PARASITOLOGY LECTURE

Tissue and Blood Nematodes

Tissue Nematodes
Angiostrongylus cantonensis
Trichinella spiralis
Dracunculus medinensis
Angiostrongylus cantonensis
rat lungworm
First described by Chen in 1935 from domestic rats in
Canton, China
Causes eosinophilic meningoencephalitis in man
Parasite Biology
Male worms:
16-19mm in length by 0.26mm in diameter
Well-developed caudal bursa (kidney shaped and single lobed)

Female worms:
21-25mm in length by 0.30 to 0.36 mm in diameter
Has uterine tubules which are wound spirally around the
intestine
barbers pole pattern (arrangement)
Parasite Biology
Eggs:
Have delicate hyaline shells
Unembryonated when oviposited
The first stage larva, found in the lungs of the rodent host, has a
distinct small knob near the tip of the tail.
Two well-developed chitinous rods below its buccal cavity
identify the infective third stage larva found in mollusks
These rods have expanded knob-like tip
Parasite Biology
Adult worms:
In the bloodstream, gravid females lay eggs which are then carried
into the smaller vessels of the lungs.
After six days, the first stage larvae hatch from the eggs. The larvae
enter the respiratory tract and migrate to the trachea where they are
swallowed and then expelled in the feces of the rat.
The larvae infect the molluscan intermediate host.
In the Philippines, the known intermediate hosts include the
following slugs and snails: Achatina fulica or giant African snail,
Hemiplecta sagittifera, Helicostyla macrostoma,Vaginilus
plebeius, and Veronicella altae.
Mode of infection: ingestion or penetration
Parasite Biology
Adult worms:
In the mollusk, the larvae undergo two molts to reach the infective third
larval stage.
When rats or humans ingests these infective mollusks, the larvae pass
through the stomach into the intestine and then enter the circulatory system
and migrate to the brain and spinal cord.
Again, they undergo two or more molts before they reach maturity in about
four weeks.
Early development occurs in the brain.
After the final molt in the rats, the young adults migrate to the pulmonary
arteries to complete their development.
After two weeks, the adult female starts laying eggs.
In humans, however, the larva probably remains in the brain for a longer
period of time and does not develop to the adult stage.
Worms have also been known to migrate to the eye.
Pathogenesis and Clinical
Manifestations
Incubation period: around 6 to 15 days but it may vary from 12 to 47
days
Acute severe intermittent occipital or bitemporal headache
Stifness of the neck, weakness of the extrimities (hands or legs),
abdominal pain, nausea, vomiting, paresthesia, peripheral eosinophilia,
facial paralysis, and low grade fever.
Ocular involvement with failing vision
Postmortem examination may show leptomeningitis, encephalomalacia,
and moderate ventricular dilation.
Immature worms may be seen in cerebellum and cerebrum.
Adult worms are also recovered from the eye and pulmonary artery of
patients.
Large numbers of Charcot-Leyden crystals have also been demonstrated
in the meninges
Diagnosis
Diagnosis is difficult since the primary site of infection is the brain
Presumptive diagnosis is made by travel and exposure history.
Examination of cells in the CSF
CSF of greater than 10% in proportion to WBC/uL will exclude
other common causes of meningitis.
The CSF protein is mildly elevated while the CSF glucose is
normal
CT scan (lesions of the meninges; also important in excluding
neurocysticercosis)
ELISA (serologic confirmation)
Treatment
No antihelminthic treatment is recommended at present
(mebendazole, thiabendazole, albendazole, and ivermectin
separately were found to be successful in animal
experiments)
Symptomatic treatment with the use of analgesics and careful
removal of about 10ml of spinal fluid at frequent intervals
can relieve headaches experienced by the patient
Prednisone 30 mg is recommended (in severe cranial nerve
involvement)
Epidemiology
Human infection was first reported by Nomura and Lin
from Taiwan
Two cases of ocular angistrongyliasis have been diagnosed at
the College of Public Health, University of the Philippines
Manila.
Transmission is usually attributed to: ingestion of raw
mollusk intermediate host, ingestion of leafy vegetables
contaminated ith mucus secretion of the mollusk carrying
infective stage (thirs larval stage) of the parasite, ingestion of
a paratenic host such as freshwater prawn or crab harboring
the infective stage of the parasite, and drinking contaminated
water.
Prevention and Control
Proper eating habits
Safe food preparation
Elimination of the intermediate hosts
Eradication of the rodent hosts
Thorough washing of leafy vegetables
Eating sufficiently cooked prawns an crabs
Drinking safe water
Avoiding ingestion of raw snails and slugs
Trichinella spiralis
First found in the muscles of patients autopsied by Peacock in
London
Before the turn of the century, German investigators were
able to prove that raw or insufficiently cooked meat was
responsible for trichinosis in humans.
Three subspecies which can infect humans: Trichinella spiralis
spiralis (found in temperate regions),Trichinella spiralis native
(found in arctic regions), and Trichinella spiralis neloni (found
in Africa).
Parasite Biology
Male worms:
Measures 1.5 mm by 0.04mm
Single testis located near the posterior end of the body and is
joined in the mid-body by the genital tube which in turn
extends back to cloaca

