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    Intestinal nematodes Intestinal nematodes Presentation Transcript

    • Intestinal NematodesDr. Devika Iddawela08/09 batchDr. Devikaddawela
    • HelminthesNemathelminthes PlatyhelminthesNematodes(round worms)Cestodes(tape worms)Trematodes(flukes)
    • Elongated,cylindrical wormsFlattened tape-like segmentedFlatten leaf-likeSexes areseparateSexes are notseparateSexes are notseparate exceptblood flukesCompleteAlimentary canal + Alimentary canalabsentAlimentary canalincompletePossess a bodycavity(psedocelome)Body cavityabsentBody cavity absent
    • NematodesNematodes have successfullyadapted to nearly everyecological niche from marine tofresh water, from the polarregions to the tropics,word "nematode" came from a Greekword nema that means "thread".
    • NematodesLong cyndrical bodyNo segmentationMales and females separate. Females larger thenmale.Similar to each other but vary in sizeEg: round worm-size of a pencilhook worm-size of a pinPin worm- smaller than the aboveDO NOT MULTIPLY IN HUMANS
    • • Parasitize the intestinal tract, tissues,tissue spaces, lymphatics• Body covered in a complex cuticleLongitudinal muscle fibers present, Nocircular muscle• Fluid filled body cavity present• Organs are suspended in the bodycavity• Reproduction & developmental stages:egg, Egg fertilization,embryonated egg,larva, 4 moults, adult
    • Small intestine - NematodeparasitesAscaris lumbricoidesAncylostoma duodenale/NecatoramericanusStrongyloides stercoralisNematodes of small intestine
    • Nematodes of the largeintestine• 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 worldover but high prevalence in countrieswith poor sanitation•Commonest age group affected –pre-schoolchildren & young school children•Prevalence due to indiscriminatedefaecation 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 sexesshows three lipsLocation in host – worms are foundfree in the lumen of small intestineMaintains position in lumen with muscularmovement against peristalsis. Can be temporarilyattached to mucosa for short periods
    • EggsFertilized eggs: (corticated, decorticated)Ovoid, 60 x 40 um.Thick shell – ( triple layered) inner non-permeablelayer, thick transparent middle layer and an outermammilated coat .
    • Unfertilized eggs - Larger, rectangular(80 - 90 x 60 um) with disorganized,vacuolated contents
    • Male and female adults in thesmall intestineFertilized eggs( non- infectivepass in thefaecesInfective L2 larva ( 2ndstage larva)developwith in the egg ( 2-3weeks )Infective eggs swallowedwith contaminated waterand foodeggs hatch in smallintestineLarva penetratethe Intestinal walland venulesLarva entersportal veinHeartReachespulmonarycapillariesLarva penetrate in to thealveolus bronchiolestrachea swallowedoesophagus smallintestinewarm moistclay soil 25-30C
    • Adults in the small intestine
    • Pathogenesis & clinical featuresDepends on• worm load• The host immune response• Effect of larval migration• Mechanical effects of adult worm• Nutritional deficiencies due to thepresence of adult wormMajority of infections are clinicallyasymptomatic
    • Migrating Larvae( larval ascariasis)Loeffler’s syndromeEosinophilic abscesses• Lungs - larval migration causespneumonitis (Loffler’s syndrome) dueto immunological(hypersensitive)reactionCLINICAL FEATURERS: Fever, cough,sputum, asthma, eosinophilia andradiological infiltration
    • On reaching general circulationRarely larvae may wander in to thebrain, eye or retina causinggranuloma
    • Adult wormsAdult worms in their normal habitatcause little pathologyBUT(Severe diseaseif worm burden 100 or >)Heavy infections can cause intestinal colic•Aggregate masses of worms causeVolvulous, Intestinal obstruction orinterssusception
    • Large worm load :Intestinal obstructionSmall bowel obstruction in kids >1000 inworm ball
    • Wandering ascaridslone adults are prone to wandering habit–block/perforate ductscause acute symptoms• Blocking the duct orificesAcute appendicitis –Pancreatic necrosis-Obstructive jaundiceAscaris liver abscess• Migrate out of the anus or come out themouth or nose
    • Immuno-pathological effects-sensitivity to ascaris ag-conjunctivitis, urticaria, asthmaIndirect effects - Micro organisms canby carried by the adult worms on theirmigration from bowel
