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Filariasis

  • Author: Siddharth Wayangankar, MD, MPH; Chief Editor: Pranatharthi Haran Chandrasekar, MBBS, MD  more...
 
Updated: Dec 10, 2015
 

Practice Essentials

Filariasis is a disease group affecting humans and animals, caused by filariae; ie, nematode parasites of the order Filariidae.[1] Of the hundreds of described filarial parasites, only 8 species cause natural infections in humans. The World Health Organization (WHO) has identified lymphatic filariasis as the second leading cause of permanent and long-term disability in the world, after leprosy.

In lymphatic filariasis, repeated episodes of inflammation and lymphedema lead to lymphatic damage, chronic swelling, and elephantiasis of the legs (see the image below), arms, scrotum, vulva, and breasts .[2, 3, 4, 5, 6, 7]

Filariasis. Unilateral left lower leg elephantiasi Filariasis. Unilateral left lower leg elephantiasis secondary to Wuchereria bancrofti infection in a boy.

Signs and symptoms

Lymphatic filariasis

  • Fever
  • Inguinal or axillary lymphadenopathy
  • Testicular and/or inguinal pain
  • Skin exfoliation
  • Limb or genital swelling - Repeated episodes of inflammation and lymphedema lead to lymphatic damage, chronic swelling, and elephantiasis of the legs, arms, scrotum, vulva, and breasts.

The following acute syndromes have been described in filariasis:

  • Acute adenolymphangitis (ADL)
  • Filarial fever - Characterized by fever without associated adenitis
  • Tropical pulmonary eosinophilia (TPE)

Onchocerciasis

The clinical triad of infection in onchocerciasis is as follows:

  • Dermatitis - Skin lesions include edema, pruritus, erythema, papules, scablike eruptions, altered pigmentation, and lichenification
  • Skin nodules (ie, onchocercomas) - Skin nodules tend to be common over bony prominences
  • Ocular lesions - Eye lesions are usually related to the duration and severity of infection and are caused by an abnormal host immune response to microfilariae; loss of visual acuity may occur

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.

Mansonella infections

These are usually asympt omatic. If symptoms are present, they may include fever, pruritus, skin lumps, lymphadenitis, and abdominal pain.

See Clinical Presentation for more detail.

Diagnosis

Microfilariae can be detected through examination of the following:

  • Blood - The microfilariae of all species that cause lymphatic filariasis and the microfilariae of Loa loa, Mansonella ozzardi, and M perstans are detected in blood [8]
  • Urine - If lymphatic filariasis is suspected, urine should be examined macroscopically for chyluria and then concentrated to examine for microfilariae
  • Skin - Onchocerca volvulus and M streptocerca infections are diagnosed when microfilariae are detected in multiple skin-snip specimens from different sites located on both sides of the body; the Mazzotti test allows a presumptive diagnosis of cutaneous filariasis to be made when skin snips are negative for microfilariae
  • Eye - Microfilariae of O volvulus may be detected in the cornea or anterior chamber of the eye using slit-lamp examination

The following imaging studies can be used in the evaluation of filariasis:

  • Chest radiography - Diffuse pulmonary infiltrates are visible in patients with TPE
  • Ultrasonography - Can be used to demonstrate and monitor lymphatic obstruction of the inguinal and scrotal lymphatics; has also been used to demonstrate the presence of viable worms
  • Lymphoscintigraphy [9]

Histologic findings include the following:

  • Lymphatic filariasis - Affected lymph nodes demonstrate fibrosis and lymphatic obstruction with the creation of collateral channels
  • Elephantiasis - The skin is characterized by hyperkeratosis, acanthosis, lymph and fatty tissue, loss of elastin fibers, and fibrosis
  • Onchocerciasis - Onchocercomas have a central stromal and granulomatous, inflammatory region where the adult worms are found and a peripheral, fibrous section; microfilariae in the skin incite a low-grade inflammatory reaction with loss of elasticity and fibrotic scarring

See Workup for more detail.

Management

Anthelmintics used in the treatment of filariasis include the following:

  • Diethylcarbamazine (DEC)
  • Ivermectin - Drug of choice for Wuchereria bancrofti
  • Suramin - Only drug in clinical use for onchocerciasis that is effective against adult worms
  • Mebendazole
  • Flubendazole
  • Albendazole

Surgery

In lymphatic filariasis, large hydroceles and scrotal elephantiasis can be managed with surgical excision. Correcting gross limb elephantiasis with surgery is less successful and may necessitate multiple procedures and skin grafting.

