- Reasons of a sudden dieback
- Symptoms of a sudden dieback
- Treatment of a sudden dieback
The sudden dieback - an acute viral infection of babies or children of early age, usually is originally shown by high fever with lack of local symptoms and the subsequent emergence of krasnukhopodobny rashes (spotty papular rash). The sudden dieback is most widespread among children from 6 to 24 months, middle age makes about 9 months. Less often, children of advanced age, teenagers and adults can be infected. The sudden dieback has some other names: children's roseola, pseudorubella, sixth disease, 3-day fever, roseola infantum, exanthema subitum, pseudorubella. It officially is called a sudden dieback as rash develops suddenly (right after fever), this disease usually is called sudden skin rash. To distinguish a sudden dieback from other children's diseases with presence of skin rash, it was once called "the sixth disease" (so it, as a rule, became the sixth disease at small children and proceeded about six days), but this name is already almost forgotten.
Reasons of a sudden dieback:
The sudden dieback is caused by a virus of herpes 6 (VGCh-6) which was allocated in 1986 from blood of the people having limfoproliferativny diseases. and is more rare a virus of herpes 7 (VGCh-7). HHV-6 is for the first time found by Salahuddin and соавт. in 1986 at adult patients with limforetikulyarny diseases and infected with the human immunodeficiency virus (HIV). In two years of Yamanishi and соавт. isolated the same virus from blood of four babies with an inborn roseola. Though this new virus was found initially in B-lymphocytes of the immunocompromised adult patients, afterwards it became clear that it has initial affinity to T lymphocytes, and its original name - a human V-lymphotropic virus (HBLV) - was changed to HHV-6. HHV-6 is a part of the sort Roseolovirus, beta-Herpesvirus subfamily. Like other viruses of herpes, HHV-6 possesses the characteristic electronic and dense kernel and an ikosaedralny capsid surrounded with a cover and an external membrane, the location of important glycoproteins and proteins of a membrane. The main component of a cellular receptor for HHV-6 - CD46 which is present at a surface of all nuclear cells and allows HHV-6 to infect a wide number of cells. The main goal of HHV-6 is a mature cell of CD4+, but the virus can infect natural killers (NK), the gamma delta T lymphocytes, monocytes, treelike cells, astrocytes and various lines T and B of cells, megacaryocytes, fabric of an epithelium and others. HHV-6 is presented by two close connected options: HHV-6A and HHV-6B which differ on cellular tropism, molecular and biological features, epidemiology and clinical associations. The roseola and other primary infections of HHV-6 are caused only by option B. Cases of primary infection connected with option A still are subject to the analysis. HHV-6A and HHV-6B are closest to human gerpesvirusa 7 types (HHV-7), but some amino acids are similar to a human cytomegalovirus (CMV).
The sudden dieback extends from the person to the person, most often, in the airborne way or at contact. The peak of incidence - spring and fall. The infection acquired by HHV-6 occurs preferential at babies of 6-18 months of life. Almost all children are infected aged up to three years and keep immunity for the rest of life. The most indicative is that HHV-6 infection acquired at children's age leads to the high frequency of a seropozitivnost at adults. In the United States of America and many other countries almost all adult seropozitivna. The main mechanisms of a HHV-6 broadcast are insufficiently studied. HHV-6 persistirut after primary infection in blood, a respiratory secret, urine and other physiological secrets. Apparently, the adults who are closely contacting to them, HHV-6 carriers become a source of infection of babies; other ways of transfer Relative protection of newborns against primary infection are also possible until there are maternal antibodies, points that antibodies of serum provide protection against HHV-6. Primary infection differs in a viremiya which stimulates products of neutralized antibodies that leads to the termination of a viremiya. Specific antibodies of IgM appear during the first five days from the beginning of clinical symptoms, in the next 1-2 months of IgM decrease and further are not defined. Specific IgM can be present at reactivation of an infection and as many authors specify, at a small amount - at healthy people. Specific IgG raise within the second and third week, with increase of their avidnost further. IgG to HHV-6 persistirut all life, but in lower quantities, than in the early childhood. Levels of antibodies can fluctuate after the postponed primary infection, perhaps, as a result of reactivation of a latent virus. Essential increase of level of antibodies, according to some scientists, is observed in case of infection with other viruses with similar DNA, for example, of HHV-7 and CMV. In observations of some researchers it is specified that children within several years after primary infection can have a quadruple increase of a caption of IgG to HHV-6 again, sometimes owing to acute infection with other agent, it is impossible to exclude also possible reactivation of latent HHV-6. In literature it is described that reinfection other option or a strain of HHV-6 is possible. Cellular immunity is important in control of primary infection of HHV-6 and afterwards in maintenance of a latent state. Reactivation of HHV-6 at immunological the compromised patients confirms importance of cellular immunity. The acute stage of primary infection is connected with the increased cellular activity of NK, perhaps, through IL-15 and induction of IFN. In studying of in vitro decrease in replication of a virus under the influence of exogenous IFN was noted. HHV-6 also induces IL-1 and TNF-, it demonstrates that HHV-6 can modulate an immune response during primary infection and reactivation by means of stimulation of products of cytokines. After primary infection the virus persistention in a latent state or in the form of persistent infection with products of a virus remains. Components of an immune response important in control of persistent infection, are unknown. Reactivation of a latent virus happens at immunological the compromised patients, but can be observed also at immunocompetent people for the unknown reasons. HHV-6 DNA often is found after primary infection in mononuclear cells of peripheral blood and secrets of healthy people, but the main location of latent infection of HHV-6 is unknown. The pilot studies conducted by scientists demonstrate that HHV-6 latentno infects monocytes and macrophages of different fabrics, and also stem cells of marrow from which afterwards there is its reactivation.
