02845nas a2200457   4500000000100000008004100001260001600042653001500058653001000073653000900083653002200092653001500114653001500129653001000144653002100154653002000175653002700195653001100222653002000233653002100253653002600274653003800300653001100338653001200349653000900361653001600370653002000386653001700406653001600423100001400439700001400453700001200467700001400479700001700493245011900510856007700629300001100706490000600717520165000723022001402373       2010                            d  c2010 Nov 1910aAdolescent10aAdult10aAged10aAged, 80 and over10aAlgorithms10aBangladesh10aChild10aCluster Analysis10aContact Tracing10aFamily Characteristics10aFemale10aGenes, Dominant10aGenes, Recessive10aGenetic Heterogeneity10aGenetic Predisposition to Disease10aHumans10aleprosy10aMale10aMiddle Aged10aModels, Genetic10aRisk Factors10aYoung Adult1 aFischer E1 ade Vlas S1 aMeima A1 aHabbema D1 aRichardus JH00aDifferent mechanisms for heterogeneity in leprosy susceptibility can explain disease clustering within households.  uhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC2988824/pdf/pone.0014061.pdf  ae140610 v53 a<p>The epidemiology of leprosy is characterized by heterogeneity in susceptibility and clustering of disease within households. We aim to assess the extent to which different mechanisms for heterogeneity in leprosy susceptibility can explain household clustering as observed in a large study among contacts of leprosy patients.We used a microsimulation model, parameterizing it with data from over 20,000 contacts of leprosy patients in Bangladesh. We simulated six mechanisms producing heterogeneity in susceptibility: (1) susceptibility was allocated at random to persons (i.e. no additional mechanism), (2) a household factor, (3, 4) a genetic factor (dominant or recessive), or (5, 6) half a household factor and half genetic. We further assumed that a fraction of 5%, 10%, and 20% of the population was susceptible, leading to a total of 18 scenarios to be fitted to the data. We obtained an acceptable fit for each of the six mechanisms, thereby excluding none of the possible underlying mechanisms for heterogeneity of susceptibility to leprosy. However, the distribution of leprosy among contacts did differ between mechanisms, and predicted trends in the declining leprosy case detection were dependent on the assumed mechanism, with genetic-based susceptibility showing the slowest decline. Clustering of leprosy within households is partially caused by an increased transmission within households independent of the leprosy susceptibility mechanism. Even a large and detailed data set on contacts of leprosy patients could not unequivocally reveal the mechanism most likely responsible for heterogeneity in leprosy susceptibility.</p>  a1932-6203