Synthesis and Reporting (Step 7)

1. How is pathophysiologi and pathogenesis of filariasis?

The filarial life cycle, like that of all nematodes, consists of 5 developmental
(larval) stages in a vertebral host and an arthropod intermediate host and
vector. Adult female worms produce thousands of first-stage larvae, or
microfilariae, which are ingested by a feeding insect vector. Some
microfilariae have a unique daily circadian periodicity in the peripheral
circulation. The arthropod vectors (mosquitoes and flies) also have a circadian
rhythm in which they obtain blood meals. The highest concentration of
microfilariae usually occurs when the local vector is feeding most actively. 
Microfilariae undergo two developmental changes in the insect. Third-stage
larvae then are inoculated back into the vertebral host during the act of feeding
for the final two stages of development. These larvae travel through the dermis
and enter regional lymphatic vessels. During the next 9 months, the larvae
develop into mature worms (20-100 mm in length). An average parasite can
survive for about 5 years.

The pre-patent period is defined as the interval between a vector bite and the
appearance of microfilariae in blood, with an estimated duration of about 12
months.

The following factors affect the pathogenesis of filariasis:

 The quantity of accumulating adult worm antigen in the lymphatics 
 The duration and level of exposure to infective insect bites 
 The number of secondary bacterial and fungal infections 
 The degree of host immune response 

Filarial infection generates significant inflammatory immune responses that

participate in the development of symptomatic lymphatic obstruction.
Increased levels of immunoglobulin E (IgE) and immunoglobulin G4 (IgG4)
secondary to antigenic (from dead worms) stimulation of Th2-type immune
response have been demonstrated. 
 Studies indicate that there is a familial tendency to lymphatic obstruction. This
provides support for the hypothesis that host genes influence lymphedema
susceptibility.  Studies also suggest that microfilaremia may be increased in
individuals with low levels of mannose-binding lectin, suggesting a genetic
predisposition. Furthermore, a propensity to develop chronic disease has been
demonstrated in patients with polymorphisms of endothelin-1 and tumor
necrosis factor receptor II. 

2. What are the types of filariasis?

Type of filariasis Clinical symptoms Diagnosis Treatment
Filariasis Bancrofti  Acute manifestation  Identification of DEC 6mg/kgBB/hari
Aetiology: Limfadenitis often micofilariaes in for 12 days, divided
Wuchereria bancrofti accompanied by local blood smear by into 3 doses, take
(tropic) pain, local tenderness, microscopic after meal
fever, headache, examination
Habitat: lymphatic vomiting, nausea  Eosinophilia
systems,blood  Chronic manifestation  Leukositosis
Hydrocele, chiluria,
Epidemiology : lymphedema,
filariasis bancrofti (it elephantiasis
can be found both in
urban and rural but
mstly can be found in
rural, risk group are
young adults
Filariasis Malayi and  The amount of  Identification of DEC 5mg/kgbb/hari
Timori microfilarias are lower microfilariaes in for 10 days
Aetiology: Brugia than filariasis bancrofti blood smear by
malayi (south east  Typical symptoms: microscopic
asia) and Brugia superficial examination
Timori (lesser sunda) lymphadenopathy  Eosinophilia up
 Do not affect urinary to 70%
Habitat: lymphatic tract and breasts  The difference
systems,blood between timori
 and malayi are in
Epidemiology: the shape of the
filariasis malayi (can microfilariaes
be found in rural only  In timori
due to its vector 1. The shape of the
especially in sumatra length of the head
untul maluku) is 3 times bigger
filariasis timori (can than the width
be found in rural only 2. The tails have 2
too but only in east additional core
indonesia (NTT) and 3. The length of the
timor timor microfilariae is
longer

3. Prevention programs for filariasis

Global Programme to Eliminate Lymphatic Filariasis by WHO
In 1997, following advances in diagnosis and treatment of the disease, WHO
classified lymphatic filariasis, along with five other infectious diseases, as
eradicable or potentially eradicable. The same year, the World Health
Assembly adopted Resolution WHA 50.29, which called on Member States to
initiate steps to eliminate lymphatic filariasis as a public health problem. In
response to this call, WHO launched the Global Programme to Eliminate
Lymphatic Filariasis (GPELF) in 2000.

The elimination strategy has two components:

1. to stop the spread of infection (interrupting transmission)
2. to alleviate the suffering of affected populations (controlling morbidity).

In order to interrupt transmission, districts in which lymphatic filariasis is

endemic must be mapped and community-wide mass treatment programmes
implemented to treat the entire at-risk population. Most of these programmes
are based on once-yearly administration of single doses of two drugs given
together. The following recommended drug regimens need to be administered
once a year for at least 5 years, with a coverage of at least 65% of the total at-
risk population: 
1. Stop the spread of infection – MDA
In order to interrupt transmission, districts in which lymphatic filariasis is
endemic must be mapped and a strategy of preventive chemotherapy called
mass drug administration (MDA) implemented to treat the entire at-risk
population. The following drug regimens are recommended for use in
annual MDA for at least 5 years with a coverage of at least 65% of the total
at-risk population: 
 6 mg/kg of body weight diethylcarbamazine citrate (DEC) + 400 mg
albendazole
 150 µg/kg of body weight ivermectin + 400 mg albendazole (in areas
that are also endemic for onchocerciasis)
 400 mg albendazole preferably twice per year (in areas that are also
endemic for Loa loa). 
An alternative and equally effective community-wide regimen in endemic
regions is the use of common table salt or cooking salt fortified with DEC.
DEC fortified salt has been used in only a few settings. 

2. Alleviate suffering – MMDP

Successful MDA will prevent new infections and no new cases of clinical
disease. To achieve the second aim of GPELF, a core strategy of morbidity
management and disability prevention (MMDP) is needed. Suffering
caused by the disease can be alleviated through a minimum recommended
package of care to manage lymphedema and hydrocele. These services
should be available within primary health care systems in all areas of
known patients.