Leishmania is a protozoan parasite that causes leishmaniasis, which exists in two main forms: visceral leishmaniasis (VL) and cutaneous leishmaniasis (CL). VL affects internal organs and is fatal without treatment, while CL typically causes skin sores. The parasite has 21 pathogenic species transmitted between mammalian hosts by sand fly bites. India carries a high burden of VL, also known as kala-azar, while CL is widespread across parts of Africa, Asia, Europe and South America. Diagnosis involves identifying the parasite microscopically or through serological tests, with treatment differing between VL and CL. Coinfection with HIV is also a concern as it can

1. LEISHMANIA

2. INTRODUCTION
• Zoonotic
• 21 species – Pathogenic
• Visceral and Cutaneous
• 2 subgenuses – Leishmania , Viannia
• KALAAZAR – BLACK SICKNESS

3. INDEX
• HISTORY
• TAXONOMY
• CLASSIFICATION
• EPIDEMIOLOGY
• MORPHOLOGY
• LIFE CYCLE
• PATHOGENICITY
• CLINICAL FEATURES
• LABORATORY DIAGNOSIS
• TREATMENT
• PROPHYLAXIS/ PREVENTIVE MEASURES
• LEISHMANIA COINFECTIONS

4. HISTORY
• Cutaneous leishmaniasis (CL) –
King Ashurbanipal from the seventh century BC
• Physicians (10th century AD) Balkh sore
• 15th and 16th century Spanish colonials "valley
sickness", "Andean sickness", "white leprosy”
• 1756, Alexander Russell, gave detailed clinical
description
• Indian doctors pronounced it kālā āzār Hindustani
phrase for "black fever”

5. • 1901, Leishman identified organisms from spleen of a patient
dead from "dum-dum fever" - in Calcutta , India
• Captain Charles Donovan (1863–1951) confirmed Leishman-
Donovan bodies - Madras, India.
• Ronald Ross proposed - name Leishmania donovani

6. TAXONOMY
• Phylum
• Subphylum
• Class
• Order
• Family
• Genus
Sarcomastigophora
Mastigophora
Zoomastigophorea
Kinetoplastida
Trypanosomatina
Leishmania

7. CLASSIFICATION
• Species Classification
based on
– Isoenzyme analysis
– DNA sequence analysis
– Antigenic structure
– Biochemical properties
– Growth properties
• Clinical Classification
based on
– Site
– The geographical
distribution

8. LEISHMANIA
Leishmania
Leishmania
donovani
complex
Viannia
•Leishmania dononvani
•Leishmania chagasi
•Leishmania infantum
•Leishmania archibaldi
Leishmania
tropica
complex
Leishmania
major
complex
Leishmania
aethiopica
complex
Leishmania
mexicana
complex
Leishmania
guyanensis
complex
Leishmania
braziliensis
complex
Leishmania
lainsoni
complex
Leishmania
naiffi
complex
• Leishmania tropica
•Leishmania mexicana

9. CLINICAL
CLASSIFICATION
MUCOCUTANEOUS
LEISHMANIASIS
VISCERAL
LEISHMANIASIS
( KALAAZAR)
CUTANEOUS
LEISHMANIASIS
Indian Kala
Azar
(L. donovani)
Mediterranean
Kala Azar
(L. infantum)
South american
Kala Azar
(L. chagasi)
African Kala
Azar
(L.archibaldi)
South America
L. braziliensis
NEW WORLD
L.mexicana ,
L.braziliensis
OLD WORLD
L.tropica ,
L.major,
L.aethiopica
Dermal
Leishmnoid
(PKDL)

10. EPIDEMIOLOGY
• Worldwide prevalence 12 million cases
• Population at risk is about 350 million.
• Endemic countries 88
• 90 % of cases with Cutaneous Leishmaniasis occur in
Afghanistan, Algeria, Brazil, Iran, Peru, Saudi Arabia
and Syria
• Ninety per cent of Visceral Leishmaniasis cases are
found in Bangladesh, Brazil, India, Nepal and Sudan

11. WORLDWIDE DISTRIBUTION OF LEISHMANIASIS
http://www.geo.arc.nasa.gov

12. EPIDEMIOLOGY IN INDIA
• 165 million people estimated to be at risk
• BIHAR state is the worst affected
• West Bengal ten districts affected Jharkhand five
districts and Uttar Pradesh with four districts

