Parasitology Lec 3.01a Intestinal Nematodes

3.01 January 6, 2017

INTESTINAL NEMATODES Dr. Malijan

Department of Microbiology and Parasitology

TOPIC OUTLINE I. Introduction: Metazoan parasites II. Overview: Intestinal Nematodes a. Ascaris lumbricoides b. Hookworms c. Strongyloides stercoralis d. Capilaria philippinensis e. Enterobius vermicularis

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Trichuris trichiura

Red italicized – from Doc Malijan Green italicized – from Transer

METAZOAN PARASITES 

Metazoan parasites are either helminths or arthropods  Helminths. 3 groups causing infection to man: o Annelids (leeches) o Nematodes  Aka roundworms  Elongated and cylindrical in shape with bilateral symmetry  Generally, with complete digestive tract and muscular pharynx which is characteristically triradiate  Separate sexes or parthenogenetic  with sensory organ in the anterior (amphids) and posterior (phasmids) ends (Amphids – A – Anterior; Phasmids – P – posterior) o Flatworms (*Platyhelminthes) Phylum Nematoda (Round Worms)  Intestinal o Acaris lumbricoides o Hookworms o Strongyloides stercoralis o Capilaria philippinensis o Enterobius vermicularis o Trichuris trichiura  Extra-intestinal o Angiostrongylus cantonensis o Filarial worms o Trichinella spiralis Phylum Cestoidea (Tapeworms)  Order Cyclophyllidea o Dipylidium caninum o Echinococcus spp. o Hymenolepis spp. o Raillientina garrisoni o Taenia spp.  Order Pseudophyllidea

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o Diphyllobothrium latum o Spirometra Phylum Trematoda (Flukes) o Artyfechinostomum malayanum o Clonorchis sinensis o Echinostoma ilocanum o Heterophyids o Opistorchis spp. o Paragonimus westermani o Schistosoma spp. Phylum Nematoda “Roundworms” Unsegmented, elongated and cylindrical Sexes are separate – females are larger than males Posterior end of male usually curved Class Aphasmidia – lacking phasmids or caudal receptor (Adenophorea) o Trichuris o Trichinella o Capilaria 2. Class Phasmidia – with phasmids or caudal papillae (Secernentia)     1.

ORDER Ascaridida Strongylida Rhabditida Oxyurida Spirurida

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GENUS/ORGANISM Ascaris Angiostrongylus and hookworms Strongyloides Enterobius Filarial worms

INTESTINAL NEMATODES Species which parasitize the small intestine o Ascaris lumbricoides o Necator americanus (hookworm) o Ancylostoma duodenale (hookworm) o Strongyloides stercoralis (threadworm) o Capilaria philippinensis Species which parasitize the large intestine o Enterobius vermicularis (pinworm) o Trichuris trichiura (whipworm) Life cycle: 1. Egg stage 2. Four larval stages 3. Adult stage Adult female may be:

Intestinal Nematodes 1.

Oviparous – eggs are oviposited and embryo develops outside the maternal body (e.g. A. lumbricoides) 2. Viviparous – female gives birth to larvae (C. philippinensis) 3. Parthogenetic – can produce visible eggs without being fertilized by the male worms (S. stercoralis) Mode of infection: o Auto-infection possible in:  Capilaria, Strongyloides, Enterobius o Transmission through inhalation: Enterobius, Ascaris Ascaris lumbricoides

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Figure 2. (L) to (R): Ascaris adult female, Ascaris Adult Male. Notice the ventrally curved posterior end of male.

