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APHASMIDS

Subclass ADENOPHOREA

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

Trichinella spiralis

Trichina worm
dead end alley infection cannot be
transmitted from human to human
Trichinosis, Trichiniasis
Discovered at autopsy in London
Parasite carnivorous/omnivorous animals (cats,
dogs, hogs,rats)
Not actually a parasite to humans
Human: accidental host

MORPHOLOGY
o ADULT

Male measures 1.6x0.04mm

Female measures 3.5x0.6mm (BIGGER)

REPRODUCTION

After mating, males are dislodged from the mucosa,


and die afterwards (males mate only ONCE)

Female burrows deeply in the mucosa (duodenum


to cecum)
Female DIES after passing the larva
Affects small to upper part of large intestine

INFECTIVE STAGE: Encysted Larva


MODE OF TRANSMISSION: Ingestion of infected muscle
with encysted larva
LIFE CYCLE:

Female

Encyst/develop only in striated muscle


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

Ingestion of improperly cooked infected meat/pork


which has an encysted larva excyst in the upper
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

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:
1300x40 microns

Maybe lodged in
various foci
(brain, heart,
body cavities)

PATHOLOGY
Depends on
o

Number of worms

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palindrome.2012

APHASMIDS
o

Size and age of patient

Thin
individuals
cannot
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
Becks 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

BACILLARY BAND: distinguishing factor from


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

MORPHOLOGY
o ADULT

Flesh colored

Fleshy posterior end

With ventral bacillary band

Male: 3.5-5mm (BIGGER)

Female: 3-4mm

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palindrome.2012

APHASMIDS
o

More than 50
heavy infection
Protoscopy of Rectal Mucosa

eggs/smear

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


aphasmids)
PATHOLOGY
Mechanical (colonic wall)
o Trauma/irritation
o
Obstruction

Not more of invasion

Due to bolus of worm

Intestinal obstruction (Colon)

Allergic
o
Presence of eosinophils
o
Presence of Charcot-Leyden Crystals
(urine)
SYMPTOMATOLOGY

Abdominal cramps and pain

Blood streaked stool (trauma to mucosal layer)

Hypochromic anemia (colon cannot


absorb nutrients)

Diarrhea (water absorption largely affected in


the colon)

Weight loss (due to diarrhea) lack of nutrient


intake

Mental problem (misdiagnosed in a psych patient);


(imbalance of nutrients)

Rectal prolapsed (also in E. vermicularis)


DIAGNOSIS

Demonstration of eggs in the feces

Direct fecal smear


o
Less than 10 eggs/smear
light infection

o
o
o

EGGS
o
o
o

Male:2.3-3.2 mm
Female: 2.5-4.3 mm (BIGGER)
Males have an extraordinarily long
spicular sheath
Pass in the feces
Embryonate in 1014 days
Developed into
infective stage in
the fish
Typical capillaria egg
Yellow egg

Moderately thick shelled with

striations
With flattened bipolar plug (-)

mucus
Peanut shaped measures

42x20 microns
With 2 segmented stages

Atypical capillaria egg


Thin shelled

Without bipolar plugs

With segmentation

Embryonated

INTERMEDIATE HOST: Freshwater fish (If man defecates in


the river or infected soil gets into the river)
INFECTIVE STAGE: Larva
MODE OF TRANSMISSION: eating of infected fish with larva
stage
DIAGNOSTIC STAGE: typical and atypical eggs (infective stage
in fish) in the feces

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palindrome.2012

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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