filaria 2012 rev

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    FILARIASIS

    DEPARTEMENT OF PARASITOLOGY

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    CLINICAL CASE2

    A 28-year old male came to Community Health Centrewith complaints swelling of right leg from thigh totoes. The swelling occurred once every 5-6 months. Itstarted 4 years ago along with hardness and swelling

    of inguinal lymph nodes. He also developed chills andfever. About 4-5 days later the fever stopped, but theswelling of the leg increased. At this stage he hadchills with severe pain in the right leg. This lasted for

    10-12 days, after which the pain subsided. During thistime he had ulcers on the swollen leg with bleedingand a yellow discharge. This remained for 2 days.Later the swelling decreased and the ulcers startedhealing.

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    3

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    Learning issues4

    1. Agents of the disease

    2. Pathogenesis

    3. Diagnosis

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    References5

    King, C.L. 2001. Transmission intensity and human immune responses to

    lymphatic filariasis. Parasite Immunology 23 (7): 363371

    Melrose, W.D. 2002. Lymphatic filariasis: new insights into an old disease.

    International Journal for Parasitology32(8), 947-960

    Muller, R. and Wakelin, D. 2002. Worm and Human Disease. 2th edition.

    London. CABI Publishing

    Palumbo, E. 2008. Filariasis: diagnosis, treatment and prevention. Acta

    biomedical. 79. 106-109

    Rahmah, N., Lim, B. H., Khairul Anuar, A., et al. 2001. A recombinant

    antigen-based igg4 ELISA for the specific and sensitive detection of brugia

    malayiinfection. Transactions of the royal society of tropical medicine andhygiene 95(3): 280-284

    World Health Organization. 1999. Collaborative global programme to

    eliminate lymphatic filariasis: Programmes backround and overview towards

    initiating a National programme to eliminate lymphatic filariasis .

    WHO/CEE/FIL World Health Organization, Geneva, 1-25

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    Lymphatic Filariasis

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    Causative agents7

    1. Brugia malayi

    2. Wuchereria bancrofti

    3. Brugia timori

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    8

    Wucherer ia banc ro ft i

    The larva was found by Demarquay (1863)

    and Wucherer (1866)

    The adult was first found by Bancroft in 1876

    Nocturnal periodicity

    Vector: CulexandAedes

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    Wucherer ia banc ro ft iMorphology

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    Adults look like thin and long threads

    Female is 80-100 mm, male is 25-45 mm with

    spiral-shaped tail

    Fertilized eggs is 30-40 x 20-25 m, the egg

    cell develops rapidly to form a larva while in

    the uterus

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    Wucherer ia banc ro ft iMorphology

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    Microfilaria is sheated and smooth-shaped,

    0.24-0.35 mm long

    Regular nucleus, no terminal nucleus

    Cephalic space: the length is equal with the

    width

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    Wucherer ia banc ro ft iMorphology

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    L3 enter human body

    13 The L3 enter the skin of the

    human host through thepuncture site of the mosquito

    when it takes its second blood

    meal.

    Details of larvae molting and

    development in humans arelargely unknown, but it is

    thought the larvae almost a

    year to:

    Migrate to the lymphatics

    Mature undergoing two molts

    and to become an adult

    Mate

    Produces microfilariae

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    Brug ia malayi14

    The larva was first observed from a native

    Sumatera by Brug (1927)

    Nocturnal periodicity

    Vector: Mansonia uniformis (rural) and

    Anopheles spp. (urban)

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    Brugia malayiMorphology

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    Adult resembles that ofW bancrofti

    Female is 43-55 mm, male is 13-23 mm with

    spiral-shaped tail

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    Brug ia malayiMorphology

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    The larva is sheated and slightly winding (kinky),

    0.18-0.23 mm long

    Irregular nucleus, 2 terminal nucleus

    Cephalic space: the length is twice as the width

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    Brugia malayiMorphology

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    Pathogenesis19

    Inflammation occurs when worms die, either drug-induced or spontaneously.

    Granulomas arise around those worms,characterized by macrophages which develop intogiant cells: as plasma cells, eosinophils andneutrophils.

    Clinical symptom is filarial fever starting when theworm died and leads to retrograde lymphangitis(painful with swelling), and lymphadenitis, whichlasts for 1 week.

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    Pathogenesis20

    Lymph vessels dilation, not obliteration, is probably theearly event following antigenic stimulation, which springlarvae are being released. These larvae are degenerateand will be taken up by phagocytic cells.

    These accompanied by triggering of the innate immunesystem, release proinflammatory cytokines andmolecules that promote lymphangiogenesis.

    The enlarge lymph vessels become less efficient attransporting lymph from the periphery, which in the legsis always oriented against gravity, more vulnerable toexogenous microorganisms.

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    Pathogenesis21

    Insufficient fluid transport will lead to fluidextravasations, particularly in the lower limbs, andeventually to lymphoedema.

    L3 preferentially stimulate IL-4 and IL-13 release frombasophils as well as histamine release. In addition,basophils comprise approximately 1% of cells in PBMCand their contribution to the observed cytokineproduction can be substantial. Therefore mast cells andbasophils may play an important role in regulating thehost response to filarial infection by affecting T-celldifferentiation, local blood flow, lymphocyte proliferationor by release of histamine or other prostanoids.

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    ManagementDiagnosis

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    Clinical manifestations

    Laboratory diagnosis

    Microscopic

    Immunodiagnosis

    Molecular technique

    Ultrasonography

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    Clinical Manifestations25

    Acute filariasis

    Chronic filariasis

    Atypical presentation

    Asymptomatic carrier

    L h ti l dil t ti l

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    Lymphatic vessel dilatation, valve

    incompetency, lymphatic back flow, pooling &

    oedema26

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    Adult worms in the lymphatic

    system

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    Microscopy for Filaria

    Nucleopore membran(Knotts concentration)

    Staining thick blood filmwith Giemsa

    Specific but not sensitive,depends on:

    Timing of sampling(periodicity)

    Volume of blood (volumeincrease sensitivityincrease)

    Nucleopore membrane(knotts concentration)

    Staining of the blood film Mor holo ical

    28

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    Periodicity

    Definition:Relative density of microfilaria in peripheralcirculation

    > 24 hours per cycle

    Nocturnal periodic: peak microfilaria at aroundmid-night but very low or absence during theday

    Diurnal periodic: peak microfilaria during the day

    but low or absence at night Nocturnal subperiodic: peak microfilaria density

    at night with lower density during the day

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    Periodicity

    Microfilariae stay in the lung during thedaytime and come rarely out to theperipheral vessels, but soon after sunsetthey begin to appear in the peripheral blood,increasing in number from 10 p.m. until 6a.m. (nocturnal periodicity)

    There are a number of theories Photodynamic substance theory by Masuya Fluorescent substances in the microfilarias

    body are injured by the sunlight (W bancroftiand B malayi)

    Microfilaria ofLoa loa has no fluorescentsubstance at all

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    Ultrasonography31

    Detect the motile adult worms within thelymphatics, scrotum and breast (term filarial

    dance signs). Detecting W bancroftionly.

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    Immunodiagnosis32

    Brugia rapid

    Antibody detection

    assay

    Detects IgG4

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    Immunodiagnosis33

    Antigen detection

    assay

    For bancroftian

    filariasis

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    THANK YOU