Chapter 57 Neonatal infections
1. What are the TORCHES infections in a neonate?
2. Describe the cutaneous findings in neonatal herpes simplex viral (HSV) infections.
HSV infection usually presents as grouped vesicles on an erythematous base. These lesions can be present on any part of the skin but are more common on the face, scalp, or buttocks (Fig. 57-1). They may also be generalized or disseminated or occur in the perianal region in a breech-delivered baby. In the intrauterine-exposed baby, they may present as atrophic areas with scarring.
3. Is neonatal herpes simplex dangerous?
Neonatal herpetic infections are usually severe (especially if lesions are disseminated or the central nervous system [CNS] is involved) and require immediate diagnosis and treatment. The majority of infants with HSV infection acquire it in the intrapartum period or postnatally. Even with adequate treatment, the mortality rate approaches 50% in infants with disseminated disease, and the incidence of long-term morbidity is significant.
Kohl S: Herpes simplex virus. In Behrman R, Kliegman R, Jenson H, editors: Nelson textbook of pediatrics. Philadelphia, 2004, WB Saunders, pp 1051–1057.
4. What percentage of herpes-infected neonates display skin or mucosal lesions?
About 65% of infected infants display lesions shortly after birth, with disseminated disease occurring during the first 2 weeks of life. This includes infants with skin, eye, and mouth lesions (40%) as well as those with disseminated disease (25%) that includes the skin. If intrauterine exposure has occurred, lesions are usually present at birth. Fortunately, intrauterine transmission of HSV occurs in fewer than 5% of cases.
Jacobs RF: Neonatal herpes simplex virus infections, Semin Perinatol 22:64–71, 1998.
6. What tests can be done to diagnose herpes infections? How should material be obtained for these tests?
To obtain specimens for diagnostic testing, scrape the base of a blister and smear the material on a microscope slide. Stain (e.g., Wright’s stain) and look for multinucleated giant cells. If available, send another slide for a HSV-fluorescein antibody test. Confirmation of a cytopathic effect can be made by immunofluorescence using antibodies specific to HSV-1 and HSV-2. Material from the blister base can be sent for viral culture. The sensitivity of performing a culture is best for a vesicular lesion. It is also advisable to culture urine, nasopharynx, conjunctiva, and cerebrospinal fluid, if indicated. The polymerase chain reaction (PCR) detects viral DNA and can be important in diagnosing HSV encephalitis.
7. What is congenital varicella syndrome?
Intrauterine infection with varicella virus that occurs in the first trimester may result in congenital varicella syndrome. These infants are born with hypoplasia of the limbs and exhibit cutaneous zosteriform scars and atrophy. Interestingly, there have been reports of neonates developing herpes zoster, which implies that they must have had chickenpox in utero. The future of varicella disease may be altered by the continued use of the varicella vaccine.
8. What is the average age of onset of lesions in a neonate exposed to varicella perinatally? When is there an increased risk of mortality?
The age of onset of varicella lesions is usually within the first 10 days of life. Neonatal varicella is fatal in about 30% of patients whose mothers developed lesions from 5 days before to 2 days after delivery.
Smith CK, Arvin AM: Varicella in the fetus and newborn, Semin Fetal Neonatal Med 14:209–217, 2009.
9. What is the treatment of neonatal HSV and varicella infection?
Early identification of infection and initiation of therapy are the most important aspects of treatment. Intravenous acyclovir or vidarabine is recommended for either infection. The usual course is 14 to 21 days. Ophthalmologic examination may be necessary and adequate isolation precautions must be instituted. For varicella infection, varicella-zoster immune globulin (VZIG) is recommended for cases with evidence of maternal infection 5 days before to 2 days after delivery (given within 48 to 96 hours after exposure). VZIG is not indicated for infants born to mothers with herpes zoster.
10. What is a “blueberry muffin baby”? What is the significance of this diagnosis?
This term applies to babies exhibiting blue-red or red indurated macules or papules on the face, trunk, or scalp present at birth, or within the first 2 days of life (Fig. 57-2). These lesions represent extramedullary dermal erythropoiesis and are seen in congenital rubella syndrome, toxoplasmosis, cytomegalovirus infection, neuroblastoma, leukemia, erythroblastosis fetalis, and twin transfusion syndrome.