    • • Protein Energy Malnutrition [PEM]Due to consumption by the wormAct as a mechanical barrier to absorbnutrients• children with 13-40 wormsloose 4g protein/day from a daily intake of 35-50g[1 egg only 6g protein]• Kwashiorkor – swelling due to low albumin [lowserum proteins]• Vitamin A deficiency – Night blindness• AFFECTS NORMAL GROWTH & EDUCATIONALDEVELOPMENTEffect of Ascariasis on Growth & Nutrition
    • Stunting = low height for ageHeight difference in 2 girls of 5 years age40% of world’s children are stuntedCHRONIC MALNUTRITION STUNTINGStunting linked to impaired intellectual developmentUNICEF – State of the World’s ChildrenThe same factors that lead to stunting cause learning deficitsMalnutrition early in life islinked to deficits in childrensintellectual developmentthat persist in spite of schoolingand impair their learning abilitygrowth retardation, poor cognitive & scholasticachievements
    • DiagnosisDemonstrating characteristic eggs in faecesIdentification wormConcentration techniques are usefulEosiniphilia – Larval ascariasis higheosinophiliaIn Adult infection – little or noneRadiography: 4 -6 hours after opaque mealdisplays worm as cylindrical filling defect
    • Long, tubular filling defects,especially in distal smallbowelThe worm ingests barium andthe barium may be seen as athin line of contrast in thecenter of the wormEspecially after the remainderof the barium exits the smallbowel
    • Epidemiology• Common backyard infection• Maintained by young children• Transmission occurs throughinfective eggs Contaminated foodand waterIn Sri Lanka prevalence is highestamong school children
    • Prevention of ingestion of infectiveeggs• Wash raw vegetables and fruits thoroughly( preferably with running water)• Wash hands with soap and waterbefore eating and after soil contact• Drink boiled cool waterPrevention & Control
    • Prevention of indiscriminateDefaecation by Providing sanitarylatrines.Treatment of infected patientsProvision of safe drinkingwater
    • Geographical distribution -Parasite ofwarmclimatesMorphology - 3 - 5 cm. Posterior 2/5th ofthe body is thick (whip handle). Anterior3/5th thin and is threaded into themucosa of the large intestine. Posteriorend of male is curved.Trichuris trichiura
    • Egg - Paddy seed shape withtwo polar plugs 50 x 20 um
    • Life cycleAdults - attached to the colon from theiranterior site embedded in mucousbetween intestinal villiEggs are laid unsegmented requireembryonation in the soilNo lung migration
    • Adults in largeintestineEggs in stoolsEggsmaturein soilMoistclay25 -30 CEggs ingested with contaminated fruits,vegetablesetc.Life cycle of whipwormLarva hatches inintestinePenetrate and mature inintestinal mucosaNo lung migration
    • PathologyFew worms – little damageHeavy infection- spreadthroughout the colon to the rectumcausing• Haemorrhages• Muco-purulent stools, dysenteryand rectal prolapse
    • clinical featuresMild infections are asymptomaticHeavy infection cause blood and mucusdiarrhoeadue to mucosal damage & rectal prolapseChildren may get ‘Trichuris dysenterysyndrome’ resulting in severe diarrhoea,malnutrition, growth retardation andimpairment of cognitive functions
    • DiagnosisFinding the characteristic eggs instool by direct smear or byconcentration methodsProctoscopy – in cases of dysentery, shownumerous worms attach to the mucosa which isredden and ulcerated
    • EpidemiologyTrichuris trichiura is primary a humaninfection but Trichuris suis of pig alsocan infect manCommon in areas of high rain fall, highhumidity, dense shade and poorsanitation.High prevalence in children of primaryschool ageOften associated with ascariasis
    • Enterobius vermicularisGeographical distribution -worldwide highprevalence in cold climates.Location in host - Adults are looselyattached to the mucosa of the largeintestineMorphology - creamy white, 1cm, spindleshaped
    • Eggs - Plano-convex 50 x 25 um,double walled with outeralbuminous layer and an innerlipoid layer
    • The ‘cervical alae’ extend right downthe sides of the body so in cut sectionseen as projection in either side of thebody
    • Adults live in the large intestine; femalesmigrate out of the anus for oviposition:Worm attached to the mucosa of large intestine,they are not blood suckersA gravid female carries about 10,000 eggs.It diesafter ovipositionNo lung migration of larvaeNo development in the soil. Therefore it is not asoil transmitted helminthe infectionLife cycle
    • Eggs become infective within 6hoursof laying
