STD Statistics

Meta note: this is a long report on STD epidemiology and risks, made possible by generous crowdfunders. I’m going to post these kinds of research projects on my blog from now on.  I am not a doctor; I’ve just found that it’s hard to find comprehensive syntheses of the medical literature that answer the questions people actually want to know.  Please don’t hesitate to correct me if you find any errors or omissions!


Incidence Age Race Gender
Chlamydia 446.6 cases per 100,000 Peaks at age 15-19, at 1852.1 cases per 100,000 rate among blacks 6.4x rate among whites; rate among Hispanics 2.1x rate among whites; rate among Asians 0.61x rate among whites more commonly reported in women (2:1 ratio) because women are more likely to have symptoms
HPV genital warts: 194.5 per 100,000
genital seroprevalence: 20-30%
Genital warts:

peaks at 20-24 for women: 300-900 cases per 100,000
peaks at 25-29 for men: 250-750 cases per 100,000

no difference between races genital warts 4x as common in men as women
Trichomoniasis 143 cases per 100,000 (in women)

prevalence: 3.1% (in women)

increases with age in black women; otherwise uncorrelated prevalence among blacks 10x rate among whites; prevalence among Hispanics and whites equal not studied in men
Gonorrhea 106.1 cases per 100,000 Peaks at age 20-24, at 541.6 cases per 100,000 in women, 459.4 cases per 100,000 in men rate among blacks 12.4x rate among whites; rate among Hispanics 1.9x rate among whites; rate among Asians 0.5x rate among whites Equal between genders
Herpes/ HSV genital herpes: 96 cases per 100,000
seroprevalence: 16.2% HSV2
Increases with age rate among blacks 3.7x rate among whites; equal among whites and Hispanics 2x as common in women as men
HIV 15 cases per 100,000 peaks at ages 20-24 rate among blacks 7.9x rate among whites; rate among Hispanics 3x rate among whites rate among men 4.2x rate among women; 78% of cases are from MSM
Syphilis 5.5 cases per 100,000 Peaks age 20-24, at 16.1 cases per 100,000 rate among blacks 5.3x rate among whites; rate among Hispanics 2.0x rate among whites; rate among Asians 0.85x rate among whites 11.4x as common in men as women; 60% of cases are from MSM
Hepatitis B 0.9 cases per 100,000 Peaks at age 30-39, at 2 cases per 100,000 no difference between races rate for males 1.7x rate for females
Per-Partner Transmission Rate Condom Effectiveness Treatability Dangerous sequelae
Chlamydia 40% male-to-female, 32% female-to-male high (reduces risk by 60%)


high (antibiotics) pelvic inflammatory disease (if untreated)
HPV 20% high (reduces risk by 58%) not treatable; preventable with vaccine cervical, oropharyngeal,  anal, and genital cancer
Trichomoniasis 60-100% male-to-female, 40-80% female-to-male low? (one study found no effect of condom use on prevalence)[87] high (antibiotics) low birth weight infants
Gonorrhea 22% very high (reduces risk by 90%)


high (antibiotics) pelvic inflammatory disease (if untreated)
Herpes 19% moderate (reduces risk by 30%)[76] genital warts are treatable symptomatically meningitis, encephalitis, Bell’s palsy
HIV 40.4%, receptive anal sex;

21.7%, insertive anal sex

28.9%, heterosexual couples

high (reduces risk by 80%)[88] moderate (anti-retroviral drugs) AIDS
Syphilis 60% high (reduces risk by 60-70%) high (antibiotics) neurosyphilis, cardiac problems
Hepatitis B 25%-59% high (reduces risk by 75%) moderate (chronic hepatitis can cause irreversible liver damage, but the vaccine is effective at preventing HBV) cirrhosis, hepatocellular carcinoma


Per-partner transmission rate means “given that you have sex with an infected partner, what is the chance that you’ll get infected?”  By default, these refer to unprotected sex. Many of the studies observe long-term partnerships (e.g. studies of married couples) and the risk of being infected after a long period of time (six months, a year, etc.) Since the time limit varies between studies, these numbers are not strictly comparable.  Clearly, the larger the total number of sex acts, the greater the risk of transmission.



Symptom Prevalence in chlamydia patients
Common Inflammation of cervix and/or urethra: causes pain while urinating and during sex, abnormal discharge, genital swelling, fever 50% in women, 2% in men
Moderate Pelvic inflammatory disease (increases risk of infertility and cancer) Roughly 1% in women. Less likely if chlamydia is treated.
Rare Reactive arthritis (causes painful inflammation of the eyes, joints, and genitals). Roughly 0.1%.

Chlamydia causes inflammation of the cervix and/or urethra; one study found that 71% of female patients with chlamydia had cervicitis or urethritis.[18]

In women, chlamydial infection of the cervix is asymptomatic 50-70% of the time; if left untreated it leads to pelvic inflammatory disease in about half of cases.

In men, chlamydia causes inflammation of the urethra about half the time, which sometimes results in symptoms such as burning while urinating, discharge from the penis, testicular pain or swelling, or fever. However, only 2-4% of men infected with chlamydia develop symptoms. [20]

Anal infections cause pain or discharge.

Chlamydia is the primary cause of pelvic inflammatory disease, which can cause infertility in women in 37% of cases in developed countries.  Across 16 studies, an average of 37% of patients diagnosed with pelvic inflammatory disease had chlamydia.  Since asymptomatic chlamydia is often not treated, testing for chlamydia is an effective way to reduce the risk of pelvic inflammatory disease.[21]  Roughly 0.14% of women of reproductive age have been treated for pelvic inflammatory disease.[22]  This yields a (very) roughly 1% chance of getting pelvic inflammatory disease given that one has chlamydia.

Chlamydia can cause reactive arthritis, an autoimmune disease which involves inflammation of the joints, eyes, and genitals.  Reactive arthritis usually develops two to three weeks after an infection. Chlamydia-induced reactive arthritis has an incidence of about 4.6 per 100,000.[23]

Incidence and Risks

Overall Prevalence 3-5%
Male-to-female per-partner transmission rate 40%
Female-to-male per-partner transmission rate 32%
Per-encounter transmission rate, across sexes 5.85%-0.16% (depending on age)
Per-encounter transmission rate with condom, across sexes 0.053%


Chlamydia has a 3-5% population prevalence in both men and women.

It has a single exposure male-to-female transmission rate of 40%, and a single exposure female-to-male transmission rate of 32%.[1]  This refers to the risk that you will get chlamydia given that you have an (unprotected) sex partner who has chlamydia. 

