Lepra Bubalorum, a Potential Reservoir of Mycobacterium leprae.

In 1926, a mycobacterial skin disease was observed in water buffaloes by researchers in Indonesia. The disease was designated as skin tuberculosis, though it was hypothesized that it might be a form of leprosy or a leprosy-like disease. In a follow-up study (Ph.D. thesis Lobel, 1934, Utrecht University, Netherlands) a similar nodular skin disease was described in Indonesian water buffaloes and named "lepra bubalorum" or "nodular leprosy." Two decades later Kraneveld and Roza (1954) reported that, so far, the diagnosis lepra bubalorum had been made in 146 cases in Indonesia. After a final series of research reports by Indonesian veterinarians in 1961, no subsequent cases were published. Based on information from these reports, it can be concluded that, even though evidence of nerve involvement in buffaloes was not reported, similarities exist between lepra bubalorum and Hansen's disease (leprosy), i.e., nodular skin lesions with a chronic course and microscopically granulomatous reactions with AFB in globi in vacuoles. This raises the question as to whether these historical cases might indeed have been caused by Mycobacterium leprae, Mycobacterium lepromatosis or another representative of the M. leprae complex. The future use of state-of-the-art molecular techniques may answer this question and may also help to answer the question whether water buffaloes should be considered as a potential natural reservoir of the causative pathogen of Hansen's disease.

La influencia del poder colonial sobre la población y la naturaleza determinaron los asentamientos de la enfermedad de Hansen en Surinam / No disponible

Los colonizadores holandeses en Surinam afirmaban que la lepra (o enfermedad de Hansen) era muy contagiosa y se transmitía entre humanos. Se construyó un "cordón sanitario" alrededor de los pacientes, sobre todo esclavos africanos y asiáticos contratados como trabajadores y sus descendientes. Se les perseguía y eran recluidos en aldeas para afectados de lepra muy remotas localizadas en la selva tropical. Algunos pacientes obedecieron a las autoridades, mientras que otros resistieron y se rebelaron. Sus historias revelan conceptos confusos sobre la enfermedad con su cultura y el medioambiente surinamés, y contienen importantes informaciones para comprender su mundo y la vida dentro y fuera de las colonias para lepra. Combinaban prácticas sanitarias tradicionales y plantas medicinales de su hábitat natural con tratamientos biomédicos (practicando un pluralismo médico). Creían en una gran variedad de explicaciones sobre la enfermedad, predominantemente los conceptos tabúes treef, tyina y animales tótem asociados con su hábitat natural (el bioma surinamés). Algunas de las explicaciones de su imaginario (por ejemplo, la lepra es transmitida por la tierra y ciertos animales) revelan una analogía sorprendente con descubrimientos científicos recientes. Nuestra investigación revela que la naturaleza contribuye a moldear el mundo de los pacientes de Hansen. Un planteamiento ecológico puede contribuir significativamente a la hora de comprender su mundo. Hay que efectuar una investigación histórica y antropológica comparativa para trazar la influencia de distintos biomas sobre los modelos locales. Las colonias de Hansen actualmente abandonadas y sus entornos naturales son lugares importantes para el patrimonio cultural

According to the Dutch colonizers in Suriname, leprosy (or Hansen's disease) was highly contagious and transmitted from human-to-human. A "cordon sanitaire" was constructed around the patients, mainly African slaves and Asian indentured laborers and their descendants. They were tracked down and incarcerated in remote leprosy settlements located in the rainforest. Some patients obeyed the authorities while others resisted and rebelled. Their narratives, revealing conceptual entanglement of the disease with their culture and the Surinamese natural environment, contain important information for understanding their world and their life inside and outside of leprosy settlements. They combined traditional health practices and medicinal plants from their natural habitat with biomedical treatments (practicing medical pluralism). They believed in a diversity of disease explanations, predominantly the taboo concepts treef, tyina, and totem animals associated with their natural habitat (the Surinamese biome). Some of their imaginary explanations (e.g., "leprosy is carried and/or transmitted through soil and certain animals") show a surprising analogy with recent findings from leprosy scientists. Our research shows that nature contributes to shaping the world of Hansen's disease patients. An ecological approach can make a valuable contribution to understanding their world. Comparative historical and anthropological research needs to be conducted to map the influence of different biomes on local explanatory models. The now deserted Hansen's disease settlements and their natural environments are interesting research sites and important places of cultural heritage

Reservoirs and transmission routes of leprosy; A systematic review.

