Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1520_Библиотеки_им_академика_М_И_Перельмана
.pdf
98
B.P. Goorney
8.2 General Principles
Anorectal STIs in common with their genital counterparts share a number of impor-
tant characteristics:
(a) Anorectal STIs are commonly asymptomatic. Rectal gonorrhea is asymptom-
atic in more than two-thirds of cases [ 1 ] . It is estimated that 80% of women and
50% of men carrying Chlamydia are asymptomatic. However, rectal lym-
phogranuloma venereum (LGV) is largely symptomatic [ 2 ] . Around a third of
cases of early syphilis are diagnosed in the asymptomatic early latent stage and
are only identifi ed on routine syphilis serology.
(b) All the above STIs will be detected on routine STI screening as carried out in a
sexual health clinic, irrespective of the presence or absence of symptoms. In con-
trast, most anogenital viral STIs (warts and herpes) are carried in a subclinical state,
and as yet there is no screening test for these asymptomatic infections. Diagnosis is
therefore on the appearance of characteristic lesions of these viral infections.
(c) The presence of anorectal symptoms and signs does not always denote trans-
mission via receptive anal sex, and such assumptions should not be made until
a full sexual history is taken (Box 8.1 ). Alternative explanations for anorectal
involvement by STIs are hematogenous spread of disease to involve the anorec-
tum, i.e., secondary syphilis (mucus ulcers, condylomata lata) or local contigu-
ous spread from the genital area, such as genital warts or herpes, in a heterosexual
male, or female.
(d) Multiple STIs commonly coexist. For example, a quarter of patients with gonor-
rhea are coinfected with Chlamydia [ 3 ] , emphasizing the importance of full STI
screen from all sites, depending on sexual history and clinical presentation.
Box 8.1: Sexual History in Relation to Anorectal STIs
1. Is the patient currently sexually active (usually relevant period within pre-
vious 3–6 months)? If so what is their sexuality? MSM, bisexual (increased
risk of anorectal STI)?
2. For males, does he have a current regular male partner? Is he symptomatic?
Or does he have casual partners? If so, when did he last have sex (neces-
sary for partner notifi cation and HIV risk assessment)?
Questions:
1. What is the most likely differential diagnosis?
2. What further investigations are required?
3. What is the subsequent management of his problem?
4. What further associated STI need to be considered?
99
8 Anorectal Sexually Transmitted Infections
8.3 Clinical Presentations
Symptomatic anorectal STIs broadly fall into three categories: acute or subacute
proctitis, perianal ulceration, and condylomatous or warty lesions. In addition to
these, HIV-associated infections and tumors occur, which may also present in any
of these three categories and are best dealt with separately.
8.3.1 Proctitis
The cardinal symptoms are rectal discharge (which can range from mucoid to
frankly purulent), rectal pain, bleeding, constipation or diarrhoea, and pruritus ani.
It is not uncommon that presentation is initially with just one of these symptoms.
(a) Gonorrhoea
Although now less common than Chlamydia, the prevalence of gonorrhoea
remains stable in the general population. Nevertheless, with its short incubation
period (2–5 days), it remains the most reliable surrogate marker of anoreceptive
sex among men who have sex with men (MSM). In women, secondary inocula-
tion from contaminated secretions from the genital tract to rectum can occur.
The presentation is usually as a nonulcerative, predominantly purulent rectal
discharge in addition to pruritus ani. Around 1–2% of patients may have dis-
seminated infection, leading to bacteremia and septic arthritis. The diagnosis is
confi rmed by rectal Gram-stained smear and culture. As antibiotic resistance is
common, treatment is based on antibiotic sensitivities, with a single dose of
intramuscular Ceftriaxone (500mg) usually as fi rst-line choice. A test of cure
swab can be offered at 1–2 weeks post–initial treatment.
(b) Chlamydia trachomatis (Serovars D-K)
Chlamydia is now the commonest bacterial STI in the UK, and while the major-
ity of cases are asymptomatic, it is one of the commonest causes of proctitis in
3. If patient admits anal sex, is it receptive, insertive, or both (indicates poten-
tial sites of infection)? Also, enquire about oro-anal sex (rimming) – risk
of enteric infections.
4. Are condoms used consistently? (Consistent and correct condom use will
preclude most STIs, except extragenital warts or herpes).
5. Any unusual sexual practices, e.g., fi sting or use of sex toys (associated
with increased risk of HIV, hepatitis C, syphilis, and LGV)?
6. Use of recreational drugs, e.g., poppers (nitrates)? (can be associated with
above practices).
