Intestinal Nematodes

Dr. Devika Iddawela

08/09 batchDr. Devika ddawela

Helminthes

Nemathelminthes Platyhelminthes

Nematodes(round worms)

Cestodes(tape worms)

Trematodes(flukes)

Elongated, cylindrical worms

Flattened tape-like segmented

Flatten leaf-like

Sexes are separate

Sexes are not separate

Sexes are not separate except blood flukesComplete

Alimentary canal + Alimentary canal absent

Alimentary canal incompletePossess a body

cavity (psedocelome)

Body cavity absent

Body cavity absent

Nematodes

Nematodes have successfully adapted to nearly every ecological niche from marine to fresh water, from the polar regions to the tropics,

word "nematode" came from a Greek word nema that means "thread".

Nematodes

Long cyndrical body

No segmentation

Males and females separate. Females larger then male.

Similar to each other but vary in size

Eg: round worm-size of a pencil

hook worm-size of a pin

Pin worm- smaller than the above

DO NOT MULTIPLY IN HUMANS

• Parasitize the intestinal tract, tissues, tissue spaces, lymphatics

• Body covered in a complex cuticle Longitudinal muscle fibers present, No circular muscle

• Fluid filled body cavity present

• Organs are suspended in the body cavity

• Reproduction & developmental stages: egg, Egg fertilization,embryonated egg, larva, 4 moults, adult

Small intestine - Nematode parasites

Ascaris lumbricoidesAncylostoma duodenale/Necator

americanusStrongyloides stercoralis

Nematodes of small intestine

Nematodes of the large intestine

• Trichuris trichiura - Whipworm

• Enterobius vermicularis - Pinworm

Orally infected Intestinal nematodes

• Ascaris lumbricoides (round worm)

• Trichiuris trichiura ( Whip worm)

• Enterobius vermicularis ( Pin worm)

Ascaris lumbricoides – (Round worm)

worm

•Common intestinal parasite world over but high prevalence in countries with poor sanitation

•Commonest age group affected – pre-school children & young school children

•Prevalence due to indiscriminate defaecation in and around home gardens

Morphology - •Sexes are separate. •Female - 20 - 40 cm•Male - 15 - 30 cm with curved tails•No. of eggs /female/day - appr. 200,000

The anterior end of both sexes shows three lips

Location in host – worms are found free in the lumen of small intestine

Maintains position in lumen with muscular movement against peristalsis. Can be temporarily attached to mucosa for short periods

Eggs

Fertilized eggs: (corticated, decorticated)Ovoid, 60 x 40 um. Thick shell – ( triple layered) inner non-permeable layer, thick transparent middle layer and an outer mammilated coat .

Unfertilized eggs - Larger, rectangular (80 - 90 x 60 um) with disorganized,

vacuolated contents

Male and female adults in the small intestine

Fertilized eggs ( non- infective

pass in the faeces

Infective L2 larva ( 2nd stage larva)develop with in the egg ( 2-3

weeks )

Infective eggs swallowed with contaminated water

and food

eggs hatch in smallintestine

Larva penetrate the Intestinal wall

and venules

Larva enters portal vein

Heart

Reaches pulmonary capillaries

Larva penetrate in to the alveolus bronchioles trachea swallowed

oesophagus small intestine

warm moist clay soil 25-

30C

Adults in the small intestine

Pathogenesis & clinical features

Depends on• worm load• The host immune response• Effect of larval migration• Mechanical effects of adult worm• Nutritional deficiencies due to the presence of adult wormMajority of infections are clinically asymptomatic

Migrating Larvae( larval ascariasis)

Loeffler’s syndromeEosinophilic abscesses

• Lungs - larval migration causes pneumonitis (Loffler’s syndrome) due to immunological(hypersensitive) reaction

CLINICAL FEATURERS: Fever, cough, sputum, asthma, eosinophilia and radiological infiltration

On reaching general circulation

Rarely larvae may wander in to the brain, eye or retina causing

granuloma

Adult worms

Adult worms in their normal habitat cause little pathology

BUT(Severe disease if worm burden 100 or >)

Heavy infections can cause intestinal colic

•Aggregate masses of worms cause

Volvulous, Intestinal obstruction or interssusception

Large worm load :Intestinal obstruction

Small bowel obstruction in kids >1000 in worm ball

Wandering ascaridslone adults are prone to wandering habit –block/perforate ductscause acute symptoms• Blocking the duct orifices

