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Sexually Transmitted
andInfectious Diarrheal Diseases
RezaArsalani-Zadeh, ChristinaCellini,
andLesterGottesman
27
Introduction
Infectious diseases of the anorectum include those
transmitted sexually and by other mechanisms.
This chapter covers sexually transmitted and
infectious diarrheal diseases. Sexually transmitted infections (STIs) have increased at an alarming rate and have expanded from a narrow group
of “classic” venereal diseases to include more
than 25 infectious bacterial, fungal, protozoan,
and viral agents. In the past three decades, more
than 50 organisms or syndrome combinations
have been identied as sexually transmitted.
To put into context, the United States has the
world’s highest rates of STIs. The annual incidence of STIs in the United States is estimated to
be around 19.7 million. Yet, the reported disease
rate likely underestimates the true burden of the
disease [1]. Many STIs are asymptomatic; in
addition, there is reluctance, even among physicians, to discuss STIs, leaving them unrecognized and untreated.
R. Arsalani-Zadeh
Department of Colorectal Surgery, University of
Rochester Medical Center, Rochester, NY, USA
C. Cellini
Department of Surgery, University of Rochester
Medical Center, Rochester, NY, USA
e-mail: christina_cellini@urmc.rochester.edu
L. Gottesman (*)
Division of Colon and Rectal Surgery, Department of
Surgery, Mount Sinai, New York, NY, USA
Surveys have produced widely varying estimates of the prevalence of anal intercourse. The
anorectum has been used with increasing frequency for sexual fulllment over the past several
decades [2], resulting in an explosive growth in
the incidence of STIs which affect the anorectum.
Anal intercourse appears to be practiced, at least
occasionally, by a substantial proportion of the
sexually active population. Peterson et al. [3]
reported that 73% of adult homosexual and bisexual black men surveyed in 1990 had engaged in
anal intercourse within the past 6 months. This
practice is not conned to the homosexual population. Among sexually active adolescents, surveys
have estimated the proportion having practiced
anal intercourse to be as high as 27% of men and
35% of women [4]. A survey of sexually active
college students in Canada reported that 14% of
men and 19% of women had anal intercourse at
some time in their lives [5]. Approximately 2–2.5
million British citizens regularly use the anorectum for sexual fulllment [6]. The National Health
and Social Life Survey conducted in 1992 estimated that 26% of men and 20% of women ages
18–59 had engaged in anal intercourse during
their lifetimes [7]. Of greatest concern is that in
several populations studied, the majority of those
who practiced anal intercourse used condoms
inconsistently or not at all [8], placing them at
increased risk for HIV and other STIs. STIs
acquired through anal intercourse are usually conned to the lower rectum. The frequency of
© Springer International Publishing AG, part of Springer Nature 2019
D. E. Beck et al. (eds.), Fundamentals of Anorectal Surgery,
https://doi.org/10.1007/978-3-319-65966-4_27
495
496
R. Arsalani-Zadeh et al.
sexually transmitted proctocolitis has declined
over the past decade, possibly due to effect of the
safer sex campaigning. There are however concerns that we are facing a new rise in the incidence
of STIs. Due to highly active antiretroviral therapy (HAART), the rate of high risk sexual behavior has been increasing in the United Stated and
other developed nations. The rates of early syphilis, gonorrhea and chlamydia have also been on
the rise [9].
STIs often present with non-specic symptoms. STIs involving the anal canal typically
present with pain, mainly due to extensive sensory innervation of the anal canal. Pain in turn
can cause reexive anal sphincter spasm and
therefore constipation and tenesmus. STIs involving the rectum usually present with bloody or
mucopurulent discharge.
Unfortunately, the clinical examination is
often inaccurate in diagnosing STIs. The majority of genital or anal ulcers in young sexually
active patients are due to syphilis or herpes.
Accurate diagnosis of sexually transmitted and
infectious disease of the anorectum is difcult
because patients commonly harbor multiple
organisms. The global epidemic of HIV and
AIDS has complicated the diagnosis and treatment of anorectal STIs, even further. It is therefore of paramount importance that physicians
have a working knowledge of each of these disorders and be familiar with the incidence of different type of STIs in their community. Laboratory
evaluation of genital, anal or perianal ulcers
should include syphilis serology or PCR testing,
culture and PCR testing for genital herpes and
serologic testing for HSV antibody. In addition,
HIV testing should be performed on everyone
with unknown HIV status. Unusual looking
ulcers or those not responding to initial therapy
should be biopsied.
