case presentation on post kala azar dermal leishmaniasis (PKDL)
1. A CASE STUDY ON POST KALA- AZAR
DERMAL LEISHMANIASIS
PRESENTED BY
1.CHRISTY THOMAS
2.GAUTAM SAHU
3.ANJAPPA
2. CONTENTS
o Introduction
o PKDL
o Patient details
o Examinations and Investigations
o Diagnosis
o Management and Treatment
o Conclusion
o References
3. INTRODUCTION
According to WHO “ Leishmaniasis is caused by the
protozoan Leishmania parasites which are transmitted
by the bite of infected female phlebotomine sandflies .”
It is classified as a neglected tropical disease.
Causative organisms:
Leishmaniasis is caused by a protozoa parasite from
over 20 Leishmania species. The main are,
L. donovani
L. arabica
L. infantum
L. maxiana
phlebotomine sand-fly
4. • RISK FACTORS
Malnutrition
Famine
Lack of financial resource
Large migration of people
Urbanization emergency situation
Environmental changes and climate changes
6. 1.VISCERAL LEISHMANIASIS
Also known as kala-azar.
Fatal if left untreated in over 95% of cases.
Incubation period 3-8 months.
Symptoms:
1. Hepatomegaly.
2. Splenomegaly.
3. Lymphadenopathy.
4. Pancytopenia.
5. hypergammaglobulimnaemia .
6. Skin pigmentation.
7. 2.CUTANEOUS LEISHMANIASIS.
most common form of Leishmaniasis.
Incubation period 2 weeks to several months.
Symptoms:
1. skin lesions.
2. mainly ulcers, on exposed parts of the body, leaving life-long
scars and serious disability.
leads to partial or total destruction of mucous membranes of the
nose, mouth and throat
Mainly in South America.
Incubation period 1-3 months.
3.MUCOCUTANEOUS LEISHMANIASIS
8. POST KALA-AZAR DERMAL LEISHMANIASIS
Post-kala-azar dermal Leishmaniasis (PKDL) is usually a sequel
of visceral Leishmaniasis.
Appears as macular, papular or nodular rash usually on face,
upper arms, trunks and other parts of the body.
It occurs mainly in East Africa and on the Indian subcontinent,
where 5–10% of patients with kala-azar develop the condition.
It usually appears 6 months to 1 or more years after kala-azar has
apparently been cured, but can occur earlier.
Not a life threatening disease.
9. • SIGN AND SYMPTOMS OF PKDL
Early hypo pigmented macules similar to macular lesions of
Lepromatous Leprosy but normally less than 1 cm.
Usually occur on face but can affect any part of the body.
Later (after a variable period of months or years) diffuse nodular
lesions on those macules.
Erythematous butterfly rash which may be aggravated by exposure
to Sunlight; an early sign of PKDL.
Papules and nodules which usually occur on face, especially the
chin. Lesions progressive over many years , seldom heal
spontaneously.
Papular rash Macular rash Nodular rash
10. PATHOPHYSIOLOGY OF PKDL
The precise immune mechanisms of PKDL are still
obscure.
Immunobiology of the Sudanese and South Asian
PKDL differ.
Proposed hypothesis for pathophysiology of PKDL
are,
1. immune reactivation after cure from VL with
involvement of IFN-gamma, IL-10,CD-8 and CD-4
cells.
2. UV light induced skin changes.
3. Organ specific memory T cell response.
4. Genetic susceptibility of host.
11. EPIDEMIOLOGY
PKDL is estimated to occur in about 5–10% of visceral
Leishmaniasis patients within 5 years of onset; it often remains
untreated.
It is mainly seen in Sudan and India .
A 2010 survey of 4323 households in a highly endemic area in
Bihar showed a local PKDL prevalence of 5/10 000 population .
12. Patient Name : XYZ
Age : 13 years
Gender : female
Date of admission : 26/ 09 / 2018
Complaint of ; papular and nodular lesion
on the face and macular lesions on her
body.
History of : kala- azar at the age of 6 yrs.
