Echovirus Infection Workup

Updated: Jun 14, 2019
  • Author: Madhu Chhanda Choudhary, MD; Chief Editor: Michael Stuart Bronze, MD  more...
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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) and nucleic acid sequence–based amplification are rapid, sensitive, and specific methods 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. [32] Quality control is essential to minimize laboratory cross-contamination and false-positive results.


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.


Imaging Studies


Myopericarditis produces enlargement of the cardiac silhouette on chest radiography in approximately 50% of cases, due to either pericardial effusion or cardiac dilatation.


Echocardiography may confirm the presence of acute ventricular dilatation, decreased cardiac ejection fraction, or pericardial effusion.


Other Tests


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.


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.