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Lymphatic Filariasis
B.Ganesh
Regional Filaria Training & Research Centre
National Institute of Communicable Diseases
Kozhikode.
Lymphatic Filariasis
Infection with 3 closely related Nematodes
Wuchereria bancrofti
Brugia malayi
Brugia timori
* Transmitted by the bite of infected mosquito
responsible for considerable sufferings/deformity
and disability
* All the parasites have similar life cycle in man
* Adults seen in Lymphatic vessels
* Offsprings seen in peripheral blood during night
Disease Manifestation
Disease manifestation range from
 None
 Acute-Filarial fever
 Chronic-Lymphangitis, Lymphadenitis,
Elephantiasis of genitals/legs/arms
 Tropical Pulmonary Eosinophilia (TPE)
 Filarial arthritis
 Epididimoorchitis
 Chyluria, etc.
Distribution
Prevalent world wide in the Tropics
and Sub-tropical regions of
Africa
Asia
Western Pacific
Parts of Central & South America
Lymphatic Filariasis Endemic Countries & Territories
Endemic Countries
Global Distribution Map
Global Scenario
Population
at risk : 1.2 Billion
No. of countries : > 80
Mf carriers : 76 Million
Diseased : 44 Million
Hydrocele : 27 Million
Lymphoedema : 16 Million
TPE : 1 Million
National Scenario
Total Population : 110 C
Population at risk : 45.4 C
(in 16 States & 5 UT’s)
Total infected : 51.7 M
(Wb - 99.4 % and Bm - 0.6 %)
No. of diseased : 22.5 M
Mf carriers : 29.2 M
Hydrocele : 12.9 M
Agent Factors
S.no Parasite Mosquito Disease
1. W.bancrofti Culex LF
2. B.malayi Mansonia LF
3. B.timori
Anopheles/
Mansonia
LF
4. O.volvulus
Simulium
flies
River
Blindness
5. L.loa Chrysops flies S/c swellings
6. M.perstans Culicoides Serous cavity
7. M.streptocerca Culicoides ”
8. M.ozzardi Culicoides ”
Host Factors
 Man – Natural Host
 Age – All age (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 and 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.
Mode of Transmission &
Incubation Period
 Lymphatic Filariasis is transmitted by the
bite of Infected mosquito which harbours 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
Lymphatic Filariasis
Diagnostic Methods
Diagnosis of Lymphatic Filariasis
 Lymphatic Filariasis can be diagnosed
clinically and through laboratory techniques.
 Clinically, diagnosis can be made on
circumstantial evidence with support from
antibody or other laboratory assays as most
of the LF patients are amicrofilaraemic and
in the absence of serological tests which is
not specific other than CFA (ICT). In TPE,
serum antibodies like IgG & IgE will be
extremely high and the presence of IgG4
antibodies indicate active infection.
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
intravenous 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 can be done by
Card test and through ELISA. Circulating
Filarial Antigen detection is regarded as
“Gold Standard” for diagnosing
Wuchereria bancrofti infection.
Specificity is near complete, sensitivity is
greater than all other parasite detection
assays, will detect antigen in
amicrofilaraemic as well as with clinical
manifestations like lymphoedema,
elephantiasis.
3. Quantitative Blood Count (QBC):
QBC will identify the microfilariae and will help
in studying the morphology. Though quick it is
not sensitive than blood smear examination.
4. Ultrasonography:
Ultrasonography using a 7.5 MHz or 10 MHz
probe can locate and visualize the movements of
living adult worms of W.b. in the scrotal
lymphatics of asymptomatic males with
microfilaraemia. The constant thrashing
movements described as “Filaria dance sign” can
be visualized.
5. Lymphoscintigraphy:
The structure and 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.
Picture will show interstial thickening, diffused
nodular mottling.
