Ascaris lumbricoides

Common name-Roundworm
-lumbricoides is derived from its resemblance with earthworm (Lumbricus, meaning earthworm
in Latin).
Adult worms live in the small intestine (85% in jejunum and 15% in ileum).
The roundworm, Ascaris lumbricoides is the largest nematode parasite in the human intestine.
LIFE CYCLE
Life cycle of Ascaris involves only one host.
Natural Host Man.
There is no intermediate host.
Infective Form-Embryonated eggs.
• Mode of transmission:
- Infection occurs when the egg containing the infective rhabditiform larva is swallowed. A
frequent mode of transmission is through fresh vegetables grown in fields manured with
human feces (night soil). Infection may also be transmitted through contaminated drinking
water.
Children playing about in mud can transmit eggs to their mouth through dirty fingers
(geophage  A creature that eats earthy substances such as clay and chalk).
Where soil contamination is heavy due to indiscriminate defecation, the eggs sometimes get
airborne along with windswept dust and are inhaled.The inhaled eggs get swallowed.
Development in Soil
The fertilized egg passed in feces is not immediately infective. It has to undergo a period of
incubation in soil before acquiring infectivity.
• The eggs are resistant to adverse conditions and can survive for several years.
• The development of the egg in soil depends on the nature of the soil and various
environmental factors. A heavy clayey soil and moist shady location, with temperature between
20°c and 30°C are optimal for rapid development of the embryo.
• The development usually takes from 10-40 days, during which time the embryo moults twice
and becomes the infective rhabditiform larva, coiled up within the egg.
Development in Man
When the swallowed eggs reach the duodenum, the larvae hatch out.
The rhabditiform larva, about 250 μm in length and 14 μm in diameter, are actively motile.
They penetrate the intestinal mucosa, enter the portal vessels and are carried to the liver.
They then pass via the hepatic vein, inferior vena cava, and the right side of the heart and in
about 4 days reach the lungs, where they grow and moult twice.
After development in the lungs, in about 10-15 days, the larvae pierce the lung capillaries and
reach the alveoli.They crawl up or are carried up the respiratory passage to the throat and are
swallowed.
The larvae moult finally and develop into adults in the upper part of the small intestine. They
become sexually mature in about 6-12 weeks and the gravid females start laying eggs to repeat
the cycle.
The adult worm has a lifespan of 12 – 20 months.
• PATHOGENICITY AND CLINICAL FEATURES
Disease caused by A. lumbricoides is called as ascariasis.
• Clinical manifestations in ascariasis can be caused either by the migrating larvae
or by the adult worms.
Symptoms Due to the Migrating Larvae
The pathogenic effects of larval migration are due to allergic reaction and not the
presence of larvae as such. Therefore, Ascaris Lumbricoides the initial exposure to
larvae is usually asymptomatic, except when the larval load is very heavy.
• When reinfection occurs subsequently, there may be intense cellular reaction to
the migrating larvae in the lungs, with infiltration of eosinophils, macrophages
and epithelioid cells.
• This Ascaris pneumonia is characterized by low grade fever, dry cough,
asthmatic wheezing, urticaria, eosinophilia and mottled lung infiltration in the
chest radiograph.
• The sputum is often blood-tinged and may contain Charcot-Leyden crystals. The
larvae may occasionally be found in the sputum, but are seen more often in
gastric washings. This condition is called Loeffler's syndrome.
• The clinical features generally clear in 1 or 2 weeks, though it may sometimes be
severe and rarely, even fatal. Loeffler's syndrome can also be caused by
hypersensitivity to other agents, both living and nonliving.
Symptoms Due to the Adult Worm
Clinical manifestations due to adult worm vary from asymptomatic infection to
severe and even fatal consequences.
• Asymptomatic infection: Generally seen in mildly infected cases; however, it is
not unusual to find children apparently unaffected in spite of heavy infestation
with the worms.
• The pathological effects, when present, are caused by spoliative action, toxic
action, mechanical effects and wandering effects .
