Updated: Oct 23, 2008
Nematode infections in humans include ascariasis, trichuriasis, hookworm, enterobiasis, strongyloidiasis, filariasis, and trichinosis, among others. The phylum Nematoda, also known as the roundworms, is the second largest phylum in the animal kingdom, encompassing up to 500,000 species. Members of Nematoda are elongated, with bilaterally symmetric bodies that contain an intestinal system and a large body cavity.
Many roundworm species are free living in nature. Recent data have demonstrated that approximately 60 species of roundworms parasitize humans. Intestinal roundworm infections constitute the largest group of helminthic diseases in humans. According to a 2005 report by the World Health Organization (WHO), approximately 0.807-1.221 billion humans have ascariasis, 604-795 million have trichuriasis, and 576-740 million have hookworm infections worldwide.1
The life cycle of parasitic nematodes is clinically important. Some nematode infections can be transmitted directly from infected to uninfected people; in others, the nematode eggs must undergo a process of maturation outside the host. In a third category, the parasites may spend a part of their life cycle in the soil before becoming infective to humans.
As with other parasitic infections, definitive diagnosis of nematode infections depends on demonstration of the stage of the life cycle in the host. Nematodes, as with most other worms infectious to humans, almost never complete their entire life cycle in the human host.
The life cycles of nematodes are complex and highly varied. Some species, including Enterobius vermicularis, can be transmitted directly from person to person, while others, such as Ascaris lumbricoides, Necator americanus, and Ancylostoma duodenale, require a soil phase for development. Because most helminthic parasites do not self-replicate, the acquisition of a heavy burden of adult worms requires repeated exposure to the parasite in its infectious stage, whether larva or egg. Hence, clinical disease, as opposed to asymptomatic infection, generally develops only with prolonged residence in an endemic region.
Unlike with protozoan infections, a casual or a low degree of exposure to infective stages of parasitic nematodes usually does not result in patent infection or pathologic findings. Repeated or intense exposure to a multitude of infective stage larvae is required for infection to be established and disease to arise.
Eosinophilia and elevated serum immunoglobulin E (IgE) levels are features of many nematode infections; when unexplained, these symptoms should always prompt a search for occult roundworm infection. Humans do not appear to develop significant protective immunity to intestinal nematodes, although the mechanisms of parasite immune evasion and host immune responses to these infections have not been elucidated in detail.
Nematode infections are usually asymptomatic or subclinical.
Several clinical signs and symptoms can occur in patients with nematode infections.
| Anemia | Leprosy |
| Anthrax | Lymphedema |
| Appendicitis | Lymphogranuloma Venereum (LGV) |
| Asthma | Pancreatitis, Acute |
| Cholecystitis | Systemic Lupus Erythematosus |
| Diverticulitis | Tuberculosis |
| Hodgkin Disease |
Nonfilarial causes of lymphangitis include acute bacterial lymphangitis, phlebitis, and plague (unusual).
Nonfilarial causes of lymphedema, chyluria, and elephantiasis include the following:
Characteristic eggs, worms, or larvae in tissue
No special diet is required.
No restrictions are necessary. In lymphatic filariasis, if edema is a problem, the patient may want to elevate legs while sitting.
The goals of pharmacotherapy are to eradicate the infestation, to reduce morbidity, and to prevent complications.
Parasite biochemical pathways are different from the human host; thus, toxicity is directed to the parasite, egg, or larvae. Mechanism of action varies within the drug class. Antiparasitic actions may include the following:
Used for hookworm, pinworm, and roundworm. Decreases ATP production in worm, causing energy depletion, immobilization, and, finally, death.
