Bien Ag Nina Ian John “G” Rachel Mark Jocelle Edo Gienah Jho Kath Aynz Je Glad Nickie

Ricobear Teacher Dadang Niňa Arlene Vivs Paul F. Rico F. Ren Mai Revs Mavis Jepay Yana Mayi Serge Hung Tope

S4 L3: NEMATODES II by Dra. Bunyi January 19, 2011

FILARIASIS o Mosquitoes: agents of lymphatic filariasis (Wuchereria

bancrofti and Brugia malayi)
Causal Agents: o Blackflies (Simulium): Onchocerca volvulus
o Nematodes (roundworms) that inhabit the lymphatics o Midges: Mansonella perstans and Mansonella streptocerca
and subcutaneous tissues.
o Both midges and blackflies: Mansonella ozzardi
8 main species infect humans:
o 3 of these cause most of the morbidity due to filariasis: o Deerflies (Chrysops): Loa loa
 Wuchereria bancrofti and Brugia malayi Inside the arthropod, microfilariae devekop in 1 to 2 weeks into infective
cause lymphatic filariasis and Onchocerca filariform (third-stage) larvae
volvulus causes onchocerciasis (river o During a subsequent blood meal by the insect, the larvae
blindness) infect the vertebrate host → migrate to the appropriate site
o 5 other species are Loa loa, Mansonella perstans, M.
& develop into adults, a slow process than can require up to
streptocerca, M. ozzardi, and Brugia timori. (The last
species also causes lymphatic filariasis.) 18 months in the case of Onchocerca.
There are four sheathed species: Wuchereria bancrofti, Brugia
malayi, Brugia timori and Loa loa. Wuchereria bancrofti Brugia malayi
(Bancroft’s filarial worm) (Malayan filarial worm)
Geographic Distribution Causes bancroftian filariasis Causes Malayan filariasis
Among the agents of lymphatic filariasis, Wuchereria bancrofti is
Causes a chronic disfiguring Chronic infection also
encountered in tropical areas worldwide.
disease presents with lymphedema
Brugia malayi is limited to Asia
Brugia timori is restricted to some islands of Indonesia. o Lymphedema or elephantiasis
The agent of river blindness, Onchocerca volvulus, occurs mainly o Elephantiasis Mosquito vectors:
in Africa, with additional foci or Latin America and the Middle o Hydrocele Mansonia
East. Vectors: Aedes, Culex, Development of
Among the other species, Loa loa and Mansonella streptocerca Anopheles microfilariae to infective
are found in Africa; Development of microfilariae stage: 2 weeks
o Mansonella perstans occurs in both Africa and South
into infective stage: 6-20 days Maturation time for 3rd
America.
o Mansonella ozzardi occurs only in the American stage larvae to become
continent. adults: 3-9 months

Life Cycle: Filaria

Infection with these filarial parasites not only causes chronic
Infective larvae are transmitted by infected biting arthropods during a debilitating disease but also:
blood meal  Acute fever
Larvae migrate to the appropriate site of the host’s body, where they  Inflammation of the lymphatic system
develop into microfilariae-producing adults.  Tropical pulmonary eosinophilia
Adults dwell in various human tissues where they can live for several
years.
o The agents of lymphatic filariasis (Wuchereria, Brugia) Wuchereria
reside in lymphatic vessels and lymph nodes: Adults: creamy, white, long and filiform
 LYMPHATICS: Brugia malayi, Wuchereria o Male worm: 2-4 cm length
bancrofti. o Female: 8-10 cm
 Onchocerca volvulus in nodules in subcutaneous Microfilariae appear as snake-like organisms & measures 270-
tissues 290µm
 Loa loa in subcutaneous tissues, where it o Enclosed in a hyaline
migrates actively sheath which is longer
 Mansonella streptocerca in the dermis and than the microfilaria itself
subcutaneous tissue o Central axis: shows dark
 Mansonella ozzardi apparently in the staining nuclei; column
subcutaneous tissues of nuclei arranged in 2 or
 Mansonella perstans in body cavities and the 3 rows and is distinctly
surrounding tissues conspicuous
The female worms produce microfilariae which circulate in the blood o Graceful appearance
except: Wuchereria bancrofti
o Onchocerca volvulus and Mansonella streptocerca- skin Microfilaria
o O. Volvulus- invade the eye. o Thick blood smears stained with hematoxylin.
The microfilariae infect biting arthropods:
 o Microfilaria is sheathed, its body is gently curved, and
the tail is tapered to a point.
The nuclear column (the cells that constitute the body of the 8.
microfilaria) is loosely packed; the
cells can be visualized individually
and do not extend to the tip of the
tail. Adult forms
The sheath is slightly stained with
hematoxylin.
Vector
Mosquito vector depends on geographic distribution
o Culex (C. annulirostris, C. bitaeniorhynchus, C.
quinquefaciatus, and C. pipiens)
o Anopheles (A. arabinensis, A. bancroftii, A farauti, A.
funestus, A. gambiae, A. koliensis, A. melas, A. merus,
A. punctulatus and A. wellcomei)
o Aedes (A. aegypti, A. aquasalis, A . bellator, A. cooki,
A. darling, A. kochi, A. polynesiensis, A.
pseudoscutellaris, A. rotumae, A. scapularis and A.
vigilax)
o Mansonia (M. pseudotitillans, M. uniformis)
o Coquillettidia (C. juxtamansonia)
Life cycle of Wuchereria bancrofti
Brugia malayi
Microfilaria
1-2. An infected mosquito introduces third-stage filarial larvae onto the skin
of the human host where they develop in adults that commonly reside
in the lymphatics.
3. Adults produce microfilariae which are sheathed and have nocturnal
periodicity, except the South Pacific microfilariae (absence of marked
periodicity). The microfilariae migrate into lymph and blood
channels moving actively through lymph and blood.
4-7. Mosquito ingests the microfilariae during a blood meal, the microfilariae
lose their sheaths and some of them work their way through the wall of
the proventriculus and cardiac portion of the mosquito's midgut and
reach the thoracic muscles where they develop into first-stage larvae
and subsequently into third-stage infective larvae.
Third-stage infective larvae migrate through the hemocoel to the
mosquito's prosbocis and can infect another human when the mosquito
takes a blood meal.
Adults produce microfilariae measuring 244 to 296 µm by 7.5 to
10µm
o Microfilariae are sheathed
o Have nocturnal periodicity (except the South Pacific
microfilariae which have the absence of marked
periodicity)
Inside the mosquito, the microfilariae, develop into first (L1),
second (L2) and 3rd (L3) stage larvae; after 6 to 20 days they
migrate into the mosquito’s head and proboscis
During a blood meal, larvae (from the mosquito) reach the
lymphatic vessels and nodes where they develop into adult
worms.
Worms usually localize in the lymph vessels of the lower
extremities, inguinal lymph nodes, epididymis of the males, labial
glands of females
Microfilariae have a nocturnal periodicity (seen in blood taken
between 8pm to 4am
Brugia
Adult male: 12-23mm length
o Female: 43-45mm
o Adult females of B. malayi and W. bancrofti are
indistinguishable
Microfilariae measures 177-230µm
o Enclosed in a sheath & with
curvatures with secondary
kinks and 2 nuclei at the tail
tip
o Column of nuclei is in 2
rows which are indistinct or
confluent
Thick blood smear hematoxylin stain
Like Wuchereria bancrofti, this species has a sheath (slightly
stained in hematoxylin.)
Differently from Wuchereria, the microfilariae in this species are
more tightly coiled, and the nuclear column is more tightly packed,
preventing the visualization of individual cells.
Development of the microfilariae to the infective stage in the
mosquito takes about 2 weeks
Maturation time for the 3rd stage larvae to become adult: 3-9
months
Microfilariae produced are seen in the circulation & have a
subperiodic periodicity.
Detail from the microfilaria of Brugia malayi
showing the tapered tail, with a subterminal
and a terminal nuclei (seen as swellings at
the level of the arrows), separated by a gap
Page 2 of 14
without nuclei. This is characteristic of B. malayi muscles where they develop into first-stage larvae and subsequently
into third-stage larvae.
8. Third-stage larvae migrate through the hemocoel to the mosquito's
proboscis and can infect another human when the mosquito takes a
Microfilaria of W. bancrofti collected by blood meal.
filtration with a Nucleopore ® membrane. The
pores of the membrane are visible
Filariasis in the Philippines

