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Saturday, February 4, 2012

Coxsackie Virus

Coxsackie Virus-What is the Coxsackie virus?

Coxsackie virus is an intestinal viruses (enteroviruses), Coxsackie virus is divided into two types of A and B, Coxsackie virus is a common type of infection with the human respiratory tract and digestive tract virus infection of the future will develop feversneezing, coughing and other flu symptoms. Pregnancy infection can cause non-paralytic polio disease, caused by intrauterine infection and teratogenicity.

Coxsackie virus - an overview of pathology

Coxsackie virus is a highly sensitive neonatal rat suckling mice infected lesions, Coxsackie virus can be divided into a, b two groups. a 23 virus, group b type virus. By type-specific antigen, and test. elisa method can be of various types were identified. All b group and a group of type 9 have a common group specific antigen, cross-reaction between group b virus, and there is no common group-specific antigen but a group of viruses. group a certain type-specific antigen at 37 ° C caused by the human o-erythrocyte agglutination.

Coxsackie virus is an enterovirus (enteroviruses) are divided into A and B are two types of infection during pregnancy can lead to non-paralytic polio lesions caused by intrauterine infection and teratogenicity.


Coxsackie virus - gene structureCoxsackie virus genetic structure of viruses as a single strand RNA viruses, gene-length 7.4kb, bases (G + C) content of about 47%. Both ends of the conserved non-coding region, in the middle of the coding region. The 5 'end of the covalent combination of a small molecule protein Vpg (about 7kDa), and viral RNA synthesis and genome assembly about; 3' end with a polyA tail. Coding region encoding the viral structural protein VP1 ~ of VP4 of EV71, the same CoxV VP1, VP2 and VP3 are exposed on the surface of the viral capsid, and in antigenic sites; of VP4 is located inside the capsid VP1 and receptor binding the VP4 is released, the capsid loose, shelling penetration of the viral genome. 5 'untranslated region of the poly-pyrimidine Area and poly-C District. Various types of featuresConstitute each of the capsid shell particles have four capsid protein, VP1-VP4, have antigenic activity. According to the specific antigen on the difference in its capsid echovirus will initially be divided into 34 subtypes, but later found that Type 1 and Type 8 antigens classified as 10 type reovirus (reovirus), 28 type classified as the nose virus, type 34 is CoxA24 variant, therefore echovirus 34 serotypes from the original re-divided into 30 serotypes. Exists between the various types of cross-immune response. Known to cause HFMD echovirus echovirus type 11, the virus has the ability to agglutinate human type O red blood cells.

Coxsackie virus - symptoms and signs
Coxsackie virus - Coxsackie A41, Coxsackie A9 is a common disease pathogens, and often popular in the summer, often accompanied by meningitis and lung damage, skin rashes common, but no specificity for sporadic erythema, rash, early in the face and neck, and gradually spread to the trunk and upper extremities and the palms and soles. Usually lasts 1-7d, short-term fever, hot back in the rash, and may occur varicella syndrome, namely fever 3-4d, 1-2mm size of the blisters and erythema on the basis of distribution, showing concentric The rash does not scab. Can also be associated with herpes angina, local lymph nodes. They can also occur urticaria and purpura, separable this virus in patients with throat secretions, cerebrospinal fluid, stool and blood.
, Coxsackie A4 can occur prodromal symptoms such as nasal congestion, pharyngitis, salivation, and often a rash of herpes pharyngitis, sustainable-10d, when the heating or hot back rash for 2-5mm size of rash or pimples, mainly in the face and torso (but never seen in the buttocks). About 1-4d of this rash subsided, but may also evolve into a 5-10mm size yellowish opaque blisters in batches found in the trunk to the limbs spread, but does not infringe the palms and soles, no itching, need 1-2 weeks to subside leaving brown pigmentation.


