Description

• Parasites are divided into 2 groups:
  • Protozoa: Single-cell organisms; typically multiply within the host. Intestinal protozoa: Transmission by direct fecal–oral route; do not cause eosinophilia.
  • Helminths (worms): Multicellular organisms; rarely multiply within the host (exceptions: Strongyloides stercoralis, Hymenolepis nana); infection may cause a degree of eosinophilia. Level of eosinophilia is associated with the degree of tissue invasiveness. Worms have a limited life span and, without reinfection, most eventually die on their own.
• Some are invasive, and some do not release their infective forms into the bowel. This latter group (e.g., Toxoplasma gondii, Echinococcus sp., Trichinella spiralis) is not reviewed here.
• Most worms require incubation outside the host before being infectious or need a vector for transmission. Enterobius vermicularis (pinworm) eggs are infectious shortly after being passed; autoinfection occurs readily.
• Person-to-person transmission of worms is uncommon, except for pinworm.
• System(s) affected: Gastrointestinal (GI)

Pediatric Considerations
Most common age group affected

Pregnancy Considerations
Many of the treatments are contraindicated.

Epidemiology

Acquisition involves personal, food, and/or water sanitation and migration from higher-prevalence areas.

• Predominant sex: Male = Female
• Predominant age: Pediatric

• US laboratory statistics: 5–30% of general population. Random testing finds at least 1 GI parasite in 5–10% of all people.
• From daycare surveys: Asymptomatic 20–30%; symptomatic 50–80%
• Intestinal protozoa account for most parasite findings in North America. Helminths account for <10% of GI parasites.
• Blastocystis hominis is a commensal enteric fungus of no clinical significance found in 20–30% of stools.

Risk Factors

• Age (children)
• Low socioeconomic status and poor sanitation: Personal, food, water; crowding: Daycare centers, institutional care
• International travel or migration
• Multiple medical conditions, pregnancy, gastric hypoacidity, immunosuppression (AIDS)

General Prevention

• Intestinal parasites are usually acquired by direct fecal–oral contact via ingested contaminated food or water. Rarely, infected arthropod vectors are involved in transmission. Person-to-person transmission may occur through this mechanism.
• Safe food and water precautions (“Wash it, cook it, peel it, or forget it”); enteric and hand hygiene is the means of preventing infections. Infrastructure systems for safe food and water processing contribute to the low prevalence of intestinal parasites.

Pathophysiology

• The pathophysiology of GI parasitic infections is host–parasite-specific.
• Most intestinal parasitic infections are eventually self-limiting. Most worms have a defined life expectancy in the host. Autoreinfection does occur in some worm infections (e.g., strongyloidiasis, pinworm).

Etiology

• Protozoan pathogens:
  • Giardia lamblia: Common
  • Entamoeba histolytica, Cryptosporidium sp., Isospora belli, Balantidium coli, Cyclospora cayetanensis, Microsporida
• Possible protozoan pathogens: Dientamoeba fragilis
• Probable nonpathogenic protozoa:
  • Amoebas: All other Entamoeba sp., Endolimax nana
  • All other intestinal flagellates
• Helminthic pathogens:
  • Nematodes (roundworms): Enterobius vermicularis, Trichuris trichiura, Ascaris lumbricoides, hookworm (Necator americanus, Ancylostoma duodenale), Strongyloides stercoralis, Capillaria philippinensis, Trichostrongylus sp.
  • Trematodes (flukes): Fasciolopsis buski, Clonorchis sinensis, Opisthorchis viverrini, Heterophyes, Fasciola hepatica, Paragonimus westermani, Schistosoma mansoni, S. japonicum, S. hematobium, S. mekongi
  • Cestodes (tapeworms): Taenia saginata, T. solium, Diphyllobothrium latum, Hymenolepis nana, H. diminuta, Dipylidium caninum

Commonly Associated Conditions

• GI parasitic infections and diseases may be associated with HIV infection or AIDS, steroid use, immune deficiencies, and blood type.
• Intestinal parasite infection appears to protect against allergic sensitization (1)[A].