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MAJOR ARTICLE

Severe Eczema Vaccinatum in a Household Contact


of a Smallpox Vaccinee
Surabhi Vora,1 Inger Damon,8 Vincent Fulginiti,10,11 Stephen G. Weber,3,4 Madelyn Kahana,2 Sarah L. Stein,5
Susan I. Gerber,7 Sylvia Garcia-Houchins,3 Edith Lederman,8 Dennis Hruby,12 Limone Collins,13 Dorothy Scott,14
Kenneth Thompson,6 John V. Barson,9 Russell Regnery,8 Christine Hughes,8 Robert S. Daum,1 Yu Li,8 Hui Zhao,8
Scott Smith,8 Zach Braden,8 Kevin Karem,8 Victoria Olson,8 Whitni Davidson,8 Giliane Trindade,8 Tove Bolken,12
Robert Jordan,12 Debbie Tien,12 and John Marcinak1

Background. We report the first confirmed case of eczema vaccinatum in the United States related to smallpox
vaccination since routine vaccination was discontinued in 1972. A 28-month-old child with refractory atopic
dermatitis developed eczema vaccinatum after exposure to his father, a member of the US military who had
recently received smallpox vaccine. The father had a history of inactive eczema but reportedly reacted normally
to the vaccine. The childs mother also developed contact vaccinia infection.
Methods. Treatment of the child included vaccinia immune globulin administered intravenously, used for the
first time in a pediatric patient; cidofovir, never previously used for human vaccinia infection; and ST-246, an
investigational agent being studied for the treatment of orthopoxvirus infection. Serological response to vaccinia
virus and viral DNA levels, correlated with clinical events, were utilized to monitor the course of disease and to
guide therapy. Burn patienttype management was required, including skin grafts.
Results. The child was discharged from the hospital after 48 days and has recovered with no apparent systemic
sequelae or significant scarring.
Conclusion. This case illustrates the need for careful screening prior to administration of smallpox vaccine
and awareness by clinicians of the ongoing vaccination program and the potential risk for severe adverse events
related to vaccinia virus.
Vaccination with vaccinia virus to protect against smallpox infection was practiced globally until the World
Health Organization declared that smallpox had been
eradicated in 1980. Recognition of adverse events associated with vaccinia vaccination and the decreased
risk of smallpox led to the discontinuation of routine
childhood immunization in the United States in 1972
[1] and for military personnel in 1990.
In December 2002, in response to the possible threat

Received 26 October 2007; accepted 6 January 2008; electronically published


3 April 2008.
Reprints or correspondence: Dr. Surabhi Vora, University of Chicago Medical
Center, Dept. of Pediatrics, Section of Infectious Diseases, 5841 S. Maryland Ave.,
Chicago, IL 60637 (sbhargav@uchicago.edu).
Clinical Infectious Diseases 2008; 46:155561
 2008 by the Infectious Diseases Society of America. All rights reserved.
1058-4838/2008/4610-0011$15.00
DOI: 10.1086/587668

of intentional release of smallpox virus, the US government implemented a program to immunize select
military and public health personnel against smallpox.
As of May 2007, more than 1.2 million vaccinations
had been administered [2].
Eczema vaccinatum is a potentially life-threatening
illness that occurs in people with atopic dermatitis or
other forms of eczema who are exposed to vaccinia
virus. Exposure may occur through smallpox vaccination or contact with a recent vaccinee. Deaths occur
most often in young children [3]. Since vaccination
programs were reinstituted in 2002, there have been no
confirmed cases of eczema vaccinatum in the United
States [2].
CASE REPORT
A 28-month-old boy with a history of refractory atopic
dermatitis and failure to thrive was transferred to the
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Sections of 1Infectious Diseases and 2Critical Care, Department of Pediatrics, and 3Infection Control Program, and Sections of 4Infectious Diseases
and 5Dermatology, and 6Department of Pathology, University of Chicago Medical Center, and 7Chicago Department of Public Health, Chicago,
Illinois; 8Poxvirus and Rabies Branch and 9Division of Bioterrorism Preparedness and Response, Centers for Disease Control and Prevention,
Atlanta, Georgia; 10University of Arizona, Tucson; 11University of Colorado, Denver; 12SIGA Technologies, Corvallis, Oregon; 13Vaccine Healthcare
Centers Network, Department of Defense, and 14US Food and Drug Administration, Washington, D.C.