In general, single-exposure transmission rates are higher than “per-encounter” or “per-coital-act” transmission rates, because people tend to have more than one sexual encounter with a given partner. 

Per-encounter transmission risk declines with age, from 5.85% at age 15 to 0.16% at age 25. One of the most robust epidemiological findings about chlamydia is that it’s more common among younger people.[2]

Estimated per-encounter male-to-female transmission risk for unprotected intercourse was determined to be 0.9%; with a condom it’s 0.053%.[3]

Chlamydia can be transmitted by vaginal, oral, and anal sex.  It can also be passed from a mother to a baby in childbirth.

 In a study of men who have sex with men seen at a gay men’s community health center, the prevalence rates of rectal, urethral, and pharyngeal chlamydia were 7.9%, 5.2%, and 1.4% respectively.[4]  Men who have sex with men have higher rates of chlamydia in general than the overall population, at 12.0%.[28]


Chlamydia is detected by nuclear acid amplification of samples from the cervix, urethra, vaginal swabs, or urine.

A meta-analysis found that pooled sensitivities for LCR (ligase chain reaction), PCR (polymerase chain reaction), gene probe and EIA (enzyme immunoassay) on urine were 96.5%, 85.6%, 92% and 38%, respectively, while on cervical swabs the corresponding sensitivities of PCR, gene probe and EIA were 88.6%, 84% and 65%. Specificities are high, often 100%.[19]


Chlamydia is treated with a week-long course of antibiotics, most often azithromycin and doxycycline.  This has a cure rate of 98%.[17]



Symptom Prevalence in HPV patients*
Common anal intraepithelial neoplasia (MSM)

Genital warts (men)

Cervical intraepithelial neoplasia

Oropharyngeal cancer (women)

Moderate Oropharyngeal cancer (men)

Cervical cancer



Rare Genital warts (women)

Anal cancer (MSM)

Vaginal cancer



*These are back-of-the-envelope calculations, and use the location of HPV most relevant to the disease. For example, for oropharyngeal cancer we take the lifetime risk of oropharyngeal cancer, multiply by the percentage of cases due to HPV, and divide by the prevalence of oral HPV.

There are over 170 types of human papilloma virus, most of which cause no physical symptoms. A subset of HPV types cause papillomas (warts) on the vulva, penis, anus, cervix, or pharynx. Others cause hand or foot warts, and are not sexually transmitted. The “high-risk” HPV types (16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68, 73, and 82) cause nearly all cases of cervical cancer.

 There are about 13,000 cervical cancer cases a year; the incidence of HPV-associated cervical cancer is about 7-10 cases per 100,000 women.[12]  Cervical intraepithelial neoplasia, a precursor to cancer, has a prevalence rate of 4-5% among women receiving cervical cancer screening.[32]  The lifetime risk of developing cervical cancer is 0.65%.[33]

HPV can cause oral and pharyngeal cancer. The incidence of HPV-associated oropharyngeal cancer is about 6.4 per 100,000 in men and 1.4 per 100,000 in women.[34]  HPV causes about 60% of cases of oropharyngeal cancer.[35]  The overall lifetime risk of oropharyngeal cancer is 1.55% for men and 0.67% for women.[33]

HPV can cause anal cancer. The prevalence of anal intraepithelial neoplasia, a precursor to cancer, is 35% among non-HIV-infected men who have sex with men.[14]  The lifetime risk of anal cancer is about 0.2%.[36]  HPV is thought to be associated with 90% of anal cancers.[37]

HPV can cause vaginal cancer. It is thought to be associated with 70% of vaginal cancers.[37]  Vaginal cancer is rare; the lifetime risk is 1/1100.[38]

 Low-risk HPV types, i.e. HPV types 6 and 11, cause genital warts. The overall prevalence of genital warts ranges from 0.13% to 0.56%.[13]  Prevalence ranges from 0.13% to 0.16% in women, and 4.1% among heterosexual, sexually active men.[31]

Incidence and Risks

Vaginal HPV prevalence (women) 26.8%
Genital HPV prevalence (men) >20%?
Oral HPV prevalence (men) 10.1%
Oral HPV prevalence (women) 3.6%
Anal HPV prevalence (MSM) 50%
Per-partner transmission rate 20%
Per-encounter transmission rate 0.2%

The overall prevalence of vaginal HPV in women is 26.8%.[39]

A systematic review of studies of men found prevalences of HPV ranging from 1.3% to 72.9%; a majority found rates of over 20%. [40]

10.1% of men and 3.6% of women have oral HPV infections.[10]

50% of men who have sex with men have anal HPV.[11]

Transmission rates from men to women and women to men are about equal and about 20% per person during a 6-month relationship period.[8] At an average of 4 sexual encounters a week, the per-sex-act transmission rate was roughly 0.2%.

Condom use protects against HPV transmission.  College freshmen women who used condoms consistently had a 37.8% per patient-year incidence of genital HPV, compared to an incidence of 89.3% among those who did not.[15]


HPV testing is not approved for men, but some healthcare providers may offer anal Pap smears for high-risk men, such as men who have HIV or receive anal sex.

Women are recommended to get a cervical HPV test at the same time they get a Pap smear, every three years.[41]  The HPV test is a DNA amplification test taken from a cervical swab.

 Oral HPV testing is commercially available, but the value of the test for predicting oral cancer has not yet been established.  Most people who test positive for salivary HPV will not get oral cancer.


Genital warts can be treated with podofilox (an anti-mitotic drug that destroys warts), imiquimod (an immune enhancer), cryotherapy, surgery, or caustic agents.

Cervical cancer is treated with surgery, radiation, and/or chemotherapy.

Asymptomatic HPV is not treated.

The cervical cancer vaccine Gardasil, when administered to young women, has a 94-100% efficacy rate in preventing persistent HPV infections.[16]  (“Young”, because it is most likely to be effective before the onset of sexual activity and thus before exposure to HPV.)  While Gardasil is not as actively promoted for young men, it is also available to men and similarly effective at preventing HPV in men.



Symptom Prevalence in Trichomoniasis Patients
Common Vaginal discharge





Low birth weight infant

42% (women)

50% (women)

22-37% (women)

50% (men)

42% (men)

11% (assuming infected while pregnant)

Trichomoniasis is caused by the protozoan Trichomonas vaginalis and is a common cause of vaginitis.  Symptoms include pain, burning, or itching in the urethra, penis, or vagina.  For women there can be an itchy, yellow-green, frothy, foul-smelling vaginal discharge.  However, nearly half of all women[64] and men[65]  are asymptomatic.