1)
Microfilaria of Brugia malayi collected by Knott
(centrifugation) concentration technique in 2%
formalin wet preparation
Note the clearly visible sheath that extends
beyond the anterior and posterior ends of the
microfilaria.
Vector
mosquito of the genus Mansonia
*Aedes is also listed as one of its vectors (CDC)
Bancroftian filariasis
o Camarines Norte, Camarines Sur, albay, Sorsogon,
Mindoro, Masbate, Romblon, Marinduque, Bohol,
Samar, Leyte, Palawan, Mountain Province (Bontoc),
and all provinces of Mindanao including Sulu, Tawi-
Tawi and Basilan
 Anopheles minimus var. flavirostis- vector in
Mt. Province, Sulu and Palawan
 Aedes poecilus (breeds in water in the axils
of abaca and banana plant)-vector in other
provinces
 Infection rate from 1989 to 1991: 0.88 to 2.5%
 Sorsogon: microfilaria rate 15%; hydrocele was present in
4% of males

2) Malayan Filariasis
o Malayan filariasis- Palawan, Eastern Samar, Agusan del Sur, and Sulu
 In these places, W. bancrofti coexists with B. malayi
 Mosquito vector: Mansonia bonnae (breeds in freshwater
swamps) and Mansonia uniformis (breeds in rice fields)
 Night biters: 5pm until 11pm
o Prevalence: <3%
o Cats are important reservoir host and transmit infection to humans by
means of cat-mosquito-man cycle.

Clinical Features of Filariasis

Lymphatic filariasis most often consists of asymptomatic
microfilaria
o Development of lymphatic dysfunction causing
lymphedema and elephantiasis (frequently in the lower
extremities)
o with Wuchereria bancrofti, there is hydrocele and
scrotal elephantiasis.
o Episodes of febrile lymphangitis and lymphadenitis
may occur.
o Persons who have newly arrived in disease-endemic
areas can develop afebrile episodes of lymphangitis
and lymphadenitis.
o An additional manifestation of filarial infection, mostly
in Asia, is pulmonary tropical eosinophilia
syndrome
1-2. An infected mosquito introduces third-stage filarial larvae onto the skin nocturnal cough and wheezing, fever, and
of the human host, where they develop into adults that commonly eosinophilia.
reside in the lymphatics. Clinical Course:
3. Adult worms resemble those of Wuchereria bancrofti but are smaller.
Adults produce microfilariae which are sheathed and have nocturnal Endemic community- different stages overlap
periodicity, migrate into lymph and enter the blood stream reaching Manifestations are caused mainly by adult worms, living, dead or
the peripheral blood. degenerating
4-7. Mosquito ingests the microfilariae during a blood meal; microfilariae o Microfilariae cause less pathology but have been
lose their sheaths and work their way through the wall of the associated with tropical pulmonary eosinophilia
proventriculus and cardiac portion of the midgut to reach the thoracic (TPE), granulomas of the skin, and allergic reactions
following destruction by drugs

Page 3 of 14
 Those who are infected after migration to endemic regions
present with “Expatriate Syndrome”: clinical and immunologic
hyperresponsiveness to the mature or maturing worms.
o Present with allergic reactions such as hive, rashes
and blood eosinophilia along with the usual
manifestations of lymphadenitis and lymphangitis
STAGES:
1. Asymptomatic stage
Characterized by the presence of thousands to millions of blood
and adult worms in the lymphatic system with no manifestations
of filariasis.
This stage is seen among those with a highly down regulated
immune system.
May have hidden lymphatic pathology and kidney damage.
Vector: Chrysops silacea and C. dimidiata (day
biting flies)
Parasite Characteristics:
Adult males: 2 to 3.5 cm long; Females: 5-7cm long
Microfilariae: 250-300µm long, sheathed and differ from
Wuchereria and Brugia in having body nuclei that are continuous
to the tip of the tail.
Adult worms migrate through subcutaneous deeper tissues
Microfilariae→bloodstream; diurnal periodicity

