infantile rash
Introduction
Introduction to children's acute rash Children's acute rash, also known as baby rose rash, burns rash, is an acute rash-borne infection commonly caused by human herpesvirus type 6 and 7 infections in infants and young children. The clinical features are high fever for 3 to 4 days, then sudden fever and rash, usually within a few hours, the endothelium begins to subside, disappears within 2 to 3 days, without pigmentation and peeling. The prognosis is good and they all heal themselves. basic knowledge The proportion of illness: 30% Susceptible people: children Mode of infection: non-infectious Complications: high fever in children, convulsion in children, thrombocytopenic purpura
Cause
Child rash cause
(1) Causes of the disease
At present, HHV-6 is considered to be the main cause of the disease, but it is not the only pathogen. HIV-7 infection can also cause this disease. HHV-6 can also cause acute febrile illness without rash in infants.
1.HHV-6 Salahuddin of the United States is equivalent to the isolation of a new virus from peripheral blood mononuclear cells (PBMCs) in 6 patients with various lymphoproliferative disorders in 1986. Subsequent studies have demonstrated that its genetic configuration is specific to human herpesviruses. It is 66% homologous to CMV and belongs to the -herpesvirus family. In 1987, it was named HHV-6.
HHV-6 was isolated from peripheral blood polymorphonuclear leukocytes in ES patients in 1988, and then isolated from ES patients with CD4+, CD8+, CD3+, monocytes/macrophages, and HHV-6 was isolated. Neutralization test was used to determine different stages of ES disease. The HHV-6 antibody has a positive rate of 18% to 100%. It has been confirmed that HHV-6 infection is the cause of ES. Most of the ES is caused by HHV-6B infection, and is rarely caused by infection in group A.
HHV-6 has the morphological characteristics of a typical herpesvirus family. The virus particles are round, consisting of 162 shells composed of a icosahedral symmetrical nucleocapsid with a diameter of 90-110 nm. The outer layer is composed of a cortex and a cortical layer. ~40nm; the outermost layer is covered with a lipid membrane, the surface has irregular glycoprotein protrusions, the core is linear double-stranded DNA entangled around a core protein to form axon; the mature released virus particles are 180-200 nm in diameter.
2. HHV-7 Frenkel is equivalent to the isolation of HHV-7 from a healthy adult peripheral blood T lymphocyte for the first time in 1990. Thereafter, the virus is isolated from a patient with chronic fatigue syndrome. The virus particle diameter is about 200 nm, HHV. -7 has a capsule, and belongs to the -herpesvirus family together with HHV-6 and CMV.
(two) pathogenesis
HHV is affinitive to lymphocytes.
1. HHV-6 HHV-6 has a genome of 163-170 kb and can encode more than 70 kinds of products, including early immediate proteins IE-A and IE-B. HHV-6 has two variants, variants A and B. The homology of the two variants at the nucleotide level is 95% to 99% in the most conserved genes, and 75% in the most differential regions. It is suggested that these two variants of HHV-6 should be included. Two different genera, different variants may have different eosinophilic effects in infecting children or adults. Similar to other herpes viruses, HHV-6 causes a primary infection in humans, and after the infection has subsided, the genome of the virus can be The host cell is chronically latent, and the virus has several glycoproteins, of which the gH glycoprotein may play a major role in the infection of the virus into the cell and the fusion of the infected cells.
The nucleic acid of HHV-6 is mainly lurking in the gland of peripheral blood mononuclear cells, salivary glands, kidneys and bronchi. Under certain conditions, HHV-6 can be activated and cause reinfection. The mechanism of HHV-6 activation is still unclear. HHV-6 can be activated when HIV, Epstein-Barr virus, measles virus, and cytomegalovirus infection are present in the body.
HHV-6 cannot be distinguished from other herpesviruses by electron microscopy, but can be distinguished from other herpes viruses by DNA hybridization, PCR or HHV-6 specific polyclonal or monoclonal antibodies by immunofluorescence antibody method. HHV- 6 Although it is closest to the cytomegalovirus in the herpesvirus genus, there is no antibody cross-reactivity between the two viruses.
2. HHV-7 gene study showed that HHV-7 has high homology with HHV-6 and HCMV DNA. HHV-7 can be cultured in cord blood mononuclear cells and normal human peripheral blood lymphocytes. The method is similar to HHV-6. HHV-7 has a strong affinity for T lymphocytes, and this virus is also often found in the saliva of healthy adults.
