MEDICAL PARASITOLOGY

PHASMID 4
DR. Roxas / Dueñas
OLFU • FUMC ½ COLLEGE OF MEDICINE
Ref: Medical Parasitology in the Philippines by: Belizario

Parasitic Biology
Miscellaneous Nematodes: • Morphology of Adult Worm:
• Angiostrongylus / Parastrongylus cantonensis § Filiform worm narrowed at both extremities
• Dracunculus medinensis § Cuticula ® smooth and slightly thickened at both
• Gnathostoma spinigerum extremities
§ Cephalic tip ® simple with 3-minute lips
ANGIOSTRONGYLUS/ PARASTRONGYLUS CANTONENSIS § 4 pairs of papillae on the external border of the head
• “Rat lung worm” – Rattus spp ® Site of infection is in the Brain § No buccal capsule
§ This also called “Tropical Eosinophilic § Mouth open directly into an esophagus
Meningoencephalitis” in human due to CNS § Body ® Pale and filiform 17 to 25mm, live in 2 main
involvement (fetal) ® cerebral angiostrongyliasis branches of the pulmonary artery of the rats
• Habitat: § Filiform worm that is tapering on both end
§ Ault parasite only in rodents (rats) in the branches of § Lack of buccal capsule, the mouth opens directly into a
pulmonary artery of rats muscular filiform type of esophagus
§ Infected rats pass larvae in feces ® Originally isolated • Male
from the bronchial tree of the domestic rats [Chen in § Kidney-shaped, well developed caudal bursa (arrow)
China, 1935] and single lobe and bursal rays (dart)
• Geographic: § 16 to 22mm x 0.25 to 0.35mm
§ 1st reported human infection (meningitis) in Taiwan § Small copulatory bursa at the end and bent ventrally
[1945] ® 4 females and 2 male worms from spinal fluid § Long spicules (long black arrow)
§ At present ® associated with outbreaks of eosinophilic
meningitis
§ In Thailand ® 3 cases involved the eyes
• Angiostrongylosis
§ Incubation period ® 1-3 weeks and can be shorter or
longer
§ MOT ® human to human transmission
§ A. cantonensis ® causing neural angiostrongyliasis • Female
(brain and eye) § 21 to 25 x 0.03 to 0.36 mm
§ A. costaricensis ® causing abdominal § “Barbers Pole” pattern – spiral uterine tubules around
angiostrongyliasis (intestinal inflammatory) intestine – the uterus coils around the blood-filled
intestine giving rise to barber’s appearance
§ Blunt posterior end with subterminal and pore on
ventral aspect
§ Anterior to the anus (dart) and vulvar opening (arrow)
§ Transparent cuticle posterior end blunt shape
§ Lay egg 15,000 daily
§ The adult female lay eggs in the bloodstream which is
now transported into the vessels of the lung

Order Strongylida
Superfamily Metastrongylida
Definitive/Primary Host Rats
Infective And Pathogenic L3 larvae
Stage
Other Primates Dogs, Horses, Birds
Mot Ingestion of raw or undercooked with
infected snails or slugs [intermediate host] • Ovoidal Eggs/Larval stage:
Paratenic Host Fresh Water Shrimps, Land Crabs, Frogs § 46 to 48 x 68 to 74um
and Toads, Monitor Lizards, Planarians ® unembryonated
Intermediate Host Snails and Slugs when oviposited
§ Elongated with
• Epidemiology delicate hyaline shells
§ Delicate hyaline shells
§ Southeast Asia, tropical Pacific Islands
§ L1 stage
§ Various species of Rats
o Definitive host o Found in lungs of the rodent rats
o Distinct small knob near the tip of the tail
o Only hosts in which the adult stage occurs
§ L3 stage ® infective and pathogenic stage
• Contributing factors for the spread of infection
§ Geographic mobility of rats o 2 well-developed chitinous rods below its
buccal cavity
§ Geographic mobility of the large African snail ®
o Expanded knob-like tips
Achatina fulica
§ The eggs hatch in the lungs of the rodent host to
§ Lack of host specify
produce the larva
§ The larva will migrate to the trachea, it is shallowed or
it can migrate directly into alimentary tract

