header logo

Risk management in sexual practices — a technical and rigorous introduction to sex education

Photo credit to Pixabay

Sex and safety

This article was conceived from an observation among several friends. Among most single adults in our social circles, condoms are viewed as more important during vaginal or anal sex than during oral sex. Lest we think the problem here is that I have some promiscuous friends, relatively recent survey studies show that condom usage is higher for anal sex [1,2] and vaginal sex [2,3] than for oral sex. When I ask around, friends regardless of education level or industry (including medical students and doctors) explain this behavior with a variant of "I don't use condoms for oral sex but they are a must for vaginal sex because everyone else thinks so." This is a lackluster explanation at best and it turns out working in the medical field does not make anyone an expert on sex ed [4]. The situation is one of three things - either STD transmission rates are significantly lower orally than with other sex practices and therefore it is sensible to use more protection for higher risk acts OR STD transmission rates are not significantly different and either we are forgoing lots of pleasure by using condoms when we are already comfortable with that level of risk (as demonstrated by condomless oral sex practices) OR we are taking risks we are not aware of or comfortable with and we all need to be wearing condoms for oral sex too. There is a rational basis for the popular practice but it is not as firm as we tend to imagine it is.

Goals of this article

The goal of this article is to present the risk management portion of sexual education with the technical rigor it deserves. Are the transmission rates of any/most/all sexually transmitted diseases (STDs or sexually transmitted infections, STIs) lower during oral, anal, or vaginal sex? How much time must elapse between exposure and testing for a disease to be detected by a screening test? How much do condoms lower transmission rates?

Author note

This article cites little original research. To write a proper literature review on a subject this broad requires a far higher word count and more subject-matter expertise than I have. Therefore, this article cites mostly review articles, peer-reviewed articles that present a subject-matter expert's view of the state of the science.

Articles like this one are extremely frustrating to compose because the data one would like to cite are often not available. For example, CDC prevalence data on various STDs is incomplete (herpes did not suddenly arrive in 1998). And the per-exposure risk of transmission has been studied for few sex acts and diseases. As I pass on to my readers this incomplete data, know that I am deeply sorry for these frustrations and more. I am acutely aware of these shortcomings and have done my best to minimize them.

A note about sexual ethics

Insofar as it is possible, the goal of this blog is not to preach about what should be; the goal is to describe the world as it is and identify the features of it that should be most relevant to our decision-making processes. However, those who reviewed this article before publication frequently had moral objections or comments. Sex is difficult to discuss in the absence of value judgments. This article is not a discussion about what kinds of sex you should have. It is a mistake on the part of the reader to interpret it as such. It is a discussion about the information you should consider as you decide what kinds of sex you choose to have.

"Only slutty people need to worry about that kind of thing. Good, decent people get married and don't have any of these problems." — This is probably my favorite quote about sex because it was said to me during a discussion about sexual risk by a person whose marriage dissolved several years later. They had several rebound relationships afterward, contracted an incurable STD, and now have a slightly different take on marriage. This is the result of thinking that impulsive, ill-informed decision-making is a substitute for the measured, informed variety. Risk tolerance concerning sex is a topic that should be of interest to everyone. Even for those in monogamous relationships, the ugly fact is not all of those relationships are monogamous. Statistics on cheating are notoriously difficult to collect. One study found a six-fold increase in infidelity by having a computer ask the questions instead of a research assistant with a clipboard [5]. I have yet to see convincing data on the incidence of infidelity in monogamous relationships but I can safely say lots of people think they are in monogamous relationships who are not.

A few definitions

Prevalence: the number or percent of people in a population currently infected with a disease

Incidence: the number or percent of people in a population with new infections per time (ie 200,000 new infections per year)

Incubation period: the time between exposure and development of symptoms (often highly variable)

Window period: the time between exposure and possible detection with a diagnostic test

Nucleic acid amplification test (NAAT): Diagnostic test which directly detects the pathogen's DNA or RNA in the sample. There are many types of NAAT tests which use different techniques to amplify the DNA/RNA.

Enzyme-linked immunosorbent assay (ELISA): Diagnostic test which detects antibodies in the body. ELISA tests give results in minutes. Most diagnostic tests in a doctor's office where they mix a few things on the counter are ELISA tests.

Enzyme immunoassay (EIA): Diagnostic test which detects antibodies in the body and proteins in the pathogen. In some literature, this is synonymous with ELISA but in HIV tests ELISAs only detect antibodies and EIAs detect antibodies + an HIV protein, p24.

What specific diseases are we talking about

There are four major STDs which compose the standard STD screening test. They are syphilis, gonorrhea, chlamydia, and human immunodeficiency virus (HIV). Some institutions and clinicians include trichomoniasis for women but it is never a part of routine screenings for men. Additionally, sexual contact is a major mechanism of transmission for hepatitis B, the two herpes simplex viruses (HSV-1 and HSV-2), human papillomavirus (HPV), chancroid, donovanosis, yeast infections, pubic lice, scabies, and bacterial vaginosis (BV). Of those, donovanosis, chancroid, and scabies are rare enough to be of no serious concern in the developed world. Hepatitis B and HPV are vaccine-preventable and therefore of less concern. Herpes, pubic lice, yeast infections, and BV are relatively low-consequence and, except for herpes, curable.

It is important to note hepatitis B, the two herpes simplex viruses (HSV-1 and HSV-2), yeast infections, pubic lice, scabies, and bacterial vaginosis (BV) can be spread by other mechanisms and all but the first two can arrise spontaneously.

STD risk analysis

Risk analysis considers the combination of probability (discussed below) and severity (discussed under the section "Severity: notes on the prognosis and transmission of STDs"). In an ideal world, we would have access to a good deal of data so we could make informed decisions about risk. Specifically, we need to know two probabilities to compute the odds of contracting a disease from random partners over \(n\) encounters.

$$ P_\text{contracting disease A} = n \left(P_\text{per-act infection risk}\right)\left( P_\text{prevalence of A}\right) $$

The \(P_\text{per-act infection risk}\) depends on several parameters such as the disease in question, use of barrier protection, type of sex act, and position in that act. For example, the risk of transmission of most diseases is higher from an infected penis to a vagina than it is from an infected vagina to a penis. Unfortunately, the literature has incomplete information on the per-act risk of transmission of most diseases and the degree to which barrier protection reduces that risk. The \( P_\text{prevalence of A}\) is something most Western countries have reliable data on.

