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Year : 2020  |  Volume : 65  |  Issue : 6  |  Page : 461-464
Histopathology of post kala-azar dermal leishmaniasis

1 Department of Dermatology and STD, Vardhman Mahavir Medical College and Safdarjang Hospital, New Delhi, India
2 Department of Dermatology, All India Institute of Medical Sciences, New Delhi, India

Date of Web Publication23-Oct-2020

Correspondence Address:
V Ramesh
Department of Dermatology and STD, Vardhman Mahavir Medical College and Safdarjang Hospital, New Delhi
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijd.IJD_307_19

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The various lesions seen in the clinical presentation of post kala-azar dermal leishmaniasis (PKDL) are reflected in the histopathology of the type of lesion biopsied. The cells that form the dermal infiltrate include lymphocytes, histiocytes, and plasma cells in varying proportions. The infiltrate, which is mild and confined to the superficial dermis in macular lesion becomes denser with the increasing severity of the lesion. Leishman–Donovan bodies (LDB) in general are rarely demonstrable in macules and somewhat infrequently in the rest, though at times they may be numerous; mucosal lesions offer a greater chance of visualizing LDB than biopsies from the skin. A characteristic histomorphology in nodules is prominent follicular plugging with a dense plasma cell-rich lymphohistiocytic dermal infiltrate that shows an abrupt cut-off in the lower dermis, an appearance highly suggestive of PKDL even in the absence of LDB. Russell bodies within plasma cells, vascular changes, and xanthoma-like hue have been seen in plaques from chronic PKDL. The histopathologic picture in some may also mimic that seen in tuberculoid and lepromatous leprosy, and other granulomatous dermatoses. In contrast to Indian PKDL, epithelioid cell granulomas with giant cells are more common in African PKDL, and vascular changes are rare though neuritis showing LDB has been described.

Keywords: Histopathology, Leishman–Donovan bodies, neuritis, post kala-azar dermal leishmaniasis, Russell bodies

How to cite this article:
Ramesh V, Ramam M. Histopathology of post kala-azar dermal leishmaniasis. Indian J Dermatol 2020;65:461-4

How to cite this URL:
Ramesh V, Ramam M. Histopathology of post kala-azar dermal leishmaniasis. Indian J Dermatol [serial online] 2020 [cited 2021 Dec 4];65:461-4. Available from:

   Introduction Top

Being an uncommon dermatosis and geographically seen in the eastern region of India, limited reports on histopathology are available about post kala-azar dermal leishmaniasis (PKDL). As the dermatosis has a range of manifestations from the early macules, which progress to form papules, plaques, and nodules, the histopathology varies depending upon the type of lesion biopsied. In case of a polymorphic presentation, the biopsy is best taken from the most indurated lesion, like plaques and papulonodules. However, this opportunity may not be available when the lesions are predominantly macular.

   Early and Late Histopathologic Changes Top

A comprehensive report[1] around the middle of the last century revealed that the infiltrate in PKDL was composed mainly of lymphocytes, macrophages, and plasma cells in varying proportions. The earliest change was noted in the sub-papillary plexus of the macule where histiocytes and lymphocytes were seen, rarely extending to the reticular dermis, and around sebaceous glands and hair follicles in chronic cases; the degree of cellular infiltration increased as the lesions became erythematous and indurated and became densest in the nodular lesions. These changes have been described as three patterns,[2] namely a mild superficial infiltrate seen in macules [Figure 1], dense upper dermal infiltrate in papules, and a diffuse dermal infiltrate in nodules [Figure 2]]. A characteristic appearance in nodules is prominent follicular plugging with a dense plasma cell-rich lymphohistiocytic dermal infiltrate that shows an abrupt cut-off in the lower dermis. This appearance is highly suggestive of PKDL even in the absence of Leishman–Donovan bodies (LDB) [Figure 3]. A grenz zone may be seen in a majority of the cases but is absent in the others. Similar observations were made in other studies with an important observation that lymphocytes and plasma cells formed the main component of the infiltrate amidst which were dispersed the macrophages; neutrophils and eosinophils could be seen. Epithelioid cell granulomas are an uncommon finding [Figure 4] and were not observed by some workers[3],[4] but were reported in 4 of 88 cases in a large recent series.[2] It was seen in one report[5] that the plasma cells were conspicuous when the infiltrate was mild to moderate in contrast to those with a heavy dermal infiltrate. The density of inflammation was maximal in the superficial dermis as compared to the mid and deep dermis, which showed moderate or sparse inflammation.[6] Large collections of plasma cells showing well-developed Russell bodies can be seen in biopsies of nodules.[7] In a study of 100 cases, edema of the papillary dermis and destruction of the basal cell layer were seen in nodular lesions, whereas hypochromic macules showed decreased melanin in basal cell layer with very little dermal infiltrate.[8] In the infiltrated areas the collagen was thick, hyalinized, seen as broad strands, and slightly basophilic in tinctorial character.[1],[4] Vascular changes in the dermis have been observed in chronic lesions. They vary from dilatation and thickening of the blood vessels in early lesions to sclerotic changes around the dermal vessel wall in chronic cases.[2],[4] In chronic plaques that have a xanthoma-like hue, fibrosis with venular constriction and subsequent dilatation have been described giving them a deeper orange color.[9] Reports from Africa on PKDL are mostly confined to Sudan. Apart from the main differences summarized in [Table 1], in isolated instances psoriasiform hyperplasia of the epidermis, a band like infiltrate similar to lichen planus, and vasculitis have been reported.[10]
Figure 1: Mild superficial perivascular infiltrate in a macule showing lymphocytes and few plasma cells (inset) (H and E, ×40; inset ×200)

