Visceral leishmaniasis is a vector-borne protozoan disease targeted for elimination from the Indian subcontinent by year 2020. Sri Lanka is a new focus of human leishmaniasis caused by a genetically distinct variant of Leishmania donovani, which is the species more widely known to cause visceral leishmaniasis (VL). The clinical entity that is most frequent in Sri Lanka is cutaneous leishmaniasis (CL), though a few cases of muco-cutaneous (MCL) and VL have also been reported in the recent past. In CL, papules, nodules, ulcerating nodules and ulcers occur mainly as single lesions on exposed body areas of affected individuals. A wide age range is affected including both sexes. The potential for visceralization in the cutaneous variant of L. donovani in Sri Lanka is not known. There is no evidence for a serological response in CL patients who have demonstrated negative for rK 39 antibodies in sera, (rk39 test being the recommended test for VL detection), while MCL and VL cases have been rK39 positive.Phlebotomus argentipes, the vector of L. donovani in other parts of the world is a widely prevalent insect in almost all parts of Sri Lanka. Studies are underway for vector identification. L.donovani is transmitted between this vector and the human host, the only known host for this species. However, domestic dogs have shown the presence of Leishmania parasites and also the presence of anti -L. donovani antibodies in their sera, providing primary evidence for the likely presence of an animal reservoir in Sri Lanka. Field-based risk factor studies have shown that there is peri-domestic as well as zoonotic/outdoor transmission cycles in different parts of the country.At present patients are detected mainly passively based on self referrals. Only a proportion of these patients proceed for pre-treatment laboratory confirmation due to the lack of freely available investigation facilities. Leishmaniasis was made a notifiable disease in Sri Lanka in 2008. Action plan for its control was drawn up with primary involvement of the Ministry of Health and other stake holders in 2008. Preventive and control activities are required to be put in place sooner rather than later. Enhanced case detection and active treatment are of prime value in controlling L.donovani infections. Availability of cost effective and field friendly diagnostic services in a decentralized manner, timely case management and vector control using appropriate protocols are necessary. To achieve this, a considerable amount of information is already available, and further research is needed to fill in the essential gaps.
Sri Lanka reports a large epidemic of cutaneous leishmaniasis (CL) caused by an atypical L. donovani while regional leishmaniasis elimination drive aims at achieving its targets in 2020. Visceralization, mucotrophism, and CL associated poor treatment response were recently reported. Long-term clinico-epidemiological trends (2001-2013) in this focus were examined for the first time. Both constant and changing features were observed. Sociodemographic patient characteristics that differ significantly from those of country profile, microchanges within CL profile, spatial expansion, constant biannual seasonal variation, and nondependency of clinical profile on age or gender were evident. Classical CL remains the main clinical entity without clinical evidence for subsequent visceralization indicating presence of parasite strain variation. These observations make a scientific platform for disease control preferably timed based on seasonal variation and highlights the importance of periodic and continued surveillance of clinic-epidemiological and other characteristics.
Cutaneous leishmaniasis caused by a genetic variant of L. donovani is being reported from Sri Lanka since year 2001. Patients presented from different geographical locations (600 patients from North or South and a minority of cases from other foci, 2001-2013) were studied. Analysis revealed two different sociodemographic and clinical profiles of leishmaniasis in Northern and Southern Sri Lanka. Also, the same different profiles were present in these foci since the onset of the recent outbreak and had independently propagated within each focus over the time. A profile of 14 parameters identified in the Northern focus was further examined with regard to other locations. Northwestern (10/14) and Central parts (9/14) of the island were more similar to Northern focus (14/14). Infection would have originated in one focus and spread to other 2 in Northern Sri Lanka. Southern focus was different from and appeared older than all others (2/14). Western focus that accommodates a large transient population had a mixed picture of North and South features (4/14). Lesions in North showed a slow progression and a nonulcerative nature (128/185, 69.2%), while those in South showed a rapid progression and less nonulcerative lesions (193/415, 46.5%). Clinical analysis favoured a parasite aetiology (considerable strain differences) rather than a host aetiology (age, gender, or genetics). Both foci demonstrated a biannual seasonal variation since the onset of the epidemic. Two peaks were observed during the early and latter parts of the year. Furthermore, long-term existence and recent spatiotemporal expansion and detection of leishmaniasis in this country rather than a recent introduction and establishment were indicated by these findings. Vigorous antimalarial activities that existed in Sri Lanka until few decades ago, lack of professional awareness, and more recent military activities that brought human population in close contact with a sylvatic cycle would have played a role in silent propagation of Leishmania parasites and subsequent increment in human cases, respectively, in this country.
Cutaneous leishmaniasis (CL) was first detected in Sri Lanka in 1992.Local disease is caused by a genetically different variant of Leishmania donovani. Early case detection and management is the mainstay of L. donovani control. High degree of clinical suspicion is critical but a clinical diagnostic tool is not available for leishmaniasis. Current study described, for the first time, a two-staged clinical algorhythm that facilitates screening of CL in Sri Lanka by primary health care worker in stage 1 and management by medical professional in stage 2.Selected clinical markers of 400 patients suspected of CL were analysed retrospectively with laboratory confirmation of leishmaniasis. Ten clinical markers predicted CL with a over 90% accuracy. Subsets of markers showed high levels of sensitivities (60-97.2%) and/or significant association with positive laboratory results as compared to negative lesions [typical onset (acne-form, painless non-itchy), (P 5 0.026), size up to 2 cm (P 5 0.046), well-defined edges (P 5 0.002), regular edges (P 5 0.018), rounded shape (P 5 0.030), and lesions at 5-8 months (P 5 0.052)]. Five of them (typical onset, number up to 2, small size, rounded edges, and rounded shape) also had w 70% sensitivity levels as compared to laboratory findings. Typical onset had the highest sensitivity of 97% and a PPV of 72%. Lesions at 5-8 months duration having defined edges (P 5 0.013, specificity 89.7%, PPV 83.1) or having regular edges (P 5 0.006, specificity 86.2%, PPV 82.4%) were also predictive of CL. Most of early laboratory-confirmed (v12 months) lesions remained v3 cm (sensitivity w 67%, PPV w 70%) and had defined edges (sensitivity of 52-71%, specificity 46.7-68.8%), (PPV 75.1-86%). Four clinical markers served as good diagnostic markers in both early (j4) and late (w12 months) lesions, viz. typical onset (91.3-98.4%), presence of j2 lesions (sensitivity 82.6-94.7%), size j2 cm (66.9-73.7%), and regular edges (68.6-76.3%). Reliability of clinical markers generally declined in chronic lesions. However, small lesions of over 12 months were highly indicative of CL (sensitivity of 66%, specificity 66.7%). None of the single/combination markers, however, were 100% sensitive or specific, highlighting the undeniable usefulness of laboratory confirmation, in diagnosis. Decision-making algorithm used 10 basic clinical features for screening and seven specific clinical markers for clinical handling and referral for investigations.
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