Sex, age, newly found leprosy patients by cluster.

1<p>M/F ratio = male/female ratio.</p>2<p>Registered prevalence (at sub-district level) per 10,000 population per September 30, 2002, before the survey.</p

Prevalence of previously undiagnosed leprosy (PPUL) per 10,000 in the subgroups of the contact population of the COLEP study [13] and in the general population sample.

1<p>95% CI = 95% confidence interval for PPUL.</p

Model structure to calculate benefits (newly diagnosed leprosy patients) and costs of chemoprophylaxis with single dose rifampicin.

<p>Model structure to calculate benefits (newly diagnosed leprosy patients) and costs of chemoprophylaxis with single dose rifampicin.</p

Summary of total costs in the two treatment arms (in US$).

<p>Summary of total costs in the two treatment arms (in US$).</p

Number of leprosy patients arising from contacts after 2 years according to physical distance of the contacts to the index patient, by intervention (standard treatment <i>vs.</i> chemoprophylaxis).

<p>Number of leprosy patients arising from contacts after 2 years according to physical distance of the contacts to the index patient, by intervention (standard treatment <i>vs.</i> chemoprophylaxis).</p

Cumulative incidence of NFI for risk groups defined by the adjusted prediction rule, using WHO leprosy classification and presence of anti-PGL-I antibodies as predictive variables.

<p>NFI = nerve function impairment, PGL-I = phenolic glycolipid I.</p

Cumulative incidence of NFI for risk groups defined by the Bands prediction rule, using WHO leprosy classification and longstanding NFI at diagnosis as predictive variables.

<p>NFI = nerve function impairment, Bands = Bangladesh acute nerve damage study.</p

Agreement between NFI risk groups according to the Bands prediction rule and the adjusted prediction rule.

<p>Table shows number of patients per risk group and (number of patients with NFI event). Totals show number of patients, (number of patients with NFI event) and percentage of NFI events in that particular group.</p><p>NFI = nerve function impairment, Bands = Bangladesh acute nerve damage study.</p

Longitudinal assessment of anti-PGL-I serology in contacts of leprosy patients in Bangladesh

<div><p>Background</p><p>Despite elimination efforts, the number of <i>Mycobacterium leprae</i> (<i>M</i>. <i>leprae</i>) infected individuals who develop leprosy, is still substantial. Solid evidence exists that individuals living in close proximity to patients are at increased risk to develop leprosy. Early diagnosis of leprosy in endemic areas requires field-friendly tests that identify individuals at risk of developing the disease before clinical manifestation. Such assays will simultaneously contribute to reduction of current diagnostic delay as well as transmission. Antibody (Ab) levels directed against the <i>M</i>.<i>leprae</i>-specific phenolic glycolipid I (PGL-I) represents a surrogate marker for bacterial load. However, it is insufficiently defined whether anti-PGL-I antibodies can be utilized as prognostic biomarkers for disease in contacts. Particularly, in Bangladesh, where paucibacillary (PB) patients form the majority of leprosy cases, anti-PGL-I serology is an inadequate method for leprosy screening in contacts as a directive for prophylactic treatment.</p><p>Methods</p><p>Between 2002 and 2009, fingerstick blood from leprosy patients’ contacts without clinical signs of disease from a field-trial in Bangladesh was collected on filter paper at three time points covering six years of follow-up per person. Analysis of anti-PGL-I Ab levels for 25 contacts who developed leprosy during follow-up and 199 contacts who were not diagnosed with leprosy, was performed by ELISA after elution of bloodspots from filter paper.</p><p>Results</p><p>Anti-PGL-I Ab levels at intake did not significantly differ between contacts who developed leprosy during the study and those who remained free of disease. Moreover, anti-PGL-I serology was not prognostic in this population as no significant correlation was identified between anti-PGL-I Ab levels at intake and the onset of leprosy.</p><p>Conclusion</p><p>In this highly endemic population in Bangladesh, no association was observed between anti-PGL-I Ab levels and onset of disease, urging the need for an extended, more specific biomarker signature for early detection of leprosy in this area.</p><p>Trial registration</p><p>ClinicalTrials.gov <a href="https://clinicaltrials.gov/ct2/show/ISRCTN61223447" target="_blank">ISRCTN61223447</a></p></div

Cross-sectional analysis of anti-PGL-I Ig antibody levels at intake.

<p>Anti-PGL-I antibodies at intake for contacts of leprosy patients who developed leprosy during the study (black circle; n = 25) and contacts who remained free of leprosy disease (white box; n = 198) were detected by ELISA using natural disaccharide of PGL-I linked to HSA (ND-O-HSA). Optical density readings were performed at 450nm (OD₄₅₀) and corrected for background levels. Median values per group are indicated by horizontal lines. The cut-off for positivity is indicated by the dashed horizontal line.</p