REVISION

Types of Life Cycle in Trematoda and Cestoda

Life cycle in human trematodes

Type of life cycles in intestinal cestodes

Life cycles in human intestinal cestodes

Life cycles in human larval cestodiases

Nematoda

Dr. Mohiedden M Abdul-Fattah

General characters• Cylindrical, round in cross section (round worm).• Body wall is formed of 3 layers• Has body cavity containing fluid, sex organs and intestine.

• Separate sexes ♀ >♂.• Single set of genitalia

in ♂ and 2 sets in ♀.• Digestive system

begins with;• Mouth with lips,

papillae or buccal capsules, followed by

• oesophagus, then • Intestine and ends by • Anus which opens

ventrally joining the genital tract to form cloaca in ♂. and separately in ♀

Esophagus types in nematodes

Adult intestinal nematodes with pre adult larval migratory phase: Ascaris lumbricoides, strongyloides stercoralis, Hookworms

Adult Intestinal nematodes without larval migratory phase: Enterobius vermicularis, Trichostrongylus colubriformis, Capillaria philippinensis and Trichuris trichiura.

Intestinal nematodes with post-adult larval tissue invasion: Trichinella.

Larval tissue nematodiases with developmental arrest: visceral and cutaneous larva migrans.

Adult tissue nematodes: Adult tissue nematodiasis: Dracunculus medinensis and filariae.

Human Nematodes

Classification of nematodes according to habitat and development.

Adult intestinal nematodes with pre adult larval migratory

phase: ,Ascaris, Hookworms, strongyloides.

Adult Intestinal nematodes without larval migratory phase:

Enterobius, Trichostrongylus, Capillaria and Trichuris.

Intestinal nematodes with post-adult larval tissue invasion:

Trichinella.

Larval tissue nematodes with developmental arrest: visceral

and cutaneous larva migrans.

Adult tissue nematodes: Adult tissue nematodiases:

Dracunculus and filariae.

Nematodes according to mode of infection

1. Ingestion of eggs: Ascaris, Enterobius, Trichuris.2. Ingestion of larva: Trichostrongylus (on vegetable), Trichinella (in pork),

Dracunculus (in cyclops), Capillaria (in fish).3. Active penetration of skin by larva: Ancylostoma, Necator, Strongyloides.4. Entrance of skin by larva transmitted by insect: Filarial worms : Wucheraria, Onchocerca, Loa,

Acanthocheilonema, Mansonella.

Nematode infection by ingestion

Nematode infection via skin

Intestinal Nematodes: with pre-adult larval lung migratory phase:

Dr Mohieddin M Abdul-Fattah

1. Ascaris

2. Hookworms

3. Strongyloides stercoralis

I. Biology1.Ascaris lumbricoides

Ascaris male and female

♂ post end with spicule

Man related biology

1. Man (especially children) act as final host.

2. Habitat: lumen of small intestine.

3. Diagnostic morphology: Intestinal nematode; 25 cm long, creamy white.

4. Exit stage: fertilized and unfertilized eggs in stool ♀ Ascaris lays 200,000 eggs per day.

II. Epidemiology Geographical distribution: moist warm

climates and temperate zones. Transmission:.

1. Intermediate host: none

2. Reservoir hosts: None, Human is the only host.

3. Infective stage: egg containing Filariform larvae.

Fertile eggs embryonate optimally in moist, warm, shaded soil and develop infective filariform larva in 2 – 5 weeks.

4. Mode of infection: Ingestion of foods mainly vegetables and carrots contaminated by eggs with (2nd stage) larvae.

III. Host parasite relationship

Immune responses

1. Adult in the lumen elicits no immune response.

2. Migrating larva stimulates humoral response with an increase of IgE.

3. Migrating larvae in the lung initiate inflammatory cellular response (eosinophilic)

4. The immune responses are not protective as reinfection occurs.

III. Host parasite relationship

Pathogenesis

1. Larvae in the lung cause pneumonitis (Loffler's syndrome)

2. Heavy worm burden (> 200 eggs/ G feces) causes intestinal obstruction.

3. Parasite secretes trypsin inhibitor, prevents host from digesting proteins → protein-calorie malnutrition.

4. Migrating adult into bile ducts causes obstructive jaundice and pancreatitis

Inflammatory eosinophilic granuloma around larva in lung

Volvulus

Ascaris extracted from liver

III. Host parasite relationship Clincal picture:

1. Migratory phase: Loffler’s syndrome: fever, cough, eosinophilia

lung infiltration; (during prepatent period).

