MICROBIOLOGY Dra. Bunyi 4th shifting Jan.

30, 2008

shar, cams, joy Class no.:

 deerflies [Chrysops] for Loa loa

FILARIASIS - Inside the arthropod, the microfilariae develop in 1 to 2
Causal Agents weeks into infective filariform (third-stage) larvae
- nematodes (roundworms) that inhabit the lymphatics and
subcutaneous tissues  During a subsequent blood meal by the insect, the
- 8 main species infect humans: larvae infect the vertebrate host → migrate to the
• 3 of these are responsible for most of the morbidity appropriate site of the host's body, where they
due to filariasis: develop into adults, a slow process than can require
up to 18 months in the case of Onchocerca.
o Wuchereria bancrofti and Brugia malayi
cause lymphatic filariasis, and
o Onchocerca volvulus causes Wuchereria bancrofti and Bancroft’s filarial
onchocerciasis (river blindness) worm
• Causes bancroftian filariasis
• other five species are Loa loa, Mansonella perstans,
• Causes a chronic disfiguring disease
M. streptocerca, M. ozzardi, and Brugia timori. (The
- Lymphedema, elephantiasis,
last species also causes lymphatic filariasis.)
hydrocoele
• Vectors: Aedes, Culex, Anopheles
There are four sheathed species: Wuchereria bancrofti,
Brugia malayi, Brugia timori, and Loa loa. • Development of microfilaria into
infective stage: 6-20days
Geographic Distribution: Brugia malayi – Malayan filarial worm
- Among the agents of lymphatic filariasis, Wuchereria • Causes Malayan filariasis
bancrofti is encountered in tropical areas worldwide • Chronic infection also presents with
- Brugia malayi is limited to Asia lymphedema and elephantiasis
- Brugia timori is restricted to some islands of Indonesia
• Mosquito vectors: Mansonia
- the agent of river blindness, Onchocerca volvulus, occurs
mainly in Africa, with additional foci in Latin America and the • Development of microfilariae to
Middle East infective stage: 2 weeks
- among the other species, Loa loa and Mansonella • Maturation time for 3rd stage larvae
streptocerca are found in Africa to become adults: 3-9 months
- Mansonella perstans occurs in both Africa and South America
- Mansonella ozzardi occurs only in the American continent Infection with these filarial parasites not only causes chronic
debilitating disease but also
Life Cycles: • Acute fever
- Infective larvae are transmitted by infected biting arthropods • Inflammation of the lymphatic system
during a blood meal • Tropical pulmonary eosinophilia
- larvae migrate to the appropriate site of the host's body,
where they develop into microfilariae-producing adults WUCHERERIA
- adults dwell in various human tissues where they can live for
several years • Adult: Creamy, white, long and filiform
- the agents of lymphatic filariasis (Wuchereria - Male worm: 2-4 cm length
bancrofti) reside in lymphatic vessels and lymph nodes; - Female: 8-10 cm
- Brugia malayi in lymphatics, as with Wuchereria bancrofti; • Microfilariae appear as snake-like organisms &
- Onchocerca volvulus in nodules in subcutaneous tissues; measures 270-290um
- Loa loa in subcutaneous tissues, where it migrates actively; - Enclosed in a hyaline sheath which is longer
- Mansonella streptocerca in the dermis and subcutaneous than the microfilaria itself
tissue; - Central axis: shows dark staining nuclei; column
- Mansonella ozzardi apparently in the subcutaneous tissues; of nuclei arranged in 2 or 3 rows and is
and indistinctly conspicuous
- M. perstans in body cavities and the surrounding tissues - Graceful appearance
- The female worms produce microfilariae which circulate in
the blood, except: BRUGIA
 Onchocerca volvulus and Mansonella • Adult male: 12-32 mm length
streptocerca, which are found in the skin, - Female: 43-45 mm
and - Adult females of B. malayi and W. bancroftiare
indistinguishable
 O. volvulus which invade the eye • Microfilariae measures 177-230um
- The microfilariae infect biting arthropods: - Enclosed in a sheath & with angular curvatures
 Mosquitoes - agents of lymphatic filariasis: with secondary kinks and 2 nuclei at the tip tail
Wuchereria & Brugia - Column of nuclei is in 2 rows which are indistinct
or confluent
 blackflies [Simulium] for Onchocerca
volvulus; W. BANCROFTI
 midges for Mansonella perstans and M. Vector
streptocerca; and • mosquito vector depends on geographic distribution
- Culex (C. annulirostns, C. bitaenicrhynchus, C.
 both midges and blackflies for Mansonella quinquefasciatus, and
ozzardi;
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 C. pipiens); 0.30 mm in diameter, while the males measure about 40 mm
- Anopheles (A. arabinensis, A. bancroftii, A. farauti, A. by .1 mm. Adults produce microfilariae measuring 244 to 296
funestus, A. gambiae, A. koliensis, A. melas, A. merus, A. μm by 7.5 to 10 μm, which are sheathed and have nocturnal
punctulatus and A. wellcomei); periodicity, except the South Pacific microfilariae which have
- Aedes (A. aegypti, A. aquasalis. A. bellator, A. cooki, A. the absence of marked periodicity. The microfilariae migrate
darlingi, A. kochi, A. polynesiensis, A. pseudoscutellaris, into lymph and blood channels moving actively through lymph
A. rotumae, A. scapularis, and A. vigilax); and blood . A mosquito ingests the microfilariae during a
- Mansonia (M. pseudatitillans, M. uniformis)
- Coquillettidia (C. juxtamansonia). blood meal . After ingestion, the microfilariae lose their
sheaths and some of them work their way through the wall of
Adult forms the proventriculus and cardiac portion of the mosquito's
• Adults produce microfilariae measuring 244 to 296 um by midgut and reach the thoracic muscles . There the
7.5 to 10 um microfilariae develop into first-stage larvae and
- Microfilariae are sheathed
subsequently into third-stage infective larvae . The third-
- have nocturnal periodicity, (except the South Pacific
stage infective larvae migrate through the hemocoel to the
microfilariae which have the absence of marked periodicity)
mosquito's prosbocis and can infect another human when
Vector mosquito the mosquito takes a blood meal .
- Aedes, Culex. Anopheles
- Other possible vectors: Mansonia , Coquillettidia (CDC)
LIFE CYCLE OF B. MALAYI
• 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 rnosquito’s head and proboscis
• During a blood meal, larvae (from the mosquito) reaches 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 penodicity (seen in blood
taken between 8pm to 4 am)

