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Helminthes

Nematodes III

Medical Parasitology – SBD2114


Intestinal Nematodes with a Tissue
stage
• Round worms - Ascaris lumbricoides, Toxocara canis
• Hookworms - Ancylostoma duodenale, Necator

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americanus
• Strongyloides stercoralis

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Strongyloides stercoralis
Distribution

• Found mainly in warm moist tropics, but may

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also occur in the temperate regions

• Common in Brazil, Columbia and in the Far East

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—Myanmar, Thailand, Vietnam, Malaysia,
Philippines

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Epidemiology and risk factors
• Known to exist on all continents except for Antarctica, but
most common in tropics, subtropics, and in warm
temperate regions

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• Global prevalence  is unknown, but experts estimate that
there are between 30–100 million infected persons

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worldwide

• Found more frequently in socioeconomically


disadvantaged, in institutionalized populations, and in
rural areas

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• Often associated with agricultural activities
Epidemiology and risk factors cont.

• Most common way of becoming infected is by contacting


soil that is contaminated with Strongyloides larvae.

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• Activities that increase contact with the soil increase the
risk of becoming infected, such as:

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• Walking with bare feet
• Contact with human waste or sewage
• Occupations that increase contact with contaminated soil
such as farming and coal mining

• Primarily infect human but ay infect other animals as well


• Ex: Dog, cattle 5
Morphology and life cycle
• Complex life cycle - multiplicity of pathways through
which it can develop
• It is unique among human nematodes in that it has, in
addition to the parasitic cycle, a free-living soil cycle, in

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which it can persist for long periods in soil, feeding on soil
bacteria, passing through several generations

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Morphology and life cycle cont.
Parasitic Phase
• Adult worm is found in human intestine embedded in the
mucosa of the duodenum and upper jejunum

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• Individual worm has a lifespan of 3 or 4 months, but
because it can cause autoinfection, the infection may
persist for years

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• Only the female worms are seen in the intestine. It was
believed that they are parthenogenetic and can produce
offspring without being fertilized by the male
• But it has since been established that parasitic males do
exist

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Morphology and life cycle cont.
• Males shorter and broader than the female
• They can be demonstrated in experimentally infected dogs

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• Majority of females are probably parthenogenetic

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• Female worm is thin, transparent, about 2.5 mm long and
has a cylindrical esophagus occupying the anterior third of
the body, and the intestines in the posterior two-thirds
opening through the anus situated ventrally, a little in front
of the pointed tail tip

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Morphology and life cycle cont.
• Eggs laid in the mucosa hatch immediately, releasing
rhabditiform (first stage) larvae, about 0.25 mm long, with
a relatively short muscular esophagus ending in an
enlarged bulb

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• Rhabditiform larvae migrate into the lumen and pass down
the gut to be released in feces

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• Rhabditiform larva of S.
stercoralis in an unstained
wet mount of stool. Notice
the rhabditoid esophagus
(blue arrow) and
prominent genital
primordium (red arrow). 10
Morphology and life cycle cont.
• On reaching the soil, they moult twice to become the
infective filariform (third stage) larvae
• Filariform larvae are slender, about 0.55 mm in size, with a
long oesophagus of uniform width

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• Filariform larvae are non-feeding and can live in soil only
for about 12 days

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• Filariform (L3) larva of 11
S. stercoralis in an
unstained wet mount
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Morphology and life cycle cont.
• When a person walks barefoot on soil containing the
infective filariform larvae, they penetrate the skin, usually
on the sides of the feet or between toes, enter the
cutaneous lymphatics or blood vessels and are carried

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along the venous circulation to the right side of the heart
and to the lungs

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• Here they escape from pulmonary capillaries into the
alveoli
• Migrate up the respiratory tract to the pharynx and are
swallowed
• Reaching their final destination, the duodenum and
jejunum, where they burrow into the mucosa 13
• There they mature in 15 to 20 days and start laying eggs
Morphology and life cycle cont.
• This mode of life cycle is called the direct development
and is the usual mode of human infection
• It resembles the life cycle of the hookworm

