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Clinical features of varicella-zoster virus infection: ChickenpoxAuthorMary A Albrecht, MDSection EditorsMartin S Hirsch, MD

Sheldon L Kaplan, MDDeputy EditorJennifer Mitty, MD, MPHDisclosures

All topics are updated as new evidence becomes available and ourpeer review processis complete.Literature review current through:Apr 2013. | This topic last updated:abr 11, 2013.

INTRODUCTIONVaricella-zoster virus (VZV) is one of eight herpesviruses known to cause human infection and is

distributed worldwide. VZV infection causes two clinically distinct forms of disease: varicella (chickenpox) and herpes

zoster (shingles). Primary VZV infection results in the diffuse vesicular rash of varicella, or chickenpox. Endogenous

reactivation of latent VZV typically results in a localized skin infection known as herpes zoster, or shingles.

Primary varicella infection in children is generally a mild disease compared to more severe presentations in adults or

immunocompromised patients of any age. The rates of infection, hospitalizations, and mortality have all declined in the US

since the introduction of thevaricella vaccinein 1995; immunization is recommended in all children before the age of five

years and in nonimmune adults. (See"Prevention of varicella-zoster virus infection: Herpes zoster"and"Epidemiology of

varicella-zoster virus infection: Chickenpox".)

The major clinical manifestations and complications of chickenpox will be reviewed here. Infection in the neonate and the

treatment and prevention of this infection, including thevaricella vaccine,and herpes zoster are discussed separately.

(See"Varicella-zoster infection in the newborn"and"Treatment of varicella-zoster virus infection:

Chickenpox"and"Prevention of varicella-zoster virus infection: Chickenpox"and"Measles-mumps-rubella vaccination in

high risk adults"and"Clinical manifestations of varicella-zoster virus infection: Herpes zoster"and"Prevention of varicella-

zoster virus infection: Herpes zoster".)

TRANSMISSION AND VIROLOGYChickenpox is highly contagious, with secondary household attack rates of >90

percent in susceptible individuals [1,2].

Infection control issues within hospitals are discussed elsewhere. (See"Prevention and control of varicella in hospitals".)

Transmission routesTransmission occurs in susceptible hosts via contact with aerosolized droplets from

nasopharyngeal secretions of an infected individual or by direct cutaneous contact with vesicle fluid from skin lesions [1].

Airborne transmission of VZV to susceptible nursing staff has also been reported in a hospital unit [3].

ViremiaVZV is a double-stranded, linear DNA virus encoding approximately 75 proteins [1,4,5]and possessing a lipid-

containing envelope with glycoprotein spikes. After gaining entry, the virus undergoes localized replication at an undefined

site with concurrent replication in regional lymph nodes by days four to six [6]. This is followed by a primary viremic phase

with seeding of the reticuloendothelial system. A secondary phase of viremia occurs after approximately nine days [7]and

persists through the development of skin lesions [8,9].

Incubation periodThe average incubation period for varicella infection is 14 to 16 days, although this interval can

range from 10 to 21 days [10]. The period of infectivity is generally considered to last from 48 hours prior to the onset of

rash until skin lesions have fully crusted.

Administration ofvaricella zoster immune globulin(VZIG) following exposure can prolong the incubation period from 21

days to 28 days. (See"Prevention and control of varicella in hospitals".)

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ReinfectionIt has been generally thought that second episodes of varicella infection in immunocompetent individuals

rarely occur [11,12], although subclinical reinfection with VZV is common [13]. However, post-vaccine surveillance

programs have suggested that a second episode of primary varicella in immunocompetent individuals might be more

common than previously thought [14]. More than 95 percent of first infections were physician diagnosed, epidemiologically

linked to another case, or had a rash consistent with varicella; the same was true for reported second infections. The

study demonstrated the following results:

While the overall incidence of primary varicella declined substantially after the introduction of vaccine (2934

versus 587 cases in 1995 and 1999, respectively), the proportion of cases of varicella in individuals with a

previous history of the disease increased from 4.5 to 13.3 percent. None of the patients with a second episode of

varicella had been vaccinated.

People who reported reinfections were generally healthy. There was a family history of repeat infections in 45

percent of people who reported reinfections.

Of note, diagnoses made within this study were clinically-based and not laboratory-confirmed.

CLINICAL MANIFESTATIONSPrimary infection with VZV routinely occurs during childhood and is usually a benign

self-limited illness in immunocompetent children. However, varicella can be a severe disease in adolescents, adults, and

immunosuppressed or immunocompromised individuals of any age. Secondary cases in household contacts appear to be

more severe than primary cases [10].