Acute appendicitis – Pancreatic necrosis-Obstructive jaundice Ascaris liver abscess

• Migrate out of the anus or come out the mouth or nose

Immuno-pathological effects-

sensitivity to ascaris ag-

conjunctivitis, urticaria, asthma

Indirect effects - Micro organisms can by carried by the adult worms on their migration from bowel

• Protein Energy Malnutrition [PEM]

Due to consumption by the worm

Act as a mechanical barrier to absorb nutrients

• children with 13-40 worms

loose 4g protein/day from a daily intake of 35-50g

[1 egg only 6g protein]• Kwashiorkor – swelling due to low albumin [low

serum proteins]• Vitamin A deficiency – Night blindness• AFFECTS NORMAL GROWTH & EDUCATIONAL

DEVELOPMENT

Effect of Ascariasis on Growth & Nutrition

Stunting = low height for ageHeight difference in 2 girls of 5 years age40% of world’s children are stunted

CHRONIC MALNUTRITION STUNTINGStunting linked to impaired intellectual developmentUNICEF – State of the World’s ChildrenThe same factors that lead to stunting cause learning deficits

Malnutrition early in life is linked to deficits in children's intellectual development that persist in spite of schooling and impair their learning ability

growth retardation, poor cognitive & scholastic achievements

Diagnosis

Demonstrating characteristic eggs in faeces Identification worm

Concentration techniques are useful

Eosiniphilia – Larval ascariasis high eosinophilia

In Adult infection – little or none

Radiography: 4 -6 hours after opaque meal displays worm as cylindrical filling defect

Long, tubular filling defects, especially in distal small bowel The worm ingests barium and the barium may be seen as a thin line of contrast in the center of the worm Especially after the remainder of the barium exits the small bowel

Epidemiology• Common backyard infection• Maintained by young children• Transmission occurs through infective eggs Contaminated food and water

In Sri Lanka prevalence is highest among school children

Prevention of ingestion of infective eggs

• Wash raw vegetables and fruits thoroughly ( preferably with running water)

• Wash hands with soap and water before eating and after soil contact

• Drink boiled cool water

Prevention & Control

Prevention of indiscriminate Defaecation by Providing sanitary latrines.

Treatment of infected patients

Provision of safe drinking water

Geographical distribution -Parasite of warmclimatesMorphology - 3 - 5 cm. Posterior 2/5th of the body is thick (whip handle). Anterior 3/5th thin and is threaded into the mucosa of the large intestine. Posterior end of male is curved.

Trichuris trichiura

Egg - Paddy seed shape with two polar plugs 50 x 20 um

Life cycle

Adults - attached to the colon from their anterior site embedded in mucous between intestinal villi

Eggs are laid unsegmented require embryonation in the soil

No lung migration

Adults in large intestine Eggs in stools

Eggs maturein soil

Moistclay

25 -30 C

Eggs ingested with contaminated fruits, vegetables

etc.

Life cycle of whipworm

Larva hatches in intestine

Penetrate and mature in intestinal mucosa

No lung migration

Pathology

Few worms – little damage

Heavy infection- spread throughout the colon to the rectum causing

• Haemorrhages

• Muco-purulent stools, dysentery and rectal prolapse

clinical features

Mild infections are asymptomatic

Heavy infection cause blood and mucus diarrhoea

due to mucosal damage & rectal prolapse

Children may get ‘Trichuris dysentery syndrome’ resulting in severe diarrhoea, malnutrition, growth retardation and impairment of cognitive functions

Diagnosis

Finding the characteristic eggs in stool by direct smear or by concentration methods

Proctoscopy – in cases of dysentery, show numerous worms attach to the mucosa which is redden and ulcerated

Epidemiology

Trichuris trichiura is primary a human infection but Trichuris suis of pig also can infect man

Common in areas of high rain fall, high humidity, dense shade and poor sanitation.

