Herpes Zoster: Pain Now, Rash Later

March 31, 2010

A 5-year-old boy was brought for evaluation of left leg pain. He had awoken with the pain 2 days earlier.


Figure 1 – This erythematous papulovesicular rash, consistent with herpes zoster, developed on the medial aspect of the left thigh, leg, and foot of a 5-year-old boy the day after he presented with leg pain.

A 5-year-old boy was brought for evaluation of left leg pain. He had awoken with the pain 2 days earlier. He identified an area just above the medial malleolus as most painful. The pain worsened with movement (eg, walking) and was alleviated minimally with acetaminophen and ibuprofen. There was no history of trauma. By age 4, the child had received all appropriate immunizations except for the second dose of varicella vaccine; he had received the first dose at the age of 1 year.

The boy was crying and would not bear weight on the left leg. His weight was 16.8 kg (37.0 lb; 25th percentile); temperature, 36.5°C (97.6°F); blood pressure, 88/63 mm Hg; respiration rate, 24 breaths per minute; and heart rate, 114 beats per minute. He had a 5-mm lesion that looked like a scab on the medial aspect of the left leg. The hip and knee joints were slightly flexed. There was no swelling or erythema and no limitation of joint movement.

The clinical impression was that of leg pain of unknown etiology. Radiographs of the hip, knee, and ankle were normal. Complete blood cell count revealed a total white blood cell (WBC) count of 9600/μL, with 66.5% neutrophils and 26.8% lymphocytes. The platelet count was 529,000/μL, and erythrocyte sedimentation rate was 4 mm/h. An oral analgesic was prescribed, and follow-up was scheduled in 2 days.


Figure 2 – A similar rash was noted on the left side of the lower back at the level of L3 to L4. Polymerase chain reaction analysis of fluid from one of the vesicles was positive for herpes zoster.

At follow-up, it was noted that the pain had continued and that an erythematous papulovesicular rash had developed on the medial aspect of the left thigh, leg, and foot (Figure 1). There was a similar rash on the left side of the lower back at the level of L3 to L4 (Figure 2). Polymerase chain reaction (PCR) analysis of fluid from one of the vesicles was positive for herpes zoster.

Further questioning revealed that the child had had no previous illness suggestive of chickenpox and had no contact with anyone with chickenpox or shingles. He was treated with oral acyclovir (30 mg/kg/d) in addition to an oral analgesic. Within 3 days, he was pain-free. One week later, the lesions had scabbed over; serum immunoglobulin levels were within normal limits.

HERPES ZOSTER: AN OVERVIEW

Herpes zoster (shingles) occurs as a result of reactivation of latent varicella-zoster virus infection.1 It is characteristically a disease of older persons and is rare in children. Immunocompromised children are affected more frequently than immunocompetent children.2 Affected persons invariably have low or absent cell-mediated immunity to the virus.3 In adults, a prodrome of fever, malaise, headache, and local pain or dysesthesia may develop 1 to 4 days before the onset of cutaneous lesions; however, zoster in children is usually only mildly painful.4

 

The differential diagnosis of localized pain in the absence of a rash would not normally include herpes zoster, especially when the patient is a child. Of note, this child pointed to the medial aspect of his thigh and leg (suggestive of dermatomal affectation) before the appearance of the rash.

 

The widespread use of the varicella vaccine since 1995 has reduced the incidence of chickenpox in children and should reduce herpes zoster later in life.5 However, herpes zoster can occur after varicella immunization; the incidence among vaccinees is about 14 cases per 100,000 person-years.6 When herpes zoster does occur after vaccination, it represents either a new infection with wild-type virus-when the patient has been in contact with a person who has chickenpox or shingles-or a reactivation of the vaccine virus.7-9 The latter scenario seems likely in this case, because the patient had no history of chickenpox infection, had received 1 dose of varicella vaccine, and had no contact with an infected person before the onset of symptoms. In addition, this patient appeared to be immunocompetent (the WBC count, lymphocyte count, and immunoglobulin levels were normal). In immunocompetent children, herpes zoster tends to develop at a younger age when it follows varicella vaccination than it does when it follows natural varicella infection.9 PCR analysis can differentiate the wild-type virus from the vaccine virus,10 although the results do not change the treatment.

KEY POINTS FOR YOUR PRACTICE

Because pain may precede the rash in herpes zoster, include zoster in the differential diagnosis of localized pain in children even when no rash is apparent.
Herpes zoster can occur in a healthy child who has no history of varicella but who has received all or part of the varicella vaccine.

 

Cases of primary vaccine failure among young children who received only 1 dose of the varicella vaccine have been reported.3 Since 2006, the CDC has recommended 2 doses of the vaccine for all children. The second dose is followed by a marked increase in both humoral and cellular immunity3 and by inference should reduce the risk of zoster developing.

 

The use of acyclovir for treatment of herpes zoster may lead to prompt resolution of the rash and pain associated with shingles. This child seemed to respond to this therapy. In immunocompetent hosts, most viral replication stops 72 hours after rash onset. Thus, oral acyclovir is not recommended for routine treatment of varicella-zoster virus infection.11 However, because some controlled studies have shown a modest benefit in children and adolescents given oral acyclovir within 24 hours of rash onset, prompt treatment is recommended for those at increased risk for moderate or severe illness.12,13

 

Varicella-zoster virus can be transmitted via contact with skin lesions of patients who have either chickenpox or zoster, although infectivity is less with zoster. Transmission occurs until all lesions have crusted. Localized zoster lesions that are covered by clothing seem to pose little risk to susceptible people.11

 

Acknowledgment: We appreciate the contribution of Osvaldo Regueira, MD, who took the photographs.

References:

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2. Wootton SH, Law B, Tan B, et al. The epidemiology of children hospitalized with herpes zoster in Canada: Immunization Monitoring Program, Active (IMPACT) 1991-2005. Pediatr Infect Dis J. 2008;27: 112-118.
3. Gershon AA. Varicella-zoster virus infections. Pediatr Rev. 2008;29:5-10.
4. Jenson AB, Leach CT. Chickenpox and zoster. In: Jenson HB, Baltimore RS, eds. Pediatric Infectious Diseases: Principles and Practice. 2nd ed. Philadelphia: WB Saunders; 2002:331-342.
5. Seward JF, Watson BM, Peterson CL, et al. Varicella disease after introduction of varicella vaccine in the United States, 1995-2000. JAMA. 2002;287:606-611.
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10. Loparev VN, Argaw T, Krause PR, et al. Improved identification and differentiation of varicellazoster virus (VZV) wild-type strains and an attenuated varicella vaccine strain using a VZV open reading frame 62-based PCR. J Clin Microbiol. 2000;38:3156-3160.
11. American Academy of Pediatrics. Varicellazoster infections. In: Pickering LK, Baker CJ, Long SS, McMillan JA, eds. Red Book: 2006 Report of the Committee on Infectious Diseases. 27th ed. Elk Grove, IL; American Academy of Pediatrics; 2006:720.
12. Balfour HH Jr, Rotbart HA, Feldman S, et al. Acyclovir treatment of varicella in otherwise healthy adolescents. J Pediatr. 1992;120:627-633.
13. Dunkle LM, Arvin AM, Whitley RJ, et al. A controlled trial of acyclovir for chickenpox in normal children. N Engl J Med. 1991;325:1539-1544.