Pathogenic herpes simplex virus can be divided into type ⅰ and type ⅱ. These two kinds of viruses can lie in the body for a long time after being inoculated in the peripheral part and detecting the virus DNA by PCR technology. Type I HSV lurks in olfactory bulb, olfactory tract and sensory ganglion of trigeminal nerve, which is easy to induce encephalitis. Type ⅱ HSV lurks in the posterior root ganglion of sacral spinal cord, which is easy to induce recurrent genital herpes infection. Therefore, in the case of host immunosuppression, HSV often becomes one of the pathogens that induce opportunistic infections.
2 disease name herpes simplex encephalitis
3 English name herpes simplex encephalitis
4. Herpes simplex encephalitis; Herpes simplex encephalitis; Herpes simplex encephalitis; Herpes encephalitis; Herpes encephalitis; Herpes simplex encephalitis
Classification of infectious diseases > virus infection > herpes virus infection
Neurology > central nervous system infection
6 ICD number B00.4
Epidemic herpes simplex encephalitis can occur at any age; Is sporadic; It is the most common type of non-epidemic viral encephalitis, accounting for about 10% ~ 20% of viral encephalitis. The condition is serious and the prognosis is poor.
Since HSV 1 is mainly related to oral and lip infections, while HSV V2 mainly causes genital infections, it is obvious that HSV 1 is easier to approach and invade the brain, so more than 95% of herpes encephalitis is caused by HSV 1 infection. HSV2 is very common in neonatal patients.
7. 1 source of infection Both acute patients and chronic carriers are sources of infection. In the general population, 5% adults are asymptomatic carriers; Herpes simplex virus (HSV) exists in herpes fluid, secretion of focus, saliva and feces of infected people. It can also be detected from patients with no obvious lesions in the external genitalia.
7.2 Transmission route Herpes simplex virus has weak resistance to the outside world, and it is mainly transmitted through direct contact between the diseased part of the patient and healthy mucosa or tiny skin lesions; Transmission through air droplets is another important way of HSVI infection. * * *, kissing is one of the important ways of disease transmission, leading to the onset of genital herpes. Therefore, genital herpes is included in the category of sexually transmitted diseases. Sick pregnant women can also cause intrauterine infection. In addition, herpes simplex virus infection can also spread through the digestive tract.
7.3 Susceptible population is generally susceptible, and the detection rate of HSV antibody in adults is high. Tischendorf reported that 80% ~ 90% of European residents had been infected with HSV 1 subtype. It is estimated that about13 of the global population has suffered from herpes simplex, most of which are recessive infections; However, the existence of herpes simplex virus antibody can not completely protect the body from repeated infection of herpes virus, and patients can also suffer from two subtypes of herpes simplex virus infection at the same time. However, those who have been infected with HSV 1 subtype can be relatively mild if they are infected with HSV V2 subtype again.
The occurrence of herpes simplex encephalitis is mostly the sporadic or recurrent attack of the original latent virus infection. Studies show that the infection rate of herpes simplex virus is higher in areas with low economic level and crowded living conditions; Children with malnutrition or immune dysfunction caused by other reasons are more likely to suffer from herpes simplex virus infection; Sometimes the epidemic will occur in areas where children are concentrated, such as children's health care institutions. Sex promiscuous sex workers are one of the high-risk groups of genital herpes, and they are easily infected with HSV because they have more opportunities to contact the source of infection. In recent years, the incidence of genital herpes in China has increased significantly.
8 Etiology Herpes is a common and ancient infectious skin disease. Relevant records can even be traced back to ancient Greece. /kloc-in the 0/8th century, the existence of genital herpes has attracted clinical attention. /kloc-After the 0/9th century, due to the industrial revolution, population density and large-scale mobility have increased the chances of herpes spreading through general contact and sexual contact, leading to an increase in the incidence of herpes-like diseases; Doctors gradually realized its infectivity and sexual transmission, and later found that herpes virus has the characteristics of latent infection.
HSV belongs to DNA virus, barringer and Swoveland 1973. In non-selective human autopsy materials, 85% ~ 90% of cadavers can display HSV type I genome in their trigeminal sensory ganglia.
