Lymphatic

Filariasis
 Lymphatic Filariasis

 Because of infection with 3 closely related

Nematodes: Wuchereria bancrofti, Brugia malayi
(both occurring in India) & Brugia timori.

 Transmitted by the bite of infected mosquito & all

the parasites have similar life cycle in man.
 Burden of Disease
 1.254 billion population at risk in 83 countries

 120 million people in tropical & subtropical areas of

the world are infected.
 2nd leading cause of disability
– Almost 25 million men suffer from genital disease (most
commonly hydrocoele)
– Around 15 million people — mainly women — have
lymphoedema
LF Endemic Countries & Territories
– 2006, WHO

Bangladesh, Democratic Republic of Congo, India,

Indonesia, Madagascar, Nigeria & Philippines are
among most highly endemic countries.
 National Scenario
• Population at risk : 45.4 C (454 million)
(in 16 States & 5 UT’s)
• Total infected : 5.17 C
(Wb - 99.4 % and Bm - 0.6 %)
• No. of diseased : 2.25 C
• Mf carriers : 2.92 C
• Hydrocele : 1.29 C
 Agent Factors
[Link] Parasite Mosquito Disease
1. [Link] Culex LF
2. [Link] Mansonia LF
Anopheles/
3. [Link] LF
Mansonia
River
4. [Link] Simulium flies
Blindness
5. [Link] Chrysops flies S/c swellings
6. [Link] Culicoides Serous cavity
7. [Link] Culicoides ”
8. [Link] Culicoides ”
 Periodicity & life cycle
 Mf are nocturnally periodic (maximum density of Mf in blood is
reported between 10 pm & 2 am) except in South pacific island
& limited foci in the Nicobar islands, Thailand & Vietnam, it is
non-periodic (sub-periodic), being detectable throughout 24
hours.
 Man is definitive & mosquito is intermediate host.

 Adult worms living in lymphatic system.

 Females are viviparous, & giving birth around 50,000Mf/d.

 Mf survives for about a year & adult worm for 15 years or

more.
 Host Factors
 Man – Natural Host

 Age – All age (even in infant <6 months) Max: 20-30

years
 Sex – Higher in men

 Migration – leading to extension of infection to non-

endemic areas
 Immunity – may develop after long year of exposure
(Basis of immunity-not known)
 Social & Environmental Factors
 Associated with Urbanization, Poverty,
Industrialization, Illiteracy & Poor sanitation.
 Climate: is an important factor which influences:
1. The breeding of mosquito
2. Longevity (Optimum temperature 20-300C &
Humidity 70%)
3. The development of parasite in the vector
4. Sanitation, Town planning, Sewage & Drainage.
 Dranage: breed profusely in polluted water.
 Town planning: Common breeding placess are:
cesspool, soakage pits, ill-maintained drains, septic
tanks, open ditches, burrow pits etc.
 Vectors of Lymphatic filariasis
• For
 W. bancrofti: Culex, Anopheles & Aedes
 Brugia species: Mansonia, Anopheles & Coquillettidia.

• Main vectors in India: for

 Bancroftian filariasis - C. quinquefasciatus (C.
fatigans)
 Brugian filariasis - Mansonia annulifers & M. unifomis
 Mode of Transmission & Incubation Period

 L. filariasis - transmitted by the bite of Infected

mosquito which harbors L3 larva. (L1: 1-3 hours, L2: 3-4

days, L3: 5-6 days)

 Pre-patent period: (L3 to Mf) Not known

 Clinical Incubation period: 8-16 months (invasion

of infective larvae to the development of clinical
manifestation)
 Lymphatic Filariasis
Diagnostic Methods

LF can be diagnosed clinically & by laboratory techniques.

