INTESTINAL NEMATODES

Infection occurs by:

a) Ingested eggs: Ascaris, Enterobius, Trichuris and Trichinella (cysts)
b) Skin penetration: Hookworms (Ancylostomata & Nector), Strongloids

ASCARIS LUMBRICOIDES

Causes: Ascariasis
Affects: Gastrointestinal and respiratory systems
Regions: tropical and subtropical regions.

Morphology
 Largest intestinal nematode:
o Females: Up to 40 cm long, 6 mm wide
o Males: Smaller, with a curved posterior end
o Color: White or pink, tapered at both ends

 Eggs (Ova):
o Oval with a thick shell and mamillated
(bumpy) outer coat
 o Extremely durable in the environment for up to 10 years under
moist, warm, and shady conditions

Epidemiology
 Affects 1.4 billion people worldwide (~25% of the global population).
 Most common regions:
o Asia: 73% of infections
o Africa: 12%
o South America: 8%
 High-risk group:
o Children aged 2 to 10 years (due to increased exposure to
contaminated soil)
o Prevalence decreases after age 15
 Clustering in families and high household density increase the worm
burden.

Transmission
 Primary route:
o Ingestion of contaminated food or water (especially raw
vegetables/fruits) containing fertilized eggs
 Inhalation of contaminated dust is rare but possible.
 Environmental reservoirs:
o Eggs can survive for years in soil.
 Transplacental transmission:
o Rare cases of larvae crossing the placenta have been reported.
 Life Cycle

1.

Egg Production
 Female Reproductive Output: Mature female Ascaris can produce approximately
200,000 eggs per day.
 Fecal Shedding: These eggs are excreted in feces in an unembryonated state, rendering
them non-infective initially.
2. Environmental Development
 Embryonation: The eggs undergo embryonation in the soil, which requires optimal
conditions of temperature (20-25ºC), moisture, and oxygen.
 Larval Development: Within a period of 3 to 6 weeks, the eggs develop into infective
larvae, becoming capable of causing infection.
3. Host Infection
 Ingestion of Infective Eggs: Humans acquire the infection by ingesting contaminated
food or water containing the infective second-stage rhabditoid larvae within the eggs.
 Egg Hatching: Upon reaching the small intestine, digestive juices dissolve the eggshell,
releasing juveniles that are approximately 0.2-0.3 mm in length and 13-15 µm in
diameter. These juveniles, while resembling adults in structure, lack fully developed
reproductive organs.
 Intestinal Penetration: The juveniles penetrate the intestinal wall and enter the
mesenteric circulation, progressing through the hepatic portal vein to the liver.
4. Migration Through the Body
 Path to the Heart: After reaching the liver, the larvae travel to the right side of the
heart via the post-caval vein.
  Lung Migration: From the heart, the larvae are transported to the lungs through the
pulmonary artery, where they remain for several days and increase in size.
 Development in the Lungs: In the lungs, juveniles rupture the blood capillaries,
entering the alveoli. During this stage, they grow larger and undergo a series of moults,
transitioning from second-stage to third-stage and then to fourth-stage larvae, with the
latter growing to a length of 2 to 3 mm.
5. Return to the Intestine
 Exit from the Lungs: The fourth-stage larvae exit the alveoli and travel through the
bronchioles and bronchus into the trachea.
 Re-swallowing: They then reach the pharynx, where they are coughed up and
subsequently swallowed for a second time into the gut.
6. Final Development
 Moulting in the Intestine: Within the small intestine, the larvae undergo their final
moult and reach maturity within approximately 60 to 75 days.
 Sexual Maturity: Adult Ascaris lumbricoides attain sexual maturity around 8 to 10
weeks after re-entering the intestine.
 Lifespan: The adult worms can live for 12 to 18 months within the host.

Pathophysiology of Ascariasis
1. Direct Tissue Damage:
o Larvae invade intestinal walls and lungs, causing localized tissue
damage.
o Migration to unusual sites (e.g., kidneys, brain) may lead to serious
complications.
2. Immune Response:
o The host’s immune system reacts to the presence of eggs, larvae,
or adult worms, causing inflammation.
o Eosinophilia (high eosinophil count) is a typical sign during larval
migration.
3. Mechanical Obstruction:
o A large worm burden can cause:
 Intestinal obstruction (particularly in children).
 Blockage of the biliary or pancreatic ducts, leading to
jaundice or pancreatitis.

4. Nutritional Impact:
 o Chronic infections can impair nutrient absorption and lead to
malnutrition, especially in children.
o The parasite competes with the host for essential nutrients, such as
vitamin A and protein.

