{
"topic": "Varicella Zoster",
"slug": "varicella-zoster",
"category_id": 15684,
"passage_count": 14,
"source_chars": 11323,
"enough_material": true,
"references": [
{
"title": "MedStudy Pediatrics Core 11th Edition 2024-2025",
"author": null,
"pages": [
790
]
},
{
"title": "Zitelli and Davis' Atlas of Pediatric Physical Diagnosis: Expert Consult - Online",
"author": null,
"pages": [
495
]
},
{
"title": "Kliegman R. Nelson Textbook of Pediatrics 2-Volume Set 22ed 2024",
"author": null,
"pages": [
1351,
2007,
2008
]
},
{
"title": "Pediatric Clinical Practice Guidelines & Policies, 18th Edition",
"author": "American Academy of Pediatrics",
"pages": [
896
]
},
{
"title": "Red Book Atlas of Pediatric Infectious Diseases",
"author": "American Academy of Pediatrics (AAP);Tan, Tina Q.;",
"pages": [
824
]
},
{
"title": "Gomella's Neonatology: Management, Procedures, On-Call Problems, Diseases, and Drugs, Eighth Edition",
"author": "Tricia Lacy Gomella, Fabien G. Eyal and Fayez Bany-Mohammed",
"pages": [
1244,
1245
]
},
{
"title": "CURRENT Diagnosis and Treatment Pediatrics, Twenty-Fourth Edition",
"author": "Hay, William W., Levin, Myron J., Deterding, Robin R., Abzug, Mark J.",
"pages": [
443
]
},
{
"title": "Netters Pediatrics (Florin \u0422., Ludwig St.)",
"author": null,
"pages": [
636
]
}
],
"passages": [
{
"source": "MedStudy Pediatrics Core 11th Edition 2024-2025, p. 790",
"text": "to varicella and has a history of exposure must be kept in a negative-pressure isolation room with airborne and contact precautions during the incubation period\u2014 specifically from days 8-21 after exposure. Remember: Individuals who receive varicella-zoster IG may have a longer incubation period\u2014up to 28 days. In the hospital setting, a child with varicella is considered infectious and remains in isolation until all lesions are crusted over or at least a minimum of 5 days if crusting occurs earlier. Herpes Zoster (Shingles) Herpes zoster is caused by reactivation of VZV. Varicella vaccine (a live attenuated virus vaccine) can also cause herpes zoster in children with immunocompetence; how- ever, it is usually mild. Most commonly, herpes zoster affects 1 or 2 adjacent dermatomes, with thoracic, cranial nerve, and lumbosacral areas most frequently involved. The lesions increase in number over 3-5 days and crust over by 2 weeks. A Tzanck smear (now of only historical value) shows"
},
{
"source": "Zitelli and Davis' Atlas of Pediatric Physical Diagnosis: Expert Consult - Online, p. 495",
"text": "Varicella in the normal pediatric host is a relatively benign, albeit highly contagious illness caused by the varicella-zoster virus. A brief prodrome of low-grade fever, upper respiratory tract symptoms, and mild malaise may occur, followed rapidly by the appearance of a pruritic exanthem. Lesions appear in crops and evolve rapidly over several hours. Most patients have three crops, although some may have only one and others may have as many as five. Initial crops involve the trunk and scalp, and subsequent crops are distributed more peripherally; thus the mode of spread is centrifugal. The presence of scalp lesions with the initial crop is often helpful in diagnosing the infection in a patient who presents early in the course of the disease. Lesions begin as tiny erythematous papules that rapidly enlarge to form thin-walled, superficial central vesicles surrounded by red halos (Fig. 12-3, _A_ ). Vesicular fluid changes promptly from clear to cloudy; then drying begins, resulting in an umbilicated"
},
{
"source": "Kliegman R. Nelson Textbook of Pediatrics 2-Volume Set 22ed 2024, p. 2008",
"text": "## **CLINICAL MANIFESTATIONS** Varicella is an acute febrile rash illness that was common in children in the United States before the universal childhood vaccination program. It has variable severity but is usually self- limited. It may be associated with severe complications, including bacterial superinfection, especially with staphylococci and group A streptococci, pneumonia, encephalitis, bleeding disorders, congenital infection, and life- threatening perinatal infection. Herpes zoster is not common in children and typically causes localized cutaneous symptoms, but may disseminate in immunocompromised patients. ## **Varicella in Unvaccinated Individuals**"
},
{
"source": "Pediatric Clinical Practice Guidelines & Policies, 18th Edition, p. 896",
"text": "Although varicella has been reported as a cause of airborne sports-related infections,[157] such reports are rare in the era of immunization with the live attenuated vaccine against the virus. The varicella-zoster virus (\u200dVZV) manifests primarily as a generalized, pruritic, vesicular rash consisting of 250 to 500 lesions in different stages (\u200dcrops) of development and crusting.[39] There is usually an associated lowgrade fever, and there may be other systemic symptoms. Disease in vaccinated children is often milder and atypical in nature compared with the wild virus infection and requires a high index of suspicion. Diagnosis is usually made on the basis of a typical clinical picture coupled with history of exposure, but vesicular fluid or scab scraping can be used for confirmation by using PCR, direct fluorescent antibody assay, or VZVspecific culture. A significant increase in serum varicella immunoglobulin G antibody between acute and convalescent serum samples can also assist in diagnosis."