Baringer and Pisani 1994 used PCR technology to study the autopsy data of patients who died of known diseases outside the nervous system, and found that HSV genome existed in the medulla oblongata, pons and olfactory bulb, but the process of how HSV lurks in human body to cause encephalitis is not completely clear.
Herpesviridae is divided into α, β and γ subfamilies, including 1 14 members, which have certain host specificity and infect humans or other animals respectively. At present, human herpesvirus includes at least 8 members (table 1).
The pathogen of herpes simplex is human herpes simplex virus, which belongs to α subfamily and herpes simplex virus genus in virus taxonomy, and is divided into HSV 1 and HSV V2 subtypes. HSV 1 subtype mainly invades the parts above the waist, especially the face and brain tissue. Type HSV2 mainly invades the parts below the waist, especially the genitals, so it is called genital herpes. But this distinction is not strict.
Herpes simplex virus (HSV) is spherical and consists of core-shell and virus outer membrane. The core-shell is icosahedron, which consists of 162 shell particles. Its core contains virus genome, which is a linear double-stranded DNA molecule with a length of 15226kb. The homology between HSV 1 and HSV V2 is only 47% ~ 50%. The genome of herpes simplex virus encodes at least 70 different protein. The mature virus core-shell contains at least seven kinds of protein. There is an inner membrane with unclear physical structure on the surface of the nuclear shell, which contains four protein components, which are related to the transcription and replication of virus genes. The outer envelope of herpes simplex virus is a bilayer lipid glycoprotein. Glycoprotein has complex components, including at least six kinds; The antigen specificity of glycoprotein gG is the serological basis for distinguishing HSV 1 or 2. After herpes simplex virus invades the host cell, the viral DNA enters the nucleus for replication, and the viral DNA transcript enters the cytoplasm to guide the synthesis of viral structural proteins in the cytoplasm. Subsequently, the progeny virus DNA returned to the cytoplasm and assembled into infectious mature virus particles. During the replication of herpes simplex virus, only a few mature virus particles were found, and the rest were rapidly degraded or became non-infectious immature virus particles because they were not treated and packaged in time.
Human herpes simplex virus has no resistance to the outside world. It can be inactivated by heating at 56℃ for 30min, ultraviolet irradiation for 5min, ether and other fatty solvents. But it can keep its biological activity for a long time at 70℃.
In vitro culture environment, herpes simplex virus can infect almost all fibroblasts and epithelial cells from embryos and newborn animals, and soon produce visible lesions; Therefore, in some difficult cases, virus isolation in vitro can be used to assist clinical diagnosis.
9 Pathogenesis The pathogenesis of herpes simplex encephalitis is complicated. Recent studies have proved that the mechanism of brain tissue damage caused by virus infection is partly the result of immunopathological reaction damage.
Type I HSV manifests encephalitis in children and adults, mainly involving medial temporal lobe, inferior frontal lobe, adjacent insular lobe and cingulate gyrus, and involving olfactory bulb and olfactory tract, but not occipital lobe and cerebellum, suggesting that brain inflammation and olfactory mucosa infection caused by HSV may spread through olfactory system and cause the above typical damage distribution.
Some scholars have suggested that HSV spreads from the sensory ganglion of trigeminal nerve to medial temporal lobe and inferior frontal lobe along the nerve supplying dura mater (Davis and Johnson, 1979), but this theory remains to be affirmed.
In children and young people, primary HSV infection can lead to encephalitis; It may be the result of viremia, but it may also be caused by herpes virus invading the brain directly through the nasopharynx and along the olfactory nerve. Animal experiments show that the toxicity of HSV2 to nervous system is greater than HSV 1. Since HSV 1 is mainly related to oral and lip infections, while HSV V2 mainly causes genital infections, it is obvious that HSV 1 is easier to approach and invade the brain, so more than 95% of herpes encephalitis is caused by HSV 1 infection. HSV2 is very common in neonatal patients. Encephalitis caused by adult herpes simplex virus is characterized by the most serious damage to the temporal lobe. Most patients have a history of herpes simplex, or the serum HSV 1 antibody is positive. The occurrence of encephalitis mainly comes from the reactivation of HSV 1 latent infection in vivo. When the immune function of the body is low, HSV lurking in the trigeminal ganglion (semilunar ganglion) or spinal ganglion invades the central nervous system along the axon, causing brain tissue damage; Or the virus lurks in the central nervous system for a long time and activates under certain conditions to cause encephalitis. Such patients may not have a viremia process.