B. MALAYI
• Vector: mosquito of the genus Mansonia
- Aedes is also listed as one of its vectors (CDC)
• 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 and have a
subperiodic periodicity

LIFE CYCLE OF W. BANCROFTI

During a blood meal, an infected mosquito 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 the lymphatics . The adult
worms resemble those of Wuchereria bancrofti but are
smaller. Female worms measure 43 to 55 mm in length by
130 to 170 μm in width, and males measure 13 to 23 mm in
length by 70 to 80 μm in width. Adults produce microfilariae,
measuring 177 to 230 μm in length and 5 to 7 μm in width,
which are sheathed and have nocturnal periodicity. The
microfilariae migrate into lymph and enter the blood stream
reaching the peripheral blood . A mosquito ingests the
microfilariae during a blood meal . After ingestion, the
microfilariae lose their sheaths and work their way through
the wall of the proventriculus and cardiac portion of the
midgut to reach the thoracic muscles . There the
microfilariae develop into first-stage larvae and
subsequently into third-stage larvae . The third-stage
larvae migrate through the hemocoel to the mosquito's
prosbocis and can infect another human when the mosquito
takes a blood meal .

During a blood meal, an infected mosquito introduces third- FILARIASIS IN THE PHILIPPINES
stage filarial larvae onto the skin of the human host, where 1. Bancroftian filariasis
they penetrate into the bite wound . They develop in • Bancroftan filariasis - Camarines Norte, Camarines Sur,
adults that commonly reside in the lymphatics . The Albay, Sorsogon, Mindoro, Masbate, Romblon,
female worms measure 80 to 100 mm in length and 0.24 to Marinduque, Bohol, Samar, Leyte, Palawan, Mountain
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 Province (Bontoc), and all provinces of Mindanao ○ s/sx reflect immunologic phenomenon
inciuding Sulu, Tawi-Tawi and Basilan
caused by sensitization to the products of
- Anopheles minimus var. flavirostris — vector in Mt. Province,
living or dead worms collectively called
Sulu, Palawan
adenolymphangitis (ADL) or
- Aedes poecilus (breeds in water in the axils of abaca and
dermatolyphangioadenitis (DLA)
banana plants) — vector in other provinces
• Chronic Stage
- Infection rate from 1989 to 1991: 0.88 to 2.5%
- Sorsogon: microfilaria rate 15%; hydrocoele was present in ○ With repeated acute episodes, acute
4% of males manifestations merge into a chronic
proliferative overgrowth of fibrous tissue
2. Malayan filariasis around the dead worms — lead to
• Malayan filariasis — Palawan, Eastern Samar, Agusan del lymphatic obstruction, recurrent attacks
of DLA and lymphedema, elephantiasis or
Sur, and Sulu
hydrocoele
- In these places W. bancrofti coexists with B. malayl
○ Cellular reaction and edema are replaced
- Mosquito vector: Mansonia bonnae (breeds in freshwater
swamps) and Mansonia uniformis (breeds in rice fields) by fibrous hyperplasia
- Night biters: 5pm until 11 pm • TPE (tropical pulmonary eosinophilia): occult filariasis —
microfilariae not found in the blood but may be found in
• Prevalence: <3%
tissues
• Cats are important reservoir host and transmit infection - immunologic hyperresponsiveness to filarial
to humans by means of cat-mosquito- man cycle infection characterized by nocturnal cough,
hypereosinophilia, elevated ESR, diffuse miliary
FILARIASIS: CLINICAL FEATURES lesions or increased vascular markings
• Lymphatic filariasis most often consists of asymptomatic • Chyluria — rupture of lymphatics in the kidney due to
microfilaremia. blockage of retroperitoneal lymph nodes
- Development of lymphatic dysfunction causing - Several reports of glomerulonephritis in
lymphedema and elephantiasis bacroftian filariasis
- with Wuchereria bancrofti there is: hydrocele & scrotal
elephantiasis
- febrile lymphangitis and lymphadenitis may occur
- Persons who have newly arrived in disease-endemic
areas can develop afebrile episodes of lymphangitis &
lymphadenitis.
- An additional manifestation of filarial infection, mostly in
Asia, is pulmonary tropical eosinophilia syndrome
- nocturnal cough and wheezing, fever, and
eosinophilia
• Clinical course
- 1. asymptomatic stage; 2. Acute stage; 3. Chronic stage
- Endemic community — different stages overlap
• Manifestations are caused mainly by adult worms, living,
dead or degenerating
- Microfilariae cause less pathology but have been
associated with tropical pulmonary LOA LOA
eosinophilia (TPE), granulomas of the skin,
Life Cycle of Loa loa:
and allergic reactions following destruction by
