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Coxsackieviruses Clinical Presentation

  • Author: Martha L Muller, MD; Chief Editor: Michael Stuart Bronze, MD  more...
 
Updated: Aug 19, 2015
 

History

More than 90% of coxsackieviruses infections are asymptomatic or cause nonspecific febrile illnesses. In neonates, they are the most common cause of febrile illnesses during the summer and fall months. Thirteen percent of newborns with fever in the first month of life were noted to have an enteroviral infection. In addition to nonspecific illnesses, various well-described illnesses have been associated with coxsackievirus infections.

Aseptic meningitis

Patients with aseptic meningitis may have rapid or gradual onset of fever and chills, nausea and vomiting, malaise, headaches, neck pain, light sensitivity, and upper respiratory symptoms. Infants younger than 3 months have been noted to have the highest incidence of clinically recognized aseptic meningitis, partly because lumbar punctures are often performed for the evaluation of fever in this age group. These infants often present with only a febrile illness characterized by irritability and anorexia. Meningismus occurs in only approximately 50% of infants with enteroviral meningitis.

Coxsackievirus B infection is more likely than coxsackievirus A to be associated with meningitis.

Seizures, lethargy, and movement disorders occur early in the course of disease and have been reported in 5-10% of patients with enteroviral meningitis. No long-term neurologic deficits appear to exist in infants with aseptic meningitis. Adults may experience a more prolonged period of fever and headache compared with infants and children.

Encephalitis

Encephalitis is an unusual manifestation of CNS infection, although it is sometimes observed in association with aseptic meningitis. Enteroviruses accounts for approximately 5% of all cases of encephalitis. Coxsackievirus types A9, B2, and B5 have been linked with encephalitis. In rare cases, it mimics encephalitis secondary to herpes simplex virus.

Neurologic diseases

Rarely, coxsackieviruses have been implicated in additional neurologic diseases such as sporadic cases of flaccid motor paralysis that closely mimic poliovirus infection. Additionally, cases of Guillain-Barré syndrome have been described with coxsackievirus serotypes A2, A5, and A9.

Myopericarditis

Myopericarditis can occur at any age although has a predilection for adolescents and young adults. Enteroviruses account for half of all cases of acute viral myopericarditis.

Manifestations of myopericarditis range from an asymptomatic presentation to heart failure and death. Between the two extremes, most patients report dyspnea, chest pain, fever, and malaise.

Symptoms may be preceded by an upper respiratory infection within the preceding 7-14 days.

Presenting signs include pericardial friction rub, gallop rhythm, and cardiomegaly and/or pericardial effusion on chest radiography.

ECG abnormalities may range from ST-segment elevations to heart block. Echocardiography may show diminished ejection fractions and left ventricular wall abnormalities. Myocardial enzyme levels in the serum are frequently elevated.

The male-to-female ratio is 2:1. The mortality rate is low, and the prognosis in children is believed to be better than that in adults. Complications include pericardial effusion, arrhythmia, heart block, valvular dysfunction, and dilated cardiomyopathy.

Diabetes

Although principally correlative, data suggest that type-1 insulin-dependent diabetes may result from group B coxsackievirus infections. Epidemiologic data note that clustering of newly onset diabetes mellitus occurs 1-3 months following infection with the virus. Similarly, animal models noted infection of pancreatic islet cells.

Exanthems

Two of the more distinctive exanthems caused by coxsackievirus hand-food-and-mouth disease (HFMD) and herpangina.

HFMD often affects children and spreads easily to other family members. Patients present with a sore throat and mouth. Vesicles that coalesce, form bullae, and then ulcerate form on the buccal mucosa and tongue. Seventy-five percent of patients have peripheral cutaneous lesions at approximately the same time. Biopsy reveals intracytoplasmic viral particles. The most common virus isolated is coxsackievirus A16. Numerous cases of a more severe HFMD caused by coxsackievirus A6 were reported between 2004 and 2011 in several Asian and European countries.[5] Additionally, between 2011 and 2012 in the United States, several cases of severe HFMD were reported, with 74% of those cases testing PCR positive for coxsackievirus A6; about 25% of reported cases were in adults.[5]

Herpangina is a vesicular enanthem of the posterior oropharynx with fever, sore throat, occasional throat exudate, odynophagia, and dysphagia, which is observed more often in young children than in adolescents and adults. Prompt recovery is typical, with almost all patients recovering completely. Group A coxsackieviruses are the most common viruses isolated from herpangina patients.

Epidemic pleurodynia

This is a muscular disease, and viral invasion of muscles, causing inflammation, is suspected; however, direct histologic evidence is lacking. Epidemic pleurodynia is usually associated with outbreaks of group B coxsackievirus infection.

