Soil Transmitted

Helminthiasis

Refference
References
1.

Roberts L, Janovy Jr J. Gerald D. Schmidt & Larry S. Roberts

Foundations of Parasitology. 7 th ed. McGraw Hill. New York. 2005 :
397-99, 417-24, 431-5

2.

Brooker S, Bundy DAP, Soil Transmitted Helminths (Geohelminths). In :

Cook GC, Zumla AI (ed). Mansons Tropical Disease. 22 nd ed. Saunders
Elsevier. 2009 : 1517-40

3.

World Health Organization. Preventive Chemotherapy in Human

Helminthiasis : Coordinated Use of Anthelminthic Drugs in Control
Intervensions : A Manual for Health Professionals and Programme
Managers. Geneva, Switzerland : World Health Organization; 2006

4.

World Health Organization. Weekly Epidemiological Record : SoilTransmitted Helminthiasis : Estimates of The Number of Children
Needing Preventive Chemotherapy and Number Treated . Geneva,
Switzerland : World Health Organization; 2011

5.

Hotez PJ, Brooker S, Bethony JM, et al. Hookworm Infection. The New
England Journal of Medicine. 2004; 351 : 799-807

Soil Transmitted Helminthiasis

Learning Objective

Agents

of the disease
Pathology
Diagnosis
Prevention

Soil Transmitted Helminthiasis

General

Nematode infections

Transmitted via soil medium either :

1.
2.

Ingestion of embryonated eggs

Skin penetration by infective
larvae

Soil Transmitted Helminthiasis

General

Etiology :
Ascaris lumbricoides
Trichuris trichiura
Common STH
Hookworms
agents
Strongyloides stercoralis
Toxocara spp.

Soil Transmitted Helminthiasis

General
o

Infections STH associated

with:
Poverty and poor
condition
Crowded living
conditions, combined
with lack of access to
health care and low
levels of education (poor
personal and health
awareness)
Soil quality and climate

Soil Transmitted Helminthiasis

Global Estimation

Ascariasis
General
o
o
o

Etiology : Ascaris lumbricoides

(roundworm)
Habitat : small intestine, especially
jejunum and upper ileum
One of the most common &
widespread human infection, about 1
billion people worldwide

Ascaris lumbricoides
Morfology

Adult Ascaris lumbricoides

Ascaris lumbricoides
Morfology
Egg of A.
lumbricoides
corticated
Fertilized

Unfertilized

decorticate
d

Ascaris lumbricoides
Morfology
Egg of A.
lumbricoides

Infectious
corticated

Ascariasis
Life Cycle
Infective stage :
fertilized egg
Diagnostic stage
:
egg & adult in
feces
Route of
infection :
ingestion

Ascariasis
Pathology
o Majority

symptomless
o May caused by migrating larva or
adult worm

Ascariasis
Pathology

Migrating Larvae
When juveniles break out of lung
cappilaries into the resp. system
small hemorrhage
Segments of 4th stage larvae can be
seen in the bronchioles associated with
infiltration with PMN and eosinophil
with scattered Charcot-Leyden crystals
and radiological pulmonary infiltration
Ascaris pneumonitis (Lfflers

Ascariasis
Pathology
Ascaris

pneumonitis (Lfflers
pneumonia) : fever, cough,
sputum, wheeze, skin rash,
eosinophilia, and radiological
pulmonary infiltration
Larvae may wander into the
brain, eye, causing granulomas

Ascariasis
Pathology

Adult
worms
Adult
can cause physiological
abnormalities in the small intestine
malabsorbtion of nutrients and
micronutrients, malnutrition, growth failure
and cognitive impairments
Intestinal ascariasis GI discomfort, colic
and vomiting are quite common

Ascariasis
Pathology
The

commonest
complication of
ascariasis among
children below 10
years is small-bowel
obstruction

Heavy

infection can
cause intestinal colic,
fatal intestinal
blockage

Ascariasis
Pathology

Wandering worms :
may reach liver, billiary
tract, appendix and
oesophagus
acute and chronic
inflammation with
infiltrations by
eosinophils, histiocytes
and mononuclear cells
at sites of ectopic
ascariasis
granuloma formation

Ascariasis
Diagnostic
o

Adult worm out of body

openings

Larvae std 4th in sputum

Eggs in feces fertilized /

unfertilized

Eosinophilia

Serology (?)