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Human Intestinal Giant Roundworm Largest and most common parasitic worm in humans Found worldwide (1/6 of the population, >1 billion infected) but prevalent in tropical countries Two separate populations and reservations o Adult ascaris – parasitizing man o Ascaris eggs – environment Ascariasis considered a disease of poverty o Contribute to impairment of cognitive performances and growth of children o Reduce work capacity and productivity of adults Parasite Biology Adult o Creamy white or pinkish yellow o Polymyarian type of somatic muscle arrangement:  Cells are numerous and project well into the body longitudinally o Covered by acid-resistant cuticle for protection against host’s GIT environment o Terminal mouth with three lips and sensory papillae anteriorly o Reside in but do not attach to the mucosa of small intestine

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Female o Bigger and longer, tapered at both ends o Large (22-35cm x 5mm) and may grow up to 45 cm long o Reproductive potential: 240,000 eggs/day o With paired reproductive organs in posterior 2/3 o Vulva in anterior end and comprises 1/3 of its whole length

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Male o Ventrally curved posterior end with two spicules in tail o 15-25cm x 3mm (10-31cm) o Reproductive organ: single, long, tortuous tubule

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Fertilized egg o Mostly oval or spherical, golden brown o Capable of further development in soil from single cell to embryonated eggs o Shell (Corticated)  Inner highly impermeable lipoidal vitelline membrane  Thick transparent middle glycogen layer  Outermost coarsely mammilated albuminoid layer o Decorticated  absent mammillated albuminous layer o At oviposition, fertile eggs have an ovoid mass of protoplasm -> larvae development in 14 days o 45-70µm x 35-50µm

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Intestinal Nematodes

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Figure 3. (L): Corticated Fertilized egg.  (R): Decorticated Fertilized egg.

Unfertilized eggs o 1st two layers absent; shell is thinner with irregular mammilated coating (only one layer) filled with refractile granules o Generally larger, narrower, more elongated o Can never undergo development in soil o 88-94µm x 39-44µm (longer and narrower)

Figure 4. Unfertilized egg (longer and narrower compared to fertilized egg)

Life Cycle

Figure 5. Life cycle of Ascaris lumbricoides.

1. Adult worms live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces 2. Unfertilized eggs may be ingested but are not infective 3. Fertile eggs embryonated and become infective after 18 days to several weeks, depending on the environmental conditions (optimum: moist, warm, shaded soil) 4. After infective eggs are swallowed, the larvae hatch, invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs 5. The larvae mature further in the lungs (10 to 14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed 6. Upon reaching the small intestine, they develop into adult worms 7. (Back to 1) Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female.  Adult worms can live 1 to 2 years  Embryonated eggs can survive in moist shaded soil for a few months to 2 years in tropical and sub-tropical areas, much longer in temperate regions  Mode of infection: ingestion of embryonated eggs  Infective stage: embryonated egg (inside is third-stage larva)

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Pathogenesis and Clinical Manifestations Larval Stage o Larval lung migration  Migratory larvae -> hemorrhages and destruction of the lung

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Intestinal Nematodes

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Larval migration to other organs  Lactose intolerance  Eosinophilia  Abdominal pain – most common complaint

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parenchyma as the larvae breaks through the capillaries Asthmatic type of respiration Cough with rales and chest pain Ascaris pneumonitis Loeffler’s syndrome:  Allergic  Eosinophilic infiltration of the lungs

Adult Stage o Intestinal  Bowel obstruction (heavy infections)  Lactose intolerance (moderate infections) o Extraintestinal  Suffocation: passage in the larynx of vomited Ascaris  Otitis media: enter Eustachian tube 10-20 worms – asymptomatic Intestinal volvulus, intussusception and obstruction Continuous biting or pricking of intestinal mucosa by a few adults may irritate nerve endings in the mucosa and result in intestinal spasm leading to intestinal obstruction Organ May become entangled in intestine Appendix Bile duct

Liver Perforate the bowel and into peritoneal cavity Gallbladder

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 Complication Intestinal obstruction  Acute appendicitis  Biliary ascariasis – presenting with severe colicky abdominal pain Multiple abscesses  Peritonitis  Gall stones (Ascaris eggs) Pancreatitis – may be  caused by even just a single Ascaris adult 

