Intestinal Nematodes

Dr. Devika Iddawela 08/09 batch

Dr. Devika ddawela

Helminthes Nemathelminthes Platyhelminthes

Cestodes Trematodes Nematodes (round worms) (tape worms) (flukes)

Elongated, Flattened tapecylindrical worms like segmented Sexes are Sexes are not separate separate Complete Alimentary canal + Alimentary canal absent Possess a body Body cavity cavity absent (psedocelome)

Flatten leaf-like Sexes are not separate except blood flukes Alimentary canal incomplete Body cavity absent

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

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

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 lumbricoides Ancylostoma duodenale/Necator americanus Strongyloides 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 including 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

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

The anterior end of both sexes shows three lips

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

Larva penetrate in to the alveolus bronchioles trachea swallowed oesophagus small intestine
Reaches pulmonary capillaries

warm moist clay soil 2530C

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

Heart Larva enters portal vein

Larva penetrate the Intestinal wall and venules

eggs hatch in small intestine

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 worm Majority of infections are clinically

asymptomatic

Migrating Larvae( larval ascariasis) Loefflers syndrome Eosinophilic abscesses Lungs - larval migration causes pneumonitis (Lofflers 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 ascarids lone adults are prone to wandering habit block/perforate ducts cause acute symptoms Blocking the duct orifices Acute appendicitis Pancreatic necrosisObstructive jaundice Ascaris liver abscess Migrate out of the anus or come out the mouth or nose

Immuno-pathological effectssensitivity to ascaris agconjunctivitis, urticaria, asthma

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

Effect of Ascariasis on Growth & Nutrition

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

CHRONIC MALNUTRITION STUNTING Stunting linked to impaired intellectual development UNICEF State of the Worlds Children The 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 Stunting = low height for age Height difference in 2 girls of 5 years age 40% of worlds children are stunted 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 & Control 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 of indiscriminate Defaecation by Providing sanitary latrines .

Provision of safe drinking water Treatment of infected patients

Trichuris trichiura
Geographical distribution -Parasite of warmclimates Morphology - 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.

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

Life cycle of whipworm Adults in large intestine

Penetrate and mature in intestinal mucosa

Eggs in stools

No lung migration Larva hatches in intestine

Moist clay 25 -30 C

Eggs mature in soil

Eggs ingested with contaminated fruits, vegetables etc.

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

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 high prevalence in cold climates. Location in host - Adults are loosely attached to the mucosa of the large intestine Morphology - 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

Life cycle
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 oviposition No lung migration of larvae No development in the soil. Therefore it is not a soil transmitted helminthe infection

Life cycle of pinworm

Adults in large intestine Gravid females moves to the anal verge

Eggs ingested

Lays eggs on the anal verge

Eggs become infective within 6 hours of laying

NO LUNG MIGRATION

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 insomnia Female worms may enter vagina urethra, can cause vulvitis, pruritis vulvi
Loss of appetite, loss of weight ,irritability, enuresis

Diagnosis
Demonstration 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

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

Adults

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 America Ancylostoma duodenale E.Europe,N.Africa, India, N.China, Japan Both species overlap in S.E.Asia, Pacific, W.Africa

Morphology N.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 The caudal expansion of certain male nematodes that functions as a claspers during copulation.

Female

Male

Egg Oval ,60 x 40 m with a thin glass like shell. Embryo usually segmented when pass out with the faeces

L3 5th
day

Obligatory lung migration

Non feeding,move on to top soil

L2 rhab.larva (3rd day) Free living,actively feeding

L1

Shade,warmth, sandy soil

24 hours

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

Pathogenesis Larvae 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/min Habitual blood sucker and need serum Secrete anticoagulant substance and may move from spot to spot increasing the damage and blood loss Blood loss N. Americarnus -0.03ml /day/worm A. Duodenale 0.15/day/worm

Iron deficiency Anaemia Hb related to worm burden 500-1000 worms Anaemia even if adequate dietary iron intake If dietary iron deficient anaemia even with light infection

