SESSION_04_WORM INFESTATION DISEASE.pptx

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INTRODUCTION.
 Taeniasis is the tape worm infection that affect the
digestive system.
 Taeniasis is the zoonotic disease caused by taenia
saginata and taenia solium.
 They are found in intestine of human host .
 They pass through two distinct phases in different host
to complete their developmental cycle.
 Adult worm live in the intestine of their definitive host.
 Larva stage found in the intermediate host.

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CLASSIFICATION OF TAENIASIS.
 Taeniasis in human are classified into three parasitic
species according to where they are obtained.
 Taenia species
 Taenia solium;are the worm found in pig called pork
tape worm.
 Taenia saginata ;are the worm found in cattles
called beef tape worm.
 Taenia asiatic;are the asian taenia affects human or
pig but found in part of asia.

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INCUBATION PERIODS
 The incubation period is appear in 8 to 10 weeks for
taenia solium.
 Also it take 10 to 14 weeks for taenia saginata after
infections.

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LIFE CYCLE OF TAENIASIS.

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MODE OF TRANSMISSION
 Through ingestion of infective cysts in undercooked
beef [T.saginata] and pork[Tsolium].
 Through ingestion of food,water or vegetables
contaminated with eggs of worm.
 Infection can also occur between individual through
contaminated hands.

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CAUSES OF TAENIASIS.
 Taeniasis is an intestinal tapeworm infection caused by;
 Eating raw or undercooked beef or pork of infected animal.
 Poor hygiene can cause disease through the fecal-oral
route
 Contaminated food can contain tape worm eggs or larvae
that grow in the intestine when eaten.
 Human tape worm carries excrete worm eggs in their
feaces and contaminate the environment when they
defecate in open areas.
 Taenia solium is the cause of 30 percentage epilepsy cases
in many endemic areas where people and roaming pigs
livein close priximity.

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SIGN AND SYMPTOMS
 Abdominal pain.
 Loss of appetite.
 Nausea and vomiting.
 Weight loss.
 Diarrhea or constipation may arise.
 Cysticercosis in muscle.
 Irritation in perianal areas.

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COMPLICATION OF TAENIASIS
 Obstruction of bile
 Interstinal obstruction.
 Acute pancreatic
 Inflamation of gallblader
 Larva can cause cysticercosis example cerebral
infection,lung infection and liver demage.

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DIAGNOSIS OF TAENIASIS
 Diagnosis of taenia tape worm infection is made by
examination of stool sample to see eggs or worms
segments are present.
 The diagnosis of neurocysticercosis usually require
MRI[magnetic resonance imaging] or
CT[computerized tomography] brain scan.
 Blood test include a complete blood count [CBC].

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TREATMENTS.
 It depend upon the number and location of cysts
and viability.
 Albendazole and praziquantel are both effective to
kill adult worm and cysticerci
 Albendazole is the drug of choice and is co-
administered with a steroid.
 Niclosarmide are drug effective agaist adult taenia
saginata and taenia solium in intestine.

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Preventive measures and controls
 Through inspection of meat and pork in the house
slaughter by veterinary surgeon.
 Adequate sewage treatment and safe disposal of
excreta.
 Do not eat undercooked meat and pork
 Improving level of sanitation and clean water supply
 Proper means of defecating should be followed and
not in an open area.
 Health education regarding improving the general
living condition of the people

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PRESENTATION OBJECTIVES
o Introduction to Hook Worms
o Disease etiology and its epidemiology
o Modes of disease transmission
o Pathogenesis and clinical manifestation of hook
worms
o Diagnostic measures
o Prevention and treatment measure

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INTRODUCTION
 Hookworm is a parasite that cause an infection in
people of all ages.
 Hookworm infestation is parasitic disease caused by
invading of hookworms in the body of host.
 The common host are human, cattle, dogs and
cats.
 It is widely spread in tropical and sub-tropical
countries

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Cont…
 Hook worms is one of the small intestine affecting
nematodes.
 It is named “hook” since the anterior end of an
adult worm is bent like a hook structure.
 There are two important human species which are ;
a) Ancylostoma duodenale
b) Necator americanus

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Ancylostoma duodenale
 This is also called world hook worm and it causes
ancylostomiasis which is the infection of the small
intestine.

