GONOCOCCAL URETHRITIS

Gonococcal urethritis, the most extensively studied sexually transmitted disease over the last 20
years, reached a peak incidence in 1975 and is now declining in frequency, while the incidence of
nongonococcal urethtritis is rising.
On the gram-stained smear of urethral scrapings, Neisseria gonorrhoeae are gram-negative
diplococcus within the neurophils. The intracellular diplococcus causes neutrophil, lymphocyte, and
plasma cell infiltration.
Concurrent infections with Chlamydia and other organisms are common. The urethra is the most
common site of infection in all men. In heterosexual men, the pharynx is infected in 7%, and in
homosexual men, the pharynx is infected in 40% and the rectum in 25% (Handshield et al, 1980). A
single episode of intercourse with an infected female partner carries a transmission risk of 17 – 20% for
the male; however, the female partner of an infected male will contract the disease about 80% of the
time (Harrison, 1984; Thin Williams, and Nicol, 1971).

Clinical Findings
A. Symptoms: In males, the usual symptoms of gonorrhea are urethral discharge and dysuria. There
may be only urethral itching. The usual incubation period is 3 – 7 weeks, with 95% of men
becoming asymptomatic after 3 months. Gonococcal urethritis with known gonorrhea (Harisson,
1984). Complications such as involvement of the prostate may lead to urinary frequency,
urgency, and nocturia. Spread down the vas deferens to the epididymis lead to acute
epididymitis.
B. Signs: The discharge with gonococcal urethritis is usually yellow or brown. There may be meatal
edema and erythema. The pendulous urethra may exhibit tenderness. Inspect the pharynx and
rectum if by history, there was contact in those regions. Anoscopy will show easy bleeding from
rectal mucosa and pus with proctitis. Pharyngeal infections are often asymptomatic.
C. Laboratory Findings: The patient is best examined 1 hour, preferably 4 hours, after last voiding,
so that discharge will not be washed away (Fig 15 - 1). A calcium alginate swab is then inserted
2 – 3 cm into the urethra and rotated gently. Do not use cotton-tipped swabs, as they are
bactericidal. The swab is then rolled onto a slide for gram staining, and the swab is plated
immediately onto a culture medium or placed in a transport medium. The gram-stained smear
should show evidence of urethritis, with 4 or more leukocytes per high-power field (magnification
x 400). Cultures of pharyngeal and rectal scrapings are required if there is a history of oral rectal
intercourse.
Do not swab the anal epithelium but instead obtain a swab from the rectal mucosa by
anoscopy. A gram-stained smear positive if gram-negative diplococcic are seen. The examination
is equivocal if diplococcic are only extracellular or if they are intracellular but atypical. The
specificity of a gram-stained smear in gonococcal urethritis is 95%. The sensitivity is nearly 100%
in urethritis and 60% rectal gonorrhea. Although cultures are not always necessary for diagnosis,
they should be obtained to determine antibiotic sensitivities, especially in populations with a high
percentage of resistant organisms. Alternative diagnostic methods based on detection of the
gonococcal enzymes, antigens, DNA, and liposachharides are available (Hook and Holmes, 1985).

Differential Diagnosis
The discharge in nongonococcal urethritis is often more and clearer than in gonococcal urethritis;
however, the discharge may appear identical in both diseases. Gram-stained smear of the urethral swab
will show only leukocytes in a male with no nongococcal urethritis.

Complications
Periurethtritis is one of the more common complications and may lead to abcess formation,
urethral fibrosis, and finally, urethral stricture. Prostatitis may develop and may cause perineal pain and
low backache; if this is left untreated, an abcess may occur. Epididymis may occur and could lead to
infertility or testicular atrophy.
Proctitis presents as anal discharge, bleeding, pain, tensmus, or constipation. Anoscopy will
reveal pus and easy bleeding from the mucosal surface. One polymorphonuclear leukocyte or more per
high-power field (magnification x 400) on gram-stained smear is

Suspicion of urethritis

Gram-stained smear of
urethral scrapings

More than 4 MPNs per Less than 4 PMNs per

high-power field high-power field

Examine early morning swab of

eurethral tiossue or first-
voided urine specimen

Positive Negative
ve No
urethritis

Gram-negative Equivocal or No gram-negative

intracellular atypical smear intracellular
diplococci diplococci

Gonococcal Mixed gonococcal and Nongococal

urethritis nongococcal urethritis urethritis

Examine and treat sexual

partners.
Repeat positive cultures at
follow up

consistent with proctitis. Gram-stained smear of the rectal mucosa is 60% sensitive but 100% specific if
intracellular dipococci are seen (Klein et al, 1977). The differential diagnosis includes infection due to
Chlaymydia, herpes simplex virus, and other agents.
 Infection may become disseminated. Fever and leukocytes are uncommon. Small, tender papules
or petechiae may appear on the arms and legs and may quickly develop into pustules, becoming
hemorrhagic or necrotic. Tenosynovitis and arthritis may occur. The knees are more commonly involved
than other joints. Synovial effusion is present in approximately 33% of patients with joint involvement. A
culture for gonococci will be positive if the synovial fluid reveals leukocytes, more than 80,000 al
(Handfield, Wiesner, and Holmes, 1976). Florid monarticular arthritis may require open drainage and
irrigation. Also rarely seen are hepatitis, myocarditis, endocarditis, and manigitis.

