Introduction
Background
Filariasis is a disease group affecting humans and animals caused by nematode parasites of the order Filariidae, commonly called filariae. Filarial parasites may be classified according to the habitat of the adult worms in the vertebral host. The cutaneous group includes Loa loa, Onchocerca volvulus, and Mansonella streptocerca. The lymphatic group includes Wuchereria bancrofti, Brugia malayi, and Brugia timori. The body-cavity group includes Mansonella perstans and Mansonella ozzardi.
Of the hundreds of described filarial parasites, only 8 species cause natural infections in humans. The parasites of the cutaneous and lymphatic groups are the most clinically significant. Other species of filariae may cause incomplete infections because they are unable to reach adult maturity in human hosts and therefore cannot produce microfilaria (eg, Dirofilaria immitis [dog heartworm], Dirofilaria [Nochtiella] repens, and Dirofilaria tenuis [raccoon heartworm]).
These infections have a significant economic and psychosocial impact in endemic areas, disfiguring and/or incapacitating more than 40 million individuals.1 Studies from the Indian subcontinent have shown that infected patients lose significant time from work because of the disease,2 costing the national treasury a minimum of $842 million per year.3
Filariae have a specific geographic distribution. For example, W bancrofti is found in sub-Saharan Africa, Southeast Asia, India, and the Pacific Islands. B malayi is found in similar locations, but not in sub-Saharan Africa. B timori is concentrated to the Timor island of Indonesia.
It has been observed (especially in endemic areas), that the prevalence of microfilaremia increases with age, as adult worms are gradually acquired over years. Lymphatic filariasis is first contracted in childhood, and most individuals in endemic areas have been exposed by the third or fourth decade of life. The proportion of infected individuals remains constant.4 As with most helminths, adult filarial parasites replicate in a secondary host. The adult worm burden in an individual cannot increase unless the host is exposed to additional microfilaria. Infected individuals cannot sustain higher levels of parasitemia once they leave the endemic area.
Because the mosquito vector is inefficient, a relatively prolonged stay in an endemic area is usually required to acquire the infection. Disorganized urbanization is adding to the vector population and hence to the increased incidence and prevalence of such diseases in developing countries.
Pathophysiology
The filarial life cycle, like that of all nematodes, consists of 5 developmental or larval stages in a vertebral host and an arthropod intermediate host and vector. Adult female worms produce thousands of first-stage larvae or microfilariae that 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.
Filariasis. This figure displays the life cycle of Wuchereria bancrofti in humans and mosquito vectors (ie, Aedes, Anopheles, Culex, Mansonia species). Life cycles of other lymphatic nematodes (ie, Brugia malayi, Brugia timori) are identical, while the life cycles for other filariae differ in the body location of adult worms, the microfilariae present, and the arthropod intermediate hosts and vectors.
Microfilariae then 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, these develop into mature worms (20-100 mm in length). An average parasite can survive for about 5 years.
The prepatent period is defined as the interval between a vector bite and the appearance of microfilaria 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 lymphatics5
- The duration and level of exposure to infective insect bites6
- The number of secondary bacterial and fungal infections5
- The degree of host immune response7
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 have shown that there is a familial tendency to lymphatic obstruction, providing support for the hypothesis that host genes influence lymphedema susceptibility.8 Prenatal exposure seems to be an important determinant in conferring greater immune tolerance to parasite antigen.9 Thus, individuals from endemic areas are often asymptomatic until late in disease when they have high worm burden, whereas nonimmune expatriates tend to have brisk immune responses and more severe early clinical symptoms, even in light infections.
Recent studies have shown that lymphatic filarial parasites contain rickettsialike Wolbachia endosymbiotic bacteria. This association has been recognized as contributing to the inflammatory reaction seen in filariasis.10
Frequency
United States
No form of human filariasis is currently endemic to the United States. W bancrofti was once prevalent in Charleston, South Carolina, because of the presence of suitable mosquito vectors. Immigrant populations and persons who have traveled long-term to the tropics are potential reservoirs of infection. Returning missionaries and Peace Corps volunteers are at particular risk for lymphatic filariasis and onchocerciasis because of the long prepatent period and relatively high intensity of exposure required between exposure to infective insect bites and the development of sexually mature adult worms.