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HOOK WORMS EPIDEMIOLOGY
 It globally affect almost 900 million people.
 The Necator spp said to have afected 835 million
and the Ancylostoma spp have affected 135 million.
 Hook worm infection is prevalent in the tropics and
subtropical countries like Asia, Africa, America
China and Southern Europe.

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Cont..
 Males and young adults are commonly affected
compared to others
 Anaemia is severe in children and pregnant women.

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MORPHOLOGY OF THE HOOK WORM
 Exhibits two structures; adult worm and egg.
 Adult worm; Is small greyish white and cylindrical
structured.
 Its anterior end bent dorsally hence named hook.
 Its oral aperture directed torwards dorsal surface.
 The buccal capsule has 6 teeth: 4 hook-like on

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CAUSES OF HOOK WORMS
 It is caused by two main species in humans which
are anyclostoma duodenale and necator
americanus.
 Anyclostoma duodenale cause anyclostomiasis
 Necator americanus causes necatoriasis

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MODE OF TRANSIMISION
 Through contaminated soil.
 Through contaminated water and food.

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PATHOGENESIS OF HOOKWORM
 Eggs are passed onto the stool and if they are
deposited in warm moist place in loose soil they
hatch in 1-2 days.
 The eggs release rhabdiform larvae which grows in
the soil and feed on the microbes.
 After few days the larvae mature to filariform larvae
which is infective.

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Cont..
 When they come into contact with human host the
penetrate through the skin and are carried within
the blood vessels to the heart then to the lungs. they
penetrate to the pulmonary alveoli ascend to the
bronchial tree to the pharynx and then swallowed.

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Cont…
 The larva reach small intestine they mature to adult
and live in the lumen of the small intestine.
 They attach to the wall and feed on blood and
produce eggs again and later excreted in the
feces.

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Cont…
 An infection starts with penetration of the filariform
larvae into the skin and through ingestion.
 It causes ground itch on site of penetration.
 At the lungs, cough and pneumotis may result as
larvae break into larvae break into the alveoli and
travel up the trachea and pharynx and later
swallowed to the small intestine.

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Clinical Features of Hook worms infection
 Itchiness.
 Localized rash.
 Abdominal pain.
 Diarrhea.
 Weight loss.
 Loss of appetite.
 Iron deficiency anemia or malnutrition.
 Breathing complication such as wheezing and a
cough.

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Diagnostic procedures of Hook Worms
 Direct methods
 Stool examination: to find the adult worm or
characteristic hook worm eggs in the stool sample.
 Stool concentration: Required to detect light hook
worm infections
 Larva can be seen in the stool sample if it is kept at
room temperature after 24 hrs (not preserved)

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Cont..
 Adult female hook worms produces 2500 to 5000
eggs per day
 Stool eggs count indicates the number of adult
hook worms present in the small intestine
 Also large number of eggs indicates severity of
infection.

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Cont..
 Indirect methods
 Blood examination: this reveals microcytic,
hypochromic anaemia and eosinophilia.
 Stool culture: it is conducted 5-7 days. During the
culture the eggs hatch out and develop into
filariform larva (L3) stage which can be observed
clearly. Hence this helps to confirm hook worms
presence in the small intestine.

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PREVENTIVE MEASURES
 Wearing shoes and improved personal hygiene
 Taking safety precautions such as wearing gloves
and shoes when gardening or farming activities.
 Avoid consuming soil or unwashed foods that may
be contaminated with hookworm.
 Sewage system should be well managed and
maintained.

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Cont…
 Do not defecate in open areas but rather in toilets
 Public health education to the community and
schools.

