Intestinal Nematodes

Lecturer: Mark M. Calban, RMT, MD, MPM | April 11, 2021

Trans by: Azurin, Columna, Lugo, Quirino, Tumamao

OUTLINE Morphology
I. Phylum Nematoda H. Anisakis simplex  Adult worms
A. Ascaris lumbricoides I. Ancylostoma caninum  Creamy white to pinkish yellow when freshly expelled.
B. Trichuris tichuria and Ancylostoma  The head is provided with 3 lips and a small triangular
C. Strongyloides braziliense buccal cavity.
stercolaris J. Angiostrongylus  Gifted with three (3) lips
D. Trichinella spiralis cantonensis  The three lips and sensory papillae are seen at anterior
E. Capillaria philippinensis II. Review Questions end.
F. Enterobius vermicularis III. References  The margin of each lip is lined with minute teeth which
G. Toxocara canis are NOT VISIBLE at this magnification
Table 1. Male and Female Morphology
I. PHYLUM NEMATODA MALE FEMALE
 True roundworms Characteristics
 Unsegmented, elongated, cylindrical  Smaller and slender  Tapered at both ends large
 Sexes are separate  Curved posteriorly  Paired reproductive organs
 Females are larger than males  Single tortuous tubule in posterior 2/3 (22-35cm
 Egg stage, 4 larval stages, adult  Equipped with copulatory long)
 Class Phasmidia/Aphasmidia spicule (10-31 cm)
Table 1. Phasmidia vs. Aphasmidia
PHASMIDIA APHASMIDIA
Small Intestine
Ascaris Lumbrocoides Trichinella spiralis
Necator americanus Capillaria philippinensis
Ancylostoma duodenale
Ancylostoma ceylanicum
Strongyloides stercoralis
Large Intestines
Enterobius vermicularis Trichuris trichiura
Filariasis
Wuchereria bancrofti Cross Section
Brugia malayi
1. Cuticle and hypodermis 1. Cuticle and hypodermis
Larva Migrans 2. Longitudinal muscle layer 2. Longitudinal muscle layer
Ancylostoma braziliense 3. Vas deferens 3. Ovary
Ancylostoma caninum 4. Testis 4. Oviduct
Angiostrongylus cantonensis 5. Lateral line with excretory 5. Uterus
A. ASCARIS LUMBRICOIDES canal 6. Intestine
 Common name: 6. Intestine
 “Large Intestinal Roundworm” 7. Pseudocoelom
 Giant roundworm
 Disease Caused: Ascariasis
 The most common helminth Infection
 Highest prevalence in Tropical and Subtropical regions
 70% from Asia
 Most common Intestinal Nematode of Man
Characteristics
 Soil Transmitted Helminth (STH)
 A Disease of Poverty
 Impairment of Cognitive performance and growth in children.
 Reduce work capacity and productivity in adults.
 Polymyarian Type of Somatic Muscle
 Arrangement.
 Final Host: Man;
Habitat: Small Intestine
 Diagnostic Stage: Ova
(fertilized/unfertilized)
 Infective Stage:
Embryonated Ova
 MOT: Ingestion
 Portal of Entry: Mouth

Figure 2. Ascaris lumbricoides: Male (Top) and Female (Bottom)

