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Condition created 2026-08-24 · updated 2026-08-24
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Anorectal Sexually Transmitted Infections

Eighth chapter of Part II ("Anorectal Disease"). Filed as a single comprehensive page — unlike Ch12/13/16, this chapter's many sub-entities (bacterial, viral, ectoparasitic STIs) share one unifying clinical framework (anorectal-STI presentation, screening/diagnostic algorithm, treatment philosophy) rather than being arbitrarily grouped unrelated conditions, so a single page mirroring the chapter's own organization was used instead of a split. Sexually transmitted infections (STIs, the term replacing "STD" as more accurate/less stigmatizing — infection doesn't necessarily mean disease/ symptoms, e.g. HPV) of the anus and rectum are an increasing public health concern: ~2.4 million reported US cases of chlamydia/gonorrhea/syphilis alone in 2018, with anorectal STIs specifically thought to be rising due to increased anal receptive intercourse — though true anorectal-specific incidence is hard to quantify. Additional risk factors: oral-anal sex, contiguous spread from genital infections (~50–60% of chlamydia/gonorrhea cases occur at non-urethral sites). Anorectal STIs are often asymptomatic and can be mistaken for hemorrhoids or other common anorectal conditions — colorectal surgeons play a critical role in diagnosis/treatment, requiring a high level of suspicion.

Anorectal immunology

Mucosal integrity of the anorectum is the critical barrier to viral/bacterial transmission, protecting the host via a locally-autonomous immune system. Infection occurs when a pathogen diffuses through this layer into circulation. In HIV, the virus can bind secretions to facilitate transport across the epithelial barrier; the GI tract's abundant T-cell population makes it a preferential target for viral replication. Anorectal-mucosa Langerhans (dendritic) cells and T cells work in concert to identify pathogens. HPV increases the number of anal-mucosa Langerhans cells, but HIV causes a dramatic decrease in Langerhans cells when coinfected with HPV — resulting in greater HPV recurrence risk; HIV is also correlated with more aggressive HPV infection (decreased T lymphocytes, suppressed Langerhans cells), allowing HPV to persist and progress toward anal dysplasia/carcinoma — demonstrating how HIV-positive patients face greater coinfection risk from local anorectal immunosuppression. Anal receptive intercourse directly delivers pathogens into abraded, vulnerable mucosa by denuding protectant cell layers and natural mucous coating. Parasitic infections (Entamoeba histolytica, Giardia lamblia) may also transmit via oroanal intercourse. Latex condoms protect against inoculation, though patients with a latex allergy may face even greater transmission risk from the immune response to alternative barriers.

Screening and prevention

Screening/testing recommendations by risk group (adapted from CDC): all people aged 13–64 should be HIV-tested at least once in their lifetime; sexually active women under 25 (or older with multiple partners) should be tested yearly for chlamydia/gonorrhea; MSM should be tested for chlamydia/ gonorrhea at least annually (every 3–6 months if high-risk), at all contact sites (urethral, rectal, pharyngeal) regardless of condom use; similar timeframes apply for syphilis screening in both populations; HSV type-specific serologic testing can be considered during initial STI screening for patients with multiple partners; HIV testing should be annual in MSM if status is negative/unknown or partners have had >1 partner since last testing; anal dysplasia screening in high-risk MSM/HIV-positive cohorts is also important (relevant to Colorectal Anatomy & Embryology's HPV-related-dysplasia content and the queued ASCRS Ch19/20 anal-neoplasia chapters).

Pre-exposure vaccination: Gardasil®9 (HPV) — recommended for both sexes beginning age 9, with 9-valent vaccine originally recommended in MSM up to 26, FDA later expanding approval to male patients up to 45. Hepatitis A and B vaccines also available.