10 pathological changes The pathology of this disease is very characteristic, and it is the change of acute necrotizing encephalitis, which is characterized by asymmetric diffuse brain injury and the formation of hemorrhagic necrotic foci of different sizes. The lesion can first damage one cerebral hemisphere and then spread to the opposite side. Necrosis was confined to one side in half cases, and about 1/3 cases were confined to temporal lobe. Even if the patient's bilateral cerebral hemispheres are damaged, they are often concentrated on one side.
Generally speaking, there will be a large area of congestion and swelling in the early brain. Moreover, the swelling of one side leads to the asymmetry of both sides of the brain, and the displacement of the midline structure leads to temporal lobe hook hernia. The areas of brain necrosis are medial temporal lobe, anterior part of parahippocampal gyrus, inferior temporal gyrus, fusiform gyrus, uncinate gyrus and fronto-orbital gyrus, especially the posterior part of orbital gyrus, which can extend to middle temporal gyrus, superior temporal gyrus, insular gyrus, cingulate gyrus, hippocampus and amygdala. The lesion not only involves cortex but also goes deep into white matter, resulting in unclear gray matter boundary. Those who survived for 1 ~ 2 weeks, the necrotic tissue disintegrated, and those who survived for several weeks or more could see temporal lobe atrophy, and the necrotic area of cortex was cystic.
Microscopically, the early nervous tissue was loose and necrotic with meningoencephalitis changes. A large number of inflammatory cells in brain tissue are mainly lymphocytes, but also larger monocytes and plasma cells. Nerve cells can autophagy, necrosis and disappear, and the lattice cells formed by phagocytosis of lipids by macrophages can be seen. Blood vessel wall necrosis, blood vessels ooze red blood cells, and some are surrounded by inflammatory cells to form blood vessel sheath. The congestion and inflammatory reaction of the pia mater are mainly lymphocytes. There may be a small number of lymphocytes and oozing red blood cells in subarachnoid space. Typical changes are eosinophilic inclusions in the nucleus, which can be seen in nerve cells, astrocytes and oligodendrocytes. HE staining can find eosinophilic inclusions in the nucleus under high magnification. Immunohistochemical staining (ABC) showed dark brown, and virus particles could be found by electron microscope (Rao Liming et al., 1987).
Clinical manifestations of herpes simplex encephalitis111mainly show that herpes simplex encephalitis can occur at any age, and more than 50% of adults are over 20 years old. It can happen all year round. Acute onset is common, but there are also subacute, chronic and recurrent cases. Have a history of oral herpes. The onset of children and adult patients is often acute or subacute, and the first symptoms are headache, fever or only behavioral and personality changes.
Local or generalized convulsions (secondary epilepsy) last for several hours or days. The most common seizure forms are simple or complex partial seizures and generalized tonic-clonic seizures after partial seizures. Patients with lesions involving the dominant hemisphere will have language disorders and hemiplegia.
A small number of patients complained of olfactory hallucination or taste hallucination in the early stage of the course of disease, and the course of disease was short, suggesting the possibility of HSV infection. Some patients have herpes on the upper lip before and after onset, which is helpful to consider herpes virus infection.
Severe cases can fall into high fever, coma, and even brain hernia due to brain edema. Neurological examination usually has meningeal signs and provides signs of brain parenchymal injury. Neonatal patients are mostly infected through the birth canal infected with HSV, even in the uterus. Newborns and infant patients are mostly infected with systemic organs, often involving skin, eyes and mouth at the same time. Intrauterine infection can lead to diffuse brain injury or deformity.
