neonatal herpes simplex virus infection
Introduction
Brief introduction of neonatal herpes simplex virus infection Herpessimplex viral infection (newborn) is a systemic infection, more common in premature infants, lesions involving multiple organs, and a serious prognosis. Herpes simplex virus is a double-stranded DNA virus, which can be divided into two types. Type I mainly causes mucosal herpes on the lips, mouth, and pharyngeal skin; type II causes genital herpes. The new HSV infection is mostly caused by type II, and even by type I. HSV has the characteristics of long-term latent, recurrent and neurotropic tissue. basic knowledge The proportion of illness: 0.001% Susceptible people: children Mode of infection: non-infectious Complications: respiratory failure, shock, cataract
Cause
Causes of neonatal herpes simplex virus infection
(1) Causes of the disease
Infants can be infected during pregnancy, childbirth and postpartum. Early infection can cause spontaneous abortion, or cause developmental disorders, congenital malformations; mid-term infection can cause stillbirth; birthtime infection is the fetus through the birth canal, scalp, eye, skin, umbilical cord Infection with direct contact with the respiratory tract; postnatal infection is caused by exposure to a virus carrier.
(two) pathogenesis
HSV firstly spreads in affected areas such as oropharynx, combined with membrane and skin. The lesions can be limited to local, neonatal immunity is low, the virus is easy to spread and cause viremia, and then spread to the central nervous system and other tissues and organs of the body, such as Liver, lung, adrenal gland, etc.; the virus can also be retrogradely transmitted to the central nervous system via axons.
The virus replicates in the cells, causing the infected cells to enlarge, inclusion bodies in the nucleus, cell lysis in the affected tissues, hemorrhagic coagulation necrosis and lymphocyte infiltration, and calcification in the brain.
Prevention
Neonatal herpes simplex virus infection prevention
A large number of candidate HSV vaccines have been prepared from infected cell extracts or recombinant viral glycoproteins and have been tested in animals and humans. To date, no vaccine has prevented HSV infection or latency; Prevention of HSV infection depends on reducing transmission and reducing recurrence, because most infections are subclinical. To prevent the spread of genital HSV infection, it is necessary to control sexual behavior or widely use condoms. There is still a lack of information on the effectiveness of condoms.
Vertical transmission of HSV can be reduced by reducing maternal HSV infection or reducing the likelihood of transmission to neonates, although prophylactic use of acyclovir may reduce clinical HSV recurrence, but does not eliminate asymptomatic viral emissions, safety for the fetus Sexuality is also unclear, so it may be inappropriate to prevent acyclovir in pregnant women with recurrent genital herpes to reduce the risk of neonatal infection, because it is impossible to identify a sexual partner who is suffering from asymptomatic infections. It is more complicated for pregnant women to get new infections during pregnancy.
It is clear that women may have viral emissions during childbirth, so the strategy of using cesarean section to prevent transmission is confusing due to the need to find clinical lesions before birth, because there are even asymptomatic viral emissions in the primary infection. This strategy has made it even more difficult. Perinatal virus culture cannot predict whether there will be virus emissions during childbirth, so it is no longer recommended.
Chronic repressive treatment with acyclovir reduces the recurrence of latent genital and lip HSV infection, and prophylactic administration of acyclovir is also effective in immunocompromised hosts, including bone marrow transplants and kidney transplant patients, cancer patients and In other immunodeficiency patients, the risk of HSV infection recurrence was significantly reduced from 60% to 80% of placebo to 0% to 10% of acyclovir in patients with impaired immune function.
Prophylactic antiviral therapy is not appropriate for newborns exposed to HSV during childbirth.
Complication
Neonatal herpes simplex virus infection complications Complications, respiratory failure, shock cataract
Respiratory distress or pause can occur, convulsions, and viremia can rapidly develop into respiratory failure, shock and DIC, etc. Survivors all have central nervous system sequelae, to small eyeballs, cataracts and so on.
Symptom
Newborn herpes simplex virus infection symptoms Common symptoms Herpes shock splenomegaly sleepiness calcified crusting respiratory failure small eye coma convulsion
Intrauterine infection with HSV can cause miscarriage, stillbirth, or birth, skin herpes, scarring, small eyeballs, keratoconjunctivitis, retinal choroiditis, microcephaly, hydrocephalus, intracranial calcification and liver, splenomegaly If the performance is poor, the prognosis is poor, and the ewes have a long-term premature rupture of the water. The mother may suffer from HSIV-type genital infection. The virus exerts intrauterine infection on the fetus. Generally, the central nervous system is not tired. Only skin or eye lesions have a good prognosis.