Symptoms of a sudden dieback:
The disease is not really infectious, the incubation interval of a disease makes 9-10 days. Signs and symptoms of VGCh-6 (or VGCh-7) can vary infections depending on age of the patient. At children of younger age temperature usually suddenly increases, irritability, increase in cervical and occipital lymph nodes, cold is noted, the century, diarrhea, a small injection in a pharynx, sometimes a dieback in the form of small makulopapulezny rash on a soft palate and a uvula, a hyperemia and puffiness of a conjunctiva swelled a century. Within 12-24 hours after temperature increase rash develops. Children of more advanced age at whom VGCh-6 develops (or VGCh-7) an infection, most often have such symptoms as high temperature within several days, is possible, cold and/or diarrhea. Children of advanced age have a rash less often. Temperature at fever can be quite high, on average 39,7 C, but can rise up to 39.4-41.2 C above. Despite high temperature the child is usually active. Temperature falls critically usually for the 4th day. The dieback appears at decrease in temperature. Sometimes rash is observed before fever, sometimes decreases after during the day the child had no temperature. Rashes of rozeolezny, makulezny or makulopapulezny character, pink coloring, to 2-3 mm in the diameter, they turn pale when pressing, seldom merge, are not followed by an itch. Rashes usually develop at once on a trunk with the subsequent distribution on a neck, a face upper and lower extremities, in certain cases they are located preferential on a trunk, a neck and a face. Rashes remain several hours or within 1-3 days, disappear completely, the dieback in the form of an erythema is sometimes noted. Primary infection of HHV-6 at newborns is shown by also sudden dieback. It can be observed at children of the first three months of life, including newborns, its clinical manifestations are generally similar to that at the senior children, but proceed easier. The feverish state without local symptoms is the most frequent form, but temperature increase is usually lower, than at children of advanced age. According to literature, more frequent manifestation of primary HHV-6 of an infection are cases of an asymptomatic infection at which find DNA HHV-6 in mononuclear cells of peripheral blood after the birth or in the neonatal period. At some sick HHV-6 DNA persistirut in cells of peripheral blood some time with the subsequent development of manifest primary infection of HHV-6. HHV-6 connect an infection with a number of manifestations. Some scientists assume HHV-6 as the reason of development of a syndrome of chronic fatigue, others - multiple sclerosis, a syndrome of multiorgan insufficiency, pink depriving, hepatitis, a virus hemophagocytosis, an idiopathic Werlhof's disease, a syndrome of excessive sensitivity to medicines, especially antibacterial. However, these data disputable also demand further deep studying. Complications of a sudden dieback of the Complication meet at a sudden dieback quite seldom, except for children reduced immune system. People with healthy immune system, in general, develop lifelong immunity to VGCh-6 (or VGCh-7).
Blood test: a leukopenia with a relative lymphocytosis Serological tests: identification of IgM, IgG to VGCh of PTsR 6 type (VGCh-6) of serum on VGCh-6. Differential diagnosis: rubella, measles, infectious erythema, enteroviral infection, otitises, meningitis, bacterial pneumonia, medicinal rash, sepsis.
Treatment of a sudden dieback:
Whether it is necessary to see a doctor if the child got sick with a sudden dieback? Yes, it is the good idea. The child with fever and rash should not contact to other children before it is examined by the doctor. After deflorescence and fever the child can return to usual life. If temperature does not deliver treatment of fever to the child of inconvenience, then treatment is not necessary. There is no need to awake the child for treatment of fever if there are no instructions of the doctor. The child with fever has to be in comfortable conditions and should not be too warmly dressed. The excess clothes can cause temperature increase. Bathing in warm water (29,5 C) can help to reduce fever. Never pound the child (or the adult) alcohol; alcoholic couples can create numerous problems at inhalation. If the child shivers in a bathtub, water temperature in a bathtub has to be increased. High temperature at a sudden dieback can initiate spasms. Febrile spasms are widespread among children from 18 months to 3 years. They arise at 5-35% of children with a sudden dieback. Spasms can look very frighteningly, but, as a rule, are not dangerous. Fibrilny spasms are not connected with long side effects, damages of a nervous system or a brain. Anticonvulsant drugs are seldom appointed for treatment or prevention at fervescence. What to do if the child has spasms caused by fever at a sudden dieback: - Keep calm and try to calm the child, weaken clothes around a neck. - Remove sharp objects which can do harm, turn the child sideways, so saliva can follow from a mouth. - Put a pillow or the curtailed coat under the child's head, but it is not necessary to place anything in the child's mouth. - Expect when spasms pass. Children are often sleepy and can sleep after spasms that is quite normal. After spasms it is necessary to see a doctor that the child was surely examined. Rash at a sudden dieback develops when the increased temperature (fever) decreases. Rash develops on a neck and a trunk, especially in a stomach and a back, but also can develop on hands and legs (extremities). Skin gains reddish color and temporarily turns pale when pressing. Rash is not itched, and does not hurt. It is not infectious. Rash passes in 2-4 days and is not returned. The forecast is favorable.