Diagnosis Direct fecal smear: o 2mg stool used Kato Technique of Cellophane Thick Smear: o 20-60mg stool, purely qualitative method recommended for mass examination Kato-Katz Technique:

modified Kato technique, 40-60mg stool to quantify number of eggs in sample  Quantitative: count number of eggs per gram of stool  Determine egg reduction rate post-treatment  Determine intensity of infection Kato technique and Kato-Katz method is useful for individual and mass screening than DFS These techniques are more sensitive, cheaper, and easier to maintain Negative Stool Exam o When patients are actually free from infection (true negative) o During larval migration via blood stream o When worms are still sexually immature o When only male worms are found in intestines Treatment Broad spectrum antihelminthics: neuromuscular blocking effect on parasite -> paralysis of worms o Albendazole  Drug of choice (DOC)  400mg single dose o Mebendazole: 500mg single dose o Pyrantel pamoate: 10mg/kg single dose o Ivermectin: effective as Albendazole at 200µg/kg single dose Community-based chemotherapy: 4-month interval or thrice a year for 3 years Among school children: twice a year of 4-6 months interval Reinfection observed 4 months posttreatment and full reinfection at 6-7 months Cure rates close to 100%, tolerance and resistance not observed Teratogenic: shouldn’t be given to pregnant women o

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Epidemiology Occurs most frequently in tropical and subtropical regions (Asia, Central and South America, Africa) Estimated to infect 1.2 billion individuals (1/5 of the world’’s population) Thrives in areas with lack of sanitation, poverty, and ignorance Most common source of infection – soilcontaminated foods esp. raw vegetables Cosmopolitan distribution 20,000 die annualy, mostly young children Risk of infection exist wherever fecal disposal is improper Factors contributing to transmission: o High density of human population

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Intestinal Nematodes o o o

Involvement of agriculture (night-soil as fertilizer) Illiteracy Poor sanitation

Prevention and Control Mass Treatment Selective Treatment o treating only those found positive for eggs on stool exam Targeted group o treating children alone Sanitary disposal of human excreta Health education and Personal hygiene Avoiding use of human feces for fertilizer Thorough cooking of food

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Hookworms Necator americanus: New world hookworm/ American murderer Ancylostoma duodenale: Old world hookworm Ancylostoma braziliense: Cat hookworm Ancyclostoma caninum: Dog hookworm

Numbers 1 and 2  Soil-transmitted helminths that infect man  Blood-sucking nematodes that attach to mucosa of small intestine (Ascaris do not attach)  Most commonly found in sub/tropical countries occurring as single or mixed infections Parasite Biology Necator americanus  Adult o Small, cylindrical, fusiform, gray-white o Females > Males o Males: posterior end broad membranous caudal bursa with rib-like rays used for copulation o Hook-like head curved opposite to body’s curvature o Buccal capsule: ventral pair of semilunar cutting plates

Figure 6. (L) adult with ventral pair of semilunar cutting plates (R top) Male with copulatory bursa. (R below) Female

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Rhabditiform larva (1st stage) o Resembles those of S. stercocoralis o Somewhat larger, more attenuated posteriorly o Longer buccal cavity o Smaller genital primordium

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Filariform larva o Buccal spears are conspicuous and parallel to body o Conspicuous transverse striations on sheath of tail o Infective stage to man

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Egg o 60-75µm x 35-40µm o Bluntly rounded ends o Single, thin, transparent, hyaline shell o Unsegmented at oviposition o Ovoidal, colorless, 4-8 cell stage o Constipated stool: embryo inside shell o Differentiation of N. americanus and A. duodenale:  Difficult and impractical

Ancylostoma duodenale  Adult o Larger than N. americanus o Single-paired male and female reproductive organs o Head continues in same direction as body o Buccal capsule: 2 pairs of curved ventral teeth

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Intestinal Nematodes

Figure 7. (L) Adult A. duodenale with 2 pairs ofcurved ventral teeth. (R) Female and Male respectively.

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Rhabditiform larva (1st stage) o Same as N. americanus

Figure 10. Hookworm egg in wet mount (L) unstained.