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TREATMENT
Most common for treatment are:
 Benzimidazoles.
 Albendazole: is much more effective during
intestinal stage and during parasites around the
skin. (400mg single dose)
 Mebendazole 100mg twice daily for 3 days
 Iron supplements if anemia is suspected.

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.
Ascariasis – is a intestinal
parasitic disease caused by
species of roundworm of the
class Nematoda, and can
cause intestinal and lung
damage

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 Ascaris lumbricoides, an intestinal
roundworm, is one of the most common
helminthic human infections worldwide.
 Highest prevalence in tropical and
subtropical regions, and areas with
inadequate sanitation. Ascariasis occurs in
rural areas of the southeastern United
States.

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EPIDEMIOLOGY

It is estimated that more than 1.4 billion people are
infected with A. lumbricoides, representing 25
percent of the world population. Transmission is
enhanced by the fact that individuals can be
asymptomatically infected and can continue to
shed eggs for years, yet prior infection does not
confer protective immunity.
The majority of people with ascariasis live in Asia
(73 %), Africa (12 %) and South America (8 %),
where some populations have infection rates as

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 Ascariasis is most common in children 2 to
10 years old, and prevalence decreases over
the age of 15 years. Infections tend to cluster
in families, and worm burden correlates
with the number of people living in a home.
 Ova can survive in the environment for
prolonged periods and prefer warm, shady,
moist conditions under which they can
survive for up to 10 years.

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 Transmission — Transmission occurs mainly via
ingestion of water or food (raw vegetables or
fruit in particular) contaminated with A.
lumbricoides eggs and occasionally via
inhalation of contaminated dust. Children
playing in contaminated soil may acquire the
parasite from their hands.
 Transplacental migration of larvae has also
occasionally been reported

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 Adult worms inhabit the lumen of the small
intestine, usually in the jejunum or ileum.
They have a life span of 10 months to 2
years and then are passed in the stool.
 The ova are passed out in the feces, and
embryos develop into infective second-stage
larvae in the environment in 2 to 4 weeks
(depending upon environmental conditions).

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LIFE CYCLE
 When ingested by humans, the ova hatch in the small intestine
and release larvae, which penetrate the intestinal wall and
migrate hematogenously or via lymphatics to the heart and lungs.
 Occasionally, larvae migrate to sites other than the lungs,
including to the kidney or brain.

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 Adult worms (1) live in the lumen of the small intestine. A
female may produce approximately 200,000 eggs per day,
which are passed with the feces (2). Unfertilized eggs may be
ingested but are not infective. Fertile eggs embryonate and
become infective after 18 days to several weeks (3), depending
on the environmental conditions (optimum: moist, warm,
shaded soil). After infective eggs are swallowed (4), the larvae
hatch (5), invade the intestinal mucosa, and are carried via the
portal, then systemic circulation to the lungs (6). The larvae
mature further in the lungs (10 to 14 days), penetrate the
alveolar walls, ascend the bronchial tree to the throat, and are
swallowed (7). Upon reaching the small intestine, they develop
into adult worms (1). Between 2 and 3 months are required
from ingestion of the infective eggs to oviposition by the adult
female. Adult worms can live 1 to 2 years.

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Pathophysiologic mechanisms
include
 Direct tissue damage
 The immunologic response of the host to infection with larvae,
eggs or adult worms
 Obstruction of an orifice or the lumen of the gastrointestinal
tract by an aggregation of worms
 Nutritional sequelae of infection

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CLINIC SYMPTOMS
 The majority of infections with A. lumbricoides are
asymptomatic.
 Clinical disease is largely restricted to individuals with a high
worm load.
 When symptoms do occur, they relate either to the larval
migration stage or to the adult worm intestinal stage.