Ascariasis, enterobiasis, hookworm, or trichuriasis: 400 mg PO as single dose, may repeat in 3 wk if necessary
Strongyloidiasis: 400 mg PO qd for 3 d, may repeat regimen in 3 wk if necessary
Trichinosis: 400 mg PO bid for 15 d
Ascariasis, enterobiasis, hookworm, or trichuriasis
<2 years: 200 mg PO as single dose, may repeat in 3 wk if necessary
>2 years: Administer as in adults
Strongyloidiasis
<2 years: 200 mg PO qd for 3 d, may repeat regimen in 3 wk if necessary
>2 years: Administer as in adults
Coadministration with carbamazepine may decrease efficacy; dexamethasone, cimetidine, and praziquantel may increase toxicity
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Teratogenic in laboratory animals; avoid in pregnancy; may increase LFTs significantly (discontinue drug, may resume when at pretest values); abdominal pain, nausea, vomiting, diarrhea, dizziness, vertigo, fever, increased intracranial pressure, and alopecia may occur
Indicated for treating E vermicularis (pinworm), T trichiura (whipworm), A lumbricoides (common roundworm), A duodenale (common hookworm), N americanus (American hookworm) in single or mixed infections. Efficacy varies as a function of such factors as preexisting diarrhea and GI transit time, degree of infection, and helminth strains. Causes worm death by selectively and irreversibly blocking uptake of glucose and other nutrients in susceptible adult intestine where helminths dwell.
Ascariasis, hookworm, or trichuriasis: 100 mg PO qd for 3 d; alternatively, 500 mg PO once
Enterobiasis: 100 mg PO once, repeat dose in 2 wk
Trichinosis: 200-400 mg PO tid for 3 d initially; followed by 400-500 mg tid for 10 d
<2 years: Not established
>2 years: Administer as adults
Carbamazepine and phenytoin may decrease effects; cimetidine may increase levels
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Avoid use in pregnancy, especially first trimester; adjust dose in hepatic impairment
Member of avermectin class (broad-spectrum antiparasitic agents). Unique mode of action. Binds selectively with high affinity to glutamate-gated chloride ion channels in invertebrate nerve and muscle cells. Increases permeability of cell membrane to chloride ions. Results in hyperpolarization of nerve or muscle cell, causing parasite paralysis and death. Also affects other ligand-gated chloride channels (eg, those gated by GABA). Active against various life-cycle stages of most nematodes. Active against O volvulus tissue microfilariae but not adult form. Activity against S stercoralis limited to intestinal stages.
Strongyloidiasis: 200 mcg/kg PO qd for 1-2 d
Cutaneous larva migrans (onchocerciasis): 150 mcg/kg PO as single dose; may repeat q6-12mo until asymptomatic
<5 years: Not established
>5 years: Administer as in adults
None reported
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in breastfeeding women; repeat courses of therapy may be required in immunocompromised patients; may cause nausea, vomiting, drowsiness, and mild CNS depression; patients with hyperreactive onchodermatitis may develop a severe immune reaction (ie, Mazzotti reaction) consisting of optic neuritis, chorioretinitis, proteinuria, pruritus, rash, and edema
Readily absorbed from GI tract, partially degraded in vivo, and excreted in urine. Paralyzes worm muscle; thus, worm expelled by normal intestinal peristalsis. Exhibits wide therapeutic index. Not available in the United States.
Ascariasis: 3.5 g/d (hexahydrate equivalent) PO as single dose for 2 d
Enterobiasis: 65 mg/d (hexahydrate equivalent) PO for 7 d; not to exceed 2.5 g/d
Ascariasis: 75 mg/kg/d (hexahydrate equivalent) PO for 2 d; not to exceed 3.5 g/d
Enterobiasis: Administer as in adults
Phenothiazines may increase risk of seizures; antagonizes pyrantel pamoate activity
Documented hypersensitivity; hepatic or renal dysfunction; seizure disorder
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Most commonly reported reactions include GI and CNS effects, discontinue drug if adverse effects become significant; avoid prolonged, repeated, and excessive therapy due to potential neurotoxicity; caution in severe malnutrition and anemia
Depolarizing neuromuscular blocking agent and cholinesterase inhibitor that results in spastic paralysis of worm. Active against E vermicularis (pinworm), A lumbricoides (roundworm), and A duodenale (hookworm).
