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The nematodes, or roundworms, that are of medical significance can be broadly classified as either tissue or intestinal parasites.

Tissue Nematode Infections

With the exception of trichinellosis, these infections are due to invasive larval stages that do not reach maturity in humans.


Microbiology and Epidemiology Eight species of Trichinella cause human infection; two—T. spiralis and T. pseudospiralis—are found worldwide.

  • Infection results when humans ingest meat (usually pork) that contains encysted Trichinella larvae.
    • The larvae invade the small-bowel mucosa.
    • After 1 week, female worms release new larvae that migrate to striated muscle via the circulation and encyst.
  • The host immune response has few deleterious effects on muscle-dwelling larvae.
  • About 12 cases of trichinellosis are reported annually in the United States.

Clinical Manifestations Most light infections (<10 larvae per gram of muscle) are asymptomatic. A burden of >50 larvae per gram can cause fatal disease.

  • In the first week of infection, large numbers of parasites invading the gut usually cause diarrhea, abdominal pain, constipation, nausea, and/or vomiting.
  • In the second week of infection, pts develop symptoms related to larval migration and muscle invasion: hypersensitivity reactions with fever and hypereosinophilia; periorbital and facial edema; and hemorrhages in conjunctivae, retina, and nail beds. Deaths are usually due to myocarditis with arrhythmias or heart failure.
  • Approximately 2–3 weeks after infection, larval encystment in muscle causes myositis, myalgias, muscle edema, and weakness (especially in extraocular muscles; the biceps; and muscles of the jaw, neck, lower back, and diaphragm).
  • Symptoms peak at 3 weeks; convalescence is prolonged.

Diagnosis Eosinophilia develops in >90% of pts, peaking at a level of >50% at 2–4 weeks after infection.

  • An increase in parasite-specific antibody titers after the third week of infection confirms the diagnosis.
  • Detection of larvae by microscopic examination of ≥1 g of fresh muscle tissue (i.e., not routine histopathologic sections) also confirms the diagnosis. Yields are highest near tendon insertions.

Intestinal Nematode Infections

Intestinal nematodes infect >1 billion persons worldwide, most commonly in regions with poor sanitation and particularly in developing countries in the tropics or subtropics. Because most helminthic parasites do not self-replicate, clinical disease (as opposed to asymptomatic infection) generally develops only with prolonged residence in an endemic area and is typically related to infection intensity.


Microbiology Ascariasis is caused by Ascaris lumbricoides, the largest intestinal nematode, which reaches lengths up to 40 cm.

  • Humans—primarily younger children—are infected by ingestion of fecally contaminated soil that contains ascarid eggs.
  • Larvae hatch in the intestine, invade the mucosa, migrate to the lungs, break into the alveoli, ascend the bronchial tree, are swallowed, mature in the small intestine, and produce up to 240,000 eggs per day that pass in the feces.

Clinical Manifestations Most infections have a low worm burden and are asymptomatic. During lung migration of the parasite (~9–12 days after egg ingestion), pts may develop a cough and substernal discomfort, occasionally with dyspnea or blood-tinged sputum, fever, and eosinophilia.

  • Eosinophilic pneumonitis (Löffler’s syndrome) may be evident.
  • Heavy infections with numerous entangled worms can occasionally cause pain, small-bowel obstruction, perforation, volvulus, biliary obstruction and colic, or pancreatitis.

Laboratory Findings Ascaris eggs (65 by 45 μm) can be found in fecal samples. Adult worms can pass in the stool or, much less commonly, through the mouth or nose.

Filarial and Related Infections

Filarial worms, which infect >170 million people worldwide, are nematodes that dwell in the SC tissue and lymphatics. Usually, infection is established only with repeated and prolonged exposures to infective larvae; however, filarial disease is characteristically more intense and acute in newly exposed individuals than in natives of endemic areas.

  • Filarial parasites have a complex life cycle, including infective larval stages carried by insects and adult worms that reside in humans.
    • The offspring of adults are microfilariae (200–250 μm long, 5–7 μm wide) that either circulate in the blood or migrate through the skin.
    • Microfilariae are ingested by the arthropod vector and develop over 1–2 weeks into new infective larvae.
  • A bacterial endosymbiont, Wolbachia, is found in all stages of Brugia, Wuchereria, Mansonella, and Onchocerca spp. and has become a target for antifilarial chemotherapy.

Lymphatic Filariasis

Microbiology Lymphatic filariasis is caused by Wuchereria bancrofti (most commonly), Brugia malayi, or B. timori, which can reside in and cause inflammatory damage to lymphatic channels or lymph nodes.

Clinical Manifestations Subclinical microfilaremia, hydrocele, acute adenolymphangitis (ADL), and chronic lymphatic disease are the main clinical presentations.

  • ADL is associated with high fever, lymphatic inflammation, and transient local edema. Both the upper and lower extremities can be involved in both bancroftian and brugian filariasis, but W. bancrofti almost exclusively affects genital lymphatics.
  • ADL may progress to more chronic lymphatic obstruction and elephantiasis with brawny edema, thickening of the SC tissues, and hyperkeratosis. Superinfection is a problem.

Diagnosis Detection of the parasite is difficult, but microfilariae can be found in peripheral blood, hydrocele fluid, and occasionally other body fluids.

  • Timing of blood collection is critical and should be based on the periodicity of the microfilariae in the endemic region involved (primarily nocturnal in many regions).
  • Two assays are available to detect W. bancrofti circulating antigens, and a PCR has been developed to detect DNA of both W. bancrofti and B. malayi in the blood.
  • High-frequency ultrasound (with Doppler techniques) of the scrotum or the female breast can identify motile adult worms.
  • The presence of antifilarial antibody supports the diagnosis, but cross-reactivity with other helminthic infections makes interpretation of this finding difficult.

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