7. Haematology : Increase in eosinophil count
Lymphatic Filariasis
Clinical Manifestations
Clinical Manifestations
 Manifestations are 2 types
1. Lymphatic Filariasis (Presence of
Adult worms)
2. Occult Filariasis (Immuno hyper
responsiveness)
Clinical Spectrum
None Asymptomatic
microfilaremia
Filarial
fever
Chronic
pathology
TPE
Stages in Lymphatic Filariasis
 There are 4 stages :
1. Asymptomatic amicrofilariaemic
stage
2. Asymptomatic microfilariaemic
stage
3. Stage of Acute manifestation
4. Stage of Obstructive (Chronic)
lesions
Stage of Asymptomatic
amicrofilaraemic
In endemic areas, 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.
Stage of Asymptomatic
Microfilariaemic
Considerable proportions are
asymptomatic for months and years,
though they have circulating
microfilariae. They are an important
source of infection. They can be
detected by Night Blood Survey and
other suitable procedures.
Stage of Acute Manifestation
 During initial months and years, there are
recurrent episodes of Acute inflammation
in the lymph vessel/node of the limb &
scrotum that are related to bacterial &
fungal super infections of the tissue that are
already compromised lymphatic function.
 Clinical manifestations are consisting of:
1. Filarial fever (ADL-DLA)
2. Lymphangitis
3. Lymphadinitis
4. Epididimo orchitis
Chronic Manifestation
Chronic (Obstructive) lesions takes 10-15 years.
This is due to the permanent damage to the lymph
vessels caused by the adult worms, the
pathological changes causing dilation of the
lymph vessels due to recurrent inflammatory
episodes leading to endothelial proliferation and
inflammatory granulomnatous reaction around
the parasite. Initially, it starts with pitting oedema
which gives rise to browny oedema leading to
hardening he tissues. Still late, hyper
pigmentation, caratosis, wart like lesions are
developed. Eg. Hydrocele (40-60%),
Elephantiasis of Scrotum, Penis, Leg, Arm,
Vulva, Breast, Chyluria.
2. Occult Filariasis (TPE)
 Occult or Cryptic filariasis, in classical
clinical manifestation mf will be absent.
Occult filariasis is believed to be the result
of hyper responsiveness to filarial antigens
derived from mf. Seen more in males.
Patients present with paroxysmal cough and
wheezing, low grade fever, scandy sputum
with occasional haemoptysis, adenopathy
and increased eosinophilia. X-ray shows
diffused nodular mottling and interstial
thickening.
Hydrocele
Scrotum
Penis
Leg
Arm
Breast
Chyluria & Haematuria
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
 The pathology associated
with lymphatic filariasis
results from a complex
interplay of the
pathogenic potential of
the parasite, the tissue
response of the host and
external bacterial and
fungal infections. Most of
the pathology associated
with LF is limited to the
lymphatics.
 The damage to the lymphatic
vessels is 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. In the absence of
inflammation, marked lymphatic
dilation with lymphoedema is seen
in experimental animals with
immune deficiency and when
immuno competent cells are
induced, it results inflammatory
granuloma reactions around the
parasite and subsequent
obstructions of the lymphatic vessel
occurs leading to lymphoedema.
Lymphatic Filariasis
Management
Twin Pillars of Lymphatic Filariasis
Elimination
Interrupt transmission
Control Morbidity (relief of suffering)
# Community-level care of those with
disease
• Lymphoedema
• Acute inflammatory attacks
• Hydrocele repair
Management of Lymphatic Filariasis
1. Treating the infection
2. Treatment and prevention of Acute
ADL attacks
3. Treatment and prevention of
Lymphoedema
Treating the infection
Remarkable advances in the treatment
of LF have recently been achieved
focusing not on individual but on
community with infection, with the
goal of reducing mf in the community,
to levels below which successful
transmission will not occur.
Chemotherapy of Filariasis
Drugs effective against filarial parasites
1. Diethyl Carbomazine citrate (DEC)
2. Ivermectin
3. Albendazole
4. Couramin compound
Treatment of microfilaraemic patients
may prevent chronic obstructive disease
and 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/12 days
 Recent dosage: 6mg/Kg single dose
 Adverse reactions are mostly due to the rapid
destruction of mf which is characterised by fever,
nausea, myalgia, sore throat, cough, headache.