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Note: Angiostrongylus/Parastrongylus
• Mode of infection
§ Ingestion or active
penetration
• Mode of transmission ® ingestion of raw
or undercooked infected snails or slugs {intermediate host}
§ ingestion of raw mollusk infected with L3
§ ingestion of leafy vegetable infected with snail
mucus secretion carrying L3
§ ingestion of paratenic host (crabs or prawn)
infected with parasite
§ drinking contaminated water
• A. cantonensis ® Neural (brain) and Ocular (eye)
Angiostrongyliasis
• A. costaricensis ® Abdominal Angiostrongyliasis
[inflammatory intestinal reactions]
• L1 larva – found in lungs of the rodent host
• L3 larva – 2 well developed chitinous rods below its buccal
cavity
• In humans ® the larva probably remains in the brain for a
longer period of time and not develop to the adult stage
• Natural host: Rats
• Accidental host: human
• Intermediate hosts: Molluscan, Garden slugs and Snails
• Infective form: L3 larvae
• Rats ® Definitive host
§ L3 larva is ingested
§ Adult in the pulmonary arteries
§ Adult lays eggs and produces L1 larva
• Mollusks ® Intermediate host
§ L1 larva is ingested from feces of rats
§ L1 ® L3 Larva
• Life cycle: CDC
§ In the Philippines, especially in the rice field, A. fulica
(land snails) and other snails is a source of food of the
rodent rats
§ Adult worms of A. cantonensis live in the pulmonary
arteries and right ventricle of the normal definitive
host (1)
§ The females lay eggs that hatch in the terminal
branches of the pulmonary arteries, yielding first-stage
larvae. The first-stage larvae migrate to the pharynx,
are swallowed, and passed in the feces. They penetrate
or are ingested by a gastropod intermediate host (2)
§ After two molts, third-stage larvae are
produced (3) which are infective to mammalian hosts.
§ When the infected gastropod is ingested by the
definitive host, the third-stage larvae migrate to the
brain where they develop into young adults (4)
§ The young adults return to the venous system and then
the pulmonary arteries where they become sexually
mature
§ Of note, various animals act as paratenic (transport)
hosts: after ingesting the infected snails, they carry the
third-stage larvae which can resume their development
when the paratenic host is ingested by a definitive host.
Humans can acquire the infection by eating raw or
undercooked snails or slugs infected with the parasite;
they may also acquire the infection by eating raw
produce that contains a small snail or slug, or part of
one (5)
§ There is some question whether or not larvae can exit
the infected gastropods in slime (which may be infective
to humans if ingested, for example, on produce).
Infection may also be acquired by ingestion of
invertebrate paratenic hosts containing L3 larvae (e.g.,
crabs, freshwater shrimp)
§ In humans, larvae migrate to the brain, or rarely to the
lungs, where the worms ultimately die (6). Larvae may
MEDICAL PARASITOLOGY
PHASMIDS 4
develop to fourth or fifth stage in the human host, but
seem to be incapable of maturing fully
Note: Life Cycle 📢📢📢
• RAT: DEFINITIVE HOST
§ HABITAT: Adult moves to the Pulmonary Arteries &
Right Ventricle.
§ Adult female lays egg at the terminal branches of the
PULMONARY ARTERIES and may go trachea.
§ L1 Larva is swallowed and pass feces.
• MOLLUSKS/PARATENIC HOST: INTERMEDIATE HOST
§ Swallows the feces of L1 Larva (RAT)
§ HABITAT: L1® L2 ® L3 Mottling Stages
(CRABS/SHRIMP/SLUGS/SNAIL)
§ Then be eaten by Mammalian Host or Rodent Host.
• HUMAN: ACCIDENTAL HOST
§ Ingesting Mollusks, Uncooked
§ Ingesting Food Items contaminated by “Snail Lime
Trails”
§ Go to the BRAIN (L4-L5 Stages) but Die. (Gives
Intense Inflammation)
§ They don’t reproduce anymore
§ They may also go back to Pulmonary System (RAT)
– Maturity
Pathogenesis and Clinical Manifestation
• When human get infected the L3 pass through stomach then enter
the circulation and migrate to the brain (remain in the brain for long
period of time and DO NOT develop into adult stage) and spinal
cord or may migrate into the eye chamber
• Clinical symptoms are caused by the presence of larva in the brain
and by local host reactions:
§ Severe headaches, nausea and vomiting, neck
stiffness, seizures and neurologic abnormalities
§ Ocular invasion ® occasionally
§ Eosinophilic ® most cases
• Abdominal angiostrongyliasis mimics appendicitis with
eosinophilia
• Acute severe, intermittent occipital or bitemporal headache
§ Illness lasts – 2 to 8 weeks
• Bacterial meningitis – presence of Charcot Leyden crystal in the
meninges
§ Nausea and vomiting
§ Neck stiffness – meningismus
§ Leg or arm paresthesia
• Tropical eosinophilic meningitis
§ Cause Parastrongylosis in humans affecting CNS (fetal)
• Ocular invasion – not fatal
§ Intraocular hemorrhage
§ Retinal detachment
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• Common in wet and tropical environment which is SE Asia
Note: Signs and Symptoms • 3 species in the Philippines:
• Asymptomatic or mild infection § G. spinigerum – human locally in Asian country
• Larva reaches the brain and induce a host responds ® § G. hispidum
eosinophilic meningitis § G. doloresi – human gnathostomiasis in Japan
• There can be ocular invasion • G. hispidum and G. doloresi
• Self-limiting infection ® 4-6 weeks § Reported in China, Japan, and Thailand
§ Philippines – reported pigs and NO human infection
• Japan:
Note:
§ “Dojo” – consumption of fish (Misgurnus
• In human cases, including cases of Ocular Parastrongylosis,
anguillicaudatus)
which are all non-fatal and presumably due to larvae of
§ G. doloresi and G. hispidum – recognized as human
P. cantonensis, have been reported locally
gnathostomiasis in Japan due to consumption of fish
“Dojo”
§ G. doloresi – this harbor the larvae
o Wild boars, salamanders, frogs, and snakes
• Philippines:
§ Both G. hispidum and G. doloresi – recorded in pigs in
the Philippines
§ Cordillera Province (Ifugao) – “Jojo”
Note: Differential Diagnosis § G. doloresi larvae
• Eosinophilic myeloencephalitis (Gnathostoma spinigerum) o Found in frogs and Ophicephalus striatus
• Other helminthic infections with high eosinophilia “dalag” ® this serves as the intermediate
§ Cerebral cysticercosis host
§ Trichinosis
§ Toxocariasis
§ Strongyloidiasis