1556 CID 2008:46 (15 May) Vora et al.

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University of Chicago Medical Center (Chicago, IL) with fever


and new-onset blistering. He experienced increased itching and
erythema on his hands and face for 45 days, and fever (temperature, up to 39C) for 2 days. On the morning of admission
to the hospital, his mother noticed blisters on his hands that
had spread to his arms and face. Initial physical examination
was remarkable for erythema over much of the face, with multiple areas of shallow erosion, small vesicles, and yellow-crusted
papules. The neck, chest, and arms demonstrated lichenified
plaques and scattered vesicles, pustules, and erosions. The lower
extremities had lichenified plaques consistent with chronic severe atopic dermatitis. The patient weighed 10 kg (less than
the third percentile for his age).
The patient was hospitalized with a presumed diagnosis of
eczema herpeticum with bacterial superinfection and was
placed on contact isolation, and therapy with intravenous clindamycin and acyclovir was initiated at weight-appropriate dosages. Results of direct fluorescent antibody tests of samples from
vesicular lesions were negative for herpes simplex virus and
varicella zoster virus. However, cytopathic effect was noted in
cell culture. Staphylococcus aureus was isolated from initial
blood and skin cultures. Subsequent cultures showed no bacterial growth. Over the next 3 days, the patients condition
worsened, with increasingly umbilicated vesicles spreading to
the legs and trunk (figure 1A).
Additional history obtained on hospital day 5 revealed that
the patients father was in the US Army serving in Iraq. He
had visited his family for 5 days, 2 weeks prior to the patients
admission and 21 days after receiving the smallpox vaccination.
According to the fathers report, his reaction to the smallpox
vaccine was within expected limits, and the resulting scab had
separated prior to his visit home. Also, he kept a bandage over
the vaccination site throughout his visit home. The father engaged in routine activities with the child that included hugging,
bathing, sharing towels, and sleeping. Both the father and patients sibling reported histories of inactive eczema.
The US Department of Defense (DoD) and Centers for Disease Control (CDC) were consulted regarding the diagnosis of
eczema vaccinatum. On hospital day 6, nonvariola orthopoxvirus was detected in vesicular scrapings and viral culture supernatant from the patients skin lesions using PCR tests performed at the Illinois Department of Public Health
(Springfield). This result was confirmed by vaccinia virusspecific PCR at the CDC. Later that day, vaccinia immune globulin
intravenous (VIGIV) obtained from the CDC was administered
to the patient at a dose of 6000 IU/kg. The patient was transferred to the Pediatric Intensive Care Unit for aggressive wound
care and fluid and electrolyte management for burn patient
type physiology. Ophthalmologic monitoring and trifluridine
ocular drop treatment were initiated. Because of recurrence of
fever, the patients antimicrobial regimen was broadened.

Figure 1. Pictures of the patient depicting the progression of skin


lesions on hospital day 5 (A), hospital day 7 (B), hospital day 13 (C), and
hospital day 28 (D).