},
{
"source": "Kliegman R. Nelson Textbook of Pediatrics 2-Volume Set 22ed 2024, p. 2007",
"text": "Varicella- zoster virus (VZV) causes primary, latent, and reactivation infections. The primary infection manifests as varicella (chickenpox) and results in establishment of a lifelong latent infection of sensory ganglionic neurons. Reactivation of the latent infection causes herpes zoster (shingles). Although often a mild illness of childhood, varicella can cause substantial morbidity and mortality in otherwise healthy children. Morbidity and mortality are higher in immunocompetent infants, adolescents, and adults, as well as in immunocompromised persons. Varicella predisposes to severe group A streptococcus and staphylococcus infections. Primary clinical disease can be prevented by immunization with live- attenuated varicella vaccine. A clinically modified disease can occur among vaccinated persons (breakthrough varicella), usually with milder presentation. Varicella and herpes zoster can be treated with antiviral drugs. Vaccines are also available to prevent herpes zoster in older adults."
},
{
"source": "Red Book Atlas of Pediatric Infectious Diseases, p. 824",
"text": "Varicella-Zoster Virus infections   **Image 161.24** Bullous varicella (uncomplicated) in a 1-year-old. courtesy of George nankervis, MD. **Image 161.23** Herpes zoster (shingles). courtesy of c. W. leung.  **Image 161.25**"
},
{
"source": "Gomella's Neonatology: Management, Procedures, On-Call Problems, Diseases, and Drugs, Eighth Edition, p. 1244",
"text": " There are 3 forms of varicella-zoster infections involving the fetus and neonate: **fetal, congenital (early neonatal), and postnatal** . ## FETAL VARICELLA SYNDROME - **I. Definition. VZV** is a teratogen that can cross the placenta and cause a pattern of congenital malformations called fetal varicella syndrome (FVS). This form occurs when the mother has her first exposure to VZV during the first half of pregnancy. The syndrome is also recognized in the literature as **congenital varicella syndrome (CVS)** . - **II. Incidence.** Only approximately 5% of women of childbearing age are susceptible to VZV. The incidence of varicella during pregnancy is estimated at 1 to 5 cases per 10,000 pregnancies. The incidence of **embryopathy and fetopathy (FVS)** after maternal varicella infection in the first 20 weeks is 1% to 2%."
},
{
"source": "CURRENT Diagnosis and Treatment Pediatrics, Twenty-Fourth Edition, p. 443",
"text": "## **2. Varicella-Zoster Infection** ## \u00bb **Clinical Findings** Grouped vesicles in a dermatome, usually on the trunk or face, suggest varicella-zoster reactivation. Zoster in children may not be painful and usually has a mild course. In patients with compromised host resistance, the appearance of an erythematous border around the vesicles is a good prognostic sign. Conversely, large bullae without a tendency to crusting and systemic illness imply a poor host response to the virus. Varicella-zoster and herpes simplex lesions undergo the same series of changes: papule, vesicle, pustule, crust, slightly depressed scar. Lesions of primary varicella appear in crops, and many different stages of lesions are present at the same time (eg, papules), eccentrically placed vesicles on **411** **SKIN** an erythematous base (\u201cdew drop\u201d on a rose petal), erosions, and crusts."
},
{
"source": "Kliegman R. Nelson Textbook of Pediatrics 2-Volume Set 22ed 2024, p. 1351",
"text": "varicella- zoster disease causing pneumonitis, encephalitis, and CNS vasculitis. Treatment is not defined, but avoiding live viral vaccines, providing antiviral prophylaxis, and providing non- live annual influenza and COVID- 19 vaccination to affected individuals and family members appear prudent."
