.

� Helminths (from theGreek Helmins,

Dr. Gaurav AgrawalAssist. ProfessorDepartment of PediatricsMGMCHJaipur

Greek meaning

Helmins,worm)

include three groupsof parasitic worm,large organisms withcomplex tissues andorgans.

� Diseases are caused by adultnematode living in the humannematode living in the humangut.

Two types:1. the hookworms, which have a soil stage in which they

develop into larvae that then penetrate the host2. a group of nematodes which survive in the soil merely

as eggs that have to be ingested for their life cycle tocontinue.

� The geographical distribution of hookworms islimited by the larval requirement for warmthand humidity.

� Soil-transmitted nematode infections can beprevented by avoidance of faecal soilcontamination (adequate sewerage disposal)or skin contact (wearing shoes), and by strictpersonal hygiene.

� Ancylostomiasis is caused byparasitisation with Ancylostoma duodenale or Necator americanus.

� The adult hookwormis 1 cm long and livesin the duodenum andupper jejunum.

� Eggs are passed in the faeces.� In warm, moist, shady soil the larvae develop

into rhabditiform and then the infectivefilariform stages; they then penetrate humanskin and are carried to the lungs.

bronchi, are swallowed and mature in� After entering the alveoli they ascend the

thesmall intestine, reaching maturity 4–7 weeks after infection.

� The worms attachthemselves to themucosa of the smallintestine by theirbuccal capsule andwithdraw blood.

� The mean daily loss of blood from one A.duodenale is 0.15 mL and from N. americanus0.03 mL.

� Hookworm infection is one of the main causes ofanaemia in the tropics and subtropics.

Clinical features:

� An allergic dermatitis, usually on the feet (grounditch), may be experienced at the time of infection.

� The passage of the larvae through the lungs in aheavy infection causes a paroxysmal cough

patchy pulmonary consolidationwith blood-stained sputum, associated with

andeosinophilia.

1

eosinophilia.

.

� When the worms have reached the intestine, vomiting occurs

small � Anaemia with high-output cardiac failure may result.

Investigations:

� There is eosinophilia.The characteristic ovum can be recognised inintestine, vomiting occurs

� Sometimes frequent loose stools are passed.� The degree of iron and protein deficiency

which develops depends not only on the loadof worms but also on the nutrition of the patientand especially on the iron stores.

result.� The mental and physical development of

children may be retarded in severe infection.

� The characteristic ovum can be recognised inthe stool.

� If hookworms are present in numbers sufficientto cause anaemia, faecal occult blood testingwill be positive and many ova will be present.

Management:

� A single dose of albendazole (400 mg) is thetreatment of choice.

� Alternatively, mebendazole 100 mg 12-hourlyfor 3 days may be used.

� Anaemia and heart failure associated withhookworm infection respond well to oral iron,even when severe; blood transfusion is rarelyrequired.

� Strongyloides stercoralis is a very smallnematode (2 mm × 0.4 mm) which parasitisesthe mucosa of the upper part of the smallintestine, often in large numbers, causingpersistenteosinophilia.

� The eggs hatch in the bowel but only larvaeare passed in the faeces.

� In moist soil they moult and become theinfective filariform larvae.

� After penetrating human skin, they undergo adevelopment cycle similar to that of hookworms, except that the female wormsburrow into the intestinal mucosa andsubmucosa.

� Some larvae in the intestine may develop intofilariform larvae, which may then penetrate themucosa or the perianal skin and lead toautoinfection and persistent infection.

� Patients with Strongyloides infection persistingfor more than 35 years have been described.

� Strongyloidiasis occurs in the tropics andsubtropics, and is especially prevalent in theFar East.

� The classic triad of symptoms consists ofabdominal pain, diarrhoea and urticaria

� Cutaneous manifestations, either urticaria orlarva currens (a highly characteristic pruritic,elevated, erythematous lesion advancingalong the course of larval migration), are

� Systemic strongyloidiasis (the Strongyloideshyperinfection syndrome), with disseminationof larvae throughout the body, occurs in

suppressionassociation with immune (intercurrent disease, HIV and HTLV-1infection, corticosteroid treatment)

� Patients presentabdominal pain,

with severe, generalisedabdominal distension and

2

along the course of larval migration), arecharacteristic and occur in 66% of patients

abdominal pain,shock

abdominal distension and

.

� Massive larval invasion of the lungs causescough, wheeze and dyspnoea; cerebral

Investigations:

� There is eosinophilia.� Serology (ELISA) is helpful, but definitive

Management:

� Ivermectin 200 μg/kg as a single dose, or twodoses of 200 μg/kg on successive days, iscough, wheeze and dyspnoea; cerebral

involvement has manifestations ranging fromsubtle neurological signs to coma.

� Gram-negative sepsis frequently complicatesthe picture.

� Serology (ELISA) is helpful, but definitivediagnosis depends upon finding the larvae.

� The faeces should be examinedmicroscopically for motile larvae; excretion isintermittent so repeated examinations may benecessary.

� Larvae can also be found in jejunal aspirate ordetected using the string test.