The child underwent extubation on hospital day 31 and was


discharged home on day 48.
The patients mother also reported a rash on hospital day 3.
She described having had a breakout of acne on her face that
began prior to the fathers visit. The mother was previously
healthy, with no history of eczema or smallpox vaccination. On
examination, she had several umbilicated vesicles on her face.
These spread to include her neck, eyelid and finger over the
next 5 days, and she developed lymphadenopathy, fatigue, and
myalgias. Vaccinia infection was confirmed by PCR analysis.
After treatment with a single dose of VIGIV (6000 IU/kg), her
lesions began to scab and systemic symptoms resolved.
LABORATORY METHODS
Vaccinia virus DNAspecific PCR assays were used to confirm
the diagnoses of both the patient and his mother. A second
real-time PCR assay, targeting the orthopoxvirus DNA polymerase gene, was used to quantitate viral DNA in tissues (figure
2B). Anti-orthopoxvirus IgM and IgG reactivities were measured using methods described elsewhere (figure 2A) [4].
Analysis of the pharmacokinetics of ST-246 therapy (figure
3) was performed at MPI Research. Serum was harvested by
centrifugation and analyzed by liquid chromatography mass
spectrometry using a validated analytical method. Pharmacokinetic parameters were determined using WinNonlin software
(Pharsight).
Multilocus sequence typing revealed that the patients S. aureus blood isolate was ST188 from clonal cluster 1. The skin
isolate was ST8 and contained SCCmec IV and the PantonValentine leukocidin genes. Methods are described elsewhere
[5, 6].
DISCUSSION
To our knowledge, this is the first confirmed case of eczema
vaccinatum related to smallpox vaccination in the United States
since routine vaccination was discontinued in 1972. A case of
eczema vaccinatum in an adult vaccinee was reported from
Israel in 2002 [7].
Much of our understanding of the frequency of adverse
events associated with smallpox vaccine is based on data from
the 1960s. Despite the high prevalence of atopic dermatitis and
eczema in the population, eczema vaccinatum has always
been rare, with an estimated incidence of 1038.5 cases per
million primary vaccinees [811]. Of note, deaths occurred only
among individuals who acquired vaccinia via contact transmission [11]. Todays population may be more susceptible to
adverse reactions because of the larger number of nonimmune
individuals, prevalence of HIV infection, increased rates of
atopic dermatitis, and increases in other immunosuppressed
populations [10].
Atopic dermatitis, regardless of severity or current activity,

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In light of the childs critical condition and need for pain


control and sedation, the patient underwent intubation on hospital day 7. Skin lesions continued to spread (figure 1B). Two
additional doses of VIGIV were administered to reach a total
cumulative dose of 24,000 IU/kg. Nevertheless, by hospital day
8, his condition had deteriorated, with worsening acidosis, hypoalbuminemia, hypothermia, and hypotension. New lesions
appeared on his shoulder and face. Because of the possibility
of ongoing viremia, cidofovir (5 mg/kg) with probenecid and
hydration was administered.
An Emergency Investigational New Drug Application was
issued, and on hospital day 9, ST-246, an investigational agent
with activity against multiple orthopoxvirus species, was administered at a dose of 5 mg/kg via nasogastric tube. The patients condition continued to worsen, with increasing edema,
anuria, rising creatinine levels, and increasing hypotension requiring vasopressor therapy. After a peritoneal catheter was
emergently placed to relieve abdominal compartment syndrome and 700 mL of sterile transudative fluid were drained,
his clinical condition stabilized. Clindamycin treatment was
restarted on hospital day 10 because of the possible contribution of staphylococcal toxin to the severity of illness. In the
next few days, renal dysfunction improved, acidosis resolved,
and the patient became normotensive.
After hospital day 8, there were no new skin lesions; the
existing lesions began to flatten and became confluent. By day
13, the lesions began to crust; some had hemorrhagic centers.
During this time, areas on his arms, hands, chin, and neck
became increasingly denuded (figure 1C). Silver sulfadiazine
cream and xeroform gauze dressings were applied to these
regions.
The patient experienced several hematologic complications,
including neutropenia, anemia, and thrombocytopenia; all
complications resolved while the child continued to receive
both VIGIV and ST-246. A basic immunologic analysis, including a complete blood cell count with differential, HIV
ELISA, and quantitative immune globulin measurements, revealed no abnormalities.
Daily teleconferences with the CDC, DoD, US Food and
Drug Administration, and ST-246 manufacturer guided therapeutic decisions. The child received 24,000 IU/kg of VIGIV
daily from hospital day 10 to 14. With stabilization of antiorthopoxvirus IgG levels, doses were administered less frequently (figure 2A). Vaccinia virus DNA load, which was measured daily, showed a decreasing trend from day 7 onward and
was undetectable at day 18 (figure 2B). The patients plasma
ST-246 level was monitored daily; and the dosage was adjusted
on the basis of pharmacokinetic data (figure 3). Antibiotic therapy was discontinued on hospital day 26. Cadaveric allografts
were eventually placed in areas where the skin had completely
denuded (figure 1D), resulting in successful epithelialization.

