THE INTESTINAL NEMATODES Phylum Nematoda Non-segmented, generally cylindrical Tapered at both ends covered by tough

covering= Cuticle Has complete digestive tract = both oral and

anal openings Separate sexes: Males smaller than female

wormsMale : - single tubule, smaller end consists of testicular cells

- Extends into a vas deferens and seminal vesicle- Terminates in an ejaculatory duct opening into

the cloaca Female : - reproductive organs are tubular and lie coiled in the body cavity

- Has 2 cylindrical ovaries which expand to the uteri

- Uteri may open to the exterior through a single vulva or there may be a common vagina between the vulva and the uteri

- Vulva commonly located near the middle of the body but varies in position in different species

Majority are free living Estimated 500,000 species of nematodes Generally light cream-white color, females appear

darker when filled with dark-colored eggs Primitive form : mouth surrounded by three lips Hookworms: buccal capsule with cutting plates or

teeth Anterior portion of digestive tract: Esophagus =

muscular form = if caliber is uniform – Filariform = if expanded posteriorly into a bulb containing a

valve mechanism – Rhabditiform Male nematodes: has a pair of copulatory

spicules, lie in pouches near the ejaculatory duct and may be inserted into the vagina of the female

Stages of life cycle: egg-- larvae which undergo several molts--- adults

Filariform type of esophagus: infective stage larvae

Ascaris = die in about a year in the absence of reinfection

Trichuris = live more than a year Hookworm = may persist as long as 8 to 16 years

Diagnosis: Demonstration of the characteristic egg in the feces

HELMINTHIC DISEASESASCARIASIS Etiology:

Ascaris lumbricoides = largest intestinal roundworm

Most prevalent human helminthiasis Female worms = 20-35 cm in length

= may be as thick as a lead pencil Male worms = seldom more than 30 cm long

= more slender and distinguished by an incurved tail

Both sexes are creamy white, sometimes with a pinkish cast and fine circular striations in the cuticle

Mature larva-containing egg = infective stage Eggs passed in the feces of infected person &

mature in 5-10 days under favorable conditions to become infective

Female life span = 1-2 years Produces 200,000 eggs/24 hrs.

Epidemiology: Promiscuous defecation & use of human manure

= unhygienic practices Mode of transmission = hand to mouth; fingers

contaminated by soil contact Eggs remain infective in soil for months

Life Cycle:Embryonated egg swallowed (infective, containing fully developed larva) ® larva escapes from egg in S.I. ® tissues and lymphatic vessels and lungs ® further development in alveoli ® larva from lung ® larva in lung pass on to the intestine via trachea, esophagus and stomach ® develop maturity ® adult in small intestine ® eggs passed in feces ® unfertilized egg ® fertilized egg ® swallowed again.

Pathogenesis: Ingestion of mature egg – larva released from egg

– penetrate intestinal wall—Via venous circulation penetrate the lungs – break through pulmonary tissues to Alveolar spaces – ascend to the bronchial tree & trachea – re-swallowed

Clinical Manifestations: Morbidity manifested during migration of the

larva thru the lungs = Pneumonitis – occur from 4 days to 2 weeks after infection ( asthma attacks)

Pulmonary ascariasis = cough blood stained sputum and eosinophilia (Loeffler’s-like syndrome)

Adult worms in the small intestine = vague abdominal pains, distention & obstruction due to mass of worms in heavily infected individuals

In obstruction = peak incidence 1-6 yrs old; abdominal pain sudden onset, severe, colicky and vomiting

Eosinophilia noted in 10% of patients

Diagnosis: Direct fecal smear Kato’s thick smear Pulmonary & GI ascariasis complicated by

obstruction = based on clinical symptoms & high index of

suspicion Fertilized egg: broadly ovoidal, 45 to75 umx35 to

50um. Albuminoid outer coveringThick yellowish inner shell

Infertile eggs: longer, narrower than fertile eggs Measures 90 x 40 um

Both inner shell and albuminoid coat are thinIf albuminoid coat is absent – may resemble Trichostrongylus eggs

Can also be diagnosed through radiography = worm-shaped radioluscent areas in a barium- filled intestine

