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Epidemic myalgia

Introduction
Cause
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Diagnosis

Introduction

Introduction Most of the epidemic myalgia is caused by Coxsackie and Echoviruses 1, 6, and 9. Sudden chest pain and/or abdominal pain suddenly appeared. It can be painful for pressure, tingling, knife cutting or tearing. More episodes of seizures, each lasting 1 to 2 hours. There may also be dull pain during the seizure period. The pain can be on one side or on both sides. It can also be accompanied by infections such as fever, sore throat and headache. Epidemic myalgia can be exacerbated by breathing, coughing or rotating position, and can be radiated to the neck and shoulders. The myalgia is different. In severe cases, it can cause shock. When muscle activity is increased, myalgia is intensified. Most of myalgia is in 3~4. After disappearing in the future, the fever will also improve, and the disease will be able to heal itself. Occasionally recurrent episodes, the course of the disease is delayed for several weeks. The clinical manifestation is sudden onset of myalgia, the pain is paroxysmal, and the activity is aggravated. In some cases, the pain is migratory. A few are accompanied by systemic symptoms such as fever, dizziness, fatigue and so on.

Cause

Cause

The Coxsackie virus belongs to the genus Enterovirus of the picornavirus family. The virus particles are spherical or oval, and have a diameter of 22 to 30 nm and are in the form of round particles. The viral genome is a single strand of linear RNA with a total length of about 6000 to 8500 bp, which constitutes the viral core. The outer shell is a 20-faceted body, which is stereo-symmetric and consists of 32 shell particles, each of which contains four shell proteins VP1 to VP4 encoded by viral nucleic acids. A viral gene protein Vpg is bound to the nucleic acid end of the 5th, followed by a non-coding region of about 740 bp in length after Vpg. Coxsackie virus is divided into two groups according to the difference in lesions in suckling mice. There were 24 serotypes in group A, of which type 23 was later classified as Echovirus type 9 and 23 serotypes remained. These serotypes can be distinguished by neutralization tests and complement binding assays. Group A viruses do not share a common antigen, but there is cross-immunity between the types, such as A3 and A8, A11 and A15, A13 and A18 can have cross-sero-reaction; on the contrary, the serotype of 6 B group of viruses There is a common group antigen between A9 and A9. Except for a few strains, Coxsackie virus does not produce hemagglutinin, so it cannot be identified by hemagglutination inhibition test.

Coxsackie virus is highly pathogenic to newborn mice, and group A viruses cause skeletal muscle myositis and flaccid paralysis and die within 1 week. Group B viruses can cause focal distribution of myositis and can cause adipose tissue inflammation, encephalitis, myocarditis, pancreatitis, hepatitis and endocarditis. Chicks often have whole body tremors, spasms and tonic spasms. Older mice can tolerate group B viral infections, but pancreatitis can be induced by the use of adrenocortical hormones. Malnutrition can cause the B3 virus to cause serious diseases in adult mice, including persistent infections in the heart, spleen, liver, and brain, and lymphoid tissue atrophy. The lymphocytes of the immunocompetent mouse are transferred to the malnourished mouse to protect the mouse against the B3 virus and prevent serious consequences. A7, A9 and A16 viruses can also be grown in monkey kidney cell culture. Some group A strains can grow in human amnion cells, Hela cells or RD cell lines, but A1, A19 and A22 viruses fail in any cells. Breeding in culture. Orangutans and monkeys may not develop after infection. The virus appears briefly in the pharynx and blood and is excreted in the feces for 2 to 5 weeks.

The A14 virus causes polio-like lesions in adult mice and monkeys, and the A7 virus causes severe central nervous system lesions and spasms in monkeys. In cell culture, Group B viruses can cause cytopathic effects. The infected cells become rounded, shrunk, the nucleus condenses, reflects, and finally degenerates and falls off. Group A viruses did not produce cytopathic effects.

Examine

an examination

Related inspection

Coxsackie virus antibody anti-Coxsackie B virus IgG antibody muscle tone examination extensor tension test flexor tension test

1. The total number of white blood cells in peripheral blood is normal or slightly increased.

2. Virus isolation is the primary method of diagnosis, with the advantages of savings, speed and accuracy, while avoiding the serotypes encountered by serological methods.