International
Lymphatic filariasis affects more than 90 million people worldwide and is found throughout the tropics and subtropics. At least 21 million people are infected with O volvulus in equatorial Africa and foci in Central and South America. Approximately 3 million people in Central Africa are infected with L loa. In 1997, the World Health Organization (WHO) initiated a program to globally eliminate lymphatic filariasis as a public health problem.
Mortality/Morbidity
- Filarial diseases are rarely fatal, but the consequences of infection can cause significant personal and socioeconomic hardship for those who are affected.
- The WHO has identified lymphatic filariasis as the second leading cause of permanent and long-term disability in the world after leprosy.
- The morbidity of human filariasis results mainly from the host reaction to microfilariae or developing adult worms in different areas of the body.
Race
Filariasis has no known racial predilection.
Sex
Both sexes are equally susceptible to filariasis. Because of different local, cultural, and social work practices, as well as differences in exposure to insect vectors, one sex or the other may be exposed to infection more often.
Age
- Individuals of all ages are susceptible and potentially microfilaremic.
- Microfilaremia rates increase with age through childhood and early adulthood, although clinical infection may not be apparent.
- The manifestation of acute and chronic filariasis usually occurs only after years of repeated and intense exposure to infected vectors in endemic areas.
Clinical
History
Symptoms of filariasis are species-dependent and body-site–dependent and can be acute or chronic in nature. Up to 70% of infected individuals remain asymptomatic. Symptoms usually do not manifest until adolescence or adulthood, when worm burden is usually the highest. Several variations have been observed.11
- Lymphatic filariasis
- The symptoms of lymphatic filariasis predominantly result from the presence of adult worms residing in the lymphatics.
- The clinical course is broadly divided into asymptomatic microfilaremia, acute phases of adenolymphangitis (ADL), and chronic irreversible lymphedema.
- Three acute syndromes have been described in filariasis, as follows:
- Acute ADL: This refers to the sudden onset of febrile painful lymphadenopathy. Pathologically, the lymph node is characterized by a retrograde lymphangitis, distinguishing it from bacterial lymphadenitis. Symptoms usually abate within one week, but recurrences are possible.12
- Filarial fever: This is characterized by fever without the associated adenitis.
- Tropical pulmonary eosinophilia (TPE): See below.
- Patients with microfilaremia are generally asymptomatic, although those with heavy microfilarial loads may develop acute and chronic inflammatory granulomas secondary to splenic destruction.
- Passage of cloudy milklike urine may denote chyluria.
- Tropical pulmonary eosinophilia
- TPE is a form of occult filariasis.
- Presenting symptoms include a paroxysmal dry cough, wheezing, dyspnea, anorexia, malaise, and weight loss.
- Symptoms of TPE are usually due to the inflammatory response to the infection. Characteristically, peripheral blood eosinophilia and abnormal findings on chest radiography are observed. TPE is usually related to W bancrofti or B malayi infection.
- Onchocerciasis
- This also is known as hanging groins, leopard skin, river blindness, or sowda.
- Symptoms result from the presence of microfilariae in the skin and include pruritus, subcutaneous lumps, lymphadenitis, and blindness.
- Patients with onchocerciasis may report impaired visual acuity due to corneal fibrosis.
- Loiasis
- The symptoms of L loa infection are usually confined to subcutaneous swellings on the extremities, localized pain, pruritus, and urticaria.
- Microfilaremia tends to be asymptomatic.
- Occasionally, the worm is observed migrating through the subconjunctiva or other tissues.
- M ozzardi, M perstans, and M streptocerca infection
- Mansonella infections are usually asymptomatic.
- If symptoms are present, they may include fever, pruritus, skin lumps, lymphadenitis, and abdominal pain.
Physical
Signs of filariasis present on examination are species-dependent and may be acute or chronic in nature.
- Lymphatic filariasis
- Acute manifestations of lymphatic filariasis usually are referred to as ADL, which is characterized by episodic attacks of fever associated with inflammation of the inguinal lymph nodes, testis, spermatic cord, lymphedema, or a combination of these. Skin exfoliation of the affected body part usually occurs with resolution of an episode.
- Repeated episodes of inflammation and lymphedema lead to lymphatic damage, chronic swelling, and elephantiasis of the legs, arms, scrotum, vulva, and breasts.
Lymphatic filariasis resulting from Wuchereria bancrofti infection, which is causing limb lymphoedema, inguinal lymphadenopathy, and hydrocele. Photograph taken by Professor Bruce McMillan and donated by John Walker, MD.