Diagnosis
• Blood analysis:
§ Peripheral Eosinophilia
• CSF analysis
§ High CSF eosinophilia, low sugar
§ Increase (pressure, protein, leukocytes, eosinophils) • Epidemiology:
§ (+) larva in the CSF § Common in Asia ® Japan and Thailand
• CT scan § 1970, >1000 cases from Latin America ® Mexico and
§ Meningeal lesion, non-specific cerebral edema and Ecuador
ventricular dilation § Endemic area ® south central Africa
§ Larva and adult worm may be seen in CSF (rare)
§ Dishes with undercooked meat in these area (sushi,
• Also, presence of Charcot-Leyden crystal in the meninges sashimi, sum-fale ceviche)
• Since the primary site of infection is in the Brain, it will result to § Increased traveling has led to increased incidence of
neurologic problem or deficit – this may result in the prognosis of this typically rare disease
the patient
Definitive host Domestic and wild felines and canines
Note: 1st intermediate host Copepods/cyclops (serrulatus, bicolor)
• CSF does not have high PMNs (Polymorphonuclear) 2nd intermediate host Fresh water fishes (glossogobius giurus,
• Eosinophils are found instead, though these cells may be Ophicephalus striatus, therapon argenteus)
absent early and late in the course of disease Paratenic host Ducks, chickens
• History and PE Infective stage L3 ® fish or frogs
• Lumbar puncture ® larva or young worm L2 ® cats and dogs
• CSF ® increase pressure, leukocytes, proteins and eosinophils L2 and L3 ® humans
Diagnostic L3 (gastric wall of pigs)
Treatment
• Symptomatic
§ Analgesics, anti-inflammatory or steroids
• No DOC ® may use thiabendazole or albendazole
• No specific treatment
• Ocular involvement ® surgical removal of the larva
• To relieve headache ® extract (lumbar tap/puncture) about 10cc
of CSF

Prevention and Control Parasitic Biology

• Health teaching – proper sanitation • Adult Spirurid
• Discouraged from eating raw poorly cooked mollusks or § Stout and Pink worm
unwashed vegetable § Adult 1-3cm long
§ With a distinct head bulb covered by a row of hooks
§ Anterior half – covered by rows of flat toothed spines
GNATHOSTOMA SPINIGERUM
(covered with leaf-like spines and trident)
• “Creeping worm”
§ Followed by a bare portion
• Genus: Gnathostoma § Posterior tip has numerous tiny, cuticular spines
• Gnathostomiasis – zoonotic infection of man

