leismaniasis

1. Topic: LEISHMANIASIS
By: DR JOHN E. AGHO
(MBBS, BSc ( Ed), NCE. Asso.Member NPMCN.)

2. Instruction:
 Answer all questions
 Choose the best of the five options
available
 45 seconds per question.
 Answers to the questions are highlighted
in red in course of the presentation
Pretest

3. Which of these is not a neglected
tropical disease?
a.HIV
b.Yaw
c.Leishmaniasis
d.Onchocerciasis
e.Buruli ulcer
1

4. Which of these is not a synonym for a
form of leishmaniasis?
a.Delhi belly
b.Baghdad sore
c.Kala- azar
d.Dumdum fever
e.Oriental sore
2

5. Globally, how many people are at risk
of Leishmaniasis?
a.350 million
b.350 thousand
c.35 million
d.3.5 billion
e.3.5 million
3

6. Which of these countries does someone
have the lowest possibility of acquiring
leishmaniasis.
a.Iraq
b.Ethiopia
c.Spain
d.Denmark
e.Malta
4

7. How can one protect himself from getting
infected with leishmania?
a.Get vaccinated
b.Wear sunscreen
c.Take vitamin supplements
d.Sleep under a ITN and use insect repellant
e.Avoid contact with rodents.
5

8. Which cells of the human body does
leishmania infect?
a.Macrophages
b.basophils
c.erythrocytes
d.T-lymphocytes
e.thrombocytes
6

9. The drug of choice for visceral
leishmaniasis, sodium stibogluconate was
first used to treat leishmaniasis in
a.1912
b.2002
c.1982
d.2016
e.2010
7

10. The vector for transmission of leishmaniasis
in northern Nigeria is
a.Lutsomyia verrucarum
b.Phlebotomus nigeriene
c.Phlebotomus duboscqi
d.Phlebotomus turanicus
e.Lutsomyia aethiopica
8

11. Post kala-azar dermal leishmaniais is a
complication of
a.Mucocutaneous leishmaniasis
b.Cutaneous leishmaniasis
c.Visceral leishmaniasis
d.Diffuse cutaneous leishmaniasis
e.Local cutaneous leishmaniasis
9

12. Leishmaniasis recidivan is a manifestation
of
a.Cutaneous leishmaniasis
b.Visceral leishmaniasis
c.Chiclero ulcer
d.Mucocutaneous leishmaniasis
e.Post kala-azar dermal leishmaniasis
10

13. Introduction
Classification
Life cycle
Clinical features
Investigations/ diagnosis
Treatment
Prevention
Conclusion
outline

14. The term leishmaniasis encompasses multiple
clinical syndromes. Most notable are visceral,
cutaneous, and mucosal leishmaniasis, which
result from infection of macrophages
throughout the reticuloendothelial system, in
the dermis, and in the naso-oropharyngeal
mucosa, respectively.
Introduction

15.  Leishmaniasis is a vector-borne
disease caused by obligate
intracellular protozoa.
 A neglected tropical disease
amongst other diseases like yaw,
Onchocerciasis, buruli ulcers,
Chagas and many others. Note HIV
is not a neglected tropical disease.

17. Leishmania donovani
 Causative agent of visceral leishmaniasis
 Identified by William Leishman in 1900 from a soldier who
died of fever in Dum-Dum, India. Charles Donovan identified
the parasites in the spleen of an infected person in 1903.
Parasite is named in honor of these two men.
William Boog LEISHMAN
(1865-1926)
Charles DONOVAN (1863-1915))

18.  Synonyms
• Dum- Dum fever
• Baghdad sore
• Oriental sore
• Delhi boil
• Aleppo boil
• Kala-azar
• Sa lak ( Iran)
• Sa ldaneh ( Afghanistan)
• Chiclero ulcer

19. Classification

22. Endemic in approx. 98 countries throughout
• Latin America,
• Africa,
• Asia,
• southern Europe
 350 million people are thought to be at risk with
worldwide prevalence of 12 million.
 An annual incidence of 1.5 million cases of CL.
Desjeux P. et al, Trans R Soc Trop Med Hyg 2001;95:239- 43.

24.  90% of cutaneous leishmaniasis
occurs in Afghanistan, Iran, Saudi
Arabia, Syria, Brazil and Peru
 90% of all visceral leishmaniasis
occurs in Bangladesh, Brazil,
India, and the Sudan
 90% of mucocutaneous
leishmaniasis occurs in Bolivia,
Brazil and Peru
Leishmaniasis

26. Population movements due to
insecurity and development
issues are the main reasons for
its spread to new countries

27.  Risk factors
 Vector:
Infection in humans is caused by ~20
Leishmania species (Leishmania and Viannia
subgenera) which are transmitted by ~30
species of phlebotomine sandflies
(Phlebotomus [Old World] and Lutzomyia
[New World]).
Etiology

