Describe the intestinal nematodes with their life cycles, clinical features and treatment.

Ascaris Lumbricoides

• The largest intestinal nematode — the female is 20 to 35 cm long — and the commonest helminth infection worldwide, with a very large burden in India
• Transmission — ingestion of embryonated eggs from soil-contaminated food, water or hands. Eggs require 2 to 4 weeks in soil to embryonate, so freshly passed eggs are not infective and direct person-to-person spread does not occur
• The eggs are remarkably resistant, surviving in soil for years and withstanding disinfectants; the fertilised egg has a thick mamillated albuminous coat

Embryonated eggs are ingested and hatch in the small intestine → Larvae penetrate the intestinal wall and enter the portal circulation → They pass through the liver, the right heart, and reach the lungs → They break into the alveoli, causing loeffler syndrome — a transient pneumonitis with cough, wheeze, fleeting radiographic shadows and marked eosinophilia → They migrate up the bronchi and trachea, are swallowed, and return to the small intestine → They mature into adults in about 2 to 3 months and live for 1 to 2 years → The female lays up to 200,000 eggs per day, passed in the faeces

• Most infections are asymptomatic; heavy burdens cause abdominal pain, malabsorption, protein-energy malnutrition and growth retardation in children, and impaired cognitive development
• Complications reflect the size and the mobility of the worm — intestinal obstruction by a bolus of worms (a classical cause of obstruction in Indian children); migration into the biliary tree causing biliary colic, cholangitis and pancreatitis; appendicitis; intestinal perforation; and emergence from the mouth, nose or anus, which is how many patients present
• Migration is provoked by fever, anaesthesia and some anthelminthics, so obstruction may follow treatment
• Diagnosis — eggs in stool, which are abundant; adult worms passed or seen on imaging (a linear filling defect with a central "double tramline" of the worm's own gut on ultrasound is characteristic); eosinophilia during migration but not during the intestinal phase
• Treatment — albendazole or mebendazole single dose; pyrantel pamoate. Obstruction is usually managed conservatively first, with anthelminthics given after decompression

Hookworm

• Two species — ancylostoma duodenale (the Old World hookworm, predominant in northern India) and necator americanus (predominant in southern India). Ancylostoma has cutting teeth and Necator has cutting plates
• Infection is percutaneous — filariform (L3) larvae in warm moist shaded soil penetrate the skin of the bare foot, causing "ground itch". A. Duodenale can also infect by ingestion and through breast milk
• Migration — skin, blood, lungs, alveoli, up the bronchi, swallowed, and thence to the duodenum — the same route as Ascaris
• The clinical problem IS iron deficiency anaemia. The adult worm attaches to the mucosa and sucks blood, secreting anticoagulant; blood is lost from the worm itself and from the bleeding site after it moves on. A. Duodenale takes about 0.15 mL and N. Americanus about 0.03 mL per worm per day, so Ancylostoma causes anaemia with a much smaller burden
• Hookworm is a leading cause of iron deficiency anaemia in India, particularly in women and children, with consequent effects on pregnancy outcome and child development; heavy chronic infection also causes hypoproteinaemia with oedema
• Diagnosis — characteristic oval, thin-shelled eggs with a clear space around a segmented ovum; the eggs of the two species are indistinguishable, and species identification requires larval culture. If the stool is left standing the eggs hatch, so a delayed specimen shows larvae and may be confused with Strongyloides
• Treatment — albendazole or mebendazole, together with iron replacement, which is as important as the anthelminthic

Trichuris and Strongyloides

• Strongyloides hyperinfection and dissemination is the reason this parasite matters disproportionately. corticosteroids (and HTLV-1 infection, transplantation and malignancy) suppress the response that limits autoinfection, allowing massive larval multiplication and spread to lung, liver and brain, with gram-negative sepsis and meningitis as the larvae carry gut bacteria with them. Mortality approaches 80%
• Eosinophilia is characteristically absent in hyperinfection, because the steroids that caused it also suppress the eosinophil response — so its absence is falsely reassuring
• Larva currens — a rapidly migrating serpiginous urticarial rash around the buttocks and trunk, moving several centimetres per hour, which is pathognomonic of autoinfection
• Screen and treat before immunosuppression — anyone from an endemic area who is to receive corticosteroids, chemotherapy or a transplant should be screened serologically or given empirical ivermectin, which is the drug of choice

Comparison of the Intestinal Nematodes

Applied Aspects

• Give iron with the anthelminthic in hookworm anaemia; the worm is the cause but the iron deficit is the disease
• Ask about steroids before treating, and treat before giving steroids, wherever Strongyloides is possible; steroid-precipitated hyperinfection is usually fatal and entirely preventable
• Do not rely on eosinophilia to exclude helminth infection in an immunosuppressed patient, since immunosuppression abolishes it
• Footwear prevents hookworm and strongyloidiasis, and sanitation prevents both these and Ascaris and Trichuris; these are the interventions that produce lasting change, deworming being a holding measure
• Consider ascariasis in a child with intestinal obstruction in an endemic area, and in biliary colic or pancreatitis with no gallstones
• Examine the stool promptly; hookworm eggs hatch on standing and the resulting larvae may be misreported as Strongyloides, which has entirely different implications
• Mebendazole is preferred for Trichuris and albendazole for the others, which is worth knowing when a child with rectal prolapse fails to respond
• Larva currens is pathognomonic of strongyloidiasis — a track advancing centimetres per hour around the buttocks — and indicates active autoinfection requiring ivermectin
• Loeffler syndrome resolves without treatment, and anthelminthics during the migratory phase are ineffective since the worms are not yet in the gut
• Rectal prolapse in an Indian child should prompt a stool examination; heavy whipworm infection is a classical and readily treatable cause
• Deworming improves growth and school performance measurably in heavily infected children, which is the justification for treating whole populations rather than individuals
• Ivermectin, not albendazole, is the drug for Strongyloides, and getting this wrong in a patient about to receive steroids can be fatal
• Ascaris migrates when provoked by fever, anaesthesia or certain drugs, so obstruction and biliary migration may follow treatment and the worms are best cleared before elective surgery
• Repeated infection is the norm in an endemic setting, and cure of the individual is temporary without sanitation — which is why programmes are periodic and why footwear and toilets are the durable answer
• Eosinophilia appears during migration and disappears once the adults settle in the lumen, so its timing is informative and its absence in established infection is expected
• Hookworm anaemia depends on species and burden — Ancylostoma takes five times as much blood per worm as Necator, so it causes anaemia with a far smaller worm load
• Screen before transplantation and chemotherapy in anyone from an endemic area; empirical ivermectin is cheap insurance against a hyperinfection that kills most of those who develop it
• Ascaris eggs need weeks in soil before becoming infective, so a patient is not infectious to household contacts — a reassurance worth giving explicitly
• Ground itch and a cough weeks later in a barefoot agricultural worker is the classical hookworm history, and the anaemia follows months afterwards