drugs
• Those who are infected after migration to endemic
regions present with “Expatriate Syndrome”: clinical and
immunologic hyperresponsiveness to the mature or
maturing worms
- Present with allergic reactions such as hive,
rashes and blood eosinohilia along with the usual
manifestations of lyphadenitis and lymphagitis
• Asymptomatic stage
- Characterized by the presence of thousands to
millions of microfilariae in the peripheral 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
• Acute stage
o Early manifestations:
- Fever, inflammation of lymph glands (especially of the male
genital organs, arms and legs)
○ Recurrent attacks:
- swelling & redness of the arms & legs, accompanied by
vomiting, headache
- affected area can be tender

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During a blood meal, an infected fly (genus Chrysops, day-
biting flies) introduces third-stage filarial larvae onto the skin
of the human host, where they penetrate into the bite wound
. The larvae develop into adults that commonly reside in
subcutaneous tissue . The female worms measure 40 to 70
mm in length and 0.5 mm in diameter, while the males
measure 30 to 34 mm in length and 0.35 to 0.43 mm in
diameter. Adults produce microfilariae measuring 250 to 300
μm by 6 to 8 μm, 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 . The 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 . There
the microfilariae develop into first-stage larvae and
subsequently into third-stage infective larvae . The third-
stage infective larvae migrate to the fly's proboscis and can
infect another human when the fly takes a blood meal .

• Vector flies — Chrysops, C. silacea and C. dimidiate

o Chrysops — day biting flies During a blood meal, an infected arthropod (midges, genus
• African eye worm: Sudan rain forest, basin of Congo and Culicoides, or blackflies, genus Simulium) introduces third-
stage filarial larvae onto the skin of the human host, where
West Africa
• Migrates throughout subcutaneous tissues of the body they penetrate into the bite wound . They develop into
• Most conspicuous and irritating when crossing the adults that commonly reside in subcutaneous tissues .
conjunctivae Adult worms are rarely found in humans. The size range for
• Loasis is similar to onchocercaisis - It can also cause females worms is 65 to 81 mm in length and 0.21 to 0.25 mm
blindness in diameter but unknown for males. Adults worms recovered
• Microfilariae has diurnal periodicity from experimentally infected Patas monkeys measured 24 to
• During the day they are found in peripheral blood, but 28 mm in length and 70 to 80 μm in diameter (males) and 32
during the noncirculation phase, they are found in the to 62 mm in length and .130 to .160 mm in diameter
lungs (females). Adults produce unsheathed and non-periodic
• Microfilariae have been recovered from spinal fluids, microfilariae that reach the blood stream . The arthropod
urine, and sputum. ingests microfilariae during a blood meal . After ingestion,
the microfilariae migrate from the arthropod's midgut through
Parasite characteristics
the hemocoel to the thoracic muscles . There the
• Adult males: 2 to 3.5 cm long; Females: 5-7cm long
microfilariae develop into first-stage larvae and
• Microfilariae: 250-300 urn long, sheathed and differ from
subsequently into third-stage infective larvae . The third-
Wuchereria and Brugia in having body nuclei that are
continuous to the tip of the tail stage infective larvae migrate to arthropod's proboscis and
• Adult worms migrate through subcutaneous deeper can infect another human when the arthropod takes a blood
tissues meal .
• Microfilariae → blood stream; diurnal periodicity • Vector: midges (genus Culicoides), or blackflies (genus
Simulium)
Symptoms: • Adults inhabit the mesenteries and visceral fat
• Loiasis (Loa loa) is often asymptomatic. • Microfilariae: unsheathed, non periodic, found in the blood;
- Episodic angioedema and subconjunctival may be obtained by skin biopsy
migration of an adult worm can occur - Nuclei do not extend to the tip of the tail
• Non painful migration through tissues (compared to M. streptocerca and M. perstans)
• Conjunctival edema; patches of localized subcutaneous - Tail shorter and less tapered than Onchocerca
edema (Calabar swellings) • Generally an asymptomatic infection
• Eosinophilia - inguinal adenopathy has been reported
- Skin lesions, arthritis, fever, marked eosinophiha
- pulmonary symptoms adenopathy,
M. OZZARDI
hepatomegaly, and pruritus
Life Cycle of Mansonella ozzardi:

M. PERSTANS
Life Cycle of Mansonella perstans:

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 M. STREPTOCERCA
Life Cycle of Mansonella streptocerca:

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 body cavities, most
commonly the peritoneal cavity or pleural cavity, but less
frequently in the pericardium . The size range for female
worms is 70 to 80 mm in length and 120 μm in diameter, and
the males measure approximately 45 mm by 60 μm. Adults
produce unsheathed and subperiodic microfilariae, measuring
200 by 4.5 μm that reach the blood stream . A midge
ingests microfilariae during a blood meal . After ingestion,
the microfilariae migrate from the midge's midgut through the
hemocoel to the thoracic muscles of the arthropod
the microfilariae develop into first-stage larvae
subsequently into third-stage infective larvae . The third-
stage infective larvae migrate to the midge's proboscis and
can infect another human when the midge takes a blood meal
.
• Vector: midges (Culicoides)
• Adult worms live in deep connective tissues
• Microfilariae: found in peripheral blood and in the skin
- no periodicity; unsheathed
- Nuclei extend to the tip of the tail
• often asymptomatic, can be associated with angioedema,
pruritus, fever, headaches, arthralgas, and neurologic
manifestations.
- Edema and inflammatory changes and
granulomas form around dead filariae
- Eosinophilia
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 . The
females measure approximately 27 mm in length. Their
diameter is 50 μm at the level of the vulva (anteriorly) and
ovaries (near the posterior end), and up to 85 μm at the mid-
body. Males measure 50 μm in diameter. Adults produce
. There unsheathed and non-periodic microfilariae, measuring 180 to
240 μm by 3 to 5 μm, which reside in the skin but can also
and
reach the peripheral blood . A midge ingests the
microfilariae during a blood meal . After ingestion, the
microfilariae migrate from the midge's midgut through the
hemocoel to the thoracic muscles . There the microfilariae
develop into first-stage larvae and subsequently into third-
stage larvae . The third-stage larvae migrate to the
midge's proboscis and can infect another human when the
midge takes another blood meal .
• Vector: small midges (Culicoides)
• Microfilariae found in the skin and blood
o Nuclei extend to the tip of the tail whd is
bent in the form of a shepherd’s crook
• skin manifestations including pruritus, papular eruptions
and pigmentation changes