Treatment: Albendazole = a nitroimidazole that binds

irreversibly to tubulin, blocking microtubule assembly and inhibiting glucose uptake by the worm

= 400mg p.o. single dose (200 mg for children <2 years old) = drug of choice

Mebendazole 100 mg BID for 3 days or 500 mg once

Pyrantel pamoate 11 mg/kg single dose Piperazine salts (citrate, adipate or phosphate)

= causes neuromuscular paralysis & rapid expulsion of the parasite; used for intestinal & biliary obstruction; given 50-75 mg/kg for 2 days

Surgical treatment for severe obstructive cases

Prevention: Treating human feces before it is used as

fertilizer Providing hygienic sewage disposal facilities Deworming every 3-6 months

ENTEROBIUS VERMICULARIS Pinworm Affects 10% of pediatric population Spread is facilitated by crowded indoor living in

temperate climates but also common in the tropics

Male : inconspicuous, 2-5 mm long and not more than 0.2 mm wide

Female : 8-13 mm in length and 0.5 mm in width Light yellowish whiteDistinguished by a long thin, sharply pointed tail

Inhabit the cecum and adjacent portions of the large and small intestines

Female worms, when fully gravid, migrate down the intestinal tract to pass out the anus and deposit their eggs

The worms may migrate several inches out of the anus, depositing eggs as they crawl or liberating masses of them as the worms dry and literally explode

Eggs are fully embryonated and are infective within a few hours of the time they are deposited

Eggs live longest under conditions of fairly high humidity and moderate temperature

Reinfection of the patient by contamination of the hand is common and makes control of the parasite very difficult

Development of adult worm = 6 weeks

Familial outbreaks : Infection through contaminated clothing and beddings

Eggs may survive for some days in dry dust

Airborne eggs may infect persons at some distance

Retrofection = a type of autoinfection, involves hatching of the embryonated eggs after their deposition in the perianal area and subsequent migration back into the rectum and large intestine

Life Cycle: Mature egg ingested by human ® egg hatch in

the duodenum ® larva develops to maturity in S. I. ® proceed to L.I. (final habitat) ® adult in large L. I. (male and female)

Diagnosis: Recovery of the characteristic eggs

Method: Scotch Tape Swab Technique Suspected in children with pruritus ani Occasionally, adult female worms seen

crawling in the perianal region or in the feces

Females do not ordinarily oviposit until they leave the intestinal tract

Eggs: 50-60 um in length, 20-32 in breadth

Translucent shell of moderate thickness Flattened on one side = flattening, consequent reduction in diameter and thicker shell – differentiates from hookworm eggs

Symptoms: Pruritus ani = migration of the female worms

from the anus In small children, worms may invade the vagina

after leaving the rectum producing a local irritation

Local itching may interfere with the sleep of children or adults = worms migrate from the anus during the resting hours

Pathogenesis: Considered as a commensal Attachment of the adult worms to the intestinal

wall may produce some inflammation Invasion of the appendix can also be expected as

a cause of appendicitis

Entrance into the peritoneal cavity via the female reproductive system may result in formation of granulomas around eggs and worms = chronic pelvic peritonitis

Occasionally reported in other sites: Liver and lungs

Treatment: Albendazole = DOC

= single dose of 400mg or 200 mg in children < 2 y.o.

= should be repeated in 2 weeks to kill any worms that migrated and hatched from eggs present at the time of initial treatment

Pyrantel pamoate = single dose of 11 mg/kg body weight and repeated in 2 weeks

HOOKWORM INFECTIONS:ANCYLOSTOMA DUEDENALE

Old World hookworm Adults : - grayish white or pinkish

- head slightly bent in relation to the rest of the body

- Male = measures nearly 1 cm x 0.5 mm- Female = longer and stouter

Mouth is well developed = pair of teeth on either side of the median line and a smaller pair in the depths of the buccal capsule

Male worm: provided with a prominent copulatory bursa posteriorly

Hookworm eggs when passed in feces = unsegmented

In sandy and moist soil, larvae develop and hatch within 24 to 48 hours

Growth and development take place in the soil as the larva feed on bacteria and organic material and undergo first molt