Filariasis. Unilateral left lower leg elephantiasis secondary to Wuchereria bancrofti infection in a boy.
Filariasis. This is a close-up view of the unilateral lower leg elephantiasis shown in Image 4. Note the lymphedema and typical skin appearance of depigmentation and verrucosities (warty changes).
Filariasis. Lateral view of the right outer aspect of a leg affected by gross elephantiasis secondary to Wuchereria bancrofti infection.
Filariasis. Inner aspect of the lower leg of the male patient in Image 6, showing gross elephantiasis secondary to Wuchereria bancrofti infection.
Filariasis. Unilateral left hydrocele and testicular enlargement secondary to Wuchereria bancrofti infection in a man who also was positive for microfilariae.
Filariasis. Bilateral hydrocele, testicular enlargement, and inguinal lymphadenopathy secondary to Wuchereria bancrofti infection in a man who also was microfilaremic.
- The WHO has developed a system to grade the severity of edema, as follows:1
- Grade 1 - Pitting edema reversible with limb elevation
- Grade 2 - Nonpitting edema irreversible with limb elevation
- Grade 3 - Severe swelling with sclerosis and skin changes
- Hydrocele is the most common manifestation of chronic W bancrofti infection in males in endemic areas but is rare with B malayi and B timori infection.
- Chyluria also may be present in chronically infected persons. Since large amounts of fat and protein are lost in the urine, these conditions can lead to nutritional deficiencies.
- Tropical pulmonary eosinophilia
- Scattered wheezes and crackles are heard in both lung fields.
- Lymphadenopathy and hepatomegaly may be present.
- D repens infection: This may result in painless subcutaneous, submucosal, or eyelid lumps.
- Onchocerciasis
- The clinical triad of infection is dermatitis, skin nodules (ie, onchocercomas), and ocular lesions.
Filariasis. Onchocercomas of the forearm skin (sowda) in a Sudanese man.
- Skin lesions include edema, pruritus, erythema, papules, scablike eruptions, altered pigmentation, and lichenification.
- Skin nodules tend to be common over bony prominences.
- Eye lesions are usually related to the duration and severity of infection and are caused by an abnormal host immune response to microfilariae. The common eye findings include punctate keratitis, pannus formation, corneal fibrosis, iridocyclitis, glaucoma, choroiditis, and optic atrophy. Loss of visual acuity may occur.
- The clinical triad of infection is dermatitis, skin nodules (ie, onchocercomas), and ocular lesions.
- Loiasis
- The diagnostic feature of loiasis is a Calabar swelling, ie, a large transient area of localized nonerythematous subcutaneous edema. This is most common around the joints.
- Other rare manifestations of infection include arthritis, breast calcification, meningoencephalopathy, endomyocardial fibrosis, peripheral neuropathy, pleural effusions, and retinopathy.
- M ozzardi, M perstans, and M streptocerca infection: Subcutaneous or conjunctival nodules and lymphadenopathy may be detected in symptomatic persons.
Causes
- Lymphatic filariasis
- Mosquitoes of the genera Aedes, Anopheles, Culex, or Mansonia are the intermediate hosts and vectors of all species that cause lymphatic filariasis.
- Acute lymphatic filariasis is related to larval molting and adult maturation to fifth-stage larvae. Adult worms are found in lymph nodes and lymphatic vessels distal to the nodes. Females measure 80-100 mm in length and males are 40 mm.
- The most commonly affected nodes are in the femoral and epitrochlear regions.
- Abscess formation may occur at the nodes or anywhere along the distal vessel.
Filarial abscess scar on the left upper thigh in a young male who is positive for Wuchereria bancrofti microfilariae
- Infection with B timori appears to result in more abscesses than infection with B malayi or W bancrofti.
- Cellular invasion, with plasma cells, eosinophils, and macrophages, together with hyperplasia of the lymphatic endothelium, occurs with repeated inflammatory episodes. The consequence is lymphatic damage and chronic leakage of protein-rich lymph in the tissues, thickening and verrucous changes of the skin, and chronic streptococcal and fungal infections, which all contribute to the appearance of elephantiasis.
- B malayi elephantiasis is more likely to affect the upper and lower limbs, with genital pathology and chyluria being rare.
- Occult filariasis
- Occult filariasis denotes filarial infection in which microfilariae are not observed in the blood but may be found in other body fluids and/or tissues.
- The occult syndromes are TPE, D immitis or D repens infection, filarial arthritis, filarial breast abscess, and filarial-associated immune-complex glomerulonephritis.
