Archival, paleopathological and aDNA-based techniques in leprosy research and the case of Father Petrus Donders at the Leprosarium 'Batavia', Suriname.

OBJECTIVE: We assessed whether Petrus Donders (died 1887), a Dutch priest who for 27 years cared for people with leprosy in the leprosarium Batavia, Suriname, had evidence of Mycobacterium (M.) leprae infection. A positive finding of M. leprae ancient (a)DNA would contribute to the origin of leprosy in Suriname. MATERIALS: Skeletal remains of Father Petrus Donders; two additional skeletons excavated from the Batavia cemetery were used as controls. METHODS: Archival research, paleopathological evaluation and aDNA-based testing of skeletal remains. RESULTS: Neither archives nor inspection of Donders skeletal remains revealed evidence of leprosy, and aDNA-based testing for M. leprae was negative. We detected M. leprae aDNA by RLEP PCR in one control skeleton, which also displayed pathological lesions compatible with leprosy. The M. leprae aDNA was genotyped by Sanger sequencing as SNP type 4; the skeleton displayed mitochondrial haplogroup L3. CONCLUSION: We found no evidence that Donders contracted leprosy despite years of intense leprosy contact, but we successfully isolated an archaeological M. leprae aDNA sample from a control skeleton from South America. SIGNIFICANCE: We successfully genotyped recovered aDNA to a M. leprae strain that likely originated in West Africa. The detected human mitochondrial haplogroup L3 is also associated with this geographical region. This suggests that slave trade contributed to leprosy in Suriname. LIMITATIONS: A limited number of skeletons was examined. SUGGESTIONS FOR FURTHER RESEARCH: Broader review of skeletal collections is advised to expand on diversity of the M. leprae aDNA database.

Control de la lepra y contagionismo en suriman / No disponible

La lepra, aunque actualmente está desapareciendo, no ha sido derrotada todavía en Surinam. En la época colonial fue un gran problema para el gobierno colonial y la población, siendo la mayoría de pacientes (en la época pre-abolicionista) esclavos. En el siglo XVIII se estableció un sistema de control que ya incluía la en la legislación la detección y el confinamiento como métodos importantes. Los médicos holandeses que ejercían en Surinam durante el siglo XVIII y primera mitad del siglo XIX propusieron modelos contagionistas de contención que sugieren que la lepra era causada por una mezcla de factores, siendo la infección uno de ellos. Pero durante la primera mitad del siglo XIX, los investigadores europeos rechazaron mayoritariamente la infección y prevaleció el anti-contagionismo, considerando la herencia y los factores medioambientales como su causa. Al mismo tiempo, en Surinam - puesto que la lepra estaba incontrolada - la lucha contra la lepra se reforzó promulgando leyes implacables para perseguir e identificar a los leprosos. A su vez, Charles Louis Drognat-Landré defendió el punto de vista (tesis Utrecht) de que solamente la infección es la causa de la lepra. Su argumento sobre el contagionismo fue rechazado en Holanda, pero posteriormente publicó sus ideas en francés y así llegaron a ser más conocidas internacionalmente e influyeron en el noruego Hansen. Este descubrió algunos años después el microorganismo causal. Se afirma que hay una relación entre el desarrollo de una forma de contagionismo típico surimanés, un sistema de control de la lepra brutal y la estructura política autocrática, no liberal (hacia los esclavos) de la colonia holandesa de Surinam

Leprosy is nowadays a disappearing but not yet defeated disease in Suriname. In colonial times it was a burden for colonial government and people, the majority of patients (in preabolition times) being slaves. In the 18th century a control system was established, with detection and isolation, anchored in legislation, as major methods. Dutch physicians working in Suriname in the 18th and first half of the 19th century proposed contingent contagionistic models, according to which leprosy was caused by a mixture of factors, infection being one of them. But in the first half of the 19th century European researchers generally denied infection as the cause of leprosy and the paradigm of anti-contagionism prevailed, considering heredity and environmental factors as its cause. At the same time in Suriname - because leprosy appeared uncontrollable - the fight against the disease was reinforced by promulgating more relentless laws to hunt and identify lepers. In line with this, the Suriname born Charles Louis Drognat-Landré defended the view (thesis Utrecht) that infection is the one and only cause of leprosy. His extreme contagionism was sharply rejected in The Netherlands, but then he published his ideas in French and so could reach the international scene and influence the Norwegian Hansen. The latter discovered the culpable micro-organism a few years later. We claim a correlation between the development of a typical Surinamese form of contagionism, the brutal leprosy control system and the autocratic, non-liberal (towards the slaves) political structure of the Dutch colony Suriname

Progressive macular hypomelanosis: an overview.

