Intestinal Nematodes (Roundworms)

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Intestinal Nematodes (Roundworms)

Objectives

1. Describe the distinguishing morphologic characteristics and basic life cycle (vectors, hosts, and stages of infectivity) for each of the parasites listed.

2. Define and identify the following parasitic structures when appropriate: mammillated ovum, gravid, rhabditiform larvae, buccal capsule, esophagus, genital primordia, polar hyaline plugs, copulatory bursa, embryonated egg, cutting plates, and filariform larvae.

3. Describe the diseases and mechanism of pathogenicity including route of transmission for each of the species listed.

4. Differentiate Ascaris lumbricoides adult male and female worms.

5. Define and differentiate direct versus indirect life cycle as related to nematodes and the routes of transmission including autoinfection and hyperinfections.

6. Identify and differentiate the characteristic morphologies and eggs for A. lumbricoides, E. vermicularis, and T. trichiura.

7. Compare clinical signs and symptoms, morphologic characteristics, and identification of hookworm’s rhabditiform larvae for Ancylostoma duodenale and Necator americanus.

8. Compare and contrast the morphologic characteristics and identification of the larval forms of Strongyloides stercoralis.

9. List the various methods used to diagnosis intestinal nematode infections.

10. Identify the appropriate intestinal nematodes where the following techniques are useful and explain the principle for each including the Baermann concentration method, agar culture, and Harada-Mori filter paper method for the recovery of intestinal nematodes.

There are more than 60 species of nematodes known to infect humans. Ascaris lumbricoides, hookworms (Ancylostoma duodenale and Necator americanus), and Trichuris trichiura are estimated to infect more than 1 billion people. Nematodes are nonsegmented, elongate, cylindrical worms with a well-developed digestive tract and reproductive system. The adult worms have separate sexes, with the male generally smaller than the female. Most nematodes are diagnosed by finding the characteristic eggs in the stool. The infective stage of the nematodes varies with species; for example, transmission may occur through the ingestion of eggs, whereas others burrow through the skin and migrate to the intestine. The nematodes have very diverse life cycles providing different routes of transmission as well as disease symptoms.

Ascaris Lumbricoides

General Characteristics

Ascaris lumbricoides is the most common and the largest roundworm. The parasite has a worldwide distribution with higher prevalence in the tropical regions. Eggs are ingested and hatch in the duodenum, penetrate the intestinal wall, and migrate to the hepatic portal circulation. The adult worms live and reproduce in the lumen of the small intestine. The ovum is a thick, oval mammillated (outer protrusions) and embryonated egg. The eggs are passed in the feces and become infective 2 to 6 weeks following deposition, depending on the environment. The general life cycle is outlined in Figure 51-1. A. lumbricoides life cycle is classified as an indirect life cycle; transmission is not via a direct route from one host to the next.

Pathogenesis and Spectrum of Disease

Many A. lumbricoides infections are asymptomatic. The presentation of symptoms correlates with the length of infection, the number of worms present, and the overall health of the host. Intestinal symptoms range from mild to severe intestinal obstruction. Some patients will develop pulmonary symptoms and present with immune-mediated hypersensitivity pneumonia. The worms may cause an immune condition known as Löffler’s syndrome characterized by peripheral eosinophilia. See Table 51-1 for a summarized detail of associated diseases.

TABLE 51-1

Pathogenesis and Spectrum of Associated Diseases

Organism Pathogenesis Mode of Transmission and Spectrum of Disease
Ascaris lumbricoides Attributed to four main factors:

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:

Pulmonary:

Intestinal:

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:

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

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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.

Enterobius Vermicularis

General Characteristics

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.