Ascaris lumbricoides: DHB202

• The topic is parasitic infections of the small intestine, focusing on Ascaris lumbricoides/Ascariasis (Giant intestinal roundworm).
• The course code is DHB202.

Learning Objectives

• Classify Ascaris lumbricoides taxonomically as a nematode.
• Determine if its habitat is as a parasite of the small intestine.
• Identify the geographical distribution of Ascaris lumbricoides, with emphasis on Egypt and WHO campaigns.
• Discuss the role of human hosts in completing the life cycle.
• Identify the mode of infection as a soil-transmitted nematode and the infective stage.
• Relate the life cycle in the human host to the pathogenesis and clinical picture.
• Discuss possible complications relative to parasite behavior.
• Select proper laboratory samples and techniques, and describe the diagnostic stage.
• Recommend other important investigations.
• Recognize the drug of choice and the MDA (Mass Drug Administration) drug.
• Outline measures for integrated prevention and control based on WHO guidelines.

Classification

• Ascaris lumbricoides is the largest and most common intestinal nematode infecting humans.
• Its taxonomy identifies it as a nematode.

Geographical Distribution

• The parasite is cosmopolitan, found in areas with inadequate sanitation.
• It is common where untreated human feces are used as an organic fertilizer.
• Soil-transmitted helminth (STH) infections, including Ascaris, are widely distributed in tropical and subtropical areas, according to the WHO.

Host and Habitat

• Humans are the definitive host.
• Adult worms live in the small intestine of humans, between the folds of the mucosa.

Morphology of Adult Worms (Diagnostic Stage)

• They are the largest intestinal nematode affecting humans and have a club-shaped esophagus.
• Male worms are 15-30 cm long, with a posterior end coiled ventrally and two copulatory spicules.
• Female worms are 20-40 cm long, with a straight posterior end and two sets of genital organs parallel in position.

Life Cycle and Host Relationship

• Infection occurs through ingesting mature embryonated eggs containing rhabditiform larvae.
• This happens via soil-contaminated food, drinks, or hands.
• Houseflies can mechanically transmit infective eggs to food.
• Eggs are laid immature and are not infective until they embryonate in the soil.
• It takes about two weeks for the eggs to embryonate in the soil.
• The eggs remain viable in the soil for years under desiccation, low temperature and chemicals; only sunlight kills them.
• Children are more commonly infected than adults due to their habits of consuming soil.
• There is no autoinfection in ascariasis due to the eggs needing a period of embryonation in the soil.

Pathogenesis and Clinical Picture of Ascariasis

• I-Prepatent Period (Larval Migration, Loffler's Syndrome)
  • Larval migration produces a transient local inflammatory and hypersensitivity reaction, like eosinophilic pneumonitis in the lungs
  • The reaction is due to the presence of larvae plus allergic mediators
  • This results in local eosinophilic infiltration around larvae
  • This results in systemic hypereosinophilia
  • This results in petechial hemorrhages at the site of the larval track that may have superimposed bacterial infection.
• Clinically, this presents as sudden rise in body temperature (up to 39°C), dyspnea, blood-tinged sputum (hemoptysis), eosinophilia, and pulmonary symptoms, may be accompanied by urticaria.
• It is often a transient and spontaneous recovery usually occurs after two weeks
• Asthmatic children with a history of playing in soil should be investigated for ascariasis.

Patent Infection (Adult Intestinal Phase)

• According to the worm burden, the intestinal phase can be asymptomatic.
• Symptoms include diffuse or epigastric abdominal pain, weight loss or retarded growth, nausea, and vomiting, with worms sometimes seen in the vomitus.
• Adult worms may be expelled from the nares or anus (expulsion phenomenon).

Complications

• Aberrant adult worm migration is usually stimulated by fever.
• It can also be stimulated by some anesthetics and/or antihelminthic drugs like pyrental pamoate, and improper dosages of antihelminthic drugs.
• This can cause acute abdomen and can include intestinal obstruction, intestinal perforation and peritonitis, severe cholangitis (obstructive jaundice), severe pancreatitis, or appendicitis.

Clinical Diagnosis of Ascariasis

• Ascariasis is difficult to diagnose due to its endemicity and similarity to other soil-transmitted nematode infections.
• If they complain of vomiting adult worms or passage from the anus or anterior nares this is pathognomonic.

Laboratory Diagnosis

I- Prepatent Period

• Complete blood count (CBC): shows marked transient eosinophilia.
• Sputum analysis: may reveal larvae (diagnostic stage) and/or Charcot-Leyden crystals.
• Stool examination: shows no Ascaris eggs.

II- Established infection (adult phase/ intestinal phase)

• Direct diagnosis via a stool examination, you'll see Ascaris eggs or expelled adult worms (diagnostic stages), Ascaris eggs may be recovered in duodenal aspirate during the intestinal phase.
• The gold standard test, is also a stool examination, where Ascaris eggs, the diagnostic stage, are examined.
  • Size: 60X 40 um.
  • Shape: Oval
  • Shell: thick with an outer coarse albuminoid mammillations.
  • Colour: Yellowish brown
  • Content: Large unsegmented embryo
• Eggs are recovered in duodenal aspirate during the intestinal phase.
• A female Ascaris may produce approximately ~200,000 eggs per day, this makes diagnosis by stool examination very feasible.
• Indirect Diagnosis (Serological Diagnosis): It has little value due to antigenic similarities with other nematodes.

Imaging Techniques

• Chest radiography may reveal patchy infiltrates of eosinophilic pneumonia, which disappear later on during Loffler's syndrome.
• Abdominal radiography may reveal adult worms (especially with contrast).
• Ultrasonography aids in detecting worms in the gallbladder.
• Cholangiopancreatography (ERCP) or magnetic resonance imaging (MRI) may detect adult worms in bile or pancreatic ducts.

Treatment

• Commonly recommended agents include albendazole and mebendazole.
• Albendazole (Vermizole) is the drug of choice, a systemic broad-spectrum antihelminthic, often used for MDA.
  • Dose: 400 mg single oral dose, repeated after 3 weeks if not cured; children under 4 get half the adult dose.
• Mebendazole (Vermox)
  • Contraindicated for children less than 2 years of age
  • Dose: 100 mg orally twice a day for 3 consecutive days, a second course can be administered after 3–4 weeks if needed.
• Levamisole (ketrax)
  • Sometimes used for mass treatment in schools.
  • Dose: 2.5 mg/kg (100-150 mg) as a single oral dose.

Integrated Prevention and Control

• WHO strategy for soil-transmitted helminthiases includes:
  • Geotargeting + Mass Drug Administration (MDA) for deworming (surveys and WHO prevalence >20%).
  • Diagnosis and Treatment (patients, especially school children in areas prevalence is <20%).

Preventative measures

• Prevention of fecal contamination of soil:
  • Good sanitation and safe water supply.
  • Prohibit promiscuous defecation, especially by children.
  • Stop using untreated human excreta as fertilizer.

Health Education measures

• Washing vegetables is a great preventable measure
• Prevent children from playing in soil.
• Washing hands before meals and engaging in housefly control.