Clinical Manifestations
 Asymptomatic infection: Common in light infections.
 Intestinal symptoms:
o Abdominal pain, bloating, nausea, diarrhea, or malnutrition.
o In severe cases: intestinal obstruction (requiring surgical
intervention).
 Respiratory symptoms:
o Cough, wheezing, or difficulty breathing during the lung
migration phase (Löffler’s syndrome).
o Hypersensitivity Reactions: Urticaria (hives) and allergic
symptoms may develop towards the end of the lung migration
phase.
 Complications:
o Biliary obstruction: Causing pain and jaundice.
o Pancreatitis: Due to worms blocking the pancreatic ducts.

Laboratory Diagnosis
1. Microscopy: Examination of fecal samples characteristic eggs with
thick shells.
2. Eosinophilia: [Elevated eosinophil counts]
(5–12%, sometimes up to 30–50% during the larval migration phase)
o Serum IgG and IgE levels are also elevated during early infection.
3. Radiologic Findings:
o Plain X-ray:
 Shows a "whirlpool" effect caused by a mass of worms.
  Barium meal: Worms ingest barium, appearing as white
threads within their bodies.
o Ultrasound: Useful in diagnosing biliary or pancreatic
ascariasis.
o CT or MRI: Can visualize worms in the liver or bile ducts, with
cross-sections showing a "bull’s eye" appearance.
4. Serology:
o Antibody detection tests may identify chronic infections, but
these are less commonly used for routine diagnosis.

Treatment
Several anti-helminthic drugs are effective in treating ascariasis.
1. First-Line Treatments:
o Albendazole:
 400 mg single dose (nearly 100% effective).
o Mebendazole:
 100 mg twice daily for 3 days or 500 mg single dose.
o Pyrantel pamoate:
 11 mg/kg (maximum 1 g) in a single dose.
2. Other Options:
o Ivermectin:
 Causes paralysis of worms but is not a first-line choice.
o Piperazine citrate:
 Rarely used due to toxicity; used at 50–75 mg/kg for 2 days.
o Levamisole:
 150 mg for adults or 5 mg/kg for children; 77–96% effective.

Prevention
 1. Sanitation:
o Preventing fecal contamination of soil through improved hygiene
and sanitation is essential.
2. Mass Deworming Programs:
o In endemic areas, mass treatment with albendazole or
mebendazole every 3–4 months targets school-aged children to
reduce infection rates.

Enterobius vermicularis (Pinworm Infection)

Disease: Pinworm infection, or

Enterobiasis
Pathogenesis:
 a) Mode of infection: The infection begins when a person ingests eggs of
the worm (usually through contaminated hands, food, or surfaces).

b) Life cycle:
o Eggs hatch in the small
intestine and release
larvae.
o These larvae
differentiate into adult
worms and migrate to
the colon, where they
mature.
o Mating occurs in the
colon.
o At night, adult female
worms migrate from
the anus to the
perianal region and
release thousands of
eggs on the skin.
o Transmission: Eggs are
easily spread via hands,
clothes, bedding, and
surfaces, causing
reinfection or infecting others.
Clinical Findings:
 The main symptom is perianal pruritis (itching around the anus),
which is often worse at night.
 The itching is thought to be an allergic reaction to the eggs or worm
secretions.
Laboratory Diagnosis and Treatment:
 Diagnosis:
 o Scotch tape technique: Adhesive tape is pressed on the perianal
skin in the morning before bathing, then transferred to a glass slide.
Microscopy is used to detect the eggs.
 Treatment:
o Mebendazole or pyrantel pamoate are the primary drugs used.
o These medications kill the adult worms but not the eggs, so
reinfection is common. Proper hygiene and treatment of all
household members is recommended to prevent reinfection.
Trichuris trichiura (Whipworm Infection)

Disease: Whipworm infection

Pathogenesis:
1. Mode of infection: Infection occurs by ingestion of eggs in
contaminated food or water.
2. Life cycle:
o Eggs hatch in the small intestine
and release larvae.
o The larvae migrate to the colon,
where they develop into mature
adult worms.
o Adult females lay thousands of
eggs, which are passed in the feces
and contaminate the environment.
o The infectious cycle continues
when new hosts ingest
contaminated food or water.
Clinical Findings:
 Mild infection: Usually asymptomatic.
 Heavy infection:
o Diarrhea.
o Rectal prolapse (a part of the rectum protruding through the anus)
may occur, especially in children with severe infections. This
happens due to increased peristalsis (contractions of the intestines
trying to expel the worms).
 Anemia is generally not significant in whipworm infections.
Laboratory Diagnosis and Treatment:
 Diagnosis:
o Stool examination reveals barrel-shaped eggs with a mucus plug
at each end under the microscope.
 Treatment:
o Mebendazole is the drug of choice.