Empirical therapy of STIs based on the clinical ndings and epidemiologic setting is recommended. Even after a complete diagnostic
evaluation up to 25% of patients will have no
laboratory conrmed diagnosis [9, 10].
Tables 27.1 and 27.2 list the diseases covered
in this chapter and include a summary of the presenting symptoms, physical ndings, suggested
diagnostic tests, and accepted treatment
modalities.
Sexually Transmitted Anorectal Disorders
Bacterial Infections
Gonorrhea
Gonorrhea, caused by Neisseria gonorrhea, a
gram-negative intracellular diplococcus, is probably the most common venereal disease affecting
the anorectum with an estimated 820,000 new
cases annually [9, 11]. The overall prevalence of
gonorrhea has shown a steady increase since
2009, resulting in a dangerously prevalent reservoir of disease carriers in the community [9, 12].
Women who have primarily gynecologic gonorrhea also will have the anorectum infected in
36–63% of cases [13]. The anorectum will be the
exclusive site of infection in 40–50% of homosexual men and in 4% of women [14]. The incubation period is usually from 5 to 7 days after
exposure, but may be as long as 30days.
At least half the male patients and up to 95%
of female patients with rectal gonorrhea are
asymptomatic. Symptomatic infections vary in
severity. Anorectal inoculation usually produces
proctitis and/or cryptitis and presents with nonspecic symptoms including pruritus, tenesmus,
and bloody or mucopurulent rectal discharge. If
untreated, the initial infection can progress to
more advanced conditions such as perihepatitis,
meningitis, endocarditis, pericarditis, and gonococcal arthritis. Gonococcal arthritis tends to be a
unilateral migratory purulent arthritis of large
joints.
The perineum is generally not involved in
gonococcal proctitis. A thick yellow mucopurulent discharge with or without proctitis is diagnostic of gonorrhea (Fig. 27.1). One classic
nding is the ability to express the purulent material from the anal crypts by applying gentle external pressure while the anoscope is in place [15].
Sigmoidoscopy often reveals diffuse congestion
and edema of the mucosa extending 8–9 cm
above the anal verge. The mucosa is frequently
covered by thick, creamy, tenacious pus, which
often exudes from inamed crypts at the dentate
line. This discharge may be mistaken for ulcerative or nonspecic proctitis or other infectious
agents. Fistulae and abscesses are an uncommon
complication.
27 Sexually Transmitted andInfectious Diarrheal Diseases
Table 27.1 Sexually transmitted anorectal disorders
Organism Symptoms Physical ndings Diagnostic tests Treatment
Gonorrhea (Neissera
gonorrhea)
Chlamydia and
lymphogranuloma
venereum (LGV)
Chancroid Hemophilus
ducreye
Donovanosis Klebsiella
granulomatis
Syphillis Rectal pain Painful anal
Herpes simplex Anorectal
Human papillomavirus
(HPV) (condylomata
acuminata)
Mulluscum contagiosum Painless
Human
immunodeciency virus
(AIDS)
NAAT nucleic acid amplication test, IM intramuscular, PO orally, BID twice a day, QID four times a day
Rectal
discharge
Tenesmus Friable, often
Anal pain Anorectal
Perianal
mass
pain,
pruritus
Pruritus,
bleeding,
discharge,
pain
dermal
lesions
See text See text Western blot AZT, HAART
Proctitis,
muco- purelent
discharge
ulcerated rectal
mucosa±rectal
mass
abscesses and
ulcers
Hard, shiny
perianal masses
ulcer
Perianal
erythema,
vesicles, ulcers,
diffusely
inamed,
friable rectal
mucosa
Perianal warts Excisional
Flattened round
umbilicated
lesions
NAAT,
Thayer-Mayer
culture of
discharge
NAAT,
Serologic
antibody titer,
Biopsy for
culture
Culture Azithromycin 1g PO or
Biopsy of mass Trimethoprim-sulfamethoxazole
Dark-eld exam
of fresh
scrapings,
serologic tests
Cytologic exam
of scrapings or
viral culture of
vesicular uid
biopsy with
viral analysis
Excisional
biopsy
Ceftriaxone 250mg IM for 1day
and Azithromycin 1g PO or
doxycycline 100mg PO BID for
7days
Azithromycin 1g PO or
doxycycline 100mg PO BID for
7days
Ceftriaxone 250mg IM for 1day
(DS) PO BID for 7days and
Azithromycin 1g PO for 21days
Benzathine penicillin 2.4million
units IM
Acyclovir 200mg ve times
daily for 5days
Destruction. See Chap. 9
Excision, cryotherapy
497
Swabs should be taken of the discharge for
both culture and grams stain. Gram stain typically shows intracellular Gram-negative diplococci, however, it is often unreliable and falsely
negative. Swabbing the mucous under direct
visualization raises the positive yield from 34%
to 79%. Lubrication of the anoscope or proctoscope with anything other than water is not
advisable since many lubricants and creams contain antibacterial agents. Biopsies are often normal and non-diagnostic. Empirical therapy is
highly recommended. Nucleic Acid
Amplication Test (NAAT) has a higher sensitivity (100%) and equivalent specicity in com-
parison to culture and is the recommended
diagnostic test. According to CDC guidelines
treatment of gonococcal proctitis is similar to
gonococcal urethritis or cervicitis. All patients
should also be tested and empirically treated for
presumed concomitant chlamydial infection.