Female worms:
Measures 3.5 mm by 0.06mm
Single ovary, situated in the posterior part of the body
Has an oviduct, a seminal receptacle, a coiled uterus, a vagina,
and vulva
Parasite Biology
Larvae:
Spear-like burrowing anterior tip
The digestive tract of a mature larva encysted in a muscle fiber
resembles that of the adult worm
The reproductive organs at this stage are not yet developed but
even then, it is already possible to identify the sex of the
parasite
 In Trichinella infection, the host (humans, rats, dogs, cats, pigs, bears, foxes, walruses, or any
other carnivore or omnivore) serves as both the final and intermediate host by harboring bot
the adult and larval stages.
Infective larvae are usually encysted in the muscle fibers of the host
When infective larvae are ingested by the host through raw or insufficiently cooked meat
(usually pork), the cysts are digested in the stomach and larvae excyst either in the stomach or
in the small intestine.
Then they burrow into the subepithelium of the villi where they mature.
Adult worms mate and after fertilization, the female begins to produce eggs that grow into the
larvae in its uterus.
After a few days, the female worm deposits larvae in the mucosa
The larvae penetrate the mucosa, pass through the lymphatic system into the circulation, and
finally into striated muscles.
In the muscles, the larvae grow and develop. After about three weeks, they start to coil into
individual cysts.
The larva in the cysts remains viable for many years.
In humans, calcification of the cysts may take place 6 to 12 months after infection.
This may lead to destruction or death of the larva.
When a carnivore or omnivore consumes meat containing infective larvae, the larvae break
out through gastric digestion of the cysts, and the cycle continues.
Pathogenesis and Clinical
Manifestations
The clinical conditions are divided into three phases: enteric phase, invasion
phase, and convalescent phase.
These correspons to the stages of 1) incubation and intestinal invasion,
2) larval migration and muscle invasion, and 3)encystment and
encapsulation

