新生儿全身播散型单纯疱疹病毒感染1例报告

新生儿单纯疱疹病毒(HSV)感染可以分为眼皮肤口腔型、脑型和全身播散型；新生儿单纯疱疹病毒感染的病死率很高，其中以全身播散型最高。现将我院收治的1例全身播散型病例报告如下。     

新生儿单纯疱疹病毒感染

美国新生儿单纯疱疹病毒(HSV)感染每年约1/5000～1/7500,主要为HSV-2型,1型占25%～30%。但50%以上患儿之母无生殖道HSV 感染病史或症状,与其性交者也无HSV 感染。生产时无症状排HSV 者约占0.2%～1%。宫内感染(胎盘血行或上行)较少约10%,主要系产时经产道感染.如母为原发性感染,其胎儿被感染的机会为40%～50%,而复发性感染者则仅4%～8%。早产,胎膜早破>4小     

新生儿单纯疱疹病毒感染

新生儿早期的病毒感染主要可分为病毒经胎盘垂直感染胎儿的先天性感染(congenitalinfections)及分娩时和围生期的短时间内的围生期感染(perinatalinfections)。母体是主要的传染源。而不同的病原体感染,表现特征有很大差异,如新生儿单纯疱疹病毒感染(HSV)多发生在分娩过程中。1　临床流行病学特征HSV属于大的疱疹病毒家族,有两种抗原类型,即HSV 1和HSV 2型,主要由糖蛋白G的氨基酸顺序所决定。国外报道新生儿HSV总的感染率为1/5 0 0 0～1/2 0 0 0 [1] ,我国尚无这方面的资料。胎儿与新生儿是否能被感染主要取决于母亲孕期的感染与免疫…     

新生儿单纯疱疹病毒感染1例

患儿男,2天,G1P1,足月剖宫产,无窒息史,无早破膜史,其母妊娠晚期心律不齐,出现频发的室性早搏.患儿出生后15h出现咽及上腭充血、发热,诊断上上感用青霉素,潘生丁治疗2天无效.体温38℃-39℃,口吐白沫,气促,双肺呼吸音粗,胸片示:间质性肺炎,改用先锋需素Ⅵ、干扰素治疗,于发病第七日开始出现出血倾向,面部、上唇、牙龈有2mm大小的数个疱疹,无脓液.     

新生儿单纯疱疹病毒感染1例

患儿男,２天,Ｇ１Ｐ１,足月剖宫产,无窒息史,无早破膜史,其母妊娠晚期心律不齐,出现频发的室性早搏。患儿出生后１５ｈ出现咽及上腭充血、发热,诊断上“上感”用青霉素,潘生丁治疗２天无效。体温３８℃一３９Ｃ,口吐白沫,气促,双肺呼吸音粗,胸片示：间质性肺炎,改用先锋需素Ⅵ、干扰素治疗,于发病第七日开始出现出血倾向,面部、上唇、牙龈有２ｍｍ大小的数个疱疹,无脓液。肝脏进行性增大,肋下３．５ｃｍ,剑下３．５ｃｍ,质中等。脾未扪及。血培养为腐生葡萄球菌生长,ＷＢＣ１２．８×１０~９／Ｌ,中性分叶１０％、杆…     

新生儿单纯疱疹病毒感染2例报告

新生儿单纯疱疹病毒感染的脑炎型及播散型预后差,病死率高,临床少见,目前国内报道较少.     

新生儿单纯疱疹病毒感染2例报告

新生儿单纯疱疹病毒感染的脑炎型及播散型预后差,病死率高,临床少见,目前国内报道较少。 临床资料 例1.患儿男,12天,因拒乳、吐沫11天,胸部及双上肢出现水疱样皮疹2天而入院,母孕38周正常分娩,无早破膜史,生后轻度     

先天性单纯疱疹病毒感染一例

单纯疱疹病毒感染在围产医学中非常重要,其感染的广泛性与巨细胞病毒相似,也多为隐性感染。有报告认为虽2.5％孕妇有活动感染而先天感染很少报告。本院出生一例临床及实验室检查证实为先天性单纯疱疹病毒1型(HSV-1)感染新生儿,现报告如下。     

新生儿单纯疱疹病毒感染的研究进展

新生儿单纯疱疹病毒 (HSV)感染病死率高 ,预后差 ,对新生儿有极大危害性。本篇综述主要介绍新生儿HSV感染的流行病学及影响因素 ,特别是母亲HSV感染对新生儿的影响及新生儿HSV感染的患病率、临床表现、干预措施等方面的研究进展     

新生儿单纯疱疹病毒感染的研究进展

新生儿单纯疱疹病毒(HSV)感染病死率高，预后差，对新生儿有极大危害性。本篇综述主要介绍新生儿HSV感染的流行病学及影响因素，特别是母亲HSV感染对新生儿的影响及新生儿HSV感染的患病率、临床表现、干预措施等方面的研究进展。     

Relapse of neonatal herpes simplex virus infection

BACKGROUND: Neonatal herpes simplex virus (HSV) infection is a severe disease with high mortality and morbidity. Recurrence of skin vesicles is common. OBJECTIVE: To determine the features of relapse and identify the factors related to relapse. DESIGN: Thirty two surviving patients with neonatal herpes virus infections were enrolled. All patients received acyclovir treatment. Clinical and virological data were analysed and compared between relapsed and non-relapsed cases. RESULTS: Thirteen (41%) had either local skin or central nervous system relapse between 4 and 63 days after completing the initial antiviral treatment. Nine patients exhibited local skin relapses, and four developed central nervous system relapses. In one skin and two central nervous system relapse cases, neurological impairment later developed. Type 2 virus infection was significantly related to relapse (odds ratio 10.4, 95% confidence interval 1.1 to 99.0). Patients with relapse had worse outcomes than those without relapse. CONCLUSION: Neonates with HSV type 2 infections have a greater risk of relapse. Relapsed patients have poorer prognoses.     

Fatal hepatic failure secondary to acute herpes simplex virus infection

Acute hepatitis with severe hepatic failure is an uncommon manifestation of herpes simplex virus (HSV) infection. It has been described in both immunocompromised and immunocompetent patients and is usually fatal. Due to the better survival after acyclovir treatment in a few reported cases, physicians need to be aware of the characteristic clinical abnormalities so that early diagnosis and treatment can be implemented. The authors describe an adolescent diagnosed with Hodgkin disease who developed fatal hepatic failure secondary to acute HSV. Typical signs and symptoms in patients at risk, when there is no other obvious cause of fulminant hepatitis, should lead to early empirical treatment with acyclovir.     

The neonatal human's immune response to herpes simplex virus infection: a critical review

The neonate has a variety of quantitative defects in its immune response in elements of both the early containment phase and the later curative phase to HSV infection (Table 2). It is likely that the combination of these defects, and possibly others yet to be delineated (IL-2 response, T cell cytotoxicity response, etc.), account for dissemination or for locally progressive illness in newborn infants. It is unlikely that all these defects can be reconstituted by current available modalities (immunoglobulin, interferons, interleukins). One would hope that improving one or a few of these mechanisms may tilt the balance away from dissemination or central nervous system disease and allow the neonate to mature immunologically.     

Disseminated neonatal herpes simplex virus infection acquired from the father

A disseminated herpes virus type 1 infection in a baby was acquired from the father, who had herpes labialis. This was shown by virus strain typing using restriction endo-nuclease DNA analysis. Labial herpes, a common infection in adults, must be recognised as a potential threat to newborn babies.Abbreviations HSV herpes simplex virus - CSF cerebrospinal fluid - IFA immunofluorescent assay