Coxsackie virus - clinical manifestationsCoxsackie virus - Coxsackie A one Coxsackie virus type A infection incubation period of 1-3 days, upper respiratory tract infections, acute onset, runny nose, cough, sore throat, fever, general malaise. The typical symptoms of angina for herpes in the nasopharynx, epiglottis, tongue and soft palate, the Ministry of small herpes, mucous membrane irritation, lymphoid follicular hyperplasia, exudate, enlarged tonsils, accompanied by difficulty swallowing, loss of appetite. According to the survey (R0binson, 1958) associated with oropharyngeal herpes acute fever and rash in 79% Ke Sake A-type virus caused.Rash for herpes and rash, mainly distributed in the peripheral side of the torso, back, limbs on the back, was the eccentric distribution, especially in the face, fingers, toes, back rash more common, so called hand, foot, mouth Triad of ( hand-foot-mouthdi-sease).Coxsackie virus type A infection in children is more common infection in adults accounted for 21.7% (Robinson, 1958). Clinical manifestations In addition to the above, the main features of acute fever, rash. Meningoencephalitis associated with Guillain-Barré syndrome and acute toxic cardiomyopathy (Bell, Grist, 1968,1969). Dominant and latent infection ratio of 1:50-100.Caused by Coxsackie virus B infection the characteristic the infectious Sternocostal pain (epide-micpleurodynia) called Bornholm,'s disease. Can be combined meningoencephalitis, myocarditis, fever, Guillain-Ba-rré syndrome, hepatitis, hemolytic anemia and pneumonia.Three of the Coxsackie virus is a virus from the 1948 Dolldorf and Sickles in Coxsackie town, New York, USA, isolated in the children with faeces from clinically diagnosed as polio. It belongs picornavirus Branch (Picornaviridas), and enterovirus (Enterovirus). Coxsackie virus virion is icosahedral, three-dimensional symmetry, was a ball shape, bare nucleocapsid diameter of about 23-30nm, no envelope, no protrusions, viral nucleic acid and protein composition.Four Coxsackie virus are known to have 30 serotypes. Pathogenic characteristics of the virus to suckling mice and cell sensitivity to the different virus group A and group B, group A viruses have 24 serotypes, ie, A1-A24, A23 type Ech09 virus; group of viruses have six serotypes B1-B6.Group A Coxsackie virus - Coxsackie B 5 Coxsackie virus can cause a flaccid paralysis of the 1-day-old neonatal rat, subsequent breathing slower, weaker, lighter ,12-14h within death, and some cause limb paralysis hair loose and paralyzed. Histopathology: skeletal muscle and extensive damage was edema, amyloidosis, focal necrosis, cell infiltration, when the mice age more than 24h, the mice decreased sensitivity to Coxsackie virus infection. Coxsackie group A virus most type strains can not be cultured cells, but in recent years, studies have reported, the group A virus can be grown on RD cells (rhabdomyosarcoma tumor cells).

Six Coxsackie B virus can cause neonatal rat body weakness, tremors, muscle spasms paralysis, dyspnea, cyanosis and other symptoms before death, generally within 48 hours of death, the survival of mice show developmental disorder and Masonic disorders. Lead to softening of the brain, associated with cysts, the naked eye is swelling of fat in the visible scapular, gray partially transparent areas, some of pancreatitis after intracerebral injection. Histologically, involuntary muscle focal necrosis, inflammatory cell infiltration, adipose tissue degeneration and necrosis. A virus does not cause such lesions, when the mice age more than 48h, the virus infection is greatly reduced. Coxsackie B virus in a variety of cell growth and induce pathological changes leading to cell death, virus release. Based on these characteristics, the most appropriate separation of group A Coxsackie virus to suckling mice, while the separation of the Coxsackie B virus while cell culture method is most appropriate.

