APHASMIDS

Subclass ADENOPHOREA  Encyst/develop only in striated muscle

  Reduced/Absent caudal papilla 
 Excretory system are without lateral canals 
 Most important distinguishing characterisic: 
ABSENT caudal chemoreceptor
 Even with the prior 2 properties but with the 3rd, it
would still be considered an aphasmid
diaphragm, laryngeal, abdominal,
 psoas,pectoral, deltoid, gluteus, biceps 
 Liberated from female worm after 4-16 weeks 
 No egg stage, born larva 

 Migrates until it finds its permanent
habitat: SKELETAL MUSCLE 

 When it migrates, it can be trapped to other
parts of the body, where they eventually die 

Trichinella spiralis REPRODUCTION

 After mating, males are dislodged from the mucosa,
  Trichina worm  and die afterwards (males mate only ONCE) 

 “dead end alley”  infection cannot be  Female burrows deeply in the mucosa (duodenum
 transmitted from human to human   to cecum) 
  Trichinosis, Trichiniasis   Female DIES after passing the larva 
  Discovered at autopsy in London   Affects small to upper part of large intestine 
 Parasite carnivorous/omnivorous animals (cats,
 dogs, hogs,rats)  INFECTIVE STAGE: Encysted Larva
 Not actually a parasite to humans  MODE OF TRANSMISSION: Ingestion of infected muscle
 Human: accidental host  with encysted larva

MORPHOLOGY LIFE CYCLE:

o ADULT  Ingestion of improperly cooked infected meat/pork
  Male measures 1.6x0.04mm  which has an encysted larva excyst in the upper
 Female measures 3.5x0.6mm (BIGGER)  small intestine  release of larva invasion of
intestinal mucosa (small and upper part of large
intestine)  maturation in 18-24 hours (sex
differentiation; by this time they are already mature)
 adult migrate encapsulation and deposition in
the muscle  larva dies and calcifies 
 It causes no symptom once it is in the muscle 

 It is encapsulated in the muscle and eventually
dies there 

Female Male

 With STICHOSOME (Stichocytes) sensory organ;

 nerve cell  only in T. spiralis
  With esophagus 
 Mouth bears protrusible stylet (only protrudes
 when eating) 
  With single testis and ovary 
 May be mistaken for Strongyloides due to
 its thread-like structure 
 Presence of stichosome is the
 differentiating characteristic 
 Stichosome – cell, a substitute receptor organ
 due to their lack of a phasmid 
 Stichocytes – group of cells/stichosomes 
o LARVA
 At birth: 120x5.6
 microns 
 In the muscles: PATHOLOGY
 1300x40 microns   Depends on
 Maybe lodged in o Number of worms
various foci
(brain, heart,
body cavities)  Page 1 of 4
© palindrome.2012

o Size and age of patient
 Thin individuals
harbor as much parasite 
o Tissues invaded
o General resistance of patients
 Five larva/gram of body muscle = patient will die 
PHASES OF THE DISEASE
 Incubation and Intestinal Invasion (during which
they excyst)
o Diarrhea/constipation
o Vomiting
o Abdominal cramps
o Nausea
 Larval migration and Muscle invasion 
o Fever
o Pain
o Weakness
o Facial edema (face has very small
muscles so when larva attaches here,
inflammatory reaction occurs)
 Encystment and Encapsulation 
o Disappearance of all symptoms
o Most cases are not treated because
signs and symptoms disappear without
medications
DIAGNOSIS (false positive result is more likely)
 Muscle Biopsy – MOST DEFINITIVE
o Taken within the group of muscles
they primarily thrive in
 Serological Test: ELISA 
o Bachman intradermal test
o BFT Bentomite Flocculation Test
o Beck’s Xenodiagnosis
TREATMENT
 Thiabendazole
o Expels the adult worm
o No effect on larva
 Mebendazole  BETTER
o Kills the larva
o Used for 2 weeks
 DOC: Both 
 Better DOC: Mebendazole 
Trichuris trichiura
Common Name: WHIPWORM
MORPHOLOGY
o ADULT
 Flesh colored 
 Fleshy posterior end 
  With ventral bacillary band 
 Male: 3.5-5mm (BIGGER)
 Female: 3-4mm 
APHASMIDS
 BACILLARY BAND: distinguishing factor from
cannot  other Aphasmid 
 With Esophagus, Intestine, and
 Reproductive organs 
 With a sheathed single spicule 
o EGG
  Barrel/Lemon/Football shaped/Japanese latern 
 With a prominent dome shaped bipolar
 mucus plugs on both ends 
 Triple sheathed
 (thick shell) 
 Measures 54x23
 microns 
 Passed in the feces
in fertilized
unsegmented stage 
  Requires 10-14 days from embryonation in the soil 
 Requires moisture (humid soil) 
 Fertilization takes place inside the body 
o LARVA
 Developed after ingestion of eggs 
 Hatches in the small intestine 
 Enters the crypts of the colon 
 Grows with an adult worm in 3 months 

