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BANCROFTIAN
FILARIASIS
Rumala Morel
Department of Parasitology
Peradeniya
Y3S2
South East Asia - ½ the global burden
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 the
National Filariasis Control Programme in Sri Lanka
OBJECTIVES - Bancroftian filariasis
Distribution of Bancroftian
filariasis in Sri Lanka
Confined to urbanized
coastal belt:
3 provinces - 9.5 million
(50% of SL population)
exposed
inland foci:
Gampaha,
Warakapola
Veyangoda
life span 7-16 yrs
Revision of Life Cycle
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
PATHOLOGY
Adult worms induce
endothelial cell proliferation
lymphatic dilatation
Death 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 lymphatics
Impairs lymphatic function
Predisposes to bacterial & fungal infections
ACUTE DERMATOLYMPHANGIOADENITIS [ADLA]
leads to CHRONIC LYMPHOEDEMA
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
Death of adult worm causes
granuloma formation
Obliterative peri/endolymphangitis
in dilated lymphatics
Clinical – ACUTE FILARIASIS
1. 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
•Clinical – CHRONIC FILARIASIS
Lymphangiectasia
Due to adult worms
lymphoedema
elephantiasis
Males: hydrocoele
11ry
bacterial
& fungal
infections
11ry bacterial
infections
Recurrent ADLA
&
Non pitting
[Grade 2]
Pitting oedema
[Grade 1]
Lymphoedema
Elephantiasis
[Grade 3]
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
CLINICAL MANIFESTATIONS IN
MALE GENITALIA
- acute funiculitis
- acute epididymo – orchitis
- hydrocoele
-Scrotal elephantiasis,
-lymph scrotum
(skin vesicles)
Tropical Pulmonary Eosinophilia - TPE
OCCULT FILARIASIS
common in India, Sri Lanka
Pathogenesis: immune destruction of mf in lungs
due to host response
to human mf / mf of animal filaria
Eosinophilic granulocytes in lung
X’ray- broncho vascular markings
 serum IgE levels (> 1000 kU/L)
filarial Ag/Ab+
peripheral blood mf - ve
and
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 diffuse
bronchopneumonia.
Early treatment can
prevent interstitial
fibrosis
Bilaterally diffuse
milliary nodules
Tropical Pulmonary Eosinophilia- TPE
OCCULT FILARIASIS
ANTI-FILARIAL TREATMENT
Diethylcarbamazine 6mg/kg tds
3 weeks
Clinical manifestations in endemic areas
mf +
subclinical
lymphangiectasia
but non reversible
40% kidney
damage
mf +/-
AFD-filarial fevers
lymphangitis
lymphadenitis
CFD-chronic
obstructive mf -
TPEAsymptomatic Symptomatic
mf - ve
Filarial Ag +/-
Ab +
Occult
filariasis
AFD = Acute Filarial Disease
CFD = Chronic Filarial Disease
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
Indirect
1. Circulating Filarial Antigen [CFA] - BEST daytime
2. Filarial Specific Antibody – won’t differentiate
from past infection
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
Now WHO recommends :-
www. who.int. lymphatic_filariasis/epidemiology
Antigen detection
Immunochromatographic [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
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 blood
using monoclonal antibody
A. Ultrasound scan – scrotum – filarial dance sign
B. Radionucleotide lymphoscintigraphy
- assessment of lymphatic damage
Imaging techniques
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
RAGFIL: Rapid Assesment of Geographical distribution of
bancroftian FILariasis. - Map endemic foci of lymphatic
filariasis - to decide on mass treatment programs.