Coxsackie virus - Pathogenesis
One pathogen Coxsackie virus, according to its biological characteristics are divided into two categories: Class A and Class B The sub-genus Enterovirus class the Exeter virus (Echovirus) and poliovirus (Poliomyelitisvirus). Now known as the "fine viruses (picoviruses,).
Second, epidemiological Dalldorf and Sickles (1948) was first  (Coxsachie) isolated the virus its name. Melnick (1949) Application of the virus inoculated animals (mice) cause movement disorders, limb flaccid paralysis. Humans caused by the the Polio change of herpes angina and non-paralytic class.Coxsackie virus - treatment
Coxsackie virus hybrid IgM enzyme-linked immunosorbent assay detection interferon group on conventional therapy plus interference injection results, the upper respiratory tract infection CV-IgM positive rate was 25.56%, 24.05% positive rate of the pneumonia group. the CV-IgM-positive children with the flu: the interferon group hot back lower than the control group, significant differences (P <0.05), the CV-IgM positive children with pneumonia: the interferon group hot back time and cure time were lower than control group, significant differences (P <0.05) Conclusion: (1) Coxsackie virus can cause respiratory infections in children, accounting for 25.56 percent of the flu, pneumonia accounted for 24.05%. ② The interferon on the respiratory tract Coxsackie virus infection treatment.

Coxsackie virus - CaseThe daily contact by oral infection is the main route of transmission. Or through water, food, and respiratory tract and through the placenta from mother to fetus. Performance:1, encephalitis and myelitisEncephalitis, fever, headache, vomiting, myalgia 1-2 days of meningeal irritation. CSF cell number (0.1-0.2) × 109 / L, a small number of> × 109 / L,; disease junior high neutrophils dominant, followed by the increased proportion of lymphocytes, normal sugar and chloride, the protein is slightly higher. Some patients have a temporary weakness. Paralyzed little faster recovery. Small number of patients have a disturbance of consciousness, and JE.2, myocarditis, pericarditisMyocarditis often occurs in newborns, more students within one week after onset, acute onset, fever, upper respiratory tract infection symptoms, anorexia, loose stools, followed by difficulty in breathing, lip cyanosis, pale face, tachycardia, re- heart failure soon. Found that adults and older children in recent years are not uncommon. Often precede respiratory symptoms, pericardial involvement, also involving the endocardium, followed by precordial pain, a pericardial friction rub, half of the muscle and joint pain. X-ray significant pericardial effusion, often accompanied by left pleural effusion, ECG showing arrhythmia, conduction block and pericarditis.3, epidemic myalgia, or chest painParoxysmal severe muscle pain, can affect the muscles. Adults and older children to have chest pain, often in the hypochondrium, may be involved in the shoulder; infants and young children abdominal pain more common, mostly in the upper abdomen, occasionally misdiagnosed as appendicitis. In addition, there are fever, sore throat, headache, anorexia, vomiting and diarrhea and so on.4, herpes anginaFever, sore throat, throat gray herpes rupture to form superficial ulcers, the minority can be seen in the vulva, may also have headache, nausea, vomiting, abdominal pain. Another for children with acute lymphoid nodules pharyngitis, throat gray or pale yellow Summary, do not form herpes and ulcers.- Respiratory tract infections, respiratory infectionsUpper respiratory tract infection is the most common, but also can cause laryngitis, tracheitis, bronchitis and bronchiolitis and pneumonia.6, infant diarrheaYellow-green water will dilute several times a day, no pus and mucus.7, rash and feverFever, rash, rash, maculopapular rash, urticaria, herpes, petechiae, etc.. Itching, desquamation. Small number of cases in the hands, feet, skin and oral mucosal herpes. Also known as hand, foot and mouth disease.8, neonatal systemic infectionRapid-onset, poor feeding, vomiting, convulsions, dyspnea, cyanosis, arrhythmias, heart and liver can be dramatically swollen. High mortality rate. The autopsy visible encephalitis, myocarditis, hepatitis, pancreatitis, and adrenal lesions.The current lack of effective antiviral drugs. Attention to rest, symptomatic treatment for the clinical manifestations. Prevent secondary infection. Do a good job of manure management, improve the environment and food hygiene and develop good personal hygiene habits.