TREPONEMATOSIS Bejel. Pinta.

1. TREPONEMATOSISBejel. Pinta.

2. Treponematosis traditionally refers to the group of nonvenereal diseases that are caused by Treponema species that are morphologically and serologically identical to each other and to Treponema pallidum subspecies pallidum. • All the nonvenereal Treponema species are transmitted, chiefly by direct contact, among children living in tropical and subtropical climates.

3. PINTASynonyms: pinta, azul, carate, endemic treponematosis, mal de pinto. • Pinta is an endemic, contagious, systemic, nonvenereal treponematosis. • Pinta is characterized by chronic skin lesions that occur primarily in young adults.

4. It is an ancient disease that was first described in the 16th century in Aztec and Carib Amerindians. • In 1938, treponemes indistinguishable from those causing yaws and syphilis were demonstrated in lesions of a Cuban patient.

5. Etiology • Family Spirochaetaceae • GenusTreponema • Species Treponema carateum • Treponema carateumis morphologically identical to Treponema pallidum.

6. Morphology • Slender spirals measuring about 0,2 µm in width and 5-15µm in length. • The organisms are actively motile, rotating steadily around their endoflagella even after attaching to cell by their tapered ends. • The long axis of the spiral is ordinarily straight but may sometimes bend, so that the organism forms a complete circle for moments at time, returning then to its normal straight position.

7. Epidemiology • Peak age of incidence is 15-30 years. • Both sexes are affected with equal frequency. • The source of infection is infected person. • Pinta is transmitted by nonsexual means, either by direct contact through cuts in the skin contact or through the agency of flies or gnats.

8. Pinta occurs endemically in all age groups in the New World, particularly the Caribbean, Central America and South America. • It is a disease of poor regions with sub-standard hygiene.

9. Clinical symptoms • Like other treponematoses, pinta is classified into an early and late stage. The early stage comprises the initial lesion and the secondary lesions, while the late stage comprises the latent phase and tertiary stage. • After an incubation period of approximately 2-3 weeks, the initial lesion appears on the skin.

10. The primary lesion • A papule or erythematosquamous plaque usually found on exposed surfaces of the legs, dorsum of the foot, forearm, or hands. • The lesion slowly enlarges and becomes pigmented and hyperkeratotic. • It is often accompanied by regional lymphadenopathy.

11. Clinical symptoms • Disseminated lesions, referred to as pintids, are similar to the primary lesion and may appear 3-9 months after infection. • These secondary lesions vary in size and location and become pigmented with age.

12. Late or tertiary pinta • Disfiguring pigmentary changes, hypochromia, achromic lesions, and hyperpigmented and atrophic lesions. • The pigmentary changes often produce a mottled appearance of the skin. • Lesions may appear red, white, blue.

13. Laboratory diagnostics • The darkfield examination of exudates from early lesions. • Organisms appear white against a dark background. May also have a directed back and forth movement.

14. Treponemes can be demonstrated in the epidermis in primary and secondary lesions using silver stain.

15. Serologic tests • Nontreponemal test results (rapid plasma reagent [RPR], Venereal Disease Research Laboratory [VDRL]) are positive in all stages of pinta except very early lesions. • Confirmatory treponemal test results (Tr. pallidum hemagglutination [TPHA], microhemagglutination Tr. pallidum [MHA-TP], fluorescent treponemal antibody absorption [FTA-Abs]) also are positive but are not practical in remote areas. Reactive VDRL Non-reactive VDRL

16. Histologic Findings • Findings of pinta and yaws are similar, but no ulcer formation occurs in pinta. • In early lesions, mild acanthosis is present with migration of lymphoid cells into the epidermis. • In the late stage, irregular acanthosis or epidermal atrophy occurs. Fibrosis, swollen venules, and granulation tissue can be seen between fat lobules and the connective tissue septa.