The current CDC recommendations are ceftriaxone 250mg in a single intramuscular dose plus
azithromycin 1g oral in a single dose. If ceftriaxone is not available an alternative regimen of
cexime 400 mg orally as a single dose plus
azithromycin 1g orally as a single dose, can be
used. Due the high prevalence of tetracycline
resistance in the United States, doxycycline is no
498
Table 27.2 Infectious diarrheal disorders
Organism Symptoms Physical ndings Diagnostic tests Treatment
Campylobacter
jejuni
Yersinia Non-bloody
Salmonella Non-bloody
Shigella Abdominal
Mycobacterium
aviumintracellulare
Cytomegalovirus
(CMV)
Amebiasis
Entomeoboa
histolytica
Cryptosporidia Profuse
Giardia lamblia Nausea,
Isospora Vomiting,
PO per os, RLQ right lower quadrant
Diarrhea,
cramps,
bloating
diarrhea,
vomiting,
tenesmus,
fever
diarrhea,
abdominal
pain, fever
cramps,
fever,
tenesmus,
bloody
diarrhea
Watery
diarrhea
Rectal
bleeding
Bloody
diarrhea
bloody
mucoid
diarrhea
bloating,
cramps,
diarrhea
fever,
abdominal
pain
Erythema, edema,
grayish-white
ulcerations of rectal
mucosa
RLQ tenderness,
mass
Mucosal hyperemia
and petechiae
Erythema, edema,
grayish-white
ulcerations of rectal
mucosa
Friable
mucosa±ulceration
Multiple small white
ulcers
Friable rectal
mucosa; shallow
ulcers with yellowish
exudate and ring of
erythrema
Normal mucosa Rectal biopsy
Normal mucosa Fresh stool exam
Normal mucosa Acid-fast stain of
Culture stool using
selective media
Stool culture Trimethoprim-sulfamethoxazole
Stool culture Fluid and electrolyte
Stool culture Ciprooxacin 500mg PO BID
Acid-fast stain of
stool, endoscopic
biopsy
Biopsy, viral
culture, antigen
assay of ulcers
Fresh stool exam
(microscopy)
(oocytes)
(microscopy)
stool; endoscopic
biopsy
Erythromycin 500mg PO QID
for 7days
(DS) PO
replacement (ampicillin if
severe)
for 7days
Quinolones, macrolide
antibiotics
Intravenous ganciclovir
Metronidazole 750mg PO TID
for 10days, then dilodohydroxyguinine 650mg PO TID for
20days
Hydration, nutritional support
(spiramycin)
Mitronidazole 250mg PO TID
for 7days
Trimethoprim- sulfamethoxazole
(double strength) PO BID for
7days
R. Arsalani-Zadeh et al.
longer recommended as a second antimicrobial
treatment regimen. Treatment does not differ in
HIV-positive patients [1, 9].