In onchocerciasis, nodulectomy with local anesthetic is a common treatment to reduce skin and eye complications.

See Treatment and Medication for more detail.

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Background

Filariasis is a disease group affecting humans and animals, caused by filariae; ie, nematode parasites of the order Filariidae.[1] Filarial parasites can be classified according to the habitat of the adult worms in the vertebral host, as follows (see Pathophysiology, Etiology, and Workup):

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 first-stage larvae, known as microfilariae (eg, Dirofilaria immitis [dog heartworm], D [Nochtiella] repens, and D tenuis [raccoon heartworm]). (See the image below.)

Filariasis. This figure displays the life cycle of 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.

Filariasis has a significant economic and psychosocial impact in endemic areas, disfiguring and/or incapacitating more than 40 million individuals.[11] Studies from the Indian subcontinent have shown that infected patients lose significant time from work because of the disease,[12] costing the national treasury a minimum of $842 million per year. (See Epidemiology, Prognosis, Clinical Presentation, and Treatment.)[13]

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 occurs on Timor island, in Indonesia. (See Epidemiology.)

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. (See Pathophysiology and Etiology.)[14]

As with most helminths, adult filarial parasites replicate in a definitive 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.

Patient education

Patients should learn to protect against insect vectors and to refrain from self-treatment regimens, especially with diethylcarbamazine (DEC), since this drug can lead to meningoencephalopathy. (See Treatment and Medication.)

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Pathophysiology

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.[15]

Microfilariae undergo 2 developmental changes in the insect. Third-stage larvae then are inoculated back into the vertebral host during the act of feeding for the final 2 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 prepatent 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 [16, 17]
  • The duration and level of exposure to infective insect bites [18]
  • The number of secondary bacterial and fungal infections [16]
  • The degree of host immune response [19]

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.[20]

Studies have shown that there is a familial tendency to lymphatic obstruction, providing support for the hypothesis that host genes influence lymphedema susceptibility.[21] Studies also suggest that microfilaremia may be increased in individuals with low levels of mannose-binding lectin, suggesting a genetic predisposition.[7] Further, a propensity to develop chronic disease has been demonstrated in patients with polymorphisms of endothelin-1 and tumor necrosis factor receptor II.[22]

Prenatal exposure seems to be an important determinant in conferring greater immune tolerance to parasite antigen.[23] Thus, individuals from endemic areas are often asymptomatic until late in the 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.

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.[24]

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Etiology

Lymphatic filariasis

Mosquitoes of the genera Aedes, Anopheles, Culex, or Mansonia are the intermediate hosts and vectors of all species that cause lymphatic filariasis.[25]

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. Infection with B timori appears to result in more abscesses than infection with B malayi or W bancrofti. (See the image below.)

Filarial abscess scar on the left upper thigh in a Filarial abscess scar on the left upper thigh in a young male who is positive for Wuchereria bancrofti microfilariae

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. (The skin of individuals with elephantiasis is characterized by hyperkeratosis, acanthosis, lymph and fatty tissue, loss of elastin fibers, and fibrosis.)

B malayi elephantiasis is more likely to affect the upper and lower limbs, with genital pathology and chyluria being rare. Secondary bacterial infection in elephantiasis can result in blindness.

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 as follows:

Tropical pulmonary eosinophilia (TPE) - Most likely results from a hyperresponsiveness to W bancrofti or B malayi antigen; symptoms result from allergic and inflammatory reactions elicited by the microfilariae and parasite antigens that the lungs clear from the bloodstream

D immitis or D repens infection - 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.

  • Filarial arthritis
  • Filarial breast abscess
  • Filaria-associated immune-complex glomerulonephritis

Onchocerciasis

O volvulus 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.[26]

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. (See the image below.)[27]

Filariasis. Microfilariae of Loa loa detected in s Filariasis. Microfilariae of Loa loa detected in skin snips.

L loa meningoencephalopathy

Meningoencephalopathy is a severe and often fatal complication of infection. This syndrome is usually related to diethylcarbamazine (DEC) administration in individuals with high-density microfilaremia but it may occur without drug therapy.[28]

DEC causes a large influx of microfilariae into the cerebrospinal fluid, leading to capillary obstruction, cerebral edema, hypoxia, and coma. Localized necrotizing granulomas are also present, in response to microfilariae. Endomyocardial fibrosis, nephritic syndrome, and venous thrombosis may also be observed.