� Larvae may also be cultured from faeces.

doses of 200 μg/kg on successive days, iseffective. Alternatively, albendazole is givenorally in a dose of 15 mg/kg body weight 12-hourly for 3 days. A second course may berequired.

� For the Strongyloides hyperinfectionsyndrome, ivermectin is given at 200 μg/kg ondays 1, 2, 15 and 16.

� This pale yellow nematode is 20–35 cm long.� Humans are infected by eating food

contaminated with mature ova.� Ascaris larvae hatch in the duodenum, migrate

through the lungs, ascend the bronchial tree,are swallowed and mature in the smallintestine.

� This tissue migration can provoke both localand general hypersensitivity reactions, withpneumonitis, eosinophilic granulomas,bronchial asthma and urticaria.

Clinical features:

� Intestinal ascariasis causes symptoms rangingfrom occasional vague abdominal pain throughto malnutrition.

� The large size of the adult worm and itstendency to aggregate and migrate can resultin obstructive complications.

� Tropical and subtropical areas are endemic forascariasis, and in these areas it causes up to35% of all intestinal obstructions, mostcommonly in the terminal ileum.

� Obstruction can be complicated further byintussusception, volvulus, haemorrhagicinfarction and perforation.

� Other complications include blockage of thebile or pancreatic duct and obstruction of the

Investigations:

� The diagnosis is made microscopically by finding ova in the faeces.

� Adult worms are frequently expelled rectally or orally.

� Occasionally, the worms are demonstrated radiographically by a barium examination.

� There is eosinophilia.

Management:

� A single dose of albendazole (400 mg),pyrantel pamoate (11 mg/kg; maximum 1 g),piperazine (4 g) or mebendazole (100 mg 12-hourly for 3 days) is effective for intestinalascariasis.

� Patients should be warned that they mightexpel numerous whole, large worms.

3

bile or pancreatic duct and obstruction of theappendix by adult worms.

.

� Obstruction due to ascariasis should betreated with nasogastric suction, piperazine

Prevention:

� Community chemotherapy programmes havebeen used to reduce Ascaris infection.

� This helminth is common throughout the world.It affects mainly children.treated with nasogastric suction, piperazine

and intravenous fluids.been used to reduce Ascaris infection.

� The whole community can be treated every 3months for several years.

� Alternatively, schoolchildren can be targeted;treating them lowers the prevalence ofascariasis in the community.

� It affects mainly children.� After the ova are swallowed, development

takes place in the small intestine, but the adultworms are found chiefly in the colon.

Clinical features:

� The gravid femaleworm lays ova aroundthe anus, causingintense itching,especially at night.

� The ova are oftencarried to the mouthon the fingers and soreinfection or human-to-human infectiontakes place.

� In females the genitalia may be involved.� The adult worms may be seen moving on the

buttocks or in the stool.

Investigations:

� Ova are detected by applying the adhesivesurface of cellophane tape to the perianal skinin the morning. This is then examined on aglass slide under the microscope.

� A perianal swab, moistened with saline, is analternative sampling method.

Management:

� A single dose of mebendazole (100 mg),albendazole (400 mg), pyrantel pamoate (11mg/kg) or piperazine (4 g) is given and may berepeated after 2 weeks to control auto-reinfection.

� If infection recurs in a family, each membershould be treated as above.

� During this period all nightclothes and bed linen are laundered.

� Fingernails must be kept short and hands washed carefully before meals.

� Subsequent therapy is reserved for those developfamily members who recurrent

infection.

� Infections with whipworm are common all overthe world under unhygienic conditions.

� Infection is contracted by the ingestion of earthor food contaminated with ova which havebecome infective after lying for 3 weeks ormore in moist soil.

� The adult worm is 3–5 cm long and has acoiled anterior end resembling a whip.

4

coiled anterior end resembling a whip.

.

� Whipworms inhabit the caecum, lower ileum,appendix, colon and anal canal.

� The diagnosis is readily made by identifying ova in faeces.

� Filarial worms are tissue-dwelling nematodes.The larval stages are inoculated by bitingappendix, colon and anal canal.

� There are usually no symptoms, but intenseinfections in children may cause persistentdiarrhoea or rectal prolapse, and growthretardation.

ova in faeces.� Treatment is with mebendazole in doses of

100 mg 12-hourly for 3–5 days or a single dose of albendazole 400 mg.

� The larval stages are inoculated by bitingmosquitoes or flies, each specific to aparticular filarial species.

� The larvae develop into adult worms (2–50 cmlong) which, after mating, produce millions ofmicrofilariae (170–320 mm long) that migratein blood or skin.

� The life cycle is completed when the vectortakes up microfilariae while feeding onhumans.

� In the insect, ingested microfilariae developinto infective larvae for inoculation in humans,normally the only host.

� Disease is due tothe host’s immuneresponse to theworms (both adultand microfilariae),particularly dyingworms, and itspattern and severityvary with the siteand stage of eachspecies.

� The worms are long-lived; microfilariae survive 2–3 years and adult worms 10–15 years.

� The infections are chronic and worst in individuals constantly exposed to reinfection.