High prevalence in children of primary school age

Often associated with ascariasis

Enterobius vermicularis

Geographical distribution -worldwide highprevalence in cold climates. Location in host - Adults are loosely attached to the mucosa of the large intestineMorphology - creamy white, 1cm, spindle shaped

Eggs - Plano-convex 50 x 25 um, double walled with outer albuminous layer and an inner lipoid layer

The ‘cervical alae’ extend right down the sides of the body so in cut section seen as projection in either side of the body

Adults live in the large intestine; females

migrate out of the anus for oviposition:

Worm attached to the mucosa of large intestine, they are not blood suckers

A gravid female carries about 10,000 eggs.It dies after ovipositionNo lung migration of larvae

No development in the soil. Therefore it is not a soil transmitted helminthe infection

Life cycle

Eggs become infective within 6 hours

of laying

clinical features

• Very little tissue damage• Rarely penetrates the gut wall causing granulomatous reactions in the liver, ovary, kidney

•Can co-exist with amoebiasis

•Causes intense perianal pruritis especially at night when gravid female moves on and lay eggs on the perianal skin

• In children this leads to insomniaFemale worms may enter vagina urethra, can cause vulvitis, pruritis vulvi

• Loss of appetite, loss of weight ,irritability, enuresis

DiagnosisDemonstration of eggs:NIH (National Institute of Health, USA) swab and Scotch Tape method a clear adhesive cellulose tape is applied to the anal area early in the morning before bathing or defecation

A simple ‘cello-tape’

Cotton wool swab

Adults

Eggs are usually collected in the folds of skin around the anus. Rarely appear in the stools

Transmission and epidemiology

1.Direct transmission from the perianal and anal region to mouth by figure nail contamination due to scratching of perianal region and by soiled night cloths ( hand to mouth)

2. Exposure to viable eggs from soiled bed linen and other contaminated objects in the environment.

3. Via mouth or nose from contaminated dust

4. Retro-infection where eggs hatch in the perianal skin and larvae migrate up the bowel

It is a household infection and is common in overcrowded houses and institutions like hostels, prisons, refugee camps, orphanages etc

Prevention

Cut figure nails short

Wash hand with soap and water regularly

Treat every one in the household

Following treatment all bed linen & personal cloths should be washed and dried in hot sun

Intestinal nematodes

Infection via skin penetration

Hook worms- Ancylostoma duodenale Necator americanus

Tread worm- Strongyloides stercoralis

HOOK WORMS

Hookworms

Necator americanus - Sri Lanka, S.Asia,Africa,

Pacific region and AmericaAncylostoma duodenale -

E.Europe,N.Africa,India, N.China, Japan

Both species overlap in S.E.Asia, Pacific, W.Africa

MorphologyN.americanus - 1 cm, head sharply bent backwards. Buccal capsule has a pair of ventral cutting plates

A.duodenale – • slightly larger• head bent backwards in a smooth curve. • Buccal capsule has two pairs of teeth

Both species - Males have expanded tails to form the copulatory bursa

Female

Male

The caudal expansion of certain male nematodes that functions as a

claspers during copulation.

Egg – Oval ,60 x 40 µm with a thin glass like shell. Embryo usually segmented when pass out with

the faeces

Shade,warmth, sandy soil

24 hours

L1

L3 5th day

L2 rhab.larva (3rd day)

Free living,actively feeding

Non feeding,move

on to top soil

Obligatory lung migration

IP= 4-7 weeks

Life cycles of Ancylostoma and Necator are similar except that

• A.duodenale can infect by ingestion as well as via the skin

• N. americana infects only through skin

• Migrating larvae of N.americana grow and develop in the lungs, where as ancylostoma do not

PathogenesisLarvae

Larvae at the site of entry –vesiculation and pustulation (ground itch)

Can be secondarily infected due to severe itching

Asthma and bronchitis during migration, can cause pneumonitis but less severe than ascariasis

Adults:

Hook worm Anaemia

Symptoms- mucous surface & skin become pale. Palpitation, breathlessness

Chronic blood loss is due to • active suction impulse 120- 200 times/minHabitual blood sucker and need serum• Secrete anticoagulant substance and •may move from spot to spot increasing the damage and blood lossBlood lossN. Americarnus -0.03ml /day/wormA. Duodenale – 0.15/day/worm

500-1000 worms • Anaemia even if adequate dietary iron intake• If dietary iron deficient – anaemia even with light infection

Iron deficiency AnaemiaHb related to worm burden

Severe iron deficiency anaemia, hypoproteinaemia, oedema withassociated circulatory problems

