The history of leishmaniasis

In this review article the history of leishmaniasis is discussed regarding the origin of the genus Leishmania in the Mesozoic era and its subsequent geographical distribution, initial evidence of the disease in ancient times, first accounts of the infection in the Middle Ages, and the discovery of Leishmania parasites as causative agents of leishmaniasis in modern times. With respect to the origin and dispersal of Leishmania parasites, the three currently debated hypotheses (Palaearctic, Neotropical and supercontinental origin, respectively) are presented. Ancient documents and paleoparasitological data indicate that leishmaniasis was already widespread in antiquity. Identification of Leishmania parasites as etiological agents and sand flies as the transmission vectors of leishmaniasis started at the beginning of the 20th century and the discovery of new Leishmania and sand fly species continued well into the 21st century. Lately, the Syrian civil war and refugee crises have shown that leishmaniasis epidemics can happen any time in conflict areas and neighbouring regions where the disease was previously endemic

Prevalence of pfmdr1, pfcrt, pfdhfr and pfdhps mutations associated with drug resistance, in Luanda, Angola

<p>Abstract</p> <p>Background</p> <p>Malaria is the infectious disease causing the highest morbidity and mortality in Angola and due to widespread chloroquine (CQ) resistance, the country has recently changed its first-line treatment recommendations for uncomplicated malaria, from CQ to artemisinin combination therapies (ACT) in adults, and sulphadoxine/pyrimethamine (S/P) in pregnant women. Loss of SP sensitivity is, however, progressing rapidly in Africa and, in this study, were investigated a number of molecular markers associated to CQ and S/P.</p> <p>Methods</p> <p>Blood samples were collected from 245 children with uncomplicated malaria, admitted at the Pediatric Hospital Dr. David Bernardino (HPDB), Angola, and the occurrence of mutations in <it>Plasmodium falciparum </it>was investigated in the <it>pfmdr1 </it>(N86Y) and <it>pfcrt </it>(K76T) genes, associated with CQ resistance, as well as in <it>pfdhfr </it>(C59R) and <it>pfdhps </it>(K540E), conferring SP resistance.</p> <p>Results</p> <p>The frequencies of <it>pfmdr1 </it>mutations in codon 86 were 28.6% N, 61.3% Y and 10.1% mixed infections (NY). The frequency of <it>pfcrt </it>mutations in codon 76 were 93.9% K, 5.7% T and 0.4% mixed infections (KT). For <it>pfdhfr </it>the results were in codon 59, 60.6% C, 20.6% R and 18.8% mixed infections (CR). Concerning <it>pfdhps</it>, 6.3% of the isolates were bearers of the mutation 540E and 5.4% mixed infections (K540E).</p> <p>Conclusion</p> <p>The results of this epidemiologic study showed high presence of CQ resistance markers while for SP a much lower prevalence was detected for the markers under study.</p

DECREASED EFFECT OF GLUCANTIME IN CUTANEOUS LEISHMANIASIS COMPLICATED WITH SECONDARY BACTERIAL INFECTION

Background: Glucantime is regarded as the first-line treatment of cutaneous leishmaniasis (CL); however, failure to treatment is a problem in many cases. Aim: The aim was to evaluate the therapeutic effect of glucantime in CL complicated with secondary bacterial infection compared to uncomplicated lesions. Methods: This experimental study was performed in Skin Diseases and Leishmaniasis Research Center, Isfahan, Iran. A total of 161 patients enrolled in the study had CL confirmed by positive smear of lesions. All the patients were treated with systemic glucantime for 3 weeks and followed for 2 months. Response to treatment was defined as loss of infiltration, reepithelization, and negative smear. Depending on the results of bacterial cultures, the lesions were divided into two groups and the efficacy of glucantime was compared. Results: A total of 123 patients (76.4%) were negative, and 38 patients (23.6%) were positive for secondary bacterial infection. In groups with negative bacterial culture response to treatment was 65% (80 patients) and in the other positive group, it was 31.6% (12 patients), with a difference (χ2 = 13.77, P < 0.01). Conclusion: Therapeutic effect of glucantime showed a decrease in CL lesions with secondary bacterial infection. Therefore, in the cases of unresponsiveness to treatment, the lesions should be evaluated for bacterial infection, before repeating the treatment

Prevalence of mutations associated with antimalarial drugs in <it>Plasmodium falciparum </it>isolates prior to the introduction of sulphadoxine-pyrimethamine as first-line treatment in Iran

<p>Abstract</p> <p>Background</p> <p>This work was carried out to assess the patterns and prevalence of resistance to chloroquine (CQ) and sulphadoxine-pyrimethamine (SP) in Iran.</p> <p>Methods</p> <p>The prevalence of <it>pfcrt </it>K76T, <it>pfmdr1 </it>N86Y, <it>pfdhfr </it>N51I, C59R, S108N/T and I164L and codons S436F/A, A437G, K540E, A581E, and A613S/T in <it>pfdhps </it>genes were genotyped by PCR/RFLP methods in 206 <it>Plasmodium falciparum </it>isolates from Chabahar and Sarbaz districts in Sistan and Baluchistan province, Iran, during 2003–2005.</p> <p>Results</p> <p>All <it>P. falciparum </it>isolates carried the 108N, while 98.5% parasite isolates carried the 59R mutation. 98.5% of patients carried both 108N and 59R. The prevalence of <it>pfdhps </it>437G mutation was 17% (Chabahar) and 33% (Sarbaz) isolates. 20.4% of samples presented the <it>pfdhfr </it>108N, 59R with <it>pfdhps </it>437G mutations. The frequency of allele <it>pfcrt </it>76T was 98%, while 41.4% (Chabahar) and 27.7% (Sarbaz) isolates carried <it>pfmdr1 </it>86Y allele. Eight distinct haplotypes were identified in all 206 samples, while the most prevalent haplotype was <b>T</b>_76/N_86/N₅₁<b>R</b>₅₉<b>N</b>_108/A₄₃₇among both study areas.</p> <p>Conclusion</p> <p>Finding the fixed level of CQ resistance polymorphisms (<it>pfcrt </it>76T) suggests that CQ must be withdrawn from the current treatment strategy in Iran, while SP may remain the treatment of choice for uncomplicated malaria.</p

Soluble CD26/CD30 levels in visceral leishmaniasis: markers of disease activity

Leishmania infantum is the causative agent of zoonotic visceral leishmaniasis (VL). If untreated the disease could be fatal; however, in some cases the infection can run a subclinical course. In subclinical infections a Th1-response predominates, while Th2-responses and/or probably Treg cells are related to unfavourable outcome of the disease in active VL. In the present study we determined the levels of soluble (s) CD26 and CD30 co-stimulatory molecules in sera from patients with active VL, asymptomatic individuals and healthy volunteers. Results showed a significant difference in both sCD26 and sCD30 between infected cases and normal individuals (P ≤ 0·001). However, there was no significant difference in sCD26 levels between asymptomatic cases and patients, although the difference was not significant. sCD30 levels were significantly higher in VL patients than asymptomatic cases (P ≤ 0·001). These findings suggest a possible association between sCD26 and sCD30 levels and the clinical manifestation of L. infantum infection