 Trichomoniasis (and other bacterial vaginosis) during pregnancy is associated with preterm delivery of a low-birth-weight infant, with an odds ratio of 1.4, according to a cohort study of 13,914 women.[69]  8% of infants are born with low birth weight,[70] so the probability given the mother has trichomoniasis is 11%.

Trichonomiasis also increases the risk of HIV infection by a factor of 1.52[71].

Incidence and Risks

Prevalence 3.1%
Male-to-female per-partner transmission rate 66-100%
Female-to-male per-partner transmission rate 40-80%


The prevalence of trichomoniasis infection is estimated to be 3.1% among women ages 14-49.[66]  2.8% of 454 men attending an STD clinic tested positive for trichonomas vaginalis.[67]

66-100% of the female partners of infected men had trichomoniasis; 40-80% of the male partners of infected women had trichomoniasis.[72]


Trichomoniasis is usually diagnosed with microscopic examination of a sample of vaginal fluid.  This has only a 60-70% sensitivity, and so often results in false negatives.[73]


Trichomoniasis is treated with metronidazole, an antibiotic typically used for protozoa.  For 95-97% of cases, a single dose resolves the infection.[68]


Symptom Prevalence in Chlamydia patients
Common Pain during urination or sex, genital discharge, (in women) abdominal pain roughly 50%
Moderate Sore throat
Pelvic inflammatory disease (increases risk of infertility and cancer in women)
Sore throat: 10%

PID: roughly 9%

Rare Gonococcal arthritis (causes joint pain, rash, and fevers) 0.5-3%


About half of women have no symptoms; the other half have vaginal discharge, lower abdominal pain, or pain during intercourse. Most men with gonorrhea have infection of the urethra, which causes burning during urination and/or discharge.

Gonorrhea in the throat causes a sore throat about 10% of the time.

Gonorrhea, if left untreated, can cause pelvic inflammatory disease in women. The risk of developing pelvic inflammatory disease from gonorrhea is somewhat unclear.  A meta-analysis found that gonococcal cases of PID outnumbered non-gonococcal PID in three-fourths of the studies, but the gonococcal-to-non-gonococcal ratio varied from 1:1.5 to 8:1.  (In other words: the distribution of STDs depends dramatically on the location of the clinic doing the epidemiological study.)  In the Women’s Health Study, women with a history of gonorrhea had an 80% increase in the risk of pelvic inflammatory disease relative to women without such a history.[24]  (Overall population prevalence of PID in US women 18-44 is roughly 5%.)

Untreated gonorrhea can spread to the joints, causing gonococcal arthritis.  This occurs in roughly 0.3-5% of cases of gonorrheal infection.  It causes joint pain, skin lesions, and fever and chills. Standard treatment is intravenous or intramuscular ceftriaxone (an antibiotic).[25]

Incidence and Risks

Overall prevalence 0.5% (among 15-25-year-olds), 0.1% (in general US population.)
Female-to-male per-partner transmission risk 22%


Prevalence is about 0.5% among 15-25-year-olds (the highest-risk population), in both men and women.  The overall US prevalence is 0.1%.[27]

Female-to-male transmission (in a 1978 study of sailors on shore leave in East Asia) was 19% for white men and 53% for black men.[5]  Another study of transmission rates among sailors found that the female-to-male transmission rate was 22%.[26]

Condoms prevent gonorrhea. Consistent condom users have lower rates of chlamydia and gonorrhea than nonusers.[6][7]

Gonorrhea can be transmitted by oral, anal, or vaginal intercourse. In a study of men who have sex with men, seen at a gay men’s community health center, prevalence rates were 6.9%, 6.0%, and 9.2% for anal, urethral, and pharyngeal chlamydia respectively.[4]  Men who have sex with men have higher than average rates of gonorrhea in general: 16.4%.[28]


Gonorrhea is treatable with antibiotics.  Standard treatment is intramuscular ceftriaxone and oral azithromycin.  This has a 99% cure rate.[29]



Symptom Prevalence in HSV patients
Common Fever, headache, malaise

Local pain and itching

Pain urinating

Tender lymph nodes

Aseptic meningitis





36% women, 13% men (HSV-2)

Moderate Bell’s palsy roughly 2% (HSV-1)
Rare Encephalitis roughly 0.001%

Herpes simplex virus 1 and 2 (HSV1 and HSV2) cause cold sores and genital herpes, respectively.  They cause watery blisters in the skin and mucous membranes of the mouth, lips, or genitals.  The virus is normally dormant and lives in the cell bodies of sensory nerves throughout a person’s lifetime. When the herpes virus reactivates (note that outbreaks may be asymptomatic), it is shed from skin and becomes contagious.

The first episode often presents with systemic symptoms (fever, malaise, swollen lymph nodes) as well as outbreaks of painful vesicular lesions.  Usually HSV-1 causes mouth lesions and HSV-2 causes genital lesions, but HSV-1 can also cause genital lesions.

One prospective study of 3438 initially HSV-negative women followed for 20 months found that most infections (74% of HSV-1 and 63% of HSV-2) were asymptomatic, that more cases of symptomatic genital herpes were caused HSV-1 than by HSV-2, and that there were no clinical differences between HSV-1-caused and HSV-2-caused genital herpes.[42]

HSV can have complications. Symptoms of aseptic meningitis (stiff neck, headache, and photophobia) were found in 36% of women and 13% of men with primary genital HSV-2 infections.[43]

HSV-1 infection is considered the likely cause of Bell’s palsy, a sudden onset facial paralysis.  HSV-1 DNA was found in 11 of 14 patients with Bell’s palsy.[45]  Lifetime risk of Bell’s palsy is about 1.5%.[46]

HSV-1 encephalitis (an infection of the membrane around the brain, causing fever, headache, seizures, and frequently death) is responsible for about 10-20% of the 20,000 yearly US cases of fatal sporadic encephalitis.[44]

There is early-stage research suggesting that HSV1 is implicated in the pathogenesis of neurological diseases such as Alzheimer’s, multiple sclerosis, and intractable focal epilepsy. The APOE4 allele is a stronger risk factor for Alzheimer’s among patients harboring HSV1 in their brains.  (Patients with HSV1 are not more likely to have Alzheimer’s across the board than patients without it.)[47]

Incidence and Risks

HSV-1 Seroprevalence 65%
HSV-2 Seroprevalence, Women 26%
HSV-2 Seroprevalence, Men 18%
Per-Partner HSV-2 Transmission Rate 19%
Per-Encounter HSV-2 Transmission Rate, Women 0.06%-0.089%
Per-Encounter HSV-2 Transmission Rate, Men 0.015%-0.053%
Per-Encounter HSV-1 Transmission Rate, Women 0.014%
Per-Encounter HSV-1 Transmission Rate, Heterosexual Men 0.024%
Per-Encounter HSV-1 Transmission Rate, MSM 0.085

Seroprevalence refers to the presence of antibodies to the virus (which may be asymptomatic.)