Hypoalbuminaemia - reduced albumin synthesis &Protein loss > RBC loss Related to worm load

Hookworm disease

Laboratory DiagnosisBy demonstrating characteristic eggs in faeces. In ‘old’ stool samples Rhabditiform larvae may be found ( distinguish them from those of Strongyloides stercoralis). Concentration techniques are helpful

Eggs can be cultured into infective larvae (Harada – Mori culture)

Transmission

• Normally acquired via the skin from filariform larvae in the soil contaminated by the human faeces or

• Orally via the ingestion of contaminated food ( A. duodenale)

• Migrating infective filariform larvae of A.duodenale are arrested in their development and migrate to the mammary gland and are excreted via milk and infect the child

Epidemiology –

varies in different parts of the world. There are geographical variations too. In Sri Lanka it is an infection of the adults due to indiscriminate defaecation in shady areas away from dwellings.

Prevention & Control

avoidance of indiscriminate defaecation & use of foot wear

provision of hygienic latrines, treatment of infected persons& health education

Strongyloides stercoralis

Distribution - Worldwide but more common in warm climates. Major opportunistic infection among immunocompromised persons.

Morphology - Females are about 2mm. Male is very small , short life span in parasitic life cycle or non- exsistant

Male exist but disappear from the bowel soon after oviposition. Eggs can be produced parthenogenetically Worm - embedded in the small intestinal mucosa

Egg output –

low and asynchronous ( not occurring at regular interval)

Eggs hatch in the mucosa itself and 1st stage rhabditiform larvae are passed in faeces

Life cycle

Two life cycles –

Parasitic cycle ( if the external conditions are unfavorable)

Free living cycle( if conditions are favorable )

Rabditiform larvae

Develop in to filariform larvae in

soil

Follow free living cycle in the soil

Penetrate the intact skin and

initiate the infection

Filariform larvae develop before

leaving the patient

Enter perianal skin & initiate autoinfection

Enter intestinal mucosa, migrate to lung & initiate

autoinfection

Multiplication in the host by two ways

1. Filariform larvae do not pass out in the stool but reinvade bowel or skin

2. Filariform larvae lodge in the bronchial epithelium and produce further progeny (offspring)

HOOK WORM TREAD WORM

Attach to small intestine

Embedded in small intestine

Both male and female

Male short living

parasitic cycle parasitic and free living cycles

no autoinfection Autoinfection+

Differences between hookworms and threadworms

clinical features

Vast majority of infections in endemic areas are symptomlessPrimary infection• a pruritic erythematous eruption ‘Ground itch’ at the site of entry to larvae, last about 3 weeks• Pneumonitis due to lung migration not common

Intestinal nematodes

Infection via skin penetration

Hook worms- Ancylostoma duodenale Necator americanus

Tread worm- Strongyloides stercoralis

HOOK WORMS

Hookworms

Necator americanus - Sri Lanka, S.Asia,Africa,

Pacific region and AmericaAncylostoma duodenale -

E.Europe,N.Africa,India, N.China, Japan

Both species overlap in S.E.Asia, Pacific, W.Africa

MorphologyN.americanus - 1 cm, head sharply bent backwards. Buccal capsule has a pair of ventral cutting plates

A.duodenale – • slightly larger• head bent backwards in a smooth curve. • Buccal capsule has two pairs of teeth

Both species - Males have expanded tails to form the

copulatory bursa

Female

Male

The caudal expansion of certain male nematodes that functions as a clasper during

copulation.

Egg - Ovoid,60 x 40 µm with a thin glass like shell. Embryo

usually segmented when pass out with the faeces

Shade,warmth, sandy soil

24 hours

L1

L3 5th day

L2 rhab.larva (3rd day)

Free living,actively feeding

Non feeding,move

on to top soil

Obligatory lung migration

IP= 4-7 weeks

Life cycle

Adults in smallintestine

Eggs passed in faeces

Eggs hatch in 24 hours into 1st stagerhabditiform larva

Moults into 2nd rhab. larva on the 3rd day

Moults into 3rd stageinfective filariform larva

Penetrates skin, enterscirculation, carried tothe lungs

Breaks into alveolimove along bronchioles,trachea, swallowed

Shady warmth

sandy soil

Life cycles of Ancylostoma and Necator are similar except that

• A.duodenale can infect by ingestion as well as via the skin

• N. americana infects only through skin

• Migrating larvae of N.americana grow and develop in the lungs, where as ancylostoma do not

