Filariasis

Filarial infections have been broadly grouped into 3 categories of disease based on the
location of disease: lymphatic, cutaneous, and body cavity. Morbidity is almost entirely
attributable to those species that cause lymphatic disease, and to a lesser extent cutaneous
disease. Body cavity infection, caused by Mansonella ozzardi, is usually asymptomatic and is
not discussed further.

EPIDEMIOLOGY
Lymphatic filariasis is caused mainly by W. bancrofti (bancroftian filariasis), which causes
90% of disease, and B. malayi (Malayan filariasis), which accounts for only 10% of all
cases.28 Infection caused by Brugia timori is rare. Lymphatic filariasis is widely distributed in
both urban and rural areas of tropical and subtropical areas, with the largest number of
infections occurring in India, South Asia, East Asia, and the Pacific Islands, and sub-Saharan
Africa. W. bancrofti is also endemic in northern parts of South America (Guyana, Surinam,
and some coastal regions of Brazil). In developed countries, infections are seen primarily in
immigrants and persons with prolonged visits to endemic areas. Infection is transmitted to
humans by mosquitoes, and can be prevented by avoidance of mosquito bites. The
incubation period is usually 5 to 18 months, during which time microfilariae migrate to the
lymphatic system, mature into adults, mate, and release microfilariae (larvae); occasionally
symptoms develop within 3 months of exposure. Lymphatic filariasis is first acquired in
childhood, often with as many as one-third of children in endemic areas infected before the
age of 5 years.29 The characteristic symptoms typically occur years after infection and the
prevalence of clinical disease increases after age 20 years in endemic areas. Adult worms
live an average of 10 to 15 years, and microfilariae probably 6 to 12 months.

Cutaneous filariasis is caused by Loa loa, M. perstans, M. streptocerca, and O. volvulus.

Loiasis is endemic in rural areas of Central and West Africa, affecting an estimated 3 to 13
million residents. Loa loa is transmitted by the day-biting Chrysops fly; infection can be
prevented by avoiding bites from Chrysops in endemic
areas, diethylcarbamazinechemoprophylaxis, and treatment of infected humans to reduce
the source of parasites. Symptoms usually begin an average of 24 months after exposure,
but can begin as early as 4 months or as late as a decade or more after infection. The adult
worm can live longer than 20 years in the human host.

Infection caused by both M. perstans and M. streptocerca is often asymptomatic. M.

perstans is endemic in sub-Saharan Africa, as well as parts of Central and South America,
where it is transmitted by Culicoides midges. Like lymphatic filariasis, infection during
childhood is common, and reinfection may occur.30 In highly endemic areas, the prevalence
of infection may be as high as 80%. M. streptocerca is endemic in forested areas of West
and Central Africa. Transmission is also by infected midges.

Onchocercosis (river blindness; erysipelas de la costa in Mexico and Guatemala; sowda in

Arabic speaking areas; craw-craw in West Africa) is concentrated in rural areas of equatorial
Africa and the Arabian peninsula, and in Latin America. Onchocerciasis is transmitted by
black-flies of the genus Simulium. In the human, infective larvae mature to adult worms that
are encapsulated in fibrous tissue and reside in nodules in the subcutaneous tissue and
deep fascia. The incubation period is usually 1 to 2 years with a range of months to several
years, although microfilariae may first appear 3 to 15 months after exposure; symptoms
may precede microfilaremia but often develop only after months or years of infection.
Microfilariae can survive in humans for up to 2 to 3 years, and adult worms for 10 to 15
years. The primary means of preventing onchocerciasis are through vector control and mass
treatment with ivermectin of the population in endemic areas.