Routine follow-up is not necessary after treatment for gonorrhea, as therapy is usually effective. In the case of recurrent symptoms, a full
history regarding compliance and re-exposure
should be obtained and the patient should be reexamined. Suspected treatment failures rst
should be retreated routinely with the recommended as reinfections are more likely than
actual treatment failures. If treatment failure is
highly suspected, specimens should be obtained
for culture (preferably with simultaneous NAAT)
and antimicrobial susceptibility testing performed before retreatment. Dual treatment with
single doses of oral gemioxacin 320 mg plus
oral azithromycin 2g or dual treatment with sin-
27 Sexually Transmitted andInfectious Diarrheal Diseases
499
Fig. 27.2 Perianal LGV ulcer. With permission from
[20] © Springer International Publishing AG 2018
Fig. 27.1 The mucopurulent discharge of gonorrheal
proctitis
gle doses of intramuscular gentamicin 240 mg
plus oral azithromycin 2g can be considered.
A test-of-cure at relevant clinical sites should be
obtained 7–14days after retreatment.
Patient with urethritis are recommended to
abstain from sexual activity for 7days. There is
no specic recommendation with regards to
gonococcal proctitis. Clinicians should ensure
that the patient’s sex partners from the preceding
60days are evaluated promptly with culture and
presumptively treated using the same regimen
used for the patient [9].
Chlamydia Trachomatis: Lymphogranuloma Venereum (LGV)
Chlamydia infection is the most common sexually transmitted bacterial infection in the world,
with an estimated 50 million new cases occurring
each year. In the United States chlamydia is
also the most frequently reported bacterial STI
with an annual incidence of 1.4 million [16].
Chlamydia is more common in young men
and women. Pelvic inammatory disease and
infertility are signicant sequelae of chlamydialinfection in women. About 20% of women will
be infertile as a result of chlamydial infection [9].
Chlamydia trachomatis is an obligate intracellular organism. The incubation period of chlamydial infection is between 5 to 14 days.
Chlamydia proctitis typically occurs within
10 days of penetrating anal sexual contact and
may co-exist with other STIs, especially gonorrhea. Prevalence of anorectal Chlamydia tracho-
matis has been reported to be as high as 24.4%
among men who have sex with men (MSM) and
17.5% among women [17–19]. A large proportion
of patients (43% of males and 79% of females)
with chlamydial infection are asymptomatic.
Symptoms of patient with chlamydial infection vary depending on the serotype involved. Of
the 15 known serotypes of Chlamydia trachoma-
tis, serotypes D through K are responsible for
proctitis, and serotypes L1, L2, and L3 are
responsible for LGV.Patients with serotypes L1–
L3 generally have a much more aggressive proctitis with perianal, anal and rectal ulceration,
which may be difcult to distinguish from Crohn’s
disease (Fig.27.2). Patients who remain untreated
may develop perirectal abscesses, rectal strictures
and/or rectovaginal stulas [12, 21]. Non-LGV
proctitis presents with pain, tenesmus, fever, and
an erythematous rectal mucosa but rarely with
mucosal ulcerations. The inguinal nodes may be
enlarged and matted. LGV patients also have
pain and tenesmus, but with associated mucosal
and perianal ulcerations and a more pronounced
friability resembling Crohn’s proctitis. The inguinal lymphadenopathy plays an important role in
differentiating LGV from Crohn’s disease. The
nodes may fuse into large, indurated masses with
overlying erythema producing a clinical picture
similar to syphilis. Chronic inammation of the
nodes may result in lymphedema. If untreated,
500
R. Arsalani-Zadeh et al.
the disease may progress to ulcerations,
rectovaginal or rectovesical stulae, abscesses,
and late rectal strictures.
Sigmoidoscopy in the non-LGV cases usually
shows a mild inammation of the distal rectal
mucosa and anal crypts, whereas in LGV a more
severe nonspecic granular proctitis is seen. The
mucosa is erythematous, friable, and ulcerated.
Biopsy of the inamed rectal mucosa should be
transported in sucrose phosphate media on ice for
immediate tissue culture inoculation. Because
chlamydia is an obligate intracellular pathogen,
culture is usually unrewarding. Antichlamydial
antibody titers are measured by complement xation and should be 1:80 or greater in order establish the diagnosis. Unfortunately, the titer
elevation often occurs more than 1month after
infection. The most sensitive serotyping test, the
immunouorescent antibody titer, is not universally available. NAAT has better sensitivity and
specicity compared with cultures and is the
diagnostic test of choice [22]. Treatment of chlamydial infection depends on the serotype.
