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Ascaris Lumbricoides
Dr. Neelam Gupta, M.D.
General Introduction
 Common name“ round worm of man”
 It is worldwide in distribution and most
prevalent through out the tropics, sub-tropics
and more prevalent in the malnourished
people.
 Habitat : Small intestine (jejunum) of man.
 Adult:
 Cylindrical tapering at ends.
 Creamy-white or pinkish in color.
 Longitudinal streaks on body.
 Mouth at ant. End. Has three toothed lips,
1dorsal and 2ventral.
 Digestive and respiratory symptoms float inside
body cavity.
 Ascaron :- toxic fluid causing allergic reactions..
Morphology
The lips of A. lumbricoides
The three lips are
seen at the anterior
end. The margin of
each lip is lined with
minute teeth which are
not visible at this
magnification

 Females measure 20-35 cm long with a
straightened tail; males are smaller at 15-31 cm
and tend to have a curved tail.
 Two equal size copulatory spicules in male.
 vulvar waist in female.
 Female lays nearly 200,000 eggs daily which are
passed in feces.
: Posterior end of a male A.
lumbricoides, showing the
curled tail.
Adult female A.
lumbricoides.
Adult worm of A. lumbricoides
Egg
 There are three kinds of the eggs
 fertilized eggs
 unfertilized eggs
 decorticated eggs
Morphology
 Fertilized egg:
 an average size 60×45µm
 Round or oval in shape
 bile stained&brown in color
 thick transparent shell
 Innermost- lipoidal vitelline membrane .
 Middle – thick transparent layer.
 Outermost – mammillated Albuminoid layer.
 large unsegmented ovum
 There is a clear crescentric space at each pole.
 Float in SSS.
Morphology
 Unfertilized egg
 Longer and slender than fertilized egg
 90*55um.
 Bile stained and brown in colour.
 The shell and albuminous coat are thinner
 Lipoidal membrane is absent,
 Small atrophied ovum.
 Do not float in SSS.
 refractable granules various in size may be
present.
Morphology
Decorticated egg:
Both fertilized and unfertilized eggs
sometimes may lack their outer albuminous
coats and are colorless
 Site of inhabitation: small intestine
 Only single host
 No intermediate host.
 Infective stage: embryonated eggs
 Route of infection: by feco-oral-route.
Life Cycle
 Adult worms , live in the lumen of the small intestine.
 Eggs passed in faeces.
 Fertile eggs embryonate and become infective after 18 days
to several weeks , depending on the environmental
conditions (optimum: moist, warm, shaded soil).
 After infective eggs are swallowed , the larvae hatch ,
invade the intestinal mucosa, and are carried via the
portal, then systemic circulation to the lungs .
 Larva moult twice in the lungs (10 to 14 days), break
capillary & penetrate the alveolar walls, ascend the
bronchial tree crawl the epiglottis, and are swallowed .
 Upon reaching the small intestine, they develop into adult
worms . After 12 weeks gravid female begin to discharge
eggs in stools.
 Cycle is repeated.
1. Cause ascariasis.
2. Due to adult worm and migrating larva.
3. Malnutrition , night blindness, vit A def,, growt
retardation.
4. Intermittent colicky pain in intestine.
5. Mechanical obstruction.
6. Worms are RESTLESS WANDERERS. Insinuate
any aperture in their way.
7. Crawl out of mouth, ear. naris
Pathogenesis
 Respiratory obstruction.
 Wandering adults may block the appendical
lumen or the common bile duct and even
perforate the intestinal wall which cause
complications of ascariasis:
 intestinal obstruction
 Appendicitis
 biliary ascariasis (the most common one)
 perforation of the intestine
 cholecystitis, pancreatitis and peritonitis
Migrating larva
1. In repeated infections ,During the migration
through the lungs, the larvae may cause a
inflammatory and hypersensitivity reactions.
 The symptoms of the pneumonia are low fever,
cough, blood-tinged sputum, asthma
 The clinical manifestation is also called
Loeffler’s syndrome
 feces are examined for the ascaris eggs
 Direct fecal film: it is simple and effective
and is the first choice
 recovery of adult worms: when adults or
adolescents are found in feces or vomit and
tissues. Barium meal can be done.
 Serology- detect ascaris antibody by IHA and
IFA.
 Eosinophilia
 Ascaris pneumonitis: examination of sputum
for Ascaris larvae is sometimes
Diagnosis
 Treatment to ascariasis: pyrantel palmoate
 Mebendazole, are effective
 Sanitary disposal of feces.
 Hygienic habits such as cleaning of hands before
meals.
 Health education.
Prevention
VISCERAL LARVA MIGRANS
 caused by: Ingestion of embryonated eggs of
nematodes of animals like :
Toxocara canis
Toxocara cati
Angiostrongylus cantonensis
Anisakis simples
Larva hatch in small intestine
and migrate to liver.
 Wherever larva settles it is attacked by phagocytic
cells: eosinophils, histiocytes, giant cells, leading
to granulomatous lesion.
 Thus their progress is arrested and unlike ascaris
they do not convert in adults worms.
 VLM: hypere-eosinophilia, hepatomegaly, or
pneumonia, fever,
 Ocular larva migrans- end ophthalmitis.
 Diagnosed by identification of larva in biopsy or
autopsy by IHA and IFA test.
Thank you.

