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Ascariasis
Anup Muni Bajracharya
Ascariasis
• infection of the small intestine
• caused by Ascaris lumbricoides
• the largest intestinal nematode to infect
human.
Habitat
• The adult worm lives in small intestine and
grow to a length of more than 30 cm.
• Human is only the natural host and reservoir
of infection.
Geographical Distribution
• occurs worldwide in areas with warm, moist
climates.
• most common in tropical and subtropical
areas where sanitation and hygiene are poor.
• Main epidemic region with prevalence rate of
approx. 10-90% includes countries on
• South east Asia, Africa and Latin America.
Morphology
• Adult:
• resembles to earthworm.
• is elongatedtapering to both end,
• anterior being thinner than
posterior.
• Freshly excreted worm is yellowish
pink in color, which gradually
changes to white.
• The worm is sexuallydiamorphic.
• Adult male: 15-30 cm in length, 3-4
mm in diameter, tailcurved
• Adult female; 20-40 cm length, 2-
6mm diameter, tail straight
Morphology
• Egg:
• round or oval,
• 60 x 40 µm size
• thick brown shell and have rough surface
• It is the infective form of parasite.
• Two types of eggs are liberated from the female worm of
Ascaris lumbricoides:
• i) fertilized egg
• ii) Unfertilized egg
•
Fertilized egg
Shape Round to oval.
Size 50-70um x 40-50um
Covering
Surrounded by a thick smooth transleucent
shell consisting of three layers:
-The outer coarsely mamillated albuminoid
coat
-A thick transparent middle layer
-Inner lipoidal vitelline membrane
Some eggs are found in feces without the
outer mamillated albuminous coat. These are
called decorticated eggs.
Bile Staining Bile stained, golden brown in saline mount.
Floatation Floats in saturated salt solution.
Ovum
Contains a large unsegmented ovum of
granular mass with clear space at both the
end.
The fertilized eggs are laid by females after
inseminatedby mating with a male. These are
embryonatedand developinto the infective eggs.
Unfertilized eggs
Size
90um x 45um
Shape Round to oval.
Covering
Albuminous coat is thin,
distorted and scanty.
Bile Staining
Bile stained, golden
brown in saline mount.
Floatation
Doesn’t float in saturated
salt solution.
Ovum
Contains an unsegmented
small atrophied ovum
with a mass of
disorganized highly
refractile granules.
The unfertilized eggs are laid by uninseminated
female. Thes are non-embryonated and cannot
become infective.
Life cycle
• The life cycle of Ascaris completes in single host human.
• Stage I: Eggs in faeces
• Sexuallymature female produces as many as 200,000 eggs
per day, which are shed along with faeces in
unembryonatedform. They are non infective.
Stage II: Development in soil
Embryonation occurs in soil as optimum temperatureof 20-25C
with sufficient moisture and oxygen
Infective larva developswithin egg in about 3-6 weeks.
Stage III: Human infection and liberation of larvae
Human get infection with ingestion of embryonated egg contaminated
food and water
Within embryonated state inside egg, first stage larvae develops into
second stage larvae. This second stage larvae is known as Rhabtitiform
larvae
Second stage larve is stimulatedto hatch out by the presence of
alkalinepH in small intestine and solubilizationof its outer layer by bile.
• Stage IV: migration of larvae through lungs
• Hatched out larvae penetrates the intestinalwall
and carried to liver through portal circulation
• It then travels via bloodto heart and to lungs by
pulmonary circulationwithin4-7 days of infection.
• The larvae in lungs molds twice, enlarge and
breaks into alveoli.
• Stage V: Re-entry to stomach and small intestine
• From alveoli,the Larvae then pass up through bronchi and into trachea and
then swallowed.
• The larvae passes down the oesophagus to the stomach and reached into
small intestine once again.
• Small intestine is the normal habitatof Ascaris and it colonises here.
• Within intestine parasitemolds twice and mature into adult worm.
• Sexual maturationoccurs with 6-10 weeks and the mature female
discharges its eggs in intestinal lumenand excreted along with faeces,
continuingthe life cycle.
• The life span of parasite is 12-18 months
Mode of transmission
• faeco-oral route, by contaminated vegetables
or water.
Pathogenesis
• Two phase in ascariasis.
• Phase I: migrating larvae
• The migrating larvae causes pathological lesions.
• The severity of lesions depends upon the sensitivity of host, nutritional
status of host and number of migrating larvae.
• During migration and molding through lungs, larvae may causes
pneumonia with low grade fever, cough and other allergic symptoms.
Pathogenesis
• Phase II: Adult worm
• Few worm in intestine produce no
major symptoms andbut some
time give abdominal pain especially
in children.
