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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. continue... • 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. continue... • 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”). continue... • 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)