    • clinical features• Very little tissue damage• Rarely penetrates the gut wall causinggranulomatous reactions in the liver,ovary, kidney•Can co-exist with amoebiasis•Causes intense perianal pruritis especially atnight when gravid female moves on and lay eggson the perianal skin
    • • In children this leads to insomniaFemale worms may enter vaginaurethra, can cause vulvitis, pruritisvulvi• Loss of appetite, loss of weight,irritability, enuresis
    • DiagnosisDemonstration of eggs:NIH (NationalInstitute of Health, USA) swab andScotch Tape method a clear adhesivecellulose tape is applied to the anal areaearly in the morning before bathing ordefecationA simple ‘cello-tape’Cotton wool swab
    • AdultsEggs are usually collected in the folds ofskin around the anus. Rarely appear inthe stools
    • Transmission andepidemiology1.Direct transmission from the perianal andanal region to mouth by figure nailcontamination due to scratching of perianalregion and by soiled night cloths ( hand tomouth)2. Exposure to viable eggs from soiled bedlinen and other contaminated objects in theenvironment.3. Via mouth or nose from contaminated dust4. Retro-infection where eggs hatch in theperianal skin and larvae migrate up the bowel
    • It is a household infection and is common inovercrowded houses and institutions likehostels, prisons, refugee camps, orphanagesetcPreventionCut figure nails shortWash hand with soap and water regularlyTreat every one in the householdFollowing treatment all bed linen & personalcloths should be washed and dried in hot sun
    • Intestinal nematodesInfection via skin penetrationHook worms- Ancylostoma duodenaleNecator americanusTread worm- Strongyloides stercoralis
    • HOOK WORMS
    • HookwormsNecator americanus - Sri Lanka,S.Asia,Africa,Pacific region and AmericaAncylostoma duodenale -E.Europe,N.Africa,India, N.China, JapanBoth species overlap in S.E.Asia,Pacific, W.Africa
    • MorphologyN.americanus - 1 cm, head sharply bentbackwards. Buccal capsule has a pair ofventral cutting plates
    • A.duodenale –• slightly larger• head bent backwards in asmooth curve.• Buccal capsule has two pairsof teeth
    • Both species - Males have expandedtails to form the copulatory bursaFemaleMaleThe caudal expansion of certainmale nematodes that functions as aclaspers during copulation.
    • Egg – Oval ,60 x 40 µm with a thinglass like shell. Embryo usuallysegmented when pass out withthe faeces
    • Shade,warmth, sandysoil24 hoursL1L3 5thdayL2rhab.larva(3rdday)Freeliving,activelyfeedingNon feeding,moveon to top soilObligatory lungmigration
    • Life cycles of Ancylostoma and Necatorare similar except that• A.duodenale can infect by ingestion aswell as via the skin• N. americana infects only through skin• Migrating larvae of N.americana grow anddevelop in the lungs, where asancylostoma do not
    • PathogenesisLarvaeLarvae at the site of entry –vesiculation andpustulation (ground itch)Can be secondarily infected due to severe itchingAsthma and bronchitis during migration, cancause pneumonitis but less severe than ascariasisAdults:Hook worm AnaemiaSymptoms- 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 thedamage and blood lossBlood lossN. Americarnus -0.03ml /day/wormA. Duodenale – 0.15/day/worm
    • 500-1000 worms• Anaemia even if adequate dietary ironintake• If dietary iron deficient – anaemia evenwith light infectionIron deficiency AnaemiaHb related to worm burden
    • Severe iron deficiency anaemia,hypoproteinaemia, oedema withassociated circulatory problemsHypoalbuminaemia - reduced albuminsynthesis &Protein loss > RBC lossRelated to worm loadHookwormdisease
    • Laboratory DiagnosisBy demonstrating characteristic eggsin faeces.In ‘old’ stool samplesRhabditiform larvae may be found( distinguish them from thoseof Strongyloides stercoralis).Concentration techniques are helpfulEggs can be cultured into infective larvae(Harada – Mori culture)
    • Transmission• Normally acquired via the skin fromfilariform larvae in the soil contaminated bythe human faeces or• Orally via the ingestion of contaminatedfood ( A. duodenale)• Migrating infective filariform larvae ofA.duodenale are arrested in theirdevelopment and migrate to the mammarygland and are excreted via milk and infectthe child
    • Epidemiology –varies in different parts of the world.There are geographical variationstoo. In Sri Lanka it is an infection ofthe adults due to indiscriminatedefaecation in shady areas awayfrom dwellings.
