The Intestinal Nematodes

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 worms Male : - 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

HELMINTHIC DISEASES ASCARIASIS 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

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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.

♦ 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 ♦

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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

Epidemiology:

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Promiscuous defecation & use of human manure = unhygienic practices

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Mode of transmission = hand to mouth; fingers contaminated by soil contact Eggs remain infective in soil for months

years

♦ Diagnosis: Demonstration of the characteristic egg in the feces

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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:

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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

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Clinical Manifestations:

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

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

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

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In obstruction = peak incidence 1-6 yrs old; abdominal pain sudden onset, severe, colicky and vomiting Eosinophilia noted in 10% of patients

Diagnosis:

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Prevention: • Treating human feces before it is used as fertilizer • Providing hygienic sewage disposal facilities • Deworming every 3-6 months ENTEROBIUS VERMICULARIS

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Pinworm

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

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Female : 8-13 mm in length and 0.5 mm in width

Direct fecal smear Kato’s thick smear

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Fertilized egg: broadly ovoidal, 45 to75 umx35 to 50um. Albuminoid outer covering Thick yellowish inner shell Infertile eggs: longer, narrower than fertile eggs Measures 90 x 40 um Both inner shell and albuminoid coat are thin If albuminoid coat is absent – may resemble Trichostrongylus eggs Can also be diagnosed through radiography = worm-shaped radioluscent areas in a bariumfilled intestine

Treatment:

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Albendazole = a nitroimidazole that binds irreversibly to tubulin, blocking microtubule

Affects 10% of pediatric population Spread is facilitated by crowded indoor living in temperate climates but also common in the tropics

Light yellowish white Distinguished by a long thin, sharply pointed tail

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Pulmonary & GI ascariasis complicated by obstruction = based on clinical symptoms & high index of suspicion

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

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

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

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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

Symptoms:

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

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

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

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Development of adult worm = 6 weeks

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Eggs may survive for some days in dry dust

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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

Familial outbreaks : Infection through contaminated clothing and beddings Airborne eggs may infect persons at some distance

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Pruritus ani = migration of the female worms from the anus

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In small children, worms may invade the vagina after leaving the rectum producing a local irritation

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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

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Attachment of the adult worms to the intestinal wall may produce some inflammation

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Invasion of the appendix can also be expected as a cause of appendicitis

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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

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Life Cycle:

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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

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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

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

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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:

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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

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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 esophagus Strongyloides = short buccal capsule Eggs = 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.

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Manifestations:

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Allergic reaction in penetrating the skin = “ ground itch”

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Do not usually cause severe pulmonary symptoms since larvae is smaller than Ascaris

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Maturation of the worms may be marked by gastrointestinal discomfort or diarrhea Chronic infections = considerable blood loss--Iron Deficiency Anemia

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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 temperature Sufficient rainfall Loose sandy loam soil Treatment: • 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

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

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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

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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

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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

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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

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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:

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Recently redescribed as Paracapillaria philippinensis

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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

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Two other capillarias causing human infections (rare): 1.C. hepatica = causing hepatic capillariasis 2.C. aerophila = causing pulmonary capillariasis Treatment:

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= 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

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Trichuris = hair tail

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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

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Diagnosis:

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Mebendazole = DOC

TRICHURIS TRICHIURA • Whipworm

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with their attenuated anterior ends embedded in the mucosa Worms found in the rectum in heavy infections

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Demonstration of the characteristic barrel or football-shaped eggs in the feces Each female worm produces 3,000 to 7,000 eggs daily

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Eggs measure 50 to 54 um in length with refractile prominences at both ends= Polar plugs

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Zinc sulfate flotation method = very efficient in demontrating the eggs

Symptoms:

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Usually asymptomatic in light infections

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Prolapse of the rectum = usual complication in chronic heavy infections

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

In heavy infections : abdominal pain and distention, bloody or mucoid diarrhea, tenesmus, weight loss and weakness

Pathogenesis: • Appendicitis = brought by blockage of the lumen by worms

Life cycle:

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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

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Edema of the rectum produced by numbers of worms embedded = rectal prolapse

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Blood loss per worm is calculated to be approximately 0.005 ml/worm/day

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Infections of 200 worms or more may cause chronic dysentery = profound anemia and growth retardation

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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

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Related to hookworms and the adults are similar in appearance

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Species infecting humans are smaller than the hookworms but the eggs are larger

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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:

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Eggs hatch in soil --- hatched larvae contaminate foodstuff --- ingested

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Larvae do not undergo pulmonary migration but when reswallowed attach themselves to the intestinal mucosa and grow to adulthood in 3-4 weeks

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

Epidemiology:

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Use of human feces as fertilizer = human to human spread of the infection

Treatment: • Mebendazole = DOC • Albendazole = equally effective

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Human infections results from ingestion of thirdstage 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

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

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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

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Symptoms:

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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

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

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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

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Diagnosis:

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A presumptive diagnosis can be made on the basis of the patient’s food habits

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

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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:

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Human infections results from the consumption of raw or insufficiently smoked or salted or marinated fish

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

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Smoking fish kills the parasite only if the

ANISAKIASIS

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Parasites of the gastrointestinal tract of animals ( seals, sea lions, whales and dolphins) Found in marine fish infected with the larval stages of nematodes

temperature of the flesh reaches 65°C during the process

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

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

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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