CLINICAL FEATURES
Lymphatic Filariasis (Brugia malayi, Brugia timori; Wuchereria bancrofti)
Clinical manifestations may be acute, chronic, or recurrent. Initial infection may be
subclinical but may also cause recurrent lymphangitis with characteristic retrograde
progression (beginning in the affected lymph node and moving distally), lymphadenitis,
orchitis, epididymitis, or, occasionally, fever. Lymphangitis typically recurs 6 to 10 times per
year, with each episode lasting 3 to 7 days. The affected body part clinically appears normal
between early episodes, although during the resolution of the acute phase of W.
bancroftifilariasis, there may be extensive exfoliation of the skin of the affected limb.
Intermittent fevers and adenolymphangitis can recur for the lifetime of the adult worm.
Travelers (>1 month) to endemic areas less frequently acquire infection but may present
with more intense inflammatory reactions to filarial parasites. The findings may include
lymphangitis, lymphadenitis, groin pain from the associated lymphatic inflammation,
urticaria, and peripheral eosinophilia.

Chronic disease with sequelae of lymphatic obstruction (lymphedema, elephantiasis,

hydrocele, and chyluria) becomes evident 10 to 15 years after infection. The skin over the
involved area can become hypertrophic, verrucous, and fibrotic with redundant skin folds
(Fig. 177-9). Fissures, ulceration, secondary bacterial infection, and gangrene may occur. The
lower extremity, scrotum, and penis are most commonly affected, and less frequently the
upper extremity, breast, and vulva are involved. Although antiparasitic treatment does not
reverse the late findings of scarring and lymphatic obstruction, a 6-week course of
doxycycline can reduce mild-to-moderate lymphedema independent of active filarial
infection by reducing vascular endothelial growth factor.31

FIGURE 177-9
Lymphatic filariasis. (Used with permission from Jay S. Keystone, MD, FRCPC.)
 View Full Size|Favorite Figure|Download Slide (.ppt)
The differential diagnosis for lymphatic filariasis includes acute infection that can resemble
bacterial lymphangitis and other causes of nodular lymphangitis (eg, sporotrichosis,
leishmaniasis). Other causes of lymphedema and elephantiasis must also be considered
during evaluation of chronic disease.

Cutaneous Filariasis
LOAISIS (LOA LOA)
The characteristic finding of loiasis is the Calabar swelling (Fig. 177-10), a localized area of
angioedema caused by migration of adult worms through subcutaneous tissues. Calabar
swellings usually begin years after infection, typically around joints of the upper extremities,
generally last 2 to 4 days, and may be associated with pruritus or pain. They range in size
from 5 to 20 cm in diameter and may recur in different locations. Fatigue, myalgias,
arthralgias, and fever are rare. Adult worms may be seen moving across the bulbar
conjunctiva of the eye (see Fig. 177-5) and eyelid. Pruritus may also occur. High-grade
peripheral eosinophilia, leukocytosis, and elevated IgE levels are often present.

FIGURE 177-10
Calabar swelling in loiasis. (Used with permission from Jay S. Keystone, MD, FRCPC.)

View Full Size|Favorite Figure|Download Slide (.ppt)

The differential diagnosis includes other causes of migratory and nodular skin lesions
(see Tables 177-2 and 177-3).

Cutaneous Filariasis
MANSONELLIASIS (MANSONELLA PERSTANS, MANSONELLA STREPTOCERCA)
Cutaneous manifestations of M. perstans infection include Calabar-like swellings, typically in
the forearms, hands and face, and pruritus with or without a papular rash. The exact
interval between infection and onset of symptoms is unclear. Pruritus, papular lesions, and
hypopigmented, hyperpigmented, or lichenified macules, typically found on the upper
chest, are seen with M. streptocerca infection. Eosinophilia is often present
in Mansonellainfections, but also may be from the high prevalence of coinfection with other
filarial or helminthic infections.
Cutaneous Filariasis
ONCHOCERCIASIS (ONCHOCERCA VOLVULUS)
Individuals with onchocerciasis may be asymptomatic. Clinical manifestations most
commonly involve the skin and eye. Heavy infections can result in blindness from chronic
keratitis or retinitis. Six different patterns of skin changes have been described in
onchocerciasis: acute and chronic papular onchodermatitis (see Fig. 177-1), lichenified
onchodermatitis, atrophy, depigmentation, and onchocercal nodules (see Fig. 177-2). More
than one pattern of skin involvement may be present simultaneously, or one pattern of skin
involvement may evolve into another pattern.