2. Intestinal stage: Asymptomatic in light infection. Heavy infection; nausea, vomiting, diarrhea and

abdominal pain. Intestinal obstruction due to intussusception and

volvulus may occur.

III. Host parasite relationship Erratic movement of the adult: occurs due to its

irritation by fever, anesthesia and drugs: Adult migrate from normal habitat through any opening,

and can even perforate the intestinal wall to:

1. Ampulla of Vater: (pancreatitis).

2. CBD: (obstructive jaundice).

3. Appendix: (appendicitis).

4. Peritoneum: (peritonitis due to intestinal bacteria)

5. Liver: granulomas around eggs and adult ♀.

6. Biliary ducts: biliary ascariasis with recurrent cholangitis.

IV. Diagnosis Direct methods: Detection of eggs in feces. Egg count by Stoll technique is

needed to estimate worm burden. Detection of larvae in sputum Indirect methods: Eosinphilia. Chest x-ray (lung infiltration). X-ray with Barium meal: filling

defects

ovoid.60 x 45 um

V. Treatment Albendazole: 200 mg for 3 days. Mebendazole: 100 mg bid for 3 days. Treatment; to be followed by purge to avoid

allergic manifestation.

Alternating streaking filling defects in barium meal

VI. Control

Personal hygiene Hand washing Vegetable washing Avoid playing in soil. Sanitary disposal of human excreta. Avoid use of human excreta as fertilizer for

vegetables Treatment of patients

Use of night soil as fertilizer

2. Hookworms: Ancylostoma and Necator BIOLOGY: Final host: human. Habitat: The adult are usually found in jejunum. Exit stage: Adult females put eggs [20,000/24h;

Ancylostoma, 4000; Necator] in the 4 cell stage. When passed in stool they develop to the morula stage and hatches in 1-2 days.

D. morphology: 9 – 12 mm x 0.4 mm, the head bends back dorsally and has a buccal capsule with teeth [Ancylostoma] or plates [Necator].

1. Egg in feces2. Rhabditiform larva Hatches

in soil

5. Adults live in small intestine

3. Filariform larva in soil

4. Penetrates skin

Life cycle of Hookworms

The 1st stage larva develops to the 2nd stage rhabditiform larvae with distal oesophageal bulb

Within 5-8 days it develop to infective 3rd stage non-feeding filariform larvae [800 µm with simple muscular esophagus and protective sheath].

The larvae penetrate skin, enter blood & migrate to lungs. They enter alveoli, pass up trachea, then swallowed to become mature worms in jejunum that lay eggs

within 5 week period from exposure.

II. Epidemiology Geographical distribution: Endemic in tropics; favoured by 1. promiscous daefecation.2. moist, shady, warm, sandy soil with decaying vegetation. 3. the presence of dung and stool burying beetles. Prolonged dry and cold climates are unsatisfactory. Transmission: Intermediate host: No. Resevoir hosts: No, Human are the only hosts. Infective stage: Filariform larvae in soil. 1. These larvae survive 3-4 weeks in the soil or moisture

films on the ground. 2. They move towards warmth, moisture, oxygen, and CO2

but away from gravity [larval tropism]. Mode of infection: Filariform larvae in soil penetrate

skin of feet.

Host-Parasite Relationship

1. Ground itch:

cutaneous penetration; associated with stinging

sensation, followed by local oedema, erythema and

papule formation.

These are more common in repeated infections and

reflect enhanced host immune reaction (type I) to

larval forms. They are more pronounced among the

expatriates.

2. Transient creeping eruption caused by larvae of

Necator americanus.