Progressive macular hypomelanosis (PMH) is a common skin disorder that is often misdiagnosed. Various authors have written about similar skin disorders, referring to them by different names, but we believe that all these similar disorders are part of the same entity.PMH is characterized by ill-defined nummular, non-scaly hypopigmented spots on the trunk, often confluent in and around the midline, and rarely extending to the proximal extremities and neck/head region. There is no itch, pain, or preceding inflammation. PMH has a worldwide distribution; however, it is more often identified in Black people living in or originating from tropical countries. It is also more often seen in young females. The natural history of PMH is stable disease or perhaps slow progression over decades, with spontaneous disappearance after mid-life. Extensive pityriasis alba is probably identical with PMH and we suggest discontinuation of use of the former term on the grounds that extensive pityriasis alba is histologically and clinically different from classical pityriasis alba, which is basically an eczematous type of disorder.PMH is characterized histologically by diminished pigment in the epidermis and a normal-looking dermis. Electron microscopy shows a shift from large melanosomes in normal-looking skin to small aggregated, membrane-bound melanosomes in hypopigmented skin. PMH should be differentiated from other disorders with hypopigmentation on the trunk such as pityriasis versicolor. We propose that Propionibacterium acnes bacteria living in hair follicles are the cause of PMH as a result of production of a hypothetical depigmenting factor. This hypothesis is based on: (i) the presence of a red follicular fluorescence in the hypopigmented spots and the absence of this phenomenon in normal skin when examined under a Wood's light in a dark room; (ii) cultivation of P. acnes from the follicles in the hypopigmented spots but not from follicles in normal-looking skin; and (iii) improvement of the disorder after elimination of these micro-organisms with topical antimicrobial treatment in combination with UVA light.Currently, the treatment of choice of PMH is application of 1% clindamycin lotion during the daytime, 5% benzoyl peroxide gel at night-time, and UVA light irradiation three times a week for a period of 12 weeks. There is insufficient information available as yet to comment on the recurrence rate after therapy.

Benzoyl peroxide/clindamycin/UVA is more effective than fluticasone/UVA in progressive macular hypomelanosis: a randomized study.

BACKGROUND: There is no effective treatment for progressive macular hypomelanosis. Recent findings indicate that Propionibacterium acnes may play a role in the pathogenesis. OBJECTIVES: We sought to compare the effectiveness of antimicrobial therapy with anti-inflammatory therapy in patients with progressive macular hypomelanosis. METHODS: A total of 45 patients were randomized to a within-patient left-right comparison study of benzoyl peroxide 5% hydrogel/clindamycin 1% lotion in combination with UVA irradiation versus fluticasone 0.05% cream in combination with UVA irradiation. Repigmentation was determined by photometric measurements of changes in skin color and by patient and dermatologist assessment using before and after photographs. RESULTS: Benzoyl peroxide 5% hydrogel, clindamycin 1% lotion, and UVA led to better repigmentation than fluticasone 0.05% cream in combination with UVA irradiation in all measurements. (Photometric measurements P = .007, patient assessment P < .0001, and dermatologist assessment P < .0001.) LIMITATIONS: There was difficult objective color measurement. Therefore, subjective assessment has important additional value. Right-left comparisons have certain inherent limitations. CONCLUSION: Antimicrobial therapy in conjunction with light was more effective in repigmentation in patients with progressive macular hypomelanosis than a combination of anti-inflammatory therapy and light.

Propionibacterium acnes and the pathogenesis of progressive macular hypomelanosis.

BACKGROUND: Progressive macular hypomelanosis is a common hypopigmentation mainly on the central parts of the trunk, predominantly in young adults, especially women. It is often mistaken for pityriasis versicolor and pityriasis alba. It occurs in all races and has been described in many parts of the world. We discovered follicular red fluorescence restricted to lesional skin. We suspected a relation with a porphyrin-producing bacteria residing in sebum of the pilosebaceous duct, and we therefore performed a study in 8 patients. Observation In all biopsy specimens taken from lesional skin of 8 women, we could demonstrate gram-positive bacteria in the pilosebaceous duct, and a mild perifollicular lymphocytic infiltrate was seen. In all but 1 patient, Propionibacterium acnes was yielded from cultured biopsy specimens taken from follicular lesional skin. Healthy follicular skin did not show bacteria in histological sections, and cultures did not yield anaerobic bacteria. CONCLUSIONS: There seems to be a relation between the presence of P acnes and the hypopigmented macules. We propose that a factor is produced by these strains of P acnes, which interfere with melanogenesis. Based on these observations, we are undertaking a clinical trial to find a treatment for this troubling, intractable disease.