Leishmania Flashcards
etio
Etiology.Many species of obligate intracellular protozoa Leishmania;predominant species are:
■ New World: Leishmania mexicana complex, Viannia subgenus.
■ Old World:L.tropica,L.major,and L.aethiopica.
Vector
Vector.Sandfies.OldWorld:Phlebotomus.NewWorld:Lutzomyia
Pathogenesis
In ection o macrophages in skin, naso-oropharyngeal mucosa, and the reticuloen-
dothelialsystem(viscera).Diversityo clinicalsyndromesresulting romaparticularparasite,vector, and host species.
characterized bydevelopmento singleormultiplecutane- ouspapulesatthesiteo asand ybite,o en evolving into nodules and ulcers, which heal spontaneously with a depressed scar.
Cutaneous leishmaniasis
stages of parasite
Stageso parasite:Promastigote: Flagellated form found in sandflies and culture; amastigote: non agellated tissue orm
transmission
Vector-borne by bite o in ected
emalephlebotominesand ies,whichbecome in ected by taking blood meal rom in ected mammalian host
incubation period
Inversely proportional to size o inoculum:Shorterinvisitorstoendemicarea. OWCL: L. tropica major, 1 to 4 weeks; L. tropica, 2 to 8 months; acute CL: 2 to 8 weeks or more
symptoms
Noduloulcerativelesionsusually asymptomatic. With secondary bacterial in ec- tion, may become painful
NEW WORLD CUTANEOUS LEISH . skin manif
Small erythema- tous papule develops at sand y bite site, evolv- ing into ulcerated nodule
elarges to 3 to 12 cm with raised border. Nonulcerating nodules may become verrucous. Lymphangitis, regional lymphadenopathy
Ear lesions may persist or years, destroying cartilage (chiclero ulcers)
Mucocutaneous leish. skin manif
Characterized by naso-oropharyngeal mucosal involvement
Edemaandin ammatorychangesleadto epistaxis and coryzal symptoms. In time, the nasal septum, oor o the mouth, and tonsil- lar areas are destroyed (Fig. 29-3). Results in marked disf gurement (re erred to as espundia inSouthAmerica).Deathmaybecausedby superimposed bacterial in ection, pharyngeal obstruction, or malnutrition.
old world cut leish. manif
Begins as small erythematous papule, which may appear immediately a er sand y bite but usually 2 to 4 weeks later. Papule slowly enlarges to 2 cm over a period o several weeks and assumes a dusky violaceous hue (Figs. 29-4 and 29-5). Eventually, lesion becomes crusted
in center with a shallow ulcer and raised indu- rated border = volcano sign. In some cases, the center o the nodule becomes hyperkera- totic, ormingacutaneoushorn
Complication
of L.tropica infection.Dusky-redplaqueswith active,spreadingbordersandhealingcenters, giving rise to gyrate and annular lesions. Most commonlya ectsthe ace;cancausetissue destruction and severe deformity.
LEISHMANIASIS RECIDIVANS(LR)
SequeltoVLthathasresolvedsponta- neously or during/a er adequate treatment. Lesionsappear≥1yeara ercourseo therapy
with macular, papular, nodular lesions, and hypopigmentedmacules/plaqueson ace (Fig.29-6),trunk,andextremities
post kala azardermal leishmaniasis
Dx
Clinical suspicion, confirmed by demonstrating:
■ Intracellular non agellated amastigote in a biopsyo skin,mucosa,liver,lymphnodesor
aspirate o spleen, bone marrow, and lymph
node.
■ Flagellated promastigote in culture o tissues
(requiresupto21days)
Tx
sodium stibogluconate
alt : amphotericin B, miltefosine,paromomycin,and pentamidine