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PHASMIDS 4
Head bulb Posterior body Anterior body Pathogenesis and Clinical Manifestation
(Cuticular spines) (Cuticular spines) • Due to L3 larvae migration ® may become dormant on abscessed
pockets
• Deep cutaneous or subcutaneous tunnels ® which the worms
migrate (cutaneous larva migrans / creeping eruptions)
• Cutaneous Larva Migrans – Gnathostomiasis externa
§ Migrating edema
§ Intermittent, migratory, painful, pruritic swellings in
subcutaneous tissues
• Egg
§ Ovoid in shape
§ Single polar thickening or a mucus plug
§ Unembryonated when laid
§ Has polar cap at only end
§ Outer shell in pitted

• Visceral Larva Migrans – Gnathostomiasis interna

§ Cough, hematuria, ocular involvement
§ Eosinophilic
§ Meningitis and myeloencephalitis

• Life cycle
§ To complete the development – require aquatic
copepods as intermediate host (fishes) and wide range
of paratenic host (snakes, frogs) may intervene as
“extension host” in the cycle Note: Gnathostoma ® differential diagnosis
§ Definitive host – G. spinigerum • Furunculosis, and other localized bacterial skin infection
o Dog, cats, pigs, flying lemurs and palm civets • Migrating larva of hookworms
§ 1st Intermediate Host ® Copepods • Eosinophilic meningitis of A. cantonensis
§ 2nd Intermediate Host ® Fresh water fisher
§ Paratenic host Diagnosis
o Water snakes (Hurria rynchops) • Excision Biopsy
o Frogs (Rana limnocharis) § Identify presence of typical larva
§ In definitive hosts, adult worms of
• Serology ® ELISA
most Gnathostoma spp. reside in a tumor-like mass in
§ Eosinophilic
the gastric wall; adult worms of some species are found
in the esophagus or kidney
Treatment
• MOT:
• Drugs
§ Ingestion of raw or uncooked fish harboring the L3 larva
§ Albendazole
§ Drinking of water contaminated by crustaceans
§ Ivermectin
harboring the L2 larva
• Treatment
§ Incision of the lesion and removal of the larva

Prevention and Control

• Cook food properly
• Avoiding contaminated freshwater
• Proper hand washing
• Adequate cooking of fish
• Immersion of strong vinegar for 5 hours

DRACUNCULUS MEDINENSIS
• “Guinea worm” “serpent worm” “dragon worm” – longest and
largest nematode roundworm about 800mm long [female]
• Neglected tropical disease
• Found in subtropics to tropical regions – especially in India, South-
West Asia (Iraq, Iran, Pakistan etc.)
• 25 to 300c – best for larval development
• Prevalence:
§ The parasite relies on people accidentally consuming
microcrustaceans of the genus Cyclops (copepods), that
dwell in stationary bodies of water such as ponds, large
open wells (with stairs), or rain-filled cistern
§ The infection occurs most during times of drought or the
“dry-season” in humid climates, or during or just after
the rain season on the “semiarid, wet-and-dry climates
in lower surface water – this results in the drinking of
unfiltered drinking water infected with L3 stage