Prevention
Condoms, if properly used, will prevent the spread of N gonorrhea. Nonoxynol-9, a vaginal
spermicide, has been shown to kill gonococcus (Jick et al, 1982).It is even more effective if used with a
contraceptive diaphragm (barlow, 1977). Antibiotic prophylaxis may be effective but may lead to selection
of resistant strains (Singh, Cutler, and Utidjian, 1972). Currently, control of gonorrhea depends on case
finding. Contacts, whether symptomatic or not, should be examined, cultured, and treated.

Treatment
The growth of plasmid-mediated beta-lactamase

Because of regional differences in antibiotic susceptibility, no single therapeutic regimen can any
longer be prescribed. The latest WHO (World Health Organization) report gives 2 lists of
recommendations applicable to industrialized countries (Centers for Disease Cintrol, 1982). The Group A
regimen is for areas where resistant strains are more prevalent.
A. Specific Measures: Specific recommendations for antibiotic treatment are listed in Table 15 – 1.
B. General Measures: sexual intercourse should be avoided until cure has been established.
C. Treatment of Complications: The WHO treatment for gonococcal epididymitis is a single dose of
amoxicillin, 3 g given intramuscularly; or aqueous procaine penicillin, 4.8 x 10 6 units given
intramuscularly; plus either tetracycline, 500 mg orally twice a day for 10 days.
The treatment for disseminated gonococcal infection is crystalline penicillin G, 10 million units given
intravenously daily for 3 days or until symptoms improve. Then, amoxicillin, 3 g orally daily, or ampicillin,
3.5 orally daily, is given to complete the 5- to 7-day course.
Urethral strictures require urethral dilations or surgical intervention.
Treatment regimens for rectal and pharyngeal gonorrhea are the same as for uncomplicated
gonococcal infection described above, except that amoxicillin and doxycycline are ineffective (Klein t al,
1977).

Prognosis
Once the infection has been treated properly, the discharge should disappear within 12 hours. In
the 10-35% of patients withn concurrent infection due to Chlamydia who do not receive a 7-day regimen
of tetracycline or doxycycline, there may remain a thin, clear urethral; discharge (postgonococcal
urethritis), which should be treated as a chlamydial infection.
Cure of gonococcal urethritis should be established by gram-stained smear of urethral tissue in
10 days. If the infection has not been cured, spectinomycin is commonly selected; it is not affected by
penicillinase producing microorganisms. The recommended dose is 2 g given intramuscularly once only.
The cure rate is about 95% (Centers for Disease Control, 1982).
Table15 – 1. Current approaches t therapy for uncomplicated gonorrhea and selected complications of gonorrhea.

Type of Gonorrhea Group of Regimist Group B Regimens

Uncomplicated gonorrhea Amoxicillin, 3 g, plus probenecid, 1 g, both orally; or Cetriaxone, 250 mg intramuscularly; or
ampicillin, 3.5 g, plus probenecid, 1 g, both orally; or cefotaxime, 1 g intramuscular, plus
aqueous procaine penicillin G, 4.8 million units probenecid, 1 g orally; or cefoxitin, 2 g
intramuscularly, plus probenecid 1 g orally ( drug of intramuscularly, plus probenecid, 1 g orally; or
choice only for pharyngeal infection or infection in spectomycin, 2 g intramuscularly.
homosexual men); or spectinomycin, 2 g
intramuscularly (recommended for patients allergic to
penicillin or for whom penicillin has failed. )
Gonococcal pelvic inflammatory disease Cefoxcitinand probenecid plus doxycycline Cefoxitin, and probenecidplus doxycycline
(Ambulatory or hospilatized patients); 500 mg 4 (ambulatory or hospitalized patients); or
times a day orally for 10 days, or doxycycline, 100 gentamicin or tobramicin plus clindaycin
mg twice a day orally for 10 days. (hospitalization patients only).
Gonococcal epididymitis Single-dose therapy for gonorrhea as above plus Cefoxitin, 2 g intramuscularly, plus probenecid,
either tetracycline, 500 mg 4 times a day orally for 10 1 g orally, plus doxcycline, 100 mg orally twice
days, or doxycycline, 100 mg twice a day orally 10 a day for 10 days.
days.
Dissiminated gonococcal infection Crystalline penicillin G omproved, then ampicillin to Cefoxcitin, 1 g 4 times a day intravenously for
complete a 7-day course. 7 days; or cefotaxime, 500 mg 4 times a day
intravenously for 7 days, or spectinomycin, 2 g
twice intramuscularly for 7 days.
*Reprocuced, with permission, from Hook EW III, Holmes KK: Gonococcal infections. Ann interm 1985;102:229.
†For use in areas where gonococci have maintained chromosomal sensitivity agents and penicillinase-producing strains of N gonorrhea comprise
less than 1% of isolates.
‡For use in areas where chromosomal resistance to antimicrobial agents in cure rates of less than 95% with group A regimens or where
penicillinase-producing strains of N gonorrhea are prevalent (5% or more than 1% and increasing).
§Add doxycyline, 100 mg twice a day orally, is cheaper and can be substituted when treating compliant patients because of increasing
chromosomal resistance and decreasing cure rates for tetracycline regimens, tetracycline is no longer recommended as the sole treatment of
gonorrhea.