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 The symptoms and complications of infection
can be classified into the following:

 1. Pulmonary and hypersensitivity manifestations
 2. Intestinal symptoms
 3. Intestinal obstruction
 4. Hepatobiliary and pancreatic symptoms

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Pulmonary and hypersensitivity
manifestations
 Transient respiratory symptoms can
occur in sensitized hosts during the stage
of larval migration through the lungs.
Symptoms associated with the
pneumonitis, which are known as
Loffler's syndrome, tend to occur one to
two weeks after ingestion of the eggs.

 Urticaria and other symptoms related to
hypersensitivity usually occur toward the
end of the period of migration through
the lungs.
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INTESTINAL SYMPTOMS
 Heavy infections with Ascaris are frequently
believed to result in:
 Abdominal discomfort,
 Anorexia,
 Nausea
 Diarrhea.

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Intestinal obstruction

 A mass of worms can obstruct the bowel lumen in heavy
Ascaris infection, leading to acute intestinal obstruction.

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Hepatobiliary and pancreatic symptoms
Symptoms related to the migration of adult worms into the biliary
tree can cause:
 abdominal pain,
 biliary colic,
 acalculous cholecystitis,
 ascending cholangitis,
 obstructive jaundice, or bile duct perforation with peritonitis.

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Complications
Complications associated with A.
lumbricoides infections are fatal in up
to five percent of cases. It is estimated
that 20,000 deaths from ascariasis
occur annually, primarily as a
consequence of intestinal obstruction.

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Laboratory diagnostic
 Microscopy — Characteristic eggs
may be seen on direct examination of
feces or following concentration
techniques.
 Eosinophilia — (during the phase of
larval migration through the lungs)..
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 Plain film of the abdomen. The
mass of worms contrasts against
the gas in the bowel, typically
producing a "whirlpool" effect.
 Radiologic detection of adult
worms is sometimes made by
detecting elongated filling defects
following barium meal
examinations of the small bowel.
Radiographs will also show when
there is associated intestinal
obstruction.
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 Ultrasound examinations can help to diagnose hepatobiliary or pancreatic ascariasis.
 Computed tomographic (CT) scanning or magnetic resonance imaging (MRI)
may also be used to identify worm(s) in the liver or bile ducts, but this is not usually
necessary. Imaging the worm in cross-section gives a "bull's eye" appearance.
 Serology — Infected individuals make antibodies to A. lumbricoides which can be
detected.

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TREATMENT
 Choice of Drugs — A number of drugs can be used in the treatment
of ascariasis:
 * Pyrantel pamoate (11 mg/kg up to a maximum of 1 g) is effective
in eradicating adult worms.
 * Mebendazole (100 mg BID for 3 days or 500 mg as a single dose).
 * Albendazole — A single dose of albendazole (400 mg) is effective
in almost 100 percent of cases.


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 Ivermectin — Ivermectin causes paralysis of adult worms and
is approximately as effective as other available therapies but is
not generally used.
 * Piperazine citrate — Piperazine citrate (50 to 75 mg/kg
QD up to a maximum of 3.5 g for 2 days) is used seldom
because of the big toxicity
 * Levamisole — Levamisole (150 mg for adults and 5 mg/kg
for children) is safe and is effective in 77 to 96 percent of cases
of ascariasis.

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PREVENTION
 Good sanitation to prevent fecal contamination of soil is required. Soil
treatments have been attempted but are generally not practical.

 Mass treatments with single dose mebendazole or albendazole for all
school-age children every three to four months has been used in
some communities.

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Introduction
 Pinworm infection is also known as enterobiasis.
 It is a human parasitic disease caused by pinworm (enterobius
vermicularis)
 It is the intestinal worm infection
 It is associated with itching in the anal area.

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Where we find Entrobius vermicularis eggs,,

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Mode of transmission
1. Infection
occurs when a heathy person ingest the infective
eggs from the environment
2. Self-infection
a person infects alone by ingestion of infective eggs
3. Retro-infection
this occurs when eggs mature and larvae hatch in
anal area and migrate back to the large intestine
through the anus, where by they grow in to mature
worms.