    • Prevention & Controlavoidance of indiscriminate defaecation & useof foot wearprovision of hygienic latrines, treatment ofinfected persons& health education
    • Strongyloides stercoralis
    • Distribution - Worldwide but morecommon in warm climates. Majoropportunistic infection amongimmunocompromised persons.Morphology - Females are about 2mm.Male is very small , short life span inparasitic life cycle or non- exsistant
    • Male exist but disappear from the bowelsoon after oviposition. Eggs can beproduced parthenogeneticallyWorm - embedded in the smallintestinal mucosaEgg output –low and asynchronous ( notoccurring at regular interval)Eggs hatch in the mucosa itself and1st stage rhabditiform larvae arepassed in faeces
    • Life cycleTwo life cycles –Parasitic cycle ( if the externalconditions are unfavorable)Free living cycle( if conditions arefavorable )
    • Rabditiform larvaeDevelop in tofilariform larvae insoilFollow freeliving cyclein the soilPenetrate theintact skin andinitiate theinfectionFilariform larvaedevelop beforeleaving the patientEnter perianalskin & initiateautoinfectionEnter intestinal mucosa,migrate to lung & initiateautoinfection
    • Multiplication in the host by two ways1. Filariform larvae do not pass out inthe stool but reinvade bowel or skin2. Filariform larvae lodge in thebronchial epithelium and producefurther progeny (offspring)
    • HOOK WORM TREAD WORMAttach to smallintestineEmbedded insmall intestineBoth male andfemaleMale short livingparasitic cycle parasitic andfree living cyclesno autoinfection Autoinfection+Differences between hookworms andthreadworms
    • clinical featuresVast majority of infections in endemicareas are symptomlessPrimary infection• a pruritic erythematous eruption ‘Grounditch’ at the site of entry to larvae, last about3 weeks• Pneumonitis due to lung migration notcommon
    • Intestinal nematodesInfection via skin penetrationHook worms- Ancylostoma duodenaleNecator americanusTread worm- Strongyloides stercoralis
    • HOOK WORMS
    • HookwormsNecator americanus - Sri Lanka,S.Asia,Africa,Pacific region and AmericaAncylostoma duodenale -E.Europe,N.Africa,India, N.China, JapanBoth species overlap in S.E.Asia,Pacific, W.Africa
    • MorphologyN.americanus - 1 cm, head sharply bentbackwards. Buccal capsule has a pair ofventral cutting plates
    • A.duodenale –• slightly larger• head bent backwards in asmooth curve.• Buccal capsule has two pairsof teeth
    • Both species - Males haveexpanded tails to form thecopulatory bursaFemaleMaleThe caudal expansion ofcertain male nematodes thatfunctions as a clasper duringcopulation.
