Leishmanin Skin Test Standardization and Evaluation of Safety, Dose, Storage, Longevity of Reaction and Sensitization

Endemic Transmission of Visceral Leishmaniasis in Bhutan

“…We hypothesized that the much higher bed net usage in Sunkosh, where the malaria control program had distributed nets to all houses, might account for the difference in transmission rates. However, we could not test this hypothesis in the data set, because the (9) systematic difference in bed net usage between the two sites was tantamount to epidemiological confounding. Further investigation is required to evaluate other possible risk factors, such as environmental determinants of vector populations and housing conditions, in addition to direct assessment of the potential protective effect of nets.…”

“…7 Following the international consensus definition, the LST was considered positive if the mean of the two measurements was 5 mm or greater. 8,9 The Institutional Review Board of the Centers for Disease Control and Prevention reviewed the protocol and determined that the activity met the criteria for an outbreak investigation, and as such was not classified as research and did not require formal Institutional Review Board approval.…”

Cutaneous leishmaniasis in the Peruvian Andes: an epidemiological study of infection and immunity

“…An (MST). The explanation usually suggested for this apparent lack of specificity is that these people were exposed to sub-clinical leishmanial transmission, possibly because they were infected with avirulent (non-pathogenic) parasites [9][10][11][12][13][14][15].…”

“…Previous studies of the proportion of leishmania parasites which are avirulent have been largely qualitative, with the notable exception of Weigle and coworkers [14], who suggested that the 'relative pathogenicity' (rp) of the parasite population in an endemic area can be estimated by 'the fraction of [MST] reactive individuals who manifest signs or a history of prior leishmanial lesions', as detected in a cross-sectional survey. The value of rp calculated from previous cross-sectional studies varies considerably, for example: 0-02 [16], 0 03 [17], 0 07 [11], 0-11 [18], 0-22 [19], 0-25 [12], 0-67 [20], and 1-0 [21].…”

“…In addition to genetic variation in parasite virulence, rp could be influenced by a number of factors [22]: (i) rp will be negatively correlated with the extent of cross-protection that a sub-clinical infection confers against subsequent clinical infection; (ii) MST sensitivity will vary with dose, antigen type and storage conditions of the leishmanin [14]; (iii) a positive MST response could be induced by cross-reacting parasitic infections, such as glandular tuberculosis, lepromatous leprosy or lizard leishmania [23]; (iv) a positive MST response could be stimulated by a previous MST [24]; (v) the clinical response to leishmania infections will depend on human susceptibility; (vi) following human infection, there may be a latent period between MST conversion and clinical response; and (vii) cryptic infections could be due to mis-diagnosis [18]: scars could be 'lost' more quickly than MST positivity, due to a combination of skin ageing and patients' inability to remember their past infections with time. Thus cross-sectional epidemiological data are likely to be an unreliable indicator of either parasite virulence or host susceptibility.…”