HPV Fast Facts. HPV: A Potential Risk for Healthcare Facilities. HPV Infections and Cancer

                HPV Fast Facts HPV: A Potential Risk for Healthcare Facilities Human papillomaviruses (HPV) are one of the most important infec...
Author: Beatrice Price
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HPV Fast Facts

HPV: A Potential Risk for Healthcare Facilities Human papillomaviruses (HPV) are one of the most important infectious causes of cancer with high-risk types accounting for 5% of all cancers worldwide.

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Cancers associated with high-risk HPV include virtually all cervical cancers, most anal cancers and some cancers of the penis, vulva and mouth and throat (oropharynx). HPV is highly prevalent: most sexually active people are infected with HPV at some point in their lives and it is the most common sexually transmitted infection in the United States.

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While HPV is generally sexually transmitted through sexual intercourse (vaginal, anal and oral) and skin-toskin contact, evidence and research shows the virus can survive and remain infectious on surfaces, even when treated with common disinfectants.

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This may have serious implications for infection prevention practices in healthcare facilities, particularly where semi-critical medical devices such as ultrasound probes and endoscopes, which contact mucous membranes, are used.

HPV Infections and Cancer To date, more than 170 HPV types have been identified and are referred to by number. A subset of these types are linked to cancer so HPV types are consequently grouped into high and low-risk categories.

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The major cancer causing types are HPV 16 and 18. Together, these can be considered especially highrisk and are responsible for the majority of HPV induced cancers including 99.7% of all cervical cancers as well as about 85% of anal cancer and close to half of vaginal, vulvar and penile cancers.

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There are a number of other ‘high-risk’ types (including HPV 31, 33, 35, 39, 45, 52 and 58) that are commonly associated with cancers globally.

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Low risk types may cause common warts on different parts of the body, such as the hands or feet. For example, HPV types 6 and 11 cause 90 percent of all genital warts. Low risk types of HPV are rarely linked to cancer. HPV16 persists longer than other types and also is especially carcinogenic; the risk of high grade cervical cancer (cervical intraepithelial neoplasia-3) is 47% at 12 years.

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HPV type 16 alone causes 50% to 60% of all cases of cervical cancer while type 18 causes 10% to 12% of all cases.

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Cervical Cancer 10

The American Cancer Society's estimates for cervical cancer in the United States for 2015 are : Approximately 12,900 new cases of invasive cervical cancer will be diagnosed. Approximately 4,100 women will die from cervical cancer. Cervical pre-cancers are diagnosed far more often than invasive cervical cancer. Cervical cancer was once one of the most common causes of cancer death for American women. But over the last 30 years, the cervical cancer death rate has gone down by more than 50%. The main reason for this change is the increased use of the Pap test. This screening procedure can find changes in the cervix before cancer develops. It can also find cervical cancer early, in its most curable stage.

Who Does HPV Infect? HPV is a common DNA virus that can affect both men and women although infection rates with high-risk types are highest for young women.

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The virus can infect cells on the surface of the skin, and mucous

membranes lining the genitals, anus, mouth and throat. About 14 million new genital HPV infections occur each year in the United States (NCI1) and around 79 million Americans are currently infected.

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At any point in time, 42.5% of women have genital HPV infections, whereas less than 7% of adults have oral HPV infections.

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In one study of female college students, 32% of those who initially had a negative result for HPV DNA tested positive two years later.

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By age 50, 80% of sexually active women will have acquired a genital HPV infection.

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How is HPV Transmitted? HPV is spread is through sex, including vaginal, anal, and even oral sex. HPV can be spread from one person to another via direct contact with skin or mucous membranes. Multiple studies carried out in laboratories and in real-world healthcare scenarios show HPV is able to remain infectious on objects and surfaces for days.

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Identified Risk Factors for HPV Infection The most consistent predictors of HPV infection are measures of sexual activity, •

Lifetime number of partners



Younger age at sexual debut



Lack of condom use



Partner with a history of multiple partners.

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such as:

However, there are potentially other non-sexual risk factors that have yet to be determined.