Pruritus is the most prominent and persistent symptom of infection. Acute papular
onchodermatitis most often involves the face, extremities, and trunk, and includes
widespread small pruritic papules, vesicles and pustules, sometimes with associated
erythema and edema. Short-term visitors to endemic regions typically present with acute
pruritus and rash (see Fig. 177-1),32 and demonstrate immune hyperresponsiveness despite
low levels of parasites33; skin nodules and eye involvement are usually absent. After
exposures in forested areas of West and Central Africa, travelers and expatriates may have
an acute form of onchocerciasis characterized by acute pruritic and erythematous swelling
of a limb known as gros bras camerounais13 or onchocerciasis-associated limb swelling.34

The skin lesions of chronic papular onchodermatitis are macules and lichenoid papules
varying in size from 3 to 9 mm in diameter. Pruritus is common, and postinflammatory
hyperpigmentation may be present. The most commonly affected anatomic areas are the
buttocks, shoulders, and waist (see Fig. 177-1). Palpable asymptomatic onchocercal nodules
containing the adult worm involve the deep dermis and subcutaneous tissue (see Fig. 177-
2), and occur over bony prominences such as the skull, iliac crest, knee, rib, sacrum, scapula,
and trochanter.

Diagnosis is made by finding microfilariae in the skin by biopsy or skin snips (superficial 2- to
4-mm snips of the upper dermis placed in saline and incubated for 24 hours; the fluid is then
examined for microfilariae). Peripheral eosinophilia and elevated IgE levels are common
findings.

The differential diagnosis for onchocercal nodules includes other parasitic causes of nodules
(see Table 177-3) and epidermal inclusion cysts. Acute onchodermatitis may resemble
miliaria, insect bites, scabies or eczema. Chronic onchodermatitis may resemble a chronic or
lichenoid eczema or atopic dermatitis. Skin changes resembling lichenified onchodermatitis
can be the result of conditions causing significant pruritus or rubbing. Atrophic changes
resemble those associated with aging. Onchocercal depigmentation may be confused with
postinflammatory hypopigmentation or depigmentation.

DIAGNOSIS
Eosinophilia, sometimes high-grade, and elevated IgE levels are common in filarial
infections. Diagnosis rests primarily on demonstration of microfilariae in blood (for
lymphatic filariasis, loiasis, and cutaneous filariasis caused by Mansonella species; note that
daytime blood specimens are appropriate for all except bancroftian filariasis, which requires
nocturnal specimens for diagnosis) or in skin snips
(for Mansonella and Onchocerca infections). However, persons with active filarial infection
may not be microfilaremic. Microfilariae may not appear in blood until 5 to 6 months after
infection in loiasis. Diagnosis also can be established through identification of the adult
worm.

Filarial serology is often very sensitive but is nonspecific because of cross-reaction with
other helminthiases. A positive serologic test for bloodborne species should be followed by
both a blood examination for larvae and test for filarial antigen, to confirm whether
serology represents an active infection or a previous one.

Infiltrates may be present on chest radiography in individuals with lymphatic filariasis and
tropical pulmonary eosinophilia, an aberrant immune response to the infection. Inguinal
lymph node ultrasonography may show active adult worms (“filarial dance sign”), more
commonly seen in men than in women. Lymph node biopsy is contraindicated.

MANAGEMENT
Management of filariasis depends on the infecting species. Table 177-8 summarizes
treatment of filariasis.

Filariasis atau kaki gajah adalah pembengkakan tungkai akibat infeksi

cacing jenis filaria. Cacing ini menyerang pembuluh getah bening dan
ditularkan melalui gigitan nyamuk. 
Penyakit kaki gajah masih ada di Indonesia, terutama di daerah Papua, Nusa
Tenggara Timur, Jawa Barat, dan Nanggroe Aceh Darussalam. Menurut data
Kementerian Kesehatan Republik Indonesia, tercatat hampir 13.000 kasus kaki
gajah di Indonesia.