Patients present with fever and sharp, paroxysmal, spasmodic pain in the chest and upper abdomen.

All patients recover completely within 1 week.

Acute hemorrhagic conjunctivitis

Pain and edema of the eyelids and subconjunctival hemorrhage are present.

Patients may also report photophobia, foreign body sensation, fever, malaise, and headache. These symptoms usually resolve spontaneously within one week.

Rare complications include keratitis and motor paralysis.

This condition is highly contagious and has resulted in epidemics and pandemics.

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Physical

Aseptic meningitis

On examination, patients may have signs of nuchal rigidity and other evidence of meningeal irritation, photophobia, pharyngitis, and rash.

Encephalitis

In contrast to patients with aseptic meningitis, whose brain function is normal, patients with encephalitis may present with cerebral dysfunction that manifests as altered mental status, personality changes, and neurologic deficits (eg, motor, sensory, speech impairment). An EEG may be helpful in localizing and characterizing the seizure focus.

Myopericarditis

The presentation in patients with myopericarditis ranges from asymptomatic to critical illness secondary to severe heart failure. Most patients report fever, malaise, upper respiratory tract symptoms, dyspnea, and chest pain. Chest pain increases when the patient is lying down and improves when the patient sits up and leans forward.

On examination, the point of maximal pulse (PMI) may be displaced, pericardial friction rub may be heard, and signs of heart failure (eg, S3 gallop, pulmonary edema) may be present.

HFMD

Physical examination findings include vesicular lesions that may appear on the tongue or buccal mucosa, as well as the hands and feet, including the palms and soles. Uncommonly, the buttocks and genitalia are involved. The vesicles are tender and may ulcerate. However, the vesicles are usually not pruritic, which helps to distinguish them from chickenpox lesions.

Epidemic pleurodynia

On physical examination, edema of the involved muscles and tenderness to palpation may occur.

Acute hemorrhagic conjunctivitis (AHC)

Physical examination findings include subconjunctival hemorrhage. Eye pain, edema of the eyelids, photophobia, and a serous discharge may be present. Slit lamp examination may reveal keratitis.

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Causes

Aseptic meningitis

Coxsackievirus B (serotypes 2-5) and echoviruses account for more than 90% of viral causes of aseptic meningitis.

Exanthems

Coxsackieviruses cause many different types of rashes. Whether the viruses directly cause the rashes or immunologic mechanisms are responsible for the rashes is not known. An exception is HFM, in which viruses are isolated directly from the lesions. HFM is predominantly caused by coxsackievirus A16. In most other instances, rashes can be attributed to coxsackieviruses only if findings on concurrent polymerase chain reaction (PCR) or serology are positive.

AHC

Coxsackievirus serotype A24 generally causes AHC. Transmission usually occurs via contact of contaminated fingers or fomites with the eyes. To prevent further transmission, strict handwashing should be encouraged and sharing of towels should be avoided.

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Contributor Information and Disclosures
Author

Martha L Muller, MD Associate Professor of Pediatrics, Division of Infectious Diseases, University of New Mexico School of Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

John W King, MD Professor of Medicine, Chief, Section of Infectious Diseases, Director, Viral Therapeutics Clinics for Hepatitis, Louisiana State University Health Sciences Center; Consultant in Infectious Diseases, Overton Brooks Veterans Affairs Medical Center

John W King, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Federation for Medical Research, Association of Subspecialty Professors, American Society for Microbiology, Infectious Diseases Society of America, Sigma Xi

Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America

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

Disclosure: Nothing to disclose.

Additional Contributors

Maria D Mileno, MD Associate Professor of Medicine, Division of Infectious Diseases, The Warren Alpert Medical School of Brown University

Maria D Mileno, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, International Society of Travel Medicine, Sigma Xi

Disclosure: Nothing to disclose.

Acknowledgements

Mashiul H Chowdhury, MD Assistant Professor, Department of Medicine, Division of Infectious Disease, Program Director, Infectious Disease Fellowship, Director, TravelHealth Center, Drexel University College of Medicine

Disclosure: Nothing to disclose.

Nhat M Doan, MD Fellow, Department of Internal Medicine, Division of Infectious Diseases, Washington Hospital Center

Disclosure: Nothing to disclose.

Parul Kaushik, MD, MPH Fellow, Department of Medicine, Division of Infectious Disease, Drexel University College of Medicine

Disclosure: Nothing to disclose.

Michael Rajnik, MD Associate Professor, Department of Pediatrics, Program Director, Pediatric Infectious Disease Fellowship Program, Uniformed Services University of the Health Sciences

Michael Rajnik is a member of the following medical societies: American Academy of Pediatrics, Armed Forces Infectious Disease Society, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society.

Disclosure: Nothing to disclose.

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