Coxsackie virus eruption refers to spots and papules caused by Coxsackie virus. Coxsackie virus A and B causes different clinical symptoms respectively.


Coxsackie virus eruption is caused by Coxsackie virus.

Coxsackie virus (CV) is an enterovirus, a small RNA virus, and can be divided into group A and B. Coxsackie virus can cause viral myocarditis, aseptic meningitis, epidemic myalgia, polymyositis, Type 1 diabetes, upper respiratory tract infection, and acute hemorrhagic conjunctivitis.


Coxsackie virus infects humans through fecal-oral, respiratory, and insect-borne transmissions, forming viremia. Main targets are meninges, heart, skin, and muscles, but any organ in the body can be involved, and clinical manifestations are varying.

Signs and Symptoms

Skin lesions caused by Coxsackie A virus

Coxsackie virus A9 is a common causative pathogen, often prevalent in summer, and patients are often accompanied by meningitis and pulmonary lesions. Skin lesions are common but not specific, can be scattered erythema, maculopapular rash, and occur initially in the neck and face, spreading gradually to the trunk, upper limbs, palms, and soles, persisting for 1 to 7 days. Short-term fever may be present, but fever is reduced after eruption. Varicella syndrome may occur, that is, after 3 - 4 days of high fever, pinhead sized centripetal blisters occur on the basis of erythema, and skin lesions cannot scab. Herpangina may occur, with local lymphadenopathy. In addition, urticaria and purpura may occur. The virus can be isolated from throat secretions, cerebrospinal fluid, stool, and blood of patients.

Coxsackie virus A4 can cause prodromal symptoms such as nasal congestion, pharyngitis, and salivation, often accompanied by herpangina, persisting for 1 to 10 days. Eruption occurs during or after fever and is manifested by pinhead sized spots or pimples, mainly in the face and torso, but never in the buttocks. Skin lesions subside in about 1 to 4 days, but can also evolve into pea sized, clustered, pale yellow opaque blisters in the trunk, spreading to the limbs, but without invasion of palms and soles, without pruritus, regressing in 1 to 2 weeks, leaving brown pigmentation.

Coxsackie virus A16 can cause Gianotti-Crosti syndrome-like lesions.

Skin lesions caused by Coxsackie B virus

Coxsackie virus B1 can cause prodromal symptoms such as fever, headache, and aseptic meningitis, can cause exanthem subitum-like spots and maculopapular rash, and can occasionally cause hand, foot, and mouth disease-like symptoms and herpangina, more common in children.

Coxsackie virus B2 can cause maculopapular rash, blisters, or ecchymosis while fever, often only in the abdomen. Ulcers can occur in the mouth, and are often complicated by muscle pain, respiratory or gastrointestinal symptoms.

Coxsackie virus B3 can cause prodromal symptoms such as fever, headache, and diarrhea, as well as hepatolienomegaly. About 25% of children patients may have eruption, mainly manifested by maculopapular rash, blisters, and petechiae, with or without nodules and ulcers, as well as hand, foot, and mouth disease-like eruption, pneumonia, myocarditis, and hepatitis. The virus can be isolated in blister fluid, pharyngeal secretions, and stool, and the neutralizing antibody titer in serum is also increased.

Coxsackievirus B5 is also a common causative pathogen and often causes encephalitis, myocarditis, pericarditis, peritonitis, sputum, orchitis, herpangina, hepatitis, and cervical and occipital lymphadenopathy. Eruption can occur after fever and is manifested by spots and pimples, initially in the face and neck, gradually expanding to the trunk and limbs in 4 to 24 hours, without invasion of palms and soles. It has also been reported that Coxsackievirus B5 can cause vesicular stomatitis with polymorphous erythema, with blisters in the mouth and lips.


On the basis of medical history, clinical manifestations, and results of viral detection, a diagnosis can be provided.


Coxsackie virus is not sensitive to antibiotics and chemicals, and specific treatment is absent.

Symptomatic treatment is applied. On the basis of general treatment and supportive therapy, interferon and ribavirin can be administered in severe patients, and digitalis therapy can be used as early as possible in the case of heart failure. Appropriate antimicrobial agents can be administered to prevent secondary bacterial infections.


In general, good prognosis is present. Even with meningitis and encephalitis, most patients can recover quickly within few days. Only a small number of patients are healed in several weeks. Although loss of muscle tone is more common, it can recover quickly. Only about 5% of patients with meningitis can have sequelae of muscle tonus and mental retardation. Systemic infections, myocarditis, and pneumonia in infants and young children have a poor prognosis and a high mortality rate. The mortality rate of serious infections in newborns can reach 80% to 90%. The prognosis of myocarditis in older children and young adults is better. Most patients recover completely after appropriate treatment, and few patients develop into chronic myocarditis. Few patients may develop progressive cardiomegaly, cardiac dysfunction, arrhythmia, and thromboembolism.


In the absence of selenium and vitamin E in the human body, Coxsackie virus is susceptible to point mutations, causing phenotypic changes, resulting in enhanced pathogenicity. Therefore, supplements of vitamins and trace elements can help to prevent Coxsackie virus infection.