2. Acute stage
Microfilaria of Loa loa (thick blood smear
Early manifestations:
stained with hematoxylin). Loa loa is sheathed
o Fever, inflammation of lymph glands (especially of the with a relatively dense nuclear column, its tail
male genital organs, arms and legs) tapers and is frequently coiled, and nuclei
Recurrent attacks: extend to the end of the tail.
o Swelling & redness of the arms & legs, accompanied
by vomiting, headache
o Affected areas can be tender Symptoms:
S/Sx reflect immunologic phenomenon caused sensitization to Loiasis (Loa loa) is often asymptomatic
the products of living or dead worms collectively called o Episodic angioedema and subconjucntival migration of
adenolymphangitis (ADL) or dermatolymphangioadenitis an adult worm can occur
(DLA) Non-painful migration through tissues
Conjunctival edema; patches of localized subcutaneous edema
3. Chronic stage (Culabar swellings)
Eosinophilia
With repeated acute episodes, acute manifestations merge into a Life cycle of Loa loa
chronic proliferative overgrowth of fibrous tissue around the dead
worm→lead to lymphatic obstruction, recurrent attacks of DLA
and lymphedema, elephantiasis or hydrocele.
Cellular reaction and edema are replaced by fibrous hyperplasia.
TPE (Tropical Pulmonary Eosinophilia)occult filariasis-
microfilariae not found in the blood but may be found in tissues.
o Immunologic hyperresponsiveness to filarial infection
characterized by nocturnal cough, hypereosinophilia,
elevated ESR, diffuse military lesions or increased
vascular markings.
Chyluriarupture of lymphatics in the kidney blockage of
retroperitoneal lymph nodes.
o Several reports of glomerulonephritis in bancroftian
filariasis

Loa loa
African eye worm: Sudan rain forest, basin of Congo and West
Africa
Migrates throughout subcutaneous tissues of the body
Most conspicuous and irritating when crossing the conjunctivae
Loasis is similar to onchocercaisis which can also cause
blindness
Microfilariae has diurnal periodicity
During the day, they are found in peripheral blood, but during the
non-circulation phase, they are found in the lungs.
Microfilariae have been recovered from spinal fluids, urine and
sputum.

Page 4 of 14
1-2. Infected fly (genus Chrysops, day- biting flies) introduces third-stage
filarial larvae onto the skin of the human host and develop into adults
that commonly reside in subcutaneous tissue.
3. Adults produce microfilariae which are sheathed and have diurnal
periodicity. Microfilariae have been recovered from spinal fluids,
urine, and sputum. During the day they are found in peripheral blood,
but during the noncirculation phase, they are found in the lungs.
4-7. Fly ingests microfilariae during a blood meal. After ingestion, the
microfilariae lose their sheaths and migrate from the fly's midgut
through the hemocoel to the thoracic muscles of the arthropod, where
they develop into first-stage larvae and subsequently into third-stage
infective larvae.
8. Third-stage infective larvae migrate to the fly's proboscis and can infect
another human when the fly takes a blood meal.
Mansonella ozzardi
Vectors: midges (genus Culicoides) or blackflies (genus
Simulium)
Adults inhabit the mesenteries and visceral fat
Microfilariae: unsheathed, non-periodic, found in the blood; may
be obtained by skin biopsy
o Nuclei do not extend to the tip of the tail (compared to
M. streptocerca and M. perstans)
o Tail shorter and less tapered than Onchocerca
Generally an asymptomatic infection
o Inguinal adenopathy has been reported
o Skin lesions, arthritis, fever, marked eosinophilia
o Pulmonary symptoms, adenopathy, hepatomegaly,
and pruritus
Life cycle of Mansonella ozzardi
1-2. During a blood meal, an infected arthropod (midges, genus Culicoides,
or blackflies, genus Simulium) introduces third-stage filarial larvae onto
the skin of the human host, where they penetrate into the bite wound.
They develop into adults that commonly reside in subcutaneous
tissues. Adult worms are rarely found in humans.
3. Adult worms recovered from experimentally infected Patas monkeys.
Adults produce unsheathed and non-periodic microfilariae that
reach the blood stream.
4-7. The arthropod ingests microfilariae during a blood meal. After
ingestion, the microfilariae migrate from the arthropod's midgut through
the hemocoel to the thoracic muscles. There the microfilariae develop
into first-stage larvae and subsequently into third-stage infective
larvae.
8. The third-stage infective larvae migrate to arthropod's proboscis and
can infect another human when the arthropod takes a blood meal.
Mansonella perstans
Vector: midges (Culicoides)
Adult worms live in deep connective tissues
Microfilariae: found in peripheral blood and in the skin
o No periodicity; unsheathed
o Nuclei extend to the tip of the tail
Microfilaria of M. perstans (thick blood smear
stained with hematoxylin). Mansonella perstans
is smaller, has no sheath and has a blunt tail
with nuclei extending to the end of the tail.
Often asymptomatic, can be associated with angioedema,
pruritus, fever, headaches, arthralgias, and neurologic
manifestations
o Edema and inflammatory changes and granulomas
form around dead filariae
o Eosinophilia
1. During a blood meal, an infected midge (genus Culicoides) introduces
third-stage filarial larvae onto the skin of the human host, where they
penetrate into the bite wound.
Page 5 of 14
2. They develop into adults that reside in body cavities, most commonly 8. Third-stage larvae migrate to the midge's proboscis and can infect
the peritoneal cavity or pleural cavity, but less frequently in the another human when the midge takes another blood meal.
pericardium.
3. Adults produce unsheathed and subperiodic microfilariae that reach Onchocerca volvulus
the blood stream. Causes onchocerciasis
4-7. A midge ingests microfilariae during a blood meal. After ingestion, the Major cause of blindness in some parts of Africa
microfilariae migrate from the midge's midgut through the hemocoel to Also known as river blindness
the thoracic muscles of the arthropod wehre they develop into first- Adult worms: wirelike, whitish, lie coiled within fibrous tissue
stage larvae and subsequently into third-stage infective larvae. capsules
8. Third-stage infective larvae migrate to the midge's proboscis and can Female: 50cm; males-5cm
infect another human when the midge takes a blood meal. Microfilariae: unsheathed; 150-350µm