HIV pre-/post-exposure prophylaxis: PrEP (pre-exposure prophylaxis) — FDA-approved 2012, one tablet daily (tenofovir disoproxil fumarate 300mg + emtricitabine 200mg) for those at high risk (MSM, heterosexual men/women with multiple partners and variable condom use, injection drug users sharing needles); requires known-negative HIV status before starting to avoid resistance. McCormack et al. (2016): 86% reduction in HIV transmission in MSM/homosexual populations. On-demand dosing (2 pills before sexual activity + 1 pill for 2 days after) showed similar reduction with improved compliance (Molina et al.) — though real-world average patient use was only 15 pills/month. Screen every 3 months for HIV/renal function/STDs once on PrEP; 99% reduction in HIV transmission risk when taken consistently. PEP (post-exposure prophylaxis): considered within 72 hours of high-risk exposure; three-drug regimen (tenofovir disoproxil fumarate 300mg + emtricitabine 200mg once daily + raltegravir 400mg twice daily or dolutegravir 50mg daily) for 28 days.

Reporting: mandatory reportable STIs in all 50 states include gonorrhea, chlamydia, syphilis, HIV, and chancroid (state-specific reporting for others); all reports confidential; all states allow minors to consent for STI care without parental permission (some limit by service type).

Diagnosis and initial evaluation

Asymptomatic presentation is common — ~85% of rectal STIs in MSM are asymptomatic; screening only the urogenital epithelium in women overlooks 12–30% of chlamydia/gonorrhea infections compared to multi-site testing. Untreated extragenital STIs create an infectious reservoir increasing HIV acquisition/transmission risk. Current guidelines recommend general multi-surface screening in asymptomatic high-risk subgroups (adolescents/young adults 15–24, incarcerated persons, gay/bisexual men, pregnant women, those failing safe-sex practices or with multiple partners, limited healthcare access).

Symptomatic presentation: anal pain, tenesmus, urgency, bleeding, mucopurulent drainage; painless or painful lesions/ulcers with or without mucosal inflammation/discharge — often mistaken for fissures, hemorrhoids, hidradenitis, fistula-in-ano, or malignancy (see Pruritus Ani for the fuller anal- pruritus differential this chapter's STI content feeds into). In adolescents/young adults, symptoms + proctitis can closely mimic IBD, specifically lymphogranuloma venereum; in patients diagnosed with IBD but not responding to appropriate therapy, infectious proctitis should be considered. Diagnosis requires a thorough workup: sexual history, prior STIs, complete anal exam with anoscopy ± endoscopy (mucosal erythema, friability, exudate, discharge). Swabs for gonorrhea/chlamydia/herpes must be obtained before introducing lubricant during anoscopy/endoscopy, as most medical lubricants are bacteriostatic. All patients with a suspected STI should undergo serologic testing for syphilis and HIV. Empiric therapy should be considered for both patient and partners while awaiting results (reduces transmission risk, improves outcomes): dual gonorrhea/chlamydia coverage (ceftriaxone 250mg IM ×1 + azithromycin 1g PO ×1 or doxycycline 100mg PO BID ×7 days) plus empiric valacyclovir for HSV while awaiting final results. Doxycycline may be superior to azithromycin for rectal-specific infections despite azithromycin's CDC-preferred status (driven by tetracycline resistance concerns and single-dose compliance advantage).

Bacterial STIs

Chlamydia

Chlamydia trachomatis — most common reportable US STI (~2 million new cases in 2018, likely underestimated given frequent asymptomatic presentation); ~1 in 20 women aged 14–24 have chlamydia. Untreated infection risks ectopic pregnancy/infertility/PID in women. Obligate intracellular bacterium with ≥15 serovars: D–K cause the common urethritis/cervicitis/PID/neonatal-disease/ proctitis spectrum; L1–L3 are more aggressive, most commonly causing lymphogranuloma venereum (LGV, below) and can mimic Crohn's disease. Diagnosis: NAAT (~97% sensitivity/specificity), first-catch urine in men, vaginal swab (or first-catch urine) in women; extragenital (rectal/pharyngeal) NAAT testing lacked FDA approval until 2019 (Aptima Combo 2 Assay, Xpert CT/NG). Treatment: azithromycin 1g PO ×1, or doxycycline 100mg BID ×7 days (may have greater efficacy than azithromycin for rectal- specific infection — reports of rectal chlamydial treatment failure with azithromycin up to 20%). Repeat testing at 3 months post-treatment (not <3 weeks, to avoid false positives from continued organism shedding); pregnant women re-tested at 3–4 weeks and again at 3 months.