    • Egg - Ovoid,60 x 40 µm with athin glass like shell. Embryousually segmented when passout with the faeces
    • Shade,warmth, sandysoil24 hoursL1L3 5thdayL2rhab.larva(3rdday)Freeliving,activelyfeedingNon feeding,moveon to top soilObligatory lungmigration
    • Life cycleAdults in smallintestineEggs passed in faecesEggs hatch in 24hours into 1st stagerhabditiformlarvaMoults into 2nd rhab.larva on the 3rd dayMoults into 3rd stageinfective filariform larvaPenetrates skin, enterscirculation, carried tothe lungsBreaks into alveolimove along bronchioles,trachea, swallowedShady warmthsandy soil
    • Life cycles of Ancylostoma and Necatorare similar except that• A.duodenale can infect by ingestion aswell as via the skin• N. americana infects only through skin• Migrating larvae of N.americana grow anddevelop in the lungs, where asancylostoma do not
    • PathogenesisLarvaeLarvae at the site of entry –vesiculation andpustulation (ground itch)Can be secondarily infected due to severe itchingAsthma and bronchitis during migration, cancause pneumonitis but less severe than ascariasisAdults:Hook worm AnaemiaSymptoms- 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 thedamage and blood lossBlood lossN. Americarnus -0.03ml /day/wormA. Duodenale – 0.15/day/worm
    • 500-1000 worms• Anaemia even if adequate dietary ironintake• If dietary iron deficient – anaemia evenwith light infectionIron deficiency AnaemiaHb related to worm burden
    • Severe iron deficiency anaemia,hypoproteinaemia, oedema withassociated circulatory problemsHypoalbuminaemia - reduced albuminsynthesis &Protein loss > RBC lossRelated to worm loadHookwormdisease
    • Laboratory DiagnosisBy demonstrating characteristic eggsin faeces.In ‘old’ stool samplesRhabditiform larvae may be found( distinguish them from thoseof Strongyloides stercoralis).Concentration techniques are helpfulEggs can be cultured into infective larvae(Harada – Mori culture)
    • Transmission• Normally acquired via the skin fromfilariform larvae in the soil contaminated bythe human faeces or• Orally via the ingestion of contaminatedfood ( A. duodenale)• Migrating infective filariform larvae ofA.duodenale are arrested in theirdevelopment and migrate to the mammarygland and are excreted via milk and infectthe child
    • Epidemiology - varies in different partsof the world. There are geographicalvariations too. In Sri Lanka it is aninfection of the adults due toindiscriminate defaecation in shady areasaway from dwellings.
    • Prevention & Controlavoidance of indiscriminate defaecation & useof foot wearprovision of hygienic latrines, treatment ofinfected persons& health education
    • Strongyloides stercoralis
    • Distribution - Worldwide but morecommon in warm climates. Majoropportunistic infection amongimmunocompromised persons.Morphology - Females are about 2mm.Male is very small , short life span inparasitic life cycle
    • Male exist but disappear from thebowel soon after oviposition. Eggscan be producedparthenogeneticallyWorm - embedded in the smallintestinal mucosaEgg output –low and asynchronous ( notoccurring at regular interval)Eggs hatch in the mucosa itself and1st stage rhabditiform larvae arepassed in faeces
    • Life cycleTwo life cycles –Parasitic cycle ( if the externalconditions are unfavorable)Free living cycle( if conditions arefavorable )
    • Rabditiform larvaeDevelop in tofilariform larvae insoilFollow freeliving cyclein the soilPenetrate theintact skin andinitiate theinfectionFilariform larvaedevelop beforeleaving the patientEnter perianalskin & initiateautoinfectionEnter intestinal mucosa,migrate to lung & initiateautoinfection
    • Multiplication in the host by two ways1. Filariform larvae do not pass out inthe stool but reinvade bowel or skin2. Filariform larvae lodge in thebronchial epithelium and producefurther progeny
    • HOOK WORM TREAD WORMAttach to smallintestineEmbedded insmall intestineBoth male andfemaleMale short livingparasitic cycle parasitic andfree living cyclesno autoinfection Autoinfection+Differences between hookworms andthreadworms
    • clinical featuresVast majority of infections in endemicareas 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 notcommon
    • Chronic uncomplicated strongyloidiasisEpigastric pain, anorexia, chronicdiarrhoea due to mucosal damage, weightlossSkin rashesTwo typesLarva currens: Occur around the anus andanywhere on the trunk. larvae migrateunder the skincauses itchy rash which is not indurate &has a red flare at the edge