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ONCHOCERCIASIS
Life Cycle of Onchocerca volvulus:
During a blood meal, an infected blackfly (genus Simulium)
introduces third-stage filarial larvae onto the skin of the
human host, where they penetrate into the bite wound . In
subcutaneous tissues the larvae develop into adult filariae,
which commonly reside in nodules in subcutaneous
connective tissues . Adults can live in the nodules for
approximately 15 years. Some nodules may contain
numerous male and female worms. Females measure 33 to
50 cm in length and 270 to 400 μm in diameter, while males
measure 19 to 42 mm by 130 to 210 μm. In the
subcutaneous nodules, the female worms are capable of
producing microfilariae for approximately 9 years. The
microfilariae, measuring 220 to 360 µm by 5 to 9 µm and
unsheathed, have a life span that may reach 2 years. They
are occasionally found in peripheral blood, urine, and sputum
but are typically found in the skin and in the lymphatics of
connective tissues . A blackfly ingests the microfilariae
during a blood meal . After ingestion, the microfilariae
migrate from the blackfly's midgut through the hemocoel to
the thoracic muscles . There the microfilariae develop into
first-stage larvae and subsequently into third-stage
infective larvae . The third-stage infective larvae migrate
to the blackfly's proboscis and can infect another human
when the fly takes a blood meal . A. Capillary
- major cause of blindness in some parts of Africa
- also known as river blindness
- adult worms: wirelike, whitish, lie coiled within fibrous tissue
capsules
- Female - 50cm; males — 5 cm
- Microfilariae: unsheathed;150-350um
o 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
LABORATORY DIAGNOSIS
- Examination of blood
o the blood sample can be a thick smear, stained with
Giemsa or hematoxylin and eosin
o For increased sensitivity, concentration techniques
can be used. These include centrifugation of the
blood sample lyzed in 2% formalin (Knott's
technique), or filtration through a Nucleopore®
membrane.
- Examination of skin snips will identify microfilariae of
Onchocerca volvulus and Mansonella streptocerca
○ Skin snips can be obtained using a corneal-scleral
punch, or more simply a scalpel and needle
○ Allowe sample to incubate for 30 minutes to 2 hours
in saline or culture medium, and then examined for
microfilariae that would have migrated from the
tissue to the liquid phase of the specimen
- Finding of microfilariae in the blood as seen in wet or thick
blood smears taken between 8 pm and 4am (nocturnal
periodioty — W. bancrofti)
○ B. malayi microfilariae — subperiodic penodicity
○ In low intensity infection Knott’s method for
concentration may be used
○ DEC (diethylcarbamazine) provocative test
stimulates microfilariae to come out to peripheral
circulation allowing blood smear collection even
during daytime
- Antigen detection techniques to detect circulating flianal
antigens (CFA) — useful in low and variable infection
- Diagnostic findings:
 Antigen detection using an immunoassay for
circulating filarial antigens - useful because
microfilaremia can be low and variable
 A rapid-format immunochromatographic
test, applicable to Wuchereria bancrofti
antigens, has been recently evaluated in the
field.
 Molecular diagnosis using PCR
 available for W. bancrofti and B. malayi.
 Identification of adult worms is possible from
tissue samples collected during nodulectomies
(onchocerciasis), or during subcutaneous biopsies or
worm removal from the eye (loiasis).
 Antibody detection - limited value
 Substantial antigenic cross reactivity exists
between filaria and other helminths, and a
positive serologic test does not distinguish
between past and current infection.
- Special Procedures for Detecting Microfilariae (Blood
microfilariae)
(fingerstick) blood
Since microfilariae concentrate in the peripheral
capillaries, thick and thin smears prepared from
fingerstick blood are recommended.
B. Anticoagulated (EDTA) venous blood (1 ml) should be
concentrated by one of the following methods:
1. Centrifugation (Knott’s technique) – uses 2%
formaldehyde
2. Filtration – uses membrane filter (Millipore® or
Nucleopore® membrane filter
- Ultrasonography, contrast lymphagiography and
Iymphscintigraphy
o May demonstrate live worms in the lymphatics
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 o Contrast lymphangiography and lympscintigraphy where humans exhibit a microfilaraemia all
using radiolabled albumin or dextran may the time with the highest numbers being
demonstrate obstructed lymphatics detected between noon and 8om

Comparison of microfilariae of W. bancrofti and B. MICROFILARIAE OF DIFFERENT

malayi
FILARIAL SPECIES
Microfilaria of W. bancrifti:

- Sheathed body is gently curved and tail is tapered

to a point
- Nuclear column (the cells that constitute the body
of the microfilaria) is loosely packed, the nuclei
can be visualized individually and do not extend
to the tip of the tail
Comparison of microfilariae sizes and morphology

Microfilaria of B. malayi

- Like W. bancrofti, this species has a sheath

PERIODICITY (slightly stained in hematoxylin)
- Unlike Wuchereria, it is more tightly coiled, and
- • PERIODICITY - FLUCTUATION IN NUMBERS OF the nuclear column is more tightly packed,
MICROFILARIAE PRESENT IN THE PERIPHERAL BLOOD preventing the visualization of individual cells
DURING A 24 HOUR PERIOD
- • Nocturnally periodic - species found in the blood Microfilaria of Onchocerca volvulus
during night-time hours but absent at other times
- e.g. W bancrofti and B. malayi
- • Diurnally periodic: present only during certain
daytime hours - e.g. Loa loa
- • Nonperiodic or aper.odic: microfilariae that
circulate in the blood throughout a 24 hour period
without significan changes in their numbers - e g - No sheath present
Mansonia spp - Tail is tapered and is sharply angled at the end
- Subperiodic: microfilariae normally present in
the blood at all hours but whose density increases
significantly during either the night or day Microfilaria of Loa loa:
o There are two strains of B. malay:
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; and
o The sub-periodic strain which is found in
Malaysia, Indonesia, and the Philippines

