in blood, CSF, tissue, or pericardial fluid. Pharyngeal and stool cultures may be helpful but are not diagnostic, as asymptomatic shedding can persists for several weeks after acute infection.
  • Polymerase chain reaction
    • Reverse transcriptase polymerase chain reaction (RT-PCR) is a rapid, sensitive, and specific method of detecting echoviral RNA in clinical specimens. The quick turnaround time offers advantages in terms of patient management decisions.
    • RT-PCR has detected echoviral RNA from CSF, throat swabs, serum, and stool samples. Quality control is essential to minimize laboratory cross-contamination and false-positive results.
  • Serology: Serologic testing for echoviral infection has limited value. The results are slow, depend on acute and convalescent titers, and are not type-specific. Regardless of titer, a single antibody result is most often useless.
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Imaging Studies

  • Radiography: Myopericarditis produces enlargement of the cardiac silhouette on chest radiography in approximately 50% of cases, due to either pericardial effusion or cardiac dilatation.
  • Echocardiography: Echocardiography may confirm the presence of acute ventricular dilatation, decreased cardiac ejection fraction, or pericardial effusion.
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Other Tests

  • Electrocardiography: Pericarditis and myocarditis produce electrocardiographic changes ranging from ST-segment elevation or nonspecific ST-segment and T-wave abnormalities. Severe myocardial disease may lead to the development of Q waves, ventricular tachyarrhythmias, and all degrees of heart block.
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Histologic Findings

In enteroviral myopericarditis, viruses reach the heart during the viremia that follows replication in the GI or respiratory tract. Experimental studies in a murine model strongly suggest that virus replication occurs in the myocytes. A chronic inflammatory response persists for weeks to months when the replicating virus is no longer present in the heart, and this lingering response is the subject of keen interest. Some investigators consider the late-phase inflammatory response to be due to virus-induced, cytotoxic T-lymphocyte destruction of myocytes. Others postulate the development of a myocardial neoantigen or cross-reactivity between viral and myocardial cell antigens. A variable degree of interstitial fibrosis and evidence of myocyte loss accompany healing.

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Contributor Information and Disclosures
Author

Mary T Busowski, MD  Infectious Disease Faculty Practice/Internal Medicine Faculty Practice, Orlando Health; Clinical Instructor of Medicine, Florida State University School of Medicine

Mary T Busowski, MD, is a member of the following medical societies: American Academy of Hospice and Palliative Medicine, American College of Physicians, American Medical Association, Florida Medical Association, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Coauthor(s)

Mark R Wallace, MD, FACP, FIDSA  Clinical Professor of Medicine, Florida State University College of Medicine; Head of Infectious Disease Fellowship Program, Orlando Regional Medical Center

Mark R Wallace, MD, FACP, FIDSA is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Tropical Medicine and Hygiene, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Larry I Lutwick, MD  Professor of Medicine, State University of New York Downstate Medical School; Director, Infectious Diseases, Veterans Affairs New York Harbor Health Care System, Brooklyn Campus

Larry I Lutwick, MD is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Specialty Editor Board

Mark R Wallace, MD, FACP, FIDSA  Clinical Professor of Medicine, Florida State University College of Medicine; Head of Infectious Disease Fellowship Program, Orlando Regional Medical Center

Mark R Wallace, MD, FACP, FIDSA is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Tropical Medicine and Hygiene, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Michael Stuart Bronze, MD  Professor, Stewart G Wolf Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Medical Association, Association of Professors of Medicine, Infectious Diseases Society of America, Oklahoma State Medical Association, and Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

Eleftherios Mylonakis, MD  Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital

Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD  Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital

Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

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