Wuchereria bancrofti

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Wuchereria bancrofti is a human parasitic roundworm that is the major cause of lymphatic filariasis. It is one of the three parasitic worms, together with Brugia malayi and B. timori, that infect the lymphatic system to cause lymphatic filariasis. These filarial worms are spread by a variety of mosquito vector species. W. bancrofti is the most prevalent of the three and affects over 120 million people, primarily in Central Africa and the Nile delta, South and Central America, the tropical regions of Asia including southern China, and the Pacific islands.[1] If left untreated, the infection can develop into a chronic disease called elephantiasis.[2] In rare conditions, it also causes tropical eosinophilia, an asthmatic disease. No vaccine is commercially available, but high rates of cure have been achieved with various antifilarial regimens and lymphatic filariasis is the target of the WHO Global Program to Eliminate Lymphatic Filariasis with the aim to eradicate the disease as a public-health problem by 2020.[3]


  • 1 History
  • 2 Morphology
  • 3 Lifecycle
  • 4 Epidemiology
  • 5 Pathology
  • 6 Diagnosis
  • 7 Treatment
  • 8 Control
  • 9 Eradication
  • 10 References
  • 11 External links


The effects of W. bancrofti were documented early in ancient texts. Ancient Greek and Roman writers noted the similarities between the enlarged limbs and cracked skin of infected individuals to that of elephants. Since then, this condition has been commonly known as elephantiasis. However, this is a misnomer, since elephantiasis literally translates to “a disease caused by elephants”.

W. bancrofti was named after physician Otto Wucherer and parasitologist Joseph Bancroft, both of whom extensively studied filarial infections.

W. bancrofti is speculated to have been brought to the New World by the slave trade.[4] Once it was introduced to the New World, this filarial worm disease persisted throughout the areas surrounding Charleston, South Carolina, until its sudden disappearance in the 1920s.[5]


As a dioecious worm, W. bancrofti exhibits sexual dimorphism. The adult worm is long, cylindrical, slender, and smooth with rounded ends. It is white in colour and almost transparent. The body is quite delicate, making removing it from tissues difficult. It has a short cephalic or head region connected to the main body by a short neck, which appears as a constriction. Dark spots are dispersed nuclei throughout the body cavity, with no nuclei at the tail tip. Males and females can be differentiated by size and structure of their tail tips. The male worm is smaller, 40 mm (1.6 in) long and 100 μm (0.0039 in) wide, and features a ventrally curved tail. The tip of the tail has 15 pairs of minute caudal papillae, the sensory organs. The anal region is an elaborate structure consisting of 12 pairs of papillae, of which eight are in front and four are behind the anus. In contrast, the female is 60 millimetres (2.4 in) to 100 millimetres (3.9 in) long and 300 micrometres (0.012 in) wide, nearly three times larger in diameter than the male. Its tail gradually tapers and rounded at the tip. No additional sensory structures are seen. Its vulva lies towards the anterior region, about 0.25 mm from the head. Adult males and females are most often coiled together and are difficult to separate. Females are ovoviviparous and can produce thousands of juveniles known as microfilariae.[6]

The microfilaria is a miniature adult, and retains the egg membrane as a sheath, and is often considered an advanced embryo. It measures 280 μm long and 25 μm wide. It appears quite structureless in vivo, but histological staining makes its primitive gut, nerve ring, and muscles apparent.[7]


Lifecycle of Wuchereria bancrofti

W. bancrofti carries out its lifecycle in two hosts. Humans serve as the definitive host and mosquitos as the intermediate host. The adult parasites reside in the lymphatics of the human host. They are found mostly in the afferent lymphatic channels of the lymph glands in the lower part of the body. The first-stage larvae, known as microfilariae, are present in the circulation. The microfilariae have a membrane “sheath”. This sheath, along with the area in which the worms reside, makes identification of the species of microfilariae in humans easier to determine. The microfilariae are found mainly in the peripheral blood and can be found at peak amounts from 10 pm to 4 am. They migrate between the deep and the peripheral, circulation exhibiting unique diurnal periodicity. During the day, they are present in the deep veins, and during the night, they migrate to the peripheral circulation. The cause of this periodicity remains unknown, but the advantages of the microfilariae being in the peripheral blood during these hours may ensure the vector, the nighttime mosquito, will have a higher chance of transmitting them elsewhere. Physiological changes also are associated with sleeping, such as lowered body temperature, oxygen tension, and adrenal activity, and an increased carbon dioxide tension, among other physical alterations, any of which could be the signals for the rhythmic behavior of microfilarial parasites. If the hosts sleep by day and are awake at night, their periodicity is reversed. In the South Pacific, where W. bancrofti shows diurnal periodicity, it is known as periodic.

