Intestinal Nematodes

Ascaris lumbricoides is the largest intestinal nematode infecting humans. Adult females reach up to 35 to 40 centimetres in length. It is one of the most common helminth infections worldwide and is transmitted by the soil-transmitted (geohelminth) faecal-oral route.

Infective stage. The embryonated egg, containing a fully developed L3 larva, is the infective form. Freshly passed eggs are unembryonated and not immediately infective. They need to mature in soil, typically for several weeks under warm, moist, shaded conditions. This delay distinguishes Ascaris from directly transmissible organisms such as Enterobius.

Route of entry. Infection follows ingestion of embryonated eggs. Sources are contaminated soil, unwashed produce grown in or fertilised with contaminated soil, or contaminated hands. Children with soil-contact behaviours (geophagia, poor hand hygiene) are particularly at risk.

Migration. Larvae hatch in the small intestine, penetrate the intestinal wall and enter the portal circulation. They travel to the liver, then via the bloodstream to the lungs. There they break into alveolar spaces, ascend the bronchial tree and trachea, and are swallowed. They return to the small intestine to mature to adulthood.

This hepato-pulmonary migration takes approximately 10 to 14 days. Passage through the lungs can produce a transient pulmonary hypersensitivity reaction (Loeffler syndrome: cough, wheeze, dyspnoea, and eosinophilic pulmonary infiltrates on imaging).

Adult location. Adult worms reside free within the lumen of the small intestine, typically the jejunum, without attaching to the mucosa. They survive by direct ingestion of luminal intestinal contents.

Diagnostic stage. Unembryonated eggs (rounded, thick mammillated shell) are identified on stool microscopy. Adult worms may occasionally be passed in stool or vomited and recognised macroscopically.

Major disease pattern. Most infections, particularly with low worm burden, are asymptomatic. Heavy infection can cause:

• Abdominal pain and malnutrition or growth impairment in children, through nutrient competition.
• Mechanical intestinal obstruction, because the large adult worm mass carries a specific risk. This is particularly seen in children with heavy burden, where a tangled bolus of worms can obstruct the bowel lumen.
• Biliary or pancreatic duct obstruction, because adult worms tend to migrate into the biliary tree or pancreatic duct. This produces biliary colic, cholangitis, or pancreatitis.
• Migration into the appendix.

Enterobius vermicularis (pinworm, threadworm) is the most common helminth infection in many temperate, industrialised settings, particularly among school-aged children. It is transmitted directly and does not require soil maturation.

Infective stage. The egg is the infective form. It becomes infective within hours of being laid, unusually rapid compared to Ascaris. Unlike most other intestinal nematode eggs, it is deposited directly on the perianal skin, not in stool.

Route of entry. Infection occurs via ingestion of eggs. The most common route is autoinoculation: a child scratches the intensely pruritic perianal area, eggs adhere to fingers and under fingernails, and are transferred to the mouth. Contaminated fomites (bedding, clothing, toys, communal surfaces) also transmit infection, as eggs can survive on surfaces for one to two weeks under favourable humidity.

Migration. Unlike Ascaris and hookworm, Enterobius has no tissue migration phase. Ingested eggs hatch in the small intestine. Larvae mature directly to adulthood while migrating distally through the gastrointestinal tract, without a bloodstream or pulmonary phase.

Adult location. Adult worms reside in the caecum, appendix, and adjacent colon. At night, gravid female worms migrate out through the anus onto the perianal skin to deposit their eggs. This behaviour causes the characteristic nocturnal pruritus of pinworm infection.

Diagnostic stage. Eggs are not reliably found on routine stool examination, since they are deposited perianally rather than passed in stool.

The standard diagnostic method is the cellophane (Scotch) tape test. Apply adhesive tape to the perianal skin first thing in the morning, before washing or defecation. Then examine the tape microscopically for the characteristic flattened, asymmetric (D-shaped) eggs.

Major disease pattern. The dominant symptom is perianal pruritus (in girls, sometimes vulvovaginal), characteristically worse at night. It can cause sleep disturbance and irritability. Scratching can cause secondary bacterial skin infection.

Vulvovaginitis and, rarely, ectopic migration of worms into the female genital tract are recognised complications in girls. Serious complications are otherwise uncommon. Infection is generally more a source of nuisance and social or hygiene concern than significant systemic disease.

Trichuris trichiura (whipworm) is a soil-transmitted nematode named for its distinctive whip-like shape, with a long, thin anterior end and a thicker posterior end.

Infective stage. The embryonated egg is the infective form. It needs several weeks of maturation in soil under warm, moist conditions before becoming infective, directly analogous to Ascaris.

Route of entry. Eggs are ingested via contaminated soil, food, or hands. The pattern is faecal-oral and soil-transmitted, as for Ascaris. The two infections frequently coexist in the same individuals and regions because of shared transmission ecology.

Migration. Trichuris has no tissue migration phase. Larvae hatch in the small intestine and migrate directly to the large intestine, where they mature to adulthood. They burrow their thin anterior end into the superficial colonic mucosa, which explains the whip shape: the thin end is embedded and the thicker posterior end is left free within the lumen.

