Acquired and congenital syphilis. Etiology & pathogenesis. Stages of development. Primary syphilitic lesion. Organ site damage.
Syphilis is a chronic infection caused by Treponema pallidum (a spirochete); its incidence varies widely between regions and population groups. Organism is transmitted via contact of mucosal lesion in sexual partner in primary or secondary stages, or across the placenta from mother to fetus. Widespread dissemination occurs within days, even before the appearance of the primary lesion. Below we will look at the stages and symptoms of syphilis.
Remember: congenital syphilis (transplacental, risk highest when the mother has primary or secondary syphilis):
- Early (first 2 years): snuffles (nasal discharge), rash with desquamation, hepatosplenomegaly, pneumonia alba, osteochondritis
- Late: Hutchinson triad - notched incisors, interstitial keratitis, eighth-nerve deafness; also saddle nose and saber shins
The first stage is the primary stage (average of 21 days after infection). Here a primary lesion known as chancre appears at the point of spirochete entry. This resolves spontaneously after 4-6 weeks. It is a ‘hard chancre’ in contrast to some differential diagnosis and in males is generally on the penis, in females, the vagina or uterine cervix. It begins as a firm papule, which becomes a painless ulcer. It is accompanied by inflammatory infiltrate rich in plasma cells.
Memory aid: the syphilitic chancre is hard and painless; the chancre of chancroid (Haemophilus ducreyi) is soft and painful - "you do cry with ducreyi".
The secondary stage occurs about two weeks after the chancre has resolved. It manifests as generalised lymph node enlargement and mucocutaneous skin lesions (usually symmetrical and maculopapular), often involves palms and soles of feet. Condylomata lata, broad flat plaques on moist skin areas, may also occur. The mucocutaneous lesions show proliferative endarteritis with lymphoplasmacytic infiltrate, with spirochetes abundant, these lesions are highly infectious.
The chancre and the mucocutaneous lesions are a result of proliferative endarteritis, that is the inflammation of the intima of the artery as a result (it is thought) of the host immune response that activates endothelial cell activation and proliferation, leading to perivascular fibrosis and luminal narrowing.