Coxsackie Virus (cont.)
Charles Patrick Davis, MD, PhD
Dr. Charles "Pat" Davis, MD, PhD, is a board certified Emergency Medicine doctor who currently practices as a consultant and staff member for hospitals. He has a PhD in Microbiology (UT at Austin), and the MD (Univ. Texas Medical Branch, Galveston). He is a Clinical Professor (retired) in the Division of Emergency Medicine, UT Health Science Center at San Antonio, and has been the Chief of Emergency Medicine at UT Medical Branch and at UTHSCSA with over 250 publications.
William C. Shiel Jr., MD, FACP, FACR
Dr. Shiel received a Bachelor of Science degree with honors from the University of Notre Dame. There he was involved in research in radiation biology and received the Huisking Scholarship. After graduating from St. Louis University School of Medicine, he completed his Internal Medicine residency and Rheumatology fellowship at the University of California, Irvine. He is board-certified in Internal Medicine and Rheumatology.
In this Article
- Coxsackie virus facts
- What is coxsackie virus?
- What are the types of coxsackie viruses, and what can they cause?
- What are coxsackie virus infection symptoms and signs?
- How do people get infected with coxsackie virus?
- What are the risk factors for coxsackie virus infection?
- How are coxsackie virus infections diagnosed?
- Is there any treatment for coxsackie virus infection?
- Can coxsackie virus infections be prevented?
- What is the prognosis of coxsackie virus infections?
- Childhood Illnesses You Should Know Slideshow
- Enterovirus D68 Slideshow
- Bacterial Infections 101 Slideshow
What are the types of coxsackie viruses, and what can they cause?
Coxsackie viruses are separable into two groups, A (CVA) and B (CVB), which are based on their effects on newborn mice (coxsackie A results in muscle injury, paralysis, and death; coxsackie B results in organ damage but less severe outcomes.) There are over 24 different serotypes of the virus (having distinct proteins on the viral surface). Coxsackie viruses infect host cells and cause host cells to break open (lyse).
Type A viruses cause herpangina (painful blisters in the mouth, throat, hands, feet, or in all these areas). Hand, foot, and mouth disease (HFMD) is the common name of this viral infection. Coxsackie A 16 (CVA16) causes the majority of HFMD infections in the U.S. It usually occurs in children (age 10 and under), but adults can also develop the condition. This childhood disease should not be confused with the "foot and mouth disease" usually found in animals with hooves (for example, cattle, pigs, and deer). Type A viruses also cause inflammation of the eyelids and white area of the eye (conjunctivitis).
Type B viruses cause epidemic pleurodynia (fever, lung, and abdominal pain with headache that lasts about two to 12 days and resolves). Epidemic pleurodynia is also termed Bornholm disease. There are six serotypes of coxsackie B (1-6, with B 4 considered by some researchers as a possible cause of diabetes in a number of individuals).
Both types of viruses (A and B) can cause meningitis, myocarditis, and pericarditis, but these occur infrequently from coxsackie infections. Some researchers suggest coxsackie virus (mainly coxsackie B4) has a role in the development of acute onset type I (formerly known as juvenile) diabetes, but this relationship is still under investigation.
Coxsackie viruses and other enteroviruses may cause the childhood disease of hand, foot, and mouth disease. However, the majority of children with coxsackie virus infections completely resolve the symptoms and infection in about 10-12 days.
Enterovirus 71, like coxsackie virus, also causes HFMD. In Asia in July 2012, particularly Cambodia, children infected with enterovirus 71 (EV-71) had a high mortality rate. This epidemic (mainly in babies, toddlers, and children under 2 years of age) is still under intense investigation, and it is likely researchers will have a better understanding of this high death rate linked to EV-71. The research is ongoing and some investigators have suggested that mortality in children occurs from a combination of enterovirus 71, Streptococcus suis, and dengue viral coinfections. Treatment with steroids was also implicated in the disease process.
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