16.2% of Americans age 14-49 are infected with HSV2. Seroprevalence increases with age, from 2.9%/0.8% for 14-19-year-old females and males respectively, to 32.3%/19.3% for 40-49-year old females and males respectively. [49]  Seroprevalence rises with number of sex partners, from 3.9% among people with one lifetime sex partner, to 26.7% among people with >10 lifetime sex partners.[49]

The current prevalence of genital herpes caused by HSV-2 in the U.S. is roughly one in four or five adults, with approximately 50 million people infected with genital herpes and an estimated 0.5 million new genital herpes infections occurring each year.[48]

65% of Americans are seropositive for HSV-1; it is commonly acquired in childhood, from contact with family members.[50]

The per-sex-act risk of acquiring HSV-2 for heterosexual women was found to be 0.089%, and the per-sex-act risk for heterosexual men was found to be 0.015%, in a study of 528 monogamous heterosexual couples.[51]  Another study, of 1843 subjects found that the per-sex-act rate of acquiring HSV-2 was 0.06% for women and 0.053% for men.  The per-sex-act rate of acquiring HSV-1 was 0.014% for women, 0.024% for heterosexual men, and 0.085% for men who have sex with men.

In a prospective study of couples where one partner had HSV-2 and the other did not, 19% of the negative partners acquired HSV-2 by the end of the study. The overall risk of acquiring HSV-2 is 10% a year.[52]

Condom use reduces the risk of acquiring HSV-2 among female subjects. When condoms were used more than 25% of the time, women’s risk of acquiring HSV-2 fell over the duration of the study with a hazard ratio of 0.085.  Men’s risk was unaffected.[51]  Because genital herpes is transmitted via a sore, condoms are only protective if they cover the area where the sore is.


HSV-2 and HSV-1 serologic blood tests can detect the presence of an immune response to the herpes simplex virus.  The CDC recommends testing for people who have symptoms of genital herpes, but not as screening for the general population.[53]  These tests have sensitivities and specificities of 97-100%.[54]


Herpes simplex, both HSV-1 and HSV-2, is treated with antiviral drugs, including acyclovir, valacyclovir, famcyclovir, and pencyclovir. No treatment can eliminate herpes simplex virus from the body, but antivirals reduce the frequency of outbreaks and the probability of transmission.  In one double-blind study, during a 120-day treatment period, 94% of placebo patients had a recurrence of herpes, while only 35% of acyclovir-treated patients did.  Recurrences in acyclovir-treated patients were shorter in duration and associated with a lower frequency of viral shedding.[55]



Symptom Prevalence in HIV Patients
Common Acute infection (fever, swollen lymph nodes, rash, throat inflammation)

Eventual progression to AIDS

Chronic diarrhea

Pneumocystis pneumonia

HIV wasting syndrome

Kaposi’s sarcoma







10-20% [83]

Human immunodeficiency virus infection leads to low levels of T cells (specifically, CD4+ helper T-cells).  The initial symptom of HIV infection is an influenza-like illness with rash, followed by a prolonged period (3-20 years) without symptoms. After this, the weakened immune system becomes much more susceptible to opportunistic infections and tumors. The late stages of infection are known as AIDS, and are characterized by certain “AIDS-defining conditions” — infections such as Pneumocystis pneumonia, cancers such as Kaposi’s sarcoma, and severe weight loss.

 Tuberculosis and pneumonia are common causes of death in AIDS patients. Esophagitis is a common symptom, often caused by viruses (HSV or cytomegalovirus) or Candida fungus.  Toxoplasmosis, leukoencephalopathy, and AIDS dementia complex are common neurological complications of AIDS.[83]

There is a very wide variety of opportunistic infections and tumors which occur in AIDS patients, and which we do not list here.

The average life expectancy for an American 20-year-old on anti-retroviral therapy is 43 years — that is, half will die by the age of 63.  The average life expectancy for an untreated AIDS patient is 9-11 years.[82]

Incidence and risks

Prevalence 0.37%
Incidence 15 per 100,000
per-partner risk, receptive anal intercourse 40.4%
per-partner risk, insertive anal intercourse 21.7%
per-partner risk, heterosexual couples 28.9%
per-act risk, receptive anal intercourse 1.4%
per-act risk, insertive anal intercourse 0.11 circumcised, 0.62% uncircumcised
per-act risk, receptive vaginal intercourse 0.08%
per-act risk, insertive vaginal intercourse 0.04%
per-act risk, receptive fellatio 0.04%

In 2011, an estimated 1,201,100 people over the age of 13 were living with HIV.[84]  This is a prevalence of 0.37% in the US population.

In 2010, there were an estimated 47,500 new HIV infections; this is an incidence of 15 per 100,000.[85]

Unprotected receptive anal intercourse has a per-partner transmission risk of 40.4% and a per-act transmission risk of 1.4%, for both heterosexuals and homosexuals.  Per-partner transmission risk of unprotected insertive anal intercourse is 21.7%.[88]  The per-act transmission risk of unprotected insertive anal intercourse is 0.11% for circumcised men and 0.62% for uncircumcised men.[91]

The per-act transmission risk of unprotected receptive vaginal intercourse is 0.08%, and the per-act transmission risk of unprotected insertive vaginal intercourse is 0.04%. [90]

In a study of heterosexual couples with one HIV-positive and one HIV-negative partner, 28.9% of the uninfected partners acquired HIV within 40 months.[92]

The per-act risk of receptive fellatio is 0-0.04%.[93]

According to a Cochrane review of 14 studies, consistent condom users have an 80% reduced incidence of HIV than non-users.[89]


HIV is diagnosed with antibody tests of blood serum, which are extremely accurate, with a sensitivity of 99.7% and specificity of 98.5%.[94]  AIDS is diagnosed by low T-cell count or an “AIDS-defining clinical condition”, one out of a list of opportunistic infections and tumors which usually occur only in immunocompromised people.


Anti-retroviral drugs are the standard treatment for AIDS.

They also serve as pre-exposure prophylaxis for HIV (they make an infected person less infectious, by a factor of 10-20 [97]) and post-exposure prophylaxis (immediately administering anti-retrovirals after exposure reduces the chance of HIV infection five-fold [96].)