The duration of the disease varies. Generally speaking, the average period from onset to coma is 1 week, and the period from coma to death is 1 week. But some last for 3-4 months. Without treatment, the mortality rate is as high as 70%, and more than half of the survivors have sequelae.
1 1.2 The duration of clinical staging is different. Generally speaking, the average period from onset to coma is 1 week, and the period from coma to death is 1 week. But some last for 3-4 months. Without treatment, the mortality rate is as high as 70%, and more than half of the survivors have sequelae.
1 1.2. 1, dizziness, headache, general pain, etc. , followed by upper respiratory tract infection, fever can reach 38 ~ 40℃, only some cases have skin herpes. This period generally does not exceed 2 weeks.
1 1.2.2 Neuropsychiatric symptoms are varied. Mental symptoms are often prominent in the early stage, including personality changes, abnormal behavior, irrelevant answers, disorientation, hallucinations, delusions, amnesia, aphasia and so on. It may be caused by the virus invading temporal lobe, frontal lobe and limbic system through trigeminal nerve and olfactory bulb in the early stage.
With the progress of the disease, brain tissue necrosis lesions appear, and patients have consciousness disorders. Such as lethargy, lethargy, delirium, coma, etc. ; Convulsion, convulsion, hemiplegia and neurological dysfunction, such as deviation of eyeball, unequal pupil, hemianopia, etc. , with intracranial hypertension. The patient has stiff neck, increased muscle tension and pathological reflex. Some cases were in the early stage of brain removal. In severe cases, brain hernia may occur.
Acute encephalomyelitis is mainly found in infants under 1 year old, who are infected with HSV at birth. Intrauterine infection can lead to diffuse brain injury or deformity.
Abnormal EEG may appear in the early stage of the disease. Typical changes are: focal periodic sharp waves on the background of diffuse high amplitude slow waves; Temporal lobe and frontal lobe often present periodic spikes and slow waves. Brain CT and MRI can show low-density lesions in temporal lobe and frontal lobe, punctate hemorrhage, brain edema and ventricular compression and displacement. Radionuclide brain scan showed increased uptake of temporal lobe and frontal lobe.
12 complications of herpes simplex encephalitis: complications of herpes simplex encephalitis can often lead to coma, and severe cases can lead to cerebral hernia.
1. intracranial hypertension.
2. Brain hernia.
3. Some cases were in the state of decerebrated rigidity in the early stage.
13 laboratory examination 1. Early examination of cerebrospinal fluid in some patients can be normal. Generally, it is colorless and transparent, with clear appearance and high pressure. The number of cells is about (20 ~ 200) × 106/L, mostly below 0.4×109/L. Most of them are lymphocytes and monocytes, but they can also be neutrophils in the early stage. Due to the hemorrhagic and necrotizing nature of brain tissue lesions, cerebrospinal fluid in some cases contains more red blood cells, which can reach (50 ~ 500) × 106/L or even more. Protein increased slightly to moderately, and the content of protein was 0.5 ~ 2.0g/L; Sugar content is normal or low. The above changes can only provide infectious diseases.
2. The detection of polymerase chain reaction (PCR) is extremely sensitive to the diagnosis of HSV pathogens, especially important for early diagnosis, but it can still appear false negative after 1 ~ 2 days and 10 ~ 14 days. Because HSV antibody appears in CSF late, it is easy to be detected 1 week after onset, but it can exist for weeks to months, so it is still valuable to make a retrospective diagnosis.
3. Indirect immunofluorescence detection of HSV antibody in serum is also helpful for etiological diagnosis. Immunological examination showed that the titer of serum neutralizing antibody or complement binding antibody gradually increased to more than 4 times; The anti-viral antibody titer of herpes simplex virus in cerebrospinal fluid was > 1 ∶ 80, and the antibody titer of early and late samples increased by more than 4 times.