>60%
Filariasis in Sri Lanka-
1937-39: Brugia malayi predominant
1947: Anti Filariasis Campaign
1960’s: Brugian filariasis eradicated
control of larval breeding
residual action of DDT on adults
treatment with DEC
Bancroftian filariasis is the ONLY lymphatic
filariasis in SL now
Filariasis control in Sri Lanka
by
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 by
killing mf and disrupting transmission - continued for 4-5 years
MOST EFFECTIVE
Morbidity control – disability management training
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-
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
Washing with soap
Proper footwear
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 antigens
D. Secondary bacterial infections are important
co-factors in pathogenesis
E. Treatment is with diethylcarbamazine [DEC]
True BCDE
MCQ

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Filariasis clinical

  • 2. South East Asia - ½ the global burden
  • 3. 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 the National Filariasis Control Programme in Sri Lanka OBJECTIVES - Bancroftian filariasis
  • 4. Distribution of Bancroftian filariasis in Sri Lanka Confined to urbanized coastal belt: 3 provinces - 9.5 million (50% of SL population) exposed inland foci: Gampaha, Warakapola Veyangoda
  • 5. life span 7-16 yrs Revision of Life Cycle
  • 6. 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
  • 7. PATHOLOGY Adult worms induce endothelial cell proliferation lymphatic dilatation Death 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 lymphatics Impairs lymphatic function Predisposes to bacterial & fungal infections ACUTE DERMATOLYMPHANGIOADENITIS [ADLA] leads to CHRONIC LYMPHOEDEMA
  • 8. 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
  • 9. Death of adult worm causes granuloma formation Obliterative peri/endolymphangitis in dilated lymphatics
  • 10. Clinical – ACUTE FILARIASIS 1. 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
  • 11. •Clinical – CHRONIC FILARIASIS Lymphangiectasia Due to adult worms lymphoedema elephantiasis Males: hydrocoele 11ry bacterial & fungal infections 11ry bacterial infections Recurrent ADLA &
  • 12. Non pitting [Grade 2] Pitting oedema [Grade 1] Lymphoedema
  • 14. 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
  • 15. CLINICAL MANIFESTATIONS IN MALE GENITALIA - acute funiculitis - acute epididymo – orchitis - hydrocoele -Scrotal elephantiasis, -lymph scrotum (skin vesicles)
  • 16. Tropical Pulmonary Eosinophilia - TPE OCCULT FILARIASIS common in India, Sri Lanka Pathogenesis: immune destruction of mf in lungs due to host response to human mf / mf of animal filaria Eosinophilic granulocytes in lung
  • 17. X’ray- broncho vascular markings  serum IgE levels (> 1000 kU/L) filarial Ag/Ab+ peripheral blood mf - ve and 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 diffuse bronchopneumonia. Early treatment can prevent interstitial fibrosis
  • 18. Bilaterally diffuse milliary nodules Tropical Pulmonary Eosinophilia- TPE OCCULT FILARIASIS ANTI-FILARIAL TREATMENT Diethylcarbamazine 6mg/kg tds 3 weeks
  • 19. Clinical manifestations in endemic areas mf + subclinical lymphangiectasia but non reversible 40% kidney damage mf +/- AFD-filarial fevers lymphangitis lymphadenitis CFD-chronic obstructive mf - TPEAsymptomatic Symptomatic mf - ve Filarial Ag +/- Ab + Occult filariasis AFD = Acute Filarial Disease CFD = Chronic Filarial Disease
  • 20. 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 Indirect 1. Circulating Filarial Antigen [CFA] - BEST daytime 2. Filarial Specific Antibody – won’t differentiate from past infection
  • 21. 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
  • 22. Now WHO recommends :- www. who.int. lymphatic_filariasis/epidemiology Antigen detection Immunochromatographic [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
  • 23. 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 blood using monoclonal antibody
  • 24. A. Ultrasound scan – scrotum – filarial dance sign B. Radionucleotide lymphoscintigraphy - assessment of lymphatic damage Imaging techniques
  • 25. 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
  • 26. RAGFIL: Rapid Assesment of Geographical distribution of bancroftian FILariasis. - Map endemic foci of lymphatic filariasis - to decide on mass treatment programs. >60%
  • 27. Filariasis in Sri Lanka- 1937-39: Brugia malayi predominant 1947: Anti Filariasis Campaign 1960’s: Brugian filariasis eradicated control of larval breeding residual action of DDT on adults treatment with DEC Bancroftian filariasis is the ONLY lymphatic filariasis in SL now
  • 28. Filariasis control in Sri Lanka by 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 by killing mf and disrupting transmission - continued for 4-5 years MOST EFFECTIVE Morbidity control – disability management training
  • 29. 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-
  • 30. 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
  • 32. 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 antigens D. Secondary bacterial infections are important co-factors in pathogenesis E. Treatment is with diethylcarbamazine [DEC] True BCDE MCQ