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Figure 2: Dense infiltrate of lymphocytes, histiocytes, and many plasma cells (H and E, ×400)

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Figure 3: Follicular plugging with a dense plasma cell-rich lymphohistiocytic dermal infiltrate that shows an abrupt cut-off in the lower dermis; a clear to less dense subepidermal grenz zone can be appreciated (H and E, ×20)

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Figure 4: Epithelioid cells and giant cells amidst an infiltrate of lymphocytes and plasma cells (H and E, ×200)

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Table 1: Main differences between Indian and African Post kala-azar dermal leishmaniasis

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The finding that confirms the diagnosis is the demonstration of LDB, which represent the amastigote form of the parasite inside the macrophages or extracellular spaces, seen most prominently immediately beneath the epidermis. The bodies show an increasing gradient from the nearly always negative status in macules to the moderate or heavily parasitized macrophages in the nodules [Figure 5]. Many times this logical conclusion appears too simple and fails to work since the demonstration of LDB is independent of the extent or type of lesion, for no organisms may be demonstrable both in the extensive macular cases[15] and in biopsies from the nodules of PKDL.[4] In the authors' experience LDB are generally sparse and are found after a patient search, though in a minority they may be abundant. Histopathological detection of LDB from macular lesions is very unusual as their numbers are so small.[1],[15] In the other types of lesions LD bodies are seen in less than half the number of patients with PKDL.[2],[5],[16] When numerous, the bodies may at times be confused with histoplasmosis.[17] Roustan et al .[18] and Singh et al .[2] found that the demonstration of organisms was higher from mucosal lesions as compared to cutaneous nodules and recommended biopsying the former if both sites were affected.[2] Special stains like iron hematoxylin[1] or Giemsa do not help much as they do not stain LDB differently from karyorrhectic nuclei.[4] A helpful aid in their differentiation is that nuclear detritus has an intense hematoxyphilic color similar to that of lymphocyte nuclei, whereas LDB are a shade paler.[2]
Figure 5: Numerous Leishman–Donovan bodies within the macrophage cytoplasm (H and E, ×1000)

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Immunohistochemical techniques using antileishmanial antibodies considerably enhance the demonstration of LDB as compared to hematoxylin and eosin-stained sections in both Indian and Sudanese PKDL,[6],[10] particularly in macular forms.[6] The same study[6] showed that the parasite load was highest in the superficial dermis, decreasing in numbers as one reached the deep dermis; more importantly all the nodular lesions studied had a low count of parasites explaining why even slit-skin smears could be negative from nodules. These observations were also made in Sudanese PKDL, a notable finding being that the parasite or parasite antigen could be seen in as high as 88% of cases in immunoperoxidase stained sections compared to 17% with sections stained by hematoxylin and eosin.[12]

Limitations and differential diagnosis

A histopathologic picture mimicking tuberculoid and lepromatous leprosy have been described in PKDL.[2] Unlike the diffuse and scattered infiltrate seen in PKDL, a granuloma composed of epithelioid cells with or without giant cells can be seen; it may be ill formed[19] or compact,[16] often seen in nodules[17] and arranged in zones with the histiocytes and giant cells in the center surrounded by lymphocytes and plasma cells.[1] The granulomatous inflammation may be seen around the nerve twigs[20] confounding the situation further. In PKDL from Sudan, granulomas have been seen more frequently in the papules and nodules and also within the dermal nerve twigs where parasites have also been visualized.[12],[13] Thus, even when the clinician has made the diagnosis of PKDL, the pathologist may report it as leprosy in the absence of LDB since both these diseases are usually endemic in the same region and leprosy tends to be commoner and more familiar to the pathologists. Additionally, other granulomatous dermatoses, particularly when the lesions in PKDL are confined to the face, may confound the diagnosis. In these situations molecular tests like PCR may be helpful, failing which a good clinicopathologic correlation must be done[21],[22] followed by a response to antileishmanial therapy.