Prevalence

Most STDs are mandatory reporting diseases meaning anytime a lab in the US obtains a positive result, they are required to report it to the Center for Disease Control (CDC). This information is used to judge the effectiveness of STD prevention programs, detect outbreaks, and inform screening guidelines. As a matter of convention in epidemiology, rare prevalence and incidence are measured on a "per 100,000" basis. Common disease prevalence and incidence are measured in percentage terms (per 100). Some papers occasionally use other bases but these are the two most common reporting metrics in epidemiology.

prevalence of STDs in US

[Caption] Prevalence of most tracked STDs in the United States. Syphilis has five stages (primary, secondary, early latent, late latent, and tertiary) of which the late latent is the least infectious. Syphilis prevalence is shown twice to illustrate an accurate picture of the disease epidemiology and the prevalence relevant to risk management. HIV estimated data 1981-2008 from [6], HIV 2010-2016 from [7], trichomoniasis from [8], HSV-1 and -2 from [9], all others from [10]. The HIV prevalence statistics from [6] and [7] are not in agreement even though both reports are from the CDC. This is likely because of different diagnostic criteria, estimation methods, and other discrepancies between the two reports. It is impossible to gather consistent figures on disease prevalence at the beginning of their discovery because the diagnostic definition of the disease is usually evolving during that time. Therefore, prevalence statistics are extrapolated and estimated to give a picture of the past. This is not an exact science and different groups working with different data sets are expected to reach slightly different figures. Trichomoniasis is only regularly diagnosed in women, the prevalence in men is not measured with the same accuracy but it is thought to be similar [11,12,13].

Normally when we are selecting partners we know more about them than "this person is a member of the US population." Even in the most sordid circumstances, we know something about the sexuality, gender, age, and race of our sexual partners. These pieces of information can place our potential sexual partner in subpopulations of the US with significantly different disease prevalences. For instance, the prevalence of HIV in African/American homosexual/bisexual men is greater than 1,400 per 100,000; heterosexual Asian females have rates under 100 per 100,000. This difference has been used to justify tremendous bigotry. However, just because a fact has historically been used to justify ugly things does not mean the fact itself must be ignored. These differences are relevant to making informed decisions about risk tolerance regardless of how else they might be used. Complete information about relative STD prevalence by age, gender, sexuality, geography, and race can be found on the CDCs website: www.cdc.gov.

A detailed, interactive map of HIV prevalence and incidence compiled from CDC data is available at map.aidsvu.org.

Disease control efforts

There have been many attempts to paint increasing STD rates as consequence of the sexual revolution or sexual education. This is hard to square with the fact that while HIV and chlamydia rates were increasing, gonnorhea rates were on the decline. The real cause is likely to be the work of public health officials and medical researchers. Gonorrhea was brought under control through the National Gonorrhea Control Program which began in 1972 shortly before gonorrhea rates in the US peaked [14]. When a society has access to accurate screening tests, chooses to use them, and treats accordingly, diseases which are often asymptomatic go into decline. By comparison, widespread chlamydia testing began in the UK in 2002 with the National Chlamydia Screening Programme [15]. Chlamydia only became a mandatory reporting disease in the US in 2010 while gonnorhea has been mandatory reporting disease since 1944.

Per-act risk of transmission

Pathogen Sex act Risk with barrier Risk w/o barrier
HIV Receptive anal intercourse 11-70 [16] 102-186 [16]
HIV Insertive anal intercourse 1-8 [16] 4-28 [16]
HIV Receptive penile-vaginal intercourse 0.63-4.1 [16] 6-11 [16]
HIV Insertive penile-vaginal intercourse 0.16-3.9 [16] 1-19 [16]
HIV Oral sex bidirectional --- 0-5 [16]
Primary/secondary syphilis Bidirectional penile-vaginal intercourse 10-20 [17] 100-200 [17]
Primary/secondary syphilis Bidirectional penile-anal intercourse >14 [17] >140 [17]
Primary/secondary syphilis Bidirectional penile-oral intercourse about 10 [17] about 100 [17]
HSV-2 Man to woman 10-45 [18] 100-750 [18]
HSV-2 Woman to man 5-25 [18] 10-50 [18]

[Caption] Odds shown are a range (95% confidence interval) of transmissions per 10,000 exposure events. HIV risks assume no antiretroviral treatment which decreases these figures by a factor of 20-30 [16]. Odds of transmission also vary with an individual's viral load at any given time. Remarkably few papers attempt to quantify the per-act transmission risk of STDs. I could not find data on other STDs and sex acts; apparently, researchers and grant organizations do not believe these are important figures to document.

Severity: notes on the prognosis and transmission of STDs

Infections, sexual or not, come in one of four broad varieties: fungi, parasites, bacteria, and viruses. STDs are represented in every category.

Fungal STDs

Yeast infections are most commonly caused by species in the Candida genus. The organisms are present in normal healthy persons but overgrowth causes symptoms. The infection can be transmitted sexually [19,20] but can also arise spontaneously [21]. Because the pathogenic organisms are normally present, treatment is based on symptoms. Screening is not performed for Candida species.

Parasitic STDs

Trichomoniasis is caused by the protozoan Trichomonas vaginalis. It is not a mandatory reporting disease so historical statistics on prevalence are noisy and include some estimation [22]. Today (2020) the CDC estimates the prevalence at 1,100 per 100,000, more than double the prevalence of gonorrhea or chlamydia. Like chlamydia and gonorrhea, trichomoniasis is not usually a serious disease when treated promptly. However, trichomoniasis infections increase the susceptibility to HIV infection [23,24] and long term infection can cause infertility in both sexes [25,26,27]. Unlike other STDs, infection is largely limited to the genitals and does not affect the mouth or anus. Trichomoniasis NAAT tests are the most commonly used screening tests. The sensitivity and specificity of NAATs are between 96-100% [28] but the window period remains unstudied.

Bacterial STDs

Syphilis is caused by Treponema pallidum. The disease progresses through four stages, primary (sores on the genitals, 3-90 days after exposure), secondary (rash on palms and soles, 4-10 weeks after exposure), latent (no symptoms, 10 weeks to 10 years after exposure), and tertiary (may attack neurological or cardiovascular systems or cause non-cancerous growths, may occur anytime after latent syphilis). Syphilis is one of the commonly screened STDs because the consequences of neuro- or cardio-syphilis are high and the diagnosis is difficult. The description of symptoms above appears in most medical textbooks but applies only to a minority of patients. Clinical diagnosis by symptoms is notoriously difficult so diagnosis is most commonly made by blood testing [29]. Fortunately, syphilis is easily treatable once diagnosed. It is one of few bacterial pathogens that has failed to develop any antibiotic resistance and is therefore still treated with penicillin.

Gonorrhea and chlamydia are caused by Neisseria gonorrhoeae and Chlamydia trachomatis, respectively. They are often considered together because from the perspective of the patient, the two are almost identical. Both are often without symptoms and can cause infertility if left untreated. Chlamydia can cause epididymitis, prostatitis, pelvic inflammatory disease, pharyngitis, conjunctivitis, perihepatic inflammation, and proctitis [30]. It is the most common cause of congenital blindness [31]. Infection with chlamydia or gonorrhea increases susceptibility to HIV [32]. Untreated gonorrhea can cause septic arthritis [30]. However, the primary concern that calls for screening is the damage to fertility and morbidity in babies born to infected mothers. Both are easily treated with antibiotics though drug-resistant gonorrhea is becoming a serious threat [33,34,35]. Although information about oral transmission is scarce, oral gonorrhea can cause a sore throat but usually causes no symptoms at all [36].