Patients with non-LGV proctitis should be treated
with either azithromycin 1g orally once or doxycycline 100 mg twice daily for 21 days. NonRCTs for rectal C. trachmotatis raised some
concern about the efcacy of azithromycin and
recommend the development of a RCT between
doxycycline and azithromycin specically for
rectal infections [8]. A recently published randomized trial has shown the efcacy of azithromycin is 97% vs. 100% for doxycycline. The
non-inferiority of azithromycin in the setting of
directly observed treatment was not established
[23]. Persons treated for chlamydia should
abstain from sexual activity for 7days after single dose therapy or after 7days of therapy. All the
sexual partners of the person during 60days preceding the onset of symptoms should be referred
and treated for presumed chlamydia infection.
Treatment of LGV includes aspiration or incision of the lymph nodes to prevent scarring and
21-day course of doxycycline 100mg twice daily
[9]. Treatment of symptomatic strictures should
initially include a 3-week course of appropriate
antibiotics. Treatment of strictures is often complicated because these strictures may be multiple
and of varying segments. A proximal diversion or
sphincter-saving excisional surgery may be the
only options for treatment failures [24].
Chancroid
Chancroid is caused by Haemophilus ducreyi, a
short gram-negative, nonmotile, aerobic bacillus.
This disease had been rarely encountered in developed countries. It has become more and more
infrequently reported in the United States with
only 6 cases reported in 2014 [12]. The incidence
is usually low in women, except in high-risk
groups such as prostitutes. The incubation period
is 1–5days. The disease is characterized by, multiple perianal abscesses, tender genital or anorectal
ulcers, and inguinal adenopathy that are usually
unilateral, painful, tender, and may suppurate.
The diagnosis of chancroid is difcult. A
recent study during an outbreak of chancroid in
New Orleans demonstrated that only on third of
patients present with the classic clinical ndings
[10]. Gram stain of ulcer exudates is only sensitive in 40–60% of cases, and culturing H. ducreyi
requires a special media that is not readily available [9]. There is no FDA-approved PCR test, but
it is available in some commercial laboratories.
The CDC considers chancroid to be the probable
diagnosis when the following criteria are met: a
patient has more than one painful genital ulcer,
no evidence of T. pallidum infection by dark eld
examination of the ulcer exudate or by a serologic test for syphilis performed at least 7days
after appearance of ulcers, and the absence of
HSV from the ulcer exudate [9].
The CDC recommends the following treatment for chancroid: azithromycin 1 g for one
dose, ceftriaxone 250mg intramuscularly for one
dose, ciprooxacin 500mg twice daily for 3days
or erythromycin 500 mg four times a day
for 7 days [9]. Antibiotic susceptibility of this
organism is unpredictable. Generally, response is
seen in 3days, with resolution of the ulcers by
day seven. However, uncircumcised individuals
or HIV positive cases typically do not respond as
rapidly. If clinical improvement is not seen after
the initial course of therapy, an alternative antibiotic should be administered. Resolution of adenopathy usually lags behind that of the ulcers.
27 Sexually Transmitted andInfectious Diarrheal Diseases
501
Granuloma Inguinale
Granuloma inguinale, also known as donovanosis, is believed to be caused by Calymmatobacterium
granulomatis, a gram-negative encapsulated
bacillus. It is rarely encountered in the United
States, but is seen more commonly in tropical climates, such as Papua New Guinea, South Africa,
India, Brazil and within the Aboriginal community in Australia. It is chronic and progressive,
transmitted by sexual and nonsexual trauma to
genital, anal, and inguinal tissues. It requires
repeated exposures in order to be transmitted. The
incubation period is from a few days to months.
Beginning as a small, innocuous papule, the
lesion progresses with four subtypes: ulcerogranulomatous variant with ulceration and slow progression to a rather orid, beefy-red granulation
tissue; hypertrophic or verrucous ulcers; necrotic
lesions or dry sclerotic ulcers with associated
brosis and scar formation. Scarring may lead to
signicant stenosis of the anorectum. Diagnosis
is conrmed by biopsy demonstrating the typical
Donovan bodies in large mononuclear cells.
Tissue should be crushed between glass slides
and stained with Wright-Giemsa stain. In addition, PCR techniques are now available.