7. Any recent travel abroad? If so, where? Africa and Southeast Asia have
high rates of HIV, syphilis, and hepatitis B.
100
B.P. Goorney
MSM [ 4 ] . The incubation period is around 10–14 days following exposure, but
the earliest it can be diagnosed using nucleic acid amplifi cation technique test
(NAAT) is around 5–7 days.
Multiple anatomical sites may be infected, i.e., pharynx and urethra if both
insertive and receptive anal sex as well as orogenital contact has taken place.
Symptoms and signs of nonspecifi c urethritis (NSU) may also be present, i.e.,
urethral discharge and dysuria. The diagnosis is based on rectal samples tested
by NAAT. Treatment is either by oral doxycycline 100 mg twice daily, for
1 week, or a single dose of azithromycin, 1 g orally. A test of cure swab may be
taken 1/12 after completion of treatment as microbiological cure rates may be
less with azithromycin [
5 ] .
There are no long-term sequelae of rectal Chlamydia infection; this is in
contrast to LGV caused by Chlamydia trachomatis serovars L1-L3, an increas-
ingly common cause of proctitis in MSM since fi rst cases were identifi ed in
Netherlands in 2004 [ 6 ] .
(c) Lymphogranuloma venereum
There is a strong association between being HIV positive and use of sexual aids
such as “toys” and “anal fi sting” with possible transmission via such methods. The
clinical presentation is usually more severe than non-LGV-associated Chlamydia,
with rectal pain a prominent symptom and a less distinct incubation period.
LGV was originally described as a tropical genital ulcer disease with enlarged
suppurating lymph nodes (buboes). Rarely, these features may also be present
with the “anorectal variant.” LGV has similarities with Crohn’s disease, both
clinically (i.e., rectal stricture, perforation, and fi stulae) and histologically (non-
caseating granulomas, cryptitis especially in untreated LGV proctocolitis) [ 7 ] .
The diagnosis is based on NAAT for Chlamydia on rectal swabs. If positive,
a DNA probe is used to identify L1-L3 serovars. A positive result confi rms the
diagnosis of LGV. Specifi c serology is helpful in selected cases where a swab
was not taken, or the patient has already received antichlamydial antibiotics.
A titer of >1:64 is suggestive of recent infection [ 8, 9 ] .
Management of LGV is as for uncomplicated chlamydia except that a 3-week
course of doxycycline is required or a 5-day course of azithromycin. Complete
cure can be expected in uncomplicated cases, and a test of cure swab is normally
taken 4 weeks following completion of therapy. Because of strong association,
HIV testing should always be offered when LGV is diagnosed.
(d) Nonspecifi c Proctitis ( NSP )
Nonspecifi c proctitis is analogous to NSU in men, and amounts to the presence
of microscopic evidence of proctitis (>10 white cells per high-power fi eld) in
addition to symptoms of proctitis, but in the absence of any other microbial
agent. Symptoms are usually mild, and treatment is the same as for uncompli-
cated chlamydial infection. Although it is uncertain if NSP is always sexually
transmissible (similar to NSU), contact tracing and treatment of recent partners,
in common with all the above infections, are carried out.
(e) Syphilis and Herpes
Syphilis and herpes may also cause an ulcerative proctitis (see below).
101
8 Anorectal Sexually Transmitted Infections
8.3.2 Anorectal Ulceration
The commonest causes of anorectal ulceration are:
(a) Herpes
Herpes simplex type 1 and 2 are the commonest cause of anogenital ulceration
in UK. Compared to other STIs, the incidence has remained stable until recently
[ 10 ] . Herpes has a tendency to establish latency in the dorsal root ganglia of the
lumbosacral plexus and to reactivate sporadically, resulting in clinical recur-
rence. It remains one of the most troublesome viral STIs which can result in
signifi cant psychosexual morbidity.
In the anorectal area, herpes may present as an acute fi rst attack, either
from direct inoculation of the virus during anal sex, or secondary contiguous
spread from genital lesions. The evolution of lesions is characteristically from
initial erythema to clusters of small vesicles (Fig. 8.1 ), which then form mul-
tiple shallow, painful ulcers around the anal area, which may extend into the
rectum causing severe “ulcerative proctitis.” During a primary episode, there
may be systemic symptoms due to viremia, with associated myalgia and
radicular leg pain. Complications include acute retention of urine or loss of
bowel function due to involvement of the autonomic plexus. Secondary bacte-
rial infection is common in perianal herpes. The lesions normally heal within
2–3 weeks; however, prompt treatment with antiviral agents will usually pro-
duce earlier resolution.