Every few years the CDC issues a new report on antibiotic resistance. The report classifies resistant pathogens as one of four stages: "urgent threats," "serious threats," "concerning threats" or "watch list." In the 2019 report [37], Neisseria gonorrhoeae is listed as "urgent" along with only four other bacteria; no other sexually transmitted pathogen was mentioned in the report. Gonorrhea is by far the scariest bacterial STD. To quote the same CDC report: "Gonorrhea has quickly developed resistance to all but one class of antibiotics, and half of all infections are resistant to at least one antibiotic. Tests to detect resistance are not available at time of treatment. . . Untreated gonorrhea can cause serious and permanent health problems in women and men, including ectopic pregnancy and infertility, and can spread to the blood resulting in cardiovascular and neurological problems." After a significant percentage of gonorrhea developed penicillin and tetracycline resistance (1980), ciprofloxacin resistance (2007), and cefixime resistance (2012), the medical community now recommends an azithromycin/ceftriaxone dual therapy. Documented cases of failure of that dual therapy now exist [38,39] and it appears to be a matter of time before they become common. Drug resistance is presenting an additional tracking problem. Because pathogen identification used to be done primarily with cell cultures and microscopy, it was trivial for labs to run antibiotic sensitivity tests at the same time. Today, a ball-park 80% of gonorrhea samples never make it to cell culture thanks to the rise of various NAAT-style diagnostic tests [40]. Not only do we know that gonorrhea presents an increasing public health challenge, we do not know precisely how big a problem it is.

Drug resistant gonorrhea - ceftriaxone concentration density resistance curves year by year in heterosexuals

[Caption] Frequency of ceftriaxone minimum inhibitory concentrations as a function of year for heterosexuals in the UK. Ceftriaxone is one of two first-line treatments for gonorrhea and resistance is rapidly developing [41].

Bacterial vaginosis (BV) is caused by a plethora of bacteria, none of which are individually sufficient to cause the disease. BV causes itching, pain, and discharge. While it is highly uncomfortable and a quality of life issue, BV does not cause significant morbidity or mortality and is usually treatable. BV can arise spontaneously but is likely also sexually transmitted. It is more common in sexually active women and the bacteria associated with it have been found on the penises [42] of the partners of women with BV. Having sex with a man who has multiple sexual partners also significantly increases the risk of developing BV [43]. BV is a risk factor for miscarriage [44,45,46].

Donovanosis (granuloma inguinale) and chancroid are caused by Klebsiella granulomatis and Haemophilus ducreyi, respectively [30]. They are both genital ulcer diseases, both treatable with antibiotics, and both extremely rare in the developed world. There are less than 100 cases of each per year in the US [30,47]. However, because of testing limitations, chancroid is thought to be underdiagnosed [30].

Viral STDs

Viral infections are generally the most dangerous. Modern antibiotics are highly effective against most bacterial infections most of the time. Treatments for fungi and parasites are similarly effective. Anti-viral drugs are the least effective class. Viruses are the most likely infection to progress to a chronic state even with treatment, the most likely to cause cancer, and the most likely to cause death.

There are 3 classes of viral hepatitis: Hep A, Hep B, and Hep C caused by Hepatovirus A, Hepatitis B virus, and Hepacivirus C, respectively. The nomeclature around hepatitis viruses is complicated and unimportant here (Hepacivirus A causes lung infections in dogs, Hepatovirus A causes severe stomach flu in humans). Hep A is a food-borne illness which a healthy individual naturally clears. For most healthy adults, this is experienced as severe stomach flu. In rare cases or the case of immune-compromised patients, Hep A causes liver failure. Hep B is spread by sexual contact among other mechanisms but it is vaccine-preventable in >90% of the population [48] and about 95% of adults clear the infection naturally [49]. Hep B is still capable of causing significant damage particularly among those infected early or late in life and in the immunocompromised. It is also a miserable disease to contract; even when it does resolve naturally, that process can take the better part of a year. Hep C is primarily spread by IV drug users sharing needles and other blood to blood transmission modes (accidental needle sticks of health care workers, etc). There are a few documented cases of Hep C spread by sexual contact but it is extremely rare [50]. For IV drug users and healthcare workers with accidental needle sticks, Hep C is a serious danger because 1% of the population is currently infected. This number is growing as more opioid addicts shift toward injectable street drugs.

HSV-1 and HSV-2 used to be strongly associated with oral and genital herpes, respectively. With the increasing practice of oral sex in recent decades, that correlation is dropping off [51]. The risk of herpes is high among those with many sexual partners because only about 10-25% of people with genital herpes are aware they have it [52]. A blood test can only indicate the presence of antibodies but without an outbreak, there is no way to identify whether the infection is genital or oral [52]. Transmission rates can be reduced with condoms [18,52,53], by having infected partners on an antiviral regimen [52], and by having the uninfected partner on an antiviral prophylaxis like PrEP [54] or valacyclovir [55]. While all of those precautions lower the risk of transmission, none of them is a guarantee, even in combination. With both partners on valacyclovir and perfect condom usage, HSV will still occasionally spread. Those with an HSV virus (70%+ of the population [52]) need to take minor precautions to avoid spreading it in unfortunate ways. Never perform oral sex on someone while you have a cold sore — you can transmit your oral herpes as genital herpes. Never touch a lesion and then rub an eye or apply a contact lens — you can transmit the infection as ocular herpes (herpes keratitis). Never allow a baby near a lesion and do not kiss a baby with a cold sore. The herpes infection is mostly harmless to adults but can kill infants. Always tell your ob/gyn if you have a herpes infection during pregnancy as it is not safe for women with primary genital herpes to deliver babies vaginally [56,57].

There is a myth that those with oral herpes are protected from genital herpes. This is absolutely not true, coinfection with both HSV-1 and -2 is common [58,59]. One study from 1978 [60] found HSV-1 to have a slightly protective effect against HSV-2 in mouse models. This has not (to my knowledge) been shown in humans and the protection for mice was partial at best.

