Body location of "New World" cutaneous leishmaniasis lesions and its impact on the quality of life of patients in Suriname.

Cutaneous leishmaniasis (CL) is a chronic skin infection caused by Leishmania parasites, causing single or multiple skin nodules and ulcers on the exposed body locations. Healing of lesions is followed by scar formation. Active and healed CL lesions may affect patient's health related quality of life (HRQL). The aim of this study was to determine whether the body location of the leishmaniasis lesions affects the HRQL of localized CL patients in Suriname. The HRQL of 163 patients with CL was assessed by Skindex-29 and EQ-5D/VAS questionnaires. Forty-six patients out of the total study population also participated in a qualitative anthropological study involving in depth interviews. All patients were allocated in 4 groups in the following hierarchy: head and face, upper limbs, lower limbs and trunk. Patients with lesions on the lower limbs had significantly higher Skindex-29 scores, indicating worse HRQL, in the symptom scale compared to lesions on head/face and trunk. The lower limb group was more likely to report problems in the dimensions self-care, mobility, daily activities and pain/discomfort of the EQ-5D. Little to no social stigma was reported in the in-depth interviews. The findings of this study indicate that Surinamese patients with CL lesions located on the lower limbs had more impairment in HRQL than on other body locations. Stigma related to CL seems to be virtually absent in Suriname.

Evaluation of point of care tests for the diagnosis of cutaneous leishmaniasis in Suriname.

BACKGROUND: Cutaneous leishmaniasis (CL) is a serious health problem in Suriname. To expand the diagnostic options, two newly developed diagnostic tests, i.e. the rapid diagnostic test CL Detect™ Rapid Test (CL Detect) and the Loopamp™ Leishmania Detection Kit (Loopamp) were evaluated. METHODS: Diagnostic test performance was compared to the routine diagnostic approach in place, i.e. clinical symptoms combined with microscopy, and to polymerase chain reaction (PCR), which was used as a reference standard. The study population (n = 93) was a typical representation of the CL affected population in Suriname and mainly infected with Leishmania guyanensis. RESULTS: CL Detect had a very low sensitivity compared to microscopy (36.7%) or PCR (35.8%), due to a high number of false negative results. The specificity of the CL Detect compared to microscopy and PCR was 85.7 and 83.3% respectively. Loopamp sensitivity was 84.8% compared to microscopy and 91.4% compared to PCR. The Loopamp test had a moderate specificity (42.9%) compared to microscopy, but a good specificity compared to PCR (91.7%). CONCLUSION: The CL Detect is not likely to be a good replacement for the routine diagnostic procedure for CL in Suriname. The high sensitivity of the easy to perform Loopamp enables the implementation of sensitive molecular diagnosis in resource limited settings.

Randomized single-blinded non-inferiority trial of 7 mg/kg pentamidine isethionate versus 4 mg/kg pentamidine isethionate for cutaneous leishmaniaisis in Suriname.

BACKGROUND: Standard treatment of cutaneous leishmaniasis (CL) in Suriname entails three injections of pentamidine isethionate (PI) 4 mg/kg per injection in 7 days (7 day regimen). Compliance to treatment is low and may contribute to increasing therapy failure. A 3 day regimen, including 2 injections of 7 mg/kg in 3 days may increase compliance. METHODS: In a randomized, single-blinded non-inferiority trial conducted in Suriname, 84 CL patients received the 7 day regimen and 79 CL patients received the 3 day regimen. Primary objective was the proportion of patients clinically cured at 6 weeks follow-up. Secondary objectives were clinical cure at 12 weeks follow-up; parasitological cure at 6 and 12 weeks; adverse and drug related toxicity events recorded one week after the end of treatment and health related quality of life. The non-inferiority margin was set at 15%, 1 sided test, α = 0.1. RESULTS: At 6 weeks follow-up 31 (39%) patients in the 3 day regimen and 41 (49%) patients in the 7 day regimen were clinically cured. Intention to treat (ITT) analyses showed that the difference in proportion clinically cured was -9.6% (90% Confidence Interval (CI): -22.3% to 3.2%). Per protocol (PP) analysis showed that the difference in proportion clinically cured was 0.2% (90% CI: -14.6% to 15.2%). ITT analysis showed that the difference in proportion parasitological cured at 6 weeks was -15.2% (90% CI:-28.0% to -2.5%). PP analyses showed similar results. Non-inferiority could not be concluded for all adverse and toxicological events. CONCLUSION: We cannot conclude that the 3 day regimen is non-inferior to the 7 day regimen regarding proportion clinically and parasitological cured. Therefore there is no evidence to change the current standard practice of the 7 day regimen for the treatment of CL in Suriname.

First case of cutaneous leishmaniasis caused by Leishmania (Viannia) braziliensis in Suriname.

The main causative agent of cutaneous leishmaniasis (CL) in Suriname is Leishmania (Viannia) guyanensis. This case report presents a patient infected with Leishmania (Viannia) braziliensis, a species never reported before in Suriname. This finding has clinical implications, because L. braziliensis has a distinct clinical phenotype characterized by mucocutaneous leishmaniasis, a more extensive and destructive form of CL that requires different treatment. Clinicians should be aware that chronic cutaneous ulcers in patients from the Guyana region could be caused by L. braziliensis.

