Microvirus B19 Infectious Rheumatism
Introduction
Introduction to microvirus B19 infectious rheumatism The microvirus B19 (parvovirus B19) is a new virus that has been gradually recognized by people. It was first identified by YvonneCossart in 1975 in the serum of the B19 HBsAg control. It was found to be a different type of HBsAg. Antigen. After electron microscopy, the antigen contained in the serum recognized a spherical particle and a typical viral enzyme shell. The new virus was originally found in the serum of healthy donors, and its antigen has a suspension density of 1.36 to 1.40 in the cesium chloride gradient electrophoresis, which is a typical micro-virus enzyme. In 1985 they studied the pathogenic role of the virus. It has been confirmed that microvirus B19 can cause rheumatism. basic knowledge The proportion of illness: 0.005% Susceptible people: no special people Mode of infection: non-infectious Complications: hemolytic anemia, thalassemia, autoimmune hemolytic anemia, glucose-6-phosphate dehydrogenase deficiency, hereditary spherocytosis, meningitis
Cause
The cause of microvirus B19 infectious rheumatism
(1) Causes of the disease
Micro-virus B19 arthropathy is a pathogenic and well-defined chronic joint disease. The micro-virus B19-specific DNA is found in the chronic micro-virus B19 joint synovial biopsy tissue and in the patient's bone marrow puncture by PCR. Other researchers are chronic. The micro-virus B19 is positive in the synovial fluid of the micro-virus B19 joint disease. The micro-virus B19 persists in the patient because the virus evades the host's immune surveillance and selective antibody-deficient state, that is, the lack of neutralization and clearance in the body. The antibody of microvirus B19, as to how microvirus B19 causes joint damage and other system damage, is the direct toxic effect of the gene product of the virus, or the immune complex of the gene product or the cross-immunization reaction of the gene product causes autoimmunity The tissue damage has not been covered in the current literature.
(two) pathogenesis
It has been confirmed that the cell receptor of B19 is a myelin glycoprotein, which is a blood group antigen, which is a major component of the erythrocyte membrane. This receptor glycoprotein acts as a membrane receptor for toxins, viruses and bacteria. It plays a pathogenic role in many infectious diseases. This receptor is present in many kinds of tissue cell membranes, especially in the mesoderm tissue membrane. Therefore, cells derived from mesoderm are easily involved, such as liver, tissue cell B19 receptor. The high correlation of expression binding to B19 envelope DNA and high affinity has been confirmed in B19-related diseases.
Pathology: There is no B19-related histopathological data in the literature.
Bone marrow examination of patients with aplastic anemia crisis showed that the red blood cell line was significantly reduced, and other cell lines did not change greatly. Therefore, it is believed that the virus mainly invades the red blood cell line in the bone marrow hematopoietic system, and the original stage of red blood cells may be the main target cell. The globoside on red blood cells is a viral receptor. After infection, the red blood cells can be lysed by the virus, which leads to the reduction of red blood cells. This inhibition of bone marrow hematopoietic function lasts for 1 week, and may have a slight effect on normal hematopoietic function. However, patients with hemolytic anemia with shortened red blood cell life may have the possibility of causing aplastic anemia. In addition, the virus can invade various organs and tissues of the body, and has died from the heart, brain, and liver of people who are seriously infected with B19. B19 DNA was detected in tissues such as kidney, lung and spleen. Electron microscopy showed a virus in the myocardium of the myocarditis. The virus was found in the vascular endothelial cells, sweat glands and ductal epithelial cells. The virus may have a direct pathogenic effect, and the B19 virus infection may cause the production of cytokines such as interferon gamma, IgM and IgG specificity. The appearance of the body can cause immune-mediated pathological changes, and joint disease may be caused by immune complexes. Many studies have shown that some patients after B19 infection may be chronic diseases and/or long-term carrying viruses, and immune function is the main reason. The immune function is also normal, there are long-term carriers, the reason is not clear, some people detected B19 DNA from the bone marrow of healthy donors, so it is possible that the bone marrow is the place where B19 virus survives for a long time.
