The document provides an overview of cutaneous leishmaniasis and neurocysticercosis, detailing their causative agents, clinical features, diagnostic methods, and treatment options. Cutaneous leishmaniasis, primarily caused by Leishmania species, presents various clinical forms and has high incidence rates in certain geographic regions, while neurocysticercosis, caused by Taenia solium, is a neurological infection characterized by the presence of cysts in the central nervous system. It emphasizes the importance of laboratory diagnosis and prevention strategies for effective management of these parasitic infections.

1. Cutaneous
Leishmaniasis
and Cystecercosis

2. CUTANEOUS
LEISHMANIASIS

3. INTRODUCTION
▰ Hemoflagellates - flagellated protozoa that are found in
peripheral blood circulation
▰ Examples - Leishmania and Trypanosoma - both are transmitted
by bite of insect vector.

4. Various morphological forms of
flagellate
A. Amastigote; B. Promastigote; C. Epimastigote; D.
Trypomastigote

5. INTRODUCTION (Cont..)
▰ In Leishmania - amastigote and promastigote forms are seen.
 Amastigotes - diagnostic form, found in man
 Promastigotes - infective stage to man, found in insect
vector

6. LEISHMANIASIS
▰ Caused by an obligatory intracellular protozoa of the genus
Leishmania - primarily affects the reticulo-endothelial system of
the host.
▰ Vector - bite of the female sandfly vector.

7. LEISHMANIASIS (Cont..)
▰ Clinical forms:
 Visceral leishmaniasis (VL)
 Post–kala-azar dermal leishmaniasis (PKDL) - occurs few
months to years following VL.
 Cutaneous forms - cutaneous leishmaniasis (CL), diffuse
cutaneous leishmaniasis (DCL), leishmaniasis recidivans (LR)
and mucocutaneous leishmaniasis (MCL).

8. LEISHMANIASIS (Cont..)
▰ Subgenera: Leishmania has two subgenera - L. Leishmania (L.L.)
and L. Viannia (L.V.).
▰ Both of the subgenera comprise of nearly 20 species.

9. Old world leishmaniasis
▰ Seen in Asia, Africa and less frequently in Europe; transmitted by
sandfly of genus Phlebotomus.
 L.L. donovani: Causes VL and PKDL
 L.L. infantum: Causes VL and PKDL
 L.L. tropica complex: Causes CL

10. New world leishmaniasis
▰ Seen in Central and South America; transmitted by sandfly of
genus Lutzomyia.
 L.L. chagasi: Causes VL and CL
 L.L. mexicana complex: Causes CL
 L. Viannia braziliensis complex: Causes MCL and CL

11. CUTANEOUS LEISHMANIASIS
▰ CL: Cutaneous leishmaniasis (CL) - most common form of
leishmaniasis.
▰ Global annual incidence of 6-10 lakh new cases.
▰ About 95% of CL cases - America, the Mediterranean basin, the
Middle East and Central Asia

12. CUTANEOUS LEISHMANIASIS
(Cont..)
▰ MCL: Over 90% of mucocutaneous leishmaniasis (MCL) cases -
Bolivia, Brazil, Ethiopia and Peru.
▰ Post kala-azar dermal leishmaniasis (PKDL) - another cutaneous
manifestation - occurs few months to years following VL

13. Various agents of cutaneous
leishmaniasis
Species Geographical
distribution
Clinical
syndrome
Vector (sandfly) Reservoir Transmission
L. L. tropica
(Oriental sore)
Western India,
North Africa, and
Middle East
CL, LR Phlebotomus
sergenti
Humans Anthroponotic
(human)
L. L. aethiopica Ethiopia,
Uganda, and
Kenya
CL, DCL P. longipes Hyraxes Zoonotic
L. L. major Middle East,
India, China,
CL P. papatasi Rodents Zoonotic

14. Old World Cutaneous
Leishmaniasis (CL)
▰ Old world CL is caused by Leishmania tropica complex -
comprises of three species—L. tropica, L. aethiopica and L. major.
▰ Vary from each other in - geographical distribution, reservoir
(human or animal) and species of sandfly vector involved in
transmission and the type of cutaneous lesions produced.

15. Life Cycle
Life cycle of the L. tropica complex is
same as L. donovani , except that:
 Vector: Sandfly, but different
species of Phlebotomus.
 Habitat: In humans, the
amastigote forms reside in
reticuloendothelial cells of skin

16. Clinical Features
▰ Cutaneous leishmaniasis: Also known as
“Oriental sore”, Delhi boil, Aleppo boil and
Baghdad Button, etc.
▰ Occurs on face and hands – painless papule,
becomes nodular and finally it ulcerates.
▰ Heals spontaneously or - leaves behind
disfigurement or scar.