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Figure 2. A, Time course of anti-orthopoxvirus IgM and IgG levels depicted as anti-orthopoxvirus ELISA optical density (OD) levels, minus background
subraction (cut-off value [COV]). Hospital day 1 corresponds with 1014 days after the patients exposure to vaccinia virus. Although, at the time of
the first serological sampling (hospital day 6), the child had no detectable orthopoxvirus-specific IgG response and was gravely ill, he did have a high
IgM antibody level and an elevated serum vaccinia virus-neutralization titer (data not shown). B, Time course of the level of intravascular orthopoxvirus
DNA in EDTA blood specimens determined by quantitative PCR using reference standards.

is a risk factor for eczema vaccinatum among vaccinees and


their contacts and is a contraindication to vaccination. In a
1964 study, two-thirds of those who developed eczema vaccinatum had only a history of atopic dermatitis. Contact exposure
to vaccinia accounted for 65% of cases. One-half of the eczema
vaccinatum cases and 73% of associated deaths occurred among
children aged !5 years [12]. An immune modulation defect,

1558 CID 2008:46 (15 May) Vora et al.

which is specifically related to T cell dysfunction, and a virtual


absence of antimicrobial peptides (cathelicidins) normally present in skin [13] appear to play critical roles in the predisposition of individuals with atopic dermatitis to the initiation and
rapid spread of vaccinia infection, even in intact skin [14]. Prior
to the advent of immunoglobulin therapy, Kempe [15] reported
an overall mortality of 30%40% among patients with eczema

vaccinatum, but it was only 7% among those who received


vaccinia immune globulin intramuscularly (VIGIM). This benefit has not been examined in a controlled trial.
This patients case emphasizes the need to exclude individuals with a history of remote or active atopic dermatitis from
smallpox vaccination or contact with vaccinees. Vaccinia infections can occur in individuals with other forms of eczema
as well, and clear guidelines need to be established [16]. It is
postulated that two-thirds of the vaccine complications that
occurred during the smallpox vaccination era in the United
States could have been avoided with improved prevaccination
screening [10]. The current systematic training and screening
program employed by the DoD considers both atopic dermatitis and eczema and may explain the low rates of adverse
events seen since 2002 [17]. However, screening cannot eliminate all risk. Vaccine recipients or contacts may have unrecognized risk factors or report an inaccurate history of skin
disease [18, 19].
According to report from the DoD, our patients father was
unsure about household contacts with eczema, but conveyed his own personal history and should not have been vaccinated. Although his vaccine reaction was reportedly normal
in size, severity, and time to resolution, viral transmission to
his son occurred 2125 days after vaccination; this was beyond
the generally accepted period of infectivity (321 days) [20].
The fathers history of eczema may have contributed to prolonged viral shedding. Findings in the child also indicate extended viral shedding; swabs from skin where scabs had recently

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Figure 3. Plasma concentrations of ST-246 in the patient during treatment. Levels of ST-246 in plasma samples acquired 3 h after each dose
are shown. The plasma sample from hospital day 16 was not available
for analysis. Doses were incrementally increased on the basis of a target
peak level of 1000 ng/mL, determined by efficacy studies in nonhuman
primates. The reason for the decrease in plasma levels after hospital day
15 is not known, but because of the improvement in the patients clinical
situation no additional increases in ST-246 dose were implemented.