Producing N gonorrhoeae and chromosome-mediated penicillin and tetracycline-resistant N gonorrhoeae has stimulated the development of more
effective antimicrobials and faster diagnostic methods. As infection does not confer immunity, the search for a vaccine continues.
NONGONOCOCCAL URETHTRITIS

Etiology
I in most sexually transmitted disease clinics and student health services, urehriis is nongococcal
more than 50% of the time. Nongococcal urethtritis is usually not reported to health authorities, and
sexual contacts are not often examined or treated. This condition more commonly affects men of higher
socioeconomic status and heterosexual men more often than homosexual men. The morbidity of
nongococcal urethritis is a syndrome with several microbial causes. The most important and potential
dangerous is Chlamydia trachomatis (Stamm et al, 1984). Within the last decade, c trachomatis has been
recognized s being responsible for an increasing number of genital syndromes. Since many practitioners
did not have access to means of isolating this organism, infections were often diagnosed and treated
without confirmation. Now there is usually access to immunoflourescent staining, so that chlamydial
infections can be confirmed (Table 15-2).

Table 15 – 2. Disease associated with N gonorrhoeae and c trachomatis.*

*reproduced, with permission, from Berger RE: Nongococcal urethritis and related syndromes. Monogr
Urol 1982;3:99
N gonorrhoeae C trachomatis
C
Urethtritis Urethtritis
Cervicitis Cervicitis
Salppingitis Salppingitis
Bartholinitis Bartholinitis
Perihepatitis Perihepatitis
Arthritis Arthritis
Urethral syndrome Urethral syndrome
Proctitis Proctitis
Conjuctivitis Conjuctivitis
Endocarditis Endocarditis
Asymptomatic disease Asymptomatic disease
Pneumonia
Otitis media
trachomatis is a small bacterium and an obligate intracellular parasite of columnaror pseucocolumnar
epithelium. Two species of Chlamydia exist: Chlamydia psttaci, which causes psittacosis, and C
trachomatis, which has 15 serotypes. Serotypes A – C case hyperendemic blin ding trachoma; serotypes
D – K cause genital tract infection; and serotypes L1 – L3 cause lymphogranulama venerum.
C trachomatis can be recovered from the urethra in 25 – 60% of heterosexual men with
nongococcal urethtritis, in 4 35% of men with gonorrhea, and in 0 – 7% of men in sexually transmitted
disease clinics without symptoms of urethtritis (tamm et al). Aymptomatic infection occurs in 28% of the
contacts of women with chlamydial cervical infections (Lycke et al, 1980).
Postgonococcal urethritis occurs in patients who probably acquire gonorrhea and chlamydial
infection simultaneously but develop biphasic illness due to the longer incubation period of the latter. This
occurs in 15 – 35% of heterosexuals with gonorrhea (Stamm rt al, 1984).
Ureaplasma urealyticum may be the cause of non-gonococcal urethritis in 20 – 50% of cases. The
pathogenic role of U urealyticum in nongococcal urethtritis is difficult to interpret because genital
colonization increases with an increasing number of sexual partners. In urethritis, the rate of U
urealyticum colonization is low (Stamm et al, 1984). Urethral cultures from 40% of men with a history of
3 – 5 sexual partners will yield U urealyticum whether or not they have urethritis.
Evidence for U urealyticum as a urethral pathogen comes from several sources. The rate of
isolation is higher in m en with nongococcal urethtritis with negative C trachomatis cultures compared to
those with positive cultures (Stam,m et al, 1984). In men with c trachomatis-negative cultures and U
urealyticum-positive cultures, the urethtritis responds poorly to sulfonamides but well to aminocyclitols
(eg, spectonomycin) (to which U urealyticum but not C trachomatis is sensitive) (Stamm et al, 1984).
Nongoicoccal urethtritis persists in a group of C trachomatyis-negative patients who have persistence of
Ureaplasma during treatment with tetracycline. Endourethral inoculation of U urealyticum into humans
and nonhuman primates has produced colonization and urethritis. Some of the 14 different serotypes of
U Urealyticum may be more pathogenic than others (Stamm et al, 1984).
Twenty to 30% of men with avute urethtitis are negative for N gonorrhoeae, C Trachomatis, and
U urealyticum. Some of these men respond to antibiotic treatment, but persistence and recurrence of
infection are common. Herpes simplex virus, cytomegalovirus, Trichomonas vaginalis, and other
organisms have not been convincingly associated with most of these cases (Stamm et al, 1984).