 No effect on the treatment of ADL
 Drug of choice in the treatment of TPE.
Ivermectin
 Mode of action: Directly acts on mf and no action
on adults.
 Very effective against mf (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
 This antihelmenthic 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 and Prevention of ADL
The most distressing aspect of LF is the
acute attacks of ADL, which results in
considerable economic loss and
deterioration of quality of life. Prompt
treatment and prevention of ADL are of
paramount importance. ADL may be seen
both in early & late stages of the disease. It
is due to the infection & inflammation of
the skin and 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 and
vomiting. Occasionally becomes
septicemic.
 First sign will be enlarged,
tender and painful L.nodes. SS
of inflammation appears later
lasting for 4-5days. Peeling &
darkening of skin is common.
Repeated attacks increase the
size of the legs. Management
includes symptomatic treatment
like relieving pain, care of
entry lesions etc. In patients
with late stages of oedema,
long term antibiotic therapy
using oral Penicillin or long
acting parentral Benzathil
Penicillin are used to prevent
ADL.
ADL
Cooling the Leg
ADL
ADL
Entry Lesions
Entry Lesions
Ulcers
Surgical Treatment
 Hydrocele: Excision
 Scrotal Elip: Surgical removal of Skin &
Tissue, preserving penis and testicles.
 Lymphoedema (Elephantiasis): Excision of
redundant tissue, Excision of subcutaneous
and fatty tissues,
 postral drainage and physiotherapy
 Treatment and Prevention of
Lymphoedema and 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 helps
 to eliminate the bad odour
 to prevent & heal entry
lesion
 to help patients self-
confident
 to reduce the size of the
lyphoedema
 to prevent disability
 to prevent economic loss
Lymphoedema Management
Basic Components and Benefits
Basic Components
1. Hygiene
2. Prevention &
cure of entry
lesions
3. Exercise
4. Elevation of foot
5. Use of proper
footwares
Hygiene
Drying the Leg
Prevention & Cure of Entry lesions
Exercise
Elevation of Foot
Elevation of Foot
Use of appropriate
Foot ware


Lymphatic Filariasis
Control
Lymphatic Filariasis Control Programme
The current strategy of filariasis control
(Elimination) is based on:
1. Interruption of transmission
2. Control of Morbidity
Interruption of the transmission can be achieved through:
a. Chemotherapy
b. Vector control
An integrated programme is in place for the
control of lymphatic filariasis. Earlier, vector
control was the main method of control. There
are three 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 )
 Case detection and treatment in low
endemic areas are suitable for preventing
transmission and controlling the disease.
 In high endemic areas, Mass chemotherapy
is the approach.
 DEC medicated salt is also a form of Mass
treatment using low dose of drug over a
long period of time (1-2 gm /Kg of Salt).
Vector Control
Vector control involves anti larval measures,
anti adult measures, personal prophylaxis. An
integrated method using all the vector control
measures alone will bring about sustained vector
control.
I. 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
Vector Control
II. Anti adult measures:
Anti adult measures as indoor residual spay
using DDT, HCH and Dieldrin. Pyrethrum
as a space spray is also followed.
III. Personal Prophylaxis:
Reduction of man mosquito contact by
using mosquito nets, screening of houses,
etc.
Morbidity Management
Control Morbidity (relief of
suffering)
# Community-level care of those
with disease
• Lymphoedema
• Acute inflammatory attacks
• Hydrocele repair
Thank you

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31201-31211.ppt

  • 1. Lymphatic Filariasis B.Ganesh Regional Filaria Training & Research Centre National Institute of Communicable Diseases Kozhikode.