13. EPIDEMICS
• Sudan a major epidemic of visceral leishmaniasis occurred
from 1984 to 1994
• Kabul in 2002
• Pakistan in 2004 , Sudanese refugee camps , Chad in 2007.
• Ethiopia (2005–06), Kenya (2008), and Southern Sudan
(2009)
• In India last major outbreak was reported around 1944 from
Assam
(1995 Outbreak of kala-azar in Bombay)

14. LEISHMANIA DONOVANI
• 1903
• Endemic – India , China, Africa
• Intracellular in Man
• Amastigote form
• RE system

15. MORPHOLOGY
• Two stages :
Amastigote Stage : Man Promastigote Stage : Sandfly,
Artificial culture
Amastigote Stage (Aflagellar)
Round /oval (2-4µ)
Cell membrane present only in FRESH specimens
Nucleus ‹ 1µ
Kinetoplast lies tangentially to nucleus
Axoneme ( extension from kinetoplast to margin of body)
Vacuole surrounds Axoneme
LEISHMAN DONOVAN (LD) BODIES

17. Promastigote Stage (Flagellar)
Initial …Pear shaped 5-10 µ length and 1-
5µ in breadth
Later ….Spindle shaped 15-20µ by 1-2µ
Nucleus is central
Kinetoplast transverse , anterior
Flagellum : anteriorly placed

19. PROMASTIGOTES AMASTIGOTES

20. SAND FLY
Subfamily Phlebotominae ( argentipes- India)
In the New World, leishmaniasis is spread
by sand flies of the genus Lutzomyia
In the Old World, the disease is spread
by Phlebotomus
Female 1.5–3 mm, yellowish in colour (hairy
body, wings and legs)
Wings are oval lanceolate
Females Haematophagus, Males sap feeders

21. MAMMALIAN HOSTS
• Rodents L. archibaldi, L.major
• Dogs L. infantum, L. chagasi, L.tropica
• Foxes L. infantum ,L. chagasi
• Humans L. donovani, L.tropica
• Gerbil L.major

22. LIFE CYCLEBLOCKED

23. PATHOGENESIS
• Incubation Period : 3-6 months
Inoculation of Promastigotes in skin
Ingestion of Promastigote by Neutrophils
Attraction of macrophages
Ingestion of infected neutrophil, Amastigote formation
(Macrophage)
Invasion by Plasma cells and lymphocytes
Amastigotes liberated in circulation after rupture
RE cells proliferate, heavily parasitised

24. CLINICAL DISEASE
• Visceral
– Fatal (90%
untreated)
– Liver
– Spleen RE
– Bone marrow
• Cutaneous
– Generally Self- healing
– Skin
– Mucous membranes

25. VISCERAL LEISHMANIASIS
Low grade fever continuous / intermittent
Hepato-splenomegaly
RE system affected
Bone marrow hyperplasia
Anemia , Leucopenia
Hypergammaglobulinnemia
Epistaxis , Proteinuria, Hematuria
If left untreated ....Fatal 75-95%

26. • A 12-year-old boy
suffering from visceral
leishmaniasis.
• The boy exhibits
splenomegaly and
severe muscle wasting.

27. • Profile view of
a teenage boy
suffering from
visceral
leishmaniasis.

28. COMPLICATIONS
• Amoebic/ Bacillary dysentry
• Pneumonia / Tuberculosis
• Cancrum oris (extreme neutropenia)
• Sepsis
• Death (untreated)

29. LABORATORY DIAGNOSIS
• KALA AZAR :
– DIRECT EVIDENCE ( Demonstration of L.donovani)
– INDIRECT EVIDENCE

31. DIRECT EVIDENCE
• PERIPHERAL BLOOD BY THICK FILM METHOD (Amastigote
form/ LD bodies)
– Leishmans stain / Giemsa stain
– Positivity rate is low – Centrifuge
– Peripheral smear : Mononuclear leucocytes
Buffy Coat : Neutrophils
BIOPSY MATERIAL :
Lymph node puncture
Sternal / Iliac crest puncture 50-85 % Positive, Safe
* Spleen puncture * 98 % Positive; Risky

32. • Blood Culture : Novy Mac Neal, later modified by
Nicolle (N.N.N.)medium
( 2 parts of salt agar , 1 part defibrinated Rabbit blood, Ascorbic
acid and Haematin )
Specimen inoculated in water of condensation
22°C – 24°C, 4 weeks
Promastigote Form
Least sensitive, Long time