Life Cycle

Figure 8. Hookworm rhabditiform larva.

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Filariform larva o Same but with inconspicuous buccal spears and transverse striations on tail region

Figure 11. Life cycle of intestinal hookworm

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Figure 9. (L) Hookworm filariform larva in wet mount. (R) Close up of posterior end of hookworm filariform larva

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Egg

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Eggs passed in stool under favorable conditions (moisture, warmth, shade) -> larvae hatch in 1 to 2 days -> rhabditiform larvae released and grow in feces and/or soil 2. Becomes infective filariform (thirdstage) larvae after 5 to 10 days (and two molts)  Survive 3-4 weeks in favorable environments 3. Contact with human host -> larvae penetrate skin and carried through circulation to heart and lungs -> penetrate into pulmonary alveoli, and ascend to bronchial tree to pharynx, and swallowed 4. Larvae reside and mature into adults in small intestine. Adults live in lumen of small

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Intestinal Nematodes

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intestine -> attach to intestinal wall -> resultant blood lost by host Most adult worm eliminated 1-2 years but longetivity may reach several years Some A. duodenale larvae after skin penetration can become dormant in intestine or muscle N. americanus infection by transpulmonary migration phase A. duodenale infection by oral and transmammary route

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Figure 12. Cutaneous larval migrans

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Cutaneous larval migrans (creeping eruption) is zoonotic with hookworm species using non-human as definitive hosts (A. braziliense – cats, and A. caninum – dogs) Cycle in definitive host is very similar Humans may be infected when filariform larvae penetrate skin Pathogenesis and Clinical Manifestations Larval Stage o Ground Itch/Coolie Itch  Intense localized itching, edema, erythema and papulovesicular eruption  Lasts up to 2 weeks  Site of entrance of filariform (L3) larvae:  Dermatitis  Dew itch related to contact with soil (on a dewy morning) o Creeping eruption/ Cutaneous Larva Migrans  Due to exposure of skin to filariform larvae of A. braziliense or A, caninum  Occasional: N. americanus and A. duodenale  Serpiginous tunnel in stratum germinativum of skin

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Larvae move several mm to few cm per fay  Pyogenic infection: pruritus Pulmonary lesions  Petechial hemorrhages  Eosinophilic and leucocytic infiltration  Bronchitis or pneumonitis Intestine  Abdominal pain, steatorrhea, diarrhea with blood and mucus  Eosinophilia 30-60% 

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Adult Stage o Hookworm Anemia  Due to continuous mechanical suction of blood from intestinal mucosa attachment  Progressive, secondary, microcytic, hypochromic anemia (irondeficiency type)  RBC loss in gut  N. americanus: 0.03-0.05mL blood/day  A. duodenale: 0.16-0.34mL blood/day o Hypoalbuminemia  Combined loss of blood, lymph and protein o Other signs and symptoms  Exertional dyspnea, weakness, dizziness and lassitude  Rapid pulse, edema, albuminuria Diagnosis Ground itch and creeping eruption: characteristic lesion, history of contact with soil DFS: for heavy infection (can’t detect 50% rates in 1990 Factors contributing to transmission: o Suitability of environment for eggs or larvae: damp, sandy or friable soil with decaying vegetation, temperature 2432⁰C o Mode and extent of fecal pollution (unsanitary disposal of feces, night soil as fertilizer)

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Mode and extent of contact between infected soil and skin or mouth

Prevention and Control Proper treatment of human excreta used as fertilizer Avoiding ingestion of raw vegetables not washed properly Sanitary disposal of feces Wearing of shoes, slipper, or boots to avoid skin contact with infected larvae Health education Treatment of infected individuals Protection of susceptible individuals: improve household, diet Trichuris trichiura Whipworm Soil-Transmitted helminth Frequently occurs together with Ascaris Holymyarian o Based on arrangement of somatic muscles in cross section o Small numerous and closely packed in narrow zone Parasite Biology Adult o Inhabit large intestine o Entire whip-like portion embedded into intestinal wall of cecum o Eggs become embryonated within 2-3 weeks o No heart-lung migration o Female  35-50mm  Bluntly rounded posterior  Lays 3,000-10,000 eggs/day o Male  30-45mm, shorter than female  Coiled posterior end with a single spicule and retractile sheath