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Life cycle
 Humans are the host.
 Infection occurs by ingesting the eggs.
 The larvae hatch from the eggs in the small intestine.
 The larvae develops into female and male worms.
 After one month female becomes gravid (Carry Eggs)
 The worms do not lay eggs in the intestinal lumen but they lay eggs in the
perianal skin(skin around the anus)
 The eggs can spread everywhere and becomes infective in 4 to 6 hours.
 Pinworm egg can survive for up to two weeks on clothing , bedding, food
and other surfaces.
 Ready to infect other people

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Symptoms of pinworm
infection
 Perianal pruritus (Often Intense Itching) is the common
symptoms.
 Is thought to be an allergic reaction to the presence
of either adult female or the eggs
 Itching of the perianal area and vagina is commonly
notable, especially during night.
 Weight loss is also observable in the severe infections.
 Scratching pre-disposes to the secondary infection.
 Insomnia
 Frequent defecation

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Laboratory diagnosis
 The eggs are recovered from the perianal skin by using the
scotch tape technique for the microscopic examination.
 Eggs are not found in the stool.
 No serological tests are available.

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Epidemiology
 Although adult can be infected but infection
is more common in children.
 Infections are more common within families
with school aged children.
 Kindergartens and nurseries
 Orphanages
 Refugees camps
 Mental institutions.

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Complications
 Appendicitis: when the worms invade
appendix.
 Vaginitis: found in female patient due to
invasion of vagina by the hatched larva
from anal area.

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Cont..
• Urethritis: Inflammation of the tube carrying urine
from the bladder to the outside of the body.
• Salpingitis: Inflammation of the fallopian tube.
• Endometritis: Inflammation of the endometrial lining
of the uterus

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Treatment
Several medications used for treatment of
pinworms are;
 Mebendazole
 Pyrantel pamoate
 Albendazole
All these drugs are to be given in a single dose
and then repeated 2 weeks later.

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Prevention and control
 Hand hygiene (after using toilet, before eating)
 Trimming the nails regularly and avoid biting the
nails
 Avoid scratching the anal area

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Cont…..
 Showering every morning and washing the
anal area to remove the eggs
 Cleaning bathrooms and toilets.
 Washing and ironing cloth and bed linens

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• Habitat: females live in the superficial tissues of the
small intestine (duodenum and jejunum)
• Definitive host: Human, dogs and cats
• Route of infection: Filariform larvae penetrate the skin of
human.
• Infective stage: Third stage larvae ( filariform).
• Diagnostic stage: First stage larvae(Rhabditiform) in feces.
• Geographical distribution: - cosmopolitan parasite, mainly in
moist and warm areas of low hygiene
Introduction

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Introduction cont……
• Human parasitic disease caused by nematode S. Stercoralis.
• Mostly in tropical, subtropical area and temperate climate.
• Affect 30-100 million annually.
• Has two unique life cycle: Free life cycle and Parasitic life cycle.
• Cause by direct contact with contaminated soil and
recreational activities.
• Children highly affected to bad sanitation.
• S. stercoralis is a 2 mm long intestinal worm

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Epidemiology
• Relatively uncommon in the US
• Usually found in tropical and subtropical countries
– Prevalence up to 40% in areas of West Africa, the Caribbean,
Southeast Asia
• Affects >100 million worldwide
• No sexual or racial disparities. All age groups.

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Eggs are laid in the mucosa, hatch into rhabditiform larvae that
penetrate the glandular epithelium and pass into the lumen of
the intestine and out the feces

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Morphology cont……

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a) parasitic female
b) free-living male
c) free-living female

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•Since the parasitic females live in the superficial tissues of the small intestine, and can
be present in high numbers, they can cause significant pathology.