Lymphogranuloma venereum (LGV)

Caused by C. trachomatis serovars L1–3 (L2 most implicated in recent increased prevalence); historically thought rare in developed countries, now surging in the MSM population (especially HIV-positive). More invasive than standard chlamydia, causing severe proctitis with ulcers that can progress to abscesses, fistulas, chronic pain, and strictures — can mimic IBD. Lymphatic involvement produces tender femoral/inguinal lymphadenopathy ("buboes," classic on exam but uncommon with genital infection); rectal pain, tenesmus, mucoid/anal discharge, fevers, fatigue, weight loss. Diagnosis: clinical suspicion + exclusion of IBD as the proctitis cause, confirmed by culture, direct immunofluorescence, or nucleic acid detection following a positive rectal/genital chlamydia NAAT. Endoscopic findings (mucosal erythema, friability, ulcers; biopsies showing lymphocytic infiltrates, crypt abscesses, even granulomatous changes) can mimic Crohn's disease. Treatment: doxycycline 100mg BID for 21 days (longer than standard chlamydia, given LGV's greater invasiveness); erythromycin regimen as an alternative (poorly tolerated — GI upset, frequent dosing). Local control of infected lymph nodes/buboes may need aspiration/incision-drainage to prevent ulceration/fistulization. HIV- positive MSM with proctitis and positive rectal chlamydial testing should be treated empirically for LGV given diagnostic-testing inconsistency and the risk of undertreatment.

Gonorrhea

Neisseria gonorrhoeae — second most common reportable US STI (>1 million cases/year, 500,000 reported to CDC in 2018). Most presentations asymptomatic (50% of men, up to 95% of women with positive cultures). Untreated risks: PID, fallopian tube involvement, infertility, ectopic pregnancy. Men: urethritis with painful urination/discharge up to 2 weeks post-inoculation; epididymitis less common. Women: cervicitis, urethritis, or proctitis (often mistaken for bladder/vaginal infection due to mild symptoms). Proctitis presents with tenesmus, hematochezia, mucopurulent discharge; untreated progression can cause pelvic pain, fever, abscess. Rare disseminated disease: polyarthritis, dermatitis, endocarditis, meningitis. Diagnosis: anoscopy shows erythema/friable mucosa/thick mucopurulent discharge from anal crypts; NAAT is definitive (100% sensitivity, >95% specificity); gram stain and culture reserved for treatment failure or symptomatic patients (allows antimicrobial susceptibility testing given gonococcal resistance concerns — Thayer-Martin media selectivity prevents overgrowth by endogenous flora). Treatment: dual therapy — ceftriaxone 250mg IM ×1 + azithromycin 1g PO ×1 (dual mechanisms reduce resistance risk and improve efficacy across genital/extragenital sites, also covers concurrent chlamydia). Abstain from intercourse until 7 days post-treatment-completion; repeat testing at 3 months; partners from the last 2 months should be counseled/treated. Treatment failure defined as persistent positive culture/NAAT or symptoms 3–5 days post-completion with no sexual contact in that window — these cases are reportable and warrant ID consultation.

