Organism	Pathogenesis	Mode of Transmission and Spectrum of Disease
Ascaris lumbricoides	Attributed to four main factors: 1. Host immune response 2. Effects from larval migration 3. Mechanical disruption and blockage by worms 4. Nutritional deficiency associated with worm burden

Fecal-oral transmission
Reinfection possible
Children and young adolescents have higher infection rate
Pregnant women, unknown impact to unborn fetus
Potential tissue damage from migration to lungs, liver, and immune cell infiltration (pneumonitis)
Peripheral eosinophilia (Löffler’s syndrome)
Nutritional impairment in young children
Hepatic ascariasis, including hepatic abscesses and obstructive cholangitis
Intestinal blockage, pancreatic or bile duct
Migration to other tissues may include kidneys, appendix, and pleural cavity Enterobius vermicularis Worm burden may be a single organism to thousands
Rarely migration occurs to nearby tissues Fecal-oral or inhalation
Sexual transmission has been reported
Reinfection and autoinfection occur
Children and women more common than men
Mild nocturnal pruritus
Migration to vagina, uterus, and fallopian tubes where organisms become encapsulated granulomas
Hemorrhagic colitis and inflammation of ileum and colon in homosexual males
Uncommon sites include peritoneal cavity, lungs, liver, urinary tract, and natal cleft Strongyloides stercoralis Varies in severity dependent on worm burden and area of body infected
Immune response affects symptoms Direct penetration
Chronic and hyperinfection may occur
May remain asymptomatic with peripheral eosinophilia
Cutaneous:

• Pruritus and erythema

• “Larva currens” tracks under skin from worm migration

Pulmonary:

• Asymptomatic to pneumonia

• Löffler’s syndrome; shortness of breath and pulmonary infiltrates

Intestinal:

• Diarrhea, constipation, anorexia, and abdominal pain may occur

• Damage to mucosa may occur in heavy infections

Trichostrongylus spp. Dependent on worm burden Diarrhea, anorexia, and general malaise
Damage to intestinal mucosa may occur, resulting in hemorrhage and tissue desquamation
Heavy worm burden may result in anemia and cholecystitis Trichuris trichiura Dependent on worm burden
Mechanical damage to intestinal mucosa and allergic reaction
Migration of parasites Fecal-oral transmission
Ingestion of embryonated eggs
Asymptomatic to mild symptoms associated with low worm burden
Heavy infections may result in hemorrhage, weight loss, abdominal pain, blood-tinged stools, and diarrhea
Rectal prolapse and hypochromic anemia in repeated heavy infections in children
Inflammation of mucosa Capillaria philippinensis Dependent on worm burden Fecal-oral transmission
Ingestion of larvae-infected seafood such as fish, crab, shrimp, and snails
Malabsorption, fluid loss, and associated loss of electrolytes
Extended infections can result in organ failure and death Hookworms:
A. duodenale
N. americanus Vary according to life cycle phase and worm burden
Production of proteins that suppress host immune response
Hyaluronidase: facilitates digestion of connective tissue and penetration of epidermis and dermis
Migration of larvae to lungs
Mechanical: attachment, feeding, and anticoagulation production Direct penetration
Mild to severe pruritus and potential secondary infections
Ground itch: Development of vesicles resulting from erythematous papular rash
Pneumonitis: decreased sensitization as compared to A. lumbricoides and S. stercoralis.
Gastrointestinal:

• Tissue damage at site of attachment

• Blood loss, anemia

• Acute gastrointestinal phase demonstrates increased eosinophilia

• Increased worm burden may result in death, particularly in young children

Ancylostoma duodenale Period of arrested development May be associated with vertical transmission and congenital infections
Eosinophilia peaks in approximately 1 month in gastrointestinal phase Necator americanus Proteolytic enzymes that degrade collagen, fibronectin, laminin, and elastin Skin-associated symptoms as described for hookworms
Eosinophilia peaks in approximately 2 months in gastrointestinal phase

Laboratory Diagnosis

Female worms have an extremely high daily output of eggs, making diagnosis relatively easy through the identification of eggs in feces. The large, broadly oval mammillated ova are typically stained brown from bile (Figure 51-2). Some eggs will be decorticated, or lacking the mammillated outer cover. Infertile eggs may be oval or irregular shaped with a thin shell and containing internal granules. Adult worms may also be identified in feces. The male is smaller (15 to 31 cm) with a curved posterior end (Figure 51-3) and contains three well-characterized lips. Larvae may be found in sputum or gastric aspirates as a result of larval migration during development within the human host.

Figure 51-2 Bile-stained mammillated *A. lumbricoides* ovum. (Courtesy Dr. Henry Travers, Sioux Falls, S.D.)

Figure 51-3 *A. lumbricoides* adult male worm. Note the curved posterior end. (Courtesy Dr. Henry Travers, Sioux Falls, S.D.)

Enterobius vermicularis (pinworm) is distributed worldwide and commonly identified in group settings of children ages 5 to 10 years. The life cycle is considered direct; transmission occurs from an infected host to another individual (Figure 51-4). During the night, the mature female worm migrates out of the anus of the infected host and lays eggs in the perianal region. The embryonated eggs will mature and a third-stage larva stage develops, resulting in infectivity within hours. Transmission occurs by ingestion or inhalation of eggs. Reinfection may also occur when the eggs hatch and larvae return to the intestine where they mature.