Anti-retroviral therapy is usually given as a cocktail of several drugs.  Anti-retroviral therapy is 95% effective at keeping HIV RNA count below 50 copies/mL.[95]



Symptom Incidence in Syphilis Patients
Common Chancre

Rash and systemic symptoms


Cardiac symptoms

Almost all

Almost all
15% (if untreated)

10% (if untreated)

Moderate Neurosyphilis 6.5% (if untreated)
Rare many n/a

Syphilis is caused by the spirochete bacterium Treponema pallidum.  

Syphilis can have many symptomatic manifestations, but it usually progresses in stages.

Primary syphilis: A painless sore (chancre) on the anus, mouth, penis, or vagina, about 21 days after infection

Secondary syphilis: diffuse, non-itchy rash, frequently including the palms and soles of the feet, consisting of small red or copper-colored macules (non-raised spots); fever, malaise, headache; usually 4-10 weeks after infection

Latent syphilis: no symptoms

Tertiary syphilis: gummas (non-cancerous necrotic growths, either on the skin or inside the body), cardiac and neurological problems.  Years after initial infection.  Without treatment, 15-40% of infected people develop tertiary disease.  People with tertiary syphilis are not infectious.[54]

Tertiary syphilis is extremely varied. Cardiac symptoms (affecting 10% of untreated syphilis patients)  usually involve the aortic arch and can lead to chest pain or aneurysm.

Gummas (affecting 15% of untreated syphilis patients) are rarely physically debilitating but can be disfiguring, and can cause collapse of the palate or nasal septum, or pressure damage to internal organs.

Neurosyphilis (affecting 6.5% of untreated syphilis patients) involves infection of the cerebrospinal fluid.  It can cause a very wide variety of neurological symptoms.  In one study of 161 patients diagnosed with neurosyphilis, 51% presented with symptoms of delirium, dementia, and other neuropsychiatric conditions; 15% had stroke; 9% had spinal cord disease; and 9% had seizures.[57]

Incidence and Risks

Total population incidence 0.018%
Incidence among men who have sex with men 0.54%
Penile-anal per-act transmission rate 1.4%
Penile-oral per-act transmission rate 1%
Per-partner transmission rate 60%


In 2013 there were 56,471 cases of syphilis, for an incidence rate of 0.018%.

Syphilis is much more common in men who have sex with men than any other group; 60% of syphilis cases are from men who have sex with men, who make up just 2% of the US population. The male-female ratio for syphilis was 5.2 in 2003.[58]

There were 21,819 cases of “late and late latent” syphilis in 2013, which includes tertiary syphilis; this is an incidence rate of 0.007%.

Syphilis is transmitted through contact with a chancre; it can happen through vaginal, anal, or oral sex.  The per-partner transmission probability is about 60%.[59]

There is a 60-70% reduction in risk of syphilis among condom users as opposed to non-condom users among non-sex-workers, but several studies of sex workers found no association between condom use and syphilis incidence.[60]  Because syphilis is transmitted via a sore, condoms are only effective at prevention if they cover the area of the sore.


Syphilis is diagnosed with a blood test. There are nontreponemal tests which recognize nonspecific antibodies, and often have false positives (due, for instance, to another infection.)  These have sensitivities of  78-86% for detecting primary syphilis, 100% for detecting secondary syphilis, and 95-98% for detecting tertiary syphilis. Specificity ranges from 85-99%.  Treponemal tests test for antibodies specific to the bacterium that causes syphilis.  They have a sensitivity of 84% for detecting primary syphilis infection and almost 100% sensitivity for detecting syphilis infection in other stages. Their specificity is 96%.[61][62]

Neurosyphilis is diagnosed by taking samples of cerebrospinal fluid and looking at serologic tests, CSF cell count, and disease symptoms.


Intramuscular penicillin injection is the standard treatment for early syphilis. The cure rate is 95%.[63]  Neurosyphilis is treated with large intravenous doses of penicillin.

Hepatitis B


Symptom Risk
Common Acute viral hepatitis 30-50%
Moderate Chronic hepatitis <5%
Rare hepatocellular carcinoma 0.1%-0.2%


Hepatitis B is caused by the hepatitis B virus (HBV), and is transmitted by infected blood and other bodily fluids. It is preventable by vaccination.

Acute viral hepatitis causes malaise, fever, nausea, vomiting, and dark urine, ultimately progressing to jaundice in 75% of reported cases. This illness usually lasts for a few weeks and then improves.  30-50% of patients with acute hepatitis B will have symptoms.

Chronic hepatitis is inflammation of the liver; in the long term, it can lead to cirrhosis, and increases the incidence of hepatocellular carcinoma. Only <5% of cases of hepatitis B lead to chronic hepatitis.[77]  The relative risk of hepatocellular carcinoma in chronic hepatitis is 18.8 for men and 33.2 for women; with an overall incidence of 6 per 100,000 in the US,[74] this is a risk of 0.2% for women and 0.1% for men.

Incidence and Risks

Incidence 0.9 per 100,000
Prevalence 4.7%
Per-partner transmission risk 25%-59%

There were 2895 cases of acute hepatitis B in the US, for a national incidence rate of 0.9 per 100,000.  42% of cases reported injection drug use; 5% reported sexual contact with a person with confirmed or suspected hepatitis infection.[77]  During the period 1999-2006, the NHANES survey found a prevalence of hepatitis B surface antigen of 4.7%. [78]

Serum, semen, and saliva can transmit HBV. The seroprevalence of HBV infection among heterosexual spouses of people with chronic HBV infection ranges from 25% to 59%. Heterosexual transmission accounts for about 39% of new infections among adults, and transmission among MSM accounts for about 24%.[80] One mathematical model of HBV transmission dynamics used an estimate of 33% transmission risk per year per partnership for heterosexual partnerships, and 42% for homosexual partnerships.[81]

Regular condom users have about a 75% reduced prevalence of hepatitis B.[86]


Hepatitis is diagnosed with serum assays that detect antibodies or viral antigens.


A hepatitis B vaccine is standard for infants in the US, and has 95% effectiveness in preventing HBV until age 40, when it drops to about 90%, and again to around 75% in people over 60.[82]

Acute hepatitis B infections are usually self-limiting; chronic infections are treated with antivirals or the immune modulator interferon-alpha.

Note on Transgender Issues

The vast majority of studies on STD epidemiology do not address transgender people. “Female” and “male” susceptibility rates here implicitly refer to cisgender women and men.

Extrapolating the available information for trans people inevitably requires judgment calls. Per-act transmission rates are based on the type of intercourse (oral, vaginal, anal, receptive or penetrative) and should be extrapolated to trans people accordingly.  Per-partner studies of heterosexual couples do not specify type of intercourse but can probably be assumed to involve chiefly vaginal intercourse.