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- Sheathed, with a relatively dense nuclear columns
- Its tail tapers and is frequently coiled
- Nuclei extend to the end of the tail
Microfilaria of Mansonella perstans:
- Smaller, no sheath, and has a blunt tail with
nuclei extending to the end of the tail
Microfilaria of M. streptocerca:
- Unsheathed
- Has a nearly straight body attitude
- Tail is typically coiled into a “shepherd’s crook”
- Terminal nuclei extend as a single row to the end
of the tail
Microfilaria of M. ozzardi
- Typically small
- Unsheathed
- Has a slender, tapered tail that is hooked
(buttonhook)
- The nuclei do not extend to the end of the tail
There are four sheathed species: Wuchereria
bancrofti, Brugia malayi, Brugia timori, and Loa loa.
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 – 3-6 mg/day up tp 36 to 72
mg/body weight
- Ivermectin – 200 to 400 µg/kg single oral dose;
as effective as 12 days of DEC
PREVENTION AND CONTROL
- Goal for endemic communities:
eliminate 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/ivremectincombination in areas where
onchocercosis or loaiasis is prevalent
- Personal protective measures
- Vector control: development of sprays and
polystyrene beads to seal latrines
TRICHINOSIS
- Causal Agents:
Trichinellosis (trichinosis) is caused by nematodes
(roundworms) of the genus Trichinella
- In addition to the classical agent T. spiralis (found
worldwide in many carnivorous and omnivorous
animals), several other species of Trichinella are
now recognized:
o T. pseudospiralis – mammals and birds
worldwide
o T. native – Arctic bears
o T. nelson – African predators and scavengers
o T. britovi – carnivores of Europe and Western
Asia
TRICHINELLA
- Adult female measures 2.2mm in length
(3.5mm by 0.06mm) – 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
- Males 1.2mm (1.5mm by 0.04mm) – single testis
located near the posterior end and is joined in the
mid-body by the genital tube, which in turn
extends back to the cloaca
o Cloaca – has a pair of caudal appendages and
2 pairs of papillae
- Larva: 80-120 µm by 5.6 µm 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
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 o Humans, rats, dogs, cats, pigs, bears, foxes, o Periorbital and facial edema, conjunctivitis,
walruses, other carnivores or omnivores fever, myalgias, splinter hemorrhages,
rashes, and blood eosinophilia
TRICHINELLA: LIFE CYCLE - Occasional life-threatening manifestations:
o Myocarditis, CNS involvement, and
- Host are infected by consuming pneumonitis
insufficiently cooked meat (containing o Larval encystment in the muscles causes
the infected larvae) myalgia and weakness, followed by
- Larvae encyst either in the stomach or small subsidence of symptoms
intestine  burrow into the villi where they - Severity of symptoms depend on intensity of
mature infection
- Adult worms mate  female produce eggs that o Light infection: patients harboring up to 10
grow into larvae in its uterus  are deposited in larvae
the mucosa, penetrates it, pass through lymphatic o Moderate infection: 50-500 worms
system into circulation  to striated muscle o Severe and potentially fatal: >1000 larvae
- After 3 weeks, larvae start to coil into individual - 3 phases of clinical conditions
cysts o Enteric phase: stage of incubation and
- Encapsulation: 4-5 weeks after infection intestinal invasion
- Larva in the cysts remain viable for years  Diarrhea or constipation, vomiting,
- In humans, calcification of cyst takes 6-12 cramps, malaise, nausea
months after infection o Invasion phase: larval migration and muscle
- Rodents maintain endemicity invasion
- Carnivores/omnivores feed on infected rodents or  Myalgia, periorbital edema and
meat eosinophilia – cardinal SSx
- Humans are accidentally infected when eating  High remittent fever, dyspnea, dysphagia,
improperly processed meat difficulty in chewing, paralysis of
extremities, GI hemorrhage,
splenomegaly
o Convalescent phase: encystment and
encapsulation
 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 or absent peripheral blood
eosinophilia – poor prognosis

TRICHINELLOSIS: 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
TRICHINELLOSIS: DIAGNOSIS
- Based on history of exposure 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
for 14 days after for female worm in the
duodenum and larvae in the muscles of
experimental host
- Laboratory Diagnosis: suspicion 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 in pressed muscle
tissue sample
- The coiled larvae can be seen inside the cysts
TREATMENT

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- Should begin as soon as possible - After 6 days, first stage larvae hatch from eggs 
o Bed rest, supportive treatment respiratory tract  up to the trachea and are
- Thiabendaole – 25mg/kg 2x/day for 7 days expels swallowed  expelled in the feces
adult worm from GIT during the 1 st 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/kg 6 hourly for 10-14 days
o Albendazole – shows promise but has not yet
been sufficiently evaluated
- Steroids are used for infections with severe
symptoms (Prednisone 20mg 3x daily tapered
over 2-3 weeks)