Mansonella streptocerca Microfilaria of Onchocerca volvulus from

Vector: small midges (Culicoides) skin snip from a patient seen in
Microfilariae found in the skin and blood Guatemala (Wet preparation).
o Nuclei extend to the tip of the tail which is bent in the form of
Important characteristics: no sheath
a shepherd’s crook
present and tail is tapered and is sharply
Skin manifestations including pruritus, popular eruptions and
angled at the end
pigmentation changes

Life cycle of Mansonella streptocerca

Often found in the skin; rarely in urine, blood and sputum
Developing worms wander through subcutaneous tissues
Most worms become encapsulated-nodules are produced.
Onchocerciasis can cause pruritus, dermatitis. Onchocercomata
(subcutaneous nodules), and lymphadenopathies.
The most serious manifestation consists of ocular lesions that can
progress to blindness.

1-2. During a blood meal, an infected midge (genus Culicoides) introduces

third-stage filarial larvae onto the skin of the human host, where they
penetrate into the bite wound They develop into adults that reside in the
dermis, most commonly less than 1 mm from the skin surface.
3. Adults produce unsheathed and non-periodic microfilariae which reside
in the skin but can also reach the peripheral blood.
4-7. A midge ingests the microfilariae during a blood meal. After ingestion, 1. During a blood meal, an infected blackfly (genus Simulium) introduces
the microfilariae migrate from the midge's midgut through the hemocoel third-stage filarial larvae onto the skin of the human host, where they
to the thoracic muscles where they develop into first-stage larvae and penetrate into the bite wound.
subsequently into third-stage larvae.

Page 6 of 14
2-4. In subcutaneous tissues the larvae develop into adult filariae, which Special Procedures for Detecting Microfilariae (Blood Microfilariae)
commonly reside in nodules in subcutaneous connective tissues; Capillary (fingerstick) blood
female worms are capable of producing microfilariae for approximately o Since microfilariae concentrate in the peripheral
9 years. The microfilariae are unsheathed, have a life span that may capillaries, thick and thin smears prepared from
reach 2 years. They are occasionally found in peripheral blood, urine, fingerstick bood are recommended.
and sputum but are typically found in the skin and in the lymphatics of
connective tissues. Anticoagulated (EDTA) venous blood (1ml) should be
5-8. Blackfly ingests the microfilariae during a blood meal and migrate from concentrated by one of the following methods:
the blackfly's midgut through the hemocoele to the thoracic muscles. 1. Centrifugation (Knott’s technique) uses 2%
There the microfilariae develop into first-stage larvae and subsequently formaldehyde
into third-stage infective larvae. 2. Filtrationuses membrane filter (Millipore ® or
9. Third-stage infective larvae migrate to the blackfly's proboscis and can Nucleopore ® membrane filter)
infect another human when the fly takes a blood meal.
Ultrasonography, contrast lymphagiography and
Laboratory Diagnosis: Filariasis lymphscintigraphy
Identification of blood samples to identify microfilariae o May demonstrate live worms in the lymphatics
o Blood sample can be a thick smear, stained with o Contrast lymphangiography using radiolabeled
Giemsa or H&E albumin or dextran may demonstrate obstructed
o For increased sensitivity, concentration techniques can lymphatics
be used: centrifugation of blood sample lyzed in 2%
formalin (Knott’s technique) or filtration through a Comparison of Microfilariae of W. bancrofti and B. malayi
Nucleopore® membrane Criteria W. bancrofti B. malayi
Examination of skin snips will identify microfilariae of Onchocerca Mean length (µm) 290 222
volvulus and Mansonella streptocerca Cephalic space: 1:1 2:1
o Skin snips are obtained using a corneal-scleral punch, broadth
or a scalpel and needle.
Sheath in Giemsa Unstained Pink
o Allow sample to incubate for 30 minutes to 2 hours in
saline or culture medium and then examined for Nuclei Regularly spaced, separately Irregularly spaced and
stunted overlapping
microfilariae that would have migrated from the tissue
to the liquid phase of the specimen. Tail Single row of nuclei that does Single row of nuclei that
Finding of microfilariae in the blood as seen in wet or thick blood not reach the tail’s ends reaches tail’s end
smears taken between 8pm and 4am
o W. Bancrofti- nocturnal periodicity Terminal Nuclei None 2 nuclei which bulge the
o B. malayi microfilariae- subperiodic periodicity cuticle, conspicuously
o In low intensity infection Knott’s method for places
concentration may be used
o DEC (Diethylcarbamazine) provocative test Appearance in Smoothly curved Kinky
blood film
stimulates microfilariae to come out to peripheral
circulation allowing blood smear collection even during
daytime. Comparison of Microfilariae sizes and morphology
Antigen detection techniques to detect circulating filarial antigens Species Size Morphology
(CFA)- useful in low and variable infection Wuchereria bancrofti 210-320µm by 8-10µm Sheathed, tail pointed and
clear
Diagnostic Findings:
Brugia malayi 170-260µm by 5-6µm Sheathed, tail pointed with 2
Antigen detection using an immunoassay for circulating filarial nuclei
antigens- useful because microfilaremia can be low and variable
o A rapid format immunochromatographic test, Loa loa 230-300µm by 6-8µm Sheathed, tail blunt with
nuclei
applicable to Wuchereria bancrofti antigens has been
recently evaluated in the field. Mansonella perstans 200µm by 6µm Unsheathed, tail blunt with
Molecular diagnosis using PCR nuclei
o Available for W. bancrofti and B. malayi Mansonella ozzardi 250µm by 5-7µm Unsheathed, tail pointed and
Identification of adult worms is possible from tissue samples clear
collected during nodulectomies (onchocerciasis) or during
subcutaneous biopsies or worm removal from the eye (loiasis).
Antibody detection- limited value Periodicity
o Substantial antigenic cross reactivity exists between Fluctuation in numbers of microfilariae present in the peripheral
filarial and other helminthes and a positive serologic blood during a 24-hour period
test does not distinguish between past and current Nocturnally Periodic
infection. species found in the blood during night-time hours but absent at
other times (e.g. W. bancrofti & B. malayi)