STD rates among trans people are poorly studied, but HIV rates among trans women appear to be very high.  11.8% of transgender women reported having HIV.[30]


[1] Current Clinical Practice: Sexually Transmitted Diseases: A Practical Guide for Primary Care Edited by: A. L. Nelson and J. A. Woodward © Humana Press, Totowa, NJ

[2]Teng, Yu, Nan Kong, and Wanzhu Tu. “Estimating age-dependent per-encounter chlamydia trachomatis acquisition risk via a Markov-based state-transition model.” Journal of clinical bioinformatics 4.1 (2014): 7.

[3] Tu, Wanzhu, Pulak Ghosh, and Barry P. Katz. “A stochastic model for assessing Chlamydia trachomatis transmission risk by using longitudinal observational data.” Journal of the Royal Statistical Society: Series A (Statistics in Society) 174.4 (2011): 975-989.

[4]Kent, Charlotte K., et al. “Prevalence of rectal, urethral, and pharyngeal chlamydia and gonorrhea detected in 2 clinical settings among men who have sex with men: San Francisco, California, 2003.” Clinical Infectious Diseases41.1 (2005): 67-74.

[5]Hooper, R. R., et al. “Cohort study of venereal disease. I: the risk of gonorrhea transmission from infected women to men.” American Journal of Epidemiology108.2 (1978): 136-144.\

[6]Gallo, Maria F., et al. “Self-reported condom use is associated with reduced risk of chlamydia, gonorrhea, and trichomoniasis.” Sexually transmitted diseases34.10 (2007): 829-833.

[7]Warner, Lee, et al. “Problems with condom use among patients attending sexually transmitted disease clinics: prevalence, predictors, and relation to incident gonorrhea and chlamydia.” American journal of epidemiology 167.3 (2008): 341-349.

[8]Burchell AN et al. Genital transmission of human papillomavirus in recently formed heterosexual couples. J Infect Dis 2011 Dec 1; 204:1723 – See more at:

[9]Burchell, Ann N., et al. “Modeling the sexual transmissibility of human papillomavirus infection using stochastic computer simulation and empirical data from a cohort study of young women in Montreal, Canada.” American journal of epidemiology 163.6 (2006): 534-543.

[10]Gillison, Maura L., et al. “Prevalence of oral HPV infection in the United States, 2009-2010.” Jama 307.7 (2012): 693-703.

[11]Chin-Hong, Peter V., et al. “Age-specific prevalence of anal human papillomavirus infection in HIV-negative sexually active men who have sex with men: the EXPLORE study.” Journal of Infectious Diseases 190.12 (2004): 2070-2076.


[13]Patel, Harshila, et al. “Systematic review of the incidence and prevalence of genital warts.” BMC infectious diseases 13.1 (2013): 39.

[14]Moscicki, Anna-Barbara, et al. “Updating the natural history of human papillomavirus and anogenital cancers.” Vaccine 30 (2012): F24-F33.

[15]Cottler L, Garvin EC, Callahan C (September 2006). “Condom use and the risk of HPV infection”. The New England Journal of Medicine 355 (13): 1388–9

[16]Lowy, Douglas R., and John T. Schiller. “Prophylactic human papillomavirus vaccines.” Journal of Clinical Investigation 116.5 (2006): 1167.

[17]Lau C-Y, Qureshi AK. Azithromycin versus doxycycline for genital chlamydial infections: A meta-analysis of randomized clinical trials. Sex Transm Dis 2002;29:497-502. PubMed Abstract Full Text

[18]Falk, Lars, Hans Fredlund, and J. S. Jensen. “Signs and symptoms of urethritis and cervicitis among women with or without Mycoplasma genitalium or Chlamydia trachomatis infection.” Sexually transmitted infections 81.1 (2005): 73-78.

[19]Watson, Emma J., et al. “The accuracy and efficacy of screening tests for Chlamydia trachomatis: a systematic review.” Journal of medical microbiology51.12 (2002): 1021-1031.

[20]Schillinger JA, Dunne EF, Chapin JB, et al. Prevalence of Chlamydia trachomatis infection among men screened in 4 U.S. cities. Sex Transm Dis. 2005;32(2):74–77.

[21]Paavonen, Jorma, and Matti Lehtinen. “Chlamydial pelvic inflammatory disease.” Human Reproduction Update 2.6 (1996): 519-529.

[22]Simms, I., and J. M. Stephenson. “Pelvic inflammatory disease epidemiology: what do we know and what do we need to know?.” Sexually Transmitted Infections 76.2 (2000): 80-87.

[23] Kvien, T.; Glennas, A.; Melby, K.; Granfors, K et al. (1994). “Reactive arthritis: Incidence, triggering agents and clinical presentation”. Journal of Rheumatology 21(1): 115–22.

[24]Grodstein, Francine, and Kenneth J. Rothman. “Epidemiology of pelvic inflammatory disease.” Epidemiology 5.2 (1994): 234-242.

[25] Rompalo AM, Hook EW 3rd, Roberts PL, et al. The acute arthritis-dermatitis syndrome. The changing importance of Neisseria gonorrhoeae and Neisseria meningitidis. Arch Intern Med 1987; 147:281.

[26] Holmes, King K., David W. Johnson, and Henry J. Trostle. “An estimate of the risk of men acquiring gonorrhea by sexual contact with infected females.”American Journal of Epidemiology 91.2 (1970): 170-174.



[29] Moran JS, Levine WC. Drugs of choice for the treatment of uncomplicated gonococcal infections. Clin Infect Dis 1995; 20 Suppl 1:S47.


[31]Patel, Harshila, et al. “Systematic review of the incidence and prevalence of genital warts.” BMC infectious diseases 13.1 (2013): 39.

[32]Insinga RP, Glass AG, Rush BB. Diagnoses and outcomes in cervical cancer screening: a population-based study. Am J Obstet Gynecol 2004; 191:105.



[35] Ang, K. K.; Harris, J.; Wheeler, R.; Weber, R.; Rosenthal, D. I.; Nguyen-Tân, P. F.; Westra, W. H.; Chung, C. H.; Jordan, R. C.; Lu, C.; Kim, H.; Axelrod, R.; Silverman, C. C.; Redmond, K. P.; Gillison, M. L. (2010). “Human Papillomavirus and Survival of Patients with Oropharyngeal Cancer”. New England Journal of Medicine 363 (1): 24–35.