17. Clinical Features (Cont..)
▰ Leishmaniasis recidivans (LR):
Granulomatous response producing new
lesions - occur years after healing of
primary sore due to L. tropica. It is
▰ Characterized by scaly, erythematous
papules and nodules - develop in center
or periphery of a previously healed sore.

18. Clinical Features (Cont..)
▰ Diffuse cutaneous leishmaniasis (DCL): Caused by L.
aethiopica. It is
▰ Characterized by - lack of CMI response to the parasite, resulting
in widespread cutaneous lesions
▰ Rare -100 cases have been reported so far - Kenya and Ethiopia
▰ Responds poorly to treatment; disease may last long.

19. Laboratory Diagnosis of CL
▰ Microscopy: Amastigotes - demonstrated from punch biopsies -
from the edge of the active lesion and touch preparation
(impression smear) stained with Giemsa
▰ Culture: Aspiration from the ulcers - cultured in NNN medium
and Schneider’s Drosophila medium - isolation of promastigote
forms

20. Laboratory Diagnosis of CL (Cont..)
▰ Montenegro test: Positive leishmanin skin test - delayed
hypersensitivity reaction to the parasite.
▰ Negative in diffuse CL.

21. Treatment of Cutaneous Leishmaniasis
(Old World)
▰ Local therapy - usually recommended. Options available are:
 (i) paromomycin (15%) or methyl benzethonium (12%)
ointment - 20 days
 (ii) intralesional antimonials
 (iii) cryotherapy
 (iv) thermotherapy.

22. Treatment of Cutaneous Leishmaniasis
(Old World) (Cont..)
▰ Systemic therapy: Only for disfiguring or scarring lesions.
 L. major—(i) fluconazole for 6 weeks, (ii) pentavalent
antimonials with or without pentoxifylline for 10–20 days
 L. tropica—pentavalent antimonials for 10–20 days. In LR
cases - combined with oral allopurinol
 L. aethiopica—pentavalent antimonials + paramomycin for 60
days or longer.

23. New World Cutaneous
Leishmaniasis
▰ Mainly caused by:
 Leishmania Leishmania (L.L.) mexicana complex
 Leishmania Viannia (L.V.) braziliensis complex
 Leishmania Leishmania (L.L.) chagasi - Causes atypical CL and
American VL.

24. New World Cutaneous
Leishmaniasis (Cont..)
▰ Morphology and life cycle - identical to
L. donovani, except:
▰ Vector: Lutzomyia species
▰ Reservoir of infection: Dogs, foxes
(zoonotic)
▰ Amastigote forms - reside in
reticuloendothelial cells of skin and
mucous membrane (do not invade

25. Chiclero ulcer
▰ L. mexicana causes - specific form of CL - chiclero ulcer (or bay
sore).
▰ Characterized by persistent ulcerations in pinna.
▰ Seen in Central America - workers living in forests harvesting
chicle plants to collect chewing gum latex.

26. Espundia (mucocutaneous
leishmaniasis or MCL)
▰ L. braziliensis infects mucous membrane
of the nose, oral cavity, pharynx or
larynx.
▰ Presents months to years after the CL.
▰ Ulcerative lesions - formed with erosion
of the soft tissue and the cartilages - loss
of lips, soft part of nose and soft palate

27. Espundia (mucocutaneous
leishmaniasis or MCL) (Cont..)
▰ Gradually, the nasal septum - destroyed, resulting in nasal
collapse with hypertrophy of upper lip and nose leading to
development of “tapir nose”.

28. Treatment New World cutaneous
leishmaniasis
▰ In contrast to Old World CL - systemic therapy – recommended
for New World CL - as lesions are more chronic, multiple and
have tendency for mucosal involvement.
▰ Local therapy - given in addition - agents used for treatment -
same as used for Old World CL

29. Treatment New World cutaneous
leishmaniasis (Cont..)
▰ The regimen for systemic therapy depends upon - causative
agent.
 L. mexicana: Ketoconazole or miltefosine for 28 days
 L. guyanensis and L. panamensis: Pentamidine or pentavalent
antimonials or miltefosine for 28 days
 L. braziliensis: Pentavalent antimonials for 20 days; or

30. Treatment New World cutaneous
leishmaniasis (Cont..)
 L. amazonensis, L. peruviana and L. venezuelensis: Pentavalent
antimonials for 20 days
 Relapse treatment: Amphotericin B or pentavalent
antimonials + topical imiquimod.