Adult location. Adult worms reside embedded by their anterior end in the mucosa of the caecum and proximal colon. Heavier infections extend further along the colon and into the rectum.

Diagnostic stage. Eggs (barrel-shaped, with characteristic bipolar mucous plugs at each end) are identified on stool microscopy.

Major disease pattern. Light infection is usually asymptomatic. Heavy infection produces chronic colitis with abdominal pain and diarrhoea, which can be mucoid or bloody.

A substantial worm burden can produce Trichuris dysentery syndrome, particularly in young children. It is characterised by chronic bloody diarrhoea, abdominal pain, and rectal prolapse.

Rectal prolapse is a distinctive and clinically recognisable complication. The inflamed, oedematous rectal mucosa, sometimes with visible adult worms attached, prolapses through the anus. It generally reflects very heavy chronic infection with malnutrition.

Chronic heavy infection is also an important contributor to growth impairment, anaemia, and cognitive and developmental effects in children in endemic settings.

Strongyloides stercoralis has the most biologically distinctive life cycle of the intestinal nematodes, because of its unique capacity for autoinfection.

Infective stage. The filariform (L3) larva is the infective form. It develops either in the external environment (free-living cycle) or, critically, within the host's own gastrointestinal tract or perianal skin (autoinfective cycle). Strongyloides differs from every other intestinal nematode here: it transmits via larvae, not eggs.

Route of entry. The primary route of externally acquired infection is skin penetration by filariform larvae from contaminated soil. In autoinfection, larvae generated within the host directly reinvade the colonic mucosa or perianal skin, with no external exposure required.

Migration. After skin penetration, larvae enter the bloodstream, migrate to the lungs, break into alveolar spaces, ascend the airway, and are swallowed. This parallels the hepato-pulmonary migration route of Ascaris and hookworm. Larvae then reach the small intestine and mature to adulthood.

Adult location. Uniquely among the intestinal nematodes, only adult female worms are found in human tissue. They reproduce by parthenogenesis, without fertilisation by a male, and are embedded within the mucosa of the duodenum and proximal jejunum.

Diagnostic stage. Larvae (rhabditiform, the non-infective first-stage larva), rather than eggs, are identified on stool examination, since eggs hatch within the intestinal mucosa before passage. This is a key distinguishing feature from the egg-based diagnosis of other intestinal nematodes.

Major disease pattern. Chronic infection is often asymptomatic or produces mild, nonspecific gastrointestinal symptoms. It can persist for decades because of the autoinfective cycle.

In immunosuppressed hosts, accelerated autoinfection can produce hyperinfection syndrome and disseminated strongyloidiasis, a life-threatening complication. Risk groups include those on corticosteroids, with HTLV-1 co-infection, or with other T-cell impairment.

Two hookworm species infect humans. Ancylostoma duodenale is found in parts of Asia, the Middle East, and North Africa. Necator americanus is the dominant hookworm species in sub-Saharan Africa, the Americas, and parts of Asia. They share essentially the same life cycle and clinical pattern and are considered together.

Infective stage. The filariform (L3) larva is the infective form. It develops from eggs passed in stool after a period of maturation in warm, moist, shaded soil.

Route of entry. Filariform larvae actively penetrate intact human skin. The most common site is the soles of the feet in individuals walking barefoot on contaminated soil. Entry produces a local pruritic papular skin reaction (ground itch). Ancylostoma duodenale can additionally infect via the oral route if larvae are ingested.

Migration. After skin penetration, larvae enter the bloodstream and follow the same hepato-pulmonary migration route as Ascaris and Strongyloides. They travel to the lungs, break into alveoli, ascend the airway, and are swallowed. They reach the small intestine and mature to adulthood.

Adult location. Adult worms attach firmly to the mucosa of the proximal small intestine (duodenum and jejunum). They use well-developed buccal cutting plates or teeth (Ancylostoma) or cutting plates (Necator), through which they actively feed on host blood.

Diagnostic stage. Eggs are identified on stool microscopy. They are oval and thin-shelled. The two species are morphologically indistinguishable on routine microscopy. Larval culture or molecular methods are needed to distinguish species when relevant.

Major disease pattern. The defining clinical consequence is chronic intestinal blood loss from the feeding activity of attached adult worms. Each worm can cause a measurable daily blood loss, with Ancylostoma generally associated with greater blood loss per worm than Necator.

This produces iron deficiency anaemia proportional to worm burden and chronicity of infection. It is the principal cause of morbidity in endemic populations. It is also a major contributor to anaemia, impaired growth and cognitive development in children, and adverse pregnancy outcomes (including low birth weight) in infected pregnant women.

Cutaneous larva migrans is a distinct, self-limited, intensely pruritic serpiginous skin eruption. It does not result from these two human hookworm species. It results from related zoonotic hookworm species, notably Ancylostoma braziliense, a dog and cat hookworm.

Their larvae penetrate human skin but cannot complete their normal migratory life cycle in the incidental human host. They wander within the skin and produce the characteristic migrating tract.