 Laboratory Diagnosis
1. Demonstration of microfilarae in the
peripheral blood
a) Thick blood smear: 2-3 drops of free flowing blood by
finger prick method, stained with JSB-II
b) Membrane filtration method: 1-2 ml IV blood filtered
through 3µm pore size membrane filter
c) DEC provocative test (2mg/Kg): After consuming
DEC, mf enters into the peripheral blood in day time
within 30 - 45 minutes.
2. Immuno Chromatographic Test (ICT): (Antigen
detection assay) “Gold Standard” for diagnosing
Wuchereria bancrofti infection.
3. Quantitative Blood Count (QBC):
Identify the microfilariae & will help in studying the
morphology.
Though quick it is not sensitive than blood smear
examination.
4. Ultrasonography:
Can locate & visualize the movements of living adult
worms of W.b. in the scrotal lymphatics (“Filaria dance
sign” ).
5. Lymphoscintigraphy:
The structure & function of the lymphatics of the
involved limbs can be assessed by lymphoscintigraphy
after injecting radio-labelled albumin or dextran in the
web space of the toes. The structural changes can be
imaged using a Gamma camera. Lymphatic dilation &
obstruction can be directly demonstrated even in early
clinically asymptomatic stage of the disease.
6. X-ray Diagnosis:
X-ray are helpful in the diagnosis of Tropical pulmonary
eosinophilia (TPE).
Picture will show interstial thickening, diffused
nodular mottling.
7. Haematology : Increase in eosinophil count
 Lymphatic Filariasis
Clinical Manifestations
 Clinical Manifestations
2 types:
1. Lymphatic Filariasis (Presence of Adult worms)

2. Occult Filariasis (Immuno hyper responsiveness)

Clinical Spectrum

None Asymptomatic Filarial Chronic TPE

microfilaremia fever pathology
 Stages in Lymphatic Filariasis
There are 4 stages
1. Stage of Asymptomatic amicrofilaraemic:
• A proportion of population does not show mf or clinical
manifestation even though they have some degree of
exposure to infective larva similar to those who become
infected.
• Laboratory diagnostic techniques are not able to determine
whether they are infected or free.
2. Stage of Asymptomatic Microfilariaemic:
• Asymptomatic for months & years, though they have
circulating microfilariae.
• They are an important source of infection. They can be
detected by Night Blood Survey & other suitable procedures.
 Stages in Lymphatic Filariasis
3. Stage of Acute Manifestation:
• Recurrent episodes of Acute inflammation in the lymph
vessel/node of the limb & scrotum.
• Clinical manifestations are consisting of:
1. Filarial fever (ADL-DLA), 3. Lymphadinitis,
2. Lymphangitis 4. Epididimoorchitis

4. Chronic Manifestation:
 It takes 10-15 years.
 It is due to the permanent damage to the lymph vessels
caused by the adult worms (dilation of the lymph vessels)
 starts with pitting oedema which gives rise to browny
oedema leading to hardening he tissues. Eg. Hydrocele (40-
60%), Elephantiasis of Scrotum, Penis, Leg, Arm, Vulva,
Breast, Chyluria.
 2. Occult or Cryptic Filariasis
 Classical clinical manifestation mf. will be absent.
 Due to (probably) hyper responsiveness to filarial antigens
derived from mf.
 More in males.
 Patients present with:
1. Paroxysmal cough & wheezing,
2. Low grade fever,
3. Scanty sputum with occasional haemoptysis,
4. Adenopathy,
5. Increased Eosinophil.
 X-ray shows - diffused nodular mottling & interstial
thickening.
 Classification of Lymphoedema
• Lymphoedema is classified into 7 stages on
the basis of the presence & absence of the
following:
1. Oedema
2. Folds
3. Knobs
4. Mossy foot
5. Disability
Stages of Lymphoedema of the
Leg (Stage I)
• Swelling reverses at
night
• Skin folds-Absent
• Appearance of Skin-
Smooth, Normal
Stages of Lymphoedema of the
Leg (Stage II)

• Swelling not
reversible at night
• Skin folds-Absent
• Appearance of skin-
Smooth, Normal
Stages of Lymphoedema of the
Leg (Stage III)

• Swelling not
reversible at night
• Skin folds-Shallow
• Appearance of skin-
Smooth, Normal
Stages of Lymphoedema of the
Leg (Stage IV)

• Swelling not reversible

at night
• Skin folds-Shallow
• Appearance of skin
- Irregular,
• * Knobs, Nodules
Stages of Lymphoedema of the
Leg (Stage V)

• Swelling not reversible

at night
• Skin folds-Deep
• Appearance of skin –
Smooth or Irregular
Stages of Lymphoedema of the
Leg (Stage VI)