Syphilis

Treponema pallidum (spirochete) — ~35,000 new US cases in 2018, >70% rise from 2014, after near-elimination-level nadir in the late 1990s/early 2000s; resurgence concentrated in MSM and HIV-positive MSM populations, but extending to women and increased congenital syphilis. Open syphilitic ulcers facilitate HIV transmission, and early syphilis diagnosis increases the likelihood of an HIV diagnosis. Three stages: primary (painless ulcer/chancre at inoculation site 1–21 days post-infection; extragenital ulcers more often painful; resolves in 3–6 weeks regardless of treatment, so few patients are diagnosed at this stage — HIV-positive patients more often asymptomatic in primary disease, presenting instead in secondary stage), secondary (weeks to months later: fever, malaise, arthralgias, diffuse lymphadenopathy, rectal mass, and a characteristic diffuse maculopapular rash often involving palms/soles — signifies hematogenous spread; untreated progresses to an asymptomatic latent stage 1–30 years), and tertiary (minority of patients: cardiac involvement, gummas — necrotic/ulcerated non-cancerous growths anywhere in the body). Neurosyphilis can occur at any stage (ocular/CNS involvement of brain, peripheral nerves, spinal cord — meningitis, cranial nerve palsies, paralysis, dementia, death); increased prevalence in HIV-positive patients, with evidence HIV may accelerate its clinical course. Diagnosis: nontreponemal testing (VDRL, RPR — inexpensive, easy, but nonspecific with false-positives in HIV/autoimmune disease/pregnancy) followed by confirmatory treponemal testing (FTA-ABS, other immunoassays/immunoblots); some labs use "reverse" testing (treponemal-specific first) — interpretation is difficult given treponemal-specific tests stay reactive lifelong regardless of treatment status, and reverse testing shows increased false-positive rates. Patients with CNS/ocular symptoms need organ-specific testing (CSF testing, slit lamp exam). All syphilis patients should be HIV-tested given high coinfection rates. Treatment: penicillin G for all stages (single IM dose of benzathine penicillin G 2.4 million units for early-stage disease; longer duration for latent/tertiary disease; penicillin-allergic patients need alternative therapy managed by ID). Patients should be counseled about the Jarisch-Herxheimer reaction — an acute febrile reaction (headache, myalgia, fever) within 24 hours of treatment initiation, which can trigger preterm labor in pregnant women if unrecognized. Repeat clinical evaluation/testing at 6 and 12 months; treatment failure/reinfection suspected with persistent symptoms or elevated antibody titers.

Chancroid

Haemophilus ducreyi — declining US incidence (only 3 reported cases in 2018), though notoriously hard to culture, making true incidence uncertain. Painful lesions hours to days post-exposure, progressing papule → pustule → open painful ulceration; often multiple, ragged borders with overlying exudate — can facilitate HIV transmission like other ulcerative STIs. Diagnosis: painful genital/anal ulcer + unilateral suppurative inguinal lymphadenopathy suggests the diagnosis. Gram stain may show "school of fish" chained gram-negative rods but has low sensitivity (40–60%); culture requires multiple non-widely-available media; PCR is most sensitive but has no FDA-approved test in the US — diagnosis is often made by exclusion criteria (painful genital ulcer(s), no syphilis evidence, regional lymphadenopathy, HSV-negative ulcer exudate). Treatment: single-dose ceftriaxone 250mg IM or azithromycin 1g PO (both one-time dosing); ciprofloxacin/erythromycin alternatives with some intermediate-resistance data. Ulcers should symptomatically improve within 3 days, objectively improve by 7 days, full healing up to 2 weeks (slower in uncircumcised men, HIV coinfection, or antimicrobial resistance).

Donovanosis (granuloma inguinale)

Klebsiella granulomatis (intracellular bacterium) — rare in the US, more prevalent in tropical/ developing regions (Brazil, South Africa, Caribbean). Typical presentation: non-tender, beefy red, highly vascular ulcer that bleeds easily; anorectal presentation can show verrucous lesions and/or deep fibrotic-ulcer fissures with subcutaneous lesions/granulomas ("pseudobuboes"). Diagnosis: identifying Donovan bodies within large mononuclear cells on Giemsa-stained smears (difficult with more fibrotic/ necrotic ulcers); PCR increasingly available. HIV coinfection testing recommended. Treatment: azithromycin 1g PO weekly ×3 weeks or 500mg daily ×3 weeks (first-line per CDC); healing proceeds outside-in requiring prolonged treatment for full epithelialization; gentamicin addition considered if no improvement within a few days.