  • 2. Lymphatic Filariasis Infection with 3 closely related Nematodes Wuchereria bancrofti Brugia malayi Brugia timori * Transmitted by the bite of infected mosquito responsible for considerable sufferings/deformity and disability * All the parasites have similar life cycle in man * Adults seen in Lymphatic vessels * Offsprings seen in peripheral blood during night
  • 3. Disease Manifestation Disease manifestation range from  None  Acute-Filarial fever  Chronic-Lymphangitis, Lymphadenitis, Elephantiasis of genitals/legs/arms  Tropical Pulmonary Eosinophilia (TPE)  Filarial arthritis  Epididimoorchitis  Chyluria, etc.
  • 4. Distribution Prevalent world wide in the Tropics and Sub-tropical regions of Africa Asia Western Pacific Parts of Central & South America
  • 5. Lymphatic Filariasis Endemic Countries & Territories Endemic Countries Global Distribution Map
  • 6. Global Scenario Population at risk : 1.2 Billion No. of countries : > 80 Mf carriers : 76 Million Diseased : 44 Million Hydrocele : 27 Million Lymphoedema : 16 Million TPE : 1 Million
  • 7. National Scenario Total Population : 110 C Population at risk : 45.4 C (in 16 States & 5 UT’s) Total infected : 51.7 M (Wb - 99.4 % and Bm - 0.6 %) No. of diseased : 22.5 M Mf carriers : 29.2 M Hydrocele : 12.9 M
  • 8. Agent Factors S.no Parasite Mosquito Disease 1. W.bancrofti Culex LF 2. B.malayi Mansonia LF 3. B.timori Anopheles/ Mansonia LF 4. O.volvulus Simulium flies River Blindness 5. L.loa Chrysops flies S/c swellings 6. M.perstans Culicoides Serous cavity 7. M.streptocerca Culicoides ” 8. M.ozzardi Culicoides ”
  • 9. Host Factors  Man – Natural Host  Age – All age (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)
  • 10. Social & Environmental Factors  Associated with Urbanization, Poverty, Industrialization, Illiteracy and 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.
  • 11. Mode of Transmission & Incubation Period  Lymphatic Filariasis is transmitted by the bite of Infected mosquito which harbours 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
  • 13. Diagnosis of Lymphatic Filariasis  Lymphatic Filariasis can be diagnosed clinically and through laboratory techniques.  Clinically, diagnosis can be made on circumstantial evidence with support from antibody or other laboratory assays as most of the LF patients are amicrofilaraemic and in the absence of serological tests which is not specific other than CFA (ICT). In TPE, serum antibodies like IgG & IgE will be extremely high and the presence of IgG4 antibodies indicate active infection.
  • 14. 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 intravenous 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.
  • 15. 2. Immuno Chromatographic Test (ICT): Antigen detection assay can be done by Card test and through ELISA. Circulating Filarial Antigen detection is regarded as “Gold Standard” for diagnosing Wuchereria bancrofti infection. Specificity is near complete, sensitivity is greater than all other parasite detection assays, will detect antigen in amicrofilaraemic as well as with clinical manifestations like lymphoedema, elephantiasis.
  • 16. 3. Quantitative Blood Count (QBC): QBC will identify the microfilariae and will help in studying the morphology. Though quick it is not sensitive than blood smear examination. 4. Ultrasonography: Ultrasonography using a 7.5 MHz or 10 MHz probe can locate and visualize the movements of living adult worms of W.b. in the scrotal lymphatics of asymptomatic males with microfilaraemia. The constant thrashing movements described as “Filaria dance sign” can be visualized.
  • 17. 5. Lymphoscintigraphy: The structure and 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. Picture will show interstial thickening, diffused nodular mottling. 7. Haematology : Increase in eosinophil count
  • 19. Clinical Manifestations  Manifestations are 2 types 1. Lymphatic Filariasis (Presence of Adult worms) 2. Occult Filariasis (Immuno hyper responsiveness) Clinical Spectrum None Asymptomatic microfilaremia Filarial fever Chronic pathology TPE
  • 20. Stages in Lymphatic Filariasis  There are 4 stages : 1. Asymptomatic amicrofilariaemic stage 2. Asymptomatic microfilariaemic stage 3. Stage of Acute manifestation 4. Stage of Obstructive (Chronic) lesions
  • 21. Stage of Asymptomatic amicrofilaraemic In endemic areas, 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.