Hookworms:
Parasitic nematodes that infect the small intestine of mammals like humans,
dogs, and cats.
The two main species that infect humans are:
 Ancylostoma duodenale (Old World hookworm)
 Necator americanus (New World hookworm)
Morphology of Ancylostoma duodenale

Adult Worm
 Size:

o Male: 8 mm, shorter with a bell-shaped copulatory bursa (for

mating).
o Female: 12.5 mm, longer with tapering posterior (no bursa).
 Buccal Capsule:
o Lined with a hard substance with 6 teeth (4 hook-like on the
ventral side and 2 triangular plates on the dorsal side).
o Secretes enzymes to prevent blood clotting, aiding in blood
feeding.
Eggs
 Oval, colorless, surrounded by a
transparent shell.
 Size: 60 µm by 40 µm.
 Contains 4 blastomeres (segments)
inside.
 Ancylostoma produces 10,000-20,000
eggs per day, whereas Necator produces
3,000-6,000 eggs per day.
Filariform Larva (Infective stage)
 Non-feeding, elongated larvae that penetrate the skin to infect the host.

Life Cycle

 Completed entirely in one host (human).

 Development Time: About 8-10 days from egg to infective stage.
  Stages:
1. Passage of eggs in feces from an infected host.
2. Development in soil:
o Eggs hatch into L1 rhabditiform larvae, which molt twice to
become L3 filariform larvae (infective stage).
3. Entry into host:
o L3 larvae penetrate the skin (cutaneous route) or enter via oral
ingestion.
4. Migration:
o Through lymphatic vessels → lungs (alveoli) → trachea and
pharynx → swallowed into the intestine.
5. Maturation & Reproduction:
o Larvae mature into adults in the small intestine and start laying
eggs after 4-5 weeks.

Transmission
1. Cutaneous: Skin penetration by L3 larvae (most common).
2. Oral ingestion: Swallowing infective larvae from contaminated soil.
3. Transmammary: Transmission through breast milk.
4. Rare cases: Trans-placental transmission (mother to fetus).

Pathogenesis & Symptoms

1. Adult Worms in Intestine
o Attach to the intestinal wall, sucking blood and causing
mechanical disruption of the mucosa.
o Blood Loss:
 A. duodenale: 0.2 ml/day per worm
 N. americanus: 0.03 ml/day per worm
o Anemia: Leads to iron-deficiency anemia and hypoalbuminemia
(low protein levels).
 2. Infective Larvae
o Ground itch: Local reaction at the site of skin penetration with
intense itching.
o Pulmonary phase: Larvae in the lungs cause mild cough, fever,
and wheezing.
o Eosinophilia (high eosinophil count) and leukocytosis (high white
blood cell count).
3. Intestinal Infection
o Symptoms: Abdominal pain, nausea, vomiting, and bloody
diarrhea.
o Chronic infection: Results in fatigue, pallor, tachycardia,
malabsorption, and stunted growth in children.

Laboratory Diagnosis
1. Stool Microscopy
o Direct wet mount to detect eggs in feces.
o For light infections, concentration techniques (e.g., formalin-ether
or salt flotation) are used.
2. Stool Culture
o Harada-Mori method: Incubating stool on moist filter paper to
hatch larvae.
3. Imaging
o Chest X-ray may show patchy infiltrates in cases of lung
involvement.
4. Blood Test
o Identifies anemia and eosinophilia.
5. Occult Blood Test
o Detects hidden blood in stool.

Treatment
 1. Anti-parasitic drugs:
o Mebendazole (100 mg twice daily for 3 days)
o Albendazole, Pyrantel pamoate, Levamisole
2. Iron replacement therapy:
o For treating anemia caused by chronic blood loss.

Prevention
 Sanitation: Proper disposal of feces, use of sanitary latrines.
 Personal hygiene: Wearing shoes to avoid skin penetration.
 Health education: Nutritional support with iron-rich diets.
 Treatment of infected individuals to break the transmission cycle.

Epidemiology
 Prevalence: Second most common helminthic infection worldwide (after
ascariasis).
 Distribution:
o A. duodenale: Europe (Mediterranean), South America, China,
India, Nepal.
o N. americanus: Africa, Southeast Asia, and the Americas.
 Affected Population: Around 1.2 billion people globally, mostly in
warm, moist climates where sanitation is poor.