Pediatric Filariasis Medication

  • Author: Robert W Tolan Jr, MD; Chief Editor: Russell W Steele, MD   more...
 
Updated: Jan 10, 2012
 

Medication Summary

Ivermectin is now considered the drug of choice for the treatment of all forms of filariasis, except Mansonella, in which its effects are unproven.

Because M perstans is resistant to standard antiparasitic treatment, doxycycline is sometimes used to eradicate Wolbachia, an endosymbiont found in most filarial species. Doxycycline treatment typically results in death or sterility of the filarial nematode. In an open-label, randomized trial, Coulibaly et al recruited patients infected with M perstans from 4 African villages in Mali.[8] Patients were randomly assigned to receive doxycycline at 200 mg orally every day for 6 weeks (n=106) or no treatment (n=110).

At 6 months, patients co-infected with W bancrofti underwent a second randomization to receive a single dose of albendazole (400 mg) plus ivermectin (150 mcg/kg) or no treatment. At 12 months, 97% of patients who received doxycycline had no detectable blood levels of M perstans compared with 16% in the group that did not receive treatment (p < 0.001). At 36 months, M perstans remained suppressed in 75% of patients who received doxycycline. This suggests that doxycycline is an effective therapy for M perstans.

In the United States, ivermectin can be obtained from the Centers for Disease Control and Prevention (CDC); in endemic areas of the world, it is provided free by the Mectizan Donation Program.

The addition of albendazole seems to improve response. More recently, 6-week and 8-week courses of doxycycline have compared favorably to ivermectin plus albendazole (a 3-week course induced amicrofilaremia but was not curative). Doxycycline therapy may be more readily available and better tolerated for some patients.

Recent studies have validated the use of single-dose regimens of ivermectin and diethylcarbamazine (DEC) or albendazole to reduce W bancrofti microfilaremia, antigenemia, and clinical manifestations for large-scale control and eradication programs.

Moxidectin, an investigational agent, is under investigation as an alternative to ivermectin for the treatment of river blindness. This agent may shorten the number of annual treatments to 6.

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Antihelmintic agents

Class Summary

Parasite biochemical pathways are different from the human host, thus toxicity is directed to the parasite, egg, or larvae. The mechanism of action varies within the drug class. Antiparasitic actions may include the following:

  • Inhibition of microtubules causing irreversible block of glucose uptake
  • Tubulin polymerization inhibition
  • Depolarizing neuromuscular blockade
  • Cholinesterase inhibition
  • Increased cell membrane permeability, resulting in intracellular calcium loss
  • Vacuolization of the schistosome tegument
  • Increased cell membrane permeability to chloride ions via alteration of chloride channels
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Ivermectin (Mectizan, 22,23-dihydroavermectin)

 

Macrocyclic lactone derivative of Avermectin. Exerts its antiparasitic action by acting as a potent agonist at GABA receptors and potentiating the inhibitory signals sent to motor neurons that paralyze the parasite. Has no paralytic action in humans because GABA is confined to CNS in humans, and ivermectin does not cross the blood brain barrier. Mechanism of action thought to involve GABA pathways and chloride ion channel permeability. Potent microfilaricide and macrofilaricidal for W bancrofti in multiple doses. Used alone or in combination with DEC.

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Diethylcarbamazine (DEC, Hetrazan)

 

Piperazine derivative. Immobilizes microfilariae by decreasing muscle activity due to hyperpolarization effects, but precise mechanism not understood. Alteration of surface membrane and enhanced destruction by host's immune system also occur. May enhance adhesion of granulocytes via antibody-dependent and antibody-independent mechanisms. Interference by microfilarial intracellular processing and transport of specific macromolecules by DEC is also hypothesized.

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Suramin (Germanin, Antrypol, Naganol)

 

Antitrypanosome and antihelminthic. Only drug currently in clinical use for onchocerciasis that is effective against adult worms. Use is restricted because of frequency of associated complications and its intrinsic toxicity. WHO advises to consider only for curative treatment of individuals in areas without transmission of onchocerciasis, for treatment of individuals leaving an endemic area, and for severe hyperreactive onchodermatitis in which symptoms are not adequately controlled with ivermectin. Only available from the CDC Drug Service.

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Mebendazole (Banworm, SQ Worm, Vermox)

 

Benzimidazole derivative. Causes worm death by selectively and irreversibly blocking uptake of glucose and other nutrients in susceptible adult intestine where helminths dwell.

Flubendazole (Flicum, Fluvermal)

 

Not available in United States. Benzimidazole carbamate antihelminthic that is an analogue of mebendazole.

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Albendazole (Albenza)

 

Methyl [5-(propylthio)-1H-benzimidazol-2yl] carbamate. Broad-spectrum antihelminthic. Action is thought to mainly be intraintestinal; although, at higher doses, sufficient amount is absorbed and metabolized to an active sulfoxide metabolite to have therapeutic effect against tissue parasites.

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Antibiotics

Class Summary

These agents may provide an alternative to anthelminthics.

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Doxycycline (Bio-Tab, Vibramycin)

 

Broad-spectrum, synthetically derived bacteriostatic antibiotic in the tetracycline class. Almost completely absorbed, concentrates in bile, and is excreted in urine and feces as a biologically active metabolite in high concentrations.

Inhibits protein synthesis and, thus, bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria. May block dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

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Contributor Information and Disclosures
Author

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

Specialty Editor Board

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.

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.

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.

Daniel Rauch, MD, FAAP  Director, Pediatric Hospitalist Program, Associate Professor, Department of Pediatrics, New York University School of Medicine

Daniel Rauch, MD, FAAP is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, and Society of Hospital Medicine

Disclosure: Baxter Honoraria Consulting

Chief Editor

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.

Additional Contributors

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors Michael D Nissen, MBBS, FRACP, FRCPA, and John Charles Walker, MSc, PhD, to the original writing and development of this article.

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The life cycle of lymphatic filarioids in humans (Wuchereria bancrofti, Brugia malayi, Brugia timori) and the mosquito vectors (Aedes, Anopheles, Culex, and Mansonia genera) is shown. Life cycles for other filarioid nematodes (Onchocerca volvulus, Loa loa, Mansonella perstans) are identical. The body location of adult worms and the microfilariae differ, as do the arthropod intermediate hosts and vectors.
Lymphatic filariasis due to Wuchereria bancrofti causing limb lymphedema, inguinal lymphadenopathy, and hydrocele. Photograph taken by Professor Bruce McMillan and donated by Dr John Walker.
Adult worms of Wuchereria bancrofti in a cross section isolated from a testicular lump.
Microfilaria of Wuchereria bancrofti in a peripheral blood smear.
Shown here are onchocercomas of the forearm skin, also called sowda, in a Sudanese man.
Adult Onchocerca volvulus contained within onchocercomas of the skin.
Microfilariae of Loa loa detected in skin snips.
Microfilariae of Mansonella perstans in peripheral blood.
 
 
 
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