Figure 1. Ascaris lumbricoides

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Table 2. Infertile eggs vs. Fertile eggs of A. lumbricoides  Penetration of worms to intestinal wall
INFERTILE EGGS FERTILE EGGS  Intestinal volvulus
88-94 um x 39-44um 45-70um x 35-50um  Intussusception
Longer and narrower Shorter and wider  Obstruction – secondary to continuous pricking of adult
Thin shell and irregular Thick transparent hyaline shell worms for food > IRRITATE NERVE ENDINGS > Intestinal
mamillated coating filled with with a thick outer layer + spasm
refractive granules vitelline, lipoidal inner Pathology
membrane (highly impermeable)
 Reactions of tissues to invading larvae.
Difficult to identify Outer, coarsely mamillated
 Irritation of the intestine by the mechanical and toxic action of
albuminous covering which
the adult.
maybe absent or lost in
decorticated eggs  Complications arising from the parasite’s extra intestinal
migration.
Table 3. Intestinal phase vs. tissue phase
INTESTINAL PHASE TISSUE PHASE
Intestinal or appendix With heavy or repeated
obstruction results from infection, pneumonia, cough,
Layers: migrating adults in heavy low-grade fever, and 30% to
1. Outer – Mamillary Coat infections. 50% eosinophilia (Löffler’s
2. Middle – Glycogen layer a. Vomiting and abdominal syndrome)
3. Inner – Vitelline Layer pain result from adult Result from migration of larvae
Life Cycle migration. through the lungs (1 to 2
1. Infective stage: Eggs embryonate in soil by one month b. Protein malnutrition can weeks after ingestion of eggs).
2. Method of infection: Infective egg (embryonated egg) occur in children with heavy Allergic asthmatic reaction
containing fully developed larva, is ingested by human infections and poor diets. may occur with reinfection
3. Larva which escapes from egg in small intestine bores into c. Some patients are
tissues and reaches the lymphatic vessels or the venules and asymptomatic.
finally the lungs LARVA ADULT
4. Further development and growth take place in the alveoli Ascaris pneumonitis / Diarrhea
5. Larva from the lung pass on to the intestine by way of trachea, Loeffler’s Syndrome
esophagus and stomach and develop to maturity DOB, Cough, Fever, Lung Malnutrition
6. Adult A. lumbricoides is present in small intestine Infiltration
7. Diagnostic stage: Unfertilized egg passed in feces May become erratic Villous Atrophy
Worm Bolus/Obstruction
 Associated infections:
 Moderate Infections: Lactose Intolerance
 Heavy Infections: Bowel Obstruction
 The major damage occurs during larval migration rather than
from the presence of the adult worm in the intestine.
 The principal site of tissue reaction is the lungs, where
inflammation with an eosinophilic exudate occurs in response
to larval antigens (Loeffler’s Syndrome)
 Because the adults derive their nourishment from ingested
food, a heavy worm burden may contribute to malnutrition,
especially in children in developing countries.
 Complications from intestinal obstruction are caused by
tangling of the large worms or migration of adults to other sites,
such as the appendix, bile duct, or liver (detectable by
radiograph).
 Migrating adults may exit by the nose, mouth, and anus.
Laboratory Diagnosis
 Direct fecal smear
Figure 3. Life cycle of A. lumbricoides
 2mg of feces + 1drop NSS
 Migration Phase: 7-10 days  LPO/ MPO
 High fever  Kato techniques
 Eosinophilia  20-60 mg feces
 Prepatent period: 6-70 days  Qualitative tech, MASS examination
 Erratic Migration:  Kato katz technique
 Gallbladder  Quantitative
 Liver  Egg counts/ gram feces
 Nostrils  Determine egg reduction after treatment
 Trachea  Determine intensity of ascaris infection
 Appendix Treatment
 Pancreas
 Albendazole
 Follows intestinal bacteria – Abscess
 Mebendazole
 Lung Migration:
 Pyrantel pamoate
 Lung Infiltration
 Ivermectin
 Asthmatic Attacks
 Pulmonary Edema Prevention
 Vague Abdominal Pain – most frequent complaint  Handwashing

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 Proper disposable of human wastes Life Cycle
 Health education 1. Infective Stage: Eggs embryonate in soil by one month
 Mass chemotherapy 2. Method of Infection: Infective egg (embryonated egg)
B. TRIHURIS TICHIURA containing fully developed larva, is ingested by human
 Whipworm 3. Larvae hatch in small intestine
 Disease Caused: Trichuriasis 4. Penetrate and develop in intestinal villi
 Cousin of Ascaris 5. Return to lumen and go to cecum
 Habitat: Large Intestine 6. Larvae mature
 Final Host: Man 7. Adults live in colon: Anterior portion embeds in mucosa by
spear-like projection
 Portal of Entry: Mouth
8. Diagnostic Stage: Unfertilized eggs in feces
 Holomyarian Type of Muscle Arrangement
Morphology
Table 4. T. Trichiura Adult and Egg Morphology
MALE WORM FEMALE WORM
Characteristics
 30-45 mm  35- 50 mm
 3,000-10,000 eggs/ day
 60 million eggs/2 years