Herpes can present in other ways that are not sexually transmitted. The most common presentation of herpes is a cold sore on the lips [61]. This can be contracted in childhood by sharing beverages or towels with adults [62]. Other presentations are less common. Herpes gladatorium appears on any part of the body and is often associated with mixed martial arts, wrestling, and other physical, close-contact sports [63,64,65]. It is colloquially known as "mat herpes". In some situations, antivirals are prescribed prophylactically to prevent outbreaks at wrestling camps [66]. Herpes keratitis is an ocular presentation of herpes affecting the cornea [67,68]. Contact lens usage increases the likelyhood of herpes keratitis and some evidence suggests lenses increase the frequency of outbreaks if it is contracted [69]. Herpetic whitlow is a herpes lesion around the fingernail. Before the arrival of HIV, dentists did not wear gloves. As a result, they were the most likely people to contract herpetic whitlow [70,71]. In doing so, they also facilitated the transmission of oral HSV from patient to patient. HSV esophagitis is herpes of the throat (commonly seen in immunocompromised patients) [72]. Herpes encephalitis and herpes meningitis are rare and often fatal infections of the brain and meninges, respectively. These rare but more severe conditions are among the many public health motivations for lowering the prevalence of HSV [61].

Human papillomavirus (HPV) affects 5-10% of the US population [73]. The CDC says "HPV is so common that nearly all sexually active men and women get the virus at some point in their lives." Transmission of HPV to males is slightly reduced by circumcision but this effect is small for individual decision making [74]. While sexual intercourse is the most common mode of transmission, it is not required; the virus has been detected in vaginal swabs of women who report no history of sexual contact [75]. In most cases, HPV resolves spontaneously without treatment within 2 years. In a minority of cases, certain strains of the virus cause genital warts, pharyngeal cancer, or cervical cancer. The HPV vaccine is currently available to the younger population.

HIV is the most well-known and deadly sexually-transmitted virus of the last century. For this reason, it is also the most well studied. HIV eventually compromises the immune system of infected individuals and allows otherwise benign infections to flourish and eventually kill the patient. HIV is becoming treatable as research into new drugs and therapies continues but it is still deadly and dangerous. Preexposure prophylaxis (PrEP) is a cocktail drug (tenofovir and emtricitabine [76]) which reduces the risk of transmission when taken by a non-infected person before exposure. Transmission rates are significantly lowered by condoms, use of antivirals in the infected person, and use of antivirals in the uninfected person (PrEP is a combination of antivirals) [77,78,79]. However, there are reports that PrEP treatment can increase the false positive rate of HIV screening tests [80].

HIV is the primary cause of concern in sexual risk management. Other STDs are, in the vast majority of cases, an inconvenience compared to HIV. They are mostly curable (all the diseases in the bacterial category, trichomoniasis, & Hep B), or vaccine-preventable (Hep B, HPV), or low consequence and often asymptomatic (HSV). HIV is not any of those things and for this reason, HIV is the most severe hazard associated with sexual activity, even with modern treatment advances. However, the risk of HIV motivates us to reduce the transmission of other STDs because infection with almost any STD is linked to increased risk of contracting HIV (chlamydia/gonorrhea [32], syphilis [81], BV [82,83], trichomoniasis [23,24], HSV [84], yeast infections [85], chancroid [86]).

The rationale for condoms during vaginal/anal sex while practicing unprotected oral sex

The original purpose of this article was to determine whether there was a sound, rational basis for using condoms during vaginal/anal sex but not oral sex. Insofar as it is reasonable to make that argument, it goes as follows:

For most healthy adults who are regularly screened for STDs, HIV is the only STD of serious concern. When captured by screening tests and treated promptly, all STDs except herpes and HIV are curable and usually cause no long-term problems. Herpes is ubiquitous and the consequences are more social than physical when taking antivirals as prescribed. In the developed world, HIV is the only dangerous STD. It is the primary motivation to practice safe sex because the consequences of contracting it dwarf the consequences of all other STDs. Because HIV is the only disease we are willing to make sacrifices in pleasure to avoid, and because HIV is significantly less transmissible by oral sex than anal/vaginal sex, we use condoms to lower the HIV risk anally/vaginally but not orally.

That justification is open to legitimate criticism. Perhaps you are more concerned about other STDs that do not appear to exhibit the same differential transmission rates between sex acts. Perhaps you are too terrified of HIV or the rise of drug-resistant gonorrhea to have sex at all. That criticism relates to what the risk tolerance of the society and/or the individual should be. It does not relate to a misunderstanding or application of the facts about STD transmission as they are currently understood by experts.

Lying to lesbians — the medical literature on STI risks and women who have sex with women

In scientific literature, the terms "women who have sex with women" (WSW) and "men who have sex with men" (MSM) describe homosexual and bisexual people. This grouping arose mostly during the study of HIV as the scientific community tried to explain the high prevalence of HIV in MSM. There is a popular myth that lesbian sex acts present a low risk of STD transmission across the board. Part of the problem is in the scientific literature. Survey studies often say things like "chlamydia, gonorrhea, and pelvic inflammatory disease were rare and diagnosed only in women who had histories of sex with men." [87] That study surveyed 708 WSW of which 82% reported sexual contact with men. Of course, chlamydia and gonorrhea were rare. They affect about 0.5% and 0.2% of the population, respectively, and this study surveyed 127 exclusive lesbians. If lesbians were just as likely as their bisexual counterparts to contract these STDs, this study had too small a sample to accurately measure the prevalence.

The problem with studies on this topic are small samples which give inconsistent results. Here [88] is a survey of 1408 WSW of which 93% had sexual contact with men. Here's another survey [89] with about 100,000 women but only 641 exclusive lesbians. The study carefully pointed out WSW had a lower risk of STIs unless they were also smokers. This is asinine because it is simply not possible to accurately measure a disease prevalence below 1% with a sample size in the hundreds. Further dividing that group by lifestyle habits is the definition of chasing noise in data.

The papers discussed here are the best papers from Google Scholar results for "WSW STI". All that can be concluded from the Google Scholar results on the topic is WSW have higher rates of BV, they can transmit other STDs without the help of a man, and we know little else. The commonly held belief that lesbian sex is low risk is unsubstantiated by the evidence we currently have. The scientific community's refusal to ask relevant questions about lesbian sex (and sex in general) is the reason so many of the questions I hoped to answer in this article are still unanswered. For example, what percentage of lesbian sex involves orogenital contact? digital-genital contact? genital-genital contact directly? genital-genital through the use of shared toys? How do such behaviors influence disease transmission?

Safe sex vs abstinence as an STD prevention strategy

Since 1981 and the Adolescent Family Life Act, abstinence-only education has been a major portion of the sexual education in US public schools. At times it has been the only version to receive federal funding. It has been championed by everyone from doctors [90] to religious zealots. There are many legitimate ways to criticize abstinence-only education programs from their scientific merit to their moral implications [91]. Criticizing the science in abstinence-only education is like shooting fish in a barrel [92] but here I will address two important things: the grossly misrepresented statistics on condoms and the value of risk in our personal lives.