The microfilariae are transferred into a vector, which are most commonly mosquito species of the genera Culex, Anopheles, Mansonia, and Aedes. Inside the mosquito, the microfilariae mature into motile larvae called juveniles; these migrate to the labium after a period around 10 days. When the infected mosquito has its next blood meal, W. bancrofti larvae are deposited from the mouthparts onto the skin of the prospective host and migrate through microcuts in the dermis or the tract created by the proboscis into the blood stream of the new human host. The larvae move through the lymphatic system to regional lymph nodes, predominantly in the legs and genital area. The larvae develop into adult worms over the course of a year, and reach sexual maturity in the afferent lymphatic vessels. After mating, the adult female worm can produce thousands of microfilariae that migrate into the bloodstream. A mosquito vector can bite the infected human host, ingest the microfilariae, and thus repeat the lifecycle. The organism notably does not multiply within its intermediate host, the mosquito.[7][8][9]


An infection in leg by W. bancrofti

W. bancrofti is responsible for 90% of lymphatic filariasis. Recently, 120 million worldwide cases of lymphatic filariasis were estimated. W. bancrofti largely affects areas across the broad equatorial belt (Africa, the Nile Delta, Turkey, India, the East Indies, Southeast Asia, Philippines, Oceanic Islands, and parts of South America).

The mosquito vectors of W. bancrofti have a preference for human blood; humans are apparently the only animals naturally infected with W. bancrofti. No reservoir host is known,[10] and the disease could, therefore, potentially be eradicated.


The pathogenesis of W. bancrofti infection is dependent on the immune system and inflammatory responses of the host. After infection, the worms mature within 6–8 months, male and female worms mate and then release the microfilariae. These microfilariae can be released for up to 10 years.

  • The asymptomatic phase usually consists of high microfilaremia infection, and individuals show no symptoms of being infected. This occurs due to cytokine IL-4 suppressing the activity of TH1 cells in the immune system. This can occur for years until the inflammatory reaction rises again.
  • In the inflammatory (acute) phase, the antigens from the female adult worms elicit inflammatory responses. The worms in the lymph channels disrupt the flow of the lymph, causing lymphedema. The individual exhibits fever, chills, skin infections, painful lymph nodes, and tender skin of the lymphedematous extremity. These symptoms often lessen after 5-7 days. Other symptoms that may occur include orchitis, an inflammation of the testes, which is accompanied by painful, immediate enlargement and epididymitis (inflammation of the spermatic cord).
  • The obstructive (chronic) phase is marked by lymph varices, lymph scrotum, hydrocele, chyluria (lymph in urine), and elephantiasis. Microfilariae are not normally present in this phase. A key feature of this phase is scar formation from affected tissue areas. Other features include thickening of the skin and elephantiasis, which develops gradually with the attack of the lymphatic system. Elephantiasis affects men mainly in the legs, arms, and scrotum. In women, the legs, arms, and breasts are affected.
  • Diagnosis[edit]

    A blood smear is a simple and fairly accurate diagnostic tool, provided the blood sample is taken during the period in the day when the juveniles are in the peripheral circulation.[11] Technicians analyzing the blood smear must be able to distinguish between W. bancrofti and other parasites potentially present.

    A polymerase chain reaction test can also be performed to detect a minute fraction, as little as 1 pg, of filarial DNA.[12]

    Some infected people do not have microfilariae in their blood. As a result, tests aimed to detect antigens from adult worms can be used.

    Ultrasonography can also be used to detect the movements and noises caused by the movement of adult worms.[13]

    Dead, calcified worms can be detected by X-ray examinations.


    The severe symptoms caused by the parasite can be avoided by cleansing the skin, surgery, or the use of anthelmintic drugs, such as diethylcarbamazine, ivermectin, or albendazole. The drug of choice is diethylcarbamazine, which can eliminate the microfilariae from the blood and also kill the adult worms with a dose of 6 mg/kg semiannually or annually.[14] A polytherapy treatment that includes ivermectin with diethylcarbamazine or albendazole is more effective than either drug alone.[15] Protection is similar to that of other mosquito-spread illnesses; one can use barriers both physical (a mosquito net), chemical (insect repellent), or mass chemotherapy as a method to control the spread of the disease.