 Coiled posterior with a single  Buntly rounded posterior

spicule and rectractile sheath end
 Attenuated anterior 3/5 traversed by a narrow esophagus
resembling string of beads
 Robust post 2/5- contains the intestines and single set of
reproductive organs
 Habitat: Large intestine (CECUM)
 Anterior 2/3- attenuated and thin
 Posterior 1/3- fleshy and robust

Figure 4. Life cycle of Trichuris Trichiura

Pathology
 Persons with slight infections are asymptomatic
 Ulcerative Colitis in children
 Inflammatory Bowel Disease in Adults
 Histology: Eosinophil Infiltrations
 No Decrease in Goblet Cells
Symptoms
 Bloody or Mucoid Diarrhea
 Weight Loss and Weakness
 Abdominal Pain and Tenderness
 Rectal Prolapse
 Gross Blood in stool and Stunting
 Enterrorhagia, RECTAL PROLAPSE (increased peristalsis that
occurs in an effort to expel the worms), Appendicitis
EGGS
 NOT cause significant anemia, unlike the hookworms.
 50-54 um x 23 um
 Lemon shape with plug- like translucent polar prominences  Differ from Ascaris: No heart & Lung migration
 Bipolar plug Notes:
 Football shape Adult worms
 Barrel- shaped  Live in the cecum and ascending colon.
 With Hyaline polar plug  Anterior portion is threaded into the mucosa.
 Transparent inner shell and yellowish outer because of bile
 Female worms shed between 3,000 – 20,000 eggs/day
contact
 More susceptible to dessication as Ascaris
 Lifespan is 1 year
 Embryo: Unicellular; undeveloped

Figure 5. Rectal Prolapse

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Laboratory Diagnosis Table 6. Male and Female Morphology of Strongyloides stercoralis
 Direct fecal smear Male Worm Female Worm
 2mg of feces + 1drop NSS 0.7mm x 0.04mm 1mm x 0.06mm
 LPO/ MPO (+) muscular double bulbed
 Kato techniques esophagus
 20-60 mg feces Ventrally curved tail, 2 Intestine is a straight cylindrical
copulatory spicules, tube
 Qualitative tech
gobernaulum but NO
 MASS examination
CAUDAL ALAE
 Kato katz technique
 Quantitative
 Egg counts/ gram feces
 Determine egg reduction after treatment
 Determine intensity of ascaris infection
Treatment
 Mebendazole
Prevention
 Handwashing
 Proper disposable of human wastes Figure 7. S. stercolralis parasitic female
 Health education
Life Cycle
 Mass chemotherapy
1. Infective Stage: Infective third-stage larvae (Filariform)
C. STRONGYLOIDES STERCORALIS 2. Method of infection: Larvae penetrate skin, enter lumpatics
 “Threadworm,” Cichin China Diarrhea or blood
 Rhabditiform Larvae - Free Living form, Diagnostic Stage 3. Migrate to lungs via bloodstream
 Filariform Larvae – Parasitic Form, Infective Stage 4. Larvae break out of lung capillaries into alveoli
 Smallest Nematode of Man 5. Travel to bronchioles, coughed up to pharynx, swallowed,
 Final Host: Man; Habitat: SI return to intestine
6. Larva mature to adults
 MC Intestinal Nematode of Man 7. Adult in mucosa of small intestine parthenogenic parasite
Epidemiology female only (no male)
 More of a focally transmitted worm than a soil transmitted 8. Eggs hatch in mucosa
helminth because it is infective shortly after passage w/ the 9. Diagnostic Stage first-stage larvae (rhabditiform,
noninfective) in feces
feces.
10.1 Indirect (Heterogenic) development: Molts 4 times
Morphology  Lives in soil and rapidly develops to free-living
Table 5. Filariform Larvae vs. Rhabditiform Larvae of S. Stercoralis nonparasitic adults
FILARIFORM LARVAE RHABDITIFORM LARVAE  Eggs
2.2mm x 0.04mm 225um x 16um  Rhabditiform larvae
Colorless, semi- transparent (+) elongated esophagus with a 10.2 Autoreinfection: larvae develop to infective stage in intestine
with a finely striated cuticle pyriform posterior bulb
Slender tapering anterior end Si smaller and less attenuated
and a short conical pointed tail posteriorly (diff from hookworm)
Short buccal cavity has 4 Shorter buccal capsule and
indistinct lips larger genital primordial
Vulva is located 1/3 the full
length of the body from the
post end