- The spoliative or nutritional effects are usually seen when the worm burden is
heavy. The worms may be present in enormous numbers, sometimes exceeding
500, in small children, occupying a large part of the intestinal tract. This interferes
with proper digestion and absorption of food. Ascariasis may contribute
to protein-energy malnutrition and vitamin A deficiency. Patients have loss of
appetite and are often restless. Abnormalities of the jejunal mucosa are often
present, including broadening and shortening of villi, elongation of crypts and
round cell infiltration of lamina propria. These changes are reversed when the
worms are eliminated.
- the toxics are due to hypersensitivity to the worm antigens and may be
manifested as fever, urticaria(a rash of round, red welts on the skin that itch intensely,
sometimes with dangerous swelling, caused by an allergic reaction, typically to specific foods),
angioneurotic edema (area of swelling of the lower layer of skin and tissue just under the skin
or mucous membranes), wheezing and conjunctivitis. These are more often seen in
persons who come into contact with the worm occupationally, as in laboratory
technicians and abattoir workers {who become sensitive to the pig ascarid, A.
suum), than in children having intestinal infestation.
- The mechanical effects are the most important manifestations of ascariasis.
Mechanical effects can be due to masses of worms causing luminal occlusion
or even a single worm infiltrating into a vital area. The adult worms live in the
upper part of the small intestine, where they maintain their position due to
their body muscle tone, spanning the lumen.They may stimulate reflex peristalsis,
causing recurrent and often severe colicky pain in the abdomen. The worms may
be clumped together into a mass, filling the lumen, leading to volvulus,
intussusception (the inversion of one portion of the intestine within another) or intestinal
obstruction and intestinal perforation
Ectopic ascariasis (Wanderlust): The worms are restless wandering which is
enhanced when the host is ill, particularly when febrile, with temperature above
39°C. The male worm is more responsive to illness of the host, than the female.
The worm may wander up or down along the gut. Going up, it may enter the
opening of the biliary or pancreatic duct causing a cute biliary obstruction or
pancreatitis. It may enter the liver parenchyma, where it may lead to liver
abscesses. The worm may go up the esophagus and come out through the mouth
or nose. It may crawl into the trachea and the lung causing respiratory
obstruction or lung abscesses. Migrating downwards, the worm may cause
obstructive appendicitis. It may lead to peritonitis when it perforates the
intestine, generally at weak spots such as typhoid or tuberculous ulcers or
through suture lines. This tendency makes preoperative deworming necessary
before gastrointestinal surgery in endemic areas. The wandering worm may also
reach kidneys.
LABORATORY DIAGNOSIS
Detection of Parasite
Adult Worm
The adult worm can occasionally be detected in stool or sputum of patient by
naked eye.
Barium meal may reveal the presence of adult worm in the small intestine.
A plain abdominal film may reveal masses of worms in gas-filled loops of bowel in
patients with intestinal obstruction.
Pancreaticobiliary worms can be detected by ultrasound (more than 50%
sensitive) and endoscopic retrograde cholangiopancreatography (ERCP; 90%
sensitive).
Larvae
In the early stages of infection, when migrating larvae cause Loeffler's syndrome,
the diagnosis may be made by demonstrating the larvae in sputum, or more often
in gastric washings.
• Presence of Charcot-Leyden crystals in sputum and an attendant eosinophilia
supports the diagnosis. At this stage, no eggs are seen in feces.
• Chest X-ray may show patchy pulmonary infiltrates.
Eggs
Definitive diagnosis of ascariasis is made by demonstration of eggs in feces.
Three eggs per mg of feces. At this concentration, the eggs can be readily seen by
microscopic examination of a saline emulsion of feces. Both fertilized and
unfertilized eggs are usually present.
• Rarely when the infestation is light, eggs are demonstrable only by
concentration methods.
• Eggs may not be seen if only male worms are present, as may occasionally be
the case. Fecal films often contain artifacts resembling Ascaris eggs and care must
be taken to differentiate them.
• Eggs may be demonstrative in the bile obtained by duodenal aspirates.
Serological Tests
Ascaris antibody can be detected by:
• Indirect hemagglutination (IHA)
• Indirect fluorescent antibody (IFA)
• Enzyme-linked immunosorbent assay (ELISA).
• Serodiagnosis is helpful in extraintestinal ascariasis like Loeffler's syndrome.
Blood Examination
Complete blood count may show eosinophilia in early stage of invasion