[39]Dunne EF, Unger ER, Sternberg M, McQuillan G, Swan DC, Patel SS, Markowitz LE (February 2007). “Prevalence of HPV infection among females in the United States”. JAMA 297 (8): 813–9.

[40]Dunne, Eileen F., et al. “Prevalence of HPV infection among men: a systematic review of the literature.” Journal of Infectious Diseases 194.8 (2006): 1044-1057.


[42]Bernstein, David I., et al. “Epidemiology, clinical presentation, and antibody response to primary infection with herpes simplex virus type 1 and type 2 in young women.” Clinical infectious diseases 56.3 (2013): 344-351.

[43]Corey, Lawrence, et al. “Genital herpes simplex virus infections: clinical manifestations, course, and complications.” Annals of internal medicine 98.6 (1983): 958-972.

[44]Levitz RE. Herpes simplex encephalitis: a review. Heart Lung 1998; 27:209.

[45]Murakami S, Mizobuchi M, Nakashiro Y, et al. Bell palsy and herpes simplex virus: identification of viral DNA in endoneurial fluid and muscle. Ann Intern Med 1996; 124:27.

[46]Marson, Anthony G., and Rodrigo Salinas. “Clinical Evidence: Bell’s palsy.”Western Journal of Medicine 173.4 (2000): 266.

[47]Steiner, Israel, Peter GE Kennedy, and Andrew R. Pachner. “The neurotropic herpes viruses: herpes simplex and varicella-zoster.” The Lancet Neurology6.11 (2007): 1015-1028.

[48]Fatahzadeh M, Schwartz RA (2007). “Human herpes simplex virus infections: epidemiology, pathogenesis, symptomatology, diagnosis, and management”. J. Am. Acad. Dermatol. 57 (5): 737–63;

[49] Xu, F; MR Sternberg, PhD, SL Gottlieb, MD, SM Berman, MD, LE Markowitz, MD, Div of STD Prevention, National Center for HIV/AIDS, Viral Hepatitis, STD, and TB Prevention; SE Forhan, MD, LD Taylor, DrPH, EIS officers, CDC (23 April 2010).”Seroprevalence of Herpes Simplex Virus Type 2 Among Persons Aged 14–49 Years—United States, 2005–2008″. Morbidity and Mortality Weekly Report (MMWR) 59 (15)

[50]Arvin, Ann, et al., eds. Human herpesviruses: biology, therapy, and immunoprophylaxis. Cambridge University Press, 2007.

[51]Wald, Anna, et al. “Effect of condoms on reducing the transmission of herpes simplex virus type 2 from men to women.” Jama 285.24 (2001): 3100-3106.

[52]Bryson, Yvonne, et al. “Risk of acquisition of genital herpes simplex virus type 2 in sex partners of persons with genital herpes: a prospective couple study.”Journal of Infectious Diseases 167.4 (1993): 942-946.


[54]Wald, Anna, and Rhoda Ashley-Morrow. “Serological testing for herpes simplex virus (HSV)–1 and HSV-2 infection.” Clinical infectious diseases 35.Supplement 2 (2002): S173-S182.

[55]Douglas, John M., et al. “A double-blind study of oral acyclovir for suppression of recurrences of genital herpes simplex virus infection.” New England Journal of Medicine 310.24 (1984): 1551-1556.

[56]Kent ME, Romanelli F (February 2008). “Reexamining syphilis: an update on epidemiology, clinical manifestations, and management”. Annals of Pharmacotherapy 42 (2): 226–36.

[57]Timmermans, M., and J. Carr. “Neurosyphilis in the modern era.” Journal of Neurology, Neurosurgery & Psychiatry 75.12 (2004): 1727-1730.

[58]Peterman, Thomas A., et al. “The changing epidemiology of syphilis.” Sexually Transmitted Diseases 32 (2005): S4-S10.

[59]Singh, Ameeta E., and Barbara Romanowski. “Syphilis: review with emphasis on clinical, epidemiologic, and some biologic features.” Clinical microbiology reviews 12.2 (1999): 187-209.


[61]Schmid GP. Serologic screening for syphilis. Rationale, cost, and realpolitik. Sex Transm Dis. Jan-Feb 1996;23(1):45-50.

[62]Young H. Syphilis. Serology. Dermatol Clin. Oct 1998;16(4):691-8

[63]Riedner, Gabriele, et al. “Single-dose azithromycin versus penicillin G benzathine for the treatment of early syphilis.” New England Journal of Medicine 353.12 (2005): 1236-1244.

[64]Schwebke, Jane R., and Donald Burgess. “Trichomoniasis.” Clinical microbiology reviews 17.4 (2004): 794-803.

[65]Swygard, H., et al. “Trichomoniasis: clinical manifestations, diagnosis and management.” Sexually transmitted infections 80.2 (2004): 91-95.

[66]Sutton M, Sternberg M, Koumans EH, McQuillan G, Berman S, Markowitz L. The prevalence of Trichomonas vaginalis infection among reproductive-age women in the United States, 2001-2004. Clin Infect Dis. 2007 Nov 15;45(10):1319-26

[67]Joyner, James L., et al. “Comparative Prevalence of Infection With Trichomonas vaginalis Among Men Attending a Sexually Transmitted Diseases Clinic.”Sexually transmitted diseases 27.4 (2000): 236-240.

[68]Niccolai LM, Kopicko JJ, Kassie A, Petros H, Clark RA, Kissinger P. Incidence and predictors of reinfection with Trichomonas vaginalis in HIV-infected women. Sex Transm Dis. 2000;27(5)

[69]Hillier, Sharon L., et al. “Association between bacterial vaginosis and preterm delivery of a low-birth-weight infant.” New England Journal of Medicine 333.26 (1995): 1737-1742.


[71]Sorvillo, Frank, et al. “Trichomonas vaginalis, HIV, and African-Americans.”Emerging infectious diseases 7.6 (2001): 927.

[72]Bowden, Francis J., and Geoffrey P. Garnett. “Trichomonas vaginalis epidemiology: parameterising and analysing a model of treatment interventions.” Sexually transmitted infections 76.4 (2000): 248-256.

[73]Fouts AC, Kraus SJ. Trichomonas vaginalis: reevaluation of its clinical presentation and laboratory diagnosis. J Infect Dis. 1980;141(2):137–143.

[74]El‐Serag, Hashem B., and Fasiha Kanwal. “Epidemiology of hepatocellular carcinoma in the United States: Where are we? Where do we go?.” Hepatology60.5 (2014): 1767-1775.


[76]Martin, E. Archives of Internal Medicine, July 13, 2009; vol 169: pp 1233-1240.