Figure 8. Strongyloides stercoralis Life Cycle

Phases of Infection
 Invasion of the skin by filariform larvae:
 Erythema
 Pruritic
 Elevated hemorrhagic papules
 Migration of larvae through the body:
 Lungs are destroyed causing LOBAR PNEUMONIA with
hemorrhage
 Penetration of the intestinal mucosa by adult female worm:
 Duodenum and Upper Jejunum
Pathology and Symptoms
 Major clinical features are
 Abdominal pain
Figure 6. Tail (filariform larvae). (A) Strongyloides stercoralis, (B) hookworm  Diarrhea

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  Urticarial with eosinophilia  In very heavy infections, eggs (less common), larvae (both
 Skin shows recurring allergic, raised, itchy, red wheals from types), and adult worms may be recovered in the stool.
larval penetration.  If agar plates are used (culture, method of choice), they must
 Migration of larvae: be dried sufficiently to eliminate free water on the agar prior to
 Primary symptoms are in the lungs use.
 Bronchial verminous (from worms) pneumonia.
 Intestinal symptoms
 Abdominal pain
 Diarrhea
 Constipation
 Vomiting
 Weight loss
 Variable anemia
 Eosinophilia
 Protein-losing enteropathy.
 Light infections are often asymptomatic; gross lesions are
usually absent.
 The bowel is edematous and congested with heavy
infection.
 S. stercoralis has caused sudden deterioration and death in
immunocompromised persons because of heavy
autoinfection and larval migration throughout body Figure 10. Eggs of Strongyloides stercoralis: Clear, thin, shell, similar to those
of hookworms (50x58um by 30-34um)
(hyperinfection), with bacterial infection secondary to larval
spread and intestinal leakage. Treatment
 Associated symptoms:  Albendazole
Light infection No intestinal symptoms
Prevention
Moderate Diarrhea with alternating constipation
Heavy Intractable  Similar to those of hookworm
Painless  Handwashing
Intermittent diarrhea (Cochin China  Proper disposable of human wastes
Diarrhea) characterized by numerous  Health education
episodes of watery and bloody stools  Mass chemotherapy
Complications Edema D. TRICHINELLA SPIRALIS (TRICHINA WORM)
Emaciation
 Trichinella spiralis spiralis- Temperate regions
Loss of appetite
 Trichinella spiralis nativa- Arctic regions
Anemia
Lobar pneumonia  Trichinella spiralis nelson- Africa
Malabsorption leading to cachexia Epidemiology
 Trichinosis occurs worldwide, especially in Eastern Europe
and West Africa.
 Related to eating home prepared sausage, usually on farms
where the pigs are fed uncooked garbage.
 Disease occurs primarily in hunters who eat undercooked
PORK.
Morphology
Table 7. Morphology of Trichinella spiralis
Adult Female Adult Male
Size: 4x0.5mm 2x0.04mm
Blunt, round posterior end; Curved posterior end with
single ovary with vulva in two rounded appendages
anterior fifth of body
Thin anterior end
Figure 9. Skin symptoms of Strongyloides stercoralis from larval penetration
Small mouth
Laboratory Diagnosis Long slender digestive tract
 Recovery of the rhabditiform (noninfective) larvae is
normally from the stool concentrate.
 Caution: Filariform (infective) larvae can also be
recovered in the stool.
 A minimum of four (4) stools are recommended before
indicating that the patient is not infected (routine formalin,
ethyl acetate sedimentation concentration);
 If the stool specimens are negative, examination of duodenal
contents is recommended (duodenal aspirates, Entero-Test
capsule); however, the overall sensitivity of the method varies.
 Eggs: Clear, thin, shell similar to those of hookworm
 Various concentrates (Baermann) and cultures (Harada-Mori,
petri dish) can also be used for larval recovery.
 Eggs are rarely seen in the stool but may be recovered from
duodenal contents. Figure 11. Adult Trichinella spiralis: (A) Male; (B) Female