Prevention
Microvirus B19 infectious rheumatism prevention
1. Remove infected lesions, pay attention to hygiene, strengthen physical exercise, and improve autoimmune function.
2. The law of life, work and rest, comfortable, avoid strong mental stimulation.
3. Strengthen nutrition, fasting and cold, pay attention to warming.
4. Secondary prevention early diagnosis, early treatment.
5. The vaccine has been developed for animal testing and is expected to be used for prevention in the future.
Complication
Microvirus B19 infectious rheumatism complications Complications hemolytic anemia thalassemia autoimmune hemolytic anemia glucose-6-phosphate dehydrogenase deficiency hereditary spherocytosis meningitis
Patients with sickle cell anemia, hemolytic anemia such as alpha-thalassemia, beta-thalassemia, autoimmune hemolytic anemia, glucose-6-phosphate dehydrogenase deficiency, hereditary spherocytosis and iron agranulocytic anemia After the recent infection with B19, a transient aplastic anemia crisis can be complicated, and aseptic meningitis and encephalopathy can also be reported.
Symptom
Micro-Virus B19 Infectious Rheumatic Symptoms Common Symptoms Skin Itching Fetus Edema Hemolysis Anemia Morning Stiffness Freckles Anorexia Chilling Pleural Effusion Toxic Bursal
Infected with B19 for one week to form viremia, peak viremia occurred on the 89th day, the incubation period is 6 to 18 days, and individual can be up to 28 days. The clinical symptoms after infection are two-way, namely viremia and antibody formation. During the viremia period, some patients are asymptomatic, and some patients have symptomatic symptoms: short-term fever, general malaise, muscle pain, headache, itchy skin and chills, followed by rash, multiple joint pain or more Arthritis, accompanied by an anti-B19 IgM antibody reaction period in vivo to eliminate viremia, most patients have no infection when they go to hospital for rash and joint symptoms. After acute infection, anti-B19 IgM antibody lasts for 23 months. After a gradual decline, the anti-B19 IgG response period can persist for a long time, but no diagnostic significance.
Main performance
(1) Transient aplastic anemia crisis: Pattison et al. first described the clinical syndrome of microvirus B19. It was confirmed by clinically that a sickle cell anemia patient developed a transient aplastic anemia crisis after newly infected B19. A transient aplastic anemia crisis occurred in other chronic hemolytic anemia and reticulocytes stopped regenerating, but after 7 to 10 days after retinal erythrocyte cessation of regeneration, it clearly rose back to a critical level in patients with chronic hemolytic anemia. In the case of periodic recurrence of reticulocytes, there should be a high degree of suspicion of viral infections, especially B19 infection. It has been confirmed that 70% of patients infected with B19 have a transient aplastic anemia crisis. In these patients, red blood cell regeneration stops in the giant red blood cell phase. At this time, marginal intracellular inclusions can be seen in giant red blood cells, other hemolytic anemia such as -thalassemia, -thalassemia, autoimmune hemolytic anemia, glucose-6-phosphate dehydrogenase deficiency, hereditary A transient aplastic anemia crisis can occur after infection with B19, such as spherocytosis and iron myocyte anemia.
(2) Infectious erythema: 80% of patients have facial infectious erythema after infection with B19. They can also be located in the trunk and limbs. The appearance of the lesions is banded and reticulated. It can also be a maculopapular rash with high local skin. Occasionally, the rash is Hemorrhagic purpura, blisters, about half of the patients have itchy skin, most patients have a tendency to relapse after the skin lesions subsided, which is induced by sun exposure, hot bath and excessive fatigue, when the systemic symptoms are fatigue, headache, sore throat, cough , fever, anorexia, vomiting, diarrhea and joint pain, etc., the recurrence of rash is directly related to viremia.
