Nematodes infections of the intestine

- Cylindrical worms (round in cross-section), unisexual (Separate

sexes),
have a body cavity.
- Male is smaller than female (♀ >♂) and commonly has a curved
posterior
end.
- The digestive system begins with the mouth with lips, papillae, or
buccal
capsules, followed by the esophagus, then intestine, and ends by the
anus.

Ascaris lumbricoides
(Giant intestinal roundworm)

Geographical distribution: cosmopolitan, especially in tropical and

subtropical
countries (moist warm climates and temperate zones) with inadequate
sanitation. It’s common in Egypt.

Life cycle and transmission:

- Definitive host (DH): Man, especially children.
- Habitat: Lumen of the small intestine.
- Diagnostic stage: Fertilized and unfertilized immature eggs pass in the
feces (200,000 eggs/female/day).
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- Intermediate host (IH): None.
- Reservoir hosts (RH): None; human is the only host.
- Infective stage: Egg containing 2nd stage larva (embryonated egg).
- Mode of infection: Ingestion of foods, mainly vegetables and carrots,
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contaminated by eggs with 2nd stage larvae (embryonated eggs).
Contaminated hands with polluted soil are another source of infection.

N.B.
In soil, fertilized eggs embryonate optimally in moist, warm, shaded soil and
develop infective larva in 2 – 5 weeks. After infective eggs are
swallowed, the larvae hatch, invade the intestinal mucosa and are carried via
the portal, then systemic circulation to the lungs. The larvae mature further
in the lungs (10 to 14 days), penetrate the alveolar walls, ascend the bronchial tree
to the throat, and are swallowed. Upon reaching the small intestine, they develop
into adult worms. Between 2 and 3 months are required from ingestion of the
infective eggs to oviposition by the adult female. Adult worms can live for 1 to 2
years

Clinical picture

1- Migratory phase:
It is caused by the passage of migrating larvae either to the lung or other
viscera.
Loffler’s syndrome: fever, cough, eosinophilia, lung infiltration (during
prepatent period). Passing larvae from pulmonary capillaries to the
alveoli leads to peticheal haemorrhage, cellular infiltrate with
polymorphonuclear cells and eosinophils, cellular exudates and
formation of Charcot leyden crystals.

Occasionally, some larvae reach the general circulation and are

distributed to various organs such as lymph nodes, brain, spleen &
kidneys, leading to granuloma formation around the larvae with
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abnormal clinical manifestations resulting from visceral larva migrans
(VLM).

2- Intestinal stage:
- Asymptomatic in light infection.

- Heavy infection: nausea, vomiting, diarrhea, and abdominal pain. The

adult worm metabolites cause gastrointestinal irritation and suppression
of digestive enzymes.

- Intestinal obstruction due to intussusception and volvulus may occur.

3- The erratic movement of the adult:

occurs due to its irritation by fever,
anesthesia, and drugs. Adult migrates from typical habitat through any
opening and can even perforate the intestinal wall to:
a- Ampulla of Vater: acute pancreatitis.
b- Common Biliary Duct (CBD): obstructive jaundice.
c- Appendix: acute appendicitis.
d- Peritoneum: peritonitis due to intestinal bacteria after perforation of
the intestinal wall.
e- Liver: granulomas around eggs and adult ♀.
f- Biliary ducts: biliary ascariasis with recurrent cholangitis.

Diagnosis:
A- Direct methods:
1- Detection of eggs or adults in feces.
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2- Egg count by Stoll’s technique is needed to estimate worm burden.
3- Detection of larvae and Charcot leyen crystals in sputum.
B- Indirect methods:
1- Eosinophilia.
2- Chest x-ray (lung infiltration).
3- X-ray with Barium meal: filling defects [ string test ]

Treatment:
- Mebendazole (vermox or antiver) is the drug
of choice as 100 mg bid (twice daily) for three days.
It acts on adult only.
- Treatment is to be followed by purge to avoid allergic manifestation.

Prevention and control:

1- Personal hygiene.
 Hand washing.
 Vegetable washing.
 Avoid playing in the soil.
2- Sanitary disposal of human excreta.
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3- Avoid the use of human excreta as fertilizer for vegetables
4- Treatment of patients.

Trichuris trichiura
(Trichocephalus trichiuris or whipworm)
Geographical distribution: Worldwide, especially in humid tropical and
subtropical countries including Egypt.
Life cycle and transmission:
- Definitive host (DH): Man
- Habitat: Large intestine (caecum, appendix, colon, and rectum) with anterior
end embedded in the intestinal wall.
- Diagnostic stage: one cell immature egg in feces.
- Intermediate host (IH): None.
- Reservoir hosts (RH): None.
- Infective stage: Embryonated egg with 2nd stage larva.
- Mode of infection: Ingestion of soil, food or drinks contaminated with
embryonated egg

Clinical picture
1- Mild infection: Asymptomatic.