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Life cycle
of
S.
stercoralis

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Life Cycle
cont….
2. Parasitic Phase
•When filariform larvae encounter a human or another suitable
host (e.g. cats and dogs), they penetrate the skin and are carried
by cutaneous veins to the vena cava
•They enter the right side of the heart and are carried to the lungs
via the pulmonary artery
•In the lungs, following a 3rd molt, the larvae rupture from the
pulmonary capillaries and enter the alveoli
•From the alveoli, the larvae move up the respiratory tree to the
epiglottis
•Abetted by coughing and subsequent swallowing by the host, they
migrate over the epiglottis to the esophagus and down into the
small intestine, where they undergo a final molt and become
sexually mature females

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Parasitic Phase cont.
•Females produce embryonated eggs
parhenogenetically
•These eggs hatch in the mucosa into 1st stage
rhabditiform larvae
•These exit the intestine with the feces, feeding down
the length of the intestine
•Larvae become established in the soil, undergo
several molts and become free-living adults
•Under adverse conditions they can revert to being
filariform larvae

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3. Autoinfection
•During passage through the host digestive system, rhabditiform
larvae may undergo 2 molts to filariform larvae and by penetrating
the intestinal mucosa, enter the circulatory system and continue
their parasitic lives without leaving the host
•Autoinfection can also occur when larvae remain on and penetrate
the perianal skin.
• Autoinfection often leads to very high worm burdens in humans

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Pathology
• Invasive : Skin Penetration.
• Pulmonary: During Cycle or
Immigration.
• Intestinal: Tissue Destruction

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Clinical Presentation/ Aspects
• Acute infection:
– Lower extremity itching (mild erythematous
maculopapular rash at the site of skin
penetration)
– Cough, dyspnea, wheezing
– Low-grade fevers
– Epigastric discomfort, nausea, vomiting, diarrhea
(n/v/d)

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Clinical Presentation/Aspects
cont….
• Chronic Infection
– Can be completely asymptomatic
– Abdominal pain that can be very vague, crampy, burning
• Often worse after eating
– Intermittent diarrhea
• Can alternate with constipation
– Occasional nausea, vomiting (n/v)
– Weight loss (if heavy infestation)
– Larva currens (“racing larva” – a recurrent maculopapular or
serpiginous rash)
• Usually begins perianally and extends up the buttocks, upper thighs,
abdomen
– Chronic urticaria

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Clinical Presentation/Aspects
cont….
• Severe infection
– Can be abrupt or insidious in onset
– N/v/d, severe abdominal pain, distention
– Cough, hemoptysis, dyspnea, wheezing, crackles
– Stiff neck, headache, MS changes
• If CNS involved
– Fever/chills
• Risk factors for severe infection
– Immunosuppressant meds (steroids, chemo, tumor necrosis factor (TNF )
modulators, tacro, etc)
– Malignancy
– Malabsorptive state
– end-stage renal disease (ESRD)
– Diabetes mellitus (DM)
– Advanced age
– human immunodeficiency virus (HIV)

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Dangerous Complications
• Hyperinfection Syndrome
– Acceleration of the normal life cycle, causing excessive
worm burden
– Autoinfection (turn into infective filariform larva within
the lumen
– Spread of larvae outside the usual migration pattern of
GI
tract and lungs
• Disseminated strongyloidiasis
– Widespread dissemination of larvae to extraintestinal
organs
• CNS (meningitis), heart, urinary tract, bacteremia, etc

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Transmission
 Direct penetration of unbroken
skin by larva
• Autoinfection - internal (larva
becomes infectious in intestinal tract) & external

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 Direct stool smears (larvae)
 Cultivation of stool. (Damp charcoal or Harada-
Mori mediums).
 Eosinophilia, is present in uncomplicated
strongyloidiasis, but is lost in hyper infection
 Histological examination of duodenal or jejunal biopsy
specimens obtained by endoscopy can demonstrate adult
worms embedded in the mucosa.
 For population screening in endemic areas, an ELISA for
IgG
anfi-Strongyloides antibodies is effective.
Laboratory
Diagnosis

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Laboratory Diagnosis cont…..
• Diagnosis rests on the microscopic identification of
larvae (rhabditiform and occasionally filariform) in
the stool or duodenal fluid.
• Examination of serial samples may be necessary, and
not always sufficient, because stool examination is
relatively insensitive.