4. Virus antigen can be detected by immunohistochemical technique; However, it is difficult to do brain biopsy in clinic. Virological testing is the gold standard for the diagnosis of this disease. However, when encephalitis occurs, most patients have no herpes lesions on their body surfaces, and it is often difficult to detect viruses in cerebrospinal fluid. Although inclusion bodies and virus particles in the nucleus can be found in brain biopsy samples under electron microscope; PCR can be used to detect HSV DNA in cerebrospinal fluid samples, which is helpful for early diagnosis, but its specificity should be paid attention to.
14 assists in the examination of EEG abnormalities, which can be asymmetrical on both sides, especially on one cerebral hemisphere; CT and MRI showed hemorrhagic necrosis of temporal lobe and frontal lobe, or diffuse lesions of brain tissue.
14. 1 EEG often shows diffuse slow waves with high amplitude, especially in unilateral or bilateral temporal frontal area, and even spikes and spikes in temporal area may appear.
14.2 imaging changes CT scan: normal and local low density areas can be seen; MRI is helpful to find the lesions with long T 1 and long T2 signal in brain parenchyma.
14.3 brain histopathological examination showed that the important feature of brain histopathology under light microscope was hemorrhagic necrosis. Under electron microscope, Cowdry A-type inclusions could be seen in the nucleus, oligodendrocytes and nerve nuclei could be seen in or near the necrotic area, and Togo inclusions could be seen in one nucleus. Pathogenic examination showed that intracellular virus particles could be seen under electron microscope; There can also be brain tissue samples for PCR, in situ hybridization and other viral nucleic acid inspection, or virus isolation and culture.
15 diagnosis of herpes simplex encephalitis is mainly based on clinical manifestations and laboratory results. The following points suggest the possibility of herpes encephalitis:
1. Acute or subacute onset, first general malaise or upper respiratory tract infection, often fever several days after onset, with headache, fever or abnormal behavior as the first symptom.
2. Then there are signs of disturbance of consciousness, mental abnormality and brain parenchymal injury; If you have upper lip herpes damage or have olfactory hallucinations and taste hallucinations in your medical history, you should consider this disease more.
3. Cerebrospinal fluid pressure increases, and protein and white blood cells increase slightly to moderately, mainly lymphocytes; A large number of red blood cells were found in cerebrospinal fluid (but diseases such as puncture injury or subarachnoid hemorrhage should be excluded), the protein content was increased, and the sugar and chlorine were normal, which was of diagnostic value.
4. EEG is abnormal, and both sides can be asymmetrical, especially in one cerebral hemisphere; CT and MRI showed hemorrhagic necrosis of temporal lobe and frontal lobe, or diffuse lesions of brain tissue.
5. If it is diagnosed as herpes simplex encephalitis, the infected pathogen should be checked in time. At present, the detection of HSV antigen in CSF by PCR is the most important for early diagnosis. If the test result is negative within 1 ~ 2 days after onset, the PCR test of CSF should be repeated after 24 ~ 48 hours. If it is still negative, we should consider other pathogens or other diseases.
The clinical manifestations of herpetic encephalitis are not specific, and only about 1/4 patients have skin herpes (cold sores). If encephalitis occurs in patients with primary herpes infection, there is no trace of past medical history to follow; Although HSV2 is very common in neonatal patients, it is not always possible to find signs of genital herpes in their biological mothers, so the clinical diagnosis of herpetic encephalitis is sometimes quite difficult. Brain biopsy showed eosinophilic inclusions in the nucleus, and virus particles were seen under electron microscope. The cultured HSV virus has diagnostic significance.
16 differential diagnosis 16. 1 Other viral encephalitis There are various pathogens of viral encephalitis, mainly including herpes virus, arbovirus and enterovirus. However, except for a few epidemic encephalitis such as Japanese encephalitis, the clinical manifestations of other sporadic viral encephalitis are relatively light, and there are few signs that the temporal lobe and frontal lobe are mainly damaged. It is helpful to identify the specific antibodies of the corresponding virus in serum and cerebrospinal fluid.
Japanese encephalitis is a serious disease with rapid progress. It often begins with sudden high fever, and quickly presents manifestations of brain parenchymal damage such as disturbance of consciousness, convulsion and convulsion. Moreover, the incidence is concentrated in the mosquito season in summer and autumn, and patients who have not been vaccinated with Japanese encephalitis vaccine can help diagnose.
