Wuchereria bancrofti

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Wuchereria bancrofti
Microfilar of Wuchereria bancrofti, from a patient seen in Haiti - the thick blood smears are stained with hematoxylin.
Scientific classification
Kingdom:Animalia
Phylum:Nematoda
Class:Secernentea
Order:Spirurida
Suborder:Spirurina
Family:Onchocercidae
Genus:Wuchereria
 
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Wuchereria bancrofti
Microfilar of Wuchereria bancrofti, from a patient seen in Haiti - the thick blood smears are stained with hematoxylin.
Scientific classification
Kingdom:Animalia
Phylum:Nematoda
Class:Secernentea
Order:Spirurida
Suborder:Spirurina
Family:Onchocercidae
Genus:Wuchereria

Wuchereria bancrofti is a parasitic filarial nematode (roundworm) spread by a mosquito vector. It is one of the three parasites that cause lymphatic filariasis, an infection of the lymphatic system by filarial worms. It affects over 120 million people, primarily in Africa, South America, and other tropical and subtropical countries.[1] If the infection is left untreated, it can develop into a chronic disease called elephantiasis. Limited treatment modalities exist and no vaccines have been developed.

Contents

History

The effects of W. bancrofti were documented early in ancient text. 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.[2] 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.[3]

Etiology

W. bancrofti exhibits considerable sexual dimorphism. The adult worm is long, slender, and smooth with rounded ends. It has a short cephalic region and dispersed nuclei throughout its body cavity, with no nuclei at the tail tip. The male worm is 40 mm long and 100 μm wide, and features a curved tail. In contrast, the female is 6 cm to 10 cm long and 300 μm wide, nearly three times larger in diameter than the male. Females are ovoviviparous and can produce thousands of juveniles known as microfilariae. Microfilariae of W. bancrofti retain the egg membrane as a sheath and are often considered advanced embryos.

Wuchereria bancrofti
Classification and external resources
ICD-10B74.0
ICD-9125.0

Life cycle

W. bancrofti carry out their life cycle in two hosts. Human beings serve as the definitive host and mosquitoes as their intermediate hosts. The adult parasites reside in the lymphatics of the human host. The first-stage larvae, known as microfilariae, are present in the circulation. They migrate between the deep and the peripheral circulation. W. bancrofti is a periodic strain that exhibits nocturnal periodicity. During the day, they are present in the deep veins, and during the night, they migrate to the peripheral circulation. Next, the microfilariae are transferred into a vector; the most common mosquito vector species are within the genera Culex, Anopheles, Mansonia, and Aedes. Inside the mosquito vector, also known as the intermediate host, the microfilariae mature into motile larvae called juveniles. When the mosquito vector has its next blood meal, W. bancrofti is egested via the mosquito’s 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 life cycle of W. bancrofti.

Epidemiology

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. There is no reservoir host.[4]

Biology

Life cycle of Wuchereria bancrofti

In humans, the adult worms reside in the lymphatic ducts and are found mostly in the afferent lymphatic channels of the lymph glands in the lower part of the body. The microfilariae produced by the female worms 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 p.m. to 2 a.m. 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.

Pathology

An Armigeres subalbatus mosquito ingesting a blood meal from a human finger

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

  1. 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.
  2. 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 will exhibit fever, chills, skin infections, painful lymph nodes, and tender skin of the lymphedematous extremity. These symptoms often lessen after five to seven 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).
  3. 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 and arms are affected.

Diagnosis

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.[5] 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.[6]

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.[7]

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

Treatment

The severe symptoms caused by the parasite can be avoided by cleansing the skin, surgery, or the use of therapeutic drugs, such as diethylcarbamazine (DEC), ivermectin, or albendazole. The drug of choice, however, is DEC, which can eliminate the microfilariae from the blood and also kill the adult worms with a dosage of 6 mg/kg semiannually or annually.[8] A polytherapy treatment that includes ivermectin with DEC or albendazole is more effective than each drug alone.[9] 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.

Control

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.

Eradication

The WHO is coordinating an effort to eradicate filarisis. 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.

See also

Tropical eosinophilia

References

  1. ^ 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. 
  2. ^ 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. 
  3. ^ Chernin E (1987). "The disappearance of bancroftian filariasis from Charleston, South Carolina". Am J Trop Med Hyg 37 (1): 111–4. PMID 3300389. 
  4. ^ 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. 
  5. ^ vanHoegaerden M, Ivanoff B (1986). "A rapid, simple method for isolation of viable microfilariae". Am J Trop Med Hyg 35 (1): 148–51. PMID 3456213. 
  6. ^ 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. PMID 8615447. 
  7. ^ 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. PMID 8024070. 
  8. ^ 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. PMID 9347968. 
  9. ^ de Kraker ME, Stolk WA, van Oortmarssen GJ, Habbema JD (2006 May). "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. 

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