},
{
"source": "Netters Pediatrics (Florin \u0422., Ludwig St.), p. 636",
"text": "  **----- Start of picture text -----**
Herpes zoster or shingles
**----- End of picture text -----**
**Figure 97-4** _Clinical presentations of varicella zoster virus._ ## **EVALUATION AND MANAGEMENT** The diagnosis of VZV can be confirmed using direct fluorescence antigen or PCR. Viral cultures can also be done from tissue sample in 3 to 4 days. A fourfold increase in VZV IgG titer can also be confirmatory. There is usually an initial leukopenia and then a lymphocytosis. In most cases, the liver enzymes are slightly elevated. Acyclovir can be used to treat varicella infections but is not currently recommended in healthy children. It can be given to adolescents, children older than 12 months old with skin or pulmonary disorders and children receiving chronic [Figure OCR, page 636, figure 2] N 614 SECTION XV \u2022 Infectious Disease"
},
{
"source": "The Harriet Lane Handbook (The Johns Hopkins Hospital), p. 559",
"text": "||Varicella zoster
virus (VZV)1
Primary varicella (chickenpox): pruritic
macules that progress to vesicles, plus
fever and malaise.
Herpes zoster: painful, vesicular, dermato-
mal rash.
SeeTable 17.1for congenital VZV.
_DNA_, Deoxyribonucleic acid;_EIA_, enzyme immunoassay;_HLH_, hemophagocytic
cell;_RT- PCR_, reverse- transcriptase polymerase chain reaction.
~~**TABLE 17.3\u2014cont\u2019d**~~
**PEDIATRIC VIRAL ILLNESSES**
**Presentation**|Airborne spread or direct contact.
Incubation period 10\u201321 days.
Reactivation of latent VZV from sensory
ganglia.
Clinical.
PCR of vesicular fuid.
Supportive care if healthy host.
Treat with acyclovir/valacyclovir
if chronic skin or lung disease,
unvaccinated and 12+ years
old, or immunocompromised.
Acyclovir/valacyclovir reduce
duration and risk of posther-
petic neuralgia.
lymphohistiocytosis;_Ig_, immunoglobulin;_IVIG_, intravenous immunoglobulin;_NSAIDs_, nonsteroidal antiinfammatory drugs;_RBC_, red"
},
{
"source": "The Harriet Lane Handbook 22nd Edition (2020) (The Johns Hopkins Hospital), p. 559",
"text": "||Varicella zoster
virus (VZV)1
Primary varicella (chickenpox): pruritic
macules that progress to vesicles, plus
fever and malaise.
Herpes zoster: painful, vesicular, dermato-
mal rash.
SeeTable 17.1for congenital VZV.
_DNA_, Deoxyribonucleic acid;_EIA_, enzyme immunoassay;_HLH_, hemophagocytic
cell;_RT- PCR_, reverse- transcriptase polymerase chain reaction.
~~**TABLE 17.3\u2014cont\u2019d**~~
**PEDIATRIC VIRAL ILLNESSES**
**Presentation**|Airborne spread or direct contact.
Incubation period 10\u201321 days.
Reactivation of latent VZV from sensory
ganglia.
Clinical.
PCR of vesicular fuid.
Supportive care if healthy host.
Treat with acyclovir/valacyclovir
if chronic skin or lung disease,
unvaccinated and 12+ years
old, or immunocompromised.
Acyclovir/valacyclovir reduce
duration and risk of posther-
petic neuralgia.
lymphohistiocytosis;_Ig_, immunoglobulin;_IVIG_, intravenous immunoglobulin;_NSAIDs_, nonsteroidal antiinfammatory drugs;_RBC_, red"
},
{
"source": "Gomella's Neonatology: Management, Procedures, On-Call Problems, Diseases, and Drugs, Eighth Edition, p. 1245",
"text": "- **A. Appearance of maternal varicella during pregnancy.** - **B. Presence of congenital skin lesions** in dermatomal distribution and/or neurologic defects, eye disease, or limb hypoplasia. - **C. Proof of intrauterine varicella-zoster virus infection** by detection of viral DNA in the infant by polymerase chain reaction (PCR), presence of VZV-specific immunoglobulin (Ig) M, persistence of VZV IgG beyond 7 months of age, or appearance of zoster (shingles) during early infancy."
},
{
"source": "Red_Book_2021_2024_Report_of_the_Comm_z_library_sk,_1lib_sk,, p. 880",
"text": "Fetal infection after maternal varicella during the first or early second trimester of pregnancy occasionally results in fetal death or varicella embryopathy, characterized by limb hypoplasia, cutaneous scarring, eye abnormalities, and damage to the central nervous system (congenital varicella syndrome). The incidence of the congenital varicella syndrome among infants born to mothers who experience gestational varicella is approximately 2% when infection occurs between 8 and 20 weeks of gestation. Rarely, cases VARICELLA-ZOSTER VIRUS INFECTIONS 832 of congenital varicella syndrome have been reported in infants of women infected after 20 weeks of pregnancy, the latest occurring at 28 weeks\u2019 gestation. Children infected with VZV in utero may develop zoster early in life without having had extrauterine varicella."
}
]
}