(3) Arthritis: mainly seen in adults, especially in adult women. Acute arthritis is mostly symmetrical. It usually starts from the hand or knee joint and affects other joints such as wrist, ankle, foot and elbow after 2 to 3 days. And the shoulder joint, but the entire spinal joint is less involved, arthritis is pain, stiffness, varying degrees of swelling, usually relieved within two weeks, but there are still varying degrees of persistent joint symptoms after remission; about half of the patients are present Joint symptoms, accompanied by general malaise, fever, skin lesions and gastrointestinal symptoms, these symptoms often occur with the deterioration of joint symptoms. Unlike rheumatoid arthritis, arthritis usually does not cause erosive damage. However, the distribution of joint involvement, symmetry and morning stiffness are similar to rheumatoid arthritis. About half of the patients have chronic progressive arthritis, which is in line with the American College of Rheumatology diagnostic criteria for rheumatoid arthritis. The typical patient's morning stiffness lasts for more than 1 hour. , upper limb knuckles, wrist joints and wrist joints are symmetrically involved, if there are different titers of autoantibodies such as RF, anti-DNA antibodies, anti-nuclear antibodies and anti-drugs in the acute phase Lymphocyte antibodies suggest a diagnosis of rheumatoid or lupus erythematosus or this autoimmunity secondary to B19 infection.
(4) fetal edema: about 30% of pregnant women infected with B19, can cause fetal infection, but 10% of the fetus in public places infected with B19 can cause serious consequences, the life of infected fetus red blood cells is shortened to 45 to 70 days, fetal infection B19 can occur again Dangerous crisis, causing high discharge heart failure, resulting in secondary soft tissue edema and ascites, pleural effusion, some pregnant women with polyhydramnios caused by fetal non-immune edema, also reported that B19 caused fetal viral cardiomyopathy and ultimately Caused by fetal edema, there are also reports of congenital syndrome in the fetus, characterized by anemia, thrombocytopenia, cardiac insufficiency and liver dysfunction.
(5) Bone marrow suppression: patients with congenital or acquired immunodeficiency may not completely clear B19 viremia; cases of congenital immunodeficiency (such as Nezelof syndrome), lymphoblastic leukemia, acute lymphocytic leukemia, chronic medulla Sexual monocytic leukemia, other cancers, AIDS and neonatal immune system hypoplasia, all of which are consistently infected with B19 and myelosuppression, while immunologically normal host anti-B19 IgM antibodies last only about 2 months, anti-B19 IgM antibodies and acute The anti-B19 IgG antibody response recognizes the Vp2 (viral surface protein 2) epitope, and the V19 (viral surface protein 1) epitope is recognized by the anti-B19 IgG antibody during convalescence.
2. Secondary performance
(1) Skin: B19 infection can cause several kinds of skin damage, mainly manifested as pustular papules with folliculitis-like changes, red blood cells infiltrating into the dermis to make pustules hemorrhagic papules, although some patients are caused by thrombocytopenia Purple spot or ecchymosis, but a similar pattern of Henoch-Schölein purpura-like rash occurs when there is no significant change in platelets. The most obvious feature of skin lesions is a clear dermatosis in the wrist and ankle. It is called a glove sock syndrome. Edema and itching occur in the damaged part, and local desquamation occurs after the skin lesion subsides, but the syndrome can also occur in other viral infections.
(2) Nervous system: manifested as peripheral neuropathy, can also be expressed as abnormal finger sensation, occasional toe numbness, progressive arm weakness, aseptic meningitis and encephalopathy can also occur, fibromyalgia can also occur disease.
(3) Reticuloendothelial system: It is reported that B19 infection can also develop benign and self-limiting systemic lymphadenopathy, and lymph node enlargement with blood cell phagocytic syndrome is similar to necrotizing lymphadenitis.