Viral STIs

Herpes simplex virus (HSV)

HSV-2 is one of the most prevalent US STDs (>20% adult carrier rate) and one of the most common causes of nongonococcal proctitis in MSM. Although HSV-2 is classically associated with genital lesions, a 2006 report demonstrated a rising proportion of anogenital herpes secondary to HSV-1 in both heterosexual women and MSM cohorts — attributed to reduced childhood HSV-1 transmission producing a larger susceptible adult population engaging in oroanal/orogenital practices. The virus establishes lifelong latency in sensory nerve ganglia after retrograde travel from the primary infection site, reactivating antegrade to shed from the mucocutaneous surface. Anorectal herpes: recurrent blistering mucous-membrane lesions, symptoms typically 4–21 days post-anal-receptive-intercourse (perianal pain, burning, or pruritus most common); small vesicles with surrounding erythema on perianal skin/anal canal, may coalesce into large ulcers. Transmission risk continues until an epithelial barrier forms over the lesion (~3 weeks). Endoscopic findings: friable mucosa, diffuse ulcerations typically limited to the distal 10cm of rectum. Lumbosacral radiculopathy may occur (urinary dysfunction, sacral paresthesia, impotence, pain). Recurrence risk in the first year post-seroconversion: up to 90% in HSV-2 patients; recurrent infections are typically less painful and shorter-duration than primary infection. Immunocompromised patients (leukemia, HIV, T-cell-compromising medications) may have exacerbated genital/mucosal effects with life-threatening ulcer disease. Diagnosis: type-specific virologic and serologic testing; cell culture detects viral presence in 90% of active vesicular lesions (traditional method, allows viral typing/antiviral sensitivity testing); Tzanck preparation/ direct immunofluorescence are insensitive and not recommended; PCR is the current gold standard for systemic HSV/CNS infections and increasingly used for all HSV-associated lesions. Treatment: oral antiviral medications (valacyclovir, acyclovir, famciclovir — all RCT-validated) are mainstay management (no cure); indicated for symptomatic onset or as daily suppressive therapy. Diaz-Mitoma et al.: daily suppressive famciclovir gave a 3× lower recurrence-interval rate vs. control, 70–80% disease-free at 1 year. Once-daily valacyclovir reduces HSV-2 transmission risk in both heterosexual couples and those with multiple partners. Severe HSV proctitis, systemic sequelae, or neurologic complications may need hospitalization/IV acyclovir. Acyclovir resistance: 5% in HIV-positive patients, <1% immunocompetent — drug-resistant infections treated with foscarnet or cidofovir (limited data for topical imiquimod/cidofovir gel).

Genital warts (condyloma acuminata)

HPV is one of the most prevalent global STIs (>20 million US patients affected, 5 million new cases annually), more prevalent in MSM (condyloma rates up to 57% in HIV-negative and >90% in HIV-positive MSM patients); HIV-positive MSM face a 2× increased risk of HPV infection/condyloma formation vs. non-MSM patients. >120 known HPV serotypes; types 6 and 11 most commonly cause benign condylomas; types 16 and 18 more commonly associated with cellular changes causing anal dysplasia and invasive carcinoma (relevant to Colorectal Anatomy & Embryology's existing HPV-related-dysplasia content at the anal transition zone, and the queued ASCRS Ch19 "Anal Intraepithelial Neoplasia"/Ch20 "Anal Cancer" chapters). Transmission: sexual contact, ~3-month incubation; autoinoculation from genitourinary warts to the perianal region without direct contact has been demonstrated. Diagnosis: typically clinical (raised gray/pink fleshy cauliflower-like growths); anoscopy recommended to evaluate anal-canal extension (small papules rarely extend proximal to the dentate line); full genitalia/perineum/groin exam with speculum exam + Pap smear in women; HPV subtyping not recommended for anogenital warts (results don't guide management). High-resolution anoscopy (colposcopy- analog) for high-risk MSM/HIV-positive populations, using 3% acetic acid or Lugol's solution — lesions that turn distinctly acetowhite or fail to take up Lugol's solution carry greater dysplasia risk (punctation, mosaicism, neovascularization, abnormal vascular pattern are dysplasia features). Histologic confirmation only recommended when the patient is immunocompromised, diagnosis is uncertain, treatment fails, or the lesion worsens.

Management focuses on destruction/clearance of visible disease while minimizing tissue harm — HPV is not eradicated by local destruction, similar to HSV, and immunocompetent patients may even clear lesions spontaneously if untreated. Recurrence rates 4–29%, varying by immune function; single treatment clears up to 75% of patients, but intra-anal lesions/extensive presentation/no HPV vaccination are risk factors for recurrence/need for additional therapy within 2 years.