2- Heavy infection:
- Dysentery with mucopurulent stools, pain in the right iliac fossa and
paraumbilical region frequently lead to rectal prolapse.

- Penetration of mucosa may predispose to 2ry bacterial infection,

appendicitis, and peritonitis.
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- Bleeding from friable mucosa leads to hypochromic iron deficiency
anemia with clubbing of fingers and growth retardation in children.
- Megaloblastic (hyperchromic) anemia may occur (Trichocephalus
pernicious anemia) due to toxins of the parasite.

.Diagnosis:
- Detection of typical eggs in stools sample.
- Proctoscopy to detect the worms.

Treatment:
• Mebendazole (ivermox or antiver) is the drug of choice in a single oral dose
of 100 mg.
Prevention and control:
- Personal hygiene:
 Washing hands before meals.
 Proper washing of raw vegetables.
 Avoid playing in the soil.
- Avoid the use of human excreta as fertilizer to vegetables.
- Proper disposal of human feces.

N.B.
Tricuris suis is a parasite of pig. Man dealing with pigs can be infected.
Egg pass in human stool without any symptoms giving a false diagnosis of
Trichuris trichiuria.

Enterobius vermicularis
(Oxyuris, thread worm, pinworm, seat-worm)
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Geographical distribution: Worldwide. Mostly in children.

Life cycle and transmission:

- DH: Man, common in children (5-14 years).

- Habitat: Caecum and colon (large intestine).
- Diagnostic stage: Mature egg (containing larva) and adult female in perianal
skin or stools.
- Infective stage: Embryonated egg (Egg containing larva).

- Mode of infection: Household transmission is common:

1- Auto infection e.g., during finger biting or thumb suckling.
2- Ingestion of food and drink contaminated with eggs
3- Handling contaminated cloths (night cloths) or bed linen as the eggs
remain viable for three weeks.
4- Airborne through inhalation of dust contaminated with eggs.
5- Retro infection: eggs hatch in the perianal region, and the newly
hatched larvae ascend through the anus to the large intestine.

Clinical picture
A- May be asymptomatic

B- Local symptoms:

- Pruritis ani at night (migration of gravid female out of the anus to lay eggs
in perianal skin). Itching causes excoriation of the skin and secondary
infection.

- Enterocolitis (inflammation of mucosa) as the adult attaches itself to

intestinal mucosa causing minute ulcerations in caecal and appendicular
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.mucosa, hemorrhage with submucosal abscess due to secondary bacterial
infection. There is nausea, vomiting, and diarrhea.

- Appendicitis.

C- General symptoms:
- Insomnia, restlessness, and nocturnal enuresis.

D- Complications:
1- Secondary bacterial dermatitis of perianal region.
2- Vulvitis with pruritis vulvae.
3- Vaginits with mucoid vaginal discharge.

Diagnosis:
1- Detection of eggs at the perianal skin in the morning, before bathing and
defecation by:
a. National Institute of Health (NIH) swab.
b. Scotch adhesive tape.
c. Toilet paper.
d. Camel hairbrush of Khalil.
2- Detection of eggs in stools: + ve in 5% only.
3- Detection of adult at the perianal skin at night.

Treatment:
- All the family must be treated.
- Albendazole (zentol) is the drug of choice as a single dose of 400 mg/kg
and repeated after two weeks.
- Local application of Mercurial ointment (white precipitate ointment) to
perianal skin at night to relieve itching, kill adult females and prevent egg
deposition.

Prevention and control:

- Mass treatment to all members of the family.
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- Personal hygiene.
Washing hands before meal.
Keeping nails short.
Avoid thumb suckling and finger nail biting.
Boiling bed linen and cloths.
181182
- Infected children must wear tight trouser at night.
- Food and drink must be protected from contamination.

Trichostrongylus colubriformis
Geographical distribution: Egypt, Central Africa, India, Japan, and Indonesia.

Life cycle and transmission:

- DH: Man.
- Habitat: Small intestine of man.
- Diagnostic stage: Trichostrongylus egg.
- RH: Herbivorous animals.
- Infective stage: Third stage filariform larva. It is sheathed, has a filariform
esophagus, and its tail is pointed.
- Mode of infection: Ingestion of filariform larvae in contaminated raw
vegetables

Pathogenicity:
- Anterior end of the worm is embedded in intestinal mucosa causing
inflammation which results in gastrointestinal disturbance.