Selain tungkai, bagian tubuh lain, seperti organ kelamin, lengan, dan dada, juga
dapat mengalami pembengkakan. Sebelum timbul pembengkakan, penyakit kaki
gajah tidak menimbulkan gejala yang spesifik, sehingga pengobatannya sering kali
terlambat.
Oleh karena itu, pencegahan kaki gajah sangat penting. Pencegahannya dapat
dilakukan dengan menghindari gigitan nyamuk dan mengikuti program pemberian
obat pencegahan massal (POPM) yang dilakukan oleh pemerintah.

Penyebab dan Penularan Kaki Gajah

Penyakit kaki gajah atau filariasis disebabkan oleh infeksi cacing jenis filaria pada
pembuluh getah bening. Cacing ini dapat menular dari satu orang ke orang lain
melalui gigitan nyamuk.
Walaupun menyerang pembuluh getah bening, cacing filaria juga beredar di
pembuluh darah penderita kaki gajah. Jika penderita kaki gajah digigit oleh nyamuk,
cacing filaria dapat terbawa bersama darah dan masuk ke dalam tubuh nyamuk.
Lalu bila nyamuk ini menggigit orang lain, cacing filaria di tubuh nyamuk akan masuk
ke dalam pembuluh darah dan pembuluh getah bening orang tersebut. Cacing filaria
kemudian akan berkembang biak di pembuluh getah bening dan menyumbat
peredaran getah bening, hingga menyebabkan kaki gajah.
Beberapa jenis cacing filaria yang menyebabkan filariasis atau kaki gajah
adalah Wuchereria bancrofti, Brugia malayi, dan Brugia timor. Sedangkan jenis
nyamuk penyebar cacing filaria adalah nyamuk jenis Culex, Aedes,
Anopheles, dan Mansonia. 
Melihat cara penularannya, seseorang akan lebih berisiko terkena penyakit kaki
gajah jika:

 Tinggal di lingkungan endemik kaki gajah.

 Tinggal di lingkungan yang tingkat kebersihannya buruk.
 Sering digigit nyamuk atau tinggal di lingkungan yang banyak nyamuk.
 

Gejala Kaki Gajah

Sesuai namanya, gejala utama kaki gajah adalah pembengkakan pada tungkai.
Selain di tungkai, pembengkakan juga bisa terjadi di bagian tubuh lainnya, seperti
lengan, kelamin, dan dada.
Kulit pada tungkai yang bengkak akan menebal, kering, menjadi lebih gelap, pecah-
pecah, dan terkadang muncul luka. Sayangnya, tungkai yang sudah mengalami
pembengkakan dan perubahan kulit tidak dapat kembali seperti semula. Pada
kondisi ini, kaki gajah sudah memasuki fase kronik.
Pada awal penyakit, penderita kaki gajah biasanya tidak mengalami gejala apa pun.
Hal ini menyebabkan penderita tidak sadar telah tertular penyakit kaki gajah
(filariasis), sehingga terlambat melakukan penanganan. Peradangan pembuluh atau
kelenjar getah bening juga dapat muncul di fase awal, berupa pembengkakan
setempat pada pembuluh dan kelenjar getah bening.

Kapan harus ke dokter

Bila Anda berencana berpergian ke daerah yang terdapat kasus kaki gajah,
berkonsultasilah terlebih dahulu dengan dokter. Tanyakan kepada dokter adakah
cara untuk mencegahnya. Anda juga perlu berkonsultasi dengan dokter bila di
lingkungan tempat tinggal Anda ada yang menderita penyakit kaki gajah.
Temui dokter bila timbul pembengkakan pada saluran dan kelenjar getah bening,
terutama bila Anda tinggal di tempat yang banyak terdapat kasus kaki gajah atau
sehabis berpergian ke daerah yang terdapat kasus kaki gajah. Apalagi bila
pembengkakan kelenjar getah bening tersebut terjadi berulang.