After 7 days, worm stop feeding and molt the second time, transforming from rhabditiform to filariform or infective larvae

Infective larvae do not feed and live for 2 weeks and if cannot find a host, live in the upper layers of the soil = contact with skin of suitable host

= can also enter percutaneous, oral, transmammary and transplacental

Humans = the only host Larvae enter adjacent venules and carried to the

lungs then to the alveoli – trachea --- reswallowed --- small intestine where they mature

Attach thru mouth parts and suck blood and tissue juices of the host = average period of 7-8 weeks

Life Cycle: Filariform larva on soil penetrate skin ® blood

stream ® alveoli ® via trachea, esophagus and stomach to S. I. ® adult worm attach to mucosa of S. I. ® Hookworm egg in soil hatches to produce rhabditiform larva ® molts in about 3 days to produce 2nd stage rhabditiform larva ® molts in about a week to produce infective filariform larva

Diagnosis: Depends on the recovery of the eggs from the stools

Eggs similar with Strongyloides: Ancylostoma = long buccal capsule between the oral opening and the esophagusStrongyloides = short buccal capsuleEggs = oval and 56-60 um long x 36 to 40 um in breadth

= shell is thin and colorless

ANCYLOSTOMA CANINUM Hookworm of dogs Can cause abortive infection in humans Larvae unable to complete the life cycle ---

migrate through the subcutaneous tissue Seen in an area heavily populated by dogs

infected with the parasite Treatment: Mebendazole

NECATOR AMERICANUS

Resemble Ancylostoma but slightly smaller Males : 5-9 mm in length Females: about 1 cm long Head is slightly bent in relation to the rest of the

body= definite hook shape at the anterior end Buccal capsule is armed with a pair of cutting

plates while Ancylostoma has teeth Eggs slightly larger, averaging 64-76um by 36x40

um.

Manifestations: Allergic reaction in penetrating the skin = “

ground itch” Do not usually cause severe pulmonary

symptoms since larvae is smaller than Ascaris

Maturation of the worms may be marked by gastrointestinal discomfort or diarrhea

Chronic infections = considerable blood loss--- Iron Deficiency Anemia

Pica = consequence of iron deficiency anemia Eosinophilia is variable = up to 70%

Pathogenesis: Anemia = Microcytic hypochromic type Bone marrow is markedly hyperplastic Erythroid and myeloid hyperplasia of the spleen A. duodenale = lives 1-5 years N. americanus = as long as 18 years

Epidemiology: Widespread infection in significant parts of which

defecate directly onto the soil and do not customarily wear shoes

Factors: appropriate ambient temperatureSufficient rainfall

Loose sandy loam soilTreatment:

Albendazole = single oral dose of 400 mg (200 mg in children under 2 years old)

= drug of choice in both Ancylostoma and Necator

Mebendazole = equally effective = 100 mg BID for 3 days Pyrantel Pamoate = also effective Ferrous sulfate = in severe infection = 200 mg daily TID = start at the time of anti helminthic teratment and continued 3 months after the hemoglobin value returns to normal

STRONGYLOIDES STERCORALIS Exist as free living nematode Adult: very small = about 1 mm long Filariform larvae = infective stage

= incapable of further development in the soil and must penetrate skin of host to continue life cycle

Rhabditiform larvae that pass out from the stool of the host can directly transform into filariform larvae without developing into free living adults

Penetration to the skin and migration to the lungs and eventually to the small intestine also takes place

Adult males = eliminated from the body in early infection

Adult females = burrow into the mucosa of the intestinal tract where they lay eggs

Eggs similar in appearance with hookworms, hatch in the mucosa and liberate rhabditiform larvae which make their way to the lumen of the intestine

Life Cycle: Rhabditiform and filariform larve in feces ® filariform larva may re-infect while in intestine or penetrate skin from soil ® rhabditiform larva may molt forming into filariform larva ® may molt twice to become free-living adult ® under favorable conditions producing infective filariform larva

Larvae molt once before being passed out in the feces

Once filariform larvae is formed, it penetrate immediately into the wall of the gut and enter

the bloodstream Diagnosis: Demonstration of characteistic larvae in

the stools= larvae resemble those hookworm but can be distinguished by their very short buccal cavity