    • Urticaria –• Allergy to larval penetration in alreadysensitized patient• Occur in the buttocks with pruritus ani&around the waist•Last 1-2 days and can recurs at regularintervals
    • Severe complicatedstrongyloidiasisSevere disease with hyper-infection in personswith immunosupression• severe watery diarrhoea, often withmalabsorption, hypoalbuminaemia.Generalized oedema, Fever,Lungs- hypereosinophilia, pneuminitis, diffusecrepitation, pulmonary abscess and grossrespiratory failure
    • Diagnosis•Demonstration of 1st stage rhab.larvae in stools• Diffentiate from hookworm 1st stage larvae• Ss 1st stage rhab larva has a short buccalcapsule compared to that of Hw•
    • Diagnosis•Microscopic identification of larvae(rhabditiform and occasionally filariform) in thestool or duodenalExamination of serial samples is necessary andnot always sufficient, because stool examinationis relatively insensitive.stool can be examined in wet mounts:•directly• after concentration (formalin-ethyl acetate)• after culture by the Harada-Mori filter papertechnique• after culture in agar plates
    • •Culture faeces by /Modified agar plateHarada-Mori technique• obtain 3rd stage filariform larvae. Sshas atriradiate tip of the tail while Hw has apointed tail•Larvae may be obtained by endoscopyor by ‘Entero test’ELISA – to detect parasite specific IgG
    • Antibody detectionIndications:When the infection is suspectedand the organism cannot bedemonstrated by duodenalaspiration, string tests, or byrepeated examinations of stool.Enzyme immunoassay (EIA) is currently recommendedbecause of its greater sensitivity (90%).Antibody test results cannot be used to differentiatebetween past and current infectionSerological test is useful in follow up of treated patients
    • In hyperinfection: larvae can found insputumHookworm L3larvaS. Stercoralis L3 larva
    • Examination of faeces forintestinal parasitesCollection of faecesInto a dry, clean, leakproof containerusing wooden spatulaAvoid contamination with urine, water,soilLabel the sample
    • Delivery and transportation :Formed faecal sample without blood andmucous should be examined during theday of passagePreservation methods:Allow faecal sample to be examinedafter delay in deliveryCommonly used preservatives: 10%aqueous formalin and PVA (polyvinylalcohol)
    • Microscopic examination of faecesDirect wet smear (saline/iodine)Quantitative faecal examination:Kato – Katz thick smear to calculatethe worm burden
    • Concentration techniquesseparate parasites from faecal debris andincrease the chances of detecting parasiticorganisms when these are in small numbers.Methodsflotation techniques andsedimentation techniquesSedimentation techniquesuse solutions of lower specific gravity thanthe parasitic organisms, concentrating thelatter in the sediment
    • Eg: formalin-ethyl acetate techniqueFlotation techniques :use solutions which have higher specificgravity than the organisms to be floated sothat the organisms rise to the top and thedebris sinks to the bottom.most frequently used: zinc sulfate ,Sheathers 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 thosestages of diagnostic importance.• Describe the pathogenesis and clinical features of parasiticnematodes• Outline laboratory methods of visualization/identification.•Identify points in the life cycle where preventive matures areapplicable.
    • Soil is essential for complete the lifecycles of followingA.A. lumbricoidesB.Hook wormsC. Enterobius vermicularisD.Strongyloides stercoralisE. Trichuris trichiura
    • Regarding transmission of intestinalnematodesA.A. lumbricodes is by ingestion ofcontaminated food and waterB. Hook worms by faeco –oral routeC. S. stercoralis is by skin penetration ofinfective larvaD.T. trichiura by transplacental routE.E. vermicularis is by retro infection
    • Match the infective stage with theorganismA.E. vermicularis – infective larvacontaining eggB. A. lumbricoides – L2 larvaeC.Hook worms – Filariform larvaeD. T. Trichiura – Infective larvacontaining egg
    • True/ false1.Hook worm infection causes blood andmucous diarrhoea2.S. stercoralis causes sever disease inimmunocompromised patients3.A.lumdricoides infection is commonamong adults in SL4. Hookworm infection is commonamong children In SL5. Whipworm infection is known causeof rectal prolapse in children6. Trichiuris trichiura and A.lumbricoides infections co-exist
    • Hook worm anemia is microcytichypoochromicAscaris lumbricoides infection causesstuntingS. Stercoralis infection can be diagnosedby detecting eggs in faecesS. Stercoralis is known to cause waterydiarrhoea