Clinical picture (Trichostrongyliasis)

- Asymptomatic in light infection.
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- In heavy infection, there is gastrointestinal disturbance and mild anemia.

Diagnosis:
Detection of eggs in stools.

Treatment:
- Levamisole is the drug of choice in a single oral dose of 2.5 mg/kg.

Prevention and control:

- Proper washing of raw vegetables.
- Proper water purification.
- Sanitary disposal of human excreta.

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 Hookworms
Ancylostoma duodenale and Necator americanus

Geographical distribution: Tropical and subtropical countries, including Egypt.

Necator Americanus is common in Africa, America, and Southern Asia
.
Life cycle and transmission:
- DH: Man.
- Habitat: Small intestine of man (jejunum).
- Diagnostic stage: Egg containing 4-cell stage in stools.
- Infective stage: Third stage filariform larva in soil.
- Modes of infection:
1. Percutaneous route: filariform larva penetrates the skin.
2. Via mucous membrane penetration when infective larvae are eaten with
contaminated vegetables.
3. Trans-mammary: Larva passes to suckling baby through milk.

- N.B. Immature eggs pass in the feces (20,000 eggs/female/day in

Ancylostoma and 10,000 eggs/female/ day in Necator americanus). Under
favorable conditions (moisture, warmth, shade), larvae hatch in 1 to 2
days. The released rhabditiform larvae grow in the feces and/or the soil, and
after 5 to 10 days (and two molts), they become filariform (third-stage) larvae
that are infective. These infective larvae can survive 3 to 4 weeks in favorable
environmental conditions. On contact with the human host, the larvae
penetrate the skin and are carried through the veins to the heart and then to the
lungs. They penetrate the pulmonary alveoli, ascend the bronchial tree to the
pharynx, and are swallowed. The larvae reach the small intestine, where they
reside and mature into adults. Adult worms live in the small intestine lumen,
where they attach to the intestinal wall with resultant blood loss by the
host. Most adult worms are eliminated in 1 to 2 years, but longevity records
can reach several years. Some A. duodenale larvae, following penetration of
the host skin, can become dormant (in the intestine or muscle). In addition,
infection by A. duodenale may probably also occur by the oral and
transmammary routes
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.
Larval tropisms:
The infective larvae are attracted to the host by different tropisms:
1. Positive thermotropism: Larva is drawn toward heat or warmth.
2. Positive hygrotropism: larva moves toward moist.
3. Positive chemotropism: larva moves toward O2.
4. Positive histotropism: larvae move toward host tissues
5. Negative geotropism: larva moves against gravity.
6. Positive phototropism: Larva moves toward light.

Clinical picture
1- Invasion stage: due to penetrating the skin by the infective larvae. There is
dermatitis, itching, erythema, papules, and pustules (ground itch). The most
affected site is the feet and hands.

2- Migration stage (Loffler’s syndrome): due to migration of the

infective
larvae to the lung leads to pneumonia. There is fever, dry cough, bronchitis,
lung infiltration, and asthma.

3- Intestinal stage: The adult attaches to intestinal wall by its buccal capsule
causing inflammation, malabsorption and sucks blood for feeding.

- Hook worm enteropathy: Epigastric pain, abdominal discomfort,

nausea, vomiting, loss of appetite, sometimesthere is geophagy or pica,
diarrhea with occult blood in stools.
- There is malabsorption, hypoalbuminemia, and edema due to
reversible changes of villi.

- Hook worm anemia (Egyptian chlorosis, Miner’s anemia):

hypochromic iron deficiency anemia as the adult sucks blood for
feeding (each worm sucks about 0.5 ml/day). Anaemia is also due to
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decreased iron intake and depletion of iron stores. Dyspnea on mild
exertion, weakness, apathy, pallor, tachycardia, and heart failure
commonly occur.

Mechanisms of anemia:
a- Tear by buccal capsule.
b- Anticoagulant
secretion by cephalic glands (continued bleeding
after detachment).
c- Toxic bone marrow depression.
d- Enteritis (due to 2ry infection) decrease absorption of iron.

Complications:
1. Myocarditis and cardiac dilatation are due to anemia.
2. Edema and ascites are caused by hypoalbuminemia.
3. Physical and mental retardation is caused by toxins secreted by the
worms. These toxins affect the endocrine glands.

Diagnosis:
1. Detection of eggs in the stools.
2. Estimation of the intensity of infection by Stoll`s technique.
3. Detection of larvae in soil by Baermann`s technique.
4. Detection of anemia by blood iron level, hemoglobin, and ferritin analysis.