17. Treatment • The goals of pharmacotherapy are to eradicate the infection, to reduce morbidity, and to prevent complications. • Drug Category: Antibiotics -- Benzathine penicillin is the DOC but should not be administered to patients who are penicillin-allergic. Alternative therapies are tetracycline or erythromycin.

18. Prognosis • The prognosis is good. • The skin is the only organ affected. Primary and secondary lesions usually heal within 6-12 months. • Pigmentary changes persist in late lesions.

19. Prophylaxis • No vaccines for the disease are available.

20. Bejel(ENDEMIC SYPHILIS ). • Synonyms and related keywords:nonvenereal syphilis of children, sibbens, radseyege, siti, therlijevo, njovera, frenjak, Tr. pallidum subsp. endemicum, nonvenereal endemic syphilis Bejel, non-venereal endemic syphilis Bejel • Endemic syphilis is also known as sibbens (Scotland), radseyege (Scandinavia), siti (Gambia), therlijevo (Croatia), njovera (Southern Rhodesia), frenjak (Balkans), and nonvenereal endemic syphilis (Bejel).

21. Etiology • Endemic syphilis is caused by a spirochete closely related to T bejel(pallidum), which is T pallidum subsp endemicum. • It is morphologically identical to Treponema pallidum.

22. Epidemiology • Endemic syphilis is transmitted through direct or indirect skin-to-skin or mouth-to-mouth contact of the infected lesion. • Children aged 2-15 years are most commonly affected; 25% of cases occur before age 6 years, and 55% of cases occur before age 16 years. • The remaining 20% of cases occur in adults who are in close contact with children who are infected. Because children are the active transmitters of the disease, infection of all members of a household is very common. • Both sexes are equally affected, especially in the pediatric population. • The common housefly, Musca domestica, • has not been established as a potential vector.

23. Endemic syphilis occurs chiefly in Africa but also in the Middle East, in Southeast Asia, and elsewhere. It is also widely spread in rural areas of poor hygiene and education.

24. Clinical symptoms • Endemic syphilis rarely involves the nervous and cardiovascular systems. • The clinical manifestation of neurosyphilis is minor and not significant. • Congenital syphilis is rarely encountered because the disease can be treated during pregnancy.

25. The incubation period is 10-90 days. The disease has 2 stages: • an early stage • a secondary stage. • The early stage consists of primary and secondary lesions very similar to those of venereal syphilis. • The secondary stage consists of late latent disease and tertiary lesions. Each stage affects different tissues and organs.

26. The primary lesions • A small, eroded or ulcerated papule is usually asymptomatic. • Primary lesions heal in 1-6 weeks and often go undiagnosed.

27. Secondary stage • Secondary stage lesions can appear as mucous patches on the lips, the palate, and the larynx. • Angular stomatitis, condylomata, oral ulcers, and generalized adenopathy can also be seen in the secondary stage. • Painful osteoperiostitis in the long bones (eg, tibia) can occur. • This stage can persist for 6-9 months.

28. Tertiary and late-stage • Tertiary and late-stage disease usually develops 6 months to years after inoculation and may manifest as gummas of the skin, the bones, or the cartilage. • Saddle nose deformity and palate perforation can occur. Neurologic involvement and cardiac involvement are rare.

29. Laboratory diagnostics Dark-field microscopy • This is the best method to confirm a treponemal disease. Although it does not specify the correct species because of similarities in morphology, the test promptly confirms that the infection is caused by a treponeme.

30. Serologic tests • The fluorescence treponemal antibody absorption (FTA-ABS) test, are positive in all stages of the disease. • Nontreponemal tests, such as the Venereal Disease Research Laboratory (VDRL) test and the rapid plasma reagent (RPR) test, are reactive 2-3 weeks after the onset of the primary lesion.

31. Treatment Drug Category: • Antibiotics – • Penicillin G benzathine (Bicillin LA); • Tetracycline (Sumycin) and • Erythromycin can be used in patients allergic to penicillin.

32. Prophylaxis • No vaccines for the disease are available.