other names of leishmania
valley fever, white leprosy, Kal Azar or black fever (visceral)
leishmania agent type and name
protozoan, phylum kinetoplastida with single flagellum and kinetoplast
different stages of leishmania...
1. express different sets of genes
2. adapt their surface structure and metabolism to survival in insect or mammal hosts
dimorphic parasite stages
intracellular = amastigote
extracellular = flagellated promastigote
mammalian host, nucleus, kinetoplast and internal flagellum
intestinal tract of the insect vector, central nucleus, kinetoplast and long free anterior flagellum
invades host cells by..
triggering phagocytosis by macrophages. it likes the lysomes and lytic enzymes/acidic environment
compare phagocytosis methods with other species
trypansoma cruzi: induces phagocytosis but escapes into cytoplasm
myobacterium tuberculosis: induces phagocytosis but blocks lysosomal maturation
leishmania: adapted to like acidic environment
sand flies (Phlebotomidae)
2-4mm, yellowish body
• Active at dusk and night
• Potential hosts:
- reptiles, mammal, birds, amphibians
leishmania ecology old world
close contact of humans with domestic animals (in rural areas zoonosis) and human to human in urban environments.
infection common in dogs in mediterranean
leishmania ecology new world
working/hunting in forest. wild animal reservoirs (rodents, monkies, sloths..also dogs), sylvatic transmission
(we get infected when we go into the forest because most of the hosts are in the forest)
intertropical zones of america and africa. temperate regions of south america, southern europe and asia
old world species
l. tropica and l. major
new world species
3 leishmania types
visceral, cutaneous, mucocutaneous
visceral leishmania definition
systematic infection of reticulo-endothelial cells (mostly macrophages) throughout multiple internal organs and the blood particularly spleen, liver, lymph nodes
kala azar incubation
up to 6 months
kala azar symptoms
abdominal swelling due to hepato and splenomegaly, high fever, progressive drastic weight loss (kachexia, anemia, darkening of skin. untreated 75-95% mortality
post kala azar
dermal leishmaniasis. lesions contain large number of parasites. relapses frequent after 'cure'
cutaenous leishmaniasis definition
infection remains restricted to the initial site of infection (bite site)
chronic, but self-limiting dry ulceration at bite site, erythematous papule similar to insect bite, enlarges over a few weeks, ulceration starts months after infection
cutaneous leishmanisis facts
parasites not found outside lesion, volcano shaped ulcer (with divet) granuloma, depresssed scar, nearly absolut resistance to reinfection, inoculation long practices in mid east
mucocutaneous leishmaniasis (espundia)
spreads to mucosea of mouth, nose, larynx, pharynx and ear creating ulcers (20% of patients develop these). destruction of all soft parts of the nose, lips, soft palate. death through secondary bacterial infection
espundia clinical features
nasal congestion and nocturnal discomfort, epistaxis (nose bleeds), septum rapidly destroyed = "tapir nose"
espundia long term problems
laryngeal extensions, respiratory tract obstruction, dysphagia and undernutrition, tisssue necrosis and disfigurement, death (pulomonary super-infections, false alimentary passage, acture respiratory obstruction, disfiguring through refractile scars
clinical presentation, epidemiological elements considered, cultures, immunological diagnosis through indirect fluoresccent antibody technique (IFAT), skin test: Montenegro
leishmania diagnosis gold standard!
parasites in blood or lymph (kala azar) or scraping of the ulcer (cutaneous versions)
drugs. visceral = pentavalent antimonials. cutaenous = amphotheracin B
prevention and control
avoid zoonotic habitat, mechanical means (nets), chemical spraying. there is no vaccine or chemoprofilaxis, forest clearance, case detection and treatment, wild reservoir control, sand fly control
life cycle 1.
bitten by sandfly infected with promastigotes
life cycle 2.
Promastigotes get eaten by macrophages. But instead of being destroyed, they divide inside macrophage until it explodes
life cyle 3.
These amastigotes can either reinfect other cells as amastigotes.... or infect an insect when a sandfly eats an infected macrophage which bursts inside the insect (where they turn back into promastigotes)
why don't we inoculate everyone like they do in the mid east?
Not practiced everywhere because you ARE actually getting the disease, and complications could arise from infection. With smallpox pricks, the person didn't actually get the disease)