28. Phlebotomine sandfly

29. The sandfly, Phlebotomus (Phlebotomus)
duboscqi is the vector of the disease in the
northern savannah zone of Nigeria
(Asimeng, 1985; Dondji et al, 1995)
Vector

30.  (zoonotic cycle: infected rodent-
sandfly-human)
Or
 (anthroponotic cycle: infected
human-sandfly-human)
Transmission

31.  Person to person occurs through the sharing
of needles, as is often the case in
intravenous drug user.
 From mother to child ( L. infantum)
Leishmania/HIV co-infections. WHO fact sheet. [28/12/05]
Transmission

32. Life cycle and Immunoregulation

33. Leishmaniasis is viewed as a model
system for exploring
immunoregulatory responses to
intracellular pathogens.

35.  Common old world reservoir host -
Domestic dogs, rodents, foxes,
Wolves, jackals, raccoons
Mammalian reservoir host

36. Mastomys natalensis and Tatera
gambiana as probable reservoirs of
human cutaneous leishmaniasis in
Nigeria
E.I. Ikeh, J.A. Ajayi and E.J. Nwana
Journal of the Royal Society of Tropical Medicine and Hygiene,
Volume 89, Issue 1, Pages 25-26

37.  Cutaneous Leishmaniasis

38.  Cutaneous leishmaniasis is
limited to certain geographical
areas the :
 Old world -Sudan, Ethiopia,
Kenya, India, Middle East ,
 New world - Brazil, Mexico and
the United States of America

39. Epidemics :
Movement from non-endemic areas
into endemic areas
Bailey MS, 2007
Weina PJ, Clin Infect Dis 2004;39:1674- 80.
Cutaneous leishmaniasis

40.  Two endemic foci of CL in northern Nigeria.
 Keana village - LST positivity -was 28.7%
 Kanana village of Langtang South local
government area of Plateau State.- LST
positivity was 54.5%
(Agwale et al. 1993 & 1997),

41. Isolated reports of Obasi (1991)
In a population study in Kaduna state,
the prevalence was found to be 6.8%.
Obasi, O.E. Int. J. Dermatol. 1991; 30:274.
OKWORI,E.N.A et al. J. Protozool. 2001;11:32-46

42.  Male = female
 children are more affected
than adults.

43. Incubation periods can vary from a
few days to many months,

44. Clinical features

45.  Morphologic variants
• Clinical forms depend on:
 the immune condition of the
patients.
 the subspecies of the Leishmania
 the areaof the localization.

46.  Subclinical- Self healing
Disseminated- Death
 The first sign is a small erythematous papule that may
appear immediately following a bite from a sand fly
but usually appears 2 to 4 weeks later.
 The papule slowly enlarges over a period of several
weeks and assumes a more dusky violaceous hue.
 The lesion eventually becomes crusted in the center.
Clinical course

47.  When the crust is removed, there is a
shallow ulcer, often with a raised and
indurated border.
 The ulcer is typically painless

48.  Small papule that enlarges and ulcerates
at its centre to produce a volcano-
shaped wet lesion
 Leishmania major

49. Typical lesion
 A painless, sharply delineated ulcer surrounded by a
purplish raised border

50.  Smooth nodule or the surface
may become hyperkeratotic.
Dry lesions

51.  Hyperkeratotic lesions, central crust, No
exudates
Dry lesions

52.  Diffuse cutaneous lesion is caused by the spread of
either parasites or their antigens away from the site of
a primary lesion

53.  Leishmaniasis recidivans
 it presents as a recurrent of lesion at the
site of an apparently healed disease, years
after the original infection
 It manifest as enlarging papule, plaque, or
coalescence of papules that heals with
central scarring.
Other manifestation of CL

55. Verruciform CL
Psoriasiform CL
Impetigenized CL
Erysipeloid CL
Sporotrichoid CL
Less common manifestation

56.  The general term visceral leishmaniasis
encompasses a broad spectrum of
severity and manifestations, with a
chronic, subacute, or acute onset and an
incubation period of weeks, months, or
sometimes years.
Visceral leishmaniasis

57. On the Indian subcontinent and in the Horn of
Africa, persons of all ages are affected by VL. In
endemic areas of the Americas and the
Mediterranean basin, immunocompetent infants
and small children as well as immunodeficient
adults are affected often.

58.  irregular bouts of fever,
 weight loss, despite good appetite
 enlargement of the spleen and liver,
 anaemia.
 Darkening of the skin of face, hands, feet and
abdomen is common in India (kala-azar=black
sickness)
 Lymphadenopathy may also occur.
Clinical features

59.  In advanced illness, hypoalbuminemia
may manifest as pedal edema and ascites.
 Anemia appears early and may become
severe enough to cause congestive heart
failure.
 Epistaxis, retinal hemorrhages, and
gastrointestinal bleeding are associated
with thrombocytopenia.

60.  Post-kala-azar dermal leishmaniasis
(PKDL)
 is a sequel of visceral leishmaniasis that
appears as macular, papular or nodular
rash usually on face, upper arms, trunks
and other parts of the body.