Uncomplicated varicellaThe clinical manifestations of varicella in healthy children generally develop within fifteen

days after the exposure and typically include a prodrome of fever, malaise, or pharyngitis, loss of appetite [1], followed by

the development of a generalized vesicular rash, usually within 24 hours.

The vesicular rash of varicella, which is usually pruritic, appears in successive crops over several days. The lesions begin

as macules that rapidly become papules followed by characteristic vesicles; these lesions can then develop a pustular

component followed by the formation of crusted papules [10](picture 1). The patient with varicella typically has lesions in

different stages of development on the face, trunk and extremities. New vesicle formation generally stops within four days,

and most lesions have fully crusted by day six in normal hosts [1]. Crusts tend to fall off within about one to two weeks

and leave a temporary area of hypopigmentation in the skin [10].

Impact of vaccine on clinical manifestationsApproximately 20 percent of children who receive one dose ofvaricella

vaccinemay develop varicella infection, known as "breakthrough disease", if exposed to VZV [15,16]. A report on the

clinical and epidemiological characteristics of varicella in populations with increasing vaccine coverage between 1997 and

2005 identified the following trends [15]:

In vaccinated children 1 to 14 years of age, varicella was more often mild and modified than in unvaccinated

children (eg, less fever and a lower number of lesions).

The accompanying rash was significantly more likely to be atypical in nature among vaccinated children (eg,

maculopapular).

Complications were less likely to be reported among vaccinated children than unvaccinated children

Neurologic complications (eg, encephalitis) continue to be rare [17].

COMPLICATIONS OF VARICELLAPrior to the introduction ofvaricella vaccinein 1995, healthy children and

adolescents accounted for 80 percent of the estimated 9300 annual varicella-related hospitalizations in the United States

[2,18].

A survey was conducted from 1990 to 1992 of over 250,000 members of a health maintenance organization to assess the

epidemiology of varicella and its complications [19]. Following a medical record review process, a total of 107 confirmed

complications were identified, including bacterial skin infections and pneumonia. Skin infections were associated with the

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most hospitalizations in the youngest age group (19 years of age. (See"Epidemiology of varicella-zoster virus infection: Chickenpox".)

After the introduction of vaccine, the number of complications in children dramatically declined, although the most

common complication has remained bacterial superinfections; in the Varicella Active Surveillance Project (VASP),

complications included skin and soft tissue infections (42 percent), dehydration (11 percent), and neurologic complications

(9 percent) [17].

Although vaccine attenuates disease manifestations substantially, complications can still occur and are discussed below

[15].

Skin/soft tissue infectionsPrimary varicella infection in children has been associated with an increased incidence of

invasive group A streptococcal soft tissue infection [20-23]. Infectious complications have included cellulitis, myositis,

necrotizing fasciitis, and toxic shock syndrome [20-25].

Neurologic complicationsEncephalitis and, mostly in the past, Reye syndrome, are the most serious complications

of VZV infection, although they are uncommonly seen [17]. Other less common neurologic complications include transient

focal deficits, aseptic meningitis, transverse myelitis, vasculitis, and hemiplegia [1].

EncephalitisIn one series of serious varicella-related complications, encephalitis accounted for 20 percent of

varicella-related hospitalizations [26]. Two distinct forms of encephalitis have been described [1,17,26]:

Acute cerebellar ataxia

Diffuse encephalitis

These disorders typically develop toward the end of the first week of the exanthem, but there are cases in which central

nervous system involvement has preceded the rash [27,28].

Acute cerebellar ataxia most often develops in children, occurring in about 1 in 4000 varicella infections in children

younger than 15 years of age [29]. It has a limited time course and is generally followed by complete recovery. These

issues are discussed in detail separately. (See"Acute cerebellar ataxia".)

Diffuse encephalitis most often occurs in adults, but young children are also at increased risk [30,31]. The clinicalmanifestations include delirium, seizures, and focal neurologic signs. Pathologic examination has revealed three main

patterns; although one usually predominates, mixed features are seen in many cases [32]:

A medium to large vessel vasculopathy with bland or hemorrhagic infarctions

A small vessel vasculopathy with mixed ischemic and demyelinating lesions

A ventriculitis or periventriculitis

Reported mortality rates approach 10 percent and long-term neurologic sequelae reported in up to 15 percent of survivors

[30,31,33]. Not surprisingly, varicella encephalitis is more severe in immunosuppressed hosts, such as patients with AIDS

and transplant recipients. Such patients typically have a fulminant course with seizures, mental status changes, and focal

deficits including stroke syndromes.

There is no proven effective therapy once encephalitis occurs. Acyclovirhas been used with anecdotal success [34,35].