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 Encysted Larvae  +++ cardiac and CNS disease
(+) Spear-like burrowing anterior tip  Cause of death: CHF and Respiratory paralysis
900-1300 x 35-40um Method of Diagnosis
Diagnostic Criteria
 Identification of encysted larvae in biopsied muscle;
 Serologic testing (ELISA) 3 to 4 weeks after infection.
 A history of eating undercooked pork or bear
 Fever, muscle pain, bilateral periorbital edema, and rising
eosinophilia

Figure 12. Encysted larvae of T. spiralis

Life Cycle
1. Method of Infection and Infective Stage: Ingestion of
undercooked, striated muscle containing encysted larvae in
pork, deer, walrus, bear, etc.
2. Tissue digested and larvae freed in intestine
3. Rapidly mature to adults in about 3 days
4. Adults in intestine
5. Female in submucosa releases larvae, which disseminate via
bloodstream
6. Diagnostic Stage: larvae encyst “nurse cells” in striated
muscle
Phases and Stages of Infection
1. Enteric Phase or Incubation and Intestinal Invasion
 Like an attack of acute food poisoning including d/a or
constipation, vomiting and abdominal cramps, malaise
and nausea
2. Invasion Phase or Larval Migration and Muscle Invasion
 Severe Myalgia, periorbital edema and eosinophilia, high
remittent fever, dyspnea, dysphagia, difficulty of chewing,
paralysis of the extremities, gastric and intestinal
hemorrhages, pericardial effusion, CHF, meningitis,
ocular disturbances
3. Convalescent Phase or Encystment and Encapsulation Figure 13. Diagnostic Criteria for T. spiralis
 Fever, weakness, pain Laboratory Diagnosis
Major Pathology and Symptoms  Based on history of exposure and PE
1. Intestinal phase shows small intestine edema and  Muscle biopsy reveals larvae within striated muscle
inflammation, nausea, vomiting, abdominal pain, diarrhea,  Done after 7 days
headache, and fever (1st week after infection).  Diaphragm, pectoral, gluteus deltoid. Biceps,
2. Migration phase shows high fever (104 F), blurred vision, gastrocnemius
edema of the face and eyes, cough pleural pains, and  Bentonite Flocculation Test
eosinophilia (15% to 40%) lasting 1 month in heavy infection;  Positive 3 weeks after infection
death can occur during this phase in 4th to 8th week after  Biochemical Tests:
infection.
 INCREASE CPK, LDH and MYOKINASE LEVELS
3. Muscular phase shows acute local inflammation with edema
 Peripheral Eosinophilia
and pain of the musculature. Other symptoms vary depending
on the location and number of larvae present. Larvae encyst  IFAT and ELISA
in skeletal muscles of limbs, diaphragm, and face, but  Beck’s Xenodiagnosis
they invade other muscles as well. Weakness and fatigue KEY POINTS:
develop. 1. The history and clinical findings may suggest possible
4. Focal lesions show periorbital edema, splinter trichinosis (consumption of rare or raw infected meat).
hemorrhages of fingernails, retinal hemorrhages, and Remember to check hematology results for a possible
rash. eosinophilia (can reach 50% or higher).
 Pigs are the most important reservoirs 2. Using compression slides, examination of suspect meat
 MOT: eating raw or undercooked meat containing encysted may reveal larvae (artificial digestion procedure) Note that
larvae in the muscle not all species of larvae form the capsule; however, the
 Small Intestine: larvae excyst and mature into adults unencapsulated larvae can still be seen in a “squash”
 Eggs hatch within the adult females, and larvae are released preparation of biopsy material.
and distributed via the bloodstream to many organs; 3. Larvae or adult worms are rarely recovered in fecal
 Striated muscle cells or “nurse cells,” they encyst within a specimens during the intestinal phase (diarrhea).
fibrous capsule and can remain viable for several years but 4. Examination of muscle tissue obtained at biopsy may
eventually calcify confirm the diagnosis (tissue compression between two
 HUMANS are the END STAGE HOSTS slides or the artificial digestion technique).
 Few days after eating undercooked PORK results to diarrhea 5. Serologic tests for antibody detection may be very helpful;
followed 1 to 2 weeks later by fever, muscle pain, periorbital coproantigen detection tests are being developed.
edema and eosinophilia. Treatment
 Subconjuctival hemorrhages are an important diagnostic  There is NO treatment for trichinosis
criterion  Bed rest and supportive treatment
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 Severe s/s: STEROIDS + MEBENDAZOLE
 THIABENDAZOLE is effective against the adult intestinal
worms early in infection.
Prevention
 The disease can be prevented by properly cooking pork and
by feeding pigs only cooked garbage.
E. CAPILLARIA PHILIPPINENSIS (PUDOC WORM)
Epidemiology
 1st recorded in Northern Luzon
 Natural Hosts: Migratory Fish, Eating birds
 The first proven case of human infection with Capillaria
philippinensis occurred in 1963 in a patient from the Philippines
who died 3 days after admission to the hospital with a diagnosis
of malabsorption syndrome.
 Although the significance was not recognized until 4 years
later, C. philippinensis eggs were found in the stools and
autopsy showed parasitism of the large and small intestines.
Morphology
Table 8. Morphology of adult Capillaria philippinensis
MALE WORM FEMALE WORM
1.5-3.9mm 2.3-5.3mm
Spicule: 230 – 300um, Vulva: at the junction of
unspined sheath anterior and middles thirds Figure 15. Life Cycle of C. spiralis
Thin filamentous anterior end and slightly thicker and shorter Pathogenesis
posterior end  Symptoms are related to the worm burden; with large numbers
Esophagus: rows of secretory cells called STICHOCYTES; entire of worms, there may be intestinal malabsorption and fluid loss
oesophageal structure is called STICHOSOME along with electrolyte and plasma protein imbalance.
Anus: subterminal  Most of the abnormality is found in the small intestine, where the
wall is thickened and indurated and contains many larval and
adult worms.
 Watery stools are passed (up to eight per day), with fluid loss of
several liters.
 Patients lose weight rapidly and develop muscle wasting,
abdominal distention, and edema.
 Death from pneumonia, heart failure, hypokalemia, or cerebral
edema may occur within several weeks to a few months.
 In some cases, patients reported chronic abdominal pain and
diarrhea over a period of many months prior to diagnosis.
 On gastroduodenoscopy and subsequent histology, the jejunal
mucosa revealed flattened villi, crypt proliferation, acute
inflammation, and eosinophilic granulomata.

