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Clinical Aspects
Published in Yamuna Deepani Siriwardana, Leishmaniasis in Sri Lanka, 2023
Some of our locally reported historical cases indicated the possible existence of leishmanial infections consistent with a clinical picture of cutaneous leishmaniasis (CL) since long. However, it is interesting to note the evidence provided by the rest of historical cases on the possibility of visceral leishmaniasis (VL) also occurring in this country. None of the reports, however, provided adequate evidence to confirm or refute the co-existence of both visceral and cutaneous manifestations or post-kala-azar dermal leishmaniasis (PKDL) in them. Subsequently, all the initial cases of the recent epidemic presented with skin lesions and appeared to be consistent with CL. Is this the only clinical form emerging or prevalent in this setting? What are the characteristics of CL in Sri Lanka? What are the sequelae of an infection caused by a genetically variant visceralizing parasite? Evidence-based information was necessary for case suspicion, diagnosis, and management in a community. Therefore, it was then necessary to study the clinical profile through scientific methods.
Inflammatory and infectious conditions
Published in Aimilios Lallas, Enzo Errichetti, Dimitrios Ioannides, Dermoscopy in General Dermatology, 2018
Vishal Gupta, Sidharth Sonthalia, Yasmeen Jabeen Bhat, Sonali Langar, Manal Bosseila
Similarly to fair-skinned patients, granulomatous skin diseases frequently show focused linear and branching vessels, while the characteristic yellowish-orange hue is generally difficult to see in skin of color (Figure 18.19).2,5,6 Additionally, in both sarcoidosis and lupus vulgaris of dark-skinned subjects, it is more common to observe whitish scar-like areas (Figure 18.19) (authors’ personal observations). Regarding the other main granulomatous dermatoses (granuloma annulare necrobiosis lipoidica, leishmaniasis, etc.), there is no relevant difference according to skin phototype (authors’ personal observations). Interestingly, the dermoscopic features of post kala-azar dermal leishmaniasis (a late cutaneous manifestation of untreated or partially treated visceral leishmaniasis caused by Leishmania donovani, commonly seen in India and Sudan) is similar to those of classic cutaneous leishmaniasis, with lesions mainly displaying erythema and whitish follicular plugs (Figure 18.20).11
Lipid-Based Nanocarriers for the Treatment of Infected Skin Lesions
Published in Andreia Ascenso, Sandra Simões, Helena Ribeiro, Carrier-Mediated Dermal Delivery, 2017
Sandra Simöes, Manuela Carvalheiro, Maria Manuela Gaspar
CL is considered the most serious protozoan skin infection in many developing countries with an annual incidence estimated between 0.7 and 1.2 million cases. Ninety percent of CL cases occur in Middle East and South American countries [29]. As shown in Fig. 11.3, the clinical CL manifestations may range from single or disseminated, nodular or ulcerative skin lesions to the destruction of mucosal tissue [27,30]. In most cases CL is limited to a single or few lesions that are localized at the site of parasite inoculation within dermal macrophages on exposed parts of the body [31]. The infection begins as an erythema that develops into a nodule and then enlarges and matures into an ulcerated lesion over 1-3 months (Fig. 11.3) [27,32]. These lesions may heal spontaneously after months or even years. Less common CL presentations include disseminated and diffuse (very rare) forms that origin multiple skin lesions over large body areas [31,32]. ML, which usually occurs after an initial cutaneous infection, involves the mucous membranes of the upper respiratory tract and oral cavity (nose, mouth, and throat) [33]. Post kala-azar dermal leishmaniasis is yet another form of CL that may arise after visceral infection caused by L. donovani [34]. In the more severe forms of CL, the lesions do not self-cure triggering significant disfigurement and social stigmatization [31].
Visceral leishmaniasis (kala-azar) caused by L. mexicana in a patient with AIDS
Published in Baylor University Medical Center Proceedings, 2023
Kacie L. Mitchell, Matt C. Smithhart, Bill R. Covington, Timothy M. Byrd, Seth J. Sullivan, Michael K. Dixon
Although our patient is from Belize, L. mexicana is endemic to Texas. Therefore, it is not unlikely that our patient contracted this parasite locally. We believe that his immunocompromised state allowed L. mexicana to manifest as VL rather than cutaneous leishmaniasis. In the years following his VL diagnosis, he developed dermatologic manifestations known as post-kala-azar dermal leishmaniasis (PKDL) (Figure 2). PKDL is a disfiguring skin condition resulting from an aberrant host immune response to vestigial parasites.1 The skin lesions of PKDL can range from hypopigmented or erythematous macules to raised plaque-like lesions. These lesions classically involve areas of the face, neck, and upper torso. Progression of VL to PKDL has been reported in 10% to 60% of individuals diagnosed with VL.10 Furthermore, there is increased frequency and severity of PKDL in patients with HIV.10,11
Small molecules as kinetoplastid specific proteasome inhibitors for leishmaniasis: a patent review from 1998 to 2021
Published in Expert Opinion on Therapeutic Patents, 2022
Mohd Imran, Shah Alam Khan, Ahmed Subeh Alshrari, Mahmoud Mudawi Eltahir Mudawi, Mohammed Kanan Alshammari, Aishah Ali Harshan, Noufah Aqeel Alshammari
Leishmaniasis is a vector-borne, protozoal infectious disease caused by a kinetoplastid parasite belonging to about 18 species of Leishmania (Family: Trypanosomatidae) [1]. This disease is mainly transmitted by infected sandflies. The intracellular replication of different Leishmania species leads to the development of different types of leishmaniasis like diffuse cutaneous leishmaniasis (DCL), localized cutaneous leishmaniasis (LCL), mucocutaneous leishmaniasis (MCL), post kala-azar dermal leishmaniasis (PKDL), and visceral leishmaniasis (VL). Leishmaniasis has also been classified as Old-World leishmaniasis (OWL) and the New-World leishmaniasis (NWL) based on the geographical distribution and the microorganism [1,2] (Table 1)3]. The untreated leishmaniasis causes about 70,000 deaths annually [2]. Despite that leishmaniasis is estimated to be one of the largest disease burdens, it is considered a neglected disease [1–4].
How can proteomics overhaul our understanding of Leishmania biology?
Published in Expert Review of Proteomics, 2020
Paul W. Denny, Karunakaran Kalesh
The development and severity of clinical manifestations of leishmaniasis depend not only on the Leishmania spp. but on the many factors pertaining to the susceptible individual such as malnutrition, comorbidities and the state of the immune system. Leishmania spp. parasites have co-evolved with humans in endemic areas and this positive selection pressure has contributed to pathogen survival by latent infection. The development of post-Kala-azar dermal leishmaniasis (PKDL) in some visceral leishmaniasis (VL) patients after recovery from the VL, and the development of mucosal lesions in some individuals after several years or even decades of developing primary cutaneous lesions, are indicative of the ability of the parasite to persist within the host even after successful treatment of the initial clinical condition. Clearly, despite years of research, many aspects of the Leishmania-host interaction remain poorly understood. In principle, all antileishmanials that work purely by targeting a parasite protein are likely to eventually fail as the extraordinary genetic plasticity of Leishmania spp. will confer fitness gains enabling the parasite to effectively evolve toward drug-resistant phenotypes. Therefore, an alternative strategy of host-directed therapeutic development has been proposed to tackle this issue. However, in the first place this requires better understanding of the Leishmania-host interaction.