  • 22. Stage of Asymptomatic Microfilariaemic Considerable proportions are asymptomatic for months and years, though they have circulating microfilariae. They are an important source of infection. They can be detected by Night Blood Survey and other suitable procedures.
  • 23. Stage of Acute Manifestation  During initial months and years, there are recurrent episodes of Acute inflammation in the lymph vessel/node of the limb & scrotum that are related to bacterial & fungal super infections of the tissue that are already compromised lymphatic function.  Clinical manifestations are consisting of: 1. Filarial fever (ADL-DLA) 2. Lymphangitis 3. Lymphadinitis 4. Epididimo orchitis
  • 24. Chronic Manifestation Chronic (Obstructive) lesions takes 10-15 years. This is due to the permanent damage to the lymph vessels caused by the adult worms, the pathological changes causing dilation of the lymph vessels due to recurrent inflammatory episodes leading to endothelial proliferation and inflammatory granulomnatous reaction around the parasite. Initially, it starts with pitting oedema which gives rise to browny oedema leading to hardening he tissues. Still late, hyper pigmentation, caratosis, wart like lesions are developed. Eg. Hydrocele (40-60%), Elephantiasis of Scrotum, Penis, Leg, Arm, Vulva, Breast, Chyluria.
  • 25. 2. Occult Filariasis (TPE)  Occult or Cryptic filariasis, in classical clinical manifestation mf will be absent. Occult filariasis is believed to be the result of hyper responsiveness to filarial antigens derived from mf. Seen more in males. Patients present with paroxysmal cough and wheezing, low grade fever, scandy sputum with occasional haemoptysis, adenopathy and increased eosinophilia. X-ray shows diffused nodular mottling and interstial thickening.
  • 28. Penis
  • 29. Leg
  • 30. Arm
  • 33. 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
  • 34. Stages of Lymphoedema of the Leg (Stage I)  Swelling reverses at night  Skin folds-Absent  Appearance of Skin- Smooth, Normal
  • 35. Stages of Lymphoedema of the Leg (Stage II)  Swelling not reversible at night  Skin folds-Absent  Appearance of skin- Smooth, Normal
  • 36. Stages of Lymphoedema of the Leg (Stage III)  Swelling not reversible at night  Skin folds-Shallow  Appearance of skin- Smooth, Normal
  • 37. Stages of Lymphoedema of the Leg (Stage IV)  Swelling not reversible at night  Skin folds-Shallow  Appearance of skin - Irregular,  * Knobs, Nodules
  • 38. Stages of Lymphoedema of the Leg (Stage V)  Swelling not reversible at night  Skin folds-Deep  Appearance of skin – Smooth or Irregular
  • 39. 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
  • 40. 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
  • 41. Pathology of Lymphatic Filariasis  The pathology associated with lymphatic filariasis results from a complex interplay of the pathogenic potential of the parasite, the tissue response of the host and external bacterial and fungal infections. Most of the pathology associated with LF is limited to the lymphatics.
  • 42.  The damage to the lymphatic vessels is 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. In the absence of inflammation, marked lymphatic dilation with lymphoedema is seen in experimental animals with immune deficiency and when immuno competent cells are induced, it results inflammatory granuloma reactions around the parasite and subsequent obstructions of the lymphatic vessel occurs leading to lymphoedema.
  • 44. Twin Pillars of Lymphatic Filariasis Elimination Interrupt transmission Control Morbidity (relief of suffering) # Community-level care of those with disease • Lymphoedema • Acute inflammatory attacks • Hydrocele repair
  • 45. Management of Lymphatic Filariasis 1. Treating the infection 2. Treatment and prevention of Acute ADL attacks 3. Treatment and prevention of Lymphoedema
  • 46. Treating the infection Remarkable advances in the treatment of LF have recently been achieved focusing not on individual but on community with infection, with the goal of reducing mf in the community, to levels below which successful transmission will not occur.