Enteric phase: attack of acute food poisoning, diarrhea or constipation,

vomiting, abdominal cramps, malaise, and nausea; Due to invasion of the
intestinal wall by the newborn larvae, appear 1-2 days after ingestion of
undercooked pork and last nearly 2-3 months
Invasion phase: sever myalgia, periorbital edema, eosinophilia, myocardial
and neurological complications; Due to invasion of the muscle by the larvae,
this is seen during 7-11 days of ingestion of the infected food
Convalescent phase: fever, weakness, pain; Marked by the beginning of the
encapsulation of the encysted larvae during the third week of infection
Diagnosis
History of exposure and physical examination
Most definitive diagnostic exam: demonstration of the larva
using muscle biopsy (this can only be done when encystment of the
parasite has started)
Biochemical tests may show chemical evidence of muscle damage
(elevated creatine phosphokinase, lactate dehydrogenase and myokinase
levels)
Serology (may provide confirmatory diagnosis)
Bentonite flocculation test (BFT) and latex flocculation test
(LFT), ELISA are now used for diagnosis of trichinosis
Becks xenodiagnoses can be done when meat is suspected of
harboring the encysted larva of Trichinella (this test involves feeding the
meat to albino rats, observation is done 14 days after inoculation for the
presence of the female worm in the duodenum and larvae in the muscles
of the experimental animal.
Treatment
Bed rest and supportive treatment
Analgesics and antipyretics are used to control the symptoms
Severe cases: Prednisone 20 mg three times daily
Epidemiology
Trichinosis is primarily a zoonosis
Humans get infected after ingestion of raw or insufficiently
cooked meat of infected animals
The infection is usually maintained in a pig-to-pig or pig-to-
rat-to-pig cycle.
Prevention and Control
Health education
Meat be cooked at 77 degrees Celsius
Freezing is another way to kill larvae
Meat inspection and keeping pigs rat-free
Dracunculus medinensis
Common name: Guinea worm, Medina worm, Dragon
worm, Fiery Serpent worm of the Israelites
Disease: Dracunculiasis or Dracontiasis
It is an ancient disease
Longest nematode (reaches up to 1 meter)
The parasite causing disease was known as Guinea worm as it was
first detected in Guinea in West Africa
It was also known as Medina worm as it was commonly found in
Medina
Russian biologist Fedtschenko (1870) discovered the role of
cyclops as vector in transmission of disease
Habitat: Subcutaneous tissues of man usually the foot or lower
limb
Parasite Biology
Adult worm
Male:
Difficult to demonstrate as they die immediately after fertilizing the
female

Female:
Milky white, slender and looks like a thick twine of thread
It has rounded anterior end and a tapering posterior end in a form of
hook-like structure
Minute triangular mouth in the anterior end
A pair of uteri, oviducts and tubules and a single unpaired vagina
constitute the female genital tract
Viviparous
Parasite Biology
First-stage larva
Unsheated and coiled with round anterior end and a long
slender filariform tail
It shows tadpole-like movement in water
It has a short life unless taken up by cyclops

Infective Form:
Third-stage larva found in the body cavity of cyclops
Pathogenesis and Clinical
Manifestation
Third-stage larvae are not pathogenic, they essentially do not produce any pathological
lesions in man
Only female worm is pathogenic. It produces blister which is formed in the site, at which
the female worm comes out of the surface of the skin, on coming in contact with water
The blister is bacteriologically sterile and contains numerous larvae and leukocytes
Diffusable toxins produced by the parasite believed to cause urticaria, dyspnea, vomiting,
mild fever and occasional fainting
Man is the only reservoir of infection
Water contaminated with infected cyclops is the main source of infection
Man acquires infection by drinking water contaminated with cyclops harboring with
third-stage larva
The condition essentially is a disease of rural poor people
Contamination of drinking water, presence of infected cyclops in shallow waters, poor
sanitation and poor personal hygiene facilitate transmission of infection in community
Diagnosis
Parasitic diagnosis
Established by observation of the typical ulcer and flooding
ulcer with water to recover the discharge of larvae
Serodiagnosis
IFA, IHA, ELISA and western blot
Imaging methods
Radiologic examination of the affected part demonstrates dead
and calcified parasites
Visceral Larva
COMMON NAME:
Toxocara canis : Dog ascaris
Toxocara cati : Cat ascaris