How is HPV Infection Treated? There is currently no medical treatment or cure for HPV infections though most people’s bodies clear the virus within 1–2 years.

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The ‘low risk’ types of HPV may cause benign growths called papillomas such as common warts that can be treated. Precancerous cervical lesions can also be treated by cryosurgery (freezing that destroys tissue). If infection with a high-risk type of HPV persists, the infection becomes chronic and this may lead to cancers.

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HPV Vaccines While there is no treatment for HPV infection, cancer risk may be reduced in part by vaccines. There are currently two vaccines which have market approval in many countries: Gardisil and Cervarix. Both vaccines are intended to produce immunity to high-risk HPV types 16 and 18 while Gardasil also offers protection against types 6 and 11. Gardisil recently introduced a 9-valent vaccine to target types 6, 11, 16, 18, 31, 33, 45, 52, and 58.

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There are potential limitations with vaccines: •

Some people are not suitable for vaccination.



There is a chance some patients will not seroconvert so will not be adequately protected



Vaccines do not treat established HPV infection or disease so must be administered prior to sexual activity commencing.



There are limited studies available on the long-term efficacy of these vaccines.



A variety of issues have led to a lower uptake of the HPV vaccines in the United States than in some other developed nations. The CDC is working to address this.

With no available treatment and the long-term efficacy of vaccines not yet fully established, prevention of exposure to HPV is a key strategy.

Transmission Risks with Ultrasound Probes Multiple studies carried out in laboratories and in real-world healthcare scenarios show HPV is able to 3

remain infectious on objects and surfaces for days.

Clinical studies have demonstrated the presence of high-risk HPV DNA on ultrasound probes following ultrasound examinations and routine disinfection.

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Disinfection Practices To Reduce HPV Ultrasound Probe Transmission Risks In the US, transvaginal and transrectal ultrasound probes are classed as “semi-critical” medical devices as they come into contact with mucous membranes. Multiple US guidelines recommend high level disinfection (HLD) of probes between patients to prevent cross contamination. HLD completely eliminates all microorganisms on the probe, except for a small number of bacterial spores. Ultrasound probe covers do not reduce the requirements for HLD. Studies show covers have a high rate of perforation before use

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and probes may become contaminated during handling, or when the cover is

placed onto, or removed from, them. Due to the difficulties of producing natural, infectious HPV for research, disinfectant efficacy testing against HPV has not previously been possible. This changed recently when a method to produce sufficient infectious HPV for testing was developed and the first HPV disinfectant efficacy study was published in 2014.

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The results showed that two disinfectants commonly used for high level disinfection in medical and healthcare facilities, glutaraldehyde and ortho-phthalaldehyde (OPA), do not kill native HPV16 - even after 24 hours of contact time. In a further study, surface carrier tests against HPV16 and HPV18 were carried out using and an ®

automated high level disinfection system, the trophon EPR.

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The testing was conducted according to

manufacturers’ instructions to simulate normal clinical use conditions (concentration, time, temperature) and met FDA requirements for virucidal testing. OPA was shown to be ineffective against both HPV16 and HPV18. The trophon EPR achieved HLD of both HPV16 and HPV18, even at the minimum concentration of its disinfectant solution.

References 1.

Parkin DM (2006). "The global health burden of infection-associated cancers in the year 2002". Int. J. Cancer 118 (12): 3030–44.

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Centers for Disease Control and Prevention. Genital HPV Infection - Fact Sheet [Internet]. 2015 [updated 2015 Feb 23; cited 2015 Mar 31]. Available from: http://www.cdc.gov/STD/HPV/STDFact-HPV.htm

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Ryndock EJ, Meyers C., A risk for non-sexual transmission of human papilloma virus? Expert Rev. Anti Infect. Ther. 12(10), 11651170 (2014)

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Bzhalava D, et al., A systematic review of the prevalence of mucosal and cutaneous human papillomavirus types. Virology 2013; 445(1-2): 224-31.

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Ault KA (2006). Epidemiology and Natural History of Human Papillomavirus Infections in the Female Genital tract. Infectious Diseases in Obstetrics and Gynecology 2006: 1–5.