The positive rate of virus isolation from feces is highest, and it can still be positive within 10 days after onset. The virus can be isolated from the blood 36 hours before onset and during fever. People with respiratory tract infections can isolate the virus from throat swabs or gargles. The positive rate of isolated virus in cerebrospinal fluid is lower, but the diagnosis is more significant. Other specimens including pleural effusion, pericardial effusion, urine, muscle biopsy tissue, and autopsy nerve tissue can be sent for examination. The stool specimens can be stored at 4 °C for many days, and other specimens should be kept below -7 °C. The isolation of viruses from the feces and respiratory tract is only of reference because it may be a co-infection. The isolation of viruses from blood, cerebrospinal fluid and pericardial effusion is diagnostic. Therefore, specimens should be collected from multiple sources as much as possible to increase the reliability of the results. In addition to the A9 and A16 serotypes, the Coxsackie A virus can be isolated from the virus by cell culture. The other serotypes need to be inoculated with milk through various routes (subcutaneous, intraperitoneal, intracerebral, etc.) to isolate the virus. Pathological changes were first observed and then confirmed by specific antiserum for neutralization test. Recently, RD cells (human rhabdomyosarcoma cells) strains have been used to isolate and culture Group A viruses other than Coxsackie A1, A19, and A22 viruses. Tissue culture was the first choice for the isolation of Coxsackie B virus. The commonly used cell strains were monkey kidney, human embryonic kidney and Hela cells. The African green monkey kidney (BGM) cell line and RD cell strain were better. After 2 to 5 days, the cytopathic effect was observed for initial diagnosis, and then the specific antiserum was used for neutralization test to identify. The whole process takes about 1 to 3 weeks, but as a clinical diagnosis, it is not necessary to wait for the identification of the serotype.

3. Serological examination due to the large number of serotypes, only in the following cases:

1 The virus has been isolated as a serotype;

2 has been found to have characteristic clinical manifestations such as epidemic chest pain, which clearly indicates when certain antibodies (such as group B viruses) are used to detect antibodies; or when hand, foot, and oral diseases are usually caused by Coxsackie A16 virus;

3 is occurring when a single serotype virus causes epidemics;

4 for sero-epidemiological investigation of a particular serotype.

In the serological test method, the neutralization test is the most specific method for identifying the isolated virus serotype. However, as an antibody for detecting enterovirus infection, the neutralization test is not sensitive enough, and the operation is complicated and expensive. The patient developed neutralizing antibodies at the 2nd week of the disease and peaked after 2 to 3 weeks and remained for 3 to 6 years. The complement binding assay is less specific and has a higher incidence of heterotypic antibodies. However, the complement-binding antibody appears simultaneously with the neutralizing antibody, but only for 2 to 3 months, which can be used as a basis for recent infection. The hemagglutination inhibition test is not very useful, because only 1/3 of the enterovirus produces erythropoietin, and even some strains can be produced in the same serotype, while the other strains do not produce erythrocyte lectin. Recently, it has been reported that IgM-type enterovirus antibodies are detected by immunoblotting, and the positive rate is 60%, most of which are group-specific (22/31), and a few are type-specific. It has been reported that the heat-treated virus is used as an antigen and the synthetic polypeptide is used as an antigen for ELISA detection of IgG antibodies, and the sensitivity (by virus isolation as a control) is 0.67 and 0.62, respectively, which is higher than the complement binding test. Among the 56 cases with negative virus isolation, IgG-ELISA double serum titers were significantly increased in 13 and 19 cases, respectively, for clinical diagnosis. In recent years, it has been reported that the detection of enterovirus RNA in serum by PCR has high sensitivity and specificity, and the positive rate is significantly higher than that of cell culture.

Other ancillary tests: The same virus is isolated from the patient's throat swab. Severe cases can be combined with myocarditis, encephalitis, meningitis, secondary bacterial infection.

Diagnosis

Differential diagnosis

(1) Progressive muscular dystrophy: polymyositis has a rapid onset, can be relieved, has systemic weakness and muscle atrophy, is particularly prone to neck muscles and dysphagia, muscle pain and tenderness, and may have skin Changes and Raynaud's phenomenon, no family history, can identify the identification of muscular dystrophy.

(B) epidemic myalgia: viral infection, the same patient in the epidemic area, mainly respiratory pain and chest muscle tenderness.

(C) myosinuria: systemic or local muscle pain, weakness, urine redness, urinary myosin positive. In addition, attention should also be paid to the differentiation of myasthenia gravis, infectious polyneuritis, and rheumatic polymyalgia.