Figure 14. C. philippinensis

Life Cycle
 Although the exact mode of transmission is unknown,
experimental infection is transmitted through small fish that
serve as the intermediate host; often, whole, small fish may be
ingested.
 Development to the infective stage in the fish takes at least 3
weeks.
 In areas of the Philippines where this infection occurs, people
also eat raw shrimp, crabs, and snails.
 They also tend to defecate in the fields or water where the fish,
shrimp, crabs, and snails are obtained, thus completing the life
cycle.
 The worms live burrowed into the mucosa of the small bowel,
mainly the jejunum.

Figure 16. Pathogenesis of C. spiralis

 Ulcerative and Degenerative Lesions:
 Malabsorption of fluid, CHON and electrolytes
 Histology:
 Flattened and denuded villi with dilated mucosal glands

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  Lamina propria infiltrated with plasma cells, lymphocytes,  Asymmetrical, elongated-ovoidal, planoconvex (D-Shaped)
macrophages, and neutrophils.  Shell is relatively thick and colorless 7 contains tadpole-like
 Eggs: larvae.
 Peanut-shaped with striated shells and flattened bipolar
plugs
 36-45um x 20um

Figure 20. Eggs of E. vermicularis

Life Cycle
Table 9. Life cycle of E. vermicularis
Transmission: Ingestion of embryonated
Figure 17. Eggs of C. spiralis egg or Inhalation of Eggs
Treatment Usual time to infective 4-6 hrs first stage larva in
 Electrolyte Replacement stage: egg
 High Protein Diet Larval Migration in None
 DOC: ALBENDAZOLE- 400 mg OD x 10 days Humans:
Habitat of Adult Worms: Cecum, Appendix,
Prevention
Rectum
 Adequate Cooking of Food especially fish Prepatent Period: 3-4 weeks
F. ENTEROBIUS VERMICULARIS Lifespan of adults: 1-2 months
 Common names: PINWORM, SEATWORM Infective Stage Embryonated egg
Morphology Diagnostic Stage Eggs on Perianal folds
 Oral end lacks a true buccal capsule. Pathogenesis
 CUTICULAR ALAR EXPANSION on the anterior end  ENTEROBIASIS/OXYURIASIS
(CEPHALIC ALAE) 1. Due to the attachment of adult worms – inflammation of the
 Prominent Esophageal Bulb intestinal mucosa
 Male: 2. Due to the migration of gravid females into the anus –
 2-5x0.1-0.2 mm female releases thousands of fertilized eggs on perianal skin
 Curved Tail and Single Spicule eggs develop into larvae causing pruritus ani or perianal
pruritus.
3. Due to the wandering adult worms – appendicitis, vaginitis,
endometritis, salpingitis, peritonitis, eosinophilic enterocolitis.
Laboratory Diagnosis
 GRAHAM’S SCOTCH TAPE SWAB or SWUBE TUBE
PROCEDURE
 D Shaped Ova with thin colorless cell wall
 Usually by seeing adults in perianum (best 2-3hr after the child
is asleep)
 Very few ova are seen in stool; so, not recommended
 Adhesive tape on perianal skin to collect eggs (90% in 3
consecutive samples) when px awakens in morning
Figure 18. Male E. vermicularis  Anal swabs (“swube tubes:” paddles coated with adhesive
 Female: material may also be used)
 8-13 x 0.4 mm; Long pointed tail Epidemiology
 Paired reproductive organs
 OTHER MOT: Inhalation, Retroinfection
 Geographical Distribution:Cosmopolitan
 Prevalence Rate in Phils: 10% in Rural,75% in Urban, 29% in
Schoolchildren
 Factors: overcrowding