Clinical Findings
A. Symptoms and Signs: Clinically, Chlamydia-positive and Chlamydia nongococcal urethtritis cannot
be differentiated on the basis of signs and symptoms alone. Both usually present after a 7- to 21-
day incubation period, with dysuria and mild to moderate whitish or clear urethral discharge.
Urethral discharge is often scant; however, it may be thick and purulent. Discharge may be
absent, and the patient may only complain of urethral itching. Asymptomatic infection is
common, especially among contacts or women with known cervical chlamydial infection.
Examination reveals no abnormalities other than discharge in most cases; associated
adenopathy, focal urethral tenderness, and meatal or penile lesions should suggest herpetic
urethritis. Tenderness on papation of the prostate has not been convincingly linked to chlamydial
urethritis.
B. Laboratoty Findings: Diagnnosis of non-gonococcal urethritis requires demonstration of urethritis
and exclusion of infection with N gonorrhoeae (Fig 15 - 1). The man suspected of having
urethritis ideally should be examined after 4 hours oof urinary continence so that the discharge
may be reliably demonstrated. On gram-stained smear of a urethral swab, the presence of more
than 4 PMNs per oil-immersion field confirms urethritis. Altenatively, thepresence of 15 or more
PMNs in 5 random high-power fields (magnification x 400) of spun urine sediment correlates with
urethritis. Many men with asymptomaic chlamydial urethral infection have urethral leukocytes
(4PMNs per high-power field) on gra-stained smear of urethral secretions. When urethritis is
suspected but urethral inflammation cannot be detected, the urethral swab should be obtained in
the early morning before voiding.
Because C trachomatis is an intracellular parasite of columnar epithelium, the best
specimen for culture is an endourethral swab rather than urethral exudate or urine. This
specimen must be taken carefully from an area 2 – 4 cm inside the urethra. Preliminary culture
results are available 2 – 3 days after inoculation. A flourescein conjugated monoclonal antibody
has been used in the diagnosis of chlamydial nongococcal urethritis. It requires less than 30
minutes to perform and is based on the detectionof extracellular chlamydial bodies. It has a
sensitivity of 93% and (Tam et al, 1984). Although many physicians believe that cultures are
unnecessary, C trachomatis is dangerous pathogen, and culture results will serve both as a guide
to therapy and as documentation of the disease.
Treatment
Since nongococcal irethritis is a syndrome that can be caused by different organisms that
respond differently to treatment, results of therapy are inconsistent. The current recommendations from
the Centers for Disease Control are based o chlamydial infection (Table 15 - 3).
Depending on the organism causing urethritis, there are different responses to therapy. Patients
with C trachomatis have the best response, and those with neither C trachomatis nor U urealyticum have
the poorest response to therapy.

Table 15 -3 . Management of nongocccal urethritis*

Initial management of diagnosed urethritis
Give tetracycline, 500 mg orally 4 times a day for 7 days; or monocycline or doxycyline, 100 mg twice
daily for 7 days; or erythromycin, 500 mg 4 times a day for 7 days. Examine and treat sexual partners
with the same regimen.
Management of persistent or recurrent urethritis
Question the patient about compliance with treatment and reexposure to infection.
Examine the patient carefully for les common causes of urethritis.
Confirm urethritis.
Treat any specific cause that can be elucidated.
If a specific cause is not found or if U urealyticum is present, treat with erythromycin base, 500 mg 4
times a day for 14 adys.
*Modified and reproduced, with permission, from Bowie WR: Nongococcal urethritis. Urol Clin North Am
1984;11:55

Every attempt should be made to treat the patient’s sexual partner promptly. In general, the
same regimen is used to treat the male and the female.
In most cases,infection due to Chlamydia is easily treated. No tetracycline resistance hs been
documented. However, complications such as apididymitis, prostatitis, proctitis, or Reiter’s syndrome do
occur.

Complications
C trachomatis has been shown to cause most cases of apididymitis in heterosexual men less than
35 years of age. Men with epididymitis who are older than 35 years generally have confirm infections
accompanied by a history of urologic disease or instrumentation (Berger, 1983).
The possibility of C trachomatis causing nonbacterial prostatitis is still controversial. In Mardh’s
study in 1978, only 13% of patients with nonbacterial prostatitis had antibodies to C trachomatis and
none had positive cultures from expressed prostatic secretions.
A recent prospective evaluation indicated that C trachomatis may be found in 15% cases of
proctitis in homosexual men (Stamm et al, 1982; Quinn et al, 1981). Lymphogranuloma venereum
immunotypes can produce a primary ulcerative proctitis and a histopathologic picture of giant cell
formation in granulomas identical to those seen in acute Crohn’s disease. Symptoms and signs may
include rectal pain, bleeding, mucus discharge, and diarrhea.Most C trachomatis-infected patients have
abnormally high numbers of PMNs in their stool and on sigmoidoscopy have friable rectal mucosa.
Reier’s syndrome (urethritis, conjuctivitis, arthritis, and characteristics mucocutaneous lesions),
reactive tenosynovitis and arthritis without the other components of Reiter’s syndrome have been
associated with genital infection with C trachomatis. Preceding or concurrent infection with C trachomatis
may be present in more than 80% of patients with Reiter’s syndrome, which occurs with increased
frequency in patients with the HLA-B27 haplotype (Brewerton et al, 19730).
Prognosis
Most nongonococcal urethritis responds promptly to tetracycline. Vigorous treatment of the man’s
sexual partner or partners is imperative.
TRICHHOMONIASIS

Etiology
Trichomonas vaginalis was described by Donne in 1836 and was long regarded as a harmless
inhabitant of the vagina. Of the 3 species of trichomonads that infect humans, only T vaginalis causes
clinical disease. The prevalence of colonization in control male populations ranges from nil in
asymptomatic men to 18% in men with gonococcal urethritis (Krieger, 1981). The median prevalence in
control male populations is 2%.
The highest is a consensus the T vaginalis is sexually transmitted in almost all instances. T
vaginalis been isolated from 14 – 60% of male partners of infected women and in 67 – 100% of female
partners of infected men. The difference is most likely attribute to the difficulty of demonstrating
trichomonads in the male genital tract, as well as the spontaneous clearance in any men (Krieger, 1981).
Many European investigators feel that trichomoniasis may be a major cause of morbidity in men
(Krieger, 1981). The cause is unknown in 30 – 50& of cases of nongococcal urethritis. The evidence for
trichomoniasis as a sole cause of urethritis is poor. T vaginalis has been claimed to cause some cases of
balanoposthitis, epididymitis, urethral stricture, prostatitis, pyelonephritis, and rarely, infertility (Lewis and
Carrol, 1928). Most infections due to T vaginalis in men are asymptomatic, and some feel that men serve
primarily as vecrors for transmission of asymptomatic disease for women.