Prevention
Childhood acute rash prevention
The isolated child was not contagious 5 days after the visit. Avoid going to public places during the epidemic.
Complication
Childhood acute rash complications Complications, children with high fever, convulsions, thrombocytopenic purpura
Can cause febrile seizures, occasional reports of concomitant encephalitis and thrombocytopenic purpura.
Symptom
Children's acute rash symptoms Common symptoms Herpes rash appetite hypothermia hyperthermia chronic congestion convulsion
The incidence of infection is mostly within 2 years old, especially within 1 year old, and the incubation period is generally 5 to 15 days.
1. During the febrile period, it usually has high fever and lasts for 3 to 5 days. It can be accompanied by convulsions in the early stage of high fever. In addition to loss of appetite, restlessness or mild cough, the signs are not obvious. Only the pharynx and tonsils are mildly congested and head and neck. Superficial lymph nodes are slightly enlarged, showing high fever and mild symptoms and signs are not commensurate.
2. On the 3rd to 5th day of the rash period, the body temperature suddenly retreats to normal, and at the same time or later, a rash appears, and the rash is scattered. It is a red rose rash or a maculopapular rash. The pressure fades, rarely merges, first appears on the torso, then Rapidly spread to the neck, upper limbs, face and lower limbs, the rash quickly subsided for 24 to 48 hours, no pigmentation, and no peeling.
Examine
Childhood acute rash examination
Blood routine examination
See a decrease in the total number of white blood cells, accompanied by neutropenia, and the subsequent increase in the total number of white blood cells.
2. Virus separation
Viral isolation is the definitive method for HHV-6,7 infection. HHV-6,7 can be propagated in fresh cord blood mononuclear cells or adult peripheral blood mononuclear cells, but phytohemagglutinin should be added to the medium ( PHA), IL-2, dexamethasone and other substances, infected cells appear lesions in about 7 days, the cells are pleomorphic, nuclear pyknosis, multinucleated cells appear, infected cells can continue to survive for 7 days, no infection The cells die within 7 days of culture. Because the virus isolation and culture takes time, it is not suitable for early diagnosis and is generally only used in laboratory research.
3. Detection of viral antigens
Viral antigen detection is suitable for early diagnosis, but viremia maintenance time is short, it is difficult to take specimens in time. At present, immunohistochemistry is widely used to detect viral antigens in cells and tissues. Antigen positive results can be used as a basis for diagnosis.
4. Determination of viral antibodies
Determination of HHV-6,7 IgG and IgM antibodies by ELISA and indirect immunofluorescence is currently the most common and simple method. IgM antibody positive, high titer IgG and recovery period IgG antibody increase 4 times can explain HHV The presence of -6,7 infection, when IgM antibody or IgG antibody is detected from cerebrospinal fluid, indicates the presence of central nervous system infection. IgM antibody is generally produced 5 days after infection and can persist for 2 to 3 weeks. IgG antibody is present. It occurs 7 days after infection and reaches a peak after 4 weeks. It can last for a long time. However, due to the presence of certain antigen crossover between herpes viruses, other herpesvirus infections can also cause antibody increase, which can be identified by anti-complement immunofluorescence assay.
5. Viral nucleic acid detection
HHV-6,7 DNA can be detected by nucleic acid hybridization method and PCR method. Due to the latent infection of HHV-6,7, the DNA of the virus is sometimes detected, and it is not confirmed that it is in a latent state or an activated state. Quantitative and semi-quantitative can be used. PCR is used to determine the amount of DNA to determine the presence of active infection, and high concentrations of viral DNA suggest the presence of active infection.
The diagnosis of HHV-6,7 infection should be combined with clinical manifestations and multiple etiological findings.
General cases do not require special examination, if necessary, can do X-ray chest X-ray, ECG and other examinations.
Diagnosis
Diagnosis and identification of children's acute rash
It is difficult to diagnose during the fever period, but the systemic symptoms of the child are slightly inconsistent with the high fever performance. The total number of cells in the peripheral blood image is reduced. It should be considered. Once the fever is retreat and the rash appears at the same time, the diagnosis is not difficult to establish. Within a day, HHV-6 can be isolated from peripheral blood lymphocytes and saliva, or nucleic acid hybridization techniques can be used to detect viral genes for pathogen diagnosis.
Consideration should be given to the identification of pneumococcal sepsis and rubella, adenovirus, enterovirus infections, sexually transmitted diseases and other rash diseases.