 Poor personal and family hygiene
 Soil transmitted helminth
 Life Cycle is confined in humans
 Most common soil transmitted helminth in developed countries.
 A Cosmopolitan Worm.


Figure 19. Female E. vermicularis Treatment

 Eggs:  Pyrantel pamoate
 55x25 um
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 G. TOXOCARA CANIS Life Cycle
 Dog Ascaris or Dog Roundworm
 Causes:
 Visceral larva migrans – which occurs mostly in preschool
children, the larvae invade multiple tissues (commonly liver,
lung, skeletal muscle, occasionally heart) and cause various
nonspecific symptoms (e.g. fever, myalgia, weight loss,
cough, rashes, hepatosplenomegaly) usually accompanied
by hypereosinophilia.
 Ocular Toxocariasis = Ocular Larva Migrans + Uveitis +
Endophthalmitis
 Migration to the central nervous system (neurotoxocariasis or
neural larva migrans (NLM)) is uncommon and can cause
eosinophilic meningoencephalitis.
 Death can occur in instances of severe cardiac, pulmonary, or
neurologic involvement.
 In OLM, the larvae produce various ophthalmologic lesions, and
may cause diffuse unilateral subacute neuroretinitis (DUSN).
Involvement is typically unilateral (affecting one eye) and
associated visual impairment usually presents with uveitis,
retinitis, or endophthalmitis; permanent visual damage or
blindness can occur.
Life Cycle

Figure 22. Life Cycle of Anisakis simplex

I. ANCYLOSTOMA CANINUM AND ANCYLOSTOMA
BRAZILIENSE
 Dog and Cat Hookworm
 Causes Creeping Eruptions or Cutaneous Larva Migrans
 The most common manifestation of zoonotic infection with
animal hookworm species is cutaneous larva migrans (CLM),
also known as creeping eruption, where migrating larvae
cause intensely pruritic and erythematous serpiginous tracks in
the upper dermis, which may occasionally become bullous.
 These tracks may spread up to a few centimeters daily, and
secondary infections can develop following excessive
scratching.
 In some cases of diffuse unilateral subacute retinitis, single
Figure 21. Life Cycle of Toxocara spp. larvae compatible in size with Ancylostoma spp. have been
visualized in the affected eye.
H. ANISAKIS SIMPLEX
 Zoonotic roundworms Life Cycle
 Transmitted in raw seafoods
 Causes eosinophilic gastroenteritis
 Involves acute abdominal symptoms, usually within hours
after ingestion of larvae. This nonspecific abdominal distress
can be mistaken for other conditions such as peptic ulcers, food
poisoning, and appendicitis.
 Occasionally, the larvae are coughed up. If the larvae pass into
the bowel, a severe eosinophilic granulomatous response
may also occur 1 to 2 weeks following infection, causing
symptoms
 mimicking Crohn’s disease, and rarely, intestinal perforation
can occur.
 Rare cases of ectopic infection are known, in sites such as the
peritoneal cavity, mesentery, esophagus, and tongue.
 Most infections are self-limiting as larvae are unable to survive
for long periods in the human host, but the associated tissue
damage can cause longer lasting symptoms.
 Antigens that remain in the fish muscle after the larvae are killed
(e.g. after freezing) can cause allergic reactions in some
individuals. Figure 23. Life Cycle of Cutaneous Larva Migrans

