Blackwell Publishing Inc

COMMENTARY
Pediatric Dermatology Vol. 23 No. 3 291– 293, 2006

Anogenital Warts in Children

Gayle Fischer, F.A.C.D
The Royal North Shore Hospital, St Leonards, New South Wales, Australia

It is a familiar situation for dermatologists: a small child desirable, range of human behavior. It means that every
presents in the clinic with her parents. She is 5 years old day in your office the probability is that many of the
and has anogenital warts (AGW). You make the children you are seeing have been, or are being, sexually
diagnosis, talk about how they might be treated, and abused. The crime goes unreported because most per-
then comes the inevitable but unavoidable question, the petrators are trusted friends or family members and few
one that really matters, at any age: how were they are unlucky enough to leave a trail, like an HPV-related
acquired? If the parents don’t ask first, you must. disease. Fear, shame, and intimidation limit the possi-
However, must you, in every instance, embark on the bility that children will disclose the abuse (3). Sexual
difficult and usually painful path of exploring the abuse may not be life threatening, but it is life ruining.
possibility of sexual abuse? Can you accept more In the short term, children may suffer from nightmares,
palatable explanations that will absolve you from this bed wetting, anxiety and depression, low self-esteem,
duty: Mom had cervical HPV, last year the child had a sexualized or aggressive behavior, school avoidance, and
wart on her finger, Dad had a plantar wart. A recent running away from home. The long-term effects include
consensus statement from the American Medical numerous behavioral problems: depression, eating disorder,
Association says “No.” Their conclusion: “All children chronic pelvic pain, aggression, sexual difficulties, drug
with AGW should be referred for evaluation of possible abuse, and of course, re-victimization (2).
sexual abuse” (1). Many authors make the point that it is only in the last
We easily accept that AGW in adults are almost 15 years that the prevalence of AGW has risen dramatically
universally acquired by sexual contact. Why should it be as evidenced by the number of reports in the medical
so different in children? Therefore, how do we judge literature. However, this may simply reflect increased
those articles that have appeared in the medical literature awareness and willingness to come forward among
that claim that AGW in children are “frequently” patients. A retrospective study of 710 randomly selected
acquired nonsexually? It is interesting that the pre- adult women from Australia, published in 1994, revealed
valence of sexual transmission of AGW in published that of the 20% who could recall being sexually abused
studies varies from 90% in children referred to specialists as children, only 10% reported the abuse, and that about
in child abuse to 10% or less in children referred to half did not do so until 10 years later (3).
dermatologists (2). Is this because referring practitioners In the long term, there is another important question.
accurately triage patients so that the abused ones go What implications do early-onset AGW have for the
straight to child abuse experts? Or is it that when your health of a child, particularly a girl? We know that
chosen field is dermatology and not child protection you rates of cervical cancer match chronic carriage with
just do not have the skill or the inclination to identify the oncogenic HPV genotypes. Are girls who had AGW at
child at risk? an early age at greater risk for early-onset cervical cancer?
Child sexual abuse is a criminal offense, reportable by When should they have their first Pap smear? Should
medical practitioners. Yet it is common. It is found in all girls with AGW have screening for oncogenic genotypes
social classes. Numerous studies tell us that 25% of girls to identify those at risk of cervical carcinoma?
and 10% of boys have been abused by the age of 16. Despite the plethora of printed information, there is
That’s a staggering figure, enough to place child sexual still a lot we do not understand about AGW. What do we
abuse in what one could consider the “normal,” if not the know? That it is caused by a virus that cannot be cultured,
Address correspondence to Gayle Fischer, F.A.C.D., P.O. Box 440, Killara 2071, NSW, Australia, or e-mail: gaylef@chw.edu.au.