Page 7 of 14

Diurnally Periodic
present only during certain daytime hours (e.g. Loa loa)
Nonperiodic or Aperiodic
microfilariae that circulate in the blood throughout a 24-hour
period without significant changes in their numbers (e.g.
Mansonia spp.)
Subperiodic
microfilariae normally present in the blood at all hours but whose
density increases significantly during either the night or day
There are two strains of B. malayi:
o The nocturnal periodic strain which is widely
distributed in Asia, the microfilariae being in their
highest concentrations between the hours of 10pm and
2am
o The sub-periodic strain which is found in Malaysia,
Indonesia and the Philippines where humans exhibit a
microfilaraemia all the time with the highest numbers
being detected between noon and 8pm
Treatment
Different drugs are recommended for the treatment of filariasis
depending on the specific causal agent.
Diethylcarbamazine citrate (DEC)- drug of choice for
bancroftian filariasis: 6mg/day orally for 12 days (given in divided
doses after meals)
o Brugian filariasis- 3-6mg/kg per day up to 36 to
72mg/body weight
Ivermectin- 200 to 400µg/kg single oral dose- as effective as 12
days of DEC
Prevention and Control
Goal for endemic communties: elimintae microfilariae in the blood
to prevent transmission of disease by vectors
Control of transmission:
o Identification of endemic areas
o Implementation of mass treatment programs using
albendazole/DEC or DEC/ivermectin combination in
areas where onchocercosis or loaiasis is prevalent
Personal protective measures
Vector control: development sprays and polystyrene beads to seal
latrines
Trichinella
Causes Trichinellosis
classical agent: T. Spiralis
other species of Trichinella:
o T. pseudospiralis (mammals and birds worldwide)
o T. native (Arctic bears)
o T. nelson (African predators and scavengers), and
o T. britovi (carnivores of Europe and West Asia)
Adult female is 2.2 mm in length (3.5 mm x 0.06 mm) – single
ovary situated in the posterior part of the body
o Has an oviduct, a seminal receptacle, coiled uterus, a
vagina and a vulva situated in the anterior fifth on the
ventral side of the body
o Viviparous females live for 30 days and can produce
1500 larvae or more
Adult males is 1.2 mm (1.5 mm x 0.04 m) – single testes located
near the posterior end and is joined in the mid-body by the genital
tube, which in turns extends back to the cloaca
o Cloaca has a pair of caudal appendages and 2 pairs of
papillae
Larvae: 80-120 um x 5.6 um at birth
o Has a spear-like burrowing anterior tip
Infective larvae are encysted in the muscle fiber of the host
Hosts serve as both the final and intermediate host by harboring
both the adult and larval stages
o Humans, rats, dogs, ctas, pigs, bears, foxes, walruses,
other carnivores or omnivores
Host are infected by consuming insufficiently cooked meat
(containing the infective larvae)
Larvae excyst either in the stomach or small intestine → burrow
into the villi where they mature
Adult worms mate → female produce eggs that grow into larvae
in its uterus → are deposited in the mucosa, penetrates it, pass
through lymphatic system into circulation → to striated muscle
After 3 weeks larvae start to coil into individual cysts
Encapsulation: 4-5 weeks after infection
Larvae in the cysts remain viable for years
In humans, calcification of cysts takes 6-12 months after infection
Life cycle of Trichinella
1. Ingesting meat containing cysts (encysted larvae) of Trichinella.
2-3. Larvae are released and invade the small bowel mucosa → they
develop into adult worms;
4-5. After 1 week, females release larvae → migrate to striated muscles
where they encyst (Trichinella pseudospiralis does not encyst)
 encystment is completed 4-5 weeks; encysted larvae may remain
viable for several years.
 Ingestion of the encysted larvae perpetuates the cycle.
 Rats/rodents maintain endemicity
 Carnivores/omnivores feed on infected rodents or meat
 Humans are accidentally infected when eating improperly
processed meat.
Page 8 of 14
Clinical Manifestations
Light infections may be asymptomatic.
Intestinal invasion
o accompanied by GI symptoms: diarrhea, abdominal
pain, vomiting
Larval migration into muscle tissues (one week after infection )
can cause
o Periorbital and facial edema, conjunctivitis, fever,
myalgias, splinter hemorrhages, rashes, and blood
eosinophilia.
Occasional life-threatening manifestations
o Myocarditis, CNS involvement, and pneumonitis
o Larval encystment in the muscles causes myalgia and
weakness, followed by subsidence of symptoms.
Severity of symptoms depends on intensity of infection:
o Light infection :patients harboring up to 10 larvae
o Moderate infection: 50-500worms
o Severe and potentially fatal:> 1,000 larvae
3 Phases of clinical conditions
1. Enteric phasestage of incubation and intestinal
invasion
o Diarrhea or constipation, vomiting, cramps,
malaise, nausea
2. Invasion phaselarval migration and muscle
invasion
o Myalgia, periorbital edema & eosinophilia –
cardinal s/s
o High remittent fever, dyspneadysphagia,
difficulty chewing, paralysis of extremities,
GI hemorrhage, splenomegaly
3. Convalescent phaseencystment and encapsulation
o Abatement of fever, pain, weakness and
other symptoms
Full recovery expected since it’s a self-limiting disease
Complications: myocardial and neurologic
o In heavy infections, ocular disturbances, deafness,
seizures and coma may occur
Prognosis is good in mild infections
o Death is uncommon except in cases with
complications (heart failure, encephalitis, pneumonia,
sepsis)
o Low-grade fever or absent peripheral blood
eosinophilia- poor prognosis.
Diagnosis
Based on history of exposures and physical exam
Most definitive diagnostic exam – demonstration of larva using
muscle biopsy
Biochemical test – elevated CPK, LDH and myokinase
High blood count and peripheral eosinophilia –strengthen
diagnosis
Serology may provide confirmatory diagnosis
Beck’s xenodiagnosiswhen meat is suspected on harboring
encysted larva
o Feeding the meat to albino rats; observe them 14 days
after for female worm in the duodenum and larvae in
the muscle of experimental host.
Laboratory Diagnosis
Suspension of trichinellosis (trichinosis) based on clinical
symptoms and eosinophilia
Can be confirmed by specific diagnostic tests: antibody detection,
muscle biopsy, and microscopy
Encysted larvae of Trichinella on pressed muscle
tissue sample
The coiled larvae can be seen inside the cysts.
Treatment:
should begin as soon as possible
o bed rest, supportive treatment
Thiabendazole – 25 mg/kg 2x/D for 7D expels adult worm from
GIT during 1st week of infection, but has no effect on migrating
larvae and is useless for infections detected 2 weeks after
exposure
o Mebendazole – larvicidal when given at 20mg/g
6hourly for 10-14 days.
o Albendazole-shows promise but has yet been
sufficienly evaluated
Steriods are used for infections with severe symtoms (Prednisone
20mg 3x daily tapered over 2-3 weeks
Epidemiology
Occurs whenever meat is part of the diet
o Canada, mexico, Holland, Hungary, Polland, Ukraine,
Lithuania, Yugoslavia, spain, Egypt, Brazil, Uruguay,
Chile, Ecuador, Vietnam, Malaysia, and Thailand
Humans get infected after ingestion of raw or insufficiently cooked
meat of infected animals.
Infection is maintained in a pig-pig or pig-rat-pig cycle.
Prevention and Control
Health education
Cook meat 77*C
Freezing at -15*C for 20 days or -30*C for 6 days can kill the
larvae
Smoking, salting, drying – not effective
Meat inspection and keeping pigs in rat-free pens
Angiostrongylus
Causal Agents: The nematode (roundworm)
Angiostrongylus cantonensis, the rat lung worm, is the most
common cause of human eosinophilic meningitis
Angiostrongylus (Parastrongylus) costaricensis is the causal
agent of abdominal, or intestinal, angiostrongyliasis
Geographic distribution:
Most cases of eosinophilic meningitis have reported from
Souheast Asia and the Pacific Basin.
Abdominal angiostrongyliasis has been reported from Costa Rica,
and occurs mainly in children less than 13 years old.
Human infection was first reported in Taiwan in 1944
First well documented fatal case of human Angiostrongyliasis was
in a 50 year old Filipino male admitted in a hospital in Hawaii
Angiostrongylus cantonensis
Adult worm: pale, filiform
Page 9 of 14
 Male worm: 16-19 mm (length) x
0.26 mm (diameter)
o well-developed caudal
bursa w/c is kidney-
shaped and single-
lobed
Female worm: 21-25 mm x 0.30 –
0.36 mm
o has uterine tubules w/c are wound spirally around the
intestine → “barbers pole” pattern
o lays up to 15,000 eggs/D