61.  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.
 People with PKDL are considered to be a
potential source of kala-azar infection.

62.  leads to partial or total
destruction of mucous
membranes of the nose, mouth
and throat.
 Caused mainly by the viannia
leishmania group
Mucocutaneous leishmaniasis

63.  Young men with chronic lesions of CL
are at particular risk.
 Overall, ~3% of infected persons
develop ML.

64.  Not every patient with ML has a history of
prior CL. ML is almost entirely confined to
the new world
 In rare cases, ML may also be caused by
Old World species like L. major, L.
infantum (L. chagasi), or L. donovani.

65.  Typically, ML presents as nasal stuffiness
and bleeding followed by destruction of
nasal cartilage, perforation of the nasal
septum, and collapse of the nasal bridge.
 Subsequent involvement of the pharynx
and larynx leads to difficulty in
swallowing and phonation.
Clinical features

66.  HIV / leishmaniasis co-infection
 The combination is deadly because of the impact
of the two infections together.
 They have high chance of developing the full-
blown clinical disease, and high relapse and
mortality rates.
 Antiretroviral treatment reduces the development
of the disease, delays relapses and increases the
survival of the coinfected patients.
 High Leishmania-HIV coinfection rates are
reported from Brazil, Ethiopia and the state of
Bihar in India.

67. Mucocutaneous leishmaniasis

68.  Visceral leishmaniasis: Identification of
amastigotes in smears of tissue aspirates is the
gold standard for diagnosis.
 The sensitivity of splenic smears is >95%, but
splenic aspiration may be very dangerous;
smears of bone marrow and lymph node
aspirates have sensitivities of 60–85% and
50%, respectively.
Diagnosis

69.  Several serologic techniques,
including a rapid test, are
available and offer good
sensitivity and specificity.

70.  Cutaneous and mucosal leishmaniasis:
 Diagnosis is made by microscopy,
culture, or PCR examination of
aspirates and biopsy specimens from
skin lesions and lymph nodes.

71. Treatment

73.  No vaccine is available for any form of
leishmaniasis.
 Inoculation with live L. major
(“leishmanization”) is practice in Iran
 Anthroponotic leishmaniasis is controlled by
case finding, treatment, and vector control with
insecticide-impregnated bed nets and curtains
and residual insecticide spraying.
Prevention

74.  Control of zoonotic leishmaniasis is more
difficult. Use of insecticide-impregnated
collars for dogs, treatment of infected
domestic dogs, and culling of street dogs
are measures that have been used with
uncertain efficacy to prevent transmission
of L. infantum.

75.  In Brazil, a canine vaccine has been found to promote a
decrease in the human and canine incidence of
zoonoticVL.
 Two vaccines, Leishmune and Leish-Tec, are licensed in
Brazil.
 Leishmune provides significant protection to
vaccinated dogs.
 Personal prophylaxis with bed nets and repellants may
reduce the risk of CL infections in the New World.

76. Leishmaniasis
 Leishmaniasis is caused by the intracellular
protozoa Leishmania,
 usually being spread by sand flies
 3 types:
A) Cutaneous leishmaniasis:
 caused by Leishmania tropica or Leishmania
mexicana
 crusted lesion at site of bite
B) Mucocutaneous leishmaniasis:
Summary

77. B) Mucocutaneous leishmaniasis:
 caused by Leishmania braziliensis
 skin lesions may spread to involve mucosae of nose, pharynx etc
C) Visceral leishmaniasis (kala-azar)
 mostly caused by Leishmania donovani
 occurs in the Mediterranean, Asia, South America, Africa
Features:
1) fever,
2) Massive splenomegaly& hepatomegaly
3) good appetite, weight loss
4) grey skin - 'kala-azar' means black sickness
5) pancytopaenia secondary to hypersplenism

78. Leishmaniasis is one of the numerous neglected tropical
diseases, which has detrimental effect in patient welfare,
ranging from cosmetics through social functioning of the
individual to life threatening condition.
It imposes a DALY loss of up to 2.4million.
Early recognition and treatment as well as good political
will would go a long way in the pursuit of the disease
eradication.
Conclusion

79. Thank you.

80.  Drusano GL. Pharmacokinetics and pharmacodynamics of antimicrobials.
Clin Infect Dis. 2007;45(suppl):89–95.
 Chemotherapy of microbial diseases. In: Chabner BA, Brunton LL,
Knollman BC, eds. Goodman and Gilman’sThe Pharmacological Basis of
Therapeutics. 12th ed. NewYork, NY:McGraw-Hill; 2011.
 US Department of Health and Human Services. Panel on Antiretroviral
Guidelines for Adults and Adolescents. Guidelines for the use of
antiretroviral agents in HIV-1-infected adults and adolescents. 1–239.
http://www.aidsinfo.nih.gov/ContentFiles/AdultandAdolescentGL pdf.
References