The most recent CDC recommendation is
azithromycin 1g orally, 1g orally once per week
or 500mg daily for at least 3weeks. Alternative
regimens include doxycycline 100 mg twice a
day for 3weeks, trimethoprim-sulfamethoxazole
one double-strength (160 mg/800 mg) tablet
orally twice a day for at least 3weeks, ciprooxacin 750mg orally twice a day for at least 3weeks
or erythromycin base 500mg orally four times a
day for at least 3weeks [9]. Treatment should be
continued and patient should be followed up until
signs and symptoms have resolved. The disease
is autoinoculable and may spread if surgical excision is mistakenly undertaken. Relapse can occur
up to 18months after treatment.
Syphilis
Primary anal syphilis is largely a disease of
homosexual men. Caused by the spirochete
Treponema pallidum, syphilis can present in the
primary form (chancre or proctitis), secondary
stage (condyloma lata), or tertiary form (gumma).
The national rate of primary and secondary syphilis cases in 200 and 2001 was 2.1 cases per
10,000 population, which is the lowest rate since
the beginning of reporting in 1941.The incidence
of syphilis however has increased almost every
year since 2000–2001 with a total of 19,999
syphilis cases reported in 2014 [12].
The organism enters the anus during anal
intercourse causing ulcers within 2–10 weeks.
However, the incubation period can be as long as
6months. In 10–20% of cases the primary chancre may be hidden within the anal canal. It often
begins as a trivial-appearing maculopapular
lesion that soon ulcerates and may be mistaken
for a common anal ssure. Unlike the classic
painless chancre, which appears on the genitalia,
chancres in the anal canal are usually painful.
Certain features should help to distinguish these
lesions from idiopathic anal ssures including
location off the midline, peripheral placement on
the perianal skin, or location proximal to the dentate line. In addition, these lesions are often irregular (Fig. 27.3a), multiple, and appear opposite
each other in a “mirror image” or “kissing” conguration. Proctitis in the absence of anogenital
lesions has been reported. Unilateral or bilateral
inguinal adenopathy may confuse the diagnosis
with lymphoma, which may also present with
rubbery adenopathy and submucosal rectal
irregularities.
If untreated, the lesion usually regresses spontaneously in 4–8weeks. Secondary lesions may
develop 2–12weeks later. Secondary syphilis can
present with systemic symptoms such as fever,
malaise, arthralgia, sore throat and headache. A
diffuse red maculopapular rash, classically on the
palms of the hands and soles of the feet, has histopathological features of hyperkeratosis of the
epidermis, capillary proliferation, and transmigration of polymorph nuclear leukocytes. The
spirochete may be found in the aqueous humor of
the eye and cerebrospinal uid.
Secondary syphilis can also present as pale
brown or pink, at verrucous lesion called condyloma latum (Fig. 27.3b). Many smooth, raised
warts may coalesce and secrete mucus causing
pruritus and a foul odor. Spirochetes can be demonstrated on dark eld examination as
502
R. Arsalani-Zadeh et al.
a
b
Fig. 27.3 Anal syphilis. (a) Primary anal chancre. (b)
Condyloma latum
ally becomes positive 4–6weeks after infection
and remains positive for life. Titers do not correlate with disease activity. Serological tests in
most HIV-infected patients are accurate and reliable for the diagnosis of syphilis. Dark eld
examination and direct uorescent antibody tests
of tissue or exudate from the lesion are considered to be the denitive tests.
The treatment is a single dose of long-acting
benzathine penicillin (Bicillin, Wyeth
Pharmaceutical, Philadelphia, PA), 2.4 million
units, given intramuscularly. There is no strong
evidence to support prolonged or augmented
therapy in treating syphilis in patients who are
HIV positive [1, 25]. Erythromycin or tetracycline can be used in penicillin-allergic patients.
All sexual contacts within 90days of the diagnosis of the index case should be prophylactically
treated and patients must abstain from all sexual
activity until proven noninfectious by low titers.
Follow-up testing with VDRL or RPR should be
done at 3-month intervals for 1year. As the spirochetes are destroyed, patients may manifest fever,
skin lesions, arthralgia, and adenopathy known
collectively as the Jarisch-Hexheimer reaction.
This is self-limiting and best treated with
analgesics.
corkscrew-shaped, motile, uorescent, yellowgreen organisms. Biopsy of rectal lesions may
show spirochetes on Warthin-Starry silver stain.
Both primary and secondary lesions are
infectious.
Tertiary syphilis is rare in developed countries.