The diagnosis is confi rmed by direct viral polymerase chain reaction testing
on swabs taken from an ulcer or vesicle prior to commencement of acyclovir.
Subsequent recurrences are usually less severe and self-limiting in nature,
requiring antiviral treatment only if symptoms are troublesome. Persistent or
aggressive herpes should always prompt HIV testing, especially in MSM.
Fig. 8.1 Clusters of vesicles
due to perianal herpes
102
B.P. Goorney
(b) Syphilis
Primary syphilis : In early syphilis, the primary stage may present with an “anal
chancre” described as a painless solitary ulcer on the anal verge, often less charac-
teristic morphologically than genital lesions, and may be confused with an anal
fi ssure (Fig. 8.2 ). The diagnosis is confi rmed by either direct dark fi eld microscopy
of an ulcer sample or NAAT identifi cation. Reactive syphilis serology with raised
rapid plasma reagin titers (RPR) helps confi rm the diagnosis further, although this
can be negative (25%) in early stages of the disease, and clinical suspicion should
prompt repeat serology to cover the seroconversion window period of 3 months.
Left untreated, the chancre will heal in a matter of weeks, and the infection
will progress over 6–12 weeks to secondary syphilis.
Secondary syphilis : During this phase of “spirochetemia,” lesions may appear in
the perianal area, with mucus ulcers or patches that may also appear on the geni-
tal area or oral cavity and are usually painless. As in primary syphilis, direct
treponemal identifi cation from these lesions and positive syphilis serology with
strongly positive RPR will confi rm the diagnosis. Contaminating rectal spiro-
chetes may be mistaken for T . pallidum on dark ground microscopy.
HIV and syphilis coinfection is common [ 11 ] and may result in more atypical
and aggressive forms of syphilis [ 12 ] as well as increasing the risk of transmis-
sion of HIV via ulcerative anogenital lesions. Enlarged, asymmetric inguinal
lymphadenopathy may be present in primary syphilis and is often generalized in
the secondary stages of the disease.
Late syphilis : Gummas of tertiary syphilis are less common now in the post-
penicillin era, but these granulomatous ulcers may present in gastrointestinal
tract with rectal ulceration and are normally confi rmed by biopsy and demon-
stration of Treponema pallidum on Warthin-Starry silver staining. Syphilis serol-
ogy will be positive.
(c) Tropical Ulcer Disease ( Buboes )
These rare primarily painful inguinogenital ulcerative conditions caused by LGV
(see above), chancroid ( H . ducreyi ), and granuloma inguinale (donovanosis) and
are usually seen in association with sexual contact from sub-Saharan Africa as a
Fig. 8.2 Chancre of primary
syphilis on anal verge
103
8 Anorectal Sexually Transmitted Infections
result of heterosexual transmission. Large suppurating unilateral inguinal lymph
nodes (buboes) may mimic a bacterial inguinal abscess.
8.3.3 Anal Warts and Condylomata
(a) Early Syphilis
Condylomata lata (Fig. 8.3 ) may appear during the secondary stage of dissemi-
nated infection. These are papular skin lesions resembling perianal warts or skin
tags but which contain spirochetes and may cause anal discharge. Diagnosis is
as described for secondary syphilis (see above).
(b) Anogenital Warts
Anogenital warts are often symptomless but may present with pruritus ani, pain,
bleeding, and anal discharge if they become necrotic. They are highly prevalent
because of low-risk HPV infection type 6 and 11 and can occur in both hetero-
sexual males and females as result of secondary contamination from the genital
tract. In most MSM, genital warts are transmitted via anoreceptive sex.
Morphologically, they are mostly perianal fl eshy, moist, condylomatous pap-
ules. Around a third of men have warts extending into the anal canal and rectum
[ 13 ] , which are visualized and treated via a proctoscope.
Treatment of anal warts is either with topical creams such as podophyllotoxin
or imiquimod, or by ablative therapies, such as cryotherapy and electrocautery.
Extensive caulifl ower-like growths are best treated with surgical excision
(Fig. 8.4 ). Recurrence rate is high following clearance, especially in immuno-
compromised patients. There is now available a quadrivalent vaccine (Gardasil)
protective against both high-risk HPV 16 and 18, associated with anal cancer,
and low-risk anogenital warts. However, it is licensed as a primary vaccine only,
i.e., with no prior exposure to HPV, and not intended as a therapeutic vaccine.