Figure 13. (L) Female and (R) Male T. trichiura

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Egg o 50-54µm x 23µm

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Intestinal Nematodes o o o o

Lemon-shaped/ barrel-shaped/ footballshaped/ like a Japanese lantern With plug-like translucent polar prominences Yellowish outer and transparent inner shell Embryonic development when eggs deposited in clayish soil

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4cm long, live and fixed in cecum and ascending colon, anterior whip-like portions threaded into mucosa Females oviposit 6-70 days after infection, shed 3,000-20,000 eggs/day Lifespan: 2 years

Pathogenesis and Clinical Manifestations Worms embedded in mucosa cause petechial hemorrhages -> predisposed to amebic dysentery (ulcers suitable for E. hystolitica “Mostly sa intestine kasi dun sila nageembed”

Figure 14. T. trichiura eggs

Life Cycle

Figure 16. Rectal Prolapse

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1. Unembryonated eggs passed in stool 2. In soil:  Eggs develop to 2-cell stage (advanced cleavage stage) then embryonated 3. Eggs become infective in 15-30 days 4. After ingestion  Eggs hatch in small intestine -> four larval stages -> mature to adults in colon 5. “Diretso na agad sa intestine, wala nang lakwatsa” 6. Adult worms

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Hyperemic and edematous mucosa Enterorhagia Trichuris dysentery syndrome: o Chronic Dysentery o Rectal Prolapse - “kasi ire nang ire” Appendicitis or granulomas 5,000 eggs/g -> symptomatic >20,000 eggs/g feces -> severe diarrhea or dysenteric syndrome Light infection o Asymptomatic Heavy parasitism o Blood-streaked stools o Abdominal pain o Anemia o Weight loss Diagnosis Heavy infections o Relies upon clinical symptoms such as rectal prolapse, blood streaked diarrhea, abdominal pain, and tenderness Light infections o DFS, Kato Thick Smear Method, Kato-Katz

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Intestinal Nematodes 

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Kato technique and Kato-Katz technique are simpler and cheaper o High sensitivity and specificity in detecting Trichiura One may see the adults in the intestinal mucosa for those with rectal prolapse Treatment Mebendazole o Drug of Choice o 100 mg twice a day for 3 days Albendazole Contraindication to Mebendazole and Albendazole: o Early pregnancy (within the 1st trimester) o Hypersensitivity Adverse effects (mild and transient): o Headache, nausea, vomiting, GI discomfort, itchiness

Eggs deposited by single female:  4,672 – 16,888 (mean 11,105/day) Male  2.5mm  Tail curves ventrad  Single copulatory spicule  Male dies after copulation (awtsu.)

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Epidemiology Children 5-15 years old frequently infected Philippines: 80-84% prevalence Infection through ingestion of embryonated eggs Prevention and Control Mass treatment if infection rate is >50% Preventive measure o Treatment of infected individuals o Sanitary disposal of human feces by constructing toilets and their proper use o Washing of hands with soap and water before and after meals o Health education on sanitation and personal hygiene o Thorough washing and scalding of uncooked vegetables especially those areas where night soil is used as fertilizer Enterobius vermicularis Human pinworm Causes Enterobiasis or Oxyuriasis characterized by perianal itching or pruritus ani Parasite Biology Adult o Small, whitish, or brownish in color o Anterior end: posterior cuticular alar expansions (lateral wings or cephalic alae) o Posterior esophageal bulb o Female  8-13mm x 0.4mm  Long pointed tail (“pinworm”)  Females die after oviposition

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Figure 17. Adult (L) Female and (R) Male E. vermicularis