� Infection with the filarial worms Wuchereriabancrofti and Brugia malayi is associated withclinical outcomes ranging from subclinicalinfection to hydrocele and elephantiasis.

� W. bancrofti is transmitted by night-biting culicine or anopheline mosquitoes in most areas.

5

� The adult worms, 4–10 cm in length, live in thelymphatics, and the females producemicrofilariae which circulate in large numbersin the peripheral blood, usually at night.

.

Pathology:

� Several factors contribute to the pathogenesis of lymphatic filariasis.

� Death of the adult worm results in acute filariallymphangitis.

� Lymphatic obstruction persists after death ofthe adult worm.of lymphatic filariasis.

� Toxins released bylymphangiectasia;

the adult worm cause this dilatation of the

lymphatic dysfunction

vessels and

leads the

to chronic

manifestations of lymphatic

lymphatic clinical

filariasis,lymphoedema and hydrocele.

lymphangitis.� The filariae are symbiotically infected with

rickettsia-like bacteria (Wolbachia spp.) andrelease of lipopolysaccharide from thesebacteria contributes to inflammation.

the adult worm.� Secondary bacterial infections cause tissue

destruction.� The host response to microfilariae is central to

the pathogenesis of tropical pulmonaryeosinophilia.

Clinical features:

� Acute filarial lymphangitis presents with fever,pain, tenderness and erythema along thecourse of inflamed lymphatic vessels.

� Inflammation of the spermatic cord, epididymisand testis is common.

� The whole episode lasts a few days but mayrecur several times a year.

� Temporary oedema becomes more persistentand regional lymph nodes enlarge.

� Progressive enlargement, coarsening,corrugation, fissuring and bacterial infection ofthe skin and subcutaneous tissue developgradually, causing irreversible ‘elephantiasis’.

� The scrotum may reach an enormous size.� Chyluria and chylous effusions are milky and

opalescent; on standing, fat globules rise tothe top.

� The acute lymphatic manifestations of filariasismust be differentiated from thrombophlebitisand infection.

� The oedema and lymphatic obstructivechanges must be distinguished fromcongestive cardiac failure, malignancy, traumaand idiopathic abnormalities of the lymphaticsystem.

� Silicates absorbed from volcanic soil can alsocause non-filarial elephantiasis.

� Tropical pulmonary eosinophilia is acomplication seen mainly in India and is likelyto be due to microfilariae trappedpulmonary capillariesallergic inflammation. Patients present

in the and destroyed by

withparoxysmal cough, wheeze and fever.

� If untreated, this progresses to debilitating chronic interstitial lung disease.

Investigations:

• diagnosis is made on clinical grounds, supported byeosinophilia and sometimes by positive filarialserology.

� Filarial infections cause the highest eosinophilcounts of all helminthic infections.

� In the earliest stages of lymphangitis the � Microfilariae can be found in the peripheralblood at night, and either are seen moving in awet blood film or are detected by microfiltrationof a sample of lysed blood.

� They are usually present in hydrocele fluid,which may occasionally yield an adult filaria.

6

chronic interstitial lung disease.

.

� By the time elephantiasis develops,microfilariae become difficult to find.

� Indirect fluorescence and ELISA detectantibodies in over 95% of active cases and

� Highly sensitive specificimmunochromatographic

and card tests for microfilariae become difficult to find.

� Calcified filariae may sometimes bedemonstrable by radiography.

� Movement of adult worms can be seen onscrotal ultrasound.

� PCR-based tests for detection of W. bancroftiand B. malayi DNA from blood have beendeveloped.

antibodies in over 95% of active cases and70% of established elephantiasis. The testbecomes negative 1–2 years after cure.

� Serological tests cannot distinguish thedifferent filarial infections.

immunochromatographicdetection ofcommercially

filarial available;

cardinfection

finger

tests for are now

prick bloodtaken at any time of the day can be used for these.

� In tropical pulmonary eosinophilia, serology isstrongly positive and IgE levels are massivelyelevated, but circulating microfilariae are notfound. The chest X-ray shows miliary changesor mottled opacities. Pulmonary function testsshow a restrictive picture.

Management:

� Treatment of the individual is aimed atreversing and halting disease progression.

� Diethylcarbamazine (DEC) kills microfilariaeand adult worms. The dose is 6 mg/ kg dailyorally in three divided doses for 12 days.

� Most adverse effects seen with DEC treatmentare due tomicrofilariae,

the host response to dying and the reaction intensity is

directly proportional to the microfilarial load.

� The main symptoms are fever, headache,nausea, vomiting, arthralgia and prostration.These usually occur within 24–36 hours of thefirst dose of DEC.

� Antihistamines or corticosteroids may berequired to control these allergic phenomena.

� Both the 12-day course and a single dose ofDEC reduce microfilaria levels by about 90%6–12 months after treatment.

� No carefully controlled trials have evaluatedthe effects of DEC treatment alone on thechronic manifestations of lymphatic filariasis.

� A single dose of either ivermectin (200 μg/kg)or albendazole (400 mg) in combination withDEC (300 mg) also eliminates microfilariae for1 year.