Host Parasite Relationship

3. Pulmonary lesions; pneumonitis and eosinophilia occurs during massive migration of larvae in the lung.

If Ancylostoma duodenale infection has occurred orally, pneumonitis is preceded by nausea, salivation, itching of the pharynx and hoarsness [Wakana disease].

4. Intestinal infection & hookworm disease; abdominal pain, diarrhea, less commonly malabsorption,

5. iron deficiency anaemia and chronic protein calorie malnutrition if the infection was heavy (>100 worms). Less than 25 worm load is insignificant.

Diagnosis Detection of eggs or larvae in faeces. Egg

count by Stoll technique is needed to estimate worm burden. Eosinphilia usually occurs.

Egg characters: thin shelled, colourless, ovoid with blunt ends, 60 x 40 µm and contain an ovum in 4 or 8 cell stage.

Rhabditoid larva: 250 µm with rhabditiform oesophagus, and buccal cavity longer than the width of the head tip.

Treatment1. Albendazole (Alzental, tablets 100, 200) 200 mg

for 3 days.

2. Mebendazole (Antiver, tablet 100mg) 100 mg twice daily for 3 days.

3. Pyrantel pamoate (Combantrin,tablets; 250, 125), a single dose of 12.5 mg/kg, i.e. 3 tablets

Control:

1.Use footwear.

2.Proper disposal of human waste

3. Strongyloides stercoralis Biology: Final host: Human. Habitat:. Adult lives and lays egg in mucosa

of small intestine . Exit stage: egg in the mucosa hatches

Rhabditiform larva that escapes into the lumen and is passed in faeces.

Diagnostic morphology: Parasitic female is larger (2.2 mm x 45 µm)

than the free-living worm (1 mm x 60 µm) .The eggs, when laid are 55 µm by 30 µm.

Life cycle of Strongyloides

2.Epidemiology:Geographical distribution: endemic in tropics and subtropics with poor sanitation. It has 2 features:

The worm has potential for autoinfection and multiplication within the host.

It has two types of cycles; free living and parasitic.Intermediate host: No.Reservoir host: NoThe infective stage: Filariform larvae.Mode of infection: Filariform larvae can penetrate either by:

The intestinal mucosa (internal autoinfection),The skin of the perianal area (external autoinfection),orContact of the skin of hands and feet with contaminated

soils.

3. Host parasite relationship: Patients with a low worm burden are asymptomatic,

otherwise; Larva currens:

A. rash caused by chronic cutaneous larval migration localized around the waist and buttocks.

B. It is a serpiginous red line that progresses 1 to 2cm/h for up to 48 h.

Larvae in the lung produce pneumonitis. Adults within the mucosa cause enteritis leading to

diarrhea. Sepsis due to enteric bacteria may occur due to damage

caused by autoinfection. Massive super infection occurs in the immune

compromised (hyper-infection)..

4.Lab diagnosis: - Detection of larvae in stool sample by direct exam.

Or by Baermann concentration. Eosinophilia in blood count Characters of the rhabditiform larva: Very short buccal cavity. The esophagus has two bulbs with narrow isthmus

between them.

5.Treatment: - Albendazole 5mg/kg/12h peroral (PO) for3d or Thiabendazole 25mg/kg/12h PO for 3d or Ivermctin (Mectizan) 200 µg/kg/d for two days.

6.Control: - Foot wear and proper disposal of human waste.

Intestinal nematodes with post-adult larval tissue invasion

•Trichinella spiralis

Trichinella spiralisA.Biology: Final host: Pigs, wild boars, rats, bears, walruses, and

many other carnivores including man. Habitat: -

i. Adult ♂ in Small intestines while females inhabit rows of epithelial cells of the mucosa of duodenum and jejunum.

ii. Larvae live in Striated muscle fibers (cells). Exit stage:

i. Males in the faecal streams.

ii. Larvae have no exit as they encyst in muscle fibers. Morphology: 2.5 mm long ♀ with tapering post. end and

1.2 mm long ♂ with 2 caudal appendages. ♀ puts 5000 larvae each 100 µm long.