Trans # 7 Intestinal Nematodes 9 of 13

 J. ANGIOSTRONGYLUS CANTONENSIS a. Ascaris lumbricoides
 RAT LUNGWORM b. Necator americanus
 Transmitted in undercooked seafoods c. Strongyloides stercoralis
 Eosinophilic meningitis – most notable symptom d. 2 of the above
e. NOTA
 Most common cause of Parasitic Meningitis 5. What parasite/s has a blood-lung phase in the life cycle?
 Somatic symptoms (e.g. headache, fever, malaise) as well as a. Ascaris
varying degrees of neurological dysfunction are usually noted. b. Entorobius
 A. cantonensis infection may occasionally prove fatal. Ocular c. Strongyloides
angiostrongyliasis is associated with uveitis, blurred vision, and d. 2 of the above
a substantial loss of visual acuity. e. NOTA
6. The encysted larva of the organism is the infective stage to
man?
a. Capillaria philippinensis
b. Trichinella spiralis
c. Ascaris lumbricoides
d. Trichuris trichura
e. NOTA
7. Ascaris Larvae may cause the following, except:
Figure 24. A. cantonensis
a. Pneumonia
b. Cough
Life Cycle c. Eosinophilia
d. Loeffler’s syndrome
e. NOTA
8. Produces autoinfection to man?
a. ANcylostoma braziliense
b. Entorobius vermicularis
c. Strongyloides stercoralis
d. AOTA
e. NOTA
9. The habitat is the small intestine?
a. Trichuris trichiura
b. Ascaris lumbricoides
c. Necator americanus
d. 2 of the above
10. A parasite with a Bipolar Plug?
a. Whipworm

Answers:
b. Pudoc worm

9D, 10A
1B, 2D,
3D, 4B,
5D, 6B,
7E, 8C,
c. Hookworm
d. NOTA

V. REFERENCES
 Dr. Calban PPT
Figure 25. Life Cyle of A. cantonensis

III. REVIEW QUESTIONS

1. An outbreak of mild intestinal distress, sleeplessness, perianal
itching, and anxiety has broken out among preschool children
in a private home. The most likely cause of this condition is
a. Trichomonas vaginalis
b. Enterobius vermicularis
c. Ascaris lumbricoides
d. Necator americanus
e. Entamoeba histolytica
2. You are working in a rural medical clinic in China and a 3-
yearold girl is brought in by her mother. The child appears
emaciatedand, upon testing, is found to have a hemoglobin
level of 5 g/dL. Her feet and ankles are swollen, and there is
an extensive rash on her feet, ankles, and knees. The most
likely parasitic infection that causes the child’s condition is
a. Schistosomiasis
b. Cercarial dermatitis
c. Cyclosporiasis
d. Hookworm infection
e. Trichuriasis
f. Ascariasis
3. The usual manner of transmission by the parasite is by skin
penetration?
a. Ascaris lumbricoides
b. Necator americanus
c. Strongyloides stercoralis
d. 2 of the above
e. none of the above
4. What parasite produces Iron deficiency anemia to man?
Trans # 7 Intestinal Nematodes 10 of 13
Trans # 7 Intestinal Nematodes 11 of 13
Trans # 7 Intestinal Nematodes 12 of 13
Trans # 7 Intestinal Nematodes 13 of 13