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PHASMIDS 4
Definitive host Human
Intermediate host Copepods or cyclops
Infective stage L3 larva
Diagnostic Female worm emerging from skin a year after
infection
MOT Drinking unfiltered water infected by copepods
harboring L3 larva
Habitat Subcutaneous tissues and skin
History:
Clinical feature Skin blistering at lower extremites
• Guinea worm has been known from antiquity. It is believed to
have been fiery serpent on the Bible, which tormented the
Israelites on the banks of the Red Sea Pathogenesis and Clinical Manifestation
• The technique of extractive the worm by twisting it on a stick, • Infection induces no illness
still practiced by patients in endemic areas is said to have been • Erythema, urticaria, pruritus ® inflammation, blister formation
devised by Moses, the picture of the serpent worm on a stick (papule with vesicular center), ulceration of the skin
may gave given rise to the physician’s symbol of caduceus • Blister formation – yellowish liquid
§ Due to toxic adult worm with many mononuclear,
eosinophilic and polymorphonuclear leukocytes
Parasitic Biology § Site: Feet (metatarsal bones or/on ankles)
• Morphology of Adult Worm • Beneath the blister ® anterior extremity of the female worm
§ L1 larva measure 400um on length and have a lying in a subcutaneous or deeper tunnel Dracunculus Medinensis 223
rhabditiform pharynx • penetrate
The larvae Dracunculiasis
the gut wall of –the
last forand
cyclops 1 to 3 Skin
months
test: An intradermal test with guinea worm antigen
§ L3 larva are longer, measuring 600um in length and •
enter its body cavity, where they moult twice.
Sequelae: elicits positive response.
In about 2–4 weeks, they develop into the infective Serological test: Enzyme-linked immunosorbent
have a filariform pharynx third-stage larvae (L3). § Secondary infectionsassay ® (ELISA)
tetanus and immunofluorescence assay (IFA) are
§ Mouth ® small triangular surrounded by The entire life cycle takes about an year, so that all the
infected persons develop Arthritis
§ the blisters and present with
frequently used to detected antibodies to D. medinensis
(Flowchart 22.1).
quadrangular, sclerotized plate clinical manifestations §at aboutSynovitis
the same time of the
year (Fig. 22.4).
§ No lips § Ankylosis Treatment
§ Esophagus has large glandular portion Pathogenicity and§Clinical Contracture
Features of the involved Antihistaminicslimbs
and steroids are of help in the initial
§ Spicule of male worm are unequal D. medinensis causes dracunculiasis or dracunculosis.
stage of allergic reaction.
Metronidazole, niridazole, and thiabendazole are useful
• Male worm Infection induces no illness till the gravid female worm in treatment.
comes to lie under the skin, ready to discharge its
§ 2 to 4cm in length with Unequal spicules embryos.
• Female worm The body fluid of the adult worm is toxic and leads to
blister formation. Parasites requiring one intermediate host to
§ Creamy white and grow up to 80cm by 2mm A few hours before the development of the blister, complete their life cycle
there may be constitutional symptoms such as nausea,
§ Contain thousands of embryos vomiting, intense pruritus, and urticarial rash. Intermediate host Parasite
• Life cycle: The blister develops initially as a reddish papule with a
• centerComplication
Man Plasmodium species
Echinococcus granulosus
vesicular and surrounding induration.
§ When the human is infected by ingesting contaminated The most common sites§for blister Secondary bacterial
formation are the feet infection Echinococcus multilocularis
Taenia multiceps
water ® infected L3 larva (copepods) between the metatarsal bones or on the ankles.
§ Disfiguring cutaneous
The fluid in the blister is a sterile yellowish liquid with Pig scars Taenia solium
§ The copepods die ® releases the larva and penetrates polymorphs, eosinophils, and mononuclear cells.
§ Pronounced inflammatory reaction ®
Taenia saginata asiatica
when suihominis
the
The local discomfort diminishes with the release of the Sarcocystis
the stomach and intestinal walls (abdominal cavity and embryos. worms die in situ and improperly removed
Trichinella(killing
spiralis in
Cow Taenia saginata
retroperitoneal spaces) Secondary bacterial infection is frequent. Sometimes, it
not good idea) Sarcocystis hominis
may lead to tetanus.
§ Adult male and female and when they copulate ® Sometimes, the worm§travels Immobility
to unusual sitesdue Snail
such to pain while on treatment Schistosoma species
process
as the pericardium, the spinal canal, or the eyes, with Cyclops Dracunculus medinensis
male dies serious effects. Sandfly Leishmania species
§ Gravid female moves to skin surface and release its Dracunculiasis lasts usually for 1–3 months. Diagnosis Tsetse fly
Chrysops
Trypanosoma species
Loa loa
larva in water source ® water may relieve the • ®
Goal finding the head of the worm in the skinWuchereria
Mosquito ulcer bancrofti
Laboratory Diagnosis Brugia spp.
discomfort (intense burning blister) • X-ray Mansonella spp.
Detection of adult worm: Diagnosis is evident when Tick Babesia species
§ from
the tip of the worm projects (+)theworm from
base of the ulcer.the skin lesion
Triatomine bug Trypanosoma cruzi
Calcified worms can be seen by radiography.
§ (+) calcified dead
Detection of larva: By bathing the ulcer with water, the
worm
Flea Hymenolepis nana
Hymenolepis diminuta
• be induced
worm can ELISAto test
release the embryos, which can Dipylidium caninum
be examined under the microscope.

Flowchart 22.1: Laboratory diagnosis of Dracunculus medinensis

Treatment
• Rolling the worm into a stick and pulling out of the skin lesion
• If there is resistance. Do not pull
• No drug treatment for disease
• No vaccine
• Niridazole 25mg/kg daily for 10 days
• Thiabendazole 50mg/kg daily for 3 days
• Metronidazole 400-500mg daily for 10 to 20 days
• Mebendazole ® causes worm tissue to breakdown of fragmented

Prevention and Control

• Use of properly treated water for consumption
• Boiling of water suspected of contamination

END

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