Strongyloides stercoralis
General
Family

Strongyloididae
Facultative parasite
Widely distributed on earth,
most densely in those areas
characterized by high
temperature and humidity and
poor hygienic conditions

Strongyloides stercoralis
Morphology

egg is 70 x 40 m with an
extremely thin eggshell
Female adult of parasitic generation:
thin and long, about 2 mm long, two
sets of genital organs, with lack of
seminal receptacles (because no
sperm is required for parthenogenesis)
Female adult of free living generation:
thicker and shorter, seminal
receptacles (+)
Male adult: smaller, about 0.7-1 mm
long, the tail end curls on the ventral
side
The

Strongyloides stercoralis
Morphology
Rhabditiform

larva:

only can be
differentiated with
those of
Ancylostomatidae
through electron
microscopy
Filariform larva: 0.40.7 mm in length, a
half is occupied
with esophagus,
forked tail

Life Cycle &

Transmission
Infective stage:
filariform larvae
Diagnostic stage
: rhabditiform
larvae in feces

Strongyloides stercoralis
Life Cycle
Direct

Cycle: filariform larva invades

human skin, proceed in the blood
stream to the heart and lung, then
return to the small intestine via
tracheal migration
Indirect cycle: when outside
conditions are favorable, rhabditiform
larvae grow become male and female
free living form, and after copulation
and lying eggs, adults die, and the
eggs give rise rhabditiform larvae, and
become infective form after two molts

Strongyloides stercoralis
Route of Infection

Internal

autoreinfection: if a host
has constipation or immune
deficiency
External autoreinfection: in poor
hygienic host, whose perianal is
contaminated by rhabditiform,
the larvae grow become infected
larvae and then invade the
perianal skin or mucosa, proceed
to the lung, etc.

Strongyloidiasis
Clinical manifestation:

Immunocompetent (Intestinal):

Acute: diarrhoea abdominal pain, nausea,

vomitting, constipation, weight loss, GIbleeding, pruritus ani.

Chronic:
protein
losing
enteropathy,
malabsorbtion, paralytic ileus.

Strongyloidiasis :
Immunocompromised (Extra Intestinal):
Pulmonary:

Cough & wheezing.

Loefflers syndrome
Haemoptysis
Bronchopneumonia
Hypereosinophilia.

Cutaneous

Rash
Pruritus
Larva currens

Neurological:
- Infection of brain & meninges

Diagnosis
Non-specific;

increased eosinophilia and IgE.

Stool FEME: larvae form more often seen than
eggs.
Concentration of larva by Baermanns method.
Stool culture by either Harada mori or Sand& charcoal
culture; wait for larva to emerge within 5-7 days.
Duodenal aspirate
Urine, sputum, cerebrospinal fluid
Specimen biopsy and autopsy.

Ancylostomiasis
General
o Etiology

: Ancylostoma
duodenale
Necator
americanus
o Habitat : small intestine
o Recent estimate suggest that
hookworms infect 740 million
people worldwide

Ancylostomiasis
Morfology

Adult Ancylostoma duodenale

Ancylostomiasis
Morfology

Adult Necator americanus

Ancylostomiasis
Morfology

Hookworm larvae

Rhabditiform larvae

Filariform larvae

Ancylostomiasis
Morfology

Egg of
Hookworm

Ancylostomiasis
Life Cycle
Infective stage :
Filariform larvae
Diagnostic stage :
Eggs in feces
Route of infection :
normally aquired by
skin penetration
Uncommon, A. duodenale
can be transmitted through
undercooked meat incl.
rabbit, lamb, beef and pork
(Wakanas disease) and
lactogenic during breastfeeding (infantile hookworm)

A.duodenale

Ancylostomiasis
Pathology

Hookworm disease manifests three

main phases of pathogenesis :
o The cutaneous or invasion
period
o The migration or pulmonary
phase
o Intestinal phase

