filariasis - year 3 - 2009 -10 batch
TRANSCRIPT
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BANCROFTIAN
FILARIASIS
Rumala Morel
Department of Parasitology
Peradeniya
Y3S2
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South East Asia - ½ the global burden
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1.Describe the geographical distribution in SL
2.Describe the pathogenesis & clinical features
3.Evaluate the laboratory methods of diagnosis
4.Name the antifilarial drug(s) used in Sri Lanka
5.State the principles underlying the prevention and control
6.Describe the preventive and control measures used in theNational Filariasis Control Programme in Sri Lanka
OBJECTIVES - Bancroftian filariasis
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Distribution of Bancroftian
filariasis in Sri Lanka
Confined to urbanizedcoastal belt:
3 provinces - 9.5 million
(50% of SL population)
exposed
inland foci:
Gampaha,Warakapola
Veyangoda
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life span 7-16 yrs
Revision of Life Cycle
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Immunopathogenesis:as yet unclear, associated with
location of adult worms in lymphatics Basic lesion
Dilatation of lymphatics = Lymphangiectasia
Granuloma
(host inflammatory reaction)
Not due to blockage by adult worm
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PATHOLOGY
Adult worms induce
endothelial cell proliferation
lymphatic dilatationDeath of adult worms – antigen leakage
formation of granulomatous nodules
activation of host inflammatory responses
Obliterative peri/endolymphangitis in dilated
lymphatics
Episodes of ACUTE FILARIAL LYMPHANGITIS [AFL]
Lymphangiectasia = dilated lymphaticsImpairs lymphatic function
Predisposes to bacterial & fungal infections
ACUTE DERMATOLYMPHANGIOADENITIS [ADLA]
leads to CHRONIC LYMPHOEDEMA
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Pathogenesis of lympoedema
Acute Dermatolymphangioadenitis[ADLA]
Lymphoedema
Pitting [Grade 1]
Non pitting [Grade 2]
Elephantiasis [Grade 3]
Obstruction &
Dilatation of lymphatics
Granuloma
Death of adult worms
Acute Filarial Lymphangitis [AFL]
11ry bacterial & fungal infections
Repeated attacks of
ADLA
No mechanical blockage by worms
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Death of adult worm causes
granuloma formation
Obliterative peri/endolymphangitisin dilated lymphatics
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Clinical – ACUTE FILARIASIS1. Acute Filarial Lymphangitis [AFL]
Due to death of adult worms
Mild Residual lymphoedema - rare
2. Acute Dermatolymphangioadenitis [ADLA]
Due to 11ry bacterial infections in limbs with
compromised lymphatics
2-6 attacks / year
Diffuse subcutaneous inflammation & oedema
Males - acute funiculitis- acute epididymo – orchitis
Extra lymphatic disease - filarial monoarthritis - KJ
- filarial fevers
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•Clinical – CHRONIC FILARIASIS
LymphangiectasiaDue to adult worms
lymphoedema
elephantiasis
Males: hydrocoele
11ry
bacterial& fungal
infections
11ry bacterial
infectionsRecurrent ADLA
&
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Non pitting
[Grade 2]
Pitting oedema
[Grade 1]
Lymphoedema
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Elephantiasis
[Grade 3]
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Clinical manifestations of lymphoedema
depend on site of obstruction
lympoedema –
Grade 1- pitting
Grade 2- non pitting
Grade 3- elephantiasis
lymph leakage into urinary tract-
chyluria
(obstruction in cisterna chyli)
lymph leakage into
peritoneal cavity
chylous peritonitis
Common sites
limbs
genitalia
breast
Kidney damage: proteinuria & /or haematuria
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CLINICAL MANIFESTATIONS IN
MALE GENITALIA
- acute funiculitis
- acute epididymo – orchitis
- hydrocoele
-Scrotal elephantiasis,
-lymph scrotum(skin vesicles)
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Tropical Pulmonary Eosinophilia - TPEOCCULT FILARIASIS
common in India, Sri LankaPathogenesis: immune destruction of mf in lungs
due to host response
to human mf / mf of animal filaria
Eosinophilic granulocytes in lung
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X’ray- broncho vascular markings
serum IgE levels (> 1000 kU/L)
filarial Ag/Ab+
peripheral blood mf - veand
clinical response to diethylcarbamazine
Diagnostic criteria for TPE
Clinical Syndrome: cough, bronchospasm (worse at night)
With eosinophila >3000/µl
& history of exposure to lymphatic filariasis
Bilaterally diffusebronchopneumonia.