separated resulted in positive virus culture results even on hospital day 29. The mothers vaccinia infection likely occurred
via tertiary transmission, and the presence of acne may have
contributed to the extent and distribution of her rash [21].
Several novel therapies were used for the treatment of this
child, including VIGIV, cidofovir, and ST-246. Vaccinia immune globulin is a sterile solution of purified g-globulin isolated from plasma containing high titers of anti-vaccinia antibody. In the 1960s, VIGIM was routinely administered for
treatment and prophylaxis of complications related to smallpox
vaccination [22]. The intravenous formulation has recently
been developed to improve tolerability and pharmacokinetic
profiles. Prior to this case, VIGIV treatment had not been given
to a child. The initial dose of 6000 IU/kg was based on a phase
I study that found that dose resulted in neutralizing antibody
activity comparable with that achieved with VIGIM [23]. Subsequent doses of 24,000 IU/kg were based on its demonstrated
safety as the largest dose tested in healthy adults, as well as a
study that indicated that the higher dose more effectively diminished the size of a smallpox vaccination lesion (Cangene
Corporation, unpublished data). VIGIV treatment was administered until anti-orthopoxvirus IgG levels stabilized (figure
2A). Our patient received a total of 3.96 g/kg of vaccinia IgG
in 11 doses. This is equivalent to more than double the maximum dose that was administered in severe cases of progressive
vaccinia or eczema vaccinatum in the era of smallpox vaccination (maximum dose, 10 mL/kg or 1.66 g/kg) [24].
Two antiviral treatments, each with different mechanisms of
action, were used. When the appearance of new lesions on
hospital day 8 indicated potentially ongoing viremia, 5 mg/kg
of cidofovir was administered on the basis of standard induction dosing for patients with AIDS who have CMV retinitis.
Because of clinical improvement over the next week, our patient
did not require another dose of cidofovir. Although no human
anti-orthopoxvirus trials with this agent have been published,
the CDC currently considers cidofovir a second-line therapy
for severe vaccinia infection [10], because extensive in vitro
and animal data demonstrate that it has activity against orthopoxviruses [2528]. Renal toxicity is the major toxicity associated with cidofovir in humans; thus, this treatment could
have contributed to the patients transient renal dysfunction.
Because of the childs critical condition, treatment with ST246, an investigational agent under development to prevent
and treat orthopoxvirus infection, was initiated on the basis of
its unique mechanism of action, current safety profile, and
promising efficacy, even when administered at later stages of
illness [29]. The drug targets an envelope protein required for
viral maturation [28]. ST-246 has shown in vitro activity against
multiple species of orthopoxviruses, as well as efficacy in animal
models, including both monkeypox and variola challenges in

Acknowledgments
We thank Kenneth Alexander, Arthur Frank, Donald Leung, Daniel Glikman, and Kirk Chan-Tack, for their critical review of the manuscript; Sue
Boonlanyagoor, for coordinating specimen transport to the CDC; Emmanuel Semmes, for facilitating the receipt and administration of therapies;
Barrett Fromme, Dana Aronson, PICU nursing staff, and many others, for
their assistance with clinical care of the patient; Lori Ferguson, for infection
control support; William Bower, for coordinating numerous conference
calls; Chris Sinclair (Cangene Corporation), for providing VIGIV data;
Wayne Staggs and Charlene Graves, for assistance with Indiana public
health aspects of the case; Mary Reynolds, Nikki Pesik, Yvonne Stifel, Joel
Price, John Nawrocki, George Dizikes, Kimberly King, and Jie Peng, for
logistics and laboratory assistance; and the Vaccine Healthcare Centers
Network and the Military Vaccine Agency staff, for their help addressing
issues regarding the service member.
Potential conflicts of interest. D.H., T.B., R.J., and D.T. own equity in
SIGA Technologies. All other authors: no conflicts.

