eMedicine Specialties > Infectious Diseases > Parasitic Infections

Filariasis

Author: Michael D Nissen, MBBS, BMedSc, 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
Coauthor(s): 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
Contributor Information and Disclosures

Updated: Jun 9, 2006

Introduction

Background

Filariasis is a disease group affecting humans and animals that is 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 these 8 species cause natural infections in humans. The parasites of the cutaneous and lymphatic groups are of the most significant clinical interest. 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]).

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 circadian periodicity in the peripheral circulation over a 24-hour period. 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. Microfilariae then 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.

Frequency

United States

No form of human filariasis currently is endemic to the United States. W bancrofti once was 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 rarely are 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 mainly results from the host reaction to microfilariae or developing adult worms in different areas of the body.

Race

No racial predilection is known.

Sex

Both sexes are equally susceptible to infection. 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 for filariasis are species-dependent and body-site–dependent and can be acute or chronic in nature.

  • Lymphatic filariasis
    • The symptoms of lymphatic filariasis predominantly result from the presence of adult worms residing in the lymphatics.
    • Symptoms include fever, inguinal or axillary lymphadenopathy, testicular and/or inguinal pain, skin exfoliation, and limb or genital swelling.
    • Patients with microfilaremia generally are asymptomatic, although subjects 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
    • Tropical pulmonary eosinophilia (TPE) is a form of occult filariasis.
    • Presenting symptoms include a paroxysmal dry cough, wheezing, dyspnea, anorexia, malaise, and weight loss.
  • D immitis infection
    • Symptoms are respiratory in nature, with chest discomfort, cough, fever, and hemoptysis.
    • Immature forms of the worm also may cause breast and subcutaneous abscesses.
  • D repens infection: Symptoms usually are a subcutaneous, submucosal, or eyelid lump.
  • 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.
  • Loaiasis
    • The symptoms of L loa infection usually are confined to subcutaneous swellings on the extremities, localized pain, pruritus, and urticaria.
    • Microfilaremia tends to be asymptomatic.
  • M ozzardi, M perstans, and M streptocerca infection
    • Infections from Mansonella species usually are 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.

  • Lymphatic filariasis
    • Acute manifestations of lymphatic filariasis usually are referred to as adenolymphangitis (ADL). ADL 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.
    • 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.
  • Tropical pulmonary eosinophilia
    • Scattered wheezes and crackles are heard in both lung fields.
    • Lymphadenopathy and hepatomegaly may be present.
  • D immitis infection: Reduced localized air entry may be detected upon chest auscultation.
  • D repens infection: Signs usually are a painless subcutaneous, submucosal, or eyelid lump.
  • Onchocerciasis
    • The clinical triad of infection is dermatitis, skin nodules (ie, onchocercomas), and ocular lesions.
    • Skin lesions include edema, pruritus, erythema, papules, scablike eruptions, altered pigmentation, and lichenification.
    • Skin nodules tend to be common over bony prominences.
    • Eye lesions usually are related to the duration and severity of infection and are caused by an abnormal host immune response to microfilariae. The common eye findings are punctate keratitis, pannus formation, corneal fibrosis, iridocyclitis, glaucoma, choroiditis, and optic atrophy.
  • Loaiasis
    • The diagnostic feature of disease 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.
    • 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 hyporesponsive to parasite antigen, have increased eosinophilia, and result in the presence of high levels of serum immunoglobulin E (IgE).
    • Patterns of onchocercal eye disease also are associated with parasite strain differences at the DNA level.
  • Loaiasis
    • Mango flies or deerflies of Chrysops transmit loaiasis.
    • 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 also are higher in nonresidents with infection.
  • L loa meningoencephalopathy
    • Meningoencephalopathy is a severe and often fatal complication of infection.
    • The syndrome usually is related to diethylcarbamazine (DEC) administration to individuals with high-density microfilaremia, but it may occur without drug therapy. DEC causes a large influx of microfilariae into the cerebrospinal fluid, leading to capillary obstruction, cerebral edema, hypoxia, and coma.
    • Localized necrotizing granulomas also are present in response to microfilariae.

More on Filariasis

Overview: Filariasis
Differential Diagnoses & Workup: Filariasis
Treatment & Medication: Filariasis
Follow-up: Filariasis
Multimedia: Filariasis
References

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Further Reading

Keywords

filariasis, bancroftian filariasis, elephantiasis, hanging groins, leopard skin, river blindness, sowda, loaiasis, Loa loa, Onchocerca volvulus, Mansonella streptocerca, Wuchereria bancrofti, Brugia malayi, Brugia timori, Mansonella perstans, Mansonella ozzardi, tropical pulmonary eosinophilia, TPE, adenolymphangitis, ADL

Contributor Information and Disclosures

Author

Michael D Nissen, MBBS, BMedSc, 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
Michael D Nissen, MBBS, BMedSc, FRACP, FRCPA is a member of the following medical societies: American Academy of Pediatrics, American Society for Microbiology, Pediatric Infectious Diseases Society, Royal Australasian College of Physicians, and Royal College of Pathologists of Australasia
Disclosure: Nothing to disclose.

Coauthor(s)

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.

Medical Editor

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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Thomas M Kerkering, MD, Professor of Medicine and Microbiology, Department of Internal Medicine, Division of Infectious Disease, Brody School of Medicine at East Carolina University
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.

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

 
 
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