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Walboomers JMM,Jacobs MV,Manos MM, et al. Human papillomavirus is a necessary cause of invasive cervical cancer worldwide. J Pathol. 1999; 189: 12–19.

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Schiffman M, Clifford G, Buonaguro FM. Classification of weakly carcinogenic human papillomavirus types: addressing the limits of epidemiology at the borderline. Infectious agents and cancer 2009; 4: 8.

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Moscicki A-B, Schiffman M, Kjaer S, Villa LL. Updating the natural history of HPV and anogenital cancer. Vaccine. 2006;24(Suppl 3):42-51.

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Bosch FX, de Sanjos¨¦ S. Chapter 1: human papillomavirus and cervical cancer¡ªburden and assessment of causality. J Natl Cancer Inst Monogr. 2003;31:3-13.

10. American Cancer Society's Cancer Facts and Figures accessed 27 March 2015. Available at: http://www.cancer.org/cancer/cervicalcancer/detailedguide/cervical-cancer-key-statistics Last Medical Review: 09/19/2014 Last Revised: 02/26/2015. 11. Hariri S, Unger ER, Sternberg M, et al. Prevalence of genital human papillomavirus among females in the United States: the National Health and Nutrition Examination Survey, 2003-2006. J Infect Dis. 2011;204(4):566-73. 12. CDC: Centers for Disease Control and Prevention. Genital HPV Infection – Fact Sheet [ONLINE]. Accessed December 5, 2014 13. Gillison ML, Broutian T, Pickard RK, et al. Prevalence of oral HPV infection in the United States, 2009–2010. JAMA 2012; 307(7):693–703.

 

 

14. Winer RL, et al. Genital human papillomavirus infection: incidence and risk factors in a cohort of female university students. Am J Epidemiol. 2003;157:218-26. 15. Centers for Disease Control and Prevention. Self-Study STD Module ¨C Genital Human Papillomavirus (HPV) Infection. Available at: http://www2a.cdc.gov/stdtraining/self-study/hpv.asp. Accessed September 11, 2012. 16. Burchell, AN, et al. Epidemiology and transmission dynamics of genital HPV infection. Vaccine 2006:24(Suppl 3):52-61. 17. Rodríguez AC, et al. (2008) Rapid clearance of human papillomavirus and implications for clinical focus on persistent infections. J Natl Cancer Inst 100: 513–517. doi: 10.1093/jnci/djn044. pmid:18364507 18. Rodríguez AC, et al. (2010) Longitudinal study of human papillomavirus persistence and cervical intraepithelial neoplasia grade 2/3: critical role of duration of infection. J Natl Cancer Inst 102: 315–324. doi: 10.1093/jnci/djq001. pmid:20157096 19. National Cancer Institute. 2014. Human Papillomavirus (HPV) Vaccines: An Interview with Douglas R. Lowy, M.D.. [ONLINE] Available at: http://www.cancer.gov/news-events/nci-update/2014/hpv-vaccines-lowy. Accessed 6 January, 2015 20. Casalegno et. Al.: High Risk HPV Contamination of Endocavity Vaginal Ultrasound Probes: An Underestimated Route of Nosocomial Infection?, PLOS ONE, Oct 2012, Volume 7, Issue 10 21. Ma et al.: Transvaginal ultrasound probe contamination by the human papillomavirus in the emergency department, Emerg Med J, 2012 22. M’Zali et al. Persistence of microbial contamination on transvaginal ultrasound probes despite low-level disinfection procedure. PLoS One 2014;9:e93368. 23. Rutala W., et. al, Guideline for Disinfection and Sterilization in Healthcare Facilities, 2008, Centers of Disease Control, 1-158, 2008. 24. Meyers, J., et al., Susceptibility of high-risk human papillomavirus type 16 to clinical disinfectants. J Antimicrob Chemother, 2014. 25. Meyers, C., et al., Efficacy of a high-level disinfectant system against high-risk human papilloma virus. Presented at SHEA 2015.

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