 Small and large intestines both affected 
 Grow to adulthood in colon 
 Hatch in the intestines 
 Do not invade colon, just hang there 
INFECTIVE STAGE: Fully embryonated egg
DIAGNOSTIC STAGE: Fertilized
Egg Permanent Habitat: Colon
Mode of Infection: Ingestion of fully embryonated egg
LIFE CYCLE
 Eggs in soil (embryonated in 2-3 weeks) ingestion
of embryonated egg (infective stage)  stays in the
small intestine for 3-10 days  goes down to the
colon (habitat)  maturation to adult  eggs in
 feces  eggs in soil 
 No intermediate host, only between soil and man 
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 APHASMIDS

o More than 50 eggs/smear

heavy infection
 Protoscopy of Rectal Mucosa 

TREATMENT
 Mebendazole – DOC (100mg; 2x/day for 3 days) 
 Pyrantel pamoate - alternative 

Capillaria Philippinensis

 Common Name: PUDOC WORM 

 Disease: Intestinal capillariasis 
 Discovered in Ilocos Norte, Philippines 
  Native in the Philippines
MORPHOLOGY 
 ADULT 
o Lives in the mucosa of the small
intestine (jejunum)

LIFESPAN
 3,000-10,000 eggs/day per female worm 
 Lifespan: 4-6 years (longest lifespan among o Male:2.3-3.2 mm
aphasmids) o Female: 2.5-4.3 mm (BIGGER)
o Males have an extraordinarily long
PATHOLOGY spicular sheath
 Mechanical (colonic wall)  EGGS
o Trauma/irritation o Pass in the feces
o Obstruction o Embryonate in 10-
 Not more of invasion  14 days
 Due to bolus of worm  o Developed into

 Intestinal obstruction (Colon)  infective stage in
 Allergic  the fish
o Presence of eosinophils o Typical capillaria egg
o Presence of Charcot-Leyden Crystals  Yellow egg
(urine)  Moderately thick shelled with
striations
SYMPTOMATOLOGY  With flattened bipolar plug (-)
 Abdominal cramps and pain  mucus
 Blood streaked stool (trauma to mucosal layer)   Peanut shaped measures
 42x20 microns
 Hypochromic anemia (colon cannot
 With 2 segmented stages
 absorb nutrients) 
 Diarrhea (water absorption largely affected in
o Atypical capillaria egg
the colon) 
 Thin shelled
 Weight loss (due to diarrhea) lack of nutrient
 Without bipolar plugs
 intake
 With segmentation
 Mental problem (misdiagnosed in a psych patient); Embryonated

 (imbalance of nutrients) 
 Rectal prolapsed (also in E. vermicularis) 
INTERMEDIATE HOST: Freshwater fish (If man defecates in
the river or infected soil gets into the river)
DIAGNOSIS
INFECTIVE STAGE: Larva
 Demonstration of eggs in the feces 
MODE OF TRANSMISSION: eating of infected fish with larva
 Direct fecal smear  stage
o Less than 10 eggs/smear  DIAGNOSTIC STAGE: typical and atypical eggs (infective stage
light infection in fish) in the feces
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 INTESTINAL NEMATODES
APHASMIDS
Note: Italicized text were taken directly from the manual

LIFE CYCLE
 Eggs in feces  passed to the water  eaten by
freshwater fish  embryonation  larval
formation  man eats infected fish  develop
in the adult  matures and lays eggs  eggs in
the feces 
  Primary resides in the JEJUNUM
 Embryonation takes place in the body of the fish 


SYMPTOMATOLOGY
 Intestinal malabsorption (OUTSTANDING SIGN)
 Severe fat malabsorption (very fatty stool) 
  Fluid and electrolyte losses 
 Free passage of plasma protein 
 Abdominal pain and distention 
 Cachexia and emancipation 

*Of all Aphasmids, Capillaria has the WORST symptoms

TREATMENT:
 Mebendazole

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© palindrome.2012