Abstinence does have a few points in its favor, namely it is the only preventative strategy with 100% effectiveness in the "perfect-use" case. (Except for HSV which can be contracted other ways, bloodborne STDs which can be contracted other ways, yeast infections & bacterial vaginosis which can arise spontaneously, . . . ) To properly describe the effectiveness of an STD or pregnancy prevention strategy requires two metrics — "perfect-use" (or "method failure") and "typical-use" (or "user-failure"). Abstinence-only advocates commonly cite condoms as 70-80% effective which is approximately accurate for the "typical-use" case. For the abstinence method, however, they cite the "perfect-use" success rate. Blatant misapplication of statistics such as these is morally equivalent to lying.

The core problem with abstinence-only advocates is their desire to impose certainty on a probablistic world. The world does not owe anyone certainty and great arrogance is required to imagine it does. No human activity is safe in absolute terms. To claim abstinence is best because the risk is 0% indicates the value of sexual activity is appalling low. All things that give human beings pleasure and happiness are worth some element of risk. They all require some element of risk. The question is how much are you willing to risk for how small a reward? Virtually no one takes this hardline stance on any other risk. 30-40k people die every year in the US in fatal car accidents; at its peak in the early 1990s HIV killed under 15k people per year. Cars are more fatal than HIV ever was. On a per-capita basis, they were probably approximately equally lethal since less than 100% of the population is sexually active. Is it therefore prudent to avoid cars altogether? Abstinence from driving is the only 100% effective way to avoid a fatal car accident (unless a car strikes you as a pedestrian but you can also catch HIV from a blood transfusion). Mature people balance the risk of the activity with the rewards. The only way to properly approach this question is to have all the facts in front of you and make the highly personal decision about what you are willing to risk and what pleasures you hope to experience as a result. Unfortunately, abstinence-only education programs make every effort to hide most of the facts.

Despite the misrepresentation of data, outright lies about sex, and ethical implications of moral proselytizing, abstinence-only education has a bigger flaw. It does not do what it is purported to do [93,94,95,96,97,98]. Some studies show that abstinence education delays the onset of sexual activity slightly but not pregnancy or STD rates. If you can find a peer-reviewed study without obvious methodology flaws showing abstinence-only sex education reduces pregnancy or STD rates, please email me.

The bureaucratic view of risk management and sex

Prostitution is legal in the United States at the federal level and is legally practiced in several Nevada counties. In legal US brothels, condoms are required by law for oral, vaginal, and anal sex acts. Barrier protection is not required for oral sex performed by the Johns on the sex workers. Legal requirements are never a foolproof guide to risk management (obviously drug laws would be unrecognizable if they were) but they are an interesting practical example of bureaucratic risk-management. As one might expect, the bureaucratic standard in the United States is more risk-averse than the standard practiced by common people. However, in Amsterdam rules and regulations are looser. Sex workers are not required to use any protection though the vast majority chose to do so.

Final thoughts

The choice of whom to have sex with, when, and with which protective measures in place to mitigate the risks of STDs is a highly personal decision. It can only be an informed decision if the person has accurate information on the risk associated with specific behaviors and the degree protective measures mitigate those risks. In the months before I wrote this, I came to the realisation no one in my (highly-educated) social circle knew half of the information germane to these decisions. Including me. Despite the fact all adults are constantly making decisions about their sexual activity. As of today, this article is longer and has more references than any other post on this blog. This is a reflection of the breadth, complexity, and importance of topic.

References

[1] J. S. Leichliter, A. Chandra, N. Liddon, K. A. Fenton, and S. O. Aral, "Prevalence and correlates of heterosexual anal and oral sex in adolescents and adults in the United States," Journal of Infectious Diseases, vol. 196, pp. 1852—1859, 2007.

[2] M. A. Habel, J. S. Leichliter, P. J. Dittus, I. H. Spicknall, and S. O. Aral, "Heterosexual anal and oral sex in adolescents and adults in the United States, 2011—2015," Sexually Transmitted Diseases, vol. 45, pp. 775—782, 2018.

[3] R. L. Fielder, and M. P. Carey, "Prevalence and characteristics of sexual hookups among first-semester female college students," Journal of Sex & Marital Therapy, vol. 36, pp. 346—359, 2010.

[4] C. Warner, S. Carlson, R. Crichlow, and M. W. Ross, "Sexual health knowledge of US medical students: A national survey," The Journal of Sexual Medicine, vol. 15, pp. 1093—1102, 2018.

[5] M. A. Whisman, and D. K. Snyder, "Sexual infidelity in a national survey of American women: Differences in prevalence and correlates as a function of method of assessment," Journal of Family Psychology, vol. 21, pp. 147, 2007.

[6] Centers for Disease Control and Prevention, "HIV surveillance—United States, 1981-2008," Morbidity and Mortality Weekly Report, vol. 60, pp. 689, 2011.

[7] Centers for Disease Control and Prevention, "Estimated HIV incidence and prevalence in the United States, 2010-2016," HIV Surveillance Supplemental Report, vol. 24, 2019.

[8] J. Braxton, D. W. Davis, B. Emerson, E. W. Flagg, J. Grey, L. Grier, A. Harvey, S. Kidd, J. Kim, and K. Kreisel, "Sexually transmitted disease surveillance 2017," 2018.

[9] G. M. McQuillan, D. Kruszon-Moran, E. W. Flagg, and R. Paulose-Ram, "Prevalence of herpes simplex virus type 1 and type 2 in persons aged 14-49: United States, 2015-2016," National Center For Health Statistics Data Brief, 2018.

[10] Centers for Disease Control and Prevention, "Sexually transmitted disease surveillance 2018," 2018.

[11] K. Wendel, E. Erbelding, C. A. Gaydos, and A. M. Rompalo, "Use of urine polymerase chain reaction to define the prevalence and clinical presentation of Trichomonas vaginalis in men attending an STD clinic," Sexually Transmitted Infections, vol. 79, pp. 151—153, 2003.

[12] S. B. Saxena, and R. R. Jenkins, "Prevalence of Trichomonas vaginalis in men at high risk for sexually transmitted diseases," Sexually Transmitted Diseases, vol. 18, pp. 138—142, 1991.

[13] W. C. Miller, H. Swygard, M. M. Hobbs, C. A. Ford, M. S. Handcock, M. Morris, J. L. Schmitz, M. S. Cohen, K. M. Harris, and J. R. Udry, "The prevalence of trichomoniasis in young adults in the United States," Sexually Transmitted Diseases, vol. 32, pp. 593—598, 2005.

[14] T. A. Peterman, K. O’Connor, H. M. Bradley, E. A. Torrone, and K. T. Bernstein, "Gonorrhea control, United States, 1972—2015, a narrative review," Sexually Transmitted Diseases, vol. 43, pp. 725, 2016.

[15] S. Szreter, "Chlamydia: A Disease without a History," The Hidden Affliction: Sexually Transmitted Infections and Infertility in History, 2019.