- TPE most likely results from a hyperresponsiveness to W bancrofti or B malayi antigen.
- Human infection with D immitis may result in pulmonary lesions of immature Dirofilaria worms in the lung periphery. If D immitis larvae lodge in branches of the pulmonary arteries, they can cause pulmonary infarcts.
- Onchocerciasis
- Microfilariae from the skin are ingested by the Simulium species of blackflies.
- Chronic onchocerciasis cases are hyperresponsive to parasite antigen, have increased eosinophilia, and result in the presence of high levels of serum IgE.
- Patterns of onchocercal eye disease also are associated with parasite strain differences at the DNA level.
- Loiasis
- Mango flies or deerflies of Chrysops transmit loiasis.
- Response to L loa infection appears to differ between residents and nonresidents in endemic areas. Nonresidents with infection appear to be more prone to symptoms than residents, despite lower levels of microfilaremia. Eosinophil, serum IgE, and antibody levels are also higher in nonresidents with infection.
- L loa meningoencephalopathy
- This severe, often fatal complication is precipitated by diethylcarbamazine (DEC) therapy in patients with a high microfilarial burden.
- Localized necrotizing granulomas, endomyocardial fibrosis, nephritic syndrome, and venous thrombosis may also be observed.
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References
[Guideline] World Health Organization. Lymphatic filariasis: the disease and its control. Fifth report of the WHO Expert Committee on Filariasis. World Health Organ Tech Rep Ser. 1992;821:1-71. [Medline].
Babu BV, Swain BK, Rath K. Impact of chronic lymphatic filariasis on quantity and quality of productive work among weavers in an endemic village from India. Trop Med Int Health. May 2006;11(5):712-7. [Medline].
Ramaiah KD, Das PK, Michael E, Guyatt H. The economic burden of lymphatic filariasis in India. Parasitol Today. Jun 2000;16(6):251-3. [Medline].
Witt C, Ottesen EA. Lymphatic filariasis: an infection of childhood. Trop Med Int Health. Aug 2001;6(8):582-606. [Medline].
Baird JB, Charles JL, Streit TG, Roberts JM, Addiss DG, Lammie PJ. Reactivity to bacterial, fungal, and parasite antigens in patients with lymphedema and elephantiasis. Am J Trop Med Hyg. Feb 2002;66(2):163-9. [Medline].
King CL. Transmission intensity and human immune responses to lymphatic filariasis. Parasite Immunol. Jul 2001;23(7):363-71. [Medline].
Lamb TJ, Le Goff L, Kurniawan A, Guiliano DB, Fenn K, Blaxter ML, et al. Most of the response elicited against Wolbachia surface protein in filarial nematode infection is due to the infective larval stage. J Infect Dis. Jan 1 2004;189(1):120-7. [Medline].
Lammie PJ, Cuenco KT, Punkosdy GA. The pathogenesis of filarial lymphedema: is it the worm or is it the host?. Ann N Y Acad Sci. Dec 2002;979:131-42; discussion 188-96. [Medline].
Ottesen EA. The Wellcome Trust Lecture. Infection and disease in lymphatic filariasis: an immunological perspective. Parasitology. 1992;104 Suppl:S71-9. [Medline].
Taylor MJ, Hoerauf A. Wolbachia bacteria of filarial nematodes. Parasitol Today. Nov 1999;15(11):437-42. [Medline].
Kazura J. Guerrant R, Walker DH, Weller PF, eds. Tropical Infectious Diseases: Principles, Pathogens and Practice. Vol 2. Philadelphia, PA: Churchill Livingstone; 1999:852.
Pani SP, Yuvaraj J, Vanamail P, Dhanda V, Michael E, Grenfell BT. Episodic adenolymphangitis and lymphoedema in patients with bancroftian filariasis. Trans R Soc Trop Med Hyg. Jan-Feb 1995;89(1):72-4. [Medline].
Chanteau S, Moulia-Pelat JP, Glaziou P, Nguyen NL, Luquiaud P, Plichart C, et al. Og4C3 circulating antigen: a marker of infection and adult worm burden in Wuchereria bancrofti filariasis. J Infect Dis. Jul 1994;170(1):247-50. [Medline].
Nguyen NL, Plichart C, Esterre P. Assessment of immunochromatographic test for rapid lymphatic filariasis diagnosis. Parasite. Dec 1999;6(4):355-8. [Medline].