• Patient Details
13. • EXAMINATIONS AND INVESTIGATIONS
1.Biochemical Test
2.Haematological Test
3.Virology Test
4.Microbiological Test
5.Clinical examination
14. 1.BIOCHEMICAL TEST
TEST Normal value
(g/dl)
26/09/2018
Total protein 6.0 - 8.3 6.63
Albumin 3.2 - 5.5 3.40
Globulin 2.8 - 3.0 3.23
Serum total albumin 1.10 0.76
Blood urea 15 - 45 22.8
Serum creatinine Men - 0.7 - 14
women -0.6-11 0.5
SGOT/ ASAT 34 34.5
SGPT/ ALAT MEN- 45
WOMEN - 35 24.0
Alkaline phosphate Adult - 279 u/l 128
15. HAEMOGRAM(CBC) REFERENCE RANGE OBSERVED VALUE
TOTAL RBC 3.9-5.7 millions/c.mm 4.41 millions/c.mm
HAEMOGLOBIN 11.0 – 12.2 gm/dL 12.5 gm/dL
TOTAL WBC 4000- 10500 /c.mm 11500 /c.mm
NEUTROPHILS 40-70 % 70%
LYMPHOCYTES 15- 40 % 25%
MONOCYTES 01-06 % 03%
EOSINOPHILS 01- 05 % 02%
BASOPHILS 00-01% 00%
TOTAL PLATELET
COUNT
1,40000 – 4,50000/c.mm 3,23000/c.mm
HCT MEN – 38.8 – 50 %
WOMEN – 34.9 – 44.5 % 38%
2.HAEMATOLOGICAL TESTS
16. 3. VIROLOGY TEST
TEST INTERPRETATION RESULT
HBsAg Cut off value (0.191) 0.056 NR
HCV antibodies Cut off value (0.361) 0.007 NR
4. MICROBIOLOGICAL INVESTIGATION
• Skin smear / Biopsy :- positive
5. CLINICAL EXAMINATION
• RK 39 Strip test :- positive
• Liver and Spleen : No Abnormalities
17. DIAGNOSIS
Based upon the clinical observations and
parasitological investigation the case was diagnosed
as Post Kala – Azar Dermal Leishmaniasis.
18. TREATMENT
Drug Name/generic name Dose Frequency
Inj. Ambisome (Liposomal
Amphotericin B)
0.25 mg in 10ml
5% dextrose.
Test dose
Inj. Ambisome (Liposomal
Amphotericin B)
128mg in
250ml 5%
dextrose.
5 times with 4 days
interval.
Syp. Meprazyme (digestive
enzymes)
1 teaspoon B.I.D
Syp. Fez XT (ferrous
ascorbate+folic acid)
1 teaspoon B.I.D
Cap. Miltefosine 50 mg bid x 21 days
19. PREVENTION AND CONTROL
Wear clothing that covers as much skin as possible. Long pants,
long-sleeved shirts tucked into pants, and high socks are
recommended.
Use insect repellent on any exposed skin and on the ends of your
pants and sleeves. The most effective insect repellants contain
DEET.
Spray indoor sleeping areas with insecticide.
Use screens and air conditioning indoors when possible. Using fans
might make it more difficult for the insects to fly.
Use a bed net tucked into your mattress. Sand flies are much smaller
than mosquitos, so you need a tightly woven net. Spray the net with
insecticide containing pyrethroid if possible.
20. • CONCLUSION
Post-kala-azar dermal Leishmaniasis (PKDL) is
usually a sequel of visceral Leishmaniasis. It is not a
life threatening disease. The availability of newer oral
agents may change the way of this disease is
managed. If development of PKDL continues after
treatment of VL, it will certainly affect the feasibility of
the Leishmaniasis elimination program. Hence, post-
treatment monitoring under a VL elimination program
needs attention.
21. • REFERENCES
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dermal leishmaniasis
(Review). Lancet Infectious Diseases 2003;3:87-98.
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RN. A Comparison
of Miltefosine and Sodium Stibogluconate for Treatment of Visceral Leishmaniasis in an
Ethiopian
Population with High Prevalence of HIV Infection. Clinical Infectious Diseases 2006;
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MM, El Hassan AM.
The natural history of Sudanese post- kala-azar dermal leishmaniasis: clinical,
immunological and
prognostic features. Annals of Tropical Medicine and Parasitology 2002;96:765-72.
4. Zijlstra EE, El-Hassan AM. Leishmaniasis in Sudan.Trans￢actions of the Royal
Society of Tropical
Medi￢cine and Hygiene 2001; 95; supplement 1: S1-S76.
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