� With the discovery of an endosymbioticbacterium, Wolbachia, in most of the filarialworms, there is a possible role for doxycyclinein eliminating the bacteria; the drug leads tointerruption of embryogenesis and hence theproduction of microfilariae.

� For tropical pulmonary eosinophilia, DEC (6mg/kg daily orally in three divided doses for 14days) is the treatment of choice.

7

.

Chronic lymphatic pathology:

� Experience in Indiaactive management

and Brazil shows that of chronic lymphatic

� Tight bandaging, massage and bed rest withelevation of the affected limb may help to

� Plastic surgery may be indicated inestablished elephantiasis.active management of chronic lymphatic

pathology can alleviate symptoms.� Patients should be taught meticulous skin care

of their lymphoedematous limbs to preventsecondary bacterial and fungal infections.

elevation of the affected limb may help tocontrol the lymphoedema.

� Prompt diagnosis and antibiotic therapy ofbacterial cellulitis are important in preventingfurther lymphatic damage and worsening ofexisting elephantiasis.

established elephantiasis.� Great relief can be obtained by removal of

excess tissue but recurrences are probableunless new lymphatic drainage is established.

� Hydroceles and chyluria can be repairedsurgically.

Prevention:

� Treatment of the whole population in endemicareas with annual single-dose DEC (6 mg/kg),either alone or in combination withalbendazole or ivermectin, can reduce filarialtransmission.

� This mass treatment should be combined withmosquito control programmes.

� Onchocerciasis is the result of infection by thefilarial Onchocerca volvulus.

� The infection is conveyed by flies of the genusSimulium, which breed in rapidly flowing, well-aerated water.

� Adult flies inflict painful bites during the day,both inside and outside houses.

� While feeding, theypick upmicrofilariae,

the which

mature into theinfective larva andare transmitted to anew host insubsequentbites.

� Humans are theonly known hosts

� Onchocerciasis is endemic in sub-SaharanAfrica, Yemen, and a few foci in Central andSouthAmerica.

� It is estimated that 17.7 million people areinfected, of whom 500 000 are visuallyimpaired and 270 000 blind.

� Due to onchocerciasis huge tracts of fertileland lie virtually untilled, and individuals and

Pathology:

� After inoculation of larvae by a bite from aninfected fly, the worms mature in 2–4 monthsand live for up to 17 years in subcutaneousand connective tissues.

� At sites of trauma, over bony prominences andaround joints, fibrosis may form nodulesaround adult worms which otherwise cause nodirect damage.

� Innumerable microfilariae, discharged by thefemale O. volvulus, move actively in thesenodules and in the adjacent tissues, are widelydistributed in the skin, and may invade theeye.

8

land lie virtually untilled, and individuals andcommunities are impoverished.

direct damage.

.

� Live microfilariae elicit little tissue reaction, butdead ones may cause severe allergic

Clinical features:

� The infection may remain symptomless formonths or years.

� This is difficult to see on dark skins, in whichthe most common signs are papules dead ones may cause severe allergic

inflammation leading to hyaline necrosis andloss of collagen and elastin.

� Death of microfilariae in the eye causesinflammation and may lead to blindness.

months or years.� The first symptom is usually itching, localised

to one quadrant of the body and laterbecoming generalised and involving the eyes.

� Transient oedema of part or all of a limb is anearly sign, followed by papular urticariaspreading gradually from the site of infection.

the mostexcoriated

common signs are by

hyperpigmentationscratching,

from

papules spotty

resolvinginflammation, and more chronic changes of a rough, thickened or inelastic, wrinkled skin.

� Both infected and uninfected superficial lymphnodes enlarge and may hang down in folds ofloose skin at the groins.

� Hydrocele, femoral hernias and scrotalelephantiasis can occur.

� Firm subcutaneous nodules > 1 cm in in chronicdiameter (onchocercomas) occur

infection.

� Eye disease is most common in highly endemicareas and is associated with chronic heavyinfections and nodules on the head.

� Early manifestations include itching, lacrimationand conjunctival injection. These lead toconjunctivitis, sclerosing keratitis with pannusformation, uveitis which may lead to glaucomaand cataract, and, less commonly, choroiditis andoptic neuritis. Classically, ‘snowflake’ deposits areseen in the edges of the cornea.

Investigations:

� The finding of nodules or characteristiclesions of the skin or eyes in a patientfrom an endemic area, associated witheosinophilia, is suggestive.

� Skin snips or shavings, taken with acorneoscleral punch or scalpel blade from calf,buttock and shoulder, are placed in salineunder a cover slip on a microscope slide andexamined after 4 hours. Microfilariae are seenwriggling free in all but the lightest infections.

� Slit-lamp examination may reveal microfilariaemoving in the anterior chamber of the eye ortrapped in the cornea.

� A nodule may be removed and incised,showing the coiled, thread-like adult worm.

� Filarial antibodies may be detected in up to 95%of patients.

� Several promising rapid strip tests based onantibody or antigen detection are under clinicalevaluation.