Herpes zoster encephalitis: This disease is rare. It mainly invades and lurks in nerve cells of dorsal root ganglion of spinal nerve or sensory ganglion of brain cells, and rarely invades the central nervous system. The clinical manifestations are symptoms and signs of confusion, ataxia and focal brain injury. The degree of lesion is mild and the prognosis is good. Most patients have a history of herpes zoster in the chest and waist, and CT shows no bleeding and necrosis. Serum and cerebrospinal fluid are positive for virus antigen, antibody and virus nucleic acid, which can be used for identification.
Intestinal viral encephalitis: it is more common in summer and autumn and can be epidemic or sporadic. Clinical manifestations include fever, disturbance of consciousness, imbalance, recurrent attacks and limb paralysis. Gastrointestinal symptoms appear in the early stage of the disease, and virus isolation from cerebrospinal fluid or PCR positive is helpful for diagnosis.
Cytomegalovirus encephalitis: rare in clinic, common in patients with immunodeficiency or long-term use of immune will agents.
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16.2 pyogenic meningoencephalitis showed severe symptoms of systemic infection and poisoning, obvious increase of white blood cells in peripheral blood, purulent changes in cerebrospinal fluid, and positive bacterial smear or culture.
16.3 more and more attention has been paid to acute disseminated encephalomyelitis, which was found in the course of acute eruptive viral infectious diseases (such as measles, rubella, smallpox, chickenpox, etc.). ); It can also be seen in the recovery period of other acute viral infection (such as infectious mononucleosis, influenza, etc.). ), called encephalitis after virus infection; Others occur within 2 ~ 3 weeks after vaccination with pertussis and rabies vaccine, which is called post-vaccination encephalitis; It can even occur due to the treatment of anthelmintics, such as levamisole encephalitis, which may be related to immune response. Acute disseminated encephalomyelitis is characterized by symptoms and signs of brain parenchyma, meninges, brain stem, cerebellum and spinal cord. Symptoms and signs are diverse, and in severe cases, consciousness disorder and mental symptoms may occur.
Pathological features are disseminated demyelination of brain and spinal cord and infiltration of inflammatory cells around venules. Clinical manifestations vary with the location and severity of the lesion, including high fever, headache, vomiting, convulsion, insanity, coma, meningeal signs and signs of local injury. The number of protein and cells detected in cerebrospinal fluid increased. Paying attention to the time when patients' neurological symptoms appear often has the significance of prompting clinical diagnosis.
16.4 toxic encephalopathy often occurs in the early or extreme stage of acute bacterial infection, and is more common in septicemia, pneumonia, bacillary dysentery, typhoid fever, diphtheria and whooping cough. The patients were mainly children aged 2 ~ 10, who were allergic to infectious toxins, resulting in cerebral congestion and edema; The clinical manifestations are high fever, headache, vomiting, delirium, convulsion, coma and meningeal sign. With the increase of cerebrospinal fluid pressure, the protein can be slightly increased, the cells are generally not increased, and the sugar and chlorine are normal. After the primary disease improves, the brain symptoms gradually disappear, and generally there will be no sequelae.
17 treatment of herpes simplex encephalitis 17. 1 general treatment should strengthen nursing to prevent complications such as bedsore and lung infection; At the same time, cooling, spasmolysis, dehydration and other treatments were taken according to the condition. If the intracranial hypertension crisis is ineffective after drug treatment, ventricular drainage and bone flap surgery can be used for emergency decompression if necessary.
17.2 antiviral therapy because the lesions occur in the central nervous system, the sooner antiviral therapy is, the better; However, because the virus only causes typical symptoms at the end of intracellular replication, the opportunity of antiviral treatment is often late, which affects the curative effect and prognosis. An ideal antiviral drug can selectively inhibit the metabolism of viral nucleic acid and protein without affecting the host cells at all. But the current antiviral drugs can't do this, and most of them have certain toxic and side effects. The following are commonly used in clinic.