1560 CID 2008:46 (15 May) Vora et al.

References
1. Lane JM, Millar JD. Routine childhood vaccination against smallpox
reconsidered. N Engl J Med 1969; 281:12204.
2. Department of Defense Smallpox Vaccination Program: safety summary. 17 May 2007. Available at: http://www.smallpox.army.mil/event/
SPSafetySum.asp. Accessed 1 October 2007.
3. Goldstein JA, Neff JM, Lane JM, Koplan JP. Smallpox vaccination
reactions, prophylaxis and therapy of complications. Pediatrics 1975;
55:3427.
4. Karem KL, Reynolds M, Braden Z, et al. Characterization of acute
phase humoral immunity to monkeypox; use of IgM ELISA for detection of monkeypox infection during the 2003 North American outbreak. Clin Diagn Lab Immunol 2005; 12:86772.
5. Enright MC, Day NP, Davies CE, Peacock SJ, Spratt BG. Multilocus
sequence typing for characterization of methicillin-resistant and methicillin susceptible clones of Staphylococcus aureus. J Clin Microbiol
2000; 38:100815.
6. Lina G, Piemont Y, Godail-Gamot F, et al. Involvement of PantonValentin leukocidinproducing Staphylococcus aureus in primary skin
infections and pneumonia. Clin Infect Dis 1999; 29:112832.
7. Moses AE, Cohen-Poradosu R. Eczema vaccinatuma timely reminder. N Engl J Med 2002; 346:1287.
8. Lane JM, Ruben FL, Neff JM, Millar JD. Complications of smallpox
vaccination, 1968: results of statewide surveys. J Infect Dis 1970; 122:
3039.
9. Lane JM, Ruben FL, Neff JM, Millar JD. Complications of smallpox
vaccination, 1968: national surveillance in the United States. N Engl
J Med 1969; 281:12018.
10. Cono J, Casey CG, Bell DM. Smallpox vaccination and adverse events:
guidelines for clinicians. Centers for Disease Control and Prevention.
MMWR Recomm Rep 2003; 52:128.
11. Aragon TJ, Ulrich S, Fernyak S, Rutherford GW. Risks of serious complications and death from smallpox vaccination: a systematic review
of the United States experience, 19631968. BMC Public Health 2003;3:
2637.
12. Copeman PWM, Wallace HJ. Eczema vaccinatum. BMJ 1964; 2:9068.
13. Howell MD, Jones JF, Kisich KO, Streib JE, Gallo RL, Leung DYM.
Selective killing of vaccinia virus by LL-37: implications for eczema
vaccinatum. J Immunol 2004; 172:17637.
14. Engler R, Kenner J, Leung D. Smallpox vaccination: risk considerations
for patients with atopic dermatitis. J Allergy Clin Immunol 2002; 110:
35765.
15. Kempe CH. Studies on smallpox and complications of smallpox vaccination. Pediatrics 1960; 26:17689.
16. Fulginiti V, Papier A, Lane JM, Neff JM, Henderson DA. Smallpox
vaccination: a review, part I. Background, vaccination technique, normal vaccination and revaccination, and expected normal reactions. Clin
Infect Dis 2003; 37:24150.
17. Grabenstein JD, Winkenwerder W. US military smallpox vaccination
program experience. JAMA 2003; 289:327882.
18. Moberg C, Meding B, Stenberg B, Svensson A, Lindberg M. Remembering childhood atopic dermatitis as an adult: factors that influence
recollection. Br J Dermatol 2006; 155:55760.
19. Naleway AL, Belongia EA, Greenlee RT, Kieke BA, Chen RT, Shay DK.
Eczematous skin disease and recall of past diagnoses: complications
for smallpox vaccination. Ann Intern Med 2003; 139:17.
20. Lane MJ, Fulginiti VA. Transmission of vaccinia virus and rationale for
measures for prevention. Clin Infect Dis 2003; 37:2814.
21. Schmitt BS, Marks MI. Acne vaccinatuma complication of smallpox vaccination. Pediatrics 1971; 48:8156.
22. Hopkins RJ, Kramer WG, Blackwelder WC, et al. Safety and pharmacokinetic evaluation of intravenous vaccinia immune globulin in
healthy volunteers. Clin Infect Dis 2004; 39:75966.
23. Vaccinia Immune Globulin Intravenous (Human; VIGIV) [package
insert], Winnipeg, Manitoba, Canada: Cangene Corporation, 2005.