31. Treatment New World cutaneous
leishmaniasis (Cont..)
▰ For MCL (all species):
 (i) pentavalent antimonials with or without oral pentoxifylline
for 30 days
 (ii) amphotericin B
 (iii) Bolivia - miltefosine - agent of choice.

32. NEUROCYSTICERCOSIS

33. NEUROCYSTICERCOSIS
▰ Neurologic infection caused by the larval stage of the tapeworm
Taenia solium

34. Life Cycle of Taenia solium
▰ Host: Man acts as both definitive and intermediate host
▰ Infective stage: Eggs of T. solium
▰ Mode of transmission: Firstly man acquires the infection by—
 (1) ingestion of contaminated food or water containing eggs of
T. solium
 (2) autoinfection

35. Cysticercus Cellulosae
▰ A mature cysticercus cellulosae - 5 mm long and 8–10 mm wide,
spherical
(or slightly oval), yellowish white, separated from the host tissue
by a thin collagenous capsule.
▰ It contains two chambers: Outer - bladder like sac filled with
0.5 mL of vesicular fluid and the inner chamber contains the
growing scolex

36. Cysticercus Cellulosae (Cont..)

37. Neurocysticercosis
▰ Most common form (60–90% cases) of cysticercosis, parasitic
CNS infection of man and adult onset epilepsy throughout the
world.
▰ NCC is of two types:
▰ 1. Parenchymal: Involves brain parenchyma
▰ 2. Extraparenchymal sites are meninges, ventricles and spinal
cord.

38. Neurocysticercosis (Cont..)
▰ Seizure (70% of cases), Hydrocephalus, Increased intracranial
pressure, Chronic meningitis, Focal neurological deficits,
Psychological disorders and dementia.
▰ Clinical presentation is variable and depends on number,
location & size of the cyst, the morphological stage of the cyst
and the host immune response.

39. Neurocysticercosis (Cont..)
▰ NCC exists in four morphological stages: It starts as vesicular
form, gradually develops into necrotic, followed by nodular and
finally into calcified stage

40. Other Forms of Cysticercosis
▰ Subcutaneous cysticercosis
▰ Muscular cysticercosis
▰ Ocular cysticercosis

41. Laboratory diagnosis of
Cysticercosis
▰ Radiodiagnosis—CT scan and MRI (useful for detecting number,
location, size of the cysticerci and the stage of the disease)
▰ Antibody detection in serum or CSF—
 ELISA (using crude extract of cysticerci)
 Western blot (using 13 kDa LLGP Ag)

42. Laboratory diagnosis of Cysticercosis
(Cont..)
▰ Antigen detection in serum or CSF—ELISA ..Lymphocyte
transformation test
▰ Histopathology of muscles, eyes, subcutaneous tissues or brain
biopsies—can detect cysticerci
▰ FNAC of the cyst and then staining with Giemsa
▰ Fundoscopy of eye—detects larvae
▰ Modified Del Brutto diagnostic criteria.

43. Laboratory diagnosis of Cysticercosis
(Cont..)
CT scan of brain showing multiple ring
enhancing lesions with eccentric scolex
(neurocysticercosis).

44. Laboratory diagnosis of Cysticercosis
(Cont..)
Cysticercus cellulosae in biopsy from
the brain (hematoxylin and eosin
stain)—An entire cysticercus seen
within the bladder walls,
[Parenchymatous portion of the
cysticercus can be better observed.
The extensive folding of the spiral
canal and one sucker of the scolex
(Arrow)].

45. Treatment of Cysticercosis
Antiparasitic agents:
▰ For brain parenchymal lesions:
 Albendazole (15 mg/kg per day for 8–28 days) or
 Praziquantel (50–100 mg/kg daily in three divided doses for 15–
30 days)
 Longer courses - in patients with multiple subarachnoid
cysticerci

46. Treatment of Cysticercosis (Cont..)
Symptomatic treatment of:
▰ Seizures by antiepileptic drugs
▰ High-dose glucocorticoids - used to reduce the inflammatory
reactions caused by dead cysticerci
▰ Hydrocephalus: Attempts should be made to reduce intrac-
ranial pressure.

47. Treatment of Cysticercosis (Cont..)
Surgery:
▰ Open craniotomy to remove cysticerci - rarely required
nowadays
▰ Surgery - indicated for ocular, spinal and ventricular lesions
because antiparasitic drugs can provoke irreversible
inflammatory damage

48. Prevention
▰ Good personal hygiene to prevent autoinfection with eggs
▰ Effective fecal disposal to prevent contamination of food and
water with eggs
▰ Treatment and prevention of human intestinal taeniasis
▰ Vaccines to prevent porcine cysticercosis