Address correspondence to Gayle Fischer, F.A.C.D., P.O. Box 440,

Killara 2071, NSW, Australia, or e-mail: gaylef@chw.edu.au

© 2006 The Author. Journal compilation © 2006 Blackwell Publishing, Inc. 291
292 Pediatric Dermatology Vol. 23 No. 3 May/June 2006
that in adults, it is most often sexually transmitted, that
it is difficult to treat, and that treated lesions can recur.
We believe that the incubation period is between
3 weeks and 8 months (4). We know that there are geno-
types that are oncogenic, but these are not usually found
in genital warts, most of which are caused by non-
oncogenic mucosal types 6 and 11 although many others,
mucosal, cutaneous, and cutaneomucosal, have been
identified. Now look at what we do not know or what
remains controversial. What is the longest latency we
would consider possible? Is latency indefinite? What is
the mode of transmission? How brief can contact be?
How infective is a patient with subclinical infection?
Can we accept transmission from fomites? Does the
finding of a nonmucosal HPV type rule out sexual trans-
mission? What is the reality of nonsexual transmission?
We are sure that vertical and horizontal transmission
occurs, but how often relative to sexual transmission? Is
auto-inoculation a reality? An epidemiologic study from
1983 showed no difference in the incidence of skin warts
between those with and without genital warts (5). Of the
numerous children we all see with common warts, how
many mention that they have lesions on the genitals? If
auto-inoculation was a reality, AGW in children ought to
be frequent. But they are not. They are rare.
The advent of techniques that identify HPV DNA in
tissue even when there is no macroscopic lesion present
has only added to our dilemma. We now have a new
entity in the HPV disease spectrum: subclinical infection
as HPV DNA detected only by polymerase chain
reaction. This technique is very sensitive. It not only
identifies but can also genotype the HPV. This is perhaps
where its true value lies: we are able to detect patients
with oncogenic strains (mainly 16 and 18). However, the
ability to detect viral DNA opens a Pandora’s box of extra
controversies. Can HPV typing assist us in determining
mode of transmission? Previous studies say no. What
does it mean to detect viral DNA where there are no
observable clinical changes, no histopathologic changes,
and no history of exposure to infection? A recent study
claims that genital HPV carriage in nonabused prepu-
bertal children is up to 15% (6). But how do the authors
know for sure these children were never abused?
Perhaps the most compelling work supporting the mode
of transmission of genital HPV as sexual was a paper
by Gutman et al (7) who reported finding HPV DNA in
33% of sexually abused girls and not at all in 17 non-
sexually abused controls. However, the validity of this
paper is, like so many on this subject, limited by the small
sample size.
The prevalence of AGW in the adult population is
about 1% to 2% but we have limited and conflicting data
on what proportion of the population carries HPV DNA
on the genitals (figures range from 10% to 80% in adult
women and is highly age dependent) and even less on
nongenital carriage (8). A large population study looking
at genital and nongenital carriage in abused and non-
abused children would be interesting. But any such work
would be confounded by the unreliability of reporting of
sexual abuse, which depends partially on the population
studied. As an example, consider these reports and
understand the dilemma: Sexual abuse is the mode of
transmission of AGW in up to 47.1% of children in a
study from Rio de Janiero, but in Belfast it is only 6.5%
and in Paris it seems HPV DNA can be acquired from
underwear (9–11)!
The article in this journal by Marcoux et al (12) tackles
two unanswered questions, namely can we draw a con-
clusion about mode of transmission first by the morphology
of the wart and second by its serotype by DNA analysis?
The conclusion drawn is that the mode of transmission
of AGW cannot be identified by either clinical appearance
or HPV typing. The authors recommend that careful
interview and examination is the best guide. But is it?
No matter how meticulous your interview technique or
how careful your examination, it can be difficult if not
impossible to positively identify the sexually abused
child (13). Sexual abuse is not necessarily violent and
does not always involve genital to genital contact. By the
time they are examined, most abused children have no
clinical signs of abuse (14). Furthermore, most children
do not disclose. Without disclosure we are frequently
left only with our suspicions. As dermatologists, unless
we have undertaken special training, we lack the skills
necessary to evaluate this situation.
A finding of AGW is not incontrovertible proof of
sexual transmission in a child, particularly in the very
young child where vertical transmission may have
occurred. Because of many conflicting published articles
that claim to prove scientifically that AGW can be
acquired vertically from mother to child, horizontally
from caregiver to child, by autoinoculation from non-
genital sites, from fomites, and even, perhaps, at insem-
ination, we cannot jump to conclusions. According to
Marcoux et al (12), neither can we conclude from the
appearance of the wart or from the finding of a mucosal
wart type on DNA analysis that sexual transmission has
occurred. Is it possible to make sense of any of this?
Until we have an understanding of the unanswered
questions, if we ever do, we will struggle with this topic.
At the moment, we are a long way from an algorithm
that enables decision making. It is tempting to be reassured
by the medical literature or simply to conclude that there
is so much controversy that it is impossible to draw a
conclusion. Until we are sure of our facts, we must, in
every case, take the difficult path. All children with

