Download Syphilis and Gonorrhea

by Chow Wen M17090880
Introduction
• Syphilis is an infection caused by Treponema pallidum
subspecies pallidum that is usually sexually transmitted.
• The most common and recognizable manifestations are
usually cutaneous.
• It can cause serious disease in persons who acquire it
after birth and especially devastating disease in persons
who acquire it in utero.
• Syphilis passes through four distinct clinical phases.
• Persons with human immunodeficiency virus infection
are at higher risk of treatment failure and to
neurosyphilis.
BIOLOGY
• Treponema pallidum subspecies pallidum is a motile, spiral-shaped
bacterium for which humans are the only natural host.
• Microscopically, the bacterium is indistinguishable from other
pathogenic treponemes that cause nonvenereal diseases, including
T. pallidum subspecies endemicum (bejel), T. pallidum subspecies.
pertenue(yaws), and T. pallidum subspecies carateum (pinta).
• The bacterium has very limited metabolic capabilities, making it
reliant on host pathways for many of its metabolic needs.
• T. pallidum does not survive more than a few hours to days outside
its host and cannot be cultured in vitro for sustained periods
• Thus,transmission of Treponema pallidum requires close personal
contact. Ex:minute abrasions of skin and mucous membranes
Typical penile chancre of primary syphillis
T. pallidum subspecies.
T. pallidum subspecies endemicum (bejel)
T. pallidum subspecies carateum (pinta).
Pathogenesis
• Following inoculation, T. pallidum attaches to host cells, including epithelial,
fibroblast-like, and endothelial cells, likely by binding to fibronectin, laminin, or
other components of host serum, cell membranes, and the extracellular matrix.
• It can invade rapidly into the bloodstream—within minutes of inoculation and
can cross many barriers in the body, such as the blood–brain barrier and the
placental barrier, to infect many tissues and organs
• That dissemination leads ultimately to manifestations of syphilis distant from the
site of the initial chancre(s) in an infected person and in a developing fetus.
• Infection at all stages leads to infiltration by lymphocytes, macrophages, and
plasma cells. CD4+ T cells predominate in chancres, and CD8+ T cells
predominate in lesions of secondary syphilis.
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• Infection leads also to elaboration of Th1 cytokines, including IL-2 and
IFN-γ, although down regulation of the Th1 response during secondary
syphilis, coincident with the peaking of antibody titers,might contribute
to the organism’s ability to evade the host immune response.
• The humoral immune response begins with production of IgM
antibodies approximately 2 weeks after exposure, followed 2 weeks
thereafter by IgG antibodies. IgM in addition to IgG continues to be
produced during infection and can lead to immune-complex formation.
• Antibody titers peak during bacterial dissemination, in secondary
syphilis
Clinical course
Diagnostic Tests
• DARKFIELD MICROSCOPY.-Darkfield microscopic examination is the
diagnostic test of choice in chancres, moist lesions of secondary
syphilis (condylomata lata and mucous patches), and the discharge
from rhinitis in congenital syphilis
• DIRECT FLUORESCENCE ANTIBODY TEST-The lesional exudate is
smeared on a glass slide and stained with fluorescein-labeled anti-T.
pallidum immunoglobulin.The sensitivity of the test is 73%–100%.
• MOLECULAR TESTS- PCR based methods have been used to detect T.
pallidum DNA from lesions.
• SEROLOGIC TESTS FOR SYPHILIS(STS)- Positive in persons with any
treponemal infection. Tests always Positive in secondary syphilis
Primary syphilis
• Primary syphilis is a stage of syphilis characterized by one or more
chancres, in the presence of laboratory evidence from tissues or sera
consistent with syphilis
• At the inoculation site, a chancre develops after an incubation period
that ranges from 10 to 90 days (average, 3 weeks)
• The chancre starts as a dusky red macule that evolves into a papule
and then a round-to-oval ulcer
• The typical chancre, also called a Hunterian chancre or “ulcus
durum” (hard ulcer)
• The base is usually clean, and the chancre is classically not painful
Secondary syphilis
• Secondary syphilis is a stage of syphilis characterized by localized or
diffuse mucocutaneous lesions, often with generalized
lymphadenopathy, in the presence of laboratory evidence from
tissues or sera consistent with syphilis. The chancre may still be
present
• Lesions of secondary syphilis, classically called “syphilids” or, when
affecting the skin, “syphiloderms,”63 typically erupt 3–12 weeks after
the chancre appears (up to 6 months after exposure)
• Rash is present in nearly all cases of secondary syphilis, although the
specific type of rash varies.
• Erythematous macules (roseola syphilitica) or maculopapules are
commonly present symmetrically on the trunk and extremities with
papular, papulosquamous, or lichenoid
• A white scaly ring on the surface of papulosquamous lesions, called
Biette’s collarette
• Crown of Venus is present sometimes
• Erythematous to copper-colored round papules, well demarcated and
sometimes with an annular scale, are present on the palms and soles
in nearly 75% of cases
• Plantar lesions can be variously mistaken for calluses (clavi syphilitici).