Clinical Findings
Urethral discharge should be mixed immediately with 1 – 2 mL f saline and studied
microscopically. This examination has less accuracy in men than the 60 – 70% accuracy that it has in
women (Rothenberg et al, 1976; Fleury, 1979).
Liquid and semisolid media cultures have proved to be most accurate for diagnosis of
trichomoniasis (Nielsen, 1973; Rothenberg et al, 1976; Cox and Nicol, 1973).

Treatment
Most cases of trichomoniasis in men are discovered and treated on the basis of contact with
women with trichomoniasis vaginitis. One the diagnosis has been made, a condom should be used during
intercourse until treatment has been successful.

Prognosis
Most trichomonad infections respond promptly to metronodazole. Vigorous treatment of theman’s
sexual or partners is imperative.

PRIMARY SYPHILIS
A. Symptoms and Signs: Syphilis is caused by treponema pallidum, a spirochete, which gains
access through the intact or abraded skin or mucous membranes. The patient usually presents
with a painless penile sore (chance) 2 – 4 weeks after sexualexposure. The chance begins as a
hyperemic or erythematous spot. This painless papule, or pustule, develops on the glans, corona,
foreskin, shaft, suprapubic area or scrotum. It may break down to form an indurated, punched-
out lesion. The syphilitic (hard) chance is relatively deep, has indurated edges and a clean base,
and is not tender on pressure. The lesion may be so small and transient that it may be missed.
Without treatment, the lesion will heal spontaneously and slowly. Discrete enlarged inguinal
nodes may be palpable. These may be in a unilateral or bilateral satellite formation. They are not
tender unless secondary infected (Table 15-4).

B. Laboratory Findings: the diagnosis is made by findings the spirochetes on the dark field
examination of scraping of the base of the chancre or by florescent antibody techniques. Where the
darkfield examination is not available, a reagin (RPR) card test may be used (Kraus, 1984). This is
equivalent to and is replacing the VDRL test. Repeated examinations daily for 3 days without local
systemic treatment and aspiration of the enlarges nodes may be necessary to demonstrate the organism.
The serologic tests may remain negative for 1-3 weeks after the appearance of the chancre. The quickest
and least expensive examination, the fluorescent treponema antibody-absorption test (FTS - ABS), is
also the most specific and sensitive. The more expensive and more difficult treponema pallidum
immobilization test has been replaced by the microhemagglutination test, which can be automated and
quantitated (Garner et al, 1972).

Differential diagnosis
Chancroid, lymphogranuloma venereum, graluma inguinale, balanitides of varying cause, carcinoma,
acabies, psoriasis, lichen planus, leukoplakia, cythroplasia, and infection due to herpes simplex virus may
resemble syphilis. Borrelia refringens is difficult to distinguish from T pallidum. Erythroplasia of Queyrat
may resemble a hard chancre. All penile lesions should be considered syphilis until proved otherwise.
Compilations
Urologic compilations are rate and occur in the tertiary form of the disease. They includes gummas of the
testis and neurogenic bladder secondary to neurosyphilis.

Prevention
If exposure has occurred, give benzathine penixcilin G, 2.4 million units intramuscularly in a single dose.

Treatment
Patients with early syphilis (primary, secondary, or latent of less than 1 year’s duration) should receive
benzathine penicillin G, 2.4 million units intramuscularly in a single dose. Patients allergic ot penicillin
should receive tetracycline hydrochloride, 500 mg orally 4 times for 15 days, or erythromycin, 500 mg
orally 4 times daily for 15 days.

Prognosis
The prognosis excellent; relapse is rate. If it occurs, more intensive penicillin therapy is required.

Chancroid
Chancroid is a sexually transmitted disease caused by Haemphilus ducreyi.

Clinical Findings
A. Symptoms: A papule is the first lesion of chancroid, usually seen a few days after sexual
exposure. One or more painful, dirty – appearing chancroid ulcers then appear. These are deep
with flat, rugged, erythematous borders that extend into the mermis and subcutaneous tissue of
the surrounding skin. Chancroid ulcers often have purulent secretions. About 50% of patients will
have fever, malaise, and headache.
B. Signs: Ulcers caused by chancroid may be indurated but are usually soft and malleable. The
base is friable and bleeds easily. Lesions may be painful. Untreated ulcers. Confluent ulcers
enlarge by peripheral extension. Painful chronic inguinal inflammation seen with chancroid may
cause lymphatic obstruction. Genital lymphedema may ensure, with the end stage being
elephantiasis.
C. Laboratory Findings: A gram – stained smear reveals H ducreyi in 50% of cases. Selective
culture for H ducreyi has greater sensitivity and specificity than clot cultures and gram – stained
smears. Biopsy is always diagnosis.