Leprosy is a chronic infectious disease caused by Mycobacterium leprae (M. leprae) and the more recently discovered Mycobacterium lepromatosis (M. lepromatosis). The two leprosy bacilli cause similar pathologic conditions. They primarily target the skin and the peripheral nervous system. Currently it is considered a Neglected Tropical Disease, being endemic in specific locations within countries of the Americas, Asia, and Africa, while in Europe it is only rarely reported. The reason for a spatial inequality in the prevalence of leprosy in so-called endemic pockets within a country is still largely unexplained. A systematic review was conducted targeting leprosy transmission research data, using PubMed and Scopus as sources. Publications between January 1, 1945 and July 1, 2019 were included. The transmission pathways of M. leprae are not fully understood. Solid evidence exists of an increased risk for individuals living in close contact with leprosy patients, most likely through infectious aerosols, created by coughing and sneezing, but possibly also through direct contact. However, this systematic review underscores that human-to-human transmission is not the only way leprosy can be acquired. The transmission of this disease is probably much more complicated than was thought before. In the Americas, the nine-banded armadillo (Dasypus novemcinctus) has been established as another natural host and reservoir of M. leprae. Anthroponotic and zoonotic transmission have both been proposed as modes of contracting the disease, based on data showing identical M. leprae strains shared between humans and armadillos. More recently, in red squirrels (Sciurus vulgaris) with leprosy-like lesions in the British Isles M. leprae and M. lepromatosis DNA was detected. This finding was unexpected, because leprosy is considered a disease of humans (with the exception of the armadillo), and because it was thought that leprosy (and M. leprae) had disappeared from the United Kingdom. Furthermore, animals can be affected by other leprosy-like diseases, caused by pathogens phylogenetically closely related to M. leprae. These mycobacteria have been proposed to be grouped as a M. leprae-complex. We argue that insights from the transmission and reservoirs of members of the M. leprae-complex might be relevant for leprosy research. A better understanding of possible animal or environmental reservoirs is needed, because transmission from such reservoirs may partly explain the steady global incidence of leprosy despite effective and widespread multidrug therapy. A reduction in transmission cannot be expected to be accomplished by actions or interventions from the human healthcare domain alone, as the mechanisms involved are complex. Therefore, to increase our understanding of the intricate picture of leprosy transmission, we propose a One Health transdisciplinary research approach.

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.

Detection of Mycobacterium leprae DNA in soil: multiple needles in the haystack.

Leprosy is an infectious disease caused by Mycobacterium leprae affecting the skin and nerves. Despite decades of availability of adequate treatment, transmission is unabated and transmission routes are not completely understood. Despite the general assumption that untreated M. leprae infected humans represent the major source of transmission, scarce reports indicate that environmental sources could also play a role as a reservoir. We investigated whether M. leprae DNA is present in soil of regions where leprosy is endemic or areas with possible animal reservoirs (armadillos and red squirrels). Soil samples (n = 73) were collected in Bangladesh, Suriname and the British Isles. Presence of M. leprae DNA was determined by RLEP PCR and genotypes were further identified by Sanger sequencing. M. leprae DNA was identified in 16.0% of soil from houses of leprosy patients (Bangladesh), in 10.7% from armadillos' holes (Suriname) and in 5% from the habitat of lepromatous red squirrels (British Isles). Genotype 1 was found in Bangladesh whilst in Suriname the genotype was 1 or 2. M. leprae DNA can be detected in soil near human and animal sources, suggesting that environmental sources represent (temporary) reservoirs for M. leprae.

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

[Coping with leprosy in the Dutch West Indies in the 19th century; opposing but meaningful views from Suriname]. / Omgang met lepra in 'de West' in de negentiende eeuw. Tegendraadse maar betekenisvolle geluiden vanuit Suriname.

Leprosy was highly prevalent among African slaves in the Dutch West Indian colony of Suriname. Largely based on observations in Suriname, Dutch physicians described the aetiology of leprosy in terms of'a substrate' to which all sorts of mixtures of infection, heredity and hygiene contributed ('seed and soil'). This explanatory model with multiple options for prevention and treatment left room for different developmental trajectories to control the spread of the disease in the various tropical colonies of the Dutch empire. In Suriname there was a growing worry in the 19th century regarding the spread of leprosy, threatening the health of slaves, settlers and colonial administrators. And this could be harmful to an already weakening plantation economy. This concern prompted the local administration to develop a rigorous policy of strict isolation of leprosy sufferers. This, in turn, intersected with a changing insight in Europe - including the Netherlands - that leprosy was non-contagious. However,'in splendid isolation' in the economically and politically marginal colony Suriname, Dutch physicians like Charles Landre and his son, Charles Louis Drognat Landré, could afford to ignore the European non-contagious approach and continue to support the strict isolation policies. Moreover, they developed a dissident radical explanation of leprosy as a disease caused only by contagion. In the absence of a receptive Dutch audience Drognat Landré published his contagion theory in French and so succeeded in inspiring the Norwegian Hansen, who subsequently discovered the culpable micro-organism. At the same time colonial administrators and physicians in the economically and politically important Dutch colonies in the East Indies adhered to the prevailing European concept and changed policies: the system of isolation was abolished. Given the rather different trajectories of leprosy health policies in the Dutch East and West Indies we point out the importance of a comparative approach.

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.