Ancylostomiasis
Pathology

Cutaneous
Phase
Begins when larva penetrates the
skin
Pruritic , erythematous, papular rash
at the site entry (ground itch)

Ancylostomiasis
Pathology
Pulmonary Phase
Occurs

when juveniles break out of the lung capillary

into alveoli and progress up bronchi to the throat
Each sites hemorrhage slightly
Usually asimptomatic, although there may be cough
and sore throat
Pulmonary hookworm infection resembles Lfflers
syndrome because of its association with
eosinophilia in the lung.
Hookworm pneumonitis may indicate severe
infection

Ancylostomiasis
Pathology
Intestinal Phase
The

attachment of hookworms cutting

organ to the intestinal mucosa and
submucosa and the subsequent rupture of
intestinal capillaries and arterioles blood
loss
Hookworm produce active suction impulses
120-200 times per minute
The secretion of anticoagulation by parasite
help to maintain continous oozing of blood
at the attachment site

Ancylostomiasis
Pathology
The

major clinical manifestations of

hookworm disease : chronic intestinal
blood loss.
Infection with A. duodenale causes
greater blood loss than does infection
with N. americanus
The blood loss has been estimated as :
0,15 ml/ day per worm in A. duodenale
inf.
0,03 ml/ day per worm in N.
americanus inf.

Ancylostomiasis
Pathology
In

very heavy infection iron

deficiency anemia,
hypoproteinemia, edema,
potbelly in children, delayed
puberty, mental dullness, impair
cognitive ability, heart failure and
death

Ancylostomiasis
Diagnostic

o Hookworm eggs or adult worm in

feces
o Rhabditiform larva cultured from
eggs by the Harada-Mori method
o Serologi

Soil Transmitted Helminthiasis

Treatment and Control

WHO has recommended three

interventions to control morbidity due
to STH infections:
1. Regular drug treatment of highrisk groups for reduction of the
worm burden over time
2. Health education
3. Sanitation supported by personal
hygiene aimed to reducing soil
contamination

Soil Transmitted Helminthiasis

Treatment and Control

Regular drug treatment of high-risk groups

The recommended drugs :
1. Albendazole (400mg) tablets given in a
single dose,
2. Levamisole (40mg) tablets given in a
single dose by weight (2.5mg/kg)
3. Mebendazole (500mg) tablets given in a
single dose;
4. Pyrantel pamoate tablets given in a
single dose by weight (10mg/kg)

Soil Transmitted Helminthiasis

Treatment and Control

CUTANEOUS LARVA
MIGRANS

Cutaneous larva migrans

Synonim:

creeping eruption, ground

itch
Causativa agents: nematodes (zoonotic
hookworms): Ancylostoma braziliense,
Ancylostoma caninum, Ancylostoma
ceylanicum, Strongyloides stercoralis
Filariform larvae penetrate human skin,
usually feet and hands invade
epithellium aimless wandering
through the skin red, itchy wound
usually infected by pyogenic bacteria

Pathogenesis
Contact

with soil containing infective larvae

(filariform larvae) that are capable of
penetrating the skin.
This cant occur after first exposure but follows
reinfection only after several weeks, this
infection suggests that the disease is due to
hypersensitivity to larval secretions (Provic and
Croese, 1996)
The larva produces a number of enzymes
which may assist in dermal invasion; such as
metaloprotease, minor protease and
hyluronidase (Hotez, Hawdon and
Capello,1995)

Pathology
Lesions

may also become vesiculated,

encrusted, or secondarily infected.
The larvae eventually die and become
absorbed without treatment.
The cutaneous symptoms typically last for
days to months.
Only 29% of patients had lesions that
persisted for 1 month, but in occasional
patients had lesions in follicles and cause
disease for as long as 2 years.
Slightly increase of eosinophilia and normal
IgE

49

50

Treatment
Application

of 15% thiabendazole
ointment for 5 days.
Systemic treatment with
albendazole or ivermectin may
also be used, especially in severe
cases.
If applicable : 2nd bacterial
infection th/.