Deteccao de determinantes antigenicos compartilhados entre a proteina de choque termico 65 do Mycobacterium leprae e proteina de choque termico 60 humana / Detection of shared antigenic determinantes between Mycobacterium leprae heat shock protein 65 and human heat shock protein 60

Nestes estudos foram investigados se o Mycobacterium leprae (M. leprae) e o homem compartilham determinantes antigenicos que podem estar localizados nas Proteinas de Choque Termico (HSPs) e que podem ser responsaveis pela destruicao tecidual. Usando-se tecnica de coloracao unica pela imunoperoxidase em cortes feitos com criostato, observaram-se tres anticorpos que eram dirigidos contra HSP-60 (anticorpos policlonais SPA-804, SP-805 e o anticorpo monoclonal SPA-807, que provavelmente reagiram especificamente com macrofagos e celular epitelioides em biopsia cutaneas de pacientes com hanseniase. No Western Blot foi observado que todos os anticorpos contra HSP-60 humana a anticorpos monoclonais (MoAbs) contra HSP-65 do M. leprae (F47-10, F67-18, F88-1) reagiram intensamente com as proteinas do M. leprae sonicado com peso molecular de 65 kDa, indicando semelhanca de alguns determinantes antigenicos entre HSP-60 humana e HSP-65 do M. leprae. Subsequentemente, um estudo imunohistoquimico comparativo dos padroes de coloracao de anticorpos contra HSP-60 humana e anticorpos contra HSP-65 do M. leprae, usando cortes cutaneos feito em criostato de hanseniase paucibacilar (PB), multibacilar (MB) e outras doencas granulomatosas, revelaram que os MoAbs F47-10 e F67-18 reagiram somente fracamente com os granulomas em hanseniase PB e em outras doencas granulomatosas cutaneas, mas coravam o granuloma da hanseniase MB intensamente. O MoAb F88-1 e os anticorpos policlonais SPA-804, SPA-805 e o MoAb SPA 807 coraram os granulomas dos pacientes PB e de outros doencas cutaneas granulomatosas com a mesma intensidade daquela nos pacientes MB. Utilizando-se uma tecnica de dupla coloracao, observou-se que os determinantes antigenicos reconhecidos pelo MoAb contra HSP-60 humana (SPA-807) e os MoBbs contra a HSP-65 do M. leprae (F67-18, F47-10, F88-1) estavam, na maioria das vezes, localizados nos macrofagos. Esses achados nao contradizem nossa hipotese de que semelhancas entre determinantes antigenicos nas HSPs no M. leprae e no hospedeiro humano podem ser, no minimo em parte, responsaveis pela inducao de uma reacao autoimune na hanseniase causando formacao de granuloma com subsequente dano tecidual. Os resultados deste estudo tambem indicaram que alguns destes determinantes estao provavelmente localizados na HSP-60. Uma explicacao similar possivelmente se aplique aos achados em...

Detection of shared antigenic determinants between Mycobacterium leprae heat shock protein 65 and human heat shock protein 60

In these studies, it was investigated whether M. leprae and man share antigenic determinants which may be located on Heat Shock Proteins (HSPs), and which may be responsible for tissue destruction. Using immunoperoxidase single-staining technique on cryostat sections it was observed that three antibodies which are directed against HSP 60 (polyclonal antibodies SPA 804 and SPA 805 and monoclonal antibody SPA 807) probably reacted specifically with macrophages and epitheloid cells in leprosy skin sections. On Western Blotting, it was observed that the antibodies againts human HSP 60 nomoclonal antibodies (MoAbs) against M. leprae HSP 65 (F 47-10, F 67-18, F 88-1) all reacted strongly with sonicated M. leprae proteins with a molecular mass of 65 kDa undicating similarity of some antigenic determinants between human HSP 60 and M. leprae HSP 65. Subsequently, a comparative immunohistochemical study of the staining patterns of antibodies against human HSP 60 and antibodies against M. leprae HSP 65 using cryostat skin section of paucibacillary (PB) leprosy multibacillary (MB) leprosy and other granulomatous skin disorders revealed that the MoAbs F 47-10 and F 67-18 reacted only weakly with the granulomas in PB leprosy and in other granulomatous skin diseases, but stained MB leprosy granuloma strongly. The MoAb F 88-1 and the polyclonal antibodies SPA 804, SPA 805 and the MoAb SPA 807 stained granulomas of PB patients and of other granulomatous skin disorders with the same intensity as that MB patients. Using a double-staining technique, it was observed that the antigenic determinants recognized by the MoAb against human HSP 60 (SPA 807) and the MoAbs against M. leprae HSP 65 (F 67-18, F 47-10, F 88-1) were mostly located in the macrophages. These findings do not contradict our suggestion, Heath Shock Proteins of M. leprae and the human host may be at least in part responsible for the induction of an autoimmune reaction causing granuloma formation with subsequent tissue damage in leprosy. The results of this study also indicated that some of these determinats are probably located on HSP 60. A similar explanation possibly applies to the findings in the other granulomatous disease e.g. sarcoidosis probably micobacterial induced and necrobiosis lipoidica related to diabetis, in which antigenic similarities between bacterial HSP 65 and human HSP 60 are considered to play a part.