Diagnosis Kaki Gajah

Dokter akan bertanya kepada penderita mengenai gejala yang dirasakan dan sejak
kapan gejala muncul. Setelah itu, dokter akan melakukan pemeriksaan fisik untuk
memeriksa gejala tersebut.
Jika menduga pasien menderita kaki gajah, dokter akan menganjurkan tes darah.
Sampel darah akan diperiksa guna mengetahui apakah terdapat cacing filaria atau
tidak. Pemeriksaan ini dilakukan dengan mikroskop atau melalui tes kimia khusus
menggunakan antigen.
Jika diperlukan, penderita juga dapat menjalani pemeriksaan penunjang lainnya
untuk melihat dampak dari penyakit kaki gajah yang dideritanya. Pemeriksaan yang
dilakukan antara lain tes pemindaian dengan USG atau foto Rontgen dan tes urine.

Pengobatan Kaki Gajah
Pengobatan yang dapat dijalani oleh pasien filariasis bertujuan untuk mencegah
infeksi bertambah buruk dan menghindari komplikasi filariasis. Untuk mengurangi
jumlah parasit dalam tubuh, pasien dapat mengonsumsi obat cacing,
seperti ivermectin, albendazole, atau diethylcarbamazine.
Bila filarisis sudah menimbulkan pembengkakan tungkai dan kaki, ukurannya tidak
dapat kembali seperti semula. Namun ada beberapa hal yang dapat dilakukan untuk
menjaga kebersihan kaki yang bengkak, antara lain:

 Istirahatkan tungkai dan selalu jaga posisi tungkai lebih tinggi, saat duduk
atau berbaring.
 Gunakan stocking kompres, sesuai anjuran dokter.
 Bersihkan bagian tungkai yang bengkak dengan air dan sabun setiap hari.
 Jika mengalami luka, segera bersihkan luka dengan antiseptik.
 Gerakkan tungkai melalui olahraga ringan untuk menjaga kelancaran aliran
getah bening di bagian yang bengkak.

Jika pembengkakan pada tungkai sudah sangat parah, atau jika terdapat
pembengkakan skrotum (hidrokel), pasien dapat menjalani operasi untuk
mengecilkan pembengkakan tersebut. Operasi yang dilakukan akan mengangkat
sebagian kelenjar dan pembuluh limfa yang mengalami infeksi.
Kaki yang sudah mengalami pembengkakan akibat filariasis tidak dapat kembali
normal. Oleh karena itu, langkah-langkah pencegahan filariasis sangat penting untuk
dijalankan, terutama bagi orang yang berisiko terkena penyakit ini.
Komplikasi Kaki Gajah
Komplikasi utama yang dapat muncul akibat kaki gajah adalah pembengkakan parah
pada bagian tubuh yang terinfeksi. Pembengkakan ini dapat menimbulkan rasa nyeri
dan menyebabkan kecacatan. Namun, rasa nyeri dan tidak nyaman yang timbul
dapat diredakan melalui langkah-langkah pengobatan kaki gajah.
Kaki yang bengkak juga dapat mengalami infeksi bakteri sekunder, karena kulit kaki
gajah sering mengalami luka.

Pencegahan Kaki Gajah

Langkah utama untuk mencegah kaki gajah adalah dengan menghindari gigitan
nyamuk. Hal ini sangat penting dilakukan, terutama di daerah endemik kaki gajah.
Untuk memaksimalkan perlindungan terhadap gigitan nyamuk, Anda dapat
melakukan langkah-langkah sederhana berikut ini:

 Mengenakan baju dan celana panjang

 Mengoleskan losion antinyamuk
 Tidur dalam kelambu
 Membersihkan genangan air di sekitar rumah

Penyebaran kaki gajah juga dapat dihentikan dengan cara mengikuti program
pemerintah untuk memberantas kaki gajah, yaitu pemberian obat pencegahan
massal (POPM).
Program ini dilakukan di daerah yang masih memiliki kasus kaki gajah, seperti
provinsi Papua, Papua Barat, Jawa Barat, Nusa Tenggara Timur, Nanggroe Aceh
Darussalam, dan Sulawesi Tenggara.