[79]Wasley, Annemarie, et al. “The prevalence of hepatitis B virus infection in the United States in the era of vaccination.” Journal of Infectious Diseases 202.2 (2010): 192-201.

[80]Mast, Eric E., et al. “A comprehensive immunization strategy to eliminate transmission of hepatitis B virus infection in the United States.” MMWR 54.16 (2005): 1-32.

[81]Williams, J. R., et al. “The transmission dynamics of hepatitis B in the UK: a mathematical model for evaluating costs and effectiveness of immunization programmes.” Epidemiology and infection 116.01 (1996): 71-89.


[83]Mandell, Gerald L.; Bennett, John E.; Dolin, Raphael, eds. (2010). Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases (7th ed.). Philadelphia, PA: Churchill Livingstone/Elsevier.

[84]aCDC. Monitoring selected national HIV prevention and care objectives by using HIV surveillance data—United States and 6 U.S. dependent areas—2011. HIV Surveillance Supplemental Report 2013;18(No. 5)

[85]CDC. Estimated HIV incidence among adults and adolescents in the United States, 2007-2010. HIV Supplemental Report 2012)

[86]Bernabe-Ortiz, Antonio, et al. “HBV infection in relation to consistent condom use: A population-based study in Peru.” PloS one 6.9 (2011): e24721.

[87]Holmes, King K., Ruth Levine, and Marcia Weaver. “Effectiveness of condoms in preventing sexually transmitted infections.” Bulletin of the World Health Organization 82.6 (2004): 454-461.

[88]Baggaley, Rebecca F., Richard G. White, and Marie-Claude Boily. “HIV transmission risk through anal intercourse: systematic review, meta-analysis and implications for HIV prevention.” International journal of epidemiology(2010): dyq057.

[89]Weller, S. C., and K. Davis-Beaty. “Condom effectiveness in reducing heterosexual HIV transmission (Review).” The Cochrane Library 4 (2007): 1-24.

[90]Boily M-C, Baggaley RF, Wang L et al. Heterosexual risk of HIV-1 infection per sexual act: systematic review and meta-analysis of observational studies. Lancet Infectious Diseases. 2009 Feb;9(2):118–29.

[91]Jin F, Jansson J, Law M et al. Per-contact probability of HIV transmission in homosexual men in Sydney in the era of HAART. AIDS. 2010 Mar 27;24(6):907–13.

[92]Wawer, Maria J., et al. “Rates of HIV-1 transmission per coital act, by stage of HIV-1 infection, in Rakai, Uganda.” Journal of Infectious Diseases 191.9 (2005): 1403-1409.

[93]Del Romero J et al. Evaluating the risk of HIV transmission through unprotected orogenital sex. AIDS 16(9): 1296-1297, 2002

[94]Chou R, Huffman LH, Fu R, Smits AK, Korthuis PT (July 2005). “Screening for HIV: a review of the evidence for the U.S. Preventive Services Task Force”. Ann. Intern. Med. 143 (1): 55–73.

[95]Vogel, Martin, et al. “The treatment of patients with HIV.” Deutsches Ärzteblatt International 107.28-29 (2010): 507.

[96] [No authors listed] (April 2012). “HIV exposure through contact with body fluids”.Prescrire Int 21 (126): 100–1, 103–5.

[97]Chou R, Selph S, Dana T et al. (November 2012). “Screening for HIV: systematic review to update the 2005 U.S. Preventive Services Task Force recommendation”.Annals of Internal Medicine 157


This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit

18 thoughts on “STD Statistics

  1. Hi! I didn’t have time to go through all the text but one thing that caught my attention and that one or both of us could improve on -and that might interest people- is the per-sex-act transmission rate for different sex acts. If I remember correctly, for HIV (and I’m guessing for most blood pathogens) the transmission rate is much greater for anal sex than it is for vaginal sex than it is for oral sex. And receptive sex is always more at risk than insertive sex. The orders of magnitude are big enough to matter, although I don’t remember them.

    • Are you sure you aren’t conflating per-act transmission rates (where my numbers are similar to yours) with per-partner transmission rates (the probability that, over a YEAR of having sex regularly with a person, you will catch the disease)?

  2. Hi!
    Thanks for great work.

    I have one question. Does use of condoms in these numbers/studies means usuall condom use practice (used just for vaginal/anal sex, and no barrier for oral and all around touching genitals and their area without any barrier) or strict “safe sex” practice (aka only touch is amongst genitals protected with condom)?

  3. Thank you for another magnificent article. Where else
    may anybody get that kind of information in such a perfect manner
    of writing? I’ve a presentation subsequent week, and I am at the search for such information.

  4. Good information. You should write for the NHS!! Don’t usually comment but you clearly spent time on that. It’s put my mind at rest and also woke me up to the dangers. Thank you

  5. Also, your Chlamydia rates are way off. You are reporting per-encounter rates as transmission probability. Go back and read the study you cite. The probability of contracting chlamydia after one sexual event with a known infected partner is much higher than you say.

  6. Hello, it is a great work.
    Do you have statistics of transmission of STIs per one act i.e. the chance of transmission of uninfected person to get the infection when he/she will be in sexual contact with an infected person per one exposure?
    Best regards

  7. Hi Sarah: I’m wondering how you arrived at your “per-encounter transmission rate” for HPV of .2%? As someone suffering from some serious HR-HPV hypochondria (from performing oral on a woman known to subsequently test positive), I’ve scoured the internet and available studies looking for any data on this. As far as I can tell, your number is WAY below reality. I’ve seen a range between 5% and nearly 100% per act. Is .2% referring to “general” risk with a person of unknown status? Or is that assuming the partner is positive for any HPV?

  8. I contacted Herpes virus from my Husband, And after so many search looking for medical cure to this illness which no medical doctor had cure to with no choice I was forced to share my pain to a friend who had same Issues and she directed me to this amazing herbal doctor who got her cured and she assured me that Robinson buckler will help me get total rid of my herpes virus and for my husband’s hpv too the help of his herbal herbal cured i and my husband, so surprising after taking his herbal treatment i and my husband was totally cured and for 2 months now we have not experienced any symptoms i am so happy today tell you all my story though it’s cost me some money but I guarantee you he is one man you can contact for help and he will help you with his great herbs. So if you have been looking for cure to whatever illness you are suffering from contact Robinson buckler by visiting his Robinsonbuckler@ hotmail. com

Leave a Reply

Fill in your details below or click an icon to log in: Logo

You are commenting using your account. Log Out /  Change )

Facebook photo

You are commenting using your Facebook account. Log Out /  Change )

Connecting to %s