Reye syndromeReye syndrome, an illness developing during the course of varicella infection in children, typically

presents with a distinct constellation of symptoms including nausea, vomiting, headache, excitability, delirium, and

combativeness with frequent progression to coma [36]. Since salicylate use was identified as a major precipitating factor

for the development of Reye syndrome [37], this complication has virtually disappeared, concomitant with advisories

against using salicylates in febrile children. In a surveillance study from 1980 through 1997, 1207 cases were reported;

the number of cases peaked in 1980 at 555 and dramatically declined, with warnings issued against the use ofaspirinin

patients with varicella or influenza [38]. From 1987 to 1993 fewer than 36 cases per year were reported; fewer than two

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cases per year were noted from 1994 to 1997. (See"Acute toxic-metabolic encephalopathy in children", section on 'Reye

syndrome'.)

PneumoniaIn immunocompetent children with varicella, pneumonia remains an uncommon complication; in contrast,

pneumonia accounts for the majority of morbidity and mortality seen in adults with varicella, although it is infrequently

seen since the introduction of vaccine (eg, 60 per 10,000 cases) [17].

In immunocompetent adults, varicella pneumonia has a reported incidence of about one in 400 cases [29,39,40]and

carries an overall mortality of between 10 and 30 percent [41,42]. However, in patients with respiratory failure who require

mechanical ventilation, mortality rates approach 50 percent despite institution of aggressive therapy and appropriate

supportive measures [43-45].

Risk factors linked to the development of varicella pneumonia include cigarette smoking [33,41,46], pregnancy [47],

immunosuppression [31], and male sex [39]. Pregnancy may be an additional risk factor for severe varicella pneumonia

although the incidence of pneumonia does not appear to be higher in pregnant patients with varicella [48]. (See"Varicella-

zoster virus infection in pregnancy".)

Varicella pneumonia typically develops insidiously within one to six days after the rash has appeared with symptoms of

progressive tachypnea, dyspnea, and dry cough; hemoptysis has occasionally been reported [42]. Patients demonstrate

impaired gas exchange with progressive hypoxemia. Chest radiographs typically reveal diffuse bilateral infiltrates; in the

early stages a nodular component may be present, which can subsequently become calcified [42,49,50]. Promptadministration of intravenousacyclovirhas been associated with clinical improvement and resolution of pneumonia in

selected series [42,44,51]. (See"Acyclovir: An overview".)

The use of steroids as adjunctive therapy for the treatment of life-threatening varicella pneumonia is controversial and has

not been well studied. An uncontrolled study evaluated 15 adult patients with varicella pneumonia; 11 of these 15 patients

(73 percent) were smokers and eight (53 percent) required mechanical ventilation [45]. All were treated with

intravenousacyclovirand supportive measures; six also received steroids. The patients who received steroids had a

shorter hospitalization (median difference of 10 days) and a shorter ICU stay (median difference eight days). The authors

of this report suggested a randomized trial, which to date has not been performed.

HepatitisBiopsy proven visceral hepatic involvement with varicella is uncommon, but when it occurs, generally affects

immunosuppressed hosts including transplant recipients and AIDS patients; the outcome is frequently fatal [52-55].

Clinical varicella hepatitis in healthy individuals is rare despite the fact that asymptomatic or subclinical transaminase

elevation, coincident with the onset of varicella, has been documented in 77 percent of children in one series [56].

In immunosuppressed hosts with varicella hepatitis, the most common presenting features have typically included

cutaneous vesicular lesions, fever, and acute abdominal or back pain [55,57]. However, the rash may precede [54],

appear coincident with [52], or follow [53]the onset of hepatitis, which can delay the diagnosis of this complication. The

development of varicella hepatitis with widespread visceral dissemination has been reported in a bone marrow transplant

patient in the absence of a rash [58]. Fulminant liver failure with disseminated intravascular coagulation (DIC) and

gastrointestinal hemorrhage with dissemination have also been reported [59,60].

OtherOther clinical manifestations among children and adults have included diarrhea, pharyngitis, and otitis media

[17].

IMMUNOSUPPRESSED HOSTSPatients with a history of underlying malignancy, steroid use or immunosuppressive

therapy, HIV infection, or solid organ transplantation are susceptible for disseminated varicella due to impaired cellular

immunity. Immunosuppressed hosts who develop varicella experience more frequent severe morbidity and higher

mortality rates compared to normal hosts. While only 0.1 percent of varicella infections develop in this population, this

group accounted for as many as 25 percent of varicella-related deaths in the prevaccine era [1].

