Leishmaniasis in rheumatology, haematology and oncology: epidemiological, immunological and clinical aspects and caveats: Figure 1

Abstract

Leishmaniasis is an intracellular protozoan infection that can lead to cutaneous, mucocutaneous, visceral or systemic manifestations depending on the parasite species and virulence and on the host immune response. It is endemic in countries of Europe (Mediterranean basin), Asia, Africa, Central and South America, but autochthonous cases begin to emerge outside classical disease areas. CD4+ T helper cells, interferon γ, dendritic cells and macrophages are the key components of antileishmanial defence. Leishmaniasis is an important differential diagnosis in patients with chronic lesions of the skin or mucous membranes or with fever, hepatosplenomegaly, lymphadenopathy, pancytopenia, histocytosis, haemophagocytic syndrome or glomerulonephritis. Organ transplant recipients and patients with autoimmune syndromes are at particular risk of developing visceral leishmaniasis following immunosuppressive therapy (eg, with steroids, methotrexate, ciclosporin or tumour necrosis factor-neutralising biological agents). Diagnosis and adequate treatment of leishmaniasis requires the combined use of culture, microscopic and nucleic acid amplication methods and species identification by sequencing and other molecular techniques. Standard regimens for the treatment of visceral leishmaniasis are intravenous liposomal amphotericin B (3 mg/kg body weight for 10 days) or oral miltefosine (150 mg/day for 28 days).

Risk factors, clinical features and outcomes of visceral leishmaniasis in solid-organ transplant recipients: a retrospective multicenter case–control study

“…Prior reports demonstrated that steroid use is related to the development of intracellular infections [17]. In our study, VL was not related to induction therapy with antilymphocyte globulins or to baseline immunosuppression.…”

Clinical and parasitological factors in parasite persistence after treatment and clinical cure of cutaneous leishmaniasis

“…Persistent infection without signs of disease in animal models has provided evidence that such infection may promote immunity to subsequent infections [23–25]. In contrast, well documented clinical cases of disease reactivation in the context of immune suppression [26–28] or local trauma [29, 30] and mucosal involvement years after an episode of CL [31–33] support parasite persistence as a risk factor for reactivation of disease. Notably, the presence of a scar typical of CL and/or a positive Montenegro skin test reaction, both indicative of prior infection, have been shown to significantly increase the risk of re-activation of infection and development of CL in a prospective investigation of incidence of infection and disease in endemically exposed communities [33].…”

Cutaneous leishmaniasis associated with TNF-α blockers: a case report

“…In particular, TNF-α increases the expression of monocyte chemoattractant protein 1, intercellular adhesion molecule 1, E-selectin and vascular cell adhesion molecule, essential cytokines in the formation of granuloma and migration of monocytes that leads to the eradication of Leishmania spp 9. The use of infliximab and other anti-TNF agents may reduce this process, which would lead to a greater probability of reactivations or primary infections in these patients 10. In view of this, serological detection may be indicated to diagnose possible latent Leishmania infection before the prescription of TNF inhibitors in countries with a high incidence of infection by aggressive Leishmania spp.…”