� In patients with strong suspicion of onchocerciasisbut negative tests, a provocative Mazzotti test, inwhich administration of 0.5–1.0 mg/kg of DECexacerbates pruritus or dermatitis, strongly

9

exacerbates pruritus or dermatitis, stronglysuggests onchocerciasis.

.

Management:

� Ivermectin, in a single dose of 100–200 μg/kg,repeated several times at 3-monthly intervals

� In the rare event of a severe reaction causingoedema or postural hypotension, prednisolone

Prevention:

� Mass treatment with ivermectin is practised. Itreduces morbidity in the community andrepeated several times at 3-monthly intervals

to prevent relapses, is recommended. It killsmicrofilariae, and is non-toxic and does nottrigger severe reactions.

oedema or postural hypotension, prednisolone20–30 mg may be given daily for 2 or 3 days.

� Eradication of Wolbachia with doxycycline(100 mg daily for 6 weeks) preventsreproduction of the worm.

reduces morbidity in the community andprevents eye disease from getting worse.

� Simulium can be destroyed in its larval stageby the application of insecticide to streams.

� Long trousers, skirts and sleeves discouragethe fly from biting.

� Infestation with the Guinea worm Dracunculusmedinensis manifests itself when the femaleworm, over a metre long, emerges from theskin.

� Humans are infected by ingesting a smallcrustacean, Cyclops, which inhabits wells andponds, and contains the infective larval stageof the worm.

Management and prevention:

� Traditionally, the protruding worm is extractedby winding it out gently over several days on amatchstick.

� The worm must never be broken.� Antibiotics for secondary infection and

prophylaxis of tetanus are also required.

� A global elimination campaign is based on theprovision of clean drinking water anderadication of water fleas from drinking water.The latter is being achieved by simple filtrationof water through a plastic mesh filter andchemical treatment of water supplies.

� Trichinella spiralis is a nematode that parasitisesrats and pigs, and is only transmitted to humansif they eat partially cooked infected pork, usuallyas sausage or ham. Bear meat is anothersource.

� Symptoms result from invasion of intestinalsubmucosa by ingested larvae, which developinto adult worms, and the secondary invasionof striated muscle by fresh larvae produced bythese adult worms.

� Outbreaks have occurred in the UK, as well asin other countries where pork is eaten.

Clinical features:

� The clinical features of trichinosis aredetermined by the larval numbers.

� A light infection with a few worms may beasymptomatic; a heavy infection causesnausea and diarrhoea 24–48 hours after theinfected meal.

10

.

� A few days later, the symptoms associatedwith larval invasion predominate: there is fever

� Larval migration may cause acute myocarditis and encephalitis.

Investigations:

� Commonly, a group of people who have eateninfected pork from a common source developwith larval invasion predominate: there is fever

and oedema of the face, eyelids andconjunctivae; invasion of the diaphragm maycause pain, cough and dyspnoea; andinvolvement of the muscles of the limbs, chestand mouth causes stiffness, pain andtenderness in affected muscles.

and encephalitis.� An eosinophilia is usually found after the 2nd

week.� An intense infection may prove fatal but those

who survive recover completely.

infected pork from a common source developsymptoms at about the same time.

� Biopsy from the deltoid or gastrocnemius afterthe 3rd week of symptoms in suspected casesmay reveal encysted larvae.

� Serological tests are also helpful.

Management:

� Treatment is with albendazole 20 mg/kg dailyfor 7 days. Given early in the infection, thismay kill newly formed adult worms in thesubmucosa and thus reduce the number oflarvae reaching the muscles.

� Corticosteroids are necessary to control theserious effects of acute inflammation.

� CLM is common lesion travellers.

seen

the most linear

in

� Intensely pruritic, linear, serpiginous lesionsresult from the larval migration of the doghookworm (Ancylostoma caninum).

� The track moves across the skin at a rate of 2–3 cm/day. This contrasts with the rash ofStrongyloides , which is fast-moving andtransient.

� Although the larvae of dog hookwormsfrequently infect humans, they do not usuallydevelop into the adult form.

� The most common site for CLM is the foot but elbows, breasts and buttocks may be affected.

� Most patients with CLM have recently visited a beach where the affected part was exposed.

� The diagnosis is clinical.

� Treatment may be local with 12-hourlyapplication of 15% thiabendazole cream, orsystemic with a single dose of albendazole(400 mg) or ivermectin (150–200 μg/kg).

� These leaf-shaped worms are parasitic tohumans and animals.

� Their complex life cycles may involve one ormore intermediate hosts, often freshwatermolluscs.

11

.

� Schistosomiasis is one of the most importantcauses of morbidity in the tropics.

� S. haematobium was discovered by TheodorBilharz in Cairo in 1861 and the disease iscauses of morbidity in the tropics.

� There are five species of the genusSchistosoma which commonly cause diseasein humans: S. haematobium, S. mansoni, S.japonicum, S. mekongi and S. intercalatum.

Bilharz in Cairo in 1861 and the disease issometimes called bilharzia or bilharziasis.

� Schistosome eggs have been found inEgyptian mummies dated 1250 BC.

� The ovum is passed in the urine or faeces ofinfected individuals and gains access to freshwater, where the ciliated miracidium inside it isliberated; it enters its intermediate host, a species of freshwater snail, in which itmultiplies.