Different Diagnosis
Chancroid msut be differentiated from other ulcerative lesions of the external genitalia (eg, genital
herpes, syphilis, granuloma inguinale, lymphogranuloma venereum, traumatic ulcer, and lesions
associated with drug reaction).
Compilations
Uncommonly, secondary infection with aerobic and anaerobic bacteria may cause marked destruction
of tissue.
 Treatment
a. Specific Measure : Response with tertracycline is excellent. The dose is 500 mg orally 4 times
daily for 10 days. Erythromycin, 500 mg orally 4 times daily, is also effective, as is trimethprinm –
sulfamethoxazole, one double – strength tablet orally twice daily. Therapy should be continued a
minimum of 10 days and until ulcers or nodes have disappeared. Sexual partners should be
examined and treated identically.
b. General Measures: Cleanliness is important washing the gentalia carefully with green soap and
water immediately after intercourse has been shown to be effective (Moore, 1920).
c. Treatment of Compilation: if a super infection complicates the picture, use penicillin or
clindamycin in addition to antibiotics described above.
Prognosis
With proper antibiotics therapy, the prognosis is excellent.
Lymphogranuloma Venereum
Chlamydia trachomatis immunotypes L1, L2, and L3 cause Lymphogranuloma Venereum. The
diseased is characterized by a transient genital lesion followed by lymphadenitis and, possibly, rectal
strictures. The inguinal and sub inguinal lymph nodes may become matted, undergo suppuration, and
form multiple sinuses.
Clinical Findings
A. Symptoms and Sings: a papulte or pastule appears 5 – 21 days after sexual exposure. The
genital lesion of lymphogranuloma venereum is so small and transient that is often goes
unnoticed. It may simply be a vesicle or a superficial erosion. An initial lesion that codes to form
an ulcer is usually superficial. Painful nodes may become fluctuant. Unilateral lymphadenopathy is
most common and may be the initial symptom. At the stage of bubo formation, constitutional
symptoms are commonly present (eg. Chills, fever, headache, generalized joint pains, nausea,
and vomiting). Skin rashes are frequent.

B. Laboratory Findings: the white blood count may reach 20.000 /ul if the lymph nodes are invaded
anemia may be present. Proteins (globulin) are elevated. Skin lesions show acute and subacute
imflammation; there is nothing specific or diagnostic in their appearance. Thwe nodes show
abscesses with heavy infiltration by neutrophils. Hyperplasia of lymphoid elements takes place,
and plasma cells appear.
The most specific test in the diagnosis of lymphogranuloma venereum is culture of C
trachomatis from an inguinal node aspirate. Serologic tests, are commonly used and have
replaced the Frei skin test. The complement fixation test is not specific for lymphogranulama
venereum because it also detects other Chlamydia infections, including urethritis and psittacosis.

Differential Diagnosis
All other cause of penile ulcers should be differentiated, especially syphilis, infection due to
herpes simplex virus, and chancroid. Always suspect lymhphogranulama venereum in patients with a
rectal stricture. The inguinal syndrome of lymphogranuloma venereum id indistinguishable from that of
chancroid in that both are unilateral in two-thirds of cases, and in both, an inguinal bubo (a firm, slightly
painful mass) may appear in 1 – 2 weeks (Kraus, 1982).

Complication
Rupture of inguinal nodes in lymphogranuloma venereum canlead to draining sinuses. Chronic
inguinal inflammation may cause lymphatic obstruction and elephantiasis. Rectal stricture is a late
complication.

Treatment
A. Specific Measures: Lymphogranuloma venereum is treated with antibiotics that are
effective in other chlamydial infections. Tetracycline is the drug of choice, 500 mg orally 4
times daily for 2 weeks. Alternatives include erythromycin, 500 mg orally 4 times daily, and
 sulfamethoxazole, 1 g orally twice daily. Treatment with any of these medications should
continue for at least 2 weeks.
B. Treatment of Complications: Aspiration of fluctuant nodes is indicated. Draining sinuses
can be excised. Rectal stenosis may require surgery.

Prognosis
The prognosis is excellent if the disease is treated promptly. The late complications are genital
elephantiasis and rectal stricture.

GRANULOMA INGUINALE
This sexually transmitted chronic infection of the skin and subcutaneous tissue of the genitalia,
perineum, and inguinal area has an incubation period of 2 – 3 months. The infective agent,
Calymmatobacterium granulamatis, is realted to Klebsielle pneumoniae and grows with difficulty on an
egg yolk medium.

Clinical Findings
A. Symptoms and Signs: A papule is the first sign of granuloma inguinale. This may from an ulcer
protruding above the level of the surrounding skin. The ulcer base is erythematous and may have
hemmorhagic secretions. It is firm, indurated, and nontender. The inguinal swelling or
pseudobubo is a subcutaneous granulomatous process rather than a true lymphadenopathy.
Untreated, it enlarges by direct extension or erodes through the skin. Chronic inguinal
inflammation may cause lymphatic obstruction and elephantiasis. The microscopic picture
includes nonspecific infiltrates of plasma cells, giant cells, neutrophils, and large monocytes. The
monocyte cytoplasm contains Donovan bodies, the intracellular stage of C granulamatis.
B. Laboratory Findings: Indentification of Donovan bodies in monocytes on a stained smear makes
the diagnosis. These organisms appear as bipolar staining rods within the monocytes. A crush
preparation for cytologic study is prepared by obtaining a small fragment of tissue from the ulcer
base and crushing it between 2 slides. Giemsa’s stain. Serial sctions are done, as histologic
visualization of Donovan bodies may not be seen on only one study. Crush preparation test are
available inminutes, whereas results of histologic studies cannot be obtained for days. In case of
doubt, biopsy may be performed. A reliable culture for C granulomatis is not available.