    Mass chemotherapy should cover the entire endemic area at the same time. This will significantly decrease the overall microfilarial titer in blood in mass, hence decreasing the transmission through mosquitoes during their subsequent bites.

    Antibiotic active against the Wolbachia symbionts of the worm have been tested as treatment.[16] Wolbachia-free worms immediately become sterile, and later die prematurely.


    Prevention focuses on protecting against mosquito bites in endemic regions. Insect repellents and mosquito nets are useful to protect against mosquito bites. Public education efforts must also be made within the endemic areas of the world to successfully lower the prevalence of W. bancrofti infections.


    The WHO is coordinating an effort to eradicate filariasis. The mainstay of this programme is the mass use of antifilarial drugs on a regular basis for at least five years.

    In April 2011, Sri Lanka was certified by the WHO as having eradicated this disease.


  • ^ Melrose WD (2002). “Lymphatic filariasis: New insights into an old disease”. Int J Parasitol. 32 (8): 947–60. doi:10.1016/S0020-7519(02)00062-0. PMID 12076624..mw-parser-output cite.citation{font-style:inherit}.mw-parser-output .citation q{quotes:”””””””‘””‘”}.mw-parser-output .citation .cs1-lock-free a{background:url(“//upload.wikimedia.org/wikipedia/commons/thumb/6/65/Lock-green.svg/9px-Lock-green.svg.png”)no-repeat;background-position:right .1em center}.mw-parser-output .citation .cs1-lock-limited a,.mw-parser-output .citation .cs1-lock-registration a{background:url(“//upload.wikimedia.org/wikipedia/commons/thumb/d/d6/Lock-gray-alt-2.svg/9px-Lock-gray-alt-2.svg.png”)no-repeat;background-position:right .1em center}.mw-parser-output .citation .cs1-lock-subscription a{background:url(“//upload.wikimedia.org/wikipedia/commons/thumb/a/aa/Lock-red-alt-2.svg/9px-Lock-red-alt-2.svg.png”)no-repeat;background-position:right .1em center}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration{color:#555}.mw-parser-output .cs1-subscription span,.mw-parser-output .cs1-registration span{border-bottom:1px dotted;cursor:help}.mw-parser-output .cs1-ws-icon a{background:url(“//upload.wikimedia.org/wikipedia/commons/thumb/4/4c/Wikisource-logo.svg/12px-Wikisource-logo.svg.png”)no-repeat;background-position:right .1em center}.mw-parser-output code.cs1-code{color:inherit;background:inherit;border:inherit;padding:inherit}.mw-parser-output .cs1-hidden-error{display:none;font-size:100%}.mw-parser-output .cs1-visible-error{font-size:100%}.mw-parser-output .cs1-maint{display:none;color:#33aa33;margin-left:0.3em}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration,.mw-parser-output .cs1-format{font-size:95%}.mw-parser-output .cs1-kern-left,.mw-parser-output .cs1-kern-wl-left{padding-left:0.2em}.mw-parser-output .cs1-kern-right,.mw-parser-output .cs1-kern-wl-right{padding-right:0.2em}
  • ^ “Wuchereria bancrofti: The causative agent of Bancroftian Filariasis”. ww.nematodes.org. Retrieved 20 February 2014.
  • ^ Ramaiah, KD; Ottesen, EA (November 2014). “Progress and impact of 13 years of the global programme to eliminate lymphatic filariasis on reducing the burden of filarial disease”. PLoS Neglected Tropical Diseases. 8 (11): e3319. doi:10.1371/journal.pntd.0003319. PMC 4239120. PMID 25412180.
  • ^ Laurence BR (1989). “The global dispersal of bancroftian filariasis”. Parasitology Today. 5 (8): 260–4. doi:10.1016/0169-4758(89)90260-3. PMID 15463229.
  • ^ Chernin E (1987). “The disappearance of bancroftian filariasis from Charleston, South Carolina”. Am J Trop Med Hyg. 37 (1): 111–4. doi:10.4269/ajtmh.1987.37.111. PMID 3300389.
  • ^ “Lymphatic Filariasis”. Stanford University. Retrieved 20 February 2014.
  • ^ a b Junghanss, Jeremy Farrar, Peter J. Hotez, Thomas (2013). Manson’s Tropical Diseases: Expert Consult – Online (23rd ed.). Oxford: Elsevier/Saunders. pp. e49–e52. ISBN 9780702053061.
  • ^ Ridley, John W. (2012). Parasitology for Medical and Clinical Laboratory Professionals. Clifton Park, N.Y.: Cengage Learning. pp. 103–104. ISBN 9781435448162.
  • ^ Rajan, T.V. (2008). Textbook of Medical Parasitology. BI Publications Pvt Ltd. pp. 73–77. ISBN 9788172253172.
  • ^ King CL, Freedman DP (2000). “Filariasis”. In G.T. Strickland. Hunter’s tropical medicine and emerging infectious diseases (8th ed.). Philadelphia: E.B. Saunders. pp. 740–53. ISBN 978-0-7216-6223-7.
  • ^ van Hoegaerden M, Ivanoff B (1986). “A rapid, simple method for isolation of viable microfilariae”. Am J Trop Med Hyg. 35 (1): 148–51. doi:10.4269/ajtmh.1986.35.148. PMID 3456213.
  • ^ Zhong M, McCarthy J, Bierwert L, Lizotte-Waniewski M, Chanteau S, Nutman TB, Ottesen EA, Williams SA (1996). “A polymerase chain reaction assay for detection of the parasite Wuchereria bancrofti in human blood samples”. Am J Trop Med Hyg. 54 (4): 357–63. doi:10.4269/ajtmh.1996.54.357. PMID 8615447.
  • ^ Amaral F, Dryer G, Figueredo-Silva J, Noroes J, Cavalcanti A, Samico SC, Santos A, Coutinho A (1994). “Live adult worms detected by ultrasonography in human Bancroftian filariasis”. Am J Trop Med Hyg. 50 (6): 753–7. doi:10.4269/ajtmh.1994.50.753. PMID 8024070.
  • ^ Eberhard ML, Hightower AW, Addiss DG, Lammine PJ (1997). “Clearance of Wuchereria bancrofti antigen after treatment with diethylcarbamazine or ivermectin”. Am J Trop Med Hyg. 57 (4): 483–6. doi:10.4269/ajtmh.1997.57.483. PMID 9347968.
  • ^ de Kraker ME, Stolk WA, van Oortmarssen GJ, Habbema JD (May 2006). “Model-based analysis of trial data: microfilaria and worm-productivity loss after diethylcarbamazine-albendazole or ivermectin-albendazole combination therapy against Wuchereria bancrofti”. Trop Med Int Health. 11 (5): 718–28. doi:10.1111/j.1365-3156.2006.01606.x. PMID 16640625.
  • ^ Taylor, MJ; Makunde, WH; McGarry, HF; Turner, JD; Mand, S; Hoerauf, A (2005). “Macrofilaricidal activity after doxycycline treatment of Wuchereria bancrofti: a double-blind, randomised placebo-controlled trial”. Lancet. 365 (9477): 2116–21. doi:10.1016/S0140-6736(05)66591-9. PMID 15964448.
  • External links[edit]