  • 47. Chemotherapy of Filariasis Drugs effective against filarial parasites 1. Diethyl Carbomazine citrate (DEC) 2. Ivermectin 3. Albendazole 4. Couramin compound Treatment of microfilaraemic patients may prevent chronic obstructive disease and may be repeated every 6 months till mf and/or symptoms disappears.
  • 48. 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/12 days  Recent dosage: 6mg/Kg single dose  Adverse reactions are mostly due to the rapid destruction of mf which is characterised by fever, nausea, myalgia, sore throat, cough, headache.  No effect on the treatment of ADL  Drug of choice in the treatment of TPE.
  • 49. Ivermectin  Mode of action: Directly acts on mf and no action on adults.  Very effective against mf (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
  • 50. Albendazole  This antihelmenthic 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.
  • 51.  Treatment and Prevention of ADL The most distressing aspect of LF is the acute attacks of ADL, which results in considerable economic loss and deterioration of quality of life. Prompt treatment and prevention of ADL are of paramount importance. ADL may be seen both in early & late stages of the disease. It is due to the infection & inflammation of the skin and 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 and vomiting. Occasionally becomes septicemic.
  • 52.  First sign will be enlarged, tender and painful L.nodes. SS of inflammation appears later lasting for 4-5days. Peeling & darkening of skin is common. Repeated attacks increase the size of the legs. Management includes symptomatic treatment like relieving pain, care of entry lesions etc. In patients with late stages of oedema, long term antibiotic therapy using oral Penicillin or long acting parentral Benzathil Penicillin are used to prevent ADL.
  • 53. ADL
  • 55. ADL
  • 56. ADL
  • 60. Surgical Treatment  Hydrocele: Excision  Scrotal Elip: Surgical removal of Skin & Tissue, preserving penis and testicles.  Lymphoedema (Elephantiasis): Excision of redundant tissue, Excision of subcutaneous and fatty tissues,  postral drainage and physiotherapy
  • 61.  Treatment and Prevention of Lymphoedema and 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.
  • 62. Lymphoedema management helps  to eliminate the bad odour  to prevent & heal entry lesion  to help patients self- confident  to reduce the size of the lyphoedema  to prevent disability  to prevent economic loss Lymphoedema Management Basic Components and Benefits Basic Components 1. Hygiene 2. Prevention & cure of entry lesions 3. Exercise 4. Elevation of foot 5. Use of proper footwares
  • 65. Prevention & Cure of Entry lesions
  • 69. Use of appropriate Foot ware  
  • 71. Lymphatic Filariasis Control Programme The current strategy of filariasis control (Elimination) is based on: 1. Interruption of transmission 2. Control of Morbidity Interruption of the transmission can be achieved through: a. Chemotherapy b. Vector control An integrated programme is in place for the control of lymphatic filariasis. Earlier, vector control was the main method of control. There are three 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 )
  • 72.  Case detection and treatment in low endemic areas are suitable for preventing transmission and controlling the disease.  In high endemic areas, Mass chemotherapy is the approach.  DEC medicated salt is also a form of Mass treatment using low dose of drug over a long period of time (1-2 gm /Kg of Salt).
  • 73. Vector Control Vector control involves anti larval measures, anti adult measures, personal prophylaxis. An integrated method using all the vector control measures alone will bring about sustained vector control. I. 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
  • 74. Vector Control II. Anti adult measures: Anti adult measures as indoor residual spay using DDT, HCH and Dieldrin. Pyrethrum as a space spray is also followed. III. Personal Prophylaxis: Reduction of man mosquito contact by using mosquito nets, screening of houses, etc.
  • 75. Morbidity Management Control Morbidity (relief of suffering) # Community-level care of those with disease • Lymphoedema • Acute inflammatory attacks • Hydrocele repair