Downloaded from http://cid.oxfordjournals.org/ by guest on January 22, 2015

pilot studies of nonhuman primates. Thus far, the drug has


shown no toxicity in animal toxicology experiments, and has
been associated with no severe adverse events in Phase I studies
in healthy adult volunteers [2830] (SIGA Technologies, unpublished data). On the basis of the decreasing viral load, the
improvement of the patients clinical and immune status, and
data from non-human primate studies, ST-246 treatment was
discontinued after 14 days.
It is difficult to precisely define the potential contributions
of each agent to the patients recovery because of the close
timing of administration. Vaccinia virus DNA levels in blood
samples decreased from pretreatment levels following VIGIV
and cidofovir treatment, then continued to decrease with the
administration of ST-246, especially with achievement of target
peak and trough ST-246 plasma concentration levels (figures
2B and 3). It appears that the patient mounted his own antiorthopoxvirus IgG response between days 9 and 10; maximum
IgG levels were achieved between hospital days 12 and 18 (figure
2A). Additionally complicating interpretation of the impact of
individual interventions, we cannot yet differentiate between
the patients own IgG and that contributed by the VIGIV treatment. Although it is difficult to assess and differentiate the
effects of specific therapeutic interventions, the childs immune
response almost certainly played a role in the eventual control
of his infection [16].
This case illustrates the need for meticulous prevaccination
screening and the potential hazards of widespread smallpox
vaccination. It provides an important model of the coordinated,
multidisciplinary effort required for the management of such
a complication. This case also exemplifies the utility of novel
treatments, as well as the role of new techniques in laboratory
diagnosis and monitoring of infection, in guiding this therapy.
The need for additional research in the areas of therapeutics
and safer vaccines is clear as long as the perceived threat of
smallpox persists.

24.

25.
26.
27.

Available at: http://www.fda.gov/cber/label/vigivcan050305LB.pdf.Accessed 24 August 2007.


Centers for Disease Control and Prevention. Medical management of
smallpox (vaccinia) vaccine adverse reactions. 21 February 2006. Available at: http://www.bt.cdc.gov/agent/smallpox/vaccination/mgmt-adv
-reactions.asp. Accessed 9 May 2007.
Bray M. Pathogenesis and potential antiviral therapy of complications
of smallpox vaccination. Antiviral Research 2003; 58:10114.
De Clercq E. Cidofovir in the treatment of poxvirus infections. Antiviral
Research 2002; 55:113.
Quenelle DV, Collins DJ, Kern ER. Efficacy of multiple or single-dose

cidofovir against vaccinia and cowpox virus infections in mice. Antimicrob Agents Chemother 2003; 47:327580.
28. Yang G, Pevear, DC, Davies MH, et al. An orally bioavailable antipoxvirus compound (ST-246) inhibits extracellular virus formation and
protects mice from lethal orthopoxvirus challenge. J Virol 2005; 79:
1313949.
29. Sbrana E, Jordan R, Hruby DE, et al. Efficacy of the antiorthopoxvirus
compound ST-246 for the treatment of severe orthopoxvirus infection.
Am J Trop Med Hyg 2007; 76:76873.
30. Quenelle DC, Buller RML, Parker S, et al. Efficacy of delayed treatment
with ST-246 given orally against systemic orthopoxvirus infections in
mice. Antimicrob Agents Chemother 2007; 51:68995.

Downloaded from http://cid.oxfordjournals.org/ by guest on January 22, 2015

Eczema Vaccinatum in a Household Contact CID 2008:46 (15 May) 1561

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