Embyonated eggs = present in severe diarrhea = differentiated with hookworm eggs since

they contain always well-developed larvae

Larvae may be concentrated with zinc sulfate Duopdenal Aspiration = occasionally reveal larvae String Capsule method or Enterotest

Symptoms: Pneumonitis may be produced by the larvae but

less severe than Ascariasis Moderate to severe diarrhea Malabsorption syndrome with steatorrhea In heavy infections, involve the large and small

bowels = give rise to ulceration of the intestinal mucosa suggestive of duodenal ulcer or ulcerative colitis

Melena may be present in massive lower gastrointestinal bleeding with passage of bright red blood per rectum

If only GIT and lungs are involved = Hyperinfection syndrome - fever, GI symptoms, dyspnea, wheezing, hemoptysis, cough and weakness

When migrating larvae are many = Disseminated strongyloidiasis – commonly affects malnourished

children, immunocompromised (AIDS), malignancy, taking high doses of corticosteroids

Pathogenesis: Patchy Pneumonitis in heavy infections = larvae

may be found in the sputum Adult female worm may be found in all parts of

the intestinal tract but more common in the jejunum

Treatment: Albendazole and Ivermectin = both are effective In hyperinfection syndrome = 400mg daily for 15

days Ivermectin = 100% cure rate when given at 200

mcg/kg body weight daily for 2 days

STRONGYLOIDES FULLEBORNI A parasite of monkeys but also infect humans Common in infants under 6 months of age Eggs are found in the feces Larvae found in the milk of nursing mothers Causes “swollen belly sickness” = abdominal

distention, respiratory distress, generalized edema, and hypoproteinemia

Therapy as recommended for S. stercoralis is curative if begun early

CAPILLARIA PHILIPPINENSIS Intestinal capillariasis = first observed in 1962 in

Ilocos Sur Adult worms: slender, 4-5 mm long Live in intestinal mucosa primarily jejunum Finding of larval stages, and of oviparous and

larviparous females in the bowel, suggests that the parasite multiplies in the intestine and overwhelming infections are the result of autoinfection

Eggs seen in infected persons = measures 45 x 21 um --- ingested by fresh water and brackish water fish where larval stages are found

Complete life cycle is not known Laboratory diagnosis is made by finding the

characteristic eggs

Symptoms: Abdominal pain, borborygmus (gurgling), and

diarrhea Diarrhea may be accompanied by anorexia,

nausea, vomiting and hypotension

Patient may become cachectic with generalized anasarca

Visible peristaltic waves may be seen over the distended abdomen

Pathogenesis: Pathologic picture : Hypoproteinuria, low blood

calcium, potassium, and cholesterol levels, features of protein wasting enteropathy

Epidemiology: Recently redescribed as Paracapillaria

philippinensis Natural life cycle is not known Experimentally: eggs hatch and develop into

larvae if fed to fresh and brackish water fish and to adult stage if the infected fish are fed to monkeys --- fresh and brackish water fish are eaten raw --- humans acquire infection

Two other capillarias causing human infections (rare):

1.C. hepatica = causing hepatic capillariasis 2.C. aerophila = causing pulmonary capillariasis

Treatment: Mebendazole = DOC

= 200 mg BID for 20 days Albendazole = alternative drug

= 400 mg for 10 days In acute illness = fluid and electrolyte

replacement and high protein diet

TRICHURIS TRICHIURA Whipworm Trichuris = hair tail Common in tropical areas and in regions where

sanitation is poor Thick posterior part of the body forming the stock

and long thin anterior portion the lash Adult worm : 3-5 cm long Females are larger than males Thin almost colorless anterior three fifths of the

body consists of the esophagus Expanded posterior part is pinkish gray and

contains the intestine and reproductive organs

Life cycle: Infection acquired by ingesteion of fully

embryonated eggs ---- passed in unsegmented condition and require 10 days or more outside the body to reach the infective stage ---- larvae pass to the cecal area where they attach permanently with their attenuated anterior ends embedded in the mucosa