Schuetz A, Addiss DG, Eberhard ML, Lammie PJ. Evaluation of the whole blood filariasis ICT test for short-term monitoring after antifilarial treatment. Am J Trop Med Hyg. Apr 2000;62(4):502-3. [Medline].
Lal RB, Ottesen EA. Enhanced diagnostic specificity in human filariasis by IgG4 antibody assessment. J Infect Dis. Nov 1988;158(5):1034-7. [Medline].
Dreyer G, Noroes J, Amaral F, Nen A, Medeiros Z, Coutinho A, et al. Direct assessment of the adulticidal efficacy of a single dose of ivermectin in bancroftian filariasis. Trans R Soc Trop Med Hyg. Jul-Aug 1995;89(4):441-3. [Medline].
Ottesen EA. Filarial infections. Infect Dis Clin North Am. Sep 1993;7(3):619-33. [Medline].
[Best Evidence] Coulibaly YI, Dembele B, Diallo AA, Lipner EM, Doumbia SS, Coulibaly SY, et al. A randomized trial of doxycycline for Mansonella perstans infection. N Engl J Med. Oct 8 2009;361(15):1448-58. [Medline].
Ottesen EA. Major progress toward eliminating lymphatic filariasis. N Engl J Med. Dec 5 2002;347(23):1885-6. [Medline].
WHO. Global programme to eliminate lymphatic filariasis. Wkly Epidemiol Rec. Sep 12 2008;83(37):333-41. [Medline].
Grieve RB, Wisnewski N, Frank GR, Tripp CA. Vaccine research and development for the prevention of filarial nematode infections. Pharm Biotechnol. 1995;6:737-68. [Medline].
Baird JK, Neafie RC, Lanoie L, Connor DH. Adult Mansonella perstans in the abdominal cavity in nine Africans. Am J Trop Med Hyg. Nov 1987;37(3):578-84. [Medline].
Bazi T, Finan R, Zourob D, Sabbagh AS, Nasnas R, Zreik TG. Filariasis infection is a probable cause of implantation failure in in vitro fertilization cycles. Fertil Steril. Jun 2006;85(6):1822.e13-5. [Medline].
Carme B, Boulesteix J, Boutes H, Puruehnce MF. Five cases of encephalitis during treatment of loiasis with diethylcarbamazine. Am J Trop Med Hyg. Jun 1991;44(6):684-90. [Medline].
Chernin E. The disappearance of bancroftian filariasis from Charleston, South Carolina. Am J Trop Med Hyg. Jul 1987;37(1):111-4. [Medline].
Connor DH, George GH, Gibson DW. Pathologic changes of human onchocerciasis: implications for future research. Rev Infect Dis. Nov-Dec 1985;7(6):809-19. [Medline].
Connor DH, Gibson DW, Neafie RC, et al. Sowda--onchocerciasis in north Yemen: a clinicopathologic study of 18 patients. Am J Trop Med Hyg. Jan 1983;32(1):123-37. [Medline].
Davidson RN, Godfrey-Faussett P, Bryceson AD. Adverse reactions in expatriates treated with ivermectin. Lancet. Oct 20 1990;336(8721):1005. [Medline].
De Sole G, Remme J, Awadzi K, et al. Adverse reactions after large-scale treatment of onchocerciasis with ivermectin: combined results from eight community trials. Bull World Health Organ. 1989;67(6):707-19. [Medline].
Dreyer G, Figueredo-Silva J, Neafie RC, et al. Lymphatic filariasis. In: Nelson AM, Horsburgh CR, eds. Pathology of Emerging Infections. Vol 2. Washington, DC: American Society for Microbiology; 1998:317-42.
Dreyer G, Noroes J, Figueredo-Silva J, Piessens WF. Pathogenesis of lymphatic disease in bancroftian filariasis: A clinical perspective. Parasitol Today. Dec 2000;16(12):544-8. [Medline].
Duke BO, Zea-Flores G, Castro J, et al. Effects of three-month doses of ivermectin on adult Onchocerca volvulus. Am J Trop Med Hyg. Feb 1992;46(2):189-94. [Medline].
Dunyo SK, Appawu M, Nkrumah FK, et al. Lymphatic filariasis on the coast of Ghana. Trans R Soc Trop Med Hyg. Nov-Dec 1996;90(6):634-8. [Medline].
