This PPT is about Leshimaniasis including its epidemiology in Ethiopia. Prepared by Temesgen Girma C1, SPHMMC, Addis Abeba Ethiopia

1. Leishmaniasis
<<The Parasite of the Poor.>>

2. Definition
 Leishmaniasis is a vector-borne disease caused by protozoan parasite of the
genus Leish mania. It is transmitted by the vector phlebotomine sandfly.
 is the second-largest parasitic killer in the world (after malaria) and is endemic in
many parts of Africa, Asia and South America.

3. There are 3 main forms of leishmaniasis
in humans
 Visceral (also known as kala-azar, which is and the most serious form of the
disease),
 Cutaneous (aka oriental sore,the most common), and
 Mucocutaneous (Espundia)

4. Etiology & Diseases
SPECIES Disease
Leishmania tropica
Leishmania major
Leishmania aethiopica
Leishmania Mexicana
Cutaneous leishmaniasis
Leishmania braziliensis Mucocutaneous leishmaniasis
Leishmania donovani
Leishmania infantum
Leishmania chagasi
Visceral leishmaniasis

5. Epidemiology
 Globally, 350 million people at risk
 12 million people are currently suffering
 Yearly incidence is 0.7 – 1.2 million cases of CL and 0.2 – 0.4 million cases
of VL.
 90% of CL infections occur in Afghanistan, Pakistan, Syria, Saudi Arabia,
Algeria, Iran, Brazil, and Peru
 90% of VL cases occur in Bangladesh, Brazil, India, Sudan, South Sudan
and Ethiopia.
 (LCL) and (DCL) are distributed all over the country, where as, VL found
mainly in lowlands of northwest, central, south and southwestern
Ethiopia.

6. Epidemiology

7. Epidemiology

8. Epidemiology of VL in Ethiopia

10. Life cycle & Pathogenesis

11. How does leshimania evades the immune
system?
Down regulate the presentation of antigines
 Down regulate the production of inflammatory
cytokines such as IL-2, IL-1 & TNF alpha
Upregulates immunosuppressive substances like IL-
10 & TGF beta

12. Life cycle & Pathogenesis
 Cellular immune mechanisms determine resistance or susceptibility to
infection with Leishmania.
 subclinical infection can be identified by hypersensitivity skin response to
leishmanial antigens (Montenegro skin test )

13. Clinical manifestations
Factors that influence the expression of leshimaniasis as either
subclinical infection or active disease
 Host factors (genetic background, concomitant disease,
nutritional status),
 parasite factors (virulence, size of the inoculum), and possibly
 vector -specific factors (vector genotype, immunomodulatory
salivary constituents)

14. LCL (Oriental sore )
 It may present as 1 or a few papular,
nodular, plaque-like, or ulcerative
lesions
 The lesions typically begin as a small
papule at the site of the sandfly bite,
which enlarges to 1-3 cm in diameter
and may ulcerate over the course of
several weeks to months.

15. Diffuse Cutaneous Leishmaniasis
 Manifests as large, nonulcerating
macules, papules, nodules, or plaques
that often involve large areas of skin and
may resemble lepromatous leprosy.
 The face and extremities are most often
involved. Dissemination from the initial
lesion usually takes place over several
years.

16. Mucosal Leishmaniasis
 Resulting from hematogenous metastasis to the nasal or oropharangeal mucosa
from a cutaneous infection
 50% have preceding hx of an acute cutaneous lesions

17. Visceral Leishmaniasis
 VL typically affects older children and young adults in Africa
and Asia (L. donovani ).
After inoculation of the organism into the skin by the sandfly,
 completely asymptomatic
 Oligosymptomatic
 active kala-azar within 2-8 mo (25%)
 During the 1st few wk to mo of disease evolution
 3-6 mo after the onset of the illness,

18. At the terminal stages of kala-azar,
 hepatosplenomegaly
 gross wasting,
 pancytopenia
 jaundice, edema, and ascites
 Sever Anemia
 Bleeding episodes
The late stage of the illness is often
complicated by secondary bacterial
infections, which frequently are a cause
of death.

19. Post Kala-azar Dermal Leishmaniasis
(PKDL)
 It is a complication of
visceral leishmaniasis characterized
by a macular, maculopapular, and
nodular rash in a patient who has
recovered from VL and who is
otherwise well.
 Usually involves the face and torso.

20. DDx for VL
 Hyperactive Tropical Splenomegaly
 Malaria
 Typhoid Fever
 Typhus
 Brucellosis
 Schistosomiasis (Bilharzia)
 Splenic Abscess
 Tuberculosis( miliary Tuberculosis)
 HIV/AIDS
 Leukaemia (Chronic Myeloid Leukaemia)

21. Diagnosis
 Clinical Diagnosis
 Laboratory Investigations

22. Clinical Diagnoses

23. Laboratory Investigations
1) Indirect evidence(CBC & Serum tests)
 hemoglobin, 5-8 mg/dL
 Thrombocytopenia
 leukopenia (2,000-3,000 cells/µL)
 elevated hepatic transaminase levels, and
 hyperglobulinemia (>5 g/dL)

24. 2) Samples collected from suspected CL
cases
Scrapes
Fluid aspirated from wet lesions

25. 3) Direct evidences(Aspiration & microscopy/
Culture )

26. Treatment
 The objectives of VL treatment are to:
1. Reduce the parasite burden,
2. Prevent drug resistance,
3. Avoid toxic drug effects, and
4. Improve the clinical condition of patients and to manage
complications (anemia, malnutrition and secondary
infections)

27. First-Line Regimens for VL
A. sodium stiogluconate + paromomycin Im for 17days
B. Sodium Stiogluconate Im for 30 days.
C. Liposomal Amphotericin B (LAmB, AmBisome)

28. Second-Line Treatment for VL
A. Liposomal Amphotericin B (AmBisome)
B. Miltefosine
C. Paromomycin (Aminosidine)

29. Prevention
Insecticide spray
Mosquito nets
Infected or stray dogs should be destroyed.
Early diagnosis & treatment.