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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