Circulation

5. Larva encysts in striated muscles

3. enter intestinal mucosa

♂ copulates ♀

4.Larva deposited in the mucosa

1. Man ingests encysted larva in undercooked

pork

RodentsCarnivorism

Pigs

Life cycle of Trichinella

1. Encysted larva from pigs

2. Larvae released in intestine, mature to adults

Trichinella Life Cycle

Circulation

5. Larva encysts in striated muscles

3. enter intestinal mucosa

♂ copulates ♀

4.Larva deposited in the mucosa

1. Man ingests encysted larva in undercooked

pork

RodentsCarnivorism

Pigs

Life cycle of Trichinella

1. Encysted larva from pigs

2. Larvae released in intestine, mature to adults

B. Epidemiology: Distribution: Worldwide; prevalent in pork

eating countries (USA and Europe). Transmission: Intermediate host (IH): Pigs. One host may serve as both final and IH. Humans

are dead end IH. Reservoir host: Pigs, wild boars, rats, bears,

walruses, and many other carnivores. Infective stage: Encysted larvae in muscles. Mode of infection: Ingestion of pork infected by

encysted larvae.

C.Host-parasite relationship:1. Intestinal stage (20-24 hours): eneteritis → nausea,

vomiting, abdominal pain and diarrhea.2. Migratory stage:A.Invading skeletal muscles (1-2 weeks): fever, facial

edema, conjunctivitis, pain, swelling and weakness of the involved muscles.

B.Invading cardiac muscles and CNS (3rd week): Myocarditis and CNS involvement are the most frequent two causes of death in trichinosis.

3.Encapsulation (3w – 4 w): symptoms subside or decrease. Myocarditis persists

and may precipitate congestive heart failure.4. If the infective dose ≥100 larvae morbidity occurs. If it

is ≥300,000 death occurs

D. Diagnosis: 1. Symptoms. 2. detection of free or encapsulated larvae.

From the 7th day onward a) In compressed (trichinoscopy) or b) Stained biopsy.c) Or digested samples from deltoid, biceps,

gastrocnemius or Pectoralis muscles. d) Or by xenodiagnosis in rats. 3. Immune-diagnosis by a. Bachman intra-dermal skin test (IDT). Or by b. Serology: from 2 weeks in heavy infection and

3-4 w in lighter ones: BFT (2w), IFAT (2-3w) and Sandwich Elisa.

E.Treatment: Prednisolone 40 mg/day for 5d, with Mebendazole 50 mg/kg/12h PO for 10

days.

F.Control: Properly cooking pork. Feeding pigs on cooked garbage.

Intestinal nematodes without lung larval migratory phase

Habitat in large intestine:

1. Enterobius vermicularis (Oxyuris)

2. Ttichuris trichiura Habitat in small intestine

1. Trichostrongylus colubriformis

2. Capillaria philipinensis.

Enterobius vermicularis (Oxyuris)

Final host: Human. Habitat: Cecum

and colon. Exit stage: mature

egg. Diagnostic

morphology: ♀ cylindrical 1 cm with pointed ends. ♂ ½ cm with curved posterior end.

I. BIOLOGY

II. Epidemiology

Distribution: worldwide. Mostly in children. Transmission: Intermediate host: No. Reservoir host: No. Infective stage: Embryonated egg. Mode of infection: Ingestion of mature eggs fro environment, with

foods, or by hand to mouth. Re-infection (auto infection).

III. Host-Parasite relationship Peri-anal pruritis and insomnia, Nausea, and loss of appetite Urinary tract infection especially in females. Worm may migrate into ♀ genital tract

inducing bacterial infection, salpingitis.

IV. Diagnosis Eggs are detected in peri-anal skin by Scotch

tape technique. Adult in the stool or diapers. Eggs are detected in stool accidentally, in 3%

of patients

V. Treatment

Mebendazol 200 mg/12 hours for one day, repeated after one week.

If aged < 2 years, piperazine; 0.3ml/kg/day for 7 days. Treat the whole family

VI. Control

Personal cleanliness. Hygiene is more important than drugs as

adults die after 6 weeks. Continued symptoms means re-infection

Trichuris Trichiura

Final host: Man Habitat: Large

intestine with ant end embedded in the intestinal wall.