Naturally parasitic in the intestines of dogs and cats that

accidentally infect human (abberant host) producing disease
known as Visceral Larva Migrans (VLM) or Toxocariasis
Life cycle in dogs and cats is the same as the human ascaris
When the embryonated is ingested by man, larvae will hatch and
cannot follow its normal course of development as seen in their
normal host.
The larvae will penetrate the intestinal mucosa and are carries by
the blood stream to the liver, lungs and other organs
Cutaneous Larva
Ancylostoma braziliense
Cat hookworm
Possesses a pair of large teeth and a pair of inconspicuous median
teeth in the buccal capsule
Ancylostoma caninum
Dog hookworm
Buccal cavity is provided with three pairs of ventral teeth
The cephalic or amphidial gland of the worm secretes an
anticoagulant that delays coagulation of blood
Ancylostoma ceylanicum
Smallest hookworm species
Common parasite of cats and less frequently of dogs
Blood Nematodes
Wuchereria bancrofti
Brugia malayi
Loa-loa
Onchocerca volvulus
Mansonella spp.
BLOOD NEMATODES
Lymphatic Filaria Parasites
Wuchereria bancrofti
Brugia malayi

Lymphatic filariasis is one of the most debilitating diseases plaguing most of the
tropical countries today.
The two most common mosquito-borne causative agents of this disease are
Wuchereria bancrofti or Bancrofts filarial worm which is the causative agent of
bancroftian filariasis or filariasis bancrofti, and Brugia malayi or the Malayan
filariar worm which causes Malayan filariasis.
W. bancrofti causes chronic disfiguring disease which may present as
lymphedema, elephantiasis, or hydrocele
B. malayi causes chronic infection which presents lymphedema or elephantiasis
Tropical pulmonary eosinophilia (acute fever, inflammation of the
lymphatic system, and the bronchial-asthmatic condition
BLOOD NEMATODES
GENERAL CHARACTERISTICS AND CLASSIFICATION
1. Adult worms are thread-like, they have simple mouth
which is circular or slightly elongated dorsoventrally and is
surrounded by papillae
2. Adult worms live in the lymphatics, subcutaneous tissues,
connective tissues, muscle and body cavities of the host
3. Female adult worms are viviparous. Larvae are called
microfilaria
4. Humans are the key definitive host
5. Filarial worms are transmitted through the bite of
arthropod
Filarial nematode

Wuchereria bancrofti Sheated without caudal nuclei

Nuclei are distinct and arranged in 2-3 rows

Brugia malayi Sheated with 2 caudal nuclei

Nuclei are indistinct and confluent

Loa loa Sheated

Caudal nuclei continuous with those of the trunk

Onchocerca volvulus Unsheated

Both anterior and posterior end are nuclei free

Mansonella perstans Unsheated

Nuclei extending up to the tip of the blunt tail

Mansonella ozzardi Unsheated

Tail tapers to a thin filament containing column of 4-6 ovoid nuclei

Mansonella streptocerca Unsheated

Posterior end is strongly bent
PERIODICITY
- refers to the rhythmical appearance of microfilaria in the peripheral
blood circulation.
1. Nocturnal Periodicity during night (10PM to 2AM)
2. Diurnal Periodicity during daytime (10AM to 2PM)
3. Subperiodic day and night time
a. Subperiodic diurnal
b. Subperiodic nocturnal

* Knowledge of microfilaria periodicity is important in determining

the proper or best time for specimen collection for laboratory
identification of the parasite.
1. Loa loa
eye worm
Causes: Fugitive swelling/Calabar Swelling
MOT: bite of Chrysops Fly (Mango fly)/Tabanid Fly
Perioicity: diurnal
Diagnosis:
Identification of the adult worm
Identification of the microfilaria
2. Onchocerca volvulus
Blinding worm
Causes:Blinding filariasis or River blindness
Habitat: Subcutaneous
Diagnosis: skin snips
MOT: Bite of Simulium (Black fly)
Clinical manifestations:
Onchocercal dermatitis
Genital elephantiasis
Iridocyclitis: fibrosis and retraction of the iris, distortion of the pupils
Periodicity: Non-periodic
3.Wuchereria bancrofti
Microfilaria appears snake like
Graceful appearance
Nuclei does not reach the tail end
Nuclei regular and spaced
Vectors: Aedes, Culex, Anopheles
Periodicity: Nocturnal
PATHOLOGY:
Lymphatic Filariasis
Caused by the juvenile and adult worms.
The clinical manifestation of the condition depend on stages
of the diseases as follows:
1. ENDEMIC NORMAL
- a certain proportion of the population living in these areas do not
show any overt clinical manifestations of the disease or any mcf in
their blood even though they are exposed