Examine
Examination of microvirus B19 infectious rheumatism
1. In the viremia period, blood routine examination can be seen with neutropenia, thrombocytopenia or anemia. Sometimes there are 3 bloodlines reduced and reticulocytes decreased with aplastic anemia. Individual cases can be normal blood. In patients with idiopathic thrombocytopenic purpura, various hemolytic anemia changes can be seen in patients with hemolytic anemia.
2. Biochemical examination Most patients showed transient transaminase elevation in acute joint disease, and individual biochemical changes of fulminant hepatic insufficiency, such as elevated blood ammonia, children's cases may show acute hepatitis changes such as elevated bilirubin , elevated transaminase, etc.
3. Specific serological examination
(1) Enzyme labeling method:
1 coated with solid anti-human IgM or IgG in solid phase;
2 after the serum containing IgM or IgG is kept warm on the reaction plate;
3, then rinse off too much antibody, finally add B19 antigen to be determined, use 125I-labeled anti-mouse B19 monoclonal antibody to determine B19 antigen, in order to detect antibody, add the test serum to b, and add virus serum known to contain B19 (positive control), the reaction plate designed for the detection of anti-B19 serum was coated with goat anti-human IgM (or lgG) antibody. After incubation for 24 h, the reaction plate was washed with a buffer containing non-ionic detergent and added to the test. Serum, after re-incubation, rinse the reaction plate, then add the antigen to the reaction well, and add the negative serum in parallel to the negative control well. After 24 hours of incubation, rinse the reaction plate again, then add anti-B19 monoclonal antibody, then keep warm and After washing, the catalase-conjugated goat anti-mouse IgM antibody is added, and then washed and incubated, the color change occurs in the presence of catalase, and the reaction is stopped with sulfuric acid. The serum sample to be tested is inactivated with the B19 antigen and exceeds the negative. The control was positive for 3 standard deviations, and the antibody capture enzyme labeling method was characterized by high specificity and strong sensitivity.
(2) Polymerase chain reaction (PCR): It is a particularly sensitive DNA amplification reaction that has been applied to the DNA of B19 specimens. This method is suitable for the original immunodeficiency disease and persistent infection with B19, and the virus level in the body is special. In low patients, the interpolated probes were found to be sensitive to the direct hybridization of the template virus, but there is still a problem in the detection of B19 in clinical specimens by PCR, that is, the inhibitor of the primer polymerase is present in the specimen, and the inhibition is eliminated. The method of pre-heating the sample before amplification, decontamination extraction of DNA and Nest amplification in the specimen.
Electromyography: In the acute phase, there is a decrease in nerve conduction velocity and a decrease in motor and sensory nerve potential.
Diagnosis
Diagnosis and identification of microvirus B19 infectious rheumatism
diagnosis
Diagnosis depends mainly on clinical manifestations and specific serum tests.
Differential diagnosis
1. Scarlet fever: a streptococcal infectious disease with early flu symptoms, diffuse dense scarlet rash, distributed in the neck, axilla, groin, and rarely seen at the extremities, generally without arthritis. It has a good effect on the treatment of penicillin. The rash of this disease is mainly located on the face, at the extremities of the extremities. It can be seen with pruritus and edema with edema, and there are always hematological changes, and there are many obvious polyarthritis, which is not effective for penicillin treatment.
2. Rheumatoid arthritis: joint swelling, pain, morning stiffness, rheumatoid factor positive, erythrocyte sedimentation rate increase, rheumatoid nodules, X-ray examination of joint erosion, the above characteristics are not seen in this disease .
3. Exudative erythema multiforme: Although there are prodromal symptoms of upper respiratory tract infection, rash also has blister, but mucosal skin may have ulcers and pseudomembrane formation, skin lesions are particularly obvious at the junction of skin and mucous membranes, generally no systemic symptoms. There is no mucosal ulcer and pseudomembrane in this disease, and there is no obvious characteristic of mucosal skin junction, so the two are not difficult to identify.
