Download 13. Medical helminthology Roundworms

Theme: Medical helminthology:
Roundworms – human parasites
Lecturer: ass. prof. Tetyana Bihunyak
The main questions:
1. General characteristic of class Nematoda.
2. Intestinal Nematodes:
2.1. Ascaris lumbricoides.
2.2. Enterobius vermicularis (Pinworm).
2.3. Trichuris trichiura (Whipworm).
2.4. Hookworms: Ancylostoma duodenale, Necator americanus.
2.5. Strongyloides stercoralis (Threadworm).
2.6. Trichinella spiralis.
3. Tissue Nematodes:
3.1. Dracunculus medinensis.
3.2. Wuchereria bancrofti.
3.3. Onchocerca volvulus.
3.4. Toxocara canis.
3.5. Loa loa.
Class Nematoda (Roundworms):
1.
Bilaterally
symmetrical,
elongate,
unsegmented worms.
2. Cylindrical, round in cross sections
(Roundworms).
3. Separate sexes. Sexual dimorphism: 1) males
are smaller than females; 2) posterior end of
male worm is rounded.
4. Pseudocoel containing body fluid.
5. Body wall is made by 3 layers:
1) Outer laminated non-cellular cuticle.
2) Subcuticular epithelium (hypodermis);
3)Muscle layer (4 groups of longitudinal cords).
6. Digestive system: mouth, pharynx,
oesophagus, intestine, anus (opens to cloaca).
7. Excretory system: special cells which function
as glands and systems of excretory canals.
8. Nervous system: peripharyngeal nervous
ring, dorsal and ventral longitudinal nerve
cords.
9. Reproductive system.
9.1. Male reproductive organs: testis (long
convoluted tube), vas deferens, seminal vesicle,
ejaculatory duct (opens to cloaca).
9.2.Female reproductive organs: two ovaries
(convoluted tubes), oviducts, uteri, vagina,
vulva.
Parasite: Ascaris lumbricoides
Disease: ascariasis
Geographical distribution: cosmopolitan
Morphology: Adult worms are creamy or pink, spindleshaped, covered by striated cuticle. Adult male about 20
cm in length, posterior end curved ventrally, adult female
about 25-40 cm in length, posterior end straight. Eggs are
brown, oval, covered by membranes. An external
membrane is tuberous.
Host: man
Mode of transmission: fecal-oral (alimentary).
Infective stage: eggs.
Localisation: small intestine (adult), liver, lungs, heart
(larvae).
Female
Male
Ascaris lumbricoides
Egg
Ascaris lumbricoides
Life cycle of Ascaris lumbricoides
1. Immature eggs pass in the feces (200,000 eggs/day).
2. Under favourable environmental conditions
(temperature 20-25 C, oxygen, humidity 70-90%) larvae
develop inside the eggs in the soil within 24 days
(infective stage).
3. Eggs may be ingested through contaminated, water or
raw vegetables, hands.
4. Eggs hatch in the small intestine.
5. Larvae migrate through the gut wall into the
bloodstream and then to the liver, heart, lungs. They enter
the alveoli, pass up the bronchi and trachea, and are
swallowed.
6. Within the small intestine, larvae become adult worms.
Eggs appear in feces about 2 months after infection.
Clinical manifestation: 1) Migrating larvae may lead to
pneumonia, eosinophilia. 2) Adults in the intestine may
cause intestinal obstruction, penetration of the intestinal
wall, occlusion of the bile duct, the pancreatic duct or the
appendix, toxic effects (nausea, vomiting). Most infection
are asymptomatic.
Laboratory diagnosis: microscopic examination of feces
(availability of eggs); larvae may be found in sputum.
Prophylaxis: washing hands before meals; proper
washing of vegetables eaten raw; treatment of patients;
health education.
Ascaris lumbricoides
Parasite: Enterobius vermicularis
Disease: enterobiasis
Geographical distribution: cosmopolitan
Morphology: Adult female worms are up to 10 mm in length,
and male worms are up to 5 mm. Eggs are transparent and
colourless, asymmetrical, with thin and smooth membrane, 40-60
micro;m.
Host: man.
Mode of transmission: fecal-oral (alimentary).
Infective stage: eggs.
Localisation: large intestine (caecum).
Male
Female
Enterobius vermicularis
Life cycle of Enterobius vermicularis:
1) The adult pinworms live in the colon approximately 30 days.