Adult worms of A. cantonensis:

measure b/w 1-7-25 mm long and
reside in the pulmonary arteries
and arterioles of the definitive host
Adult worm live in the pulmonary
arteries of the rat.
After 6 days first stage larvae hatch from eggs → respiratory tract
→ up to trachea and are swallowed → expelled in the feces
The 1st stage larvae of A. cantonensis. The larvae are found in the
faeces of rats.

Angiostrongylus Life cycle:

Adult worm of A. cantonensis live in the pulmonary arteries of rats
and rodents
Females lay eggs that hatch, yielding first stage larvae, in the
terminal branches of pulmonary arteries → migrate to the
pharynx, are swallowed and are passed in the feces → invade an
intermediate host (snail or slug); after 2 molts, 3rd stage larvae are
produced, which are infective to mammalian hosts
Known intermediate hosts in the Phil.:
o slugs and snails:
 Acnatina fulica
 Hemiplecta sagittifer
 Helicostyla macrostoma
 Vaginilus plebeius
 Veronicella altae
Mollusk is ingested by the definitive host, the 3rd stage larvae
migrate to the brain where they develop into young adults →
young adults return to venous system and then pulmonary
arteries where they become sexually mature.
o Various animals act as paratenic (transport) hosts:
after ingesting the infected nails, they carry the third
stage larvae which can resume their development
when the paratenic host is ingested by a definitive host
Human acquire the infection by eating uncooked snails or slugs,
vegetables contaminated with mollusks secretion, or infected
paratenic animals (crabs, freshwater shrimps).
o Development of the third stage larvae is stalled in the
brain while they die.
Life cycle of Angiostrongylus (parastrongylus) costaricensis is
similar, except that the adult worm reside in the arterioles of the
ileocecal area of the definitive host
In humans, the eggs and larvae degenerate and cause local inflammatory
reactions.
1. Adult worms in the rat lungs lay eggs & yield L1→ pharynx, swallowed →
rat feces
2. Invade IH (snail/slug) → L3; mollusk are ingested by definitive hosts &L3
migrate to brain → young adults, return to venous system and pulmonary
arteries where they become sexually mature.
o In humans, A. cantonensis juvenile worms migrate to brain, or
rarely in the lungs, where the worms ultimately die.
O In humans, A. costaricensis often reaches sexual maturity and
release eggs into the intestinal tissues. The eggs and larvae
degenerate and cause intense local inflammatory reactions and
do not appear to be shed in the stool.
Clinical features
Clinical symptoms of eosinophilic meningitis are caused by the
presence of larvae in the brain and by local host reaction.
o Severe headaches, nausea, vomiting, neck stiffness,
seizures, and neurologic abnormalities.
o Occasionally, ocular invasion occurs.
o Eosinophilia is present in most cases
o Most patient recover fully
Abdominal angiostrongyliasis (eosinophilic enteritis) mimics
appendicitis, with eosinophilia.
In eosinophiic meningitis the CSF is abnormal (↑ pressure, PRO
and leukocytes; eosinophilia).
o On rare occasions, larvae have been found on CSF
o CT scans- may show meningeal lesions
o Serologic confirmation – ELISA
In abdominal angiostrongyliasis, eggs and larvae can be identified
in the tissues removed at surgery.