Patients with rheumatologic diseases treated with tumor necrosis factor (TNF) antagonists remain at selectively increased

risk for more severe primary varicella infections compared with the general population [61]. A retrospective review utilizing

a hospital database and national patient registry of rheumatologic diseases, conducted in Spain, evaluated

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hospitalizations due to chickenpox in patients with rheumatic diseases. In rheumatologic patients exposed to TNF

antagonists, the estimated incidence rate of hospitalization due to chickenpox was 26 cases per 100,000 (95% CI 10-69)

compared with the expected rate of 1.9 (95% CI 1.8-2.0) in the general population.

Clinical manifestations in the immunosuppressed host can include ongoing development of crops of vesicles over weeks,

large and hemorrhagic skin lesions, pneumonia, or widespread disease with disseminated intravascular coagulation [10].

Varicella vaccineprograms appear to have had a positive impact on severe varicella infection in this patient subset.

Surveillance mortality data compiled from the National Center for Health Statistics during the period from 1990-2001 [62]

reviewed mortality rates in high-risk individuals for which varicella was identified as the underlying cause of death. High-

risk individuals were defined as those with conditions for which vaccination is contraindicated: cancer, HIV infection or

AIDS, and other immunodeficiencies:

Between 1990 and 2001, cancer accounted for the greatest proportion of high-risk conditions among those

younger than 20 years (71 percent) and those of 50 years of age or older (90 percent). Among high-risk persons

20 to 49 years of age, HIV infection or AIDS were the most common conditions (58 percent).

Overall, however, patients with high-risk conditions accounted for few of the varicella deaths in this study

(approximately 20 percent).

The authors surmised that patients who were identified to be at high risk for severe varicella may have received earlyaggressive therapy with intravenousacyclovirthat favorably impacted survival. A higher rate of varicella vaccination

among close contacts of persons ineligible for vaccination may also have occurred; thus herd immunity may have

prevented some cases of primary infection [62]. (See"Acyclovir: An overview".)

There are few data on varicella in HIV-infected children. One natural history in 57 HIV-infected children included patients

with primary varicella or HIV-infected controls without a history of varicella (matched by age and CD4 count) [63]. Thirty

children developed varicella, but only one case was judged to be severe; 22 of 30 had received acyclovirtherapy.

While the outcome of primary infection was favorable in this population of HIV-infected children, the incidence of later

herpes zoster infection was high. Of the children with a history of varicella, eight (27 percent) developed herpes zoster an

average of 1.9 years after the episode of primary varicella [63].

INFORMATION FOR PATIENTSUpToDate offers two types of patient education materials, The Basics and Beyond

the Basics. The Basics patient education pieces are written in plain language, at the 5th

to 6thgrade reading level, and

they answer the four or five key questions a patient might have about a given condition. These articles are best for

patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education

pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th

to 12thgrade reading level

and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to

your patients. (You can also locate patient education articles on a variety of subjects by searching on patient info and th e

keyword(s) of interest.)

Basics topics (see"Patient information: Chickenpox (The Basics)")

Beyond the Basics topics (see"Patient information: Chickenpox prevention and treatment (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Primary varicella infection in children is generally a mild disease compared to more severe presentations in adults

or immunocompromised patients of any age. The incidences of infection, hospitalizations, and mortality have all

declined since the introduction of thevaricella vaccinein 1995. (See'Introduction'above.)

Chickenpox is highly contagious, with secondary household attack rates of >90 percent in susceptible individuals.

Transmission occurs in susceptible hosts via contact with aerosolized droplets from nasopharyngeal secretions of

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ate.com/contents/clinical-features-of-varicella-zoster-virus-infection-chickenpox/abstract/62http://www.uptodate.com/contents/varicella-virus-vaccine-drug-information?source=see_linkhttp://www.uptodate.com/contents/clinical-features-of-varicella-zoster-virus-infection-chickenpox/abstract/10

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an infected individual or by direct cutaneous contact with vesicle fluid from skin lesions. (See'Transmission and

virology'above.)

The clinical manifestations of varicella generally develop within fifteen days after the exposure and typically

include a prodrome of fever, malaise, or pharyngitis, followed by the development of a generalized vesicular rash.

(See'Clinical manifestations'above.)

Complications of varicella in children can include bacterial superinfection while pneumonia is more common in

adults. (See'Complications of varicella'above.)

Patients with a history of underlying malignancy, steroid use or immunosuppressive therapy, HIV infection, or

solid organ transplantation are susceptible for disseminated varicella due to impaired cellular immunity.

(See'Immunosuppressed hosts'above.)

Use of UpToDate is subject to theSubscription and License Agreement.

REFERENCES

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