PathogenesisLarvae

Larvae at the site of entry –vesiculation and pustulation (ground itch)

Can be secondarily infected due to severe itching

Asthma and bronchitis during migration, can cause pneumonitis but less severe than ascariasis

Adults:

Hook worm Anaemia

Symptoms- mucous surface & skin become pale. Palpitation, breathlessness

Chronic blood loss is due to • active suction impulse 120- 200 times/minHabitual blood sucker and need serum• Secrete anticoagulant substance and •may move from spot to spot increasing the damage and blood lossBlood lossN. Americarnus -0.03ml /day/wormA. Duodenale – 0.15/day/worm

500-1000 worms • Anaemia even if adequate dietary iron intake• If dietary iron deficient – anaemia even with light infection

Iron deficiency AnaemiaHb related to worm burden

Severe iron deficiency anaemia, hypoproteinaemia, oedema withassociated circulatory problems

Hypoalbuminaemia - reduced albumin synthesis &Protein loss > RBC loss Related to worm load

Hookworm disease

Laboratory DiagnosisBy demonstrating characteristic eggs in faeces. In ‘old’ stool samples Rhabditiform larvae may be found ( distinguish them from those of Strongyloides stercoralis). Concentration techniques are helpful

Eggs can be cultured into infective larvae (Harada – Mori culture)

Transmission

• Normally acquired via the skin from filariform larvae in the soil contaminated by the human faeces or

• Orally via the ingestion of contaminated food ( A. duodenale)

• Migrating infective filariform larvae of A.duodenale are arrested in their development and migrate to the mammary gland and are excreted via milk and infect the child

Epidemiology - varies in different parts of the world. There are geographical variations too. In Sri Lanka it is an infection of the adults due to indiscriminate defaecation in shady areas away from dwellings.

Prevention & Control

avoidance of indiscriminate defaecation & use of foot wear

provision of hygienic latrines, treatment of infected persons& health education

Strongyloides stercoralis

Distribution - Worldwide but more common in warm climates. Major opportunistic infection among immunocompromised persons.

Morphology - Females are about 2mm. Male is very small , short life span in parasitic life cycle

Male exist but disappear from the bowel soon after oviposition. Eggs can be produced parthenogenetically Worm - embedded in the small intestinal mucosa

Egg output –

low and asynchronous ( not occurring at regular interval)

Eggs hatch in the mucosa itself and 1st stage rhabditiform larvae are passed in faeces

Life cycle

Two life cycles –

Parasitic cycle ( if the external conditions are unfavorable)

Free living cycle( if conditions are favorable )

Rabditiform larvae

Develop in to filariform larvae in

soil

Follow free living cycle in the soil

Penetrate the intact skin and

initiate the infection

Filariform larvae develop before

leaving the patient

Enter perianal skin & initiate autoinfection

Enter intestinal mucosa, migrate to lung & initiate

autoinfection

Multiplication in the host by two ways

1. Filariform larvae do not pass out in the stool but reinvade bowel or skin

2. Filariform larvae lodge in the bronchial epithelium and produce further progeny

HOOK WORM TREAD WORM

Attach to small intestine

Embedded in small intestine

Both male and female

Male short living

parasitic cycle parasitic and free living cycles

no autoinfection Autoinfection+

Differences between hookworms and threadworms

clinical features

Vast majority of infections in endemic areas are symptomlessPrimary infection• a pruritic erythematous eruption ‘Ground itch’ at the site of entry to larvae, last about 3 weeks• Pneumonitis due to lung migration not common

Chronic uncomplicated strongyloidiasisEpigastric pain, anorexia, chronic diarrhoea due to mucosal damage, weight lossSkin rashesTwo typesLarva currens: Occur around the anus and anywhere on the trunk. larvae migrate under the skin causes itchy rash which is not indurate & has a red flare at the edge

Urticaria –

• Allergy to larval penetration in already sensitized patient• Occur in the buttocks with pruritus ani& around the waist

•Last 1-2 days and can recurs at regular intervals

Severe complicated strongyloidiasis

Severe disease with hyper-infection in persons with immunosupression • severe watery diarrhoea, often with malabsorption, hypoalbuminaemia. Generalized oedema, Fever,