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Egg o 50-60µm x 20-30µm o Elongated, ovoid, flattened on ventral side o Similar to letter D o Translucent shell (two layers):  Outer, triple, thick hyaline albuminous shell: mechanical protection  Inner embryonic lipoidal membrane: chemical protection o Outside host, eggs become infective/embryonated within 6 hours o Ovum develops into tadpole-like embryo o Resistant to putrefaction and disinfectants but succumb to dehydration in dry air within a day o Cool and moist conditions: eggs remain viable for several days

Figure 18. E. vermicularis eggs in wet mount. (R) iodine-stained wet mount

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Intestinal Nematodes 

Larvae o Folded once within shell, creating a visible line along egg’s long axis o Rhabditiform larvae  Characteristic esophageal bulb but has no cuticular expansion on anterior end

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Life Cycle

Figure 19. Life cycle of E. vermicularis

1. Eggs deposited on perianal folds 2. Autoinfection o Transferring infective eggs to mouth with hands that have scratched perianal area 3. Person-to-person transmission o Handling of contaminated clothes or bed linens o Contaminated clothes (e.g. underwear) – beddings -> fixing your bed -> ingestion ( tumatawa kasi habang pinapag-pag) o Enterobiasis acquired through ingestion of embryonated eggs and contact with egg-contaminated surfaces o Some may become airborne and inhaled 4. Ingestion of infective embryonated eggs -> larva hatch in small intestine -> adults establish themselves in colon o Ingestion of infective eggs -> oviposition of adult females is abouth 1 month (lifespan: 2 months) 5. Gravid females migrate nocturnally outside the anus and oviposit on perianal area 6. (Back to 1) Larvae in eggs develop and become infective 4-6 hours under optimal conditions  Retroinfection o Migration of newly hatched larvae from anal skin back to rectum Pathogenesis and Clinical Manifestations

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1/3 asymptomatic Forms: o Pathology at the site of attachment of worm  Mild catarrhal inflammation of the mucosa due to attachment of the worms  Mechanical irritations and secondary bacterial infection  Minute ulceration or abscesses in cecal mucosa o Pathology due to egg deposition in perianal area  Intense itching or pruritus in perianal region -> scarified  Pruritus ani -> hemorrhage, eczema, bacterial infection of anal and perianal regions and perineum o Pathology caused by migrating adults  Migrating worms lay eggs in genital organs causing vulvovaginitis, worms enter fallopian tube causing salpingitis  “Pregnant female is responsible for signs and symptoms” Children suffer insomnia due to pruritus “Hinahanap ni female yung pinagmulan niya kaya kung saan-saang butas pumasok…” vaginitis, endometriasis, salpingitis, peritonitis, appendicitis Other s/sx: poor appetite, weight loss, irritability, teeth grinding, abdominal pain Diagnosis History and physical exam Direct Fecal Smear o Eggs are found only in 5% of infected persons Perianal Cellulose Tape Swab or Graham’s Scotch Adhesive Tape Swab o D-shaped ova o Best time: soon after patient awakens and before bathing Worms seen migrating out of child’s anus at right Treatment Pyrantel pamoate o Drug of Choice o 10mg/kg with second dose 2-4 weeks later Albendazole o 400 mg, single dose Mebendazole o 500mg, single dose A second dose is necessary for heavy infection

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Intestinal Nematodes 

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Egg reduction rate as a parameter for cure is difficult because eggs are hardly found in stools Epidemiology Mode of Transmission: o Hand-to-mouth transmission: most common o Inhalation of airborne eggs in dust o Retroinfection through anus Enterobiasis is the only intestinal nematode condition that cannot be controlled through proper sanitary disposal of feces because eggs are deposited in perianal region Local prevalence o 29% among school children from exclusive private schools o 56% among those from public schools Local prevalence higher in females than males Collected from fingertips and fingernails of school children Adult female worms migrate to perianal area even during daytime but more migration occurs at night