� Large numbers of fork-tailed cercariae arethen liberated into the water, where they maysurvive for 2–3 days.

� Cercariae can penetrate the skin or themucous membrane of the mouth of humans.

� They transform into schistosomulae and moultas they pass through the lungs; thence theyare carried by the blood stream to the liver,and so to the portal vein, where they mature.

� The male worm is up to 20 mm in length andthe more slender cylindrical female, usuallyenfolded longitudinally by the male, is ratherlonger.

� Within 4–6 weeks of infection they migrate tothe venules draining the pelvic viscera, wherethe females deposit ova.

Pathology:

� This depends on thespecies and thestage of infection.

12

� Most disease is due to the passage of eggsthrough mucosa and to the granulomatousreaction to eggs deposited in tissues.

� The eggs of S. haematobium pass mainlythrough the wall of the bladder, but may alsoinvolve rectum, seminal vesicles, vagina,cervix and uterine tubes.

.

� S. mansoni and S. japonicum eggs passmainly through the wall of the lower bowel or

� Later there is fibrosis and eggs calcify, often insufficient numbers to become radiologically

Clinical features:

� Recent travellers, especially those overlandingthrough Africa, may present with allergicmainly through the wall of the lower bowel or

are carried to the liver.� The most serious, although rare, site of ectopic

deposition of eggs is in the CNS.� Granulomas are composed of macrophages,

eosinophils, and epithelioid and giant cellsaround an ovum.

sufficient numbers to become radiologicallyvisible.

� Eggs of S. haematobium may leave thevesical plexus and be carried directly to thelung.

through Africa, may present with allergicmanifestations and eosinophilia; residents ofschistosomiasis-endemic areas are more likelyto present with chronic urinary tract pathologyor portal hypertension.

� During the early stages of infection there maybe itching lasting 1–2 days at the site ofcercarial penetration.

� After a symptom-free period of 3–5 weeks,acute schistosomiasis (Katayama syndrome)may present with allergic manifestations suchas urticaria, fever, muscle aches, abdominalpain, headaches, cough and sweating.

� On examination hepatomegaly, splenomegaly,lymphadenopathy and pneumonia may bepresent.

� These allergic phenomena may be severe ininfections with S. mansoni and S. japonicum,but are rare with S. haematobium.

� The features subside after 1–2 weeks.

Schistosoma mansoni:

� S. mansoni is endemic throughout Africa, theMiddle East, Venezuela, Brazil and theCaribbean.

� Characteristic symptoms begin 2 months ormore after infection.

� They may be slight, no more than malaise, orconsist of abdominal pain and frequent stoolswhich contain blood-stained mucus.

� With severe advanced disease, polyps

increased may befrom rectaldiscomfort

experienced.� The early hepatomegaly is reversible, but

portal hypertension may cause massivesplenomegaly, fatal haematemesis from oesophageal varices, or progressive ascites.

� Liver function is initially preserved because the

� S. mansoni and other schistosoma infectionspredispose to the carriage of Salmonella, inpart because Salmonella may attach to theschistosomes and in part because sharedantigens on schistosomes may induceimmunological tolerance to Salmonella.

Schistosoma japonicum, S. mekongiand S. intercalatum:

� In addition to humans, the adult worm of S.japonicum infects the dog, rat, field mouse,water buffalo, ox, cat, pig, horse and sheep.

� Although other Schistosoma spp. Can infectspecies other than humans, the non-humanreservoir seems to be particularly important intransmission for S. japonicum but not for S.haematobium or S. mansoni.

13

� Liver function is initially preserved because the pathology is fibrotic rather than cirrhotic.

haematobium or S. mansoni.

.

� S. japonicum is prevalent in the Yellow Riverand Yangtze–Jiang basins in China, where the

� The pathology of S. japonicum is similar to thatof S. mansoni, but as this worm produces

� The small and large bowel may be affected,and hepatic fibrosis with splenic enlargementand Yangtze–Jiang basins in China, where the

infection is a major public health problem. Italso has a focal distribution in the Philippines,Indonesia and Thailand.

� The related S. mekongi occurs in Laos,Thailand and Myanmar, and S. intercalatum inWest and CentralAfrica.

of S. mansoni, but as this worm producesmore eggs, the lesions tend to be moreextensive and widespread.

� The clinical features resemble those of severeinfection with S. mansoni, with addedneurological features.

and hepatic fibrosis with splenic enlargementis usual.

� Deposition of eggs or worms in the CNS,especially in the brain or spinal cord, causessymptoms in about 5% of infections, notablyepilepsy, blindness, hemiplegia or paraplegia.

Investigations:

� There is marked eosinophilia.are� Serological

screeningtests (ELISA)

tests but remain positiveuseful as

afterchemotherapeuticcure.

� In S. haematobiuminfection, dipstickurine testing showsblood and albumin.The eggs can be

byfound microscopic examination centrifuged

of thedeposit

of terminal streamurine.

� Ultrasound is useful for assessing the urinarytract; bladder wall thickening, hydronephrosisand bladder calcification can be detected.