Plantar lesions can also extend to the lateral and posterior aspects of
the foot
• Patchy nonscarring alopecia, described as “moth-eaten” or, less
commonly, a diffuse alopecia of the scalp.
Secondary syphilis: papulosquamous lesion Typical red keratotic papules on the palm.
(A) Subtle solitary papule on one palm only. (B) Multiple keratotic papules on palm.
Secondary syphilis: annular
facial lesions
Secondary syphilis:
papulosquamous lesions
Secondary syphilis: condylomata
lata
Syphilids
“moth-eaten” or, less commonly, a diffuse
alopecia of the scalp.
Latent syphilis
• The secondary stage is followed by an asymptomatic stage with no clinical
findings, with seroreactivity by definition the only evidence of infection
• Latent syphilis therefore is a diagnosis of exclusion, after signs of syphilis,
including those that can be present on accessible mucosal surfaces (e.g., oral
cavity, perineum,perianal area, underneath the foreskin, labia, vaginal walls,
cervix), have been excluded
• For disease surveillance purposes, CDC divides latent syphilis into three
subcategories, early latent, late latent, and latent syphilis of unknown
duration.
• Clinical management of patients with late latent syphilis and latent syphilis of
unknown duration is identical and differs from clinical management of
patients with early latent syphilis.
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• Early latent syphilis can be diagnosed if, within the year preceding discovery of
the reactive serologic test, a person had one of the following:
1. Documented seroconversion or fourfold or greater increase in titer of a
nontreponemal test;
2. Unequivocal symptoms of primary or secondary syphilis;
3. A sex partner documented to have primary, secondary, or early latent
syphilis; or
4. Reactive nontreponemal and treponemal tests from a person whose only
possible exposure occurred within the previous 12 months
• Late latent syphilis, , is diagnosed in a patient with latent syphilis who cannot
be diagnosed with one of the other two subcategories.
Tertiary syphilis
• It is“syphilis, late, with clinical manifestations other than neurosyphilis
(late benign syphilis and cardiovascular syphilis),” which is
characterized by inflammatory lesions of the cardiovascular system,
skin, bone, and rarely, other structures, in the presence of laboratory
evidence from tissues or sera consistent with syphilis
• Because of effective antibiotic therapy, progression to tertiary syphilis
is now very rare in the developed world.
• The hallmark of late benign syphilis is the gumma, a granulomatous
nodular lesion with variable central necrosis, which most commonly
affect the skin or mucous membranes
• They are common on the scalp, forehead, buttocks, and presternal,
supraclavicular, or pretibial areas.
• Other manifestations of late benign
syphilis affecting the skin include
granulomatous nodular and
noduloulcerative lesions and psoriasiform
plaques
• Cardiovascular manifestations of tertiary
syphilis affected 10%–40% of those
infected and were thought to be
responsible for most deaths caused by
syphilis.
• Syphilis typically causes syphilitic aortitis,
leading to aortic regurgitation in 10% of
individuals with untreated disease, and
can also cause coronary ostial stenosis
and saccular aneurysm.
Summary
• Syphilis passes through four distinct clinical phases:
1. Primary stage, characterized by a chancre.
2. Secondary stage, characterized typically by skin eruption(s) with or
without lymphadenopathy and organ disease.
3. A latent period of varied duration, characterized by the absence of
signs or symptoms of disease, with only reactive serologic tests as
evidence of infection.
4. Tertiary stage, with cutaneous, neurologic, or cardiovascular
manifestations.
Neurosyphilis
• infection of the central nervous system (CNS) by T. pallidum—is commonly considered to
be a manifestation of “tertiary syphilis,”
• “Neuroinvasion,” in which T. pallidum disseminates to cerebrospinal fluid and meninges,
occurs very early in syphilis.
• Early symptomatic neurosyphilis typically manifests as meningitis
• Uveitis is the most common ophthalmic manifestation of early neurosyphilis, presenting
as eye pain, redness, and photophobia, and sensorineural hearing loss is the most
common manifestation of otologic syphilis
• The two syndromes commonly associated with late neurosyphilis are
• 1) general paresis of the insane/dementia paralytica-presents as a rapidly progressive
dementia, accompanied by personality changes
2) tabes dorsalis-presents with sensory ataxia and bowel and bladder dysfunction can be
accompanied by an Argyll–Robertson pupil (which accommodates but does not react to
light) and optic atrophy.
Congenital syphilis
• Congenital syphilis refers to syphilis caused by infection in utero with
T. pallidum.
• Transplacental fetal infection can occur at any time during pregnancy
and at any stage of maternal infection
• Probability of transmission of infection depends on the stage of
infection in an untreated mother, ranging from 70%–100% in primary
syphilis, 40% for early latent syphilis and 10% for late latent syphilis.
• Clinical findings in symptomatic infants are similar to congenital
infections caused by cytomegalovirus, toxoplasmosis, herpes simplex
virus, rubella, and other infections
Early congenital syphilis(Infectious)
• The most prominent manifestations of early
congenital syphilis defined as syphilis in a
child aged <2 years, include:
• fever, rash, hepatosplenomegaly, and
persistent rhinitis (“snuffles”)
Hydrops fetalis (edema), lymphadenopathy,
neurosyphilis, leukocytosis,
thrombocytopenia, and periostitis and
osteochondritis may also be present, with the
pain associated with osteochondritic lesions
causing the infant to refuse to move the
affected anatomic area (“pseudoparalysis of
Parrot”).
