Classical PKDL from Sudan showing a papular rash on the face.

<p>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 <a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0003258#pntd.0003258-Zijlstra2" target="_blank">[36]</a>.)</p

Immune (re-)constitution and post-kala-azar dermal leishmaniasis (PKDL).

<p><i>Panel A</i>: 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) <i>Panel B</i>: 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). <i>Panel C</i>: Theoretical overlap in mechanisms of PKDL occurring during VL and HIV co-infection treated with combined antileishmanial and antiretroviral therapy.</p

Diffuse or disseminated cutaneous leishmaniasis in an HIV-positive patient from Rajasthan, India (endemic for CL, not VL).

<p>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 <a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0003258#pntd.0003258-Chaudhary1" target="_blank">[97]</a>.</p

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).

<p>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.</p

Clinical entities particular to HIV and <i>Leishmania</i> 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.

<p>The corresponding terminology with PKDL as a starting point is indicated.</p><p>*can only be diagnosed retrospectively</p><p>Clinical entities particular to HIV and <i>Leishmania</i> 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.</p

Comparison of PKDL and PKDL-like lesions in immunocompetent and in immunocompromised patients.

<p>Comparison of PKDL and PKDL-like lesions in immunocompetent and in immunocompromised patients.</p

Examples of terminology used in the literature to describe (muco-)cutaneous involvement by <i>Leishmania</i> in HIV co-infected patients.

<p>Examples of terminology used in the literature to describe (muco-)cutaneous involvement by <i>Leishmania</i> in HIV co-infected patients.</p

Post-kala-azar dermal leishmaniasis in the Indian subcontinent: A threat to the South-East Asia Region Kala-azar Elimination Programme.

<div><p>Background</p><p>The South-East Asia Region Kala-azar Elimination Programme (KAEP) is expected to enter the consolidation phase in 2017, which focuses on case detection, vector control, and identifying potential sources of infection. Post-kala-azar dermal leishmaniasis (PKDL) is thought to play a role in the recurrence of visceral leishmaniasis (VL)/kala-azar outbreaks, and control of PKDL is among the priorities of the KAEP.</p><p>Methodology and principal finding</p><p>We reviewed the literature with regard to PKDL in Asia and interpreted the findings in relation to current intervention methods in the KAEP in order to make recommendations. There is a considerable knowledge gap regarding the pathophysiology of VL and PKDL, especially the underlying immune responses. Risk factors (of which previous VL treatments may be most important) are poorly understood and need to be better defined. The role of PKDL patients in transmission is largely unknown, and there is insufficient information about the importance of duration, distribution and severity of the rash, time of onset, and self-healing. Current intervention methods focus on active case detection and treatment of all PKDL cases with miltefosine while there is increasing drug resistance. The prevention of PKDL by improved VL treatment currently receives insufficient attention.</p><p>Conclusion and significance</p><p>PKDL is a heterogeneous and dynamic condition, and patients differ with regard to time of onset after VL, chronicity, and distribution and appearance of the rash, as well as immune responses (including tendency to self-heal), all of which may vary over time. It is essential to fully describe the pathophysiology in order to make informed decisions on the most cost-effective approach. Emphasis should be on early detection of those who contribute to transmission and those who are in need of treatment, for whom short-course, effective, and safe drug regimens should be available. The prevention of PKDL should be emphasised by innovative and improved treatment for VL, which may include immunomodulation.</p></div

Endemic area for VL in India (Muzaffarpur).

<p>(A) People live in close contact with animals that may attract sand flies. (B) Typical houses with walls made of mud. VL, visceral leishmaniasis.</p

PKDL from Bangladesh: confluent macular rash involving most of the face (courtesy of Dr. Dinesh Mondal).

<p>PKDL; post-kala-azar dermal leishmaniasis.</p