    • History of Wuchereria Bancrofti
    • Animal Diversity Web
    •  ”Filaria” . Collier’s New Encyclopedia. 1921.

    (Tapeworm infection)Roundworm/

    • Hookworm infection
    • Ancylostoma duodenale/Ancylostoma braziliense
      • Ancylostomiasis
      • Cutaneous larva migrans
    • Necator americanus
      • Necatoriasis
    • Angiostrongylus cantonensis
      • Angiostrongyliasis
    • Metastrongylus
      • Metastrongylosis


    • Ascaris lumbricoides
      • Ascariasis
    • Anisakis
      • Anisakiasis
    • Toxocara canis/Toxocara cati
      • Visceral larva migrans/Toxocariasis
    • Baylisascaris
    • Dioctophyme renale
      • Dioctophymosis
    • Parascaris equorum


    • Strongyloides stercoralis
      • Strongyloidiasis
    • Trichostrongylus spp.
      • Trichostrongyliasis
    • Halicephalobus gingivalis


    • Enterobius vermicularis
      • Enterobiasis
      • Pinworm


    • Trichinella spiralis
      • Trichinosis
    • Trichuris trichiura (Trichuriasis
      * Whipworm)
    • Capillaria philippinensis
      • Intestinal capillariasis
    • Capillaria hepatica

    Source: https://en.wikipedia.org/wiki/Wuchereria_bancrofti