Figure 1.
Classical PKDL from Sudan showing a papular rash on the face.
The identity of the photographer was known to the patient, who gave permission. (Further images of PKDL can be found in the WHO PKDL atlas: A manual for health workers [36].)
Figure 2.
A simplified, theoretical presentation of the relationship between Th1 and Th2 responses, and parasite load, with the influence of HIV and antileishmanial and antiretroviral treatment on cutaneous leishmaniasis (CL), post-kala-azar dermal leishmaniasis (PKDL), diffuse cutaneous leishmaniasis (DCL) and visceral leishmaniasis (VL).
The Th17 response is not shown but is similar in polarity to the Th1 response. Mucocutaneous leishmaniasis (MCL) and leishmaniasis recidivans (LR) are indicated as reference points.
Figure 3.
Immune (re-)constitution and post-kala-azar dermal leishmaniasis (PKDL).
Panel A: Immune constitution in PKDL in immunocompetent patients. Theoretical relationship between changes in parasite load and immune response as the result of antileishmanial treatment, with associated clinical syndromes (visceral leishmaniasis [VL], PKDL) Panel B: Immune reconstitution in HIV infection. Theoretical relationship between changes in viral load and CD4 count as a result of antiretroviral therapy, with examples of associated immune reconstitution disease (cryptococcal meningitis, Kaposi's sarcoma, tuberculosis). Panel C: Theoretical overlap in mechanisms of PKDL occurring during VL and HIV co-infection treated with combined antileishmanial and antiretroviral therapy.
Table 1.
Examples of terminology used in the literature to describe (muco-)cutaneous involvement by Leishmania in HIV co-infected patients.
Table 2.
Comparison of PKDL and PKDL-like lesions in immunocompetent and in immunocompromised patients.
Figure 4.
Diffuse or disseminated cutaneous leishmaniasis in an HIV-positive patient from Rajasthan, India (endemic for CL, not VL).
There are florid nodules mainly on the face and on the extremities and back; oral and nasopharyngeal infiltrations were also found. There was no previous ulcer nor were there signs of visceralization. The parasite was not typed. Reproduced with permission from Chaudhary et al., the Indian Journal for Dermatology, Venereology and Leprology [97].
Table 3.
Clinical entities particular to HIV and Leishmania co-infection and with reported causative parasite and region: a new terminology based on the presence and time of presentation of VL in relation to the development of the cutaneous lesions.