Femal e

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Prevention and Control All members of household who are positive should be treated At least 7 consecutive post-treatment perianal smears using scotch-tape swab method should be negative to declare negative infection Personal hygiene Cut fingernails short Bed linens and clothing of infected persons sterilized by boiling

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2.2mm x 0.04mm Colorless, semitransparent with a finely striated cuticle Slender tapering anterior end and a short conical pointed tail Short buccal cavity with four indistinct lips Uteri with single file of 8-12 thinshelled, transparent, segmented ova Long, slender esophagus extends to the anterior fourth of the body Intestine is continuous Subterminal anus Vulva located 1/3 of body from posterior end

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Gubernaculu m but no caudal alae

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1mm x 0.06mm Smaller than parasitic female With muscular doublebulbed esophagus Intestine is a straight cylindrical tube

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Strongyloides stercoralis Causes Strongyloides, Cochin-China Diarrhea, threadworm infection Epidemiology: infections run parallel with hookworm infection Infective stage: filariform larvae via skin penetration Parasite Biology

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Adults Male

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PARASITIC  None

FREE LIVING  0.7mm x 0.04mm  Smaller than female  With ventrally curved tail, 2 copulatory spicules

Figure 20. (L) Free-living adult male S. stercoralis with spicules (red arrow) (R) Free-living adult female with row of eggs inside the body .

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Rhabditiform larvae o 225µm x 16µm

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Intestinal Nematodes o o o

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Elongated esophagus with a pyriform posterior bulb Differs from hookworm rhabditiform larva in being slightly smaller and less attenuated posteriorly Also, shorter buccal capsule and a larger genital primordium

Filariform larvae o Infective stage o Non-feeding, slender, 550µm o Usually smaller than hookworm filariform larvae, with distinct cleft at tip of tail

Figure 23. Life cycle of S. stercoralis

Figure 21. (L) Rhabditiform and (R) Filariform larva of S. Stercoralis.

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Egg o Clear thin shell o Similar to egg or hookworm but is only 50-58µm x 30-34µm

Figure 22. (L) Eggs of S. Stercoralis.

Life Cycle

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Free-living cycle o The rhabditiform larvae passed in the stool  Molt twice and become infective filariform larvae (direct development)  Molt four times and become free living adult males and females that mate and produce eggs from which more rhabditiform larvae hatch

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Parasitic cycle o Begins when filariform larvae in contaminated soil penetrate the human skin -> lungs -> alveolar spaces -> bronchial tree -> pharynx -> swallowed -> small intestine o Duodenum: molt twice, become adult female worms o The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs, which yield rhabditiform larvae o The rhabditiform larvae can either be  passed in the stool (free living), or  cause autoinfection o In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either:  the intestinal mucosa (internal autoinfection) or  the skin of the perianal area (external autoinfection) o Autoinfection in humans with helminthic infections:  Strongyloides stercoralis  Capilaria philippinensis only *Strong Capi (coffee)

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Intestinal Nematodes o

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Mode of infection: skin penetration (filariform larvae)

Pathogenesis and Clinical Manifestations Filariform larvae o Skin penetration, petechial hemorrhage, congestion and edema, pruritus o Lungs -> pneumonitis (cough), lobar pneumonia, pleural effusion Filariform and adult o Intestine -> GIT disturbances o Stool: watery mucous, diarrhea depends on intensity of infection, duration, host-tissue reaction (encapsulate the worms) Blood Picture o Leukocytosis (WBC = 25,000) o Eosinophilia (40%) Three Phases of Infection 1. Invasion of the skin by filariform larvae o Erythema o Pruritic elevated hemorrhagic papules 2. Migration of larva through body o Lungs are destroyed -> lobar pneumonia with hemorrhage 3. Penetration of the intestinal mucosa by adult female worms o Pylorus to rectum o Greatest number in duodenum and jejunum Intensity of infection o Light infection  no intestinal symptoms; good prognosis o Moderate infection  diarrhea alternating constipation o Heavy infection  Intractable, painless, intermittent diarrhea (Cochin China diarrhea) -> numerous episodes of watery and bloody stool o High mortality rates for moderate and heavy infections Diagnosis Direct or Concentration Methods o Finding rhabditiform larvae in feces or duodenal aspirate  Eggs only obtained by drastic purge/NGT duodenal aspirates  Eosinophilia as a clue Harada mori culture o For use in field Baermann funnel, Beales’s string Test, Duodenal aspiration, Small bowerl biopsy Serology