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• If present at delivery, the rash is
usually bullous (“syphilitic
pemphigus”) and very infectious.
• Other cutaneous lesions present
can include condyloma lata,
mucous patches, fissures around
the lips, nares, or anus, and
petechiae from
thrombocytopenia. The skin of
the syphilitic neonate is often dry
and wrinkled and, in newborns
with fair skin, may have a café-aulait hue
Late congenital syphilis(Non-infectious)
• Late congenital syphilis is defined as disease occurring in a child at least
2 years old that typically manifests over the first two decades of life
• Causes manifestations like scars (“rhagades”) ; a saddle-nose
deformity, ; frontal bossing (Olympian brow), thickening of the
sternoclavicular portion of the clavicle (Higoumenakis sign), anterior
bowing of the midtibia (saber shins), and scaphoid scapula, ; and pegshaped notched central incisors (Hutchinson teeth) and mulberry
molars
• Other manifestation include Hutchinson’s triad- refers to Hutchinson
teeth, interstitial keratitis, and eighth nerve deafness.
Gonorrhea
Geerthanaa
• Etiology : N. gonorrhoeae, the gonococcus.
• Colonize mucoso : oropharynx, anogenital sites.
• Epidemiology. STI. Shares clinical spectrum of Chlamydia trachomatis;
symptoms are usually more severe with gonococcal infections.
• Transmission
Sexually- from partner who either is asymptomatic or has minimal symptoms
Vertical transmission - Neonate exposed to infected secretions in birth canal
(Ophatalmia neonatrum)
Risk factor
• Sexually active women younger than 25 and men who have sex with
men are at increased risk of getting gonorrhea.
• Other factors that can increase your risk include:
•
•
•
•
Having a new sex partner
Having a sex partner who has other partners
Having more than one sex partner
Having had gonorrhea or another sexually transmitted infection
Pathogenesis
• Gonococcus has affinity for columnar epithelium; stratified and squamous
epithelia are more resistant to attack.
• Gonococcus penetrates between epithelial cells, causing a submucosal
inflammation with polymorphonuclear (PMN) leukocyte reaction with
resultant purulent discharge.
• Strains of gonococcus that cause disseminated infection tend to cause little
genital inflammation and thereby escape detection.
• Most signs and symptoms of disseminated infection are manifestations of
immune complex formation and deposition.
• Multiple episodes of disseminated infection may be associated with
abnormality of terminal complement component factors
Clinical manifestation
• Genitalia.
• Men: Urethral discharge ranging from scanty and clear to purulent and copious
• Women: Periurethral edema, urethritis. Purulent discharge from cervix but no
vaginitis. In prepubescent females, vulvovaginitis. Bartholin abscess.
• Anorectum.
• Proctitis with pain and purulent discharge.
• Pharynx
• Pharyngitis with erythema occurs secondary to oral-genital sexual exposure. Always
coexists with genital infection.
• Neonate
• Conjunctivitis, swollen eyelid, severe hyperemia, chemosis, profuse purulent
discharge; rarely, corneal ulcer and perforation.
Gonorrhea Purulent,
creamy urethral
discharge from the distal
urethra.
Disseminated gonococcal
infection
Hemorrhagic, painful pustules
on erythematous bases on
the palm and the finger of the
other hand. These lesions
occur at acral sites and are
few in number
Gonococcal ophthalmia
neonatorum
Laboratory diagnosis
• Gram Stain
• Gram-negative diplococci intracellularly in PMN leukocytes in exudate
• Culture
• Men: Urethra, rectum, oropharynx.
• Women: Cervix, rectum, oropharynx. DGI:
• Blood
• Isolation on gonococcal-selective media, chocolatized blood agar, Martin–
Lewis medium, Thayer–Martin medium.
• Antimicrobial susceptibility testing important due to resistant strains
Neisseria gonorrhoeae –
gram-negative diplococci within
polymorphonuclear leukocytes as well
as in the extracellular areas of a
smear from a urethral discharge
Treatment
• Localized uncomplicated gonorrhea.
• Single dose intramuscular ceftriaxone 125 mg or oral cefixime 400
mg. Alternatives: intramuscular ceftizoxime 500 mg, or
intramuscular cefotaxime 500 mg, or intramuscular cefoxitin 2 g
with oral probenecid 1 g.
• Penicillin Allergy. intramuscular spectinomycin 2 mg.
• Disseminated gonococal infection.
• Intramuscular or intravenous ceftriaxone 1 g every 24 hours.
• Alternatives: intravenous cefotaxime or ceftizoxime 1 g every 8
hours or intramuscular spectinomycin 2 g every 12 hours.
Complications of delayed therapy in
gonorrhoea
• Acute prostatitis
• Epididymo-orchitis
• Bartholin’s gland abscess
• PID (may lead to infertility or ectopic pregnancy)