  • Electrosurgical ablation — usable for lesions in any location, full-thickness destruction; requires mechanical debridement after cauterization; care needed to avoid deep dermis/subcutaneous fat burns (scarring/poor cosmesis risk). CO2 laser is an alternative ablative technique, beneficial for large/multiple/recurrent or intraurethral lesions (tissue-sparing). Electrodesiccation should be performed in a well-ventilated room with smoke-evacuator technique. No FDA-approved topical therapies exist for intra-anal lesions.
  • Provider-applied agents: trichloroacetic/bichloroacetic acid 80–90% (caustic protein coagulation; small perianal/anal-canal lesions; sodium bicarbonate/soap/talc can neutralize unwanted acid contact) and cryotherapy (thermal-induced cytolysis; pain/blistering common). Less- utilized alternatives: podophyllum resin, intralesional interferon, photodynamic therapy, topical cidofovir (limited outcomes data, greater side-effect profile — not first-line).
  • Patient-applied topicals (non-intra-anal lesions only): imiquimod 5% cream (immune-response modifier, antiviral via interferon/cytokine stimulation; up to 87% success alone over 16 weeks; combination with laser ablation improves sustained clearance; applied bedtime 3×/week, left 6–8 hours; side effects: pain, burning, itching, induration, ulceration, erosion, vesicle formation; patients must fully wash off product before sex, as it weakens latex condom protection) and podofilox 0.5% (antimitotic, wart-necrosis-inducing; applied twice daily ×3 days then 1-day break, repeatable ×4 cycles; total daily volume capped at 0.5mL for systemic-toxicity/skin-irritation risk; 37% clearance, 4–38% recurrence).
  • Topical imiquimod suppositories post-ablation have been investigated for intra-anal lesions with complete clearance/minimal side effects.
  • Intralesional immunotherapy with recall antigens (Candida albicans, MMR, Trichophyton, tuberculin antigens) is an adjunct under investigation, inducing a local T-cell-mediated immune response. HPV vaccine (Gardasil®9) as an off-label therapeutic (not just prophylactic) agent has limited but growing supporting literature.

Giant condyloma (Buschke-Löwenstein tumor)

Also covered from the oncology side, as "verrucous carcinoma," on Anal Cancer (ASCRS Ch20) — that page explicitly reconciles the two chapters' framing of this same entity: Ch20 flags an unresolved classification controversy (benign lesion with invasive potential vs. slow-growing SCC variant) and reports a malignant-transformation rate of 40–60%, close to but not identical to this chapter's "up to 56%" figure below; the two are not reconciled against each other, reported as each source states.

First described 1925, first perianal case reported 1967. Associated with HPV types 6, 11, 16, and 18, but distinguished from ordinary condyloma by marked papillomatosis, acanthosis, and thickened rete ridges with greater mitotic activity; more prevalent in immunosuppressed patients. Represents a continuum from benign condyloma to invasive squamous cell carcinoma, with malignant transformation risk reported up to 56%. Treatment: wide local excision with 1cm margins is standard; recurrence rate 65% (higher in HIV-positive patients) makes aggressive resection with complete histologic margin examination important. Large surgical defects may need secondary-intent healing, rotational S flaps, advancement flaps, V-Y flaps, or skin grafts; abdominoperineal resection required if the anal sphincter is involved. Chemoradiation alone has shown successful outcomes in poor surgical candidates or when complete margins can't be safely achieved. A sleeve-resection technique (cylindrical mucocutaneous excision with radiofrequency dissection, positioning the dentate line correctly to avoid mucosal ectropion) has shown short hospital stay with no anal stenosis/recurrence at 1 year in one series.