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Not useful in endemic areas Strongyloides cross react with filarial worm antigens Culture technique o Practical, low cost, recommended for mass screening and individual diagnosis o o

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Epidemiology Found throughout the world with same distribution pattern as hookworms More of a fecally-transmitted worm than soil-transmitted helminth because it is infective shortly after passage with the feces Low local prevalence More frequently found among male children 7-14 years old than among females and adults Prevention and Control Proper waste disposal Protection of the skin from contact with contaminated soil Early detection and treatment of cases Capilaria philippinensis Family Trichuroidea o Thin filamentous anterior end and slightly thicker and shorter posterior end Adults have subterminal anus Parasite Biology Adult o Female  2.3-5.3mm  Esophagus has rows of secretory cells (stichocytes)  Entire esophageal structure (stichosome)  Vulva at the junction of anterior and middle third o Male  1.5-3.9mm  Spicule 230-300µm long and has unspined sheath  Chitinized spicule and a long spicule Egg o Peanut-shaped with striated shells, flattened bipolar plugs o 36-45µm x 20µm o Passed in feces, embryonated in soil or water o In water, ingested by freshwater or brackish water fish

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Intestinal Nematodes Hyperinfection: massive number of adult worms 7. Definitive natural hosts: migratory fisheating birds Pathogenesis and Clinical Manifestations Sypmtoms: o abdominal pain, o gurgling stomach (borborygmus) o chronic diarrhea o weight loss, malaise o anorexia o vomiting o edema  Lab findings: o sever protein-losing enteropathy o malabsorption of fats and sugars o decreased excretion of xylose o low electrolyte (K+) levels o high IgE levels  Histology o Flattened and denuded villi o dilated mucosal glands o lamina propria infiltrated with plasma cells o lymphocytes, macrophages, neutrophils  No invasion of intestinal tissue but with micro-ulcers in epithelium and compressive degeneration and mechanical compression of cells

 Figure 24. Egg of C. philippinensis in an unstained wet mount of stool.

Life Cycle

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Figure 23. Life cycle of C. philippinensis

1.-2. Unembryonated eggs passed in stool become embryonated externally 3. Ingested freshwater fish -> larvae hatch -> penetrate intestine -> migrate to tissues 4. Humans ingest raw or uncooked fish -< infection by infective 3rd stage larvae -> inhabit jejunum 5. Adults burrow in mucosa where females deposit embryonated eggs 6. Autoinfection o Some become embryonated and releases larvae in the intestine ->

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Diagnosis Finding rhabditiform larvae o Feces or duodenal aspirate direct or concentration methods Eggs only obtained by drastic purge/NGY duodenal aspirates Treatment Electrolyte replacement and high protein diet Anti-diarrheal agents Antihelminthic drugs o Albendazole  400mg once daily for 10 days  Preferred as it destroys larvae more readily o Mebendazole  200mg twice daily for 20 days Epidemiology 1967-1968 epidemic: 1,000 cases with almost 100 deaths In Northern Luzon, Zambales, South Leyte, Compostela Valley, Zamboanga del Norte Compostela Valley Province (1998): “mystery disease” that causes death of villagers due to misdiagnosis

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Intestinal Nematodes   

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Only intestinal nematode with Bagsit fish as intermediate host Also found in Thailand, Iran, Japan, Egypt, Korea, Taiwan, and India Transmission by eating uncooked small freshwater/brackish water fish Prevention and Control Discouraging people from rural areas to eat raw fish Good sanitary practices Education Infected people: treated quickly and feces disposed properly

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