Worms found in the rectum in heavy infections

Diagnosis: Demonstration of the characteristic barrel or

football-shaped eggs in the feces Each female worm produces 3,000 to 7,000 eggs

daily Eggs measure 50 to 54 um in length with

refractile prominences at both ends= Polar plugs

Zinc sulfate flotation method = very efficient in demontrating the eggs

Symptoms: Usually asymptomatic in light infections In heavy infections : abdominal pain and

distention, bloody or mucoid diarrhea, tenesmus, weight loss and weakness

Prolapse of the rectum = usual complication in chronic heavy infections

Anemia and moderate eosinophilia and nutritional deficiencies may be seen in heavy infections

Pathogenesis: Appendicitis = brought by blockage of the

lumen by worms Edema of the rectum produced by numbers of

worms embedded = rectal prolapse Blood loss per worm is calculated to be

approximately 0.005 ml/worm/day Infections of 200 worms or more may cause

chronic dysentery = profound anemia and growth retardation

Mimics inflammatory bowel disease but is readily curable

Treatment: Albendazole = DOC Mebendazole = alternative drug Loperamide hydrochloride = may help by increasing

contact time between drug and parasites

TRICHOSTRONGYLUS SPECIES T. orientalis Related to hookworms and the adults are similar

in appearance Species infecting humans are smaller than the

hookworms but the eggs are larger Eggs: Symmetrical and thin shelled and differ

from hookworm egg in size ( 73 to 95 by 40 – 50 um) and their more pointed ends

Symptoms and Pathogenesis: Eggs hatch in soil --- hatched larvae contaminate

foodstuff --- ingested Larvae do not undergo pulmonary migration but

when reswallowed attach themselves to the intestinal mucosa and grow to adulthood in 3-4 weeks

They ingest blood = clinically apparent blood loss only seen in heavy infections

Epidemiology: Use of human feces as fertilizer = human to

human spread of the infection

Treatment: Mebendazole = DOC Albendazole = equally effective

ANISAKIASIS Parasites of the gastrointestinal tract of animals

( seals, sea lions, whales and dolphins) Found in marine fish infected with the larval

stages of nematodes Human infections results from ingestion of third-

stage larvae belonging to genera Anisakis or Pseudoterranova

Larvae reach a length of 50 mm and a diameter of 1-2 mm

Classification is difficult but generally identified by “type” on the basis of the structure of the digestive tract

Larvae of Anisakis usually found in mackerel and salmon

Larvae of Pseudoterranova = usually parasitize cod, halibut, rockfish (Pacific red snapper), sardine, and squid

Most human infections have been reported from Japan and Netherlands = consumption of sushi and sashimi in Japan and pickled herring in Netherlands

Invades the gastric mucosa and intestinal tract

Symptoms: Abrupt onset 1-5 days after ingestion of raw fish,

abdominal pain, nausea, and sometimes vomiting or diarrhea, with signs of peritoneal irritation and incomplete ileus of the small intestine

Perforation of the bowel has been reported = finding of an anisakid larva in an inflammatory omental mass

Gastric anisakiasis = severe epigastric pain, nausea, and vomiting sometimes within a few hours after ingestion of contaminated raw fish

Gastroscopic removal of the worm is usually needed

Diagnosis: A presumptive diagnosis can be made on the

basis of the patient’s food habits

Definitive diagnosis: Demonstration of worms obtained by gastroscopy, or vomited by the patient

If vomited larvae are well preserved, they may be cleared in glycerin and identified by the structure of the digestive tract which differs in three types of anisakid larvae

Epidemiology: Human infections results from the consumption of

raw or insufficiently smoked or salted or marinated fish

Fish kept frozen at –20°C for at least 5 days are considered safe for consumption in dishes such as sashimi and sushi

Smoking fish kills the parasite only if the temperature of the flesh reaches 65°C during the process

Salting or marinating fish cannot be depended on to kill the parasites

Larvae may be found in the gut, visceral cavity and the flesh of the fish

When fish are iced ( but not frozen) for transportation to harbor processing plants, larvae may migrate from the gut into the muscles

Treatment: No treatment needed in transient anisakiasis Albendazole = 400mg BID for 21 days

Comparative morphology of the digestive tracts of the three types of anisakine larvae