Page 10 of 14
 Presumptive dx is made by travel and exposure history. o Fertilized egg (R); Egg containing a well-developed
In humans, eggs and larvae are not normally excreted, but remain larvae; this will be infective if ingested by a human
sequestered in tissues. (frequently a child) (L)
Both eggs and larvae (occasionally adult worms) of A.
costaricensis can be identified in biopsy of surgical specimens of Life cycle of Toxocara
intestinal tissue.
The larvae need to be distinguished from larvae of Strongyloides
stercoralis; however, the presence of granulomas containing thin
shelled eggs and/ or larvae serve to distinguish A. costaricensis
infections.

Eggs and Larva of A. costaricensis

Management and Prognosis:

No antihelminthic treatment is recommended at resent although
mebendazole, thiabendazole and ivermectin were found to be
successful in animal experiments
o Antihelminthics usually not necessary bec. Disease is
self-limiting and killing the worms may bring about
Ingestion by dogs→ infective eggs hatch→larvae penetrate the
greater inflammatory reactions.
gut wall and migrate into various tissues, where they encyst if the
o Analgesics; removal of spinal fluid at regular intervals
dog is older than 5 weeks.
can relieve headache
In younger dogs larvae migrate thru the lungs, bronchial tree, and
o Prednisone 30 mg daily: recommended in severe
esophagus; adult worms develop and oviposit in the small
cases with cranial nerve involvement
intestine
o Surgical removal: when parasite is lodge in the anterior
In older dogs, encysted stages are reactivated during pregnancy
chamber of the eye
and infect by the transplacental and transmammary routes the
o Prognosis is usually good
puppies, in those small intestine adult worms become
o Infection is self-limiting, complete recovery usually
established.
occurs
Humans are accidental hosts, become infected by ingesting
o Permanent neurologic deficits do not occur
infective eggs in contaminated soil
o Occasionally fatal.
After ingestion, eggs hatch & larvae penetrate intestinal wall & are
carried by the circulation to different tissues (liver, heart, lungs,
Toxocara
brain, muscle, eyes) & can cause severe local reactions
Causes toxocariasis 2 main clinical presentations: visceral larvae migrans (VLM) &
o larvae of Toxocara canis (dog roundworm) ocular larvae migrans (OLM)
o T. cati (cat roundworm)
Clinical Features
Toxocara canis accomplishes its life cycle in dogs, with humans
acquiring the infection as accidental host. Puppies are infected w/ Many humans infections are asymptomatic, w/ only eosinophilia
T. canis as early as the fetal stage or at birth due to transplacental and positive serology
and transmammary transmission (important source of eggs) 2 main clinical presentations
Man becomes infected by ingestion of embryonated eggs thru 1. VMLlarvae invade multiple tissues (liver, heart,
contaminated food and water lungs, brain, muscle) and cause various symptoms
o fever, anorexia, weight loss, cough,
Other mammals and birds may serve as paratenic hosts
wheezing,rashes, hepatosplenomegaly,
Geographic Distribution: worldwide
and hypereosinophilia
The eggs are passed in the dog feces, especially puppies’ feces.
o occurs mostly in preschool children
Human infections with
2. OLMlarvae produce various ophthalmologic lesions,
Toxocara do not produce
w/c in some cases has been misdiagnosed as
or excrete eggs, and
retinoblastoma, resulting in surgical enucleation
therefore eggs are not a
o often occurs in older children and young
diagnostic finding in human
adults, w/ only rare eosinophilia or visceral
toxocariasis
manifestations
Eggs of Toxocara canis

Page 11 of 14
 Death can occur rarely, by severe cardiac, pulmonary or predation, the larvae are transferred from fish to fish until ingested
neurologic involvement by humans and marine mammals.
Upon ingestion by marine mammals, the larvae molt 2x & develop
Toxocariasis: Laboratory Diagnosis into adults → adult females produce eggs that are shed by
Diagnosis does not rest on identification of the parasite marine mammals
Since the larvae do not develop into adults in humans, a stool Human are infected by eating raw or undercooked infected
examination would not detect any Toxocara eggs marine fish →larvae penetrate the gastric and intestinal mucosa,
o presence of Ascaris and Trichuris eggs in feces, causing symptoms
indicating fetal exposure, increases the probability of
Toxocara in the tissues.
For both VLM and OLM, a presumptive diagnosis rests on clinical
signs, history of exposure to puppies, laboratory findings
(including eosinophilia0, & detection of antibodies to Toxocara.
Antibody detection
o The only means of confirmation of clinical dx of VML,
OML and CT (covert toxocariasis)), the most clinical
syndromes associated with Toxocara infections
o The currently recommended serologic test for
toxocariasis is EIA.