• The adult worm produce trauma in
host tissue
• The wandering adults mayblock
the appendical lumen or common
bile duct and even small intestine.
• Large number of adult worms
affects the nutritional status of host
causing malnutrition and growth
retardation in children.
• The metabolites of living or dead
worm are toxic and immunogenic.
• The worm also produces various
allergic toxin, which manifests fever,
conjunctivitis and irritation.
Picture Extraction of Ascarislumbricoidesfromjejunum
via enterotomy.
source- CaseReport, Published: 17 June 2009
Rare cause of intestinal obstruction, Ascarislumbricoides
infestation:twocase reports
Yetim et al
Clinical manifestation
• Most of the Ascaris infection is asymptomatic.
• Symptomatic ascariasis; two types
• Intestinal Ascariasis
• Pulmonary Ascariasis
2. Pulmonary ascariasis;
Transienteosinophilicpneumonitis
(loeffler’s disease); elevatedIgE
Bronchospasm
Dyspnea and wheezing
Fever
Non-productivecough and chest
pain
1. Intestinal ascariasis;
Nausea
Vomiting
Colicky abdominalpain
Abdominaldistention
Weight loss and diarrhea
Malabsorption ofnutrition
Growth retardation
Heavy worm in childrenleads to intussusceptionand
total obstruction
Complications:Appendicitis,Biliarycolic and
perforation of bile duct, Hepatomegaly
Lab diagnosis
• Specimen: stool, sputum
• Microscopy: examination of
stool by saline emulsion or
concentrationby floatation
methods employed to
unembryonated egg
• X-ray
Lab diagnosis
• Serodiagnosis:
• Indirect
haemagglutination
test,
• Immuno-fluorescence
assay
• Ultrasonography and
CT scan
• Other test: blood
count shown
peripheral eosinophilia
Picture source- Sonographicimages of
hepato-pancreatico-biliaryand intestinal
ascariasis: A pictorialreview
Lynser D et al Published: 16 September
2015
Treatment
• Mebendazole
• Albendazole
• Pyrantel pamoate
• Piperazine citrate
Prevention
• Avoid ingesting soil that may be contaminated with human feces.
• Wash hands with soap and water before handling food.
• Teach children the importance of washing hands to prevent
infection.
Prevention
• Wash, peel, or cook all raw vegetables and fruits before eating,
particularly those that have been grown in soil that has been
fertilized with manure.
• Transmission of Ascaris lumbricoides infection to others in a
community setting can be prevented by:
– Not defecating outdoors.
– Effective sewage disposal systems.
Ascariasis- Roundworm Infection

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Ascariasis- Roundworm Infection

  • 2. Ascariasis • infection of the small intestine • caused by Ascaris lumbricoides • the largest intestinal nematode to infect human.
  • 3. Habitat • The adult worm lives in small intestine and grow to a length of more than 30 cm. • Human is only the natural host and reservoir of infection.
  • 4. Geographical Distribution • occurs worldwide in areas with warm, moist climates. • most common in tropical and subtropical areas where sanitation and hygiene are poor. • Main epidemic region with prevalence rate of approx. 10-90% includes countries on • South east Asia, Africa and Latin America.
  • 5. Morphology • Adult: • resembles to earthworm. • is elongatedtapering to both end, • anterior being thinner than posterior. • Freshly excreted worm is yellowish pink in color, which gradually changes to white. • The worm is sexuallydiamorphic. • Adult male: 15-30 cm in length, 3-4 mm in diameter, tailcurved • Adult female; 20-40 cm length, 2- 6mm diameter, tail straight
  • 6. Morphology • Egg: • round or oval, • 60 x 40 µm size • thick brown shell and have rough surface • It is the infective form of parasite. • Two types of eggs are liberated from the female worm of Ascaris lumbricoides: • i) fertilized egg • ii) Unfertilized egg •
  • 7. Fertilized egg Shape Round to oval. Size 50-70um x 40-50um Covering Surrounded by a thick smooth transleucent shell consisting of three layers: -The outer coarsely mamillated albuminoid coat -A thick transparent middle layer -Inner lipoidal vitelline membrane Some eggs are found in feces without the outer mamillated albuminous coat. These are called decorticated eggs. Bile Staining Bile stained, golden brown in saline mount. Floatation Floats in saturated salt solution. Ovum Contains a large unsegmented ovum of granular mass with clear space at both the end. The fertilized eggs are laid by females after inseminatedby mating with a male. These are embryonatedand developinto the infective eggs.
  • 8. Unfertilized eggs Size 90um x 45um Shape Round to oval. Covering Albuminous coat is thin, distorted and scanty. Bile Staining Bile stained, golden brown in saline mount. Floatation Doesn’t float in saturated salt solution. Ovum Contains an unsegmented small atrophied ovum with a mass of disorganized highly refractile granules. The unfertilized eggs are laid by uninseminated female. Thes are non-embryonated and cannot become infective.
