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APHASMID NEMATODES

Dr. Ayochok
*Phasmids =receptors located at anterior portion of
parasite

when encysted, digestive tract has the same level of


maturity with that of the adult
causes much of the pathology of Trichinosis

Subclass Adenophora (Aphasmid Nematodes)


reduced/absent caudal papillae (also fxn as
receptor)
no lateral excretory canal
esophageal area: cylindrical with esophageal
gland forming stichosome (composed of
stichocytes)
egg: unsegmented (FERTILIZED but
unembryonated/immature) with plug at either
pole
Order Trichinata
I. Trichinella spiralis
II. Trichuris trichuria
III. Capillaria philippinensis
! Note: in all the three, male adult worms are smaller with
coiled posterior ends.

Life Cycle

I. Trichinella spiralis

common name: Trichina worm

disease caused: Trichinosis or Trichiniasis


Morphology
1. Adult worms

anterior end: w/ protrusible stylet inside the


papillated mouth (papilae- important for
sensing stimuli)

anterior portion: filled with stichosomes


which are composed of stichocytes (linearly
arranged strand-like cells)

esophagus: begins anterior to stichosome

intestine: posterior to esophagus, simple


tube that leads to the anus/cloaca

cloaca: serves as an opening to both


digestive and reporductive systems of the
worm

1.
2.
3.
4.

5.

a. Male Worms
delicate anterior end with cephalic papillae
posterior portion: 2 caudal/copulatory appendages
reproductive tract: single testes with its own tube that
will run anteriorly and go down posteriorly to open in the
cloaca
cloaca: evertible during copulation
b. Female Worms
Simple reproductive system: single ovary which starts
posteriorly then goes anteriorly to join with other
reproductive structures
Vulva: located at the anterior 5th of the body
Viviparous
1 adult female capable of producing 500 larvae in a
month
2. Larva
equipped with spear-like burrowing tip which is seen at
the anterior end

Trichinellosis is acquired by ingesting meat


containing cysts (encysted larvae) of Trichinella.
(infective stage)
After exposure to gastric acid and pepsin, the
larvae are released from the cysts and
invade/burrow into the intestinal mucosa
In the small bowel mucose, they develop into
adult worms (female 2.2 mm in length, males 1.2
mm; life span in the small bowel: 4 weeks)
After 1 week, the females release larvae that
migrate trhough the lymphatics, then the
bloodstream to finally reach the skeletal muscles.
! Skeletal muscle biopsy: deltoids, biceps,
pectorals since they are more accessible
Encystation in the muscles. Encystment is
completed in 4 to 5 weeks and the encysted
larvae may remain viable for several years.
Hence, man can serve as a dead-end host.
! Encapsulation takes place on the 3rd week from
the onset of infection
! Capsule is induced and not secreted, meaning,
the capsule is not produced by the larva but
comes from the skeletal muscle of the host.
! Capsule is penetrable
! Nurse cell- larva complex = Trichinella larva +
host skeletal muscle; calcifies in time
! includes other cycles for maintenance of
survival
o
Pig-to-pig
o
Rat-to-rat
o
Sylvatic cycle- maintained by wild
rodents

Epidemiology

Cosmopolitan distribution

Rare; absent in Australia

main reservoir: pig

Pathology and Symptomatology


3 Clinical Manifestations
1. Intestinal phase

From time of pork ingestion to GI


symptoms

Inflammation of duodenal and jejunal


mucosa

Non-specific symptoms: abdominal pain,


nausea, body malaise

Lasts up to 3 days
2. Muscle invasion phase

Muscle fibers: increase in size,


edematous, basophilic degeneration

Nuclei increase in size and number

Fever (remittent, up to 40C)

Periorbital edema, Generalized facial


edema

Tender lymphadenopathy

CBC: eosinophilia (prominent feature)


50 to 60% but can go as high as 90%

Myocarditis: most common grave


manifestation

Elevated cardiac markers

Takes place up to the 3rd week


3. Convalescence Phase

Larval encapsulation

Fever subsides

Muscular symptoms decrease

Diuresis, appetite returns


Diagnosis

History of poorly cooked or raw meat ingestion


CPK, LDH
CBC: Eoosinophilia (progressively increasing as
disease progresses until Convalescence phase
Bachman intradermal test: if result is (+),
supplement with any serologic test
Inject diluted solution with antigen of parasite
(+): white swelling surrounded by a wheal which
is not raised (5cm)
Serologic test: Bentonite flocculation (standard
test in some countries)
Muscle biopsy: definitive diagnosis; look for
free/encapsulated larva

Treatment

Mebendazole

Thiabendazole

Steroids: for allergic reaction and myocarditis


Prognosis

Generally good, except with Myocarditis

Absent/ low grade eosinophilia makes the


prognosis WORSE
Prevention

Freezing of pork

Avoid feeding raw garbage to hogs

Proper cooking of pork

Extermination of rats in farms


Notetaker: Stephanie Abnasan

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