Fig. 8.3 Condylomata lata of
secondary syphilis
104
B.P. Goorney
In HIV coinfection, persistent anal warts should be referred for biopsy to exclude
anal cancer, as the risk is increased twofold compared with HIV-negative MSM
[ 14 ] . Anal warts are commonly misdiagnosed as fi broepithelial skin tags, exter-
nal hemorrhoids, and perianal hematomas.
8.4 HIV Infection
HIV infection may coexist with all the above conditions and is independently asso-
ciated with STIs such as early syphilis and LGV [ 15 ] . There is a wide range of
indicator conditions for HIV which affect the GI tract and that may present with
anorectal symptoms (Box 8.2 ). These consist of either opportunistic infections or
tumors as a result of declining immune function, such as Kaposi’s sarcoma (Fig. 8.5 ),
which can present as a rectal lesion, causing bleeding and pain.
Fig. 8.4 Giant condylomata
requiring excision
105
8 Anorectal Sexually Transmitted Infections
As a result of the success of treatment with highly active antiretroviral therapy
(HAART), HIV is now regarded as a controllable chronic disease. Routine HIV
testing is clinically indicated for the above conditions (Box 8.2 ) without need for
lengthy counseling [ 16 ] . Advice on testing can be sought from local sexual health
clinics, with prompt referral required if HIV test result is positive.
Fig. 8.5 Cutaneous Kaposi’s
sarcoma presenting in
HIV-positive patient
Key Points
Consideration as to whether anorectal symptoms could be due to STIs •
based on a sexual history taken in a nonjudgmental and sensitive manner.
Establish involvement of anorectum, perianal area in addition to genital •
and inguinal involvement.
Consider common syndromic causes: herpes/syphilis for ulcers, viral warts/con-•
dylomata lata for warty lesions, and gonorrhoea/chlamydia/LGV for proctitis.
Be aware of potential similarity between infl ammatory bowel disease and •
certain STI, i.e., Crohn’s and LGV proctitis.
Box 8.2: Anorectal Conditions Which are Clinical Indicators of HIV
Infection
Proctitis Anorectal ulceration
Condylomata/
masses
Cytomegalovirus Cytomegalovirus
Anal cancer
Specifi c enteropathogens, i.e.,
Salmonella , Shigella , Entamoeba
Idiopathic HIV ulceration Condylomata
accuminata
(viral warts)
Atypical mycobacteria, cryptosporidi-
osis, isosporiasis, microsporidia
Non-Hodgkin’s
lymphoma
Kaposi’s sarcoma
106
B.P. Goorney
Always consider underlying HIV coinfection, and encourage testing on •
clinical grounds with informed consent.
Seek advice and consider early referral to sexual health clinics for appropriate •
swabs and serological tests, even if to exclude potential anorectal infections.
Case Scenario Answers
1. The most likely diagnosis is an infective proctitis, caused by an STI, as sug-
gested from the sexual history (see Box 8.1 ). The commonest infective causes
of proctitis seen in UK are gonorrhoea, Chlamydia (strains D-K), lym-
phogranuloma venereum, herpes simplex, and nonspecifi c proctitis. In addi-
tion in HIV positive individuals, the differential diagnosis widens to involve
additional causes (see Table 8.2 ), caused by opportunistic infections such as
Cytomegalovirus. The clinical presentation is suggestive of either anorectal
LGV, Chlamydia (non-LGV), or possibly gonococcal proctitis: the former
seems most likely given the sexual history, with rectal pain a prominent
symptom, and the duration of symptoms. The lack of visible ulceration makes
herpetic or syphilitic proctitis unlikely. The relatively long incubation period
(4 weeks after suspected sexual exposure) makes gonorrhea less likely.
2. As with most STIs the diagnosis cannot be made entirely on clinical grounds,
and several STIs may co-exist as with genital tract infection in general. These
must be confi rmed with appropriate microbiological, virological, and serologi-
cal tests. Referral to a sexual health clinic would be appropriate at this stage for
full STI swabs including from urethra and pharynx. Rectal swabs are taken via
a proctoscope for gonorrhoeal identifi cation. In many cases immediate micros-
copy will give a provisional diagnosis pending culture confi rmation. Chlamydia
rectal swabs will be tested for LGV if positive. In cases where all tests returned
are negative but microscopy of rectal swab indicates microscopic proctitis
(>10 white cells per high-power fi eld) then a diagnosis of “nonspecifi c procti-
tis” can be made, analogous to nonspecifi c urethritis in men.
