Professional Documents
Culture Documents
Filariasis
Filariasis
Filariasis
30, 2008
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
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 .
M. PERSTANS
Life Cycle of Mansonella perstans:
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M. STREPTOCERCA
Life Cycle of Mansonella streptocerca:
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• 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
ONCHOCERCIASIS - Examination of blood
Life Cycle of Onchocerca volvulus: 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 a blood meal, an infected blackfly (genus Simulium) during daytime
introduces third-stage filarial larvae onto the skin of the - Antigen detection techniques to detect circulating flianal
antigens (CFA) — useful in low and variable infection
human host, where they penetrate into the bite wound . In - Diagnostic findings:
subcutaneous tissues the larvae develop into adult filariae, Antigen detection using an immunoassay for
which commonly reside in nodules in subcutaneous circulating filarial antigens - useful because
connective tissues . Adults can live in the nodules for microfilaremia can be low and variable
approximately 15 years. Some nodules may contain A rapid-format immunochromatographic
numerous male and female worms. Females measure 33 to test, applicable to Wuchereria bancrofti
50 cm in length and 270 to 400 μm in diameter, while males antigens, has been recently evaluated in the
measure 19 to 42 mm by 130 to 210 μm. In the field.
subcutaneous nodules, the female worms are capable of
producing microfilariae for approximately 9 years. The Molecular diagnosis using PCR
microfilariae, measuring 220 to 360 µm by 5 to 9 µm and available for W. bancrofti and B. malayi.
unsheathed, have a life span that may reach 2 years. They Identification of adult worms is possible from
are occasionally found in peripheral blood, urine, and sputum tissue samples collected during nodulectomies
but are typically found in the skin and in the lymphatics of (onchocerciasis), or during subcutaneous biopsies or
connective tissues . A blackfly ingests the microfilariae worm removal from the eye (loiasis).
during a blood meal . After ingestion, the microfilariae Antibody detection - limited value
migrate from the blackfly's midgut through the hemocoel to Substantial antigenic cross reactivity exists
the thoracic muscles . There the microfilariae develop into between filaria and other helminths, and a
first-stage larvae and subsequently into third-stage positive serologic test does not distinguish
between past and current infection.
infective larvae . The third-stage infective larvae migrate - Special Procedures for Detecting Microfilariae (Blood
to the blackfly's proboscis and can infect another human microfilariae)
when the fly takes a blood meal . A. Capillary (fingerstick) blood
Since microfilariae concentrate in the peripheral
- major cause of blindness in some parts of Africa capillaries, thick and thin smears prepared from
- also known as river blindness fingerstick blood are recommended.
- adult worms: wirelike, whitish, lie coiled within fibrous tissue B. Anticoagulated (EDTA) venous blood (1 ml) should be
capsules concentrated by one of the following methods:
- Female - 50cm; males — 5 cm 1. Centrifugation (Knott’s technique) – uses 2%
- Microfilariae: unsheathed;150-350um formaldehyde
o Often found in the skin; rarely in urine, blood and 2. Filtration – uses membrane filter (Millipore® or
sputum Nucleopore® membrane filter
•Developing worms wander through subcutaneous tissues
•Most worms become encapsulated — nodules are produced - 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
Microfilaria of B. malayi
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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)
- Unsheathed
- Has a nearly straight body attitude TRICHINELLA
- Tail is typically coiled into a “shepherd’s crook”
- Terminal nuclei extend as a single row to the end
- Adult female measures 2.2mm in length
of the tail (3.5mm by 0.06mm) – single ovary
situated in the posterior part of the body
Microfilaria of M. ozzardi 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
- Typically small o Cloaca – has a pair of caudal appendages and
- Unsheathed 2 pairs of papillae
- Has a slender, tapered tail that is hooked - Larva: 80-120 µm by 5.6 µm at birth
(buttonhook) o Has a spear-like burrowing anterior tip
- The nuclei do not extend to the end of the tail
- Infective larvae are encysted in the muscle fiber
of the host
There are four sheathed species: Wuchereria - Hosts serve as both the final and intermediate
bancrofti, Brugia malayi, Brugia timori, and Loa loa. 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: 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
TRICHINELLOSIS: CLINICAL (trichinosis): based on clinical symptoms and
MANIFESTATIONS eosinophilia
- Can be confirmed by specific diagnostic tests:
- Light infections may be asymptomatic antibody detection, muscle biopsy, and
- Intestinal invasion microscopy
o Accompanied by GI symptoms: - Encysted larvae of Trichinella in pressed muscle
Diarrhea, abdominal pain, vomiting tissue sample
- Larval migration into muscle tissues (one week - The coiled larvae can be seen inside the cysts
after infection) can cause
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
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
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)
- Ingestion by dogs infective eggs hatch larvae
penetrate the gut wall and migrate into various TOXOCARIASIS: TREATMENT
tissues, where they encyst if the dog is older than - VLM is treated with antiparasitic drugs,
5 weeks usually in combination with anti-
- In younger dogs, larvae migrate through the
lungs, bronchial tree, and esophagus; adult worms inflammatory medications
develop and oviposit in the small intestine - Treatment of OLM is more difficult and usually
- In older dogs, encysted stages are reactivated consists of measures to prevent progressive
during pregnancy and infect by the transplacental damage to the eye
and transmammary routes the puppies in whose o Albendazole
small intestines the adult worms become o Mebendazole
established
- Humans are accidental hosts, becoming infected ANISAKIASIS
by ingesting infective eggs in contaminated soil - Caused by larval stages of anisakine
- After ingestion, eggs hatch and the larvae
penetrate the intestinal wall and are carried by nematodes persisting in the alimentary
the circulation to different tissues (liver, heart, canal or penetrating the tissues of
lungs, brain, muscle, eyes) and cause severe local humans after consuming raw or semi-
reactions raw fish
- 2 main clinical manifestations: visceral larva
- Conditions is caused by the accidental ingestion
migrans (VLM) and ocular larva migrans (OLM)
of larvae of the nematodes Anisakis simplex and
Pseudoterranova decipiens
TOXOCARIASIS: CLINICAL FEATURES - Fish species acts as intermediate/transport hosts
- Many human infections are for the larva
asymptomatic, with only eosinophilia o Larva matures into adults in warm-blooded
marine mammals
and positive serology - No human case yet reported in the Philippines but
- 2 main clinical presentations the potential for infection is great
o Visceral larva migrans (VLM): larva invade
multiple tissues (liver, heart, lungs, brain,
muscle) and cause various symptoms 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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