Molluscum contagiosum

Poxvirus-family member causing small contagious skin lesions; incubation 1 week to 6 months, may last multiple months untreated. Transmission via direct skin/mucous-membrane contact or fomites (towels, clothing); associated with pools/bathing facilities; autoinoculation to other body sites occurs. Lesions: flesh-colored or gray-white, itching/pain. Typically self-limiting in immunocompetent hosts; in HIV or other immunocompromised states, lesions become large, verrucous, and hyperkeratotic. Treatment: phenol, trichloroacetic acid, tangential excision, electrocautery, or cryotherapy all effective; patient-applied topicals (podophyllotoxin, imiquimod) also used — controlling transmission risk and improving cosmetic outcomes.

Human immunodeficiency virus (HIV)

Recognized as an epidemic since 1981 (though transmission reported prior to 1980). Single-stranded RNA retrovirus incorporating into the host genome via reverse transcriptase; attacks CD4 receptors, causing abnormal immune activation and eventual T-lymphocyte destruction; capable of viral latency for years, complicating eradication. ~1.7 million people infected in the US since initial reporting,

500,000 deaths, 1.2 million currently living with disease, 14% unaware of infectious status. Annual incidence declined 9% 2010–2016, but prevalence remains greatest in MSM, especially African American MSM. Three disease stages: acute (HIV-1 infection syndrome, within weeks of transmission — flu-like symptoms, rash, as multiple immune-system cells/lymphatic tissue are targeted); dormancy phase (low-level ongoing reproduction; untreated, CD4 counts fall — below 500/mm³ risks HSV/HPV reactivation, below 200/mm³ risks opportunistic infection/cancer = AIDS/end-stage HIV disease); disease progression influenced by physiologic and psychosocial factors (drug use, high-risk sexual behavior, mental health). HAART (highly active antiretroviral therapy) has significantly reduced HIV-related morbidity/mortality by suppressing viral load and preserving/restoring immune function (both adaptive and innate parameters).

Anorectal disease in HIV: though HIV itself is not a specific anorectal disorder, benign anorectal pathology is the most common operative indication in HIV-infected patients, presenting three ways: (1) HIV-specific condition (anal ulcer), (2) routine condition (hemorrhoid, fissure, fistula, perirectal abscess — see Hemorrhoids, Anal Fissure, Anal Fistula, Anorectal Abscess), and (3) routine condition manifesting differently due to HIV status (anal condylomas, herpetic anal ulcers). HIV is also associated with malignancies including anal squamous cell carcinoma, lymphoma, and Kaposi's sarcoma. Surgeons should understand the patient's disease stage/medication regimen — concerns about delayed/poor wound healing in AIDS patients largely predate the HAART era; T4-cell count has shown no predictive value for wound healing, and HIV-positive patients on appropriate virus-targeted therapy face no increased complication risk from anorectal surgery and should be treated in standard fashion regardless of immune status.

  • Anorectal abscess — drain via small incision close to the anal verge, culture, antibiotics in immunocompromised patients.
  • Anal fistula — typically cryptoglandular in origin; treated with setons or sphincter-preserving operations; fistulotomy in low uncomplicated fistulas, but thorough bowel-habit/diarrhea/sphincter evaluation is warranted before any sphincter-sacrificing procedure.
  • Anal fissures among MSM may result from anal receptive intercourse and must be distinguished from HIV-/AIDS-related ulcers and other ulcerating infections (HSV, syphilis) more prevalent in this population — HIV-related ulcers are typically tender, necrotic, exudative with deep irregular overhanging borders, often off-midline (when midline, more proximal in the anal canal/closer to the dentate line vs. simple fissures), most disabling of any anal disease, associated with a hypotonic sphincter, occasionally with a superficial purulent layer mimicking an abscess. Anal ulcers remain a common disorder in this population as they are not affected by antiviral medications. Internal sphincterotomy is not advised for HIV-population fissures unless clearly distinguished from ulcerating disease. Intralesional steroids have shown significant improvement in six patients with anal ulcers in one series; ulcer excision + mucosal advancement flap reserved for medical-treatment failures, with a more aggressive surgical approach associated with symptomatic relief and successful wound healing.