• Swelling not reversible

at night
• Skin folds-Absent,
Shallow, Deep
• Appearance of skin
*Wart-like lesions on
foot or top of the toes
Stages of Lymphoedema of the
Leg (Stage VII)
• Swelling not reversible
at night
• Skin folds-Deep
• Appearance of skin-
Irregular
• Needs help for daily
activities - Walking,
bathing, using bathrooms,
dependent on family or
health care systems
Pathology of Lymphatic Filariasis
• A complex interplay of the
pathogenic potential of the
parasite, the tissue response of
the host & external bacterial &
fungal infections.
• Most of the pathology
associated with LF is limited to
the lymphatics.
• lymphatic vessels damage:
mediated both by an immune
response to the adult worms as
well as by a direct action of the
parasite or the product released
by them.
• Lymphoedema :
inflammatory granuloma
reactions around the parasite
and subsequent obstructions of
the lymphatic vessel occurs
leading to lymphoedema.
Prevention & control of
Lymphatic Filariasis
 Prevention & Control measures
A. Management of Lymphatic Filariasis
1. Treating the infection (Chemotherapy of
Filariasis)
2. Treatment & prevention of Acute
Dermatolymphangioadenitis (ADLA) attacks
3. Treatment & prevention of Lymphoedema

B. Vector controle:
 1. Chemotherapy of Filariasis
Drugs effective against filarial parasites:
1. Diethyl Carbomazine citrate (DEC)
2. Ivermectin
3. Albendazole
4. Couramin compound

Treatment prevent chronic obstructive

disease & may be repeated every 6 months
till mf and/or symptoms disappears.
 Diethyl Carbomazine Citrate
(Hetrazan, Banocide, Notezine)
 Mode of action: DEC do not have direct action of parasite but
mediate through host immune system.
 Very effective against mf (Microfilariacidal)
 Lowers mf level even in single dose
 Effective against adult worms in 50% of patients in sensitive
cases.
 Dose: 6mg/Kg/d for 12 days
 Adverse reactions:
Mostly due to the rapid destruction of mf:
characterised by fever, nausea, myalgia, sore throat, cough,
headache.
 No effect on the treatment of ADL
 Drug of choice for Tropical Pulmonary Eosinophilia (TPE)
 Ivermectin
 Mode of action: Directly acts on mf & no action on adults.

 Microfilariacidal

 Lowers mf level even in single dose of 200µg – 400µg/Kg body

weight
 No action on TPE

 Drug of choice in Co-endemic areas of Onchocerciasis with LF.

 Adverse reactions are lesser but similar to that of DEC

 Microfilariae reappears faster than DEC

 Albendazole
 kills adult worms

 No action on microfilariae

 Dose: 400mg/twice day /2 weeks

 With combination of DEC & Ivermectin, it enhances

the action of the drugs.
 It induces severe adverse reactions in hydrocele
cases due to the death of adult worms.
 Treatment & Prevention of of Acute
Dermatolymphangioadenitis (ADLA) attacks

 ADLA is due to the infection & inflammation of the

skin & affected area due to entry of bacteria or
fungus through the entry lesions.
 The skin becomes warm, tender, painful, swollen,
red. Patient develops fever, headache, chills and
sometimes nausea & vomiting.
 Occasionally becomes septicemic.
 Treatment & Prevention of of Acute
Dermatolymphangioadenitis (ADLA) attacks
Sign & symptoms:
 First sign will be enlarged, tender & painful [Link].
 Peeling & darkening of skin is common. Repeated attacks
increase the size of the legs.
Management (symptomatic):
1. Analgesic - relieving pain,
2. Long term antibiotic therapy - oral amoxycillin/
Erythromycine or Or parentral in severe disease.
3. Care of entry lesions.
4. Cooling the Leg
5. Do not give any anti-filarial medicine
ADL
ADL
 Entry Lesions
for entry of bacteria or fungus
Entry Lesions
Ulcers
Cooling the Leg
 Treatment & Prevention of
Lymphoedema & Elephantiasis
 Early treatment with drugs may destroy the adult
worms and logically prevent the later development
of lymphoedema.

