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© 2007 American Public Health Association
DOI: 10.2105/AJPH.2007.119446
LETTER |
Yin Ling Woo is with the Department of Pathology, University of Cambridge, Cambridge, England, and the Department of Gynaecological Oncology, Addenbrooke’s Hospital, Cambridge. Jane Carolyn Sterling is with the Department of Medicine, University of Cambridge, and the Department of Dermatology, Addenbrooke’s Hospital, Cambridge.
Correspondence: Requests for reprints should be sent to Jane Carolyn Sterling, Department of Medicine, University of Cambridge, Tennis Court Road, Cambridge CB2 1QP, UK (e-mail: jcs12{at}mole.bio.cam.ac.uk).
We read with interest the study by Brogly et al.1 of the genital infections of girls and adolescents who were infected perinatally with HIV. They reported a higher-than-expected incidence of warts in the anogenital area, especially in prepubertal children, highlighting this as a cause for concern and suggesting that the distribution of the warts implies a sexual mode of transmission.
This conclusion as to the mode of acquisition of human papillomavirus (HPV) infection omits the possibility that warts in children may be contracted by means other than sexual contact, such as horizontal transmission. Perinatal vertical transmission of HPV to mucosae is common, but in immunocompetent individuals the infection is likely to clear within 3 years,2 at least from the buccal mucosa. Furthermore, there are data demonstrating that persistent anogenital HPV infection in young children may have been acquired peri- or postnatally.3
In the cohort of children and adolescents studied, the incidence of genital condylomata was higher than that of definitely sexually transmitted infections, such as chlamydia and gonorrhea. This suggests that sexual transmission may not have been the mode of acquisition for these girls—an idea supported by observations in children known to have been abused, in whom HPV does not appear to be the most common or the most infectious sexually transmitted disease.4
Brogly et al. did not report HPV typing of the observed warts. Several studies have suggested that up to 40% of anogenital warts in children arise from infection with cutaneous HPV types, such as HPV 2, and that other modes of transmission, such as horizontal or self-inoculation, may account for the infection.5–7 Information regarding the presence or absence of hand warts in the children or in their close relatives is important to include, as hand-to-genital transfer may be common in young children.
The distribution of the warts is suggested to be evidence that sexual contact was likely. In girls with anogenital warts, vulval and peri-anal lesions commonly coexist,6 and warts at any anogenital site may harbor genital or cutaneous HPV types.8
One further detail that could lend weight to the possibility that anogenital warts in the older children and young adults arise from sexual activity would be a correlation between HPV infection of the vulva and cervical smear result. Cervical disease is often associated with external HPV,9 and such a link could support the idea that the warts were acquired sexually.
Footnotes
Contributors
Both authors contributed equally to this letter.
Accepted for publication May 29, 2007.
References
1. Brogly SB, Watts H, Ylitalo N, et al. Reproductive health of adolescent girls perinatally infected with HIV. Am J Public Health. 2007;97:1047–1052.
2. Mant C, Kell B, Rice P, Best JM, Bible JM, Cason J. Buccal exposure to human papillomavirus type 16 is a common yet transitory event of childhood. J Med Virol. 2003;71:593–598.[CrossRef][Web of Science][Medline]
3. Sinclair KA, Woods CR, Kirse DJ, Sinal SH. Anogenital and respiratory tract human papillomavirus infections among children: age, gender, and potential transmission through sexual abuse. Pediatrics. 2005; 116:815–825.
4. White ST, Loda FA, Ingram DL, Pearson A. Sexually transmitted disease in sexually abused children. Pediatrics. 1983;72:16–21.
5. Fleming KA, Venning V, Evans M. DNA typing of genital warts and diagnosis of sexual abuse in children. Lancet. 1987;2(8556):454.[Web of Science][Medline]
6. Marcoux D, Nadeau K, McCuaig C, Powell J, Oligny LL. Pediatric anogenital warts: a 7-year review of children referred to a tertiary-care hospital in Montreal, Canada. Pediatr Dermatol. 2006;23:199–207.[CrossRef][Web of Science][Medline]
7. Aquilera-Barrantes I, Magro C, Nuovo GJ. Verruca vulgaris of the vulva in children and adults: a non-venereal type of vulval wart. Am J Surg Pathol. 2007; 31:529–535.[CrossRef][Web of Science][Medline]
8. Padel AF, Venning VA, Evans MF, Quantrill AM, Fleming KA. Human papillomaviruses in anogenital warts in children: typing by in situ hybridisation. BMJ. 1990;300:1491–1494.
9. Gutman LT, St Claire KK, Everett VD, et al. Cervical-vaginal and intraanal human papillomavirus infection of young girls with external genital warts. J Infect Dis. 1994;170:339–344.[Web of Science][Medline]
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  S. B. Brogly, E. L. Franco, D. H. Watts, and R. Van Dyke BROGLY ET AL. RESPOND Am J Public Health, November 1, 2007; 97(11): 1930 - 1930. [Full Text] [PDF]
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