Treatment
VLM is treated with antiparasitic drugs, usually in combination
with anti-inflammatory medications.
Treatment of OLM is more difficult and usually consists of
measures to prevent progressive damage to the eye
o Albendazole
o Mebendazole

Anisakis
Causes anisakiasis
Caused by larval stages anisakine nematodes persisting in the
alimentary canal or penetrating the tissues of humans after
consuming raw or semi raw fish
Conditions is caused by accidental ingestion of larvae f
nematodes (roundworms) Anisakis simplex and Pseudoterranova Clinical features:
decipiens Within hours after ingestion of infected larvae, violent abdominal
Fish species acts as intermediate/transport host for the larva pain, nausea, and vomiting may occur.
o Larva matures into adults in warm blooded marine Occasionally the larvae are coughed up
mammals If the larvae pass into the bowel 1 – 2 weeks following infection, a
No human case yet reported in the Phil but the potential for severe eosinophilic granulomatous response may also occur,
infection is great. causing symptoms mimicking Crohn’s disease
Laboratory Diagnosis:
Geographical distribution: Can be made by gastroscopic examination during which the 2 cm
Worldwide, with higher incidence in areas where raw fish is eaten larvae are visualized and removed, or by
(Japan, Pacific Coast of South America, Netherlands) Histopathologic examination of tissue removed at biopsy or during
Increasing incidence in US due to increased consumption of raw surgery
fish Treatment
Treatment of choice is surgical or endoscopic removal.
Life cycle of Anisakis
Adult stages reside in the stomach of marine mammals→ adult -------------------------------------------END OF TRANS-------------------------------------
female produce unembryonated eggs and passed in the feces of
marine animals (sorry wala ng space for filler,
Eggs become embryonated in water, and 1st stage larvae are overwhelming ang trans na ito eh.
hehehe )
formed in the eggs → larvae molt → 2nd stage larvae and after it
hatches from the eggs, become free swimming
Released larvae are ingested by crustaceans→ develop into 3rd
stage larvae that are infective to fish and squid
Larvae migrate from intestine to tissues in the peritoneal cavity;
upon host’s death, larvae migrate to muscle tissue → thru

Page 12 of 14
 BLOOD AND TISSUE NEMATODES
Species Common name Habitat Mode of Transmission Arthropod Vector Periodicity

Wucheria bancrofti Bancroft’s Filaria Lower lymphatics Skin Inoculation Mosquitoes (Aedes, Culex, Anopheles and Mansonia) Nocturnal periodic

Brugia malayi Malayan Filaria Upper lymphatics Skin Inoculation Mosquitoes (Mansonia spp.) Nocturnal subperiodic

Loa loa Eyeworm Subcutaneous tissues Skin Inoculation Chrysops fly/ Deerfly/ Mango fly Diurnal periodic

Onchocerca Convoluted Filaria Body cavities Skin Inoculation Simulium fly/ Black fly Non-periodic
volvulus

Dipetalonema Persistent Filaria Body cavities Skin Inoculation Culicoides fly Non-periodic
perstan

Mansonella ozzardi Ozzard’s Filaria Body cavities Skin Inoculation Culicoides fly Non-periodic

MORPHOLOGY OF MICROFILARIA
Species Possession of Sheath Distinguishing Feature

Wucheria bancrofti Nuclei do not extend to the tip of the tail

Sheathed
Brugia malayi With 2 distinct terminal nuclei

Loa loa Nuclei extend to the tip of the tail

Onchocerca volvulus Nuclei do not extend to the tip of the tail and microfilaria does not appear in the peripheral
Unsheathed blood

Dipetalonema perstans Nuclei extend to the tip of the tail

Mansonella ozzardi Nuclei do not extend to the tip of the tail

Source: CEU Review notes in parasitology by Ma. Cristina Liwanag

Page 13 of 14
DIFFERENCES AMONG THE SIX BLOOD AND TISSUE NEMATODES
Species
Wuchereria bancrofti
Brugia malayi
Loa loa
Onchocerca volvulus
Mansonella perstans (or
Dipetalonema perstans
Mansonella ozzardi
Source: CEU Review notes in parasitology by Ma. Cristina Liwanag
Geographic distribution
Indigenous throughout the warmer regions of the
globe. It is hyperendemic in South East Asia and
Polynesian Islands
Found only in South East Asia
Indigenous in Central and West Africa
Occurs in equatorial Africa, with the exception of the
east coast, and in Guatemala and Southern Mexico
Widely distributed in the tropical areas of Africa and
Central and South America
Occurs in South America and the western Indian
Islands
Morphology of adult
Adults are long, female 8-10 cm x
0.25 mm being larger than male, 4
cm x 0.1 mm
Adult worms are 2-5 cm x 0.1-0.2
mm
Adults range in size from 3-7 cm x
0.3- 0.5 mm. The female being
slightly larger than the male
Adult worms are long, female
being markedly larger (30-50 cm x
0.3-0.4 mm) than the male (2-4 cm
x 0.1-0.2 mm)
The adult worms are slightly larger
than tha adults of Loa loa. Inhabits
the connective tissue of the
mesenteries and the peritoneal
cavities; more rarely they occur in
the pericardial and pleural cavities
Adult worms are similar in size to
those of D. perstans
Pathogenesis
Bancroftian filariasis
Adult worms provoke inflammatory response and obstructive changes in the lymph glands.
Inflammation results in toxemia, fever and local pain. Obstruction of the lymph channels
results in stagnation of the lymph and dilatation of the vessels with following hypertrophy
and fibrosis of the affected tissues, leading eventually to elephantiasis especially of the
limbs and scrotum
Malayan Filariasis
The elephantic lesions are more frequent in the upper limbs and are rarely observed in the
lower limbs of the scrotum
Temporary inflammatory swelling (Calabar/ Fugitive swelling)
Provoked by migratory adults. They cause pain and inconvenience especially when in the
neighborhood of the eyes or bridge of the nose
Onchocerciasis or blinding Filariasis
Adult worms in the subcutaneous tissue give rise to inflammatory reactions and fibrotic
nodules, each of which generally contains a male and female worm. The characteristic
nodules are not usually painful unless situated over a joint but they may be intensely
pruritic. Much more serious are the ocular lesions which results from the invasion of the eye
by microfilaria and their death therein give rise to inflammatory reactions,, Blindness not
infrequently follows.
Infection is essentially symptomless
Page 14 of 14