 Once lymphoedema is established there is no cure

and the “foot care programme” may offer relief and
prevent acute attacks thus preventing further
progression of the swelling.
 Lymphoedema Management
Basic Components & Benefits
Basic Components:
1. Hygiene - to eliminate the bad odour

2. Prevention & cure of entry lesions –

to prevent & heal entry lesion
to help patients self-confident

3. Exercise  to reduce the size of the

4. Elevation of foot lyphoedema
5. Use of proper footwares  to prevent disability
 to prevent economic loss
Hygiene
Drying the Leg
Prevention & Cure of Entry lesions
Exercise
Elevation of Foot
Elevation of Foot
 Use of appropriate
Foot ware

 
 Surgical Treatment
Hydrocele: Excision

Scrotal Elip: Surgical removal of Skin & Tissue, preserving

penis and testicles.

Lymphoedema (Elephantiasis):

1. Excision of redundant tissue, Excision of subcutaneous

& fatty tissues,

2. Postral drainage & physiotherapy

 B. Vector Control
A. Anti larval measures:
1. Chemical control
a. Mosquito larvicidal oil
b. Pyrosene oil
c. Organo phosphorous compounds such as
Temephos, Fenthion,
2. Removal of pistia plants
3. Minor environmental measures
B. Anti-adult measurees
C. Personal prophylaxis
 Lymphatic Filariasis Control Programme
The current strategy based on:
1. Interruption of transmission - achieved through:
a. Chemotherapy
b. Vector control - integrated vector control
programme

2. Control of Morbidity:
 Low endemic areas - Case detection & treatment
 High endemic areas:
- Mass chemotherapy.
- DEC medicated salt over a long period of time (1-2
gm /Kg of Salt).
 Assesment of Filariasis Control Programme
1. Clinical parameters:
 Incidence of acute infections (adeno-lymphangitis, epididymoorchitis)
 Prevention of chronic menifestations (elephantiasis, hydrocele,
lymphoedema)
2. Parasitological parameters:
 Microfilari rate: % of persons showing Mf in their peripheral blood
([Link])
 Filaria endemicity rate: % of persons examined showing Mf. In their
blood, or disease or both.
 Microfilaria density: No. of Mf. /unit volume (20cu. mm) of blood from
individual person – indicate intensity of infection.
 Average infestation rate: Average no. of Mf./positive slide – indicate
prevalence of Mf. In the population.
 Assesment of Filariasis Control Programme

3. Entomological parameters:
 Vector density / 10 man-hour catch
 % of mosquitoes positive for all stages of development
 % of mosquitoes positive for infective (stage 3) larvae.
 Annual breading rate – for assesment of transmission
 Type of larval breading places
There are 3 main reasons why filariasis
never causes explosive epidemics

1. The microfilariae does not multiply in the

vector

2. Infective larvae do not multiply in man

3. Life cycle of the parasite is relatively long

(>15 )
Factors Favorable for Elimination of LF -
WHO

1. Biological factors

2. Available tools

3. Operational feasibility
 Biological Factors

 Man is the only reservoir host

 Prolonged exposure with multiple mosquito bites is

required to establish infection in a new host
 Vectors are not efficient biological transmitters
hence feasible to interrupt transmission once the
parasite load in the individual is reduced.
 Available Tools

 Low cost, safe & very effective drugs for prevention of

infection & treatment of morbid cases

 Diagnostic kits & monitoring tools to detect infection

in man & mosquito

 Cost-effective control technology has been developed

for elimination of LF in endemic countries
 Operational Feasibility
1. Some countries achieved time-bound successful elimination of
LF
2. Community cooperation has been found to be very encouraging.
3. The infrastructure for implementation of the programme is
available in endemic countries
4. The recommended interventions strategy is simple, safe &
effective, and is well accepted
5. Reasonable cost of interventions, - MDA drugs - interventions
strategy is simple, safe & effective, and is well accepted
6. Clear guidelines are available for all aspects of programme
implementation.
 Mass Drug Administration (MDA)

• To interrupt the transmission of lymphatic filariasis,

WHO recommends MDA* with diethylcarbamazine
(DEC) & albendazole to the entire endemic
population.

• A single dose is administered annually for 4-6

years.

* Excluded are children below 2 years & pregnant women.

 Issues/Challenges/Constraints

 Availability of DEC for nationwide MDA

 MDA coverage of 68%

 Prevention & alleviation of disability

 Commitment of all stakeholders

Thank you