3. LGV is the most likely diagnosis if rectal smear and culture are negative
for Neisseria gonorrhoea , and are positive for Chlamydia with L1-L3
DNA detected in the rectal sample. Normally treatment is commenced
prior to a positive Chlamydia swab being received and treatment is assumed
to be for LGV with fi rst-line antibiotic therapy (see 1,c above). In addition
to clinical resolution of symptoms a further test of cure (rectal Chlamydia
swab) should be performed not less than a month after completing therapy,
as nonviable organisms may still be detectable by highly sensitive NAAT
tests currently used.
4. All patients in “high-risk groups” such as MSM should be offered HIV
testing; this can be carried out outside of a conventional sexual health
clinic, in this case on clinical grounds. HIV positivity is strongly associated
107
8 Anorectal Sexually Transmitted Infections
References
1. Robertson DHH, McMillan A, Young H. Gonorrhoea: clinical features and treatment. In:
Clinical practice in sexually transmissible diseases, 2nd edn. Edinburgh: Churchill and
Livingstone; 1989. Ch 16: p. 215.
2. Tinmouth J, Gilmour MW, Kovacs S, et al. Sub-clinical LGV and non-LGV chlamydia infec-
tion in MSM. Int J STD AIDS. 2008;19:805–9.
3. Creighton S, Tenant-Flowers M, Taylor CB, et al. Co-infection with gonorrhoea and Chlamydia:
how much is there and what does it mean? Int J STD AIDS. 2003;14:109–13.
4. Manavi K, Mcmillan A, Young H. The prevalence of rectal Chlamydia infection amongst men
who have sex with men attending the genitourinary medicine clinic in Edinburgh. Int J STD
AIDS. 2004;15:162–4.
5. Steedman NM, McMillan A. Treatment of asymptomatic rectal Chlamydia trachomatis:is
single dose azithromycin effective? Int J STD AIDS. 2009;20:16–8.
6. Niewenhuis RF, Ossewaarde JM, Gotz HM, et al. Resurgence of lymphogranuloma venereum
in Western Europe: an outbreak of Chlamydia trachomatis serovar L2 proctitis in the
Netherlands among men who have sex with men. Clin Infects Dis. 2004;39:996–1003.
7. Mabey D, Peeling RW. Lymphogranuloma venereum. Sex Transm Infect. 2002;78:90–2.
8. Forrester B, Pawade S, Horner P. The potential role of serology in diagnosing chronic lym-
phogranuloma venereum (LGV): a case of LGV mimicking Crohn’s disease. Sex Transm
Infect. 2006;82:139–40.
9. Martin IM, Alexander SA, Ison CA, Macdonald N, et al. Diagnosis of lymphogranuloma
venereum from biopsy samples. Gut. 2006;55:1522–3.
10. Bruhga R, Keersmaekers K, Renton A, Meheus A. Geniral Herpes infection: a review. Int J
Epidemiol. 1997;26(4):698–709.
11. Higgins SP, Sukthankar A, Mahto N, Jarvis R, Lacey H. Syphilis increases in Manchester, UK.
Lancet. 2000;355(9213):1466.
12. Hutchinson CM, Hook EW, Shepherd M, et al. Clinical syphilis in patients with HIV infection.
Ann Intern Med. 1994;121:94–100.
13. Goorney BP, Waugh MA, Clarke J. Anal warts in heterosexual men. Genitourin Med.
1987;63:216.
14. Goedert JJ. The epidemiology of acquired immunodefi ciency syndrome malignancies. Semin
Oncol. 2000;27:390–401.
15. Health Proitection Agency report. Syphilis and lymphogranuloma venereum: resurgent STIs in
UK. 2009.
www.hpa.org.uk/Topics/Infectious.Diseases./Infections.AZ/LGV/. Accessed Nov 2010.
16. BHIVA guidelines on HIV testing.UK guidelines for HIV testing. 2008.
http://www.bhiva.org/
documents/Guidelines/Testing/GlinesHIVTest08.pdf
. Accessed Nov 2010
with LGV infection. Other associated STIs are Hepatitis C and early syphi-
lis. Rectal mucosal trauma from activities such as “fi sting” and use of sex
toys can enhances the transmission of these infections. Although infl am-
matory bowel disease may present in a similar manner, or indeed in co-
existance with anorectal STI, it is imperative to exclude STI fi rst.
The similarity between LGV and Crohn’s disease is striking both clinically
and histologically. The consequences using steroids or other immunosuppres-
sives in a patient with undiagnosed LGV co-infected with HIV could be
catastrophic.
Соседние файлы в папке Библиотека им академика М.И. Перельмана