� Cystoscopy reveals ‘sandy’ patches, bleedingmucosa and later distortion.

� In a heavy infection with S. mansoni or S.japonicum the characteristic egg with its lateralspine can usually be found in the stool.

� When the infection is light or of long duration,a rectal biopsy can be examined.

� Sigmoidoscopy may show inflammation orbleeding.Biopsies should be examined for ova.

Management:

� The object of specific treatment is to kill the adult schistosomes and so stop egg-laying.

� Praziquantel is the drug of choice for all formsof schistosomiasis.parasitological cure

The drugin 80% of

produces treated

individuals and over 90% reduction in egg counts in the remainder.

� Side-effects are uncommon but includenausea and abdominal pain.

� Praziquantel therapy in early infectionreverses pathologies such as hepatomegalyand bladder wall thickening and granulomas.

14

� Biopsies should be examined for ova.

.

� Surgery may be required to deal with residuallesions such as ureteric stricture, small fibrotic

Prevention:

� So far no controlling

satisfactory single means ofschistosomiasis has been

� Furthermore, S. japonicum has so many hostsbesides humans that latrines would be of littlelesions such as ureteric stricture, small fibrotic

urinary bladders, or granulomatous masses inthe brain or spinal cord.

� Removal of rectal papillomas by diathermy orby other means may provide symptomaticrelief.

controlling established.

schistosomiasis has been

� The life cycle is terminated if the ova in urineor faeces are not allowed to contaminate freshwater containing the snail host.

� The provision of latrines and of a safe watersupply, however, remains a major problem inrural areas throughout the tropics.

besides humans that latrines would be of littleavail.

� Annual mass treatment of the population helpsagainst S. haematobium and S. mansoni, butthis method has so far had little success withS. japonicum.

� Attack on the intermediate host, the snail,presents many difficulties and has not on itsown proved successful on any scale. Forpersonal protection, contact with infectedwater must be avoided.

� Liver flukes infect at least 20 million peopleand remain an important public health problemin many endemic areas.

� They are associated with abdominal pain,hepatomegaly and relapsing cholangitis.

� Clonorchis sinensis is a major aetiologicalagent of bile duct cancer.

� The three major liver flukes have similar life cycles and pathologies.

� Other flukes of medical importance include lung and intestinal flukes

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� Cestodes are ribbon-shaped worms which inhabit the intestinal tract.

� They have no alimentary system and absorb nutrients through the tegumental surface.

� The anterior end, or scolex, has suckers for attaching to the host.

� From theprogressively developing segments,

scolex arises a series ofthe

proglottides, which, when shed, may continue to show active movements.

� Cross-fertilisation takes place between segments.

.

� Ova, present in large numbers in matureproglottides, remain viable for weeks and

� Taenia saginata (beef tapeworm) andDiphyllobothrium latum (fish tapeworm) cause

� Taenia solium causes intestinal infection if acysticerci-containing intermediate host isproglottides, remain viable for weeks and

during this period they may be consumed bythe intermediate host.

� Larvae liberated from the ingested ova passinto the tissues, forming larval cysticerci.

� Tapeworms cause two distinct patterns ofdisease, either intestinal infection or systemiccysticercosis.

Diphyllobothrium latum (fish tapeworm) causeonly intestinal infection, following humaningestion of intermediate hosts that containcysticerci (the larval stage of the tapeworm).

cysticerci-containing intermediate host isingested, and cysticercosis (systemic infectionfrom larval migration) if ova are ingested.

� Echinococcus granulosus (dog tapeworm)does not cause human intestinal infection, butcauses hydatid disease (which is analogous tocysticercosis) following ingestion of ova andsubsequent larval migration.

� Humans acquire tapeworm by eatingundercooked beef infected with the larval

� Usually only one adult tapeworm is present in the gut but up to ten have been reported.

� The ova of T. saginata and T. solium are indistinguishable microscopically.

� However, examination of scolex and proglottides can differentiate between them.

� T. solium has a rostellum and two rows ofhooklets on the scolex, and dischargesmultiple proglottides (3–5) attached togetherwith lower degrees of uterine branching(approximately 10); T. saginata has only foursuckers in its scolex, and discharges singleproglottids with greater uterine branching (upto 30).

� Infection with T. saginata occurs in all parts ofthe world.

� The adult worm may be several metres longand produces little or no intestinal upset inhuman beings, but knowledge of its presence,by noting segments in the faeces or onunderclothing, may distress the patient.

16

to 30).

.

� Ova may be found in the stool.Praziquantel is the drug of choice; niclosamide

� T. solium, the pork tapeworm, is commonin central Europe, South Africa, South

� The adultonly

worm isinfound � Praziquantel is the drug of choice; niclosamide

or nitazoxanide are alternatives.� Prevention depends on efficient meat

inspection and the thorough cooking of beef.

in central Europe, South Africa, SouthAmerica and parts of Asia.

� It is not as large as T. saginata.

only infound humans followingthe eating of undercooked pork containing cysticerci.

� Niclosamide, followed by a mild laxative (after1–2 hours) to prevent retrograde intestinal

intestinalautoinfection, is effective for infection.