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Laboratory Diagnosis cont…..
• CBC
– WBC usually wnl for acute and chronic cases, can
be elevated in severe cases
– Eosinophilia common during acute infection, +/- in
chronic infection (75%), usually absent in severe
infection

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Strongyloides stercoralis in
transplant patients

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Prevention
• Good sanitation with specific care of human
waste disposal.
• Wearing permanent shoes.
• screening prior to transplantation
• Education Program for community.

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⦿Known as the whipworm is
also a soil- transmitted
helminth.
⦿Ascaris and Trichuris are
frequently observed as
occuring together.
⦿ .

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The female
worm is about
35 to 50 mm
The male
worm
measures
30 to 45 mm

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Posterior part of
male
Trichuris trichuria
Posterior part of
female Trichuris
trichuria

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⦿ Trichuris worm inhabit the large intestine.
⦿ After copulation, the female worm lays
eggs, which are passed out with feces
and deposited in the soil.
⦿ Under favorable conditions, the eggs
develop and become embryonated
within two to three weeks.
⦿ If swallowed, the infective embryonated
eggs go to small intestine and undergo
four larval stages to become adult worm.
⦿ Unlike Ascaris, there is no heart
lung migration.

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⦿ The anterior portion of the worm, which
is embedded in the mucosa, cause
petechial hemorrhages, which may
predispose to amebic dysentery.
⦿ The mucosa is hyperemic and
edematous; enterorrhagia is common
and there may even be rectal
prolapse.
⦿ The lumen may be filled with worms,
and irritation and inflammation may

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⦿ Infection with over 5,000 T. trichuria
eggs per gram of feces are usually
symptomatic.
⦿ Those with more than 20,000 eggs
per gram feces often develop
severe diarrhea or dysenteric
syndrome.
⦿ Light infections, usually
asymptomatic, and the presence of
the parasite is discovered in stool
examination.
⦿ I
n heavily parasitized individuals,
the worm may be found

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Heavy chronic trichuriasis are
often marked by:
⦿ Frequent blood-streaked
diarrheal stools
⦿ Abdominal pain and
tenderness
⦿ Nausea
⦿ Vomiting
⦿ Anemia

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⦿ Clinical diagnosis is possible
only in heavy chronic
Trichuris infection.
⦿ In light infection, where
symptoms are absent,
laboratory diagnosis is essential.

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 Direct fecal smear (DFS) with a drop
of saline.
 Kato thick smear method – highly
recommended in diagnosis of
trichuriases

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⦿ Mebendazole – drug of choice for
Trichuris.
⦿ Albendazole – may be used as
an alternative drug.
⦿ Ivermectin in combination with
albendazole – exhibit better cure
and egg reduction rate than
albendazole alone.

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⦿ Trichuris occurs in both temperate
and tropical countries, but is more
widely distributed in warm, moist
areas of t ranges he world.

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⦿ Factors affecting transmission are
the same as that of Ascariasis
namely:
 Indiscriminate defecation of
children around yards
 Frequent contact between fingers
and soil among children at play
 Poor health education
 Poor personal and community
hygiene

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⦿ Mass treatment may be indicated id
infection rates are higher than 50%
⦿ Infection in highly endemic areas may
be prevented by:
 Treatment of infected individuals
 Sanitary disposal of human feces
by construction of toilets
 Washing of hands with soap and water
before meal
 Health education on sanitation and
personal hygiene
 Washing and scalding of uncooked
vegetables especially if night soils is used
as fertilizers

SESSION_04_WORM INFESTATION DISEASE.pptx

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