Exit stage: one cell immature egg.

Morphology: Whip like with narrow ant part is half the length of thick posterior part in ♂ and double the length in ♀.

I. BIOLOGY

II. Epidemiology Distribution: worldwide, esp. in the

tropics. Transmission: Intermediate host: None. Reservoir host: None. Infective stage:

embryonated egg with 2nd stage larva.

Mode of infection: Ingestion of soil, food or drinks contaminated with embryonated egg.

III. Host Parasite Relationship

1. Mild infection is asymptomatic, 2. In heavy infection: Penetration of mucosa may predispose to 2ry

bacterial infection, appendicitis and peritonitis. Bleeding from friable mucosa → hypochromic

iron deficiency anemia and growth retardation in children.

Megaloblastic (hyperchromic) anaemia may occur

3. Severe infection: dysentery→ frequently lead to rectal prolapse

IV. Diagnosis

Detection of typical eggs in stool sample.

Counting eggs with Stoll technique

Characters of egg:

1. 50 x 25 µm,

2. Barrel shaped with mucoid plug at both ends,

3. brownish, 4. unsegmented with one cell

V. Treatment

Mebendazole 200 mg/ 12h pero–oral (PO) for 6 days

VI. Control Personal hygiene Proper disposal of human faeces

Capillaria Philippinensis

1. Man or birds ingest larvae in fish & larvae develop to adults in intestinal mucosa

2.♀ lay Immature eggs3. Mature egg

4. Infective larva develops in fish

5. Some ♀ lay larvae 6.These reinvade mucosa & develop to adults

Internal auto- infection

Capillaria Philippinensis Life Cycle

C. philippinensis

Final host: Humans, fish.

Habitat: mucosa of the small intestine (the jejunum).

Exit stage: Eggs, larvae, and adults passed in feces.

Basic morphology and life cycle: adult 2-4 mm long.

I. BIOLOGY

II. Epidemiology

Distribution: worldwide but more in the Orientals ;

Philippines and Thailand. TransmissionI. Reservoir hosts: Fish and Birds.

II. Intermediate hosts: fish

III. Infective stage: infective larva in the mucosa of fish.

IV. Mode of infection: ingestion of undercooked fish infected with the larvae or by internal autoinfection.

III. Host Parasite Relationship

1. Watery diarrhea with excessive fluid loss.

2. Malabsorption with weight loss, abdominal

distension, oedema and muscle wasting.

3. Death due to heart failure, pneumonia or

hyperkalaemia in severe infection.

IV. Diagnosis Clinical picture in endemic areas gives a clue

to diagnosis. Detection of eggs in the stool:1. Thick shelled with polar plugs 2. 40x20µ in size. Detection of larvae or adults in stool.

V. Treatment Mebendazole: 400mg daily for 20 days

VI. Control Health education, proper cooking of fish.

Trichostrongylus

Final host: - herbivorous animals (sheep, goats). Occasionally, found in man.

Habitat:- small intestine; with anterior end embedded in the mucosa.

Exit stage: Egg with 16 -32 cell morula stage. Morphology: 4mm long ♂, 8mm long ♀, slender hair like

worm with narrow anterior extremity. Male adult is with post. copulatory bursa.

I. Biology

I. Biology: Life cycle

II. Epidemiology Distribution: Middle East and Far East. Transmission:1. Intermediate host: No.2. Reservoir host:- Sheep, camels and

goats.3. Infective stage:- Filariform larvae on

vegetables.4. Mode of infection:- Ingestion of

vegetables contaminated with filariform larvae.

III. Host-Parasite relationship Slight enteritis and diarrhea

IV. DiagnosisDetection of typical eggs in stool sample.

Characters of egg: 90 x 45 µm, thin shelled, pointed at one end, brownish, and segmented embryo with 16 -32 cells.

V.Treatment: Mebendazole 200 mg/ 12h peroral (PO) for three days.

VI.Control:- Personal hygiene, washing vegetables and water sanitation