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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
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
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
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