EPIDEMIOLOGY
- Occurs whenever meat is part of the diet
o Canada, mexico, Holland, hungary, Poland,
Ukraine, Lithuania, Yugoslavia, spain, egypt,
Lebanon, Syria, brazil, Uruguay, chile, LIFE CYCLE
ecuafor, 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 at 77®C
- Freezing at -15®C for 20 days or -30®C for six
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 lungworm, is the most common
cause of human eosinophilic meningitis
- Angiostrongylus (Parastrongylus) costaricensis is
the causal agent of abdominal, or intestinal
angiostrongyliasis
- Geographic distribution:
o Most cases of eosinophilic meningitis have
been reported from SE Asia and the Pacific
Basin
o Abdominal angiostrongyliasis has been
reported from Costa Rica, and occurs mainly
in children <13y/o
- Human infection was first reported in Taiwan in
1944
- First well documented fatal case of human
angiostrongylosis was in a 50y/o Filipino male
- Adult worms of A.cantonensis live in the
admitted in a hospital in Hawaii
pulmonary arteries of rats and rodents
- Females lay eggs that hatch, yielding first stage
A. CANTONENESIS larvae in the terminal branches of the pulmonary
- Adult worm: pale, filiform arteries  migrate to the pharynx, are swallowed
- Male worm: 16-19mm (length) X 0.26mm and are passed in the feces  invade an
(diameter) intermediate host (snail or slug)  after two
o Well-developed caudal bursa which is kidney molts, third stage larvae are produced, which are
shaped and single-lobed infective to mammalian hosts
- Female worm: 21-25mm X 0.30-0.36mm - Known intermediate hosts in the Philippines:
o Has uterine tubules which are wound spirally o Slugs and snails
around the intestine  “barber’s pole”  Achatina fulica, Hemiplecta sagittifera,
pattern Helicostyla macrostoma, Vaginilus
o Lays up to 15,000 eggs per day plebeius, Veronicella altae
- Adult worms measure between 17-25mm long and - Mollusk is ingested by the definitive host, the
reside in the pulmonary arteries and arterioles of third stage larvae migrate to the brain where they
the definitive hosts develop into young adults  young adults return
- Adult worms live in the pulmonary arteries of the
rat
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 to venous system and then the pulmonary arteries MANAGEMENT AND PROGNOSIS
where they become sexually mature
o Various animals act as paratenic (transport)
- No antihelminthic treatment is
hosts: after ingesting the infected snails, they recommended at present although
carry the third stage larvae which can resume mebendazole, thiobendazole,
their development when the paratenic host is albendazole, and ivermectin were found
ingested by a definitive host
- Humans acquire the infection by eating
to be successful in animal experiments
o Antihelminthics are usually not necessary
undercooked snails or slugs, vegetables
contaminated with mollusk secretions, or infected because the disease is self-limiting and killing
paratenic animals (crabs, freshwater shrimps) the worms may bring about greater
o Development of the third stage larvae is inflammatory reactions
o Analgesics and removal of spinal fluid at
stalled in the brain where they die
- Life cycle of Angiostrongylus (Parastrongylus) regular intervals can relieve headaches
costaricensis is similar, except that the adult o Prednisone 30mg daily is recommended in
worms reside in the arterioles of the ileocecal severe cases with cranial nerve involvement
area of the definitive host o Surgical removal indicated when parasite is
- In humans, the eggs and larvae degenerate and lodged in the anterior chamber of the eye
cause local inflammatory reactions - Prognosis is usually good
- In humans, A. cantonensis juvenile worms migrate o Infection is self-limiting, complete recovery
to the brain, or rarely in the lungs, where the usually occurs
worms ultimately dies o Permanent neurologic deficits do occur
- In humans, A. costaricensis often reaches sexual o Occasionally fatal
maturity and release eggs into the intestinal
tissues. The eggs and larvae degenerate and TOXOCARIASIS
cause intense local inflammatory reactions and do
not appear to be shed in the stool.
- Causal Agents
Larvae of Toxocara canis (dog roundworm) and less
frequently of T. cati (cat roundworm), two nematode
parasites of animals
- Toxocara canis accomplishes its life cycle in dogs,
ANGIOSTRONGYLUS: CLINICAL with humans acquiring the infection as accidental
FEATURES hosts
- Clinical symptoms of eosinophilic - Puppies are infected with T. camis as early as the
fetal stage or at birth due to transplacental and
meningitis are caused by the presence transmammary transmission (important source of
of larvae in the brain and by local host eggs)
reactions - Man becomes infected by ingestion of
o Severe headaches, nausea, vomiting, neck embryonated eggs through contaminated food
stiffness, seizures, and neurologic and water
abnormalities - Other mammals and birds may serve as paratenic
o Occasionally, ocular invasion occurs hosts
o Eosinophilia is present in most cases - Geographic distribution is worldwide
o Most patients fully recover
- Abdominal angiostrongyliasis (eosinophilic
enteritis) mimics appendicitis with eosinophilia

ANGIOSTRONGYLUS: LABORATORY
DIAGNOSIS
- In eosinophilic meningitis, the CSF is
abnormal (elevated pressure, proteins
and leukocytes; eosinophilia) LIFE CYCLE
o On rare occasions, larvae have been found in
the 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
- Presumptive diagnosis is made by travel and
exposure history
- In humans, eggs and larvae are not normally
excreted, but remain sequestered in tissues
- Both eggs and larvae (occasionally adult worms)
of A. costaricensis can be identified in biopsy or
surgical specimens of intestinal tissues
- The larvae need to be distinguished from larvae of
Strongyloides stercoralis; however, the presence
of granulomas containing thin shelled eggs and/or
lavae serve to distinguish A. costaricensis
infections