Dunyo SK, Nkrumah FK, Simonsen PE. Single-dose treatment of Wuchereria bancrofti infections with ivermectin and albendazole alone or in combination: evaluation of the potential for control at 12 months after treatment. Trans R Soc Trop Med Hyg. Jul-Aug 2000;94(4):437-43. [Medline].
Eberhard ML, Lammie PJ. Laboratory diagnosis of filariasis. Clin Lab Med. Dec 1991;11(4):977-1010. [Medline].
Garcia LS, Bruckner DA. Filarial nematodes. In: Diagnostic Medical Parasitology. 3rd ed. Washington, DC: American Society for Microbiology; 1997:275-307.
Grove DI. Tissue nematodes (Trichinosis, Dracunculiasis, Filariasis). In: Mandell GL, Bennett JE, Dolin R, eds. Principles and Practice of Infectious Diseases. 5th ed. New York, NY: Churchill Livingstone; 2000:2946-7.
Gutierrez Y, Catellier MJ, Wicker DL, et al. Extrapulmonary Dirofilaria immitis-like infections in the Western Hemisphere. Am J Surg Pathol. Mar 1996;20(3):299-305. [Medline].
Iqbal J, Sher A. Determination of the prevalence of lymphatic filariasis among migrant workers in Kuwait by detecting circulating filarial antigen. J Med Microbiol. Apr 2006;55(Pt 4):401-5. [Medline].
Klion AD, Massougbodji A, Sadeler BC, et al. Loiasis in endemic and nonendemic populations: immunologically mediated differences in clinical presentation. J Infect Dis. Jun 1991;163(6):1318-25. [Medline].
Limaye AP, Abrams JS, Silver JE, et al. Interleukin-5 and the posttreatment eosinophilia in patients with onchocerciasis. J Clin Invest. Oct 1991;88(4):1418-21. [Medline].
McMahon JE. The examination--time/dose interval in the provocation of nocturnally periodic microfilariae of Wuchereria bancrofti with diethylcarbamazine and the practical uses of the test. Tropenmed Parasitol. Mar 1982;33(1):28-30. [Medline].
McMahon JE, Simonsen PE. Filariases. In: Cook GC, ed. Manson's Tropical Diseases. 20th ed. London, England: WB Saunders Co; 1996:1321-68.
Muro A, Genchi C, Cordero M, Simon F. Human dirofilariasis in the European Union. Parasitol Today. Sep 1999;15(9):386-9. [Medline].
Nanduri J, Kazura JW. Clinical and laboratory aspects of filariasis. Clin Microbiol Rev. Jan 1989;2(1):39-50. [Medline].
Neva FA, Ottesen EA. Tropical (filarial) eosinophilia. N Engl J Med. May 18 1978;298(20):1129-31. [Medline].
Newland HS, White AT, Greene BM, et al. Ocular manifestations of onchocerciasis in a rain forest area of west Africa. Br J Ophthalmol. Mar 1991;75(3):163-9. [Medline].
Noireau F, Apembet JD, Nzoulani A, Carme B. Clinical manifestations of loiasis in an endemic area in the Congo. Trop Med Parasitol. Mar 1990;41(1):37-9. [Medline].
Noireau F, Pichon G. Population dynamics of Loa loa and Mansonella perstans infections in individuals living in an endemic area of the Congo. Am J Trop Med Hyg. Jun 1992;46(6):672-6. [Medline].
Nutman TB. Experimental infection of humans with filariae. Rev Infect Dis. Sep-Oct 1991;13(5):1018-22. [Medline].
Nutman TB, Nash TE, Ottesen EA. Ivermectin in the successful treatment of a patient with Mansonella ozzardi infection. J Infect Dis. Oct 1987;156(4):662-5. [Medline].
Ottesen EA, Duke BO, Karam M, Behbehani K. Strategies and tools for the control/elimination of lymphatic filariasis. Bull World Health Organ. 1997;75(6):491-503. [Medline].
Ottesen EA, Ismail MM, Horton J. The role of albendazole in programmes to eliminate lymphatic filariasis. Parasitol Today. Sep 1999;15(9):382-6. [Medline].
Ottesen EA, Vijayasekaran V, Kumaraswami V, et al. A controlled trial of ivermectin and diethylcarbamazine in lymphatic filariasis. N Engl J Med. Apr 19 1990;322(16):1113-7. [Medline].