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Conflicts of interest

There are no conflicts of interest.

   References Top

Sen Gupta PC, Bhattacharjee B. Histopathology of post-kala-azar dermal leishmaniasis. J Trop Med Hyg 1953;56:110-6.  Back to cited text no. 1
Singh A, Ramesh V, Ramam M. Histopathological characteristics of post kala-azar dermal leishmaniasis: A series of 88 patients. Indian J Dermatol Venereol Leprol 2015;81:29-34.  Back to cited text no. 2
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Mukherjee A, Ramesh V, Misra RS. Post-kala-azar dermal leishmaniasis: A light and electron microscopic study of 18 cases. J Cutan Pathol 1993;20:320-5.  Back to cited text no. 3
Singh N, Ramesh V, Arora VK, Bhatia A, Kubba A, Ramam M. Nodular post-kala-azar dermal leishmaniasis: A distinct histopathological entity. J Cutan Pathol 1998;25:95-9.  Back to cited text no. 4
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Ramesh V, Misra RS, Saxena U, Mukherjee A. Post-kala-azar dermal leishmaniasis: A clinical and therapeutic study. Int J Dermatol 1993;32:272-5.  Back to cited text no. 7
Singh RP. Observation on dermal leishmanoid in Bihar. Indian J Dermatol 1968;13:59-63.  Back to cited text no. 8
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Ismail A, Kharazami A, Permin H, el Hassan AM. Detection and characterization of Leishmania in tissues of patients with post-kala-azar dermal leishmaniasis using a specific monoclonal antibody. Trans R Soc Trop Med Hyg 1997;91:283-5.  Back to cited text no. 10
Ghosh MK, Nandy A, Addy M, Maitra TK, Ghose AC. Subpopulations of T lymphocytes in the peripheral blood, dermal lesions and lymph nodes of post-kala-azar dermal leishmaniasis patients. Scand J Immunol 1995;41:11-7.   Back to cited text no. 11
Ismail A, Gadir AFA, Theander TG, Kharazmi A, el-Hassan AM. Pathology of post-kala-azar dermal leishmaniasis: A light microscopical, mmunohistochemical, and ultrastructural study of skin lesions and draining lymph nodes. J Cutan Pathol 2006;33:778-87.  Back to cited text no. 12
el-Hassan AM, Ghalib HW, Zijlstra EE, Eltoum IA, Satti M, Ali MS, et al. Post-kala-azar dermal leishmaniasis in the Sudan: Clinical features, pathology and treatment. Trans R Soc Trop Med Hyg 1992;86:245-8.  Back to cited text no. 13
Zijlstra EE, Musa AM, Khalil EAG, el-Hassan IM, el-Hassan AM. Post-kala-azar dermal leishmaniasis. Lancet Inf Dis 2003;3:87-98.  Back to cited text no. 14
Ramesh V, Singh N. A clinical and histopathological study of the macular type of post-kala-azar dermal leishmaniasis. Trop Doct 1999;29:205-7.  Back to cited text no. 15
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Roustan G, Jimencz JA, Gutierrez-Solar B, Gallego JL, Alvar J, Patron M. Post-kala-azar dermal leishmaniasis with mucosal involvement in a kidney transplant recipient: Treatment with liposomal amphotericin B. Br J Dermatol 1998;138:526-8.  Back to cited text no. 18
Garg VK, Agrawal S, Rani S, Joshi A, Agarwalla A, Das ML, et al. Post-kala-azar dermal leishmaniasis in Nepal. Int J Dermatol 2001;40:179-84.  Back to cited text no. 19
Khandpur S, Ramam M, Sharma VK, Salotra P, Singh MK, Malhotra A. Nerve involvement in Indian post-kala-azar dermal leishmaniasis. Acta Derm Venereol 2003;84:245-6.  Back to cited text no. 20
Bhandare P, Shukla P, Bhobe M, Pai VV. Post-kala-azar dermal leishmaniasis: A diagnostic dilemma in a non-endemic area. Indian Dermatol Online J 2018;5(Suppl 2):S122-4.  Back to cited text no. 21
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  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]

  [Table 1]


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