Acyclovir only works on cells infected with the virus, but has no effect on uninfected cells, making it the first choice. The dosage is 5 ~ 10 mg/kg body weight each time, and intravenous drip 1 time /8h, 14 ~ 2 1 day is a course of treatment; When it is less than 10 days, repetition often occurs. Adverse reactions include tremor, rash, hematuria, transient renal insufficiency and elevated transaminase. Recently, the number of strains resistant to acyclovir has increased, especially HSV 1 type.
The dose of arabinoside was15 mg/(kg d), *** 10 day. When in use, it must be diluted and then slowly infused intravenously, so that its concentration does not exceed 700mg/L, and the infusion time is not less than 12h. Adverse reactions include nausea and vomiting, hematopoietic dysfunction and so on.
Children were given ribavirin intravenously at a dose of 0.5 ~ 1g/d and 20 ~ 30mg/kg body weight for 7 ~ 10 days.
17.3 Although there are some controversies about adrenocortical hormones, most scholars still advocate the use of hormones to treat this disease in view of the fact that immune damage is involved in the pathogenesis of this disease. Corticosteroids can reduce inflammatory reaction, detoxify and stabilize lysosomal system, reduce capillary permeability, protect blood-brain barrier, eliminate brain edema and overcome rebound caused by dehydrating agent. Once diagnosed, hormones can be used early, in large quantities and for a short time. Dexamethasone is the first choice. Generally, it is 15 ~ 20 mg, and it is diluted and given intravenously. After 1 time /d, 10 ~ 14 days, it gradually decreases.
Interferon 17.4 and its inducer interferon have inhibitory effects on many viruses. Clinically, 3 million to 5 million U, 1 time /d, intramuscular injection, about 4 weeks as a course of treatment.
Interferon inducers, such as poly-myocytes, induce human body to produce endogenous interferon, and the curative effect of treating this disease is uncertain.
17.5 Traditional Chinese medicine mainly treats viral encephalitis by clearing away heat and toxic materials, and adopts the principles of aromatic turbidity, promoting blood circulation and dredging collaterals. Prescriptions include rhinoceros horn Dihuang decoction, Baihu decoction, Qingwen Baidu decoction, Yinqiao powder and so on. Chinese patent medicines include Zixuedan and Angong Niuhuang Pill.
The prognosis of 18 is that the mortality rate of herpes encephalitis can be as high as 70%, and most of them die within 2 weeks after onset. Those with deep coma, severe intracranial hypertension and late antiviral treatment often have poor prognosis. Half of the survivors have different degrees of neurological sequelae, such as memory loss or amnesia, language disorder, mental disorder, labor loss, and even vegetative state.
19 prevention of herpes simplex encephalitis patients with herpes simplex should be informed to be isolated at home after they appear in nurseries, and can only return after treatment. Pregnant women with genital herpes should give birth by cesarean section. Pregnant women with a recent history of genital herpes should take amniotic fluid samples to detect IgM HSV antibody. If it is positive, it indicates that the fetus has intrauterine infection. We can discuss with the couple whether to choose 0. 1% eye drops and isolate them from the sick mother to avoid being fed by the sick mother until the sick mother recovers. During the period of hospital labor and postpartum observation, mothers and their newborns should be isolated from other mothers and newborns.
Adhere to the premarital physical examination system, avoid multiple sexual partners, and advocate safe sex; If necessary, using condoms will help to control or reduce the prevalence of genital herpes infection. Acyclovir was used immediately after organ transplantation (including bone marrow transplantation). For patients with recurrent herpes, the inducing factors should be removed or avoided as much as possible. All the above measures are helpful to prevent the occurrence of herpes simplex infection or the onset of the original recessive infection. At present, the vaccine to prevent herpes simplex has entered the clinical trial stage.
20 related drugs: acyclovir, cytarabine, adenosine, ribavirin, dexamethasone, interferon, polyinosine, Zixuedan and Angong Niuhuang Pill.
2 1 plasma cells, herpes simplex virus antibody, cerebrospinal fluid pressure, interferon related examination
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