Lungs- hypereosinophilia, pneuminitis, diffuse crepitation, pulmonary abscess and gross respiratory failure

Diagnosis •Demonstration of 1st stage rhab. larvae in stools • Diffentiate from hookworm 1st stage larvae• Ss 1st stage rhab larva has a short buccal capsule compared to that of Hw•

Diagnosis •Microscopic identification of larvae (rhabditiform and occasionally filariform) in the stool or duodenal

Examination of serial samples is necessary and not always sufficient, because stool examination is relatively insensitive.

stool can be examined in wet mounts:•directly• after concentration (formalin-ethyl acetate)• after culture by the Harada-Mori filter paper technique• after culture in agar plates

•Culture faeces by /Modified agar plate Harada-Mori technique

• obtain 3rd stage filariform larvae. Ss has a

triradiate tip of the tail while Hw has a

pointed tail

•Larvae may be obtained by endoscopy or by ‘Entero test’

ELISA – to detect parasite specific IgG

Antibody detectionIndications

:When the infection is suspected and the organism cannot be demonstrated by duodenal aspiration, string tests, or by repeated examinations of stool. 

Enzyme immunoassay (EIA) is currently recommended because of its greater sensitivity (90%). 

Antibody test results cannot be used to differentiate between past and current infection

Serological test is useful in follow up of treated patients

In hyperinfection: larvae can found in sputum

Hookworm L3 larvaS. Stercoralis L3 larva

Examination of faeces for intestinal parasites

Collection of faecesInto a dry, clean, leakproof container using wooden spatulaAvoid contamination with urine, water, soilLabel the sample

Delivery and transportation :Formed faecal sample without blood and mucous should be examined during the day of passage

Preservation methods:Allow faecal sample to be examined after delay in deliveryCommonly used preservatives: 10% aqueous formalin and PVA (polyvinyl alcohol)

Microscopic examination of faeces

Direct wet smear (saline/iodine)

Quantitative faecal examination:Kato – Katz thick smear to calculate

the worm burden

Concentration techniquesseparate parasites from faecal debris and increase the chances of detecting parasitic organisms when these are in small numbers.  Methods

flotation techniques and sedimentation techniques

Sedimentation techniques use solutions of lower specific gravity than the parasitic organisms, concentrating the latter in the sediment

Eg: formalin-ethyl acetate technique

Flotation techniques : use solutions which have higher specific gravity than the organisms to be floated so that the organisms rise to the top and the debris sinks to the bottom. 

most frequently used: zinc sulfate , Sheather's sugar

Objectives:

•List the different groups of parasitic helminthes.•List the major characteristics of parasitic nematodes.•List the common intestinal nematodes in humans.•Outline the life cycles (LC) with stages and events.•Write a comparative account of the different LSs(SGL)•State the stages that cause pathogenic effects and identify those stages of diagnostic importance.• Describe the pathogenesis and clinical features of parasitic nematodes• Outline laboratory methods of visualization/identification.•Identify points in the life cycle where preventive matures are applicable.

Soil is essential for complete the life cycles of following A.A. lumbricoidesB.Hook wormsC. Enterobius vermicularisD.Strongyloides stercoralisE. Trichuris trichiura

Regarding transmission of intestinal nematodesA.A. lumbricodes is by ingestion of contaminated food and waterB. Hook worms by faeco –oral routeC. S. stercoralis is by skin penetration of infective larvaD.T. trichiura by transplacental routE.E. vermicularis is by retro infection

Match the infective stage with the organismA.E. vermicularis – infective larva containing eggB. A. lumbricoides – L2 larvaeC.Hook worms – Filariform larvaeD. T. Trichiura – Infective larva containing egg

True/ false1.Hook worm infection causes blood and mucous diarrhoea2.S. stercoralis causes sever disease in immunocompromised patients3.A.lumdricoides infection is common among adults in SL4. Hookworm infection is common among children In SL5. Whipworm infection is known cause of rectal prolapse in children6. Trichiuris trichiura and A. lumbricoides infections co-exist

Hook worm anemia is microcytic hypoochromicAscaris lumbricoides infection causes stunting S. Stercoralis infection can be diagnosed by detecting eggs in faecesS. Stercoralis is known to cause watery diarrhoea