Updated: Dec 08, 2020
  • Author: Irina Petrache, MD; Chief Editor: Zab Mosenifar, MD, FACP, FCCP  more...
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Pleurodynia (formerly called Bornholm disease) is a form of viral myalgia defined by the sudden occurrence of lancinating chest pain or abdominal pain, commonly associated with fever, malaise, and headaches. It is usually an uncommon complication of coxsackievirus B infection; however, cases of pleurodynia secondary to other enteroviruses have been reported (eg, enteric cytopathogenic human orphan [ECHO] virus). Coxsackievirus B is an RNA Enterovirus, which usually causes an asymptomatic or brief upper respiratory tract or gastroenteric infection. In rare cases, other severe sequelae of coxsackievirus B infection develop, including meningitis and carditis. [1]

Diagnosis of pleurodynia is made on clinical grounds. Negative serology does not rule out the disease. No specific treatment exists. The pain typically lasts 1 to 4 days, although pain lasting as long as 45 days has been described. [2] Management is supportive and includes nonsteroidal anti-inflammatory drugs (NSAIDs) for pain and pleurisy (if present) or peripheral nerve block (eg, intercostal nerve) with 1% lidocaine (Xylocaine) infusion.

Also see the article Coxsackieviruses.

For patient education resources, see the Lungs Center and Coxsackievirus Infection.



The striated muscle is the actual anatomic structure targeted by the coxsackievirus B and is responsible for the attacks of severe chest pain. Therefore, the term pleurodynia may be a misnomer because only some patients with the condition actually develop pleuritis (ie, inflammation of the pleural surface). In patients with pleurodynia, the striated intercostal muscles necrose, which explains the frequent elevations in serum creatine kinase levels. Some of the more chronic sequelae, such as myocarditis, dermato-polymyositis, chronic fatigue syndrome, and possibly, juvenile-onset diabetes type I, are believed to be immune mediated.

The virus has an incubation time of 1 week in the gastrointestinal tract and then, through hematogenous dissemination, involves the target organs, most commonly the skeletal muscles but also the central nervous system (CNS) (ie, meningitis, encephalitis) and myocardium (ie, carditis with or without associated pericarditis). Coxsackievirus B can be recovered in the stool or pharynx for up to 2 weeks after the resolution of the symptoms.



The classic etiologic agent for pleurodynia is coxsackievirus B, serotypes B1, B2, B3, B4, and B5, [3] which are small, nonenveloped RNA viruses, in which an icosahedral capsid encloses the single-stranded RNA genome. Other nonpolio enteroviruses, including echoviruses type 6 and 19, coxsackievirus A, and human parechovirus type 3 (HPeV3), [4] are also reported to cause syndromes very similar to that of coxsackievirus B infection, including pleurodynia.

A rare case of echovirus 1-caused pleurodynia was reported in a 31 year old woman in the Netherlands who fell is a few days after returning from a 1 month backpacking trip to Thailand, Indonesia and Malaysia. The cause was determined by stool culture and confirmed by polymerase chain reaction (PCR) and direct genotyping. [5]

Humans are the only known reservoir of the enteroviruses; transmission occurs via the fecal-oral route. The incubation time is usually 2-5 days. Potential risk factors for the transmission of the enteroviruses are poor sanitation and overcrowding. Intrafamilial spread is common.



United States

Coxsackievirus B was present in 24% of the 18,000 enteroviruses isolated and reported in the United States from 1970-1979. [6] The estimated number of nonpolio enteroviral symptomatic infections is 5-10 million per year. In regions of temperate climate, the infection is seasonal, with about 90% of infections occurring in the summer and early fall, and sometimes infections occur in epidemics.


Antibodies to coxsackievirus B serotypes are present in 75% of the population in developed countries. In the tropical and subtropical climate areas, the prevalence of the enteroviral infections is year-round.

Sex- and age-related demographics

Males are more commonly affected than females.

The incidence of coxsackievirus B infection in neonates is 1 in 2000 live births. Coxsackievirus B infection occurs most commonly in children younger than 15 years; half of these patients are younger than 5 years, and 30% are younger than 1 year. The disease is rare in patients older than 60 years. However, pleurodynia most commonly affects adults infected with the virus, with fewer than 10% of cases occurring in patients younger than 20 years. Of 372 prospectively studied children aged 4-18 years with nonpolio enteroviral infections, only 3% developed pleurodynia. [7] In contrast, 30 of 78 mostly adult patients with coxsackievirus B-associated cardiac disease had pleurodynia. [8] Therefore, the location of pain is believed to be predominantly abdominal in children and thoracic in adults.



The prognosis for pleurodynia is good, with complete recovery in most cases. The return to normal health may be gradual after a period of weakness and fatigue. No deaths are reported as a direct result of pleurodynia. The severity of the coxsackievirus B infection is highest in infants and children. In infants who develop coxsackievirus B infection, 10% die, usually within the first 4 weeks of life most commonly from cardiac involvement. Fulminant hepatic failure, sepsis syndrome, and severe CNS involvement with seizures and apnea are also potential complications in this age group. [9]


Direct complications of pleurodynia are rare. Splinting from pain may result in atelectasis and shortness of breath.

A postviral syndrome, also called fatigue-dysphoria syndrome, is described in children who were seropositive for coxsackievirus B and who complained of fatigue, weakness, sore throats, and dysphoria. This syndrome may also complicate the patient's recovery.

In rare cases, coxsackievirus B infection may be complicated by carditis, [10] aseptic meningitis, constrictive pericarditis, orchitis, myalgic encephalomyelitis, severe neonatal encephalitis with seizures, [11] hemorrhagic conjunctivitis, hepatitis, pancreatitis, and juvenile-onset diabetes mellitus.

Dilated cardiomyopathy is a complication of viral myocarditis. It may be acute or related to severe muscle necrosis, or it may occur several years later, possibly due to chronic inflammation and fibrosis as a result of an immune-mediated process. [10]