Ectoparasitic STIs

  • Pediculosis pubis (pubic lice) — Pthirus pubis infestation of pubic hair/perianal region via close sexual contact; primary symptom is pruritus; skin becomes crusted with rust-colored fecal flecks visible; diagnosis clinical, dermascope can visualize parasites within hair follicles; 30% coinfection risk with other STIs including HIV warrants screening. Treatment: permethrin 1% cream or pyrethrins with piperonyl butoxide (first-line); malathion 0.5% lotion or ivermectin 250μg/kg orally ×2 weeks (alternatives); lindane is a further alternative but carries aplastic anemia/seizure risk. Clothing/bedding should be washed; shaving generally unnecessary; clear of infestation if no parasites present 1 week post-treatment.
  • Scabies — Sarcoptes scabiei, an 8-legged mite, frequently sexually transmitted in adults; can survive up to 36 hours at room temperature and transmit via fomites. Nocturnal pruritus with symmetrical papules/pustules/excoriations, classically interdigital webs/nipples/genitals. Diagnosis by identifying the mite in its burrow (challenging) or fecal-material findings (more typical). Treatment: permethrin 5% cream or oral ivermectin ×2 weeks; lindane an alternative in limited refractory cases given toxicity. Crusted (Norwegian) scabies — increased transmission ease and aggressive infestation rate in HIV/immunocompromised patients; combination therapy recommended (25% benzyl benzoate or 5% permethrin cream + oral ivermectin); lindane avoided given increased systemic- toxicity risk in this population; close follow-up at 2 weeks with additional therapy if needed.

Conclusion

Anorectal STIs remain a public health concern despite diagnostic/therapeutic advances. The most effective treatment method is prevention, starting with patient/provider education. High-risk populations (MSM, low socioeconomic status) should be screened and offered appropriate vaccines and prevention strategies. All patients presenting with STI concerns require specific testing/screening for all related organisms and HIV. Effective antibiotic/antiviral therapies exist for most of these conditions and operative intervention may not be required for the majority — the colorectal surgeon should provide a supportive environment ensuring patients receive required treatment and sexual health counseling.

  • Pruritus Ani — this chapter's STI content backs that page's existing "STIs more broadly" differential subsection (gonorrhea, syphilis, herpes, pinworms, scabies, pediculosis); that page's brief STI mentions are superseded/expanded here.
  • Anal Fissure — STI-related/HIV-related fissures already flagged on that page; this chapter provides the fuller HIV-anal-ulcer differential and management detail.
  • Hemorrhoids — that page's HIV/immunocompromise hemorrhoidectomy-safety content; this chapter provides the broader HIV-anorectal-disease framework it sits within.
  • Anorectal Abscess, Anal Fistula — HIV/immunocompromise already named as a factor on both pages; this chapter's HIV section provides fuller context (no increased complication risk on appropriate HAART).
  • Anal Stenosis — condyloma excision/fulguration already named as a stenosis cause; this chapter's Genital Warts and Giant Condyloma sections provide the fuller underlying disease content.
  • Colorectal Anatomy & Embryology — HPV types 16/18 and anal-transition-zone dysplasia.
  • Anal Intraepithelial Neoplasia — the fuller dysplasia/precancer content this chapter's HPV 16/18 mention and HRA-screening note set up background for.
  • Anal Cancer — closes this page's Ch20 forward reference; also see the Giant condyloma section above for the direct content overlap with that page's Verrucous carcinoma section (same entity, two chapters' framing).

Open items / gaps

  • Anal dysplasia/AIN content is intentionally kept brief here (screening mention, HPV 16/18 oncogenic-subtype note) — see Anal Intraepithelial Neoplasia (ASCRS Ch19) for the full dysplasia/precancer content, now ingested. Anal Cancer (Ch20) is also now ingested — see the Giant condyloma section above for the malignancy-side reconciliation of that entity.
  • No primary-literature source yet for the cited trial/cohort data (McCormack PrEP trial, Molina on-demand PrEP trial, Diaz-Mitoma famciclovir RCT, giant condyloma sleeve-resection series) — known only via this textbook chapter's synthesis.
  • Donovanosis and chancroid are both explicitly noted as rare/declining in current US incidence but diagnostically difficult (hard to culture) — true incidence for both is likely underestimated per the chapter.