Hookworm disease Severe iron deficiency anaemia, hypoproteinaemia, oedema with associated circulatory problems Hypoalbuminaemia - reduced albumin synthesis &Protein loss > RBC loss Related to worm load

Laboratory Diagnosis By 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

Filariform larvae develop before leaving the patient

Follow free living cycle in the soil

Penetrate the intact skin and initiate the infection

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)

Differences between hookworms and threadworms

HOOK WORM Attach to small intestine Both male and female parasitic cycle

TREAD WORM Embedded in small intestine Male short living

parasitic and free living cycles no autoinfection Autoinfection+

clinical features
Vast majority of infections in endemic areas are symptomless Primary 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 America Ancylostoma duodenale E.Europe,N.Africa, India, N.China, Japan Both species overlap in S.E.Asia, Pacific, W.Africa

Morphology N.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 The caudal expansion of certain male nematodes that functions as a clasper during copulation.
Female

Male

Egg - Ovoid,60 x 40 m with a thin glass like shell. Embryo usually segmented when pass out with the faeces

L3 5th
day

Obligatory lung migration

Non feeding,move on to top soil

L2 rhab.larva (3rd day) Free living,actively feeding

L1

Shade,warmth, sandy soil

24 hours

Life cycle

Eggs passed in faeces

Shady warmth

Adults in small intestine

Eggs hatch in 24 sandy soil hours into 1st stage rhabditiform larva

Breaks into alveoli move along bronchioles, trachea, swallowed

Penetrates skin, enters circulation, carried to the lungs

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

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

Pathogenesis Larvae 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/min Habitual blood sucker and need serum Secrete anticoagulant substance and may move from spot to spot increasing the damage and blood loss Blood loss N. Americarnus -0.03ml /day/worm A. Duodenale 0.15/day/worm

Iron deficiency Anaemia Hb related to worm burden 500-1000 worms Anaemia even if adequate dietary iron intake If dietary iron deficient anaemia even with light infection

Hookworm disease Severe iron deficiency anaemia, hypoproteinaemia, oedema with associated circulatory problems Hypoalbuminaemia - reduced albumin synthesis &Protein loss > RBC loss Related to worm load

Laboratory Diagnosis By 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

Filariform larvae develop before leaving the patient

Follow free living cycle in the soil

Penetrate the intact skin and initiate the infection

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

Differences between hookworms and threadworms

HOOK WORM Attach to small intestine Both male and female parasitic cycle

TREAD WORM Embedded in small intestine Male short living

parasitic and free living cycles no autoinfection Autoinfection+

clinical features
Vast majority of infections in endemic areas are symptomless Primary 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 strongyloidiasis Epigastric pain, anorexia, chronic diarrhoea due to mucosal damage, weight loss Skin rashes Two types Larva 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 detection

Indications 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

S. Stercoralis L3 larva

Hookworm L3 larva

In hyperinfection: larvae can found in sputum

Examination of faeces for intestinal parasites Collection of faeces Into a dry, clean, leakproof container using wooden spatula Avoid contamination with urine, water, soil Label 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 delivery Commonly 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 techniques separate 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. lumbricoides B. Hook worms C. Enterobius vermicularis D. Strongyloides stercoralis E. Trichuris trichiura

Regarding transmission of intestinal nematodes A. A. lumbricodes is by ingestion of contaminated food and water B. Hook worms by faeco oral route C. S. stercoralis is by skin penetration of infective larva D. T. trichiura by transplacental rout E. E. vermicularis is by retro infection

Match the infective stage with the organism A. E. vermicularis infective larva containing egg B. A. lumbricoides L2 larvae C. Hook worms Filariform larvae D. T. Trichiura Infective larva containing egg

True/ false 1. Hook worm infection causes blood and mucous diarrhoea 2. S. stercoralis causes sever disease in immunocompromised patients 3. A.lumdricoides infection is common among adults in SL 4. Hookworm infection is common among children In SL 5. Whipworm infection is known cause of rectal prolapse in children 6. Trichiuris trichiura and A. lumbricoides infections co-exist

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