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• Worm also has a cycle of autoinfection
• Here the rhabditiform larvae mature into the infective

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third stage larvae during their passage down the gut
• These filariform larvae cause reinfection by piercing the
perianal and perianal skin during defecation
• Larvae wander in the dermis of the perianal region for
sometime, causing a radiating perianal creeping eruption,
a form of cutaneous larva migrans
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Morphology and life cycle cont.
• They ultimately enter the lymphatics or venules and are
carried to the right heart and the lungs to complete the life
cycle as above
• This ability to cause autoinfection explains the persistence

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of the infection in patients for long periods, even 30 to 40
years, after leaving the endemic areas

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Morphology and life cycle cont.
• In another type of autoinfection, seen typically in
immunodeficient hosts, the rhabditiform larvae released
into the bowel walls mature into the infective filariform
larvae there itself

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• They penetrate the deeper layers of the intestine, to reach
the mesenteric venules and are carried in circulation to
complete the life cycle

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• This mode of autoinfection is called internal reinfection
• It may lead to very heavy infection causing serious and
sometimes even fatal illness

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Morphology and life cycle cont.
Free-living Phase
• Rhabditiform larvae passed in stools develop in moist soil
into free-living males and females
• Female is 1 mm and the male 0.7 mm long

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• They mate in soil
• Fertilised female lays eggs which hatch to release the next

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generation of rhabditiform larvae
• These may repeat the free-living cycle, or may develop into
the filariform larvae which infect humans and initiate the
parasitic phase
• Humans are the natural host of S. stercoralis.

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Pathogenesis and Clinical Features
• Generally asymptomatic, blood eosinophilia and larvae in
stools being the only indications of infection

• But it may sometimes cause clinical manifestations, which

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may be severe and even fatal, particularly in those with
defective immune response

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• Clinical disease may be classified as cutaneous, pulmonary
and intestinal
• Severe disease seen in the immune compromised is known
as hyperinfection

• Generalised Strongyloidosis may be seen in AIDS 18


Pathogenesis and Clinical Features
Cutaneous
• There may be dermatitis, with erythema and itching at the
site of penetration of the filariform larvae, particularly
when large numbers of larvae enter the skin

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Pulmonary

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• During escape of the larvae from the pulmonary capillaries
into the alveoli, small haemorrhages occur, along with
cellular infiltration into alveoli and bronchioles
• Bronchopneumonia may be present, which may, in some
go on to chronic bronchitis and asthmatic symptoms
• Larvae may be found in the sputum
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Pathogenesis and Clinical Features
Intestinal
• Symptoms may resemble those of peptic ulcer or of
malabsorption syndrome
• Mucus diarrhoea is often present

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• In heavy infection causing dysenteric stools

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Diagnosis
• Demonstration of the rhabditiform larvae in freshly
passed stools is the most important method of specific
diagnosis
• Larvae found in stale stools have to be differentiated from

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larvae hatched from hookworm eggs

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Diagnosis cont.
• Larvae may sometimes be present in sputum and gastric
aspirates
• When larvae are scanty in stools, diagnosis may be
facilitated by stool culture

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• Larvae develop into free-living forms and multiply in
charcoal cultures set up with stools
• Large numbers of

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free-living larvae
and adults can be
seen after 7 to 10
days

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Diagnosis cont.
• Serological tests have been described, using strongyloides
or filarial antigens
• Complement fixation, indirect haemagglutination and
ELISA have been reported

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• But the antigens are not freely available, and extensive
cross reactions limit the utility of these tests
• Peripheral eosinophilia is a constant finding

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• However, in severe hyperinfection eosinophilia may
sometimes be absent

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Treatment
• All cases of strongyloidosis, whether symptomatic or not
should be treated to prevent severe invasive disease
• Thiabendazole, mebendazole and ivermectin are effective

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Prevention
• Prevention of soil contamination with faeces
• Avoiding contact with infective soil and contaminated
surface waters constitute the general methods of
prevention

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