Tertiary lesions are caused by obliterative small
vessel arteritis and can affect the cardiovascular
or central nervous systems and cause syphilitic
renal or hepatic dysfunction. Although rarely seen
in the United States, tabes dorsalis can produce
anal sphincter paralysis and severe perianal pain.
Of patients with anal syphilis, one third proceed
to spontaneous cure, one third have latent disease,
and one-third progress to late or tertiary disease.
In untreated primary syphilis, the Venereal
Disease Research Laboratory (VDRL) assay is
reactive in about 75% of cases. In the secondary
stage, 100% should react. The uorescent treponemal antibody absorption test (FTA-ABS) usu-
Viral Infections
Herpes Simplex
Herpes simplex type I and II are very common
STIs in the United States. The majority of anorectal herpes infections are caused by HSV-2, with
only 10% caused by HSV-1 [26]. Seropositivity
rate for HSV 2 decreased between 1988–1994
and 2007–2010, from 21.2% to 15.5%. However,
the prevalence of HSV-I is increasing especially
among young women and MSMs [9]. Serologic
tests indicate that more than 95% of male homosexual patients may have been infected with herpes simplex virus type 2 (HSV-2).
Transmission occurs through autoinoculation
or direct contact with an infected person. In the
normal human, only mucocutaneous sites and the
neuronal nuclei of sensory ganglion are affected.
After local inoculation, the virus is transported
27 Sexually Transmitted andInfectious Diarrheal Diseases
503
along peripheral nerves to the neuron’s nucleus.
The viral invasion of neurons leads to a latency
state [27].
A primary infection may cause an initial tingling sensation at the viral entry point with subsequent eruption of one or more pruritic vesicles
in a cluster on any mucous membrane surface or
skin area within 24 h. The normal incubation
period averages 6days. Cell-mediated responses
appear to be important in controlling the severity
of mucocutaneous outbreaks of the virus, which
explains the severity of HSV infections in HIVpositive patients. The majority of patients with
genital herpes however do not report classic
symptoms of infection [28]. Prior infection with
HSV in any site modies the clinical manifestations of subsequent exposures, which is usually
most severe at the time of initial infection. The
risk of recurrence after primary infection with
genital herpes is greater than 80% and may be
frequent despite high antibody titers.
HSV is the second most common STI affecting the anorectal area. HSV infection may begin
4–21 days after anorectal intercourse. The prodromal symptoms may be minor and include
mild local irritation, burning and paresthesia in
the anorectal area. Within a short period of time
the pain becomes increasingly intense. A sacral
root radiculitis, manifested by pain involving the
buttocks, posterior thighs and perineum, together
with constipation, tenesmus, urinary retention,
and temporary impotence is quite characteristic.
The symptoms of radiculopathy and deep pelvic
pain often outlast the active clinical infection
[29]. Anal itching, bleeding, and mucopurulent
anorectal discharge are common symptoms.
Systemic manifestations include fever, chills, and
malaise. Bilateral tender inguinal lymphadenopathy may sometimes occur. Recurrent episodes are
generally milder, lasting 4.5days on average. The
median time to rst recurrence is shorter in
HSV-2 compared to HSV-1, 49 and 330 days
respectively [29]. Nearly all men and 85% of
women will experience recurrent HSV-2 infection within the rst year, with an estimate of continuous 4–5 recurrences annually.
The initial herpetic lesion is a small vesicle surrounded by a red areola, usually scattered or in
clusters in the perianal skin, anal canal, and
perineum. Carefully spreading the buttocks for
inspection may reveal acute lesions ranging from
these small vesicles to larger ruptured vesicles,
which have coalesced (Fig.27.4). Shallow perianal
ulcers may coalesce and extend to the sacrococcygeal region in a buttery distribution [30, 31].
Anoscopy reveals friable epithelium, ulceration, and mucopurulent discharge. Viral culture
of a suspicious vesicle is positive in up to 90% of
clinical HSV-2 infections. Proctoscopy reveals
friable mucosa, diffuse ulcerations, and occasional vesicles and pustules limited to the distal
10cm of the rectum. Ulcerations in the anal canal
may become secondarily infected, and appear as
grayish crypts with erythematous borders.
Crusting of the lesions is followed by healing
within 2weeks.
Presumptive diagnosis is based on the clinical
examination, nding multinucleated giant cells
with intranuclear inclusion bodies in Papanicolaou
Fig. 27.4 Perianal herpes simplex virus