Partono F, Pribadi PW, Soewarta A. Epidemiological and clinical features of Brugia timori in a newly established village. Karakuak, West Flores, Indonesia. Am J Trop Med Hyg. Sep 1978;27(5):910-5. [Medline].
Poltera AA, Reyna O, Zea-Flores G, et al. Use of an ophthalmologic ultrasound scanner in human onchocercal skin nodules for non-invasive sequential assessment during a macrofilaricidal trial with amocarzine in Guatemala. The first experiences. Trop Med Parasitol. Sep 1991;42(3):303-7. [Medline].
Ramzy RM, Gad AM, Faris R, Weil GJ. Evaluation of a monoclonal-antibody based antigen assay for diagnosis of Wuchereria bancrofti infection in Egypt. Am J Trop Med Hyg. Jun 1991;44(6):691-5. [Medline].
Rao RU, Atkinson LJ, Ramzy RM, Helmy H, Farid HA, Bockarie MJ. A real-time PCR-based assay for detection of Wuchereria bancrofti DNA in blood and mosquitoes. Am J Trop Med Hyg. May 2006;74(5):826-32. [Medline].
Sabry M, Gamal H, el-Masry N, Kilpatrick ME. A placebo-controlled double-blind trial for the treatment of bancroftian filariasis with ivermectin or diethylcarbamazine. Trans R Soc Trop Med Hyg. Sep-Oct 1991;85(5):640-3. [Medline].
Scheiber P, Braun-Munzinger RA, Southgate BA. A new technique for the determination of microfilarial densities in onchocerciasis. Bull World Health Organ. 1976;53(1):130-3. [Medline].
Shah MK. Human pulmonary dirofilariasis: review of the literature. South Med J. Mar 1999;92(3):276-9. [Medline].
Srividya A, Pani SP, Rajagopalan PK, et al. The dynamics of infection and disease in bancroftian filariasis. Trans R Soc Trop Med Hyg. Mar-Apr 1991;85(2):255-9. [Medline].
Stingl P, Ross M, Gibson DW, et al. A diagnostic "patch test" for onchocerciasis using topical diethylcarbamazine. Trans R Soc Trop Med Hyg. 1984;78(2):254-8. [Medline].
Taylor AER, Denham DA. Diagnosis of filarial infections. Trop Dis Bull. 1992;89:R1-R33.
Turner JD, Mand S, Debrah AY, Muehlfeld J, Pfarr K, McGarry HF. A randomized, double-blind clinical trial of a 3-week course of doxycycline plus albendazole and ivermectin for the treatment of Wuchereria bancrofti infection. Clin Infect Dis. Apr 15 2006;42(8):1081-9. [Medline].
Wamae CN, Roberts JM, Eberhard ML, et al. Kinetics of circulating human IgG4 after diethylcarbamazine and ivermectin treatment of bancroftian filariasis. J Infect Dis. Jun 1992;165(6):1158-60. [Medline].
Wartmann WB. Filariasis in American armed forces in World War II. Medicine. 1947;26:334-94.
Wegesa P, McMahon JE, Abaru DE, et al. Tanzania filariasis project. Survey methodology and clinical manifestations of bancroftian filariasis. Acta Trop. Dec 1979;36(4):369-77. [Medline].
Weil GJ, Lammie PJ, Richards FO Jr, Eberhard ML. Changes in circulating parasite antigen levels after treatment of bancroftian filariasis with diethylcarbamazine and ivermectin. J Infect Dis. Oct 1991;164(4):814-6. [Medline].
Weil GJ, Lammie PJ, Weiss N. The ICT Filariasis Test: A rapid-format antigen test for diagnosis of bancroftian filariasis. Parasitol Today. Oct 1997;13(10):401-4. [Medline].
Weil GJ, Steel C, Liftis F, et al. A rapid-format antibody card test for diagnosis of onchocerciasis. J Infect Dis. Dec 2000;182(6):1796-9. [Medline].
World Health Organization. The World Health Report 1995--bridging the gaps. World Health Forum. 1995;16(4):377-85. [Medline].
Further Reading
Keywords
filariasis, bancroftian filariasis, elephantiasis, hanging groins, leopard skin, river blindness, sowda, loaiasis, loiasis, Loa loa, Onchocerca volvulus, Mansonella streptocerca, Wuchereria bancrofti, Brugia malayi, Brugia timori, Mansonella perstans, Mansonella ozzardi, tropical pulmonary eosinophilia, TPE, adenolymphangitis, ADL