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Ascariasis

  • 2. General Introduction  Common name“ round worm of man”  It is worldwide in distribution and most prevalent through out the tropics, sub-tropics and more prevalent in the malnourished people.  Habitat : Small intestine (jejunum) of man.
  • 3.  Adult:  Cylindrical tapering at ends.  Creamy-white or pinkish in color.  Longitudinal streaks on body.  Mouth at ant. End. Has three toothed lips, 1dorsal and 2ventral.  Digestive and respiratory symptoms float inside body cavity.  Ascaron :- toxic fluid causing allergic reactions.. Morphology
  • 4. The lips of A. lumbricoides The three lips are seen at the anterior end. The margin of each lip is lined with minute teeth which are not visible at this magnification
  • 5.   Females measure 20-35 cm long with a straightened tail; males are smaller at 15-31 cm and tend to have a curved tail.  Two equal size copulatory spicules in male.  vulvar waist in female.  Female lays nearly 200,000 eggs daily which are passed in feces.
  • 6. : Posterior end of a male A. lumbricoides, showing the curled tail. Adult female A. lumbricoides.
  • 7. Adult worm of A. lumbricoides
  • 8. Egg  There are three kinds of the eggs  fertilized eggs  unfertilized eggs  decorticated eggs Morphology
  • 9.  Fertilized egg:  an average size 60×45µm  Round or oval in shape  bile stained&brown in color  thick transparent shell  Innermost- lipoidal vitelline membrane .  Middle – thick transparent layer.  Outermost – mammillated Albuminoid layer.  large unsegmented ovum  There is a clear crescentric space at each pole.  Float in SSS. Morphology
  • 10.  Unfertilized egg  Longer and slender than fertilized egg  90*55um.  Bile stained and brown in colour.  The shell and albuminous coat are thinner  Lipoidal membrane is absent,  Small atrophied ovum.  Do not float in SSS.  refractable granules various in size may be present. Morphology
  • 11. Decorticated egg: Both fertilized and unfertilized eggs sometimes may lack their outer albuminous coats and are colorless
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  • 13.  Site of inhabitation: small intestine  Only single host  No intermediate host.  Infective stage: embryonated eggs  Route of infection: by feco-oral-route. Life Cycle
  • 14.  Adult worms , live in the lumen of the small intestine.  Eggs passed in faeces.  Fertile eggs embryonate and become infective after 18 days to several weeks , depending on the environmental conditions (optimum: moist, warm, shaded soil).  After infective eggs are swallowed , the larvae hatch , invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs .  Larva moult twice in the lungs (10 to 14 days), break capillary & penetrate the alveolar walls, ascend the bronchial tree crawl the epiglottis, and are swallowed .  Upon reaching the small intestine, they develop into adult worms . After 12 weeks gravid female begin to discharge eggs in stools.  Cycle is repeated.
  • 15.
  • 16. 1. Cause ascariasis. 2. Due to adult worm and migrating larva. 3. Malnutrition , night blindness, vit A def,, growt retardation. 4. Intermittent colicky pain in intestine. 5. Mechanical obstruction. 6. Worms are RESTLESS WANDERERS. Insinuate any aperture in their way. 7. Crawl out of mouth, ear. naris Pathogenesis
  • 17.  Respiratory obstruction.  Wandering adults may block the appendical lumen or the common bile duct and even perforate the intestinal wall which cause complications of ascariasis:  intestinal obstruction  Appendicitis  biliary ascariasis (the most common one)  perforation of the intestine  cholecystitis, pancreatitis and peritonitis
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  • 19. Migrating larva 1. In repeated infections ,During the migration through the lungs, the larvae may cause a inflammatory and hypersensitivity reactions.  The symptoms of the pneumonia are low fever, cough, blood-tinged sputum, asthma  The clinical manifestation is also called Loeffler’s syndrome
  • 20.  feces are examined for the ascaris eggs  Direct fecal film: it is simple and effective and is the first choice  recovery of adult worms: when adults or adolescents are found in feces or vomit and tissues. Barium meal can be done.  Serology- detect ascaris antibody by IHA and IFA.  Eosinophilia  Ascaris pneumonitis: examination of sputum for Ascaris larvae is sometimes Diagnosis
  • 21.  Treatment to ascariasis: pyrantel palmoate  Mebendazole, are effective  Sanitary disposal of feces.  Hygienic habits such as cleaning of hands before meals.  Health education. Prevention
  • 22. VISCERAL LARVA MIGRANS  caused by: Ingestion of embryonated eggs of nematodes of animals like : Toxocara canis Toxocara cati Angiostrongylus cantonensis Anisakis simples Larva hatch in small intestine and migrate to liver.
  • 23.  Wherever larva settles it is attacked by phagocytic cells: eosinophils, histiocytes, giant cells, leading to granulomatous lesion.  Thus their progress is arrested and unlike ascaris they do not convert in adults worms.  VLM: hypere-eosinophilia, hepatomegaly, or pneumonia, fever,  Ocular larva migrans- end ophthalmitis.  Diagnosed by identification of larva in biopsy or autopsy by IHA and IFA test.