Complications
Secondary infection may cause deep ulceration and tissue destruction. Sinuses may result.
Phimosis may occur. A change in bowel habits suggests a rectal stricture.

Prevention
The use of condom does not prevent pregenital spread.

Treatment
Neither controlled granuloma inguinale therapy trials nor in vitro susceptibilities of C granulomatis
are available. Treatment has been successful with tetracycline, 500 mg orally 4 times daily, or
trimethoprimsulfamethoxazole, one double-strength tablet orally twice daily. These doses are continued
until the lesion has healed. Gentamicin and chloramphenicol, although more toxic, are also effective.

Prognosis
The antibiotics are effective, the complications few, and the prognosis good.
GENITAL HERPES INFECTION

Etiology
Genital herpes is a disease of great concern to physician and patients. The increasing prevalence
of infection in men and women, the risk of transmission to sexual partners, the high rates of morbidity
and even death associated with cervical cancer, and the absence of curative therapy have made it
diagnose, counsel, and treat patients with genital herpes.
Herpes simplex virus is a double –stranded DNA virus that may cause persistent or latent
infections. Most genital herpes infections are due to type 2 virus, although infection due to type 1 herpes
virus, which has been reported in 10 – 25% of cases of genital herpes. Herpes simplex is seen in 5% of
patients seeking help at clinics for sexually transmitted disease (Corey and Holmes, 1983). In college
students, herpes simples virus infections are 10 times more common than gonorrhea or syphilis (Corey et
al, 1983). Although it is not inevitable that the sexual partner of an infected patient will also become
infected, partners are at rick even when the infection is asymptomatic.

Clinical Findings
A. Symptoms and Signs: Retrospective studies that 50 – 70% of herpes type 2 infections are
asymptomatic, but prospective studies to determine the percentage of asymptomatic infections
have not been undertaken. Herpes simplex virus types 1 and 2 produce primary genital lesions of
equal severity. The first episode of disease is much more severe in persons without prior oral
herpes. The incubation period is 2 – 10 days. Approximately 2% of patients with primary genital
herpes develop severe sacral or autonomic nervous system dysfunction resulting in urinary
retention (Corey et al, 1983). Vesicles grouped on an erythematous base, not following a neural
distribution, and associated with a revious history of such eruptions are pathognomonic for
genital herpes. The lesions are tender to touch. Adenophaty is usually bilateral, and the lymph
nodes are mildly tender, nonfixed, and slightly firm. Dysuria is present in 44% of men. Herpes
simplex virus can be isolated from the urethra in most of these patients (Corey and Holmes,
1983). Extragenital skin lesions, usually from autoinoculation, are found in approximately 10% of
men with genital herpes.
B. Laboratory Findings: Virus isolation by culture is the most sensitive of techniques for
diagnosing herpes infections. In recurrent disease, urethral isolation can be obtained in fewer
than 2% of men. Results can be available in 5 days. Tzanck or Papanicolaou smears of lesions
will demonstrate intranuclear inclusions in 50 – 60% of culture-positive cases (Moseley et al,
1981). Serum antibody to herpes simplex virus infections can be measured by a number of
methods. No test presently available is completely reliable in differentiating type 1 from type 2
infections. Serologic tests are now used only to document a history of past infection.