[16] P. Patel, C. B. Borkowf, J. T. Brooks, A. Lasry, A. Lansky, and J. Mermin, "Estimating per-act HIV transmission risk: a systematic review," AIDS (London, England), vol. 28, pp. 1509, 2014.

[17] R. T. Gray, A. Hoare, G. P. Prestage, B. Donovan, J. M. Kaldor, and D. P. Wilson, "Frequent testing of highly sexually active gay men is required to control syphilis," Sexually Transmitted Diseases, vol. 37, pp. 298—305, 2010.

[18] A. S. Magaret, A. Mujugira, J. P. Hughes, J. Lingappa, E. A. Bukusi, G. DeBruyn, S. Delany-Moretlwe, K. H. Fife, G. E. Gray, and S. Kapiga, "Effect of condom use on per-act HSV-2 transmission risk in HIV-1, HSV-2-discordant couples," Clinical Infectious Diseases, vol. 62, pp. 456—461, 2015.

[19] B. J. Horowitz, S. W. Edelstein, and L. Lippman, "Sexual transmission of Candida," Obstetrics and Gynecology, vol. 69, pp. 883—886, 1987.

[20] J. D. Sobel, "Genital candidiasis," Sexually Transmitted Infections and Sexually Transmitted Diseases, pp. 613—624, 2011.

[21] J. D. Sobel, "Patient education: Vaginal yeast infection (Beyond the Basics)," UpToDate, 2019.

[22] W. C. Miller, and J. M. Zenilman, "Epidemiology of chlamydial infection, gonorrhea, and trichomoniasis in the United States —2005," Infectious Disease Clinics, vol. 19, pp. 281—296, 2005.

[23] P. Kissinger, and A. Adamski, "Trichomoniasis and HIV interactions: a review," Sexually Transmitted Infections, vol. 89, pp. 426—433, 2013.

[24] R. S. McClelland, L. Sangaré, W. M. Hassan, L. Lavreys, K. Mandaliya, J. Kiarie, J. Ndinya-Achola, W. Jaoko, and J. M. Baeten, "Infection with Trichomonas vaginalis increases the risk of HIV-1 acquisition," The Journal of Infectious Diseases, vol. 195, pp. 698—702, 2007.

[25] A. El-Shazly, H. El-Naggar, M. Soliman, M. El-Negeri, H. El-Nemr, A. Handousa, and T. Morsy, "A study on Trichomoniasis vaginalis and female infertility," Journal of the Egyptian Society of Parasitology, vol. 31, pp. 545—553, 2001.

[26] I. El-Sharkawy, S. Hamza, and M. El-Sayed, "Correlation between trichomoniasis vaginalis and female infertility," Journal of the Egyptian Society of Parasitology, vol. 30, pp. 287—294, 2000.

[27] F. Gimenes, R. P. Souza, J. C. Bento, J. J. Teixeira, S. S. Maria-Engler, M. G. Bonini, and M. E. Consolaro, "Male infertility: a public health issue caused by sexually transmitted pathogens," Nature Reviews Urology, vol. 11, pp. 672, 2014.

[28] M. M. Hobbs, and A. C. Seña, "Modern diagnosis of Trichomonas vaginalis infection," Sexually Transmitted Infections, vol. 89, pp. 434—438, 2013.

[29] C. B. Hicks, and M. Clement, "Syphilis: Screening and diagnostic testing," UpToDate, 2019.

[30] V. Kumar, A. Abbas, and J. Aster, "Infectious diseases," in Robbins & Cotran Pathologic Basis of Disease, pp. 370, 2014.

[31] P. Mallika, T. Asok, H. Faisal, S. Aziz, A. Tan, and G. Intan, "Neonatal conjunctivitis—a review," Malaysian Family Physician: the Official Journal of the Academy of Family Physicians of Malaysia, vol. 3, pp. 77, 2008.

[32] K. Workowski, "Chlamydia and gonorrhea," Annals of Internal Medicine, vol. 158, pp. ITC2—1, 2013.

[33] J. Stephenson, "Rise in Drug-Resistant Gonorrhea Cases," JAMA, vol. 291, pp. 2420—2420, 2004.

[34] J. Melendez, J. Hardick, M. Barnes, K. Page, and C. Gaydos, "Antimicrobial susceptibility of Neisseria gonorrhoeae isolates in Baltimore, Maryland, 2016: the importance of sentinel surveillance in the era of multi-drug-resistant gonorrhea," Antibiotics, vol. 7, pp. 77, 2018.

[35] M. Bodie, M. Gale-Rowe, S. Alexandre, U. Auguste, K. Tomas, and I. Martin, "Preventing the spread of extensively drug-resistant gonorrhea," Canada Communicable Disease Report, vol. 45, 2019.

[36] H. Swygard, A. C. Seña, and M. S. Cohen, "Patient education: Gonorrhea (Beyond the Basics)," UpToDate, 2018.

[37] Centers for Disease Control and Prevention, "Antibiotic Resistance Threats in the United States," pp. 65—108, 2019.

[38] C. Ison, J. Hussey, K. Sankar, J. Evans, and S. Alexander, "Gonorrhoea treatment failures to cefixime and azithromycin in England, 2010," Eurosurveillance, vol. 16, pp. 19833, 2011.

[39] D. W. Eyre, N. D. Sanderson, E. Lord, N. Regisford-Reimmer, K. Chau, L. Barker, M. Morgan, R. Newnham, D. Golparian, and M. Unemo, "Gonorrhoea treatment failure caused by a Neisseria gonorrhoeae strain with combined ceftriaxone and high-level azithromycin resistance, England, February 2018," Eurosurveillance, vol. 23, 2018.

[40] M. Bodie, M. Gale-Rowe, S. Alexandre, U. Auguste, K. Tomas, and I. Martin, "Multidrug resistant gonorrhea: Addressing the rising rates of gonorrhea and drug-resistant gonorrhea: There is no time like the present," Canada Communicable Disease Report, vol. 45, pp. 54, 2019.

[41] K. Town, C. Obi, N. Quaye, S. Chisholm, and G. Hughes, "Drifting towards ceftriaxone treatment failure in gonorrhoea: risk factor analysis of data from the Gonococcal Resistance to Antimicrobials Surveillance Programme in England and Wales," Sexually Transmitted Infections, vol. 93, pp. 39—45, 2017.

[42] C. M. Liu, B. A. Hungate, A. A. Tobian, J. Ravel, J. L. Prodger, D. Serwadda, G. Kigozi, R. M. Galiwango, F. Nalugoda, and P. Keim, "Penile microbiota and female partner bacterial vaginosis in Rakai, Uganda," MBio, vol. 6, pp. e00589—15, 2015.