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Epidemiology

Occurrence in the 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.

Two cases of ocular onchocerciasis have been reported in the United States,[29] as has a single case of spinal mass in a toddler due to Onchocerca lupi infection.[30]

International occurrence

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.[31, 27]

Sex- and age-related demographics

Both sexes are equally susceptible to filariasis. Because of different local and cultural practices, however, as well as differences in exposure to insect vectors, one sex or the other may be exposed to infection more often.

Individuals of all ages are susceptible to infection and are 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.

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Prognosis

The prognosis in filariasis is good if infection is recognized and treated early. Filarial diseases are rarely fatal, but the consequences of infection can cause significant personal and socioeconomic hardship for those who are affected.

The morbidity of human filariasis results mainly from the host reaction to microfilariae or developing adult worms in different areas of the body. The WHO has identified lymphatic filariasis as the second leading cause of permanent and long-term disability in the world, after leprosy.

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Contributor Information and Disclosures
Author

Siddharth Wayangankar, MD, MPH Resident Physician, Department of Internal Medicine, Oklahoma University Health Sciences Center

Siddharth Wayangankar, MD, MPH is a member of the following medical societies: American College of Physicians

Disclosure: Nothing to disclose.

Coauthor(s)

Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, Oklahoma State Medical Association, Southern Society for Clinical Investigation, Association of Professors of Medicine, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Rhett L Jackson, MD Associate Professor and Vice Chair for Education, Department of Medicine, Director, Internal Medicine Residency Program, University of Oklahoma College of Medicine; Assistant Chief, Medicine Service, Oklahoma City Veterans Affairs Hospital

Rhett L Jackson, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, American Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Pranatharthi Haran Chandrasekar, MBBS, MD Professor, Chief of Infectious Disease, Program Director of Infectious Disease Fellowship, Department of Internal Medicine, Wayne State University School of Medicine

Pranatharthi Haran Chandrasekar, MBBS, MD is a member of the following medical societies: American College of Physicians, American Society for Microbiology, International Immunocompromised Host Society, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Acknowledgements

Rosemary Johann-Liang, MD Medical Officer, Infectious Diseases and Pediatrics, Division of Special Pathogens and Immunological Drug Products, Center for Drug Evaluation and Research, Food and Drug Administration

Rosemary Johann-Liang, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Thomas M Kerkering, MD Chief of Infectious Diseases, Virginia Tech Carilion School of Medicine

Thomas M Kerkering, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Public Health Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Medical Society of Virginia, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Charles S Levy, MD Associate Professor, Department of Medicine, Section of Infectious Disease, George Washington University School of Medicine

Charles S Levy, MD is a member of the following medical societies: American College of Physicians, Infectious Diseases Society of America, and Medical Society of the District of Columbia

Disclosure: Nothing to disclose.

Michael D Nissen, MBBS, FRACP, FRCPA Associate Professor in Biomolecular, Biomedical Science & Health, Griffith University; Director of Infectious Diseases and Unit Head of Queensland Paediatric Infectious Laboratory, Sir Albert Sakzewski Viral Research Centre, Royal Children's Hospital

Disclosure: Nothing to disclose.

Russell W Steele, MD Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Robert W Tolan Jr, MD Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine

Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility

Disclosure: Novartis Honoraria Speaking and teaching

John Charles Walker, MSc, PhD Head, Department of Parasitology, Center for Infectious Diseases and Microbiology, Westmead Hospital, Westmead, Australia; Senior Lecturer, Department of Medicine, University of Sydney, Australia

Disclosure: Nothing to disclose.

Martin Weisse, MD Program Director, Associate Professor, Department of Pediatrics, West Virginia University

Martin Weisse, MD is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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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.
Filarial abscess scar on the left upper thigh in a young male who is positive for Wuchereria bancrofti microfilariae
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 the previous image. 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 the previous image, 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.
Filariasis. Adult worms of Wuchereria bancrofti in cross section isolated from a testicular lump.
Filariasis. Microfilaria of Wuchereria bancrofti in a peripheral blood smear.
Filariasis. Appearance of microfilariae after concentration of venous blood with a Nuclepore filter.
Filariasis. Onchocercomas of the forearm skin (sowda) in a Sudanese man.
Filariasis. Adult Onchocerca volvulus contained within onchocercomas of the skin.
Filariasis. Microfilariae of Loa loa detected in skin snips.
Filariasis. Microfilariae of Mansonella perstans in peripheral blood.
 
 
 
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