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  Fever, anorexia, weight loss, cough,
wheezing, rashes, hepatosplenomegaly,
and hypereosinophilia
 Occurs mostly in preschool children
o Ocular larva migrans (OLM): larvae produce
various ophthalmologic lesions, which in some
cases have been misdiagnosed as
retinoblastoma, resulting in surgical
enucleation
 Often occurs in older children or young
adults, with only rare eosinophilia or
visceral manifestations
- Death can occur rarely by severe crdiac,
pulmonary or neurologic involvement

- Ingestion by dogs  infective eggs hatch  larvae
penetrate the gut wall and migrate into various
tissues, where they encyst if the dog is older than
5 weeks
- In younger dogs, larvae migrate through the
lungs, bronchial tree, and esophagus; adult worms
develop and oviposit in the small intestine
- In older dogs, encysted stages are reactivated
during pregnancy and infect by the transplacental
and transmammary routes the puppies in whose
small intestines the adult worms become
established
- Humans are accidental hosts, becoming infected
by ingesting infective eggs in contaminated soil
- After ingestion, eggs hatch and the larvae
penetrate the intestinal wall and are carried by
the circulation to different tissues (liver, heart,
lungs, brain, muscle, eyes) and cause severe local
reactions
- 2 main clinical manifestations: visceral larva
migrans (VLM) and ocular larva migrans (OLM)
TOXOCARIASIS: CLINICAL FEATURES
- Many human infections are
asymptomatic, with only eosinophilia
and positive serology
- 2 main clinical presentations
o Visceral larva migrans (VLM): larva invade
multiple tissues (liver, heart, lungs, brain,
muscle) and cause various symptoms
TOXOCARIASIS: LABORATORY
DIAGNOSIS
- Diagnosis does not rest on identification
of the parasite
- Since the larvae do not develop into adults in
humans, a stoll examination would not detect any
Toxocara eggs
o Presence of Ascaris and Trichuris eggs in
feces, indicating fecal 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
eosinophilia), and the detection of antibodies to
Toxocara
- Antibody Detection
o The only means of confirmation of a clinical
diagnosis of visceral larva migrans (VLM),
ocular larva migrans (OLM), and covert
toxocariasis (CT), the most common clinical
syndromes associated with Toxocara
infections
o The currently recommended serologic test for
toxocariasis is enzyme immunoassay (EIA)
TOXOCARIASIS: 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
ANISAKIASIS
- Caused by larval stages of anisakine
nematodes persisting in the alimentary
canal or penetrating the tissues of
humans after consuming raw or semi-
raw fish
- Conditions is caused by the accidental ingestion
of larvae of the nematodes Anisakis simplex and
Pseudoterranova decipiens
- Fish species acts as intermediate/transport hosts
for the larva
o Larva matures into adults in warm-blooded
marine mammals
- No human case yet reported in the Philippines but
the potential for infection is great
LIFE CYCLE

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- Adult stages of A. simplex or P. o If the larvae pass into the bowel 1-2 weeks
decipiens reside in the stomach of following infection, a severe eosinophilic
granulomatous response may also occur,
marine mammals, where they are causing symptoms mimicking Crohn’s disease
embedded in the mucosa in cluters - Laboratory Diagnosis:
- Eggs produced by the adult females are passed in o Diagnosis can be made by gastroscopic
the feces, hatch and yield second stage larvae examination during which the 2cm larvae are
- Upon ingestion by crustaceans, third stage larvae visualized and removed, or by
develop that are infective to fish and squid o Histopathologic examination of tissue
- After ingestion by the fish and squid hosts, the removed at biopsy or during surgery
larvae migrate from the intestine to the peritoneal - Treatment:
cavity to (upon the host’s death) the muscle o The treatment of choice is surgical or
tissues endoscopic removal
- Through predation, the larvae are transferred
from fish to fish until they are ingested by the
marine mammal
- In this definitive host, the larvae develop into
adults, thus closing the cycle
- Humans become infected by eating raw or
undercooked marine fish. After ingestion, the
anisakid larvae penetrate the gastric and
intestinal mucosa causing the symptoms of
anisakiasis

ANISAKIASIS
- Geographic distribution: worldwide, with
higher incidence in areas where raw fish
is eaten (e.g., Japan, Pacific coast of
South America, the Netherlands)
- Increasing incidence in the United States due to
increased consumption of raw fish
- Clinical features:
o Within hours after ingestion of infected
larvae, violent abdominal pain, nausea, and
vomiting may occur
o Occasionally, the larvae are coughed up

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