[43] L. E. Manhart, C. M. Khosropour, C. Liu, C. W. Gillespie, K. Depner, T. Fiedler, J. M. Marrazzo, and D. N. Fredricks, "Bacterial vaginosis—associated bacteria in men: Association of leptotrichia/sneathia spp. with nongonococcal urethritis," Sexually Transmitted Diseases, vol. 40, pp. 944, 2013.

[44] S. Ralph, A. Rutherford, and J. Wilson, "Influence of bacterial vaginosis on conception and miscarriage in the first trimester: cohort study," BMJ, vol. 319, pp. 220—223, 1999.

[45] H. Leitich, and H. Kiss, "Asymptomatic bacterial vaginosis and intermediate flora as risk factors for adverse pregnancy outcome," Best Practice & Research: Clinical Obstetrics & Gynaecology, vol. 21, pp. 375—390, 2007.

[46] B. Guerra, T. Ghi, S. Quarta, A. M. Morselli-Labate, T. Lazzarotto, G. Pilu, and N. Rizzo, "Pregnancy outcome after early detection of bacterial vaginosis," European Journal of Obstetrics & Gynecology and Reproductive Biology, vol. 128, pp. 40—45, 2006.

[47] J. J. Wu, D. B. Huang, K. R. Pang, and S. K. Tyring, "Selected sexually transmitted diseases and their relationship to HIV," Clinics in Dermatology, vol. 22, pp. 499—508, 2004.

[48] E. Teo, and A. S. Lok, "Hepatitis B virus immunization in adults," UpToDate, 2019.

[49] G. Fattovich, F. Bortolotti, and F. Donato, "Natural history of chronic hepatitis B: special emphasis on disease progression and prognostic factors," Journal of Hepatology, vol. 48, pp. 335—352, 2008.

[50] O. Nguyen, V. Sheppeard, M. W. Douglas, E. Tu, and W. Rawlinson, "Acute hepatitis C infection with evidence of heterosexual transmission," Journal of Clinical Virology, vol. 49, pp. 65—68, 2010.

[51] A. Birkmann, and H. Zimmermann, "HSV antivirals—current and future treatment options," Current Opinion in Virology, vol. 18, pp. 9—13, 2016.

[52] R. Gupta, T. Warren, and A. Wald, "Genital herpes," The Lancet, vol. 370, pp. 2127—2137, 2007.

[53] J. D. Stanaway, A. Wald, E. T. Martin, S. L. Gottlieb, and A. S. Magaret, "Case-crossover analysis of condom use and HSV-2 acquisition," Sexually Transmitted Diseases, vol. 39, pp. 388, 2012.

[54] C. Celum, R. A. Morrow, D. Donnell, T. Hong, C. W. Hendrix, K. K. Thomas, K. H. Fife, E. Nakku-Joloba, A. Mujugira, and J. M. Baeten, "Daily oral tenofovir and emtricitabine-tenofovir preexposure prophylaxis reduces herpes simplex virus type 2 acquisition among heterosexual HIV-1-uninfected men and women: a subgroup analysis of a randomized trial," Annals Internal Medicine, vol. 161, pp. 11—19, 2014.

[55] L. Corey, A. Wald, R. Patel, S. L. Sacks, S. K. Tyring, T. Warren, J. M. Douglas Jr, J. Paavonen, R. A. Morrow, and K. R. Beutner, "Once-daily valacyclovir to reduce the risk of transmission of genital herpes," New England Journal of Medicine, vol. 350, pp. 11—20, 2004.

[56] P. Street, "Genital Herpes in Pregnancy (GL849)," National Health Service — Royal Berkshire, 2015.

[57] Z. A. Brown, A. Wald, R. A. Morrow, S. Selke, J. Zeh, and L. Corey, "Effect of serologic status and cesarean delivery on transmission rates of herpes simplex virus from mother to infant," JAMA, vol. 289, pp. 203—209, 2003.

[58] A. M. Casto, P. Roychoudhury, H. Xie, S. Selke, G. A. Perchetti, H. Wofford, M. Huang, G. M. Verjans, G. S. Gottlieb, A. Wald, K. R. Jerome, D. M. Koelle, C. Johnston, and A. L. Greninger, "Large, stable, contemporary interspecies recombination events in circulating human herpes simplex viruses," The Journal of Infectious Diseases, pp. jiz199, 2019.

[59] N. W. Anderson, W. Sistrunk, and M. J. Binnicker, "Simultaneous detection of herpes simplex virus 1 and 2 in the cerebrospinal fluid of a patient with seizures and encephalitis," Journal of Clinical Microbiology, vol. 53, pp. 343—345, 2015.

[60] B. Sturn, and K. Schneweis, "Protective effect of an oral infection with herpes simplex virus type 1 against subsequent genital infection with herpes simplex virus type 2," Medical Microbiology and Immunology, vol. 165, pp. 119—127, 1978.

[61] C. Johnston, and A. Wald, "Epidemiology, clinical manifestations, and diagnosis of herpes simplex virus type 1 infection," UpToDate, 2019.

[62] J. M. Drugge, and P. J. Allen, "A nurse practitioner's guide to the management of herpes simplex virus-1 in children," Dermatology Nursing, vol. 20, pp. 455, 2008.

[63] B. Selling, and S. Kibrick, "An outbreak of herpes simplex among wrestlers (herpes gladiatorum)," New England Journal of Medicine, vol. 270, pp. 979—982, 1964.

[64] T. M. Becker, R. Kodsi, P. Bailey, F. Lee, R. Levandowski, and A. J. Nahmias, "Grappling with herpes: herpes gladiatorum," The American Journal of Sports Medicine, vol. 16, pp. 665—669, 1988.

[65] E. Y. Wei, and D. T. Coghlin, "Beyond folliculitis: recognizing herpes Gladiatorum in adolescent athletes," The Journal of Pediatrics, vol. 190, pp. 283, 2017.

[66] B. Anderson, D. P. McGuire, M. Reed, M. Foster, and D. Ortiz, "Prophylactic valacyclovir to prevent outbreaks of primary herpes gladiatorum at a 28-day wrestling camp: a 10-year review," Clinical Journal of Sport Medicine, vol. 26, pp. 272—278, 2016.

[67] S. Kaye, and A. Choudhary, "Herpes simplex keratitis," Progress in Retinal and Eye Research, vol. 25, pp. 355—380, 2006.

[68] A. Rowe, A. S. Leger, S. Jeon, D. Dhaliwal, J. Knickelbein, and R. Hendricks, "Herpes keratitis," Progress in Retinal and Eye Research, vol. 32, pp. 88—101, 2013.

[69] J. J. Mucci, V. M. Utz, A. Galor, W. Feuer, and B. H. Jeng, "Recurrence rates of herpes simplex virus keratitis in contact lens and non-contact lens wearers," Eye & Contact Lens, vol. 35, pp. 185—187, 2009.