2. ASYMPTOMATIC STAGE
- persons in this stage have mcf in their blood but do not show any
clinical manifestation of filariasis

3. ACUTE FILARIASIS
- caused by antigens released by female adult worms. Mcf cause no
inflammatory changes. The condition is characterized by Filarial Fever,
Lymphoedema, Lymphadenitis, adenolymphagitis.
4. CHRONIC FILARIASIS
- or obstructive phase, usually takes 10 to 15 years to develop. Types of chronic
filariasis include:
4.1. Hydrocele most common feature. Caused by the obstruction of
the lymph vessel of the spermatic cord and exudation from the inflammed testes
and Epidydimis
4.2. Elephantiasis caused by a complex immune reaction of long
duration and repeated super infection over many years. Elephantiasis of the
scrotum legs and arms in males, legs and arms in females.
4.3. Granuloma of the female breast caused by the adult worms
present in the lymphatic of the breast. Characterized by the presence of a firm
solitary mass in the breast.
4.4. Chyluria urine shows chyle mixed with blood and occasionally
with mcf. It is caused by the obstruction of lymphatic vessels of the kidney and the
abdomen
4.5. Lymph varices
5. OCCULT FILARIASIS
- denotes a condition of hypersensitivity reaction of the host to
microfilarial antigens. Mcf are not found in the peripheral
blood and the classical features of lymphatic filariasis are absent.
TROPICAL PULMONARY EOSINOPHILIA is the most
important manifestation of occult filariasis

6. LESS FREQUENT LESIONS

- include granuloma of the spleen and other organs and the
presence of adult worm in the anterior chamber of the eye
Diagnosis:
1. Blood microscopy
2. QBC
3. Urine microscopy

TREATMENT: Diethyl carbamazine citrate(DEC)

4. Brugia malayi
With secondary kinks
With 2 nuclei at the tip of the tail
Nuclei irregular and overlapping
Vector: Mansonia
Periodicity: Subperiodic
Clinical manifestations:
Tropical Pulmonary Eosinophilia
Elephantiasis
Hydrocele/Chylocele
Diagnosis:
DEC Provocation Test: stimulate the microfilaria to come out to the peripheral blood
Detection of CFA
Nucleopore filter
Knotts concentration technique
Thick smear
 Brugia malayi Wuchereria bancrofti
Common name Malayan filarial worm Bancrofts filarial worm
Disease Malayan filariasis or Brugian filariasis Bancroftian filariasis
Wucheriasis
Elephantiasis
Prevalence Less than 3% 4 to 10%
Intermediate host / Vector Swamps = Mansonia bonneae Urban type = Aedes poecilus
Rice fields = Mansonia uniformis (abaca/banana)
Rural type = Anopheles minismus
flavirostris
Specimen Blood Blood
Life span 5 years 5 years
Periodicity Nocturnal subperiodic (10 pm to 2 Nocturnal subperiodic
am)
Appearance Sheathed Sheathed
Angular curve / kinky appearance Moves in graceful manner/sweeping
curves
Anal pore 82.28% (smaller) 82.48% (bigger)
Nucleus overlapping Discrete/separate
Genital cell big Small
Excretory cell big Small
Cephalic space Twice as long as broad Long as broad
Tail end Slightly bulb with nuclei Tapering without nuclei
Habitat Upper lymphatic Lower lymphatic