33. LEISHMANIA DONOVANI - AMASTIGOTES -
HUMAN LIVER

34. INDIRECT EVIDENCE
• Blood count : Neutropenia, Anaemia, Relative Lymphocytosis
• Serological Tests :
Aldehyde ( Formal gel) Test (Napier) To detect gamma globulin
Antimony test : Increase in globulin levels ( Not used now)
Complement Fixation Test : Utilises W.K.K. antigen ( Witebsky,
Klinenstein and Kuhn ) Early diagnosis ( Not used now )

35. • Other serological tests :
ELISA ,
Latex particle agglutination,
CIE,
IFA
Ig G Ab detection
• Molecular diagnosis : PCR ,
Western Blot - CHOICE

36. DIRECT AGGLUTINATION TEST (DAT)
Semi-quantitative test
Microtitre plates : increasing dilutions of patient's serum or blood
is mixed with stained killed L. donovani promastigotes.
Agglutination visible after 18 hours
A titre greater than 1:3200 is positive

38. TREATMENT
• VISCERAL LEISHMANIASIS:
– Aggressive management of associated bacterial or viral
infections, anaemia, hypovolemia and malnutrition.
– Sodium Stibogluconate 20 mg/kg/day for 30 days
– Miltefosine 2.5 mg/kg/day for 28 days. Cure rate is 94%
– Second line: Liposomal Amphotericin B, 1 mg/kg/day for 15
days.

39. POST KALAAZAR DERMAL
LEISHMANOID (PKDL)
• Normally develops <2 years after recovery from VL(10-20%)
• L.donovani
• Non ulcerative
• Restricted to skin
• India ...Bengal & Assam , Africa
• Clinical Presentation
– Macular and hypopigmented,
– Erythematous patch
– Nodules
• Treatment : Pentavalent antimonials

40. CUTANEOUS LEISHMANIASIS
"Aleppo boil," "Baghdad boil," "Bay sore," "Biskra button,"
"Chiclero ulcer," "Delhi boil," "Kandahar sore," "Lahore sore," "Leishmaniasis
tropica," "Oriental sore," "Pian bois," and "Uta"
BISKRA BUTTON
UTA

41. • A raised, red nodule develops at site of bite Central crust
Ulcerative lesion
or Dry scales
• Old World (OWCL)
– Anthroponotic/ Urban Cutaneous Leishmaniasis (ACL) L.tropica : self
healing with scarring
– Zoonotic/Rural Cutaneous Leishmaniasis (ZCL) L.major : painless
lesions, rapid self healing ( Non immune person – scarring)
– Diffuse cutaneous leishmaniasis (DCL) L. aethiopica : diminished cell
mediated - disfiguring nodular lesions
• New World (NWCL)
– Bay sore :L.mexicana ,
– Uta :L.peruviana

45. (MCL)
•L.braziliensis
• Central and South america
• 2 Stages
Primary cutaneous lesion
Secondary mucosal lesion
• 5% cases
• Nasal septum is destroyed
• Lymphatic / Hematogenous
spread
• Death due to respiratory
distress

46. TREATMENT
• CUTANEOUS LEISHMANIASIS:
– Intralesional antimonials,
– Fluconazole 200-400 mg daily
– Rifampicin
– Cryosurgery
– Radiofrequency heat therapy

47. PREVENTION
• STRATEGY FOR CONTROL
1. Interruption of transmission by reducing vector
population through indoor residual insecticides (DDT)
2. Early diagnosis and complete treatment of Kala-azar
cases
3. Health education programme for community awareness

49. LEISHMANIA /HIV COINFECTION
• Since 1990, cases of co-infection have been
reported from 34 countries worldwide
• 70 % reported in South-Western Europe
• V.L is MC associated with HIV CD4 <
200cells/mm
• Mode of transmission IV drug users
60-70 % Europe ; 15 % rest
• In India HIV-Leishmania co-infection is
estimated to occur in less than 1% of
patients

50. The triad of HIV, tuberculosis and VL has been reported (Pandey et at,
2005).
Poverty, overcrowding, malnutrition, polygamy, illiteracy, and poor domestic
conditions facilitate the growth of these diseases
The Mantoux test / Purified protein derivative test : Negative in HIV infection
Hence ELISA and PCR ( utmost importance )
Both visceral leishmaniasis (VL) and tuberculosis (TB) increasing in Sudan
Mycobacteria/Leishmania share common Antigen
LEISHMANIA / TUBERCULOSIS
COINFECTION

52. THANK YOU