General Characteristics

• Superfamily : Ascaridoidea
• Family: Ascarididae
• Ascaridids largest the nematodes some species 18
inches
• Originally a parasite of pigs that adapted to
humans (When Swine domesticated)
• Two populations of this parasite exist:
One in human A. lumbricoides, other A. suum in pigs
 Morphology
• Males are 15-31 cm long and 2-4 mm width, posterior end curved
ventrally and tail is bluntly pointed, spicule are simple 2-3 mm long.
• In both sexes the mouth is surrounded by one dorsal and 2 ventrolateral
lips
• Female are 20-49 cm long and 3-6 mm width. Ovaries are extensive
and uteri contains 27 million eggs at a time and lay 200,000 eggs per
day
• Fertilized eggs are oval to round 45-75 um long by 35-50 um wide
with thick outer shell proteinaceous layer contributed by uterine wall
(When pass out side the host body darkly stained to golden brown).
• Female before inseminated lay unfertilized eggs.
Biology
• A period 9-13 days embryo to develop into a
active J1.
• Embryo extremely resistant to low temperature,
desiccation and strong chemicals.
• Embryogenesis is retarded by sunlight and high
temperatures as they are lethal.
• Infection occurs when shelled juveniles are
swallowed with contaminated food and water.
• Hatch in duodenum, juvenile penetrate the mucosa Female and male Ascaris lumbricoides
and submucosa and enter into lymphatic or
venules.
• After passing through heart they enter pulmonary
circulation and enter into alveolus of lungs.
• Many worms lost during this migration and
accumulate in every body organs to cause acute
tissue reactions.
• In lungs they (1.4-1.8 mm long) molt twice and
move up to pharynx (10 days) and enter
esophagus. In lungs they molts L4 which is
resistant to gastric juice, then pass to intestine
where they mature. The anterior end of Ascaris
lumbricoides. Notice the
• Lay eggs after 60-65 days
three prominent "lips".
Life Cycle
• Adult worms live in the lumen of the small intestine and get
nourishment from semidigested food in the host
• Copulation occurs here and eggs are passed with the feces
• The outer, albuminous coat of the egg is brown in color due to
bile pigment absorbed from the feces
• The zygote does not begin development until the egg has reached
the soil
• Eggs are fairly resistant to desiccation and low temperatures
• With proper temperatures and oxygen levels the embryo molts at
least once in the shell and develops to an infective larva
• Eggs can remain viable in the soil for 2 years
 Ascaris
Life Cycle
Life Cycle cont.
• After being ingested, infective eggs hatch in the duodenum
• Larvae actively burrow into the mucosal lining, enter the circulatory system,
and are carried to the liver, through the right side of the heart, and on to the
lungs by way of pulmonary arterial flow
• Larvae remain in the
lungs several days, but
eventually rupture from
the pulmonary capillaries
and enter the alveoli
• From here they move up
the lungs and trachea to
the epiglottis, are coughed
up, swallowed, and passed
into the small intestine
• After molting the worms
grow to sexual maturity
Epidemiology
 Distribution of A. lumbricoides is worldwide, but it is prevalent in warmer
climates
 It depends upon poor sanitation for its proliferation
 It is most prevalent in children; they are exposed to contaminated soil, do
not wash before eating, put hands in mouth, etc. Abundant and world wide
distribution
 Children more infective as they eat dirt or placing soiled fingers and toys in
their mouth.
 More prevalent in countries where night soil is used as fertilizer eastern
Asia, Germany and Mediterranean countries
 Cockroaches carries their eggs
 Wind can spread eggs
 1 billion persons one quarter of the world population are infected
 Brudastove kept eggs 10 years in which 30-35% still infective.
Sympatamology
• Most cases of ascariasis are symptomless
• The most frequent symptom is upper abdominal discomfort
• Little damage results from larval penetration of the host’s mucosa
• However, aberrant larvae migrating in such organs as the spleen, liver, lymph
nodes, and brain usually result in an inflammatory response
• Also, larvae escaping from capillaries in the lungs and entering the respiratory
system cause small, hemorrhagic foci accompanied by coughing, fever, and
difficulty in breathing
• Worms sometimes cause mechanical blockage of the intestinal tract
• Also, worms may penetrate the intestinal wall or appendix causing local
hemorrhaging
• Overcrowding may also lead to wandering; worms can enter the appendix and
cause blockage; worms have been known to migrate all he way to the anus
• Some worms migrate anteriorly and have been known to block pancreatic and
bile ducts; others have gotten into the stomach and some even as far as the
esophagus and tracheae
Toxocara canis
• Found in the small intestine of dogs and other canines
• Causes visceral larval migrans among humans (an accidental
host); most common among children
• It usually results from the ingestion of eggs and the subsequent
migration of second stage larvae within the internal organs
• The second stage larvae hatching from the eggs penetrate the
intestinal wall and quickly invade the liver
• Although a majority of these larvae remain in the liver, some pass
on to the lungs and, sometimes, the CNS and eyes
• Although most of the larvae eventually gravitate to a single
location and become encapsulated by host tissues, for a period of
time they actively migrate through the tissues, leaving long trails
of inflammatory reaction cells
 Visceral Larval Migrans

• When juveniles of several species of nematodes

gain entry to an improper host, the juveniles begin
the typical tissue migration.
• Don’t complete the normal migration but under go
developmental arrest.
• Random wondering through the body of the host
• Toxocara canis is one of them
Visceral Larval Migrans Case Study
• A previously healthy 37-year-old black man
had fever, abdominal cramping, vomiting, and
diarrhea. After 1 week of symptoms, a chest
radiograph showed multiple noncavitating
pulmonary nodules
• On further questioning, the patient stated that
he had acquired a puppy 1 month before onset
of the abdominal pain. The puppy was being
house-trained, and the patient had had no
previous household exposure to dogs.
Subsequently, tests for serum antibodies against
• T canis IgG and IgM were obtained and were
A chest radiograph showing
positive at 11.5 and 9.3 standard deviations multiple noncavitating
above the mean of a reference group of normal pulmonary nodules
subjects. The Toxocara IgM titer indicated acute
infection with T canis.