Treatment:
- Elimination of adult worms by Albendazole (zentol), the drug of
choice in a single oral dose of 400 mg (80% cure); or 200mg daily for
three successive days (100% cure).
- Treatment of anemia: Replacement therapy of iron by ferrous sulphate
or gluconate 200 mg tds and folic acid 5 mg for three months.

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Prevention and control:
1. Personal prophylaxis: People work in mines or handling mud as farmers
must wear shoes and gloves.
2. Health education:
a. Abstinence from walking barefooted
b. Abstinence from defecation on the ground.
3. Sanitary disposal of human excreta.
4. Mass treatment of cases.
.

Strongyloides stercoralis
(Dwarf thread worm)
- Geographical distribution: Worldwide.

Life cycle and transmission:

- DH: Man.
- Habitat: The parasitic males and females live in the small intestine of
man (duodenum and jejunum).
- Diagnostic stage: The rhabditiform larvae.
- RH: Dogs and Chimpanzees have been found infected with strains like
those of man.
- The infective stage: Filariform larvae.
- Mode of infection:
1- Filariform larvae penetrate the skin of hands and the feet, getting in contact
with contaminated soils.
2- Autoinfection: If the rhabditiform larvae change into filariform larvae in the
lumen of the intestine and penetrate the intestinal mucosa (Internal
autoinfection). In other cases, these larvae come out and penetrate the
perianal skin (External autoinfection).

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N.B. It has two types of cycles; free-living and parasitic.
a- Parasitic cycle: When the external environmental conditions are unfavorable
for free-living, rhabditiform larvae grow and molt in 2-3 days to filariform
larvae that infect man
b- Free-living cycle: If the external environmental conditions are favorable for
free-living, the rhabditiform larvae molt in two days to free-living males and
females

- So, larvae join the venous circulation by auto-infection and complete their
direct life cycle. More and more adults are formed in the intestine until they
reach the state of hyper-infection.
- Sometimes the filariform larvae reaching the lung may stay for a few days and
develop to adults (in cases of immunosuppression of man). Adults mate, so
worms, eggs, and rhabditiform larvae may be detected in the bronchial
epithelium and may be found in the sputum.

- Strongyloidiasis in individuals receiving immunosuppressive therapy, which

reduces the body's natural resistance, is considered an opportunistic
helminthic infection due to the extensive invasion by the adult worms.

Clinical picture
- It depends on the intensity of infection and the host immunity, so:

1- During the invasive stage, skin irritation and creeping eruption sometimes
ground itching, occurs due to the secretory products of the penetrating
filariform larvae. There may be dermatitis, papular, vesicular, or pustular
eruption.

2- On the migration phase: fever, cough, expectoration, hemoptysis,

leukocytosis, and eosinophilia due to petechial hemorrhage in the pulmonary
tissue caused by the metabolites and end products of the larvae in the lungs.
In severe infection, lobar pneumonitis and consolidation may result.

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3- During the intestinal phase:
- The mature females invade and penetrate the intestinal mucosa to lay eggs
then larvae, leading to acute mucosal inflammation, sloughing, secondary
infection, and necrosis. Mucosa heals by fibrosis which affects the intestine's
physiological functions.
- Nausea, vomiting, and diarrhea (cochin-china diarrhea) alternating with
constipation.
- Epigastric pain and tenderness due to duodenitis.
- Anorexia, loss of weight and weakness.
- Eosinophilia.
- Skin manifestations during the chronic course of infection are linear tortuous
urticarial lesions over thighs, back, and trunk resembling cutaneous larva
migrans (CLM).

4- In immunosuppressed case, massive penetration of the perianal skin by

the filariform larvae causes linear urticarial lesions over the thigh and trunk; this
is called larva currens (racing larvae). The filariform larvae in the lung
alveoli gain access to the general circulation and may invade the brain,
intestine, lymph glands, liver, and rarely the myocardium.

Diagnosis: as hock worm

1- Rhabditiform larvae in stools (diagnostic) or the sputum by direct simple
smear.
2- Baermann's technique increase the chance of detection of larvae.
3- Stools culture.
4- Eosinophilia (blood picture).
5- Serological tests as IHAT and ELISA.

Treatment
: Thiabendazole: 25 mg/kg twice daily for 2-3 days. A 5-7 days course
for disseminated infection.

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Prevention and control:
1- Personal prophylaxis: Wearing shoes and other protective clothes as gloves
for people handling mud or working in mines, gardening2- Health education:
a. Abstinence from walking barefooted.
b. Abstinence from defecation on the ground.
3- Sanitary disposal of human feces: Usage as fertilizer should be after storage
or chemical disinfection of feces.
4- Mass treatment: Periodic mass treatment of the population.

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