Hookworm: 11 mg/kg PO qd for 3 d; not to exceed 1 g/d
Ascariasis: 11 mg/kg PO as single dose; not to exceed 1 g/d
Enterobiasis: 11 mg/kg PO as single dose; not to exceed 1 g/d; repeat q2wk for 2 regimens
<2 years: Not established
>2 years: Administer as in adults
Pyrantel and piperazine are mutually antagonistic in ascariasis; may increase theophylline serum levels
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in liver impairment, anemia, pregnancy, and malnutrition
Effective in treating filariasis specific for W bancrofti, B malayi, and L loa. Does not contain any toxic metallic elements. Not recommended as DOC because of severe adverse effects. Recommended if therapy with mebendazole fails or unavailable.
6 mg/kg/d PO divided tid for 14 d
Administer as in adults
None reported
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in renal dysfunction (reduce dose); gradual dose titration may be needed over first 3 d to reduce allergic reaction in patients with microfilariae in blood or skin; patients with hyperreactive onchodermatitis or L loa infection may develop a severe immune reaction (ie, Mazzotti reaction) consisting of optic neuritis, chorioretinitis, proteinuria, pruritus, rash, and edema
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nematode infections, roundworms, helminths, helminthic infection, intestinal parasites, ascariasis, enterobiasis, trichuriasis, strongyloidiasis, filariasis, parasitic diseases, larva migrans, river blindness, dracunculiasis, whipworm, loiasis, Guinea worm, onchocerciasis, Strongyloides stercoralis, Enterobius vermicularis, Ascaris lumbricoides, Necator americanus, Ancylostoma duodenale, Dracunculus medinensis, Wuchereria bancrofti, Onchocerca volvulus, Loa loa, Brugia malayi, Brugia timori, Trichuris trichiura, Toxocara canis, Toxocara cati, Ancylostoma braziliense, S stercoralis, E vermicularis, A lumbricoides, N americanus, A duodenale, D medinensis, W bancrofti, B malayi, B timori, L Loa, O volvulus, T trichiura, T canis, T cati, A braziliense
Murat Hökelek, MD, PhD, Technical Consultant of Parasitology Laboratory, Associate Professor, Department of Clinical Microbiology, Ondokuz Mayis University Medical School, Turkey
Murat Hökelek, MD, PhD is a member of the following medical societies: Turkish Society for Parasitology
Disclosure: Nothing to disclose.
Larry I Lutwick, MD, Professor of Medicine, State University of New York, Downstate Medical School; Director, Infectious Diseases, Veterans Affairs New York Harbor Health Care System, Brooklyn Campus
Larry I Lutwick, MD is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America
Disclosure: Nothing to disclose.
Arnold C Cua, MD, Physician, Department of Infectious Diseases, Renown Medical Center
Arnold C Cua, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine and Infectious Diseases Society of America
Disclosure: Nothing to disclose.
Joseph Richard Masci, MD, Chief of Infectious Diseases, Associate Director, Associate Professor, Department of Internal Medicine, Division of Infectious Diseases, Elmhurst Hospital Center, Mount Sinai School of Medicine
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
Ronald A Greenfield, MD, Professor, Department of Internal Medicine, Section of Infectious Diseases, University of Oklahoma College of Medicine
Ronald A Greenfield, MD is a member of the following medical societies: American College of Physicians, American Federation for Medical Research, American Society for Microbiology, Central Society for Clinical Research, Infectious Diseases Society of America, Medical Mycology Society of the Americas, Phi Beta Kappa, Southern Society for Clinical Investigation, and Southwestern Association of Clinical Microbiology
Disclosure: Pfizer Honoraria Speaking and teaching; Gilead Honoraria Speaking and teaching; Ortho McNeil Honoraria Speaking and teaching; Wyeth Honoraria Speaking and teaching; Abbott Honoraria Speaking and teaching; Astellas Honoraria Speaking and teaching; Cubist Speaking and teaching
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.
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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