  • 9. Life cycle • The life cycle of Ascaris completes in single host human. • Stage I: Eggs in faeces • Sexuallymature female produces as many as 200,000 eggs per day, which are shed along with faeces in unembryonatedform. They are non infective. Stage II: Development in soil Embryonation occurs in soil as optimum temperatureof 20-25C with sufficient moisture and oxygen Infective larva developswithin egg in about 3-6 weeks. Stage III: Human infection and liberation of larvae Human get infection with ingestion of embryonated egg contaminated food and water Within embryonated state inside egg, first stage larvae develops into second stage larvae. This second stage larvae is known as Rhabtitiform larvae Second stage larve is stimulatedto hatch out by the presence of alkalinepH in small intestine and solubilizationof its outer layer by bile.
  • 10.
  • 11. • Stage IV: migration of larvae through lungs • Hatched out larvae penetrates the intestinalwall and carried to liver through portal circulation • It then travels via bloodto heart and to lungs by pulmonary circulationwithin4-7 days of infection. • The larvae in lungs molds twice, enlarge and breaks into alveoli. • Stage V: Re-entry to stomach and small intestine • From alveoli,the Larvae then pass up through bronchi and into trachea and then swallowed. • The larvae passes down the oesophagus to the stomach and reached into small intestine once again. • Small intestine is the normal habitatof Ascaris and it colonises here. • Within intestine parasitemolds twice and mature into adult worm. • Sexual maturationoccurs with 6-10 weeks and the mature female discharges its eggs in intestinal lumenand excreted along with faeces, continuingthe life cycle. • The life span of parasite is 12-18 months
  • 12. Mode of transmission • faeco-oral route, by contaminated vegetables or water.
  • 13. Pathogenesis • Two phase in ascariasis. • Phase I: migrating larvae • The migrating larvae causes pathological lesions. • The severity of lesions depends upon the sensitivity of host, nutritional status of host and number of migrating larvae. • During migration and molding through lungs, larvae may causes pneumonia with low grade fever, cough and other allergic symptoms.
  • 14. Pathogenesis • Phase II: Adult worm • Few worm in intestine produce no major symptoms andbut some time give abdominal pain especially in children. • The adult worm produce trauma in host tissue • The wandering adults mayblock the appendical lumen or common bile duct and even small intestine. • Large number of adult worms affects the nutritional status of host causing malnutrition and growth retardation in children. • The metabolites of living or dead worm are toxic and immunogenic. • The worm also produces various allergic toxin, which manifests fever, conjunctivitis and irritation. Picture Extraction of Ascarislumbricoidesfromjejunum via enterotomy. source- CaseReport, Published: 17 June 2009 Rare cause of intestinal obstruction, Ascarislumbricoides infestation:twocase reports Yetim et al
  • 15. Clinical manifestation • Most of the Ascaris infection is asymptomatic. • Symptomatic ascariasis; two types • Intestinal Ascariasis • Pulmonary Ascariasis 2. Pulmonary ascariasis; Transienteosinophilicpneumonitis (loeffler’s disease); elevatedIgE Bronchospasm Dyspnea and wheezing Fever Non-productivecough and chest pain 1. Intestinal ascariasis; Nausea Vomiting Colicky abdominalpain Abdominaldistention Weight loss and diarrhea Malabsorption ofnutrition Growth retardation Heavy worm in childrenleads to intussusceptionand total obstruction Complications:Appendicitis,Biliarycolic and perforation of bile duct, Hepatomegaly
  • 16. Lab diagnosis • Specimen: stool, sputum • Microscopy: examination of stool by saline emulsion or concentrationby floatation methods employed to unembryonated egg • X-ray
  • 17. Lab diagnosis • Serodiagnosis: • Indirect haemagglutination test, • Immuno-fluorescence assay • Ultrasonography and CT scan • Other test: blood count shown peripheral eosinophilia Picture source- Sonographicimages of hepato-pancreatico-biliaryand intestinal ascariasis: A pictorialreview Lynser D et al Published: 16 September 2015
  • 18. Treatment • Mebendazole • Albendazole • Pyrantel pamoate • Piperazine citrate
  • 19. Prevention • Avoid ingesting soil that may be contaminated with human feces. • Wash hands with soap and water before handling food. • Teach children the importance of washing hands to prevent infection.
  • 20. Prevention • Wash, peel, or cook all raw vegetables and fruits before eating, particularly those that have been grown in soil that has been fertilized with manure. • Transmission of Ascaris lumbricoides infection to others in a community setting can be prevented by: – Not defecating outdoors. – Effective sewage disposal systems.