11. At what time during pregnancy is there the highest risk of congenital rubella following maternal infection?
The risk is highest if maternal exposure occurs during the first 20 weeks of pregnancy. The risk of fetal infection is 90% during the first trimester; the majority of these infants suffer from congenital defects. Between the 12th and 20th weeks of gestation, the infection risk drops to 50%, and about one third of these infants have sequelae.
13. Are any precautions necessary for infants with congenital rubella syndrome at the time of hospital discharge?
14. Why is human parvovirus infection important to a pregnant woman?
Human parvovirus B19, the etiologic agent of erythema infectiosum, readily infects erythroblasts and may, therefore, result in hydrops fetalis and fetal death. This risk is small, with current studies showing a 2% to 9% risk after infection during the first 16 to 28 weeks of pregnancy. Fortunately, about 50% of pregnant women have serologic evidence of prior exposure to parvovirus B19.
Tolfvenstam T, Broliden K: Parvovirus B19 infection, Semin Fetal Neonatal Med 14:218–221, 2009.
Key Points: Neonatal Infection
1. The TORCHES infections are toxoplasmosis; other (varicella-zoster virus, parvovirus B19); rubella; cytomegalovirus; herpes simplex virus and HIV; enteroviruses and Epstein-Barr virus; and syphilis.
15. Are most infants with congenital cytomegalovirus (CMV) infection symptomatic?
No. Ninety percent of congenitally CMV-infected infants are asymptomatic. The other 5% to 10% usually have disease manifested by hepatosplenomegaly, hemorrhagic diatheses, and jaundice. The mortality rate in overtly symptomatic infants is almost 30%.
DeVries J: The ABC’s of CMV, Adv Neonatal Care 7:248–255, 2007.
18. Describe a clinical presentation of congenital human papillomavirus infection.
The infant can present with voice changes or a persistent abnormal hoarse cry, due to laryngeal papillomas thought to be acquired during passage through the infected birth canal. The time between rupture of the amnion and delivery seems to be a critical factor in vertical transmission rate. These signs of infection may not be evident for several months to several years of age.
Anogenital warts in young children can also be acquired as a congenital infection, through sexual abuse, or by other postnatal, nonsexual contact with affected adults (Fig. 57-3).
19. What is the risk of HIV infection transmission to an infant born from an HIV-positive mother?
The risk of transmission ranges from 2% for HIV-infected mothers receiving multidrug antiretroviral therapies up to 30% for mothers with no previous preventative treatment during pregnancy. By 2005, in the United States, almost 8500 children had been diagnosed with acquired immunodeficiency syndrome (AIDS) who were infected perinatally. Since 1994, studies show the risk of perinatal transmission to be even less than 2% (as published by the Pediatric AIDS Clinical Trials Group 076). Most often, infected and uninfected infants cannot be clinically distinguished at birth.
20. What is Hutchinson’s triad?
Interstitial keratitis, Hutchinson’s teeth, and eighth nerve deafness. These are common findings in late congenital syphilis. Interstitial keratitis is the most common lesion in this triad. It is rare before age 8 and after age 40. Both eyes are usually affected, and the corneal clouding may be spotty or diffuse. Hutchinson’s teeth are due to deficient development of the permanent teeth buds and are characterized by conical central incisors with notching of the distal free margin. Eighth nerve deafness usually occurs after interstitial keratitis, is usually bilateral, and is often preceded by tinnitus and vertigo.
21. Are there any other stigmata of late congenital syphilis?
Bone involvement is common with periostitis of long bones, resulting in thickened and bent tibias (saber shins) and other bony abnormalities. Other stigmata include scarring and wrinkling at the corners of the mouth (rhagades), saddle nose, dish facies, Parrot’s nodes on the skull, and salt-and-pepper fundi.
Weston WL, Lane AT, Morelli JG: Color textbook of pediatric dermatology, St Louis, 2002, Mosby.
22. What are the physical findings of early congenital syphilis?
Syphilitic rhinitis is the most important and frequent physical finding in early congenital syphilis. It is characterized by a profuse serous nasal discharge (snuffles) that is teeming with spirochetes. The inflammatory process leads to eventual cartilage and bone deformity. Other findings include papulosquamous skin lesions, perianal erosions (Fig. 57-4), blistering of the hands and feet, hepatosplenomegaly, meningitis, meningoencephalitis, and osteochondritis. Congenital syphilis is a serious infection that, if untreated, has significant mortality.