� Cooking pork well prevents intestinal infection.� Great care must be taken by nurses and other

adults while attending a patient harbouring anadult worm to avoid ingestion of ova orsegments.

Cysticercosis:� Human cysticercosis is acquired by ingesting T.

solium tapeworm ova, from either contaminatedfingers or food.

� The larvae are liberated from eggs in thestomach, penetrate the intestinal mucosa and arecarried to many parts of the body where theydevelop and form cysticerci, 0.5–1 cm cysts thatcontain the head of a young worm.

� They do not grow further or migrate.� Common locations are the subcutaneous tissue,

skeletal muscles and brain.

Clinical features:

� When superficially placed, cysts can bepalpated under the skin or mucosa as pea-likeovoid bodies.

� Here they cause few or no symptoms, and willeventually die and become calcified.

� Heavy brain infections, especially in children,may cause features of encephalitis.

� More commonly, however, cerebral signs donot occur until the larvae die, 5–20 years later.

� Epilepsy, personality changes, staggering gaitor signs of internal hydrocephalus are the mostcommon features.

Investigations:

� Calcified cysts in muscles can be recognisedradiologically.

� In the brain, however, less calcification takesplace and larvae are only occasionally visibleby plain X-ray; usually CT or MRI will showthem.

� Epileptic fits starting in adult life suggest thepossibility of cysticercosis if the patient has

� The subcutaneous tissue should be palpated and any nodule excised for histology.

� Radiological examination of the skeletal muscles may be helpful.

� Antibody detection is available for serodiagnosis.

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possibility of cysticercosis if the patient haslived in or travelled to an endemic area.

.

Management and prevention:

� Albendazole, 15 mg/kg daily for a minimum of8 days, has now become the drug of choice for

� In addition, anti-epileptic drugs should begiven until the reaction in the brain has

� Dogs are the definitive hosts of the tinytapeworm E. granulosus.8 days, has now become the drug of choice for

parenchymal neurocysticercosis.� Praziquantel is another option, 50 mg/kg in

three divided doses daily for 10 days.� Prednisolone, 10 mg 8-hourly, is also given for

14 days, starting 1 day before the albendazoleor praziquantel.

given until the reaction in the brain hassubsided.

� Operative intervention is indicated forhydrocephalus.

� Studies from India and Peru suggest that mostsmall solitary cerebral cysts will resolvewithout treatment.

tapeworm E. granulosus.� The larval stage, a hydatid cyst, normally

occurs in sheep, cattle, camels and otheranimals that are infected from contaminatedpastures or water.

� By handling a dog or drinking contaminatedwater, humans may ingest eggs.

� The embryo is liberated from the ovum in thesmall intestine and gains access to the bloodstream and thus to the liver.

� The resultant cyst grows very slowly, sometimesintermittently.

� It is composed of an enveloping fibrous pericyst,laminated hyaline membrane (ectocyst) and innergerminal layers (endocyst) which gives rise todaughter cysts, or germinating cystic broodcapsule in which larvae (protoscolices) develop.

� Over time some cysts may calcify and becomenon-viable.

� The disease is common in the Middle East,North and East Africa, Australia and Argentina.Foci of infection persist in rural Wales andScotland.

� E. multilocularis, which has a cycle betweenfoxes and voles, causes a similar but moresevere infection, ‘alveolar hydatid disease’,which invades the liver like cancer.

Clinical features:

� A hydatid cyst is typically acquired in childhoodand may, after growing for some years, causepressure symptoms. These vary, depending onthe organ or tissue involved.

� In nearly 75% of patients with hydatid diseasethe right lobe of the liver is invaded andcontains a single cyst.

� In others a cyst may be found in lung, bone,

Investigations:

� The diagnosis depends on the clinical,radiological and ultrasound findings in apatient who has lived in close contact withdogs in an endemic area.

� Complement fixation and ELISA are positive in70–90% of patients.

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� In others a cyst may be found in lung, bone,brain or elsewhere.

.

Management and prevention:

� Hydatid cysts should be excised possible.

wherever � Albendazole (400 mg 12-hourly for 3 months)should also be used. The drug is now often

� Prevention is difficult in situations where thereis a close association with dogs and sheep.possible.

� Great care is taken to avoid spillage andcavities are sterilised with 0.5% silver nitrate or2.7% sodium chloride.

should also be used. The drug is now oftencombined with PAIR (percutaneous puncture,aspiration, injection of scolicidal agent and re-aspiration) to good effect.

� Praziquantel 20 mg/kg 12-hourly for 14 daysalso kills protoscolicesperioperatively.

is a close association with dogs and sheep.� Personal hygiene, satisfactory disposal of

carcasses, meat inspection and deworming ofdogs can greatly reduce the prevalence ofdisease.

Other tapeworms:

� There are many other cestodes whose adult orlarval stages may infect humans.

� Sparganosis is a condition in which animmature worm develops in humans, usuallysubcutaneously, as a result of eating orapplying to the skin the secondary or tertiaryintermediate host.

�Ectoparasites only interact with the outermost surfaces of the host.

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