2) After fertilisation female worm migrates from the anus and
releases thousands of fertilized eggs on perianal skin.
3) Within 6 hours, eggs develop into larvae and become infectious.
4) Reinfection can occur if they are carried to the mouth by
fingers after scratching of the itching skin.
Clinical manifestation: Infection is frequent among children.
Perianal pruritus (itching) is most common symptom.
Laboratory diagnosis: the eggs are recovered from perianal skin
by using the “Scotch tape” technique and can be microscopically.
Prophylaxis: keep sanitary condition, dehelminthization of the
population.
Parasite: Trichuris trichiura
Disease: trichocephaliasis (whipworm infection)
Geographical distribution: cosmopolitan
Morphology: Adult female worms are up to 5,5 cm in
length, and male are up to 4 cm. The front end of the body
is thread-like extend. The eggs are brown, barrel-shaped
with a plug at each end, 20-50 micro;m in size.
Host: man.
Mode of transmission: fecal-oral (alimentary).
Infective stage: eggs.
Localisation: caecum, appendix, first 1/3 part of large
intestine.
Trichuris trichiura
Egg
Life cycle of Trichuris trichiura:
1. Immature eggs pass in the feces (2,000 eggs/day).
2. Under favourable environmental conditions (temperature 26-28 C,
oxygen, humidity 80-90%) larvae develop inside the eggs in the soil
within 4 weeks (infective stage).
3.Embryonated eggs may be ingested through contaminated, water, raw
vegetables and hands.
4. Eggs hatch in the small intestine; larvae become adults in few days,
then migrate to the large intestine.
5. Eggs appear in feces about 2 months after infection.
Pathogenesis and clinical manifestation: Adult worms burrow their
hairlike anterior ends into the intestinal mucosa. They feed blood.
Trichuris may cause diarrhea, abdominal pain, nausea, acute
appendicitis. Most infections are asymptomatic.
Laboratory diagnosis: microscopic examination of feces
(availability of eggs).
Prophylaxis: washing hands before meals; proper washing of
vegetables eaten raw; treatment of patients; health education.
Parasites: Ancylostoma duodenale, Necator americanus
Disease: ancylostomiasis
Morphology: 1) Adult worms about 1 cm in length;
2) Eggs are translucent, oval with blunt poles,
40-60 micro;m in size;
3) the rhabditiform larva is about 0.25-0.5
micro;m with rhabditiform oesophagus
(1/3 body length), pointed tail end;
4) the filariform larva is about 0.6-0.7 micro;m
with cylindrical oesophagus (1/4 body length),
sharply pointed tail.
Host: man.
Mode of transmission: penetration of skin by filariform larva
Infective stage: filariform larva.
Buccal capsule
of Ancylostoma duodenale
Life cycle of Ancylostoma and Necator:
1. Filariform larvae penetrate the skin, usually of feet or legs in
moist soil.
2. They are carried by the blood to the lungs, migrate into the
alveoli and up the bronchi and trachea, and then are swallowed.
3. They develop into adults in the small intestine, attaching to the
wall with either cutting plates (Necator) or teeth (Ancylostoma).
They feed blood.
4. Immature eggs pass in the feces about 2 months after infection.
5.Under favourable environmental conditions in the soil eggs
develop into rhabditiform larva and then into filariform larvae.
(infective stage).
Clinical manifestation: 1) invasion stage: dermatitis and itching
(“ground itch”); 2) migration stage: pneumonia, eosinophilia;
3) intestinal stage: anemia, diarrhea, abdominal pain, nausea.
Laboratory diagnosis: microscopic examination of feces
(availability of eggs). Blood in the stool is frequent.
Prophylaxis: disposing of sewage properly and wearing shoes.
Parasites: Strongyloides stercoralis
Disease: strongyloidiasis
Geographical distribution: cosmopolitan
Morphology: 1) adults;
2) eggs;
3) rhabditiform larvae;
4) filariform larvae;
5) free-living female and male.
Localisation: small intestine.
Host: man.
Mode of transmission: penetration of the skin by
filariform larva.
Infective stage: filariform larva.
Life cycle of Strongyloides stercoralis
1) within the human body:
1. Filariform larvae penetrate the skin, usually of feet or legs in
moist soil.
2. They migrate to the lungs, enter the alveoli, pass up the bronchi
and trachea, and then are swallowed.
3. Larvae develop into adults in the small intestine and produce
eggs.