Most of the sick children are infected at the time of birth or shortly after delivery. The baby is born with no abnormalities, and most of them occur 5 to 10 days after birth. The clinical manifestations include systemic dissemination and local lesions:
1. Systemic dissemination type: about 50%, the incidence of more than the first weekend, from viremia to organs are more widely involved, may involve skin, lung, central nervous system, adrenal gland, trachea, esophagus, heart, kidney and Spleen and other clinical symptoms are similar to neonatal sepsis, which can be expressed as fever, pale, respiratory distress or pause, convulsions, lethargy, irritability, hypercholemia, shock and DIC, etc. In most cases, shingles can be seen in the skin, sometimes in the case of The first exposed part, herpes base is red, the edge is clear, the diameter is 1~3mm, and even can develop into bullae, the diameter is >1cm, about 20%~30% of the sick children have no herpes in the whole course, making the diagnosis of this disease difficult. The prognosis of this type of case is poor, and the mortality rate can reach 80%. Survivors have left sequelae such as nervous system. In recent years, antiviral drugs have been used, and the mortality rate has dropped to 15% to 20%, but 40% to 55% of cases have sequelae.
2. Limited type: more than the second week after birth, can be expressed in the following two types:
(1) The lesion is confined to the skin, eye and mouth mucosa: about 20%. If antiviral treatment is not used in time, it can also develop into a systemic dissemination type. The skin lesions are as described above; the ocular lesions are keratoconjunctivitis, late onset. Retinal choroiditis, with or without small eyeballs, cataract, about one-third of the cases in this group, there is no manifestation of encephalitis in the course of the disease, but long-term follow-up observation, can be found to cause central nervous system sequelae, may be related to the disease The primary central nervous system is associated with subclinical infection.
(2) Encephalitis type: about 30%, different from the disseminated type, the central nervous system symptoms appear later, rare complicated with viremia, a few cases have skin mucosal herpes, the blood of sick children mostly from the mother HSV And antibody and antibody-dependent cellular cytotoxic antibodies, supporting the idea that the virus spreads along the axons rather than through the viremia to the central nervous system. The clinical manifestations of the sick children are fever, lethargy, irritability, screaming, coma, convulsions, and anterior Bulging, etc., B ultrasound, CT or EEG often show focal lesions of temporal lobe.
(3) cause pneumonia: In addition, HSV can cause pneumonia or disseminated pneumonia, which is manifested as respiratory distress, can rapidly develop into respiratory failure, and the lung X-rays are mostly interstitial or reticular granular lesions.
Examine
Examination of neonatal herpes simplex virus infection
HSV is easily isolated from active lesions, such as herpes fluid, nasopharynx, conjunctiva, respiratory secretion, cerebrospinal fluid, urine and feces, and tissue culture takes only 1 to 3 days.
Exfoliated cells or herpes base smear cytology, lesions increased, there are intranuclear inclusions or multinucleated giant cells, although the positive rate can reach 60% to 70%, but the positive change is not unique to herpes simplex lesions, recent years Stain with monoclonal or polyclonal antibodies with high specificity and sensitivity.
HSV antigen or DNA detection, such as polymerase chain reaction (PCR), can be quickly diagnosed, serological tests are of little help to the diagnosis, and there is a cross-immunity between HSV types.
In patients with hepatic lesions, serum bilirubin and transaminase increased; brain lesions increased cerebrospinal fluid cell count (including red blood cells, lymphocytes and monocytes), protein increased, but normal patients can not exclude this disease, EEG can be periodic Slow wave, sharp wave or multifocal discharge, mostly limited to temporal lobe, CT scan can be seen in temporal lobe lesions or low density changes around the cerebral cortex and ventricles, and bleeding or calcification can be seen in some cases.
B-ultrasound, CT or EEG examination often showed focal lesions of the intracranial temporal lobe; the lung X-ray showed multiple interstitial or reticular granular lesions.
Diagnosis
Diagnosis and diagnosis of neonatal herpes simplex virus infection
diagnosis
The earlier the treatment, the better the prognosis is. Therefore, early diagnosis is very important. For example, if the above clinical manifestations are present in the neonatal period, and the herpes on the skin mucosa occurs, the disease should be suspected. The blood routine can be found to shift left neutrophils, platelets. Can be reduced, often immunoglobulin G decreased, nervous system involvement, cerebrospinal fluid may have increased protein, lymphocyte count increased or no change, but the diagnosis of HSV infection requires antigen or antibody examination.
Differential diagnosis
The disease must be differentiated from sepsis and differentiated from TORCH syndrome.