[70] N. H. Rowe, C. S. Heine, and C. J. Kowalski, "Herpetic whitlow: an occupational disease of practicing dentists," Journal of the American Dental Association, vol. 105, pp. 471—473, 1982.

[71] M. Lewis, "Herpes simplex virus: an occupational hazard in dentistry," International Dental Journal, vol. 54, pp. 103—111, 2004.

[72] K. E. Mönkemüller, and C. M. Wilcox, "Diagnosis and treatment of esophagitis in AIDS," Comprehensive Therapy, vol. 26, pp. 163—168, 2000.

[73] A. K. Chaturvedi, B. I. Graubard, T. Broutian, W. Xiao, R. K. Pickard, L. Kahle, and M. L. Gillison, "Prevalence of oral HPV infection in unvaccinated men and women in the United States, 2009-2016," JAMA, vol. 322, pp. 977—979, 2019.

[74] B. Hernandez, L. Wilkens, X. Zhu, K. McDuffie, P. Thompson, Y. Shvetsov, L. Ning, and M. Goodman, "Circumcision and human papillomavirus infection in men: a site-specific comparison," The Journal of Infectious Diseases, vol. 197, pp. 787—794, 2008.

[75] M. L. Shew, B. Weaver, W. Tu, Y. Tong, J. D. Fortenberry, and D. R. Brown, "High frequency of human papillomavirus detection in the vagina before first vaginal intercourse among females enrolled in a longitudinal cohort study," The Journal of Infectious Diseases, vol. 207, pp. 1012—1015, 2012.

[76] P. L. Anderson, J. J. Kiser, E. M. Gardner, J. E. Rower, A. Meditz, and R. M. Grant, "Pharmacological considerations for tenofovir and emtricitabine to prevent HIV infection," Journal of Antimicrobial Chemotherapy, vol. 66, pp. 240—250, 2010.

[77] B. Varghese, J. E. Maher, T. A. Peterman, B. M. Branson, and R. W. Steketee, "Reducing the risk of sexual HIV transmission: quantifying the per-act risk for HIV on the basis of choice of partner, sex act, and condom use," Sexually Transmitted Diseases, vol. 29, pp. 38—43, 2002.

[78] J. Castilla, J. Del Romero, V. Hernando, B. Marincovich, S. García, and C. Rodríguez, "Effectiveness of highly active antiretroviral therapy in reducing heterosexual transmission of HIV," Journal of Acquired Immune Deficiency Syndromes, vol. 40, pp. 96—101, 2005.

[79] S. C. Weller, and K. Davis-Beaty, "Condom effectiveness in heterosexual HIV transmission," Cochrane Database of Systematic Reviews, 2002.

[80] J. D. Stekler, L. R. Violette, L. Niemann, V. M. McMahan, D. A. Katz, J. M. Baeten, R. M. Grant, and K. P. Delaney, "Repeated false-positive HIV test results in a patient taking HIV pre-exposure prophylaxis," Open Forum Infectious Diseases, vol. 5, pp. ofy197, 2018.

[81] G. Karp, F. Schlaeffer, A. Jotkowitz, and K. Riesenberg, "Syphilis and HIV co-infection," European Journal of Internal Medicine, vol. 20, pp. 9—13, 2009.

[82] J. Atashili, C. Poole, P. M. Ndumbe, A. A. Adimora, and J. S. Smith, "Bacterial vaginosis and HIV acquisition: a meta-analysis of published studies," AIDS (London, England), vol. 22, pp. 1493, 2008.

[83] L. Myer, L. Denny, R. Telerant, M. de Souza, T. C. Wright Jr, and L. Kuhn, "Bacterial vaginosis and susceptibility to HIV infection in South African women: a nested case-control study," The Journal of Infectious Diseases, vol. 192, pp. 1372—1380, 2005.

[84] T. Schacker, "The role of HSV in the transmission and progression of HIV," Herpes: the Journal of the IHMF, vol. 8, pp. 46—49, 2001.

[85] R. A. Hester, and S. B. Kennedy, "Candida infection as a risk factor for HIV transmission," Journal of Women's Health, vol. 12, pp. 487—494, 2003.

[86] D. Lewis, "Chancroid: clinical manifestations, diagnosis, and management," Sexually Transmitted Infections, vol. 79, pp. 68—71, 2003.

[87] J. V. Bailey, C. Farquhar, C. Owen, and P. Mangtani, "Sexually transmitted infections in women who have sex with women," Sexually Transmitted Infections, vol. 80, pp. 244—246, 2004.

[88] K. Fethers, C. Marks, A. Mindel, and C. S. Estcourt, "Sexually transmitted infections and risk behaviours in women who have sex with women," Sexually Transmitted Infections, vol. 76, pp. 345—349, 2000.

[89] S. Molin, B. F. De Blasio, and A. O. Olsen, "Is the risk for sexually transmissible infections (STI) lower among women with exclusively female sexual partners compared with women with male partners? A retrospective study based on attendees at a Norwegian STI clinic from 2004 to 2014," Sexual Health, vol. 13, pp. 257—264, 2016.

[90] R. C. Noble, "There is no safe sex," Newsweek, 1991.

[91] H. Waxman, "The content of federally funded abstinence-only education programs," Washington, DC: US House of Representatives Committee On Government Reform-Minority Staff Special Investigations Division , 2004.

[92] A. J. Lin, and J. S. Santelli, "The accuracy of condom information in three selected abstinence-only education curricula," Sexuality Research & Social Policy, vol. 5, pp. 56, 2008.

[93] C. Dailard, "Understanding abstinence: implications for individuals, programs and policies," Guttmacher Report On Public Policy, vol. 6, pp. 4—6, 2003.

[94] P. K. Kohler, L. E. Manhart, and W. E. Lafferty, "Abstinence-only and comprehensive sex education and the initiation of sexual activity and teen pregnancy," Journal of Adolescent Health, vol. 42, pp. 344—351, 2008.

[95] D. B. Kirby, "The impact of abstinence and comprehensive sex and STD/HIV education programs on adolescent sexual behavior," Sexuality Research & Social Policy, vol. 5, pp. 18, 2008.

[96] H. Brückner, and P. Bearman, "After the promise: the STD consequences of adolescent virginity pledges," Journal of Adolescent Health, vol. 36, pp. 271—278, 2005.

[97] C. S. Haignere, R. Gold, and H. J. McDanel, "Adolescent abstinence and condom use: Are we sure we are really teaching what is safe?" Health Education & Behavior, vol. 26, pp. 43—54, 1999.

[98] L. M. Kantor, J. S. Santelli, J. Teitler, and R. Balmer, "Abstinence-only policies and programs: An overview," Sexuality Research & Social Policy, vol. 5, pp. 6, 2008.

Follow @domesticengine7

© MC Byington