Early treatment canprevent interstitialfibrosis
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Bilaterally diffuse
milliary nodules
Tropical Pulmonary Eosinophilia- TPE
OCCULT FILARIASIS
ANTI-FILARIAL TREATMENT
Diethylcarbamazine 6mg/kg tds
3 weeks
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Clinical manifestations in endemic areas
mf +subclinical
lymphangiectasia
but non reversible40% kidney
damage
mf +/- AFD-filarial fevers
lymphangitis
lymphadenitisCFD-chronic
obstructive mf -
TPEAsymptomatic Symptomatic
mf - ve
Filarial Ag +/-
Ab +
Occult
filariasis
AFD = Acute Filarial Disease
CFD = Chronic Filarial Disease
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Laboratory Diagnosis of Filariasis:
Direct- detection of microfilaria in blood
Thick film- 10pm-2 am (20-60µl)wet mount/ stain Giemsa
Not sensitive!
Concentration-
•Knott’s method (old)•Membrane filtration- pore size 5µm
Detection of adults in biopsy- rare
Indirect1. Circulating Filarial Antigen [CFA] - BEST daytime
2. Filarial Specific Antibody – won’t differentiate
from past infection
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Useful in occult filariasis - TPE
Indirect immunofluorescent test- IFA/FAT
ELISA (enzyme linked immunosorbent assay)
Disadvantage: Can’t diagnose acute
lymphatic disease.
Antibodies long lasting. May be past infection.
Detection of filarial
antibodies in serum
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Now WHO recommends :-www. who.int. lymphatic_filariasis/epidemiology
Antigen detectionImmunochromatographic [ICT] card
test
high sensitivity [100% sensitive in mf +ves ]
high specificity
100 μl of fingerprick blood drawn at any time, day
or night.
simple, no equipment required
quick results <15 min
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Antigen detection strip (card) tests- RDTs
Sample origin
(whole blood
serum/plasma)
polyclonal Ab
+ colloidal gold
Mab
W bancrofti
T C
absorbent pad
test control
Immunochromatographic [ICT] card test
Detects specific
circulating W bancrofti Ag
in serum/whole bloodusing monoclonal antibody
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A. Ultrasound scan – scrotum – filarial dance sign
B. Radionucleotide lymphoscintigraphy
- assessment of lymphatic damage
Imaging techniques
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The Global Programme to Eliminate
Lymphatic Filariasis (GPELF) - 2000
--• Global Alliance to Eliminate Lymphatic Filariasis - 2000
– public-private partnership
– WHO & national Ministries of Health,
–
Private drug companies donating albendazole & ivermectin(Mectizan®)
– NGOs
• 1 billion at risk population
• > 120 million people are already infected
• > 40 million incapacitated or disfigured
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RAGFIL: Rapid Assesment of Geographical distribution of
bancroftian FILariasis. - Map endemic foci of lymphatic
filariasis - to decide on mass treatment programs.
>60%
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Filariasis in Sri Lanka-
1937-39: Brugia malayi predominant1947: Anti Filariasis Campaign
1960’s: Brugian filariasis eradicated
control of larval breedingresidual action of DDT on adults
treatment with DEC
Bancroftian filariasis is the ONLY lymphaticfilariasis in SL now
Fil i i t l i S i L k
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Filariasis control in Sri Lankaby
Anti Filariasis Campaign
Vector control: prevent mosquito breeding
clear drains, cess pits, sealing of septic tanks
larviciding with insecticides, larvivorous fish
Selective treatment of mf + cases
2-weeks diethylcarbamazine [DEC] (6 mg/kg)
Mass Drug Administration- eradicate parasite bykilling mf and disrupting transmission - continued for 4-5 years
MOST EFFECTIVE
Morbidity control – disability management training
M D Ad i i t ti
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started in Oct/1999 in SL
covering endemic area-3 provinces.
In 2004 - coverage 80% compliance 71% (WHO)
Exclude infants & pregnant females
Pregnancy- treat 1 month after delivery
Mf + and clinical filariasis treated with full course DEC
Effect on intestinal geohelminths
– Gunawardena NK et al - Ceylon Med J. 2008 Mar;53(1):13-6
Treat all persons in endemic areas with
Diethylcabamazine [DEC] +albendazole
annually
Mass Drug Administration-
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Motivate & train pts & care givers on :-washing
elevation
preventing & treating entry lesions
-topical antibiotics & antifungals using proper footwear
WHO morbidity control strategy
Community Home Based Care
by Filariasis Morbidity Control Clinics
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Washing with soap
Proper footwear
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1. Regarding lymphatic filariasis
A. Adult worms block lymphatics
B. Wucheraria bancrofti microfilaria show nocturnal periodicity
C. Immunochromatographic card test is used to detect
circulating filarial antigensD. Secondary bacterial infections are important
co-factors in pathogenesis
E. Treatment is with diethylcarbamazine [DEC]
True BCDE
MCQ