AGW should be suspected of having been the subject of
sexual abuse. If your experience with interviewing
families with this in mind is limited, refer to someone
with this skill. Your actions could make a difference to a
child’s future. If you doubt the wisdom of this, just
reflect on the statistics on the prevalence of child sexual
abuse. Kids with AGW are just the tip of the iceberg.
ACKNOWLEDGMENTS
I would like to express my thanks to Professor Suzanne
Garland for valuable advice on the microbiologic aspects
of this subject.
REFERENCES
1. Beutner KR, Reitano MV, Richwald GA et al. External
genital warts: report of the American Medical Association
Consensus Conference. Clin Infect Dis 1998;27:796–
806.
2. Wissow LS. Child abuse and neglect. N Engl J Med
1995;332:1425 –1431.
3. Fleming JM. Prevalence of childhood sexual abuse in a
community sample of Australian women. Med J Aust
1996;166: 65 – 68.
4. Barrett TJ, Silbar JD, McGinley JP. Genital warts: a
venereal disease. JAMA 1954;154:333 –334.
5. Gissman L, Wolnick L, Ikenberg H et al. Human pap-
illomavirus type 6 and 11 DNA sequences in genital and
Fischer: Anogenital Warts in Children 293
laryngeal papillomas and some cervical cancer. Proc Natl
Acad Sci USA 1983;80:560–563.
6. Powell J, Strauss S, Gray J et al. Genital carriage of
human papillomavirus (HPV) DNA in prepubertal girls
with and without vulval disease. Pediatr Dermatol
2003;20:191–194.
7. Gutman LT, St.Claire K, Herman-Giddens PA et al.
Evaluation of sexually abused and nonabused girls for
intravaginal human papilomavirs infection. Am J Child
Dis 1992;146:694–699.
8. Siegfried E, Rasnck-Conley J, Cook S et al. Human
papillomavirus screening in pediatric victims of sexual
abuse. Pediatrics 1998;101:43–47.
9. DeJesus LE, Cirne Neto OL, Monteiro DO et al. Anogenital
warts in children: sexual abuse or unintentional contamina-
tion? Cadernis de Saude Publica 2001;7:1383–1391.
10. Armstrong DKB, Bingham EA, Dinsmore WW et al.
Anogenital warts in prepubertal children: a follow-up
study. Br J Dermatol 1998;138:544–545.
11. Bergeron C, Ferenczy A, Richart R. Underwear: contami-
nation by human papillomaviruses. Am J Obstet Gynecol
1990;162:25–29.
12. Marcoux D, Nadeau K, McCuaig C et al. Pediatric ano-
genital warts: a 7-year review of children referred to a
tertiary-care hospital in Montreal, Canada. Pediatr Dermatol
2006;23:199–207.
13. Weinberg R, Sybert VP, Feldman KW et al. Outcome of
CPS referral for sexual abuse in children with condyloma
acuminate. Adolesc Pediatr Gynecol 1994;7:19–24.
14. Merritt DF. Vulvar and genital trauma in pediatric and
adolescent gynecology. Curr Opin Obset Gynecol
2004;16:371–381.