4. The eggs form rhabditiform larvae that are passed in the feces
and appear in stool within 4 weeks of infection.
5. Some rhabditiform larvae form filariform larvae, which
penetrate the intestinal wall directly without leaving the host and
migrate to the lungs (autoreinfection).
6. In the soil, the rhabditiform larvae develop into filariform
larvae (infective for man).
2) free-living in the soil:
1. The rhabditiform larvae molt into free-living males
and females.
2. Female worms lay eggs in the soil.
3. The eggs develop into rhabditiform larvae;
rhabditiform larvae form filariform larvae (infective for
man).
Clinical manifestation: 1) invasion stage: pruritis
(ground itch) at the site of larval penetration of the skin;
2) migration stage: pneumonia, eosinophilia; 3) intestinal
stage: diarrhea, abdominal pain.
Laboratory diagnosis: microscopic examination of
faeces (availability of rhabditiform larvae).
Prophylaxis: disposing of sewage properly and
wearing shoes.
Parasites: Trichinella spiralis
Disease: trichinosis
Geographical distribution: especially Europe, west Africa
Morphology: 1) The adult female worms are up to 3-4  0.6
mm; the adult male worms are up
to 1.5  0.04 mm;
2) the incysted larvae (1 mm) is enclosed in a
fibrous cyst wall.
Localisation: small intestine (adult worms) and striated
muscles (larvae).
Hosts: man, pig, rat, bear, fox.
Infective stage: larva
Mode of transmission: alimentary (eating raw or undercooked
meat (usually pork), containing larvae.
Larva of Trichinella spiralis
Life cycle of Trichinella spiralis:
1. The larvae excyst and mature into adults within the small intestine
of host.
2. Male worms die after fertilization, female worms lay larvae.
3. Larvae are released and distributed via the bloodstream to striated
muscles
(diaphragm,
tongue,
m.deltoideus,
m.pectoralis,
m.intercostalis).
4. Larvae encyst in the muscles within fibrous capcule and can
remain viable for several years.
Clinical manifestation: initially diarrhea, abdominal pain; by 1-2
weeks later – fever, muscle pain, periorbital edema, eosinophilia.
Laboratory diagnosis: muscle biopsy reveals larvae within striated
muscle; serologic test (become positive 3 weeks after infection).
Prophylaxis: by properly cooking pork and by feeding pigs only
cooked garbage; pork inspection in slaughter houses using a
trichinoscope.
Pork inspection in
slaughter houses
using
a trichinoscope.
Species: Wuchereria bancrofti
Common Name of Disease: Filariasis
Endemic Areas: Tropics primarily
Mode of Transmission: Mosquito bite
Clinical Findings: Obstruction of lymphatic vessels,
causing edema of legs and genitalia (elephantiasis).
Diagnosis: Blood smear (microfilariae can be
demonstrated).
Wuchereria bancrofti
causes elephantiasis
Wuchereria
bancrofti causes
edema of leg
and genitalia
Species: Onchocerca volvulus
Common Name of Disease: Onchocerciasis (river
blindness)
Endemic Areas: Africa, Central America
Mode of Transmission: Blackfly bite
Clinical Findings: Inflammation of subcutaneous tissue,
formation of pruritic papules and nodules; lesions of the
eyes (blindness).
Diagnosis: Skin biopsy.
Species: Loa loa
Common Name of Disease: Loiasis
Endemic Areas: Tropical Africa
Mode of Transmission: Deer fly bite
Clinical Findings: Transient, localized, nonerythematous,
subcutaneous edema (Calabar swellings); adult worm
crawling across the conjuctiva of the eye.
Diagnosis: Blood smear (microfilariae can be
demonstrated).
Species: Dracunculus medinensis
Common Name of Disease: Dracunculiasis
Endemic Areas: Tropical Africa and Asia
Mode of Transmission: Ingestion of copepods in
water
Clinical Findings: Inflammation, blistering, and
ulceration of the skin; papule itches.
Diagnosis: Clinical (by finding the head of the
worm in the skin ulcer).
Dracunculus medinensis causes dracunculiasis
Species: Toxocara canis
Common Name of Disease: Visceral larva
migrans
Endemic Areas: Woldwide
Mode of Transmission: Ingestion of eggs
Clinical Findings: Fever, hepatomegaly,
blindness, eosinophilia.
Diagnosis: Clinical and serologic.
Life cycle
of Toxocara
canis
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