Treatment
Acyclovir is the only drug that has shown efficacy in the treatment of genital herpes. Topical,
intravenous, an doral forms are effective for first-episode genital herpes.
Acyclovir acts on viral thymidine kinase as a guanine analog. It is selectively phosporylated in
the virus, acts as an inhibitor of viral DNA polymerase, and acts as a chain terminator (Colby et al, 1980).
Oral acyclovir, 200 mg 5 times daily for 5 – 10 days, and intravenous acyclovir appear more effective
than topical therapy in the treatment of primary genital herpes. Acyclovir decreases the duration of viral
shedding, the time to crusting of lesions, during which there is pain or itching, or both. Only the oral and
intravenous forms decrease dysuria, vaginal discharge, systemic symptoms, and the development of new
lesions (Corey and Holmes, 1983). Prophylactic treatment with acyclovir, 200 mg orally 2 – 5 times daily,
may sufficiently decrease recurrence, but more information on the long-term side effects is needed
before this form of therapy can be recommended (Bryson et al, 1983).
Table 15 – 5. Sexually transmitted diseases that cause infections of the liver, intestines, and rectum.*
Organ Agents
Liver Hepatitis B virus
Hepatitis A virus
Hepatitis non-A, non-B agents
Intestines Giardia lamblia
Entamoeba histolytica
Cryptosporidium species
Shigella species
Campylobacter species
Strongyloides species
Rectum Neisseria gohorrhoeae
Chlamydia trachomatis
Treponema pallidum
Herpes simplex virus
Human papillomavirus
*Reproduced, with permission, from Judson FN: Sexually transmitted viral hepatitis and enteric
pathogens. Urol Clin North Am 1984;11:178.
 Table 15 – 4. General ulcer
Disease Cause Preferred Test Type of Ulcer Anacillary Type of Drug of Choice Alternative Drug
Tests Adenopathy
Genital Herpes Herpes Siplex Viral Culture Grouped vesicles; Tzanck Firm, tender Acyclovir ointment 5% 6t times
Virus type 1 or 2 small, painful when smear. when a days for 7 days (initial
scraped; soft. palpated period). Acyclovir, 5 mg/kg
intraveniously every 8 hours for
5 days.
Chancroid Haemophilus Selective Deep, undermined Fluctuant Erythromycin, 500 mg orally 4 Trimethoprim –
ducreyi medium culture border; painful, soft tender overly times a day for 10 days. sulfamethoxazole, 1
or indurated, double strength tablet
purulent twice a day for 10 days.
Granuloma Calymmatobacte Crush Firm, painless; Histology No Tetracycline, 500 mg orally 4 Erythromycin, 500 mg
inguinale rium preparation rolled elevated adenopathy times a day for 2 weeks or until orally 4 times a day for 2
granulomatis border; chronic, healed. week; or timethoprim –
speading. sul- famethxazole, 1
double- strength tablet
twice a day for 2 weeks
or until healed.
Lymphogranulo Chlamydia Complement Usually absent. C Fluctuant Tetracycline, 500 mg 4times a Erythromycin, 500 mh
ma trachomatis (L1, Fixation or trachomatis tender. day for 2 weeks. orally 4 times a day for 2
L2, L3 subtypes) Immunofluores culture weeks.
cene.
Traumatic ulcer None Onset during sexual
activity.
Fixed drug None Recurrences
reaction associated with the
same systemic
medicine.
Syphilis Treponema Darkfield Painless, firm, RPR, VDRL,
Firm, Non- Benzatherine penicillin G, 2.4 Tetracyline, 500 mg
(primary) pallidum microscopy “hard,” indurated. FTS – ABStender or million units intramuscularly orally 4 times a day for
MHA-TP. tender 15 days.
“rubbery.”
Modified and reproduced, with permission, from Kraus SJ: Evaluation and management of acute genital ulcers in sexually active patients. Urol Clin
North Am 1984;11;155
HEPATITIS & ENTERIC INFECTIONS
In the past, viral hepatitis and erectic infections were not viewed as sexually transmitted
diseases. Now, however, many of these infections are known to be sexually transmitted in some cases
(table 15 – 5). Hepatitis A and B may be transmitted by sexual contact and through other close physical
contact. Enteric infections such as amebiasis, giardiasis, shigellosis, and campylobacteriosis may be
transmitted sexually. Most of these sexually transmitted enteric infections occur in homosexual men.
Contacts is made through anal intercourse or anilingus. Enteric disease may also be transmitted to female
partners.
Approximately one-third of Hepatitis B cases may be attribute to homosexual contacts. Thirty to
80% of homosexual men test seropositive for hepatitis B (Shreeder et al, 1982). Hepatitis A is also
spread by sexual contact and is more prevalent in homosexual men than in heterosexual men. At this
time, there is little evidence that non-A, non-B hepatitis has a sexual mode of transmission (Hentzer et al,
1980).

ACQUIRED IMMUNODEFICIENCY SYNDROME

Acquired immonodifficiency syndrome (AIDS), first reported in 1981, has as its basis acquired
immunoincompetence. The retrovirus (human T cell leukemia virus, lymhphotropic virus tyoe 3, or human
immonudefficiency virus type 3, or human immonudefficiency virus [HIV] appears to be transmitted by
sexual contact, contaminated syringes, or blood transfusion. Most patients are homosexuals with multiple
partners, abusers of intravenous drugs, hemophiliacs receving factor VIII concentrate, or recipients of
multiple transfusions. Vertical transmission from male-to-male and male-to-female penile-vaginal
transmission (Harris et al, 1983). The disease is transmitted only by sexual contact; normal physical
contact, even within a household, will not spread disease (Curran, Gold, and Jaffe, 1984).
The prodromal syndrome includes fatigue, weight loss, fever, and diarrhea. Four AIDS syndromes
have been reported: lymphadenopathy syndrome, Kaposi’s sarcoma, increased susceptibility to
opportunistic infections, and cancer (lymphoma, squamous cell carcinoma, or Burkitt’s lymphoma)
(Ziegler et al, 1984).
The physician may find generalized lymphadenophaty, multiple purple “bruises” on the legs
(Kaposi’s sacroma), or recurring infections (bacterial, viral or fungal). Be on the alert for the chronic
cough of Pneumocystis carinii pneumonia.
Laboratory data reveal the depressed immune system. There is an abnormal ratio or even a
reversal in the ratio of helper T cells to suppressor T cells. One should search for antibodies to hepatitis B
virus and cytomegalovirus, as these organisms infect compromised hosts. An enzyme-linked immune
sorbent assay (ELISA) has been developed to detect antibodies to HIV. Serum antibody to HIV was found
in 95% of patients with AIDS, 87% of those with lymphadenopathy syndrome, and less than 1% of
controls (Sarngad-haran et al, 1984).
The spermicide nonoxynol-9 is inhibitory to HIV and, if used in combination with condoms, may
decrease transmission of the virus. There is no therapeutic intervention to date that has permanently
reversed the immunodeficiency. The patients often succumb to aggressive Kaposi’s sarcoma or other
runaway infections, such as P carinii pneumonia.
The overall mortality rate in the first 1500 cases is close to 40%; this rate will probably increase
on follow-up studies (Curran, Gold, and Jaffe, 1984).